Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Acetaminophen Toxicity Treatment & Management

  • Author: Susan E Farrell, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: May 18, 2016
 

Approach Considerations

In addition to antidote therapy, supportive care is essential in acetaminophen toxicity. Immediate assessment of the patient's airway, breathing, and hemodynamic status (ie, ABCs) is critical, while considering and initiating treatment for suspected acetaminophen overdose. As with any ingestion, assessing for other potential life-threatening co-ingestants is very important.

Administer activated charcoal (AC) if the patient has a stable mental and clinical status, patent airway, and presents to the emergency department within 1 hour of ingestion. Measure a 4-hour serum acetaminophen concentration to assess the potential risk for hepatotoxicity, using the Rumack-Matthew nomogram.

Patients with acetaminophen concentrations below the “possible” line for hepatotoxicity on the Rumack-Matthew nomogram may be discharged home after they are medically cleared. If the ingestion occurred with intent to do self-harm, a thorough psychosocial, psychological and/or psychiatric evaluation is indicated before the patient can be discharged safely from the medical care facility.

Admit patients with acetaminophen concentrations above the "possible" line on the Rumack-Matthew nomogram for treatment with N-acetylcysteine (NAC). Treat patients with evidence of hepatic failure, metabolic acidosis, coagulopathy, and/or encephalopathy in an intensive care unit (ICU). Transfer patients with evidence of clinically significant hepatotoxicity to a medical facility with intensive care support and liver transplant services.

Early administration of NAC after suspected acetaminophen overdose is most essential.[30] NAC is nearly 100% hepatoprotective when it is given within 8 hours after an acute acetaminophen ingestion. Guidelines from the American College of Emergency Physicians recommend the use of NAC to treat acute acetaminophen overdose in patients with either possible or probable risk for hepatotoxicity, according to the Rumack-Matthew nomogram, and ideally within 8-10 hours post ingestion.[31]

Because of the relatively benign nature of NAC administration, and the risk of adverse effects from acetaminophen toxicity, NAC should be given even if the history is unclear but a potentially toxic acetaminophen ingestion is suspected. NAC should be administered while awaiting an acetaminophen concentration if the patient presents close to, or later than, 8 hours after an acute ingestion, or if the patient is pregnant.

A late presentation should not preclude NAC administration if the history or presentation suggests potential toxicity.[32] Failure to administer NAC because of late presentation is considered medically and legally inappropriate.

Surgical evaluation for possible liver transplantation is indicated for patients who have severe hepatotoxicity and potential to progress to hepatic failure. Criteria for liver transplantation include the following:

  • Metabolic acidosis, unresponsive to resuscitaton
  • Renal failure
  • Coagulopathy
  • Encephalopathy
Next

Gastric Decontamination

Oral activated charcoal (AC) avidly adsorbs acetaminophen and may be administered if the patient presents within 1 hour after ingesting a potentially toxic dose. AC should not be administered if the patient is mentally compromised and does not have an intact or protected airway.[33]

Oral AC may be of potential benefit longer than 1 hour after the ingestion if the ingestion involves an agent that delays gastric emptying or slows gastrointestinal (GI) motility. In one case series, oral AC administered with NAC 4 hours after ingestion was shown to be effective in reducing the incidence of transaminitis after toxic APAP ingestion.[32] However, it is well documented that the effectiveness of oral AC diminishes over time, especially beyond 60 minutes after a toxic ingestion.  Administration of NAC is of highest priority in this case.

Previous
Next

Oral N-Acetylcysteine

The oral formulation of NAC (Mucomyst) is the drug of choice for the treatment of acetaminophen overdose. GI decontamination with activated charcoal prior to starting NAC therapy does not change the recommended NAC administration schedule. The FDA-approved dosage regimen for oral NAC starts with a loading dose of 140 mg/kg, followed by 17 doses, each at 70 mg/kg, given every 4 hours. The total duration of the treatment course is 72 hours.[23]

A national multicenter study found that oral NAC is safe and effective for as long as 24 hours after a toxic ingestion.[34] Treatment with oral NAC effectively prevented hepatotoxicity, regardless of the initial serum acetaminophen level, if it was started within 8 hours of the ingestion. NAC's treatment effectiveness did not depend on whether it was started 0-4 or 4-8 hours after ingestion.[34]

Previous
Next

Intravenous N-Acetylcysteine

In 2004, the FDA approved an intravenous (IV) formulation of NAC (Acetadote) for use in adults. In February 2006, this FDA approval was modified to include children (patients <40 kg). IV NAC is the therapeutic formulation used in many hospitals. Additional indications for IV administration of NAC include the following:

  • Altered mental status
  • GI bleeding and/or obstruction
  • A history of caustic ingestion
  • Potential acetaminophen toxicity in a pregnant woman
  • Inability to tolerate oral NAC because of emesis refractory to proper use of antiemetics

Pharmaceutical guidelines for IV NAC administration depend on the patient's body weight and/or on whether the ingestion is acute or chronic. Continuous IV infusion is recommended for acute ingestion, as follows:

  • Loading dose: 150 mg/kg IV; mix in 200 mL of 5% dextrose in water (D5W) and infuse over 1 h
  • Dose 2: 50 mg/kg IV in 500 mL D5W over 4 h
  • Dose 3: 100 mg/kg IV in 1000 mL D5W over 16 h

In patients who weigh more than 100 kg, limited data suggest a loading dose of 15,000 mg infused IV over 1 hours, then a first maintenance dose of 5,000 mg IV over 4 hours and a second maintenance dose of 10,000 mg over 16 hours.

To reduce the risk of reconstitution and administration errors, simpler IV NAC regimens have been developed.[35]  One such off-label regimen consists of a loading dose of 150 mg/kg, given over 60 minutes, followed by a maintenance infusion of 15 mg/kg/hr, which is continued until the serum acetaminophen concentration measures less than 10 mg/L and the liver enzyme concentrations remain normal or are trending downward.[36]

In a retrospective study in 59 pediatric patients, age 2 months to 18 years, the above described regimen appeared effective and well tolerated. Treatment durations ranged from 4.25 to 89 hours.Two patients developed hepatoxicity, but none experienced liver failure. The only documented adverse reactions to NAC were minor anaphylactoid reactions, including flushing, facial redness, and itching. These reactions occurred at the end of the loading dose infusion of IV NAC, and responded to IV diphenhydramine or slowing of the infusion rate.[36]

Intermittent IV infusion may be considered for late-presenting or chronic ingestion. A loading dose of 140 mg/kg IV (diluted in 500 mL D5W) is infused over 1 h. Maintenance doses of 70 mg/kg IV are given every 4 hours for at least 12 doses (dilute each dose in 250 mL of D5W and infuse over a minimum of 1 hour).

Adverse side effects associated with IV administration include flushing, pruritus, and rash (seen in about 15% of patients). Stopping the infusion, administering an antihistamine, and restarting NAC at a slower infusion rate remedy those adverse effects. Bronchospasm and hypotension can occur, but those adverse effects are rare (<2% of patients).[37]

Previous
Next

NAC and AC Interaction and Administration

In cases of acetaminophen overdose, early administration of NAC takes priority over GI decontamination with oral AC. Although AC does bind to NAC, AC adsorbs APAP more avidly. Therefore, any decrease in the bioavailability of oral NAC that may result from the administration of AC is clinically inconsequential. Importantly, AC administration may prevent significant APAP absorption from the GI tract and obviate the need for NAC if AC is administered within 60 minutes of an acute ingestion.[38]

Oral NAC administration may be staggered with AC administration in the rare cases where the patient needs multiple doses of AC for the treatment of a co-ingestant.[39] Treatment with intravenous NAC is preferable in this situation.

Consider and evaluate for possible co-ingestants and consider the possible effects of decreased GI motility on the absorption of APAP, because the predictive value of the treatment nomogram may be less reliable in these situations. Therefore, in the absence of good data on multidrug ingestions or co-ingestions involving APAP, administer NAC as early as possible and consult the regional poison control center for guidance on a treatment regimen.

Previous
Next

Delayed Presentation

If a patient presents 8-24 hours or later after an acute ingestion, initiate NAC therapy immediately and evaluate for laboratory evidence of hepatotoxicity. If evidence of hepatotoxicity exists, continue NAC therapy and consult a regional poison control center for guidance on a treatment regimen.

NAC administration in cases of hepatic failure has been associated with a decreased incidence of cerebral edema and improved survival. Therefore, NAC therapy should be initiated if concern exists for potential toxicity while awaiting confirmatory laboratory studies.

Because NAC can be beneficial for acetaminophen-induced hepatic failure when patients present more than 24 hours after a single ingestion, medical toxicologists recommend initiating treatment with NAC in patients who present after 24 hours if an acetaminophen concentration is detected and if hepatic injury is evident from liver function studies.

The beneficial effect of NAC in late treatment, when liver damage has already occurred, suggests that additional local hepatic repair mechanisms may be result from NAC administration. Proposed mechanisms of NAC in this setting include an antioxidant effect, decreased neutrophil accumulation, and improved microcirculatory blood flow supporting increased oxygen delivery to hepatic tissue.

