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Management of myasthenia gravis in pregnancy

Management of myasthenia gravis in pregnancy
Literature review current through: Jan 2024.
This topic last updated: Aug 11, 2023.

INTRODUCTION — Myasthenia gravis (MG) is an autoimmune disorder characterized by a fluctuating degree and variable combination of weakness in ocular, bulbar, limb, and respiratory muscles. Affected patients (most often young females and older males) usually present with fatigable weakness after repetitive muscle use.

This topic will discuss the effect of pregnancy on MG and management of MG in pregnancy. It will also briefly review clinical and treatment issues related to MG that are discussed in greater detail separately.

(See "Pathogenesis of myasthenia gravis".)

(See "Clinical manifestations of myasthenia gravis".)

(See "Diagnosis of myasthenia gravis".)

(See "Differential diagnosis of myasthenia gravis".)

(See "Overview of the treatment of myasthenia gravis".)

CLINICAL ASPECTS — MG is a relatively uncommon autoimmune disorder characterized by weakness and fatigability of skeletal muscles due to dysfunction of the neuromuscular junction. It can occur at any age, but there is a bimodal distribution to the age of onset with an early peak in the second and third decades (female predominance) and a late peak in the sixth to eighth decade (male predominance). (See "Pathogenesis of myasthenia gravis".)

There are two clinical forms of myasthenia: ocular and generalized. In ocular MG (OMG), the weakness is limited to the eyelids and extraocular muscles. In generalized MG disease, the weakness commonly affects the ocular muscles, but it also involves a variable combination of bulbar, limb, and respiratory muscles. (See "Clinical manifestations of myasthenia gravis" and "Ocular myasthenia gravis".)

More than 50 percent of patients with MG present with ocular symptoms of ptosis and/or diplopia. Of those who present with ocular manifestations, about half will remain purely ocular. About 15 percent of patients present with bulbar symptoms. These include fatigable chewing, dysphagia, and dysarthria. Less than 5 percent present with proximal limb weakness alone. Involvement of the muscles of respiration produces the most serious symptoms in MG, such as respiratory insufficiency and pending respiratory failure, termed myasthenic crisis. (See "Myasthenic crisis".)

Many patients with acetylcholine receptor (AChR) antibody-positive MG have thymic abnormalities, including hyperplasia in 60 to 70 percent and thymoma in 10 to 12 percent.

In all patients with clinically suspected MG, the diagnosis should be confirmed, if possible, by immunologic and/or electrodiagnostic testing (table 1). (See "Diagnosis of myasthenia gravis".)

EFFECT OF PREGNANCY — Pregnancy has a variable effect on the course of MG [1-3]. However, patients with MG that is under good control before pregnancy can be reassured that they are likely to remain stable throughout pregnancy, although a small proportion may have worsening in the postpartum period [4]. For patients with active MG before pregnancy, flares are most likely to occur in the first trimester and the postpartum period. Some patients may be diagnosed with MG after developing initial symptoms during pregnancy [5-7].

In a metanalysis including over 32 studies and 824 pregnant patients where an MG exacerbation occurred in 34 percent, remission occurred in 20 percent, and no change in disease was reported by 48 percent. Postpartum exacerbations were noted in 30 percent of all patients. In addition, myasthenic crisis occurred during pregnancy in 8 percent and in the postpartum period in 8 percent. Similar findings have been reported in other studies as well [1,5,8-12].

As already noted, the first trimester and the acute postpartum period are times of highest risk for exacerbation [13]. Mortality risk of the mother with MG is inversely proportional to the duration of disease, with the highest risk being within the first year after disease onset [14]. Myasthenic flare may occur after therapeutic abortion secondary to the stress of surgery, but it usually remits following spontaneous abortion [5,8].

NEONATAL MYASTHENIA GRAVIS — Transient neonatal MG develops in 10 to 20 percent of infants born to myasthenic mothers due to transplacental passage of IgG anti-acetylcholine receptor antibodies (AChR-Ab). Though definitive data are lacking, a small retrospective study found no correlation between neonatal MG and the maternal IgG anti-AChR titer [15]. In addition, a small prospective study found that the duration of maternal disease and medication usage for MG were not associated with the occurrence of neonatal MG [16].

Among mothers with a child affected by transient neonatal MG, the risk of recurrence with subsequent pregnancies is approximately 75 percent. (See "Neuromuscular junction disorders in newborns and infants", section on 'Neonatal myasthenia gravis'.)

