Hypoglicemia almost kills — Review of a case

Objectives: Brain function depends on a continuous supply of glucose from blood, and oxidative metabolism is the only source of energy except in extreme starvation. This is the basis of the high frequency of cerebral dysfunction in cases of transient hypoglycemia. Neuronal death can occur when plasma glucose levels fall below 18 mg/dL. Typically, MRI in hypoglycemic encephalopathy demonstrates T2 white matter lesions in the cortex, hippocampus, and basal ganglia. Prolonged, severe hypoglycemia can cause permanent neurologic damage. Complications include permanent brain damage leading to persistent vegetative state and death. This is usually seen in diabetic patients and rarely in prolonged starvation. This case is presented with the goal of alert for a common pathology, somethimes not considered. Material and method: Retrospective analysis of the patient chart, blood analysis and image exams. Case report: A 31-year-old male was admitted after three days of no food ingestion, just alcohool abuse. He was admitted in the emergency room for seizures. He had no past history of diabetes, epilepsy or any other neurologic problems. A finger stick glucometer reading showed a serum glucose level of 11 mg/dL. At entrance he scored 6 at Glasgow coma score. He had no extra-ocular movement abnormalities or pyramidal signs at examination. A CT scan performed at D1 showed diffuse cerebral edema and no focal lesions. An electroencephalogram (EEG) was done at D3 and showed diffuse large theta–delta waves. The MRI scan at D18 revealed T2 white matter lesion of the caudate nucleus, hippocampus and putamina, and diffuse global parenchyma atrophy but no evidence of cortical laminar necrosis. The analytic workup was unremarkable, namely for hepatic function, thyroid function, viral serologies, auto-immune research and CSF studies. There was no evidence of insulinoma. No other metabolic disorder was found during admission. There were no other records of severe hypoglycemia. The clinical findings were admitted to be related to hypoglycemic encephalopathy. He was discharged at D25, maintaining language and gait disturbance. Discussion/conclusions: Hypoglycemic encephalopathy is a serious condition that can lead to death and permanent severe neurologic deficits. Prompt recognition and adequate treatment carry the only chance of good recovery. Diabetes and poor nutritional status are the more prevalent risk factors but other causes must be excluded. Awareness of the presenting features and typical EEG and MRI findings of this entity are of critical importance.