Skip to main content

Main menu

  • Home
  • Content
    • Current issue
    • Past issues
    • Early releases
    • Collections
    • Sections
    • Blog
    • Infographics & illustrations
    • Podcasts
    • COVID-19 articles
    • Obituary notices
  • Authors & Reviewers
    • Overview for authors
    • Submission guidelines
    • Submit a manuscript
    • Forms
    • Editorial process
    • Editorial policies
    • Peer review process
    • Publication fees
    • Reprint requests
    • Open access
    • Patient engagement
  • Physicians & Subscribers
    • Benefits for Canadian physicians
    • CPD Credits for CMA Members
    • Subscribe to CMAJ Print
    • Subscription prices
    • Obituary notices
  • Alerts
    • Email alerts
    • RSS
  • JAMC
    • À propos
    • Numéro en cours
    • Archives
    • Sections
    • Abonnement
    • Alertes
    • Trousse média 2023
    • Avis de décès
  • CMAJ JOURNALS
    • CMAJ Open
    • CJS
    • JAMC
    • JPN

User menu

Search

  • Advanced search
CMAJ
  • CMAJ JOURNALS
    • CMAJ Open
    • CJS
    • JAMC
    • JPN
CMAJ

Advanced Search

  • Home
  • Content
    • Current issue
    • Past issues
    • Early releases
    • Collections
    • Sections
    • Blog
    • Infographics & illustrations
    • Podcasts
    • COVID-19 articles
    • Obituary notices
  • Authors & Reviewers
    • Overview for authors
    • Submission guidelines
    • Submit a manuscript
    • Forms
    • Editorial process
    • Editorial policies
    • Peer review process
    • Publication fees
    • Reprint requests
    • Open access
    • Patient engagement
  • Physicians & Subscribers
    • Benefits for Canadian physicians
    • CPD Credits for CMA Members
    • Subscribe to CMAJ Print
    • Subscription prices
    • Obituary notices
  • Alerts
    • Email alerts
    • RSS
  • JAMC
    • À propos
    • Numéro en cours
    • Archives
    • Sections
    • Abonnement
    • Alertes
    • Trousse média 2023
    • Avis de décès
  • Visit CMAJ on Facebook
  • Follow CMAJ on Twitter
  • Follow CMAJ on Instagram
  • Listen to CMAJ podcasts
Practice

Dermatologic emergencies

Anatoli Freiman, Daniel Borsuk and Denis Sasseville
CMAJ November 22, 2005 173 (11) 1317-1319; DOI: https://doi.org/10.1503/cmaj.050783
Anatoli Freiman
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Daniel Borsuk
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Denis Sasseville
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Responses
  • Metrics
  • PDF
Loading

Dermatologic problems represent about 15%–20% of visits to family physicians and emergency departments. It is often a challenge for a primary care provider to differentiate mundane skin ailments from more serious, life-threatening conditions that require immediate intervention. The purpose of this article is to highlight some dermatologic emergencies.

Figure

Figure. Photo by: Dr. Brenda Moroz

Staphylococcal toxic shock syndrome: This toxin-mediated disease is characterized by rapid onset of generalized erythema with desquamation, fever, hypotension and potential mutisystem failure. The illness occurs in the setting of Staphylococcus aureus infection, for example in women using menstrual tampons of high absorbency, or in patients with superficial skin or surgical wound infections. S. aureus produces exotoxins, which induce massive cytokine secretion by T cells; fever, hypotension and multi-organ failure result. After a 2–3 day prodrome period of malaise, patients typically present with fever, chills, nausea and abdominal pain. A diffuse erythematous, nonpruritic, maculopapular or petechial rash ensues, with subsequent desquamation. The rash initially appears on the trunk and spreads peripherally to the palms and soles. Multi-system involvement includes arrhythmias, hepatic and renal failure, disseminated intravascular coagulation and acute respiratory distress syndrome.

Management: Aggressive supportive management is required to treat hypotension and potential multi-organ failure. Inciting factors should be removed. Once culture specimens are obtained, treatment with a β-lactamase-resistant anti-staphylococcal antibiotic is recommended.

