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PRACTICE EMPRACTICE NET
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
September 2002
Dermatologic Emergencies: Volume 4, Number 9
W HILE most rashes seen in the ED are benign, some indicate a serious
or even life-threatening medical illness. This issue of Emergency
Medicine Practice provides a systematic approach to managing dangerous
CME Objectives
Editor-in-Chief Center School of Medicine, Emergency Medicine, Morristown Professor and Chief of the Division Medical Service, Orlando, FL.
Albuquerque, NM. Memorial Hospital. of Family Medicine, Mount Sinai Alfred Sacchetti, MD, FACEP,
Stephen A. Colucciello, MD, FACEP, School of Medicine, New York, NY. Research Director, Our Lady of
W. Richard Bukata, MD, Assistant Michael A. Gibbs, MD, FACEP, Chief,
Assistant Chair, Department of Clinical Professor, Emergency Department of Emergency John A. Marx, MD, Chair and Chief, Lourdes Medical Center, Camden,
Emergency Medicine, Carolinas Medicine, Los Angeles County/ Medicine, Maine Medical Center, Department of Emergency NJ; Assistant Clinical Professor
Medical Center, Charlotte, NC; USC Medical Center, Los Angeles, Portland, ME. Medicine, Carolinas Medical of Emergency Medicine,
Associate Clinical Professor, CA; Medical Director, Emergency Center, Charlotte, NC; Clinical Thomas Jefferson University,
Department of Emergency Gregory L. Henry, MD, FACEP,
Department, San Gabriel Valley Professor, Department of Philadelphia, PA.
Medicine, University of North CEO, Medical Practice Risk
Medical Center, San Gabriel, CA. Emergency Medicine, University Corey M. Slovis, MD, FACP, FACEP,
Carolina at Chapel Hill, Chapel Assessment, Inc., Ann Arbor,
Francis M. Fesmire, MD, FACEP, MI; Clinical Professor, Department of North Carolina at Chapel Hill, Professor of Emergency Medicine
Hill, NC. Chapel Hill, NC.
Director, Chest PainStroke of Emergency Medicine, and Chairman, Department of
Associate Editor Center, Erlanger Medical Center; University of Michigan Medical Emergency Medicine, Vanderbilt
Michael S. Radeos, MD, MPH,
Assistant Professor of Medicine, School, Ann Arbor, MI; President, University Medical Center;
Attending Physician, Department
Andy Jagoda, MD, FACEP, Professor UT College of Medicine, American Physicians Assurance Medical Director, Metro Nashville
of Emergency Medicine,
of Emergency Medicine; Director, Chattanooga, TN. Society, Ltd., Bridgetown, EMS, Nashville, TN.
Lincoln Medical and Mental
International Studies Program, Barbados, West Indies; Past Health Center, Bronx, NY; Mark Smith, MD, Chairman,
Valerio Gai, MD, Professor and Chair,
Mount Sinai School of Medicine, President, ACEP. Assistant Professor in Emergency Department of Emergency
Department of Emergency
New York, NY. Medicine, University of Turin, Italy. Jerome R. Hoffman, MA, MD, FACEP, Medicine, Weill College of Medicine, Washington Hospital
Professor of Medicine/Emergency Medicine, Cornell University, Center, Washington, DC.
Michael J. Gerardi, MD, FACEP,
Medicine, UCLA School of New York, NY.
Editorial Board Clinical Assistant Professor, Charles Stewart, MD, FACEP,
Medicine; Attending Physician, Colorado Springs, CO.
Medicine, University of Medicine Steven G. Rothrock, MD, FACEP, FAAP,
UCLA Emergency Medicine Center;
Judith C. Brillman, MD, Residency and Dentistry of New Jersey; Associate Professor Thomas E. Terndrup, MD, Professor
Co-Director, The Doctoring
Director, Associate Professor, Director, Pediatric Emergency of Emergency Medicine, University and Chair, Department of
Program, UCLA School of Medicine,
Department of Emergency Medicine, Childrens Medical of Florida; Orlando Regional Emergency Medicine, University
Los Angeles, CA.
