Posted: October 8th, 2024

Acetaminophen Poisoning Case Study Analysis

Acetaminophen Poisoning Case Study Analysis

Acetaminophen, commonly known as Tylenol, is a widely used analgesic and antipyretic. Despite its therapeutic benefits, overdose can lead to severe hepatotoxicity. This case study examines a 20-year-old female who ingested a significant amount of Tylenol Extra Strength® in a suicide attempt. The analysis focuses on critical historical information, diagnostic testing, immediate treatment, patient disposition, and the mechanism of acetaminophen toxicity.

Historical Information
In cases of suspected acetaminophen overdose, confirming the time of ingestion is crucial. This information allows healthcare providers to accurately assess the risk of toxicity using the Rumack-Matthew nomogram (Rumack & Matthew, 1975). Additionally, verifying the absence of coingestants is essential, as it influences both the clinical presentation and management strategy.

Diagnostic Testing
The primary diagnostic test required is a serum acetaminophen level. This test should be performed at least four hours post-ingestion to ensure accuracy in risk assessment (Dart et al., 2006). A pregnancy test is also recommended due to the patient’s age and potential implications for treatment. While baseline liver function tests (LFTs) and coagulation profiles (PT/PTT) may be considered if toxicity is confirmed, they are not immediately necessary given the early presentation and lack of underlying liver disease.

Immediate Treatment
Given the eight-hour delay since ingestion, immediate administration of N-acetylcysteine (NAC) is warranted. NAC acts as an antidote by replenishing glutathione stores, thereby neutralizing the toxic metabolite NAPQI (Prescott, 1983). The loading dose of 140 mg/kg should be administered promptly, as NAC is most effective within the first 8-10 hours post-ingestion (Smilkstein et al., 1988).

Patient Disposition
The patient’s acetaminophen level at eight hours post-ingestion places her in the “probable hepatotoxicity” category. Consequently, she should be admitted for a full course of NAC treatment. Additionally, given the context of a suicide attempt, inpatient psychiatric evaluation and suicide precautions are necessary to ensure her safety and address underlying mental health issues.

Mechanism of Acetaminophen Toxicity
Acetaminophen is primarily metabolized in the liver. In therapeutic doses, a small fraction is converted by the cytochrome P450 system into NAPQI, a toxic metabolite. Normally, NAPQI is detoxified by glutathione. However, in overdose situations, excessive NAPQI depletes glutathione stores, leading to hepatocyte damage and potential liver failure (Mitchell et al., 1973). Understanding this mechanism underscores the importance of timely NAC administration to prevent irreversible liver injury.

Conclusion
This case highlights the critical steps in managing acetaminophen overdose, emphasizing the importance of timely diagnosis and treatment. By understanding the pharmacokinetics and toxicology of acetaminophen, healthcare providers can effectively mitigate the risk of severe outcomes in overdose scenarios.

References
Dart, R. C., Erdman, A. R., Olson, K. R., Christianson, G., Manoguerra, A. S., Chyka, P. A., … & Woolf, A. D. (2006). Acetaminophen poisoning: an evidence-based consensus guideline for out-of-hospital management. Clinical Toxicology, 44(1), 1-18.

Mitchell, J. R., Jollow, D. J., Potter, W. Z., Davis, D. C., Gillette, J. R., & Brodie, B. B. (1973). Acetaminophen-induced hepatic necrosis. I. Role of drug metabolism. Journal of Pharmacology and Experimental Therapeutics, 187(1), 185-194.

Prescott, L. F. (1983). Paracetamol overdosage: pharmacological considerations and clinical management. Drugs, 25(3), 290-314.

Rumack, B. H., & Matthew, H. (1975). Acetaminophen poisoning and toxicity. Pediatrics, 55(6), 871-876.

Smilkstein, M. J., Knapp, G. L., Kulig, K. W., & Rumack, B. H. (1988). Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the national multicenter study (1976 to 1985). New England Journal of Medicine, 319(24), 1557-1562.

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PHARMACOLOGY/TOXICOLOGY CASE STUDY.

History: A 20-year-old female presents to the Emergency Department after
ingesting over 50 tablets of Tylenol Extra Strength® eight hours prior to
arrival in a suicide attempt. She denies coingestants and complains of
nausea.
PMH: None.
Physical Examination:
T: 99 °F HR: 90 bpm RR: 12 breaths per minute BP: 120/72 mm Hg
General: Tearful female in no acute distress.
HEENT: Pupils 4 mm and reactive, moist mucus membranes.
Pulmonary: Clear to auscultation.
CV: Tachycardic with regular rhythm.
Abdomen: Normal bowel sounds, nontender to palpation.
Neurologic: Unremarkable.

QUESTIONS CASE STUDY
1. What is the most important historical information that should be obtained?
2. What diagnostic testing, if any, would you perform?
3. What treatment, if any, should be initiated immediately?
4. What is the appropriate disposition of this patient?
5. Explain the mechanism of toxicity of acetaminophen.

CASE STUDY : ACETAMINOPHEN POISONING
1. The presence of coingestants and confirmation of the time of ingestion is the most
important historical information to obtain. The time of ingestion should be
determined so that accurate plotting of the level on the Rumack-Matthew
nomogram can be accomplished to determine the risk of toxicity. Tylenol Extra
Strength® contains 500 mg of acetaminophen (APAP) per tablet; however there is
no reliable way to predict toxicity based on the patient’s report of the quantity
ingested.
2. The only initial laboratory tests that should be obtained are a serum APAP level
and a pregnancy test. Because the Rumack-Matthew nomogram does not risk
stratify patients based on levels obtained prior to four hours after ingestion,
obtaining acetaminophen levels prior to this time is not useful except possibly to
substantiate a claim of overdose. One may consider ordering baseline LFTs and
PT/PTT if the APAP level is in the toxic range, but this early after the ingestion,
one would expect those to be normal if the patient has no underlying disease. A
toxicology screen would not be useful because the patient is relatively
asymptomatic and has a normal exam.
3. Because the ingestion occurred eight hours earlier, N-acetylcysteine (loading dose
140 mg/kg) should be administered prior to the laboratory results. The antidote is
most effective if administered within the first 8-10 hours. If the level is non-toxic,
further doses are not indicated. If the patient presents prior to the eight hour
mark, there is no known advantage to administering NAC before the level returns.
In this patient, the eight hour level is 250 mcg/ml.
4. Because the patient’s eight hour acetaminophen level places her in the “probable
hepatotoxicity” category, she should be admitted for the full course of NAC.
Suicide precautions should be continued as an inpatient.
5. Hepatic metabolism of acetaminophen occurs via the cytochrome p450 system
and produces a highly reactive metabolite called N-acetyl-p-benzoquinone imine,
(NAPQI). In therapeutic doses, approximately 4% of APAP is metabolized via the
P450 system and the resultant NAPQI is detoxified by the glutathione stores in the
liver. In the presence of toxic doses, the amount of acetaminophen metabolized
by the cytochrome p450 system increases, subsequently depleting glutathione
stores and leading to an increased amount of NAPQI. NAPQI acts to cause
toxicity by binding to the hepatocyte and resulting in cell death

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Tags: Acetaminophen Toxicity, Hepatotoxicity, N-acetylcysteine Treatment, Overdose Management