A 30-year-old woman, gravida 1, para 0, at 38 weeks gestation is admitted to the labor and… — USMLE Step 2 CK

A $30$ -year-old woman, gravida 1, para 0, at $38$ weeks gestation is admitted to the labor and delivery unit for induction of labor due to preeclampsia with severe features. She is receiving continuous intravenous infusions of oxytocin and magnesium sulfate. Maintenance intravenous fluids are running concurrently at $125\text{ mL/hr}$ . Approximately $12$ hours into her induction, she reports the sudden onset of severe shortness of breath, anxiety, and a cough productive of pink, frothy sputum.

Vital signs are:
- Temperature: $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ )
- Blood pressure: $152/100\text{ mmHg}$
- Heart rate: $118/\text{min}$
- Respiratory rate: $28/\text{min}$
- Oxygen saturation: $86\%$ on room air

Physical examination reveals prominent jugular venous distension and diffuse, bilateral crackles on lung auscultation. Deep tendon reflexes are $2+$ and symmetric bilaterally. Urine output has been $50\text{ mL}$ over the last $2$ hours. The fetal heart rate tracing demonstrates a baseline of $145/\text{min}$ with moderate variability and no decelerations. Supplemental oxygen is administered via a non-rebreather mask.

Which of the following is the most appropriate next step in management?

Administer intravenous furosemideAnswer
B
Administer intravenous calcium gluconate
C
Perform an emergent cesarean delivery
D
Administer intravenous labetalol
E
Administer a rapid intravenous fluid bolus

Answer

The most appropriate next step is to administer intravenous furosemide to treat the acute pulmonary edema.

This patient has developed acute pulmonary edema, a life-threatening complication of severe preeclampsia. The pathophysiology involves increased systemic vascular resistance, increased capillary permeability, and decreased plasma oncotic pressure, which is often exacerbated by intravenous fluid administration during labor induction. Her clinical presentation (hypoxia, pink frothy sputum, jugular venous distension, bilateral crackles, and tachypnea) is classic for fluid overload and alveolar fluid accumulation. The most appropriate immediate next step, in addition to the supplemental oxygen she is already receiving, is the administration of an intravenous loop diuretic such as furosemide to reduce intravascular volume and relieve the pulmonary congestion.

Step-by-Step Solution

Evaluate the patient's acute respiratory distress in the context of severe preeclampsia.

The presence of tachypnea, hypoxia, pink frothy sputum, jugular venous distension, and bilateral crackles indicates acute decompensated heart failure resulting in pulmonary edema.

Preeclampsia causes endothelial damage, increased capillary permeability, and increased systemic vascular resistance, making patients highly susceptible to pulmonary edema, particularly during fluid-heavy labor inductions.

Differentiate pulmonary edema from magnesium toxicity.

The patient has a respiratory rate of 28/min and 2+ deep tendon reflexes. Magnesium toxicity presents with respiratory depression (rate < 12/min) and absent reflexes.

Ruling out magnesium toxicity ensures that the correct antidote (calcium gluconate) is avoided and proper treatment is initiated.

Select the immediate therapeutic intervention.

Intravenous loop diuretics (furosemide) are indicated.

Furosemide provides rapid venodilation (decreasing preload) and diuresis (removing excess fluid), which directly addresses the life-threatening alveolar fluid accumulation.

Key Concept

Acute pulmonary edema is a severe complication of preeclampsia that presents with tachypnea, hypoxia, and crackles, requiring immediate management with supplemental oxygen and intravenous furosemide. It must be clinically distinguished from magnesium toxicity, which presents with respiratory depression and areflexia.

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