Pediatric Fulminant Hepatic Failure

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Pediatric Fulminant Hepatic Failure

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Fulminant hepatic failure (FHF) is usually defined as the severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of preexisting liver disease. However, unlike in adults, encephalopathy may be absent, late, or apparent in children only at the terminal stages. Thus, the emphasis in children is placed on the presence of significant coagulopathy in the absence of sepsis or disseminated intravascular coagulation that is not correctable by the administration of parenteral vitamin K within 8 hours.

The exact etiology remains unidentified in many cases of pediatric FHF. Likewise, the pathophysiologic mechanism that leads to hepatic encephalopathy in children with FHF has not been fully defined (see Pathophysiology and Etiology). [1]

FHF affects previously healthy children with no recognized risk factors for liver disease. Children usually present with a hepatitis-like clinical picture; jaundice is the presenting symptom in most patients. Children with FHF are critically ill, and symptoms and level of consciousness rapidly deteriorate. Over a few days to weeks, the condition progresses to coma, with development of ascites, cerebral edema, and decorticate and decerebrate posturing (see Presentation).

A range of laboratory studies is required to determine the etiology, severity, and prognosis in pediatric patients with FHF. Liver biopsy is usually an essential procedure to consider in the management of this condition (see Workup).

Symptomatic treatment and life support should be provided to patients. Direct treatment is toward the specific cause of FHF when an identifiable etiology is found. An intensive care unit (ICU) and pediatric hepatology setting with facilities for liver transplantation should be available for proper diagnosis and management. Orthotopic liver transplantation remains the only effective mode of treatment of FHF (see Treatment and Management). [2]

Pharmacologic intervention is usually directed at causative agents or the treatment of complications (see Medication).

See Acute Liver Failure for more information on this topic.

FHF usually begins with exposure of a susceptible person to an agent capable of producing severe hepatic injury, although the exact etiology remains unidentified in many cases of FHF. Likewise, the pathophysiologic mechanism that leads to hepatic encephalopathy in children with FHF has not been fully defined.

One theory highlights the effect of accumulation of neurotoxic or neuroactive substances as a consequence of hepatocellular failure. These substances include false neurotransmitters, ammonia, increased gamma-aminobutyric acid receptor activity, and increased circulating levels of endogenous benzodiazepine-like substances. Decreased hepatic clearance of these neurotoxins and increased absorption may contribute to the encephalopathy. Serum ammonia levels may be normal or slightly elevated, even in patients who are deeply comatose, thus not the sole explanation to the impaired cerebral function.

Viral agents may cause damage to hepatocytes either by direct cytotoxic effect or as a result of hyperimmune response to viral antigens. Apparently, the interaction between agent and host determines the incidence of FHF.

Hepatotoxic metabolites, which accumulate as a result of errors in metabolism or of taking hepatotoxic drugs, may cause injury to the hepatocytes. Etiology

The etiology of pediatric fulminant hepatic failure differs significantly from adults in developed countries. Viral hepatitis and drug-induced hepatotoxicity are the 2 most common identifiable causes of FHF. The cause remains unknown (ie, idiopathic) in a large proportion of patients. [3]

In approximately 50% of patients, FHF is caused by acute viral hepatitis, commonly caused by hepatitis viruses A, B, C, D, or E. Acute viral hepatitis A and E are usually self-limiting diseases. However, acute liver failure, prolonged cholestasis, ascites, and hemolysis are common atypical manifestations of acute viral hepatitis A and E. [4] Many other viruses are also recognized causes of FHF in childhood, including Epstein-Barr virus; cytomegalovirus (CMV); paramyxovirus; varicella-zoster virus; herpesvirus types 1, 2, and 6; parvovirus; and adenovirus. [5]

Hepatitis B virus (HBV) is the most common cause of FHF in endemic areas. Recognized sources of infection include women with positive anti-hepatitis B e antigen (HBe) who give birth and carriers of subdeterminants of hepatitis B surface antigen (HBsAg) and donate blood.

The presence of immunoglobulin M (IgM) antibody to HBV core antigen (IgM anti-HBcAg) or HBsAg in serum is supportive of the diagnosis of acute HBV infection. However, in patients with FHF caused by HBV infection, serum findings may be negative for hepatitis HBsAg. In more than one third of patients, no HBV DNA is detectable in the serum.

Hepatitis A virus infection is a recognized cause of FHF in individuals of all ages, with an estimated prevalence of 1.5-31%. All cases should therefore be followed up until complete recovery. [6] Diagnosis of HAV infection is made by the presence of anti-HAV IgM in the patient’s serum.

