First described in 1962, the dialysis disequilibrium syndrome (DDS) is a central nervous system disorder described in dialysis patients [1,2]. It is characterized by neurologic symptoms of varying severity that are thought to be due primarily to cerebral edema.
New patients just being started on hemodialysis are at greatest risk, particularly if the BUN is markedly elevated (above 175 mg/dL or 60 mmol/L). Other predisposing factors include severe metabolic acidosis, older age, pediatric patients, and the presence of other central nervous system disease such as a preexisting seizure disorder .
This topic review will discuss dialysis disequilibrium syndrome. Issues related to mental status changes and acute problems during dialysis are presented separately. (See "Acute complications during hemodialysis" and "Psychiatric illness in dialysis patients" and "Seizures in patients undergoing hemodialysis".)
The symptoms of DDS are caused by water movement into the brain, leading to cerebral edema. Two theories have been proposed to explain why this occurs: a reverse osmotic shift induced by urea removal [1,3-5]; and a fall in cerebral intracellular pH .
Reverse osmotic shift — Hemodialysis rapidly removes small solutes such as urea, particularly in patients who have marked azotemia. The reduction in BUN lowers the plasma osmolality, thereby creating a transient osmotic gradient that promotes water movement into the cells. In the brain, this water shift produces cerebral edema and a variable degree of acute neurologic dysfunction. The loss of extracellular water can also cause extracellular volume depletion which can contribute to the development of hypotension. (See "Renal replacement therapy (dialysis) in acute kidney injury (acute renal failure): Metabolic and hemodynamic considerations".)