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2. V ad eme c um LANDES BIOSCIENCE V ad e me c u mEmergency MedicineEmergency Medicine HendersonSean O. Henderson 3. v a d e m e c u mEmergency MedicineSean O. Henderson, M.D. Department of Emergency Medicine Keck School of MedicineUniversity of Southern California Los Angeles, California, U.S.A.LANDESBIOSCIENCEGEORGETOWN, TEXASU.S.A. 4. VADEMECUM Emergency Medicine LANDES BIOSCIENCE Georgetown, Texas, U.S.A.Copyright 2006 Landes BioscienceAll rights reserved.No part of this book may be reproduced or transmitted in any form or by anymeans, electronic or mechanical, including photocopy, recording, or anyinformation storage and retrieval system, without permission in writing from thepublisher.Printed in the U.S.A.Please address all inquiries to the Publisher:Landes Bioscience, 810 S. Church Street, Georgetown, Texas 78626, U.S.A.Phone: 512/ 863 7762; Fax: 512/ 863 0081ISBN: 1-57059-668-9Cover artwork by Kristen Shumaker Library of Congress Cataloging-in-Publication DataEmergency medicine / [edited by] Sean O. Henderson. p. ; cm. -- (Vademecum)Includes bibliographical references and index.ISBN 1-57059-668-9 1. Emergency medicine. I. Henderson, Sean O. II. Title. III. Series.[DNLM: 1. Emergency Treatment--Handbooks. 2. Emergencies--Handbooks. WB 39E5321 2006]RC86.7.E5794 2006616.025--dc222006005514While the authors, editors, sponsor and publisher believe that drug selection and dosage andthe specifications and usage of equipment and devices, as set forth in this book, are in accordwith current recommendations and practice at the time of publication, they make nowarranty, expressed or implied, with respect to material described in this book. In view of theongoing research, equipment development, changes in governmental regulations and therapid accumulation of information relating to the biomedical sciences, the reader is urged tocarefully review and evaluate the information provided herein. 5. Dedication Dedicated to the aspiring Emergency Physician.Thanks to Drs. Greenspan, Calder, Swadron and Brown for their invalu-able aid, and to all the authors, for their efforts on behalf of, and patiencewith, this project. Sean O. Henderson, M.D. 6. Contents Preface ............................................................................ xix 1. Emergency Resuscitation .................................................. 1 Stuart P. Swadron, Peter C. Benson and William K. Mallon 2. Cardiovascular Disorders ................................................ 16Jason Greenspan, Shahram Tabib and Stuart P. Swadron Part A: Hypertension and Hypertensive Emergencies ............................... 16 Part B: Acute Coronary Syndromes .......................................................... 23 Part C: Congestive Heart Failure ............................................................... 34 Part D: Endocarditis .................................................................................. 39 Part E: Pericardial Diseases ....................................................................... 41 Part F: Structural Heart Disease ............................................................... 43 Part G: Aortic Emergencies ....................................................................... 49 3. Pulmonary Emergencies .................................................. 53Deborah B. Diercks, Steven Offerman, Mark Thoma and Peter E. Sokolove Part A: Acute Respiratory Failure (ARF) ................................................... 53 Part B: Asthma ......................................................................................... 56 Part C: Chronic Obstructive Pulmonary Disease ...................................... 61 Part D: Pneumonia ................................................................................... 63 Part E: Hemoptysis ................................................................................... 67 Part F: Pleural Effusions ........................................................................... 70 Part G: Pneumothorax .............................................................................. 72 Part H: Pulmonary Embolism ................................................................... 73 4. Neurologic Emergencies .................................................. 77Jacquelyn Hasler Salas Part A: Headache ...................................................................................... 77 Part B: Motor Deficits .............................................................................. 83 Part C: Altered Level of Consciousness ..................................................... 88 Part D: Infections of the Central Nervous System ..................................... 93 Part E: Cerebrovascular Emergencies ...................................................... 101 Part F: Dizziness and Vertigo .................................................................. 110 Part G: Seizures ....................................................................................... 115 5. GI Emergencies ............................................................. 121 Susan Stone and Andrew S. Kassinove 6. Genitourinary Emergencies........................................... 136 Chi Lee, Sean O. Henderson and Sabrina Grassl 7. OB/GYN Emergencies .................................................. 158Stephen D. Docherty Part A: Selected Obstetric Emergencies ................................................... 158 Part B: Selected Gynecologic Emergencies .............................................. 169 7. 8. Orthopedic Emergencies ............................................... 175Susan Zapalac and Mark G. Richmond 9. Endocrine and Electrolyte Emergencies ........................ 225 Jeffrey Denham and Wendy DenhamPart A: Endocrine Emergencies ............................................................... 225Part B: Electrolyte Emergencies .............................................................. 24310. Hematologic Emergencies ............................................. 251 Alicia HaglundPart A: Transfusion in the Emergency Department ................................. 251Part B: Thrombocytopenia ..................................................................... 255Part C: Sickle Cell Anemia ...................................................................... 259Part D: Oncologic Emergencies ............................................................... 264Part E: Congenital Bleeding Disorders .................................................... 27111. Infectious Disease Emergencies ..................................... 278Ellen M. Slaven, Fred A. Lopez and James Rhorer12. General Management of the Poisoned Patient .............. 294 Kathryn ChallonerPart A: Initial Management .................................................................... 294Part B: Individual Toxins ........................................................................ 29713. Selected Environmental Emergencies ............................ 327Paul Silka14. ENT, Maxillofacial and Dental Emergencies ................. 357Kirsten Calder and Jason Ruben15. Ophthalmologic Emergencies ....................................... 388Kirsten Calder and Jason Ruben16. Trauma .......................................................................... 408Stephen D. Docherty and Carla Valentine17. Psychiatric Emergencies ................................................ 450Carrie S. Korn, Adam J. Trenton and Glenn W. Currier18. Special Imaging Studies for the EmergencyDepartment: Angiography MRI V/Q and Sestamibi ..... 471Matt Hendrickson19. Computed Tomography: Emergency DepartmentApplications .................................................................. 492Sujal Mandavia and Diku Mandavia 8. 20. Bedside Ultrasound in Emergency Medicine ................ 515Diku Mandavia and Sujal Mandavia21. Disaster Management ................................................... 533Mark Hollinger22. Special Pediatric Considerations ................................... 545 David Leader, Marilyn Hicks, Russell Karten, Lance Brownand Olly DuckettPart A: Pediatric Cardiopulmonary Arrest ............................................... 545Part B: Cardiac Problems in Children ..................................................... 550Part C: Genitourinary Problems in Children ........................................... 561Part D: Orthopedic Problems in Children ............................................... 570Part E: Infectious Disease Problems in Children ..................................... 577Part F: ENT and Respiratory Problems in Children ............................... 586Part G: Sickle Cell Disease in Children ................................................... 595Part H: Neurologic Problems in Children ............................................... 599Index ............................................................................. 615 9. EditorSean O. Henderson Department of Emergency Medicine Keck School of MedicineUniversity of Southern California Los Angeles, California, U.S.A. Email: sohender@usc.eduChapter 6Associate EditorKirsten Calder Department of Emergency Medicine Keck School of MedicineUniversity of Southern California Los Angeles, California, U.S.A.Email: kcalder@usc.eduChapters 14, 15Assistant Editors Lance BrownDivision of Pediatric Emergency MedicineDepartment of Emergency Medicine Loma Linda University Medical Center and Childrens Hospital Loma Linda, California, U.S.A. Email: lbrownmd@aol.com Chapter 22 Jason Greenspan Department of Emergency Medicine Keck School of MedicineUniversity of Southern California Los Angeles, California, U.S.A.Email: greenspanj@adelphia.net Chapter 2 Stuart P. Swadron Department of Emergency Medicine Keck School of MedicineUniversity of Southern California Los Angeles, California, U.S.A.Email: swadron@usc.eduChapters 1, 2 10. Contributors Peter C. Benson Olly Duckett Department of Emergency MedicineDepartment of Emergency Medicine Keck School of Medicine WakeMed University of Southern California University of North Carolina - Chapel Hill Los Angeles, California, U.S.A. Raleigh, North Carolina, U.S.A. Email: pbenson@sbcglobal.netEmail: Duckett@weppa.org Chapter 1 Chapter 22 Kathryn Challoner Sabrina Grassl Department of Emergency MedicineDepartment of Emergency Medicine Keck School of Medicine Keck School of Medicine University of Southern California University of Southern California Los Angeles, California, U.S.A. Los Angeles, California, U.S.A. Email: challone@usc.edu