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SURGICAL RECALL6th Edition

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SURGICAL RECALL6th Edition

RECALL SERIES EDITOR AND SENIOR EDITOR

Lorne H. Blackbourne, M.D., F.A.C.S.Trauma, Burn, and Critical Care Surgeon

San Antonio,Texas

“In the operating room we can save more lives, cure more

cancer, restore more function, and relieve more suffering

than anywhere else in the hospital.”

—R. SCOTT JONES, M.D.

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Acquisitions Editor: Susan RhynerProduct Manager: Joyce MurphyMarketing Manager: Joy Fisher-WilliamsManufacturing Manager: Margie OrzechDesign Coordinator: Holly Reid McLaughlinCompositor: Aptara, Inc.

Sixth Edition

Copyright © 2012, 2009, 2006, 2002, 1998, 1994 Lippincott Williams & Wilkins, a Wolters Kluwer business.

351 West Camden Street Two Commerce Square, 2001 Market StreetBaltimore, MD 21201 Philadelphia, PA 19103

Printed in China

All rights reserved. This book is protected by copyright. No part of this book may be reproduced or trans-mitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, orutilized by any information storage and retrieval system without written permission from the copyrightowner, except for brief quotations embodied in critical articles and reviews. Materials appearing in this bookprepared by individuals as part of their official duties as U.S. government employees are not covered by theabove-mentioned copyright. To request permission, please contact Lippincott Williams & Wilkins at 530 Walnut Street, Philadelphia, PA 19106, via email at [email protected], or via website at lww.com(products and services).

9 8 7 6 5 4 3 2 1

Library of Congress Cataloging-in-Publication Data

Surgical recall / Recall series editor and senior editor, Lorne H.Blackbourne, M.D., F.A.C.S., Trauma, Burn, and Critical Care Surgeon,San Antonio, Texas. – 6th edition.

p. ; cm. – (Recall series)Includes index.Summary: “Written by students, residents, and experts in the field,

Surgical Recall faciliatates rapid review and memorization with aconcise question-and-answer format”–Provided by publisher.

ISBN 978-1-60831-421-8 (alkaline paper)1. Surgery–Examinations, questions, etc. I. Blackbourne, Lorne H.,

editor. II. Series: Recall series. [DNLM: 1. Surgical Procedures, Operative–Examination Questions. WO

18.2]RD37.2.S9748 2012617.0076–dc22

2010044314

DISCLAIMER

Care has been taken to confirm the accuracy of the information present and to describe generallyaccepted practices. However, the authors, editors, and publisher are not responsible for errors or omissionsor for any consequences from application of the information in this book and make no warranty, expressedor implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Appli-cation of this information in a particular situation remains the professional responsibility of the practitioner;the clinical treatments described and recommended may not be considered absolute and universal recom-mendations.

The authors, editors, and publisher have exerted every effort to ensure that drug selection and dosageset forth in this text are in accordance with the current recommendations and practice at the time of publi-cation. However, in view of ongoing research, changes in government regulations, and the constant flow ofinformation relating to drug therapy and drug reactions, the reader is urged to check the package insert foreach drug for any change in indications and dosage and for added warnings and precautions. This is partic-ularly important when the recommended agent is a new or infrequently employed drug.

Some drugs and medical devices presented in this publication have Food and Drug Administration (FDA)clearance for limited use in restricted research settings. It is the responsibility of the health care provider toascertain the FDA status of each drug or device planned for use in their clinical practice.

To purchase additional copies of this book, call our customer service department at (800) 638-3030 or faxorders to (301) 223-2320. International customers should call (301) 223-2300.

Visit Lippincott Williams & Wilkins on the Internet: http://www.lww.com. Lippincott Williams & Wilkinscustomer service representatives are available from 8:30 am to 6:00 pm, EST.

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mailto:[email protected]

http://www.lww.com

This book is dedicated to the memory of Leslie E. Rudolf,Professor of Surgery and Vice-Chairman of the Depart-ment of Surgery at the University of Virginia. Dr. Rudolfwas born on November 12, 1927, in New Rochelle, NewYork. He served in the U.S. Army Counter-IntelligenceCorps in Europe after World War II.

He graduated from Union College in 1951 andattended Cornell Medical College, where he graduatedin 1955. He then entered his surgical residency atPeter Brigham Hospital in Boston, Massachusetts,

and completed his residency there, serving as Chief Resident Surgeon in 1961.

Dr. Rudolf came to Charlottesville, Virginia as an Assistant Professor ofSurgery in 1963. He rapidly rose through the ranks, becoming Professor ofSurgery and Vice-Chairman of the Department in 1974 and a Markle Scholarin Academic Medicine from 1966 until 1971. His research interests includedorgan and tissue transplantation and preservation. Dr. Rudolf was instrumen-tal in initiating the Kidney Transplant Program at the University of VirginiaHealth Sciences Center. His active involvement in service to the Char-lottesville community is particularly exemplified by his early work with theCharlottesville/Albemarle Rescue Squad, and he received the Governor’s Citationfor the Commonwealth of Virginia Emergency Medical Services in 1980.

His colleagues at the University of Virginia Health Sciences Center, includ-ing faculty and residents, recognized his keen interests in teaching medicalstudents, evaluating and teaching residents, and helping the young surgicalfaculty. He took a serious interest in medical student education, and he wouldhave strongly approved of this teaching manual, affectionately known as the“Rudolf” guide, as an extension of ward rounds and textbook reading.

In addition to his distinguished academic accomplishments, Dr. Rudolf wasa talented person with many diverse scholarly pursuits and hobbies. His adviceand counsel on topics ranging from Chinese cooking to orchid raising weresought by a wide spectrum of friends and admirers.

This book is a logical extension of Dr. Rudolf’s interests in teaching. No onebook, operation, or set of rounds can begin to answer all questions of surgicaldisease processes; however, in a constellation of learning endeavors, this effortwould certainly have pleased him.

John B. Hanks, M.D.Professor of Surgery

University of VirginiaCharlottesville, Virginia

Dedication

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Editors and Contributors

vi

ADVISOR:

Curtis G. Tribble, M.D.Professor of SurgeryUniversity of MississippiJackson, Mississippi

PAST EDITORS ANDCONTRIBUTORS:

Bruce Crookes, M.D.

C. Suzanne Cutter, M.D.

Alfa O. Diallo, M.D.

Matthew Edwards, M.D.

Ara J. Fienstein, M.D.

E. William Johnson, M.D.

Peter Lopez, M.D.

Martin I. Newman, M.D.

Carl Schulman, M.D.

David Shatz, M.D.

Nicholas R. Alverez, B.S.

Jos Amortequi, M.D.

Joshua I. Bleier, M.D.

Andrew Cameron, M.D.

Diane Diesen, M.D.

Gladys L. Giron, M.D.

Lawerence V. Gulotta, M.D.

Fahim Habib, M.D.

Jennifer Hall, M.D.

David King, M.D.

Joseph Michaels V, M.D.

Rupen G. Modi, M.B.A.

Paymann Moin, B.S.

Todd M. Morgan, M.D.

Andrew Newman, B.S.

Louis Pizano, M.D.

Dimitris G. Placantonakis, M.D. PH.D.

Justin Yovino, M.D.

Esteban Ambrad-Chalela, M.D.

David Chessin, M.D.

Owen Johnson, B.S.

Peter T. Kennealy, M.D.

Geoffery Lam, M.D.

Garrett Nash, M.D.

Inderpal Sarkaria, M.D.

Alysandra Schwarz, M.D.

Ali Vafa, M.D.

Nabil Wasif, M.D.

INTERNATIONAL EDITORS:

Mohammad Azfar, M.B.B.S.,F.R.C.S.General SurgeonAbu Dhabi, United Arab Emirates

Gwinyai Masukume, M.B.CH.B.University of ZimbabweCollege of Health SciencesHarare, Zimbabwe

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Surgical Recall represents the culmination of several years’ effort by LorneBlackbourne and his friends, who began the project when they were third-yearmedical students. Lorne, who completed his residency in General Surgery atthe University of Virginia, has involved other surgical residents and medicalstudents to provide annual updates and revisions.

This reflects the interest, enthusiasm, and true dedication to learning andteaching that permeates the medical school classes and surgical residencies inour institution. It is an honor, privilege, and a continuing stimulus to work inthe midst of this group of dedicated young people. I congratulate all the stu-dents and residents involved in this project and also acknowledge the leader-ship of the surgical faculty. The professor’s ultimate satisfaction occurs whenall the learners assume ownership of learning and teaching.

This book encompasses the essential information in general surgery and sur-gical specialties usually imparted to students in our surgical clerkship andreviewed and developed further in electives. Developed from the learner’sstandpoint, the text includes fundamental information such as a description ofthe diseases, signs, symptoms, essentials of pathophysiology, treatments, andpossible outcomes. The unique format of this study guide uses the Socraticmethod by employing a list of questions or problems posed along the left side ofthe page with answers or responses on the right. In addition, the guide includesnumerous practical tips for students and junior residents to facilitate compre-hensive and effective management of patients. This material is essential forstudents in the core course of surgery and for those taking senior electives.

R. Scott Jones, M.D.University of Virginia

Charlottesville, Virginia

Foreword

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viiiviii

Surgical Recall began as a source of surgical facts during my Surgery Clerkshipwhen I was a third-year medical student at the University of Virginia. My goalhas been to provide concise information that every third-year surgical studentshould know in a “rapid fire,” two-column format.

The format of Surgical Recall is conducive to the recall of basic surgicalfacts because it relies on repetition and positive feedback. As one repeats thequestion-and-answer format, one gains success.

We have dedicated our work to the living memory of Professor LeslieRudolf. It is our hope that those who knew Dr. Rudolf will remember him andthose who did not will ask.

Lorne H. Blackbourne, M.D., F.A.C.STrauma, Burn, and Critical Care Surgeon

San Antonio, Texas

P.S. We would like to hear from you if you have any corrections, acronyms, andclassic ward or operating room questions (all contributors will be credited).You can reach me via e-mail in care of Lippincott Williams & Wilkins [email protected].

Preface

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mailto:[email protected]

ixix

Dedication . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .vEditors and Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .viForeword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .viiPreface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .viii

SECTION IOVERVIEW AND BACKGROUND SURGICALINFORMATION

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1Surgical Notes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9Common Abbreviations You Should Know . . . . . . . . . . . . . . . . . . . . .15Glossary of Surgical Terms You Should Know . . . . . . . . . . . . . . . . . . .18Surgery Signs,Triads, etc.You Should Know . . . . . . . . . . . . . . . . . . . .25

2. Surgical Syndromes . . . . . . . . . . . . . . . . . . . . . . . . . . .32

3. Surgical Most Commons . . . . . . . . . . . . . . . . . . . . . . .35

4. Surgical Percentages . . . . . . . . . . . . . . . . . . . . . . . . . . .38

5. Surgical History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .40

6. Surgical Instruments . . . . . . . . . . . . . . . . . . . . . . . . . .42

7. Sutures and Stitches . . . . . . . . . . . . . . . . . . . . . . . . . . .53

8. Surgical Knot Tying . . . . . . . . . . . . . . . . . . . . . . . . . . . .61

9. Procedures for the Surgical Ward and Clinic . . . . . . . .66

10. Incisions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .73

11. Surgical Positions . . . . . . . . . . . . . . . . . . . . . . . . . . . . .78

12. Surgical Speak . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .79

13. Preoperative 101 . . . . . . . . . . . . . . . . . . . . . . . . . . . . .80

14. Surgical Operations You Should Know . . . . . . . . . . . . .82

Contents

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15. Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .91

16. Drains and Tubes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .93

17. Surgical Anatomy Pearls . . . . . . . . . . . . . . . . . . . . . . .103

18. Fluids and Electrolytes . . . . . . . . . . . . . . . . . . . . . . . .107

19. Blood and Blood Products . . . . . . . . . . . . . . . . . . . . .124

20. Surgical Hemostasis . . . . . . . . . . . . . . . . . . . . . . . . . .128

21. Common Surgical Medications . . . . . . . . . . . . . . . . .130

22. Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .138

23. Common Causes of Ward Emergencies . . . . . . . . . .156

24. Surgical Respiratory Care . . . . . . . . . . . . . . . . . . . . .158

25. Surgical Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . .160

26. Shock . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .164

27. Surgical Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . .170

28. Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .180

29. Surgical Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . .181

30. Surgical Radiology . . . . . . . . . . . . . . . . . . . . . . . . . . .183

31. Anesthesia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .190

32. Surgical Ulcers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .195

33. Surgical Oncology . . . . . . . . . . . . . . . . . . . . . . . . . . . .197

SECTION IIGENERAL SURGERY

34. GI Hormones and Physiology . . . . . . . . . . . . . . . . . . .199

35. Acute Abdomen and Referred Pain . . . . . . . . . . . . . .203

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Contents xi

36. Hernias . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .209

37. Laparoscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .223

38. Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .226

39. Burns . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .246

40. Upper GI Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . .254

41. Stomach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .270

42. Bariatric Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . .281

43. Ostomies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .284

44. Small Intestine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .286

45. Appendix . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .293

46. Carcinoid Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . .301

47. Fistulas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .305

48. Colon and Rectum . . . . . . . . . . . . . . . . . . . . . . . . . . .308

49. Anus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .325

50. Lower GI Bleeding . . . . . . . . . . . . . . . . . . . . . . . . . . .334

51. Inflammatory Bowel Disease:Crohn’s Disease and Ulcerative Colitis . . . . . . . . . .338

52. Liver . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .345

53. Portal Hypertension . . . . . . . . . . . . . . . . . . . . . . . . . .357

54. Biliary Tract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .364

55. Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .382

56. Breast . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .399

57. Endocrine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .418

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58. Thyroid Gland . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .438

59. Parathyroid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .452

60. Spleen and Splenectomy . . . . . . . . . . . . . . . . . . . . . .458

61. Surgically Correctable HTN . . . . . . . . . . . . . . . . . . . .463

62. Soft Tissue Sarcomas and Lymphomas . . . . . . . . . . .464

63. Skin Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .469

64. Melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .471

65. Surgical Intensive Care . . . . . . . . . . . . . . . . . . . . . . . .476

66. Vascular Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . .489

SECTION IIISUBSPECIALTY SURGERY

67. Pediatric Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . .517

68. Plastic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .572

69. Hand Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .578

70. Otolaryngology: Head and Neck Surgery . . . . . . . . .586

71. Thoracic Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . .621

72. Cardiovascular Surgery . . . . . . . . . . . . . . . . . . . . . . .648

73. Transplant Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . .671

74. Orthopaedic Surgery . . . . . . . . . . . . . . . . . . . . . . . . .690

75. Neurosurgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .721

76. Urology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .743

Rapid Fire Power Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .767Figure Credits . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .775Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .776

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PREPARING FOR THE SURGERY CLERKSHIP

USING THE STUDY GUIDE

This study guide was written to accompany the surgical clerkship. It hasevolved over the years through student feedback and continued updating. Inthis regard, we welcome any feedback (both positive and negative) or sugges-tions for improvement. The objective of the guide is to provide a rapid overviewof common surgical topics. The guide is organized in a self-study/quiz format.By covering the information/answers on the right with the bookmark, you canattempt to answer the questions on the left to assess your understanding of theinformation. Keep the guide with you at all times, and when you have even afew spare minutes (e.g., between cases) hammer out a page or at least a fewquestions. Many students read this book as a primer before the clerkship evenbegins!

Your study objectives in surgery should include the following four points:1. O.R. question-and-answer periods2. Ward questioning3. Oral exam4. Written exam

The optimal plan of action would include daily reading in a text,anatomy review prior to each O.R. case, and Surgical Recall. But remem-ber, this guide helps you recall basic facts about surgical topics. Readingshould be done daily! The advanced student should read AdvancedSurgical Recall.

To facilitate learning a surgical topic, first break down each topic into thefollowing categories and, in turn, master each category:1. What is it?2. Incidence3. Risk factors

1

Section I Overview and

Background Surgical

Information

IntroductionChapter 1

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4. Signs and symptoms5. Laboratory and radiologic tests6. Diagnostic criteria7. Differential diagnoses8. Medical and surgical treatment9. Postoperative care

10. Complications11. Stages and prognosis

Granted, it is hard to read after a full day in the O.R. For a change, go tosleep right away and wake up a few hours early the next day and read beforegoing to the hospital. It sounds crazy, but it does work.

Remember—REPETITION is the key to learning for most adults.

2 Section I / Overview and Background Surgical Information

Why is your appearance soimportant?

The patient sees only the wounddressing, the skin closure, and you. Youcan wear whatever you want, but youmust look clean. Do not wearreligious or political buttons becausethis is not fair to your patients withdifferent beliefs!

APPEARANCE

WHAT THE PERFECT SURGICAL STUDENT CARRIES IN HER LAB COAT

StethoscopePenlightScissorsMinibook on medications (e.g., trade names, doses)Tape/4 � 4sSutures to practice tyingPen/notepad/small notebook to write down pearlsNotebook or clipboard with patient’s data (always write down chores with a

box next to them so you can check off the box when the chore iscompleted)

Small calculatorList of commonly used telephone numbers (e.g., radiology)(Oh, and of course, Surgical Recall!)

THE PERFECT PREPARATION FOR ROUNDS

Interview your patient (e.g., problems, pain, wishes)Talk with your patient’s nurse (e.g., “Were there any events during the last

shift?”)Examine patient (e.g., cor/pulm/abd/wound)


Chapter 1 / Introduction 3

Record vital signs (e.g., Tmax)Record input (e.g., IVF, PO)Record output (e.g., urine, drains)Check labsCheck microbiology (e.g., culture reports, Gram stains)Check x-raysCheck pathology reports.Know the patient’s allergiesCheck allied health updates (e.g., PT, OT)Read chartCheck medication (don’t forget H2 blocker in hyperalimentation)Check nutritionAlways check with the intern for chores, updates, or insider information

before rounds

PRESENTING ON ROUNDS

Your presentation on rounds should be like an iceberg. State important pointsabout your patient (the tip of the iceberg visible above the ocean), but knoweverything else about your patient that your chief might ask about (that partof the iceberg under the ocean). Always include:

NamePostoperative day s/p-procedureConcise overall assessment of how the patient is doingVital signs/temp status/antibiotics dayInput/output-urine, drains, PO intake, IVFChange in physical examinationAny complaints (not yours—the patient’s)PlanYour presentation should be concise, with good eye contact (you should not

simply read from a clipboard). The intangible element of confidence cannotbe overemphasized; if you do not know the answer to a question about apatient, however, the correct response should be “I do not know, but I will findout.” Never lie or hedge on an answer because it will only serve to make theremainder of your surgical rotation less than desirable. Furthermore, do yourbest to be enthusiastic and motivated. Never, ever whine. And remember tobe a team player. Never make your fellow students look bad! Residents pickup on this immediately and will slam you.

THE PERFECT SURGERY STUDENT

Never whinesNever pimps his residents or fellow students (or attendings)Never complainsIs never hungry, thirsty, or tired



Is always enthusiasticLoves to do scut work and can never get enoughNever makes a fellow student look badIs always clean (a patient sees only you and the wound dressing)Is never lateSmiles a lot and has a good sense of humorMakes things happenIs not a “know-it-all”Never corrects anyone during rounds unless it will affect patient careMakes the intern/resident/chief look good at all times, if at all possibleKnows more about her patients than anyone elseLoves the O.R.Never wants to leave the hospitalTakes correction, direction, and instruction very wellSays “Sir” and “Ma’am” to the scrub nurses (and to the attending, unless

corrected)Never asks questions he can look up for himselfKnows the patient’s disease, surgery, indication for surgery, and the anatomy

before going to the O.R.Is the first one to arrive at clinic and the last one to leaveAlways places x-rays up in the O.R.Reads from a surgery text every dayIs a team playerAsks for feedbackNever has a chip on her shoulderLoves to sutureIs honest and always admits fault and errorsKnows when his patient is going to the O.R. (e.g., by calling)Is confident but not cockyHas a “Can-Do” attitude and can figure out things on her ownIs not afraid to get help when neededNever says “No” or “Maybe” to involvement in patient careTreats everyone (e.g., nurses, fellow students) with respectAlways respects patients’ modesty (e.g., covers groin with a sheet as soon as

possible in the trauma bay)Follows the chain of commandPraises others when appropriateChecks with the intern beforehand for information for rounds (test results/

surprises)RUNS for materials, lab values, test results, etc., during rounds before any

house officerGives credit where credit is dueDresses and undresses wounds on roundsHas a steel bladder, a cast-iron stomach, and a heart of gold



Always writes the OP note without questionAlways checks with the intern after rounds for choresAlways makes sure there is a medical student in every caseAlways follows the patient to the recovery roomIn the O.R., always asks permission to ask a questionAlways reviews anatomy prior to going to the O.R.Does what the intern asks (i.e., the chief will get feedback from the

intern)Is a high-speed, low-drag, hardcore HAMMERHEAD

Define HAMMERHEAD. A hammerhead is an individual who placeshis head to the ground and hammersthrough any and all obstacles to get a jobdone and then asks for more work. Onewho gives 110% and never complains.One who desires work.

OPERATING ROOM

Your job in the O.R. will be to retract (water-skiing) and answer questions posedby the attending physicians and residents. Retracting is basically idiot-proof.Many students emphasize anticipating the surgeon’s next move, but stick tofollowing the surgeon’s request. More than 75% of the questions asked in theO.R. deal with anatomy; therefore, read about the anatomy and pathophysiologyof the case, which will reduce the “I don’t knows.”

Never argue with the scrub nurses—they are always right. They are theselfless warriors of the operating suite’s sterile field, and arguing with one willonly make matters worse.

Never touch or take instruments from the Mayo tray (tray with instru-ments on it over the patient’s feet) unless given explicit permission to do so.Each day as you approach the O.R. suite door, STOP and ask yourself if youhave on scrubs, shoe covers, a cap, and a mask to avoid the embarrassing situationof being yelled at by the O.R. staff (a.k.a. the 3 strikes test: strike 1 � no mask,strike 2 � no headcover, strike 3 � no shoe covers . . . any strikes and you areoutta here—place a mental stop sign outside of the O.R. with the 3 strikes ruleon it)! Always wear eye protection. When entering the O.R., first introduceyourself to the scrub nurse and ask if you can get your gloves or gown. If youhave questions in the O.R., first ask if you can ask a question because it maybe a bad time and this way it will not appear as though you are pimping theresident/attending.

Other thoughts on the O.R.:If you feel faint, ask if you can sit down (try to eat prior to going to the

O.R.). If your feet swell in the O.R., try wearing support hose socks. If yourback hurts, try taking some ibuprofen (with a meal) prior to the case. Also, sit-ups or abdominal crunches help to relieve back pain by strengthening theabdominal muscles. At the end of the case, ask the scrub nurse for some


What if I have to sneeze?

What if I feel faint?

What should I say when Ifirst enter the O.R.?

Should I wear my ID taginto the O.R.?

Can I wear nail polish?

Can I wear my rings and mywatch when scrubbed in theO.R.?

Can I wear earrings?

When scrubbed, is my backsterile?

When in the surgical gown,are my underarms sterile?

How far down my gown isconsidered part of the sterile field?

How far up my gown is considered sterile?


Back up STRAIGHT back; do not turnyour head, as the sneeze exits throughthe sides of your mask!

Do not be a hero—say, “I feel faint. MayI sit down?” This is no big deal and isvery common (Note: It helps to alwayseat before going to the O.R.)

Introduce yourself as a student; state thatyou have been invited to scrub and ask ifyou need to get out your gloves and/orgown

Yes

Yes, as long as it is not chipped

No

No

No

No; do not put your hands under yourarms

Just to your waist

Up to the nipples

OPERATING ROOM FAQS

leftover ties (clean ones) to practice tying knots with and, if there is time, startwriting your OP note.


How do I stand if I am waiting for the case to start?

Hands together in front above your waist


Can I button up a surgicalgown (when I am notscrubbed!) with bare hands?

How many pairs of glovesshould I wear whenscrubbed?

What is the normal order ofsizes of gloves: small pair,then larger pair?

What is a “scrub nurse” versus a “circulating nurse”?

What items comprise thesterile field in the operatingroom?

Yes (Remember: the back of the gown isNOT sterile)

2 (2 layers)

No; usually the order is a larger size followed by a smaller size (e.g., mencommonly wear a size #8 covered by asize #7.5; women commonly wear a size#7 covered by a size #6.5)

The scrub nurse is “scrubbed” and handsthe surgeon sutures, instruments,and so forth; this person is often anOperating Room Technician (a.k.a.“Scrub Tech”)

The circulating nurse “circulates” andgets everything needed before andduring the procedure

The instrument table, the Mayo tray, andthe anterior drapes on the patient


What is the tray with theinstruments called?


Mayo tray

Can I grab things off theMayo tray?

How do you remove bloodwith a laparotomy pad (“lap pad”)?

Can you grab the skin withDeBakey pickups?

How should you cut thesutures after tying a knot?

No; ask the scrub nurse/tech for permission

Dab; do not wipe, because wipingremoves platelet plugs

NO; pickups for the skin must have teeth(e.g., Adson, rat-tooth) because it is “better to cut the skin than crush it”

1. Rest the cutting hand on the noncutting hand

2. Slip the scissors down to the knot andthen cant the scissors at a 45-degreeangle so you do not cut the knot itself

45°


What are the two wordsmost commonly misspelledin a surgical history note?

1. Guaiac2. Abscess


Favorite Trick Questions

What should you do whenyou are scrubbed and someone is tying a suture?

Why always wipe the Betadine® (povidone-iodine)off your patient at the endof the procedure?

Ask the scrub nurse for a pair of suturescissors, so you are ready if you are askedto cut the sutures

Betadine® can become very irritating anditchy

SURGICAL NOTES

HISTORY AND PHYSICAL REPORT

The history and physical examination report, better known as the H & P, can makethe difference between life and death. You should take this responsibility veryseriously. Fatal errors can be made in the H & P, including the incorrect diagno-sis, the wrong side, the wrong medications, the wrong allergies, and the wrong pastsurgical history. Operative reports of the patient’s past surgical procedures areinvaluable! The surgical H & P needs to be both accurate and concise. To savespace, use � for a negative sign/symptom and � for a positive sign/symptom.

What is the most commonintra-operative bladder“tumor”?

Describe a stool with melena.

Is amylase part of Ranson’scriteria?

Can a patient in shock have“STABLE” vital signs?

What is the most commonlypimped, yet the rarest,cause of pancreatitis?

Where can you go to obtainan abdominal CT scan on a600-pound, morbidly obesepatient?

Foley catheter

Melenic—not melanotic

Amylase is NOT part of Ranson’s criteria!

Yes—stable vital signs are any vital signsthat are not changing! Always say“normal” vital signs, not “stable!”

Pancreatitis from a scorpion bite(scorpion found on island of Trinidad)

The ZOO (used in the past, but now raredue to liability)



Example H & P (very brief—for illustrative purposes only—see belowor next section for abbreviation key):

Mr. Smith is a 22-year-old African American man who was in his normal state ofexcellent health until he noted the onset of periumbilical pain 1 day prior toadmission. This pain was followed �4 hours later by pain in his right lower quad-rant that any movement exacerbated. � vomiting, anorexia. � fever, urinary tractsymptoms, change in bowel habits, constipation, BRBPR, hematemesis, ordiarrhea.Medications: ibuprofen prn headachesAllergies: NKDAPMH: nonePSH: noneSH: EtOH, tobaccoFH: �CAROS: �resp disease, �cardiac disease,

�renal diseasePhysical Exam: V/S 120/80 85 12 T 37� C

HEENT ncat, tms clearcor nsr, �m, r, gpulm clear b/labd nondistended, �bs, �tender RLQ,

�rebound RLQrectal guaiac �nl tone, �massext nt, �c, c, eneuro wnl

LABS: urinalysis (ua) normal, chem 7, PT/PTT,CBC pending

X-RAYS: noneASSESSMENT: 22 y.o. m with Hx and physical findings of

right lower quadrant peritoneal signsconsistent with (c/w) appendicitis

Plan: NPOConsentIVF with Lactated Ringer’sIV cefoxitinTo O.R. for appendectomy

Wilson Tyler cc III/

NKDA � no known drug allergies; PMH � past medical history; PSH � past sur-gical history; SH � social history; FH � family history; ROS � review of systems;V/S � vital signs; ncat � normocephalic atraumatic; tms � tympanic membranes;cor � heart; m, r, g � murmur, rub, gallop; NSR � normal sinus rhythm; b/l �bilateral; bs � bowel sounds; ext � extremity; nt � nontender; c, c, e � cyanosis,clubbing, or erythema; wnl � within normal limits; cc III � clinical clerk, thirdyear



PREOP NOTE

The preop note is written in the progress notes the day before the operationExample:

Preop Dx: colon CALabs: CBC, chem 7, PT/PTTCXR: �infiltrateBlood: T & C � 2 unitsEKG: NSR, wnlAnesthesia: preop completedConsent: signed and on front of chartOrders: 1. Void OCTOR

2. 1 gm cefoxitin OCTOR3. Hibiclens scrub this p.m.4. Bowel prep today5. NPO p- MN

NPO � nothing by mouth; OCTOR � on call to O.R.; p-� after; MN � midnight

OP NOTE

The OP note is written in the progress note section of the chart in the O.R.before the patient is in the PACU (or recovery room).Example:

Preop Dx: acute appendicitisPostop Dx: sameProcedure: appendectomySurgeon: HalstedAssistants: Cushing, TribbleOP findings: no perforationAnesthesia: GET*I/O: 1000 mL LR/uo 600 mL*EBL: 50 mLSpecimen: appendix to pathologyDrains: noneComplications: none (Note: If there are complications,

ask what you should write.)

To PACU in stable condition

GET � general endotracheal; I/O � ins and outs; uo � urine output; EBL �estimated blood loss; PACU � postanesthesia care unit*Ask the anesthesiologist or Certified Registered Nurse Anesthetist (CRNA)for this information.



How do I remember what isin the OP note when I am inthe O.R.?

Remember the acronym “PPP SAFEDISC”:

Preop DxPostop DxProcedure

Surgeon (and assistants)AnesthesiaFluidsEstimated blood loss (EBL)

DrainsIV FluidsSpecimenComplications

POSTOP NOTE

The postop note is written on the day of the operation in the progress notesExample:

Procedure: appendectomyNeuro: A&O � 3V/S: wnl/afebrileI/O: 1 L LR/uo 600 mLLabs: postop Hct: 36PE: cor RRR

pulm CTA abd drsg dry and intact

Drains: JP 30 mL serosanguinous fluidAssess: stable postopPlan: 1. IV hydration

2. 1 g cefoxitin q 8 hr

A&O � 3 � alert and oriented times 3; V/S � vital signs; uo � urine output; Hct � hematocrit; RRR � regular rhythm and rate; JP � Jackson-Pratt; wnl �within normal limits

ADMISSION ORDERS

The admission orders are written in the physician orders section of the patient’schart on admission, transfer, or postopExample:

Admit to 5E Dr. DeBakeyDx: AAACondition: stableV/S: q 4 hr or q shift; if postop, q 15 min � 2 hr,

then q 1 hr � 4, then q 4 hrAllergies: NKDA



Activity: bedrest or OOB to chairNursing: daily wgt; I/O; change drsg q shiftCall HO for: temp �38.5

UO �30 mL/hrSBP �180 �90DBP �100HR �60 �110

Diet: NPOIVF: D5 1/2 NS c- 20 KCLDrugs: ANCEFLabs: CBC

OOB � out of bed; I/O � ins and outs; HO � House Officer; SBP � systolicblood pressure; DBP � diastolic blood pressure; HR � heart rate; KCL �potassium chloride

ADMISSION ORDERS/POSTOP ORDERS

“AC/DC AVA PAIN DUD”:Admit to 5ECare ProviderDiagnosisCondition

AllergiesVitalsActivity

Pain medsAntibioticsIVF/Incentive SpirometryNursing (Drains, etc.)

DVT prophylaxisUlcer prophylaxisDiet

DAILY NOTE—PROGRESS NOTE

Basically a SOAP note, but it is not necessary to write out SOAP; for many rea-sons, make your notes very OBJECTIVE and, as a student, do not mentiondischarge because this leads to confusionExample:

10/1/90 Blue SurgeryPOD #4 s/p appendectomyDay #5 cefoxitinPt without c/o



V/S: 120/80 76 12 afebrile (Tmax 38)I/O: 1000/600Drains: JP #1 60 last shiftPE: cor RRR—no m, g, r

pulm CTAabd �BS, �flatus, �rigidityext nt, �cyanosis, �erythema

ASSESS: Stable POD #4 on IV antibioticsPLAN:

1. Increase PO intake2. Increase ambulation3. Follow cultures

Grayson Stuart, cc III/Important: Always date, time, and sign your notes and leave space for them to

be cosigned!

POD � Postop day (Note: The day after operation is POD #1. The day ofoperation is the operative day. But: Antibiotic day #1 is the day the antibioticswere started.); c/o � complains of; nt � nontender; cc III � clinical clerk,third year

The following is an acronym for what should be checked on your patient dailybefore rounding with the surgical team: “AVOID WTE”:

Appearance—any subjective complaintsVital signsOutput—urine/drainsIntake—IV/PODrains—# of/output/character

Wound/dressing/weightTemperatureExam—cor, pulm, abd, etc.

INTENSIVE CARE NOTE

This note is by systems:

Neurologic (GCS, MAE)Pulmonary (vent settings, etc.)CVS (pressors, swann numbers, etc.)Heme (CBC)FEN (Chem 10, nutrition, etc.)Renal (urine output, BUN, Cr, etc.)I & D (Tmax, WBC, antibiotics, etc.)AssessmentPlan



BeforeAbdominal aortic aneurysm; “triple A”Army battle dressingArterial blood gasAnkle to brachial indexAbove the knee amputationAlso known asAortaAbdominoperineal resectionAcute respiratory distress syndromeAspirinAbdominal x-rayBillroth 1 gastroduodenostomyBillroth 2 gastrojejunostomyBirth control pillBarium enemaBilateral inguinal herniaBelow the knee amputationBright red blood per rectumBowel sounds; Breath sounds; Blood sugarBreast self-examinationWithCancerCoronary artery bypass graft (“CABBAGE”)Complete blood cell count

aAAAABDABGABIAKAa.k.a.AoAPRARDSASAAXRB1B2BCPBEBIHBKABRBPRBSBSEcCACABGCBC

CVS � current vital signs; FEN � fluids, electrolytes, nutrition; BUN � bloodurea nitrogen; Cr � creatinine; I & D � incision and drainage (Note: PE, labs,radiology studies, etc. are included in each section. This is also an excellent way towrite progress notes for the very complicated floor patient.)

CLINIC NOTE

Often the clinic note is a letter to the referring doctor. It should always include:1. Patient name, history #, date2. Brief Hx, current complaints/symptoms3. PE, labs, x-rays4. Assessment5. Plan

How is a medicationprescription written?

Tylenol® 500 mg tabletDisp (dispense): 100 tabletssig: 1–2 PO q 4 hrs PRN pain

COMMON ABBREVIATIONS YOU SHOULD KNOW

(Check with your hospital for approved abbreviations!)



Common bile ductComplains ofChronic obstructive pulmonary diseaseChest painClear to auscultation; CT angiogramCerebral vascular accidentCostovertebral angle tendernessCentral venous pressureChest x-rayDiagnosisDifferential diagnosisDiabetes insipidusDorsalis pedalisDiagnostic peritoneal lavageDelayed primary closureDelirium tremensDeep venous thrombosisEstimated blood lossExtracorporeal membrane oxygenationEsophagogastroduodenoscopy (UGI scope)Electrocardiogram (also ECG)Exploratory laparotomyExtraocular muscles intactEndoscopic retrograde cholangiopancreatographyAlcoholExam under anesthesiaExploratory laparotomyFamilial adenomatous polyposisFocused abdominal sonogram for traumaFluids, electrolytes, nutritionFine needle aspirationFecal occult blood testGlasgow Coma ScaleGastroesophageal reflux diseaseGeneral endotracheal (anesthesia)GenitourinaryHematocritHead, eyes, ears, nose, and throatHouse officerHistoryIntra-aortic balloon pumpInflammatory bowel diseaseIntensive care unitIncision and drainageIns and outs, in and outIntermittent mandatory ventilation

CBDc/oCOPDCPCTACVACVATCVPCXRDxDDxDIDPDPLDPCDTDVTEBLECMOEGDEKGELAPEOMIERCPEtOHEUAEX LAPFAPFASTFENFNAFOBTGCSGERDGET(A)GUHCTHEENTHOHxIABPIBDICUI & DI & OIMV



Inferior vena cavaIntravenous fluidsIntravenous pyelographyIntravenous piggybackJugular venous distentionLeftLower extremityLower esophageal sphincterLeft inguinal herniaLeft lower quadrantLactated Ringer’sLeft upper quadrantMoving all extremitiesMilitary antishock trousersMultiple endocrine neoplasiaMyocardial infarctionMorphine sulfateNasogastric tubeNothing per osNormal salineOrtho bowel routineOn call to O.R.Out of bedOpen reduction internal fixationAfterPulmonary capillary wedge pressurePulmonary embolism; Physical examinationPositive end-expiratory pressurePercutaneous endoscopic gastrostomy (via EGD and skin

incision)Pupils equal and react to lightPulmonary function testsPeripherally inserted central catheterProximal gastric vagotomy (i.e., leaves fibers to pylorus intact

to preserve emptying)Pelvic inflammatory diseasePer os (by mouth)Postoperative dayPer rectumAs needed, literally, pro re nataPhysical therapy; Patient; Posterior tibial; Prothrombin timePercutaneous transhepatic cholangiogram (dye injected via a

catheter through skin and into dilated intrahepatic bile duct)Percutaneous transluminal coronary angioplastypneumothorax

IVCIVFIVPIVPBJVDLLELESLIHLLQLRLUQMAEMASTMENMIMSO4NGTNPONSOBROCTOROOBORIFpPCWPPEPEEPPEG

PERRLPFTPICCPGV

PIDPOPODPRPRNPTPTC

PTCAPTX


Abscess Localized collection of pus anywhere inthe body, surrounded and walled off bydamaged and inflamed tissues


EveryRightRight inguinal herniaRight lower quadrantTreatmentReturn to clinicWithoutSmall bowel obstructionSequential compression deviceSyndrome of inappropriate antidiuretic hormoneSurgical intensive care unitSubjective, objective, assessment, and planStatus postSplit thickness skin graftSuperior vena cavaSymptomsTransesophageal echocardiographyType and crossType and screenMaximal temperatureTotal parenteral nutritionTransurethral resection of the prostateUpper extremityUpper gastrointestinalUrine outputUltrasoundUrinary tract infectionVentricular assist deviceVoid on call to O.R.Wet-to-dry dressingX-ray therapyNo; negativeYes; positiveIncrease; moreDecrease; lessLess thanGreater thanApproximately

q or qRRIHRLQRxRTCsSBOSCDSIADHSICUSOAPS/PSTSGSVCSxTEET & CT & STmax

TPNTURPUEUGIUOU/SUTIVADVOCTORWSDXRT��cT��

GLOSSARY OF SURGICAL TERMS YOU SHOULD KNOW



Achlorhydria

Acholic stool

Adeno-

Adhesion

Adnexa

Adventitia

Afferent

-algia

Amaurosis fugax

Ampulla

Analgesic

Anastomosis

Angio-

Anomaly

Apnea

Atelectasis

Bariatric

Bifurcation

Absence of hydrochloric acid in the stomach

Light-colored stool as a result ofdecreased bile content

Prefix denoting gland or glands

Union of two normally separate surfaces

Adjoining parts; usually means ovary/fallopian tube

Outer coat of the wall of a vein or artery(composed of loose connective tissue)

Toward

Suffix denoting pain

Transient visual loss in one eye

Enlarged or dilated ending of a tube orcanal

Drug that prevents pain

Connection between two tubular organsor parts

Prefix denoting blood or lymph vessels

Any deviation from the normal (i.e., con-genital or developmental defect)

Cessation of breathing

Collapse of alveoli

Weight reduction; bariatric surgery isperformed on morbidly obese patients toeffect weight loss

Point at which division into two branchesoccurs


Bile salts

Bili-

Boil

Bovie

Calculus

Carbuncle

Cauterization

Celiotomy

Cephal-

Chole-

Cholecyst-

Choledocho-

Cleido-

Colic

Colloid

Colonoscopy

Colostomy

Constipation


Alkaline salts of bile necessary for theemulsification of fats

Prefix denoting bile

Tender inflamed area of the skin containing pus

Electrocautery

Stone

Collection of boils (furuncles) with multiple drainage channels (CARbuncle � car � big)

Destruction of tissue by directapplication of heat

Surgical incision into the peritoneal cavity(laparotomy � celiotomy)

Prefix denoting the head

Prefix denoting bile

Prefix denoting gallbladder

Prefix denoting the common bile duct

Prefix denoting the clavicle

Intermittent abdominal pain usually indicating pathology in a tubular organ(e.g., small bowel)

Fluid with large particles (e.g., albumin)

Endoscopic examination of the colon

Surgical operation in which part of thecolon is brought through the abdominalwall

Infrequent or difficult passage of stool


Cor pulmonale

Curettage

Cyst

Direct bilirubin

-dynia

Dys-

Dyspareunia

Dysphagia

Ecchymosis

-ectomy

Efferent

Endarterectomy

Enteritis

Enterolysis

Eschar

Enlargement of the right ventricle causedby lung disease and resultant pulmonaryhypertension

Scraping of the internal surface of anorgan or body cavity by means of aspoon-shaped instrument

Abnormal sac or closed cavity lined with epithelium and filled with fluid orsemisolid material

Conjugated bilirubin (indirect �unconjugated)

Suffix denoting pain

Prefix: difficult/painful/abnormal

Painful sexual intercourse

Difficulty in swallowing

Bruise

Suffix denoting the surgical removal of apart or all of an organ (e.g., gastrectomy)

Away from

Surgical removal of an atheroma and theinner part of the vessel wall to relieve anobstruction (carotid endarterectomy �CEA)

Inflammation of the small intestine, usually causing diarrhea

Lysis of peritoneal adhesions; not to beconfused with enteroclysis, which is acontrast study of the small bowel

Scab produced by the action of heat or acorrosive substance on the skin



Excisional biopsy

Fascia

Fistula

Foley

Frequency

Furuncle

Gastropexy

Hemangioma

Hematemesis

Hematoma

Hemoptysis

Hemothorax

Hepato-

Herniorrhaphy

Hesitancy

Hiatus

Hidradenitis

Icterus


Biopsy with removal of entire tumor(Think: Excisional � Entire removal)

Sheet of strong connective tissue

Abnormal communication between twohollow, epithelialized organs or betweena hollow organ and the exterior (skin)

Bladder catheter

Abnormally increased frequency (e.g.,urinary frequency)

Boil, small subcutaneous staphylococcalinfection of follicle (Think: Furuncle �follicle � car � carbuncle)

Surgical attachment of the stomach tothe abdominal wall

Benign tumor of blood vessels

Vomiting of blood

Accumulation of blood within the tissues,which clots to form a solid swelling

Coughing up blood

Blood in the pleural cavity

Prefix denoting the liver

Surgical repair of a hernia

Difficulty in initiating urination

Opening or aperture

Inflammation of the apocrine glands,usually caused by blockage of the glands

Jaundice


Ileostomy

Ileus

Incisional biopsy

Induration

Inspissated

Intussusception

-itis

Lap appy

Laparoscopy

Laparotomy

Lap chole

Leiomyoma

Leiomyosarcoma

Lieno-

Melena

Necrotic

Obstipation

Odynophagia

-orraphy

Surgical connection between the lumenof the ileum and the skin of the abdominal wall

Abnormal intestinal motility (usually paralytic)

Biopsy with only a “slice” of tumorremoved

Abnormal hardening of a tissue or organ

Hard

Telescoping of one part of the bowel intoanother

Suffix denoting inflammation of an organ,tissue, etc. (e.g., gastritis)

Appendectomy via laparoscopy

Visualization of the peritoneal cavity via alaparoscope

Surgical incision into the abdominal cavity(laparotomy � celiotomy)

Cholecystectomy via laparoscopy

Benign tumor of smooth muscle

Malignant tumor of smooth muscle

Denoting the spleen

Black tarry stool (melenic, not melanoticstools)

Dead

Failure to pass flatus or stool

Painful swallowing

Surgical repair (e.g., herniorrhaphy)



-ostomy

-otomy

Percutaneous

-pexy

Phleb-

Phlebolith

Phlegmon

Plica

Plicae circulares

Plicae semilunares

Pneumaturia

Pneumothorax

Pseudocyst

Pus


General term referring to any operationin which an artificial opening is createdbetween two hollow organs or betweenone viscera and the abdominal wall fordrainage purposes (e.g., colostomy) or forfeeding (e.g., gastrostomy)

Suffix denoting surgical incision into anorgan

Performed through the skin

Suffix denoting fixation

Prefix denoting vein or relating to veins

Calcification in a vein—a vein stone

Diffuse inflammation of soft tissue,resulting in a swollen mass of tissue(most commonly seen with pancreatic tissue)

Fold or ridge

Circular (complete circles) folds in thelumen of the small intestine (a.k.a. valvulae conniventes)

Folds (semicircular) into lumen of thelarge intestine

Passage of urine containing air

Collapse of lung with air in pleural space

Fluid-filled cavity resembling a true cyst,but not lined with epithelium

Liquid product of inflammation, consisting of dying leukocytes and other fluids from the inflammatoryresponse


Rubor

Steatorrhea

Stenosis

Sterile field

Succus

Tenesmus

Thoracotomy

Transect

Trendelenburg

Urgency

Wet-to-dry dressing

Redness; a classic sign of inflammation

Fatty stools as a result of decreased fatabsorption

Abnormal narrowing of a passage oropening

Area covered by sterile drapes or preppedin sterile fashion using antiseptics (e.g.,Betadine®)

Fluid (e.g., succus entericus is fluid fromthe bowel lumen)

Urge to defecate with ineffectual straining

Surgical opening of the chest cavity

To divide transversely (to cut in half)

Patient posture with pelvis higher thanthe head, inclined about 45� (a.k.a.“headdownenburg”)

Sudden strong urge to urinate; often seenwith a UTI

Damp gauze dressing placed on a wound and removed after the dressingdries to the wound, providingmicrodébridement


What are the ABCDs ofmelanoma?

Signs of melanoma:AsymmetricBorder irregularitiesColor variationDiameter �0.6 cm and Dark color

SURGERY SIGNS,TRIADS, ETC. YOU SHOULD KNOW



Ulnarartery

Radialartery

Define the following terms: Ballance’s sign

Barrett’s esophagus

Battle’s sign

Constant dullness to percussion in theleft flank/LUQ and resonance topercussion in the right flank seen withsplenic rupture/hematoma

Columnar metaplasia of the distal esophagus (GERD related)

Ecchymosis over the mastoid process inpatients with basilar skull fractures

Battle’ssign

What is the Allen’s test? Test for patency of ulnar artery prior toplacing a radial arterial line or perform-ing an ABG: Examiner occludes bothulnar and radial arteries with fingersas patient makes fist; patient opensfist while examiner releases ulnarartery occlusion to assess blood flowto hand



Beck’s triad

Bergman’s triad

Blumer’s shelf

Boas’ sign

Borchardt’s triad

Carcinoid triad

Charcot’s triad

Chvostek’s sign

Courvoisier’s law

Seen in patients with cardiac tamponade:1. JVD2. Decreased or muffled heart sounds3. Decreased blood pressure

Seen with fat emboli syndrome:1. Mental status changes2. Petechiae (often in the axilla/thorax)3. Dyspnea

Metastatic disease to the rectouterine(pouch of Douglas) or rectovesical pouchcreating a “shelf” that is palpable on rectal examination

Right subscapular pain resulting fromcholelithiasis

Seen with gastric volvulus: 1. Emesis followed by retching2. Epigastric distention3. Failure to pass an NGT

Seen with carcinoid syndrome (Think:“FDR”):

1. Flushing2. Diarrhea3. Right-sided heart failure

Seen with cholangitis:1. Fever (chills)2. Jaundice3. Right upper quadrant pain

(Pronounced “char-cohs”)

Twitching of facial muscles upon tapping thefacial nerve in patients with hypocalcemia(Think: CHvostek’s � CHeek)

Enlarged nontender gallbladder seen withobstruction of the common bile duct,most commonly with pancreatic cancerNote: not seen with gallstone obstructionbecause the gallbladder is scarred secondary to chronic cholelithiasis (Pronounced “koor-vwah-ze-ay”)


Cullen’s sign


Bluish discoloration of the periumbilicalarea due to retroperitoneal hemorrhagetracking around to the anterior abdominalwall through fascial planes (e.g., acutehemorrhagic pancreatitis)

Umbilicus

Cushing’s triad

Dance’s sign

Fothergill’s sign

Fox’s sign

Goodsall’s rule

Signs of increased intracranial pressure:1. Hypertension2. Bradycardia3. Irregular respirations

Empty right lower quadrant in childrenwith ileocecal intussusception

Used to differentiate an intra-abdominalmass from one in the abdominal wall; ifmass is felt while there is tension on themusculature, then it is in the wall (i.e.,sitting halfway upright)

Ecchymosis of inguinal ligament seenwith retroperitoneal bleeding

Anal fistulae course in a straight pathanteriorly and a curved path posteriorlyfrom midline (Think of a dog with astraight anterior nose and a curved posterior tail)


Grey Turner’s sign

Hamman’s sign/crunch

Homans’ sign

Howship-Romberg sign

Kehr’s sign

Kelly’s sign

Krukenberg tumor

Laplace’s law

Ecchymosis or discoloration of the flankin patients with retroperitonealhemorrhage as a result of dissectingblood from the retroperitoneum (Think:TURNer’s � TURN side-to-side � flank)

Crunching sound on auscultation of theheart resulting from emphysematousmediastinum; seen with Boerhaave’s syndrome, pneumomediastinum, etc.

Calf pain on forced dorsiflexion of thefoot in patients with DVT

Pain along the inner aspect of the thigh;seen with an obturator hernia as theresult of nerve compression

Severe left shoulder pain in patientswith splenic rupture (as a result ofreferred pain from diaphragmatic irritation)

Visible peristalsis of the ureter inresponse to squeezing or retraction; used to identify the ureter during surgery

Metastatic tumor to the ovary (classicallyfrom gastric cancer)

Wall tension � pressure � radius (thus,the colon perforates preferentially at thececum because of the increased radiusand resultant increased wall tension)


Anterior

Goodsall

Posterior


McBurney’s point

McBurney’s sign

Meckel’s diverticulumrule of 2s

Mittelschmerz

Murphy’s sign

Obturator sign


One third the distance from the anterioriliac spine to the umbilicus on a line connecting the two

Tenderness at McBurney’s point inpatients with appendicitis

2% of the population have a Meckel’sdiverticulum, 2% of those are symptomatic,and they occur within �2 feet of the ileocecal valve

Lower quadrant pain due to ovulation

Cessation of inspiration while palpatingunder the right costal margin; thepatient cannot continue to inspiredeeply because it brings an inflamedgallbladder under pressure (seen inacute cholecystitis)

Pain upon internal rotation of the legwith the hip and knee flexed; seen inpatients with appendicitis/pelvic abscess

PheochromocytomaSYMPTOMS triad

Pheochromocytoma ruleof 10s

Think of the first three letters in theword pheochromocytoma—“P-H-E”:

PalpitationsHeadacheEpisodic diaphoresis

10% bilateral, 10% malignant, 10% inchildren, 10% extra-adrenal, 10% havemultiple tumors


Raccoon eyes Bilateral black eyes as a result of basilarskull fracture

Reynold’s pentad

Rovsing’s sign

Saint’s triad

Silk glove sign

1. Fever2. Jaundice3. Right upper quadrant pain4. Mental status changes5. Shock/sepsisThus, Charcot’s triad plus #4 and #5; seen

in patients with suppurative cholangitis

Palpation of the left lower quadrantresulting in pain in the right lower quadrant; seen in appendicitis

1. Cholelithiasis2. Hiatal hernia3. Diverticular disease

Indirect hernia sac in the pediatricpatient; the sac feels like a finger of a silkglove when rolled under the examiningfinger


Psoas sign Pain elicited by extending the hip withthe knee in full extension, seen withappendicitis and psoas inflammation


Sister Mary Joseph’s sign(a.k.a. Sister MaryJoseph’s node)

Virchow’s node

Virchow’s triad

Trousseau’s sign

Valentino’s sign

Westermark’s sign

Whipple’s triad


Metastatic tumor to umbilical lymphnode(s)

Metastatic tumor to left supraclavicularnode (classically due to gastric cancer)

Risk factors for thrombosis:1. Stasis2. Abnormal endothelium3. Hypercoagulability

Carpal spasm after occlusion of blood tothe forearm with a BP cuff in patientswith hypocalcemia

Right lower quadrant pain from a perforated peptic ulcer due to succus/pus draining into the RLQ

Decreased pulmonary vascular markings onCXR in a patient with pulmonary embolus

Evidence for insulinoma:1. Hypoglycemia (�50)2. CNS and vasomotor symptoms

(e.g., syncope, diaphoresis)3. Relief of symptoms with

administration of glucose

What is afferent loopsyndrome?

What does ARDS stand for?

SurgicalSyndromes

Chapter 2

Obstruction of the afferent loop of a Billroth II gastrojejunostomy

Acute Respiratory Distress Syndrome(poor oxygenation caused by leaky capillaries)


What is blind loop syndrome?

What is Boerhaave’ssyndrome?

What is Budd-Chiarisyndrome?

What is carcinoid syndrome?

What is compartmentsyndrome?

What is Cushing’s syndrome?

What is dumping syndrome?

What is Fitz-Hugh-Curtissyndrome?

What is Gardner’ssyndrome?

What is HITT syndrome?

Bacterial overgrowth of intestine causedby stasis

Esophageal perforation

Thrombosis of hepatic veins

Syndrome of “B FDR”:Bronchospasm

FlushingDiarrheaRight-sided heart failure (caused by

factors released by carcinoidtumor)

Compartmental hypertension caused byedema, resulting in muscle necrosis ofthe lower extremity, often seen in thecalf; patient may have a distal pulse

Excessive cortisol production

Delivery of a large amount ofhyperosmolar chyme into the smallbowel, usually after vagotomy and a gastric drainage procedure (pyloroplasty/gastrojejunostomy); results in autonomicinstability, abdominal pain, and diarrhea

Perihepatic gonorrhea infection

GI polyps and associated findings ofSebaceous cysts, Osteomas, and Desmoidtumors (SOD); polyps have high malig-nancy potential (Think: A Gardnerplants SOD)

Heparin-Induced ThrombocytopenicThrombosis syndrome: Heparin-inducedplatelet antibodies cause platelets tothrombose vessels, often resulting in lossof limb or life

Chapter 2 / Surgical Syndromes 33


What is Leriche’s syndrome?

What is Mallory-Weisssyndrome?

What is Mendelson’ssyndrome?

What is Mirizzi’s syndrome?

What is Munchausensyndrome?

What is Ogilvie’s syndrome?

What is Peutz-Jegherssyndrome?

What is Plummer-Vinsonsyndrome?

What is RED reactionsyndrome?

What is refeedingsyndrome?

What is Rendu-Osler-Weber(ROW) syndrome?

What is short-gut syndrome?


Claudication of buttocks and thighs,Impotence, Atrophy of legs (seen withiliac occlusive disease) (Think: CIA)

Post-emesis/-retching tears in the gastricmucosa (near gastroesophageal junction)

Chemical pneumonitis after aspiration ofgastric contents

Extrinsic obstruction of the commonhepatic bile duct from a gallstone in thegallbladder or cystic duct

Self-induced illness

Massive nonobstructive colonic dilatation

Benign GI polyps and buccal pigmenta-tion (Think: Peutz � Pigmentation)

Syndrome of:1. Esophageal web2. Iron-deficiency anemia3. Dysphagia4. Spoon-shaped nails5. Atrophic oral and tongue mucosa

Typically occurs in elderly women; 10%develop squamous cell carcinoma

Syndrome of rapid vancomycin infusion,resulting in skin erythema

Hypokalemia, hypomagnesemia, andhypophosphatemia after refeeding astarved patient

Syndrome of GI tract telangiectasia/A-Vmalformations

Malnutrition resulting from �200 cm ofviable small bowel


What is SIADH?

What is another name forSipple’s syndrome?

What is superior vena cava(SVC) syndrome?

What is thoracic outlet syndrome?

What is Tietze’s syndrome?

What is toxic shocksyndrome?

What is Trousseau’ssyndrome?

What is another name forWermer’s syndrome?

What is Zollinger-Ellisonsyndrome?

Chapter 3 / Surgical Most Commons 35

Syndrome of Inappropriate AntiDiureticHormone (Think: InappropriatelyIncreased ADH)

MEN II

Obstruction of the SVC (e.g., by tumor,thrombosis)

Compression of the structures exitingfrom the thoracic outlet

Costochondritis of rib cartilage; aseptic(treat with NSAIDs)

Staphylococcus aureus toxin-induced syndrome marked by fever, hypotension,organ failure, and rash (desquamation—especially palms and soles)

Syndrome of deep venous thrombosis(DVT) associated with carcinoma

MEN I

Gastrinoma and PUD

What is the most common:Indication for surgerywith Crohn’s disease?

Type of melanoma?

Type of breast cancer?

Surgical MostCommons

Chapter 3

Small bowel obstruction (SBO)

Superficial spreading

Infiltrating ductal


Site of breast cancer?

Vessel involved with ableeding duodenal ulcer?

Cause of common bileduct obstruction?

Cause of cholangitis?

Cause of pancreatitis?

Bacteria in stool?

Cause of SBO in adults inthe United States?

Cause of SBO in children?

Cause of emergencyabdominal surgery in theUnited States?

Site of GI carcinoids?

Abdominal x-ray (AXR)finding with SBO?

Electrolyte deficiencycausing ileus?

Cause of transfusionhemolysis?

Cause of blood transfusionresulting in death?

Site of distant metastasisof sarcoma?

Cause of shock in a surgical patient?

Position of anal fissure?


Upper outer quadrant

Gastroduodenal artery

Choledocholithiasis

Bile duct obstruction resulting fromcholedocholithiasis

EtOH

Bacteroides fragilis (“B. frag”)

Postop peritoneal adhesions

Hernias

Acute appendicitis

Appendix

Air-fluid levels

Hypokalemia

Clerical error

Clerical error (wrong blood types)

Lungs

Hypovolemia

Posterior


Cause of large bowelobstruction?

Type of colonic volvulus?

Cause of fever �48 post-operative hours?

Bacterial cause of urinarytract infection (UTI)?

Chest x-ray (CXR) findingwith traumatic thoracicaortic injury?

Abdominal organ injuredin blunt abdominaltrauma?

Abdominal organ injuredin penetrating abdominaltrauma?

Benign tumor of the liver?

Malignancy of the liver?

Pneumonia in the ICU?

Cause of epiduralhematoma?

Cause of lower GI bleeding?

Hernia?

Cause of esophageal perforation?

Cancer in females?

Cancer in males?

Chapter 3 / Surgical Most Commons 37

Colon cancer

Sigmoid volvulus

Atelectasis

Escherichia coli

Widened mediastinum

Liver (not the spleen, as noted in recentstudies!)

Small bowel

Hemangioma

Metastasis

Gram-negative bacteria

Middle meningeal artery injury

Upper GI bleeding

Inguinal hernia (right more than left)

Iatrogenic instrumentation (e.g., EGD)

Lung cancer

Prostate cancer



Type of cancer causingDEATH in males andfemales?

Cause of free peritonealair?

Symptom with gastriccancer?

Site of colon cancerhematogenousmetastasis?

Cause of death ages1�44?

LUNG cancer

Perforated PUD

Weight loss

Liver

TRAUMA

SurgicalPercentages

Chapter 4

What percentage of peoplein the United States willdevelop acute appendicitis?

What is the acceptable percentage of normalappendices removed withthe preoperative diagnosisof appendicitis?

In what percentage of casescan ultrasound diagnosecholelithiasis?

In what percentage of casesdoes a lower GI bleed stopspontaneously?

In what percentage of casesdoes a UGI bleed stop spontaneously?

�7%

Up to 20%; it is better to remove somenormal appendices than to miss a case ofacute appendicitis, which could result ina ruptured appendix

98%

�90%

�80%


What percentage of patientsundergoing laparotomydevelop a postoperativesmall bowel obstruction atsome time later?

What percentage of American women developbreast cancer?

What percentage of patientswith acute appendicitis willhave a radiopaque fecalithon abdominal x-ray (AXR)?

What percentage of patientswith gallstones will have ra-diopaque gallstones on AXR?

What percentage of kidneystones are radiopaque onAXR?

At 6 weeks, wounds haveachieved what percentage oftheir total tensile strength?

What percentage of patientswith ARDS will die?

What percentage of the population have a Meckel’sdiverticulum?

What is the risk ofappendiceal rupture 24 hours after the onset ofsymptoms?

What percentage of colonicvillous adenomas containcancer?

One unit of packed RBCsincreases the hematocrit byhow much?

�5%

10%

Only about 5%

�10%

�90%

�90%

�40%

2%

�25%

�40% (Think: VILLous � VILLain)

3%

Chapter 4 / Surgical Percentages 39

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Additional 1 liter by nasalcannula increases FIO2 byhow much?

What percentage of porce-lain gallbladders will containcancer?

What percentage of patientswith gastric ulcers have cancer on biopsy?


3%

�50%

10%

Identify the following:First to use antiseptic(carbolic acid)

First to advocate surgicalgloves

Father of antiseptic surgery

Father of American neurosurgery

Developer of vasculargrafts

Developed electrocauteryfor surgery with Dr.Cushing

The Mayo Brothers’scrub nurse

Surgical HistoryChapter 5Lister (British surgeon)

Halsted (made by GOODYEAR®)

Lister (1827–1912)

Harvey Cushing

DeBakey (he hand-sewed them!)

Bovie (1928)

Sister Joseph (of St. Mary’s hospital)


Developed the cardio-pulmonary bypass

Identify the year the follow-ing procedures were firstperformed and the physicianwho performed them:

Renal transplant

CABG

CEA

Heart transplant

Artificial heart valve

Liver transplant

Total parenteral nutrition(TPN)

Vascular anastomosis

Lung transplant

Pancreatic transplant

Heart-lung transplant

AAA Rx

First lap chole

First appendectomy

First gastric resection

First lap appy

Who was the only surgeon towin the Pulitzer Prize?

Gibbon

1954; Murray

1962; Sabiston

1953; DeBakey

1967; Barnard

1960; Starr

1963; Starzl

1968; Rhoades

1902; Carrel

1964; Hardy

1966; Najarian

1982; Reitz

1951; Dubost

1987; Mouret and Dubois in France

1848; Hancock

1881; Billroth

1983; Semm (GYN DOCTOR!)

Cushing (for his biography on Osler)

Chapter 5 / Surgical History 41


Which surgeons have wonthe Nobel Prize? (9)

When was the Dakinsolution developed?


Kocher 1909 (thyroid surgery)Gullstrand 1911 (ophthalmology)Carrel 1912 (transplantation/vascular

anastomosis)Bárány 1914 (inner ear disease/vestibular

disease)Banting 1922 (insulin)Hess 1949 (brain physiology)Forssman 1956 (cardiac catheterization)Huggins 1966 (oncology)Murray 1990 (kidney transplant)

World War I; Dakin developed the solution to treat dirty combat wounds

How should a pair ofscissors/needle-driver/clampbe held?

SurgicalInstruments

Chapter 6

With the thumb and fourth finger, usingthe index finger to steady

Is it better to hold the skinwith a DeBakey or anAdson, or toothed, forcep?

What helps steady the scissor- or Bovie-hand?

Better to use an Adson, or toothed,pickup because it is better to cut the skinrather than crush it!

Resting it on the opposite hand

What can be done to guar-antee that you do not cut theknot when cutting sutures?

Slide the scissors down to the knot, thenturn the scissors at a 45� angle, and cut


Chapter 6 / Surgical Instruments 43

How should a pair offorceps be held?

Like a pencil

What are forceps alsoknown as?

“Pickups”

Identify the following instru-ments:

Forcep

DeBakey pickup



Adson pickup

Iris scissors

Bandage scissors



Needle-driver

Right-angle clamp

Kelly clamp



Babcock clamp

Tonsil clamp

Metzenbaum scissors



Mayo scissors (heavy scissors)

Straight Curved

GIA stapler

What does “GIA” stand for? GastroIntestinal Anastomosis

TA stapler

What does “TA” stand for? ThoracoAbdominal



What is the Poole suckerused for?

Suctioning fluid (often irrigation) fromperitoneal cavity

Gigli saw

Poole sucker



EEA stapler

What does “EEA” stand for? End-to-End Anastomosis

Pott’s scissors

Allis clamp



Kocher clamp, for very thick tissue (e.g., fascia)

Bovie electrocautery

Yankauer suction (sucker)



Number 10

10

Number 11

Number 15

Define the following scalpelblades:

What does it mean to “toe in”the retractor?

Identify the followingretractors:

To angle the tip of the retractor in byangling the retractor handle up

Deaver retractor

RETRACTORS (YOU WILL GET TO KNOW THEM WELL!)



Sweetheart retractor (Harrington)

Army–Navy retractor

Weitlaner retractor also known as a“WHEATY” (self-retaining retractor;sorry, operates without a student!)

Bookwalter retractor


Chapter 7 / Sutures and Stitches 53

Richardson retractor, also known as a“RICH”

Metal retractor that can be bent to customize to the situation at hand

What is a “malleable”retractor?

What is a suture?

How are sutures sized?

Which is thicker, 1-O sutureor 3-O suture?

Sutures andStitches

Chapter 7

Any strand of material used to ligateblood vessels or to approximate tissues

By diameter; stated as a number of O’s:the higher the number of O’s, the smallerthe diameter (e.g., 2-O suture has alarger diameter than 5-O suture)

1-O suture (pronounced “one oh”)

SUTURE MATERIALS

GENERAL INFORMATION



What is it?

How long does it retain itsstrength?

Should you ever usePURPLE-colored Vicryl®

for skin closure?

Absorbable, braided, multifilamentouscopolymer of lactide and glycoside

60% at 2 weeks, 8% at 4 weeks

NO—it may cause purple tattooing

Vicryl® Suture

PDS®

What is it?

How long does it maintainits tensile strength?

How long does it take tocomplete absorption?

Absorbable, monofilament polymer ofpolydioxanone (absorbable fishing line)

70% to 74% at 2 weeks, 50% to 58% at 4 weeks, 25% to 41% at 6 weeks

180 days (6 months)

CLASSIFICATION

What are the two most basicsuture types?

What is an absorbablesuture?

What is a nonabsorbablesuture?

Absorbable and nonabsorbable

Suture that is completely broken downby the body (dissolving suture)

Suture is not broken down (permanentsuture)

SUTURES

Catgut

What are “catgut” suturesmade of?

What are the two types ofgut sutures?

What is the differencebetween plain and chromicgut?

Purified collagen fibers from the intestinesof healthy cows or sheep (sorry, no cats)

Plain and chromic

Chromic gut is treated with chromium salts(chromium trioxide), which results in morecollagen crosslinks, making the suture moreresistant to breakdown by the body



WOUND CLOSURE

GENERAL INFORMATION

What is the purpose of asuture closure?

What are the three types ofwound healing?

What is primary intention?

What is secondary intention?

What is tertiary intention?

What is another term fortertiary intention?

To approximate divided tissues toenhance wound healing

1. Primary closure (intention)2. Secondary intention3. Tertiary intention (Delayed Primary

Closure � DPC)

When the edges of a clean wound areclosed in some manner immediately (e.g., suture, Steri-Strips®, staples)

When a wound is allowed to remain openand heal by granulation, epithelization,and contraction—used for dirty wounds,otherwise an abscess can form

When a wound is allowed to remain openfor a time and then closed, allowing fordébridement and other wound care toreduce bacterial counts prior to closure(i.e., delayed primary closure)

DPC � Delayed Primary Closure

What is silk?

What is Prolene?

What is nylon?

What is monocryl?

What kind of suture shouldbe used for the biliary tractor the urinary tract?

Braided protein filaments spun by thesilkworm larva; known as a nonabsorb-able suture

Nonabsorbable suture (used for vascularanastomoses, hernias, abdominal fascialclosure)

Nonabsorbable “fishing line”

Absorbable monofilament

ABSORBABLE—otherwise the suturewill end up as a nidus for stone formation!



SUTURE TECHNIQUES

What is a taper-pointneedle?

Round body, leaves a round hole in tissue(spreads without cutting tissue)

Classic time to wait beforeclosing an open abdominalwound by DPC?

What rule is constantly toldto medical students aboutwound closure?

5 days

“Approximate, don’t strangulate!” Translation: If sutures are pulled too tight, then the tissue becomes ischemic because the blood supply is decreased,possibly resulting in necrosis, infection,and/or scar

What is it used for?

What is a conventional cutting needle?

Suturing of soft tissues other than skin(e.g., GI tract, muscle, nerve, peritoneum,fascia)

Triangular body with the sharp edgetoward the inner circumference; leaves atriangular hole in tissue

What are its uses?

What is a simple interruptedstitch?

Suturing of skin



What is a vertical mattressstitch?

Simple stitch is made, the needle isreversed, and a small bite is taken fromeach wound edge; the knot ends up onone side of the wound

What is the vertical mattressstitch also known as?

What is it used for?

What is a horizontalmattress stitch?

Far-far, near-near stitch—orientedperpendicular to wound

Difficult-to-approximate skin edges;everts tissue well

Simple stitch is made, the needle isreversed, and the same size bite is takenagain—oriented parallel to wound

What is a simple running(continuous) stitch?

Stitches made in succession without knotting each stitch



What is a subcuticularstitch?

Stitch (usually running) placed justunderneath the epidermis, can be eitherabsorbable or nonabsorbable (pull-outstitch if nonabsorbable)

What is a pursestringsuture?

Stitch that encircles a tube perforating ahollow viscus (e.g., gastrostomy tube),allowing the hole to be drawn tight andthus preventing leakage

What are metallic skinstaples?



What is a staple removaldevice?

What is a gastrointestinalanastomosis (GIA) device?

Stapling device that lays two rows ofsmall staples in a hemostatic row andautomatically cuts in between them



What is a pop-off suture? Suture that is not permanently swaged tothe needle, allowing the surgeon to “popoff” the needle from the suture withoutcutting the suture

What is a suture ligature(a.k.a. stick tie)?

Suture is anchored by passing it throughthe vessel on a needle before wrapping itaround and occluding the vessel; preventsslippage of knot-use on larger vessels

What is a retention suture? Large suture (#2) that is full thicknessthrough the entire abdominal wallexcept the peritoneum; used to buttressan abdominal wound at risk fordehiscence


Chapter 8 / Surgical Knot Tying 61

What is the basic surgicalknot?

Surgical KnotTying

Chapter 8

Square knot

KNOTS AND EARS

What is the first knot thatshould be mastered?

What is a “surgeon’s knot”?

Instrument knot

Double-wrap throw followed by singlesquare knot throws

How many (correct) throwsare necessary to ensure thatyour knots do not slip?

What are the guidelines forthe number of minimalthrows needed?

As many as the attending surgeon wants

Depends on the suture materialSilk—3Gut—4Vicryl®, Dexon®, other braided

synthetics—4Nylon, polyester, polypropylene,

PDS, Maxon—6

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How long should the ears ofthe knot be cut?

When should skin sutures beremoved?

How can strength be addedto an incision during andafter suture removal?

In general, in which groupof patients should skinsutures be left in longerthan normal?

How should the sutures be cut?

How is an instrument knottied?

Does a student need toknow a one-hand tie?


Some guidelines are:Silk vessel ties—1 to 2 mmAbdominal fascia closure—5 mmSkin sutures, drain sutures—5 to

10 mm (makes them easier to findand remove)

As soon as the wound has healed enoughto withstand expected mechanicaltrauma

Any stitch left in more than �10 days willleave a scar

Guidelines are:Face—3 to 5 daysExtremities—10 daysJoints—10–14 daysBack—14 daysAbdomen—7 days

With Steri-Strips®

Patients on steroids

Use the tips of the scissors to avoid cutting other tissues

Try to remove the cut ends (less foreignmaterial decreases risk of infection)

Rest the scissor-hand on the non–scissor-hand to steady

Always start with a double wrap, known as a “surgeon’s knot,” and then use a single wrap, pulling the suture inthe opposite directions after every“throw”

No! Master the two-hand tie and theinstrument tie



Then continue with single throws

INSTRUMENT TIE

1.

2.

3.

4.

5.

6.

7.

8.

9.



TWO-HAND TIE

What is the basic positionfor the two-hand tie?

“C” position, formed by the thumb andindex finger; the suture will alternateover the thumb and then the index fingerfor each throw

How is a two-hand knottied?

First, use the index finger to lead



Ask a resident or intern to help you after you have tried for a while.Open book to this page for guidance.Place the Surgical Recall bookmark at back of book to use as a suture anchor.

Then use thumb to lead:


How do you place a peripheral intravenous (IV)catheter?

Procedures forthe Surgical Wardand Clinic

Chapter 9

1. Place a rubber tourniquet above thesite

2. Use alcohol antiseptic3. Place IV into vein with “flash” of blood4. Remove inner needle while advancing

IV catheter5. Secure with tape

COMMON PROCEDURES


How do you draw bloodfrom the femoral vein?

Remember “NAVEL”: In the lateral tomedial direction—Nerve, Artery, Vein,Empty space, Lymphatics—and thusplace needle medial to the femoralpulse


Chapter 9 / Procedures for the Surgical Ward and Clinic 67

How do you remove staples?

How do you removestitches?

How do you place Steri-Strips®?

Use a staple remover (see Chapter 7),then place Steri-Strips®

1. Cut the suture next to the knot2. Pull end of suture out by holding onto

the knot3. Place Steri-Strips®

1. Dry the skin edges of the wound2. Place adhesive (e.g., benzoin)3. With the Adson pickup or with your

fingers, place strips to gently apposeepidermis (Note: Avoid any tension orblisters will appear!)

Femoralnerve

Femoralvein

Femoralartery

Saphenousvein

HRF '04



How do you place a Foleycatheter?

1. Stay sterile2. Apply Betadine® to the urethral

opening (meatus)3. Lubricate the catheter4. Place catheter into urethra5. As soon as urine returns, inflate

balloon with saline (balloon size isgiven in cc on the catheter)

HRF '?04

Catheter

Bladder

Balloon inflation tipUrinary drainage tip

Externalurinarysphincter

Inflatedballoontip

Prostate


How do you find the urethrain females?


First find the clitoris and clitoral hood:The urethra is just below thesestructures; wiping a Betadine®-soakedsponge over this area will often result inhaving the urethra “wink” open

Vagina

ClitorisLabiaUrethralmeatus

HRF '04

Can you inflate the Foleyballoon before you get urinereturn?

No, you might blow up a balloon in theurethra!

NASOGASTRIC TUBE (NGT) PROCEDURES

How do you determine howmuch of the NGT should beadvanced into the body forthe correct position?

Rough guide: from nose, around ear, to 5 cm below the xiphoid


How do you place the NGTin a nare?


First place lubrication (e.g., Surgilube®)then place NGT straight back—not up or down!

What is the best neck position for advancing the NGT?

Neck FLEXED! Also have the patientdrink some water (using a straw)

What if there is 3 liters/24 hours drainage from anNGT?

Think DUODENUM—the NGT may bein the duodenum and not the stomach!Check an x-ray


How can you clinically confirm that an NGT is inthe stomach?


Use a Toomey syringe to “inject” airwhile listening over the stomach with astethoscope; you will hear the “swish” ifthe NGT is in place

How do you tape an NGT?

What MUST you obtain andexamine before using anNGT for feeding?

LOWER chest/upper abdominal x-ray toabsolutely verify placement into thestomach and NOT the LUNG—patientshave died from pulmonary tube feeding!


How do you draw a radialarterial blood gas (ABG)?


Feel for the pulse and advance directlyinto the artery; ABG syringes do not haveto have the plunger withdrawn manually

Radialartery

How do you drain anabscess?

By incision and drainage (or “I & D”):After using local anesthetic, use a #11blade to incise and then open the abscesspocket; large abscesses are best drainedwith a cruciate incision or removal of apiece of skin; pack the open wound


How do you remove an epidermal cyst or sebaceouscyst?

Chapter 10 / Incisions 73

1. Administer local anesthetic2. Remove the ellipse of skin overlying

the cyst, including the pore3. Remove the cyst with the encompass-

ing sac lining

If a patient has an old incision, is it best to make asubsequent incision next toor through the old incision?

What is used to incise theepidermis?

What is used to incise thedermis?

IncisionsChapter 10Through the old incision, or excise the oldincision, because it has scar tissue that lim-its the amount of collaterals that would beneeded to heal an incision placed next to it

Scalpel blade

Scalpel or electrocautery


Describe the following incisions:

Kocher


Right subcostal incision for open cholecystectomy:

Midline laparotomy Incision down the middle of abdomenalong and through the linea alba:

McBurney’s Small, oblique right lower quadrant incisionfor an appendectomy through McBurney’spoint (one third from the anterior superioriliac spine to the umbilicus):


Rocky-Davis


Like a McBurney’s incision except transverse (straight across):

hrf

Pfannenstiel(“fan-en-steel”)

Low transverse abdominal incision withretraction of the rectus muscles laterally;most often used for gynecologicprocedures:

Kidney transplant Lower quadrant; kidney placed extraperitoneally:


Liver transplant


Chevron or Mercedes-Benz® incision inthe upper abdomen:

Median sternotomy Midline sternotomy incision for heartprocedures; less painful than a lateralthoracotomy:

Thoracotomy Usually through the fourth or fifth intercostal space; may be anterior orposterior lateral incisions

Very painful, but many are performedwith muscle sparing (muscle retractionand not muscle transection):


CEA (carotid endarterectomy)


Incision down anterior border of the sternocleidomastoid muscle to expose thecarotid:

Sternocleidomastoidmuscle

Incision

hrf'02

Inguinal hernia repair(open)

Laparoscopic cholecystectomy

Four trocar incisions:


Define the followingpositions:

Supine

Prone

Left lateral decubitus

Surgical PositionsChapter 11

Patient lying flat, face up

Patient lying flat, face down

Patient lying down on his left side (Think:left lateral decubitus � left side down)


Right lateral decubitus

Lithotomy

Patient lying down on his right side(Think: right lateral decubitus � rightside down)

Patient lying supine with legs spread


Chapter 12 / Surgical Speak 79

Trendelenburg Patient supine with head lowered (a.k.a.“headdownenburg”—used during placement of a subclavian vein catheteras the veins distend with blood fromgravity flow)

Define the suffix:-ectomy

-orraphy

-otomy

-ostomy

-plasty

Surgical SpeakChapter 12

To surgically remove part of or an entirestructure/organ

Surgical repair

Surgical incision into an organ

Surgically created opening between twoorgans, or organ and skin

Surgical “shaping” or formation

The language of surgery is quite simple if you master a few suffixes.

Reverse Trendelenburg

What is the best positionfor a pregnant patient?

Patient supine with head elevated (usualposition for laparoscopic cholecystectomyto make the intestines fall away from theoperative field)

Left side down to take gravid uterus offof the IVC


Now test your knowledge ofsurgical speak:

Word for the surgicalrepair of a hernia

Word for the surgicalremoval of the stomach

Word for the surgical creation of an openingbetween the colon andthe skin

Word for the surgical for-mation of a “new” pylorus

Word for the surgicalopening of the stomach

Surgical creation of anopening (anastomosis)between the common bileduct and jejunum

Surgical creation of anopening (anastomosis)between the stomach andjejunum


Herniorrhaphy

Gastrectomy

Colostomy

Pyloroplasty

Gastrotomy

Choledochojejunostomy

Gastrojejunostomy

When can a patient eat priorto major surgery?

What risks should be dis-cussed with all patients anddocumented on the consentform for a surgical procedure?

If a patient is on antihyper-tensive medications, shouldthe patient take them on theday of the procedure?

Preoperative 101Chapter 13Patient should be NPO after midnightthe night before or for at least 8 hoursbefore surgery

Bleeding, infection, anesthesia, scar;other risks are specific to the individualprocedure (also MI, CVA, and death ifcardiovascular disease is present)

Yes, (remember clonidine “rebound”)


If a patient is on an oralhypoglycemic agent (OHA),should the patient take theOHA on the day of surgery?

If a patient is taking insulin,should the patient take it onthe day of surgery?

Should a patient whosmokes cigarettes stopbefore an operation?

What laboratory test mustall women of childbearingage have before enteringthe O.R.?

What is a preop colonsurgery “bowel prep”?

Has a preop bowel prepbeen shown conclusively todecrease postop infectionsin colon surgery?

What preoperative medication can decreasepostoperative cardiac eventsand death?

What must you always orderpreoperatively for yourpatient undergoing a majoroperation?

What electrolyte must youcheck preoperatively if apatient is on hemodialysis?

Who gets a preoperativeECG?

Chapter 13 / Preoperative 101 81

Not if the patient is to be NPO on theday of surgery

No, only half of a long-acting insulin(e.g., lente) and start D5 NS IV; checkglucose levels often preoperatively, operatively, and postoperatively

Yes, improvement is seen in just 2 to 4 weeks after smoking cessation

�-HCG and CBC because of the possibilityof pregnancy and anemia from menses

Bowel prep with colon cathartic (e.g.,GoLYTELY), oral antibiotics (neomycinand erythromycin base), and IV antibioticbefore incision

No, there is no data to support its use

�-blockers!

1. NPO/IVF2. Preoperative antibiotics3. Type and cross blood (PRBCs)

Potassium

Patients older than 40 years of age


Define the following procedures:

Billroth I

SurgicalOperations YouShould Know

Chapter 14

Antrectomy with gastroduodenostomy


Billroth II Antrectomy with gastrojejunostomy

How can the differencebetween a Billroth I and aBillroth II be remembered?

Billroth 1 has one limb; Billroth 2 hastwo limbs


Chapter 14 / Surgical Operations You Should Know 83

Describe the following procedures:

Roux-en-Y limb Jejunojejunostomy forming a Y-shapedfigure of small bowel; the free end canthen be anastomosed to a second hollowstructure (e.g., esophagojejunostomy)

RouxlimbCommon

bile duct

Brooke ileostomy

CEA

Bassini herniorrhaphy

McVay herniorrhaphy

Lichtenstein herniorrhaphy

Standard ileostomy that is folded onitself to protrude from the abdomen �2 cm to allow easy appliance placementand collection of succus

Carotid EndArterectomy; removal of ath-erosclerotic plaque from a carotid artery

Repair of inguinal hernia by approximat-ing transversus abdominis aponeurosisand the conjoint tendon to the reflectionof Poupart’s (inguinal) ligament

Repair of inguinal hernia by approximating the transversus abdominisaponeurosis and the conjoint tendon toCooper’s ligament (which is basically thesuperior pubic bone periosteum)

“Tension-free” inguinal hernia repair usingmesh (synthetic graft material)



Shouldice herniorrhaphy

Plug and patch herniarepair

APR

LAR

Hartmann’s procedure

Mucous fistula

Kocher (“koh-ker”)maneuver

Repair of inguinal hernia by imbricationof the transversalis fascia, transversusabdominis aponeurosis, and the conjointtendon and approximation of the trans-versus abdominis aponeurosis and theconjoint tendon to the inguinal ligament

Prosthetic plug pushes hernia sac in andthen is covered with a prosthetic patch torepair inguinal hernias

AbdominoPerineal Resection; removal of the rectum and sigmoid colon throughabdominal and perineal incisions (patientis left with a colostomy); used for lowrectal cancers �8 cm from the anal verge

Low Anterior Resection; resection oflow rectal tumors through an anteriorabdominal incision

1. Proximal colostomy2. Distal stapled-off colon or rectum that

is left in peritoneal cavity

Distal end of the colon is brought to theabdominal skin as a stoma (proximal endis brought up to skin as an end colostomy)

Dissection of the duodenum from theright-sided peritoneal attachment toallow mobilization and visualization ofthe back of the duodenum/pancreas

AB



Seldinger technique

Cricothyroidotomy

Hepaticojejunostomy

Puestow procedure

Placement of a central line by first placinga wire in the vein, followed by placing thecatheter over the wire

Emergent surgical airway through thecricoid membrane

Anastomosis between a jejunal roux limband the hepatic ducts

Side-to-side anastomosis of the pancreasand jejunum (pancreatic duct is filletedopen)

Stamm gastrostomy Gastrostomy placed by open surgical incision and tacked to the abdominalwall



Highly selectivevagotomy

Transection of vagal fibers to the body of the stomach without interruption offibers to the pylorus (does not needpyloroplasty or other drainage procedurebecause the pylorus should still function)

Enterolysis

LOA

Appendectomy

Lap appy

Cholecystectomy

Lap chole

Nissen

Lysis of peritoneal adhesions

Lysis Of Adhesions (enterolysis)

Removal of the appendix

Laparoscopic removal of the appendix

Removal of the gallbladder

Laparoscopic removal of the gallbladder

Nissen fundoplication; 360� wrap of thestomach by the fundus of the stomacharound the distal esophagus to preventreflux



Lap Nissen

Simple mastectomy


Graham patch

Heineke-Mikulicz pyloroplasty

Nissen fundoplication with laparoscopy

Removal of breast and nipple withoutremoval of nodes

Anastomosis of the common bile duct tothe jejunum (end to side)

Placement of omentum with stitches overa gastric or duodenal perforation (i.e.,omentum is used to plug the hole)

Longitudinal incision through all layers ofthe pylorus, sewing closed in a transversedirection to make the pylorus nonfunctional(used after truncal vagotomy)

Pringle maneuver Temporary occlusion of the porta hepatis(for temporary control of liver blood flowwhen liver parenchyma is actively bleeding)


Modified radical mastectomy

Lumpectomy and radiation

I & D

Exploratory laparotomy

TURP

Fem pop bypass


Removal of the breast, nipple, and axillarylymph nodes (no muscle is removed)

Removal of breast mass and axillarylymph nodes; normal surrounding breasttissue is spared; patient then undergoespostoperative radiation treatments

Incision and Drainage of pus; the woundis then packed open

Laparotomy to explore the peritoneal cav-ity looking for the cause of pain, peritonealsigns, obstruction, hemorrhage, etc.

TransUrethral Resection of the Prostate;removal of obstructing prostatic tissue viascope in the urethral lumen

FEMoral artery to POPliteal arterybypass using synthetic graft or saphenousvein; used to bypass blockage in thefemoral artery



Ax Fem Long prosthetic graft tunneled under theskin placed from the AXillary artery tothe FEMoral artery

hrf'02

Triple A repair

CABG

Repair of an AAA (Abdominal AorticAneurysm): Open aneurysm and placeprosthetic graft; then close old aneurysmsac around graft

Coronary Artery Bypass Grafting; viasaphenous vein graft or internal mammaryartery bypass grafts to coronary arteriesfrom aorta (cardiac revascularization)

Veingrafts

IMAgraft

Hartmann’s pouch Oversewing of a rectal stump (or distalcolonic stump) after resection of acolonic segment; patient is left with aproximal colostomy


PEG


Percutaneous Endoscopic Gastrostomy:Endoscope is placed in the stomach,which is then inflated with air; a needle ispassed into the stomach percutaneously,wire is passed through the needle traversing the abdominal wall, and thegastrostomy is then placed by using theSeldinger technique over the wire

Guidewire

Snare

Tube

Ileoanal pull-through

Hemicolectomy

Truncal vagotomy

Anastomosis of the ileum to the anusafter total proctocolectomy

Removal of a colonic segment (i.e., partial colectomy)

Transection of the vagus nerve trunks;must provide drainage procedure tostomach (e.g., gastrojejunostomy orpyloroplasty) because after truncal vagotomy, the pylorus does not relax

Truncal vagotomy

Vagus nerves


Chapter 15 / Wounds 91

Antrectomy

Whipple procedure

Removal of stomach antrum

Pancreaticoduodenectomy:CholecystectomyTruncal vagotomyPancreaticoduodenectomy—removal

of the head of the pancreas andduodenum

CholedochojejunostomyPancreaticojejunostomy (anastomosis

of distal pancreas remnant to thejejunum)

Gastrojejunostomy (anastomosis ofstomach to jejunum)

hrf'02

Excisional biopsy

Incisional biopsy

Tracheostomy

Biopsy with complete excision of all suspect tissue (mass)

Biopsy with incomplete removal ofsuspect tissue (incises tissue from mass)

Placement of airway tube into tracheasurgically or percutaneously

WoundsChapter 15Define the following terms:

Primary wound closure Suture wound closes immediately (a.k.a.“first intention”)



Secondary wound closure

Delayed primary closure(DPC)

How long until a suturedwound epithelializes?

After a primary closure,when should the dressing be removed?

When can a patient take ashower after a primary closure?

What is a wet-to-drydressing?

What inhibits woundhealing?

What reverses the deleteriouseffects of steroids on woundhealing?

What is an abdominalwound dehiscence?

What is Dakin solution?

Wound is left open and heals over timewithout sutures (a.k.a. “secondaryintention”); it heals by granulation, con-traction, and epithelialization over weeks(leaves a larger scar)

Suture wound closes 3 to 5 days AFTERincision (classically 5 days)

24–48 hours

POD #2

Anytime after POD #2 (after woundepithelializes)

Damp (not wet) gauze dressing placedover a granulating wound and thenallowed to dry to the wound; removalallows for “microdébridement” of thewound

Infection, ischemia, diabetes mellitus,malnutrition, anemia, steroids, cancer,radiation, smoking

Vitamin A

Opening of the fascial closure (not skin);treat by returning to the O.R. for immediate fascial reclosure

Dilute sodium hypochlorite (bleach)used in contaminated wounds


Chapter 16 / Drains and Tubes 93

What is the purpose ofdrains?

What is a Jackson-Pratt (JP)drain?

Drains and TubesChapter 161. Withdrawal of fluids2. Apposition of tissues to remove a

potential space by suction

Closed drainage system attached to a suction bulb (“grenade”)

What are the “three S’s” ofJackson-Pratt drain removal?

What is a Penrose drain?

1. Stitch removal2. Suction discontinuation3. Slow, steady pull

Open drainage system composed of a thinrubber hose; associated with increasedinfection rate in clean wounds

Gastrostomy tube; used for drainage orfeeding

Define the following terms:G-tube



J-tube

Cholecystostomy tube

T-tube

Jejunostomy tube; used for feeding; maybe a small-needle catheter (remember toflush after use or it will clog) or a large,red rubber catheter

Tube placed surgically or percutaneouslywith ultrasound guidance to drain thegallbladder

Tube placed in the common bile duct withan ascending and descending limb thatforms a “T”

Drains percutaneously; placed after com-mon bile duct exploration

CHEST TUBES

What is a thoracostomy tube?

What is the purpose of achest tube?

How is a chest tube inserted?

Chest tube

To appose the parietal and visceral pleuraby draining blood, pus, fluid, chyle, or air

1. Administer local anesthetic2. Incise skin in the fourth or fifth inter-

costal space between the mid- andanterior-axillary lines

3. Perform blunt Kelly-clamp dissectionover the rib into the pleural space

4. Perform finger exploration to confirmintrapleural placement

5. Place tube posteriorly and superiorly



Is the chest tube placedunder or over the rib?

What are the goals of chesttube insertion?

In most cases, where shouldthe chest tube be positioned?

How can you tell on CXR ifthe last hole on the chesttube is in the pleural cavity?

What are the cm measure-ments on a chest tube?

Over to avoid the vessels and nerves

Drain the pleural cavityAppose parietal and visceral pleura to

seal any visceral pleural holes

Posteriorly into the apex

Last hole is cut through the radiopaqueline in the chest tube and is seen on CXRas a break in the line, which should bewithin the pleural cavity

Centimeters from the last hole on thechest tube


What is the chest tube connected to?

Suction, waterseal, collection system(three-chambered box, e.g., Pleuravac®)


From patient/chest tube

Tosuction

Suctioncontrol

Waterseal

Collectionchamber

What are the three chambersof the Pleuravac®?

Describe how each chamberof the Pleuravac® box worksas the old three-bottle system:

Collection chamber

1. Collection chamber2. Water seal3. Suction control

Collects fluid, pus, blood, or chyle andmeasures the amount; connects to thewater seal bottle and to the chest tube



Water-seal chamber One-way valve—allows air to be removedfrom the pleural space; does not allow airto enter pleural cavity; connects to thesuction control bottle and to the collectionchamber

Suction-control chamber Controls the amount of suction by theheight of the water column; sucking inroom air releases excessive suction; connects to wall suction and to the waterseal bottle



Give a good example of awater seal.

How is a chest tube placedon water seal?

Should a chest tube ever beclamped off?

What does it mean to “runthe system” of a chest tube?

How can you tell if the chesttube is “tidling”?

How can you check for anair leak?

What is the usual course forremoving a chest tubeplaced for a PTX?

How fast is a small, stablePTX absorbed?

Place a straw in a cup of water—you canblow air out but if you suck in, the straw fillswith water and thus forms a one-way valvefor air just like the chest tube water seal

By removing the suction; a tension pneumothorax (PTX) cannot formbecause the one-way valve (water seal)allows release of air buildup

No, except to “run the system” momentarily

To see if the air leak is from a leak in thepleural cavity (e.g., hole in lung) orfrom a leak in the tubing

Momentarily occlude the chest tubeand if the air leak is still present, it isfrom the tubing or tubing connection,not from the chest

Take the Pleuravac® off of suction and lookat the water seal chamber: Fluid shouldmove with respiration/ventilation (called“tidling”); this decreases and ceases if thepleura seals off the chest tube

Look at the water seal chamber on suction:If bubbles pass through the water seal

fluid, a large air leak (i.e., air leakinginto chest tube) is present; if no airleak is evident on suction, removesuction and ask the patient to cough

If air bubbles through the water seal,a small air leak is present

1. Suction until the PTX resolves and theair leak is gone

2. Water seal for 24 hours3. Remove the chest tube if no PTX or

air leak is present after 24 hours ofwater seal

�1% daily; therefore, a 10% PTX by volume will absorb in �10 days



How should a chest tube beremoved?

What is a Heimlich valve?

1. Cut the stitch2. Ask the patient to exhale or inhale

maximally3. Rapidly remove the tube (split second)

and at same time, place petroleumjelly gauze covered by 4 � 4’s andthen tape

4. Obtain a CXR

One-way flutter valve for a chest tube

Directionof flow

NASOGASTRIC TUBES (NGT)

How should an NGT beplaced?

How should an NGT beremoved?

1. Use lubrication and have suction upon the bed

2. Use anesthetic to numb nose3. Place head in flexion4. Ask patient to drink a small amount of

water when the tube is in the back ofthe throat and to swallow the tube; ifthe patient can talk without difficultyand succus returns, the tube should bein the stomach (Get an x-ray if there isany question about position)

Give patient a tissue, discontinue suction,untape nose, remove quickly, and tellpatient to blow nose


What test should beperformed before feedingvia any tube?

How does an NGT work?


High abdominal x-ray to confirm place-ment into the GI tract and NOT the lung!

Sump pump, dual lumen tube—thelarge clear tube is hooked to suction andthe small blue tube allows for air sump(i.e., circuit sump pump with air in theblue tube and air and succus sucked outthrough the large clear lumen)

Air

Air

Air andgastric contents

Air andgastriccontents

Tosuctioncanister

How can you check to see ifthe NGT is working?

Should an NGT be placedon continuous orintermittent suction?

What happens if the NGT isclogged?

How should an NGT beunclogged?

Blue port will make a sucking noise;always keep the blue port opening abovethe stomach

Continuous low suction—side holes disengage if they are against mucosabecause of the sump mechanism andmultiple holes

Tube will not decompress the stomach and will keep the low esophageal sphincter (LES) open (i.e., a setup foraspiration)

Saline-flush the clear port, reconnect tosuction, and flush air down the bluesump port



What is a common cause ofexcessive NGT drainage?

What is the differencebetween a feeding tube(Dobbhoff tube) and anNGT?

What is a Foley catheter?

What is a coudé catheter?

Tip of the NGT is inadvertently placedin the duodenum and drains the pancre-atic fluid and bile; an x-ray should betaken and the tube repositioned into thestomach

A feeding tube is a thin tube weighted atthe end that is not a sump pump but asimple catheter; usually placed past thepylorus, which is facilitated by theweighted end and peristalsis

Catheter into the bladder, allowing accurate urine output determination

Foley catheter with a small, curved tip tohelp maneuver around a large prostate

FOLEY CATHETER

If a Foley catheter cannotbe inserted, what are thenext steps?

1. Anesthetize the urethra with a sterilelocal anesthetic (e.g., lidocaine jelly)

2. Try a larger Foley catheter

Coudé catheter


What are they?

What major complicationsresult from placement?

In long-term central lines,what does the “cuff” do?

What is a Hickman® orHickman-type catheter?

What is a Port-A-Cath®?

What is a “cordis”?

If you try to place a subcla-vian central line unsuccess-fully, what must you dobefore trying the other side?


Catheters placed into the major veins(central veins) via subclavian, internaljugular, or femoral vein approaches

PTX (always obtain postplacement CXR),bleeding, malposition (e.g., into the neckfrom subclavian approach), dysrhythmias

Allows ingrowth of fibrous tissue, which:Holds the line in placeForms a barrier to the advance of

bacteria

External central line tunneled under theskin with a “cuff”

Central line that has a port buried underthe skin that must be accessed throughthe skin (percutaneously)

Large central line catheter; used for massive fluid resuscitation or for placinga Swan-Ganz catheter

Get a CXR—a bilateral pneumothoraxcan be fatal!

CENTRAL LINES

HRF '04

What if a patient has a urethral injury and a Foleycannot be placed?

A suprapubic catheter will need to beplaced


Chapter 17 / Surgical Anatomy Pearls 103

MISCELLANEOUS

How can diameter in mm bedetermined from a Frenchmeasurement?

How can needle-gauge sizebe determined?

What is a Tenckhoffcatheter?

Divide the French size by � or 3.14 (e.g., a 15 French tube has a diameter of5 mm)

14-gauge needle is 1/14 of an inch (Thus, a 14-gauge needle is larger than a21-gauge needle)

Catheter placed into the peritoneal cavityfor peritoneal dialysis

What is the drainage of theleft testicular vein?

What is the drainage of theright testicular vein?

What is Gerota’s fascia?

What are the prominent collateral circulations seenin portal hypertension?

What parts of the GI tractare retroperitoneal?

What is the gubernaculum?

Surgical AnatomyPearls

Chapter 17

Left renal vein

IVC

Fascia surrounding the kidney

Esophageal varices, hemorrhoids (inferiorhemorrhoidal vein to internal iliac vein),patent umbilical vein (caput medusa),and retroperitoneal vein via lumbar tributaries

Most of the duodenum, the ascendingcolon, the descending colon, and the pancreas

Embryologic structure that adheres thetestes to the scrotal sac; used to helpmanipulate the testes during indirect hernia repair


Which artery bleeds inbleeding duodenal ulcers?

What is the name of thelymph nodes between thepectoralis minor and majormuscles?

Is the left vagus nerve anterior or posterior?

What is Morrison’s pouch?

Give the locations of the following structures:

Foregut

Midgut

Hindgut

Where are the blood vesselson a rib?

What is the order of thefemoral vessels?

What is Hesselbach’s triangle?

What nerve is located on topof the spermatic cord?

What is Calot’s triangle?


Gastroduodenal artery

Rotter’s lymph nodes

Anterior; remember that the esophagusrotates during development

Hepatorenal recess; the most posteriorcavity within the peritoneal cavity

Mouth to ampulla of Vater

Ampulla of Vater to distal third of transverse colon

Distal third of transverse colon to theanus

Vein, Artery, and Nerve (VAN) are under-neath the rib (thus, place chest tubes andthoracentesis needles above the rib!)

Femoral vein is medial to the femoralartery (Think: “NAVEL” for the order ofthe right femoral vessels—Nerve, Artery,Vein, Empty space, Lymphatics)

The area bordered by:1. Inguinal ligament2. Epigastric vessels3. Lateral border of the rectus sheath

Ilioinguinal nerve

The area bordered by:1. Cystic duct2. Common hepatic duct3. Cystic artery

(Pronounced “kal-ohs”)


What is Calot’s node?

What separates the rightand left lobes of the liver?

What is the gastrinoma triangle?

Which artery is responsiblefor anterior spinalsyndrome?

Where is McBurney’s point?

How can you find the appendix after you find thececum?

Where is the space of Retzius?

What are the white lines ofToldt?

What is the strongest layerof the small bowel?

Which parts of the GI tractdo not have a serosa?

What is the vein thatoverlies the pylorus?

What is the pouch ofDouglas?

What does the thoracic ductempty into?

Chapter 17 / Surgical Anatomy Pearls 105

Lymph node found in Calot’s triangle

Cantle’s line—a line drawn from the IVCto just left of the gallbladder fossa

Triangle where �90% of gastrinomas arelocated, bordered by:

1. Junction of the second and thirdportions of the duodenum

2. Cystic duct3. Pancreatic neck

Artery of Adamkiewicz

One third the distance from the anteriorsuperior iliac spine to the umbilicus (estimate of the position of the appendix)

Trace the taeniae back as they convergeon the origin of the appendix

Preperitoneal space anterior to the bladder

Lateral peritoneal reflections of theascending and descending colon

Submucosa (not the serosa, think: SUbmucosa � SUperior)

EsophagusMiddle and distal rectum

Vein of Mayo

Pouch between the rectum and bladderor uterus

Left subclavian vein; left internal jugularvein junction


What is the coronary vein?

What is the hypogastricartery?

Which is longer, the left orright renal vein?

What are the layers of theabdominal wall?

What are the plicaecirculares?

What is another name forthe plicae circulares?

What are the majorstructural differencesbetween the jejunum andileum?

What are the major anatomicdifferences between thecolon and the small bowel?

How far up does thediaphragm extend?

What dermatome is at theumbilicus?


Left gastric vein

Internal iliac artery

Left

1. Skin, then fat2. Scarpa’s fascia, then more fat3. External oblique4. Internal oblique5. Transversus abdominis6. Transversalis fascia7. Preperitoneal fat8. Peritoneum

Plicae � folds, circulares � circular;thus, the circular folds of mucosa of thesmall bowel

Valvulae conniventes

Jejunum—long vasa rectae; large plicaecirculares; thicker wall

Ileum—shorter vasa rectae; smaller plicae circulares; thinner wall (Think:Ileum � Inferior vasa rectae, Inferiorplicae circulares, and Inferior wall)

Colon has taeniae coli, haustra, andappendices epiploicae (fat appendages),whereas the small intestine is smooth

To the nipples in men (fourth intercostalspace; thus, the abdomen extends to thelevel of the nipples)

T10


What are the major layers ofan artery?

Chapter 18 / Fluids and Electrolytes 107

Adventitia

Media

Intima

What are the two majorbody fluid compartments?

What are the twosubcompartments ofextracellular fluid?

What percentage of bodyweight is in fluid?

Fluids andElectrolytes

Chapter 18

1. Intracellular2. Extracellular

1. Interstitial fluid (in between cells)2. Intravascular fluid (plasma)

60%

hrf ‘07

60%



What percentage of bodyfluid is intracellular?

What percentage of bodyfluid is extracellular?

What is the composition ofbody fluid?

How can body fluid distribution by weight beremembered?

On average, what percentageof body weight does bloodaccount for in adults?

How many liters of bloodare in a 70-kg man?

What are the fluid requirements every 24 hoursfor each of the followingsubstances:

Water

Potassium

Chloride

Sodium

What are the levels andsources of normal dailywater loss?

What are the levels andsources of normal daily electrolyte loss?

66%

33%

Fluids � 60% total body weight:Intracellular � 40% total body weightExtracellular � 20% total body weight

(Think: 60, 40, 20)

“TIE”:T � Total body fluid � 60% of body

weightI � Intracellular � 40% of body weightE � Extracellular � 20% of body

weight

�7%

0.07 � 70 � 5 liters

�30 to 35 mL/kg

�1 mEq/kg

�1.5 mEq/kg

�1–2 mEq/kg

Urine—1200 to 1500 mL (25–30 mL/kg)Sweat—200 to 400 mLRespiratory losses—500 to 700 mLFeces—100 to 200 mL

Sodium and potassium � 100 mEqChloride � 150 mEq



THIRD SPACING

What is it?

When does “third-spacing”occur postoperatively?

What are the classic signs ofthird spacing?

What is the treatment?

What are the surgical causesof the following conditions:

Metabolic acidosis

Hypochloremic alkalosis

Fluid accumulation in the interstitium oftissues, as in edema, e.g., loss of fluid intothe interstitium and lumen of a paralyticbowel following surgery (think of theintravascular and intracellular spaces asthe first two spaces)

Third-spaced fluid tends to mobilize backinto the intravascular space around POD#3 (Note: Beware of fluid overload oncethe fluid begins to return to the intravas-cular space); switch to hypotonic fluidand decrease IV rate

TachycardiaDecreased urine output

IV hydration with isotonic fluids

Loss of bicarbonate: diarrhea, ileus,fistula, high-output ileostomy,carbonic anhydrase inhibitors

Increase in acids: lactic acidosis(ischemia), ketoacidosis, renal failure,necrotic tissue

NGT suction, loss of gastric HCl throughvomiting/NGT

What are the levels of sodiumand chloride in sweat?

What is the major electrolytein colonic feculent fluid?

What is the physiologicresponse to hypovolemia?

�40 mEq/L

Potassium—65 mEq/L

Sodium/H2O retention via renin Saldosterone, water retention via ADH,vasoconstriction via angiotensin II andsympathetics, low urine output andtachycardia (early), hypotension (late)


Metabolic alkalosis

Respiratory acidosis

Respiratory alkalosis

What is the “classic” acid-base finding with significantvomiting or NGT suctioning?

Why hypokalemia with NGTsuctioning?

What is the treatment forhypokalemic hypochloremicmetabolic alkalosis?

What is paradoxic alkaloticaciduria?

How does paradoxicalkalotic aciduria occur?

With paradoxic alkaloticaciduria, why is H�

preferentially lost?

What can be followed toassess fluid status?

With hypovolemia, whatchanges occur in vital signs?


Vomiting, NG suction, diuretics, alkaliingestion, mineralocorticoid excess

Hypoventilation (e.g., CNS depression),drugs (e.g., morphine), PTX, pleural effusion, parenchymal lung disease, acute airway obstruction

Hyperventilation (e.g., anxiety, pain, fever,wrong ventilator settings)

Hypokalemic hypochloremic metabolicalkalosis

Loss in gastric fluid—loss of HCl causesalkalosis, driving K� into cells

IVF, Cl�/K� replacement

Seen in severe hypokalemic, hypovolemic,hypochloremic metabolic alkalosis withparadoxic metabolic alkalosis of serumand acidic urine

H� is lost in the urine in exchange forNa� in an attempt to restore volume

H� is exchanged preferentially into theurine instead of K� because of the lowconcentration of K�

Urine output, base deficit, lactic acid,vital signs, weight changes, skin turgor,jugular venous distention (JVD), mucosalmembranes, rales (crackles), central venouspressure, PCWP, chest x-ray findings

Tachycardia, tachypnea, initial rise indiastolic blood pressure because ofclamping down (peripheral vasoconstric-tion) with subsequent decrease in bothsystolic and diastolic blood pressures


What are the insensible fluidlosses?

What are the quantities ofdaily secretions:

Bile

Gastric

Pancreatic

Small intestine

Saliva

How can the estimated levelsof daily secretions from bile,gastric, and small-bowelsources be remembered?


Loss of fluid not measured:Feces—100 to 200 mL/24 hoursBreathing—500 to 700 mL/24 hours

(Note: increases with fever andtachypnea)

Skin—�300 mL/24 hours, increasedwith fever; thus, insensible fluidloss is not directly measured

�1000 mL/24 hours

�2000 mL/ 24 hours

�600 mL/ 24 hours

�3000 mL/day

�1500 mL/24 hours (Note: almost all secretions are reabsorbed)

Alphabetically and numerically: BGS and123 or B1, G2, S3, because Bile, Gastric,and Small bowel produce roughly 1 L, 2 L, and 3 L, respectively!

COMMON IV REPLACEMENT FLUIDS (ALL VALUESARE PER LITER)

What comprises normalsaline (NS)?

What comprises 1/2 NS?

What comprises 1/4 NS?

What comprises lactatedRinger’s (LR)?

What comprises D5W?

154 mEq of Cl�

154 mEq of Na�

77 mEq of Cl�

77 mEq of Na�

39 mEq of Cl�

39 mEq of Na�

130 mEq Na�

109 mEq Cl�

28 mEq lactate4 mEq K�

3 mEq Ca�

5% dextrose (50 g) in H2O


What accounts for tonicity?

What happens to the lactatein LR in the body?

IVF replacement by anatomicsite:

Gastric (NGT)

Biliary

Pancreatic

Small bowel (ileostomy)

Colonic (diarrhea)


Mainly electrolytes; thus, NS and LR areboth isotonic, whereas 1/2 NS is hypotonicto serum

Converted into bicarbonate; thus, LRcannot be used as a maintenance fluidbecause patients would become alkalotic

D5 1/2 NS � 20 KCl

LR�/�sodium bicarbonate


LR


CALCULATION OF MAINTENANCE FLUIDS

What is the 100/50/20 rule?

What is the 4/2/1 rule?

What is the maintenance fora 70-kg man?

Maintenance IV fluids for a 24-hour period:100 mL/kg for the first 10 kg50 mL/kg for the next 10 kg20 mL/kg for every kg over 20 (divide

by 24 for hourly rate)

Maintenance IV fluids for hourly rate:4 mL/kg for the first 10 kg2 mL/kg for the next 10 kg1 mL/kg for every kg over 20

Using 100/50/20:100 � 10 kg � 100050 � 10 kg � 50020 � 50 kg � 1000Total � 2500Divided by 24 hours � 104 mL/hr

maintenance rate

Using 4/2/1:4 � 10 kg � 402 � 10 kg � 201 � 50 kg � 50Total � 110 mL/hr maintenance rate


What is the common adultmaintenance fluid?

What is the common pediatricmaintenance fluid?

Why should sugar (dextrose)be added to maintenancefluid?

What is the best way toassess fluid status?

What is the minimal urineoutput for an adult on maintenance IV?

What is the minimal urineoutput for an adult traumapatient?

How many mL are in 12 oz(beer can)?

How many mL are in 1 oz?

How many mL are in 1 tsp?

What are common isotonicfluids?

What is a bolus?

Why not combine bolus fluidswith dextrose?


D5 1/2 NS with 20 mEq KCl/L

D5 1/4 NS with 20 mEq KCl/L (use 1/4 NS because of the decreased abilityof children to concentrate urine)

To inhibit muscle breakdown

Urine output (unless the patient has cardiac or renal dysfunction, in whichcase central venous pressure or wedgepressure is often used)

30 mL/hr (0.5 cc/kg/hr)

50 mL/hr

356 mL

30 mL

5 mL

NS, LR

Volume of fluid given IV rapidly (e.g., 1 Lover 1 hour); used for increasing intravas-cular volume, and isotonic fluids shouldbe used (i.e., NS or LR)

Hyperglycemia may result


What is the possible conse-quence of hyperglycemia inthe patient with hypovolemia?

Why not combine bolus fluidswith a significant amount ofpotassium?

Why should isotonic fluidsbe given for resuscitation(i.e., to restore intravascularvolume)?

What portion of 1 L NS willstay in the intravascularspace after a laparotomy?

What is the most commontrauma resuscitation fluid?

What is the most commonpostoperative IV fluid aftera laparotomy?

After a laparotomy, whenshould a patient’s fluid be“mobilized”?

What IVF is used to replaceduodenal or pancreatic fluidloss?


Osmotic diuresis

Hyperkalemia may result (the potassiumin LR is very low: 4 mEq/L)

If hypotonic fluid is given, the tonicity ofthe intravascular space will be decreasedand H2O will freely diffuse into the interstitial and intracellular spaces; thus,use isotonic fluids to expand the intra-vascular space

In 5 hours, only �200 cc (or 20%) willremain in the intravascular space!

LR

LR or D5LR for 24 to 36 hours, followedby maintenance fluid

Classically, POD #3; the patient begins to“mobilize” the third-space fluid back intothe intravascular space

LR (bicarbonate loss)

ELECTROLYTE IMBALANCES

What is a common cause ofelectrolyte abnormalities?

What is a major extracellularcation?

What is a major intracellularcation?

Lab error!

Na�

K�


What is the normal rangefor potassium level?

What are the surgical causesof hyperkalemia?

What are the signs/symptoms?

What are the ECG findings?

What are the critical values?

What is the urgenttreatment?

What is the nonacute treatment?

What is the acronym for the treatment of acutesymptomatic hyperkalemia?

What is “pseudohyper-kalemia”?


3.5–5.0 mEq/L

Iatrogenic overdose, blood transfusion,renal failure, diuretics, acidosis, tissuedestruction (injury/hemolysis)

Decreased deep tendon reflex (DTR) orareflexia, weakness, paraesthesia, paralysis,respiratory failure

Peaked T waves, depressed STsegment, prolonged PR, wide QRS,bradycardia, ventricular fibrillation

K� �6.5

IV calcium (cardioprotective), ECG monitoring

Sodium bicarbonate IV (alkalosis drivesK� intracellularly)

Glucose and insulinAlbuterolSodium polystyrene sulfonate

(Kayexalate) and furosemide (Lasix)Dialysis

Furosemide (Lasix), sodium polystyrenesulfonate (Kayexalate)

“CB DIAL K”:CalciumBicarbonate

DialysisInsulin/dextroseAlbuterolLasix

Kayexalate

Spurious hyperkalemia as a result offalsely elevated K� in sample from sample hemolysis

HYPERKALEMIA


What acid-base change lowers the serum potassium?

What nebulizer treatmentcan help lower K� level?


Alkalosis (thus, give bicarbonate forhyperkalemia)

Albuterol

HYPOKALEMIA

What are the surgicalcauses?



What is a U wave?

Diuretics, certain antibiotics, steroids,alkalosis, diarrhea, intestinal fistulae, NGaspiration, vomiting, insulin, insufficientsupplementation, amphotericin

Weakness, tetany, nausea, vomiting,ileus, paraesthesia

Flattening of T waves, U waves,ST segment depression, PAC, PVC, atrialfibrillation

U

What is the rapid treatment?

What is the maximumamount that can be giventhrough a peripheral IV?

What is the maximumamount that can be giventhrough a central line?

What is the chronictreatment?

What is the most commonelectrolyte-mediated ileus inthe surgical patient?

KCl IV

10 mEq/hour

20 mEq/hour

KCl PO

Hypokalemia


What electrolyte conditionexacerbates digitalis toxicity?

What electrolyte deficiencycan actually causehypokalemia?

What electrolyte must youreplace first before replacing K�?

Why does hypomagnesemiamake replacement of K�

with hypokalemia nearlyimpossible?


Hypokalemia

Low magnesium

Magnesium

Hypomagnesemia inhibits K� reabsorptionfrom the renal tubules

HYPERNATREMIA

What is the normal rangefor sodium level?



What is the usual treatmentsupplementation slowly overdays?

How fast should you lower the sodium level in hyperna-tremia?

What is the major complica-tion of lowering the sodiumlevel too fast?

135–145 mEq/L

Inadequate hydration, diabetes insipidus,diuresis, vomiting, diarrhea, diaphoresis,tachypnea, iatrogenic (e.g., TPN)

Seizures, confusion, stupor, pulmonary orperipheral edema, tremors, respiratoryparalysis

D5W, 1/4 NS, or 1/2 NS

Guideline is �12 mEq/L per day

Seizures (not central pontine myelinolysis)

HYPONATREMIA

What are the surgical causesof the following types:

Hypovolemic Diuretic excess, hypoaldosteronism, vomiting, NG suction, burns, pancreatitis,diaphoresis



Euvolemic

Hypervolemic


What is the treatment of thefollowing types:

Hypovolemic

Euvolemic

Hypervolemic

How fast should youincrease the sodium level inhyponatremia?

What may occur if you correcthyponatremia too quickly?

What are the signs of centralpontine myelinolysis?

What is the most commoncause of mild postoperativehyponatremia?

How can the sodium level inSIADH be remembered?

SIADH, CNS abnormalities, drugs

Renal failure, CHF, liver failure(cirrhosis), iatrogenic fluid overload (dilutional)

Seizures, coma, nausea, vomiting, ileus,lethargy, confusion, weakness

NS IV, correct underlying cause

SIADH: furosemide and NS acutely, fluidrestriction

Dilutional: fluid restriction and diuretics

Guideline is �12 mEq/L per day

Central pontine myelinolysis!

1. Confusion2. Spastic quadriplegia3. Horizontal gaze paralysis

Fluid overload

SIADH � Sodium Is Always DownHere � Hyponatremia

“PSEUDOHYPONATREMIA”

What is it? Spurious lab value of hyponatremia as aresult of hyperglycemia, hyperlipidemia,or hyperproteinemia



HYPERCALCEMIA

What are the causes?



What is the acute treatmentof hypercalcemic crisis?

What are other options forlowering Ca� level?

“CHIMPANZEES”:Calcium supplementation IVHyperparathyroidism (1/3)

hyperthyroidismImmobility/Iatrogenic (thiazide

diuretics)Mets/Milk alkali syndromePaget’s disease (bone)Addison’s disease/AcromegalyNeoplasm (colon, lung, breast,

prostate, multiple myeloma)Zollinger-Ellison syndrome (as part of

MEN I)Excessive vitamin DExcessive vitamin ASarcoid

Hypercalcemia—“Stones, bones, abdomi-nal groans, and psychiatric overtones”

Polydipsia, polyuria, constipation

Short QT interval, prolonged PR interval

Volume expansion with NS, diuresis withfurosemide (not thiazides)

Steroids, calcitonin, bisphosphonates(pamidronate, etc.), mithramycin, dialysis(last resort)

HYPOCALCEMIA

How can the calcium levelbe determined with hypoalbuminemia?


What is Chvostek’s sign?

(4-measured albumin level) � 0.8, thenadd this value to the measured calciumlevel

Short bowel syndrome, intestinal bypass,vitamin D deficiency, sepsis, acutepancreatitis, osteoblastic metastasis,aminoglycosides, diuretics, renal failure,hypomagnesemia, rhabdomyolysis

Facial muscle spasm with tapping offacial nerve (Think: CHvostek � CHeek)


What is Trousseau’s sign?



What is the acutetreatment?


What is the possible compli-cation of infused calcium ifthe IV infiltrates?

What is the best way to checkthe calcium level in the ICU?


Carpal spasm after occluding blood flowin forearm with blood pressure cuff

Chvostek’s and Trousseau’s signs, perioralparaesthesia (early), increased deep tendonreflexes (late), confusion, abdominalcramps, laryngospasm, stridor, seizures,tetany, psychiatric abnormalities (e.g.,paranoia, depression, hallucinations)

Prolonged QT and ST interval (peaked Twaves are also possible, as in hyperkalemia)

Calcium gluconate IV

Calcium PO, vitamin D

Tissue necrosis; never administerperipherally unless absolutely necessary(calcium gluconate is less toxic than calcium chloride during an infiltration)

Check ionized calcium

HYPERMAGNESEMIA

What is the normal rangefor magnesium level?

What is the surgical cause?



1.5–2.5 mEq/L

TPN, renal failure, IV over supplementation

Respiratory failure, CNS depression,decreased deep tendon reflexes

Calcium gluconate IV, insulin plusglucose, dialysis (similar to treatment ofhyperkalemia), furosemide (Lasix)

HYPOMAGNESEMIA


TPN, hypocalcemia, gastric suctioning,aminoglycosides, renal failure, diarrhea,vomiting



What is the acute treatment?