PREPREGNANCY PLANNING — The following general principles apply to the management of patients with MG during pregnancy [4,13,17].

For patients with MG, pregnancy should be planned well in advance with multidisciplinary management including, where available, maternal-fetal medicine specialists with expertise for managing high-risk, complicated pregnancies. (See "Prenatal care: Initial assessment", section on 'Care provider'.)

Prepregnancy counseling should include a discussion concerning safety of therapies for MG, with avoidance or discontinuation of known teratogenic medications (methotrexate and mycophenolate mofetil). (See 'Symptomatic therapy' below.)

Thymectomy in the year prior to conception is unlikely to result in clinical remission of MG in the mother before pregnancy, and its impact on the risk of neonatal MG is undetermined. Most experts advise young patients to proceed with thymectomy as soon as possible, with the exception of those who are already pregnant. In such cases, thymectomy should be performed when feasible after pregnancy [4].

Retrospective analysis of data from the Medical Birth Registry of Norway found that neonates of mothers with MG who had undergone thymectomy were less likely to develop neonatal MG than those born to mothers without thymectomy (9/72 [13 percent] versus 17/63 [27 percent], relative risk 0.4, 95% CI 0.16-0.94) [18]. These results suggest that thymectomy has a protective effect against neonatal MG. Of note, 25 of the 41 thymectomized mothers had undergone thymectomy an average of five years before the first birth, allowing more time for the benefit of thymectomy to accumulate. However, the strength of this study is limited by the retrospective design, lack of randomization and blinding, and wide confidence intervals.

It is important to note that the beneficial effects thymectomy are delayed for all patients and may take years to accrue, as discussed separately. (See "Role of thymectomy in patients with myasthenia gravis", section on 'Generalized AChR-positive myasthenia'.)

MANAGEMENT DURING PREGNANCY

General measures — Baseline and surveillance clinical evaluations of pregnant patients with MG includes assessment of neurologic status and risks for neurologic deterioration.

Initial evaluation of the pregnant patient with MG includes assessment of baseline motor strength, respiratory status, and pulmonary function tests. Cardiac status should be followed with electrocardiograms, since rare occurrences of focal myocardial necrosis have been recorded in patients with MG [19,20]. Thyroid function tests should be performed since there is an association between MG and other autoimmune diseases [21].

All infections should be treated promptly. In one study of 65 pregnant females with MG, four who had underlying infection (pyelonephritis, endometritis, or mastitis) all developed MG exacerbations [5].

Complaints of dyspnea or cough call for prompt evaluation of possible myasthenic flare with diaphragm and respiratory muscle weakness [22].

Physical and emotional stress can exacerbate MG.

Medications for myasthenia gravis — Although the normal physiologic changes associated with pregnancy may affect the course of MG, the treatment of MG in pregnancy is similar to that in patients who are not pregnant. (See "Overview of the treatment of myasthenia gravis".)

A number of medications may exacerbate weakness in the myasthenic patient and should be avoided whenever possible (table 2).

Symptomatic therapy — Acetylcholinesterase inhibitors such as pyridostigmine are the standard first-line symptomatic treatment for MG, including during pregnancy [4]. Dose adjustment may be required in pregnancy as a result of increased renal clearance, expanded maternal blood volume, delayed gastric emptying, and frequent emesis [22]. Increasing the dose of pyridostigmine should first be accomplished by decreasing the interval of administration, followed by increasing the dose if symptoms persist. (See "Overview of the treatment of myasthenia gravis", section on 'Initial symptomatic therapy'.)

Intravenous acetylcholinesterase inhibitors may produce uterine contractions and should not be used during pregnancy prior to delivery [17]. During labor, however, anticholinesterase medications should be administered parenterally to avoid erratic gastrointestinal absorption. (See 'Labor and delivery' below.)

Immunomodulatory therapy — Prednisone is the immunomodulatory agent of choice in pregnancy [4]. In addition to glucocorticoids, azathioprine, tacrolimus, and cyclosporine may be used if anticholinesterases fail to control MG exacerbations [4]. These medications have been well studied in pregnancy, mainly in transplant recipients and patients with autoimmune diseases other than MG and have been found to be relatively safe [23,24]. However, high doses of cyclosporine and azathioprine have been linked to spontaneous abortion, preterm labor, low birth weight, chromosomal damage [2,23,24], and hematologic suppression; they should be reserved for pregnant patients who are not controlled, cannot tolerate glucocorticoids, or have significant comorbidities that may worsen with glucocorticoid administration [2,23-25]. The risk of continuing these medications in high doses should be weighed against the benefit of controlling myasthenic symptoms. Mycophenolate mofetil and methotrexate increase the risk of teratogenicity and should not be used in pregnancy [4]. (See "Safety of rheumatic disease medication use during pregnancy and lactation" and "Chronic immunotherapy for myasthenia gravis".)

