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Surgery_Schwartz_5002
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J Thorac Cardiovasc Surg. 1994;107(4):1087-1093; discussion 1093-1094. 49. Bedetti B, Bertolaccini L, Rocco R, Schmidt J, Solli P, Scarci M. Segmentectomy versus lobectomy for stage I non-small cell lung cancer: a systematic review and meta-analysis. J Thorac Dis. 2017;9(6):1615-1623. 50. Schuchert MJ, Pettiford BL, Keeley S, et al. Anatomic seg-mentectomy in the treatment of stage I non-small cell lung cancer. Ann Thorac Surg. 2007;84(3):926-932; discussion 932-923. 51. Sienel W, Stremmel C, Kirschbaum A, et al. Frequency of local recurrence following segmentectomy of stage IA non-small cell lung cancer is influenced by segment localisation and width of resection margins–implications for patient selec-tion for segmentectomy. Eur J Cardiothorac Surg. 2007;31(3): 522-527; discussion 527-528. 52. Shapiro M, Weiser TS, Wisnivesky JP, Chin C, Arustamyan M, Swanson SJ. Thoracoscopic segmentectomy compares favorably with thoracoscopic lobectomy for patients with small stage I lung cancer.
Surgery_Schwartz. J Thorac Cardiovasc Surg. 1994;107(4):1087-1093; discussion 1093-1094. 49. Bedetti B, Bertolaccini L, Rocco R, Schmidt J, Solli P, Scarci M. Segmentectomy versus lobectomy for stage I non-small cell lung cancer: a systematic review and meta-analysis. J Thorac Dis. 2017;9(6):1615-1623. 50. Schuchert MJ, Pettiford BL, Keeley S, et al. Anatomic seg-mentectomy in the treatment of stage I non-small cell lung cancer. Ann Thorac Surg. 2007;84(3):926-932; discussion 932-923. 51. Sienel W, Stremmel C, Kirschbaum A, et al. Frequency of local recurrence following segmentectomy of stage IA non-small cell lung cancer is influenced by segment localisation and width of resection margins–implications for patient selec-tion for segmentectomy. Eur J Cardiothorac Surg. 2007;31(3): 522-527; discussion 527-528. 52. Shapiro M, Weiser TS, Wisnivesky JP, Chin C, Arustamyan M, Swanson SJ. Thoracoscopic segmentectomy compares favorably with thoracoscopic lobectomy for patients with small stage I lung cancer.
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M, Weiser TS, Wisnivesky JP, Chin C, Arustamyan M, Swanson SJ. Thoracoscopic segmentectomy compares favorably with thoracoscopic lobectomy for patients with small stage I lung cancer. J Thorac Cardiovasc Surg. 2009;137(6):1388-1393. 53. Oizumi H, Kanauchi N, Kato H, et al. Total thoracoscopic pulmonary segmentectomy. Eur J Cardiothorac Surg. 2009;36(2):374-377; discussion 377. 54. Schuchert MJ, Pettiford BL, Pennathur A, et al. Anatomic seg-mentectomy for stage I non-small-cell lung cancer: compari-son of video-assisted thoracic surgery versus open approach. J Thorac Cardiovasc Surg. 2009;138(6):1318-1325. e1311. 55. Watanabe A, Ohori S, Nakashima S, et al. Feasibility of video-assisted thoracoscopic surgery segmentectomy for selected peripheral lung carcinomas. Eur J Cardiothorac Surg. 2009;35(5):775-780; discussion 780. 56. Fuwa N, Mitsudomi T, Daimon T, et al. Factors involved in lymph node metastasis in clinical stage I non-small cell lung cancer–from studies of 604 surgical
Surgery_Schwartz. M, Weiser TS, Wisnivesky JP, Chin C, Arustamyan M, Swanson SJ. Thoracoscopic segmentectomy compares favorably with thoracoscopic lobectomy for patients with small stage I lung cancer. J Thorac Cardiovasc Surg. 2009;137(6):1388-1393. 53. Oizumi H, Kanauchi N, Kato H, et al. Total thoracoscopic pulmonary segmentectomy. Eur J Cardiothorac Surg. 2009;36(2):374-377; discussion 377. 54. Schuchert MJ, Pettiford BL, Pennathur A, et al. Anatomic seg-mentectomy for stage I non-small-cell lung cancer: compari-son of video-assisted thoracic surgery versus open approach. J Thorac Cardiovasc Surg. 2009;138(6):1318-1325. e1311. 55. Watanabe A, Ohori S, Nakashima S, et al. Feasibility of video-assisted thoracoscopic surgery segmentectomy for selected peripheral lung carcinomas. Eur J Cardiothorac Surg. 2009;35(5):775-780; discussion 780. 56. Fuwa N, Mitsudomi T, Daimon T, et al. Factors involved in lymph node metastasis in clinical stage I non-small cell lung cancer–from studies of 604 surgical
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2009;35(5):775-780; discussion 780. 56. Fuwa N, Mitsudomi T, Daimon T, et al. Factors involved in lymph node metastasis in clinical stage I non-small cell lung cancer–from studies of 604 surgical cases. Lung Cancer. 2007;57(3):311-316. 57. Fernando HC, De Hoyos A, Landreneau RJ, et al. Radiofre-quency ablation for the treatment of non-small cell lung cancer in marginal surgical candidates. J Thorac Cardiovasc Surg. 2005;129(3):639-644. 58. Pennathur A, Luketich JD, Abbas G, et al. Radiofrequency ablation for the treatment of stage I non-small cell lung cancer in high-risk patients. J Thorac Cardiovasc Surg. 2007;134(4):857-864. 59. Lencioni R, Crocetti L, Cioni R, et al. Response to radiofre-quency ablation of pulmonary tumours: a prospective, inten-tion-to-treat, multicentre clinical trial (the RAPTURE study). Lancet Oncol. 2008;9(7):621-628. 60. Fakiris AJ, McGarry RC, Yiannoutsos CT, et al. Stereotactic body radiation therapy for early-stage non-small-cell lung car-cinoma:
Surgery_Schwartz. 2009;35(5):775-780; discussion 780. 56. Fuwa N, Mitsudomi T, Daimon T, et al. Factors involved in lymph node metastasis in clinical stage I non-small cell lung cancer–from studies of 604 surgical cases. Lung Cancer. 2007;57(3):311-316. 57. Fernando HC, De Hoyos A, Landreneau RJ, et al. Radiofre-quency ablation for the treatment of non-small cell lung cancer in marginal surgical candidates. J Thorac Cardiovasc Surg. 2005;129(3):639-644. 58. Pennathur A, Luketich JD, Abbas G, et al. Radiofrequency ablation for the treatment of stage I non-small cell lung cancer in high-risk patients. J Thorac Cardiovasc Surg. 2007;134(4):857-864. 59. Lencioni R, Crocetti L, Cioni R, et al. Response to radiofre-quency ablation of pulmonary tumours: a prospective, inten-tion-to-treat, multicentre clinical trial (the RAPTURE study). Lancet Oncol. 2008;9(7):621-628. 60. Fakiris AJ, McGarry RC, Yiannoutsos CT, et al. Stereotactic body radiation therapy for early-stage non-small-cell lung car-cinoma:
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trial (the RAPTURE study). Lancet Oncol. 2008;9(7):621-628. 60. Fakiris AJ, McGarry RC, Yiannoutsos CT, et al. Stereotactic body radiation therapy for early-stage non-small-cell lung car-cinoma: four-year results of a prospective phase II study. Int J Radiat Oncol Biol Phys. 2009;75(3):677-682. 61. Potters L, Kavanagh B, Galvin JM, et al. American Society for Therapeutic Radiology and Oncology (ASTRO) and American College of Radiology (ACR) practice guideline for the per-formance of stereotactic body radiation therapy. Int J Radiat Oncol Biol Phys. 2010;76(2):326-332. 62. Timmerman R, Paulus R, Galvin J, et al. Stereotactic body radiation therapy for inoperable early stage lung cancer. JAMA. 2010;303(11):1070-1076. 63. Simon CJ, Dupuy DE, DiPetrillo TA, et al. Pulmonary radio-frequency ablation: long-term safety and efficacy in 153 patients. Radiology. 2007;243(1):268-275. 64. Abbas G, Pennathur A, Landreneau RJ, Luketich JD. Radio-frequency and microwave ablation of lung tumors. J
Surgery_Schwartz. trial (the RAPTURE study). Lancet Oncol. 2008;9(7):621-628. 60. Fakiris AJ, McGarry RC, Yiannoutsos CT, et al. Stereotactic body radiation therapy for early-stage non-small-cell lung car-cinoma: four-year results of a prospective phase II study. Int J Radiat Oncol Biol Phys. 2009;75(3):677-682. 61. Potters L, Kavanagh B, Galvin JM, et al. American Society for Therapeutic Radiology and Oncology (ASTRO) and American College of Radiology (ACR) practice guideline for the per-formance of stereotactic body radiation therapy. Int J Radiat Oncol Biol Phys. 2010;76(2):326-332. 62. Timmerman R, Paulus R, Galvin J, et al. Stereotactic body radiation therapy for inoperable early stage lung cancer. JAMA. 2010;303(11):1070-1076. 63. Simon CJ, Dupuy DE, DiPetrillo TA, et al. Pulmonary radio-frequency ablation: long-term safety and efficacy in 153 patients. Radiology. 2007;243(1):268-275. 64. Abbas G, Pennathur A, Landreneau RJ, Luketich JD. Radio-frequency and microwave ablation of lung tumors. J
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ablation: long-term safety and efficacy in 153 patients. Radiology. 2007;243(1):268-275. 64. Abbas G, Pennathur A, Landreneau RJ, Luketich JD. Radio-frequency and microwave ablation of lung tumors. J Surg Oncol. 2009;100(8):645-650. 65. Lanuti M, Sharma A, Digumarthy SR, et al. Radiofre-quency ablation for treatment of medically inoperable stage I nonsmall cell lung cancer. J Thorac Cardiovasc Surg. 2009;137(1):160-166. 66. Pua BB, Solomon SB. Radiofrequency ablation of primary and metastatic lung cancers. Semin Ultrasound CT MR. 2009;30(2):113-124. 67. Casal RF, Tam AL, Eapen GA. Radiofrequency ablation of lung tumors. Clin Chest Med. 2010;31(1):151-163. 68. Crocetti L, Lencioni R. Radiofrequency ablation of pulmonary tumors. Eur J Radiol. 2010;75(1):23-27. 69. Fernando HC, Schuchert M, Landreneau R, Daly BT. Approaching the high-risk patient: sublobar resection, stereo-tactic body radiation therapy, or radiofrequency ablation. Ann Thorac Surg. 2010;89(6):S2123-2127. 70. Timmerman
Surgery_Schwartz. ablation: long-term safety and efficacy in 153 patients. Radiology. 2007;243(1):268-275. 64. Abbas G, Pennathur A, Landreneau RJ, Luketich JD. Radio-frequency and microwave ablation of lung tumors. J Surg Oncol. 2009;100(8):645-650. 65. Lanuti M, Sharma A, Digumarthy SR, et al. Radiofre-quency ablation for treatment of medically inoperable stage I nonsmall cell lung cancer. J Thorac Cardiovasc Surg. 2009;137(1):160-166. 66. Pua BB, Solomon SB. Radiofrequency ablation of primary and metastatic lung cancers. Semin Ultrasound CT MR. 2009;30(2):113-124. 67. Casal RF, Tam AL, Eapen GA. Radiofrequency ablation of lung tumors. Clin Chest Med. 2010;31(1):151-163. 68. Crocetti L, Lencioni R. Radiofrequency ablation of pulmonary tumors. Eur J Radiol. 2010;75(1):23-27. 69. Fernando HC, Schuchert M, Landreneau R, Daly BT. Approaching the high-risk patient: sublobar resection, stereo-tactic body radiation therapy, or radiofrequency ablation. Ann Thorac Surg. 2010;89(6):S2123-2127. 70. Timmerman
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Landreneau R, Daly BT. Approaching the high-risk patient: sublobar resection, stereo-tactic body radiation therapy, or radiofrequency ablation. Ann Thorac Surg. 2010;89(6):S2123-2127. 70. Timmerman R, McGarry R, Yiannoutsos C, et al. Excessive toxicity when treating central tumors in a phase II study of B stereotactic body radiation therapy for medically inoperable early-stage lung cancer. J Clin Oncol. 2006;24(30):4833-4839. 71. Pisters KM, Ginsberg RJ, Giroux DJ, et al. Induction chemo-therapy before surgery for early-stage lung cancer: a novel approach. Bimodality Lung Oncology Team. J Thorac Car-diovasc Surg. 2000;119(3):429-439. 72. Rosell R, Gomez-Codina J, Camps C, et al. A randomized trial comparing preoperative chemotherapy plus surgery with sur-gery alone in patients with non–small-cell lung cancer. N Engl J Med. 1994;330(3):153-158. 73. Brouchet L, Bauvin E, Marcheix B, et al. Impact of induc-tion treatment on postoperative complications in the treat-ment of non–small cell
Surgery_Schwartz. Landreneau R, Daly BT. Approaching the high-risk patient: sublobar resection, stereo-tactic body radiation therapy, or radiofrequency ablation. Ann Thorac Surg. 2010;89(6):S2123-2127. 70. Timmerman R, McGarry R, Yiannoutsos C, et al. Excessive toxicity when treating central tumors in a phase II study of B stereotactic body radiation therapy for medically inoperable early-stage lung cancer. J Clin Oncol. 2006;24(30):4833-4839. 71. Pisters KM, Ginsberg RJ, Giroux DJ, et al. Induction chemo-therapy before surgery for early-stage lung cancer: a novel approach. Bimodality Lung Oncology Team. J Thorac Car-diovasc Surg. 2000;119(3):429-439. 72. Rosell R, Gomez-Codina J, Camps C, et al. A randomized trial comparing preoperative chemotherapy plus surgery with sur-gery alone in patients with non–small-cell lung cancer. N Engl J Med. 1994;330(3):153-158. 73. Brouchet L, Bauvin E, Marcheix B, et al. Impact of induc-tion treatment on postoperative complications in the treat-ment of non–small cell
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lung cancer. N Engl J Med. 1994;330(3):153-158. 73. Brouchet L, Bauvin E, Marcheix B, et al. Impact of induc-tion treatment on postoperative complications in the treat-ment of non–small cell lung cancer. J Thorac Oncol. 2007;2(7):626-631. 74. Rusch VW. Management of Pancoast tumours. Lancet Oncol. 2006;7(12):997-1005. 75. Rusch VW, Giroux DJ, Kraut MJ, et al. Induction chemoradia-tion and surgical resection for superior sulcus non–small-cell lung carcinomas: long-term results of Southwest Oncol-ogy Group Trial 9416 (Intergroup Trial 0160). J Clin Oncol. 2007;25(3):313-318. 76. Dillman RO, Herndon J, Seagren SL, et al. Improved survival in stage III non–small-cell lung cancer: seven-year follow-up of Cancer and Leukemia Group B (CALGB) 8433 trial. J Natl Cancer Inst. 1996;88(17):1210-1215. 77. Okawara G, Mackay JA, Evans W, et al. Management of unresected stage III non-small cell lung cancer: a systematic review. J Thorac Oncol. 2006;1:377-393. 78. Swanson SJ, Herndon JE 2nd, D’Amico
Surgery_Schwartz. lung cancer. N Engl J Med. 1994;330(3):153-158. 73. Brouchet L, Bauvin E, Marcheix B, et al. Impact of induc-tion treatment on postoperative complications in the treat-ment of non–small cell lung cancer. J Thorac Oncol. 2007;2(7):626-631. 74. Rusch VW. Management of Pancoast tumours. Lancet Oncol. 2006;7(12):997-1005. 75. Rusch VW, Giroux DJ, Kraut MJ, et al. Induction chemoradia-tion and surgical resection for superior sulcus non–small-cell lung carcinomas: long-term results of Southwest Oncol-ogy Group Trial 9416 (Intergroup Trial 0160). J Clin Oncol. 2007;25(3):313-318. 76. Dillman RO, Herndon J, Seagren SL, et al. Improved survival in stage III non–small-cell lung cancer: seven-year follow-up of Cancer and Leukemia Group B (CALGB) 8433 trial. J Natl Cancer Inst. 1996;88(17):1210-1215. 77. Okawara G, Mackay JA, Evans W, et al. Management of unresected stage III non-small cell lung cancer: a systematic review. J Thorac Oncol. 2006;1:377-393. 78. Swanson SJ, Herndon JE 2nd, D’Amico
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G, Mackay JA, Evans W, et al. Management of unresected stage III non-small cell lung cancer: a systematic review. J Thorac Oncol. 2006;1:377-393. 78. Swanson SJ, Herndon JE 2nd, D’Amico TA, et al. Vid-eoassisted thoracic surgery lobectomy: report of CALGB 39802—a prospective, multi-institution feasibility study. J Clin Oncol. 2007;25(31):4993-4997. 79. Demmy TL, James TA, Swanson SJ, McKenna RJ Jr, D’Amico TA. Troubleshooting video-assisted thoracic sur-gery lobectomy. Ann Thorac Surg. 2005;79(5):1744-1752; discussion 1753. 80. Fry WA. Thoracic incisions. Chest Surg Clin N Am. 1995;5:177-188. 81. Dewey TM, Mack MJ. Lung cancer. Surgical approaches and incisions. Chest Surg Clin N Am. 2000;10:803-820. 82. Cerfolio RJ, Bryant AS. Results of a prospective algorithm to remove chest tubes after pulmonary resection with high out-put. J Thorac Cardiovasc Surg. 2008;135(2):269-273. 83. Cerfolio RJ, Bass C, Katholi CR. Prospective randomized trial compares suction versus water seal for air
Surgery_Schwartz. G, Mackay JA, Evans W, et al. Management of unresected stage III non-small cell lung cancer: a systematic review. J Thorac Oncol. 2006;1:377-393. 78. Swanson SJ, Herndon JE 2nd, D’Amico TA, et al. Vid-eoassisted thoracic surgery lobectomy: report of CALGB 39802—a prospective, multi-institution feasibility study. J Clin Oncol. 2007;25(31):4993-4997. 79. Demmy TL, James TA, Swanson SJ, McKenna RJ Jr, D’Amico TA. Troubleshooting video-assisted thoracic sur-gery lobectomy. Ann Thorac Surg. 2005;79(5):1744-1752; discussion 1753. 80. Fry WA. Thoracic incisions. Chest Surg Clin N Am. 1995;5:177-188. 81. Dewey TM, Mack MJ. Lung cancer. Surgical approaches and incisions. Chest Surg Clin N Am. 2000;10:803-820. 82. Cerfolio RJ, Bryant AS. Results of a prospective algorithm to remove chest tubes after pulmonary resection with high out-put. J Thorac Cardiovasc Surg. 2008;135(2):269-273. 83. Cerfolio RJ, Bass C, Katholi CR. Prospective randomized trial compares suction versus water seal for air
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pulmonary resection with high out-put. J Thorac Cardiovasc Surg. 2008;135(2):269-273. 83. Cerfolio RJ, Bass C, Katholi CR. Prospective randomized trial compares suction versus water seal for air leaks. Ann Thorac Surg. 2001;71(5):1613-1617. 84. Bauer C, Hentz JG, Ducrocq X, et al. Lung function after lobectomy: a randomized, double-blinded trial compar-ing thoracic epidural ropivacaine/sufentanil and intravenous morphine for patient-controlled analgesia. Anesth Analg. 2007;105(1):238-244. 85. Casati A, Alessandrini P, Nuzzi M, et al. A prospective, randomized, blinded comparison between continuous Brunicardi_Ch19_p0661-p0750.indd 74601/03/19 7:02 PM
Surgery_Schwartz. pulmonary resection with high out-put. J Thorac Cardiovasc Surg. 2008;135(2):269-273. 83. Cerfolio RJ, Bass C, Katholi CR. Prospective randomized trial compares suction versus water seal for air leaks. Ann Thorac Surg. 2001;71(5):1613-1617. 84. Bauer C, Hentz JG, Ducrocq X, et al. Lung function after lobectomy: a randomized, double-blinded trial compar-ing thoracic epidural ropivacaine/sufentanil and intravenous morphine for patient-controlled analgesia. Anesth Analg. 2007;105(1):238-244. 85. Casati A, Alessandrini P, Nuzzi M, et al. A prospective, randomized, blinded comparison between continuous Brunicardi_Ch19_p0661-p0750.indd 74601/03/19 7:02 PM
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CHAPTER 19747CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAthoracic paravertebral and epidural infusion of 0.2% ropi-vacaine after lung resection surgery. Eur J Anaesthesiol. 2006;23(12):999-1004. 86. Inderbitzi RG, Leiser A, Furrer M, Althaus U. Three years’ experience in video-assisted thoracic surgery (VATS) for spontaneous pneumothorax. J Thorac Cardiovasc Surg. 1994;107(6):1410-1415. 87. Warner BW, Bailey WW, Shipley RT. Value of computed tomography of the lung in the management of primary spon-taneous pneumothorax. Am J Surg. 1991;162(1):39-42. 88. Mansharamani N, Balachandran D, Delaney D, Zibrak JD, Silvestri RC, Koziel H. Lung abscess in adults: clinical com-parison of immunocompromised to non-immunocompromised patients. Respir Med. 2002;96(3):178-185. 89. Laheij RJ, Sturkenboom MC, Hassing RJ, Dieleman J, Stricker BH, Jansen JB. Risk of community-acquired pneu-monia and use of gastric acid-suppressive drugs. JAMA. 2004;292(16):1955-1960. 90. Conant EF, Wechsler RJ. Actinomycosis
Surgery_Schwartz. CHAPTER 19747CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAthoracic paravertebral and epidural infusion of 0.2% ropi-vacaine after lung resection surgery. Eur J Anaesthesiol. 2006;23(12):999-1004. 86. Inderbitzi RG, Leiser A, Furrer M, Althaus U. Three years’ experience in video-assisted thoracic surgery (VATS) for spontaneous pneumothorax. J Thorac Cardiovasc Surg. 1994;107(6):1410-1415. 87. Warner BW, Bailey WW, Shipley RT. Value of computed tomography of the lung in the management of primary spon-taneous pneumothorax. Am J Surg. 1991;162(1):39-42. 88. Mansharamani N, Balachandran D, Delaney D, Zibrak JD, Silvestri RC, Koziel H. Lung abscess in adults: clinical com-parison of immunocompromised to non-immunocompromised patients. Respir Med. 2002;96(3):178-185. 89. Laheij RJ, Sturkenboom MC, Hassing RJ, Dieleman J, Stricker BH, Jansen JB. Risk of community-acquired pneu-monia and use of gastric acid-suppressive drugs. JAMA. 2004;292(16):1955-1960. 90. Conant EF, Wechsler RJ. Actinomycosis
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RJ, Dieleman J, Stricker BH, Jansen JB. Risk of community-acquired pneu-monia and use of gastric acid-suppressive drugs. JAMA. 2004;292(16):1955-1960. 90. Conant EF, Wechsler RJ. Actinomycosis and nocardiosis of the lung. J Thorac Imaging. 1992;7(4):75-84. 91. Thomson RM, Armstrong JG, Looke DF. Gastroesopha-geal reflux disease, acid suppression, and Mycobacterium avium complex pulmonary disease. Chest. 2007;131(4): 1166-1172. 92. Koh WJ, Lee JH, Kwon YS, et al. Prevalence of gastroesopha-geal reflux disease in patients with nontuberculous mycobac-terial lung disease. Chest. 2007;131(6):1825-1830. 93. Angrill J, Agusti C, de Celis R, et al. Bacterial colonisation in patients with bronchiectasis: microbiological pattern and risk factors. Thorax. 2002;57(1):15-19. 94. Barker AF. Bronchiectasis. N Engl J Med. 2002;346(18):1383-1393. 95. Ilowite J, Spiegler P, Chawla S. Bronchiectasis: new find-ings in the pathogenesis and treatment of this disease. Curr Opin Infect Dis.
