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Agglutination of blood cardioplegia by cold reacting autoantibodies
Agglutination of Blood Cardioplegia by ColdReacting Autoantibodies William L. Holman, MD, Shirley H. Smith, MD, Rosemary Edwards, MD, and Shu T. Huang, MD Division of Cardiothoracic Surgery and Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama
Cold-reacting autoantibodies occasionally occur in patients requiring cardiac operations. This report describes the clinical course of 1 patient with cold-reacting autoantibodies and intracoronary agglutination of the blood cardioplegia solution. Observations made in vivo and in
vitro are considered in discussing recommendations for the management of extracorporeal circulation and cardioplegic arrest in patients with clinically silent coldreacting autoantibodies. (Ann Thoruc Surg 2991;52:833-6)
C
Postoperatively there was no grossly evident hemolysis and no inotropic support was required. There was no evidence for myocardial necrosis by serial electrocardiographic or creatine kinase isoenzyme determinations (postoperative total creatine kinase: 76, 380, 227 UL; creatine kinase-MB: 5, 11, 5 U/L). The patient's subsequent convalescence was uneventful. In vitro mixing of the patient's blood with cold cardioplegia solution (4"C, 15 minutes) resulted in agglutination (Fig 1). Warming the agglutinated blood to 37°C resulted in dispersion of the erythrocytes (Fig 2). Further agglutination of the patient's blood occurred with continued hypothermia (Fig 3). Subsequent analysis showed that the patient was blood type A Rh+ with an anti-I cold agglutinin titer of 1:256 at 4°C. The patient's blood agglutinated at 24°C (titer, 1:4)but not at 30" or 37°C. The direct antiglobulin test was negative using polyspecific antiglobulin serum, as well as nonspecific anti-immunoglobulin G and anticomplement serum. Additional in vitro tests were performed to better understand the effect of agglutination on erythrocytes passing through small-caliberconduits. Serum from 3 patients with anti-I titers ranging from 1:4 to 1:32 at room temperature was mixed with red cells and incubated at room temperature and 4°C for 30 minutes. 1+ to 4+ visual agglutination was demonstrated before passing the agglutinated blood through an 18+m filter (Hemonate-filter, Gesco International Medical, San Antonio, TX). Sixty millimeters of mercury pressure was constantly applied to the agglutinated blood as it passed through the filter by the attachment of a pressurizing syringe to a sphygmomanometer. The blood passed through the filter without hemolysis as determined by testing a 1:lOO dilution of serum with an Ames Bililabstix (MilesInc, Ames Division, Elkhart, IN). Anti-Lewis b reagent antiserum, another cold-reacting antibody, was mixed with Lewis b positive cells and subjected to the same procedure without evidence of hemolysis. Finally, serum from a patient with clinically severe hemolytic agglutinin disease was mixed with adult red blood cells (incubated for 30 minutes at 4°C
old-reacting autoantibodies are usually of the immunoglobulin M class and are most commonly directed against the human erythrocyte I antigen. Patients with cold-reacting autoantibodies may show the development of acrocyanosis, severe hemolytic anemia, and hemoglobinuria after exposure to cold temperatures; however, cold-reacting autoantibodies with low thermal amplitude are usually clinically silent and may only be detected by preoperative blood typing [l]. The management of patients with cold-reacting autoantibodies who are exposed to hypothermic extracorporeal circulation remains controversial [2-8]. This report describes the clinical course of l patient who had cold-reacting autoantibodies with resultant intracoronary agglutination of the blood cardioplegia solution. Our in vivo and in vitro observations serve as the basis for a discussion of existing protocols for the treatment of similar patients.
Case History and In Vitro Observations The patient is a 69-year-old man with severe pulmonary dysfunction and class IV angina pectoris who was referred for bypass grafting of a proximal stenosis in the anterior descending artery. Angioplasty of this long lesion spanning a large first diagonal branch was considered unsafe. Extracorporeal circulation was conducted at 28°C and a flow of 1.8 L . min-' m-'. The heart was arrested using a 4°C blood cardioplegia solution. Agglutinated blood was found when the anterior descending artery was incised. Two proximal and two distal saphenous vein anastomoses were constructed during a 38-minute ischemic interval. Rewarming to 37°C was initiated during the last proximal anastomosis. The postcardioplegia reperfusion of the heart was begun with a blood cardioplegia solution delivered at 37°C under controlled conditions of flow and pressure. Accepted for publication Oct 23, 1990. Address reprint requests to Dr Holman, Department of Surgery, University Station, Birmingham, AL 35294.
