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THE OFFICIAL CME PUBLICATION OF THE AMERICAN COLLEGE OF EMERGENCY PHYSICIANS

Volume 30 Number 7 July 2016

Lumbar puncture (LP) is used in the diagnostic evaluation of central nervous system (CNS) processes, most commonly in cases of suspected infection and subarachnoid hemorrhage. Less commonly, the procedure is used for therapeutic purposes (eg, in cases of idiopathic intracranial hypertension).

Breathe EasyRespiratory complaints in infants and children can be as terrifying to health care teams as they are to family members. Bronchiolitis, one such common diagnosis, typically is self-limiting; however, some of these children will die. Emergency physicians must rely on their clinical acumen to recognize high-risk patients and initiate appropriate treatment.

Tiny BubblesAlthough the vast majority of rashes that present to the emergency department stem from relatively benign etiologies, vesiculobullous lesions warrant particular consideration. A rapid diagnosis is essential to the effective management of these patients, and clinicians must be prepared to identify red flags suggesting a more ominous disease process.

Contributor Disclosures. In accordance with the ACCME Standards for Commercial Support and policy of the American College of Emergency Physicians, all individuals with control over CME content (including but not limited to staff, planners, reviewers, and authors) must disclose whether or not they have any relevant financial relationship(s) to learners prior to the start of the activity. These individuals have indicated that they have a relationship which, in the context of their involvement in the CME activity, could be perceived by some as a real or apparent conflict of interest (eg, ownership of stock, grants, honoraria, or consulting fees), but these individuals do not consider that it will influence the CME activity. Sharon E. Mace, MD, FACEP; Baxter Healthcare, consulting fees, fees for non-CME services, and contracted research; Gebauer Company, contracted research; Halozyme, consulting fees. Joshua S. Broder, MD, FACEP; GlaxoSmithKline; his wife is employed by GlaxoSmithKline as a research organic chemist. All remaining individuals with control over CME content have no significant financial interests or relationships to disclose.

Method of Participation. This educational activity consists of two lessons, a post-test, and evaluation questions; as designed, the activity it should take approximately 5 hours to complete. The participant should, in order, review the learning objectives, read the lessons as published in the print or online version, and complete the online post-test (a minimum score of 75% is required) and evaluation questions. Release date July 1, 2016. Expiration June 30, 2019.

Accreditation Statement. The American College of Emergency Physicians is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The American College of Emergency Physicians designates this enduring material for a maximum of 5 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Each issue of Critical Decisions in Emergency Medicine is approved by ACEP for 5 ACEP Category I credits. Approved by the AOA for 5 Category 2-B credits.

Commercial Support. There was no commercial support for this CME activity.Target Audience. This educational activity has been developed for emergency physicians.

Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American College of Emergency Physicians, PO Box 619911, Dallas, TX 75261-9911. Send address changes and comments to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas, TX 75261-9911, or to [email protected]; call toll-free 800-798-1822, or 972-550-0911.

Copyright 2016 © by the American College of Emergency Physicians. All rights reserved. No part of this publication may be reproduced, stored, or transmitted in any form or by any means, electronic or mechanical, including storage and retrieval systems, without permission in writing from the Publisher. Printed in the USA.

The American College of Emergency Physicians (ACEP) makes every effort to ensure that contributors to its publications are knowledgeable subject matter experts. Readers are nevertheless advised that the statements and opinions expressed in this publication are provided as the contributors’ recommendations at the time of publication and should not be construed as official College policy. ACEP recognizes the complexity of emergency medicine and makes no representation that this publication serves as an authoritative resource for the prevention, diagnosis, treatment, or intervention for any medical condition, nor should it be the basis for the definition of, or standard of care that should be practiced by all health care providers at any particular time or place. Drugs are generally referred to by generic names. In some instances, brand names are added for easier recognition. Device manufacturer information is provided according to style conventions of the American Medical Association. ACEP received no commercial support for this publication.

To the fullest extent permitted by law, and without limitation, ACEP expressly disclaims all liability for errors or omissions contained within this publication, and for damages of any kind or nature, arising out of use, reference to, reliance on, or performance of such information.

Lesson 13 n Vesiculobullous Rashes . . . . . . . . . . . . . . . . . . . . . . . 3

LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Critical Procedure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Lesson 14 n Bronchiolitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15

Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Drug Box/Tox Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

Critical Decisions in Emergency Medicine is the official CME publication of the American College of Emergency Physicians. Additional volumes are available to keep emergency medicine professionals up to date on relevant clinical issues.

EDITOR-IN-CHIEFLouis G. Graff, IV, MD, FACEP

University of Connecticut, Farmington, CT [email protected]

EDITOR-ELECTMichael S. Beeson, MD, MBA, FACEP

Northeastern Ohio Universities, Rootstown, OH

SECTION EDITORSJ. Stephen Bohan, MD, MS, FACEP

Brigham & Women’s Hospital/Harvard Medical School, Boston, MA

Joshua S. Broder, MD, FACEP Duke University, Durham, NC

Amal Mattu, MD, FACEP University of Maryland, Baltimore, MD

Lynn P. Roppolo, MD, FACEP University of Texas Southwestern Medical Center,

Dallas, TX

Christian A. Tomaszewski, MD, MS, MBA, FACEP University of California Health Sciences, San Diego, CA

Steven J. Warrington, MD Kaweah Delta Medical Center, Visalia, CA

ASSOCIATE EDITORSWalter L. Green, MD, FACEP

University of Texas Southwestern Medical Center, Dallas, TX

John C. Greenwood, MD University of Pennsylvania, Philadelphia, PA

Daniel A. Handel, MD, MPH, FACEP Medical University of South Carolina, Charleston, SC

Frank LoVecchio, DO, MPH, FACEP Maricopa Medical Center/Banner Phoenix Poison

and Drug Information Center, Phoenix, AZ

Sharon E. Mace, MD, FACEP Cleveland Clinic Lerner College of Medicine/Case

Western Reserve University, Cleveland, OH

Jennifer L. Martindale, MD SUNY Downstate Medical Center/

Kings County Hospital Center, Brooklyn, NY

Robert A. Rosen, MD, FACEP University of Virginia, Charlottesville, VA

George Sternbach, MD, FACEP Stanford University Medical Center, Stanford, CA

Kathleen Wittels, MD Brigham & Women’s Hospital/

Harvard Medical School, Boston, MA

RESIDENT EDITORNathaniel Mann, MD

University of Cincinnati Medical Center, Cincinnati, OH

EDITORIAL STAFFRachel Donihoo, Managing Editor

[email protected] Hamilton, Educational Products Assistant

Lexi Schwartz, Subscriptions CoordinatorMarta Foster, Director, Educational Products

ISSN2325-0186(Print) ISSN2325-8365(Online)

n Syncope

n Swollen Joint

I N T H I S I S S U E

N E X T M O N T H

mailto:cdem%40acep.org?subject=

July 2016 n Volume 30 Number 7 3

FROM THE EM MODEL4.0 Cutaneous Disorders

4.7 Vesicular/Bullous Lesions

LESSON 13

By Brit Long, MD; Drew A. Long, BS; and Alex Koyfman, MDDr. Brit Long is a physician in the Department of Emergency Medicine at San Antonio Military Medical Center in Fort Sam Houston, Texas. Mr. Drew Long is a medical student at the Vanderbilt University School of Medicine in Nashville, Tennessee. Dr. Koyfman is a clinical assistant professor in the Department of Emergency Medicine at the University of Texas Southwestern Medical Center, and an attending emergency medicine physician at Parkland Memorial Hospital in Dallas, Texas.

Reviewed by Walter L. Green, MD, FACEP

n What red flags may indicate a life-threatening rash?

n What factors differentiate erythema multiforme from severe, life-threatening rashes?

n What critical signs should raise suspicion for Stevens-Johnson syndrome and toxic epidermal necrolysis?

n How can bullous pemphigoid be distinguished from pemphigus vulgaris?

n What high-risk features should raise suspicion for staphylococcal scalded skin syndrome, and what treatments can be initiated in the emergency department?

CRITICAL DECISIONSOBJECTIVESOn completion of this lesson, you should be able to:

1. Recognize red flags in the history and physical examination that may indicate a life-threatening rash.

2. Recognize key factors that differentiate erythema multiforme from other rashes.

3. Understand the various etiologies, diagnoses, and management of Stevens-Johnson syndrome and toxic epidermal necrolysis.

4. Differentiate bullous pemphigoid from pemphigus vulgaris.

5. Discuss the diagnosis and management of staphylococcal scalded skin syndrome.

Vesiculobullous Rashes

Tiny Bubbles

Rashes are common complaints in the emergency department, and — despite the innocuous nature of most — some presentations portend a serious risk of morbidity and even mortality. Vesiculobullous rashes, which are characterized by fluid-filled lesions, are among the most concerning dermatologic disorders.

Critical Decisions in Emergency Medicine4

CASE PRESENTATIONS■ CASE ONE

A 2-year-old girl with no medical history presents with a diffuse erythematous rash that began 3 days ago. Her parents deny fever, vomiting, diarrhea, or upper respiratory symptoms. The patient’s vaccinations are up to date, and she has no history of new lotions, detergents, or travel; however, she was given amoxicillin 1 week ago for right otitis media.

The physical examination shows a well-appearing, afebrile child with normal vital signs. The rash, which involves the patient’s upper and lower extremities, back, and chest, consists of multiple erythematous, serpiginous, raised lesions. The lesions have dark red peripheries with central clearing (Figure 2). No mucosal involvement is found.

■ CASE TWOA 55-year-old man presents

with a pruritic, blistering rash that began one 1 month ago with redness and pruritus over his chest. The patient initially attempted to control his symptoms with an oral antihistamine, but the rash intensified and spread to his upper axillae, upper extremities, chest, and abdomen. The lesions have become slightly painful, but he denies arthralgia, fever, or other systemic symptoms; his vital signs are normal.

The rash is confluent with denuded skin between the tense, fluid-filled blisters (Figure 3). The Nikolsky sign is negative, and no mucosal lesions are found on examination.

Among the disorders marked by

vesiculobullous lesions are erythema

multiforme (EM), Stevens-Johnson

syndrome (SJS), toxic epidermal

necrolysis (TEN), bullous pemphigoid,

pemphigus vulgaris (PV), and

staphylococcal scalded skin syndrome

(SSSS).

Structure and FunctionThe skin is comprised of several

layers, including the epidermis, dermis, and subcutaneous tissue. The epidermis, a protective sheet of basal cells and keratinocytes, can be further subdivided into four layers (Figure 1). An understanding of these components is essential, as different disease processes target specific layers of the skin.

The dermis, which provides strength and elasticity, is comprised of collagen, elastin, and reticular fibers; the subcutaneous layer contains fat and connective tissue. The majority of vesiculobullous diseases affect the dermal-epidermal junction. (Deposition of immunoglobulin [Ig] and complement destroys these junctions, leading to blister formation.)1-3

CRITICAL DECISIONWhat red flags may indicate a life-threatening rash?

Any rash warrants a complete head-to-toe evaluation of the oral mucosa, conjunctiva, hair, neck, lymph nodes, lungs, chest, abdomen, trunk, extremities, joints, palms and soles, and nails and fingers.

