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Thromboelastogram and postoperative hemorrhage
810
CORRESPONDENCE
surgery maintain, to speed, simplify, and magnify the exchange of ideas, methods, and techniques.
Ann Thorac Surg 1992;54:809-16
n OXYGEMJM
Richard A. Hopkins, M D Department of Surgery Georgetown University Medical Center 3800 Reservoir Road NW Washington, DC 20007-2197
Reply
PUMP
PUMP
Fig 1 . Simple delivery circuit for continuous normothermic blood cardioplegia.
To the Editor:
I am grateful to Mr Gunning for researching the history of the aortic homograft so thoroughly. I have no doubt that in every field of endeavour there will be prior claims registered or uncovered as far back probably as Leonard0 da Vinci. I must confess that I was not aware of Heimbecker and Bigelow's attempt, but knowing these two pioneers, I am not surprised. We like to credit Conrad Lam with the concept of using the homograft aortic valve, which he published in 1952. It was his work that stimulated us and we followed it up in the dog laboratory in Guy's Hospital under the auspices of Lord Brock (Brewin) [l]. The rest is history.
Donald Ross, FRCS 25 Upper Wimpole St London W 1 M 7 T A England
Reference 1. Brewin EG. The use of tissue transplants in the surgery of cardiac valve disease-an experimental study. Guy's Hosp Rep 1956;105:328-39.
Continuous Normothermic Blood Cardioplegia: Simplified Delivery Circuit To the Editor: We have been following with keen interest the development of "warm" blood cardioplegia [l-31. We have used this method of myocardial protection in 50 patients. Patients with congenital heart disease formed a predominant group in our experience, besides those with coronary and valvular procedures. In the first 25 patients we used the pump circuit and dilution of blood as reported by Lichtenstein and associates. However, in the last 25 patients we have adopted the following modifications in the method of cardioplegia delivery which, we believe, have simplified the pump circuit considerably: (1)use of blood directly from oxygenator for continuous perfusion of aortic root, (2) fixed flow rate of aortic root perfusion (1to 2 mL * kg-' * min-' to maintain aortic root pressure at 80 mm Hg) and varying potassium concentration for induction and maintenance of cardiac arrest, and (3) use of a syringe pump for infusing potassium chloride solution into the cardioplegia line just beyond the cardioplegia delivery pump (Fig 1). The syringe infusion pump is filled with the commercially available potassium chloride solution, and it is connected to the side port of the straight connector interposed in the cardioplegia line just beyond the cardioplegia pump. Once full flows are achieved on standard cardiopulmonary bypass the aorta is clamped and the syringe pump is switched on at a predetermined setting to deliver a 0.1 mEq . kg-' . min-' dose of potassium chloride solution to stop the heart in 3 to 5 minutes (induction
dose), and then the infusion rate is adjusted to give 0.005 to 0.01 mEq * kg-' . min-' potassium to sustain the cardiac arrest (maintenance dose). Small purges may be needed occasionally to sustain the arrest. In the final stages of intracardiac repair the potassium infusion is stopped but continuous normothermic infusion is continued for some time, and the aorta is declamped with suction on the aortic root. In our practice, we believe that this is a much simpler circuit to handle and it allows more precise control over the amount of potassium that is being delivered. Because we are using blood directly from the oxygenator, there is no need for any further heat exchanger in the circuit. The use of additional crystalloid solution for dilution and the use of solutions containing varying quantities of potassium are also avoided [l, 3, 41.
