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cancer. Breast Cancer Res Treat. 1993;28:115-120. 56. Kerlikowske K, Ichikawa L, Miglioretti DL, et al. Longitudi-nal measurement of clinical mammographic breast density to improve estimation of breast cancer risk. J Natl Cancer Inst. 2007;99:386-395. 57. Berry DA, Parmigiani G, Sanchez J, et al. Probability of car-rying a mutation of breast-ovarian cancer gene BRCA1 based on family history. J Natl Cancer Inst. 1997;89:227-238. 58. Parmigiani G, Berry D, Aguilar O. Determining carrier prob-abilities for breast cancer-susceptibility genes BRCA1 and BRCA2. Am J Hum Genet. 1998;62:145-158.Brunicardi_Ch17_p0541-p0612.indd 60301/03/19 5:06 PM 604SPECIFIC CONSIDERATIONSPART II 59. Tyrer J, Duffy SW, Cuzick J. A breast cancer prediction model incorporating familial and personal risk factors. Stat Med. 2004;23:1111-1130. 60. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxi-fen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study.
Surgery_Schwartz. cancer. Breast Cancer Res Treat. 1993;28:115-120. 56. Kerlikowske K, Ichikawa L, Miglioretti DL, et al. Longitudi-nal measurement of clinical mammographic breast density to improve estimation of breast cancer risk. J Natl Cancer Inst. 2007;99:386-395. 57. Berry DA, Parmigiani G, Sanchez J, et al. Probability of car-rying a mutation of breast-ovarian cancer gene BRCA1 based on family history. J Natl Cancer Inst. 1997;89:227-238. 58. Parmigiani G, Berry D, Aguilar O. Determining carrier prob-abilities for breast cancer-susceptibility genes BRCA1 and BRCA2. Am J Hum Genet. 1998;62:145-158.Brunicardi_Ch17_p0541-p0612.indd 60301/03/19 5:06 PM 604SPECIFIC CONSIDERATIONSPART II 59. Tyrer J, Duffy SW, Cuzick J. A breast cancer prediction model incorporating familial and personal risk factors. Stat Med. 2004;23:1111-1130. 60. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxi-fen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study.
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Stat Med. 2004;23:1111-1130. 60. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxi-fen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. 1998;90:1371-1388. 61. Grodstein F, Stampfer MJ, Colditz GA, et al. Postmeno-pausal hormone therapy and mortality. N Engl J Med. 1997;336:1769-1775. 62. Hartmann LC, Schaid DJ, Woods JE, et al. Efficacy of bilat-eral prophylactic mastectomy in women with a family history of breast cancer. N Engl J Med. 1999;340:77-84. 63. Kerlikowske K, Grady D, Rubin SM, et al. Efficacy of screening mammography. A meta-analysis. JAMA. 1995;273:149-154. 64. Rowe TC, Chen GL, Hsiang YH, et al. DNA damage by anti-tumor acridines mediated by mammalian DNA topoisomer-ase II. Cancer Res. 1986;46:2021-2026. 65. Sakorafas GH. The management of women at high risk for the development of breast cancer: risk estimation and preven-tative strategies. Cancer Treat Rev. 2003;29:79-89. 66. Schrag D,
Surgery_Schwartz. Stat Med. 2004;23:1111-1130. 60. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxi-fen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. 1998;90:1371-1388. 61. Grodstein F, Stampfer MJ, Colditz GA, et al. Postmeno-pausal hormone therapy and mortality. N Engl J Med. 1997;336:1769-1775. 62. Hartmann LC, Schaid DJ, Woods JE, et al. Efficacy of bilat-eral prophylactic mastectomy in women with a family history of breast cancer. N Engl J Med. 1999;340:77-84. 63. Kerlikowske K, Grady D, Rubin SM, et al. Efficacy of screening mammography. A meta-analysis. JAMA. 1995;273:149-154. 64. Rowe TC, Chen GL, Hsiang YH, et al. DNA damage by anti-tumor acridines mediated by mammalian DNA topoisomer-ase II. Cancer Res. 1986;46:2021-2026. 65. Sakorafas GH. The management of women at high risk for the development of breast cancer: risk estimation and preven-tative strategies. Cancer Treat Rev. 2003;29:79-89. 66. Schrag D,
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GH. The management of women at high risk for the development of breast cancer: risk estimation and preven-tative strategies. Cancer Treat Rev. 2003;29:79-89. 66. Schrag D, Kuntz KM, Garber JE, et al. Decision analysis—effects of prophylactic mastectomy and oophorectomy on life expectancy among women with BRCA1 or BRCA2 mutations. N Engl J Med. 1997;336:1465-1471. 67. Vogel VG. Management of the high-risk patient. Surg Clin North Am. 2003;83:733-751. 68. Wu K, Brown P. Is low-dose tamoxifen useful for the treat-ment and prevention of breast cancer? J Natl Cancer Inst. 2003;95:766-767. 69. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collabora-tive reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women with-out breast cancer. Lancet. 1997;350:1047-1059. 70. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in
Surgery_Schwartz. GH. The management of women at high risk for the development of breast cancer: risk estimation and preven-tative strategies. Cancer Treat Rev. 2003;29:79-89. 66. Schrag D, Kuntz KM, Garber JE, et al. Decision analysis—effects of prophylactic mastectomy and oophorectomy on life expectancy among women with BRCA1 or BRCA2 mutations. N Engl J Med. 1997;336:1465-1471. 67. Vogel VG. Management of the high-risk patient. Surg Clin North Am. 2003;83:733-751. 68. Wu K, Brown P. Is low-dose tamoxifen useful for the treat-ment and prevention of breast cancer? J Natl Cancer Inst. 2003;95:766-767. 69. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collabora-tive reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women with-out breast cancer. Lancet. 1997;350:1047-1059. 70. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in
