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Ann Thorac Surg 1996;62:1431-1441
© 1996 The Society of Thoracic Surgeons
Departments of Cardiothoracic Surgery, Pathology, and Anesthesiology, The New York Hospital-Cornell Medical Center, New York, New York
Accepted for publication June 17, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentReferences |
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Methods. Ninety patients undergoing coronary artery bypass grafting or valvular operations were prospectively randomized to either have (IAD group) or not have (control group) calculated maximum volume IAD performed. Treatment was otherwise identical. Transfusion guidelines were uniformly applied to all patients.
Results. An average volume of 1,540 ± 302 mL of fresh autologous blood was removed and reinfused in the IAD group. Postoperative hematocrits were significantly greater at 12 and 24 hours postoperatively in the IAD group versus the control group despite a significant decrease in both the percentage of patients in whom allogeneic red blood cells were transfused (17% versus 52%; p < 0.01) and the number of red blood cell units transfused per patient per group (0.28 ± 0.66 and 1.14 ± 1.19 units; p < 0.01). Conversely, chest tube output, incidence of excessive postoperative bleeding, postoperative prothrombin time, and platelet and coagulation factor transfusion requirement did not differ between groups.
Conclusions. These results indicate that intraoperative autologous donation serves to preserve red blood cell mass. Its routine use in eligible patients is therefore justified. However, the removal and reinfusion of an individually calculated maximum volume of fresh autologous blood had no effect on postoperative bleeding or platelet and coagulation factor transfusion requirement. This lack of hemostatic effect belies the beliefs of many about the primary action of IAD, helps to delineate the optimal way in which to perform IAD, and carries implications regarding the use of allogeneic platelet and coagulation factors for the treatment of early postoperative bleeding.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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One of the oldest blood conservation techniques involves the removal of a portion of a patient's blood intraoperatively before cardiopulmonary bypass (CPB), and reinfusion of this blood immediately after CPB. Known as acute hemodilution, acute autologous donation, blood pooling, and more recently, and perhaps more accurately, as intraoperative autologous donation (IAD), this technique was first described for use in cardiac surgery by Dodrill and associates in 1957 [1]. Theoretically, IAD serves to (1) preserve the portion of withdrawn blood from degradation and destruction by the CPB circuit; (2) decrease the percentage of autologous components lost into lap pads, discard suckers, and field drapes; and (3) provide a volume of fresh autologous red blood cells, platelets, and coagulation factors for reinfusion after CPB. The technique is simple, cost-effective, and intuitively appealing. In Dodrill and associates' words: "The advantages ... are so great and so protean that time and space do not permit a complete statement of its advantages."
Since these words, many studies have appeared in the literature attempting to document the normalization of platelet and coagulation parameters, the reduction in postoperative bleeding, and the decrease in homologous transfusion requirement that the technique appears to promise. Results, however, have been inconsistent. Improvements in platelet number, platelet function, postoperative bleeding, and transfusion requirement have been reported by some investigators, but others have not found these benefits (Table 1
). Further analysis reveals that although these conflicting results are partly attributable to differences in study design and in attention to details that lend validity to studies of blood conservation [2], they are also due to inconsistent and often suboptimal application of the IAD technique itself. Shortcomings in respect to the IAD technique employed in previous studies can be grouped into three categories: (1) removal of insufficient volume to cause a measurable effect, (2) use of an inadequately low transfusion trigger during CPB, thereby triggering potentially unnecessary transfusion, and (3) reinfusion of banked blood before IAD blood during CPB, thereby potentially triggering unnecessary allogeneic transfusion.
