09/10/2026

68-year-old woman with paresthesias and cramping

A 68-year-old woman is evaluated in the emergency department for a 3-day history of tingling around her mouth and in her fingertips. This morning, her hand cramped painfully while her daughter was using a home blood pressure cuff. Her history is notable for GERD managed with omeprazole for the past 10 years. She recently recovered from a 4-day bout of watery diarrhea after a family picnic. In the ED, she was given 1 gram of intravenous calcium gluconate with transient improvement; her symptoms have now returned. Temperature is 37.1°C (98.8°F), blood pressure is 134/82 mm Hg, pulse is 88/min, and respirations are 16/min. She is alert and anxious. Neurologic examination is nonfocal. An ECG shows a corrected QT interval of 510 ms. Laboratory studies show: Sodium: 138 mEq/L Potassium: 3.4 mEq/L Chloride: 99 mEq/L Bicarbonate: 26 mEq/L BUN: 24 mg/dL Creatinine: 1.1 mg/dL Calcium, total: 6.7 mg/dL Albumin: 3.8 g/dL Magnesium: 0.7 mg/dL Which of the following is the most appropriate next step in management?

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The Correct Answer

A


Explanation

Clinical Pearl:
Severe hypomagnesemia causes functional hypoparathyroidism by impairing parathyroid hormone (PTH) secretion and inducing end-organ resistance to PTH action. The resulting hypocalcemia is often refractory to calcium repletion until the magnesium deficit is corrected.


Explanation:
This patient presents with symptomatic hypocalcemia (perioral paresthesias, Trousseau sign, prolonged QTc) in the setting of severe hypomagnesemia. The long-term use of a proton pump inhibitor and recent diarrheal illness are risk factors for magnesium depletion. This clinical picture indicates hypomagnesemia-induced hypocalcemia. The most appropriate next step is to administer intravenous magnesium sulfate. Correcting the severe magnesium deficiency is essential, as it restores parathyroid hormone secretion and sensitivity, allowing for normalization of the serum calcium. Administering a continuous infusion of calcium gluconate without addressing the magnesium deficit will likely be ineffective, as suggested by the patient's transient response to an initial bolus. Measuring the intact parathyroid hormone level is a diagnostic step that should not delay urgent management of a symptomatic electrolyte emergency. Oral calcium and vitamin D are not appropriate for acute, symptomatic hypocalcemia due to their slow onset of action. While mild hypokalemia is present, the patient's life-threatening symptoms are due to hypocalcemia, making magnesium repletion the immediate priority over administering intravenous potassium.

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