0 1991 by The Society of Thoracic Surgeons
0003-4975/91/$3.50
834
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
Ann Thorac Surg 1991:51:83M
antibody. It is possible that the transcapillary perfusion pressure caused disaggregation of the erythrocytes or that disaggregation occurred with rewarming before the onset of irreversible myocardial ischemic injury. Warm (23°C) cardioplegic arrest [8], preoperative plasma exchange [4,8], intraoperative blood exchange [ 5 ] , and infusion of warm nonoxygenated crystalloid cardioplegia followed by cold crystalloid cardioplegia infusion [3, 5, 7, 81 have all been used in patients with a preoperative finding of cold-reacting autoantibodies. These interventions are intended to decrease the titer of the cold-reacting antibody and maintain the patient’s temperature above the thermal amplitude of the antibody. Such interventions may be crucial in patients with complement-fixing antibodies that can cause hemolysis; however, the observations in our case question the necessity for these interventions in patients with clinically silent nonhemolytic cold-reacting autoantibodies. Although a single infusion of agglutinated blood cardioplegia did not cause myocardial injury in this case, a second infusion of cold (4°C)blood cardioplegia cannot be considered safe in the absence of more complete data. The in vivo and in vitro observations of this report predict that subsequent infusions of cold (4°C)crystalloid cardioplegia solution would be safe if the duration of the procedure
Fig 1 . Agglutination of the patient’s blood by hypothermia at 4°C for 15 minutes ( ~ 1 0 before 0 30% reduction.)
and room temperature). A portion of these samples was passed through the same test system. A large amount of hemolysis was demonstrated in all samples. The mechanism for red cell destruction for this in vitro test was therefore complement activation by cold-reacting autoantibodies rather than agglutination and mechanical destruction.
Comment Our comments are confined to the management of perfusion and hypothermic cardioplegic arrest in patients with the clinically silent, low thermal amplitude, nonhemolytic (ie, benign) variety of cold-reacting autoantibodies. Agglutination of the blood cardioplega solution in our patient did not cause any discernable myocardial damage, and exposure of the blood to temperatures below 24°C during the initial phases of cooling (water bath = 4°C)did not cause hemolysis or malfunction of the hollow-fiber oxygenator (Bentley BCM-7). The cold-reacting autoantibody in this case caused intracoronary agglutination of the blood cardioplegia solution; however, adverse clinical sequelae of hemolysis or myocardial necrosis did not occur. The agglutination of erythrocytes by antibody probably did not result in capillary occlusion even at temperatures well below the thermal amplitude of the
Fig 2 . Dispersion of patient’s blood by rewarming at 37°C for 15 minutes ( ~ 2 0before 0 30% reduction.)
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
Ann Thorac Surg 1991;51:833-6
835
warrants additional doses of cardioplegia. If the presence of nonhemolytic cold-reacting autoantibodies is detected before operation, our experience suggests that 4°C crystalloid cardioplegia could be used safely. The risks of infection and destabilizing fluid shifts associated with plasma exchange are probably not justified in patients with benign cold-reacting autoantibodies.
References
Fig 3 . Further agglutination of the patient’s blood by continued hypothermiu for 30 minutes (x40 before 30% reduction.)