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) and our own previous findings [3]. In fact, outcome analysis reveals that the transfusion of banked red cells during CPB while autologous (IAD) red blood cells are available may actually lead to an unnecessary increase in allogeneic transfusion, particularly when large volumes of IAD blood are removed. This is because the removal of IAD blood necessarily lowers the hematocrit during CPB. If banked cells are used to restore this low hematocrit, the patient is automatically committed to banked blood exposure. For this exposure to be justified the preservation and post-CPB reinfusion of the corresponding IAD unit must consistently either reduce the use of platelets or coagulation factors, or decrease postoperative bleeding by at least 450 mL (the equivalent of one unit of red blood cells). In addition, this bleeding and red blood cell loss must occur in a patient whose postoperative hematocrit is in the range of the stated postoperative transfusion trigger, so that the reduction in bleeding actually prevents post-CPB allogeneic red blood cell transfusion. A central issue, therefore, both in delineating the benefit of IAD and in determining the optimal way in which to perform IAD, becomes whether or not IAD leads to a reduction in postoperative bleeding. Based on analysis of the literature and our own clinical experience, we developed a logically optimized three-principle IAD technique that involves (1) removal and preservation of a calculated safe maximum volume of autologous blood, (2) adherence to the lowest safe transfusion trigger during CPB, and (3) use of IAD blood before banked blood for hematocrits below this trigger. Only by integrating the first and second of these principles can the largest possible volume of fresh autologous blood be removed and safely preserved until after CPB. And only by reinfusing IAD blood before banked blood during CPB-during the time that the hematocrit has been iatrogenically lowered by the IAD process itself-can potentially unnecessary allogeneic transfusion be avoided.
To determine the clinical effectiveness of this optimized form of IAD in respect to allogeneic transfusion requirement and postoperative bleeding, a prospective, randomized, controlled trial was performed. To accurately assess the former a strict set of red blood cell, platelet, and coagulation factor transfusion guidelines was applied to all patients. To appropriately address the latter, patients selected for this study were those in whom it could be predicted (by preoperative hematocrit and red blood cell mass parameters) that at least two units of IAD blood would be available for reinfusion after the completion of CPB, even if IAD reinfusion was required during CPB.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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The amount of blood removed in the IAD group was calculated using the patient's estimated blood volume (EBV), the CPB circuit prime volume (2,100 mL), the initial hematocrit (Hct) value obtained in the operating room, and a target Hct of 18% during CPB. The following two equations were used to perform this calculation:
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After anesthetic induction, but before initiation of CPB, the calculated blood volume was removed by gravity drainage via a wide-bore side port 9.0F internal jugular venous line (Arrow International Inc, Reading, PA) into standard citrate-phosphate-dextrose collection bags (Baxter Healthcare Corp, Deerfield, IL). Bags were filled while resting on an electronic scale to ensure proper filling and maintenance of the proper blood to citrate-phosphate-dextrose ratio (450 g blood per bag). The blood was stored at room temperature (25°C) without agitation until the time of reinfusion. Systolic blood pressure was maintained greater than 95 mm Hg with simultaneous crystalloid infusion through a distal Swan-Ganz catheter port or peripheral line, typically in a 2:1 ratio of crystalloid to blood removed. In both groups crystalloid infusion was augmented by alpha support (phenylephrine, 0.1 mg bolus injections) when hemodynamically indicated. The CPB circuit included a COBE membrane oxygenator (COBE Laboratories Inc, Lakewood, CO) and either a COBE roller pump or Biomedicus centrifugal pump (Biomedicus, Eden Prairie, MN). The circuit was primed with 2,100 mL of crystalloid solution (200 mL 25% albumin, 0.5 mg/kg mannitol, 1,700 mL lactated Ringer's solution). Intermittent anterograde cold blood cardioplegia with moderate systemic cooling (28° to 32°C) was used for all cases. Patients were anticoagulated after IAD removal but before CPB with 2 U/kg heparin sulfate. Additional heparin was administered to achieve and maintain an activated clotting time of 400 seconds. In the large-volume group one-unit aliquots of IAD blood were returned during CPB when needed to maintain a minimum hematocrit of 16%. Banked red blood cells were only used in this group after all IAD blood had been returned. In the control group the same minimum hematocrit was maintained using banked blood only. After CPB, following heparin reversal (2 mg/kg protamine sulfate), all remaining IAD blood was immediately returned to the patient centrally through a blood warming device at 38°C as rapidly as clinically possible, generally over a 20- to 30-minute period. Salvaged and residual circuit blood was processed using a cell-saving apparatus (Haemonetics Corp, Braintree, MA), and this blood was reinfused immediately after reinfusion of IAD blood in the large-volume IAD group, and at the equivalent time in the control group. In both groups, banked blood was used after CPB only after all available blood from the cell-saving device and IAD blood had been returned to the patient. Except for collection and reinfusion of IAD blood, all aspects of preoperative, intraoperative, and postoperative care were identical between groups. Shed mediastinal blood was returned to all patients for a maximum of 12 hours postoperatively using the Pleurovac ATS (Deknatel Inc, Fall River, MA) noncontinuous reinfusion system.