Ponangi V . Satyanarayana, M S , MCh Podila Sita Rama Rao, M S , MCh Kesavaram Madhusudhana Rao, BSc, CCP Alluru Sarath Chandra, M S Kanchumarthi Sudhakar Rao, M S Karri Venkat Reddy, M S Department of Cardio Thoracic Surgery Nitam's Znstitute of Medical Sciences Hyderabad, 500 482 India
References 1. Lichtenstein SV, Ashe KA, El Dalati H, Cusimano RJ, Panos A, Slutsky AS. Warm heart surgery. J Thorac Cardiovasc Surg 1991;101:269-74. 2. Lichtenstein SV, Fremes SE, Abel JG, Christakis GT, Salerno TA. Technical asuects of warm heart surgery. " , .I Card Sura 1991;6:2:278-84. 3. Lichtenstein SV, El Dalati H, Panos A, Slutskv AS. Long " cross-clamp with warm heart surgery. Lancet 1989;1:1443. 4. Tutassaura H. Continuous warm blood cardioplegia. Ann Thorac Surg 1991;51:866. v
Thromboelastogram and Postoperative Hemorrhage To the Editor: The recent article "Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients" by Wang and associates [ l ] provides an interesting contrast to most prior work in this area [2-51. Indeed, this represents the only report that finds no predictive accuracy or advantage of thromboelastography (TEG) over routine coagulation testing. Perhaps some of the following discussion and points may explain this obvious discrepancy. Wang and associates note the most common abnormalities before cardiopulmonary bypass were hypocoagulability and fibrinolysis. The mean values for TEG reaction time values were considerably higher than postbypass values, and the mean
CORRESPONDENCE
Ann Thorac Surg
811
1992;54809-16
activated clotting time values were higher (156 2 28.5 seconds) than values routinely considered as normal. These two facts suggest that some patients must have been receiving preoperative heparin infusions. Low-dose preoperative heparin infusions may cause profound prolongations of the reaction time value and also affect the coagulation time and maximum amplitude. The reaction time value may be of infinite length with such therapy, and if this occurred in any of the 101 patients studied, then correlations between activated clotting time, activated partial thromboplastin time, and the TEG reaction time value would be largely dependent on how the statistical analysis of these data was handled. The demographics given do not allow one to decide if that was actually a problem for the investigators. Other pertinent pieces of information such as the incidence of emergency cases and use of platelet inhibitors and fibrinolytics are missing. The preoperative data show a tendency toward fibrinolysis (mean amplitude 60 minutes after the maximum amplitude was 20% less than the maximum amplitude). This alone suggests that some patients must have received streptokinase tissue plasminogen activators or urokinase therapy before entrance into the operating rooms. The large standard deviation in the amplitude 60 minutes after the maximum amplitude also suggests that some subpopulation of patients (n = 16) had profound lysis. If patients on thrombolytic therapy and heparin therapy are included in the study population, it would be unlikely that the maximum amplitude would have any correlation with platelet count, as both of these therapies greatly affect platelet function. The TEG tests not only platelet count, but also platelet function. Our prior studies wherein some weak correlations were demonstrated before bypass avoided patients with heparin or thrombolytic therapy specifically to avoid these compounding variables [31. After bypass the only coagulation data collected were from the time immediately after protamine administration. Those coagulation data were correlated with measured chest tube drainage for periods over the subsequent 24 hours. Once again, a great deal of pertinent information is lacking. There is no report of the mean, median, and standard deviations for chest tube blood loss at each measured time interval. All patients were lumped together in the overall correlation data. There are populations of patients that exhibit extremes of hemorrhage, and there is no way of knowing if "severe bleeders" affected the overall correlations. Conspicuously absent is any discussion of the use of factor and platelet therapy in the immediate postoperative period. In 101 patients it would be nearly impossible to avoid the use of these blood bank products. Once they are administered, the correlation of prior coagulation data (TEG, platelet count) with subsequent chest tube hemorrhage would be negated. Without simultaneous testing and a clearly defined and rigidly followed algorithm for administration, the use of any such blood products seriously damages any conclusions drawn from such correlations. Patients were reexplored for chest tube bleeding based on surgical criteria-a combination of the speed of blood loss and its hemodynamic consequences. Unfortunately, probably some element of surgical bleeding occurred in the "undefined" population. We will never know what the impact of such blood loss was because these patients were never reexplored. No separate correlations were done between coagulation tests and those patients with abnormal bleeding. Would there have been a differenceas compared with the patients with routine chest tube losses? Data for abnormal coagulation do not agree between Tables 4 and 5. In Table 4, 42 patients have abnormal TEG data after
cardiopulmonary bypass, whereas, in Table 5, only 34 are reported to have abnormalities. Why does this discrepancy exist? No criteria are described for inclusion versus exclusion of patients for the group reported. Were these 101 consecutive patients as a clinical series? The above-described concerns lead to the conclusion that this was performed as exactly that-a clinical series of patients without tight experimental control. As a series, the reported data correspond somewhat with what has been found in one series of more than 500 patients. A surprisingly high incidence of hypercoagulability and fibrinolysis exist. These coagulopathies are heretofore unstudied, and the problem of hypercoagulability is particularly worrisome. In conclusion, the article by Wang and associates does not prove or disprove the usefulness of TEG monitoring, but it does point out that we have a lot of study remaining regarding coagulation and cardiopulmonary bypass before we understand all the problems.
