Alcohol is a central nervous system depressant. In large amounts it decreases the level of consciousness and ultimately causes respiratory depression. Impaired consciousness sometimes results in aspiration of vomitus and death. Acute intoxication may also be associated with acute or acute erosive gastritis and Mallory-Weiss tear.

Alcoholic liver disease

Alcohol is the most common cause of chronic liver disease in Western countries. Females show increased susceptibility to the hepatotoxic effects of alcohol. Maximum recommended daily intakes are 30-40 gm/day for women and 50-60 gm/day for men. Toxicity may be related to the metabolic breakdown product acetaldehyde.

Fatty liver (steatosis) — Fatty change occurs rapidly after alcohol intake. With chronic ingestion, the liver becomes pale, weighing up to 4-6 kg, and feels soft and greasy. Histologically rounded clear vacuoles pushing the nucleus to the cell periphery are seen in affected hepatocytes. Initially, the distribution is perivenular. Fatty liver is fully reversible unless associated with perivenular subsinusoidal fibrosis.

Alcoholic hepatitis — Usually associated with binge drinking, this causes increased serum gamma glutamyltranspeptidase and transaminases and presents similarly to acute viral hepatitis. It is associated with hepatocyte cell death, eosinophilic globular material (Mallory’s hyaline) comprising condensed cytokeratins in the cytoplasm of hydropic hepatocytes and an inflammatory infiltrate in which neutrophils predominate. There is associated perivenular subsinusoidal and sometimes periportal fibrosis.

Alcoholic cirrhosis — Only about 10 per cent of chronic alcoholics develop cirrhosis. It may present as alcoholic hepatitis or insidiously with end stage liver disease. Causes of death include liver failure, gastrointestinal haemorrhage, infection and hepatorenal syndrome. Hepatocellular carcinoma develops in 5-6 per cent of cases.

Initially the liver is yellow-tan in colour, fatty and enlarged. Later it is brown, shrunken and non-fatty. It begins with fibrous dissection of hepatic acini and hepatocyte regeneration resulting in a micronodular pattern. Later, with cessation of drinking, it takes on a mixed macro- and micronodular form.

Gallstones are responsible for 35-60 per cent of acute pancreatitis and alcohol up to 65 per cent. The ratio biliary tract disease/alcohol is 3 : 1 in women and 1 : 6 in males. It is unclear if alcohol causes de novo acute pancreatitis or acute exacerbations of underlying chronic pancreatitis. Alcohol results in protein rich pancreatic fluid that forms protein plugs which block small ducts. These undergo secondary calcification and cause local atrophy and fibrosis. Alcohol may also directly injure acinar cells or result in deranged intracellular transport of pancreatic enzymes with their premature activation.

Acute pancreatitis manifests as parenchymal necrosis, oedema and enzymatic fat necrosis. Acute haemorrhagic pancreatitis is more severe with more extensive necrosis as well as haemorrhage. In chronic pancreatitis, the pancreas appears shrunken and fibrotic. It may be associated with malabsorption, diabetes mellitus and pain.

Alcohol is a cause of dilated cardiomyopathy. The appearances of the heart are similar to those in idiopathic dilated cardiomyopathy. The aetiology may be direct toxicity of alcohol on the myocardium or thiamine deficiency (known as beri beri) or both. Low levels of alcohol increase plasma high density lipoprotein protecting against atheroma whereas high levels of alcohol have the opposite effect.

Acute gastritis has already been mentioned. Vomiting following binge drinking may result in a Mallory-Weiss tear at the gastro-oesophageal junction. Typically blood is not present initially. Major blood loss may result. Alcoholic cirrhosis is associated with an increased occurrence of chronic peptic ulcer.

Brain injury may be associated with cognative decline, ataxia or the Wernicke-Korsakoff syndrome (secondary to thiamine deficiency). The latter presents acutely with ataxia, global confusion, opthalmoplegia and nystagmus and chronically with loss of short-term memory (Korsakoff’s syndrome).

The pathological manifestations include generalized cerebral atrophy, cerebellar atrophy with loss of Purkinje cells and changes of Wernicke’s encephalopathy. The latter include symmetrical discoloration, softening, congestion and punctate haemorrhages in the paraventricular regions of the thalamus and hypothalamus, mamillary bodies, about the aqueduct in the midbrain, in the floor of the fourth ventricle and in the anterior cerebellum. Histologically blood vessels are dilated with endothelial proliferation and ringed by haemorrhages. There is some demyelination, loss of neuropil and gliosis.

A symmetric, nonspecific polyneuropathy (peripheral neuropathy) involving motor, sensory, and reflex arcs beginning in the nerves of the feet and lower legs may develop secondary to thiamine deficiency or direct alcohol injury. It extends proximally with progression. It begins with myelin degeneration but may progress to disruption of nerves.

Alcohol ingestion in pregnancy can result in the fetal alcohol syndrome. The components of this include growth retardation, microcephaly with mental retardation, atrial septal defect, short palpebral fissures and maxillary hypoplasia. It can occur with relatively modest alcohol intake.

Infection

Alcohol liver disease is associated with increase susceptibility to infection particularly primary peritonitis. Associated factors may delay diagnosis and treatment of infections such as pneumonia.

Alcohol ingestion is associated with driver and pedestrian road trauma and injury resulting from fights.

Binge drinking may precipitate alcoholic myopathy involving rhabdomyolysis, myoglobinuria and renal failure.