- Email: [email protected]
Autotransfusion of shed mediastinal blood
CORRESPONDENCE
Coronary-Subclavian Steal After Coronary Artery Bypass Grafting Using the Internal Mammary Artery To the Editor: In a recent issue, Olsen and colleagues (11 described the syndrome of coronary-subclavian steal through an internal mammary artery graft after coronary artery bypass grafting. They also collected 8 cases from the world literature. In May 1985, my colleagues and I at De Stadsmaten Hospital, Enschede, the Netherlands, encountered such a syndrome in a 53-year-old woman. She underwent coronary artery bypass grafting in September 1964 because of worsening angina pectoris. The left internal mammary artery was used to revascularize the distal left anterior descending coronary artery and a saphenous vein graft was placed to the distal right coronary artery. In January 1985 the patient was rehospitalized with onset of recurrent angina after having been asymptomatic for some weeks. Digital subtraction angiogram showed a patency of the left IMA and saphenous vein graft. However, total occlusion was found at the origin of the left subclavian artery. To bypass this occlusion a left carotid-subclavian artery bypass (21 was performed (May 1985) and up to the present the patient is symptom free. As the internal mammary artery is now an essential element in myocardial revascularization, it is our opinion, in agreement with that of Olsen and colleagues, that preoperative measurement of a possible difference in upper extremity blood pressure is a simple and effective means to screen for clinically significant stenosis of the subclavian artery. It is our policy to perform a digital subtraction angiogram or an angiography of the aortic arch-carotic-subclavian system only when there are signs of obstruction based on history and physical examination. If there are signs of obstruction the use of the ipsilateral internal mammary artery as a free graft, if possible the contralateral internal mammary artery, or a venous graft are alternatives in these patients. This case mentioned here has been published in the Dutch Hart Bulletin [3], so up to the present 10 cases of this condition have been described.
Rent M . H. 1. Brouwer, M D Department of Thoracic Surgery Academic Hospital of Groningen Groningen, the Netherlands
References 1. Olsen CO, Dunton RF, Maggs PR, Lahey SJ. Review of coronary-subclaviansteal following internal mammary arterycoronary artery bypass surgery. Ann Thorac Surg 1988; 46:6756. 2. Tarazi RY, OHara PJ, Loop FD. Symptomatic coronarysubclavian steal syndrome corrected by carotid-subclavian bypass. J Vasc Surg 1986;3:669. 3. Kerbert C, Delwig H, Donders HPC, et al. Recidieve angina pectoris na een mammaria-coronary-bypass-operatie als gevolg van stenosering van de arterie subclavia (coronarysubclavian steal). Hart Bull 1987;18:127.
Reply To the Editor: Certainly more cases of coronary-subclavian steal through an internal mammary artery graft after coronary artery bypass grafting will become evident as manifestations of this syndrome are systematically searched for in patients who have undergone myocardial revascularization. Hopefully, with careful and thorough evaluation of patients before coronary bypass grafting, 0 1989 by The Society of Thoracic Surgeons
those with clinically significant subclavian stenosis can be properly identified and alternative conduits can be used. Dr Brouwer points out another excellent modality for diagnosing clinically significant subclavian artery stenosis, that of digital subtraction angiography,
Craig 0. Olsen, M D Cardiovascular and Chest Surgical Associates, P A 333 N Ist, Suite 280 Boise, ID 83702
Autotransfusion of Shed Mediastinal Blood To the Editor: A recent paper by Griffith and associates [l]advocates the use of a cell washing device before autotransfusion of shed mediastinal blood. Recent work from our department, presented at the Surgical Research Society, has also focused on this phenomenon
PI.
The study was part of a prospective randomized evaluation of intraoperative salvage autotransfusion using either the Solcotrans system or bank blood controls in elective aortic reconstruction. The Solcotrans device is similar in principle to the Sorensen system, and does not employ cell washing; salvaged blood is reinfused through a 4O-pm filter. Systemic heparinization (2 mg/kg, controlled with the activated clotting time) was used during blood salvage.
