Acute haemorrhagic leukoencephalitis (AHL) is a fulminant inflammatory disease of cerebral white matter, characterised by demyelination and haemorrhagic necrosis. The outcome is usually fatal with only few survivors.An unusual presentation of a 44-year-old South Indian farmer who developed AHL following a snake bite is reported. Though the initial brain imaging showed extensive involvement of the white matter with multiple haemorrhagic foci, the patient improved spontaneously with no specific therapy. A repeat magnetic resonance imaging of the brain 28 days after the snake bite confirmed radiological improvement. KeywordsAcute haemorrhagic leukoencephalitis, Hurst's disease, snake bite Case reportA 44-year-old farmer from India was working in the fields when he was bitten on his right foot by a snake which he readily identified to be a Russell's viper (Daboia russelii). A few minutes after the bite, he developed severe pain, swelling and bleeding from the site, followed by diplopia and ptosis. He was brought to our centre and was initiated on intravenous polyvalent antisnake serum (Serum Institute of India Limited). He showed no immediate reaction to the anti-venom. While in the hospital he developed bleeding gums and oliguria. On examination, the vital signs were stable. The right foot was markedly swollen with two deep fang marks on the dorsum. Neurological examination revealed a normal sensorium, bilateral ptosis with ophthalmoparesis and normal deep tendon reflexes. He was admitted to the intensive care unit (ICU) where he developed anuria and respiratory failure within 24 h of admission. He was ventilated for respiratory failure and was transfused multiple blood products for various bleeding manifestations. His respiratory status gradually improved and he was extubated. His renal failure persisted and required maintenance haemodialysis.Following transfer to the ward from the ICU, on the seventh day following the snake bite, he was detected to have a low sensorium with bi-pyramidal signs. Neurological examination revealed a conscious but drowsy state and resolution of the ptosis and ophthalmoplegia. The limbs were spastic with a hypereflexic quadriparesis. Sensory examination was normal and Babinski reflex was positive bilaterally. Investigations revealed normal hemoglobin, white blood cell and platelet counts. His coagulation profile was deranged (prothrombin time 63.4 s [13-15 s], activated partial thromboplastin time 41.6 s [28-39 s]). He had severe renal failure, with serum creatinine 654mM [44-124 mM], microscopic haematuria and granular casts on urine microscopy. His serum electrolytes were normal (sodium: 145 meq/dl, potassium 3.6 meq/dl). Non-contrast computed tomography (CT) and magnetic resonance imaging (MRI) scans of the brain were done on the 10th day post snake bite.