Medicine, The University of Center, Atlantic Health System; Medical Center; Medical Director of of Alabama at Birmingham,
New Mexico Health Sciences Vice-Chairman, Department of Francis P. Kohrs, MD, MSPH, Associate Orange County Emergency Birmingham, AL.
these conditions as variants of erythema multiforme. evolution or various external factors such as scratching,
healing, medications, and infections transform primary
Epidemiology lesions into secondary lesions.
Pattern recognition is the key to the correct diagnosis
Dermatologic complaints account for approximately 5% of an unknown rash. Peter Lynch developed a taxonomy
of all ED visits. However, there are limited epidemiologic in which an unknown rash is classified based on its major
data that analyze the types of rashes seen in EDs. One
pediatric ED reported that 31% of the cases primarily
involved the skin. Most cases were classified as contu- Table 1. Common Skin Lesions.
sions, lacerations, and burns; non-traumatic causes
included viral exanthems, bacterial infections, and Lesion type Description
contact dermatitis.2 In one survey, the most common skin Macule Circumscribed area of change in normal
complaints diagnosed by internists were dermatitis (16% skin color with no skin elevation
of all diagnoses), bacterial skin infections (14%), fungal Papule Solid, raised lesion up to 0.5 cm in
infections (5%), and acne vulgaris (5%).3 The emergency diameter; variable color
physician is more likely to encounter the life-threatening
Nodule Similar to papule but located deeper in
rashes, such as meningococcemia, toxic epidermal the dermis and subcutaneous tissue;
necrolysis, or toxic shock syndrome. more than 0.5 cm in diameter
A thick skin is a gift from God. Plaque Circumscribed elevation of skin more
Konrad Adenauer (1876-1976), German statesman than 0.5 cm in diameter; often a
confluence of papules
Pathophysiology
Pustule Circumscribed area of skin containing
The skin is comprised of three layers: the epidermis, the purulent fluid
dermis, and the subcutaneous layer. The epidermis
Vesicle Circumscribed, elevated, fluid-filled
contains basal cells and keratinocytes, which form a
lesion up to 0.5 cm in diameter
protective barrier. Melanocytes produce the pigment that
filters ultraviolet radiation. The dermis is comprised of Bulla Circumscribed, elevated, fluid-filled
connective tissuescollagen, elastin, and reticular lesion greater than 0.5 cm in diameter
fiberswhich provide strength and elasticity to the skin. Petechiae Small red or brown macules up to 0.5
The subcutaneous layer contains mostly fat cells and cm in diameter that do not blanch
connective tissue. Sweat glands, hair follicles, nerves, with pressure
capillaries, and veins are dispersed within these
Purpura Circumscribed petechiae more than
three layers.
0.5 cm in diameter
When these capillaries leak blood into the skin,
petechiae appear. Leakage results from perivascular Scales Excess dead epidermal cells produced
inflammation and/or thrombocytopenia. Petechiae are by abnormal keratinization; scaling in
often first seen in dependent areas such as the ankles and sheets is desquamation
wrists. If the petechiae are greater than 0.5 cm in size,
they become purpura. In vasculitis, the purpura can Table 2. Secondary Skin Lesions.
become palpable.
The dermal-epidermal junction deserves special Lesion type Description
mention. It is the site of immunoglobulin and comple- Erosion Focal loss of epidermis; heals
ment deposition and is the origin of blisters in diseases without scarring
such as pemphigus and Stevens-Johnson syndrome. Ulcer Focal loss of epidermis and dermis;
Immunofluorescence assays performed at the dermal- heals with scar
epidermal junction can help diagnose vesiculo-bullous
Excoriation Linear or angular erosions due
skin disease.
to scratching
Laboratory results
Table 7. Drugs Commonly Implicated In Cutaneous
Eosinophil count >1000/mm3
Lymphocytosis with atypical lymphocytes
Allergic Reactions.
