Lucio phenomenon is a rare, potentially fatal vasculonecrotic reaction seen predominantly in untreated diffuse lepromatous leprosy. It presents with characteristic angulated purpuric lesions that evolve into painful necrotic ulcers and heal with stellate atrophic scars. Although classically reported from Mexico and Central America, sporadic cases are increasingly recognised in India. Pregnancy and the postpartum period may alter immune responses and precipitate leprosy reactions.

A 36-year-old woman from rural Bihar presented one month after an uneventful vaginal delivery with multiple painful ulcers over both upper and lower limbs and buttocks for four weeks. She reported progressive sensory loss in both lower limbs, recurrent nasal stuffiness, epistaxis and pedal oedema for one year, with rapid worsening within five days postpartum. Her mother had previously received multidrug therapy for multibacillary leprosy.

Examination showed diffuse shiny infiltration of the face and earlobes giving a lepra bonita appearance, complete ciliary and superciliary madarosis, and multiple irregular, jagged necrotic ulcers with healed hypopigmented stellate scars. Bilateral ulnar, greater auricular and common peroneal nerves were thickened, with glove-and-stocking hypoesthesia. Slit-skin smear showed abundant acid-fast bacilli with a bacteriological index of 6+ and morphological index of 25%. Histopathology from the ulcer edge demonstrated dermal vessel thrombosis, perivascular inflammation and acid-fast bacilli within vascular walls on Fite-Faraco staining. A diagnosis of Lucio phenomenon secondary to diffuse lepromatous leprosy was made. She was treated with multibacillary multidrug therapy, tapering oral prednisolone, wound care and iron supplementation, with no new lesions after two weeks and partial re-epithelialisation by four weeks.

Lucio phenomenon should be considered in patients with diffuse lepromatous leprosy who develop widespread, angulated necrotic ulcers. The combination of lepra bonita, madarosis, high bacillary load and endothelial acid-fast bacilli is highly suggestive. Histologically, vascular endothelial invasion and thrombosis help distinguish it from vasculonecrotic erythema nodosum leprosum. The postpartum onset in this case supports the role of pregnancy-related immune modulation and subsequent immune rebound in precipitating reactional states. Early recognition, prompt multibacillary multidrug therapy, appropriate anti-inflammatory treatment and meticulous wound care are needed to limit morbidity and mortality.

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