oa Unexpected complication of a common therapy in a pregnant patient

Background: Pre-eclampsia/eclampsia is a life-threatening disease with considerable risks on maternal and neonatal health. Globally, it affects between 2–8% of all pregnancies. Worldwide, approximately 63,000 pregnant women die each year due to pre-eclampsia/eclampsia. The MAGPIE (Magnesium sulphate for Prevention of Eclampsia) trial stated that the risk of developing convulsions was lowered significantly (58%) in severe pre-eclampsia patients who received magnesium sulfate in comparison to the placebo group.¹ The exact mechanism of action of magnesium sulfate (MgSO4) is not completely understood, blocking calcium channels and decreasing availability of calcium for smooth muscle contractions has been suggested. Pritchard advocated that therapeutic concentration of MgSO4 should be between 2-4 mmol/l.² Despite strong evidence of the effectiveness of MgSO4, concerns have been expressed about the risk of hypocalcemia to the patient when used alone or concomitantly with nifedipine as both of them affect calcium metabolism.³ Hypermagnesemia causes hypocalcemia by inhibiting parathyroid hormone secretion and increases urinary excretion of calcium. Severe hypocalcemia is a life-threatening condition and may lead to focal or generalized tonic muscle cramps, convulsions, arrhythmia, and laryngospasm and stridor which is common in the pediatric population but has also been reported in adults.⁴ A case of symptomatic hypocalcemia secondary to hypermagnesemia is extremely rare, and to the best of our knowledge, only a few cases have been reported.⁵ We believe this is the only case in the literature with stridor and potential airway obstruction. Case: A 30-year old black South African woman, gravida 5, para 3+1, presented with severe preeclampsia (BP 215/145 mmHg, proteinuria +2), and preterm premature rupture of membrane at 33 weeks of gestation. General and obstetric examinations were unremarkable. Laboratory parameters on admission showed acute kidney injury, anemia and elevated lactate dehydrogenase and alkaline phosphatase. Other investigations were normal (Table 1). She was admitted to the high dependent unit and received 10 grams of intramuscular MgSO4, followed by continuous intravenous infusion at a rate of 2 g/hour for 24 hours. Her blood pressure dropped to 145/95 mmHg. Three hours post-admission, her blood pressure raised to 186/124 mmHg and was controlled with a labetalol intravenous infusion and nifedipine 10 mg orally. Her blood pressure then dropped to 150/90 mmHg. Six hours post-admission, the patient had an uneventful emergency caesarean section under spinal anesthesia for fetal distress. Nine hours post-admission, the patient had dyspnea, respiratory distress, and inspiratory stridor, and chest examination was unremarkable. While checking her blood pressure, the patient had carpopedal spasm (Trousseau's sign) and masseter muscle spasm (Chvostek's sign). MgSO4 infusion was stopped. She received 10 ml of 10% calcium chloride over 10 minutes and responded dramatically to resuscitation and calcium chloride. Investigations (arterial blood gas, FBC, urea and electrolytes) were performed and showed low ionized calcium 0.89 mmol/l and her magnesium level was 2.74 mmol/l. Conclusion: Although MgSO4 is considered as the treatment of choice for the prevention of convulsions in pre-eclampsia/eclampsia patients, concerns have been raised regarding the risk of severe hypocalcemia, especially when used concomitantly with calcium channel blockers. Prospective studies designed in a controlled fashion are needed to assess the safe combination of magnesium sulfate and nifedipine.