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Recovery from end-stage ischemic cardiomyopathy during long-term LVAD support
Ann Thorac Surg 1998;66:555–7
wall to the SVC, ascending aorta, and right pulmonary artery. The massive cardiac neurilemoma seen in our patient compressed the SVC and appeared to increase its thickness; it had no symptoms or signs except for slight jugular venous dilatation and elevation of the SVC pressure. Because benign cardiac neoplasms may compress or occupy the cardiac chambers, their manifestations are not type-specific but rather an effect of their size and location [5, 6]. Cardiovascular symptoms of such a tumor may include chest pain, syncope, heart failure, cardiac tamponade, arrhythmias, and conductive disorders. Chronic obstruction may cause cardiac failure, with intermittent obstruction representing one cause of syncope. A right-sided tumor may produce obstruction of the SVC [6]. Among the reported occurrences of cardiac neurilemoma, two right-sided tumors have produced right ventricular outflow tract obstruction and subsequent dyspnea [3, 6], and a left-sided tumor has caused atrial fibrillation [4]. Clinical differentiation of cardiac neurilemoma from other cardiac tumors is impossible except by histologic examination. In our case the possibilities of sudden death, syncope, heart failure, arrhythmia, and malignant tumor all demanded prompt surgical treatment, and the resected specimen provided the diagnosis. The prognosis of benign cardiac tumor depends on resectability. After complete resection the prognosis is excellent, and adjuvant therapy is not needed. Among reported cases of cardiac neurilemoma, only 3 have required cardiopulmonary bypass [3–5]. Cardiopulmonary bypass provides a stable hemodynamic state and satisfactory visualization to excise the tumor. In our case cardiopulmonary bypass facilitated complete resection of the tumor from the heart and great vessels, particularly the SVC.
References 1. Factor S, Turi G, Biempica L. Primary cardiac neurilemoma. Cancer 1976;37:883–90. 2. Gleason TH, Dillard DH, Gould VE. Cardiac neurilemoma. NY State J Med 1972;72:2435– 6. 3. Kodama M, Aoki M, Sakai K. Primary cardiac neurilemoma. Circulation 1995;92:274–5. 4. Forbes AD, Schmidt RA, Wood DE, Cochran RP, Munkenbeck F, Verrier ED. Schwannoma of the left atrium: diagnostic evaluation and surgical resection. Ann Thorac Surg 1994;57: 743– 6. 5. Monroe B, Federman M, Balogh K. Cardiac neurilemoma. Report of a case with electron microscopic examination. Arch Pathol Lab Med 1984;108:300– 4. 6. Betancourt B, Defendini EA, Johnson C, et al. Severe right ventricular outflow tract obstruction caused by an intracavitary cardiac neurilemoma. Successful surgical removal and postoperative diagnosis. Chest 1979;75:522– 4. 7. Hallman GL, Cooley DA, Webb JA. Primary tumors of the heart: results of surgical treatment in ten patients. J Cardiovasc Surg 1966;7:447–57. 8. Cayten CG, Kastor JA, Park CD. Unusual presentation of © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
555
intrathoracic malignant schwannoma. J Thorac Cardiovasc Surg 1973;66:601– 6.
