Transient cerebral oedema associated to hypoglycaemia

• Published in: Revista de neurologiá Vol. 39; no. 11; pp. 1030 - 1033
• Main Authors: Berbel-García, A, Porta-Etessam, J, Martínez-Salio, A, Ballesta, F, Sáiz-Díaz, R A, Pérez-Martínez, D A, de Toledo, M
• Format: Journal Article
• Language: Spanish
• Published: Spain 01-12-2004
• Subjects: Blood Glucose - metabolism; Brain Edema - etiology; Brain Edema - pathology; Female; Humans; Hypoglycemia - complications; Hypoglycemia - pathology; Middle Aged
• ISSN: 0210-0010
• DOI: 10.33588/rn.3911.2004333

In the adult, hypoglycaemia is documented as a consequence of overdose of insulin or oral hypoglycaemic agents. Neonatal hypoglycaemia is common but rarely symptomatic due to protective mechanisms. Very few reports on hypoglycaemic injury are available in adults and most of them in patients with poor outcome.
Woman, 45 years old. She is referred to emergency room due to insulin overdose and coma of unknown duration. Glucose level was 15 mg% without other metabolic anomalies. Computerized tomography revealed brain oedema most obvious in the parieto-occipital lobes. Therapy with manitol and glucose was started with total functional recovery.
Brain imaging in neonatal hypoglycaemia shows similar findings. In the acute phase oedema in the parieto-occipital cortex and underlying white matter and atrophy or malacic cysts in the chronic phase have been described. Chronic changes are related to long-term sequelae that vary from development delay and epilepsy to persistent vegetative state. In adults lesions involve hippocampus and basal ganglia. The reasons of different sensitivity of these regions are not fully clear. Differences in regional blood flow autoregulation or in excitotoxins receptors of aspartate have been postulated. Hypoglycaemia may induce blood-brain-barrier permeability and subsequently brain oedema.