Magnesium Sulfate-Induced Ophthalmoplegia: A Rare Postnatal Complication

Magnesium sulfate (MgSO₄) is widely used in managing eclampsia, but its neurological side effects are often overlooked. A 25-year-old woman with a second gravida pregnancy developed eclampsia in her third trimester and underwent an emergency cesarean section. In the immediate postoperative period, she presented with bilateral ophthalmoplegia, ptosis, and neck flexion weakness, though her pupillary reflexes remained intact. Initial concerns included myasthenia gravis and Miller-Fisher syndrome, but further investigations, including repetitive nerve stimulation (RNS), acetylcholine receptor (AChR), and muscle-specific kinase (MuSK) antibody testing, were negative. Three Tesla MRI brains with constructive interference in steady state (CISS) sequences of III, IV, and VI were normal, and laboratory results revealed elevated serum magnesium levels (5.5 meq/L). A diagnosis of hypermagnesemia-induced ophthalmoplegia was confirmed, and MgSO₄ therapy was promptly discontinued. Within 36 hours, her symptoms began to resolve, highlighting the transient yet significant neuromuscular effects of magnesium toxicity. This case underscores the importance of recognizing early signs of magnesium toxicity in postpartum patients receiving MgSO₄ therapy. While mild hypermagnesemia can cause headache and diminished reflexes, severe cases may progress to muscle paralysis, respiratory failure, and even cardiac arrest. Ophthalmoplegia, though rare, should raise suspicion, prompting timely magnesium level monitoring and treatment adjustments. Withholding MgSO₄ at the appropriate time can prevent further complications, ensuring safer management of eclampsia and postpartum neurological health.