48: Alcohol and Substance Abuse

Published on 06/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1245 times

CHAPTER 48 Alcohol and Substance Abuse

James Duke, MD, MBA

1 How is alcohol absorbed and metabolized?

Alcohol is absorbed across the gastrointestinal mucosa, more so in the small intestine than in the stomach. The volume of distribution (Vd) of alcohol is that of body water. Alcohol easily crosses the blood-brain barrier. Arterial blood levels of alcohol correlate well with concentrations in lung alveoli, thus the basis of the breathalyzer test used by law-enforcement officers.

Alcohol is metabolized primarily in the liver. Most consumed alcohol is converted to acetaldehyde by the enzyme alcohol dehydrogenase. Alcohol metabolism follows Michaelis–Menten zero-order kinetics. When alcohol dehydrogenase is saturated with ethanol, the rate of metabolism is constant, although alcohol concentration may increase. A 5% to 10% amount of consumed alcohol is excreted unchanged in the breath and urine.

2 What are the acute and chronic effects of alcohol on the nervous system?

Acutely alcohol depresses the central nervous system by inhibiting polysynaptic function, which is characterized by generalized blunting and loss of higher motor, sensory, and cognitive function. Although the behavioral effects of alcohol consumption may seem excitatory or stimulating to observers and users, this impression is probably caused by a depressive effect on inhibitory pathways (disinhibition).

Chronic alcohol use is associated with peripheral nerve and neuropsychiatric disorders, many of which (e.g., Wernicke’s encephalopathy and Korsakoff’s psychosis) may be linked to nutritional deficiencies. Alcohol-related neuropathy usually involves pain and numbness in the lower extremities, often with concomitant weakness of the intrinsic muscles of the feet. Patients may exhibit hypalgesia in a stocking-foot distribution, and the Achilles tendon reflex may be absent. Generalized weakness in the proximal limb musculature may also be noted.

3 What are the effects of alcohol on the cardiovascular system?

Moderate acute ingestion of alcohol produces no significant changes in blood pressure or myocardial contractility. Cutaneous vasodilation occurs, and heart rate increases. At toxic levels of acute alcohol ingestion, a decrease in central vasomotor activity causes respiratory and cardiac depression.

The leading cause of death in chronic users of alcohol is cardiac dysfunction. Consumption of 60 oz of ethanol per month (8 pints of whiskey or 55 cans of beer) may lead to alcohol-induced hypertension. An intake >90 oz per month over a 10-year period may result in congestive cardiomyopathy with associated pulmonary hypertension, right-heart failure, and dysrhythmias (usually atrial fibrillation and premature ventricular contractions). Ventricular tachydysrhythmias, ventricular fibrillation, and sudden death are also risks.

4 How does alcohol affect the respiratory system?

Acute alcohol intake may cause hyperventilation via disinhibition of central respiratory regulation centers and increases in dead-space ventilation. Despite hyperventilation, alcohol depresses the ventilatory response to carbon dioxide. Aspiration of gastric contents is a risk. Chronic alcohol users are susceptible to pulmonary infections, often by staphylococci or gram-negative organisms. There is also a generalized decrease in all lung capacities (vital, functional residual, and inspiratory capacity).

5 How does alcohol affect the gastrointestinal and hepatobiliary systems?

Acute alcohol use may cause esophagitis, gastritis, and pancreatitis. Chronic alcohol use leads to delayed gastric emptying and relaxation of the lower esophageal sphincter, increasing the risk of aspiration. The liver undergoes transient and reversible fatty infiltration during acute alcohol use. Although such changes resolve with abstinence and the cycle can repeat itself many times, prolonged alcohol exposure leads to chronic infiltration of fat, which over time progresses to necrosis and fibrosis of liver tissue. The initial presentation of fatty liver is hepatomegaly. When necrosis, fibrosis, and cirrhosis become apparent, the liver regresses in size. Chronic severe consumption of alcohol leads to irreversible cirrhosis and alcohol-induced hepatitis. Hepatic synthetic function is also impaired. Production of albumin and coagulation factors II, V, VII, X, and XIII is decreased. Reduction of albumin results in lower intravascular oncotic pressure and may lead to tissue edema. A reduction in circulating coagulation factors may predispose to bleeding, which is evidenced by a prolonged prothrombin time.