Email: grasslss@hotmail.com Chapter 12Chapter 6 Glenn W. CurrierAlicia Haglund Department of PsychiatryLAC+USC Medical Center University of Rochester University of Southern California Rochester, New York, U.S.A. Los Angeles, California, U.S.A. Email: glenn_currier@urmc.rochester.edu Email: aliciahaglund@hotmail.com Chapter 17Chapter 10 Jeffrey DenhamMatt Hendrickson LAC+USC Medical CenterCedars-Sinai Medical Center University of Southern California and Los Angeles, California, U.S.A. Department of Emergency Medicine Email: jdwmd@aol.comHarbor-UCLA Chapter 9 Los Angeles, California, U.S.A. Email: mhendrickson@sbcglobal.net Wendy DenhamChapter 18 Huntington Memorial Hospital Pasadena, California, U.S.A.Marilyn Hicks Email: jdwmd@aol.comDepartment of Emergency Medicine Chapter 9 WakeMed University of North Carolina - Chapel Hill Deborah B. DiercksRaleigh, North Carolina, U.S.A. Department of Emergency MedicineEmail: lynhicks@earthlink.net University of CaliforniaChapter 22Davis Medical Center Sacramento, California, U.S.A.Mark Hollinger Email: dbdiercks@ucdavis.eduDepartment of Emergency Medicine Chapter 3 LAC+USC Medical Center Los Angeles County College of Nursing Stephen D. Docherty Los Angeles, California, U.S.A. Department of ClinicalEmail: mhollinger@dhs.co.la.ca.usEmergency Medicine Chapter 21 Keck School of Medicine University of Southern California Los Angeles, California, U.S.A. Email: magicdocs@aol.com Chapters 7, 16 11. Russell Karten William K. MallonDepartment of Emergency Medicine Department of Emergency MedicineLankenau HospitalKeck School of MedicineWynnewood, Pennsylvania, U.S.A.University of Southern CaliforniaEmail: Russell_Karten@hotmail.comLos Angeles, California, U.S.A.Chapter 22 Email: wkmallon@yahoo.com Chapter 1Andrew S. KassinoveEncino-Tarzana Medical CenterDiku MandaviaTarzana, California, U.S.A.Department of Emergency MedicineEmail: kassinove@yahoo.com Cedars-Sinai Medical CenterChapter 5and Keck School of MedicineCarrie S. Korn University of Southern CaliforniaDepartment of Emergency Medicine Los Angeles, California, U.S.A.Keck School of MedicineEmail: mandavia@usc.eduandChapters 19, 20LAC+USC Medical CenterUniversity of Southern CaliforniaSujal MandaviaLos Angeles, California, U.S.A.Department of Emergency MedicineEmail: ckorn@usc.edu Cedars-Sinai Medical CenterChapter 17 and Keck School of MedicineDavid Leader University of Southern CaliforniaDepartment of Emergency Medicine Los Angeles, California, U.S.A.WakeMedEmail: smandavia@mac.comUniversity of North Carolina - Chapel Hill Chapters 19, 20Raleigh, North Carolina, U.S.A.Email: Leader@weppa.orgSteven OffermanChapter 22 Department of Emergency Medicine University of CaliforniaChi Lee Davis Medical CenterDepartment of Emergency Medicine Sacramento, California, U.S.A.Keck School of MedicineChapter 3University of Southern CaliforniaLos Angeles, California, U.S.A.James RhorerEmail: chiyonglee@hotmail.comOur Lady of the Lake HospitalChapter 6Baton Rouge, Louisiana, U.S.A. Chapter 11Fred A. LopezDepartment of Medicine Mark G. RichmondLouisiana State University Department of Emergency MedicineandLoma Linda University Medical CenterMedical Center of LouisianaandNew Orleans, Louisiana, U.S.A. Childrens HospitalEmail: alopez1@lsuhsc.eduLoma Linda, California, U.S.A.Chapter 11 Email: mrichmond@cox.net Chapter 8 12. Jason Ruben Susan StoneLAC+USC Medical CenterDepartment of Emergency MedicineUniversity of Southern California Keck School of MedicineLos Angeles, California, U.S.A. University of Southern CaliforniaEmail: Ruben@usc.eduLos Angeles, California, U.S.A.Chapters 14, 15 Email: sstone_90064@yahoo.comChapter 5Jacquelyn Hasler SalasLompoc District HospitalShahram TabibLompoc, California, U.S.A.LAC+USC Medical CenterEmail: salasjh@hotmail.comUniversity of Southern CaliforniaChapter 4 Los Angeles, California, U.S.A.Chapter 2Paul SilkaDepartment of Emergency MedicineMark ThomaCedars Sinai Medical Center Department of Emergency Medicineand Davis Medical CenterKeck School of Medicine University of CaliforniaUniversity of Southern California Davis, California, U.S.A.Los Angeles, California, U.S.A. Email: togden@hotmail.comEmail: paul.silka@cshs.orgChapter 3Chapter 13Adam J. TrentonEllen M. Slaven Department of PsychiatryDepartment of Emergency MedicineUniversity of RochesterLouisiana State University Health Rochester, New York, U.S.A. Sciences CenterChapter 17Charity HospitalNew Orleans, Louisiana, U.S.A.Carla ValentineEmail: eslaven@aol.comDepartment of Emergency MedicineChapter 11Santa Barbara Cottage HospitalSanta Barbara, California, U.S.A.Peter E. Sokolove Email: carlavalentine@gmail.comDepartment of Emergency MedicineChapter 16University of California Davis Medical Center Susan ZapalacSacramento, California, U.S.A.Department of Emergency MedicineEmail: pesokolove@ucdavis.edu Keck School of MedicineChapter 3 University of Southern CaliforniaLos Angeles, California, U.S.A.Email: zapalac@cox.netChapter 8 13. PrefaceThe idea when we started was to collect the core Emergency Medicineinformation and present it in an abbreviated, succinct manner, useful tohousestaff and medical students. As we progressed it became obvious thatthe very breadth of the specialty prevented any one person from accomplish-ing this task. It also became obvious that our specialty had advanced past thepoint where succinctness was possible. We peeled, boiled and pared, andcame up with this. We hope you find it useful. 14. Acknowledgments To Carrie S. Korn, R.N., for her help in keeping track of all that paper. 15. CHAPTER 1 CHAPTER 1Emergency ResuscitationStuart P. Swadron, Peter C. Benson and William K. MallonWhat Is Resuscitation? Resuscitation, a word derived from the Latin word meaning to set in motion, isthe term most commonly used to describe the emergent treatment of the most se-verely ill and injured patients. To the emergency physician, the term encompassesnot only attempts to reanimate those patients in cardiopulmonary arrest, but thetreatment of virtually any diseases in the extremes of presentation. Resuscitation isan active process that is intervention-oriented and often invasive. The emergencyphysician (EP) confronted with a resuscitation must multitask and set into mo-tion a team of health care workers which includes nurses, technologists and con-sultants.Resuscitation and the Downward Spiral of Disease Most disease processes move through stages of severity, beginning with an asymp-tomatic phase and progressing toward their end-stage. Generally speaking, distur-bances in one physiologic function lead to disturbances in others and, through asort of pathologic multiplier effect, diseases gain momentum as they progress.Diseases that have reached their end-stage often have such momentum that theyrequire intensive and rapid intervention if there is to be any hope of reversing theunderlying pathology. Although patients may present to the emergency departmentat any stage in the continuum, it is those patients at the bottom of the spiral, thosewith decompensated and end-stage disease, that will require resuscitation. In general, attempts are made to tailor the treatment of a particular patient to thetempo of their disease. The treatment of these processes should ideally occur at asimilar pace, because abrupt changes may cause additional risk to the patient. None-theless, the momentum of end-stage disease will often force the emergency physicianto use drastic and potent therapy, and such therapy is usually not without adverseconsequences. The effect of the unwanted effects of therapy, together with the pow-erful and synergistic downward forces of multiply deranged physiologic functions,make resuscitation among the most challenging tasks of the emergency physician.Shock: The Final Common Pathway The final common pathway of most severe disease states is that of shock. Simplydefined, shock is the failure of the circulation to provide adequate tissue perfusion.Although shock may not be present in all patients requiring emergent resuscitation,if untreated or treated inadequately, most will eventually deteriorate into a shockstate. Once an illness progresses to a shock state, further deterioration involves acomplex interaction between the underlying disease, host factors and the patho-physiology of the shock state itself. Because of its central role in severe decompensated disease, a working knowledgeof the classification and approach to shock is essential. When the diagnosis is known,Emergency Medicine, edited by Sean Henderson. 2006 Landes Bioscience. 16. 2Emergency MedicineTable 1.1. Classification and causes of shock1 Cardiogenic (inadequate pump function)Cardiac ruptureCongestive heart failureDysrhythmiaIntracardiac shunt (e.g., septal defect)Ischemia/infarctionMyocardial contusionMyocarditisValvular dysfunctionDistributive (misdistrubution of the circulating volume)Adrenal crisisAnaphylaxisCapillary leak syndromesNeurogenicSepsisToxicologicObstructive (extracardiac obstruction to circulation)Air embolismCardiac tamponadeMassive pulmonary embolusTension pneumothoraxHypovolemic (Inadequate circulating volume)Adrenal crisisHemorrhageSevere dehydrationtreatment is directed at both the underlying cause as well as the shock state itself. Forthose patients in whom the diagnosis is unknown, general resuscitative measuresand treatment of shock proceeds alongside the diagnostic evaluation. Table 1.1 out-lines the major classes of shock and gives examples of individual etiologies of eachclass. Many patients have compound presentations when more than one root causeis present.The Recognition of Occult Shock Many of the traditional clinical indicators of shock, such as blood pressure (BP)and heart rate (HR), lack the sensitivity to identify all patients in shock. In fact,more sophisticated indices, such as pooled venous oxygen saturation measuredthrough a central catheter, can demonstrate a mismatch between the delivery ofoxygen to the tissues and its consumption in some patients with normal or elevatedBPs. Moreover, evidence suggests that using such indices to guide therapy in septicshock (not simply the BP) results in better outcomes. Thus, the early identificationof shock before the traditional vital signs are grossly deranged (in its so-called oc-cult form) is essential to management and disposition. In the ED, shock is still most often recognized by the presence of persistent hy-potension (e.g., systolic BP of 100 in non-pregnant adults) is present in most patients with shock; however, its presence may be masked by multiple factors including spinal cord injury, medications, intra-abdominal catastrophe, older age and cardiac conduction abnormalities.Blood pressure Hypotension (arbitrarily systolic BP 0.9 is a more sensitive indicator of shock than either blood pressure or heart rate alone.Pulsus paradoxus A wide variation of blood pressure with respiration (>10 mm Hg) may indicate obstructive shock (e.g., cardiac tamponade)Respirations Either high (>24/min) or low (2 seconds) is another sign of shock.Urine output Most often reduced (105 F), aggressive mechanical cooling measures may be necessary. Ster-ile dressings should be applied to patients with burns.Resuscitation PhaseHistory Historical information should be elicited from either prehospital personnel, fam-ily members as well as patients themselves. Historical elements may point to a par-ticular class of shock or underlying process. Some findings, however, such as alteredmental status and chest pain, may be simply a result of inadequate tissue perfusionand not the key to determining the cause. Identification of a class of shock presentwill help guide the initial resuscitation. For example, a history of bleeding, vomit-ing, diarrhea or trauma will immediately alert the clinician to the possibility ofhypovolemic shock and the need for rapid volume administration. A history of heartdisease, especially with the symptoms of paroxysmal nocturnal dyspnea or orthop-nea, are highly suggestive of a cardiogenic shock state. A history of infection, fever 24. 