Caution should be exercised when initiating therapy with glucocorticoids, since a transient worsening of MG may occur. Glucocorticoids may also produce carbohydrate intolerance, especially during pregnancy. Even though there are no teratogenic effects from glucocorticoids, pregnant patients with MG who rely on these medications should be maintained on the lowest possible dose [2,19]. The use of glucocorticoids to treat MG, including dosing and tapering schedules, is discussed in detail separately. (See "Chronic immunotherapy for myasthenia gravis", section on 'Glucocorticoids'.)

MuSK antibody positive MG – Patients with anti-acetylcholine receptor antibodies (AChR-Ab)-negative MG who are muscle-specific receptor tyrosine kinase (MuSK) antibody positive share most of the clinical manifestations of generalized myasthenia but are generally less responsive to acetylcholinesterase inhibitors. For patients with MuSK antibody-associated MG, treatment with prednisone, plasma exchange, or other immunomodulatory therapies may be required [6]. For those with severe and progressive MG, rituximab may be used as a first line immunomodulatory therapy. However, the data are limited for rituximab use during conception and pregnancy; the risks and benefits must be weighed carefully and discussed with the patient. (See "Safety of rheumatic disease medication use during pregnancy and lactation" and "Chronic immunotherapy for myasthenia gravis".)

Myasthenic crisis – Plasmapheresis and high-dose intravenous immune globulin are safe in pregnancy and have also been used for myasthenic crisis with variable results [2,5,13,19,26]. These interventions should be reserved for cases where conventional therapy has failed and developing respiratory failure or profound dysphagia and weakness threatens the mother and fetus [11,27]. (See "Myasthenic crisis", section on 'Rapid therapies'.)

The data are limited regarding the use of infusion therapies during pregnancy for generalized, acetylcholine receptor-positive MG patients. These agents include efgartigimod, ravulizumab, and eculizumab. (See "Chronic immunotherapy for myasthenia gravis", section on 'Eculizumab' and "Chronic immunotherapy for myasthenia gravis", section on 'Ravulizumab' and "Chronic immunotherapy for myasthenia gravis", section on 'Efgartigimod'.)

Patients with preeclampsia and eclampsia — Magnesium sulfate is commonly administered in contemporary obstetrics for management of preeclampsia/eclampsia and preterm labor but is contraindicated in patients who have MG since it can precipitate a severe myasthenic crisis (table 2) [28,29]. Severe hypertension can be treated with methyldopa or hydralazine, while beta blockers and calcium channel blockers should be avoided if possible [28,29]. Levetiracetam or valproic acid can be used for seizure prophylaxis, whereas phenytoin can potentially exacerbate weakness and is therefore reserved for refractory seizures [20,22]. The patient with preeclampsia and myasthenia on high-dose glucocorticoids is at high risk for pulmonary edema and should be monitored closely. In addition, decreased urine output is often found in patients with preeclampsia and may require dosing modifications in order to avoid toxicity [22].

Fetal assessment — The development of fetal abnormalities related to transplacental passage of IgG AChR-Abs is a major concern during pregnancy in mothers with MG. (See "Neuromuscular junction disorders in newborns and infants", section on 'Neonatal myasthenia gravis'.)

Assessment of fetal well-being may include the nonstress test or biophysical profile. Methods of fetal assessment are discussed in detail separately. (See "Overview of antepartum fetal assessment", section on 'Fetal assessment techniques' and "Nonstress test and contraction stress test".)

The perception of fetal movement may be altered in patients with MG. Continuous fetal monitoring is indicated during a myasthenic crisis if the fetus is at a viable gestational age (eg, at least 23 menstrual weeks of gestation) given the high risk of maternal and fetal hypoxia.

Abnormal sonographic findings in affected pregnancies may include polyhydramnios due to impaired fetal swallowing [30,31]. Decreased fetal movement and breathing have also been described [30].