To ensure valid comparisons between groups a strict set of guidelines for the use of red blood cells, platelets, and coagulation factors was uniformly applied to all patients (Table 2). The time and criteria used for each transfusion were recorded (eg, 4 hours postoperatively; hematocrit, 21.4%) to confirm this uniformity.
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In addition to assessment of red blood cell, platelet, and coagulation function, a series of 95 other variables possibly affecting hematocrits, bleeding, or transfusion requirement were recorded for each patient. Patients were sequentially randomized by odd-even history number. All data were statistically analyzed using analysis of variance, Student's t test, 
2, and Fisher's exact tests where applicable. Results are expressed as either percent of total or mean plus or minus standard deviation. The study was approved by the hospital review board, and informed consent was obtained from all patients entered into the study.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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) [4]. Of the 90 patients enrolled, 1 patient (control group) was excluded from analysis after return to the operating room for bleeding and identification of a clear surgical source.
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In the IAD group 17% of patients required homologous red blood cell transfusions versus 52% in the control group (p < 0.01) (Fig 1), with an average number of units transfused per patient per group of 0.28 ± 0.66 and 1.14 ± 1.19 units, respectively (p < 0.01) (Fig 2). A total of 13 allogeneic red blood cell units were transfused in the IAD group versus 45 in the control group (p < 0.01). The timing of red blood cell transfusions is seen in Figure 3. No patient in either group required banked red blood cells during CPB. The majority of red blood cell transfusions in both groups (71.4%) occurred during the first 24 postoperative hours, with the major difference between groups also occurring during this period. Analysis of the red blood cell transfusion triggers used revealed no significant difference between the IAD and control groups in respect to the average trigger used (22.0% ± 2.4% versus 21.2% ± 1.5%, respectively). Five of the nine red cell transfusions (56%) in the IAD group were given for hematocrits above the established postoperative transfusion trigger of 21.9% (administered for clinically symptomatic anemia). In the control group 5 of 32 transfusions (16%) were given above this trigger, indicating that relative overtransfusion did not contribute to the increase in red blood cell transfusion observed in the control group.
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. During bypass the mean low hematocrit was significantly lower in the IAD group than in controls (17.6% ± 2.6% versus 21.6% ± 3.5%; p < 0.001). Eleven patients in the IAD group experienced hematocrits on bypass of 15% or less, versus no patients in the control group. The lowest hematocrit experienced on CPB was 13% (1 patient, IAD group). Reinfusion of part or all of the withdrawn IAD blood elevated the hematocrit to more than 15% in all 11 IAD patients with low hematocrits. After reinfusion of the remaining IAD blood and blood processed in the cell-saving device, hematocrits were significantly greater at 4 and 12 hours after CPB in the IAD group (32.5% ± 3.2% versus 29.8% ± 3.8%, and 30.7% ± 3.6 versus 28.2% ± 4.1; p < 0.05). From postoperative day 1 to postoperative day 7 there was a suggested but not significant difference in hematocrits between groups, despite the marked difference in red blood cell transfusions. When the hematocrit at each time point is corrected for the number of homologous red blood cell units transfused up to that time (by subtracting three percentage points for each unit transfused), the autologous red blood cell mass remaining in the patient at any given time is estimated, and the difference between groups made more apparent (Fig 5).
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). In addition, the incidence of moderately increased bleeding, delineated as chest tube output greater than 200 mL after the first postoperative hour (24% versus 25%) or 300 mL after the second postoperative hour (29% versus 25%), did not differ between the IAD and control groups. Likewise, the incidence of excessive bleeding requiring treatment with homologous platelet and coagulation factors, as defined by a chest tube output greater than 300 mL after the first postoperative hour (8.9% versus 11.4%) and 500 mL after the second postoperative hour (6.7% versus 6.8%), did not differ between the two groups. To further emphasize the lack of effect of IAD on postoperative bleeding, when the 13 patients who had four or more units of fresh autologous blood reinfused (mean, 1,925 ± 135 mL; 36% EBV; 4.3 ± 0.3 red cell unit equivalents; range, 1,800 to 2,250 mL) were compared with the remaining 76 patients in the study, no significant difference in postoperative bleeding was seen (Fig 7).