1. Pruzanski W, Shumak KH. Biologic activity of cold-reacting autoantibodies. N Engl J Med 1977;297538-42, 583-9. 2. AuBuchon AJ, Stofan BA, Davey RJ. Hemolysis during extracorporeal circulation: significance of cold-reactive auto-antibodies and mechanical trauma. Blood 1983;62(Suppl 1):42a. 3. Shahian DM, Wallach SR, Bern MM. Open heart surgery in patients with cold-reactive proteins. Surg Clin North Am 1985;65:315-22. 4. Klein HG, Faltz LL, McIntosh CL, Appelbaum FR, Deisseroth AB, Holland PV. Surgical hypothermia in a patient with a cold agglutinin. Management by plasma exchange. Transfusion 1980;20:354-7. 5. Lee MC, Chang CH, Hsieh MJ. Use of a total wash-out method in an open heart operation. Ann Thorac Surg 1989;47 57-8. 6. Moore RA, Geller EA, Mathews ES, Botros SB, Jose AB, Clark DL. The effect of hypothermic cardiopulmonary bypass on patients with low-titer, nonspecific cold agglutinins. Ann Thorac Surg 1984;37233-8. 7. Berreklouw E, Moulijn AC, Pegels JG, Meijne NG. Myocardial protection with cold cardioplegia in a patient with cold agglutinins and hemolysins. Ann Thorac Surg 1982;33:521-2. 8. Paccagnella A, Simini G, Nieri A. Cardiopulmonary bypass and cold agglutinin [Letter]. J Thorac Cardiovasc Surg 1988; 95:543.
INVITED COMMENTARY Patients with cold-reacting antibodies are theoretically at risk for hemolysis or microvascular obstruction by red cell aggregates when hypothermic techniques, including cold cardioplegia, are employed during open heart operations. The degree of antibody-mediated hemolysis that occurs in vivo depends on the extent of complement activation. Complement activation through to C3d will result in normal cell survival, activation to C3b will result in extravascular hemolysis, and activation to C9 will result in intravascular hemolysis. Overt hemolysis is unusual, probably as a result of natural inhibitors of the complement cascade. The incidence of microvascular obstruction by red cell aggregates is not known but may be underestimated. For example, red cell aggregates in the coronary circulation after infusion of cold blood cardioplegia might interfere with cardioplegia distribution, leading to poor myocardial protection and depressed left ventricular function. The relationship of these complications to cold agglutinins may not be recognized. In this case report by Holman and associates, two factors served to mitigate against the development of
these complications, even in the presence of gross erythrocyte agglutination. First, the antibody was of low thermal amplitude and midrange titer. Second, the patient had limited coronary disease and the period of systemic and cardiac hypothermia was limited. The favorable outcome in this report cannot necessarily be extrapolated to patients with complex multivessel disease who may require a prolonged hypothermic period. We also have several reservations about the in vitro methodology employed by Holman and associates. First, there is no evidence that the lack of mechanical trauma to agglutinated red cells when passed through an 18-pm filter under 60 mm Hg pressure accurately simulates the passage of red cells through the coronary microcirculation. Second, the absence of in vitro hemolysis in the three sera tested may be a function of the activity of complement in their test system and may not reflect what would have occurred in vivo. Finally, we are curious as to why the patient’s own blood was never subjected to the in vitro testing described. What then should be the approach to patients with cold
836
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
agglutinins who undergo coronary operations? Routine preoperative cold temperature screening of all patients' sera is probably not justified owing to the lack of serious clinical sequelae in most instances. For patients undergoing elective procedures who have known potent cold agglutinins, the thermal amplitude and titer of the antibody should be determined. Knowledge of the thermal amplitude can allow the surgeon to control the degree of autoagglutination by manipulation of cardiac, systemic, and infusate temperatures. More complex preoperative and intraoperative techniques should be reserved for the rare patient with the syndrome of cold autoimmune hemolytic anemia. When red cell agglutination is encountered unexpectedly, the following suggestions may be useful: (1) verification by the blood bank that a cold agglutinin and not an unrecognized alloantibody is present; (2) the use of crystalloid cardioplegia to dilute the
Ann Thorac Surg 1991;51:8W
titer of antibody in the coronary circulation; (3) the use of noncardioplegic techniques; (4) maintenance of systemic temperature greater than 28" to M"C, at which levels significant agglutination is unlikely to occur; and (5) vigilant inspection of the extracorporeal circuit and oxygenators for aggregates. David M . Shahian, M D Department of Thoracic and Cardiovascular Surgery h h e y Clinic Medical Center 41 Mall Rd Burlington, M A 01805 Walter H . Dzik, M D Blood Bank and Tissue Typing Laboratory .Vew England Deaconess Hospital Boston, M A
REVIEW OF RECENT BOOKS
AIDS and Surgery Edited by Andrew 1. W . Sim and Donald I . Ieferies London, Blackwell Scientific Publications, 1990 142 pp, illustrated, $54.95
and control of tuberculosis. This transition reminds all readers new to the area that the true extent of the current epidemic and the real occupational risks are reflected by HIV-infected individuals-not just those with full-blown AIDS. Because the editors . . have altered the manuscripts as httle as possible, . . . individual authors' approaches (and attitudes) . . permeate the text." The professional and ethical conflicts engendered by governmental policies of treating HIV infection and HIV-related illness as social problems rather than as a fatal mfectious disease are readily apparent throughout the book, both by direct comment and through inference. Among these conflicts IS the impediment to infection control, public health, and occupational risk identification imposed by undue emphasis on individual rather than societal rights. Also evident is the paradox between that which seems medically and epidemiologically sound and that which is "legal." This book should be mandatory reading for two identifiable groups of surgeons: (1) "those who either ignore or do not believe there are aspects of surgery which will be affected by HIV infection" and (2) "those who take an active stance and refuse to operate on any individual who carries or might carry the virus." It will be a welcome source of information to "those surgeons who recognize that HIV infection will be with us for the foreseeable future, that there are risks involved, and that something can be done to reduce the chance of occupational infection." 'I.
