Acute alcoholic hepatitis: Difference between revisions

 
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==Clinical Features==
==Clinical Features==
[[File:Jaundice08.jpg|thumb|Jaundice of the skin]]
[[File:SpiderAngioma.jpg|thumb|Spider angioma]]
[[File:SpiderAngioma.jpg|thumb|Spider angioma]]
[[File:Hepaticfailure.jpg|thumb|[[Ascites]] secondary to cirrhosis.]]
===Symptoms===
===Symptoms===
*[[Abdominal pain]]
*[[Abdominal pain]]
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==Evaluation==
==Evaluation==
[[File:Auscities.png|thumb|Ascites appearance on ultrasound]]
[[File:CirrhosisWithAscitesMark.png|thumb|Liver cirrhosis with ascites on CT]]
===Work Up===
===Work Up===
====Labs====
====Labs====
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**Supporting laboratory abnormalities  
**Supporting laboratory abnormalities  
***May be nondiagnostic in patients with mild disease or early cirrhosis
***May be nondiagnostic in patients with mild disease or early cirrhosis
*May also have electrolyte abnormalities from malnutrition or [[alcoholic ketoacidosis]]


==Management==
==Management==
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***If '''Lille score >0.45''', considered as non-responder and prednisolone should be discontinued<ref name=Singal2018 />
***If '''Lille score >0.45''', considered as non-responder and prednisolone should be discontinued<ref name=Singal2018 />
*[[Pentoxifylline]] - evidence does not support its use<ref>Mathurin P, Louvet A, Duhamel A, et al. Prednisolone with vs without pentoxifylline and survival of patients with severe alcoholic hepatitis: a randomized clinical trial. JAMA. 2013;310(10):1033-41.</ref>
*[[Pentoxifylline]] - evidence does not support its use<ref>Mathurin P, Louvet A, Duhamel A, et al. Prednisolone with vs without pentoxifylline and survival of patients with severe alcoholic hepatitis: a randomized clinical trial. JAMA. 2013;310(10):1033-41.</ref>
*Discontinue nonselective beta blockers (e.g., propranolol) to lower incidence of AKI<ref> Sersté T, Njimi H, Degré D, Deltenre P, Schreiber J, Lepida A, Trépo E, Gustot T, Moreno C. The use of beta-blockers is associated with the occurrence of acute kidney injury in severe alcoholic hepatitis. Liver Int. 2015 Aug;35(8):1974-82. doi: 10.1111/liv.12786. Epub 2015 Feb 4. PMID: 25611961.</ref>


==Disposition==
==Disposition==
*Discharge
===Discharge===
**Mild disease/low risk
*Mild disease/low risk
**Nutritional assessment and intervention
*Nutritional assessment and intervention
**Discuss [[alcohol]] use and recommend strict abstinence
*Discuss [[alcohol]] use and recommend strict abstinence
*Admit
 
**High risk defined as MDF ≥ 32, MELD ≥ 18, or presence of [[hepatic encephalopathy]]
===Admit===
*High risk defined as MDF ≥ 32, MELD ≥ 18, or presence of [[hepatic encephalopathy]]
*Admission should be considered for the above as well as any of the following complications:
**Evidence of active infection
**Renal failure
**Severe coagulopathy and/or liver failure
**Alcohol withdrawal/delirium tremens


==Prognosis==
==Prognosis==
*Maddrey Discriminant Function score ([http://www.mdcalc.com/maddreys-discriminant-function-for-alcoholic-hepatitis/ MDF])
*Maddrey Discriminant Function score ([http://www.mdcalc.com/maddreys-discriminant-function-for-alcoholic-hepatitis/ MDF])
*Model for End-Stage Liver Disease score ([http://www.mdcalc.com/meld-score-model-for-end-stage-liver-disease-12-and-older/ MELD])
*Model for End-Stage Liver Disease score ([http://www.mdcalc.com/meld-score-model-for-end-stage-liver-disease-12-and-older/ MELD])
*High risk: MDF ≥ 32, MELD ≥ 18, or presence of hepatic encephalopathy<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>
*High risk: MDF ≥ 32, MELD ≥ 18, or presence of [[hepatic encephalopathy]]<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>


==See Also==
==See Also==

Latest revision as of 23:36, 7 February 2024

Background

Acute alcoholic hepatitis is inflammatory liver disease secondary to alcohol use.