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) or the number of units transfused per patient per group (see Fig 2). No platelet or coagulation factors were administered intraoperatively, either before or after CPB, in either patient group. Transfusion trigger analysis revealed that 4 patients in each of the two groups met the criteria for platelet and fresh frozen plasma administration, and all 8 of these patients received appropriate transfusions. Platelets, fresh frozen plasma, or both were administered for bleeding rates lower than those stated in the transfusion guidelines to 2 patients in the IAD group and 1 patient in the control group. No patient in either group met the criteria for, or received, cryoprecipitate. Platelet counts did not differ between groups after IAD removal or during CPB, but were significantly higher in the IAD group at 24 hours postoperatively (138.1 ± 38.3 versus 117.9 ± 29.3 x 103/µL; p < 0.05). From postoperative day 2 to postoperative day 7 there was no significant difference between groups. Prothrombin times measured 2 hours postoperatively were significantly elevated over preoperative values in both groups, with no difference between groups (15.2 ± 1.6 versus 15.0 ± 1.6 seconds for control and IAD groups; p = not significant).
Because of the large difference in the percentage of patients receiving red blood cell transfusion in the IAD group, the percentage of patients exposed to any homologous blood (28% versus 59%; p < 0.05) was significantly less in the IAD group (see Fig 1). A decrease in the total number of homologous exposures for all blood products was suggested in the IAD group, but because of the lack of difference in platelet and coagulation factor use, this did not reach statistical significance (1.3 ± 2.8 versus 2.6 ± 4.1; p = 0.09) (see Fig 2).
There were no deaths in either patient group. One patient in the IAD group whose lowest hematocrit on CPB was 18% experienced an embolic stroke and postoperative renal insufficiency. Respirator time, inotrope requirement, length of intensive care unit stay, and postoperative length of stay did not differ between groups.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentReferences |
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), and have often removed this blood in a procedural context that may not have allowed for full expression of its effects. The results of these studies have therefore conflicted over the relative benefit of IAD in respect to measures of blood conservation such as transfusion requirement, postoperative bleeding, and platelet and coagulation number and function. It was our hypothesis that removal and preservation of a maximum volume of autologous blood would allow for the fullest expression of the effects of IAD, and therefore optimal evaluation of its benefit as a blood conservation technique. There are three essential elements to safely preserving the maximum amount of autologous blood while at the same time minimizing allogeneic exposure: (1) removal of a calculated safe maximum amount of blood from each individual patient based on the lowest acceptable level of anemia, (2) identification and use of the lowest safe level of anemia during CPB, and (3) reinfusion of IAD blood before banked blood for hematocrits below the lowest safe level to prevent potentially unnecessary homologous transfusion. These three elements are integrally linked to one another.
The IAD calculation takes into account the patient's EBV [9], the starting hematocrit in the operating room, the CPB circuit prime volume, and a target hematocrit on CPB of 18%. A target hematocrit of 18% is used to allow for both a one-unit margin of error and the typical 2 to 3 percentage point drift downward in hematocrit as CPB proceeds. By taking into consideration these parameters, the amount of blood withdrawn is safely maximized for each individual patient. The average mean low hematocrit on CPB of 17.6% ± 2.6% and the need for return of only a small portion of the total withdrawn IAD blood (16 of 131 total units removed; 12%) attest to the accuracy and safety of this method of IAD volume calculation and removal.
The lowest safe level of anemia has never been definitively established, and transfusion triggers used during CPB by surgeons and institutions differ widely. Clinical data regarding tolerance to anemia during CPB are largely anecdotal [4, 5] but point to a lower acceptable hematocrit level of 15%. Because the heart is relatively protected during CPB, other organs such as the brain serve as better markers of the adequacy of oxygen delivery. Recent data suggest that a hematocrit of 15% is adequate to maintain cerebral oxygen delivery under conditions of moderate hypothermia [6]. Laboratory data also support the safety of this level of anemia [7]. It has been our clinical experience that a hematocrit during CPB of 15% to 16% is well tolerated [3, 8], and we routinely use this number as the trigger for red blood cell transfusion during CPB employing moderate hypothermia.
