Chapter 30: Deep Venous Thrombosis and Pulmonary Embolism

INTRODUCTION

Pregnancy is a hypercoagulable state secondary to blood stasis in the lower extremities, increased liver production of clotting factors, decreased fibrinolysis, and endothelial injury mostly at the time of delivery.¹ The risk of deep venous thrombosis (DVT) and pulmonary embolism (PE) is five to six times higher than the nonpregnant population. Thromboembolic disease constitutes the most common cause of maternal mortality in developed nations.¹ The risk of developing a thromboembolic complication is highest during the postpartum period. Particularly, the risk for PE is most pronounced in the postpartum.

CLINICAL PRESENTATION

The clinical presentation of DVT and PE during pregnancy is essentially the same as outside pregnancy. Importantly, many physiological symptoms of pregnancy resemble the clinical presentation of these conditions including physiologic dyspnea of pregnancy and bilateral leg swelling. The astute clinician should individualize each case presentation and decide based on the preclinical probability if further workup is needed. The vast majority of DVT cases during pregnancy (up to 80%) affect the left lower extremity secondary to decreased venous return as the result of compression of the right iliac artery over the left iliac vein as the latter crosses to drain into the inferior vena cava (similar pathophysiology as that seen in the May Thurner Syndrome).²

DVT is characterized by unilateral swelling of the affected extremity and pain. Pain may be elicited by flexion of the foot (Homan’s sign) and palpation of the calf muscles (Pratt sign). PE is characterized by a sudden onset of chest pain and shortness of breath. In addition, patients may present with tachypnea with resultant respiratory alkalosis, tachycardia, and rarely with hypotension and hemodynamic instability due to acute right ventricular failure. The latter leads to acute right ventricular dilation with leftward displacement of the interventricular septum resulting in obliteration of the left ventricular cavity and consequently impaired cardiac output and hemodynamic shock. The acute dilation of the right ventricle compresses the ventricular wall with coronary compression increasing also the risk of an acute right ventricular infarct. The latter two mechanisms explain the hemodynamic compromise seen in cases of massive PE. Hypoxemia may also be present but normal oxygenation does not rule out the possibility of a PE.

DIAGNOSIS

Clinical suspicion of DVT or PE must be confirmed with imaging studies. When suspicion exists for a DVT in the lower extremities, ultrasound Doppler is the initial test of choice. If the initial ultrasound is negative, serial further imaging at days 3 and 7 is recommended. Alternatively, the use of a sensitive D-dimer assay may be considered. If the assay is negative, no further workup is required. If the assay is positive, repeat imaging at days 3 and 7 is recommended.³ Elevated levels of D-dimer are physiologic during pregnancy and should not by themselves trigger extensive diagnostic workups.⁴ However, a negative D-dimer during pregnancy has ...