Hepatitis C virus (HCV) infection is not a significant cause of FHF in children. HCV infection is diagnosed by detecting anti-HCV antibody or HCV RNA in the serum. Children with acute leukemia are at a high risk of hepatitic C infection, either by immunosuppression from therapy or from multiple transfusions of blood products. HCV in leukemia could be virtually eliminated by proper testing of the blood transfusion pool. [7]

Hepatitis D virus (HDV) also is not a significant cause of FHF in children. The diagnosis of HDV is confirmed by the presence of anti-HDV antibody in serum. Superinfection with HDV can result in FHF in chronic carriers of HBV, with or without chronic hepatitis.

Hepatitis E virus mainly affects adolescents and young adults in endemic areas.

These agents are the second most common cause of FHF, responsible for approximately 20% of cases. [8] Hepatotoxic drugs include acetaminophen (paracetamol), chlorinated hydrocarbons, salicylates, methanol, isoniazid, intravenous tetracycline, and sodium valproate. [9] The most common drug involved is acetaminophen, and in some locations, it is the most common cause of FHF. Overdose of acetaminophen causes direct hepatotoxicity and hepatocellular necrosis. [5, 10]

These causes vary according to the age of the patient. Because patients with metabolic causes have preexisting liver disease, the inclusion of metabolic causes in the etiology of FHF in children is not uniformly approved.

In neonates, inborn errors of metabolism, including tyrosinemia, hereditary fructose intolerance, galactosemia, and neonatal hemochromatosis, are the major metabolic causes of FHF. In older children and adolescents with FHF, Wilson disease, which is the most common metabolic cause in that age group, should be considered. [11, 12, 13, 14]

Circulatory causes are uncommon in FHF. They include congestive heart failure, cardiomyopathy, sepsis, shock, cyanotic heart disease, obstructive lesions of the aorta, vascular occlusions, myocarditis, and severe asphyxia.

Non–A-E hepatitis has been found in a heterogeneous group of patients in both adult and pediatric series. Prevalence in American and European patients with FHF is approximately 24%. Patients usually present with symptoms similar to those found in other forms of hepatitis. Non–A-E hepatitis is a diagnosis of exclusion, assigned when other identifiable causes have been eliminated. Patients have the same biochemical and histologic manifestations, but no viral markers are detected, and no history of drug exposure or other cause of FHF is found. Non–A-E hepatitis is characterized by its high fatality rate, low rate of spontaneous recovery, and unique complication of aplastic anemia, as compared with other causes of FHF.

Other conditions also include Hodgkin disease, leukemic infiltration, and autoimmune hepatitis.

At least several hundred children of all ages develop FHF each year in the United States, if all etiologies, including infections, drugs, inborn errors of metabolism, and unknown causes, are considered.

Acute liver failure in children is a potentially devastating disease. [15] The mortality rate may reach 80-90% in the absence of liver transplantation. In some pediatric series, survival rates of 50-75% have been reported.

Prognostic criteria include patient’s age, etiology of liver disease, degree and onset of encephalopathy, serum bilirubin level, prothrombin time (PT) or international normalized ratio (INR), serum creatinine level, factor V level, and arterial pH level.

Presence of jaundice for at least 1 week before the onset of encephalopathy is associated with a poor prognosis. Patients with illness lasting longer than 8 weeks before the onset of encephalopathy have a higher likelihood of developing portal hypertensive manifestations such as renal failure. Increased incidence of cerebral edema is associated with illness lasting fewer than 4 weeks before disease. Hemorrhagic diathesis and systemic collapse indicate a poor prognosis.

The maximum INR reached during the course of illness is a sensitive predictor of outcome. With an INR of 4 or more, the mortality rate reaches 86%; with an INR of less than 4, it is as low as 27%.

Children with FHF who have severe coagulopathy, prolonged duration of illness prior to the onset of encephalopathy, and lower alanine aminotransferase on admission are more likely to require liver transplantation. [16] Early referral to a specialized center for consideration of liver transplantation is vital in these patients. Shortage of organ donors affects survival rate.

