Hypercoagulability in pregnancy is the tendency of pregnant women to develop thrombosis (blood clotting). Pregnancy itself is a factor of hypercoagulability (pregnancy induced hypercoagulability), as a mechanism of physiological adaptation to prevent postpartum hemorrhage. However, when combined with an additional underlying hypercoagulation state, the risk of thrombosis or embolism may be substantial.
Video Hypercoagulability in pregnancy
Cause
Hypercoagulability induced by pregnancy may be a physiological adaptation mechanism to prevent postpartum hemorrhage. Pregnancy alters the plasma levels of many clotting factors, such as fibrinogen, which can rise up to three times its normal value. Thrombin level increases. Protein S, anticoagulant, decreases. However, other major anticoagulants, protein C and antithrombin III, remain constant. Fibrinolysis is impaired by increased inhibitor plasminogen inhibitor-1 (PAI-1 or PAI) and plasminogen activator inhibitor-2 (PAI-2), the latter synthesized from the placenta. Venous stasis may occur at the end of the first trimester, due to increased vascular wall adherence by hormonal effects.
In addition, pregnancy can cause hypercoagulability by other factors, eg. frequent bed rest that occurs in post-partum cases occurring in cases of labor with forceps, vacuum extractor or caesarean section. A study of more than 200,000 women came to the outcome that admission to hospitalization during pregnancy was associated with an 18-fold increase in risk of venous thromboembolism (VTE) during stay, and a 6-fold increase in risk at four weeks after return, compared with women pregnant women who do not require hospitalization. The study included women hospitalized for one or more days for reasons other than delivery or venous thromboembolism.
Pregnancy after age 35 increases the risk of VTE, as do multiple multigravidities over four pregnancies.
Pregnancy itself causes about five times the increased risk of deep vein thrombosis. Some pregnancy complications, such as preeclampsia, lead to substantial hypercoagulability.
Hypercoagulability conditions as pre-existing conditions in pregnancy include those obtained, such as antiphospholipid antibodies, and congenital ones, including V Leiden factor, prothrombin mutation, protein C and S deficiency, and antithrombin III deficiency.
Maps Hypercoagulability in pregnancy
Complications
Hypercoagulability in pregnancy, mainly due to inherited thrombophilia, can cause placental vascular thrombosis. This in turn can lead to complications such as premature hypertensive disorder of pregnancy, pre-eclampsia and minor for infant gestational age (SGA). Among other causes of hypercoagulability, the antiphospholipid syndrome has been associated with adverse pregnancy outcomes including recurrent miscarriage. Deep venous thrombosis has one in every 1,000 to 2,000 pregnancies in the United States, and is the second leading cause of maternal death in developed countries after bleeding.
Prevention of thrombosis with anticoagulants
Unfractionated heparin, low molecular weight heparin, warfarin (not used during pregnancy) and aspirin remain the basis of antithrombotic and prophylactic treatment both before and during pregnancy.
While consensus among physicians is maternal safety in place of developing fetal safety, changes in anticoagulation regimens during pregnancy can be done to minimize the risk to developing fetus while maintaining anticoagulant levels in the mother.
A major problem with anticoagulation in pregnancy is that warfarin, the most commonly used anticoagulant in chronic administration, is known to have a teratogenic effect on the fetus if given early in pregnancy. However, there appears to be no teratogenic effect of warfarin before six weeks of pregnancy. However, unfractionated heparin and low molecular weight heparin do not cross the placenta.
Indication
In general, the indications for anticoagulants during pregnancy are similar to the general population. These include (but are not limited to) new history of deep venous thrombosis (DVT) or pulmonary embolism, metal prosthetic heart valves, and atrial fibrillation in the regulation of structural heart disease.
In addition to these indications, anticoagulation may be beneficial in individuals with lupus erythematosus, individuals with a history of DVT or PE associated with previous pregnancies, and even with individuals with a history of COPD and DVT-related deficiency not previously associated. pregnancy
In pregnant women with a history of recurrent miscarriage, anticoagulation appears to increase the level of live birth among them with antiphospholipid syndrome and possibly those with congenital thrombofilia but not those with unexplained miscarriage.