10 Emergency MedicineTable 1.5. Important clues on history1 Critical historical elementsBystander resuscitation Rescue breathingChest compressionsAutomated external defibrillationMedical alert/identification braceletsMedications brought in by paramedicsOld medical records/electrocardiogramsOrgan donor identification/drivers licenseParamedic and bystander observationsPatients clothing/belongings for medications/devices/recreational drug paraphernaliaPresence of possible toxins on sceneResponse to prehospital interventions OxygenFluid challengeElectrical therapyMedicationsPositioningVital sign trends and neurological status changes in prehospital phaseHistorical clues in shock states:History Possible Class Of ShockPreceding chest pain, Cardiogenicshortness of breath ObstructiveOrthopnea CardiogenicAny new medicationDistributive (anaphylactic)Vomiting and diarrhea HypovolemicHemorrhageHypovolemicRashDistributive (anaphylactic, septic)Intravenous drug useDistributive (septic)CardiogenicIndwelling devices (catheters, lines) Distributive (septic)Chronic debility/neurologic disease Distributive (septic)HypovolemicTraumaHypovolemic (hemorrhage)Diagnostic investigationsor the use of a new medication may suggest distributive shock. Table 1.5 reviewscritical historical elements and clues that may lead to life-saving interventions in theresuscitation of the critically ill patient.Bedside Diagnostic Investigations The nature of emergency resuscitation precludes the type of methodical diagnos-tic workup that is possible in less critically ill patients. Each diagnostic tool must beevaluated for its ability to change the course of the resuscitation. Near immediateresults are essential, and tests should not interfere with life-saving interventions.Table 1.6 outlines diagnostic investigations that are useful during the initial phasesof resuscitation.Secondary Survey As the severity patients condition on presentation increases, so does the relativeimportance of the physical examination. Thus, both primary and secondary surveysin resuscitation are primarily directed at physical findings. There is a significant 25. Emergency Resuscitation 11Table 1.6. Diagnostic investigations in resuscitationContinuous monitoring 1Pulse oximetry Pulse oximetry is considered a fifth vital sign. It is tremendously helpful when it can be recorded accurately; however, in severe shock states diminished pulses and cool extremities may make it impossible to obtain. Pulse oximetry probes can be placed on the earlobes as well as the extremities. Falsely reassuring readings may occur with abnormal hemoglobins, such as with CO toxicity or methemoglobinemia.Neurological statusMental status has also been referred to as a vital sign. A progres- sive alteration in mental status has a broad differential diagnosis, but within the context of an individual resuscitation its signifi- cance is often clear. In shock states, it may represent worsening cerebral perfusion or hypoxia and the need for more aggressive resuscitative efforts. In patients with intracranial pathology, it may represent brain herniation and the need for lowering intracranial pressure, especially when combined with localizing signs. When toxic, metabolic and endocrinologic derangements are present, worsening electrolyte abnormalities or hypoglycemia may be present and a multitude of interventions, ranging from simple dextrose administration to hemodialysis may be necessary.Pain scalesSigns of pain, both verbal and non-verbal, should not be ignored. These may indicate the need to search for an occult injury such as a fracture or penetrating trauma that may change the direction of the resuscitation. Pain can also be used as a guide to the success of resuscitation, as is the case when chest pain and dyspnea resolve with adequate treatment of myocardial ischemia or pulmonary edema.Continuous cardiac Continuous telemetry is essential in any resuscitation to monitor monitor for life-threatening dysrhythmias and responses to treatment.Electrocardiography12-lead EKGThe 12-lead EKG is enormously helpful in resuscitation. It has utility in both cardiac and non-cardiac emergencies. EKG findings may be either the cause or result of the underlying condition requiring resuscitation. Attention is directed at signs of myocardial infarction and ischemia, electrolyte derangements and clues to other life threatening pathologies such as decreased voltage in cardiac tamponade or signs of acute right-sided heart strain in pulmonary embolus. Certain drug toxicities have characteristic EKG findings as well.Additional EKG leads Right-sided precordial leads (RV3 and RV4) may be critical in identifying the cause of cardiogenic shock as right ventricular MI. Posterior leads (V8 and V9) may unmask the presence of posterior MI.Bedside laboratory testsBlood glucoseCritically low blood glucose results from many different life- threatening processes and must be addressed immediately. The finding of high blood glucose is similarly important and may help tailor early resuscitative efforts. Blood glucose should be measured in all patients with altered mental status and, when abnormal, frequent rechecks are indicated. continued on next page 26. 12 Emergency MedicineTable 1.6. ContinuedHemoglobin orBoth of these tests express hemoglobin concentration and, as1hematocritsuch, can appear misleadingly high in acute hemorrhage before volume resuscitation has occurred. These tests are subject to error, and repeat and serial values should be obtained when they are utilized to guide resuscitation.Pregnancy test A positive serum or urine pregnancy test may lead to a diagnosis of the underlying pathology in a critically ill female. In addition, this finding may affect decisions made during resuscitation with respect to monitoring, emergent procedures, the selection of medications and imaging studies and disposition.Blood type and This is an essential test that must be performed to facilitate crossmatchtreatment with blood and blood products in a multitude of resuscitations, both traumatic and non-traumatic. The infusion of fresh frozen plasma and platelets also requires crossmatching.Bedisde electrolytes The availability of blood electrolyte analysis at the bedside is increasing and very helpful. Knowledge of the electrolytes in the first few minutes may enable critical interventions to be started early. In some cases, such therapies should be started even before electrolytes are available (e.g., giving emergent treatment for hyperkalemia in the presence of a typical EKG and history)Arterial blood gases Although an assessment for hypoxia and hypercarbia should be made clinically, arterial blood gases have a special role when pulse oximetry is not possible or unreliable, to assess for certain toxins such as carbon monoxide and methemoglobin, and to assist with mechanical ventilation management. The pH and base excess values obtained from blood gases (including venous gases) may also be used as an adjunct to gauge the severity of shock states and response to resuscitative efforts.Pooled venousRequires the placement of central venous line with a special oxygen levels probe. May be used to gauge the severity and response to resuscitation.Other bedside assays Although there are many potential pitfalls in their application and interpretation, bedside assays may be extremely helpful. In some cases, elevated cardiac markers may confirm suspicion of an MI. A variety of toxicological tests are now available, and, in the appropriate circumstances, bedside screening assays for various bioterrorism agents.Diagnostic imagingChest film An early portable chest X-ray is of paramount importance. It may, by itself, identify the type of shock state present (e.g., the finding of cardiomegaly and pulmonary edema in cardiogenic shock, tension pneumothorax in obstructive shock, hemothorax or pleural effusion in hypovolemic shock). It may also be helpful in pulmonary embolismless for the presence of rare signs such as Hamptons Hump and Westermarks sign than for the absence of significant findings pointing to alternative diagnoses such as pulmonary edema and pneumonia. A widened or abnormal mediastinum may represent aortic rupture or dissection.Cervical spine films The presence of cervical spine trauma may help explain the findings of shock, neurological deficits and ventilatory failure. continued on next page 27. Emergency Resuscitation 13Table 1.6. ContinuedPelvis This is an important film that may identify a source of hemor- rhage and occult trauma.1Lateral soft tissue neck This film may identify mechanical airway obstruction, a source of septic shock or foreign bodies.Abdominal filmsAlthough rarely helpful in resuscitation, a single abdominal film may show a pattern of calcification of the aorta in the case of a ruptured aortic aneurysm and the presence of radiopaque toxic ingestions such as iron, phenothiazines and enteric release tablets.UltrasonographyBedside ultrasound is ideal for use in resuscitation