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* '''[[Acute liver failure]]''' - development of [[hepatic encephalopathy]] (confusion, stupor and coma) and decreased production of [[protein]]s (such as [[human serum albumin|albumin]] and [[coagulation|blood clotting proteins]]) within four weeks of the first symptoms (such as [[jaundice]]) of a liver problem. [["Hyperacute"]] liver failure is said to be present if this interval is 7 days or less, while [["subacute"]] liver failure is said to be present if the interval is 5-12 weeks.<ref name="pmid8101303">{{cite journal |vauthors=O'Grady JG, Schalm SW, Williams R |title=Acute liver failure: redefining the syndromes |journal=Lancet |volume=342 |issue=8866 |pages=273–5 |date=July 1993 |pmid=8101303 |doi=10.1016/0140-6736(93)91818-7 |url=}}</ref> | * '''[[Acute liver failure]]''' - development of [[hepatic encephalopathy]] (confusion, stupor and coma) and decreased production of [[protein]]s (such as [[human serum albumin|albumin]] and [[coagulation|blood clotting proteins]]) within four weeks of the first symptoms (such as [[jaundice]]) of a liver problem. [["Hyperacute"]] liver failure is said to be present if this interval is 7 days or less, while [["subacute"]] liver failure is said to be present if the interval is 5-12 weeks.<ref name="pmid8101303">{{cite journal |vauthors=O'Grady JG, Schalm SW, Williams R |title=Acute liver failure: redefining the syndromes |journal=Lancet |volume=342 |issue=8866 |pages=273–5 |date=July 1993 |pmid=8101303 |doi=10.1016/0140-6736(93)91818-7 |url=}}</ref> | ||
* '''[[Chronic liver failure]]''' - usually occurs in the context of '''[[cirrhosis]]''', itself potentially the result of many possible causes, such as excessive [[alcoholic beverage|alcohol]] intake, [[hepatitis B]] or [[hepatitis C|C]], autoimmune, hereditary and metabolic causes (such as [[hemochromatosis|iron]] or [[Wilson's disease|copper]] overload or [[non-alcoholic fatty liver disease]]). | * '''[[Chronic liver failure]]''' - usually occurs in the context of '''[[cirrhosis]]''', itself potentially the result of many possible causes, such as excessive [[alcoholic beverage|alcohol]] intake, [[hepatitis B]] or [[hepatitis C|C]], autoimmune, hereditary and metabolic causes (such as [[hemochromatosis|iron]] or [[Wilson's disease|copper]] overload or [[non-alcoholic fatty liver disease]]).[[Encephalopathy]] develops after 6 months. | ||
* '''[[Acute on Chronic Liver Failure]]''' - when acute hepatic decompensation observed in patients with preexisting [[chronic liver disease]] characterized by one or more extrahepatic organ failures with a significantly increased risk of death.<ref name="pmid23474284">{{cite journal |vauthors=Moreau R, Jalan R, Gines P, Pavesi M, Angeli P, Cordoba J, Durand F, Gustot T, Saliba F, Domenicali M, Gerbes A, Wendon J, Alessandria C, Laleman W, Zeuzem S, Trebicka J, Bernardi M, Arroyo V |title=Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis |journal=Gastroenterology |volume=144 |issue=7 |pages=1426–37, 1437.e1–9 |date=June 2013 |pmid=23474284 |doi=10.1053/j.gastro.2013.02.042 |url=}}</ref> | * '''[[Acute on Chronic Liver Failure]]''' - when acute hepatic decompensation observed in patients with preexisting [[chronic liver disease]] characterized by one or more extrahepatic organ failures with a significantly increased risk of death.<ref name="pmid23474284">{{cite journal |vauthors=Moreau R, Jalan R, Gines P, Pavesi M, Angeli P, Cordoba J, Durand F, Gustot T, Saliba F, Domenicali M, Gerbes A, Wendon J, Alessandria C, Laleman W, Zeuzem S, Trebicka J, Bernardi M, Arroyo V |title=Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis |journal=Gastroenterology |volume=144 |issue=7 |pages=1426–37, 1437.e1–9 |date=June 2013 |pmid=23474284 |doi=10.1053/j.gastro.2013.02.042 |url=}}</ref> | ||
Revision as of 22:08, 30 July 2020
| Hepatic failure | |
| ICD-10 | K72.9 |
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| DiseasesDB | 5728 |
| MeSH | D017093 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: Liver failure; fulminating hepatic failure
Overview
Liver failure is the inability of the liver to perform its normal synthetic and metabolic function as part of normal physiology.