■ CASE THREEA 77-year-old man with new-onset

seizures arrives with diffuse erythema and small blister formation (Figure 4). He began taking a prescription for phenytoin 3 weeks ago, and noticed diffuse redness 1 week after starting the medication. His symptoms have escalated to include eye redness, and decreased oral intake (due to the painful rash).

The patient is febrile and tachycardic (110 beats per minute), and appears to be in mild distress. The examination reveals diffuse pain to palpation, with a positive Nikolsky sign. His conjunctiva and sclera are erythematous and injected, and several intraoral lesions are discovered. Intravenous fluids are initiated, and laboratory tests are ordered.

A rapid diagnosis is essential to the effective management of these patients, and emergency physicians must be prepared to identify red flags that suggest a more ominous disease process. While many of these patterns stem from relatively benign etiologies such as poison ivy or mild varicella zoster, others may herald life-threatening pathologies.

FIGURE 1. Layers of the Epidermis


Specifics about the patient’s personal and medical history can offer valuable clues about a potential etiology, including information about when the rash appeared and how it has progressed (Table 1). Symptoms such as blisters, mucosal involvement, and the presence of pain or pruritus can help narrow the differential diagnosis, as can details about the patient’s travel history, occupation, and current medications.

Fevers suggest infection or inflam-mation, which pose the greatest risk to very young and elderly populations due to their decreased immune function. Although viral exanthema is the most likely culprit of rash in febrile patients, fever also can portend a deadly vesiculobullous rash.1-4 Lesions in the oral or genital mucosa suggest a systemic process such as SJS or TEN.

Altered mental status and confusion suggest central nervous involvement or critical illness. Systemic illness should be suspected in any patient with extensive blistering. The presence of a Nikolsky sign, defined by the dislodgement of epidermis with lateral pressure on normal skin adjacent to a bullous lesion, is concerning for SSSS, SJS, TEN, or PV.3

CRITICAL DECISIONWhat factors differentiate erythema multiforme from severe, life-threatening rashes?

Erythema multiforme, a normally self-limited inflammatory rash, can arise from a multitude of causes; however, an etiology is successfully pinpointed in only 50% of cases.1,5 Although rare (1.2 to 6 cases per 1 million per year), it most frequently is seen in young males in the second to fourth decades of life.

The most common culprit is

infection (often herpes simplex, Epstein-Barr virus, or mycoplasma) followed by medications, including penicillin, nonsteroidal anti-inflammatory drugs (NSAIDs), and sulfonamides. The likely mechanism of EM is an immune complex hypersensitivity reaction, specifically type IV hypersensitivity involving T lymphocytes.1,5

Clinical PresentationPatients may present with fever and

joint pain, or a prodrome of upper-respiratory symptoms, including malaise and congestion. A cutaneous eruption, which occurs 3 to 5 days after symptom onset, first appears on the extremities, including the palms and soles of the feet.

Initial symptoms include dull-red macules, which expand over 48 hours and develop a central clearing with vesicle or bullae formation. The

periphery of the lesions becomes cyanotic or violaceous in color, forming a classic target lesion — the disorder’s hallmark sign (Figure 5). The lesions, which often are symmetrical and spread centripetally to include the trunk, appear in crops over 2 to 4 weeks; the rash typically resolves within 1 week.1,5-8

Erythema multiforme can be

FIGURE 2. Rash from Case 1

Generalized

Acute onset

Painful

Nonpruritic

Associated fever in adult

Altered mental status

Presence of blistering, erosive, or mucosal lesions

Positive Nikolsky sign

TABLE 1. Red Flags of Rashes



FIGURE 5. Classic Target Lesion of Erythema Multiforme


divided into two types — major and minor — which are differentiated by mucosal involvement. Both forms lead to epidermal detachment on less than 10% of the body surface area; however, EM minor does not involve the mucosa, and EM major includes one mucous membrane system.1,5,6

The disease, especially the major form, easily can be confused with more severe rashes, including Stevens-Johnson syndrome or toxic epidermal necrolysis. There are, however, several important distinctions. Although EM may lead to extensive skin involvement, it will not present with the Nikolsky sign, and the lesions differ from those of SJS and TEN (Table 2).1,5-7 Additionally, infectious agents such as herpes simplex virus are the likely culprit behind most cases of EM, while SJS and TEN more commonly are triggered by medications.

Erythema multiforme must be

diagnosed clinically, based on a patient’s history and the appearance of the rash. The patient should not appear toxic; if other complaints are present, including fever, an alternative diagnosis should be considered.

EM usually resolves without treatment or residual scarring. Systemic antihistamines can provide symptomatic relief, and patients should be cautioned to return to the emergency department if they develop fever, new systemic symptoms, or large blisters.1,5

CRITICAL DECISIONWhat critical signs should raise suspicion for Stevens-Johnson syndrome and toxic epidermal necrolysis?

Stevens-Johnson syndrome is defined by epidermal detachment on less than 10% of the body surface area, while toxic epidermal necrolysis displays epidermal involvement greater than 30%.1,2,9 The overlap between the two diseases, which likely are a continuum of the same pathophysiologic process, falls between these two percentages. The incidence ranges from 1 to 7 per million people per year for SJS, and 0.4 to 1.5 per million for TEN. Male and female pediatric patients are affected equally; however, the disorder is more common in adult women than in men (2:1).9-11

The vast majority of cases are triggered by medication, most commonly trimethoprim-sulfamethoxazole, cephalosporin, quinolones, penicillin, carbamazepine, nonsteroidal anti-inflammatory agents, corticosteroids, phenytoin, allopurinol, phenobarbital, or

valproic acid.1,3 The risk increases with higher doses and the rapid introduction of the drug.1,11-15

Infection is the second most common etiology of SJS and TEN, including human immunodeficiency virus, herpes virus, mycoplasma, and hepatitis A (Table 3). Other less common causes include lupus, radiotherapy, and vasculitis.9,13,14

Clinical PresentationPatients with medication-induced

SJS/TEN may present with fever, myalgia, headache, and diffuse pain that develops 1 to 3 weeks following the introduction of a medication. Mucous membrane involvement can occur several days later. Lesions begin as macules with purpuric centers that give way to large blisters, vesicles, and bullae (Figure 6). This phase may be followed 3 to 5 days later with the epidermal detachment of bullae, which can leave behind large denuded areas of skin.

The most reliable indicator of SJS/TEN is a positive Nikolsky sign. The lesions can lead to extreme pain, loss of fluid and protein, electrolyte disorders, renal failure, bleeding, hypothermia, and infection.1,9,13,14

The disorder can affect multiple organ systems. Gastrointestinal complications include ileus, mucosal breakdown, and stenosis/stricture. Pulmonary involvement includes edema and progressive respiratory failure with large areas of ulceration and necrosis of bronchial epithelium. Hypoxemia and hypercarbia are common; respiratory support with intubation may be required.9,13,15,16

Ophthalmic involvement, which occurs in 70% of adults and 30% of children, can include erythema, conjunctivitis, keratitis, and endophthalmitis.8 Pancreatitis, hepatocellular necrosis, and glomerulonephritis also may result.1,9,13,14 The most concerning complication is serious bacterial infection due to loss of the natural skin barrier.1,14,17 Sepsis and septic shock are the most common cause of death in these patients, with S. aureus or Pseudomonas the most likely culprits.1,9,14

TABLE 2. Differentiated Characteristics of Erythema Multiforme, Stevens-Johnson Syndrome, and Toxic Epidermal Necrolysis

ReactionErythema

MultiformeStevens-Johnson

SyndromeToxic Epidermal

Necrolysis

Epidermal detachment <10% <10% >30%

Typical target lesions Yes No No

Atypical target lesions Flat Flat Flat

Mucosal involvement Only in EM major Yes Yes

Patient appearance Nontoxic May appear toxic Toxic appearing with high likelihood

of mortality

Nikolsky sign Negative Positive Positive

TABLE 3. Common Causes of SJS/TEN

Etiology Agent

Medications BactrimCephalosporins

QuinolonesPenicillins

CarbamazepineNSAIDSSteroids

PhenytoinAllopurinol

PhenobarbitalValproic acid

Infectious HIVHerpes virusMycoplasmaHepatitis A

Lupus

Other RadiotherapyVasculitis


Disease ManagementThe first step in treatment is cessation

of the suspected agent. Admission to a burn unit also is required, and has been proven to decrease the risk of mortality, bacteremia, and septicemia, and reduce the length of hospitalization in these patients. Fluid resuscitation (2 mL/kg/% body surface area) is recommended; higher rates increase the risk of pulmonary edema and fluid overload.

Analgesia should be provided, and skin lesions may be treated with antimicrobial agents, biologic materials, or synthetic agents. Nutritional support, temperature management, ocular care, and a pulmonary toilet are required.1,12-14 Corticosteroids have been studied extensively, but most literature fails to support their use.22 Other immunosuppressant agents that have shown benefit include intravenous immunoglobulin, cyclosporine, metho-trexate, N-acetylcysteine, infliximab, azathioprine, and cyclophosphamide.1,9,14

CRITICAL DECISIONHow can bullous pemphigoid be distinguished from pemphigus vulgaris?

Bullous PemphigoidBullous pemphigoid is the most

common blistering autoimmune disorder, with an incidence of 7 cases per 1 million patients. The disease, which affects both women and men at equal rates, is most common in patients older than 60 years.1-3 The majority of cases have no precipitating factor (85%); however, 15% stem from culprits such as radiation therapy, burns, vaccines, trauma, surgery, and medications. Furosemide is the most frequently implicated medication.1,23-25

The disease is caused by immuno-globulin type G (IgG) auto-antibodies that target the dermal-epidermal junction by attaching to the basement membrane hemidesmosome. This leads to complement activation, mast cell degranulation, and enzyme breakdown of the basement membrane, resulting in blister formation.1,23,26

Bullous pemphigoid is divided into several phases. The first, which can last

for several months, is associated with erythematous or urticarial lesions that cause severe pruritus (Figure 8). Lesions often are found in flexural surfaces such as the axillae and groin. This initial phase is followed by the formation of tense blisters (either localized or generalized). Although skin involvement usually isn’t painful, it often is pruritic — a presentation that may be the only symptom in older patients.1,23,26-28 A minority of patients will experience oral involvement, and the Nikolsky sign is absent.26-29

A diagnosis of bullous pemphigoid requires tense blisters, histologic/biopsy findings of subepidermal blisters with eosinophils, and direct immunofluorescence with IgG and complement deposits.23,24,26,27

Treatment includes topical and systemic corticosteroids, beginning

A definitive diagnosis requires a biopsy, which will reveal apoptosis, necrosis, and vacuolization of keratin-ocytes; dermal-epidermal separation; and lymphocytic infiltration of perivascular regions (Figure 7).1,9,14

Mortality due to multi-organ failure is seen in 1% to 3% of patients with SJS; however, the rate is significantly higher in patients with TEN (30% to 50%).14,18

The Severity of Illness Score for TEN (SCORTEN) assesses seven risk factors according to their predicted risk of mortality. The greater the number of risk factors, the higher the SCORTEN score — and the higher the mortality rate, as indicated below.1,19,20

