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| | | [[File:Siren.gif|30px|link=Acute liver failure resident survival guide]]|| <br> || <br> |
| | | [[Acute liver failure resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| | |} |
| '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' | | '''For patient information click [[{{PAGENAME}} (patient information)|here]]''' |
| {{Infobox_Disease | | | {{Acute liver failure}} |
| Name = {{PAGENAME}} |
| | {{CMG}}; '''Associate Editor(s)-In-Chief:''' {{HS}}, [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com], {{ADI}} |
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| ICD10 = {{ICD10|K|72|9|k|70}} |
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| MeshID = D017114 |
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| {{CMG}} | |
| ==Overview==
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| '''Acute liver failure''' is the appearance of severe complications rapidly after the first signs of liver disease (such as [[jaundice]]), and indicates that the liver has sustained severe damage (loss of function of 80-90% of liver cells). The complications are [[hepatic encephalopathy]] and impaired [[protein synthesis]] (as measured by the levels of [[serum albumin]] and the [[prothrombin time]] in the blood).
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| ==Classification==
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| '''1)''' The 1993 classification defines <ref>O'Grady JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. ''[[The Lancet|Lancet]] 1993;342:273-5. PMID 8101303.</ref> It reflects the fact that the pace of disease evolution strongly influence prognosis. Underlying [[aetiology]] is the other significant determinant of outcome.<ref name="ogredy1">{{cite journal |author=O'Grady JG |title=Acute liver failure |journal=Postgraduate medical journal |volume=81 |issue=953 |pages=148-54 |year=2005 |pmid=15749789 |doi=10.1136/pgmj.2004.026005}}</ref> | |
| * ''Hyperacute'' as within 1 week,
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| * ''Acute'' as 8-28 days and
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| * ''Subacute'' as 4-12 weeks
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| '''2)''' Acute liver failure may be fulminant or subfulminant. Both the forms have poor prognosis
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| * ''Fulminant hepatic failure'' - Development of [[hepatic encephalopathy]] within 2 months after the onset of acute liver disease.
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| * ''Subfulminant hepatic failure'' - Development of hepatic encephalopathy within 2 months to 6 months after the onset of acute liver disease
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| ==Causes==
| | {{SK}} ALF, acute hepatic failure, fulminant hepatic failure, fulminant liver failure, fulminant hepatitis |
| Common causes for acute liver failure are:
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| * [[Paracetamol]] (acetaminophen) overdose is the commonest cause. The commonest causes for paracetamol poisoning is suicidal intent. Additionally, the toxic threshold dose of paracetamol decreases in some cases like chronic alcoholics, and fasting.
| | ==[[Acute liver failure overview|Overview]]== |
| * Idiosyncratic reaction to medication is the second commonest cause. Common culprit drugs are: [[tetracycline]], [[troglitazone]], antituberculosis drugs, and anti-epileptic drugs
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| * Excessive [[alcoholic beverage|alcohol intake]] (severe [[alcoholic hepatitis]])
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| * Viral hepatitis ([[hepatitis A]] or [[hepatitis B|B]] - it is extremely uncommon in [[hepatitis C]]). The incidences of acute liver failure post viral hepatitis has decreased due to the extensive vaccination against these infections.
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| * [[Acute fatty liver of pregnancy]]
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| * [[Reye syndrome]] is acute liver failure in a child with a viral infection (e.g. [[chickenpox]]); it appears that [[aspirin]] use may play a significant role
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| * [[Wilson's disease]] (hereditary copper accumulation) may infrequently present with acute liver failure
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| * Idiopathic (without an obvious cause)
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| * Budd–Chiari syndrome
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| * Malignancy (lymphomas)
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| * Shock
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| * Hyperthermia
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| * Hypothermia
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| == Pathophysiology== | | ==[[Acute liver failure historical perspective|Historical Perspective]]== |
| In the majority of acute liver failure (ALF) there is widespread hepatocellular necrosis beginning in the [[hepatic lobule|centrizonal distribution]] and progressing towards portal tracts. The degree of [[parenchyma]]l inflammation is variable and is proportional to duration of [[disease]]<ref>{{cite journal |author=Boyer JL, Klatskin G |title=Pattern of necrosis in acute viral hepatitis. Prognostic value of bridging (subacute hepatic necrosis) |journal=N. Engl. J. Med. |volume=283 |issue=20 |pages=1063-71 |year=1970 |pmid=4319402 |doi=}}</ref><ref name="gimson"/>.
