Derm diagnoses you can’t afford to miss

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Applied Evidence

Derm diagnoses you can’t afford to miss

J Fam Pract. 2009 June;58(6):298-306

By

Ribhi Hazin, MD

Jamil Y. Abuzetun, MD

Khalil A. Khatri, MD

Innocuous or serious? Patients’ lives may depend on your ability to recognize dangerous dermatologic conditions.

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References

1. Noe R, Cohen AL, Lederman E, et al. Skin disorders among construction workers following Hurricane Katrina and Hurricane Rita: an outbreak investigation in New Orleans, Louisiana. Arch Dermatol. 2007;143:1393-1398.

2. Kulthanan K, Jiamton S, Thumpimukvatana N, et al. Chronic idiopathic urticaria: prevalence and clinical course. J Dermatol. 2007;34:294-301.

3. Stanway AD, Cohen SN, Chen C, et al. H1-antihistamines for chronic urticaria. Cochrane Database Syst Rev. 2008(2):CD006137.-

4. Grattan CE, Humphreys F. British Association of Dermatologists Therapy Guidelines and Audit Subcommittee. Guidelines for evaluation and management of urticaria in adults and children. Br J Dermatol. 2007;157:1116-1123.

5. Kozel MM, Mekkes JR, Bossuyt PM, et al. Natural course of physical and chronic urticaria and angioedema in 220 patients. J Am Acad Dermatol. 2001;45:387-391.

6. Nettis E, Colanardi MC, Soccio AL, et al. Double-blind, placebo-controlled study of sublingual immunotherapy in patients with latex-induced urticaria: a 12-month study. Br J Dermatol. 2007;156:674-681.

7. Lee EE, Maibach HI. Treatment of urticaria. An evidence-based evaluation of antihistamines. Am J Clin Dermatol. 2001;2:27-32.

8. Humphreys F, Hunter JA. The characteristics of urticaria in 390 patients. Br J Dermatol. 1998;138:635-638.

9. Serhat Inaloz H, Ozturk S, Akcali C, et al. Low-dose and short-term cyclosporine treatment in patients with chronic idiopathic urticaria: A clinical and immunological evaluation. J Dermatol. 2008;35:276-282.

10. Erbagci Z. The leukotriene receptor antagonist montelukast in the treatment of chronic idiopathic urticaria. A single-blind, placebo-controlled, crossover clinical study. J Allergy Clin Immunol. 2002;110:484-488.

11. Kostis JB, Kim HJ, Rusnak J, et al. Incidence and characteristics of angioedema associated with enalapril. Arch Intern Med. 2005;165:1637-1642.

12. Yusuf S, Teo KK, Pogue J, et al. ONTARGET Investigators. Telmisartan, ramipril, or both in patients at high risk for vascular events. N Engl J Med 2008;358:1547-1559.

13. Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. The diagnosis and management of anaphylaxis: an updated practice parameter. J Allergy Clin Immunol. 2005;115(3 Suppl 2):s483-s523.

14. Bas M, Kirchhartz N, Hochfeld J, et al. Potential role of vasomotor effects of fibrinogen in bradykinin-induced angioedema. J Allergy Clin Immunol. 2008;121:969e2-975e2.

15. Sica DA, Black HR. Angioedema in heart failure: occurrence with ACE inhibitors and safety of angiotensin receptor blocker therapy. Congest Heart Fail. 2002;8:334-341.

16. Banerji A, Clark S, Blanda M, et al. Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Ann Allergy Asthma Immunol. 2008;100:327-332.

17. Cicardi M, Zingale LC, Zanichelli A, et al. The use of plasma-derived C1 inhibitor in the treatment of hereditary angioedema. Expert Opin Pharmacother. 2007;8:3173-3181.

18. Bork K, Bygum A, Hardt J. Benefits and risks of danazol in hereditary angioedema: a long-term survey of 118 patients. Ann Allergy Asthma Immunol. 2008;100:153-161.

19. US Food and Drug Administration. Advisory Committee Briefing Document. Kalbitor (ecallantide) for acute attacks of hereditary angioedema. Available at: http://www.fda.gov/ohrms/dockets/AC/09/briefing/2009-4413b1-03-Dyax.pdf. Accessed May 5, 2009.