Hypomagnesemia maymake it impossible tocorrect what otherelectrolyte abnormality?


Increased deep tendon reflexes, tetany,asterixis, tremor, Chvostek’s sign, ventricular ectopy, vertigo, tachycardia,dysrhythmias

MgSO4 IV

Magnesium oxide PO (side effect:diarrhea)

Hypokalemia (always fix hypomagnesemiawith hypokalemia)

HYPERGLYCEMIA




What is the Weiss protocol?

What is the goal glucoselevel in the ICU?

Diabetes (poor control), infection, stress,TPN, drugs, lab error, drawing over IVsite, somatostatinoma, glucagonoma

Polyuria, hypovolemia, confusion/coma,polydipsia, ileus, DKA (Kussmaul breathing), abdominal pain, hyporeflexia

Insulin

Sliding scale insulin

80–110 mg/dL

HYPOGLYCEMIA




Excess insulin, decreased caloric intake,insulinoma, drugs, liver failure, adrenalinsufficiency, gastrojejunostomy

Sympathetic response (diaphoresis,tachycardia, palpitations), confusion,coma, headache, diplopia, neurologicdeficits, seizures

Glucose (IV or PO)


What is the normal rangefor phosphorus level?


What is a complication ofsevere hypophosphatemia?


What is the critical value?



2.5–4.5 mg/dL

Weakness, cardiomyopathy, neurologicdysfunction (e.g., ataxia), rhabdomyolysis,hemolysis, poor pressor response

Respiratory failure

GI losses, inadequate supplementation,medications, sepsis, alcohol abuse, renalloss

�1.0 mg/dL

Supplement with sodium phosphate orpotassium phosphate IV (depending onpotassium level)

HYPERPHOSPHATEMIA




Calcification (ectopic), heart block

Renal failure, sepsis, chemotherapy,hyperthyroidism

Aluminum hydroxide (binds phosphate)

MISCELLANEOUS

This ECG pattern is consistent with which electrolyte abnormality?

Hyperkalemia: peaked T waves

HYPOPHOSPHATEMIA


If hyperkalemia is leftuntreated, what can occur?


Ventricular tachycardia/fibrillation Sdeath

Which electrolyte is aninotrope?

What are the major cardiacelectrolytes?

Which electrolyte must bemonitored closely in patientson digitalis?

What is the most commoncause of electrolyte-mediated ileus?

What is a colloid fluid?

What is the rationale forusing an albumin-furosemide “sandwich”?

An elderly patient goes intoCHF (congestive heart failure) on POD #3 after alaparotomy. What is going on?

What fluid is used to replaceNGT (gastric) aspirate?

What electrolyte is associatedwith succinycholine?

Calcium

Potassium (dysrhythmias), magnesium(dysrhythmias), calcium (dysrhythmias/inotrope)

Potassium

Hypokalemia

Protein-containing fluid (albumin)

Albumin will pull interstitial fluid into theintravascular space and the furosemidewill then help excrete the fluid as urine

Mobilization of the “third-space” fluidinto the intravascular space, resulting influid overload and resultant CHF (butalso must rule out MI)

D5 1/2 NS with 20 KCl

Hyperkalemia



Define the following terms:PT

PTT

INR

Packed red blood cells(PRBCs)

Platelets

Fresh frozen plasma (FFP)

Cryoprecipitate (cryo)

Which electrolyte is mostlikely to fall with the infusionof stored blood? Why?

What changes occur in thestorage of PRBCs?

What are general guidelinesfor blood transfusion?

What is the rough formulafor converting Hgb to Hct?

One unit of PRBC increasesHct by how much?

Blood and BloodProducts

Chapter 19

Prothrombin Time: Tests extrinsic coagulation pathway

Partial Thromboplastin Time: Testsintrinsic coagulation pathway

International Normalized Ratio (reportsPT results)

One unit equals �300 ml (�50 ml); noplatelets or clotting factors; can be mixedwith NS to infuse faster

Replace platelets with units of platelets(6–10 units from single donor or randomdonors)

Replaces clotting factors; (no RBCs/WBCs/platelets)

Replaces fibrinogen, von Willebrand factor, and some clotting factors

Ionized calcium; the citrate preservativeused for the storage of blood binds serumcalcium

T Ca�, c K�, T 2,3-DPG, c H� (T pH), T PMNs

Acute blood loss, Hgb �10, and historyof CAD/COPD or healthy symptomaticpatient with Hgb �7

Hgb � 3 � Hct

�3% to 4%


Which blood type is the“universal” donor for PRBCs?

Which blood type is the“universal” donor for FFP?

What is a type and screen?

What is a type and cross?

Define thrombocytopenia.

What are the commoncauses of thrombocytopeniain the surgical patient?

What can be given to helpcorrect platelet dysfunctionfrom uremia, aspirin, orbypass?

What common medicationcauses platelets toirreversibly malfunction?

What is Plavix®?

What platelet count is associated with spontaneousbleeding?

What should the plateletcount be before surgery?

When should “prophylactic”platelet transfusions begiven?

Chapter 19 / Blood and Blood Products 125

O negative

AB

Patient’s blood type is determined andthe blood is screened for antibodies; atype and cross from that sample can thenbe ordered if needed later

Patient’s blood is sent to the blood bankand cross-matched for specific donorunits for possible blood transfusion

Low platelet count (�100,000)

Sepsis, H2 blockers, heparin, massivetransfusion, DIC, antibiotics, spurious labvalue, Swann-Ganz catheter

DDAVP (desmopressin)

Aspirin (inhibits cyclooxygenase)

Clopidogrel—irreversibly inhibits plateletP2Y12 ADP receptor (blocks fibrincrosslinking of platelets)

�20,000

�50,000

With platelets �10,000 (old recommendation was 20,000)



What is microcytic anemia“until proven otherwise” ina man or postmenopausalwoman?

Why not infuse PRBCs withlactated Ringer’s?

For how long can packedRBCs be stored?

What is the most commoncause of transfusion hemolysis?

What is the risk of receivinga unit of blood infected withHIV?

What are the symptoms of atransfusion reaction?

What is the treatment fortransfusion hemolysis?

What component of theblood transfusion can causea fever?

What is the transfusion“trigger” Hct in younghealthy patients?

What is the widelyconsidered “optimal” Hct ina patient with a history ofheart disease or stroke?

When should aspirin admin-istration be discontinuedpreoperatively?


Colon cancer

Calcium in LR may result in coagulationwithin the IV line (use NS)

About 6 weeks (42 days)

ABO incompatibility as a result of clerical error

�1 in 1,000,000

Fever, chills, nausea, hypotension, lumbarpain, chest pain, abnormal bleeding

Stop transfusion; provide fluids; performdiuresis (Lasix) to protect kidneys; alkalinize urine (bicarbonate); give pressors as needed

WBCs

21%

�30%

At 1 week because platelets live 7 to 10 days (must use judgment if patient isat risk for stroke or MI; it may be betterto continue and use excellent surgicalhemostasis in these patients)


What can move theoxyhemoglobin dissociationcurve to the right?

What is the normal life ofRBCs?

What is the normal life ofplatelets?

What factor is deficient inhemophilia A?

How can the clotting factorfor hemophilia A be remembered?

What is the preoperativetreatment of hemophilia A?

What coagulation study iselevated with hemophilia A?

How do you rememberwhich coagulation study isaffected by the hemophilias?

What factor is deficient inhemophilia B?

How do you rememberwhich factors are deficientwith hemophilia A andhemophilia B?

How are hemophilias A andB inherited?

What is von Willebrand’s disease?

How is von Willebrand’s disease inherited?

What is used to correct vonWillebrand’s disease?

Chapter 19 / Blood and Blood Products 127

Acidosis, 2,3-DPG, fever, elevated PCO2

(to the right means greater ability torelease the O2 to the tissues)

120 days

7 to 10 days

Factor VIII

Think: “Eight” sounds like “A”

Factor VIII infusion to �100% normalpreoperative levels

PTT

There are two major hemophilias andtwo t’s in PTT

Factor IX

Think alphabetically and chronologically:A before B—8 before 9Hemophilia A � factor VIIIHemophilia B � factor IX

Sex-linked recessive

Deficiency of von Willebrand factor(vWF) and factor VIII:C

Autosomal dominant

DDAVP or cryoprecipitate


What coagulation is abnormalwith the following disorders:

Hemophilia A

Hemophilia B

von Willebrand’s disease

What is the effect on thecoagulation system if thepatient has a deficiency inprotein C, protein S, orantithrombin III?

What is a “left shift” on aCBC?

What is the usual “therapeutic” PT?

What is the acronym basisfor the word WARFARIN?

What is the most commoninherited hypercoagulablestate?

What is Xigris®?


PTT (elevated)

PTT (elevated)

Bleeding time

A hypercoagulable state

Juvenile polymorphonuclear leukocytes(bands); legend has it that the old counters for all the blood cells had thelever for bands on the LEFT of thecounter

With coumadin, usually shoot for an INRof 2.0–3.0

Wisconsin Alumni Research Foundation-ARIN

Factor V Leiden (Think: LEiden � LEader)

Activated protein C, which is used insevere sepsis

What motto is associatedwith surgical hemostasis?

What is the most immediatemethod to obtain hemostasis?

SurgicalHemostasis

Chapter 20

“All bleeding stops”

Pressure (finger)


Chapter 20 / Surgical Hemostasis 129

Electrocautery (designed by Bovie withCushing for neurosurgery in the 1920s)

Continuous electrical current (20,000 Hz); cuts well with a decreasedability to coagulate

Intermittent electrical current (20,000 Hz); results in excellent vesselcoagulation with decreased ability to cut

What is the “Bovie”?

What is the CUT mode onthe Bovie?

What is the COAG mode onthe Bovie?

Where should a Bovie beapplied to a clamp or pick-up to coagulate a vessel?

Anywhere on the clamp/pick-up

Should you ever “blindly”place a clamp in a wound tostop bleeding?

Define the following terms:Figure-of-eight suture

No, you may injure surrounding tissuessuch as nerves

Suture ligature placed twice in the tissueprior to being tied



Surgicel®

Fibrin glue

Harmonic scalpel

Clips

Cellulose sheets—act as a framework forclotting factors/platelets to adhere to(Think: SurgiCEL � CELlulose)

Fibrinogen and thrombin sprayed simultaneously and mixed to produce afibrin “glue”

Ultrasonic scalpel that vibrates �50,000 times per second; seals vesselsand cuts tissue

Metallic clips for clipping vessels

Vessel “tied in continuity” Tie, tie, cut in between

Which antibiotics arecommonly used for anaerobic infections?

Which antibiotics arecommonly used for gram-negative infections?

Common SurgicalMedications

Chapter 21

Metronidazole, clindamycin, cefoxitin,cefotetan, imipenem, ticarcillin-clavulanicacid, Unasyn®, Augmentin®

Gentamicin and other aminoglycosides,ciprofloxacin, aztreonam, third-generationcephalosporins, sulfamethoxazole-trimethoprim

ANTIBIOTICS


Which antibiotic, if takenwith alcohol, will produce adisulfiram-like reaction?

What is the drug of choicefor treating amoebic infections?

Which antibiotic is associatedwith cholestasis?

Which antibiotic cannot begiven to children or pregnantwomen?

With which common anti-biotics must serum levels be determined?

Is rash (only) in response topenicillins a contraindicationto cephalosporins?

Describe the following medications:

Augmentin®

Unasyn®

Cefazolin (Ancef ®)

Cefoxitin (Mefoxin®)

Ceftazidime (Ceftaz®)

Clindamycin

Chapter 21 / Common Surgical Medications 131

Metronidazole (Flagyl®) (disulfiram isAntabuse®)

Metronidazole (Flagyl®)

Ceftriaxone (Rocephin®)

Ciprofloxacin (interferes with the growthplate)

Aminoglycosides and vancomycin

No, but breathing problems, urticaria,and edema in response to penicillins arecontraindications to the cephalosporins

Amoxicillin and clavulanic acid

Ampicillin and sulbactam

First-generation cephalosporin; surgicalprophylaxis for skin flora

Second-generation cephalosporin; usedfor mixed aerobic/anaerobic infections;effective against Bacteroides fragilis andanaerobic bacteria

Third-generation cephalosporin; strongactivity against Pseudomonas

Strong activity against gram-negativeanaerobes such as B. fragilis; adequategram-positive activity


Gentamicin

Imipenem and cilastatin(Primaxin®)


Nafcillin (Nafcil®)

Vancomycin

Ciprofloxacin (Cipro®)

Aztreonam (Azactam®)

Amphotericin

Fluconazole (Diflucan®)

Nystatin


Aminoglycoside used to treat gram-negative bacteria; nephrotoxic, ototoxic;blood peak/trough levels should be monitored

Often used as a last resort against serious,multiresistant organisms

Usually combined with cilastin, whichinhibits renal excretion of imipenem

Has a very wide spectrum

Used for serious anaerobic infections(e.g., diverticulitis); also used to treatamebiasis; patient must abstain fromalcohol use during therapy

Antistaphylococcal penicillin commonlyused for cellulitis

Used to treat methicillin-resistantStaphylococcus aureus (MRSA); usedorally to treat C. difficile pseudomembra-nous colitis (poorly absorbed from thegut); with IV administration, peak/troughlevels should be monitored

Quinoline antibiotic with broad-spectrumactivity, especially against gram-negativebacteria, including Pseudomonas

Monobactam with gram-negative spectrum

IV antifungal antibiotic associated withrenal toxicity, hypokalemia

Antifungal agent (IV or PO) not associatedwith renal toxicity

PO and topical antifungal


What are the side effects?

What are its uses?

Can steroids be stoppedabruptly?

Which patients need stress-dose steroids beforesurgery?

What is the “stress dose” forsteroids?

Which vitamin helpscounteract the deleteriouseffects of steroids on woundhealing?


Adrenal suppression, immunosuppression,weight gain with central obesity, cushingoidfacies, acne, hirsutism, purple striae,hyperglycemia, sodium retention/hypokalemia, hypertension, osteopenia,myopathy, ischemic bone necrosis(avascular necrosis of the hip), GIperforations

Immunosuppression (transplant), autoimmune diseases, hormone replacement (Addison’s disease), spinalcord trauma, COPD

No, steroids should never be stoppedabruptly; always taper

Those who are on steroids, were onsteroids in the past year, have suspectedhypoadrenalism, or are about to undergoadrenalectomy

100 mg of hydrocortisone IV every 8 hours and then taper (adults)

Vitamin A

STEROIDS

HEPARIN

Describe the action.

What are its uses?

What are the side effects?

What reverses the effects?

Heparin binds with and activatesantithrombin III

Prophylaxis/treatment—DVT, pulmonaryembolism, stroke, atrial fibrillation, acutearterial occlusion, cardiopulmonary bypass

Bleeding complications; can cause thrombocytopenia

Protamine IV (1:100, 1 mg of protamineto every 100 units of heparin)


What laboratory test shouldbe used to follow effect?

What is the standard lab target for therapeuticheparinization?

Who is at risk for a protamineanaphylactic reaction?

What is the half-life ofheparin?

How long before surgeryshould it be discontinued?

Does heparin dissolve clots?

What is LMWH?

What laboratory test do youneed to follow LMWH?


aPTT—activated partial thromboplastintime

1.5–2.5 times control or measuredantifactor X level

Patients with type 1 diabetes mellitus, s/p prostate surgery

�90 minutes (1–2 hours)

From 4 to 6 hours preoperatively

No; it stops the progression of clotformation and allows the body’s own fibrinolytic systems to dissolve the clot

Low Molecular Weight Heparin

None, except in children, patients withobesity, and those with renal failure,which is the major advantage of LMWH(check factor X levels)

WARFARIN (COUMADIN®)

ACRONYM basis for name?

Describe its action.

What are its uses?

What are its associated risks?

What laboratory test shouldbe used to follow its effect?

What is INR?

Wisconsin Alumni Research Foundation

Inhibits vitamin K–dependent clottingfactors II, VII, IX, and X, (i.e., 2, 7, 9and 10 [Think: 2 � 7 � 9 and 10]),produced in the liver

Long-term anticoagulation (PO)

Bleeding complications, teratogenic inpregnancy, skin necrosis, dermatitis

PT (prothrombin time) as reported as INR

International Normalized Ratio


What is the classic therapeuticINR?

What is the half-life ofeffect?

What reverses the action?

How long before surgeryshould it be discontinued?

How can warfarin cause skinnecrosis when first started?


INR of 2–3

40 hours; thus, it takes about 2 days toobserve a change in the PT

Cessation, vitamin K, fresh-frozenplasma (in emergencies)

From 3 to 5 days preoperatively and IVheparin should be begun; heparin shouldbe discontinued from 4 to 6 hours preoperatively and can be restarted postoperatively; Coumadin® can berestarted in a few days

Initially depressed protein C and S result ina HYPERcoagulable state! Avoid by usingheparin concomitantly when starting

MISCELLANEOUS AGENTS

Describe the followingdrugs:

Sucralfate (Carafate®)

Cimetidine (Tagamet®)

Ranitidine (Zantac®)

Ondansetron (Zofran®)

PPI

Promethazine(Phenergan®)

Treats peptic ulcers by forming an acid-resistant barrier; binds to ulcer craters;needs acid to activate and thus shouldnot be used with H2 blockers

H2 blocker (ulcers/gastritis)

H2 blocker (ulcers/gastritis)

AntinauseaAnti-emetic

Proton-Pump Inhibitor: Gastric acid–secretion inhibitor; works by inhibitingthe K�/H�-ATPase (e.g., omeprazole[Prilosec®])

Acute antinausea agent; used postoperatively


Metoclopramide (Reglan®)

Haloperidol (Haldol®)

Ondansetron (Zofran®)

Albumin

Albuterol

Octreotide

Famotidine (Pepcid®)

Aspirin

Furosemide (Lasix®)

Dantrolene (Dantrium®)

Misoprostol (Cytotec®)

What is an antibiotic optionfor colon/appendectomy coverage if the patient isallergic to penicillin?

If the patient does notrespond to a dose offurosemide, should the dosebe repeated, increased, ordecreased?


Increases gastric emptying with increasein LES pressure; dopamine antagonist;used in diabetic gastroparesis and to helpmove feeding tubes past the pylorus

Sedative/antipsychotic (side effects �extrapyramidal symptoms, QT prolongation)

Anti-emetic/serotonin receptor blocker

5% albumin25% albumin—draws extravascular fluid

into intravascular space by oncoticpressure

Inhaled 2 agonist (bronchodilator)

Somatostatin analog

H2 blocker

Irreversibly inhibits platelets byirreversibly inhibiting cyclooxygenase

Loop diuretic (watch for hypokalemia)

Medication used to treat malignanthyperthermia

Prostaglandin E1 analogGastroduodenal mucosal protection

1. IV ciprofloxacin (Cipro) AND2. IV clindamycin or IV Flagyl

Dose should be doubled if there is noresponse to the initial dose


What medication is used totreat promethazine-induceddystonia?

Which medication is classically associated withmesenteric ischemia?

What type of antihypertensivemedication is contraindicatedin patients with renal arterystenosis?

Does acetaminophen(Tylenol®) inhibit platelets?

What medications are usedto stop seizures?

List examples of preopantibiotics for:

Vascular prosthetic graft

Appendectomy

Colon surgery


Diphenhydramine hydrochloride IV(Benadryl®)

Digitalis

ACE inhibitors

No

Benzodiazepines (e.g., lorazepam[Ativan®]); phenytoin (Dilantin®)

Ancef ® (gram-positive coverage)

Cefoxitin, Unasyn® (anaerobic coverage)

Cefoxitin, Unasyn® (anaerobic coverage)

NARCOTICS

What are common postoper-ative IV narcotics?

What is Percocet®

What is Demerol’s claim tofame?

What are side effects of narcotics?

Morphine (most common), meperidine(Demerol®), fentanyl, Percocet®, Dilaudid®

PO narcotic pain reliever with acetaminophen and oxycodone

Used commonly with acute pancreatitis/biliary pathology because classically morphine may cause sphincter of Oddispasm/constriction

Respiratory depression, hypotension,itching, bradycardia, nausea


What is it?

What is the etiology?

ComplicationsChapter 22

Collapse of the alveoli

Inadequate alveolar expansion (e.g., poorventilation of lungs during surgery, inability to fully inspire secondary topain), high levels of inspired oxygen

ATELECTASIS

What is the danger ofprolonged use of Demerol?

What medication reversesthe effects of narcotic overdose?

Narcotic used to decreasepostoperative shivering?


Accumulation of metabolite norme-peridine (especially with renal/hepaticdysfunction), which may result in overse-dation, hallucinations, and seizures!

Naloxone (Narcan®), 0.4 mg IV

Demerol®

MISCELLANEOUS

What reverses the effects ofbenzodiazepines?

What is Toradol®?

What are the risks ofToradol®?

Why give patients IV Ciproif they are eating a regulardiet?

What is clonidine“rebound”?

Flumazenil (Romazicon®), 0.2 mg IV

Ketorolac � IV NSAID

GI bleed, renal injury, platelet dysfunction

No reason—500 mg of Cipro PO givesthe same serum level as 400 mg CiproIV! And PO is much cheaper!

Abruptly stopping clonidine can cause the patient to have severe “rebound”hypertension (also seen with -blockers)


Chapter 22 / Complications 139

POSTOPERATIVE RESPIRATORY FAILURE

What is it?

What is the differential diagnosis?


What is the initial workup?

What are the indications forintubation and ventilation?

Respiratory impairment with increasedrespiratory rate, shortness of breath, dyspnea

Hypovolemia, pulmonary embolism,administration of supplemental O2 to a patient with COPD, atelectasis, pneumonia, aspiration, pulmonaryedema, abdominal compartment syndrome,pneumothorax, chylothorax, hemothorax,narcotic overdose, mucous plug

Supplemental O2, chest PT; suctioning,intubation, and ventilation if necessary

ABG, CXR, EKG, pulse oximetry, andauscultation

Cannot protect airway (unconscious),excessive work of breathing, progressivehypoxemia (PaO2 �55 despite supplemental O2), progressive acidosis(pH �7.3 and PCO2 �50), RR �35

What are the signs?

What are the risk factors?

What is its claim to fame?

What prophylactic measurescan be taken?


Fever, decreased breath sounds withrales, tachypnea, tachycardia, andincreased density on CXR

Chronic obstructive pulmonary disease(COPD), smoking, abdominal or thoracicsurgery, oversedation, poor pain control(patient cannot breathe deeplysecondary to pain on inspiration)

Most common cause of fever during PODs #1 to #2

Preoperative smoking cessation, incentivespirometry, good pain control

Postoperative incentive spirometry,deep breathing, coughing, early ambulation, NT suctioning, and chest PT


What are the possible causesof postoperative pleuraleffusion?

What is the treatment ofpostoperative wheezing?

Why may it be dangerous togive a patient with chronicCOPD supplemental oxygen?


Fluid overload, pneumonia, anddiaphragmatic inflammation with possiblesubphrenic abscess formation

Albuterol nebulizer

This patient uses relative hypoxia for respiratory drive, and supplemental O2

may remove this drive!

PULMONARY EMBOLISM

What is a pulmonaryembolism (PE)?

What is DVT?

Is DVT more common in theright or left iliac vein?

What are the signs/symptomsof DVT?

What is Homan’s sign?

What test is used to evaluatefor DVT?

What is Virchow’s triad?

What are the risk factors forDVT and PE?

DVT that embolizes to the pulmonaryarterial system

Deep Venous Thrombosis—a clot formingin the pelvic or lower extremity veins

Left is more common (4:1) because theaortic bifurcation crosses and possiblycompresses the left iliac vein

Lower extremity pain, swelling, tenderness,Homan’s sign, PE

Up to 50% can be asymptomatic!

Calf pain with dorsiflexion of the footseen classically with DVT, but actuallyfound in fewer than one third of patientswith DVT

Duplex ultrasonography

1. Stasis2. Endothelial injury3. Hypercoagulable state (risk factors for

thrombosis)

Postoperative status, multiple trauma,paralysis, immobility, CHF, obesity, BCP/tamoxifen, cancer, advanced age,polycythemia, MI, HIT syndrome,hypercoagulable state (protein C/protein Sdeficiency)


What are the signs/symptomsof PE?

What are the associated labfindings?

Which diagnostic tests areindicated?

What are the associatedCXR findings?

What are the associatedEKG findings?

What is a “saddle” embolus?

What is the treatment if thepatient is stable?

What is a Greenfield filter?


Shortness of breath, tachypnea, hypotension, CP, occasionally fever, loudpulmonic component of S2, hemoptysiswith pulmonary infarct

ABG—decreased PO2 and PCO2

(from hyperventilation)

CT angiogram, V-Q scan (ventilation-perfusion scan), pulmonary angiogram isthe gold standard

1. Westermark’s sign (wedge-shaped areaof decreased pulmonary vasculatureresulting in hyperlucency)

2. Opacity with base at pleural edge frompulmonary infarction

�50% are abnormal; classic finding is corpulmonale (S1Q3T3 RBBB and right-axisdeviation); EKG most commonly showsflipped T waves or ST depression

PE that “straddles” the pulmonary arteryand is in the lumen of both the right andleft pulmonary arteries

Anticoagulation (heparin followed bylong-term [3–6 months] Coumadin®) orGreenfield filter

Metallic filter placed into IVC via jugularvein to catch emboli prior to lodging inthe pulmonary artery


ASPIRATION PNEUMONIA

Where did Dr. Greenfield getthe idea for his IVC filter?

When is a Greenfield filterindicated?

What is the treatment if thepatient’s condition is unstable?

What is the Trendelenburgoperation?

What is a “retrievable” IVCfilter?

What percentage of retrievable IVC filter areactually removed?

What prophylactic measurescan be taken for DVT/PE?


Oil pipeline filters!

If anticoagulation is contraindicated orpatient has further PE on adequate anticoagulation or is high risk (e.g., pelvicand femur fractures)

Consider thrombolytic therapy; consultthoracic surgeon for possible Trendelenburg operation; considercatheter suction embolectomy

Pulmonary artery embolectomy

IVC filter that can be removed(“retrieved”)

Only about 20%

LMWH (Lovenox®) 40 mg SQ QD; or30 mg SQ b.i.d.; subQ heparin (5000 units subQ every 8 hrs; must be started preoperatively), sequential compressiondevice BOOTS beginning in O.R. (oftenused with subQ heparin), early ambulation

What is it?



Pneumonia following aspiration of vomitus

Intubation/extubation, impairedconsciousness (e.g., drug or EtOH overdose), dysphagia (esophageal disease),nonfunctioning NGT, Trendelenburgposition, emergent intubation with fullstomach, gastric dilatation

Respiratory failure, CP, increased sputumproduction, fever, cough, mental statuschanges, tachycardia, cyanosis, infiltrateon CXR


What are the associatedCXR findings?

Which lobes are commonlyinvolved?

Which organisms arecommonly involved?



What is Mendelson’ssyndrome?

Are prophylatic antibioticsindicated for aspirationpneumonitis?


Early—fluffy infiltrate or normal CXRLate—pneumonia, ARDS

Supine—RULSitting/semirecumbent—RLL

Community acquired—gram-positive/mixed

Hospital/ICU—gram-negative rods

CXR, sputum, Gram stain, sputumculture, bronchoalveolar lavage

Bronchoscopy, antibiotics if pneumoniadevelops, intubation if respiratory failureoccurs, ventilation with PEEP if ARDSdevelops

Chemical pneumonitis secondary to aspiration of stomach contents (i.e., gastric acid)

NO

What are possible NGT complications?

Aspiration-pneumonia/atelectasis (especially if NGT is clogged)

SinusitisMinor UGI bleedingEpistaxisPharyngeal irritation, gastric irritation

GASTROINTESTINAL COMPLICATIONS

GASTRIC DILATATION




Abdominal surgery, gastric outletobstruction, splenectomy, narcotics

Abdominal distension, hiccups,electrolyte abnormalities, nausea

NGT decompression


What is it?

What is the initialtreatment?

Malabsorption and diarrhea resulting fromextensive bowel resection (120 cm ofsmall bowel remaining)

TPN early, followed by many small mealschronically

SHORT BOWEL SYNDROME

POSTOPERATIVE SMALL BOWEL OBSTRUCTION (SBO)/ILEUS

What causes SBO? Adhesions (most of which resolve spontaneously), incarcerated hernia(internal or fascial/dehiscence)


POSTOPERATIVE PANCREATITIS

What is it?

What lab tests areperformed?


Pancreatitis resulting from manipulationof the pancreas during surgery or lowblood flow during the procedure (i.e., cardiopulmonary bypass), gallstones,hypercalcemia, medications, idiopathic

Amylase and lipase

Same as that for the other causes of pancreatitis (e.g., NPO, aggressive fluidresuscitation, � NGT PRN)

CONSTIPATION

What are the postoperativecauses?


What is OBR?

Narcotics, immobility

OBR

Ortho Bowel Routine: docusate sodium(daily), dicacodyl suppository if no bowelmovement occurs, Fleet® enema if suppository is ineffective

What do you do if you havea patient with high NGToutput?

Check high abdominal x-ray and, if theNGT is in duodenum, pull back the NGTinto the stomach



JAUNDICE

What are the causes of thefollowing types of postoperative jaundice:

Prehepatic

Hepatic

Posthepatic

What blood test results wouldsupport the assumption thathemolysis was causing jaundice in a patient?

Hemolysis (prosthetic valve), resolvinghematoma, transfusion reaction, postcardiopulmonary bypass, blood transfusions (decreased RBC complianceleading to cell rupture)

Drugs, hypotension, hypoxia, sepsis,hepatitis, “sympathetic” hepaticinflammation from adjacent right lowerlobe infarction of the lung or pneumonia,preexisting cirrhosis, right-sided heartfailure, hepatic abscess, pylephlebitis(thrombosis of portal vein), Gilbertsyndrome, Crigler-Najjar syndrome,Dubin-Johnson syndrome, fatty infiltratefrom TPN

Choledocholithiasis, stricture, cholangitis,cholecystitis, biliary-duct injury, pancreatitis, sclerosing cholangitis, tumors(e.g., cholangiocarcinoma, pancreatic cancer, gallbladder cancer, metastases), biliary stasis (e.g., ceftriaxone [Rocephin®])

Decreased—Haptoglobin, HctIncreased—LDH, reticulocytesAlso, fragmented RBCs on a peripheral

smear

What causes ileus?

What are the signs of resolving ileus/SBO?

What is the order of recoveryof bowel function afterabdominal surgery?

When can a postoperativepatient be fed through a J-tube?

Laparotomy, hypokalemia or narcotics,intraperitoneal infection

Flatus PR, stool PR

First—small intestineSecond—stomachThird—colon

From 12 to 24 postoperative hoursbecause the small intestine recovers function first in that period


What is it?

With what conditions is itassociated?


How is the diagnosis made?

What is the medicaltreatment?

Delivery of hyperosmotic chyme to thesmall intestine causing massive fluidshifts into the bowel (normally the stomach will decrease the osmolality ofthe chyme prior to its emptying)

Any procedure that bypasses the pylorusor compromises its function (i.e.,gastroenterostomies or pyloroplasty); thus,“dumping” of chyme into small intestine

Postprandial diaphoresis, tachycardia,abdominal pain/distention, emesis,increased flatus, dizziness, weakness

History; hyperosmolar glucose load willelicit similar symptoms

Small, multiple, low-fat/carbohydratemeals that are high in protein content;also, avoidance of liquids with meals toslow gastric emptying; surgery is a lastresort

DUMPING SYNDROME


BLIND LOOP SYNDROME

What is it?


What are the surgical causesof B12 deficiency?

Bacterial overgrowth in the small intestine

Anything that disrupts the normal flow ofintestinal contents (i.e., causes stasis)

Blind loop syndrome, gastrectomy(decreased secretion of intrinsic factor)and excision of the terminal ileum (site ofB12 absorption)

POSTVAGOTOMY DIARRHEA

What is it?

What is the cause?

Diarrhea after a truncal vagotomy

It is thought that after truncal vagotomy,a rapid transport of bile salts to the colonresults in osmotic inhibition of waterabsorption in the colon, leading to diarrhea



ENDOCRINE COMPLICATIONS

DIABETIC KETOACIDOSIS (DKA)

What is the surgicaltreatment?

What is a reversed jejunalinterposition loop?

Conversion to Roux-en-Y (� reversedjejunal interposition loop)

Segment of jejunum is cut and thenreversed to allow for a short segment ofreversed peristalsis to slow intestinaltransit

What is it?

What are the signs of DKA?

What are the associated labvalues?


What electrolyte must bemonitored closely in DKA?

What must you rule out in adiabetic with DKA?

Deficiency of body insulin, resulting inhyperglycemia, formation of ketoacids,osmotic diuresis, and metabolic acidosis

Polyuria, tachypnea, dehydration, confusion, abdominal pain

Elevated glucose, increased anion gap,hypokalemia, urine ketones, acidosis

Insulin drip, IVF rehydration, K�

supplementation, � bicarbonate IV

Potassium and HYPOkalemia (Remember correction of acidosis andGLC/insulin drive K� into cells and aretreatment for HYPERkalemia!)

Infection (perirectal abscess is classicallymissed!)

ADDISONIAN CRISIS

What is it?

How can you rememberwhat it is?

What is the cause?

Acute adrenal insufficiency in the face of a stressor (i.e., surgery, trauma, infection)

Think: ADDisonian � ADrenal Down

Postoperatively, inadequate cortisolrelease usually results from steroidadministration in the past year



What is its clinical claim toinfamy?

Which lab values are classic?

How can the electrolyteswith ADDisonian � ADrenalDown be remembered?

Tachycardia, nausea, vomiting, diarrhea,abdominal pain, � fever, progressivelethargy, hypotension, eventual hypovolemic shock

Tachycardia and hypotension refractoryto IVF and pressors!

Decreased Na�, increased K� (secondaryto decreased aldosterone)

Think: DOWN the alphabeticalelectrolyte stairs

J

L

M

O

K+

Na+


What is fludrocortisone?

IVFs (D5 NS), hydrocortisone IV, fludrocortisone PO

Mineralocorticoid replacement(aldosterone)

SIADH

What is it?

What does ADH do?

Syndrome of Inappropriate AntiDiureticHormone (ADH) secretion (think ofinappropriate increase in ADH secretion)

ADH increases NaCl and H2O resorptionin the kidney, increasing intravascular volume (released from posteriorpituitary)






How can the serum sodiumlevel in SIADH beremembered?


Mainly lung/CNS: CNS trauma, oat-celllung cancer, pancreatic cancer, duodenalcancer, pneumonia/lung abscess, increasedPEEP, stroke, general anesthesia, idio-pathic, postoperative, morphine

Low sodium, low chloride, low serum osmolality; increased urine osmolality

Remember, SIADH � Sodium Is AlwaysDown Here � hyponatremia

Treat the primary cause and restrict fluidintake

DIABETES INSIPIDUS (DI)

What is it?

What is the source of ADH?

What are the two majortypes?

What is the mechanism ofthe two types?

What are the classic causesof central DI?

What are the classic causesof nephrogenic DI?

What lab values are associated with DI?


Failure of ADH renal fluid conservationresulting in dilute urine in large amounts(Think: DI � Decreased ADH)

POSTERIOR pituitary

1. Central (neurogenic) DI2. Nephrogenic DI

1. Central DI � decreased production ofADH

2. Nephrogenic DI � decreased ADHeffect on kidney

BRAIN injury, tumor, surgery, and infection

Amphotericin B, hypercalcemia, andchronic kidney infection

HYPERnatremia, decreased urinesodium, decreased urine osmolality, andincreased serum osmolality

Fluid replacement; follow NA� levels andurine output; central DI warrantsvasopressin; nephrogenic DI mayrespond to thiazide diuretics


What are the arterial linecomplications?

What is an Allen test?

What are the commoncauses of dyspnea followingcentral line placement?

What is the differential diagnosis of postoperativechest pain?

What is the differential diagnosis of postoperativeatrial fibrillation?

Infection; thrombosis, which can lead tofinger/hand necrosis; death/hemorrhagefrom catheter disconnection (rememberto perform and document the Allen testbefore inserting an arterial line or obtaining a blood gas sample)

Measures for adequate collateral blood flowto the hand via the ulnar artery:

Patient clenches fist; clinicianoccludes radial and ulnar arteries;patient opens fist and clinicianreleases only the ulnar artery

If the palm exhibits immediate strongblush upon release of ulnar artery,then ulnar artery can be assumedto have adequate collateral flow ifthe radial artery were to thrombose

Pneumothorax, pericardial tamponade,carotid puncture (which can cause ahematoma that compresses the trachea),air embolism

MI, atelectasis, pneumonia, pleurisy,esophageal reflux, PE, musculoskeletalpain, subphrenic abscess, aortic dissection,pneumo/chyle/hemothorax, gastritis

Fluid overload, PE, MI, pain (excesscatecholamines), atelectasis, pneumonia,digoxin toxicity, hypoxemia, thyrotoxicosis,hypercapnia, idiopathic, acidosis,electrolyte abnormalities

MYOCARDIAL INFARCTION (MI)

What is the most dangerousperiod for a postoperativeMI following a previous MI?

What are the risk factors forpostoperative MI?

Six months after an MI

History of MI, angina, Qs on EKG, S3,JVD, CHF, aortic stenosis, advanced age,extensive surgical procedure, MI within 6 months, EKG changes


CARDIOVASCULAR COMPLICATIONS



How do postoperative MIspresent?

What EKG findings are associated with cardiacischemia/MI?

Which lab tests areindicated?

What is the treatment ofpostoperative MI?

How can the treatment ofpostoperative MI be remembered?

When do postoperative MIsoccur?

Often without chest painNew onset CHF, new onset cardiac

dysrhythmia, hypotension, chestpain, tachypnea, tachycardia, nausea/vomiting, bradycardia, neck pain, armpain

Flipped T waves, ST elevation, STdepression, dysrhythmias (e.g., new onset A fib, PVC, V tach)

Troponin I, cardiac isoenzymes (elevatedCK mb fraction)

Nitrates (paste or drip), as toleratedAspirinOxygenPain control with IV morphine-blocker, as toleratedHeparin (possibly; thrombolytics are

contraindicated in the postoperativepatient)

ICU monitoring

“BEMOAN”:BEta-blocker (as tolerated)MorphineOxygenAspirinNitrates

Two thirds occur on PODs #2 to #5 (often silent and present with dyspneaor dysrhythmia)

POSTOPERATIVE CVA

What is a CVA?


What is the workup?

CerebroVascular Accident (stroke)

Aphasia, motor/sensory deficits usuallylateralizing

Head CT scan; must rule out hemorrhageif anticoagulation is going to be used;carotid Doppler ultrasound study to evaluate for carotid occlusive disease



What is the perioperativeprevention?

ASA, � heparin if feasible postoperativelyThrombolytic therapy is not usually postoperative option

Avoid hypotension; continue aspirin ther-apy preoperatively in high-risk patients iffeasible; preoperative carotid Dopplerstudy in high-risk patients

MISCELLANEOUS

POSTOPERATIVE RENAL FAILURE

What is it?

Define the following terms:Anuria

Oliguria


Prerenal

Renal

Postrenal

What is the workup?

What is FENa?

Increase in serum creatinine anddecrease in creatinine clearance; usuallyassociated with decreased urine output

�50 cc urine output in 24 hours

Between 50 cc and 400 cc of urineoutput in 24 hours

Inadequate blood perfusing kidney:inadequate fluids, hypotension, cardiacpump failure (CHF)

Kidney parenchymal dysfunction:acute tubular necrosis, nephrotoxic contrast or drugs

Obstruction to outflow of urine fromkidney: Foley catheter obstruction/stone,ureteral/urethral injury, BPH, bladderdysfunction (e.g., medications, spinalanesthesia)

Lab tests: electrolytes, BUN, Cr, urinelytes/Cr, FENa, urinalysis, renal ultrasound

Fractional Excretion of Na� (sodium)




What is the formula forFENa?

Define the lab results withprerenal vs renal failure:

BUN/Cr ratio

Specific gravity

FENa

Urine Na� (sodium)

Urine osmolality

What are the indications fordialysis?

“YOU NEED PEE” � UNP(UNa� � Pcr / PNa� � Ucr) � 100

(U � urine, cr � creatinine, Na� �sodium, P � plasma)

Prerenal: �20:1Renal: �20:1

Prerenal: �1.020 (as the body tries tohold on to fluid)

Renal: �1.020 (kidney has decreasedability to concentrate urine)

Prerenal: �1%Renal: �2%

Prerenal: �20Renal: �40

Prerenal: �450Renal: �300 mOsm/kg

Fluid overload, refractory hyperkalemia,BUN �130, acidosis, uremic complication(encephalopathy, pericardial effusion)

DIC

What is it?


Activation of the coagulation cascadeleading to thrombosis and consumptionof clotting factors and platelets and activation of fibrinolytic system (fibrinolysis), resulting in bleeding

Tissue necrosis, septic shock, massivelarge-vessel coagulation, shock, allergicreactions, massive blood transfusion reaction, cardiopulmonary bypass, cancer,obstetric complications, snake bites,trauma, burn injury, prosthetic material,liver dysfunction





Acrocyanosis or other signs of thrombosis,then diffuse bleeding from incision sites,venipuncture sites, catheter sites, ormucous membranes

Increased fibrin-degradation products,elevated PT/PTT, decreased platelets,decreased fibrinogen (level correlates wellwith bleeding), presence of schistocytes(fragmented RBCs), increased D-dimer

Removal of the cause; otherwise supportive: IVFs, O2, platelets, FFP,cryoprecipitate (fibrin), Epsilon-aminocaproic acid, as needed in predominantly thrombotic cases

Use of heparin is indicated in cases thatare predominantly thrombotic withantithrombin III supplementation asneeded

ABDOMINAL COMPARTMENT SYNDROME

What is it?


How to measure intra-abdominal pressure?

What is normal intra-abdominal pressure?

What intra-abdominal pressure indicates need fortreatment?


Increased intra-abdominal pressure usually seen after laparotomy or aftermassive IVF resuscitation (e.g., burnpatients)

Tight distended abdomen, decreasedurine output, increased airway pressure,increased intra-abdominal pressure

Read intrabladder pressure (Foleycatheter hooked up to manometry afterinstillation of 50–100 cc of water)

�15 mm Hg

�25 mm Hg, especially if signs of compromise

Release the pressure by placing drainand/or decompressive laparotomy (leaving fascia open)




What is it?

How is it diagnosed?


With massive bladder distention, how much urinecan be drained immediately?

What is the classic sign ofurinary retention in anelderly patient?

Enlarged urinary bladder resulting frommedications or spinal anesthesia

Physical exam (palpable bladder), bladderresidual volume upon placement of aFoley catheter

Foley catheter

Most would clamp after 1 L and thendrain the rest over time to avoid a vasovagal reaction

Confusion

URINARY RETENTION

WOUND INFECTION



What is fascial dehiscence?


Erythema, swelling, pain, heat (rubor,tumor, dolor, calor)

Open wound, leave open with wet to drydressing changes, antibiotics if cellulitispresent

Acute separation of fascia that has beensutured closed

Bring back to the O.R. emergently forreclosure of the fascia

WOUND HEMATOMA

What is it?


Collection of blood (blood clot) in operative wound

Acute: Remove with hemostasisSubacute: Observe (heat helps resorption)

What is a “Bogata Bag”? Sheet of plastic (empty urology irrigationbag or IV bag) used to temporarily closethe abdomen to allow for more intra-abdominal volume



What is the incidence ofbloody diarrhea?

What classic antibioticcauses C. difficile?



What is the indication foremergent colectomy?

Diarrhea, fever, hypotension/tachycardia

10%

Clindamycin (but almost all antibioticscan cause it)

C. diff toxin in stool, fecal WBC, flex sig(see a mucous pseudomembrane inlumen of colon � hence the name)

1. Flagyl (PO or IV)2. PO vancomycin if refractory to Flagyl

Toxic megacolon

PSEUDOMEMBRANOUS COLITIS

What can causehypotension?

Common Causes of WardEmergencies

Chapter 23

Hypovolemia (iatrogenic, hemorrhage),sepsis, MI, cardiac dysrhythmia, hypoxia,false reading (e.g., wrong cuff/arterialline twist or clot), pneumothorax, PE,cardiac tamponade, medications (e.g.,morphine)


WOUND SEROMA

What is it?


Postoperative collection of lymph andserum in the operative wound

Needle aspiration, repeat if necessary(prevent with closed drain)


Chapter 23 / Common Causes of Ward Emergencies 157

How do you act?

What are the commoncauses of postoperativehypertension?

What can cause hypoxia/shortness of breath?

How do you act?

What can cause mental status change?

What are the signs ofalcohol withdrawal?

What are the causes oftachycardia?

ABCs, examine, recheck BP, IV access,IV bolus, labs (e.g., HCT), EKG, pulseox/vital signs monitoring, CXR, supple-mental oxygen, check medications/history,give IV antibiotics “stat” if sepsis likely,compress all bleeding sites

Pain (from catecholamine release), anxiety,hypercapnia, hypoxia (which may alsocause hypotension), preexisting condition,bladder distention

Atelectasis, pneumonia, mucous plug,pneumothorax, PE, MI/dysrhythmia,venous blood in ABG syringe, SAT%machine malfunction/probe malposition,iatrogenic (wrong ventilator settings),severe anemia/hypovolemia, low cardiac output, CHF, ARDS, fluid overload

ABCs, physical exam, vital signs/pulseoximetry monitoring, supplemental oxygen, IV access, ABG, EKG, CXR

Hypoxia until ruled out, hypotension(e.g., cardiogenic shock), hypovolemia,iatrogenic (narcotics/benzodiazepines),drug reaction, alcohol withdrawal, drugwithdrawal, seizure, ICU psychosis, CVA, sepsis, metabolic derangements, intracranial bleeding, urinary retentionin the elderly

Confusion, tachycardia/autonomic instability, seizure, hallucinations

Hypovolemia/third-spacing, pain, alcohol withdrawal, anxiety/agitation, urinary retention, cardiac dysrhythmia(e.g., sinoventricular tachycardia, atrial fibrillation with rapid rate), MI, PE, -blocker withdrawal, anastomotic leak


What are the causes ofdecreased urine output?

How do you act initially in acase of decreased urine output?

Hypovolemia, urinary retention, Foleycatheter malfunction, cardiac failure, MI, acute tubular necrosis (ATN),ureteral/urethral injury, abdominal compartment syndrome, sepsis

Examine, vital signs, check or place Foleycatheter, irrigate Foley catheter, IV fluidbolus

What is the most commoncause of fever in the first 48 hours postop?

What is absorption atelectasis?

What is incentivespirometry?

SurgicalRespiratory Care

Chapter 24

Atelectasis

Elevated inhaled oxygen replaces thenitrogen in the alveoli resulting in collapseof the air sac (atelectasis); nitrogen keepsalveoli open by “stenting” them

Patient can document tidal volume andwill have an “incentive” to increase it

hrf '04



Chapter 24 / Surgical Respiratory Care 159

What is oxygen-inducedhypoventilation?

Why give supplemental oxygen to a patient with apneumothorax?

What is a nonrebreathermask?

Some patients with COPD have low oxygen as the main stimulus for the respiratory drive; if given supplementaloxygen, they will have a decreased respiratory drive and hypoventilation

Pneumothorax is almost completely nitrogen—thus increasing the oxygen inthe alveoli increases the nitrogen gradientand results in faster absorption of thepneumothorax!

100% oxygen with a reservoir bag

Exhalationvalveopens

Reservoir bagexpands fully

Valvecloses

Why do nonrebreathermasks have a “reservoir”bag?

What is the maximumoxygen FiO2 delivered by anonrebreather mask?

How do you figure out thePaO2 from an O2 sat?

Inhalation flow will exceed the deliveryrate of the tubing and the bag allows forextra oxygen stores

�80% to 90%

PaO2 of 40, 50, 60 roughly equals 70, 80,90 in sats


What is an oxygen nasal cannula?

Oxygen delivered via tubing with prongsinto nares

How much do you increasethe FiO2 by each liter addedto the nasal cannula?

What is the max effectiveflow for a nasal cannula?

�3%

6 liters

Surgical NutritionChapter 25What is the motto of surgicalnutrition?

What are the normal dailydietary requirements foradults of the following:

Protein

Calories

“If the gut works, use it”

1 g/kg/day

30 kcal/kg/day



Chapter 25 / Surgical Nutrition 161

By how much is basalenergy expenditure (BEE)increased or decreased inthe following cases:

Severe head injury

Severe burns

What are the calorie contentsof the following substances:

Fat

Protein

Carbohydrate

What is the formula for converting nitrogen requirement/loss to proteinrequirement/loss?

What is RQ?

What is the normal RQ?

What can be done todecrease the RQ?

What dietary change can bemade to decrease CO2 pro-duction in a patient in whomCO2 retention is a concern?

What lab tests are used tomonitor nutritional status?

Where is iron absorbed?

Increased �1.7 �

Increased �2–3 �

9 kcal/g

4 kcal/g

4 kcal/g

Nitrogen � 6.25 � protein

Respiratory Quotient: ratio of CO2

produced to O2 consumed

0.8

More fat, less carbohydrates

Decrease carbohydrate calories andincrease calories from fat

Blood levels of:Prealbumin (t1/2�2–3 days)—acute

change determinationTransferrin (t1/2�8–9 days)Albumin (t1/2�14–20 days)—more

chronic determinationTotal lymphocyte count AnergyRetinol-binding protein (t1/2�12

hours)

Duodenum (some in proximal jejunum)


Where is vitamin B12absorbed?

What are the surgical causesof vitamin B12 deficiency?

Where are bile saltsabsorbed?

Where are fat-solublevitamins absorbed?

Which vitamins are fat soluble?

What are the signs of thefollowing disorders:

Vitamin A deficiency

Vitamin B12/folatedeficiency

Vitamin C deficiency

Vitamin K deficiency

Chromium deficiency

Zinc deficiency

Fatty acid deficiency

What vitamin increases thePO absorption of iron?

What vitamin lessens thedeleterious effects ofsteroids on wound healing?

What are the common indications for totalparenteral nutrition (TPN)?

Terminal ileum

Gastrectomy, excision of terminal ileum,blind loop syndrome

Terminal ileum

Terminal ileum

K, A, D, E (“KADE”)

Poor wound healing

Megaloblastic anemia

Poor wound healing, bleeding gums

T in the vitamin K–dependent clottingfactors (II, VII, IX, and X); bleeding; elevated PT

Diabetic state

Poor wound healing, alopecia, dermatitis,taste disorder

Dry, flaky skin; alopecia

PO vitamin C (ascorbic acid)

Vitamin A

NPO �7 daysEnterocutaneous fistulasShort bowel syndromeProlonged ileus



Chapter 25 / Surgical Nutrition 163

What is TPN?

What is in TPN?

How much of each in TPN:Lipids

Protein

Carbohydrates

What are the possible complications of TPN?

What are the advantages ofenteral feeding?

What is the major nutrientof the gut (small bowel)?

What is “refeedingsyndrome”?

What are the vitaminK–dependent clotting factors?

What is an elemental tubefeed?

Where is calcium absorbed?

Total Parenteral Nutrition � IV nutrition

ProteinCarbohydratesLipids (H2O, electrolytes, minerals/vitamins,

� insulin, � H2 blocker)

20% to 30% of calories (lipid fromsoybeans, etc.)

1.7 g/kg/day (10%–20% of calories) asamino acids

50% to 60% of calories as dextrose

Line infection, fatty infiltration of theliver, electrolyte/glucose problems, pneumothorax during placement of central line, loss of gut barrier, acalculuscholecystitis, refeeding syndrome, hyperosmolality

Keeps gut barrier healthy, thought tolessen translocation of bacteria, not associated with complications of lineplacement, associated with fewerelectrolyte/glucose problems

Glutamine

Decreased serum potassium,magnesium, and phosphate afterrefeeding (via TPN or enterally) a starving patient

2, 7, 9, 10 (Think: 2 � 7 � 9, and then 10)

Very low residue tube feed in whichalmost all the tube feed is absorbed

Duodenum (actively)Jejunum (passively)


What is the major nutrientof the colon?

What must bind B12 forabsorption?

What sedative medicationhas caloric value?

Why may all the insulinplaced in a TPN bag not getto the patient?

What is the best way to deter-mine the caloric requirementsof a patient on the ventilator?

How can serum bicarbonatebe increased in patients onTPN?

What are “trophic” tubefeeds?

When should PO feedings bestarted after a laparotomy?

What is the best parameterto check adequacy of nutritional status?

Butyrate (and other short-chain fattyacids)

Intrinsic factor from the gastric parietalcells

Propofol delivers 1 kcal/cc in the form oflipid!

Insulin will bind to the IV tubing

Metabolic chart

Increase acetate (which is metabolizedinto bicarbonate)

Very low rate of tube feeds (usually10–25 cc/hr), which are thought to keepmucosa alive and healthy

Classically after flatus or stool PR (usually postoperative days 3–5)

Prealbumin


What is the definition ofshock?

What are the different types (5)?

ShockChapter 26Inadequate tissue perfusion

HypovolemicSepticCardiogenicNeurogenicAnaphylactic


Chapter 26 / Shock 165

HYPOVOLEMIC SHOCK

What is the definition?

What are the commoncauses?

What are the signs?

What are the signs/symptoms with:

Class I hemorrhage(�15% or 750 cc bloodloss)?

Class II hemorrhage(15%–30% or 750–1500 cc blood loss)?

Class III hemorrhage(30%–40% or 1500–2000 cc blood loss)?

Decreased intravascular volume

HemorrhageBurnsBowel obstructionCrush injuryPancreatitis

Early—Orthostatic hypotension, mildtachycardia, anxiety, diaphoresis, vaso-constriction (decreased pulse pressurewith increased diastolic pressure)

Late—Changed mental status, decreasedBP, marked tachycardia

Mild anxiety, normal vital signs

Normal systolic BP with decreased pulsepressure, tachycardia, tachypnea, anxiety

Tachycardia (heart rate �120), tachypnea(respiratory rate �30), decreasedsystolic BP, decreased pulse pressure,confusion

What are the signs of shock?

What are the best indicatorsof tissue perfusion?

What lab tests help assesstissue perfusion?

Pale, diaphoretic, cool skinHypotension, tachycardia, tachypneaT mental status and pulse pressurePoor capillary refillPoor urine output

Urine output, mental status

Lactic acid (elevated with inadequate tissue perfusion), base deficit, pH fromABG (acidosis associated with inadequatetissue perfusion)



Class IV hemorrhage(�40% or �2000 ccblood loss)?


How is the effectiveness oftreatment evaluated:

Bedside indicator?

Labs?

What usually causes failureof resuscitation?

Why does decreased pulsepressure occur with earlyhypovolemic shock?

What is the most commonvital sign change associatedwith early hypovolemicshock?

What type of patient does not mount a normaltachycardiac response tohypovolemic shock?

Should vasopressors beused to treat hypovolemicshock?

Should patients with hypovolemic shock be putinto the Trendelenburgposition?

Decreased systolic BP, tachycardia (heartrate �140), tachypnea (respiratory rate�35), decreased pulse pressure, confusedand lethargic, no urine output

1. Stop the bleeding2. Volume: IVF (isotonic LR) then

blood products as needed

Urine output, BP, heart rate, mental status, extremity warmth, capillary refill,body temperature

pH, base deficit, and lactate level

Persistent massive hemorrhage, requiringemergent surgical procedure

Pulse pressure (systolic–diastolic BP)decreases because of vasoconstriction,resulting in an elevated diastolic BP

Tachycardia

Patients on -blockers, spinal shock (loss of sympathetic tone), enduranceathletes

No

No



SEPTIC SHOCK


What is the specificetiology?

What factors increase thesusceptibility to septicshock?

What complications aremajor risks in septic shock?


What percentage of bloodcultures is positive inpatients with bacterial septic shock?

What are the associatedfindings?



Documented infection and hypotension

Most common—gram-negativesepticemia

Less common—gram-positive septicemia,fungus

Any mechanism that increases susceptibility to infection (e.g., trauma,immunosuppression, corticosteroids,hematologic disease, diabetes)

Multiple organ failure, DIC, death

Initial—vasodilation, resulting in warmskin and full pulses; normal urine output

Delayed—vasoconstriction and poorurine output; mental status changes;hypotension

Only about 50%!

Fever, hyperventilation, tachycardia

Early—hyperglycemia/glycosuria,respiratory alkalosis,hemoconcentration, leukopenia

Late—leukocytosis, acidosis, elevated lactic acid

(Note: Identifying organism is importantto direct treatment/antibiotics)

1. Volume (IVF)2. Antibiotics (empiric, then by cultures)3. Drainage of infection4. Pressors PRN5. Zygris® PRN



What is Zygris®? Activated protein C, shown to decreasemortality in septic shock and multipleorgan failure

CARDIOGENIC SHOCK



What are the signs/symptomson exam?

What are the associated vitalsigns/parameters?

What are the signs on CXR?


What are the last resort support mechanisms?

Cardiac insufficiency; left ventricular failure (usually), resulting in inadequatetissue perfusion

MI, papillary muscle dysfunction, massivecardiac contusion, cardiac tamponade,tension pneumothorax, cardiac valve failure

DyspneaRalesPulsus alternans (increased pulse with

greater filling following a weak pulse)Loud pulmonic component of S2

Gallop rhythm

Hypotension, decreased cardiac output,elevated CVP/wedge pressure, decreasedurine output (low renal blood flow),tachycardia (possibly)

Pulmonary edema

Based on diagnosis/mechanism:1. CHF: diuretics and afterload

reduction (e.g., ACE inhibitors),with or without pressors

2. Left ventricular failure (MI): pressors, afterload reduction

Intra-aortic balloon pump (IABP),ventricular assist device (VAD)

NEUROGENIC SHOCK



Inadequate tissue perfusion from loss ofsympathetic vasoconstrictive tone

Spinal cord injury:Complete transection of spinal cordPartial cord injury with spinal shockSpinal anesthesia



Why are heart rate and BPdecreased?

What are the associatedfindings?

What MUST be ruled out inany patient where spinalshock is suspected?


What percentage of patientswith hypotension and spinalneurologic deficits havehypotension of purely neurogenic origin?

What is spinal shock?

What is the lowest reflexavailable to the examiner?

What is the lowest level voluntary muscle?

What are the classic findingsassociated with spinal cordshock?


Hypotension and bradycardia, neurologic deficit

Loss of sympathetic tone (but hypovolemia [e.g., hemoperitoneum]must be ruled out)

Neurologic deficits suggesting cord injury

Hemorrhagic shock!

IV fluids (vasopressors reserved for hypo-tension refractory to fluid resuscitation)

About 67% (two thirds) of patients

Complete flaccid paralysis immediatelyfollowing spinal cord injury; may or maynot be associated with circulatory shock

Bulbocavernous reflex: checking for contraction of the anal sphincter uponcompression of the glans penis or clitoris

External anal sphincter

HypotensionBradycardia or lack of compensatory

tachycardia

MISCELLANEOUS

What is the acronym fortreatment options foranaphylactic shock?

“BASE”:BenadrylAminophyllineSteroidsEpinephrine



Surgical InfectionChapter 27What are the classic signs/symptoms of inflammation/infection?

Define:Bacteremia

SIRS

Sepsis

Septic shock

Cellulitis

Abscess

Superinfection

Nosocomial infection

Empiric

Prophylactic

What is the most commonnosocomial infection?

What is the most commonnosocomial infection causingdeath?

Tumor (mass � swelling/edema)Calor (heat)Dolor (pain)Rubor (redness � erythema)

Bacteria in the blood

Systemic Inflammatory ResponseSyndrome (fever, tachycardia, tachypnea,leukocytosis)

Documented infection and SIRS

Sepsis and hypotension

Blanching erythema from superficialdermal/epidermal infection (usually strepmore than staph)

Collection of pus within a cavity

New infection arising while a patient isreceiving antibiotics for the originalinfection at a different site (e.g., C. difficilecolitis)

Infection originating in the hospital

Use of antibiotic based on previous sensitivity information or previous experience awaiting culture results in an established infection

Antibiotics used to prevent an infection

Urinary tract infection (UTI)

Respiratory tract infection (pneumonia)


Chapter 27 / Surgical Infection 171

URINARY TRACT INFECTION (UTI)

What diagnostic tests areused?

What constitutes a POSITIVEurine analysis?

What number of colony-forming units (CFU)confirms the diagnosis ofUTI?

What are the commonorganisms?


What is the treatment ofbladder candidiasis?

Urinalysis, culture, urine microscopy forWBC

Positive nitrite (from bacteria)Positive leukocyte esterase (from WBC)�10 WBC/HPFPresence of bacteria (supportive)

On urine culture, classically 100,000 or105 CFU

Escherichia coli, Klebsiella, Proteus(Enterococcus, Staphylococcus aureus)

Antibiotics with gram-negative spectrum(e.g., sulfamethoxazole/trimethoprim[Bactrim™], gentamicin, ciprofloxacin,aztreonam); check culture and sensitivity

1. Remove or change Foley catheter2. Administer systemic fluconazole or

amphotericin bladder washings

CENTRAL LINE INFECTIONS

What are the signs of a central line infection?

What is the most commoncause of “catheter-relatedbloodstream infections”?

When should central linesbe changed?

What central line infusionincreases the risk ofinfection?

Unexplained hyperglycemia, fever,mental status change, hypotension,tachycardia S shock, pus, and erythemaat central line site

Coagulase-negative staphylococcus (33%),followed by enterococci, Staphylococcusaureus, gram-negative rods

When they are infected; there is NOadvantage to changing them every 7 daysin nonburn patients

Hyperal (TPN)



WOUND INFECTION (SURGICAL SITE INFECTION)

What is it?

When do these infectionsarise?



What are the most commonbacteria found in postopera-tive wound infections?

Which bacteria cause feverand wound infection in the first 24 hours after surgery?

Infection in an operative wound

Classically, PODs #5 to #7

Pain at incision site, erythema, drainage,induration, warm skin, fever

Remove skin sutures/staples, rule out fascial dehiscence, pack wound open, sendwound culture, administer antibiotics

Staphylococcus aureus (20%)Escherichia coli (10%)Enterococcus (10%)Other causes: Staphylococcus epidermidis,

Pseudomonas, anaerobes, other gram-negative organisms, Streptococcus

1. Streptococcus2. Clostridium (bronze-brown weeping

tender wound)

CLASSIFICATION OF OPERATIVE WOUNDS

What is a “clean” wound?

What is the infection rate ofa clean wound?

Elective, nontraumatic wound withoutacute inflammation; usually closed primarily without the use of drains

�1.5%

What is the treatment forcentral line infection?

When should peripheral IVshort angiocatheters bechanged?

1. Remove central line (send for culture)�/� IV antibiotics

2. Place NEW central line in a differentsite

Every 72 to 96 hours



What is a clean-contaminatedwound?

Without infection present,what is the infection rate of aclean-contaminated wound?

What is a contaminatedwound?

What is the infection rate ofa contaminated wound?

What is a dirty wound?

What is the infection rate ofa dirty wound?

What are the possible complications of woundinfections?

What factors influence thedevelopment of infections?

What patient factorsinfluence the developmentof infections?

Operation on the GI or respiratory tractwithout unusual contamination or entryinto the biliary or urinary tract

�3%

Acute inflammation, traumatic wound,GI tract spillage, or a major break in sterile technique

�5%

Pus present, perforated viscus, or dirtytraumatic wound

�33%

Fistula, sinus tracts, sepsis, abscess, suppressed wound healing, superinfection(i.e., a new infection that develops duringantibiotic treatment for the original infection), hernia

Foreign body (e.g., suture, drains, grafts)Decreased blood flow (poor delivery of

PMNs and antibiotics)Strangulation of tissues with excessively

tight suturesNecrotic tissue or excessive local tissue

destruction (e.g., too much Bovie)Long operations (�2 hrs)Hypothermia in O.R.Hematomas or seromasDead space that prevents the delivery of

phagocytic cells to bacterial fociPoor approximation of tissues

UremiaHypovolemic shockVascular occlusive statesAdvanced ageDistant area of infection


What are examples of animmunosuppressed state?

Which lab tests areindicated?


What are the indications forantibiotics after drainage ofa subcutaneous abscess?

Immunosuppressant treatmentChemotherapySystemic malignancyTrauma or burn injuryDiabetes mellitusObesityMalnutritionAIDSUremia

CBC: leukocytosis or leukopenia (as anabscess may act as a WBC sink), bloodcultures, imaging studies (e.g., CT scanto locate an abscess)

Incision and drainage—an abscess mustbe drained (Note: fluctuation is a signof a subcutaneous abscess; mostabdominal abscesses are drained percutaneously)

Antibiotics for deep abscesses

Diabetes mellitus, surrounding cellulitis,prosthetic heart valve, or an immunocom-promised state


PERITONEAL ABSCESS

What is a peritonealabscess?


What are the sites of occurrence?



Abscess within the peritoneal cavity

Postoperative status after a laparotomy,ruptured appendix, peritonitis, anyinflammatory intraperitoneal process,anastomotic leak

Pelvis, Morison’s pouch, subphrenic,paracolic gutters, periappendiceal, lesser sac

Fever (classically spiking), abdominalpain, mass

Abdominal CT scan (or ultrasound)



When should an abdominalCT scan be obtained look-ing for a postoperativeabscess?

What CT scan findings areassociated with abscess?


What is an option fordrainage of pelvic abscess?

All abscesses must bedrained except which type?

After POD #7 (otherwise, abscess willnot be “organized” and will look like anormal postoperative fluid collection)

Fluid collection with fibrous rind, gas influid collection

Percutaneous CT–guided drainage

Transrectal drainage (or transvaginal)

Amebiasis!

NECROTIZING FASCIITIS

What is it?

What are the causativeagents?



Is necrotizing fasciitis anemergency?

Bacterial infection of underlying fascia(spreads rapidly along fascial planes)

Classically, group A Streptococcuspyogenes, but most often polymicrobialwith anaerobes/gram-negative organisms

Fever, pain, crepitus, cellulitis, skin discoloration, blood blisters (hem-orrhagic bullae), weeping skin, increasedWBCs, subcutaneous air on x-ray, septicshock

IVF, IV antibiotics and aggressive earlyextensive surgical débridement, cultures,tetanus prophylaxis

YES, patients must be taken to the O.R.immediately!

CLOSTRIDIAL MYOSITIS

What is it?

What is another name forthis condition?

Clostridial muscle infection

Gas gangrene



SUPPURATIVE HIDRADENITIS

What is it?

In what three locations doesit occur?

What is the most commoncausative organism?


Infection/abscess formation in apocrinesweat glands

Perineum/buttocks, inguinal area, axillae(site of apocrine glands)

Staphylococcus aureus

AntibioticsIncision and drainage (excision of skin

with glands for chronic infections)

PSEUDOMEMBRANOUS COLITIS

What is it?


What causes the diarrhea?


Antibiotic-induced colonic overgrowth of C. difficile, secondary to loss ofcompetitive nonpathogenic bacteria thatcomprise the normal colonic flora(Note: it can be caused by any antibiotic,but especially penicillins, cephalosporins,and clindamycin)

Diarrhea (bloody in 10% of patients), � fever, � increased WBCs, � abdominalcramps, � abdominal distention

Exotoxin released by C. difficile

Assay stool for exotoxin titer; fecalleukocytes may or may not be present; on colonoscopy you may see an exudatethat looks like a membrane (hence,“pseudomembranous”)




Clostridium perfringens

Pain, fever, shock, crepitus, foul-smellingbrown fluid, subcutaneous air on x-ray

IV antibiotics, aggressive surgicaldébridement of involved muscle, tetanusprophylaxis



What is the treatment? PO metronidazole (Flagyl®; 93% sensitive)or PO vancomycin (97% sensitive);discontinuation of causative agent

Never give antiperistaltics

What are the indications forprophylactic IV antibiotics?

What must a prophylacticantibiotic cover forprocedures on the largebowel/abdominaltrauma/appendicitis?

What commonly used antibiotics offer anaerobiccoverage?

What antibiotic is used prophylactically for vascularsurgery?

When is the appropriatetime to administer prophylactic antibiotics?

Accidental wounds with heavy contamination and tissue damage

Accidental wounds requiring surgicaltherapy that has had to be delayed

Prosthetic heart valve or valve diseasePenetrating injuries of hollow

intra-abdominal organsLarge bowel resections and anastomosisCardiovascular surgery with the use of a

prosthesis/vascular proceduresPatients with open fractures (start in ER)Traumatic wounds occurring �8 hours

prior to medical attention

Anaerobes

Cefoxitin (Mefoxin®), clindamycin,metronidazole (Flagyl®), cefotetan, ampicillin-sulbactam (Unasyn®), Zosyn™,Timentin®, Imipenem®

Ancef (if patient is significantly allergic to PCN—hives/swelling/shortness ofbreath—then erythromycin orclindamycin are options)

Must be in adequate levels in the bloodstream prior to surgical incision!

PROPHYLACTIC ANTIBIOTICS



What is it?


What are the associated riskfactors?

What is the most commontime of occurrence?

What are the signs?


Infection of the parotid gland

Staphylococcus

Age older than 65 years, malnutrition,poor oral hygiene, presence of NG tube,NPO, dehydration

Usually 2 weeks postoperative

Hot, red, tender parotid gland andincreased WBCs

Antibiotics, operative drainage as necessary

MISCELLANEOUS

What is a “stitch” abscess?

Which bacteria can be foundin the stool (colon)?

Which bacteria are found ininfections from human bites?

What are the most commonICU pneumonia bacteria?

What is Fournier’sgangrene?

Does adding antibiotics toperitoneal lavage solutionlower the risk of abscess formation?

Subcutaneous abscess centered around asubcutaneous stitch, which is a “foreignbody”; treat with drainage and stitchremoval

Anaerobic—Bacteroides fragilisAerobic—Escherichia coli

Streptococcus viridans, S. aureus, Peptococcus, Eikenella (treat with Augmentin®)

Gram-negative organisms

Perineal infection starting classically inthe scrotum in patients with diabetes;treat with triple antibiotics and widedébridement—a surgical emergency!

No (“Dilution is the solution topollution”)

PAROTITIS


What is the classic finding associated with aPseudomonas infection?

What are the classic antibiotics for “triple”antibiotics?

Which antibiotic is used totreat amoeba infection?

Which bacteria commonlyinfect prosthetic materialand central lines?

What is the antibiotic ofchoice for Actinomyces?

What is a furuncle?

What is a carbuncle?

What is a felon?

What microscopic finding isassociated with Actinomyces?

What organism causestetanus?

What are the signs oftetanus?

What are the appropriateprophylactic steps intetanus-prone (dirty) injuryin the following patients:

Three previousimmunizations?


Green exudate and “fruity” smell

Ampicillin, gentamycin, and metronidazole (Flagyl®)


Staphylococcus epidermis

Penicillin G (exquisitely sensitive)

Staphylococcal abscess that forms in ahair follicle (Think: Follicle � Furuncle)

Subcutaneous staphylococcal abscess(usually an extension of a furuncle), mostcommonly seen in patients with diabetes(i.e., rule out diabetes)

Infection of the finger pad (Think: Felon �Finger printing)

Sulfur granules

Clostridium tetani

Lockjaw, muscle spasm, laryngospasm,convulsions, respiratory failure

None (tetanus toxoid only if �5 yearssince last toxoid)


Two previous immunizations?

One previous immunization?

No previousimmunizations?

What is Fitz-Hugh-Curtissyndrome?

Tetanus toxoid

Tetanus immunoglobulin IM and tetanustoxoid IM (at different sites!)

Tetanus immunoglobulin IM and tetanustoxoid IM (at different sites!)

Right upper quadrant pain fromgonococcal perihepatitis in women


Define postoperative fever.

What are the classic W’s ofpostoperative fever? (5)

Give the classic postoperativetiming for the followingcauses of postoperative fever:

Atelectasis (Wind)

UTI (Water)

Wound infection (Wound)

DVT/PE/thrombophlebitis(Walking)

Drug fever (Wonderdrugs)

What is the most commoncause of fever on postoperative days 1 to 2?

FeverChapter 28Temperature �38.5� C or 101.5� F

Wind—atelectasisWater—urinary tract infection (UTI)Wound—wound infectionWalking—DVT/thrombophlebitisWonder drugs—drug fever

First 24 to 48 hours

Anytime after POD #3

Usually after POD #5 (but it can be anytime!)

PODs #7 to #10

Anytime

Atelectasis


Chapter 29 / Surgical Prophylaxis 181

What is a “complete” feverworkup?

What causes fever before 24 postoperative hours?

What causes fever frompostoperative days 3 to 5?

What is an anesthetic causeof fever INTRAoperatively?

What causes fever frompostoperative days 5 to 10?

What causes woundinfection on postoperativedays 1 to 2?

What can cause fever at anytime?

Physical exam (look at wound, etc.),CXR, urinalysis, blood cultures, CBC

Atelectasis, -hemolytic streptococcal orclostridial wound infections, anastomoticleak

UTI, pneumonia, IV site infection,wound infection

Malignant hyperthermia—treat withdantrolene

Wound infection, pneumonia, abscess,infected hematoma, C. difficile colitis,anastomotic leak

DVT, peritoneal abscess, drug feverPulmonary embolism, abscess, parotitis

StreptococcusClostridia (painful bronze-brown weeping

wound)

1. IV site infection2. Central line infection3. Medications

SurgicalProphylaxis

Chapter 29

What medications provideprotection from postoperativeGI bleeding?

What measures provide protection from postoperativeatelectasis/pneumonia?

What treatments provideprotection from postoperativeDVT?

H2 blockers, PPI (proton-pump inhibitor)

Incentive spirometry, coughing, smokingcessation, ambulation

Low-molecular-weight heparin (LMWH),subcutaneous low-dose unfractionatedheparin, sequential compression device(SCD) for lower extremities, or both;early ambulation



What measures provide protection from woundinfection?

Why not use a razor toremove hair?

How long should “prophylac-tic antibiotics” be given?

What treatment provides pro-tection from oral/esophagealfungal infection during IVantibiotic treatment?

What measures prevent ventilator-associated pneumonia (VAP)?

What is the classic preoperative “bowel prep”?

Is there any evidence that a“bowel prep” decreasesinfections?

What treatment providesprotection from OPSS aftersplenectomy?

What treatment providesprotection from endocarditiswith faulty heart valve orprosthetic heart valve?

Shower the night before surgery withchlorhexidine scrub

Never use a razor for hair removal(electric shavers only)

Ensure adequate skin prep in O.R.Do not close the skin in a contaminated caseEnsure preoperative antibiotics in the

bloodstream before incisionEnsure no excess Bovie (necrotic tissue)

Micro cuts are a nidus for bacteria and subsequent wound infection

�24 hrs

PO nystatin

Head of bed �30�, handwashing, patientoral hygiene, avoidance of gastric overdistention

1. Bowel prep: Lower bacterial count incolon by catharsis (GoLYTELY orFleets)

2. PO antibiotics (neomycin, erythromycin)preoperatively

3. Preoperative IV antibiotic with spectrumversus anaerobes (e.g., Cefoxitin)

NO

Immunization against H. influenzae,Streptococcus, Meningococcus, and penicillin when illness/fever occurs

Antibiotics prior to dental procedure orany surgery


Chapter 30 / Surgical Radiology 183

What treatment providesprotection from tetanusinfection?

What treatment providesprotection from EtOH withdrawal?

What treatment providesprotection from Wernicke’sencephalopathy?

What is Wernicke’sencephalopathy?

What treatment decreasesthe risk of perioperativeadrenal crisis in a patient onchronic steroids?

Tetanus toxoid (and tetanus immuneglobulin, if one or no previous toxoidwith dirty wound)

Chlordiazepoxide (Librium®), also giveRally pack

Rally pack (a.k.a. banana bag becausethe IV is yellow with the vitamins in it);pack includes thiamine, folate, andmagnesium

Condition resulting from thiamine deficiency in patients with alcoholism,causing a triad of symptoms; think “COA”:

1. Confusion2. Ophthalmoplegia3. Ataxia

“Stress-dose” steroids: 100 mg hydrocor-tisone administered preoperatively, continued postoperatively q 8 hours, and then tapered off

Surgical RadiologyChapter 30

What defines a technicallyadequate CXR?

The film must be “RIPE”:Rotation: Clavicular heads are

equidistant from the thoracic spinous processes

Inspiration: Diaphragm is at or belowribs 8–10 posteriorly and ribs 5–6anteriorly

Penetration: Disk spaces are visiblebut there is no bony detail of thespine; bronchovascular structuresare seen through the heart

Exposure: Make sure all of the lungfields are visible

CHEST



How should a CXR be read?

What CXR is better: P-A orA-P?

Classically, how much pleuralfluid can the diaphragmhide on upright CXR?

How can CXR confirm thatthe last hole on a chest tubeis in the pleural cavity?

How can a loculated pleuraleffusion be distinguished froma free-flowing pleural effusion?

How do you recognize apneumothorax on CXR?

What x-ray should be obtainedbefore feeding via a nasogas-tric or nasoduodenal tube?

What C-spine views are usedto rule out bony injury?

Check the following:Tubes and lines: Check placementPatient data: Name, date, history

numberOrientation: Up/down, left-rightTechnique: AP or PA, supine or

erect, decubitusTrachea: Midline or deviated, caliberLungs: CHF, massPulmonary vessels: Artery or vein

enlargementMediastinum: Aortic knob, nodesHila: Masses, lymphadenopathyHeart: Transverse diameter should be

less than half the transthoracicdiameter

Pleura: Effusion, thickening,pneumothorax

Bones: Fractures, lesionsSoft tissues: Periphery and below the

diaphragm

P-A, less magnification of the heart (heartis closer to the x-ray plate)

It is said that the diaphragm canovershadow up to 500 cc

Last hole is through the radiopaque lineon the chest tube; thus, look for the breakin the radiopaque line to be in the rib cage

Ipsilateral decubitus CXR; if fluid is notloculated (or contained), it will layer out

Air without lung markings is seen outsidethe white pleural line—best seen in theapices on an upright CXR

Low CXR to ensure the tube is in the GItract and not in the lung

CT scan



What is used to look for ligamentous C-spine injury?

What CXR findings may provide evidence oftraumatic aortic injury?

How should a CT scan beread?

Lateral flex and extension C-spine films,MRI

Widened mediastinum �8 cm (mostcommon)

Apical pleural cappingLoss of aortic knobInferior displacement of left main

bronchus; NG tube displaced to theright, tracheal deviation, hemothorax

Cross section with the patient in supineposition looking up from the feet

Posterior

Anterior

PatientRight

PatientLeft

How should an abdominal x-ray (AXR) be read?

Check the following:Patient data: name, date, history

numberOrientation: up/down, left-rightTechnique: A-P or P-A, supine or

erect, decubitusAir: free air under diaphragm,

air-fluid levelsGas dilatation (3, 6, 9 rule)Borders: psoas shadow, preperitoneal

fat stripeMass: look for organomegaly, kidney

shadowStones/calcification: urinary, biliary,

fecalithStoolTubesBonesForeign bodies

ABDOMEN



Air

Fluid

Air-fluidlevel

How can you tell the difference between a smallbowel obstruction (SBO) andan ileus?

What is the significance ofan air-fluid level?

In SBO there is a transition point (cut-off sign) between the distendedproximal bowel and the distal bowel ofnormal caliber (may be gasless), whereasthe bowel in ileus is diffusely distended

Seen in obstruction or ileus on an uprightx-ray; intraluminal bowel diameterincreases, allowing for separation of fluidand gas

What are the normalcalibers of the small bowel,transverse colon, andcecum?

What is the “rule of 3s” forthe small bowel?

How can the small and largebowel be distinguished onAXR?

Where does peritoneal fluidaccumulate in the supineposition?

What percentage of kidneystones are radiopaque?

Use the “3, 6, 9 rule”:Small bowel �3 cmTransverse colon �6 cmCecum �9 cm

Bowel wall should be �3 mm thickBowel folds should be �3 mm thickBowel diameter should be �3 cm wide

By the intraluminal folds: The smallbowel plicae circulares are complete,whereas the plicae semilunares of thelarge bowel are only partially around theinner circumference of the lumen

Morison’s pouch (hepatorenal recess), thespace between the anterior surface of theright kidney and the posterior surface ofthe right lobe of the liver

�90%


What percentage ofgallstones are radiopaque?

What percentage of patientswith acute appendicitis havea radiopaque fecalith?

What are the radiographicsigns of appendicitis?

What does KUB stand for?

What is the “parrot’s beak”or “bird’s beak” sign?

What is a “cut-off sign”?

What are “sentinel loops”?

What is loss of the psoasshadow?

What is loss of the peritonealfat stripe (a.k.a. preperitonealfat stripe)?

What is “thumbprinting”?

What is pneumatosis intestinalis?


�10%

�5%

Fecalith; sentinel loops; scoliosis awayfrom the right because of pain; masseffect (abscess); loss of psoas shadow; loss of preperitoneal fat stripe; and, veryrarely, a small amount of free air, if perforated

Kidneys, Ureters, and Bladder—commonly used term for a plain filmAXR (abdominal flat plate)

Evidence of sigmoid volvulus on bariumenema; evidence of achalasia on bariumswallow

Seen in obstruction, bowel distention,and distended bowel that is “cut-off”from normal bowel

Distention or air-fluid levels (or both)near a site of abdominal inflammation(e.g., seen in RLQ with appendicitis)

Loss of the clearly defined borders of thepsoas muscle on AXR; loss signifiesinflammation or ascites

Loss of the lateral peritoneal/preperitonealfat interface; implies inflammation

Nonspecific colonic mucosal edemaresembling thumb indentations on AXR

Gas within the intestinal wall (usuallymeans dead gut) that can be seen inpatients with congenital variant orchronic steroids



Diaphragm

Free air

What is free air? Air free within the peritoneal cavity (air or gas should be seen only within thebowel or stomach); results from bowel orstomach perforation

What is the best position forthe detection of FREE AIR(free intraperitoneal air)?

If you cannot get an uprightCXR, what is the secondbest plain x-ray for free air?

How long after a laparotomycan there be free air on AXR?

What is Chilaiditi’s sign?

When should a postoperativeabdominal/pelvic CT scanfor a peritoneal abscess beperformed?

What is the best test to evaluate the biliary systemand gallbladder?

Upright CXR—air below the rightdiaphragm

Left lateral decubitus, because it preventsconfusion with gastric air bubble; withfree air both sides of the bowel wall canbe seen; can detect as little as 1 cc of air

Usually 7 days or less

Transverse colon over the liver simulatingfree air on x-ray

POD #7 or later, to give time for theabscess to form

Ultrasound (U/S)



What is the normal diameterof the common bile ductwith gallbladder present?

What is the normal commonbile duct diameter afterremoval of the gallbladder?

What U/S findings are associated with acute cholecystitis?

What type of kidney stone isnot seen on AXR?

What medication should begiven prophylactically to apatient with a true history ofcontrast allergy?

What is a C-C mammogram?

�4 mm until age 40, then add 1 mm perdecade (e.g., 7 mm at age 70)

8 to 10 mm

Gallstones, thickened gallbladder wall(�3 mm), distended gallbladder (�4 cmA-P), impacted stone in gallbladder neck,pericholecystic fluid

Uric acid (Think: Uric acid � Unseen)

Methylprednisolone or dexamethasone;the patient should also receive nonioniccontrast (associated with one fifth asmany reactions as ionic contrast, the lessexpensive standard)

Cranio-Caudal mammogram, in whichthe breast is compressed top to bottom



What is an MLOmammogram?

MedioLateral Oblique mammogram, inwhich the breast is compressed in a 45�angle from the axilla to the lowersternum

What are the best studies toevaluate for a pulmonaryembolus?

Spiral thoracic CT scan, V-Q scan,pulmonary angiogram (gold standard)

Define the following terms:Anesthesia

Local anesthesia

Epidural anesthesia

Spinal anesthesia

Regional anesthesia

AnesthesiaChapter 31Loss of sensation/pain

Anesthesia of a small confined area ofthe body (e.g., lidocaine for an elbowlaceration)

Anesthetic drugs/narcotics infused intoepidural space

Anesthetic agents injected into the thecalsac

Blocking of the sensory afferent nervefibers from a region of the body (e.g.,radial nerve block)


General anesthesia

GET or GETA

Give examples of the following terms:

Local anesthetic

Regional anesthetic

General anesthesia

Dissociative agent

What is cricoid pressure?

What is “rapid-sequence”anesthesia induction?

Give examples of inductionagents.

What are contraindicationsof the depolarizing agentsuccinylcholine?

Why is succinylcholine contraindicated in thesepatients?

Why doesn’t lidocaine workin an abscess?

Chapter 31 / Anesthesia 191

Triad:1. Unconsciousness/amnesia2. Analgesia3. Muscle relaxation

General EndoTracheal Anesthesia

Lidocaine, bupivacaine (Marcaine®)

Lidocaine, bupivacaine (Marcaine®)

Isoflurane, enflurane, sevoflurane, desflurane

Ketamine

Manual pressure on cricoid cartilageoccluding the esophagus and thusdecreasing the chance of aspiration ofgastric contents during intubation (a.k.a. Sellick’s maneuver)

1. Oxygenation and short-actinginduction agent

2. Muscle relaxant3. Cricoid pressure4. Intubation5. Inhalation anesthetic (rapid: boom,

boom, boom S to lower the risk ofaspiration during intubation)

Propofol, midazolam, sodium thiopental

Patients with burns, neuromuscular diseases/paraplegia, eye trauma, orincreased ICP

Depolarization can result in life-threateninghyperkalemia; succinylcholine alsoincreases intraocular pressure

Lidocaine does not work in an acidicenvironment



Why does lidocaine burn on injection and what can be done to decrease theburning sensation?

Why does some lidocainecome with epinephrine?

In what locations is lidocainewith epinephrine contraindi-cated?

What are the contraindica-tions to nitrous oxide?

What is the feared side effectof bupivacaine (Marcaine®)?

What are the side effects ofmorphine?

What are the side effects ofmeperidine?

Limit to the duration ofDemerol® postoperatively?

What medication is acontraindication toDemerol®?

What metabolite of Demerol®

breakdown causes side effects(e.g., seizures)?

Lidocaine is acidic, which causes theburning; add sodium bicarbonate todecrease the burning sensation

Epinephrine vasoconstricts the smallvessels, resulting in a decrease in bleedingand blood flow in the area; this prolongsretention of lidocaine and its effects

Fingers, toes, penis, etc., because of thepossibility of ischemic injury/necrosisresulting from vasoconstriction

Nitrous oxide is poorly soluble in serumand thus expands into any air-filled bodypockets; avoid in patients with middle earocclusions, pneumothorax, small bowelobstruction, etc.

Cardiac dysrhythmia after intravascularinjection leading to fatal refractorydysrhythmia

Constipation, respiratory failure, hypotension (from histamine release),spasm of sphincter of Oddi (useDemerol® in pancreatitis and biliary surgery), decreased cough reflex

Similar to those of morphine but causesless sphincteric spasm and can causetachycardia and seizures

Build up of the metabolites (normeperidine)

Monoamine oxidase inhibitor

Normeperidine


Chapter 31 / Anesthesia 193

What is the treatment oflife-threatening respiratorydepression with narcotics?

What are the side effects ofepidural analgesia?

What is the advantage ofepidural analgesia?

What are the side effects ofspinal anesthesia?

What is the side effect ofinhalational (volatile) anesthesia?

Narcan® IV (naloxone)

Orthostatic hypotension, decreasedmotor function, urinary retention

Analgesia without decreased cough reflex

Urinary retentionHypotension (neurogenic shock)

Halothane—hypotension (cardiacdepression, decreased baroreceptorresponse to hypotension, and peripheralvasodilation), malignant hyperthermia

What is it?

What is the incidence?




Inherited predisposition to an anestheticreaction, causing uncoupling of the excitation–contraction system in skeletalmuscle, which in turn causes malignanthyperthermia; hypermetabolism is fatalif untreated

Very rare

General anesthesia, succinylcholine

Increased body temperature; hypoxia;acidosis; tachycardia, c PCO2 (c end tidalCO2)

IV dantrolene, body cooling, discon-tinuation of anesthesia

MALIGNANT HYPERTHERMIA

What are some of thenondepolarizing muscleblockers?

VecuroniumPancuronium

MISCELLANEOUS


What are the antidotes tothe nondepolarizing neuro-muscular blocking agents?

How do these agents work?

Which muscle blocker isdepolarizing?

What is the duration ofaction of succinylcholine?

What is the antidote toreverse succinylcholine?

What is the maximum doseof lidocaine:

With epinephrine?

Without epinephrine?

What is the duration of lidocaine local anesthesia?

What are the early signs oflidocaine toxicity?

What are the signs oflidocaine toxicity with largeoverdose (�10 mcg/mL)?

When should the Foleycatheter be removed in apatient with an epiduralcatheter?

What is a PCA pump?


EdrophoniumNeostigminePyridostigmine

They inhibit anticholinesterase

Succinylcholine

�6 minutes

Time; endogenous blood pseudocholines-terase (patients deficient in this enzymemay be paralyzed for hours!)

7 mg/kg

4 mg/kg

30 to 60 minutes (up to 4 hours with epinephrine)

Tinnitus, perioral/tongue numbness,metallic taste, blurred vision, muscletwitches, drowsiness

Seizures, coma, respiratory arrestLoss of consciousnessApnea

Several hours after the epidural catheteris removed (to prevent urinary retention)

Patient-Controlled Analgesia; a pumpdelivers a set amount of pain relieverwhen the patient pushes a button (e.g., 1 mg of morphine every 6 minutes)


Chapter 32 / Surgical Ulcers 195

What are the advantages ofa PCA pump?

What is a “basal rate” on thePCA?

What is used to reverse narcotics?

What is used to reverse benzodiazepines?

What is fentanyl?

Name an IV NSAID.

Better pain controlPatients actually use less pain medication

with a PCA!If given a moderate dose without a basal

rate, patients should not be able tooverdose (They will fall asleep and notbe able to push the button!)

Steady continuous infusion rate of the narcotic (e.g., 1–2 mg of morphine) continuously infused per hour; patient can supplement with additional doses as needed

Naloxone (Narcan®)

Flumazenil

Very potent narcotic (#1 drug of abuse byanesthesiologists)

Ketorolac (has classic side effects ofNSAIDs: PUD, renal insufficiency)

Define the following terms:Peptic ulcer

Gastric ulcer

General term for gastric/duodenal ulcerdisease

Ulcer in the stomach

Surgical UlcersChapter 32



Curling’s ulcer Gastric ulcer after burn injury (Think:Curling’s—curling iron burn—burn)

OUCH!

Cushing’s ulcer

Dieulafoy’s ulcer

Marjolin’s ulcer

Aphthous ulcer

Marginal ulcer

Decubitus ulcer

Venous stasis ulcer

LE arterial insufficiencyulcer

Peptic ulcer after neurologic insult(Think: Cushing—famous neurosurgeon)

Pinpoint gastric mucosal defect bleeding from underlying arterial vessel malformation

Squamous cell carcinoma ulcerationoverlying chronic osteomyelitis or burnscar

GI tract ulcer seen in Crohn’s disease

Mucosal ulcer seen at a site of GI tractanastomosis

Skin/subcutaneous ulceration from pressure necrosis, classically on the buttocks/sacrum

Skin ulceration on medial malleoluscaused by venous stasis of a lower extremity

Skin ulcers usually located on the toes/feet


Chapter 33 / Surgical Oncology 197

Define:Surgical oncology

XRT

In situ

Benign

Malignant

Adjuvant RX

Neoadjuvant RX

Brachytherapy

Metachronous tumors

Synchronous tumors

What do the T, M, and N stand for in TMN staging?

What tumor marker is associated with colon cancer?

What tumor marker is associated with hepatoma?

What tumor marker is associated with pancreaticcarcinoma?

Surgical treatment of tumors

Radiation therapy

Not invading basement membrane

Nonmalignant tumor—does not invadeor metastasize

Tumors with anaplasia that invade andmetastasize

Treatment that aids or assists surgicaltreatment � Chemo or XRT

Chemo, XRT, or both BEFORE surgicalresection

XRT applied directly or very close to thetarget tissue (e.g., implantable adioactiveseeds)

Tumors occurring at different times

Tumors occurring at the same time

T-Tumor sizeM-Mets (distant)N-Nodes

CEA

-Fetoprotein

CA 19-9

Surgical OncologyChapter 33



What is paraneoplasticsyndrome?

What are the most com-mon cancers in women?

What are the mostcommon cancers in men?

What is the most commoncancer causing death inboth men and women?

Syndrome of dysfunction not directlyassociated with tumor mass or mets(autoimmune or released substance)

1. Lung2. Breast3. Colorectal

1. Prostate2. Lung3. Colorectal

Lung!


Define the products of thefollowing stomach cells:

Gastric parietal cells

Chief cells

G cells

Mucous neck cells

What is pepsin?

What is intrinsic factor?

Name three receptors on theparietal cell that stimulateHCl release.

What is the enterohepaticcirculation?

Where are most of the bileacids absorbed?

HClIntrinsic factor

PEPsinogen (Think: “a PEPpy chief”)

Gastrin, G cells are found in the antrum(Think: G � Gastrin)

Bicarbonate mucus

Proteolytic enzyme that hydrolyzes peptide bonds

Protein secreted by the parietal cells thatcombines with vitamin B12 and enablesabsorption in the terminal ileum

Think: “HAG”:1. Histamine2. Acetylcholine3. Gastrin

Circulation of bile acids from the liver to the gut and back to the liver via theportal vein

Terminal ileum

199

Section II General Surgery

GI Hormones and Physiology

Chapter 34

OVERVIEW

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How many times is the entirebile acid pool circulated during a typical meal?

What are the stimulators ofgallbladder emptying?

What are the inhibitors ofgallbladder emptying?

200 Section II / General Surgery

Twice

Cholecystokinin, vagal input

Somatostatin, sympathetics (it is impossibleto flee and digest food at the same time),vasoactive intestinal polypeptide (VIP)

CHOLECYSTOKININ (CCK)

What is its source?

What stimulates its release?

What inhibits its release?

What are its actions?

Duodenal mucosal cells

Fat, protein, amino acids, HCl

Trypsin and chymotrypsin

Empties gallbladderOpens ampulla of VaterSlows gastric emptyingStimulates pancreatic acinar cell growth

and release of exocrine products

SECRETIN

What is its source?




Duodenal cells (specifically theargyrophilic S cells)

pH �4.5 (acid), fat in the duodenum

High pH in the duodenum

Releases pancreatic bicarbonate/enzymes/H2O

Releases bile/bicarbonateDecreases lower esophageal sphincter

(LES) toneDecreases release of gastric acid

GASTRIN

What is its source? Gastric antrum G cells


Chapter 34 / GI Hormones and Physiology 201




Stomach peptides/amino acidsVagal inputCalcium

pH �3.0Somatostatin

Release of HCl from parietal cellsTrophic effect on mucosa of the stomach

and small intestine

SOMATOSTATIN

What is its source?



Pancreatic D cells

Food

Globally inhibits GI function

MISCELLANEOUS

What is the purpose of thecolon?

What is the main smallbowel nutritional source?

What is the main nutritionalsource of the colon?


Where is iron absorbed?

Where is vitamin B12absorbed?

Which hormone primarilycontrols gallbladder contraction?

What supplement does apatient need after removalof the terminal ileum orstomach?

Reabsorption of H2O and storage of stool

Glutamine

Butyrate (short-chain fatty acid)

Duodenum actively, jejunum passively

Duodenum

Terminal ileum

CCK

Vitamin B12


Name the main constituentsof bile.

What are most gallstonesmade of?

How do opiates affect thebowel?

Which type of muscle fibers,smooth or striated, does theesophagus contain?

Which electrolytes does thecolon actively absorb?

Which electrolyte does thecolon actively secrete?

Which electrolyte does thecolon passively secrete?

What is the gastrocolicreflex?

What is the blood supply tothe liver?

What are Peyer patches?


Water, phospholipids (lecithins), bileacids, cholesterol, and bilirubin

Cholesterol

By stimulating sodium absorption andinhibiting secretion in the ileum as well asdecreasing GI motility by incoordinatedperistalsis (Therefore, place patients onstool softeners when dispensing pain medication)

Both:Upper third—striated muscle control

of motor nervesMiddle third—mixedLower third—smooth muscle, primarily

under control of vagal motor fibers

Na�, Cl�

HCO3� (plays a role in diarrhea causing

the patient to have a normal anion gapacidosis)

K�

Increased secretory and motor functionsof the stomach result in increased colonicmotility

75% from the portal vein, rich in productsof digestion

25% from the hepatic artery, rich in O2

(but each provide for 50% of oxygen)

Nodules of lymphoid tissue with B and Tlymphocytes in the small intestine thatselectively sample lumenal antigensfound in the terminal ileum


Chapter 35 / Acute Abdomen and Referred Pain 203

What is an “acuteabdomen”?

What are peritoneal signs?

Define the following terms:Rebound tenderness

Motion pain

Voluntary guarding

Involuntary guarding

Colic

What conditions can maskabdominal pain?

What is the most commoncause of acute abdominalsurgery in the UnitedStates?

Acute Abdomenand Referred Pain

Chapter 35

Acute abdominal pain so severe that thepatient seeks medical attention(Note: Not the same as a “surgicalabdomen,” because most cases of acuteabdominal pain do not require surgicaltreatment)

Signs of peritoneal irritation: extremetenderness, percussion tenderness,rebound tenderness, voluntary guarding,motion pain, involuntary guarding/rigidity (late)

Pain upon releasing the palpating handpushing on the abdomen

Abdominal pain upon moving, pelvicrocking, moving of stretcher, or heelstrike

Abdominal muscle contraction with palpation of the abdomen

Rigid abdomen as the muscles “guard”involuntarily

Intermittent severe pain (usually becauseof intermittent contraction of a hollowviscus against an obstruction)

Steroids, diabetes, paraplegia

Acute appendicitis (7% of the populationwill develop it sometime during theirlives)

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What important questionsshould be asked whenobtaining the history of apatient with an acuteabdomen?

What should the acuteabdomen physical examinclude?

What is the best way to havea patient localize abdominalpain?

What is the classic positionof a patient with peritonitis?


“Have you had this pain before?”“On a scale from 1 to 10, how would you

rank this pain?”“Fevers/chills?”“Duration?” (comes and goes vs. constant)“Quality?” (sharp vs. dull)“Does anything make the pain better or

worse?”“Migration?”“Point of maximal pain?”“Urinary symptoms?”“Nausea, vomiting, or diarrhea?”“Anorexia?”“Constipation?”“Last bowel movement?”“Any change in bowel habits?”“Any relation to eating?”“Last menses?”“Last meal?”“Vaginal discharge?”“Melena?”“Hematochezia?”“Hematemesis?”“Medications?”“Allergies?”“Past medical history?”“Past surgical history?”“Family history?”“Tobacco/EtOH/drugs?”

Inspection (e.g., surgical scars,distention)

Auscultation (e.g., bowel sounds, bruits)Palpation (e.g., tenderness, R/O hernia,

CVAT, rectal, pelvic exam, rebound,voluntary guard, motion tenderness)

Percussion (e.g., liver size, spleen size)

“Point with one finger to where the painis worse”

Motionless (often with knees flexed)


What is the classic positionof a patient with a kidneystone?

What is the best way toexamine a scared child orhistrionic adult’s abdomen?

What lab tests are used toevaluate the patient with anacute abdomen?

What is a “left shift” on CBCdifferential?

What lab test should everywoman of childbearing agewith an acute abdomenreceive?

Which x-rays are used toevaluate the patient with anacute abdomen?

How is free air ruled out ifthe patient cannot stand?

What diagnosis must be considered in every patientwith an acute abdomen?

What are the differentialdiagnoses by quadrant?

RUQ


Cannot stay still, restless, writhing in pain

Use stethoscope to palpate abdomen

CBC with differential, chem-10,amylase, type and screen, urinalysis,LFTs

Sign of inflammatory response:Immature neutrophils (bands) Note: Many call �80% of WBCs as

neutrophils a “left shift”

Human chorionic gonadotropin (�-hCG)to rule out pregnancy/ectopic pregnancy

Upright chest x-ray, upright abdominalfilm, supine abdominal x-ray (if patientcannot stand, left lateral decubitusabdominal film)

Left lateral decubitus—free air collectsover the liver and does not get confusedwith the gastric bubble

Appendicitis!

Cholecystitis, hepatitis, PUD, perforatedulcer, pancreatitis, liver tumors, gastritis,hepatic abscess, choledocholithiasis,cholangitis, pyelonephritis, nephrolithiasis,appendicitis (especially duringpregnancy); thoracic causes (e.g.,pleurisy/pneumonia), PE, pericarditis,MI (especially inferior MI)


LUQ

LLQ

RLQ

What is the differential diagnosis of epigastric pain?

What is the differentialdiagnosis of gynecologicpain?

What is the differentialdiagnosis of thoracic causesof abdominal pain?

What is the differentialdiagnosis of scrotal causesof lower abdominal pain?


PUD, perforated ulcer, gastritis, splenicinjury, abscess, reflux, dissecting aorticaneurysm, thoracic causes, pyelonephritis,nephrolithiasis, hiatal hernia (strangulatedparaesophageal hernia), Boerhaave’s syndrome, Mallory-Weiss tear, splenicartery aneurysm, colon disease

Diverticulitis, sigmoid volvulus, perforated colon, colon cancer, urinary tract infection, small bowelobstruction, inflammatory boweldisease, nephrolithiasis, pyelonephritis,fluid accumulation from aneurysm orperforation, referred hip pain, gynecologiccauses, appendicitis (rare)

Appendicitis! And same as LLQ; also mesenteric lymphadenitis, cecaldiverticulitis, Meckel’s diverticulum,intussusception

PUD, gastritis, MI, pancreatitis, biliarycolic, gastric volvulus, Mallory-Weiss

Ovarian cyst, ovarian torsion, PID,mittelschmerz, tubo-ovarian abscess(TOA), uterine fibroid, necrotic fibroid,pregnancy, ectopic pregnancy,endometriosis, cancer of the cervix/uterus/ovary, endometrioma, gynecologictumor, torsion of cyst or fallopian tube

MI (especially inferior), pneumonia, dissecting aorta, aortic aneurysm,empyema, esophageal rupture/tear, PTX,esophageal foreign body

Testicular torsion, epididymitis, orchitis,inguinal hernia, referred pain fromnephrolithiasis or appendicitis


What are nonsurgical causesof abdominal pain?

What is the unique differentialdiagnosis for the patient withAIDS and abdominal pain?

What are the possible causesof suprapubic pain?

What causes pain limited tospecific dermatomes?

What is referred pain?

What is gastroenteritis?

What is classically stated tobe the “great imitator”?

Name the classic locations ofreferred pain:

Cholecystitis

Appendicitis

Diaphragmatic irritation(from spleen, perforatedulcer, or abscess)

Pancreatitis/cancer


Gastroenteritis, DKA, sickle cell crisis,rectus sheath hematoma, acuteporphyria, PID, kidney stone,pyelonephritis, hepatitis, pancreatitis,pneumonia, MI, C. difficile colitis

In addition to all common abdominalconditions:

CMV (most Common)Kaposi’s sarcomaLymphomaTBMAI (Mycobacterium Avium

Intracellulare)

Cystitis, colonic pain, gynecologic causes(and, of course, appendicitis)

Early zoster before vesicles erupt

Pain felt at a site distant from a diseaseprocess; caused by the convergence ofmultiple pain afferents in the posteriorhorn of the spinal cord

Viral or bacterial infection of the GI tract,usually with vomiting and diarrhea, pain(usually after vomiting), nonsurgical

Constipation

Right subscapular pain (also epigastric)

Early: periumbilicalRarely: testicular pain

Shoulder pain (� Kehr’s sign on the left)

Back pain


Rectal disease

Nephrolithiasis

Rectal pain

Small bowel

Uterine pain

Give the classic diagnosis forthe following cases:

“Abdominal pain out ofproportion to exam”

Hypotension andpulsatile abdominal mass

Fever, LLQ pain, andchange in bowel habits

Give the test of choice forthe following conditions:

Cholelithiasis

Bile duct obstruction

Mesenteric ischemia

Ruptured abdominal aortic aneurysm

AAA

Abdominal abscess

Severe diverticulitis

What is the most commoncause of RUQ pain?

What is the most commoncause of surgical RLQ pain?


Pain in the small of the back

Testicular pain/flank pain

Midline small of back pain

Periumbilical pain

Midline small of back pain

Rule out mesenteric ischemia

Ruptured AAA; go to the O.R.

Diverticulitis

Ultrasound (U/S)

U/S

Mesenteric A-gram

NONE—emergent laparotomy

Abdominal CT scan or U/S

Abdominal CT scan

Abdominal CT scan

Cholelithiasis

Acute appendicitis


What is the most commoncause of GI tract LLQ pain?

Classically, what endocrineproblems can cause abdomi-nal pain?

Chapter 36 / Hernias 209

Diverticulitis

1. Addisonian crisis2. DKA (Diabetic KetoAcidosis)

What is a hernia?


What are the precipitatingfactors?

Why should hernias berepaired?

What is more dangerous: asmall or large hernia defect?

Define the followingdescriptive terms:

Reducible

Incarcerated

HerniasChapter 36(L. rupture) Protrusion of a peritonealsac through a musculoaponeurotic barrier(e.g., abdominal wall); a fascial defect

5%–10% lifetime; 50% are indirectinguinal, 25% are direct inguinal, and�5% are femoral

Increased intra-abdominal pressure:straining at defecation or urination (rectal cancer, colon cancer, prostaticenlargement, constipation), obesity,pregnancy, ascites, valsavagenic (coughing)COPD; an abnormal congenital anatomicroute (i.e., patent processus vaginalis)

To avoid complications of incarceration/strangulation, bowel necrosis, SBO, pain

Small defect is more dangerous because atight defect is more likely to strangulate ifincarcerated

Ability to return the displaced organ ortissue/hernia contents to their usualanatomic site

Swollen or fixed within the hernia sac (incar-cerated � imprisoned); may cause intestinalobstruction (i.e., an irreducible hernia)


Strangulated


Incarcerated hernia with resultingischemia; will result in signs andsymptoms of ischemia and intestinalobstruction or bowel necrosis (Think:strangulated � choked)

Complete

Incomplete

What is reducing a hernia“en masse”?

Hernia sac and its contents protrude allthe way through the defect

Defect present without sac or contentsprotruding completely through it

Reducing the hernia contents and hernia sac



Define the following typesof hernias:

Sliding hernia Hernia sac partially formed by the wall ofa viscus (i.e., bladder/cecum)

Littre’s hernia

Spigelian hernia

Internal hernia

Petersen’s hernia

Obturator hernia

Lumbar hernia

Petit’s hernia

Grynfeltt’s hernia

Hernia involving a Meckel’s diverticulum(Think alphabetically: Littre’s Meckel’s �LM)

Hernia through the linea semilunaris (or spigelian fascia); also known as spontaneous lateral ventral hernia (Think:Spigelian � Semilunaris)

Hernia into or involving intra-abdominalstructure

Seen after bariatric gastric bypass—internal herniation of small bowelthrough the mesenteric defect from theRoux limb

Hernia through obturator canal (females� males)

Petit’s hernia or Grynfeltt’s hernia

(Rare) hernia through Petit’s triangle(a.k.a. inferior lumbar triangle) (Think:petite � small � inferior)

Hernia through Grynfeltt-Lesshaft triangle (superior lumbar triangle)


Pantaloon hernia


Hernia sac exists as both a direct andindirect hernia straddling the inferiorepigastric vessels and protruding throughthe floor of the canal as well as the internal ring (two sacs separated by theinferior epigastric vessels [the pantcrotch] like a pair of pantaloon pants)

Indirecthernia

Directhernia

Inferiorepigastricvessels

Incisional hernia

Ventral hernia

Parastomal hernia

Sciatic hernia

Richter’s hernia

Hernia through an incisional site; mostcommon cause is a wound infection

Incisional hernia in the ventral abdominalwall

Hernia adjacent to an ostomy (e.g.,colostomy)

Hernia through the sciatic foramen

Incarcerated or strangulated hernia involving only one sidewall of the bowel,which can spontaneously reduce, resultingin gangrenous bowel and perforation withinthe abdomen without signs of obstruction


Epigastric hernia

Umbilical hernia

Intraparietal hernia

Femoral hernia

Hesselbach’s hernia

Bochdalek’s hernia

Morgagni’s hernia

Properitoneal hernia

Cooper’s hernia

Indirect inguinal

Direct inguinal

Hiatal hernia

Amyand’s hernia


Hernia through the linea alba above theumbilicus

Hernia through the umbilical ring, inadults associated with ascites, pregnancy,and obesity

Hernia in which abdominal contentsmigrate between the layers of theabdominal wall

Hernia medial to femoral vessels (underinguinal ligament)

Hernia under inguinal ligament lateralto femoral vessels

Hernia through the posterior diaphragm,usually on the left (Think: Boch da lek � “back to the left” on thediaphragm)

Anterior parasternal diaphragmatic hernia

Intraparietal hernia between theperitoneum and transversalis fascia

Hernia through the femoral canal and tracking into the scrotum or labiamajus

Inguinal hernia lateral to Hesselbach’striangle

Inguinal hernia within Hesselbach’s triangle

Hernia through esophageal hiatus

Hernia sac containing a ruptured appendix(Think: Amyand’s � Appendix)


What are the boundaries ofHesselbach’s triangle?

What are the layers of theabdominal wall?

What is the differential diagnosis for a mass in ahealed C-section incision?


1. Inferior epigastric vessels2. Inguinal ligament (Poupart’s)3. Lateral border of the rectus sheathFloor consists of internal oblique and the

transversus abdominis muscle

SkinSubcutaneous fatScarpa’s fasciaExternal obliqueInternal obliqueTransversus abdominusTransversalis fasciaPreperitoneal fatPeritoneumNote: All three muscle layer aponeuroses

form the anterior rectus sheath, withthe posterior rectus sheath being deficient below the arcuate line

Hernia, ENDOMETRIOMA

GROIN HERNIAS

What is the differential diagnosis of a groin mass?

Lymphadenopathy, hematoma, seroma,abscess, hydrocele, femoral arteryaneurysm, EIC, undescended testicle,sarcoma, hernias, testicle torsion

DIRECT INGUINAL HERNIA

What is it?

What is the cause?


What nerve runs with thespermatic cord in theinguinal canal?

Hernia within the floor of Hesselbach’striangle, i.e., the hernia sac does not traverse the internal ring (think directlythrough the abdominal wall)

Acquired defect from mechanical breakdown over the years

�1% of all men; frequency increaseswith advanced age

Ilioinguinal nerve



INDIRECT INGUINAL HERNIA

What is it? Hernia through the internal ring of theinguinal canal, traveling down toward theexternal ring; it may enter the scrotumupon exiting the external ring (i.e., ifcomplete); think of the hernia sac travelingindirectly through the abdominal wallfrom the internal ring to the external ring

External ring

Internal ring

What is the cause?


How is an inguinal herniadiagnosed?

What is the differential diagnosis of an inguinal hernia?

What is the risk of strangulation?

Patent processus vaginalis (i.e., congenital)

�5% of all men; most common hernia inboth men and women

Relies mainly on history and physicalexam with index finger invaginated intothe external ring and palpation of hernia;examine the patient standing up if diagnosis is not obvious(Note: if swelling occurs below the inguinalligament, it is possibly a femoral hernia)

Lymphadenopathy, psoas abscess, ectopictestis, hydrocele of the cord, saphenousvarix, lipoma, varicocele, testicular torsion,femoral artery aneurysm, abscess

Higher with indirect than direct inguinalhernia, but highest in femoral hernias




Emergent herniorrhaphy is indicated if strangulation is suspected or acuteincarceration is present; otherwise, electiveherniorrhaphy is indicated to prevent thechance of incarceration/strangulation

INGUINAL HERNIA REPAIRS

Define the following procedures:

Bassini

McVay

Lichtenstein

Shouldice

Plug and patch

High ligation

TAPP procedure

TEPA procedure

What are the indications forlaparoscopic inguinal herniarepair?

Sutures approximate reflection ofinguinal ligament (Poupart’s) to the transversus abdominis aponeurosis/conjoint tendon

Cooper’s ligament sutured to transversusabdominis aponeurosis/conjoint tendon

“Tension-free repair” using mesh

Imbrication of the floor of the inguinalcanal (a.k.a. “Canadian repair”)

Placing a plug of mesh in hernia defectand then overlaying a patch of mesh overinguinal floor (requires few if any suturesin mesh!)

Ligation and transection of indirect hernia sac without repair of inguinal floor(used only in children)

TransAbdominal PrePeritoneal inguinalhernia repair

Totally ExtraPeritoneal Approach

1. Bilateral inguinal hernias2. Recurring hernia3. Need to resume full activity as soon as

possible

CLASSIC INTRAOPERATIVE INGUINAL HERNIA QUESTIONS

What is the first identifiablesubcutaneous named layer?

Scarpa’s fascia (thin in adults)



What is the name of the sub-cutaneous vein that is ligated?

What happens if you cut theilioinguinal nerve?

From what abdominal muscle layer is the cremastermuscle derived?

From what abdominal muscle layer is the inguinalligament (a.k.a. Poupart’sligament) derived?

To what does the inguinal(Poupart’s) ligament attach?

Which nerve travels on thespermatic cord?

Why do some surgeonsdeliberately cut theilioinguinal nerve?

What is in the spermaticcord (6)?

What is the hernia sac made of?

What attaches the testicle tothe scrotum?

What is the most commonorgan in an inguinal herniasac in men?

What is the most commonorgan in an inguinal herniasac in women?

Superficial epigastric vein

Numbness of inner thigh or lateral scrotum; usually goes away in 6 months

Internal oblique muscle

External oblique muscle aponeurosis

Anterior superior iliac spine to the pubictubercle

Ilioinguinal nerve

First they obtain preoperative consentand cut so as to remove the risk ofentrapment and postoperative pain

1. Cremasteric muscle fibers2. Vas deferens3. Testicular artery4. Testicular pampiniform venous plexus5. � hernia sac6. Genital branch of the genitofemoral

nerve

Peritoneum (direct) or a patent processusvaginalis (indirect)

Gubernaculum

Small intestine

Ovary/fallopian tube


What lies in the inguinalcanal in the female insteadof the VAS?

Where in the inguinal canaldoes the hernia sac lie in rela-tion to the other structures?

What is a “cord lipoma”?

What is a small outpouchingof testicular tissue off of thetesticle?

What action should betaken if a suture is placedthrough the femoral arteryor vein during an inguinalherniorrhaphy?

What nerve is found on topof the spermatic cord?

What nerve travels withinthe spermatic cord?

What are the borders ofHesselbach’s triangle?


Round ligament

Anteromedially

Preperitoneal fat on the cord structures(pushed in by the hernia sac); not a reallipoma; remove surgically, if feasible

Testicular appendage (a.k.a. the appendixtestes); remove with electrocautery

Remove the suture as soon as possibleand apply pressure (i.e., do not tie thesuture down!)

Ilioinguinal nerve

Genital branch of the genitofemoralnerve

1. Epigastric vessels2. Inguinal ligament3. Lateral border of the rectus

1. Epigastric vessels

3. Rectus

2. Inguinal ligament


What type of hernia goesthrough Hesselbach’s triangle?

What is a “relaxingincision”?

What is the conjoint tendon?

Define inguinal anatomy.


Direct hernia due to a weak abdominalfloor

Incision(s) in the rectus sheath to relaxthe conjoint tendon so that it can beapproximated to the reflection of theinguinal ligament without tension

Aponeurotic attachments of the“conjoining” of the internal oblique andtransversus abdominis to the pubic tubercle

1. Inguinal ligament (Poupart’s ligament)2. Transversus aponeurosis3. Conjoint tendon

Should allow entrance of the tip of aKelly clamp but not a finger (the newexternal inguinal ring should not be tightand should allow entrance of a finger)

ZERO

1

2

3

How tight should the newinternal inguinal ring be?

What percentage of thestrength of an inguinal floorrepair does the externaloblique aponeurosis represent?

FEMORAL HERNIA

What is it? Hernia traveling beneath the inguinal ligament down the femoral canal medialto the femoral vessels (Think: FM radio,or Femoral hernia � Medial)



What are the boundaries ofthe femoral canal?

What factors are associatedwith femoral hernias?

What percentage of all hernias are femoral?

What percentage of patientswith a femoral hernia arefemale?

What are the complications?

What is the most commonhernia in women?

What is the repair of afemoral hernia?

1. Cooper’s ligament posteriorly2. Inguinal ligament anteriorly3. Femoral vein laterally4. Lacunar ligament medially

Women, pregnancy, and exertion

5%

85%!

Approximately one third incarcerate (due to narrow, unforgiving neck)

Indirect inguinal hernia

McVay (Cooper’s ligament repair), meshplug repair

HERNIA REVIEW QUESTIONS

Should elective TURP orelective herniorrhaphy beperformed first?

Which type of esophagealhiatal hernia is associatedwith GE reflux?

Classically, how can anincarcerated hernia bereduced in the ER?

TURP

Sliding esophageal hiatal hernia

1. Apply ice to incarcerated hernia2. Sedate3. Use the Trendelenburg position for

inguinal hernias4. Apply steady gentle manual pressure5. Admit and observe for signs of

necrotic bowel after reduction6. Perform surgical herniorrhaphy

ASAP


What is appropriate if you cannot reduce an incarcerated hernia withsteady, gentle compression?

What is the major differencein repairing a pediatric indirect inguinal hernia andan adult inguinal hernia?

What is the Howship-Romberg sign?

What is the “silk glove”sign?

What must you do beforeleaving the O.R. after aninguinal hernia repair?


Go directly to O.R. for repair

In babies and children it is rarelynecessary to repair the inguinal floor;repair with “high ligation” of the hernia sac

Pain along the medial aspect of theproximal thigh from nerve compressioncaused by an obturator hernia

Inguinal hernia sac in an infant/toddlerfeels like a finger of a silk glove whenrolled under the examining finger

Pull the testicle back down to thescrotum

ESOPHAGEAL HIATAL HERNIAS

Define type I and type IIhiatal hernias.

Type I � slidingType II � paraesophageal

SLIDING ESOPHAGEAL HIATAL HERNIA

What is it? Both the stomach and GE junction herniate into the thorax via theesophageal hiatus; also known as type Ihiatal hernia



What are the symptoms?






�90% of all hiatal hernias

Most patients are asymptomatic, but thecondition can cause reflux, dysphagia(from inflammatory edema), esophagitis,and pulmonary problems secondary toaspiration

UGI series, manometry, esophagogastroduodenoscopy (EGD)with biopsy for esophagitis

Reflux S esophagitis S Barrett’s esophagusS cancer and stricture formation; aspiration pneumonia; it can also result inUGI bleeding from esophageal ulcerations

85% of cases treated medically withantacids, H2 blockers/PPIs, headelevation after meals, small meals, and nofood prior to sleeping; 15% of casesrequire surgery for persistent symptomsdespite adequate medical treatment

Laparoscopic Nissen fundoplication (LAPNISSEN) involves wrapping the fundusaround the LES and suturing it in place

PARAESOPHAGEAL HIATAL HERNIA

What is it? Herniation of all or part of the stomachthrough the esophageal hiatus into thethorax without displacement of the gastroesophageal junction; also known astype II hiatal hernia






What is a type III hiatal hernia?

What is a type IV hiatal hernia?

Chapter 37 / Laparoscopy 223

�5% of all hiatal hernias (rare)

Derived from mechanical obstruction;dysphagia, stasis gastric ulcer, and strangulation; many cases are asymptomaticand not associated with reflux because ofa relatively normal position of the GEjunction

Hemorrhage, incarceration, obstruction,and strangulation

Surgical, because of frequency and severity of potential complications

Combined type I and type II

Organ (e.g., colon or spleen) �/�stomach in the chest cavity

What is laparoscopy?