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To exclude the contribution of primary fibrinogenolysis, a latex immunoagglutination test for D-dimer, which is specific for fibrin split products, was used (MAbCO Ltd, Brisbane, Australia). Assays were performed on paired samples from autotransfusion reservoirs and from patients preoperatively and at 0, 4, and 24 hours postoperatively. Normal levels (less than 200 ng/mL) were found in all patients preoperatively, whereas 28 of 32 reservoirs had raised levels of D-dimer (median, 3,770 ng/mL; range, 400 to 24,000 ng/mL). These levels are seen in high-grade disseminated intravascular coagulopathy. After reinfusion of salvaged blood, however, only 4 patients had elevated levels of D-dimer, not exceeding 500 ng/mL. No patients had raised levels of D-dimer 24 hours postoperatively. No evidence of coagulopathy was seen, and in particular there was no bleeding tendency, as evidenced by normal template bleeding times (Simplate-11, venous occlusion, single observer) and by wound drainage volume, which was less than that of bank blood controls. The crux of both our study and that of Griffith and associates is the distinction between the detection of fibrin(ogen) split products in the autotransfusate or recipient and a clinical coagulopathy. Fibrinolytic products in chest drainage fluid derive from the action of tissue plasminogen activator secreted by the pleura, but coagulopathy has not been a problem with either the Sorensen or Solcotrans systems. Although high levels of fibrin degradation products have been shown to interfere with platelet function, bleeding times were normal in our study. In established disseminated intravascular coagulopathy, the dynamic balance between coagulation and clot lysis is tipped in favor of coagulation, with a secondary activation of fibrinolysis, and a vicious circle is established. In contrast, in postoperative patients, there is a shutdown of fibrinolysis, with high levels of tissue plasminogen activator inhibitors [3]. Any plasmin infused during autotransfusion is presumably inactivated by circulating antiplasmins. In summary, it would appear that our work is in agreement with that of the San Diego group, but we feel that the available evidence does not support the use of cell washing of shed Ann Thorac Surg 1989;48:887-90
0003-4975/89/$3.50
888
CORRESPONDENCE
mediastinal blood before reinfusion, which would entail extra cost and operator time.
1. F . Thompson, MB, FRCS(Ed), FRCS A. D . B. Chant, MS, FRCS
Vascular Surgical Unit Royal South Hunts Hospital Graham Road Southampton 509 4PE United Kingdom
References 1. Griffith LD, Billman GF, Daily PO, Lane TA. Apparent coagulopathy caused by infusion of shed mediastinal blood and its prevention by washing of the infusate. Ann Thorac Surg 1989;47400-6. 2. Thompson JF, Clifford PC, Webster JHH, Chant ADB. Monoclonal antibody detection of fibrinolytic activation during salvage autotransfusion. Br J Surg 1989;76:646. 3. Gomez MG, Carroll RC, Hansard MR, Kidd M, Goldman MH. Regulation of fibrinolysis in aortic surgery. J Vasc Surg 1988; 83384-8.
Ann Thorac Surg 1989;48:887-90
preclude showing significant differences between experimental conditions using this variable alone. My colleagues and I applaud the attempts of Thompson and associates to advance knowledge on the hematologic effects of autotransfusion of shed blood but cannot accept their conclusions as applying to our experiment. The collected product, the timing of data collection, and the measurement tools are not similar to our experiment. When infusing large quantities of fibrin split products, there may still be unmeasurable negative effects that can be reduced by washing. In addition, the effects of infusing high levels of activated complement (which can be reduced by washing) are also unknown at the current time. Continued experimentation should be encouraged to assure administering to the patient the highest quality autotransfusion product with the lowest attainable risk.
b e D . Griffith, M D Cardiac Surgery Dominican Santa Cruz Hospital 1555 Soquel Drive Santa Cruz. CA 95065
References 1. Markovitz MJ, Smith PC, Brown M, Bloom R, Mammen EF.
