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{{Acute liver failure}}
{{Acute liver failure}}
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{{CMG}} {{AE}} {{HS}}
==Overview==
==Overview==
Acute liver failure is a serious condition which can rapidly progress to death if left untreated. Complications of the illness include [[cerebral edema]], [[brain herniation]], [[multi-organ failure]], [[systemic inflammatory response syndrome]], [[metabolic derangements]], [[coagulopathy]], [[hemodynamic instability]], [[coma]], and [[death]].Several prognostic scoring systems have been devised to predict mortality and to identify who will require early liver transplant. Mortality due to acute liver failure used to be as high as 80%, however this statistic has decreased with the advent of liver transplantation, and better intensive care. There are several prognostic indicator scores used for the prediction of mortality, and to assess the suitability of the patient for transplantation. These include [[King's College Criteria|kings college hospital criteria]], [[Model for End-Stage Liver Disease|MELD score]], [[APACHE II]] and Clichy criteria.
Acute liver failure is a sudden and severe loss of liver function with evidence of [[encephalopathy]] and [[coagulopathy]] with elevated [[prothrombin time (PT)]] and [[INR|(INR)]] in a person without preexisting liver disease. The commonly used time duration for an acute liver disease is < 26 weeks. Acute liver failure can be hyperacute, acute or subacute depending upon how long the patient has signs and symptoms of liver failure. If left untreated, patients with acute liver failure can eventually progress to develop [[confusion]], [[Comatose|comatose state]], and death. Common complications of acute liver failure are [[hepatic encephalopathy]], [[cerebral edema]], [[coagulopathy]], a [[systemic inflammatory response syndrome]], [[acute renal failure]] and [[Pulmonary failure|acute pulmonary failure]]. The important factors in determining the prognosis of acute liver failure include patients' age, the severity of [[encephalopathy]] and the underlying cause of acute liver failure. The commonly used [[prognostic]] indicators to predict [[mortality]] in patients with acute liver failure and to identify patients who are likely to benefit from [[liver transplantation]] include kings college criteria ( used for [[liver transplantation]] ) and [[Model for end stage liver disease|model for end-stage liver disease]] ([[MELD]]) score (to predict mortality in patients with chronic and acute liver disease).
==Natural History==
Acute liver failure is a sudden and severe loss of liver function with evidence of [[encephalopathy]] and [[coagulopathy]] with elevated [[prothrombin time (PT)]] and [[INR|(INR)]] in a person without preexisting liver disease. The commonly used time duration for an acute liver disease is < 26 weeks.<ref name="pmid17608778">{{cite journal| author=Bower WA, Johns M, Margolis HS, Williams IT, Bell BP| title=Population-based surveillance for acute liver failure. | journal=Am J Gastroenterol | year= 2007 | volume= 102 | issue= 11 | pages= 2459-63 | pmid=17608778 | doi=10.1111/j.1572-0241.2007.01388.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17608778  }} </ref>
* Acute liver failure can be hyperacute, acute or subacute depending upon how long the patient has signs and symptoms of liver failure.
* The natural history of acute liver failure depends on the etiology but generally, [[cerebral edema]] mainly presents in hyperacute or acute liver failure, whereas [[Renal failure|renal shutdown]] and [[portal hypertension]] are the main concerns in the subacute liver failure.
* If left untreated, patients with acute liver failure may initially having nonspecific symptoms such as [[anorexia]], [[fatigue]], [[Nausea and vomiting case study one|nausea and vomiting]], diffuse or [[Right upper quadrant abdominal pain resident survival guide|right upper quadrant abdominal pain]] or [[jaundice]] and can eventually progress to develop [[confusion]] and the [[comatose]] state and death.  A [[systemic inflammatory response syndrome]] may also develop. [[Acute renal failure]] occurs in up to 50% of cases. The condition can also worsen to the point of causing [[Hemodynamics|hemodynamic]] and [[cardiovascular]] compromise.
* The timely recognition and treatment of some of the causes of acute liver failure can reverse the condition and may improve the patient's prognosis. The timely evaluation can also help in identifying patients who may require [[Liver transplantation|liver transplantation.]]  
* In [[acetaminophen toxicity]] patients, the time duration between [[acetaminophen]] ingestion and treatment with [[acetylcysteine]] greatly influence the outcome.