Surgery_Schwartz. RJ, Dieleman J, Stricker BH, Jansen JB. Risk of community-acquired pneu-monia and use of gastric acid-suppressive drugs. JAMA. 2004;292(16):1955-1960. 90. Conant EF, Wechsler RJ. Actinomycosis and nocardiosis of the lung. J Thorac Imaging. 1992;7(4):75-84. 91. Thomson RM, Armstrong JG, Looke DF. Gastroesopha-geal reflux disease, acid suppression, and Mycobacterium avium complex pulmonary disease. Chest. 2007;131(4): 1166-1172. 92. Koh WJ, Lee JH, Kwon YS, et al. Prevalence of gastroesopha-geal reflux disease in patients with nontuberculous mycobac-terial lung disease. Chest. 2007;131(6):1825-1830. 93. Angrill J, Agusti C, de Celis R, et al. Bacterial colonisation in patients with bronchiectasis: microbiological pattern and risk factors. Thorax. 2002;57(1):15-19. 94. Barker AF. Bronchiectasis. N Engl J Med. 2002;346(18):1383-1393. 95. Ilowite J, Spiegler P, Chawla S. Bronchiectasis: new find-ings in the pathogenesis and treatment of this disease. Curr Opin Infect Dis.
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AF. Bronchiectasis. N Engl J Med. 2002;346(18):1383-1393. 95. Ilowite J, Spiegler P, Chawla S. Bronchiectasis: new find-ings in the pathogenesis and treatment of this disease. Curr Opin Infect Dis. 2008;21(2):163-167. 96. Xu L, Zhang F, Du S, et al. Inhaled antibiotics in non-cystic fibrosis bronchiectasis: a meta-analysis. Pharmazie. 2016;71:491-498. 97. Steinfort DP, Steinfort C. Effect of long-term nebulized colis-tin on lung function and quality of life in patients with chronic bronchial sepsis. Intern Med J. 2007;37(7):495-498. 98. Kellett F, Robert NM. Nebulised 7% hypertonic saline improves lung function and quality of life in bronchiectasis. Respir Med. 2011;105:1831-1835. 99. Frieden TR, Sterling TR, Munsiff SS, Watt CJ, Dye C. Tuber-culosis. Lancet. 2003;362(9387):887-899. 100. Haque AK. The pathology and pathophysiology of mycobac-teria infections. J Thorac Imaging. 1990;5:8-16. 101. Iseman MD. Treatment of multidrug-resistant tuberculosis. N Engl J Med.
Surgery_Schwartz. AF. Bronchiectasis. N Engl J Med. 2002;346(18):1383-1393. 95. Ilowite J, Spiegler P, Chawla S. Bronchiectasis: new find-ings in the pathogenesis and treatment of this disease. Curr Opin Infect Dis. 2008;21(2):163-167. 96. Xu L, Zhang F, Du S, et al. Inhaled antibiotics in non-cystic fibrosis bronchiectasis: a meta-analysis. Pharmazie. 2016;71:491-498. 97. Steinfort DP, Steinfort C. Effect of long-term nebulized colis-tin on lung function and quality of life in patients with chronic bronchial sepsis. Intern Med J. 2007;37(7):495-498. 98. Kellett F, Robert NM. Nebulised 7% hypertonic saline improves lung function and quality of life in bronchiectasis. Respir Med. 2011;105:1831-1835. 99. Frieden TR, Sterling TR, Munsiff SS, Watt CJ, Dye C. Tuber-culosis. Lancet. 2003;362(9387):887-899. 100. Haque AK. The pathology and pathophysiology of mycobac-teria infections. J Thorac Imaging. 1990;5:8-16. 101. Iseman MD. Treatment of multidrug-resistant tuberculosis. N Engl J Med.
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BS, Scheithauer BW, Piepgras DG, Reiman HM, Ilstrup DM. Malignant peripheral nerve sheath tumors. A clinicopathologic study of 120 cases. Cancer. 1986;57(10):2006-2021. 165. Nichols CR, Saxman S, Williams SD, et al. Primary medi-astinal nonseminomatous germ cell tumors. A modern single institution experience. Cancer. 1990;65(7):1641-1646. 166. Kesler KA, Rieger KM, Hammoud Z, et al. A 25-year sin-gle institution experience with surgery for primary medias-tinal nonseminomatous germ cell tumors. Ann Thorac Surg. 2008;85:371-378. 167. Rice TW. Benign neoplasms and cysts of the mediastinum. Semin Thorac Cardiovasc Surg. 1992;4(1):25-33. 168. Di Lorenzo M, Collin PP, Vaillancourt R, Duranceau A. Bron-chogenic cysts. J Pediatr Surg. 1989;24(10):988-991. 169. Ribet ME, Copin MC, Gosselin B. Bronchogenic cysts of the mediastinum. J Thorac Cardiovasc Surg. 1995;109(5):1003-1010. 170. St-Georges R, Deslauriers J, Duranceau A, et al. Clinical spec-trum of bronchogenic cysts of the mediastinum
Surgery_Schwartz. BS, Scheithauer BW, Piepgras DG, Reiman HM, Ilstrup DM. Malignant peripheral nerve sheath tumors. A clinicopathologic study of 120 cases. Cancer. 1986;57(10):2006-2021. 165. Nichols CR, Saxman S, Williams SD, et al. Primary medi-astinal nonseminomatous germ cell tumors. A modern single institution experience. Cancer. 1990;65(7):1641-1646. 166. Kesler KA, Rieger KM, Hammoud Z, et al. A 25-year sin-gle institution experience with surgery for primary medias-tinal nonseminomatous germ cell tumors. Ann Thorac Surg. 2008;85:371-378. 167. Rice TW. Benign neoplasms and cysts of the mediastinum. Semin Thorac Cardiovasc Surg. 1992;4(1):25-33. 168. Di Lorenzo M, Collin PP, Vaillancourt R, Duranceau A. Bron-chogenic cysts. J Pediatr Surg. 1989;24(10):988-991. 169. Ribet ME, Copin MC, Gosselin B. Bronchogenic cysts of the mediastinum. J Thorac Cardiovasc Surg. 1995;109(5):1003-1010. 170. St-Georges R, Deslauriers J, Duranceau A, et al. Clinical spec-trum of bronchogenic cysts of the mediastinum
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cysts of the mediastinum. J Thorac Cardiovasc Surg. 1995;109(5):1003-1010. 170. St-Georges R, Deslauriers J, Duranceau A, et al. Clinical spec-trum of bronchogenic cysts of the mediastinum and lung in the adult. Ann Thorac Surg. 1991;52(1):6-13. 171. Agostoni E. Mechanics of the pleural space. In: Fisherman AP, Macklem PT, Mead J, et al, eds. Mechanics of Breathing: Handbook of Physiology. Vol 3. Bethesda, MD: American Physiological Society; 1986. 172. Lawrence GH. Considerations of the anatomy and physiology of the pleural space. In: Lawrence GH, ed. Problems of the Pleural Space. Philadelphia: WB Saunders; 1983. 173. Rusch VW. Pleural effusion: benign and malignant. In: Pear-son FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1157. 174. Gammie JS, Banks MC, Fuhrman CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a
Surgery_Schwartz. cysts of the mediastinum. J Thorac Cardiovasc Surg. 1995;109(5):1003-1010. 170. St-Georges R, Deslauriers J, Duranceau A, et al. Clinical spec-trum of bronchogenic cysts of the mediastinum and lung in the adult. Ann Thorac Surg. 1991;52(1):6-13. 171. Agostoni E. Mechanics of the pleural space. In: Fisherman AP, Macklem PT, Mead J, et al, eds. Mechanics of Breathing: Handbook of Physiology. Vol 3. Bethesda, MD: American Physiological Society; 1986. 172. Lawrence GH. Considerations of the anatomy and physiology of the pleural space. In: Lawrence GH, ed. Problems of the Pleural Space. Philadelphia: WB Saunders; 1983. 173. Rusch VW. Pleural effusion: benign and malignant. In: Pear-son FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1157. 174. Gammie JS, Banks MC, Fuhrman CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a
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CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a prospective evaluation of pain management. Clin J Pain. 1998;14(2):152-154. 176. Johnston WW. The malignant pleural effusion. A review of cytopathologic diagnoses of 584 specimens from 472 consecu-tive patients. Cancer. 1985;56(4):905-909.Brunicardi_Ch19_p0661-p0750.indd 74801/03/19 7:02 PM
Surgery_Schwartz. CR, et al. The pigtail cath-eter for pleural drainage: a less invasive alternative to tube thoracostomy. JSLS. 1999;3(1):57-61. 175. Luketich JD, Kiss M, Hershey J, et al. Chest tube insertion: a prospective evaluation of pain management. Clin J Pain. 1998;14(2):152-154. 176. Johnston WW. The malignant pleural effusion. A review of cytopathologic diagnoses of 584 specimens from 472 consecu-tive patients. Cancer. 1985;56(4):905-909.Brunicardi_Ch19_p0661-p0750.indd 74801/03/19 7:02 PM
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CHAPTER 19749CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA 177. Ocaña I, Martinez-Vazquez JM, Segura RM, et al. Adenosine deaminase in pleural fluids. Test for diagnosis of tuberculous pleural effusion. Chest. 1983;84(1):51-53. 178. Lee YC, Rogers JT, Rodriguez RM, Miller KD, Light RW. Adenosine deaminase levels in nontuberculous lymphocytic pleural effusions. Chest. 2001;120(2):356-361. 179. Tremblay A, Michaud G. Single-center experience with 250 tunneled pleural catheter insertions for malignant pleural effu-sion. Chest. 2006;129(2):362-368. 180. Light RW. Parapneumonic effusions and empyema. Clin Chest Med. 1985;6(1):55-62. 181. Rahman NM, Maskell NA, West A, et al. Intrapleural use of tissue plasminogen activator and DNase in pleural infection. N Engl J Med. 2011;365:518-526. 182. Miller JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of
Surgery_Schwartz. CHAPTER 19749CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA 177. Ocaña I, Martinez-Vazquez JM, Segura RM, et al. Adenosine deaminase in pleural fluids. Test for diagnosis of tuberculous pleural effusion. Chest. 1983;84(1):51-53. 178. Lee YC, Rogers JT, Rodriguez RM, Miller KD, Light RW. Adenosine deaminase levels in nontuberculous lymphocytic pleural effusions. Chest. 2001;120(2):356-361. 179. Tremblay A, Michaud G. Single-center experience with 250 tunneled pleural catheter insertions for malignant pleural effu-sion. Chest. 2006;129(2):362-368. 180. Light RW. Parapneumonic effusions and empyema. Clin Chest Med. 1985;6(1):55-62. 181. Rahman NM, Maskell NA, West A, et al. Intrapleural use of tissue plasminogen activator and DNase in pleural infection. N Engl J Med. 2011;365:518-526. 182. Miller JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of
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JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of chylothorax. Chest Surg Clin N Am. 1996;6(1):139-148. 184. Malthaner RA, Inculet RI. The thoracic duct and chylotho-rax. In: Pearson FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1228. 185. Rusch VW. A proposed new international TNM staging system for malignant pleural mesothelioma. From the International Mesothelioma Interest Group. Chest. 1995;108(4):1122-1128. 186. Khalil MY, Mapa M, Shin HJ, Shin DM. Advances in the management of malignant mesothelioma. Curr Oncol Rep. 2003;5(4):334-341. 187. Fletcher CDM, Unni KK, Mertens F. World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the
Surgery_Schwartz. JI Jr. The history of surgery of empyema, thoracoplasty, Eloesser flap, and muscle flap transposition. Chest Surg Clin N Am. 2000;10(1):45-53. 183. Miller JI Jr. Diagnosis and management of chylothorax. Chest Surg Clin N Am. 1996;6(1):139-148. 184. Malthaner RA, Inculet RI. The thoracic duct and chylotho-rax. In: Pearson FG, ed. Thoracic Surgery. 2nd ed. New York: Churchill Livingstone; 2002:1228. 185. Rusch VW. A proposed new international TNM staging system for malignant pleural mesothelioma. From the International Mesothelioma Interest Group. Chest. 1995;108(4):1122-1128. 186. Khalil MY, Mapa M, Shin HJ, Shin DM. Advances in the management of malignant mesothelioma. Curr Oncol Rep. 2003;5(4):334-341. 187. Fletcher CDM, Unni KK, Mertens F. World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the
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of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the pleura. A clinicopathologic review of 223 cases. Am J Surg Pathol. 1989;13(8):640-658.Brunicardi_Ch19_p0661-p0750.indd 74901/03/19 7:02 PM
Surgery_Schwartz. of Tumours. Pathology and Genetics of Tumours of Soft Tissue and Bone. Lyon, France: IARC Press; 2002. 188. England DM, Hochholzer L, McCarthy MJ. Localized benign and malignant fibrous tumors of the pleura. A clinicopathologic review of 223 cases. Am J Surg Pathol. 1989;13(8):640-658.Brunicardi_Ch19_p0661-p0750.indd 74901/03/19 7:02 PM
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Congenital Heart DiseaseRaghav Murthy, Tabitha G. Moe, Glen S. Van Arsdell, John J. Nigro, and Tara Karamlou20chapterINTRODUCTIONCongenital heart surgery is a dynamic and evolving field. The last 20 years have brought about rapid developments in technol-ogy, emphasis on a multidisciplinary approach to treatment, and a more thorough understanding of both the anatomy and patho-physiology of congenital heart disease, leading to the improved care of these challenging patients.These advancements have created a sustained paradigm shift in the field of congenital heart surgery. The traditional strategy of initial palliation followed by definitive correction at a later age, which had pervaded the thinking of most surgeons, began to evolve into emphasizing early repair. Defects such as hypoplastic left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is
Surgery_Schwartz. Congenital Heart DiseaseRaghav Murthy, Tabitha G. Moe, Glen S. Van Arsdell, John J. Nigro, and Tara Karamlou20chapterINTRODUCTIONCongenital heart surgery is a dynamic and evolving field. The last 20 years have brought about rapid developments in technol-ogy, emphasis on a multidisciplinary approach to treatment, and a more thorough understanding of both the anatomy and patho-physiology of congenital heart disease, leading to the improved care of these challenging patients.These advancements have created a sustained paradigm shift in the field of congenital heart surgery. The traditional strategy of initial palliation followed by definitive correction at a later age, which had pervaded the thinking of most surgeons, began to evolve into emphasizing early repair. Defects such as hypoplastic left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is
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left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is appropriate timing of complete repair. Rather than subdivid-ing lesions into cyanotic or noncyanotic lesions, a more appro-priate classification divides defects into three categories based on the feasibility of achieving complete repair: (a) defects that have no reasonable palliation and for which repair is the only option; (b) defects for which repair is not possible and for which palliation is the only option; and (c) defects that can either be repaired or palliated in infancy. It bears mentioning that all defects in the second category are those in which the appropriate anatomic components either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some
Surgery_Schwartz. left heart syndrome (HLHS) are now successfully managed with staged palliation, resulting in excellent survival outcomes for these children.The goal in most cases of congenital heart disease (CHD) is appropriate timing of complete repair. Rather than subdivid-ing lesions into cyanotic or noncyanotic lesions, a more appro-priate classification divides defects into three categories based on the feasibility of achieving complete repair: (a) defects that have no reasonable palliation and for which repair is the only option; (b) defects for which repair is not possible and for which palliation is the only option; and (c) defects that can either be repaired or palliated in infancy. It bears mentioning that all defects in the second category are those in which the appropriate anatomic components either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some
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either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some form of CHD, most of which, however, are mild.1 In the United States nearly 40,000 infants are affected each year.2 As of 2010, it is estimated that there are about 2 million people living with CHD in the United States, and as of 2011 there are more adults (>18) than children.2 CHD is the most common birth defect and the most common cause of infant death related to birth defects, accounting for 28% of deaths due to birth defects in the first month of life. There are currently 127 centers in North America that perform congenital heart surgery. The Society for Thoracic Surgeons (STS) reports an overall national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing
Surgery_Schwartz. either are not present, as in hypoplastic left heart syndrome, or cannot be created from existing structures, i.e., unguarded tricuspid orifice.1Eight out of every 1000 live births will have some form of CHD, most of which, however, are mild.1 In the United States nearly 40,000 infants are affected each year.2 As of 2010, it is estimated that there are about 2 million people living with CHD in the United States, and as of 2011 there are more adults (>18) than children.2 CHD is the most common birth defect and the most common cause of infant death related to birth defects, accounting for 28% of deaths due to birth defects in the first month of life. There are currently 127 centers in North America that perform congenital heart surgery. The Society for Thoracic Surgeons (STS) reports an overall national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing
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national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing of blood between the systemic venous and pulmonary venous circulations.Embryology. The atrial and ventricular septa form between the third and sixth weeks of fetal development. After the paired heart tubes fuse into a single tube folded onto itself, the distal por-tion of the tube indents to form the roof of the common atrium. Near this portion of the roof, the septum primum originates and descends in a crescentic formation toward the atrioventricular (AV) junction. The ostium primum is situated superiorly to the crux of the heart at the atrioventricular junction. Prior to completion of endocardial cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis /
Surgery_Schwartz. national mortality of 3.1%.3DEFECTS AMENABLE TO COMPLETE REPAIRAtrial Septal DefectAn atrial septal defect (ASD) is defined as discontinuity of the interatrial septum that permits direct mixing of blood between the systemic venous and pulmonary venous circulations.Embryology. The atrial and ventricular septa form between the third and sixth weeks of fetal development. After the paired heart tubes fuse into a single tube folded onto itself, the distal por-tion of the tube indents to form the roof of the common atrium. Near this portion of the roof, the septum primum originates and descends in a crescentic formation toward the atrioventricular (AV) junction. The ostium primum is situated superiorly to the crux of the heart at the atrioventricular junction. Prior to completion of endocardial cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis /
