脊髓损伤scippt课件

脊髓损伤（SCI） Leading causes 80(9):1044-6. 1999 Sep;80(9):1044-6 DVT: Pathophysiology Predisposing risk factors for the development of DVT following SCI can be classified with the Virchow triad nVenous stasis results from loss of pumping function provided by contracting muscles. nHypercoagulability 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 nIntimal 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 nSwelling nFever of unknown origin nIncreased spasticity and AD nClinically apparent DVT occurs in approximately 15% to 50%. nDVT can lead to pulmonary embolism (5-10%) and death. DVT Treatment nAnticoagulation with Lovenox, Heparin, and or coumadin nIf clinically contraindicated place venacaval filter nContinue activity and compression garments DVT/PE Prevention Guidelines nAll patients will be on Lovenox or Heparin to prevent blood clot: nNon-complicated spinal cord injury (no co- morbidity) will have 8 weeks of treatment nComplicated spinal cord injury (having at least one co-morbidity) will have 12 weeks of treatment nStandard of care to prevent DVT: Anticoagulation Therapy at therapeutic doses (Lovenox 30mg SQ BID or Heparin 5000 units SQ BID/TID), SCDs 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 incomplete injuries, tetraplegic versus paraplegic, or traumatic versus nontraumatic causes. Thus, all SCI patients are at risk of developing a DVT. Powell M, Powell M, KirshblumKirshblum S, OConnor KC. Arch P Med S, OConnor KC. Arch P Med RehabilRehabil. 1999 Sep;80(9):1044-6. 1999 Sep;80(9):1044-6 Pulmonary Embolism Venacaval Filter Coronary Heart Disease nCoronary Heart Disease is thought to increase after SCI due to: physical inactivity obesity hyperlipidemia insulin resistance diabetes nCHD accounts for approximately 20% of deaths in the SCI population. nModifiable risk factors for CHD prevention include high blood pressure, smoking, obesity, physical inactivity, and cholesterol and/or lipid control. nThis risk may be increasingly important as the life expectancy of people with SCI lengthens. Response to exercise nLesions above T1-4 can compromise increases in heart rate and stroke volume. nCO = HR x SV nStroke volume is determined by: 1. Preload (return of