Prognostic scoring systems still may fail to successfully establish an accurate prognosis in acute liver failure. Studies have been launched to evaluate the prognostic accuracy of the pediatric end-stage liver disease score in children with acute liver failure. Such a score may help establish the optimal timing for liver transplantation evaluation and listing. [17, 18, 19]

Increasing public awareness of potential hepatotoxins, including over-the-counter medications such as acetaminophen (ie, paracetamol) and ibuprofen, is essential. Despite an effective antidote, acetaminophen overdose remains a frequent cause of acute liver failure in children. [5]

For patient education information, see the Hepatitis Center and the Liver, Gallbladder, and Pancreas Center, as well as Hepatitis A, Hepatitis B, Hepatitis C, and Cirrhosis.

Hackl C, Schlitt HJ, Melter M, Knoppke B, Loss M. Current developments in pediatric liver transplantation. World J Hepatol. 2015 Jun 18. 7 (11):1509-20. [Medline].

Kirnap M, Akdur A, Ozcay F, Soy E, Yildirim S, Moray G, et al. Liver Transplant for Fulminant Hepatic Failure: A Single-Center Experience. Exp Clin Transplant. 2015 May 30. [Medline].

Gotthardt D, Riediger C, Weiss KH, Encke J, Schemmer P, Schmidt J, et al. Fulminant hepatic failure: etiology and indications for liver transplantation. Nephrol Dial Transplant. 2007 Sep. 22 Suppl 8:viii5-viii8. [Medline].

Jain J, Jain M. Atypical manifestations of viral hepatitis A and E. Trop Doct. 2013 Jan. 43(1):17-8. [Medline].

Furuichi M, Fujiwara T, Fukuda A, Kasahara M, Miyairi I. Fulminant hepatic failure as a risk factor for cytomegalovirus infection in children receiving preemptive therapy after living donor liver transplantation. Transplantation. 2016 Aug 5. [Medline].

Kumar KJ, Kumar HC, Manjunath VG, Anitha C, Mamatha S. Hepatitis A in children- clinical course, complications and laboratory profile. Indian J Pediatr. 2014 Jan. 81(1):15-9. [Medline].

El-Ashry R, Malek HA, Ghayaty EA, El-Gendy AA, Darwish A, Al-Tonbary Y. Treatment for hepatitis C virus-induced portal hypertension in leukemic children. Med Oncol. 2013. 30(2):559. [Medline].

Amin MD, Harpavat S, Leung DH. Drug-induced liver injury in children. Curr Opin Pediatr. 2015 Aug 13. [Medline].

Alonso EM, James LP, Zhang S, Squires RH, Pediatric Acute Liver Failure Study Group. Acetaminophen Adducts Detected in Serum of Pediatric Patients With Acute Liver Failure. J Pediatr Gastroenterol Nutr. 2015 Jul. 61 (1):102-7. [Medline].

Kasmi I, Sallabanda S, Kasmi G. Fulminate Hepatic Failure in a 5 Year Old Female after Inappropriate Acetaminophen Treatment. Open Access Maced J Med Sci. 2015 Sep 15. 3 (3):443-6. [Medline].

Nazer H, Larcher VF, Ede RJ, Mowat AP, Williams R. Wilson’s disease: a diagnostic dilemma. Br Med J (Clin Res Ed). 1983 Jul 30. 287(6388):313-4. [Medline]. [Full Text].

Nazer H, Ede RJ, Mowat AP, Williams R. Wilson’s disease in childhood. Variability of clinical presentation. Clin Pediatr (Phila). 1983 Nov. 22(11):755-7. [Medline].

Nazer H, Ede RJ, Mowat AP, Williams R. Wilson’s disease: clinical presentation and use of prognostic index. Gut. 1986 Nov. 27(11):1377-81. [Medline].

Kido J, Matsumoto S, Momosaki K, Sakamoto R, Mitsubuchi H, Inomata Y, et al. Plasma exchange and chelator therapy rescues acute liver failure in Wilson disease without liver transplantation. Hepatol Res. 2016 Mar 23. [Medline].

Cochran JB, Losek JD. Acute liver failure in children. Pediatr Emerg Care. 2007 Feb. 23(2):129-35. [Medline].

Lee WS, McKiernan P, Kelly DA. Etiology, outcome and prognostic indicators of childhood fulminant hepatic failure in the United kingdom. J Pediatr Gastroenterol Nutr. 2005 May. 40(5):575-81. [Medline].

El-Karaksy HM, El-Shabrawi MM, Mohsen NA, El-Koofy NM, El-Akel WA, Fahmy ME. Study of predictive value of pediatric risk of mortality (PRISM) score in children with end stage liver disease and fulminant hepatic failure. Indian J Pediatr. 2011 Mar. 78(3):301-6. [Medline].