Abnormal liver function tests
Aminopenicillins
Sulfonamides
Table 6. Guidelines For The Assessment Of A Possible Cephalosporins
Adverse Drug Reaction. Allopurinol
Phenobarbital
1.Alternative causes should be excluded, especially NSAIDs
infection. Many infections (especially viral) are difficult to Quinolones
distinguish clinically from adverse drug reactions. Phenytoin
2.The interval between introduction of a drug and the Valproic acid
onset of a reaction should be examined (e.g., 1-3 weeks ACE inhibitors
for TEN/SJS, 2-6 weeks for hypersensitivity syndrome). Thiazide diuretics
3.Any improvement after drug withdrawal should Beta-blockers
be noted. Oral contraceptives
4.The caregiver should determine whether similar reactions Phenothiazines
have been associated with the same compound. Corticosteroids
5.Any reaction on re-administration of a drug should
be noted. Source: Bigby M, Jick S, Jick H, et al. Drug-induced cutaneous
reactions. A report from the Boston Collaborative Drug Surveillance
Adapted from: Roujeau JC, Stern RS. Severe adverse cutaneous Program on 15,438 consecutive inpatients, 1975 to 1982. JAMA 1986
reactions to drugs. N Engl J Med 1994;331:1272-1285. Dec 26;256(24):3358-3363.
Table 8. Classification Of Erythema Multiforme, Stevens-Johnson Syndrome, And Toxic Epidermal Necrolysis.
Sources: Bastuji-Garin S, Rzany B, Stern RS, et al. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and
erythema multiforme. Arch Dermatol 1993 Jan;129(1):92-96; Roujeau JC. The spectrum of Stevens-Johnson syndrome and toxic epidermal necrolysis:
a clinical classification. J Invest Dermatol 1994 Jun;102(6):28S-30S.
Medications
Penicillin
Sulfonamides
Phenytoin
Barbiturates
Phenylbutazone Reproduced with permission from: Habif T, ed. Clinical Dermatology:
A Color Guide to Diagnosis and Therapy. 3rd ed. St. Louis: Mosby; 1996.
Diagnosis Pathophysiology
The diagnosis of EM is clinical. The diagnosis is most The pathophysiology of SJS and TEN is not completely
ensured when classic target lesions are present. If the understood. Some studies suggest it is the result of an
patient does not have target lesions, another diagnosis altered metabolism and immune-mediated response.39,40
should be considered. Similarly, if the patient looks toxic,
has systemic complaints, or has abnormal vital signs, Epidemiology
consider an alternative diagnosis. The incidence of TEN varies from 0.4-1.2 cases per
million per year.38 TEN occurs in all age groups but is
Management more common in adults over 40. SJS commonly occurs in
EM minor and major generally resolve without treatment children and young adults. While HIV patients are
in 2-3 weeks. Any underlying infection should be treated. predisposed to TEN, HIV is not considered to be a
While many physicians treat EM with prednisone, causative factor.41
supporting data remain weak to nonexistent, involving
just a handful of patients. A prospective study of 16 Morbidity And Mortality
children with EM major treated with steroids showed a The leading causes of death in TEN are sepsis from
significant reduction in the period of fever and reduction Staphylococcus aureus or Pseudomonas aeruginosa and
in the period of the eruption.33 Another prospective study fluid/electrolyte abnormalities.38,42 The severity of
of three patients with EM minor showed a rapid response complications is proportional to the extent of skin
to steroid therapy.34 However, other larger studies necrosis. Massive transepidermal fluid losses can
suggest minimal to no benefit from treatment with produce significant electrolyte imbalance; prerenal
steroids.35,36 Based on a review of the literature, there is no azotemia is common. Bacterial colonization of the skin
strong evidence that steroids are beneficial in EM minor or and decreased immune responsiveness leads to sepsis.
