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{{Acute liver failure}}
{{Acute liver failure}}
{{CMG}} {{AE}}
{{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==
==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.
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.
* 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 shutdown and portal hypertension are the main concerns in the subacute 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 or vomiting, diffuse or 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 hemodynamic and cardiovascular compromise.
* 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.  
* 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.
* In [[acetaminophen toxicity]] patients, the time duration between [[acetaminophen]] ingestion and treatment with [[acetylcysteine]] greatly influence the outcome.
 
==Complications==
==Complications==
Complications that can develop as a result of acute liver failure are:
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>
===Cerebral Edema and Encephalopathy===
* [[Cerebral edema]]
* Complications of acute liver failure can include [[cerebral edema]] and [[hepatic encephalopathy]].
* [[Encephalopathy]]
* The detection of encephalopathy is central to the diagnosis of acute liver failure. It may vary from subtle deficits in higher brain function (e.g. mood, concentration in grade I) to deep coma (grade IV).
* [[Coagulopathy]]  
* The patients presenting as acute and hyperacute liver failure are at greater risk of developing cerebral edema and grade IV encephalopathy.  
* [[Renal failure]]
* Cerebral edema in acute liver failure can be due to vasogenic and cytotoxic effects. The increased ammonia concentration in liver failure in combination with the glutamine produced by the astrocytes causes excess levels of glutamine with the help of enzyme glutamine synthetase. The excess glutamine is cytotoxic and can disturb the osmotic gradient which can result in brain swelling. In acute liver failure, the increased levels of nitric oxide in the circulation can also disrupt the cerebral autoregulation.<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> The aim is to maintain intracranial pressures below 25 mmHg, cerebral perfusion pressures above 50 mm Hg.
* [[Renal failure]]  
===Coagulopathy===
* [[Systemic inflammatory response syndrome|Systemic inflammatory response]]
* [[Coagulopathy]] is also seen in acute liver failure. The liver has a central role in the synthesis of coagulation factors and some inhibitors of [[coagulation]] and [[fibrinolysis]].
* Metabolic derrangements
* The hepatocyte [[necrosis]] leads to impaired [[synthesis]] of [[Coagulation|coagulation factors]] and their inhibitors. The former produces a prolongation in [[Prothrombin time]] which is widely used to monitor the severity of [[hepatic]] injury.
* [[Pulmonary]] complications
===Renal Failure===
 
* [[Renal failure]] is present in more than 50% of acute liver failure 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.  
==Prognosis==
* Once the renal failure develops, it is progressive and has a poor prognosis without liver transplantation.
* 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>


===Inflammation and Infection===
* 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:
* About 60% of all acute liver failure 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]].
*The impaired host defence mechanisms due to impaired [[Opsonin|opsonisation]], [[chemotaxis]] and intracellular killing substantially increases the risk of sepsis. The sepsis is mostly due  [[Gram-positive bacteria|gram positive]] (80%)and fungal (30%) sepsis.<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===
* The metabolic derrangements seen with acute liver failure include hyponatremia which is 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]] stores.
* [[Hypokalaemia]], [[hypophosphataemia]] and [[metabolic alkalosis]] are often present independent of renal function.
* [[Lactic acidosis]] is seen 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 also a compensatory increase in [[cardiac output]].
*  [[Adrenal insufficiency]] has been documented in 60% of acute liver failure 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 such as pulmonary edema and pulmonary infections are seen in approximately 30 % of patients with acute liver failure.<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>.


==Prognosis==
**[[King's College Criteria]] (mostly used for [[liver transplantation]])
* 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.
**[[Model for End-Stage Liver Disease]] ([[MELD]]) score (used to predict mortality in patients with chronic and acute liver disease)
* The survival rate is greater than 60 % in patients treated for acute liver failure.
**Sequential Organ Failure Assessment (SOFA score)
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:
**Clichy criteria
*King's College Criteria ( most widely use for liver transplantation)
**Acute Liver Failure Study Group (ALFSG) index
*Model for End-Stage Liver Disease (MELD) score (use 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


==References==
==References==

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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