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Ann Thorac Surg 1997;63:1828-1830
© 1997 The Society of Thoracic Surgeons
Section of Cardiothoracic Surgery, Guthrie Clinic, Guthrie Square, Sayre,Pa 18840
To the Editor:
I read with interest the recent article by Christenson and associates [1]. My colleagues and I have also investigated different methods to decrease the risks of homologous blood transfusion during open heart operations [2, 3].
In a prospective, randomized manner, we evaluated the effectiveness of platelet sequestration on postoperative blood transfusion requirement in 126 consecutive patients. Unlike the Swiss patients, the majority of our patients would not hemodynamically tolerate preoperative platelet sequestration cycles. Consequently we designed a technique of intraoperative platelet-rich plasma (PRP) sequestration that occurs during the initial period of cardiopulmonary bypass after the patient's circulation is supported and heparin has been given (PRP+). The process does not require any additional hardware, personnel, or expense and it can be performed without difficulty or complication [3]. To demonstrate that the PRP+ platelets were functionally no different than platelets harvested from conventional pheresis techniques, we performed a series of platelet aggregation and activation studies. Percent aggregation of PRP+ platelets in response to adenosine diphosphate was not significantly different than that of PRP platelets. Similarly, there was no significant difference in platelet activation (CD62) between the two groups. In our study, we observed a statistically higher transfusion requirement in the control group (no PRP+) compared with the patient group that received PRP+. However, there was no difference in mediastinal tube drainage.
The average platelet count of PRP+ was 6.6 ± 3.2 x 1010/mL, which is less than that reported in Christenson and associates' report by a factor of 10. Christenson and associates state in their Comment section that for this technique to be efficacious a minimum of 3 x 1011 platelets is required. This number was based on a recommendation of the American Blood Bank Association. In our study, we found that comparative platelet aggregation studies between PRP+ and blood bank platelets, using several different agonists (adenosine diphosphate, arachidonic acid, and collagen) always showed PRP+ to be superior (p < 0.05). These data suggest that the American Blood Bank Association quantity recommendations may not be applicable to the different-quality PRP+ platelets. Furthermore, this sheds some light on the conclusions of references 8 and 9 in Christenson and associates' article.
Finally, Christenson and associates described the "frequent" occurrence of bacterial and endotoxin contamination of blood from cell conservation devices used for autologous transfusions during cardiac operations. We have recently reported that the maintenance of high flow and perfusion pressures during nonpulsatile cardiopulmonary bypass reduces the incidence of any "acute phase response" of clinical significance including endotoxin or cytokine production [4]. During this latter study, blood conservation devices were used routinely in our institution.
Obviously, our ultimate goal is open heart surgery without any blood loss. I think this is no longer an unrealistic idea but rather may be quite possible in the near future by using a combination of pharmacologic agents, concentrated autologous factors, and completely inert extracorporeal hardware circuitry.
References
The Cardiovascular Surgery Unit, Columbia Hospital de la Tour, 1 Avenue J.-D-Maillard, Ch-1217 Meyrin-Geneva, Switzerland
To the Editor:
I have read with great interest the remarks made by Dr Quigley and I thank him for his interest in our research. Nevertheless, I found it somewhat difficult to understand why their patients, in contrast to ours, would not hemodynamically tolerate preoperative PRP harvest, because I believe their patients are not different from ours, and as we have reported the PRP harvest was not discontinued in any of our patients due to hemodynamic instability. However, it should be emphasized that, during each sequestration cycle, the volume loss must be carefully counterbalanced by infusion of colloid fluids. If this is correctly done, undesirable hemodynamic fluctuations can be avoided.
When describing his intraoperative PRP sequestration method [1], Dr Quigley claims that there were no significant differences in platelet function (aggregation response to adenosine diphosphate) between PRP harvested before cardiopulmonary bypass and heparin administration as compared with conventional plateletpheresis techniques. This is in contrast to what has been reported by others [2]. It also should be stressed that platelet function is a very complex issue, thus extremely difficult to evaluate. Aggregation response covers only one facet of this complexity.
In their study, Dr Quigley and associates demonstrated a higher transfusion requirement in the control group (no PRP+) compared with patients receiving PRP harvested intraoperatively, without showing any differences in mediastinal tube drainage. I fail to understand this statement entirely, and one must ask the question: what was the transfusion algorithm used in their study? I believe this has to be thoroughly addressed in all future studies using bleeding, blood transfusion, or both as end point(s).
