Abstract
Dialysis disequilibrium syndrome (DDS) is a rare but potentially fatal complication of renal replacement therapy, typically characterized by cerebral edema and often precipitated by the rapid correction of severe azotemia. Clinical symptoms are often non-specific, and, in some cases, the condition can be fatal. While the role of azotemia in DDS is well established, alternative mechanisms, such as the brain acidosis paradox, have also been proposed. We present the case of a 57-year-old African American woman with chronic kidney disease who was admitted with urosepsis and respiratory distress. Initial laboratory evaluation revealed a serum bicarbonate level <5 mEq/L and blood urea nitrogen of 116 mg/dL (baseline = 40-50 mg/dL). Due to the severity of her metabolic acidosis and signs of impending hypoxic respiratory failure, she underwent urgent hemodialysis. After 80 minutes of treatment, the patient became hypotensive and was transferred to the intensive care unit. Subsequent imaging revealed worsening cerebral edema with associated herniation, which was refractory to osmotherapy. The patient was transitioned to palliative care, and organ procurement was arranged. Most reported cases of fatal DDS are associated with chronic azotemia >150 mg/dL, a threshold not reached in this case. While preventive strategies for DDS emphasize limiting the urea reduction ratio (URR), there are currently no established guidelines for the safe rate of bicarbonate correction. In this case, the URR was 57% using a standard blood flow rate, and the bicarbonate level increased by more than 10 mEq/L. We hypothesize that rapid correction of metabolic acidosis may contribute to fatal DDS by worsening cerebral edema through mechanisms such as the brain acidosis paradox.