| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1996;62:1908-1917
© 1996 The Society of Thoracic Surgeons
Department of Anesthesia, Montreal Heart Institute, and University of Montreal, Montreal, Quebec, Canada
Abstract
Background. Several patient-, procedure-, and prescriber-related factors are thought to influence the decision to administer allogeneic blood products. We reexamine a number of assertions applied commonly to the practice of transfusion in cardiac operations.
Methods. More than 50 original articles including a total of more than 10,000 patients from 70 centers were reviewed. Data from 5,426 patients operated on between 1990 and 1994 at the Montreal Heart Institute are presented.
Results. From our review of the literature, we conclude that postoperative mediastinal fluid drainage averages 917 mL and that aspirin therapy increases drainage by less than 300 mL in most studies, which should not increase use of blood products, insofar as a strict transfusional protocol is adhered to. Across centers, transfusions can vary eightfold for the same postoperative drainage. Data from our institution show that postoperative mediastinal drainage per se is not influenced by reoperation or by the type of operation. However, total blood losses and transfusion requirements remain increased in reoperative and complex procedures. Excessive mediastinal drainage resulting in increased transfusions occurs in 29% of patients.
Conclusions. Exposure to allogeneic transfusions remains institution dependent. Constant reevaluation of local practice is essential to implement efficient blood conservation strategies.
The collective unconscious that underlies the practice of cardiac surgery is a rich melting pot, fed by numerous opinions, experiences, and, often, a small number of studies. Medical history, however, has repeatedly shown that a reappraisal of our beliefs can lead to more precise knowledge. Therefore, although the factors influencing postoperative mediastinal drainage are numerous and differentiating the chimera from truth remains difficult, we must attempt to sort through the conflicting evidence.
Since the clinical introduction of the cardiopulmonary bypass machine in 1953, cardiac operations have been associated with major requirements for allogeneic blood products. Forty years later, cardiac operation is the primary clinical circumstance requiring the transfusion of blood products for male patients and the secondary one for female patients (Canadian Red Cross, unpublished data). According to a multicenter survey conducted in 1991, 68% of patients undergoing primary coronary artery bypass grafting (CABG) required allogeneic blood transfusion [1].
Bleeding associated with cardiac procedures is a constant concern for a number of reasons. First, hemorrhaging reduces the adaptive capacity of the cardiovascular system to support the systemic and myocardial oxygen demand. The immediate postoperative period is particularly critical in this respect. Second, initial volume repletion with crystalloids or colloids, although maintaining intravascular volume, hemodilutes the normal components of blood. Third, although transfusional repletion seems needed when some 20% of blood volume is lost, particularly to restore oxygen transport capacity and hemostatic competence, the point at which the risks of transfusion outweigh the expected gains remains ill defined. Of concern, too, is the increasingly limited availability of specific blood products anticipated at the turn of the next century.
In everyone's mind, exposure to allogeneic blood products implies significant risks of disease transmission. Nonetheless, the risk of viral transmission has markedly declined over the years. Today, the overall risk of posttransfusional viral exposure is calculated to be 29.12 per million units of allogeneic blood products for human immunodeficiency virus, hepatitis C virus, hepatitis B virus, and human T-cell lymphoma virus combined [2]. Viral exposure has a 90% probability of transmitting the disease for human immunodeficiency virus, hepatitis B virus, and hepatitis C virus, and of 30% for human T-cell lymphoma virus [2]. Clinical outcomes after transfusion-associated hepatitis C remain disturbing. It is estimated that 60% of posttransfusional infections with acute hepatitis C virus result in chronic hepatitis. Of these patients, 51% will present with cirrhosis after 20 years and 5% will be diagnosed with hepatocellular carcinoma after a mean of 28 years [3].
Blood transfusion is also associated with less recognized viral hazards. A serious and frequent complication for the immunocompromised host is cytomegalovirus infection, the risk being that of reactivation (approaching 80%) or primary infection in a seronegative recipient. There is also the risk of cytomegalovirus infection after transplantation of a solid organ in a seropositive recipient, the rate ranging anywhere from 8% to 83% [4]. The greater infection rates are usually associated with major exposure to allogeneic blood [5]. Severity of infection and mortality rates are proportional to the level of immunosuppressive therapy, with mortality as high as 10% being reported [4]. Exposure to cytomegalovirus-seronegative blood products after cardiac transplantation, compared with administration of unscreened blood products, decreases cytomegalovirus infection from 20% to 0% in seronegative patients and grafts, and from 100% to 83% in seronegative recipients of seropositive heart transplants [6].