major. The best ED intervention is to determine (and if The mortality rate is 5%-10% for SJS and 23%-30%
possible treat) the cause of the rash and provide for TEN.42 The mortality rate is higher still in elderly
symptomatic relief using systemic antihistamines patients51% in one retrospective study of 77 elderly
and possibly analgesia. patients with TEN.43 Variables associated with a poor
prognosis include increased age, extent of disease, extent
Disposition of disease at time of transfer to a burn center, azotemia,
Essentially all patients diagnosed with EM minor or multiple medication use, thrombocytopenia, and neutro-
major can be safely discharged home. Follow-up with penia.38,44 Ophthalmologic sequelae such as keratitis and
the primary medical doctor or dermatologist is corneal ulcerations, cornel scarring, and blindness occur
helpful. Patients must return to the ED if there is in 40%-50% of patients.45
rapid progression of the rash or new systemic
symptoms. Follow-up with an ophthalmologist is Clinical Presentation
essential in cases of ocular involvement. In both SJS and TEN, patients present with a chief
complaint of a rash. Some experience prodromal symp-
You know what happens to scar tissue. toms similar to a viral illness such as myalgias, fever,
Its the strongest part of your skin.Michael R. Mantell cough, or sore throat. If a new drug is the cause, the
prodrome usually begins within days of ingestion. Skin
Vesiculo-Bullous Rashes lesions then develop suddenly, after 1-2 weeks of
prodromal symptoms.
Vesicles and bullae appear in many disorders. Some of Skin lesions in SJS look like atypical target lesions or
these disorders are benignsuch as poison ivy or a mild purpuric macules on the trunk. (This is in contrast to EM
case of varicella zosterwhereas others are potentially minor and major, where the majority of the distribution is
life-threatening, such as SJS, TEN, and pemphigus
vulgaris (PV).
Table 10. Etiologic Agents In Stevens-Johnson
Stevens-Johnson Syndrome Syndrome And Toxic Epidermal Necrolysis.
And Toxic Epidermal Necrolysis
Sulfonamides
Etiology Penicillins
SJS and TEN are related to the use of certain medications. Quinolones
Anticonvulsants, sulfonamides, other antibiotics, and Phenytoin
non-steroidal anti-inflammatory drugs (NSAIDs) are the Phenobarbital
main offenders.22 (See Table 10.) In one retrospective Carbamazepine
study, sulfonamides were found to be the etiology in 30 NSAIDs
cases, NSAIDs in 29 cases, anticonvulsants in seven cases, Allopurinol
Figure 2. A positive Nikolskys sign in toxic epidermal Figure 3. Toxic epidermal necrolysis.
necrolysis.
Solid Fluid-filled
Erythematous Non-erythematous Clear Pustular
(see below (see below
for differential for differential
diagnosis) diagnosis)
Vesiculo-bullous
(see below
for differential
diagnosis)
Maculopapular Petechial/purpuric Diffuse
(see below (see below erythematous
for differential for differential (see below for
diagnosis) diagnosis) differential
diagnosis)
Adapted from: Lynch PJ, Edminster SC. Dermatology for the nondermatologist: a problem-oriented system. Ann Emerg Med
1984 Aug;13(8):603-606.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
Central Peripheral
Yes No Yes No
disease
Has the patient been using a new drug?
Has there been any travel, or local incidence
Yes No of tick-borne disease?
Pityriasis rosea
Consider: Consider:
Rocky Mountain Erythema
spotted fever multiforme
Ehrlichiosis Secondary syphilis
Anthrax
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
If the patient is ill-appearing, consider empiric treatment
for meningococcemia and Rocky Mountain spotted fever
Does the patient have any sick contacts?
Yes No
Consider: Has there been any travel, or local incidence of tick-borne disease?
Meningococcemia
Rubella
Epstein-Barr virus Yes No
Enterovirus
Hepatitis B Is there palpable purpura?
Consider:
Gonococcemia
Rocky Mountain
Rheumatic fever
spotted fever Yes No
Dengue fever
Typhus
Rat bite fever Consider vasculitis Possible
thrombocytopenia:
Idiopathic
thrombocytopenic
purpura
Thrombotic
thrombocytopenic
purpura
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2002 EB Practice, LLC. 1-800-249-5770. No part of this publication may be reproduced in any format
without written consent of EB Practice, LLC.