No. of Risk Factors Mortality Rate

0-1 3.2%

2 12.1%

3 35.3%

4 58.3%

5 or more >90%

Patients with scores of 0 or 1 do not necessitate specialized treatment, while those with scores greater than 2 should be transferred to an intensive care or burn unit.20,21

FIGURE 6. Lesions of Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis

FIGURE 7. Biopsy of Stevens-Johnson Syndrome/Toxic Epidermal NecrolysisDepicting separation of the dermis and epidermis and keratinocyte apoptosis

FIGURE 8. Bullous Pemphigoid Skin LesionsAge ≥40 years

HR ≥120/min

History of cancer or hematologic malignancy

Involved surface area detachment ≥10%

Serum urea >10 mmol/L OR 28 mg/dL

Serum bicarbonate <20 mmol/L

Serum glucose >252 mg/dL OR 14 mmol/L

TABLE 4. SCORTEN Score


with prednisone (1 mg/kg/day). Other effective medications include mycophenolate, azathioprine, leflunomide, cyclophosphamide, intravenous immunoglobulin, dapsone, and plasmapharesis.1,26,29-31

Unfortunately, bullous pemphigoid typically is a chronic disease, marked by exacerbations and remissions. Complications include secondary skin infections due to blister formation and loss of the protective skin barrier. Non-toxic patients with localized skin involvement may be discharged home with close follow up; more serious cases warrant admission.1,29-31

Pemphigus VulgarisUnlike bullous pemphigoid,

pemphigus vulgaris is indicated by a positive Nikolsky sign, and — frequently — mucosal involvement. Incidence of the disease varies from 0.5 to 3.2 per 100,000 persons, and is most common in those between the ages of 40 and 60 years.1,24,25, 27,32-34 It affects women and men equally, but patients with autoimmune conditions (eg, lupus, rheumatoid arthritis, or myasthenia gravis) are at greatest risk. Medications such as penicillin, NSAIDs, ACE inhibitors, and pyrazolones frequently are associated with the disease. Other causes include stress, burns, ultraviolet exposure, infections, and myasthenia.1,24,32

PV is caused by the formation of IgG antibodies that bind keratinocyte cell surface molecules desmoglein-1 and desmoglein-3, with disease activity correlated to levels of antibodies. This autoantibody binding results in loss of the cell-to-cell adhesions (ie, acantholysis).24,27,32,33

Oral mucosal involvement (typically,

• Vitreous hemorrhage• Retinal detachment• Acute maculopathy• Central retinal artery occlusion• Central retinal vein occlusion• Ischemic optic neuropathy

painful, irregular erosions) is noted in 50% to 70% of patients with PV; almost all experience mucosal lesions at some point in their clinical course. The conjunctiva and esophagus also may be involved.1,24,27,32

The majority of those with PV develop skin lesions characterized by a flaccid blister filled with clear fluid on an erythematous base — a contrast to the tense blisters seen in cases of bullous pemphigoid. The blisters and lesions usually are painful and not pruritic (Figure 9); nail involvement also is common, with dystrophies, subungual hematomas, and chronic paronychia.35

A biopsy, which is required to confirm the diagnosis, will reveal intraepidermal blister formation and eosinophilic infiltrates. Direct immunofluorescence demonstrates IgG on keratinocytes. Autoantibodies circulate in up to 90% of patients, with higher autoantibody levels correlating with disease activity.27,32,36

Systemic and topical corticosteroids are the mainstays of treatment for PV. Before these agents became commonplace, the disease posed a mortality risk of 50% to 90%; that rate has since dropped to approximately 10%.32,37,38 A single oral or intravenous dose of prednisone (1 mg/kg per day) is the initial treatment.38,39

As in cases of bullous pemphigoid, other immunosuppressive agents can be used to induce remission.1,40 Non-toxic patients with localized blisters usually can be discharged home with dermatology follow up. However, admission is required for those who appear toxic or have extensive blisters with erosions; these patients necessitate fluid resuscitation and electrolyte management.1,40

CRITICAL DECISIONWhat high-risk features should raise suspicion for staphylococcal scalded skin syndrome, and what treatments can be initiated in the emergency department?

Staphylococcal infections are among the most common skin disorders diagnosed in infants and children.1,42

Both SSSS and bullous impetigo are exfoliative conditions mediated by a toxin released by staphylococcus. The disease may present in adults as a nosocomial infection, or may occur in immunocompromised individuals. Children younger than 5 years typically respond well to treatment; however, mortality approaches 60% in adult patients, who often are plagued by severe illness accompanied by positive blood cultures.43,44

Both SSSS and bullous impetigo are caused by a specific strain of staphylococcus that carries exfoliative exotoxins. Exotoxins A and B cause an epidermolytic breakdown through cleavage of desmoglein-1, a pathophysiologic process similar to that of pemphigus vulgaris. Although this targeting of the cell-to-cell adhesion molecules allows the bacteria to proliferate beneath the skin barrier, only 5% of S. aureus species produce these exotoxins.42-45

In bullous impetigo, the toxin produces blisters at the site of the infection (locally); while in SSSS, dissemination of the toxin through the bloodstream leads to lesions distant from the site of infection.

SSSS stems from a focus of infection, most commonly otitis media, nasopharyngeal infection, or conjunctivitis. A prodrome of sore throat or purulent conjunctivitis may be present for 48 hours, followed by fever; malaise; and erythematous, painful skin. In young children, the disease may progress from widespread erythema to blister formation and desquamation within 48 hours — a course that is not dissimilar to that of SJS and TEN.

Clinical PresentationThe epidermis, which may appear

thin and tissue paper-like, often is followed by the appearance of large, flaccid bullae that affect flexural surfaces (Figure 10). Notably, mucous membrane involvement is absent. Unlike the necrotic lesions seen in cases of SJS and TEN, rashes caused by SSSS never appear dusky or purpuric due to the exotoxin cleavage of intracellular desmoglein-1-mediated connections. Although both syndromes will produce

FIGURE 9. Pemphigus Vulgaris Lesion


positive Nikolsky signs, SSSS will not demonstrate this symptom on unaffected skin.42-46

Physicians must rely on visual clues and clinical acumen to diagnosis SSSS in the emergency department. Cultures obtained from the rash’s bullae are sterile and of little evidentiary value; however, the lesions have been associated with bacteremia in adult patients. A culture and biopsy demonstrating positive exotoxin assays is required to confirm the diagnosis.43,45

Treatment for both SSSS and impetigo includes eradicating the focus of infection. Oral corticosteroids can be used for patients who are non-toxic and well-appearing. The majority of patients with diffuse skin involvement require intravenous therapy with medications such as nafcillin, penicillin, amoxicillin/clavulanate, cefazolin, or cephalexin.

If there is a concern for methicillin-resistant S. aureus, clindamycin, trimethoprim-sulfamethoxazole, or

n An aggressive approach may be warranted when managing a rash that is generalized; sudden; painful and nonpruritic; associated with a fever and/or altered mental status; or characterized by a positive Nikolsky sign or blistering, erosive, or mucosal lesions.

n SJS and TEN are associated with a host of complications and potential mortality. It is important to diagnose these conditions rapidly, stop the suspected agent, and admit the patient to a burn care unit.

n Severe autoimmune rashes include bullous pemphigoid and PV; the mainstay of treatment for both conditions is corticosteroids.

n SSSS is a common pediatric rash that typically follows a prodromal period after an infection with S. aureus; intravenous antibiotic treatment often is required.

FIGURE 10. Scalded Skin Syndrome

vancomycin should be initiated. Severe infections also may require intravenous immunoglobulin or plasmapheresis to help facilitate toxin clearance. Patients with localized infections may be discharged home with close follow up; however, those with diffuse involvement should be transferred to a burn center.42,43,46,47

SummaryAlthough the vast majority of

rashes that present to the emergency department are relatively benign, vesiculobullous lesions warrant particular consideration. Clinicians must be aware of factors in a patient’s history and physical examination that indicate the need for further management and a higher level of care.

Among the most concerning symptoms are rashes characterized by generalized distribution; acute onset; diffuse pain; nonpruritic lesions; associated fever, and/or altered mental status; blistering, erosive, or mucosal lesions; and a positive Nikolsky sign.

Vesiculobullous rashes such as erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, bullous pemphigoid, pemphigus vulgaris, and staphylococcal scalded skin syndrome often necessitate admission. Patients with SJS and TEN, in particular, may require referral to a burn center. Patients with EM, limited SSSS, or local bullous pemphigoid or PV may be discharged with close follow

up; however, treatment and disposition ultimately relies on the bedside assessment and the patient’s appearance.

REFERENCES1. Nguyen T, Freedman J. Dermatologic emergencies:

diagnosing and managing life-threatening rashes. Emerg Med Practice. 2002;4(9):1-28.

2. Lynch PJ, Edminster SC. Dermatology for the nondermatologist: a problem-oriented system. Ann Emerg Med. 1984;13(8):603-606.

3. Juneja M. Nikolsky’s sign revisited. J Oral Sci. 2008;50(2):213-214.

4. McKinnon HD Jr, Howard T. Evaluating the febrile patient with a rash. Am Fam Physician. 2000;62(4):804-816.

5. Sokumbi O, Wetter DA. Clinical features, diagnosis, and treatment of erythema multiforme: a review for the practicing dermatologist. Int J Dermatol. 2012;51(8):889-902.

6. Paquet P, Piérard GE. Erythema multiforme and toxic epidermal necrolysis: a comparative study. Am J Dermatopathol. 1997;19(2):127-132.

7. Wolf R, Lipozencic J. Shape and configuration of skin lesions: targetoid lesions. Clin Dermatol. 2011;29(5):504-508.

8. Power WJ, Ghoraishi M, Merayo-Lloves J, et al. Analysis of the acute ophthalmic manifestations of the erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis disease spectrum. Ophthalmology. 1995;102(11):1669-1676.

9. Letko E, Papaliodis DN, Papliodis GN, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: a review of the literature. Ann Allergy Asthma Immunol. 2005;94(4):419-436.

10. Rzany B, Mockenhaupt M, Baur S, et al. Epidemiology of erythema exsudativum multiforme majus, Stevens-Johnson syndrome, and toxic epidermal necrolysis in Germany (1990-1992): structure and results of a population-based registry. J Clin Epidemiol. 1996;49(7):769-773.

11. Roujeau JC, Stern RS. Severe adverse cutaneous reactions to drugs. N Engl J Med. 1994;331(19):1272-1285.

12. Spies M, Sanford AP, Aili Low JF, et al. Treatment of extensive toxic epidermal necrolysis in children. Pediatrics. 2001;108(5):1162-1168.

13. Roujeau JC, Chosidow O, Saiag P, et al. Toxic epidermal necrolysis (Lyell syndrome). J Am Acad Dermatol. 1990;23(6 Pt 1):1039-1058.

14. French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome: our current understanding. Allergol Int. 2006;55(1):9-16.

15. Knowles SR, Shapiro LE, Shear NH. Drug Eruptions. In: Schachner LA, Hansen RC, eds. Pediatric Dermatology. 3rd edition. London, UK: Mosby; 2003;1267-1276.