Since the major decline in transfusion-transmitted viral infections, several persistent but often underemphasized risks have moved to the forefront of transfusion medicine concerns. For example, it has been estimated that approximately 1 in 1,000 platelet concentrates is contaminated by bacteria. Thus, the risk of infection from contaminated platelets exceeds that of transmission of hepatitis B, hepatitis C, and human immunodeficiency virus combined. Moreover, the associated mortality rate resulting from sepsis has been estimated at 1 per 106 units transfused [7]. Certainly, until platelet bacteria can be screened rapidly and effectively, the septic events or deaths resulting from platelet contamination will remain underreported, inadvertently attributed to other causes such as catheter-related sepsis, for example.
Transfusion therapy must be considered as the transplantation of an imperfectly matched organ. In recent years, numerous cases of graft-versus-host disease have been recognized in immunocompetent individuals who received transfusions during cardiac operations [8, 9]. Not only do a high fever and an erythematous maculopapular rash develop, usually 3 to 30 days after transfusion, but also sepsis and hemorrhage, secondary to bone marrow hypoplasia, resulting in high morbidity and mortality rates (90%). The etiology of graft-versus-host disease involves the transfusion of donor cells homozygous for a human lymphocyte antigen haplotype shared by the recipient [10]. Of concern, in the white American population, the likelihood of this combination is 1 in 500. Directed donation from first- and second-degree family members, without previous irradiation of blood products, increases the risk of graft-versus-host disease.
The immunomodulation induced by allogeneic blood transfusion has been shown to favorably influence the prognosis of renal allograft transplantation, decrease the rate of relapse of inflammatory bowel diseases, and reduce the incidence of recurrent spontaneous abortion [11]. In contrast, a comparison of allogeneic blood transfusions with syngeneic (autologous) blood exposure has shown the former to result in a greater rate of postoperative septic complications [12]. Allogeneic blood transfusions significantly increase the risk of postoperative infections after cardiac operations [13–15], and this risk increases with the number of units transfused [13]. The combined immunosuppressive effect of allogeneic blood transfusion and hemorrhage is, presumably, involved in the high infection rate associated with late mediastinal reexploration for hemostasis [16].
Clearly, no matter how safe blood products may become, physicians must always consider them a potential vector for new diseases. Our fundamental goal must be to minimize and, ultimately, eliminate altogether the need for allogeneic blood products. Blood loss should be recognized for what it is-merely an intermediate outcome of the blood transfusion issue.
Determinants of Allogeneic Blood Product Use
The exact circumstances requiring blood product transfusion remain controversial and empiric. By and large, though, the decision to transfuse is influenced by the clinical knowledge and practice style of the prescribing doctor, the organizational context [17], and the degree of medical consensus [18]. Approximately 18% of blood products are transfused inappropriately [19]. Undoubtedly, continuing medical education in effective management of blood products is of utmost importance.
The need to transfuse is directly influenced by the hematologic reserve. One clear transfusion predictor is preoperative red blood cell (RBC) volume [20, 21]. This predictor is influenced by the age, sex, body surface area, and weight of the patient, as well as by the preoperative hematocrit [20]. Urgent operation, catheterization-induced coronary occlusion, cardiogenic shock, older age, and associated medical conditions are other preoperative predictors of RBC transfusions after CABG [22], possibly because these patients are perceived as having a decreased capacity to compensate for anemia and, consequently, are given transfusions more readily. Unfortunately, in most cases, these factors cannot be modified (corrected) before the anticipated operation. This explains the strong emphasis in the literature on the second major predictor of transfusion, ie, blood lost during and after the surgical procedure. The volume of postoperative mediastinal fluid collected in the drainage system during a given period of time is the usual element of comparison in a majority of studies.
