Explores CSF glucose levels and hypoglycaemic encephalopathy in adults, indicating potential diagnostic value.
Hypoglycaemia as the cause of unwitnessed coma may go unrecognised when the hypoglycaemia has already been partially corrected. A woman in her early 60s was found unresponsive after several days of heavy alcohol intake and poor oral intake. Emergency services had given intravenous 50% glucose; on arrival, her blood glucose was only mildly low (3.1 mmol/L (56 mg/dL)). MR scan of the brain showed cortical-predominant signal change with cortical hyperperfusion. Lumbar puncture 1.5 hours after arrival showed profound hypoglycorrhachia (cerebrospinal fluid (CSF) glucose 0.8 mmol/L (15 mg/dL)) without pleocytosis or protein elevation; multiplex CSF PCR and cultures were negative. The CSF finding suggested severe prehospital hypoglycaemia and supported a diagnosis of hypoglycaemic encephalopathy despite non-specific early imaging and electrophysiology. She required tracheostomy and remained severely disabled at 6 months. Profoundly low CSF glucose with non-inflammatory CSF can be an objective, time-integrated marker of antecedent severe hypoglycaemia and can help attribute unwitnessed coma to hypoglycaemic encephalopathy when plasma glucose at presentation is misleading.
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Sanpei et al. (2026) studied this question.
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