Reply To the Editor: I am pleased by Dr Thompson’s discussion of our paper conceming the effects of infusion of fibrin split products from shed mediastinal blood collected from postoperative cardiac surgery patients. He adds healthy fuel to the fire of a yet unsettled debate over whether or not reinfusion of shed mediastinal blood has harmful effects. However, although he is correct in stating that the Solcotrans and Sorensen collection devices are fundamentally similar, unfortunately the conditions of his experiment are not the same as those in our experiment. Thompson and associates collected systemically heparinized blood (2 mgkg) from elective aortic reconstructions and tested the postinfusion data at 4 and 24 hours. On the other hand, we collected blood that was not heparinized, and tested the patient for fibrin split product levels one-half hour after infusion. These markedly discrepant time periods already make any comparative conclusions difficult, even if the blood in the study by Thompson and associates was not anticoagulated. Thompson and associates mehsured levels of u-dimer fragments in the shed blood before reinfusion and found median levels of 3,770 nglmL. In his letter, Dr Thompson states that only 4 patients had elevated serum levels of u-dimers after infusion but fails to state the volume of the infusate. This is a crucial piece of data, as a small infusate volume, regardless of the elevated u-dimer levels, would produce a low serum concentration and thus perhaps account for the negative results. Also, his results are at variance with those of Marcovitz and co-workers [l], who found u-dimer levels were elevated in patients 15 minutes after the reinfusion of shed mediastinal blood. Lawrence-Brown and colleagues [2] have confirmed that the elevated u-dimer levels in salvaged blood can be washed to normal levels, which gives credence to our results. Dr Thompson purports an absence of bleeding tendency after reinfusion of the shed Solcotrans blood and, because of this, that washing is not justified. Unfortunately, Thompson and associates chose to use the template bleeding time and the volume of wound drainage to justify this conclusion. Bleeding times have little correlation with postoperative bleeding, especially in cardiac surgical patients [3], and there is generally sufficient variability in the postoperative blood loss of surgical patients to
Hemostasis markers in cardiac surgery patients following postoperative autotransfusion. Anesth Analg 1988;67S140. 2. Lawrence-Brown MM, Couch C, Halliday M, Hellings M, Barr A, Marshall L. D-dimer levels in blood salvage for autotransfusion. Aust NZ J Surg 1989;59(1):67-70. 3. Simon TL, AH BF, Murphy W. Controlled trial of routine administration of platelet concentrates in cardiopulmonary bypass surgery. Ann Thorac Surg 1984;37359-64.
Impairment in Right Ventricular Performance After Left Ventricular Aneurysm Operation To the Editor: We read with interest the article of Mangschau and co-workers [l]. We have studied right ventricular performance after coronary artery bypass grafting in our center with the use of a multilumen pulmonary artery catheter modified with a fast-response thermistor (Edward Laboratories, Santa Ana, CA) for measuring thermodilution right ventricular ejection fraction [2]. Unlike that of Mangschau and co-workers, our study included 34 patients scheduled for coronary artery bypass grafting without ventricular aneurysm during the first 48 hours of their postoperative course. Despite the differences in methods, our results are similar to those of Mangschau and co-workers. In particular, we note the following. 1. We do not observe any correlation between right ventricular ejection fraction and pulmonary artery pressure. Other authors found the same results [3], probably because of the small dispersion of pulmonary artery pressure values and the alterations of the diastolic properties and compliance of the ischemic myocardium [4]. 2. There is a significant decrease in right ventricular ejection fraction from 48% preoperatively to 37% four hours after coronary artery bypass grafting and 36% in the first postoperative day. This decrease is accompanied by a significant increase in heart rate and a significant decrease in right ventricular stroke work index during the same period. The right ventricular end-systolic volume index is unchanged, and we note a small decrease in right ventricular end-diastolic volume index.