==Natural History==
In acute liver failure, [[cerebral edema]] leads to [[hepatic encephalopathy]], [[coma]], [[brain herniation]] and eventually death. A systemic inflammatory reponse syndrome may also develop. [[Acute renal failure]] occurs in up to 50% of cases. The condition can also worsen to the point of causing hemodynamic and cardiovascular compromise.
==Complications==
==Complications==
====Cerebral Edema and Encephalopathy====
Complications that can develop as a result of acute liver failure are:<ref name="pmid20196116">{{cite journal| author=Kumar R, Shalimar. Bhatia V, Khanal S, Sreenivas V, Gupta SD et al.| title=Antituberculosis therapy-induced acute liver failure: magnitude, profile, prognosis, and predictors of outcome. | journal=Hepatology | year= 2010 | volume= 51 | issue= 5 | pages= 1665-74 | pmid=20196116 | doi=10.1002/hep.23534 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20196116  }} </ref><ref name="pmid9250851">{{cite journal |vauthors=Riordan SM, Williams R |title=Treatment of hepatic encephalopathy |journal=N. Engl. J. Med. |volume=337 |issue=7 |pages=473–9 |year=1997 |pmid=9250851 |doi=10.1056/NEJM199708143370707 |url=}}</ref><ref name="pmid8305063">{{cite journal |vauthors=Lee WM |title=Acute liver failure |journal=N. Engl. J. Med. |volume=329 |issue=25 |pages=1862–72 |year=1993 |pmid=8305063 |doi=10.1056/NEJM199312163292508 |url=}}</ref><ref name="pmid8303321">{{cite journal |vauthors=Muñoz SJ |title=Difficult management problems in fulminant hepatic failure |journal=Semin. Liver Dis. |volume=13 |issue=4 |pages=395–413 |year=1993 |pmid=8303321 |doi= |url=}}</ref><ref>{{cite journal |author=Hazell AS, Butterworth RF |title=Hepatic encephalopathy: An update of pathophysiologic mechanisms |journal=Proc. Soc. Exp. Biol. Med. |volume=222 |issue=2 |pages=99-112 |year=1999 |pmid=10564534 |doi=}}</ref><ref>{{cite journal |author=Larsen FS, Wendon J |title=Brain edema in liver failure: basic physiologic principles and management |journal=Liver Transpl. |volume=8 |issue=11 |pages=983-9 |year=2002 |pmid=12424710 |doi=10.1053/jlts.2002.35779}}</ref><ref>{{cite journal |author=Armstrong IR, Pollok A, Lee A |title=Complications of intracranial pressure monitoring in fulminant hepatic failure |journal=Lancet |volume=341 |issue=8846 |pages=690-1 |year=1993 |pmid=8095592 |doi=}}</ref><ref>{{cite journal |author=Schmidt LE, Larsen FS |title=Prognostic implications of [[Lactate|hyperlactatemia]], multiple organ failure, and systemic inflammatory response syndrome in patients with acetaminophen-induced acute liver failure |journal=Crit. Care Med. |volume=34 |issue=2 |pages=337-43 |year=2006 |pmid=16424712 |doi=}}</ref><ref>{{cite journal |author=Harry R, Auzinger G, Wendon J |title=The clinical importance of adrenal insufficiency in acute hepatic dysfunction |journal=Hepatology |volume=36 |issue=2 |pages=395-402 |year=2002 |pmid=12143048 |doi=10.1053/jhep.2002.34514}}</ref><ref>{{cite journal |author=Bihari D, Gimson AE, Waterson M, Williams R |title=Tissue hypoxia during fulminant hepatic failure |journal=Crit. Care Med. |volume=13 |issue=12 |pages=1034-9 |year=1985 |pmid=3933911 |doi=}}</ref><ref>{{cite journal |author=Trewby PN, Warren R, Contini S, ''et al'' |title=Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure |journal=Gastroenterology |volume=74 |issue=5 Pt 1 |pages=859-65 |year=1978 |pmid=346431 |doi=}}</ref>
Complications of acute liver failure can include [[cerebral edema]], [[hepatic encephalopathy]], [[brain herniation]] and [[death]]. Detection of encephalopathy is central to the diagnosis of ALF. It may vary from subtle defecit in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV). Patients presenting as acute and hyperacute liver failure are at greater risk of developing cerebral oedema and grade IV encephalopathy. The [[pathogenesis]] remains unclear but is likely to be a consequence of several phenomena. There is a build up of toxic substances like [[ammonia]], [[Thiol|mercaptan]], endogenous [[benzodiazepines]] and [[serotonin]]/[[tryptophan]] in the brain. This affects [[neurotransmitter]] level and [[neuroreceptor]] activation. Autoregulation of cerebral blood flow is impaired and is associated with [[Fermentation (biochemistry)|anaerobic glycolysis]] and [[oxidative stress]]. Neuronal cell [[astrocyte]]s are susceptible to these changes and they swell up, resulting in increased intracranial pressure. Inflammatory mediators also play important role<ref>{{cite journal |author=Hazell AS, Butterworth RF |title=Hepatic encephalopathy: An update of pathophysiologic mechanisms |journal=Proc. Soc. Exp. Biol. Med. |volume=222 |issue=2 |pages=99-112 |year=1999 |pmid=10564534 |doi=}}</ref><ref>{{cite journal |author=Larsen FS, Wendon J |title=Brain edema in liver failure: basic physiologic principles and management |journal=Liver Transpl. |volume=8 |issue=11 |pages=983-9 |year=2002 |pmid=12424710 |doi=10.1053/jlts.2002.35779}}</ref>.
* [[Cerebral edema]]
* [[Encephalopathy]]
* [[Coagulopathy]]
* [[Renal failure]]
* [[Renal failure]]
* [[Systemic inflammatory response syndrome|Systemic inflammatory response]]
* Metabolic derrangements
* [[Pulmonary]] complications