Recovery From End-Stage Ischemic Cardiomyopathy During LongTerm LVAD Support Lars Pietsch, MD, Horst Laube, MD, Gerd Baumann, MD, PhD, and Wolfgang Konertz, MD, PhD Departments of Cardiac Surgery and Cardiology, Charite´, Humboldt University, Berlin, Germany
A patient with ischemic cardiomyopathy and extremely reduced left ventricular function (left ventricular ejection fraction 5 0.10) presented to our institution for cardiac transplantation. Because of his worsening condition he was placed on the Novacor left ventricular assist device. During 3 months of support his left ventricular function recovered and he successfully underwent percutaneous transluminal coronary angioplasty and minimally invasive direct coronary artery bypass grafting procedures; subsequently he could be weaned from the left ventricular assist device and discharged. The patient is no longer considered for cardiac transplantation. (Ann Thorac Surg 1998;66:555–7) © 1998 by The Society of Thoracic Surgeons
T
here is increasing evidence that some patients’ hearts recover during long-term left ventricular (LV) assist [1]. This has been observed with patients after heterotopic heart transplantation [2], as well as after mechanical circulatory assist. Successful coronary revascularization is highly dependent on the presence of viable myocardium. Tools for discriminating hibernating myocardium from scar and nonviable tissue are not perfect. Currently no technique shows 100% accuracy, especially in extremely dysfunctional hearts [3]. A 54-year-old patient was transferred to our institution with cardiac failure. An intensified medical regimen including diuretics, b-blockers, digitalis, and angiotensin-converting enzyme inhibitors failed to improve his situation. Cardiac catheterization showed two-vessel disease with occlusion of the proximal left anterior descending artery and a 75% stenosis of the circumflex artery. Left ventricular function was extremely reduced, with an LV ejection fraction of 0.10. The LV end-diastolic volume Accepted for publication Feb 25, 1998. Address reprint requests to Dr Pietsch, Universita¨tsklinikum Charite, Klinik fu¨r Herzchirurgie, Schumannstr 20-21, 10717 Berlin, Germany (e-mail: cardiac&rz.charite.hu-berlin.de).
0003-4975/98/$19.00 PII S0003-4975(98)00507-4
556
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
Ann Thorac Surg 1998;66:555–7
the left internal mammary artery to the left anterior descending artery on the beating heart was performed. After recovery from the operation, the Novacor LV assist device was set on the fixed-rate mode at 60 beats/ min, and slowly during three subsequent weeks the rate was slowed down to 40 beats/min. As the patient tolerated this gradual decrease of support well, he underwent elective removal of the device 4 weeks after revascularization. Six weeks later the patient was discharged home. The LV ejection fraction at this time had increased to 0.50. Six months later the patient is doing well with medication of digitalis, angiotensin-converting enzyme inhibitor, b-blocker, and aspirin. Echocardiographic estimation of LV function in the outpatient clinic showed an unchanged LV ejection fraction of 0.50.
Comment
Fig 1. Left ventriculogram at admission showing severe left ventricular dysfunction and increased left ventricular volumes (EF 5 ejection fraction.)
was 287 mL, and the end-systolic volume was 258 mL (Fig 1). Cardiac index was calculated as 1.3 L z min21 z m22 by the Fick method. Pulmonary hypertension with a mean pressure of 45 mm Hg, a wedge pressure of 24 mm Hg, and a pulmonary vascular resistance of 8 Wood units were present. Scintigraphy showed no viable myocardium. Because of the elevated pulmonary vascular resistance, cardiac transplantation seemed to be contraindicated and the patient was placed on the wearable Novacor LV assist device (Baxter Healthcare Corporation, Irvine, CA) for improvement of the peripheral circulation and to see whether his pulmonary hypertension was reversible with long-term unloading of the left ventricle. Implantation and postoperative course were uneventful, and the patient could be transferred to a partial outpatient status after 6 weeks. Two months later cardiac recatheterization, which is our routine institutional protocol for patients on long-term chronic LV assist devices, showed an unforeseen recovery of the myocardium. The LV ejection fraction was 0.46 with the device on and fell to 0.36 after the Novacor device was switched off (Fig 2). Left ventricular volumes had returned to near normal. Pulmonary artery pressure had dropped to normal on the device and showed no increase when the LV assist device was switched off. This, the increase in contractility, and the improved LV function made treatment of the underlying coronary artery disease possible. The patient underwent a successful percutaneous transluminal coronary angioplasty of the circumflex artery, and the next day minimally invasive direct coronary artery bypass grafting of
Several points in this report seem noteworthy. First is the inability of nuclear scan to detect viable myocardium in this patient. This could be caused by two mechanisms: (1) the metabolic status of hibernating myocardium and (2) high wall tension and stretch on the epicardial vessels making perfusion indetectable. There is evidence that myocardial perfusion is limited not only by hypertrophy but also by dilatation of the left ventricle [3]. Chronic LV unloading leads to a decrease in LV size, wall tension, and intramyocardial pressurizing force, which subsequently improves perfusion and function, a pathophysiologic pathway that is currently being thoroughly investigated for the LV size reduction operation
Fig 2. Left ventriculogram after recovery with the left ventricular assist device switched off showed remarkable recovery of left ventricular function and dimensions.
