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Abstract
Thrombophilia can be defined as a predisposition to form clots inappropriately. Thrombotic events during infancy and childhood are increasingly recognized as a significant source of mortality and morbidity. Neonates are at greater risk of thromboembolic complications than older children . The incidence of vascular accidents decreases significantly after the first year of life, with a second peak during puberty
The predisposition to form clots can arise from genetic factors, acquired changes in the clotting mechanism, or, more commonly, an interaction between genetic and acquired factors .
Current treatment for thrombophilias involves both prophylaxis with low-molecular-weight heparin and treatment involving heparin, warfarin or purified factor concentrate. The presence of an inherited thrombophilia should not alter the intensity of anticoagulant therapy, given that antithrombin, protein C, or protein S deficiency, factor V Leiden, and the prothrombin G20210A mutation are not unusually anticoagulant resistant. However, they can increase the optimal treatment duration after a first thromboembolic event
Acute therapy aims to prevent extension or embolism of an acute thrombosis, and needs to continue for a sufficient duration of time and intensity to insure that the acute thrombus has either lysed or become organized, and the ”activated” acute inflammatory/innate immunity system has returned to baseline. The total duration of anticoagulation for acute therapy should be individualized based on the circumstances of the thrombotic event. .