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cancer and 108,411 women with-out breast cancer. Lancet. 1997;350:1047-1059. 70. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women’s Health Ini-tiative Randomized Trial. JAMA. 2003;289:3243-3253. 71. Beral V. Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet. 2003;362:419-427. 72. Glasziou P, Houssami N. The evidence base for breast cancer screening. Prev Med. 2011;53:100-102. 73. Olsen O, Gotzsche PC. Cochrane review on screening for breast cancer with mammography. Lancet. 2001;358:1340-1342. 74. Siu AL. Screening for Breast Cancer: U.S. Preventive Ser-vices Task Force recommendation statement. Ann Intern Med. 2016;164:279-296. 75. Oeffinger KC, Fontham ET, Etzioni R, et al. Breast can-cer screening for women at average risk: 2015 guide-line update from the American Cancer Society. JAMA. 2015;314:1599-1614. 76. National Comprehensive Cancer
Surgery_Schwartz. cancer and 108,411 women with-out breast cancer. Lancet. 1997;350:1047-1059. 70. Chlebowski RT, Hendrix SL, Langer RD, et al. Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women’s Health Ini-tiative Randomized Trial. JAMA. 2003;289:3243-3253. 71. Beral V. Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet. 2003;362:419-427. 72. Glasziou P, Houssami N. The evidence base for breast cancer screening. Prev Med. 2011;53:100-102. 73. Olsen O, Gotzsche PC. Cochrane review on screening for breast cancer with mammography. Lancet. 2001;358:1340-1342. 74. Siu AL. Screening for Breast Cancer: U.S. Preventive Ser-vices Task Force recommendation statement. Ann Intern Med. 2016;164:279-296. 75. Oeffinger KC, Fontham ET, Etzioni R, et al. Breast can-cer screening for women at average risk: 2015 guide-line update from the American Cancer Society. JAMA. 2015;314:1599-1614. 76. National Comprehensive Cancer
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Fontham ET, Etzioni R, et al. Breast can-cer screening for women at average risk: 2015 guide-line update from the American Cancer Society. JAMA. 2015;314:1599-1614. 76. National Comprehensive Cancer Network. Breast cancer screening and diagnosis, version 1.2016. Available at: https://www.nccn.org/professionals/physician_gls/pdf/breast-screening.pdf. Accessed July 9, 2018. 77. US Preventive Services Task Force. Screening for breast cancer: US Preventive Services Task Force recommenda-tion statement. Ann Intern Med. 2009;151:716-726, W-236. 78. Powles TJ, Ashley S, Tidy A, Smith IE, Dowsett M. Twenty-year follow-up of the Royal Marsden randomized, double-blinded tamoxifen breast cancer prevention trial. J Natl Cancer Inst. 2007;99:283-290. 79. Independent UK Panel on Breast Cancer Screening. The ben-efits and harms of breast cancer screening: an independent review. Lancet. 2012;380:1778-1786. 80. Nyström L, Andersson I, Bjurstam N, Frisell J, Norden-skjöld B, Rutqvist LE. Long-term
Surgery_Schwartz. Fontham ET, Etzioni R, et al. Breast can-cer screening for women at average risk: 2015 guide-line update from the American Cancer Society. JAMA. 2015;314:1599-1614. 76. National Comprehensive Cancer Network. Breast cancer screening and diagnosis, version 1.2016. Available at: https://www.nccn.org/professionals/physician_gls/pdf/breast-screening.pdf. Accessed July 9, 2018. 77. US Preventive Services Task Force. Screening for breast cancer: US Preventive Services Task Force recommenda-tion statement. Ann Intern Med. 2009;151:716-726, W-236. 78. Powles TJ, Ashley S, Tidy A, Smith IE, Dowsett M. Twenty-year follow-up of the Royal Marsden randomized, double-blinded tamoxifen breast cancer prevention trial. J Natl Cancer Inst. 2007;99:283-290. 79. Independent UK Panel on Breast Cancer Screening. The ben-efits and harms of breast cancer screening: an independent review. Lancet. 2012;380:1778-1786. 80. Nyström L, Andersson I, Bjurstam N, Frisell J, Norden-skjöld B, Rutqvist LE. Long-term
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The ben-efits and harms of breast cancer screening: an independent review. Lancet. 2012;380:1778-1786. 80. Nyström L, Andersson I, Bjurstam N, Frisell J, Norden-skjöld B, Rutqvist LE. Long-term effects of mammography screening: updated overview of the Swedish randomised trials. Lancet. 2002;359:909-919. 81. Moss S, Thomas I, Evans A, Thomas B, Johns, L. Ran-domised controlled trial of mammographic screening in women from age 40: results of screening in the first 10 years. Br J Cancer. 2005;92:949-954. 82. Veronesi U, Maisonneuve P, Sacchini V, Rotmensz N, Boyle P. Tamoxifen for breast cancer among hysterectomised women. Lancet. 2002;359:1122-1124. 83. Cuzick J, Forbes JF, Sestak I, et al. Long-term results of tamoxifen prophylaxis for breast cancer–96-month follow-up of the randomized IBIS-I trial. J Natl Cancer Inst. 2007;99: 272-282. 84. Gail MH, Costantino JP, Bryant J, et al. Weighing the risks and benefits of tamoxifen treatment for preventing breast cancer. J Natl Cancer Inst.
Surgery_Schwartz. The ben-efits and harms of breast cancer screening: an independent review. Lancet. 2012;380:1778-1786. 80. Nyström L, Andersson I, Bjurstam N, Frisell J, Norden-skjöld B, Rutqvist LE. Long-term effects of mammography screening: updated overview of the Swedish randomised trials. Lancet. 2002;359:909-919. 81. Moss S, Thomas I, Evans A, Thomas B, Johns, L. Ran-domised controlled trial of mammographic screening in women from age 40: results of screening in the first 10 years. Br J Cancer. 2005;92:949-954. 82. Veronesi U, Maisonneuve P, Sacchini V, Rotmensz N, Boyle P. Tamoxifen for breast cancer among hysterectomised women. Lancet. 2002;359:1122-1124. 83. Cuzick J, Forbes JF, Sestak I, et al. Long-term results of tamoxifen prophylaxis for breast cancer–96-month follow-up of the randomized IBIS-I trial. J Natl Cancer Inst. 2007;99: 272-282. 84. Gail MH, Costantino JP, Bryant J, et al. Weighing the risks and benefits of tamoxifen treatment for preventing breast cancer. J Natl Cancer Inst.