Unfortunately, signs of elevated [[intracranial pressure]] such as [[Papilledema|papilloedema]] and loss of [[pupil]]lary reflexes are not reliable and occur late in the disease process. [[Computed tomography|CT]] imaging of the brain is also unhelpful in detecting early cerebral oedema but is often performed to rule out [[Intracranial_hemorrhage|intra-cerebral bleeding]]. Invasive intracranial pressure monitoring via [[Dura mater|subdural]] route is often recommended, however the risk of complications must be weighed against the possible
==Prognosis==
benefit (1% fatal haemorrhage).<ref>{{cite journal |author=Armstrong IR, Pollok A, Lee A |title=Complications of intracranial pressure monitoring in fulminant hepatic failure |journal=Lancet |volume=341 |issue=8846 |pages=690-1 |year=1993 |pmid=8095592 |doi=}}</ref> The aim is to maintain intracranial pressures below 25 mmHg, cerebral perfusion pressures above 50 mm Hg.  
* The important factors in determining the prognosis of acute liver failure include patients' age, the severity of [[encephalopathy]] and the underlying cause of acute liver failure.<ref name="pmid9635624">{{cite journal |vauthors=Dhiman RK, Seth AK, Jain S, Chawla YK, Dilawari JB |title=Prognostic evaluation of early indicators in fulminant hepatic failure by multivariate analysis |journal=Dig. Dis. Sci. |volume=43 |issue=6 |pages=1311–6 |year=1998 |pmid=9635624 |doi= |url=}}</ref><ref name="pmid8792311">{{cite journal |vauthors=Huo TI, Wu JC, Sheng WY, Chan CY, Hwang SJ, Chen TZ, Lee SD |title=Prognostic factor analysis of fulminant and subfulminant hepatic failure in an area endemic for hepatitis B |journal=J. Gastroenterol. Hepatol. |volume=11 |issue=6 |pages=560–5 |year=1996 |pmid=8792311 |doi= |url=}}</ref><ref name="pmid8175127">{{cite journal |vauthors=Takahashi Y, Kumada H, Shimizu M, Tanikawa K, Kumashiro R, Omata M, Ehata T, Tsuji T, Ukida M, Yasunaga M |title=A multicenter study on the prognosis of fulminant viral hepatitis: early prediction for liver transplantation |journal=Hepatology |volume=19 |issue=5 |pages=1065–71 |year=1994 |pmid=8175127 |doi= |url=}}</ref><ref name="pmid7875687">{{cite journal |vauthors=Lake JR, Sussman NL |title=Determining prognosis in patients with fulminant hepatic failure: when you absolutely, positively have to know the answer |journal=Hepatology |volume=21 |issue=3 |pages=879–82 |year=1995 |pmid=7875687 |doi= |url=}}</ref><ref name="pmid8445211">{{cite journal |vauthors=Pauwels A, Mostefa-Kara N, Florent C, Lévy VG |title=Emergency liver transplantation for acute liver failure. Evaluation of London and Clichy criteria |journal=J. Hepatol. |volume=17 |issue=1 |pages=124–7 |year=1993 |pmid=8445211 |doi= |url=}}</ref><ref name="pmid22885329">{{cite journal |vauthors=Rutherford A, King LY, Hynan LS, Vedvyas C, Lin W, Lee WM, Chung RT |title=Development of an accurate index for predicting outcomes of patients with acute liver failure |journal=Gastroenterology |volume=143 |issue=5 |pages=1237–43 |year=2012 |pmid=22885329 |pmc=3480539 |doi=10.1053/j.gastro.2012.07.113 |url=}}</ref>