Ann Thorac Surg 1998;66:557– 8
[4]. Recovery of LV function in our patient made possible treatment of the underlying coronary artery disease, which could be performed rather atraumatically by a so-called hybrid procedure, which means a combination of percutaneous catheter techniques and a minimally invasive cardiac operation. Surgical revascularization of the posterior wall with the Novacor device in situ would have been extremely technically demanding. Cardiopulmonary bypass, cardioplegic arrest, and extensive dissection of the heart were avoided by use of the hybrid procedure. Recovery of the heart after chronic LV assist has been observed in the setting of myocarditis [5] and occasionally in idiopathic dilative cardiomyopathy. Also, we and others found reversal of LV dysfunction in patients with ischemic dilative cardiomyopathy after heterotopic cardiac transplantation and concomitant repair of the recipient’s heart [2, 6]. In 1 pediatric patient with a large anterior myocardial infarction caused by an anomalous left coronary artery from the pulmonary artery, it was possible to explant the donor heart after near-complete recovery of the native heart had occurred 3 years after revascularization and simultaneous heterotopic cardiac transplantation [6]. This case report indicates that some high-risk patients may benefit from LV assist device implantation as a “bridge to repair” rather than a “bridge to transplantation,” which has been shown to work well recently for other surgical procedures, for example, partial left ventriculectomy [7].
References 1. Levin HR, Oz MC, Chen JM, Packer M, Rose EA, Burkhoff D. Reversal of chronic ventricular dilation in patients with end stage cardiomyopathy by prolonged mechanical unloading. Circulation 1995;91:2717–20. 2. Konertz W, Sheikzadeh A, Weigand M, Friedl A, Bernhard A. Heterotopic heart transplantation— current indications for the procedure with results in 10 patients. Tex Heart Inst J 1988;15:159– 62. 3. Soha GB, Macintyre J, Brunken R, et al. Present assessment of myocardial viability by nuclear imaging. Semin Nucl Med 1996;26:315–35. 4. Lunkenheimer PP, Redmann K, Dietl LH, et al. The assessment of intramural stress alignment on the beating heart in situ using microergometry: functional implications. Technol Healthcare 1997;5:115–22. 5. Martin G, Kogpani S, Schindler M, van de Loo A, Yoshitoke M, Beyersdorf F. MEDOS HIA-VAD biventricular assist device for bridge to recovery in fulminant myocarditis. Ann Thorac Surg 1997;63:1145– 6. 6. Schmid C, Kececioglu D, Konertz W, Mo¨llhoff T, Scheld H. Biological bridging after repair of an anomolous origin of a left coronary artery. Ann Thorac Surg 1996;62:1839– 41. 7. Frazier OH, Radovancevic B, Odegaard P, Hernandez P, Wilansky S, Cook P. Left ventricular reduction in patients with idiopathic cardiomyopathy awaiting heart transplantation—preliminary results [Abstract]. J Heart Lung Transplant 1997;16:80. © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT NODA ET AL ABDOMINAL HEMORRHAGE DURING CPB
557
Intraabdominal Hemorrhage During Combined Coronary Artery Bypass and Carotid Endarterectomy Seiichi Noda, MD, Michael J. Buckmaster, MD, Charles W. Hogue, Jr, MD, Brian G. Rubin, MD, and Thoralf M. Sundt III, MD Divisions of Cardiothoracic Surgery and Vascular Surgery, Department of Surgery, and Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri
Intraabdominal complications during cardiopulmonary bypass are extremely rare, with an incidence of less than 1% in multiple retrospective studies. These complications are associated with a high mortality, and their rapid diagnosis is critical to the outcome of the patient. We present a case of spontaneous intraabdominal hemorrhage after combined carotid endarterectomy and fourvessel coronary artery bypass grafting, which was diagnosed through a diaphragmatic window. (Ann Thorac Surg 1998;66:557– 8) © 1998 by The Society of Thoracic Surgeons
