The patient is admitted to the hospital, and an intravenous line and urinary catheter are placed. She receives corticosteroids to accelerate fetal lung maturity and magnesium sulfate for fetal neuroprotection. Three hours later, the patient develops dyspnea and has a drop in arterial oxygen saturation. Temperature is 36.7 C (98.1 F), blood pressure is 150/80 mm Hg, pulse is 112/min, and respirations are 24/min. Pulse oximetry is 91% on room air. Examination shows bibasilar crackles and use of accessory muscles for breathing. Heart sounds are tachycardic and without murmur. There is 3+ pitting edema of the lower extremities, and deep tendon reflexes are 2+ bilaterally. The remainder of the examination is normal. Urine output is 60 mL/hr. What is the most likely cause of this patient's respiratory symptoms?

Question

The patient is admitted to the hospital, and an intravenous line and urinary catheter are placed.  She receives corticosteroids to accelerate fetal lung maturity and magnesium sulfate for fetal neuroprotection.  Three hours later, the patient develops dyspnea and has a drop in arterial oxygen saturation.  Temperature is 36.7 C (98.1 F), blood pressure is 150/80 mm Hg, pulse is 112/min, and respirations are 24/min.  Pulse oximetry is 91% on room air.  Examination shows bibasilar crackles and use of accessory muscles for breathing.  Heart sounds are tachycardic and without murmur.  There is 3+ pitting edema of the lower extremities, and deep tendon reflexes are 2+ bilaterally.  The remainder of the examination is normal.  Urine output is 60 mL/hr.  What is the most likely cause of this patient's respiratory symptoms?

Quizplus · Accepted Answer

11ec25c8_da6d_3667_bc81_0bcf07d08fa2_MD0003_00 This patient's dyspnea, hypoxia, and bibasilar crackles on examination are most likely due to acute pulmonary edema, a life-threatening complication of preeclampsia with severe features. Patients with preeclampsia typically have generalized arterial vasospasm, leading to increased systemic vascular resistance and high cardiac afterload. In response, the heart becomes hyperdynamic to attempt to overcome the systemic hypertension. This causes increased pulmonary capillary pressure, which drives fluid from the capillaries into the interstitium. Preeclampsia with severe features predisposes to acute pulmonary edema because it causes endothelial damage, leading to increased capillary permeability. This increased permeability promotes decreased serum albumin levels and decreased capillary oncotic pressure that enables third spacing (eg, peripheral pitting edema). In addition, normal diuresis is impeded due to decreased renal function. Management includes supplemental oxygen, fluid restriction, and diuretic medications in severe cases. Fluid restriction and diuretic medications are used with caution because patients have overall decreased plasma volume (due to third spacing) and aggressive treatment may compromise placental perfusion and fetal wellbeing. (Choice A) Amniotic fluid embolism, caused by amniotic fluid entering the maternal circulation, can cause sudden hypoxemic respiratory failure. However, patients typically develop circulatory collapse with severe hypotension, making this diagnosis less likely. (Choice B) Bronchospasm may cause dyspnea and hypoxemia, but it usually causes wheezing instead of bibasilar crackles. (Choice C) Excessive magnesium sulfate can cause neuromuscular depression, resulting in decreased respiratory effort/apnea, muscle paralysis, and somnolence. Unlike this patient, those with magnesium sulfate toxicity typically have decreased deep tendon reflexes and decreased respiratory effort. (Choice D) Peripartum cardiomyopathy can cause left ventricular failure and acute pulmonary edema with bibasilar lung crackles. However, patients typically have an S3 and murmur (ie, mitral regurgitation) and elevated jugular venous pressure. (Choice F) The risk for pulmonary embolus is increased peripartum due to the prothrombotic effects of estrogen. Although pulmonary embolism can cause tachycardia, tachypnea, and hypoxia, it does not typically cause acute bibasilar crackles and is not usually associated with pitting edema. Educational objective: Pulmonary edema is a life-threatening complication of preeclampsia with severe features. It is caused by increased systemic vascular resistance, capillary permeability, and pulmonary capillary hydrostatic pressure in addition to decreased serum albumin levels. References: Acute pulmonary edema in an obstetric intensive care unit: a case series study. (http://www.ncbi.nlm.nih.gov/pubmed/29995818) 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)

The Patient Is Admitted to the Hospital, and an Intravenous