Acute alcoholic hepatitis: Difference between revisions
ClaireLewis (talk | contribs) No edit summary |
|||
| Line 1: | Line 1: | ||
==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 | ||
| Line 21: | Line 21: | ||
*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== | ||
| Line 38: | Line 38: | ||
====Labs==== | ====Labs==== | ||
*CBC | *CBC | ||
**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> | ||
*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 | ||
==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=== | ===High risk, severe cases=== | ||
Revision as of 18:19, 29 September 2019
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 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
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