In nephrology, dialysis disequilibrium syndrome, commonly abbreviated DDS, is the occurrence of neurologic signs and symptoms, attributed to cerebral edema, during or following shortly after intermittent hemodialysis.
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Classically, DDS arises in individuals starting hemodialysis due to chronic renal failure and is associated, in particular, with "aggressive" (high solute removal) dialysis. However, it may also arise in fast onset, i.e. acute, renal failure in certain conditions.
Etiology
The cause of DDS is currently not well understood. There are two theories to explain it; the first theory postulates that urea transport from the brain cells is slowed in chronic renal failure, leading to a large urea concentration gradient, which results in reverse osmosis. The second theory postulates that organic compounds are increased in uremia to protect the brain and result in injury by, like in the first theory, reverse osmosis. More recent studies on rats noted that brain concentrations of organic osmolytes were not increased relative to baseline after rapid dialysis. Cerebral edema was thus attributed to osmotic effects related to a high urea gradient between plasma and brain.
Diagnosis
Clinical signs of cerebral edema, such as focal neurological deficits, papilledema and decreased level of consciousness, if temporally associated with recent hemodialysis, suggest the diagnosis. A computed tomography of the head is typically done to rule-out other intracranial causes.
MRI of the head has been used in research to better understand DDS.
Treatment
Avoidance is the primary treatment. Better alternatives are Nocturnal or Daily Dialysis, which are far more gentle processes for the new dialysis patient. Dialysis disequilibrium syndrome is a reason why hemodialysis initiation should be done gradually, i.e. it is a reason why the first few dialysis sessions are shorter and less aggressive than the typical dialysis treatment for end-stage renal disease patients.