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Substance Abuse in Pregnancy
Recreational drug abuse has increased dramatically in recent years. Approximately 250,000 women in the United States abuse intravenous (IV) drugs, and nearly 90% of them are of childbearing age. Maternal drug addiction may result in life-threatening complications for both the mother and baby. Because social trends affect women with heart disease in the same way as the general population, physicians caring for pregnant women with heart disease will encounter patients who are also abusing illicit drugs. Furthermore, because most pregnant women using illicit drugs deny it, physicians should exercise caution and a high degree of skepticism. Tobacco use, absence of prenatal care, and a history of premature births are associated with substance abuse. The illicit drugs most commonly abused in pregnancy include cocaine, amphetamines, opioids, ethanol, marijuana, and toluene-based solvents. Polysubstance abuse is very common. In some states, exposing a fetus to illicit drugs is considered a form of child neglect or abuse.
This chapter reviews substances commonly abused during pregnancy, including tobacco, alcohol, opioids, cocaine, amphetamines, and marijuana.
Tobacco
Cigarette smoking remains surprisingly common among pregnant women. An estimated 15% of women smoke during pregnancy. Maternal cigarette smoking increases the fetal death rate. It is the leading cause of fetal growth restriction, and it has been shown to impair growth of the fetal brain and kidney. The risk to fetuses occurs in part because smoking increases the risk of bleeding during pregnancy, abruptio placenta, placenta previa, and premature and prolonged rupture of the membranes. Tobacco smoke contains over 4000 chemical compounds, 40 of which are known carcinogens. Two that are leading contenders for the toxic effects of smoke to fetuses are nicotine and carbon monoxide. Both cross the placenta. Compared with maternal blood levels, nicotine levels in amniotic fluid may be up to 88% higher, and fetal blood levels are 15% higher. Nicotine causes vasoconstriction of the uteroplacental blood vessel, which may result in uteroplacental underperfusion. It also impairs growth in the fetal nervous system. Carbon monoxide binds to hemoglobin, impairing oxygen delivery to the fetus. Cigarette smoking also is associated with the use of illicit drugs. Pregnant women who are smokers should be encouraged to quit. It is not clear that nicotine replacement therapy is successful in pregnant women, and because nicotine is a fetal toxin, it is difficult to advocate its use in any form in pregnant women.
Alcohol
Maternal alcohol use, even in small amounts, has been shown to increase the risk of fetal death in the first trimester. The hazard ratio associated with 2.0 to 3.5 drinks per week is 1.66. The hazard ratio associated with four or more drinks per week is 2.82. The risk is greatest during gestational weeks 13 to 16. There seems to be little or no increased risk of fetal death after 16 weeks. However, because ethanol readily crosses the placenta, heavy maternal alcohol intake may result in a specific pattern of neonatal malformation known as fetal alcohol syndrome. This pattern involves prenatal growth deficiency, developmental delay, craniofacial anomalies, and limb defects. Ethanol is detrimental to the developing brain and remains the leading cause of mental retardation in developing countries. The mechanism of alcohol brain damage remains elusive. Neurologic effects of ethanol appear to be mediated by its actions on the receptor for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). The overall neonatal mortality rate in pregnancies complicated by heavy alcohol intake is estimated at 18%. No safe level of alcohol consumption in pregnancy has been established. Regardless of the gestational period, ethanol adversely affects fetuses; therefore, abstinence from alcohol is the safest approach in pregnancy.
Parturients who abuse alcohol may present to labor and delivery with a variety of clinical manifestations, depending on degree of chemical dependency and timing of the most recent consumption. Physiologic dependence on alcohol is manifested as a withdrawal syndrome when the drug is abruptly discontinued or when there is a significant decrease in consumption. The most common and earliest manifestations of acute withdrawal include generalized tremor, hypertension, tachycardia, cardiac arrhythmias, nausea, vomiting, insomnia, confusion, agitation, and hallucinations. Symptoms of acute withdrawal usually begin 6 to 48 hours after cessation of alcohol consumption, although delay as long as 10 days after last use has been reported. Withdrawal symptoms may be suppressed by administering benzodiazepines or α 2 -adrenergic agonists or by resuming alcohol consumption. Delirium tremens is a rare but life-threatening medical emergency in ethanol-addicted parturients.
