The role of inherited thrombophilias in RPL has generated a great deal of interest. This heterogeneous group of disorders results in increased venous or arterial thrombosis. Their associations with pregnancy loss rest on both proved and hypothetical alterations in placental growth and development particularly placental vascular development. Abnormal placental vascularization and inappropriate placental thrombosis would link these thrombophilic states to pregnancy loss. Although some thrombophilic states may be acquired most are heritable. Those heritable thrombophilias most often linked with reference to RPL include hyperhomocyteinemia. Activated protein C resistance associated with mutations in factor V deficiencies in proteins C and S mutations in the prothrombin gene promoter mutations in prothrombin and mutations in antithrombin III. Inherited thrombophilic mutations have been estimated to be causative in 50% of VTE during pregnancy. Approximately 40% of episodes of venous or arterial thromboembolic phenomena occur in patients carrying a heritable mutation. Associations between thrombophilias and adverse fetal outcomes cover a range of early gestational and obstetric disorders. These disorders include isolated and recurrent early and late spontaneous pregnancy losses intrauterine growth restriction (IUGR) intrauterine fetal demise (IUFD). Placental abruption and pregnancy- induced hypertension (PIH). This discussion will focus on pathophysiologic mechanisms diagnostic tesing and treatment strategies for patients with RPL who may have an inherited or acquired predisposition to thrombosis (excluding the antiphospholipid syndrome). The basis for the association between adverse fetal outcomes and heritable thrombophilias has focused on the mechanisms of impaired placental development and function secondary to venous or arterial thrombosis at the maternal-fetal interface.