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cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis / 755Patent Ductus Arteriosus / 759Aortic Coarctation / 761Truncus Arteriosus / 764Total Anomalous Pulmonary Venous Connection / 765Cor Triatriatum / 768Aortopulmonary Window / 769Vascular Rings and Pulmonary Artery Slings / 769Defects Requiring Palliation 770Tricuspid Atresia / 770Hypoplastic Left Heart Syndrome / 773Defects That May be Palliated or Repaired 777Ebstein’s Anomaly / 777Transposition of the Great Arteries / 780Double-Outlet Right Ventricle / 783Double-Outlet Right Ventricle With Noncommitted Ventricular Septal Defect / 783Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis /
Surgery_Schwartz. cushion fusion with the septum pri-mum, a sequence of fenestrations appear that coalesce into the Introduction 751Defects Amenable to Complete Repair 751Atrial Septal Defect / 751Aortic Stenosis / 755Patent Ductus Arteriosus / 759Aortic Coarctation / 761Truncus Arteriosus / 764Total Anomalous Pulmonary Venous Connection / 765Cor Triatriatum / 768Aortopulmonary Window / 769Vascular Rings and Pulmonary Artery Slings / 769Defects Requiring Palliation 770Tricuspid Atresia / 770Hypoplastic Left Heart Syndrome / 773Defects That May be Palliated or Repaired 777Ebstein’s Anomaly / 777Transposition of the Great Arteries / 780Double-Outlet Right Ventricle / 783Double-Outlet Right Ventricle With Noncommitted Ventricular Septal Defect / 783Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis /
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or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis / 784Taussig–Bing Syndrome Without Pulmonary Stenosis / 784Taussig–Bing Syndrome With Pulmonary Stenosis / 784Tetralogy of Fallot / 784Ventricular Septal Defect / 786Atrioventricular Canal Defects / 789Interrupted Aortic Arch / 790Pediatric Mechanical Circulatory Support / 790Pediatric Heart Transplantation / 791Public Reporting and the STS Database in Congenital Heart Surgery / 792Future Directions / 793Brunicardi_Ch20_p0751-p0800.indd 75122/02/19 2:54 PM 752ostium secundum. During this coalescence, the septum secun-dum grows downward from the roof of the atrium, parallel to and to the right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure
Surgery_Schwartz. or Doubly Committed Ventricular Septal Defect Without Pulmonary Stenosis / 784Double-Outlet Right Ventricle With Subaortic or Doubly Committed Ventricular Septal Defect With Pulmonary Stenosis / 784Taussig–Bing Syndrome Without Pulmonary Stenosis / 784Taussig–Bing Syndrome With Pulmonary Stenosis / 784Tetralogy of Fallot / 784Ventricular Septal Defect / 786Atrioventricular Canal Defects / 789Interrupted Aortic Arch / 790Pediatric Mechanical Circulatory Support / 790Pediatric Heart Transplantation / 791Public Reporting and the STS Database in Congenital Heart Surgery / 792Future Directions / 793Brunicardi_Ch20_p0751-p0800.indd 75122/02/19 2:54 PM 752ostium secundum. During this coalescence, the septum secun-dum grows downward from the roof of the atrium, parallel to and to the right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure
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right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure associated with an increase in SVR relative to PVR typically closes this pathway in approximately 80% of the population, obliterating the interatrial communication.Anatomy. ASDs can be classified into three different types (Fig. 20-1): (a) ostium secundum type defect (Fig. 20-1B,C) (deficiency of septum primum), which are the most prevalent subtype, comprising 80% of all ASDs; (b) ostium primum defects (Fig. 20-1A), which may also be described as partial or transitional AV canal defect; and (c) sinus venosus type defects, comprising approximately 5% to 10% of all ASDs.4Pathophysiology. ASDs result in an increase in pulmonary blood flow secondary to primarily left-to-right shunting through the defect. The direction of the intracardiac shunt is predomi-nantly determined by the compliance of
Surgery_Schwartz. right of the septum primum. The septum primum does not fuse, but creates an oblique pathway, called the foramen ovale, within the interatrial septum. After birth, the increase in left atrial pressure associated with an increase in SVR relative to PVR typically closes this pathway in approximately 80% of the population, obliterating the interatrial communication.Anatomy. ASDs can be classified into three different types (Fig. 20-1): (a) ostium secundum type defect (Fig. 20-1B,C) (deficiency of septum primum), which are the most prevalent subtype, comprising 80% of all ASDs; (b) ostium primum defects (Fig. 20-1A), which may also be described as partial or transitional AV canal defect; and (c) sinus venosus type defects, comprising approximately 5% to 10% of all ASDs.4Pathophysiology. ASDs result in an increase in pulmonary blood flow secondary to primarily left-to-right shunting through the defect. The direction of the intracardiac shunt is predomi-nantly determined by the compliance of
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in an increase in pulmonary blood flow secondary to primarily left-to-right shunting through the defect. The direction of the intracardiac shunt is predomi-nantly determined by the compliance of the respective ventri-cles. In utero, the distensibility, or compliance, of the right and left ventricles is equal, but postnatally the left ventricle (LV) becomes less compliant than the right ventricle (RV). This shift occurs because the resistance of the downstream vascular beds changes after birth. The pulmonary vascular resistance falls with the infant’s first breath, decreasing RV pressure, whereas the systemic vascular resistance rises dramatically, increasing LV pressure. The increase in LV pressure promotes hypertrophy with a thicker muscle mass, which offers a greater resistance to diastolic filling than does the RV; thus, the majority of flow through the ASD occurs from left to right. The greater volume of blood returning to the right atrium causes volume overload in the RV, but
Surgery_Schwartz. in an increase in pulmonary blood flow secondary to primarily left-to-right shunting through the defect. The direction of the intracardiac shunt is predomi-nantly determined by the compliance of the respective ventri-cles. In utero, the distensibility, or compliance, of the right and left ventricles is equal, but postnatally the left ventricle (LV) becomes less compliant than the right ventricle (RV). This shift occurs because the resistance of the downstream vascular beds changes after birth. The pulmonary vascular resistance falls with the infant’s first breath, decreasing RV pressure, whereas the systemic vascular resistance rises dramatically, increasing LV pressure. The increase in LV pressure promotes hypertrophy with a thicker muscle mass, which offers a greater resistance to diastolic filling than does the RV; thus, the majority of flow through the ASD occurs from left to right. The greater volume of blood returning to the right atrium causes volume overload in the RV, but
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filling than does the RV; thus, the majority of flow through the ASD occurs from left to right. The greater volume of blood returning to the right atrium causes volume overload in the RV, but because of its lower muscle mass and low-resistance output, it easily distends to accommodate the increased volume.The long-term consequences of RV volume overload include hypertrophy with elevated RV end-diastolic pressure and a relative pulmonary stenosis across the pulmonary valve because it cannot accommodate the increased RV flow. Com-pliance gradually decreases as the right ventricular pressure approaches systemic pressure, and the size of the left-to-right shunt decreases. Patients at this stage have a balanced circula-tion and may deceptively appear less symptomatic.Key Points1 Congenital heart disease comprises a wide morphologic spec-trum. In general, lesions can be conceptualized as those that can be completely repaired, those that should be palliated, and those that can be either
Surgery_Schwartz. filling than does the RV; thus, the majority of flow through the ASD occurs from left to right. The greater volume of blood returning to the right atrium causes volume overload in the RV, but because of its lower muscle mass and low-resistance output, it easily distends to accommodate the increased volume.The long-term consequences of RV volume overload include hypertrophy with elevated RV end-diastolic pressure and a relative pulmonary stenosis across the pulmonary valve because it cannot accommodate the increased RV flow. Com-pliance gradually decreases as the right ventricular pressure approaches systemic pressure, and the size of the left-to-right shunt decreases. Patients at this stage have a balanced circula-tion and may deceptively appear less symptomatic.Key Points1 Congenital heart disease comprises a wide morphologic spec-trum. In general, lesions can be conceptualized as those that can be completely repaired, those that should be palliated, and those that can be either
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heart disease comprises a wide morphologic spec-trum. In general, lesions can be conceptualized as those that can be completely repaired, those that should be palliated, and those that can be either repaired or palliated depending on particular patient and institutional characteristics.2 Percutaneous therapies for congenital heart disease are quickly becoming important adjuncts, and in some cases, alternatives, to standard surgical therapy. Important exam-ples include percutaneous closure of atrial and ventricular septal defects, the hybrid approach to hypoplastic left heart syndrome, radiofrequency perforation of the pulmonary valve, and percutaneous pulmonary valve placement. Further studies are necessary to establish criteria and current bench-marks for the safe integration of these novel approaches into the care of patients with congenital heart surgery.3 Patients with critical left ventricular outflow tract obstruc-tion, such as neonatal critical aortic stenosis, represent a
Surgery_Schwartz. heart disease comprises a wide morphologic spec-trum. In general, lesions can be conceptualized as those that can be completely repaired, those that should be palliated, and those that can be either repaired or palliated depending on particular patient and institutional characteristics.2 Percutaneous therapies for congenital heart disease are quickly becoming important adjuncts, and in some cases, alternatives, to standard surgical therapy. Important exam-ples include percutaneous closure of atrial and ventricular septal defects, the hybrid approach to hypoplastic left heart syndrome, radiofrequency perforation of the pulmonary valve, and percutaneous pulmonary valve placement. Further studies are necessary to establish criteria and current bench-marks for the safe integration of these novel approaches into the care of patients with congenital heart surgery.3 Patients with critical left ventricular outflow tract obstruc-tion, such as neonatal critical aortic stenosis, represent a
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novel approaches into the care of patients with congenital heart surgery.3 Patients with critical left ventricular outflow tract obstruc-tion, such as neonatal critical aortic stenosis, represent a challenging population. It is critical that the correct decision (whether to pursue univentricular or biventricular repair) be made prior to the initial operation, as attrition when the incorrect decision is made is high. There are several pub-lished criteria (Congenital Heart Surgeons’ Society critical stenosis calculator) to help surgeons decide which strategy to pursue.4 Optimum strategy for repair of total anomalous pulmonary venous connection (TAPVC) remains a topic of some con-tention. Sutureless repair, formerly reserved for initial reste-nosis after conventional repair, has evolved in many centers to be the primary approach for high-risk patients. Defining whether sutureless repair should be considered in all patients with TAPVC will require further study.5 Vascular rings and
Surgery_Schwartz. novel approaches into the care of patients with congenital heart surgery.3 Patients with critical left ventricular outflow tract obstruc-tion, such as neonatal critical aortic stenosis, represent a challenging population. It is critical that the correct decision (whether to pursue univentricular or biventricular repair) be made prior to the initial operation, as attrition when the incorrect decision is made is high. There are several pub-lished criteria (Congenital Heart Surgeons’ Society critical stenosis calculator) to help surgeons decide which strategy to pursue.4 Optimum strategy for repair of total anomalous pulmonary venous connection (TAPVC) remains a topic of some con-tention. Sutureless repair, formerly reserved for initial reste-nosis after conventional repair, has evolved in many centers to be the primary approach for high-risk patients. Defining whether sutureless repair should be considered in all patients with TAPVC will require further study.5 Vascular rings and
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in many centers to be the primary approach for high-risk patients. Defining whether sutureless repair should be considered in all patients with TAPVC will require further study.5 Vascular rings and pulmonary artery slings often require multidisciplinary approaches for management. They can be associated with complete tracheal rings and tracheobronchomalacia.6 A recent prospective, randomized, multi-institutional trial sponsored by the National Institutes of Health, the Systemic Ventricle Reconstruction (SVR) trial, compared the out-comes of neonates with hypoplastic left heart syndrome hav-ing either a modified Blalock–Taussig shunt (MBTS) versus a right ventricle-to-pulmonary artery (RV-PA) shunt. The SVR trial demonstrated that transplantation-free survival 12 months after randomization was higher with the RV-PA shunt than with the MBTS. However, data collected over a mean follow-up period of 32 ± 11 months showed a nonsig-nificant difference in transplantation-free survival between
Surgery_Schwartz. in many centers to be the primary approach for high-risk patients. Defining whether sutureless repair should be considered in all patients with TAPVC will require further study.5 Vascular rings and pulmonary artery slings often require multidisciplinary approaches for management. They can be associated with complete tracheal rings and tracheobronchomalacia.6 A recent prospective, randomized, multi-institutional trial sponsored by the National Institutes of Health, the Systemic Ventricle Reconstruction (SVR) trial, compared the out-comes of neonates with hypoplastic left heart syndrome hav-ing either a modified Blalock–Taussig shunt (MBTS) versus a right ventricle-to-pulmonary artery (RV-PA) shunt. The SVR trial demonstrated that transplantation-free survival 12 months after randomization was higher with the RV-PA shunt than with the MBTS. However, data collected over a mean follow-up period of 32 ± 11 months showed a nonsig-nificant difference in transplantation-free survival between
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was higher with the RV-PA shunt than with the MBTS. However, data collected over a mean follow-up period of 32 ± 11 months showed a nonsig-nificant difference in transplantation-free survival between the two groups.7 Outcomes have improved substantially over time in congeni-tal heart surgery, and most complex lesions can be operated in early infancy. Neurologic protection, however, remains a key issue in the care of neonates undergoing surgery with cardiopulmonary bypass and deep hypothermic circulatory arrest. New monitoring devices and perioperative strategies are currently under investigation. Attention in the field has shifted from analyses of perioperative mortality, which for most lesions is under 10%, to longer-term outcomes, includ-ing quality of life and neurologic function.8 Pediatric mechanical circulatory support and heart transplan-tation is an upcoming and rapidly evolving component of congenital heart surgery. These are offering options for res-cue, palliation, and
Surgery_Schwartz. was higher with the RV-PA shunt than with the MBTS. However, data collected over a mean follow-up period of 32 ± 11 months showed a nonsig-nificant difference in transplantation-free survival between the two groups.7 Outcomes have improved substantially over time in congeni-tal heart surgery, and most complex lesions can be operated in early infancy. Neurologic protection, however, remains a key issue in the care of neonates undergoing surgery with cardiopulmonary bypass and deep hypothermic circulatory arrest. New monitoring devices and perioperative strategies are currently under investigation. Attention in the field has shifted from analyses of perioperative mortality, which for most lesions is under 10%, to longer-term outcomes, includ-ing quality of life and neurologic function.8 Pediatric mechanical circulatory support and heart transplan-tation is an upcoming and rapidly evolving component of congenital heart surgery. These are offering options for res-cue, palliation, and
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mechanical circulatory support and heart transplan-tation is an upcoming and rapidly evolving component of congenital heart surgery. These are offering options for res-cue, palliation, and treatment of complex defects or children who were palliated and failing.9 Public reporting has become an integral part of this subspe-cialty. The Society of Thoracic Surgeons Congenital Heart Surgery Database (STS CHSD) remains the largest database in the world for congenital and pediatric heart surgery. Transparency in overall outcomes, mortality, and morbidity is allowing patients and their families an insight into the complexity of their diagnoses as well as the level of perfor-mance of different centers.Brunicardi_Ch20_p0751-p0800.indd 75222/02/19 2:54 PM 753CONGENITAL HEART DISEASECHAPTER 20ABCFigure 20-1. A. Echocardiogram of a patient with primum type artial septal defect (‘*’ points to the atrial septal defect). B. Echocardiogram of a large secundum type ASD (‘*’ points to the defect).