The third element of effectively preserving the maximum amount of blood from the CPB circuit is the return of IAD blood before banked blood if the lowest safe hematocrit transfusion trigger is breached during CPB. This aspect of optimally applied IAD at first appears counterintuitive, until it is realized that the selective preservation of IAD blood for reinfusion after CPB, as practiced by many previous clinicians and investigators, relies upon the assumption that IAD blood is hemostatically useful. Three pieces of evidence reveal the assumption that IAD helps to decrease postoperative bleeding to be invalid, however. First, all prospective, randomized trials that have evaluated the prophylactic reinfusion of banked platelets and coagulation factors have revealed no significant benefit in respect to postoperative blood loss with the use of these products [10]. Second, the few IAD and platelet plasmapheresis studies that used a prospective, randomized format with adequate transfusion guidelines revealed no significant reduction in postoperative bleeding with prophylactic reinfusion of either fresh whole IAD blood or fresh platelet product [11, 12]. Third, and similarly, the present study demonstrates a clear lack of benefit in respect to bleeding, even when those patients who had the largest volume of blood removed and reinfused are analyzed separately (see Fig 7). Additional indirect evidence is provided by the fact that the postoperative chest tube output of those 11 patients in whom all or part of their IAD blood was transfused during CPB was not significantly greater than that of the remainder of the study (IAD and control) patients. This indicates that not having part or all of the IAD blood available after CPB did not lead to a relative detriment in coagulation function-even when one might clearly have been anticipated, given the more difficult bypass runs/operative procedures likely experienced by this patient group (as indicated by the increased need for intraoperative blood). Withholding IAD blood for reinfusion after CPB, therefore, cannot be justified on this basis of providing for improved postoperative hemostasis.
The second difficulty with reinfusing banked red blood cells before IAD blood during CPB is the potential to paradoxically increase homologous red blood cell use, particularly when large-volume IAD is used. Removal of such large volumes necessarily decreases the hematocrit during CPB. The chances of reaching hematocrits below the transfusion trigger are markedly increased by performing IAD, particularly if a sufficiently low transfusion trigger is not used. If banked blood is used for these breaches, patients with adequate overall autologous red blood cell mass (the IAD volume plus the volume remaining in the patient) may be transfused simply because the hematocrit was transiently and iatrogenically lowered during CPB by the IAD process. Adoption of the strategy of preferentially reinfusing IAD blood before banked blood in the present study allowed 5 of the 11 patients in the IAD group who required return of part or all of their IAD blood during CPB to be spared unnecessary homologous red blood cell transfusion, as postoperatively, after reinfusion of the remaining IAD blood, no additional homologous red blood cells or other blood products were required. Additional support can be found by assessing total red blood cell transfusion requirements in the two groups. Thirteen allogeneic red blood cell units were transfused in the IAD group, versus 45 in the control group. However, 16 units of IAD blood were returned during CPB in the IAD group. Had banked blood been given preferentially (and this autologous blood saved for post-CPB reinfusion), then the total number of allogeneic red blood cell transfusions administered in the IAD group would have been increased to 29, and the significant difference between groups in respect to this parameter would have been eliminated.
We found the use of large-volume IAD to be simple and safe. With judicious fluid replacement (1.9:1 crystalloid to blood removed ratio in the present study), hemodynamic stability and fluid status were adequately maintained, while at the same time unnecessary hemodilution was minimized. The average post-IAD/pre-CPB hematocrit of 32.5% ± 3.9% indicates that adequate oxygen carrying capacity was available both during and after the IAD process. A lack of ischemic changes on continuous electrocardiographic monitoring and urine output greater than 30 mL per hour in all patients during the pre-CPB period suggest the safety of removing large volumes of blood during the pre-CPB period. The lack of difference in postoperative outcome (ventilator time, length of intensive care unit stay, and length of hospital stay) between the two groups supports the overall safety of large-volume IAD, and of the blood conservation program in which it was employed.
