Physical exam – Look for evidence of liver disease and anemia. Pallor, jaundice, scleral icterus, telangiectasia, ascites, fetor hepaticus (“breath of the dead”), caput medusa, palmar erythema, peripheral edema, and splenomegaly.

Hepatic function – Can see a spectrum of changes from reversible fatty changes to cirrhosis. Increased serum transaminases (AST, ALT) due to cell injury and death, hyperbilirubinemia, and decreased production of clotting factors. Hypoproteinemia due to albumin depletion. Immunosuppression due to depletion of the reticuloendothelial system.

Hematology – Anemia (GI bleeds, bone marrow depression, or nutritional deficiencies), thrombocytopenia (bleeding), leukopenia, and abnormal leukocyte chemotaxis (both cause impaired wound healing and increased risk of infection).

Neurologic function – CNS depressant and can cause respiratory depression and death. Effects potentiated by concomitant use of narcotics, benzodiazepines, and barbiturates. Chronic alcohol abuser may require more anesthetic agents to produce desired level of anesthesia (but with greater risk).

Nutritional deficiencies – Chronic alcoholics are frequently malnourished. Ethanol interferes with absorption, metabolism, and storage of vitamins (specifically thiamine, folate, and vitamin B6). Thiamine deficiency may produce ophthalmoplegia, ataxia, confusion (Wernicke’s encephalopathy puts patients at risk for Wernicke-Korsakoff syndrome). Thiamine deficiency may also cause weakness, fatigue, myalgias, and anorexia. Folate deficiency may contribute to megaloblastic anemia.

Cardiac – May have an associated cardiomyopathy or low-output heart failure (leading cause of death).

Endocrine – Hypogonadism, testicular failure, and gynecomastia.

GI – Increased incidence of gastritis, pancreatitis, and liver failure.

Respiratory – Acute alcohol ingestion can cause hyperventilation and an increase in dead space ventilation. Aspiration of gastric contents with chemical pneumonitis and pulmonary infections is an increased risk with chronic alcoholism.

Begins 6–24 hours after the last intake of alcohol.

The signs and symptoms include tremors, agitation, nausea, sweating, vomiting, hallucinations, insomnia, tachycardia, hypertension, delirium, and seizures.

The most dreaded complication is delirium tremens (hyperthermia, tremors, and seizures), which has a high mortality rate.

Labs-CBC, Basic Metabolic Panel, LFTs.

Postpone surgery for acutely intoxicated patient.

Preoperative labs: CBC, BMP, and LFTs.

EKG – for patients with known alcohol-induced cardiomyopathy.

Evidence of active hepatitis – postpone surgery and obtain a medical consult.

Replenish electrolytes as required.

Monitor glucose levels closely.

Delirium tremens prophylaxis with benzo-diazepines.

Antibiotic prophylaxis due to immunosuppression.

Patients are often volume depleted secondary to dehydration and will require fluid resus-citation.

Patients are more prone to hypotension as a result of hypoalbuminemia that causes third spacing.

Patients are less sensitive to endogenous or parenteral catecholamines which can contribute to hemodynamic instability.

During emergency anesthesia with presumed alcohol intoxication, rapid sequence induction is indicated due to possible aspiration of stomach contents. Alcohol, opioids, and trauma are high risk factors for aspiration.

Esophageal varices are a concern for rupture in unsuccessful endotracheal intubation.

Chronic alcohol use increases dose requirements for general anesthetic agents as the minimal alveolar concentration is increased.

Intravenous drug doses that are increased (e.g., propofol, thiopental, and opioids) can exacerbate the risk of cardiovascular instability in patients who may be suffering from cardiomyopathy, heart failure, or dehydration.

In acutely intoxicated, non-habituated patients, the minimal alveolar concentration (MAC) of inhalational agents is reduced. Acutely intoxicated patients are more sensitive to the effects of opioids, benzodiazepines, and barbiturates. Sensitivity to other drugs may occur due to competitive inhibition from elevated blood ethanol concentration. Volatile agents compete with ethanol for binding on neuronal gamma-aminobutyric acid (GABA) and glycine receptors.

The distribution and metabolism of anesthetic drugs are altered by hypoalbuminemia and hepatic impairment. Neuromuscular blocking agents that undergo hepatic metabolism may have a prolonged duration of action.

Increased risk of postoperative infection due to immune deficiency resulting from alcohol adverse effects on hematologic system causing leukopenia and altered cytokine production.

Acute confusion or delirium after an operation can be mitigated by attention to pain control measures, oxygenation, and correction of metabolic disturbances. Consider intravenous haloperidol (0.5–10 mg may be repeated after 20–30 minutes) for acute agitation. Other medications include chlorpromazine, risperidone, and olanzapine.

An amphetamine that blocks the reuptake of norepinephrine, serotonin, and dopamine transporting mechanisms in the CNS leading to intense stimulation, euphoria, and pleasure. Cocaine has a negative impact on several different systems.

Cardiovascular system – The majority of concern is the patient’s cardiovascular system and changes in vasculature due to cocaine’s effects and especially with the risk of developing cocaine-induced cardiomyopathy in chronic abusers. Acute cocaine use can cause coronary vasospasm, myocardial ischemia/infarction, and ventricular dysrhythmias. EKG findings may show prolonged QRS and QT intervals and premature ventricular contractions, which can degenerate into deadly ventricular dysrhythmias. The myocardium is also sensitized to endogenous catecholamines.

Respiratory system – There is a risk of alveolar hemorrhaging and pulmonary edema from crack cocaine (smoked) use. Snorting cocaine can lead to mucosal ulcerations which can cause epistaxis and nasal septal destruction. Cocaine users also can have chronic coughs with an increased risk of bronchospasm and diffusion capacity abnormalities.

Hematologic system – Cocaine activates platelets, increases platelet aggregation, and promotes thrombus formation. This adds further risk for cardiac and cerebrovascular events intra-operatively. Cocaine-induced thrombocytopenia can also occur which is similar to idiopathic thrombocytopenia purpura.

Nervous system – Cocaine alters pain perception, leading to potentially lower pain thresholds. This creates challenges in analgesia administration, both intra-operatively and postoperatively. Presynaptic reuptake of norepinephrine, dopamine, serotonin, and tryptophan is prevented, leading to intense activation of the sympathetic nervous system. May see an acute elevation in blood pressure, tachycardia, and predisposition to ventricular tachyarrhythmias and seizures.

Gastrointestinal system – Chronic cocaine use also causes delayed gastric emptying, which is a risk for aspiration. As a result, aspiration prevention is an important consideration preoperatively.