Pemphigus Vulgaris
Etiology
Pemphigus vulgaris (PV) is a rare but potentially lethal
blistering condition predominantly seen in the elderly.
This autoimmune disease is characterized by erosions
and blistering of epithelial surfaces of the oral mucosa
and skin.
Clinical Presentation
The rash typically appears on the fourth day after the bite Reproduced with permission from: Habif T, ed. Clinical Dermatology:
(range, 1-15 days), erupting first on the wrist and ankles. A Color Guide to Diagnosis and Therapy. 3rd ed. St. Louis: Mosby; 1996.
2. That elderly fellow kept returning to the ED with mouth 5. I didnt think about antibiotic prophylaxis for his
sores and complained it was painful to eat. I referred him to dorm mates.
his dentist. You did a splendid job in quickly diagnosing and treating
Well, you neglected to check out the rest of his body for the index case of meningococcemia, but you neglected to
lesions or ask about personal or family history of bullous prophylax his roommates with ciprofloxacin or rifampin.
diseases. This patient had pemphigus vulgaris. Early Now two other students have contracted meningitis.
treatment can significantly improve outcome.
6. I diagnosed the patient with Stevens-Johnson syndrome
3. I thought that alcoholic, drug-abusing homeless person because he came in with denuded skin and lesions of the
was seeking narcotics. He kept on saying he had severe mouth, eyes, and rectum. I put silver sulfadiazene on the
pain in his leg, but I didnt see any physical signs that denuded areas, but he got worse.
anything was wrong. He was probably drunk. Drugs are usually the inciting agent in SJS and TEN. This
Pain out of proportion to physical examination in a toxic patient was started on sulfonamides the week he
person should raise suspicion for early necrotizing fasciitis. developed symptoms. You should have stopped the drug
This patient was toxic with altered mental statusnot (and not given silver sulfadiazene) as soon as the diagnosis
drunk. History of alcohol abuse, diabetes, peripheral of SJS was considered.
vascular disease, and a debilitated state are all risk factors
for necrotizing fasciitis. 7. I thought the patient might have TEN because she had a
really bad rash that was sloughing off and fever. It was 3:00
4. I thought the patient might have had cellulitis of his face a.m. and I didnt want to wake up the dermatologist, so I
and chest. He had fever and lymphadenopathy, so I started Continued on page 21
just started the steroids in the ED. I admitted the patient 9. She was 68 years old and had a high fever and a red
to the floor and figured the dermatologist could see her rash on her trunk. She said she had decreased energy
in the morning. and myalgias for the past few days with low-grade
This emergency physician made two big mistakes: 1) He fever. She had a past medical history of hypertension.
should have called the on-call dermatologist. 2) The patient I thought she had a viral syndrome and sent her home
should have been admitted to the ICU. Retrospective with follow-up with her primary care physician the
studies have shown that steroids may increase the rate next day.
of morbidity and mortality of patients with TEN. Steroids This patients rash worsened, and when she went to her
are generally not given for TEN and should only be given primary care physician the next day, the patient was found
in consultation with a dermatologist. Patients with TEN to have a high fever, hypotension, and upon admission to
should be treated like burn patients and admitted either the hospital she had increased BUN/Cr, CPK, and bilirubin.
to a burn unit or an ICU setting. The mortality rate from The patient had a nosebleed approximately one week prior
TEN is 25%-30%. to presentation that required nasal packing. The emergency
physician failed to obtain this history. She was admitted to
8. The patient came in complaining of severe leg pain and the hospital with the diagnosis of staphylococcal toxic
malaise. He was febrile and hypotensive but responded to shock syndrome.
fluids and acetaminophen. I diagnosed him with cellulitis,
started him on cefazolin, and admitted him to the floor. I 10. I suspected meningococcemia from the start. It takes
had no idea he would deteriorate so quickly and require time to get blood and urine cultures. I also needed to get a
transfer to the ICU. CT before I did the lumbar puncture. Plus, the nurses
This patient had streptococcal toxic shock syndrome. couldnt find a vein to stick.