20. Schneider L, Lumry W, Vegh A, et al. Critical role of kallikrein in hereditary angioedema pathogenesis: a clinical trial of ecallantide, a novel kallikrein inhibitor. J Allergy Clin Immunol. 2007;120:416-422.

21. Ellis Simonsen SM, van Orman ER, Hatch BE, et al. Cellulitis incidence in a defined population. Epidemiol Infect. 2006;134:293-299.

22. Stevens DL, Bisno AL, Chambers HF, et al. Infectious Diseases Society of America. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41:1373-1406.

23. Morris A. What are the benefits of treatments? Cellulitis and erysipelas. BMJ Clin Evid. 2005;13:2066-2069.

24. Murray H, Stiell I, Wells G. Treatment failure in emergency department patients with cellulitis. CJEM. 2005;7:228-234.

25. Meier DE, Nkor SK, Aasa D, et al. Prospective randomized comparison of two preoperative skin preparation techniques in a developing world country. World J Surg. 2001;25:441-443.

26. Giordano PA, Elston D, Akinlade BK, et al. Cefdinir vs. cephalexin for mild to moderate uncomplicated skin and skin structure infections in adolescents and adults. Curr Med Res Opin. 2006;22:2419-2428.

27. Halpern J, Holder R, Langford NJ. Ethnicity and other risk factors for acute lower limb cellulitis: a U.K.-based prospective case-control study. Br J Dermatol. 2008;158:1288-1292.

28. Lin YT, Lu PW. Retrospective study of pediatric facial cellulitis of odontogenic origin. Pediatr Infect Dis J. 2006;25:339-342.

29. Rajendran PM, Young D, Maurer T, et al. Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection. Antimicrob Agents Chemo. 2007;51:4044-4048.

30. Schneck J, Fagot JP, Sekula P, et al. Effects of treatments on the mortality of Stevens-Johnson syndrome and toxic epidermal necrolysis: a retrospective study on patients included in the prospective EuroSCAR Study. J Am Acad Dermatol. 2008;58:33-40.

31. Chan HL, Stern RS, Arndt KA, et al. The incidence of erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A population-based study with particular reference to reactions caused by drugs among outpatients. Arch Dermatol. 1990;126:43-47.

32. Hazin R, Ibrahimi OA, Hazin MI, et al. Stevens-Johnson syndrome: pathogenesis, diagnosis, and management. Ann Med, 2008;40:129-138.

33. Chung WH, Hung SI, Hong HS, et al. Medical genetics: a marker for Stevens-Johnson syndrome. Nature. 2004;428:486.-

34. Jette N, Hemming K, Hutton JL, et al. Topiramate add-on for drug-resistant partial epilepsy. Cochrane Database Syst Rev. 2008;(3):DC001417.-

35. Gürcan HM, Ahmed AR. Efficacy of various intravenous immunoglobulin therapy protocols in auto-immune and chronic inflammatory disorders. Ann Pharmacother. 2007;41:812-523.

36. Strom BL, Carson JL, Halpern AC, et al. A population-based study of Stevens-Johnson syndrome. Incidence and antecedent drug exposures. Arch Dermatol. 1991;127:831-838.

37. Gravante G, Delogu D, Marianetti M, et al. Toxic epidermal necrolysis and Steven-Johnson syndrome: 11-years experience and outcome. Eur Rev Med Pharmacol Sci. 2007;11:119-127.

Practice recommendations

Management of hereditary angioedema should include fresh frozen plasma containing C1 inhibitor (C1-INH), whenever possible; if C1-INH-containing plasma is unavailable, fresh frozen plasma can be used instead (SOR: A).
Do not give neomycin to patients with suspected cellulitis; the drug may promote antibiotic resistance in Staphylococcus aureus, a pathogen often associated with this condition (SOR: A).
Whenever a patient presents with erythematous skin lesions and a recent history of receiving penicillin or a cephalosporin antibiotic, a sulfa derivative, or an anticonvulsant, the suspected medication should be stopped until Stevens-Johnson syndrome is ruled out (SOR: A).

