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Anaesthesia and chronic alcohol abuse

Anaesthesia and chronic alcohol abuse
Colin Berry
Anaesthetists may assist in the management of patients who have ingested alcohol acutely or chronically:
  • trauma (vehicle related, violence, domestic accidents, child abuse)
  • complications of drinking (coma, GI bleeding, portal hypertension, pancreatitis)
  • unrelated surgical procedures in alcoholics.
Physical complications of alcohol abuse
  • Acute intoxication and coma. Blood alcohol concentration >400 mg/ 100 ml risks respiratory arrest and carries a 5% mortality.
  • Alcoholic liver disease. Earliest form is reversible fatty liver progressing to alcoholic hepatitis, characterized by abdominal pain, weight loss, jaundice, and fever. Histological changes can be reversed by abstinence. Alcoholic cirrhosis is characterized by jaundice, ascites, portal hypertension, and hepatic failure. Cirrhosis is irreversible but abstinence may result in stabilization and increased life expectancy.
  • Pancreatitis.
  • Upper gastrointestinal bleeding—gastritis, erosive gastric ulcers, and Mallory-Weiss oesophageal tears. Oesophageal varices in those with severe liver disease and portal hypertension.
  • Cardiac arrhythmias including atrial fibrillation (may complicate binge drinking and chronic misuse). Ventricular arrhythmias.
  • Ischaemic heart disease and hypertension. Modest alcohol intake may offer cardioprotection. Alcoholic cardiomyopathy is characterized by a dilated hypokinetic left ventricle with a decreased ejection fraction. Patients may present with congestive cardiac failure and oedema, exacerbated by low serum albumin. Cardiac failure is a feature of heavy alcohol ingestion.
  • Hypoglycaemia may complicate acute alcohol intoxication, alcoholic liver disease, and pancreatic disease. More common in children and adolescents.
  • Ketoacidosis may present after binge drinking in association with vomiting and fasting. Blood alcohol concentrations may not be elevated at the time.
  • Convulsions are most commonly seen 7–48 h after cessation of drinking. Typically tonic-clonic with loss of consciousness. Several fits over a period of a few days are common. Normally self-limiting unless associated with trauma or sustained unconsciousness. Hypokalaemia and hypomagnesaemia predispose to convulsions. Exclude other causes such as intracranial bleeds, tumours, or abscesses.
  • Anaemia (macrocytic—direct toxic alcohol effect; megaloblastic—folate deficiency; iron deficiency—poor diet, upper GI blood loss). Neutropenia (due to marrow toxicity or folate deficiency). Thrombocytopenia.
  • Immunodeficiency with increased prevalence of respiratory infections (including TB).
  • Skin diseases: psoriasis, eczema, rosacea, fungal infections, and acne are commoner in heavy drinkers.


Pharmacological considerations
Patients with acute alcohol ingestion are partially anaesthetized and reduced concentrations of volatile agents are required to produce anaesthesia (and respiratory and cardiac side-effects). Chronic exposure to alcohol induces tolerance to some anaesthetic agents. Serious liver pathology may result in depressed metabolism and drug clearance, which increases drug half-life (see liver failure p. 127).
Preoperative assessment
  • Quantify excessive drinking and lifestyle. History of other drug misuse.
  • Ask about weight loss and history of GI bleeding.
  • Recurrent chest infections (smoking, repeated pulmonary aspiration, reduced ciliary activity).
  • Examine for hypertension, cardiac failure, arrhythmias, fetor, spider naevi, ascites, jaundice, bruising, malnutrition, neglect, tremor, peripheral neuropathy, psychosis, encephalopathy, convulsions (withdrawal).
  • FBC (increased MCV, iron deficiency, bone marrow depression).
  • Blood alcohol concentration.
  • Glucose and electrolytes (hypokalaemia, hypernatraemia, and hypomagnesaemia).
  • Liver enzymes: raised γ-glutamyl-transpeptidase and aminotransferases. Albumin is often reduced.
  • Coagulation may be abnormal due to clotting factor deficiency (reduced synthesis of factors II, V, VII, X, and XIII).
  • ECG: conduction defects, bifid T wave, ST changes (similar to digoxin changes), arrhythmias (commonly AF).
  • Echocardiogram if suspicion of alcoholic cardiomyopathy: dilated LV, decreased ejection fraction, reduced LV function.
  • Chest radiograph may show aspiration pneumonia, TB, or lung cancer.
Preoperative management
  • Avoid non-emergency surgery in the presence of acute alcohol toxicity.
  • If emergency surgical intervention is unavoidable, ensure adequate rehydration with careful attention to electrolyte and blood glucose disturbances. Give intravenous vitamins (e.g. Pabrinex slow IV twice daily for up to 7 days).
  • Correct clotting abnormalities. Treat anaemia with appropriate transfusion.
  • Patients with liver failure require intensive care if surgery is planned.
Anaesthetic management
  • Patients with GI bleeding and cirrhosis are in danger of developing hepatic failure. Insert a gastric tube (with care in the presence of varices) to stop digestion of blood.
  • Regional anaesthesia may avoid the need for large doses of sedative opioids (see below).


Postoperative management
  • Anticipate alcohol withdrawal symptoms. Most patients can tolerate 24–48 h abstinence perioperatively. With major surgery it is often easiest not to complicate management by attempting alcohol withdrawal perioperatively.
  • If problems occur, an infusion of ethanol 5% (add 50 g ethanol to 1 litre 0.9% saline or 5% dextrose) can be used to prevent alcohol withdrawal in the immediate perioperative period. Alternatively, oral or nasogastric administration of alcoholic drinks may be appropriate (within limits)!
  • Alternatively treat with chlordiazepoxide (10–50 mg four times a day) if the patient can take oral medication or chlormethiazole if intravenous therapy is required. An infusion of chlormethiazole 0.8% (8 mg/ml) is initially given at 3–7.5 ml (24–60 mg)/min until the patient is lightly sleeping, and then reduced to 0.5–1 ml (4–8 mg)/min to maintain sedation. Overdosage with chlormethiazole can cause profound respiratory depression and should be used with great care if other sedatives/opioids are being used. Manage these patients in HDU. This should not be a reason to provide inadequate analgesia.
Further reading
Chick J (1993). Alcohol problems in the general hospital. British Medical Bulletin, 50, 200–10.

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