  • Spectrum from hepatic steatosis to alcoholic hepatitis to cirrhosis
  • History of (usually chronic) alcohol abuse (~80 grams of ethanol daily for 5 years)
  • Ranges from subclinical cases to severe multisystem dysfunction

Clinical Features

Jaundice of the skin
Spider angioma
Ascites secondary to cirrhosis.

Symptoms

Signs

Cirrhosis is found in 50-60% of cases of alcoholic hepatitis[1]

Differential Diagnosis

Causes of acute hepatitis

Evaluation

Ascites appearance on ultrasound
Liver cirrhosis with ascites on CT

Work Up

Labs

  • CBC
  • Chemistry including magnesium and phosphate
  • LFTs
    • Very high elevations possibly more suggestive of viral or drug-induced hepatitis
    • Elevated AST/ALT (characteristically >2:1 and < 500 IU/L)
    • GGT alone is less reliable (low sensitivity and specificity)[3]
  • Coagulation factors
    • Elevated PT/INR
  • Lipase if suspect pancreatitis
  • Consider viral hepatitis panel

Imaging

Evaluation

  • Diagnosis is difficult and relies on a good history[4]
    • History of significant alcohol intake
    • Clinical evidence of liver disease
    • Supporting laboratory abnormalities
      • May be nondiagnostic in patients with mild disease or early cirrhosis
  • May also have electrolyte abnormalities from malnutrition or alcoholic ketoacidosis

Management

Severe Alcoholic Hepatitis

  • Defined as Maddrey's DF score ≥32[5]
    • Confers mortality of 20-50% in 30 days
  • 1st line therapy: Prednisolone 40mg PO qDay x4wks[5]
    • Must assess response to treatment at 7 days with Lille score
      • If Lille score >0.45, considered as non-responder and prednisolone should be discontinued[5]
  • Pentoxifylline - evidence does not support its use[6]
  • Discontinue nonselective beta blockers (e.g., propranolol) to lower incidence of AKI[7]

Disposition

Discharge

  • Mild disease/low risk
  • Nutritional assessment and intervention
  • Discuss alcohol use and recommend strict abstinence

Admit

  • High risk defined as MDF ≥ 32, MELD ≥ 18, or presence of hepatic encephalopathy
  • Admission should be considered for the above as well as any of the following complications:
    • Evidence of active infection
    • Renal failure
    • Severe coagulopathy and/or liver failure
    • Alcohol withdrawal/delirium tremens

Prognosis

  • Maddrey Discriminant Function score (MDF)
  • Model for End-Stage Liver Disease score (MELD)
  • High risk: MDF ≥ 32, MELD ≥ 18, or presence of hepatic encephalopathy[8]

See Also

External Links

References

  1. Basra, Gurjot,et. al. "Symptoms and Signs of Acute Alcoholic Hepatitis." World J Hepatol. 2011 May 27; 3(5): 118–120.
  2. Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002 Dec 17; 137(12): 947-54.
  3. O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258
  4. O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258
  5. 5.0 5.1 5.2 Singal AK, et. al. ACG clinical guideline: alcoholic liver disease. Am J Gastro. 2018; 113: 175-194.
  6. Mathurin P, Louvet A, Duhamel A, et al. Prednisolone with vs without pentoxifylline and survival of patients with severe alcoholic hepatitis: a randomized clinical trial. JAMA. 2013;310(10):1033-41.
  7. Sersté T, Njimi H, Degré D, Deltenre P, Schreiber J, Lepida A, Trépo E, Gustot T, Moreno C. The use of beta-blockers is associated with the occurrence of acute kidney injury in severe alcoholic hepatitis. Liver Int. 2015 Aug;35(8):1974-82. doi: 10.1111/liv.12786. Epub 2015 Feb 4. PMID: 25611961.
  8. O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258