Surgery_Schwartz. mechanical circulatory support and heart transplan-tation is an upcoming and rapidly evolving component of congenital heart surgery. These are offering options for res-cue, palliation, and treatment of complex defects or children who were palliated and failing.9 Public reporting has become an integral part of this subspe-cialty. The Society of Thoracic Surgeons Congenital Heart Surgery Database (STS CHSD) remains the largest database in the world for congenital and pediatric heart surgery. Transparency in overall outcomes, mortality, and morbidity is allowing patients and their families an insight into the complexity of their diagnoses as well as the level of perfor-mance of different centers.Brunicardi_Ch20_p0751-p0800.indd 75222/02/19 2:54 PM 753CONGENITAL HEART DISEASECHAPTER 20ABCFigure 20-1. A. Echocardiogram of a patient with primum type artial septal defect (‘*’ points to the atrial septal defect). B. Echocardiogram of a large secundum type ASD (‘*’ points to the defect).
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20-1. A. Echocardiogram of a patient with primum type artial septal defect (‘*’ points to the atrial septal defect). B. Echocardiogram of a large secundum type ASD (‘*’ points to the defect). C. Intra-operative picture during repair of atrial septal defect. A large fenestrated atrial septum is seen. Bicaval venous cannulation has been performed and a right atriotomy provides exposure to the atrial septum.Patients with large ASDs gradually develop progressive pulmonary vascular changes as a result of chronic overcircu-lation. The increased pulmonary vascular resistance in these patients leads to an equalization of left and right ventricular pressures, and their ratio of pulmonary (Qp) to systemic flow (Qs), Qp to Qs, will approach 1.5 This does not mean, however, that there is no intracardiac shunting, only that the ratio between the left-to-right component and the right-to-left component is equal.The ability of the RV to recover normal function is related to the duration of chronic
Surgery_Schwartz. 20-1. A. Echocardiogram of a patient with primum type artial septal defect (‘*’ points to the atrial septal defect). B. Echocardiogram of a large secundum type ASD (‘*’ points to the defect). C. Intra-operative picture during repair of atrial septal defect. A large fenestrated atrial septum is seen. Bicaval venous cannulation has been performed and a right atriotomy provides exposure to the atrial septum.Patients with large ASDs gradually develop progressive pulmonary vascular changes as a result of chronic overcircu-lation. The increased pulmonary vascular resistance in these patients leads to an equalization of left and right ventricular pressures, and their ratio of pulmonary (Qp) to systemic flow (Qs), Qp to Qs, will approach 1.5 This does not mean, however, that there is no intracardiac shunting, only that the ratio between the left-to-right component and the right-to-left component is equal.The ability of the RV to recover normal function is related to the duration of chronic
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shunting, only that the ratio between the left-to-right component and the right-to-left component is equal.The ability of the RV to recover normal function is related to the duration of chronic overload because those undergoing ASD closure before age 10 years have a better likelihood of achieving normal RV volumes and function in the postopera-tive period.6The physiology of sinus venosus ASDs is similar to that discussed earlier, except that these are frequently accompanied by anomalous pulmonary venous drainage. This often results in significant hemodynamic derangements that accelerate the clinical course of these infants.The same increase in symptoms is true for those with ostium primum defects because the associated mitral insuffi-ciency from the “cleft” mitral valve can lead to more atrial vol-ume load and increased atrial level shunting.Diagnosis. Patients with ASDs upon auscultation may reveal prominence of the first heart sound with fixed splitting of the second heart sound.
Surgery_Schwartz. shunting, only that the ratio between the left-to-right component and the right-to-left component is equal.The ability of the RV to recover normal function is related to the duration of chronic overload because those undergoing ASD closure before age 10 years have a better likelihood of achieving normal RV volumes and function in the postopera-tive period.6The physiology of sinus venosus ASDs is similar to that discussed earlier, except that these are frequently accompanied by anomalous pulmonary venous drainage. This often results in significant hemodynamic derangements that accelerate the clinical course of these infants.The same increase in symptoms is true for those with ostium primum defects because the associated mitral insuffi-ciency from the “cleft” mitral valve can lead to more atrial vol-ume load and increased atrial level shunting.Diagnosis. Patients with ASDs upon auscultation may reveal prominence of the first heart sound with fixed splitting of the second heart sound.
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atrial vol-ume load and increased atrial level shunting.Diagnosis. Patients with ASDs upon auscultation may reveal prominence of the first heart sound with fixed splitting of the second heart sound. This results from the relatively fixed left-to-right shunt throughout all phases of the cardiac cycle. A diastolic flow murmur indicating increased flow across the tricuspid valve may be discerned, and frequently, an ejection flow mur-mur can be heard across the pulmonary valve. A right ventricu-lar heave and increased intensity of the pulmonary component of the second heart sound indicates pulmonary hypertension.Chest radiographs in the patient with an ASD demonstrate increased pulmonary vascularity, with prominent hilar mark-ings and cardiomegaly. The electrocardiogram shows right axis deviation with an incomplete bundle-branch block. When right bundle-branch block is associated with a leftward or superior axis, an AV canal defect should be strongly suspected.Diagnosis is clarified by
Surgery_Schwartz. atrial vol-ume load and increased atrial level shunting.Diagnosis. Patients with ASDs upon auscultation may reveal prominence of the first heart sound with fixed splitting of the second heart sound. This results from the relatively fixed left-to-right shunt throughout all phases of the cardiac cycle. A diastolic flow murmur indicating increased flow across the tricuspid valve may be discerned, and frequently, an ejection flow mur-mur can be heard across the pulmonary valve. A right ventricu-lar heave and increased intensity of the pulmonary component of the second heart sound indicates pulmonary hypertension.Chest radiographs in the patient with an ASD demonstrate increased pulmonary vascularity, with prominent hilar mark-ings and cardiomegaly. The electrocardiogram shows right axis deviation with an incomplete bundle-branch block. When right bundle-branch block is associated with a leftward or superior axis, an AV canal defect should be strongly suspected.Diagnosis is clarified by
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with an incomplete bundle-branch block. When right bundle-branch block is associated with a leftward or superior axis, an AV canal defect should be strongly suspected.Diagnosis is clarified by two-dimensional echocardiogra-phy (Fig. 20-1A,C), and use of color-flow mapping facilitates an understanding of the physiologic derangements created by the defects. Older children and adults with unrepaired ASDs may present with stroke or systemic embolism from paradoxical embolism or atrial arrhythmias from dilation of the right atrium.Echocardiography also enables the clinician to estimate the amount of intracardiac shunting, and it can demonstrate the degree of mitral regurgitation in patients with ostium primum defects. With the addition of an agitated saline injection (bubble study), it can also assist in the detection of sinus venosus defects.The advent of two-dimensional echocardiography with color-flow Doppler has largely superseded the use of cardiac catheterization because the ASD can
Surgery_Schwartz. with an incomplete bundle-branch block. When right bundle-branch block is associated with a leftward or superior axis, an AV canal defect should be strongly suspected.Diagnosis is clarified by two-dimensional echocardiogra-phy (Fig. 20-1A,C), and use of color-flow mapping facilitates an understanding of the physiologic derangements created by the defects. Older children and adults with unrepaired ASDs may present with stroke or systemic embolism from paradoxical embolism or atrial arrhythmias from dilation of the right atrium.Echocardiography also enables the clinician to estimate the amount of intracardiac shunting, and it can demonstrate the degree of mitral regurgitation in patients with ostium primum defects. With the addition of an agitated saline injection (bubble study), it can also assist in the detection of sinus venosus defects.The advent of two-dimensional echocardiography with color-flow Doppler has largely superseded the use of cardiac catheterization because the ASD can
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assist in the detection of sinus venosus defects.The advent of two-dimensional echocardiography with color-flow Doppler has largely superseded the use of cardiac catheterization because the ASD can be well defined by echo-cardiography alone. However, in cases where the right ventric-ular systolic pressure is elevated, or patient is older than age 40 years, catheterization can quantify the degree of pulmonary hypertension because those with a fixed pulmonary vascular resistance greater than 12 U/mL may be considered inoperable.7 Cardiac catheterization also can be useful in that it provides data that enable the calculation of Qp and Qs so that the magnitude of the intracardiac shunt can be determined. The ratio (Qp to Qs) can then be used to determine whether closure is indicated in equivocal cases, because a ratio of Qp to Qs greater than 1.5:1 Brunicardi_Ch20_p0751-p0800.indd 75322/02/19 2:54 PM 754SPECIFIC CONSIDERATIONSPART IIis generally accepted as the threshold for surgical
Surgery_Schwartz. assist in the detection of sinus venosus defects.The advent of two-dimensional echocardiography with color-flow Doppler has largely superseded the use of cardiac catheterization because the ASD can be well defined by echo-cardiography alone. However, in cases where the right ventric-ular systolic pressure is elevated, or patient is older than age 40 years, catheterization can quantify the degree of pulmonary hypertension because those with a fixed pulmonary vascular resistance greater than 12 U/mL may be considered inoperable.7 Cardiac catheterization also can be useful in that it provides data that enable the calculation of Qp and Qs so that the magnitude of the intracardiac shunt can be determined. The ratio (Qp to Qs) can then be used to determine whether closure is indicated in equivocal cases, because a ratio of Qp to Qs greater than 1.5:1 Brunicardi_Ch20_p0751-p0800.indd 75322/02/19 2:54 PM 754SPECIFIC CONSIDERATIONSPART IIis generally accepted as the threshold for surgical
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cases, because a ratio of Qp to Qs greater than 1.5:1 Brunicardi_Ch20_p0751-p0800.indd 75322/02/19 2:54 PM 754SPECIFIC CONSIDERATIONSPART IIis generally accepted as the threshold for surgical intervention. Finally, in patients older than age 40 years, cardiac catheteriza-tion can be important to evaluate for the presence of coronary artery disease.In general, ASDs are closed when patients are between 4 and 5 years of age. Children of this size can usually be oper-ated on without the use of blood transfusion and have excellent outcomes. Patients who are symptomatic may require repair earlier, even in infancy. Some surgeons advocate routine repair in infants and children especially in cases where prematurity-related lung disease may accelerate damage to the pulmonary vascular bed, though this philosophy may not be widespread. In a review by Reddy and colleagues, 116 neonates weighing less than 2500 g who underwent repair of simple and complex cardiac defects with the use of
Surgery_Schwartz. cases, because a ratio of Qp to Qs greater than 1.5:1 Brunicardi_Ch20_p0751-p0800.indd 75322/02/19 2:54 PM 754SPECIFIC CONSIDERATIONSPART IIis generally accepted as the threshold for surgical intervention. Finally, in patients older than age 40 years, cardiac catheteriza-tion can be important to evaluate for the presence of coronary artery disease.In general, ASDs are closed when patients are between 4 and 5 years of age. Children of this size can usually be oper-ated on without the use of blood transfusion and have excellent outcomes. Patients who are symptomatic may require repair earlier, even in infancy. Some surgeons advocate routine repair in infants and children especially in cases where prematurity-related lung disease may accelerate damage to the pulmonary vascular bed, though this philosophy may not be widespread. In a review by Reddy and colleagues, 116 neonates weighing less than 2500 g who underwent repair of simple and complex cardiac defects with the use of
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though this philosophy may not be widespread. In a review by Reddy and colleagues, 116 neonates weighing less than 2500 g who underwent repair of simple and complex cardiac defects with the use of cardiopulmonary bypass were found to have no intracerebral hemorrhages, no long-term neu-rologic sequelae, and a low operative mortality rate (10%). These results correlated with the length of cardiopulmonary bypass and the complexity of repair.8 These investigators also found an 80% actuarial survival at 1 year and, more importantly, that growth following complete repair was equivalent to weight-matched neonates free from cardiac defects.8Treatment. Simple secundum type ASDs can frequently be repaired via a transcatheter technique, and assessment for trans-catheter closure with TTE assessment is generally indicated prior to consideration of a surgical repair. The most common surgical approach requires standard cardiopulmonary bypass (CPB) tech-nique through a midline sternotomy approach.
Surgery_Schwartz. though this philosophy may not be widespread. In a review by Reddy and colleagues, 116 neonates weighing less than 2500 g who underwent repair of simple and complex cardiac defects with the use of cardiopulmonary bypass were found to have no intracerebral hemorrhages, no long-term neu-rologic sequelae, and a low operative mortality rate (10%). These results correlated with the length of cardiopulmonary bypass and the complexity of repair.8 These investigators also found an 80% actuarial survival at 1 year and, more importantly, that growth following complete repair was equivalent to weight-matched neonates free from cardiac defects.8Treatment. Simple secundum type ASDs can frequently be repaired via a transcatheter technique, and assessment for trans-catheter closure with TTE assessment is generally indicated prior to consideration of a surgical repair. The most common surgical approach requires standard cardiopulmonary bypass (CPB) tech-nique through a midline sternotomy approach.
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is generally indicated prior to consideration of a surgical repair. The most common surgical approach requires standard cardiopulmonary bypass (CPB) tech-nique through a midline sternotomy approach. The details of the repair itself are generally straightforward. An oblique atriotomy is made, the position of the coronary sinus and all systemic and pulmonary veins are determined, and the rim of the defect is completely visualized. Closure of an ostium secundum defect is accomplished either by primary repair or by insertion of a patch that is sutured to the rim of the defect. The decision of whether patch closure is necessary can be determined by the size and shape of the defect as well as by the quality of the edges.The type of repair used for sinus venosus ASDs associated with partial anomalous pulmonary venous connection is dictated by the location of the anomalous pulmonary vein. If the anoma-lous veins connect to the atria or to the superior vena cava cau-dal to where the cava is
Surgery_Schwartz. is generally indicated prior to consideration of a surgical repair. The most common surgical approach requires standard cardiopulmonary bypass (CPB) tech-nique through a midline sternotomy approach. The details of the repair itself are generally straightforward. An oblique atriotomy is made, the position of the coronary sinus and all systemic and pulmonary veins are determined, and the rim of the defect is completely visualized. Closure of an ostium secundum defect is accomplished either by primary repair or by insertion of a patch that is sutured to the rim of the defect. The decision of whether patch closure is necessary can be determined by the size and shape of the defect as well as by the quality of the edges.The type of repair used for sinus venosus ASDs associated with partial anomalous pulmonary venous connection is dictated by the location of the anomalous pulmonary vein. If the anoma-lous veins connect to the atria or to the superior vena cava cau-dal to where the cava is
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pulmonary venous connection is dictated by the location of the anomalous pulmonary vein. If the anoma-lous veins connect to the atria or to the superior vena cava cau-dal to where the cava is crossed by the right pulmonary artery, the ASD can be repaired by inserting a patch, with redirection of the pulmonary veins behind the patch to the left atrium. Care must be taken with this approach to avoid obstruction of the pulmonary veins or the superior vena cava, although usually the superior vena cava is dilated and provides ample room for patch insertion. If the anomalous vein connects to the superior vena cava cranial to the right pulmonary artery, an alternative technique, the Warden procedure, may be necessary. In this operation, the superior vena cava is transected cranial to the connection of the anomalous vein (usually the right superior pulmonary vein). The caudal end of the transected cava is over-sewn. The cranial end of the transected cava is anastomosed to the auricle of the
Surgery_Schwartz. pulmonary venous connection is dictated by the location of the anomalous pulmonary vein. If the anoma-lous veins connect to the atria or to the superior vena cava cau-dal to where the cava is crossed by the right pulmonary artery, the ASD can be repaired by inserting a patch, with redirection of the pulmonary veins behind the patch to the left atrium. Care must be taken with this approach to avoid obstruction of the pulmonary veins or the superior vena cava, although usually the superior vena cava is dilated and provides ample room for patch insertion. If the anomalous vein connects to the superior vena cava cranial to the right pulmonary artery, an alternative technique, the Warden procedure, may be necessary. In this operation, the superior vena cava is transected cranial to the connection of the anomalous vein (usually the right superior pulmonary vein). The caudal end of the transected cava is over-sewn. The cranial end of the transected cava is anastomosed to the auricle of the
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of the anomalous vein (usually the right superior pulmonary vein). The caudal end of the transected cava is over-sewn. The cranial end of the transected cava is anastomosed to the auricle of the right atrium. Inside the atrium, a patch is used to redirect pulmonary venous blood flow to the left atrium. In contrast to the repair for a defect where the pulmonary veins enter the right atrium or the superior vena cava below the right pulmonary artery, the patch covers the superior vena caval right atrial junction so that blood from the anomalous pulmonary vein that enters the cava is directed to the left atrium. Blood returning from the upper body enters the right atrium via the anastomosis between the superior vena cava and the right atrial appendage.Results and Complications of Surgical ASD Closure. Tra-ditional operative strategies, such as pericardial or synthetic patch closure, have been well established, with a low complica-tion rate and a mortality rate of zero among patients
Surgery_Schwartz. of the anomalous vein (usually the right superior pulmonary vein). The caudal end of the transected cava is over-sewn. The cranial end of the transected cava is anastomosed to the auricle of the right atrium. Inside the atrium, a patch is used to redirect pulmonary venous blood flow to the left atrium. In contrast to the repair for a defect where the pulmonary veins enter the right atrium or the superior vena cava below the right pulmonary artery, the patch covers the superior vena caval right atrial junction so that blood from the anomalous pulmonary vein that enters the cava is directed to the left atrium. Blood returning from the upper body enters the right atrium via the anastomosis between the superior vena cava and the right atrial appendage.Results and Complications of Surgical ASD Closure. Tra-ditional operative strategies, such as pericardial or synthetic patch closure, have been well established, with a low complica-tion rate and a mortality rate of zero among patients
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ASD Closure. Tra-ditional operative strategies, such as pericardial or synthetic patch closure, have been well established, with a low complica-tion rate and a mortality rate of zero among patients without pulmonary hypertension.9 The most frequently reported imme-diate complications include postpericardiotomy syndrome and atrial arrhythmias. Beyond immediate postoperative outcomes, long-term outcomes following surgical closure (up to 20 years) document the low mortality rates and durability of functional status benefit. Importantly, however, atrial arrhythmias, par-ticularly atrial fibrillation, are not completely mitigated by closure and can occur in 10% to 40% of patients, especially in older patients (>40 years) or those with preexisting arrhyth-mias.10 Kutty and colleagues11 followed 300 patients from their institution, 152 of whom had surgical closure. Late mortality at 10 years was 3%, and functional health status had declined in only 15 patients during follow-up. Recently,
