VTE is a major contributor to maternal morbidity and mortality in the United States.¹ The risk of VTE during pregnancy and the postpartum period is substantially increased compared to the nonpregnant state.² Deep venous thrombosis (DVT) accounts for approximately three-quarters of thromboembolic events in pregnancy, with pulmonary embolism cases being the remainder. As there is limited high-quality data on which to base the evaluation, treatment, and prevention of VTE in the obstetric population, recommendations are often extrapolated from the nonobstetric literature.

Physiologic changes in pregnancy, such as impaired venous return due to hormonal and structural factors, as well as an increase in procoagulant factors, amplify the propensity for VTE. Factors VII, VIII, X, and XII, as well as von Willebrand factor (VWF), are all increased, as is fibrinogen.³

The elevated risk for VTE begins in the first trimester, although the risk appears to be greatest in the postpartum period.⁴ One theory for the increased risk during the postpartum period is that endothelial damage (the third component of Virchow’s triad) occurs during delivery. While the first 6 weeks postpartum appears to confer the greatest risk, recent data suggests that a small increase in risk remains until 12 weeks after delivery.⁵

A personal history of previous VTE is the most significant risk factor for developing the condition in pregnancy. Approximately 15% to 25% of VTE cases in pregnancy are recurrent.⁶ The magnitude of risk for recurrent VTE during pregnancy depends on the circumstances surrounding the initial VTE and the presence of a thrombophilia. Aside from pregnancy, other notable risk factors that have been described include surgery (including cesarean delivery), prolonged immobility, air travel, obesity, age, smoking, and malignancy.

In addition, inherited or acquired thrombophilias are associated with varying degrees of risk for VTE. Those inherited thrombophilias that carry the greatest risk of developing VTE for patients are antithrombin III deficiency, homozygous Factor V Leiden or prothrombin gene mutations, or compound heterozygosity with both Factor V Leiden mutation and prothrombin gene mutation. Protein C and S deficiencies, as well as heterozygosity for Factor V Leiden or the prothrombin gene, confer a lesser degree of risk.

Symptoms of VTE are often nonspecific and may overlap with symptoms commonly encountered in a routine pregnancy, which is why a high index of suspicion is necessary when evaluating these patients. Symptoms of DVT may include edema, pain with ambulation, or potentially lower abdominal pain in the setting of more proximal clots. In addition to normal pregnancy symptoms, calf strain could cause symptoms similar to distal lower-extremity DVT. Abdominal pain has a fairly broad differential in pregnancy, but a possible proximal DVT should be considered. When compared to nonpregnant patients, DVT in pregnancy more commonly occurs in the left leg, and proximal DVT is more likely.⁷ One proposed reason for this is the compression by the gravid uterus of the left iliac vein where it crosses behind the right iliac artery.⁸

Patients with pulmonary embolism may report shortness of breath or chest pain. They may be noted to have tachypnea, tachycardia, or hypoxia. Significant alternative diagnoses that should also be considered, depending upon the presentation, are symptomatic anemia, peripartum cardiomyopathy, iatrogenic pulmonary edema, or amniotic fluid embolism.

Prevention of VTE involves identifying those subgroups at the highest risk for VTE, as described earlier. In the nonobstetric literature, recommendations for how to prevent VTE involve weighing the risks of bleeding with the risks of VTE in individual patients;⁹ it is logical to take a similar approach during pregnancy.

There is considerable ambiguity regarding which patients are appropriate candidates to receive anticoagulation for the prevention of VTE. Furthermore, different regimens for prevention of VTE have not been rigorously evaluated to determine the optimal dose. The care of antepartum patients is complicated by the uncertainty of when and how delivery may occur. Thus the decision regarding the administration of pharmacologic prophylaxis needs to be individualized. One multicenter study did not show a reduction in VTE events with prophylactic anticoagulation, but the study population was mixed and included patients receiving anticoagulation because of a history of pregnancy complications who may have had a lower risk for VTE than those patients on anticoagulation for a history of a prior VTE event.¹⁰

Current guidelines from the American College of Chest Physicians (ACCP) and the American Congress of Obstetrics and Gynecology (ACOG) do not recommend universal administration of pharmacologic prophylaxis to reduce the risk of VTE after C-section delivery.^6,11 ACOG suggests the use of intermittent pneumatic compression devices for low risk patients undergoing C-section is sufficient; the data regarding the merit of this intervention is limited to decision analyses and cost-effectiveness studies. The ACCP does not recommend anything beyond early ambulation for the low-risk patient.

While there are theoretical concerns about risk of bleeding complications with the use of thromboprophylaxis after cesarean delivery, existing data suggest this risk is relatively low.^12,13 Women who undergo cesarean delivery and have additional factors that increase their risk for VTE should receive thromboprophylaxis postpartum, ideally with low-molecular-weight heparin (LMWH); alternatively, in those in whom the bleeding risk associated with anticoagulation is too great, mechanical prophylaxis should be employed.¹¹

Table 49-1 summarizes the ACOG recommendations for thromboprophylaxis during pregnancy; for many situations, there is a fair amount of latitude in selecting a management plan. Take, for example, a patient who has previously had a VTE while on oral contraceptives. She is not on lifelong anticoagulation and her thrombophilia testing is negative, but her prior VTE would be considered estrogen-related. Thus the recommendation would be for her to be on prophylactic anticoagulation during pregnancy and postpartum. The ACCP recommendations are generally similar to these, although management is further stratified based upon family history.

As is always the case, patients should first be evaluated for hemodynamic and respiratory stability. Oxygen saturation should be determined and supplemental oxygen used as needed to maintain a level of 92% or greater.

Most clinical prediction tools for VTE, such as the Wells rule,¹⁴ have not been rigorously validated in pregnant women. A difference in calf circumference of ≥2 cm is suggestive of lower-extremity DVT. Compression ultrasonography is the initial diagnostic test of choice for DVT because it is noninvasive and involves no radiation exposure. Notably, a greater percentage of DVTs diagnosed in pregnancy are proximal than outside of pregnancy.¹⁵ If the results are negative or equivocal, but there is high clinical suspicion for DVT, then magnetic resonance imaging (MRI) should be considered; alternatively, surveillance with serial Doppler ultrasonography can be performed.

Electrocardiogram (ECG) and chest x-ray are of limited utility in the diagnosis of pulmonary embolism, as they are often normal or have nonspecific (e.g. sinus tachycardia) findings. While D-dimer levels are useful in the nonpregnant population, this acute phase reactant physiologically increases during pregnancy, making its utility in excluding VTE more limited, as mean levels in normal pregnancy, particularly in the third trimester, exceed the thresholds for excluded VTE in nonpregnant populations.