Electroconvulsive Therapy During Pregnancy

Brattleboro Retreat Psychiatric Review
June 1996
Sarah K. Lentz - Dartmouth Medical School - Class of 1997

Introduction

Psychiatric illness during pregnancy often presents a clinical dilemma. Pharmacologic interventions that are usually effective for these disorders have teratogenic potential and are therefore contraindicated during pregnancy. However, for depression, mania, catatonia, and schizophrenia, an alternative treatment exists: electroconvulsive therapy (ECT), the induction of a series of generalized seizures.

Psychiatric Treatment during Pregnancy

Pharmacologic therapies pose risks to the fetus in pregnant patients. Antipsychotics, particularly phenothiazines, have been noted to cause congenital anomalies in babies born to women treated with these medications during pregnancy (Rumeau-Rouquette 1977). Congenital defects have also been associated with the use of lithium, especially when administered during the first trimester (Weinstein 1977). However, in a recent study by Jacobson et al. (1992), no association between lithium and congenital anomalies was found. Tricyclic antidepressants have been associated with limb reduction deformities (McBride 1972) and, moreover, take four to six weeks to affect depression. During this time, risk to the fetus and woman may be substantial, depending on the mental and psychologic condition of the mother, her ability to care for herself, and possible suicidality. In a crisis situation in which the risks of untreated symptoms are extreme, the patient is known to be refractory to medications, or the medication represents a substantial risk to the fetus, ECT represents a valuable alternative in the pregnant patient. When administered by trained staff, and when precautions germane to pregnancy are taken into account, ECT is a relatively safe and effective treatment during pregnancy.

ECT: The History

Electroconvulsive therapy was first introduced as an effective treatment option for psychiatric illness in 1938 by Cerletti and Bini (Endler 1988). Several years earlier in 1934, Ladislas Meduna introduced the induction of generalized seizures with the pharmacological agents camphor and then pentylenetetrazol as effective treatment in a number of psychiatric illnesses. Prior to this time, no effective biological treatment for psychiatric illness was in use. The work of Meduna therefore, opened a new era of psychiatric practice and was quickly accepted throughout the world (M. Fink, personal communication). With the discovery that more predictable and effective seizures could be induced by ECT, the pharmacological method fell into disuse. ECT persisted as a mainstay of therapy until the 1950s and 1960s, when effective antipsychotic, antidepressant, and antimanic drugs were discovered (Weiner 1994). ECT was largely replaced by medications from this point until the early 1980s, when its usage level stabilized. However, a renewed interest in ECT in the medical community, prompted by failures of pharmacotherapy, has led to an increase in its judicious use in treatment-refractory patients with several psychiatric illnesses, including depression, mania, catatonia, and schizophrenia and also in circumstances in which psychopharmacological treatment is contraindicated, such as during pregnancy (Fink 1987 and personal communication).

ECT: The Procedure

Standard procedure. During the procedure, the patient is administered a short-acting barbiturate, typically methohexital or thiopental, which puts the patient to sleep, and succinylcholine, which induces paralysis. Paralysis suppresses the peripheral manifestations of the seizure, protecting the patient from fractures caused by muscular contractions and other injuries induced by the seizure. The patient is ventilated with 100% oxygen through a bag and hyperventilated before the electrical stimulus is administered. An EEG should be monitored. The stimulus is applied either unilaterally or bilaterally, inducing a seizure that should last at least 35 seconds by EEG. The patient is asleep for 2 to 3 minutes and awakens gradually. Vital signs are monitored throughout (American Psychiatric Association 1990).

Systemic changes that may occur during ECT include a brief episode of hypotension and bradycardia, followed by sinus tachycardia and sympathetic hyperactivity with an increase in blood pressure. These changes are transient and typically resolve over the course of minutes. The patient may experience some confusion, headache, nausea, myalgia, and anterograde amnesia following the treatment. These side effects generally clear over the course of several weeks following completion of the treatment series but can take up to six months to resolve. In addition, the incidence of side effects has been decreasing over the years as ECT technique has improved (American Psychiatric Association 1990). Finally, the mortality rate associated with ECT is approximately only 4 per 100,000 treatments and is generally cardiac in origin (Fink 1979).

During pregnancy. ECT has been found safe during all trimesters of pregnancy by the American Psychiatric Association. However, all ECT on pregnant women should occur in a hospital with facilities to manage a fetal emergency (Miller 1994). During pregnancy, several recommendations are added to the standard procedure to decrease potential risks. An obstetric consultation should be considered in high-risk patients. Vaginal exam is not obligatory, though, since it is relatively contraindicated during pregnancy. Furthermore, nothing about the vaginal exam would affect ECT. In the past, external fetal cardiac monitoring during the procedure was recommended. However, no alteration in fetal heart rate has been observed. Therefore, fetal monitoring as a routine part of the procedure is not warranted given its expense and lack of utility (M. Fink, personal communication). In high-risk cases, the presence of an obstetrician during the procedure is recommended.