Fetal arthrogryposis multiplex congenita is the most severe finding in the fetus with neonatal MG; lack of generalized fetal movement and diaphragmatic excursion may rarely produce joint contractures and pulmonary hypoplasia [30,32]. Several studies describe a direct relationship between high maternal titers of AChR-Abs and fetal arthrogryposis multiplex congenital [30,32]. Whereas ultrasound may be able to detect these abnormalities during the antepartum period, its utility for predicting clinical outcome is not well defined.

LABOR AND DELIVERY

Mode of delivery — Spontaneous vaginal delivery is the objective and should be encouraged [4]. Cesarean delivery should be reserved for the usual obstetrical indications. Appropriate steps should be taken to circumvent the effects of maternal fatigue on delivery, since stress and exertion can precipitate a myasthenic crisis [21]. The first stage of labor is not affected by MG because the uterus is composed of smooth muscle and lacks the postsynaptic acetylcholine receptor. In contrast, the second stage of labor may be affected because the voluntary striated muscles used during expulsive efforts may easily weaken. Excessive maternal fatigue may result. Operative vaginal delivery may reduce maternal fatigue and weakness. In a systematic review that included 824 pregnancies, spontaneous vaginal delivery was performed for 56 percent of births, operative vaginal delivery for 10 percent, and cesarean birth represented only 3 percent of deliveries [33].

Monitoring and management of neuromuscular status

Anesthesiology consultation – Consultation with an anesthesiologist before labor is recommended, since patients with MG who undergo general anesthesia may be at increased risk for requiring mechanical ventilation [34,35]. Selection of anesthetic technique is dependent on several factors. Regional anesthesia is recommended for mild to moderate disease when vaginal delivery is anticipated, allowing for adequate anesthesia if vacuum or forceps are needed; it also can reduce fatigue associated with the second stage of labor. General endotracheal anesthesia is recommended for the patient with severe disease and compromised respiratory or bulbar status [19].

Medications – Neuromuscular blocking agents should be avoided if neuromuscular monitoring and sugammadex are unavailable since patients with MG have altered acetylcholinesterase activity. Due to the relative resistance to succinylcholine, larger doses are often required leading to a prolonged block [19]. Patients with MG are more sensitive to inhaled anesthetics including sevoflurane, desflurane, halothane, and isoflurane [19,36].

Sedatives, opioids, and tranquilizers can potentiate respiratory depression in this population and should be administered judiciously. When using opioids or other sedatives for pain control, pulse oximetry and frequent assessment of respiratory rate is recommended. Nonsteroidal anti-inflammatory drugs such as ketorolac tromethamine may also be used for postpartum or postoperative pain.

During labor, anticholinesterase medications should be administered parenterally to avoid erratic gastrointestinal absorption. The dose of pyridostigmine is individualized based on patient symptoms. The parenteral dose of pyridostigmine is equivalent to one-thirtieth of the patient's oral dose.

The periprocedural anesthetic management of patients with MG is discussed in greater detail separately. (See "Anesthesia for the patient with myasthenia gravis", section on 'Anesthesia management'.)

Respiratory status – The maternal respiratory status (respiratory rate, pulse oximetry) should be monitored carefully because stress and fatigue associated with labor and delivery may precipitate worsening of disease. Another issues is that chronic glucocorticoid therapy can suppress the hypothalamic-pituitary-adrenal axis and lead to adrenal insufficiency during times of stress such as labor and delivery. Therefore, some experts suggest that patients on long-term glucocorticoids who take prednisone or equivalent at a dose >7.5 mg/day should receive stress-dose hydrocortisone during the intrapartum period [17]. Other experts use somewhat different thresholds to determine the need for glucocorticoid coverage based upon the patient's history of glucocorticoid intake and likelihood of hypothalamic-pituitary-adrenal axis suppression, as discussed elsewhere. (See "The management of the surgical patient taking glucocorticoids".)

Complications — Pregnant patients with MG have an increased incidence of preterm labor and birth in some studies [37,38], although this is not confirmed by other studies [8]. In one review, the rates of preterm birth occurring prior to 37 and 34 weeks gestation were 12 and 4 percent, respectively [33].

Estimates of perinatal mortality rates for infants born of patients with MG vary widely [1,37]. In a retrospective population study, perinatal mortality was not significantly higher among 127 births by Norwegian females with MG compared with those of a reference group without MG (2.4 versus 1.4 percent) [37]. However, females with MG had a significantly higher risk of delivery complications than the reference group (41 versus 33 percent); the most common complication was premature rupture of membranes. Cesarean deliveries were also performed more frequently in females with MG (17 versus 9 percent of deliveries); half were elective. In contrast, a population based study from Taiwan found no significant differences between pregnant patients with MG and controls for the risk of delivery complicated by low birth weight, small for gestational age, or cesarean delivery [39].

