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 | ||
* | *History of (usually chronic) alcohol abuse (~80 grams of ethanol daily for 5 years) | ||
* | *Ranges from subclinical cases to severe multisystem dysfunction | ||
==Clinical Features== | ==Clinical Features== | ||
===Symptoms=== | ===Symptoms=== | ||
*[[ | *[[Abdominal pain]] | ||
*[[Nausea and vomiting]] | *[[Nausea and vomiting]] | ||
* | *Weight loss / fatigue / anorexia | ||
===Signs=== | ===Signs=== | ||
*[[RUQ tenderness]] | *[[RUQ tenderness]] | ||
*[[ | *[[Jaundice]] | ||
*[[ | *[[Fever]] | ||
*[[ | *[[Hepatomegaly]] | ||
*[[ | *[[Ascites]] | ||
*[[ | *[[Encephalopathy]] | ||
* | *Spider angioma | ||
*[[GI bleed]]/varices | *[[GI bleed]]/varices | ||
* | *Malnutrition | ||
* | *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== | ||
* | *Alcoholic [[pancreatitis]] | ||
*[[ | *[[Gallstones]] | ||
*[[Budd-Chiari syndrome]] | *[[Budd-Chiari syndrome]] | ||
*[[Viral hepatitis]] | |||
*Drug-induced hepatitis | |||
{{Acute hepatitis causes}} | {{Acute hepatitis causes}} | ||
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**Leukocytosis with elevated ANC | **Leukocytosis with elevated ANC | ||
*Chemistry including magnesium and phosphate | *Chemistry including magnesium and phosphate | ||
*LFTs | *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> | ||
Revision as of 03:09, 12 October 2018
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
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 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
Management
- Control of withdrawal symptoms
- Nutritional support for malnutrition: especially thiamine, folate, pyridoxine, magnesium, phosphate, glucose, and protein
High risk, severe cases
- Steroids
- Pentoxifylline- may not provide any added benefit[5]
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
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[6]
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
- ↑ 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.
- ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258