Acute alcoholic hepatitis: Difference between revisions
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==Background== <!--T:1--> | |||
<!--T:2--> | |||
Acute alcoholic hepatitis is inflammatory liver disease secondary to alcohol use. | |||
*Spectrum from hepatic steatosis to alcoholic hepatitis to [[Special:MyLanguage/cirrhosis|cirrhosis]] | |||
*History of (usually chronic) [[Special:MyLanguage/alcohol Abuse|alcohol abuse]] (~80 grams of ethanol daily for 5 years) | |||
*Ranges from subclinical cases to severe multisystem dysfunction | |||
== | ==Clinical Features== <!--T:3--> | ||
<!--T:4--> | |||
[[File:Jaundice08.jpg|thumb|Jaundice of the skin]] | |||
[[File:SpiderAngioma.jpg|thumb|Spider angioma]] | |||
[[File:Hepaticfailure.jpg|thumb|[[Special:MyLanguage/Ascites|Ascites]] secondary to cirrhosis.]] | |||
== | ===Symptoms=== <!--T:5--> | ||
<!--T:6--> | |||
*[[Special:MyLanguage/Abdominal pain|Abdominal pain]] | |||
*[[Special:MyLanguage/Nausea and vomiting|Nausea and vomiting]] | |||
*Weight loss / fatigue / anorexia | |||
== | |||
===Signs=== <!--T:7--> | |||
<!--T:8--> | |||
*[[Special:MyLanguage/RUQ tenderness|RUQ tenderness]] | |||
*[[Special:MyLanguage/Jaundice|Jaundice]] | |||
*[[Special:MyLanguage/Fever|Fever]] | |||
*[[Special:MyLanguage/Hepatomegaly|Hepatomegaly]] | |||
*[[Special:MyLanguage/Ascites|Ascites]] | |||
*[[Special:MyLanguage/Encephalopathy|Encephalopathy]] | |||
*Spider angioma | |||
*[[Special:MyLanguage/GI bleed|GI bleed]]/varices | |||
*[[Special:MyLanguage/Malnutrition|Malnutrition]] | |||
*Symptoms of [[Special:MyLanguage/alcohol withdrawal|alcohol withdrawal]] | |||
<!--T:9--> | |||
[[Special:MyLanguage/Cirrhosis|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== <!--T:10--> | |||
<!--T:11--> | |||
*Alcoholic [[Special:MyLanguage/pancreatitis|pancreatitis]] | |||
*[[Special:MyLanguage/Gallstones|Gallstones]] | |||
*[[Special:MyLanguage/Budd-Chiari syndrome|Budd-Chiari syndrome]] | |||
*[[Special:MyLanguage/Viral hepatitis|Viral hepatitis]] | |||
*Drug-induced hepatitis | |||
</translate> | |||
{{Acute hepatitis causes}} | |||
<translate> | |||
==Evaluation== <!--T:12--> | |||
<!--T:13--> | |||
[[File:Auscities.png|thumb|Ascites appearance on ultrasound]] | |||
[[File:CirrhosisWithAscitesMark.png|thumb|Liver cirrhosis with ascites on CT]] | |||
===Work Up=== <!--T:14--> | |||
====Labs==== <!--T:15--> | |||
<!--T:16--> | |||
*CBC | |||
**[[Special:MyLanguage/Leukocytosis|Leukocytosis]] with elevated ANC | |||
*Chemistry including magnesium and phosphate | |||
*[[Special:MyLanguage/LFTs|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)<ref>O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258</ref> | |||
*Coagulation factors | |||
**Elevated PT/INR | |||
*Lipase if suspect [[Special:MyLanguage/pancreatitis|pancreatitis]] | |||
*Consider [[Special:MyLanguage/viral hepatitis|viral hepatitis]] panel | |||
====Imaging==== <!--T:17--> | |||
<!--T:18--> | |||
*Consider [[ultrasound: Abdomen|transabdominal ultrasound]] if concern for: | |||
**[[Special:MyLanguage/biliary disease|Biliary obstruction]] | |||
**[[Special:MyLanguage/Budd-Chiari syndrome|Budd-Chiari syndrome]] | |||
**Hepatic or biliary neoplasms | |||
===Evaluation=== <!--T:19--> | |||
<!--T:20--> | |||
*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 | |||
**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 [[Special:MyLanguage/alcoholic ketoacidosis|alcoholic ketoacidosis]] | |||
==Management== <!--T:21--> | |||
<!--T:22--> | |||
*Control of withdrawal symptoms | |||
*Nutritional support for malnutrition: especially [[Special:MyLanguage/thiamine|thiamine]], [[Special:MyLanguage/folate|folate]], [[Special:MyLanguage/pyridoxine|pyridoxine]], [[Special:MyLanguage/magnesium|magnesium]], [[Special:MyLanguage/hypophosphatemia|phosphate]], [[Special:MyLanguage/dextrose|glucose]], and protein | |||
