The effect of toxicologic screening on management of minimally symptomatic overdoses.
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Biomedical subjects
Publications and source records attributed to K A Sporer.
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The purpose of the study was to determine the incidence of ethanol-induced hypoglycemia. All nondiabetic patients who had blood alcohol levels above 0.10% and a random serum chemistry drawn (including glucose) were included. Over a 6-month study period, 378 patients were included in the study. Fifteen patients (4%) presented with hypoglycemia (glucose less than 67 mg%). Of these, four (1%) were profoundly hypoglycemic (glucose less than 50 mg%). Two hundred and fifty three patients (67%) patients were normoglycemic (glucose 67-106 mg%) and 110 patients (29%) were hyperglycemic (glucose greater than 106 mg%). Nonfasting glucose measurements from a control group of 96 nondiabetic, nonintoxicated patients were compared with those of the study group. Two patients (2%) presented with hypoglycemia and none (0%) presented with profound hypoglycemia. Forty-five patients (47%) presented with normoglycemia, and 49 (51%) with hyperglycemia. There were no statistically significant differences found in the hypoglycemia rate between the intoxicated patients and nonintoxicated control population (odds ratio of 0.75; P greater than .05). Four of 378 intoxicated patients (1%) had profound hypoglycemia (less than 50 mg/dL) compared with none (0%) of the 96 nonintoxicated patients. Intoxicated patients had a statistically significant lower rate of hyperglycemia in comparison with the nonintoxicated control group (29% versus 51%; P less than .0001). Age, sex, race, ethanol level, and serum electrolyte measurement had no predictive value for hypoglycemia in intoxicated patients. The anion gap was consistently elevated in hypoglycemic patients in comparison with normoglycemic patients (P less than .05). Hypoglycemia appears to occur as frequently in an ethanol-intoxicated population as in a population without elevated ethanol levels.(ABSTRACT TRUNCATED AT 250 WORDS)
A 57-year-old woman ingested 15 to 17 tablets of carbidopa-levodopa 10/100 tablets (carbidopa 150 mg and levodopa 1,500 mg) along with ibuprofen, carisoprodol, hydrocodone, and acetaminophen. The patient developed choreiform movements that persisted despite obtundation and attempts to extinguish them with naloxone, morphine, and diazepam. When the patient developed a rising level of creatine phosphokinase and myoglobinuria, she was treated with ventilatory support and pancuronium. She required paralysis for 60 hours, when her chorea resolved.
A 37-year-old man presented to the emergency department after an attempt to self-treat his priapism with saltpeter (K+NO3). Initially he had a potassium of 7.6 with electrocardiographic changes and a markedly elevated CO2. The potassium and carbon dioxide normalized in less than 24 hours with standard treatment for hyperkalemia. Hyperkalemia is expected with large oral potassium ingestion; and the elevated CO2 was spurious, caused by the misreading of serum nitrates by the Ektachrom 700 system. Ingestion of K+NO3 should be added to the differential of hyperkalemia with a markedly elevated CO2.