Perioperative Venous Thromboembolism
Autor: | Frederick W. Lombard, Ronald J. Gordon |
---|---|
Rok vydání: | 2017 |
Předmět: |
medicine.medical_specialty
Hemorrhage Disease 030204 cardiovascular system & hematology Risk Assessment 03 medical and health sciences Postoperative Complications 0302 clinical medicine Fibrinolytic Agents Risk Factors Humans Medicine cardiovascular diseases 030212 general & internal medicine Thrombus Endothelial dysfunction Hypoxia Perioperative Period Intensive care medicine Aspirin business.industry Incidence Anticoagulants Lidocaine Thrombosis Venous Thromboembolism Perioperative medicine.disease Venous Valves Anesthesiology and Pain Medicine Hydroxymethylglutaryl-CoA Reductase Inhibitors Pulmonary Embolism business Risk assessment Platelet Aggregation Inhibitors medicine.drug |
Zdroj: | Anesthesia & Analgesia. 125:403-412 |
ISSN: | 0003-2999 |
Popis: | Venous thromboembolism (VTE) is a significant problem in the perioperative period, increasing patient morbidity, mortality, and health care costs. It is also considered the most preventable of the major postoperative complications. Despite widespread adoption of prophylaxis guidelines, it appears that morbidity from the disease has not substantially changed within the past 2 decades. It is becoming clear that current prophylaxis efforts are not sufficient. Using more potent anticoagulants may decrease the incidence of VTE, but increase the risk for bleeding and infection. Much has been learned about the pathophysiology of venous thrombogenesis in recent years. Beyond the "traditional coagulation cascade," which anticoagulants modulate, there is a growing appreciation for the roles of tissue factor, monocytes, neutrophils, neutrophil extracellular traps, microvesicles, and platelets in thrombus initiation and propagation. These recent studies explain to some degree why aspirin appears to be remarkably effective in preventing thrombus propagation. Endothelial dysfunction, traditionally thought of as a risk factor for arterial thrombosis, plays an important role within the cusps of venous valves, a unique environment where the majority of venous thrombi originate. This suggests a role for newer treatment modalities such as statins. Not all patients have an equal likelihood of experiencing a VTE, even when undergoing high-risk procedures, and better tools are required to accurately predict VTE risk. Only then will we be able to effectively individualize prophylaxis by balancing the risks for VTE against the risks associated with treatment. Given the different cell types and pathways involved in thrombogenesis, it is likely that multimodal treatment regimens will be more effective, enabling the use of lower and safer doses of hemostatic modulating therapies such as anticoagulants, antithrombotics, and antiplatelet medications. |
Databáze: | OpenAIRE |
Externí odkaz: |