Blood loss associated with cardiac surgery is the sum of two factors: (1) the quality of surgical hemostasis, keeping in mind it is not possible to coagulate or ligate each and every blood vessel severed during the surgical procedure; and (2) the physiologic mechanisms involved in the compensation and correction of active bleeding (essentially the hemostatic system). Imbalance between these factors may result in excessive bleeding. However, given the dynamic and potent action of the hemostatic system in reaction to aggression or in response to treatment of hypocoagulable states, postoperative prothrombotic states may become prevalent in a significant number of patients and must be anticipated and treated also.
"Normal" Blood Losses Associated With Cardiac Operations
Obviously, excessive bleeding after a cardiac operation is a stressful event for patients and for physicians. The concern though, is how to differentiate "excessive" from the "usual, normal, or expected" blood losses after a cardiac operation. "Normal or expected" mediastinal drainage is the result of an optimal surgical control of potential bleeding sites and of the appropriate physiologic response to bleeding. Rupture of this equilibrium can result in hemorrhage or thrombosis.
After reviewing 52 cardiac surgical studies* conducted since 1987 and involving approximately 10,000 patients in 70 centers, we calculated patients in the control groups bled an average of 917 mL (range, 400 to 2,200 mL). The wide range of values reported suggests a multifactorial origin of bleeding, ie, both defective surgical hemostasis and coagulation may be responsible for the increased post–cardiopulmonary bypass (CPB) mediastinal drainage observed. Unfortunately, it is impossible to isolate the contribution of surgical hemostasis to these figures. To the mean value of 917 mL must be added the losses occurring during the operation, the precise measurement of which is much more difficult. Based on the data available from the Montreal Heart Institute (Table 1
), mean intraoperative blood losses may be (cautiously) estimated to range from 500 to 1,200 mL. Lower intraoperative blood losses occur in first-time cardiac operations, the greater intraoperative blood losses being associated with reinterventions. Thus, the mean total blood losses anticipated during a primary cardiac intervention will be approximately 1,400 mL, a value of the same order of magnitude as those reported for total hip arthroplasty [23].
|
Excessive mediastinal drainage after CPB is secondary to either a coagulopathy (congenital, acquired, or drug-induced) or a surgical failure. Although the literature has no standardized definition of excessive bleeding, it does present possible indicators (guidelines) of the need for a reoperation. For example, Kirklin and Barratt-Boyes [24] advise mediastinal exploration for a chest tube drainage of more than 10 mL/kg in the first hour after operation or of more than 20 mL/kg over the first 3 hours after operation. As well, a drainage of greater than 300 mL/h after minimal previous blood loss usually indicates surgical failure, thereby warranting intervention. More detailed algorithms are also used: 200 mL/m2 or more during a 1-hour period, greater than or equal to 150 mL/m2 per hour, during a 2-hour period, greater than or equal to 100 mL/m2 per hour during a 4-hour period, or greater than or equal to 80 mL/m2 per hour during a 12-hour period [25]. Etiology aside, the occurrence of different speeds of blood loss during different periods of time has also been used as a criterion of excessive bleeding (250 to 400 mL/h during the first 2 to 8 postoperative hours, for example). With moderate rates of bleeding (50 to 150 mL/h), a coagulopathy is usually suspected [26].
Mediastinal exploration, as an indicator of excessive chest tube drainage, is required in 0% to 14% of cases [20, 25, 27–30] (Table 2). Unsurprisingly, resternotomy for postoperative bleeding is a significant predictor of allogeneic blood transfusion [20]. However, reoperation for bleeding should be considered as a marker rather than a determinant of unfavorable outcomes such as increased blood requirements, infection, and increased mortality. Early reoperation to control surgical bleeding and decrease local fibrinolysis [31] should be considered an important aspect of a multimodal approach to postoperative hemorrhage.
|
In practice, the definition of profuse mediastinal drainage remains extremely variable. Rather than adopt any arbitrary definition, it would appear more rational to define excessive mediastinal drainage as it relates to final outcome, eg, exposure to allogeneic blood products. Ferraris and Gildengorin [21] identified, albeit empirically, excessively transfused patients as those requiring more than 5 units of allogeneic blood products. A review of 3,022 patients operated on at the Montreal Heart Institute between November 1990 and December 1994 showed that a postoperative chest drainage of more than 1,000 mL is associated with an accelerating rate of exposure to blood products [33]. Consequently, 1,000 mL is our local definition of profuse mediastinal drainage after CPB, being associated with transfusional needs greater than 5 units of allogeneic blood products. Smaller blood losses could, conceivably, be managed without allogeneic blood transfusions in a majority of our patients. Thus, depending on local practice, excessive mediastinal drainage may be different in terms of the absolute volume of blood lost.
