Related Therapeutic strategies

Herpes simplex virus (HSV) occurs in 2 common locations: orofacial (usually due to HSV-1) and genital (usually due to HSV-2).

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Seborrheic dermatitis can be limited to the scalp, but it also can involve the face and any hairy or intertriginous area and rarely can even progress to a generalized erythroderma.

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Chancroid

Timothy Berger Bruce Wintroub

Saturday, January 01, 2011

The diagnosis of chancroid is usually clinical, although improved culture techniques allow isolation of the causative organism H. ducreyi. The therapeutic strategy is to eliminate the pathogenic microorganism.

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Case Note

Case Note: Asymptomatic Lesions

History

A 24-year-old woman with history of recurrent orolabial herpes infection, presents with asymptomatic lesions on the palms (approximately eight on each hand) and soles (approximately four to five on each foot) that developed 1 day after new vesicles developed on her lips. This is the first time that she has developed skin lesions in association with her orolabial herpes. She reports no fever, respiratory or gastrointestinal symptoms.

Initial evaluation

  • Exam reveals target lesions, approximately 1 cm in size on the palms and soles
  • Four small erosions on the lower left lip with hemorrhagic crusting

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Enter your diagnosis

Diagnosis

  • A diagnosis of herpes simplex virus-associated erythema multiforme (EM) minor is rendered 
  • As it has been several days since her orolabial herpetic flare, no antiviral therapy is given
  • The patient is counseled that if she develops frequent herpes simplex virus (HSV) recurrences with EM minor, she should return to the clinic for consideration of viral suppressive therapy
  • She is also counseled to use photoprotection, especially over the lips, to avoid triggering recurrent herpetic flares

Initial Treatment

No patient treatment details are available; however, the general treatment strategy for EM is provided below.

First-line treatment is supportive care. Diagnostic management should entail consideration of a skin biopsy and a reasonable search for potential triggers that can be eliminated or treated. Diagnostic considerations include: Viral direct fluorescence antibody (DFA) testing, viral culture, herpes serologies, mycoplasma serologies or cold agglutinins and chest X-ray.

  • For bullous skin lesions, aluminum acetate compresses (such as Domeboro's or Burow's soak compresses, made by dissolving one packet or tablet in one cup of tap water) applied b.i.d. for 10-20 minutes followed by applications of silver sulfadiazine (Silvadene) cream b.i.d. Silvadene should be avoided if there is any concern for a sulfadiazine drug-related EM or Stevens-Johnson syndrome (SJS)
  • For oral lesions, an antiseptic mouthwash or hydrogen peroxide 30%, diluted 1:10, should be used t.i.d. Pain-alleviating mouthwash containing viscous lidocaine, diphenhydramine and aluminum and magnesium hydroxide can be used b.i.d. to t.i.d.
  • For ocular lesions, the most devastating potential complication of EM and/or SJS, ophthalmology referral is paramount. There currently is no evidence that either systemic or intraocular steroids can prevent progression of ocular disease. Note: Sulfa-containing eye drops should be avoided if there is any concern for a sulfa drug-related EM or SJS

Ancillary therapy

  • EM is triggered by either infection (most commonly, either Type I or II herpes simplex, but also Mycoplasma pneumoniae and a variety of other organisms) or, more rarely, drugs. Therefore, a search for the underlying cause is indicated. When a drug-related EM is suspected, it is worthwhile to exclude the possibility of an infectious cause as part of a complete diagnostic evaluation. Although therapy for coexistent or antecedent herpes infections (eg, with acyclovir) will not impact on the course of an individual episode of EM, suppressive therapy with acyclovir may prevent subsequent attacks. Implement treatment of other infectious causes because rarely epidemics of EM follow transmission of pathogens to other individuals
  • Patients receiving sulfonamides, anti-epileptics, analgesics or antibiotics may have drug-induced disease. Discontinue the offending agent and monitor the patient for progression to toxic epidermal necrolysis (a rare event that occurs after infection-related disease). Cutaneous tenderness and widespread bulla formation (epidermolysis) are important clues. Immediate skin biopsy with frozen sections is indicated and therapy then becomes that for toxic epidermal necrolysis (TEN)
  • Parenteral fluid replacement may be needed for patients with extensive erosions, particularly if oral lesions compromise fluid intake. Monitor fluid requirements by observing blood pressure, urine output, daily weights and assessment of central venous pressure, if necessary
  • Monitor for sepsis: With a compromised skin barrier, patients with bullous EM are prone to become septic. However, prophylactic antibiotics are not routinely indicated; antibiotic choice should be directed by bacterial culture data taken from the skin

