Flashcards in Hepatology - Alcoholic liver disease Deck (13):
In what group of patients is alcoholic liver disease more commonly found?
ALD = inflammatory liver injury caused by chronic, heavy intake of alcohol.
Alcohol is the most common cause of chronic liver disease in the Western world. Alcoholic liver disease occurs more commonly in men, usually in their 4th and 5th decades, although subjects can present in there 20s with advanced disease.
What level of alcohol consumption is associated with a risk of ALD?
Although alcohol acts as a hepatotoxin, the exact mechanism leading to hepatitis and cirrhosis is unknown. As only 10-20% of people who drink excessively develop cirrhosis, genetic predisposition and immunological mechanisms have been proposed. The risk of ALD begins at around 30g/day. There is no clear relationship been dose and liver damage.
What are the risk factors for alcoholic liver disease?
Drinking patterns - ALD occurs in contiguous rather than binge drinkers
Gender - women are at higher risk for a given volume of alcohol due to their lower volume of distribution
Genetics - alcoholism is more common in monozygotic than dizygotic twins
Nutrition - obesity increases the incidence of liver related death fivefold in heavy drinkers
What are the three clinical syndromes of alcoholic liver disease?
1) Alcoholic fatty liver
2) Alcoholic hepatitis
3) Alcoholic cirrhosis
There is some overlap between the three.
What is fatty change?
This is the most common finding on liver biopsy in alcoholic individuals. Regular alcohol use even for several weeks can result in steatosis, a disorder in which hepatocytes contain macrovesicular droplets of triglycerides (substrates of alcohol metabolism are used to synthesise liver triglycerides). Fat disappears on cessation of alcohol intake, but with continued drinking there may be progress to fibrosis and cirrhosis.
What are the clinical features of fatty change?
Symptoms are usually absent, and on examination there may be hepatomegaly. There is no fever or neutrophilic leucocytosis.
Laboratory tests are often normal, although and elevated MCV often indicates heavy drinking (in the absence of macrocytic anaemia). The gamma GGT level is usually elevated.
What is alcoholic hepatitis?
Alcoholic hepatitis generally occurs after years of heavy drinking and may coexist with cirrhosis. Histologically, in addition to steatosis, there are ballooned (swollen) hepatocytes that often contain amorphous eosinophilic material called Mallory bodies, surrounded by neutrophils. There may be fibrosis and foamy degeneration of hepatocytes. 35% of heavy drinkers develop this form of disease.
What is the history of alcoholic hepatitis?
May remain asymptomatic and undetected unless they present for other reasons. May be mild illness with nausea, malaise, epigastric or right hypochondrial pain and a low-grade fever.
May be more severe with rapid onset jaundice (cardinal sign), abdominal discomfort or swelling, swollen ankles or GI bleeding. Women tend to present with more florid illness than men. There is a history of heavy alcohol intake ( 15–20 years of excessive intake necessary for development of alcoholic hepatitis). There may be trigger events (e.g. aspiration pneumonia or injury).
What are the important features on examination of a patient with alcoholic hepatitis?
1) SIGNS OF ALCOHOL EXCESS: Malnourished, palmar erythema, Dupuytrens contracture, facial telangiectasia, parotid enlargement, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising
2) SIGNS OF SEVERE ALCOHOLIC HEPATITIS: Febrile (50% of patients), tachycardia, jaundice (>50% of patients), bruising, encephalopathy (e.g. hepatic foetor, liver flap, drowsiness, unable to copy a five-pointed star, disoriented), ascites (30–60% of patients), hepato- megaly (liver is usually mild–moderately enlarged and may be tender on palpation), splenomegaly.
How should alcoholic hepatitis be investigated?
i) FBC: decr. Hb, incr. MCV, incr. WCC, decr. platelets
ii) LFT (incr. transminases, incr. bilirubin, decr. albumin, incr. AlkPhos, incr. GGT).
- AST:ALT ratio is >2)
- absolute values are usually <500 IU/L
iii) U&E: Urea and K+ levels tend to be low, unless significant renal impairment. Raised creatinine is an ominous sign and may predict the development of hepatorenal syndrome
iv) Clotting: Prolonged PT is a sensitive marker of significant liver damage.
2) Ultrasound scan: For other causes of liver impairment (e.g. malignancies).
3) Upper GI endoscopy: To investigate for varices.
4) Liver biopsy: Percutaneous or transjugular (in the presence of coagulopathy) may be helpful
to distinguish from other causes of hepatitis.
5) Electroencephalogram: For slow-wave activity indicative of encephalopathy.
How do I manage alcoholic hepatitis?
Patients with severe alcoholic hepatitis require supportive treatment:
- thiamine, vitamin C and other multivitamins
- monitor and correct K+, Mg++ and glucose abnormalities
- ensure adequate urine output
- treat encephalopathy with oral lactulose and phosphate enemas
- ascites managed by diuretics (spironolactone +/- furosemide) or therapeutic paracentesis
- glypressin or NAC for hepatorenal syndrome
- oral or nasogastric feeding
- protein restriction should be avoided unless the patient is encephalopathic
- TPN may also be considered as this improves mortality
- nutritional supplements and vitamins (B group, thiamine, folic acid) should be started parenterally initially, then continued orally afterwards
When should steroids be given in alcoholic hepatitis?
Corticosteroids (40 mg per day for four weeks) reduce the in ammatory process and are indicated if Maddrey’s discriminant function ≥32, indicating severe disease:
[4.6 × (prothrombin time above control in seconds) + bilirubin (mg/dL)]
Bilirubin mmol/L ÷ 17 to convert to mg/dL
Steroids are contraindicated if renal failure, infection or bleeding. Pentoxifylline, a phosphodiesterase inhibitor with many effects including modulation of TNF-α transcription, also reduces mortality, thought mainly by prevention of hepatorenal syndrome.