Case Presentation: A 70yo female with bipolar disorder and type 2 DM on metformin presented to the hospital with altered mental status, nausea/vomiting and diarrhea for 3 days. Per report the patient had self-administered laxatives and had consumed expired deli meat. On presentation, the patient was obtunded with at blood glucose of <10 and the following vital signs: T:36.2, BP: 112/47, HR: 97, RR: 29, saturating 96% on room air. After IV dextrose she became arousable, able to answer simple questions and follow simple commands. She appeared to be in mild respiratory distress but denied dyspnea and was noted to have dry mucous membranes with a slightly distended abdomen. Admission labs included acute kidney injury (BUN= 83, Cr=6.1), hyperkalemia (K=6.5) and anion gap metabolic acidosis (pH= 7.01, bicarb=7, AG=41) with a lactic acid = 14. The patient was admitted to the medical intensive care unit. Given severe metabolic acidosis and hyperkalemia, emergent hemodialysis was initiated.
Two hours into her dialysis session the patient became unresponsive, staring straight ahead with decorticate posturing. An emergent head CT scan demonstrated cerebral edema. Dialysis was discontinued and she was started on IV hypertonic saline for presumed dialysis disequilibrium syndrome. A follow up head CT scan showed resolution of cerebral edema accompanied by clinical improvement in the patient’s mental status. One week later she was discharged to home with normal renal function.
Discussion: Dialysis disequilibrium syndrome (DDS) is a rare but devastating consequence of dialysis initiation resulting in cerebral edema. During dialysis, osmole concentrations such as urea and lactic acid are reduced more rapidly in the blood than in the central nervous system owing to the relative impermeability of the blood-brain barrier. This may result in an osmole gradient favoring water shifts into the brain, resulting in cerebral edema and increased intracranial pressure. Mild forms of DDS present with nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma and even death. In mild cases discontinuation of dialysis results in complete reversal of symptoms over several hours. Little evidence exists to guide management of severe cases but some experts have advocated the use of hyperosmolar solutions such as hypertonic saline and/or mannitol to reduce intracranial pressure. Historically, DDS was seen in patients with very high urea levels initiated on hemodialysis with rapid hemofiltration rates. Clinical practice changes in dialysis initiation methods such as slower hemofiltration rates have resulted in a reduced incidence of this disorder.
Conclusions: We suspect our patient experienced a rapid reduction in urea and lactic acid levels, resulting in a significant osmotic gradient between the systemic circulation and the CNS and consequent cerebral edema. Prompt recognition of DDS and administration of hypertonic saline allowed for a favorable outcome. Although the exact pathophysiology of DDS is not fully understood, it is recommended, that for patients felt to be at high risk for the disorder, to use lower efficiency renal replacement over a longer treatment period (CVVH) or utilize a high osmole dialysate (urea-enriched vs. mannitol) when aggressive dialysis is required. While DDS is rare, hospitalists should be aware of this devastating disorder, identify those patients at most risk, and recognize early signs of cerebral edema to trigger the life–saving discontinuation of hemodialysis.