29.1 Acute Intoxication, Withdrawal Syndromes & Perioperative Complications

Why This Topic Matters on the NCE

Domain IV.B.5 of the content outline is the substance use disorder population, with four sub-topics: medication-assisted therapy, pharmacologic interactions including acute intoxication, pain management, and management of complications. Medication-assisted therapy and pain management are covered in the chronic pain chapter. This section covers acute intoxication and withdrawal — the situations where the drug in the patient's system right now changes the anesthetic.

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1. Alcohol

The MAC paradox

Getting these backwards is one of the most common errors on this topic. The acutely intoxicated trauma patient needs less anesthetic; the chronic drinker who arrives sober needs more.

Systemic consequences of chronic use

• Alcoholic cardiomyopathy with reduced ejection fraction, and alcohol-related atrial fibrillation
• Cirrhosis with coagulopathy, thrombocytopenia, hypoalbuminemia, ascites, esophageal varices, encephalopathy, and altered drug metabolism
• Malnutrition: thiamine, folate, magnesium, and phosphate deficiency
• Peripheral neuropathy — document it before any regional technique
• Increased perioperative infection, bleeding, and cardiopulmonary complication rates; even 4 weeks of preoperative abstinence measurably reduces complications

Alcohol withdrawal: a timeline you must know

Delirium tremens carries a mortality of roughly 5 to 15 percent with treatment, and historically up to about 20 percent untreated. The distinguishing feature from alcoholic hallucinosis is the globally altered sensorium — a patient with hallucinosis knows where they are.

Treatment

• Benzodiazepines are first-line and are the only agents shown to reduce seizures and mortality. Symptom-triggered dosing guided by a CIWA-Ar score is preferred to fixed schedules. Lorazepam is favored in hepatic impairment because it lacks active metabolites.
• Dexmedetomidine is an adjunct only. It controls autonomic hyperactivity and agitation but does not prevent seizures and must never replace benzodiazepines.
• Phenobarbital is an alternative or adjunct in benzodiazepine-refractory withdrawal.
• Thiamine must be given before any glucose-containing fluid to prevent precipitating Wernicke encephalopathy (the triad of ophthalmoplegia, ataxia, and confusion) in a thiamine-depleted patient. Add folate, magnesium, and phosphate.
• Beta-blockers and clonidine mask the autonomic signs without treating the underlying process; they are adjuncts at most.

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2. Cocaine

Acute intoxication

Cocaine blocks presynaptic reuptake of norepinephrine, dopamine, and serotonin, producing a sympathomimetic state: hypertension, tachycardia, coronary vasospasm, dysrhythmias, hyperthermia, agitation, seizures, and a genuine risk of myocardial infarction and aortic dissection in young patients with normal coronary arteries.

Delay elective surgery in an acutely intoxicated patient. Cocaine has a short plasma half-life of roughly 45 to 90 minutes, but its metabolites and clinical effects persist far longer, and a urine screen remains positive for days.

The management rule

Do not give a pure beta-blocker. Beta-blockade in the presence of high circulating catecholamines leaves unopposed alpha stimulation, worsening hypertension and coronary vasospasm. The management order is:

1. Benzodiazepines first — they reduce central sympathetic outflow and treat agitation, hypertension, tachycardia, and seizure risk simultaneously
2. Nitroglycerin for coronary vasospasm and hypertension
3. Phentolamine (alpha-blocker) for refractory hypertension
4. Calcium channel blockers such as nicardipine
5. Aggressive cooling for hyperthermia

Labetalol has combined alpha and beta blockade but its beta effect predominates roughly seven to one, so it is not a satisfactory substitute for a pure alpha-blocker in this setting.

Chronic use

Chronic cocaine and methamphetamine use depletes presynaptic catecholamine stores. The clinical consequence is that indirect-acting sympathomimetics such as ephedrine may fail, and refractory intraoperative hypotension should be treated with direct-acting agents — phenylephrine, norepinephrine, and vasopressin. Chronic users also have cardiomyopathy, accelerated atherosclerosis, and, with nasal use, septal perforation that complicates nasal instrumentation.

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3. Methamphetamine and Other Stimulants

The same principles as cocaine, with a longer duration of action (plasma half-life of roughly 10 to 12 hours). Chronic methamphetamine use adds severe dental disease complicating airway management and intubation, cardiomyopathy, pulmonary hypertension, malnutrition, and psychosis. Refractory hypotension from catecholamine depletion is common and responds to direct-acting vasopressors and vasopressin.

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4. Opioids

Withdrawal

Opioid withdrawal in an adult is intensely unpleasant but not usually life threatening, which distinguishes it from alcohol, benzodiazepine, and barbiturate withdrawal.

Features: mydriasis, lacrimation, rhinorrhea, yawning, piloerection, diaphoresis, myalgias, abdominal cramping, diarrhea, vomiting, restlessness, and hypertension with tachycardia. Severity is scored with the COWS scale.

Two important exceptions:

• Neonatal abstinence syndrome in the infant of an opioid-dependent mother is life threatening, with seizures and feeding failure.
• Withdrawal in a critically ill patient can precipitate cardiovascular decompensation.

Precipitated withdrawal — from naloxone, or from giving nalbuphine, butorphanol, or buprenorphine to a full-agonist-dependent patient — is far more severe and abrupt than spontaneous withdrawal.

Overdose

Miosis, respiratory depression with a reduced rate, and depressed consciousness. Naloxone is titrated in small increments (40 to 80 mcg) in the postoperative setting to restore ventilation without abolishing analgesia and precipitating a hypertensive, tachycardic, agonizing withdrawal state that has caused pulmonary edema. Naloxone's duration is shorter than that of most opioids, so re-sedation is the predictable danger and an infusion or repeated dosing with continued monitoring is required.

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5. Sedative-Hypnotic Withdrawal

Benzodiazepine and barbiturate withdrawal are life threatening, producing seizures, delirium, and autonomic instability much like alcohol withdrawal, because all three act on the GABA-A receptor complex. Chronic benzodiazepine therapy should be continued perioperatively or covered with an equivalent, never abruptly stopped. The same reasoning applies to the herbal GABAergic valerian.

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6. Nicotine and Tobacco

The time course of benefit from cessation is directly testable:

The nuance worth knowing is that the large pulmonary benefit requires weeks, while the carboxyhemoglobin and nicotine benefit appears within a day — so even overnight abstinence is worthwhile and should be encouraged, and there is no evidence that brief preoperative cessation increases complications.

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Exam Traps

• Acute alcohol lowers MAC; chronic alcohol raises it.
• Delirium tremens is at 48 to 96 hours; hallucinosis is earlier and has an intact sensorium.
• Benzodiazepines are first-line for both alcohol withdrawal and cocaine toxicity. Dexmedetomidine does not prevent seizures.
• Thiamine before glucose.
• No pure beta-blocker after cocaine — unopposed alpha.
• Chronic stimulant use depletes catecholamines — use direct-acting vasopressors.