Reviewed by Carey P. Page, M D The authors of this 1990 publication have collated the proceedings from a 1987 conference entitled AIDS and Surgery. It represents a "snapshot" of the thoughts and recommendations of scientists and practitioners from the UK and the USA on dealing with a myriad of human immunodeficiency virus (HIV) infection-related issues. Though some of the information is dated, most remains quite applicable and timely. The book is concise and readable. Particularly strong chapters include those concerning the virology of HIV and laboratory and prognostic tests, sterilization and disinfection of equipment including fiberoptic devices, and HIV as an occupational hazard to surgeons. The chapter concerning the legal aspects of acquired immunodeficiency syndrome (AIDS) is as disappointing as the current laws in the UK and USA. The term AZDS (only a portion of the spectrum of HIV infection) and HZV infection are used with approximately equal frequency in this book. This refreshing change is perhaps evidence of maturation of our collective thought processes and similar to transitionally discarding the term consumption once we had a clearer understanding of the bacteriology, epidemiology,
San Antonio, Texas
Cold-reacting autoantibodies occasionally occur in patients requiring cardiac operations. This report describes the clinical course of 1 patient with cold-reacting autoantibodies and intracoronary agglutination of the blood cardioplegia solution. Observations made in vivo and in
vitro are considered in discussing recommendations for the management of extracorporeal circulation and cardioplegic arrest in patients with clinically silent coldreacting autoantibodies. (Ann Thoruc Surg 2991;52:833-6)
C
Postoperatively there was no grossly evident hemolysis and no inotropic support was required. There was no evidence for myocardial necrosis by serial electrocardiographic or creatine kinase isoenzyme determinations (postoperative total creatine kinase: 76, 380, 227 UL; creatine kinase-MB: 5, 11, 5 U/L). The patient's subsequent convalescence was uneventful. In vitro mixing of the patient's blood with cold cardioplegia solution (4"C, 15 minutes) resulted in agglutination (Fig 1). Warming the agglutinated blood to 37°C resulted in dispersion of the erythrocytes (Fig 2). Further agglutination of the patient's blood occurred with continued hypothermia (Fig 3). Subsequent analysis showed that the patient was blood type A Rh+ with an anti-I cold agglutinin titer of 1:256 at 4°C. The patient's blood agglutinated at 24°C (titer, 1:4)but not at 30" or 37°C. The direct antiglobulin test was negative using polyspecific antiglobulin serum, as well as nonspecific anti-immunoglobulin G and anticomplement serum. Additional in vitro tests were performed to better understand the effect of agglutination on erythrocytes passing through small-caliberconduits. Serum from 3 patients with anti-I titers ranging from 1:4 to 1:32 at room temperature was mixed with red cells and incubated at room temperature and 4°C for 30 minutes. 1+ to 4+ visual agglutination was demonstrated before passing the agglutinated blood through an 18+m filter (Hemonate-filter, Gesco International Medical, San Antonio, TX). Sixty millimeters of mercury pressure was constantly applied to the agglutinated blood as it passed through the filter by the attachment of a pressurizing syringe to a sphygmomanometer. The blood passed through the filter without hemolysis as determined by testing a 1:lOO dilution of serum with an Ames Bililabstix (MilesInc, Ames Division, Elkhart, IN). Anti-Lewis b reagent antiserum, another cold-reacting antibody, was mixed with Lewis b positive cells and subjected to the same procedure without evidence of hemolysis. Finally, serum from a patient with clinically severe hemolytic agglutinin disease was mixed with adult red blood cells (incubated for 30 minutes at 4°C