The incidence of excessive mediastinal drainage in 5,426 patients operated on during a 4-year period at the Montreal Heart Institute (presented in more detail below) is presented in Figure 1. Excessive postoperative mediastinal drainage, defined in this case as a total volume of more than 1,000 mL, occured in 29% of cardiac procedures. No distinction, vis-à-vis excessive postoperative drainage, characterized the type of operation and the reoperation group (p > 0.07).
|
Intuitively, one expects greater blood losses after more complex surgical procedures and after reinterventions. Four studies, each with a large number of patients, have compared postoperative mediastinal drainage associated with various cardiac procedures [25, 27, 28, 34]. Postoperative blood losses and requirement for allogeneic blood products of patients in the control groups of these studies are shown in Table 3.
|
Subsequently, postoperative and total blood losses as they relate to different cardiac operations were reevaluated at the Montreal Heart Institute (5,426 procedures between November 1990 and December 1994). Data were collected, processed, and analyzed as reported in 1991 [34]. Nevertheless, two major differences exist between the present cohort and that described previously. First, cardioplegia is now performed using a sanguineous rather than a crystalloid solution. Second, temperature during CPB is maintained between 32°C and 34°C instead of 28°C as was the case between 1988 and 1990. Antifibrinolytics were not administered systematically during either study period. This reevaluation has shown results similar to those reported in the original study (see Table 1
).
The four studies described in Table 3 [25272834] and the data presented in Table 1 suggest that postoperative chest tube drainage no longer differs after revascularization, valvular, or combined surgical procedures. Also, contrary to firmly entrenched convictions, reoperations in general do not entail supplemental postoperative mediastinal drainage, despite a significantly longer exposure to CPB (see Table 1). Even more interesting, postoperative blood loss associated with reoperative CABG in particular is significantly reduced, as compared with first-time procedures (see Table 1). These findings agree with those of Øvrum and associates [28]. No doubt the increasing availability of different pharmacologic and nonpharmacologic therapeutic modalities partially accounts for this improvement. However, intraoperative and total blood losses are still related to the type of operation performed, increasing in parallel with the extent of the operation (see Table 1).
Other, less obvious factors may influence significantly blood losses after cardiac operations. Blood accumulated in the pericardial and pleural spaces during CPB shows altered hemostatic function secondary to tissue contact, stagnation, and air/pressure trauma. The retransfusion of this collected and highly activated blood is potentially hazardous to hemostasis [35], inasmuch as it is associated with a systemic stimulus of the clotting and fibrinolytic systems. De Haan and associates [35] reported blood losses of 822 ± 76 mL during the first 24 postoperative hours in patients retransfused with this blood, compared with 611 ± 75 mL in patients in whom this blood was retained (p < 0.05). Despite wastage of the suctioned blood (780 ± 210 mL), the volume of transfused erythrocytes and particularly plasma in the retainment group was smaller, although not significantly so. There is no major doubt that shed mediastinal blood is hemostatically inadequate [36]. The study by de Haan and associates [35] is the first to describe the impact on hemostasis and postoperative bleeding of retransfusing the blood shed and collected during full heparinization and CPB. As for the studies on the retransfusion of mediastinal blood shed after CPB, the impact on bleeding and the need for allogeneic blood products may vary from center to center.
