Models of thrombosis risk. In each panel, the figure shows the thrombosis (black) potential of each risk factor present during an individual's life and the resultant thrombosis potential (red). (From FR Rosendaal: Venous thrombosis: A multicausal disease. Lancet 353:1167, 1999; with permission.) Several acquired risk factors are very strong, causing thrombosis in several percent of those afflicted, which implies a relative risk of ≥50. These are orthopedic, neurosurgical, and major abdominal interventions; major trauma with multiple fractures; central venous catheters; and metastasized cancer, particularly adenocarcinomas. Moderate risk factors are antiphospholipid antibody syndrome, puerperium, prolonged bedrest, and nonmetastasized cancers; pregnancy, oral contraceptive. | Chapter 112. Venous Thrombosis Part 2 Figure 111-1 Models of thrombosis risk. In each panel the figure shows the thrombosis black potential of each risk factor present during an individual s life and the resultant thrombosis potential red . From FR Rosendaal Venous thrombosis A multicausal disease. Lancet 353 1167 1999 with permission. Several acquired risk factors are very strong causing thrombosis in several percent of those afflicted which implies a relative risk of 50. These are orthopedic neurosurgical and major abdominal interventions major trauma with multiple fractures central venous catheters and metastasized cancer particularly adenocarcinomas. Moderate risk factors are antiphospholipid antibody syndrome puerperium prolonged bedrest and nonmetastasized cancers pregnancy oral contraceptive use hormone replacement therapy obesity and long-distance travel are mild risk factors with a two- to fivefold increased risk. Homozygous protein C or protein S deficiency leads to potentially fatal purpura fulminans directly after birth while homozygous antithrombin deficiency is not compatible with life. These are exceedingly rare except in communities with a high frequency of consanguinity. Heterozygous antithrombin deficiency and homozygous factor V Leiden are the strongest genetic risk factors increasing the risk of thrombosis 20- to 50-fold. Heterozygous protein C and protein S deficiencies are moderate contributors to risk with a relative risk of 10. Other genetic factors that are associated with venous thrombosis are either mild and increase the risk two- to fivefold as is the case for factor V Leiden prothrombin 20210A and non-O blood groups or have negligible effects on risk that are only of academic interest MTHFR 677T factor V HR2 FXIII val34leu PAI-1 4G 5G . Mildly increased risks are also present for abnormalities in the coagulation system of which the origin is unclear such as elevated levels of procoagulant factors fibrinogen II von Willebrand factor VIII