Coronary-Subclavian Steal After Coronary Artery Bypass Grafting Using the Internal Mammary Artery To the Editor: In a recent issue, Olsen and colleagues (11 described the syndrome of coronary-subclavian steal through an internal mammary artery graft after coronary artery bypass grafting. They also collected 8 cases from the world literature. In May 1985, my colleagues and I at De Stadsmaten Hospital, Enschede, the Netherlands, encountered such a syndrome in a 53-year-old woman. She underwent coronary artery bypass grafting in September 1964 because of worsening angina pectoris. The left internal mammary artery was used to revascularize the distal left anterior descending coronary artery and a saphenous vein graft was placed to the distal right coronary artery. In January 1985 the patient was rehospitalized with onset of recurrent angina after having been asymptomatic for some weeks. Digital subtraction angiogram showed a patency of the left IMA and saphenous vein graft. However, total occlusion was found at the origin of the left subclavian artery. To bypass this occlusion a left carotid-subclavian artery bypass (21 was performed (May 1985) and up to the present the patient is symptom free. As the internal mammary artery is now an essential element in myocardial revascularization, it is our opinion, in agreement with that of Olsen and colleagues, that preoperative measurement of a possible difference in upper extremity blood pressure is a simple and effective means to screen for clinically significant stenosis of the subclavian artery. It is our policy to perform a digital subtraction angiogram or an angiography of the aortic arch-carotic-subclavian system only when there are signs of obstruction based on history and physical examination. If there are signs of obstruction the use of the ipsilateral internal mammary artery as a free graft, if possible the contralateral internal mammary artery, or a venous graft are alternatives in these patients. This case mentioned here has been published in the Dutch Hart Bulletin [3], so up to the present 10 cases of this condition have been described.
Rent M . H. 1. Brouwer, M D Department of Thoracic Surgery Academic Hospital of Groningen Groningen, the Netherlands
References 1. Olsen CO, Dunton RF, Maggs PR, Lahey SJ. Review of coronary-subclaviansteal following internal mammary arterycoronary artery bypass surgery. Ann Thorac Surg 1988; 46:6756. 2. Tarazi RY, OHara PJ, Loop FD. Symptomatic coronarysubclavian steal syndrome corrected by carotid-subclavian bypass. J Vasc Surg 1986;3:669. 3. Kerbert C, Delwig H, Donders HPC, et al. Recidieve angina pectoris na een mammaria-coronary-bypass-operatie als gevolg van stenosering van de arterie subclavia (coronarysubclavian steal). Hart Bull 1987;18:127.
Reply To the Editor: Certainly more cases of coronary-subclavian steal through an internal mammary artery graft after coronary artery bypass grafting will become evident as manifestations of this syndrome are systematically searched for in patients who have undergone myocardial revascularization. Hopefully, with careful and thorough evaluation of patients before coronary bypass grafting, 0 1989 by The Society of Thoracic Surgeons
those with clinically significant subclavian stenosis can be properly identified and alternative conduits can be used. Dr Brouwer points out another excellent modality for diagnosing clinically significant subclavian artery stenosis, that of digital subtraction angiography,
Craig 0. Olsen, M D Cardiovascular and Chest Surgical Associates, P A 333 N Ist, Suite 280 Boise, ID 83702
Autotransfusion of Shed Mediastinal Blood To the Editor: A recent paper by Griffith and associates [l]advocates the use of a cell washing device before autotransfusion of shed mediastinal blood. Recent work from our department, presented at the Surgical Research Society, has also focused on this phenomenon
PI.
The study was part of a prospective randomized evaluation of intraoperative salvage autotransfusion using either the Solcotrans system or bank blood controls in elective aortic reconstruction. The Solcotrans device is similar in principle to the Sorensen system, and does not employ cell washing; salvaged blood is reinfused through a 4O-pm filter. Systemic heparinization (2 mg/kg, controlled with the activated clotting time) was used during blood salvage.