====Coagulopathy====
* Several [[prognostic]] scoring systems to predict [[mortality]] in patients with acute liver failure and to identify patients who are likely to benefit from liver transplantation include:
[[Coagulopathy]] is another cardinal feature of ALF. Liver has central role in synthesis of almost all coagulation factors and some inhibitors of [[coagulation]] and [[fibrinolysis]]. Hepatocellular [[necrosis]] leads to impaired [[synthesis]] of many [[Coagulation|coagulation factors]] and their inhibitors. the former produces a prolongation in [[Prothrombin time]] which is widely used to monitor severity of [[hepatic]] injury.There is significant platelet dysfunction (with both quantitative and qualitative platelet defects). Progressive [[thrombocytopenia]] with loss of larger and more active [[platelet]] is almost universal. Thrombocytopenia with or without [[disseminated intravascular coagulation|DIC]] increases risk of intracerebral bleeding<ref name="gimson"/>.
===Renal Failure===
[[Renal failure]] is common, present in more than 50% of ALF patients, either due to original insult such as paracetamol resulting in [[acute tubular necrosis]] or from [[hyperdynamic circulation]] leading to [[hepatorenal syndrome]] or functional renal failure. Because of impaired production of urea, blood urea do not represent degree of renal impairment.
====Inflammation and Infection====
About 60% of all ALF patients fulfil the criteria for [[Systemic inflammatory response syndrome|systemic inflammatory syndrome]] irrespective of presence or absence of infection<ref>{{cite journal |author=Schmidt LE, Larsen FS |title=Prognostic implications of [[Lactate|hyperlactatemia]], multiple organ failure, and systemic inflammatory response syndrome in patients with acetaminophen-induced acute liver failure |journal=Crit. Care Med. |volume=34 |issue=2 |pages=337-43 |year=2006 |pmid=16424712 |doi=}}</ref>. This often contributes towards [[Multiple organ dysfunction syndrome|multi organ failure]]. Impaired host defence mechanism due to impaired [[Opsonin|opsonisation]], [[chemotaxis]] and intracellular killing substantially increase risk of sepsis. Bacterial sepsis mostly due to [[Gram-positive bacteria|gram positive]] organisms and fungal sepsis are observed in up to 80% and 30% patients respectively<ref name="gimson">{{cite journal |author=Gimson AE |title=Fulminant and late onset hepatic failure |journal=British journal of anaesthesia |volume=77 |issue=1 |pages=90-8 |year=1996 |pmid=8703634 |doi=}}</ref>.
====Metabolic Derangements====
[[Hyponatraemia]] is almost universal finding due to water retention and shift in [[intracellular]] sodium transport from inhibition of [[Na+/K+-ATPase|Na/K ATPase]]. [[Hypoglycaemia]] (due to depleted hepatic [[glycogen]] store and [[insulin|hyperinsulinaemia]]), [[hypokalaemia]], [[hypophosphataemia]] and [[Metabolic alkalosis]] are often present independent of renal function. [[Lactic acidosis]] occurs predominantly in paracetamol overdose. 
====Hemodynamic and Cardio-respiratory Compromise====
[[Hyperdynamic circulation]] with peripheral [[vasodilator|vasodilatation]] from low [[systemic vascular resistance]] leads to [[hypotension]]. There is a compensatory increase in [[cardiac output]]. [[Adrenal insufficiency]] has been documented in 60% of ALF and is likely to contribute in haemodynamic compromise<ref>{{cite journal |author=Harry R, Auzinger G, Wendon J |title=The clinical importance of adrenal insufficiency in acute hepatic dysfunction |journal=Hepatology |volume=36 |issue=2 |pages=395-402 |year=2002 |pmid=12143048 |doi=10.1053/jhep.2002.34514}}</ref>. There is also abnormal [[oxygen]] transport and utilization. Although delivery of oxygen to the tissues is adequate, there is a decrease in tissue oxygen uptake, resulting in [[tissue]] [[hypoxia]] and lactic acidosis<ref>{{cite journal |author=Bihari D, Gimson AE, Waterson M, Williams R |title=Tissue hypoxia during fulminant hepatic failure |journal=Crit. Care Med. |volume=13 |issue=12 |pages=1034-9 |year=1985 |pmid=3933911 |doi=}}</ref>.