Follow-up evaluation strategy

In this case, no follow-up evaluation details are available. However, in general, consideration should be given to the following:

  • Drug-induced EM rarely may progress to toxic epidermal necrolysis
  • There is a tendency for recurrent EM in patients with recurrent herpes simplex infections. Recurrent EM stemming from HSV may be associated with HLA-B15. Prophylactic acyclovir 400-800 mg/day may prevent flares of both herpes and resultant episodes of EM
  • If the patient was treated with systemic steroids before being seen, the possibility that complications of steroid therapy (eg, sepsis) are already present must be considered

General discussion

The presence of annular lesions, often acrally distributed, with a central target or bulla, is characteristic of EM. True target lesions are tripartite and consist of sharply marginated circular or polycyclic lesions with central dusky erythema, concentric edematous blanching, rimmed by a macular erythematous border. Atypical lesions may be flatter and consist of two instead of three zones. The central portion may be bullous in both true target lesions and atypical lesions. Mucosal lesions are seen in 25% of cases and typically affect the oral mucosa. EM may be seen in association with herpes simplex infection, mycoplasma pneumonial infection, contact dermatitis, medications, radiation or be idiopathic. Rare associations with EM include orf, vaccinia, varicella zoster, adenovirus, Epstein-Barr virus (EBV), cytomegalovirus (CMV), hepatitis, coxsackievirus, parvovirus, HIV, chlamydia, salmonella, tuberculosis, leprosy, histoplasma and dermatophyte infections (Hughey SL, 2010). Atypical forms with urticarial plaques or oral lesions alone, however, can present diagnostic dilemmas. Urticarial lesions with target-like central duskiness are often misdiagnosed as EM; this likely represents a clinical syndrome of 'urticaria multiforme' seen in children that has distinct clinical and histologic features (Shah KN et al, 2007). The classification and terminology of EM in the literature is controversial, and at times, confusing. EM may be clinically subdivided into EM minor and EM major, connoting distinct disease associations. EM minor is typified by minimal skin and/or mucosal disease, with minimal systemic symptoms, in association with either HSV or mycoplasma pneumonial infection. Therapy is generally not required or helpful for EM minor (limited to skin and/or one mucosal surface without systemic symptoms). Because this form of EM invariably follows infection and is self-limited, usually lasting only days to weeks, in the majority of cases the therapeutic strategy is symptom control or no treatment at all. However, if the problem is recurrent, the therapeutic strategy is to prevent and/or treat the causative herpes virus infection to prevent additional episodes. EM major (sometimes alternatively termed infection or drug-related SJS), however, requires inpatient management because of significant systemic symptoms and involvement of one and usually more mucosal surfaces. Unfortunately, specific therapy does not exist, and administration of systemic steroids may cause complications. Fortunately, like EM minor, the disease is self-limited regardless of severity, and supportive care is the mainstay of treatment.

Further reading

Hughey SL. Approach to the hospitalized patient with targetoid lesions. Dermatol Ther 2011;24:196-206.

Shah KN, et al. Urticaria multiforme: a case series and review of acute annular urticarial hypersensitivity syndromes in children. Pediatrics 2007;119;e1177.

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