Cerebral oedema during treatment of diabetic ketoacidosis: are we any nearer finding a cause?
Cerebral oedema remains the leading cause of death and morbidity in children with Type 1 diabetes mellitus. Around seven per thousand episodes of diabetic ketoacidosis (DKA) are complicated by cerebral oedema, and one-quarter of those children will die from it. The cause or causes of cerebral oedema are still very poorly understood, but lawyers are already keen to implicate various aspects of the management of DKA. There have been many theories as to the pathophysiology of cerebral oedema, and possible contributing factors may be excessive rate of rehydration, falling plasma osmolality (particularly that due to a reduction in plasma sodium concentration), hypoxia and insulin dosage. There is some supportive evidence for all of these factors in some cases, but there have been no sizeable case-control studies, in part because of the rarity of the condition. Furthermore, cerebral oedema can still occur even when the management of DKA follows current 'best practice' guidelines. As the mechanisms of cell volume regulation within the brain are increasingly understood, different questions may provide greater insights. For example, what is it about children that makes them so much more susceptible to cerebral oedema than adults? And why does one child treated in a certain way develop cerebral oedema whereas another does not? The anxiety over causing cerebral oedema has driven most of the changes in the management of DKA over recent decades, yet there is no evidence that the incidence has reduced. Until the causes are understood, we cannot be dogmatic about treatment recommendations.
Edge
J A
JA
John Radcliffe Hospital, Oxford, UK. julie.edge@paediatrics.ox.ac.uk
D000328:Adult; D001929:Brain Edema / Q000453:epidemiology / Q000209:etiology* / Q000517:prevention & control; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000150:complications* / Q000401:mortality / Q000503:physiopathology; D016883:Diabetic Ketoacidosis / Q000150:complications* / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D009017:Morbidity