Patients may go on to develop fulminant liver failure requiring a transplant or, if they survive Stage III, they enter a recovery stage (Stage IV - four days to two weeks post ingestion). Acute renal failure may also occur during this stage. During Stage III (72 to 96 hours after ingestion) nausea, vomiting, and malaise return and patients may also exhibit jaundice and confusion. There may also be hepatomegaly on physical exam. However, patients generally are asymptomatic during Stage II although they may develop some right upper quadrant pain and tenderness. Laboratory evidence of hepatotoxicity usually becomes evident by Stage II (24 to 72 hours after acute ingestion). There is a broad spectrum of overdose presentation depending on whether the intoxication is acute or chronic, the amount of acetaminophen ingested, and time since ingestion. In Stage 1 (0.5-24 hours after ingestion) patients may complain of nausea, vomiting, lethargy and general malaise. It is also the most common cause of acute liver failure (ALF) in the United States, accounting for 50% of all ALF cases. This activity reviews the evaluation and treatment of common overdoses, and highlights the role of the interprofessional team in evaluating and treating patients that have experienced an overdose.Īcetaminophen: Acetaminophen overdose is the most commonly reported overdose in both the UK and in the United States. This activity will focus on updating the health team on sixteen of the most common overdose presentations and their corresponding antidotes. Identifying the ingestion and prompt administration of the correct antidote can prevent significant morbidity and mortality for many patients. While for many overdoses and intoxications the treatment involves supportive care and treatment of the sequelae there are specific antidotes available for a variety of substances. In the United States in 2015 antidotes for various overdoses were used 184,742 times. With more than 2.4 million toxic exposures each year, poisoning is the second most common cause of injury-related morbidity and mortality in the United States. The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance.Overdoses and accidental ingestions or exposures are common throughout the world. Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia. The doses of glucagon required to reverse severe beta-blockade are 50 micrograms/kg iv loading dose, followed by a continuous infusion of 1-15 mg/h, titrated to patient response. Because it may bypass the beta-receptor site, glucagon can be considered as an alternative therapy for profound beta-blocker intoxications. This suggests that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. These effects are unchanged by the presence of beta-receptor blocking drugs. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose. Medical complications of beta-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. The effects of glucagon in reversing the cardiovascular depression of profound beta-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Two cases of severe beta-blocker overdose are presented that were treated successfully with glucagon therapy.
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