Hypoglycemic encephalopathy

Case contributed by Francis Deng
Diagnosis certain

Presentation

History of prior partial pancreatectomy for alcoholic pancreatitis and subsequent brittle type 2 diabetes mellitus. Long-acting insulin (glargine) dose was increased the night prior from 10 units to 14 units. They were found in bed in the morning unresponsive with blood glucose 48 mg/dL. Hypothermic, bradycardic, and unresponsive (Glasgow coma scale 3) on arrival.

Patient Data

Age: 75 years
Gender: Male
mri

There are areas of cortical restricted diffusion involving the posterior left superior frontal gyrus, as well as bilateral parietal, occipital, and posterior lateral temporal lobes. These findings are associated with faint FLAIR hyperintensity.

Generalized parenchymal volume loss and periventricular white matter T2 hyperintensities.

Case Discussion

The subtle findings of cortical restricted diffusion raised the possibilities of hypoglycemic encephalopathy, seizure-related changes, hypoxic-ischemic injury, and Creutzfeldt-Jakob disease. Electroencephalography showed no seizures but did show generalized delta more than theta slowing of the background consistent with an encephalopathic state. The acute onset was not compatible with Creutzfeldt-Jakob disease. The imaging pattern of posterior cerebral predominance and sparing of the thalami and cerebellum favored hypoglycemic encephalopathy over hypoxic-ischemic brain injury, consistent with the clinical history of profound hypoglycemia on presentation. A repeat MRI four days later showed unchanged findings. The neurological prognosis was poor and the patient was discharged in a persistent vegetative state.

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