===Severe Alcoholic Hepatitis=== <!--T:23--> | |||
<!--T:24--> | |||
*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> | |||
**Confers mortality of 20-50% in 30 days | |||
*1st line therapy: '''[[Special:MyLanguage/Prednisolone|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 /> | |||
*[[Special:MyLanguage/Pentoxifylline|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== <!--T:25--> | |||
===Discharge=== <!--T:26--> | |||
<!--T:27--> | |||
*Mild disease/low risk | |||
*Nutritional assessment and intervention | |||
*Discuss [[Special:MyLanguage/alcohol|alcohol]] use and recommend strict abstinence | |||
===Admit=== <!--T:28--> | |||
<!--T:29--> | |||
*High risk defined as MDF ≥ 32, MELD ≥ 18, or presence of [[Special:MyLanguage/hepatic encephalopathy|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== <!--T:30--> | |||
<!--T:31--> | |||
*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]) | |||
*High risk: MDF ≥ 32, MELD ≥ 18, or presence of [[Special:MyLanguage/hepatic encephalopathy|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== <!--T:32--> | |||
<!--T:33--> | |||
*[[Special:MyLanguage/Acute hepatitis|Acute hepatitis]] | |||
*[[Special:MyLanguage/Alcohol|Alcohol]] | |||
==External Links== <!--T:34--> | |||
<!--T:35--> | |||
*http://www.aasld.org/sites/default/files/guideline_documents/AlcoholicLiverDisease1-2010.pdf | |||
==References== <!--T:36--> | |||
<!--T:37--> | |||
<references/> | <references/> | ||
<!--T:38--> | |||
[[Category:GI]] | |||
</translate> | |||
Latest revision as of 16:57, 6 January 2026
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
Ascites secondary to cirrhosis.
Symptoms
- Abdominal pain
- Nausea and vomiting
- Weight loss / fatigue / anorexia
Signs
- RUQ tenderness
- Jaundice
- Fever
- Hepatomegaly
- Ascites
- Encephalopathy
- Spider angioma
- GI bleed/varices
- Malnutrition
- Symptoms of alcohol withdrawal
Cirrhosis is found in 50-60% of cases of alcoholic hepatitis[1]
Differential Diagnosis
- Alcoholic pancreatitis
- Gallstones
- Budd-Chiari syndrome
- Viral hepatitis
- Drug-induced hepatitis
Causes of acute hepatitis
- Acetaminophen toxicity (most common cause of acute liver failure in the US[2])
- Viral hepatitis
- Toxoplasmosis
- Acute alcoholic hepatitis
- Toxins
- Ischemic hepatitis
- Autoimmune hepatitis
- Wilson's disease
Evaluation
Work Up
Labs
- CBC
- Leukocytosis with elevated ANC
- 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
- Consider transabdominal ultrasound if concern for:
- Biliary obstruction
- Budd-Chiari syndrome
- Hepatic or biliary neoplasms
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
- Control of withdrawal symptoms
- Nutritional support for malnutrition: especially thiamine, folate, pyridoxine, magnesium, phosphate, glucose, and protein
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]
- Must assess response to treatment at 7 days with Lille score
- 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
- ↑ Basra, Gurjot,et. al. "Symptoms and Signs of Acute Alcoholic Hepatitis." World J Hepatol. 2011 May 27; 3(5): 118–120.
- ↑ 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.
- ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258
- ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258
- ↑ 5.0 5.1 5.2 Singal AK, et. al. ACG clinical guideline: alcoholic liver disease. Am J Gastro. 2018; 113: 175-194.
- ↑ 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.
- ↑ 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.
- ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258