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trial. J Natl Cancer Inst. 2007;99: 272-282. 84. Gail MH, Costantino JP, Bryant J, et al. Weighing the risks and benefits of tamoxifen treatment for preventing breast cancer. J Natl Cancer Inst. 1999;91:1829-1846. 85. Vogel VG, Costantino JP, Wickerham DL, et al. Effects of tamoxifen vs. raloxifene on the risk of developing inva-sive breast cancer and other disease outcomes: the NSABP Study of Tamoxifen and Raloxifene (STAR) P-2 trial. JAMA. 2006;295:2727-2741. 86. Vogel VG, Costantino JP, Wickerham DL, et al. Update of the National Surgical Adjuvant Breast and Bowel Project Study of Tamoxifen and Raloxifene (STAR) P-2 Trial: Preventing breast cancer. Cancer Prev Res (Phila). 2010;3:696-706. 87. Goss PE, Ingle JN, Ales-Martinez JE, et al. Exemestane for breast-cancer prevention in postmenopausal women. N Engl J Med. 2011;364:2381-2391. 88. Cuzick J. IBIS II: a breast cancer prevention trial in post-menopausal women using the aromatase inhibitor anastro-zole. Expert Rev Anticancer
Surgery_Schwartz. trial. J Natl Cancer Inst. 2007;99: 272-282. 84. Gail MH, Costantino JP, Bryant J, et al. Weighing the risks and benefits of tamoxifen treatment for preventing breast cancer. J Natl Cancer Inst. 1999;91:1829-1846. 85. Vogel VG, Costantino JP, Wickerham DL, et al. Effects of tamoxifen vs. raloxifene on the risk of developing inva-sive breast cancer and other disease outcomes: the NSABP Study of Tamoxifen and Raloxifene (STAR) P-2 trial. JAMA. 2006;295:2727-2741. 86. Vogel VG, Costantino JP, Wickerham DL, et al. Update of the National Surgical Adjuvant Breast and Bowel Project Study of Tamoxifen and Raloxifene (STAR) P-2 Trial: Preventing breast cancer. Cancer Prev Res (Phila). 2010;3:696-706. 87. Goss PE, Ingle JN, Ales-Martinez JE, et al. Exemestane for breast-cancer prevention in postmenopausal women. N Engl J Med. 2011;364:2381-2391. 88. Cuzick J. IBIS II: a breast cancer prevention trial in post-menopausal women using the aromatase inhibitor anastro-zole. Expert Rev Anticancer
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women. N Engl J Med. 2011;364:2381-2391. 88. Cuzick J. IBIS II: a breast cancer prevention trial in post-menopausal women using the aromatase inhibitor anastro-zole. Expert Rev Anticancer Ther. 2008;8:1377-1385. 89. Sestak I, Singh S, Cuzick J, et al. Changes in bone mineral density at 3 years in postmenopausal women receiving anas-trozole and risedronate in the IBIS-II bone substudy: an inter-national, double-blind, randomised, placebo-controlled trial. Lancet Oncol. 2014;15:1460-1468. 90. Jenkins VA, Ambroisine LM, Atkins L, et al. Effects of anas-trozole on cognitive performance in postmenopausal women: a randomised, double-blind chemoprevention trial (IBIS II). Lancet Oncol. 2008;9:953-961. 91. Nelson HD, Smith ME, Griffin JC, et al. Use of medications to reduce risk for primary breast cancer: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2013;158:604-614. 92. Visvanathan K, Hurley P, Bantug E, et al. Use of pharmaco-logic interventions for
Surgery_Schwartz. women. N Engl J Med. 2011;364:2381-2391. 88. Cuzick J. IBIS II: a breast cancer prevention trial in post-menopausal women using the aromatase inhibitor anastro-zole. Expert Rev Anticancer Ther. 2008;8:1377-1385. 89. Sestak I, Singh S, Cuzick J, et al. Changes in bone mineral density at 3 years in postmenopausal women receiving anas-trozole and risedronate in the IBIS-II bone substudy: an inter-national, double-blind, randomised, placebo-controlled trial. Lancet Oncol. 2014;15:1460-1468. 90. Jenkins VA, Ambroisine LM, Atkins L, et al. Effects of anas-trozole on cognitive performance in postmenopausal women: a randomised, double-blind chemoprevention trial (IBIS II). Lancet Oncol. 2008;9:953-961. 91. Nelson HD, Smith ME, Griffin JC, et al. Use of medications to reduce risk for primary breast cancer: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2013;158:604-614. 92. Visvanathan K, Hurley P, Bantug E, et al. Use of pharmaco-logic interventions for
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breast cancer: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2013;158:604-614. 92. Visvanathan K, Hurley P, Bantug E, et al. Use of pharmaco-logic interventions for breast cancer risk reduction: american society of clinical oncology clinical practice guideline. J Clin Oncol. 2013;31:2942-2962. 93. Domchek SM, Friebel TM, Singer CF, et al. Association of risk-reducing surgery in BRCA1 or BRCA2 mutation carriers with cancer risk and mortality. JAMA. 2010;304: 967-975. 94. Ford D, Easton DF, Stratton M, et al. Genetic heterogeneity and penetrance analysis of the BRCA1 and BRCA2 genes in breast cancer families. The Breast Cancer Linkage Consor-tium. Am J Hum Genet. 1998;62:676-689. 95. Gowen LC, Avrutskaya AV, Latour AM, et al. BRCA1 required for transcription-coupled repair of oxidative DNA damage. Science. 1998;281:1009-1012. 96. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92:1126-1135. 97. Oddoux
Surgery_Schwartz. breast cancer: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med. 2013;158:604-614. 92. Visvanathan K, Hurley P, Bantug E, et al. Use of pharmaco-logic interventions for breast cancer risk reduction: american society of clinical oncology clinical practice guideline. J Clin Oncol. 2013;31:2942-2962. 93. Domchek SM, Friebel TM, Singer CF, et al. Association of risk-reducing surgery in BRCA1 or BRCA2 mutation carriers with cancer risk and mortality. JAMA. 2010;304: 967-975. 94. Ford D, Easton DF, Stratton M, et al. Genetic heterogeneity and penetrance analysis of the BRCA1 and BRCA2 genes in breast cancer families. The Breast Cancer Linkage Consor-tium. Am J Hum Genet. 1998;62:676-689. 95. Gowen LC, Avrutskaya AV, Latour AM, et al. BRCA1 required for transcription-coupled repair of oxidative DNA damage. Science. 1998;281:1009-1012. 96. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92:1126-1135. 97. Oddoux
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repair of oxidative DNA damage. Science. 1998;281:1009-1012. 96. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92:1126-1135. 97. Oddoux C, Struewing JP, Clayton CM, et al. The carrier frequency of the BRCA2 6174delT mutation among Ash-kenazi Jewish individuals is approximately 1%. Nat Genet. 1996;14:188-190. 98. Roa BB, Boyd AA, Volcik K, et al. Ashkenazi Jewish pop-ulation frequencies for common mutations in BRCA1 and BRCA2. Nat Genet. 1996;14:185-187.Brunicardi_Ch17_p0541-p0612.indd 60401/03/19 5:06 PM 605THE BREASTCHAPTER 17 99. Rosen EM, Fan S, Pestell RG, et al. BRCA1 gene in breast cancer. J Cell Physiol. 2003;196:19-41. 100. Wooster R, Weber BL. Breast and ovarian cancer. N Engl J Med. 2003;348:2339-2347. 101. Petrij-Bosch A, Peelen T, van Vliet M, et al. BRCA1 genomic deletions are major founder mutations in Dutch breast cancer patients. Nat Genet. 1997;17:341-345. 102. Gorski B, Byrski T, Huzarski T, et al. Founder
Surgery_Schwartz. repair of oxidative DNA damage. Science. 1998;281:1009-1012. 96. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. 2000;92:1126-1135. 97. Oddoux C, Struewing JP, Clayton CM, et al. The carrier frequency of the BRCA2 6174delT mutation among Ash-kenazi Jewish individuals is approximately 1%. Nat Genet. 1996;14:188-190. 98. Roa BB, Boyd AA, Volcik K, et al. Ashkenazi Jewish pop-ulation frequencies for common mutations in BRCA1 and BRCA2. Nat Genet. 1996;14:185-187.Brunicardi_Ch17_p0541-p0612.indd 60401/03/19 5:06 PM 605THE BREASTCHAPTER 17 99. Rosen EM, Fan S, Pestell RG, et al. BRCA1 gene in breast cancer. J Cell Physiol. 2003;196:19-41. 100. Wooster R, Weber BL. Breast and ovarian cancer. N Engl J Med. 2003;348:2339-2347. 101. Petrij-Bosch A, Peelen T, van Vliet M, et al. BRCA1 genomic deletions are major founder mutations in Dutch breast cancer patients. Nat Genet. 1997;17:341-345. 102. Gorski B, Byrski T, Huzarski T, et al. Founder
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A, Peelen T, van Vliet M, et al. BRCA1 genomic deletions are major founder mutations in Dutch breast cancer patients. Nat Genet. 1997;17:341-345. 102. Gorski B, Byrski T, Huzarski T, et al. Founder mutations in the BRCA1 gene in Polish families with breast-ovarian can-cer. Am J Hum Genet. 2000;66:1963-1968. 103. Sarantaus L, Huusko P, Eerola H, et al. Multiple founder effects and geographical clustering of BRCA1 and BRCA2 families in Finland. Eur J Hum Genet. 2000;8:757-763. 104. Gayther SA, Harrington P, Russell P, et al. Frequently occurring germ-line mutations of the BRCA1 gene in ovarian cancer families from Russia. Am J Hum Genet. 1997;60:1239-1242. 105. Szabo CI, King MC. Population genetics of BRCA1 and BRCA2. Am J Hum Genet. 1997;60:1013-1020. 106. Abeliovich D, Kaduri L, Lerer I, et al. The founder muta-tions 185delAG and 5382insC in BRCA1 and 6174delT in BRCA2 appear in 60% of ovarian cancer and 30% of early-onset breast cancer patients among Ashkenazi women. Am J Hum Genet.
