Saturday, 25 July 2020

Venous throboembolism


For DNB/MD Candidates:- Thromboembolic disease is linked with both adverse maternal and fetal/neonatal out­comes. The term venous thromboembolism (VTE) encompasses deep vein throm­bosis (DVT) and pulmonary embolism (PE).Pregnant women are four to five times more likely to experience a VTE than age- matched nonpregnant women. Incidence of VTE ranges from 0.76 to 2.0 episodes per 1,000 pregnancies. VTEs account for 9% of all maternal deaths in the United States. Approximately 80% of VTEs in pregnancy are DVT and 20% are PE.
Approximately half of all VTEs occur in the antepartum period and appear to be evenly divided among the three trimesters. PE  occurs more frequently postpartum. Cesarean delivery imparts a three to five times greater risk than a vaginal delivery.
Pregnancy ?  Ans: These are  hypercoagulable state sue mainly to increase of A) Fibrinogen, B)  coagulation factors, and C) plasminogen activator inhibitor-1 (PA1-1) levels. Associated with decrese of  free protein S levels and fibrinolytic activity. Additionally, VTE risk is increased by anatomic changes in pregnancy including increased venous stasis and compression of the inferior vena cava and pelvic veins by the enlarging uterus.
One of the most significant risk factors is a personal history of VTE. Maternal medical conditions including 1)  heart disease, 2)  SCD,3)  lupus, 4) obesity, 5) diabetes, and 6)  hypertension increase risk. Other risk (actors include 7) recent surgery, 8) family history of VTE, 9) bed rest or prolonged immobilization,  10) smoking, 11) age older than 35 years, 12) multiple gestations, 13) preeclampsia, and 14) postpartum infection.
Thrombophilias may be inherited or acquired.
Pregnancy may trigger an event in women with an underlying thrombophilia.
Fetal death in utero, severe IUGR, abruption, and severe early-onset preeclampsia have been correlated with underlying thrombophilias that affect uteroplacental circulation; however, this is controversial and recent studies fail to reliably estab­lish causal links between thrombophilias and these adverse pregnancy outcomes.
Inherited thrombophilias
A)                  Increase the risk of prior maternal thromboembolic event approximately eightfold. This history is present in over half of all maternal thrombotic events.
B)                  Antithrombin deficiency and homozygosity for factor V Leiden mutation are the most potent of the inherited thrombophilias. Double or compound het­erozygotes (for both factor V Leiden and prothrombin G20219A) are also at greater risk of VTE.
Acquired thrombophilias:
Include persistent antiphospholipid antibody syndromes (APS) (lupus antico­agulants or anticardiolipin antibodies). APS is present in 15% to 17% of women with recurrent pregnancy loss.
Routine screening for thrombophilias is not recommended in all pregnant women and screening indications are controversial. ACOG no longer recommends thrombophilia testing in women with recurrent fetal loss, placental abruption, IUGR, or preeclampsia. A thrombophilia workup should be consid­ered for the following:
 VTE during pregnancy (workup after delivery) or VTE associated with a non­recurrent risk factor such as prolonged immobilization.

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