I
ntraabdominal complications occur infrequently during procedures involving cardiopulmonary bypass (CPB) but are associated with high mortality. Multiple retrospective studies have identified gastrointestinal bleeding and intestinal ischemia as the most common intraabdominal complications after CPB [1– 4]. The mortality associated with these complications approaches 100%, in part because of a delay in diagnosis resulting in irreversible end-organ injury in these critically ill patients. To obviate adverse patient outcomes, a high level of suspicion is required for early diagnosis of intraabdominal complications. In this report, we present a case in which a small diaphragmatic window created from the inferior aspect of a median sternotomy incision was used to facilitate the diagnosis of an acute intraperitoneal hemorrhage. A 60-year-old man presented with symptoms of increasing fatigability and chest fluttering. Past medical history was significant for non–insulin-dependent diabetes mellitus and a left hemispheric stroke 2 years before the present admission with minimal residual deficit. His laboratory values and renal function were within normal limits. Serum creatine kinase enzyme levels were consistent with an acute myocardial infarction. He was found to have severe three-vessel disease with severely impaired left ventricular function on cardiac catheterization. Duplex examination demonstrated 80% to 99% stenosis of his carotid arteries bilaterally. Neuroangiog-
Accepted for publication Feb 26, 1998. Address reprint requests to Dr Sundt, Division of Cardiothoracic Surgery, Washington University School of Medicine, One Barnes Hospital Plaza, Suite 3108 Queeny Tower, St. Louis, MO 63110.
0003-4975/98/$19.00 PII S0003-4975(98)00474-3
wall to the SVC, ascending aorta, and right pulmonary artery. The massive cardiac neurilemoma seen in our patient compressed the SVC and appeared to increase its thickness; it had no symptoms or signs except for slight jugular venous dilatation and elevation of the SVC pressure. Because benign cardiac neoplasms may compress or occupy the cardiac chambers, their manifestations are not type-specific but rather an effect of their size and location [5, 6]. Cardiovascular symptoms of such a tumor may include chest pain, syncope, heart failure, cardiac tamponade, arrhythmias, and conductive disorders. Chronic obstruction may cause cardiac failure, with intermittent obstruction representing one cause of syncope. A right-sided tumor may produce obstruction of the SVC [6]. Among the reported occurrences of cardiac neurilemoma, two right-sided tumors have produced right ventricular outflow tract obstruction and subsequent dyspnea [3, 6], and a left-sided tumor has caused atrial fibrillation [4]. Clinical differentiation of cardiac neurilemoma from other cardiac tumors is impossible except by histologic examination. In our case the possibilities of sudden death, syncope, heart failure, arrhythmia, and malignant tumor all demanded prompt surgical treatment, and the resected specimen provided the diagnosis. The prognosis of benign cardiac tumor depends on resectability. After complete resection the prognosis is excellent, and adjuvant therapy is not needed. Among reported cases of cardiac neurilemoma, only 3 have required cardiopulmonary bypass [3–5]. Cardiopulmonary bypass provides a stable hemodynamic state and satisfactory visualization to excise the tumor. In our case cardiopulmonary bypass facilitated complete resection of the tumor from the heart and great vessels, particularly the SVC.