[[Pulmonary]] complications occur in up to 50% patients<ref>{{cite journal |author=Trewby PN, Warren R, Contini S, ''et al'' |title=Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure |journal=Gastroenterology |volume=74 |issue=5 Pt 1 |pages=859-65 |year=1978 |pmid=346431 |doi=}}</ref>. Severe lung injury and [[hypoxemia]] result in high mortality. Most cases of severe lung injury is due to [[ARDS]] with or without[[ sepsis]]. Pulmonary [[haemorrhage]], [[pleural effusion]]s, [[atelectasis]], and intrapulmonary shunts also contribute to respiratory difficulty.
**[[King's College Criteria]] (mostly used for [[liver transplantation]])
**[[Model for End-Stage Liver Disease]] ([[MELD]]) score (used to predict mortality in patients with chronic and acute liver disease)
**Sequential Organ Failure Assessment (SOFA score)
**Clichy criteria
**Acute Liver Failure Study Group (ALFSG) index


==Prognosis==
==References==
Historically mortality has been unacceptably high, being in excess of 80%<ref>{{cite journal |author=Rakela J, Lange SM, Ludwig J, Baldus WP |title=Fulminant hepatitis: Mayo Clinic experience with 34 cases |journal=Mayo Clin. Proc. |volume=60 |issue=5 |pages=289-92 |year=1985 |pmid=3921780 |doi=}}</ref>. In recent years the advent of liver transplantation and multidisciplinary intensive care support have improved survival significantly. At present overall short term survival with transplant is more than 65%<ref>{{cite journal |author=Ostapowicz G, Fontana RJ, Schiødt FV, ''et al'' |title=Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States |journal=Ann. Intern. Med. |volume=137 |issue=12 |pages=947-54 |year=2002 |pmid=12484709 |doi=}}</ref>.
{{Reflist|2}}


Several prognostic scoring systems have been devised to predict mortality and to identify who will require early liver transplant. These include [[King's College Criteria|kings college hospital criteria]], [[Model for End-Stage Liver Disease|MELD score]], [[APACHE II]] and Clichy criteria.
[[Category:Hepatology]]
[[Category:Gastroenterology]]


==References==
{{reflist|2}}
{{WH}}
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[[Category:Organ failure]]
[[Category:Causes of death]]
[[Category:Hepatology]]
[[Category:Gastroenterology]]
[[Category:Intensive care medicine]]

Latest revision as of 20:54, 18 December 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Husnain Shaukat, M.D [2]

Overview

Acute liver failure is a sudden and severe loss of liver function with evidence of encephalopathy and coagulopathy with elevated prothrombin time (PT) and (INR) in a person without preexisting liver disease. The commonly used time duration for an acute liver disease is < 26 weeks. Acute liver failure can be hyperacute, acute or subacute depending upon how long the patient has signs and symptoms of liver failure. If left untreated, patients with acute liver failure can eventually progress to develop confusion, comatose state, and death. Common complications of acute liver failure are hepatic encephalopathy, cerebral edema, coagulopathy, a systemic inflammatory response syndrome, acute renal failure and acute pulmonary failure. The important factors in determining the prognosis of acute liver failure include patients' age, the severity of encephalopathy and the underlying cause of acute liver failure. The commonly used prognostic indicators to predict mortality in patients with acute liver failure and to identify patients who are likely to benefit from liver transplantation include kings college criteria ( used for liver transplantation ) and model for end-stage liver disease (MELD) score (to predict mortality in patients with chronic and acute liver disease).

