Later in pregnancy, risk of aortocaval compression becomes a concern. As the uterus increases in size and weight, it may compress the inferior vena cava and lower aorta when the patient is in the supine position, as she is during ECT treatment. With compression of these major vessels, increased heart rate and peripheral resistance compensate but perhaps insufficiently to maintain placental perfusion. This can be prevented, however, by elevating the patient's right hip during the ECT treatment, which displaces the uterus to the left, relieving pressure on the major vessels. Assuring hydration with adequate fluid intake or intravenous hydration with Ringer's lactate or normal saline before ECT treatment will also reduce this risk of reduced placental perfusion (Miller 1994).

ECT During Pregnancy:

Risks and Complications

Reported complications. In a retrospective study of ECT use during pregnancy by Miller (1994), 28 of 300 cases (9.3%) reviewed from the literature from 1942 to 1991 reported complications associated with ECT. The most common complication found by this study is fetal cardiac arrhythmia. Noted in five cases (1.6%), disturbances in fetal cardiac rhythm included irregular fetal heart rate up to 15 minutes postictally, fetal bradycardia, and reduced variability in fetal heart rate. The latter is hypothesized to have been in response to barbiturate anesthetic. The disturbances were transient and self-limited, and a healthy baby was born in each case.

Five cases (1.6%) also reported known or suspected vaginal bleeding related to ECT. Mild abruptio placentae was the cause of bleeding in one case and recurred after each of a weekly series of seven ECT treatments. No source of bleeding was identified in the remaining cases. However, in one of these cases, the patient had experienced similar bleeding in a previous pregnancy during which she received no ECT. In all these cases, the baby was again born healthy.

Two cases (0.6%) reported uterine contraction following shortly after ECT treatment. Neither resulted in any noticeable adverse consequences. Three cases (1.0%) reported severe abdominal pain directly following ECT treatment. The etiology of the pain, which resolved following the treatment, was unknown. In all cases, healthy babies were born.

Four cases (1.3%) reported premature labor after the patient received ECT during pregnancy; however, labor did not immediately follow ECT treatment, and it appears ECT was not related to the premature labors. Similarly, five cases (1.6%) reported miscarriage in pregnant patients who received ECT during their pregnancy. One case appeared to be due to an accident. However, as Miller (1994) points out, even including this latter case, a miscarriage rate of 1.6 percent is still not significantly higher than that of the general population, suggesting that ECT does not increase the risk of miscarriage. Three cases (1.0%) of stillbirth or neonatal death in patients undergoing ECT during pregnancy were reported, but these appear to be due to medical complications unrelated to the ECT treatment.

Medication risks

Succinylcholine, the muscle relaxant most commonly used to induce paralysis for ECT, has undergone limited study in pregnant women. It does not cross the placenta in detectable amounts (Moya and Kvisselgaard 1961). Succinylcholine is inactivated by the enzyme pseudocholinesterase. Approximately four percent of the population is deficient in this enzyme and could, consequently, have a prolonged response to succinylcholine. In addition, during pregnancy, pseudocholinesterase levels are low, so this prolonged response is not infrequent and could occur in any patient (Ferrill 1992). In the Collaborative Perinatal Project (Heinonen et al. 1977), 26 births to women exposed to succinylcholine during the first trimester of pregnancy were assessed after birth. No abnormalities were noted. However, several case reports noted complications in the use of succinylcholine during the third trimester of pregnancy. The most notable complication studied in women undergoing caesarian section was development of prolonged apnea that required continuous ventilation and lasted several hours to days. In nearly all the infants, respiratory depression and low Apgar scores were seen after birth (Cherala 1989).

Pharyngeal secretions and excessive vagal bradycardia can also occur during ECT treatments. To prevent these effects during the procedure, anticholinergic agents are often administered prior to ECT. The two anticholinergics of choice are atropine and glycopyrrolate. In the Collaborative Perinatal Project (Heinonen et al. 1977), 401 women received atropine, and four women received glycopyrrolate during their first trimester of pregnancy. In the women who received atropine, 17 infants (4%) with malformations were born, while in the glycopyrrolate group, no malformations were seen. The incidence of malformations in the atropine group was not greater than would be expected in the general population. Likewise, studies of these two anticholinergics used in the third trimester of pregnancy or during labor did not reveal any adverse effects (Ferrill 1992).

To induce sedation and amnesia prior to the treatment, a short-acting barbiturate is typically used. The agents of choice, methohexital, thiopental, and thiamylal, have no known adverse effects associated with pregnancy (Ferrill 1992). The only known exception is that administration of a barbiturate to a pregnant woman with acute porphyria may trigger an attack. Elliot et al. (1982) conclude that the recommended dose of methohexital in nonpregnant adults appears to be safe for use during the third trimester of pregnancy.

Teratogenicity. In the retrospective study by Miller (1994), five cases (1.6%) of congenital abnormalities were reported in children of patients who underwent ECT during pregnancy. The cases with noted abnormalities include an infant with hypertelorism and optic atrophy, an anencephalic infant, another infant with clubfoot, and two infants demonstrating pulmonary cysts. In the case of the infant with hypertelorism and optic atrophy, the mother received only two ECT treatments during the course of her pregnancy; however, she had received 35 insulin coma therapy treatments, which are suspected of teratogenic potential. As Miller notes, no information on other potential teratogenic exposures was included in these studies. Based on the number and pattern of congenital anomalies in these cases, she concludes that ECT does not appear to have an associated teratogenic risk.