References 1. Factor S, Turi G, Biempica L. Primary cardiac neurilemoma. Cancer 1976;37:883–90. 2. Gleason TH, Dillard DH, Gould VE. Cardiac neurilemoma. NY State J Med 1972;72:2435– 6. 3. Kodama M, Aoki M, Sakai K. Primary cardiac neurilemoma. Circulation 1995;92:274–5. 4. Forbes AD, Schmidt RA, Wood DE, Cochran RP, Munkenbeck F, Verrier ED. Schwannoma of the left atrium: diagnostic evaluation and surgical resection. Ann Thorac Surg 1994;57: 743– 6. 5. Monroe B, Federman M, Balogh K. Cardiac neurilemoma. Report of a case with electron microscopic examination. Arch Pathol Lab Med 1984;108:300– 4. 6. Betancourt B, Defendini EA, Johnson C, et al. Severe right ventricular outflow tract obstruction caused by an intracavitary cardiac neurilemoma. Successful surgical removal and postoperative diagnosis. Chest 1979;75:522– 4. 7. Hallman GL, Cooley DA, Webb JA. Primary tumors of the heart: results of surgical treatment in ten patients. J Cardiovasc Surg 1966;7:447–57. 8. Cayten CG, Kastor JA, Park CD. Unusual presentation of © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
555
intrathoracic malignant schwannoma. J Thorac Cardiovasc Surg 1973;66:601– 6.
Recovery From End-Stage Ischemic Cardiomyopathy During LongTerm LVAD Support Lars Pietsch, MD, Horst Laube, MD, Gerd Baumann, MD, PhD, and Wolfgang Konertz, MD, PhD Departments of Cardiac Surgery and Cardiology, Charite´, Humboldt University, Berlin, Germany
A patient with ischemic cardiomyopathy and extremely reduced left ventricular function (left ventricular ejection fraction 5 0.10) presented to our institution for cardiac transplantation. Because of his worsening condition he was placed on the Novacor left ventricular assist device. During 3 months of support his left ventricular function recovered and he successfully underwent percutaneous transluminal coronary angioplasty and minimally invasive direct coronary artery bypass grafting procedures; subsequently he could be weaned from the left ventricular assist device and discharged. The patient is no longer considered for cardiac transplantation. (Ann Thorac Surg 1998;66:555–7) © 1998 by The Society of Thoracic Surgeons
T
here is increasing evidence that some patients’ hearts recover during long-term left ventricular (LV) assist [1]. This has been observed with patients after heterotopic heart transplantation [2], as well as after mechanical circulatory assist. Successful coronary revascularization is highly dependent on the presence of viable myocardium. Tools for discriminating hibernating myocardium from scar and nonviable tissue are not perfect. Currently no technique shows 100% accuracy, especially in extremely dysfunctional hearts [3]. A 54-year-old patient was transferred to our institution with cardiac failure. An intensified medical regimen including diuretics, b-blockers, digitalis, and angiotensin-converting enzyme inhibitors failed to improve his situation. Cardiac catheterization showed two-vessel disease with occlusion of the proximal left anterior descending artery and a 75% stenosis of the circumflex artery. Left ventricular function was extremely reduced, with an LV ejection fraction of 0.10. The LV end-diastolic volume Accepted for publication Feb 25, 1998. Address reprint requests to Dr Pietsch, Universita¨tsklinikum Charite, Klinik fu¨r Herzchirurgie, Schumannstr 20-21, 10717 Berlin, Germany (e-mail: cardiac&rz.charite.hu-berlin.de).
0003-4975/98/$19.00 PII S0003-4975(98)00507-4
556
CASE REPORT PIETSCH ET AL RECOVERY FROM END-STAGE CARDIOMYOPATHY
Ann Thorac Surg 1998;66:555–7
the left internal mammary artery to the left anterior descending artery on the beating heart was performed. After recovery from the operation, the Novacor LV assist device was set on the fixed-rate mode at 60 beats/ min, and slowly during three subsequent weeks the rate was slowed down to 40 beats/min. As the patient tolerated this gradual decrease of support well, he underwent elective removal of the device 4 weeks after revascularization. Six weeks later the patient was discharged home. The LV ejection fraction at this time had increased to 0.50. Six months later the patient is doing well with medication of digitalis, angiotensin-converting enzyme inhibitor, b-blocker, and aspirin. Echocardiographic estimation of LV function in the outpatient clinic showed an unchanged LV ejection fraction of 0.50.