6 Which nutritional deficiencies are seen in chronic alcohol users?

Deficiency of thiamine leads to Wernicke’s encephalopathy, polyneuropathy, and cardiac failure characterized by high cardiac output, low systemic vascular resistance, and loss of vasomotor tone. Folic acid deficiency causes bone-marrow depression and thrombocytopenia, leukopenia, and anemia.

7 What are the effects of alcohol on inhalational anesthetics?

In acutely intoxicated, nonhabituated patients, the minimal alveolar concentration (MAC) of inhalational agents is reduced. For chronic users of alcohol the MAC for inhalational agents is increased.

Acutely intoxicated patients are more sensitive to the effects of barbiturates, benzodiazepines, and opioids. Cross-tolerance develops to intravenous agents with chronic alcohol exposure.

8 How does alcohol affect muscle relaxants?

Patients with liver disease may have decreased levels of circulating plasma cholinesterase, and the effects of succinylcholine may be prolonged. Cirrhotic patients with poor liver function have a greater Vd for injected drugs and thus require a larger dose of nondepolarizing relaxants. Relaxants that rely on hepatic clearance may have a prolonged duration of action. Muscle relaxants that are metabolized independently of organ function (e.g., cisatracurium) are good choices for patients with liver disease.

9 Describe special considerations in the perioperative assessment of alcohol-abusing patients

Special consideration must be given to the cardiovascular system of chronic alcohol users. Tachycardia, dysrhythmias, or cardiomegaly may indicate alcohol-related cardiac dysfunction; and a 12-lead electrocardiogram (ECG) should be evaluated. Patients with alcohol-induced cardiac disease are less sensitive to endogenous or parenteral catecholamines. Hypokalemia and hypoglycemia are common, as are anemia, thrombocytopenia, and altered coagulation. These patients are often volume depleted and will require fluid resuscitation. Insert a urinary catheter to follow urine output. Intravascular monitoring should be individualized. Instrumentation of the esophagus should be avoided in patients with known liver disease because of the possibility of rupturing esophageal varices.

10 How should sober chronic alcohol abusers be anesthetized?

Sober chronic alcohol users can tolerate intravenous and inhalational anesthetics. Isoflurane may be the best inhalational agent for maintaining hepatic blood flow. In general, a balanced anesthetic technique using amnestics, opioids, muscle relaxants, and an inhalational agent will suffice.

11 What are the signs and symptoms of alcohol withdrawal?

Alcohol withdrawal presents as anorexia, insomnia, weakness, combativeness, tremors, disorientation, auditory and visual hallucinations, and convulsions. Onset is usually 10 to 30 hours after abstinence, and the symptoms may last for 40 to 50 hours. Prolonged abstinence may lead to delirium tremens or autonomic hyperactivity (tachycardia, diaphoresis, fever, anxiety, and confusion). Alcohol withdrawal syndrome may occur while under anesthesia and manifest as uncontrolled tachycardia, diaphoresis, and hyperthermia. The treatment is administration of benzodiazepines or intravenous infusion of ethanol.

KEY POINTS: Concerns in Chronic Alcoholics image

1. May have cardiomyopathy and dysrhythmias
2. Predisposed to aspiration and have diminished pulmonary function
3. Portal hypertension and varices (avoid orogastric and nasogastric tubes)
4. Impaired synthetic liver function (important screening tests are albumin and prothrombin time)
5. Alcohol withdrawal may cause seizures.