Historical Perspective
- The original definition of Acute liver failure by Trey and Davidson was in 1959.[1]
- In the late 1980s and early 1990s, more terminologies of Acute liver failure proposed in.[2][3]
- Term of Acute-on-chronic Liver failure suggested by Jalan and willimas in 2002.[4]
Classification
Three forms are recognized:
- Acute liver failure - development of hepatic encephalopathy (confusion, stupor and coma) and decreased production of proteins (such as albumin and blood clotting proteins) within four weeks of the first symptoms (such as jaundice) of a liver problem. "Hyperacute" liver failure is said to be present if this interval is 7 days or less, while "subacute" liver failure is said to be present if the interval is 5-12 weeks.[3]
- Chronic liver failure - usually occurs in the context of cirrhosis, itself potentially the result of many possible causes, such as excessive alcohol intake, hepatitis B or C, autoimmune, hereditary and metabolic causes (such as iron or copper overload or non-alcoholic fatty liver disease).Encephalopathy develops after 6 months.
- Acute on Chronic Liver Failure - when acute hepatic decompensation observed in patients with preexisting chronic liver disease characterized by one or more extrahepatic organ failures with a significantly increased risk of death.[5]
Pathophysiology
- The pathophysiology depends on the etiology of the Acute liver failure.
- Most cases of Acute liver failure (except acute fatty liver of pregnancy and Reye syndrome) will have massive hepatocyte necrosis and/or apoptosis leading to liver failure. Hepatocyte necrosis occurs due to ATP depletion causing cellular swelling and cell membrane disruption.
- The pathophysiology of cerebral edema and hepatic encephalopathy is seen in Acute Liver Failure is multi-factorial and includes altered blood-brain barrier secondary to inflammatory mediators leading to microglial activation, accumulation of glutamine secondary to ammonia crossing the BBB and subsequent oxidative stress leading to depletion of adenosine triphosphate (ATP) and guanosine triphosphate (GTP). This ultimately leads to astrocyte swelling and cerebral edema.
- Chronic liver failure is the result of Cirrhosis which is is an advanced stage of liver fibrosis that is accompanied by distortion of the hepatic vasculature.[6]
Causes
Etiology of Acute Liver disease
Viruses
- Hepatitis A virus
- Hepatitis B virus ± delta virus
- Hepatitis E virus
- Herpes simplex virus
- Varicella-zoster virus
- Cytomegalovirus
- Epstein-Barr virus
- Human herpesvirus-6
- Adenovirus, Coxsackie B virus,
- hemorrhagic fever virus
Drugs
- Beractant
- Carfilzomib
- Caspofungin acetate
- Cefadroxil
- Ceftazidime
- Chlordiazepoxide
- Dactinomycin
- diclofenac (patch)
- Didanosine
- Diflunisal
- Efavirenz
- Fulvestrant
- gadoxetate
- Gemcitabine
- Indinavir
- Interferon gamma
- Ixabepilone
- Meropenem
- Micafungin sodium
- Nitisinone
- Oxaprozin
- Oxazepam
- Sorafenib
- Sulfasalazine
- Trovafloxacin mesylate
- Zafirlukast
Metabolic Disease
Toxins
Cardiovascular disease
Autoimmune diseases
Malignant infiltration
Differential Diagnosis
Autoimmune hepatitis must be differentiated from other diseases that cause jaundice, nausea and vomiting, abdominal pain, arthragia, and hepatomegaly such as Hepatitis A,B,C, E, drug induced hepatitis, CMV hepatitis, EBV hepatitis, alcoholic hepatitis, Primary biliary cirrhosis and Primary sclerosing cholangitis.[7][8][9][10][11][12][13][14][15]
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Prognosis
The King's College criteria (KCC) may be used.