16. de Prost N, Mekontso-Dessap A, Valeyrie-Allanore L, et al. Acute respiratory failure in patients with toxic epidermal necrolysis: clinical features and factors associated with mechanical ventilation. Crit Care Med. 2014;42(1):118-128.

17. de Prost N, Ingen-Housz-Oro S, Duong Ta, et al. Bacteremia in Stevens-Johnson syndrome and toxic epidermal necrolysis: epidemiology, risk factors, and predictive value of skin cultures. Medicine (Baltimore). 2010;89(1):28-36.

18. Sekula P, Dunant A, Mockenhaupt M, et al. Comprehensive survival analysis of a cohort of patients with Stevens-Johnson syndrome and toxic epidermal necrolysis. J Invest Dermatol. 2013;133(5):1197-1204.

19. Trent JT, Kirsner RS, Romanelli P, Kerdel FA. Use of SCORTEN to accurately predict mortality in patients with toxic epidermal necrolysis in the United States. Arch Dermatol. 2004;140(7):890-892.

20. Valeyrie-Allanore L RJ-C. Epidermal necrolysis (Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis). In: Goldsmith LA KS, Gilchrest BA, Paller AS, eds. Fitzpatrick’s Dermatology in General Medicine. 8th ed: McGraw-Hill; 2012.

21. Palmieri TL, Greenhalgh DG, Saffle JR, et al. A multicenter review of toxic epidermal necrolysis treated in U.S. burn centers at the end of the twentieth century. J Burn Care Rehabil. 2002;23(2):87-96.


22. Letko E, Papaliodis DN, Papaliodis GN, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: a review of the literature. Ann Allergy Asthma Immunol. 2005;94(4):419-436; quiz 436-438, 456.

23. Lo Schiavo A, Ruocco E, Brancaccio G, et al. Bullous pemphigoid: etiology, pathogenesis, and inducing factors: facts and controversies. Clin Dermatol. 2013;31(4):391-399.

24. Baum S, Sakka N, Artsi O, et al. Diagnosis and classification of autoimmune blistering diseases. Autoimmun Rev. 2014;13(4-5):482-489.

25. Langan SM, Smeeth L, Hubbard R, et al. Bullous pemphigoid and pemphigus vulgaris—incidence and mortality in the UK: population based cohort study. BMJ. 2008;337:a180.

26. Yancey KB, Egan CA. Pemphigoid: clinical, histological, immunopathologic, and therapeutic considerations. JAMA. 2000;248(3):350-356.

27. Kershenovich R, Hodak E, Mimouni D. Diagnosis and classification of pemphigus and bullous pemphigoid. Autoimmun Rev. 2014;13(4-5):477-481.

28. Bakker CV, Terra JB, Pas HH, Jonkman MF. Bullous pemphigoid as pruritus in the elderly: a common presentation. JAMA Dermatol. 2013;149(8):950-953.

CASE RESOLUTIONS■ CASE ONE

The well-appearing toddler showed no red flags or signs of hemodynamic instability; she was playful and active during her visit. The emergency physician did not perceive her to be at risk for systemic illness, and declined to order any laboratory studies. The patient received a diagnosis of erythema multiforme, and the parents were given strict return precautions (eg, fever, or the development of blisters or oral lesions), and were advised to follow up with the child’s pediatrician.

■ CASE TWOConcerned about the middle-aged

man’s extensive tense blister formation, the emergency physician ordered a renal function panel and other laboratory studies. Dermatology was consulted, and — based on the patient’s extensive skin involvement — recommended admission for a further workup and fluid/electrolyte monitoring. A diagnosis of bullous pemphigoid was made, and prednisone (1 mg/kg) was administered. The patient was admitted to an inpatient floor with dermatology follow up.

■ CASE THREEThe elderly toxic-appearing man’s

symptoms were suspicious for TEN, and initial laboratory test results revealed elevated creatinine. The emergency physician contacted a specialist at the local burn center, who recommended transferring the patient for further management. Intravenous fluids and pain medi-cation were administered, and the patient’s wounds were covered with gauze prior to transporting him to the burn center.

29. Ruocco E, Wolf R, Caccavale S, et al. Bullous pemphigoid: associations and management guidelines: facts and controversies. Clin Dermatol. 2013;31(4):400-412.

30. Joly P, Roujeau JC, Benichou J, et al. A comparison of two regimens of topical corticosteroids in the treatment of patients with bullous pemphigoid: a multicenter randomized study. J Invest Dermatol. 2009;129(7):1681-1687.

31. Kirtschig G, Middleton P, Bennett C, et al. Interventions for bullous pemphigoid. Cochrane Database Syst Rev. 2010;(10):CD002292.

32. Santoro FA, Stoopler ET, Werth VP. Pemphigus. Dent Clin North Am. 2013;57(4):597-610.

33. Mignogna MD, Fortuna G, Leuci S. Oral pemphigus. Minerva Stomatol. 2009;58(10):501-518.

34. Hietanen J, Salo OP. Pemphigus: an epidemiological study of patients treated in Finnish hospitals between 1969 and 1978. Acta Derm Venereol. 1982;62(6):491-496.

35. Engineer L, Norton LA, Ahmed AR. Nail involvement in pemphigus vulgaris. J Am Acad Dermatol. 2000;43(3):529-535.

36. Mentink LF, de Jong MC, Kloosterhuis GJ, et al. Coexistence of IgA antibodies to desmogleins 1 and 3 in pemphigus vulgaris, pemphigus foliaceus and paraneoplastic pemphigus. Br J Dermatol. 2007;156(4):635-641.

37. Seidenbaum M, David M, Sandbank M. The course and prognosis of pemphigus. A review of 115 patients. Int J Dermatol 1988;27(8):580-584.

38. Rosenberg FR, Sanders S, Nelson CT. Pemphigus: a 20-year review of 107 patients treated with corticosteroids. Arch Dermatol. 1976;112(7):962-970.

39. Chams-Davatchi C, Daneshpazhooh M. Prednisolone dosage in pemphigus vulgaris. J Am Acad Dermatol. 2005;53(3):547.

40. Camisa C, Warner M. Treatment of pemphigus. Dermatol Nurs. 1998;10(2):115-118, 123-131.

41. Aberer W, Wolff-Schreiner EC, Stingl G, Wolff K. Azathioprine in the treatment of pemphigus vulgaris. A long-term follow-up. J Am Acad Dermatol. 1987;16(3 Pt 1):527-533.

42. Stanley JR, Amagai M. Pemphigus, bullous impetigo, and the staphylococcal scalded-skin syndrome. N Engl J Med. 2006;355(17):1800-1810.

43. Patel GK, Finlay AY. Staphylococcal scalded skin syndrome: diagnosis and management. Am J Clin Dermatol. 2003;4(3):165-175.

44. Mockenhaupt M, Idzko M, Grosber M, et al. Epidemiology of staphylococcal scalded skin syndrome in Germany. J Invest Dermatol. 2005;124(4):700-703.

45. Murono K, Fujita K, Yoshioka H. Microbiologic characteristics of exfoliative toxin-producing Staphylococcus aureus. Pediatr Infect Dis J. 1988;7(5):313-315.

46. Hubiche T, Bes M, Roudiere L, et al. Mild staphylococcal scalded skin syndrome: an underdiagnosed clinical disorder. Br J Dermatol. 2012;166(1):213-215.

47. Johnston GA. Treatment of bullous impetigo and the staphylococcal scalded skin syndrome in infants. Expert Rev Anti Infect Ther. 2004;2(3):439-446.

ADDITIONAL READINGMcKinnon HD Jr, Howard T. Evaluating the febrile patient

with a rash. Am Fam Physician. 2000;62(4):804-816.

Nguyen T, Freedman J. Dermatologic emergencies: diagnosing and managing life-threatening rashes. Emerg Med Practice. 2002;4(9):1-28.

n Mistaking erythema multiforme for a more serious rash such as Stevens-Johnson syndrome or toxic-epidermal necrolysis. A negative Nikolsky sign, otherwise well appearance, and skin biopsy with lack of epidermal detachment can help distinguish EM.

n Withholding broad-spectrum antibiotics in the setting of suspected sepsis, the most common cause of death in patients with SJS/TEN.

n Failing to warn patients about the likelihood of remissions and exacerbations associated with bullous pemphigoid. It is a chronic disease, and patients must be educated about which recurring symptoms necessitate a return to the emergency department.

n Neglecting to provide coverage of methicillin-resistant S. aureus in the pediatric patient with SSSS who fails to improve after initial intravenous antibiotic therapy.


Two distinct clinical entities underlie “hyperglycemic crisis” — diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS). Although both cause diffuse metabolic derangement and severe dehydration, they have completely different patho physiologic origins. The incidence of these syndromes will increase concomitantly with the escalating number of patients with type 1 and type 2 diabetes. (In 2010, there were 26 million people in the US living with type 2 diabetes; and the incidence of type 1 diabetes has grown, particularly in children younger than 5 years.)

The diagnostic criteria for DKA include a blood glucose level greater than 250 mg/dL, moderate ketonuria or ketonemia, arterial pH of 7.3, and bicarbonate less than 15 mEq/L. The criteria for HHS are altered sensorium, a glucose level greater than 600 mg/dL, minimal or no ketonemia, serum osmolality greater than 320 MOsm/kg, arterial pH higher than 7.3, and a bicarbonate greater than 15 mEq/L.

DKA, which is characterized by symptoms that have been present for hours to days, often is precipitated by some other pathologic event. HHS, on the other hand, is more insidious and evolves over days to weeks. Ketoacidosis can occur with normal or minimally elevated glucose levels — an entity that comprises about 10% of these cases. The

The LLSA Literature Review

Critical Decisions in Emergency Medicine’s series of LLSA reviews features articles articles from ABEM’s 2016 Lifelong Learning and Self-Assessment Reading List. Available online at acep.org/llsa and on the ABEM website.

presence of acidemia should always raise suspicion for a toxidrome.

Since severe dehydration is present in all patients with either syndrome, hydration is the first therapeutic intervention; infusions should start at 20 mL/kg/hr, with a goal of achieving urine output of 1 mL/kg/hr.

Electrolyte perturbations are ubiquitous in these syndromes, with both sodium and potassium being elevated or decreased. An ECG is a quick and reliable way to assess for severe hyperkalemia. The patient’s potassium status should be confirmed by laboratory testing before the initiation of insulin therapy, which can exacerbate hypokalemia. If hypokalemia is confirmed, potassium should be restored to at least 3.3mEq/L prior to insulin administration.

An IV infusion of insulin is standard

By J. Stephen Bohan, MS, MD, FACEP Brigham and Women’s Hospital/Harvard Medical School, Boston, Massachusetts

n Type 1 diabetes, and — consequently — DKA are increasing in young children, and should be included in the differential diagnosis for a newly ill child. A finger stick glucose, an IV infusion of saline, and an ECG are the first important steps in diagnosis and treatment. If severe signs of hyperkalemia are absent on ECG, insulin therapy should be withheld until the patient’s serum potassium level is known and significant deficits are corrected.

n An intravenous infusion of insulin is the standard treatment.n HHS should be considered in any elderly patient with altered mental status.n Institutional guidelines should be in place for the management of elevated

glucose, including protocols for fluid administration, insulin therapy, and electrolyte derangement.

