Introduction: Cerebral edema (CE), a rare but lethal complication of diabetic ketoacidosis (DKA), is more common in children than adults. The estimated incidence of CE in adults is 0.03% and the overall mortality from CE in DKA is 20-40%. The mechanism by which CE develops in DKA remains unclear, and the risk factors associated with CE in adult DKA have not been well studied. Description: A 29-year-old woman with history of hypertension and recent sinusitis presented to the emergency department for altered mentation, headaches, and left ear pain and discharge. She was found to be in severe DKA and was administered intravenous crystalloids and insulin. A head computed tomography (CT) done 20 min after the initiation of insulin showed diffuse cerebral edema with effacement of sulci and basal cisterns without mass lesions or hydrocephalus, as well as extensive sinusitis. She received mannitol and 3% hypertonic saline for CE, along with antibiotics and steroids for suspected meningitis. She was admitted to the Intensive Care Unit, and lumbar puncture the following day revealed an opening pressure of 15 cm H2O. Cerebrospinal fluids studies were not consistent with meningitis, so antibiotics were changed for sinusitis treatment. The patient’s anion gap closed within 14 hours of presentation, but she remained with severe metabolic acidosis so was started on oral sodium bicarbonate. On hospital day 3, brain magnetic resonance imaging showed complete resolution of the CE seen on initial head CT. By hospital day 4, her mental status had markedly improved, and she was ultimately discharged home on hospital day 7. Discussion: Risk factors and mechanisms of CE in adult DKA remain poorly understood. There is controversy in the literature, which is largely based on pediatric studies, as to whether CE in DKA arises from the underlying metabolic derangement or from rapid correction of glucose. This case is notable for the very early onset of cerebral edema at the initiation of glucose correction, with complete resolution following hyperosmolar therapy and anion gap closure, suggesting that CE was due to severe DKA rather than its treatment. Early recognition of CE in DKA in adults is important and further studies are needed to clarify the underlying mechanisms.
Jones et al. (Sun,) studied this question.