Case Presentation: A 53 year old man presented with a global headache and difficulty concentrating for one week. The patient’s past medical history included systemic amyloidosis status post autologous stem cell transplant, hypertension, and end stage kidney disease, not yet on dialysis. Admission vital signs were within normal limits and physical exam was unremarkable. Computerized tomography of the head was significant for a subdural hematoma with subfalcine herniation and midline shift. Prior to initiating dialysis, the patient’s blood urea nitrogen was 65 mg/dL (normal 7-20 mg/dL), creatinine was 5.9 mg/dL (normal 0.6-1.2 mg/dL), INR was 0.97 (normal <1.1), and platelets were 207 10^3/µL (normal 150-450 10^3/ µL). Given concern for uremic platelet dysfunction, hemodialysis was initiated via an existing arteriovenous fistula. Shortly after initiation of dialysis, the patient complained of worsening headache and vomiting. Dialysis was stopped and the patient received an infusion of hypertonic saline and mannitol. The patient’s neurological exam was unremarkable and computed tomography of the head was unchanged. The patient was taken for craniotomy and evacuation of the subdural hematoma given symptoms of increased intracranial pressure.

Discussion: This clinical vignette highlights the importance of recognizing emergencies during dialysis, particularly in patients who have not previously undergone dialysis. Our patient experienced manifestations of dialysis disequilibrium syndrome (DDS), a disorder characterized by protean central nervous system effects attributed to cerebral edema. The pathogenesis of DDS is thought to be secondary to reverse osmotic shift. The rapid reduction in blood urea nitrogen lowers plasma osmolality, creating a transient osmotic gradient that promotes water movement into cells, which can result in cerebral edema. Important risk factors for DDS, many of which were present in our patient, are first-time dialysis treatment and central nervous system pathology such as hemorrhage or infection. Blood urea nitrogen levels above 75 mg/dL can also predispose to DDS. Clinical manifestations of DDS can vary from mild, self-limited symptoms such as headache or lethargy to seizure and coma. DDS can be prevented by utilizing shorter dialysis sessions, continuous renal replacement therapy, or concurrent mannitol infusions. Patients at high risk may benefit from frequent neurological monitoring.

Conclusions: Recognizing and anticipating emergencies during dialysis, such as dialysis disequilibrium syndrome (DDS) is crucial to preventing neurological sequelae in patients at high risk. First-time dialysis, extremes of age, and intracranial pathology can predispose patients to DDS. The incidence of ischemic and hemorrhagic stroke in dialysis patients has increased over the last decade as more elderly patients are receiving dialysis. Incidence of subdural hematomas has also risen, likely due to widespread use of anticoagulation. Reducing the duration and speed of initial dialysis sessions could prevent DDS in these populations.