Continuation of NAC therapy is based on the patient's clinical status, on detectable serum acetaminophen, and liver function test results. The Rumack-Matthew nomogram is not valid in cases of late presentation and should not be used to guide medical management in these cases.

Previous
Next

Chronic Ingestion

If a patient presents after multiple ingestions or chronic ingestion of supratherapeutic doses of acetaminophen over hours or days, evaluate for the presence of a persistent serum APAP concentration and laboratory indicators of hepatotoxicity. Begin NAC therapy if the patient has elevated aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels or a measurable serum APAP concentration. Consult a regional poison control center for guidance on a treatment regimen.

Previous
Next

Extended-Release Acetaminophen Overdose

Extended-release acetaminophen (Tylenol ER) consists of acetaminophen 325 mg in immediate release (IR) form surrounding a matrix of acetaminophen 325 mg formulated for slow release. Some alteration of the elimination kinetics of this preparation may affect the reliability of the Rumack-Matthew nomogram to predict potential hepatotoxicity and subsequent treatment based on serum APAP concentrations.

Several studies show that the elimination of ER and IR APAP preparations is nearly identical after 4 hours. However, some case reports have documented APAP levels that are above the potential toxicity and treatment line on the nomogram as late as 11-14 hours after the ingestion of the ER preparation.

Given these findings, recommended management for overdose of ER preparations includes the measurement of 4-, 6-, and 8-hour APAP concentrations. Begin NAC therapy if any level crosses above the nomogram treatment line. If the 6-hour level is greater than the 4-hour level, begin NAC therapy. More prolonged monitoring of APAP levels may be necessary if the patient has food in his or her stomach or has taken co-ingestants that delay gastric emptying.

Consult a regional poison control center for guidance in the evaluation and optimal treatment regimen for these cases.

Previous
Next

Consultations

Consultation with a medical toxicologist is recommended for patients who have a complicated or late presentation, hepatic or renal dysfunction, or a history of potentially toxic co-ingestants. Medical toxicologists are available through consultation with a regional poison control center. For ingestions seen as a "cry for help" or as an intent to self-harm, psychosocial, psychological and/or psychiatric evaluations are required.

A hepatologist who is directly affiliated with a transplantation medical center should be consulted in the setting of hepatic dysfunction and liver failure. Concurrently, consult a transplantation surgeon in the setting of clinical and laboratory indicators that are highly predictive of death unless urgent transplantation is undertaken (see Prognosis). The United Kingdom King's College Hospital criteria for the determination of the urgent need for transplantation after acetaminophen-induced fulminant hepatic failure include any one of the following:

  • Arterial pH less than 7.3 after fluid resuscitation
  • Grade III or IV encephalopathy
  • Prothrombin time (PT) greater than 100 seconds
  • Serum creatinine level greater than 3.4 mg/dL
Previous
 
 
Contributor Information and Disclosures
Author

Susan E Farrell, MD Assistant Professor of Medicine, Harvard Medical School; Program Director, Partners HealthCare International; Attending Physician, Department of Emergency Medicine, Brigham and Women's Hospital

Susan E Farrell, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Germaine L Defendi, MD, MS, FAAP Associate Clinical Professor, Department of Pediatrics, Olive View-UCLA Medical Center

Germaine L Defendi, MD, MS, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

Michael J Burns, MD Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Clinical Toxicologists, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association

Disclosure: Nothing to disclose.

Halim Hennes, MD, MS Division Director, Pediatric Emergency Medicine, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director of Emergency Services, Children's Medical Center

Halim Hennes, MD, MS is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

References
  1. [Guideline] Acetaminophen toxicity in children. Pediatrics. 2001 Oct. 108(4):1020-4. [Medline].

  2. Penna A, Buchanan N. Paracetamol poisoning in children and hepatotoxicity. Br J Clin Pharmacol. 1991 Aug. 32(2):143-9. [Medline]. [Full Text].

  3. US Food and Drug Administration. June 29-30, 2009: Joint meeting of the Drug Safety and Risk Management Advisory Committee with the Anesthetic and Life Support Drugs Advisory Committee and the Nonprescription Drugs Advisory Committee: meeting announcement. Available at http://www.fda.gov/AdvisoryCommittees/Calendar/ucm143083.htm. Accessed: September 10, 2015.

  4. US Food and Drug Administration. Organ-specific warnings: internal analgesic, antipyretic, and antirheumatic drug products for over-the-counter human use. Federal Register. 2009 Apr 29;74(81). Available at http://edocket.access.gpo.gov/2009/pdf/E9-9684.pdf. Accessed: September 9, 2015.

