Acetaminophen-induced liver necrosis has been studied extensively, but the extrahepatic manifestations of acetaminophen toxicity are currently not described well in the literature. Renal insufficiency occurs in approximately 1-2% of patients with acetaminophen overdose. The pathophysiology of renal toxicity in acetaminophen poisoning has been attributed to cytochrome P-450 mixed function oxidase isoenzymes present in the kidney, although other mechanisms have been elucidated, including the role of prostaglandin synthetase and N-deacetylase enzymes. Paradoxically, glutathione is considered an important element in the detoxification of acetaminophen and its metabolites; however, its conjugates have been implicated in the formation of nephrotoxic compounds. Acetaminophen-induced renal failure becomes evident after hepatotoxicity in most cases, but can be differentiated from the hepatorenal syndrome, which may complicate fulminant hepatic failure. The role of N-acetylcysteine therapy in the setting of acetaminophen-induced renal failure is unclear. This review will focus on the pathophysiology, clinical features, and management of renal insufficiency in the setting of acute acetaminophen toxicity.Case: A 47-year-old female was found lethargic at home and brought by ambulance to an emergency department. History from family members suggested an inadvertent acetaminophen overdose, and she had last been seen a few hours earlier. She reportedly ingested 18 tablets of 500 mg acetaminophen (APAP) over the previous two days because she had run out of her prescription pain medication. Her past medical history was significant for fibromyalgia, arthritis, and a prior gastric bypass procedure. She had no history of alcohol abuse or renal insufficiency. She was lethargic. Vital signs: BP 128/96 mmHg, pulse 112/min, respirations 32/min; pulse oximetry 98% on 2L nasal cannula oxygen. Laboratory studies: BUN 9 mg/dL, creatinine 0.9 mg/dl, acetaminophen 12 mcg/mL, AST 5409 u/L and ALT 1085 u/L. A urinalysis was negative for blood with trace protein and ketones. A urine drug screen was positive for marijuana and opioid metabolites. At the initial hospital, she was treated with N-acetylcysteine (NAC) orally. Subsequently, she developed fulminant hepatic failure with elevated transaminases, hypoglycemia, and coagulopathy (Tables 1A and 1B). She was transferred

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The increasing trend of DXM abuse cases noted in the first half of the decade by previous studies seems to have peaked at 17.6 calls per million population in 2006. It is likely that a combination of legislative, educational, and economic initiatives are responsible for the observed plateau.

Objectives: Medication error prevention has become a priority in health care. The Joint Commission recommends that a list of medications, dosages, and allergies be obtained from all patients. The authors sought to determine the accuracy of medication history taking in emergency department (ED) triage. The hypothesis was that there would be significant discrepancies between medications listed in triage and those the patient was actually taking. Methods: This was a prospective, cross-sectional survey of adult patients presenting to the ED. As a part of regular care, nurses recorded a medication list during triage in the electronic medical record (EMR). For this study, the triage medication list was rechecked during an independent patient interview. Results: Of 1,797 patients approached, 1,657 completed the survey (92%). The mean age was 39 years (standard deviation [SD] ±16 years). Discrepancies in medication lists obtained during triage were documented in 626 (37%) patients. Discontinued medications (163, 9.8%) were included, additional medications (463, 27.9%) were omitted, and 632 patients (38%) reported taking a nonprescription medication not listed in the EMR. Conclusions: Medication histories performed in ED triage are inaccurate and incomplete. ACADEMIC EMERGENCY MEDICINE 2011; 18:102-104 ª 2011 by the Society for Academic Emergency Medicine M edication errors are a major cause of morbidity and mortality. It is estimated that 9.7% of patients involved in an adverse drug event (ADE) have a resulting disability. 1 Patients who experience an ADE have twice the risk of death as those who do not. 2 The Institute of Medicine (IOM) estimates 1.5 million preventable ADEs occur annually, costing $3.5 billion per year. 3 ADEs translate into increased emergency department (ED) utilization. Approximately 177,000 ED visits by elders are attributed to drug misadventures annually. 4 These numbers are considered an underestimate, as many ADEs go unrecognized or unre-ported. The IOM report and the Joint Commission have made medication safety a priority in health care. Medication errors and adverse effects can occur any time in the patient encounter, 5 and the majority of ADEs can be prevented. 6 The Joint Commission recommends a list of medications, route, frequency, dosage, allergies, and adverse reactions be recorded, a process called medication reconciliation. It is hypothesized that accurate reconciliation prevents therapeutic duplications, drug omissions, drug-drug and drug-disease interactions , dosing errors, allergic reactions, and adverse effects. Medication lists are often inaccurate, and the limited available data suggest that medication reconciliation is often not complete in the ED. 7 This study attempts to evaluate the accuracy of medication histories performed during ED triage. We hypothesized that there would be significant discrepancies between medication lists obtained at triage and those medications patients were actually taking. We sought to determine the frequency of omitted medications , discontinued m...