Myasthenia gravis during pregnancy


  • Management of myasthenia gravis during pregnancy requires an MDT approach, disease optimisation prior to pregnancy and management in a tertiary or specialist centre
  • 1/3rd of patients experience an improvement in symptoms
  • 1/3rd of patients experience no change in disease state
  • 1/3rd of patients experience a worsening of symptoms

  • Exacerbations are most likely to occur either:
    • Early i.e. in the first trimester
    • Post-partum

  • The aspiration risk is higher in MG during pregnancy owing to the combination of:
    • Pregnancy-associated relaxation of the lower oesophageal sphincter, increasing gastric reflex
    • MG-associated bulbar dysfunction

  • There is an increased risk of respiratory failure due to:
    • Pregnancy-associated reduction in RV and FRC due to anatomical changes
    • MG-associated intercostal muscle weakness
  • Fortunately this rarely manifests

  • Management of pre-eclampsia is affected as myasthenia gravis relatively contraindicates a number of first-line pharmacological agents

  • β-blockers i.e. labetalol and calcium channel blockers i.e. nifedipine should be avoided
  • Methyldopa or hydralazine should be used instead

  • Magnesium impairs NMJ transmission and should only be used if absolutely necessary
  • If given IV for eclampsia it can cause respiratory failure necessitating I&V
  • Such a patient should be managed in an HDU setting

  • MG alone doesn't mandate LSCS, though exertion, stress or prolonged labour can trigger myasthenic crisis and should be avoided

Labour care

  • Drugs including anticholinesterases and steroids should be continued throughout
  • The first stage is typically unaffected as the uterus (non-striated smooth muscle) is not affected by MG
  • Muscle fatigue in pushing muscles during the second stage may increase need for instrumental delivery

Labour analgesia

  • Early epidural analgesia benefits from:
    • Reducing need for systemic opioids
    • Minimal motor block of low-dose mixture used
    • Ability for top-ups
  • 1:1 monitoring is advised

  • Systemic opioids (IM/IV/PCA) should be avoided, especially if pre-existing respiratory disease

LSCS

  • Standard measures apply:
    • Premedication with antacid prophylaxis and metoclopramide
    • Optimised fluid status and left-lateral tilt to avoid hypotension from aortocaval compression
    • Consider arterial line if autonomic dysfunction
    • Cautious use of oxytocin boluses as can exacerbate hypotension from autonomic dysfunction; infusion is better

  • Neuraxial technique
    • Neuraxial techniques benefit from earlier return to oral intake of MG medications
    • Mid-thoracic anaesthesia from neuraxial blockade may, however, be poorly tolerated in those with respiratory or bulbar symptoms
    • In such patients GA + TAP blocks may be advisable

    • A well-titrated epidural top-up may be the best technique owing to better CV stability and avoidance of excessively high block
    • Spinals are associated with greater CV instability and higher block, though theoretically cause less potentiation of neuromuscular blockade via systemic absorption of LA than epidurals
    • CSE carries the benefits of both; rapidly attainable anaesthesia which is relatively stable from a cardio-respiratory standpoint

  • General anaesthetic technique
    • A GA technique with TAP blocks may be advisable in those with respiratory/bulbar symptoms who won't tolerate mid-thoracic neuraxial block
    • NMBA doses may need to be reduced and full reversal with sugammadex is required
    • The aspiration risk is even higher than the standard obstetric risk
    • Depth of anaesthesia monitoring is a useful adjunct to balance excessive MAC (muscle-relaxant properties) and too little MAC (high rates of AAGA)

Post-operative care

  • Obstetric HDU
  • Focus on normalising respiratory function with:
    • Suitable positioning
    • Early physiotherapy
    • ± use of NIV
  • Recommence oral medications as soon as possible

  • 10 - 20% of neonates have transient disease because of placental transfer of maternal antibodies
  • Presents in the first days of life with poor feeding, weakness and respiratory issues
  • May require invasive ventilation although the disease is often short-lived and resolves within 8 weeks
  • Breastfeeding is ill-advised owing to:
    • Anti-AChR autoantibodies present in breastmilk
    • Immunosuppressants such as azathioprine or MMF present in breastmilk
    • Anticholinesterases are not found in breastmilk