Figure

Figure. Photo by: Dr. Shabaz Janjua, DermNet NZ

Angioedema: Characterized by well-circumscribed areas of edema caused by increased vascular permeability, this condition affects mostly the skin, and the gastrointestinal and respiratory tracts. Patients typically present with acute subcutaneous swelling, usually of the face, extremities or genitalia.

A generalized anaphylactic reaction may occur, which is potentially fatal if the upper airway is compromised. Urticaria can be associated with angioedema in 50% of cases; the angioedema is usually nonpruritic but burning. Although often idiopathic, angioedema can be induced by medications, allergens (e.g., food) or physical agents (e.g., vibration, cold). Typically, 10%–25% of cases are due to angiotensin-converting-enzyme (ACE) inhibitor therapy, occurring in 1–2 per 1000 new users. Penicillins, NSAIDs and radiographic contrast media are other potential triggers. Angioedema can occur as a result of C1 esterase inhibitor (C1INH) deficiency. Two rare but well-described categories exist: hereditary angioedema, which is transmitted in autosomal-dominant fashion, and acquired angioedema, which can be associated with autoimmune disorders and B-cell lymphoproliferative malignant disease.

Management: Treatment is largely supportive. Airway patency must be ensured if the respiratory system is involved. Cool, moist compresses and antihistamines can be used to control local burning. Referral to an allergy specialist for appropriate investigations should be considered. Avoidance of known triggers, such as associated medications, is paramount. ACE inhibitors are contraindicated in patients with C1INH deficiency. Attenuated androgens danazol and stanozolol increase the amount of active C1INH and are used for the prevention of hereditary angioedema. An algorithm for the diagnosis and management of hereditary angioedema was recently published.1

Figure

Figure.

Exfoliative erythroderma: This is a generalized scaly erythematous skin eruption involving more than 90% of the cutaneous surface. Although many cases are idiopathic, it can be associated with a diverse range of underlying dermatoses, including eczema, psoriasis, drug reaction (e.g., allopurinol, calcium-channel blockers, anticonvulsants and lithium), cutaneous T-cell lymphoma or leukemia, pityriasis rubra pilaris, paraneoplastic syndrome and dermatomyositis. Pruritus is usually the initial symptom, and malaise and fever may subsequently develop owing to excessive vasodilation. Fluid and protein loss through the skin can lead to life-threatening hypotension, electrolyte imbalance, congestive heart failure and enteropathy. In a study involving 91 patients with erythroderma, the disease-specific mortality was 18%;2 53% of the cases were associated with exacerbation of an existing dermatosis, which underscores the need for a thorough history and skin examination to identify a potential underlying skin condition.

Management: The cause should be determined and, if a drug reaction is suspected, the offending medication stopped. Skin biopsies can be obtained to help establish the diagnosis. Supportive therapy includes hospital admission, proper hydration, nutrition, electrolyte and cardiac monitoring, and temperature support. Skin care involves the use of emollients and compresses as well as topical corticosteroid therapy and antihistamines for pruritus. Antibiotic therapy should be administered if signs of infection develop.

Figure

Figure. Photo by: Dr. Benjamin Barankin

Necrotizing fasciitis: This rapidly spreading infection of the deep fascia can cause necrosis of the subcutaneous tissues. Type II necrotizing fasciitis is caused by group A streptococci, whereas mixed anaerobes, gram-negative aerobic bacilli and enterococci are implicated in type I. The organisms can be introduced through minor cuts, burns, blunt trauma or surgical procedures. Risk factors include diabetes mellitus, peripheral vascular disease and immunosuppression. The first cutaneous manifestation of streptococcal necrotizing fasciitis is diffuse swelling of the affected skin area followed by the development of bullae, which rapidly become burgundy in colour. Without prompt treatment, the infection may develop into frank cutaneous gangrene. Shock and organ failure can ensue and portend a poor prognosis. When skin necrosis is not obvious, diagnosis of necrotizing fasciitis must be suspected if there are signs of severe sepsis or some of the following local symptoms and signs: severe pain, indurated edema, skin hyperesthesia, crepitation, muscle weakness and foul-smelling exudate.

