History and exam
Key diagnostic factors
common
presence of risk factors
Key risk factors include prolonged heavy alcohol consumption, presence of hepatitis C, and female sex.
abdominal pain
Right upper abdominal discomfort is most common in patients with acute alcohol-related hepatitis.
hepatomegaly
May be present in patients with alcohol-related steatosis or alcohol-related hepatitis. Hepatomegaly may be an ominous sign in patients with cirrhosis, suggesting the presence of hepatocellular carcinoma.
uncommon
haematemesis and melaena
Signs of gastrointestinal bleeding, possibly related to oesophageal or gastric varices, gastric irritation, and coagulopathy.
venous collaterals
Engorged para-umbilical veins (caput medusae), present in advanced ARLD.
splenomegaly
May be present in advanced liver disease patients with portal hypertension.
hepatic mass
Ominous sign; may portend presence of hepatocellular carcinoma.
jaundice
Common in severe alcohol-related hepatitis and in decompensated severe alcohol-related cirrhosis. Uncommon in compensated alcohol-related cirrhosis or alcohol-related steatosis. However, co-existent intra- or extrahepatic cholestasis should also be considered.
palmar erythema
Affects the thenar and hypothenar eminences while sparing the central portions of the palm. It may be present in patients with ARLD.
cutaneous telangiectasia
Vascular spiders with central arteriole flanked by smaller vessels. Usually seen on the trunk, face, and upper limbs. It may be present in patients with advanced ARLD.
asterixis
Flapping motions of outstretched, dorsiflexed hands; quick test for encephalopathic state. It is one of the manifestations of hepatic encephalopathy present in advanced ARLD.
Other diagnostic factors
common
ascites
Very common clinical complication of cirrhosis. It can be evaluated by the presence of shifting dullness or fluid wave examination.
weight loss
High tumour necrosis factor (TNF)-alpha and inflammatory response is associated with ARLD and can lead to loss of appetite and weight loss.[64]
weight gain
Ascites and/or oedema can cause gradual unintentional weight gain in patients with ARLD with portal hypertension.
malnutrition and wasting
May manifest as loss of weight and muscle mass, or as vitamin deficiency.
anorexia
fatigue
Common in patients with co-existing chronic hepatitis. May be caused by the activation of peripheral pathways between the brain and liver, which leads to changes in brain neurotransmission.[66]
uncommon
confusion
Hepatic encephalopathy in advanced cirrhosis may manifest as impaired mentation.[67]
Agitation, loss of concentration, and impaired judgement may be part of mental confusion.
Thiamine deficiency associated with ARLD can lead to mental confusion and neurological complications, such as Wernicke-Korsakoff syndrome.
pruritus
Present in association with jaundice due to accumulation of bile salts in the skin layers. It may be significant enough to cause sleep disturbances.
fever
Low-grade fever can be present in patients with alcohol-related hepatitis in the absence of infection.[41]
nausea and vomiting
May be due to gastric irritation from alcohol- or cirrhosis-associated gastroparesis.
finger clubbing
Distal portion of digit takes on drumstick appearance.
Dupuytren's contracture
Characteristic palmar fascia contracture and thickening associated with severe liver disease.
leg swelling
Peripheral oedema commonplace in both renal and liver disease from salt retention, hypoalbuminaemia, osmotic changes.
parotid gland enlargement
Fatty infiltration of the gland with fibrosis and oedema, probably due to the extrahepatic toxicity of alcohol.
gynaecomastia
Present in nearly two-thirds of patients. Common symptom of chronic liver disease, manifestation of altered sex hormone metabolism.[68]
hypogonadism
Multifactorial in nature, and a common finding in advanced ARLD.
dementia
Warrants careful evaluation for thiamine deficiency.
peripheral neuropathy
Focal defects, including altered reflexes, may be present.
Peripheral neuropathy might be associated with the direct toxic effect of alcohol on nerve tissue but is more likely to be associated with nutritional deficiencies.
Risk factors
strong
prolonged and heavy alcohol consumption
The quantity of alcohol ingested and the duration are the most important risk factors for ARLD development.[1]
Although alcohol-induced liver injury is somewhat dose dependent, there is no set alcohol consumption threshold that reliably predicts the development of ARLD.[1][13] One meta-analysis reported increased risk for ARLD with alcohol consumption ≥280 g/week.[29]
Most heavy alcohol drinkers will never develop clinical liver disease. Only about 10% to 20% of chronic heavy drinkers develop severe forms of ARLD, such as alcohol-related hepatitis or cirrhosis.[1][14][15]
hepatitis C
weak
obesity
The risk of ARLD is at least 2 times higher in patients with obesity than in patients with a normal body mass index.[1][18][19] Even if abstinent, people with obesity are at an increased risk of steatotic liver disease. Obesity seems to be an independent risk factor for both alcohol-related hepatitis and alcohol-related cirrhosis.[18]
age >65 years
Alcohol metabolism and distribution change with age. An older person's liver is more susceptible to alcohol-related toxicity. However, within the spectrum of ARLD, the symptoms and signs are similar in patients of all ages. Prognosis for ARLD in older people (age >65 years) is poor.[34]
genetic predisposition
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