Bruce D. Spiess, M D Division of Cardiothoracic Anesthesia University of Washington School of Medicine RN-10 Seattle, W A 98195
References 1. Wang J-S, Lin C-Y, Hung W-T, et al. Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients. Ann Thorac Surg 1992;53:435-9. 2. Martin P, Horkay F, Rajah SM, Walker DR. Monitoring of coagulation status using thromboelastography during paediatric open heart surgery. Int J Clin Monit Comput 1991;8: 18%7. 3. Spiess BD, Tuman KJ, McCarthy RJ, DeLaria GA, Schillo R, Ivankovich AD. Thromboelastography as an indicator of postcardiopulmonary bypass coagulopathies. J Clin Monit 1987;3: 25-30. 4. Tuman KJ, Spiess BD, McCarthy RJ, Ivankovich AD. Comparison of viscoelastic measures of coagulation after cardiopulmonary bypass. Anesth Analg 1989;69:69-75. 5. Whitten C, Allison P, Latson T, Elmore J, Gulden R, Burkhardt D. Thromboelastographic fibrinolysis does not correlate with levels of D-dimers after cardiopulmonary bypass. Anesthesiology 1991;75:A-432.
To the Editor: In the recent article entitled "Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients" by Wang and associates [l], TEG as well as routine coagulation studies were unable to reliably predict postoperative hemorrhage. Because of the differences in the findings of this study with others examining the predictive effects of TEG after cardiopulmonary bypass [24], particular attention should be made to assure the reader that the technical aspects of the coagulation studies performed in this series were similar to those used by other investigators. We are especially concerned about the specific methods used to obtain TEG data because this study uniquely reports a manyfold greater incidence of hypocoagulability before operation in patients undergoing elective cardiac operations compared with previously reported TEG data in this setting. In our experience, obtaining TEG samples from arterial lines connected to flush devices containing heparin to maintain patency may result in a significant number of samples exhibiting a "factor deficiency"-like tracing when an inadequate volume of blood is withdrawn before obtaining blood for the TEG. In the study by Wang and associates, a larger than expected number of patients (17; 46%) exhibited prebypass TEG tracings consistent
CORRESPONDENCE
surgery maintain, to speed, simplify, and magnify the exchange of ideas, methods, and techniques.
Ann Thorac Surg 1992;54:809-16
n OXYGEMJM
Richard A. Hopkins, M D Department of Surgery Georgetown University Medical Center 3800 Reservoir Road NW Washington, DC 20007-2197
Reply
PUMP
PUMP
Fig 1 . Simple delivery circuit for continuous normothermic blood cardioplegia.
To the Editor:
I am grateful to Mr Gunning for researching the history of the aortic homograft so thoroughly. I have no doubt that in every field of endeavour there will be prior claims registered or uncovered as far back probably as Leonard0 da Vinci. I must confess that I was not aware of Heimbecker and Bigelow's attempt, but knowing these two pioneers, I am not surprised. We like to credit Conrad Lam with the concept of using the homograft aortic valve, which he published in 1952. It was his work that stimulated us and we followed it up in the dog laboratory in Guy's Hospital under the auspices of Lord Brock (Brewin) [l]. The rest is history.
Donald Ross, FRCS 25 Upper Wimpole St London W 1 M 7 T A England
Reference 1. Brewin EG. The use of tissue transplants in the surgery of cardiac valve disease-an experimental study. Guy's Hosp Rep 1956;105:328-39.
