Brattleboro Retreat Psychiatric
Review
June 1996 Electroconvulsive Therapy During Pregnancy
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
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* Jacobson SJ, Jones K, Johnson K, et al. 1992. Prospective multicentre study
of pregnancy outcome after lithium exposure during first trimester. Lancet.
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* 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
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* 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.
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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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