Surgery_Schwartz. ASD Closure. Tra-ditional operative strategies, such as pericardial or synthetic patch closure, have been well established, with a low complica-tion rate and a mortality rate of zero among patients without pulmonary hypertension.9 The most frequently reported imme-diate complications include postpericardiotomy syndrome and atrial arrhythmias. Beyond immediate postoperative outcomes, long-term outcomes following surgical closure (up to 20 years) document the low mortality rates and durability of functional status benefit. Importantly, however, atrial arrhythmias, par-ticularly atrial fibrillation, are not completely mitigated by closure and can occur in 10% to 40% of patients, especially in older patients (>40 years) or those with preexisting arrhyth-mias.10 Kutty and colleagues11 followed 300 patients from their institution, 152 of whom had surgical closure. Late mortality at 10 years was 3%, and functional health status had declined in only 15 patients during follow-up. Recently,
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300 patients from their institution, 152 of whom had surgical closure. Late mortality at 10 years was 3%, and functional health status had declined in only 15 patients during follow-up. Recently, there have been an increasing number of reports regarding the results follow-ing surgical closure among elderly patients (>60 years of age), which demonstrate equivalent survival to younger patients, albeit with slightly higher complication rates.11-13 Hanninen and colleagues14 studied 68 patients between 68 and 86 years at their institution undergoing either surgical (n = 13) or device (n = 54) closure. Although the 23% incidence of major complications (including pneumothorax, heart failure, and pneumonia) was higher than that recently reported by Mascio et al15 using the Society of Thoracic Surgeons’ Congenital Database (20%) or a single-institution review by Hopkins et al16 (12%), there were no operative deaths among the elderly cohort. Moreover, after ASD closure, echocardiographic
Surgery_Schwartz. 300 patients from their institution, 152 of whom had surgical closure. Late mortality at 10 years was 3%, and functional health status had declined in only 15 patients during follow-up. Recently, there have been an increasing number of reports regarding the results follow-ing surgical closure among elderly patients (>60 years of age), which demonstrate equivalent survival to younger patients, albeit with slightly higher complication rates.11-13 Hanninen and colleagues14 studied 68 patients between 68 and 86 years at their institution undergoing either surgical (n = 13) or device (n = 54) closure. Although the 23% incidence of major complications (including pneumothorax, heart failure, and pneumonia) was higher than that recently reported by Mascio et al15 using the Society of Thoracic Surgeons’ Congenital Database (20%) or a single-institution review by Hopkins et al16 (12%), there were no operative deaths among the elderly cohort. Moreover, after ASD closure, echocardiographic
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Surgeons’ Congenital Database (20%) or a single-institution review by Hopkins et al16 (12%), there were no operative deaths among the elderly cohort. Moreover, after ASD closure, echocardiographic indices of right ventricular size and function were significantly improved from preoperative val-ues, and functional capacity as measured by standardized survey instruments was also significantly improved.New and Future Approaches to Traditional Surgical ASD Closure. Because of the uniformly excellent outcomes with traditional surgery, attention has shifted to improving the cos-metic result and minimizing hospital stay and convalescence. Multiple strategies have been described to achieve these aims, including the right submammary incision with anterior thora-cotomy, limited bilateral submammary incision with partial sternal split, and limited midline incision with partial sternal split. Some surgeons use either video-assisted thoracic surgery (VATS) in conjunction with the submammary and
Surgery_Schwartz. Surgeons’ Congenital Database (20%) or a single-institution review by Hopkins et al16 (12%), there were no operative deaths among the elderly cohort. Moreover, after ASD closure, echocardiographic indices of right ventricular size and function were significantly improved from preoperative val-ues, and functional capacity as measured by standardized survey instruments was also significantly improved.New and Future Approaches to Traditional Surgical ASD Closure. Because of the uniformly excellent outcomes with traditional surgery, attention has shifted to improving the cos-metic result and minimizing hospital stay and convalescence. Multiple strategies have been described to achieve these aims, including the right submammary incision with anterior thora-cotomy, limited bilateral submammary incision with partial sternal split, and limited midline incision with partial sternal split. Some surgeons use either video-assisted thoracic surgery (VATS) in conjunction with the submammary and
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incision with partial sternal split, and limited midline incision with partial sternal split. Some surgeons use either video-assisted thoracic surgery (VATS) in conjunction with the submammary and transxiphoid approaches to facilitate closure within a constricted operative field or totally endoscopic repair in selected patients.17-20 Use of robotics has also been reported in a small series of 12 adult patients by Argenziano and colleagues.18 The morbidity and mortality of all of these approaches are comparable to those of the traditional median sternotomy; however, each has technical drawbacks. Operative precision must be maintained with limited exposure in any minimally invasive technique. Extended CPB and aortic cross-clamp times, coupled with increased cost, may limit the utility of totally endoscopic or robotic-assisted ASD closure except at specific centers. Moreover, certain approaches have a specific patient population in whom they are most appli-cable. For example, the
Surgery_Schwartz. incision with partial sternal split, and limited midline incision with partial sternal split. Some surgeons use either video-assisted thoracic surgery (VATS) in conjunction with the submammary and transxiphoid approaches to facilitate closure within a constricted operative field or totally endoscopic repair in selected patients.17-20 Use of robotics has also been reported in a small series of 12 adult patients by Argenziano and colleagues.18 The morbidity and mortality of all of these approaches are comparable to those of the traditional median sternotomy; however, each has technical drawbacks. Operative precision must be maintained with limited exposure in any minimally invasive technique. Extended CPB and aortic cross-clamp times, coupled with increased cost, may limit the utility of totally endoscopic or robotic-assisted ASD closure except at specific centers. Moreover, certain approaches have a specific patient population in whom they are most appli-cable. For example, the
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of totally endoscopic or robotic-assisted ASD closure except at specific centers. Moreover, certain approaches have a specific patient population in whom they are most appli-cable. For example, the anterolateral thoracotomy should not be employed in prepubescent girls because it will interfere with breast development. Most totally endoscopic approaches are not feasible in very young patients because of the size of the tho-racoscopic ports. Despite these potential drawbacks, however, in carefully selected patients, minimally invasive techniques have demonstrated benefits. Luo and associates performed Brunicardi_Ch20_p0751-p0800.indd 75422/02/19 2:54 PM 755CONGENITAL HEART DISEASECHAPTER 20ABFigure 20-2. A. Picture of the Amplatzr device after open retrieval from the heart (dislodged during percutaenous catheter placement). B. Echocardiographic view of the septum after transcatheter closure of the atrial septal defect with an Amplatzar device.a prospective randomized study comparing
Surgery_Schwartz. of totally endoscopic or robotic-assisted ASD closure except at specific centers. Moreover, certain approaches have a specific patient population in whom they are most appli-cable. For example, the anterolateral thoracotomy should not be employed in prepubescent girls because it will interfere with breast development. Most totally endoscopic approaches are not feasible in very young patients because of the size of the tho-racoscopic ports. Despite these potential drawbacks, however, in carefully selected patients, minimally invasive techniques have demonstrated benefits. Luo and associates performed Brunicardi_Ch20_p0751-p0800.indd 75422/02/19 2:54 PM 755CONGENITAL HEART DISEASECHAPTER 20ABFigure 20-2. A. Picture of the Amplatzr device after open retrieval from the heart (dislodged during percutaenous catheter placement). B. Echocardiographic view of the septum after transcatheter closure of the atrial septal defect with an Amplatzar device.a prospective randomized study comparing
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percutaenous catheter placement). B. Echocardiographic view of the septum after transcatheter closure of the atrial septal defect with an Amplatzar device.a prospective randomized study comparing ministernotomy (division of the upper sternum for aortic and pulmonary lesions and the lower sternum for septal lesions) to full sternotomy in 100 consecutive patients undergoing repair of septal lesions.19 The patients in the ministernotomy group had longer procedure times (by 15 to 20 minutes) but had less bleeding and shorter hospital stays. Consistent with these initiatives, conversion of “low-risk” patients undergoing minimally invasive ASD closure to an ambulatory population (discharge from hospital within 24 hours) has recently been described.21First performed in 1976, transcatheter closure of ASDs with the use of various occlusion devices is gaining widespread accep-tance.22 Certain types of ASDs, including patent foramen ovale, secundum defects, and some fenestrated secundum
Surgery_Schwartz. percutaenous catheter placement). B. Echocardiographic view of the septum after transcatheter closure of the atrial septal defect with an Amplatzar device.a prospective randomized study comparing ministernotomy (division of the upper sternum for aortic and pulmonary lesions and the lower sternum for septal lesions) to full sternotomy in 100 consecutive patients undergoing repair of septal lesions.19 The patients in the ministernotomy group had longer procedure times (by 15 to 20 minutes) but had less bleeding and shorter hospital stays. Consistent with these initiatives, conversion of “low-risk” patients undergoing minimally invasive ASD closure to an ambulatory population (discharge from hospital within 24 hours) has recently been described.21First performed in 1976, transcatheter closure of ASDs with the use of various occlusion devices is gaining widespread accep-tance.22 Certain types of ASDs, including patent foramen ovale, secundum defects, and some fenestrated secundum
Surgery_Schwartz_5063
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closure of ASDs with the use of various occlusion devices is gaining widespread accep-tance.22 Certain types of ASDs, including patent foramen ovale, secundum defects, and some fenestrated secundum defects, are amenable to device closure, as long as particular ana-tomic criteria (e.g., an adequate superior and inferior rim for device seating and distance from the AV valve) are met. Since the introduction of percutaneous closure (Fig. 20-2A,B), there has been a dramatic rise in device closure prevalence to the point where device closure has supplanted surgical therapy as the domi-nant treatment modality for secundum ASD.23 A study from Karamlou et al23 found that ASD and patent foramen ovale clo-sures per capita increased dramatically from 1.08 per 100,000 population in 1988 to 2.59 per 100,000 population in 2005, an increase of 139%. When analyzed by closure type, surgical clo-sure increased by only 24% (from 0.86 per 100,000 population in 1988 to 1.07 per 100,000 in 2005), whereas
Surgery_Schwartz. closure of ASDs with the use of various occlusion devices is gaining widespread accep-tance.22 Certain types of ASDs, including patent foramen ovale, secundum defects, and some fenestrated secundum defects, are amenable to device closure, as long as particular ana-tomic criteria (e.g., an adequate superior and inferior rim for device seating and distance from the AV valve) are met. Since the introduction of percutaneous closure (Fig. 20-2A,B), there has been a dramatic rise in device closure prevalence to the point where device closure has supplanted surgical therapy as the domi-nant treatment modality for secundum ASD.23 A study from Karamlou et al23 found that ASD and patent foramen ovale clo-sures per capita increased dramatically from 1.08 per 100,000 population in 1988 to 2.59 per 100,000 population in 2005, an increase of 139%. When analyzed by closure type, surgical clo-sure increased by only 24% (from 0.86 per 100,000 population in 1988 to 1.07 per 100,000 in 2005), whereas
Surgery_Schwartz_5064
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100,000 population in 2005, an increase of 139%. When analyzed by closure type, surgical clo-sure increased by only 24% (from 0.86 per 100,000 population in 1988 to 1.07 per 100,000 in 2005), whereas transcatheter closure increased by 3475% (from 0.04 per 100,000 population in 1988 to 1.43 per 100,000 in 2005). Importantly, this study determined that the paradigm shift favoring transcatheter closure has occurred mainly due to increased prevalence of closure in adults over age 40 years rather than an increase in closure in infants or children.Despite the simplicity of ASD repair, there are a myriad of options for patients and physicians who care for patients with CHD. The patient population that might benefit from closure (whether device or surgical) is likely to increase, challenging current ideas and treatment algorithms that optimize outcomes.2Aortic StenosisAnatomy and Classification. The spectrum of aortic valve abnormality represents the most common form of CHD, with the great
Surgery_Schwartz. 100,000 population in 2005, an increase of 139%. When analyzed by closure type, surgical clo-sure increased by only 24% (from 0.86 per 100,000 population in 1988 to 1.07 per 100,000 in 2005), whereas transcatheter closure increased by 3475% (from 0.04 per 100,000 population in 1988 to 1.43 per 100,000 in 2005). Importantly, this study determined that the paradigm shift favoring transcatheter closure has occurred mainly due to increased prevalence of closure in adults over age 40 years rather than an increase in closure in infants or children.Despite the simplicity of ASD repair, there are a myriad of options for patients and physicians who care for patients with CHD. The patient population that might benefit from closure (whether device or surgical) is likely to increase, challenging current ideas and treatment algorithms that optimize outcomes.2Aortic StenosisAnatomy and Classification. The spectrum of aortic valve abnormality represents the most common form of CHD, with the great
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ideas and treatment algorithms that optimize outcomes.2Aortic StenosisAnatomy and Classification. The spectrum of aortic valve abnormality represents the most common form of CHD, with the great majority of patients being asymptomatic until midlife. Obstruction of the left ventricular outflow tract (LVOT) occurs at multiple levels: subvalvular, valvular, and supravalvular (Fig. 20-3A-D). The critically stenotic aortic valve in the neo-nate or infant is commonly unicommissural or bicommissural, with thickened, dysmorphic, and myxomatous leaflet tissue and a reduced cross-sectional area at the valve level. Associ-ated left-sided lesions are often present. In a review of 32 cases from the Children’s Hospital in Boston, 59% had unicommis-sural valves, and 40% had bicommissural valves.24 Associated lesions were frequent, occurring in 88% of patients, most com-monly patent ductus arteriosus, mitral regurgitation, and hypo-plastic LV. Endocardial fibroelastosis (EFE) also is common among
Surgery_Schwartz. ideas and treatment algorithms that optimize outcomes.2Aortic StenosisAnatomy and Classification. The spectrum of aortic valve abnormality represents the most common form of CHD, with the great majority of patients being asymptomatic until midlife. Obstruction of the left ventricular outflow tract (LVOT) occurs at multiple levels: subvalvular, valvular, and supravalvular (Fig. 20-3A-D). The critically stenotic aortic valve in the neo-nate or infant is commonly unicommissural or bicommissural, with thickened, dysmorphic, and myxomatous leaflet tissue and a reduced cross-sectional area at the valve level. Associ-ated left-sided lesions are often present. In a review of 32 cases from the Children’s Hospital in Boston, 59% had unicommis-sural valves, and 40% had bicommissural valves.24 Associated lesions were frequent, occurring in 88% of patients, most com-monly patent ductus arteriosus, mitral regurgitation, and hypo-plastic LV. Endocardial fibroelastosis (EFE) also is common among
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lesions were frequent, occurring in 88% of patients, most com-monly patent ductus arteriosus, mitral regurgitation, and hypo-plastic LV. Endocardial fibroelastosis (EFE) also is common among infants with critical aortic stenosis (AS). In this condi-tion, the LV is usually prohibitively hypoplastic and noncom-pliant, rendering these patients poor candidates for recruitment of the LV into the systemic circulation with techniques that can be utilized in those with more normal sized LVs. In some neonates with critical AS, a dilated LV with poor diastolic com-pliance rather than a hypertrophied LV is encountered.24Neonates with critical AS are a challenging population because one must make a decision about the suitability of the left-sided structures to support a biventricular circulation. There are recent approaches that include techniques, such as aortic valvotomy coupled with EFE resection and mitral valve inter-vention, that are directed at LV rehabilitation. The advent of fetal
Surgery_Schwartz. lesions were frequent, occurring in 88% of patients, most com-monly patent ductus arteriosus, mitral regurgitation, and hypo-plastic LV. Endocardial fibroelastosis (EFE) also is common among infants with critical aortic stenosis (AS). In this condi-tion, the LV is usually prohibitively hypoplastic and noncom-pliant, rendering these patients poor candidates for recruitment of the LV into the systemic circulation with techniques that can be utilized in those with more normal sized LVs. In some neonates with critical AS, a dilated LV with poor diastolic com-pliance rather than a hypertrophied LV is encountered.24Neonates with critical AS are a challenging population because one must make a decision about the suitability of the left-sided structures to support a biventricular circulation. There are recent approaches that include techniques, such as aortic valvotomy coupled with EFE resection and mitral valve inter-vention, that are directed at LV rehabilitation. The advent of fetal
Surgery_Schwartz_5067
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There are recent approaches that include techniques, such as aortic valvotomy coupled with EFE resection and mitral valve inter-vention, that are directed at LV rehabilitation. The advent of fetal valvotomy for critical AS may also increase the number of infants who are candidates for biventricular repair.Pathophysiology. The unique intracardiac and extracardiac shunts present in fetal life allow even neonates with critical AS to survive. In utero, left ventricular hypertrophy and ischemia cause left atrial hypertension, which reduces the right-to-left flow across the foramen ovale. In severe cases, a reversal of Brunicardi_Ch20_p0751-p0800.indd 75522/02/19 2:54 PM 756SPECIFIC CONSIDERATIONSPART IIFigure 20-3. A. Congenital aortic valve stenosis, en fosse echocardiographic view of the stenotic bicuspid aortic valve. Parasternal long axis view of the same valve with a gradient of 60 mm of Hg (‘*’ points to the valve). B. Parasternal long axis ecocardiographic view of a patient with
Surgery_Schwartz. There are recent approaches that include techniques, such as aortic valvotomy coupled with EFE resection and mitral valve inter-vention, that are directed at LV rehabilitation. The advent of fetal valvotomy for critical AS may also increase the number of infants who are candidates for biventricular repair.Pathophysiology. The unique intracardiac and extracardiac shunts present in fetal life allow even neonates with critical AS to survive. In utero, left ventricular hypertrophy and ischemia cause left atrial hypertension, which reduces the right-to-left flow across the foramen ovale. In severe cases, a reversal of Brunicardi_Ch20_p0751-p0800.indd 75522/02/19 2:54 PM 756SPECIFIC CONSIDERATIONSPART IIFigure 20-3. A. Congenital aortic valve stenosis, en fosse echocardiographic view of the stenotic bicuspid aortic valve. Parasternal long axis view of the same valve with a gradient of 60 mm of Hg (‘*’ points to the valve). B. Parasternal long axis ecocardiographic view of a patient with
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stenotic bicuspid aortic valve. Parasternal long axis view of the same valve with a gradient of 60 mm of Hg (‘*’ points to the valve). B. Parasternal long axis ecocardiographic view of a patient with discrete subaortic membrane (‘*’ points to the membrane). C. Parasternal long axis ecocardiographic view of a patient with diffuse tunnel like subvalvar aortic stenosis with membrane. Doppler revealed a gradient of 81 mm of hg (‘*’ represents the area of diffuse narrowing). D. Appearance of supravalvar aortic stenosis on an aortogram performed in the cardiac catheterization lab (‘*’ points to the stenosis). E. Appearance after four patch reconstruction of the same patient shown in Figure 20.3 d. (Re-formatted images obtained from a CT angiogram).ABCDEBrunicardi_Ch20_p0751-p0800.indd 75622/02/19 2:54 PM 757CONGENITAL HEART DISEASECHAPTER 20flow may occur, causing right ventricular volume loading. The RV then provides the entire systemic output via the patent duc-tus arteriosus