What gas is used and why?

Which operations areperformed with the laparoscope?

LaparoscopyChapter 37Minimally invasive surgical techniqueusing gas to insufflate the peritoneumand instruments manipulated throughports introduced through small incisionswith video camera guidance

CO2 because of better solubility in bloodand, thus, less risk of gas embolism; noncombustible

Frequently—cholecystectomy;appendectomy; inguinal hernia repair; ventral hernia repair, Nissenfundoplication

Infrequently—bowel resection,colostomy, surgery for PUD (PGV,perforation), colectomy, splenectomy,adrenalectomy


What are the contraindications?

What are the associatedcomplications?

What are the classic findingswith a CO2 gas embolus?

What prophylactic measureshould every patient getwhen they are going to havea laparoscopic procedure?

What are the cardiovascular effects of apneumoperitoneum?

What is the effect of CO2

insufflation on end tidal CO2 levels?

What are the advantagesover laparotomy?

What is the Veress needle?

How can it be verified thatthe Veress needle is in theperitoneum?


Absolute—hypovolemic shock, severecardiac decompensation

Relative—extensive intraperitoneal adhesions, diaphragmatic hernia, COPD

Pneumothorax, bleeding, perforatinginjuries, infection, intestinal injuries,solid organ injury, major vascular injury,CO2 embolus, bladder injury, hernia atlarger trocar sites, DVT

Triad:1. Hypotension2. Decreased end tidal CO2 (low flow

to lung)3. Mill-wheel murmur

SCD boots—Sequential CompressionDevice (and most add an OGT to decompress the stomach; Foley catheteris usually used for pelvic procedures)

Increased afterload and decreasedpreload (but the CVP and PCWP aredeceivingly elevated!)

Increased as a result of absorption ofCO2 into the bloodstream; the body compensates with increased ventilationand blows the extra CO2 off and thusthere is no acidosis

Shorter hospitalization, less pain andscarring, lower cost, decreased ileus

Needle with spring-loaded, retractable,blunt inner-protective tube thatprotrudes from the needle end when itenters peritoneal cavity; used for blindentrance and then insufflation of CO2

through the Veress needle

Syringe of saline; saline should flow freelywithout pressure through the needle“drop test”


If the Veress needle is not inthe peritoneal cavity, whathappens to the CO2 flow/pressure?

What is the Hassontechnique?

What is the cause of post-laparoscopic shoulder pain?

What is a laparoscopic-assisted procedure?

What is FRED®?

Give some tips for “driving”the camera duringlaparoscopy.

Chapter 37 / Laparoscopy 225

Flow decreases and pressure is high

No Veress needle—cut down and placetrocar under direct visualization

Referred pain from CO2 on diaphragmand diaphragm stretch

Laparoscopic dissection; then, part of theprocedure is performed through an openincision

Fog Reduction Elimination Device:sponge with antifog solution used to coatthe camera lens

1. Keep the camera centered on theaction

2. Watch all trocars as they enter theperitoneal cavity (and the tissuesbeyond, so they can be avoided!)

3. Watch all instruments as they comethrough the trocars (unless directedotherwise)

4. Ask if you want to come out andclean and re-FRED the lens

5. Look outside the body at the trocarsand instrument angles to reorientyourself

6. Keep the camera oriented at alltimes (i.e., up and down); usually thecamera cord is on the bottom of thecamera—orient yourself to the camerabefore entering the abdomen

7. You may clean the camera lens attimes by lightly touching the lens tothe liver or peritoneum

8. Never let the camera lens come intocontact with the bowel because thecamera may get very hot and you canburn a hole in the bowel or burn thedrapes!


At what length must youclose trocar sites?

How do you get the spleenout through a trocar site aftera laparoscopic splenectomy?

What is an IOC?

What is the safest time forlaparoscopy duringpregnancy?


9. Put your helmet on (i.e., expect toget yelled at!)

10. Never act agitated when the surgeonsare a little abrupt (e.g., “Center—center the camera!”)

11. Always watch the trocars as they areremoved from the abdominal wallfor bleeding from the site and viewthe layers of the abdominal wall,looking for bleeding as you pull thecamera trocar out at the end of thecase

�5 mm should be closed

Morcellation in a bag, then removepiecemeal

IntraOperative Cholangiogram (doneduring a lap chole to evaluate thecommon bile duct anatomy and to lookfor any retained duct stone)

Second trimester

TraumaChapter 38What widely accepted protocol does trauma care in the United States follow?

What are the three mainelements of the ATLS protocol?

Advanced Trauma Life Support (ATLS)precepts of the American College of Surgeons

1. Primary survey/resuscitation2. Secondary survey3. Definitive care


Chapter 38 / Trauma 227

PRIMARY SURVEY

Think: “ABCDEs”:Airway (and C-spine stabilization)BreathingCirculationDisabilityExposure and Environment

Life-threatening problems discoveredduring the primary survey are alwaysaddressed before proceeding to the next step

What are the five steps ofthe primary survey?

What principles are followedin completing the primarysurvey?

AIRWAY

What are the goals duringassessment of the airway?

In addition to the airway,what MUST be consideredduring the airway step?

What comprises spinalimmobilization?

In an alert patient, what isthe quickest test for an adequate airway?

What is the first maneuverused to establish an airway?

If these methods are unsuccessful, what is thenext maneuver used toestablish an airway?

Securing the airway and protecting thespinal cord

Spinal immobilization

Use of a full backboard and rigid cervicalcollar

Ask a question: If the patient can speak,the airway is intact

Chin lift, jaw thrust, or both; if successful,often an oral or nasal airway can beused to temporarily maintain the airway

Endotracheal intubation

How and when should thepatient history be obtained?

It should be obtained while completingthe primary survey; often the rescuesquad, witnesses, and family membersmust be relied upon


If all other methods areunsuccessful, what is thedefinitive airway?


Cricothyroidotomy, a.k.a. “surgical airway”:Incise the cricothyroid membranebetween the cricoid cartilage inferiorlyand the thyroid cartilage superiorly andplace an endotracheal or tracheostomytube into the trachea

What must always be kept in mind during difficultattempts to establish an airway?

Spinal immobilization and adequate oxygenation; if at all possible, patientsmust be adequately ventilated with 100%oxygen using a bag and mask before anyattempt to establish an airway

BREATHING

What are the goals in assessing breathing?

What comprises adequateassessment of breathing?

What are the life-threateningconditions that MUST bediagnosed and treated during the breathing step?

Securing oxygenation and ventilationTreating life-threatening thoracic injuries

Inspection—for air movement, respiratoryrate, cyanosis, tracheal shift, jugularvenous distention, asymmetric chestexpansion, use of accessory muscles of respiration, open chest wounds

Auscultation—for breath soundsPercussion—for hyperresonance or

dullness over either lung fieldPalpation—for presence of subcutaneous

emphysema, flail segments

Tension pneumothorax, open pneumothorax, massive hemothorax



Pneumothorax

What is it?


What is the treatment of atension pneumothorax?

What is the medical term fora “sucking chest wound”?

What is a tube thoracostomy?

How is an open pneumothorax diagnosedand treated?

What does a pneumothoraxlook like on chest X-ray?

Injury to the lung, resulting in release of airinto the pleural space between the normallyapposed parietal and visceral pleura

Tension pneumothorax is a clinicaldiagnosis: dyspnea, jugular venousdistention, tachypnea, anxiety, pleuriticchest pain, unilateral decreased or absentbreath sounds, tracheal shift away fromthe affected side, hyperresonance on theaffected side

Rapid thoracostomy incision or immedi-ate decompression by needle thoracos-tomy in the second intercostal spacemidclavicular line, followed by tube thoracostomy placed in the anterior/midaxillary line in the fourth intercostalspace (level of the nipple in men)

Open pneumothorax

“Chest tube”

Diagnosis: usually obvious, with airmovement through a chest wall defectand pneumothorax on CXR

Treatment in the ER: tube thoracostomy(chest tube), occlusive dressing overchest wall defect

Loss of lung markings (Figure shows aright-sided pneumothorax; arrows pointout edge of lung-air interface)


Flail Chest

What is it?


Two separate fractures in three or moreconsecutive ribs


What is the major cause ofrespiratory compromise withflail chest?


Cardiac Tamponade

What is it?

What are the signs andsymptoms?

Flail segment of chest wall that movesparadoxically (sucks in with inspirationand pushes out with expiration oppositethe rest of the chest wall)

Underlying pulmonary contusion!

Intubation with positive pressure ventilation and PEEP PRN (let ribs healon their own)

Bleeding into the pericardial sac, resultingin constriction of heart, decreasing inflowand resulting in decreased cardiac output(the pericardium does not stretch!)

Tachycardia/shock with Beck’s triad,pulsus paradoxus, Kussmaul’s sign


Define the following:Beck’s triad

Kussmaul’s sign

How is cardiac tamponadediagnosed?


Massive Hemothorax



What are indications foremergent thoracotomy forhemothorax?


1. Hypotension2. Muffled heart sounds3. JVD

JVD with inspiration

Ultrasound (echocardiogram)

Pericardial window—if blood returnsthen median sternotomy to rule out andtreat cardiac injury

Unilaterally decreased or absent breathsounds; dullness to percussion; CXR, CTscan, chest tube output

Volume replacementTube thoracostomy (chest tube)Removal of the blood (which will allow

apposition of the parietal and visceralpleura, sealing the defect and slowingthe bleeding)

Massive hemothorax �1. �1500 cc of blood on initial

placement of chest tube2. Persistent �200 cc of bleeding via

chest tube per hour 4 hours

CIRCULATION

What are the goals in assessing circulation?

What is the initial test foradequate circulation?

What comprises adequateassessment of circulation?

Securing adequate tissue perfusion; treatment of external bleeding

Palpation of pulses: As a rough guide, if a radial pulse is palpable, then systolicpressure is at least 80 mm Hg; if afemoral or carotid pulse is palpable, thensystolic pressure is at least 60 mm Hg

Heart rate, blood pressure, peripheralperfusion, urinary output, mental status,capillary refill (normal �2 seconds), examof skin: cold, clammy � hypovolemia


Who can be hypovolemicwith normal blood pressure?

Which patients may notmount a tachycardicresponse to hypovolemicshock?

How are sites of externalbleeding treated?

What is the best andpreferred intravenous (IV)access in the traumapatient?

What are alternate sites ofIV access?

For a femoral vein catheter,how can the anatomy of theright groin be remembered?

What is the trauma resuscitation fluid of choice?

What types of decompressiondo trauma patients receive?

What are the contraindications toplacement of a Foley?


Young patients; autonomic tone canmaintain blood pressure untilcardiovascular collapse is imminent

Those with concomitant spinal cord injuries

Those on �-blockersWell-conditioned athletes

By direct pressure; �/� tourniquets

“Two large-bore IVs” (14–16 gauge), IV catheters in the upper extremities(peripheral IV access)

Percutaneous and cutdown catheters inthe lower leg saphenous; central accessinto femoral, jugular, subclavian veins

Lateral to medial “NAVEL”:NerveArteryVeinEmpty spaceLymphatics

Thus, the vein is medial to the femoralartery pulse (Or, think: “venous close to penis”)

Lactated Ringer’s (LR) solution (isotonic, and the lactate helps buffer thehypovolemia-induced metabolic acidosis)

Gastric decompression with an NG tubeand Foley catheter bladder decompressionafter normal rectal exam

Signs of urethral injury:Severe pelvic fracture in menBlood at the urethral meatus (penile

opening)“High-riding” “ballotable” prostate

(loss of urethral tethering)Scrotal/perineal injury/ecchymosis


What test should beobtained prior to placing aFoley catheter if urethralinjury is suspected?

How is gastricdecompression achievedwith a maxillofacialfracture?


Retrograde UrethroGram (RUG): dye inpenis retrograde to the bladder and x-raylooking for extravasation of dye

Not with an NG tube because the tubemay perforate through the cribriformplate into the brain; place an oral-gastrictube (OGT), not an NG tube

DISABILITY

What are the goals in assessing disability?

What comprises adequateassessment of disability?

Describe the GCS scoringsystem.

Determination of neurologic injury(Think: neurologic disability)

Mental status—Glasgow Coma Scale(GCS)

Pupils—a blown pupil suggests ipsilateralbrain mass (blood) as herniation of thebrain compresses CN III

Motor/sensory—screening exam for lateralizing extremity movement, sensory deficits

Eye opening (E)4—Opens spontaneously3—Opens to voice (command)2—Opens to painful stimulus1—Does not open eyes

(Think: Eyes � “four eyes”)

Motor response (M)6—Obeys commands5—Localizes painful stimulus4—Withdraws from pain3—Decorticate posture2—Decerebrate posture1—No movement

(Think: Motor � “6-cylinder motor”)

Verbal response (V)5—Appropriate and oriented4—Confused3—Inappropriate words2—Incomprehensible sounds1—No sounds

(Think: Verbal � “Jackson 5”)


What is a normal humanGCS?

What is the GCS score for adead man?

What is the GCS score for apatient in a “coma”?

How does scoring differ ifthe patient is intubated?


GCS 15

GCS 3

GCS 8

Verbal evaluation is omitted and replacedwith a “T”; thus, the highest score for anintubated patient is 11 T

EXPOSURE AND ENVIRONMENT

What are the goals inobtaining adequateexposure?

What is the “environment”of the E in ABCDEs?

Complete disrobing to allow a thoroughvisual inspection and digital palpation ofthe patient during the secondary survey

Keep a warm Environment (i.e., keep thepatient warm; a hypothermic patient canbecome coagulopathic)

SECONDARY SURVEY

What principle is followed in completing the secondarysurvey?

Why look in the ears?

Examination of what part ofthe trauma patient’s body isoften forgotten?

What are typical signs ofbasilar skull fracture?

What diagnosis in the anterior chamber must not be missed on the eyeexam?

Complete physical exam, including allorifices: ears, nose, mouth, vagina,rectum

Hemotympanum is a sign of basilar skullfracture; otorrhea is a sign of basilar skullfracture

Patient’s back (logroll the patient andexamine!)

Raccoon eyes, Battle’s sign, clear otorrheaor rhinorrhea, hemotympanum

Traumatic hyphema � blood in the anterior chamber of the eye



Nasal septal hematoma: Hematoma mustbe evacuated; if not, it can result inpressure necrosis of the septum!

Dental malocclusion: Tell the patient to“bite down” and ask, “Does that feel normal to you?”

Crepitus or subcutaneous emphysema fromtracheobronchial disruption/PTX; trachealdeviation from tension pneumothorax;jugular venous distention from cardiactamponade; carotid bruit heard withseatbelt neck injury resulting in carotidartery injury

Lateral and anterior-posterior compressionof the thorax to elicit pain/instability

None: Diagnosis of great vessel injuryrequires a high index of suspicion basedon the mechanism of injury, associatedinjuries, and CXR/radiographic findings(e.g., widened mediastinum)

CT angiogram

Concomitant injury to the abdomen:Remember, the diaphragm extends to thelevel of the nipples in the male on fullexpiration

Indicates PTX, until proven otherwise

Logrolling the patient to allow completevisualization of the back and palpationof the spine to elicit pain over fractures,step off (spine deformity)

Alert patient without any evidence ofhead/spinal cord injury or drug/EtOHintoxication (even then, the abdominalexam is not 100% accurate)

What potentially destructivelesion must not be missed onthe nasal exam?

What is the best indicationof a mandibular fracture?

What signs of thoracictrauma are often found onthe neck exam?

What is the best physical examfor broken ribs or sternum?

What physical signs arediagnostic for thoracic greatvessel injury?

What is the best way to diagnose or rule out aorticinjury?

What must be considered inevery penetrating injury ofthe thorax at or below thelevel of the nipple?

What is the significance ofsubcutaneous air?

What is the physical examtechnique for examining thethoracic and lumbar spine?

What conditions must existto pronounce an abdominalphysical exam negative?


What physical signs mayindicate intra-abdominalinjury?

What is the seatbelt sign?

What must be documentedfrom the rectal exam?

What is the best physicalexam technique to test forpelvic fractures?

What is the “halo” sign?

What physical signs indicatepossible urethral injury, thuscontraindicating placementof a Foley catheter?

What must be documentedfrom the extremity exam?

What complication afterprolonged ischemia to thelower extremity must betreated immediately?

What is the treatment forthis condition?

What injuries must besuspected in a traumapatient with a progressivedecline in mental status?


Tenderness; guarding; peritoneal signs;progressive distention (always use a gastric tube for decompression of air);seatbelt sign

Ecchymosis on lower abdomen fromwearing a seatbelt (�10% of patients withthis sign have a small bowel perforation!)

Sphincter tone (as an indication of spinalcord function); presence of blood (as anindication of colon or rectal injury); prostateposition (as an indication of urethral injury)

Lateral compression of the iliac crestsand greater trochanters and anterior-posterior compression of the symphysispubis to elicit pain/instability

Cerebrospinal fluid from nose/ear will forma clear “halo” around the blood on a cloth

High-riding ballotable prostate onrectal exam; presence of blood at themeatus; scrotal or perineal ecchymosis

Any fractures or joint injuries; any openwounds; motor and sensory exam,particularly distal to any fractures; distalpulses; peripheral perfusion

Compartment syndrome

Fasciotomy (four compartments belowthe knee)

Epidural hematoma, subdural hematoma,brain swelling with rising intracranialpressure

But hypoxia/hypotension must beruled out!



TRAUMA STUDIES

What are the classic blunttrauma ER x-rays?

What are the commontrauma labs?

Will the hematocrit be low after an acute massivehemorrhage?

How can a C-spine be evaluated?

What patients can have their C-spines cleared by a physical exam?

How do you rule out a C-spine bony fracture?

What do you do if no bonyC-spine fracture is apparenton CT scan and you cannotobtain an MRI in aCOMATOSE patient?

Which x-rays are used forevaluation of cervical spineLIGAMENTOUS injury?

What findings on chest filmare suggestive of thoracicaortic injury?

1. AP (anterior-to-posterior) chest film2. AP pelvis film

Blood for complete blood count,chemistries, amylase, liver function tests,lactic acid, coagulation studies, and typeand crossmatch; urine for urinalysis

No (no time to equilibrate)

1. Clinically by physical exam2. Radiographically

No neck pain on palpation with full rangeof motion (FROM) with no neurologicinjury (GCS 15), no EtOH/drugs, no distracting injury, no pain meds

With a CT scan of the C-spine

This is controversial; the easiest answer isto leave the patient in a cervical collar

MRI, lateral flexion and extension C-spine films

Widened mediastinum (most commonfinding), apical pleural capping, loss of aortic contour/KNOB/AP window,depression of left main stem bronchus,nasogastric tube/tracheal deviation, pleural fluid, elevation of right mainstembronchus, clinical suspicion, high-speedmechanism


What study is used to ruleout thoracic aortic injury?

What is the most commonsite of thoracic aortictraumatic tear?

What studies are available toevaluate for intra-abdominalinjury?

What is a FAST exam?

What does the FAST examlook for?

What does DPL stand for?

What diagnostic test is thetest of choice for evaluationof the unstable patient withblunt abdominal trauma?

What is the indication forabdominal CT scan in blunttrauma?

What is the indication forDPL or FAST in blunttrauma?

How is a DPL performed?

What is a “grossly positive”DPL?


Spiral CT scan of mediastinum lookingfor mediastinal hematoma with CTA

Thoracic arch aortogram (gold standard)

Just distal to the take-off of the left subclavian artery

FAST, CT scan, DPL

Ultrasound: Focused Assessment withSonography for Trauma � FAST

Blood in the peritoneal cavity looking atMorison’s pouch, bladder, spleen, andpericardial sac

Diagnostic Peritoneal Lavage

FAST

Normal vital signs with abdominalpain/tenderness/mechanism

Unstable vital signs (hypotension)

Place a catheter below the umbilicus (inpatients without a pelvic fracture) intothe peritoneal cavity

Aspirate for blood and if �10 cc are aspirated, infuse 1 L of saline or LR

Drain the fluid (by gravity) and analyze

�10 cc blood aspirated


Where should the DPLcatheter be placed in apatient with a pelvicfracture?

What constitutes a positiveperitoneal tap?

What are the indicators of apositive peritoneal lavage inblunt trauma?

What must be in placebefore a DPL is performed?

What injuries does CT scanmiss?

What injuries does DPLmiss?

What study is used toevaluate the urethra in casesof possible disruption due toblunt trauma?


Above the umbilicus

Common error: If you go below theumbilicus, you may get into a pelvichematoma tracking between the fascialayers and thus obtain a false-positiveDPL

Prior to starting a peritoneal lavage, theDPL catheter should be aspirated; if �10 mL of blood or any enteric contentsare aspirated, then this constitutes a positive tap and requires laparotomy

Classic: Inability to read newsprint through

lavaged fluidRBC �100,000/mm3

WBC �500/mm3 (Note: mm3, notmm2)

Lavage fluid (LR/NS) drained fromchest tube, Foley, NG tube

Less common:Bile presentBacteria presentFeces presentVegetable matter presentElevated amylase level

NG tube and Foley catheter (to removethe stomach and bladder from the line of fire!)

Small bowel injuries and diaphragminjuries

Retroperitoneal injuries

Retrograde urethrogram (RUG)


What are the most emergentorthopaedic injuries?

What findings would requirea celiotomy in a blunt traumavictim?

What is the treatment of agunshot wound to the belly?

What is the evaluation of astab wound to the belly?


1. Hip dislocation—must be reducedimmediately

2. Exsanguinating pelvic fracture (binderor external fixator)

Peritoneal signs, free air on CXR/CTscan, unstable patient with positive FASTexam or positive DPL results

Exploratory laparotomy

If there are peritoneal signs, heavybleeding, shock, perform exploratorylaparotomy; otherwise, many surgeonseither observe the asymptomatic stabwound patient closely, use local woundexploration to rule out fascialpenetration, or use DPL

PENETRATING NECK INJURIES

What depth of neck injurymust be further evaluated?

Define the anatomy of theneck by trauma zones:

Zone III

Zone II

Zone I

Penetrating injury through the platysma

Angle of the mandible and up

Angle of the mandible to the cricoid cartilage

Below the cricoid cartilage


How do most surgeons treatpenetrating neck injuries(those that penetrate theplatysma) by neck zone:

Zone III

Zone II

Zone I

What is selectiveexploration?

What are the indications forsurgical exploration in allpenetrating neck wounds(Zones I, II, III)?

How can you remember theorder of the neck traumazones and Le Fortefractures?


Selective exploration

Surgical exploration vs. selectiveexploration

Selective exploration

Selective exploration is based on diagnosticstudies that include A-gram or CT A-gram,bronchoscopy, esophagoscopy

“Hard signs” of significant neck damage:shock, exsanguinating hemorrhage,expanding hematoma, pulsatilehematoma, neurologic injury, subQemphysema

In the direction of carotid blood flow

MISCELLANEOUS TRAUMA FACTS

What is the “3-for-1” rule?

What is the minimal urineoutput for an adult traumapatient?

Trauma patient in hypovolemic shockacutely requires 3 L of crystalloid (LR)for every 1 L of blood loss

50 mL/hr

Carotid

Neck zones Le Forte fracture

IIIIII III

II

I


How much blood can be lostinto the thigh with a closedfemur fracture?

Can an adult lose enoughblood in the “closed” skullfrom a brain injury to causehypovolemic shock?

Can a patient behypotensiveafter an isolated head injury?

What is the brief ATLS history?

In what population is a surgical cricothyroidotomynot recommended?

What are the signs of alaryngeal fracture?

What is the treatment ofrectal penetrating injury?

What is the treatment ofEXTRAperitoneal minorbladder rupture?

What intra-abdominal injury isassociated with seatbelt use?

What is the treatment of apelvic fracture?

Bleeding from pelvic fracturesis most commonly caused byarterial or venous bleeding?


Up to 1.5 L of blood

Absolutely not! But infants can loseenough blood from a brain injury tocause shock

Yes, but rule out hemorrhagic shock!

“AMPLE” history:AllergiesMedicationsPMHLast meal (when)Events (of injury, etc.)

Any patient younger than 12 years; insteadperform needle cricothyroidotomy

Subcutaneous emphysema in neckAltered voicePalpable laryngeal fracture

Diverting proximal colostomy; closureof perforation (if easy, and definitely ifintraperitoneal); and presacral drainage

“Bladder catheter” (Foley) drainage andobservation; intraperitoneal or large bladder rupture requires operative closure

Small bowel injuries (L2 fracture,pancreatic injury)

�/� pelvic binder until the external fixator is placed; IVF/blood; �/� A-gramto embolize bleeding pelvic vessels

Venous (�85%)


If a patient has a lacerationthrough an eyebrow, shouldyou shave the eyebrow priorto suturing it closed?

What is the treatment ofextensive irreparable biliary,duodenal, and pancreatichead injury?

What is the most commonintra-abdominal organinjured with penetratingtrauma?

How high up do thediaphragms go?

Classic trauma question: “If you have only one vial ofblood from a trauma victimto send to the lab, what testshould be ordered?”

What is the treatment ofpenetrating injury to thecolon?

What is the treatment ofsmall bowel injury?

What is the treatment ofminor pancreatic injury?

What is the most commonlyinjured abdominal organwith blunt trauma?

What is the treatment forsignificant duodenal injury?


No—20% of the time, the eyebrow willnot grow back if shaved!

Trauma Whipple

Small bowel

To the nipples (intercostal space #4);thus, intra-abdominal injury withpenetrating injury below the nipplesmust be ruled out

Type and cross (for blood transfusion)

If the patient is in shock, resection andcolostomy

If the patient is stable, the trend is primary anastomosis/repair

Primary closure or resection and primaryanastomosis

Drainage (e.g., JP drains)

Liver (in recent studies)

Pyloric exclusion:1. Close duodenal injury2. Staple off pylorus3. Gastrojejunostomy


What is the treatment formassive tail of pancreasinjury?

What is “damage control”surgery?

What is the “lethal triad”?

What comprises the workup/treatment of a stableparasternal chest gunshot/stab wound?

What is the diagnosis withNGT in chest on CXR?


Distal pancreatectomy (usually performsplenectomy also)

Stop major hemorrhage and GI soilagePack and get out of the O.R. ASAP to

bring the patient to the ICU to warm,correct coags, and resuscitate

Return patient to O.R. when stable,warm, and not acidotic

“ACH”:1. Acidosis2. Coagulopathy3. Hypothermia

(Think: ACHe � Acidosis, Coagulopathy,Hypothermia)

1. CXR2. FAST, chest tube, �/� O.R. for sub-

xiphoid window; if blood returns, thensternotomy to assess for cardiac injury

Ruptured diaphragm with stomach inpleural cavity (go to ex lap)

hrf ‘07

Stomach

NG tube instomach

Diaphragm

What films are typicallyobtained to evaluate extremity fractures?

Complete views of the involved extremity,including the joints above and below thefracture


What finding on ABD/pelvicCT scan requires ex lap inthe blunt trauma patientwith normal vital signs?

Can you rely on a negativeFAST in the unstable patientwith a pelvic fracture?


Free air; also strongly consider in thepatient with no solid organ injury but lotsof free fluid � both to rule out hollowviscus injury

No—perform DPL (above umbilicus)

Outline basic workup for a victim of severe blunt traumaIn ER: Airway, physical exam. IV X 2, labs, type and cross,

OGT/NGT, Foley, chest tube PRNX-rays: CXR, pelvic, femur (if femur fracture is suspected)

+/� bloodtransfusion

Hypotension Normal vital signs

+ Pelvic fracture Chest CTC-spine/head CT, ABD/pelvic CT

Extremity films PRN

ICU PRN

Flex/ext latC-spine films orMRI C-spine orphysical examC-spine

FASTFAST

(+)FAST

O.R. ex lapO.R. ex lap

Ext fixatorPRNExternal

pelvic fixator

PelvicA-gram PRN

Chest CTABD/pelvic CT

Pelvic A-gram PRN

Ext films PRN

[Note: AP = anteroposterior; Ext = extremity; OGT = orogastric tube;FAST = Focused Assessment Sonogram for Trauma; lat = lateral; C = cervical.]

Ext films PRNICU

ICU

C-spine/head CT

Chest CT

Chest CTABD/pelvic CTC-spine/head CT

Ext films PRN

Ext filmsPRN

ICU

ICU

C-spine/head CT

(�)FAST (+)FAST (�)FAST

� Pelvic fracture

(+) DPL (–)

Chest CTC-spine/head CT


What lab tests are used tolook for intra-abdominalinjury in children?

What is the only real indica-tion for MAST trousers?

What is the treatment forhuman and dog bites?

What percentage of pelvicfracture bleeding isexclusively venous?

What is sympatheticophthalmia?

What can present after blunttrauma with neurologicaldeficits and a normal brainCT scan?


Liver function tests (LFTs) � cASTand/or cALT

Prehospitalization, pelvic fracture

Leave wound open, irrigation, antibiotics

85%

Blindness in one eye that results in subsequent blindness in the contralateraleye (autoimmune)

Diffuse Axonal Injury (DAI), carotidartery injury

BurnsChapter 39Define:

TBSA Total Body Surface Area

STSG Split Thickness Skin Graft

Are acid or alkali chemical In general, ALKALI burns are more burns more serious? serious because the body cannot buffer

the alkali, thus allowing them to burn formuch longer

Why are electrical burns so Most of the destruction from electricaldangerous? burns is internal because the route of

least electrical resistance follows nerves,blood vessels, and fascia; injury is usually worse than external burns atentrance and exit sites would indicate;cardiac dysrhythmias, myoglobinuria,acidosis, and renal failure are common


How is myoglobinuria To avoid renal injury, think “HAM”:treated? Hydration with IV fluids

Alkalization of urine with IV bicarbonate

Mannitol diuresis

Define level of burn injury:First-degree burns Epidermis only

Second-degree burns Epidermis and varying levels of dermis

Third-degree burns A.k.a. “full thickness”; all layers of theskin including the entire dermis (Think:“getting the third degree”)

Fourth-degree burns Burn injury into bone or muscle

How do first-degree burns Painful, dry, red areas that do not form present? blisters (think of sunburn)

How do second-degree burns Painful, hypersensitive, swollen, mottledpresent? areas with blisters and open weeping

surfaces

How do third-degree burns Painless, insensate, swollen, dry, mottledpresent? white, and charred areas; often described

as dried leather

What is the major clinical Third-degree burns are painless, anddifference between second- second-degree burns are painfuland third-degree burns?

By which measure is burn Depth of burn and TBSA affected byseverity determined? second- and third-degree burns

TBSA is calculated by the “rule of nines” in adults and by a modifiedrule in children to account for the disproportionate size of the head andtrunk

Chapter 39 / Burns 247


What is the “rule of nines”? In an adult, the total body surface areathat is burned can be estimated by thefollowing:

Each upper limb � 9%Each lower limb � 18%Anterior and posterior trunk � 18% eachHead and neck � 9%Perineum and genitalia � 1%


What is the “rule of the palm”? Surface area of the patient’s palm is �1%of the TBSA used for estimating size ofsmall burns

What is the burn center referralcriteria for the following?

Second-degree burns �20% TBSA

Third-degree burns �5% TBSASecond degree �10% TBSA in children

and the elderlyAny burns involving the face, hands, feet,

or perineumAny burns with inhalation injuryAny burns with associated traumaAny electrical burns


What is the treatment of Keep clean, � Neosporin®, pain medsfirst-degree burns?

What is the treatment of Remove blisters; apply antibioticsecond-degree burns? ointment (usually Silvadene®) and

dressing; pain medsMost second-degree burns do not require

skin grafting (epidermis grows fromhair follicles and from margins)

What are some newer 1. Biobrane® (silicone artificialoptions for treating a epidermis—temporary)second-degree burn? 2. Silverlon® (silver ion dressings)

What is the treatment of Early excision of eschar (within first weekthird-degree burns? postburn) and STSG

How can you decrease Tourniquets as possible, topical bleeding during excision? epinephrine, topical thrombin

What is an autograft STSG? STSG from the patient’s own skin

What is an allograft STSG? STSG from a cadaver (temporarycoverage)

What thickness is the STSG? 10/1000 to 15/1000 of an inch (down tothe dermal layer)

What prophylaxis should the Tetanusburn patient get in the ER?

What is used to evaluate the Fluoresceineyes after a third-degree burn?

What principles guide the ABCDEs, then urine output; check forinitial assessment and eschar and compartment syndromesresuscitation of the burn patient?

What are the signs of Smoke and soot in sputum/mouth/nose,smoke inhalation? nasal/facial hair burns, carboxyhemoglobin,

throat/mouth erythema, history of loss ofconsciousness/explosion/fire in smallenclosed area, dyspnea, low O2 saturation,confusion, headache, coma



What diagnostic imaging is Bronchoscopyused for smoke inhalation?

What lab value assesses Carboxyhemoglobin level (a carboxy-smoke inhalation? hemoglobin level of �60% is associated

with a 50% mortality); treat with 100%O2 and time

How should the airway be With a low threshold for intubation;managed in the burn patient oropharyngeal swelling may occlude thewith an inhalational injury? airway so that intubation is impossible;

100% oxygen should be administeredimmediately and continued until signifi-cant carboxyhemoglobin is ruled out

What is “burn shock”? Burn shock describes the loss of fluidfrom the intravascular space as a resultof burn injury, which causes “leakingcapillaries” that require crystalloid infusion

What is the “Parkland V � TBSA Burn (%) � Weight (kg) � 4formula”? Formula widely used to estimate the

volume (V) of crystalloid necessary forthe initial resuscitation of the burnpatient; half of the calculated volumeis given in the first 8 hours, the restin the next 16 hours

What burns qualify for the �20% TBSA second- and third-degreeParkland formula? burns only

What is the Brooke formula Replace 2 cc for the 4 cc in the Parklandfor burn resuscitation? formula

How is the crystalloid given? Through two large-bore peripheralvenous catheters

Can you place an IV or central YESline through burned skin?

What is the adult urine 30–50 cc (titrate IVF)output goal?



Why is glucose-containing Patient’s serum glucose will be elevatedIVF contraindicated in burn on its own because of the stress responsepatients in the first 24 hours postburn?

What fluid is used after the Colloid; use D5W and 5% albumin atfirst 24 hours postburn? 0.5 cc/kg/% burn surface area

Why should D5W IV be Because of the massive sodium load inadministered after 24 hours the first 24 hrs of LR infusion andpostburn? because of the massive evaporation of

H2O from the burn injury, the patientwill need free water; after 24 hours, thecapillaries begin to work and then thepatient can usually benefit from albuminand D5W

What is the minimal urine Adults 30 cc; children 1–2 cc/kg/hroutput for burn patients?

How is volume status Urine output, blood pressure, heartmonitored in the burn rate, peripheral perfusion, and mentalpatient? status; Foley catheter is mandatory and

may be supplemented by central venouspressure and pulmonary capillary wedgepressure monitoring

Why do most severely Patients with greater than 20% TBSAburned patients require burns usually develop a paralytic ileus →nasogastric decompression? vomiting → aspiration risk → pneumonia

What stress prophylaxis must H2 blocker to prevent burn stress ulcerbe given to the burn patient? (Curling’s ulcer)

What are the signs of burn Increased WBC with left shift, wound infection? discoloration of burn eschar (most

common sign), green pigment, necroticskin lesion in unburned skin, edema,ecchymosis tissue below eschar, second-degree burns that turn into third-degreeburns, hypotension

Is fever a good sign of NOinfection in burn patients?



What are the common Staphylococcus aureus, Pseudomonas,organisms found in burn Streptococcus, Candida albicanswound infections?

How is a burn wound Send burned tissue in question to theinfection diagnosed? laboratory for quantitative burn wound

bacterial count; if the count is �105/gram,infection is present and IV antibioticsshould be administered

How are minor burns Gentle cleaning with nonionic detergentdressed? and débridement of loose skin and broken

blisters; the burn is dressed with a topicalantibacterial (e.g., neomycin) andcovered with a sterile dressing

How are major burns Cleansing and application of topicaldressed? antibacterial agent

Why are systemic IV antibi- Bacteria live in the eschar, which isotics contraindicated in avascular (the systemic antibiotic willfresh burns? not be delivered to the eschar); thus,

apply topical antimicrobial agents

Note some advantages and disadvantages of the following topical antibiotic agents:

Silver sulfadiazine Painless, but little eschar penetration, (Silvadene®) misses Pseudomonas, and has idiosyncratic

neutropenia; sulfa allergy is contraindi-cation

Mafenide acetate Penetrates eschars, broad spectrum (but(Sulfamylon®) misses Staphylococcus), causes pain on

application; triggers allergic reaction in7% of patients; may cause acid-baseimbalances (Think: Mafenide ACetate �Metabolic ACidosis); agent of choice inalready-contaminated burn wounds

Polysporin® Polymyxin B sulfate; painless, clear, usedfor facial burns; does not have a wideantimicrobial spectrum



Are prophylactic systemic No—prophylactic antibiotics have notantibiotics administered to been shown to reduce the incidenceburn patients? of sepsis, but rather have been shown to

select for resistant organisms; IVantibiotics are reserved for established wound infections, pneumonia, urinary tract infections, etc.

Are prophylactic antibiotics Noadministered for inhalational injury?

Circumferential, full- Distal neurovascular impairmentthickness burns to the extremities are at risk for what complication?

How is it treated? Escharotomy: full-thickness longitudinalincision through the eschar with scalpelor electrocautery

What is the major infection Pneumonia, central line infection (change complication (other than central lines prophylactically every 3 towound infection) in burn 4 days)patients?

Is tetanus prophylaxis Yes, it is mandatory in all patients exceptrequired in the burn patient? those actively immunized within the past

12 months (with incomplete immunization:toxoid � 3)

From which burn wound is Third degreewater evaporation highest?

Can infection convert a Yes!partial-thickness injury into a full-thickness injury?

How is carbon monoxide 100% O2 (� hyperbaric O2)inhalation overdose treated?

Which electrolyte must be Na� (sodium)closely followed acutely after a burn?



When should central lines be Most burn centers change them everychanged in the burn patient? 3 to 4 days

What is the name of the Curling’s ulcer (Think: CURLING iron gastric/duodenal ulcer burn � CURLING’s burn ulcer)associated with burn injury?

How are STSGs nourished IMBIBITION (fed from wound bedin the first 24 hours? exudate)


Upper GI BleedingChapter 40What is it? Bleeding into the lumen of the proximal

GI tract, proximal to the ligament of Treitz

What are the signs/ Hematemesis, melena, syncope,symptoms? shock, fatigue, coffee-ground emesis,

hematochezia, epigastric discomfort,epigastric tenderness, signs ofhypovolemia, guaiac-positive stools

Why is it possible to have Blood is a cathartic and hematochezia hematochezia? usually indicates a vigorous rate of

bleeding from the UGI source

Are stools melenic or Melenic (melanotic is incorrect)melanotic?

How much blood do you �50 cc of bloodneed to have melena?

What are the risk factors? Alcohol, cigarettes, liver disease, burn/trauma, aspirin/NSAIDs, vomiting, sepsis, steroids, previous UGI bleeding,history of peptic ulcer disease (PUD),esophageal varices, portal hypertension,splenic vein thrombosis, abdominal aorticaneurysm repair (aortoenteric fistula),burn injury, trauma


What is the most common PUD—duodenal and gastric ulcers (50%)cause of significant UGI bleeding?

What is the common 1. Acute gastritisdifferential diagnosis of 2. Duodenal ulcerUGI bleeding? 3. Esophageal varices

4. Gastric ulcer5. Esophageal6. Mallory-Weiss tear

What is the uncommon Gastric cancer, hemobilia, duodenal differential diagnosis of diverticula, gastric volvulus, Boerhaave’sUGI bleeding? syndrome, aortoenteric fistula,

paraesophageal hiatal hernia, epistaxis,NGT irritation, Dieulafoy’s ulcer,angiodysplasia

Which diagnostic tests are History, NGT aspirate, abdominal x-ray,useful? endoscopy (EGD)

What is the diagnostic test of EGD (�95% diagnosis rate)choice with UGI bleeding?

What are the treatment Coagulation, injection of epinephrineoptions with the endoscope (for vasoconstriction), injection of during an EGD? sclerosing agents (varices), variceal ligation

(banding)

Which lab tests should be Chem-7, bilirubin, LFTs, CBC,performed? type & cross, PT/PTT, amylase

Why is BUN elevated? Because of absorption of blood by the GItract

What is the initial treatment? 1. IVFs (16 G or larger peripheral IVS � 2), Foley catheter (monitorfluid status)

2. NGT suction (determine rate andamount of blood)

3. Water lavage (use warm H2O—willremove clots)

4. EGD: endoscopy (determine etiology/location of bleeding and possibletreatment—coagulate bleeders)

Chapter 40 / Upper GI Bleeding 255


Why irrigate in an upper To remove the blood clot so you can seeGI bleed? the mucosa

What test may help identify Selective mesenteric angiographythe site of MASSIVE UGI bleeding when EGD fails to diagnose cause and blood continues per NGT?

What are the indications for Refractory or recurrent bleeding and sitesurgical intervention in UGI known, �3 u PRBCS to stabilize orbleeding? �6 u PRBCs overall

What percentage of patients �10%require surgery?

What percentage of patients �80% to 85%spontaneously stop bleeding?

What is the mortality of acute Overall 10%, 60–80 years of age 15%, UGI bleeding? older than 80 years of age 25%

What are the risk factors for Age older than 60 yearsdeath following UGI bleed? Shock

�5 units of PRBC transfusionConcomitant health problems

PEPTIC ULCER DISEASE (PUD)

What is it? Gastric and duodenal ulcers

What is the incidence in the �10% of the population will suffer from United States? PUD during their lifetime!

What are the possible Pain, hemorrhage, perforation, obstructionconsequences of PUD?

What percentage of patients �20%with PUD develops bleeding from the ulcer?

Which bacteria are Helicobacter pyloriassociated with PUD?



What is the treatment? Treat H. pylori with MOC or ACO 2-week antibiotic regimens:

MOC: Metronidazole, Omeprazole,Clarithromycin (Think: MOCk)

orACO: Ampicillin, Clarithromycin,

Omeprazole

What is the name of the sign Valentino’s signwith RLQ pain/peritonitis as a result of succus collecting from a perforated peptic ulcer?

DUODENAL ULCERS

In which age group are 40–65 years of age (younger thanthese ulcers most common? patients with gastric ulcer)

What is the ratio of male to Men � women (3:1)female patients?

What is the most common Most are within 2 cm of the pylorus in location? the duodenal bulb

What is the classic pain Food classically relieves duodenal ulcerresponse to food intake? pain (Think: Duodenum � Decreased

with food)

What is the cause? Increased production of gastric acid

What syndrome must you Zollinger-Ellison syndromealways think of with a duodenal ulcer?

What are the associated Male gender, smoking, aspirin and otherrisk factors? NSAIDs, uremia, Z-E syndrome,

H. pylori, trauma, burn injury

What are the symptoms? Epigastric pain—burning or aching, usuallyseveral hours after a meal (food, milk,or antacids initially relieve pain)

BleedingBack painNausea, vomiting, and anorexia↓ appetite



What are the signs? Tenderness in epigastric area (possibly),guaiac-positive stool, melena,hematochezia, hematemesis

What is the differential Acute abdomen, pancreatitis, cholecystitis,diagnosis? all causes of UGI bleeding, Z-E

syndrome, gastritis, MI, gastric ulcer,reflux

How is the diagnosis made? History, PE, EGD, UGI series (if patient is not actively bleeding)

When is surgery indicated Most surgeons use: �6 u PRBCwith a bleeding duodenal transfusions, �3 u PRBCs needed toulcer? stabilize, or significant rebleed

What EGD finding is Visible vessel in the ulcer crater, recentassociated with rebleeding? clot, active oozing

What is the medical PPIs (proton pump inhibitors) or H2

treatment? receptor antagonists—heal ulcers in 4 to 6 weeks in most cases

Treatment for H. pylori

When is surgery indicated? The acronym “I HOP”:Intractability

Hemorrhage (massive or relentless)Obstruction (gastric outlet obstruction)Perforation

How is a bleeding duodenal Opening of the duodenum through theulcer surgically corrected? pylorus

Oversewing of the bleeding vessel

What artery is involved with Gastroduodenal arterybleeding duodenal ulcers?

What are the common surgical options for the following conditions:

Truncal vagotomy? Pyloroplasty



Duodenal perforation? Graham patch (poor candidates, shock,prolonged perforation)

Truncal vagotomy and pyloroplasty incorporating ulcer

Graham patch and highly selective vagotomy

Truncal vagotomy and antrectomy(higher mortality rate, but lowest recurrence rate)

Duodenal obstruction Truncal vagotomy, antrectomy, andresulting from duodenal gastroduodenostomy (BI or BII)ulcer scarring (gastric Truncal vagotomy and drainage procedureoutlet obstruction)? (gastrojejunostomy)

Duodenal ulcer PGV (highly selective vagotomy)intractability? Vagotomy and pyloroplasty

Vagotomy and antrectomy BI or BII (especially if there is a coexistent pyloric/prepyloric ulcer) but associated with a higher mortality

Which ulcer operation has PGV (proximal gastric vagotomy)the highest ulcer recurrence rate and the lowest dumping syndrome rate?

Which ulcer operation has Vagotomy and antrectomythe lowest ulcer recurrence rate and the highest dumping syndrome rate?

Why must you perform a Pylorus will not open after a truncaldrainage procedure vagotomy(pyloroplasty, antrectomy) after a truncal vagotomy?

Which duodenal ulcer PGV (1/200 mortality), truncal vagotomyoperation has the lowest and pyloroplasty (1–2/200), vagotomy mortality rate? and antrectomy (1%–2% mortality)

Thus, PGV is the operation of choicefor intractable duodenal ulcers with the cost of increased risk of ulcer recurrence



What is a “kissing” ulcer? Two ulcers, each on opposite sides of thelumen so that they can “kiss”

Why may a duodenal rupture Fluid can be sterile, with a nonirritatingbe initially painless? pH of 7.0 initially

Why may a perforated Fluid from stomach/bile drains downduodenal ulcer present as paracolic gutters to lower quadrants and lower quadrant abdominal causes localized irritationpain?

GASTRIC ULCERS

In which age group are these 40–70 years old (older than the duodenalulcers most common? ulcer population)

Rare in patients younger than 40 years

How does the incidence in Men � womenmen compare with that of women?

Which is more common Duodenal ulcers are more than twice asoverall: gastric or duodenal common as gastric ulcers (Think:ulcers? Duodenal � Double rate)

What is the classic pain Food classically increases gastric ulcerresponse to food? pain

What is the cause? Decreased cytoprotection or gastricprotection (i.e., decreased bicarbonate/mucous production)

Is gastric acid production Gastric acid production is normal or low!high or low?

Which gastric ulcers are Prepyloricassociated with increased Pyloricgastric acid? Coexist with duodenal ulcers

What are the associated risk Smoking, alcohol, burns, trauma, CNS factors? tumor/trauma, NSAIDs, steroids, shock,

severe illness, male gender, advanced age

What are the symptoms? Epigastric pain�/� Vomiting, anorexia, and nausea



How is the diagnosis made? History, PE, EGD with multiple biopsy(looking for gastric cancer)

What is the most common �70% are on the lesser curvature; 5% arelocation? on the greater curvature

When and why should biopsy With all gastric ulcers, to rule out gastric be performed? cancer

If the ulcer does not heal in 6 weeks aftermedical treatment, rebiopsy (alwaysbiopsy in O.R. also) must be performed

What is the medical Similar to that of duodenal ulcer—PPIs ortreatment? H2 blockers, Helicobacter pylori treatment

When do patients with 1. For diagnosis with biopsiesgastric ulcers need to have 2. 6 weeks postdiagnosis to confirman EGD? healing and rule out gastric cancer!

What are the indications for The acronym “I CHOP”:surgery? Intractability

Cancer (rule out)Hemorrhage (massive or relentless)Obstruction (gastric outlet obstruction)Perforation

(Note: Surgery is indicated if gastric cancer cannot be ruled out)

What is the common Distal gastrectomy with excision of theoperation for hemorrhage, ulcer without vagotomy unless there isobstruction, and perforation? duodenal disease (i.e., BI or BII)

What are the options for Resect (BI, BII) and truncal vagotomyconcomitant duodenal and gastric ulcers?

What is a common option Truncal vagotomy and antrectomyfor surgical treatment of a (i.e., BI or BII)pyloric gastric ulcer?

What is a common option for Graham patcha poor operative candidate with a perforated gastric ulcer?



What must be performed in Biopsy looking for gastric cancerevery operation for gastric ulcers?

Define the following terms:Cushing’s ulcer PUD/gastritis associated with neurologic

trauma or tumor (Think: Dr. Cushing �NeuroSurgeon � CNS)

Curling’s ulcer PUD/gastritis associated with major burninjury (Think: curling iron burn)

Marginal ulcer Ulcer at the margin of a GI anastomosis

Dieulafoy’s ulcer Pinpoint gastric mucosal defect bleedingfrom an underlying vascular malformation

PERFORATED PEPTIC ULCER

What are the symptoms? Acute onset of upper abdominal pain

What causes pain in the Passage of perforated fluid along coliclower quadrants? gutters

What are the signs? Decreased bowel sounds, tympanicsound over the liver (air), peritonealsigns, tender abdomen

What are the signs of Bleeding from gastroduodenal arteryposterior duodenal erosion/ (and possibly acute pancreatitis)perforation?

What sign indicates anterior Free air (anterior perforation is moreduodenal perforation? common than posterior)

What is the differential Acute pancreatitis, acute cholecystitis,diagnosis? perforated acute appendicitis, colonic

diverticulitis, MI, any perforated viscus

Which diagnostic tests are X-ray: free air under diaphragm or inindicated? lesser sac in an upright CXR (if upright

CXR is not possible, then left lateraldecubitus can be performed because aircan be seen over the liver and notconfused with the gastric bubble)



What are the associated lab Leukocytosis, high amylase serumfindings? (secondary to absorption into the blood

stream from the peritoneum)

What is the initial treatment? NPO: NGT (↓ contamination of the peritoneal cavity)

IVF/Foley catheterAntibiotics/PPIsSurgery

What is a Graham patch? Piece of omentum incorporated into thesuture closure of perforation

What are the surgical Graham patch (open or laparoscopic)options for treatment of a Truncal vagotomy and pyloroplastyduodenal perforation? incorporating ulcer

Graham patch and highly selective vagotomy

What are the surgical options Antrectomy incorporating perforatedfor perforated gastric ulcer? ulcer, Graham patch or wedge resection

in unstable/poor operative candidates

What is the significance of May indicate two ulcers (kissing); hemorrhage and perforation posterior is bleeding and anterior is with duodenal ulcer? perforated with free air

What type of perforated Posterior perforated duodenal ulcer ulcer may present just like into the pancreas (i.e., epigastric painacute pancreatitis? radiating to the back; high serum

amylase)

What is the classic difference Duodenal � decreased painbetween duodenal and Gastric � increased paingastric ulcer symptoms as (Think: Duodenal � Decreased pain)related to food ingestion?



TYPES OF SURGERIES

Define the following terms:Graham patch For treatment of duodenal perforation in

poor operative candidates/unstablepatients

Place viable omentum over perforationand tack into place with sutures

Truncal vagotomy Resection of a 1- to 2-cm segment ofeach vagal trunk as it enters theabdomen on the distal esophagus,decreasing gastric acid secretion

What other procedure must “Drainage procedure” (pyloroplasty, be performed along with a antrectomy, or gastrojejunostomy), truncal vagotomy? because vagal fibers provide relaxation of

the pylorus, and, if you cut them, thepylorus will not open

Define the following terms:Vagotomy and pyloroplasty Pyloroplasty performed with vagotomy to

compensate for decreased gastric emptying



Vagotomy and antrectomy Remove antrum and pylorus in addition to vagotomy; reconstruct as a Billroth I or II

What is the goal of duodenal Decrease gastric acid secretion (and fix ulcer surgery? IHOP)

What is the advantage of No drainage procedure is needed; vagalproximal gastric vagotomy fibers to the pylorus are preserved; rate (highly selective of dumping syndrome is lowvagotomy)?

What is a Billroth I (BI)? Truncal vagotomy, antrectomy, and gastroduodenostomy (Think: BI � ONElimb off of the stomach remnant)

What are the contraindica- Gastric cancer or suspicion of gastrictions for a Billroth I? cancer



What is a Billroth II (BII)? Truncal vagotomy, antrectomy, and gastrojejunostomy (Think: BII � TWOlimbs off of the stomach remnant)

What is the Kocher Dissect the left lateral peritoneal maneuver? attachments to the duodenum to allow

visualization of posterior duodenum

STRESS GASTRITIS

What is it? Superficial mucosal erosions in thestressed patient

What are the risk factors? Sepsis, intubation, trauma, shock, burn,brain injury

What is the prophylactic H2 blockers, PPIs, antacids, sucralfatetreatment?

What are the signs/symptoms? NGT blood (usually), painless (usually)

How is it diagnosed? EGD, if bleeding is significant

What is the treatment for LAVAGE out blood clots, give a maximumgastritis? dose of PPI in a 24-hour IV drip

MALLORY-WEISS SYNDROME

What is it? Post-retching, postemesis longitudinaltear (submucosa and mucosa) of thestomach near the GE junction; approxi-mately three fourths are in the stomach



For what percentage of all �10%upper GI bleeds does this syndrome account?

What are the causes of Increased gastric pressure, often a tear? aggravated by hiatal hernia

What are the risk factors? Retching, alcoholism (50%), �50% ofpatients have hiatal hernia

What are the symptoms? Epigastric pain, thoracic substernal pain,emesis, hematemesis

What percentage of patients 85%will have hematemesis?

How is the diagnosis made? EGD

What is the “classic” history? Alcoholic patient after binge drinking—first, vomit food and gastric contents, followed by forceful retching and bloodyvomitus

What is the treatment? Room temperature water lavage (90% ofpatients stop bleeding), electrocautery,arterial embolization, or surgery forrefractory bleeding

When is surgery indicated? When medical/endoscopic treatment fails(�6 u PRBCs infused)

Can the Sengstaken- No, it makes bleeding worseBlakemore tamponade Use the balloon only for bleedingballoon be used for from esophageal varicestreatment of Mallory-Weiss tear bleeding?

ESOPHAGEAL VARICEAL BLEEDING

What is it? Bleeding from formation of esophagealvarices from back up of portal pressurevia the coronary vein to the submucosalesophageal venous plexuses secondary toportal hypertension from liver cirrhosis



What is the “rule of two Two thirds of patients with portalthirds” of esophageal hypertension develop esophageal variceal hemorrhage? varices

Two thirds of patients with esophagealvarices bleed

What are the signs/ Liver disease, portal hypertension, symptoms? hematemesis, caput medusa, ascites

How is the diagnosis made? EGD (very important because only 50%of UGI bleeding in patients with knownesophageal varices are bleeding from thevarices; the other 50% have bleedingfrom ulcers, etc.)

What is the acute medical Lower portal pressure with somatostatintreatment? and vasopressin

In the patient with CAD, Nitroglycerin—to prevent coronary what must you give in artery vasoconstriction that may result addition to the vasopressin? in an MI

What are the treatment Sclerotherapy or band ligation via options? endoscope, TIPS, liver transplant

What is the Sengstaken- Tamponades with an esophageal balloonBlakemore balloon? and a gastric balloon



What is the problem with Decreased portal pressure, but increasedshunts? encephalopathy


BOERHAAVE’S SYNDROME

What is it? Postemetic esophageal rupture

Who was Dr. Boerhaave? Dutch physician who first described thesyndrome in the Dutch Grand AdmiralVan Wassenaer in 1724

Why is the esophagus No serosasusceptible to perforation and more likely to break down an anastomosis?

What is the most common Posterolateral aspect of the esophagus (onlocation? the left), 3 to 5 cm above the GE junction

What is the cause of rupture? Increased intraluminal pressure, usuallycaused by violent retching and vomiting

What is the associated risk Esophageal reflux disease (50%)factor?

What are the symptoms? Pain postemesis (may radiate to the back,dysphagia)

What are the signs? Left pneumothorax, Hamman’s sign, leftpleural effusion, subcutaneous/mediastinalemphysema, fever, tachypnea, tachycardia,signs of infection by 24 hours, neck crepitus,widened mediastinum on CXR

What is Mackler’s triad? 1. Emesis2. Lower chest pain3. Cervical emphysema (subQ air)

What is Hamman’s sign? “Mediastinal crunch or clicking”produced by the heart beating against air-filled tissues

How is the diagnosis made? History, physical examination, CXR,esophagram with water-soluble contrast


What is the treatment? Surgery within 24 hours to drain themediastinum and surgically close the perforation and placement of pleuralpatch; broad-spectrum antibiotics

What is the mortality rate �15%if less than 24 hours until surgery for perforated esophagus?

What is the mortality rate �33%if more than 24 hours until surgery for perforated esophagus?

Overall, what is the Iatrogenic (most commonly cervical most common cause of esophagus)esophageal perforation?


ANATOMY

StomachChapter 41

1. Cardia2. Fundus3. Body4. Antrum5. Incisura angularis6. Lesser curvature7. Greater curvature8. Pylorus

Identify the parts of thestomach:


Chapter 41 / Stomach 271

What space lies behind thestomach?

What is the opening into thelesser sac?

What are the folds of gastricmucosa called?

Lesser sac; the pancreas lies behind thestomach

Foramen of Winslow

Rugae

Identify the blood supply tothe stomach:

1. Left gastric artery2. Right gastric artery3. Right gastroepiploic artery4. Left gastroepiploic artery5. Short gastrics (from spleen)

GASTRIC PHYSIOLOGY

Define the products of thefollowing stomach cells:

Gastric parietal cells

Chief cells

Mucous neck cells

G cells

Where are G cells located?

What is pepsin?

What is intrinsic factor?

HClIntrinsic factor

PEPsinogen (Think: “a PEPpy chief”)

BicarbonateMucus

Gastrin (Think: G cells � Gastrin)

Antrum

Proteolytic enzyme that hydrolyzes pep-tide bonds

Protein secreted by the parietal cells thatcombines with vitamin B12 and allowsfor absorption in the terminal ileum



GASTROESOPHAGEAL REFLUX DISEASE (GERD)

What is it?

What is pyrosis?



What disease must be ruledout when the symptoms ofGERD are present?

What tests are included inthe workup?


What are the indications forsurgery?

What is Barrett’s esophagus?

Excessive reflux of gastric contents intothe esophagus, “heartburn”

Medical term for heartburn

Decreased lower esophageal sphincter(LES) tone (�50% of cases)

Decreased esophageal motility to clearrefluxed fluid

Gastric outlet obstructionHiatal hernia in �50% of patients

Heartburn, regurgitation, respiratoryproblems/pneumonia from aspiration ofrefluxed gastric contents; substernal pain

Coronary artery disease

EGDUGI contrast study with esophagogram24-hour acid analysis (pH probe in

esophagus)Manometry, EKG, CXR

Small mealsPPIs (proton-pump inhibitors) or

H2 blockersElevation of head at night and no meals

prior to sleeping

Intractability (failure of medical treatment)Respiratory problems as a result of reflux

and aspiration of gastric contents (e.g.,pneumonia)

Severe esophageal injury (e.g., ulcers,hemorrhage, stricture, � Barrett’sesophagus)

Columnar metaplasia from the normalsquamous epithelium as a result ofchronic irritation from reflux


What is the major concernwith Barrett’s esophagus?

What type of cancer devel-ops in Barrett’s esophagus?

What percentage of patientswith GERD developsBarrett’s esophagus?

What percentage of patientswith Barrett’s esophagus willdevelop adenocarcinoma?

What is the treatment ofBarrett’s esophagus withdysplasia?

Define the following surgical options for severeGERD:

Lap Nissen


Developing cancer

Adenocarcinoma

10%

7% lifetime (5%–10%)

Nonsurgical: endoscopic mucosal resection and photodynamic therapy;other options include radiofrequencyablation, cryoablation (these methodsare also often used for mucosal adenocarcinoma)

360 fundoplication—2 cm long (laparoscopically)

hrf ‘07


Belsey mark IV


240� to 270� fundoplication performedthrough a thoracic approach

hrf ‘07

Hill Arcuate ligament repair (close largeesophageal hiatus) and gastropexy todiaphragm (suture stomach to diaphragm)

hrf ‘

07

LWBK758-c39-42_p246-283.qxd 3/17/11 7:30 PM Page 274 Aptara

Toupet


Incomplete (around 200�) posterior wrap(laparoscopic) often used with severedecreased esophageal motility

hrf ‘

07

How does the Nissen wrapwork?

In what percentage ofpatients does Lap Nissenwork?

What are the postoperativecomplications of Lap Nissen?

What is gas-bloat syndrome?

Thought to work by improving the loweresophageal sphincter:

1. Increasing LES tone2. Elongating LES �3 cm3. Returning LES into abdominal cavity

85% (70%–95%)

1. Gas-bloat syndrome2. Stricture3. Dysphagia4. Spleen injury requiring splenectomy5. Esophageal perforation6. Pneumothorax

Inability to burp or vomit

GASTRIC CANCER



Low in United States (10/100,000); highin Japan (78/100,000)

Diet—smoked meats, high nitrates, lowfruits and vegetables, alcohol, tobacco

Environment—raised in high-risk area,poor socioeconomic status, atrophicgastritis, male gender, blood type A,previous partial gastrectomy, perniciousanemia, polyps, Helicobacter pylori



What is the average age atthe time of discovery?

What is the ratio of male tofemale patients?

Which blood type is associated with gastric cancer?


What are the most commonearly symptoms?

What is the most commonsymptom?

What are the signs?

What does the patient withgastric cancer have if he or she has proximal colondistension?

What is the symptom ofproximal gastric cancer?

What is a Blumer’s shelf?

What is a Virchow’s node?

�60 years

3:2

Blood type A (there is an “A” in gastricbut no “O” or “B” � gAstric � type “A”)

“WEAPON”:Weight lossEmesisAnorexiaPain/epigastric discomfortObstructionNausea

Mild epigastric discomfort andindigestion

Weight loss

Anemia, melena, heme occult, epigastricmass (in advanced disease), hepatomegaly,coffee-ground emesis, Blumer’s shelf,Virchow’s node, enlarged ovaries, axillaryadenopathy

Colonic obstruction by direct invasion(rare)

Dysphagia (gastroesophagealjunction/cardia)

Solid peritoneal deposit anterior to therectum, forming a “shelf,” palpated onrectal examination

Metastatic gastric cancer to the nodes inthe left supraclavicular fossa


What is Sister Mary Joseph’ssign?

What is a Krukenberg’stumor?

What is “Irish’s” node?

What is a surveillance laboratory finding?

What is the initial workup?

What is the histology?

What is the differential diag-nosis for gastric tumors?

What are the two histologictypes?

What is the morphology?

Are gastric cancers morecommon on the lesser orgreater curvatures?

What is more common,proximal or distal gastriccancer?

Which morphologic type is named after a “leatherbottle”?

How do gastric adenocar-cinomas metastasize?


Periumbilical lymph node gastric cancermetastases; presents as periumbilical mass

Gastric cancer (or other adenocarcinoma)that has metastasized to the ovary

Left axillary adenopathy from gastric cancermetastasis

CEA elevated in 30% of cases (if �, usefulfor postoperative surveillance)

EGD with biopsy, endoscopic U/S toevaluate the level of invasion, CT ofabdomen/pelvis for metastasis, CXR, labs

Adenocarcinoma

Adenocarcinoma, leiomyoma, leiomyosar-coma, lymphoma, carcinoid, ectopic pan-creatic tissue, gastrinoma, benign gastriculcer, polyp

1. Intestinal (glands)2. Diffuse (no glands)

Ulcerative (75%)Polypoid (10%)Scirrhous (10%)Superficial (5%)

Lesser (“less is more”)

Proximal

Linitis plastica—the entire stomach isinvolved and looks thickened (10% ofcancers)

Hematogenously and lymphatically


Which patients with gastriccancer are NONoperative?

What is the role oflaparoscopy?

What is the geneticalteration seen in �50% ofpatients with gastric cancer?

How can you remember P53for gastric cancer?


What operation is performedfor tumor in the:

Antrum?

Midbody?

Proximal?

What is a subtotalgastrectomy?


1. Distant metastasis (e.g., liver metastasis)2. Peritoneal implants

To rule out peritoneal implants and toevaluate for liver metastasis

P53

Gastric Cancer � GC � P53; or, think:“GCP . . . 53”—it sings!

Surgical resection with wide (�5 cmchecked by frozen section) margins andlymph node dissection

Distal subtotal gastrectomy

Total gastrectomy

Total gastrectomy

Subtotal gastrectomy � 75% of stomachremoved

hrf ‘07


What is a total gastrectomy?


Stomach is removed and a Roux-en-Ylimb is sewn to the esophagus

RouxlimbCommon

bile duct

What type of anastomosis?

When should splenectomybe performed?

Define “extended lymphnode dissection.”

What percentage of patientsare inoperable at presentation?

What is the adjuvanttreatment?

What is the 5-year survivalrate for gastric cancer?

Billroth II or Roux-en-Y (never use aBillroth I)

When the tumor directly invades thespleen/splenic hilum or with splenic hilaradenopathy

Usually D1 and D2:D1 are perigastric LNsD2 include: splenic artery LNs,

hepatic artery LNs, anteriormesocolon LNs, anterior pancreas LNs, crural LNs

�10% to 15%

Stages II and III: postoperativechemotherapy and radiation

25% of patients are alive 5 years afterdiagnosis in the United States (in Japan,50% are alive at 5 years)


Why is it thought that thepostoperative survival is somuch higher in Japan?


Aggressive screening and capturing earlycancers

GIST

What is it?

What was it previouslyknown as?

What is the cell of origin?

Where is it found?



How are distant metastasesdiagnosed?

What is the tumor marker?

What is the prognosis?


Is there a need for lymphnode dissection?

What is the chemotherapyfor metastatic or advanceddisease?

GastroIntestinal Stromal Tumor

Leiomyosarcoma

CAJAL, interstitial cells of Cajal

GI tract—“esophagus to rectum”—mostcommonly found in stomach (60%), small bowel (30%), duodenum (5%), rectum (3%), colon (2%), esophagus (1%)

GI bleed, occult GI bleed, abdominalpain, abdominal mass, nausea, distention

CT scan, EGD, colonoscopy

PET scan

C-KIT (CD117 antigen)

Local spread, distant metastasesPoor long-term prognosis: size �5cm,

mitotic rate �5 per 50 HPF (highpower field)

Resect with negative margins, �/�chemotherapy

NO

Imatinib—tyrosine kinase inhibitor


Chapter 42 / Bariatric Surgery 281

MALTOMA

What is it?

What is the most commonsite?

What is the causative agent?


Mucosal-Associated LymphoproliferativeTissue

Stomach (70%)

H. pylori

Nonsurgical—treat for H. pylori withtriple therapy and chemotherapy/XRT inrefractory cases

GASTRIC VOLVULUS

What is it?



Twisting of the stomach

Borchardt’s triad:1. Distention of epigastrium2. Cannot pass an NGT3. Emesis followed by inability to

vomit

Exploratory laparotomy to untwist, andgastropexy

Bariatric SurgeryChapter 42What is it?

Define morbid obesity.

What is the BMI?

What is the formula for BMI?

Weight reduction surgery for themorbidly obese

1. BMI �40 (basically, �100 poundsabove ideal body weight) or

2. BMI �35 with a medical problemrelated to morbid obesity

Body Mass Index

Body weight in kg divided by height inmeters squared



What is a formula for arough estimate of BMI without using metric measures?

What medical conditions are associated with morbidobesity?

What are the currentoptions for surgery?

Define gastric bypass.

Wt (pounds) � 703(Ht in inches)2

Sleep apnea, coronary artery disease, pul-monary disease, diabetes mellitus, venousstasis ulcers, arthritis, infections, sex-hormone abnormalities, HTN, breastcancer, colon cancer

Gastric bypass (malabsorptive)Vertical-banded gastroplasty

Stapling off of small gastric pouch(restrictive)

Roux-en-Y limb to gastric pouch (bypass)

How does gastric bypasswork?

1. Creates a small gastric reservoir2. Causes dumping symptoms when a

patient eats too much food or high-calorie foods; the food is “dumped”into the Roux-en-Y limb

3. Bypass of small bowel by Roux-en-Ylimb


Which operation works bestoverall?

What are the possible postoperative complicationsafter weight reduction surgery?

What is the most commonsign of an anastomotic leakafter a gastric bypass?

What is the incidence ofanastomotic leak?

What is the mortality rate ofan anastomotic leak?

What is a lap-band?

Chapter 42 / Bariatric Surgery 283

Gastric bypass (mean weight loss 50% ofexcess weight)

Gallstones (if gallbladder in situ), anastomotic leak, marginal ulcer, stenosisof pouch/anastomosis, malnutrition,incisional hernia, spleen injury, irondeficiency, B12 deficiency

Tachycardia

�3% (1%–5%)

�10%

Laparoscopically placed band aroundstomach with a subcutaneous port toadjust constriction; results in smaller gastric reservoir

What is a Petersen’s hernia? Seen after bariatric gastric bypass—internal herniation of small bowel throughthe mesenteric defect from the Roux-en-Ylimb



Define the following terms:Ostomy

Stoma

Gastrostomy

Jejunostomy

Kock pouch

Colostomy

End colostomy

Mucous fistula

Hartmann’s pouch

Double-barrel colostomy

OstomiesChapter 43Operation that connects the GI tract toabdominal wall skin or the lumen ofanother hollow organ; a man-made fistula

Opening of the ostomy (Gr. “mouth”)

G-tube through the abdominal wall tothe stomach for drainage or feeding

J-tube through the abdominal wall to thejejunum for feeding

“Continent ileostomy”Pouch is made of several ileal loopsPatient must access the pouch with a

tube intermittently

Connection of colon mucosa to theabdominal wall skin for stool drainage

Proximal end of colon brought to the skinfor stool drainage

Distal end of transected colon brought tothe skin for decompression; the mucosa pro-duces mucus, an ostomy is a fistula, and,hence, the term mucous fistula (proximalcolon brought up as a colostomy or, if theproximal colon is removed, an ileostomy)

Distal end of transected colon stapledand dropped back into the peritonealcavity, resulting in a blind pouch; mucusis decompressed through the anus (proximal colon is brought up as an endcolostomy or, if proximal colon isremoved, an end ileostomy)

End colostomy and a mucous fistula (i.e., two barrels brought up to the skin)


Loop colostomy

Chapter 43 / Ostomies 285

Loop of large bowel is brought up to theabdominal wall skin and a plastic rod isplaced underneath the loop; the colon isthen opened and sewn to the abdominalwall skin as a colostomy

Ileal conduit

Brooke ileostomy

Loops of stapled-off ileum made into apouch, anastomosed to the ureters, andthen brought to the abdominal wall skinto allow drainage of urine in patientswho undergo removal of the bladder(cystectomy)

Ileostomy folded over itself to provideclearance from skin


Why doesn’t an ileostomy orcolostomy close?

Why doesn’t a gastrostomyclose?

If the plastic tube, G-tube,or J-tube is removed, howfast can the hole to thestomach or jejunum close?

What is a “tube check”?


Epithelialization (mucosa to skin) fromthe acronym FRIEND (see page 305)

Foreign body (the plastic tube) from theacronym FRIEND

In a matter of hours! (Thus, if it comesout inadvertently from a well-establishedtract, it must be replaced immediately)

Gastrografin contrast study to confirm thata G-tube or J-tube is within the lumen ofthe stomach or jejunum, respectively

SMALL BOWEL

ANATOMY

What comprises the smallbowel?

How long is the duodenum?

What marks the end of theduodenum and the start ofthe jejunum?

What is the length of theentire small bowel?

What provides blood supplyto the small bowel?

What does the small bowel do?

What are the plicaecirculares?

Small IntestineChapter 44

Duodenum, jejunum, and ileum

�12 inches—thus the name: duodenum!

Ligament of Treitz

�6 meters (20 feet)

Branches of the superior mesentericartery

Major site of digestion and absorption

Plicae means “folds,” circulares means “circular”; thus, circular folds of mucosa(a.k.a. valvulae conniventes) in small bowellumen


What are the majorstructural differencesbetween the jejunum andthe ileum?

What does the terminalileum absorb?

Chapter 44 / Small Intestine 287

Jejunum—long vasa rectae, large plicaecirculares, thicker wall

Ileum—shorter vasa rectae, smaller plicae circulares, thinner wall(Think: Ileum � Inferior vasa rectae,

Inferior plicae circulares, andInferior wall thickness in comparisonto the jejunum)

B12, fatty acids, bile salts

SMALL BOWEL OBSTRUCTION

What is small bowel obstruction (SBO)?


What lab tests areperformed with SBO?

What are classic electrolyte/acid-base findings with proximal obstruction?

What must be ruled out onphysical exam in patientswith SBO?

What major AXR findingsare associated with SBO?

Mechanical obstruction to the passage ofintraluminal contents

Abdominal discomfort, cramping, nausea, abdominal distention, emesis,high-pitched bowel sounds

Electrolytes, CBC, type and screen, urinalysis

Hypovolemic, hypochloremic,hypokalemia, alkalosis

Incarcerated hernia (also look for surgicalscars)

Distended loops of small bowel air-fluidlevels on upright film

Air-fluidlevel



Define complete SBO.

What is the danger of complete SBO?

Define partial SBO.

What is initial managementof all patients with SBO?

What tests can differentiatepartial from complete bowelobstruction?

What are the ABCs of SBO?

What are other causes of SBO?

What is superior mesentericartery (SMA) syndrome?

What is the treatment ofcomplete SBO?

What is LOA?

Complete obstruction of the lumen; usually paucity or no colon gas

Closed loop strangulation of the bowelleading to bowel necrosis

Incomplete SBO; some colon gas

NPO, NGT, IVF, Foley

CT with oral contrast, small bowelfollow-through

Causes of SBO:1. Adhesions2. Bulge (hernias)3. Cancer and tumors

The acronym “GIVES BAD CRAMPS”:Gallstone ileusIntussusceptionVolvulusExternal compressionSMA syndrome

Bezoars, Bowel wall hematomaAbscessesDiverticulitis

Crohn’s diseaseRadiation enteritisAnnular pancreas Meckel’s diverticulumPeritoneal adhesions Stricture

Seen with weight loss—SMA compressesduodenum, causing obstruction

Laparotomy and lysis of adhesions

Lysis Of Adhesions


What is the treatment ofincomplete SBO?

Intraoperatively, how canthe level of obstruction bedetermined in patients withSBO?

What is the most commonindication for abdominalsurgery in patients withCrohn’s disease?

Can a patient have completeSBO and bowel movementsand flatus?

After a small bowel resection,why should the mesentericdefect always be closed?

What may cause SBO ifpatient is on coumadin?

What is the #1 cause of SBOin adults (industrializednations)?

What is the #1 cause of SBOaround the world?

What is the #1 cause of SBOin children?

What are the signs of strangulated bowel withSBO?

What are the clinical parameters that will lowerthe threshold to operate ona partial SBO?


Initially, conservative treatment with closeobservation plus NGT decompression

Transition from dilated bowel proximal tothe decompressed bowel distal to theobstruction

SBO

Yes; the bowel distal to the obstructioncan clear out gas and stool

To prevent an internal hernia

Bowel wall hematoma

Postoperative adhesions

Hernias

Hernias

Fever, severe/continuous pain,hematemesis, shock, gas in the bowelwall or portal vein, abdominal free air,peritoneal signs, acidosis (increasedlactic acid)

Increasing WBCFeverTachycardia/tachypneaAbdominal pain


What is an absolute indication for operation with partial SBO?

What classic saying is associated with completeSBO?

What condition commonlymimics SBO?

What is the differential diagnosis of paralytic(nonobstructive) ileus?

What tumor classicallycauses SBO due to “mesenteric fibrosis”?


Peritoneal signs, free air on AXR

“Never let the sun set or rise on completeSBO”

Paralytic ileus (AXR reveals gas distentionthroughout, including the colon)

Postoperative ileus after abdominal surgery (normally resolves in 3–5 days)

Electrolyte abnormalities (hypokalemia ismost common)

Medications (anticholinergic, narcotics)Inflammatory intra-abdominal processSepsis/shockSpine injury/spinal cord injuryRetroperitoneal hemorrhage

Carcinoid tumor

SMALL BOWEL TUMORS

What is the differential diag-nosis of benign tumors ofthe small intestine?

What are the signs andsymptoms of small boweltumors?

What is the most commonbenign small bowel tumor?

What is the most commonmalignant small bowel tumor?

What is the differential diagnosis of malignanttumors of the smallintestine?

Leiomyoma, lipoma, lymphangioma,fibroma, adenomas, hemangiomas

Abdominal pain, weight loss, obstruction(SBO), and perforation

Leiomyoma

Adenocarcinoma

1. Adenocarcinoma (50%)2. Carcinoid (25%)3. Lymphoma (20%)4. Sarcomas (�5%)


What is the workup of asmall bowel tumor?

What is the treatment formalignant small boweltumor?

What malignancy isclassically associated withmetastasis to small bowel?


UGI with small bowel follow-through,enteroclysis, CT scan, enteroscopy

Resection and removal of mesentericdraining lymph nodes

Melanoma

MECKEL’S DIVERTICULUM

What is it? Remnant of the omphalomesenteric duct/vitelline duct, which connects the yolk sacwith the primitive midgut in the embryo


What is the usual location?

What is the major differential diagnosis?

Is it a true diverticulum?


Most common small bowel congenitalabnormality

Within �2 feet of the ileocecal valve onthe antimesenteric border of the bowel

Appendicitis

Yes; all layers of the intestine are foundin the wall

�2% of the population at autopsy


What is the gender ratio?

What is the average age atonset of symptoms?

What are the possible complications?


What is the most commoncomplication of Meckel’sdiverticulum in adults?

In what percentage of casesis heterotopic tissue foundin the diverticulum?

What heterotopic tissue typeis most often found?

What is the “rule of 2s”?

What is the role of incidental Meckel’s diverticulectomy (surgicalremoval upon findingasymptomatic diverticulum)?


Twice as common in men

Most frequently in the first 2 years oflife, but can occur at any age

Intestinal hemorrhage (painless)—50%; accounts for half of all lower GI bleeding in patients younger than 2 years

Bleeding results from ectopic gastricmucosa secreting acid S ulcer Sbleeding

Intestinal obstruction—25%; mostcommon complication in adults;includes volvulus and intussusception

Inflammation (� perforations)—20%

Lower GI bleeding, abdominal pain, SBO

Intestinal obstruction

�50%

Gastric mucosa (60%), but duodenal,pancreatic, and colonic mucosa are alsofound

2% of patients are symptomaticFound �2 feet from the ileocecal valveFound in 2% of the populationMost symptoms occur before age 2 yearsEctopic tissue found in 1 of 2 patientsMost diverticula are �2 inches long2 to 1 male:female ratio

Most experts would remove in children(very controversial in adults)


What is a Meckel’s scan?

What is the treatment of aMeckel’s diverticulum that is causing bleeding andobstruction?

What is the name of the hernia associated with incarcerated Meckel’s diverticulum?

In patients with guaiac-positive stools and anegative upper- and lower-GI workup, what must beruled out?

What is the most commoncause of small bowel bleeding?

Chapter 45 / Appendix 293

Scan for ectopic gastric mucosa inMeckel’s diverticulum; uses technetiumpertechnetate IV, which is preferentiallytaken up by gastric mucosa

Surgical resection, with small bowelresection as the actual ulcer is usually on the mesenteric wall opposite thediverticulum!

Littre’s hernia (Think alphabetically: Littre’s, then Meckel’s)

Small bowel tumor; evaluate withenteroclysis (small bowel contrast study)

Small bowel angiodysplasia

What vessel provides bloodsupply to the appendix?

Name the mesentery of theappendix.

How can the appendix belocated if the cecum hasbeen identified?

AppendixChapter 45Appendiceal artery—branch of the ileocolic artery

Mesoappendix (contains the appendicealartery)

Follow the taenia coli down to the appendix; The taeniae converge on theappendix



APPENDICITIS

What is it?


What is the lifetimeincidence of acuteappendicitis in the UnitedStates?

What is the most commoncause of emergent abdominalsurgery in the United States?

How does appendicitis classically present?

Why does periumbilical painoccur?

Why does RLQ pain occur?


Define the following terms:Obturator sign

Inflammation of the appendix caused byobstruction of the appendiceal lumen,producing a closed loop with resultantinflammation that can lead to necrosisand perforation

Lymphoid hyperplasia, fecalith(a.k.a. appendicolith)

Rare—parasite, foreign body, tumor (e.g., carcinoid)

�7%!

Acute appendicitis

Classic chronologic order:1. Periumbilical pain (intermittent and

crampy)2. Nausea/vomiting3. Anorexia4. Pain migrates to RLQ (constant and

intense pain), usually in �24 hours

Referred pain

Peritoneal irritation

Signs of peritoneal irritation may be present: guarding, muscle spasm,rebound tenderness, obturator and psoassigns, low-grade fever (high grade if perforation occurs), RLQ hyperesthesia

Pain upon internal rotation of the legwith the hip and knee flexed; seen inpatients with pelvic appendicitis


Psoas sign

Rovsing’s sign

Valentino’s sign

McBurney’s point


Pain elicited by extending the hip withthe knee in full extension or by flexingthe hip against resistance; seen classicallyc retrocecal appendicitis

Palpation or rebound pressure of theLLQ results in pain in the RLQ; seen inappendicitis

RLQ pain/peritonitis from succus draining down to the RLQ from a perforated gastric or duodenal ulcer

Point one third from the anteriorsuperior iliac spine to the umbilicus(often the point of maximal tenderness)

What is the differential diagnosis for:

Everyone?

Females?

Meckel’s diverticulum, Crohn’s disease, perforated ulcer, pancreatitis,mesenteric lymphadenitis, constipation,gastroenteritis, intussusception, volvulus,tumors, UTI (e.g., cystitis), pyelonephritis,torsed epiploicae, cholecystitis, cecaltumor, diverticulitis (floppy sigmoid)

Ovarian cyst, ovarian torsion, tuboovarianabscess, mittelschmerz, pelvic inflamma-tory disease (PID), ectopic pregnancy,ruptured pregnancy


What lab tests should beperformed?

Can you have an abnormalurinalysis with appendicitis?

Does a positive urinalysisrule out appendicitis?

What additional tests can beperformed if the diagnosis isnot clear?

In acute appendicitis, whatclassically precedes vomiting?

What radiographic studiesare often performed?

What are the radiographicsigns of appendicitis onAXR?

With acute appendicitis, inwhat percentage of caseswill a radiopaque fecalith beon AXR?

What are the CT findingswith acute appendicitis?


CBC: increased WBC (�10,000 per mm3

in �90% of cases), most often with a“left shift”

Urinalysis: to evaluate for pyelonephritisor renal calculus

Yes; mild hematuria and pyuria are common in appendicitis with pelvicinflammation, resulting in inflammationof the ureter

No; ureteral inflammation resulting fromthe periappendiceal inflammation cancause abnormal urinalysis

Spiral CT, U/S (may see a large, noncompressible appendix or fecalith),AXR

Pain (in gastroenteritis, the painclassically follows vomiting)

CXR: to rule out RML or RLL pneumonia, free air

AXR: abdominal films are usuallynonspecific, but calcified fecalith present in about 5% of cases

Fecalith, sentinel loops, scoliosis awayfrom the right because of pain, mass effect(abscess), loss of psoas shadow, loss ofpreperitoneal fat stripe, and (very rarely) asmall amount of free air if perforated

Only �5% of the time!

Periappendiceal fat stranding,appendiceal diameter �6 mm,periappendiceal fluid, fecalith


What are the preoperativemedications/preparation?

What is a lap appy?

What is the treatment for nonperforated acuteappendicitis?

What is the treatment forperforated acuteappendicitis?

How is an appendicealabscess that is diagnosedpreoperatively treated?

If a normal appendix isfound upon exploration,should you take out the normal appendix?

How long after removal of aNONRUPTURED appendixshould antibiotics continuepostoperatively?

Which antibiotic is used for NONPERFORATEDappendicitis?

What antibiotic is used for aPERFORATED appendix?


1. Rehydration with IV fluids (LR)2. Preoperative antibiotics with

anaerobic coverage (appendix is considered part of the colon)

Laparoscopic appendectomy; used inmost cases in women (can see adnexa) orif patient has a need to quickly return tophysical activity, or is obese

Nonperforated—prompt appendectomy(prevents perforation), 24 hours of antibiotics, discharge home usually onPOD #1

Perforated—IV fluid resuscitation andprompt appendectomy; all pus is drainedwith postoperative antibiotics continuedfor 3 to 7 days; wound is left open inmost cases of perforation after closing thefascia (heals by secondary intention ordelayed primary closure)

Usually by percutaneous drainage of theabscess, antibiotic administration, andelective appendectomy �6 weeks later(a.k.a. interval appendectomy)

Yes

For 24 hours

Anaerobic coverage: Cefoxitin®, Cefotetan®, Unasyn®, Cipro®, and Flagyl®

Broad-spectrum antibiotics (e.g.,Amp/ Cipro®/Clinda or a penicillin suchas Zosyn®)


How long do you give antibiotics for perforatedappendicitis?

What is the risk of perforation?

What is the most commongeneral surgical abdominalemergency in pregnancy?

What are the possible complications of appendicitis?

What percentage of the population has a retrocecal,retroperitoneal appendix?

What percentage of negativeappendectomies isacceptable?

Who is at risk of dying fromacute appendicitis?

What bacteria are associatedwith “mesenteric adenitis”that can closely mimic acuteappendicitis?

What is an “incidentalappendectomy”?

What are complications ofan appendectomy?

What is the most commonpostoperative complication?


Until the patient has a normal WBCcount and is afebrile, ambulating, andeating a regular diet (usually 3–7 days)

�25% by 24 hours from onset of symptoms, �50% by 36 hours, and�75% by 48 hours

Appendicitis (about 1/1750; appendixmay be in the RUQ because of theenlarged uterus)

Pelvic abscess, liver abscess, free perforation, portal pylethrombophlebitis(very rare)

�15%

Up to 20%; taking out some normalappendixes is better than missing a caseof acute appendicitis that eventually ruptures

Very old and very young patients

Yersinia enterolytica

Removal of normal appendix duringabdominal operation for different procedure

SBO, enterocutaneous fistula, woundinfection, infertility with perforation inwomen, increased incidence of rightinguinal hernia, stump abscess

Wound infection



CLASSIC INTRAOPERATIVE QUESTIONS

What is the differencebetween a McBurney’s incision and a Rocky-Davisincision?

What are the layers of theabdominal wall during aMcBurney incision?

What are the steps inlaparoscopic appendectomy(lap appy)?

Do you routinely getperitoneal cultures for acute appendicitis (nonperforated)?

How can you find the appendix after identifyingthe cecum?

Which way should your finger sweep trying to findthe appendix?

How do you get to a retrocecal andretroperitoneal appendix?

Why use electrocautery onthe exposed mucosa on theappendiceal stump?

McBurney’s is angled down (follows extoblique fibers), and Rocky-Davis isstraight across (transverse)

1. Skin2. Subcutaneous fat3. Scarpa’s fascia4. External oblique5. Internal oblique6. Transversus muscle7. Transversalis fascia8. Preperitoneal fat9. Peritoneum

1. Identify the appendix2. Staple the mesoappendix (or coagulate)3. Staple and transect the appendix at

the base (or use Endoloop® and cutbetween)

4. Remove the appendix from theabdomen

5. Irrigate and aspirate until clear

No

Follow the taeniae down to where theyconverge on the appendix

Lateral to medial along the lateralperitoneum—this way you will not tearthe mesoappendix that lies medially!

Divide the lateral peritoneal attachmentsof the cecum

To kill the mucosal cells so they do notform a mucocele


If you find Crohn’s diseasein the terminal ileum, willyou remove the appendix?

If the appendix is normalwhat do you inspect intraoperatively?

Who first described the classic history and treatmentfor acute appendicitis?

Who performed the firstappendectomy?

Who performed the first lapappy?


Yes, if the cecal/appendiceal base is notinvolved

Terminal ileum: Meckel’s diverticulum,Crohn’s disease, intussusception

Gynecologic: Cysts, torsion, etc.Groin: hernia, rectus sheath hematoma,

adenopathy (adenitis)

Reginald Fitz

Harry Hancock in 1848 (McBurney popularized the procedure in 1880s)

Dr. Semm (GYN) in 1983

APPENDICEAL TUMORS

What is the most commonappendiceal tumor?

What is the treatment ofappendiceal carcinoid lessthan 1.5 cm?

What is the treatment ofappendiceal carcinoid largerthan 1.5 cm?

What percentage of appendiceal carcinoids aremalignant?

What is the differential diagnosis of appendicealtumor?

What type of appendicealtumor can cause the dreadedpseudomyxoma peritonei ifthe appendix ruptures?

Carcinoid tumor

Appendectomy (if not through the bowelwall)

Right hemicolectomy

�5%

Carcinoid, adenocarcinoma, malignantmucoid adenocarcinoma

Malignant mucoid adenocarcinoma


What is “mittelschmerz”?

Should one remove the normal appendix withCrohn’s disease found intraoperatively?

Chapter 46 / Carcinoid Tumors 301

Pelvic pain caused by ovulation

Yes, unless the base of the appendix isinvolved with Crohn’s disease, the normalappendix should be removed to avoiddiagnostic confusion with appendicitis inthe future

What is a carcinoid tumor?

Why is it called “carcinoid”?

How can you remember thatKulchitsky cells are found incarcinoid tumors?


What are the common sitesof occurrence?


Why SBO with carcinoid?

Carcinoid TumorsChapter 46Tumor arising from neuroendocrine cells(APUDomas), a.k.a. Kulchitsky cells;basically, a tumor that secretes serotonin

Suffix “-oid” means “resembling”; thus,carcinoid resembles a carcinoma but isclinically and histologically less aggressivethan most GI carcinomas

Think: “COOL CAR” or KULchitskyCARcinoid

Between 0.2% and 1.0% and about 25%of all small bowel tumors

“AIR”:1. Appendix (most common)2. Ileum3. Rectum4. BronchusOther sites: jejunum, stomach,

duodenum, colon, ovary, testicle,pancreas, thymus

Depends on location; most cases areasymptomatic; also SBO, abdominal pain, bleeding, weight loss, diaphoresis,pellagra skin changes, intussusception,carcinoid syndrome, wheezing

Classically � severe mesenteric fibrosis


What are the pellagra-likesymptoms?

What causes pellagra in carcinoid patients?

What is carcinoid syndrome?

What are the symptoms ofcarcinoid syndrome?

What is a complete memoryaid for carcinoid?


Think “3-D”:1. Dermatitis2. Diarrhea3. Dementia

Decreased niacin production

Syndrome of symptoms caused by releaseof substances from a carcinoid tumor

Remember the acronym “B FDR”:Bronchospasm

Flushing (skin)DiarrheaRight-sided heart failure (from valve

failure)

Think: B FDR � CARcinoid, or “Be FDRin a cool CAR” (COOL � KULchitsky cells)

Why does right-sided heartfailure develop but not left-sided heart failure?

What is the incidence ofcarcinoid SYNDROME inpatients who have acarcinoid TUMOR?

What released substancescause carcinoid syndrome?

What is the medical treatmentfor carcinoid syndrome?

What is the medicaltreatment of diarrhea alone?

Lungs act as a filter (just like the liver);thus, the left heart doesn’t see all thevasoactive compounds

�10%

Serotonin and vasoactive peptides

Octreotide IV

Odansetron (Zofran®)—serotonin antagonist


How does the liver preventcarcinoid syndrome?

Why does carcinoidsyndrome occur in sometumors and not in others?

What tumors can producecarcinoid syndrome?

What does the liver breakdown serotonin into?

What percentage of patientswith a carcinoid have an elevated urine 5-HIAA level?

What are the associateddiagnostic lab findings?

How do you remember 5-HIAA for carcinoid?

Chapter 46 / Carcinoid Tumors 303

By degradation of serotonin and theother vasoactive peptides when thetumor drains into the portal vein

Occurs when venous drainage from thetumor gains access to the systemic cir-culation by avoiding hepatic degradationof the vasoactive substances

Liver metastasesRetroperitoneal disease draining into

paravertebral veinsPrimary tumor outside the GI tract,

portal venous drainage (e.g., ovary,testicular, bronchus), or both

5-hydroxyindoleacetic acid (5-HIAA)

50%

Elevated urine 5-HIAA as well as elevated urine and blood serotoninlevels

Think of a 5-HIGH CAR pile up �5-HIAA CARcinoid

hrf ‘07

5

4

3

2

1

What stimulation test canoften elevate serotonin levels and cause symptomsof carcinoid syndrome?

Pentagastrin stimulation


How do you localize a GIcarcinoid?

What are the special radiologic (scintigraphy)localization tests?



How effective is octreotide?

What is a common antiserotonin drug?

What is the overall prognosis?

What is the prognosis ofpatients with liver metastasisor carcinoid syndrome?

What does carcinoid tumorlook like?

For appendiceal carcinoid,when is a righthemicolectomy indicatedversus an appendectomy?

Which primary site has thehighest rate of metastasis?

Can a carcinoid tumor beconfirmed malignant bylooking at the histology?


Barium enema, upper GI series withsmall bowel follow-through, colonoscopy,enteroscopy, enteroclysis, EGD, radiologytests

131I-MIBG (131 metaiodobenzylguanidine)111In-octreotidePET scan utilizing 11C-labeled HTP

Excision of the primary tumor and singleor feasible metastasis in the liver (livertransplant is an option with unresectableliver metastasis); chemotherapy foradvanced disease

Medical therapy for palliation of the carcinoid syndrome (serotonin antagonists,somatostatin analogue [octreotide])

It relieves diarrhea and flushing in morethan 85% of cases and may shrink tumorin 10% to 20% of cases

Cyproheptadine

Two thirds of patients are alive at 5 years

50% are alive at 3 years

Usually intramural bowel mass; appearsas yellowish tumor upon incision

If the tumor is �1.5 cm, righthemicolectomy is indicated; if there areno signs of serosal or cecal involvementand tumor is �1.5 cm, appendectomyshould be performed

Ileal primary tumor

No, metastasis must be present to diagnose malignancy


What is the correlationbetween tumor size andmalignancy potential?

What treatments might youuse for the patient withunresectable liver metastasisthat is refractory to medicaltreatment?

What are the overall survivalrates for carcinoid tumors at5 years? 10 years?

What are the side effects ofcolorectal carcinoid?

Chapter 47 / Fistulas 305

Vast majority of tumors �2 cm arebenign; in tumors �2 cm, malignancypotential is significant

Chemoembolization or radiofrequencyablation

5 years � 70%; 10 years � 50%

Most common side effect is rectal bleeding�/� vague abdominal pain/discomfort

FistulasChapter 47What is a fistula?

What are the predisposingfactors and conditions thatmaintain patency of afistula?

Abnormal communication between twohollow organs or a hollow organ and theskin (i.e., two epithelial cell layers)

The acronym “HIS FRIEND”:High output fistula (�500 cc/day)Intestinal destruction (�50% of

circumference)Short segment fistula �2.5 cm

Foreign body (e.g., G-tube)RadiationInfectionEpithelization (e.g., colostomy)NeoplasmDistal obstruction

SPECIFIC TYPES OF FISTULAS

ENTEROCUTANEOUS

What is it? Fistula from GI tract to skin (entero—cutaneous � bowel to skin)



COLONIC FISTULAS

What are they?

What are the most commoncauses?

What is the most commontype?



What is a cholecystentericfistula?

Include colovesical, colocutaneous, colovaginal, and coloenteric fistulas

Diverticulitis (most common cause),cancer, IBD, foreign body, and irradiation

Colovesical fistula, which oftenpresents with recurrent urinary tractinfections; other signs includepneumaturia, dysuria, and fecaluria

Via BE and cystoscopy

Surgery: segmental colon resection andprimary anastomosis; repair/resection ofthe involved organ

Connection between gallbladder andduodenum or other loop of small boweldue to large gallstone erosion, oftenresulting in SBO as the gallstone lodgesin the ileocecal valve (gallstone ileus)


What is the workup?



Which enterocutaneous fistulacloses faster: short or long?

Anastomotic leak, trauma/injury to thebowel/colon, Crohn’s disease, abscess,diverticulitis, inflammation/infection,inadvertent suture through bowel

1. CT scan to rule out abscess/inflammatory process

2. Fistulagram

High-output fistulas, malnutrition, skinbreakdown

NPO; TPN; drain abscesses, rule out andcorrect underlying causes; may feed distally(or if fistula is distal, feed elemental dietproximally); half will close spontaneously,but the other half require operation andresection of the involved bowel segment

Long fistula (may be counterintuitive—but true)


Chapter 47 / Fistulas 307

PANCREATIC ENTERIC FISTULA

What is it? Decompression of a pseudocyst or abscessinto an adjacent organ (a rare complication);usually done surgically or endoscopically totreat a pancreatic pseudocyst

What are the common causesof a gastrocolic fistula?

What are the possiblecomplications of gastrocolicfistulas?

Penetrating ulcers, gastric or coloniccancer, and Crohn’s disease

Malnutrition and severe enteritis due toreflux of colonic contents into the stomachand small bowel with subsequent bacterialovergrowth

EXTERNAL PANCREATIC FISTULA

What is it?


What is a “refractory” pancreatic fistula?

What is the diagnostic testfor “refractory” pancreaticfistulas?

How is refractory tail of apancreas fistula treated?

How is refractory head of apancreas fistula treated?

Pancreaticocutaneous fistula; drainage ofpancreatic exocrine secretions through toabdominal skin (usually through draintract/wound)

NPO, TPN, skin protection, octreotide

Pancreaticocutaneous fistula that doesnot resolve with conservative medicalmanagement (the minority of cases)

ERCP to define site of fistula tract (i.e., tail versus head of pancreas)

Resection of the tail of the pancreas andthe fistula

Pancreaticojejunostomy

BLADDER FISTULAS

What are the specific types? Vesicoenteric (50% due to sigmoiddiverticulitis); signs includepneumaturia, fecaluria

Vesicovaginal (most are secondary togynecologic procedures); signs includeurinary leak through vagina


1. Ileocolic artery2. Right colic artery3. Superior mesenteric artery (SMA)4. Middle colic artery5. Inferior mesenteric artery (IMA)6. Left colic artery7. Sigmoidal artery8. Superior hemorrhoidal artery

(superior rectal)9. Middle hemorrhoidal artery

10 Inferior hemorrhoidal artery11. Marginal artery of Drummond12. Meandering artery of Gonzalez


ANATOMY

Identify the arterial blood supply to the colon:

Colon and RectumChapter 48


Chapter 48 / Colon and Rectum 309

What are the white lines ofToldt?

What parts of the GI tractdo not have a serosa?

What are the major anatomicdifferences between thecolon and the small bowel?

What is the blood supply tothe rectum:

Proximal?

Middle?

Distal?

What is the venous drainageof the rectum:

Proximal?

Middle?

Distal?

Lateral peritoneal reflections of theascending and descending colon

Esophagus, middle and distal rectum

Colon has taeniae coli, haustra, andappendices epiploicae (fat appendages),whereas the small intestine is smooth

Superior hemorrhoidal (or superior rectal) from the IMA

Middle hemorrhoidal (or middle rectal)from the hypogastric (internal iliac)

Inferior hemorrhoidal (or inferior rectal)from the pudendal artery (a branch ofthe hypogastric artery)

Via the IMV to the splenic vein, then tothe portal vein

Via the iliac vein to the IVC

Via the iliac vein to the IVC

COLORECTAL CARCINOMA

What is it?


How common is it as a causeof cancer deaths?

Adenocarcinoma of the colon or rectum

Most common GI cancerSecond most common cancer in the

United StatesIncidence increases with age starting at

40 and peaks at 70 to 80 years

Second most common cause of cancerdeaths



What is the lifetime risk ofcolorectal cancer?

What is the male to femaleratio?


What is Lynch’s syndrome?

What are current ACS recommendations forpolyp/colorectal screening in asymptomatic patientswithout family (first-degree)history of colorectal cancer?

What are the current recom-mendations for colorectalcancer screening if there is ahistory of colorectal cancerin a first-degree relative less than 60 years old?

What percentage of adultswill have a guaiac-positivestool test?

What percentage of patientswith a guaiac-positive stool test will have coloncancer?

6%

�1:1

Dietary: Low-fiber, high-fat diets correlate with increased rates

Genetic: Family history is importantwhen taking historyFAP, Lynch’s syndrome

IBD: Ulcerative colitis � Crohn’sdisease, age, previous colon cancer

HNPCC � Hereditary NonPolyposisColon Cancer—autosomal-dominantinheritance of high risk for developmentof colon cancer

Starting at age 50, at least one of thefollowing test regimens is recommended:

Colonoscopy q 10 yrsDouble contrast barium enema

(DCBE) q 5 yrsFlex sigmoidoscopy q 5 yrsCT colonography q 5 yrs

Colonoscopy at age 40, or 10 years beforethe age at diagnosis of the youngest first-degree relative, and every 5 yearsthereafter

�2%

�10%


What signs/symptoms areassociated with the followingconditions:

Right-sided lesions?

Left-sided lesions?

From which site is melenamore common?

From which site ishematochezia morecommon?

What is the incidence of rectal cancer?

What are the signs/symptoms of rectal cancer?

What is the differential diagnosis of a colon tumor/mass?

Which diagnostic tests arehelpful?


Right side of bowel has a large luminaldiameter, so a tumor may attain alarge size before causing problems

Microcytic anemia, occult/melena morethan hematochezia PR, postprandialdiscomfort, fatigue

Left side of bowel has smaller lumen andsemisolid contents

Change in bowel habits (small-caliberstools), colicky pain, signs of obstruction, abdominal mass,heme(�) or gross red blood

Nausea, vomiting, constipation

Right-sided colon cancer

Left-sided colon cancer

Comprises 20% to 30% of all colorectalcancer

Most common symptom is hematochezia(passage of red blood � stool) or mucus;also tenesmus, feeling of incompleteevacuation of stool (because of the mass),and rectal mass

Adenocarcinoma, carcinoid tumor, lipoma,liposarcoma, leiomyoma, leiomyosarcoma,lymphoma, diverticular disease, ulcerativecolitis, Crohn’s disease, polyps

History and physical exam (Note: �10%of cancers are palpable on rectalexam), heme occult, CBC, bariumenema, colonoscopy


What disease does microcytic anemia signifyuntil proven otherwise in aman or postmenopausalwoman?

What tests help find metastases?

What is the preoperativeworkup for colorectalcancer?

What are the means bywhich the cancer spreads?

Is CEA useful?

What unique diagnostic testis helpful in patients withrectal cancer?

How are tumors staged?

Give the TNM stages:Stage I

Stage II


Colon cancer

CXR (lung metastases), LFTs (livermetastases), abdominal CT (livermetastases), other tests based onhistory and physical exam (e.g., headCT for left arm weakness looking forbrain metastasis)

History, physical exam, LFTs, CEA, CBC,Chem 10, PT/PTT, type and cross 2 uPRBCs, CXR, U/A, abdominopelvic CT

Direct extension: circumferentially andthen through bowel wall to laterinvade other abdominoperineal organs

Hematogenous: portal circulation to liver;lumbar/vertebral veins to lungs

Lymphogenous: regional lymph nodesTransperitonealIntraluminal

Not for screening but for baseline andrecurrence surveillance (but offers noproven survival benefit)

Endorectal ultrasound (probe is placedtransanally and depth of invasion andnodes are evaluated)

TMN staging system

Invades submucosa or muscularis propria(T1–2 N0 M0)

Invades through muscularis propria orsurrounding structures but with negativenodes (T3–4, N0, M0)


Stage III

Stage IV

What is the approximate 5-year survival by stage:

Stage I?

Stage II?

Stage III?

Stage IV?

What percentage of patients with colorectal cancer have liver metastaseson diagnosis?

Define the preoperative“bowel prep.”

What are the common preoperative IVantibiotics?

If the patient is allergic (hives,swelling), what antibioticsshould be prescribed?

What are the treatmentoptions?


Positive nodes, no distant metastasis(any T, N1–3, M0)

Positive distant metastasis (any T, anyN, M1)

90%

70%

50%

10%

�20%

Preoperative preparation for colon/rectalresection:

1. Golytely colonic lavage or Fleets Phospho-Soda until clear effluentper rectum

2. PO antibiotics (1 gm neomycin and 1 gm erythromycin � 3 doses)

Note: Patient should also receive preop-erative and 24-hr IV antibiotics

Cefoxitin, Unasyn®

IV Cipro® and Flagyl®

Resection: wide surgical resection oflesion and its regional lymphatic drainage


What decides low anteriorresection (LAR) versusabdominal perinealresection (APR)?

What do all rectal canceroperations include?

What is the lowest LAR possible?

What do some surgeons do with any anastomosisless than 5 cm from theanus?

What surgical margins are needed for coloncancer?

What is the minimal surgicalmargin for rectal cancer?

How many lymph nodesshould be resected with acolon cancer mass?

What is the adjuvanttreatment of stage III coloncancer?

What is the adjuvant treatment for T3–T4 rectal cancer?

What is the most common site of distant(hematogenous) metastasisfrom colorectal cancer?

What is the treatment ofliver metastases fromcolorectal cancer?


Distance from the anal verge, pelvis size

Total mesorectal excision—remove therectal mesentery, including the lymphnodes (LNs)

Coloanal anastomosis (anastomosis normal colon directly to anus)

Temporary ileostomy to “protect” theanastomosis

Traditionally �5 cm; margins must be atleast 2 cm

2 cm

12 LNs minimum � for staging, and mayimprove prognosis

5-FU and leucovorin (or levamisole)chemotherapy (if there is nodal metastasis postoperatively)

Preoperative radiation therapy and 5-FU chemotherapy as a “radiosensitizer”

Liver

Resect with 1-cm margins and administer chemotherapy if feasible


What is the surveillance regimen?

Why is follow-up so important the first 3 postoperative years?

What are the most commoncauses of colonic obstructionin the adult population?

What is the 5-year survivalrate after liver resectionwith clean margins for coloncancer liver metastasis?

What is the 5-year survivalrate after diagnosis of unresectable colon cancerliver metastasis?


Physical exam, stool guaiac, CBC, CEA,LFTs (every 3 months for 3 years, thenevery 6 months for 2 years), CXR every 6 months for 2 years and then yearly,colonoscopy at years 1 and 3 postopera-tively, CT scans directed by exam

�90% of colorectal recurrences arewithin 3 years of surgery

Colon cancer, diverticular disease,colonic volvulus

�33% (28%–50%)

0%

COLONIC AND RECTAL POLYPS

What are they?

How are they anatomicallyclassified?

What are the histologic classifications of the following types:

Inflammatory(pseudopolyp)?

Hamartomatous?

Hyperplastic?

Tissue growth into bowel lumen, usuallyconsisting of mucosa, submucosa, or both

Sessile (flat)Pedunculated (on a stalk)

As in Crohn’s disease or ulcerative colitis

Normal tissue in abnormal configuration

Benign—normal cells—no malignantpotential


Neoplastic?

What are the subtypes ofneoplastic polyps?

What determines malignantpotential of an adenomatouspolyp?

What is the most commontype of adenomatous polyp?

What is the correlationbetween size andmalignancy?

What about histology andcancer potential of an adenomatous polyp?

What is the approximatepercentage of carcinomasfound in the followingpolyps overall:

Tubular adenoma?

Tubulovillous adenoma?

Villous adenoma?

Where are most polyps found?


What are the diagnostictests?


Proliferation of undifferentiated cells;premalignant or malignant cells

Tubular adenomas (usually pedunculated)Tubulovillous adenomasVillous adenomas (usually sessile and look

like broccoli heads)

SizeHistologic typeAtypia of cells

Tubular 85%

Polyps larger than 2 cm have a high riskof carcinoma (33%–55%)

Villous � tubovillous � tubular (Think:VILLous � VILLain)

5%

20%

40%

Rectosigmoid (30%)

Bleeding (red or dark blood), change inbowel habits, mucus per rectum,electrolyte loss, totally asymptomatic

Best � colonoscopy Less sensitive for small polyps � barium

enema and sigmoidoscopy




Endoscopic resection (snared) if polyps;large sessile villous adenomas should beremoved with bowel resection and lymphnode resection

POLYPOSIS SYNDROMES

FAMILIAL POLYPOSIS

What is another name forthis condition?

What are the characteristics?

What is the inheritance pattern?

What is the genetic defect?


Familial adenomatous polyposis (FAP)

Hundreds of adenomatous polyps withinthe rectum and colon that begin developingat puberty; all undiagnosed; untreatedpatients develop cancer by ages 40 to 50

Autosomal dominant (i.e., 50% ofoffspring)

APC (adenomatous polyposis coli) gene

Total proctocolectomy and ileostomyTotal colectomy and rectal mucosal

removal (mucosal proctectomy) andileoanal anastomosis

GARDNER’S SYNDROME

What are thecharacteristics?

What are the otherassociated findings?

How can the findings associated with Gardner’ssyndrome be remembered?

Neoplastic polyps of the small boweland colon; cancer by age 40 in 100% ofundiagnosed patients, as in FAP

Desmoid tumors (in abdominal wall orcavity), osteomas of skull (seen on x-ray),sebaceous cysts, adrenal and thyroidtumors, retroperitoneal fibrosis, duodenaland periampullary tumors

Think of a gardener planting “SOD”:Sebaceous cystsOsteomasDesmoid tumors


What is a desmoid tumor?

What medications may slow the growth of adesmoid tumor?


What is the treatment ofcolon polyps in patients withGardner’s syndrome?


Tumor of the musculoaponeurotic sheath,usually of the abdominal wall; benign, butgrows locally; treated by wide resection

Tamoxifen, sulindac, steroids

Varying degree of penetrance from anautosomal-dominant gene

Total proctocolectomy and ileostomyTotal colectomy and rectal mucosal

removal (mucosal proctectomy) andileoanal anastomosis

PEUTZ-JEGHERS’ SYNDROME

What are thecharacteristics?

What is the associated cancer risk from polyps?

What is the associated cancer risk for women withPeutz-Jeghers?


What are the other signs?


What are juvenile polyps?

Hamartomas throughout the GI tract(jejunum/ileum � colon � stomach)

Increased

Ovarian cancer (granulosa cell tumor ismost common)

Autosomal dominant

Melanotic pigmentation (black/brown) of buccal mucosa (mouth), lips, digits,palms, feet (soles)

(Think: Peutz � Pigmented)

Removal of polyps, if symptomatic (i.e.,bleeding, intussusception, or obstruction)or large (�1.5 cm)

Benign hamartomas in the small boweland colon; not premalignant; also knownas “retention polyps”


What is Cronkhite-Canadasyndrome?

What is Turcot’s syndrome?


Diffuse GI hamartoma polyps (i.e., nocancer potential) associated withmalabsorption/weight loss, diarrhea, andloss of electrolytes/protein; signs includealopecia, nail atrophy, skin pigmentation

Colon polyps with malignant CNStumors (glioblastoma multiforme)

DIVERTICULAR DISEASE OF THE COLON

DIVERTICULOSIS

What is diverticulosis? Condition in which diverticula can befound within the colon, especially the sigmoid; diverticula are actually falsediverticula in that only mucosa and submucosa herniate through the bowelmusculature; true diverticula involve alllayers of the bowel wall and are rare inthe colon

Blood vessel

Diverticula

Describe the pathophysiology.



Weakness in the bowel wall develops atpoints where nutrient blood vessels enterbetween antimesenteric and mesenterictaeniae; increased intraluminal pressuresthen cause herniation through these areas

�50% to 60% in the United States byage 60, with only 10% to 20% becomingsymptomatic

95% of people with diverticulosis havesigmoid colon involvement


Who is at risk?

What are the symptoms/complications?

What is the diagnosticapproach:

Bleeding?

Pain and signs of inflammation?

What is the treatment ofdiverticulosis?

What are the indications for operation with diverticulosis?

When is it safe to get a colonoscopy or bariumenema/sigmoidoscopy?


People with low-fiber diets, chronicconstipation, and a positive familyhistory; incidence increases with age

Bleeding: may be massiveDiverticulitis, asymptomatic (80% of cases)

Without signs of inflammation: colonoscopy

Abdominal/pelvic CT scan

High-fiber diet is recommended

Complications of diverticulitis (e.g., fistula, obstruction, stricture); recurrentepisodes; hemorrhage; suspected carci-noma; prolonged symptoms; abscess notdrainable by percutaneous approach

Due to risk of perforation, this isperformed 6 weeks after inflammationresolves to rule out colon cancer

DIVERTICULITIS

What is it?

What is thepathophysiology?



What are the associatedradiographic findings?

Infection or perforation of a diverticulum

Obstruction of diverticulum by afecalith leading to inflammation andmicroperforation

LLQ pain (cramping or steady), change inbowel habits (diarrhea), fever, chills, ano-rexia, LLQ mass, nausea/vomiting, dysuria

Increased WBCs

On x-ray: ileus, partially obstructed colon,air-fluid levels, free air if perforated

On abdominal/pelvic CT scan: swollen,edematous bowel wall; particularlyhelpful in diagnosing an abscess


What are the associated barium enema findings?

Is colonoscopy safe in anacute setting?


What is the most commonfistula with diverticulitis?

What is the best test fordiverticulitis?

What is the initial therapy?

When is surgery warranted?

What is the lifelong risk ofrecurrence after:

First episode?

Second episode?

What are the indications forelective resection?

What surgery is usually performed ELECTIVELYfor recurrent bouts?

What type of surgery is usually performed for anacute case of diverticulitiswith a complication (e.g.,perforation, obstruction)?


Barium enema should be avoided inacute cases

No, there is increased risk of perforation

Abscess, diffuse peritonitis, fistula,obstruction, perforation, stricture

Colovesical fistula (to bladder)

CT scan

IV fluids, NPO, broad-spectrumantibiotics with anaerobic coverage, NG suction (as needed for emesis/ileus)

Obstruction, fistula, free perforation,abscess not amenable to percutaneousdrainage, sepsis, deterioration with initialconservative treatment

33%

50%

Two episodes of diverticulitis; should beconsidered after the first episode in ayoung, diabetic, or immunosuppressedpatient

One-stage operation: resection of involvedsegment and primary anastomosis (withpreoperative bowel prep)

Hartmann’s procedure: resection ofinvolved segment with an end colostomyand stapled rectal stump (will need subsequent reanastomosis of colon usually after 2–3 postoperative months)


What is the treatment ofdiverticular abscess?

How common is massivelower GI bleeding withdiverticulitis?

What are the most commoncauses of massive lower GIbleeding in adults?

What must you rule out inany patient with diverticulitis/diverticulosis?


Percutaneous drainage; if abscess is notamenable to percutaneous drainage, thensurgical approach for drainage is necessary

Very rare! Massive lower GI bleeding isseen with diverticulosis, not diverticulitis

Diverticulosis (especially right sided),vascular ectasia

Colon cancer

COLONIC VOLVULUS

What is it?

What is the most commontype of colonic volvulus?

Twisting of colon on itself about itsmesentery, resulting in obstruction and, ifcomplete, vascular compromise withpotential necrosis, perforation, or both

Sigmoid volvulus (makes sense because thesigmoid is a redundant/“floppy” structure!)

SIGMOID VOLVULUS

What is it? Volvulus or “twist” in the sigmoid colon



What are the etiologicfactors?


What findings are evidenton abdominal plain film?

What are the signs of necroticbowel in colonic volvulus?


Under what conditions isgastrografin enema useful?

What are the signs of strangulation?


What is the percentage of recurrence after nonoperative reduction of a sigmoid volvulus?


�75% of colonic volvulus cases (Think:Sigmoid � Superior)

High-residue diet resulting in bulky stoolsand tortuous, elongated colon; chronicconstipation; laxative abuse; pregnancy;seen most commonly in bedridden elderlyor institutionalized patients, many ofwhom have history of prior abdominalsurgery or distal colonic obstruction

Acute abdominal pain, progressiveabdominal distention, anorexia, obstipation, cramps, nausea/vomiting

Distended loop of sigmoid colon, often inthe classic “bent inner tube” or “omega”sign with the loop aiming toward the RUQ

Free air, pneumatosis (air in bowel wall)

Sigmoidoscopy or radiographic exam withgastrografin enema

If sigmoidoscopy and plain films fail toconfirm the diagnosis; “bird’s beak” ispathognomonic seen on enema contraststudy as the contrast comes to a sharp end

Discolored or hemorrhagic mucosa onsigmoidoscopy, bloody fluid in therectum, frank ulceration or necrosis atthe point of the twist, peritoneal signs,fever, hypotension, c WBCs

Nonoperative: If there is no strangulation,sigmoidoscopic reduction is successful in �85% of cases; enema study will occasionally reduce (5%)

�40%!




Emergently if strangulation is suspectedor nonoperative reduction unsuccessful(Hartmann’s procedure); most patientsshould undergo resection during samehospitalization of redundant sigmoid aftersuccessful nonoperative reductionbecause of high recurrence rate (40%)

CECAL VOLVULUS

What is it?

What is a cecal “bascule”volvulus?





What diagnostic studiesshould be performed?


Twisting of the cecum upon itself and themesentery

Instead of the more common axial twist, the cecum folds upward (lies on theascending colon)

�25% of colonic volvulus (i.e., much lesscommon than sigmoid volvulus)

Idiopathic, poor fixation of the rightcolon, many patients have history ofabdominal surgery

Acute onset of abdominal or colicky painbeginning in the RLQ and progressing toa constant pain, vomiting, obstipation,abdominal distention, and SBO; manypatients will have had previous similarepisodes

Abdominal plain film; dilated, ovoidcolon with large air/fluid level in theRLQ often forming the classic “coffeebean” sign with the apex aiming towardthe epigastrium or LUQ (must rule outgastric dilation with NG aspiration)

Water-soluble contrast study (gastrografin),if diagnosis cannot be made by AXR

Emergent surgery, right colectomy withprimary anastomosis or ileostomy andmucous fistula (primary anastomosis maybe performed in stable patients)


What are the majordifferences in theEMERGENT managementof cecal volvulus versus sigmoid?

Chapter 49 / Anus 325

Patients with cecal volvulus require surgical reduction, whereas the vastmajority of patients with sigmoid volvulusundergo initial endoscopic reduction ofthe twist

ANATOMY

Identify the following:

AnusChapter 49

1

2

3

4

5

6

1. Anal columns2. Dentate line3. Rectum4. External sphincter5. Internal sphincter6. Levator ani muscle



ANAL CANCER

What is the most commoncarcinoma of the anus?

What cell types are found incarcinomas of the anus?

What is the incidence ofanal carcinoma?

What is anal Bowen’s disease?

How is Bowen’s diseasetreated?

What is Paget’s disease ofthe anus?

How is Paget’s diseasetreated?

What are the risk factors foranal cancer?

What is the most commonsymptom of anal carcinoma?

What are the othersigns/symptoms of anal carcinoma?

What percentage of patientswith anal cancer is asymptomatic?

To what locations do analcanal cancers metastasize?

Squamous cell carcinoma (80%)(Think: ASS � Anal Squamous Superior)

1. Squamous cell carcinoma (80%)2. Cloacogenic (transitional cell)3. Adenocarcinoma/melanoma/

mucoepidermal

Rare (1% of colon cancers incidence)

Squamous cell carcinoma in situ(Think: B.S. � Bowen Squamous)

With local wide excision

Adenocarcinoma in situ of the anus(Think: P.A. � Paget’s Adenocarcinoma)

With local wide excision

Human papilloma virus, condyloma, herpes, HIV, chronic inflammation (fistulae/Crohn’s disease) immunosuppres-sion, homosexuality in males, cervical/vaginal cancer, STDs, smoking

Anal bleeding

Pain, mass, mucus per rectum, pruritus

�25%

Lymph nodes, liver, bone, lung


What is the lymphaticdrainage below the dentateline?

