Pregnancy and myasthenia gravis: Clinical course, delivery, and postpartum management, a clinical pharmacist’s report

Samyuktha D V

Group Clinical Pharmacist, Kauvery Hospital, Trichy, Tamil Nadu

Abstract

Myasthenia Gravis (MG) is an autoimmune neuromuscular disorder characterized by fluctuating skeletal muscle weakness, posing unique challenges in pregnancy and delivery. We present the case of a 32-year-old multiparous woman with a history of MG, who experienced complications during labor necessitating cesarean section under spinal anaesthesia, followed by postpartum exacerbation of symptoms, requiring plasmapheresis. The case highlights the importance of multidisciplinary coordination for the management of MG in pregnancy to optimize maternal and fetal outcomes.

Introduction

Myasthenia Gravis (MG) is a persistent autoimmune disorder affecting the neuromuscular junction, characterized by fluctuating weakness in voluntary muscles. This condition results from the immune system producing antibodies that target acetylcholine receptors. MG predominantly affects younger women, particularly those in their twenties and thirties, which coincides with their reproductive years. Globally, the incidence of MG is estimated to be between 5 and 10 cases per million people annually. In India, available data suggest a comparably low but likely underreported prevalence, with localized studies indicating an incidence ranging from 5 to 8 cases per million per year (1,2).

Pregnancy in women diagnosed with MG introduces distinctive clinical difficulties due to complex interactions between the disease process and gestational physiological changes. While MG generally does not impact fertility, the course of the disease during pregnancy is variable and unpredictable. Approximately 30 to 50 percent of pregnant women with MG experience worsening symptoms during pregnancy or in the postpartum phase, especially during the first trimester and within the month following childbirth. Conversely, a subset of patients may observe improvement in symptoms, possibly attributable to the immunological modulation that occurs during pregnancy. Additionally, anatomical and physiological changes in pregnancy—such as upward displacement of the diaphragm and altered respiratory mechanics—may increase the risk of MG exacerbations or myasthenic crisis, underscoring the need for vigilant multidisciplinary care (3,4).

From a maternal health perspective, MG is not associated with a significantly elevated risk of miscarriage, fetal growth restriction, or preterm birth. However, there is a reported increase in the incidence of premature rupture of membranes and more complicated labor due to muscle weakness. Fatigue of the striated muscles involved in the second stage of labor can further challenge delivery in affected patients (3,4).

The fetus is susceptible to transient neonatal myasthenia gravis, which occurs in roughly 10 to 20 percent of infants born to mothers with MG. This condition is caused by the passive transfer of maternal autoantibodies across the placenta, leading to clinical features such as muscle hypotonia, feeding difficulties, and respiratory distress. These neonatal symptoms are typically self-limiting and resolve within a few weeks. Breastfeeding is generally considered safe for mothers on medications like pyridostigmine and corticosteroids; however, certain immunosuppressive drugs may contraindicate lactation (1,3,6).

Figure 1: General principles apply to the management of women with MG during pregnancy

At present, no definitive cure exists for MG, but effective management includes the use of immunosuppressive agents—such as corticosteroids and azathioprine—and acetylcholinesterase inhibitors like pyridostigmine. In cases of disease exacerbation, treatments such as plasmapheresis and intravenous immunoglobulin therapy are employed. During pregnancy, therapeutic strategies are tailored carefully to ensure optimal control of maternal symptoms while minimizing risks to the fetus (1,3,6).

Although MG usually develops independently of pregnancy, immune system fluctuations related to pregnancy and delivery can precipitate the initial onset or worsen existing symptoms. Nonetheless, there is no established causal relationship between the first pregnancy and the onset of MG. Women of reproductive age, particularly females, are more susceptible to MG due to underlying autoimmune tendencies (1,3,5).

Epidemiologically, MG is more frequently diagnosed in females compared to males, with an approximate female-to-male ratio of 2:1. This sex disparity varies with age and different subtypes of the disease. Typically, women manifest symptoms in their second and third decades, while males tend to present with MG later in life, often after the age of 50 (7,8).