because of its availability, repeatability and speed. Bedside echocardiography can be used to reveal the presence of various shock states by identifying cardiac tamponade, global hypokinesis or right ventricular outflow obstruction. In the future, it may be utilized by emergency physicians to evaluate valvular lesions and dyskinesis. It can also assist with the distinction between pulseless electrical activity and cardiac standstill (electromechanical dissociation). This may help to determine when resuscitation efforts should be terminated. Abdominal ultrasound may quickly identify free-fluid (most importantly, hemorrhage) in the peritoneal cavity. Hemothorax, as well as pleural effusions, may also be identified during the focused assessment with sonography for trauma (FAST) examination. The aorta may be quickly imaged to assess for abdominal aortic aneurysm. Pelvic ultrasonography in the female patient with intraperitoneal hemorrhage may further delineate the source of shock. The absence of an intrauterine gestation in a pregnant female may represent ectopic pregnancy, whereas its presence may indicate a bleeding cyst, heterotopic ectopic pregnancy or occult trauma. Ultrasonography also has a role in assisting with emergency procedures, such as line placement and pericardiocentesis.Cranial CT Of all CT studies, cranial CT, because of its speed and lack of need for contrast, may be performed even in the unstable patient. It may identify the need for emergent surgical decom- pression, measures to lower intracranial pressure or the search for other causes of altered mental status, all which may change the course of a resuscitation.overlap in the examination during the primary and secondary surveys, but the sec-ondary survey tends to reveal those features which would be missed unless specifi-cally looked for. In the context of an individual resuscitation, some of these findingsmay be very important or even critical. Simply stated, the secondary survey is a complete, compulsive physical examina-tion. Once resuscitative measures are underway, every critically ill patient shouldhave such an examination. Several examples of secondary survey findings that mayalter acute management are given below: 28. 14 Emergency MedicineFindings Possible Diagnostic SignificanceImpaired visual acuity Occult trauma Arterial thromboembolism1(cerebrovascular accident, aortic dissection)Hemotympanum Occult head traumaNuchal rigidity, meningeal signs Meningitis Subarachnoid hemorrhageThyroidectomy scar Myxedema comaRight ventricular heaveObstructive shock (acute right heart strain, massive pulmonary embolism)Absent bowel soundsDistributive or hypovolemic shock (peritonitis) Occult spinal cord injuryRetained vaginal foreign bodyDistributive shock (toxic shock syndrome)Dysmetria, ataxia limb movements Cerebellar lesionUnilateral upgoing plantar responseCerebrovascular accident Non-convulsive status epilepticusDefinitive Care Phase Definitive care phase of the resuscitated patient may begin in the ED and con-tinue in various inpatient settings (the operating room, intensive care unit, cardiaccatheterization or interventional radiology suite, etc.). Transfer to another facilityfor specialized care may be necessary. The importance of the family of the critically ill patient should not be forgotten.Many patients requiring extensive resuscitation in the ED may have been previouslywell. In the case of patients with chronic, controlled disease, family members maybe quite shaken by the sudden decompensation in their loved ones condition. It isthe responsibility of the EP and other members of the primary resuscitation team(nursing staff, social services) to make themselves available to the family as soon as itis possible. Early communication with family and friends serves several purposes: toobtain additional relevant history, to explain the current condition and resuscitativeefforts that are taking place, to clarify any advance directives or previously expressedwishes of the patient, and to express the concern and support of the resuscitativeteam. Although controversy exists as to whether family members should be permit-ted to view resuscitative efforts, there is little doubt that interacting with familymembers in these situations is a skill that requires training, practice and flexibility. Other individuals that may become involved as indirect members of the resusci-tation team include religious or spiritual counselors, organ procurement specialists,law enforcement, forensic specialists, sexual assault and domestic violence person-nel. It is the responsibility of the EP to understand the reporting requirements forvictims of violence, abuse, neglect and organ procurement in their respective prac-tice jurisdictions.Ethical and Legal Aspects of ResuscitationMany ethical issues are magnified and intensified during a resuscitation. Howaggressive should resuscitation efforts be when there is a low likelihood of survival?How should resources in the ED be distributed between critically ill patients withpoor prognoses and less severely ill patients? Under what circumstances is a patientthat is still communicating in a position to refuse resuscitative efforts when they are 29. Emergency Resuscitation 15emergently needed? What process should be followed to obtain consent for organdonation? There are, however, certain legal realities that the EP and other members of the 1resuscitation team need to be compliant with. Moreover, laws and guidelines thatapply to medical emergencies differ from jurisdiction to jurisdiction. These includelaws relating to Do Not Resuscitate (DNR) orders, advance directives, living wills,consent or refusal of treatment and mandatory reporting laws to police, coroner andvarious social agencies. In general, resuscitative efforts should not be initiated when obvious signs ofdeath are apparent, such as dependent lividity, rigor mortis or trauma inconsistentwith life. Although statutes regarding DNR directives vary, the fundamental right ofan individual to make decisions about their medical care, including end-of-life care,should be honored by medical personnel. This right was recognized in the UnitedStates by the Patient Self-Determination Act of 1991. Similar legislation exists inother countries. The decision of when to cease resuscitative efforts once they have begun is oftenmore difficult. Survival after prolonged loss of spontaneous circulation and, perhapsmore importantly, survival with neurological function that would be acceptable tothe patient, becomes less likely as time elapses, with the rare exception of miraculoussurvival such as sometimes occurs with victims of accidental hypothermia. Ulti-mately, a judgment must be made by the responsible physician, weighing the likeli-hood of benefit against the disadvantages of continuing aggressive resuscitative efforts. 30. CHAPTER 2Cardiovascular DisordersJason Greenspan, Shahram Tabib and Stuart P. SwadronPart A: Hypertension and HypertensiveEmergencies Hypertension is one of the most common conditions affecting patients in devel-oped countries. As the population ages and the emergency department continues toserve populations without access to appropriate primary care, issues regarding hy-pertension will become more important. Emergency Physicians must be comfort-able in evaluating and treating patients with conditions associated with an acute risein blood pressure, conditions secondary to long-standing hypertension, as well aswith the complications of medications used to control hypertension.Definitions Essential Hypertension is a persistently elevated blood pressure measured on two sepa-rate occasions. The Joint National Committee on Prevention, Detection, Evaluation,and Treatment of High Blood Pressure has classified hypertension based on the degreeof elevation (Table 2A.1). Hypertensive Urgency is the presence of an elevated BP without signs or symptoms ofend organ damage. Blood pressure should be reduced gradually over 24-48 h in hyper-tensive urgencies. Hypertensive Emergency is the presence of an elevated BP with evidence of end-organdamage. Table 2A.2 lists conditions regarded as true hypertensive emergencies. Theseconditions necessitate the careful reduction of blood pressure in minutes to hours.Epidemiology/Pathophysiology The majority of hypertensive emergencies occur in previously hypertensive patients.In these patients, the ability of the body to autoregulate blood pressure is adjusted toaccommodate for the chronic elevation of blood pressure. A hypertensive emergencyoccurs with an acute elevation in blood pressure over baseline. While the actual blood pressure is important in the evaluation and diagnosis of theseconditions, it is the presence of end-organ damage and not the actual blood pressuremeasurement that indicates the need for emergent lowering of blood pressure. The rate of elevation of the blood pressure may be more important in the pathogenesisof end-organ damage than the actual blood pressure.Diagnosis and EvaluationHistory and Physical Examination The evaluation of the hypertensive patient involves a careful history focused on evalu-ating the presence of symptoms suggestive of end-organ damage, the risk of develop-ing subsequent end-organ damage if untreated, and any past treatment for hyperten-sion or associated conditions.Emergency Medicine, edited by Sean Henderson. 2006 Landes Bioscience. 31. Cardiovascular Disorders17Table 2A.1. JNC-VI classification of blood pressure in adultsCategory Systolic BPDiastolic BPOptimal6 L 142. 