By evaluating the individual blood compartments and using large IAD volumes that presumably served to magnify any effects that the technique might have, we were able to help discern the effects of IAD on these blood compartments. The first significant finding could perhaps be predicted: IAD preserves autologous red blood cell mass, as evidenced by decreased homologous red blood cell transfusion requirement in the IAD group. The decrease in red blood cell transfusion cannot be attributed to overtransfusion in the control group because (1) hematocrits were equal or higher in the IAD group at all postoperative time points and (2) analysis of transfusion triggers reveals that more transfusions (56% versus 16%) were given for hematocrits above the transfusion trigger in the IAD group than in the control group (these transfusions were given for clinically symptomatic anemia). Red blood cell preservation in the IAD group can be explained by two basic mechanisms. First, when one third of a patient's blood volume is removed and set aside, this portion of blood does not suffer the percentage loss (from hemorrhage and hemolysis) that it would suffer if left in the body and extracorporeal circuit [13, 14]. Second, because the remaining two thirds of the patient's red blood cell mass that does remain in the body are redistributed in the full blood volume, when blood losses do occur into lap pads and discard suckers, the number of red blood cells lost per milliliter of blood lost is decreased. Together these two processes could well account for the approximately one unit in red blood cell savings per patient in the IAD group (0.28 versus 1.18 units per patient per group). This one-unit savings was appreciated with removal and preservation of an average IAD of 3.4 red blood cell units. Removal of smaller IAD volumes would be expected to yield proportionately less red blood cell savings. This volume dependency of the red blood cell preserving effects of IAD may help to explain the lack of benefit seen in studies of IAD that have used smaller blood volumes.
The second important finding of this study is that IAD did not help to decrease postoperative bleeding. Neither the mean total chest tube drainage nor the incidence of excessive postoperative bleeding differed between the two groups. This finding persisted even when the 13 patients who had the largest volume of fresh red blood cells, platelets, and coagulation factors removed and reinfused (all greater than 4 units) were analyzed separately. Although this result is counterintuitive, and not fully supported by the previous literature (see Table 3), nor by the traditional reliance on allogeneic platelet and coagulation factor use during the postoperative period, there are at least two plausible explanations for this lack of benefit. First, the IAD withdrawal, storage, and reinfusion process may induce its own degree of platelet and coagulation factor loss and dysfunction. This could occur from multiple processes not unlike the exposure to the CPB circuit that is its purpose to avoid (eg, traumatic flow through needles and stop-cocks, activation by synthetic surfaces, exposure to standard hypothermic operating room temperature). Not supporting this first explanation for the ineffectiveness of IAD in decreasing postoperative bleeding is a large body of blood banking literature describing the appropriate collection, storage, and preparation of whole blood collected for component separation. The American Association of Blood Banks allows up to 8 hours of static room temperature citrate-phosphate-dextrose whole blood storage before component separation is performed [15]. Platelet and coagulation factor function and yield have been shown to be well preserved up to this time [16, 17]. Although shorter term autologous whole blood storage (without subsequent component processing) in the operating room setting has not been directly evaluated, it technically differs little from standard donor blood collection, and therefore platelet and coagulation factor numeric and functional yield would be expected to be at least as good.
A second explanation for the lack of benefit of large-volume IAD in respect to postoperative bleeding is that the coagulopathic process that accompanies all cardiopulmonary bypass-and that is still allowed to occur in the two thirds of the blood that remains in the patient-overwhelms the fresh IAD blood as it is returned to the patient. Cardiopulmonary bypass leads to a coagulopathic state [18]. This coagulopathy is multifactorial and can be attributed to platelet dysfunction, continuous low-level thrombin activation, fibrinolysis, white blood cell and inflammatory cascade activation, and abnormal red blood cell–white blood cell–platelet interactions. The reduction in postoperative bleeding seen clinically with the use of the serine protease inhibitor aprotinin, which blocks steps in several of the coagulation and inflammatory cascades, and which helps to preserve platelet function, provides evidence that varying degrees of this coagulopathy exist in every patient after CPB [19, 20]. It is well established that the antifibrinolytic agents are significantly more effective at decreasing postoperative bleeding if their use is begun before the initiation of CPB, rather than in the postoperative period once excessive bleeding has been identified [21]. This suggests that the prevention of the development of the coagulopathic state is likely more effective than attempts at correction once it has begun-whether this correction be with fresh autologous or allogeneic blood. Studies evaluating the randomized prophylactic administration of allogeneic and autologous platelets and coagulation factors during or immediately after CPB have not found such transfusions to be of benefit, and provide additional support for the use of preventive strategies, whether these be pharmacologic, technologic, or both [22–25]. If it is assumed that IAD blood is adequately preserved (ie, if a storage lesion that limits the hemostatic effectiveness of fresh whole IAD blood reinfusion does not develop), then the present study provides confirmation of the relative importance of coagulopathy prevention.
