Erythema multiforme

Erythema multiforme

Erythema Multiforme DIAGNOSTIC SUMMARY • Sudden onset of symmetric, erythematous, edematous, macular, papular, urticarial, bullous, or purpuric skin l...

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Erythema Multiforme DIAGNOSTIC SUMMARY • Sudden onset of symmetric, erythematous, edematous, macular, papular, urticarial, bullous, or purpuric skin lesions • Evolves into “target lesions” (“bull’s eye” lesions with clear centers and concentric erythematous rings) • Characteristic first site: dorsum of hand • Characteristic distribution: extensor surfaces of extremities with relative sparing of head and trunk • Rare oral manifestations: range from tender superficial erythematous and hyperkeratotic plaques to painful, deep, hemorrhagic bullae and erosions • Tendency to recur in spring and fall

GENERAL CONSIDERATIONS • The term erythema multiforme (EM) includes a wide range of expressions, from exclusive oral erosions (oral EM) to mucocutaneous lesions ranging from mild (EM minor) to severe multiple mucosal membranes (EM major, Stevens-Johnson syndrome [SJS]) or large area of total body surface (toxic epidermal necrolysis [TEN]). But the term erythema multiforme is not accepted worldwide; various clinical categories have overlapping features. EM minor, EM major, SJS, and TEN differ in severity and expression. All variants share two common features: cutaneous target lesions and satellite cell or more widespread necrosis of epithelium. Clinically, EM major is characterized by typical or raised atypical targets located on extremities and/or face. SJS is diagnosed when lesions are flat, atypical targets or purpuric maculae that are widespread or distributed on trunk. • Suspected etiologic factors: herpes simplex or Mycoplasma are linked to 90% of cases of EM minor; SJS and TEN (80% of cases) arise from drugs—anticonvulsants, sulfonamides, nonsteroidal anti-inflammatories, and antibiotics. Vaccines (e.g., vaccinia, bacille Calmette-Guérin, polio), food allergy, and other infectious 310

EM initiating pharmaceutical

DETERMINE NEED FOR CONVENTIONAL INTERVENTION

Coordinate discontinuation of offending agent with prescribing practitioner

Underlying infection

Immune support and indicated antimicrobial therapy

Identify and decrease exposure

Identify and coordinate cessation of offending agent. Cease all unnecessary medicines

Medications

Environmental exposure

Elimination diet with monitored reintroduction of suspected allergens

Food allergy

Identify initiating factor

MINIMIZE OBSTACLES TO HEALING

ERYTHEMA MULTIFORME

Herpetic infection

Initiate anti-inflammatory program

TAILOR NATURAL INTERVENTIONS TO PATIENT NEEDS

Zinc sulfate locally

Potassium iodide

Erythema Multiforme

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organisms have all induced EM minor. Common factor: highly reactive, polymorphonuclear leukocyte oxygen intermediates trigger hypersensitivity and immune system–mediated tissue damage. • Human leukocyte antigen (HLA) DQ3 correlates closely with recurrent EM and may be a marker to distinguish herpes-associated EM from other skin diseases. Biopsy can help predict disease progression from EM lesions to SJS or TEN.

THERAPEUTIC CONSIDERATIONS • Potassium iodide: historically used to treat a variety of erythematous disorders, including EM, erythema nodosum, nodular vasculitis, acute febrile neutrophilic dermatosis, and subacute nodular migratory panniculitis. Potassium iodide has documented dramatic success. Mechanism: suppression of generation of oxygen intermediates (hydrogen peroxide, hydroxyl radical) by stimulated polymorphonuclear antibodies. Iodine therapy is occasionally associated with adverse skin reactions and gastrointestinal discomfort. Never use in pregnant women in last trimester because of suppression of fetal thyroid. • Zinc: zinc sulfate (0.025% to 0.05%) is used locally at site of herpetic infection to prevent relapse of postherpetic EM.

THERAPEUTIC APPROACH Carefully search to determine initiating factor; treat underlying infections; cease all unnecessary medicines; initiate anti-inflammatory program. In herpes-associated EM, antiviral treatment initiated after EM has erupted has no benefit. Symptomatic treatment—local skin care, analgesics, and soothing mouthwashes—is important. Liquid antiseptics help prevent superinfection. Liquid diet may be necessary. Intravenous fluid replacement with electrolytes and nutrients should be started as early as possible. Systemic corticosteroids are controversial, some believing that it may increase risk of complications. • Supplements: — Potassium iodide: 100 mg t.i.d. for 4 to 6 weeks. Discontinue if adverse reactions occur. — Zinc sulfate: 0.025% to 0.05% solution applied locally to postherpetic lesions.