الفهرس | Only 14 pages are availabe for public view |
Abstract Platelets are essential for primary hemostasis and repair of the endothelium, but they also play a key role in the development of acute coronary syndromes and contribute to cerebrovascular events. In addition, they participate in the process of forming and extending atherosclerotic plaques. Atherosclerosis is a chronic inflammatory process, and inflammation is an important component of acute coronary syndromes. The relation between chronic and acute vascular inflammation is unclear, but platelets are a source of inflammatory mediators, and the activation of platelets by inflammatory triggers may be a critical component of atherothrombosis. Platelets have emerged as key cellular determinants of physiologic vascular repair and its pathologic derangement. Anesthesiologists frequently encounter patients with atherothrombotic disease who are receiving drugs deliberately designed to impair the normal function of the coagulation system. The platelet is integral to the initiation of thrombosis. Drugs that affect platelet function are a fundamental part of primary and secondary management of atherosclerotic thrombotic disease including stroke, acute myocardial infarction (AMI), acute coronary syndrome (ACS), angina, percutaneous coronary intervention (PCI), cardiac surgery, primary and secondary cardiovascular disease prevention, peripheral vascular disease, and thrombotic disorders such as atrial fibrillation. There are several antiplatelet drugs available for use in clinical practice and several under investigation. Anti-platelet and anticoagulants are be useful in the treatment and prophylaxis of arterial thrombotic conditions, but must be carefully administered without increasing the risk of bleeding to an unacceptable level. The main use of platelet function tests has been traditionally to identify the potential causes of abnormal bleeding, to monitor pro-haemostatic therapy in patients with a high risk of bleeding and to ensure normal platelet function either prior to or during surgery. However, they are increasingly being utilized to monitor the efficacy of antiplatelet and anticoagulants therapy and to potentially identify platelet hyperfunction to predict thrombosis. The perioperative management of patients receiving anticoagulations and antiplatelets agents can be problematic. It is important that the benefit of surgery is first weighed against the risk of altering the anticoagulation regimen. where doubt exists, there should be a discussion involving the physician managing the anticoagulation, the surgeon and the anesthetist about the risks and benefits of continuing the anticoagulation or the antiplatelets agents. It may also be wise to involve the patient in the decisionmaking process and to consider an individual plan for complex situations. A multidisciplinary approach helps to manage the perioperative anticoagulation therapy safely and effectively. Management of patients who are receiving antiplatelets and anticoagulants drugs during the perioperative period requires an understanding of the underlying pathology and rationale for their administration, pharmacology and pharmacokinetics, and drug interactions. Knowledge of the pharmacodynamics and pharmacokinetics may allow practitioners to anticipate difficulties associated with drug withdrawal and administration in the perioperative period including the potential for drug interactions. The risk versus benefit assessment of continuing or discontinuing these drugs should be made bearing in mind the proposed surgery and its inherent risk for bleeding or thrombotic complications as well as decisions relating to appropriate use of general or some form of regional anesthesia. In the patient requiring urgent surgery, the options to treat an elevated INR are fresh frozen plasma and prothrombin concentrate complex. Vitamin K takes 1-2 days to achieve the target INR and is considered an adjunct in this setting. In the case of semi-urgent surgery, vitamin K can reverse the INR in 1-3 days. Oral administration is preferred, and the dose is based on the INR at presentation. In elective procedures, Coumadin can be discontinued 5 days prior to surgery to achieve a target INR of 1.3 or less. Bridging therapy with unfractionated heparin or low molecular weight heparin is indicated in patients with a high or intermediate risk of thromboembolism. In patients requiring surgery with a high risk of bleeding, there may be a role for a temporary inferior vena cava filter. In general, Coumadin can be restarted on the first post-operative evening at the maintenance dose. Bridging therapy may be used in post-operatively until the INR is therapeutic. |