The lack of effect of the reinfusion of up to 5 units of fresh whole blood on decreasing postoperative bleeding points toward the complex nature of the coagulopathy of CPB, and demonstrates that the simple addition of platelets and coagulation factors to the post-CPB hematologic system is not enough to alter the course of this coagulopathy. This carries important implications regarding the transfusion of allogeneic platelet and coagulation factor concentrates in the early postoperative period (even if given according to recently advocated near-patient testing algorithms), indicating that these multiple donor exposures may be of limited value in cases in which platelet and coagulation factor levels are numerically sufficient. The lack of benefit seen with large-volume fresh whole blood reinfusion suggests that homologous platelet and coagulation factor concentrates administered for early post-CPB bleeding may provide physician comfort, and may often give the appearance of helping to terminate this bleeding, when in reality cessation of bleeding is only attributable to the passage of time, blood cell and plasma protein functional recovery, and clearance by the body of factors responsible for the initial coagulopathic state. The optimal method of treating the patient with early excessive postoperative bleeding indeed may not be one of immediate platelet and coagulation factor transfusion, with its attendant risks and costs, but one of careful observation (while limiting red blood cell losses during this observation period through shed blood reinfusion), combined with a low threshold for return to the operating theater for early severe or continued excessive bleeding. In our own clinical practice we have found that adherence to a set of transfusion guidelines that virtually eliminates the use of platelets and coagulation factors in the operating room, and that elevates the triggers for platelet and coagulation factor transfusion in the early postoperative period, has markedly decreased our need for these products, without compromising patient care. The low rates for platelet and coagulation factor use in the present study (which used a similar set of guidelines), coupled with the low incidence of return to the operating room for bleeding (1 patient) or other postoperative morbidity, attests to the safety and effectiveness of this simple overall approach.
In summary, maximum-volume IAD preserves as much autologous blood as possible from the detrimental effects of the CPB circuit. It therefore magnifies any impact that IAD might have on preserving the structure and function of blood, and on decreasing homologous transfusion requirement. By employing a prospective, randomized, and controlled trial format with a standardized set of transfusion guidelines, the present study clearly reveals that the primary effect of IAD is to prevent the loss of autologous red blood cell mass, as indicated by higher or equal postoperative hematocrits despite a significant reduction in homologous red blood cell transfusion. The routine use of IAD in all eligible patients can therefore be justified. However, our results indicate that the benefit of IAD is limited to the red blood cell compartment. Although an average of 3
units of fresh whole blood were reinfused after CPB, no decrease in postoperative bleeding could be appreciated. This carries important implications in respect to the treatment of the coagulopathy of CPB, concurring with previous studies suggesting that blood product transfusion in the early postoperative period provides limited benefit.
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L. Y. Lee, W. J. DeBois, K. H. Krieger, and O. W. Isom Transfusion Therapy and Blood Conservation Card. Surg. Adult, January 1, 2003; 2(2003): 389 - 400. [Full Text]
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K. Kottke-Marchant and S. Sapatnekar Hemostatic Abnormalities in Cardiopulmonary Bypass: Pathophysiologic and Transfusion Considerations Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 187 - 206. [Abstract] [PDF]
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W. J. DeBois and T. K. Rosengart Retrograde autologous priming reduces blood use Ann. Thorac. Surg., September 1, 1998; 66(3): 987 - 987. [Full Text] [PDF]
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T. K. Rosengart, W. DeBois, M. O'Hara, R. Helm, M. Gomez, S. J. Lang, N. Altorki, W. Ko, G. S. Hartman, O. W. Isom, et al. Retrograde Autologous Priming For Cardiopulmonary Bypass: A Safe And Effective Means Of Decreasing Hemodilution And Transfusion Requirements J. Thorac. Cardiovasc. Surg., February 1, 1998; 115(2): 426 - 439. [Abstract] [Full Text] [PDF]
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R. E. Helm, T. K. Rosengart, M. Gomez, J. D. Klemperer, W. J. DeBois CPP, F. Velasco, J. P. Gold, N. K. Altorki, S. Lang, S. Thomas, et al. Comprehensive Multimodality Blood Conservation: 100 Consecutive CABG Operations Without Transfusion Ann. Thorac. Surg., January 1, 1998; 65(1): 125 - 136. [Abstract] [Full Text] [PDF]
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