Surgery_Schwartz. A, Peelen T, van Vliet M, et al. BRCA1 genomic deletions are major founder mutations in Dutch breast cancer patients. Nat Genet. 1997;17:341-345. 102. Gorski B, Byrski T, Huzarski T, et al. Founder mutations in the BRCA1 gene in Polish families with breast-ovarian can-cer. Am J Hum Genet. 2000;66:1963-1968. 103. Sarantaus L, Huusko P, Eerola H, et al. Multiple founder effects and geographical clustering of BRCA1 and BRCA2 families in Finland. Eur J Hum Genet. 2000;8:757-763. 104. Gayther SA, Harrington P, Russell P, et al. Frequently occurring germ-line mutations of the BRCA1 gene in ovarian cancer families from Russia. Am J Hum Genet. 1997;60:1239-1242. 105. Szabo CI, King MC. Population genetics of BRCA1 and BRCA2. Am J Hum Genet. 1997;60:1013-1020. 106. Abeliovich D, Kaduri L, Lerer I, et al. The founder muta-tions 185delAG and 5382insC in BRCA1 and 6174delT in BRCA2 appear in 60% of ovarian cancer and 30% of early-onset breast cancer patients among Ashkenazi women. Am J Hum Genet.
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et al. The founder muta-tions 185delAG and 5382insC in BRCA1 and 6174delT in BRCA2 appear in 60% of ovarian cancer and 30% of early-onset breast cancer patients among Ashkenazi women. Am J Hum Genet. 1997;60:505-514. 107. Johannesdottir G, Gudmundsson J, Bergthorsson JT, et al. High prevalence of the 999del5 mutation in Icelandic breast and ovarian cancer patients. Cancer Res. 1996;56:3663-3665. 108. Hakansson S, Johannsson O, Johansson U, et al. Moder-ate frequency of BRCA1 and BRCA2 germ-line mutations in Scandinavian familial breast cancer. Am J Hum Genet. 1997;60:1068-1078. 109. Infante M, Duran M, Acedo A, et al. The highly prevalent BRCA2 mutation c.2808_2811del (3036delACAA) is located in a mutational hotspot and has multiple origins. Carcinogenesis. 2013;34:2505-2511. 110. Warner E, Foulkes W, Goodwin P, et al. Prevalence and pen-etrance of BRCA1 and BRCA2 gene mutations in unselected Ashkenazi Jewish women with breast cancer. J Natl Cancer Inst.
Surgery_Schwartz. et al. The founder muta-tions 185delAG and 5382insC in BRCA1 and 6174delT in BRCA2 appear in 60% of ovarian cancer and 30% of early-onset breast cancer patients among Ashkenazi women. Am J Hum Genet. 1997;60:505-514. 107. Johannesdottir G, Gudmundsson J, Bergthorsson JT, et al. High prevalence of the 999del5 mutation in Icelandic breast and ovarian cancer patients. Cancer Res. 1996;56:3663-3665. 108. Hakansson S, Johannsson O, Johansson U, et al. Moder-ate frequency of BRCA1 and BRCA2 germ-line mutations in Scandinavian familial breast cancer. Am J Hum Genet. 1997;60:1068-1078. 109. Infante M, Duran M, Acedo A, et al. The highly prevalent BRCA2 mutation c.2808_2811del (3036delACAA) is located in a mutational hotspot and has multiple origins. Carcinogenesis. 2013;34:2505-2511. 110. Warner E, Foulkes W, Goodwin P, et al. Prevalence and pen-etrance of BRCA1 and BRCA2 gene mutations in unselected Ashkenazi Jewish women with breast cancer. J Natl Cancer Inst.