Figure 2: Treatment options for MG during pregnancy

Case Presentation

A 32-year-old woman, gravida 2 para 1, presented to MAA Kauvery Hospital at term with intermittent mild lower abdominal pain, seeking safe confinement. She had a known diagnosis of myasthenia gravis since 2018, managed with oral pyridostigmine (Gravitor) 60 mg thrice daily. Her menstrual cycles were regular (3–5 days per 28-day cycle). She was married since 2014 to a partner with a history of neurocutaneous melanocytosis. Her obstetric record included one previous healthy male child aged 10 years, with the current pregnancy conceived spontaneously.

On admission, she was conscious, oriented, and afebrile, with no pallor or pedal edema. She was diagnosed as G2P1L1 at 9 months’ amenorrhea, with stable myasthenia gravis. Neurological evaluation including acetylcholine receptor antibody testing showed a titre greater than 8.00, consistent with active MG. The neurologist advised continuation of pyridostigmine at 90 mg thrice daily and advised against the use of oxytocin, given its potential to exacerbate MG symptoms.

Induction of labor was attempted but failed owing to nonprogress of labor. Subsequently, a lower segment cesarean section (LSCS) was performed under spinal anesthesia, resulting in delivery of a healthy male infant. Postoperatively, the patient developed a spinal headache which was managed conservatively. Prophylactic intravenous antibiotics, deep vein thrombosis (DVT) prophylaxis, and supportive care were administered.

Within days, she experienced worsening MG symptoms, including limb fatigability, neck pain, and difficulty in speaking, and swallowing. She was transferred to a Neurological care center (Kauvery-Cantonment, Trichy) for specialized management.

On admission, vital signs were stable, Glasgow Coma Scale was 15, and clinical examination revealed restricted upward and horizontal extraocular movement with intact limb strength (5/5). Investigations showed leukocytosis (total count 11,630), platelet count of 276,000, normal renal parameters, and hemoglobin 9.9 g/dL, Chest computed tomography confirmed bilateral basal atelectasis. Point-of-care cardiac and pulmonary ultrasound evaluations were unremarkable.

Due to symptomatic exacerbation, plasmapheresis was planned. During the initial session, the patient developed pruritus involving the face, bilateral upper limbs, trunk, abdomen, and periorbital swelling. The procedure was halted, and she was treated promptly with intravenous chlorpheniramine (Avil) and hydrocortisone, after which plasmapheresis was restarted and completed.

She underwent a total of five plasmapheresis cycles, alongside management with intravenous pantoprazole (40 mg once daily), subcutaneous heparin (1 ml three times daily), oral prednisolone (Wysolone 5 mg once daily), calcium supplementation (Shelcal 500 mg once daily), and continued pyridostigmine every six hours.

The patient’s condition improved gradually, and she was discharged in stable condition with no further complications noted during follow-up. Upon discharge, her prescribed medications were Tab. Pantoprazole 40 mg OD, Tab. Prednisolone 20 mg OD, Tab. Pyridostigmine 60 mg TDS, and Tab. Azathioprine 50 mg OD.

 

Discussion

This case underscores the challenges posed by MG in pregnancy, requiring meticulous planning and multidisciplinary coordination involving obstetricians, neurologists, and anesthetists. Pregnancy may unpredictably influence MG course, requiring vigilance for exacerbations, especially postpartum. Avoidance of medications like oxytocin, which may worsen MG symptoms, is critical during labor.

Anesthesia choice is also paramount; spinal anesthesia was successfully employed in this case, minimizing neuromuscular complications. Postpartum exacerbation demands prompt immunomodulatory interventions such as plasmapheresis, which can be complicated by hypersensitivity reactions but remains essential for symptom control. The balance between maternal disease control and fetal safety governs therapy choices, with close monitoring for neonatal myasthenia gravis.

Our patient’s favorable outcomes illustrate the effectiveness of coordinated care and timely intervention, reaffirming evidence from previous literature that plasmapheresis alongside immunosuppressive therapy improves prognosis in flare-ups.

Conclusion

Myasthenia gravis in pregnancy presents significant management complexities requiring individualized, multidisciplinary care throughout the peripartum period. Recognizing potential exacerbations, avoiding contraindicated medications, and providing prompt immunomodulatory treatment such as plasmapheresis can ensure positive outcomes for mother and child. Careful follow-up is essential to maintain long-term stability.

Reference

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