Comment
Fig 1. Left ventriculogram at admission showing severe left ventricular dysfunction and increased left ventricular volumes (EF 5 ejection fraction.)
was 287 mL, and the end-systolic volume was 258 mL (Fig 1). Cardiac index was calculated as 1.3 L z min21 z m22 by the Fick method. Pulmonary hypertension with a mean pressure of 45 mm Hg, a wedge pressure of 24 mm Hg, and a pulmonary vascular resistance of 8 Wood units were present. Scintigraphy showed no viable myocardium. Because of the elevated pulmonary vascular resistance, cardiac transplantation seemed to be contraindicated and the patient was placed on the wearable Novacor LV assist device (Baxter Healthcare Corporation, Irvine, CA) for improvement of the peripheral circulation and to see whether his pulmonary hypertension was reversible with long-term unloading of the left ventricle. Implantation and postoperative course were uneventful, and the patient could be transferred to a partial outpatient status after 6 weeks. Two months later cardiac recatheterization, which is our routine institutional protocol for patients on long-term chronic LV assist devices, showed an unforeseen recovery of the myocardium. The LV ejection fraction was 0.46 with the device on and fell to 0.36 after the Novacor device was switched off (Fig 2). Left ventricular volumes had returned to near normal. Pulmonary artery pressure had dropped to normal on the device and showed no increase when the LV assist device was switched off. This, the increase in contractility, and the improved LV function made treatment of the underlying coronary artery disease possible. The patient underwent a successful percutaneous transluminal coronary angioplasty of the circumflex artery, and the next day minimally invasive direct coronary artery bypass grafting of
Several points in this report seem noteworthy. First is the inability of nuclear scan to detect viable myocardium in this patient. This could be caused by two mechanisms: (1) the metabolic status of hibernating myocardium and (2) high wall tension and stretch on the epicardial vessels making perfusion indetectable. There is evidence that myocardial perfusion is limited not only by hypertrophy but also by dilatation of the left ventricle [3]. Chronic LV unloading leads to a decrease in LV size, wall tension, and intramyocardial pressurizing force, which subsequently improves perfusion and function, a pathophysiologic pathway that is currently being thoroughly investigated for the LV size reduction operation
Fig 2. Left ventriculogram after recovery with the left ventricular assist device switched off showed remarkable recovery of left ventricular function and dimensions.
Ann Thorac Surg 1998;66:557– 8
[4]. Recovery of LV function in our patient made possible treatment of the underlying coronary artery disease, which could be performed rather atraumatically by a so-called hybrid procedure, which means a combination of percutaneous catheter techniques and a minimally invasive cardiac operation. Surgical revascularization of the posterior wall with the Novacor device in situ would have been extremely technically demanding. Cardiopulmonary bypass, cardioplegic arrest, and extensive dissection of the heart were avoided by use of the hybrid procedure. Recovery of the heart after chronic LV assist has been observed in the setting of myocarditis [5] and occasionally in idiopathic dilative cardiomyopathy. Also, we and others found reversal of LV dysfunction in patients with ischemic dilative cardiomyopathy after heterotopic cardiac transplantation and concomitant repair of the recipient’s heart [2, 6]. In 1 pediatric patient with a large anterior myocardial infarction caused by an anomalous left coronary artery from the pulmonary artery, it was possible to explant the donor heart after near-complete recovery of the native heart had occurred 3 years after revascularization and simultaneous heterotopic cardiac transplantation [6]. This case report indicates that some high-risk patients may benefit from LV assist device implantation as a “bridge to repair” rather than a “bridge to transplantation,” which has been shown to work well recently for other surgical procedures, for example, partial left ventriculectomy [7].