  5. US Food and Drug Administration. Acetaminophen information. Available at http://www.fda.gov/Drugs/DrugSafety/InformationbyDrugClass/ucm165107.htm. Accessed: September 10, 2015.

  6. Brooks M. FDA Asks Docs to Limit Acetaminophen in Prescription Meds. Medscape Medical News. Available at http://www.medscape.com/viewarticle/819216. Accessed: September 9, 2015.

  7. FDA. Acetaminophen Prescription Combination Drug Products with more than 325 mg: FDA Statement - Recommendation to Discontinue Prescribing and Dispensing. U.S. Food and Drug Administration. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm381650.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery.. Accessed: September 9, 2015.

  8. FDA. FDA Drug Safety Communication: FDA warns of rare but serious skin reactions with the pain reliever/fever reducer acetaminophen. US Food and Drug Administration. Available at http://www.fda.gov/Drugs/DrugSafety/ucm363041.htm#. Accessed: March 9, 2016.

  9. Lowes R. Acetaminophen Poses Risk for Rare but Fatal Skin Reactions. Medscape Medical News. Aug 1 2013. [Full Text].

  10. Dart RC, Rumack BH. Intravenous acetaminophen in the United States: iatrogenic dosing errors. Pediatrics. 2012 Feb. 129(2):349-53. [Medline].

  11. Berling I, Anscombe M, Isbister GK. Intravenous paracetamol toxicity in a malnourished child. Clin Toxicol (Phila). 2012 Jan. 50(1):74-6. [Medline].

  12. Anker AL, Smilkstein MJ. Acetaminophen. Concepts and controversies. Emerg Med Clin North Am. 1994 May. 12(2):335-49. [Medline].

  13. McNeil Consumer Healthcare. TYLENOL® Dosage for Adults. Available at https://www.tylenol.com/safety-dosing/usage/dosage-for-adults. 2016; Accessed: May 18, 2016.

  14. US Food and Drug Administration. Public health problem of liver injury related to the use of acetaminophen in both over-the-counter (OTC) and prescription (RX) products. Available at http://www.fda.gov/AdvisoryCommittees/Calendar/ucm143083.htm. Accessed: June 26, 2013.

  15. Health and Human Services. Undefined. Federal Register. April 29, 2009. 74(81).:[Full Text].

  16. Department of Health and Human Services; Food and Drug Administration. Organ-Specific Warnings; Internal Analgesic, Antipyretic, and Antirheumatic Drug Products for Over-the-Counter Human Use; Final Monograph. Federal Register [serial online]. April 29, 2009. 74:19385-409. [Full Text].

  17. Important: Transition to Single Concentration — Pediatric Liquid Acetaminophen Products. Tylenol for Healthcare Professionals. Available at https://www.tylenolprofessional.com/letter_pediatric_liquid_acetaminophen_products.html. May 4, 2011; Accessed: March 9, 2016.

  18. Heard K, Bui A, Mlynarchek SL, Green JL, Bond GR, Clark RF, et al. Toxicity From Repeated Doses of Acetaminophen in Children: Assessment of Causality and Dose in Reported Cases. Am J Ther. 2012 Mar 8. [Medline]. [Full Text].

  19. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 32nd Annual Report. Clin Toxicol (Phila). 2015 Dec. 53 (10):962-1147. [Medline]. [Full Text].

  20. Mitchell I, Bihari D, Chang R, Wendon J, Williams R. Earlier identification of patients at risk from acetaminophen-induced acute liver failure. Crit Care Med. 1998 Feb. 26(2):279-84. [Medline].

  21. Schmidt LE, Dalhoff K. Serum phosphate is an early predictor of outcome in severe acetaminophen-induced hepatotoxicity. Hepatology. 2002 Sep. 36(3):659-65. [Medline].

  22. Bernal W, Donaldson N, Wyncoll D, Wendon J. Blood lactate as an early predictor of outcome in paracetamol-induced acute liver failure: a cohort study. Lancet. 2002 Feb 16. 359(9306):558-63. [Medline].

  23. McNeil Consumer and Specialty Pharmaceuticals. Guidelines for the Management of Acetaminophen Overdose. Available at http://www.tylenolprofessional.com/assets/Overdose_Monograph.pdf. Accessed: July 11, 2013.

  24. FDA Consumer Health Information: US Food and Drug Administration. Acetaminophen and Liver Injury: Q & A for Consumers. June 2009. 1-3. Available at http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm168830.htm. Accessed: September 10, 2015.