If the patient is in the second half of pregnancy, intubation is the standard of anesthetic care to reduce the risk of pulmonary aspiration and resultant aspiration pneumonitis. During pregnancy, gastric emptying is prolonged, increasing the risk of aspiration of regurgitated gastric contents during ECT. Pneumonitis may result following aspiration of particulate matter or acidic fluid from the stomach. Standard procedure requires the patient to take nothing by mouth after midnight the night preceding ECT. However, in the pregnant patient this is often insufficient to prevent regurgitation. In the second half of pregnancy, intubation is performed routinely to isolate the airway and reduce the risk of aspiration. In addition, administering a nonparticulate antacid, such as sodium citrate, to raise gastric pH, may be considered as optional adjuvant therapy, but its usefulness is debated (Miller 1994, M. Fink, personal communication).

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.

Long-term effects in children. Literature examining the long-term effects of ECT treatment during pregnancy is limited. Smith (1956) examined 15 children between the ages of 11 months and five years whose mothers had undergone ECT during pregnancy. None of the children demonstrated intellectual or physical abnormalities. Sixteen children, aged 16 months to six years, whose mothers had received ECT during the first or second trimester of pregnancy, were examined by Forssman (1955). None of the children was found to have a defined physical or mental defect. Impastato et al. (1964) describes follow-up on eight children whose mothers had received ECT during pregnancy. The children ranged in age from two weeks to 19 years at the time of examination. No physical deficits were noted; however, mental deficiencies were noted in two and neurotic traits in four. Whether ECT contributed to the mental deficits is questionable. The mothers of the two mentally deficient children had received ECT after the first trimester, and one received insulin coma treatment during the first trimester, which could have contributed to the mental deficit.

Summary

ECT offers a valuable alternative for treating the pregnant patient suffering from depression, mania, catatonia, or schizophrenia. Pharmacological therapy for these psychiatric illnesses carries inherent risks of side effects and adverse consequences to the unborn child. Medications often require a long time to take effect, or the patient may be refractory to them. Additionally, these psychiatric conditions themselves are a risk to the mother and fetus. An effective, expeditious, and relatively safe alternative for pregnant patients requiring psychiatric treatment is ECT. The risk of the procedure can be minimized by modifying the technique. Medications used during the procedure are reportedly safe to use during pregnancy. In addition, complications reported in pregnant patients who received ECT during pregnancy have not been conclusively associated with the treatment. Research conducted to date suggests that ECT is a useful resource in psychiatric treatment of the pregnant patient.

Bibliography
References
* American Psychiatric Association. 1990. The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging. Convulsive Therapy. 6:85-120.
* Cherala SR, Eddie DN, Sechzer PH. 1989. Placental transfer of succinylcholine causing transient respiratory depression in the newborn. Anaesth Intens Care. 17:202-4.
* Elliot DL, Linz DH, Kane JA. 1982. Electroconvulsive therapy: pretreatment medical evaluation. Arch Intern Med. 142:979-81.
* Endler NS. 1988. The origins of electroconvulsive therapy (ECT). Convulsive Therapy. 4:5-23.
* Ferrill MJ, Kehoe WA, Jacisin JJ. 1992. ECT during pregnancy. Convulsive Therapy. 8(3):186-200.
* Fink M. 1987. Is ECT usage decreasing? Convulsive Therapy. 3:171-3.
* Fink M. 1979. Convulsive Therapy: Theory and Practice. New York: Raven.
* Forssman H. 1955. Follow-up study of sixteen children whose mothers were given electric convulsive therapy during gestation. Acta Psychiatr Neurol Scand. 30:437-41.
* Heinonen OP, Slone D, Shapiro S. 1977. Birth defects and drugs in pregnancy. Littleton, MA: Publishing Sciences Group.
* Impastato DJ, Gabriel AR, Lardaro HH. 1964. Electric and insulin shock therapy during pregnancy. Dis Nerv Syst. 25:542-6.
* Jacobson SJ, Jones K, Johnson K, et al. 1992. Prospective multicentre study of pregnancy outcome after lithium exposure during first trimester. Lancet. 339:530-3.
* McBride WG. 1972. Limb deformities associated with iminobenzyl hydrochloride. Med J Aust. 1:492.
* Miller LJ. 1994. Use of electroconvulsive therapy during pregnancy. Hosp Community Psychiatry. 45(5):444-450.
* Moya F, Kvisselgaard N. 1961. The placental transmission of succinylcholine. J Amer Society Anesthesiology. 22:1-6. * Nurnberg HG. 1989. An overview of somatic treatment of psychosis during pregnancy and postpartum. Gen Hosp Psychiatry. 11:328-338.
* Rumeau-Rouquette C, Goujard J, Huel G. 1977. Possible teratogenic effect of phenothiazines in human beings. Teratology. 15:57-64.
* Smith S. 1956. The use of electroplexy (ECT) in psychiatric syndromes complicating pregnancy. J Ment Sci. 102:796-800.
* Walker R, Swartz CD. 1994. Electroconvulsive therapy during high-risk pregnancy. Gen Hosp Psychiatry. 16:348-353.
* Weiner RD, Krystal AD. 1994. The present use of electroconvulsive therapy. Annu Rev Med 45:273-81.
* Weinstein MR. 1977. Recent advances in clinical psycopharmacology. I. Lithium carbonate. Hosp Formul. 12:759-62.

Brattleboro Retreat Psychiatry Review
Volume 5 - Number 1 - June 1996
Publisher Percy Ballantine, MD
Editor Susan Scown
Invited Editor Max Fink, MD

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