old-reacting autoantibodies are usually of the immunoglobulin M class and are most commonly directed against the human erythrocyte I antigen. Patients with cold-reacting autoantibodies may show the development of acrocyanosis, severe hemolytic anemia, and hemoglobinuria after exposure to cold temperatures; however, cold-reacting autoantibodies with low thermal amplitude are usually clinically silent and may only be detected by preoperative blood typing [l]. The management of patients with cold-reacting autoantibodies who are exposed to hypothermic extracorporeal circulation remains controversial [2-8]. This report describes the clinical course of l patient who had cold-reacting autoantibodies with resultant intracoronary agglutination of the blood cardioplegia solution. Our in vivo and in vitro observations serve as the basis for a discussion of existing protocols for the treatment of similar patients.
Case History and In Vitro Observations The patient is a 69-year-old man with severe pulmonary dysfunction and class IV angina pectoris who was referred for bypass grafting of a proximal stenosis in the anterior descending artery. Angioplasty of this long lesion spanning a large first diagonal branch was considered unsafe. Extracorporeal circulation was conducted at 28°C and a flow of 1.8 L . min-' m-'. The heart was arrested using a 4°C blood cardioplegia solution. Agglutinated blood was found when the anterior descending artery was incised. Two proximal and two distal saphenous vein anastomoses were constructed during a 38-minute ischemic interval. Rewarming to 37°C was initiated during the last proximal anastomosis. The postcardioplegia reperfusion of the heart was begun with a blood cardioplegia solution delivered at 37°C under controlled conditions of flow and pressure. Accepted for publication Oct 23, 1990. Address reprint requests to Dr Holman, Department of Surgery, University Station, Birmingham, AL 35294.
0 1991 by The Society of Thoracic Surgeons
0003-4975/91/$3.50
834
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
Ann Thorac Surg 1991:51:83M
antibody. It is possible that the transcapillary perfusion pressure caused disaggregation of the erythrocytes or that disaggregation occurred with rewarming before the onset of irreversible myocardial ischemic injury. Warm (23°C) cardioplegic arrest [8], preoperative plasma exchange [4,8], intraoperative blood exchange [ 5 ] , and infusion of warm nonoxygenated crystalloid cardioplegia followed by cold crystalloid cardioplegia infusion [3, 5, 7, 81 have all been used in patients with a preoperative finding of cold-reacting autoantibodies. These interventions are intended to decrease the titer of the cold-reacting antibody and maintain the patient’s temperature above the thermal amplitude of the antibody. Such interventions may be crucial in patients with complement-fixing antibodies that can cause hemolysis; however, the observations in our case question the necessity for these interventions in patients with clinically silent nonhemolytic cold-reacting autoantibodies. Although a single infusion of agglutinated blood cardioplegia did not cause myocardial injury in this case, a second infusion of cold (4°C)blood cardioplegia cannot be considered safe in the absence of more complete data. The in vivo and in vitro observations of this report predict that subsequent infusions of cold (4°C)crystalloid cardioplegia solution would be safe if the duration of the procedure
Fig 1 . Agglutination of the patient’s blood by hypothermia at 4°C for 15 minutes ( ~ 1 0 before 0 30% reduction.)
and room temperature). A portion of these samples was passed through the same test system. A large amount of hemolysis was demonstrated in all samples. The mechanism for red cell destruction for this in vitro test was therefore complement activation by cold-reacting autoantibodies rather than agglutination and mechanical destruction.
