A 22-year-old woman with type 1 diabetes mellitus is evaluated in the labor and delivery department due to drowsiness. The patient is somnolent but rouses to sternal rub. An hour ago, the patient underwent a cesarean delivery after a failed induction of labor for preeclampsia with severe features. Her delivery was complicated by postpartum hemorrhage with an estimated blood loss of 2,000 mL due to a torn uterine artery. She is currently receiving a magnesium sulfate infusion and a basal-bolus insulin regimen. Temperature is 99.7 F (37.6 C), blood pressure is 148/96 mm Hg, pulse is 70, and respirations are 10/min. The lungs are clear to auscultation bilaterally. Abdominal examination shows a firm uterus with normal tenderness to palpation. The Pfannenstiel incision is intact and has minimal bleeding. The patellar reflexes are absent bilaterally. There is minimal, dark urine in the Foley catheter. Fingerstick blood glucose level is 240 mg/dL. Which of the following is the most likely cause of this patient's symptoms?
Magnesium toxicity | |
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Treatment |
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Patients with preeclampsia with severe features are administered magnesium sulfate to prevent eclamptic seizures because magnesium acts as a calcium channel blocker on the CNS, thereby raising the seizure threshold. Therapeutic serum magnesium levels (ie, 4.8-8.4 mEq/L), which are 2-4 times higher than normal concentrations, are required to prevent eclampsia. Normally, this therapeutic range is maintained between the balance of magnesium sulfate infusion and renal excretion of magnesium. However, in patients with abnormal renal function—as evidenced by either an elevated creatinine level or decreased urine output (as in this patient with minimal, dark urine)—magnesium can be retained and increase to toxic levels.
High levels of magnesium inhibit presynaptic acetylcholine release, thereby causing neuromuscular inhibition. Therefore, the first sign of magnesium sulfate toxicity is often hyporeflexia. As magnesium levels increase, patients can develop areflexia (eg, loss of patellar reflexes) and respiratory depression (eg, drowsiness, respirations ≤12/min). If untreated, patients are at risk for respiratory paralysis and cardiac arrest. Treatment is immediate cessation of magnesium sulfate and administration of calcium gluconate.
(Choice A) Acute blood loss anemia (eg, postpartum hemorrhage) may present with drowsiness due to hypoxia and decreased urine output due to hypovolemia. However, these patients typically have tachycardia, tachypnea, and hypotension, which are not seen in this patient. In addition, anemia does not cause absent patellar reflexes.
(Choice B) Amniotic fluid embolism (AFE) is an obstetric emergency that causes sudden cardiopulmonary collapse and possible disseminated intravascular coagulopathy. In contrast to this patient, those with an AFE have an abnormal lung examination (eg, bilateral crackles) and tachypnea, rather than respiratory depression. In addition, there is no associated areflexia.
(Choice C) Diabetic ketoacidosis (DKA) can cause neurologic changes (eg, somnolence), but it typically occurs when hyperglycemia is severe (eg, >350 mg/dL). In contrast to this patient, DKA usually causes tachypnea and increased urine output.
(Choice D) Patients with preeclampsia are at increased risk for eclamptic seizure, and an eclamptic postictal state can present with drowsiness. However, affected patients typically have hyperreflexia (eg, clonus) rather than areflexia.
Educational objective:
Patients with magnesium sulfate toxicity typically have absent patellar reflexes and respiratory depression; toxicity can progress to respiratory paralysis and cardiac arrest. Treatment is cessation of magnesium sulfate and administration of calcium gluconate.