KEY POINTS

Hyperglycemic Crisis Van Ness-Otunnu R, Hack JB. J Emerg Med. 2013;45(50):797-805.

therapy (regular insulin at 0.14 units/kg/hr); there appears to be no difference in outcomes between bolus or intravenous therapies. Glucose levels should be measured hourly; if a 10% reduction in serum glucose has not been achieved after the first hour, additional insulin should be given (a bolus of 0.14 units/kg), and the infusion should be continued.

Subsequent care should be rendered according to a hospital-wide protocol, which will guide the continued administration of IV fluids (both amount and constituents) and insulin therapy based on blood glucose levels. The same rule applies to the management of potassium and sodium derangements. These treatment recommendations apply to both DKA and HHS.

http://www.acep.org/llsa


The Critical Procedure

POSTERIOR TIBIAL NERVE BLOCK

Benefits and RisksA successful posterior tibial nerve

block eliminates the need for local anesthesia. Injections to the plantar surface of the foot can be painful, and often must be repeated multiple times in larger procedures. When combined with topical anesthetics, nerve blocks can create a near pain-free patient experience.

Nerve blocks of the ankle pose little additional risk compared to local anesthesia; however, potential complications include neurological injury or permanent neuropathy. Albeit rare (<1%), these injuries can arise from direct damage to the posterior tibial nerve. Other risks include injection or injury to the posterior vessels.

In addition to risks specific to the nerve block, patients also should be educated about the general dangers associated with local anesthesia. In

By Steven J. Warrington, MDDr. Warrington is a core faculty member of the general surgery and emergency medicine residency programs, and the associate medical director for emergency department outreach and education at Kaweah Delta Medical Center in Visalia, California.

CONTRAINDICATIONSn Allergy to anesthetic/medication n Overlying infected tissuen Relative – An uncooperative patientn Relative – Severe coagulopathy

A posterior tibial nerve block can make

an otherwise difficult and uncomfortable

procedure on the sole of a patient’s foot

relatively quick and painless. By providing

anesthesia to the plantar surface, this

approach obviates the need for local

infiltration or a large volume of anesthetic. Transverse section of lower leg

Ankle block involves anesthetizing five separate nerves: two deep, and three superficial. The two deep nerves are tibial and deep peroneal nerve. The superficial nerves are superficial peroneal, sural and saphenous.

PHOTO COURTESY OF SONOSIM, INC.


TECHNIQUE1. Obtain consent from the patient and notify the

staff of the procedure(s).

2. Perform a thorough neurovascular examination of the ankle and foot.

3. Consider applying topical anesthetic to the site of expected needle insertion (ie, the area between medial malleolus and Achilles tendons).

If using ultrasound:

4. Pinpoint the posterior tibial artery, which can aid in the identification of the nerve. The nerve will sit just posterior (toward the Achilles tendon) to the artery.

5. Clean the area, insert the needle just outside of the nerve on ultrasound, and inject approximately 5 ml of anesthetic. Consider injecting half of the medication deep to the nerve, and the remainder superficial to the nerve.

If not using ultrasound:

4. Identify the posterior tibial artery, just posterior to the medial malleolus. The insertion site will be approximately 0.5 to 1 cm superior/proximal.

5. Clean the area, insert the needle approximately 1 cm deep, and gently move it. If the patient feels paresthesias, withdraw slightly and inject up to 5 ml of anesthetic. If no paresthesias are felt, advance the needle until it reaches the posterior tibia. Withdraw slightly, and inject approximately 5 ml of anesthetic, while slowly withdrawing.

6. Allow the patient to sit for 10 minutes.

7. Determine if the patient can feel the onset of the anesthetic. It may take more time for the block to completely take effect; however, consider a second attempt or an alternate route of anesthesia if no effects are felt after 10 minutes.

addition, patients should be warned that these procedures sometimes fail, necessitating local anesthesia or sedation.

Reducing Side EffectsWhile the risk of complications is

minimal, ultrasound guidance may help decrease the likelihood of injury to nerves and vessels. Additionally, ultrasound-guided posterior tibial nerve blocks have been found to have a higher success rate than landmark-guided (blind) attempts.

As with any injection of medication,

the clinician should aspirate first to avoid

injecting intravascularly.

AlternativesLocal anesthesia may be a more

suitable alternative to nerve block when

managing a small wound involving only

the edge of expected distribution of the

posterior tibial sensory region. Sedation

may be a better option in patients who

are uncooperative or unable to tolerate

the procedure.

Special Considerations Lidocaine typically is the anesthetic

of choice for short procedures. However, bupivacaine may be considered if prolonged pain is a concern (due to its longer duration of action). Regardless of the type of anesthetic chosen, a thorough neurovascular examination should be documented before and after the procedure, recognizing that the block may still be in effect. Topical anesthetic also can be considered prior to attempting a nerve block, and can make needle insertion more tolerable.


A 46-year-old man with chest pressure and lightheadedness.

The Critical ECGSinus rhythm, rate 70, left ventricular hypertrophy, acute inferior-posterior-lateral myocardial infarction (MI), probable right ventricular MI.

ST-segment elevation is present in the inferior leads (with early q-wave formation) and lateral precordial leads, consistent with acute inferior and lateral MI. Posterior MI is strongly suggested by the presence of tall R waves in leads V2-V3. Tall R waves in the right precordial leads in the setting of an acute MI are analogous to q waves, or infarction, in the posterior region of the heart. Right ventricular extension of an inferior MI is strongly suggested when the magnitude of ST-segment elevation in lead III is significantly greater than the ST-segment elevation in lead II, as is the case here. Approximately one-third of inferior MIs will extend to the posterior region of the heart, and one-third will extend to the right ventricle (RV). Posterior extension of the MI can be confirmed by placement of additional leads in the left mid-back area just inferior to the inferior pole of the scapula. When the ECG is repeated with these posterior leads, acute posterior MI demonstrates typical acute MI findings of q-wave formation and STE in those leads. RV extension of the MI can be confirmed by placing precordial leads across the right side of the chest (mirror image of their normal left-sided placement) and then repeating the ECG. RV MI will then demonstrate ST-segment elevation in those right precordial leads. LVH is diagnosed based on the presence of an R wave in lead aVL >11 mm in height. See figure below.

From Mattu A, Brady W, ECGs for the Emergency Physician 2. London: BMJ Publishing; 2008:11,23. Reprinted with permission.

By Amal Mattu, MD, FACEPDr. Mattu is a professor, vice chair, and director of the Emergency Cardiology Fellowship in the Department of Emergency Medicine at the University of Maryland School of Medicine in Baltimore.

Right ventricular (RV) myocardial infarction most often occurs in the setting of inferior wall acute MI. (Of note, approximately 30% of patients with inferior wall MI also will suffer an RV infarction.) In this setting, clinical and electrocardiographic findings will suggest the diagnosis. Clinically, systemic hypotension spontaneously or after a vasodilating agent (nitroglycerin or morphine) with clear lung fields suggests RV infarction. Electrocardiographically, numerous findings are supportive of RV infarction in the setting of an inferior wall MI. a) Right-sided ECG leads will demonstrate STE. b) Disproportionate ST-segment elevation in lead III relative to leads II and aVF. c) ST-segment elevation in lead V1.


FROM THE EM MODEL16.0 Thoracic-Respiratory Disorders

16.4 Obstructive/Restrictive Lung Disease

LESSON 14

By Steven J. Warrington, MD and Matt Poliakoff, DODr. Warrington is a core faculty member of the general surgery and emergency medicine residency programs, and the associate medical director for emergency department outreach and education; and Dr. Poliakoff is chief resident in the Emergency Medicine Residency Program at Kaweah Delta Medical Center in Visalia, California.

Reviewed by Lou Graff, MD, FACEP

n What red flags in a child’s medical and social history should raise suspicion for bronchiolitis?

n How should the physical examination be approached when assessing a child for bronchiolitis?

n What diagnostic tests should be initiated in the emergency department?

n What treatments can be administered in the emergency department?

n Which high-risk factors indicate the need for further observation or hospital admission?

CRITICAL DECISIONSOBJECTIVESOn completion of this lesson, you should be able to:

1. Describe the typical presentation of a patient with bronchiolitis.

2. Identify characteristics of patients with bronchiolitis that place them at high risk.

3. List recommended treatment options for bronchiolitis.

4. Define which patients with bronchiolitis warrant radiographic imaging.

5. Recognize which patients with bronchiolitis may require admission.

Bronchiolitis

Breathe Easy

Respiratory complaints in infants and children can be as terrifying to health care teams as they are to family members. Bronchiolitis, one such common diagnosis, typically is self-limiting; however, some of these children will die. Emergency physicians must rely on their clinical acumen to recognize high-risk patients and initiate appropriate treatments.


CASE PRESENTATIONS

■ CASE ONEA previously healthy 8-month-

old boy is brought to the emergency department by his mother, who says the baby is having difficulty breathing. He was born at 38 weeks, and his immunizations are up to date. There are two older children in the household, who recently have been sick with coughs and congestion. When the patient’s congestion began 2 days ago, the mother assumed he had contracted the same illness as his siblings. Today, however, his symptoms have progressed to include “noisy breathing,” which worsens when he becomes upset.

No medications have been given at home. Aside from an episode of post-tussive emesis yesterday and a fever that was not checked with a thermometer, the mother reports no other associated symptoms. The patient is well-appearing, and seems content when sitting in his mother’s lap. His vital signs are blood pressure 84/37, pulse 140, respiratory rate 29, temperature 37.2°C (99°F), and oxygen saturation 97% on room air.

Pulmonary auscultation shows diffuse coarseness to the anterior and posterior chest without any areas of focality and with good aeration bilaterally. No nasal flaring or retractions are noted, and he

does not appear to be tachypneic or have increased work of breathing. The tympanic membranes are within normal limits, and he produces plenty of tears. The rest of the examination is unremarkable.

■ CASE TWOThe emergency department is

notified about an ambulance en route carrying a 4-month-old boy in respiratory distress. Respiratory therapy is called, and the staff prepares a room with equipment for intubation and resuscitation. On arrival, emergency medical services reports the child has had a cough and congestion, which started yesterday; wheezing developed overnight, and a fever accompanied by quick, shallow respirations began this morning.

The difficult breathing has prevented the child from eating, and he has produced no wet or dirty diapers today. He has been otherwise healthy, was born “on time,” and is up to date on immunizations. On arrival, his vital signs are blood pressure 72/34, pulse 190, respiratory rate 55, temperature 38.4°C (101.2°F), and oxygen satur-ation 93% on 0.5 L nasal cannula.

The patient appears in distress with supraclavicular, intercostal, and substernal retractions. Auscultation of the lungs shows diffuse wheezing with coarseness to the right posterior

inferior chest. The cardiac assessment is remarkable only for a tachycardic rate. The physician requests nasal continuous positive airway pressure (CPAP), an intravenous fluid bolus of normal saline (20 mL/kg), rectal dose of acetaminophen (15 mg/kg), chest x-ray, complete blood count (CBC), basic metabolic panel, and blood cultures.

