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Early use of aspirin after coronary bypass surgery is safe and is associated with a reduced risk of death and ischemic complications involving the heart, brain, kidneys, and gastrointestinal tract.
Early use of aspirin after coronary bypass surgery is safe and is associated with a reduced risk of death and ischemic complications involving the heart, brain, kidneys, and gastrointestinal tract.
The literature does not consistently support the importance of anticoagulation monitoring techniques during CPB. This is best reflected by studies that have evaluated the impact of the ACT method on blood loss and transfusion outcomes. Inconsistent findings from studies that evaluated the impact of ACT monitoring may be related to either suboptimal study design (i.e., retrospective, unblinded, nonrandomized) or possibly the diagnostic inprecision of the ACT method used in these studies. There are a small number of well-controlled studies, some of which suggest that bleeding and transfusion outcomes can be improved by refining heparin monitoring techniques, either by sustaining better anticoagulation during CPB or by optimizing protamine doses (i.e., when empiric protocols result in excessive protamine doses). More well-controlled studies are needed to better define the importance of anticoagulation management during CPB.
A pproximately 10 to 14 million red blood cell (RBC) units 1 and 1.5 million platelet (PLT) transfusions (approx. 85%, single-donor plateletpheresis products; the remainder, pools of six whole-blood-donor PLT concentrates) are administered in the United States each year. Transfusion-related adverse (20% of transfusions) and serious adverse (0.5%) events were estimated by Walker in the 1980s. 2 More recently, serious adverse events have been estimated to occur in 0.1 percent of RBCs and 0.04 percent of PLT transfusions. With early estimates, transfusion-associated adverse events were thought to lead to a short-term (i.e., not including disease transmission-related deaths) mortality of 1 to 1.2 per 100,000 patients, or approximately 35 transfusion-related deaths per year in the United States. With more recent estimates, long-term or total mortality (i.e., including disease transmission-related deaths) is probably higher due to unrecognized or unreported transfusion-related deaths. 1,3 Perioperative signs and symptoms (e.g., fever, hypotension, tachycardia, hypoxemia, microvascular bleeding, hemoglobinuria, low urine output) can accompany any of several serious transfusion-related complications such as acute hemolytic transfusion reactions (HTRs), bacterial contamination, anaphylaxis, transfusion-related acute lung injury (TRALI), or other events (e.g. hyperkalemia, fluid overload, air embolus). Current risks associated with blood and blood component transfusion can be characterized as immune-mediated versus non-immunemediated, hemolytic versus nonhemolytic, or acute versus delayed transfusion reactions, as well as bloodborne disease transmission. Another approach would involve subdividing transfusion risks into those that are the leading causes of mortality versus those that are uncommon causes of transfusion-related mortality. The leading causes of transfusion-related mortalityReports to the US Food and Drug Administration (FDA) 4 and quoted mathematical estimates 1 of transfusionrelated mortality indicate that the leading causes of transfusion-related mortality are (in decreasing order): TRALI, bacterial or viral contamination of blood and blood components, and transfusion of ABO-mismatched blood. Transfusion-associated respiratory distress can be related to one of the following (in order of decreasing frequency): fluid overload (also called transfusion-associated circulatory overload or TACO), allergic reactions, or TRALI. Although the exact incidence of circulatory overload related to transfusion is unknown (e.g., 1 in every 200-10,000 units), 5 it is more likely in older patients with a history of congestive heart failure. Reported estimates of the frequency of TRALI range from 1:400 to 1:50,000 units transfused (i.e., involving plasma, PLTs, or RBCs). 6 This extremely wide estimated range reflects the difficulties in clinical recognition of TRALI with resultant underreporting. Both one-hit (white blood cell [WBC] antibodies) and two-hit mechanisms have been proposed as the etiology of TRALI. Indeed, as TRALI ...
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