Acute alcoholic hepatitis: Difference between revisions

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==Background==
==Background==
Acute alcoholic hepatitis is inflammatory liver disease secondary to alcohol use.   
Acute alcoholic hepatitis is inflammatory liver disease secondary to alcohol use.   
*Spectrum from hepatic steatosis to alcoholic hepatitis to cirrhosis
*Spectrum from hepatic steatosis to alcoholic hepatitis to [[cirrhosis]]
*History of (usually chronic) alcohol abuse (~80 grams of ethanol daily for 5 years)
*History of (usually chronic) [[alcohol Abuse|alcohol abuse]] (~80 grams of ethanol daily for 5 years)
*Ranges from subclinical cases to severe multisystem dysfunction
*Ranges from subclinical cases to severe multisystem dysfunction


==Clinical Features==
==Clinical Features==
[[File:Jaundice08.jpg|thumb|Jaundice of the skin]]
[[File:SpiderAngioma.jpg|thumb|Spider angioma]]
[[File:Hepaticfailure.jpg|thumb|[[Ascites]] secondary to cirrhosis.]]
===Symptoms===
===Symptoms===
*[[Abdominal pain]]
*[[Abdominal pain]]
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*Spider angioma
*Spider angioma
*[[GI bleed]]/varices
*[[GI bleed]]/varices
*Malnutrition  
*[[Malnutrition]]
*Symptoms of [[alcohol withdrawal]]
*Symptoms of [[alcohol withdrawal]]


Cirrhosis is found in 50-60% of cases of alcoholic hepatitis<ref>Basra, Gurjot,et. al.  "Symptoms and Signs of Acute Alcoholic Hepatitis." World J Hepatol. 2011 May 27; 3(5): 118–120.</ref>
[[Cirrhosis]] is found in 50-60% of cases of alcoholic hepatitis<ref>Basra, Gurjot,et. al.  "Symptoms and Signs of Acute Alcoholic Hepatitis." World J Hepatol. 2011 May 27; 3(5): 118–120.</ref>


==Differential Diagnosis==
==Differential Diagnosis==
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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====
*CBC
*CBC
**Leukocytosis with elevated ANC  
**[[Leukocytosis]] with elevated ANC  
*Chemistry including magnesium and phosphate
*Chemistry including magnesium and phosphate
*LFTs - very high elevations possibly more suggestive of viral or drug-induced hepatitis
*[[LFTs]]
**Very high elevations possibly more suggestive of viral or drug-induced hepatitis
**Elevated AST/ALT (characteristically >2:1 and < 500 IU/L)
**Elevated AST/ALT (characteristically >2:1 and < 500 IU/L)
**GGT alone is less reliable (low sensitivity and specificity)<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>
**GGT alone is less reliable (low sensitivity and specificity)<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>
*Coagulation factors
*Coagulation factors
**Elevated PT/INR
**Elevated PT/INR
*Lipase if suspect pancreatitis
*Lipase if suspect [[pancreatitis]]
*Consider hepatitis panel
*Consider [[viral hepatitis]] panel


====Imaging====
====Imaging====
Consider transabdominal ultrasound if concern for:
*Consider [[ultrasound: Abdomen|transabdominal ultrasound]] if concern for:
*Biliary obstruction
**[[biliary disease|Biliary obstruction]]
*Budd-Chiari syndrome  
**[[Budd-Chiari syndrome]]
*Hepatic or biliary neoplasms
**Hepatic or biliary neoplasms


===Evaluation===
===Evaluation===
Diagnosis is difficult and relies on a good history<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>
*Diagnosis is difficult and relies on a good history<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref>
*History of significant alcohol intake
**History of significant alcohol intake
*Clinical evidence of liver disease
**Clinical evidence of liver disease
*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==
*Control of withdrawal symptoms
*Control of withdrawal symptoms
*Nutritional support for malnutrition: especially thiamine, folate, pyridoxine, magnesium, phosphate, glucose, and protein
*Nutritional support for malnutrition: especially [[thiamine]], [[folate]], [[pyridoxine]], [[magnesium]], [[hypophosphatemia|phosphate]], [[dextrose|glucose]], and protein


===High risk, severe cases===
===Severe Alcoholic Hepatitis===
*[[Steroids]]
*Defined as '''Maddrey's DF score ≥32'''<ref name=Singal2018>Singal AK, et. al. ACG clinical guideline: alcoholic liver disease. Am J Gastro. 2018; 113: 175-194.</ref>
*[[Pentoxifylline]]- may not provide any added benefit<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>
**Confers mortality of 20-50% in 30 days
*1st line therapy: '''[[Prednisolone]] 40mg PO qDay x4wks'''<ref name=Singal2018 />
**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<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>
*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
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