This term refers to a group of symptoms that may occur during and following hemodialysis or peritoneal dialysis as a by-product of some degree of cerebral edema. The symptoms include headache, nausea, muscle cramps, nervous irritability, agitation, drowsiness, and convulsions. The headache, which may be bilateral and throbbing and resemble common migraine, develops in approximately 70 percent of patients, whereas the other symptoms are observed in 5 to 10 percent, usually in those undergoing rapid dialysis or in the early stages of a dialysis program. The symptoms tend to occur in the third or fourth hour of dialysis and last for several hours. Sometimes they appear 8 to 48 h after the completion of dialysis. Originally, these symptoms were attributed to the rapid lowering of serum urea, leaving the brain with a higher concentration of urea than the serum and resulting in a shift of water into the brain to equalize the osmotic gradient (reverse urea syndrome). Now it is believed that the shift of water into the brain is akin to water intoxication and is a result of the inappropriate secretion of antidiuretic hormone.
The symptoms of subdural hematoma, which in the past occurred in 3 to 4 percent of patients undergoing dialysis, now being less frequent, may still be mistakenly attributed to the disequilibrium syndrome.
This is a subacutely progressive syndrome that in the past complicated chronic hemodialysis. Characteristically, the condition begins with a hesitant, stuttering dysarthria and aphasia, to which are added facial and then generalized myoclonus, focal and generalized seizures, personality and behavioral changes, and intellectual decline. The EEG is invariably abnormal, taking the form of paroxysmal and sometimes periodic sharp-wave or spike-and-wave activity (up to 500 mV and lasting 1 to 20 s), intermixed with abundant theta and delta activity. The CSF is normal except occasionally for increased protein.
At first the myoclonus and speech disorders are intermittent, occurring during or immediately after dialysis and lasting for only a few hours, but gradually they become more persistent and eventually permanent. Once established, the syndrome is usually steadily progressive over a 1to 15-month period (average survival of 6 months in the 42 cases analyzed by Lederman and Henry). A characteristic feature is a transient improvement in speech with the administration of intravenous diazepines.
The neuropathologic changes are said to be subtle and consist of a mild degree of microcavitation of the superficial layers of the cerebral cortex. Although the changes are diffuse, they have been found in one study to be more severe in the left (dominant) hemisphere than in the right and more severe in the left frontotemporal operculum than in the surrounding cortex (Winkelman and Ricanati). The disproportionate affection of the left frontotemporal opercular cortex putatively explains the distinctive disorder of speech and language. In the one case, we have studied carefully, we could not be certain of any microscopic changes.
The most plausible view of the pathogenesis of dialysis encephalopathy is that it represented a form of aluminum intoxication (Alfrey et al), the aluminum being derived from the dialysate or from orally administered aluminum gels. In recent years, this disorder has disappeared, the result, in all likelihood, of the universal practice of purifying the water used in dialysis and thereby removing aluminum from the dialysate. This subject has been reviewed by Parkinson and coworkers.
Complications of Renal Transplantation