Sanchez MC, D’Agostino DE. Pediatric end-stage liver disease score in acute liver failure to assess poor prognosis. J Pediatr Gastroenterol Nutr. 2012 Feb. 54(2):193-6. [Medline].

Wlodzimirow KA, Eslami S, Abu-Hanna A, Nieuwoudt M, Chamuleau RA. A systematic review on prognostic indicators of acute on chronic liver failure and their predictive value for mortality. Liver Int. 2013 Jan. 33(1):40-52. [Medline].

Baker A, Alonso ME, Aw MM, et al. Hepatic failure and liver transplant: Working Group report of the second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2004 Jun. 39 Suppl 2:S632-9. [Medline].

Dhawan A, Cheeseman P, Mieli-Vergani G. Approaches to acute liver failure in children. Pediatr Transplant. 2004 Dec. 8(6):584-8. [Medline].

Latif N, Mehmood K. Risk factors for fulminant hepatic failure and their relation with outcome in children. J Pak Med Assoc. 2010 Mar. 60(3):175-8. [Medline].

Alpert O, Sharma V, Cama S, Spencer S, Huang H. Liver transplant and quality of life in the pediatric population: a review update (2013-2014). Curr Opin Organ Transplant. 2015 Apr. 20 (2):216-21. [Medline].

Goss JA, Shackleton CR, Maggard M, et al. Liver transplantation for fulminant hepatic failure in the pediatric patient. Arch Surg. 1998 Aug. 133(8):839-46. [Medline].

Nakazawa A, Nakano N, Fukuda A, Sakamoto S, Imadome K, Kudo T, et al. Use of serial assessment of disease severity and liver biopsy for indication for liver transplantation in pediatric Epstein-Barr virus-induced fulminant hepatic failure. Liver Transpl. 2015 Mar. 21 (3):362-8. [Medline].

Baccarani U, Adani GL, Sainz M, et al. Human hepatocyte transplantation for acute liver failure: state of the art and analysis of cell sources. Transplant Proc. 2005 Jul-Aug. 37(6):2702-4. [Medline].

Lee HS, Choi GH, Joo DJ, Kim MS, Kim SI, Han KH, et al. Prognostic value of model for end-stage liver disease scores in patients with fulminant hepatic failure. Transplant Proc. 2013 Oct. 45(8):2992-4. [Medline].

Faraj W, Dar F, Bartlett A, Melendez HV, Marangoni G, Mukherji D, et al. Auxiliary liver transplantation for acute liver failure in children. Ann Surg. 2010 Feb. 251(2):351-6. [Medline].

Hattori H, Higuchi Y, Tsuji M, et al. Living-related liver transplantation and neurological outcome in children with fulminant hepatic failure. Transplantation. 1998 Mar 15. 65(5):686-92. [Medline].

Squires RH, Dhawan A, Alonso E, Narkewicz MR, Shneider BL, Rodriguez-Baez N, et al. Intravenous N-acetylcysteine in pediatric patients with non-acetaminophen acute liver failure: A placebo-controlled clinical trial. Hepatology. 2012 Aug 10. [Medline].

Hisham Nazer, MBBCh, FRCP, DTM&H Professor of Pediatrics, Consultant in Pediatric Gastroenterology, Hepatology and Clinical Nutrition, University of Jordan Faculty of Medicine, Jordan

Hisham Nazer, MBBCh, FRCP, DTM&H is a member of the following medical societies: American Association for Physician Leadership, Royal College of Paediatrics and Child Health, Royal College of Surgeons in Ireland, Royal Society of Tropical Medicine and Hygiene, Royal College of Physicians and Surgeons of the United Kingdom

Disclosure: Nothing to disclose.

Dena Nazer, MD, FAAP Assistant Professor of Pediatrics, Wayne State University School of Medicine; Chief, Child Protection Team, Children’s Hospital of Michigan

Dena Nazer, MD, FAAP is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Professional Society on the Abuse of Children, Ray E Helfer Society

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.

Carmen Cuffari, MD Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine

Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Prometheus Laboratories for speaking and teaching; Received honoraria from Abbott Nutritionals for speaking and teaching. for: Abbott Nutritional, Abbvie, speakers’ bureau.

Jayant Deodhar, MD Associate Professor in Pediatrics, BJ Medical College, India; Honorary Consultant, Departments of Pediatrics and Neonatology, King Edward Memorial Hospital, India

Disclosure: Nothing to disclose.

Pediatric Fulminant Hepatic Failure

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Pediatric Fulminant Hepatic Failure

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