Blood Losses and Aspirin Therapy
Aspirin has been shown to improve venous graft patency after CABG [37] and to reduce the incidence of myocardial infarction in primary and secondary prevention trials [3839]. Discontinuation of aspirin therapy results in abnormally high platelet activity, and it has been proposed that, in patients with advanced coronary artery disease, aspirin not be withdrawn to avoid the risk of thrombosis [40]. Thus, a large number of patients coming for myocardial revascularization may be on aspirin therapy at the time of operation. The widespread clinical impression is that aspirin therapy is associated with increased postoperative bleeding and transfusion of allogeneic blood products. However, the data presented in Table 4 show that the effects of aspirin on bleeding and transfusion requirements are inconsistent [41–53]. Several factors may explain this inconsistency of aspirin effect.
|
Also, aspirin ingestion can reveal a preexisting "Intermediate syndrome of platelet dysfunction" [56], resulting in an insufficient hemostatic reserve. This state, combined with the hemostatic trauma secondary to exposure to the CPB circuit, may be associated with excessive postoperative bleeding [21]. Presumably, this subgroup of patients is, for the most part, responsible for the bad reputation of aspirin in cardiac surgery.
So, should aspirin administration be stopped preoperatively? Presumably, this is not necessary in the majority of patients, considering the limited increase in postoperative blood loss, as shown by most of the recent studies detailed in Table 4 [41, 43, 45–47, 53]. This small increase in postoperative bleeding (<300 mL in most cases) should not result in increased exposure to allogeneic blood products if a strict transfusion protocol is adhered to. On the other hand, it appears prudent to discontinue aspirin administration in those patients who are particularly sensitive to its effects (tentatively defined by a prolongation of the bleeding time greater than 10 minutes), or those scheduled for high-risk surgical procedures [57]. Alternatively, when aspirin cannot be withdrawn for fear of precipitating an acute coronary event, the intraoperative administration of aprotinin has been shown to decrease bleeding and transfusion requirements after CPB in these patients [51].
Requirements for Allogeneic Blood Products and Type of Cardiac Operation
Despite the above, exposure to allogeneic blood products remains dependent mainly on the type of procedure performed. As shown by Hardy and associates [34], patients undergoing combined CABG and valve replacement operations received significantly more allogeneic RBC units. Combined CABG and valve operations were associated with increased platelet transfusions [34]. Also of interest, reoperations were associated with increased transfusions of allogeneic RBCs, except in reoperations for combined CABG and valvular procedures [34]. Table 5 illustrates the dichotomy observed between postoperative mediastinal drainage and allogeneic blood exposure. These apparently increased requirements for allogeneic blood products after reoperations, despite similar postoperative blood losses, may be explained in several ways. First and clearly, the additional blood lost during the operation (see Table 1) has to be compensated for by additional RBCs. This increased requirement for RBCs is probably appropriate, considering hemoglobin concentrations at the time of discharge were similar in patients undergoing primary and reoperative procedures [34]. Second, however, as described previously [158], it may reflect inappropriate transfusional habits regarding RBCs and hemostatic blood products.
|
Transfusion Trigger
Increasingly, it is recommended that the transfusion trigger be adapted to the dynamic physiologic condition and reserve of the patient. Consequently, additional parameters for erythrocyte transfusion must be introduced, subject to rigorous evaluation. These may include measures of oxygen delivery and consumption, arteriovenous gradient in pH, venoarterial gradient in carbon dioxide tension, and circulating lactate concentration. All these parameters may be applied to whole body or specific organ function.
Empiric or subjective approaches to transfusions can no longer be justified. Hematocrit values alone are not a proper transfusion trigger, as RBC transfusion protocols based exclusively on a critical hematocrit value cannot distinguish between true blood losses and the effect of hemodilution (factitious anemia). Acceptance of a lower transfusion trigger has a significant impact on the requirement for allogeneic blood products and is well tolerated by patients after a cardiac procedure. A prospective study of 24 institutions (2,375 patients) conducted by the Multiple Centers Study of Perioperative Ischemia research group [59] examined the influence of the intensive care unit entry hematocrit on the risk of myocardial infarction and death after CABG. Patients with a very low hematocrit (<18%, n = 18) had no myocardial infarction or death. Moderate anemia (hematocrit 
34%) upon entering the intensive care unit actually reduced the risk of perioperative myocardial infarction.