Continuous Normothermic Blood Cardioplegia: Simplified Delivery Circuit To the Editor: We have been following with keen interest the development of "warm" blood cardioplegia [l-31. We have used this method of myocardial protection in 50 patients. Patients with congenital heart disease formed a predominant group in our experience, besides those with coronary and valvular procedures. In the first 25 patients we used the pump circuit and dilution of blood as reported by Lichtenstein and associates. However, in the last 25 patients we have adopted the following modifications in the method of cardioplegia delivery which, we believe, have simplified the pump circuit considerably: (1)use of blood directly from oxygenator for continuous perfusion of aortic root, (2) fixed flow rate of aortic root perfusion (1to 2 mL * kg-' * min-' to maintain aortic root pressure at 80 mm Hg) and varying potassium concentration for induction and maintenance of cardiac arrest, and (3) use of a syringe pump for infusing potassium chloride solution into the cardioplegia line just beyond the cardioplegia delivery pump (Fig 1). The syringe infusion pump is filled with the commercially available potassium chloride solution, and it is connected to the side port of the straight connector interposed in the cardioplegia line just beyond the cardioplegia pump. Once full flows are achieved on standard cardiopulmonary bypass the aorta is clamped and the syringe pump is switched on at a predetermined setting to deliver a 0.1 mEq . kg-' . min-' dose of potassium chloride solution to stop the heart in 3 to 5 minutes (induction
dose), and then the infusion rate is adjusted to give 0.005 to 0.01 mEq * kg-' . min-' potassium to sustain the cardiac arrest (maintenance dose). Small purges may be needed occasionally to sustain the arrest. In the final stages of intracardiac repair the potassium infusion is stopped but continuous normothermic infusion is continued for some time, and the aorta is declamped with suction on the aortic root. In our practice, we believe that this is a much simpler circuit to handle and it allows more precise control over the amount of potassium that is being delivered. Because we are using blood directly from the oxygenator, there is no need for any further heat exchanger in the circuit. The use of additional crystalloid solution for dilution and the use of solutions containing varying quantities of potassium are also avoided [l, 3, 41.
Ponangi V . Satyanarayana, M S , MCh Podila Sita Rama Rao, M S , MCh Kesavaram Madhusudhana Rao, BSc, CCP Alluru Sarath Chandra, M S Kanchumarthi Sudhakar Rao, M S Karri Venkat Reddy, M S Department of Cardio Thoracic Surgery Nitam's Znstitute of Medical Sciences Hyderabad, 500 482 India
References 1. Lichtenstein SV, Ashe KA, El Dalati H, Cusimano RJ, Panos A, Slutsky AS. Warm heart surgery. J Thorac Cardiovasc Surg 1991;101:269-74. 2. Lichtenstein SV, Fremes SE, Abel JG, Christakis GT, Salerno TA. Technical asuects of warm heart surgery. " , .I Card Sura 1991;6:2:278-84. 3. Lichtenstein SV, El Dalati H, Panos A, Slutskv AS. Long " cross-clamp with warm heart surgery. Lancet 1989;1:1443. 4. Tutassaura H. Continuous warm blood cardioplegia. Ann Thorac Surg 1991;51:866. v
Thromboelastogram and Postoperative Hemorrhage To the Editor: The recent article "Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients" by Wang and associates [ l ] provides an interesting contrast to most prior work in this area [2-51. Indeed, this represents the only report that finds no predictive accuracy or advantage of thromboelastography (TEG) over routine coagulation testing. Perhaps some of the following discussion and points may explain this obvious discrepancy. Wang and associates note the most common abnormalities before cardiopulmonary bypass were hypocoagulability and fibrinolysis. The mean values for TEG reaction time values were considerably higher than postbypass values, and the mean
CORRESPONDENCE
Ann Thorac Surg
811
1992;54809-16
activated clotting time values were higher (156 2 28.5 seconds) than values routinely considered as normal. These two facts suggest that some patients must have been receiving preoperative heparin infusions. Low-dose preoperative heparin infusions may cause profound prolongations of the reaction time value and also affect the coagulation time and maximum amplitude. The reaction time value may be of infinite length with such therapy, and if this occurred in any of the 101 patients studied, then correlations between activated clotting time, activated partial thromboplastin time, and the TEG reaction time value would be largely dependent on how the statistical analysis of these data was handled. The demographics given do not allow one to decide if that was actually a problem for the investigators. Other pertinent pieces of information such as the incidence of emergency cases and use of platelet inhibitors and fibrinolytics are missing. The preoperative data show a tendency toward fibrinolysis (mean amplitude 60 minutes after the maximum amplitude was 20% less than the maximum amplitude). This alone suggests that some patients must have received streptokinase tissue plasminogen activators or urokinase therapy before entrance into the operating rooms. The large standard deviation in the amplitude 60 minutes after the maximum amplitude also suggests that some subpopulation of patients (n = 16) had profound lysis. If patients on thrombolytic therapy and heparin therapy are included in the study population, it would be unlikely that the