A 21-year-old woman, gravida 1 para 0, at 36 weeks gestation comes to the labor and delivery unit for a blood pressure of 190/110 mm Hg in the office. On arrival, her blood pressure is 184/106 mm Hg. Initial laboratory results show elevated serum creatinine and transaminases. Urinalysis shows 4+ proteinuria. Nifedipine and magnesium sulfate are administered. Induction of labor is started with oxytocin. Six hours later, the patient's blood pressure is 150/90 mm Hg. Laboratory results are as follows: Which of the following is the most likely cause of this patient's hypermagnesemia?

Question

A 21-year-old woman, gravida 1 para 0, at 36 weeks gestation comes to the labor and delivery unit for a blood pressure of 190/110 mm Hg in the office.  On arrival, her blood pressure is 184/106 mm Hg.  Initial laboratory results show elevated serum creatinine and transaminases.  Urinalysis shows 4+ proteinuria.  Nifedipine and magnesium sulfate are administered.  Induction of labor is started with oxytocin.  Six hours later, the patient's blood pressure is 150/90 mm Hg.  Laboratory results are as follows:  Which of the following is the most likely cause of this patient's hypermagnesemia?

Quizplus · Accepted Answer

11ec25c8_da6a_c560_bc81_f94b2bcb72fb_MD0003_00 Magnesium sulfate is the treatment of choice for the prevention of eclamptic seizures. It is also administered to patients for whom preterm delivery is imminent because it decreases the risk for cerebral palsy in premature infants (ie, fetal neuroprotection at <32 weeks gestation). Common adverse effects include headache, nausea, fatigue, and diaphoresis. Signs of magnesium toxicity include loss of deep tendon reflexes, somnolence, and respiratory depression. Because magnesium is primarily excreted by the kidneys, a common risk factor for toxicity is renal insufficiency (ie, elevated serum creatinine), as seen in this patient. Patients with known renal insufficiency or suspected toxicity require monitoring of serum magnesium levels and adjustments in magnesium infusion rates (ie, lowered). Calcium gluconate is the first-line treatment for toxicity. (Choice A) Antihypertensive therapy is indicated for severe hypertension (eg, ≥160/110 mm Hg), and concomitant use of calcium channel blockers (eg, nifedipine) and magnesium can potentiate hypotension. However, this patient is hypertensive. (Choice B) Although this patient's transaminase elevation indicates hepatic damage from preeclampsia, the liver is not involved in magnesium excretion. (Choice C) Hypocalcemia is a potential adverse effect, rather than a cause, of hypermagnesemia because moderate hypermagnesemia can cause temporary suppression of parathyroid hormone secretion. Calcium levels typically normalize after stopping magnesium sulfate therapy. (Choice D) Oxytocin can enhance antidiuretic hormone release and cause the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Patients with SIADH have hyponatremia, not hypermagnesemia. Educational objective: Magnesium sulfate is commonly administered for eclamptic seizure prevention and fetal neuroprotection. All patients on magnesium should be monitored for signs of toxicity (eg, somnolence, areflexia, respiratory suppression). Because magnesium is excreted primarily by the kidneys, patients with renal insufficiency are at increased risk for toxicity. References: An integrative review of the side effects related to the use of magnesium sulfate for pre-eclampsia and eclampsia management. (http://www.ncbi.nlm.nih.gov/pubmed/23383864) Magnesium sulfate: past, present, and future. (http://www.ncbi.nlm.nih.gov/pubmed/22060216)

A 21-Year-Old Woman, Gravida 1 Para 0, at 36 Weeks