Allogeneic blood products are indicated mainly to correct anemia and defective hemostasis. Physicians confronted with a clinical coagulopathy require monitoring of hemostasis in a timely manner to guide transfusional practice. Even if this approach is still far from perfect, hemostatic blood products should be administered only after the results of coagulation testing have been interpreted comprehensively. Despotis and associates [58] suggest the perioperative use of a transfusion algorithm with on-site coagulation data (platelet count, prothrombin time, and activated partial thromboplastin time) to decrease intraoperative and postoperative exposure to allogeneic blood products. As mentioned previously, despite the varying number of blood products transfused, the total RBC volume lost during hospitalization remained constant [58], indicating, once more, the inappropriateness of the "shotgun therapy" approach.
Blood Loss, Transfusion Practice, and Institutional Variability
Mediastinal blood loss associated with elective CABG varies notably. A survey of 18 tertiary-care hospitals in 1991 reported wide-ranging means of estimated RBC volumes lost during hospitalization (mean for all patients = 1,016 ± 25 mL, with institutional means ranging from 672 to 1,445 mL) whereas patient-related factors, such as age, RBC volume, and whole blood volume, were similar [1]. Surgical factors may explain part of these differences because both the duration of CPB and estimated total blood lost during hospitalization (means ranging from 744 to 1,564 mL) varied significantly among the 19 surgeons studied [1]. However, in a single institution, this influence of the attending surgeon (n = 8) on postoperative mediastinal drainage may not be observed [34]. Perhaps the quality of surgical hemostasis and a number of small variations in technique difficult to appreciate with precision at present may explain the variability observed between surgeons and institutions.
Transfusion practices also vary widely among institutions despite similar patient characteristics. Using the data presented in Goodnough and associates' [1] study, we calculated the ratio of mediastinal bleeding to RBCs transfused for the institutions surveyed. This ratio ranged from 229 mL to 1,882 mL of blood shed per unit of RBCs transfused. Interestingly, these eightfold variations of the bleeding/transfusion ratio were inversely related to the mediastinal bleeding reported after CPB, suggesting that the institutions where bleeding was most important also tended to overtransfuse blood products. Transfusion of RBCs remained different among institutions after controlling for patient and surgical variables, confirming the above and suggesting the application of different transfusion protocols (including autologous blood predonation or acute hemodilution) or the inappropriate application of accepted protocols.
Transfusion practices change over time. The science of transfusion medicine has accelerated the development and the application of transfusional protocols. The introduction of different blood-conservation techniques in a transfusional protocol requires a precise evaluation of their impact, ideally under the supervision of a multidisciplinary transfusion committee [60]. A quality assessment program to study transfusion practices has a number of advantages: data are collected and transfusion practices can be monitored; it can contribute to education and research, resulting in improved patient care; and blood products can be used more efficiently. Parameters to establish a quality assessment program and a transfusion committee have been reviewed elsewhere [60]. Table 6 [3058616263] illustrates the significant impact of different institutional commitments on total allogeneic blood exposure. Use of a comprehensive blood conservation program allowed 97% of 2,298 patients undergoing primary CABG to avoid any allogeneic blood product [28]. Clearly, each institution should be evaluating its own practice continuously to identify and improve its profile. Inappropriate institutional practice may minimize and even negate the results of otherwise efficacious, often expensive blood-sparing modalities.
|
Both empiric and prophylactic transfusion of blood components in adult cardiac operations are not supported by the literature. Rather, the ultimate goal is to reduce or eliminate altogether exposure of patients to allogeneic blood products. Many factors (either known, suspected, or unidentified at present) influence the achievement of this goal, thereby necessitating a constant monitoring of transfusional practices by multidisciplinary transfusion committees in all cardiac centers. The two major prerequisites for effective control of allogeneic blood exposure, however, are meticulous surgical hemostasis and adherence to widely accepted transfusion protocols. These two elements must absolutely be in place before the addition of pharmacologic or nonpharmacologic blood-sparing strategies is adopted.
Is bloodless cardiac surgery a chimera? In a number of cases, surely. Nonetheless, the judicious choice of different blood conservation approaches and a constant concern over transfusions may allow clinicians to achieve this objective, at least in part. At the dawn of the third millennium it is now reasonable to think that primary CABG will indeed be recognized shortly as a bloodless surgical procedure.