12 Review the differences between addiction, dependence, pseudoaddiction, and tolerance

According to the American Pain Society:

image Dependence implies “a state of adaptation that is manifested by a drug class–specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of the drug, and/or administration of an antagonist.”
image Opioid tolerance is “a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time.”
image Addiction “is a primary, chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing its development and manifestations. It is characterized by behaviors that include one or more of the following: impaired control over drug use, compulsive use, continued use despite harm, and craving.”
image Pseudoaddiction refers to an iatrogenic state in which the patient displays addiction-type behaviors, but the cause is inadequate treatment of a painful condition. Often the setting is an acute pain condition superimposed on a chronic pain state. Patients on prolonged opioid therapy develop physical dependence and potentially tolerance, but they usually do not develop addictive behaviors.

13 List complications of chronic opioid abuse

Cellulitis Pneumonia
Adrenal suppression Tetanus
Abscess formation Subacute bacterial endocarditis
Thrombophlebitis Hepatitis
Atelectasis Acute pulmonary edema
Anemia Systemic and pulmonary emboli
Pulmonary hypertension Acquired immunodeficiency syndrome
Sepsis Sclerosing glomerulonephritis
Death from overdose

14 Discuss perioperative problems associated with the chronic opioid abuser

The perioperative period is not an appropriate time to attempt opioid withdrawal. It is necessary to know the patient’s usual opioid requirements to avoid undermedication. Associated behavioral and psychologic problems may make general anesthesia a better option than regional or local anesthesia. These patients may be in acute withdrawal and be uncooperative. Intravenous access may be difficult, and central venous catheterization may be necessary. A substantially increased dose of opioids to achieve the desired effect is the norm. Consultation with a pain-management team may help with development of a realistic postoperative pain-management strategy.

15 Describe the time frame and stages of opioid withdrawal

The onset and duration of withdrawal vary with the drug used. For example, meperidine withdrawal symptoms peak in 8 to 12 hours and last for 4 to 5 days. Heroin withdrawal symptoms usually peak within 36 to 72 hours and may last for 7 to 14 days. Symptoms of withdrawal include restlessness, sweating, nausea, rhinorrhea, nasal congestion, abdominal cramping, lacrimation, and drug craving. Overt withdrawal results in piloerection, emesis, diarrhea, muscle spasms (thus the term kicking the habit), fever, chills, tachycardia, and hypertension.

16 What medications are used to stabilize and detoxify the withdrawing opioid patient?

Long-acting medications (e.g., methadone and sustained-release morphine) are used because they have a slower onset of action and the high experienced with rapid-onset medications is less prominent. Autonomic hyperactivity and other symptoms of acute opiate withdrawal are treated with β-adrenergic antagonists and α2-agonists such as clonidine.

17 To what arrhythmias are methadone-treated patients prone?

There are multiple reports of these patients having prolonged correct QT intervals, torsades de pointes, and sudden death.

Other important facts about methadone are that it has no effect on seizure disorders, has no active metabolites, is relatively safe in renal failure, and has not been associated with hepatic toxicity.

18 What are the various forms of cocaine and routes of administration?

A hydrochloride salt of cocaine is a powdery, white crystalline, water-soluble substance that can be sniffed or injected. A lipid-soluble form, called crack or free-base cocaine, is inexpensively manufactured by mixing the hydrochloride salt with an alkali. Crack is more stable on heating, vaporizes readily, and has high bioavailability when smoked.

19 How is cocaine metabolized and excreted?

Peak plasma concentrations occur 15 to 60 minutes after intranasal ingestion; its biologic half-life is about 45 to 90 minutes. Plasma (pseudocholinesterase) and liver esterases hydrolyze cocaine to ecgonine methyl ester (EME) and benzoylecgonine. EME and benzoylecgonine constitute 80% of the metabolites of cocaine and are detected in urine for 14 to 60 hours after cocaine use. Only 1% to 5% is cleared unmetabolized in the urine.

