الفهرس 
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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.