Strength of recommendation (SOR)

Good-quality patient-oriented evidence
Inconsistent or limited-quality patient-oriented evidence
Consensus, usual practice, opinion, disease-oriented evidence, case series

Skin eruptions are a common reason for visits to primary care physicians. While most are innocuous, some are associated with—or are early warning signs of—severe allergic reactions or other emergent conditions. A 9-year-old patient I’ll call Julie is a case in point.

The first time Julie’s parents brought her to our clinic, she’d been complaining of a sore throat and had a fever that hovered between 102° and 103°F for several days. The physician who examined Julie found mild maxillary tenderness. A rapid streptococcal throat swab was negative; her doctor prescribed a 10-day course of trimethoprim/sulfamethoxazole (TMP/SMX) for presumed acute sinusitis.

FAST TRACK

In up to 80% of cases of chronic urticaria, no identifiable trigger is found.

Thirteen days later (3 days after the patient completed the course of antibiotics), Julie’s parents brought her back to the clinic. Her throat still hurt, and she had erythematous oval lesions on her trunk and upper extremities. Her physician diagnosed scarlet fever and wrote a prescription for penicillin.

The following day, Julie was taken to the emergency department (ED) with bilateral conjunctival hyperemia and diffuse, confluent erythematous macules throughout her body. The ED physician who examined Julie found a 2.5 × 2.0 cm targetoid lesion with a necrotic, purpuric center on her lower back—a diagnostic clue to the cause of her signs and symptoms.

If you had been Julie’s physician, would you have been alert to that clue?

For family physicians accustomed to seeing relatively mild skin disorders, recognizing and responding to dermatologic conditions with potentially dire outcomes can be challenging. This review, and the images that accompany it, will help you sharpen your dermatologic diagnostic and treatment skills, both for benign disorders and those that are less common and more severe. We’ll also tell you more about Julie and her diagnosis.

Urticaria: A simple case of hives?

This common allergic reaction affects close to 10% of the population at some point in their lives. The affected areas are itchy and have raised, circumscribed red welts with surrounding erythema.¹ Urticaria can occur throughout the body, with new lesions often erupting as the old ones disappear.^2,3

Despite the persistent itchiness that patients typically complain of, however, urticaria is usually self-limiting, and rarely life-threatening. Acute urticaria normally resolves within 2 to 6 weeks.^2,4

In most cases, urticaria arises secondary to exposure to an allergenic substance, chemical, or emotional stress.^4,5 In rare instances, systemic diseases, such as hematologic malignancies, can also cause urticarial lesions to erupt throughout the body.⁴

Body piercing, cosmetics, latex exposure, Helicobacter pylori, insects, and angiotensin-converting enzyme (ACE) inhibitors have been identified as common triggers of urticaria, as have nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, animal dander, and foods such as shellfish, nuts, and dairy products.^4,6

FAST TRACK

Hereditary angioedema typically occurs in children with no underlying disease; acquired angioedema generally affects adults with an underlying disorder that disrupts the complement pathway.

Treatment of all forms of urticaria should be based on identification and strict avoidance of the causative agent, if it’s known.⁷ Following withdrawal of the specific agent, symptomatic treatment with medications such as histamine antagonists and corticosteroids remains the mainstay of therapy.^4,8 A daily dose of 40 to 60 mg prednisone for 5 days is a reasonable therapeutic regimen for adults; a 5-day course of 1 mg/kg per day is suitable for pediatric patients.^4,8,9

In the event that topical or oral therapy is ineffective in mild cases of urticaria, intravenous (IV) diphenhydramine (50 mg) can be administered every 6 to 8 hours.^4,8 IV diphenhydramine typically takes 30 minutes to work, while corticosteroids take at least 2 hours to reach full effect.^4,8

In an emergency setting, subcutaneous epinephrine (0.3-0.5 mg) can be useful in treating severe urticaria.^4,8 And recent clinical trials have demonstrated complete clearance of urticaria with leukotriene inhibitors, such as montelukast (10 mg).¹⁰