SEIZURES: I
Authors: Kaupke C J. , Vaziri N. D. 
Published: October 2007

A 25‐year‐old man with end‐stage renal disease (ESRD) secondary to obstructive uropathy suffered a generalized tonic‐clonic seizure 3 hr after a routine hemodialysis treatment. The associated conditions included well‐controlled mild hypertension and typical anemia of renal disease. There was no prior history of seizures, loss of consciousness, headaches, tremor, symptomatic neuropathy, or notable head trauma. His medications included nifedipine, recombinant erythropoietin, ferrous sulfate, folate, calcitriol, aluminum hydroxide, and calcium carbonate. Physical examination was remarkable only for the presence of a grade I/VI systolic ejection murmur and a patent dialysis access in the left arm. Routine predialysis laboratory data obtained two weeks previously revealed the following: Na 141, K 4.9, Cl 112, CO2 13 (all electrolyte values are mmol/ l), blood urea nitrogen (BUN) 68 mg/dl, calcium 6.8 mg/dl, phosphorus 4.6 mg/dl, albumin 3.5 g/dl, hematocrit 29, aluminum <1 μg/l. The electrocardiogram was within normal limits. On the day of admission the patient underwent a routine dialysis treatment for 3 hr using a new cellulose acetate dialyzer, bicarbonate‐based dialysate containing potassium 1 mmol/l and calcium 2.5 mmol/l. The patient was well and asymptomatic during dialysis, and his arterial blood pressure was stable at approximately 140/90 mm Hg. Three hours after leaving the dialysis center, he began to experience facial twitching and numbness in his fingers, followed by a single 30‐sec generalized tonic‐clonic seizure. Upon arrival at the emergency department, he was alert and oriented, and complained only of paresthesias in his hands. Review of his medications revealed that he had failed to take the prescribed calcitriol and calcium carbonate for several weeks. Physical examination was unchanged from the previous evaluation except for the presence of Chvostek and Trousseau signs. Laboratory studies revealed the following: Na 145, K 4.6, Cl 110, CO2 27 (all electrolyte values are mmol/l), BUN 43 mg/dl, glucose 100 mg/dl, albumin 4.9 g/dl, total Ca 7.5 mg/dl, ionized Ca 3.0 mg/dl, magnesium 3.0 mg/dl, and phosphorus 7.0 mg/dl. EKG was normal except for a prolonged QT interval. Upon admission to the hospital, the patient was treated with intravenous calcium gluconate, followed by oral calcium carbonate and calcitriol. Within 48 hr, the patient's serum total and ionized calcium concentrations increased to 8.5 and 4.0 mg/dl, respectively. A CT scan of the head showed no abnormalities. The seizure was felt to be due to hypocalcemia, exacerbated by rapid correction of acidosis with dialysis, leading to further reduction in the ionized calcium concentration. The observed hypocalcemia was attributable to the patient's discontinuation or oral calcium and calcitriol and the absence of a high calcium dialysate, which is appropriate when combined with calcitriol and calcium supplementation, but necessary in their absence. Since discharge, the patient has experienced no further seizure activity and with consistent use of the prescribed oral calcium and calcitriol, his serum calcium has remained above 8 mg/dl, with phosphorus levels ranging from 5–6 mg/dl.