Abstract Diabetic Ketoacidosis (DKA) is a life-threatening complication of diabetes. The two most common causes of mortality in DKA are sepsis and cerebral edema, the latter uncommon in adult populations with a mortality rate of 35%.1The mechanism of cerebral edema in DKA may be due to osmolar shifts resulting from rapid fluid resuscitation from the correction of glucose levels and acidosis during treatment in pediatric populations.2 An alternative hypothesis is that a relative reduction in cerebral blood flow causes ischemia-reperfusion injury and inflammatory changes from decreased cerebral blood flow caused by hyperventilation.3 Here we present a rare and life-threatening case of adult DKA complicated by cerebral edema. A 44-year-old male presented with acute encephalopathy and shock. He was found to have a blood glucose of 2033 mg/dL and severe metabolic acidosis (pH of 7.11, anion gap of 29) consistent with DKA, without a history of type 1 or type 2 diabetes mellitus. With glucose levels over 600 mg/dL, we noted discrepancy between point of care (POC) fingerstick glucose and venous blood glucose levels. Venous glucose measurements were preferred and monitored every 4 hours. Initial Head Computerized Tomography (CT) demonstrated a diffuse decrease in white matter differentiation and cerebral edema. For the management of his cerebral edema, a bolt intracranial pressure monitor (ICP) was placed by neurosurgery. Initial readings were 14-16 mmHg and decreased to 8 mmHg over 18 hours. Continuous renal replacement therapy (CRRT) was initiated for refractory acidosis, anuria, and volume overload with hypoxic respiratory failure. On CRRT, acidosis improved, osmotic shifts were controlled, glucose levels normalized, and cerebral edema resolved. Neurologic function returned to normal. Cerebral edema is a rare complication of hyperglycemic crisis in adults. This case highlights that with ICP monitoring, CRRT, and careful volume resuscitation, the deleterious effects of cerebral edema complicating diabetic ketoacidosis can be mitigated. CRRT reduces unpredictable fluid shifts and electrolyte imbalances from sodium and glucose. ICP monitoring allows for real-time adjustments to therapy in critically ill patients with coma without relying solely on neurologic examinations or serial CT scans. The discrepancy between glucose readings potentially contributed to refractory acidosis, switching to venous glucose levels rather than POC glucose readings allowed for greater accuracy in blood glucose correction. While the etiology of cerebral edema in adults with DKA remains unclear, in addition to conventional management for DKA, attention to osmotic and electrolyte shifts and close neurologic monitoring portends a favorable outcome. This abstract is funded by: None
Hopkins et al. (Fri,) studied this question.