Hypothermia: an unusual indication for gastric lavage.

BACKGROUND: Previous reports suggest that gastric lavage holds many risks and is not routinely indicated for decontamination of the overdose patient. OBJECTIVE: To present a case of overdose with concurrent accidental hypothermia where gastric decontamination was utilized. CASE REPORT: A 50-year-old hypothermic, comatose patient was transported to the Emergency Department with a concurrent, massive medication ingestion diagnosed incidentally on a routine abdominal computed tomography scan. Both active and passive rewarming measures, in conjunction with gastric lavage and retrieval of multiple pill fragments, were performed, and the patient survived to hospital discharge without sequelae. Interestingly, the patient admitted to an intentional ingestion of both labetalol and lorazepam. CONCLUSION: Due to hypothermia-mediated changes in metabolism, including gastric atony and decreased hepatic metabolism, gastric lavage may provide additional benefit in the management of severely hypothermic patients with potentially lethal, massive pill ingestions.

Fatal intoxication with labetalol (Trandate).

The dead body of a 44-year-old woman, previously known for depression and alcoholism, has been discovered at her place of residence by her husband. A forensic autopsy has been carried out. The results indicated unspecific histological lesions (alveolar oedema, liver steatosis and interstitial nephritis) but did not reveal any apparent cause of death. Several boxes of medicines have been found near the body, justifying a toxicological analysis. This has been performed on peripheral blood and urine samples using liquid chromatography with diode array and mass spectrometric detections, in conjunction with gas chromatography coupled with mass spectrometry. Ethanol has been found (1.24 g/L in blood, 2.63 g/L in urine and 1.33 g/kg in gastric content), as well as therapeutic concentrations of meprobamate (14.1mg/L) and low concentrations of nordazepam (0.12 mg/L) in blood. On the other hand, particularly high levels of labetalol, a widely used beta-blocker, have been found both in blood (1.7 mg/L) and urine (20.2mg/L), which led us to measure labetalol levels in available viscera samples (liver, heart, kidney, and lung) and gastric content. Measured concentrations were 14.2 microg/g, 7.8 microg/g, 5.4 microg/g, 5.2 microg/g and 31.1 microg/g, respectively. We describe here the first report of a fatal intoxication attributed to labetalol that is linked to its acute toxicity, with tissue distribution of this beta-blocker.

Electrocardiographic changes associated with beta-blocker toxicity.

STUDY OBJECTIVE: We sought to characterize the ECG changes associated with symptomatic beta-blocker overdose. METHODS: The study population consisted of a prospective cohort of patients reporting to 2 regional poison centers with beta-blocker overdose. Each patient received an ECG on presentation and a structured follow-up. The inclusion criteria for symptomatic overdose included heart rate of less than 60 beats/min or systolic blood pressure of less than 90 mm Hg; symptoms consistent with decreased end-organ perfusion; therapeutic intervention with cardioactive medication; and corroboration by 2 of the authors that this was a clear-cut case of symptomatic beta-blocker overdose with cardiovascular toxicity. Exclusion criteria included cardioactive coingestants, age younger than 6 years, and no available ECG. RESULTS: Of 167 patients, 13 were determined to have symptomatic exposures. First-degree heart block (>200 ms) was the most common ECG finding (10/12) and also had the greatest likelihood ratio (5.31) when comparing those with symptomatic exposures with those with asymptomatic exposures. Comparing the asymptomatic with the symptomatic groups, the mean PR interval was 167 ms (95% confidence interval [CI] 162 to 171 ms) versus 216 ms (95% CI 193 to 238 ms), the mean QRS interval was 89 ms (95% CI 87 to 91 ms) versus 112 ms (95% CI 92 to 132 ms), the mean QTc interval was 422 ms (95% CI 417 to 428) versus 462 ms (95% CI 434 to 490 ms), and the mean heart rate was 72 beats/min (95% CI 69 to 74 beats/min) versus 66 beats/min (95% CI 59 to 73 beats/min). Two cases of symptomatic acebutolol exposure appeared unique by demonstrating disproportionate prolongation of the QTc interval, an RaVR height of 3 mm or greater, and associated ventricular tachydysrhythmia. CONCLUSION: The majority of clinically significant beta-blocker intoxications demonstrate negative dromotropic effects on ECG. Several ECG differences in acebutolol intoxication might reflect unique pathophysiologic processes relative to other beta-blockers.

Labetalol overdose successfully treated with amrinone and alpha-adrenergic receptor agonists.

Circulatory collapse and obtundation occurred in a 37-year-old woman following an iatrogenic overdose of labetalol. Conventional therapy with glucagon and alpha-adrenergic receptor-stimulating agents was ineffective in raising the patient's cardiac output or improving her mental status despite increasing the arterial pressure. The administration of amrinone was temporally associated with significant increases in the cardiac output accompanied by improved mental status. This case suggests that amrinone may be effective adjunctive therapy for beta-adrenergic receptor blocker overdoses by reversing their negative inotropic effects.

Acute renal failure associated with a labetalol overdose.

A case of acute renal failure in association with a deliberate labetalol overdose is described. The possible pathogenetic mechanisms behind the deterioration in renal function are discussed. Treatment of beta-blockade overdose, with special emphasis on the place of glucagon in such poisoning, is reviewed.

Survival following massive overdose of adrenergic blocking agents (acebutolol and labetalol).

Massive overdosage of adrenergic blocking drugs is associated with severe morbidity and a high mortality rate. We report the case of a 24-year-old medical intern who ingested 9.6 g acebutolol, 7.2 g labetalol and 0.625 g trimipramine in an attempted suicide. Blood samples drawn on admission were shown to contain markedly elevated plasma levels of acebutolol and its major metabolite and of labetalol. The patient was deeply comatose on admission. The heart rate was 60 min-1 (sinus rhythm) and the blood pressure was clinically unrecordable. Atropine, isoproterenol and dopamine initially had no effect on either heart rate or blood pressure. Only following the administration of inordinately large doses of isoproterenol and dopamine, together with glucagon was a clinical response obtained. The patient remained haemodynamically dependent on dopamine for 12 h and isoproterenol for 65 h. The total dose of isoproterenol administered was 260 mg, two thirds of this during the first 12 h. The patient left hospital well after 7 days but was readmitted after 26 days because of intestinal obstruction due to ischemic bowel necrosis.