Management: Early recognition, aggressive management of sepsis and surgical débridement of the necrotic tissue are essential for effective treatment of necrotizing fasciitis. Antistreptococcal antimicrobial therapy should be administered; however, if the causal agents cannot be definitively identified, the patient should be given broad-spectrum antibiotics, as dictated by the clinical picture.

Figure

Figure. Photo by: Dr. Brenda Moroz

Meningococcemia: Neisseria meningitidis is a leading cause of meningitis and septicemia among North American youth. The incidence of invasive meningococcal disease is about 1.1 cases per 100 000, with the peak incidence at 6–12 months of age, when protective antibodies have not yet developed. The classic presentation of meningococcemia is the abrupt onset of maculopapular or petechial rash and flu-like symptoms, including fever, chills, malaise and disorientation. Over several hours, the disease may rapidly progress to purpura, disseminated intravascular coagulation, shock and death.

Management: Any febrile patient with a petechial rash should be suspected of having meningococcemia and treated promptly after blood cultures are obtained. Besides supportive management, therapy with a third-generation cephalosporin (e.g., ceftriaxone) or intravenous penicillin G therapy are the treatments of choice. Chloramphenicol may be used for patients allergic to penicillin.

Figure

Figure. Photo by: Dr. Benjamin Barankin

Stevens–Johnson syndrome and toxic epidermal necrolysis: These conditions represent a spectrum of drug-induced or idiopathic mucocutaneous reaction patterns, characterized by skin tenderness, erythema, epidermal necrosis and desquamation. The pathogenesis is thought to involve an impaired capacity to detoxify intermediate drug metabolites and genetic susceptibility. Common medications responsible for Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) include sulfonamides, anticonvulsants, allopurinol and NSAIDs. Drug administration typically precedes the rash by 1–3 weeks. Patients may present with a prodrome of fever, stinging eyes and pain on swallowing, followed by the development of dusky erythematous macules that progress to flaccid blisters. Two or more mucous membranes are usually involved, with erythema and erosions of buccal, genital and ocular mucosa. Severe ophthalmic involvement may lead to permanent scarring and blindness. Epidermal detachment is common, which may lead to massive fluid loss and electrolyte imbalance. Less than 10% of the epidermis sloughs off in SJS and more than 30% in TEN. These conditions are potentially life-threatening because of their multisystem involvement and skin-barrier breakdown. Epithelial loss results in vulnerability to bacterial and fungal infections and predisposes patients to septicemia and severe fluid loss. Mortality ranges from 5% in SJS to 30% in TEN.

Management: SJS and TEN should be managed by an experienced physician. Supportive measures include identification and removal of the offending medication, admission to a burn unit if necessary, intravenous fluid administration, maintenance of electrolyte and temperature homeostasis, and ophthalmologic assessment in case of ocular involvement. Skin care consists of proper wound dressings, oral hygiene (i.e., chlorhexidine rinses), antihistamine and topical corticosteroid therapy for pruritus, and antimicrobial therapy in cases of superinfection due to skin-barrier breakdown. Some centres use high doses of immunoglobulin intravenously as mainstay therapy for TEN; however, more evidence of its effectiveness is needed.

Figure

Figure. Photo by: Dr. Bernice Krafchik

Rocky Mountain spotted fever: This condition is potentially life-threatening and is most commonly introduced to humans through tick bites carrying the Rickettsia rickettsii parasite. Canadian vectors of R. rickettsii include Dermacentor variabilis (dog tick) in eastern Canada and Dermacentor andersoni (wood tick) in western Canada. Rocky Mounted spotted fever is associated with a mortality of 3%– 7% among treated patients and 30%– 70% among those not treated promptly or adequately. In about 60% of cases, patients present with a triad of fever, headache and rash following a tick bite. The classic rash with this condition appears within the first 2 weeks on the wrists and ankles and rapidly spreads to the palms and soles and eventually to the trunk and face. Purpuric macules and papules can be observed. Multiorgan involvement may lead to a variety of symptoms, which makes the diagnosis challenging. Complications of Rocky Mounted spotted fever include myocarditis and cardiogenic shock, peripheral edema due to hepatic failure and hypoalbuminemia, acute renal failure, altered mental status, seizures or coma, meningismus and disseminated intravascular coagulation.

