Acute alcoholic hepatitis: Difference between revisions
No edit summary |
|||
| Line 8: | Line 8: | ||
===Symptoms=== | ===Symptoms=== | ||
*[[abdominal pain]] | *[[abdominal pain]] | ||
*[[ | *[[Nausea and vomiting]] | ||
*weight loss / fatigue / anorexia | *weight loss / fatigue / anorexia | ||
Revision as of 08:08, 20 January 2016
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
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
Diagnosis
Work Up
Labs
- CBC
- Leukocytosis with elevated ANC
- Chemistry including magnesium and phosphate
- LFTs
- 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
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[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
See Also
External Links
References
- Privette TW Jr, Carlisle MC, Palma JK. Emergencies of the liver, gallbladder, and pancreas. Emerg Med Clin North Am. 2011 May;29(2):293-317, viii-ix. doi: 10.1016/j.emc.2011.01.008.
- Amini, Maziyar; Runyon, Bruce. "Alcoholic Hepatitis 2010: A clinician's Guide to Diagnosis and Therapy." World of Gatstroenterol 2010 October 21; 16(39):4905-4912
- ↑ 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
- ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010) Alcoholic liver disease. Hepatology 51: 307–328. doi: 10.1002/hep.23258