Footnotes
Address reprint requests to Dr Bélisle, Department of Anesthesia, Montreal Heart Institute, 5000 Bélanger St E, Montreal, PQ H1T 1C8, Canada.
* A complete bibliography is available from the authors upon request. 
References
This article has been cited by other articles:
|
|
 |
|
  A. J. Chapman, A. L. Blount, A. T. Davis, and R. L. Hooker Recombinant factor VIIa (NovoSeven RT) use in high risk cardiac surgery Eur J Cardiothorac Surg, December 1, 2011; 40(6): 1314 - 1319. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Hacquard, M. Durand, T. Lecompte, S. Boini, S. Briancon, and J.-P. Carteaux Off-label use of recombinant activated factor VII in intractable haemorrhage after cardiovascular surgery: an observational study of practices in 23 French cardiac centres (2005-7) Eur J Cardiothorac Surg, December 1, 2011; 40(6): 1320 - 1327. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Vuylsteke, C. Pagel, C. Gerrard, B. Reddy, S. Nashef, P. Aldam, and M. Utley The Papworth Bleeding Risk Score: a stratification scheme for identifying cardiac surgery patients at risk of excessive early postoperative bleeding Eur J Cardiothorac Surg, June 1, 2011; 39(6): 924 - 930. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. S. Myles Stopping Aspirin Before Coronary Artery Surgery: Between the Devil and the Deep Blue Sea Circulation, February 15, 2011; 123(6): 571 - 573. [Full Text] [PDF]
|
|
|
|
 |
|
 T.-H. Chen and R. Matyal The Management of Antiplatelet Therapy in Patients With Coronary Stents Undergoing Noncardiac Surgery Seminars in Cardiothoracic and Vascular Anesthesia, December 1, 2010; 14(4): 256 - 273. [Abstract] [PDF]
|
|
|
|
 |
|
 A. C. Logan and L. T. Goodnough Recombinant Factor VIIa: An Assessment of Evidence Regarding Its Efficacy and Safety in the Off-Label Setting Hematology, December 1, 2010; 2010(1): 153 - 159. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Mollmann, H. M. Nef, and C. W. Hamm Antiplatelet therapy during surgery Heart, June 1, 2010; 96(12): 986 - 991. [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Reddy, S. Talwar, D. Velayoudam, P. Gharde, V. Mallick, R. K. Jha, L. Kumar, and S. K. Arkalgud Multi-modality blood conservation strategy in open-heart surgery: an audit Interact CardioVasc Thorac Surg, September 1, 2009; 9(3): 480 - 482. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. O'Riordan, R. J. Margey, G. Blake, and P. R. O'Connell Antiplatelet Agents in the Perioperative Period Arch Surg, January 1, 2009; 144(1): 69 - 76. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Y. Lee, W. J. DeBois, K. H. Krieger, and O. W. Isom Transfusion Therapy and Blood Conservation Card. Surg. Adult, January 1, 2008; 3(2008): 415 - 430. [Full Text]
|
|
|
|
 |
|
 P.-G. Chassot, A. Delabays, and D. R. Spahn Perioperative antiplatelet therapy: the case for continuing therapy in patients at risk of myocardial infarction Br. J. Anaesth., September 1, 2007; 99(3): 316 - 328. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 The Society of Thoracic Surgeons Blood Conservatio, V. A. Ferraris, S. P. Ferraris, S. P. Saha, E. A. Hessel II, C. K. Haan, B. D. Royston, C. R. Bridges, R. S.D. Higgins, G. Despotis, et al. Perioperative Blood Transfusion and Blood Conservation in Cardiac Surgery: The Society of Thoracic Surgeons and The Society of Cardiovascular Anesthesiologists Clinical Practice Guideline Ann. Thorac. Surg., May 1, 2007; 83(5_Supplement): S27 - S86. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Dial, E. Delabays, M. Albert, A. Gonzalez, J. Camarda, A. Law, and D. Menzies Hemodilution and surgical hemostasis contribute significantly to transfusion requirements in patients undergoing coronary artery bypass J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 654 - 654. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. P. Cannon, S. R. Mehta, and S. F. Aranki Balancing the Benefit and Risk of Oral Antiplatelet Agents in Coronary Artery Bypass Surgery Ann. Thorac. Surg., August 1, 2005; 80(2): 768 - 779. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. K. Banbury, J. A. White, E. H. Blackstone, and D. M. Cosgrove III Vacuum-assisted venous return reduces blood usage J. Thorac. Cardiovasc. Surg., September 1, 2003; 126(3): 680 - 687. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Karski and J. T. Balatbat Blood Conservation Strategies in Cardiac Surgery Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2003; 7(2): 175 - 188. [Abstract] [PDF]
