Deaths from cerebral edema and herniation have been reported in the past, but are rare with newer dialysis techniques.3
The mechanism of dialysis disequilibrium syndrome is that urea is more rapidly cleared from the plasma than from the brain.8 After dialysis, water enters the brain following an osmotic gradient. This results in an increase in brain extracellular water and brain edema.8,9 Decrease in intracellular pH and generation of osmolar molecules may contribute to cerebral edema.3,10,11
Between dialysis sessions, the EEG may show background slowing.12,13 During dialysis, increased slow activity, bursts of bilaterally symmetrical slow waves, and increased photic sensitivity may be seen.12,13 The EEG can determine whether abnormal movements are due to seizures or movement disorder by the presence or absence of paroxysmal activity.
Other disorders that can cause seizures in renal insufficiency need to be excluded. These are the same disorders to be ruled out in diagnosing uremic encephalopathy:3
Dialysis must be discontinued until the seizure and vital signs have been stabilized. Antiepileptic drug (AED) therapy may help to reduce seizures. A drug not removed by dialysis should be selected. (See Table: Risk of Drug Removal By Hemodialysis)
Most often, phenytoin is used. It is effective for tonic-clonic and partial seizures, and it can be given intravenously in loading doses to maintain a desired plasma concentration (e.g., after hemodialysis). Therapy begins with a loading dose of intravenous phenytoin (15-20 mg/kg). After dialysis, additional intravenous loading doses of phenytoin may be administered, if necessary. (See Correction for drug loss during hemodialysis)
Hypocalcemic seizures may be controlled with calcium gluconate.3
Reviewed and revised February 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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