The document discusses alcoholic hepatitis, including its clinical presentation, diagnostic testing, and management. It reviews that alcoholic hepatitis typically presents with jaundice, anorexia, fever, abdominal pain, and sometimes encephalopathy in patients with a history of heavy alcohol use over 100g per day. Diagnostic testing includes liver function tests showing elevated AST and ALT with an AST:ALT ratio over 2, as well as elevated bilirubin and INR. Management involves alcohol abstinence, treatment of withdrawal if needed, nutritional support, and steroids or supportive care depending on disease severity. The most common cause of acute liver failure is alcoholic hepatitis.
Alcoholic liver disease includes a spectrum of dysplastic and inflammatory changes to hepatic tissues including steatosis, inflammation, fibrosis, and cirrhosis
These stages of alcoholic liver disease may be simultaneously present
Steatosis or fatty liver is relatively mild and potentially reversible
In alcoholic hepatitis, there is liver inflammation and impaired liver function caused by extended excessive alcohol intake
Cirrhosis can be compensated or decompensated, with clinically significant portal HTN, ascites, encephalopathy, and bleeding varices
Typically have a history of daily heavy alcohol use (>100 g per day) for more than 20 years
Standard drink is 14 g, so about 7 drinks daily
Patients often stop drinking as they become ill, so it is common for patients to have ceased alcohol intake several weeks prior to presentation
Age 40-60 years old
Symptoms
Jaundice: developed within 3 months prior to presentation
Anorexia
Fever: important to exclude other sources of infection e.g. SBP
RUQ/epigastric pain: with tender hepatomegaly on exam
Ascites: due to underlying cirrhosis w/ portal HTN OR transient portal venous obstruction from hepatic swelling
Hepatic encephalopathy: if severe or if underlying cirrhosis
Elevated AST and ALT, but usually less than 300, rarely higher than 500
Higher transaminase levels should raise suspicion of concurrent liver injury due to viral or ischemic hepatitis or acetaminophen use (which can be toxic even at therapeutic doses in patients who abuse alcohol)
AST:ALT ratio >2
Elevated serum bilirubin: >5
Leukocytosis with neutrophilic predominance, usually <20k
Elevated INR
Low albumin: due to malnutrition and decreased synthesis due to liver dysfunction
Elevated creatinine due to hepatorenal syndrome
Diagnosis can be made based on supportive clinical and lab findings in the setting of significant alcohol intake
Want to rule out other causes of acute hepatitis, including:
Tylenol toxicity
Drug-induced liver injury
Nonalcoholic steatohepatitis
Acute viral hepatitis (HAV, HBV, HCV, HDV, HEV, HSV, EBV, CMV)
Ischemic hepatitis
Budd-Chiari syndrome
HELLP
Acute fatty liver of pregnancy
Wilson disease
Alpha-1 antitrypsin deficiency
Toxin-induced hepatitis (mushroom poisoning, carbon tetrachloride)
Obtain a thorough history and identify risk factors
Order hepatitis serologies to rule out acute viral hepatitis
Abdominal US with doppler to rule out Budd-Chiari or biliary obstruction
Imaging with US, CT, MRI can also identify fatty changes, cirrhosis, ascites
Liver biopsy: not necessary but can help with diagnosis if there is uncertainty
Liver biopsy
Steatosis: micro or macrovesicular
Hepatocellular ballooning
Neutrophilic infiltration
Mallory-Denk bodies: eosinophilic accumulations of intracellular protein aggregates within cytoplasm of hepatocytes
Important marker of alcohol related injury
Findings aren’t specific for alcoholic hepatitis
3 features of acute liver failure are INR >1.5, encephalopathy, and no pre-existing liver disease (symptoms within 26 weeks)
Acetaminophen is the most common cause of ALF in the US, Australia, Denmark, and UK
Viral hepatitis is the most common cause in Asia and other parts of Europe
Hepatitis A, B. Hepatitis C and D in patients with HBV infection
Idiosyncratic drug reaction: antibiotics, NSAIDs, anticonvulsants
A few scoring systems can be used to determine disease severity
Maddrey discriminant function
Calculated by 4.6 x PT – control PT + bilirubin
>32 have high short-term mortality of 50% within 30 days
<32 have lower short term mortality
MELD score
Usually used to predict survival in patients with cirrhosis, but can also be used to predict mortality in patients hospitalized for alcoholic hepatitis
DF 102.3
Patients should be counseled to stop drinking
They should be treated for alcohol withdrawal
Most patients with severe alcoholic hepatitis are malnourished and require nutritional support
Thiamine, folate, phosphate, magnesium
They are also often dehydrated and need fluid management, usually with albumin
Stop nonselective beta blockers: increased risk of AKI
Management of complications of cirrhosis
Hepatic encephalopathy: lactulose, rifaximin
Supportive care for mild/moderate disease
Treatment with glucocorticoids for patients with severe alcoholic hepatitis
Prednisolone as long as there are no contraindications (active infection, chronic HCV or HBV infection)
40 mg daily for 28 days with taper
Stop therapy in patients who do not show signs of improvement after 1 week
Prednisolone is preferred over prednisone because the latter requires conversion to prednisolone in the liver, which can be impaired in alcoholic hepatitis
Lille score: used to determine if a patient is responding to steroid treatment
Incorporates age, renal insufficiency, albumin, PT, bilirubin, and change in bilirubin at day 7
Pentoxifylline: alternative to steroids for patients who have contraindications, who are at risk for sepsis, or who are at risk for failing to follow up after discharge and can’t be tapered
Good safety profile
Data is inconsistent regarding mortality benefit
Stop when bilirubin <5
Liver transplantation if fail to respond to steroids or pentoxifylline, but usually unable to receive transplant due to alcohol abuse