20 What are the mechanism of action and physiologic effects of cocaine?

There is inhibition of the norepinephrine, dopamine, and serotonin transporter mechanisms. However, the physiologic effects are caused principally by increases in norepinephrine levels. At adrenergic nerve endings cocaine inhibits the reuptake of norepinephrine into the neuron. Increases in serum norepinephrine levels increase systolic, diastolic, and mean arterial pressure; heart rate; and body temperature.

21 List the common signs and symptoms of acute cocaine intoxication

Nausea and vomiting Headache
Rapid or irregular heartbeat High or low blood pressure
Hallucinations Chest pain
Convulsions and stroke Mydriasis

22 What is the most life-threatening toxic side effect and its treatment?

Cardiac ischemia and subsequent acute myocardial infarction are present in approximately 6% of all hospital admissions for chest pain secondary to cocaine ingestion. Although acute vasoconstriction with or without thrombus formation has been considered the principal cause, it is now believed to be the result of sympathetic stimulation associated with increased norepinephrine levels. Treatment of cocaine-induced chest pain includes the use of selective β1-adrenergic blockade, nitrates, calcium channel blockers, and α-adrenergic blockers. Selective β2-blockade should generally be avoided since it may lead to unopposed α1-mediated coronary and peripheral vasoconstriction.

23 List the signs and symptoms of cocaine withdrawal

Agitation Anxiety and depression
Fatigue Irritability and disturbed sleep
Tremors Myalgias

24 What are the anesthetic concerns in the acutely intoxicated cocaine user?

Preoperative sedation and a deep level of general anesthesia inhibit adrenal release of catecholamines, potentially reducing the dysrhythmic effects of cocaine. The patient should be well anesthetized before airway instrumentation to avoid severe tachycardia and hypertension. Cocaine sensitizes the cardiovascular system to the effects of endogenous catecholamines. Ketamine and pancuronium potentiate the cardiovascular toxicity of cocaine and should be avoided. The MAC of inhalational anesthetic agents is increased in the setting of acute intoxication. Should hypotension require pressor therapy, direct-acting agents such as phenylephrine may be better since these patients may be catecholamine depleted.

25 Can the nonacutely intoxicated patient who has used cocaine be safely anesthetized?

A recent study in a large urban public hospital determined that general anesthesia can be safely administered. However, cocaine is known to prolong the QT interval, predisposing the patient to ventricular arrhythmias, including torsades de pointes. Thus an ECG must be obtained before surgery, and, if the QT interval is less than 500 msec, the patient may be anesthetized.

KEY POINTS: Concerns in Patients Taking Cocaine image

1. Myocardial ischemia is not uncommon in cocaine-abusing patients, and selective β2-blockade should be avoided because it may cause vasoconstriction and worsen the ischemia.
2. Severe hypertension and tachycardia are risks during airway management unless the patient is deeply anesthetized.
3. Cocaine sensitizes the cardiovascular system to the effects of endogenous catecholamines. Ketamine and pancuronium potentiate the cardiovascular toxicity of cocaine and should be avoided.

26 What is crystal methamphetamine and what are its properties?

This refers to the synthetic stimulant methamphetamine. Most methamphetamine users are white and young adult. Most users are male, but it is the most common drug of abuse among women. Use of methamphetamine is common among homosexual males, and there is a strong relationship between its use and having the human immunodeficiency virus.

Methamphetamine use produces a rapid pleasurable rush followed by euphoria, heightened attention, and increased energy. These effects are caused by release of norepinephrine, dopamine, and serotonin. It is quite similar to cocaine in its manifestations, and its relatively lower costs may account for its increasing abuse.

Recommendations for anesthetizing a methamphetamine-abusing patient are similar to those for cocaine. Avoid anesthetizing the acutely intoxicated patient for elective procedures. Anesthesia is probably safely started in patients who are chronic users but not acutely intoxicated. There may be an increased incidence of dental trauma because of the common finding of dental decay.