maximum amplitude would have any correlation with platelet count, as both of these therapies greatly affect platelet function. The TEG tests not only platelet count, but also platelet function. Our prior studies wherein some weak correlations were demonstrated before bypass avoided patients with heparin or thrombolytic therapy specifically to avoid these compounding variables [31. After bypass the only coagulation data collected were from the time immediately after protamine administration. Those coagulation data were correlated with measured chest tube drainage for periods over the subsequent 24 hours. Once again, a great deal of pertinent information is lacking. There is no report of the mean, median, and standard deviations for chest tube blood loss at each measured time interval. All patients were lumped together in the overall correlation data. There are populations of patients that exhibit extremes of hemorrhage, and there is no way of knowing if "severe bleeders" affected the overall correlations. Conspicuously absent is any discussion of the use of factor and platelet therapy in the immediate postoperative period. In 101 patients it would be nearly impossible to avoid the use of these blood bank products. Once they are administered, the correlation of prior coagulation data (TEG, platelet count) with subsequent chest tube hemorrhage would be negated. Without simultaneous testing and a clearly defined and rigidly followed algorithm for administration, the use of any such blood products seriously damages any conclusions drawn from such correlations. Patients were reexplored for chest tube bleeding based on surgical criteria-a combination of the speed of blood loss and its hemodynamic consequences. Unfortunately, probably some element of surgical bleeding occurred in the "undefined" population. We will never know what the impact of such blood loss was because these patients were never reexplored. No separate correlations were done between coagulation tests and those patients with abnormal bleeding. Would there have been a differenceas compared with the patients with routine chest tube losses? Data for abnormal coagulation do not agree between Tables 4 and 5. In Table 4, 42 patients have abnormal TEG data after
cardiopulmonary bypass, whereas, in Table 5, only 34 are reported to have abnormalities. Why does this discrepancy exist? No criteria are described for inclusion versus exclusion of patients for the group reported. Were these 101 consecutive patients as a clinical series? The above-described concerns lead to the conclusion that this was performed as exactly that-a clinical series of patients without tight experimental control. As a series, the reported data correspond somewhat with what has been found in one series of more than 500 patients. A surprisingly high incidence of hypercoagulability and fibrinolysis exist. These coagulopathies are heretofore unstudied, and the problem of hypercoagulability is particularly worrisome. In conclusion, the article by Wang and associates does not prove or disprove the usefulness of TEG monitoring, but it does point out that we have a lot of study remaining regarding coagulation and cardiopulmonary bypass before we understand all the problems.
Bruce D. Spiess, M D Division of Cardiothoracic Anesthesia University of Washington School of Medicine RN-10 Seattle, W A 98195
References 1. Wang J-S, Lin C-Y, Hung W-T, et al. Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients. Ann Thorac Surg 1992;53:435-9. 2. Martin P, Horkay F, Rajah SM, Walker DR. Monitoring of coagulation status using thromboelastography during paediatric open heart surgery. Int J Clin Monit Comput 1991;8: 18%7. 3. Spiess BD, Tuman KJ, McCarthy RJ, DeLaria GA, Schillo R, Ivankovich AD. Thromboelastography as an indicator of postcardiopulmonary bypass coagulopathies. J Clin Monit 1987;3: 25-30. 4. Tuman KJ, Spiess BD, McCarthy RJ, Ivankovich AD. Comparison of viscoelastic measures of coagulation after cardiopulmonary bypass. Anesth Analg 1989;69:69-75. 5. Whitten C, Allison P, Latson T, Elmore J, Gulden R, Burkhardt D. Thromboelastographic fibrinolysis does not correlate with levels of D-dimers after cardiopulmonary bypass. Anesthesiology 1991;75:A-432.
To the Editor: In the recent article entitled "Thromboelastogram fails to predict postoperative hemorrhage in cardiac patients" by Wang and associates [l], TEG as well as routine coagulation studies were unable to reliably predict postoperative hemorrhage. Because of the differences in the findings of this study with others examining the predictive effects of TEG after cardiopulmonary bypass [24], particular attention should be made to assure the reader that the technical aspects of the coagulation studies performed in this series were similar to those used by other investigators. We are especially concerned about the specific methods used to obtain TEG data because this study uniquely reports a manyfold greater incidence of hypocoagulability before operation in patients undergoing elective cardiac operations compared with previously reported TEG data in this setting. In our experience, obtaining TEG samples from arterial lines connected to flush devices containing heparin to maintain patency may result in a significant number of samples exhibiting a "factor deficiency"-like tracing when an inadequate volume of blood is withdrawn before obtaining blood for the TEG. In the study by Wang and associates, a larger than expected number of patients (17; 46%) exhibited prebypass TEG tracings consistent