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Aetiology of cerebral oedema in diabetic ketoacidosis
  1. A F T Brown
  1. Department of Emergency Medicine, Royal Brisbane Hospital, Herston, Brisbane, Queensland 4029, Australia;

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    The excellent evidence based review of the emergency management of diabetic ketoacidosis (DKA) in adults by Hardern and Quinn perpetuates the premise that “unnecessarily large volumes of intravenous fluids should be avoided because of the high case fatality rate of cerebral oedema”.1 This presupposes that the rate of fluid delivery is causally related to the development of cerebral oedema, which has not been proved. The large 15 year paediatric study in the USA that analysed 6977 hospitalisations for DKA found among the 61 cases of cerebral oedema (0.9%) that after multiple logistic-regression analysis with random and matched controls, the only variables statistically associated with cerebral oedema were higher initial serum urea nitrogen concentrations and lower partial pressures of carbon dioxide at presentation.2 In addition, smaller increases in serum sodium concentration during treatment and the use of bicarbonate were also implicated. Importantly, the rate of fluid, sodium, and insulin administration were not associated with the development of cerebral oedema, nor was the initial serum glucose or its rate of change.

    Clearly these findings relate to patients aged 18 years or less but most occurrences of cerebral oedema in DKA are in children and adolescents, with only rare cases in adults. However, the underlying aetiology should be no different. One unifying hypothesis is that the cerebral oedema is related to cerebral vasoconstriction, brain ischaemia, and hypoxia, as hypocapnoea causing cerebral vasoconstriction and extreme dehydration would both decrease cerebral perfusion. In addition, as children’s brains have higher oxygen requirements than adults this may explain their unique susceptibility.

    Perhaps clinicians should focus more on recognising the warning signs of cerebral oedema such as headache, lethargy, and deterioration in conscious level, prior to seizures, incontinence, pupillary changes, bradycardia, and respiratory arrest as brain stem herniation occurs.3 Early hyperosmolar treatment and presumably supplemental oxygen with exemplary supportive care are then essential. Finally, accepting that cerebral oedema may well be idiosyncratic rather than iatrogenic could have important medicolegal connotations too.