■ CASE THREEA 47-day-old girl is carried in by

her parents with a chief complaint of worsening respiratory symptoms and poor feeding since last night. The baby was seen in the emergency department yesterday for 1 week of difficult breathing and congestion, but was discharged home. Her laboratory workup had been unremarkable; a chest x-ray, which was interpreted by radiology, showed mild peribronchial thickening.

Today, she is in obvious respiratory distress with retractions and nasal flaring. Her vital signs are blood pressure 70/40, heart rate 195, respiratory rate 70, oral temperature 38.1°C (100.7°F), and oxygen saturation 84% on room air. She immediately is placed on nasal cannula (2 liters) and is given nebulized albuterol, a fluid bolus, intravenous methylprednisolone, and broad-spectrum antibiotics.

Bronchiolitis, which is responsible for approximately 3.1% of emergency department visits, is associated with viral infections that typically present through the late fall, winter, and early spring.1 The diagnosis generally is considered a malady of children younger than 2 years, although that criterion varies (the upper age limit can range from 12 months to 3 years). Patients typically present with prodromal viral symptoms, including rhinorrhea or congestion, which transpire into associated respiratory difficulties.

Wheezing is a common finding, as are

crackles — although neither is universal. Other characteristics of bronchiolitis include apnea (in neonates), tachypnea, cough, and retractions.2 Because the disease stems from a viral illness that affects the child’s lower airways, however, the respiratory auscultatory findings are diffuse and non-focal.

Although the diagnosis a familiar one to most emergency physicians, antibiotics and resources (eg, radio-graphs and mechanical ventilation) frequently are overutilized when managing bronchiolitis. In addition, hospital charges associated with the

disease rose 30% from 2000 to 2009, costing more than $1.7 billion in 2009 alone.3

CRITICAL DECISIONWhat red flags in a child’s medical and social history should raise suspicion for bronchiolitis?

The importance of the history and physical examination cannot be overstated. A thorough clinical assessment is the only reliable method for diagnosing bronchiolitis and gauging the severity of a patient’s disease.


A timeline of respiratory symptoms, including rhinorrhea, congestion, and abnormal breathing patterns/sounds, is necessary to confirm the diagnosis. Information about any associated fever is important to obtain, as it may indicate the need for blood tests or a full septic evaluation in certain populations (eg, non-immunized patients).

The patient’s hydration level should be assessed by gathering details about the child’s recent feeding history and urinary output, examining the mucous membranes, and noting the presence of tears upon crying.2 Dehydration is a factor that may prompt hospitalization or require specific therapy.

Additional details about events that may be related to alternate diagnoses also should be sought (eg, an aspirated foreign body). Past medical history, including birth history, plays a major role in the risk stratification of patients. Existing disorders such as cardiopulmonary or immune disease, congenital genetic disorders, and prior wheezing increase the likelihood of severe bronchiolitis.

Prematurity and smoke exposure in utero both place a child at risk for a more severe course.4 Factors such as low birth weight, lack of breastfeeding, male sex, prenatal corticosteroid exposure, and surfactant therapy are associated with an increased rate of hospitalization.5

The social history also can help predict the patient’s risk of complications. In particular, exposure to smoke should be identified, and clinicians are encouraged to counsel families on the importance of smoking cessation when caring for a child with bronchiolitis.4

Patients who have siblings younger than 10 years and live in crowded environments also may be at an increased risk for hospitalization, although these factors cannot be modified easily.5

CRITICAL DECISIONHow should the physical examination be approached when assessing a child for bronchiolitis?

A physical examination of the child should start with the vital signs, including pulse oximetry measurements. An elevated temperature may prompt a further diagnostic workup. Pulse oximetry measurements can help identify hypoxemia that otherwise would be undetectable; however, they should not be considered a sole marker of respiratory distress. Continuous pulse oximetry monitoring is not always necessary in cases of bronchiolitis, and can lead to alarm fatigue and less effective monitoring of other clinical findings.4

While a complete examination is necessary to evaluate for other possible infections and processes, this lesson will focus on the respiratory examination, which is used most often in risk stratification, and followed serially as a marker of the presence and progression of the disease.6

The pulmonary examination includes multiple steps, including evaluating for cyanosis, and assessments of accessory muscle use and auscultation. Cyanosis can be graded based on its absence, presence during crying, and location

(eg, perioral or generalized). An assessment of the accessory muscles includes evaluating for tracheal tug, head bobbing, intercostal retractions, substernal retractions, and nasal flaring. Auscultation should be done in the anterior and posterior chest bilaterally, while evaluating for the presence and characteristics of the patient’s breath sounds.

Inspiratory breath sounds should be evaluated based on their equality, amount of aeration, and presence of a wheeze or other abnormality. Expiratory breath sounds should be evaluated for equality (focality), the degree of wheezing, and the presence of any other abnormal expiratory sounds.7 These pulmonary examination findings can be used to provide patients with a clinical score that can help evaluate the severity of their disease (Table 1).6,7

CRITICAL DECISIONWhat diagnostic tests should be initiated in the emergency department?

Viral TestingAmong the most common

precipitants of bronchiolitis are respiratory syncytial virus (found in approximately 70% of cases), influenza, parainfluenza, and rhinoviruses. Viral testing is not necessary; however, admitting or observing patients may help prevent nosocomial infections.2

BloodworkLaboratory studies often are

unnecessary in such cases. A complete blood count may be beneficial if pneumonia is suspected, although the

TABLE 1. Clinical Severity Scoring System Tool6,7

Score 0 1 2 3

Respiratory rate <30 30 — 45 46 — 60 >60

Wheezing None Terminal expiration with stethoscope only

Entire expiration and inspiration with stethoscope only

Entire expiration and inspiration without stethoscope

Cyanosis None Perioral on crying only Perioral at rest Generalized at rest

Accessory muscle use None Presence of mild intercostal use (just visible), no head bobbing or tracheal tug

Moderate amount of intercostal use, no head bobbing or tracheal tug

Moderate/marked intercostal use, presence of head bobbing or tracheal tug


white blood cell count cannot be used to predict the presence of concurrent serious bacterial infections in patients admitted for lower-respiratory RSV infections and bronchiolitis.2,4 A metabolic panel may be considered in patients who are significantly dehydrated.

Blood cultures are warranted in any patient who appears toxic, has a fever higher than 38.5°C (101.3°F), requires admission to an intensive care unit, or requires a septic evaluation. Blood gas measurements may be helpful in assessing children who appear to tire, show signs of severe respiratory distress, or require inspired oxygen concentrations greater than 40%.2

RadiographyAlthough they are obtained in

approximately 72% of suspected bronchiolitis cases, routine chest radiographs are unwarranted and may even be misleading. Associated abnormalities such as atelectasis commonly are noted on x-ray, and may lead to an overuse of antibiotics. However, radiographs may be considered in patients with severe disease requiring ICU admission; oxygen saturations lower than 92%; or complications such as pneumothorax, pneumonia, or other pulmonary disease process.4,8

CRITICAL DECISIONWhat treatments can be administered in the emergency department?

There are few presentations in the emergency department more terrifying than the infant in distress. Physicians understandably will want to do everything in their power to hasten a patient’s recovery; however, this impetus can lead to the overuse of several potentially harmful medications and contribute to poor resource utilization.9 Current practice guidelines do not recommend the routine use of any medication in the emergency department for the treatment of bronchiolitis.

Parental education, IV hydration, and respiratory support continue

to be the mainstays of treatment for this particular disease process. In the emergency department, the sole clinical focus should be on supportive care, with an aim to maintain hydration and oxygenation.4 Oftentimes, this care includes intubation for pending hypercarbic/hypoxic respiratory failure — a practice that increased from 2000 to 2009.3

It is absolutely necessary for emergency physicians to understand the pathophysiology behind bronchiolitis, and familiarize themselves with appropriate treatments.

Common MedicationsAlbuterol (β-agonists)

According to the American Academy of Pediatrics’ (AAP) 2014 guidelines, albuterol should not be administered to infants with a diagnosis of bronchiolitis. This is a departure from earlier protocols, which endorsed a trial of β-agonists.

The new recommendation came after a recently updated Cochrane review of 30 randomized trials, in which bronchodilators showed no benefit in children with the disease. In addition, the cost of these agents and their potential adverse effects (eg, tachycardia and tremors) appear to outweigh any potential advantages.4 With that noted, there is controversy surrounding the recommendation against albuterol, with some authors and literature maintaining that a trial of the drug may offer some potential benefit.10,11

EpinephrineEpinephrine also is unwarranted in

children and infants with bronchiolitis. A recent Cochrane meta-analysis found no evidence to support its utility in the inpatient setting, and two large multicenter trials comparing nebulized epinephrine to placebo and albuterol showed no improvement in length of stay.4

The studies demonstrated a mild improvement in clinical scores, but no change in admission rates — a finding that suggests that although nebulized epinephrine may lead to transient clinical improvement in the emergency department, symptoms can escalate after a patient has been discharged home. Epinephrine may have potential value as a rescue agent in severe disease; however, formal studies are needed before it can be recommended in this setting.4

Hypertonic SalineAlthough it increasingly is being

studied as a potential treatment for bronchiolitis, hypertonic saline should not be used to treat these patients in the emergency department or in hospital stays shorter than 3 days.4 The agent, which increases mucociliary clearance in both healthy and diseased lungs, appears to be safe and effective in the treatment of mild to moderate bronchiolitis after 24 hours of use, and may reduce the length of stay for hospitalizations longer than 3 days.

n A trial of humidified, high-flow nasal cannula may be indicated for patients in respiratory distress. The treatment, which acts as continuous positive airway pressure, may spare the patient from mechanical ventilation.

n Educate the parents by making them aware of the natural disease course. Symptoms typically are at their worst between days 5 and 7; upper-respiratory symptoms may last up to 4 weeks.

n Demonstrate appropriate use of a nasal aspirator or bulb suction device before discharge. When used properly at home by parents, these devices can provide temporary relief by clearing thick secretions and upper-airway obstructions.


CorticosteroidsCorticosteroids should not be used

to manage infants with bronchiolitis in any setting. There is no evidence that the drug can decrease admission rates when compared to placebo, or reduce inpatient length of stay. Although corticosteroids are relatively safe, they may prolong viral shedding in patients with bronchiolitis.4

PalivizumabPalivizumab, a monoclonal antibody

that can be administered for 5 months to a specific subset of high-risk patients, should not be given routinely in the emergency department. The drug is recommended for otherwise healthy infants younger than 1 year who were born earlier than 29 weeks’ gestation; or those born earlier than 32 weeks’ gestation who required supplemental oxygen greater than 21% for at least 28 days of life.4

Alternative TherapiesHumidified, high-flow nasal cannula

can help decrease a patient’s work of breathing by providing continuous positive airway pressure. It has been shown to reduce intubation rates (from 37% to 7%) in the emergency department, ICU, and general inpatient settings in infants with bronchiolitis.4,12

Suctioning of the nasopharynx (eg, via a nasal aspirator or bulb suction device) is a simple, minimally invasive technique that can provide temporary relief by clearing thick secretions and upper-airway obstructions. In addition,

suction techniques can be explained easily to parents and included in discharge instructions if the patient is well enough to go home. It should be noted, however, that lapses greater than 4 hours between nasal suctioning and deep suctioning have been associated with longer hospital stays.4

The AAP has offered no formal recommendations about suctioning.Other therapies such as chest physio-therapy with percussion/vibration and deep suctioning have been shown to be of little benefit and are not recommended.

