Overview of chronic alcohol use

Last reviewed: 6 Sep 2022
Last updated: 04 Feb 2022



Problematic alcohol use is classified in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, 5th ed., (DSM-5) as alcohol-use disorder, with severity specified as mild, moderate, or severe, depending on the number of diagnostic criteria that have been met;[2] and as harmful use of alcohol and alcohol dependence in the ICD-11[2][3] Alcohol-use disorder results from a variety of genetic, psychosocial, and environmental factors.[4] It is characterised by increased tolerance to the effects of alcohol, the presence of characteristic withdrawal signs and symptoms, and impaired control over the quantity and frequency of drinking.[2]

Alcohol withdrawal occurs in patients who are alcohol dependent and who have stopped or reduced their alcohol intake within hours or days of presentation. Symptoms typically begin 6 to 12 hours after the patient's last drink.[5][6] Common symptoms are anxiety, nausea or vomiting, autonomic dysfunction, and insomnia. These may progress to severe withdrawal with seizures, psychiatric disturbance, and delirium tremens.[7][8][9]

Comprises three stages of liver damage: fatty liver (steatosis), alcoholic hepatitis (inflammation and necrosis), and alcoholic liver cirrhosis (fibrosis). All are caused by chronic heavy alcohol ingestion. Clinical presentation is highly variable. There is no specific laboratory test to identify alcohol as a cause of liver damage.

The pathological end stage of any chronic liver disease. The most common causes of cirrhosis in the Western world are alcohol-related liver disease, non-alcoholic fatty liver disease (NAFLD and associated steatohepatitis), and chronic viral hepatitis.[10][11][12] The main complications of cirrhosis are related to the development of liver insufficiency and portal hypertension, and include ascites, variceal haemorrhage, jaundice, portosystemic encephalopathy, acute kidney injury and hepatopulmonary syndromes, and the development of hepatocellular carcinoma.

A rare syndrome defined by a rapid decline in hepatic function, characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease.[13][14][15] Chronic alcohol misuse is a significant risk factor for the development of ALF.

A brain dysfunction caused by liver insufficiency and/or portosystemic shunt. It manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma.[16] Causation is thought to be multi-factorial, resulting in brain exposure to ammonia that has bypassed the liver through portosystemic shunting.

A disorder of the exocrine pancreas and associated with acinar cell injury with local and systemic inflammatory responses.[17] The most common presenting symptom is mid-epigastric or left upper quadrant pain that radiates to the back. Epigastric tenderness is typical. Ethanol causes 40% to 45% of cases of acute pancreatitis and is the most common cause of acute pancreatitis in men. There is no threshold for the development of acute pancreatitis. The average amount of alcohol intake in patients with acute pancreatitis is 150 to 175 g per day.[18][19]

Characterised by recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures, resulting in scarring and loss of function. Unlike recurrent acute pancreatitis, chronic pancreatitis is characterised by reduced pancreatic exocrine function, malabsorption, diabetes, and pancreatic calcifications. Worldwide, alcohol is the major risk factor for chronic pancreatitis (70% to 80%). Co-factors required to induce alcoholic pancreatitis include anatomical, environmental, and/or genetic factors, as few people with chronic alcohol dependence develop the disease (no more than 10%, and likely <3%).[20][21][22]

A neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations, typically involving mental status changes and gait and oculomotor dysfunction. In people with chronic alcohol dependence, thiamine deficiency is a result of a combination of factors: poor intake, low content of vitamins in alcohol, low storage capacity of the liver, decreased intestinal absorption, impaired conversion of thiamine to its active form (thiamine pyrophosphate), and increased demand to metabolise the carbohydrates in alcohol.[23]

Refers to a group of conditions that may result from fetal exposure to alcohol.[24] Disorders include fetal alcohol syndrome (FAS), partial FAS, alcohol-related neurodevelopmental disorder, and alcohol-related birth defects. FAS is characterised by antenatal and postnatal growth retardation, specific facial dysmorphology and structural and/or functional abnormalities of the central nervous system.

Assessment of patients with abnormal liver tests should be guided by history, risk for liver disease, duration and severity of clinical findings, presence of comorbidities, and the nature of the liver test abnormality noted. Chronic alcoholic liver disease and acute alcoholic hepatitis are associated with elevation of serum aminotransferases.[25] Elevated gamma-GT correlates with excessive alcohol consumption; however, isolated elevations in gamma-GT are so common, and so often unhelpful, that many institutions have chosen to delete this test from their liver test panel.

Delirium is an acute, fluctuating change in mental status, with inattention, disorganised thinking and altered levels of consciousness.[26] Alcohol intoxication and withdrawal are frequently associated with delirium. Recent binge drinking can cause alcoholic ketoacidosis.

Polyneuropathy is a generalised disease of the peripheral nerves due to damage to the axon and/or the myelin sheath. It most commonly presents as symmetric numbness, paraesthesias, and dysaesthesias in the feet and distal lower extremities (distal symmetrical sensorimotor polyneuropathy). In severe cases, sensory symptoms and signs progress proximally to fit a stocking-glove distribution. Balance and gait may be impaired. Thiamine and pyridoxine deficiencies caused by alcoholism are possible causes of polyneuropathy. Ethanol-polyneuropathy, associated with alcohol-use disorder, may be caused by direct toxicity of ethanol on the nerve and/or concomitant nutritional deficiencies.

Upper gastrointestinal bleeding refers to gastrointestinal blood loss whose origin is proximal to the ligament of Treitz at the duodenojejunal junction. Causes are multiple, but in developed countries bleeding is usually secondary to peptic ulcer disease, erosions, oesophagitis, or varices. Any history of chronic and excessive alcohol use, intravenous drug use (or other behaviour that places people at risk of contracting hepatitis), or underlying liver disease strongly suggests a variceal bleed.



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