  25. Zyoud SH, Awang R, Sulaiman SA, Al-Jabi SW. Impact of serum acetaminophen concentration on changes in serum potassium, creatinine and urea concentrations among patients with acetaminophen overdose. Pharmacoepidemiol Drug Saf. 2011 Feb. 20(2):203-8. [Medline].

  26. Ozkaya O, Genc G, Bek K, Sullu Y. A case of acetaminophen (paracetamol) causing renal failure without liver damage in a child and review of literature. Ren Fail. 2010. 32(9):1125-7. [Medline].

  27. Crowell C, Lyew RV, Givens M, Deering SH. Caring for the mother, concentrating on the fetus: intravenous N-acetylcysteine in pregnancy. Am J Emerg Med. 2008 Jul. 26(6):735.e1-2. [Medline].

  28. Ferner RE, Dear JW, Bateman DN. Management of paracetamol poisoning. BMJ. 2011 Apr 19. 342:d2218. [Medline].

  29. James LP, Capparelli EV, Simpson PM, Letzig L, Roberts D, Hinson JA, et al. Acetaminophen-associated hepatic injury: evaluation of acetaminophen protein adducts in children and adolescents with acetaminophen overdose. Clin Pharmacol Ther. 2008 Dec. 84(6):684-90. [Medline]. [Full Text].

  30. Whyte IM, Francis B, Dawson AH. Safety and efficacy of intravenous N-acetylcysteine for acetaminophen overdose: analysis of the Hunter Area Toxicology Service (HATS) database. Curr Med Res Opin. 2007 Oct. 23(10):2359-68. [Medline].

  31. Wolf SJ, Heard K, Sloan EP, Jagoda AS. Clinical policy: critical issues in the management of patients presenting to the emergency department with acetaminophen overdose. Ann Emerg Med. 2007 Sep. 50(3):292-313. [Medline].

  32. Spiller HA, Winter ML, Klein-Schwartz W, Bangh SA. Efficacy of activated charcoal administered more than four hours after acetaminophen overdose. J Emerg Med. 2006 Jan. 30(1):1-5. [Medline].

  33. Chyka PA, Seger D, Krenzelok EP, Vale JA. Position paper: Single-dose activated charcoal. Clin Toxicol (Phila). 2005. 43(2):61-87. [Medline].

  34. Smilkstein MJ, Knapp GL, Kulig KW, Rumack BH. Efficacy of oral N-acetylcysteine in the treatment of acetaminophen overdose. Analysis of the national multicenter study (1976 to 1985). N Engl J Med. 1988 Dec 15. 319(24):1557-62. [Medline].

  35. Chyka PA. Acetylcysteine and Acetaminophen Overdose: The Many Shades of Gray. J Pediatr Pharmacol Ther. 2015 May-Jun. 20 (3):160-2. [Medline]. [Full Text].

  36. Pauley KA, Sandritter TL, Lowry JA, Algren DA. Evaluation of an Alternative Intravenous N-Acetylcysteine Regimen in Pediatric Patients. J Pediatr Pharmacol Ther. 2015 May-Jun. 20 (3):178-85. [Medline]. [Full Text].

  37. Blackford MG, Felter T, Gothard MD, Reed MD. Assessment of the clinical use of intravenous and oral N-acetylcysteine in the treatment of acute acetaminophen poisoning in children: a retrospective review. Clin Ther. 2011 Sep. 33(9):1322-30. [Medline].

  38. Spiller HA, Krenzelok EP, Grande GA, Safir EF, Diamond JJ. A prospective evaluation of the effect of activated charcoal before oral N-acetylcysteine in acetaminophen overdose. Ann Emerg Med. 1994 Mar. 23(3):519-23. [Medline].

  39. Betten DP, Cantrell FL, Thomas SC, Williams SR, Clark RF. A prospective evaluation of shortened course oral N-acetylcysteine for the treatment of acute acetaminophen poisoning. Ann Emerg Med. 2007 Sep. 50(3):272-9. [Medline].

  40. Tsai CL, Chang WT, Weng TI, Fang CC, Walson PD. A patient-tailored N-acetylcysteine protocol for acute acetaminophen intoxication. Clin Ther. 2005 Mar. 27(3):336-41. [Medline].

 
Previous
Next
 
Semilogarithmic plot of plasma acetaminophen levels vs time. From: Rumack BH, Matthew H. Acetaminophen Poisoning and Toxicity. Pediatrics. 1975 (55)871-876.
Acetaminophen metabolism.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.