Are most patients with analcancer diagnosed early orlate?

What is the workup of apatient with suspected analcarcinoma?

Define:Margin cancer

Canal cancer

How is an anal canal epidermal carcinomatreated?

What percentage of patientshave a “complete” responsewith the NIGRO protocol?

What is the 5-year survivalwith the NIGRO protocol?

What is the treatment forlocal recurrence of anal cancer after the NIGROprotocol?

How is a small (�5 cm) analmargin cancer treated?

How is a large (�5 cm) analmargin cancer treated?


Below to inguinal lymph nodes (above topelvic chains)

Late (diagnosis is often missed)

HistoryPhysical exam: digital rectal exam,

proctoscopic exam, and colonoscopyBiopsy of massAbdominal/pelvic CT scan, transanal U/SCXRLFTs

Anal verge out 5 cm onto the perianal skin

Proximal to anal verge up to the borderof the internal sphincter

NIGRO protocol:1. Chemotherapy (5-FU and mitomycin C)2. Radiation3. Postradiation therapy scar biopsy

(6–8 weeks post XRT)

90%

85%

May repeat chemotherapy/XRT orsalvage APR

Surgical excision with 1-cm margins

Chemoradiation


What is the treatment ofanal melanoma?

What is the 5-year survivalrate with anal melanoma?

How many patients withanal melanoma have anamelanotic anal tumor?

What is the prognosis ofanal melanoma?


Wide excision or APR (especially if tumor is large) �/� XRT, chemotherapy,postoperatively

�10%

Approximately one third, thus makingdiagnosis difficult without pathology

�5% 5-year survival rate

FISTULA IN ANO

What is it?



What disease should be considered with fistula inano?


What is Goodsall’s rule?

Anal fistula, from rectum to perianal skin

Usually anal crypt/gland infection (usuallyperianal abscess)

Perianal drainage, perirectal abscess,recurrent perirectal abscess, “diaperrash,” itching

Crohn’s disease

Exam, proctoscope

Fistulas originating anterior to a transverseline through the anus will course straightahead and exit anteriorly, whereas thoseexiting posteriorly have a curved tract


How can Goodsall’s rule beremembered?


Think of a dog with a straight nose(anterior) and curved tail (posterior)

Anterior

Goodsall

Posterior

What is the management ofanorectal fistulas?

What is a seton?

1. Define the anatomy2. Marsupialization of fistula tract

(i.e., fillet tract open)3. Wound care: routine Sitz baths and

dressing changes4. Seton placement if fistula is through

the sphincter muscle

Thick suture placed through fistula tractto allow slow transection of sphinctermuscle; scar tissue formed will hold thesphincter muscle in place and allow forcontinence after transection


What percentage of patientswith a perirectal abscessdevelop a fistula in ano afterdrainage?

How do you find theinternal rectal opening of ananorectal fistula in the O.R.?

What is a sitz bath?


�50%

Inject H2O2 (or methylene blue) in externalopening—then look for bubbles (or bluedye) coming out of internal opening!

Sitting in a warm bath (usually done afterbowel movement and TID

PERIRECTAL ABSCESS

What is it?



What is the cause?


What is the indication forpostoperative IV antibioticsfor drainage?

What percentage of patientsdevelops a fistula in anoduring the 6 months aftersurgery?

Abscess formation around the anus/rectum

Rectal pain, drainage of pus, fever, perianal mass

Physical/digital exam reveals perianal/rectal submucosal mass/fluctuance

Crypt abscess in dentate line with spread

As with all abscesses (except simple liveramebic abscess) drainage, sitz bath, anal hygiene, stool softeners

Cellulitis, immunosuppression, diabetes,heart valve abnormality

�50%

ANAL FISSURE

What is it?


What is the cause?

Tear or fissure in the anal epithelium

Posterior midline (comparatively lowblood flow)

Hard stool passage (constipation), hyperactive sphincter, disease process(e.g., Crohn’s disease)



What is a sentinel pile?

What is the anal fissure triadfor a chronic fissure?


Pain in the anus, painful (can be excruciating) bowel movement, rectalbleeding, blood on toilet tissue afterbowel movement, sentinel tag, tear in theanal skin, extremely painful rectal exam,sentinel pile, hypertrophic papilla

Thickened mucosa/skin at the distal endof an anal fissure that is often confusedwith a small hemorrhoid

1. Fissure2. Sentinel pile3. Hypertrophied anal papilla

Hypertrophicpapilla

Fissure

Sentinelpile

What is the conservativetreatment?

What disease processes mustbe considered with a chronicanal fissure?


What is one surgical option?

What is the “rule of 90%”for anal fissures?

Sitz baths, stool softeners, high fiber diet,excellent anal hygiene, topical nifedipine,Botox®

Crohn’s disease, anal cancer, sexuallytransmitted disease, ulcerative colitis,AIDS

Chronic fissure refractory to conservativetreatment

Lateral internal sphincterotomy (LIS)—cut the internal sphincter to release itfrom spasm

90% occur posteriorly90% heal with medical treatment alone90% of patients who undergo an LIS heal

successfully



PERIANAL WARTS

What are they?

What is the cause?

What is the major risk?

What is the treatment ifwarts are small?

What is the treatment ifwarts are large?

Warts around the anus/perineum

Condyloma acuminatum (humanpapilloma virus)

Squamous cell carcinoma

Topical podophyllin, imiquimod (Aldara®)

Surgical resection or laser ablation

HEMORRHOIDS

What are they?

Why do we have “healthy”hemorrhoidal tissue?


Which type, internal orexternal, is painful?

If a patient has excruciatinganal pain and history ofhemorrhoids, what is thelikely diagnosis?

What are the causes of hemorrhoids?

What is an internal hemorrhoid?

What is an external hemorrhoid?

What are the three “hemorrhoid quadrants”?

Engorgement of the venous plexuses of the rectum, anus, or both; with protrusionof the mucosa, anal margin, or both

It is thought to be involved with fluid/aircontinence

Anal mass/prolapse, bleeding, itching, pain

External, below the dentate line

Thrombosed external hemorrhoid (treat by excision)

Constipation/straining, portal hypertension, pregnancy

Hemorrhoid above the (proximal)dentate line

Hemorrhoid below the dentate line

1. Left lateral2. Right posterior3. Right anterior


Classification by Degrees

Define the following termsfor internal hemorrhoids:

First-degree hemorrhoid


Hemorrhoid that does not prolapse

hrf ‘07

1st degreehemorrhoid

Second-degreehemorrhoid

Prolapses with defecation, but returns onits own

2nd degreehemorrhoid

hrf ‘07

Third-degree hemorrhoid Prolapses with defecation or any type ofValsalva maneuver and requires activemanual reduction (eat fiber!)

hrf ‘07

3rd degreehemorrhoid



Fourth-degreehemorrhoid


What is a “closed” vs. an“open” hemorrhoidectomy?

What are the dreaded complications ofhemorrhoidectomy?

What condition is acontraindication for hemorrhoidectomy?

Classically, what must beruled out with lower GIbleeding believed to becaused by hemorrhoids?

Prolapsed hemorrhoid that cannot bereduced

High-fiber diet, anal hygiene, topicalsteroids, sitz baths

Rubber band ligation (in most cases anesthetic is not necessary for internalhemorrhoids)

Surgical resection for large refractoryhemorrhoids, infrared coagulation,harmonic scalpel

Closed (Ferguson) “closes” the mucosa withsutures after hemorrhoid tissue removal

Open (Milligan-Morgan) leaves mucosa“open”

Exsanguination (bleeding may poolproximally in lumen of colon withoutany signs of external bleeding)

Pelvic infection (may be extensive andpotentially fatal)

Incontinence (injury to sphincter complex)Anal stricture

Crohn’s disease

Colon cancer (colonoscopy)

What is the definition oflower GI bleeding?


Lower GI BleedingChapter 50Bleeding distal to the ligament of Treitz;vast majority occurs in the colon

Hematochezia (bright red blood perrectum [BRBPR]), with or withoutabdominal pain, melena, anorexia, fatigue,syncope, shortness of breath, shock


What are the signs?


What medicines should belooked for causally with alower GI bleed?

What are the most commoncauses of massive lower GIbleeding?


What is the initial treatment?

What diagnostic tests shouldbe performed for all lowerGI bleeds?

What must be ruled out inpatients with lower GIbleeding?

How can you have a UGIbleed with only clear succusback in the NGT?

Chapter 43 / Ostomies 335

BRBPR, positive hemoccult, abdominaltenderness, hypovolemic shock, orthostasis

Diverticulosis (usually right-sided insevere hemorrhage), vascular ectasia,colon cancer, hemorrhoids, trauma,hereditary hemorrhagic telangiectasia,intussusception, volvulus, ischemic colitis,IBD (especially ulcerative colitis), anticoagulation, rectal cancer, Meckel’sdiverticulum (with ectopic gastricmucosa), stercoral ulcer (ulcer from hardstool), infectious colitis, aortoenteric fistula, chemotherapy, irradiation injury,infarcted bowel, strangulated hernia, analfissure

Coumadin®, aspirin, Plavix®

1. Diverticulosis2. Vascular ectasia

CBC, Chem-7, PT/PTT, type and cross

IVFs: lactated Ringer’s; packed red bloodcells as needed, IV � 2, Foley catheter tofollow urine output, d/c aspirin, NGT

History, physical exam, NGT aspiration(to rule out UGI bleeding; bile or bloodmust be seen; otherwise, perform EGD),anoscopy/proctoscopic exam

Upper GI bleeding! Remember, NGTaspiration is not 100% accurate (even ifyou get bile without blood)

Duodenal bleeding ulcer can bleed distalto the pylorus with the NGT sucking normal nonbloody gastric secretions! Ifthere is any question, perform EGD

Chapter 50 / Lower GI Bleeding 335


What would an algorithmfor diagnosing and treatinglower GI bleeding look like?


History, physical exam, labs

NGT

Bile, no bloodBlood Clear: no bile/no blood

Anoscopy/proctoscopy

EGD EGD*

(–)

Significant bleed Slow bleed

Colonoscopy

Tagged RBC study Rx

RxRx

+

(+)Rx

– –

– +

+

(+) Tagged RBC scan

–Arteriogram

*Based on clinical suspicion

Massive bleed

What is the diagnostic testof choice for localizing aslow to moderate lower GIbleeding source?

Colonoscopy


What test is performed tolocalize bleeding if there istoo much active bleeding tosee the source with acolonoscope?

What is more sensitive for aslow, intermittent amount ofblood loss: A-gram or taggedRBC study?

What is the colonoscopictreatment option for bleedingvascular ectasia or polyp?

What is the treatment ifbleeding site is KNOWN andmassive or recurrent lowerGI bleeding continues?

What is the surgicaltreatment of massive lowerGI bleeding WITHOUTlocalization?

What percentage of casesspontaneously stop bleeding?

What percentage of patientsrequire emergent surgeryfor lower GI bleeding?

Does melena always signifyactive colonic bleeding?

What is the therapeuticadvantage of doing acolonoscopy?

What is the therapeuticadvantage of doing an A-gram?

Chapter 50 / Lower GI Bleeding 337

A-gram (mesenteric angiography)

Radiolabeled RBC scan is more sensitivefor blood loss at a rate of 0.5 mL/minor intermittent blood loss because it has a longer half-life (for arteriography,bleeding rate must be 1.0 mL/min)

Laser or electrocoagulation; localepinephrine injection

Segmental resection of the bowel

Exploratory laparotomy with intraopera-tive enteroscopy and total abdominalcolectomy as last resort

80%–90% stop bleeding with resuscitativemeasures only (at least temporarily)

Only �10%

NO—the colon is very good at storingmaterial and often will store melena/maroon stools and pass them days later(follow patient, UO, HCT, and vital signs)

Options of injecting substance (epinephrine) or coagulating vessels is anadvantage with C-scope to control bleeding

Ability to inject vasopressin and/orembolization, with at least temporarycontrol of bleeding in �85%



What is IBD?

What are the two inflammatory boweldiseases?

What is another name forCrohn’s disease?

What is ulcerative colitisoften called?

What is the cause of IBD?


What are the extraintestinalmanifestations seen in bothtypes of IBD?

InflammatoryBowel Disease:Crohn’s Diseaseand UlcerativeColitis

Chapter 51

Inflammatory Bowel Disease, inflammatory disease of the GI tract

Crohn’s disease and ulcerative colitis

Regional enteritis

UC

No one knows, but probably an autoimmune process with environmentalfactors contributing

Crohn’s versus ulcerative colitis, infectiouscolitis (e.g., C. difficile, amebiasis, shigellosis), ischemic colitis, irritable bowelsyndrome, diverticulitis, Zollinger-Ellisonsyndrome (ZES), colon cancer, carcinoid,ischemic bowel

Ankylosing spondylitis, aphthous (oral)ulcers, iritis, pyoderma gangrenosum,erythema nodosum, clubbing of fingers,sclerosing cholangitis, arthritis, kidneydisease (nephrotic syndrome, amyloiddeposits)


How can thesemanifestations beremembered?

Chapter 51 / Inflammatory Bowel Disease: Crohn’s Disease and Ulcerative Colitis 339

Think of the acronym “A PIE SACK”:Aphthous ulcers

Pyoderma gangrenosumIritisErythema nodosum

Sclerosing cholangitisArthritis, Ankylosing spondylitisClubbing of fingersKidney (amyloid deposits, nephrotic

syndrome)

COMPARISON OF CROHN’S DISEASE AND ULCERATIVE COLITIS

INCIDENCE

Crohn’s disease:Incidence

At-risk population

Sex?

Distribution?

Ulcerative colitis:Incidence?

At-risk population

Sex?

Distribution?

3–6/100,000

High in the Jewish population, low in theAfrican black population, similar ratesbetween African American and U.S.white population

Female � male

Bimodal distribution (i.e., two peaks inincidence): peak incidence at 25 to 40years of age; second bimodal distributionpeak at 50 to 65 years of age

10/100,000

High in the Jewish population, low in the African American population

Positive family history in 20% of cases

Male � female

Bimodal distribution at 20 to 35 and 50 to 65 years of age



INITIAL SYMPTOMS

Crohn’s disease?

Ulcerative colitis?

Abdominal pain, diarrhea, fever,weight loss, anal disease

Bloody diarrhea (hallmark), fever,weight loss

ANATOMIC DISTRIBUTION

Crohn’s disease?

Ulcerative colitis?

Classic phrasing “mouth to anus”Small bowel only (20%)Small bowel and colon (40%)Colon only (30%)

Colon only (Think: ulcerative COLitis� COLon alone)

ROUTE OF SPREAD

Crohn’s disease?

Ulcerative colitis?

What is “backwash” ileitis?

Small bowel, colon, or both with “skipareas” of normal bowel; hence, thename “regional enteritis”

Almost always involves the rectum andspreads proximally always in a continuousroute without “skip areas”

Mild inflammation of the terminal ileumin ulcerative colitis; thought to be “backwash” of inflammatory mediatorsfrom the colon into the terminal ileum

BOWEL WALL INVOLVEMENT

Crohn’s disease?

Ulcerative colitis?

Full thickness (transmural involvement)

Mucosa/submucosa only

ANAL INVOLVEMENT

Crohn’s disease?

Ulcerative colitis?

Common (fistulae, abscesses, fissures,ulcers)

Uncommon



RECTAL INVOLVEMENT

Crohn’s disease?

Ulcerative colitis?

Rare

100%

MUCOSAL FINDINGS

Crohn’s disease (6)?

Ulcerative colitis (5)?

How can ulcerative colitisand Crohn’s anal and wallinvolvement be remembered?

1. Aphthoid ulcers2. Granulomas3. Linear ulcers4. Transverse fissures5. Swollen mucosa6. Full-thickness wall involvement

1. Granular, flat mucosa2. Ulcers3. Crypt abscess4. Dilated mucosal vessels5. Pseudopolyps

“CAT URP”:Crohn’s � Anal–TransmuralUC � Rectum–Partial wall thickness

DIAGNOSTIC TESTS

Crohn’s disease?

Ulcerative colitis?

Colonoscopy with biopsy, barium enema,UGI with small bowel follow-through,stool cultures

Colonoscopy, barium enema, UGI withsmall bowel follow-through (to look forCrohn’s disease), stool cultures

COMPLICATIONS

Crohn’s disease?

Ulcerative colitis?

Anal fistula/abscess, fistula, stricture,perforation, abscesses, toxic megacolon,colovesical fistula, enterovaginal fistula,hemorrhage, obstruction, cancer

Cancer, toxic megacolon, colonic perforation, hemorrhage, strictures,obstruction, complications of surgery



CANCER RISK

Crohn’s disease?

Ulcerative colitis?

Overall increased risk, but about half thatof ulcerative colitis

�5% risk of developing colon cancer at10 years; then, risk increases �1% peryear; thus, an incidence of �20% after 20 years of the disease (30% at 30 years)

INCIDENCE OF TOXIC MEGACOLON

Crohn’s disease?

Ulcerative colitis?

�5%

�10%

INDICATIONS FOR SURGERY

Crohn’s disease?

Ulcerative colitis?

What are the common surgical options for ulcerative colitis?

What is “toxic megacolon”?

Obstruction, massive bleeding, fistula,perforation, suspicion of cancer, abscess(refractory to medical treatment), toxicmegacolon (refractory to medicaltreatment), strictures, dysplasia

Toxic megacolon (refractory to medicaltreatment); cancer prophylaxis; massivebleeding; failure of child to maturebecause of disease and steroids; perforation; suspicion of or documentedcancer; acute severe symptoms refractoryto medical treatment; inability to weanoff of chronic steroids; obstruction; dysplasia; stricture

1. Total proctocolectomy, distal rectalmucosectomy, and ileoanal pullthrough

2. Total proctocolectomy and Brookeileostomy

Toxic patient: sepsis, febrile, abdominalpain

Megacolon: acutely and massivelydistended colon


What are the medicationoptions for treating IBD?

What is infliximab?

What is the active metaboliteof sulfasalazine?

What is the medicaltreatment of choice for perianal Crohn’s disease?

What are the treatmentoptions for long-term remission of IBD?

What medication is used forIBD “flare-ups”?

What is a unique medicationroute option for ulcerativecolitis?

Which disease has “cobblestoning” more often on endoscopic exam?

Which disease haspseudopolyps oncolonoscopic exam?

Which disease has a “lead pipe” appearance onbarium enema?

Rectal bleeding/bloody diarrhea is a hallmark ofwhich disease?


Sulfasalazine, mesalamine (5-aminosalicylic acid)

Steroids, metronidazole (Flagyl®), azathioprine, 6-mercaptopurine (6-mp), infliximab

Antibody vs. TNF-� (tumor necrosis factor-alpha)

5’-aminosalicylate (5’-ASA), which isreleased in the colon

PO metronidazole (Flagyl®)

6-mercaptopurine (6-mp), azathioprine,mesalamine

Steroids

Enemas (steroids, 5-ASA)

Crohn’s disease (Think: Crohn’s �Cobblestoning)

Ulcerative colitis; pseudopolyps arepolyps of hypertrophied mucosasurrounded by mucosal atrophy

Chronic ulcerative colitis

Ulcerative colitis (rare in Crohn’s disease)


What is the most commonindication for surgery inpatients with Crohn’s disease?

What are the intraoperativefindings of Crohn’s disease?

Why do you see fistulas andabscesses with Crohn’s andnot ulcerative colitis?

What is the operation forshort strictures of the smallbowel in Crohn’s disease?

Should the appendix be removed during a laparotomy for abdominalpain if Crohn’s disease is discovered?

What is pouchitis?

Do you need a frozensection for margins during abowel resection for Crohn’sdisease?

What is it called when theentire colon is involved?


Small bowel obstruction (SBO)

Mesenteric “fat creeping” onto theantimesenteric border of the smallbowel

Shortened (and thick) mesenteryThick bowel wallFistula(e)Abscess(es)

Crohn’s disease is transmural

Stricturoplasty; basically a Heineke-Mikulicz pyloroplasty on the stricturedsegment (i.e., opened longitudinally andsewn closed in a transverse direction)

Yes, if the cecum is not involved withactive Crohn’s disease

Inflammation of the pouch of an ileoanalpull through; treat with metronidazole(Flagyl®)

No, you need only grossly negative margins

Pancolitis


Chapter 52 / Liver 345

ANATOMY

LiverChapter 52

Glisson’s capsule

Posterior section of the liver against thediaphragm that is “bare” without peritonealcovering

Line drawn from the gallbladder to apoint just to the left of the inferior venacava, which transects the liver into theright and left lobes

What is the name of theliver capsule?

What is the “bare” area?

What is Cantle’s line?

Which ligament goes fromthe anterior abdominal wallto the liver?

What does the falciform ligament contain?

What is the coronaryligament?

What are the triangular ligaments of the liver?

Falciform ligament

Ligamentum teres (obliterated umbilicalvein)

Peritoneal reflection on top of the liverthat crowns (hence “coronary”) the liverand attaches it to the diaphragm

Right and left lateral extents of the coronary ligament, which form triangles


What is the origin of thehepatic arterial supply?

Identify the arterialbranches of the celiac trunk:


From the proper hepatic artery off of theceliac trunk (celiac trunk to commonhepatic artery to proper hepatic artery)

1. Celiac trunk2. Splenic artery3. Left gastric artery4. Common hepatic artery5. Gastroduodenal artery6. Proper hepatic artery7. Left hepatic artery8. Right hepatic artery

What is the venous supply?

What is the hepatic venousdrainage?

Portal vein (formed from the splenicvein and the superior mesenteric vein)

Via the hepatic veins, which drain intothe IVC (three veins: left, middle, andright)


What sources provideoxygen to the liver?

From what sources does theliver receive blood?

Identify the segments of theliver (French system).


Portal vein blood—50%Hepatic artery blood—50%

Portal system—75%Hepatic artery system—25%

What is the overall arrange-ment of the segments in theliver?

Clockwise, starting at segment 1

What is the maximumamount of liver that can beresected while retainingadequate liver function?

What are the signs/symptomsof liver disease?

�80%; if given adequate recovery time,the original mass can be regenerated(Remember Prometheus!)

Hepatomegaly, splenomegaly, icterus,pruritus (from bile salts in skin), blanchingspider telangiectasia, gynecomastia, testicular atrophy, caput medusae, darkurine, clay-colored stools, bradycardia,edema, ascites, fever, fetor hepaticus(sweet musty smell), hemorrhoids,variceal bleeding, anemia, body hair loss,liver tenderness, palmar erythema


Which liver enzymes aremade by hepatocytes?

What is the source ofalkaline phosphatase?

What is Child’s class? (Child-Turcotte-Pugh)

What comprises the Child’sclassification?

How can the criteriacomprising the modifiedChild’s classification beremembered?

Define Child’s classification:ABC

What is the operative mortality for a portocavalshunt vs. overall intra-abdominal operations withcirrhosis in the followingChild’s classes:

A?B?C?

What does the MELD scorestand for?

What is measured in theMELD score?


AST and ALT (aspartate aminotransferaseand alanine aminotransferase)

Ductal epithelium (thus, elevated withductal obstruction)

Classification system that estimateshepatic reserve in patients with hepaticfailure and mortality

Laboratory: bilirubin, albuminClinical: encephalopathy, ascites,

prothrombin time (PT)

Use the acronym: “A BEAP”:Ascites

BilirubinEncephalopathyAlbuminPT (prothrombin time)

Ascites Bili Enceph ALB PT INRnone �2 none �3.5 �1.7controlled 2–3 minimal 2.8–3.5 1.7–2.2uncontrolled �3 severe �2.8 �2.2(Think: As in a letter grading system, A isbetter than B, B is better than C)

�5% vs. overall � 10%�15% vs. overall � 30%�33% vs. overall � 75%

Model for End-stage Liver Disease

INR, T.Bili, serum creatinine (SCR);find good MELD calculators online


What is the mortality in cirrhotic patients for nonemergent nontransplantsurgery?

What is the mortality in cirrhotic patients for emergent nontransplant surgery?


Increase in mortality by 1% per 1 pointin the MELD score until 20, then 2% foreach MELD point

14% increase in mortality per 1 point ofthe MELD score

TUMORS OF THE LIVER

What is the most commonliver cancer?

What is the most commonprimary malignant livertumor?

What is the most commonprimary benign liver tumor?

What lab tests comprise theworkup for liver metastasis?

What are the associatedimaging studies?

What is a right hepaticlobectomy?

What is a left hepatic lobectomy?

What is a righttrisegmentectomy?

What are the three commontypes of primary benignliver tumors?

Metastatic disease outnumbers primarytumors 20:1; primary site is usually theGI tract

Hepatocellular carcinoma (hepatoma)

Hemangioma

LFTs (AST and alkaline phosphatase aremost useful), CEA for suspected primarycolon cancer

CT scan, ultrasound, A-gram

Removal of the right lobe of the liver(i.e., all tissue to the right of Cantle’s lineis removed)

Removal of the left lobe of the liver (i.e., removal of all the liver tissue to theleft of Cantle’s line)

Removal of all the liver tissue to the rightof the falciform ligament

1. Hemangioma2. Hepatocellular adenoma3. Focal nodular hyperplasia


What are the four commontypes of primary malignantliver tumors?

What chemical exposuresare risk factors for angiosarcoma?

What is a “hepatoma”?

What are the other benignliver masses?

What is a liver “hamartoma”?


1. Hepatocellular carcinoma (hepatoma)2. Cholangiocarcinoma (when

intrahepatic)3. Angiosarcoma (associated with chemical

exposure)4. Hepatoblastoma (most common in

infants and children)

Vinyl chloride, arsenic, thorotrast contrast

Hepatocellular carcinoma

Benign liver cyst, bile duct hamartomas,bile duct adenoma

White hard nodule made up of normalliver cells

HEPATOCELLULAR ADENOMA

What is it?

Describe the histology.


What is the female:maleratio?

What is the average age ofoccurrence?




Benign liver tumor

Normal hepatocytes without bile ducts

Women, birth control pills (Think: ABC � Adenoma Birth Control),anabolic steroids, glycogen storagedisease

9:1

30–35 years of age

RUQ pain/mass, RUQ fullness, bleeding (rare)

Rupture with bleeding (33%), necrosis,pain, risk of hepatocellular carcinoma

CT scan, U/S, �/– biopsy (rule outhemangioma with RBC-tagged scan!)


What is the treatment:Small?

Large (�5 cm), bleeding,painful, or ruptured?


Stop birth control pills—it may regress; if not, surgical resection is necessary

Surgical resection

FOCAL NODULAR HYPERPLASIA (FNH)

What is it?

Describe the histology.

What is the average age ofoccurrence?

What are the associated risk factors?

Are the tumors associatedwith birth control pills?


What is the classic CT scanfinding?


Is there a cancer risk withFNH?


Why does embolization workwith FNH?

Benign liver tumor

Normal hepatocytes and bile ducts(adenoma has no bile ducts)

�40 years

Female gender

Yes, but not as clearly associated as withadenoma

Nuclear technetium-99 study, U/S, CT scan, A-gram, biopsy

Liver mass with “central scar”(Think: focal � central)

Pain (no risk of cancer, very rarely hemorrhage)

No (there is a cancer risk with adenoma)

Resection or embolization if patient is symptomatic; otherwise, follow if diagnosis is confirmed; stop birth control pills

FNH tumors are usually fed by onemajor artery



HEPATIC HEMANGIOMA

What is it?




Define Kasabach-Merrittsyndrome?


Should biopsy be performed?


What are the indications forresection?

Benign vascular tumor of the liver

Most common primary benign livertumor (up to 7% of population)

RUQ pain/mass, bruits

Pain, congestive heart failure, coagulopathy,obstructive jaundice, gastric outletobstruction, Kasabach-Merritt syndrome,hemorrhage (rare)

Hemangioma and thrombocytopenia andfibrinogenopenia

CT scan with IV contrast, tagged redblood scan, MRI, ultrasound

No (risk of hemorrhage with biopsy)

Observation (�90%)

Symptoms, hemorrhage, cannot make adiagnosis

HEPATOCELLULAR CARCINOMA

What is it?

By what name is it alsoknown?

What is its incidence?

What are the geographichigh-risk areas?


Most common primary malignancy of theliver

Hepatoma

Accounts for 80% of all primarymalignant liver tumors

Africa and Asia

Hepatitis B virus, cirrhosis, aflatoxin(fungi toxin of Aspergillus flavus); Otherrisk factors: �-1-antitrypsin deficiency,hemochromatosis, liver fluke (Clonorchissinensis), anabolic steroids, polyvinylchloride, glycogen storage disease (type I)


What percentage of patientswith cirrhosis will develophepatocellular carcinoma?


What tests should beordered?

What is the tumor marker?

What is the most commonway to get a tissue diagnosis?

What is the most commonsite of metastasis?

What is the treatment ofhepatocellular carcinoma?

What are the treatmentoptions if the patient is not asurgical candidate?

What are the indications forliver transplantation?

What is the prognosis underthe following conditions:

Unresectable?

Resectable?

Which subtype has the bestprognosis?


�5%

Dull RUQ pain, hepatomegaly (classicpresentation: painful hepatomegaly),abdominal mass, weight loss,paraneoplastic syndromes, signs of portalhypertension, ascites, jaundice, fever,anemia, splenomegaly

Ultrasound, CT scan, angiography, tumormarker elevation

Elevated �-fetoprotein

Needle biopsy with CT scan, ultrasound,or laparoscopic guidance

Lungs

Surgical resection, if possible (e.g., lobectomy); liver transplant

Percutaneous ethanol tumor injection,cryotherapy, and intra-arterialchemotherapy

Cirrhosis and NO resection candidacy as well as no distant or lymph node metastases and no vascular invasion; the tumor must be single, �5-cm tumor or have three nodules, with none �3 cm

Almost none survive a year

�35% are alive at 5 years

Fibrolamellar hepatoma (young adults)



ABSCESSES OF THE LIVER

What is a liver abscess?

What are the types of liverabscess?

What is the most commonlocation of abscess in theliver?

What are the sources?

What are the two most common types?

Abscess (collection of pus) in the liverparenchyma

Pyogenic (bacterial), parasitic (amebic),fungal

Right lobe � left lobe

Direct spread from biliary tract infectionor

Portal spread from GI infection (e.g., appendicitis, diverticulitis)

Systemic source (bacteremia)Liver trauma (e.g., liver gunshot wound)Cryptogenic (unknown source)

Bacterial (most common in the UnitedStates) and amebic (most common worldwide)

BACTERIAL LIVER ABSCESS

What are the three mostcommon bacterial organismsaffecting the liver?

What are the most commonsources/causes of bacterialliver abscesses?



What are the indications foroperative drainage?

Gram negatives: E. coli, Klebsiella, andProteus

Cholangitis, diverticulitis, liver cancer,liver metastasis

Fever, chills, RUQ pain, leukocytosis,increased liver function tests (LFTs),jaundice, sepsis, weight loss

IV antibiotics (triple antibiotics withmetronidazole), percutaneous drainagewith CT scan or U/S guidance

Multiple/loculated abscesses or if multiple percutaneous attempts havefailed



How does it spread?



Which lobe is mostcommonly involved?

Classic description ofabscess contents?




What are the indications forpercutaneous surgicaldrainage?

What are the possible complications of large leftlobe liver amebic abscess?


Entamoeba histolytica (typically reachesliver via portal vein from intestinal amebiasis)

Fecal–oral transmission

Patients from countries south of theU.S.–Mexican border, institutionalizedpatients, homosexual men, alcoholicpatients

RUQ pain, fever, hepatomegaly, diarrheaNote: chills are much less common with

amebic abscesses than with pyogenicabscesses

Right lobe of the liver

“Anchovy paste” pus

Lab tests, ultrasound, CT scan

Indirect hemagglutination titers for Entamoeba antibodies elevated in �95%of cases, elevated LFTs

Metronidazole IV

Refractory to metronidazole, bacterial co-infection, or peritoneal rupture

Erosion into the pericardial sac(potentially fatal!)

HYDATID LIVER CYST

What is it? Usually a right lobe cyst filled withEchinococcus granulosus

AMEBIC LIVER ABSCESS





What are the findings on AXR?

What are the major risks?

What is the risk of surgicalremoval of echinococcal(hydatid) cysts?

When should percutaneousdrainage be performed?


Which toxic irrigations areused?


Travel; exposure to dogs, sheep, and cattle (carriers)

RUQ abdominal pain, jaundice, RUQ mass

Indirect hemagglutination antibody test(serologic testing), Casoni skin test, ultrasound, CT, radiographic imaging

Possible calcified outline of cyst

Erosion into the pleural cavity,pericardial sac, or biliary tree

Rupture into the peritoneal cavity causing fatal anaphylaxis

Rupture or leakage of cyst contents into the abdomen may cause a fatal anaphylactic reaction

Never; may cause leaking into theperitoneal cavity and anaphylaxis

Mebendazole, followed by surgicalresection; large cysts can be drained and then injected with toxic irrigant (scoliocide) into the cyst unless aspirate isbilious (which means there is a biliaryconnection) followed by cyst removal

Hypertonic saline, ethanol, or cetrimide

HEMOBILIA

What is it?

What is the diagnostic triad?


Blood draining via the common bile ductinto the duodenum

Triad:1. RUQ pain2. Guaiac positive/upper GI bleeding3. Jaundice

Trauma with liver laceration, percutaneoustranshepatic cholangiography (PTC), tumors




Chapter 53 / Portal Hypertension 357

EGD (blood out of the ampulla of Vater),A-gram

A-gram with embolization of the bleedingvessel

Identify the anatomy of theportal venous system:

PortalHypertension

Chapter 53

1. Portal vein2. Coronary vein3. Splenic vein4. IMV (inferior mesenteric vein)5. SMV (superior mesenteric vein)6. Superior hemorrhoidal vein


Describe drainage of blood from the superiorhemorrhoidal vein.

Where does blood drain intofrom the IMV?

Where does the portal veinbegin?

What are the (6) potentialroutes of portal–systemic collateral blood flow (as seenwith portal hypertension)?

What is the pathophysiologyof portal hypertension?

What level of portalpressure is normal?


What is the most commoncause of portal hypertensionin the United States?

How many patients withalcoholism develop cirrhosis?


To the IMV, the splenic vein, and thenthe portal vein

Into the splenic vein

At the confluence of the splenic vein andthe SMV

1. Umbilical vein2. Coronary vein to esophageal venous

plexuses3. Retroperitoneal veins (veins of Retzius)4. Diaphragm veins (veins of Sappey)5. Superior hemorrhoidal vein to middle

and inferior hemorrhoidal veins andthen to the iliac vein

6. Splenic veins to the short gastricveins

Elevated portal pressure resulting fromresistance to portal flow

�10 mm Hg

Prehepatic—Thrombosis of portal vein/atresia of portal vein

Hepatic—Cirrhosis (distortion of normal parenchyma by regeneratinghepatic nodules), hepatocellular carcinoma, fibrosis

Posthepatic—Budd-Chiari syndrome:thrombosis of hepatic veins

Cirrhosis (�90% of cases)

Surprisingly, �1 in 5


What percentage of patientswith cirrhosis developesophageal varices?

How many patients with cirrhosis develop portalhypertension?

What is the most commonphysical finding in patientswith portal hypertension?

What are the associatedCLINICAL findings in portal hypertension (4)?


�40%

Approximately two thirds

Splenomegaly (spleen enlargement)

1. Esophageal varices2. Splenomegaly3. Caput medusae (engorgement of

periumbilical veins)4. Hemorrhoids

Varices

Hemorrhoids

Caputmedusae

Splenomegaly

What other physical findingsare associated with cirrhosisand portal hypertension?

What is the name of theperiumbilical bruit heardwith caput medusae?

Spider angioma, palmar erythema,ascites, truncal obesity and peripheralwasting, encephalopathy, asterixis (liverflap), gynecomastia, jaundice

Cruveilhier-Baumgarten bruit


What constitutes the portal–systemic collateral circulationin portal hypertension in thefollowing conditions:

Esophageal varices?

Caput medusae?

Retroperitoneal varices?

Hemorrhoids?


What is the most commoncause of portal hypertensionoutside North America?

What is Budd-Chiarisyndrome?

What is the most fearedcomplication of portalhypertension?

What are esophagealvarices?

What is the “rule of 2/3” ofportal hypertension?


Coronary vein backing up into theazygous system

Umbilical vein (via falciform ligament)draining into the epigastric veins

Small mesenteric veins (veins of Retzius)draining retroperitoneally into lumbar veins

Superior hemorrhoidal vein (which normally drains into the inferior mesen-teric vein) backing up into the middleand inferior hemorrhoidal veins

Cirrhosis (90%), schistosomiasis, hepatitis, Budd-Chiari syndrome,hemochromatosis, Wilson’s disease, portal vein thrombosis, tumors, splenicvein thrombosis

Schistosomiasis

Thrombosis of the hepatic veins

Bleeding from esophageal varices

Engorgement of the esophageal venousplexuses secondary to increased collateralblood flow from the portal system as aresult of portal hypertension

2/3 of patients with cirrhosis will developportal hypertension

2/3 of patients with portal hypertensionwill develop esophageal varices

2/3 of patients with esophageal variceswill bleed from the varices


In patients with cirrhosis andknown varices who aresuffering from upper GIbleeding, how often does thatbleeding result from varices?


What is the mortality ratefrom an acute esophagealvariceal bleed?

What is the initial treatmentof variceal bleeding?

What is the diagnostic testof choice?

If esophageal varices causebleeding, what are the EGDtreatment options?

What are the pharmacologicoptions?

What is a Sengstaken-Blakemore tube?

What is the next therapy afterthe bleeding is controlled?


Only �50% of the time

Hematemesis, melena, hematochezia

�50%

As with all upper GI bleeding: large bore IVs � 2, IV fluid, Foley catheter,type and cross blood, send labs, correctcoagulopathy (vitamin K, fresh frozenplasma), �/ – intubation to protect fromaspiration

EGD (upper GI endoscopy)Remember, bleeding is the result of

varices only half the time; must ruleout ulcers, gastritis, etc.

1. Emergent endoscopic sclerotherapy: a sclerosing substanceis injected into the esophageal varicesunder direct endoscopic vision

2. Endoscopic band ligation: elasticband ligation of varices

Somatostatin (Octreotide) or IVvasopressin (and nitroglycerin, to avoid MI) to achieve vasoconstriction of themesenteric vessels; if bleeding continues,consider balloon (Sengstaken-Blakemoretube) tamponade of the varices, �-blocker

Tube with a gastric and esophagealballoon for tamponading an esophagealbleed (see page 268)

Repeat endoscopic sclerotherapy/banding


What are the options if sclerotherapy and conservative methods fail tostop the variceal bleeding orbleeding recurs?

What is a “selective” shunt?

What does the acronymTIPS stand for?

What is a TIPS procedure?

What is a “partial shunt”?

What is a Warren shunt?


Repeat sclerotherapy/banding and treatconservatively

TIPSSurgical shunt (selective or partial)Liver transplantation

Shunt that selectively decompresses thevarices without decompressing the portalvein

Transjugular Intrahepatic PortosystemicShunt

Angiographic radiologist places a smalltube stent intrahepatically between thehepatic vein and a branch of the portalvein via a percutaneous jugular vein route

Shunt that directly decompresses theportal vein, but only partially

Distal splenorenal shunt with ligation of thecoronary vein—elective shunt procedureassociated with low incidence ofencephalopathy in patients postoperativelybecause only the splenic flow is divertedto decompress the varices


What is a contraindication tothe Warren “selective”shunt?

Define the following shunts:End-to-side portocavalshunt

Side-to-side portocavalshunt

Synthetic portocaval H-graft

Synthetic mesocaval H-graft

What is the most commonperioperative cause of deathfollowing shunt procedure?

What is the major postoperative morbidityafter a shunt procedure?

What medication is infusedto counteract the coronaryartery vasoconstriction of IVvasopressin?

What lab value roughly correlates with degree ofencephalopathy?

What medications are used totreat hepatic encephalopathy?


Ascites

“Total shunt”—portal vein (end) to IVC(side)

Side of portal vein anastomosed to side ofIVC—partially preserves portal flow(“partial shunt”)

“Partial shunt”—synthetic tube graftfrom the portal vein to the IVC (good option for patients with alcoholism;associated with lower incidence of encephalopathy and easier transplantation later)

Synthetic graft from the SMV to the IVC

Hepatic failure, secondary to decreasedblood flow (accounts for two thirds ofdeaths)

Increased incidence of hepatic encephalopathy because of decreasedportal blood flow to the liver anddecreased clearance of toxins/metabolitesfrom the blood

Nitroglycerin IV drip

Serum ammonia level (Note: Thought to correlate with but not causeencephalopathy)

Lactulose PO, with or without neomycin PO



ANATOMY

Name structures 1 through 8 (below) of the biliary tract:

Biliary TractChapter 54

1. Intrahepatic ducts2. Left hepatic duct3. Right hepatic duct4. Common hepatic duct5. Gallbladder6. Cystic duct7. Common bile duct8. Ampulla of Vater

Which is the proximal andwhich is the distal bile duct?

What is the name of thenode in Calot’s triangle?

What are the small ducts thatdrain bile directly into thegallbladder from the liver?

Which artery is susceptibleto injury during cholecystectomy?

What is the name of thevalves of the gallbladder?

Where is the infundibulumof the gallbladder?

Where is the fundus of thegallbladder?

Proximal is close to the liver (bile and theliver is analogous to blood and the heart;they both flow distally)

Calot’s node

Ducts of Luschka

Right hepatic artery, because of its proximity to the cystic artery and Calot’striangle

Spiral valves of Heister

Near the cystic duct

At the end of the gallbladder

LWBK758-c54_p364-381.qxd 03/17/2011 8:44 AM Page 364 Aptara

What is “Hartmann’s pouch”?

What are the boundaries ofthe triangle of Calot?

Chapter 54 / Biliary Tract 365

Gallbladder infundibulum

The 3 C’s:1. Cystic duct2. Common hepatic duct3. Cystic artery

1

3

2

PHYSIOLOGY

What is the source ofalkaline phosphatase?

What is in bile?

What does bile do?

What is the enterohepaticcirculation?

Where are most of the bileacids absorbed?

What stimulates gallbladderemptying?

What is the source of cholecystokinin?

What stimulates the releaseof cholecystokinin?

Bile duct epithelium; expect alkalinephosphatase to be elevated in bile ductobstruction

Cholesterol, lecithin (phospholipid), bileacids, and bilirubin

Emulsifies fats

Circulation of bile acids from liver to gutand back to the liver

In the terminal ileum

Cholecystokinin and vagal input

Duodenal mucosal cells

Fat, protein, amino acids, and HCl

“Dr. Blackbourne, are youabsolutely sure that the Trian-gle of Calot includes the cysticartery and not the liver edge?”

Yes, look up Gastroenterology, 2002;123(5):1440





Trypsin and chymotrypsin

Gallbladder emptyingOpening of ampulla of VaterSlowing of gastric emptyingPancreas acinar cell growth and release

of exocrine products

PATHOPHYSIOLOGY

At what level of serum totalbilirubin does one start toget jaundiced?

Classically, what is thoughtto be the anatomic locationwhere one first findsevidence of jaundice?

With good renal function,how high can the serumtotal bilirubin go?

What are the signs andsymptoms of obstructivejaundice?

What causes the itching inobstructive jaundice?

Define the following terms:Cholelithiasis

�2.5

Under the tongue

Very rarely, �20

JaundiceDark urineClay-colored stools (acholic stools)Pruritus (itching)Loss of appetiteNausea

Bile salts in the dermis (not bilirubin!)

Gallstones in gallbladder

hrf ‘

07

Cholethiasis


Choledocholithiasis


Gallstone in common bile duct

Cholecystitis Inflammation of gallbladder

hrf ‘07

Gallstone incommon bileduct

hrf ‘07

Inflammation

Stonein neck

Cholangitis

Cholangiocarcinoma

Klatskin’s tumor

Biliary colic

Infection of biliary tract

Adenocarcinoma of bile ducts

Cholangiocarcinoma of bile duct at thejunction of the right and left hepaticducts

Pain from gallstones, usually from a stoneat cystic duct: The pain is located in theRUQ, epigastrium, or right subscapularregion of the back; it usually lasts minutesto hours but eventually goes away; it is often postprandial, especially after fatty foods


Biloma


Hepaticojejunostomy


Intraperitoneal bile fluid collection

Anastomosis between common bile ductand jejunum

Anastomosis of hepatic ducts or commonhepatic duct to jejunum

DIAGNOSTIC STUDIES

What is the initial diagnosticstudy of choice for evaluationof the biliary tract/gall-bladder/cholelithiasis?

Define the followingdiagnostic studies:

ERCP

PTC

IOC

HIDA/PRIDA scan

How does the HIDA scanreveal cholecystitis?

How often will plain x-rayfilms see gallstones?

Ultrasound!

Endoscopic RetrogradeCholangioPancreatography

Percutaneous TranshepaticCholangiogram

IntraOperative Cholangiogram (donelaparoscopically or open to rule outcholedocholithiasis)

Radioisotope study; isotope concentratedin liver and secreted into bile; willdemonstrate cholecystitis, bile leak, orCBD obstruction

Non-opacification of the gallbladder fromobstruction of the cystic duct

10% to 15%

BILIARY SURGERY

What is a cholecystectomy? Removal of the gallbladder laparoscopically or through a standardKocher incision


What is the Kocher incision?

What is a sphincterotomy?

How should postoperativebiloma be treated after a lapchole?

What is the treatment ofmajor CBD injury after alap chole?


Right subcostal incision

Cut through sphincter of Oddi to allowpassage of gallstones from the commonbile duct; most often done at ERCP; alsoknown as papillotomy

1. Percutaneous drain bile collection2. ERCP with placement of biliary stent

past leak (usually cystic duct remnantleak)


What is a “lap chole”? LAParoscopic CHOLEcystectomy

hrf ‘07

OBSTRUCTIVE JAUNDICE

What is it?

What is the differential diagnosis of proximal bileduct obstruction?

Jaundice (hyperbilirubinemia �2.5) fromobstruction of bile flow to the duodenum

CholangiocarcinomaLymphadenopathyMetastatic tumorGallbladder carcinomaSclerosing cholangitisGallstonesTumor embolusParasitesPostsurgical strictureHepatomaBenign bile duct tumor


What is the differentialdiagnosis of distal bile ductobstruction?

What is the initial study of choice for obstructivejaundice?

What lab results are associatedwith obstructive jaundice?


Choledocholithiasis (gallstones)Pancreatic carcinomaPancreatitisAmpullary carcinomaLymphadenopathyPseudocystPostsurgical strictureAmpulla of Vater dysfunction/strictureLymphomaBenign bile duct tumorParasites

Ultrasound

Elevated alkaline phosphatase, elevatedbilirubin with or without elevated LFTs

CHOLELITHIASIS

What is it?


What are the “Big 4” riskfactors?

What are other less commonrisk factors for gallstones?

Formation of gallstones

�10% of U.S. population will developgallstones

The “four Fs”: FemaleFatFortyFertile (multiparity)

Oral contraceptivesBile stasisChronic hemolysis (pigment stones)CirrhosisInfectionNative American heritageRapid weight loss/gastric bypassObesityInflammatory bowel disease (IBD)Terminal ileal resectionTotal parenteral nutrition (TPN)VagotomyAdvanced ageHyperlipidemiaSomatostatin therapy


What are the types ofstones?

What are the types ofpigmented stones?

What are the causes ofblack-pigmented stones?

What is the pathogenesis ofcholesterol stones?

Is hypercholesterolemia a riskfactor for gallstone formation?


Is biliary colic pain really“colic”?

What percentage of patients with gallstones areasymptomatic?

What is thought to cause biliary colic?

What is Boas’ sign?

What are the five majorcomplications of gallstones?


Cholesterol stones (75%) Pigment stones (25%)

Black stones (contain calcium bilirubinate)Brown stones (associated with biliarytract infection)

Cirrhosis, hemolysis

Secretion of bile supersaturated withcholesterol (relatively decreased amountsof lecithin and bile salts); then, cholesterolprecipitates out and forms solid crystals,then gallstones

No (but hyperlipidemia is)

Symptoms of: biliary colic, cholangitis,choledocholithiasis, gallstone, pancreatitis

No, symptoms usually last for hours;therefore, colic is a misnomer!

80% of patients with cholelithiasis areasymptomatic!

Gallbladder contraction against a stonetemporarily at the gallbladder/cystic ductjunction; a stone in the cystic duct; or astone passing through the cystic duct

Referred right subscapular pain of biliarycolic

1. Acute cholecystitis2. Choledocholithiasis3. Gallstone pancreatitis4. Gallstone ileus5. Cholangitis


How is cholelithiasisdiagnosed?

How often does ultrasounddetect cholelithiasis?

How often does ultrasounddetect choledocholithiasis?

How are symptomatic orcomplicated cases ofcholelithiasis treated?

What are the possible complications of a lap chole?

What are the indications forcholecystectomy in theasymptomatic patient?

Define IOC.

What are the indications foran IOC (6)?

What is choledocholithiasis?

What is the management ofcholedocholithiasis?

What medication maydissolve a cholesterolgallstone?


HistoryPhysical examinationUltrasound

�98% of the time!

About 33% of the time . . . not a verygood study for choledocholithiasis!

By cholecystectomy

Common bile duct injury; right hepaticduct/artery injury; cystic duct leak;biloma (collection of bile)

Sickle-cell diseaseCalcified gallbladder (porcelain

gallbladder)Patient is a child

IntraOperative Cholangiogram (dye inbile duct by way of the cystic duct withfluoro/x-ray)

1. Jaundice2. Hyperbilirubinemia3. Gallstone pancreatitis (resolved)4. Elevated alkaline phosphatase5. Choledocholithiasis on ultrasound6. To define anatomy

Gallstones in the common bile duct

1. ERCP with papillotomy andbasket/balloon retrieval of stones (pre- or postoperatively)

2. Laparoscopic transcystic duct or transcommon bile duct retrieval

3. Open common bile duct exploration

Chenodeoxycholic acid, ursodeoxycholicacid (Actigall®); but if medication isstopped, gallstones often recur


What is the major fearedcomplication of ERCP?


Pancreatitis

ACUTE CHOLECYSTITIS

What is the pathogenesis ofacute cholecystitis?



What is Murphy’s sign?

What are the complicationsof acute cholecystitis?

What lab results are associated with acute chole-cystitis?

What is the diagnostic test of choice for acutecholecystitis?

What are the signs of acutecholecystitis on ultrasound?

Obstruction of cystic duct leads toinflammation of the gallbladder; �95% of cases result from calculi, and �5%from acalculous obstruction

Gallstones

Unrelenting RUQ pain or tendernessFeverNausea/vomitingPainful palpable gallbladder in 33%Positive Murphy’s signRight subscapular pain (referred)Epigastric discomfort (referred)

Acute pain and inspiratory arrest elicitedby palpation of the RUQ during inspiration

AbscessPerforationCholedocholithiasisCholecystenteric fistula formationGallstone ileus

Increased WBC; may have:Slight elevation in alkaline

phosphatase, LFTsSlight elevation in amylase, T. Bili

Ultrasound

Thickened gallbladder wall (�3 mm) Pericholecystic fluidDistended gallbladderGallstones present/cystic duct stoneSonographic Murphy’s sign (pain on

inspiration after placement ofultrasound probe over gallbladder)


What is the differencebetween acute cholecystitisand biliary colic?

What is the treatment ofacute cholecystitis?

What are the steps in lapchole (6)?

How is an IOC performed?

What percentage of patientshas an accessory cysticartery?

Why should the gallbladderspecimen be opened in theoperating room?


Biliary colic has temporary pain; acutecholecystitis has pain that does not resolve,usually with elevated WBCs, fever, andsigns of acute inflammation on U/S

IVFs, antibiotics, and cholecystectomyearly

1. Dissection of peritoneum overlyingthe cystic duct and artery

2. Clipping of cystic artery and transect3. Division of cystic duct between clips4. Dissection of gallbladder from the

liver bed5. Cauterization; irrigation; suction, to

obtain hemostasis of the liver bed6. Removal of the gallbladder through

the umbilical trocar site

1. Place a clip on the cystic duct–gallbladder junction

2. Cut a small hole in the distal cysticduct to cannulate

3. Inject half-strength contrast and take an x-ray or fluoro

10%

Looking for gallbladder cancer, anatomy

ACUTE ACALCULOUS CHOLECYSTITIS

What is it?

What is the pathogenesis?

Acute cholecystitis without evidence ofstones

It is believed to result from sludge andgallbladder disuse and biliary stasis,perhaps secondary to absence ofcholecystokinin stimulation (decreasedcontraction of gallbladder)



What are the diagnostic testsof choice?

What are the findings onHIDA scan?

What is the management of acute acalculous cholecystitis?


Prolonged fastingTPNTraumaMultiple transfusionsDehydrationOften occurs in prolonged postoperative

or ICU setting

1. Ultrasound; sludge and inflammationusually present with acute acalculouscholecystitis

2. HIDA scan

Nonfilling of the gallbladder

Cholecystectomy, or cholecystostomytube if the patient is unstable (placedpercutaneously by radiology or open surgery)

CHOLANGITIS

What is it?


What is the most commoncause of cholangitis?


What lab results are associ-ated with cholangitis?

Bacterial infection of the biliary tractfrom obstruction (either partial or complete); potentially life-threatening

CholedocholithiasisStricture (usually postoperative)Neoplasm (usually ampullary carcinoma)Extrinsic compression (pancreatic

pseudocyst/pancreatitis)Instrumentation of the bile ducts (e.g.,

PTC/ERCP)Biliary stent

Gallstones in common bile duct(choledocholithiasis)

Charcot’s triad: fever/chills, RUQ pain,and jaundice

Reynold’s pentad: Charcot’s triad plusaltered mental status and shock

Increased WBCs, bilirubin, and alkalinephosphatase, positive blood cultures


Which organisms are mostcommonly isolated withcholangitis?


What is suppurative cholangitis?

What is the management ofcholangitis?


Gram-negative organisms (E. coli, Klebsiella, Pseudomonas, Enterobacter,Proteus, Serratia) are the most common

Enterococci are the most common gram-positive bacteria

Anaerobes are less common (B. fragilismost frequent)

Fungi are even less common (Candida)

Ultrasound and contrast study (e.g., ERCPor IOC) after patient has “cooled off” withIV antibiotics

Severe infection with sepsis—“pus underpressure”

Nonsuppurative: IVF and antibiotics,with definitive treatment later (e.g.,lap chole �/– ERCP)

Suppurative: IVF, antibiotics, anddecompression; decompression can beobtained by ERCP with papillotomy,PTC with catheter drainage, orlaparotomy with T-tube placement

SCLEROSING CHOLANGITIS

What is it?

What is its natural history?


What is the major riskfactor?

What type of IBD is themost common risk factor?

Multiple inflammatory fibrousthickenings of bile duct walls resulting inbiliary strictures

Progressive obstruction possibly leadingto cirrhosis and liver failure; 10% ofpatients will develop cholangiocarcinoma

Unknown, but probably autoimmune

Inflammatory bowel disease

Ulcerative colitis (�66%)


What are the signs andsymptoms of sclerosingcholangitis?



What are the managementoptions?

What percentage of patientswith IBD develops sclerosingcholangitis?


Same as those for obstructive jaundice:JaundiceItching (pruritus)Dark urineClay-colored stoolsLoss of energyWeight loss(Many patients are asymptomatic)

CirrhosisCholangiocarcinoma (10%)CholangitisObstructive jaundice

Elevated alkaline phosphatase, and PTCor ERCP revealing “beads on a string”appearance on contrast study

Hepatoenteric anastomosis (if primarilyextrahepatic ducts are involved) and resection of extrahepatic bile ducts because of the risk ofcholangiocarcinoma

Transplant (if primarily intrahepatic disease or cirrhosis)

Endoscopic balloon dilations

�5%

GALLSTONE ILEUS

What is it?

What is the classic site ofobstruction?

Small bowel obstruction from a largegallstone (�2.5 cm) that has erodedthrough the gallbladder and into the duodenum/small bowel

Ileocecal valve (but may causeobstruction in the duodenum, sigmoidcolon)


What are the classic findingsof gallstone ileus?


Gallstone ileus is most commonly seen inwomen older than 70 years

Symptoms of SBO: distention, vomiting,hypovolemia, RUQ pain

�1%

Abdominal x-ray: occasionally revealsradiopaque gallstone in the bowel;40% of patients show air in thebiliary tract, small bowel distention,and air fluid levels secondary to ileus

UGI: used if diagnosis is in question; willshow cholecystenteric fistula and theobstruction

Abdominal CT: reveals air in biliarytract, SBO �/– gallstone in intestine

Surgery: enterotomy with removal of thestone � interval cholecystectomy (interval-delayed)

hrf ‘07

SBO withair fluidlevels

Air in thehepaticbile ducts

Gallstonein ileocecalvalve

What is the population atrisk?


Gallstone ileus causes whatpercentage of cases of SBO?


What is the management?

CARCINOMA OF THE GALLBLADDER

What is it? Malignant neoplasm arising in thegallbladder, vast majority are adenocarcinoma (90%)



What is the female:male ratio?

What is the most commonsite of gallbladder cancer inthe gallbladder?

What is a porcelain gallbladder?

What percentage of patientswith a porcelain gallbladderwill have gallbladder cancer?



What are the signs?


What is the route of spread?

What is the managementunder the followingconditions?

Confined to mucosa

Confined to muscularis/serosa

What is the main complication of a lap cholefor gallbladder cancer?


Gallstones, porcelain gallbladder,cholecystenteric fistula

4:1

60% in fundus

Calcified gallbladder

�50% (20%–60%)

�1% of all gallbladder specimens

Biliary colic, weight loss, anorexia; manypatients are asymptomatic until late; maypresent as acute cholecystitis

Jaundice (from invasion of the common ductor compression by involved pericholedochallymph nodes), RUQ mass, palpablegallbladder (advanced disease)

Ultrasound, abdominal CT, ERCP

Contiguous spread to the liver is mostcommon

Cholecystectomy

Radical cholecystectomy:cholecystectomy and wedge resectionof overlying liver, and lymph node dis-section � chemotherapy/XRT

Trocar site tumor implants (Note: ifknown preoperatively, perform opencholecystectomy)


What is the prognosis forgallbladder cancer?


Dismal overall: �5% 5-year survival asmost are unresectable at diagnosis

T1 with cholecystectomy: 95% 5-yearsurvival

CHOLANGIOCARCINOMA

What is it?


Average age at diagnosis?


What is the most commonlocation?


What is a Klatskin tumor?

Malignancy of the extrahepatic or intrahepatic ducts—primary bile ductcancer

Almost all are adenocarcinomas

�65 years, equally affects male/female

Those of biliary obstruction: jaundice,pruritus, dark urine, clay-coloredstools, cholangitis

Proximal bile duct

Choledochal cystsUlcerative colitisThorotrast contrast dye (used in 1950s)Sclerosing cholangitisLiver flukes (clonorchiasis)Toxin exposures (e.g., Agent Orange)

Tumor that involves the junction of theright and left hepatic ducts



What is an MRCP?

What is the management of proximal bile duct cholangiocarcinoma?

What is the management ofdistal common bile ductcholangiocarcinoma?


Ultrasound, CT scan, ERCP/PTC withbiopsy/brushings for cytology, MRCP

MRI with visualization of pancreatic andbile ducts

Resection with Roux-en-Y hepaticoje-junostomy (anastomose bile ducts tojejunum) � unilateral hepatic lobectomy

Whipple procedure

MISCELLANEOUS CONDITIONS

What is a porcelain gallbladder?

What is hydrops of the gallbladder?

What is Gilbert’s syndrome?

What is Courvoisier’sgallbladder?

What is Mirizzi’s syndrome?

Calcified gallbladder seen on abdominal x-ray; results from chroniccholelithiasis/cholecystitis with calcified scar tissue in gallbladder wall;cholecystectomy required because ofthe strong association of gallbladdercarcinoma with this condition

Complete obstruction of the cystic duct by a gallstone, with filling of thegallbladder with fluid (not bile) from thegallbladder mucosa

Inborn error in liver bilirubin uptake and glucuronyl transferase resulting inhyperbilirubinemia (Think: Gilbert’s �Glucuronyl)

Palpable, nontender gallbladder (unlikegallstone disease) associated with cancerof the head of the pancreas; able to distendbecause it has not been “scarred down”by gallstones

Common hepatic duct obstruction as aresult of extrinsic compression from agallstone impacted in the cystic duct



Identify the regions of thepancreas:

PancreasChapter 55

What structure is the tail ofthe pancreas said to “tickle”?

Name the two pancreaticducts.

Which duct is the mainduct?

How is blood supplied to thehead of the pancreas?

Why must the duodenum beremoved if the head of thepancreas is removed?

1. Head2. Neck (in front of the SMV)3. Uncinate process4. Body5. Tail

Spleen

1. Wirsung duct2. Santorini duct

Duct of Wirsung is the major duct(Think: Santorini � Small duct)

1. Celiac trunk S gastroduodenal SAnterior superior pancreaticoduodenal

arteryPosterior superior pancreaticoduodenal

artery2. Superior mesenteric artery S

Anterior inferior pancreaticoduodenalartery

Posterior inferior pancreaticoduodenalartery

3. Splenic artery SDorsal pancreatic artery

They share the same blood supply (gastroduodenal artery)


What is the endocrine function of the pancreas?

What is the exocrinefunction of the pancreas?

What maneuver is used tomobilize the duodenum andpancreas and evaluate theentire pancreas?

Chapter 55 / Pancreas 383

Islets of Langerhans:�-cells: glucagon�-cells: insulin

Digestive enzymes: amylase, lipase,trypsin, chymotrypsin, carboxypeptidase

Kocher maneuver: Incise the lateralattachments of the duodenum and thenlift the pancreas to examine the posteriorsurface

PANCREATITIS

ACUTE PANCREATITIS

What is it?

What are the most commonetiologies in the UnitedStates?

What is the acronym toremember all of the causesof pancreatitis?


What are the signs ofpancreatitis?

Inflammation of the pancreas

1. Alcohol abuse (50%)2. Gallstones (30%)3. Idiopathic (10%)

“I GET SMASHED”:Idiopathic

GallstonesEthanolTrauma

Scorpion biteMumps (viruses)AutoimmuneSteroidsHyperlipidemiaERCPDrugs

Epigastric pain (frequently radiates toback); nausea and vomiting

Epigastric tendernessDiffuse abdominal tendernessDecreased bowel sounds (adynamic ileus)FeverDehydration/shock



What lab tests should beordered?

What are the associateddiagnostic findings?

What is the most commonsign of pancreatitis on AXR?



Gastritis/PUDPerforated viscusAcute cholecystitisSBOMesenteric ischemia/infarctionRuptured AAABiliary colicInferior MI/pneumonia

CBCLFTAmylase/lipaseType and crossABGCalciumChemistryCoagsSerum lipids

Lab—High amylase, high lipase, highWBC

AXR—Sentinel loop, colon cutoff, possibly gallstones (only 10% visibleon x-ray)

U/S—Phlegmon, cholelithiasisCT—Phlegmon, pancreatic necrosis

Sentinel loop(s)

NPOIVFNGT if vomiting�/– TPN vs. postpyloric tube feedsH2 blocker/PPIAnalgesia (Demerol®, not morphine—

less sphincter of Oddi spasm)Correction of coags/electrolytes�/– Alcohol withdrawal prophylaxis“Tincture of time”




Are postpyloric tube feedssafe in acute pancreatitis?

What are Ranson’s criteriafor the following stages:

At presentation?

During the initial 48 hours?

What is the mortality perpositive criteria:

0 to 2?

3 to 4?

5 to 6?

7 to 8?


PseudocystAbscess/infectionPancreatic necrosisSplenic/mesenteric/portal vessel rupture

or thrombosisPancreatic ascites/pancreatic pleural

effusionDiabetesARDS/sepsis/MOFCoagulopathy/DICEncephalopathySevere hypocalcemia

Based on Ranson’s criteria

YES

1. Age �552. WBC �16,0003. Glc �2004. AST �2505. LDH �350

1. Base deficit �42. BUN increase �5 mg/dL3. Fluid sequestration �6 L4. Serum Ca2� �85. Hct decrease �10%6. PO2 (ABG) �60 mm Hg

(Amylase value is NOT one ofRanson’s criteria!)

�5%

�15%

�40%

�100%


How can the admission Ranson criteria be remembered?

How can Ranson’s criteria at less than 48 hours beremembered?

How can the AST versusLDH values in Ranson’s criteria be remembered?

What is the etiology ofhypocalcemia withpancreatitis?

What complication is associated with splenic veinthrombosis?

Can TPN with lipids be givento a patient with pancreatitis?

What is the least commoncause of acute pancreatitis(and possibly the most commonly asked cause onrounds!)


“GA LAW (Georgia law)”:Glucose �200Age �55

LDH �350AST �250WBC �16,000(“Don’t mess with the pancreas anddon’t mess with the Georgia law”)

“C HOBBS (Calvin and Hobbes)”:Calcium �8 mg/dL

Hct drop of �10%O2 �60 (PaO2)Base deficit �4Bun �5 increaseSequestration �6 L

Alphabetically and numerically: A beforeL and 250 before 350

Therefore, AST �250 and LDH �350

Fat saponification: fat necrosis binds tocalcium

Gastric varices (treatment with splenectomy)

Yes, if the patient does not suffer fromhyperlipidemia (triglycerides �300)

Scorpion bite (found on the island ofTrinidad)



CHRONIC PANCREATITIS

What is it?

What are the subtypes?



What are the associatedsigns?

What are the signs ofpancreatic exocrine insufficiency?

What are the signs ofpancreatic endocrine insufficiency?

What are the common painpatterns?


What percentage of patientswith chronic pancreatitis haveor will develop pancreaticcancer?

Chronic inflammation of the pancreasregion causing destruction of theparenchyma, fibrosis, and calcification,resulting in loss of endocrine andexocrine tissue

1. Chronic calcific pancreatitis2. Chronic obstructive pancreatitis (5%)

Alcohol abuse (most common; 70% of cases)Idiopathic (15%)Hypercalcemia (hyperparathyroidism)HyperlipidemiaFamilial (found in families without any

other risk factors)TraumaIatrogenicGallstones

Epigastric and/or back pain, weight loss,steatorrhea

Type 1 diabetes mellitus (up to one third)Steatorrhea (up to one fourth), weight loss

Steatorrhea (fat malabsorption from lipaseinsufficiency—stools float in water)

Malnutrition

Diabetes (glucose intolerance)

Unrelenting painRecurrent pain

PUD, biliary tract disease, AAA, pancreatic cancer, angina

�2%


What are the appropriatelab tests?

Why may amylase/lipase benormal in a patient withchronic pancreatitis?

What radiographic testsshould be performed?



What is the Frey procedure?

What is the indication forsurgical treatment ofchronic pancreatitis?

What are the possible complications of chronicpancreatitis?


Amylase/lipase72-hour fecal fat analysisGlc tolerance test (IDDM)

Because of extensive pancreatic tissueloss (“burned-out pancreas”)

CT—Has greatest sensitivity for glandenlargement/atrophy, calcifications,masses, pseudocysts

KUB—Calcification in the pancreasERCP—Ductal irregularities with

dilation and stenosis (Chain of Lakes),pseudocysts

Discontinuation of alcohol use—canreduce attacks, though parenchymaldamage continues secondary to ductalobstruction and fibrosis

Insulin for type 1 diabetes mellitusPancreatic enzyme replacementNarcotics for pain

Puestow—longitudinal pancreaticojejunos-tomy (pancreatic duct must be dilated)

Duval—distal pancreaticojejunostomyNear-total pancreatectomy

Longitudinal pancreaticojejunostomy withcore resection of the pancreatic head

Severe, prolonged/refractory pain

Insulin dependent diabetes mellitusSteatorrheaMalnutritionBiliary obstructionSplenic vein thrombosisGastric varicesPancreatic pseudocyst/abscessNarcotic addictionPancreatic ascites/pleural effusionSplenic artery aneurysm



GALLSTONE PANCREATITIS

What is it?


What radiologic tests shouldbe performed?


Why should early intervalcholecystectomy beperformed on patients withgallstone pancreatitis?

What is the role of ERCP?

Acute pancreatitis from a gallstone in orpassing through the ampulla of Vater (theexact mechanism is unknown)

Acute pancreatitis and cholelithiasisand/or choledocholithiasis and no othercause of pancreatitis (e.g., no history ofalcohol abuse)

U/S to look for gallstonesCT to look at the pancreas, if symptoms

are severe

Conservative measures and early interval cholecystectomy (laparoscopiccholecystectomy or open cholecystectomy) and intraoperative cholangiogram (IOC) 3 to 5 days (after pancreatic inflammation resolves)

Pancreatitis will recur in �33% ofpatients within 8 weeks (so alwaysperform early interval cholecystectomyand IOC in 3 to 5 days when pancreatitisresolves)

1. Cholangitis2. Refractory choledocholithiasis

HEMORRHAGIC PANCREATITIS

What is it?

What are the signs?

Define the following terms:Cullen’s sign

Bleeding into the parenchyma andretroperitoneal structures with extensivepancreatic necrosis

Abdominal pain, shock/ARDS, Cullen’ssign, Grey Turner’s sign, Fox’s sign

Bluish discoloration of the periumbilical area from retroperitonealhemorrhage tracking around to the anterior abdominal wall through fascialplanes


Grey Turner’s sign

Fox’s sign

What are the significant labvalues?

What radiologic test shouldbe performed?


Ecchymosis or discoloration of theflank in patients with retroperitonealhemorrhage from dissecting blood fromthe retroperitoneum (Think: GreyTURNer � TURN side to side � flank[side] hematoma)

Ecchymosis of the inguinal ligamentfrom blood tracking from theretroperitoneum and collecting at theinguinal ligament

Increased amylase/lipaseDecreased HctDecreased calcium levels

CT scan with IV contrast

PANCREATIC ABSCESS

What is it?


What radiographic testsshould be performed?


Which organisms are foundin pancreatic abscesses?


Infected peripancreatic purulent fluidcollection

Fever, unresolving pancreatitis, epigastricmass

Abdominal CT with needle aspiration Ssend for Gram stain/culture

Positive Gram stain and culture of bacteria

Gram negative (most common):Escherichia coli, Pseudomonas, Klebsiella

Gram positive: Staphylococcus aureus,Candida

Antibiotics and percutaneous drainplacement or operative débridement and placement of drains



PANCREATIC NECROSIS

What is it?


What is the treatment:Sterile?

Suspicious of infection?

Toxic, hypotensive?

Dead pancreatic tissue, usually followingacute pancreatitis

Abdominal CT with IV contrast; deadpancreatic tissue does not take up IVcontrast and is not enhanced on CT scan(i.e., doesn’t “light up”)

Medical management

CT-guided FNA

Operative débridement

PANCREATIC PSEUDOCYST

What is it? Encapsulated collection of pancreaticfluid

hrf ‘07

Communicatingpseudocyst

Non-communicatingpseudocyst

What makes it a “pseudo”cyst?



What is the most commoncause of pancreatic pseudocyst in the UnitedStates?

Wall is formed by inflammatory fibrosis,NOT epithelial cell lining

�1 in 10 after alcoholic pancreatitis

Acute pancreatitis � chronic pancreatitis from alcohol

Chronic alcoholic pancreatitis



What are the signs?


What are the diagnosticfindings?

What is the differential diagnosis of a pseudocyst?

What are the possible complications of apancreatic pseudocyst?


What is the waiting periodbefore a pseudocyst shouldbe drained?

What percentage of pseudocysts resolvespontaneously?

What is the treatment forpseudocyst with bleedinginto cyst?


Epigastric pain/massEmesisMild feverWeight lossNote: Should be suspected when a

patient with acute pancreatitis fails toresolve pain

Palpable epigastric mass, tender epigastrium, ileus

Amylase/lipaseBilirubinCBC

Lab—High amylase, leukocytosis, highbilirubin (if there is obstruction)

U/S—Fluid-filled massCT—Fluid-filled mass, good for showing

multiple cystsERCP—Radiopaque contrast material

fills cyst if there is a communicatingpseudocyst (i.e., pancreatic duct communicates with pseudocyst)

Cystadenocarcinoma, cystadenoma

Infection, bleeding into the cyst, fistula,pancreatic ascites, gastric outlet obstruction, SBO, biliary obstruction

Drainage of the cyst or observation

It takes 6 weeks for pseudocyst walls to“mature” or become firm enough to holdsutures and most will resolve in thisperiod of time if they are going to

�50%

Angiogram amd embolization


What is the treatment forpseudocyst with infection?

What size pseudocyst shouldbe drained?

What are three treatmentoptions for pancreaticpseudocyst?

What are the surgicaloptions for the followingconditions:

Pseudocyst adherent tothe stomach?

Pseudocyst adherent tothe duodenum?

Pseudocyst not adherentto the stomach or duodenum?

Pseudocyst in the tail ofthe pancreas?

What is an endoscopicoption for drainage of apseudocyst?

What must be done during asurgical drainage procedurefor a pancreatic pseudocyst?

What is the most commoncause of death due topancreatic pseudocyst?


Percutaneous external drainage/IV antibiotics

Most experts say:Pseudocysts larger than 5 cm have a

small chance of resolving and havea higher chance of complications

Calcified cyst wallThick cyst wall

1. Percutaneous aspiration/drain2. Operative drainage3. Transpapillary stent via ERCP

(pseudocyst must communicate withpancreatic duct)

Cystogastrostomy (drain into thestomach)

Cystoduodenostomy (drain into the duodenum)

Roux-en-Y cystojejunostomy (drain intothe Roux limb of the jejunum)

Resection of the pancreatic tail with thepseudocyst

Endoscopic cystogastrostomy

Biopsy of the cyst wall to rule out a cysticcarcinoma (e.g., cystadenocarcinoma)

Massive hemorrhage into the pseudocyst



PANCREATIC CARCINOMA

What is it?



What is the African Americanto white ratio?

What is the average age?

What are the differenttypes?

What percentage arise inthe pancreatic head?

Why are most pancreaticcancers in the tailnonresectable?

What are the signs/symptoms of tumors basedon location:

Head of the pancreas?

Body or tail?

What are the most commonsymptoms of cancer of thepancreatic HEAD?

Adenocarcinoma of the pancreas arisingfrom duct cells

Smoking 3� risk, diabetes mellitus, heavyalcohol use, chronic pancreatitis, diet highin fried meats, previous gastrectomy

3:2

2:1

�60 years

�80% are duct cell adenocarcinomas;other types include cystadenocarcinomaand acinar cell carcinoma

66% arise in the pancreatic head; 33%arise in the body and tail

These tumors grow without symptoms untilit is too late and they have already spread—head of the pancreas tumors draw attentionearlier because of biliary obstruction

Painless jaundice from obstruction ofcommon bile duct; weight loss; abdominalpain; back pain; weakness; pruritus frombile salts in skin; anorexia; Courvoisier’ssign; acholic stools; dark urine; diabetes

Weight loss and pain (90%); migratorythrombophlebitis (10%); jaundice(�10%); nausea and vomiting; fatigue

1. Weight loss (90%)2. Pain (75%)3. Jaundice (70%)


What is “Courvoisier’s sign”?

What percentage of patientswith cancers of the pancreaticHEAD have Courvoisier’ssign?

What is the classic presentation of pancreaticcancer in the head of thepancreas?

What metastatic lymph nodesdescribed classically for gastric cancer can be foundwith metastatic pancreaticcancer?


Which tumor markers areassociated with pancreaticcancer?

What does CA-19-9 stand for?

What diagnostic studies areperformed?

What are the pancreaticcancer STAGES:

Stage I?

Stage II?

Stage III?


Palpable, nontender, distended gallbladder

33%

Painless jaundice

Virchow’s node; Sister Mary Joseph’s nodule

Increased direct bilirubin and alkalinephosphatase (as a result of biliaryobstruction)

Increased LFTsElevated pancreatic tumor markers

CA-19-9

Carbohydrate Antigen 19-9

Abdominal CT, U/S, cholangiography(ERCP to rule out choledocholithiasis andcell brushings), endoscopic U/S with biopsy

Tumor is limited to pancreas, with nonodes or metastases

Tumor extends into bile duct, peripancreatic tissues, or duodenum;there are no nodes or metastases

Same findings as stage II plus positivenodes or celiac or SMA involvement


Stage IVA?

Stage IVB?

What is the treatment basedon location:

Head of the pancreas?

Body or tail?

What factors signify inoperability?

Is portal vein or SMVinvolvement an absolutecontraindication forresection?

Should patients undergopreoperative biliarydrainage (e.g., ERCP)?

Define the Whipple procedure(pancreaticoduodenectomy).

What is the complication rateafter a Whipple procedure?


Tumor extends to stomach, colon, spleen,or major vessels, with any nodal statusand no distant metastases

Distant metastases (any nodal status,any tumor size) are found

Whipple procedure(pancreaticoduodenectomy)

Distal resection

Vascular encasement (SMA, hepatic artery)Liver metastasisPeritoneal implantsDistant lymph node metastasis

(periaortic/celiac nodes)Distant metastasisMalignant ascites

No—can be resected and reconstructedwith vein interposition graft at some centers

No (exceptions for symptoms/preoperative XRT, trials, etc.)

CholecystectomyTruncal vagotomyAntrectomyPancreaticoduodenectomy—removal of

head of pancreas and duodenumCholedochojejunostomy—anastomosis of

common bile duct to jejunumPancreaticojejunostomy—anastomosis of

distal pancreas remnant to jejunumGastrojejunostomy—anastomosis of

stomach to jejunum

�25%


What mortality rate is associated with a Whippleprocedure?

What is the “pylorus-preserving Whipple”?

What are the possible post-Whipple complications?

Why must the duodenum beremoved if the head of thepancreas is resected?

What is the postoperativeadjuvant therapy?

What is the palliative treatment if the tumor isinoperable and biliaryobstruction is present?

What is the prognosis at 1 year after diagnosis?

What is the survival rate at 5 years after resection?


�5% at busy centers

No antrectomy; anastomose duodenumto jejunum

Delayed gastric emptying (if antrectomyis performed); anastomotic leak (fromthe bile duct or pancreatic anastomosis),causing pancreatic/biliary fistula; woundinfection; postgastrectomy syndromes;sepsis; pancreatitis

They share the same blood supply

Chemotherapy �/– XRT

PTC or ERCP and placement of stentacross obstruction

Dismal; 90% of patients die within 1 yearof diagnosis

20%

MISCELLANEOUS

What is an annularpancreas?

What is pancreatic divisum?

Pancreas encircling the duodenum; ifobstruction is present, bypass, do notresect

Failure of the two pancreatic ducts tofuse; the normally small duct (Small �Santorini) of Santorini acts as the mainduct in pancreatic divisum (Think: thetwo pancreatic ducts are Divided �Divisum)


What is heterotopic pancreatic tissue?

What is a Puestowprocedure?

What medication decreasesoutput from a pancreatic fistula?

Which has a longer half-life:amylase or lipase?

What is the WDHA syndrome?

What is the Whipple triad ofpancreatic insulinoma?

What is the most commonislet cell tumor?

What pancreatic tumor isassociated with gallstoneformation?

What is the triad found withpancreatic somatostatinomatumor?

What are the two classicfindings with pancreaticglucagonoma tumors?


Heterotopic pancreatic tissue usuallyfound in the stomach, intestine,duodenum

Longitudinal filleting of the pancreas/pancreatic duct with a side-to-side anastomosis with the small bowel

Somatostatin (GI-inhibitory hormone)

Lipase; therefore, amylase may be normaland lipase will remain elevated longer

Pancreatic VIPoma (Vasoactive IntestinalPolypeptide tumor)

Also known as Verner-Morrison syndromeTumor secretes VIP, which causes:

WateryDiarrheaHypokalemiaAchlorhydria (inhibits gastric acid

secretion)

1. Hypoglycemia (Glc �50)2. Symptoms of hypoglycemia: mental

status changes/vasomotor instability3. Relief of symptoms with

administration of glucose

Insulinoma

Somatostatinoma (inhibits gallbladdercontraction)

1. Gallstones2. Diabetes3. Steatorrhea

1. Diabetes2. Dermatitis/rash (necrotizing migratory

erythema)


Chapter 56 / Breast 399

ANATOMY OF THE BREAST AND AXILLA

BreastChapter 56

Axillary vein

Long thoracic nerve

Latissimus dorsi muscle

Lateral to, deep to, or medial to pectoralminor muscle, depending on level ofnodes taken

1. Long thoracic nerve2. Thoracodorsal nerve3. Medial pectoral nerve4. Lateral pectoral nerve

Courses along lateral chest wall inmidaxillary line on serratus anterior muscle;innervates serratus anterior muscle

Courses lateral to long thoracic nerve on latissimus dorsi muscle; innervateslatissimus dorsi muscle

Runs lateral to or through the pectoralminor muscle, actually lateral to the lateralpectoral nerve; innervates the pectoralminor and pectoral major muscles

Runs medial to the medial pectoralnerve (names describe orientation fromthe brachial plexus!); innervates the pectoral major

Name the boundaries of theaxilla for dissection:

Superior boundary

Posterior boundary

Lateral boundary

Medial boundary

What four nerves must thesurgeon be aware of duringan axillary dissection?

Describe the location ofthese nerves and the muscleeach innervates:

Long thoracic nerve

Thoracodorsal nerve

Medial pectoral nerve

Lateral pectoral nerve


Identify the nerves in theaxilla on the illustration below:


1. Thoracodorsal nerve2. Long thoracic nerve3. Medial pectoral nerve4. Lateral pectoral nerve5. Axillary vein

5 12

3

4

What is the name of thedeformity if you cut the longthoracic nerve in this area?

What is the name of theCUTANEOUS nerve thatcrosses the axilla in a trans-verse fashion? (Many surgeonstry to preserve this nerve.)

What is the name of thelarge vein that marks theupper limit of the axilla?

What is the lymphaticdrainage of the breast?

What are the levels of axillarylymph nodes?

“Winged scapula”

Intercostobrachial nerve

Axillary vein

Lateral: axillary lymph nodesMedial: parasternal nodes that run with

internal mammary artery

Level I (low): lateral to pectoral minorLevel II (middle): deep to pectoral minorLevel III (high): medial to pectoral minorIn breast cancer, a higher level of

involvement has a worse prognosis,but the level of involvement is lessimportant than the number of positivenodes (Think: Levels I, II, and III arein the same inferior–superior anatomicorder as the Le Fort facial fracturesand the trauma neck zones; I dare youto forget!)

I

II

III


What are Rotter’s nodes?

What are the suspensorybreast ligaments called?

What is the mammary “milkline”?

What is the “tail of Spence”?

Which hormone is mainlyresponsible for breast milkproduction?


Nodes between the pectoralis major andminor muscles; not usually removedunless they are enlarged or feelsuspicious intraoperatively

Cooper’s ligaments

Embryological line from shoulder tothigh where “supernumerary” breast areolar and/or nipples can be found

“Tail” of breast tissue that tapers into theaxilla

Prolactin

What is the incidence ofbreast cancer?

What percentage of womenwith breast cancer have noknown risk factor?

What percentage of all breastcancers occur in womenyounger than 30 years?

What percentage of allbreast cancers occur inwomen older than 70 years?

What are the major breastcancer susceptibility genes?

What option exists todecrease the risk of breastcancer in women with BRCA?

What is the most commonmotivation for medicolegalcases involving the breast?

12% lifetime risk

75%!

�2%

33%

BRCA1 and BRCA2 (easily remembered:BR � BReast and CA � CAncer)

Prophylactic bilateral mastectomy

Failure to diagnose a breast carcinoma

BREAST CANCER


What is the “TRIAD OFERROR” for misdiagnosedbreast cancer?

What are the history riskfactors for breast cancer?

What are physical/anatomicrisk factors for breastcancer?

What is the relative risk ofhormone replacement therapy?

Is “run of the mill” fibrocystic disease a risk factor for breast cancer?

What are the possible symptoms of breast cancer?


1. Age �45 years2. Self-diagnosed mass3. Negative mammogramNote: �75% of cases ofMISDIAGNOSED breast cancer havethese three characteristics

“NAACP”:NulliparityAge at menarche (younger than 13 years)Age at menopause (older than 55 years)Cancer of the breast (in self or family)Pregnancy with first child (�30 years)

“CHAFED LIPS”:Cancer in the breast (3% synchronous

contralateral cancer)Hyperplasia (moderate/florid)

(2� risk)Atypical hyperplasia (4�)Female (100� male risk)ElderlyDCIS

LCISInherited genes (BRCA I and II)Papilloma (1.5�)Sclerosing adenosis (1.5�)

1–1.5

No

No symptomsMass in the breastPain (most are painless)Nipple dischargeLocal edemaNipple retractionDimpleNipple rash


Why does skin retractionoccur?

What are the signs of breastcancer?

What is the most commonsite of breast cancer?

What are the different typesof invasive breast cancer?

What is the most commontype of breast cancer?

What is the differentialdiagnosis?

Describe the appearance ofthe edema of the dermis ininflammatory carcinoma ofthe breast.

What are the screeningrecommendations for breastcancer:

Breast examrecommendations?


Tumor involvement of Cooper’s ligamentsand subsequent traction on ligamentspull skin inward

Mass (1 cm is usually the smallest lesionthat can be palpated on examination)

DimpleNipple rashEdemaAxillary/supraclavicular nodes

Approximately one half of cancersdevelop in the upper outer quadrants

Infiltrating ductal carcinoma (�75%)Medullary carcinoma (�15%)Infiltrating lobular carcinoma (�5%)Tubular carcinoma (�2%)Mucinous carcinoma (colloid) (�1%)Inflammatory breast cancer (�1%)

Infiltrating ductal carcinoma

Fibrocystic disease of the breastFibroadenomaIntraductal papillomaDuct ectasiaFat necrosisAbscessRadial scarSimple cyst

Peau d’orange (orange peel)

Self-exam of breasts monthlyAges 20 to 40 years: breast exam every

2 to 3 years by a physician�40 years: annual breast exam by

physician


Mammograms?

When is the best time forbreast self-exams?

Why is mammography amore useful diagnostic toolin older women than inyounger?

What are the radiographictests for breast cancer?

What is the classic picture of breast cancer on mammogram?


Recommendations are controversial, butmost experts say:

Baseline mammogram between 35 and40 years

Mammogram every year or everyother year for ages 40 to 50

Mammogram yearly after age 50

1 week after menstrual period

Breast tissue undergoes fatty replacementwith age, making masses more visible;younger women have more fibrous tissue,which makes mammograms harder tointerpret

Mammography and breast ultrasound,MRI

Spiculated mass

Which option is best toevaluate a breast mass in a woman younger than 30 years?

What are the methods forobtaining tissue forpathologic examination?

Breast ultrasound

Fine needle aspiration (FNA), corebiopsy (larger needle core sample),mammotome stereotactic biopsy, andopen biopsy, which can be incisional(cutting a piece of the mass) orexcisional (cutting out the entire mass)


What are the indications for biopsy?

What is the process forperforming a biopsy when anonpalpable mass is seen onmammogram?

What is a needle loc biopsy(NLB)?

What is a mammotomebiopsy?

What is obtained first, themammogram or the biopsy?

What would be suspiciousmammographic findings?

What is a “radial scar” seenon mammogram?

What tumor is associatedwith a radial scar?

What is the “workup” for abreast mass?


Persistent mass after aspirationSolid massBlood in cyst aspirateSuspicious lesion by mammography/

ultrasound/MRIBloody nipple dischargeUlcer or dermatitis of nipplePatient’s concern of persistent breast

abnormality

Stereotactic (mammotome) biopsy orneedle localization biopsy

Needle localization by radiologist,followed by biopsy; removed breast tissue must be checked by mammogramto ensure all of the suspicious lesion hasbeen excised

Mammogram-guided computerizedstereotatic core biopsies

Mammogram is obtained first;otherwise, tissue extraction (core oropen) may alter the mammographic findings (fine needle aspiration may bedone prior to the mammogram becausethe fine needle usually will not affect themammographic findings)

Mass, microcalcifications, stellate/spiculated mass

Spiculated mass with central lucency, �/– microcalcifications

Tubular carcinoma; thus, biopsy is indicated

1. Clinical breast exam2. Mammogram or breast ultrasound3. Fine needle aspiration, core biopsy, or

open biopsy


How do you proceed if themass appears to be a cyst?

Is the fluid from a breastcyst sent for cytology?

When do you proceed toopen biopsy for a breastcyst?

What is the preoperativestaging workup in a patientwith breast cancer?

What hormone receptorsmust be checked for in thebiopsy specimen?

What staging system is usedfor breast cancer?

Describe the staging(simplified):

Stage I

Stage IIA

Stage IIB


Aspirate it with a needle

Not routinely; bloody fluid should be sentfor cytology

1. In the case of a second cyst recurrence2. Bloody fluid in the cyst3. Palpable mass after aspiration

Bilateral mammogram (cancer in onebreast is a risk factor for cancer in thecontralateral breast!)

CXR (to check for lung metastasis)LFTs (to check for liver metastasis)Serum calcium level, alkaline

phosphatase (if these tests indicatebone metastasis/“bone pain,” proceedto bone scan)

Other tests, depending on signs/symptoms (e.g., head CT if patienthas focal neurologic deficit, to look forbrain metastasis)

Estrogen and progesteronereceptors—this is key for determiningadjuvant treatment; this informationmust be obtained on all specimens(including fine needle aspirates)

TMN: Tumor/Metastases/Nodes (AJCC)

Tumor �2 cm in diameter withoutmetastases, no nodes

Tumor �2 cm in diameter with mobileaxillary nodes or

Tumor 2 to 5 cm in diameter, no nodes

Tumor 2 to 5 cm in diameter with mobileaxillary nodes or

Tumor �5 cm with no nodes


Stage IIIA

Stage IIIB

Stage IIIC

Stage IV

What are the sites ofmetastases?

What are the majortreatments of breast cancer?

What are the indications forradiation therapy after amodified radical mastectomy?

What breast carcinomas arecandidates for lumpectomyand radiation (breast-conserving therapy)?


Tumor �5 cm with mobile axillary nodes or

Any size tumor with fixed axillary nodes,no metastases

Peau d’orange (skin edema) orChest wall invasion/fixation orInflammatory cancer orBreast skin ulceration orBreast skin satellite metastases orAny tumor and � ipsilateral internal

mammary lymph nodes

Any size tumor, no distant metsPOSITIVE: supraclavicular,

infraclavicular, or internal mammary lymph nodes

Distant metastases (including ipsilateralsupraclavicular nodes)

Lymph nodes (most common)Lung/pleuraLiverBonesBrain

Modified radical mastectomyLumpectomy and radiation � sentinel

lymph node dissection(Both treatments either �/– postop

chemotherapy/tamoxifen)

Stage IIIAStage IIIBPectoral muscle/fascia invasion Positive internal mammary LNPositive surgical margins�4 positive axillary LNs postmenopausal

Stage I and stage II (tumors �5 cm)


What approach may allow apatient with stage IIIA cancerto have breast-conservingsurgery?

What is the treatment ofinflammatory carcinoma ofthe breast?

What is a “lumpectomy andradiation”?

What is the major absolutecontraindication tolumpectomy and radiation?

What are othercontraindications tolumpectomy and radiation?

What is a modified radicalmastectomy?

Where are the drains placedwith an MRM?

When should the drains beremoved?


NEOadjuvant chemotherapy—if the preop chemo shrinks the tumor

Chemotherapy first! Then oftenfollowed by radiation, mastectomy, orboth

Lumpectomy (segmental mastectomy:removal of a part of the breast); axillarynode dissection; and a course of radiationtherapy after operation, over a period ofseveral weeks

Pregnancy

Previous radiation to the chestPositive marginsCollagen vascular disease (e.g.,

scleroderma)Extensive DCIS (often seen as diffuse

microcalcification)Relative contraindications:

Lesion that cannot be seen on themammograms (i.e., earlyrecurrence will be missed onfollow-up mammograms)

Very small breast (no cosmeticadvantage)

Breast, axillary nodes (level II, I), andnipple–areolar complex are removed

Pectoralis major and minor muscles are not removed (Auchincloss modification)

Drains are placed to drain lymph fluid

1. Axilla2. Chest wall (breast bed)

�30 cc/day drainage


What are the potential complications after a modifiedradical mastectomy?

During an axillary dissection,should the patient be paralyzed?

How can the long thoracicand thoracodorsal nerves beidentified during an axillarydissection?

When do you remove thedrains after an axillarydissection?

What is a sentinel nodebiopsy?

How is the sentinel lymphnode found?

What follows a positivesentinel node biopsy?

What is now considered thestandard of care for lymphnode evaluation in womenwith T1 or T2 tumors (stages Iand IIA) and clinicallynegative axillary lymphnodes?

What do you do with amammotome biopsy thatreturns as “atypicalhyperplasia”?

How does tamoxifen work?


Ipsilateral arm lymphedema, infection,injury to nerves, skin flap necrosis,hematoma/seroma, phantom breastsyndrome

NO, because the nerves (long thoracic/thoracodorsal) are stimulated with resultant muscle contraction to helpidentify them

Nerves can be stimulated with aforceps, which results in contraction ofthe latissimus dorsi (thoracodorsal nerve)or anterior serratus (long thoracic nerve)

When there is �30 cc of drainage per day,or on POD #14 (whichever comes first)

Instead of removing all the axillary lymph nodes, the primary draining or“sentinel” lymph node is removed

Inject blue dye and/or technetium-labeledsulfur colloid (best results with both)

Removal of the rest of the axillary lymphnodes

Sentinel lymph node dissection

Open needle loc biopsy as many will haveDCIS or invasive cancer

It binds estrogen receptors


What is the treatment forlocal recurrence in breastafter lumpectomy andradiation?

Can tamoxifen preventbreast cancer?

What are common optionsfor breast reconstruction?

What is a TRAM flap?


“Salvage” mastectomy

Yes. In the Breast Cancer PreventionTrial of 13,000 women at increased riskof developing breast cancer, tamoxifenreduced risk by �50% across all ages

TRAM flap, implant, latissimus dorsi flap

Transverse Rectus Abdominis Myocutaneous flap

What are side effects oftamoxifen?

In high-risk women, is therea way to reduce the risk ofdeveloping breast cancer?

Endometrial cancer (2.5� relativerisk), DVT, pulmonary embolus,cataracts, hot flashes, mood swings

Yes, tamoxifen for 5 years will lower therisk by up to 50%, but, with an increasedrisk of endometrial cancer and clots, it must be an individual patient determination


Give the common adjuvanttherapy for the followingpatients with breast cancer.(These are rough guidelines;check for current uidelines,as they are always changing.)(ER � estrogen receptor):

Premenopausal, node �,ER �



Postmenopausal, node �,ER �

Postmenopausal, node �,ER �

What type of chemotherapyis usually used for breastcancer?

Chemotherapy for high-risktumors with negative lymphnodes should be considered. What makes a tumor “HIGHRISK”?


Chemotherapy

Chemotherapy and tamoxifen

Tamoxifen

Tamoxifen, �/ chemotherapy

Chemotherapy, �/ tamoxifen

CMF (Cyclophosphamide, Methotrexate,5-Fluorouracil) or CAF(Cyclophosphamide, Adriamycin, 5-Fluorouracil)

High risk:�1 cm in sizeLymphatic/vascular invasion Nuclear grade (high)S phase (high)ER negativeHER-2/neu overexpression

DCIS

What does DCIS stand for?

What is DCIS also known as?

Describe DCIS.

Ductal Carcinoma In Situ

Intraductal carcinoma

Cancer cells in the duct without invasion(In situ: Cells do not penetrate the basement membrane)



What are the mammographicfindings?


What is the most aggressivehistologic type?

What is the risk of lymphnode metastasis with DCIS?

What is the major risk withDCIS?

What is the treatment forDCIS in the following cases:

Tumor �1 cm (lowgrade)?

Tumor �1 cm?

What is a total (simple)mastectomy?

When must a simplemastectomy be performedfor DCIS?

What is the role of axillarynode dissection with DCIS?

What is adjuvant for DCIS?

What is the role oftamoxifen in DCIS?


Usually none; usually nonpalpable

Microcalcifications

Core or open biopsy

Comedo

�2% (usually when microinvasion isseen)

Subsequent development of infiltratingductal carcinoma in the same breast

Remove with 1 cm margins �/ XRT

Perform lumpectomy with 1 cm marginsand radiation or total mastectomy (noaxillary dissection)

Removal of the breast and nipple withoutremoval of the axillary nodes (alwaysremove nodes with invasive cancer)

Diffuse breast involvement (e.g., diffusemicrocalcifications), �1 cm andcontraindication to radiation

No role in true DCIS (i.e., withoutmicroinvasion); some perform a sentinellymph node dissection for high-gradeDCIS

1. Tamoxifen2. Postlumpectomy XRT

Tamoxifen for 5 years will lower the riskup to 50%, but with increased risk ofendometrial cancer and clots; it must bean individual patient determination



Cancer arises in the same breast asDCIS (Think: DCIS � Directly in samebreast)

LCIS

What is LCIS?


What are the mammographicfindings?


What is the major risk?

Which breast is most at riskfor developing an invasivecarcinoma?

What percentage of womenwith LCIS develop aninvasive breast carcinoma?

What type of invasive breastcancer do patients with LCISdevelop?

What medication may lowerthe risk of developing breastcancer in LCIS?

What is the treatment ofLCIS?

What is the major difference in the subsequentdevelopment of invasivebreast cancer with DCISand LCIS?

Lobular Carcinoma In Situ (carcinomacells in the lobules of the breast withoutinvasion)

There are none

There are none

LCIS is found incidentally on biopsy

Carcinoma of either breast

Equal risk in both breasts! (Think ofLCIS as a risk marker for future development of cancer in either breast)

�30% in the 20 years after diagnosis ofLCIS!

Most commonly, infiltrating ductalcarcinoma, with equal distribution inthe contralateral and ipsilateral breasts

Tamoxifen for 5 years will lower the riskup to 50%, but with an increased risk ofendometrial cancer and clots; it must bean individual patient determination

Close follow-up (or bilateral simple mastectomy in high-risk patients)

LCIS cancer develops in either breast;DCIS cancer develops in the ipsilateralbreast

What is a memory aid forthe breast in which DCISbreast cancer arises?



What is the most commoncause of bloody nippledischarge in a young woman?

What is the most commonbreast tumor in patientsyounger than 30 years?

What is Paget’s disease ofthe breast?

What are the commonoptions for breastreconstruction after amastectomy?

Intraductal papilloma

Fibroadenoma

Scaling rash/dermatitis of the nipplecaused by invasion of skin by cells from aductal carcinoma

Saline implantTRAM flap

MALE BREAST CANCER

What is the incidence ofbreast cancer in men?

What is the average age atdiagnosis?


Is benign gynecomastia arisk factor for male breastcancer?

What type of breast cancerdo men develop?

�1% of all breast cancer cases (1/150)

65 years of age

Increased estrogenRadiationGynecomastia from increased estrogenEstrogen therapyKlinefelter’s syndrome (XXY)BRCA2 carriers

No

Nearly 100% of cases are ductalcarcinoma (men do not usually havebreast lobules)

MISCELLANEOUS

How do you rememberwhich breast is at risk forinvasive cancers in patientswith LCIS?

Think: LCIS � Liberally in either breast



What are the signs/symptoms of breast cancerin men?

What is the most commonpresentation?

How is breast cancer in mendiagnosed?


Breast mass (most are painless), breastskin changes (ulcers, retraction), and nipple discharge (usually blood or ablood-tinged discharge)

Painless breast mass

Biopsy and mammogram

1. Mastectomy2. Sentinel LN dissection of clinically

negative axilla3. Axillary dissection if clinically positive

axillary LN

BENIGN BREAST DISEASE

What is the most commoncause of green, straw-colored, or brown nippledischarge?

What is the most commoncause of breast mass afterbreast trauma?

What is Mondor’s disease?

What must be ruled out withspontaneous galactorrhea(�/� amenorrhea)?

Fibrocystic disease

Fat necrosis

Thrombophlebitis of superficial breast veins

Prolactinoma (check pregnancy test andprolactin level)

CYSTOSARCOMA PHYLLODES

What is it?

What is the usual age of thepatient with this tumor?

Mesenchymal tumor arising from breastlobular tissue; most are benign (Note:

“sarcoma” is a misnomer, as the vastmajority are benign; 1% of breast cancers)

35–55 years (usually older than thepatient with fibroadenoma)






What is the role of axillarydissection with cystosarcomaphyllodes tumor?

Is there a role forchemotherapy withcystosarcoma phyllodes?

Mobile, smooth breast mass thatresembles a fibroadenoma on exam,mammogram/ultrasound findings

Through core biopsy or excision

If benign, wide local excision; ifmalignant, simple total mastectomy

Only if clinically palpable axillary nodes,as the malignant form rarely spreads tonodes (most common site of metastasis isthe lung)

Consider chemotherapy if large tumor�5 cm and “stromal overgrowth”

FIBROADENOMA

What is it?

What is the clinicalpresentation of afibroadenoma?

How is fibroadenomadiagnosed?


What is this tumor’s claim to fame?

Benign tumor of the breast consisting ofstromal overgrowth, collagen arranged in“swirls”

Solid, mobile, well-circumscribed roundbreast mass, usually �40 years of age

Negative needle aspiration looking forfluid; ultrasound; core biopsy

Surgical resection for large or growinglesions; small fibroadenomas can beobserved closely

Most common breast tumor in women �30 years

FIBROCYSTIC DISEASE

What is it?


Common benign breast conditionconsisting of fibrous (rubbery) and cysticchanges in the breast

Breast pain or tenderness that varies withthe menstrual cycle; cysts; and fibrous(“nodular”) fullness




What is the treatment forsymptomatic fibrocysticdisease?

What is done if the patienthas a breast cyst?

Through breast exam, history, and aspiratedcysts (usually straw-colored or green fluid)

Stop caffeinePain medications (NSAIDs)Vitamin E, evening primrose oil (danazol

and OCP as last resort)

Needle drainage: If aspirate is bloody ora palpable mass remains after aspira-tion, an open biopsy is performed

If the aspirate is straw colored or green,the patient is followed closely; then, if there is recurrence, a second aspiration is performed

Re-recurrence usually requires open biopsy

MASTITIS

What is it?

In what circumstance does itmost often occur?

What bacteria are mostcommonly the cause?

How is mastitis treated?

Why must the patient withmastitis have close follow-up?

Superficial infection of the breast (cellulitis)

Breast-feeding


Stop breast-feeding and use a breast pumpinstead; apply heat; administer antibiotics

To make sure that she does not haveinflammatory breast cancer!

BREAST ABSCESS


What is the most commonbacteria?

What is the treatment ofbreast abscess?

Mammary ductal ectasia (stenosis ofbreast duct) and mastitis

Nursing � Staphylococcus aureusNonlactating � mixed infection

Antibiotics (e.g., dicloxacillin)Needle or open drainage with cultures

takenResection of involved ducts if recurrentBreast pump if breast-feeding


What is lactational mastitis?

What must be ruled out with a breast abscess in anonlactating woman?


Infection of the breast during breast-feeding—most commonly caused by S. aureus; treat with antibiotics andfollow for abscess formation

Breast cancer!

MALE GYNECOMASTIA

What is it?


What is the major differentialdiagnosis in the older patient?


Enlargement of the male breast

MedicationsIllicit drugs (marijuana)Liver failureIncreased estrogenDecreased testosterone

Male breast cancer

Stop or change medications; correct under-lying cause if there is a hormonal imbal-ance; and perform biopsy or subcutaneousmastectomy (i.e., leave nipple) if refractoryto conservative measures and time

ADRENAL GLAND

ANATOMY

EndocrineChapter 57

Left renal vein

Inferior vena cava (IVC)

Where is the drainage of theleft adrenal vein?

Where is the drainage of theright adrenal vein?


Chapter 57 / Endocrine 419

NORMAL ADRENAL PHYSIOLOGY

What is CRH?

What is ACTH?

What feeds back to inhibitACTH secretion?

Corticotropin-Releasing Hormone:released from anterior hypothalamus andcauses release of ACTH from anteriorpituitary

AdrenoCorticoTropic Hormone: releasednormally by anterior pituitary, which inturn causes adrenal gland to releasecortisol

Cortisol

CUSHING’S SYNDROME

What is Cushing’s syndrome?

What is the most commoncause?

What is the second mostcommon cause?

What is Cushing’s disease?

What is an ectopic ACTHsource?

What are the signs/symptoms of Cushing’ssyndrome?

How can cortisol levels beindirectly measured over ashort duration?

What is a direct test ofserum cortisol?

Excessive cortisol production (Think:Cushing’s � Cortisol

Iatrogenic (i.e., prescribed prednisone)

Cushing’s disease (most common noniatrogenic cause)

Cushing’s syndrome caused by excessproduction of ACTH by anterior pituitary

Tumor not found in the pituitary thatsecretes ACTH, which in turn causesadrenal gland to release cortisol withoutthe normal negative feedback loop

Truncal obesity, hirsutism, “moon” facies, acne, “buffalo hump,” purplestriae, hypertension, diabetes, weakness,depression, easy bruising, myopathy

By measuring urine cortisol or the breakdown product of cortisol, 17 hydroxycorticosteroid (17-OHCS),in the urine

Serum cortisol level (highest in the morn-ing and lowest at night in healthy patients)


What initial tests should beperformed in Cushing’ssyndrome?

What is the low-dosedexamethasone suppressiontest?

After the dexamethasonetest, what is next?

Can plasma ACTH levels bechecked directly?

What is the workup in apatient suspected of havingCushing’s syndrome?


ElectrolytesSerum cortisolUrine-free cortisol, urine 17-OHCSLow-dose dexamethasone suppression test

Dexamethasone is a synthetic cortisolthat results in negative feedback onACTH secretion and subsequent cortisolsecretion in healthy patients; patientswith Cushing’s syndrome do notsuppress their cortisol secretion

Check ACTH levels

Yes

Cushing’s syndrome

Check ACTH (plasma)

Adrenal tumor ACTH dependent process

Dexamethasone

Cortisol suppression

Normal

Pituitary source Ectopic ACTH

Normal or elevated ACTHLow ACTH

YESNO

Signs/symptoms of Cushing’s syndrome

High-dose dexamethasone

Cortisol suppression

YES NO


In ACTH-dependentCushing’s syndrome, how doyou differentiate between apituitary vs. an ectopicACTH source?

Summarize the “Cushing’ssyndrome” lab values foundin the majority of patientswith the following conditions:

Healthy patients

Cushing’s disease(pituitary ACTHhypersecretion)

Adrenal tumor

Ectopic ACTH-producingtumor

What is the test forequivocal results fordifferentiating pituitary vs.ectopic ACTH tumor?

What is the most common site of ectopicACTH-producing tumor?

How are the followingtumors treated:

Adrenal adenoma?

Adrenal carcinoma?

Ectopic ACTH-producingtumor?

Cushing’s disease?


High-dose dexamethasone test:Pituitary source—cortisol is

suppressedEctopic ACTH source—no cortisol

suppression

Normal cortisol and ACTH, suppression with low-dose or high-dose dexamethasone (�1/2)

High cortisol and ACTH, no suppressionwith low-dose dexamethasone, suppressionwith high-dose dexamethasone

High cortisol, low ACTH, no suppression with low-dose or high-dosedexamethasone

High cortisol and ACTH, no suppressionwith low-dose or high-dose dexamethasone

Bilateral petrosal vein sampling,especially with CRH infusion

�66% are oat cell tumors of the lung (#2 is carcinoid)

Adrenalectomy (almost always unilateral)

Surgical excision (only 33% of cases areoperable)

Surgical excision, if feasible

Transphenoidal adenomectomy


What medication must begiven to a patient who isundergoing surgicalcorrection of Cushing’ssyndrome?

What medications inhibitcortisol production?

Give the mechanism of action:Ketoconazole (an antifungal)

Aminoglutethimide (an anticonvulsant)

Mitotane

Metyrapone

What is a complication of BILATERALadrenalectomy?

What is Nelson’s syndrome?


Cortisol (usually hydrocortisone until POis resumed)

1. Ketoconazole2. Metyrapone3. Aminoglutethimide4. Mitotane

Inhibits 11 -hydroxylase, c17-20 lyase,and cholesterol side-chain cleavage

Inhibits cleavage of cholesterol sidechains

Inhibits 11 -hydroxylase and cholesterolside-chain cleavage; causes irreversibleadrenocortical cells (and thus can beused for “medical adrenalectomy”)

Inhibits 11 -hydroxylase

Nelson’s syndrome—occurs in 10% ofpatients after bilateral adrenalectomy

Functional pituitary adenoma producingexcessive ACTH and mass effect producing visual disturbances, hyperpigmentation, amenorrhea, withelevated ACTH levels

Think: Nelson � Nuclear reaction in thepituitary

ADRENAL INCIDENTALOMA

What is an incidentaloma?

What is the incidence ofincidentalomas?

Tumor found in the adrenal glandincidentally on a CT scan performed foran unrelated reason

4% of all CT scans (9% of autopsies)


What is the most commoncause of incidentaloma?

What is the differentialdiagnosis of incidentaloma?

What is the risk factor forcarcinoma?


What are the indications for removal of adrenalincidentaloma less than 6 cm?

What tumor must be ruledout prior to biopsy or surgeryfor any adrenal mass?


Nonfunctioning adenoma (�75% ofcases)

Nonfunctioning adenomaPheochromocytomaAdrenocortical carcinomaAldosteronomaMetastatic diseaseNodular hyperplasia

Solid tumor �6 cm in diameter

Controversial for smaller/medium-sizedtumors, but almost all surgeons wouldagree that resection is indicated for solidincidentalomas �6 cm in diameterbecause of risk of cancer

MRI T2 signal �2Hormonally active � hyperfunctioning

tumorEnlarging cystic lesionDoes not look like an adenoma

Pheochromocytoma (24-hour urine forcatecholamine, VMA, metanephrines)

PHEOCHROMOCYTOMA

What is it?


Which age group is mostlikely to be affected?


Tumor of the adrenal MEDULLA andsympathetic ganglion (from chromaffincell lines) that produces catecholamines(norepinephrine � epinephrine)

Cause of hypertension in �1/500hypertensive patients (�10% of U.S.population has hypertension)

Any age (children and adults); averageage is 40 to 60 years

MEN-II, family history, von Recklinghausendisease, von Hippel-Lindau disease



How can thepheochromocytoma SYMPTOMS triad beremembered?

What is the most commonsign of pheochromocytoma?


What diagnostic tests shouldbe performed?

What are the other commonlab findings?

What is the most common site of apheochromocytoma?

What are the other sites forpheochromocytoma?

What are the tumorlocalization tests?


“Classic” triad:1. Palpitations2. Headache3. Episodic diaphoresis

Also, hypertension (50%), pallor Sflushing, anxiety, weight loss, tachycardia,hyperglycemia

Think of the first three letters in theword PHEochromocytoma:

PalpitationsHeadacheEpisodic diaphoresis

Hypertension

Renovascular hypertension, menopause,migraine headache, carcinoid syndrome,preeclampsia, neuroblastoma, anxiety disorder with panic attacks,hyperthyroidism, insulinoma

Urine screen: VanillylMandelic Acid(VMA), metanephrine, andnormetanephrine (all breakdownproducts of the catechols)

Urine/serum epinephrine/norepinephrine levels

Hyperglycemia (epinephrine increases glucose, norepinephrine decreasesinsulin)

Polycythemia (resulting from intravascularvolume depletion)

Adrenal �90%

Organ of Zuckerkandl, thorax(mediastinum), bladder, scrotum

CT scan, MRI, 131I-MIBG, PET scan,OctreoScan (111In-pentetreotide scan)


What does 131I-MIBG stand for?

How to remember MIBGand pheochromocytoma?

How does the 131I-MIBGscan work?

What is the role of PETscan?

What is the scan for imaging adrenal corticalpheochromocytoma?

What is the localizing optionif a tumor is not seen on CT,MRI, or I-MIBG?

What is the tumor site ifepinephrine is elevated?

What percentage of patientshave malignant tumors?

Can histology be used todetermine malignancy?

What is the classicpheochromocytoma “rule of 10’s”?

What is the preoperative/medical treatment?


Iodine131MetaIodoBenzylGuanidine

Think: MIBG � My Big � and thus “My Big Pheo” � MIBG Pheo

131I-MIBG is a norepinephrine analogthat collects in adrenergic vesicles and,thus, in pheochromocytomas

Positron Emission Tomography is helpfulin localizing pheochromocytomas that donot accumulate MIBG

NP-59 (a cholesterol analog)

IVC venous sampling for catecholamines(gradient will help localize the tumor)

Must be adrenal or near the adrenal gland(e.g., organ of Zuckerkandl), becausenonadrenal tumors lack the capability tomethylate norepinephrine to epinephrine

�10%

No; only distant metastasis or invasioncan determine malignancy

10% malignant10% bilateral10% in children10% multiple tumors10% extra-adrenal

Increase intravascular volume with �-blockade (e.g., phenoxybenzamine or prazosin) to allow reduction incatecholamine-induced vasoconstrictionand resulting volume depletion; treatmentshould start as soon as diagnosis is made�/ -blockers


How can you rememberphenoxybenzamine as amedical treatment ofpheochromocytoma?


What are the possibleperioperative complications?

In the patient withpheochromocytoma, whatmust be ruled out?

What is the organ ofZuckerkandl?


PHEochromocytoma �PHEnoxybenzamine

Tumor resection with early ligation ofvenous drainage (lower possibility of catecholamine release/crisis by tying offdrainage) and minimal manipulation

Anesthetic challenge: hypertensive crisiswith manipulation (treat with nitroprus-side), hypotension with total removal ofthe tumor, cardiac dysrhythmias

MEN type II (almost all cases arebilateral)

Body of embryonic chromaffin cells aroundthe abdominal aorta (near the inferiormesenteric artery); normally atrophies during childhood, but is the most commonsite of extra-adrenal pheochromocytoma

CONN’S SYNDROME

What is it?

How do you remember whatConn’s syndrome is?

Primary hyperaldosteronism due tohigh aldosterone production

CONn’s disease � HYPERALdosterone� “CON HYPER AL”

Al-How’d ya liketo buy theBrooklyn Bridge?

JAVA JAVAJAVA JAVA

JAVA JAVAJAVA JAVA

‘Hyper AI’


What are the commonsources?

What is the normalphysiology for aldosteronesecretion?

What is the normalphysiologic effect ofaldosterone?


What are the two classicclues of Conn’s syndrome?

Classically, what kind ofhypertension?

What are the renin levelswith Conn’s syndrome?

What percentage of allpatients with hypertensionhave Conn’s syndrome?

What diagnostic tests shouldbe ordered?

What ratio of thesediagnostic tests is associated with primaryhyperaldosteronism?


Adrenal adenoma or adrenalhyperplasia; aldosterone is abnormallysecreted by an adrenal adenoma (66%) � hyperplasia � carcinoma

BP in the renal afferent arteriole is lowLow sodium and hyperkalemia cause

renin secretion from juxtaglomerularcells

Renin then converts angiotensinogen toangiotensin I

Angiotensin converting enzyme in thelung then converts angiotensin I toangiotensin II

Angiotensin II then causes the adrenalglomerulosa cells to secretealdosterone

Aldosterone causes sodium retention forexchange of potassium in the kidney, result-ing in fluid retention and increased BP

Hypertension, headache, polyuria,weakness

1. Hypertension2. Hypokalemia

Diastolic hypertension

Normal or decreased!

1%

1. Plasma aldosterone concentration2. Plasma renin activity

Aldosterone to renin ratio of �30


What is secondaryhyperaldosteronism?


What is the saline infusiontest?

What is the preoperativetreatment?

What is spironolactone?

What are the causes ofConn’s syndrome?

What is the treatment of thefollowing conditions:

Adenoma?

Unilateral hyperplasia?

Bilateral hyperplasia?

What are the renin levels inpatients with PRIMARYhyperaldosteronism?


Hyperaldosteronism resulting fromabnormally high renin levels (reninincreases angiotensin/aldosterone)

CT scan, adrenal venous sampling foraldosterone levels, saline infusion

Saline infusion will decrease aldosteronelevels in normal patients but not inConn’s syndrome

Spironolactone, K� supplementation

Antialdosterone medication (works at thekidney tubule)

Adrenal adenoma (66%)Bilateral idiopathic adrenal hyperplasia

(30%)Adrenal cancer (�1%)

Unilateral adrenalectomy (laparoscopic)

Unilateral adrenalectomy (laparoscopic)

Spironolactone (usually no surgery)

Normal or low (key point!)

ADDISON’S DISEASE

What is it?

What are the electrolytefindings?

How do you remember whatADDISON’s disease is?

Acute adrenal insufficiency

HYPERkalemia, hyponatremia

Think: ADDison’s disease � ADrenalDown

INSULINOMA

What is it? Insulin-producing tumor arising from cells




What are the associatedrisks?


What are the neurologicsymptoms?

What is Whipple’s triad?




#1 Islet cell neoplasm; half of celltumors of the pancreas produce insulin

Associated with MEN-I syndrome (PPP � Pituitary, Pancreas, Parathyroidtumors)

Sympathetic nervous system symptomsresulting from hypoglycemia:palpitations, diaphoresis, tremulousness,irritability, weakness

Personality changes, confusion, obtundation, seizures, coma

1. Hypoglycemic symptoms produced byfasting

2. Blood glucose �50 mg/dL duringsymptomatic attack

3. Relief of symptoms by administrationof glucose

Reactive hypoglycemiaFunctional hypoglycemia with

gastrectomyAdrenal insufficiencyHypopituitarismHepatic insufficiencyMunchausen syndrome (insulin

self-injections)Nonislet cell tumor causing hypoglycemiaSurreptitious administration of insulin or

OHAs

Glucose and insulin levels during fast; C-peptide and proinsulin levels (if self-injection of insulin is a concern, as insulininjections have no proinsulin or C-peptides)

Fasting hypoglycemia withinappropriately high levels of insulin

72-hour fast, then check glucose andinsulin levels every 6 hours (monitorvery closely because patient candevelop hypoglycemic crisis)


What is the diagnostic fastinginsulin to glucose ratio?

What localizing tests shouldbe performed?





�0.4

CT scan, A-gram, endoscopic U/S, venouscatheterization (to sample blood alongportal and splenic veins to measure insulinand localize tumor), intraoperative U/S

Diazoxide, to suppress insulin release

Surgical resection

�80% of patients have a benign solitaryadenoma that is cured by surgical resection

GLUCAGONOMA

What is it?

Where is it located?


What are the skin findings?


What is the classic findingon CBC?

What is the classic nutritionalfinding?

What stimulation test is usedfor glucagonoma?

What test is used forlocalization?

Glucagon-producing tumor

Pancreas (usually in the tail)

Necrotizing migratory erythema(usually below the waist), glossitis,stomatitis, diabetes

Necrotizing migratory erythema is a red,often psoriatic-appearing rash with serpig-inous borders over the trunk and limbs

Hyperglycemia, low amino acid levels,high glucagon levels

Anemia

Low amino acid levels

Tolbutamide stimulation test: IV tolbutamide results in elevatedglucagon levels

CT scan


What is the medicaltreatment of necrotizingmigratory erythema?



Somatostatin, IV amino acids

Surgical resection

SOMATOSTATINOMA

What is it?

What is the diagnostic triad?

What is used to make thediagnosis?


What is the medicaltreatment if the tumor isunresectable?