Surgery_Schwartz. stenotic bicuspid aortic valve. Parasternal long axis view of the same valve with a gradient of 60 mm of Hg (‘*’ points to the valve). B. Parasternal long axis ecocardiographic view of a patient with discrete subaortic membrane (‘*’ points to the membrane). C. Parasternal long axis ecocardiographic view of a patient with diffuse tunnel like subvalvar aortic stenosis with membrane. Doppler revealed a gradient of 81 mm of hg (‘*’ represents the area of diffuse narrowing). D. Appearance of supravalvar aortic stenosis on an aortogram performed in the cardiac catheterization lab (‘*’ points to the stenosis). E. Appearance after four patch reconstruction of the same patient shown in Figure 20.3 d. (Re-formatted images obtained from a CT angiogram).ABCDEBrunicardi_Ch20_p0751-p0800.indd 75622/02/19 2:54 PM 757CONGENITAL HEART DISEASECHAPTER 20flow may occur, causing right ventricular volume loading. The RV then provides the entire systemic output via the patent duc-tus arteriosus
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75622/02/19 2:54 PM 757CONGENITAL HEART DISEASECHAPTER 20flow may occur, causing right ventricular volume loading. The RV then provides the entire systemic output via the patent duc-tus arteriosus (ductal-dependent systemic blood flow). Although cardiac output is maintained, the LV suffers continued damage as the intracavitary pressure precludes adequate coronary perfu-sion, resulting in LV infarction and subendocardial fibroelas-tosis. The presentation of the neonate with critical AS is then determined by the morphology of the LV and other left-sided heart structures, the degree of left ventricular dysfunction, and the completeness of the transition from a parallel circulation to an in-series circulation (i.e., on closure of the foramen ovale and the ductus arteriosus). Those infants with mild-to-moderate AS in whom LV function is preserved are asymptomatic at birth. The only abnormalities may be a systolic ejection murmur and electrocardiogram (ECG) evidence of left ventricular
Surgery_Schwartz. 75622/02/19 2:54 PM 757CONGENITAL HEART DISEASECHAPTER 20flow may occur, causing right ventricular volume loading. The RV then provides the entire systemic output via the patent duc-tus arteriosus (ductal-dependent systemic blood flow). Although cardiac output is maintained, the LV suffers continued damage as the intracavitary pressure precludes adequate coronary perfu-sion, resulting in LV infarction and subendocardial fibroelas-tosis. The presentation of the neonate with critical AS is then determined by the morphology of the LV and other left-sided heart structures, the degree of left ventricular dysfunction, and the completeness of the transition from a parallel circulation to an in-series circulation (i.e., on closure of the foramen ovale and the ductus arteriosus). Those infants with mild-to-moderate AS in whom LV function is preserved are asymptomatic at birth. The only abnormalities may be a systolic ejection murmur and electrocardiogram (ECG) evidence of left ventricular
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with mild-to-moderate AS in whom LV function is preserved are asymptomatic at birth. The only abnormalities may be a systolic ejection murmur and electrocardiogram (ECG) evidence of left ventricular hypertro-phy. However, those neonates with severe AS and compromised LV function are unable to provide adequate cardiac output at birth and will present in circulatory collapse once the ductus closes, with dyspnea, tachypnea, irritability, narrowed pulse pressure, oliguria, and profound metabolic acidosis.24 If ductal patency is maintained, systemic perfusion will be provided by the RV via ductal flow, and cyanosis may be the only finding.Diagnosis. Neonates and infants with severe valvular AS may have a relatively nonspecific history of irritability and failure to thrive. Angina, if present, is usually manifested by episodic, inconsolable crying that coincides with feeding. As discussed previously, evidence of poor peripheral perfusion, such as extreme pallor, indicates severe LVOT
Surgery_Schwartz. with mild-to-moderate AS in whom LV function is preserved are asymptomatic at birth. The only abnormalities may be a systolic ejection murmur and electrocardiogram (ECG) evidence of left ventricular hypertro-phy. However, those neonates with severe AS and compromised LV function are unable to provide adequate cardiac output at birth and will present in circulatory collapse once the ductus closes, with dyspnea, tachypnea, irritability, narrowed pulse pressure, oliguria, and profound metabolic acidosis.24 If ductal patency is maintained, systemic perfusion will be provided by the RV via ductal flow, and cyanosis may be the only finding.Diagnosis. Neonates and infants with severe valvular AS may have a relatively nonspecific history of irritability and failure to thrive. Angina, if present, is usually manifested by episodic, inconsolable crying that coincides with feeding. As discussed previously, evidence of poor peripheral perfusion, such as extreme pallor, indicates severe LVOT
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is usually manifested by episodic, inconsolable crying that coincides with feeding. As discussed previously, evidence of poor peripheral perfusion, such as extreme pallor, indicates severe LVOT obstruction. Differen-tial cyanosis is an uncommon finding, but it is present when enough antegrade flow occurs only to maintain normal upper body perfusion, while a large patent ductus arteriosus produces blue discoloration of the abdomen and legs.Physical findings include a systolic ejection murmur, although a quiet murmur may paradoxically indicate a more severe condition with reduced cardiac output. A systolic click correlates with a valvular etiology of obstruction. As LV dys-function progresses, evidence of congestive heart failure occurs.The chest radiograph is variable but may show dilatation of the aortic root, and the ECG often demonstrates LV hypertro-phy. Echocardiography with Doppler flow is extremely useful in establishing the diagnosis, as well as quantifying the transvalvular
Surgery_Schwartz. is usually manifested by episodic, inconsolable crying that coincides with feeding. As discussed previously, evidence of poor peripheral perfusion, such as extreme pallor, indicates severe LVOT obstruction. Differen-tial cyanosis is an uncommon finding, but it is present when enough antegrade flow occurs only to maintain normal upper body perfusion, while a large patent ductus arteriosus produces blue discoloration of the abdomen and legs.Physical findings include a systolic ejection murmur, although a quiet murmur may paradoxically indicate a more severe condition with reduced cardiac output. A systolic click correlates with a valvular etiology of obstruction. As LV dys-function progresses, evidence of congestive heart failure occurs.The chest radiograph is variable but may show dilatation of the aortic root, and the ECG often demonstrates LV hypertro-phy. Echocardiography with Doppler flow is extremely useful in establishing the diagnosis, as well as quantifying the transvalvular
Surgery_Schwartz_5072
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of the aortic root, and the ECG often demonstrates LV hypertro-phy. Echocardiography with Doppler flow is extremely useful in establishing the diagnosis, as well as quantifying the transvalvular gradient. Furthermore, echocardiography can facilitate evaluation for the several associated defects that can be present in critical neonatal AS, including mitral stenosis, LV hypoplasia, LV endo-cardial fibroelastosis, subaortic stenosis, VSD, or coarctation. The presence of any or several of these defects has important impli-cations related to treatment options for these patients. Although cardiac catheterization is not routinely performed for diagnostic purposes, it can be invaluable as part of the treatment algorithm if the lesion is amenable to balloon valvotomy. Magnetic resonance imaging (MRI) is another very useful technique for assessing the adequacy of the left-sided structures and is increasingly utilized to determine candidacy for biventricular repairs.Treatment. As alluded to
Surgery_Schwartz. of the aortic root, and the ECG often demonstrates LV hypertro-phy. Echocardiography with Doppler flow is extremely useful in establishing the diagnosis, as well as quantifying the transvalvular gradient. Furthermore, echocardiography can facilitate evaluation for the several associated defects that can be present in critical neonatal AS, including mitral stenosis, LV hypoplasia, LV endo-cardial fibroelastosis, subaortic stenosis, VSD, or coarctation. The presence of any or several of these defects has important impli-cations related to treatment options for these patients. Although cardiac catheterization is not routinely performed for diagnostic purposes, it can be invaluable as part of the treatment algorithm if the lesion is amenable to balloon valvotomy. Magnetic resonance imaging (MRI) is another very useful technique for assessing the adequacy of the left-sided structures and is increasingly utilized to determine candidacy for biventricular repairs.Treatment. As alluded to
Surgery_Schwartz_5073
Surgery_Schwartz
(MRI) is another very useful technique for assessing the adequacy of the left-sided structures and is increasingly utilized to determine candidacy for biventricular repairs.Treatment. As alluded to previously, the first decision that must be made in the neonate with critical LVOT obstruction is whether the patient is a candidate for biventricular or univen-tricular repair. Central to this decision is assessment of the degree of hypoplasia of the LV and other left-sided structures. Alsoufi and colleagues25 have described a rational approach to the neonate with critical LVOT obstruction. The options vary depending on whether the infant follows a single or a 3biventricular pathway. The options for a single ventricle include the Norwood operation, a hybrid strategy (initial ductal stent and bilateral pulmonary artery bands followed by later completion of the Norwood operation) or heart transplantation. The options for a biventricular heart include balloon valvuloplasty, surgical
Surgery_Schwartz. (MRI) is another very useful technique for assessing the adequacy of the left-sided structures and is increasingly utilized to determine candidacy for biventricular repairs.Treatment. As alluded to previously, the first decision that must be made in the neonate with critical LVOT obstruction is whether the patient is a candidate for biventricular or univen-tricular repair. Central to this decision is assessment of the degree of hypoplasia of the LV and other left-sided structures. Alsoufi and colleagues25 have described a rational approach to the neonate with critical LVOT obstruction. The options vary depending on whether the infant follows a single or a 3biventricular pathway. The options for a single ventricle include the Norwood operation, a hybrid strategy (initial ductal stent and bilateral pulmonary artery bands followed by later completion of the Norwood operation) or heart transplantation. The options for a biventricular heart include balloon valvuloplasty, surgical
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and bilateral pulmonary artery bands followed by later completion of the Norwood operation) or heart transplantation. The options for a biventricular heart include balloon valvuloplasty, surgical val-votomy, neonatal Ross operation, or a Yasui operation. Often valvotomy is accompanied by LV rehabilitation techniques, including EFE resection and mitral valve interventions. Fetal aortic valvotomy, which is now offered at specialized centers, is another promising strategy to decompress the LV in fetal life and potentially allow growth of the left-sided structures sufficient to permit a biventricular circulation. Regardless of whether the baby is triaged to a single or biventricular strategy, any infant with severe AS requires urgent intervention. Preoperative stabi-lization, however, has dramatically altered the clinical algorithm and outcomes for this patient population.25 The preoperative strategy begins with endotracheal intubation and inotropic sup-port. Prostaglandin infusion is
Surgery_Schwartz. and bilateral pulmonary artery bands followed by later completion of the Norwood operation) or heart transplantation. The options for a biventricular heart include balloon valvuloplasty, surgical val-votomy, neonatal Ross operation, or a Yasui operation. Often valvotomy is accompanied by LV rehabilitation techniques, including EFE resection and mitral valve interventions. Fetal aortic valvotomy, which is now offered at specialized centers, is another promising strategy to decompress the LV in fetal life and potentially allow growth of the left-sided structures sufficient to permit a biventricular circulation. Regardless of whether the baby is triaged to a single or biventricular strategy, any infant with severe AS requires urgent intervention. Preoperative stabi-lization, however, has dramatically altered the clinical algorithm and outcomes for this patient population.25 The preoperative strategy begins with endotracheal intubation and inotropic sup-port. Prostaglandin infusion is
Surgery_Schwartz_5075
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dramatically altered the clinical algorithm and outcomes for this patient population.25 The preoperative strategy begins with endotracheal intubation and inotropic sup-port. Prostaglandin infusion is initiated to maintain ductal patency, and confirmatory studies are performed prior to opera-tive intervention. Therapy is generally indicated in the presence of a transvalvular gradient of 50 mmHg with associated symp-toms including syncope, CHF, or angina, or if a gradient of 50 to 75 mmHg exists with concomitant ECG evidence of LV strain or ischemia. In the critically ill neonate, a gradient across the aortic valve may not be present because of poor LV function. However, the decision regarding treatment options must be based on a complete understanding of associated defects. For example, in the presence of a hypoplastic LV (left ventricular end-diastolic volume <20 mL/m2) or a markedly abnormal mitral valve, iso-lated aortic valvotomy should not be performed because studies have
Surgery_Schwartz. dramatically altered the clinical algorithm and outcomes for this patient population.25 The preoperative strategy begins with endotracheal intubation and inotropic sup-port. Prostaglandin infusion is initiated to maintain ductal patency, and confirmatory studies are performed prior to opera-tive intervention. Therapy is generally indicated in the presence of a transvalvular gradient of 50 mmHg with associated symp-toms including syncope, CHF, or angina, or if a gradient of 50 to 75 mmHg exists with concomitant ECG evidence of LV strain or ischemia. In the critically ill neonate, a gradient across the aortic valve may not be present because of poor LV function. However, the decision regarding treatment options must be based on a complete understanding of associated defects. For example, in the presence of a hypoplastic LV (left ventricular end-diastolic volume <20 mL/m2) or a markedly abnormal mitral valve, iso-lated aortic valvotomy should not be performed because studies have
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in the presence of a hypoplastic LV (left ventricular end-diastolic volume <20 mL/m2) or a markedly abnormal mitral valve, iso-lated aortic valvotomy should not be performed because studies have demonstrated high mortality in this population following isolated valvotomy.26Patients who have an LV capable of providing systemic output are candidates for intervention to relieve AS, generally through balloon valvotomy. Occasionally, if catheter-based therapy is not an option, relief of valvular AS in infants and children can be accomplished with surgical valvotomy using standard techniques of CPB and direct exposure to the aortic valve. A transverse incision is made in the ascending aorta above the sinus of Valsalva, extending close to, but not into, the noncoronary sinus. Exposure is attained with placement of a retractor into the right coronary sinus. After inspection of the valve, the chosen commissure is incised to within 1 to 2 mm of the aortic wall (Fig. 20-4A,B).Balloon valvotomy
Surgery_Schwartz. in the presence of a hypoplastic LV (left ventricular end-diastolic volume <20 mL/m2) or a markedly abnormal mitral valve, iso-lated aortic valvotomy should not be performed because studies have demonstrated high mortality in this population following isolated valvotomy.26Patients who have an LV capable of providing systemic output are candidates for intervention to relieve AS, generally through balloon valvotomy. Occasionally, if catheter-based therapy is not an option, relief of valvular AS in infants and children can be accomplished with surgical valvotomy using standard techniques of CPB and direct exposure to the aortic valve. A transverse incision is made in the ascending aorta above the sinus of Valsalva, extending close to, but not into, the noncoronary sinus. Exposure is attained with placement of a retractor into the right coronary sinus. After inspection of the valve, the chosen commissure is incised to within 1 to 2 mm of the aortic wall (Fig. 20-4A,B).Balloon valvotomy
Surgery_Schwartz_5077
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with placement of a retractor into the right coronary sinus. After inspection of the valve, the chosen commissure is incised to within 1 to 2 mm of the aortic wall (Fig. 20-4A,B).Balloon valvotomy performed in the catheterization lab is generally the procedure of choice for reduction of transvalvular gradients in symptomatic infants and children without signifi-cant aortic insufficiency. Balloon valvotomy provides relief of the valvular gradient and allows future surgical intervention (which is generally required in most patients when a larger prosthesis can be implanted) to be performed on an unscarred chest. An important issue when planning aortic valvotomy, whether percutaneously or via open surgical technique, is the risk of inducing hemodynamically significant aortic regurgita-tion. Induction of more than moderate aortic regurgitation is poorly tolerated in the infant with critical AS and may require an urgent procedure to replace or repair the aortic valve. Most often in these
Surgery_Schwartz. with placement of a retractor into the right coronary sinus. After inspection of the valve, the chosen commissure is incised to within 1 to 2 mm of the aortic wall (Fig. 20-4A,B).Balloon valvotomy performed in the catheterization lab is generally the procedure of choice for reduction of transvalvular gradients in symptomatic infants and children without signifi-cant aortic insufficiency. Balloon valvotomy provides relief of the valvular gradient and allows future surgical intervention (which is generally required in most patients when a larger prosthesis can be implanted) to be performed on an unscarred chest. An important issue when planning aortic valvotomy, whether percutaneously or via open surgical technique, is the risk of inducing hemodynamically significant aortic regurgita-tion. Induction of more than moderate aortic regurgitation is poorly tolerated in the infant with critical AS and may require an urgent procedure to replace or repair the aortic valve. Most often in these
Surgery_Schwartz_5078
Surgery_Schwartz
Induction of more than moderate aortic regurgitation is poorly tolerated in the infant with critical AS and may require an urgent procedure to replace or repair the aortic valve. Most often in these patients, a Ross procedure represents the only real option as mechanical valve replacement in a neonate has exceptionally poor outcome.In general, catheter-based balloon valvotomy has supplanted open surgical valvotomy. The decision regarding Brunicardi_Ch20_p0751-p0800.indd 75722/02/19 2:54 PM 758SPECIFIC CONSIDERATIONSPART IIFigure 20-4. A. Intra-operative picture of a stenotic bicuspid aortic valve (as seen through an aortotomy). B. Intra-operative picture of the valve after a controlled valvotomy if performed. Note the forceps is across the opening of the aortic valve (‘*’ points to the valvotomy).the most appropriate method to use depends on several factors, including the available medical expertise, the patient’s overall status and hemodynamics, and the presence of associated
Surgery_Schwartz. Induction of more than moderate aortic regurgitation is poorly tolerated in the infant with critical AS and may require an urgent procedure to replace or repair the aortic valve. Most often in these patients, a Ross procedure represents the only real option as mechanical valve replacement in a neonate has exceptionally poor outcome.In general, catheter-based balloon valvotomy has supplanted open surgical valvotomy. The decision regarding Brunicardi_Ch20_p0751-p0800.indd 75722/02/19 2:54 PM 758SPECIFIC CONSIDERATIONSPART IIFigure 20-4. A. Intra-operative picture of a stenotic bicuspid aortic valve (as seen through an aortotomy). B. Intra-operative picture of the valve after a controlled valvotomy if performed. Note the forceps is across the opening of the aortic valve (‘*’ points to the valvotomy).the most appropriate method to use depends on several factors, including the available medical expertise, the patient’s overall status and hemodynamics, and the presence of associated
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the valvotomy).the most appropriate method to use depends on several factors, including the available medical expertise, the patient’s overall status and hemodynamics, and the presence of associated cardiac defects requiring repair.25 Although evidence is emerging to the contrary, simple valvotomy, whether performed using percutaneous or open technique, is generally considered a palliative procedure. The goal is to relieve LVOT obstruction without producing clinically significant regurgitation, in order to allow sufficient annular growth for eventual aortic valve replacement. The reintervention rate is higher if balloon valvuloplasty is performed as the initial palliation (54%) compared to a surgical valvolomy (23%) as the latter is a more controlled division of the aortic commissure25 (Fig. 20-4C). The majority of infants who undergo aortic valvotomy will require further intervention on the aortic valve within 10 years following initial intervention.26Neonates with severely
Surgery_Schwartz. the valvotomy).the most appropriate method to use depends on several factors, including the available medical expertise, the patient’s overall status and hemodynamics, and the presence of associated cardiac defects requiring repair.25 Although evidence is emerging to the contrary, simple valvotomy, whether performed using percutaneous or open technique, is generally considered a palliative procedure. The goal is to relieve LVOT obstruction without producing clinically significant regurgitation, in order to allow sufficient annular growth for eventual aortic valve replacement. The reintervention rate is higher if balloon valvuloplasty is performed as the initial palliation (54%) compared to a surgical valvolomy (23%) as the latter is a more controlled division of the aortic commissure25 (Fig. 20-4C). The majority of infants who undergo aortic valvotomy will require further intervention on the aortic valve within 10 years following initial intervention.26Neonates with severely