STSS often presents with pain out of proportion to This child arrested before antibiotics were ever given. When
physical exam findings. About 80% of patients with you suspect meningococcemia, set a timer. If the cultures,
STSS have an associated soft-tissue infection, and bloodwork, lumbar puncture, etc., are not done by 30
60% develop bacteremia. The emergency physician minutes, give the antibiotics anyway (the lesions can be
must have a high index of suspicion for STSS when biopsied and successfully Grams-stained the next day
patients present with a soft-tissue infection or injury, and the cerebrospinal fluid will not be sterilized for hours).
high fever, and hypotension. IV penicillin combined Cant get a peripheral IV or a central line? If you cant get
with clindamycin is the initial treatment of choice. access within a reasonable time, consider IM or
Get a surgical consult if there is suspicion of a intraosseous antibiotics for the first dose and give the IV
necrotizing infection. dose as soon as a line is established.
37. A patient who presents with a rash and fever: 44. Diseases that produce diffuse erythematous rashes
a. should receive a full, head-to-toe examination. include all of the following except:
b. only requires a skin examination. a. staphylococcal scalded skin syndrome.
c. should receive acetaminophen for presumed b. toxic epidermal necrolysis.
viral syndrome. c. Kawasaki disease.
d. is considered low-risk unless he or she also has d. the toxic shock syndromes.
difficulty breathing. e. necrotizing fasciitis.
38. When performing the skin examination, the 45. Antibiotic prophylaxis for all close contacts of
emergency physician should evaluate: patients with meningococcemia, including house-
a. the type of lesion. hold members and medical personnel in contact
b. the shape of the individual lesion. with respiratory droplets, is mandatory.
c. the arrangement of multiple lesions. a. True
d. the pattern of the rash. b. False
e. all of the above.
46. Henoch-Schnlein purpura:
39. Patients who are not toxic or febrile and who have a. rarely affects children.
a rash that appears benign should receive: b. is a constellation of cutaneous purpura,
a. a CBC. arthritis, abdominal pain, gastrointestinal
b. a CBC, chemistry panel, and liver function tests. bleeding, and nephritis.
c. a Grams stain. c. requires hospital admission.
d. a punch biopsy. d. treatment should include antibiotics and
e. none of the above. not corticosteroids.
a. They can be due to viral, bacterial, or Date of Original Release: This issue of Emergency Medicine Practice was published
September 1, 2002. This activity is eligible for CME credit through September
non-infectious causes. 1, 2005. The latest review of this material was August 7, 2002.
b. They include some of the most rapidly Discussion of Investigational Information: As part of the newsletter, faculty may
lethal rashes. be presenting investigational information about pharmaceutical products that
is outside Food and Drug Administration approved labeling. Information
c. They are usually caused by toxic
presented as part of this activity is intended solely as continuing medical
shock syndrome. education and is not intended to promote off-label use of any pharmaceutical
d. They should be presumed to be caused product. Disclosure of Off-Label Usage: This issue of Emergency Medicine Practice
discusses the use of doxycycline in young children with Rocky Mountain
by Rocky Mountain spotted fever or
spotted fever. Although it is not approved for this use, clinical studies indicate it
meningococcal disease until ruled out. is safe and effective for this condition. (See text.)
Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and
Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Nguyen, Dr.
Class Of Evidence Definitions Freedman, Dr. Burke, and Dr. Playe report no significant financial interest or
other relationship with the manufacturer(s) of any commercial product(s)
Each action in the clinical pathways section of Emergency Medicine Practice
discussed in this educational presentation.
receives an alpha-numerical score based on the following definitions.
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Always acceptable, safe consensus panels education for physicians.
Definitely useful Occasionally positive results
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effectiveness
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