Pancreatic tumor that secretes somatostatin

DDD:1. Diabetes2. Diarrhea (steatorrhea)3. Dilation of the gallbladder with

gallstones

CT scan and somatostatin level

Resection (do not enucleate)

Streptozocin, dacarbazine, or doxorubicin

ZOLLINGER-ELLISON SYNDROME (ZES)

What is it?


What is the associatedsyndrome?

What percentage of patientswith ZES have MEN-Isyndrome?

What percentage of patientswith MEN-I will have ZES?

Gastrinoma: nonislet cell tumor of thepancreas (or other locale) that producesgastrin, causing gastric hypersecretion ofHCl acid, resulting in GI ulcers

1/1000 in patients with peptic ulcer disease, but nearly 2% in patients withrecurrent ulcers

MEN-I syndrome

�25% (75% of cases of Z-E syndromeare “sporadic”)

�50%


With gastrinoma, what labtests should be ordered toscreen for MEN-I?


What causes the diarrhea?

What are the signs?

What are the possiblecomplications?

What is the differentialdiagnosis of increasedgastrin?

Which patients should havea gastrin level checked?


What are the associatedgastrin levels?

What is the secretinstimulation test?


1. Calcium level2. Parathyroid hormone level

Peptic ulcers, diarrhea, weight loss,abdominal pain

Massive acid hypersecretion and destruction of digestive enzymes

PUD (epigastric pain, hematemesis,melena, hematochezia), GERD, diarrhea,recurrent ulcers, ulcers in unusuallocations (e.g., proximal jejunum)

GI hemorrhage/perforation, gastric outletobstruction/stricture, metastatic disease

PostvagotomyGastric outlet obstructionG-cell hyperplasiaPernicious anemiaAtrophic gastritisShort gut syndromeRenal failureH2 blocker, PPI

Those with recurrent ulcer; ulcer inunusual position (e.g., jejunum) or refractory to medical management;before any operation for ulcer

Fasting gastrin levelPostsecretin challenge gastrin levelCalcium (screen for MEN-I)Chem 7

NL fasting � 100 pg/mlZES fasting � 200–1000 pg/mlBasal acid secretion; (ZES �15 mEq/hr,

nl �10mEq/hr)

IV secretin is administered and thegastrin level is determined; patients withZES have a paradoxic increase in gastrin


What are the classic secretinstimulation results?

How can you remember thediagnostic stimulation testfor Z-E syndrome?

What tests are used toevaluate ulcers?

What tests are used tolocalize the tumor?


What is the most commonNONpancreatic site?

What are some other sites?

Define “Passaro’s triangle.”


Lab results with secretin challenge:NL—Decreased gastrinZES—Increased gastrin (increased by

�200 pg/ml)

Think: “Secret Z-E GAS”: SECRETin� Z-E GAStrin

EGD, UGI, or both

Octreotide scan (somatostatin receptorscan), abdominal CT, MRI, endoscopicultrasonography (EUS)

Pancreas

Duodenum

Stomach, lymph nodes, liver, kidney, ovary

A.k.a. “gastrinoma triangle,” a triangledrawn from the following points:

1. Cystic duct/CBD junction2. Junction of the second and third

portions of the duodenum3. Neck of the pancreas


What percentage ofgastrinomas are in Passaro’striangle?

What is the next step if thetumor cannot be localized?


What is the surgicaltreatment needed for each of the following:

Tumor in head ofpancreas?

Tumor in body or tail ofpancreas?

Tumor in duodenum?

Unresectable tumor?

What percentage havemalignant tumors?


What is the treatment of patients with livermetastasis?

What is the surgical option if gastrinoma is induodenum/head of pancreas and is too largefor local resection?


�80%

Exploratory surgery (if tumor is not in pancreas, open duodenum and look), proximal gastric vagotomy if not found

H2 blockers, omeprazole, somatostatin

1. Enucleation of tumor2. Whipple procedure if main pancreatic

duct is involved

Distal pancreatectomy

Local resection

High selective vagotomy

66%

Liver

Excision, if technically feasible

Whipple procedure



What is the prognosis withthe following procedures:

Complete excision?

Incomplete excision?

90% 10-year survival

25% 10-year survival

MULTIPLE ENDOCRINE NEOPLASIA

What is it also known as?

What is it?

How is it inherited?

Which patients should bescreened for MEN?

MEN syndrome

Inherited condition of propensity todevelop multiple endocrine tumors

Autosomal dominant (but with a significantdegree of variation in penetrance)

All family members of patients diagnosedwith MEN

MEN TYPE I

What is the commoneponym?

What is the gene defect inMEN type I?

What are the most commontumors and their incidences?

How can tumors for MEN-Ibe remembered?

How can the P’s associatedwith MEN-I be remembered?

What percentage of patientswith MEN-I haveparathyroid hyperplasia?

Wermer’s syndrome (Think: Wermer �Winner � #1 � type 1)

Chromosome 11 (Think: 11 � 1)

“PPP”:Parathyroid hyperplasia (�90%)Pancreatic islet cell tumors (�66%)

Gastrinoma: ZES (50%)Insulinoma (20%)

Pituitary tumors (�50%)

Think: type 1 � Primary, Primary,Primary � PPP � Parathyroid, Pancreas,Pituitary

All the P’s are followed by a vowel: PA,PA, PI

�90%



What percentage of patientswith MEN-I have agastrinoma?

What other tumors (in addition to PPP) areassociated with MEN-I?

�50%

Adrenal (30%) and thyroid (15%)adenomas

MEN TYPE IIa

What is the commoneponym?

What is the gene defect inMEN type IIa?

What are the most commontumors and their incidences?

How can the tumorsinvolved with MEN-IIa beremembered?

How can the P of MPH beremembered?

What percentage of patients with MEN-IIa havemedullary carcinoma of thethyroid?

Sipple’s syndrome (Think: Sipple �Second � #2 � type 2)

RET (Think: reT � Two)

“MPH”:Medullary thyroid carcinoma (100%);

Calcitonin secretedPheochromocytoma (�33%);

Catecholamine excessHyperparathyroidism (�50%);

Hypercalcemia

Think: type 2 � 2 MPH or 2 Miles Per Hour � MPH � Medullary,Pheochromocytoma, Hyperparathyroid

Followed by the consonant “H”—PHEOCHROMOCYTOMA (remember,the P’s of MEN-I are followed by vowels)

100%

MEN TYPE IIb

What are the most commonabnormalities, theirincidences, and symptoms?

“MMMP”:Mucosal neuromas (100%)—in the

nasopharynx, oropharynx, larynx,and conjunctiva

Medullary thyroid carcinoma (�85%)—more aggressive than in MEN-IIa

Marfanoid body habitus (long/lanky)Pheochromocytoma (�50%) and

found bilaterally


How can the features ofMEN-IIb be remembered?

How can you remember that MEN-IIb is marfanoidhabitus?

What is the anatomicdistribution of medullarythyroid carcinoma in MEN-II?

What are the physicalfindings/signs of MEN-IIb?

What is the most commonGI complaint of patientswith MEN-IIb?

What percentage ofpheochromocytomas inMEN-IIa/b are bilateral?

What is the major differencebetween MEN-IIa andMEN-IIb?

What type of parathyroiddisease is associated withMEN-I and MEN-IIa?

What percentage of patientswith Z-E syndrome haveMEN-I?


MMMP (Think: 3M Plastics)

Think: “TO BE marfanoid” � II Bmarfanoid

Almost always bilateral (non–MEN-IIcases are almost always unilateral!)

Mucosal neuromas (e.g., mouth, eyes)Marfanoid body habitusPes cavus/planum (large arch of foot/

flatfooted)Constipation

Constipation resulting fromganglioneuromatosis of GI tract

�70% (but found bilaterally in only 10%of all patients diagnosed withpheochromocytoma)

MEN-IIa � parathyroid hyperplasiaMEN-IIb � no parathyroid hyperplasia

(and neuromas, marfanoid habitus,pes cavus [extensive arch of foot],etc.)

Hyperplasia (treat with removal of allparathyroid tissue with autotransplant ofsome of the parathyroid tissue to theforearm)

�25%



THYROID DISEASE

ANATOMY

Thyroid GlandChapter 58

1. Pyramidal lobe2. Right lobe3. Isthmus4. Left lobe

Identify the followingstructures:

Define the arterial bloodsupply to the thyroid.

Two arteries:1. Superior thyroid artery (first branch

of the external carotid artery)2. Inferior thyroid artery (branch of

the thyrocervical trunk) (IMAartery rare)1

2

Thyrocervicaltrunk

LWBK758-c58-61_p438-463.qxd 3/15/11 1:55AM Page 438 Aptara

Name the thyroid lobeappendage coursing towardthe hyoid bone from aroundthe thyroid isthmus.

What percentage of patientshave a pyramidal lobe?

What veins do you first seeafter opening the platysmamuscle when performing athyroidectomy?

Name the lymph node group around the pyramidalthyroid lobe.

What is the thyroid isthmus?

Which ligament connects thethyroid to the trachea?

What is the IMA (not I.M.A.)artery?

What percentage of patientshave an IMA artery?

Chapter 58 / Thyroid Gland 439

Pyramidal lobe

�50%

Anterior jugular veins

Delphian lymph node group

Midline tissue border between the leftand right thyroid lobes

Ligament of Berry

Small inferior artery to the thyroid fromthe aorta or innominate artery

�3%

What is the venous drainageof the thyroid?

Three veins:1. Superior thyroid vein2. Middle thyroid vein3. Inferior thyroid vein


Name the most posteriorextension of the lateralthyroid lobes.

Which paired nerves mustbe carefully identifiedduring a thyroidectomy?

What other nerve is at riskduring a thyroidectomy andwhat are the symptoms?

What is the name of thefamous opera singer whose superior laryngealnerve was injured duringthyroidectomy?


Tubercle of Zuckerkandl

Recurrent laryngeal nerves, which arefound in the tracheoesophageal groovesand dive behind the cricothyroid muscle;damage to these nerves paralyzes laryngealabductors and causes hoarseness if unilateral, and airway obstruction ifbilateral

Superior laryngeal nerve; if damaged,patient will have a deeper and quietervoice (unable to hit high pitches)

Urban legend has it that it was AmelitaGalli-Curci, but no objective data supportsuch a claim (Ann Surg 233:588, April2001)

PHYSIOLOGY

What is TRH?

What is TSH?

What are the thyroidhormones?

What is the most active formof thyroid hormone?

What is a negative feedbackloop?

What is the most commonsite of conversion of T4 to T3?

Thyrotropin-Releasing Hormonereleased from the hypothalamus; causesrelease of TSH

Thyroid-Stimulating Hormone releasedby the anterior pituitary; causes release ofthyroid hormone from the thyroid

T3 and T4

T3

T3 and T4 feed back negatively on theanterior pituitary (causing decreasedrelease of TSH in response to TRH)

Peripheral (e.g., liver)


What is Synthroid®

(levothyroxine): T3 or T4?

What is the half-life ofSynthroid® (levothyroxine)?

What do parafollicular cellssecrete?


T4

7 days

Calcitonin

THYROID NODULE

What percentage of peoplehave a thyroid nodule?

What is the differentialdiagnosis of a thyroidnodule?

Name three types ofnonthyroidal neck masses.

What studies can be used toevaluate a thyroid nodule?

What is the DIAGNOSTICtest of choice for thyroidnodule?

What is the percentage offalse negative results onFNA for thyroid nodule?

�5%

Multinodular goiterAdenomaHyperfunctioning adenomaCystThyroiditisCarcinoma/lymphomaParathyroid carcinoma

1. Inflammatory lesions (e.g., abscess,lymphadenitis)

2. Congenital lesions (i.e., thyroglossalduct [midline], branchial cleft cyst[lateral])

3. Malignant lesions: lymphoma, metastases, squamous cell carcinoma

U/S—solid or cystic noduleFine Needle Aspirate (FNA) S

cytology123I scintiscan—hot or cold nodule

FNA

�5%


What is meant by a hotversus a cold nodule?

What are the indications fora 123I scintiscan?

What is the role of thyroidsuppression of a thyroidnodule?

In evaluating a thyroidnodule, which of thefollowing suggest thyroidcarcinoma:

History?

Signs?

Symptoms?

What is the most commoncause of thyroid enlargement?

What are indications forsurgery with multinodulargoiter?

What is Plummer’s disease?


Nodule uptake of IV 131I or 99mTHot—Increased 123I uptake � functioning/

hyperfunctioning noduleCold—Decreased 123I uptake �

nonfunctioning nodule

1. Nodule with multiple “nondiagnostic”FNAs with low TSH

2. Nodule with thyrotoxicosis and low TSH

Diagnostic and therapeutic; administration of thyroid hormone suppresses TSH secretion, and up to half ofthe benign thyroid nodules will disappear!

1. Neck radiation2. Family history (thyroid cancer, MEN-II)3. Young age (especially children)4. Male � female

1. Single nodule2. Cold nodule3. Increased calcitonin levels4. Lymphadenopathy5. Hard, immobile nodule

1. Voice change (vocal cord paralysis)2. Dysphagia3. Discomfort (in neck)4. Rapid enlargement

Multinodular goiter

Cosmetic deformity, compressivesymptoms, cannot rule out cancer

Toxic multinodular goiter



MALIGNANT THYROID NODULES

What percentage of coldthyroid nodules aremalignant?

What percentage ofmultinodular masses aremalignant?

What is the treatment of apatient with a history ofradiation exposure, thyroidnodule, and negative FNA?

What should be done withthyroid cyst aspirate?

�25% in adults

�1%

Most experts would remove the nodulesurgically (because of the high risk ofradiation)

Send to cytopathology

THYROID CARCINOMA

Name the FIVE main typesof thyroid carcinoma andtheir relative percentages.


What comprises theworkup?

What oncogenes areassociated with thyroidcancers?

1. Papillary carcinoma: 80% (Popular �Papillary)

2. Follicular carcinoma: 10%3. Medullary carcinoma: 5%4. Hürthle cell carcinoma: 4%5. Anaplastic/undifferentiated

carcinoma: 1% to 2%

Mass/nodule, lymphadenopathy; most areeuthyroid

FNA, thyroid U/S, TSH, calcium level,CXR, �/� scintiscan 123I

Ras gene family and RET proto-oncogene

PAPILLARY ADENOCARCINOMA

What is papillarycarcinoma’s claim to faim?

What is the environmentalrisk?

Most common thyroid cancer (Think:Papillary � Popular) � 80% of all thyroid cancers

Radiation exposure



What is the average age?

What is the sex distribution?

What are the associatedhistologic findings?

Describe the route and rateof spread.

131I uptake?

What is the 10-year survivalrate?

What is the treatment for:�1.5 cm and no historyof neck radiationexposure?

�1.5 cm, bilateral, �cervical node metastasisOR a history of radiationexposure?

What is the treatment for:Lateral palpable cervicallymph nodes?

Central?

Do positive cervical nodesaffect the prognosis?

What is a “lateral aberrantthyroid” in papillary cancer?

What postoperativemedication should beadministered?

What is a postoperativetreatment option forpapillary carcinoma?

30–40 years

Female � male; 2:1

Psammoma bodies (Remember, P � Psammoma � Papillary)

Most spread via lymphatics (cervicaladenopathy); spread occurs slowly

Good uptake

�95%

Options:1. Thyroid lobectomy and isthmectomy2. Near-total thyroidectomy3. Total thyroidectomy

Total thyroidectomy

Modified neck dissection (ipsilateral)

Central neck dissection

NO!

Misnomer—it is metastatic papillary carcinoma to a lymph node

Thyroid hormone replacement, tosuppress TSH

Postoperative 131I scan can locate residualtumor and distant metastasis that can betreated with ablative doses of 131I


What is the most commonsite of distant metastases?

What are the “P’s” ofpapillary thyroid cancer (7)?


Pulmonary (lungs)

Papillary cancer:Popular (most common)Psammoma bodiesPalpable lymph nodes (spreads most

commonly by lymphatics, seen in�33% of patients)

Positive 131I uptakePositive prognosisPostoperative 131I scan to

diagnose/treat metastasesPulmonary metastases

FOLLICULAR ADENOCARCINOMA

What percentage of thyroidcancers does it comprise?

Describe the noduleconsistency.

What is the route of spread?

What is the male:femaleratio?

131I uptake?

What is the overall 10-yearsurvival rate?

Can the diagnosis be madeby FNA?

What histologic findingsdefine malignancy infollicular cancer?

What is the most commonsite of distant metastasis?

What is the treatment forfollicular cancer?

�10%

Rubbery, encapsulated

Hematogenous, more aggressive thanpapillary adenocarcinoma

1:3

Good uptake

�85%

No; tissue structure is needed for adiagnosis of cancer

Capsular or blood vessel invasion

Bone

Total thyroidectomy


What is the postoperativetreatment option ifmalignant?

What are the 4 “F’s” of follicular cancer?


Postoperative 131I scan for diagnosis/treatment

Follicular cancer:Far-away metastasis (spreads

hematogenously)Female (3 to 1 ratio)FNA . . . NOT (FNA CANNOT

diagnose cancer)Favorable prognosis

HÜRTHLE CELL THYROID CANCER

What is it?

What percentage of thyroidcancers does it comprise?


131I uptake?


What is the route ofmetastasis?



Thyroid cancer of the Hürthle cells

�5%

Follicular cells

No uptake

FNA can identify cells, but malignancycan be determined only by tissuehistology (like follicular cancer)

Lymphatic � hematogenous

Total thyroidectomy

80%

MEDULLARY CARCINOMA

What percentage of allthyroid cancers does itcomprise?

With what other conditionsis it associated?

Histology?

What does it secrete?

�5%

MEN type II; autosomal-dominantgenetic transmission

Amyloid (aMyloid � Medullary)

Calcitonin (tumor marker)



What is the appropriatestimulation test?

Describe the route ofspread.


131I uptake?

What is the associatedgenetic mutation?

What is the female/male ratio?


What should all patientswith medullary thyroidcancer also be screened for?

If medullary thyroidcarcinoma and pheochromo-cytoma are found, whichone is operated on first?


What are the “M’s” ofmedullary carcinoma?

Pentagastrin (causes an increase in calcitonin)

Lymphatic and hematogenous distantmetastasis

FNA

Poor uptake

RET proto-oncogene

Female � male; 1.5:1

80% without LN involvement45% with LN spread

MEN II: pheochromocytoma,hyperparathyroidism

Pheochromocytoma

Total thyroidectomy and median lymphnode dissection

Modified neck dissection, if lateral cervical nodes are positive

Medullary cancer:MEN IIaMyloidMedian lymph node dissectionModified neck dissection if lateral

nodes are positive

ANAPLASTIC CARCINOMA


What is it?

Undifferentiated carcinoma

Undifferentiated cancer arising in �75%of previously differentiated thyroid cancers(most commonly, follicular carcinoma)


What percentage of allthyroid cancers does itcomprise?

What is the genderpreference?

What are the associatedhistologic findings?

131I uptake?


What is the majordifferential diagnosis?

What is the treatment of thefollowing disorders:

Small tumors?

Airway compromise?



�2%

Women � men

Giant cells, spindle cells

Very poor uptake

FNA (large tumor)

Thyroid lymphoma (much betterprognosis!)

Total thyroidectomy � XRT/chemotherapy

Debulking surgery and tracheostomy,XRT/chemotherapy

Dismal, because most patients are atstage IV at presentation (3% alive at 5 years)

MISCELLANEOUS

What laboratory value mustbe followed postoperativelyafter a thyroidectomy?

What is the differentialdiagnosis of postoperativedyspnea after athyroidectomy?

What is a “lateral aberrantrest” of the thyroid?

Calcium decreased secondary toparathyroid damage; during lobectomy,the parathyroids must be spared andtheir blood supply protected; if bloodsupply is compromised intraoperatively,they can be autografted into thesternocleidomastoid muscle or forearm

Neck hematoma (remove sutures andclot at the bedside)

Bilateral recurrent laryngeal nervedamage

Misnomer: It is papillary cancer of alymph node from metastasis



BENIGN THYROID DISEASE

What is the most commoncause of hyperthyroidism?

What is Graves’ disease?


What is the female:maleratio?

What specific physicalfinding is associated withGraves’?


Name treatment optionmodalities for Graves’disease.

What are the possibleindications for surgicalresection?

What is the majorcomplication of radioiodideor surgery for Graves’disease?

What does PTU stand for?

Graves’ disease

Diffuse goiter with hyperthyroidism,exophthalmos, and pretibial myxedema

Caused by circulating antibodies thatstimulate TSH receptors on follicularcells of the thyroid and cause deregulatedproduction of thyroid hormones (i.e.,hyperthyroidism)

6:1

Exophthalmos

Increased T3, T4, and anti-TSH receptorantibodies, decreased TSH, global uptakeof 131I radionuclide

1. Medical blockade: iodide,propranolol, propylthiouracil (PTU),methimazole, Lugol’s solution (potassium iodide)

2. Radioiodide ablation: most populartherapy

3. Surgical resection (bilateral subtotalthyroidectomy)

Suspicious nodule; if patient isnoncompliant or refractory to medicines,pregnant, a child, or if patient refusesradioiodide therapy

Hypothyroidism

PropylThioUracil


How does PTU work?

How does methimazolework?


1. Inhibits incorporation of iodine intoT4/T3 (by blocking peroxidaseoxidation of iodide to iodine)

2. Inhibits peripheral conversion of T4 to T3

Inhibits incorporation of iodine intoT4/T3 only (by blocking peroxidase oxidation of iodide to iodine)

TOXIC MULTINODULAR GOITER


What is it?

What medication may bringon hyperthyroidism with amultinodular goiter?

How is the hyperfunctioningnodule(s) localized?


What is Pemberton’s sign?

Plummer’s disease

Multiple thyroid nodules with one ormore nodules producing thyroid hormone,resulting in hyperfunctioning thyroid(hyperthyroidism or a “toxic” thyroid state)

Amiodarone (or any iodine-containingmedication/contrast)

131I radionuclide scan

Surgically remove hyperfunctioningnodule(s) with lobectomy or near totalthyroidectomy

Large goiter causes plethora of head withraising of both arms

THYROIDITIS

What are the features ofACUTE thyroiditis?

What is the cause of ACUTEthyroiditis?

What is the treatment ofACUTE thyroiditis?

Painful, swollen thyroid; fever; overlyingskin erythema; dysphagia

Bacteria (usually Streptococcus orStaphylococcus), usually caused by athyroglossal fistula or anatomic variant

Antibiotics, drainage of abscess, needleaspiration for culture; most patients needdefinitive surgery later to remove the fistula



What are the features ofSUBACUTE thyroiditis?

What is the cause of SUBACUTE thyroiditis?

What is the treatment ofSUBACUTE thyroiditis?

What is De Quervain’sthyroiditis?

How can the differencesbetween etiologies ofACUTE and SUBACUTEthyroiditis be remembered?

What are the commoncausative bacteria in acutesuppurative thyroiditis?

What are the two types ofchronic thyroiditis?

What are the features ofHashimoto’s (chronic)thyroiditis?

What is the claim to fame ofHashimoto’s disease?

What is the etiology ofHashimoto’s disease?

What lab tests should beperformed to diagnoseHashimoto’s disease?

What is the medicaltreatment for Hashimoto’sthyroiditis?

Glandular swelling, tenderness, often follows URI, elevated ESR

Viral infection

Supportive: NSAIDS, � steroids

Just another name for SUBACUTEthyroiditis caused by a virus (Think: De QuerVain � Virus)

Alphabetically: A before S, B before V(i.e., Acute before Subacute and Bacterial before Viral and thus: Acute �Bacterial and Subacute � Viral)

Streptococcus or Staphylococcus

1. Hashimoto’s thyroiditis2. Riedel’s thyroiditis

Firm and rubbery gland, 95% in women,lymphocyte invasion

Most common cause of hypothyroidismin the United States

Autoimmune (Think: HashimOTO �AUTO; thus, Hashimoto � autoimmune)

Antithyroglobulin and microsomalantibodies

Thyroid hormone replacement ifhypothyroid (surgery is reserved forcompressive symptoms and/or if cancerneeds to be ruled out)


What is Riedel’s thyroiditis?

What is the treatment forRiedel’s thyroiditis?


Benign inflammatory thyroidenlargement with fibrosis of thyroid

Patients present with painless, large thyroidFibrosis may involve surrounding tissues

Surgical tracheal decompression, thyroidhormone replacement as needed—possibly steroids/tamoxifen if refractory

ANATOMY

ParathyroidChapter 59

Usually four (two superior and twoinferior)

�5% (Think: 5 � 5)

�10%

Posterior and lateral behind the thyroidand below the inferior thyroid artery

Thymus gland

�1%

Thyroid glandThymus/mediastinumCarotid sheathTracheoesophageal grooveBehind the esophagus

How many parathyroids arethere?

What percentage of patientshave five parathyroid glands?

What percentage of patientshave three parathyroidglands?

What is the usual position ofthe inferior parathyroidglands?

What is the most commonsite of an “extra” gland?

What percentage of patientshave a parathyroid gland inthe mediastinum?

If only three parathyroidglands are found at surgery,where can the fourth one be hiding?


What is the embryologicorigin of the followingstructures:

Superior parathyroidglands?

Inferior parathyroidglands?

What supplies blood to theparathyroid glands?

What percentage of patientshave all four parathyroidglands supplied by theinferior thyroid arteriesexclusively?

What is DiGeorge’ssyndrome?

What is the most commoncause of hypercalcemia inhospitalized patients?

What is the most commoncause of hypercalcemia inoutpatients?

Chapter 59 / Parathyroid 453

Fourth pharyngeal pouch

Third pharyngeal pouch(counterintuitive)

Inferior thyroid artery

�80%

Congenital absence of the parathyroidglands and the thymus

Cancer

Hyperparathyroidism

PHYSIOLOGY

What cell type producesPTH?

What are the major actionsof PTH?

How does vitamin D work?


Chief cells produce ParaThyroidHormone (PTH)

Increases blood calcium levels (takesfrom bone breakdown, GI absorption,increased resorption from kidney,excretion of phosphate by kidney),decreases serum phosphate

Increases intestinal absorption of calciumand phosphate

Duodenum and proximal jejunum



HYPERPARATHYROIDISM (HPTH)

Define primary HPTH.

Define secondary HPTH.

Define tertiary HPTH.

What are the methods ofimaging the parathyroids?

What are the indications fora localizing preoperativestudy?

What is the most commoncause of primary HPTH?

What are the etiologies of primary HPTH andpercentages?

What is the incidence ofprimary HPTH in theUnited States?

What are the risk factors forprimary HPTH?

Increased secretion of PTH by parathyroidgland(s); marked by elevated calcium,low phosphorus

Increased serum PTH resulting fromcalcium wasting caused by renal failureor decreased GI calcium absorption,rickets or osteomalacia; calcium levelsare usually low

Persistent HPTH after correction ofsecondary hyperparathyroidism; resultsfrom autonomous PTH secretion notresponsive to the normal negativefeedback due to elevated Ca�� levels

Surgical operationUltrasoundSestamibi scan201TI (technetium)–thallium subtraction

scanCT/MRIA-gram (rare)Venous sampling for PTH (rare)

Reoperation for recurrenthyperparathyroidism

Adenoma (�85%)

Adenoma (�85%)Hyperplasia (�10%)Carcinoma (�1%)

�1/1000–4000

Family history, MEN-I and MEN-IIa,irradiation


What are the signs/symptoms of primary HPTHhypercalcemia?

What is the “33 to 1” rule?

What plain x-ray findings areclassic for HPTH?

How is primary HPTHdiagnosed?

What is familial hypocalciurichypercalcemia?

How many of the glands areUSUALLY affected by thefollowing conditions:

Hyperplasia?

Adenoma?

Carcinoma?

What percentage of adenomasare not single but found inmore than one gland?


“Stones, bones, groans, andpsychiatric overtones”:

Stones: Kidney stonesBones: Bone pain, pathologic

fractures, subperiosteal resorptionGroans: Muscle pain and weakness,

pancreatitis, gout, constipationPsychiatric overtones: Depression,

anorexia, anxietyOther symptoms: Polydipsia, weight

loss, HTN (10%), polyuria, lethargy

Most patients with primary HPTH have aratio of serum (Cl�) to phosphate �33

Subperiosteal bone resorption (usually inhand digits; said to be “pathognomonic”for HPTH!)

Labs—elevated PTH (hypercalcemia, T phosphorus, c chloride); urine calciumshould be checked for familialhypocalciuric hypercalcemia

Familial (autosomal-dominant)inheritance of a condition ofasymptomatic hypercalcemia and low urine calcium, with or without elevated PTH; in contrast,hypercalcemia from HPTH results inhigh levels of urine calcium

Note: Surgery to remove parathyroidglands is not indicated for this diagnosis

4

1

1

�5%


What is the differentialdiagnosis of hypercalcemia?

What is the initial medicaltreatment of hypercalcemia(1� HPTH)?

What is the definitivetreatment of HPTH in thefollowing cases:

Primary HPTH resultingfrom HYPERPLASIA?

Primary HPTH resultingfrom parathyroidADENOMA?

Primary HPTH resultingfrom parathyroidCARCINOMA?

Secondary HPTH?


“CHIMPANZEES”:Calcium overdoseHyperparathyroidism (1�/2�/3�),Hyperthyroidism, Hypocalciuric

Hypercalcemia (familial)Immobility/Iatrogenic (thiazide

diuretics)Metastasis/Milk alkali syndrome (rare)Paget’s disease (bone)Addison’s disease/acromegalyNeoplasm (colon, lung, breast,

prostate, multiple myeloma)Zollinger-Ellison syndromeExcessive vitamin DExcessive vitamin ASarcoid

Medical—IV fluids, furosemide—NOTthiazide diuretics

Neck exploration removing allparathyroid glands and leaving at least 30 mg of parathyroid tissue placed in theforearm muscles (nondominant arm, ofcourse!)

Surgically remove adenoma (send forfrozen section) and biopsy all abnormallyenlarged parathyroid glands (someexperts biopsy all glands)

Remove carcinoma, ipsilateral thyroidlobe, and all enlarged lymph nodes (modified radical neck dissection for LN metastases)

Correct calcium and phosphate; performrenal transplantation (no role forparathyroid surgery)



Tertiary HPTH?

Why place 30 to 40 mg ofsliced parathyroid gland inthe forearm?

What must be ruled out inthe patient with HPTH fromhyperplasia?

What carcinomas arecommonly associated withhypercalcemia?

What is the most likelydiagnosis if a patient has aPALPABLE neck mass,hypercalcemia, and elevatedPTH?

Correct calcium and phosphate; performsurgical operation to remove all parathyroidglands and reimplant 30 to 40 mg in theforearm if REFRACTORY to medicalmanagement

To retain parathyroid function; if HPTHrecurs, remove some of the parathyroidgland from the easily accessible forearm

MEN type I and MEN type IIa

Breast cancer metastases, prostatecancer, kidney cancer, lung cancer,pancreatic cancer, multiple myeloma

Parathyroid carcinoma (vast majority of other causes of primary HPTH havenonpalpable parathyroids)

PARATHYROID CARCINOMA

What is it?

What is the number ofglands usually affected?


What is the common tumormarker?


Primary carcinoma of the parathyroidgland

1

Hypercalcemia, elevated PTH, PALPABLE parathyroid gland (50%),pain in neck, recurrent laryngeal nerveparalysis (change in voice), hypercalcemiccrisis (usually associated with calciumlevels �14)

Human Chorionic Gonadotropin (HCG)

Surgical resection of parathyroid masswith ipsilateral thyroid lobectomy,ipsilateral lymph node resection


What percentage of all cases of primary HPTH are caused by parathyroidcarcinoma?


1%

POSTOPERATIVE COMPLICATIONS OF PARATHYROIDECTOMY

What are the possiblepostoperative complicationsafter a parathyroidectomy?

What is “hungry bonesyndrome”?

What are the signs/symptoms of postoperativehypocalcemia?

What is the treatment ofhypoparathyroidism?

What is parathyromatosis?

Recurrent nerve injury (unilateral: voicechange; bilateral: airway obstruction),neck hematoma (open at bedside ifbreathing is compromised), hypocalcemia,superior laryngeal nerve injury

Severe hypocalcemia seen after surgicalcorrection of HPTH as chronicallycalcium-deprived bone aggressivelyabsorbs calcium

Perioral tingling, paresthesia,�Chvostek’s sign, �Trousseau’s sign, �tetany

Acute: IV calciumChronic: PO calcium, and vitamin D

Multiple small hyperfunctioningparathyroid tissue masses found over theneck and mediastinum—thought to befrom congenital rests or spillage duringsurgery—remove surgically (RARE)

Which arteries supply thespleen?

What is the venous drainageof the spleen?

Spleen andSplenectomy

Chapter 60

Splenic artery (a branch of the celiactrunk) and the short gastric arteries thatarise from the gastroepiploic arteries

Portal vein, via the splenic vein and theleft gastroepiploic vein


What is said to “tickle” thespleen?

What percentage of peoplehave an accessory spleen?

What percentage of the totalbody platelets are stored inthe spleen?

What are the functions ofthe human spleen?

What is “delayed splenicrupture”?

What are the signs/symptomsof ruptured/injured spleen?

What is Kehr’s sign?

What is Ballance’s sign?

What is Seagesser’s sign?

How is a spleen injurydiagnosed?


Chapter 60 / Spleen and Splenectomy 459

Tail of the pancreas

�20%

33%

Filters abnormal RBCs (does NOT storeRBCs like canine spleen!), stores platelets,produces tuftsin and properdin (opsins),produces antibodies (especially IGM) andis site of phagocytosis

Subcapsular hematoma orpseudoaneurysm may rupture some timeafter blunt trauma, causing “delayedsplenic rupture”; rupture classicallyoccurs about 2 weeks after the injury andpresents with shock/abdominal pain

Hemoperitoneum and Kehr’s sign, LUQabdominal pain, Ballance’s sign

Left shoulder pain seen with splenicrupture

LUQ dullness to percussion

Phrenic nerve compression causing necktenderness in splenic rupture

Abdominal CT, if the patient is stable;DPL or FAST exam if the patient isunstable

1. Nonoperative in a stable patient withan isolated splenic injury without hilarinvolvement/complete rupture

2. If patient is unstable, DPL/FASTlaparotomy with splenorrhaphy orsplenectomy

3. Embolization is an option in selectedpatients


What is a splenorrhaphy?

What are the otherindications for splenectomy:

Malignant diseases?

Anemias?

Thrombocytopenia?

Miscellaneousindications?

Is G6PD deficiency anindication for splenectomy?

What are the possiblepostsplenectomycomplications?

What causes OPSS?


Splenic salvage operation: wrapping vicralmesh, aid of topical hemostatic agents orpartial splenectomy, sutures (buttressed)

Hodgkin’s staging not conclusive by CTscan (rare)

Splenic tumors (primary/metastatic/locally invasive)

Hypersplenism caused by otherleukemias/non-Hodgkin’s lymphomas

Medullary fibrosis with myeloidmetaplasia

Hereditary elliptocytosisSickle cell anemia (rare, most

autosplenectomize)Pyruvate kinase deficiencyAutoimmune hemolytic anemiaHereditary spherocytosisThalassemias (e.g., -thalassemia major

a.k.a. Cooley’s)

ITP (Idiopathic Thrombocytopenic Purpura)

TTP (Thrombotic ThrombocytopenicPurpura)

Variceal bleeding with splenic veinthrombosis, Gaucher’s disease, splenicabscess, refractory splenic cysts,hypersplenism, Felty’s syndrome

NO

Thrombocytosis, subphrenic abscess,atelectasis, pancreatitis gastric dilation,and Overwhelming PostSplenectomySepsis (OPSS)

Increased susceptibility to fulminant bacteremia, meningitis, or pneumoniabecause of loss of splenic function


What is the incidence ofOPSS in adults?

What is the incidence andoverall mortality of OPSS inchildren?

What is the typicalpresentation of OPSS?

What are the commonorganisms associated withOPSS?

What is the most commonbacteria in OPSS?

What is the preventivetreatment of OPSS?

What is the best time to give immunizations tosplenectomy patients?

What lab tests are abnormalafter splenectomy?

What are the findings onpostsplenectomy RBCsmear?

When and how shouldthrombocytosis be treated?

What is the most commoncause of splenic veinthrombosis?

What opsonins does thespleen produce?

Chapter 60 / Spleen and Splenectomy 461

1%

1% to 2% with 50% mortality rate

Fever, lethargy, common cold, sorethroat, URI followed by confusion, shock,and coma with death ensuing within 24hours in up to 50% of patients

Encapsulated: Streptococcuspneumoniae, Neisseria meningitides, H. influenzae

Streptococcus pneumoniae

Vaccinations for pneumococcus, H. influenzae, and meningococcus

Prophylactic penicillin for all minorinfections/illnesses and immediatemedical care if febrile illness develops

Preoperatively, if at all possibleIf emergent, then 2 weeks

postoperatively

WBC count increases by 50% over the baseline; marked thrombocytosisoccurs; RBC smear is abnormal

Peripheral smear will showPappenheimer bodies, Howell-Jollybodies, and Heinz bodies

When platelet count is �1 million, mostsurgeons will treat with aspirin

Pancreatitis

PROperdin, TUFtsin (Think:“PROfessionally TUF spleen”)


What is the most commoncause of ISOLATEDGASTRIC varices?

What is the treatment ofgastric varices caused bysplenic vein thrombosis?

Which patients develophyposplenism?

What vaccinations shouldevery patient with asplenectomy receive?

Define hypersplenism.

Define splenomegaly.

What is idiopathic thrombocytopenic purpura (ITP)?

What is the most commoncause of failure to correctthrombocytopenia aftersplenectomy for ITP?

What are the “I’s” of ITP?

What is TTP?


Splenic vein thrombosis (usually frompancreatitis)

Splenectomy

Patients with ulcerative colitis

PneumococcusMeningococcusHaemophilus influenzae type B

Hyperfunctioning spleenDocumented loss of blood elements

(WBC, Hct, platelets)Large spleen (splenomegaly)Hyperactive bone marrow (trying to keep

up with loss of blood elements)

Enlarged spleen

Autoimmune (antiplatelet antibodies IgGin �90% of patients) platelet destructionleading to troublesome bleeding andpurpura

Missed accessory spleen

Immune etiology (IgG antiplatelets ABs)Immunosuppressive treatment (initially

treated with steroids)Immune globulinImprovement with splenectomy (75% of

patients have improved platelet countsafter splenectomy)

Thrombotic Thrombocytopenic Purpura


What is the treatment ofchoice for TTP?

What is the most commonphysical finding of portalhypertension?

Chapter 61 / Surgically Correctable Hypertension 463

Plasmapheresis (splenectomy reserved asa last resort—very rare)

Splenomegaly

What is it?

What percentage of patientswith HTN have a surgicallycorrectable cause?

What diseases that causeHTN are surgicallycorrectable?

What is the formula forpressure?

SurgicallyCorrectable HTN

Chapter 61

Hypertension caused by conditions thatare amenable to surgical correction

�7%

Think “CAN I CHURP?”:Cushing’s syndromeAortic coarctationNeuroblastoma/neoplasia

Increased intracranial pressure

Conn’s syndrome (primaryhyperaldosteronism)

Hyperparathyroidism/hyperthyroidismUnilateral renal parenchymal diseaseRenal artery stenosisPheochromocytoma

Pressure � flow � resistance or P �F � R (Think: Power FoRward); thus, an increase in flow, resistance, or both,results in an increase in pressure



SOFT TISSUE SARCOMAS

Soft TissueSarcomas andLymphomas

Chapter 62

Soft tissue tumors, derived from mesoderm

“Fish flesh”

50% of sarcomas are in the extremitiesand are 3.5� more common in thelower extremity (thigh)

0.6% of malignant tumors

55 years

“RALES”:RadiationAIDS (Immunosuppression)LymphedemaExposure to chemicalsSyndromes (e.g., Gardner’s/Li-Fraumeni)

Liposarcoma

GIST (GastroIntestinal Stromal Tumor)

Malignant fibrous histiocytoma

Rhabdomyosarcoma

Angiosarcoma

Fibrosarcoma

What are they?

Sarcoma means what inGREEK?

Sarcomas are more commonin upper or lowerextremities?

How common are they?

What is the median age atdiagnosis?


Name the following types ofmalignant sarcoma:

Fat

Gastrointestinal

Myofibroblast

Striated muscle

Vascular endothelium

Fibroblast


Lymph vessel

Peripheral nerve

AIDS

Lymphedema


How do most sarcomasmetastasize?

What is the most commonlocation and route ofmetastasis?

What tests should be donein the preoperative workup?

What are the three mostcommon malignant sarcomasin adults?

What are the two mostcommon in children?

What is the most commontype to metastasize to thelymph nodes?

What is the most common sarcoma of theretroperitoneum?

How do sarcomas locallyinvade?


Chapter 62 / Soft Tissue Sarcomas and Lymphomas 465

Lymphangiosarcoma

Malignant neurilemmoma orschwannoma

Kaposi’s sarcoma

Lymphangiosarcoma

Soft tissue mass; pain from compressionof adjacent structures, often noticed afterminor trauma to area of mass

Hematogenously (i.e., via blood)

Lungs via hematogenous route

CXR, � chest CT, LFTs

Fibrous histiocytoma (25%)Liposarcoma (20%)Leiomyosarcoma (15%)

Rhabdomyosarcoma (about 50%),fibrosarcoma (20%)

Malignant fibrous histiocytoma

Liposarcoma

Usually along anatomic planes such asfascia, vessels, etc.

Imaging workup—MRI is superior to CT at distinguishing the tumor fromadjacent structures

Mass �3 cm: excisional biopsyMass �3 cm: incisional biopsy or core

biopsy


Define excisional biopsy.

Define incisional biopsy.

What is the orientation ofincision for incisional biopsyof a suspected extremitysarcoma?

Define core biopsy.

What determines histologicgrade of sarcomas?

Define the followingAmerican Joint Committeefor Cancer Staging (AJCC)Sarcoma Stages:

Stage I

Stage IIA

Stage IIB

Stage III

Stage IV

What is a pseudocapsule andwhat is its importance?

What is the most importantfactor in the prognosis?


Biopsy by removing the entire mass

Biopsy by removing a piece of the mass

Longitudinal, not transverse, so that theincision can be incorporated in a futureresection if biopsy for sarcoma is positive

Large-bore needle that takes a core oftissue (like a soil sample)

1. Differentiation2. Mitotic count3. Tumor necrosisGrade 1 � well differentiatedGrade 2 � moderately differentiatedGrade 3 � poorly differentiated

Well differentiated (grade 1), any size, nonodes, no metastases

�5 cm, grade 2 or grade 3

�5 cm, grade 2

Positive nodes or �5 cm and grade 3

Distant metastases

Outer layer of a sarcoma that representscompressed malignant cells; microscopicextensions of tumor cells invade throughthe pseudocapsule into adjacentstructures—thus, definitive therapy mustinclude a wide margin of resection toaccount for this phenomenon and notjust be “shelled-out” like a benign growth

Histologic grade of the primary lesion



What surgical margins areobtained?

What is the “limb-sparing”surgery for extremitysarcoma?

What is the treatment ofpulmonary metastasis?

What tests should be donein the follow-up?

What syndrome of lymphan-giosarcoma arises in chroniclymphedema after axillarydissection for breast cancer?

What syndrome is associatedwith breast cancer and softtissue sarcoma?

Chapter 62 / Soft Tissue Sarcomas and Lymphomas 467

Surgical resection and radiation (with orwithout chemotherapy)

2 cm (1 cm minimum)

Avoidance of amputation with localresection and chemoradiation

Surgical resection for isolated lesions

Physical examination, CXR, repeat CT/MRI of the area of resection to look forrecurrence

Stewart-Treves syndrome

Li-Fraumeni syndrome (p53 tumorsuppressor gene mutation)

LYMPHOMA


What cell type is associatedwith the histology ofHodgkin’s disease?

What are the fourhistopathologic types of Hodgkin’s disease?

What are the indications fora “staging laparotomy” inHodgkin’s disease?

Cervical or axillary node excisional biopsy

Reed-Sternberg cells

1. Nodular sclerosing (most common;�50% of cases)

2. Mixed cellularity3. Lymphocyte predominant (best

prognosis)4. Lymphocyte depleted

Rarely performedMost experts rely on CT scans, PET

scans, bone marrow biopsy, and otherdirected imaging and biopsies


Define the stages (Ann Arbor)of Hodgkin’s disease:

Stage I

Stage II

Stage III

Stage IV

What is stage A Hodgkin’s?

What is stage B Hodgkin’s?

What is the “E” on thestaging?

What treatments are usedfor low versus advancedstage Hodgkin’s lymphoma?

What percentage of patientswith Hodgkin’s disease canbe cured?


Single lymph node region (Think: Stage 1 � 1 region)

Two or more lymph node regions on the same side of the diaphragm(Think: Stage 2 � �2 regions)

Involvement on both sides of thediaphragm

Diffuse and/or disseminated involvement

Asymptomatic (Think: Asymptomatic �stage A)

Symptomatic: weight loss, fever, nightsweats, etc. (Think: Stage B � Bad)

Extralymphatic site involvement (E � Extralymphatic)

Low stage: radiotherapyAdvanced stage: chemotherapy

�80%

GI LYMPHOMA

What is it?

What is the risk factor forgastric lymphoma?


What is the treatment ofintestinal lymphoma?

What is the most commonsite of primary GI tractlymphoma?

Non-Hodgkin’s lymphoma arising in theGI tract

Helicobacter pylori

Abdominal pain, obstruction, GIhemorrhage, GI tract perforation, fatigue

Surgical resection with removal ofdraining lymph nodes and chemotherapy

Stomach (66%) (see Maltoma, p. 281)


Chapter 63 / Skin Lesions 469

Skin LesionsChapter 631. Basal cell carcinoma (75%)2. Squamous cell carcinoma (20%)3. Melanoma (4%)

Melanoma

A redundancy! All melanomas are considered malignant!

What are the most commonskin cancers?

What is the most commonfatal skin cancer?

What is malignantmelanoma?

SQUAMOUS CELL CARCINOMA

What is it?

What are the most commonsites?


What is a precursor skinlesion?




What is the dreaded sign ofmetastasis?

What is Marjolin’s ulcer?

Carcinoma arising from epidermal cells

Head, neck, and hands

Sun exposure, pale skin, chronic inflammatory process, immunosuppression,xeroderma pigmentosum, arsenic

Actinic keratosis

Raised, slightly pigmented skin lesion;ulceration/exudate; chronic scab; itching

Small lesion—excisional biopsyLarge lesions—incisional biopsy

Small lesion (�1 cm): Excise with 0.5-cmmargin

Large lesion (�1 cm): Resect with 1- to 2-cm margins of normal tissue (largelesions may require skin graft/flap)

Palpable lymph nodes (remove involvedlymph nodes)

Squamous cell carcinoma that arises in anarea of chronic inflammation (e.g., chronicfistula, burn wound, osteomyelitis)



What is the treatment forsolitary metastasis?


Excellent if totally excised (95% cure rate);most patients with positive lymph nodemetastasis eventually die from metastaticdisease

Surgical resection

BASAL CELL CARCINOMA

What is it?






What is the risk of metastasis?

Carcinoma arising in the germinatingbasal cell layer of epithelial cells

Sun exposure, fair skin, radiation, chronicdermatitis, xeroderma pigmentosum

Head, neck, and hands

Slow-growing skin mass (chronic, scaly);scab; ulceration, with or without pigmen-tation, often described as “pearl-like”

Excisional or incisional biopsy

Resection with 5-mm margins (2-mmmargin in cosmetically sensitive areas)

Very low (recur locally)

MISCELLANEOUS SKIN LESIONS

What is an Epidermal Inclusion Cyst?

What is a sebaceous cyst?

EIC � Benign subcutaneous cyst filledwith epidermal cells (should be removedsurgically) filled with waxy material; noclinical difference from a sebaceous cyst

Benign subcutaneous cyst filled withsebum (waxy, paste-like substance) from a blocked sweat gland (should beremoved with a small area of skin thatincludes the blocked gland); may becomeinfected; much less common than EIC


What is actinic keratosis?

What is seborrheickeratosis?

How to remember actinickeratosis vs. seborrheic keratosis malignantpotential?

What is Bowen’s disease ofthe skin?

What is “Mohs” surgery?

Chapter 64 / Melanoma 471

Premalignant skin lesion from sun exposure; seen as a scaly skin lesion (surgical removal eliminates the 20% riskof cancer transformation)

Benign pigmented lesion in the elderly;observe or treat by excision (especially if there is any question of melanoma),curettage, or topical agents

Actinic Keratosis � AK � Asset Kicker �premalignant

Seborrheic Keratosis � SK � Soft Kicker � benign

Squamous carcinoma in situ (should beremoved or destroyed, thereby removingthe problem)

Mohs technique or surgery: repeats thin excision until margins are clear by microscopic review (named after Dr. Mohs)—used to minimize collateralskin excision (e.g., on the face)

What is it?

Which patients are at greatest risk?

What are the most commonsites (3)?

MelanomaChapter 64Neoplastic disorder produced by malignant transformation of themelanocyte; melanocytes are derivedfrom neural crest cells

White patients with blonde/red hair, fairskin, freckling, a history of blisteringsunburns, blue/green eyes, actinic keratosis

Male � female

1. Skin2. Eyes3. Anus(Think: SEA � Skin, Eyes, Anus)


What is the most commonsite in African Americans?

What characteristics aresuggestive of melanoma?

What are the “ABCDs” ofmelanoma?


How does location differ inmen and women?

Which locations areunusual?

What is the most commonsite of melanoma in men?

What is the most commonsite of melanoma in women?

What are the four major histologic types?

Define the following terms:Superficial spreadingmelanoma


Palms of the hands, soles of the feet(acral lentiginous melanoma)

Usually a pigmented lesion with an irregular border, irregular surface, orirregular coloration

Other clues: darkening of a pigmentedlesion, development of pigmentedsatellite lesions, irregular margins orsurface elevations, notching, recent or rapid enlargement, erosion orulceration of surface, pruritus

AsymmetryBorder irregularityColor variationDiameter �6 mm and Dark lesion

Severe sunburn before age 18, giant congenital nevi, family history, race(White), ultraviolet radiation (sun), multiple dysplastic nevi

Men get more lesions on the trunk;women on the extremities

Noncutaneous regions, such as mucousmembranes of the vulva/vagina, anorectum,esophagus, and choroidal layer of the eye

Back (33%)

Legs (33%)

1. Superficial spreading2. Lentigo maligna3. Acral lentiginous4. Nodular

Occurs in both sun-exposed andnon-exposed areas; most commonof all melanomas (75%)


Lentigo malignamelanoma

Acral lentiginousmelanoma

Nodular melanoma

Amelanotic melanoma

What is the most commontype of melanoma?

What type of melanomaarises in Hutchinson’sfreckle?

What is Hutchinson’sfreckle?


Malignant cells that are superficial, foundusually in elderly patients on the heador neck

Called “Hutchinson’s freckle” if noninvasive

Least aggressive type; very good prognosis

Accounts for �10% of all melanomas

Occurs on the palms, soles, subungualareas, and mucous membranes

Accounts for �5% of all melanomas (most common melanoma in African American patients; �50%)

Vertical growth predominatesLesions are usually darkMost aggressive type/worst prognosisAccounts for �15% of all melanomas

Melanoma from melanocytes but withobvious lack of pigment

Superficial spreading (�75%) (Think:SUPERficial � SUPERior)

Lentigo maligna melanoma

Lentigo maligna melanoma in the radialgrowth phase without vertical extension (noninvasive); usually occurs on the faces of elderly women

STAGING

What are the American JointCommittee on Cancer(AJCC) stages simplified:

IA?

IB?

�1 mm without ulceration

�1 mm with ulceration or 1–2 mm without ulceration


IIA?

IIB?

IIC?

III?

IV?

What are the common sitesof metastasis?

What are the metastaticroutes?


What is the role of shavebiopsy?

What is the “sentinel node”biopsy?

When is elective lymph nodedissection recommended?


1–2 mm with ulceration or 2–4 mm without ulceration

2–4 mm with ulceration or �4 mm without ulceration

�4 mm with ulceration

Positive nodes

Distant metastases

Nodes (local)Distant: lung, liver, bone, heart, and

brainMelanoma has a specific attraction for

small bowel mucosa and distant cutaneous sites

Brain metastases are a common cause ofdeath

Both lymphatic and hematogenous

Excisional biopsy (complete removalleaving only normal tissue) or incisionedbiopsy for very large lesions(Note: Early diagnosis is crucial)

No role

Inject Lymphazurin® blue dye, colloidwith a radiolabel, or both around themelanoma; the first LN in the drainingchain is identified as the “sentinel lymphnode” and reflects the metastatic status ofthe group of lymph nodes

Controversial—possible advantage inmelanomas 1 to 2 mm in depth but jurystill out; sentinel node biopsy if �1 mmis becoming very common


What is the recommendedsize of the surgical marginfor depth of invasion:

Melanoma in situ?

�1 mm thick?

1–4 mm thick?

�4 mm thick?

What is the treatment fordigital melanoma?

What is the treatment ofpalpable lymph node metastasis?

What factors determine theprognosis?

What is the workup tosurvey for metastasis in thepatient with melanoma?

What is the treatment ofintestinal metastasis?

Which malignancy is mostlikely to metastasize to thebowel?

What is the surgicaltreatment of nodal metastasis?

What is FDA-approved adjuvant therapy?


0.5-cm margin

1-cm margin

2-cm margin

3-cm margin

Amputation

Lymphadenectomy

Depth of invasion and metastasis are the most important factors (Superficialspreading and lentigo maligna have a better prognosis because they have alonger horizontal phase of growth andare thus diagnosed at an earlier stage;nodular has the worst prognosis becauseit grows predominantly vertically andmetastasizes earlier)

Physical exam, LFTs, CXR (bonescan/CT/MRI reserved for symptoms)

Surgical resection to preventbleeding/obstruction

Melanoma

Lymphadenectomy

Interferon alpha-2b (for stages IIB/III)


What is the treatment ofunresectable brain metastasis?

What is the treatment of isolated adrenal metastasis?

What is the treatment of isolated lung metastasis?

What is the most commonsymptom of anal melanoma?

What is the treatment ofanal melanoma?

What other experimentaltherapy is available formetastatic disease?

What is the median survivalwith distant metastasis?


Radiation

Surgical resection

Surgical resection

Bleeding

APR or wide excision (no survival benefitfrom APR, but better local control)

1. Monoclonal antibodies2. Chemotherapy (e.g., dacarbazine)3. Vaccinations

�6 months

INTENSIVE CARE UNIT (ICU) BASICS

Surgical IntensiveCare

Chapter 65

By systems:Neurologic (e.g., GCS, MAE, pain

control)Pulmonary (e.g., vent settings)CVS (e.g., pressors, Swan numbers)GI (gastrointestinal)Heme (CBC)FEN (e.g., Chem 10, nutrition)Renal (e.g., urine output, BUN, Cr)ID (e.g., Tmax, WBC, antibiotics)AssessmentPlan(Note: physical exam included in eachsection)

How is an ICU note written?


What is the best way toreport urine output in theICU?

What are the possible causesof fever in the ICU?

What is the most commonbacteria in ICU pneumonia?

What is the acronym for thebasic ICU care checklist (Dr. Vincent)?

Chapter 65 / Surgical Intensive Care 477

24 hrs/last shift/last 3 hourly rate �“urine output has been 2 liters over last24 hrs, 350 last shift, and 45, 35, 40 ccover the last 3 hours”

Central line infectionPneumonia/atelectasisUTI, urosepsisIntra-abdominal abscessSinusitisDVTThrombophlebitisDrug feverFungal infection, meningitis, wound

infectionEndocarditis

Gram-negative rods

“FAST HUG”:FeedingAnalgesiaSedationThromboembolic prophylaxis

Head-of-bed elevation (pneumonia prevention)

Ulcer preventionGlucose control

INTENSIVE CARE UNIT FORMULAS AND TERMSYOU SHOULD KNOW

What is CO?

What is the normal CO?

What factors increase CO?

What is CI?

Cardiac Output: HR (heart rate) � SV(stroke volume)

4–8 L/min

Increased contractility, heart rate, andpreload; decreased afterload

Cardiac Index: CO/BSA (body surfacearea)


What is the normal CI?

What is SV?

What is the normal SV?

What is CVP?

What is the normal CVP?

What is PCWP?

What is the normal PCWP?

What is anion gap?

What are the normal valuesfor anion gap?

Why do you get anincreased anion gap?

What are the causes ofincreased anion gap acidosisin surgical patients?

Define MODS.

What is SVR?

What is SVRI?


2.5–3.5 L/min/M2

Stroke Volume: the amount of bloodpumped out of the ventricle each beat;simply, end diastolic volume minus theend systolic volume or CO/HR

60–100 cc

Central Venous Pressure: indirect measurement of intravascular volume status

4–11

Pulmonary Capillary Wedge Pressure:indirectly measures left atrial pressure,which is an estimate of intravascular volume (LV filling pressure)

5–15

Na� � (Cl– � HCO–3)

10–14

Unmeasured acids are unmeasuredanions in the equation that are part of the“counterbalance” to the sodium cation

Think “SALUD”:StarvationAlcohol (ethanol/methanol)Lactic acidosisUremia (renal failure)DKA

Multiple Organ Dysfunction Syndrome

Systemic Vascular Resistance: MAP – CVP / CO � 80 (remember, P � F � R, Power FoRward; and calculating resistance: R � P/F)

Systemic Vascular Resistance Index:SVR/BSA


What is the normal SVRI?

What is MAP?

What is PVR?

What is the normal PVR value?

What is the formula for arterial oxygen content?

What is the basic formulafor oxygen delivery?

What is the full formula foroxygen delivery?

What factors can increaseoxygen delivery?

What is mixed venousoxygen saturation?

Which lab values help assessadequate oxygen delivery?

What is FENa?

What is the memory aid forcalculating FENa?


1500–2400

Mean Arterial Pressure: diastolic bloodpressure � 1/3 (systolic–diastolic pressure) (Note: Not the mean between diastolicand systolic blood pressure because diastole lasts longer than systole)

Pulmonary Vascular Resistance:PA(MEAN) – PCWP / CO � 80 (PA ispulmonary artery pressure and LA is leftatrial or PCWP pressure)

100 � 50

Hemoglobin � O2 saturation (SaO2) � 1.34

CO � (oxygen content)

CO � (1.34 � Hgb � SaO2) � 10

Increased CO by increasing SV, HR, orboth; increased O2 content by increasingthe hemoglobin content, SaO2, or both

SvO2; simply, the O2 saturation of theblood in the right ventricle or pulmonaryartery; an indirect measure of peripheraloxygen supply and demand

SvO2 (low with inadequate delivery), lactic acid (elevated with inadequatedelivery), pH (acidosis with inadequatedelivery), base deficit

Fractional Excretion of Sodium (Na�):(UNa� � Pcr / PNa� � Ucr) � 100

Think: YOU NEED PEE � U (Urine) N (Na�) P (Plasma); UNa� � Pcr; for the denominator, switch everything, PNa� � Ucr (cr � creatinine)


What is the prerenal FENavalue?

How long does Lasix® effectlast?

What is the formula forflow/pressure/resistance?

What is the “10 for 0.08 rule”of acid-base?

What is the “40, 50, 60 for70, 80, 90 rule” for O2 sats?

One liter of O2 via nasal cannula raises FiO2 by howmuch?

What is pure respiratory acidosis?

What is pure respiratoryalkalosis?

What is pure metabolic acidosis?

What is pure metabolic alkalosis?

List how the body compensates for each of the following:

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

What does MOF stand for?

What does SIRS stand for?


�1.0; renal failure from decreased renalblood flow (e.g., cardiogenic, hypovolemia,arterial obstruction, etc.)

6 hours � LASIX � LAsts SIX hours

Remember Power FoRward: Pressure �Flow � Resistance

For every increase of PaCO2 by 10 mm Hg,the pH falls by 0.08

PaO2 of 40, 50, 60 corresponds roughlyto an O2 sat of 70, 80, 90, respectively

�3%

Low pH (acidosis), increased PaCO2, normal bicarbonate

High pH (alkalosis), decreased PaCO2,normal bicarbonate

Low pH, low bicarbonate, normal PaCO2

High pH, high bicarbonate, normalPaCO2

Increased bicarbonate

Decreased bicarbonate

Decreased PaCO2

Increased PaCO2

Multiple Organ Failure

Systemic Inflammatory ResponseSyndrome



SICU DRUGS

DOPAMINE

What is the site of actionand effect at the followinglevels:

Low dose (1–3 �g/kg/min)?

Intermediate dose (4–10 �g/kg/min)?

High dose (�10 �g/kg/min)?

Has “renal dose” dopaminebeen shown to decreaserenal failure?

�� dopa agonist; renal vasodilation(a.k.a. “renal dose dopamine”)

� 1, �� 1; positive inotropy and somevasoconstriction

�� 1 agonist; marked afterloadincrease from arteriolar vasoconstriction

NO

DOBUTAMINE

What is the site of action?

What is the effect?

�� 1 agonist, �� 2

c inotropy; c chronotropy, decrease insystemic vascular resistance

ISOPROTERENOL


What is the effect?

�� 1 and 2 agonist

c inotropy; c chronotropy; (� vasodilationof skeletal and mesenteric vascular beds)

EPINEPHRINE (EPI)


What is the effect?

What is the effect at highdoses?

�� 1, 2, �� 1, and 2 agonist

c inotropy; c chronotropy

Vasoconstriction

NOREPINEPHRINE (NE)


What is the effect?

�� 1, 2, �� 1, and 1 agonist

c inotropy; c chronotropy; �� increasein blood pressure



VASOPRESSIN

What is the action?

What are the indications?

Vasoconstriction (increases MAP, SVR)

Hypotension, especially refractory toother vasopressors (low-dose infusion—0.01–0.04 units per minute) or as a bolusduring ACLS (40 u)

NITROGLYCERINE (NTG)


What is the effect?

�� venodilation; � arteriolar dilation

Increased venous capacitance, decreasedpreload, coronary arteriole vasodilation

SODIUM NITROPRUSSIDE (SNP)


What is the effect?

What is the major toxicity ofSNP?

�� venodilation; �� arteriolardilation

Decreased preload and afterload (allowing blood pressure titration)

Cyanide toxicity

INTENSIVE CARE PHYSIOLOGY

Define the following terms:Preload

Afterload

Contractility

Compliance

What is the Frank-Starlingcurve?

Load on the heart muscle that stretchesit to end-diastolic volume (end-diastolicpressure) � intravascular volume

Load or resistance the heart must pumpagainst � vascular tone � SVR

Force of heart muscle contraction

Distensibility of heart by the preload

Cardiac output increases with increasingpreload up to a point

What is the effect at highdoses?

Severe vasoconstriction


What is the clinicalsignificance of the steepslope of the Starling curverelating end-diastolicvolume to cardiac output?

What factors influence theoxygen content of wholeblood?

What factors influencemixed venous oxygen saturation?

What lab test for tissueischemia is based on theshift from aerobic to anaerobic metabolism?

Define the following terms:Dead space

Shunt fraction

What causes increased deadspace?

At high shunt fractions, whatis the effect of increasingFiO2 on arterial PO2?


Demonstrates the importance of preloadin determining cardiac output

Oxygen content is composed largely ofthat oxygen bound to hemoglobin, and is thus determined by the hemoglobinconcentration and the arterial oxygen saturation; the partial pressure of oxygendissolved in plasma plays a minor role

Oxygen delivery (hemoglobinconcentration, arterial oxygen saturation,cardiac output) and oxygen extractionby the peripheral tissues

Serum lactic acid levels

That part of the inspired air that does notparticipate in gas exchange (e.g., thegas in the large airways/ET tube notin contact with capillaries)

Think: space � air

That fraction of pulmonary venous bloodthat does not participate in gas exchange

Think: shunt � blood

Overventilation (emphysema, excessivePEEP) or underperfusion (pulmonaryembolus, low cardiac output, pulmonaryartery vasoconstriction)

At high shunt fractions (�50%), changesin FiO2 have almost no effect on arterialPO2 because the blood that does “see” theO2 is already at maximal O2 absorption;thus, increasing the FiO2 has no effect(FiO2 can be minimized to preventoxygen toxicity)


Define ARDS.

What is the ARDS diagnostictriad?

What does the classic chestx-ray look like with ARDS?

How can you remember thePaO2 to FiO2, or PF, ratio?

At what concentration doesO2 toxicity occur?

What are the ONLY ventilatory parameters thathave been shown to decreasemortality in ARDS patients?

What are the main causes ofcarbon dioxide retention?

Why are carbohydrates minimized in the diet/TPNof patients having difficultywith hypercapnia?


Acute Respiratory Distress Syndrome:lung inflammation causing respiratoryfailure

“CXR”:Capillary wedge pressure �18X-ray of chest with bilateral infiltratesRatio of PaO2 to FiO2 �200

Bilateral fluffy infiltrates

Think: “PUFF” ratio: PF ratio � PaO2:FiO2 ratio

FiO2 of �60% � 48 hours; thus, try tokeep FiO2 below 60% at all times

Low tidal volumes (�6 cc/kg) and lowplateau pressures �30

Hypoventilation, increased dead spaceventilation, and increased carbon dioxideproduction (as in hypermetabolic states)

Respiratory Quotient (RQ) is the ratio ofCO2 production to O2 consumption andis highest for carbohydrates (1.0) andlowest for fats (0.7)

HEMODYNAMIC MONITORING

Why are indwelling arteriallines used for blood pressuremonitoring in critically illpatients?

Which pressures/values areobtained from a Swan-Ganzcatheter?

Because of the need for frequent measurements, the inaccuracy offrequently repeated cuff measurements,the inaccuracy of cuff measurements inhypotension, and the need for frequentarterial blood sampling/labs

CVP, PA pressures, PCWP, CO, PVR,SVR, mixed venous O2 saturation


Identify the Swan-Ganzwaveforms:


1. CVP/right atrium2. Right ventricle3. Pulmonary artery4. Wedge

What does the abbreviationPCWP stand for?

Give other names for PCWP.

What is it?

Pulmonary Capillary Wedge Pressure

Wedge or wedge pressure, pulmonaryartery occlusion pressure (PAOP)

Pulmonary capillary pressure afterballoon occlusion of the pulmonaryartery, which is equal to left atrialpressure because there are no valvesin the pulmonary system

Left atrial pressure is essentially equal toleft ventricular end diastolic pressure(LVEDP): left heart preload, and,thus, intravascular volume status.


What is the primary use ofthe PCWP?

Has the usage of a Swan-Ganz catheter been shownto decrease mortality in ICUpatients?


As an indirect measure of preload �intravascular volume

NO

MECHANICAL VENTILATION

Define ventilation.

Define oxygenation.

What can increaseventilation to decreasePCO2?

What is minute ventilation?

Define tidal volume.

Are ventilation and oxygenation related?

What can increase PO2

(oxygenation) in theventilated patient?

What can decrease PCO2 inthe ventilated patient?

Define the following modes:IMV

Air through the lungs; monitored by PCO2

Oxygen delivery to the alveoli; monitoredby O2 sats and PO2

Increased respiratory rate (RR),increased tidal volume (minuteventilation)

Volume of gas ventilated through thelungs (RR � tidal volume)

Volume delivered with each breath;should be 6 to 8 cc/kg on the ventilator

Basically no; you can have an O2 sat of100% and a PCO2 of 150; O2 sats do not tellyou anything about the PCO2 (key point!)

Increased FiO2

Increased PEEP

Increased RRIncreased tidal volume (i.e., increase

minute ventilation)

Intermittent Mandatory Ventilation:mode with intermittent mandatory ventilations at a predetermined rate;patients can also breathe on their ownabove the mandatory rate without helpfrom the ventilator


SIMV

A-C

CPAP

Pressure support

APRV

HFV

What are the effects of positive pressure ventilationin a patient with hypovolemiaor low lung compliance?

Define PEEP.


Synchronous IMV: mode of IMV that delivers the mandatory breathsynchronously with patient’s initiatedeffort; if no breath is initiated, the ventilator delivers the predeterminedmandatory breath

Assist-Control ventilation: mode in whichthe ventilator delivers a breath whenthe patient initiates a breath, or the ventilator “assists” the patient to breathe;if the patient does not initiate a breath,the ventilator takes “control” and deliv-ers a breath at a predetermined rate

In contrast to IMV, all breaths are by theventilator

Continuous Positive Airway Pressure:positive pressure delivered continu-ously (during expiration and inspira-tion) by ventilator, but no volumebreaths (patient breathes on own)

Pressure is delivered only with an initiated breath; pressure supportdecreases the work of breathing by overcoming the resistance in the ventilator circuit

Airway Pressure Release Ventilation:high airway pressure intermittentlyreleased to a low airway pressure(shorter period of time)

High Frequency Ventilation: rapid ratesof ventilation with small tidal volumes

Venous return and cardiac output aredecreased

Positive End Expiration Pressure: positive pressure maintained at the endof a breath; keeps alveoli open


What is “physiologic PEEP”?

What are the side effects ofincreasing levels of PEEP?

What are the typical initialventilator settings:

Mode?

Tidal volume?

Ventilator rate?

FiO2?

PEEP?

What is a normal I:E (ins-piratory to expiratory time)?

When would you use aninverse I:E ratio (e.g., 2:1,3:1, etc.)?

When would you use a pro-longed I:E ratio (e.g., 1:4)?

What clinical situationscause increased airwayresistance?

What are the presumedadvantages of PEEP?

What are the possible disadvantages of PEEP?


PEEP of 5 cm H2O; thought to approximate normal pressure in normalnonintubated people caused by theclosed glottis

Barotrauma (injury to airway �pneumothorax), decreased CO fromdecreased preload

Intermittent mandatory ventilation

6–8 ml/kg

10 breaths/min

100% and wean down

5 cm H2OFrom these parameters, change

according to blood-gas analysis

1:2

To allow for longer inspiration in patientswith poor compliance, to allow for “alveolar recruitment”

COPD, to allow time for complete exhalation (prevents “breath stacking”)

Airway or endotracheal tube obstruction,bronchospasm, ARDS, mucous plug,CHF (pulmonary edema)

Prevention of alveolar collapse andatelectasis, improved gas exchange,increased pulmonary compliance,decreased shunt fraction

Decreased cardiac output, especially inthe setting of hypovolemia; decreased gasexchange; T compliance with high levelsof PEEP, fluid retention, increasedintracranial pressure, barotrauma


What parameters must be evaluated in deciding if a patient is ready to beextubated?

What is the Rapid-ShallowBreathing (a.k.a. Tobin)index?

What is a possible source offever in a patient with an NGor nasal endotracheal tube?

What is the 35�45 rule ofblood gas values?

Which medications can bedelivered via anendotracheal tube?

What conditions should youthink of with c peak airwaypressure and T urineoutput?

Chapter 66 / Vascular Surgery 489

Patient alert and able to protect airway,gas exchange (PaO2 �70, PaCO2 �50),tidal volume (�5 cc/kg), minute ventilation (�10 L/min), negative inspiratory pressure (��20 cm H2O,or more negative), FiO2 �40%, PEEP 5,PH �7.25, RR �35, Tobin index �105

Rate: Tidal volume ratio; Tobin index�105 is associated with successful extubation (Think: Respiratory Therapist� RT � Rate: Tidal volume)

Sinusitis (diagnosed by sinus films/CT)

Normal values:pH � 7.35�7.45PCO2 � 35�45

Think “NAVEL”:NarcanAtropineVasopressinEpinephrineLidocaine

1. Tension pneumothorax2. Abdominal compartment syndrome

What is atherosclerosis?

Vascular SurgeryChapter 66Diffuse disease process in arteries;atheromas containing cholesterol andlipid form within the intima and innermedia, often accompanied by ulcerationsand smooth muscle hyperplasia


What is the common theoryof how atherosclerosis is initiated?

What are the risk factors foratherosclerosis?

What are the common sitesof plaque formation in arteries?

What must be present for asuccessful arterial bypassoperation?

What is the major principleof safe vascular surgery?

What does it mean to“POTTS” a vessel?

What is the suture needleorientation through graftversus diseased artery in agraft to artery anastomosis?

What are the three layers ofan artery?

Which arteries supply theblood vessel itself?

What is a true aneurysm?

What is a false aneurysm(a.k.a pseudoaneurysm)?


Endothelial injury S platelets adhere Sgrowth factors released S smooth muscle hyperplasia/plaque deposition

Hypertension, smoking, diabetes mellitus, family history, hyper-cholesterolemia, high LDL, obesity, and sedentary lifestyle

Branch points (carotid bifurcation), tethered sites (superficial femoral artery[SFA] in Hunter’s canal in the leg)

1. Inflow (e.g., patent aorta)2. Outflow (e.g., open distal popliteal

artery)3. Run off (e.g., patent trifurcation

vessels down to the foot)

Get proximal and distal control of thevessel to be worked on!

Place a vessel loop twice around a vesselso that if you put tension on the vesselloop, it will occlude the vessel

Needle “in-to-out” of the lumen indiseased artery to help tack down theplaque and the needle “out-to-in” on thegraft

1. Intima2. Media3. Adventitia

Vaso vasorum

Dilation (�2� nL diameter) of all threelayers of a vessel

Dilation of artery not involving all threelayers (e.g., hematoma with fibrouscovering)

Often connects with vessel lumen andblood swirls inside the false aneurysm


What is “ENDOVASCULAR”repair?


Placement of a catheter in artery andthen deployment of a graft intraluminally

HR

Fis c

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‘05

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5

PERIPHERAL VASCULAR DISEASE

Define the arterial anatomy: 1. Aorta2. Internal iliac (hypogastric)3. External iliac4. Common femoral artery5. Profundi femoral artery6. Superficial femoral artery (SFA)7. Popliteal artery8. Trifurcation9. Anterior tibial artery

10. Peroneal artery11. Posterior tibial artery12. Dorsalis pedis artery


How can you remember theorientation of the lowerexterior arteries below theknee on A-gram?

What is peripheral vasculardisease (PVD)?

What is the most common site of arterial atherosclerotic occlusion inthe lower extremities?

What are the symptoms ofPVD?

What is intermittent claudication?

What is rest pain?

What classically resolves restpain?

How can vascular causes ofclaudication be differentiatedfrom nonvascular causes,such as neurogenic claudication or arthritis?

What is the differential diagnosis of lower extremityclaudication?


Use the acronym “LAMP”:Lateral Anterior tibialMedial Posterior tibial

Occlusive atherosclerotic disease in thelower extremities

Occlusion of the SFA in Hunter’s canal

Intermittent claudication, rest pain, erectile dysfunction, sensorimotorimpairment, tissue loss

Pain, cramping, or both of the lowerextremity, usually the calf muscle, afterwalking a specific distance; then thepain/cramping resolves after stopping fora specific amount of time while standing;this pattern is reproducible

Pain in the foot, usually over the distalmetatarsals; this pain arises at rest (classically at night, awakening thepatient)

Hanging the foot over the side of the bedor standing; gravity affords some extraflow to the ischemic areas

History (in the vast majority of patients)and noninvasive tests; remember, vascular claudication appears after a specific distance and resolves after a specific time of rest while standing (notso with most other forms of claudication)

Neurogenic (e.g., nerve entrapment/discs), arthritis, coarctation of the aorta,popliteal artery syndrome, chronic compartment syndrome, neuromas, anemia, diabetic neuropathy pain


What are the signs of PVD?

What is the site of a PVDulcer vs. a venous stasisulcer?

What is the ABI?

What ABIs are associatedwith normals, claudicators,and rest pain?

Who gets false ABIreadings?

What are PVRs?

Prior to surgery for chronicPVD, what diagnostic testwill every patient receive?

What is the bedside management of a patientwith PVD?


Absent pulses, bruits, muscular atrophy,decreased hair growth, thick toenails, tissue necrosis/ulcers/infection

PVD arterial insufficiency ulcer—usuallyon the toes/foot

Venous stasis ulcer—medial malleolus(ankle)

Ankle to Brachial Index (ABI); simply, the ratio of the systolic bloodpressure at the ankle to the systolic bloodpressure at the arm (brachial artery) A:B;ankle pressure taken with Doppler; theABI is noninvasive

Normal ABI— �1.0Claudicator ABI— �0.6Rest pain ABI— �0.4

Patients with calcified arteries, especiallythose with diabetes

Pulse Volume Recordings; pulse waveforms are recorded from lowerextremities representing volume ofblood per heart beat at sequentialsites down leg

Large wave form means good collateralblood flow

(Noninvasive using pressure cuffs)

A-gram (arteriogram: dye in vessel andx-rays) maps disease and allows forbest treatment option (i.e., angioplastyvs. surgical bypass vs. endarterectomy)

Gold standard for diagnosing PVD

1. Sheep skin (easy on the heels)2. Foot cradle (keeps sheets/blankets off

the feet)3. Skin lotion to avoid further cracks in

the skin that can go on to form afissure and then an ulcer


What are the indications forsurgical treatment in PVD?

What is the treatment ofclaudication?

How can the medicalconservative treatment forclaudication be remembered?

How does aspirin work?

How does Trental®

(pentoxifylline) work?

What is the risk of limb losswith claudication?

What is the risk of limb losswith rest pain?

In the patient with PVD, whatis the main postoperativeconcern?


Use the acronym “STIR”:Severe claudication refractory to

conservative treatment that affects quality of life/livelihood (e.g., can’t work because of the claudication)

Tissue necrosisInfectionRest pain

For the vast majority, conservative treatment, including exercise, smokingcessation, treatment of HTN, diet, aspirin, with or without Trental (pentoxifylline)

Use the acronym “PACE”:PentoxifyllineAspirinCessation of smokingExercise

Inhibits platelets (inhibits cyclooxygenaseand platelet aggregation)

Results in increased RBC deformity andflexibility (Think: pentoXifylline � RBCfleXibility)

5% limb loss at 5 years (Think: 5 in 5),10% at 10 years (Think: 10 in 10)

�50% of patients will have amputation ofthe limb at some point

Cardiac status, because most patientswith PVD have coronary arterydisease; �20% have an AAA

MI is the most common cause of postoperative death after a PVD operation


What is Leriche’s syndrome?

What are the treatmentoptions for severe PVD?

What is a FEM-POP bypass?


Buttock Claudication, Impotence (erectiledysfunction), and leg muscle Atrophy from occlusive disease of the iliacs/distalaortaThink: “CIA”:

ClaudicationImpotenceAtrophy(Think: CIA spy Leriche)

1. Surgical graft bypass2. Angioplasty—balloon dilation3. Endarterectomy—remove diseased

intima and media4. Surgical patch angioplasty (place patch

over stenosis)

Bypass SFA occlusion with a graft from theFEMoral artery to the POPliteal artery


What graft material has thelongest patency rate?

What is an “in situ” veingraft?

What type of graft is usedfor above-the-knee FEM-POPbypass?

What type of graft is usedfor below-the-knee FEM-POPor FEM-DISTAL bypass?

What is DRY gangrene?


Autologous vein graft

Saphenous vein is more or less left inplace, all branches are ligated, and thevein valves are broken with a small hookor cut out; a vein can also be used ifreversed so that the valves do not cause aproblem

Either vein or Gortex® graft; vein still hasbetter patency

Must use vein graft; prosthetic graftshave a prohibitive thrombosis rate

Dry necrosis of tissue without signs ofinfection (“mummified tissue”)

What is a FEM-DISTALbypass?

Bypass from the FEMoral artery to aDISTAL artery (peroneal artery, anteriortibial artery, or posterior tibial artery)


What is WET gangrene?

What is blue toe syndrome?


Moist necrotic tissue with signs of infection

Intermittent painful blue toes (or fingers)due to microemboli from a proximal arterial plaque

LOWER EXTREMITY AMPUTATIONS


Identify the level of the following amputations:

Irreversible tissue ischemia (no hope forrevascularization bypass) and necrotic tissue, severe infection, severe pain withno bypassable vessels, or if patient is notinterested in a bypass procedure

1. Above-the-Knee Amputation (AKA)2. Below-the-Knee Amputation (BKA)3. Symes amputation4. Transmetatarsal amputation5. Toe amputation

5

4

3

2

1

What is a Ray amputation? Removal of toe and head of metatarsal



ACUTE ARTERIAL OCCLUSION

What is it?

What are the classicsigns/symptoms of acutearterial occlusion?

What is the classic timing ofpain with acute arterialocclusion from an embolus?

What is the immediate preoperative management?

What are the sources ofemboli?

What is the most commoncause of embolus from theheart?

What is the most commonsite of arterial occlusion byan embolus?

What diagnostic studies arein order?

Acute occlusion of an artery, usually byembolization; other causes include acutethrombosis of an atheromatous lesion,vascular trauma

The “six P’s”:PainParalysisPallorParesthesiaPolar (some say Poikilothermia—you

pick)Pulselessness (You must know these!)

Acute onset; the patient can classicallytell you exactly when and where ithappened

1. Anticoagulate with IV heparin (bolusfollowed by constant infusion)

2. A-gram

1. Heart—85% (e.g., clot from AFib, clotforming on dead muscle after MI,endocarditis, myxoma)

2. Aneurysms3. Atheromatous plaque (atheroembolism)

AFib

Common femoral artery (SFA is the mostcommon site of arterial occlusion fromatherosclerosis)

1. A-gram2. ECG (looking for MI, AFib)3. Echocardiogram (�) looking for clot,

MI, valve vegetation



What is a Fogarty?

How is a Fogarty catheterused?

How many mm in diameteris a 12 French Fogartycatheter?

What must be looked forpostoperatively after reperfusion of a limb?

What is compartmentsyndrome?

What are the signs/symptoms of compartmentsyndrome?

Can a patient have a pulseand compartment syndrome?



Surgical embolectomy via cutdown andFogarty balloon (bypass is reserved forembolectomy failure)

Fogarty balloon catheter—catheter witha balloon tip that can be inflated withsaline; used for embolectomy

Insinuate the catheter with the balloondeflated past the embolus and then inflatethe balloon and pull the catheter out; theballoon brings the embolus with it

Simple: To get mm from Frenchmeasurements, divide the French number by , or 3.14; thus, a 12 Frenchcatheter is 12/3 � 4 mm in diameter

Compartment syndrome,hyperkalemia, renal failure from myoglobinuria, MI

Leg (calf) is separated into compartmentsby very unyielding fascia; tissue swellingfrom reperfusion can increase the intracompartmental pressure, resulting in decreased capillary flow, ischemia, andmyonecrosis; myonecrosis may occurafter the intracompartment pressurereaches only 30 mm Hg

Classic signs include pain, especially afterpassive flexing/extension of the foot,paralysis, paresthesias, and pallor; pulsesare present in most cases because systolic pressure is much higher than the minimal 30 mm Hg needed for thesyndrome!

YES!

History/suspicion, compartment pressuremeasurement


What is the treatment ofcompartment syndrome?


Treatment includes opening compartmentsvia bilateral calf-incision fasciotomies ofall four compartments in the calf

ABDOMINAL AORTIC ANEURYSMS


What is it?

AAA, or “triple A”

Abnormal dilation of the abdominal aorta(�1.5–2� normal), forming a trueaneurysm


By far, who is at the highestrisk?

What is the commonetiology?



What percentage of patientswith AAA have a peripheralarterial aneurysm?

�6:1

White males

Believed to be atherosclerotic in 95%of cases; 5% inflammatory

Infrarenal (95%)

5% of all adults older than 60 years of age

20%




Classically, what do testicularpain and an AAA signify?

What are the risk factors forrupture?

What are the signs ofrupture?

By how much each year doAAAs grow?

Why do larger AAAs rupturemore often and grow fasterthan smaller AAAs?

What is the risk of ruptureper year based on AAAdiameter size?

What are other risks forrupture?

Where does the aorta bifurcate?



Atherosclerosis, hypertension, smoking,male gender, advanced age, connectivetissue disease

Most AAAs are asymptomatic and discovered during routine abdominalexam by primary care physicians; in the remainder, symptoms range fromvague epigastric discomfort to back andabdominal pain

Retroperitoneal rupture with ureteralstretch and referred pain to the testicle

Increasing aneurysm diameter, COPD,HTN, recent rapid expansion, largediameter, hypertension, symptomatic

Classic triad of ruptured AAA:1. Abdominal pain2. Pulsatile abdominal mass3. Hypotension

�3 mm/year on average (larger AAAsgrow faster than smaller AAAs)

Probably because of Laplace’s law (wall tension � pressure � diameter)

�5 cm � 4%5–7 cm � 7%�7 cm � 20%

Hypertension, smoking, COPD

At the level of the umbilicus; therefore,when palpating for an AAA, palpateabove the umbilicus and below thexiphoid process

Acute pancreatitis, aortic dissection,mesenteric ischemia, MI, perforatedulcer, diverticulosis, renal colic, etc.



What is the limitation of A-gram?

What are the signs of AAAon AXR?

What are the indications forsurgical repair of AAA?



Use U/S to follow AAA clinically; othertests involve contrast CT scan and A-gram;A-gram will assess lumen patency andiliac/renal involvement

AAAs often have large mural thrombi,which result in a falsely reduced diameterbecause only the patent lumen is visualized

Calcification in the aneurysm wall, bestseen on lateral projection (a.k.a.“eggshell” calcifications)

AAA �5.5 cm in diameter, if the patientis not an overwhelming high risk for surgery; also, rupture of the AAA, anysize AAA with rapid growth, symptoms/embolization of plaque

1. Prosthetic graft placement, withrewrapping of the native aneurysmadventitia around the prosthetic graftafter the thrombus is removed; whenrupture is strongly suspected, proceedto immediate laparotomy; there isno time for diagnostic tests!

What is endovascularrepair?

2. Endovascular repair

Repair of the AAA by femoral catheterplaced stents


Why wrap the graft in thenative aorta?

What type of repair shouldbe performed with AAA andiliacs severely occluded oriliac aneurysm(s)?

What is the treatment if thepatient has abdominal pain,pulsatile abdominal mass,and hypotension?

What is the treatment if thepatient has known AAA andnew onset of abdominal painor back pain?

What is the mortality rateassociated with the followingtypes of AAA treatment:

Elective?

Ruptured?

What is the leading cause of postoperative death in apatient undergoing electiveAAA treatment?

What are the otheretiologies of AAA?

What is the mean normalabdominal aortic diameter?

What are the possible operative complications?

Why is colonic ischemia aconcern in the repair ofAAAs?


To reduce the incidence of enterograftfistula formation

Aortobi-iliac or aortobifemoral graftreplacement (bifurcated graft)

Take the patient to the O.R. for emergentAAA repair

CT scan:1. Leak S straight to OR2. No leak S repair during next elec-

tive slot

Good; �4% operative mortality

≈50% operative mortality

Myocardial infarction (MI)

Inflammatory (connective tissuediseases), mycotic (a misnomer becausemost result from bacteria, not fungi)

2 cm

MI, atheroembolism, declampinghypotension, acute renal failure(especially if aneurysm involves the renalarteries), ureteral injury, hemorrhage

Often the IMA is sacrificed duringsurgery; if the collaterals are not adequate,the patient will have colonic ischemia


What are the signs ofcolonic ischemia?

What is the study of choice to diagnose colonicischemia?

When is colonic ischemiaseen postoperatively?

What is the treatment ofnecrotic sigmoid colon fromcolonic ischemia?

What is the possible long-term complication that oftenpresents with both upperand lower GI bleeding?

What are the other possiblepostoperative complications?

What is anterior spinalsyndrome?

Which artery is involved in anterior spinal cord syndrome?

What are the most commonbacteria involved in aorticgraft infections?

How is a graft infection withan aortoenteric fistulatreated?


Heme-positive stool, or bright red bloodper rectum (BRBPR), diarrhea, abdominal pain

Colonoscopy

Usually in the first week

1. Resection of necrotic colon2. Hartmann’s pouch or mucous fistula3. End colostomy

Aortoenteric fistula (fistula between aortaand duodenum)

Erectile dysfunction (sympathetic plexusinjury), retrograde ejaculation, aortovenousfistula (to IVC), graft infection, anteriorspinal syndrome

Classically:1. Paraplegia2. Loss of bladder/bowel control3. Loss of pain/temperature sensation

below level of involvement4. Sparing of proprioception

Artery of Adamkiewicz—supplies theanterior spinal cord

1. Staphylococcus aureus2. Staphylococcus epidermidis

(usually late)

Perform an extra-anatomic bypass withresection of the graft


What is an extra-anatomicbypass graft?


Axillofemoral bypass graft—graft not in a normal vascular path; usually, the graft goes from the axillary artery tothe femoral artery and then from onefemoral artery to the other (fem-fembypass)

hrf'02

CLASSIC INTRAOP QUESTIONS DURING AAA REPAIR

Which vein crosses the neckof the AAA proximally?

What part of the smallbowel crosses in front of the AAA?

Which large vein runs to theleft of the AAA?

Which artery comes off themiddle of the AAA and runsto the left?

Renal vein (left)

Duodenum

IMV

IMA

What is an endovascularrepair?

Placement of a stent proximal and distalto an AAA through a distant percutaneousaccess (usually through the groin); lessinvasive; long-term results pending


Which vein runs behind theRIGHT common iliac artery?

Which renal vein is longer?


LEFT common iliac vein

Left

MESENTERIC ISCHEMIA

CHRONIC MESENTERIC ISCHEMIA

What is it?


What is “intestinal angina”?

What are the signs?


What supplies blood to thegut?

What is the classic findingon A-gram?


Chronic intestinal ischemia from long-term occlusion of the intestinalarteries; most commonly results fromatherosclerosis; usually in two or morearteries because of the extensive collaterals

Weight loss, postprandial abdominal pain, anxiety/fear of food because of postprandial pain, � heme occult, � diarrhea/vomiting

Postprandial pain from gut ischemia

Abdominal bruit is commonly heard

A-gram, duplex, MRA

1. Celiac axis vessels2. SMA3. IMA

Two of the three mesenteric arteries areoccluded, and there is atheroscleroticnarrowing of the third patent artery

Bypass, endarterectomy, angioplasty,stenting

ACUTE MESENTERIC ISCHEMIA

What is it?


Acute onset of intestinal ischemia

1. Emboli to a mesenteric vessel fromthe heart

2. Acute thrombosis of long-standingatherosclerosis of mesenteric artery


What are the causes ofemboli from the heart?

What drug has been associated with acute intestinal ischemia?

To which intestinal artery doemboli preferentially go?

What are the signs/symptoms of acutemesenteric ischemia?

What is the classic triad ofacute mesenteric ischemia?

What is the gold standarddiagnostic test?

What is the treatment of amesenteric embolus?

What is the treatment ofacute thrombosis?


AFib, MI, cardiomyopathy, valve disease/endocarditis, mechanical heart valve

Digitalis

Superior Mesenteric Artery (SMA)

Severe pain—classically “pain out ofproportion to physical exam,” no peritoneal signs until necrosis, vomiting/diarrhea/hyperdefecation, � heme stools

1. Acute onset of pain2. Vomiting, diarrhea, or both3. History of AFib or heart disease

Mesenteric A-gram

Perform Fogarty catheter embolectomy,resect obviously necrotic intestine, andleave marginal looking bowel until a “second look” laparotomy is performed 24 to 72 hours postoperatively

Papaverine vasodilator via A-gramcatheter until patient is in the OR;then, most surgeons would perform asupraceliac aorta graft to the involvedintestinal artery or endarterectomy; intestinal resection/second look asneeded

MEDIAN ARCUATE LIGAMENT SYNDROME

What is it?

What is the median arcuateligament comprised of?

Mesenteric ischemia resulting from narrowing of the celiac axis vessels byextrinsic compression by the medianarcuate ligament

Diaphragm hiatus fibers



What are the signs?




Postprandial pain, weight loss

Abdominal bruit in almost all patients

A-gram

Release arcuate ligament surgically

CAROTID VASCULAR DISEASE

ANATOMY

Identify the following structures:

1. Internal carotid artery2. External carotid artery3. Carotid “bulb”4. Superior thyroid artery5. Common carotid artery(Shaded area: common site of plaque

formation)


Define the following terms:Amaurosis fugax

TIA

Amaurosis fugax, TIA, RIND, CVA

Temporary monocular blindness (“curtaincoming down”): seen with microembolito retina; example of TIA

Transient Ischemic Attack: focal neurologic deficit with resolution of allsymptoms within 24 hours


RIND

CVA

What is the risk of a CVA inpatients with TIA?

What is the noninvasivemethod of evaluating carotiddisease?

What is the gold standardinvasive method of evaluating carotid disease?

What is the surgicaltreatment of carotid stenosis?

What are the indications forCEA in the ASYMPTOMATICpatient?

What are the indications forCEA in the SYMPTOMATIC(CVA, TIA, RIND) patient?

Before performing a CEA inthe symptomatic patient, whatstudy other than the A-gramshould be performed?

In bilateral high-grade carotidstenosis, on which side shouldthe CEA be performed in theasymptomatic, right-handedpatient?

What is the dreaded complication after a CEA?


Reversible Ischemic Neurologic Deficit:transient neurologic impairment (withoutany lasting sequelae) lasting 24 to 72 hours

CerebroVascular Accident (stroke): neurologic deficit with permanent braindamage

�10% a year

Carotid ultrasound/Doppler: givesgeneral location and degree of stenosis

A-gram

Carotid EndArterectomy (CEA): theremoval of the diseased intima and mediaof the carotid artery, often performedwith a shunt in place

Carotid artery stenosis �60% (greatestbenefit is probably in patients with �80%stenosis)

Carotid stenosis �50%

Head CT

Left CEA first, to protect the dominanthemisphere and speech center

Stroke (CVA)


What are the possible postoperative complicationsafter a CEA?

What is the mortality rateafter CEA?

What is the perioperativestroke rate after CEA?

What is the postoperativemedication?

What is the most commoncause of death during theearly postoperative periodafter a CEA?

Define “Hollenhorstplaque”?


CVA, MI, hematoma, wound infection,hemorrhage, hypotension/hypertension,thrombosis, vagus nerve injury (change invoice), hypoglossal nerve injury (tonguedeviation toward side of injury—“wheel-barrow” effect), intracranial hemorrhage

�1%

Between 1% (asymptomatic patient) and5% (symptomatic patient)

Aspirin (inhibits platelets by inhibitingcyclo-oxygenase)

MI

Microemboli to retinal arterioles seen asbright defects

CLASSIC CEA INTRAOP QUESTIONS

What thin muscle is cut rightunder the skin in the neck?

What are the extracranialbranches of the internalcarotid artery?

Which vein crosses thecarotid bifurcation?

What is the first branch ofthe external carotid?

Which muscle crosses the common carotid proximally?

Which muscle crosses thecarotid artery distally?

Platysma muscle

None

Facial vein

Superior thyroidal artery

Omohyoid muscle

Digastric muscle (Think: Digastric �Distal)


Which nerve crosses approximately 1 cm distal tothe carotid bifurcation?

Which nerve crosses theinternal carotid near the ear?

What is in the carotid sheath?


Hypoglossal nerve; cut it and the tonguewill deviate toward the side of the injury(the “wheelbarrow effect”)

Facial nerve (marginal branch)

1. Carotid artery2. Internal jugular vein3. Vagus nerve (lies posteriorly in 98%

of patients and anteriorly in 2%)4. Deep cervical lymph nodes

SUBCLAVIAN STEAL SYNDROME

What is it? Arm fatigue and vertebrobasilar insufficiency from obstruction of the leftsubclavian artery or innominate proximal tothe vertebral artery branch point; ipsilateralarm movement causes increased blood flowdemand, which is met by retrograde flowfrom the vertebral artery, thereby “stealing”from the vertebrobasilar arteries


Which artery is mostcommonly occluded?


What are the signs?



Left subclavian

Upper extremity claudication, syncopalattacks, vertigo, confusion, dysarthria,blindness, ataxia

Upper extremity blood pressure discrepancy, bruit (above the clavicle),vertebrobasilar insufficiency

Surgical bypass or endovascular stent

RENAL ARTERY STENOSIS

What is it?


What is the etiology of thestenosis?

What is the classic profile ofa patient with renal arterystenosis from fibromusculardysplasia?

What are the associatedrisks/clues?

Stenosis of renal artery, resulting indecreased perfusion of the juxtaglomerularapparatus and subsequent activation of therenin-angiotensin-aldosterone system (i.e.,hypertension from renal artery stenosis)

�10% to 15% of the U.S. population haveHTN; of these, �4% have potentiallycorrectable renovascular HTN

Also note that 30% of malignant HTNhave a renovascular etiology

�66% result from atherosclerosis (men � women), �33% result from fibromuscular dysplasia (women �men, average age 40 years, and 50%with bilateral disease)

Note: Another rare cause is hypoplasia ofthe renal artery

Young woman with hypertension

Family history, early onset of HTN, HTNrefractory to medical treatment



What are the diagnostic tests?A-gram

IVP

Renal vein renin ratio(RVRR)

Captopril provocation test

Are renin levels in serumALWAYS elevated?

What is the invasive nonsurgical treatment?


What antihypertensive medication isCONTRAINDICATED inpatients with hypertensionfrom renovascular stenosis?


Most patients are asymptomatic but mayhave headache, diastolic HTN, flankbruits (present in 50%), and decreasedrenal function

Maps artery and extent of stenosis (goldstandard)

80% of patients have delayed nephrogramphase (i.e., delayed filling of contrast)

If sampling of renal vein renin levelsshows ratio between the two kidneys �1.5, then diagnostic for a unilateralstenosis

Will show a drop in BP

No: Systemic renin levels may also bemeasured but are only increased inmalignant HTN, as the increasedintravascular volume dilutes the elevatedrenin level in most patients

Percutaneous Renal Transluminal Angioplasty (PRTA)/stenting:

With FM dysplasia: use PRTAWith atherosclerosis: use PRTA/stent

Resection, bypass, vein/graftinterposition, or endarterectomy

ACE inhibitors (result in renalinsufficiency)

SPLENIC ARTERY ANEURYSM

What are the causes? Women—medial dysplasiaMen—atherosclerosis



What is the risk factor forrupture?

What are the indications forsplenic artery aneurysmremoval?

What is the treatment forsplenic aneurysm?


Usually by abdominal pain S U/S or CTscan, in the O.R. after rupture, orincidentally by eggshell calcificationsseen on AXR

Pregnancy

Pregnancy, �2 cm in diameter, symptoms,and in women of childbearing age

Resection or percutaneous catheterembolization in high-risk (e.g., portalhypertension) patients

POPLITEAL ARTERY ANEURYSM

What is it?


Why examine the contralateral poplitealartery?

What are the indications forelective surgical repair of apopliteal aneurysm?

Why examine the rest of thearterial tree (especially theabdominal aorta)?

What size of the followinganeurysms are usually considered indications forsurgical repair:

Thoracic aorta?

Abdominal aorta?

Aneurysm of the popliteal artery causedby atherosclerosis and, rarely, bacterialinfection

Usually by physical exam S A-gram, U/S

50% of all patients with a popliteal arteryaneurysm have a popliteal artery aneurysmin the contralateral popliteal artery

1. �2 cm in diameter2. Intraluminal thrombus3. Artery deformation

75% of all patients with poplitealaneurysms have additionalaneurysms elsewhere; �50% of these are located in the abdominalaorta/iliacs

�6.5 cm

�5.5 cm


Iliac artery?

Femoral artery?

Popliteal artery?


�4 cm

�2.5 cm

�2 cm

MISCELLANEOUS

Define the following terms:“Milk leg”

Phlegmasia ceruleadolens

Raynaud’s phenomenon

Takayasu’s arteritis

Buerger’s disease

What is the treatment forBuerger’s disease?

What is blue toe syndrome?

A.k.a. phlegmasia alba dolens (alba �white): often seen in pregnant womenwith occlusion of iliac vein resulting from extrinsic compression by the uterus(thus, the leg is “white” because of subcutaneous edema)

In comparison, phlegmasia cerulea dolensis secondary to severe venous outflowobstruction and results in a cyanotic leg;the extensive venous thrombosis resultsin arterial inflow impairment

Vasospasm of digital arteries with colorchanges of the digits; usually initiatedby cold/emotion

White (spasm), then blue (cyanosis), thenred (hyperemia)

Arteritis of the aorta and aortic branches,resulting in stenosis/occlusion/aneurysms

Seen mostly in women

A.k.a. thromboangiitis obliterans: occlusion of the small vessels of thehands and feet; seen in young men who smoke; often results in digital gangrene S amputations

Smoking cessation, �/– sympathectomy

Microembolization from proximal atherosclerotic disease of the aorta resulting in blue, painful, ischemic toes


What is a “paradoxicalembolus”?

What size iliac aneurysmshould be repaired?

What is Behçet’s disease?


Venous embolus gains access to the leftheart after going through an intracardiacdefect, most commonly a patent foramenovale, and then lodges in a peripheralartery

�4 cm diameter

Genetic disease with aneurysms from lossof vaso vasorum; seen with oral, ocular, andgenital ulcers/inflammation (c incidence inJapan, Mediterranean)


What is the motto ofpediatric surgery?

What is a simple way to distract a pediatric patientwhen examining theabdomen for tenderness?

“Children are NOT little adults!”

Listen to the abdomen with thestethoscope and then push down on theabdomen with the stethoscope to checkfor tenderness

517

Section III Subspecialty Surgery

Pediatric SurgeryChapter 67

PEDIATRIC IV FLUIDS AND NUTRITION

What is the estimated bloodvolume of infants and children?

What is the maintenance IVfluid for children?

Why 1/4 NS?

How are maintenance fluidrates calculated in children?

What is the minimal urineoutput for children?

�8% of body weight or �80 cc/kg

D5 1/4 NS � 20 mEq KCl

Children (especially those younger than 4 years of age) cannot concentrate theirurine and cannot clear excess sodium

4, 2, 1 per hour:4 cc/kg for the first 10 kg of body

weight2 cc/kg for the second 10 kg of

body weight1 cc/kg for every kilogram over

the first 20 (e.g., the rate for achild weighing 25 kg is 4 � 10 � 40plus 2 � 10 � 20 plus 1 � 5 � 5,for an IVF rate of 65 cc/hr)

From 1 to 2 mL/kg/hr


What is the best way to present urine outputmeasurements on rounds?

What is the major differencebetween adult and pediatricnutritional needs?

What are the caloricrequirements by age for thefollowing patients:

Premature infants?

Children younger than 1 year?

Children ages 1 to 7?


Youths ages 12 to 18

What are the proteinrequirements by age for thefollowing patients:

Children younger than 1 year?



Youths ages 12 to 18?

How many calories are inbreast milk?

518 Section III / Subspecialty Surgery

Urine output total per shift, THEN cc/kg/hr

Premature infants/infants/children needmore calories and protein/kg/day

80 Kcal/kg/day and then go up

�100 Kcal/kg/day (90–120)

�85 Kcal/kg/day (75–90)

�70 Kcal/kg/day (60–75)

�40 Kcal/kg/day (30–60)

3 g/kg/day (2–3.5)

2 g/kg/day (2–2.5)

2 g/kg/day

1.5 grams/kg/day

20 Kcal/30 cc (same as most formulas)

PEDIATRIC BLOOD VOLUMES

Give blood volume per kilogram:

Newborn infant?

Infant 1–3 months of age?

Child?

85 cc

75 cc

70 cc


Chapter 67 / Pediatric Surgery 519

What is the number ofumbilical veins?

What is the number ofumbilical arteries?

Which umbilical vessel carries oxygenated blood?

The oxygenated blood travelsthrough the liver to the IVCthrough which structure?

Oxygenated blood passesfrom the right atrium to theleft atrium through whichstructure?

Unsaturated blood goesfrom the right ventricle tothe descending aortathrough which structure?

Define the overall fetal circulation.

1 (usually)

2

Umbilical vein

Ductus venosus

Foramen ovale

Ductus arteriosum

Carotid arteries

To armTo arm

Foramenovale

Femoral artery

Femoral artery

Liver

Placenta

Lung

Kidney

Lung

Gut

Ductus arteriosis

FETAL CIRCULATION


What are the ADULT structures of the followingfetal structures:

Ductus venosus?

Umbilical vein?

Umbilical artery?

Ductus arteriosus?

Urachus?

Tongue remnant ofthyroid’s descent?

Persistent remnant ofvitelline duct?


Ligamentum venosum

Ligamentum teres

Medial umbilical ligament

Ligamentum arteriosum

Median umbilical ligament

Foramen cecum

Meckel’s diverticulum

ECMO

What is ECMO?

What are the types ofECMO?



ExtraCorporeal Membrane Oxygenation:chronic cardiopulmonary bypass—forcomplete respiratory support

Venovenous: Blood from vein Soxygenated S back to vein

Venoarterial: Blood from vein (IJ) Soxygenated S back to artery (carotid)

Severe hypoxia, usually from congenitaldiaphragmatic hernia, meconium aspiration, persistent pulmonary hypertension, sepsis

Weight �2 kg, IVH (IntraVentricularHemorrhage in brain contraindicatedbecause of heparin in line)



NECK

What is the majordifferential diagnosis of apediatric neck mass?

Thyroglossal duct cyst (midline), branchialcleft cyst (lateral), lymphadenopathy,abscess, cystic hygroma, hemangioma,teratoma/dermoid cyst, thyroid nodule,lymphoma/leukemia (also parathyroidtumors, neuroblastoma, histiocytosis X,rhabdomyosarcoma, salivary gland tumors,neurofibroma)

THYROGLOSSAL DUCT CYST

What is it? Remnant of the diverticulum formed by migration of thyroid tissue; normaldevelopment involves migration ofthyroid tissue from the foramen cecum atthe base of the tongue through the hyoidbone to its final position around the tracheal cartilage




Usually presents around 5 years of age

Ultrasound

Enlargement, infection, and fistulaformation between oropharynx orsalivary gland; aberrant thyroid tissuemay masquerade as thyroglossal ductcyst, and if it is not cystic, deserves a thyroid scan


What is the anatomiclocation?

How can one remember theposition of the thyroglossalduct cyst?


Almost always in the midline

Think: thyroGLOSSAL � TONGUEmidline sticking out

What is the treatment? Antibiotics if infection is present, thenexcision, which must include the midpor-tion of the hyoid bone and entire tract toforamen cecum (Sistrunk procedure)

BRANCHIAL CLEFT ANOMALIES

What is it?

What is the common presentation?

What is the anatomicposition?

Remnant of the primitive branchial cleftsin which epithelium forms a sinus tractbetween the pharynx (second cleft), orthe external auditory canal (first cleft),and the skin of the anterior neck; if thesinus ends blindly, a cyst may form

Infection because of communicationbetween pharynx and external ear canal

Second cleft anomaly—lateral to themidline along anterior border of thesternocleidomastoid, anywhere fromangle of jaw to clavicle

First cleft anomaly—less common thansecond cleft anomalies; tend to belocated higher under the mandible


What is the most commoncleft remnant?


What is the major anatomicdifference betweenthyroglossal cyst andbranchial cleft cyst?


Second; thus, these are found most oftenlaterally versus thyroglossal cysts, which arefound centrally (Think: Second � Superior)

Antibiotics if infection is present, thensurgical excision of cyst and tract onceinflammation is resolved

Thyroglossal cyst � midlineBranchial cleft cyst � lateral(Think: brAnchial � lAteral)

STRIDOR

What is stridor?



What are the symptoms ofvascular rings?

How is the diagnosis of vascular rings made?

What is the treatment ofvascular rings?

Harsh, high-pitched sound heard onbreathing caused by obstruction of thetrachea or larynx

Dyspnea, cyanosis, difficulty withfeedings

Laryngomalacia—leading cause of stridorin infants; results from inadequatedevelopment of supporting laryngealstructures; usually self-limited andtreatment is expectant unlessrespiratory compromise is present

Tracheobronchomalacia—similar tolaryngomalacia, but involves the entiretrachea

Vascular rings and slings—abnormaldevelopment or placement of thoraciclarge vessels resulting in obstructionof trachea/bronchus

Stridor, dyspnea on exertion, or dysphagia

Barium swallow revealing typical configuration of esophageal compression

Echo/arteriogram

Surgical division of the ring, if the patientis symptomatic



CYSTIC HYGROMA

What is it?




Congenital abnormality of lymph sacresulting in lymphangioma

Occurs in sites of primitive lymphaticlakes and can occur virtually anywhere inthe body, most commonly in the floor ofmouth, under the jaw, or in the neck,axilla, or thorax

Early total surgical removal because theytend to enlarge; sclerosis may be neededif the lesion is unresectable

Enlargement in critical regions, such asthe floor of the mouth or paratrachealregion, may cause airway obstruction;also, they tend to insinuate onto majorstructures (although not malignant), making excision difficult and hazardous

ASPIRATED FOREIGN BODY (FB)

Which bronchus do FBs gointo more commonly (left orright)?

What is the most commonlyaspirated object?

What is the associated riskwith peanut aspiration?

How can an FB result in “airtrapping and hyperinflation”?

How can you tell on A-P CXR if a coin is in theesophagus or the trachea?

Younger than age 4—50/50Age 4 and older—most go into right

bronchus because it develops into astraight shot (less of an angle)

Peanut

Lipoid pneumonia

By forming a “ball valve” (i.e., air in, noair out) as seen on CXR as a hyperinflatedlung on expiratory film

Coin in esophagus results in the coin lying“en face” with face of the coin viewed asa round object because of compressionby anterior and posterior structures

If coin is in the trachea, it is viewed as aside projection due to the U-shapedcartilage with membrane posteriorly


What is the treatment of tracheal or esophageal FB?


Remove FB with rigid bronchoscope orrigid esophagoscope

CHEST

What is the differential diagnosis of a lung mass?

What is the differential diagnosis of mediastinaltumor/mass?

Bronchial adenoma (carcinoid is mostcommon), pulmonary sequestration, pulmonary blastoma, rhabdomyosarcoma,chondroma, hamartoma, leiomyoma,mucus gland adenoma, metastasis

1. Neurogenic tumor (ganglioneuromas,neurofibromas)

2. Teratoma3. Lymphoma4. Thymoma(Classic “four T’s”: Teratoma, Terrible

lymphoma, Thymoma, Thyroid tumor)Rare: pheochromocytoma, hemangioma,

rhabdomyosarcoma, osteochondroma

PECTUS DEFORMITY

What heart abnormality is associated with pectusabnormality?

Mitral valve prolapse (many patientsreceive preoperative echocardiogram)

Pectusexcavatum

PECTUS EXCAVATUM

What is it? Chest wall deformity with sternum cavinginward (Think: exCAVatum � CAVE)


What is the cause?



What is the NUSSprocedure?


Abnormal, unequal overgrowth of rib cartilage

Often asymptomatic; mental distress, dyspnea on exertion, chest pain

Open perichondrium, remove abnormalcartilage, place substernal strut; new cartilage grows back in the perichondriumin normal position; remove strut 6 monthslater

Placement of metal strut to elevate sternum without removing cartilage

PECTUS CARINATUM

What is it?

What is the cause?


Chest wall deformity with sternum outward(pectus � chest, carinatum � pigeon);much less common than pectus excavatum

Pectuscarinatum

Abnormal, unequal overgrowth of ribcartilage

Open perichondrium and removeabnormal cartilage

Place substernal strutNew cartilage grows into normal positionRemove strut 6 months later



ESOPHAGEAL ATRESIA WITHOUT TRACHEOESOPHAGEAL

(TE) FISTULA

What is it?

What are the signs?


What is the primarytreatment?

What is the definitive treatment?

Blind-ending esophagus from atresia

Excessive oral secretions and inability tokeep food down

Inability to pass NG tube; plain x-rayshows tube coiled in upper esophagusand no gas in abdomen

Suction blind pouch, IVFs, (gastrostomy todrain stomach if prolonged preoperativeesophageal stretching is planned)

Surgical with 1� anastomosis, often with preoperative stretching of blindpouch (other options include colonic orjejunal interposition graft or gastric tubeformation if esophageal gap is long)

ESOPHAGEAL ATRESIA WITH TRACHEOESOPHAGEAL (TE) FISTULA

What is it?


Define the following typesof fistulas/atresias:

Type A

Esophageal atresia occurring with afistula to the trachea; occurs in �90% ofcases of esophageal atresia

One in 1500 to 3000 births

Esophageal atresia without TE fistula (8%)


Type B


Proximal esophageal atresia with proximalTE fistula (1%)

Type C Proximal esophageal atresia with distalTE fistula (85%); most common type

Type D Proximal esophageal atresia with bothproximal and distal TE fistulas (2%)(Think: D � Double connection to trachea)


Type E


“H-type” TE fistula without esophagealatresia (4%)

How do you rememberwhich type is most common?


What are the signs?




Simple: Most Common type is type C

Excessive secretions caused by an accumulation of saliva (may not occurwith type E)

Obvious respiratory compromise, aspiration pneumonia, postprandialregurgitation, gastric distention as airenters the stomach directly from the trachea

Failure to pass an NG tube (although thiswill not be seen with type E); plain filmdemonstrates tube coiled in the upperesophagus; “pouchogram” (contrast inesophageal pouch); gas on AXR(tracheoesophageal fistula)

Directed toward minimizingcomplications from aspiration:

1. Suction blind pouch (NPO/TPN)2. Upright position of child3. Prophylactic antibiotics (Amp/gent)

Surgical correction via a thoracotomy,usually through the right chest withdivision of fistula and end-to-endesophageal anastomosis, if possible


What can be done tolengthen the proximalesophageal pouch?

Which type should be fixedvia a right neck incision?

What is the workup of apatient with a TE fistula?

What are the associatedanomalies?

What is the significance ofa “gasless” abdomen onAXR?


Delayed repair: with or without G-tubeand daily stretching of proximal pouch

“H-Type” (type E) is high in the thoraxand can most often be approached via aright neck incision

To evaluate the TE fistula and associatedanomalies: CXR, AXR, U/S of kidneys,cardiac echo (rest of workup directed byphysical exam)

VACTERL cluster (present in about 10%of cases):

Vertebral or vascular, Anorectal, Cardiac,TE fistula, Esophageal atresia

Radial limb and renal abnormalities,Lumbar and limb

Previously known as VATER:Vertebral, Anus, TE fistula, Radial

No air to the stomach and, thus, no tracheoesophageal fistula

CONGENITAL DIAPHRAGMATIC HERNIA

What is it?


What are the types ofhernias?

What are the associatedpositions?

Failure of complete formation of thediaphragm, leading to a defect throughwhich abdominal organs are herniated

One in 2100 live births; males are morecommonly affected

Bochdalek and Morgagni

Bochdalek—posterolateral with L � RMorgagni—anterior parasternal hernia,

relatively uncommon


How to remember the position of the Bochdalekhernia?


Think: BOCH DA LEK � “BACK TOTHE LEFT”

Largebowel

Spleen

Hernia

What are the signs?

What are the effects on thelungs?

What inhaled agent is oftenused?


Respiratory distress, dyspnea, tachypnea,retractions, and cyanosis; bowel sounds inthe chest; rarely, maximal heart soundson the right; ipsilateral chest dullness topercussion

1. Pulmonary hypoplasia2. Pulmonary hypertension

Inhaled nitric oxide (pulmonary vasodilator), which decreases the shuntand decreases pulmonary hypertension

NG tube, ET tube, stabilization, and ifpatient is stable, surgical repair; if patientis unstable: nitric oxide �� ECMO thento the O.R. when feasible

PULMONARY SEQUESTRATION

What is it?

Define the following terms:Interlobar

Abnormal benign lung tissue with separate blood supply that DOES NOTcommunicate with the normaltracheobronchial airway

Sequestration in the normal lung tissuecovered by normal visceral pleura


Extralobar



What is the treatment ofeach type:

Extralobar?

Intralobar?

What is the major risk during operation for sequestration?


Sequestration not in the normal lung covered by its own pleura

Asymptomatic, recurrent pneumonia

CXR, chest CT, A-gram, U/S withDoppler flow to ascertain blood supply

Surgical resection

Lobectomy

Anomalous blood supply from below thediaphragm (can be cut and retracted intothe abdomen and result in exsanguination!);always document blood supply by A-gramor U/S with Doppler flow

ABDOMEN

What is the differential diagnosis of pediatric upperGI bleeding?

What is the differential diagnosis of pediatric lowerGI bleeding?

What is the differential diagnosis of neonatal bowelobstruction?

Gastritis, esophagitis, gastric ulcer, duodenal ulcer, esophageal varices,foreign body, epistaxis, coagulopathy, vascular malformation, duplication cyst

Upper GI bleeding, anal fissures, NEC(premature infants), midgut volvulus(usually children younger than 1 year),strangulated hernia, intussusception,Meckel’s diverticulum, infectiousdiarrhea, polyps, IBD, hemolytic uremicsyndrome, Henoch-Schönlein purpura,vascular malformation, coagulopathy

Malrotation with volvulus, intestinalatresia, duodenal web, annular pancreas,imperforate anus, Hirschsprung’s disease, NEC, intussusception (rare),Meckel’s diverticulum, incarceratedhernia, meconium ileus, meconium plug,maternal narcotic abuse (ileus), maternalhypermagnesemia (ileus), sepsis (ileus)


What is the differential diagnosis of infant constipation?


Hirschsprung’s disease, CF (cystic fibrosis),anteriorly displaced anus, polyps

INGUINAL HERNIA

What is the most commonlyperformed procedure byU.S. pediatric surgeons?

What is the most commoninguinal hernia in children?

What is an indirect inguinalhernia?

What is Hesselbach’s triangle?

What type of hernia goesthrough Hesselbach’s triangle?

What is the incidence ofindirect inguinal hernia inall children?

What is the incidence inpremature infants?


What are the risk factors foran indirect inguinal hernia?

Indirect inguinal hernia repair

Indirect

Hernia lateral to Hesselbach’s triangleinto the internal inguinal ring and downthe inguinal canal (Think: through theabdominal wall indirectly into the internalring and out through the externalinguinal ring)

Triangle formed by:1. Epigastric vessels2. Inguinal ligament3. Lateral border of the rectus sheath

Direct hernia from a weak abdominalfloor; rare in children (0.5% of allinguinal hernias)

�3%

Up to 30%

6:1

Male gender, ascites, V-P shunt, prematurity, family history, meconiumileus, abdominal wall defect elsewhere,hypo/epispadias, connective tissue disease,bladder exstrophy, undescended testicle,CF


Which side is affected morecommonly?

What percentage arebilateral?

What percentage have a family history of indirecthernias?


What is the silk glove sign?

Why should it be repaired?

How is a pediatric inguinalhernia repaired?

Which infants need overnightapnea monitoring/observation?

What is the risk ofrecurrence after highligation of an indirect pediatric hernia?

Describe the steps in therepair of an indirect inguinalhernia from skin to skin.


Right (�60%)

�15%

�10%

Groin bulge, scrotal mass, thickenedcord, silk glove sign

Hernia sac rolls under the finger like thefinger of a silk glove

Risk of incarcerated/strangulated bowelor ovary; will not go away on its own

High ligation of hernia sac (no repair ofthe abdominal wall floor, which is a bigdifference between the procedure in children vs. adults; high refers to highposition on the sac neck next to the peritoneal cavity)

Premature infants; infants younger than 3months of age

�1%

Cut skin, then fat, then Scarpa’s fascia,then external oblique fascia through theexternal inguinal ring; find hernia sacanteriomedially and bluntly separatefrom the other cord structures; ligate sachigh at the neck at the internal inguinalring; resect sac and allow sac stump toretract into the peritoneal cavity; closeexternal oblique; close Scarpa’s fascia;close skin


Define the following terms:Cryptorchidism

Hydrocele

Communicatinghydrocele

Noncommunicatinghydrocele

Can a hernia be ruled out if an inguinal masstransilluminates?