128Emergency Medicine Lipase has higher diagnostic accuracy and is more cost effective compared to amylase.Amylase is both of salivary and pancreatic origin, but most labs do not differentiatebetween the two. Therefore the results of an elevated amylase are misleading. Lipasehas a higher sensitivity. Imaging studies are indicated in patients with intrabdominal sepsis and to rule outcomplications. CT scan and ultrasound can be used. If suspect pancreatitis but no labdiagnosis may be indicated.Treatment Patients with pancreatitis may have baseline hypoxemia which progresses to ARDS if not managed early. Once ARDS develops, pancreatic injury is exacerbated. Therefore application of oxygen early on is preferred.. Caution should be used with administration of insulin as there is exaggerated response with pancreatitis and profound hypoglycemia may result.5 These patients tend to be hypocalcemic and may benefit from supplementation. Nasogastric suction is no longer recommended as it prolongs hyperamylasemia and increases pain medication requirement. However, it may be necessary in the case of duodenal obstruction. Cimetidine, glucagon and atropine fail to show any benefit in alleviating symptoms or complications. Patients will require admission and monitoring for complications such as pseudocyst, gastrointestinal bleeding, cholangitis, ARDS, metabolic disturbances, encephalopa- thy and DIC. CT scanning in patients with overwhelming sepsis without a source may identify cases of pancreatitis. Autopsy studies have shown many missed cases of fatal pancreatitis in this subgroup of patients. Mild cases without evidence of biliary tract involvement or systemic involvement may be candidates for outpatient management if close follow-up is available.Peptic Ulcer Disease and GastritisRisk Factors/Etiology H. pylori (most common cause of ulceration) NSAIDs, aspirin common cause of bleeding ulcers and gastritis Alcohol Bile reflux Pancreatic enzyme reflux Gastrinoma (Zollinger-Ellison syndrome) Severe stress (e.g., trauma, burns)Clinical Presentation and Diagnosis Gastritis and PUD usually are indistinguishable in the ED without endoscopy. Typically epigastric/left upper quadrant burning pain that may radiate to the backafter meals. May be relieved by food, antacids (duodenal), or vomiting (gastric). A type and cross match should be sent if the patient is actively bleeding. Helicobacter testing is useful in the primary care setting to guide treatment.Treatment Iced saline lavage should never be performed. This is a dangerous action. It had beenthought that cooling would cause vasoconstriction and accelerate cessation of bleed-ing, but this is now known to cause arrhythmias without decreasing bleeding. Nasogastric tube. While evacuation of blood from the gut may be one benefit fromnasogastric lavage, this procedure can cause great discomfort. It may also be 143. GI Emergencies 129nondiagnostic in a large number of cases, and ultimately the patient will need endos-copy. Therefore early consultation with the gastroenterologist is key. Etiology of gastrointestinal bleeds on endoscopy in those with history of varices foundthe majority of patients with bleeding were bleeding from acute gastric duodenitisfollowed by gastric ulcer then duodenal ulcer, varices, Mallory Weiss, esophagitis.H2 Blockers and Proton Pump Inhibitors Proton pump inhibitors and H2 blockers are not effective in the acute phase of bleed-ing. However proton pump inhibitors may help decrease rebleeding after endoscopy.Vasoconstrictors Vasopressin not too beneficial and risk of hypertension, stroke, coronary ischemia Dose-related decrease in coronary flow and cardiac output Octreotide has a similar mechanism as somatostatin but is more potent and longeracting decreasing splanchnic blood flow and inhibiting gastric acid secretion 5 Patients required less blood transfusion, fewer required surgical and endoscopic inter-vention after a 100 mcg bolus followed by 25 mcg/h when compared to H2 blockers Given to patients with hematemisis and/or tarry stool and evidence of bleeding pepticulcer on early endoscopysubset to which it is applicableOutpatient Management of UGILow risk criteria that have been identified that may warrant outpatient man-agement: No high risk endoscopic feature/varices/portal hypertenisve gastropathy No debilitation No orthostatic vital sign change No liver disease or concomitant disease No anticoagulation or coagulopathy No fresh hematemesis No severe anemia Adequate home supportHigh Risk Criteria BLEED criteria good screening tool to decide which groups are likely to developrelated in-hospital complication. Bleeding, Low systolic blood pressure, Elevated pro-thrombin time, Erratic mental status, Disease comorbid. 33% of patients with BLEED criteria had complications. Patients with an upper gastrointestinal bleed with signs of hypoperfusion such as syncope, confusion, dizziness or hypotension should have myocardial ischemia ex- cluded. Upper GI bleed Peptic ulcer disease: Risk groups include alcohol use, cigarette use, medications such as NSAID use. Variceal bleeds: Risk groups include those with liver failure and portal hypertension. Variceal bleeds are frightening but remember that most UGI bleeds in patientswith varices are from sources other than the varices. If do have variceal bleed, drug therapy to decrease splanchnic flow is first line therapy(vasopressin and octreotide): Vasopressin decreases cardiac output, increases systolic hypertension, arrhythmias and bradycardia. inhibits fibrinolysis and may therefore interfere with hemostasis. Requires a continuous infusion due to short half life (20 min) 144. 130Emergency Medicine Somatostatin is more effective in many regardslocalized to splanchnic vascula-ture and produces fewer effects but no difference in all cause hospital mortality When compared, long acting vasopressin and somatostatin (octreotide) equiva- lent Given the longer half life of octreotide and fewer adverse risks then may be better In last abstract initial control of bleeding achieved in 90% of patients with scle- rotherapy and 84% octreotide groupMassive GI Hemorrhage Treatment Massive upper GI bleeding is a far more common emergency than lower GI bleed-ing. It may present as hematemesis, melena or simply shock with a positive stool testfor blood or NG aspirate. Sources include peptic ulcer and gastroesophageal varices.Massive lower GI bleeding is caused by angiodysplasia and diverticular disease.5 Primary Survey Will Require Vigorous Suctioning of the Airway Wide open normal saline with multiple large bore IVs (16 gauge or greater) are indi-cated to treat shock. Type O blood should follow the first 2 L via rapid transfuser, untiltype-specific and then cross-matched blood is available. Fresh frozen plasma is indicated for suspected coagulopathy (e.g., with stigmata ofchronic liver disease). NG tube for lavage and gastric emptying is indicated and maybe used as one gauge of active bleeding. Emergency endoscopy for hemostasis can beperformed by qualified personnel. In addition to emergent consultation for endoscopy, emergent surgical consultationshould be sought. Octreotide (50-100 mcg IV bolus followed by an infusion of 50 mcg/h) is indicated asan adjunct to other therapies or when other therapies are unavailable for massive up-per GI bleeding. Balloon tamponade via Sengstaken/Blakemore or similar tube should be attempted inthe event of severe uncontrolled upper GI hemorrhage. Apparent massive lower GI hemorrhage may be from an upper GI source (which maybe revealed by NG tube or upper GI endoscopy). If these are negative, either interventional radiological methods or laparotomy will berequired to stop bleeding. Although not entirely reliable in acute hemorrhage, serial bedside hemoglobin deter-minations are helpful in guiding resuscitations. Hypothermia should be avoided by covering the patient with warm blankets and us-ing warmed IV fluids and blood products. Stigmata of chronic liver disease as well as purpura and petechiae should be soughton initial survey. This may assist in predicting the site of bleeding (e.g., the possibil-ity of esophageal and gastric varices) and need for factor replacement during theresuscitation. A history of aortic repair surgery may indicate a aortoenteric fistula, which is managedoperatively.CholecystitisRisk Factors/Etiology Common illness with over 15 million Americans affected. Present frequently for pain control. Typically in adult females. Tends to be associated with fatty meal. Incidence rises withage. While uncommon in children, presence may suggest underlying disorder (sicklecell, hemolytic anemia). 145. GI Emergencies131Clinical Presentation and Diagnoses May present with abdominal pain in right upper quadrant or epigastrium which tendsto be constant and severe. Pain can radiate to shoulder or back. Nausea and vomiting common. Murphys sign: inspiratory arrest during palpation of RUQ. If fever or refractory pain is present or consider cholecystitis. Gallstones are either cholesterol (most common), pigment (associated with hemolyticanemia). Elevated liver function studies suggest common duct obstruction, cholangitis, chole-cystitis or hepatic involvement. Ultrasound should be initial imaging study since it is over 90% sensitive and allowsvisualization of common bile duct: Duct size over 10 mm suggests obstruction5 Gallbladder wall thickening over 5 mm or pericolic fluid suggestive of cholecystitis. HIDA scanning may detect obstruction or cholecystitis if stone is at neck of gallblad-der and nonvisualized on ultrasound. Routine abdominal films are of no utility.Treatment The first priority is analgesia. NSAIDs have been used with great success. Narcoticanalgesics with antiemetic are also part of the initial therapy. Unsuccessful pain con-trol or cholecystitis needs hospital admission. Surgical consultation is required in patients requiring admission or those diagnosedwith cholangitis, common bile duct dilatation and/or cholecystitis. Antibiotics are indicated for acute cholecystitis, cholangitis, or common bile duct di-latation. First line antibiotics include amp/sulbactam, flouroquinolone and flagyl orpipercillin/tz.HerniasRisk Factors/Etiology A hernia occurs when a viscus internally or externally protrudes from its normal cavity. Risk factors include prematurity, family history, genitourinary abnormalities, ascites,peritoneal dialysis, ventriculoperitoneal shunt, cystic fibrosis, lung disease, pregnancy,or wound sites. Most hernias are inguinal and most occur in men. An indirect inguinal hernia occurs lateral to the inferior epigastric vessels. These arethe most common hernias in both men and women. A direct inguinal hernia is an acquired defect medial to the inferior epigastric vesselsand occurs mostly in older adults. A femoral hernia occurs below the inguinal ligament in the femoral canal, occursmostly in women, is very rare, and often becomes strangulated. An umbilical hernia occurs in infants. Most close spontaneously by one year of age. Spigelian hernias occur just lateral to the rectus sheath in the abdominal wall and arevery rare. A Richter hernia involves incarceration of the wall of a hollow viscus. An incisional hernia occurs at the site of a previous wound.Clinical Presentation and Diagnosis An asymptomatic hernia presents without pain or tenderness, is reducible, and willenlarge with standing or increased intra-abdominal pressure. 146. 