Comment Our comments are confined to the management of perfusion and hypothermic cardioplegic arrest in patients with the clinically silent, low thermal amplitude, nonhemolytic (ie, benign) variety of cold-reacting autoantibodies. Agglutination of the blood cardioplega solution in our patient did not cause any discernable myocardial damage, and exposure of the blood to temperatures below 24°C during the initial phases of cooling (water bath = 4°C)did not cause hemolysis or malfunction of the hollow-fiber oxygenator (Bentley BCM-7). The cold-reacting autoantibody in this case caused intracoronary agglutination of the blood cardioplegia solution; however, adverse clinical sequelae of hemolysis or myocardial necrosis did not occur. The agglutination of erythrocytes by antibody probably did not result in capillary occlusion even at temperatures well below the thermal amplitude of the
Fig 2 . Dispersion of patient’s blood by rewarming at 37°C for 15 minutes ( ~ 2 0before 0 30% reduction.)
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
Ann Thorac Surg 1991;51:833-6
835
warrants additional doses of cardioplegia. If the presence of nonhemolytic cold-reacting autoantibodies is detected before operation, our experience suggests that 4°C crystalloid cardioplegia could be used safely. The risks of infection and destabilizing fluid shifts associated with plasma exchange are probably not justified in patients with benign cold-reacting autoantibodies.
References
Fig 3 . Further agglutination of the patient’s blood by continued hypothermiu for 30 minutes (x40 before 30% reduction.)
1. Pruzanski W, Shumak KH. Biologic activity of cold-reacting autoantibodies. N Engl J Med 1977;297538-42, 583-9. 2. AuBuchon AJ, Stofan BA, Davey RJ. Hemolysis during extracorporeal circulation: significance of cold-reactive auto-antibodies and mechanical trauma. Blood 1983;62(Suppl 1):42a. 3. Shahian DM, Wallach SR, Bern MM. Open heart surgery in patients with cold-reactive proteins. Surg Clin North Am 1985;65:315-22. 4. Klein HG, Faltz LL, McIntosh CL, Appelbaum FR, Deisseroth AB, Holland PV. Surgical hypothermia in a patient with a cold agglutinin. Management by plasma exchange. Transfusion 1980;20:354-7. 5. Lee MC, Chang CH, Hsieh MJ. Use of a total wash-out method in an open heart operation. Ann Thorac Surg 1989;47 57-8. 6. Moore RA, Geller EA, Mathews ES, Botros SB, Jose AB, Clark DL. The effect of hypothermic cardiopulmonary bypass on patients with low-titer, nonspecific cold agglutinins. Ann Thorac Surg 1984;37233-8. 7. Berreklouw E, Moulijn AC, Pegels JG, Meijne NG. Myocardial protection with cold cardioplegia in a patient with cold agglutinins and hemolysins. Ann Thorac Surg 1982;33:521-2. 8. Paccagnella A, Simini G, Nieri A. Cardiopulmonary bypass and cold agglutinin [Letter]. J Thorac Cardiovasc Surg 1988; 95:543.
INVITED COMMENTARY Patients with cold-reacting antibodies are theoretically at risk for hemolysis or microvascular obstruction by red cell aggregates when hypothermic techniques, including cold cardioplegia, are employed during open heart operations. The degree of antibody-mediated hemolysis that occurs in vivo depends on the extent of complement activation. Complement activation through to C3d will result in normal cell survival, activation to C3b will result in extravascular hemolysis, and activation to C9 will result in intravascular hemolysis. Overt hemolysis is unusual, probably as a result of natural inhibitors of the complement cascade. The incidence of microvascular obstruction by red cell aggregates is not known but may be underestimated. For example, red cell aggregates in the coronary circulation after infusion of cold blood cardioplegia might interfere with cardioplegia distribution, leading to poor myocardial protection and depressed left ventricular function. The relationship of these complications to cold agglutinins may not be recognized. In this case report by Holman and associates, two factors served to mitigate against the development of
these complications, even in the presence of gross erythrocyte agglutination. First, the antibody was of low thermal amplitude and midrange titer. Second, the patient had limited coronary disease and the period of systemic and cardiac hypothermia was limited. The favorable outcome in this report cannot necessarily be extrapolated to patients with complex multivessel disease who may require a prolonged hypothermic period. We also have several reservations about the in vitro methodology employed by Holman and associates. First, there is no evidence that the lack of mechanical trauma to agglutinated red cells when passed through an 18-pm filter under 60 mm Hg pressure accurately simulates the passage of red cells through the coronary microcirculation. Second, the absence of in vitro hemolysis in the three sera tested may be a function of the activity of complement in their test system and may not reflect what would have occurred in vivo. Finally, we are curious as to why the patient’s own blood was never subjected to the in vitro testing described. What then should be the approach to patients with cold