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(Fig. 20-4C). The majority of infants who undergo aortic valvotomy will require further intervention on the aortic valve within 10 years following initial intervention.26Neonates with severely hypoplastic LVs or significant LV endocardial fibroelastosis may not be candidates for biventricu-lar repair and are treated the same as infants with the hypoplas-tic left heart syndrome (HLHS), which is discussed later (see “Hypoplastic Left Heart Syndrome”).As mentioned previously, fetal intervention for the aortic valve has been described with the goal being to improve the growth of the left ventricle. The group at Boston Children’s Hospital have reported fairly favorable results in a small cohort.34Many surgeons previously avoided aortic valve replace-ment for AS in early childhood because the more commonly used mechanical valves would be outgrown and require replace-ment later and the obligatory anticoagulation for mechanical valves resulted in a substantial risk for complications. In
Surgery_Schwartz. (Fig. 20-4C). The majority of infants who undergo aortic valvotomy will require further intervention on the aortic valve within 10 years following initial intervention.26Neonates with severely hypoplastic LVs or significant LV endocardial fibroelastosis may not be candidates for biventricu-lar repair and are treated the same as infants with the hypoplas-tic left heart syndrome (HLHS), which is discussed later (see “Hypoplastic Left Heart Syndrome”).As mentioned previously, fetal intervention for the aortic valve has been described with the goal being to improve the growth of the left ventricle. The group at Boston Children’s Hospital have reported fairly favorable results in a small cohort.34Many surgeons previously avoided aortic valve replace-ment for AS in early childhood because the more commonly used mechanical valves would be outgrown and require replace-ment later and the obligatory anticoagulation for mechanical valves resulted in a substantial risk for complications. In
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the more commonly used mechanical valves would be outgrown and require replace-ment later and the obligatory anticoagulation for mechanical valves resulted in a substantial risk for complications. In addi-tion, prosthetic valves have an incidence of bacterial endocardi-tis or perivalvular leak requiring reintervention.The use of allografts and the advent of the Ross procedure have largely obviated these issues and made early definitive cor-rection of critical AS a viable option.23,27,28 Donald Ross first described transposition of the pulmonary valve into the aortic position with allograft reconstruction of the pulmonary outflow tract in 1967.27 The result of this operation is a normal trileaf-let semilunar valve made of a patient’s native tissue with the potential for growth to adult size in the aortic position in place of the damaged aortic valve (Fig. 20-5). The Ross procedure has become a useful option for aortic valve replacement in children because it has improved durability and
Surgery_Schwartz. the more commonly used mechanical valves would be outgrown and require replace-ment later and the obligatory anticoagulation for mechanical valves resulted in a substantial risk for complications. In addi-tion, prosthetic valves have an incidence of bacterial endocardi-tis or perivalvular leak requiring reintervention.The use of allografts and the advent of the Ross procedure have largely obviated these issues and made early definitive cor-rection of critical AS a viable option.23,27,28 Donald Ross first described transposition of the pulmonary valve into the aortic position with allograft reconstruction of the pulmonary outflow tract in 1967.27 The result of this operation is a normal trileaf-let semilunar valve made of a patient’s native tissue with the potential for growth to adult size in the aortic position in place of the damaged aortic valve (Fig. 20-5). The Ross procedure has become a useful option for aortic valve replacement in children because it has improved durability and
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in the aortic position in place of the damaged aortic valve (Fig. 20-5). The Ross procedure has become a useful option for aortic valve replacement in children because it has improved durability and can be performed with acceptable morbidity and mortality rates. The placement of a pulmonary conduit, which does not grow and becomes calci-fied and stenotic over time, does obligate the patient to rein-tervention (either surgically or using transcatheter techniques) to replace the RV-to-pulmonary artery conduit. Karamlou and colleagues29 have reviewed the outcomes and associated risk factors for aortic valve replacement in 160 children from the Hospital for Sick Children in Toronto. They found that younger age, lower operative weight, concomitant performance of aortic root replacement or reconstruction, and use of prosthesis type other than a pulmonary autograft were significant predictors of death, whereas the use of a bioprosthetic or allograft valve type and earlier year of operation
Surgery_Schwartz. in the aortic position in place of the damaged aortic valve (Fig. 20-5). The Ross procedure has become a useful option for aortic valve replacement in children because it has improved durability and can be performed with acceptable morbidity and mortality rates. The placement of a pulmonary conduit, which does not grow and becomes calci-fied and stenotic over time, does obligate the patient to rein-tervention (either surgically or using transcatheter techniques) to replace the RV-to-pulmonary artery conduit. Karamlou and colleagues29 have reviewed the outcomes and associated risk factors for aortic valve replacement in 160 children from the Hospital for Sick Children in Toronto. They found that younger age, lower operative weight, concomitant performance of aortic root replacement or reconstruction, and use of prosthesis type other than a pulmonary autograft were significant predictors of death, whereas the use of a bioprosthetic or allograft valve type and earlier year of operation
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and use of prosthesis type other than a pulmonary autograft were significant predictors of death, whereas the use of a bioprosthetic or allograft valve type and earlier year of operation were identified as significant risk factors for repeated aortic valve replacement. Autograft use was associated with a blunted progression of the peak prosthetic valve gradient and a rapid decrease in the left ventricular end-diastolic dimension. In agreement with these findings, Lupinetti and Jones28 compared allograft aortic valve replacement with the Ross procedure and found a more significant transvalvular gradient reduction and regression of left ventricular hypertro-phy in those patients who underwent the Ross procedure. In some cases, the pulmonary valve may not be usable because of associated defects or congenital absence. These children are not candidates for the Ross procedure and can be treated with cryopreserved allografts (cadaveric human aortic valves) or prosthetic aortic valve
Surgery_Schwartz. and use of prosthesis type other than a pulmonary autograft were significant predictors of death, whereas the use of a bioprosthetic or allograft valve type and earlier year of operation were identified as significant risk factors for repeated aortic valve replacement. Autograft use was associated with a blunted progression of the peak prosthetic valve gradient and a rapid decrease in the left ventricular end-diastolic dimension. In agreement with these findings, Lupinetti and Jones28 compared allograft aortic valve replacement with the Ross procedure and found a more significant transvalvular gradient reduction and regression of left ventricular hypertro-phy in those patients who underwent the Ross procedure. In some cases, the pulmonary valve may not be usable because of associated defects or congenital absence. These children are not candidates for the Ross procedure and can be treated with cryopreserved allografts (cadaveric human aortic valves) or prosthetic aortic valve
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defects or congenital absence. These children are not candidates for the Ross procedure and can be treated with cryopreserved allografts (cadaveric human aortic valves) or prosthetic aortic valve replacement. At times, there may be a size discrepancy between the right ventricular outflow tract (RVOT) and the LVOT, especially in cases of severe critical AS in infancy. For these cases, the pulmonary autograft is placed in a manner that also provides enlargement of the aortic annulus (Ross/Konno).Subvalvular AS occurs beneath the aortic valve and may be classified as discrete or tunnel-like (diffuse). A thin, ABBrunicardi_Ch20_p0751-p0800.indd 75822/02/19 2:54 PM 759CONGENITAL HEART DISEASECHAPTER 20fibromuscular diaphragm immediately proximal to the aortic valve characterizes discrete subaortic stenosis. This diaphragm typically extends for 180o or more in a crescentic or circular fash-ion, often attaching to the mitral valve as well as the interven-tricular septum. The aortic valve
Surgery_Schwartz. defects or congenital absence. These children are not candidates for the Ross procedure and can be treated with cryopreserved allografts (cadaveric human aortic valves) or prosthetic aortic valve replacement. At times, there may be a size discrepancy between the right ventricular outflow tract (RVOT) and the LVOT, especially in cases of severe critical AS in infancy. For these cases, the pulmonary autograft is placed in a manner that also provides enlargement of the aortic annulus (Ross/Konno).Subvalvular AS occurs beneath the aortic valve and may be classified as discrete or tunnel-like (diffuse). A thin, ABBrunicardi_Ch20_p0751-p0800.indd 75822/02/19 2:54 PM 759CONGENITAL HEART DISEASECHAPTER 20fibromuscular diaphragm immediately proximal to the aortic valve characterizes discrete subaortic stenosis. This diaphragm typically extends for 180o or more in a crescentic or circular fash-ion, often attaching to the mitral valve as well as the interven-tricular septum. The aortic valve
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stenosis. This diaphragm typically extends for 180o or more in a crescentic or circular fash-ion, often attaching to the mitral valve as well as the interven-tricular septum. The aortic valve itself is usually normal in this condition, although the turbulence imparted by the subvalvular stenosis may affect leaflet morphology and valve competence.Diffuse subvalvular AS results in a long, tunnel-like obstruction that may extend to the left ventricular apex. In some individuals, there may be difficulty in distinguishing between hypertrophic cardiomyopathy and diffuse subaortic steno-sis. Operation for subvalvular AS is indicated with a gradient exceeding 30 mmHg, in the presence of aortic valve insuffi-ciency, or when symptoms indicating LVOT obstruction are present.30 Given that repair of isolated discrete subaortic ste-nosis can be done with low rates of morbidity and mortality, some surgeons advocate repair in all cases of discrete AS to avoid progression of the stenosis and the
Surgery_Schwartz. stenosis. This diaphragm typically extends for 180o or more in a crescentic or circular fash-ion, often attaching to the mitral valve as well as the interven-tricular septum. The aortic valve itself is usually normal in this condition, although the turbulence imparted by the subvalvular stenosis may affect leaflet morphology and valve competence.Diffuse subvalvular AS results in a long, tunnel-like obstruction that may extend to the left ventricular apex. In some individuals, there may be difficulty in distinguishing between hypertrophic cardiomyopathy and diffuse subaortic steno-sis. Operation for subvalvular AS is indicated with a gradient exceeding 30 mmHg, in the presence of aortic valve insuffi-ciency, or when symptoms indicating LVOT obstruction are present.30 Given that repair of isolated discrete subaortic ste-nosis can be done with low rates of morbidity and mortality, some surgeons advocate repair in all cases of discrete AS to avoid progression of the stenosis and the
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of isolated discrete subaortic ste-nosis can be done with low rates of morbidity and mortality, some surgeons advocate repair in all cases of discrete AS to avoid progression of the stenosis and the development of aortic insufficiency, although more recent data demonstrate that sub-aortic resection should be delayed until the LV gradient exceeds 30 mmHg because most children with an initial LV gradient less than 30 mmHg have quiescent disease.31 Diffuse AS is a more complex lesion and often requires aortoventriculoplasty. Results are generally excellent, with operative mortality less than 5%.32Supravalvular AS occurs more rarely and also can be clas-sified into a discrete type, which produces an hourglass defor-mity of the aorta, and a diffuse form that can involve the entire arch and brachiocephalic arteries. The aortic valve leaflets are usually normal, but in some cases, the leaflets may adhere to the supravalvular stenosis, thereby narrowing the sinuses of Valsalva in diastole
Surgery_Schwartz. of isolated discrete subaortic ste-nosis can be done with low rates of morbidity and mortality, some surgeons advocate repair in all cases of discrete AS to avoid progression of the stenosis and the development of aortic insufficiency, although more recent data demonstrate that sub-aortic resection should be delayed until the LV gradient exceeds 30 mmHg because most children with an initial LV gradient less than 30 mmHg have quiescent disease.31 Diffuse AS is a more complex lesion and often requires aortoventriculoplasty. Results are generally excellent, with operative mortality less than 5%.32Supravalvular AS occurs more rarely and also can be clas-sified into a discrete type, which produces an hourglass defor-mity of the aorta, and a diffuse form that can involve the entire arch and brachiocephalic arteries. The aortic valve leaflets are usually normal, but in some cases, the leaflets may adhere to the supravalvular stenosis, thereby narrowing the sinuses of Valsalva in diastole
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brachiocephalic arteries. The aortic valve leaflets are usually normal, but in some cases, the leaflets may adhere to the supravalvular stenosis, thereby narrowing the sinuses of Valsalva in diastole and restricting coronary artery perfusion. In addition, accelerated intimal hyperplastic changes in the coronary arteries can be demonstrated in these patients because the proximal position of the coronary arteries subjects them to abnormally high perfusion pressures.The signs and symptoms of supravalvular AS are similar to other forms of LVOT obstruction. An asymptomatic murmur is the presenting manifestation in approximately half of these patients. Syncope, poor exercise tolerance, and angina may all occur with nearly equal frequency. Supravalvar AS is associated with Williams’ syndrome, a constellation of elfin facies, mental retardation, and hypercalcemia.33 Following routine evaluation, cardiac catheterization should be performed in order to delin-eate coronary anatomy, as well as to
Surgery_Schwartz. brachiocephalic arteries. The aortic valve leaflets are usually normal, but in some cases, the leaflets may adhere to the supravalvular stenosis, thereby narrowing the sinuses of Valsalva in diastole and restricting coronary artery perfusion. In addition, accelerated intimal hyperplastic changes in the coronary arteries can be demonstrated in these patients because the proximal position of the coronary arteries subjects them to abnormally high perfusion pressures.The signs and symptoms of supravalvular AS are similar to other forms of LVOT obstruction. An asymptomatic murmur is the presenting manifestation in approximately half of these patients. Syncope, poor exercise tolerance, and angina may all occur with nearly equal frequency. Supravalvar AS is associated with Williams’ syndrome, a constellation of elfin facies, mental retardation, and hypercalcemia.33 Following routine evaluation, cardiac catheterization should be performed in order to delin-eate coronary anatomy, as well as to
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of elfin facies, mental retardation, and hypercalcemia.33 Following routine evaluation, cardiac catheterization should be performed in order to delin-eate coronary anatomy, as well as to delineate the degree of obstruction. A gradient of 50 mmHg or greater is an indication for operation. However, the clinician must be cognizant of any coexistent lesions, most commonly pulmonic stenosis, which may add complexity to the repair.The localized form of supravalvular AS can be treated by creating an inverted Y-shaped aortotomy across the area of ste-nosis, straddling the right coronary artery. The obstructing shelf is then excised, and a pantaloon-shaped patch (Doty technique) or individual sinus patch enlargement (Brom technique) is used (Fig. 20-3E).The diffuse form of supravalvular stenosis is more vari-able (Fig. 20-6), and the particular operative approach must be tailored to each specific patient’s anatomy. In general, either an aortic endarterectomy with patch augmentation can be
Surgery_Schwartz. of elfin facies, mental retardation, and hypercalcemia.33 Following routine evaluation, cardiac catheterization should be performed in order to delin-eate coronary anatomy, as well as to delineate the degree of obstruction. A gradient of 50 mmHg or greater is an indication for operation. However, the clinician must be cognizant of any coexistent lesions, most commonly pulmonic stenosis, which may add complexity to the repair.The localized form of supravalvular AS can be treated by creating an inverted Y-shaped aortotomy across the area of ste-nosis, straddling the right coronary artery. The obstructing shelf is then excised, and a pantaloon-shaped patch (Doty technique) or individual sinus patch enlargement (Brom technique) is used (Fig. 20-3E).The diffuse form of supravalvular stenosis is more vari-able (Fig. 20-6), and the particular operative approach must be tailored to each specific patient’s anatomy. In general, either an aortic endarterectomy with patch augmentation can be
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is more vari-able (Fig. 20-6), and the particular operative approach must be tailored to each specific patient’s anatomy. In general, either an aortic endarterectomy with patch augmentation can be per-formed or if the narrowing extends past the aorta arch, a pros-thetic graft can be placed between the ascending and descending aorta. Operative results for discrete supravalvular AS are gen-erally good, with a hospital mortality of less than 1% and an actuarial survival rate exceeding 90% at 20 years.35 In contrast, however, the diffuse form is more hazardous to repair and car-ried a mortality of 15% in a recent series.35,36Patent Ductus ArteriosusAnatomy. The ductus arteriosus is derived from the sixth aor-tic arch and normally extends from the main or left pulmonary artery to the upper descending thoracic aorta, distal to the left subclavian artery. In the normal fetal cardiovascular system, ductal flow is considerable (approximately 60% of the com-bined ventricular output) and is
Surgery_Schwartz. is more vari-able (Fig. 20-6), and the particular operative approach must be tailored to each specific patient’s anatomy. In general, either an aortic endarterectomy with patch augmentation can be per-formed or if the narrowing extends past the aorta arch, a pros-thetic graft can be placed between the ascending and descending aorta. Operative results for discrete supravalvular AS are gen-erally good, with a hospital mortality of less than 1% and an actuarial survival rate exceeding 90% at 20 years.35 In contrast, however, the diffuse form is more hazardous to repair and car-ried a mortality of 15% in a recent series.35,36Patent Ductus ArteriosusAnatomy. The ductus arteriosus is derived from the sixth aor-tic arch and normally extends from the main or left pulmonary artery to the upper descending thoracic aorta, distal to the left subclavian artery. In the normal fetal cardiovascular system, ductal flow is considerable (approximately 60% of the com-bined ventricular output) and is
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descending thoracic aorta, distal to the left subclavian artery. In the normal fetal cardiovascular system, ductal flow is considerable (approximately 60% of the com-bined ventricular output) and is directed exclusively from the pulmonary artery to the aorta. In infancy, the length of the duc-tus may vary from 2 to 8 mm, with a diameter of 4 to 12 mm.Locally produced and circulating prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2) induce active relaxation of the duc-tal musculature, maintaining maximal patency during the fetal period.38 At birth, increased pulmonary blood flow metabo-lizes these prostaglandin products, and absence of the placenta removes an important source of them, resulting in a marked decrease in these ductal-relaxing substances. In addition, release of histamines, catecholamines, bradykinin, and acetylcholine all promote ductal contraction. Despite all of these complex Figure 20-5. Appearance of the stenotic aortic valve during aortography performed in the
Surgery_Schwartz. descending thoracic aorta, distal to the left subclavian artery. In the normal fetal cardiovascular system, ductal flow is considerable (approximately 60% of the com-bined ventricular output) and is directed exclusively from the pulmonary artery to the aorta. In infancy, the length of the duc-tus may vary from 2 to 8 mm, with a diameter of 4 to 12 mm.Locally produced and circulating prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2) induce active relaxation of the duc-tal musculature, maintaining maximal patency during the fetal period.38 At birth, increased pulmonary blood flow metabo-lizes these prostaglandin products, and absence of the placenta removes an important source of them, resulting in a marked decrease in these ductal-relaxing substances. In addition, release of histamines, catecholamines, bradykinin, and acetylcholine all promote ductal contraction. Despite all of these complex Figure 20-5. Appearance of the stenotic aortic valve during aortography performed in the