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| == Differential Diagnosis == | | ==[[Acute liver failure classification|Classification]]== |
| * Acute fatty liver of pregnancy
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| * Autoimmune chronic active hepatitis
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| * [[Budd-Chiari Syndrome]]
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| * [[Cytomegalovirus]]
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| * [[Drug]]s
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| * [[Epstein-Barr Virus]]
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| * [[Heatstroke]]
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| * Hepatic arterial occlusion or [[Hepatic venous occlusion]]
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| * [[Hepatitis A]] - [[Hepatitis G]]
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| * [[Herpes simplex]] 1, 2
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| * [[Hypotension]]
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| * [[Ddx:Hypothermia|Hypothermia]]
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| * Massive malignant infiltration of the liver
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| * [[Parainfluenza virus]]
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| * [[Paramyxovirus]]
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| * Primary graft nonfunction post liver transplantation
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| * [[Reye's Syndrome]]
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| * [[Sepsis]]
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| * [[Ddx:Shock|Shock]]
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| * [[Wilson's Disease]]
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| == Clinical consequence == | | ==[[Acute liver failure pathophysiology|Pathophysiology]]== |
| ;Cerebral oedema and encephalopathy
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| In ALF, [[Cerebral edema|cerebral oedema]] leads to [[hepatic encephalopathy]], [[coma]], [[brain herniation]] and eventually 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 phenomenon. 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><ref name="ogredy1"/>.
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| 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
| | ==[[Acute liver failure causes|Causes]]== |
| 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<ref name="ogredy1"/>.
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| ;Coagulopathy
| | ==[[Acute liver failure differential diagnosis|Differentiating Acute Liver Failure from other Diseases]]== |
| [[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"/>.
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| ;Renal failure
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| [[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.
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| ;Inflammation and infection
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| 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>.
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| ;Metabolic derangements
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| [[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.
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| ;Haemodynamic and cardio-respiratory compromise
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| [[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>.
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| [[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. | | ==[[Acute liver failure epidemiology and demographics|Epidemiology and Demographics]]== |
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| ==Lab diagnosis== | | ==[[Acute liver failure risk factors|Risk Factors]]== |
| All patients with clinical or laboratory evidence of moderate to severe acute hepatitis should have immediate measurement of prothrombin time and careful evaluation of mental status. If the prothrombin time is prolonged by ≈ 4-6 seconds or more (INR ≥1.5)
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| and there is any evidence of altered [[sensorium]], the diagnosis of ALF should be strongly suspected and hospital admission is mandatory<ref name="Polson">{{cite journal |author=Polson J, Lee WM |title=AASLD position paper: the management of acute liver failure |journal=Hepatology |volume=41 |issue=5 |pages=1179-97 |year=2005 |pmid=15841455 |doi=10.1002/hep.20703}}</ref>. Initial laboratory examination must be extensive in order to evaluate both the aetiology and severity.
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| ;Initial laboratory analysis<ref name="Polson"/>
| | ==[[Acute liver failure screening|Screening]]== |
| *[[Prothrombin time]]/INR
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| *[[Complete blood count]]
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| *Chemistries
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| **Liver function test: [[Aspartate transaminase|AST]], [[Alanine transaminase|ALT]], [[alkaline phosphatase]], [[Gamma-glutamyl transpeptidase|GGT]], total [[bilirubin]], [[albumin]]
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| **[[Creatinine]], urea/[[blood urea nitrogen]], sodium, potassium, chloride, bicarbonate, calcium, magnesium, phosphate
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| **[[Blood sugar|glucose]]
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| **[[Amylase]] and [[lipase]]
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| *[[Arterial blood gas]], [[lactate]]
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| *Blood type and screen
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| *[[Paracetamol]] (Acetaminophen) level, Toxicology screen
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| *[[Viral hepatitis]] serologies: anti-HAV IgM, HBSAg, anti-HBc IgM, anti-HEV
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| *[[Autoimmune]] markers: [[Anti-nuclear antibody|ANA]], [[Anti-actin antibodies|ASMA]], LKMA, [[Antibody|Immunoglobulin]] levels
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| *[[Ceruloplasmin]] Level ( when Wilson's disease suspected)
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| *[[Pregnancy test]] (females)
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| *[[Ammonia]] (arterial if possible)
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| *[[HIV]] status (has implication for [[transplantation]])
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| History taking should include careful review of possible exposures to viral infection and drugs or other toxins. From history and clinical examination possibility of underlying chronic disease should be ruled out as it may have different management. | | ==[[Acute liver failure natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| A [[liver biopsy]] done via the [[jugular|transjugular]] route because of [[coagulopathy]] is not usually necessary other than in occasional malignancies. As the evaluation continues, several important decisions have to be made such as whether to admit the patient to an ICU, or whether to transfer the patient to a transplant facility. Consultation with the transplant centre as early as possible is critical due to possibility of rapid progression of ALF.