CRITICAL DECISIONWhich high-risk factors indicate the need for further observation or hospital admission?

Is the patient safe to go home? Being able to answer this seemingly simple question and identify patients who are at increased risk for poor outcomes is one of many essential skills in emergency medicine. The decision seldom is straightforward, and it can be very difficult to determine if the patient in front of you is “sick” or “not sick.” Answering these questions becomes even more anxiety provoking when encountering children who cannot describe how they are feeling or how long their symptoms have been present.

Bronchiolitis carries an average cost of more than $3,000 per admission, and is the leading cause

of hospitalizations in infants younger than 1 year.1,13 Although every patient should be managed on an individual basis, it is important for care providers to recognize patterns and characteristics that place patients at risk for poor outcomes, and even death.

Researchers have failed to formulate a clear set of discharge criteria for infants presenting with the disease.14 However, there are certain elements in the physical examination and birth history that have been shown to place patients at increased risk, necessitating hospitalization to prevent significant morbidity and mortality. High-risk factors include:4

• Age younger than 12 weeks• Born earlier than 34 weeks’

gestation• Existing cardiopulmonary

disease• Genetic abnormalities• In utero smoke exposure• Respiratory rate greater than

70 breaths per minute• Oxygen saturation less than

95% on room airPerhaps the most important factor

to consider when deciding whether to send a patient home is the competence and reliability of the parents. Family education is a crucial component of successful treatment.

The child’s caregivers must leave the emergency department with a thorough understanding of the disease process; their comfort level in providing further care will be a major determinant in the disposition of the patient. If there is any doubt that the parents will be able to provide appropriate supportive care at home, admission strongly should be considered.

SummaryBronchiolitis is a clinical diagnosis

of children younger than 2 years with viral symptoms and lower airway signs on examination. Many of these patients do well, and only require parental reassurance without any focused treatment. Radiographic imaging typically is unwarranted for patients with the disease, but may be considered in children with suspected bacterial infections or underlying

n Sending a high-risk patient home because they are well appearing on your initial examination. These patients often will return with a much more concerning presentation.

n Ordering chest imaging on patients with non-complicated bronchiolitis. Nonspecific x-ray findings can lead to unwarranted antibiotic treatment and hospital admissions.

n Administering maintenance fluid with hypotonic saline. Patients with bronchiolitis produce excess amounts of antidiuretic hormone, which places them at risk for hyponatremia. The addition of hypotonic saline has been shown to cause significant iatrogenic hyponatremia when compared to those who received isotonic fluid replacement.


CASE RESOLUTIONS

■ CASE ONEA diagnosis of bronchiolitis was

made in the emergency department, and the mother received a detailed explanation about the illness. She was comfortable with the decision to not perform an x-ray or start antibiotics.

Prior to discharging the child, the mother was instructed on adequate hydration and fever control, and was given strict return precautions that she was asked to repeat back to the physician. A follow-up appointment was arranged with the family’s primary care physician for the next afternoon.

■ CASE TWOThe child was monitored closely

in the emergency department for the next hour; his vital signs improved to pulse 168, respiratory rate 46, temperature 37.2°C (99°F), and oxygen saturation 97%. The boy’s

overall appearance also improved, and his retractions resolved almost completely.

A chest x-ray revealed a right lower lobe infiltrate, which was concerning for pneumonia, and he was started on ampicillin. Laboratory test results showed a leukocytosis with mild electrolyte abnormalities.

The boy continued to improve on nasal CPAP, and improved enough to be admitted to the pediatric intensive care unit for further monitoring and care. Over the next 72 hours, he was weaned off of oxygen, and the amount of his oral intake and wet diapers returned to normal. He could then be discharged home; his parents were instructed to finish the course of antibiotics and schedule a follow-up visit with their pediatrician.

■ CASE THREEConcerned for a diagnosis of

bronchiolitis and reactive airway

disease, the clinician administered albuterol breathing treatments, but the child became lethargic and apneic. The baby, was intubated, sedated, given an IV fluid bolus, and admitted to the pediatric intensive care unit. A post-intubation chest x-ray revealed a right upper-lobe atelectasis with a nearly complete whiteout of the left lung.

The patient improved clinically with respiratory support on mechanical ventilation, and could be extubated 5 days after admission. Her respiratory panel was positive for rhinovirus, which confirmed a final diagnosis of rhinovirus bronchiolitis. She was transferred back to the hospitalist floor, and was discharged home 10 days later. This case highlights the importance of understanding the characteristics of patients who are at high risk for poor outcomes.

processes, and those admitted to the intensive care unit.

Treatment options are limited for most patients with this diagnosis as albuterol, antibiotics, steroids, and epinephrine are not recommended for use in the emergency department. Supplemental oxygen and fluids are the mainstays of treatment; nasal CPAP, nebulized hypertonic saline, and palivizumab are options in certain settings.

Hospitalization is indicated for patients with high-risk characteristics, or if there is a concern that the child’s caregivers might fail to monitor the child or seek appropriate medical attention if needed. High-risk characteristics include a young patient or mother, prematurity, chronic health problems, low birth weight, and dehydration.

REFERENCES1. Mansbach JM, Emond JA, Camargo CA Jr.

Bronchiolitis in US emergency departments 1992 to 2000: epidemiology and practice variation. Pediatr Emerg Care. 2005;21(4):242-247.

2. Fitzgerald DA. Viral bronchiolitis for the clinician. J Paediatr Child Health. 2011;47(4):160-166.

3. Hasegawa K, Tsugawa Y, Brown DF, et al. Trends in bronchiolitis hospitalizations in the United States, 2000-2009. Pediatrics. 2013;132(1):28-36.

4. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014;134(5):1474-1502.

5. Lanari M, Prinelli F, Adorni F, et al. Risk factors for bronchiolitis hospitalization during the first year of life in a multicenter Italian birth cohort. Ital J Pediatr. 2015;41:40.

6. Duarte-Dorado DM, Madero-Orostegui DS, Rodriguez-Martinez CE, Nino G. Validation of a scale to assess the severity of bronchiolitis in a population of hospitalized infants. J Asthma. 2013;50(10):1056-1061.

7. Tal A, Bavilski C, Yohai D, et al. Dexamethasone and salbutamol in the treatment of acute wheezing in infants. Pediatrics. 1983;71(1):13-18.

8. Schuh S, Lalani A, Allen U, et al. Evaluation of the utility of radiography in acute bronchiolitis. J Pediatr. 2007;150(4):429-433.

9. Knapp JF, Simon SD, Sharma V. Quality of care for common pediatric respiratory illnesses in United States emergency departments: analysis of 2005 National Hospital Ambulatory Medical Care Survey Data. Pediatrics. 2008;122(6):1165-1170.

10. Walsh P, Rothenberg SJ. American Academy of Pediatrics 2014 bronchiolitis guidelines: bonfire of the evidence. West J Emerg Med. 2015;16(1):85-88. doi:10.5811/westjem.2015.1.24930.

11. Walsh P, Rothenberg SJ. The recommendation to not use bronchodilators is not supported by the evidence. Pediatrics. 2015;135(2):e556.

12. Kallapa C, Hufton M, Millen G, Ninan TK. Use of high flow nasal cannula oxygen (HFNCO) in infants with bronchiolitis on a paediatric ward: a 3-year experience. Arch Dis Child. 2014;99(8):790-791.

13. Leader S, Kohlhase K. Recent trends in severe respiratory syncytial virus (RSV) among US infants, 1997 to 2000. J Pediatr. 2003;143(5 Suppl): S127-S132.

14. Bronchiolitis Guideline Team, Cincinnati Children’s Hospital Medical Center: Evidence-based care guideline for management of bronchiolitis in infants 1 year of age or less with a first time episode, http://www.cincinnatichildrens.org/svc/alpha/h/health-policy/ev-based/bronchiolitis.htm, Guideline 1, pages 1-13, August 15, 2005.


The Critical Image

CASE A 10-year-old boy with no significant medical history presents following a motocross accident in which his motorcycle collided with another bike. The patient fell to the ground at high speed. He was wearing a helmet and denies loss of consciousness, but complains of thoracic pain. His vital signs are blood pressure 101/63, pulse 76, temperature 36.7°C (98.1°F), respiratory rate 22, and oxygen saturation 100% on room air.

The patient is alert with a Glasgow Coma Scale score of 15. He appears slightly tachypneic, and has tenderness to palpation of the chest wall, with no crepitus. The remainder of the examination is normal.

CASE RESOLUTIONThe patient was admitted for observation, and improved over 2 days without developing hypoxia.

By Joshua S. Broder, MD, FACEPDr. Broder is an associate professor and the residency program director in the Division of Emergency Medicine at Duke University Medical Center in Durham, North Carolina.

KEY POINTSPulmonary contusion is the most common lung injury from blunt chest trauma, although the range of reported prevalence is broad (17% to 70%).1 The plain radiographic appearance of increased density (indistinguishable from other fluids such as alveolar pus or aspirated material) results from blood within alveoli. The distribution of pulmonary contusion characteristically is nonsegmental or patchy, whereas pneumonia or aspiration often follows bronchopulmonary segmental anatomy.1 Depending on the severity of pulmonary injury, findings of pulmonary contusion may be present immediately or evolve over ≥6 hours. Radiographic resolution of the diagnosis begins at 24 to 48 hours and concludes by 3 to 10 days. In contrast, new areas of pulmonary density that occur ≥24 hours after injury are more suggestive of alternative diagnoses such as pneumonia. Pulmonary contusion can occur without associated rib fractures, particularly in young patients whose ribs have not fully calcified.

A. Initial chest x-ray (day 0). Multiple nonsegmental areas of increased density are seen, representing pulmonary contusion; and no rib fractures.

B. Follow-up chest x-ray (day 2), showing interval resolution of pulmonary contusions.

C and D (zoomed from C). Axial plane CT image of the chest, lung windows. Peripheral nonsegmental or patchy parenchymal densities typical of pulmonary contusion are visible. Subpleural sparing (an absence of parenchymal density) occurs within 1 to 2 mm of the pleural surface, classic for pulmonary contusion.

REFERENCE1. Kaewlai R, Avery LL, Asrani AV, et al. Multidetector CT of blunt thoracic trauma. Radiographics. 2008;28:

1555-1570.

