DIFFICULT MANAGEMENT PROBLEMS IN DIALYSIS .2. SEIZURE

A 60-year-old African-American man was admitted to the hospital in Oct ober 1991 with seizures and right hemiparesis. He had end-stage renal disease (ESRD), presumed due to hypertension and/or analgesic nephropa thy, and had been on maintenance hemodialysis since July 1987. Noncont rast CAT of the brain revealed mild cortical atrophy and nonspecific w hile matter ischemic changes. Contrast CAT showed a right hemisphere C VA, and magnetic resonance imaging (MRI) suggested a right frontal men ingioma. Cerebral arteriogram was confirmatory, and he underwent resec tion of the fronto-parietal tumor in early November 1991. Past medical history included over 20 years of hypertension, angina for five years , gout, and peptic ulcer disease. Cardiovascular evaluation of exertio nal dyspnea and bilateral calf weakness included a negative thallium s tress test and minimal to moderate flow impairment of tibial-peroneal vessels by Doppler. Low iron stores led to upper and lower endoscopy a nd a colonic polypectomy. There was a question of an allergic reaction to intravenous iron administration (the patient reported lip swelling ), and erythropoietin therapy was started in December 1990 (starting h ematocrit was 23%). Hemodialysis access was achieved via a Brescia-Cim ino arteriovenous fistula in his left arm, which developed extensive u pper arm and shoulder collaterals, leading to a fistulogram and a diag nosis of subclavian stenosis in January 1989. Angioplasty was successf ul, and repeat fistulogram was unremarkable in February 1991. Blood pr essure control was usually adequate, ranging from 140-180/80-100 on di ltiazem, clonidine, and captopril. Occasional elevation to 210/120 wer e seen. In the months prior to the seizure, his treatments were adjust ed because of low Kt/V (by increased dialyzer surface area and increas ed time). Hematocrit had risen to 30%-33% with erythropoietin therapy (2000 Units thrice weekly). Hemodialysis was accomplished without hepa rin use, due to his gastrointestinal bleeding history. He was felt to be gaining ''flesh'' weight. In late March 1992, he had a tonic-clonic seizure. Repeat CAT scan of the brain was unchanged. He was started o n phenytoin thrice daily, but he discontinued therapy and had two more seizures (with negligible serum levels of phenytoin) in April 1992. I n May, he was readmitted after another tonic-clonic seizure. Phenytoin levels were in the therapeutic range, and CAT scan was again unchange d. Phenobarbital was added to his regimen. Drowsiness limited his comp liance, and he had several additional seizures. In late July, he suffe red a respiratory arrest shortly after a seizure.