27 What are the signs of symptoms of methamphetamine intoxication and withdrawal?

Signs and symptoms of intoxication include anorexia, diaphoresis, hypertension, tachycardia, hyperthermia, agitation, and psychosis. Patients can also have myocardial infarctions, seizures, strokes, rhabdomyolysis, and renal failure. The withdrawing patient will experience fatigue, irritability, insomnia, anxiety, and psychotic reactions. An unusual sign seen in chronic methamphetamine users is dental decay, known as meth mouth.

28 What is ecstasy and what are its mechanism of action and route of administration?

Ecstasy, or 3,4-methylenedioxymethamphetamine, is a synthetic, psychoactive drug similar to the stimulant methamphetamine and the hallucinogen mescaline. It increases the activity of multiple neurotransmitters, including serotonin, dopamine, and norepinephrine. It is taken orally in capsule or tablet form. Its effects last 3 to 6 hours. Additional doses slow its enzymatic degradation, resulting in increased duration of action and increased risk of toxicity.

29 What are the cognitive, physical, and psychologic effects of ecstasy?

Abusers experience a sense of well-being and decreased anxiety. Memory impairment may occur. Physical effects include nausea, chills, involuntary teeth clenching, muscle cramping, and blurred vision. Hypertension, loss of consciousness, and seizures are also frequent. Rarely hyperthermia develops, which may precipitate cardiovascular collapse and multiorgan failure. Withdrawal may involve drug craving, depression, confusion, and severe anxiety. In nonhuman primates as little as a 4-day exposure has been associated with damage to neurons involved in mood, thinking, and judgment.

30 What is phencyclidine and what is its mechanism of action?

Phencyclidine (PCP) is a cyclohexylamine that was developed in the 1950s as an anesthetic but was subsequently taken off the market because of its tendency to produce hallucinations. The precise mechanism of action of PCP is unknown, but it is thought to depress cortical and thalamic function while stimulating the limbic system. PCP may block afferent impulses associated with the affective component of pain perception and suppress spinal cord activity. PCP can also inhibit pseudocholinesterase. Of note, the intravenous anesthetic ketamine is produced by chemical modification of PCP.

31 Discuss the physical and psychologic effects of phencyclidine

PCP produces a dissociative state or out-of-body experience. It crosses the blood–brain barrier to produce amnesia, delirium, disordered thought processes, paranoia, hostility, and delusions. Dissociation may resemble schizophrenia. Nystagmus, ataxia, and difficulty speaking may occur. Autonomic stimulation and cerebral vasodilation are also effects. No significant ventilatory depression is observed, and airway reflexes are maintained. Copious oral secretions may be noted. General anesthesia is preferable in these patients because of their frequent dissociative state and unpredictable violent behavior.

32 How do you increase clearance of phencyclidine?

Clearance is increased by acidification of the urine and nasogastric suction.

KEY POINTS: Concerns in Patients Taking Ecstasy and Phencyclidine image

1. Hyperthermia and cardiovascular collapse with ecstasy
2. Dissociative state, severe behavior disturbances, and enhanced sympathomimetic effects with phencyclidine

Websites image

American Pain Society

http://www.ampainsoc.org

World Health Organization: Management of Substance Abuse

http://www.who/int/substance_abuse

SUGGESTED READINGS

1. Hill G.E., Ogunnaike B.O., Johnson E.R. General anesthesia for the cocaine abusing patient. Is it safe? Br J Anaesth. 2006;97:654-657.

2. Tetrault J.M., O’Connor P.G. Substance abuse and withdrawal in the critical care setting. Crit Care Clin. 2008;24:767-788.

Related posts:

31: Temperature Disturbances 61: High-Risk Obstetrics 46: Malignant Hyperthermia and Other Motor Diseases 5: Electrolytes 76: Electroconvulsive Therapy 41: Acute Respiratory Distress Syndrome (ARDS)