Failure of the testicle to descend into thescrotum

Fluid-filled sac (i.e., fluid in a patentprocessus vaginalis or in the tunicavaginalis around the testicle)

Hydrocele that communicates with theperitoneal cavity and thus fills and drainsperitoneal fluid or gets bigger, thensmaller

Hydrocele that does not communicatewith the peritoneal cavity; stays about thesame size

NO; baby bowel is very thin and willoften transilluminate

CLASSIC INTRAOPERATIVE QUESTIONS DURING REPAIR

OF AN INDIRECT INGUINAL HERNIA

From what abdominal muscle layer is the cremastermuscle derived?

From what abdominal muscle layer is the inguinalligament (a.k.a. Poupart’sligament) derived?

What nerve travels with thespermatic cord?

Name the 5 structures in thespermatic cord.

What is the hernia sac madeof?

Internal oblique muscle

External oblique

Ilioinguinal nerve

1. Cremasteric muscle fibers2. Vas deferens3. Testicular artery4. Testicular pampiniform venous plexus5. With or without hernia sac

Basically peritoneum or a patentprocessus vaginalis


What is the name of thefossa between the testicleand epididymis?

What attaches the testicle tothe scrotum?

How can the opposite sidebe assessed for a herniaintraoperatively?

Name the remnant of theprocessus vaginalis aroundthe testicle.

What is a Littre’s inguinalhernia?

What may a yellow/orangetissue that is not fat be onthe spermatic cord/testicle?

What is the most commonorgan in an inguinal herniasac in boys?

What is the most commonorgan in an inguinal herniasac in girls?

What lies in the inguinal canalin girls instead of the vas?

Where in the inguinal canaldoes the hernia sac lie in rela-tion to the other structures?

What is a “cord lipoma”?


Fossa of Geraldi

Gubernaculum

Many surgeons operatively explore theopposite side when they repair theaffected side

Laparoscope is placed into theabdomen via the hernia sac and theopposite side internal inguinal ringis examined

Tunica vaginalis

Hernia with a Meckel’s diverticulum inthe hernia sac

Adrenal rest

Small intestine

Ovary/fallopian tube

Round ligament

Anteriomedially

Preperitoneal fat on the cord structures(pushed in by the hernia sac); not areal lipoma

Should be removed surgically, if feasible


Within the spermatic cord,do the vessels or the vas liemedially?

What is a small outpouchingof testicular tissue off of thetesticle?

What is a “blue dot sign”?

How is a transected vastreated?

How do you treat atransected ilioinguinalnerve?

What happens if you cut theilioinguinal nerve?


Vas is medial to the testicular vessels

Testicular appendage (a.k.a. the appendixtestes); should be removed with electrocautery

Blue dot on the scrotal skin from atwisted testicular appendage

Repair with primary anastomosis

Should not be repaired; many surgeonsligate it to inhibit neuroma formation

Loss of sensation to the medial aspect ofthe inner thigh and scrotum/labia; loss ofcremasteric reflex

UMBILICAL HERNIA

What is it?


What are the indications forsurgical repair?

Fascial defect at the umbilical ring

1. African American infant2. Premature infant

1. �1.5 cm defect2. Bowel incarceration3. �4 years of age

GERD

What is it?


GastroEsophageal Reflux Disease

LES malfunction/malposition, hiatal hernia,gastric outlet obstruction, partial bowelobstruction, common in cerebral palsy




What cytologic aspirate finding on bronchoscopy candiagnose aspiration ofgastric contents?

What is the medical/conservative treatment?




Spitting up, emesis, URTI, pneumonia,laryngospasm from aspiration of gastriccontents into the tracheobronchial tree,failure to thrive

24-hour pH probe, bronchoscopy, UGI(manometry, EGD, U/S)

Lipid-laden macrophages (from phagocytosis of fat)

H2 blockersSmall meals/rice cerealElevation of head

“SAFE”:StrictureAspiration, pneumonia/asthmaFailure to thriveEsophagitis

Nissen 360� fundoplication, with orwithout G tube

CONGENITAL PYLORIC STENOSIS

What is it? Hypertrophy of smooth muscle of pylorus,resulting in obstruction of outflow


Family history, firstborn males are affectedmost commonly, decreased incidence inAfrican American population



What is the average age atonset?


Why is the vomiting nonbilious?

What are the signs?






1 in 750 births, M:F ratio � 4:1

Usually from 2 weeks after birth to about2 months (“2 to 2”)

Increasing frequency of regurgitation,leading to eventual nonbilious projectilevomiting

Obstruction is proximal to the ampulla ofVater

Abdominal mass or “olive” in epigastricregion (85%), hypokalemic hypochloremicmetabolic alkalosis, icterus (10%), visiblegastric peristalsis, paradoxic aciduria,hematemesis (�10%)

Pylorospasm, milk allergy, increased ICP, hiatal hernia, GERD, adrenal insufficiency, uremia, malrotation, duodenal atresia, annular pancreas, duodenal web

Usually by history and physical examalone

U/S—demonstrates elongated (�15 mm)pyloric channel and thickened musclewall (�3.5 mm)

If U/S is nondiagnostic, then bariumswallow—shows “string sign” or “double railroad track sign”

Hydration and correction of alkalosis with D10 NS plus 20 mEq of KCl (Note: the infant’s liver glycogen storesare very small; therefore, use D10; Cl

and hydration will correct the alkalosis)

Surgical, via Fredet-Ramstedt pyloromyotomy (division of circular muscle fibers without entering thelumen/mucosa)


What are the postoperativecomplications?

What is the appropriatepostoperative feeding?

Which vein crosses thepylorus?


Unrecognized incision through the duodenal mucosa, bleeding, wound infection, aspiration pneumonia

Start feeding with Pedialyte® at 6 to 12hours postoperatively; advance to full-strength formula over 24 hours

Vein of Mayo

DUODENAL ATRESIA

What is it?


What are the signs?




What are the associatedabnormalities?

Complete obstruction or stenosis of duodenum caused by an ischemic insult during development or failure ofrecanalization

85% are distal to the ampulla of Vater,15% are proximal to the ampulla of Vater(these present with nonbilious vomiting)

Bilious vomiting (if distal to the ampulla),epigastric distention

Malrotation with Ladd’s bands, annularpancreas

Plain abdominal film revealing “doublebubble,” with one air bubble in the stomach and the other in the duodenum

Duodenoduodenostomy orduodenojejunostomy

50% to 70% have cardiac, renal, or othergastrointestinal defects; 30% havetrisomy 21

MECONIUM ILEUS

What is it?


Intestinal obstruction from solidmeconium concretions

Occurs in �15% of infants with CF



What percentage of patientswith meconium ileus haveCF (cystic fibrosis)?

What are the signs/symptomsof meconium ileus?

What is Neuhauser’s sign?




What should you removeduring all operative cases?

What is the long-term medical treatment?

What is cystic fibrosis (CF)?

What is DIOS?

�95%

Bilious vomiting, abdominal distention,failure to pass meconium, Neuhauser’ssign, peritoneal calcifications

A.k.a. “soap bubble” sign: ground glassappearance in the RLQ on AXR from viscous meconium mixing with air

Family history of CF, plain abdominalfilms showing significant dilation of similar-sized bowel loops, but few if anyair-fluid levels, BE may demonstrate“microcolon” and inspissated meconiumpellets in the terminal ileum

70% nonoperative clearance ofmeconium using gastrografin enema,�� acetylcysteine, which is hypertonicand therefore draws fluid into lumen,separating meconium pellets from bowelwall (60% success rate)

If enema is unsuccessful, then enterotomywith intraoperative catheter irrigationusing acetylcysteine (Mucomyst®)

Appendix

Pancreatic enzyme replacement

Inherited disorder of epithelial Cl

transport defect affecting sweat glands,airways, and GI tract (pancreas, intestine);diagnosed by sweat test (elevated levels ofNaCl �60 mEq/liter) and genetic testing

Distal Intestinal Obstruction Syndrome:intestinal obstruction in older patients withCF from inspissated luminal contents



MECONIUM PERITONITIS

What is it?

What are the signs?

Sign of intrauterine bowel perforation;sterile meconium leads to an intenselocal inflammatory reaction with eventualformation of calcifications

Calcifications on plain films

MECONIUM PLUG SYNDROME

What is it?



What is the nonoperativetreatment?


Is meconium plug highlyassociated with CF?

Colonic obstruction from unknown factors that dehydrate meconium, forming a “plug”

Neonatal small left colon syndrome

Abdominal distention and failure to passmeconium within first 24 hours oflife; plain films demonstrate many loopsof distended bowel and air-fluid levels

Contrast enema is both diagnostic andtherapeutic; it demonstrates “microcolon”to the point of dilated colon (usually intransverse colon) and reveals copiousintraluminal material

Hirschsprung’s disease

No; �5% of patients have CF, in contrastto meconium ileus, in which nearly allhave CF (95%)

ANORECTAL MALFORMATIONS

What are they? Malformations of the distal GI tract inthe general categories of anal atresia,imperforate anus, and rectal atresia

IMPERFORATE ANUS

What is it? Congenital absence of normal anus (complete absence or fistula)



Define a “high” imperforateanus.

Define “low” imperforateanus.

Which type is much morecommon in women?





Low imperforate anuswith anal fistula?

High imperforate anus?

Rectum patent to level abovepuborectalis sling

Rectum patent to below puborectalissling

Low

Vertebral abnormalities, Anal abnormalities,Cardiac, TE fistulas, Esophageal Atresia,Radial/Renal abnormalities, Lumbarabnormalities (VACTERL; mostcommonly TE fistula)

No anus, fistula to anal skin or bladder,UTI, fistula to vagina or urethra, bowelobstruction, distended abdomen, hyperchloremic acidosis

Physical exam, the classic Cross table“invertogram” plain x-ray to see level ofrectal gas (not very accurate), perinealultrasound

Dilatation of anal fistula and subsequentanoplasty

Diverting colostomy and mucous fistula;neoanus is usually made at 1 year of age

HIRSCHSPRUNG’S DISEASE


What is it?


Aganglionic megacolon

Neurogenic form of intestinal obstructionin which obstruction results from inadequate relaxation and peristalsis;absence of normal ganglion cells of therectum and colon

Family history; 5% chance of having asecond child with the affliction





What is the classic history?


What imaging studies shouldbe ordered?

What is needed fordefinitive diagnosis?

What is the “colonic transition zone”?


4:1

Aganglionosis begins at the anorectal lineand involves rectosigmoid in 80% of cases(10% have involvement to splenic flexure,and 10% have involvement of entire colon)

Abdominal distention and bilious vomiting;�95% present with failure to pass meconium in the first 24 hours; may alsopresent later with constipation, diarrhea,and decreased growth

Failure to pass meconium in the first 24 hours of life

Meconium plug syndrome, meconiumileus, sepsis with adynamic ileus, colonicneuronal dysplasia, hypothyroidism,maternal narcotic abuse, maternal hypermagnesemia (tocolysis)

AXR: reveals dilated colonUnprepared barium enema: reveals

constricted aganglionic segment with dilated proximal segment, butthis picture may not develop for 3 to 6 weeks; BE will also demonstrateretention of barium for 24 to 48 hours(normal evacuation � 10 to 18 hours)

Rectal biopsy: for definitive diagnosis,submucosal suction biopsy is adequate in90% of cases; otherwise, full-thicknessbiopsy should be performed to evaluateAuerbach’s plexus

Transition (taper) from aganglionic smallcolon into the large dilated normal colonseen on BE

In neonates, a colostomy proximal to thetransition zone prior to correction, to allowfor pelvic growth and dilated bowel toreturn to normal size




What is a “leveling”colostomy?

Describe the following procedures:

Swenson

Colostomy performed for Hirschsprung’sdisease at the level of normally innervatedganglion cells as ascertained on frozensection intraoperatively

Primary anastomosis between the analcanal and healthy bowel (rectum removed)

Duhamel Anterior, aganglionic region of therectum is preserved and anastomosed toa posterior portion of healthy bowel; afunctional rectal pouch is thereby created(Think: duha � dual barrels side by side)

HRF

'07

“Dual barrels”


What is the new trend insurgery for Hirschsprung’sdisease?


No colostomy; remove aganglionic colon(as confirmed on frozen section) and perform pull-through anastomosis at thesame time (Boley modification)

Overall survival rate �90%; �96% of patients continent; postoperativesymptoms improve with age


Soave A.k.a. endorectal pull-through; this pro-cedure involves bringing proximal normalcolon through the aganglionic rectum,which has been stripped of its mucosa butotherwise present (Think: SOAVE �SAVE the rectum, lose the mucosa)

MALROTATION AND MIDGUT VOLVULUS

What is it?

Where is the cecum?

Failure of the normal bowel rotation,with resultant abnormal intestinal attachments and anatomic positions

With malrotation, the cecum usually endsup in the RUQ



Ladd’sbands

HRF ‘07

What is the usual age atonset?

What is the usual presentation?

Why is the vomiting bilious?




33% are present by 1 week of age, 75%by 1 month, and 90% by 1 year

Sudden onset of bilious vomiting (biliousvomiting in an infant is malrotationuntil proven otherwise!)

“Twist” is distal to the ampulla of Vater

Upper GI contrast study showing cutoffin duodenum; BE showing abnormalposition of cecum in the upper abdomen

Volvulus with midgut infarction, leading todeath or necessitating massive enterectomy(rapid diagnosis is essential!)

IV antibiotics and fluid resuscitation withLR, followed by emergent laparotomy withLadd’s procedure; second-look laparotomyif bowel is severely ischemic in 24 hours todetermine if remaining bowel is viable

What are Ladd’s bands? Fibrous bands that extend from theabnormally placed cecum in the RUQ,often crossing over the duodenum andcausing obstruction


What is the Ladd’sprocedure?

In what direction is thevolvulus reduced—clockwiseor counterclockwise?

Where is the cecum afterreduction?

What is the cause of biliousvomiting in an infant untilproven otherwise?


1. Counterclockwise reduction ofmidgut volvulus

2. Splitting of Ladd’s bands3. Division of peritoneal attachments to

the cecum, ascending colon4. Appendectomy

Rotation of the bowel in a counterclockwise direction

LLQ

Malrotation with midgut volvulus

OMPHALOCELE

What is it?

How is it diagnosed prenatally?

What comprises the “sac”?

What organ is often found protruding from an omphalocele, but isalmost never found with agastroschisis?





Defect of abdominal wall at umbilicalring; sac covers extruded viscera

May be seen on fetal U/S after 13 weeks’gestation, with elevated maternal AFP

Peritoneum and amnion

The liver

�1 in 5000 births

Prenatal U/S

Malrotation of the gut, anomalies

1. NG tube for decompression2. IV fluids3. Prophylactic antibiotics4. Surgical repair of the defect


What is the treatment of asmall defect (�2 cm)?

What is the treatment of amedium defect (2–10 cm)?


Closure of abdominal wall

Removal of outer membrane and placementof a silicone patch to form a “silo,” tem-porarily housing abdominal contents; thesilo is then slowly decreased in size over 4to 7 days, as the abdomen accommodatesthe viscera; then the defect is closed

Omphalocelereduced

Omphalocele

Silastic silo

HRF

'04

What is the treatment of“giant” defects (�10 cm)?

Skin flaps or treatment with Betadine®

spray, mercurochrome, or silver sulfadiazine(Silvadene®) over defect; this allows aneschar to form, which epithelializes overtime, allowing opportunity for futurerepair months to years later



Of what “pentalogy” isomphalocele a part?

What is the pentalogy ofCantrell?


50% of cases occur with abnormalities of the GI tract, cardiovascular system, GU tract, musculoskeletal system, CNS, and chromosomes

Pentalogy of Cantrell

“D COPS”:Diaphragmatic defect (hernia)

Cardiac abnormalityOmphalocelePericardium malformation/absenceSternal cleft

GASTROSCHISIS

What is it?

How is it diagnosed prenatally?

Where is the defect?

On what side of the umbilicus is the defect most commonly found?

What is the usual size of thedefect?



Defect of abdominal wall; sac does notcover extruded viscera

Possible at fetal ultrasound after 13 weeks’gestation, elevated maternal AFP

Lateral to the umbilicus (Think:gAstrochisis � lAteral)

Right

2 to 4 cm

Thick edematous peritoneum fromexposure to amnionic fluid;malrotation of the gut

Other complications include hypothermia;hypovolemia from third-spacing; sepsis;and metabolic acidosis from hypovolemiaand poor perfusion, NEC, prolongedileus

Prenatal U/S



What is a “silo”?



What are the majordifferences compared withomphalocele?

How can you remember theposition of omphalocele vs.gastroschisis?

How do you remember thatomphalocele is associatedwith abnormalities in 50% ofcases?


Primary—NG tube decompression, IVfluids (D10 LR), and IV antibiotics

Definitive—surgical reduction of visceraand abdominal closure; may requirestaged closure with silo

Silastic silo is a temporary housing forexternal abdominal contents; silo is slowlytightened over time

�90% survival rate

Unlike omphalocele, relatively uncommonexcept for intestinal atresia, which occursin 10% to 15% of cases

No membrane coveringsUncommon associated abnormalitiesLateral to umbilicus—not on umbilicus

Think: OMphalocele � ON the umbilicus

Think: Omphalocele � “Oh no, lots ofabnormalities”

POWER REVIEW OF OMPHALOCELE AND GASTROSCHISIS

What are the differencesbetween omphalocele andgastroschisis in terms of thefollowing characteristics:

Anomalies?

Peritoneal/amnion covering (sac)?

Position of umbilicalcord?

Common in omphalocele (50%),uncommon in gastroschisis

Always with omphalocele—never with gastroschisis

On the sac with omphalocele, from skinto the left of the gastroschisis defect


Thick bowel?

Protrusion of liver?

Large defect?


Common with gastroschisis, rare withomphalocele (unless sac ruptures)

Common with omphalocele, almost neverwith gastroschisis

Omphalocele

APPENDICITIS

What is it?


What is the affected age?





Obstruction of the appendiceal lumen(fecalith, lymphoid hyperplasia), producing a closed loop with resultantinflammation that can lead to necrosisand perforation

Most common surgical disease requiringemergency surgery in children

Very rare before 3 years of age

Onset of referred or periumbilical painfollowed by anorexia, nausea, and vomiting (Note: Unlike gastroenteritis,pain precedes vomiting, thenmigrates to the RLQ, where itintensifies from local peritonealirritation)

If the patient is hungry and can eat,seriously question the diagnosis ofappendicitis

History and physical exam

Signs of peritoneal irritation may be present—guarding, muscle spasm, reboundtenderness, obturator and Psoas signs;low-grade fever rising to high grade ifperforation occurs

Intussusception, volvulus, Meckel’s diverticulum, Crohn’s disease, ovariantorsion, cyst, tumor, perforated ulcer,pancreatitis, PID, ruptured ectopic pregnancy, mesenteric lymphadenitis


What is the common bacterial cause of mesentericlymphadenitis?

What are the associated labfindings with appendicitis?

What is the role of urinalysis?

What is the “hamburger”sign?

What radiographic studiesmay be performed?


How long should antibioticsbe administered if nonperforated?

How long if perforated?

If a normal appendix isfound upon exploration,what must be examined/ruled out?


Yersinia enterocolitica

Increased WBC (�10,000 per mm3 in�90% of cases, with a left shift in most)

To evaluate for possible pyelonephritis orrenal calculus, but mild hematuria andpyuria are common in appendicitisbecause of ureteral inflammation

Ask patients with suspected appendicitisif they would like a hamburger or favoritefood; if they can eat, seriously questionthe diagnosis

Often none; CXR to rule out RML orRLL pneumonia; abdominal films areusually nonspecific, but calcified fecalithis present in 5% of cases; U/S to evaluatefor ovarian/gynecologic pathology

Nonperforated—prompt appendectomyand cefoxitin to avoid perforation

Perforated—triple antibiotics, fluid resuscitation, and prompt appendectomy; all pus is drained andcultures obtained, with postoperativeantibiotics continued for 5 to 7 days, drain

24 hours

Usually 5 to 7 days or until WBCs arenormal and patient is afebrile

Meckel’s diverticulum, Crohn’s disease,intussusception, gynecologic disease


What is the approximate riskof perforation?


�25% after 24 hours from onset ofsymptoms

�50% by 36 hours�75% by 48 hours

INTUSSUSCEPTION

What is it?


What is the usual age atpresentation?




What is the intussuscipiens?

What is the intussusceptum?

Identify locations 1 and 2 onthe following illustration:

Obstruction caused by bowel telescopinginto the lumen of adjacent distal bowel;may result when peristalsis carries a“leadpoint” downstream

Most common cause of small bowelobstruction in toddlers (�2 years old)

Disease of infancy; 60% present from 4 to12 months of age, 80% by 2 years of age

Terminal ileum involving ileocecal valveand extending into ascending colon

Hypertrophic Peyer’s patches, which actas a lead point; many patients have priorviral illness

Alternating lethargy and irritability (colic),bilious vomiting, “currant jelly” stools,RLQ mass on plain abdominal film,empty RLQ on palpation (Dance’s sign)

Recipient segment of bowel (Think:recipiens � intussuscipiens)

Leading point or bowel that enters theintussuscipiens

1. Intussuscipiens2. Intussusceptum


How can the spelling of intussusception beremembered?


What are the causes ofintussusception in olderpatients?


Imagine a navy ship named TheU.S.S. U.S.—INTUSSUSCEPTION

Air or barium enema; 85% reduce with hydrostatic pressure (i.e., barium � meter elevation air � maximum of 120 mm Hg); if unsuccessful, thenlaparotomy and reduction by “milking”the ileum from the colon should be performed

Meckel’s diverticulum, polyps, andtumors, all of which act as a lead point

MECKEL’S DIVERTICULUM

What is it?


What is the major differentialdiagnosis?

Is it a true diverticulum?



What is the usual age atonset of symptoms?

Remnant of the omphalomesenteric duct/vitelline duct, which connects theyolk sac with the primitive midgut in theembryo

Between 45 and 90 cm proximal to theileocecal valve on the antimesenteric border of the bowel

Appendicitis

Yes; all layers of the intestine are foundin the wall

2% of the population at autopsy, but�90% of these are asymptomatic

2 to 3� more common in males

Most frequently in the first 2 years of life,but can occur at any age



What percentage of caseshave heterotopic tissue?

What is the most commonectopic tissue in a Meckel’sdiverticulum?

What other pediatric diseaseentity can also present withGI bleeding secondary toectopic gastric mucosa?

What is the most commoncause of lower GI bleedingin children?

What is the “rule of 2s”?

What is a Meckel’s scan?


Intestinal hemorrhage (painless)—50%Accounts for 50% of all lower GI

bleeding in patients younger than2 years; bleeding results fromectopic gastric mucosa secretingacid S ulcer S bleeding

Intestinal obstruction—25%Most common complication in

adults; includes volvulus and intussusception

Inflammation ( perforation)—20%

�50%; usually gastric mucosa (85%), butduodenal, pancreatic, and colonic mucosahave been described

Gastric mucosa

Enteric duplications

Meckel’s diverticulum with ectopicgastric mucosa

2% are symptomaticFound �2 feet from ileocecal valveFound in 2% of the populationMost symptoms occur before age 2One of 2 will have ectopic tissueMost diverticula are about 2 inches longMale:female ratio � 2:1

Scan for ectopic gastric mucosa inMeckel’s diverticulum; uses technetiumTc 99m pertechnetate IV, which is preferentially taken up by gastric mucosa



NECROTIZING ENTEROCOLITIS


What is it?

What are the predisposingconditions?

What is the pathophysiologicmechanism?



What are the radiographicfindings?

What are the lab findings?


What are the surgical indications?

NEC

Necrosis of intestinal mucosa, often withbleeding; may progress to transmuralintestinal necrosis, shock/sepsis, and death

PREMATURITYStress: shock, hypoxia, RDS, apneic

episodes, sepsis, exchange transfusions,PDA and cyanotic heart disease,hyperosmolar feedings, polycythemia,indomethacin

Probable splanchnic vasoconstriction withdecreased perfusion, mucosal injury, andprobable bacterial invasion

Most common cause of emergent laparotomy in the neonate

Abdominal distention, vomiting, hemepositive or gross rectal bleeding, fever orhypothermia, jaundice, abdominal wallerythema (consistent with perforationand abscess formation)

Fixed, dilated intestinal loops; pneumatosisintestinalis (air in the bowel wall); freeair; and portal vein air (sign of advanceddisease)

Low hematocrit, glucose, and platelets

Most are managed medically:1. Cessation of feedings2. OG tube3. IV fluids4. IV antibiotics5. Ventilator support, as needed

Free air in abdomen revealingperforation, and positive peritoneal taprevealing transmural bowel necrosis


Operation?

What is an option for bowelperforation in �1000 gramNEC patients?

Is portal vein gas orpneumatosis intestinalisalone an indication for operation with NEC?

What are the indications forperitoneal tap?




1. Resect2. Stoma

Placement of percutaneous drain (without laparotomy!)

No

Severe thrombocytopenia, distendedabdomen, abdominal wall erythema,unexplained clinical downturn

Bowel necrosis, gram-negative sepsis,DIC, wound infection, cholestasis, shortbowel syndrome, strictures, SBO

�80% overall survival rate

BILIARY TRACT

What is “physiologicjaundice”?

What enzyme is responsiblefor conjugation of bilirubin?

How is hyperbilirubinemiafrom “physiologic jaundice”treated?

What is Gilbert’s syndrome?

What is Crigler-Najjarsyndrome?

Hyperbilirubinemia in the first 2 weeksof life from inadequate conjugation ofbilirubin

Glucuronyl transferase

UV light

Partial deficiency of glucuronyltransferase, leading to intermittentasymptomatic jaundice in the second orthird decade of life

Rare genetic absence of glucuronyl transferase activity, causing unconjugatedhyperbilirubinemia, jaundice, and deathfrom kernicterus (usually within the firstyear)



BILIARY ATRESIA

What is it?



What are the lab findings?

What is the classic “rule of 5s” of indirectbilirubinemia?




How does a Kasai work?

Obliteration of extrahepatic biliary tree

One in 16,000 births

Persistent jaundice (normal physiologicjaundice resolves in �2 weeks),hepatomegaly, splenomegaly, ascites and other signs of portal hypertension,acholic stools, biliuria

Mixed jaundice is always present (i.e.,both direct and indirect bilirubinincreased), with an elevated serum alkaline phosphatase level

Bizarre: with progressive hyperbilirubinemia, jaundice progressesby levels of 5 from the head to toes: 5 mg/dL � jaundice of head, 10 mg/dL � jaundice of trunk, 15 mg/dL �jaundice of leg/feet

Neonatal hepatitis (TORCH); biliaryhypoplasia

1. U/S to rule out choledochal cyst andto examine extrahepatic bile ducts andgallbladder

2. HIDA scan—shows no excretion intothe GI tract (with phenobarbitalpreparation)

3. Operative cholangiogram and liverbiopsy

Early laparotomy by 2 months of agewith a modified form of the Kasaihepatoportoenterostomy

Anastomosis of the porta hepatis and thesmall bowel allows drainage of bile viamany microscopic bile ducts in thefibrous structure of the porta hepatis


What if the Kasai fails?

What are the possible postoperative complications?



Revise or liver transplantation

Cholangitis (manifested as decreased bile secretion, fever, leukocytosis, and recurrence of jaundice), progressive cirrhosis (manifested as portal hypertension with bleeding varices, ascites, hypoalbuminemia,hypothrombinemia, and fat-soluble vitamin K, A, D, E deficiencies)

Between 25% and 30% have other anomalies, including annular pancreas,duodenal atresia, malrotation, polysplenicsyndrome, situs inversus, and preduodenalportal vein; 15% have congenital heartdefects

CHOLEDOCHAL CYST

What is it?



What are the anatomic variants:

I?

Cystic enlargement of bile ducts; mostcommonly arises in extrahepatic ducts, butcan also arise in intrahepatic ducts

50% present with intermittent jaundice,RUQ mass, and abdominal pain; may alsopresent with pancreatitis

Cholelithiasis, cirrhosis, carcinoma, andportal HTN

Dilation of common hepatic and commonbile duct, with cystic duct entering thecyst; most common type (90%)


III? Choledochocele represented by anintraduodenal cyst

IV? Multiple extrahepatic cysts, intrahepaticcysts, or both

V? Single or multiple intrahepatic cysts

II?


Lateral saccular cystic dilation




What condition are thesepatients at increased risk of developing?


U/S

Operative cholangiogram to clarifypathologic process and delineate thepancreatic duct, followed by completeresection of the cyst and a Roux-en-Yhepatojejunostomy

Cholangiocarcinoma often arises inthe cyst; therefore, treat by completeprophylactic resection of the cyst

CHOLELITHIASIS

What is it?

What are the commoncauses in children?




Formation of gallstones

Etiology differs somewhat from that of adults; the most common cause is cholesterol stones, but there is anincreased percentage of pigmentedstones from hemolytic disorders

Hereditary spherocytosis, thalassemia,pyruvate kinase deficiency, sickle-cell disease, cystic fibrosis, long-termparenteral nutrition, idiopathic

Use of oral contraceptives, teenage, positive family history

Cholecystectomy is recommended for allchildren with gallstones

ANNULAR PANCREAS

What is an annularpancreas?



Congenital pancreatic abnormality withcomplete encirclement of the duodenumby the pancreas

Duodenal obstruction

Duodenoduodenostomy bypass ofobstruction (do not resect the pancreas!)



TUMORS

What is the differential diagnosis of pediatricabdominal mass?

Wilms’ tumor, neuroblastoma, hernia,intussusception, malrotation with volvulus,mesenteric cyst, duplication cyst, livertumor (hepatoblastoma/hemangioma),rhabdomyosarcoma, teratoma

WILMS’ TUMOR

What is it?





What are the signs?

What are the diagnosticradiologic tests?

Define the stages:Stage I

Stage II

Stage III

Stage IV

Stage V

Embryonal tumor of renal origin

Very rare: 500 new cases in the UnitedStates per year

Usually between 1 and 5 years of age

Usually asymptomatic except for abdominal mass; 20% of patients presentwith minimal blunt trauma to mass

Found during dressing or bathing

Abdominal mass (most do not cross themidline); hematuria (10%–15%); HTN in20% of cases, related to compression ofjuxtaglomerular apparatus; signs of Beckwith-Wiedemann syndrome

Abdominal and chest CT

Limited to kidney and completely resected

Extends beyond kidney, but completelyresected; capsule invasion and perirenaltissues may be involved

Residual nonhematogenous tumor afterresection

Hematogenous metastases (lung, distallymph nodes, and brain)

Bilateral renal involvement


What are the best indicatorsof survival?


What is the neoadjuvanttreatment?


What is the Beckwith-Wiedemann syndrome?


Stage and histologic subtype of tumor; 85%of patients have favorable histology (FH);15% have unfavorable histology (UH);overall survival for FH is 85% for all stages

Radical resection of affected kidney with evaluation for staging, followed bychemotherapy (low stages) and radiation(higher stages)

Large tumors may be shrunk withchemotherapy/XRT to allow for surgicalresection

Aniridia, hemihypertrophy, Beckwith-Wiedemann syndrome,neurofibromatosis, horseshoe kidney

Syndrome of:1. Umbilical defect2. Macroglossia (big tongue)3. Gigantism4. Visceromegaly (big organs) (Think:

Wilms’ � Beckwith-Wiedemann)

NEUROBLASTOMA

What is it?

What are the anatomic locations?

With which types of tumordoes a patient with Horner’ssyndrome present?



Embryonal tumor of neural crest origin

Adrenal medulla—50%Paraaortic abdominal paraspinal

ganglia—25%Posterior mediastinum—20%Neck—3%Pelvis—3%

Neck, superior mediastinal tumors

One in 7000 to 10,000 live births; mostcommon solid malignant tumor ofinfancy; most common solid tumor inchildren outside the CNS

�50% are diagnosed by 2 years of age�90% are diagnosed by 8 years of age



What are the signs?

LABS?

What are the diagnosticradiologic tests?

What is the classic abdominalplain x-ray finding?

How do you access bonemarrow involvement?

What is the difference inposition of tumors inneuroblastoma versusWilms’ tumors?


Vary by tumor location—anemia, failureto thrive, weight loss, and poor nutritionalstatus with advanced disease

Asymptomatic abdominal mass (palpablein 50% of cases), respiratory distress(mediastinal tumors), Horner’s syndrome(upper chest or neck tumors), proptosis(with orbital metastases), subcutaneoustumor nodules, HTN (20%–35%)

24-hour urine to measure VMA, HVA,and metanephrines (elevated in �85%);neuron-specific enolase, N-myc oncogene,DNA ploidy

CT scan, MRI, I-MIBG, somatostatinreceptor scan

Calcifications (�50%)

Bone marrow aspirate

Neuroblastoma may cross the midline,but Wilms’ tumors do so only rarely

Lateraltomidline

Midline

Adrenal:Neuroblastoma

KidneyWilms

Crossesmidline

What is the treatment? Depends on staging


Define the stages:Stage I

Stage II

Stage III

Stage IV

Stage IVS

What is the treatment ofeach stage:

Stage I?

Stage II?

Stage III?

Stage IV?

Stage IVS?

What is the survival rate ofeach stage:

Stage I?

Stage II?

Stage III?

Stage IV?

Stage IVS?


Tumor is confined to organ of origin

Tumor extends beyond organ of originbut not across the midline

Tumor extends across the midline

Metastatic disease

Infants: Localized primary tumor doesnot cross the midline, but remotedisease is confined to the liver, subcutaneous/skin, and bone marrow

Surgical resection

Resection and chemotherapy �� XRT

Resection and chemotherapy/XRT

Chemotherapy/XRT S resection

In the infant with small tumor andasymptomatic � observe as many willregress “spontaneously”

�90%

�80%

�40%

�15%

Survival rate is �80%! Note: these tumorsare basically stage I or II with metastasis toliver, subcutaneous tissue, or bone marrow;most of these patients, if younger than 1 year of age, have a spontaneous cure(Think: Stage IVS � Special condition)


What are the laboratoryprognosticators?

Which oncogene is associatedwith neuroblastoma?


Aneuploidy is favorable! The lower thenumber of N-myc oncogene copies, thebetter the prognosis

N-myc oncogeneThink: N-myc � Neuroblastoma

RHABDOMYOSARCOMA

What is it?


What is the age distribution?




What is the treatment:Resectable?

Unresectable?

Highly malignant striated muscle sarcoma

Most common sarcoma in children

Bimodal:1. 2–5 years2. 15–19 years

1. Head and neck (40%)2. GU tract (20%)3. Extremities (20%)

Mass

Tissue biopsy, CT scan, MRI, bone marrow

Surgical excision, �� chemotherapy andradiation therapy

Neoadjuvant chemo/XRT, then surgicalexcision

HEPATOBLASTOMA

What is it?



Malignant tumor of the liver (derivedfrom embryonic liver cells)

Presents in the first 3 years of life

2:1



What percentage will havean elevated �-fetoproteinlevel?


What is the overall survivalrate?

What is the major differencein age presentationbetween hepatoma andhepatoblastoma?


Physical exam—abdominal distention;RUQ mass that moves with respiration

Elevated serum �-fetoprotein and ferritin(can be used as tumor markers)

CT scan of abdomen, which oftenpredicts resectability

�90%

Resection by lobectomy or trisegment-ectomy is the treatment of choice (plus postoperative chemotherapy); large tumors may require preoperativechemotherapy and subsequent hepaticresection

�50%

Hepatoblastoma presents at youngerthan 3 years of age; hepatoma presentsat older than 3 years of age and in adolescents

PEDIATRIC TRAUMA

What is the leading cause ofdeath in pediatric patients?

How are the vast majority of splenic and liver injuriestreated in children?

What is a common simulatorof peritoneal signs in theblunt pediatric trauma victim?

How do you estimate normalsystolic blood pressure (SBP)in a child?

Trauma

Observation (i.e., nonoperatively)

Gastric distention (place an NG tube)

80 � 2 � age (e.g., a 5-year-old childshould have an SBP of about 90)


What is the 20–20–10 rulefor fluid resuscitation of theunstable pediatric traumapatient?

What CT scan findings suggest small bowel injury?

What is the treatment forduodenal hematoma?


First give a 20-cc/kg LR bolus followedby a second bolus of 20-cc/kg LR bolus if needed; if the patient is still unstableafter the second LR bolus, then administera 10-cc/kg bolus of blood

Free fluid with no evidence of liver or spleen injury; free air, contrast leak,bowel thickening, mesentery streaking

Observation with NGT and TPN

OTHER PEDIATRIC SURGERY QUESTIONS

What is bilious vomiting inan infant?

What does TORCHES standfor?

What is the commonpediatric sedative?

What are the contraindications to circumcision?

When should an umbilicalhernia be repaired?

What is the cancer risk inthe cryptorchid testicle?

When should orchidopexybe performed?

Malrotation, until proven otherwise!(About 90% of patients with malrotationpresent before the first year of life)

Nonbacterial fetal and neonatal infections:TOxoplasmosis, Rubella, Cytomegalovirus(CMV), HErpes, Syphilis

Chloral hydrate

Hypospadias, etc., because the foreskinmight be needed for future repair of theabnormality

�1.5 cm, after 4 years of age; otherwise observe, because most closespontaneously; repair before school ageif it persists

�10� the normal testicular cancer rate

All patients with undescended testicleundergo orchidopexy after 1 year of age


What are some signs of childabuse?

What is the treatment ofchild abuse?

What is Dance’s sign?

What is the treatment ofhemangioma?

What are the indications foroperation in hemangiomas?

What are treatment optionsfor hemangiomas?

What is the most commonbenign liver tumor inchildren?

What is Eagle-Barrett’s syndrome?

What is the Pierre-Robinsyndrome?

What is the major concernwith Pierre-Robin syndrome?

What are the most commoncancers in children?

What is the most commonsolid neoplasm in infants?

What is the most commonsolid tumor in children?


Cigarette burns, rope burns, scald to posterior thighs and buttocks, multiplefractures/old fractures, genital trauma,delay in accessing health care system

Admit the patient to the hospital

Empty RLQ in patients with ileocecalintussusception

Observation, because most regress spontaneously

Severe thrombocytopenia, congestiveheart failure, functional impairment(vision, breathing)

Steroids, radiation, surgical resection,angiographic embolization

Hemangioma

A.k.a. prune belly; congenital inadequateabdominal musculature (very lax and thin)

Classic triad:1. Big, protruding tongue (glossoptosis)2. Small mandible (micrognathia)3. Cleft palate

Airway obstruction by the tongue!

1. Leukemia2. CNS tumors3. Lymphomas

Neuroblastoma

CNS tumors


What syndrome must youconsider in the patient withabdominal pain, hematuria,history of joint pain, and apurpuric rash?

What is Apley’s law?

What is the most commoncause of SBO in children?

What is a patent urachus?

What is a “Replogle tube”?

What are “A’s and B’s”?

What is the “double bubble”sign on AXR?

What is Poland’s syndrome?

What is the treatment ofATYPICAL mycobacteriallymph node infection?

What is the most commoncause of rectal bleeding ininfants?


Henoch-Schönlein syndrome; patientmay also have melena (50%) or at leastguaiac-positive stools (75%)

The further a chronically recurrentabdominal pain is from the umbilicus, thegreater the likelihood of an organic causefor the pain

Hernias

Persistence of the urachus, a communication between the bladder andumbilicus; presents with urine out of theumbilicus and recurrent UTIs

10 French sump pump NG tube forbabies (originally designed by Dr. Reploglefor suction of the esophageal blind pouch of esophageal atresia)

Apnea and Bradycardia episodes inbabies

Gastric bubble and duodenal bubbleon AXR; seen with duodenal obstruction(web, annular pancreas, malrotation withvolvulus, duodenal atresia, etc.)

Absence of pectoralis major muscleAbsence of pectoralis minor muscleOften associated with ipsilateral hand

malformationNipple/breast/right-breast hypoplasia

Surgical removal of the node

Anal fissure


What chromosomalabnormality is associatedwith duodenal web/atresia/stenosis?

Which foreign body past thepylorus must be surgicallyremoved?


Trisomy 21

Batteries!

POWER REVIEW

What is the usual age atpresentation of the followingconditions:

Pyloric stenosis?

Intussusception?

Wilms’ tumor?

Malrotation?

Neuroblastoma?

Hepatoblastoma?

Appendicitis?

2 weeks to 2 months

4 months to 2 years (�80%)

1 to 5 years

Birth to 1 year (�85%)

�50% present by 2 years; �80% present by 8 years

Younger than 3 years

Older than 3 years (but must beconsidered at any age!)

Define the following terms:Blepharoplasty

Face lift

FTSG

Plastic SurgeryChapter 68Eyelid surgery—removing excessskin/fat

Removal of excess facial skin via hairline/chin/ear incisions

Full Thickness Skin Graft


Langer’s lines

Chapter 68 / Plastic Surgery 573

Natural skin lines of minimal tension(e.g., lines across the forehead), incisionsperpendicular to Langer’s lines result inlarger scars than incision parallel to thelines

hrf'02

Mammoplasty

Polydactyly

Rhinoplasty

STSG

Syndactyly

Breast surgery (reduction/augmentation)

Extra fingers

Nose surgery, after trauma or cosmetic

Split Thickness Skin Graft

Webbed fingers

WOUND HEALING

What are the phases ofwound healing?

Think: “In Every Fresh Cut” � IEFC:1. Inflammation2. Epithelialization3. Fibroplasia4. Contraction


What are the actions of thefollowing phases:

Inflammation?

Epithelialization?

Fibroplasia?

Wound contraction?

What is the maximalcontraction of a wound inmm/day?


Vasoconstriction followed by vasodilation,capillary leak

Epithelial coverage of wound

Fibroblasts and accumulation of collagen,elastin, and reticulin

Myofibroblasts contract wound

0.75 mm/day

EPITHELIALIZATION

What degree of bacterialcontamination preventsepithelialization?

In which structures does theepithelium grow fromsuperficial burns/wounds?

In full-thickness burns?

What malignant ulcer isassociated with a long-standing scar/burn?

�100,000 organisms/gm tissue (105)

Epithelial lining of sweat glands and hairfollicles

From wound margins, grows in �1 cmfrom wound edge because no sweatglands or hair follicles remain; thisepithelium has no underlying dermis

Marjolin’s ulcer (a.k.a. burn scarcarcinoma)

WOUND CONTRACTION

What are myofibroblasts?

Which contracts more: anSTSG or an FTSG?

Specialized fibroblasts that behave likesmooth muscle cells to pull the woundedges together following granulation

STSG contracts up to 41% in surfacearea, whereas an FTSG contracts little, if at all


What is granulation tissue?

Name the local factors thatimpair wound healing.

What generalized conditionsinhibit wound healing?

What helps wound healingin patients taking steroids?

When does a wound gainmore than 90% of its maximal tensile strength?

Define the following terms:Laceration

Abrasion

Contusion

Hypertrophic scar

Keloid

Why not clean lacerationswith Betadine®?

What is the best way toclean out a laceration?


Within 4 to 6 days after an open wound,development of capillary beds and fibroblasts provides a healthy base forepithelial growth from wound edges; thistissue also resists bacterial infection

Hematoma, seroma, infection, tight sutures,tight wrap, movement/disturbance of thewound (i.e., poking it with a finger)

AnemiaMalnutritionSteroidsCancerRadiationHypoxiaSepsis

Vitamin A is thought to counteract thedeleterious effect of steroids on woundhealing

After �6 weeks

Jagged wound

Superficial skin removal

Bruise without a break in the skin

Hypertrophic scar within original woundmargins

Proliferative scar tumor progressivelyenlarging scar beyond original woundmargins

Betadine® is harmful to and inhibits normal healthy tissue

Normal saline irrigation; remember,“The solution to pollution is dilution”



SKIN GRAFTS

What is an STSG?

How thick is it?

What is an FTSG?

What are the prerequisitesfor a skin graft to take?

What is a better bed for askin graft: fascia or fat?

How do you increase surfacearea of an STSG?

How does an STSG getnutrition for the first 24 hours?

Split thickness: includes the epidermisand a variable amount of the dermis

10/1000 to 18/1000 of an inch

Full thickness: includes the entire epidermis and dermis

Bed must be vascularized; a graft to abone or tendon will not take

Bacteria must be �100,000Shearing motion and fluid beneath the

graft must be minimized

Fascia (much better blood supply)

Mesh it (also allows for blood/serum tobe removed from underneath the graft)

Imbibition

FLAPS

Where does a random skinflap get its blood supply?

Where does an axial skinflap get its blood supply?

Name some axial flaps andtheir arterial supply.

From the dermal-subdermal plexus

It is vascularized by direct cutaneousarteries

Forehead flap—superficial temporalartery; often used for intraoral lesions

Deltopectoral flap—second, third, andfourth anterior perforators of theinternal mammary artery; often usedfor head and neck wounds

Groin flap—superficial circumflex iliacartery; allows coverage of hand andforearm wounds


What is the most commoncause of flap loss?

What is a simpleadvancement flap?

What is a rotational flap?

What is a “free flap”?

What is a TRAM flap?

What is a “Z-plasty”?


Venous thrombosis

Defect

Pivotpoint

Defect

Flap separated from all vascular supplythat requires microvascular anastomosis(microscope)

Transverse Rectus AbdominisMyocutaneous flap (see page 410)


What is a “V-Y advancementflap”?


Defect

Who operates on hands?

What are the bones of thehand?

What is the distal finger joint?

What is the middle finger joint?

What is the proximal fingerjoint?

What are the “intrinsic”hand muscles?

What is ADDuction andABDuction of the fingers?

Hand SurgeryChapter 69Plastic surgeons and orthopaedic surgeons

Phalanges (fingers)Metacarpal bonesCarpal bones

Distal InterPhalangeal (DIP) joint

Proximal InterPhalangeal (PIP) joint

Metacarpal Phalangeal (MP) joint

Lumbricals, interosseous muscle

ADDuction is to midline and ABDuctionis separation from midline

Midline

AB

Duction ADDuction


What are the trauma zonesof the hand?

Chapter 69 / Hand Surgery 579

5

4

3

3

1

1 2

2

Zone 2:“No Man’s Land”

Where is “no man’s land”? Zone extending from the distal palmarcrease to just beyond the PIP joint (zone 2)

5

4

3

3

1

1 2

2

SENSORY SUPPLY TO THE HAND

What is the ulnar nerve distribution?

What is the significance ofthe “no man’s land”?

Flexor tendon injuries here have a poorprognosis; a hand expert needs to repairthese injuries


What is the radial nerve distribution?


What is the median nervedistribution?

How can the radial nerve motor function betested?

How can the ulnar nervemotor function be tested?

How can the median nervefunction be tested?

1. Wrist and MCP extension2. Abduction and extension of thumb

1. Spread fingers apart against resistance

2. Check ability to cross index and middle fingers

1. Touch the thumb to the pinky (distalmedian nerve)

2. Squeeze examiner’s finger (proximalmedian nerve)


How can the flexordigitorum profundus

(FDP) apparatus be tested?


Check isolated flexion of the finger DIP joint

FDP

FDS

hrf

How can the flexordigitorum superficialis

(FDS) apparatus be tested?

Check isolated flexion of the finger at theMP joint

Where do the digital arteries run?

What hand laceration shouldbe left unsutured?

Should a clamp ever be usedto stop a laceration bleeder?

On medial and lateral sides of the digit

Lacerations from human bites or animalbites

No; use pressure and then tourniquet fordefinitive repair if bleeding does not ceasebecause nerves run with blood vessels!


What is a felon?

What is a paronychia?

What is tenosynovitis?

What are Kanavel’s signs?

Most common bacteria intenosynovitis and paronychia?

How are human and animalhand bites treated?

What unique bacteria arefound in human bites?

What unique bacteria arefound in dog and cat bites?

What is the most commonhand/wrist tumor?

What is an extremely painfultype of subungual tumor?

What is a “boxer’s fracture”?

What is a “drop finger” injury?


Infection in the tip of the finger pad(Think: felon � fingerprints � infectionin pad); treat by incision and drainage

Infection on the side of the fingernail(nail fold); treat by incision and drainage

Tendon sheath infection

Four signs of tenosynovitis:1. Affected finger held in flexion2. Pain over volar aspect of affected

finger tendon sheath upon palpation3. Swelling of affected finger (fusiform)4. Pain on passive extension of

affected finger


Débridement/irrigation/administration ofantibiotics; leave wound open

Eikenella corrodens

Pasteurella multocida

Ganglion cyst

Glomus tumor (subungual: under the nail)

Fracture of the fourth or fifth metacarpal

Laceration of extensor tendon over theMP joint

Cut


What is the classic deformityresulting from laceration ofthe extensor tendon over theDIP joint?


Mallet finger

Cut

What is the classic deformityresulting from laceration ofthe extensor tendon over thePIP joint?

Boutonniere deformity

Cut

Which fracture causes painin the “anatomic snuffbox”?

What is the “safe position”of hand splinting?

Scaphoid fracture; often not seen on x-ray at presentation, usually seen at alater date (2 weeks) on x-ray

Can result in avascular necrosisPlace in a cast if clinically suspected,

regardless of x-ray findings


What is Dupuytren’scontracture?

What is Gamekeeper’sthumb?


Fibrosis of palmar fascia, causingcontracture of and inability to extend digits

Injury to the ulnar collateral ligament ofthe thumb

How should a subungualhematoma be treated?

Release pressure by burning a hole in the nail (use hand-held disposablebattery-operated coagulation probe)

CARPAL TUNNEL SYNDROME

What is it? Compression of the median nerve in thecarpal tunnel

HR

F ‘0

7

Carpaltunnel



What are other causes?


What are the signs?

What is Wartenberg’s sign?

What is the workup?

What is initial treatment?

What are indications for surgery?

What surgery is performed?


Synovitis

“MEDIAN TRAPS”:Median artery (persistent)Edema of pregnancyDiabetesIdiopathicAcromegalyNeoplasm (e.g., ganglioneuroma)

Thyroid (myxedema)Rheumatoid arthritisAmyloidPneumatic drill usageSLE

Pain and numbness in the median nervedistribution

Tinel’s sign (symptoms with percussionover median nerve), Phalen’s test (symptoms with flexion of wrists), thenaratrophy, Wartenberg’s sign

With hand resting on a surface, the fifth digit (“pinky”) rests in ABductioncompared to the other 4 fingers

EMG, nerve conduction study

Nonoperative, rest, wrist splint, NSAIDs

Refractory symptoms, thenar atrophy,thenar weakness

Release transverse carpal ligament



Define:Anosmia

Otorrhea

Dysphagia

Odynophagia

Globus

Otalgia

Trismus

Otolaryngology:Head and NeckSurgery

Chapter 70

Inability to smell

Fluid discharge from ear

Difficulty swallowing

Painful swallowing

Sensation of a “lump in the throat”

Ear pain (often referred from throat)

Difficulty opening mouth

ANATOMY

Define the cranial nerves:I

II

III

IV

V

VI

VII

VIII

IX

X

Olfactory nerve

Optic nerve

Oculomotor nerve

Trochlear nerve

Trigeminal nerve

Abducens nerve

Facial nerve

Vestibulocochlear nerve

Glossopharyngeal nerve

Vagus nerve


XI

XII

Define motor/sensoryactions of the following cranial nerves:

I

II

III

IV

V

VI

VII

VIII

IX

X

XI

XII

What are the three divisionsof the trigeminal nerve (cranial nerve V)?

Chapter 70 / Otolaryngology: Head and Neck Surgery 587

Accessory nerve

Hypoglossal nerve

Smell

Sight (sensory pupil reaction)

Eyeball movement, pupil sphincter,ciliary muscle (motor pupil reaction)

Superior oblique muscle movement

Motor: chewing (masseter muscle)Sensory: face, teeth, sinuses, cornea

Lateral rectus muscle (lateral gaze)

Motor: facial muscles, lacrimal/sublingual/submandibular glands

Sensory: anterior tongue/soft palate, taste

Hearing, positioning

Motor: stylopharyngeus, parotid, pharynxSensory: posterior tongue, pharynx,

middle ear

Motor: vocal cords, heart, bronchus, GI tract

Sensory: bronchus, heart, GI tract,larynx, ear

Motor: trapezius muscle,sternocleidomastoid muscle

Motor: tongue, strap muscles (ansacervicalis branch)

1. Ophthalmic2. Maxillary3. Mandibular


What happens when thehypoglossal nerve (cranialnerve XII) is cut?

Name the duct of thesubmandibular gland.

Name the duct of theparotid gland.

What is the source of bloodsupply to the nose?

Name the three bones thatmake up the posterior nasalseptum.

Name the seven bones ofthe bony eyeball orbit.

Name the four strap muscles.

Which muscle crosses theexternal and internal carotidarteries?

In a neck incision, what isthe first muscle incised?

Which nerve supplies thestrap muscles?


When the patient sticks out the tongue, itdeviates to the same side as the injury(wheelbarrow effect)

Wharton’s duct

Stensen’s duct

1. Internal carotid artery: anterior andposterior ethmoidal arteries viaophthalmic artery

2. External carotid artery: superior labial artery (via facial artery) andsphenopalatine artery (via internalmaxillary artery)

1. Ethmoid (perpendicular plate)2. Vomer (Latin for “plow”)3. Palatine (some also include maxillary

crest)

1. Frontal2. Zygoma3. Maxillary4. Lacrimal5. Ethmoid6. Palatine7. Sphenoid

“TOSS”:1. Thyrohyoid2. Omohyoid3. Sternothyroid4. Sternohyoid

Digastric muscle

Platysma

Ansa cervicalis (XII)


What are the anterior andposterior neck triangles?


Two regions of the neck, divided by thesternocleidomastoid muscle

Posteriortriangle

Sternocleidomastoidmuscle

Anteriortriangle

Which nerve runs with thecarotid in the carotid sheath?

Which nerve crosses theinternal carotid artery atapproximately 1 to 2 cmabove the bifurcation?

Name the three auditoryossicle bones.

What comprises the middleear?

What comprises the innerear?

Vagus

Hypoglossal nerve

1. Malleus (hammer)2. Incus (anvil)3. Stapes (stirrup)

Eustachian tube, ossicle bones, tympanicmembrane (“ear drum”), mastoid air cell

Cochlea, semicircular canals, internalauditory canal

EAR

OTITIS EXTERNA (SWIMMER’S EAR)

What is it? Generalized infection involving the external ear canal and often the tympanicmembrane


What is the usual cause?

What are the typicalpathogens?




Prolonged water exposure and damagedsquamous epithelium of the ear canal(e.g., swimming, hearing aid use)

Most frequently Pseudomonas, may beProteus, Staphylococcus, occasionallyEscherichia coli, fungi (Aspergillus, Candida), or virus (herpes zoster or herpes simplex)

Ear pain (otalgia); swelling of externalear, ear canal, or both; erythema; pain onmanipulation of the auricle; debris incanal; otorrhea

Keep the ear dry; mild infections respondto cleaning and dilute acetic acid drops;most infections require complete removalof all debris and topical antibiotics with orwithout hydrocortisone (anti-inflammatory)

MALIGNANT OTITIS EXTERNA (MOE)

What is it?

Is it malignant cancer?

Who is affected?

What are the causativeorganisms?

What is the classic feature?

What are the other signs/symptoms?

Fulminant bacterial otitis externa

NO!

Most common scenario: elderly patientwith poorly controlled diabetes (otherforms of immunosuppression do notappear to predispose patients to MOE)

Usually Pseudomonas aeruginosa

Nub of granulation tissue on the floor of the external ear canal at the bony–cartilaginous junction

Severe ear pain, excessive purulentdischarge, and usually exposed bone






1. CT scan: shows erosion of bone,inflammation

2. Technetium-99 scan: temporal boneinflammatory process

3. Gallium-tagged white blood cell scan:to follow and document resolution

Invasion of surrounding structures toproduce a cellulitis, osteomyelitis of temporal bone, mastoiditis; later, a facialnerve palsy, meningitis, or brain abscess

Control of diabetes, meticulous localcare with extensive debridement, hospitalization and IV antibiotics (anti-Pseudomonas: usually an aminoglycosideplus a penicillin)

TUMORS OF THE EXTERNAL EAR

What are the most commontypes?

From what location do theyusually arise?

What is the associated riskfactor?


Cancers of the auricle?

Extension to the canal?

Middle ear involvement?

Squamous cell most common; occasionally,basal cell carcinoma or melanoma

Auricle, but occasionally from theexternal canal

Excessive sun exposure

Usually wedge excision

May require excision of the external earcanal or partial temporal bone excision

Best treated by en bloc temporal boneresection and lymph node dissection

TYMPANIC MEMBRANE (TM) PERFORATION

What is the etiology? Usually the result of trauma (direct orindirect) or secondary to middle earinfection; often occurs secondary to slapto the side of the head (compressioninjury), explosions



What are the signs?




Pain, bleeding from the ear, conductivehearing loss, tinnitus

Clot in the meatus, visible tear in the TM

Keep dry; use systemic antibiotics if thereis evidence of infection or contamination

Most (90%) heal spontaneously, thoughlarger perforations may require surgery(e.g., fat plug, temporalis fasciatympanoplasty)

CHOLESTEATOMA

What is it?


What other condition is itoften associated with?

What is the usual history?

What is the appearance?

What are the associatedproblems?


Epidermal inclusion cyst of the middleear or mastoid, containing desquamatedkeratin debris; may be acquired or congenital

Negative middle ear pressure fromeustachian tube dysfunction (primaryacquired) or direct growth of epitheliumthrough a TM perforation (secondaryacquired)

Chronic middle ear infection

Chronic ear infection with chronic,malodorous drainage

Grayish-white, shiny keratinous massbehind or involving the TM; oftendescribed as a “pearly” lesion

Ossicular erosion, producing conductivehearing loss; also, local invasion resulting in:

Vertigo/sensorineural hearing lossFacial paresis/paralysisCNS dysfunction/infection

Surgery (tympanoplasty/mastoidectomy)aimed at eradication of disease andreconstruction of the ossicular chain



BULLOUS MYRINGITIS

What is it?



What are the findings onotoscopic examination?

Is hearing affected?


Vesicular infection of the TM andadjacent deep canal

Unknown; viral should be suspectedbecause of frequent association with viralURI (in some instances, Mycoplasmapneumoniae has been cultured)

Acute, severe ear pain; low-grade fever;and bloody drainage

Large, reddish blebs on the TM, wall ofthe meatus, or both

Rarely; occasional reversible sensorineuralloss

Oral antibiotics (erythromycin ifMycoplasma is suspected); topical analgesics may be used, with resolution ofsymptoms usually occurring in 36 hours

ACUTE SUPPURATIVE OTITIS MEDIA (OM)

What is it?

What is the cause?

What are the predisposingfactors?


Bacterial infection of the middle ear,often following a viral URI; may be associated with a middle ear effusion

Dysfunction of the eustachian tube thatallows bacterial entry from nasopharynx;often associated with an occluded eustachiantube, although it is uncertain whetherthis is a cause or a result of the infection

Young age, male gender, bottle feeding,crowded living conditions (e.g., day care),cleft palate, Down’s syndrome, cystic fibrosis

1. Streptococcus pneumoniae (33% ofcases)

2. Haemophilus influenzae3. Moraxella catarrhalis4. Staphylococcus5. �-hemolytic strep6. Pseudomonas aeruginosa7. Viral/no culture


What is the etiology ininfants younger than 6 months?


What are the signs?

If pain disappears instantly,what may have happened?



What is the usual course?

What are the indications formyringotomy and PE tubeplacement?

What is a PE tube?

What is a Bezold’s abscess?

What are causes of chronicotitis media?


1. Staphylococcus aureus2. E. coli3. Klebsiella

Otalgia, fever, decreased hearing, infantpulls on ear, increased irritability; as manyas 25% of patients are asymptomatic

Early, redness of the TM; later, TMbulging with loss of the normal landmarks;finally, impaired TM mobility on pneumaticotoscopy

TM perforation!

TM perforation, acute mastoiditis,meningitis, brain abscess, extraduralabscess, labyrinthitis; if recurrent orchronic, OM may have adverse effects onspeech and cognitive development as aresult of decreased hearing

10-day course of antibiotics; amoxicillin isthe first-line agent; if the patient is allergicto PCN, trimethoprim-sulfamethoxazoleor erythromycin should be administered

Symptoms usually resolve in 24 to 36 hours

1. Persistent middle ear effusion over 3 months

2. Debilitated or immunocompromisedpatient

3. More than three episodes over 6 months (especially if bilateral)

Pneumatic Equalization tube (tube placedacross tympanic membrane)

Abscess behind the superior attachmentof the sternocleidomastoid muscle result-ing from extension of a mastoid infection

Mixed, S. aureus, P. aeruginosa


What are the signs/symptomsof chronic otitis media?


Otorrhea and hearing loss

OTOSCLEROSIS

What is it?



What is the usual age ofonset?


What is Schwartze’s sign?


Genetic disease characterized by abnormalspongy and sclerotic bone formation inthe temporal bone around the footplateof the stapes, thus preventing its normalmovement

Autosomal dominant with incompleteone-third penetrance

Painless, progressive hearing loss (may beunilateral or bilateral), tinnitus

Second through fourth decade

Normal TM with conductive hearing lossand no middle-ear effusion (though maybe mixed or even sensorineural if bone ofcochlea is affected)

Erythema around the stapes fromhypervascularity of new bone formation

Frequently surgical (stapedectomy withplacement of prosthesis), hearing aids, orobservation; sodium fluoride may be usedif a sensorineural component is presentor for preoperative stabilization

MISCELLANEOUS

FACIAL NERVE PARALYSIS

How is the defect localized? Supranuclear—paralysis of lower faceonly, forehead muscles are sparedbecause of bilateral corticobulbar supply

Intratemporal bone—paralysis of upperand lower face, decreased tearing,altered taste, absent stapedius reflex

Distal to stylomastoid foramen—paralysisof facial muscles only



What is the most commoncause of bilateral facialnerve palsy?


Bell’s palsyTraumaCholesteatomaTumor (carcinoma, glomus jugulare)Herpes zoster inflammation of geniculate

ganglion (Ramsay-Hunt syndrome)Peripheral lesions are usually parotid

gland tumors

Lyme disease (Borrelia burgdorferi)

BELL’S PALSY

What is it?

What is the clinical course?


What is the pathogenesis?

What is the common preceding event?



Sudden onset, unilateral facial weaknessor paralysis in absence of CNS, ear, orcerebellopontine angle disease (i.e., noidentifiable cause)

Acute onset, with greatest muscle weakness reached within 3 weeks

Most common cause of unilateral facialweakness/paralysis

Unknown; most widely accepted hypothesisis viral etiology (herpes virus); ischemic andimmunologic factors are also implicated

URI

Pathology is related to swelling of thefacial nerve; may present with total facialparalysis, altered lacrimation, increasedtearing on affected side, change in taste ifregion above chorda tympani is affected,dry mouth, and hyperacusis

Usually none is required, as most casesresolve spontaneously in 1 month;protect eye with drops and tape closedas needed; most otolaryngologistsadvocate steroids and acyclovir

Surgical decompression of CN VII isindicated if paralysis progresses ortests indicate deterioration




Overall, 90% of patients recover completely; if paralysis is incomplete,95% to 100% will recover without sequelae

SENSORINEURAL HEARING LOSS

What is it?


What are the signs?

What is the Weber vs. Rinnetest?


What is the most commoncause in children?

Hearing loss from a lesion occurring inthe cochlea or acoustic nerve, rather thanthe external or middle ear

Distortion of hearing, impaired speechdiscrimination, tinnitus

Air conduction is better than bone conduction (positive Rinne test), Weberlateralizes to the side without the defect;audiogram most commonly shows greatest loss in high-frequency tones

Weber: tuning fork on middle of head(lateral louder � either ipsilateralconductive loss or contralateralsensorineural)

Rinne: tuning fork on mastoid and thennext to ear (conductive loss louder onmastoid)

Aging (presbycusis)—leading causeAcoustic injury from sudden or

prolonged exposure to loud noisesPerilymph fistulaCongenital (TORCHES: maternal

TOxoplasmosis, Rubella, CMV,HErpes, and Syphilis)

Ménière’s diseaseDrug/toxin-inducedAcoustic neuromaPseudotumor cerebriCNS diseaseEndocrine disordersSarcoidosis

Meningitis (bacterial)




Treatment of underlying cause, hearingaids, lip reading, cochlear implant

VERTIGO

What is it?

What is the cause?

What is the history ofperipheral vertigo?

What are the risk factors forperipheral vertigo?

What is the history of centralvertigo?

What are the steps in diagnostic evaluation?

What is the most commonetiology?


Sensation of head/body movement, ormovement of surroundings (usually rotational)

Asymmetric neuronal activity betweenright and left vestibular systems

Severe vertigo, nausea, vomiting, alwaysaccompanied by horizontal or rotatorynystagmus (fast component almost alwaysto side opposite disease), other evidenceof inner ear disease (tinnitus, hearing loss)

Frequently associated with a previouslyoperated ear, a chronic draining ear,barotrauma, or head trauma

Found in brainstem or cerebellum: insidious onset, less intense and moresubtle sensation of vertigo; occasionally,vertical nystagmus

Depends on probability of central versusperipheral; careful neurologic andotologic examinations are required

May need FTA/VDRL (syphilis), temporalbone scans/CT scan/MRI, ENG,position testing, audiometric testing

Benign Paroxysmal Positional Vertigo(BPPV); history of brief spells of severevertigo with specific head positions

Central: vertebral basilar insufficiency(often in older patients with DJD ofspine), Wallenberg syndrome, MS,epilepsy, migraine

Peripheral: BPPV, motion sickness,syphilis, Ménière’s disease, vestibularneuronitis, labyrinthitis, acoustic neuroma, syphilis, perilymph fistula


What is Tullio’sphenomenon?


Induction of vertigo by loud noises;classically, result of otosyphilis

MÉNIÈRE’S DISEASE

What is it?

What is the classic triad?

What is thepathophysiology?



What are the surgicaloptions?

Disorder of the membranous labyrinth,causing fluctuating sensorineural hearingloss, episodic vertigo, nystagmus, tinnitus,and aural fullness, N/V

Hearing loss, Tinnitus, Vertigo (H, T, V)

Obscure, but most experts believe excessive production/defective resorptionof endolymph

Salt restriction, diuretics (thiazides),antinausea agents; occasionally diazepamis added; 80% of patients respond tomedical management, antihistamines

Surgery is offered to those who fail medicaltreatment or who have incapacitating vertigo (60%–80% effective)

1. Shunt from membranous labyrinth tosubarachnoid space

2. Vestibular neurectomy3. Severe cases with hearing loss:

labyrinthectomy

GLOMUS TUMORS

What are they?


How common are they?

Benign, slow-growing tumors arising inglomus bodies found in the adventitiallayer of blood vessels; often associatedwith cranial nerves IX and X in the middleear

Middle ear, jugular bulb, course of CNIX to XII

Most common benign tumor of the temporal bone




Surgical resection, radiation therapy forpoor operative candidates or forrecurrences

NOSE AND PARANASAL SINUSES

EPISTAXIS

What is it?




Which type is more serious?


What is the treatment of lastresort?

What infectious disease syndrome is seen with nasalpacking?

What is the treatment of thissyndrome?

Bleeding from the nose

Trauma, “nose picking,” sinus infection,allergic or atrophic rhinitis, blooddyscrasias, tumor, environmentalextremes (hot, dry climates; winters)

Rupture of superficial mucosal bloodvessels (Kiesselbach’s plexus if anterior,sphenopalatine artery if posterior)

Anterior (90%); usually the result oftrauma

Posterior; usually occurs in the elderly oris associated with a systemic disorder(hypertension, tumor, arteriosclerosis)

Direct pressure; if this fails, proceed toanterior nasal packing with gauze strips,followed if necessary by posterior packingwith Foley catheter or lamb’s wool; packsmust be removed in �5 days to preventinfectious complications

Ligation or embolization of thesphenopalatine artery (posterior) or ethmoidal artery (anterior)

Toxic shock syndrome: fever, shock, rashcaused by exotoxin from Staphylococcusaureus

Supportive with removal of nasal packing,IV hydration, oxygen, and antistaphylococcalantibiotics



ACUTE RHINITIS

What is it?


Inflammation of nasal mucous membrane

URI infection; rhinovirus is the mostcommon agent in adults (other nonallergiccauses: nasal deformities and tumors,polyps, atrophy, immune diseases, vasomotor problems)

ALLERGIC RHINITIS


How is the condition characterized?

What are the findings onphysical examination?


Nasal stuffiness; watery rhinorrhea;paroxysms of morning sneezing; and itching of nose, conjunctiva, or palate

Early onset (before 20 years of age),familial tendency, other allergic disorders(eczema, asthma), elevated serum IgE,eosinophilia on nasal smear

Pale, boggy, bluish nasal turbinatescoated with thin, clear secretions; in children, a transverse nasal crease sometimes results from repeated “allergicsalute”

Allergen avoidance, antihistamines,decongestants; steroids or sodium cromylate in severe cases; desensitizationvia allergen immunotherapy is the only“cure”

ACUTE SINUSITIS

What is the typical history?


Previously healthy patient with unrelenting progression of a viral URI orallergic rhinitis beyond the normal 5- to7-day course

Periorbital pressure/pain, nasal obstruction,nasal/postnasal mucopurulent discharge,fatigue, fever, headache


What are the signs?

What is the pathophysiology?



What is the treatment forfungal sinusitis?


Tenderness over affected sinuses, pus inthe nasal cavity; may also see reason forobstruction (septal deviation, spur, tightosteomeatal complex); transilluminationis unreliable

Thought to be secondary to decreasedciliary action of the sinus mucosa andedema causing obstruction of the sinusostia, lowering intrasinus oxygen tensionand predisposing patients to bacterialinfection

Up to 50% of patients have negative cultures and cause is presumably(initially) viral; pneumococcus, S. aureus,group A streptococci, and H. influenzaeare the most common bacteria cultured

14-day course of antibiotics (penicillin G,amoxicillin, Ceclor®, and Augmentin® arecommonly used), topical and systemicdecongestants, and saline nasal irrigation

Fungal sinusitis is commonly caused byMucor and seen in immunosuppressedpatients; treatment is IV antifungals (e.g., amphotericin or caspofungin) andsurgical débridement of all necrotictissue

CHRONIC SINUSITIS

What is it?

What is the pathology?

Infection of nasal sinuses lasting longerthan 4 weeks, or pattern of recurrentacute sinusitis punctuated by briefasymptomatic periods

Permanent mucosal changes secondary to inadequately treated acute sinusitis,consisting of mucosal fibrosis, polypoidgrowth, and inadequate ciliary action,hyperostosis (increased bone density onCT scan)





What is FESS?

What are the complicationsof sinusitis?


Chronic nasal obstruction, postnasal drip,mucopurulent rhinorrhea, low-gradefacial and periorbital pressure/pain

Usually anaerobes (such as Bacteroides,Veillonella, Rhinobacterium); also H. influenzae, Streptococcus viridans,Staphylococcus aureus, Staphylococcusepidermidis

Medical management with decongestants,mucolytics, topical steroids, andantibiotics; if this approach fails, proceedto endoscopic or external surgical intervention

Functional Endoscopic Sinus Surgery

Orbital cellulitis (if ethmoid sinusitis),meningitis, epidural or brain abscess(frontal sinus), cavernous sinus thrombosis(ethmoid or sphenoid), osteomyelitis(a.k.a. Pott’s puffy tumor if frontal)

CANCER OF THE NASAL CAVITY AND PARANASAL SINUSES

What are the usuallocations?

What are the associated celltypes?

What rare tumor arises fromolfactory epithelium?


Maxillary sinus (66%)Nasal cavityEthmoid sinusRarely in frontal or sphenoid sinuses

Squamous cell (80%)Adenocellular (15%)Uncommon: sarcoma, melanoma

Esthesioneuroblastoma; usually ariseshigh in the nose (cribriform plate) and islocally invasive

Early—nasal obstruction, blood-tingedmucus, epistaxis

Late—localized pain, cranial nervedeficits, facial/palate asymmetry, looseteeth






CT scan can adequately identify extent ofthe disease and local invasion; MRI is oftenalso used to evaluate soft-tissue disease

Surgery with or without x-ray therapy

5-year survival for T1 or T2 lesionsapproaches 70%

JUVENILE NASOPHARYNGEAL ANGIOFIBROMA

What is it?



Into what can the masstransform?


What are indications forbiopsy?


Most commonly encountered vascularmass in the nasal cavity; locally aggressivebut nonmetastasizing

Adolescent boys who present with nasalobstruction, recurrent massive epistaxis,possibly anosmia

Site of origin is the roof of the nasal cavity at the superior margin ofsphenopalatine foramen

Fibrosarcoma (rare cases reported)

Carotid arteriography, CT scan; biopsy iscontraindicated secondary to risk ofuncontrollable hemorrhage

None!

Surgery via lateral rhinotomy or sublabialmaxillotomy with bleeding controlled by internal maxillary artery ligation orpreoperative embolization, in the settingof hypotensive anesthesia; preoperative irradiation has also been used to shrinkthe tumor



ORAL CAVITY AND PHARYNX

PHARYNGOTONSILLITIS

What is the common site ofreferred throat pain?

What is it?



What are the signs?



EAR

Acute or chronic infection of thenasopharynx or oropharynx and/orWaldeyer’s ring of lymphoid tissue (consisting of palatine, lingual, and pharyngeal tonsils and the adenoids)

Acute attacks can be viral (adenovirus,enterovirus, coxsackievirus, Epstein-Barrvirus in infectious mononucleosis) or bacterial (group A �-hemolytic streptococciare the leading bacterial agent); chronictonsillitis often with mixed population,including streptococci, staphylococci, andM. catarrhalis

Acute—Sore throat, fever, locallymphadenopathy, chills, headache,malaise

Chronic—Noisy mouth breathing, speechand swallowing difficulties, apnea, halitosis

Viral—Injected tonsils and pharyngealmucosa; exudate may occur, but lessoften than with bacterial tonsillitis

Bacterial—Swollen, inflamed tonsils withwhite-yellow exudate in crypts and onsurface; cervical adenopathy

CBC, throat culture, Monospot test

Peritonsillar abscess (quinsy), retropharyngeal abscess (causing airway compromise), rheumatic fever,poststreptococcal glomerulonephritis(with �-hemolytic streptococci)



What are the indications fortonsillectomy?



Viral—Symptomatic S acetaminophen,warm saline gargles, anesthetic throatspray

Bacterial—10 days PCN (erythromycin ifPCN-allergic)

Sleep apnea/cor pulmonale secondary to airway obstruction, suspicion of malignancy, hypertrophy causing malocclusion, peritonsillar abscess, recurrent acute or chronic tonsillitis

Acute or delayed hemorrhage

PERITONSILLAR ABSCESS

What is the clinical setting?

What is the associatedmicrobiology?

What is the site of formation?


What is the classic description of voice?

What are the signs?


Inadequately treated recurrent acute orchronic tonsillitis

Mixed aerobes and anaerobes (whichmay be PCN resistant)

Begins at the superior pole of the tonsil

Severe throat pain, drooling dysphagia,odynophagia, trismus, cervical adenopathy,fever, chills, malaise

“Hot-potato voice”

Bulging, erythematous, edematoustonsillar pillar; swelling of uvula anddisplacement to contralateral side

IV antibiotics and surgical evacuation by incision and drainage; most expertsrecommend tonsillectomy afterresolution of inflammatory changes

LUDWIG ANGINA

What is it? Infection and inflammation of the floor ofthe mouth (sublingual and submandibular)


What is the source?



Dental infection

Antibiotics, emergency airway, I & D

CANCER OF THE ORAL CAVITY

What is the usual cell type?



What is the frequency of thefollowing conditions:

Regional metastasis?

Second primary?

Nodal metastasis?

Distant metastasis?



Squamous cell (�90% of cases)

Lip, tongue, floor of mouth, gingiva,cheek, and palate

Linked to smoking, alcohol, and smokelesstobacco products (alcohol and tobaccotogether greatly increase the risk)

�30%

�25%

Depends on size of tumor and rangesfrom 10% to 60%, usually to jugular andjugulodigastric nodes, submandibularnodes

Infrequent

Full history and physical examination,dental assessment, Panorex or bone scanif mandible is thought to be involved,CT scan/MRI for extent of tumor andnodal disease, FNA (often U/S guided)

Radiation, surgery, or both for smalllesions; localized lesions can usually be treated surgically; larger lesionsrequire combination therapy, possiblemandibulectomy and neck dissection




Depends on stage and site:Tongue: 20% to 70% survivalFloor of mouth: 30% to 80% survival

Most common cause of death insuccessfully treated head and neck cancer is development of a second primary (occurs in 20%–40% of cases)

SALIVARY GLAND TUMORS

What is the frequency ofgland involvement?

What is the potential formalignancy?

How do benign andmalignant tumors differ in terms of history and physical examination?

What is the diagnostic procedure?


What are the indications forpostop XRT?

What is the most commonbenign salivary tumor?


Parotid gland (80%)Submandibular gland (15%)Minor salivary glands (5%)

Greatest in minor salivary glandtumors (80% are malignant) and least inparotid gland tumors (80% are benign);the smaller the gland, the greater thelikelihood of malignancy

Benign—mobile, nontender, no nodeinvolvement or facial weakness

Malignant—painful, fixed mass with evidence of local metastasis and facialparesis/paralysis

FNA; never perform excisional biopsy ofa parotid mass; superficial parotidectomyis the procedure of choice for benignlesions of the lateral lobe

Involves adequate surgical resection,sparing facial nerve if possible, neck dissection for node-positive necks

Postoperative radiation therapy if high-grade cancer, recurrent cancer, residualdisease, invasion of adjacent structures,any T3 or T4 parotid tumors

Pleomorphic adenoma (benign mixedtumor) 66%

Think: Pleomorphic � Popular

Parotid gland


What is the clinical course?

What is the second mostcommon benign salivarygland tumor?


Describe the lesion.

What is the most commonmalignant salivary tumor?

What is the second mostcommon malignant salivarytumor in adults?


They are well delineated and slow growing

Warthin’s tumor (1% of all salivary glandtumors)

95% are found in parotid; 3% arebilateral

Slow-growing, cystic mass is usuallylocated in the tail of the superficial portion of the parotid; it rarely becomesmalignant

Mucoepidermoid carcinoma (10% ofall salivary gland neoplasms) Think:Mucoepidermoid � Malignant

Most common parotid malignancySecond most common submandibular

gland malignancy

Adenoid cystic carcinoma; most commonmalignancy in submandibular and minorsalivary glands

LARYNX ANATOMY

Define the three parts. 1. Glottis: begins halfway between thetrue and false cords (in the ventricle)and extends inferiorly 1.0 cm belowthe edge of the vocal folds

2. Supraglottis: extends from superiorglottis to superior border of hyoid andtip of epiglottis

3. Subglottis: extends from lower borderof glottis to inferior edge of cricoidcartilage


Innervation?


Vagus nerve: superior laryngeal andrecurrent laryngeal nerves; superiorlaryngeal supplies sensory to supraglottisand motor to inferior constrictor andcricothyroid muscle; recurrent laryngealsupplies sensory to glottis and subglottisand motor to all remaining intrinsiclaryngeal muscles

CROUP (LARYNGOTRACHEOBRONCHITIS)

What is it?


What age group is affectedmost?

Is the condition consideredseasonal?

What are the precipitatingevents?

What is the classic symptom?

What are the othersymptoms?

What are the signs?



Viral infection of the larynx and trachea,generally affecting children (boys � girls)

Parainfluenza virus (Think: crouP �Parainfluenza)

6 months to 3 years of age

Yes; outbreaks most often occur inautumn

Usually preceded by URI

Barking (seal-like), nonproductive cough

Respiratory distress, low-grade fever

Tachypnea, inspiratory retractions,prolonged inspiration, inspiratory stridor,expiratory rhonchi/wheezes

Epiglottitis, bacterial tracheitis, foreignbody, diphtheria, retropharyngealabscess, peritonsillar abscess, asthma

A-P neck x-ray shows classic “steeple sign,”indicating subglottic narrowing; ABGmay show hypoxemia plus hypercapnia



What are the indications forintubation?

What is the usual course?

What type of secondaryinfection occurs?


Keep child calm (agitation only worsensobstruction); cool mist; steroids; aerosolizedracemic EPI may be administered toreduce edema/airway obstruction

If airway obstruction is severe or childbecomes exhausted

Resolves in 3 to 4 days

Secondary bacterial infection(streptococcal, staphylococcal)

EPIGLOTTITIS

What is it?

What is the usual causativeagent?

What age group is affected?




Severe, rapidly progressive infection ofthe epiglottis

Haemophilus influenzae type B

Children 2 to 5 years of age

Sudden onset, high fever (40�C); “hot-potato” voice; dysphagia (S drooling); no cough; patient prefersto sit upright, lean forward; patientappears toxic and stridulous

Can usually be made clinically and doesnot involve direct observation of theepiglottis (which may worsen obstructionby causing laryngospasm)

Involves immediate airway support in theO.R.: intubation or possibly tracheostomy,medical treatment is comprised of steroidsand IV antibiotics against H. influenzae

MALIGNANT LESIONS OF THE LARYNX



Accounts for �2% of all malignancies,more often in males

Glottis (66%)


What is the second mostcommon type?

Which type has the worstprognosis?


What is the pathology?



Supraglottis (33%)

Subglottic tumors (infrequent)

Tobacco, alcohol

90% are squamous cell carcinoma

Hoarseness, throat pain, dysphagia,odynophagia, neck mass, (referred) ear pain

SUPRAGLOTTIC LESIONS


What area is often involved?

Extension?

What is the associated typeof metastasis?


Laryngeal surface of epiglottis

Pre-epiglottic space

Tend to remain confined to supraglotticregion, though may extend to vallecula orbase of tongue

High propensity for nodal metastasis

Early stage � XRTLate stage � laryngectomy

GLOTTIC LESIONS


Extension?

What is the associated typeof metastasis?


Anterior part of true cords

May invade thyroid cartilage, cross midline to invade contralateral cord, orinvade paraglottic space

Rare nodal metastasis

Early stage � XRTLate stage � laryngectomy



NECK MASS

What is the usual etiology ininfants?

What is the usual etiology inadolescents?

What is the usual etiology inadults?

What is the “80% rule”?

What are the seven cardinalsymptoms of neck masses?

What comprises the workup?


What is the workup of node-positive squamous cellcarcinoma and no primarysite?


Congenital (branchial cleft cysts,thyroglossal duct cysts)

Inflammatory (cervical adenitis is #1),with congenital also possible

Malignancy (squamous is #1), especiallyif painless and immobile

In general, 80% of neck masses arebenign in children; 80% are malignantin adults older than 40 years of age

Dysphagia, odynophagia, hoarseness, stridor (signifies upper airway obstruction),globus, speech disorder, referred ear pain(via CN V, IX, or X)

Full head and neck examination, indirectlaryngoscopy, CT scan and MRI, FNA fortissue diagnosis; biopsy contraindicatedbecause it may adversely affect survival ifmalignant

Inflammatory: cervical lymphadenitis,cat-scratch disease, infectiousmononucleosis, infection in neckspaces

Congenital: thyroglossal duct cyst (midline,elevates with tongue protrusion),branchial cleft cysts (lateral), dermoidcysts (midline submental), hemangioma,cystic hygroma

Neoplastic: primary or metastatic

Triple endoscopy (laryngoscopy,esophagoscopy, bronchoscopy) and blind biopsies

Surgical excision for congenital orneoplastic; two most importantprocedures for cancer treatment are radical and modified neck dissection


What is the role of adjuvanttreatment in head and neckcancer?


Postoperative chemotherapy/XRT

RADICAL NECK DISSECTION

What is involved?


What are thecontraindications?

Classically, removal of nodes from clavicle to mandible, sternocleidomastoidmuscle, submandibular gland, tail ofparotid, internal jugular vein,digastric muscles, stylohyoid andomohyoid muscles, fascia within theanterior and posterior triangles, CN XI,and cervical plexus sensory nerves

1. Clinically positive nodes that likelycontain metastatic cancer

2. Clinically negative nodes in neck, buthigh probability of metastasis from aprimary tumor elsewhere

3. Fixed cervical mass that is resectable

1. Distant metastasis2. Fixation to structure that cannot be

removed (e.g., carotid artery)3. Low neck masses

MODIFIED NECK DISSECTION

What are the types:Type I?

Type II?

Type III?

What are the advantages?

Spinal accessory nerve preserved

Spinal accessory and internal jugular veinpreserved

Spinal accessory, IJ, andsternocleidomastoid nerves preserved

Increased postoperative function anddecreased morbidity (especially ifbilateral), most often used in NO lesions;these modifications are usuallyintraoperative decisions based on thelocation and extent of tumor growth



FACIAL FRACTURES

MANDIBLE FRACTURES


What are the signs?



Gross disfigurement, pain, malocclusion,drooling

Trismus, fragment mobility andlacerations of gingiva, hematoma in floorof mouth

Malunion, nonunion, osteomyelitis, TMJankylosis

Open or closed reductionMMF � MaxilloMandibular Fixation

(wire jaw shut)

MIDFACE FRACTURES

How are they evaluated?

Classification

Le Fort I?

Careful physical examination and CT scan

Transverse maxillary fracture above thedental apices, which also traverses thepterygoid plate; palate is mobile, butnasal complex is stable

What are the disadvantages? May result in increased mortality fromlocal recurrence


Le Fort II?


Fracture through the frontal process ofthe maxilla, through the orbital floor andpterygoid plate; midface is mobile

Le Fort III? Complete craniofacial separation;differs from II in that it extends throughthe nasofrontal suture and frontozygomaticsutures

What is a “tripod” fracture? Fracture of the zygomatic complex;involves four fractures:

1. Frontozygomatic suture2. Inferior orbital rim3. Zygomaticomaxillary suture4. Zygomaticotemporal suture


What is a “blowout” fracture?

What is “entrapment”?

What is a “step off”?

Are mandibular fracturesusually a single fracture?

What is the best x-ray studyfor mandibular fractures?

What must be ruled out andtreated with a broken nose(nasal fracture)?


Orbital fracture with “blowout” ofsupporting bony structural support oforbital floor; patient has enophthalmos(sunken-in eyeball)

Orbital fracture with “entrapment” ofperiorbital tissues within the fractureopening, including entrapment ofextraocular muscles; loss of extraocularmuscle mobility (e.g., lateral tracking)and diplopia (double vision)

Fracture of the orbit with palpable “step off” of bony orbital rim (inferioror lateral)

No; because the mandible forms ananatomic ring, �95% of mandiblefractures have more than one fracturesite

Panorex

Septal hematoma; must drain to removechance of pressure-induced septal necrosis

ENT WARD QUESTIONS

How can otitis externa bedistinguished from otitismedia on examination?

What causes otitis media?

What causes otitis externa?

What must be considered inunilateral serous otitis?

What is the most commoncause of facial paralysis?

Otitis externa is characterized by severepain upon manipulation of the auricle

Most cases are caused by pneumococciand H. influenzae

Pseudomonas aeruginosa

Nasopharyngeal carcinoma

Bell’s palsy, which has an unidentifiedetiology


What is the single mostimportant prognostic factorin Bell’s palsy?

What is the most commoncause of parotid swelling?

What is Heerfordt’ssyndrome?

Which systemic diseasecauses salivary gland stones?

What is the most commonsalivary gland site of stoneformation?

What is Mikulicz’ssyndrome?

What are the three majorfunctions of the larynx?

What is a cricothyroidotomy?

Name the four major indications for atracheostomy.

What is a ranula?

What is Frey’s syndrome?

What causes Frey’ssyndrome?


Whether the affected muscles are completely paralyzed (if not, prognosis is�95% complete recovery)

Mumps

Sarcoidosis with parotid enlargement,facial nerve paralysis, and uveitis

Gout

Submandibular gland

Any cause of bilateral enlargement of theparotid, lacrimal, and submandibular glands

1. Airway protection2. Airway/respiration3. Phonation

Emergent surgical airway by incising thecricothyroid membrane

1. Prolonged mechanical ventilation(usually �2 weeks)

2. Upper airway obstruction3. Poor life-threatening pulmonary toilet4. Severe obstructive sleep apnea

Sublingual retention cyst arising fromsublingual salivary glands

Flushing, pain, and diaphoresis in theauriculotemporal nerve distribution initiated by chewing

Cutting the auriculotemporal nervecauses abnormal regeneration of the sympathetic/parasympathetic nerves,which, once destined for the parotidgland, find new targets in skin sweatglands; thus, people sweat when eating


What is the classic triad ofMénière’s disease?

What is the most common posterior fossatumor and where is itlocated?

What is the most commonsite of sinus cancer?

What tumor arises fromolfactory epithelium?

What cell type is most common in head and neckcancer?

What are the mostimportant predisposing factors to head and neckcancer?

What is the most frequentsite of salivary gland tumor?

What is the most commonsalivary gland neoplasm:

Benign?

Malignant?

What is the classic feature ofcroup?

What are the classic featuresof epiglottitis?

What comprises the workupof neck mass?


Hearing loss, tinnitus, vertigo (HTV)

Acoustic neuroma, usually occurring atthe cerebellopontine angle

Maxillary sinus

Esthesioneuroblastoma

Squamous cell

Excessive alcohol use and tobacco abuseof any form

Parotid gland

Pleomorphic adenoma

Mucoepidermoid carcinoma

Barking, seal-like cough

“Hot-potato” voice, sitting up, drooling,toxic appearance, high fever, leaningforward

Do not biopsy; obtain tissue via FNAand complete head and neck examination


What is Ramsay-Hunt syndrome?

What is the most commonmalignant neck mass in children, adolescents, andyoung adults?

What is the most commonprimary malignant solidtumor of the head and neckin children?

Throat pain is often referredto what body area?

What ENT condition isdescribed as “crocodiletears”?

What is Brown’s sign?


Painful facial nerve paralysis from herpeszoster of the ear

Lymphoma

Rhabdomyosarcoma

Ear

Frey’s syndrome!

Tympanic membrane pulsations thatcease with positive pressure (from a“pneumatic” otoscope); seen with middleear tumor mass

RAPID-FIRE REVIEW OF MOST COMMON CAUSESOF ENT INFECTIONS

Croup?

Otitis externa?

Epiglottitis?

Malignant otitis externa?

Parotitis?

Acute suppurative otitismedia?

Parainfluenza virus

Pseudomonas

H. influenzae

Pseudomonas

Staphylococcus

S. pneumoniae (33%)


Chapter 71 / Thoracic Surgery 621

Thoracic SurgeryChapter 71Video-Assisted Thoracic SurgeryWhat does VATS stand for?

THORACIC OUTLET SYNDROME (TOS)

What is it?

What are the causes (3)?


What are the most commonsymptoms with TOS?

Which nerve is most ofteninvolved?

Compression of the:Subclavian arterySubclavian vein orBrachial plexus at the superior outlet

of the thorax

1. Various congenital anomalies,including cervical rib or abnormal fascial bands to the first rib, or abnormal anterior scalene muscle

2. Trauma:Fracture of clavicle or first ribDislocation of humeral headCrush injuries

3. Repetitive motor injuries (baseballpitchers)

Paresthesias (neck, shoulder, arm, hand);90% in ulnar nerve distribution

Weakness (neural/arterial)Coolness of involved extremity (arterial)Edema, venous distension, discoloration

(venous)

Neurologic

Ulnar nerve

LWBK758-c71-c74_p621-720.qxd 03/17/2011 8:55 AM Page 621 Aptara

What are the signs?

What is the Adsonmaneuver?

What is Tinel’s test?



Paget-von Schroetter syndrome—venousthrombosis leading to edema, arm discoloration, and distension of thesuperficial veins

Weak brachial and radial pulses in theinvolved arm

Hypesthesia/anesthesiaOccasionally, atrophy in the distribution

of the ulnar nervePositive Adson maneuver/Tinel’s signEdema

Evaluates for arterial compromisePatient:

1. Extends neck (lifts head)2. Takes a deep breath and holds3. Turns head toward examined side

Physician:Monitors radial pulse on examined sideTest finding is positive if the radial

pulse decreases or disappears during maneuver

Tapping of the supraclavicular fossa producing paresthesias

Physical therapy (vast majority of cases)Decompression of the thoracic outlet by

resecting the first rib and cervical rib(if present) if physical therapy failsand as a last resort

CHEST WALL TUMORS

BENIGN TUMORS



1. Fibrous rib dysplasia (posterolateral rib)2. Chondroma (at costochondral

junction)3. Osteochondroma (any portion of rib)

Wide excision and reconstruction withautologous or prosthetic grafts



MALIGNANT TUMORS



What is Tietze’s syndrome?

1. Fibrosarcoma2. Chondrosarcoma3. Osteogenic sarcoma4. Rhabdomyosarcoma5. Myeloma6. Ewing’s sarcoma

Excision with or without radiation

Noninfectious costochondral cartilageinflammation

DISEASES OF THE PLEURA

PLEURAL EFFUSION

What is it?



What are the signs?

What are the properties of atransudate?

What are the properties ofan exudate?

Fluid in the pleural space

1. Pulmonary infections (pneumonia)2. Congestive heart failure (CHF)3. SLE or rheumatoid arthritis4. Pancreatitis (sympathetic effusion)5. Trauma6. Pulmonary embolism7. Renal disease8. Cirrhosis9. Malignancy (mesothelioma,

lymphoma, metastasis)10. Postpericardiotomy syndrome

Dyspnea, pleuritic chest pain

Decreased breath sounds, dullness topercussion, egophony at the upper limit

Specific gravity �1.016Protein �3 g/dLFew cells

Specific gravity �1.016Protein �3 g/dLMany cells


What is the key diagnostictest?


What is an empyema?

What is a decortication?


Thoracentesis (needle drainage) withstudies including cytology

1. Pigtail catheter or thoracostomy (chesttube)

2. Treat underlying condition3. Consider sclerosis

Infected pleural effusion; must bedrained, usually with chest tube(s)

Decortication may be necessary if theempyema is solid

Thoracotomy and removal of an infectedfibrous rind from around the lung (thinkof it as taking off a fibrous “cortex” fromthe lung)

LUNG ABSCESS


What are the associateddiagnostic studies?



What are the surgicaloptions?

What is middle lobesyndrome?

Fever, sputum, sepsis, fatigue

CXR: air-fluid levelCT scan to define position and to

differentiate from an empyemaBronchoscopy (looking for

cancer/culture)

Antibiotics and bronchoscopy for cultureand toilet, with or without surgery

Underlying cancer/tumorRefractory to antibiotics

Lobectomy of lobe with abscessTube drainage

Recurrent right middle lobe pneumoniacaused most commonly by intermittentextrinsic bronchial obstruction

HEMOPTYSIS

What is it? Bleeding into the bronchial tree



Define MASSIVE hemoptysis.

What comprises the workup?

What is the treatment ifmassive?

What is the treatment ofmoderate to mild bleeding?


1. Bronchitis (50%)2. Tumor mass (20%)3. TB (8%)Other causes: bronchiectasis, pulmonary

catheters, trauma

�600 cc/24 hours

CXRBronchoscopyBronchial A-gram

Bronchoscopy, intubation of unaffectedside, Fogarty catheter occlusion of bleeding bronchus, bronchial A-gramwith or without embolization, surgicalresection of involved lung

Laser coagulation, �� epinephrineinjection

SPONTANEOUS PNEUMOTHORAX

What is it?


What body habitus is associated with spontaneouspneumothorax?



What are the options ifrefractory, recurrent, orbilateral?

Who might also need a pleurodesis after the firstepisode?

Atraumatic spontaneous development ofa pneumothorax

Idiopathic (primary), bleb disease,emphysema, etc. (secondary)

Thin and tall

CXR

Chest tube

Pleurodesis: scar the lung to the parietalpleura with a sclerosant (talc) via chesttube/thoracoscopy, or by thoracotomyand mechanical abrasion

Those whose lifestyles place them atincreased risk for pneumothorax (e.g.,pilots, scuba divers)


What is a catamenial pneumothorax?


Pneumothorax due to intrathoracicendometriosis

MESOTHELIOMA

Malignant Mesothelioma

What is it?

What are the two types?



What are the signs?

What are the associatedradiographic tests?


What is the treatment iflocalized?

What is the treatment if diffuse?


Benign Mesothelioma

What is it?

What pleura is usuallyinvolved?

Primary pleural neoplasm

1. Localized2. Diffuse (highly malignant)

Exposure to asbestosSmoking

Dyspnea and pain � 90%Localized: pleuritic pain, joint pain and

swelling, dyspneaDiffuse: chest pain, malaise, weight loss,

cough

Pleural effusion:Localized (10%–15%)Diffuse (�75%)

X-ray may reveal a peripheral mass, oftenforming an obtuse angle with the chestwall; CT scan is also performed

Pleural biopsy, pleural fluid cytology

Surgical excision

Early stages may be resected, followedby radiation; for more advanced stages,radiation, chemotherapy, or both are done

Localized: poorDiffuse: dismal (average life span after

diagnosis is about 1 year)

Benign pleural mesothelioma

Visceral pleura


What is the gross appearance?




Pedunculated “broccoli or cauliflower”tumor on a stalk coming off of the lung

Surgical resection with at least 1 cm clearmargin

In contrast to malignant mesothelioma, thebenign mesothelioma has an excellent prog-nosis with cure in the vast majority of cases

DISEASES OF THE LUNGS

BRONCHOGENIC CARCINOMA

What is the annual incidenceof lung cancer in the UnitedStates?

What is the number of annualdeaths from lung cancer?

What is the #1 risk factor?

Does asbestos exposureincrease the risk in patientswho smoke?

What type of lung cancerarises in nonsmoking?

Cancer arises more often inwhich lung?


170,000 new cases/year

150,000; most common cancer death inthe United States in men and women

Smoking (85%!)

Yes

Adenocarcinoma

Right � left; upper lobes � lower lobes

Change in a chronic coughHemoptysis, chest pain, dyspneaPleural effusion (suggests chest wall

involvement)Hoarseness (recurrent laryngeal nerve

involvement)Superior vena cava syndromeDiaphragmatic paralysis (phrenic nerve

involvement)Symptoms of metastasis/paraneoplastic

syndromeFinger clubbing


What is Pancoast’s tumor?

What is Horner’s syndrome?

What are the four most common sites of extrathoracicmetastases?

What are paraneoplasticsyndromes?

Name five general types ofparaneoplastic syndromes.

What are the associatedradiographic tests?

How is the tumordiagnosed?


Tumor at the apex of the lung or superiorsulcus that may involve the brachialplexus, sympathetic ganglia, and vertebralbodies, leading to pain, upper extremityweakness, and Horner’s syndrome

Injury to the cervical sympathetic chain;Think: “MAP”

1. Miosis (small pupil)2. Anhydrosis of ipsilateral face3. Ptosis

1. Bone2. Liver3. Adrenals4. Kidney

Syndromes that are associated withtumors but may affect distant parts of thebody; they may be caused by hormonesreleased from endocrinologically activetumors or may be of uncertain etiology

1. Metabolic: Cushing’s, SIADH, hypercalcemia

2. Neuromuscular: Eaton-Lambert, cerebellar ataxia

3. Skeletal: hypertrophic osteoarthropathy4. Dermatologic: acanthosis nigricans5. Vascular: thrombophlebitis

CXR, CT scan, PET scan

1. Sputum cytology2. Needle biopsy (CT or fluoro guidance)3. Bronchoscopy with brushings, biopsies,

or both4. With or without mediastinoscopy,

mediastinotomy, scalene node biopsy,or open lung biopsy for definitivediagnosis


For each tumor listed, recallits usual site in the lung andits natural course:

Squamous cell?

Adenocarcinoma?

Small (oat) cell?

Large cell?

What are the AJCC stages ofcarcinoma of the lungs:

Stage Ia?

Stage Ib?

Stage IIa?

Stage IIb?


66% occur centrally in lung hilus; mayalso be a Pancoast’s tumor; slow growth,late metastasis; associated with smoking(Think: Squamous � Sentral)

Peripheral, rapid growth with hematogenous/nodal metastasis,associated with lung scarring

Central, highly malignant, usually notoperable

Usually peripheral, very malignant

Tumor �3 cm, no nodes, no metastases

Tumor 3–5 cm, no nodes, no metastases

1. Tumor �5 cm and positive nodes to lung or ipsilateral hilum; nometastases, or

2. Tumor 5–7 cm, no nodes, nometastases

1. Tumor 5–7 cm and positive nodes inlung or ipsilateral hilum, or

2. Tumor that invades chest wall,diaphragm, mediastinal pleura,phrenic nerve, pericardial sac, orbronchus (not carina) and no nodes,no metastases


Stage IIIa?

Stage IIIb?

Stage IV?

What are the surgicalcontraindications for NON-small cell carcinoma?

What is the treatment bystage for NON-small celllung carcinoma:

Stage I?

Stage II?

Stage IIIa?

Stage IIIb?

Stage IV?

What is the treatment forisolated brain metastasis?


1. Tumor �7 cm and � nodes in ipsilateral mediastinum or subcarinawith no metastases

2. Tumor �7 cm or extends into chestwall, parietal pleura, diaphragm,phrenic nerve, or pericardium and � lymph node metastases to ipsilateral,mediastinal, or subcarinal nodes

3. Any size tumor that invades heart,great vessels, trachea, esophagus,carina, or ipsalateral lobe, or � nodesperibronchial and/or ipsilateral hilum,or intrapulmonary nodes

Any tumor, � lymph node metastases tocontralateral hilum or mediastinum

Supraclavicular/scalene nodes, NOdistant metastases

Distant metastases

Stage IV, Stage IIIb, poor lung function(FEV1 �0.8L)

Surgical resection

Surgical resection

Chemotherapy and XRT �� surgicalresection

Chemotherapy and XRT

Chemotherapy �� XRT

Surgical resection


What is the approximateprognosis (5-year survival)after treatment of NON-smallcell lung carcinoma by stage:

Stage I?

Stage II?

Stage III?

Stage IV?

How is small cell carcinomatreated?

What are the contraindications to surgeryfor lung cancer?

What postoperative FEV1

must you have?

What is hypertrophicpulmonaryosteoarthropathy?


50%

30%

�10%

1%

Chemotherapy �� XRT (very small isolated lesions can be surgically resected)

Think: “STOP IT”Superior vena cava syndrome,Supraclavicular node metastasis, Scalene node metastasisTracheal carina involvementOat cell carcinoma (treat with

chemotherapy �� radiation)Pulmonary function tests show

FEV1 �0.8LInfarction (myocardial); a.k.a. cardiac

crippleTumor elsewhere (metastatic disease)

FEV1 �800 cc; thus, a preoperativeFEV1 �2L is usually needed for apneumonectomy

If FEV1 is �2L, a ventilation perfusionscan should be performed

Periosteal proliferation and new boneformation at the end of long bones and in the bones of the hand (seen in 10% of patients with lung cancer)

SOLITARY PULMONARY NODULES (COIN LESIONS)

What are they? Peripheral circumscribed pulmonarylesions



What percentage are malignant?

Is there a gender risk?


What are the signs?


What is the significance of“popcorn” calcification?

What are the risk factors formalignancy?

What are the associated labtests?

Which method of tissuediagnosis is used?


Granulomatous disease, benignneoplasms, malignancy

Overall, 5% to 10% (but �50% aremalignant in smokers �50 years)

Yes; the incidence of coin lesions is 3 to 9� higher and malignancy is nearlytwice as common in men as in women

Usually asymptomatic with solitary nodules, but may include coughing,weight loss, chest pain, and hemoptysis

Physical findings are uncommon; clubbingis rare; hypertrophic osteoarthropathyimplies �80% chance of malignancy

CXR, chest CT

Most likely benign (i.e., hamartoma)

1. Size: lesions �1 cm have a significantchance of malignancy, and those �4 cmare very likely to be malignant

2. Indistinct margins (corona radiata)3. Documented growth on follow-up

x-ray (if no change in 2 years, mostlikely benign)

4. Increasing age

1. TB skin tests, etc.2. Sputum cultures3. Sputum cytology is diagnostic in 5% to

20% of cases

Chest CT scan with needle biopsy, bronchoscopy (�� transtracheal biopsy),excisional biopsy (open or thoracoscopic)



Which solitary nodule canbe followed without a tissuediagnosis?


What if the patient has an SPN and pulmonary hypertrophicosteoarthropathy?

What is hypertrophicpulmonary osteoarthropathy?

What is its incidence?

What are the signs?


Surgical excision is the mainstay of treatment

Excisional biopsy is therapeutic forbenign lesions, solitary metastasis, andfor primary cancer in patients who arepoor risks for more extensive surgery

Lobectomy for centrally placed lesionsLobectomy with node dissection for

primary cancer (if resectable by preop evaluations)

Popcorn calcificationsMass unchanged for 2 years on previous

CXR

For malignant coin lesions �2 cm, 5-yearsurvival is �70%

�75% chance of carcinoma

Periosteal proliferation and new boneformation at the end of long bones and inbones of the hand

�7% of patients with lung cancer(2%–12%)

Associated with clubbing of the fingers;diagnosed by x-ray of long bones, revealing periosteal bone hypertrophy

CARCINOID TUMOR

What is it?

What is its natural course inthe lung?

What are the primary localfindings?

APUD (Amine-Precursor Uptake andDecarboxylation) cell tumor of the bronchus

Slow growing (but may be malignant)

Wheezing and atelectasis caused bybronchial obstruction/stenosis


What condition can it beconfused with?



What is a sleeve resection?

What is the prognosis (5-year survival) after complete surgical resectionof carcinoid:

Negative nodes?

Positive nodes?

What is the most commonbenign lung tumor?


Asthma

Bronchoscopy reveals round red-yellow-purple mass covered by epithelium thatprotrudes into bronchial lumen

Surgical resection (lobectomy with lymphnode dissection)

Sleeve resection is also an option forproximal bronchial lesions

Resection of a ring segment of bronchus(with tumor inside) and then end-to-endanastomosis of the remaining ends, allowing salvage of lower lobe

�90% alive at 5 years

66% alive at 5 years

Hamartoma (normal cells in a weird configuration)

PULMONARY SEQUESTRATION

What is it?

Define the following terms:Interlobar

Extralobar



Abnormal benign lung tissue with separate blood supply that DOES NOTcommunicate with the normaltracheobronchial airway

Sequestration in normal lung tissue covered by normal visceral pleura

Sequestration not in normal lung coveredby its own pleura

Asymptomatic, recurrent pneumonia

CXR, chest CT, A-gram, U/S withDoppler flow to ascertain blood supply


What is the treatment in thefollowing cases:

Extralobar?

Intralobar?

What is the major dangerduring surgery forsequestration?


Surgical resection

Lobectomy

Anomalous blood supply from below thediaphragm (these can be cut andretract into the abdomen resulting inexsanguination!)

Always document blood supply by A-gram or U/S with Doppler flow

DISEASES OF THE MEDIASTINUM

MEDIASTINAL ANATOMY

What structures lie in thefollowing locations:

Superior mediastinum?

Anterior mediastinum?

Middle mediastinum?

Posterior mediastinum?

What is the major differentialdiagnosis for tumors of themediastinum:

Anterior mediastinum?

Middle mediastinum?

Aortic arch, great vessels, upper trachea,esophagus

Thymus, ascending aorta, lymph nodes

Heart, lower trachea and bifurcation,lung hila, phrenic nerves, lymph nodes

Esophagus, descending aorta, thoracicduct, vagus and intercostal nerves, sympathetic trunks, azygous and hemizygous veins, lymph nodes

Classic “four Ts”: Thyroid tumor, Thymoma, Terrible lymphoma,Teratoma; also parathyroid tumor,lipoma, vascular aneurysms

Lymphadenopathy (e.g., lymphoma, sarcoid), teratoma, fat pad, cysts, hernias, extension of esophageal mass,bronchogenic cancer


Posterior mediastinum?

What is the most commontype of tumor arising in themediastinum?

What is the differential diagnosis for a neurogenictumor?


Neurogenic tumors, lymphoma, aorticaneurysm, vertebral lesions, hernias

Neurogenic (most commonly in posteriormediastinum)

Schwannoma (a.k.a. neurolemmoma),neurofibroma, neuroblastoma,ganglioneuroma, ganglioneuroblastoma,pheochromocytoma

PRIMARY MEDIASTINAL TUMORS

Thymoma

Where are they found in themediastinum?



What are the indications forpostop radiation therapy?

What are the indications forpreop chemotherapy?

What percentage of thymomas are malignant?

How is a malignantthymoma diagnosed?

What is myasthenia gravis?

What percentage of patientswith myasthenia gravis havea thymoma?

What percentage of patientswith thymoma have or willhave myasthenia gravis?

Anterior

CT scan

All thymomas should be surgically resectedvia midline sternotomy

Invasive malignant tumor

Tumor �6 cm and CT scan with invasion

�25%

At surgery with invasion into surroundingstructures (not by histology!)

Autoimmune disease with antibodiesagainst the muscle acetylcholine receptors

�15%

�75%!


Teratomas

What are they?

What is a dermoid cyst?

Which age group is affected?

Where in the mediastinumdo they occur?

What are the characteristicx-ray findings?


What is the treatment ofbenign dermoid cysts?

What is the treatment ofmalignant teratoma?

Which tumor markers areassociated with malignantteratomas?

Neurogenic Tumors


Where in the mediastinumdo they occur?



Tumors of branchial cleft cells; thetumors contain ectoderm, endoderm, andmesoderm

Teratoma made up of ectodermal derivatives (e.g., teeth, skin, hair)

Usually adolescents, but can occur at any age

Anterior

Calcifications or teeth; tumors may becystic

�15%

Surgical excision

Preoperative chemotherapy until tumormarkers are normal, then surgical resection

AFP, CEA

Most common mediastinal tumors in allage groups

Posterior, in the paravertebral gutters

50% in children10% in adults


What are the histologic types(5)? (Note cells of origin andwhether benign or malignant.)


1. Neurilemmoma or schwannoma(benign)—arise from Schwann cellsheaths of intercostal nerves

2. Neurofibroma (benign)—arise fromintercostal nerves; may degenerate into:

3. Neurosarcoma (malignant)4. Ganglioneuroma (benign)—from

sympathetic chain5. Neuroblastoma (malignant)—also

from sympathetic chain

LYMPHOMA

Where in the mediastinumdoes it occur?

What percentage oflymphomas involvemediastinal nodes?




Anywhere, but most often in the anterosuperior mediastinum or hilum in the middle mediastinum

�50%

Cough, fever, chest pain, weight loss,SVC syndrome, chylothorax

1. CXR, CT scan2. Mediastinoscopy or mediastinotomy

with node biopsy

Nonsurgical (chemotherapy, radiation, or both)

MEDIASTINITIS

Acute Mediastinitis

What is it?

Name the six etiologies.

Acute suppurative mediastinal infection

1. Esophageal perforation (Boerhaave’ssyndrome)

2. Postoperative wound infection3. Head and neck infections4. Lung or pleural infections5. Rib or vertebral osteomyelitis6. Distant infections


What are the clinicalfeatures?


Chronic Mediastinitis

What is it?

What is the most commonetiology?

What are the clinicalfeatures?




Fever, chest pain, dysphagia (especiallywith esophageal perforation), respiratorydistress, leukocytosis

1. Wide drainage2. Treatment of primary cause3. Antibiotics

Mediastinal fibrosis secondary to chronicgranulomatous infection

Histoplasma capsulatum

50% are asymptomatic; symptoms arerelated to compression of adjacent structures: SVC syndrome, bronchial and esophageal strictures, constrictivepericarditis

CXR or CT may be helpful, but surgery/biopsy often makes the diagnosis

Antibiotics; surgical removal of the granulomas is rarely helpful

SUPERIOR VENA CAVA SYNDROME

What is it?

What is the #1 cause?

What are the clinical manifestations?

Obstruction of the superior vena cava,usually by extrinsic compression

Malignant tumors cause �90% of cases;lung cancer is by far the most common;other tumors include thymoma,lymphoma, and Hodgkin’s disease

1. Blue discoloration and puffiness of theface, arms, and shoulders

2. CNS manifestations may includeheadache, nausea, vomiting, visual distortion, stupor, and convulsions.

3. Cough, hoarseness, and dyspnea





1. Diuretics and fluid restriction2. Prompt radiation therapy ��

chemotherapy for any causative cancer

SVC obstruction itself is fatal in �5% ofcases; mean survival time in patients withmalignant obstruction is �7 months

DISEASES OF THE ESOPHAGUS

ANATOMIC CONSIDERATIONS

What are the primary functions of the Upper and Lower EsophagealSphincters?

The esophageal venousplexus drains inferiorly intothe gastric veins. Why is thisimportant?

Identify the esophagealmuscle type:

Proximal 1/3

Middle 1/3

Distal 1/3

Identify the blood supply tothe esophagus:

Proximal 1/3

Middle 1/3

Distal 1/3

What is the length of theesophagus?

Why is the esophagus notorious for anastomoticleaks?

UES: swallowingLES: prevention of reflux

Gastric veins are part of the portal venoussystem; portal hypertension can thus bereferred to the esophageal veins, leadingto varices

Skeletal muscle

Smooth muscle � skeletal muscle

Smooth muscle

Inferior thyroid, anterior intercostals

Esophageal arteries, bronchial arteries

Left gastric artery, left inferior phrenic artery

�25 cm in the adult (40 cm from teeth toLES)

Esophagus has no serosa (same as the distalrectum)


What nerve runs with theesophagus?


Vagus nerve

ZENKER’S DIVERTICULUM

What is it? Pharyngoesophageal diverticulum; a false diverticulum containing mucosa and submucosa at the UES at thepharyngoesophageal junction throughKillian’s triangle

Zenker’sdiverticulum

What is the disease’s “claimto fame”?




Most common esophageal diverticulum

Dysphagia, neck mass, halitosis, foodregurgitation, heartburn

Barium swallow

1. Diverticulectomy2. Cricopharyngeus myotomy, if �2 cm

ACHALASIA

What is it?

What are the proposedetiologies?

1. Failure of the LES to relax duringswallowing

2. Loss of esophageal peristalsis

1. Neurologic (ganglionic degenerationof Auerbach’s plexus, vagus nerve, orboth); possibly infectious in nature

2. Chagas’ disease in South America


What are the associatedlong-term conditions?



Esophageal carcinoma secondary to Barrett’s esophagus from food stasis

Dysphagia for both solids and liquids, followed by regurgitation; dysphagia forliquids is worse

Trappedfood

Esophagus

Contractedmuscle

Diaphragm

What are the diagnosticfindings?


Radiographic contrast studies revealdilated esophageal body with narrowing inferiorly

Manometry: motility studies revealincreased pressure in the LES andfailure of the LES to relax duringswallowing

1. Balloon dilation of the LES2. Medical treatment of reflux versus

Belsey Mark IV 270 fundoplication(do not perform 360 Nissen)

3. Myotomy of the lower esophagus andLES

DIFFUSE ESOPHAGEAL SPASM

What is it?

What is the associated condition?


Strong, nonperistaltic contractions of theesophageal body; sphincter function isusually normal

Gastroesophageal reflux

Spontaneous chest pain that radiates tothe back, ears, neck, jaw, or arms



What are the associateddiagnostic tests?

What is the classic findingon esophageal contrast study(UGI)?



Angina pectorisPsychoneurosisNutcracker esophagus

Esophageal manometry: Motility studies reveal repetitive, high-amplitude contractions with normalsphincter response

Upper GI may be normal, but 50% showsegmented spasms or corkscrewesophagus

Endoscopy

“Corkscrew esophagus”

Medical (antireflux measures, calciumchannel blockers, nitrates)

Long esophagomyotomy in refractory cases

NUTCRACKER ESOPHAGUS


What is it?



What are the associateddiagnostic tests?


Hypertensive peristalsis

Very strong peristaltic waves

Spontaneous chest pain that radiates tothe back, ears, neck, jaw, or arms

Angina pectorisPsychoneurosisDiffuse esophageal spasm

1. Esophageal manometry: motility studiesreveal repetitive, high-amplitude contractions with normal sphincterresponse

2. Results of UGI may be normal (ruleout mass)

3. Endoscopy

Medical (antireflux measures, calciumchannel blockers, nitrates)

Long esophagomyotomy in refractory cases



ESOPHAGEAL REFLUX

What is it?


Name four associated conditions/factors.




Which four complicationsrequire surgery?

Describe each of thefollowing types of surgery:

Nissen

Reflux of gastric contents into the loweresophagus resulting from the decreasedfunction of the LES

1. Decreased LES tone2. Decreased esophageal motility3. Hiatal hernia4. Gastric outlet obstruction5. NGT

1. Sliding hiatal hernia2. Tobacco and alcohol3. Scleroderma4. Decreased endogenous gastrin

production

Substernal pain, heartburn, regurgitation;symptoms are worse when patient issupine and after meals

1. pH probe in the lower esophagusreveals acid reflux

2. EGD shows esophagitis3. Manometry reveals decreased LES

pressure4. Barium swallow

Medical: H2-blockers, antacids, metoclopramide, omeprazole

Elevation of the head of the bed; small,multiple meals

1. Failure of medical therapy2. Esophageal strictures3. Progressive pulmonary insufficiency

secondary to documented nocturnalaspiration

4. Barrett’s esophagus

360 fundoplication: wrap fundus of stomach all the way around the esophagus


Belsey Mark IV

Hill

Lap Nissen

Lap Toupet

What is Barrett’s esophagus?

Why is it significant?



270 fundoplication: wrap fundus ofstomach, but not all the way around

Tighten arcuate ligament around esophagus and tack stomach to diaphragm

Nissen via laparoscope

Lap fundoplication posteriorly with lessthan 220 to 250 wrap used with decreasedesophageal motility; disadvantage is morepostoperative reflux

Replacement of the lower esophagealsquamous epithelium with columnarepithelium secondary to reflux

This lesion is premalignant

People with significant reflux should befollowed with regular EGDs withbiopsies, H2-blockers, and antireflux precautions; many experts believe thatpatients with severe dysplasia shouldundergo esophagectomy

CAUSTIC ESOPHAGEAL STRICTURES

Which agents may causestrictures if ingested?



Lye, oven cleaners, drain cleaners, batteries,sodium hydroxide tablets (Clinitest)

History; EGD is clearly indicated earlyon to assess the extent of damage (�24 hrs); scope to level of severe injury(deep ulcer) only, water soluble contraststudy for deep ulcers to rule out perforation

1. NPO/IVF/H2-blocker2. Do not induce emesis3. Corticosteroids (controversial—

probably best for shallow/moderateulcers), antibiotics (penicillin/gentamicin) for moderate ulcers

4. Antibiotic for deep ulcers5. Upper GI at 10 to 14 days


What is the treatment if astricture develops?

What is the long-termfollow-up?

What is a Maloney dilator?


Dilation with Maloney dilator/ballooncatheter

In severe refractory cases, esophagectomywith colon interposition or gastric pull-up

Because of increased risk of esophagealsquamous cancer (especially with ulceration), patients endoscopies everyother year

Mercury-filled rubber dilator

ESOPHAGEAL CARCINOMA

What are the two maintypes?

What is the most commonhistology?

What is the age and genderdistribution?

What are the etiologicfactors (5)?


What comprises theworkup?


1. Adenocarcinoma at the GE junction2. Squamous cell carcinoma in most of

the esophagus

Worldwide: squamous cell carcinoma(95%!)

USA: adenocarcinoma

Most common in the sixth decade of life;men predominate, especially black men

1. Tobacco2. Alcohol3. GE reflux4. Barrett’s esophagus5. Radiation

Dysphagia, weight lossOther symptoms include chest pain,

back pain, hoarseness, symptoms ofmetastasis

1. UGI2. EGD3. Transesophageal ultrasound (TEU)4. CT scan of chest/abdomen

Leiomyoma, metastatic tumor, lymphomas,benign stricture, achalasia, diffuseesophageal spasm, GERD



Describe the stages of adenocarcinoma esophagealcancer:

Stage I

Stage IIa

Stage IIb

Stage III

Stage IV


What is an Ivor-Lewis procedure?

Treatment options withmetastatic disease(unresectable)?

What is a “blunt esophagectomy”?


