Complications
Mallory-Weiss syndrome is a common cause of upper gastrointestinal bleeding in patients with recurrent and active alcohol use. Nearly one half of the patients have no antecedent symptoms and present initially with upper gastrointestinal bleeding after vomiting.
Endoscopic therapy is effective and safe in producing hemostasis in these patients.[132]
Delirium tremens (DT) is a clinical condition that appears in about 5% of patients affected by severe alcohol withdrawal syndrome. It usually develops 2-4 days after decrease or discontinuation of chronically high alcohol intake.
DT is characterized by signs and symptoms including confusion, perceptual disturbances, and hallucinations (in particular micropsia and macropsia), tremor, altered sleep-wake cycle, changes of psychomotor activity, paroxysmal sweating, emotional lability, fever, autonomic hyperresponsiveness with hypertension, and tachycardia.
Respiratory complications or cardiac arrhythmias are the most common cause of death in patients with DT. Aggressive treatment with benzodiazepines is the recommended intervention.[127]
Alcohol-related seizures are defined as adult-onset seizures that occur as a complication of a severe alcohol withdrawal syndrome.
Concurrent risk factors, including preexisting epilepsy, structural brain lesions, and the use of other substances, may contribute to their development in some patients.[128]
While alcohol affects virtually all of the body systems, the liver is one of the sites of greatest impact. Excessive alcohol use can lead to both acute and chronic liver disease.
The three conditions most associated with alcohol use are fatty liver (steatosis), hepatitis (acute and chronic), and cirrhosis. These conditions can occur separately or concurrently. Definitive treatment requires abstinence from alcohol.
Women are at higher risk of developing alcohol-related liver disease, due to decreased metabolism of alcohol compared with men.
Persistent alcohol intake in patients with alcohol-related cirrhosis is associated with a significant increase in risk of death due to bleeding esophageal varices, infection, renal failure, and/or hepatic failure.
Although some medications may be helpful once the condition is established, the most effective strategy for these patients is alcohol abstinence, because medical and surgical treatments have limited success while drinking continues.
Total alcohol abstinence is able to improve both histologic and clinical outcome measures of all stages of alcohol-related liver disease.[42]
Alcohol consumption increases the risk of mouth, oropharynx, larynx, esophagus, colon, rectum, liver, and breast cancer, compared with never-drinkers.[129]
Alcohol use increases the risk of hypertension.[129]
Alcohol use increases the risk of both hemorrhagic and ischemic stroke.[129]
Alcohol consumption is associated with increased risk of hippocampal atrophy, in a dose-dependent manner.[134]
Alcohol-related cardiomyopathy is characterized by cardiomegaly, disruptions of myofibrillary architecture, reduced myocardial contractility, decreased ejection fraction, and enhanced risk of stroke and hypertension.[133]
Alcohol consumption >48 g of ethanol per day (2 standard drinks) is associated with an elevated risk of pancreatitis.[129]
Alcohol use disorder is often associated with thiamine deficiency. Severe thiamine deficiency may result in the development of Wernicke encephalopathy, which is characterized by ocular motility disorders, ataxia, and mental status changes (confusion).
When patients with Wernicke encephalopathy are untreated or undertreated with low doses of thiamine, mortality rates average about 20% and Korsakoff psychosis develops in about 85% of survivors. Korsakoff psychosis is characterized by anterograde and retrograde amnesia, disorientation, and confabulation.
Because of the close relationship between these clinical entities, the two disorders are usually referred to as the Wernicke-Korsakoff syndrome.[130][131]
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