-
To exclude the contribution of primary fibrinogenolysis, a latex immunoagglutination test for D-dimer, which is specific for fibrin split products, was used (MAbCO Ltd, Brisbane, Australia). Assays were performed on paired samples from autotransfusion reservoirs and from patients preoperatively and at 0, 4, and 24 hours postoperatively. Normal levels (less than 200 ng/mL) were found in all patients preoperatively, whereas 28 of 32 reservoirs had raised levels of D-dimer (median, 3,770 ng/mL; range, 400 to 24,000 ng/mL). These levels are seen in high-grade disseminated intravascular coagulopathy. After reinfusion of salvaged blood, however, only 4 patients had elevated levels of D-dimer, not exceeding 500 ng/mL. No patients had raised levels of D-dimer 24 hours postoperatively. No evidence of coagulopathy was seen, and in particular there was no bleeding tendency, as evidenced by normal template bleeding times (Simplate-11, venous occlusion, single observer) and by wound drainage volume, which was less than that of bank blood controls. The crux of both our study and that of Griffith and associates is the distinction between the detection of fibrin(ogen) split products in the autotransfusate or recipient and a clinical coagulopathy. Fibrinolytic products in chest drainage fluid derive from the action of tissue plasminogen activator secreted by the pleura, but coagulopathy has not been a problem with either the Sorensen or Solcotrans systems. Although high levels of fibrin degradation products have been shown to interfere with platelet function, bleeding times were normal in our study. In established disseminated intravascular coagulopathy, the dynamic balance between coagulation and clot lysis is tipped in favor of coagulation, with a secondary activation of fibrinolysis, and a vicious circle is established. In contrast, in postoperative patients, there is a shutdown of fibrinolysis, with high levels of tissue plasminogen activator inhibitors [3]. Any plasmin infused during autotransfusion is presumably inactivated by circulating antiplasmins. In summary, it would appear that our work is in agreement with that of the San Diego group, but we feel that the available evidence does not support the use of cell washing of shed Ann Thorac Surg 1989;48:887-90
0003-4975/89/$3.50
888
CORRESPONDENCE
mediastinal blood before reinfusion, which would entail extra cost and operator time.
1. F . Thompson, MB, FRCS(Ed), FRCS A. D . B. Chant, MS, FRCS
Vascular Surgical Unit Royal South Hunts Hospital Graham Road Southampton 509 4PE United Kingdom
References 1. Griffith LD, Billman GF, Daily PO, Lane TA. Apparent coagulopathy caused by infusion of shed mediastinal blood and its prevention by washing of the infusate. Ann Thorac Surg 1989;47400-6. 2. Thompson JF, Clifford PC, Webster JHH, Chant ADB. Monoclonal antibody detection of fibrinolytic activation during salvage autotransfusion. Br J Surg 1989;76:646. 3. Gomez MG, Carroll RC, Hansard MR, Kidd M, Goldman MH. Regulation of fibrinolysis in aortic surgery. J Vasc Surg 1988; 83384-8.
Ann Thorac Surg 1989;48:887-90
preclude showing significant differences between experimental conditions using this variable alone. My colleagues and I applaud the attempts of Thompson and associates to advance knowledge on the hematologic effects of autotransfusion of shed blood but cannot accept their conclusions as applying to our experiment. The collected product, the timing of data collection, and the measurement tools are not similar to our experiment. When infusing large quantities of fibrin split products, there may still be unmeasurable negative effects that can be reduced by washing. In addition, the effects of infusing high levels of activated complement (which can be reduced by washing) are also unknown at the current time. Continued experimentation should be encouraged to assure administering to the patient the highest quality autotransfusion product with the lowest attainable risk.
b e D . Griffith, M D Cardiac Surgery Dominican Santa Cruz Hospital 1555 Soquel Drive Santa Cruz. CA 95065
References 1. Markovitz MJ, Smith PC, Brown M, Bloom R, Mammen EF.
