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Acetaminophen (Tylenol) Poisoning
Published in Charles Theisler, Adjuvant Medical Care, 2023
Acetaminophen (Tylenol) overdose, or poisoning, is one of the most common poisonings. Mild poisoning may not cause any symptoms. When present, however, symptoms of acute acetaminophen poisoning are typically minor until about 48 hours or longer after ingestion. Symptoms include anorexia, nausea, vomiting, and right upper quadrant abdominal pain. Acetaminophen toxicity in the U.S. has replaced viral hepatitis as the most common cause of acute hepatic failure and is the second most common cause of liver failure requiring transplantation.1
Drug Overdoses during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Importantly, acetaminophen per se is not the toxic agent in overdoses, it a proximate metabolite that is toxic, and preventing the drug’s metabolism is key to antidote treatment, and the reason for urgency in NAC administration. In acetaminophen overdose, metabolic pathways (sulfation and glucuronidation) become saturated, causing an increased metabolic demand on cytochrome P-450 oxidases. The P-450 system oxidizes the drug and produces a highly reactive intracellular metabolite (N-acetyl-p-benzoquinone imine, or NAPBQI) that complexes with hepatic glutathione. The P-450 metabolite NAPBQI binds to hepatocellular macromolecules when glutathione is depleted and hepatotoxicity ensues (Andrews et al., 1976; Davis et al., 1976). Normally, NAPBQI is produced in small amounts and degraded by the liver almost immediately. Fetal P-450 has <10 percent of adult activity, resulting in negligible production of the toxic metabolite. Some authorities speculate that the increased risk of maternal hepatotoxicity compared to fetal hepatotoxicity may be related to the largely inactive fetal enzyme complement, i.e., fetal liver has a much lower capacity to metabolize the drug to NAPBQI. As the fetal liver matures, it is likely fetuses of more advanced gestational age are at greater risk for acetaminophen toxicity than less mature fetuses. In the largest series published, this relationship was not readily apparent (Table 14.6). Maternal-fetal outcomes are generally better with expedient NAC administration following acetaminophen overdose.
Analgesia And Anesthesia
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Michele Mele, Valentina Bellussi, Laura Felder
Following surgery, scheduled NSAIDs and acetaminophen have been shown to decrease opioid use and improve pain scores [88–90]. While the optimal dose and route of these medications are unclear, IM or IV administration of NSAIDs does appear to be more effective than oral administration [91]. Acetaminophen may also be administered intravenously, although there is conflicting data on the efficacy of the IV route when compared to oral or rectal administration [92–96]. Because IV acetaminophen is significantly more expensive than other formulations, many institutions opt to use oral acetaminophen. In general, medications that combine acetaminophen with an opioid should be avoided. Compared to scheduled acetaminophen, combination medications, such as oxycodone-acetaminophen (Percocet), have been shown to increase opioid consumption overall [97], and such medications are known to have higher associated street value, making them more prone to abuse by other community members.
Decision tree algorithm can determine the outcome of repeated supratherapeutic ingestion (RSTI) exposure to acetaminophen: review of 4500 national poison data system cases
Published in Drug and Chemical Toxicology, 2023
Omid Mehrpour, Christopher Hoyte, Foster Goss, Farshad M. Shirazi, Samaneh Nakhaee
While it is one of the most common analgesics in the world, acetaminophen (APAP) is also one of the most common drugs resulting in overdose with an estimation of 26,000 hospitalizations and 56,000 emergency visits per year being caused by overdoses of acetaminophen (Kaufman et al.2002, Nourjah et al.2006). In addition, overdoses of acetaminophen may result in acute liver and kidney failure (Chun et al.2009, Mour et al.2005). Besides, overdose of acetaminophen is the most common cause behind acute cases of liver failure in the US (Ostapowicz et al.2002, Wong et al.2022). Overdoses of acetaminophen can be classified into two types: repeated supra-therapeutic ingestion (RSTI) overdose or acute overdose (this is the most common type of overdose documented in medicine) (Alhelail et al.2011, Bond et al.2015).
Provider-directed analgesia for dental pain
Published in Expert Review of Clinical Pharmacology, 2023
Globally, acetaminophen is a commonly prescribed (and self-prescribed) therapeutic to reduce fever (antipyretic) and lower pain (analgesic). Acetaminophen is available in a variety of pharmaceutical formulations (e.g. capsules, tablets, syrups, suspensions, suppositories, intravenous), making it a readily adaptable agent in a variety of medical and dental settings. Despite its long history of pharmacotherapeutic use, the full elucidation of acetaminophen’s mechanism of action is still unclear and continues to be studied [26]. Although initially thought to act peripherally as a NSAID, further evaluations showed it lacks peripheral effects seen with traditional NSAIDs, such as acetylsalicylic acid (aspirin) and ibuprofen [27]. A major site of acetaminophen action appears to be located in the central nervous system (CNS), where it nonspecifically inhibits COX enzymes (Table 1) [26]. Unlike NSAIDs, which act via direct binding to the bioactive site of COX enzymes, acetaminophen reduces the bioactive form of COX, rendering it catalytically deficient [26]. There is also some evidence for the role of peroxides in the mechanism of acetaminophen. For example, acetaminophen preferably acts in areas of low peroxides, such as the brain, versus in the periphery that harbors greater concentrations of peroxides [28].
Circulating miR-122 in patients with non-toxic acute acetaminophen ingestions
Published in Clinical Toxicology, 2022
Jacob A. Lebin, Anita Mudan, Yu Zhang, Alan H. B. Wu, Craig G. Smollin
Ten patients met inclusion criteria during the study period, of whom six (60%) were female. The mean age was 27 years old (range: 13–89). The mean reported amount of ingested acetaminophen was 7837 mg (range: 4000–13000 mg) and all patients had an acetaminophen concentration obtained four hours after reported ingestion. The mean four-hour serum acetaminophen concentration was 73.4 µg/mL (range: 12–110). The mean AST and ALT at presentation were 20 U/L (range: 11–32) and 18 U/L (range: 7–38), respectively. The mean fold change in expression of miR-122 was not significantly different in patients with acetaminophen exposure versus negative controls [(0.82, IQR: 0.27, 0.77) vs (1.24, IQR: 0.54, 1.98), p = 0.33]. The mean fold change in expression of miR-122 in positive controls was 1025.59 (Figure 1).