Accounting for 20% to 30% of maternal deaths, pulmonary embolism ranks as the most frequent cause of maternal death in developed countries. Its incidence during pregnancy is 5 to 10 times that of the general population. Originating mostly from the venous system of the lower extremities, undiagnosed or untreated thrombosis can embolize through the heart into the pulmonary vasculature, leading to right-sided heart failure, hypoxemia, and vascular collapse. The early presentation of this disease may be obscured by common symptoms and signs attributable to pregnancy or to the early puerperium, necessitating diagnostic consideration of this entity throughout gestation.
Case 1: Thromboembolism
A 23-year-old nulliparous patient at 31 weeks’ gestation presented with contractions and pelvic pressure for 2 days. Her past medical history included asthma that was well controlled on a low-dose corticosteroid inhaler and obesity (body mass index 40 kg/m 2 ). On physical examination her weight was 278 lb, temperature 98° F, pulse 87 beats per minute (bpm), respiratory rate 12 breaths/min, and blood pressure 130/78 mm Hg. Generally she appeared anxious and in moderate distress during uterine contractions. Cardiovascular and pulmonary findings were unremarkable. Her abdomen was obese, nontender and the cervical examination revealed 3 cm dilation and 1.5 cm in length, and the presenting part was at –3 station. The fetal heart rate was reactive and uterine contractions occurred at 3-minute intervals.
The patient was admitted to labor and delivery, a urinary catheter was placed, IV fluids were administered along with IM betamethasone and IV magnesium sulfate. Rapid testing for group B β–hemolytic streptococci was sent and later reported as negative. Over the next 24 hours the contractions abated despite cervical dilation progressing to 4 cm. She was transferred to the antepartum unit 36 hours after betamethasone therapy and remained on bed rest with allowance to use the bathroom. On hospital day 4, uterine contractions returned and the patient was transferred to labor and delivery, where labor ensued. A vigorous female infant was delivered spontaneously and the patient was transferred to the postpartum unit 6 hours after delivery.
On day 5 of the hospitalization, she reported having chest tightness and difficulty breathing over the past 2 hours. The patient felt this was likely to be an “asthma attack.” Examination revealed an alert, anxious patient in moderate respiratory distress. Vital signs indicated temperature 98.8° F, pulse 117 bpm, respiratory rate 20 breaths/min, and blood pressure 140/82 mm Hg. Bilateral breath sounds were heard without wheezes, and tachycardia was noted on cardiac auscultation with no murmurs. Extremities revealed 2+ pedal edema bilaterally and the abdominal examination was benign. Reassurance was provided and a short-acting β–agonist inhaler was prescribed. A helical computed axial tomographic scan was ordered to “cover all the bases.”
Fours hours after receiving the inhalation treatment, the physician was called because of increased respiratory effort. Vital signs revealed temperature 98.7° F, pulse 132 bpm, respiratory rate 26 breaths/min, and blood pressure 80/30 mm Hg. One liter of normal saline was administered and repeat blood pressure was 92/48 mm Hg. A computed tomographic (CT) scan had not been performed at this time. IV heparin was administered and dosed on a weight-based nomogram. The patient was transferred to the intensive care unit (ICU), where on arrival she became obtunded and progressively hypotensive. She went into a pulseless tachycardic rhythm and respiratory arrest. Advanced cardiac life support was initiated including chest compressions, endotracheal intubation, and the administration of epinephrine and fluid boluses. A femoral venous catheter was inserted during the resuscitative efforts and multiple doses of epinephrine were given as well as vasopressin. The rhythm deteriorated into asystole and external pacing was attempted. After a total of 41 minutes of circulatory collapse and unsuccessful resuscitative efforts, the patient was pronounced deceased.
Discussion
Notably, the patient had numerous risk factors for having a thromboembolic event: obesity, pregnancy, hospitalization with limited ambulatory activity, pregnancy and delivery. Consideration should have been given to thromboembolic prophylaxis using a sequential compression device and thromboembolic deterrent stockings throughout her admission. For patients at high risk for thromboembolism, with multiple risk factors (including two of the following: age >35 years, obesity, medical illness, cesarean section, infection, immobility, or gross varicosities) heparin prophylaxis should be considered as well. In patients who have had a prior thromboembolism or thrombophilia, prophylactic heparin should be considered. For the patient described, clinical indicators suggesting a pulmonary embolism occurred early in her course. Anticoagulation should not have been withheld pending the results of thoracic imaging. Had a pulmonary embolism not been confirmed, further anticoagulation could have been discontinued.
Pathophysiology and Risk Factors
The pathophysiology of a pulmonary embolism begins with the hypercoagulable state induced in the gravida: increased clotting factors, decreased fibrinolysis, platelet activation, and venous stasis. A reduction in venous flow in the lower extremities is not uncommon beginning in the late second trimester and lasting until several weeks postdelivery. Risk factors for thromboembolic disease are widely known and are listed in Table 6-1 . A preponderance of lower extremity deep venous thromboses occurs on the left side due to compression of the left iliac vein by the right iliac artery as shown in the schematic in Figure 6-1 .
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Fifteen percent of untreated deep venous thrombi embolize to the lungs causing death in 15% of patients. Once an embolism occurs, vasoactive substances are released into the pulmonary vasculature causing bronchoconstriction and vasoconstriction ( Fig. 6-2 ). Further, the mechanical obstructive effects of the clot produce right ventricular failure. Right ventricular dysfunction has been described in this setting using echocardiography with evidence of ventricular dilatation, free-wall hypokinesia or paradoxical movement, a 30 mm Hg pressure gradient between the right ventricular and right atrial chambers, or a decreased pulmonary flow acceleration time. Sometimes a clot can be visualized within the right side of the heart (atrium, ventricle, or pulmonary artery), as well as visualized sonographically protruding through a patent foramen ovale. In severe cases, cardiac output is not able to be sustained and cardiopulmonary arrest occurs.