Reply To the Editor: I am pleased by Dr Thompson’s discussion of our paper conceming the effects of infusion of fibrin split products from shed mediastinal blood collected from postoperative cardiac surgery patients. He adds healthy fuel to the fire of a yet unsettled debate over whether or not reinfusion of shed mediastinal blood has harmful effects. However, although he is correct in stating that the Solcotrans and Sorensen collection devices are fundamentally similar, unfortunately the conditions of his experiment are not the same as those in our experiment. Thompson and associates collected systemically heparinized blood (2 mgkg) from elective aortic reconstructions and tested the postinfusion data at 4 and 24 hours. On the other hand, we collected blood that was not heparinized, and tested the patient for fibrin split product levels one-half hour after infusion. These markedly discrepant time periods already make any comparative conclusions difficult, even if the blood in the study by Thompson and associates was not anticoagulated. Thompson and associates mehsured levels of u-dimer fragments in the shed blood before reinfusion and found median levels of 3,770 nglmL. In his letter, Dr Thompson states that only 4 patients had elevated serum levels of u-dimers after infusion but fails to state the volume of the infusate. This is a crucial piece of data, as a small infusate volume, regardless of the elevated u-dimer levels, would produce a low serum concentration and thus perhaps account for the negative results. Also, his results are at variance with those of Marcovitz and co-workers [l], who found u-dimer levels were elevated in patients 15 minutes after the reinfusion of shed mediastinal blood. Lawrence-Brown and colleagues [2] have confirmed that the elevated u-dimer levels in salvaged blood can be washed to normal levels, which gives credence to our results. Dr Thompson purports an absence of bleeding tendency after reinfusion of the shed Solcotrans blood and, because of this, that washing is not justified. Unfortunately, Thompson and associates chose to use the template bleeding time and the volume of wound drainage to justify this conclusion. Bleeding times have little correlation with postoperative bleeding, especially in cardiac surgical patients [3], and there is generally sufficient variability in the postoperative blood loss of surgical patients to
Hemostasis markers in cardiac surgery patients following postoperative autotransfusion. Anesth Analg 1988;67S140. 2. Lawrence-Brown MM, Couch C, Halliday M, Hellings M, Barr A, Marshall L. D-dimer levels in blood salvage for autotransfusion. Aust NZ J Surg 1989;59(1):67-70. 3. Simon TL, AH BF, Murphy W. Controlled trial of routine administration of platelet concentrates in cardiopulmonary bypass surgery. Ann Thorac Surg 1984;37359-64.
Impairment in Right Ventricular Performance After Left Ventricular Aneurysm Operation To the Editor: We read with interest the article of Mangschau and co-workers [l]. We have studied right ventricular performance after coronary artery bypass grafting in our center with the use of a multilumen pulmonary artery catheter modified with a fast-response thermistor (Edward Laboratories, Santa Ana, CA) for measuring thermodilution right ventricular ejection fraction [2]. Unlike that of Mangschau and co-workers, our study included 34 patients scheduled for coronary artery bypass grafting without ventricular aneurysm during the first 48 hours of their postoperative course. Despite the differences in methods, our results are similar to those of Mangschau and co-workers. In particular, we note the following. 1. We do not observe any correlation between right ventricular ejection fraction and pulmonary artery pressure. Other authors found the same results [3], probably because of the small dispersion of pulmonary artery pressure values and the alterations of the diastolic properties and compliance of the ischemic myocardium [4]. 2. There is a significant decrease in right ventricular ejection fraction from 48% preoperatively to 37% four hours after coronary artery bypass grafting and 36% in the first postoperative day. This decrease is accompanied by a significant increase in heart rate and a significant decrease in right ventricular stroke work index during the same period. The right ventricular end-systolic volume index is unchanged, and we note a small decrease in right ventricular end-diastolic volume index.