title: Calcium channel blocker toxicity.
abstract: A retrospective review was conducted of all patients who were reported to a regional poison control center after "overdose" of a calcium channel blocker during a two-year period (1987 and 1988). An analysis of 91 patient cases is presented after excluding allergic reactions, cases involving coingestants, and patients lost to follow-up. Patients who developed any symptoms after ingestion were defined as manifesting toxicity. There were 38 cases of verapamil ingestion with toxicity developing in 18 patients. The mean nontoxic dose was 320 mg, whereas the mean toxic ingestion was 3.2 g. Nine patients became hypotensive, 13 developed conduction system abnormalities (sinus node suppression, atrioventricular nodal block, or bundle branch block), and 11 manifested arrhythmias. Ten developed neurological symptoms. There were 31 cases of nifedipine ingestion with toxicity developing in seven patients. The mean nontoxic dose was 19 mg, while the mean toxic ingestion was 340 mg. Four patients were hypotensive, only one developed cardiac conduction abnormalities, and four developed arrhythmias. Three had neurological symptoms. There were 24 cases of diltiazem ingestion with only minor toxicity developing in four patients. There was no statistically significant difference in the frequency of hypotension, arrhythmias, or neurological symptoms in patients who overdosed with verapamil as compared with nifedipine (by Fisher's exact test). However, conduction system abnormalities were more common with verapamil ingestion (P less than .05). Toxic manifestations after diltiazem over-dose were uncommon in our study. Eighteen of the 29 patients who developed toxicity required treatment in excess of gastrointestinal decontamination. Calcium was administered to 14 patients and was helpful in five.
authors.affiliation: Division of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania.
authors.forename: E A
authors.initials: EA
authors.lastname: Ramoska
authors.forename: H A
authors.initials: HA
authors.lastname: Spiller
authors.forename: A
authors.initials: A
authors.lastname: Myers
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000453:epidemiology / Q000628:therapy; D002648:Child; D002675:Child, Preschool; D003691:Delaware; D004110:Diltiazem / Q000008:administration & dosage / Q000506:poisoning*; D005260:Female; D006801:Humans; D007022:Hypotension / Q000139:chemically induced* / Q000453:epidemiology / Q000628:therapy; D007223:Infant; D008297:Male; D008875:Middle Aged; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000453:epidemiology / Q000628:therapy; D009543:Nifedipine / Q000008:administration & dosage / Q000506:poisoning*; D010414:Pennsylvania; D011039:Poison Control Centers; D012189:Retrospective Studies; D014700:Verapamil / Q000008:administration & dosage / Q000506:poisoning*
chemical_list: D014700:Verapamil; D004110:Diltiazem; D009543:Nifedipine