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E, Foulkes W, Goodwin P, et al. Prevalence and pen-etrance of BRCA1 and BRCA2 gene mutations in unselected Ashkenazi Jewish women with breast cancer. J Natl Cancer Inst. 1999;91:1241-1247. 111. Khatcheressian JL, Hurley P, Bantug E, et al. Breast can-cer follow-up and management after primary treatment: American Society of Clinical Oncology clinical practice guideline update. J Clin Oncol. 2013;31:961-965. 112. Schneider KA. Genetic counseling for BRCA1/BRCA2 test-ing. Genet Test. 1997;1:91-98. 113. Kriege M, Brekelmans CT, Boetes C, et al. Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. N Engl J Med. 2004;351:427-437. 114. Saslow D, Boetes C, Burke W, et al. American Cancer Soci-ety guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007; 57:75-89. 115. King MC, Wieand S, Hale K, et al. Tamoxifen and breast cancer incidence among women with inherited mutations in BRCA1 and BRCA2:
Surgery_Schwartz. E, Foulkes W, Goodwin P, et al. Prevalence and pen-etrance of BRCA1 and BRCA2 gene mutations in unselected Ashkenazi Jewish women with breast cancer. J Natl Cancer Inst. 1999;91:1241-1247. 111. Khatcheressian JL, Hurley P, Bantug E, et al. Breast can-cer follow-up and management after primary treatment: American Society of Clinical Oncology clinical practice guideline update. J Clin Oncol. 2013;31:961-965. 112. Schneider KA. Genetic counseling for BRCA1/BRCA2 test-ing. Genet Test. 1997;1:91-98. 113. Kriege M, Brekelmans CT, Boetes C, et al. Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. N Engl J Med. 2004;351:427-437. 114. Saslow D, Boetes C, Burke W, et al. American Cancer Soci-ety guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin. 2007; 57:75-89. 115. King MC, Wieand S, Hale K, et al. Tamoxifen and breast cancer incidence among women with inherited mutations in BRCA1 and BRCA2:
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WB Saunders; 1998:1416. 371. Khan SA, Badve S. Phyllodes tumors of the breast. Curr Treat Options Oncol. 2001;2:139-147. 372. Chittoor SR, Swain SM. Locally advanced breast cancer: Role of medical oncology. In: Bland KI, Copeland EMI, eds. The Breast: Comprehensive Management of Benign and Malignant Diseases. Philadelphia: WB Saunders; 1998:1403. 373. Mies C. Mammary sarcoma and lymphoma. In: Bland KI, Copeland EMI, eds. The Breast: Comprehensive Management of Benign and Malignant Diseases. Philadelphia: WB Saunders; 1998:307. 374. Stewart FW, Treves N. Lymphangiosarcoma in postmas-tectomy lymphedema; a report of six cases in elephantiasis chirurgica. Cancer. 1948;1:64-81.Brunicardi_Ch17_p0541-p0612.indd 61201/03/19 5:06 PM
Surgery_Schwartz. WB Saunders; 1998:1416. 371. Khan SA, Badve S. Phyllodes tumors of the breast. Curr Treat Options Oncol. 2001;2:139-147. 372. Chittoor SR, Swain SM. Locally advanced breast cancer: Role of medical oncology. In: Bland KI, Copeland EMI, eds. The Breast: Comprehensive Management of Benign and Malignant Diseases. Philadelphia: WB Saunders; 1998:1403. 373. Mies C. Mammary sarcoma and lymphoma. In: Bland KI, Copeland EMI, eds. The Breast: Comprehensive Management of Benign and Malignant Diseases. Philadelphia: WB Saunders; 1998:307. 374. Stewart FW, Treves N. Lymphangiosarcoma in postmas-tectomy lymphedema; a report of six cases in elephantiasis chirurgica. Cancer. 1948;1:64-81.Brunicardi_Ch17_p0541-p0612.indd 61201/03/19 5:06 PM
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Disorders of the Head and NeckAntoine Eskander, Stephen Y. Kang, Michael S. Harris, Bradley A. Otto, Oliver Adunka, Randal S. Weber, and Theodoros N. Teknos 18chapterCOMPLEX ANATOMY AND FUNCTIONThe anatomy of the head and neck is complex because of the proximity of vital structures such as framework, nerves, and arteries. Functionally, these structures afford most of the human senses: vision, taste, smell, and hearing. Even more fundamental, the upper aerodigestive tract is critical for breathing, speech, and swallowing. Otolaryngology—head and neck surgery is the field that predominantly deals with disorders of the head and neck; however, a multidisciplinary approach is required to achieve optimal outcomes. The multidisciplinary team can include audi-ology, speech language pathology, allergy/immunology, neurol-ogy, neurosurgery, radiation, and medical oncology. This chapter aims to provide an overview of the most common diseases pre-senting to and treated by the otolaryngologist—head
Surgery_Schwartz. Disorders of the Head and NeckAntoine Eskander, Stephen Y. Kang, Michael S. Harris, Bradley A. Otto, Oliver Adunka, Randal S. Weber, and Theodoros N. Teknos 18chapterCOMPLEX ANATOMY AND FUNCTIONThe anatomy of the head and neck is complex because of the proximity of vital structures such as framework, nerves, and arteries. Functionally, these structures afford most of the human senses: vision, taste, smell, and hearing. Even more fundamental, the upper aerodigestive tract is critical for breathing, speech, and swallowing. Otolaryngology—head and neck surgery is the field that predominantly deals with disorders of the head and neck; however, a multidisciplinary approach is required to achieve optimal outcomes. The multidisciplinary team can include audi-ology, speech language pathology, allergy/immunology, neurol-ogy, neurosurgery, radiation, and medical oncology. This chapter aims to provide an overview of the most common diseases pre-senting to and treated by the otolaryngologist—head
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neurol-ogy, neurosurgery, radiation, and medical oncology. This chapter aims to provide an overview of the most common diseases pre-senting to and treated by the otolaryngologist—head and neck surgeon. It reviews benign conditions, trauma, malignancies, reconstruction, tracheotomy, and rehabilitation.BENIGN CONDITIONS OF THE HEAD AND NECKOtologyInfectious. Infectious processes of the ear may be consid-ered by their location (external, middle, or inner ear), their time course (acute or chronic), and the presence of complications. The external ear or pinna consists of a cartilaginous frame-work, perichondrium, and a relatively thin layer of skin. Ery-sipelas (St Anthony’s Fire) or impetigo are causes of external ear infection affecting the dermis or hypodermis of the auricle, typically caused by Streptococcus pyogenes or Staphylococcus aureus, respectively, that may be encountered posttraumatically or related to ear piercing. Treatment is oral antibiotic therapy targeting these
Surgery_Schwartz. neurol-ogy, neurosurgery, radiation, and medical oncology. This chapter aims to provide an overview of the most common diseases pre-senting to and treated by the otolaryngologist—head and neck surgeon. It reviews benign conditions, trauma, malignancies, reconstruction, tracheotomy, and rehabilitation.BENIGN CONDITIONS OF THE HEAD AND NECKOtologyInfectious. Infectious processes of the ear may be consid-ered by their location (external, middle, or inner ear), their time course (acute or chronic), and the presence of complications. The external ear or pinna consists of a cartilaginous frame-work, perichondrium, and a relatively thin layer of skin. Ery-sipelas (St Anthony’s Fire) or impetigo are causes of external ear infection affecting the dermis or hypodermis of the auricle, typically caused by Streptococcus pyogenes or Staphylococcus aureus, respectively, that may be encountered posttraumatically or related to ear piercing. Treatment is oral antibiotic therapy targeting these
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caused by Streptococcus pyogenes or Staphylococcus aureus, respectively, that may be encountered posttraumatically or related to ear piercing. Treatment is oral antibiotic therapy targeting these organisms. History and clinical features such as presence of bullae and golden crusting distinguish erysipelas and impetigo from other benign entities causing erythema and edema of the auricle, such as relapsing polychondritis, which is typically diffuse, lobule-sparing, and steroid-responsive.Acute otitis externa, often referred to as “swimmer’s ear,” denotes infection of the skin of the external auditory canal.1 Typically, the pathology is incited by moisture within the canal leading to skin maceration and pruritus. Subsequent trauma to the canal skin by scratching (i.e., instrumentation with a cot-ton swab or fingernail), erodes the normally protective skin/cerumen barrier. Hearing aid use and comorbid dermatologic conditions such as eczema or other forms of dermatitis may similarly serve
