Pregnancy and thromboembolism

Venous thromboembolism (VTE) in pregnancy is more common and more complex to diagnose in patients with pregnancy than those individuals are not.

Incidence of venous thromboembolism 0.76-1.72 per 1000 pregnancies, four times greater than in non pregnant populations (Heit).

Venous thromboembolism is a leading cause of nonobstetric cause of maternal death in the US.

VTE is responsible for more than 9% of the maternal deaths in the US.

VTE incidence during hospitalization for vaginal delivery has increased to almost 30 per hundred thousand deliveries.

VTE risk increases 4-6 fold during pregnancy and is highest in the immediate postpartum period.

Two-thirds of cases of deep vein thrombosis occurs in the antepartum period.

Venous thromboembolism is increaed in pregnancy due to physiologic and anatomic changes including: hypercoagulability, progesterone induced venous stasis, decreased venous outflow, compression of the inferior vena cava and pelvic veins by the enlarged uterus and decreased mobility.

Pregnancy associated with hypercoagulability due to increaed levels of factor I, VII.VIII and X and von Willebrand factor, with decreased free protein S, acquired resistance to activated protein C, and decreased fibrinolysis due to increased levels of plasminogen activator inhibitor-1 and-2.

Risk factors that increase the risk for VTE during pregnancy include: prior history of estrogen related or unprovoked VTE, being a carrier of inherited thrombophilia,, having anti-thrombin, protein C, protein S deficiencies in the presence of antiphospholipid antibodies, progesterone induced venous stasis, compression of the inferior vena cava and pelvic  wins  due to an enlarged uterus, decreased mobility.

Women with SLE, diabetes, sickle cell anemia, and heart disease have a higher risk for VTE during pregnancy.

Other risk factors predisposing to thrombosis include black etnicity, smoking abuse, operative procedures, conception after assisted reproductive techniques, high body mass index, antepartum immobilization, severe pre-eclampsia, advanced age and parity and a family history of VTE.

Risk factors for thrombosis include: hospitalization, infection, hyperemesis, multiple pregnancies, preeclampsia, obesity, C-section, major postpartum hemorrhage, Intrauterine growth restriction, and fetal death.

The combination of more than one risk factors increases the risk for VTE in pregnancy.

Antepartum deep vein thrombosis occurs relatively equally in each of the trimesters of pregnancy.

Pulmonary embolism associated with pregnancy occurs in 43-60% of cases in the postpartum period (James).

An elevated risk of thrombosis persists until at least 12 weeks after delivery, and the absolute increase in risk beyond six weeks after delivery is, however, low (Kamel H et al).

As compared with the nonpregnant state the six weeks post partum period is associated with an increase of 3 to 9 times in the risk of stroke, 3 to 6 times the risk of myocardial infarction, and by a factor of 9-22 in the risk of venous thromboembolism.

The risk of VTE is greatest in the first 3 weeks postpartum among women with preeclampsia/eclampsia and in women who experience postpartum acute systemic infection in an evaluation of 168,077 women (Sultan AA et al).

Pulmonary embolism is the leading cause of maternal death in the developed world.

Deaths from pulmonary embolism 1.1-1.5 per 100,000 deliveries (Heit).

Delay in diagnosis, delayed or inadequate thromboprophylaxis account for many deaths.

Majority of deep vein thromboses during pregnancy occur in the left leg.

Occurs in the left leg in approximately 70-90% of cases in pregnancy, perhaps related to compressive effects in the left iliac vein being crossed by the right iliac artery.

Isolated deep vein thrombosis in the iliac vein occurs more often in pregnant than non pregnant women.

More than 70% of pregnancy associated DVTs are located in the ileofemoral region, as compared with 95 in nonpregnant patients.

Pregnancy associated with increases fibrin generation, impaired fibrinolysis activity, increased levels of coagulation factors II, VII, VIII and X, free protein s levels are decreased and acquired resistance to activated protein C is common.

Pregnancy accompanied by hemostatic activation with findings of increased fragment F1+2 and D-dimer.

A reduction in venous blood flow occurs in pregnancy with a 50% decrease in the legs by 25-29 weeks of gestation and lasts until approximately 6 weeks after delivery.

If inherited thrombophilias exist or the antiphospholipid syndrome is present, or a previous history of thrombosis is present the risk of venous thromboembolism in pregnancy and postpartum period increases.

Increased risk factors include the black race, heart disease, diabetes, systemic lupus erythromatosus, sickle cell disease, smoking abuse, multiple pregnancy age greater than 35 years, obesity and cesarean section.

Relation to age greater than 35 years, obesity and cesarean section contribute the most to increased risk because of their high prevalence.

Serial ultrasound may be necessary in pregnancy when there is a high clinical suspicion of DVT but negative initial investigation.

Pregnancy associated Doppler studies should include imaging of the iliac veins if there is a high suspicion of DVT, and the ultrasound of the leg is negative for femoral DVT.

Ileofemoral vein thrombosis accounts for approximately 90% of proximal thromboses in pregnancy, and occurs most often in the left lower extremity.

Ovarian vein thrombosis is rare, and occurs mostly in the postpartum period, mainly after Ceserean delivery, and usually affects the right ovarian vein.

In pregnancy, pulmonary embolism is more difficult to diagnose than DVT because clinical signs are unreliable in such patients.

The mortality untreated PE during pregnancy ranges from 18 to 38%, and so proximatelt 1/3 of patients with untreated thromboembolic disease recurrent embolism.

The prevalence of PE is between 1.4 and 4.2% is those with suspected clinical diagnosis of PE.

The main anticoagulants used in pregnancy are unfractionated heparin and low molecular weight heparin.
Owing  teratogenicity during the first trimester vitamin K antagonists are avoided.
Direct oral anticoagulants are not recommended in pregnancy due to potential crossing of the placenta.
Heparin and vitamin K antagonists are safe during lactation but direct oral anti-coagulants are not.

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