| | ==Diagnosis== |
| | [[Acute liver failure diagnostic study of choice|Diagnostic Study of Choice]] | [[Acute liver failure history and symptoms|History and Symptoms]] | [[Acute liver failure physical examination|Physical Examination]] | [[Acute liver failure laboratory findings|Laboratory Findings]] | [[Acute liver failure x ray|X Ray]] | [[Acute liver failure CT|CT]] | [[Acute liver failure echocardiography or ultrasound|Ultrasound ]] | [[Acute liver failure other imaging findings|Other Imaging Findings]] | [[Acute liver failure other diagnostic studies|Other Diagnostic Studies]] |
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| ==Treatment== | | ==Treatment== |
| {|style="padding:0.3em; float:right; margin-left:5px;border:1px solid #ffa508;"
| | [[Acute liver failure medical therapy|Medical Therapy]] | [[Acute liver failure surgery|Surgery]] | [[Acute liver failure primary prevention|Primary Prevention]] | [[Acute liver failure secondary prevention|Secondary Prevention]] | [[Acute liver failure cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Acute liver failure future or investigational therapies|Future or Investigational Therapies]] |
| |-style="background-color:#FFE4E1; align:center; color:#8B4513; text-align: center"
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| |'''King's College Hospital criteria''' <br />
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| '''for liver transplantation in acute liver failure<ref>{{cite journal |author=O'Grady JG, Alexander GJ, Hayllar KM, Williams R |title=Early indicators of prognosis in fulminant hepatic failure |journal=Gastroenterology |volume=97 |issue=2 |pages=439-45 |year=1989 |pmid=2490426 |doi=}}</ref>'''
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| |'''Patients with [[paracetamol]] toxicity'''<br />
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| pH <7.3 or<br />
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| [[Prothrombin time]] >100 seconds and<br /> [[serum creatinine]] level >3.4 mg/dL (>300 μmol/l)<br /> | |
| if in grade III or IV [[hepatic encephalopathy|encephalopathy]]
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| |- | |
| |'''Other patients'''<br />
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| Prothrombin time >100 seconds or <br />
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| ''Three of the following variables'':<br />
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| *Age <10 yr or >40 yr
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| *Cause:
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| ** non-A, non-B hepatitis
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| ** [[halothane]] hepatitis
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| ** idiosyncratic drug reaction
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| *Duration of jaundice before encephalopathy >7 days
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| *prothrombin time >50 seconds
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| *Serum [[bilirubin]] level >17.6 mg/dL (>300 μmol/l)
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| |} | |
| ===Aim of therapy is to correct===
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| * Metabolic abnormalities
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| * Coagulation defects
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| * Electrolyte and acid-base disturbances
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| * Advanced chronic kidney disease
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| * Hypoglycemia
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| * Encephalopathy
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| ===Treatment strategies===
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| ====General measures====
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| * Treatment involves admission to hospital; often [[intensive care unit]] admission or very close observation are required.
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| * Supportive treatment with adequate nutrition and, optimization of the [[fluid balance]] should be done
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| * [[Mechanical ventilation]], [[intubation]] is indicated for stage 3 or 4 encephalopathy
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| * [[Sepsis]] and infections are common with [[fulminant liver failure]]. Though prophylactic antibiotic decreases the risk of infection, but is not routinely recommended as no survival benefits have been proved. Nevertheless, broad coverage with antibiotics is recommended for suspected cases of sepsis.
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| * Routine administration of steroids for [[adrenal insufficiency]] is not recommended.
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| * [[H2 receptor blocker]] and [[proton pump inhibitors]] are indicated to prevent and treat [[stress gastropathy]].
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| * Early transfer to a liver transplantation center should be decided based on patient's clinical status.
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| ====Management of increased intracranial pressure====
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| * [[Intracranial pressure]] monitoring in severe encephalopathy and impending cerebral edema should be done with extradural sensors
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| * The goal should be to maintain the intracranial pressure below 20 mm Hg and the cerebral perfusion pressure above 70 mm Hg.
| | ==Case Studies== |
| * [[Lactulose]] is indicated in cases of encephalopathy.
| | :[[Acute liver failure case study one|Case #1]] |
| * Mannitol, 0.5 g/kg, or 100–200 mL of a 20% solution by intravenous infusion over 10 minutes for reducing cerebral edema
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| * [[Mannitol]] should be avoided in patients with advanced chronic kidney diseases.