Surgery_Schwartz. caused by Streptococcus pyogenes or Staphylococcus aureus, respectively, that may be encountered posttraumatically or related to ear piercing. Treatment is oral antibiotic therapy targeting these organisms. History and clinical features such as presence of bullae and golden crusting distinguish erysipelas and impetigo from other benign entities causing erythema and edema of the auricle, such as relapsing polychondritis, which is typically diffuse, lobule-sparing, and steroid-responsive.Acute otitis externa, often referred to as “swimmer’s ear,” denotes infection of the skin of the external auditory canal.1 Typically, the pathology is incited by moisture within the canal leading to skin maceration and pruritus. Subsequent trauma to the canal skin by scratching (i.e., instrumentation with a cot-ton swab or fingernail), erodes the normally protective skin/cerumen barrier. Hearing aid use and comorbid dermatologic conditions such as eczema or other forms of dermatitis may similarly serve
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cot-ton swab or fingernail), erodes the normally protective skin/cerumen barrier. Hearing aid use and comorbid dermatologic conditions such as eczema or other forms of dermatitis may similarly serve as predisposing factors. The milieu of the exter-nal ear canal—dark, warm, humid—is ideal for rapid microbial proliferation. The most common offending organism is Pseu-domonas aeruginosa, although other bacteria and fungi may also be involved. Symptoms and signs of otitis externa include itching during the initial phases and pain with marked swelling of the canal soft tissues as the infection progresses. Treatment involves removal of debris under otomicroscopy and applica-tion of appropriate ototopical antimicrobials, such as neomycin/polymyxin or quinolone-containing eardrops. The topical ste-roid component of these drops (e.g., hydrocortisone or dexa-methasone) addresses swelling and, as a result, decreases the often intense pain associated with this infection. In cases of marked ear
Surgery_Schwartz. cot-ton swab or fingernail), erodes the normally protective skin/cerumen barrier. Hearing aid use and comorbid dermatologic conditions such as eczema or other forms of dermatitis may similarly serve as predisposing factors. The milieu of the exter-nal ear canal—dark, warm, humid—is ideal for rapid microbial proliferation. The most common offending organism is Pseu-domonas aeruginosa, although other bacteria and fungi may also be involved. Symptoms and signs of otitis externa include itching during the initial phases and pain with marked swelling of the canal soft tissues as the infection progresses. Treatment involves removal of debris under otomicroscopy and applica-tion of appropriate ototopical antimicrobials, such as neomycin/polymyxin or quinolone-containing eardrops. The topical ste-roid component of these drops (e.g., hydrocortisone or dexa-methasone) addresses swelling and, as a result, decreases the often intense pain associated with this infection. In cases of marked ear
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ste-roid component of these drops (e.g., hydrocortisone or dexa-methasone) addresses swelling and, as a result, decreases the often intense pain associated with this infection. In cases of marked ear canal edema, the use of an otowick is required to facilitate delivery of ototopical medication medially into the ear canal. Fungal infections may call for the addition of 2% acetic acid to reestablish the premorbid pH balance. Patients with otitis externa should also be instructed to keep the ear dry. Systemic antibiotics are reserved for those with severe infections, diabet-ics, and immunosuppression.Complex Anatomy and Function 613Benign Conditions of the Head and Neck 613Otology / 613Sinonasal Inflammatory Disease / 617Pharyngeal and Adenotonsillar Disease / 622Benign Conditions of the Larynx / 624Vascular Lesions / 626Trauma of the Head and Neck 627Soft Tissue / 627Facial Fractures / 628Temporal Bone Fractures / 629Tumors of the Head and Neck 629Etiology and Epidemiology /
Surgery_Schwartz. ste-roid component of these drops (e.g., hydrocortisone or dexa-methasone) addresses swelling and, as a result, decreases the often intense pain associated with this infection. In cases of marked ear canal edema, the use of an otowick is required to facilitate delivery of ototopical medication medially into the ear canal. Fungal infections may call for the addition of 2% acetic acid to reestablish the premorbid pH balance. Patients with otitis externa should also be instructed to keep the ear dry. Systemic antibiotics are reserved for those with severe infections, diabet-ics, and immunosuppression.Complex Anatomy and Function 613Benign Conditions of the Head and Neck 613Otology / 613Sinonasal Inflammatory Disease / 617Pharyngeal and Adenotonsillar Disease / 622Benign Conditions of the Larynx / 624Vascular Lesions / 626Trauma of the Head and Neck 627Soft Tissue / 627Facial Fractures / 628Temporal Bone Fractures / 629Tumors of the Head and Neck 629Etiology and Epidemiology /
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of the Larynx / 624Vascular Lesions / 626Trauma of the Head and Neck 627Soft Tissue / 627Facial Fractures / 628Temporal Bone Fractures / 629Tumors of the Head and Neck 629Etiology and Epidemiology / 630Anatomy and Histopathology / 630Second Primary Tumors in the Head and Neck / 631Staging / 632Upper Aerodigestive Tract / 632Nose and Paranasal Sinuses / 643Nasopharynx / 644Ear and Temporal Bone / 645Neck / 646Salivary Gland Tumors / 650Reconstruction 651Local Flaps and Skin Grafts / 651Regional Flaps / 651Free Tissue Transfer / 651Tracheotomy 652Indications and Timing / 652Technique and Complications / 652Speech with Tracheotomy and Decannulation / 653Long Term Management and Rehabilitation 654Palliative Care / 654Follow-Up Care / 654Brunicardi_Ch18_p0613-p0660.indd 61301/03/19 5:22 PM 614Figure 18-1. Acute otitis media.Malignant otitis externa, a fulminant necrotizing infec-tion of the soft tissues of the external ear canal combined with osteomyelitis of the temporal bone, is
Surgery_Schwartz. of the Larynx / 624Vascular Lesions / 626Trauma of the Head and Neck 627Soft Tissue / 627Facial Fractures / 628Temporal Bone Fractures / 629Tumors of the Head and Neck 629Etiology and Epidemiology / 630Anatomy and Histopathology / 630Second Primary Tumors in the Head and Neck / 631Staging / 632Upper Aerodigestive Tract / 632Nose and Paranasal Sinuses / 643Nasopharynx / 644Ear and Temporal Bone / 645Neck / 646Salivary Gland Tumors / 650Reconstruction 651Local Flaps and Skin Grafts / 651Regional Flaps / 651Free Tissue Transfer / 651Tracheotomy 652Indications and Timing / 652Technique and Complications / 652Speech with Tracheotomy and Decannulation / 653Long Term Management and Rehabilitation 654Palliative Care / 654Follow-Up Care / 654Brunicardi_Ch18_p0613-p0660.indd 61301/03/19 5:22 PM 614Figure 18-1. Acute otitis media.Malignant otitis externa, a fulminant necrotizing infec-tion of the soft tissues of the external ear canal combined with osteomyelitis of the temporal bone, is
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PM 614Figure 18-1. Acute otitis media.Malignant otitis externa, a fulminant necrotizing infec-tion of the soft tissues of the external ear canal combined with osteomyelitis of the temporal bone, is a potentially life-threatening form of otitis externa seen most commonly among elderly patients with insulin-dependent diabetes mellitus or immunodeficiency.2,3 The classic physical finding is granulation tissue along the floor of the external auditory canal near the bony cartilaginous junction. Symptoms include persistent otalgia for longer than one month and purulent otorrhea. Biopsy is called for in order to exclude malignancy. Computed tomography (CT) and magnetic resonance imaging (MRI) define the extension of disease. Technetium 99-m scans are useful in gauging extend of bony involvement in early disease. Gallium-67 scans are valu-able for monitoring disease during the course of treatment and for determining duration of antibiotic therapy. These patients require aggressive medical
