Hepatic failure: Difference between revisions
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* '''[[Acute liver failure]]''' -loss of liver function that occurs rapidly. 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]]) starts within four weeks of the first symptoms (such as [[jaundice]]) of a liver problem. Three types are defined: "Hyperacute " liver failure is said to be present if this interval is 7 days or less, [[Acute]] as 8-28 days, while [["subacute"]] liver failure is said to be present if the interval is 5-12 weeks after the first symptom of a liver problem.<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]]''' -loss of liver function that occurs rapidly. 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]]) starts within four weeks of the first symptoms (such as [[jaundice]]) of a liver problem. Three types are defined: "Hyperacute " liver failure is said to be present if this interval is 7 days or less, [[Acute]] as 8-28 days, while [["subacute"]] liver failure is said to be present if the interval is 5-12 weeks after the first symptom of a liver problem.<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]]).[[Encephalopathy]] develops after 6 months. | * '''[[Chronic liver failure]]''' - [[Hepatic encephalopathy]] develps after 6 months and it 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 22:21, 1 August 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 -loss of liver function that occurs rapidly. Development of hepatic encephalopathy (confusion, stupor and coma) and decreased production of proteins (such as albumin and blood clotting proteins) starts within four weeks of the first symptoms (such as jaundice) of a liver problem. Three types are defined: "Hyperacute " liver failure is said to be present if this interval is 7 days or less, Acute as 8-28 days, while "subacute" liver failure is said to be present if the interval is 5-12 weeks after the first symptom of a liver problem.[3]
- Chronic liver failure - Hepatic encephalopathy develps after 6 months and it 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
Causes for Acute liver failure:
Category | Etiology of Acute liver failure |
---|---|
Viruses |
|
Drugs |
|
Metabolic diseases | |
Toxins |
|
Vascular diseases | |
Malignant Infiltration |
|
Autoimmune disease |
- Chronic liver failure usually occurs in the context of cirrhosis. The most common causes are hepatitis and other viruses, and alcohol abuse.
Differential Diagnosis
- Acute liver failure is a distinctive syndrome that is not confused with other conditions. The major differential diagnosis is in the cause of acute liver failure, whether viral (hepatitis A, B, C, D or E), autoimmune, metabolic (Wilson disease), drug-induced or idiopathic.[7][8]
Epidemiology and Demographics
- Acute liver failure affects approximately 2,000–3,000 Americans each year.[9]
- Chronic liver disease and Cirrhosis are the 12(th) leading cause of death in the United States.[10]
- Liver transplantation is the second most common solid organ transplantation, yet less than 10% of global transplantation needs are met at current rates.
Natural History, Complications and Prognosis
Natural History
- Acute liver failure (Hyperacute and subacute) is a rare but serious clinical syndrome characterized by the sudden loss of hepatic function in a person without evidence of preexisting liver disease (Exceptions to this definition include Wilson's disease, reactivation of hepatitis B virus infection, and autoimmune hepatitis).[9]
- Signs and symptoms of acute liver failure may include:
- Sudden jaundice, Hepatic encephalopathy( Mental confusion, difficulty concentrating and disorientation), Muscle tremors, Ascites, Right upper quadrant pain and Tenderness, Abdominal distention, Nausea, Vomiting, malaise, Bleeding easily, Hematemesis, Melena, Tachycardia, Hypotension, Brain herniation, Coma
Complications
- Neurological complications, Abnormal hemostasis, and bleeding complications, Multiorgan failure,infection.[11]
Prognosis
- The King's College Criteria (KCC) may be used.This scoring system is generally quite accurate in predicting poor prognosis and, along with clinical judgment, is useful for ensuring timely transfer to a liver transplant center.[9][12]
Diagnosis
The following evaluation is recommended to help determine the etiology of liver failure. Determination of etiology assists in directing therapy and estimating prognosis:
History and Symptoms
- Obtain a detailed medical history from the patient and/or family, including the first onset of the symptom(s); all medications used over the last 6 months, including prescription medications, over-the-counter agents, herbal supplements, wild mushrooms, or other alternatives/complementary therapies;
- Obtain a detailed history of current and prior substance use; current or prior depression (including assessment of suicidality), anxiety, psychosis, or other mental illness; viral prodrome; and recent travel.
