Neuropathology of hypoglycaemic brain injury

Abstract

It has long been recognised that the neurobiochemistry of hypoglycaemic brain injury differs markedly from that of hypoxic-ischaemic brain injury. The neuropathology of hypoglycaemic brain injury may also be distinctive. Such distinctive changes, aiding discrimination from hypoxic-ischaemic brain injury, are though commonly absent even in cases of biochemically proved profound hypoglycaemia. Neuronal depletion or necrosis may only be observed in 29% of cases. Autopsy findings in cases of suspected insulin overdose or overdose from oral hypoglycaemic agents may not uncommonly be non-specific. It should be appreciated that neuronal death due to hypoglycaemic brain injury may only intervene after a sustained period of blood glucose levels below 1 mmol/l and after EEG tracing has become silent. The neuropathology of hypoglycaemic brain injury may also be modified by concurrent hypoxia resulting from concomitant cardiorespiratory depression and by seizures. Atypical presentations also include strikingly asymmetric involvement of the cerebral hemispheres. It should further be appreciated that the postmortem findings in cases of hypoglycaemic brain injury may include neurogenic pulmonary oedema (seen in over half of cases). The majority of cases of suspected hypoglycaemic drug overdose represent suicides (66%) with the remainder representing accidental poisoning and homicide, with insulin the most commonly drug implicated (around 95%). In paediatric practice, hypoglycaemia frequently occurs in newborn infants who previously suffered asphyxia, offspring of diabetic mothers and with a low birth weight for gestational age. The immature brain is relatively resistant to the damaging effects of hypoglycaemia. Hypoglycaemia in this age group combined with hypoxic-ischaemic injury, in particular asphyxia, may though be more deleterious to the immature brain than either condition alone.