References 1. Levin HR, Oz MC, Chen JM, Packer M, Rose EA, Burkhoff D. Reversal of chronic ventricular dilation in patients with end stage cardiomyopathy by prolonged mechanical unloading. Circulation 1995;91:2717–20. 2. Konertz W, Sheikzadeh A, Weigand M, Friedl A, Bernhard A. Heterotopic heart transplantation— current indications for the procedure with results in 10 patients. Tex Heart Inst J 1988;15:159– 62. 3. Soha GB, Macintyre J, Brunken R, et al. Present assessment of myocardial viability by nuclear imaging. Semin Nucl Med 1996;26:315–35. 4. Lunkenheimer PP, Redmann K, Dietl LH, et al. The assessment of intramural stress alignment on the beating heart in situ using microergometry: functional implications. Technol Healthcare 1997;5:115–22. 5. Martin G, Kogpani S, Schindler M, van de Loo A, Yoshitoke M, Beyersdorf F. MEDOS HIA-VAD biventricular assist device for bridge to recovery in fulminant myocarditis. Ann Thorac Surg 1997;63:1145– 6. 6. Schmid C, Kececioglu D, Konertz W, Mo¨llhoff T, Scheld H. Biological bridging after repair of an anomolous origin of a left coronary artery. Ann Thorac Surg 1996;62:1839– 41. 7. Frazier OH, Radovancevic B, Odegaard P, Hernandez P, Wilansky S, Cook P. Left ventricular reduction in patients with idiopathic cardiomyopathy awaiting heart transplantation—preliminary results [Abstract]. J Heart Lung Transplant 1997;16:80. © 1998 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
CASE REPORT NODA ET AL ABDOMINAL HEMORRHAGE DURING CPB
557
Intraabdominal Hemorrhage During Combined Coronary Artery Bypass and Carotid Endarterectomy Seiichi Noda, MD, Michael J. Buckmaster, MD, Charles W. Hogue, Jr, MD, Brian G. Rubin, MD, and Thoralf M. Sundt III, MD Divisions of Cardiothoracic Surgery and Vascular Surgery, Department of Surgery, and Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri
Intraabdominal complications during cardiopulmonary bypass are extremely rare, with an incidence of less than 1% in multiple retrospective studies. These complications are associated with a high mortality, and their rapid diagnosis is critical to the outcome of the patient. We present a case of spontaneous intraabdominal hemorrhage after combined carotid endarterectomy and fourvessel coronary artery bypass grafting, which was diagnosed through a diaphragmatic window. (Ann Thorac Surg 1998;66:557– 8) © 1998 by The Society of Thoracic Surgeons
I
ntraabdominal complications occur infrequently during procedures involving cardiopulmonary bypass (CPB) but are associated with high mortality. Multiple retrospective studies have identified gastrointestinal bleeding and intestinal ischemia as the most common intraabdominal complications after CPB [1– 4]. The mortality associated with these complications approaches 100%, in part because of a delay in diagnosis resulting in irreversible end-organ injury in these critically ill patients. To obviate adverse patient outcomes, a high level of suspicion is required for early diagnosis of intraabdominal complications. In this report, we present a case in which a small diaphragmatic window created from the inferior aspect of a median sternotomy incision was used to facilitate the diagnosis of an acute intraperitoneal hemorrhage. A 60-year-old man presented with symptoms of increasing fatigability and chest fluttering. Past medical history was significant for non–insulin-dependent diabetes mellitus and a left hemispheric stroke 2 years before the present admission with minimal residual deficit. His laboratory values and renal function were within normal limits. Serum creatine kinase enzyme levels were consistent with an acute myocardial infarction. He was found to have severe three-vessel disease with severely impaired left ventricular function on cardiac catheterization. Duplex examination demonstrated 80% to 99% stenosis of his carotid arteries bilaterally. Neuroangiog-
Accepted for publication Feb 26, 1998. Address reprint requests to Dr Sundt, Division of Cardiothoracic Surgery, Washington University School of Medicine, One Barnes Hospital Plaza, Suite 3108 Queeny Tower, St. Louis, MO 63110.
0003-4975/98/$19.00 PII S0003-4975(98)00474-3