Dermatology MCQ - Inflammatory Dermatoses - Erythema multiforme

A 22-year-old man presents with an acute eruption of multiple, sharply demarcated, erythematous plaques, many of which have a dark red center and a pale red outer ring. He reports a mild burning sensation but no significant pruritus. The most characteristic and pathognomonic feature of the individual lesions is:

A. Wickham's striae
B. A collarette of scale
C. A central blister or duskiness within a targeted lesion
D. Auspitz sign
E. Koebner phenomenon

Correct Answer: C. A central blister or duskiness within a targeted lesion

Answer & Explanation

Explanation:

The description is classic for erythema multiforme (EM). The hallmark lesion is the "target lesion," which has a very specific appearance.

• True Target Lesion: A true or "typical" target lesion has three zones:

  1. A central dusky purpura or blister (representing epidermal necrosis).

  2. A middle pale edematous ring.

  3. An outer rim of erythema.
     The presence of this central duskiness or blister is what makes the lesion "targetoid" and is pathognomonic for EM. Lesions can also be "raised atypical targets" with two zones.

The other options are associated with different conditions:

• A. Wickham's striae: These are the fine, white, reticulate lines seen on the surface of papules in lichen planus.

• B. A collarette of scale: This is a ring of scale at the periphery of a lesion, characteristic of pityriasis rosea.

• D. Auspitz sign: Pinpoint bleeding after scale removal is seen in psoriasis.

• E. Koebner phenomenon: The development of new lesions at sites of trauma, seen in psoriasis, lichen planus, and vitiligo, but is not a defining feature of EM.

Key Associations for Erythema Multiforme

• Pathophysiology: EM is considered an immune-complex mediated, type IV hypersensitivity reaction. It is most frequently triggered by infections, most notably Herpes simplex virus (HSV), which is implicated in over 50% of cases. Mycoplasma pneumoniae is another major infectious trigger.

• Clinical Presentation:

  • Distribution: Acral and symmetrical, with a strong predilection for the backs of the hands, palms, soles, and extensor surfaces of the extremities. The face is also commonly involved.

  • Mucosal Involvement: Limited mucosal involvement (usually one mucosal surface, e.g., the lips) can occur in EM minor. Widespread mucosal erosions suggest a more severe condition like Stevens-Johnson Syndrome (SJS).

• Differential Diagnosis: The key is to distinguish it from its more severe cousins:

  • Urticaria: Lesions are migratory, pruritic, and last <24 hours, lacking central blistering.

  • Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis (SJS/TEN): These are severe, life-threatening conditions characterized by widespread blisters and epidermal detachment, involving >10% of the body surface area in SJS-TEN overlap and TEN. They are typically drug-induced and have significant mucosal involvement.

• Histopathology: The hallmark is individual keratinocyte necrosis (apoptosis) at all levels of the epidermis, with a superficial perivascular lymphocytic infiltrate. Satellite cell necrosis (a lymphocyte adjacent to a dying keratinocyte) may be seen.

• Prognosis & Management:

  • EM is typically self-limited, resolving in 2-4 weeks, but can be recurrent, especially if associated with recurrent HSV.

  • Management focuses on: 1) Identifying and treating the underlying trigger (e.g., antiviral prophylaxis for HSV-associated EM), 2) Supportive care (e.g., analgesics, topical corticosteroids for plaques, mouthwashes for oral involvement). Systemic corticosteroids are controversial and are generally avoided, especially if an infection like Mycoplasma is suspected.