132 Emergency Medicine An incarcerated hernia is not reducible and is painful. It may or may not present withsymptoms of bowel obstruction, including nausea and vomiting. A strangulated hernia presents as a toxic appearing incarcerated hernia. Systemic tox-icity secondary to ischemic bowel may be present. If necrotic bowel is suspected donot attempt to reduce the hernia and return the dead bowel into the abdomen. A femoral hernia will present with medial thigh and or groin pain. Diagnosis is based on clinical exam. Abdominal radiographs are useful to exclude abowel obstruction. A hernia must be distinguished from a scrotal hydrocoele, which will transilluminatewith a light source, while a hernia will not.Treatment An incarcerated hernia without signs of bowel obstruction may be reduced with painmeds and gravity and referred for surgical follow-up.5 Infants with inguinal hernias are at high risk for incarceration and should be urgentlyreferred to a pediatric surgeon for repair. In contrast, umbilical hernias often have abenign course and do not require urgent referral. Strangulated hernias or any toxic-appearing patient should be started on broad spec-trum antibiotics, IV fluids, nasogastric decompression, and receive emergent surgicalconsultation.Esophageal EmergenciesRisk/Factors Etiology 75% of esophageal perforations are due to iatrogenic perforations. Boerhaave syndrome is the cause of 10% of esophageal perforations with 10% of thesedue to trauma. Boerhaave syndrome occurs because the esophagus lacks a serosal layer, Thus, the wallis weaker and may rupture at a lower intraluminal pressure, usually with severe vomit-ing. Most perforations occurs in the lower third of the esophagus in the left posterolat-eral region. All other cases of esophageal perforation are caused by foreign bodies or traumaticperforations. Boerhaave syndrome is more common in middle-aged men after a drinking and eat-ing binge. Esophageal foreign bodies are most common in children. Most objects pass spontane-ously. The most common site of obstruction is the cricopharyngeal narrowing (C6).Clinical Presentation and Diagnosis Delay in diagnoses of Boerhaave syndrome is common and leads to a high mortalityrate. Classic presentation for spontaneous rupture is vomiting followed by severe chestpain. However, many patients have less dramatic presentations. Patients may presentwith abdominal pain, dyspnea, and hematemesis. Subcutaneous emphysema may be palpable in the neck or chest. Hammans crunchmay be heard in 20% of cases over the heart. Patients usually appear acutely ill, hy-potensive, and septic depending on the delay in presentation. Esophageal foreign bodies usually present in adults with retching, vomiting, coughing,dysphagia or choking. In kids, common symptoms also include refusal to eat and stridor. Diagnosis of foreign body ingestion includes plain radiographs. Patients with foreignbody sensation and negative radiographs should undergo direct laryngoscopy. Spe-cialty consultation should be obtained prior to contrast radiographs. Coins are visible on AP radiographs with the flat side visible if in the esophagus and onend if in the trachea. 147. GI Emergencies 133Treatment Treatment of Boerhaave syndrome or a delayed iatrogenic perforation in the emer-gency department includes rescusitation of shock, broad spectrum antibiotics, andemergent surgical consultation. Esophageal foreign bodies require emergent surgical consultation if the patient ap-pears toxic, has an acute abdomen, bloody stools, or persistent vomiting. Button battery ingestion requires emergent GI consultation as esophageal burns canoccur within 4 h and perforation within 6 h. Food impaction can be treated conservatively if the patient can tolerate their own secre-tions. Intravenous glucagon, 1 mg, can be used to relax esophageal smooth muscle.Sublingual nitroglycerin can be used to relax lower esophageal sphincter pressure.Anal/Rectal DisordersRisk Factors/Etiology 5 Hemorrhoids are more common in pregnancy and are associated with constipationand straining bowel movements, obesity, and chronic liver disease. Internal hemor-rhoids are located above the dentate line and are painless. External hemorrhoids arelocated below the dentate line and are painful. Anal fissures are the most common cause of painful rectal bleeding. Pilonidal cysts usually occur in young people and are a chronic recurring reaction toan ingrown hair. Perirectal and perianal abscesses are common in diabetics and drug abusers.Clinical Presentation and Diagnoses Internal hemorrhoids cause painless bright red blood with defecation. They are onlyvisible through an anoscope. External hemorrhoids cause pain with defecation and are usually visible on exam. Rectal bleeding must be referred for further evaluation for malignancy. Other causes of rectal pain include foreign body, venereal proctitis, trauma, abscesses,and anal fissures. Anal fistulas present with malodorous bloody discharge through the fistula. Anal fissures present with painful bowel movements, with the pain resolving betweenbowel movements. Perianal and perirectal abscesses present as a tender red mass and may have concurrentfever and leukocytosis.Treatment Most hemorrhoid patients may be managed conservatively with sitz baths, good hy-giene, bulk laxatives, and stool softeners. Thrombosed external hemorrhoids shouldbe referred to a surgeon, or may be excised and the clots removed in the ED if conser-vative measures have failed. Surgical referral is needed for anal fistulas. Anal fissures may be treated conservatively with sitz baths and local analgesics. All but the most simple perianal abscesses should be drained and followed by a sur-geon. Perianal abscesses should be drained and packed, with antibiotics only necessaryin diabetics and other immunocompromised hosts. Most rectal foreign bodies can be removed in the ED after adequate analgesia. Antibi-otics and surgical or gastroenterological consultation should only be obtained in casesof high risk or perforation or with peritoneal or other toxic signs. Pilonidal cysts may be drained and packed in the ED, with surgical referral appropri-ate for definitive removal of the cyst. 148. 134Emergency MedicineSpecial ConsiderationsElderly Patients with Abdominal Pain Elderly patients presenting with abdominal complaints warrant a complete evalu-ation. Up to 50% of those over 65 yr of age will ultimately have a process evolving thatrequires medical or surgical intervention. Therefore, it is judicious to check laboratoryand imaging studies. While physical examination is important, elderly patients frequently present atypi-cally. They will often lack fever and leukocytosis. For instance, it is well documentedthat elderly patients will have perforated appendicitis at an early time and with a lessobvious exam, than their younger counterparts. Higher morbidity and mortality fromhigher rates appendiceal perforation is the rule. After 50 yr of age perforation rates are5 from 32-70%!Delays in the diagnosis are typically due to: Atypical presentations Anatomy Less blood supply to appendix most likely One-third of perforations are in those with symptoms 15,000 suggests an infectious etiology, while mild leukocytosis without concominantfever usually represents demargination. Some authors also recommend obtaining a serum uric acid level, as it will be elevatedin 50% of all patients with uric acid stones, and a serum calcium to screen forhyperparathroidism and other disorders of calcium metabolism. Other important laboratory tests include CBC, serum electrolytes, BUN and creatinine.Radiographic Studies The IVP has both high sensitivity and specificity, establishing the diagnosis of calcu-6 lous disease 96% of the time. While a flat plate of abdomen (kidney, ureter, and bladder, or KUB) is the standardscout film done prior to an IVP, alone the KUB is not a reliable study to diagnose renalstone disease. Contraindications to radiocontrast medium are known allergy to contrast dye andrenal insufficiency. Other studies that can be used in patients who cannot tolerate IV are helical CT,ultrasound and renal scan. (See Renal Colic on page 507 of this volume.)Differential Diagnosis The key is not to miss a life-threatening condition, such as rupturing abdominal aorticaneurysm (Table 6.2). A careful history and physical exam can frequently elucidate the underlying pathology.Management The mainstay of therapy for ureterolithiasis is IV hydration, analgesia, and antiemetics,if needed. Hydration can be initiated with IV crystalloid infusion of 1 L NS over 30-60 min, andthen 200-500 ml/h. Patients presenting with renal colic are in severe pain and often require significantamounts of narcotic analgesics (morphine sulfate or meperidine in age and weightdetermined doses). NSAIDs, particularly ketorolac, are frequently used in conjunction with narcotics asthey are thought to decrease pain by diminishing ureterospasm and renal capsularpressure. Pain medication should be administered promptly while awaiting the results of fur-ther tests. Most patients with uncomplicated renal stone disease, whose pain is adequately con-trolled and can tolerate oral fluids can be discharged home without patient urologicfollow-up and careful instructions. All patients should be given a urinary strainer and instructed to strain all urine for upto 72 h following cessation of pain. Patients should be instructed to return to the ED immediately for any fever and chills,persistent nausea and vomiting, or for intractable pain, not relieved by prescriptionoral narcotics. Urologic follow-up should be arranged within 1-2 wk. 161. Genitourinary Emergencies147Table 6.2. Differential diagnosis of renal colicAbdominal Aortic May have similar clinical presentation,Contrast CT scan orAneurysm with gross or microscopic hematuriaangiogram, if stable(dissecting or More likely in older malesrupturing) May present with hypotension Palpate for pulsatile abdominal mass with focal tenderness Listen for bruit Palpate distant extremity pulsesAcuteMild to severe flank pain, althoughIVP (or other radio-Pyelonephritis typically not as acute as renal colicgraphic imaging) if More prolonged prodrome, with feverobstruction suspended Urinalysis shows pyuria and bacteruria CAUTION: renal obstruction with pyelonephritis is a urologic emergency requiring prompt consultationPapillary Necrosis Secondary to passage of sloughed IVPmay show 6 papillae down ureter sloughed renal papillae Seen in patients with sickle cellas a lucency within disease, diabetes, NSAID abuse,renal pelvis, but may or history of acute or chronic UTI also mimic a stone UA can show hematuria and pyuria Requires urologic consultation with possible admissionRenal Infarction1. Renal arteryPresents with acute flank pain IVP shows absent embolismand hematuriarenal function Most common acute renal vascular event Most often of cardiac originatrial fibrillation, acute bacterial endocarditis mural thrombus2. Renal arteryAlso presents with acute flank painEmergent angiography aneurysmand hematuriaindicated Usually small and clinically not significant Dissection or rupture is rarebut will cause shock3. Renal veinAcute flank pain with hematuriaIVP shows decreased thrombosisand proteinuriarenal function and Predisposing factors are nephrotic increased renal size syndrome, malignancy, and pregnancy Emergent urologic consultation is required for all cases of renal infarctionEctopic PregnancyUnilateral abdominal painPregnancy test History of amenorrhea, abnormalrequired in all women vaginal bleeding of child-bearing years May present with shockAppendicitis Unilateral presentationLaboratory tests and Subacute prodromephysical exam; if Abdominal tenderness withdiagnosis still in guarding or reboundquestionCT scanwith oral contrast 162. 