History and exam
Key diagnostic factors
common
presence of risk factors
withdrawal
Central nervous system hyperexcitability develops when alcohol use is reduced greatly or suddenly stopped. Increased autonomic activity, agitation, and nervousness are common symptoms. Generalised seizures and a confusional state (delirium) are seen in more severe cases of alcohol withdrawal. Alcohol withdrawal may occur in a patient with alcohol still present in the serum, even at relatively high levels, if those levels represent a reduction in blood level for that individual.
tolerance
This is an adaptation in which the central nervous system becomes less responsive to the chronic presence of alcohol. Both the pleasurable and impairing (e.g., poor co-ordination, sedation) effects of alcohol are attenuated in response to chronic drinking, which can lead to increased alcohol consumption by a person seeking to replicate the initial pleasurable effects experienced with alcohol use.
increased/decreased liver size, jaundice, ascites
These signs are indicators of significant alcohol-related liver disease. Liver damage is very common in people with alcohol-use disorder; it may present in a variety of ways (e.g., steatosis, hepatitis, liver cirrhosis).[42]
Other diagnostic factors
common
insomnia
While alcohol can promote sleep onset with infrequent use, chronic use disrupts sleep quality, including REM sleep, sleep continuity, and total sleep time.[43]
erectile dysfunction
The majority of men with alcohol-use disorder have some sexual dysfunction, including erectile dysfunction or low sexual desire.[44]
nicotine-use disorder
gastrointestinal distress
muscle cramps, pain, tenderness, altered sensory perception
Peripheral neuropathy is a common finding in patients with alcohol-use disorder. It is typically related to poor nutritional status (thiamine deficiency) and is often more prominent in the lower extremities.
hypertension and tachycardia
Common sequelae of alcohol-use disorder, intoxication, and withdrawal. An elevation of 20-30 mmHg over baseline in systolic blood pressure and 10-20 mmHg over baseline in diastolic blood pressure is common with alcohol-use disorder. Even greater elevations are seen in alcohol withdrawal.
Blood pressure often reverts to normal without antihypertensives after several weeks of abstinence.[49]
impaired nutritional status
Both overweight and underweight status can be a sign of alcohol-use disorder. Reduced fat mass is related to metabolic changes induced by alcohol (increased lipid peroxidation); return to a normal metabolic state appears to require at least 3 months of total abstinence.[50][51] It has also been suggested that different kinds of alcoholic beverage and some hormones may play a role in these changes.[52][53][54]
uncommon
broad-based gait
Cerebellar degeneration can occur in people with alcohol-use disorder. It may occur as a result of direct alcohol toxic effect and/or nutritional (thiamine) deficiency.
Risk factors
strong
family history of alcohol-use disorder
It is well established that alcohol-use disorder occurs more frequently in people with a family history of alcohol-use disorder.[19] The heritability of alcohol-use disorder has been estimated to be between 40% and 70%, but concordance between twins is less than 50%.[14] Thus, though genetics play an important role, other environmental factors are important, and no individual gene is necessary or sufficient for the development of alcohol-use disorder.
antisocial behaviour (pre-morbid)
high trait anxiety level
High trait anxiety strongly increases the risk of alcohol-use disorder.[23] The presence of social phobia or panic disorder is associated with a higher risk of developing alcohol-use disorder.
weak
lack of facial flushing on exposure to alcohol
The risk of alcohol-use disorder is reduced in individuals who show alcohol-induced facial flushing. The flushing is due to an accumulation of acetaldehyde, a toxic metabolite of alcohol, in people who carry a gene for a version of the enzyme aldehyde dehydrogenase that metabolises acetaldehyde more slowly. The gene is common in some East Asian populations. A less potent variant (in terms of reduced acetaldehyde-metabolising capacity) has also been found in some white populations.[24]
low responsivity to the effects of alcohol
Low responsivity to alcohol (i.e., high tolerance) has been found to predict the incidence of alcohol-use disorder in a follow-up study.[25] It is hypothesised that individuals with a low response to alcohol consume more alcohol to feel its effects and are, therefore, more likely to develop alcohol-use disorder.
history of gastric bypass
The risk of alcohol-use disorder is increased in individuals after bariatric surgery to correct obesity.[26] Alcohol is metabolised more quickly in patients with gastric bypass due to altered gastric metabolism, leading to more sensitivity to the effects of alcohol. Patients undergoing gastric bypass should be counselled on the sensitisation to alcohol that they will experience, and the increased risk of alcohol-use disorder, which remains elevated several years after the operation.
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