Case Contributor: Cathleen Bury, MD

On CT, pulmonary contusion often is peripherally located within the thorax with a nonsegmental distribution, and may demonstrate subpleural sparing.1 The interpretation is guided by the clinical presentation, including the time of onset of imaging abnormalities relative to the time of injury. Pulmonary contusion is often visible on CT immediately after injury.1

Nonsegmental peripheral

lung opacityParenchymal opacity

Subpleural sparing

A B

C

D


CME QUESTIONS

1 Which of these features should raise suspicion for a life-threatening rash?A. Any rash in a 6-month-old infantB. Pruritic lesionsC. Rash that develops slowly over 6 monthsD. Rash with associated oral lesions

2 Which characteristic differentiates erythema multiforme from Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)?A. Direct immunofluorescence showing IgG

autoantibodies on keratinocytesB. Lack of oral lesionsC. Negative Nikolsky signD. Skin involvement ≤10%

3 What is the most common cause of death in patients with SJS/TEN?A. HypovolemiaB. PancreatitisC. Respiratory failureD. Sepsis

4 Which of the following describes the standard treatment for SJS/TEN?A. Discharge home with dermatology follow upB. Rapid sequence intubation and mechanical

ventilation, ICU admission, lesion managementC. Removal of the suspected agent agent, burn unit

admission, fluid resuscitation, analgesia, lesion management

D. Removal of the suspected agent, fluid resuscitation, pain management, inpatient admission

5 What is the predominant cause of bullous pemphigoid?A. Exfoliative exotoxins cleaving desmoglein-1B. IgG autoantibodies targeting desmogleinsC. IgG autoantibodies targeting hemidesmosomesD. Type IV hypersensitivity reaction involving T lymphocytes

6 How can be pemphigus vulgaris (PV) be differentiated from bullous pemphigoid (BP)?A. BP rarely occurs in individuals older than 60 yearsB. In BP, direct immunofluorescence reveals IgG

antibodies on keratinocytesC. Patients with PV will have a positive Nikolsky sign and

oral lesions with mucosal involvementD. Skin involvement in PV is ≥30%; in BP, it is ≤10%

7 What is the first-line therapy for managing PV?A. Broad-spectrum antibioticsB. CorticosteroidsC. Fluid supportD. Intravenous immunoglobulin

8 Which diagnostic tool is most reliable in assessing for staphylococcal scalded skin syndrome (SSSS)?A. A skin biopsy that is positive for intraepidermal

blister formation and eosinophilic infiltratesB. Clinical judgment, including a head-to-toe

physical examination and detailed historyC. Cultures taken from skin lesionsD. Two positive blood cultures

9 Which treatment is most appropriate for SSSS?A. CorticosteroidsB. Intravenous antibiotic therapyC. None; lesions will resolve spontaneouslyD. Stop the suspected medication, administer fluid

resuscitation, and admit patient to a burn unit

Which of the following rashes is characterized by a positive Nikolsky sign?A. BPB. EMC. ImpetigoD. SSSS

A previously healthy 6-month-old presents with gradual-onset increased work of breathing and poor appetite. He was born full term by vaginal delivery, and his immunizations are current. He developed a runny nose and cough 4 days ago. Vital signs are heart rate 160, respiratory rate 70, and oxygen saturation 93% on 2 liters nasal cannula. He does not improve with nebulized albuterol. The pediatric hospitalist recommends admission to the pediatric intensive care unit (PICU). Which factor is an appropriate indication for a chest radiograph?A. Admission to the PICU/patient’s clinical pictureB. Low oxygen saturationC. Low respiratory rateD. Treatment failure with nebulized albuterol

Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category 1 Credits™, and 5 AOA Category 2-B credits for completing this activity in its entirety. Submit your answers online at acep.org/newcriticaldecisionstesting; a score of 75% or better is required. You may receive credit for completing the CME activity any time within three years of its publication date. Answers to this month’s questions will be published in next month’s issue.

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Reviewed by Lynn Roppolo, MD, FACEP


ANSWER KEY FOR JUNE 2016, VOLUME 30, NUMBER 6

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20A B A D D A B A A C D B D B A A B A C C

Which of the following elements in a patient’s history should raise suspicion for bronchiolitis?A. Age older than 4 months B. Antibiotic useC. Prematurity and smoke exposure in uteroD. Vaginal delivery

Blood cultures are warranted in which of the following scenarios?A. The patient appears toxic or requires a septic

evaluationB. The patient has a history of lower-respiratory

infectionsC. The patient has complications such as

pneumothorax or pneumoniaD. The patient is younger than 3 weeks

Which treatment previously was endorsed in the American Academy of Pediatrics for bronchiolitis, but is not recommended in the organization’s 2014 guidelines?A. AlbuterolB. EpinephrineC. Hypertonic salineD. Pneumonia prophylaxis for high-risk patients

Which of the following patients with bronchiolitis is at high risk for a poor outcome?A. A previously healthy 4-month-old girl with

3 days of coughing, post-tussive emesis, and a temperature of 39.5°C (103.1°F). She is tolerating bottle feeds.

B. A well-appearing 9-month-old girl with 3 days of upper-respiratory symptoms and mild wheezing. Her two siblings have asthma. Her mother notes that she had “a hole in her heart,” which closed on its own after birth.

C. An afebrile 1-month old boy with 4 days of poor feeding, rhinorrhea, and a cough. Vital signs are normal, but he was born at 31 weeks’ gestation by cesarean delivery.

D. An afebrile 9-month-old boy with clear lungs and normal vital signs. He has dry mucous at the nares bilaterally, and a history of ear infections.

A 6-month-old with increased work of breathing is given a diagnosis of bronchiolitis. Which treatment should be considered prior to initiating intubation?A. A trial of steroidsB. Chest physiotherapyC. Nasal continuous positive airway pressureD. Ribavirin

A previously healthy 1-month-old girl presents with 48 hours of congestion and a rectal temperature of 37.7°C (100.0°F). Her immunizations are up to date, and she has been eating and urinating normally. Her older sibling shows signs of a similar illness. Vital signs are blood pressure 74/48, pulse 142, respiratory rate 33, and oxygen saturation 98% on room air. What is the most appropriate next step?A. Initiate antiviral therapyB. Order a trial of albuterolC. Start antibiotic therapy with amoxicillinD. Strongly consider admitting the patient for 24-

hour observation

Which of the following factors makes the patient in question 17 “high risk?”A. Age of 1 monthB. Oxygen saturation of 98%C. Respiratory rate of 33D. Sibling in the household

An 8-month-old boy with bronchiolitis is struggling to eat due to congestion and coughing. What is the most appropriate recommendation?A. Administer nebulized hypertonic salineB. Administer supplemental oxygen by nasal cannulaC. Attempt to clear nasal secretionsD. Bottle-feed until the congestion improves

Which presentation is typical for bronchiolitis?A. A 4-year-old with 1 day of coughing, congestion,

and diffuse wheezing. Vital signs are blood pressure 88/30, pulse 160, respiratory rate 30, temperature 38.9°C (102°F), and oxygen saturation 93%

B. A 6-year-old with 2 days of coughing and coarseness to the left superior posterior chest. Vital signs are blood pressure 82/40, pulse 150, respiratory rate 48, temperature 38.9°C (102°F), and oxygen saturation 93%

C. An 8-month-old with sudden-onset respiratory difficulty with wheezing. Vital signs are blood pressure 78/32, pulse 180, respiratory rate 60, temperature 37°C (98.6°F), and oxygen saturation 96%

D. A 9-month-old with 2 days of congestion with diffuse coarseness. Vital signs are blood pressure 78/40, pulse 162, respiratory rate 38, temperature 37.3°C, (99.2°F), and oxygen saturation 96%

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Drug Box Tox BoxILLICIT OPIOID USEBy Bryan Corbett, MD, University of California Health Sciences, San Diego

Despite their value as an analgesic, opioids (particularly heroin [Di-acetylated morphine]) are being abused recreationally with alarming frequency. Unique complications stemming from specific compounds and routes of administration can be dangerously unpredictable. The increasing number of overdose deaths in recent years is partially attributable to the substitution of heroin with fentanyl and its analogs, which can be far more potent.

NALOXONEBy Frank Lovecchio, DO, MPH; and Ranvir Singh, MD, Maricopa and Banner University Medical Centers, Phoenix, ArizonaNaloxone is a pure opioid-antagonist that acts in the central nervous system (CNS) to block opiate receptors; it has no agonist activity. The drug can completely or partially reverse opioid overdose and other medication toxicities. It frequently is used to empirically treat patients in extremis from an unknown cause. The drug is particularly appealing to emergency physicians, as it can be safely administered IV/IM/SC/ETT/IO, and recent studies show its efficacy as a nebulized solution. There is growing support for the provision of outpatient prescriptions/kits for at-risk patients.

Mechanism of Action

Opioid antagonist that competitively blocks mu, kappa, and delta opiate receptors within the central nervous system

Indications Complete or partial reversal of opioid toxicity, including respiratory depression, sedation, or hypotension. Empiric use in altered patients with suspected overdose.

Dosing Opioid Overdose (known or suspected): Adults: 0.4-2 mg IV/IM/SQ q2-3 minutes; reassess if no response after 2-10 mgChildren: 0.01 mg/kg IV/IM/SQ initial dose; if no response, increase to 0.1 mg/kg2 mg in 3 mL normal saline in nebulizerEndotracheal administration is the least desirable route. No dose adjustments required for patients with renal or hepatic impairment.

Side Effects Most common: Confusion, headache, vomiting, agitation, tachycardiaMost serious, but extremely rare (<.2%): ventricular fibrillation, cardiac arrest, pulmonary edema, seizures

Precautions Contraindications: Hypersensitivity Precautions: Complete reversal of opioids may precipitate acute withdrawal. Administer with caution, especially in pregnant patients. Pregnancy and lactation: Pregnancy category C. Crosses the placenta and may cause withdrawal in the fetus. Unknown if excreted in breast milk.

Complications• Parenteral administration: Local cellulitis, abscesses (MRSA), bloodborne

pathogens (HCV & HIV), endocarditis, sepsis, and botulism (black tar heroin)• Opioid tablets (crushed and diluted in water to be injected intravenously):

Binding and filler ingredients (eg, talc, starch, and microcrystalline cellulose) can cause a pulmonary granulomatous reaction, progressing to pulmonary fibrosis and hypertension; extra-pulmonary deposition in the heart, liver, and spleen (undetermined clinical significance)

• “Free basing” (smoking heroin off of aluminum foil): Associated with spon-giform encephalopathy (bradykinesia, ataxia, and speech abnormalities)

Toxic DoseToxicity threshold unspecified. Although the risks increase with higher doses, outcomes depend on individual factors (eg, genetics and tolerance).Clinical EvaluationDiagnosis of acute opioid intoxication is a clinical toxidrome, including respiratory depression (decreased tidal volume, then rate), CNS depression, miosis (not seen with meperidine and some agonist-antagonist opioids), hypotension (severe cases), and evidence or a history of drug abuse.Note: Urine drug screens can confirm exposure, but not intoxication. They are inconsistent in recognizing fentanyl, and are not useful in patient management.Treatment• Good supportive care with attention to airway, breathing, and circulation• Naloxone to reverse CNS, respiratory, and cardiovascular depression;

see Drug Box for dosing. Repeated dosing usually is unwarranted for heroin overdose, but may be required for ingestions of methadone or sustained-release oral formulations.

Decontamination and Elimination• Not useful for parenteral overdoses• Questionable use in ingestions due to availability of an effective antidote• Extracorporeal drug removal (ie, hemodialysis) not indicated DispositionNaloxone has a short duration of action; awake, alert patients can be discharged post-administration. Repeated dosing of naloxone generally necessitates continued observation and repeated or continuous infusions of the medication.

Reviewed by Christian A. Tomaszewski, MD, MS, MBA, FACEP

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