Surgery_Schwartz. PM 614Figure 18-1. Acute otitis media.Malignant otitis externa, a fulminant necrotizing infec-tion of the soft tissues of the external ear canal combined with osteomyelitis of the temporal bone, is a potentially life-threatening form of otitis externa seen most commonly among elderly patients with insulin-dependent diabetes mellitus or immunodeficiency.2,3 The classic physical finding is granulation tissue along the floor of the external auditory canal near the bony cartilaginous junction. Symptoms include persistent otalgia for longer than one month and purulent otorrhea. Biopsy is called for in order to exclude malignancy. Computed tomography (CT) and magnetic resonance imaging (MRI) define the extension of disease. Technetium 99-m scans are useful in gauging extend of bony involvement in early disease. Gallium-67 scans are valu-able for monitoring disease during the course of treatment and for determining duration of antibiotic therapy. These patients require aggressive medical
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in early disease. Gallium-67 scans are valu-able for monitoring disease during the course of treatment and for determining duration of antibiotic therapy. These patients require aggressive medical therapy including ototopical and IV antibiotics targeting Pseudomonas. Other gram-negative bacteria and fungi are occasionally implicated, necessitating culturedirected therapy. Patients who do not respond to medical management require surgical debridement. This condition may progress to involvement of the adjacent skull base and soft tissues, meningitis, brain abscess, and death.Acute otitis media (AOM) typically implies a bacterial infec-tion of the middle ear.4 This diagnosis accounts for 25% of pedi-atric antibiotic prescriptions and is the most common bacterial infection of childhood. Most cases occur before 2 years of age and are secondary to immaturity of the Eustachian tube. Well-recog-nized contributing factors include upper respiratory viral infection and daycare attendance, as
Surgery_Schwartz. in early disease. Gallium-67 scans are valu-able for monitoring disease during the course of treatment and for determining duration of antibiotic therapy. These patients require aggressive medical therapy including ototopical and IV antibiotics targeting Pseudomonas. Other gram-negative bacteria and fungi are occasionally implicated, necessitating culturedirected therapy. Patients who do not respond to medical management require surgical debridement. This condition may progress to involvement of the adjacent skull base and soft tissues, meningitis, brain abscess, and death.Acute otitis media (AOM) typically implies a bacterial infec-tion of the middle ear.4 This diagnosis accounts for 25% of pedi-atric antibiotic prescriptions and is the most common bacterial infection of childhood. Most cases occur before 2 years of age and are secondary to immaturity of the Eustachian tube. Well-recog-nized contributing factors include upper respiratory viral infection and daycare attendance, as
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cases occur before 2 years of age and are secondary to immaturity of the Eustachian tube. Well-recog-nized contributing factors include upper respiratory viral infection and daycare attendance, as well as craniofacial conditions affect-ing Eustachian tube function, such as cleft palate.It is important to distinguish between acute otitis media and otitis media with effusion (OME). The later denotes unin-fected serous fluid accumulation within the middle ear space. In children not already considered “at risk” for developmen-tal difficulties, OME is generally observed for resolution for a period of 3 months.5 Age-appropriate hearing testing should be performed when OME persists for ≥3 months or at any time when language delay, learning problems, or a significant hear-ing loss is suspected. In the absence of these factors, the child with OME should be reexamined at 3to 6-month intervals until the effusion is no longer present or until significant hear-ing loss is identified or structural
Surgery_Schwartz. cases occur before 2 years of age and are secondary to immaturity of the Eustachian tube. Well-recog-nized contributing factors include upper respiratory viral infection and daycare attendance, as well as craniofacial conditions affect-ing Eustachian tube function, such as cleft palate.It is important to distinguish between acute otitis media and otitis media with effusion (OME). The later denotes unin-fected serous fluid accumulation within the middle ear space. In children not already considered “at risk” for developmen-tal difficulties, OME is generally observed for resolution for a period of 3 months.5 Age-appropriate hearing testing should be performed when OME persists for ≥3 months or at any time when language delay, learning problems, or a significant hear-ing loss is suspected. In the absence of these factors, the child with OME should be reexamined at 3to 6-month intervals until the effusion is no longer present or until significant hear-ing loss is identified or structural
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the absence of these factors, the child with OME should be reexamined at 3to 6-month intervals until the effusion is no longer present or until significant hear-ing loss is identified or structural abnormalities of the eardrum or middle ear are suspected. When hearing, speech, or structural concerns exist, myringotomy with tympanostomy tube place-ment is indicated.Signs and symptoms of infectious otitis media occurring for <3 weeks denote AOM. In this phase, otalgia and fever are the most common symptoms and physical exam reveals a bulging, opaque tympanic membrane (Fig. 18-1). If the process lasts 3 to 8 weeks, it is deemed subacute. Chronic otitis media, lasting more than 8 weeks, usually results from an unresolved acute otitis media. The most common organisms responsible are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.In order to minimize antibiotic resistance and obviate complications of antimicrobial therapy such as allergic reaction and diarrhea,
Surgery_Schwartz. the absence of these factors, the child with OME should be reexamined at 3to 6-month intervals until the effusion is no longer present or until significant hear-ing loss is identified or structural abnormalities of the eardrum or middle ear are suspected. When hearing, speech, or structural concerns exist, myringotomy with tympanostomy tube place-ment is indicated.Signs and symptoms of infectious otitis media occurring for <3 weeks denote AOM. In this phase, otalgia and fever are the most common symptoms and physical exam reveals a bulging, opaque tympanic membrane (Fig. 18-1). If the process lasts 3 to 8 weeks, it is deemed subacute. Chronic otitis media, lasting more than 8 weeks, usually results from an unresolved acute otitis media. The most common organisms responsible are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.In order to minimize antibiotic resistance and obviate complications of antimicrobial therapy such as allergic reaction and diarrhea,
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pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.In order to minimize antibiotic resistance and obviate complications of antimicrobial therapy such as allergic reaction and diarrhea, guidelines have been established for the treatment of AOM.6,7 Pain associated with AOM should be recognized and treated with oral analgesics. In children older than 6 months who are not otherwise considered “high risk” for complications (e.g., immunocompromised, previous cochlear implantation, developmental anomalies of the inner ear) with symptoms con-sistent with unilateral AOM without otorrhea, an initial period of observation is offered. If initial observation is selected by the physician and family, a mechanism for reexamination in 48 to 72 hours to evaluate for clinical improvement must be in place. When these criteria are not met, or clinical improvement is not observed within 48 to 72 hours, oral antibiotics are begun. First-line therapy is high-dose amoxicillin or
