0838 Cerebral oedema in diabetic ketoacidosis – an update

In summary 0737 of this series it was reported that narrowing of the lateral ventricles is evident in >50% of children with diabetic ketoacidosis (DKA) and this is frequently associated with mild mental status abnormalities (GCS scores <15) and a low initial pCO2. Risk factors included younger age, lower pH, degree of hypocapnia and severity of the dehydration. DKA is accompanied by increased cerebral blood flow, suggesting a vasogenic process, and intervention that includes mannitol, intubation and hyperventilation should be reviewed since the latter in particular may adversely affect the situation. Researchers from California and Colorado have added a little more to this potentially lethal complication through their MRI-based study of 26 children presenting with DKA. Using diffusion-weighted imaging to quantify oedema formation they measured the apparent diffusion coefficient (ADC) of brain water during and after DKA treatment, and related ADC changes to clinical and biochemical variables. ADC was elevated during DKA treatment vs. baseline (8.13 ± 0.47 vs 7.74 ± 0.49 × 10−4 mm2/sec; p < .001). While a recent and comprehensive systematic review concluded that the causes and mechanisms of cerebral oedema in DKA are unknown and the complication may be due as much to individual biological variance as to severity of underlying metabolic derangement and/or treatment risk factors, the ADC results support previous data by showing that patients with altered mental status had greater elevation in ADC. ADC elevation during DKA was also positively correlated with initial serum urea nitrogen concentration (correlation coefficient 0.41, p = .03) and initial respiratory rate (correlation coefficient 0.61, p < .001). ADC elevation was not significantly correlated with initial serum glucose, sodium or effective osmolality, nor with changes in these parameters during treatment. Multivariate analyses confirmed that the initial urea nitrogen concentration and respiratory rate were independently associated with ADC elevation. These data support the view that cerebral oedema in DKA is related to cerebral hypoperfusion, and that osmotic fluctuations during DKA treatment do not play a primary causal role.

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