A 32-year-old G2P1 at 35 weeks gestation is hospitalized for preeclampsia with severe feat… — USMLE Step 2 CK

A $32$ -year-old G2P1 at $35$ weeks gestation is hospitalized for preeclampsia with severe features. She is receiving continuous intravenous magnesium sulfate and oxytocin for labor induction. Over the past $4$ hours, her total urine output has been $45$ mL. She now reports profound weakness and blurry vision. Her blood pressure is $155/95$ mmHg, and heart rate is $88$ /min. Her respiratory rate is $10$ /min, and oxygen saturation is $91\%$ on room air. Neurologic examination reveals no muscle contraction upon percussion of the patellar tendons. Fetal heart rate monitoring demonstrates a baseline of $130$ /min, minimal variability, and recurrent late decelerations with $60\%$ of contractions.

Arterial blood gas (room air):
pH: $7.29$
pCO $_2$ : $54$ mmHg
pO $_2$ : $62$ mmHg
HCO $_3^-$ : $25$ mEq/L

Serum chemistry from $1$ hour ago:
Creatinine: $1.5$ mg/dL (baseline $0.7$ mg/dL)

What is the most appropriate next step in management?

Intravenous calcium gluconate administrationAnswer
B
Emergent cesarean delivery
C
Intravenous fluid bolus and maternal repositioning
D
Intravenous furosemide administration
E
Observation, as arterial blood gas findings are physiologic

Answer

The correct answer is intravenous calcium gluconate administration.

The correct answer is intravenous calcium gluconate administration. This patient is exhibiting classic signs of severe magnesium toxicity, including areflexia, profound weakness, and hypoventilation leading to respiratory acidosis. Magnesium is cleared exclusively by the kidneys; her oliguria and renal insufficiency have led to toxic drug accumulation. Her respiratory failure has caused maternal hypoxemia, which is the direct cause of the fetal hypoxia (evidenced by minimal variability and late decelerations). The immediate life-saving intervention is to discontinue the magnesium infusion and administer intravenous calcium gluconate, which directly antagonizes the neuromuscular blockade, restores maternal respiratory drive, and thereby improves fetal oxygenation.

Step-by-Step Solution

Evaluate the maternal clinical presentation and laboratory findings.

The patient has oliguria, an elevated creatinine level, areflexia, and profound weakness.

Oliguria and renal insufficiency impair the excretion of magnesium, leading to toxic serum levels which present initially as loss of deep tendon reflexes.

Analyze the maternal respiratory status and arterial blood gas.

The patient has a respiratory rate of 10/min and uncompensated respiratory acidosis (pH 7.29, pCO2 54 mmHg).

Magnesium toxicity causes progressive neuromuscular blockade, leading to hypoventilation, hypercapnia, and hypoxemia. This contrasts sharply with the normal physiologic respiratory alkalosis of pregnancy.

Interpret the fetal heart rate tracing in the context of the maternal condition.

The tracing shows late decelerations and minimal variability, indicating fetal hypoxia.

The fetus is hypoxic because the mother is hypoventilating and hypoxic (pO2 62 mmHg). The primary issue is maternal respiratory failure, not primary placental dysfunction.

Determine the prioritized next step in management.

Discontinue magnesium sulfate and administer intravenous calcium gluconate.

Maternal resuscitation is the absolute priority. Reversing the magnesium toxicity with its direct antidote (calcium gluconate) will restore maternal respiratory drive, correct the maternal hypoxemia, and consequently resolve the fetal hypoxia.

Key Concept

Maternal magnesium toxicity can cause life-threatening respiratory depression that secondarily leads to fetal hypoxia; administration of intravenous calcium gluconate to stabilize the mother must precede any operative intervention for fetal distress.

Estimated Time:1m 30s

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