1. Upper GI localizes tumor2. EGD obtains biopsy and assesses

resectability3. Full metastatic workup (CXR, bone

scan, CT scan, LFTs)

Tumor: invades lamina propria, muscularis mucosae, or submucosa

Nodes: negative

Tumor: invades muscularis propria (grade 3)

Nodes: negative

1. Tumor: invades up to muscularis propria

Nodes: positive regional nodes2. Invades adventitia with negative nodes

1. Tumor: invades adventitiaNodes: positive regional nodes

2. Tumor: invades adjacent structures

Distant metastasis

Esophagectomy with gastric pull-up orcolon interposition

Laparotomy and right thoracotomy withgastroesophageal anastomosis in the chestafter esophagectomy

Chemotherapy and XRT �� dilation,stent, laser, electrocoagulation, brachytherapy, photodynamic laser therapy

Esophagectomy with “blunt” transhiataldissection of esophagus from abdomenand gastroesophageal anastomosis in theneck


What is the operativemortality rate?

Has radiation therapy and/orchemotherapy been shownto decrease mortality?

What is the postop complication rate?

What is the prognosis (5-yearsurvival) by stage:

I?

II?

III?

IV?


�5%

No

�33%!

66%

25%

10%

Basically 0%

What do the followingabbreviations stand for:

AI?

AS?

ASD?

CABG?

CAD?

CPB?

IABP?

LAD?

CardiovascularSurgery

Chapter 72

Aortic Insufficiency/regurgitation

Aortic Stenosis

Atrial Septal Defect

Coronary Artery Bypass Grafting

Coronary Artery Disease

CardioPulmonary Bypass

IntraAortic Balloon Pump

Left Anterior Descending coronaryartery


IMA?

MR?

PTCA?

VAD?

VSD?

Define the following terms:Stroke volume (SV)

Cardiac output (CO)

Cardiac Index (CI)

Ejection fraction

Compliance

SVR

Preload

Afterload

PVR

MAP

What is a normal CO?

What is a normal CI?

Chapter 72 / Cardiovascular Surgery 649

Internal Mammary Artery

Mitral Regurgitation

Percutaneous Transluminal CoronaryAngioplasty (balloon angioplasty)

Ventricular Assist Device

Ventricular Septal Defect

mL of blood pumped per heartbeat (SV � CO/HR)

Amount of blood pumped by the hearteach minute: heart rate � SV

CO/BSA (body surface area)

Percentage of blood pumped out of theleft ventricle: SV end diastolic volume(nl 55%–70%)

Change in volume/change in pressure

Systemic Vascular Resistance �

MAP – CVPCO � 80

Left ventricular end diastolic pressure orvolume

Arterial resistance the heart pumpsagainst

Pulmonary Vascular Resistance �PA(mean) – PCWP/CO � 80

Mean Arterial Pressure � diastolic BP �1/3 (systolic BP – diastolic BP)

4 to 8 L/minute

2.5 to 4 L/minute


What are the ways toincrease CO?

When does most of the coronary blood flow takeplace?

Name the three major coronary arteries.

What are the three main“cardiac electrolytes”?


Remember “MR. PAIR”:1. Mechanical assistance (IABP, VAD)2. Rate—Increase heart rate

3. Preload—Increase preload4. Afterload—Decrease afterload5. Inotropes—Increase contractility6. Rhythm—Normal sinus

During diastole (66%)

1. Left Anterior Descending (LAD)2. Circumflex3. Right coronary

1. Calcium (inotropic)2. Potassium (dysrhythmias)3. Magnesium (dysrhythmias)

ACQUIRED HEART DISEASE

CORONARY ARTERY DISEASE (CAD)

What is it?



Who classically gets “silent”MIs?

Atherosclerotic occlusive lesions of thecoronary arteries; segmental naturemakes CABG possible

CAD is the #1 killer in the Westernworld; �50% of cases are triple vesseldiseases involving the LAD, circumflex,and right coronary arteries

If ischemia occurs (low flow, vasospasm,thrombus formation, plaque rupture, or acombination), patient may experiencechest pain, crushing, substernal shortnessof breath, nausea/upper abdominal pain,sudden death, or may be asymptomaticwith fatigue

Patients with diabetes (autonomicdysfunction)



Which diagnostic testsshould be performed?



HTNSmokingHigh cholesterol/lipids (�240)ObesityDiabetes mellitusFamily history

Exercise stress testing ( � thallium)EchocardiographyLocalize dyskinetic wall segmentsValvular dysfunctionEstimate ejection fractionCardiac catheterization with coronary

angiography and left ventriculography(the definitive test)

Medical therapy (�-blockers, aspirin,nitrates, HTN medications), angioplasty(PTCA), �� stents, surgical therapy: CABG

CABG

What is it? Coronary Artery Bypass Grafting

Veingrafts

hrf'0

2

What are the indications? Left main disease 2-vessel disease (especially diabetics)Unstable or disabling angina unresponsive

to medical therapy/PTCAPostinfarct anginaCoronary artery rupture, dissection,

thrombosis after PTCA


CABG vs. PTCA �� stents?

What procedures are mostoften used in the treatment?

What other vessels are occasionally used for grafting?


What is the operative mortality?

What medications shouldalmost every patient begiven after CABG?

Can a CABG be performedoff cardiopulmonary bypass?


CABG � Survival improvement for diabetics and 2-vessel disease, c short-term morbidity

PTCA � T short-term morbidity, T cost, T hospital stay, c reintervention, c postprocedure angina

Coronary arteries grafted (usually 3–6):internal mammary pedicle graft andsaphenous vein free graft are most oftenused (IMA 95% 10-year patency vs. 50%with saphenous)

Radial artery, inferior epigastric vein

HemorrhageTamponadeMI, dysrhythmiasInfectionGraft thrombosisSternal dehiscencePostpericardiotomy syndrome, stroke

1% to 3% for elective CABG (vs. 5%–10% for acute MI)

Aspirin, �-blocker

Yes, today they are performed with orwithout bypass

POSTPERICARDIOTOMY SYNDROME

What is it?


Pericarditis after pericardiotomy(unknown etiology), occurs weeks to 3 months postoperatively

FeverChest pain, atrial fibrillationMalaisePericardial friction rubPericardial effusion/pleural effusion



What is pericarditis after anMI called?


NSAIDs, �/� steroids

Dressler’s syndrome

CARDIOPULMONARY BYPASS (CPB)

What is it? Pump and oxygenation apparatus removeblood from SVC and IVC and return it tothe aorta, bypassing the heart and lungsand allowing cardiac arrest for open-heartprocedures, heart transplant, lung transplant, or heart-lung transplant as well as procedures on the proximalgreat vessels

Is anticoagulation necessary?

How is anticoagulationreversed?

What are the ways to manipulate cardiac outputafter CPB?

What mechanical problemscan decrease CO after CPB?

What is “tamponade physiology”?

Yes, just before and during the procedure,with heparin

Protamine

Rate, rhythm, afterload, preload, inotropes,mechanical (IABP and VAD)

Cardiac tamponade, pneumothorax

T Cardiac output, c heart rate, hypotension,c CVP � c wedge pressure



What are the options fortreating postop CABG mediastinal bleeding?

What is “heparin rebound”?

What is the method of lowering SVR after CPB?

What are the options if apatient cannot be weanedfrom CPB?

What percentage of patientsgoes into AFib after CPB?

What is the workup of apostoperative patient withAFib?

What is a MIDCAB?

What is TMR?


Trauma to formed blood elements (especially thrombocytopenia andplatelet dysfunction)

Pancreatitis (low flow)Heparin reboundCVAFailure to wean from bypassTechnical complications (operative

technique)MI

Protamine, c PEEP, FFP, platelets,aminocaproic acid

Increased anticoagulation after CPBfrom increased heparin levels, as increasein peripheral blood flow after CPBreturns heparin residual that was in theperipheral tissues

Warm the patient; administer sodiumnitroprusside (SNP) and dobutamine

Inotropes (e.g., epinephrine)VAD, IABP

Up to 33%

Rule out PTX (ABG, CT scan), acidosis(ABG), electrolyte abnormality (LABS),and ischemia (EKG), CXR

Minimally Invasive Direct Coronary ArteryBypass—LIMA to LAD bypass withoutCPB and through a small thoracotomy

TransMyocardial laser Revascularization:laser through groin catheter makes smallholes (intramyocardial sinusoids) incardiac muscle to allow blood to nourishthe muscle


What is OPCAB?


Off Pump Coronary Artery Bypass—median sternotomy but no bypass pump

AORTIC STENOSIS (AS)

What is it?



What is the memory aid for the aortic stenosis complications?

What are the signs?

What tests should beperformed?


What are the indications forsurgical repair?

What are the pros/cons ofmechanical valve?

Destruction and calcification of valveleaflets, resulting in obstruction of leftventricular outflow

Calcification of bicuspid aortic valveRheumatic feverAcquired calcific AS (7th to 8th decades)

Angina (5 years life expectancy if leftuntreated)

Syncope (3 years life expectancy if leftuntreated)

CHF (2 years life expectancy if leftuntreated)

Often asymptomatic until late

Aortic Stenosis Complications � AnginaSyncope CHF—5,3,2

Murmur: crescendo-decrescendo systolicsecond right intercostal space withradiation to the carotids

Left ventricular heave or lift from leftventricular hypertrophy

CXR, ECG, echocardiographyCardiac catheterization—needed to plan

operation

Valve replacement with tissue or mechanical prosthesis

If patient is symptomatic or valve cross-sectional area is �0.75 cm2 (normal 2.5to 3.5 cm2) and/or gradient �50 mm Hg

Mechanical valve is more durable, butrequires lifetime anticoagulation


What is the treatment optionin poor surgical candidates?

Why is a loud murmur oftena good sign?

Why might an AS murmurdiminish over time?


Balloon aortic “valvuloplasty”(percutaneous)

Implies a high gradient, which indicatespreserved LV function

It may imply a decreasing gradient froma decline in LV function

AORTIC INSUFFICIENCY (AI)

What is it?




What are the signs?

Incompetency of the aortic valve (regurgitant flow)

Bacterial endocarditis (Staphylococcusaureus, Streptococcus viridans)

Rheumatic fever (rare)Annular ectasia from collagen vascular

disease (especially Marfan’s syndrome)

Bicuspid aortic valve, connective tissuedisease

Palpitations from dysrhythmias anddilated left ventricle

Dyspnea/orthopnea from left ventricularfailure

Excess fatigueAngina from T diastolic BP and coronary

flow (Note: Most coronary blood flowoccurs during diastole and aortarebound)

Musset sign (bobble-head)

c diastolic BPMurmur: blowing, decrescendo diastolic

at left sternal borderAustin-Flint murmur: reverberation of

regurgitant flowIncreased pulse pressure: “pistol shots,”

“water-hammer” pulse palpated over peripheral arteries

Quincke sign (capillary pulsations ofuvula)




What are the indications forsurgical treatment?



1. CXR: increasing heart size can beused to follow progression

2. Echocardiogram3. Catheterization (definitive)4. TEE

Aortic valve replacement

Symptomatic patients (CHF, PND, etc.),left ventricle dilatation, decreasing LVfunction, decreasing EF, acute AI onset

Surgery gives symptomatic improvementand may improve longevity; low operativerisk

MITRAL STENOSIS (MS)

What is it?


What are the signs?


What are the indications forintervention?

Calcific degeneration and narrowing ofthe mitral valve resulting from rheumaticfever in most cases

1. Dyspnea from increased left atrialpressure, causing pulmonary edema(i.e., CHF)

2. Hemoptysis (rarely life-threatening)3. Hoarseness from dilated left atrium

impinging on the recurrent laryngealnerve

4. Palpations (AFib)

Murmur: crescendo diastolic rumble at apexIrregular pulse from AFib caused by

dilated left atriumStroke caused by systemic emboli from

left atrium (AFib and obstructed valveallow blood to pool in the left atriumand can lead to thrombus formation)

EchocardiogramCatheterization

1. Symptoms (severe)2. Pulmonary HTN and mitral valve area

�1 cm2/m2

3. Recurrent thromboembolism



What is the medicaltreatment for mildsymptomatic patients?



1. Open commissurotomy (open heartoperation)

2. Balloon valvuloplasty: percutaneous3. Valve replacement

Diuretics

�80% of patients are well at 10 yearswith successful operation

MITRAL REGURGITATION (MR)

What is it?


What are the most commoncauses?


What are the signs?

What are the indications fortreatment?


Incompetence of the mitral valve

Severe mitral valve prolapse (some prolapse is found in 5% of the population, with women men)

Rheumatic feverPost-MI from papillary muscle

dysfunction/ruptureRuptured chordae

Rheumatic fever (#1 worldwide), rupturedchordae/papillary muscle dysfunction

Often insidious and late: dyspnea, palpitations, fatigue

Murmur: holosystolic, apical radiating tothe axilla

1. Symptoms2. LV �45 mm end-systolic dimension

(left ventricular dilation)

1. Valve replacement2. Annuloplasty: suture a prosthetic ring

to the dilated valve annulus



ARTIFICIAL VALVE PLACEMENT

What is it?

What are the types of artificial valves?

What are the pros and cons:Tissue?

Mechanical?

Contraindications for tissue valve?

Contraindications formechanical valve?


What must patients with anartificial valve receive beforedental procedures?

Define the Ross procedure.

Replacement of damaged valves with tissue or mechanical prosthesis

Tissue and mechanical

NO anticoagulation but shorter duration(20%–40% need replacement in 10 years);good for elderly

Last longer (�15 years) but requireANTICOAGULATION

Dialysis (calcify), youth

Pregnancy (or going to be pregnant due to anticoagulation), bleeding risk(alcoholic, PUD)

From 1% to 5% in most series

Antibiotics

Aortic valve replacement with a pulmonaryautograft (i.e., patient’s own valve!)

INFECTIOUS ENDOCARDITIS

What is it?


What are the commoncausative agents?

Microbial infection of heart valves

Preexisting valvular lesion, proceduresthat lead to bacteremia, IV drug use

S. viridans: associated with abnormalvalves

S. aureus: associated with IV drug useS. epidermidis: associated with prosthetic

valves







Murmur (new or changing)PetechiaeSplinter hemorrhage (fingernails)Roth spots (on retina)Osler nodes (raised, painful on soles and

palms; Osler � Ouch!)Janeway lesions (similar to Osler nodes,

but flat and painless) (JaneWAY �pain aWAY)

Echocardiogram, TEESerial blood cultures (definitive)

Prolonged IV therapy with bactericidalantibiotics, to which infecting organisms are sensitive

Infection can progress, requiring valvereplacement

CONGENITAL HEART DISEASE

VENTRICULAR SEPTAL DEFECT (VSD)


What is it?

What is pulmonary vascularobstructive disease?

What is Eisenmenger’s syndrome?

What is the treatment ofEisenmenger’s syndrome?

Most common congenital heart defect

Failure of ventricular septum tocompletely close; 80% of cases involvethe membranous portion of theseptum, resulting in left-to-right shunt,increased pulmonary blood flow, and CHFif pulmonary to systemic flow is �2:1

Pulmonary artery hyperplasia fromincreased pulmonary pressure caused bya left to right shunt (e.g., VSD)

Irreversible pulmonary HTN from chronicchanges in pulmonary arterioles andincreased right heart pressures; cyanosisdevelops when the shunt reverses(becomes right to left across the VSD)

Only option is heart-lung transplant; otherwise, the disease is untreatable


What is the incidence ofVSD?


30% of heart defects (most commondefect)

PATENT DUCTUS ARTERIOSUS (PDA)

What is it?

What are the factorspreventing closure?


What are the signs?




Physiologic right-to-left shunt in fetal circulation connecting the pulmonaryartery to the aorta bypassing fetal lungs;often, this shunt persists in the neonate

Hypoxia, increased prostaglandins,prematurity

Often asymptomaticPoor feedingRespiratory distressCHF with respiratory infections

Acyanotic, unless other cardiac lesionsare present; continuous “machinery”murmur

Physical examinationEchocardiogram (to rule out associated

defects)Catheter (seldom required)

Indomethacin is an NSAID:prostaglandin (PG) inhibitor (PG keepsPDA open)

Surgical ligation or cardiaccatheterization closure at 6 months to 2 years of age

TETRALOGY OF FALLOT (TOF)

What is it? Misalignment of the infundibular septumin early development, leading to thecharacteristic tetrad:

1. Pulmonary stenosis/obstruction ofright ventricular outflow

2. Overriding aorta3. Right ventricular hypertrophy4. VSD



What are the signs?




Hypoxic spells (squatting behaviorincreases SVR and increases pulmonaryblood flow)

CyanosisClubbingMurmur: SEM at left third intercostal

space

CXR: small, “boot-shaped” heart anddecreased pulmonary blood flow

Echocardiography

95% survival at specialized centers

IHSS

What is IHSS?

What is it?


Idiopathic Hypertrophic SubaorticStenosis

Aortic outflow obstruction from septaltissue

Similar to aortic stenosis

COARCTATION OF THE AORTA

What is it?

What are the three types?

What percentage are associated with othercardiac defects?

What is the major route ofcollateral circulation?


Narrowing of the thoracic aorta, with orwithout intraluminal “shelf” (infolding ofthe media); usually found near ductus/ligamentum arteriosum

1. Preductal (fatal in infancy if untreated)2. Juxtaductal3. Postductal

60% (bicuspid aortic valve is most common)

Subclavian artery to the IMA to theintercostals to the descending aorta

Turner’s syndrome, male � female



What are the signs?




What are the possible postoperative complications?

What are the long-term concerns?


HeadacheEpistaxisLower extremity fatigue S claudication

Pulses: decreased lower extremity pulsesMurmurs:

1. Systolic—from turbulence acrosscoarctation, often radiating to infra-scapular region

2. Continuous—from dilated collaterals

CXR: “3” sign is aortic knob, coarctation,and dilated poststenotic aorta; ribnotching is bony erosion from dilatedintercostal collaterals

EchocardiogramCardiac catheterization if cardiac defects

Surgery:Resection with end-to-end anastomosisSubclavian artery flapPatch graft (rare)Interposition graftEndovascular repair an option in adults

Symptomatic patientAsymptomatic patient �3 to 4 years

Paraplegia“Paradoxic” HTNMesenteric necrotizing panarteritis (GI

bleeding), Horner’s syndrome, injuryto recurrent laryngeal nerve

Aortic dissection, HTN

TRANSPOSITION OF THE GREAT VESSELS

What is it? Aorta originates from the right ventricleand the pulmonary artery from the leftventricle; fatal without PDA, ASD, orVSD—to allow communication betweenthe left and right circulations







From 5% to 8% of defects

Most common lesion that presents withcyanosis and CHF in neonatal period(�90% by day 1)

CXR: “egg-shaped” heart contourCatheterization (definitive)

Arterial switch operation—aorta and pulmonary artery are moved to the correctventricle and the coronaries are reimplanted

EBSTEIN’S ANOMALY

What is it?



Tricuspid valve is placed abnormally lowin the right ventricle, forming a largeright atrium and a small right ventricle,leading to tricuspid regurgitation anddecreased right ventricular output

Cyanosis

400� the risk if the mother has takenlithium

VASCULAR RINGS

What are they?

How are they diagnosed?


Many types; represent an anomalous devel-opment of the aorta/pulmonary artery fromthe embryonic aortic arch that surroundsand obstructs the trachea/esophagus

Barium swallow, MRI

Most prominent is stridor from trachealcompression

CYANOTIC HEART DISEASE

What are the causes? Five “Ts” of cyanotic heart disease:Tetralogy of FallotTruncus arteriosusTotally anomalous pulmonary venous

return (TAPVR)Tricuspid atresiaTransposition of the great vessels



CARDIAC TUMORS

What is the most commonbenign lesion?



What is the most commonmalignant tumor in children?

Myxoma in adults

Left atrium with pedunculated morphology

Dyspnea, emboli

Rhabdomyosarcoma

DISEASES OF THE GREAT VESSELS

THORACIC AORTIC ANEURYSM

What is the cause?


What percentage of patientshave aneurysms of the aortaat a different site?


How is it most commonlydiscovered?


What are the indications fortreatment?

Vast majority result from atherosclerosis,connective tissue disease

Aortic dissection

�33%! (Rule out AAA)

Most are asymptomaticChest pain, stridor, hemoptysis (rare),

recurrent laryngeal nerve compression

Routine CXR

CXR, CT scan, MRI, aortography

�6 cm in diameterSymptomsRapid increase in diameterRupture



What are the dreaded complications aftertreatment of a thoracic aortic aneurysm?

What is anterior spinal syndrome?

What is the cause?


Replace with graft, open or endovascularstent

Paraplegia (up to 20%)Anterior spinal syndrome

Syndrome characterized by:ParaplegiaIncontinence (bowel/bladder)Pain and temperature sensation loss

Occlusion of the great radicular artery of Adamkiewicz, which is one of theintercostal/lumbar arteries from T8 to L4

AORTIC DISSECTION

What is it?

What are the aorticdissection classifications?

Define the DeBakey classifications:

DeBakey type I

Separation of the walls of the aorta froman intimal tear and disease of the tunicamedia; a false lumen is formed and a“reentry” tear may occur, resulting in“double-barrel” aorta

DeBakey classificationStanford classification

Involves ascending and descendingaorta


DeBakey type II


Involves ascending aorta only

DeBakey type III Involves descending aorta only

Define the Stanford classifications:

Type A Ascending aorta (requires surgery)� Descending aorta (includes DeBakey

types I and II)


Type B


Descending aorta only (nonoperative,except for complications) (same asDeBakey type III)



Note three other sequelae.


HTN (most common)Marfan’s syndromeBicuspid aortic valveCoarctation of the aortaCystic medial necrosisProximal aortic aneurysm

Abrupt onset of severe chest pain,most often radiating/“tearing” to theback; onset is typically more abrupt thanthat of MI; the pain can migrate as thedissection progresses; patient describes a“tearing pain”

1. Cardiac tamponade; Beck’s triad— distant heart sounds, c CVP with JVD,T BP

2. Aortic insufficiency—diastolic murmur3. Aortic arterial branch occlusion/

shearing, leading to ischemia in theinvolved circulation (i.e., unequal pulses,CVA, paraplegia, renal insufficiency,bowel ischemia, claudication)

CXR:1. Widened mediastinum2. Pleural effusion

TEECTA (CT angiography)Aortography (definitive gold standard but

time-consuming!)


What is the treatment of thevarious types:

Types I and II (Stanfordtype A)?

Type III (Stanford type B)?

Describe the surgery for anaortic dissection (Type I, II,Stanford A).

What is the preoperativetreatment?

What is the postoperativetreatment?

What is the possible cause ofMI in a patient with aorticdissection?

What is a dissecting aorticaneurysm?

What are the EKG signs ofthe following disorders:

Atrial fibrillation?


Surgical because of risk of:1. Aortic insufficiency2. Compromise of cerebral and coro-

nary circulation3. Tamponade4. Rupture

Medical (control BP), unless complicatedby rupture or significant occlusions

Open the aorta at the proximal extent ofdissection, and then sew—graft to— intimalflap and adventitia circumferentially(endovascular an option)

Control BP with sodium nitroprussideand �-blockers (e.g., esmolol); �-blockersdecrease shear stress

Lifetime control of BP and monitoring ofaortic size

Dissection involves the coronary arteriesor underlying LAD

Misnomer! Not an aneurysm!

Irregularly irregular


PVC?


Premature Ventricular Complex:Wide QRS

Ventricular aneurysm?

Ischemia?

Infarction?

ST elevation

ST elevation/ST depression/flipped T waves

Q waves

Pericarditis?

RBBB?

LBBB?

Wolff-Parkinson-White?

First degree A-V block?

Second degree A-V block?

Wenckebachphenomenon?

ST elevation throughout leads

Right Bundle Branch Block: wide QRSand “rabbit ears” or R-R in V1 or V2

Left Bundle Branch Block: wide QRSand “rabbit ears” or R-R in V5 or V6

Delta wave � slurred upswing on QRS

Prolonged P-R interval (0.2 second)

Dropped QRS; not all P waves transmitto produce ventricular contraction

Second-degree block with progressivedelay in P-R interval prior to dropped beat


Third-degree A-V block?

Chapter 73 / Transplant Surgery 671

Complete A-V dissociation; random P wave and QRS

MISCELLANEOUS

What is Mondor’s disease?

What is a VAD?

How does an IABP work?

What electrolyte must bemonitored during diuresisafter CPB?

How is extent/progress ofpostbypass diuresis followed?

What is an Austin Flint murmur?

Where is the least oxygenatedblood in the body?

What is the most commoncause of a cardiac tumor?

Thrombophlebitis of the thoracoepigastric veins

Ventricular Assist Device

IntraAortic Balloon Pump has a balloontip resting in the aorta

Balloon inflates in diastole, increasingdiastolic BP and coronary blood flow; in systole the balloon deflates,creating a negative pressure, loweringafterload, and increasing systolic BP

K�

I’s and O’s, CXR, JVD, edema, dailyweight

Diastolic murmur of AI secondary toregurgitant turbulent flow

Coronary sinus

Metastasis

Define the following terms:Autograft

Isograft

Transplant SurgeryChapter 73Same individual is both donor and recipient

Donor and recipient are genetically identical (identical twins)


Allograft

Xenograft

Orthotopic

Heterotopic

Paratopic

Chimerism


Donor and recipient are geneticallydissimilar, but of the same species

Donor and recipient belong to differentspecies

Donor organ is placed in normalanatomic position (liver, heart)

Donor organ is placed in a different sitethan the normal anatomic position (kidney, pancreas)

Donor organ is placed close to originalorgan

Sharing cells between the graft and donor

BASIC IMMUNOLOGY

What are histocompatibilityantigens?

Why are they important?

Which cells have class I antigens?

Which cells have class IIantigens?

What are the gene productsof MHC called in humans?

What is the location of theMHC complex?

What is a haplotype?

Distinct (genetically inherited) cellsurface proteins of the human leukocyteantigen system (HLA)

They are targets (class I antigens) andinitiators (class II antigens) of immuneresponse to donor tissue (i.e., distinguishing self from nonself)

All nucleated cells (Think: class 1 � ALLcells and thus “ONE for ALL”)

Macrophages, monocytes, B cells,activated T cells, endothelial cells

HLA (Human Leukocyte Antigen)

Short arm of chromosome 6

Combination of HLA genes on a chromosome inherited from one parent;therefore, two siblings have a 25%chance of being “haploidentical”


Does HLA matching matterin organ transplantation?


With recent improvements inimmunosuppression (i.e., cyclosporine),the effect is largely obscured, but it stilldoes matter; the most important ones tomatch in order to improve renal allograftsurvival are HAL-B and HLA-DR

CELLS

T CELLS

What is the source?

What is the function?

What are the types?

Thymus

Cell-mediated immunity/rejection

Th (CD4): helper T—help B cellsbecome plasma cells

Ts (CD8): suppressor T—regulateimmune response

Tc (CD8): cytotoxic T—kill cell by directcontact

B CELLS

What is the function?

What is the cell type thatproduces antibodies?

Humoral immunity

B cells differentiate into plasma cells

MACROPHAGE

What is it?

What is its function?


Briefly describe the eventsleading to antibody production.

Monocyte in parenchymal tissue

Processes foreign protein and presents itto lymphocytes

Antigen-Presenting Cell (APC)

1. Macrophage engulfs antigen andpresents it to Th cells; themacrophage produces IL-1

2. Th cells then produce IL-2, and theTh cells proliferate

3. Th cells then activate (via IL-4) B cellsthat differentiate into plasma cells,which produce antibodies against theantigen presented



IMMUNOSUPPRESSION

Who needs to beimmunosuppressed?

What are the major drugsused for immunosuppression?

What are the other drugs?

What is the advantage of“triple therapy”?

What is “induction therapy”?

All recipients (except autograft or isograft)

Triple therapy: corticosteroids,azathioprine, cyclosporine/tacrolimus

OKT3, ATGAM, mycophenolate

Employs three immunosuppressive drugs;therefore, a lower dose of each can be used,decreasing the toxic side effects of each

High doses of immunosuppressive drugsto “induce” immunosuppression

CORTICOSTEROIDS

Which is most commonlyused in transplants?

How does it function?

What is the associated toxicity?

What is the relative potency of the following corticosteroids:

Cortisol?

Prednisone?

Methylprednisolone?

Dexamethasone?

Prednisone

Primarily blocks production of IL-1 bymacrophage and stabilizes lysosomalmembrane of macrophage

“Cushingoid,” alopecia, striae, HTN, diabetes, pancreatitis, ulcer disease,osteomalacia, aseptic necrosis (especiallyof the femoral head)

1

4

5

25

AZATHIOPRINE (AZA [IMURAN®])

How does it function? Prodrug that is cleaved intomercaptopurine; inhibits synthesis of DNAand RNA, leading to decreased cellular(T/B cells) production



CYCLOSPORINE (CSA)

What is its function?


What drugs increase CSAlevels?

What drugs decrease CSAlevels?

What are the drugs ofchoice for HTN from CSA?

“Calcineurin inhibitor” inhibits production of IL-2 by Th cells

Toxicity for cyclosporine includes the 11 “H’s” and three “N’s”: Hepatitis,

Hypertrichosis, gingival Hyperplasia,Hyperlipidemia (worse than FK), Hyperglycemia, Hypertension (worsethan FK), Hemolytic uremic syndrome,Hyperkalemia, Hypercalcemia, Hypomagnesemia, Hyperuricemia,Nephrotoxicity, Neurotoxicity (headache,tremor), Neoplasia (lymphoma, KS,squamous cell skin cancers)

DiltiazemKetoconazoleErythromycin, fluconazole, ranitidine

By inducing the p450 system: dilantin,Tegretol®, rifampin, isoniazid, barbiturates

Clonidine, calcium channel blockers


When should a lower doseof AZA be administered?

What is the associated druginteraction?

Toxic to bone marrow (leukopenia �thrombocytopenia), hepatotoxic, associated with pancreatitis

When WBC is �4

Decrease dose if patient is also on allopurinol, because allopurinol inhibitsthe enzyme xanthine oxidase, which is necessary for the breakdown ofazathioprine

ATGAM/ANTITHYMOCYTE GLOBULIN

How does it function?

When is it typically used?

Antibody against thymocytes,lymphocytes (polyclonal)

For induction



OKT3

How does it work?

What is a major problemwith multiple doses?

What are basiliximab anddaclizumab?

MONOclonal antibody that binds CD3receptor (on T cells)

Blocking antibodies develop, and OKT3is less effective each time it is used

Anti-CD25 monoclonal antibodies

TACROLIMUS

What is tacrolimus alsoknown as?

How does it work?

What is its potencycompared to CSA?

What are its side effects?

Prograf®(FK506)

Similar to CSA—“calcineurin inhibitor,”blocks IL-2 receptor expression, inhibitsT cells

100� more potent than CSA

Nephrotoxicity and CNS toxicity (tremor, seizure, parasthesia, coma),hyperkalemia, alopecia, diabetes

SIROLIMUS

What is sirolimus also known as?

How does it work?

Toxicity?

Rapamycin, Rapamune®

Like CSA and tacrolimus, it does notbind to and inhibit calcineurin; rather, itblocks T-cell signaling

Hypertriglyceridemia, thrombocytopenia,wound/healing problems, anemia, oralulcers

MYCOPHENOLATE MOFETIL (MMF)

What is MMF also known as? CellCept®


Thrombocytopenia, leukopenia, serumsickness, rigors, fever, anaphylaxis,increased risk of viral infection, arthralgia



OVERVIEW OF IMMUNOSUPPRESSION MECHANISMS

What drug acts at thefollowing sites:

Mφ

A?

B?

C?

D?

B

Tn Tc

IL-1

IL-2

Lymphocyte

TNF-αIL-1IL-6

Clonalexpansion

T-B cellinteraction

How does it work? Inhibitor of inosine monophosphatedehydrogenase required for de novopurine synthesis which expanding T andB cells depend on; also inhibits adhesionmolecule and antibody production

A?

B?

C?

D?

Corticosteroids

CSA/tacrolimus

AZA/MMF

OKT3/ATGAM



MATCHING OF DONOR AND RECIPIENT

How is ABO crossmatchingperformed?

What is the purpose of lymphocytotoxic cross-matching?

How is the test performed?

Is HLA crossmatchingimportant?

Same procedure as in blood typing

Tests for HLA antibodies in serum; most important in kidney and pancreastransplants

Mix recipient serum with donor lymphocyte and rabbit complement

Yes, for kidney and pancreas transplants

REJECTION

How many methods of rejection are there?

Name the four types of rejection and their associatedtime courses.

What happens in hyperacuterejection?

What happens in acuterejection?

What type of rejection isresponsible for chronicrejection?

What is the treatment ofhyperacute rejection?

Two: humoral and cell-mediated

1. Hyperacute—immediate in O.R.2. Accelerated acute—7 to 10 days

post-transplant3. Acute—weeks to months post-transplant4. Chronic—months to years

post-transplant

Antigraft antibodies in recipientrecognize foreign antigen immediatelyafter blood perfuses transplanted organ

T cell–mediated rejection

Cellular, antibody (humoral), or both

Remove transplanted organ


What is the treatment ofacute rejection?

What is the treatment ofchronic rejection?


High-dose steroids/OKT3

Not much (irreversible) or retransplant

ORGAN PRESERVATION

What is the optimal storage temperature of an organ?

Why should it be kept cold?

What is U-W solution?

What is in it?

Why should it be used?

4C—keep on ice in a cooler

Cold decreases the rate of chemical reactions; decreased energy useminimizes effects of hypoxia and ischemia

University of Wisconsin solution; used toperfuse an organ prior to removal fromthe donor

Potassium phosphate, buffers, starch,steroids, insulin, electrolytes, adenosine

Lengthens organ preservation time

MAXIMUM TIME BETWEEN HARVEST AND TRANSPLANT OF ORGAN

Heart?

Lungs?

Pancreas?

Liver?

Kidney?

6 hours

6 hours

24 hours

24 hours

Up to 72 hours

KIDNEY TRANSPLANT

In what year was the firsttransplant performed in man?

By whom?

1954

Joseph E. Murray—1990 Nobel Prizewinner in Medicine


What are the indications forkidney transplant?

Define renal failure.

What is the most commoncause for kidney transplant?


Irreversible renal failure from:1. Glomerulonephritis (leading cause)2. Pyelonephritis3. Polycystic kidney disease4. Malignant HTN5. Reflux pyelonephritis6. Goodpasture’s syndrome

(antibasement membrane)7. Congenital renal hyperplasia8. Fabry’s disease9. Alport’s syndrome

10. Renal cortical necrosis11. Damage caused by type 1

diabetes mellitus

GFR �20% to 25% of normal; as GFRdrops to 5% to 10% of normal, uremicsymptoms begin (e.g., lethargy, seizures,neuropathy, electrolyte disorders)

Diabetes (25%)

STATISTICS

What are the sources ofdonor kidneys?

What survival rate is associated with deceaseddonor source?

What survival rate is associated with LRD?

What are the tests for compatibility?

If a choice of left or rightdonor kidney is available,which is preferred?

Should the placement of the kidney be hetero- ororthotopic?

Deceased donor (70%)Living related donor (LRD; 30%)

90% at 1 year if HLA matched; 80% at 1 year if not HLA matched; 75% graftsurvival at 3 years

95% patient survival at 1 year; 75% to85% graft survival at 3 years

ABO, HLA typing

Left—longer renal vein allows for easieranastomosis

Heterotopic—retroperitoneal in the RLQor LLQ above the inguinal ligament


Why?

Define anastomoses of a heterotopic kidney transplant.


Preserves native kidneys, allows easyaccess to iliac vessels, places ureter closeto the bladder, easy to biopsy kidney

1. Renal artery to iliac artery2. Renal vein to iliac vein3. Ureter to bladder

Renal artery

Renal vein

External iliac vein

UreterBladder

External iliac artery

hrf'0

What is the correctplacement of the ureter?

What is the differential diagnosis of post–renaltransplant fluid collection?

Why keep native kidneys?

What is the indication forremoval of native kidneys?

Submucosally through the bladder wall—decreases reflux

“HAUL”:Hematoma AbscessUrinoma Lymphocele

Increased morbidity if they are removed

Uncontrollable HTN, ongoing renal sepsis

REJECTION

What is the red flag thatindicates rejection?

c creatinine


What is the differential diagnosis of increased creatinine?


What is the workup for thefollowing tests:

U/S with Doppler?

Radionuclide scan?

Biopsy?

What is the time course forreturn of normal renal function after transplant?


(Remember: “-TION”) obstrucTION,dehydraTION, infecTION, intoxicaTION(CSA); plus lymphocele, ATN

Fever, malaise, HTN, ipsilateral legedema, pain at transplant site, oliguria

Look for fluid collection around the kidney, hydronephrosis, flow in vessels

Look at flow and function

Distinguish between rejection andcyclosporine toxicity

LRD—3 to 5 daysDeceased donor—7 to 15 days

LIVER TRANSPLANT

Who performed the firstliver transplant?


Thomas Starzl (1963)

Liver failure from:1. Cirrhosis (leading indication in

adults)2. Budd-Chiari3. Biliary atresia (leading indication

in children)4. Neonatal hepatitis5. Chronic active hepatitis6. Fulminant hepatitis with drug

toxicity—acetaminophen7. Sclerosing cholangitis8. Caroli’s disease9. Subacute hepatic necrosis

10. Congenital hepatic fibrosis11. Inborn errors of metabolism12. Fibrolamellar hepatocellular

carcinoma


What is the MELD score?

What is the test for compatibility?

What is the placement?

What are the options for biliary drainage?

What is the “piggyback technique”?

How does Living DonorLiver Transplantation(LDLT) work?

What is a split livertransplant?

What is chronic liver rejection called?


“Model for End Stage Liver Disease” isthe formula currently used to assignpoints for prioritizing position on thewaiting list for deceased donor liver transplant; based on INR, bilirubin, andcreatinine with extra points given for thepresence of liver cancer

ABO typing

Orthotopic

1. Donor common bile to recipient common bile duct end to end

2. Roux-en-Y choledochojejunostomy

Recipient vena cava is left in place; thedonor infrahepatic IVC is oversewn; thedonor superior IVC is anastomosed ontoa cuff made from the recipient hepaticveins (allows for greater hemodynamicstability of the recipient during OLT)

Adult donates a left lateral segment to achild or an adult donates a right lobe toanother adult

Deceased donor liver is harvested and divided into two “halves” for tworecipients

“Vanishing bile duct syndrome”

REJECTION

What are the red flags indicating rejection?

What is the site of rejection?

Decreased bile drainage, increasedserum bilirubin, increased LFTs

Rejection involves the biliary epitheliumfirst, and later, the vascular endothelium


What is the workup with thefollowing tests:

U/S with Doppler?

Cholangiogram?

Biopsy?

Does hepatorenal syndromerenal function improve afterliver transplant?


Look at flow in portal vein, hepaticartery; rule out thrombosis, leaky anastomosis, infection (abscess)

Look at bile ducts (easy to do; patientsusually have a T-tube if they haveprimary biliary anastomosis)

Especially important 3 to 6 weekspostoperatively, when CMV is of greatest concern

Yes

SURVIVAL STATISTICS


What percentage of patientsrequires retransplant?

Why?

�80% to 85%

�20%

Usually primary graft dysfunction, rejection, infection, vascular thrombosis,or recurrence of primary disease

PANCREAS TRANSPLANT

Who performed the firstpancreas transplant?




Richard C. Lillehei and William D. Kelly(1966)

Type I (juvenile) diabetes mellitus associated with severe complications(renal failure, blindness, neuropathy) orvery poor glucose control

ABO, DR matching (class II)

Heterotopic, in iliac fossa or paratopic


Where is anastomosis of theexocrine duct in heterotopicplacement?


To the bladder

Iliac artery

Portal vein

Graftduodenum

Iliac vein

hrf'02

Bladder

Why?

What is the associated electrolyte complication?

Where is anastomosis of theexocrine duct in paratopicplacement?

Why?

What is the advantage ofparatopic placement?

What are the red flags indicating rejection?

Why should the kidney andpancreas be transplantedtogether?

Why is hyperglycemia not agood indicator for rejectionsurveillance?

Measures the amount of amylase inurine, gives an indication of pancreaticfunction (i.e., high urine amylaseindicates good pancreatic function)

Loss of bicarbonate

To the jejunum

It is close by and physiologic

Endocrine function drains to the portalvein directly to the liver, and pancreaticcontents stay within the GI tract (noneed to replace bicarbonate)

Hyperamylasemia, hyperglycemia,hypoamylasuria, graft tenderness

Kidney function is a better indicator ofrejection; also better survival of graft isassociated with kidney-pancreastransplant than pancreas alone

Hyperglycemia appears relatively latewith pancreatic rejection



HEART TRANSPLANT

Who performed the firstheart transplant?





What is sewn together in aheart transplant?

Christiaan Barnard (1967)

Age birth to 65 years with terminalacquired heart disease—class IV of New York Heart Association classification(inability to do any physical activity without discomfort � 10% chance of surviving 6 months)

Active infectionPoor pulmonary functionIncreased pulmonary artery resistance

ABO, size

Orthotopic anastomosis of atria, aorta,pulmonary artery

Donor heart atriums, pulmonary artery,and aorta are sewn to the recipientheart atriums, pulmonary artery, andaorta

Left atrium

Donor Recipient

What are the red flags ofrejection?

What is coronary artery vasculopathy?

Fever, hypotension or hypertension,increased T4/T8 ratio

Small vessel occlusion from chronicrejection—often requires retransplant


What are the tests for rejection?

What are survival statisticsfor:

1 year?

5 years?


Endomyocardial biopsy—much moreimportant than clinical signs/symptoms;patient undergoes routine biopsy

85%

65%

INTESTINAL TRANSPLANTATION

What is it?

What types of donors arethere?

Anastomosis:Living donor?

Deceased donor?

What are indications?

What is a common postoperative problem other than rejection?

CMV status of donor?

What is the most common cause of deathpostoperatively?

How is rejection surveillanceconducted?

What is the clinical clue torejection?

Transplantation of the small bowel

Living donor, deceased donor

Ileocolic artery and vein

SMA, SMV

Short gut syndrome, motility disorders,and inability to sustain TPN (liver failure,lack of venous access, etc.)

GVHD (Graft-Versus-Host Disease) fromlarge lymphoid tissue in transplantedintestines

Must be CMV negative if recipient isCMV negative

Sepsis

Endoscopic biopsies

Watery diarrhea



LUNG TRANSPLANT

Who performed the firstlung transplant?



What tests comprise the pretransplant assessment ofthe recipient?

What are the donor requirements?

What are necessary anastomoses?

What are the postop complications?

What are the red flags ofrejection (4)?

What is chronic lung rejection called?

James Hardy (1963)

Generally, a disease that substantially limits activities of daily living and is likelyto result in death within 12 to 18 months:

Pulmonary fibrosisCOPDEosinophilic granulomaPrimary pulmonary HTNEisenmenger’s syndromeCystic fibrosis

Current smokingActive infection

1. Pulmonary—PFTs, V/Q scan2. Cardiac—Echo, cath, angiogram3. Exercise tolerance test

1. 55 years of age or younger2. Clear chest film3. PA oxygen tension of 300 on 100%

oxygen and 5 cm PEEP4. No purulent secretions on

bronchoscopy

Bronchi, PA, pulmonary veins(Bronchial artery is not necessary)

Bronchial necrosis/stricture, reperfusion,pulmonary edema, rejection

1. Decreased arterial O2 tension2. Fever3. Increased fatigability4. Infiltrate on x-ray

Obliterative Bronchiolitis (OB)


What are the survival rates:1 year?

3 yrs?


80%

70%

TRANSPLANT COMPLICATIONS

What are four major complications?

1. Infection2. Rejection3. Post-transplant lymphoproliferative

disease4. Complications of steroids

INFECTION

What are the usual agents?

When should CMV infectionbe suspected?

What is the time of peakincidence of CMV infections?

What are the signs/symptoms of CMV?

How is CMV diagnosed?

What is the treatment ofCMV?

What are the complicationsof ganciclovir?

What are the signs/symptoms of HSV?

What is the treatment of HSV?

DNA viruses, especially CMV, HSV, VZV

�21 days post-transplant

4 to 6 weeks post-transplant

Fever, neutropenia, signs of rejection of transplant; also can present as viralpneumonitis, hepatitis, colitis

Biopsy of transplant to differentiaterejection, cultures of blood, urine

Ganciclovir, with or without immunoglobin; foscarnet

Bone marrow suppression

Herpetic lesions, shingles, fever,neutropenia, rejection of transplant

Acyclovir until patient is asymptomatic

MALIGNANCY


Skin/lip cancer (40%), B-cell cancer, cervical cancer in women, T-celllymphoma, Kaposi’s sarcoma


Which epithelial cancers areimportant after transplant?

What is post-transplant lymphoma associated with?

What is the treatment forpost-transplant lympho-proliferative disease (PTLD)?


Skin/lip cancer, especially basal cell andsquamous cell

Multiple doses of OKT3EBVYoung � elderly

1. Drastically reduce immunosuppression2. � Radiation3. � Chemotherapy

OrthopaedicSurgery

Chapter 74

ORTHOPAEDIC TERMS

What do the followingabbreviations stand for:

ORIF?

ROM?

FROM?

ACL?

PCL?

MCL?

PWB?

FWB?

WBAT?

Open Reduction Internal Fixation

Range Of Motion

Full Range Of Motion

Anterior Cruciate Ligament

Posterior Cruciate Ligament

Medial Collateral Ligament

Partial Weight Bearing

Full Weight Bearing

Weight Bearing As Tolerated


THA?

TKA?

THR?

TKR?

PROM?

AROM?

AFO?

AVN?

Define the following terms:Supination

Pronation

Plantarflexion

Foot dorsiflexion

Adduction

Abduction

Inversion

Eversion

Volarflexion

Wrist dorsiflexion

Allograft bone

Chapter 74 / Orthopaedic Surgery 691

Total Hip Arthroplasty

Total Knee Arthroplasty

Total Hip Replacement

Total Knee Replacement

Passive Range Of Motion

Active Range Of Motion

Ankle Foot Orthotic

AVascular Necrosis

Palm up

Palm down

Foot down at ankle joint (plant foot inground)

Foot up at ankle joint

Movement toward the body (ADDuction � ADD to the body)

Movement away from the body

Foot sole faces midline

Foot sole faces laterally

Hand flexes at wrist joint toward flexortendons

Hand flexes at wrist joint toward extensortendons

Bone from human donor other thanpatient


Reduction

Closed reduction

Open reduction

Fixation

Tibial pin


Maneuver to restore proper alignment tofracture or joint

Reduction done without surgery (e.g., casts, splints)

Surgical reduction

Stabilization of a fracture after reductionby means of surgical placement of hardware that can be external or internal(e.g., pins, plates, screws)

Pin placed in the tibia for treating femuror pelvic fractures by applying skeletaltraction

Traction bow

Traction cable

Traction

Trans-tibialtraction pin

Tibia

Fracturedfemur

Unstable fracture or dislocation

Fracture or dislocation in which furtherdeformation will occur if reduction is notperformed


Varus


Extremity abnormality with apex ofdefect pointed away from midline(e.g., genu varum � bowlegged; withvalgus, this term can also be used todescribe fracture displacement)

(Think: knees are very varied apart)

Valgus Extremity abnormality with apex ofdefect pointed toward the midline (e.g., genu valgus � knock-kneed)

Dislocation

Subluxation

Total loss of congruity and contactbetween articular surfaces of a joint

Loss of congruity between articular surfaces of a joint; articular contact stillremains


Arthroplasty

Arthrodesis

Osteotomy

Non-union

Define each of thefollowing:

Diaphysis

Metaphysis

Physis


Total joint replacement (most last 10 to15 years)

Joint fusion with removal of articular surfaces

Cutting bone (usually wedge resection) tohelp realigning of joint surfaces

Failure of fractured bone ends to fuse

Main shaft of long bone

Flared end of long bone

Growth plate, found only in immaturebone

TRAUMA GENERAL PRINCIPLES

Define extremityexamination in fracturedextremities.

Which x-rays should beobtained?

How are fracturesdescribed?

How do you define thedegree of angulation,displacement, or both?

1. Observe entire extremity (e.g., open,angulation, joint disruption)

2. Neurologic (sensation, movement)3. Vascular (e.g., pulses, cap refill)

Two views (also joint above and belowfracture)

1. Skin status (open or closed)2. Bone (by thirds: proximal/middle/

distal)3. Pattern of fracture (e.g., comminuted)4. Alignment (displacement, angulation,

rotation)

Define lateral/medial/anterior/posteriordisplacement and angulation of the distalfragment(s) in relation to the proximalbone


Identify each numberedstructure:


1. Diaphysis2. Metaphysis3. Physis4. Epiphysis

4

4

2

2

1

3

3

FRACTURES

Define the followingpatterns of fracture:

Closed fracture

Open fracture

Simple fracture

Comminuted fracture

Intact skin over fracture/hematoma

Wound overlying fracture, through whichfracture fragments are in continuity withoutside environment; high risk of infection(Note: Called “compound fracture” in

the past)

One fracture line, two bone fragments

Results in more than two bone fragments;a.k.a. fragmentation


Oblique fracture


Fracture line creates an oblique anglewith long axis of bone

Segmental fracture Two complete fractures with a “segment”in between

Transverse fracture Fracture line perpendicular to long axisof bone

Segmental fracture


Spiral fracture


Severe oblique fracture in which fractureplane rotates along the long axis of bone;caused by a twisting injury

Longitudinal fracture

Impacted fracture

Pathologic fracture

Stress fracture

Greenstick fracture

Fracture line parallel to long axis of bone

Fracture resulting from compressive force;end of bone is driven into contiguousmetaphyseal region without displacement

Fracture through abnormal bone (e.g.,tumor-laden or osteoporotic bone)

Fracture in normal bone from cyclicloading on bone

Incomplete fracture in which cortex ononly one side is disrupted; seen inchildren

Greenstick fracture


Torus fracture

Avulsion fracture


Impaction injury in children in whichcortex is buckled but not disrupted (a.k.a. buckle fracture)

Fracture in which tendon is pulled frombone, carrying with it a bone chip

Periarticular fracture

Intra-articular fracture

Define the following specificfractures:

Colles’ fracture

Fracture close to but not involving the joint

Fracture through the articular surface ofa bone (usually requires ORIF)

Distal radius fracture with dorsaldisplacement and angulation, usuallyfrom falling on an outstretched hand (a common fracture!)

Smith’s fracture “Reverse Colles’ fracture”—distal radialfracture with volar displacement andangulation, usually from falling on thedorsum of the hand (uncommon)


Jones’ fracture

Bennett’s fracture


Fracture at the base of the fifthmetatarsal diaphysis

Fracture-dislocation of the base of thefirst metacarpal (thumb) with disruptionof the carpometacarpal joint

Bennett’sfracture

Boxer’s fracture Fracture of the metacarpal neck, “classically” of the small finger

Boxer’sfracture

Nightstick fracture

Clay shoveler’s avulsionfracture

Hangman’s fracture

Transcervical fracture

Ulnar fracture

Fracture of spinous process of C6–C7

Fracture of the pedicles of C2

Fracture through the neck of the femur


Tibial plateau fracture

Monteggia fracture

Galeazzi fracture

Tibial “plateau” fracture


Intra-articular fracture of the proximal tibia(the plateau is the flared proximal end)

Fracture of the proximal third of the ulnawith dislocation of the radial head

Fracture of the radius at the junction ofthe middle and distal thirds accompaniedby disruption of the distal radioulnar joint

Proximal tibial fracture

Tibial “plateau”fracture

“Pilon” fracture Distal tibial fracture

“Pilon” fracture

Pott’s fracture

Pott’s disease

Fracture of distal fibula

Tuberculosis of the spine



ORTHOPAEDIC TRAUMA

What are the majororthopaedic emergencies?

What is the main risk whendealing with an open fracture?

Which fracture has the highest mortality?

What factors determine theextent of injury (3)?

What is the acronym forindications for OPEN reduction?

Define open fractures by Gustilo-Anderson classification:

Grade I?

Grade II?

1. Open fractures/dislocations2. Vascular injuries (e.g., knee

dislocation)3. Compartment syndromes4. Neural compromise, especially spinal

injury5. Osteomyelitis/septic arthritis; acute,

i.e., when aspiration is indicated6. Hip dislocations—require immediate

reduction or patient will develop avascu-lar necrosis; “reduce on the x-ray table”

7. Exsanguinating pelvic fracture (binder,external fixator)

Infection

Pelvic fracture (up to 50% with openpelvic fractures)

1. Age: suggests susceptible point inmusculoskeletal system:

Child—growth plateAdolescent—ligamentsElderly—metaphyseal bone

2. Direction of forces3. Magnitude of forces

“NO CAST”:NonunionOpen fracture

Compromise of blood supplyArticular surface malalignmentSalter-Harris grade III, IV fractureTrauma patients who need early ambulation

�1-cm laceration

�1 cm, minimal soft tissue damage


Grade IIIA?

Grade IIIB?

Grade IIIC?

What are the five steps inthe initial treatment of anopen fracture?

What structures are at riskwith a humeral fracture?

What must be done whenboth forearm bones are broken?

How have femoral fracturesbeen repaired traditionally?

What is the newer technique?

What are the advantages?

What is the chief concernfollowing tibial fractures?

What is suggested by pain inthe anatomic snuff-box?

What is the most commoncause of a “pathologic” fracture in adults?


Open fracture with massive tissuedevitalization/loss, contamination

Open fracture with massive tissuedevitalization/loss and extensiveperiosteal stripping, contamination, inadequate tissue coverage

Open fracture with major vascular injuryrequiring repair

1. Prophylactic antibiotics to include IVgram-positive � anaerobic coverage:

Grade I—cefazolin (Ancef ®) Grade II or III—cefoxitin/gentamicin

2. Surgical débridement3. Inoculation against tetanus4. Lavage wound �6 hours postincident

with high-pressure sterile irrigation5. Open reduction of fracture and stabi-

lization (e.g., use of external fixation)

Radial nerve, brachial artery

Because precise movements are needed,open reduction and internal fixation aremusts

Traction for 4 to 6 weeks

Intramedullary rod placement

Nearly immediate mobility withdecreased morbidity/mortality

Recognition of associated compartmentsyndrome

Fracture of scaphoid bone (a.k.a. navicular fracture)

Osteoporosis



COMPARTMENT SYNDROME

What is acute compartmentsyndrome?



What are common causes of forearm compartmentsyndrome?

What is Volkmann’s contracture?

What is the most commonsite of compartmentsyndrome?

What situations shouldimmediately alert one to beon the lookout for adeveloping compartmentsyndrome (4)?

What are the symptoms ofcompartment syndrome?

What are the signs of compartment syndrome?

Increased pressure within an osteofascialcompartment that can lead to ischemicnecrosis

Clinically, using intracompartmentalpressures is also helpful (especially inunresponsive patients); fasciotomy isclearly indicated if pressure in the compartment is �40 mm Hg (30 to 40 mm Hg is a gray area)

Fractures, vascular compromise, reperfusion injury, compressive dressings;can occur after any musculoskeletalinjury

Supracondylar humerus fracture, brachialartery injury, radius/ulna fracture, crushinjury

Final sequela of forearm compartmentsyndrome; contracture of the forearmflexors from replacement of dead musclewith fibrous tissue

Calf (four compartments: anterior,lateral, deep posterior, superficial posterior compartments)

1. Supracondylar elbow fractures in children

2. Proximal/midshaft tibial fractures3. Electrical burns4. Arterial/venous disruption

Pain, paresthesias, paralysis

Pain on passive movement (out ofproportion to injury), cyanosis or pallor,hypoesthesia (decreased sensation,decreased two point discrimination), firmcompartment



Can a patient have acompartment syndrome with a palpable or Doppler-detectable distal pulse?

What are the possible complications ofcompartment syndrome?

What is the initial treatmentof the orthopaedic patientdeveloping compartmentsyndrome?

What is the definitive treatment of compartmentsyndrome?

YES!

Muscle necrosis, nerve damage, contractures, myoglobinuria

Bivalve and split casts, remove constricting clothes/dressings, placeextremity at heart level

Fasciotomy within 4 hours (6–8 hoursmaximum) if at all possible

MISCELLANEOUS TRAUMA INJURIES AND COMPLICATIONS

Name the motor and sensation tests used to assessthe following peripheralnerves:

Radial

Ulnar

Median

Axillary

Musculocutaneous

How is a peripheral nerveinjury treated?

What fracture is associatedwith a calcaneus fracture?

Wrist extension; dorsal web space; sensation: between thumb and index finger

Little finger abduction; sensation: littlefinger-distal ulnar aspect

Thumb opposition or thumb pinch sensation: index finger-distal radial aspect

Arm abduction; sensation: deltoid patchon lateral aspect of upper arm

Elbow (biceps) flexion; lateral forearmsensation

Controversial, although clean lacerationsmay be repaired primarily; most injuriesare followed for 6 to 8 weeks (EMG)

L-spine fracture (usually from a fall)



Name the nerves of thebrachial plexus.

What are the two indicationsfor operative explorationwith a peripheral nerveinjury?

Think: “morning rum” or “A.M. RUM” �Axillary, Median, then Radial, Ulnar, andMusculocutaneous nerves

1. Loss of nerve function after reductionof fracture

2. No EMG signs of nerve regenerationafter 8 weeks (nerve graft)

DISLOCATIONS

SHOULDER


Which two structures are atrisk?


What are the threetreatment steps?

95% are anterior (posterior are associatedwith seizures or electrical shock)

1. Axillary nerve2. Axillary artery

Indentation of soft tissue beneathacromion

1. Reduction via gradual traction2. Immobilization for 3 weeks in internal

rotation3. ROM exercises

ELBOW


Which three structures areat risk?


Posterior

1. Brachial artery2. Ulnar nerve3. Median nerve

Reduce and splint for 7 to 10 days

HIP

When should hipdislocations be reduced?

What is the most commoncause of a hip dislocation?

Immediately, to decrease risk of avascularnecrosis; “reduce on the x-ray table!”

High velocity trauma (e.g., MVC)




Which structures are at risk?


Posterior—“dashboard dislocation”—often involves fracture of posterior lip ofacetabulum

Sciatic nerve; blood supply to femoralhead—avascular necrosis (AVN)

Closed or open reduction

KNEE

What are the common types?

Which structures are at risk?


Anterior or posterior

Popliteal artery and vein, peronealnerve—especially with posterior dislocation, ACL, PCL (Note: need arteriogram)

Immediate attempt at relocation (do not wait to x-ray), arterial repair, and then ligamentous repair (delayed or primary)

THE KNEE

What are the five ligamentsof the knee?

1. Anterior Cruciate Ligament (ACL), 2. Posterior Cruciate Ligament (PCL), 3. Medial Collateral Ligament (MCL), 4. Lateral Collateral Ligament (LCL), 5. Patellar Ligament

Anteriorcruciateligament

Patellarligament

Posteriorcruciateligament

Lateralcollateralligament

Medialcollateralligament

HR

F '0

4



What is the Lachman testfor a torn ACL?

Thigh is secured with one hand while theother hand pulls the tibia anteriorly

ACHILLES TENDON RUPTURE

What are the signs of anAchilles tendon rupture?

Severe calf pain, also bruised swollencalf, two ends of ruptured tendon may befelt, patient will have weak plantar flexionfrom great toe flexors that should beintact; patient often hears a “pop”

20- to 30-degreeknee flexion

What is the meniscus of theknee?

What is McMurray’s sign?

What is the “unhappytriad”?

What is a “locked knee”?

What is a “bucket-handletear”?

In collateral ligament andmenisci injuries, which aremore common, the medialor the lateral?

Cartilage surface of the tibia plateau (lateral and medial meniscus); tears arerepaired usually by arthroscopy withremoval of torn cartilage fragments

Seen with a medial meniscus tear: medialtenderness of knee with flexion and internal rotation of the knee

Lateral knee injury resulting in:1. ACL tear2. MCL tear3. Medial meniscus injury

Meniscal tear that displaces andinterferes with the knee joint andprevents complete extension

Meniscal tear longitudinally along contourof normal “C” shape of the meniscus

Medial



Name the test for anINTACT Achilles tendon.

Thompson’s test: a squeeze of the gastrocnemius muscle results in plantarflexion of the foot

Plantar flexion

Achillestendon tear

What is the treatment for anAchilles tendon rupture?

Young � surgical repairElderly � many can be treated with

progressive splints

ROTATOR CUFF

What four muscles form the rotator cuff?

When do tears usually occur?



What is Volkmann’s contracture?

Think: “SITS”:1. Supraspinatus, etc. 2. Infraspinatus3. Teres minor4. Subscapularis

Fifth decade

Intermittent shoulder pain especiallywith overhead activity, followed by anepisode of acute pain corresponding to atendon tear; weak abduction

Most tears: symptomatic pain reliefLater: if poor muscular function persists,

surgical repair is indicated

Contracture of forearm flexors secondaryto forearm compartment syndrome



What is the usual cause ofVolkmann’s contracture?

Brachial artery injury, supracondylarhumerus fracture, radius/ulnar fracture,crush injury, etc.

MISCELLANEOUS

Define the following terms:Dupuytren’s contracture

Charcot’s joint

Tennis elbow

Turf toe

Shin splints

Heel spur

Nightstick fracture

Kienbock’s disease

What is traumatic myositis?

How does a “cast saw” cut the cast but not theunderlying skin?

Thickening and contracture of palmarfascia; incidence increases with age

Joint arthritis from peripheral neuropathy

Tendonitis of the lateral epicondyle ofthe humerus; classically seen in tennisplayers

Hyperextension of the great toe (tear ofthe tendon of the flexor hallucis brevis);classically seen in football players

Exercise-induced anterior compartmenthypertension (compartment syndrome);seen in runners

Plantar fasciitis with abnormal bone growthin the plantar fascia; classically seen inrunners and walkers

Ulnar fracture

Avascular necrosis of the lunate

Abnormal bone deposit in a muscle afterblunt trauma deep muscle contusion(benign)

It is an “oscillating” saw (designed by Dr. Homer Stryker in 1947) that goesback and forth cutting anything hardwhile moving the skin back and forthwithout injuring it



ORTHOPAEDIC INFECTIONS

OSTEOMYELITIS

What is osteomyelitis?

What are the most likelycausative organisms?

What is the most commonorganism isolated inosteomyelitis in the generaladult population?

What is the most commonisolated organism in patientswith sickle cell disease?

What is seen on physicalexamination?

What are the diagnostic steps?


What is a Marjolin’s ulcer?

Inflammation/infection of bone marrowand adjacent bone

Neonates: Staphylococcus aureus, gram-negative streptococcus

Children: S. aureus, Haemophilusinfluenzae, streptococci

Adults: S. aureusImmunocompromised/drug addicts:

S. aureus gram-negativeSickle cell: Salmonella

S. aureus

Salmonella

Tenderness, decreased movement,swelling

History and physical examination, needleaspirate, blood cultures, CBC, ESR, bonescan

Antibiotics with or without surgicaldrainage

Squamous cell carcinoma that arises in achronic sinus from osteomyelitis

SEPTIC ARTHRITIS

What is it? Inflammation of a joint beginning as synovitis and ending with destruction ofarticular cartilage if left untreated




What are the findings onphysical examination?

What are the diagnosticsteps?


Same as in osteomyelitis, except thatgonococcus is a common agent in theadult population

Joint pain, decreased motion, jointswelling, joint warm to the touch

Needle aspirate (look for pus; culture plusGram stain), x-ray, blood cultures, ESR

Decompression of the joint via needleaspiration and IV antibiotics; hip, shoulder,and spine must be surgically incised,débrided, and drained

ORTHOPAEDIC TUMORS

What is the most commontype in adults?

What are the commonsources?


What is the most commonprimary malignant bonetumor?

What is the differential diagnosis of a possible bonetumor?

What are the benign bonetumors (8)?

Metastatic!

Breast, lung, prostate, kidney, thyroid,and multiple myeloma

Bone pain or as a pathologic fracture

Multiple myeloma (45%)

Metastatic diseasePrimary bone tumorsMetabolic disorders (e.g.,

hyperparathyroidism)Infection

1. Osteochondroma2. Enchondroma3. Unicameral/aneurysmal bone cysts4. Osteoid osteoma5. Chondroblastoma6. Fibroxanthoma7. Fibrous dysplasia8. Nonossifying fibroma



What are the malignantbone tumors (7)?

Compare benign and malignant bone tumors interms of:

Size

Bone reaction

Margins

Invasive

Are most pediatric bonetumors benign or malignant?

Are most adult bone tumorsbenign or malignant?

What are the four diagnosticsteps?

What are the radiographicsigns of malignant tumors?

What are the radiographicsigns of benign tumors?

1. Multiple myeloma2. Osteosarcoma3. Chondrosarcoma4. Ewing’s sarcoma5. Giant cell tumor (locally malignant)6. Malignant melanoma7. Metastatic

Benign—small; �1 cmMalignant— �1 cm

Benign—sclerotic bone reactionMalignant—little reaction

Benign—sharpMalignant—poorly defined

Benign—confined to boneMalignant—often extends to surrounding

tissues

80% are benign (most common is osteochondroma)

66% are malignant (most commonlymetastatic)

1. PE/lab tests2. Radiographs3. CT scan, technetium scan, or both4. Biopsy

Large sizeAggressive bone destruction, poorly

defined marginsIneffective bone reaction to tumorExtension to soft tissues

SmallWell circumscribed, sharp marginsEffective bone reaction to the tumor

(sclerotic periostitis)No extension—confined to bone



What are some specific radiographic findings of thefollowing:

Osteosarcoma?

Fibrous dysplasia

Ewing’s sarcoma

What is the mainstay oftreatment for bone tumors?

“Sunburst” pattern

Bubbly lytic lesion, “ground glass”

“Onion skinning”

Surgery (excision plus débridement) forboth malignant and benign lesions; radiation therapy and chemotherapy asadjuvant therapy for many malignanttumors

OSTEOSARCOMA


What is the gender distribution?


What is the radiographicsine qua non?




What is the most commonbenign bone tumor?

What is a chondrosarcoma?

10 to 20 years

Male � female

�66% in the distal femur, proximal tibia

Bone formation somewhere within tumor

Resection (limb sparing if possible) pluschemotherapy

�70%

Lungs

Osteochondroma; it is cartilaginous in origin and may undergo malignantdegeneration

Malignant tumor of cartilaginous origin;presents in middle-aged and olderpatients and is unresponsive tochemotherapy and radiotherapy



EWING’S SARCOMA




What are the associatedradiographic findings?

What is a memory aid forEwing’s sarcoma?


How can Ewing’s sarcomamimic the appearance ofosteomyelitis?

What is a unicameral bonecyst?



What is an aneurysmal bonecyst?

Pain, swelling in involved area

Around the knee (distal femur, proximal tibia)

Evenly spread among those younger than20 years of age

Lytic lesion with periosteal reactiontermed “onion skinning,” which is calcified layering

Central areas of tumor can undergo liquefaction necrosis, which may beconfused with purulent infection (particularly in a child with fever,leukocytosis, and bone pain)

“TKO Ewing”:Twenty years old or youngerKnee joint“Onion skinning”

50%

Bone cysts

Fluid-filled cyst most commonly found inthe proximal humerus in children 5 to 15years of age

Asymptomatic until pathologic fracture

Steroid injections

Hemorrhagic lesion that is locallydestructive by expansile growth, but doesnot metastasize





Pain and swelling; pathologic fracturesare rare

Curettage and bone grafting

ARTHRITIS

Which arthritides are classified as degenerative?

What signs characterizeosteoarthritis?

What are Bouchard’s nodes?

What are Heberden’s nodes?

What is post-traumaticarthritis?

What are the treatmentoptions for degenerativearthritis (3)?

What are the characteristicsof rheumatoid arthritis?

What is pannus?

What are the classic handfindings with rheumatoidarthritis?

What are the surgical management options forjoint/bone diseases (3)?

OsteoarthritisPost-traumatic arthritis

Heberden’s nodes/Bouchard’s nodesSymmetric destruction, usually of the

hip, knee, or spine

Enlarged PIP joints of the hand fromcartilage/bone growth

Enlarged DIP joints of the hand fromcartilage/bone growth

Usually involves one joint of past trauma

1. NSAIDS for acute flare-ups, not forlong-term management

2. Local corticosteroid injections3. Surgery

Autoimmune reaction in which invasivepannus attacks hyaline articular cartilage;rheumatoid factor (anti-IgG/IgM) in 80%of patients; 3� more common inwomen; skin nodules (e.g., rheumatoidnodule)

Inflammatory exudate overlying synovialcells inside the joint

Wrist: radial deviationFingers: ulnar deviation

1. Arthroplasty2. Arthrodesis (fusion)3. Osteotomy



What is the major differencebetween gout andpseudogout?

What is a Charcot’s joint?

Gout: caused by urate deposition, negative birefringent, needle crystal

Pseudogout: caused by calcium pyrophosphate positive birefringentsquare crystals (Think: PositiveSquare crystals � PSeudogout)

Arthritic joint from peripheral neuropathy

PEDIATRIC ORTHOPAEDICS

What are the majordifferences betweenpediatric and adult bones?

What types of fractures areunique to children?

Children: increased bone flexibility and bone healing (thus, many fracturesare treated closed, whereas an adultwould require O.R.I.F.), physis (weakpoint)

Greenstick fractureTorus fractureFracture through physis

SALTER-HARRIS CLASSIFICATION

What does it describe?

What does it indicate highrisk of?

Define the following terms:Salter I

Salter II

Salter III

Salter IV

Salter V

Fractures in children involving physis

Potential growth arrest

Through physeal plate only

Involves metaphysis and physis

Involves physis and epiphysis

Extends from metaphysis through physis,into epiphysis

Axial force crushes physeal plate



Define the following fracturesby Salter-Harris grade:

Salter III

Salter IV

Salter I

Salter V



What acronym can help you remember the Salterclassifications?

What is the simple numerical method forremembering the Salter-Harris classification?

Salter II

“SALTR”:Separated � type IAbove � type IILower � type IIIThrough � type IVRuined � type V

(N � normal)

Why is the growth plate ofconcern in childhoodfractures?

Growth plate represents the “weak link”in the child’s musculoskeletal system;fractures involving the growth plate oflong bones may compromise normalgrowth, so special attention should begiven to them



What is a chief concernwhen oblique/spiralfractures of long bones areseen in children?

What is usually done duringreduction of a femoral fracture?

What is unique aboutligamentous injury inchildren?

What two fractures have ahigh incidence of associatedcompartment syndrome?

Child abuse is a possibility; other signs ofabuse should be investigated

Small amount of overlap is allowedbecause increased vascularity from injurymay make the affected limb longer ifoverlap is not present; treatment afterreduction is a spica cast

Most “ligamentous” injuries are actuallyfractures involving the growth plate!

1. Tibial fractures2. Supracondylar fractures of humerus

(Volkmann’s contracture)

CONGENITAL HIP DISLOCATION

What is the epidemiology?

What percentage arebilateral?


What is Barlow’s maneuver?

What is Ortolani’s sign?


Female � male, firstborn children,breech

Presentation, 1 in 1000 births

10%

Barlow’s maneuver, Ortolani’s signRadiographic confirmation is required

Detects unstable hip: patient is placed inthe supine position and attempt is madeto push femurs posteriorly with knees at90/hip flexed and hip will dislocate(Think: push Back � Barlow)

“Clunk” produced by relocation of a dislocated femoral head when the examiner abducts the flexed hip and liftsthe greater trochanter anteriorly; detectsa dislocated hip (Think: Out � Ortolani’s)

Pavlik harness—maintains hip reductionwith hips flexed at 100 to 110



SCOLIOSIS


What are three treatmentoptions?

What are the indications forsurgery for scoliosis?

Lateral curvature of a portion of the spineNonstructural: corrects with positional

changeStructural: does not correct

1. Observation2. Braces (Milwaukee brace)3. Surgery

Respiratory compromiseRapid progressionCurves �40Failure of brace

MISCELLANEOUS

Define the following terms:Legg-Calvé-Perthes disease

Slipped capital femoralepiphysis

Blount’s disease

Nursemaid’s elbow

Little League elbow

Osgood-Schlatter’sdisease

What is the most commonpediatric bone tumor?

Idiopathic avascular necrosis of femoralhead in children

Migration of proximal femoral epiphysison the metaphysis in children; the proximal femoral epiphysis externallyrotates and displaces anteriorly fromthe capital femoral epiphysis, whichstays reduced in the acetabulum

(Note: Hip pain in children oftenpresents as knee pain)

Idiopathic varus bowing of tibia

Dislocation of radial head (from pullingtoddler’s arm)

Medial epicondylitis

Apophysitis of the tibial tubercle resultingfrom repeated powerful contractions ofthe quadriceps; seen in adolescents withan open physis

Treatment of mild cases: activityrestriction

Treatment of severe cases: cast

Osteochondroma (Remember, 80% ofbone tumors are benign in children)


Chapter 75 / Neurosurgery 721

NeurosurgeryChapter 75HEAD TRAUMA


What percentage of traumadeaths result from headtrauma?

Identify the dermatomes:

70,000 fatal injuries/year in the UnitedStates, 500,000 head injuries per year

50%

S4

hrf'04

L5

C7C6

C5

S2S3

C4C3

CN VC2

C8T1T2

L4L3

L2L1

S1

T12T11

T10T9

T8

T6

T4T3

T5

T7Nipples T4

Umbilicus T10

What is the Glasgow ComaScale (GCS)?

GCS is an objective assessment of thelevel of consciousness after trauma

GCS SCORING SYSTEM

Eyes? Eye Opening (E)4—opens spontaneously3—opens to voice (command)2—opens to painful stimulus1—does not open eyes(Think: “4 eyes”)


Motor?

Verbal?

What indicates coma by GCSscore?

What does unilateral,dilated, nonreactive pupilsuggest?

What do bilateral fixed anddilated pupils suggest?

What are the four signs ofbasilar skull fracture?

What is the initialradiographic neuroimagingin trauma?

Should the trauma head CTscan be with or without IVcontrast?

What is normal ICP?


Motor Response (M)6—obeys commands5—localizes painful stimulus4—withdraws from pain3—decorticate posture2—decerebrate posture1—no movement(Think: 6-cylinder motor)

Verbal Response (V)5—appropriate and oriented4—confused3—inappropriate words2—incomprehensible sounds1—no sounds(Think: Jackson 5 � verbal 5)

�8 (Think: “less than eight—it may betoo late”)

Focal mass lesion with ipsilateral herniation and compression of CN III

Diffusely increased ICP

1. Raccoon eyes—periorbitalecchymoses

2. Battle’s sign—postauricularecchymoses

3. Hemotympanum4. CSF rhinorrhea/otorrhea

1. Head CT scan (if LOC or GCS �15)2. C-spine CT3. T/L spine AP and lateral

Without!

5 to 15 mm H2O


What is the worrisome ICP?

What determines ICP (Monroe-Kelly hypothesis)?

What is the CPP?

What is Cushing’s reflex?

What are the three general indications to monitor ICPafter trauma?

What is Kocher’s point?


�20 mm H2O

1. Volume of brain2. Volume of blood3. Volume of CSF

Cerebral Perfusion Pressure � meanarterial pressure—ICP (normal CPP is�70)

Physiologic response to increased ICP:1. Hypertension2. Bradycardia3. Decreased RR

1. GCS �92. Altered level of consciousness or

unconsciousness with multiple systemtrauma

3. Decreased consciousness with focalneurologic examination abnormality

Landmark for placement of ICP monitorbolt:

Coronal suture

Kocher’s point

Midpoint between

external auditory

meatus and

lateral canthus

Midpupillary line


What nonoperativetechniques are used todecrease ICP?

What is the acronym for thetreatment of elevated ICP?

Can a tight c-collar increasethe ICP?

Why is prolonged hyperventilation dangerous?

What is a Kjellberg?(pronounced “shellberg”)

How does cranial nerveexamination localize theinjury in a comatose patient?

What is acute treatment ofseizures after head trauma?

What is seizure prophylaxisafter severe head injury?


1. Elevate head of bed (HOB) 30�(if spine cleared)

2. Diuresis-mannitol (osmotic diuretic),Lasix®, limit fluids

3. Intubation (PCO2 control)4. Sedation5. Pharmacologic paralysis6. Ventriculostomy (CSF drainage)

“ICP HEAD”:INTUBATE CALM (sedate)PLACE DRAIN (ventriculostomy)/

PARALYSIS

HYPERVENTILATE TO PCO2 �35ELEVATE headADEQUATE BLOOD PRESSURE

(CPP �70)DIURETIC (e.g., mannitol)

Yes (it blocks venous drainage frombrain!)

It may result in severe vasoconstrictionand ischemic brain necrosis!

Use only for very brief periods

Decompressive bifrontal craniectomywith removal of frontal bone frozen for possible later replacement

CNs proceed caudally in the brain stemas numbered: Presence of corneal reflex(CN 5 � 7) indicates intact pons; intactgag reflex (CN 9 � 10) shows functioningupper medulla (Note: CN 6 palsy is oftena false localizing sign)

Benzodiazepines (Ativan®)

Give phenytoin for 7 days



EPIDURAL HEMATOMA

What is an epiduralhematoma?

What causes it?

Which artery is associatedwith epidural hematomas?

What is the most commonsign of an epiduralhematoma?

What is the classic historywith an epidural hematoma?

What are the classic CT scanfindings with an epiduralhematoma?

Collection of blood between the skull anddura

Usually occurs in association with a skullfracture as bone fragments laceratemeningeal arteries

Middle meningeal artery

�50% have ipsilateral blown pupil

LOC followed by a “lucid interval”followed by neurologic deterioration

Lenticular (lens)-shaped hematoma(Think: Epidural � LEnticular)

=

What is the surgical treatmentfor an epidural hematoma?

What are the indications forsurgery with an epiduralhematoma?

Surgical evacuation

Any symptomatic epidural hematoma;any epidural hematoma �1 cm

What is the significance ofhyponatremia (low sodiumlevel) after head injury?

SIADH must be ruled out; remember,SIADH � Sodium Is Always Down Here



=

TRAUMATIC SUBARACHNOID HEMORRHAGE

What is it?


Head trauma resulting in blood below thearachnoid membrane and above the pia

Anticonvulsants and observation

CEREBRAL CONTUSION

What is it? Hemorrhagic contusion of brain parenchyma

SUBDURAL HEMATOMA

What is it?

What causes it?

What are the three types ofsubdurals?

What is the treatment ofepidural and subduralhematomas?

What classic findings appearon head CT scan for a subdural hematoma?

Blood collection under the dura

Tearing of “bridging” veins that passthrough the space between the corticalsurface and the dural venous sinuses orinjury to the brain surface with resultantbleeding from cortical vessels

1. Acute—symptoms within 48 hours ofinjury

2. Subacute—symptoms within 3 to 14 days3. Chronic—symptoms after 2 weeks or

longer

Mass effect (pressure) must be reduced;craniotomy with clot evacuation is usuallyrequired

Curved, crescent-shaped hematoma(Think: sUbdural � cUrved)


What are coup and contrecoup injuries?

What is DAI?

What is the best diagnostictest for DAI?

What can present after blunttrauma with neurologicaldeficits and a normal brainCT scan?


Coup—injury at the site of impactContrecoup—injury at the site opposite

the point of impact

Diffuse Axonal Injury (shear injury to brain parenchyma) from rapid deceleration injury; 33% mortality; long-term coma

MRI

DAI, carotid artery injury

SKULL FRACTURE

What is a depressed skullfracture?


What is the treatment foropen skull fractures?

Fracture in which one or more fragmentsof the skull are forced below the innertable of the skull

1. Contaminated wound requiring cleaning and débridement

2. Severe deformity3. Impingement on cortex4. Open fracture5. CSF leak

1. Antibiotics2. Seizure prophylaxis (phenytoin)3. Surgical therapy

SPINAL CORD TRAUMA

What are the two generaltypes of injury?

Define “spinal shock.”

1. Complete—no motor/sensory functionbelow the level of injury

2. Incomplete—residual function belowthe level of injury

Loss of all reflexes and motor function,hypotension, bradycardia


Define “sacral sparing.”

What initial studies/intervention are important?

What are the diagnosticstudies?

What are the indications foremergent surgery withspinal cord injury?

What is the indication for IV high-dose steroids withspinal cord injury?

Have steroids been proven tohelp after PENETRATINGspine injury?

Describe the following conditions:

Anterior cord syndrome


Sparing of sacral nerve level: anal sphinc-ter intact, toe flexion, perianal sensation

1. ABCs—obtain airway and ventilate ifneeded

2. Maintain BP (IVF, pressors if refractoryto fluids)

3. NG tube—prevents aspiration4. Foley5. High-dose steroids—proven to

improve outcome if given �8 hourspost injury

6. Complete cervical x-rays and those oflower levels as indicated by examination

Plain films, CT scan, MRI

Unstable vertebral fractureIncomplete injury with extrinsic

compressionSpinal epidural or subdural hematoma

Controversial: Blunt spinal cord injury withneurologic deficit (methylprednisolone:high-dose bolus [30 mg/kg] followed by continuous infusion [5.4 mg/kg] for 23 hours)

No

Affects corticospinal and lateralspinothalamic tracts, paraplegia, loss ofpain/temperature sensation, preservedtouch/vibration/proprioception


Central cord syndrome


Preservation of some lower extremitymotor and sensory ability with upperextremity weakness

Brown-Séquard syndrome Hemisection of cord resulting in ipsilateral motor weakness and touch/proprioception loss with contralateralpain/temperature loss

Posterior cord syndrome

How can the findings associated with Brown-Séquard syndrome beremembered?

Define the following terms:Jefferson’s fracture

Hangman’s fracture

Odontoid fracture

Priapism

Injury to posterior spinal cord with lossof proprioception distally

Think: CAPTAIN Brown-Séquard �“CPT”:

ContralateralPainTemperature loss

Fracture through C1 arches from axialloading (unstable fracture)

Fracture through the pedicles of C2 fromhyperextension; usually stable

Think: A hangman (C2) is below stature ofPresident T. Jefferson (C1)

Fracture of the odontoid process of C2(view with open-mouth odontoid x-ray)

Penile erection seen with spinal cordinjury


Chance fracture

Clay shoveler’s fracture

Odontoid fractures


Transverse vertebral fracture

Fracture of spinous process of C7

A: Type I—fracture through tip of densB: Type II—fracture through base of

densC: Type III—fracture through body

of C2

TUMORS

GENERAL

What is the incidence ofCNS tumors?

What is the usual location ofprimary tumors in adults/children?

What is the differential diagnosis of a ring-enhancing brain lesion?

What are the adverse effectsof tumors on the brain?

What are the signs/symptomsof brain tumors?

�1% of all cancers; third leading cause ofcancer deaths in people 15 to 34 years ofage; second leading cause of cancerdeaths in children

In adults, �66% of tumors are supratentorial, �33% are infratentorial;the reverse is true in children (i.e., �66% infratentorial)

Metastatic carcinoma, abscess, GBM,lymphoma

1. Increased ICP2. Mass effect on cranial nerves3. Invasion of brain parenchyma,

disrupting nuclei/tracts4. Seizure foci5. Hemorrhage into/around tumor mass

1. Neurologic deficit (66%)2. Headache (50%)3. Seizures (25%)4. Vomiting (classically in the morning)




What are the most commonintracranial tumors in adults?

What are the three mostcommon in children?


CT scan or MRI is the standard diagnostic study

1. Establishing a tissue diagnosis2. Relief of increased ICP3. Relief of neurologic dysfunction

caused by tissue compression4. Attempt to cure in the setting of

localized tumor

Metastatic neoplasms are most common;among primaries, gliomas are #1 (50%)and meningiomas are #2 (25%)

1. Medulloblastomas (33%)2. Astrocytomas (33%)3. Ependymomas (10%)

GLIOMAS

What is a glioma?

What are the characteristicsof a LOW-grade astrocytoma?

What is the most commonprimary brain tumor inadults?

What are its characteristics?

What is the average age ofonset?



General name for several tumors of neuroglial origin (e.g., astrocytes, ependymal, oligodendrocytes)

Nuclear atypia, high mitotic rate, high signal on T2 weighted images,nonenhancing with contrast CT scan

Glioblastoma multiforme (GBM)(Think: GBM � Greatest BrainMalignancy)

Poorly defined, highly aggressive tumorsoccurring in the white matter of the cere-bral hemispheres; spread extremely rapidly

Fifth decade

Surgical debulking followed by radiation

Without treatment, �90% of patients die within 3 months of diagnosis; withtreatment, 90% die within 2 years



MENINGIOMAS

What is the layer of origination?


What are the associated histologic findings?

What is the histologic malignancy determination?

What is the peak age ofoccurrence?


What is the clinical presentation?


Arachnoid cap cells

Radiation exposureNeurofibromatosis type 2Female gender

Psammoma bodies (concentric calcifications), whorl formations (“onion skin” pattern)

Brain parenchymal invasion

40 to 50 years

Females predominate almost 2:1

Variable depending on location; lateralcerebral convexity tumors can cause focaldeficits or headache; sphenoid tumorscan present with seizures; posterior fossatumors with CN deficits; olfactory groovetumors with anosmia

Preoperative embolization and surgicalresection

CEREBELLAR ASTROCYTOMAS




5 to 9 years

Usually in the cerebellar hemispheres;less frequently in the vermis

Usually lateral cerebellar signs occur:ipsilateral incoordination or dysmetria(patient tends to fall to side of tumor) aswell as nystagmus and ataxia; CN deficitsare also frequently present, especially inCNs VI and VII


What are the treatment andprognosis?


Completely resectable in 75% of cases,which usually results in a cure; overall 5-year survival rate exceeds 90%

MEDULLOBLASTOMA





What are the treatment andprognosis?

First decade (3 to 7 years)

External granular cells of cerebellum

Cerebellar vermis in children; cerebellarhemispheres of adolescents and adults

Headache, vomiting, and other signs ofincreased ICP; also usually truncal ataxia

Best current treatment includes surgeryto debulk the tumor, cranial and spinalradiation, and chemotherapy; 5-year survival rate is �50%

PITUITARY TUMORS

What is the most commonpituitary tumor?

What is the most commonpresentation of a prolactinoma?

Prolactinoma

Bitemporal hemianopsia (lateral visualfields blind)


What are the blood prolactinlevels with a prolactinoma?

Medical treatment of a prolactinoma?

Surgical treatment for a prolactinoma?

What is the treatment of arecurrent prolactinoma aftersurgical resection?


�300 mg/L is diagnostic for prolactinoma(�100 mg/L is abnormal)

Bromocriptine

Transsphenoidal resection of the pituitarytumor (in cases refractory to bromocriptine)

Radiation therapy

VASCULAR NEUROSURGERY

SUBARACHNOID HEMORRHAGE (SAH)

What are the usual causes?

What is a berry aneurysm?

What is the usual location ofa berry aneurysm?

What medical diseaseincreases the risk of berryaneurysms?

What is an Arterio-VenousMalformation (AVM)?

Where do they occur?

What are the signs/symptoms of SAH?

Most cases are due to trauma; ofnontraumatic SAH, the leading cause isruptured berry aneurysm, followed byarteriovenous malformations

Saccular outpouching of vessels in thecircle of Willis, usually at bifurcations

Anterior communicating artery is #1 (30%),followed by posterior communicatingartery and middle cerebral artery

Polycystic kidney disease and connectivetissue disorders (e.g., Marfan’s syndrome)

Congenital abnormality of the vasculaturewith connections between the arterialand venous circulations withoutinterposed capillary network

�75% are supratentorial

Classic symptom is “the worst headacheof my life”; meningismus is documentedby neck pain and positive Kernig’s andBrudzinski’s signs; occasionally LOC,vomiting, nausea, photophobia


What comprises the workupof SAH?

What are the possible complications of SAH?

What is the treatment forvasospasm?

What is the treatment ofaneurysms?

What is the treatment ofAVMs?


If SAH is suspected, head CT should be the first test ordered to look forsubarachnoid blood; LP may showxanthochromic CSF, but is not necessaryif CT scan is definitive; this test shouldbe followed by arteriogram to look foraneurysms or AVMs

1. Brain edema leading to increased ICP2. Rebleeding (most common in the first

24 to 48 hours posthemorrhage)3. Vasospasm (most common cause of

morbidity and mortality)

Nimodipine (calcium channel blocker)

Surgical treatment by placing a metal clip on the aneurysm is the mainstay oftherapy; alternatives include balloonocclusion or coil embolization

Many are on the brain surface and accessible operatively; preoperativeembolization can reduce the size of theAVM; for surgically inaccessible lesions,radiosurgery (gamma knife) has beeneffective in treating AVMs �3 cm indiameter

INTRACEREBRAL HEMORRHAGE

What is it?


Where does it occur?

Bleeding into the brain parenchyma

#1 is hypertensive/atherosclerotic diseasegiving rise to Charcot-Bouchardaneurysms (small tubular aneurysmsalong smaller terminal arteries); othercauses include coagulopathies, AVMs,amyloid angiopathy, bleeding into atumor, and trauma

66% occur in the basal ganglia; putamenis the structure most commonly affected


How often does bloodspread to the ventricularsystem?


What is the associated diagnostic study?




66% of cases

66% present with coma; large putamen bleeding classically presentswith contralateral hemiplegia andhemisensory deficits, lateral gaze preference, aphasia, and homonymoushemianopsia

CT scan

CN III palsy, progressive alteration ofconsciousness

Poor, especially with ventricular or diencephalons involvement

SPINE

LUMBAR DISC HERNIATION

What is it?

Which nerve is affected?

Who is affected?



What is the usual presentingsymptom?

Extrusion of the inner portion of theintervertebral disc (nucleus pulposus)through the outer annulus fibrosis, causing impingement on nerve roots exiting the spinal canal

Nerve exiting at the level below (e.g., anL4–L5 disc impinges on the L5 nerveexiting between L5–S1)

Middle-aged and older individuals

Loss of elasticity of the posterior longitudinal ligaments and annulus fibrosis as a result of aging

L5–S1 (45%)L4–L5 (40%)

Low back pain


What are the signs:L5–S1?

L4–L5?

L3–L4?



What are the indications foremergent surgery?

What is cauda equinasyndrome?

What is “sciatica”?


Decreased ankle jerk reflexWeakness of plantar flexors in footPain in back/midgluteal region to

posterior calf to lateral footIpsilateral radiculopathy on straight leg

raise

Decreased biceps femoris reflexWeak extensors of foot

Decrease or absence of knee jerks,weakness of the quadriceps femoris,pain in lower back/buttock, pain inlateral thigh and anterior thigh

Pain in hip/groin region to posterolateralthigh, lateral leg, and medial toes

CT scan, CT myelogram, or MRI

Conservative—bed rest and analgesicsSurgical—partial hemilaminectomy and

discectomy (removal of herniated disc)

1. Cauda equina syndrome2. Progressive motor deficits

Herniated disc compressing multiple S1, S2, S3, S4 nerve roots, resulting inbowel/bladder incontinence, “saddleanesthesia” over buttocks/perineum, lowback pain, sciatica

Radicular or nerve root pain

CERVICAL DISC DISEASE

What is it? Basically the same pathology as lumbardisc herniation, except in the cervicalregion; the disc impinges on the nerveexiting the canal at the same level of thedisease (e.g., a C6–C7 disc impinges onthe C7 nerve root exiting at the C6–C7foramen)



What are the signs/symptoms:

C7?

C6?

C8?



What are the symptoms of central cervical cord compression from disc fragments?

What is Spurling’s sign?


C6–C7 (70%)C5–C6 (20%)C7–T1 (10%)

Decreased triceps reflex/strength, weakness of forearm extension

Pain from neck, through triceps and intoindex and middle finger

Decreased biceps and brachioradialisreflex

Weakness in forearm flexionPain in neck, radial forearm, and thumb

Weakness in intrinsic hand muscles, painin fourth/fifth fingers

CT scan or MRI

Anterior or posterior discectomy withfusion PRN

Myelopathic syndrome with LMN signsat level of compression and UMN signsdistally; e.g., C7 compression may causebilateral loss of triceps reflex and bilateralhyperreflexia, clonus, and Babinski signsin lower extremities

Reproduction of radicular pain by havingthe patient turn his head to the affectedside and applying axial pressure to thetop of the head

SPINAL EPIDURAL ABSCESS


What is the commonly associated medical condition?

Hematogenous spread from skin infectionsis most common; also, distant abscesses/infections, UTIs, postoperative infections,spinal surgery, epidural anesthesia

Diabetes mellitus


What are the three mostcommon sites?

What is the most commonorganism?



Which test iscontraindicated?




1. Thoracic2. Lumbar3. Cervical


Fever; severe pain over affected area and with flexion/extension of spine; weakness can develop, ultimately leadingto paraplegia; 15% of patients have a backfuruncle

MRI� test of choice

LP, because of the risk of seeding CSFwith bacteria, causing meningitis

Surgical drainage and appropriate antibiotic coverage

Depends on preop condition; severe neurologic deficits (e.g., paraplegia) showlittle recovery; 15% to 20% of cases arefatal

PEDIATRIC NEUROSURGERY

HYDROCEPHALUS

What is it?

What are the three generalcauses?

What is the normal dailyCSF production?

What is the normal volumeof CSF?

Abnormal condition consisting of anincreased volume of CSF along with distension of CSF spaces

1. Increased production of CSF2. Decreased absorption of CSF3. Obstruction of normal flow of CSF

(90% of cases)

�500 mL

�150 mL in the average adult


Define “communicating”versus “noncommunicating”hydrocephalus.

What are the specific causesof hydrocephalus?




What is the prognosis ifuntreated?

What are the possible complications of treatment?

What is hydrocephalus exvacuo?

What is a “shunt series”?


Communicating—unimpaired connectionof CSF pathway from lateral ventricleto subarachnoid space

Noncommunicating—complete orincomplete obstruction of CSF flowwithin or at the exit of the ventricularsystem

Congenital malformationAqueductal stenosisMyelomeningoceleTumors obstructing CSF flowInflammation causing impaired

absorption of fluidSubarachnoid hemorrhageMeningitisChoroid plexus papilloma causing

c production of CSF

Signs of increased ICP: HA, nausea,vomiting, ataxia, increasing head circumference exceeding norms for age

CT scan, MRI, measurement of head circumference

1. Remove obvious offenders2. Perform bypass obstruction with

ventriculoperitoneal shunt or ventriculoatrial shunt

50% mortality; survivors show decreasedIQ (mean � 69); neurologic sequelae:ataxia, paraparesis, visual deficits

1. Blockage/shunt malfunction2. Infection

Increased volume of CSF spaces frombrain atrophy, not from any pathology in the amount of CSF absorbed orproduced

Series of x-rays covering the entire shuntlength—looking for shunt disruption/kinking to explain malfunction of shunt



SPINAL DYSRAPHISM/NEURAL TUBE DEFECTS


What are the race/genderdemographics?

Define spina bifida occulta.


What is the most commonclinically significant defect?

What are the three mostcommon anatomic sites?




Which vitamin is thought tolower the rate of neuraltube defects in utero?

�1/1000 live births in the United States

More common in white patients andfemale patients

Defect in the development of the posterior portion of the vertebrae

Usually asymptomatic, though it may beassociated with other spinal abnormalities;usually found incidentally on x-rays

Myelomeningocele: herniation of nerveroots and spinal cord through a defect inthe posterior elements of the vertebra(e);the sac surrounding the neural tissue maybe intact, but more commonly is rupturedand therefore exposes the CNS to theexternal environment

1. Lumbar region2. Lower thoracic region3. Upper sacral region

Variable from mild skeletal deformities toa complete motor/sensory loss; bowel/bladder function is difficult to evaluate,but often is affected and can adverselyaffect survival

With open myelomeningoceles, patientsare operated on immediately to preventinfection

�95% survival for the first 2 years, compared with 25% in patients notundergoing surgical procedures

Folic acid



CRANIOSYNOSTOSIS

What is it?


What are the types?



What is the timing ofsurgery?


Premature closure of one or more of thesutures between the skull plates

1/200 live births in the United States

Named for the suture that is fused (e.g.,sagittal, coronal, lambdoid); sagittal craniosynostosis accounts for �50% of allcases; more than one suture can befused, and all or part of a suture may beaffected

Physical examination can reveal ridgesalong fused sutures and lessened suturemobility; plain x-rays can show a lack oflucency along the fused suture, but arerarely required

Most often the reasons are cosmetic, asthe cranial vault will continue to deformwith growth; occasionally, a child willpresent with increased ICP secondary torestricted brain growth

Usually 3 to 4 months of age; earlier surgery increases the risk of anesthesia;later surgeries are more difficult becauseof the worsening deformities anddecreasing malleability of the skull

�1%

MISCELLANEOUS

What is the most common bacteria causingpostneurosurgery meningitis?

What classically presents asthe “worst headache of mylife”?

What classically has a “lucidinterval”?

Staphylococcus aureus (skin flora)

Spontaneous subarachnoid hemorrhage

Epidural hemorrhage


What is the most commonlocation of a hypertensiveintracerebral hemorrhage?

What is Horner’s syndrome?

What is a third-nerve palsy?

What is Millard-Gublersyndrome?

What is syringomyelia?

Chapter 76 / Urology 743

Putamen

Cervical sympathetic chain lesion;Think: “MAP”:

MiosisAnhydrosis of ipsilateral facePtosis

Think: Third nerve does three things:1. Diplopia2. Ptosis3. Mydriasis

Pons infarction:1. VI nerve palsy2. VII nerve palsy3. Contralateral hemiplegia

Central pathologic cavitations of thespinal cord

Define the following terms:Cystogram

Ureteral stents

Cystoscope

Perc nephrostomy

Retrograde pyelogram

UrologyChapter 76Contrast study of the bladder

Plastic tubes placed via cystoscope intothe ureters for stenting, identification, etc.

Scope placed into the urethra and intothe bladder to visualize the bladder

Catheter placed through the skin into thekidney pelvis to drain urine with distalobstruction, etc.

Dye injected into the ureter up into thekidney, and films taken


RUG

Gomco clamp

Bell clapper’s deformity

Fournier’s gangrene

Foley catheter

Coudé catheter

Suprapubic catheter

Posthitis

Hydrocele

Communicating hydrocele


Retrograde UrethroGram (dye injectedinto the urethra and films taken; rules outurethral injury, usually in trauma patients)

Clamp used for circumcision; protectspenis glans

Condition of congenital absence ofgubernaculum attachment to scrotum

Extensive tissue necrosis/infection of theperineum in patients with diabetes

Straight bladder catheter placed throughthe urethra

Basically, a Foley catheter with hook onthe end to get around a large prostate

Bladder catheter placed through the skinabove the pubic symphysis into the bladder

Foreskin infection

Clear fluid in the processus vaginalismembrane

Hydrocele that communicates with peritoneal cavity and, thus, gets smallerand larger as fluid drains and then reaccumulates


Noncommunicatinghydrocele


Hydrocele that does not communicatewith the peritoneal cavity; hydroceleremains the same size

Varicocele

Spermatocele

Epididymitis

Prehn’s sign

TRUS

DRE

Orchitis

Pseudohermaphroditism

Urgency

Dysuria

Frequency

Abnormal dilation of the pampiniformplexus to the spermatic vein in the sper-matic cord; described as a “bag of worms”

Dilatation of epididymis or vas deferens

Infection of the epididymis

Elevation of the painful testicle thatreduces the pain of epididymitis

TransRectal UltraSound

Digital Rectal Examination

Inflammation/infection of the testicle

Genetically one sex; partial or completeopposite-sex genitalia

Overwhelming sensation to void immediately

Painful urination (usually burning sensation)

Urination more frequently than usual


Polyuria

Nocturia

Hesitancy

Pneumaturia

Pyuria

Cryptorchidism

IVP

Hematuria

Space of Retzius

Enuresis

Incontinence

TURP

PVR

Priapism

Paraphimosis

Phimosis

Balanitis

Balanoposthitis

UTI

Peyronie’s disease


Urination in larger amounts than usual

Awakening to urinate

Delay in urination

Air passed with urine via the urethra

WBCs in urine; UTI �10 WBCs/HPF

Undescended testicle

IntraVenous Pyelogram (dye is injectedinto the vein, collects in the renal collecting system, and an x-ray is taken)

RBCs in urine

Anatomic extraperitoneal space in frontof the bladder

Involuntary urination while asleep

Involuntary urination

TransUrethral Resection of the Prostate

PostVoid Residual

Prolonged, painful erection

Foreskin held (stuck) in the retractedposition

Inability to retract the foreskin

Inflammation/infection of the glans penis

Inflammation/infection of the glans andprepuce of the penis

Urinary Tract Infection

Abnormal fibrosis of the penis shaft,resulting in a bend upon erection


BPH

Epispadias

Hypospadiasis

Erectile dysfunction

Sterility

Appendix testis

VUR


Benign Prostatic Hyperplasia

Abnormal urethral opening on the dorsalsurface of the penis

Abnormal urethral opening on theventral surface of the penis; may occur inanterior, middle, or posterior of penis

Inability to achieve an erection

Inability to reproduce

Common redundant testicular tissue

VesicoUreteral Reflux

SCROTAL ANATOMY

What are the layers of thescrotum?

Skin

DartosExternalspermaticfascia

Internalspermatic fascia

Parietal andvisceral layers oftunica vaginalis

Tunica albuginea

Cremastermuscle

UROLOGIC DIFFERENTIAL DIAGNOSIS

What is the differential diagnosis of scrotal mass?

Cancer, torsion, epididymitis, hydrocele,spermatocele, varicocele, inguinal hernia,testicular appendage, swollen testicle aftertrauma, nontesticular tumor (paratesticulartumor: e.g., rhabdomyosarcoma,leiomyosarcoma, liposarcoma)


What are the causes ofhematuria?

What is the most commoncause of severe gross hematuria without traumaor chemotherapy/radiation?

What is the differential diagnosis for bladder outletobstruction?

What is the differential diagnosis for ureteralobstruction?

What is the differential diagnosis for kidney tumor?


Bladder cancer, trauma, UTI, cystitisfrom chemotherapy or radiation, stones,kidney lesion, BPH

Bladder cancer

BPH, stone, foreign body, urethral stricture, urethral valve

Stone, tumor, iatrogenic (suture),stricture, gravid uterus, radiation injury,retroperitoneal fibrosis

Renal cell carcinoma, sarcoma, adenoma,angiomyolipoma, hemangiopericytoma,oncocytoma

RENAL CELL CARCINOMA (RCC)

What is it?


What percentage of thetumors are bilateral?



What is the classic TRIAD ofrenal cell carcinoma?

Most common solid renal tumor (90%);originates from proximal renal tubularepithelium

Primarily a tumor of adults 40 to 60 yearsof age with a 3:1 male:female ratio; 5% ofcancers overall in adults

1%

Male sex, tobacco, von Hippel-Lindausyndrome, polycystic kidney

Pain (40%), hematuria (35%), weight loss(35%), flank mass (25%), HTN (20%)

1. Flank pain2. Hematuria3. Palpable mass (triad occurs in only

10%–15% of cases)


How are most casesdiagnosed these days?

What radiologic tests areperformed?

Define the stages (AJCC):Stage I?

Stage II?

Stage III?

Stage IV?

What is the metastaticworkup?

What are the sites of metastases?

What is the unique route ofspread?

What is the treatment ofRCC?

What gland is removed witha radical nephrectomy?

What is the uniquetreatment for metastaticspread?

What is a syndrome of RCCand liver disease?


Found incidentally on an imaging study(CT, MRI, U/S) for another reason

1. IVP2. Abdominal CT scan with contrast

Tumor �2.5 cm, no nodes, no metastases

Tumor �2.5 cm limited to kidney, nonodes, no metastases

Tumor extends into IVC or main renalvein; positive regional lymph nodes but�2 cm in diameter and no metastases

Distant metastasis or positive lymph node�2 cm in diameter, or tumor extends pastGerota’s fascia

CXR, IVP, CT scan, LFTs, calcium

Lung, liver, brain, bone; tumor thrombusentering renal vein or IVC is not uncommon

Tumor thrombus into IVC lumen

Radical nephrectomy (excision of the kidney and adrenal, including Gerota’sfascia) for stages I through IV

Adrenal gland

1. �-interferon2. LAK cells (lymphokine-activated

killer) and IL-2 (interleukin-2)

Stauffer’s syndrome


What is the concern in anadult with new onset leftvaricocele?


Left RCC—the left gonadal vein drainsinto the left renal vein

BLADDER CANCER


What is the most commonhistology?



What is the classic presenta-tion of bladder cancer?

What tests are included inthe workup?

Define the AJCC transitionalcell bladder cancer stages:

Stage 0?

Stage I?

Stage II?

Stage III?

Stage IV?

Second most common urologic malignancyMale:female ratio of 3:1White patients are more commonly affected

than are African American patients

Transitional Cell Carcinoma (TCC)—90%; remaining cases are squamous or adenocarcinomas

Smoking, industrial carcinogens (aromaticamines), schistosomiasis, truck drivers,petroleum workers, cyclophosphamide

Hematuria, with or without irritativesymptoms (e.g., dysuria), frequency

“Painless hematuria”

Urinalysis and culture, IVP, cystoscopywith cytology and biopsy

Superficial, carcinoma in situ

Invades subepithelial connective tissue,no positive nodes, no metastases

Invades superficial or deep muscularispropria, no positive nodes, no metastases

Invades perivesical tissues, no positivenodes, no metastases

Positive nodal spread with distant metastases and/or invades abdominal/pelvic wall


What is the treatmentaccording to stage:

Stage 0?

Stage I?

Stages II and III?

Stage IV?

What are the indications fora partial cystectomy?

What is TURB?

If after a TURB the tumorrecurs, then what?

What is and how does bacillusCalmette-Guérin work?


TURB and intravesical chemotherapy

TURB

Radical cystectomy, lymph node dissection, removal of prostate/uterus/ovaries/anterior vaginal wall, and urinarydiversion (e.g., ileal conduit) �� chemo

�� Cystectomy and systemicchemotherapy

Superficial, isolated tumor, apical with 3-cm margin from any orifices

TransUrethral Resection of the Bladder

Repeat TURB and intravesicalchemotherapy (mitomycin C) or bacillus Calmette-Guérin

Attenuated TB vaccine—thought to workby immune response

PROSTATE CANCER




Most common GU cancer (�100,000new cases per year in the United States); most common carcinoma in men in theU.S.; second most common cause of deathin men in the U.S.

“Disease of elderly men” present in 33% of men 70 to 79 years of age and in66% of men 80 to 89 years of age atautopsy; African American patients havea 50% higher incidence than do whitepatients

Adenocarcinoma (95%)



What percentage of patientshave metastasis at diagnosis?

What are the common sitesof metastasis?

What provides lymphaticdrainage?

What is the significance ofBatson’s plexus?

What are the steps in earlydetection?

When should men get aPSA-level check?

What percentage of patientswith prostate cancer willhave an elevated PSA?

What is the imaging test forbladder cancer?


What is the Gleason score?

What are the indications fortransrectal biopsy with normal rectal examination?


Often asymptomatic; usually presents as a nodule found on routine rectal examination; in 70% of cases, cancerbegins in the periphery of the gland and moves centrally; thus, obstructivesymptoms occur late

40% of patients have metastatic diseaseat presentation, with symptoms of bonepain and weight loss

Osteoblastic bony lesions, lung, liver,adrenal

Obturator and hypogastric nodes

Spinal cord venous plexus; route ofisolated skull/brain metastasis

1. Prostate-specific antigen (PSA)—mostsensitive and specific marker

2. Digital rectal examination (DRE)

Controversial:1. All men �50 years old2. �40 years old if first-degree family

history or African American patient

�60%

TransRectal UltraSound (TRUS)

Transrectal biopsy

Histologic grades 2–10:Low score � well differentiatedHigh score � poorly differentiated

PSA �10 or abnormal transrectal ultrasound


Staging (AJCC):Stage I?

Stage II?

Stage III?

Stage IV?

What does a “radical prostatectomy” remove?

What is “androgen ablation”therapy?

How do LHRH agonistswork?

What are the generalizedtreatment options accordingto stage:

Stage I?

Stage II?

Stage III?

Stage IV?

What is the medicaltreatment for systemicmetastatic disease?


Tumor involves �50% of 1 lobe, no nodes,no metastases, PSA �10, Gleason 6

Tumor within prostate; lobe �50% butPSA �10, or Gleason �6; or �50% of 1 lobe, no nodes, no metastases

Tumor through prostate capsule or intoseminal vesicles, no nodes, no metastases

Tumor extends into adjacent structures(other than seminal vesicles) or � nodesor � metastases

1. Prostate gland2. Seminal vesicles3. Ampullae of the vasa deferentia

1. Bilateral orchiectomy or2. Luteinizing Hormone-Releasing

Hormone (LHRH) agonists

Decrease LH release from pituitary,which then decreases testosteroneproduction in the testes

Radical prostatectomy

Radical prostatectomy, �� lymph nodedissection

Radiation therapy, �� androgen ablation

Androgen ablation, radiation therapy

Androgen ablation


What is the option for treatment in the early stageprostate cancer patient �70years old with comorbidity?


XRT

BENIGN PROSTATIC HYPERPLASIA


What is it?

What is the size of a normalprostate?

Where does BPH occur?






BPH

Disease of elderly men (average age is 60 to 65 years); prostate graduallyenlarges, creating symptoms of urinaryoutflow obstruction

20 to 25 gm

Periurethrally (Note: prostate cancer occurs in theperiphery of the gland)

Obstructive-type symptoms: hesitancy,weak stream, nocturia, intermittency,UTI, urinary retention

History, DRE, elevated PostVoid Residual(PVR), urinalysis, cystoscopy, U/S

Urinalysis, PSA, BUN, CR

Prostate cancer (e.g., nodular)—biopsyNeurogenic bladder—history of

neurologic diseaseAcute prostatitis—hot, tender glandUrethral stricture—RUG, history of STDStoneUTI

Pharmacologic—�-1 blockadeHormonal—antiandrogensSurgical—TURP, TUIP, open prostate

resectionTransurethral balloon dilation


Why do �-adrenergic blockers work?

What is Proscar®?

What is Hytrin®?

What are the indications forsurgery in BPH?

What is TURP?

What is TUIP?

What percentage of tissueremoved for BPH will havemalignant tissue on histology?

What are the possible complications of TURP?


1. Relax sphincter2. Relax prostate capsule

Finasteride: 5-�-reductase inhibitor;blocks transformation of testosterone todihydrotestosterone; may shrink and slowprogression of BPH

Terazosin: �-blocker; may increase urineoutflow by relaxing prostatic smooth muscles

Due to obstruction:Urinary retentionHydronephrosisUTIsSevere symptoms

TransUrethral Resection of Prostate:resection of prostate tissue via a scope

TransUrethral Incision of Prostate

Up to 10%!

Immediate:Failure to voidBleedingClot retentionUTIIncontinence

TESTICULAR CANCER




Rare; 2 to 3 new cases per 100,000 menper year in the United States

Most common solid tumor of young adultmales (20 to 40 years)

Cryptorchidism (6% of testicular tumorsdevelop in patients with a history of cryptorchidism)


What is cryptorchidism?

Does orchiopexy as an adultremove the risk of testicularcancer?


What percentage of patientspresent with an acute hydrocele?

What percentage presentwith symptoms of metastaticdisease (back pain, anorexia)?

What are the classifications?

What is the major classifica-tion based on therapy?

What are the tumor markersfor testicular tumors?

What are the tumor markersby tumor type?


Failure of the testicle to descend into thescrotum

NO

Most patients present with a painless lump,swelling, or firmness of the testicle; they oftennotice it after incidental trauma to the groin

10%

�10%

Germ cell tumors (95%):Seminomatous (�35%)Nonseminomatous (�65%)Embryonal cell carcinoma

TeratomaMixed cellChoriocarcinoma

Nongerminal (5%):Leydig cellSertoli cellGonadoblastoma

Seminomatous and nonseminomatoustumors

1. Beta-human chorionic gonadotropin (�-HCG)

2. Alpha-fetoprotein (AFP)

�-HCG—c in choriocarcinoma (100%),embryonal carcinoma (50%), andrarely in pure seminomas (10%); nonseminomatous tumors (50%)

AFP—c in embryonal carcinoma andyolk sac tumors; nonseminomatoustumors (50%)


Define the differencebetween seminomatous andNONseminomatous germ celltesticular tumor markers.

Which tumors almost never

have an elevated AFP?

In which tumor is �-HCGalmost always found elevated?

How often is �-HCG elevatedin patients with pureseminoma?

How often is �-HCG elevatedwith nonseminoma?

What other tumor markersmay be elevated and usefulfor recurrence surveillance?

What are the steps inworkup?

Define the stages accordingto TMN staging (AJCC):

Stage I?

Stage II?

Stage III?

What is the initial treatmentfor all testicular tumors?

What is the treatment ofseminoma at the variousstages:

Stage I and II?

Stage III?


NONseminomatous common � 90%have a positive AFP and/or �-HCG

Seminomatous rare � only 10% areAFP positive

Choriocarcinoma and seminoma

Choriocarcinoma

Only about 10% of the time!

≈65%

LDH, CEA, Human ChorionicSomatomammotropic (HCS), Gamma-Glutamyl Transpeptidase (GGT),PLacental Alkaline Phosphate (PLAP)

PE, scrotal U/S, check tumor markers,CXR, CT (chest/pelvis/abd)

Any tumor size, no nodes, no metastases

Positive nodes, no metastases, any tumor

Distant metastases (any nodal status,any size tumor)

Inguinal orchiectomy (removal of testicle through a groin incision)

Inguinal orchiectomy and radiation toretroperitoneal nodal basins

Orchiectomy and chemotherapy


What is the treatment ofNONseminomatous diseaseat the various stages:

Stages I and II?

Stage III?

What percentage of stage Iseminomas are cured aftertreatment?

Which type is most radiosensitive?

Why not remove testis withcancer through a scrotalincision?

What is the major side effectof retroperitoneal lymphnode dissection?


Orchiectomy and retroperitoneal lymphnode dissection versus close follow-upfor retroperitoneal nodal involvement

Orchiectomy and chemotherapy

95%

Seminoma (Think: Seminoma � Sensitiveto radiation)

It could result in tumor seeding of thescrotum

Erectile dysfunction

TESTICULAR TORSION

What is it?


What is a “bell clapper”deformity?

Torsion (twist) of the spermatic cord,resulting in venous outflow obstruction,and subsequent arterial occlusion Sinfarction of the testicle

Acute onset of scrotal pain usually aftervigorous activity or minor trauma

Bilateral nonattachment of the testiclesby the gubernaculum to the scrotum(free like the clappers of a bell)



What are the signs?




How much time is availablefrom the onset of symptomsto detorse the testicle?

What are the chances of tes-ticle salvage after 24 hours?


Pain in the scrotum, suprapubic pain

Very tender, swollen, elevated testicle;nonillumination; absence of cremastericreflex

Testicular trauma, inguinal hernia,epididymitis, appendage torsion

Surgical exploration, U/S (solid mass) andDoppler flow study, cold Tc-99m scan(nuclear study)

Surgical detorsion and bilateral orchiopexyto the scrotum

�6 hours will bring about the best results;�90% salvage rate

�10%

EPIDIDYMITIS

What is it?

What are thesigns/symptoms?

What is the cause?

What are the common bugs inthe following types of patients:

Elderly patients/children?

Young men?


What is the workup?


Infection of the epididymis

Swollen, tender testicle; dysuria; scrotalache/pain; fever; chills; scrotal mass

Bacteria from the urethra

Escherichia coli

STD bacteria: Gonorrhea, chlamydia

Testicular torsion

U/A, urine culture, swab if STD suspected,�� U/S with Doppler or nuclear studyto rule out torsion

Antibiotics



PRIAPISM

What is priapism?

What are its causes?

What is first-line treatment?

Persistent penile erection

Low flow: leukemia, drugs (e.g., prazosin),sickle-cell disease, erectile dysfunctiontreatment gone wrong

High flow: pudendal artery fistula, usuallyfrom trauma

1. Aspiration of blood from corporus cavernosum

2. �-Adrenergic agent

ERECTILE DYSFUNCTION

What is it?

What are the six majorcauses?


Inability to achieve an erection

1. Vascular: decreased blood flow orleak of blood from the corpuscavernosus (most common cause)

2. Endocrine: low testosterone3. Anatomic: structural abnormality of

the erectile apparatus (e.g., Peyronie’sdisease)

4. Neurologic: damage to nerves (e.g.,postoperative, IDDM)

5. Medications (e.g., clonidine)6. Psychologic: performance anxiety,

etc. (very rare)

Fasting GLC (rule out diabetes and thusdiabetic neuropathy)

Serum testosteroneSerum prolactin

CALCULUS DISEASE



1 in 10 people will have stones

Poor fluid intake, IBD, hypercalcemia(“CHIMPANZEES”), renal tubular acidosis, small bowel bypass


What are the four types ofstones?

What type of stones are notseen on AXR?

What stone is associatedwith UTIs?

What stones are seen inIBD/bowel bypass?

What are the symptoms ofcalculus disease?

What are the classicfindings/symptoms?

Diagnosis?

What is the significance ofhematuria and pyuria?

Treatment?


1. Calcium oxalate/calcium PO4 (75%)—secondary to hypercalciuria (c intestinalabsorption, T renal reabsorption, c bone reabsorption)

2. Struvite (MgAmPh)(15%)—infectionstones; seen in UTI with urea-splittingbacteria (Proteus); may cause staghorncalculi; high urine pH

3. Uric acid (7%)—stones are radiolucent(Think: Uric � Unseen); seen in gout,Lesch-Nyhan, chronic diarrhea, cancer; low urine pH

4. Cystine (1%)—genetic predisposition

Uric acid (Think: Uric � Unseen)

Struvite stones (Think: Struvite � Sepsis)

Calcium oxalate

Severe pain; patient cannot sit still: renalcolic (typically pain in the kidney/ureterthat radiates to the testis or penis), hematuria (remember, patients with peritoneal signs are motionless)

Flank pain, stone on AXR, hematuria

KUB (90% radiopaque), IVP, urinalysisand culture, BUN/Cr, CBC

Stone with concomitant infection

Narcotics for pain, vigorous hydration,observation

Further options: ESWL (lithotripsy),ureteroscopy, percutaneous lithotripsy,open surgery; metabolic workup forrecurrence


What are the indications forintervention?

What are the contraindications of outpatient treatment?

What are the three commonsites of obstruction?


Urinary tract obstructionPersistent infectionImpaired renal function

Pregnancy, diabetes, obstruction, severedehydration, severe pain, urosepsis/fever,pyelonephritis, previous urologic surgery,only one functioning kidney

1. UreteroPelvic Junction (UPJ)2. UreteroVesicular Junction (UVJ)3. Intersection of the ureter and the iliac

vessels

INCONTINENCE

What are the common typesof incontinence?

Define the following terms:Stress incontinence

Overflow incontinence

Urge incontinence

Mixed incontinence

Enuresis


Stress incontinence, overflowincontinence, urge incontinence

Loss of urine associated with coughing,lifting, exercise, etc.; seen most often inwomen, secondary to relaxation of pelvicfloor following multiple deliveries

Failure of the bladder to empty properly;may be caused by bladder outlet obstruction (BPH or stricture) or detrusor hypotonicity

Loss of urine secondary to detrusor instability in patients with stroke, dementia, Parkinson’s disease, etc.

Stress and urge incontinence combined

Bedwetting in children

History (including meds), physical examination (including pelvic/rectalexamination), urinalysis, postvoid residual(PR), urodynamics, cystoscopy/vesicocystourethrogram (VCUG) may be necessary


What is the “Marshall test”?

What is the treatment of thefollowing disorders:

Stress incontinence?

Urge incontinence?

Overflow incontinence?


