Treatment in the puerperium may require larger doses of anticoagulant. Brooks and colleagues (2002) compared antico agulation in postpartum women with that of age-matched non pregnant controls. The former required a significantly larger median total dose of warfarin-45 versus 24 mg-and a longer time-7 versus 4 days-to achieve the target INR.
Of newer oral anticoagulants, dabigatran (Pradaxal) inhibits thrombin. Rivaroxaban (Xarelto) and apixaban (Eliquis) inhibit factor Xa. Currently, very few reports address these newer agents during pregnancy, and thus the human reproductive risks are essentially unknown (Bates, 2012). Dabigatran crosses the human placenta (Bapat, 2014). However, it is unknown whether any of these agents are excreted in breast milk. Because of the potential for infant harm, a decision should be made to either avoid breastfeeding or use an alternative anticoagulant, such as warfarin, in postpartum women (Burnett, 2016).
• Complications of Anticoagulation hree significant complications associated with anticoagulation are hemorrhage, thrombocytopenia, and osteoporosis. he latter two are unique to heparin, and their risk may be reduced with LMWHs. The most serious complication is hemorrhage, which is more likely if there has been recent surgery or lacerations. Troublesome bleeding also is more likely if the heparin dosage is excessive. Unfortunately, management schemes using laboratory testing to identiY when a heparin dosage is suicient to inhibit further thrombosis, yet not cause serious hemorrhage, have been discouraging.
There are two types-the most common is a nonimmune, benign, reversible thrombocytopenia that develops within the first few days of therapy and resolves in approximately 5 days without therapy cessation. The second is the severe form of heparin-induced thrombocytopenia (HIT), which results from an immune reaction involving IgG antibodies directed against complexes of platelet factor 4 and heparin. The diagnosis of HIT is based on a drop in the platelet count of more than 50 percent or thrombosis beginning 5 to 10 days after the start of heparin in association with the appearance of platelet-activating HIT antibodies. The fall in platelet count in HIT occurs rapidly-over a period of 1 to 3 days-and is assessed relative to the highest platelet count after the start of heparin. he typical nadir is 40,000 to 80,000 platelets per microliter (Greinacher, 2015).
Although the incidence of HIT is approximately 3 to 5 percent in nonpregnant individuals, it is <0.a1 percent in obstetrical patients (Linkins, 2012). Fausett and coworkers (2001) reported no cases among 244 heparin-treated gravidas compared with 10 among 244 nonpregnant patients. Accordingly, the American College of Chest Physicians recommends against platelet count monitoring when the risk of HIT is considered to be less than 1 percent. In others, they sug (Linkins, 2012).