An earlier study found that the death rate due to fetal anomalies was higher in the myasthenic population compared with the normal population (18 versus 2.2 per 1000 live births) [1].

POSTPARTUM MANAGEMENT

Monitoring for neonatal MG — All infants of myasthenic mothers should be observed and monitored in a special care nursery for the first 48 to 72 hours of life for any evidence of weakness caused by transient neonatal MG [13]. Symptoms of respiratory distress, poor feeding, and flaccid tone can appear within hours after birth and may persist for up to three months.

Breastfeeding — Glucocorticoids can be used safely in lactation. Anticholinesterase drugs are found in breast milk in low levels and are therefore considered safe in lactation unless high doses are required [2]. Breastfeeding may continue along with the use of azathioprine, cyclosporine, tacrolimus, IVIG, or plasma exchange. Breastfeeding is not recommended for patients with MG taking mycophenolate or methotrexate [13,40].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Myasthenia gravis" and "Society guideline links: Thymomas and thymic carcinomas".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Myasthenia gravis (The Basics)")

SUMMARY AND RECOMMENDATIONS

Clinical features – Myasthenia gravis (MG) is an autoimmune disorder characterized by weakness and fatigability of skeletal muscles due to dysfunction of the neuromuscular junction. The diagnosis is confirmed by immunologic and/or electrodiagnostic testing (table 1). (See 'Clinical aspects' above.)

Transient neonatal MG develops in 10 to 20 percent of infants born to myasthenic mothers due to transplacental passage of IgG anti-acetylcholine receptor antibodies (AChR-Abs). (See 'Neonatal myasthenia gravis' above.)

Effect of pregnancy on MG – Pregnancy has a variable effect on the course of MG. The first trimester and the acute postpartum period are times of highest risk for exacerbation. (See 'Effect of pregnancy' above.)

Prepregnancy planning – For patients with MG, pregnancy should be planned well in advance with multidisciplinary communication among specialists to optimize the clinical management of MG and to minimize risks to the fetus. (See 'Prepregnancy planning' above.)

Treatment during pregnancy

MG treatment – Anticholinesterase agents such as pyridostigmine are the standard first-line symptomatic treatment for MG. Dose adjustment may be required in pregnancy. Prednisone is the immunomodulatory agent of choice in pregnancy. (See 'Medications for myasthenia gravis' above.)

The use of other immunomodulatory agents for patients unresponsive to first-line options should be individualized based on assessment of overall risks and benefits. These agents include azathioprine, tacrolimus, and cyclosporine. Mycophenolate mofetil and methotrexate increase the risk of teratogenicity and should not be used in pregnancy.

Contraindications and use of specific medications Magnesium sulfate is contraindicated in patients who have MG, since it can precipitate a severe myasthenic crisis (table 2). For management of preeclampsia or eclampsia in patients with MG, severe hypertension can be treated with methyldopa or hydralazine. Levetiracetam or valproic acid can be used for seizure prophylaxis, whereas phenytoin can potentially exacerbate weakness and is therefore reserved for refractory seizures. Non-depolarizing muscle relaxants should be avoided. (See 'Symptomatic therapy' above.)

Management during labor – The second stage of labor may be affected in patients with MG because the voluntary striated muscles used during expulsive efforts may easily weaken. Appropriate steps should be taken to circumvent the effects of maternal fatigue on delivery since stress and exertion can precipitate a myasthenic crisis. During labor, anticholinesterase medications should be administered parenterally to avoid erratic gastrointestinal absorption. (See 'Labor and delivery' above.)

Postpartum management

Monitoring for neonatal MG – All infants of myasthenic mothers should be observed in a special care nursery for the first 48 to 72 hours of life, as transient neonatal MG develops in 10 to 20 percent of infants born to myasthenic mothers. (See 'Neonatal myasthenia gravis' above and "Neuromuscular junction disorders in newborns and infants", section on 'Neonatal myasthenia gravis'.)

Breastfeeding – Glucocorticoids can be used safely in lactation. Anticholinesterase drugs are found in breast milk in low levels and are therefore considered safe in lactation unless high doses are required. Mycophenolate, methotrexate, and some other immunotherapeutic agents can cause immunosuppression in the infant and are therefore contraindicated in breastfeeding mothers. (See 'Breastfeeding' above.)

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References

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