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| * Hypernatremia (145-155 mEq/L) through intravenous hypertonic saline infusion to induce hypernatremia may be used to reduce intracranial hypertension.
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| * Hypothermia (32–34 °C) may reduce intracranial pressure in refractory cases can be tried.
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| * Other measures like elevation of head end to 30 degrees, hyperventilation and intravenous prostaglandin E1can also be used.
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| * Short-acting barbiturate, propofol, or i/v indomethacin for refractory intracranial hypertension.
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| ===Treatment for specific underlying cause===
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| ====Acetaminophen or Paracetamol poisoning====
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| ** [[Acetylcysteine]] for [[paracetamol poisoning]] up to 72 hours after ingestion
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| ** It improves cerebral blood flow and increases transplant-free survival in patients with stage 1 or 2 [[encephalopathy]] due to hepatic failure of any cause.
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| ** Its treatment can increase [[prothrombin time]] giving a false alarm of worsening liver failure.
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| *** 140 mg/kg orally followed by 70 mg/kg orally every 4 hours for an additional 17 doses or
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| *** 150 mg/kg in 5% dextrose intravenously over 15 minutes followed by 50 mg/kg over 4 hours and then 100 mg/kg over 16 hours
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| ====Mushroom poisoning====
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| * Penicillin G - 300,000 to 1 million units/kg/day or
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| * Silibinin/silymarin/milk thistle (not licensed in the United States)
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| ====Chronic viral hepatitis====
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| * Nucleoside analogs - Fulminant hepatitis B
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| ====Herpes simplex hepatitis====
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| * Intravenous acyclovir
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| ====Wilson disease====
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| * [[Plasmapheresis]] + [[D-penicillamine]]
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| ===Other supportive measures===
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| * Drainage of [[ascites]].
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| * While many people who develop acute liver failure recover with supportive treatment, [[liver transplant]]ation is often required in people who continue to deteriorate or have adverse [[Prognosis|prognostic]] factors.
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| * "[[Liver dialysis]]" (various measures to replace normal liver function) is evolving as a treatment modality and is gradually being introduced in the care of patients with liver failure.
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| ==Prognosis==
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| 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>.
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| 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.
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| ==Historical perspective==
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| To date no universally accepted nomenclature has been adopted. Trey and Davidson introduced the term ''fulminant hepatic failure'' in 1970 to describe "potentially reversible condition, the consequence of severe liver injury, with an onset of encephalopathy within 8 weeks of the appearance of the first symptoms and in the absence of pre-existing liver disease"<ref>{{cite journal |author=Trey C, Davidson CS |title=The management of fulminant hepatic failure |journal=Progress in liver diseases |volume=3 |issue= |pages=282-98 |year=1970 |pmid=4908702 |doi=}}</ref>. Later it was suggested that the term ''fulminant'' should be confined to patients who develop jaundice to encephalopathy within 2 weeks. Terms ''subfulminant'' hepatic failure and ''late onset'' hepatic failure were coined for onset between 2 weeks to 3 months and for 8 weeks to 24 weeks respectively<ref>{{cite journal |author=Bernuau J, Goudeau A, Poynard T, ''et al'' |title=Multivariate analysis of prognostic factors in fulminant hepatitis B |journal=Hepatology |volume=6 |issue=4 |pages=648-51 |year=1986 |pmid=3732998 |doi=}}</ref><ref>{{cite journal |author=Gimson AE, O'Grady J, Ede RJ, Portmann B, Williams R |title=Late onset hepatic failure: clinical, serological and histological features |journal=Hepatology |volume=6 |issue=2 |pages=288-94 |year=1986 |pmid=3082735 |doi=}}</ref>. The umbrella term of ''acute liver failure'' was proposed by Kings college group which has been adopted in this article. Paradoxically in this classification the best prognosis is in the ''hyperacute'' group<ref>{{cite journal |author=Sass DA, Shakil AO |title=Fulminant hepatic failure |journal=Liver Transpl. |volume=11 |issue=6 |pages=594-605 |year=2005 |pmid=15915484 |doi=10.1002/lt.20435}}</ref>.
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| ==References==
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| {{Reflist|2}}
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| {{Gastroenterology}}
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| {{Intensive care medicine}}
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| [[Category:Organ failure]]
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| [[Category:Causes of death]]
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| [[Category:Hepatology]] | | [[Category:Hepatology]] |
| [[Category:Gastroenterology]] | | [[Category:Gastroenterology]] |
| [[Category:Intensive care medicine]]
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| [[it:Insufficienza epatica fulminante]]
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| [[pl:Ostra niewydolność wątroby]]
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| [[ur:فشل جگری خاطف]]
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