Woman with urinary stress incontinenceplaced in the lithotomy position with afull bladder leaks urine when asked tocough

Bladder neck suspension

Pharmacotherapy (anticholinergics, �-agonists)

Self-catheterization, surgical relief ofobstruction, �-blockers

URINARY TRACT INFECTION (UTI)


What are the three commonorganisms?




When should workup beperformed?


Ascending infection, instrumentation,coitus in females

1. E. coli (90%)2. Proteus3. Klebsiella, Pseudomonas

Stones, obstruction, reflux, diabetes mellitus, pregnancy, indwelling catheter/stent

Lower UTI—frequency, urgency, dysuria,nocturia

Upper UTI—back/flank pain, fever, chills

Symptoms, urinalysis (�10 WBCs/HPF,�105 CFU)

After first infection in male patients(unless Foley is in place)

After first pyelonephritis in prepubescentfemale patients

Lower: 1 to 4 days of oral antibioticsUpper: 3 to 7 days of IV antibiotics



MISCELLANEOUS UROLOGY QUESTIONS

Why should orchiopexy beperformed?

In which area of theprostate does BPH arise?

In which area of theprostate does prostate cancer arise?

What type of bony lesions isseen in metastatic prostatecancer?

What percentage of renalcell carcinoma showevidence of metastaticdisease at presentation?

What is the most commonsite of distant metastasis inrenal cell carcinoma?

What is the most commonsolid renal tumor ofchildhood?

What type of renal stone isradiolucent?

What are posterior urethralvalves?

What is the most commonintraoperative bladder tumor?

What provides drainage of the left gonadal (e.g., testicular) vein?

T the susceptibility to blunt traumac the ease of follow-up examinations

Periurethral

Periphery

Osteoblastic (radiopaque)

�33%

Lung

Wilms’ tumor

Uric acid (Think: Uric � Unseen)

Most common obstructive urethral lesionin infants and newborns; occurs only inmales; found at the distal prostatic urethra

Foley catheter—don’t fall victim!

Left renal vein


What provides drainage ofthe right gonadal vein?

What are the signs ofurethral injury in thetrauma patient?

What is the evaluation forurethral injury in the traumapatient?

What is the evaluation for a transected ureterintraoperatively?

What aid is used to helpidentify the ureters in a previously radiatedretroperitoneum?

How can a small traumaticEXTRAperitoneal bladderrupture be treated?

How should a traumaticINTRAperitoneal bladderrupture be treated?

What percentage of patientswith an injured ureter willhave no blood on urinalysis?

What is the classic historyfor papillary necrosis?

What is Fournier’s gangrene?

What unique bleeding problem can be seen withprostate surgery?

What is the scrotal “bluedot” sign?


IVC

“High-riding, ballottable” prostate, bloodat the urethral meatus, severe pelvic fracture, ecchymosis of scrotum

RUG (Retrograde UrethroGram)

IV indigo carmine and then look for leakof blue urine in the operative field

Ureteral stents

Foley catheter

Operative repair

33%

Patient with diabetes taking NSAIDs orpatient with sickle cell trait

Necrotizing fasciitis of perineum, polymicrobial, diabetes � major risk factor

Release of TPA and urokinase (treat with�-aminocaproic acid)

Torsed appendix testis


What is Peyronie’s disease?

What is a ureterocele?

What is a “three-way”irrigating Foley catheter?


Curved penile orientation with erectiondue to fibrosis of corpora cavernosa

Dilation of the ureter—treat with endoscopic incision or operative excision

Foley catheter that irrigates and thendrains

Irrigationinlet

3-way Foley catheter

Containerof irrigationfluid

Irrigantoutlet


Rapid Fire Power Review

767

1. Elderly woman, SBO,and air in biliary tract

2. Elderly woman withpain down inner aspectof thigh

3. Abdominal pain,hypotension, andabdominal pulsatilemass

4. Abdominal pain “out of proportion” toabdominal exam

5. Arm pain and syncopewith arm movement

6. Increasing creatinine on ACE inhibitor

7. Child with MIDLINEneck mass

8. Child with LATERALneck mass

9. Crush injury and darkurine

10. Emesis, chest painradiating to back, andmediastinal air

11. Lower GI bleed � technetium pertechnetate scan

Gallstone ileus

Obturator hernia (Howship-Romberg sign)

Ruptured abdominal aortic aneurysm(AAA)

Mesenteric ischemia

Subclavian steal syndrome

Renal artery stenosis

Thyroglossal duct cyst

Branchial cleft cyst

Myoglobinuria

Boerhaave’s

Meckel’s diverticulum

TOP 100 CLINICAL SURGICAL MICROVIGNETTES

LWBK758-BM_p767-775.qxd 16/03/2011 02:28 PM Page 767 Aptara

12. Flushing, diarrhea, and right-sided heartfailure

13. Pneumaturia and LLQpain

14. Desmoid tumor, oste-oma, and colon cancer

15. Epigastric pain radiating to back andflank ecchymosis

16. Pancreatitis and palpable epigastric mass

17. Liver abscess with“anchovy paste”

18. RUQ pain, travel, andexposure to sheep

19. Caput medusa

20. 45-year-old woman withRUQ pain for 12 hours,fever, and leukocytosis

21. Elderly man with largenontender palpablegallbladder

22. Female taking birth con-trol pills with liver mass

23. Liver tumor with “central scar”

24. Pancreatic mass, gallstones, diabetes,and diarrhea

25. RUQ bruit and CHF inyoung adult

768 Rapid Fire Power Review

Carcinoid

Colovesicular fistula

Gardner’s syndrome

Hemorrhagic pancreatitis

Pancreatic pseudocyst

Amebic abscess

Hydatid cyst

Portal hypertension

Acute cholecystitis

Pancreatic cancer (Courvoisier’s sign)

Hepatic adenoma

Focal nodular hyperplasia

Somatostatinoma

Liver hemangioma


26. Excruciating pain withbowel movement

27. Abdominal pain, diar-rhea, and anal fistulae

28. EKG with “peaked” T waves

29. Buccal mucosa withpigmentation

30. LLQ pain, fever, andchange in bowel habits

31. Elevated urine 5-HIAA

32. Institutionalized, abdo-minal pain, vomiting,and distention, withproximal colonic dilation

33. Infant with projectilevomiting

34. Newborn with failureto pass meconium infirst 24 hours

35. Infant with biliousvomiting

36. Newborn with abdominal defect andumbilical cord on sac

37. Teenager with kneepain and “onionskinning” on x-ray

38. Pulmonary capillarywedge pressure �18,CXR with bilateral pul-monary infiltrates, andPaO2:FiO2 ratio �200

Anal fissure

Crohn’s disease

Hyperkalemia

Peutz-Jeghers syndrome

Diverticulitis

Carcinoid

Sigmoid volvulus

Pyloric stenosis

Hirschsprung’s

Malrotation

Omphalocele

Ewing’s sarcoma

Acute respiratory distress syndrome(ARDS)

Rapid Fire Power Review 769


39. Increased peak airwaypressure, low urineoutput, and urinarybladder �25 mmHg

40. Newborn with inabilityto “pass an NGT”

41. Traumatic blinding in one eye followed by blindness in thecontralateral eye 2 weeks later

42. Mitotic pupil, ptosis,and anhydrosis

43. Traumatic head injury, conscious in ER followed byunconsciousness

44. “Worst headache of mylife”

45. Hematuria, flank pain,and abdominal mass(palpable)

46. 60-year-old white man with painlesshematuria

47. RUQ pain, jaundice,and fever

48. Epigastric pain radiating to back, withnausea and vomiting

49. Chest pain radiating toback and described asa “tearing” pain


Abdominal compartment syndrome

Esophageal atresia

Sympathetic ophthalmia

Horner’s syndrome

Epidural hematoma (“lucid interval”)

Subarachnoid hemorrhage

Renal cell carcinoma

Bladder cancer

Cholangitis

Pancreatitis

Aortic dissection


50. 40-year-old man with tachycardia/hypertension and confusion on postoperative day #2

51. Marfanoid body habitusand mucosal neuromas

52. Psammoma bodies

53. Sulphur granules

54. Thyroid tumor withAMYLOID tissue

55. PALPABLE neck tumorand hypercalcemia

56. Hypertension,diaphoresis (episodic),and palpitations

57. Jejunal ulcers

58. Pituitary tumor,pancreatic tumor, andparathyroid tumor

59. Necrotizing migratoryerythema

60. Medullary thyroid cancer, pheochro-mocytoma, and hyperparathyroidism

61. Hypokalemia refractoryto IV potassium supplementation

62. Newborn withpneumatosis

63. Child with abdominalmass that crosses midline

Alcohol withdrawal

MEN II-b

Papillary thyroid cancer

Actinomyces infection

Thyroid medullary cancer

Parathyroid cancer

Pheochromocytoma

Zollinger-Ellison syndrome

MEN- I

Glucagonoma

MEN-IIa

Hypomagnesemia

Necrotizing enterocolitis (NEC)

Neuroblastoma



64. Child �4 years of agewith abdominal tumorthat does NOT crossmidline

65. “Currant jelly” stoolsand abdominal colic

66. Femur fracture, respiratory failure,petechiae, and mentalstatus changes

67. Hearing loss, tinnitus,and vertigo

68. Adolescent boy withnasal obstruction andrecurrent epistaxis

69. Child �5 years of agesitting upright anddrooling, with “hot-potato” voice

70. Angina, syncope, andCHF

71. Tobacco use, asbestosexposure, and pleuriticchest pain

72. Supracondylar fractureand contracture offorearm flexors

73. Tibia fracture, “pain outof proportion,” pain onpassive foot movement,and palpable pulses

74. 25-year-old man withliver mass with fibrousseptae and NO historyof cirrhosis or hepatitis


Wilms’ tumor

Intussusception

Fat embolism

Ménière’s disease

Juvenile nasopharyngeal angiofibroma

Epiglottitis

Aortic stenosis

Mesothelioma

Volkmann’s contracture

Compartment syndrome

Fibrolamellar hepatocellular carcinoma


75. EKG with flattening ofT waves and U waves

76. Central pontine myelinosis

77. Polydipsia, polyuria,and constipation

78. Factor VIII deficiency

79. Abdominal pain, fever, hypotension,HYPERkalemia, andHYPOnatremia

80. Massive urine outputand HYPERnatremia

81. Increased urine osmolality,HYPOnatremia, andlow serum osmolality

82. IV antibiotics, fever,diarrhea

83. Bleeding gums andwound dehiscence

84. Fever, central line, andHYPERglycemia

85. Appendectomyfollowed by fever andabdominal pain on post-operative day #7

86. Advancing crepitus,fever, and blood blisters

87. High INTRAoperativefever

88. Confusion, ataxia, andophthalmoplegia

Hypokalemia

Too-rapid correction of hyponatremia

Hypercalcemia

Hemophilia A

Adrenal insufficiency (Addisonian crisis)

Diabetes insipidus

SIADH

Clostridium difficile pseudomembranouscolitis

Vitamin C deficiency

Central line infection

Peritoneal abscess

Necrotizing fasciitis

Malignant hyperthermia

Wernicke’s encephalopathy



89. Tracheal deviation,decreased breathsounds, and hyperresonance

90. Hypotension, decreasedheart sounds, and JVD

91. Four ribs broken intwo places andpulmonary contusion

92. Otorrhea (clear) andBattle’s sign

93. Ulcer and decreasedpain with food

94. Vomiting, retching, andepigastric pain

95. Fever on postoperativeday #1, with “bronze”weeping, tender wound

96. Hematochezia andtenesmus

97. Upper GI bleed, jaundice, and RUQpain

98. Gallstones, epigastricpain radiating to back,and nausea

99. 18-year-old womanwith bloody nipple discharge

100. Irritability, diaphoresis,weakness, tremulousness,and palpitations


Tension pneumothorax

Pericardial tamponade

Flail chest

Basilar skull fracture

Duodenal ulcer

Mallory-Weiss tear

Clostridial wound infection

Rectal cancer

Hemobilia

Gallstone pancreatitis

Ductal papilloma

Insulinoma


Chapter 6 (Poole sucker)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:55.Chapter 6 (Gigli saw)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:51.Chapter 10 (carotid endarterectomy)Lawrence PF, Bell RM, Dayton MT. Essentials of General Surgery. 3rd ed. Philadelphia, PA: LippincottWilliams & Wilkins; 2000:545.Chapter 14 (Pringle maneuver)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:93.Chapter 14 (percutaneous endoscopic gastrostomy)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:55.Chapter 30 (craniocaudal view and MLO view mammograms)Gay SB, Woodcock RJ Jr. Radiology Recall. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:522.Chapter 30 (free air seen on chest radiograph)Lawrence PF, Bell RM, Dayton MT. Essentials of General Surgery. 3rd ed. Philadelphia, PA: LippincottWilliams & Wilkins; 2000:267, Fig 7-19A.Chapter 38 (anatomy of the larynx)Doherty GM, Meko JB, Olson JA, et al. The Washington Manual of Surgery, 2nd ed. Philadelphia, PA: LippincottWilliams & Wilkins; 1999:635, Fig 42-6.Chapter 38 (pneumothorax)Daffner RH. Clinical Radiology. The Essentials. 2nd ed. Baltimore, MD: Williams & Wilkins; 1999:154, Fig 4-91B.Chapter 38 (widened mediastinum)Greenfield LJ, Mulholland MW, Oldham KT, et al. Surgery: Scientific Principles and Practice. 3rd ed. Philadelphia,PA: Lippincott Williams & Wilkins; 2001:330, Fig 11-40.Chapter 56 (rectus abdominis flap reconstruction)Greenfield LJ, Mulholland M, Oldham KT, et al. Surgery: Scientific Principles and Practice. 2nd ed. Philadelphia, PA:Lippincott-Raven; 1997:2238, Fig 114-4.Chapter 40 (Sengstaken-Blakemore balloon)Lawrence PF, Bell RM, Dayton MT. Essentials of General Surgery. 3rd ed. Philadelphia, PA: LippincottWilliams & Wilkins; 2000:353, Fig 18-8.Chapter 42 (lap-band)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:329.Chapter 52 (French system)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:137.Chapter 52 (liver segments)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:137.Chapter 57 (gastrinoma triangle)Greenfield LJ, Mulholland M, Oldham KT, et al. Surgery: Scientific Principles and Practice. 2nd ed. Philadelphia,PA: Lippincott-Raven; 1997:924, Fig 34-8.Chapter 56 (mammogram showing breast cancer)Daffner RH. Clinical Radiology: The Essentials. 2nd ed. Baltimore, MD: Williams & Wilkins; 1999:245, Fig 6-9A.Chapter 66 (endovascular repair)Zelenock GB, Huber TS, Messina LM, et al. Mastery of Vascular and Endovas-cular Surgery. Philadelphia, PA:Lippincott Williams & Wilkins; 2005.Chapter 74 (Colles’ fracture)McKenney MG, Mangonon PC, Moylan JA. Understanding Surgical Disease: The Miami Manual of Surgery. Philadel-phia PA: Lippincott-Raven; 1998:355, Fig 4.Chapter 74 (Lachman test)Redrawn from Spindler KP, Wright RW. “Anterior Cruciate Ligament Tear.” N Engl J Med November 13, 2008;359:2135, Fig 2.Chapter 75 (Kocher’s point)Spector SA. Clinical Companion in Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 1999:430, Fig 33-1.Chapter 75 (bitemporal hemianopsia)Blackbourne, LH. Advanced Surgical Recall, 3rd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2007:747.

Figure Credits

775


776

AA BEAP acronym, 348A-C mode, 487A-gram, 337, 493A PIE SACK acronym, 339A-V block, 670–671AAAs (abdominal aortic aneurysms), 41, 89,

208, 500–505, 514, 767AB blood, 125Abbreviations, 10, 15–18ABCDs of melanoma, 25, 472Abdomen

examination of, 235–236pain related to, 203–204, 206, 207pediatric patients, 532–533sutures, 62traumatic injuries to, 37, 235, 238, 240wound dehiscence, 92

Abdominal aortic aneurysms (AAAs), 41, 89,208, 500–505, 514, 767

Abdominal compartment syndrome,154–155, 770

Abdominal fascia closure, 62Abdominal pain, 203, 204, 206, 207Abdominal perineal resection (APR),

314Abdominal wall

defect in, 548–550layers of, 106, 214

Abdominal x-rays, 185–190AAA on, 502in acute abdomen, 205double bubble sign, 571eggshell calcifications, 514gallstone ileus on, 378gasless abdomen on, 530Hirschsprung’s disease on, 544liver cysts on, 356pancreatitis on, 383, 384reading of, 185small bowel obstruction on, 36, 287

Abduction, 578, 691ABI (ankle to brachial index), 493Abrasions, 575Abscesses, 18, 170

abdominal, 208breast, 417–418drainage of, 72hepatic, 354–356lung, 624

pancreatic, 390pelvic, 175peritoneal, 174–175, 773peritonsillar, 606postoperative fever and, 181spinal epidural, 738–739

Absorbable sutures, 54Absorption atelectasis, 158AC/DC AVA PAIN DUD acronym, 13Accessory spleen, 459, 462ACE inhibitors, 137, 513Acetaminophen (Tylenol®), 137Acetylcholine, 199ACH acronym, 244Achalasia, 641–642Achilles tendon rupture, 707–708Achlorhydria, 19Acholic stool, 19Acid burns, 246ACL (anterior cruciate ligament), 690, 706,

707Acoustic neuromas, 619Acral lentiginous histology, 473ACTH (adrenocorticotropic hormone), 419,

420, 421Actinic keratosis, 471Actinomyces, 179, 771Active range of motion (AROM), 691Acute abdomen, 203–209Acute acalculous cholecystitis, 374–375Acute appendicitis, 203Acute arterial occlusion, 498–500Acute cholecystitis, 373–374, 768Acute gastritis, 255Acute respiratory distress syndrome

(ARDS), 32, 39, 484, 769Acute rhinitis, 601Acute suppurative otitis media, 593–595,

620Addisonian crisis, 147–148, 209, 773Addison’s disease, 119, 428Adduction, 578, 691Adeno-, 19Adenocarcinomas

Barrett’s esophagus and, 273gallbladder, 378–380gastric, 277small bowel, 290

Adenocellular cancer, 603Adenoid cystic carcinoma, 609

Index

LWBK758-IND_p776-808.qxd 16/03/2011 10:00 AM Page 776 Aptara

Adhesions, 19, 144–145Adjuvant RX, 197Admission orders, 12–13Admission orders/postop orders, 13Adnexa, 19Adolescents, dietary requirements, 518Adrenal adenoma, 421, 427Adrenal carcinoma, 421Adrenal crisis, 183Adrenal gland, 418–428, 564Adrenal hyperplasia, 427Adrenal incidentaloma, 422–423Adrenal insufficiency, 773Adrenocorticotropic hormone (ACTH), 419,

420, 421Adson maneuver, 622Adson pickup, 42, 44Advanced Trauma Life Support (ATLS),

226Advancement flaps, 577Adventitia, 19Afferent, 19Afferent loop syndrome, 32AFib (atrial fibrillation), 498, 507Aflatoxin, 352AFO (ankle foot orthotic), 691Afterload, 482, 649Aganglionic megacolon. See Hirschsprung’s

diseaseAI (aortic insufficiency), 648, 656–657AIDS, 207AIR acronym, 301Air trapping, 524Airway management, 227–228Albumin, 123, 161, 251Albumin-furosemide sandwich, 123Albuterol, 115, 116, 136Alcohol intake, 36, 157, 619Alcohol withdrawal, 183, 771Alcoholism, 358Aldosterone, 427-algia, 19Alkali burns, 246Alkaline phosphatase, 365Allen’s test, 26, 150Allergic rhinitis, 601Allis clamps, 49Allograft bone, 691Allografts, 672�-cells, 383�-fetoprotein, 197, 353, 568, 756A.M. RUM acronym, 705Amaurosis fugax, 19, 506Ambulation, prophylactic, 181Amebiasis, 175Amebic abscess, 768Amelantoic melanoma, 473American College of Surgeons, 226

American Joint Committee for Cancer(AJCC)

bladder cancer staging, 750lung carcinoma staging, 629–630melanoma staging, 473–474prostate cancer staging, 753RCC staging, 749sarcoma stages, 466testicular cancer staging, 757

Aminocaproic acid, 654Aminoglutethimide, 422Aminoglycosides, 130, 1315�-Aminosalicylate, 343Amiodarone, 450Ammonia levels, 363Amoebic infections, 131Amoxicillin, 131Amphotericin, 132Ampicillin, 131, 179Ampicillin-sulbactam (Unasyn®), 177AMPLE acronym, 242Ampulla, 19Amputation, lower extremity, 497Amyand’s hernia, 213Amylase, 144, 398Amylase/lipase test, 388, 390Anaerobic infections, 130, 132, 177Anal cancer, 326–335Anal fissures, 36, 330–331, 571,

769Anal fistulae, 28–29Analgesia, epidural, 193Analgesic, definition of, 19Anaphylactic shock, 169Anaplastic carcinoma, thyroid,

447–448Anastomosis, 19, 80Anatomic snuff box, 583, 702Ancef®, 137, 177Androgen ablation therapy, 753Anemia

preop testing, 81splenectomy for, 460

Anergy, 161Anesthesia, 190–195Aneurysmal bone cysts, 714Aneurysms. See also Pseudoaneurysms

AAAs, 41, 89, 208, 500–505, 767description of, 490femoral artery, 515iliac artery, 515popliteal artery, 514–515splenic artery, 513–514thoracic aorta, 665–677

Angio-, definition of, 19Angiocatheters, 172Angiodysplasia, small bowel,

293

Index 777


Angiogramsfor arterial occlusion, 498limitations of, 502pulmonary, 190renal artery stenosis, 513

Angiosarcoma, 350, 464Anion gap, 478Ankle foot orthotic (AFO), 691Ankle to brachial index (ABI), 493Annular pancreas, 397, 562Anomaly, definition of, 19Anorectal fistulas, 329Anorectal malformations, 542–543Anosmia, definition of, 586Ansa cervicalis, 588Anterior cord syndrome, 728Anterior cruciate ligament (ACL), 690, 706,

707Anterior spinal syndrome, 105, 504Antibiotics, 130–132

in appendicitis, 297for burn victims, 252–253preoperative, 81, 137prophylactic, 177topical, 252triple, 179wound infections and, 182

Anticholinesterase inhibition, 194Antidiuretic hormone (ADH), 148–149Antigen-presenting cells, 673Antihypertensive medications, 80Antiseptic, history, 40Antithrombin III, 128Antithymocyte globulin (ATGAM), 675–676Antrectomy, 82, 259, 261, 265Anuria, 152Anus, 325–334, 542–543Aorta. See also AAAs

bifurcation of, 501coarctation of, 662–663traumatic injury to, 185, 235

Aortic dissection, 666–671, 770Aortic insufficiency (AI), 648, 656–657Aortic stenosis (AS), 648, 655–656, 772Aortic valve, 655–656, 659Aortobiliac graft, 503Aortoenteric fistula, 504Aphthous ulcer, 196Apley’s law, 571Apnea, 19, 534Appearance, 2Appendectomy, 86

complications of, 298history, 41intraoperative questions, 299–300laparoscopic, 297, 299preop antibiotics, 137

Appendiceal tumors, 300–301

778 Index

Appendicitis, 294–298, 552–554abdominal surgery and, 36acute, 203acute abdomen and, 205age at presentation, 572differential diagnosis, 291incidence of, 38McBurney’s sign in, 30obturator sign, 30presentation of, 294psoas sign, 31radiopaque fecaliths in, 39, 187referred pain from, 207risk of rupture, 39, 298RLQ pain in, 208Rovsing’s sign, 31

Appendix, 293–301. See also Appendicitiscarcinoids, 36location of, 105, 299removal of normal tissue, 38

Appendix testis, 747APR (abdominoperineal resection), 84APRV mode, 487APUD (amine-precursor uptake and

decarboxylation) tumor, 633ARDS. See Acute respiratory distress

syndromeArmy-Navy retractors, 52AROM (active range of motion), 691Arterial blood gases (ABG), 72, 479Arterial bypass, 490Arterial occlusion, acute, 498–500Arteries, anatomy of, 107, 491Arteriography, 493Arteriovenous malformations (AVMs), 734,

735Artery of Adamkiewicz, 105, 504Arthritis, 715–716Arthrodesis, 694Arthroplasty, 694Artificial valve placement, 659As and Bs, 571AS (aortic stenosis), 648, 655–656, 772ASD (atrial septal defect), 648Aspergillus, 590Aspiration, foreign body, 524–525Aspiration pneumonia, 142–143Aspirin, 125, 126, 136, 494ASS acronym, 326Atelectasis, 19, 37, 138–139, 158, 180, 181ATGAM (antithymocyte globulin), 675–676Atherosclerosis, 489–490, 500–501, 512Ativan®, 724Atrial fibrillation (AFib), 498, 507, 669Atrial septal defect (ASD), 648Augmentin®, 130, 131Auricle, 591Austin Flint murmur, 671


Autografts, 671Autoimmune hemolytic anemia, 460Autologous vein graft, 496Avascular necrosis (AVN), 691AVMs (arteriovenous malformations), 734,

735AVN (avascular necrosis), 691AVOID WTE acronym, 14Avulsion fractures, 698Ax fem, 89Axilla, anatomy of, 399–401Axillary artery, 89Axillary nerve, 704Axillary vein, 399, 400Azathioprine (AZA [Imuran®]), 343,

674Aztreonam (Azactam®), 130, 132

BB cells, 673B FDR acronym, 33, 302Babcock clamps, 46Back, 62, 234“Backwash” ileitis, 340Bacteremia, 170Bacteroides fragilis, 36, 131, 178Balanitis, 746Balanoposthitis, 746Ballance’s sign, 26, 459Banana bag

See Rally packBandage scissors, 44Bariatric, definition of, 19Bariatric surgery, 281–283Barium enemas, 321Barium swallow exam, 641Barlow’s maneuver, 719Barrett’s esophagus, 26, 272–273, 645Basal cell carcinoma, 469, 470Basal energy expenditure (BEE), 161BASE acronym, 169Basilar skull fractures, 31, 234, 722, 774Basilizimab, 676Bassini herniorrhaphy, 83Bassini procedure, 216Batson’s plexus, 752Batteries, ingestion of, 572Battle’s sign, 26, 234, 722Beck’s triad, 27, 230–231Beckwith-Wiedemann syndrome, 564Behçet’s disease, 516Bell clapper deformity, 744, 758Bell’s palsy, 596–597, 617–618Belsey Mark IV, 274, 645BEMOAN acronym, 151Benign, definition of, 197Benign prostatic hyperplasia (BPH), 747,

754–755, 764

Bennett’s fractures, 699Benzodiazepines, 137, 138, 195, 724Bergman’s triad, 27Berry aneurysms, 734Beta-human chorionic gonadotropin

(�-HCG), 756�-cells, 38311�-hydroxylase, 422Betadine® (povidone-iodine),

9, 575�-blockers, 81Bicarbonate mucus, 199Bifurcation, definition of, 19Bile, 111, 202, 365Bile acids, 199, 200, 365Bile ducts

cancer of, 380cholangiocarcinoma of, 367obstruction of, 208, 369

Bile salts, 20, 162Bili-, definition of, 20Biliary atresia, 559–560Biliary colic, 367, 371Biliary stasis, 374Biliary tract, 364–381

anatomy, 364–365diagnostic studies, 368evaluation of, 188pathophysiology of, 366–368pediatric, 558–562physiology, 365–366sutures used in, 55

Bilirubin, 366, 381, 390Billroth I procedure, 82, 265Billroth II procedure, 32, 82, 266Biloma, 368, 369Biobrane®, 249“Bird’s beak” sign, 187Birth control pills, 350Bitemporal hemianopsia, 733Bites

cat, 582dog, 246, 582human, 178, 246, 582

Bladdercancer of, 750–751, 770fistulas, 307pheochromocytoma of, 424rupture of, 242tumors of, 9

Bleeding, external, 232Blepharoplasty, 572Blind loop syndrome, 33, 146Blisters, removal of, 249Blood pressure, 232, 484. See also

Hypertension; HypotensionBlood transfusions, 36, 124, 126Blood types, 125

Index 779


Blood urea nitrogen (BUN), 255Blood volume, 108, 517, 518Blount’s disease, 720Blowout fractures, 617Blue dot sign, 536Blue toe syndrome, 515Blumer’s shelf, 27, 276Blunt esophagectomy, 647Blunt force trauma, 245, 246Boas’ sign, 27, 371Bochdalek hernia, 530–531Body fluid compartments, 107Body fluids, 108, 110, 112–114Body mass index, 281–282Body temperature, 193Body weight, 107, 108, 517Boerhaave’s syndrome, 33, 269–270,

767“Bogata Bag,” 155Boils, 20Boley modification, 546Bolus, definition, 113Bones. See also Fractures; Specific bones

pain related to, 711pediatric vs. adult, 716

Bookwalter retractors, 52Borchardt’s triad, 27, 281Bouchard’s nodules, 715Boutonniere deformity, 583Bovie electrocautery, 20, 40, 50, 129Bowel prep, 81, 182, 313Bowen’s disease, 326, 471Boxer’s fractures, 582, 699BPH (benign prostatic hyperplasia), 747,

754–755, 764Brachial plexus, 705Brachytherapy, 197Brain, tumors of, 630, 730Branchial cleft anomalies, 522–523Branchial cleft cysts, 523, 767BRCA genes, 401Breast

abscesses, 417–418anatomy of, 399–401benign disease, 415malignant disease of, 399–418

Breast cancer, 399–418in American women, 39hypercalcemia and, 457infiltrating ductal, 35in men, 414–415sites, 36

Breast milk, calories in, 518Breast self-exams, 403–404Breathing, 111, 228–231Bromocriptine, 734Bronchogenic carcinoma,

627–631

780 Index

Bronchoscopy, 250, 633Brooke formula, 250Brooke ileostomy, 83, 285Brown-Séquard syndrome, 729Brown’s sign, 620Bucket-handle tears, 707Budd-Chiari syndrome, 33, 360Buerger’s disease, 515Bulbocavernous reflex, 169Bullous myringitis, 593Bupivacaine (Marcaine®), 191, 192Burn center referrals, 248Burn shock, 250Burns, 246–254

antibiotics for, 252–253basal energy expenditure in, 161contraction of, 574–575epithelialization of, 574levels of injury, 247severity of, 247wound infections, 251

Butyrate, 164Bypass surgery, 125

CC-collars, 724C HOBBS acronym, 386C-Kit marker, 280C-spine, trauma studies, 237CA 19-9, 197, 395CABG (coronary artery bypass grafting), 41,

89, 648, 651–652CAD (coronary artery disease), 268, 648,

650–660Caffeine, 417Cajal cells, 280Calcaneus fractures, 704Calcitonin, 441, 446Calcium

absorption of, 201, 453inotropic function, 123IV, 115levels after thyroidectomy, 448supplementation, 119

Calcium oxalate stones, 761Calculi, definition of, 20Calculus disease, 760–762Calmette-Guérin bacillus, 751Calories

adolescent requirements, 518in breast milk, 518child requirements, 518daily dietary requirements, 160infant requirements, 518premature infants requirements, 518

Calot’s node, 105, 364Calot’s triangle, 104, 364, 365CAN I CHURP acronym, 463


Cancer. See also Specific cancersafter transplants, 689–690in children, 570spread of, 312

Candida, 390, 590Candidiasis, 171Cantle’s line, 105, 345Captopril provocation test, 513Caput medusae, 359, 360Carbohydrate, 484Carbohydrate antigen (CA) 19-9, 197, 395Carbohydrates, 161Carbolic acid, 40Carbon dioxide, 224, 484Carbon monoxide, 253Carboxyhemoglobin, 250Carbuncles, 20, 179Carcinoid syndrome, 27, 33, 302, 303, 768,

769Carcinoid triad, 27Carcinoid tumors, 301–305, 633–634Carcinoma of the gallbladder, 378–380Cardiac dysrhythmias, 246Cardiac index (CI), 477–478, 649Cardiac output (CO), 477, 483, 649, 650Cardiac tamponade, 27, 230–231, 653Cardiac tumors, 664Cardiogenic shock, 168Cardiopulmonary bypass (CPB), 41, 648,

653–655Cardiovascular surgery, 648–671Carotid artery stenosis, 509Carotid endarectomy (CEA), 509–511Carotid sheath, 511Carotid stenosis, 509Carotid ultrasound/Doppler, 509Carotid vascular disease, 508–510Carpal bones, 578Carpal spasm, 32Carpal tunnel syndrome, 584–585Cast saws, 709CAT URP acronym, 341Catamenial pneumothorax, 626Catecholamines, 423Catgut sutures, 54Catheter infections, 171–172Cauda equina syndrome, 737Caustic esophageal strictures, 645–646Cauterization, 20CB DIAL K acronym, 115CBC, left shift, 128CD3 receptors, 676CD25 antibodies, 676CD117, 280CEA (carotid endarterectomy), 41, 77, 83,

312CEA tumor marker, 197Cecal bascule, 324

Cecal volvulus, 324–325Cecum, 186, 546Cefazolin (Ancef®), 131Cefotetan®, 130, 177, 297Cefoxitin (Mefoxin®), 130, 137, 177, 297,

313Ceftazidime (Ceftaz®), 131Ceftriaxone (Rocephin®), 131Celiac trunk, 346Celiotomy, 20, 240CellCept®, 676–677Cellulitis, 132, 170Central cord syndrome, 729, 738Central lines, 102, 171–172, 253, 254, 773Central nervous system tumors, 570Central pontine myelinolysis, 118, 773Central venous pressure (CVP), 478Cephal-, definition of, 20Cephalosporins, 130, 131Cerebellar astrocytomas, 732–733Cerebral contusions, 726–727Cerebral perfusion pressure (CPP), 723Cerebrovascular accident (CVA), 151–152,

509Cervical disc disease, 737–738Cervical spine, 184, 237CHAFED LIPS acronym, 402CHAMPANZEES acronym, 119, 456Chance fractures, 730Charcot-Bouchard aneurysms, 735Charcot’s joint, 709, 716Charcot’s triad, 27, 375Chemical burns, 246Chenodeoxycholic acid, 372Chest, pediatric, 525–531Chest tubes, 94–99, 184Chest wall tumors, 622–623Chest x-ray, 183–185

in ARDS, 484in aspiration pneumonia, 143cardiogenic shock on, 168chest tube placement on, 95foreign body aspiration on, 524metastatic disease on, 312nasogastric tubes on, 244pneumothorax on, 229in pulmonary emboli, 141sarcomas on, 465trauma studies, 237traumatic thoracic aorta injury, 37

Chief cells, 199Chilaiditi’s sign, 188Child abuse, signs of, 570, 719Child’s-Turcotte-Pugh classification, 348Chimerism, 672Chloral hydrate, 569Chloride, daily requirements, 108Chloride ion absorption, 202

Index 781


Cholangiocarcinoma, 350, 367, 380–381,562

Cholangiograms, 684Cholangitis, 27, 31, 36, 367, 375–377Chole-, definition of, 20Cholecyst-, definition of, 20Cholecystectomy, 77, 86, 364, 368, 369, 562Cholecystitis, 207, 367, 373–375Cholecystokinin (CCK), 200, 201, 365Cholecystostomy tubes, 94Choledochal cysts, 560–562Choledocho-, definition of, 20Choledochojejunostomy, 80, 87, 368, 369Choledocholithiasis, 36, 367, 372, 374–375Cholelithiasis, 27, 38, 208, 366, 370–373,

562Cholesteatoma, 592Cholesterol stones, 202, 371, 372Chondroma, 622Chondrosarcoma, 713Choriocarcinoma, 757Chromaffin cells, embryonic, 426Chromium deficiency, 162Chronic pancreatitis, 387–388Chvostek’s sign, 27, 119, 120CI (cardiac index), 477–478, 649CIA acronym, 34, 495Cilastatin (Primaxin®), 132Cimetidine (Tagamet®), 135Ciprofloxacin (Cipro®), 130, 132, 136, 138,

297, 313Circulating nurses, 7Circulation, assessment of, 231–233Circumcision, contraindications, 569Circumflex artery, 650Cirrhosis, 352, 358, 359, 360Clamps, 42, 49Claudication, 492Clavulanic acid, 131Clay shoveler’s avulsion fracture, 699Clay shoveler’s fracture, 730“Clean” wounds, 172–173Cleido-, definition of, 20Clindamycin, 130, 131, 136, 177Clinic notes, 15Clips, 130Clonidine rebound, 138Clopidogrel (Plavix®), 125Closed fractures, 695Closed reduction, 692Clostridial myositis, 175–176Clostridium spp., 172

C. difficile, 132, 156, 176C. perfringens, 176C. tetani, 179

Clotting factors, 124, 127CO (cardiac output), 469, 477, 483, 650COA acronym, 183

782 Index

COAG mode, 129Coarctation of the aorta, 662–663Coffee bean sign, 324Coin lesions, 631–633Colic, 20, 203Colles’ fractures, 698Colloids, 20, 123, 251Colon

anatomy of, 106, 308–309blood supply, 308diverticular disease of, 319–325electrolyte absorption in, 202nutrient of, 162perforation of, 29polyps of, 315–317preop preparation, 81, 137purpose of, 201volvulus, 37

Colon cancer, 37, 38, 126, 197, 314Colonic feculent fluid, 109Colonic fistulas, 306–307Colonic ischemia, 503–504Colonic villous adenoma, 39Colonic volvulus, 322Colonoscopy, 20, 336, 504Colony-forming units (CFUs), 171Colorectal carcinoma, 309–315Colostomy, 20, 80, 284, 545Colovesicular fistulas, 306, 321, 768Coma, GCS scoring, 722Comedo DCIS, 412Comminuted fractures, 695Common bile duct, 27, 34, 36, 189Communicating hydrocele, 535, 744Communicating hydrocephalus, 740Communication with patients, 80Compartment syndrome, 33, 236, 499–500,

702–704, 772abdominal, 154–155

Complete blood count (CBC) shift, 205Complete hernias, 210Compliance, 482, 649Computed tomography (CT)

abdominal scans, 208, 238C-spine views, 184gallstone ileus on, 378of pancreas, 389pancreatic pseudocysts on, 392in pancreatitis, 384for pulmonary emboli, 190reading of, 185

Condé catheter, 744Congenital diaphragmatic hernias, 530–531Congenital heart disease, 660–664Congenital hip dislocation, 719Congenital pyloric stenosis, 538–540Congestive heart failure (CHF), 123Conjoint tendon, 219


Conn’s syndrome, 426–428Consent, 80Constipation, 20, 144, 207, 533“Contaminated” wounds, 173Contractility, definition of, 482Contrast media, 189Contusions, 575COOL CAR acronym, 301Cooper’s hernia, 213Cooper’s ligaments, 220, 401, 403Cor pulmonale, 21Cord lipomas, 218, 536Cordis, 102Coronary artery bypass grafting (CABG),

41, 89, 648, 651–652Coronary artery disease (CAD), 268, 648,

650–660Coronary ligament, 345Coronary vein, 106Corrigan’s pulse, 656Corticosteroids, 674Corticotropin-releasing hormone (CRH),

419Cortisol, 33, 419–422, 674Costochondritis, 35Coudé catheters, 101Cough reflex, 193Coumadin, 128, 289Courvoisier’s gallbladder, 381Courvoisier’s law, 27Courvoisier’s sign, 395, 768CPAP mode, 487CPB (cardiopulmonary bypass), 648, 653–655CPP (cerebral perfusion pressure), 723Cranial nerves, 586–589, 724Craniosynostosis, 742Creatinine levels, 681–682Crepitus, 235CRH, 419Cricoid pressure, 191Cricothyroidotomy, 85, 242, 618Crigler-Najjar syndrome, 558Crocodile tears, 620Crohn’s disease, 35, 289, 300, 328, 339–344,

769Cronkhite-Canada Syndrome, 319Croup (laryngotracheobronchitis), 610–611,

619, 620Cruveilhier-Baumgarten bruit, 359Cryoprecipitate (cryo), 124Cryptorchid testicles, 569Cryptorchidism, 535, 746, 755–756Crystalloid, administration of, 250Cullen’s sign, 28, 389Curettage, 21Curling’s ulcer, 196, 251, 254, 262Cushing, Henry, 40Cushing’s reflex, 723

Cushing’s syndrome, 33, 419–422Cushing’s triad, 28Cushing’s ulcer, 196, 262CUT mode, 129Cut-off sign, 186Cutting needles, 56CVA (cerebrovascular accident), 151–152, 509CVP (central venous pressure), 478Cyanide toxicity, 482Cyanotic heart disease, 664Cyclooxygenase inhibition, 125Cyclosporine A (CSA), 675Cyproheptadine, 304Cystic fibrosis, 542Cystic hygroma, 524Cystine stones, 761Cystogastrostomy, 393Cystograms, 743Cystosarcoma phylloides, 415–416Cystoscopes, 743Cysts, definition of, 21Cytomegalovirus (CMV), 689

DD cells, pancreatic, 201D COPS acronym, 550Daclizumab, 676DAI (diffuse axonal injury), 727Daily notes, 13–14Dakin solution, 42, 92“Damage control” surgery, 244Dance’s sign, 28, 570Dantrolene, 181, 193DCIS (ductal carcinoma in situ), 411–413DDAVP (desmopressin), 125, 127De Quervain’s thyroiditis, 451Dead gut, 187Dead space, 483Deaver retractor, 51DeBakey classification, 666–667DeBakey pickups, 8, 42, 43Decompression, nasogastric, 251Decubitus ulcers, 196Deep vein thrombosis (DVT), 29, 35, 140,

180, 181Defoxitin (Mefoxin®), 131Delayed primary closure (DPC), 55–56, 92,

245Delphian lymph node group, 439Deltopectoral flaps, 576Dental malocclusion, 235Dentate line, 327Depolarizing muscle blockage and, 194Dermatomes, 207, 721Desflurane, 191Desmoid tumors, 317, 318Dexamethasone, 189, 420, 674Dexamethasone suppression test, 420

Index 783


Dexon® sutures, 61Dextrose solutions, 111, 113Diabetes insipidus (DI), 149, 773Diabetes mellitus, 490, 650, 680, 684Diabetic ketoacidosis (DKA), 147, 209Diagnostic peritoneal lavage (DPL),

238–239Diaphragm, 106, 243Diaphragmatic irritation, 207Diaphysis, 694, 695Diarrhea, bloody, 156DIC, 153–154Dieulafoy’s ulcer, 196, 262Diffuse axonal injury (DAI), 246, 727Diffuse esophageal spasm, 642–643Digastric muscle, 510, 588DiGeorge syndrome, 453Digital arteries, 581Digital rectal examination (DRE),

745Digitalis, 137Digitalis toxicity, 117Dilaudid®, 137DIOS (distal intestinal obstruction

syndrome), 540Diphenhydramine hydrochloride

(Benadryl®), 137Direct bilirubin, 21Direct inguinal hernia, 213, 214“Dirty” wounds, 173Disability assessment, 233–234Dislocations, 692, 693, 705–706Dissociative agents, 191Distal interphalangeal (DIP) joint, 578, 583,

715Distal intestinal obstruction syndrome

(DIOS), 540Distal pancreatectomy, 244Disulfiram (Antabuse®), 131Diverticulitis, 208, 209, 306, 320–322, 769Diverticulosis, 319–320, 335Diverting proximal colostomy, 242Dobutamine, 481, 654Documentation

admission orders, 12–13admission orders/postop orders, 13clinic notes, 15daily notes, 13–14examination of extremities, 236ICU notes, 476–477informed consent, 80intensive care notes, 14–15NPO orders, 80operative notes, 11–12postoperative notes, 12preoperative notes, 11preoperative orders, 81prescriptions, 15

784 Index

progress notes, 13–14surgical notes, 9–15

Dog bites, 246Dopamine, 481Double-barrel colostomy, 284Double bubble sign, 571DPC (delayed primary closure), 55–56, 92,

245DPL (diagnostic peritoneal lavage),

238–239Drains, 62, 93–94DRE (digital rectal examination), 745Dressings, removal of, 92Dressler’s syndrome, 653Drop finger injury, 582Drug fever, postoperative, 180, 181Dry gangrene, 496Ductal papilloma, 774Ducts of Luschka, 364Ductus arteriosus, 519, 520Ductus venosus, 519, 520Duhamel procedure, 545Dumping syndrome, 33, 146–147, 259Duodenal atresia, 540Duodenal hematoma, 569Duodenal perforation, 259Duodenal ulcers, 36, 104, 254, 255,

257–260, 774Duodenoduodenostomy bypass, 562Duodenum, 243, 453Dupuytren’s contracture, 584, 709Dys-, definition of, 21-dysnia, 21Dyspareunia, 21Dysphagia, 21, 586Dyspnea, 448Dysrhythmias, 123Dysuria, 745

EEagle-Barrett’s syndrome, 570Ears, 234, 589–590, 591Ebstein’s anomaly, 664Ecchymosis, 21Echinococcus granulosus, 355Echocardiograms, 498ECMO (extracorporeal membrane

oxygenation), 520-ectomy, 21, 79Edema, compartment syndrome and, 33Edrophonium, 194EEA stapler, 49Efferent, definition of, 21Eikenella corrodens, 582Eisenmenger’s syndrome, 660Ejection fraction, 649Elbow, 705, 709Electrical burns, 246


Electrocardiograms (EKGs)for arterial occlusion, 498examples of, 670in hypercalcemia, 119in hyperkalemia, 115, 122in hypocalcemia, 120in hypokalemia, 116, 773preoperative, 81in pulmonary emboli, 141

Electrocautery, 40, 50, 73, 129Electrolytes

absorption in colon, 202cardiac, 650checking, 81daily loss of, 108deficiency in ileus, 36imbalances, 114–123

Embolectomy, 499Emboli, arterial occlusion and, 498Empiric, definition of, 170Encephalopathy, 363End colostomy, 284End-to-end anastomoses (EEA), 49Endarterectomy, 21Endocarditis, 182, 659–660Endocrine systems, 418–437Endoscopic retrograde

cholangiopancreatography (ERCP),368, 369, 373, 389, 392

Endovascular repairs, 491, 502, 505Enflurane, 191Entamoeba histolytica, 355Enteritis, 21Enterocutaneous fistulas, 305–306Enterograft fustulas, 503Enterohepatic circulation, 199Enterolysis, 21, 86Entrapment, 617Enuresis, 746, 762Environment, trauma patients and, 234Epidermal cysts, 73Epidermal inclusion cysts (EICs), 470Epididymitis, 745, 759Epidural analgesia, 193Epidural anesthesia, 190Epidural hematoma, 37, 236, 725, 770Epidural hemorrhage, 742Epigastric hernia, 213Epigastric pain, 206Epiglottitis, 611, 619, 620, 772Epinephrine (EPI), 192, 194, 481Epiphysis, 695Epispadias, 747Epitaxis, 600Epithelialization, 92, 574Erectile dysfunction, 747, 760Erythromycin, 177Eschar, 21, 251, 252

Escharotomy, 253Escherichia coli, 172, 178

ear infection, 590epididymitis and, 759liver abscesses and, 354in otitis media, 594in pancreatic abscesses, 390UTIs related to, 763

Esophageal atresia, 527–530, 770Esophageal carcinoma, 646–648Esophageal hiatal hernias, 220–223Esophageal reflux, 644–645Esophageal varices, 267–269, 359, 360Esophagus, 105

anatomy, 640–641diseases of, 640–648muscle fibers in, 202perforation of, 33, 37

Esthesioneuroblastoma, 619Estrogen receptors, 406Euvolemia, 118Eversion, 691Ewing’s sarcoma, 713, 714, 769Excisional biopsies, 22, 91Exophthalmos, 449Exploratory laparotomy, 88External oblique muscle aponeurosis,

217External pancreatic fistulas, 307Extra-anatomic bypass graft, 504–505Extracellular fluids, 107, 108Extracorporeal membrane oxygenation

(ECMO), 520Extralobar, definition of, 532Extremities

examination of, 236, 694radiography of, 244sutures, 62

Eyebrow lacerations, 242Eyes, 233, 234, 249, 721

FFace, sutures, 62Face lifts, 572Facial fractures, 615–617Facial nerve, 511Facial nerve paralysis, 595–596Facial vein, 510Factor IX, 127Factor V Leiden, 128Factor VIII, 127Faintness, 5, 6Falciform ligament, 345Fallopian tubes, 217, 536Familial adematous polyposis (FAP), 317Familial hypocalciuric hypercalcemia, 455Famotidine (Pepcid®), 136Fascia, definition of, 22

Index 785


Fascial dehiscence, 155Fasciotomy, 236, 704FAST exams, 238, 245FAST HUG acronym, 477Fat, calorie content, 161Fat emboli syndrome, 27, 772Fat necrosis, 386, 415Fat saponification, 386Fatty acid deficiency, 162FDR acronym, 27Fecal fat analysis, 388Fecaliths, 187, 294Feces, fluid losses, 111Felons, 179, 582Fem-distal bypass, 496Fem pop bypass, 88, 495Femoral artery, 88, 89, 218, 515Femoral canal, 220Femoral fractures, 702, 719Femoral hernia, 213, 219–220Femoral pulse, 231Femoral vein, 66Femoral vein catheters, 232Femoral vessels, 104FENa (fractional excretion of sodium),

152–153, 479–480Fentanyl, 195FESS (functional endoscopic sinus surgery),

603Fetal circulation, 519–520Fevers, 37, 158, 180, 251, 477Fibrin glue, 130Fibroadenoma, breast, 416Fibrocystic disease, breast, 415, 416–417Fibrolamellar hepatocellular carcinoma,

772Fibrolamellar hepatoma, 353Fibromuscular dysplasia, 512Fibroplasia, 574Fibrosarcoma, 464Fibrous dysplasia, 713Fibrous histiocytoma, 465Fibrous rib dysplasia, 622Figure-of-eight sutures, 129Fine needle aspirate (FNA), 441Fingers (phalanges), 578FiO2, 40, 160First-degree burns, 247, 249First-degree hemorrhoids, 333First lap appy, 41First lap chole, 41Fistula in ano, 328–330Fistulas, 22, 305–307, 398Fitz-Hugh-Curtis syndrome, 33, 180Fixation, definition of, 692FK506, 676Flagyl®. See MetronidazoleFlail chest, 230, 774

786 Index

Flaps, 576–578Flexor digitorum profundus (FDP), 581Flexor digitorum superficialis (FDS), 581Flow/pressure/resistance formula, 480Fluconazole (Diflucan®), 132Fludrocortisone, 148Fluid requirements, 108Fluid resuscitation, 569Flumazenil, 195Fluorescein, 249Focal nodular hyperplasia, 349, 351, 768Fog reduction elimination device (FRED),

225Fogarty catheters, 499Folate, Rally pack, 183Foley balloons, 68, 232Foley catheters, 9, 101–102, 155, 744

contraindications, 232, 236decompression using, 232definition of, 22embolectomy, 507epidural catheters and, 194irrigation of, 766placement of, 68precautions, 232–233

Folic acid, 741Follicular adenocarcinoma, 445–446Foot dorsiflexion, 691Foramen cecum, 520Foramen of Winslow, 271Foramen ovale, 519Forceps, 42, 43Foregut, 104Forehead flaps, 576Foreign body aspiration, 524–525Foreign body ingestion, 572Fossa of Geraldi, 536Fothergill’s sign, 28Fournier’s gangrene, 178, 744Fourth-degree burns, 247Fourth-degree hemorrhoids, 334Fox’s sign, 28, 390Fractional excretion of sodium (FENa),

152–153, 479–480Fractures, 695–700. See also Specific bones

description of, 694examination in, 694Gustilo-Anderson classification, 701–702Salter classification, 716–718unstable, 692

Frank-Starling curve, 482–483FRED (fog reduction elimination device), 225Free air, 38, 188, 205, 245“Free” flaps, 577French Fogarty catheter, 499French sizes, 103Frequency, 22, 745Fresh frozen plasma (FFP), 124


Frey procedure, 388Frey’s syndrome, 618, 620FRIEND acronym, 286FROM (full range of motion), 690FTSGs (full thickness skin grafts), 572, 576Full range of motion (FROM), 690Full thickness skin grafts (FTSGs), 572, 576Full weight bearing (FWB), 690Functional endoscopic sinus surgery

(FESS), 603Fungal infections, 132Furosemide (Lasix), 115, 136Furuncles, 22, 179FWB (full weight bearing), 690

GG cells, 199, 200, 271G-tubes, 93GA LAW acronym, 386Galeazzi fractures, 700Gallbladder

cancer of, 40, 378–380contraction of, 201emptying of, 200, 365evaluation of, 188fundus, 364hydrops of, 381infundibulum, 364laparoscopic removal, 86Murphy’s sign, 30porcelain, 40, 381

Gallstone ileus, 377–378, 767Gallstone pancreatitis, 389, 774Gallstones. See also Cholelithiasis

after weight reduction surgery, 283complications of, 371constituents of, 202cystic duct, 34pigmented, 371radiopaque, 39, 187risk factors, 370types of, 371

Gamekeeper’s thumb, 584Ganciclovir, 689Ganglion cysts, 582Gangrene, 496–497Gardner’s syndrome, 33, 317–318, 768Gastrectomy, 80, 278, 279Gastric acid, 260Gastric bypass, 282Gastric cancer, 262, 275–280, 279Gastric decompression, 233Gastric dilatation, 143–144Gastric mucosa, 292Gastric parietal cells, 164, 199, 271

199Gastric resection, 41Gastric secretions, 111

Gastric ulcers, 40, 195, 254, 260–262Gastric varices, 386, 462Gastric volvulus, 27, 281Gastrin, 199, 200–201, 432Gastrinoma triangle, 105Gastrinomas, 431–435Gastritis, stress-related, 266Gastrocolic fistulas, 307Gastrocolic reflex, 202Gastroduodenal artery, 36Gastroduodenostomy, 82Gastroenteritis, 207Gastroesophageal reflux disease (GERD),

272–275, 537–538, 642Gastrointestinal anastomosis (GIA), 47, 60Gastrointestinal stromal tumor (GIST), 280,

464Gastrointestinal tract

bleeding, 37, 38, 181, 532carcinoids, 36hormones, 199–202lymphoma of, 468malformations, 542pediatric tumors, 563–568retroperitoneal portions of, 103

Gastrojejunostomy, 80, 82, 259Gastronomy tubes, 93Gastropexy, 22Gastroschisis, 550–551Gastrostomy, 90, 284Gastrotomy, 80General anesthesia, 191General endotracheal anesthesia, 191Genitofemoral nerve, 218Gentamicin, 130, 132, 179GERD (gastroesophageal reflux disease),

272–275, 537–538, 642Gerota’s fascia, 103GET/GETA, 191GIA staplers, 47, 60Gigli saw, 48Gilbert’s syndrome, 381, 558GIST, 280, 464GIVES BAD CRAMPS acronym, 288Glasgow Coma Scores (GCSs), 233–234,

721–725Gleason scores, 752Glioblastoma multiforme (GBM), 731Gliomas, 731Glisson’s capsule, 345Globus, 586Glomus tumors, 582, 599–600Glottic lesions, 612Glottis, 611Gloves, 7, 40Glucagonoma, 771Glucagonoma tumors, 398–399, 430–431Glucose, 115, 121, 251

Index 787


Glucuronyl transferase, 381, 558Glutamine, 201Goiter, toxic multinodular, 442Gomco clamp, 744Gonorrhea, 33Goodsall’s rule, 28, 328–329Gout, 618Graham patch, 87, 259, 261, 263, 264Gram-negative infections, 130, 132, 178Granulation tissue, 575Graves’ disease, 449Great vessels, 235Greenfield filter, 141–142Greenstick fractures, 697Grey Turner’s sign, 29, 390Groin, 214–220, 232Groin flaps, 576Growth plate fractures, 718Grynfeltt’s hernia, 211Gubernaculum, 103, 217, 536Gunshot wounds, 240, 244Gustilo-Anderson classification, 701–702Gut, sutures, 61Gynecomastia, 414

HHaemophilus influenzae

epiglottitis and, 611, 620OPSS and, 461osteomyelitis and, 710in otitis media, 593vaccination for, 462

HAG acronym, 199“Halo” sign, 236Haloperidol (Haldol®), 136Halothane, 193HAM acronym, 247Hamartomas, 318, 633Hamburger sign, 553Hamman’s sign/crunch, 29, 269Hammerheads, 5Hands

anatomy of, 578–582“no man’s land,” 579sensory supply to, 579–584splinting of, 583steadiness of, 42surgery on, 578–585

Hangman’s fractures, 699, 729Haplotypes, 672Harmonic scalpels, 130Harrington retractors, 52Hartmann’s pouch, 89, 284, 365Hartmann’s procedure, 84, 321Hashimoto’s thyroiditis, 451Hasson technique, 225HAUL acronym, 681Hct, optimal, 126

788 Index

Head and neck surgery, 586–620Head injuries

basal energy expenditure in, 161traumatic, 721–727

Hearing loss, sensorineural, 597–598Heart

artificial valves, 41harvest to transplant times, 679tumors of, 664

Heart-lung transplantation, 41Heart transplantation, 41, 686–687Heberden’s nodes, 715Heel spurs, 709Heerfordt’s syndrome, 618Heimlich valves, 99Heineke-Mikulicz pyloroplasty, 87Helicobacter pylori, 256–257, 468Hemangiomas, 22, 349, 352, 570Hematemesis, 22, 254Hematochezia, 254, 311, 334Hematocrit, 39, 237Hematomas, 22, 235, 569, 584Hematuria, 746, 748, 750Hemicolectomy, 90, 300, 304Hemobilia, 356–357, 774Hemodialysis, 81, 153Hemophilia A, 127, 128, 773Hemophilia B, 127, 128Hemoptysis, 22, 624–625Hemorrhages, shock and, 165–166Hemorrhagic pancreatitis, 389–390, 768Hemorrhoidectomy, 334Hemorrhoids, 332–334, 360Hemostasis, 128–130Hemothorax, 22, 231Hemotympanum, 234, 722Henoch-Schönlein syndrome, 571Heparin, 133–134, 181, 654Hepatic adenoma, 768Hepatic artery, 202Hepatic hemangioma, 352Hepatic lobectomy, 349Hepatic vein thrombosis, 33Hepaticojejunostomy, 85, 368Hepatitis B virus (HBV), 352Hepato-, definition of, 22Hepatoblastoma, 350, 567–568, 572Hepatocellular adenoma, 349, 350–351Hepatocellular carcinoma, 350, 352–353, 772Hepatocytes, function of, 348Hepatomas, 197Hepatomegaly, 352Hereditary elliptocytosis, 460Hereditary nonpolyposis colon cancer

(HNPCC), 310Hernia sac, 217, 535Hernias, 209–223

common site of, 37


description of, 209groin, 214–220incidence, 209inguinal, 37, 533–537obturator, 29plug and patch treatment, 84reduction “en masse,” 210repair of, 80, 209review questions, 220–221small bowel obstruction and, 36, 289strangulation of, 209umbilical, 537

Herniorrhaphy, 22, 80, 83–84Herpes simplex virus (HSV), 689Hesitancy, 22, 746Hesselach’s hernia, 213Hesselbach’s triangle, 104, 214, 218, 219, 533Heterotopic grafts, 672Heterotopic pancreatic tissue, 398HFV mode, 487Hiatal hernia, 213Hiatus, 22Hickman® catheters, 102HIDA/PRIDA scan, 368, 375Hidradenitis, 22High ligation of hernias, 216Hill procedure, 274, 645Hindgut, 104Hip dislocation, 240, 705–706Hip replacement, 691Hirschsprung’s disease, 542–546, 769HIS FRIEND acronym, 305Histamine, 199Histamine (H2) blockers, 181, 434Histocompatibility antigens, 672–673, 678History, 9–10, 40–42HITT syndrome, 33Hodgkin’s disease, 467–468Hollenhorst plaque, 510Homan’s sign, 29, 140Horizontal mattress stitches, 57Hormone replacement therapy, 402Hormones, GI tract, 199–202Horner’s syndrome, 564, 628, 743, 770Howship-Romberg sign, 29, 221HTN. See HypertensionHuman chorionic gonadotrophin, 457Humeral fractures, 702“Hungry bone syndrome,” 458Hürthle cell thyroid cancer, 446Hydatid cysts, 355–356, 768Hydrocele, 535, 744, 756Hydrocephalus, 739–740Hydrocephalus ex vacuo, 740Hydrocortisone therapy, 133, 183Hydrops, gallbladder, 3815-hydroxyindoleacetic acid (5-HIAA), 303Hyperaldosteronism, 426–428

Hyperbilirubinemia, 558Hypercalcemia, 119, 453, 455, 457, 773Hypercapnia, diet in, 484Hypercholesteremia, 490Hyperglycemia, 113–114, 121, 424Hyperinflation, 524Hyperkalemia, 114, 115–116, 122, 123, 769Hypermagnesemia, 120Hypernatremia, 117Hyperparathyroidism (HPTH), 119, 453–457Hyperphosphatemia, 122Hypersplenism, 462Hypertension

atherosclerosis and, 490postoperative, 157preoperative medications, 80renal artery stenosis and, 512–513surgically-correctable, 463

Hyperthyroidism, 449Hypertrophic scars, 575Hyperventilation, 724Hypervolemia, 118Hyphema, traumatic, 234Hypoalbuminemia, 119Hypocalcemia, 27, 32, 119–120, 386Hypochloremic alkalosis, 109Hypogastric artery, 106Hypoglossal nerve, 511, 588, 589Hypoglycemia, 121Hypokalemia, 36, 116–117, 773Hypomagnesemia, 117, 120–121, 771Hyponatremia, 117–118, 118Hypophosphatemia, 122Hypospadiasis, 747Hypotension, 156, 193Hypoventilation, oxygen-induced, 159Hypovolemia

hyponatremia and, 117, 118normal blood pressure and, 232physiologic response to, 109shock and, 36, 165–166, 232vital signs in, 110

Hypoxia, causes of, 157Hytrin®, 755

II & D (incision and drainage), 88I CHOP acronym, 261I GET SMASHED acronym, 383I HOP acronym, 258IABP (intraaortic balloon pump), 648,

671ICP. See Intracranial pressureICP HEAD acronym, 724Icterus, 22ID tags, 6Idiopathic hypertrophic subaortic stenosis

(IHSS), 662

Index 789


IHSS (idiopathic hypertrophic subaorticstenosis), 662

Ileal conduit, 285Ileoanal pull-through, 90Ileocecal intussusception, 28Ileostomy, 23Ileum, 106, 162, 287Ileus

on abdominal x-rays, 186air-fluid level, 186causes of, 145definition of, 23electrolyte-mediated, 123hypokalemia and, 36

Iliac artery aneurysms, 515, 516Ilioinguinal nerve, 104, 217, 536IMA (internal mammary artery), 439, 649Imatinib, 280Imipenem®, 130, 132, 177Immunology basics, 672–673Immunosuppressed states, 174Immunosuppression, 673–677Impacted fractures, 697Imperforate anus, 542–543IMV mode, 486In situ, definition of, 197Incarcerated hernias, 209, 220Incentive spirometry, 158, 181Incidental Meckel’s diverticulectomy, 292Incidentaloma, 422–423Incisional biopsy, 23, 91Incisional hernia, 212Incisions, 73–77, 88Incomplete hernias, 210Incontinence, 746, 762–763Incus, 589Indirect inguinal hernias, 213, 215, 533–537Induction agents, 191Induration, 23Infants

blood volumes, 518constipation, 533dietary protein requirement, 518estimated blood volume, 517osteomyelitis in, 710otitis media in, 594

Infections, 170–180after transplants, 689signs of, 170

Infectious endocarditis, 659–660Inferior vena cava (IVC), 418Inflammation

signs of, 170wound healing and, 574

Inflammatory bowel disease (IBD), 338Inflammatory carcinoma, 403Infliximab, 343Informed consent, 80

790 Index

Inguinal hernias, 37, 77, 216–219, 533–537Inguinal ligament, 28, 217, 219, 390Inhalational anesthesia, 193Inhalational injury, 250Inner ear, 589INR (international normalized ratios), 124,

134–135Inspissated, definition of, 23Instrument knots, 61, 62, 63Insulin, 81, 115, 383Insulinoma, 32, 398, 428–430, 774Intavenous fluid (IVF), 251Intensive care notes, 14–15Intensive care units (ICUs), 476–477

checking calcium levels in, 120glucose levels in, 121hemodynamic monitoring, 484–486mechanical ventilation in, 486–489notes written in, 476–477pneumonia in, 37terms used, 477–480

Intercostobrachial nerve, 400Interferon alpha-2b, 475Interleukins, 673Interlobar, definition of, 531Intermittent claudication, 492Internal hernias, 211Internal iliac artery, 106Internal inguinal ring, 219Internal mammary artery (IMA), 439, 649Internal oblique muscles, 217Interosseous muscles, 578Intestinal angina, 506Intestinal stasis, 33Intestinal transplantation, 687Intra-abdominal pressure, 209Intra-articular fractures, 698Intraaortic balloon pump (IABP), 648, 671Intracellular fluids, 108Intracerebral hemorrhage, 735–736Intracranial pressure (ICP)

increased, 28Monroe-Kelly hypothesis, 723normal, 722techniques to decrease, 724

Intraductal carcinoma, 411Intramedullary rods, 702Intraoperative cholangiogram (IOC), 226,

368, 372, 374Intraparietal hernia, 213Intravenous access sites, 232Intravenous (IV) fluids, 517–518Intravenous pyelogram (IVP), 746Intrinsic factor, 199, 271Intubation, indications for, 250Intussusception, 23, 554–555, 572, 772Intussuscipiens, 554Invasive ductal carcinoma, 403


Invasive lobular carcinoma, 403Inversion, definition of, 691Involuntary guarding, 203Iodide, therapeutic, 449131I-MIBG, 425Iris scissors, 44Irish’s node, 277Iron, absorption of, 161, 162, 201Irrigation, of wounds, 575Ischemia

colonic, 503–504ECG, 670to lower extremities, 236mesenteric, 137, 208, 506–507, 767tissue, 483

Islet cell tumors, 398Islets of Langerhans, 383Isoflurane, 191Isografts, 671Isoproterenol, 481Isotonic fluids, 113-itis, definition of, 23ITP, 462IV therapy, replacement fluids, 111–112IVC, 103Ivor-Lewis procedure, 647IVP (intravenous pyelogram), 746

JJ-tubes, 94Jackson-Pratt (JP) drains, 93Jaundice, 145

definition of, 369first evidence of, 366obstructive, 366, 369–370painless, 394, 395physiologic, 558

Jefferson’s fracture, 729Jejunostomy, 284Jejunostomy tubes, 94Jejunum, 106, 287, 453Jejunum interposition loop, 147Joints, sutures, 62Jones’ fractures, 699Juvenile nasopharyngeal angiofibroma,

604, 772

KKanavel’s signs, 582Kaposi’s sarcoma, 465Kasai, 559–560Kehr’s sign, 29, 459Kelly, William D., 684Kelly clamps, 45Kelly’s sign, 29Keloids, definition of, 575Ketamine, 191Ketoconazole, 422

Ketorolac, side effects, 195Kidney

Gerota’s fascia, 103tumor of, 748

Kidney stonespatient position in, 205radiopaque, 39, 186uric acid, 189

Kidney transplantation, 679–682harvest to transplant times, 679incision, 75rejection, 681–682

Kienbock’s disease, 709Kissing ulcer, 260Kjelberg procedure, 724Klatskin’s tumor, 367, 380Klebsiella, 354, 390, 594, 763Knee, 691, 706–707Knots, 61–65Kocher clamps, 50Kocher incision, 74, 369Kocher maneuver, 84, 266, 383Kocher’s point, 723Kock pouch, 284Krukenberg’s tumor, 29, 277KUB acronym, 187Kulchitsky cells, 301Kussmaul’s sign, 231

LLab coats, 2Lacerations, 575, 581Lachman’s test, 707Lactated Ringer’s solution, 111, 112, 114,

126, 232Lactational mastitis, 418Lactic acid, 165Lactic acid levels, 483Lactulose, 363LAD (left anterior descending coronary

artery), 648, 650Ladd’s bands, 540, 547Ladd’s procedure, 548LAMP acronym, 492Langer’s lines, 573Lap appy, 23, 86Lap-bands, 283Lap chole, 23, 86Lap Nissen procedure, 87, 645Lap Toupet procedure, 645Laparoscoic Nissen fundoplication, 222, 273Laparoscopic cholecystectomy, 77, 369Laparoscopy, 23, 223–226Laparotomy, 114

definition of, 23exploratory, 88, 240PO feedings after, 164small bowel obstruction after, 39

Index 791


Laparotomy pads, 8Laplace’s law, 29, 501LAR (low anterior resection), 84Large bowel obstruction, 37Laryneal fractures, 242Laryngomalacia, 523Laryngotracheobronchitis (croup), 610–611,

619, 620Larynx, 242, 609–611Lasix®, 480Lateral aberrant rest, thyroid, 448Lateral internal sphincterotomy (LIS),

331Lateral pectoral nerve, 399–400LCIS (lobar carcinoma in situ), 413–414LE arterial insufficiency ulcers, 196Le Fort fractures, 615–616Left anterior descending coronary artery

(LAD), 648, 650Left bundle branch block (LBBB), 670Left gastric vein, 106Left iliac vein, 140Left internal jugular vein, 105Left lateral decubitus position, 78Left renal vein, 103, 106Left subclavian vein, 105Left testicular vein, 103Left vagus nerve, 104Legg-Calvé-Perthes disease, 720Leiomyomas, 23, 290Leiomyosarcomas, 23, 280, 465Lentigo maligna histology, 473Leriche’s syndrome, 34, 495“Lethal triad,” 244Leukemias, 570Leveling colostomy, 545Li-Fraumeni syndrome, 467Lichtenstein herniorrhaphy, 83, 216Lidocaine, 191–192, 194Lieno-, definition of, 23Lifestyle, atherosclerosis and, 490Ligament of Treitz, 286Ligamentous injuries, 719Ligamentum arteriosum, 520Ligamentum teres, 345, 520Ligamentum venosum, 520Lillehei, Richard C., 684“Limb-sparing” surgery, 467Lipases, 144, 398Liposarcomas, 464, 465Lithotomy position, 78Little league elbow, 720Littre’s hernia, 211, 536Liver, 345–357

abscesses, 354–356anatomy of, 345–349benign cysts of, 350benign tumors of, 570

792 Index

blood supply of, 202harvest to transplant times, 679lobes of, 105metastatic disease, 37, 38, 303, 313protrusion of, 552traumatic injury to, 37, 243tumors of, 349–350

Liver failure, 682Liver function tests (LFTs), 246Liver hemangioma, 768Liver transplantation, 41, 76, 268,

682–684Living Donor Liver Transplantation

(LDLT), 683LLQ, 206, 209, 320LOA (lysis of adhesions; enterolysis), 86Local anesthesia, 190, 191Locked knee, 707Long thoracic nerve, 399–400, 409Longitudinal fractures, 697Loop colostomy, 285Low anterior resection (LAR), 314Low-dose unfractionated heparin, 181Low molecular weight heparin (LMWH),

134, 181Lower abdominal pain, 206Lower esophageal sphincter, 200Lower extremities

amputation of, 497prolonged ischemia, 236

Lower gastrointestinal bleeding, 334–337Lower GI bleeding, 532Ludwig angina, 606–607Lugol’s solution, 449Lumbar disc herniation, 736–737Lumbar hernia, 211Lumbar spine, 235Lumbrical muscles, 578Lumpectomy, 88, 407–408Lung cancer, 37, 38, 198Lung transplantation, 41, 688–689Lungs

abscesses, 624diseases of, 627–635harvest to transplant times, 679mass in, 525metastatic disease, 36

LUQ, 206Luteinizing hormone-releasing hormone

(LHRH) agonists, 753Lymph nodes

axillary, 400mycobacterial infection, 571umbilical, 32

Lymphadenectomy, 475Lymphangiosarcoma, 465Lymphazurin®, 474Lymphoid hyperplasia, 294


Lymphomas, 467–468in children, 570head and neck, 620mediastinal, 638post-transplant, 690

Lynch’s syndrome, 310Lysis of adhesions (LOA), 86, 288

MMackler’s triad, 269Macrophages, 673Mafenide acetate (Sulfamylon®), 252Magnesium, 117, 120, 183Magnetic resonance imaging (MRI), 185Major histocompatibility complexes

(MHCs), 672Male breast cancer, 414–415Male gynecomastia, 418Malignant, definition of, 197Malignant fibrous histiocytoma, 464Malignant hyperthermia, 181, 193, 773Malignant melanoma. See MelanomaMalignant neurilemmoma, 465Malignant otitis externa (MOE), 590–591,

620“Malleable” retractors, 53Mallet finger, 583Malleus, 589Mallory-Weiss syndrome, 34, 266–267,

774Malrotation, 546–548, 572, 769Maltoma, 281Mammary ductal ectasia, 417Mammary “milk line,” 401Mammograms, 189, 190, 403–404Mammoplasty, 573Mandibular fractures, 235, 615, 617MAP (mean arterial pressure), 479, 649Marginal ulcers, 196, 262Marjolin’s ulcer, 196, 469Marshall test, 763MAST trousers, 246Mastectomy, 87, 88, 401, 408Mastitis, 417Maxillary sinus cancer, 619Maxillofacial fracture, 233Maxon sutures, 61Mayo scissors, 47Mayo trays, 8McBurney’s incision, 74, 299McBurney’s point, 30, 105, 295McBurney’s sign, 30MCL (medial collateral ligament), 690, 706McMurray’s sign, 707McVay herniorrhaphy, 83, 216, 220Mean arterial pressure (MAP), 479, 649Mebendazole, 356Mechanical ventilation, ICU, 486–489

Meckel’s diverticulum, 30, 39, 291–293,520, 555–556, 767

Meckel’s scan, 293, 556Meconium ileus, 540–541Meconium peritonitis, 542Meconium plug syndrome, 542Medial collateral ligament (MCL), 690, 706Medial epicondylitis, 720Medial malleolus, 196Medial pectoral nerve, 399–400Medial umbilical ligament, 520Median arcuate ligament syndrome,

507–508Median nerve, 580, 584, 704Median sternotomy, 76MEDIAN TRAPS acronym, 585Mediastinal tumors, 525Mediastinitis, 638–639Mediastinum

anatomy of, 635–636diseases of, 635–640emphysematous, 29neuroblastoma, 564tumors of, 636–638widened, 37, 237

Medications, 15, 130–138Medullary carcinoma, thyroid, 446–447Medullary fibrosis with myeloid metaplasia,

460Medulloblastoma, 733Melanoma, 471–476

anal, 328signs of, 25small bowel tumors and, 291staging, 473–476superficial spreading, 35

MELD score, 348–349, 683Melena, 9, 23, 254, 311Melenic stools, 254MEN. See Multiple endocrine neoplasia

(MEN)Men

common cancers in, 198prostate cancer in, 37

Mendelson’s syndrome, 34, 143Ménière’s disease, 599, 619, 772Meningiomas, 732Meningitis, 597, 742Meniscus, 707Mental state, decline in, 236Mental status, 157, 233–234Meperidine (Demerol®), 137, 138, 1926-mercaptopurine, 343Mesalamine (5-aminosalicyclic acid), 343Mesenteric ischemia, 137, 208, 506–507,

767Mesothelioma, 626–627, 772Metabolic acidosis, 109, 480

Index 793


Metabolic alkalosis, 110, 480Metacarpal bones, 578Metacarpal fractures, 582Metacarpal phalangeal (MP) joint, 578Metachronous tumors, 197Metaiodobenzylguanidine, 425Metallic skin staples, 58Metaphysis, 694, 695Metastatic disease, 312, 711Methicillin-resistant Staphylococcus aureus

(MRSA), 132Methimazole, 449, 450Methylprednisolone, 189, 674, 728Metoclopramide (Reglan®), 136Metronidazole (Flagyl®), 130–132, 136, 156,

177, 179, 297, 313, 343, 355Metyrapone, 422Metzenbaum scissors, 46Microcytic anemia, 126, 312Microembolization, 515Midazolam, 191MIDCAB (minimally invasive direct

coronary artery bypass), 654Middle ear, 589

tumors of, 591Middle meningeal artery, 37, 725Midgut, 104Midgut volvulus, 546–548Midline laparotomy, 74Mikulicz’s syndrome, 618Milk alkali syndrome, 119“Milk leg,” 515Millard-Gubler syndrome, 743Minimally invasive direct coronary artery

bypass (MIDCAB), 654Mirizzi’s syndrome, 34, 381Misoprostol (Cytotec®), 136Mitotane, 422Mitral regurgitation (MR), 649, 658Mitral stenosis (MS), 657–658Mitral valve, 658, 659Mittleschmerz, 30MMMP acronym, 436–437Modified radical mastectomy, 408–409MODS (multiorgan dysfunction syndrome),

478MOF (multiple organ failure), 480Mohs surgery, 471Mondor’s disease, 415, 671Monocryl, 55Monroe-Kelly hypothesis, 723Monteggia fractures, 700Moraxella catarrhalis, 593Morbid obesity, CT scans and, 9Morgagni’s hernia, 213, 530Morphine, 137, 192Morrison’s pouch, 104, 186Motion pain, 203

794 Index

Motor function, 193, 233–234, 722MPH acronym, 436MR. PAIR acronym, 650MR (mitral regurgitation), 649, 658Mucoepidermoid carcinoma, 609Mucous fistulae, 84, 284Mucous neck cells, 199, 271Multidrug resistance, 132Multiorgan dysfunction syndrome (MODS),

478Multiple endocrine neoplasia (MEN)

MEN-I syndrome, 35, 431, 435–437, 771

MEN-II syndrome, 35, 771MEN-IIA syndrome, 436, 446, 771

Multiple myeloma, 711Multiple organ failure (MOF), 480Munchausen syndrome, 34Murphy’s sign, 30, 373Murray, Joseph E., 679Muscle blockers, nondepolarizing, 193–194Musculocutaneous nerve, 704Myasthenia gravis, 636Mycophenolate mofetil (MMF), 676–677Myelomeningocele, 741Myocardial infarction (MI), 150–151, 503,

650, 670Myofibroblasts, 574Myoglobinuria, 247, 767Myxoma, 664

NN-myc oncogene, 567NAACP acronym, 402Nafcillin (Nafcil®), 132Nail polish, 6Naloxone (Narcan®), 138, 193, 195Narcotics, 137–138

reversal of, 195Nasal cavity cancer, 603–604Nasal septum, 235, 588Nasogastric decompression, 251Nasogastric tubes (NGTs), 99–101

advancement of, 69, 70on chest x-ray, 244complications, 143confirmation of placement, 71CXR timing and, 184drainage from, 70hypokalemia and, 110placement in nare, 70procedures, 69–71taping of, 71

Nasopharyngeal angiofibroma, 604NAVEL acronym, 66, 104, 232Nebulizer treatment, 116NEC (necrotizing enterocolitis), 557–558,

771


Neckexamination of, 235masses, 613–614modified dissection of, 614–615neuroblastoma, 564pediatric surgery, 521–523penetrating injuries, 240–241radical dissection of, 614triangles, 587zones, 240–241

Necrotic, definition of, 23Necrotizing enterocolitis (NEC), 557–558,

771Necrotizing fasciitis, 175, 773Necrotizing migratory erythema, 430Needle drivers, 42, 45Needle thoracostomy, 229Needles, 56, 103Neisseria meningitides, 461Nelson’s syndrome, 422Neoadjuvant RX, 197Neomycin, 363Neonates

blood volumes, 518bowel obstruction in, 532

Neoplasms, hypercalcemia and, 119Neostigmine, 194Nephrectomy, radical, 749Nephrolithiasis, 208Neuhauser’s sign, 540Neural tube defects, 741Neurilemmoma, 465Neuroblastomas, 564–567, 570, 572,

771Neurogenic shock, 168–169, 193Neurogenic tumors, mediastinal, 637–638Neurologic disability, 233–234Neurosurgery, 40, 721–743NG tubes, 232Nightstick fractures, 699, 709NIGRO protocol, 327Nimodipine, 735Nissen fundoplication, 86, 222, 644Nissen wrap, 275Nitroglycerine (NTG), 363, 482Nitrous oxide, 192NO CAST acronym, 701Nobel Prize winners, 42Nocturia, 746Nodular melanoma, 473Non-small cell lung carcinoma (NSCLC),

630–631Non-union, 694Nonabsorbable sutures, 54Noncommunicating hydrocele, 535, 745Nonrebreather mask, 159Nonsteroidal antiinflammatory drugs

(NSAIDs), 195

Norepinephrine (NE), 481–482Normal saline (NS), 111Normeperidine, 192Nose, 600–604Nosocomial infection, 170Notes. See DocumentationNP-59, 425NPO orders, 80Nursemaid’s elbow, 720Nuss procedure, 526Nutcracker esophagus, 643Nutrition, 160–164

pediatric patients, 517–518Nylon, 55Nylon sutures, 61Nystatin, 132, 182

OO negative blood, 125Obesity, 9, 282, 490Oblique fractures, 696Obliterative bronchiolitis (OB), 688OBR (ortho bowel routine), 144Obstipation, 23Obstructive jaundice, 366, 369–370Obturator hernia, 29, 211, 767Obturator sign, 30, 294Octreotide, 136, 302, 304, 307Octreotide scan, 433Odansetron (Zofran®), 302123I scintiscan, 440, 441Odontoid fractures, 729, 730Odynophagia, 23, 586Off pump coronary artery bypass (OPCAB),

655Ogilvie’s syndrome, 34OKT3, 676Oliguria, 152Omeprazole, 434Omohyoid muscle, 510Omphalocele, 548–552, 769Ondansetron (Zofran®), 135, 136OPCAB (off pump coronary artery bypass),

655Open fractures, 695, 701–702, 727Open reduction, 692, 701Open reduction internal fixation (ORIF),

690Operating rooms, 5–9Operative notes, 11–12Operative wounds, 172–174Opiates, 202Opsonins, 461OPSS, after splenectomy, 182Oral cavity, 605–615Oral cavity cancer, 607–608Oral hypoglycemic agents (OHA),

81

Index 795


Orbit, 588Orbital fractures, 617Orchiopexy, 569, 756, 764Orchitis, 745Orders, preoperative, 81Organ of Zuckerkandl, 424, 426Organ preservation, 679ORIF (open reduction internal fixation),

690-orraphy, 23, 79Orthopaedic injuries, emergent, 240,

701Orthopaedic surgery, 690–720Orthopaedic trauma, 701–705Orthopaedic tumors, 711–713Orthostatic hypertension, 193Orthotopic grafts, 672Ortolani’s sign, 719Osgood-Schlatter’s disease, 720Osmotic diuresis, 114Ossicle bones, 589Osteoarthritis, 715Osteochondromas, 622, 712, 713,

720Osteomas, 317Osteomyelitis, 710Osteoporosis, 702Osteosarcomas, 713Osteotomy, 694Ostomies, 284–286-ostomy, 24, 79Otalgia, 586Otitis externa (swimmer’s ear), 589–590,

617, 620Otitis media, 593–595, 617Otolaryngology, 586–620-otomy, 24, 79Otorrhea, 234, 586, 590, 722Otoscherosis, 595Ovaries

cancer of, 318in hernia sac, 217inguinal hernias and, 536metastatic tumor to, 29

Overflow incontinence, 762, 763Overwhelming postsplenectomy sepsis

(OPSS), 460–461Ovulation, mittleschmerz, 30Oxygen

delivery of, 479–480supplemental, 159toxicity of, 484in whole blood, 483

Oxygen nasal cannula, 160Oxygen saturation, 159, 480,

483Oxygenation, 486Oxyhemoglobin dissociation, 127

796 Index

Pp53 gene, 278p53 mutation, 467PACE acronym, 494Packed red blood cells (PRBCs), 124, 126Paget-von Schroetter syndrome, 622Paget’s disease, 119, 326, 414Pain, suprapubic, 207Pancoast’s tumor, 628Pancolitis, 344Pancreas, 382–398. See also Pancreatitis

abscesses, 390anatomy, 382–383harvest to transplant times, 679transplantation of, 41, 684–685traumatic injury to, 243, 244

Pancreatic cancer, 27, 197, 207, 394–397,768

Pancreatic divisum, 397Pancreatic enteric fistulas, 307Pancreatic fistula, 398Pancreatic necrosis, 391Pancreatic pseudocysts, 391–393, 768Pancreatic secretions, 111Pancreatic VIP syndrome, 398Pancreaticoduodenectomy, 91. See also

Whipple procedurePancreaticojejunostomy, 307Pancreatitis, 9, 770

acute, 383–386causes of, 36chronic, 387–388gallstone-related, 389hemorrhagic, 389–390postoperative, 144referred pain from, 207splenic vein thrombosis and, 461

Pancuronium, 193Pannus, 715Pantaloon hernia, 212PaO2, 159Papaverine, 507Papillary adenocarcinoma, 443–445Papillary thyroid cancer, 445, 771Paraaortic abdominal paraspinal ganglia,

564Paradoxic alkalotic aciduria, 110Paradoxical emboli, 516Paraesophageal hiatal hernia, 222–223Parafollicular cells, 441Parainfluenza virus, 620Paralytic ileus, 251Paranasal sinus cancer, 603–604Paranasal sinuses, 600–604Paraneoplastic syndrome, 198Paraphimosis, 746Parastomal hernia, 212Parathyroid carcinoma, 457–458, 771


Parathyroid gland, 452–458Parathyroid hormone (PTH), 453Parathyroid hyperplasia, 435Parathyroidectomy, 458Parathyromatosis, 458Paratopic grafts, 672Parkland formula, 250Paronychia, 582Parotid gland, 588, 608, 619Parotitis, 178, 620“Parrot’s beak” sign, 187Partial shunts, 362Partial weight bearing (PWB), 690Passaro’s triangle, 433Passive range of motion (PROM), 691Pasturella multocida, 582Patellar ligament, 706Patent ductus arteriosus (PDA), 661Patent urachus, 571Pathologic fractures, 697, 702Patient-controlled analgesia (PCA), 194,

195Patient positioning, surgical, 78–79PCL (posterior cruciate ligament), 690, 706PCWP (pulmonary capillary wedge

pressure), 478, 485–486PDA (patent ductus arteriosus), 661PDS®, 54, 61Peanuts, aspiration of, 524Peau d’orange, 403Pectus carinatum, 526Pectus deformity, 525Pectus excavatum, 525–526Pediatric patients

abdomen, 532–533abdominal injuries, 246blood volume, 518bone tumors in, 712caloric requirements, 518chest, 525–531dietary protein requirement, 518estimated blood volume, 517frightened, 205GI tumors, 563–568maintenance fluid, 113neurosurgery, 739–743orthopaedics, 616–720osteomyelitis in, 710urine output after burns, 251

Pediatric surgery, 517–572PEEP (positive end expiration pressure),

487–488PEG (percutaneous endoscopic

gastrostomy), 90Pellagra, 301–302Pelvic abscesses, 175Pelvic fractures, 236, 701

bleeding from, 242, 246

DPL in, 239exsanguinating, 240

Pelvis, neuroblastoma, 564Penicillins, 131, 136, 179Penrose drains, 93Pentagastrin stimulation, 303, 447Pentalogy of Cantrell, 550Pepsin, 199, 271Peptic ulcer disease (PUD), 256–257Peptic ulcers, 32, 195, 262–263Perc nephrostomy, 743Percocet®, 137Percutaneous, definition of, 24Percutaneous endoscopic gastrostomy

(PEG), 90Percutaneous renal transluminal angioplasty

(PRTA), 513Percutaneous transhepatic cholangiogram

(PTC), 368Percutaneous transluminal coronary

angioplasty (PTCA), 649Perianal warts, 332Periarticular fractures, 698Pericardial tamponade, 774Pericarditis, 653, 670Peripheral intravenous catheters, 66Peripheral nerve injuries, 704Peripheral vascular disease (PVD), 491–497Perirectal abscesses, 330Peritoneal abscesses, 174–175, 188, 773Peritoneal cavity, 188Peritoneal fat stripe, 187Peritoneal signs, 203Peritoneal taps, 239, 558Peritonitis, 204Peritonsillar abscess, 606Petersen’s hernia, 211, 283Petit’s hernia, 211Peutz-Jeghers syndrome, 34, 318–319, 769-pexy, definition of, 24Peyer patches, 202Peyronie’s disease, 766Pfannenstiel incision, 75Phalanges (fingers), 578Phalen’s test, 585Pharyngotonsillitis, 605–606Pharynx, 605–615PHE acronym, 30Phenytoin (Dilantin®), 137, 724Pheochromocytoma, 30, 423–426, 447, 771Phimosis, 746Phleb-, definition of, 24Phleboliths, 24Phlegmasia alba dolens, 515Phlegmasia cerulea dolens, 515Phlegmons, 24Physical reports, 9–10Physiologic jaundice, 558

Index 797


Physis, 694, 695Pickups. See ForcepsPierre-Robin syndrome, 570Pilon fractures, 700Pituitary tumors, 733–734Plantar fasciitis, 709Plantarflexion, 691Plaque formation, 490Plasmapheresis, 463Plastic surgery, 572–578-plasty, definition of, 79Platelets, 124, 125Platysma muscle, 510, 588Plavix®, 125, 335Pleomorphic adenoma, 608, 619Pleura, diseases of, 623–627Pleural effusion, 623–624Pleuravac®, 96Pleurodesis, 625Plica, definition of, 24Plicae circularis, 24, 106, 186, 286Plicae semilunares, 24, 186Plug and patch hernia treatment, 84, 216Plummer-Vinson syndrome, 34Plummer’s disease, 442, 450Pneumatic equilization tube, 594Pneumatosis intestinalis, 187Pneumaturia, 24, 746Pneumonia

after burns, 251aspiration-related, 142–143in burn victims, 253in the ICU, 37, 477postoperative, 181

Pneumonitis, chemical, 34Pneumoperitoneum, 224Pneumothorax (PTX), 24, 98, 102, 159, 184,

229, 235Poland’s syndrome, 571Polycythemia, 424Polydactyly, 573Polyester sutures, 61Polyposis syndromes, 317–319Polypropylene sutures, 61Polyps, 315–317Polysporin®, 252Polyuria, 746Poole sucker, 48Pop-off sutures, 60Popliteal artery, 88, 514–515Porcelain gallbladder, 381Port-A-Cath®, 102Portal hypertension, 103, 357–363, 463, 768Portal vein, 202, 346, 358Portal venous system, 357–358Portocaval shunts, 363Positive end expiration pressure (PEEP),

487–488

798 Index

Post-transplant lymphoproliferative disease(PTLD), 690

Post-traumatic arthritis, 715Posterior cord syndrome, 729Posterior cruciate ligament (PCL), 690, 706Posthitis, 744Postoperative fevers, 180–181Postoperative notes, 12Postoperative pancreatitis, 144Postoperative respiratory failure, 139–140Postpericardiotomy syndrome, 652–653Postvagotomy diarrhea, 146Postvoid residual (PVR), 746Potassium, 671. See also Hyperkalemia;

Hypokalemiaalkalosis and, 116in colonic feculent fluid, 109daily requirements, 108dysrhythmias and, 123preoperative testing, 81

Potassium iodide, 449Potassium ions, 114, 202Pott’s disease, 700Pott’s fractures, 700Pott’s scissors, 49Potts technique, 490Pouch of Douglas, 105Pouchitis, 344Poupart’s ligament, 217, 219, 535PPIs (proton-pump inhibitors), 135PPP SAFE DISC acronym, 12Prealbumin, 161, 164Prednisone, 674Pregnancy

appendicitis in, 298laparoscopy during, 226testing for, 81

Prehn’s sign, 745Preload, 482, 649Premature infants

caloric requirements, 518inguinal hernias in, 533risk of NEC in, 557

Premature ventricular complexes (PVCs), 670Preoperative care, 78–81, 137Preoperative notes, 11Preperitoneal fat stripe, 187Presacral drainage, 242Prescriptions, form of, 15Pressure support mode, 487Priapism, 729, 746, 760Primary hyperaldosteronism, 426Primary intention, 55Primary survey, 227–234Primary wound closure, 91Pringle maneuver, 87Procedures, 66–73, 80, 82–91. See also

Specific procedures


Progesterone receptors, 406Prograf®, 676Progress notes, 13–14Prolactin, 401Prolactinomas, 415, 733–734Prolene, 55PROM (passive range of motion), 691Promethazine-induced dystonia, 137Promethazine (Phenergan®), 135Pronation, 691Prone position, 78Properdin, 461Properitoneal hernia, 213Prophylactic, definition, 170Propofol, 164, 191Propranolol, 449Proprioperception, 504Propylthiouracil (PTU), 449–450Proscar®, 755Prostate cancer, 37, 751–754Prostate gland, 88Prostate-specific antigen (PSA), 752Prostatectomy, radical, 753Protamine, 653, 654Protamine IV, 133Protein, dietary, 160, 161, 518Protein C deficiency, 128Protein S deficiency, 128Proteus, 354, 590, 763Proton-pump inhibitors (PPI), 181Proximal esophageal pouch, 530Proximal gastric vagotomy, 259Proximal interphalangeal (PIP) joint, 578,

583, 715PSA (prostate-specific antigen), 752Pseudoaneurysms, 490Pseudocapsules, 466Pseudocysts, 24, 391–393Pseudogout, 716Pseudohermaphroditism, 745Pseudohyperkalemia, 115Pseudohyponatremia, 118Pseudomembranous colitis, 156, 176–177,

773Pseudomonas spp., 131, 132, 172, 179, 390,

620, 763P. aeruginosa, 590, 593

Pseudopolyps, 343Psoas shadow, 187Psoas sign, 31, 295PT (prothrombin time), 124, 128PTCA (percutaneous transluminal coronary

angioplasty), 649PTT (partial thromboplastin time), 124,

127, 128PTU (propylthiouracil), 449–450PUD, 38Puestow procedure, 85, 398

Pulmonary angiograms, 190Pulmonary artery embolectomy, 142Pulmonary artery occlusion pressure

(PAOP). See PCWPPulmonary capillary wedge pressure

(PCWP), 478, 485–486Pulmonary emboli (PE), 32, 140–142, 190Pulmonary sequestration, 531–532, 634–635Pulmonary vascular obstructive disease, 660Pulmonary vascular resistance (PVR), 479,

649Pulses, palpation of, 231Pupils, 233–234, 722Pursestring stitches, 58Pus, 24Putamen, 743PVR (postvoid residual), 746PVR (pulmonary vascular resistance), 479,

649PWB (partial weight bearing), 690Pyeronie’s disease, 746Pyloric stenosis, 538–540, 572, 769Pyloroplasty, 80, 258, 259, 264Pyridostigmine, 194Pyrosis, 272Pyruvate kinase deficiency, 460Pyuria, 746

RRaccoon eyes, 31, 234, 722Race/ethnicity

Crohn’s disease and, 339pancreatic cancer and, 394prostate cancer and, 751

Radial artery, 26, 72Radial nerve, 580, 704Radial pulse, 231Radiation therapy

abbreviations used, 197in breast cancer, 407–408lumpectomy and, 88for rectal cancer, 314

Radical prostatectomy, 753Radiology

in acute abdomen, 205surgical, 183–190

Radius, fracture of, 698RALES acronym, 464Rally pack, 183Ramsay Hunt’s syndrome, 620Range of motion (ROM), 690Ranitidine (Zantac®), 135, 675Ranson’s criteria, 9, 385–386Rapamune®, 676Rapamycin, 676Rapid-sequence anesthesia induction, 191Rapid-Shallow Breathing, 489Ray amputation, 497

Index 799


Raynaud’s phenomenon, 515Razors, wound infections and, 182Rebound tenderness, 203Rectal cancer, 311, 774Rectum, 105

blood supply to, 309diseases of, 208pain referred from, 208penetrating injury, 242polyps of, 315–317

Recurrent laryngeal nerves, 440, 610Red blood cells, 39, 124, 127RED reaction syndrome, 34Reducible hernias, 209Reduction, 692Reed-Sternberg cells, 467Refeeding syndrome, 34Regional anesthesia, 190, 191Regional enteritis. See Crohn’s diseaseRejection, 678–679, 681–682Relaxing incisions, 219Renal artery stenosis, 137, 512–513, 767Renal cell carcinoma (RCC), 748–750, 770Renal failure, 152–153, 680Renal transplant, 41Renal vein, 505Renal vein renin ratio (RVRR), 513Rendu-Osler-Weber syndrome, 34Renin levels, 513Replacement fluids, 111–112Replogle tube, 571Respiratory acidosis, 110, 480Respiratory alkalosis, 110, 480Respiratory care, 158–160Respiratory quotient (RQ), 161Respiratory tract infection, 170Rest pain, 492Resuscitation, 114, 232, 249Retention sutures, 60Retinol-binding protein, 161Retractors, 51–53Retrocecal appendix, 299Retrograde urethrogram (RUG), 233, 239,

744, 765Retrogram pyelogram, 743Retroperitoneal appendix, 299Retroperitoneal hemorrhage, 28, 29Retroperitoneal varices, 360Reverse Trendelenburg position, 79Reversible ischemic neurologic deficit

(RIND), 509Reynold’s pendad, 31, 375Rhabdomyosarcoma, 464, 567, 620, 664Rheumatoid arthritis (RA), 715Rhinitis, 601Rhinoplasty, 573Rhinorrhea, 234, 722Ribs, 104, 235

800 Index

Richardson retractors, 53Richter’s hernia, 212Ridel’s thyroiditis, 452Right-angle clamps, 45Right bundle branch block (RBBB), 670Right coronary artery, 650Right iliac vein, 140Right lateral decubitus position, 78Right renal vein, 106Right testicular vein, 103RIND (reversible ischemic neurologic

deficit), 509Rings, wearing of, 6Rinne test, 597RIPE acronym, 184RLQ, 206, 208Rocky-Davis incision, 75, 299ROM (range of motion), 690Ross procedure, 659Rotational flaps, 577Rotator cuff, 708–709Rotter’s lymph nodes, 104, 401Round ligament, 218Rounds, 2–3Roux-en-Y limb, 83Rovsing’s sign, 31, 295RTUS (transrectal ultrasound), 752Rubor, 25RUG (retrograde urethrogram), 233, 239,

744, 765Rugae, gastric mucosa, 271Rule of 2s, 556Rule of 2/3s, 360Rule of 3-for-1, 241Rule of 3,6,9, 186Rule of 3s, 186Rule of 4/2/1, 112Rule of 5s, 559Rule of 10 for 0.08, 480Rule of 20-20-10, 569Rule of 33 to 1, 455Rule of 40,50,60, 480Rule of 70,80,90, 480Rule of 90%, 331Rule of 100/50/20, 112Rule of nines, 248Rule of the palm, 248RUQ, 205, 208

SSacral sparing, 728“Saddle” emboli, 141SAFE acronym, 538Saint’s triad, 31Saliva, daily quantities, 111Salivary gland stones, 618Salivary gland tumors, 608–609Salmonella, 710


Salter-Harris classification, 716–718SALTR acronym, 718SALUD acronym, 478Salvage mastectomy, 410Santorini duct, 382Sarcoid, hypercalcemia and, 119Sarcomas, 36, 464–467Scalpels, 51, 73, 130Scaphoid fracture, 583, 702Scar tissue, 73Scarpa’s fascia, 216SCD boots, 224Schwannoma, 465Schwartze’s sign, 595Sciatic hernia, 212Sciatica, 737Scissors, 42, 44, 47, 49Sclerosing cholangitis, 376–377Sclerotherapy, 268, 361–362Scoliosis, 720Scorpion bites, 386Screening, colorectal, 310Scrotal blue dot sign, 765Scrotum

anatomy, 747lower abdominal pain and, 206mass in, 747–748pheochromocytoma of, 424

Scrub nurses, 5, 7, 40Seagesser’s sign, 459Seatbelt sign, 236Seatbelts, 242Sebaceous cysts, 73, 317, 470Seborrheic keratosis, 471Second-degree burns, 247, 248, 249Second-degree hemorrhoids, 333Secondary hyperaldosteronism, 426Secondary intention, 55Secondary wound closure, 92Secretin, 200Secretin stimulation test, 432–433Segmental fractures, 696Seizures, 137, 724Seldinger technique, 85Sellick’s maneuver, 191Seminoma, 757Sengstaken-Blakemore balloon, 267, 268Sengstaken-Blakemore tube, 361Sensorineural hearing loss, 597–598Sensory function assessment, 233–234Sentinel loops, 187Sentinel node biopsies, 409, 474Sentinel piles, 331Sepsis, 170Septic arthritis, 710–711Septic shock, 167–168, 170Sequential compression devices (SCDs),

181, 224

Serotonin antagonists, 302Serous otitis, 617Seton, 329Sevoflurane, 191Shin splints, 709Shock, 9, 36, 164–170Short bowel syndrome, 144Short-gut syndrome, 34Shoulder dislocation, 705Shouldice herniorrhaphy, 84, 216Shunt fraction, 483Shunt series, 740Shunts, 362–363SIADH. See Syndrome of inappropriate

antidiuretic hormoneSickle cell anemia, 460, 710Sigmoid colon, 504Sigmoid volvulus, 37, 322–324, 769Sigmoidoscopy, 323Silk glove sign, 31, 221, 534Silk sutures, 55, 61, 62Silver sulfadiazine (Silvadene®), 252Silverlon®, 249Simple interrupted stitches, 56Simple running stitches, 57SIMV mode, 487Sinuses, cancer of, 619Sinusitis, 601–603Sipple’s syndrome, 35, 436Sirolimus, 676SIRS (systemic inflammatory response

syndrome), 170, 480Sister Mary Joseph’s node, 395Sister Mary Joseph’s sign, 32, 277Sitz baths, 330“Six Ps,” 498Skin

burned, 250fluid losses, 111grafts, 576lesions of, 469–476pickups for, 8

Skin prep, infections and, 182Skull fractures, 31, 727Sliding esophageal hiatal hernia, 221–222Sliding hernias, 211, 220Small bowel

3,6,9 rule, 186anatomy of, 106, 286–287Gardner’s syndrome, 317normal caliber of, 186nutritional source for, 201penetrating injury, 243plicae circularis, 186referred pain from, 208rule of 3’s, 186submucosa, 105traumatic injury to, 243, 569

Index 801


Small bowel obstruction (SBO), 287–290on abdominal x-rays, 186after laparotomy, 39in children, 36in Crohn’s disease, 35, 344gallstone ileus, 377–378hernias and, 571postoperative, 144–145

Small bowel tumors, 290–291Small cell lung carcinoma (SCLC), 631Small intestine, 217, 286–293Smith’s fracture, 698Smoke inhalation, 249–250Smoking

atherosclerosis and, 490Buerger’s disease, 515lung adenocarcinoma and, 627pancreatic carcinoma risk and, 394

Smoking cessation, 81, 181Sneezing, 6Soave procedure, 546SOD acronym, 33, 317Sodium bicarbonate, 115, 164Sodium chloride, in sweat, 109Sodium hypochlorite, 92Sodium ions, 108, 114, 202, 253Sodium nitroprusside (SNP), 482, 654Sodium polystyrene sulfonate (Kayexalate),

115Sodium thiopental, 191Soft tissues

sarcomas of, 464–467suturing of, 56

Solitary pulmonary nodules, 631–633Somatostatin (Octreotide), 200, 201, 361, 434Somatostatinomas, 398, 431, 768Space of Retzius, 105, 746Spermatic cord, 104, 217, 535, 536Spermatocele, 745Sphincterotomy, 369Spigelian hernia, 211Spina bifida occulta, 741Spinal anesthesia, 190, 193Spinal cord injury, 168–169, 727–730Spinal dysraphism, 741Spinal epidural abscesses, 738–739Spinal shock, 169, 727Spine, 736–739

immobilization of, 227Pott’s disease, 700

Spiral fractures, 697Spiral valves of Heister, 364Spleen, 458–463Splenectomy, 279, 458–463

follow-up, 461indications for, 460laparoscopic, 226OPSS after, 182

802 Index

Splenic artery aneurysm, 513–514Splenic rupture, 29Splenic vein thrombosis, 386, 461, 462Splenomegaly, 462, 463Splenorrhaphy, 460Splinting, hand, 583Split thickness skin grafts (STSG), 246, 249,

576Spontaneous galactorrhea, 415Spontaneous pneumothorax, 625–626Spurling’s sign, 738Squamous cell carcinoma (SCC), 469–470

anal, 326external ear, 591head and neck, 619nasal cavity, 603ulceration in, 196

Square knots, 61Stab wounds, 240, 244Stamm gastrostomy, 85Stanford classification, 666–669Stapes, 589Staphylococcus spp.

ear infection, 590osteomyelitis and, 710parotitis and, 620S. aureus, 172, 176, 390, 417, 582, 594,

659, 742S. aureus toxin, 35S. epidermidis, 172, 179, 659S. viridans, 659

Staplers, 47, 49Staples, 58, 59, 67Stauffer’s syndrome, 749Steatorrhea, 25, 387Stenosis, definition of, 25Stensen’s duct, 588Stents, 652, 743Step off fractures, 617Steri-Strips®, 62, 67Sterile fields, 6, 7, 25Sterility, 747Sternum, fractured, 235Steroids, 133

in spinal cord injury, 728wound healing and, 62, 92, 575

Stewart-Treves syndrome, 467STIR acronym, 494“Stitch” abscesses, 178Stitches, 56–58, 67Stoma, definition of, 284Stomach, 80, 270–281Stool, 9, 36, 178STOP IT acronym, 631Strangulated hernias, 210Streptococcus spp., 172

S. pneumoniae, 461, 593, 620Stress fractures, 697


Stress gastritis, 266Stress incontinence, 762, 763Stress responses, 251Stress ulcers, 251Stridor, 523Stroke. See Cerebrovascular accident (CVA)Stroke volume (SV), 478, 649Struvite stones, 761Stryker, Homer, 709STSG (split thickness skin grafts), 246, 249,

576Subarachnoid hemorrhage (SAH), 726,

734–735, 742, 770Subclavian steal syndrome, 511–512, 767Subcutaneous air, 235Subcutaneous emphysema, 235Subcuticular stitches, 58Subdural hematoma, 236, 726Subluxation, 693Submandibular gland, 588, 618Succinylcholine, 123, 191, 194Succus, definition of, 25Sucralfate (Carafate®), 135Suction-control chambers, 97Suffixes, 79–80Sulbactam, 131Sulfamethoxazole-trimethoprim, 130Sulfasalazine, 343Sump pumps, 100Superficial epigastric vein, 217Superficial spreading melanoma, 35, 472,

473Superinfections, 170Superior hemorrhoidal vein, 358Superior laryngeal nerve, 440, 610Superior mesenteric artery (SMA)

syndrome, 288Superior thyroidal artery, 510Superior vena cava syndrome, 35, 639–640Supination, definition of, 691Supine position, 78Suppurative cholangitis, 376Suppurative hidradenitis, 176Supracondylar humerus fracture, 709Supraglottic lesions, 612Suprapubic catheter, 744Suprapubic pain, 207Surgeon’s knot, 61Surgical clerkship, 1–9Surgical gowns, 6, 7Surgical instruments, 42–53Surgical intensive care, 476–489Surgical notes, 9–15Surgical oncology, 197–198Surgical positions, 78–79Surgical radiology, 183–190Surgical site infections, 172Surgical speak, 79–80

Surgical syndromes, 32–35Surigel®, 130Suture ligature, 60Sutures, 8, 42, 53–60, 62, 129SV (stroke volume), 478, 649SVR (systemic vascular resistance), 478, 649SVRI (systemic vascular resistance index),

478–479Swan-Ganz catheters, 484–485Sweat, 109Sweetheart retractors, 52Swenson procedure, 545Swimmer’s ear (otitis externa), 589–590Sympathetic ophthalmia, 246, 770Synchronous tumors, 197Syndactyly, 573Syndrome of inappropriate antidiuretic

hormone (SIADH), 35, 118, 148–149,725, 773

Synovitis, 585Synthroid® (levothyroxine), 441Syringomyelia, 743Systemic inflammatory response syndrome

(SIRS), 480Systemic vascular resistance index (SVRI),

478–479Systemic vascular resistance (SVR), 478, 649Systolic blood pressure estimation, 568

TT cells, 673T-tubes, 94TA staplers, 47Tachycardia, 157, 232Tacrolimus (Prograf®, FK506), 676Tail of Spence, 401Takayasu’s arteritis, 515Tamoxifen, 409, 410, 412Taper-point needles, 56TAPP procedure, 216TBSA, 246Temporary monocular blindness, 506Tendonitis, 709Tenesmus, 25Tennis elbow, 709Tenosynovitis, 582Tension pneumothorax, 229, 774TEPA procedure, 216Teratomas, mediastinal, 637Terminal ileum, 287Terminology, 79–80Tertiary intention, 55Testicles

cancer of, 755–758cryptorchid, 569outpouching, 218torsion, 758–759

Testicular appendage, 218

Index 803


Tetanus, 179, 183, 253Tetanus toxoid, 179, 180, 249Tetralogy of Fallot (TOF), 661–662THA (total hip arthroplasty), 691Thalassemias, 460Thenar atrophy, 585Thermoregulation, 193Thiamine, 183Third-degree burns, 247, 248, 249Third-degree hemorrhoids, 333Third-nerve palsy, 743Third spacing, 109–111Thompson’s test, 708Thoracic aorta

aneurysm of, 665–677aneurysm repair, 514coarctation of, 662–663ruling out injury to, 238sites of tears, 238traumatic injury, 37

Thoracic duct drainage, 105Thoracic outlet syndrome (TOS), 35,

621–622Thoracic spine, 235Thoracic surgery, 621–648Thoracoabdominal staplers, 47Thoracodorsal nerve, 399–400, 409Thoracostomy, 229Thoracostomy tubes, 94Thoracotomy, 25, 76Thorax, 235, 424THR (total hip replacement), 691Thrombocytopenia, 125, 460Thrombophlebitis, 180Thrombosis risk factors, 32Thrombotic thrombocytopenic purpura

(TTP), 462Thumbprinting, AXR, 187Thymoma, 636Thymus gland, 452Thyroglossal duct cysts, 521–523, 767Thyroid carcinoma, 442, 443Thyroid gland, 438–452Thyroid hormones, 440–441Thyroid medullary cancer, 771Thyroid nodules, 441–442, 443, 450Thyroid-stimulating hormone (TSH), 440Thyroidectomy, 440, 448Thyroiditis, 450–452Thyrotropin-releasing hormone (TRH), 440TIA (transient ischemic attack), 506Tibial fractures, 702Tibial pins, 692Tibial plateau fractures, 700Ticarcillin-clavulanic acid, 130Tidal volume, 486TIE acronym, 108Tietze’s syndrome, 35, 623

804 Index

Timentin®, 177Tinel’s sign, 585Tinel’s test, 622TIPS acronym, 362Tissue ischemia, 483Tissue perfusion, 165TKA (total hip arthroplasty), 691TKO Ewing, 714TMN staging, 197, 406–407. See also

American Joint Committee for Cancer(AJCC)

TMR (transmyocardial laserrevascularization), 654

Tobacco abuse, 619Tolbutamide stimulation test, 430Tonicity, 112Tonsil clamps, 46Tonsillectomy, 606Toradol®, 138TORCHES, 569Torus fractures, 698TOSS acronym, 588Total body surface area (TBSA), 246Total hip arthroplasty (THA), 691Total hip replacement (THR), 691Total knee arthroplasty (TKA), 691Total lymphocyte counts, 161Total parenteral nutrition (TPN), 41, 162Totally extraperitoneal approach, 216Toupet procedure, 275Toxic megacolon, 156, 342Toxic multinodular goiter, 450Toxic shock syndrome, 35Tracheobronchomalacia, 523Tracheoesophageal fistula, 527–530Tracheostomy, 91, 618TRAM flaps, 410, 414, 577Transabdominal preperitoneal inguinal

hernia repair, 216Transcervical fractures, 699Transect, definition of, 25Transferrin levels, 161Transfusion hemolysis, 36, 126Transient ischemic attack (TIA), 506Transjugular intrahepatic portosystemic

shunts (TIPS), 362Transmyocardial laser revascularization

(TMR), 654Transphenoidal adenomectomy, 421Transplant surgery, 671–690

complications, 689–690donor/recipient matching, 678harvest to transplant times, 679organ preservation, 679

Transposition of the great vessels, 663–664Transrectal ultrasound (TRUS), 745, 752Transurethral incision of the prostate

(TUIP), 755


Transurethral resection of the bladder(TURB), 751

Transurethral resection of the prostate(TURP), 88, 220, 746, 755

Transverse carpal ligament release, 585Transverse colon, 186Transverse fractures, 696Transverse rectus abdominis myocutaneous

flaps, 410, 414, 577Transversus aponeurosis, 219Trauma, 226–246

general principles, 694–695head injuries, 721–727miscellaneous facts, 241–246orthopaedic, 701–705pediatric, 568–569penetrating neck injuries, 240–241primary survey, 227–234secondary survey, 234–236studies, 237–240zones of the hand, 579

Trauma Whipple, 243Traumatic myositis, 709Trenckhoff catheters, 103Trendelenburg operation, 142Trendelenburg position, 25, 79, 166Trental®, 494TRH, 440“Triad of error,” 402Trigeminal nerve, 586, 587Triple A repair, 89Tripod fractures, 616Trisegmentectomy, 349Trismus, definition of, 586Trisomy 21, 572Trochar sites, 226Trousseau’s sign, 32, 120Trousseau’s syndrome, 35Truncal vagotomy, 90, 259, 261, 264TRUS (transrectal ultrasound), 745TSH, 440TTP, 462–463Tube thoracostomy, 229Tuberculosis, 700, 751Tubular adenoma, 316Tubulovillous adenoma, 316Tuftsin, 461TUIP (transurethral incision of the

prostate), 755Tullio’s phenomenon, 599Tunica vaginalis, 536TURB (transurethral resection of the

bladder), 751Turcot’s syndrome, 319Turf toe, 709TURP (transurethral resection of the

prostate), 88, 220, 746, 755Two-hand tie, 64–66

Tympanic membrane (TM) perforation,591–592

Type and cross, 125

UU waves, 116Ulcerative colitis (UC), 338–344, 376Ulcers, surgical, 195–196Ulnar artery, 26Ulnar fracture, 709Ulnar nerve, 580, 621, 704

distribution of, 579Ultrasound diagnosis

bile duct obstruction, 208biliary system evaluation, 188of cholelithiasis, 38, 208gallbladder evaluation, 188gallstones, 389pancreatic pseudocysts on, 392in pancreatitis, 384

Umbilical arteries, 519, 520Umbilical cord, 551Umbilical hernia, 213, 537, 569Umbilical veins, 519, 520Umbilicus, dermatome, 106Unasyn®, 130, 131, 137, 297, 313Unhappy triad, 707Unicameral bone cysts, 714Universal donors, 125Unstable fracture or dislocation, 692Upper GI bleeding, 254–271

cause of, 255pediatric patients, 532spontaneous stop of, 38treatment of, 255–256varices and, 361

Urachus, 520, 571Uremia, 125Ureter, peristalsis of, 29Ureteral stents, 743, 765Ureterocele, 766Urethra, female, 68Urge incontinence, 762, 763Urgency, 25, 745Uric acid stones, 189, 761, 764Urinary retention, 155, 193Urinary tract infection (UTI), 170–171,

180–181, 746, 763Urinary tract sutures, 55Urine

daily output, 113decreased output, 158minimal output, 241, 251, 517output goals for adults, 250reporting of output, 477volume status and, 251

Urine analysis, 171Urology, 743–766

Index 805


Ursodeoxycholic acid (Actigall®), 372Uterus, referred pain from, 208UTI. See Urinary tract infection

VV-Q scans, 190V-Y advancement flaps, 578Vaccinations, 462VACTERL acronym, 530VAD (ventricular assist device),

649, 671Vagotomy, 86, 90, 146Vagus nerve, 589, 610, 641Valentino’s sign, 32, 295Valgus, definition of, 693Vancomycin, 34, 131, 132, 156Vanishing bile duct syndrome, 683Varicocele, 745, 750Varus, definition of, 693Vascular anastomosis, 41Vascular prosthetic grafts, 137Vascular rings, 523Vascular slings, 523Vascular surgery, 489–516Vasoactive intestinal peptide (VIP), 200Vasopressin, 363, 482Vasospasm, 735Vein grafts, 495–496Vein of Mayo, 105Venous stasis ulcers, 196, 493Venous thrombosis, 577Ventilation, definition of, 486Ventilator-associated pneumonia (VAP),

182Ventral hernia, 212Ventricular aneurysm, 670Ventricular assist device (VAD), 649, 671Ventricular septal defect (VSD), 649,

660–661Ventricular tachycardia, 123Verbal responses, 233–234, 722Vercuronium, 193Veress needles, 224–225Verner-Morrison syndrome, 398Vertical mattress stitches, 57Vertigo, 598–599Vesicoenteric fistulas, 307Vesicoureteral reflux (VUR), 747Vesicovaginal fistulas, 307Vicryl® sutures, 54, 61Villous adenoma, 316Vinyl chloride, 350Virchow’s node, 32, 276, 395Virchow’s triad, 140Vital signs

in hypovolemia, 110in shock, 9

Vitamin A, 92, 119, 133, 162, 575

806 Index

Vitamin A deficiency, 162Vitamin B12, 162, 164, 199, 201Vitamin B12 deficiency, 162Vitamin C, 162Vitamin C deficiency, 162, 773Vitamin D, 119, 162, 453Vitamin E, 162Vitamin K, 162Vitamin K deficiency, 162Vitamins, fat-soluble, 162Vitelline duct, 520Volarflexion, 691Volkmann’s contracture, 703, 708–709, 772Voluntary guarding, 203Vomiting, 539, 547Von Willebrand’s disease, 127, 128VSD (ventricular septal defect), 649,

660–661VUR (vesicoureteral reflux), 747

WWARFARIN acronym, 128Warfarin (Coumadin®), 134–135Warren shunts, 362–363Wartenberg’s sign, 585Watches, wearing of, 6Water requirements, 108Water-seal chambers, 97WBAT (weight bearing as tolerated), 690WDHA syndrome, 398WEAPON acronym, 276Weber test, 597Wedge pressure. See PCWPWeight bearing as tolerated (WBAT), 690Weiss protocol, 121Weitlaner retractors, 52Wenckebach phenomenon, 670Wermer’s syndrome, 35Wernicke’s encephalopathy, 183, 773Westermark’s sign, 32Wet gangrene, 497Wet-to-dry dressing, 25, 92Wharton’s duct, 588WHEATY retractors, 52Whipple procedure, 91, 396–397, 434.

See also PancreaticoduodenectomyWhipple’s triad, 32, 398, 429White blood cells (WBCs), 126White lines of Toldt, 105Whole blood, oxygen content, 483Wilm’s tumor, 563–564, 572, 764, 772“Winged scapula,” 400Wirsing duct, 382Women

common cancers in, 198hernias in, 220lung cancer in, 37preop lab testing, 81


Wound closure, 55–56, 91–92Wound contraction, 574Wound dehiscence, 92Wound healing

inhibition of, 92, 575phases of, 573–575tensile strength after, 39types of, 55

Wound hematomas, 155Wound infections, 155,

180burn, 251clostridial, 774postoperative fever and, 180prophylaxis, 182surgical site, 172

Wound seroma, 156Wrist dorsiflexion, 691

XX-rays, indications for, 694Xenografts, 672Xigris®, 128XRT, definition of, 197

YYankauer suction instrument, 50Yersinia enterolytica, 298, 553

ZZ-platy, 577Zenker’s diverticulum, 641Zinc deficiency, 162Zollinger-Ellison syndrome, 35, 119, 257,

431–435, 771Zosyn ™, 177Zygris®, 168

Index 807


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