Management: Besides symptomatic support, appropriate antibiotic treatment should be initiated immediately when this condition is suspected. Doxycycline is the drug of choice and should be continued for at least 3 days after fever subsides and until clinical improvement. The tick should be removed if embedded in the skin at the time of presentation.

Footnotes

  • This article has been peer reviewed.

REFERENCES

  1. 1.↵
    Bowen T, Cicardi M, Farkas H, et al. Canadian 2003 international consensus algorithm for the diagnosis, therapy, and management of hereditary angioedema. J Allergy Clin Immunol 2004;114(3):629-37.
    OpenUrlCrossRefPubMed
  2. 2.↵
    Sigurdsson V, Toonstra J, Hezemans-Boer M, et al. Erythroderma. A clinical and follow-up study of 102 patients, with special emphasis on survival. J Am Acad Dermatol 1996;35(1):53-7.
    OpenUrlCrossRefPubMed
PreviousNext
Back to top

In this issue

Canadian Medical Association Journal: 173 (11)
CMAJ
Vol. 173, Issue 11
22 Nov 2005
  • Table of Contents
  • Index by author

Article tools

Respond to this article
Print
Download PDF
Article Alerts
To sign up for email alerts or to access your current email alerts, enter your email address below:
Email Article

Thank you for your interest in spreading the word on CMAJ.

NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.

Enter multiple addresses on separate lines or separate them with commas.
Dermatologic emergencies
(Your Name) has sent you a message from CMAJ
(Your Name) thought you would like to see the CMAJ web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Dermatologic emergencies
Anatoli Freiman, Daniel Borsuk, Denis Sasseville
CMAJ Nov 2005, 173 (11) 1317-1319; DOI: 10.1503/cmaj.050783

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
‍ Request Permissions
Share
Dermatologic emergencies
Anatoli Freiman, Daniel Borsuk, Denis Sasseville
CMAJ Nov 2005, 173 (11) 1317-1319; DOI: 10.1503/cmaj.050783
Digg logo Reddit logo Twitter logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Footnotes
    • REFERENCES
  • Responses
  • Metrics
  • PDF

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Cited By...

  • A review of causes of Stevens-Johnson syndrome and toxic epidermal necrolysis in children
  • Reporting communicable diseases
  • Google Scholar

More in this TOC Section

  • SARS-CoV-2 vaccination in pregnancy
  • Infantile perianal pyramidal protrusion
  • Topical nonsteroidal anti-inflammatory drugs
Show more Practice

Similar Articles

Collections

  • Topics
    • Dermatology

 

View Latest Classified Ads

Content

  • Current issue
  • Past issues
  • Collections
  • Sections
  • Blog
  • Podcasts
  • Alerts
  • RSS
  • Early releases

Information for

  • Advertisers
  • Authors
  • Reviewers
  • CMA Members
  • CPD credits
  • Media
  • Reprint requests
  • Subscribers

About

  • General Information
  • Journal staff
  • Editorial Board
  • Advisory Panels
  • Governance Council
  • Journal Oversight
  • Careers
  • Contact
  • Copyright and Permissions
CMAJ Group

Copyright 2023, CMA Impact Inc. or its licensors. All rights reserved. ISSN 1488-2329 (e) 0820-3946 (p)

All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association or its subsidiaries.

To receive any of these resources in an accessible format, please contact us at CMAJ Group, 500-1410 Blair Towers Place, Ottawa ON, K1J 9B9; p: 1-888-855-2555; e: [email protected]

CMA Civility, Accessibility, Privacy

 

Powered by HighWire