Possible mechanism for cerebral oedema in diabetic ketoacidosis.
This hypothesis, presented to explain the cerebral oedema that sometimes occurs during treatment of diabetic ketoacidosis (DKA), is based on activation of the Na+/H+ exchanger, a ubiquitous plasma-membrane transport system that functions in the regulation of cytoplasmic pH. Experimental acidification of the cytoplasm with weak organic acids activates the exchanger and, in the presence of extracellular Na+, leads to cell swelling. This swelling is osmotic, secondary to a net gain in Na+ and the anion of the weak organic acid. In DKA, cytoplasmic acidification results from high levels of circulating weak organic acids (ketoacids and free fatty acids) and activation of Na+/H+ exchange would similarly be expected. Conditions during conventional treatment of DKA should favour even greater activation of the exchanger and additional cell swelling would be predicted. The hypothesis is consistent with the clinical observation that clinically apparent cerebral oedema occurs with improvement in the patient's acid-base status rather than at the peak of the ketoacidosis.
D000137:Acid-Base Imbalance / Q000209:etiology; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000209:etiology*; D016883:Diabetic Ketoacidosis / Q000150:complications*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007427:Intracranial Pressure; D007474:Ion Exchange; D008954:Models, Biological; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D011188:Potassium