Halothane Hepatotoxicity Follow-up

  • Author: Ruben Peralta, MD, FACS; Chief Editor: Michael R Pinsky, MD, CM, FCCP, FCCM   more...
 
Updated: Jul 20, 2010
 

Further Inpatient Care

Because clinical deterioration may be rapid and because of the high risk of mortality, patients may require monitoring in an intensive care unit.

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Transfer

  • Hospitalized patients may be discharged when the following criteria are met:
    • Significant improvement in symptoms
    • Normalization of prothrombin time
    • A substantial downward trend in the serum aminotransferase and bilirubin values occurs. Mildly elevated aminotransferase levels should not be considered contraindications to the gradual resumption of normal activity as tolerated.
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Deterrence/Prevention

  • The most conservative approach is to avoid halothane when reasonable alternatives exist. For example, because of the medicolegal climate in the United States, halothane is infrequently used in adults since several alternatives exist and any postanesthetic liver dysfunction is likely to be ascribed to halothane. In many other countries with different medicolegal climates, halothane is still widely used because of economic reasons.
  • The anesthesia profession is becoming more aware of the occupational exposure and adverse environmental impact of inhalational anesthetics, which includes ozone damage and greenhouse gas effect. A call for the modification in anesthetics procedures and the role of total intravenous anesthesia in selected procedures is being advocated by some.[5]
  • Carefully consider halothane use in any adult patient with recent exposure in the past 6 weeks. Recent exposure is the most important risk factor for type II fulminant hepatotoxicity.
  • In patients with a history of jaundice and fever following previous halothane exposure, all volatile anesthetics (ie, halothane, enflurane, isoflurane, sevoflurane, desflurane) should be used with caution and indications should be documented.
  • Patients with unexplained elevations of liver functions should not undergo anesthesia and elective surgery until a diagnosis has been confirmed. Any type of surgery and anesthesia in the setting of acute hepatitis carries the potential for increased mortality and morbidity.
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Complications

  • Fulminant liver failure is possible.
  • In rare cases, cirrhosis may develop following halothane hepatitis. However, in most cases, liver function returns to normal.
  • Halothane given with succinylcholine for induction anesthetic is associated with masseter spasm.
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Prognosis

  • If fulminant liver failure does not occur, patients usually make a full recovery.
  • If fulminant liver failure occurs, the mortality rate can be 50%.
  • If hepatic encephalopathy is present, the mortality rate can be 80%.
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Patient Education

  • Full informed consent should always be obtained and should include the indications for use and the possible risk of hepatotoxicity.
  • Patients with a history of fever and jaundice following halothane exposure should be sure to communicate this to anesthesiologists and surgeons.
  • General anesthesia is not contraindicated for future surgery because it can be provided without the use of volatile agents.
  • For excellent patient education resources, visit eMedicine's Hepatitis Center and Liver, Gallbladder, and Pancreas Center. Also, see eMedicine's patient education articles Hepatitis A, Hepatitis B, Hepatitis C, and Cirrhosis.
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Contributor Information and Disclosures
Author

Ruben Peralta, MD, FACS  Professor of Surgery, Anesthesia and Emergency Medicine, Senior Medical Advisor, Board of Directors, Program Chief of Trauma, Emergency and Critical Care, Consulting Staff, Professor Juan Bosch Trauma Hospital, Dominican Republic

Ruben Peralta, MD, FACS is a member of the following medical societies: American Association of Blood Banks, American College of Healthcare Executives, American College of Surgeons, American Medical Association, Association for Academic Surgery, Eastern Association for the Surgery of Trauma, Massachusetts Medical Society, Society of Critical Care Medicine, and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Karl A Poterack, MD  Consulting Staff, Department of Anesthesiology, Mayo Clinic Scottsdale

Karl A Poterack, MD is a member of the following medical societies: American Society of Anesthesiologists

Disclosure: Nothing to disclose.

Specialty Editor Board

Laurie Robin Grier, MD  Medical Director of MICU, Professor of Medicine, Emergency Medicine, Anesthesiology and OBGYN, Section of Pulmonary and Critical Care Medicine, Louisiana State University Health Science Center at Shreveport

Laurie Robin Grier, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Society for Parenteral and Enteral Nutrition, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Harold L Manning, MD  Associate Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School

Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, FCCP, FCCM  Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center

Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine

Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting

References

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  2. Feng D, Wang Y, Xu Y, Luo Q, Lan B, Xu L. Interleukin 10 deficiency exacerbates halothane induced liver injury by increasing interleukin 8 expression and neutrophil infiltration. Biochem Pharmacol. Jan 15 2009;77(2):277-84. [Medline].

  3. Kobayashi E, Kobayashi M, Tsuneyama K, Fukami T, Nakajima M, Yokoi T. Halothane-induced liver injury is mediated by interleukin-17 in mice. Toxicol Sci. Oct 2009;111(2):302-10. [Medline].

  4. Unsal C, Celik JB, Toy H, Esen H, Otelcioglu S. Protective role of zinc pretreatment in hepatotoxicity induced by halothane. Eur J Anaesthesiol. Oct 2008;25(10):810-5. [Medline].

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  15. Kharasch ED, Hankins DC, Fenstamaker K, Cox K. Human halothane metabolism, lipid peroxidation, and cytochromes P(450)2A6 and P(450)3A4. Eur J Clin Pharmacol. Feb-Mar 2000;55(11-12):853-9. [Medline].

  16. Masubuchi Y, Horie T. Toxicological significance of mechanism-based inactivation of cytochrome p450 enzymes by drugs. Crit Rev Toxicol. Jun 2007;37(5):389-412. [Medline].

  17. Mikatti NE, Healy TE. Hepatic injury associated with halogenated anaesthetics: cross- sensitization and its clinical implications. Eur J Anaesthesiol. Jan 1997;14(1):7-14. [Medline].

  18. Ray DC, Drummond GB. Halothane hepatitis. Br J Anaesth. Jul 1991;67(1):84-99. [Medline].

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  22. You Q, Cheng L, Reilly TP, Wegmann D, Ju C. Role of neutrophils in a mouse model of halothane-induced liver injury. Hepatology. Dec 2006;44(6):1421-31. [Medline].

 
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