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catecholamines, bradykinin, and acetylcholine all promote ductal contraction. Despite all of these complex Figure 20-5. Appearance of the stenotic aortic valve during aortography performed in the cardiac catheterization lab. (left). Balloon valvuloplasty being performed. (right). The ‘*’ points to the the “waist” created by the stenotic valve during dilation. (Used with permission from Kelly Rosso MD.)Brunicardi_Ch20_p0751-p0800.indd 75922/02/19 2:54 PM 760SPECIFIC CONSIDERATIONSPART IIFigure 20-6. Reformatted image obtained after CT angiography of a child with diffuse supravalvar aortic stenosis (‘*’ points to the transverse aortic arch).interactions, the rising oxygen tension in the fetal blood is the main stimulus causing smooth muscle contraction and ductal closure within 10 to 15 hours postnatally.39 Anatomic closure by fibrosis produces the ligamentum arteriosum connecting the pulmonary artery to the aorta.Delayed closure of the ductus is termed prolonged patency, whereas
Surgery_Schwartz. catecholamines, bradykinin, and acetylcholine all promote ductal contraction. Despite all of these complex Figure 20-5. Appearance of the stenotic aortic valve during aortography performed in the cardiac catheterization lab. (left). Balloon valvuloplasty being performed. (right). The ‘*’ points to the the “waist” created by the stenotic valve during dilation. (Used with permission from Kelly Rosso MD.)Brunicardi_Ch20_p0751-p0800.indd 75922/02/19 2:54 PM 760SPECIFIC CONSIDERATIONSPART IIFigure 20-6. Reformatted image obtained after CT angiography of a child with diffuse supravalvar aortic stenosis (‘*’ points to the transverse aortic arch).interactions, the rising oxygen tension in the fetal blood is the main stimulus causing smooth muscle contraction and ductal closure within 10 to 15 hours postnatally.39 Anatomic closure by fibrosis produces the ligamentum arteriosum connecting the pulmonary artery to the aorta.Delayed closure of the ductus is termed prolonged patency, whereas
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15 hours postnatally.39 Anatomic closure by fibrosis produces the ligamentum arteriosum connecting the pulmonary artery to the aorta.Delayed closure of the ductus is termed prolonged patency, whereas failure of closure causes persistent patency, which may occur as an isolated lesion or in association with more complex congenital heart defects. In many of these infants with more complex congenital heart defects, either pulmonary or systemic perfusion may depend on ductal flow, and these infants may decompensate if exogenous PGE is not administered to maintain ductal patency.Natural History. The incidence of patent ductus arteriosus (PDA) is approximately 1 in every 2000 births; however, it increases dramatically with increasing prematurity.39 In some series, PDAs have been noted in 75% of infants of 28 to 30 weeks gestation. Persistent patency occurs more commonly in females, with a 2:1 ratio.40PDA is not a benign entity, although prolonged survival has been reported. The estimated
Surgery_Schwartz. 15 hours postnatally.39 Anatomic closure by fibrosis produces the ligamentum arteriosum connecting the pulmonary artery to the aorta.Delayed closure of the ductus is termed prolonged patency, whereas failure of closure causes persistent patency, which may occur as an isolated lesion or in association with more complex congenital heart defects. In many of these infants with more complex congenital heart defects, either pulmonary or systemic perfusion may depend on ductal flow, and these infants may decompensate if exogenous PGE is not administered to maintain ductal patency.Natural History. The incidence of patent ductus arteriosus (PDA) is approximately 1 in every 2000 births; however, it increases dramatically with increasing prematurity.39 In some series, PDAs have been noted in 75% of infants of 28 to 30 weeks gestation. Persistent patency occurs more commonly in females, with a 2:1 ratio.40PDA is not a benign entity, although prolonged survival has been reported. The estimated
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of infants of 28 to 30 weeks gestation. Persistent patency occurs more commonly in females, with a 2:1 ratio.40PDA is not a benign entity, although prolonged survival has been reported. The estimated death rate for infants with iso-lated, untreated PDA is approximately 30%.41 The leading cause of death is congestive heart failure, with respiratory infection as a secondary cause. Endocarditis is more likely to occur with a small ductus and is rarely fatal if aggressive antibiotic therapy is initiated early.Clinical Manifestations and Diagnosis. After birth, in an otherwise normal cardiovascular system, a PDA results in a left-to-right shunt that depends on both the size of the ductal lumen and its total length. As the pulmonary vascular resistance falls 8 to 10 weeks postnatally, the shunt will increase, and its flow will ultimately be determined by the relative resistances of the pulmonary and systemic circulations.The hemodynamic consequences of an unrestrictive duc-tal shunt are
Surgery_Schwartz. of infants of 28 to 30 weeks gestation. Persistent patency occurs more commonly in females, with a 2:1 ratio.40PDA is not a benign entity, although prolonged survival has been reported. The estimated death rate for infants with iso-lated, untreated PDA is approximately 30%.41 The leading cause of death is congestive heart failure, with respiratory infection as a secondary cause. Endocarditis is more likely to occur with a small ductus and is rarely fatal if aggressive antibiotic therapy is initiated early.Clinical Manifestations and Diagnosis. After birth, in an otherwise normal cardiovascular system, a PDA results in a left-to-right shunt that depends on both the size of the ductal lumen and its total length. As the pulmonary vascular resistance falls 8 to 10 weeks postnatally, the shunt will increase, and its flow will ultimately be determined by the relative resistances of the pulmonary and systemic circulations.The hemodynamic consequences of an unrestrictive duc-tal shunt are
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will increase, and its flow will ultimately be determined by the relative resistances of the pulmonary and systemic circulations.The hemodynamic consequences of an unrestrictive duc-tal shunt are left ventricular volume overload with increased left atrial and pulmonary artery pressures and right ventricular strain from the augmented afterload. These changes result in increased sympathetic discharge, tachycardia, tachypnea, and ventricular hypertrophy. The diastolic shunt results in lower aortic diastolic pressure and increases the potential for myo-cardial ischemia and underperfusion of other systemic organs, while the increased pulmonary flow leads to increased work of breathing and decreased gas exchange. Unrestrictive ductal flow may lead to pulmonary hypertension within the first year of life. These changes will be significantly attenuated if the size of the ductus is only moderate, and they will be completely absent if the ductus is small.Physical examination of the afflicted
Surgery_Schwartz. will increase, and its flow will ultimately be determined by the relative resistances of the pulmonary and systemic circulations.The hemodynamic consequences of an unrestrictive duc-tal shunt are left ventricular volume overload with increased left atrial and pulmonary artery pressures and right ventricular strain from the augmented afterload. These changes result in increased sympathetic discharge, tachycardia, tachypnea, and ventricular hypertrophy. The diastolic shunt results in lower aortic diastolic pressure and increases the potential for myo-cardial ischemia and underperfusion of other systemic organs, while the increased pulmonary flow leads to increased work of breathing and decreased gas exchange. Unrestrictive ductal flow may lead to pulmonary hypertension within the first year of life. These changes will be significantly attenuated if the size of the ductus is only moderate, and they will be completely absent if the ductus is small.Physical examination of the afflicted
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of life. These changes will be significantly attenuated if the size of the ductus is only moderate, and they will be completely absent if the ductus is small.Physical examination of the afflicted infant will reveal evi-dence of a hyperdynamic circulation with a widened pulse pres-sure and a hyperactive precordium. Auscultation demonstrates a systolic or continuous murmur, often termed a machinery mur-mur. Cyanosis is not present in uncomplicated isolated PDA.The chest radiograph may reveal increased pulmonary vascularity or cardiomegaly, and the ECG may show LV strain, left atrial enlargement, and possibly RV hypertrophy. Echocar-diogram with color mapping reliably demonstrates the patency of the ductus as well as estimates the shunt size. Cardiac cath-eterization is necessary only when pulmonary hypertension is suspected.Therapy. The presence of a persistent PDA is sufficient indica-tion for closure because of the increased mortality and risk of endocarditis.40 In older patients with
Surgery_Schwartz. of life. These changes will be significantly attenuated if the size of the ductus is only moderate, and they will be completely absent if the ductus is small.Physical examination of the afflicted infant will reveal evi-dence of a hyperdynamic circulation with a widened pulse pres-sure and a hyperactive precordium. Auscultation demonstrates a systolic or continuous murmur, often termed a machinery mur-mur. Cyanosis is not present in uncomplicated isolated PDA.The chest radiograph may reveal increased pulmonary vascularity or cardiomegaly, and the ECG may show LV strain, left atrial enlargement, and possibly RV hypertrophy. Echocar-diogram with color mapping reliably demonstrates the patency of the ductus as well as estimates the shunt size. Cardiac cath-eterization is necessary only when pulmonary hypertension is suspected.Therapy. The presence of a persistent PDA is sufficient indica-tion for closure because of the increased mortality and risk of endocarditis.40 In older patients with
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hypertension is suspected.Therapy. The presence of a persistent PDA is sufficient indica-tion for closure because of the increased mortality and risk of endocarditis.40 In older patients with pulmonary hypertension, closure may not improve symptoms and is associated with much higher mortality.In premature infants, aggressive intervention with indometh-acin or ibuprofen to achieve early closure of the PDA is beneficial unless contraindications such as necrotizing enterocolitis or renal insufficiency are present.41 Term infants, however, are gener-ally unresponsive to pharmacologic therapy with indomethacin, so mechanical closure must be undertaken once the diagnosis is established. This can be accomplished either surgically (Fig. 20-7) or with catheter-based therapy.15,42,43 Currently, transluminal placement of various occlusive devices, such as the Rashkind double-umbrella device or embolization with Gianturco coils, is in widespread use.42 However, there are a number of
Surgery_Schwartz. hypertension is suspected.Therapy. The presence of a persistent PDA is sufficient indica-tion for closure because of the increased mortality and risk of endocarditis.40 In older patients with pulmonary hypertension, closure may not improve symptoms and is associated with much higher mortality.In premature infants, aggressive intervention with indometh-acin or ibuprofen to achieve early closure of the PDA is beneficial unless contraindications such as necrotizing enterocolitis or renal insufficiency are present.41 Term infants, however, are gener-ally unresponsive to pharmacologic therapy with indomethacin, so mechanical closure must be undertaken once the diagnosis is established. This can be accomplished either surgically (Fig. 20-7) or with catheter-based therapy.15,42,43 Currently, transluminal placement of various occlusive devices, such as the Rashkind double-umbrella device or embolization with Gianturco coils, is in widespread use.42 However, there are a number of
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transluminal placement of various occlusive devices, such as the Rashkind double-umbrella device or embolization with Gianturco coils, is in widespread use.42 However, there are a number of complications inherent with the use of percutaneous devices, such as thromboem-bolism, endocarditis, incomplete occlusion, vascular injury, and hemorrhage secondary to perforation.43 In addition, these tech-niques may not be applicable in very young infants because the peripheral vessels do not provide adequate access for the delivery devices. Attempts are being made to develop such devices for pre-mature infants with early successful results in study populations.44Surgical closure can be achieved via either open or video-assisted approaches. The open approach employs a muscle-sparing posterior lateral thoracotomy in the third or fourth intercostal space on the side of the aorta (generally the left). The lung is then retracted anteriorly. In the neonate, the PDA is singly ligated with a surgical
Surgery_Schwartz. transluminal placement of various occlusive devices, such as the Rashkind double-umbrella device or embolization with Gianturco coils, is in widespread use.42 However, there are a number of complications inherent with the use of percutaneous devices, such as thromboem-bolism, endocarditis, incomplete occlusion, vascular injury, and hemorrhage secondary to perforation.43 In addition, these tech-niques may not be applicable in very young infants because the peripheral vessels do not provide adequate access for the delivery devices. Attempts are being made to develop such devices for pre-mature infants with early successful results in study populations.44Surgical closure can be achieved via either open or video-assisted approaches. The open approach employs a muscle-sparing posterior lateral thoracotomy in the third or fourth intercostal space on the side of the aorta (generally the left). The lung is then retracted anteriorly. In the neonate, the PDA is singly ligated with a surgical
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thoracotomy in the third or fourth intercostal space on the side of the aorta (generally the left). The lung is then retracted anteriorly. In the neonate, the PDA is singly ligated with a surgical clip or permanent suture. Care must be taken to avoid the recurrent laryngeal nerve, which courses around the PDA. The PDA can also be ligated via a median sternotomy; however, this approach is generally reserved for patients who have additional cardiac or great vessel lesions requiring repair. Occasionally, a short, broad ductus, in which the dimension of Brunicardi_Ch20_p0751-p0800.indd 76022/02/19 2:54 PM 761CONGENITAL HEART DISEASECHAPTER 20its width approaches that of its length, will be encountered. In this case, division between vascular clamps with oversewing of both ends is advisable (Fig. 20-8). In extreme cases, the use of CPB to decompress the large ductus during ligation is an option.Video-assisted thoracoscopic occlusion, using metal clips, also has been described, although
Surgery_Schwartz. thoracotomy in the third or fourth intercostal space on the side of the aorta (generally the left). The lung is then retracted anteriorly. In the neonate, the PDA is singly ligated with a surgical clip or permanent suture. Care must be taken to avoid the recurrent laryngeal nerve, which courses around the PDA. The PDA can also be ligated via a median sternotomy; however, this approach is generally reserved for patients who have additional cardiac or great vessel lesions requiring repair. Occasionally, a short, broad ductus, in which the dimension of Brunicardi_Ch20_p0751-p0800.indd 76022/02/19 2:54 PM 761CONGENITAL HEART DISEASECHAPTER 20its width approaches that of its length, will be encountered. In this case, division between vascular clamps with oversewing of both ends is advisable (Fig. 20-8). In extreme cases, the use of CPB to decompress the large ductus during ligation is an option.Video-assisted thoracoscopic occlusion, using metal clips, also has been described, although
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(Fig. 20-8). In extreme cases, the use of CPB to decompress the large ductus during ligation is an option.Video-assisted thoracoscopic occlusion, using metal clips, also has been described, although it offers few advantages over the standard surgical approach. Preterm newborns and children may do well with a surgical technique, while older patients (older than age 5 years) and those with smaller ducts (<3 mm) do well with coil occlusion. In fact, Moore and colleagues recently concluded from their series that coil occlusion is the procedure Figure 20-7. Chest x-ray before and after PDA ligation showing the dramatic improvement in the lung fields after ligation (arrow points to the clip used for PDA ligation).Figure 20-8. Surgical PDA ligation. A clip has been applied to occlude the ductus arteriosus. Note the relationship of the recurrent laryngeal nerve to the ductus arteriosus. (Used with permission from Kelly Rosso MD.)of choice for ducts smaller than 4 mm.45 Complete closure rates
Surgery_Schwartz. (Fig. 20-8). In extreme cases, the use of CPB to decompress the large ductus during ligation is an option.Video-assisted thoracoscopic occlusion, using metal clips, also has been described, although it offers few advantages over the standard surgical approach. Preterm newborns and children may do well with a surgical technique, while older patients (older than age 5 years) and those with smaller ducts (<3 mm) do well with coil occlusion. In fact, Moore and colleagues recently concluded from their series that coil occlusion is the procedure Figure 20-7. Chest x-ray before and after PDA ligation showing the dramatic improvement in the lung fields after ligation (arrow points to the clip used for PDA ligation).Figure 20-8. Surgical PDA ligation. A clip has been applied to occlude the ductus arteriosus. Note the relationship of the recurrent laryngeal nerve to the ductus arteriosus. (Used with permission from Kelly Rosso MD.)of choice for ducts smaller than 4 mm.45 Complete closure rates
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arteriosus. Note the relationship of the recurrent laryngeal nerve to the ductus arteriosus. (Used with permission from Kelly Rosso MD.)of choice for ducts smaller than 4 mm.45 Complete closure rates using catheter-based techniques have steadily improved.Outcomes. In premature infants, the surgical mortality is very low, although the overall hospital death rate is significant as a consequence of other complications of prematurity. In older infants and children, mortality is less than 1%. Bleeding, chylo-thorax, vocal cord paralysis, and the need for reoperation occur infrequently. With the advent of muscle-sparing thoracotomy, the risk of subsequent arm dysfunction or breast abnormalities is virtually eliminated.46Aortic CoarctationAnatomy. Coarctation of the aorta (COA) is defined as a lumi-nal narrowing in the aorta that causes an obstruction to blood flow. This narrowing is most commonly located distal to the left subclavian artery. The embryologic origin of COA is a sub-ject of
Surgery_Schwartz. arteriosus. Note the relationship of the recurrent laryngeal nerve to the ductus arteriosus. (Used with permission from Kelly Rosso MD.)of choice for ducts smaller than 4 mm.45 Complete closure rates using catheter-based techniques have steadily improved.Outcomes. In premature infants, the surgical mortality is very low, although the overall hospital death rate is significant as a consequence of other complications of prematurity. In older infants and children, mortality is less than 1%. Bleeding, chylo-thorax, vocal cord paralysis, and the need for reoperation occur infrequently. With the advent of muscle-sparing thoracotomy, the risk of subsequent arm dysfunction or breast abnormalities is virtually eliminated.46Aortic CoarctationAnatomy. Coarctation of the aorta (COA) is defined as a lumi-nal narrowing in the aorta that causes an obstruction to blood flow. This narrowing is most commonly located distal to the left subclavian artery. The embryologic origin of COA is a sub-ject of
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lumi-nal narrowing in the aorta that causes an obstruction to blood flow. This narrowing is most commonly located distal to the left subclavian artery. The embryologic origin of COA is a sub-ject of some controversy. One theory holds that the obstructing shelf, which is largely composed of tissue found within the duc-tus, forms as the ductus involutes.47 The other theory holds that a diminished aortic isthmus develops secondary to decreased aortic flow in infants with enhanced ductal circulation.Extensive collateral circulation develops, predominantly involving the intercostals and mammary arteries as a direct result of aortic flow obstruction. This translates into the well-known finding of “rib-notching” on chest radiograph, as well as a prominent pulsation underneath the ribs.Other associated anomalies, such as ventricular septal defect, PDA, and ASD, may be seen with COA, but the most common is that of a bicuspid aortic valve, which can be demon-strated in 25% to 42% of
Surgery_Schwartz. lumi-nal narrowing in the aorta that causes an obstruction to blood flow. This narrowing is most commonly located distal to the left subclavian artery. The embryologic origin of COA is a sub-ject of some controversy. One theory holds that the obstructing shelf, which is largely composed of tissue found within the duc-tus, forms as the ductus involutes.47 The other theory holds that a diminished aortic isthmus develops secondary to decreased aortic flow in infants with enhanced ductal circulation.Extensive collateral circulation develops, predominantly involving the intercostals and mammary arteries as a direct result of aortic flow obstruction. This translates into the well-known finding of “rib-notching” on chest radiograph, as well as a prominent pulsation underneath the ribs.Other associated anomalies, such as ventricular septal defect, PDA, and ASD, may be seen with COA, but the most common is that of a bicuspid aortic valve, which can be demon-strated in 25% to 42% of