Drug
Effect on MAC
Detection in urine
Effect on fetus
Alcohol
Acute, decrease; chronic, increase
Blood level measured
Fetal alcohol syndrome (FAS)
Opioids
Acute, decrease; chronic, increase
1–3 days
Neonatal abstinence syndrome (NAS)
Cocaine
Increase
2–3 days
Placental abruption, preterm labor, spontaneous abortion, IUGR
Tobacco
Not significantly affected
2–4 days
IUGR, low birth weight
Marijuana
Acute, decrease; chronic, increase
1–2 days
IUGR
Toxicity:
Acute toxicity is mediated by agonism of γ-aminobutyric acid type A (GABAA) receptors. Signs usually vary with blood alcohol level and are progressive, causing impaired judgment, psychomotor retardation, impaired balance, anterograde amnesia (blackout), coma, and respiratory failure. The effects of long-term ethanol use are profound and may include cognitive impairment, cerebellar degeneration, Wernicke–Korsakoff syndrome (from thiamine deficiency), peripheral neuropathy, dilated cardiomyopathy, dysrhythmias, hypertension, cirrhosis (including esophageal varices), gastritis, pancreatitis, malnutrition, hypoglycemia, hypoalbuminemia, electrolyte imbalances (hypomagnesemia, hypophosphatemia, hypocalcemia, and hypokalemia), ketoacidosis, anemia, thrombocytopenia, leukopenia, and myopathy.
Withdrawal:
Alcohol withdrawal can be lethal. The signs and symptoms of alcohol withdrawal are the opposite of acute intoxication and are, therefore, adrenergic in nature. Anxiety, insomnia, tachycardia, hypertension, diaphoresis, nausea, and mild tremors can be seen as early as 6–8 h after the last drink. Delirium tremens can occur 2–3 days later and is distinguished by completely altered sensorium, pronounced adrenergic signs, and, occasionally, fevers. The mainstay of treatment is benzodiazepines, treatment of electrolyte abnormalities, prevention of any seizure activity, airway maintenance if required, and supportive care.
Anesthetic Implications:
A thorough preoperative evaluation to determine the extent of alcohol use is paramount. Further testing should focus on affected organ systems. EKG and echocardiography may reveal dysrhythmias and decreased cardiac function, respectively. Electrolytes should be measured and abnormalities corrected. If hypoglycemia is present, thiamine should be included with glucose administration, to prevent Wernicke–Korsakoff syndrome. Liver tests typically reveal an AST/ALT ratio greater than 2 and decreased albumin. CBC and coagulation testing are also important.
Acute intoxication decreases MAC due to GABA activation. In contrast, chronic alcohol use increases MAC, due to induction of the cytochrome P-450 system or cross-tolerance to anesthetics. Therefore, anesthetic plans need to be adjusted accordingly. Other manifestations of alcohol use can also affect the anesthetic plan. Hypoalbuminemia affects both oncotic pressure and pharmacokinetics, whereas anemia and coagulopathy may necessitate administration of blood products.
Opioids
Examples of opioids include: morphine, codeine, heroin, hydromorphone, oxycodone, meperidine, fentanyl, methadone, and buprenorphine. It is important to know that, besides street use, prescription opioid abuse is very common.
Toxicity:
Opioid toxicity classically presents with a triad of sedation, hypoventilation, and miosis (though mydriasis may be present with hypoxia). Other effects include decreased gastric motility and constipation, urinary retention, sense of euphoria, hypotension, bradycardia, and, rarely, seizures. These effects however can vary, depending on the opioid type, route of administration, and with tolerance (however little tolerance develops for miosis and constipation). Acute toxicity is managed with ventilatory support and the opioid receptor antagonist naloxone, titrated to reverse ventilatory depression.
Withdrawal:
Opioid withdrawal, while not life threatening in most adults, can be long and extremely unpleasant. Signs and symptoms include extreme pain, irritability, tachycardia, nausea, vomiting, diarrhea, rhinorrhea, lacrimation, diaphoresis, and cardiovascular collapse. Naloxone administration can cause acute withdrawal. Withdrawal is treated with long-acting opioids such as methadone and the μ-opioid receptor partial agonist buprenorphine.
Anesthetic Implications:
In the preoperative assessment, the type, amount, frequency, and route of opioid use should be determined. Routes of administration include enteral (oral, rectal) and parenteral (intravenous, subcutaneous, transdermal, transmucosal, inhalational). Scabbing and/or scarring (track marks) particularly on the extremities may indicate intravenous abuse. Intravenous drug users are susceptible to infectious diseases such as HBV, HCV, HIV, and bacterial endocarditis. Vascular access can be difficult and, in addition, these patients may be malnourished. It is important to remember that chronic opioid use can cause secondary adrenal insufficiency. In the intraoperative phase, patients may exhibit tolerance to opioids and cross-tolerance to anesthetics. Special attention should be paid to patients on methadone, which may cause QT prolongation and precipitate cardiac dysrhythmias.
In general, these patients require higher doses of opioids for adequate analgesia and are also prone to hyperalgesia and allodynia. Perioperative management strategies include calculation and continuation of baseline methadone or buprenorphine requirements, increasing opioid doses to account for tolerance as well as maximizing other strategies such as peripheral nerve blocks and non-opioid medications.
Central Nervous System Stimulants
Cocaine and Amphetamine
Cocaine and amphetamines (α-methylphenethylamine or amfetamine) are sympathomimetics, as they cause CNS excitation. In general, these substances work by causing release of epinephrine, norepinephrine, dopamine, and serotonin from nerve terminals, as well as inhibiting reuptake of these neurotransmitters, allowing them to remain within the synaptic cleft in greater concentration and for a longer duration. Cocaine is now rarely used as a local anesthetic. Amphetamines are used to treat narcolepsy, attention-deficit hyperactivity disorder, enuresis, and incontinence.
Toxicity:
The clinical features of both cocaine and amphetamine toxicity and chronic abuse are similar. CNS effects include euphoria, mydriasis, stroke, and cerebral edema. Cardiac effects include hypertension, dysrhythmia, tachycardia, cardiomyopathy, and even death. Another important consequence of toxicity is coronary artery vasospasm, which, when combined with increased myocardial oxygen demand, can lead to cardiac ischemia. Cocaine-induced dysrhythmias arise from sodium and potassium channel blockade and subsequent prolongation of the QT interval. When smoked, cocaine can cause pulmonary problems, including cough, dyspnea, and pneumonitis. Other features of cocaine abuse include diaphoresis, hyperthermia, thrombocytopenia, and malnutrition. In the parturient, cocaine use can cause fetal abnormalities as well as preterm labor, premature rupture of membranes, and abruptio placentae.
Withdrawal:
Withdrawal from stimulants is unpleasant and can be life threatening. Symptoms (sometimes referred to as “crashing”) include anxiety, irritability, depression, fatigue, lethargy, malaise, and increased appetite.
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