Magnesium toxicity and an extreme uterine atony: are you ready for the consequences?
Abstract Number: F-57
Abstract Type: Case Report/Case Series
Introduction: Magnesium sulfate is widely used for seizure prophylaxis in preeclampsia. Magnesium (Mg) prevents seizures, by vasodilation, protecting the blood-brain barrier, preventing cerebral edema, and acting as an anticonvulsant through NMDA receptor antagonism. Mg has proven beneficial effects at therapeutic levels. Toxic levels, on the other hand, can have adverse affects on the parturient’s neurological, pulmonary and cardiovascular systems. In extreme cases, magnesium toxicity may lead to uterine atony and the cascade of uncontrolled postpartum hemorrhage and emergent peripartum hysterectomy.
Case description: Our case involves a 31-year-old G3P2A0 female with severe pre-eclampsia who presented at term gestation with spontaneous rupture of membranes in active labor. Magnesium sulfate was administered for seizure prophylaxis but a few hours later the patient was found to have altered mental status and diminished reflexes. A serum magnesium level of 11.5 mg/dL was discovered. Labor became further complicated by an arrest of descent. Consequently, a primary low-transverse cesarean section was performed. One hour after surgery, our patient began to hemorrhage from uterine atony and also suspected to have concurrent disseminated intravascular coagulation. Massive blood transfusion, uterotonics, Bakri balloon placement and correction of coagulopathy failed to stop her hemorrhage. Emergent hysterectomy had to be performed in order to stop the bleeding.
Discussion: Magnesium has been used in parturients for decades now, for various reasons, but its particular use in preeclampsia has gained widespread popularity in preventing seizure, and also as a tocolytic agent for per-term labor. Evidence to support the role of tocolysis in preventing pre-term labor is scarce, but the thinking is that these properties are due to calcium antagonism by magnesium administration which can perhaps lead to a decrease, in intra-cellular calcium as well as in actin-myosin complex activity, leading to uterine muscle relaxation. Many studies have confirmed that magnesium can slow the rate of labor progression. Our patient developed a supra-therapeutic magnesium level of 11.5 mg/dl with signs of magnesium toxicity. In our case, magnesium toxicity can be one of the reason for arrest of labor which then lead to cesarean section and eventual uterine atony, for which patient had peripartum hysterectomy. It becomes prudent to identify early magnesium toxicity which relies on clinical suspicion by experienced medical personal to prevent life altering complications. Ultimately, a toxicity monitoring strategy should be chosen based upon a variety of logistic considerations and patient risk factors.
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