Arguments for the PRP harvest preoperatively (before cardiopulmonary bypass and heparin administration) are to save the PRP and all its clotting factors from being damaged by the extracorporeal circulation system and to allow it to be reinfused after cardiopulmonary bypass when optimal coagulation is required.
As for Dr Quigley's comments on platelet count, Dr Quigley and his associates reported that there was no difference in mediastinal tube drainage between PRP+ and controls [1]. In contrast to this, we have clearly shown, using a much higher platelet yield in the PRP, a significantly larger total blood loss in the control group compared with the total blood loss observed in patients undergoing preoperative PRP harvest followed by reinfusion of the PRP after cardiopulmonary bypass and heparin reversal was done. This suggests that not only platelet function, but also the amount of platelets harvested has an impact on the result. These conclusions have been previously demonstrated by others [2, 3].
In the Comment section of our article, we discuss the possibility of bacterial and endotoxin contamination of blood from cell conservation devices as a procedural risk recently reported on [4]. I do agree with Dr Quigley that this is a very rare complication. We have also reported in the article that there were no sequestration-related infectious complications in our series.
I entirely agree with Dr Quigley's conclusions about the possibility of cardiac surgery without blood transfusions in the near future.
I thank Dr Quigley for his interest and comments on our article. However, it must be emphasized that none of the available blood conservation techniques (pharmacologic or mechanical), alone or in various combinations, can replace good surgical skills, including atraumatic surgical techniques and meticulous hemostasis, in preserving blood.
References
Anesthesia Pain Consultants Pc, Mississippi Medical Plaza, 3400 Dexter Court, Davenport Ia 52807
To the Editor:
I agree with Dr Quigley that there appears to be an opportunity to salvage platelets while the patient is on cardiopulmonary bypass. In addition to Dr Quigley's studies on platelet aggregation there is additional evidence that platelets collected after the onset of cardiopulmonary bypass (CPB) should still be effective: (1) Platelet dysfunction associated with CPB is highly variable between patients, and some patients tolerate more than 2 hours of CPB without major coagulopathy due to platelet dysfunction. (2) Coagulopathy is a problem in around 20% of patients, and it is difficult to predict those who will respond poorly to CPB. (3) Platelet dysfunction appears to increase with time on CPB. Platelet dysfunction may well be related to the total time that the cells are outside the patient's circulation because the presence of an intact endothelium with its secretion of prostacyclin prevents spontaneous platelet activation.
However, it is doubtful that 1 unit of platelets (4% of the circulating platelets) is sufficient to prevent coagulopathy in all of the estimated 20% of patients in whom post-CPB coagulopathy develops, and many studies have failed to show benefits from 2 units of plateletpheresis. In addition, there are other reasons to desire "platelet protection" while on CPB: The final common pathway for perioperative injury after an open heart operation where the use of a heart-lung bypass machine is required appears to be the inflammatory cascade [1, 2], with platelet activation and subsequently the activation of complement cascades and cytokines along with leukocyte activation and aggregate sequestration in lungs and other organs. Present techniques of CPB prevent the generation of frank blood clots in the CPB circuit but do not prevent these other important aspects of the coagulation process [1–4].
High-yield plateletpheresis, which accomplishes significant depletion of the platelet count before bypass, has the potential to not only prevent coagulopathy but also ameliorate the inflammatory and microembolic complications of cardiopulmonary bypass, which contribute to significant morbidity and mortality of heart operations.
There is evidence from several retrospective and prospective studies that withdrawal of a large percentage of the platelet mass before CPB with reinfusion after CPB can ameliorate some of the deleterious effects of CPB, particularly microembolic phenomena and coagulopathy [5–7]. Doctor Quigley's observation of hemodynamic instability is a concern. Plateletpheresis on cardiac patients before CPB is a complex medical procedure performed on high-risk patients demanding added vigilance, monitoring, additional central venous access, and, even for routine cases, far greater pharmacologic intervention by the anesthesiologist. The potential risks include hypovolemia, hypothermia, and citrate-induced hypocalcemia. To ensure cardiovascular stability we use a combination of norepinephrine or phenylephrine, calcium chloride, and hydroxyethyl starch as a volume expander. However, if autologous donation is to be performed at all in this patient population it is arguable that the open heart surgery operating room is the safest place for it.
References
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