Natural History

Acute liver failure is a sudden and severe loss of liver function with evidence of encephalopathy and coagulopathy with elevated prothrombin time (PT) and (INR) in a person without preexisting liver disease. The commonly used time duration for an acute liver disease is < 26 weeks.[1]

Complications

Complications that can develop as a result of acute liver failure are:[2][3][4][5][6][7][8][9][10][11][12]

Prognosis

  • The important factors in determining the prognosis of acute liver failure include patients' age, the severity of encephalopathy and the underlying cause of acute liver failure.[13][14][15][16][17][18]
  • Several prognostic scoring systems to predict mortality in patients with acute liver failure and to identify patients who are likely to benefit from liver transplantation include:

References

  1. ↑ Bower WA, Johns M, Margolis HS, Williams IT, Bell BP (2007). "Population-based surveillance for acute liver failure". Am J Gastroenterol. 102 (11): 2459–63. doi:10.1111/j.1572-0241.2007.01388.x. PMID 17608778.
  2. ↑ Kumar R, Shalimar. Bhatia V, Khanal S, Sreenivas V, Gupta SD; et al. (2010). "Antituberculosis therapy-induced acute liver failure: magnitude, profile, prognosis, and predictors of outcome". Hepatology. 51 (5): 1665–74. doi:10.1002/hep.23534. PMID 20196116.
  3. ↑ Riordan SM, Williams R (1997). "Treatment of hepatic encephalopathy". N. Engl. J. Med. 337 (7): 473–9. doi:10.1056/NEJM199708143370707. PMID 9250851.
  4. ↑ Lee WM (1993). "Acute liver failure". N. Engl. J. Med. 329 (25): 1862–72. doi:10.1056/NEJM199312163292508. PMID 8305063.
  5. ↑ Muñoz SJ (1993). "Difficult management problems in fulminant hepatic failure". Semin. Liver Dis. 13 (4): 395–413. PMID 8303321.
  6. ↑ Hazell AS, Butterworth RF (1999). "Hepatic encephalopathy: An update of pathophysiologic mechanisms". Proc. Soc. Exp. Biol. Med. 222 (2): 99–112. PMID 10564534.
  7. ↑ Larsen FS, Wendon J (2002). "Brain edema in liver failure: basic physiologic principles and management". Liver Transpl. 8 (11): 983–9. doi:10.1053/jlts.2002.35779. PMID 12424710.
  8. ↑ Armstrong IR, Pollok A, Lee A (1993). "Complications of intracranial pressure monitoring in fulminant hepatic failure". Lancet. 341 (8846): 690–1. PMID 8095592.
  9. ↑ Schmidt LE, Larsen FS (2006). "hyperlactatemia". Crit. Care Med. 34 (2): 337–43. PMID 16424712.
  10. ↑ Harry R, Auzinger G, Wendon J (2002). "The clinical importance of adrenal insufficiency in acute hepatic dysfunction". Hepatology. 36 (2): 395–402. doi:10.1053/jhep.2002.34514. PMID 12143048.
  11. ↑ Bihari D, Gimson AE, Waterson M, Williams R (1985). "Tissue hypoxia during fulminant hepatic failure". Crit. Care Med. 13 (12): 1034–9. PMID 3933911.
  12. ↑ Trewby PN, Warren R, Contini S; et al. (1978). "Incidence and pathophysiology of pulmonary edema in fulminant hepatic failure". Gastroenterology. 74 (5 Pt 1): 859–65. PMID 346431.
  13. ↑ Dhiman RK, Seth AK, Jain S, Chawla YK, Dilawari JB (1998). "Prognostic evaluation of early indicators in fulminant hepatic failure by multivariate analysis". Dig. Dis. Sci. 43 (6): 1311–6. PMID 9635624.
  14. ↑ Huo TI, Wu JC, Sheng WY, Chan CY, Hwang SJ, Chen TZ, Lee SD (1996). "Prognostic factor analysis of fulminant and subfulminant hepatic failure in an area endemic for hepatitis B". J. Gastroenterol. Hepatol. 11 (6): 560–5. PMID 8792311.
  15. ↑ Takahashi Y, Kumada H, Shimizu M, Tanikawa K, Kumashiro R, Omata M, Ehata T, Tsuji T, Ukida M, Yasunaga M (1994). "A multicenter study on the prognosis of fulminant viral hepatitis: early prediction for liver transplantation". Hepatology. 19 (5): 1065–71. PMID 8175127.
  16. ↑ Lake JR, Sussman NL (1995). "Determining prognosis in patients with fulminant hepatic failure: when you absolutely, positively have to know the answer". Hepatology. 21 (3): 879–82. PMID 7875687.
  17. ↑ Pauwels A, Mostefa-Kara N, Florent C, Lévy VG (1993). "Emergency liver transplantation for acute liver failure. Evaluation of London and Clichy criteria". J. Hepatol. 17 (1): 124–7. PMID 8445211.
  18. ↑ Rutherford A, King LY, Hynan LS, Vedvyas C, Lin W, Lee WM, Chung RT (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.

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