Anesthesia Concerns Related to Alcohol Abuse
Regional anesthesia can be administered safely in parturients with a history of alcohol abuse as long as no other contraindications exist. Intravascular fluid volume should be optimized before induction of regional anesthesia to avoid adverse consequences of sympathetic blockade. If general anesthesia is needed, patients should be evaluated for alcohol-associated hepatic dysfunction, hypoalbuminemia, and cardiac dysfunction. The chronic use of alcohol is usually associated with resistance to the actions of central nervous system (CNS) depressants, including volatile anesthetics. Suggestions that chronic ethanol consumption necessitates increased requirements of barbiturates, however, have not been confirmed. Acutely intoxicated patients generally require lower doses of anesthetic agents.
Opioids
Opioid use and abuse have risen considerably in recent years. A number of related drugs are referred to as opioids. These include “natural” opiates such as heroin and morphine as well as synthetic opioids such as fentanyl, carfentanil, methadone, hydromorphone, oxycodone, and hydromorphone. There are also synthetic opioid agonist–antagonists such as buprenorphine. Opioids may be injected intravenously, swallowed, nasally inhaled, smoked, chewed, or used as suppositories. Opioid use disorder is defined by the American College of Obstetricians and Gynecologists as “a pattern of opioid use characterized by tolerance, craving, inability to control use, and continued use despite adverse consequences.” When the drugs are injected, it can lead to complications of cellulitis, superficial skin abscesses, septic thrombophlebitis, and infective endocarditis. Patients are also at risk for malnutrition, HIV/AIDS, and hepatitis. Opioid abuse may also be accompanied by the abuse of other substances. Lack of prenatal care is common in this population.
Opioid-abusing women may present with symptoms of opioid overdose or acute opioid withdrawal. Patients with opioid overdose present with unconsciousness and respiratory depression. Pinpoint pupils are a characteristic finding on physical examination. Acute opioid withdrawal syndrome is manifested by a range of symptoms, including restlessness, anxiety, abdominal pain, nausea, diarrhea, piloerection and sweating, rhinorrhea, diffuse muscle pain, and symptoms of increased sympathetic nervous system activity, such as tachycardia, tachypnea, and hypertension. CNS manifestations range from dysphoria to various forms of bizarre behavior and unconsciousness. Withdrawal symptoms usually occur 4 to 6 hours after the last opioid intake and peak in 48 to 72 hours. Generally, opioid withdrawal is not considered life threatening.
Intravenous opioid abuse in pregnancy may affect the fetus indirectly (e.g., maternal malnutrition or infection) or directly (e.g., transplacental opioid transfer and direct effect on the fetus). Fetal intrauterine growth restriction (IUGR) and various forms of fetal distress are known consequences of intrauterine drug exposure. Symptoms of neonatal opioid withdrawal are common in neonates exposed in utero.
Currently, opioid replacement therapy with methadone or buprenorphine is recommended for the treatment of pregnant patients addicted to opioids. It helps prevent withdrawal syndrome, and it is better tolerated by fetuses than continued nonmedical opioid abuse. Avoid administering opioid antagonists or agonist–antagonists, such as naloxone or nalbuphine, because they can precipitate acute withdrawal syndrome. Opioid withdrawal syndrome usually develops within minutes after naloxone administration. Patients with symptoms of withdrawal from opioids may be treated with clonidine, diphenhydramine, or doxepin. Clonidine attenuates the opioid withdrawal symptoms by replacing opioid-mediated inhibition with α 2 -agonist–mediated inhibition of the CNS. It is possible to reverse the withdrawal syndrome by reinstituting the abused opioid or by substituting methadone.
Anesthesia Concerns Related to Opioid Abuse
Epidural and spinal anesthesia may be administered safely to opioid-abusing parturients. An increased tendency for hypotension should be anticipated after the induction of epidural or spinal anesthesia. In patients who abuse IV opioids, peripheral IV access can be difficult, necessitating central venous access. Chronic opioid use leads to tolerance to other opioids, as well as cross-tolerance to other CNS depressants, including anesthetic agents. Cross-tolerance usually results from chronic receptor stimulation, and decreased pain tolerance is secondary to decreased production of endogenous opioid peptides. If cesarean section is necessary, it is often difficult to effectively control postoperative pain in a parturient who uses opioids chronically. Patients on methadone or suboxone therapy present a similar challenge in the postoperative period. These medications do not have strong enough analgesic activity to effectively control postoperative pain, but they do have a high affinity for opioid receptors, rendering traditional opioid analgesics less efficacious. Therefore, in difficult cases, it is important to use multimodal analgesia, which includes the use of spinal opioids and the maximal use of nonopioid analgesics, such as nonsteroidal antiinflammatory drugs, dexamethasone, and gabapentin. Transversus abdominus plane blocks can provide some degree of pain relief, although they do not relieve visceral pain. Continuous epidural analgesia with local anesthetics, opioids, or both also may be considered, but it is not preferred because the patient is confined to bed while local anesthetic is being infused into the epidural catheter.
