PATHOGENESIS OF CEREBRAL EDEMA AFTER TREATMENT OF DIABETIC-KETOACIDOSIS

We studied the roles of acidosis, plasma osmolality, and organic osmol ytes in the pathogenesis of cerebral edema in an animal model of diabe tes mellitus. Normonatremic rats with streptozotocin-induced nonketoti c (NKD) and ketotic (DKA) diabetes were sacrificed before or after tre atment with hypotonic saline and insulin. Brains were analyzed for wat er, electrolyte, and organic osmolyte content. Brain water decreased b y 2% in untreated DKA and NKD despite a 12% increase in plasma osmolal ity due to hyperglycemia. After treatment of both NKD and DKA, brain w ater increased equivalently by 8%. The cerebral edema that occurred af ter treatment was associated with decreased brain sodium content and n o change in total major brain organic osmolytes in both NKD and DKA. H owever, brain content of the individual osmolytes glutamine and taurin e increased after treatment of DKA. In a separate study, brain water a nd solute content of rats with DKA were compared after treatment with either hypotonic or isotonic fluid. Animals treated with isotonic flui d had significantly less cerebral edema and higher brain sodium conten t than those treated with hypotonic fluid. In our studies, brain swell ing after treatment of DKA and NKD was primarily due to a rapid reduct ion of plasma glucose and osmolality, and was not caused by sodium mov ement into the brain. Acidosis did nor appear to play a major role in the pathogenesis of cerebral edema after treatment of DKA.