148 Emergency Medicine There are several situations in which admission is indicated:1. Acute obstruction with concurrent infection. The finding of fever, pyuria, or bacteruria in a patient with renal colic requires further work-up and admission. Urine and blood cultures should be obtained and intravenous antibiotics, covering the usual urinary pathogens, should be promptly started while in the ED. Urologic consultation is required.2. Solitary kidney with complete obstruction. Patients with only one kidney become essentially anephric with complete obstruction and may require surgical drainage. Emergent urologic consultation and admission are required.3. Uncontrolled pain. Patients whose pain can only be controlled by intravenous anal- gesia require admission.4. Intractable emesis. Patients who are unable to tolerate oral fluids must be admitted for IV hydration. Other scenarios, which may or may not require hospitalization, but should be dis-cussed in consultation with a urologist are: patient with underlying renal insufficiency,dye extravasasation demonstrated on IVP, large stone size, and high grade obstruction.6Testicular Torsion The acute scrotum is a common urologic complaint, and the differential diagnosisrests between testicular torsion and other causes of pain. While epididymitis, orchitis, torsion of the appendix testis, hydrocoele and her-nias all represent entities seen by emergency physicians, and are real emergenciesto the patients that present with them, testicular torsion represents the true uro-logic emergency.Epidemiology/Pathophysiology Testicular torsion occurs at a baseline frequency with two additional significant peaksoccurring at infancy and puberty. The baseline frequency is due to the presence of a so-called bellclappers deformityin a subset of the population. This lack of physical tethering system for the testicle places these individuals at aunique risk for the disease and is responsible for the reports of torsion in all age groups. In one series as many as 40% of individuals with torsion were found to have such anabnormality. The two peaks are seen at times during maturation when the testicle grows relativelyfaster than its tethering gubernaculum. The result is a testes that can rotate about its axis, pinching off the blood supply. When torsion occurs, the venous blood supply is obstructed resulting in edema andhemorrhage. These in turn lead to occlusion of the arterial blood supply to the gonad. Although reported in all age groups from neonates to the elderly, the peak incidence isin individuals between the ages of 12 and 18 yr, with an incidence of 1 in 4000 inthose below the age of 25 yr of age.Diagnosis The initial evaluation of a patient with acute scrotal pain or swelling should focus onruling out the presence of testicular torsion. A history of an acute onset of pain, and the absence of dysuria, suggest torsion oversuch entities as epididymitis or orchitis. The pain of torsion is usually described as thunderclap in onset and is not associatedwith a discrete mass such as might be seen in an inguinal hernia. The testicle is tender over its entirety unlike torsion of the appendix testis, and thepain is continuous and unremitting. 163. Genitourinary Emergencies 149 The absence of a high-riding testicle or the presence of a cremasteric reflex should notbe used as evidence that torsion does not exist. Of interest to the emergency physician is the phenomenon of torsion/detorsion of thetesticle. The classic presentation is of a young man who presents with a history of significantscrotal pain that has resolved by the time he arrives in the emergency department. Hedenies any dysuria or urethral discharge; however he states that he has two such epi-sodes in the past two days. The emergency department workup is normal. The concept of an intermittently torsing testicle should be entertained in this settingand appropriate referral to Urology should be given as well as discharge instructionsfor immediate return in the face of any returning pain. From a laboratory standpoint, the only mandatory test would be a dip urinalysis look-ing for hematuria/pyuria. The presence of either of these might suggest an infectiousetiology of the patients pain. Urologic consultation should be obtained early as surgi-cal exploration is definitive therapy. Imaging of the testicle and its blood supply may be accomplished using color flow6doppler or radionuclide imaging. Although the former is considered the standard of care by many, studies have shown ithas important limitations especially in the pediatric population. In one study, up to 40% of normal testes in a pediatric population scanned showed noblood flow. Overall the specificity is reported to be between 83-100% and the sensi-tivity 89-100% for decreased or absent testicular blood flow when compared to thecontralateral testicle. Radionuclide imaging has been reported to have a sensitivity of87-100% and a specificity of 93-100%. Despite these impressive numbers, radionu-clide imaging is considered an alternative in those cases where doppler is not practicalor the results are inconclusive. In one study, the color flow doppler had a sensitivity of only 57% for torsion. There-fore, it should be stressed once again that the diagnosis of this disease should not relyon any single test. The long term ramifications are of enough significance that clinical judgment andsurgical intervention may be all that is necessary to make and confirm the diagnosis.Treatment Emergency department therapy for patients with a suspected torsion focuses on anal-gesia and preparation for surgical exploration. In the mid-1990s there was a group of authors that suggested conservative manage-ment protocol of the patient with the acute scrotum. Overwhelmingly the follow-upliterature was not supportive for such a treatment strategy. Orchipexy by the urologist should be done emergently and should involve both tes-ticles. In some rare cases there have been reports of torsion after orchipexy, a phenom-enon which appears to be related to the use of absorbable sutures. As an aside, in the event that no urologist is available to perform the surgery, and giventhe time sensitive nature of the disease (4-6 h of ischemia time), a general surgeon maybe consulted to perform the procedure.Prognosis Overall, testicular torsion carries a relatively poor prognosis with regards to the in-volved side. The literature reports a salvage rate of 55% to as low as 18% with time to surgerybeing the single most important prognostic factor. Within 10 h, >80% of testes are 164. 150 Emergency Medicinelost and by 24 h the number reaches almost 100%. Reasons for delay include hesita-tion in seeking medical advice as well as misdiagnosis. Ipsilateral torsion not only places the affected testicle at risk but also the contralateraltesticles. It has been demonstrated that torsion of one testicle leads to decreased bloodflow to the contralateral side, with relative hypoxia and apoptosis. The subsequentdecrease in germ cells has been implicated in decreased fertility of these patients. One suggested solution is to increase blood flow via capsaicin which has been shownto decrease the apoptosis which occurs after testicular torsion in rats. Glucocorticoids and nitric oxide have also been suggested as anti-apoptotic agents andhave also been shown to be effective in rats, but no studies of these agents have yetbeen carried out in human subjects.Periuethral AbscessBackground Periurethral abscess is a rare but life-threatening infection of the male urethra andperiurethral areas.6 The spectrum of disease varies from a small isolated abscess to an extending necrotiz-ing fasciitis. Periurethral abscess is classically known to be a complication of stricture disease andgonococcal urethritis. The most common predisposing factors include: urethral stricture disease urinary obstruction previous periurethral abscess gonorrhea recent urinary tract infection diabetes mellitus urethral trauma or surgery chronic indwelling Foley catheter The danger in this seemingly benign process is that if the abscess perforates Bucksfascia, extensive necrotizing fasciitis may ensue.Diagnosis Clinical presentation depends largely on the area affected. If the abscess is confined to Bucks fascia, scrotal and penile swelling is the mainsymptomology. If Bucks fascia is perforated, necrotizing fasciitis may extend throughout the inguinalarea. Fever is a common presenting symptom and may be accompanied by sepsis and shock,depending on the extent of the disease. Extravasation of infected urine has been linked to urethral strictures, which can resultin subsequent urethral disruption. Therefore, it is no surprise that the organisms responsible for urinary tract infectionsare found on abscess evaluation, the most common being E. coli, Proteus mirabilis,Enterococcus species, Morganella morganii, Pseudomonas aeruginosa, Staphylococcus epi-dermis and Bacteriodes species Diagnosis of periurethral abscess is suggested largely by clinical examination. However, urethral sonography and doppler imaging have been shown to offer theadvantages of avoiding radiation to the testes, providing real-time evaluation of thedistensibility of the urethra, and having the capacity of assessing spongiosum andperiurethral tissue involvement and urethral artery location in urethral strictures. 