OBJECTIVE: Analysis of prognostic factors and treatment of a large epidemic of ethylene glycol intoxication. DESIGN: Retrospective case review comparing 16 survivors with 6 patients who died. SETTING: Cooperative study between county hospitals, a university hospital, and a poison information centre. PATIENTS AND PARTICIPANTS: Survival review of 36 serious cases and chart review of 17 cases. INTERVENTION: Time to initial treatment with intravenous fluids, sodium, bicarbonate, ethanol, and dialysis. MEASUREMENTS: Clinical data at admission and blood chemistry at 0, 24, 48, and 72 h. RESULTS: 6 of 36 patients (17%) died; 11 of 17 patients whose charts were reviewed survived and 3 had chronic renal failure. All but 2 patients had acute renal failure. Neither delay to admission, intravenous dialysis, HCO3 or alcohol was related to outcome. At admission more patients who subsequently died had seizures, were comatose, were more acidotic, and had lower base excess and higher potassium levels than those who survived. Urine contained oxalate crystals in 10 of 14 cases. At 24 h the potassium level was higher and the base excess lower in those who died. Blood ethylene glycol levels for the patients who died and survived were no different. All survivors were dialyzed, but 2 patients who died had no dialysis. No survivor needed chronic dialysis and none had organic brain lesions. CONCLUSION: In patients with severe ethylene glycol intoxication, severe acidosis, hyperkalemia, seizures, and coma at admission carry a dismal prognosis. We believe very large amounts of intravenous HCO3 should be used immediately for rapid correction of the metabolic acidosis. Intravenous ethanol and hemodialysis should be started early and continued until acidosis is corrected.
OBJECTIVE: Analysis of prognostic factors and treatment of a large epidemic of ethylene glycol intoxication. DESIGN: Retrospective case review comparing 16 survivors with 6 patients who died. SETTING: Cooperative study between county hospitals, a university hospital, and a poison information centre. PATIENTS AND PARTICIPANTS: Survival review of 36 serious cases and chart review of 17 cases. INTERVENTION: Time to initial treatment with intravenous fluids, sodium, bicarbonate, ethanol, and dialysis. MEASUREMENTS: Clinical data at admission and blood chemistry at 0, 24, 48, and 72 h. RESULTS: 6 of 36 patients (17%) died; 11 of 17 patients whose charts were reviewed survived and 3 had chronic renal failure. All but 2 patients had acute renal failure. Neither delay to admission, intravenous dialysis, HCO3 or alcohol was related to outcome. At admission more patients who subsequently died had seizures, were comatose, were more acidotic, and had lower base excess and higher potassium levels than those who survived. Urine contained oxalate crystals in 10 of 14 cases. At 24 h the potassium level was higher and the base excess lower in those who died. Blood ethylene glycol levels for the patients who died and survived were no different. All survivors were dialyzed, but 2 patients who died had no dialysis. No survivor needed chronic dialysis and none had organic brain lesions. CONCLUSION: In patients with severe ethylene glycol intoxication, severe acidosis, hyperkalemia, seizures, and coma at admission carry a dismal prognosis. We believe very large amounts of intravenous HCO3 should be used immediately for rapid correction of the metabolic acidosis. Intravenous ethanol and hemodialysis should be started early and continued until acidosis is corrected.