Strategy
A consensus about the correct anticoagulation regimen during pregnancy is lacking. Treatment is tailored to specific individuals based on the risk of complications. Warfarin and other vitamin K inhibitors are contraindicated during the first trimester of pregnancy due to teratogenic effects, and should not be given when the pregnancy is confirmed. In contrast, women who are on chronic anticoagulation may be given the option of converting either unfractionated heparin or low molecular weight heparin (LMWH), such as tinzaparin, before the planned conception. LMWH is safe and efficacious as unfractionated heparin. Blood tests including platelets and freezing screens should be performed before anticoagulant regimens in pregnancy.
Subcutaneous tinzaparin may be administered at a dose of 175 units of antifactor activity Xa per kg, based on pre-pregnancy or weight of orders about 16 weeks, and not current weight. While non-fractionated heparin is typically administered in intravenous formulations, it is uncomfortable for the long period of administration required in pregnancy.
Whether warfarin can be re-initiated after the 12th week of pregnancy is unclear. In the latest retrospective analysis, the return of warfarin after the first trimester was completed was associated with an increased risk of fetal loss. However, this analysis only involves individuals treated with anticoagulants for mechanical heart valves, which generally require high levels of anticoagulation.
In pregnant women with mechanical heart valves, optimal anticoagulation regimens are very unclear. Anticoagulation with subcutaneous heparin in this setting is associated with high incidence of valve thrombosis and death. Similar problems may be related to the use of enoxaparin (LMWH) in these high-risk individuals.
With a risk score
Prevention of DVT and other types of venous thrombosis may be necessary if certain predisposing risk factors are present. One example from Sweden is based on the following points system, where points are summed to provide the appropriate prophylactic regimen.
After adding the risk factors together, a total of one or more points indicates no necessary precautions. Two points show short-term prophylaxis, e.g. with LMWH, may be used in temporary risk factors, as well as administering prophylactic treatment seven days postpartum, beginning a few hours after birth. A total of 3 points increases the required duration of postpartum prophylaxis by up to six weeks.
A risk score of four points or higher means prophylaxis during the ante partum period is required, as well as at least six weeks of post partum . The previous distal DVT showed a minimum of 12 weeks (three months) of therapeutic anticoagulation therapy. Proximal DVT or previous pulmonary embolism requires a minimum of 26 weeks (6.5 months) of therapy If the duration of therapy reaches the delivery time, the remaining duration may be given after delivery, possibly extending a minimum of six weeks post-partum therapy. In very high risk, high doses of prophylactic antibody partum should be continued at least 12 weeks after delivery.
Women with antiphospholipid syndrome should have additional low-dose aspirin treatment.
Caution
All anticoagulants (including LMWH) should be used with caution in women with suspected coagulopathy, thrombocytopenia, liver disease and nephropathy.
The main side effects of tinzaparin are osteoporosis (occurring in 1% of cases), thrombocytopenia (heparin-induced thrombocytopenia), bleeding, hair loss and drug allergies. However, LMWH is much less likely to cause heparin-induced thrombocytopenia than non-fractionated heparin.
Regional anesthesia is contraindicated in women taking anticoagulation therapy, and should not be used within 24 hours of the last dose of tinzaparin.
Monitoring
Anticoagulant therapy with LMWH is usually not monitored. LMWH therapy does not affect prothrombin (PT) or INR time, and anti-Xa is unreliable. May prolong partial thromboplastin (APTT) time in some women, but still, APTT is not useful for monitoring.
To examine the presence of thrombocytopenia, platelet count should be checked before starting anticoagulant therapy, then seven to 10 days after commencement, and every month thereafter. The platelet count should also be checked if unexpected bruises or bleeding occur.
Inversion
Protamin reverses the unfractionated heparin effect, but only partially binds and reverses LMWH. The dose of 1 mg of protamin/100 IU LMWH reverses 90% of anti-IIa and 60% of anti-Xa activity, but the clinical effect of residual anti-Xa activity is unknown. The anti-IIa and anti-Xa activity can come back up to three hours after the reversal of the protamin, possibly because of the additional LMWH release from the depot network.
Anticoagulant in breastfeeding
Warfarin, heparin and LMWH do not seem to pass to breast milk, so this is not contraindicated in breastfeeding.
See also
- Valvular heart disease and pregnancy
References
Further reading
- [3] Anticoagulant therapy in pregnancy. Norfolk Hospital and Norwich University (NHS Trust). CA3017 reference number. June 9, 2006 [preview June 2009]
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