To explore whether the carbon dioxide-bicarbonate (Pco2-HCO3) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema.
Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967.
A clinical vignette is used—a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated—as a basis for discussion of integrative metabolic and vascular physiology.
Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available.
We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO3]CSF and rising Paco2; hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Paco2; and mechanical ventilation.
The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the Pco2-HCO3 hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology.
University of Cambridge School of Clinical Medicine, Department of Paediatrics, Addenbrooke's Hospital, Cambridge, UK (RCT); Children's Acute Transport Service, London (DL); and Paediatric Intensive Care Unit, Great Ormond Street Hospital for Children NHS Trust, London (MJP).
*See also p. 490.