Cocaine
Cocaine is an alkaloid (benzoylmethylecgonine) prepared from the leaves of the coca plant. The common pharmaceutical form is prepared by dissolving the alkaloid in hydrochloric acid to form a water-soluble salt. “Crack” is an almost pure cocaine obtained by converting the hydrochloride form back into the alkalinized form.
Cocaine produces prolonged adrenergic stimulation by blocking the presynaptic uptake of sympathomimetic neurotransmitters including norepinephrine, serotonin, and dopamine. The euphoric effects of cocaine also result from the prolongation of dopamine’s activity in the limbic system and the cerebral cortex. The use of cocaine rapidly leads to physical dependence. Sudden discontinuation of cocaine intake results in craving for the drug, fatigue, and mental depression. Catecholamine accumulation after acute cocaine intake may cause life-threatening cardiovascular complications, including hypertension, tachycardia, malignant arrhythmias, myocardial ischemia, and infarction. Mechanisms of cocaine-induced myocardial ischemia or infarction include thrombosis, vasospasm, or both. Direct myocardial depression also occurs. Cocaine-induced cardiovascular complications do not seem to be dose dependent, and even small recreational doses can lead to significant morbidity or mortality. Pregnancy is associated with increased sensitivity of the cardiovascular system to cocaine.
Identifying cocaine abuse in a pregnant woman may be difficult. Symptoms may include seizures, hyperreflexia, fever, dilated pupils, emotional instability, proteinuria, and edema. The combination of hypertension, proteinuria, and convulsions resulting from acute cocaine intake may be mistaken for eclampsia. Placental abruption is more common in cocaine-abusing parturients. Drug screening and evaluation of liver and kidney function tests may aid in the differential diagnosis.
Anesthesia Concerns Related to Cocaine
Cocaine-abusing parturients can present anesthetic challenges. In laboring patients, neuraxial analgesia is preferred, provided the patient is able to cooperate and there are no contraindications such as low platelets. It may be more difficult to achieve satisfactory analgesia in cocaine-abusing patients.
In the cocaine-abusing parturient undergoing cesarean delivery, both regional and general anesthesia are associated with risks. Although neuraxial anesthesia is generally preferred for cesarean section, patients abusing cocaine may experience thrombocytopenia, which precludes use of this technique. In addition, acutely intoxicated patients may exhibit combative behavior and have altered pain perception, which make it difficult for them to tolerate the operation despite a technically sufficient sensory block.
Chronic cocaine abuse depletes stores of sympathetic neurotransmitters. Therefore, the treatment of patients with hypotension should be with a direct-acting medication such as phenylephrine. Indirectly acting medications, such as ephedrine, are ineffective.
If general anesthesia is used, attention must be paid to multiple interactions between cocaine and commonly used anesthetic and adjunct medications. Patients may experience hypertension, cardiac arrhythmias, and myocardial ischemia, particularly during times of significant stimulation, such as laryngoscopy and intubation. Generally, beta blockers are contraindicated in cocaine-intoxicated parturients because of the potential for unopposed α-adrenergic stimulation after beta blockade. Labetalol is an exception because it has partial α-agonist activity. Hypertension can be managed by the administration of hydralazine or nitrates. Certain hypnotic induction agents, such as ketamine, may heighten sympathetic nervous system activity and predispose the arrhythmias if used in these patients. Some volatile anesthetic agents (particularly halothane) increase the heart’s sensitivity to epinephrine, therefore increasing the chance of arrhythmia; however, the volatile agents in use clinically today have a very low risk of this. Coronary artery vasospasm and the resulting myocardial ischemia is a continual risk in these patients. Nitroglycerine is safe and effective in the treatment of chest pain secondary to acute cocaine ingestion.
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