Physical Examination
- Complete physical examination should be performed.
- Assessment of mental status, the neurologic examination, and the fundoscopic examination in patients with Hepatic Encephalopathy of stage 2 or greater.
Laboratory Findings
laboratory tests are recommended for establishing an etiology and determining the prognosis of Acute liver failure:
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Imaging
- Abdominal ultrasound with Doppler to confirm portal and hepatic vein patency
- Non-contrast computed tomography (CT) scan of the head for patients with Hepatic encephalopathy
Treatment
Effective medical Therapies for specific causes of liver failure and hepatic encephalopathy. Medical therapy includes antidotes to reverse the effect of Acute liver failure and various medications to Reduce ICP[9]
- Acetaminophen intoxication Oral NAC: 140 mg/kg loading dose, then 70 mg/kg every 4 hours until discontinued by hepatology or transplantation surgery attending physician
IV NAC: 150 mg/kg loading dose, then 50 mg/kg IV over 4 hours, then 100 mg/kg IV over 16 hours as a continuous infusion until discontinued by hepatology or transplantation surgery attending physician
- Amanita phalloides(mushroom intoxication) Charcoal: via NGT every 4 hours alternating with silymarin, Penicillin G: 1 g/kg/day IV and NAC (Dosing as for acetaminophen
overdose.),Silymarin: 300 mg PO/NGT every 12 hours,Legalon-SIL: 5 mg/kg/day IV (given in 4 divided doses) or 5 mg/kg IV loading dose followed by 20 mg/kg/day via continuous infusion
- Herpes simplex virus infectionAcyclovir: 10 mg/kg IV every 8 hours (using IBW) adjusted for kidney function
- Cytomegalovirus infection Ganciclovir: 5 mg/kg IV every 12 hours (using IBW) adjusted for kidney function
- Autoimmune hepatitis Methylprednisolone: 60 mg/day IV Kessler WR, et al73
- Hepatitis B virus infection Entecavir (taken on an empty stomach) or tenofovir at standard renal adjusted doses
- Acute fatty liver of pregnancy /HELLP Delivery of the fetus
- Treatment of Hepatic Encephalopathy:
- Liver transplantation: One of the most important, yet difficult, aspects of care for patients with Acute Liver failure is the determination of the need for urgent liver transplantation. We recommend early and rapid evaluation for transplantation candidacy.
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.[13]
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.
- ↑ Chayanupatkul M, Schiano TD (February 2020). "Acute Liver Failure Secondary to Drug-Induced Liver Injury". Clin Liver Dis. 24 (1): 75–87. doi:10.1016/j.cld.2019.09.005. PMID 31753252.
- ↑ Murray KF, Hadzic N, Wirth S, Bassett M, Kelly D (October 2008). "Drug-related hepatotoxicity and acute liver failure". J. Pediatr. Gastroenterol. Nutr. 47 (4): 395–405. doi:10.1097/MPG.0b013e3181709464. PMID 18852631.
- ↑ 9.0 9.1 9.2 9.3 Patton H, Misel M, Gish RG (March 2012). "Acute liver failure in adults: an evidence-based management protocol for clinicians". Gastroenterol Hepatol (N Y). 8 (3): 161–212. PMC 3365519. PMID 22675278.
- ↑ Asrani SK, Larson JJ, Yawn B, Therneau TM, Kim WR (August 2013). "Underestimation of liver-related mortality in the United States". Gastroenterology. 145 (2): 375–82.e1–2. doi:10.1053/j.gastro.2013.04.005. PMC 3890240. PMID 23583430.
- ↑ Munoz SJ (October 2014). "Complications of Acute Liver Failure". Gastroenterol Hepatol (N Y). 10 (10): 665–8. PMC 4988224. PMID 27540338.
- ↑ McDowell Torres D, Stevens RD, Gurakar A (July 2010). "Acute liver failure: a management challenge for the practicing gastroenterologist". Gastroenterol Hepatol (N Y). 6 (7): 444–50. PMC 2933761. PMID 20827368.
- ↑ 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.