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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