Abstract

A 62-year-old man with a history of petrol consumption was admitted to the accident and emergency department of an adjacent district general hospital by paramedics. He complained of headache and difficulty in breathing. On admission his Glasgow Coma Scale was 10/15 which rapidly deteriorated to 4/15. An unenhanced computed tomography (CT) scan was performed immediately which showed obliteration of basal cisterns consistent with brainstem oedema. He was mechanically ventilated with inotropic support and then transferred to the intensive care unit of the authors' institution. Relevant past history included alcohol abuse, manic depressive psychosis and carbamazepine overdose. Following transfer, sedation was withdrawn and the patient reassessed. He had fixed dilated pupils, no respiratory effort, absent gag reflex and response to pain. He was also hypernatraemic with a serum sodium level of 170 mmol/litre (normal range 133–144 mmol/litre). Toxicology for paracetamol and salicylates was negative. A repeat unenhanced CT scan was performed at this stage. This showed high attenuation in the tentorium (Figure 1a), basal cisterns (Figures 1b and c) and in the sylvian fissures (Figure 1d). There was no history of injection of intravascular or intrathecal iodinated contrast media. This was initially interpreted as subarachnoid haemorrhage. On subsequent review, the diagnosis was changed to diffuse cerebral oedema. In view of a failing brainstem and after discussion with the patient's family, treatment was withdrawn. A post mortem examination performed by the coroner showed no evidence of subarachnoid haemorrhage.

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