|
|
|
|
 |
|
 A. Sedrakyan, K. Gondek, D. Paltiel, and J. A. Elefteriades Volume Expansion With Albumin Decreases Mortality After Coronary Artery Bypass Graft Surgery Chest, June 1, 2003; 123(6): 1853 - 1857. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Durand and O. Chavanon Does hydroxyethyl starch increase blood loss in cardiac operations Ann. Thorac. Surg., May 1, 2003; 75(5): 1682 - 1683. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
B. Collier, J. Kolff, R. Devineni, and L. S. Gonzalez III Prophylactic positive end-expiratory pressure and reduction of postoperative blood loss in open-heart surgery Ann. Thorac. Surg., October 1, 2002; 74(4): 1191 - 1194. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Johnell, G. Elgue, R. Larsson, A. Larsson, S. Thelin, and A. Siegbahn Coagulation, fibrinolysis, and cell activation in patients and shed mediastinal blood during coronary artery bypass grafting with a new heparin-coated surface J. Thorac. Cardiovasc. Surg., August 1, 2002; 124(2): 321 - 332. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. M. Wilkes Reply Ann. Thorac. Surg., May 1, 2002; 75(5): 1683 - 1683. [Full Text] [PDF]
|
|
|
|
|
|
P. R. Belcher and E. W. Muriithi Coronary artery bypass grafting surgery without the routine application of blood products: is it feasible? Eur J Cardiothorac Surg, November 1, 2001; 20(5): 1078 - 1078. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
M. M. Wilkes, R. J. Navickis, and W. J. Sibbald Albumin versus hydroxyethyl starch in cardiopulmonary bypass surgery: a meta-analysis of postoperative bleeding Ann. Thorac. Surg., August 1, 2001; 72(2): 527 - 533. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Lehman, R. C. Blaylock, D. P. Alexander, and G. M. Rodgers Discontinuation of the Bleeding Time Test without Detectable Adverse Clinical Impact Clin. Chem., July 1, 2001; 47(7): 1204 - 1211. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. W. Muriithi, P. R. Belcher, S. P. Day, V. C. Menys, and D. J. Wheatley Heparin-induced platelet dysfunction and cardiopulmonary bypass Ann. Thorac. Surg., June 1, 2000; 69(6): 1827 - 1832. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. D. Williams, S. L. Bratton, and C. Ramamoorthy Factors Associated with Blood Loss and Blood Product Transfusions: A Multivariate Analysis in Children After Open-Heart Surgery Anesth. Analg., July 1, 1999; 89(1): 57 - 57. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. R. Dalrymple-Hay, L. Pack, C. D. Deakin, S. Shephard, S. K. Ohri, M. P. Haw, S. A. Livesey, and J. L. Monro Autotransfusion of washed shed mediastinal fluid decreases the requirement for autologous blood transfusion following cardiac surgery: a prospective randomized trial Eur J Cardiothorac Surg, June 1, 1999; 15(6): 830 - 834. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. D. Williams, S. L. Bratton, E. C. Riley, and C. Ramamoorthy Association between age and blood loss in children undergoing open heart operations Ann. Thorac. Surg., September 1, 1998; 66(3): 870 - 875. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Gammie, M. Zenati, R. L. Kormos, B. G. Hattler, L. M. Wei, R. V. Pellegrini, B. P. Griffith, and C. M. Dyke Abciximab and Excessive Bleeding in Patients Undergoing Emergency Cardiac Operations Ann. Thorac. Surg., February 1, 1998; 65(2): 465 - 469. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