836
CASE REPORT HOLMAN ET AL BLOOD CARDIOPLEGIA AGGLUTINATION
agglutinins who undergo coronary operations? Routine preoperative cold temperature screening of all patients' sera is probably not justified owing to the lack of serious clinical sequelae in most instances. For patients undergoing elective procedures who have known potent cold agglutinins, the thermal amplitude and titer of the antibody should be determined. Knowledge of the thermal amplitude can allow the surgeon to control the degree of autoagglutination by manipulation of cardiac, systemic, and infusate temperatures. More complex preoperative and intraoperative techniques should be reserved for the rare patient with the syndrome of cold autoimmune hemolytic anemia. When red cell agglutination is encountered unexpectedly, the following suggestions may be useful: (1) verification by the blood bank that a cold agglutinin and not an unrecognized alloantibody is present; (2) the use of crystalloid cardioplegia to dilute the
Ann Thorac Surg 1991;51:8W
titer of antibody in the coronary circulation; (3) the use of noncardioplegic techniques; (4) maintenance of systemic temperature greater than 28" to M"C, at which levels significant agglutination is unlikely to occur; and (5) vigilant inspection of the extracorporeal circuit and oxygenators for aggregates. David M . Shahian, M D Department of Thoracic and Cardiovascular Surgery h h e y Clinic Medical Center 41 Mall Rd Burlington, M A 01805 Walter H . Dzik, M D Blood Bank and Tissue Typing Laboratory .Vew England Deaconess Hospital Boston, M A
REVIEW OF RECENT BOOKS
AIDS and Surgery Edited by Andrew 1. W . Sim and Donald I . Ieferies London, Blackwell Scientific Publications, 1990 142 pp, illustrated, $54.95
and control of tuberculosis. This transition reminds all readers new to the area that the true extent of the current epidemic and the real occupational risks are reflected by HIV-infected individuals-not just those with full-blown AIDS. Because the editors . . have altered the manuscripts as httle as possible, . . . individual authors' approaches (and attitudes) . . permeate the text." The professional and ethical conflicts engendered by governmental policies of treating HIV infection and HIV-related illness as social problems rather than as a fatal mfectious disease are readily apparent throughout the book, both by direct comment and through inference. Among these conflicts IS the impediment to infection control, public health, and occupational risk identification imposed by undue emphasis on individual rather than societal rights. Also evident is the paradox between that which seems medically and epidemiologically sound and that which is "legal." This book should be mandatory reading for two identifiable groups of surgeons: (1) "those who either ignore or do not believe there are aspects of surgery which will be affected by HIV infection" and (2) "those who take an active stance and refuse to operate on any individual who carries or might carry the virus." It will be a welcome source of information to "those surgeons who recognize that HIV infection will be with us for the foreseeable future, that there are risks involved, and that something can be done to reduce the chance of occupational infection." 'I.
Reviewed by Carey P. Page, M D The authors of this 1990 publication have collated the proceedings from a 1987 conference entitled AIDS and Surgery. It represents a "snapshot" of the thoughts and recommendations of scientists and practitioners from the UK and the USA on dealing with a myriad of human immunodeficiency virus (HIV) infection-related issues. Though some of the information is dated, most remains quite applicable and timely. The book is concise and readable. Particularly strong chapters include those concerning the virology of HIV and laboratory and prognostic tests, sterilization and disinfection of equipment including fiberoptic devices, and HIV as an occupational hazard to surgeons. The chapter concerning the legal aspects of acquired immunodeficiency syndrome (AIDS) is as disappointing as the current laws in the UK and USA. The term AZDS (only a portion of the spectrum of HIV infection) and HZV infection are used with approximately equal frequency in this book. This refreshing change is perhaps evidence of maturation of our collective thought processes and similar to transitionally discarding the term consumption once we had a clearer understanding of the bacteriology, epidemiology,
San Antonio, Texas