165. Genitourinary Emergencies151 Retrograde urethrography can show the presence of urine extravasation but providesoverall much less information and diagnostic data than ultrasonography of anteriorurethral strictures.Management The mainstay of treatment for periurethral abscesses consists of surgical drainage andantibiotics. Wide debridement and immediate suprapubic urinary diversion must not be delayed. Empiric antibiotics with broad-spectrum coverage should be started immediately andshould be modified appropriately once organisms are isolated with wound, urine, andblood cultures. Walther and colleagues showed that IV cephalosporin and aminoglycoside given for 8days followed by oral antibiotics with prompt surgical intervention decreased mortalityto 1.6% in 63 cases, whereas mortality was as high as 50% in the preantibiotic era, 6%with penicillin and sulfonamides, and 4% with oxytetracycline.Fourniers Gangrene6Epidemiology First described in 1764 by Jean-Alfred Fournier as a gangrene of the penis and scro-tum, necrotizing fasciitis of the perineum, genital or perianal area affects both sexesand is a true emergency. Failure to recognize the entity, delay in treatment and lack of aggressive medical and surgi-cal therapy are all contributors to the high morbidity and mortality seen with this disease. The mortality rate varies by report from 3-45%, and causes of death have includedsepsis, coagulopathy, renal failure, diabetic ketoacidosis and multiple organ failure. Older age, renal or hepatic dysfunction, and anorectal infectious source, are associatedwith higher mortality. Although glycosuria is present in over two-thirds of these patients, the presence ofdiabetes mellitus appears to have no affect on the outcome of the disease and is onlyassociated with approximately 20% of the cases. In addition, the chronic use of alcohol has been associated with 25-50% of the cases.Pathophysiology Although seen in children and women, Fourniers gangrene is more common in males(10:1) and was originally described as a severe gangrenous infection of the scrotum. The most common sources of infectious agents are the local skin (24%), anorectal(21%), and urologic (19%). The disease appears to affect the affluent as well as the socioeconomically depressedindividuals, and the average age of presentation is older than originally described, inone recent series the mean age of patients was 50 yr. The bacteriology of confirmed cases reveals as a rule mixed aerobic and anaerobicorganisms including Clostridia, Klebsiella, Streptococcus, coliforms and Staphylcocci spe-cies. These organisms work synergistically, with the aerobic bacteria keeping the oxy-gen tension low enough to allow anaerobic growth. Initially a cellulitis develops, superficial vessels are thrombosed and gangrene of thesuperficial skin and subcutaneous fat results. While extension of the infection into the muscle layers may lead to myonecrosis, thisis not a characteristic of classic Fourniers gangrene. In addition, while the scrotum may often be affected, the underlying testicles, whichreceive blood from an independent source, are usually not affected. If such involvement does occur, it should prompt a search for a retroperitoneal orintra-abdominal source. 166. 152 Emergency MedicineDiagnosis Clinical presentation of perineal necrotizing fasciitis, while often described as sudden,is more likely insidious over the span of several days. Given its location, some patients may present later than usual due to embarrassment. In its early stages, the disease presents with pain, erythema, and scrotal swelling. Advanced cases are described as rapidly advancing (up to 1 in/h) woody indurationsextending up the anterior abdominal wall, associated with crepitus and purulent, mal-odorous discharge. Diabetes mellitus is a comorbidity in more than two-thirds of these patients. Laboratory findings include leukocytosis, anemia, thrombocytopenia and hyperglyce-mia as mentioned above. Hypocalcemia, caused by chelation of calcium by the bacte-rial lipases, has been reported as an important diagnostic clue, and hyponatremia mayalso be present. Imaging may reveal free air in the scrotum or dissecting upward through the fascialplanes. Ultrasound may demonstrate gas in the scrotum, and CT scan may allow definition of6 the spread of the disease. In reality however, none of these imaging studies should delay the institution of therapyonce there is suspicion of disease.Treatment Treatment of Fourniers gangrene is aimed at stabilizing the thermodynamics of thepatients and beginning antimicrobial infection as rapidly as possible. Appropriate antibiotics include any broad-based regimen. Classically, penicillins were given to combat the streptococcal sp., metronidazole for anaerobic organisms and gentamicin or a third generation cephalosporin for coliforms. Current recommendations replace this cocktail with medications such as imipenem or meropenem as single agents in the patient with confirmed polymicrobial infection. Urologic or surgical consultation is mandatory and should precede any laboratory orimaging results. Replacement of fluids, blood transfusion and antibiotics in isolation cannot replacesurgical debridment of the infectious nidus. Hyperbaric oxygen, recommended by some as an adjunct after the initial debride-ment, has not been shown to improve outcomes when used in this setting.Penile EmergenciesPhimosis Condition in which the foreskin cannot be retracted behind the glans penis By 3 yr of age, 90% of foreskins can be retracted Fewer than 1% of males have phimosis by age 17 Usually not painful, but may produce urinary obstruction with ballooning of foreskin May occur as a result of recurrent balanitis May lead to chronic inflammation and carcinoma Treatment in boys older than 4 or 5 yr of age and in those who develop balanitis orbalanoposthitis is topical corticosteroids (0.1% dexamethasone) to the foreskin threeto four times daily for 6 wk. This loosens the phimotic ring in two-thirds of cases andusually allows the foreskin to be retracted manually. In uncircumcised boys older than 7 or 8 yr old with corticosteroid-resistant phimosisor in boys with ballooning of the foreskin or recurrent balanitis, circumcision or dor-sal slit is recommended. 167. Genitourinary Emergencies 153Paraphimosis Condition in which the foreskin has been retracted and left behind the glans penis,constricting the glans and causing painful vascular engorgement and edema of theforeskin distal to the phimotic ring. Can occur iatrogenically and frequently occurs after penis has been examined or ure-thral catheter has been inserted Can result in marked swelling of the glans penis such that the foreskin can no longerbe drawn forward, which may lead to arterial compromise and gangrene Reduction of paraphimosis can be initiated with gentle, steady pressure to the foreskinto decrease the swelling. Elastic bandage wrap (2 x 2 in) used for 5 min may be helpfulin some cases. Short-term ice-packing may help as an analgesic or a local anestheticblock of the penis may be indicated in marked discomfort. Marked or irreducible cases may necessitate an emergency dorsal slit or circumcisionby a urologist. Reduced paraphimosis should be scheduled for a dorsal slit or circum-cision at a later date, as paraphimosis tends to recur.Balanitis6 Inflammation of the glans, which occurs usually as a result of poor hygiene, fromfailure to retract and clean under the foreskin. Usually responds to local care and antibiotic ointment. Occasionally oral antibiotictherapy may be necessary. Recurrent balanitis may result in phimosis. Balanitis in older patients may be a presenting sign of diabetes, in which cases, circum-cision may be necessary.Balanoposthitis Severe balanitis, in which the phimotic band is tight enough to retain inflammatorysecretions, creating a preputial cavity abscess. Treatment includes cleansing and application of antifungal creams (clotrimazole bid) Urologic follow-up and possible circumcision may be indicated. In the presence of secondary bacterial infection, an oral cephalosporin should be pre-scribed. On occasion, an emergent dorsal slit is required.Penile Fracture Acute tear of the tunica albuginea, presenting with acute swelling, discoloration, andtenderness. Usually caused by trauma during intercourse accompanied by a snapping sound. Urologic consultation is indicated.Peyronies Disease Condition that results in fibrosis of the tunica albuginea, the elastic membrane thatsurrounds each corpus cavernosum, producing curvature of the penis during erection. Difficult to diagnose in flaccid state; however patients prior history of buckling traumamay establish the diagnosis. Physical exam reveals fibrous plaques or ridges along the dorsal shaft of the penis. Benign condition that may resolve or stabilize spontaneously without treatment. Complication may include erectile dysfunction. Reassurance and urologic follow-up are indicated.Priapism Prolonged painful and tender erection that persists beyond or is not related to sexualactivity 168. 154Emergency Medicine Occurs most commonly in patients with sickle cell disease but can also occur in thosewith advanced malignancy or coagulation disorders, those on total parenteral nutri-tion, certain drug therapy, and after trauma or idiopathically. Classified as primary/idiopathic and secondary, or ischemic/veno-occlusive andnonischemic/arterial. Ischemic priapism beyond 4 h is a compartment syndrome requiring emergent medical intervention Nonischemic priapism is less common and is caused by unregulated cavernous in- flow, which usually presents with an erection that is not fully rigid and is painless Drugs reported to cause priapism include but are not restricted to: Antidepressantsbupropion, trazadone, fluoxetine, setraline, lithium Antipsychoticsclozapine Tranquilizersmesoridazine, perphenazine Anxiolyticshydroxyzine Psychotropicschlorpromazine Alpha-adrenergic blockersprazosin6 HormonesGnRH Anticoagulantsheparin, warfarin Recreational drugscocaine, alcohol Complications include urinary retention, infection, and impotence Initial therapy includes terbutaline 0.25-0.5 mg subcutaneously in the deltoid area Corporal aspiration (corpus cavernosum) and irrigation with normal saline or-adrenergic blocker is the next step by a urologist.Suggested Reading1. Ahlering, TE, Boyd SD, Hamilton CL et al. 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