Contraindicated medications
Severe hepatic failure is considered an absolute contraindication to the use of the following medications:
- Carvedilol
- Conjugated estrogens/bazedoxifene
- Diclofenamide
- Dronedarone
- Nebivolol
- Rosuvastatin
- Simvastatin
- Spironolactone
- Sulfamethoxazole/Trimethoprim
- Doxorubicin Hydrochloride
- Tipranavir
The ALFSG index is a newer option that may be more accurate.[16]
References
- ↑ Riordan SM, Williams R (May 2008). "Perspectives on liver failure: past and future". Semin. Liver Dis. 28 (2): 137–41. doi:10.1055/s-2008-1073113. PMID 18452113.
- ↑ Bernuau J, Rueff B, Benhamou JP (May 1986). "Fulminant and subfulminant liver failure: definitions and causes". Semin. Liver Dis. 6 (2): 97–106. doi:10.1055/s-2008-1040593. PMID 3529410.
- ↑ 3.0 3.1 O'Grady JG, Schalm SW, Williams R (July 1993). "Acute liver failure: redefining the syndromes". Lancet. 342 (8866): 273–5. doi:10.1016/0140-6736(93)91818-7. PMID 8101303.
- ↑ Jalan R, Williams R (2002). "Acute-on-chronic liver failure: pathophysiological basis of therapeutic options". Blood Purif. 20 (3): 252–61. doi:10.1159/000047017. PMID 11867872.
- ↑ Moreau R, Jalan R, Gines P, Pavesi M, Angeli P, Cordoba J, Durand F, Gustot T, Saliba F, Domenicali M, Gerbes A, Wendon J, Alessandria C, Laleman W, Zeuzem S, Trebicka J, Bernardi M, Arroyo V (June 2013). "Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis". Gastroenterology. 144 (7): 1426–37, 1437.e1–9. doi:10.1053/j.gastro.2013.02.042. PMID 23474284.
- ↑ Schuppan D, Afdhal NH (March 2008). "Liver cirrhosis". Lancet. 371 (9615): 838–51. doi:10.1016/S0140-6736(08)60383-9. PMC 2271178. PMID 18328931.
- ↑ Selmi C, Bowlus CL, Gershwin ME, Coppel RL (2011). "Primary biliary cirrhosis". Lancet. 377 (9777): 1600–9. doi:10.1016/S0140-6736(10)61965-4. PMID 21529926.
- ↑ Lindor KD, Gershwin ME, Poupon R, Kaplan M, Bergasa NV, Heathcote EJ (2009). "Primary biliary cirrhosis". Hepatology. 50 (1): 291–308. doi:10.1002/hep.22906. PMID 19554543.
- ↑ Koff RS (1998). "Hepatitis A". Lancet. 351 (9116): 1643–9. doi:10.1016/S0140-6736(98)01304-X. PMID 9620732.
- ↑ Ciocca M (2000). "Clinical course and consequences of hepatitis A infection". Vaccine. 18 Suppl 1: S71–4. PMID 10683554.
- ↑ Fargo MV, Grogan SP, Saguil A (2017). "Evaluation of Jaundice in Adults". Am Fam Physician. 95 (3): 164–168. PMID 28145671.
- ↑ Leevy CB, Koneru B, Klein KM (1997). "Recurrent familial prolonged intrahepatic cholestasis of pregnancy associated with chronic liver disease". Gastroenterology. 113 (3): 966–72. PMID 9287990.
- ↑ Hov JR, Boberg KM, Karlsen TH (2008). "Autoantibodies in primary sclerosing cholangitis". World J. Gastroenterol. 14 (24): 3781–91. PMC 2721433. PMID 18609700.
- ↑ Bond LR, Hatty SR, Horn ME, Dick M, Meire HB, Bellingham AJ (1987). "Gall stones in sickle cell disease in the United Kingdom". Br Med J (Clin Res Ed). 295 (6592): 234–6. PMC 1247079. PMID 3115390.
- ↑ Malakouti M, Kataria A, Ali SK, Schenker S (2017). "Elevated Liver Enzymes in Asymptomatic Patients - What Should I Do?". J Clin Transl Hepatol. 5 (4): 394–403. doi:10.14218/JCTH.2017.00027. PMC 5719197. PMID 29226106.
- ↑ Rutherford A, King LY, Hynan LS, Vedvyas C, Lin W, Lee WM; et al. (2012). "Development of an accurate index for predicting outcomes of patients with acute liver failure". Gastroenterology. 143 (5): 1237–43. doi:10.1053/j.gastro.2012.07.113. PMC 3480539. PMID 22885329.