脊髓损伤sci课件.pptVIP

DVT: Pathophysiology Predisposing risk factors for the development of DVT following SCI can be classified with the Virchow triad Venous stasis results from loss of pumping function provided by contracting muscles. Hypercoagulability can occur as a result of stimulation of thrombogenic factors following injury, with resultant increase in platelet aggregation and adhesion (reduced fibrinolytic activity along with higher levels of von Willebrand factor antigen and Factor VIII-related antigen and resulting in hyperactive platelet aggregation Intimal injury may result directly from the release of vasoactive amines with trauma or surgery, or indirectly from external pressure on the paralyzed leg. Deep Venous Thrombosis Swelling Fever of unknown origin Increased spasticity and AD Clinically apparent DVT occurs in approximately 15% to 50%. DVT can lead to pulmonary embolism (5-10%) and death. DVT Treatment Anticoagulation with Lovenox, Heparin, and or coumadin If clinically contraindicated place venacaval filter Continue activity and compression garments DVT/PE Prevention Guidelines All patients will be on Lovenox or Heparin to prevent blood clot: Non-complicated spinal cord injury (no co-morbidity) will have 8 weeks of treatment Complicated spinal cord injury (having at least one co-morbidity) will have 12 weeks of treatment Standard of care to prevent DVT: Anticoagulation Therapy at therapeutic doses (Lovenox 30mg SQ BID or Heparin 5000 units SQ BID/TID), SCD’s while in bed, and Tedhose and/or Ace Wraps when out of bed. Pearls DVT occurs in 40-90% of patients depending on the degree of prophylaxis. Risk factors decline in 8-12 weeks. Proximal progression of DVT and pulmonary embolism occur in 20-50%. Historicaly clinical factors believed to be associated with DVT include motor complete injuries, paraplegia, and male gender. In a recent study by Powell et al, there was no statistical difference in incidence of DVT between motor complete versus motor