Muscle Weakness of the Lower Limbs After Epidural Anesthesia in a Pregnant Woman with Undiscovered Systemic Lupus Erythematosus

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Muscle Weakness of the Lower Limbs After Epidural Anesthesia in a Pregnant Woman with Undiscovered Systemic Lupus Erythematosus

A 29-year-old nulliparous woman at 31 ± 1 gestational weeks presented to the West China Second Hospital with progressive dyspnea, orthopnea, and bilateral lower limb edema over three months. Initial symptoms included anemia detected at 18 gestational weeks (hemoglobin [Hb] 77 g/L), which improved marginally with iron supplementation (Hb 81 g/L). By 30 gestational weeks, she developed worsening chest discomfort, palpitations, and fatigue, prompting hospitalization. Laboratory findings revealed severe anemia (Hb 67 g/L), elevated cardiac biomarkers (NT-BNP 10,300 pg/mL, troponin 0.098 mg/L), renal dysfunction (creatinine 138 mmol/L, urea nitrogen 11.64 mmol/L), hypoalbuminemia (25.7 g/L), and proteinuria (3+). Transthoracic echocardiography identified mitral stenosis with regurgitation and pericardial effusion. Left pleural effusion was confirmed via ultrasound. Due to deteriorating multisystem involvement, the pregnancy was terminated via cesarean section under epidural anesthesia to stabilize her condition.

Clinical Course and Interventions

Epidural anesthesia was administered via a catheter inserted at the L1-L2 intervertebral space. A test dose of 3 mL 1% lidocaine was followed by incremental doses (6 mL and 3 mL of 2% lidocaine). The procedure was uneventful. Postoperatively, electrolyte management, transfusions, and diuresis were initiated. By postoperative day 1 (POD 1), dyspnea resolved, but laboratory markers worsened: NT-BNP surged to 24,600 pg/mL, creatinine rose to 212 mmol/L, and potassium levels normalized (4.85 mmol/L). On POD 1, the patient reported bilateral lower limb weakness (strength 3/5) with preserved sensory function. Lumbar spine MRI ruled out structural lesions.

Immunological testing on POD 2 revealed systemic lupus erythematosus (SLE): antinuclear antibodies (ANA+), anti-dsDNA (+++), anti-Sm (+), hypocomplementemia (C3 0.38 g/L, C4 0.06 g/L), and elevated immunoglobulins (IgG 15.10 g/L). A retrospective history uncovered preexisting symptoms: facial rash, frostbite-like hand lesions, and alopecia over 10 months. Rheumatological evaluation confirmed SLE with neuropsychiatric and renal involvement. Immediate treatment included methylprednisolone and hydroxychloroquine. By POD 5, limb strength improved to 4/5, fully recovering by POD 7.

Complications and Fatal Outcome

Despite initial neurological recovery, the patient developed severe systemic complications: nephritis, serositis, seizures, psychosis, and recurrent lung infections. Aggressive therapies (plasmapheresis, antimicrobials, continuous renal replacement therapy) failed to halt disease progression. She succumbed to multiorgan failure on POD 38.

Pathophysiological Considerations

The case highlights diagnostic challenges in distinguishing SLE exacerbation from pregnancy-related physiological changes. Early signs (anemia, edema, proteinuria) were initially attributed to gestational adaptations. Delayed recognition of SLE led to critical delays in immunosuppressive therapy. The temporal association between epidural anesthesia and lower limb weakness raised suspicion of procedural complications. However, MRI excluded epidural hematoma or infection. Lidocaine neurotoxicity, though reported in animal studies, lacks conclusive human evidence. Transient neurologic syndrome (TNS) was unlikely due to absent back pain.

Neuropsychiatric SLE (NPSLE), particularly peripheral nervous system (PNS) involvement, is rare but associated with significant morbidity. Acute axonal polyneuropathy or mononeuritis multiplex, secondary to vasculitis, can mimic neuraxial anesthesia complications. In this patient, SLE-induced vasculitic neuropathy likely precipitated limb weakness, exacerbated by metabolic derangements (uremia, hypoalbuminemia) and fluid shifts.

Lessons for Clinical Practice

  1. Multidisciplinary Collaboration: Complex pregnancies with multisystem abnormalities necessitate early involvement of rheumatologists, neurologists, and nephrologists.
  2. SLE Diagnostic Vigilance: Features such as malar rash, photosensitivity, unexplained cytopenias, and hypocomplementemia warrant SLE screening, even in asymptomatic pregnant women.
  3. Anesthesia Considerations: Neuraxial techniques remain safe for most pregnancies, but underlying autoimmune disorders require meticulous risk stratification. Post-procedural neurological deficits should prompt systemic evaluation beyond local causes.
  4. Timely Immunosuppression: Early corticosteroid and antimalarial therapy may mitigate SLE flares, underscoring the importance of rapid diagnosis.

Data and Laboratory Findings

Key laboratory trends included:

  • Hematologic: Persistent anemia (Hb 77 → 81 → 67 → 73 g/L) unresponsive to iron.
  • Renal: Progressive azotemia (creatinine 138 → 212 mmol/L; urea nitrogen 11.64 → 14.38 mmol/L) and proteinuria.
  • Cardiac: Elevated NT-BNP (10,300 → 24,600 pg/mL) reflecting volume overload and myocardial stress.
  • Immunologic: Hypocomplementemia (C3 0.38 g/L, C4 0.06 g/L), anti-dsDNA (+++), and anti-Sm antibodies.

Imaging findings (echocardiography, pleural ultrasound, lumbar MRI) correlated with clinical deterioration but lacked evidence of direct neural compression or infection.

Conclusion

This case underscores the lethality of undiagnosed SLE in pregnancy and the diagnostic pitfalls in distinguishing its manifestations from gestational physiology. Anesthesia-related neurological complications, though rare, necessitate thorough systemic evaluation, particularly in high-risk populations. Early immunosuppression and multidisciplinary care are critical to improving outcomes in SLE pregnancies.

doi.org/10.1097/CM9.0000000000000665

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