Case 3-1995. Three patients requiring both coronary artery bypass surgery and orthotopic liver transplantation.
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Biomedical subjects
Publications and source records attributed to L Shore-Lesserson.
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Preoperative platelet-rich plasmapheresis has been suggested as a means of reducing homologous blood transfusions in cardiac surgical patients. The current study evaluated this technique in patients undergoing repeat cardiac operations. Fifty-two patients undergoing repeat myocardial revascularization and/or valve replacement were evaluated in a prospective randomized controlled study design. Autologous platelet-rich plasma (PRP) was harvested after the induction of anesthesia in the experimental group. After reversal of heparin, each patient received his or her autologous plasma. Patients in the control group did not have plasmapheresis and received standard transfusion therapy if coagulation variables were abnormal and a coagulopathy was clinically evident. Routine coagulation tests, thromboelastography (TEG), perioperative bleeding, and transfusion requirements were compared in the two groups. Forty-four patients completed the study. A significantly larger volume of packed red blood cells (PRBCs) was transfused in the PRP group than in the control group (P = 0.03). Platelet and fresh frozen plasma (FFP) transfusions did not differ between the two groups. Mediastinal tube drainage did not differ between the two groups. During PRP infusion, 60% of the patients required treatment for moderate hypotension (mean arterial pressure [MAP] < 60 mm Hg). Only 16% of control patients required treatment for hypotension during the comparable time period (P < 0.05). No patient who completed the study returned to the operating room for postoperative bleeding. These data suggest that PRP did not reduce postbypass bleeding or transfusion requirements in repeat cardiac surgical patients. Moreover, the incidence of hypotension during PRP reinfusion introduces a potential risk to the procedure in the absence of any obvious benefit.
Anesthetic agents may significantly alter the patient's blood pressure, and thus affect the intraoperative assessment of mitral regurgitation. This study examined the impact of an increase in afterload on a variety of parameters thought to reflect the severity of mitral regurgitation, and related them to changes in hemodynamic parameters. Twenty-four patients with mitral regurgitation undergoing cardiac surgery were studied. Following the induction of anesthesia, color-flow mapping of the entire left atrium was performed, and pulmonary vein flow was then measured. Phenylephrine was administered to increase the patients' blood pressures to their preoperative values, and the assessment was repeated. Regurgitant jet area increased 56% (482 +/- 405 v 750 +/- 440 mm2 P < 0.001), and there were significant reductions in systolic pulmonary venous velocity (0.33 +/- 0.17 v 0.18 +/- .31 m/s P < .01) with increases in diastolic flow (0.43 +/- 12 v 0.58 +/- 0.18 m/s P < .001). These changes in pulmonary venous flow were not related to the changes in the driving force across the incompetent mitral valve. Also, an additional six patients developed systolic flow reversal after phenylephrine administration. Intraoperative hemodynamic variations can significantly alter the apparent severity of mitral regurgitation, and this factor must be considered during decision making.
Hemostasis abnormalities in cardiovascular and aortic surgery remain a major source of morbidity and mortality in patients undergoing such complex procedures. The need for frequent transfusions of red cell and other blood products increases risks and costs to patients and institutions providing patient care. Specifically in cardiovascular and aortic surgery, the nature of the surgery is, at best, semi-elective, and careful preparation to preserve the hemostatic mechanisms of the body is essential. Contact of blood with the extracorporeal circuit induces a hemorrhagic diathesis through a variety of different mechanisms. Dilution of the patient's blood volume by the extracorporeal circuit prime causes depletion of platelets and coagulation factor levels. Aorto intimal disease initiates fibrinolysis by the release of tissue plasminogen activator. Due to the numerous etiologies of bleeding, a combination of blood conservation strategies is suggested. The ideal combination of interventions has yet to be determined and is currently dependent on patient variables, physician and institutional practices, and economic pressures.