Surgery_Schwartz. pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.In order to minimize antibiotic resistance and obviate complications of antimicrobial therapy such as allergic reaction and diarrhea, guidelines have been established for the treatment of AOM.6,7 Pain associated with AOM should be recognized and treated with oral analgesics. In children older than 6 months who are not otherwise considered “high risk” for complications (e.g., immunocompromised, previous cochlear implantation, developmental anomalies of the inner ear) with symptoms con-sistent with unilateral AOM without otorrhea, an initial period of observation is offered. If initial observation is selected by the physician and family, a mechanism for reexamination in 48 to 72 hours to evaluate for clinical improvement must be in place. When these criteria are not met, or clinical improvement is not observed within 48 to 72 hours, oral antibiotics are begun. First-line therapy is high-dose amoxicillin or
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must be in place. When these criteria are not met, or clinical improvement is not observed within 48 to 72 hours, oral antibiotics are begun. First-line therapy is high-dose amoxicillin or amoxicillin-clavulanate, for β-lactamase coverage. Chronic otitis media is frequently Key Points1 One of the most common benign head and neck disorders includes sinonasal inflammatory disease which can present as acute or chronic rhinosinusitis.2 Acute adeno-tonsillitis is a major cause of morbidity in children and adenotonsillectomy can significantly improve symptoms of both sleep disordered breathing and of symp-toms during acute infections.3 Squamous cell carcinoma comprises >90% of all of the malignant pathology of the mucosal lining of the upper aerodigestive tract.4 The ideal treatment protocol for these cancers varies by subsite, stage, patient comorbidity, and center preference/experience. Early stage disease is treated with unimodality and late stage disease is treated with multiple
Surgery_Schwartz. must be in place. When these criteria are not met, or clinical improvement is not observed within 48 to 72 hours, oral antibiotics are begun. First-line therapy is high-dose amoxicillin or amoxicillin-clavulanate, for β-lactamase coverage. Chronic otitis media is frequently Key Points1 One of the most common benign head and neck disorders includes sinonasal inflammatory disease which can present as acute or chronic rhinosinusitis.2 Acute adeno-tonsillitis is a major cause of morbidity in children and adenotonsillectomy can significantly improve symptoms of both sleep disordered breathing and of symp-toms during acute infections.3 Squamous cell carcinoma comprises >90% of all of the malignant pathology of the mucosal lining of the upper aerodigestive tract.4 The ideal treatment protocol for these cancers varies by subsite, stage, patient comorbidity, and center preference/experience. Early stage disease is treated with unimodality and late stage disease is treated with multiple
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for these cancers varies by subsite, stage, patient comorbidity, and center preference/experience. Early stage disease is treated with unimodality and late stage disease is treated with multiple modalities in the form of primary surgery with adjuvant radiotherapy or primary concurrent chemoradiotherapy.5 Free flap reconstruction of head and neck defects is integral to help improve patient-reported quality of life and to re-establish form and function.Brunicardi_Ch18_p0613-p0660.indd 61401/03/19 5:22 PM 615DISORDERS OF THE HEAD AND NECKCHAPTER 18treated with myringotomy and tube placement (Fig. 18-2). This treatment is indicated for frequent acute episodes and in the set-ting of COME as discussed previously. The purpose of this pro-cedure is to remove the effusion and provide a route for middle ear ventilation. Episodes of AOM following tube placement are still possible. Myringotomy tubes, however, allow for preven-tion of painful tympanic membrane distension, risk of perfora-tion
Surgery_Schwartz. for these cancers varies by subsite, stage, patient comorbidity, and center preference/experience. Early stage disease is treated with unimodality and late stage disease is treated with multiple modalities in the form of primary surgery with adjuvant radiotherapy or primary concurrent chemoradiotherapy.5 Free flap reconstruction of head and neck defects is integral to help improve patient-reported quality of life and to re-establish form and function.Brunicardi_Ch18_p0613-p0660.indd 61401/03/19 5:22 PM 615DISORDERS OF THE HEAD AND NECKCHAPTER 18treated with myringotomy and tube placement (Fig. 18-2). This treatment is indicated for frequent acute episodes and in the set-ting of COME as discussed previously. The purpose of this pro-cedure is to remove the effusion and provide a route for middle ear ventilation. Episodes of AOM following tube placement are still possible. Myringotomy tubes, however, allow for preven-tion of painful tympanic membrane distension, risk of perfora-tion
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middle ear ventilation. Episodes of AOM following tube placement are still possible. Myringotomy tubes, however, allow for preven-tion of painful tympanic membrane distension, risk of perfora-tion and other complications, and permit delivery of ototopicals into the middle ear space, in most cases obviating the need for systemic antibiotic therapy.Spontaneous tympanic membrane perforation during acute otitis media provides for drainage of purulent fluid and middle ear ventilation and frequently results in immediate resolution of severe pain. In the majority of cases, these perforations will heal spontaneously after the infection has resolved.8 Chronic otitis media, however, may be associated with nonhealing tympanic membrane perforations. Patients may have persistent otorrhea, which is treated with topical drops. Preparations containing ami-noglycoside are avoided because this class of drugs is toxic to the inner ear. Solutions containing alcohol or acetic acid may be irritating or
Surgery_Schwartz. middle ear ventilation. Episodes of AOM following tube placement are still possible. Myringotomy tubes, however, allow for preven-tion of painful tympanic membrane distension, risk of perfora-tion and other complications, and permit delivery of ototopicals into the middle ear space, in most cases obviating the need for systemic antibiotic therapy.Spontaneous tympanic membrane perforation during acute otitis media provides for drainage of purulent fluid and middle ear ventilation and frequently results in immediate resolution of severe pain. In the majority of cases, these perforations will heal spontaneously after the infection has resolved.8 Chronic otitis media, however, may be associated with nonhealing tympanic membrane perforations. Patients may have persistent otorrhea, which is treated with topical drops. Preparations containing ami-noglycoside are avoided because this class of drugs is toxic to the inner ear. Solutions containing alcohol or acetic acid may be irritating or
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treated with topical drops. Preparations containing ami-noglycoside are avoided because this class of drugs is toxic to the inner ear. Solutions containing alcohol or acetic acid may be irritating or caustic to the middle ear and are also avoided in the setting of a perforation. Nonhealing perforation requires surgical closure (tympanoplasty) after medical treatment of any residual acute infection.Chronic inflammatory changes from otitis media intersect with and share common etiological factors with cholesteatoma. Cholesteatoma is an epidermoid cyst of the middle ear and/or mastoid cavity that develops as result of Eustachian tube dysfunction. While several theories exist regarding causes of cholesteatoma, most cholesteatoma arises from squamous epi-thelium drawn into the middle ear via retraction pockets, most commonly in the pars flaccida.9 Squamous epithelium may also migrate into the middle ear via a perforation. Chronic mastoid-itis that fails medical management or is associated
Surgery_Schwartz. treated with topical drops. Preparations containing ami-noglycoside are avoided because this class of drugs is toxic to the inner ear. Solutions containing alcohol or acetic acid may be irritating or caustic to the middle ear and are also avoided in the setting of a perforation. Nonhealing perforation requires surgical closure (tympanoplasty) after medical treatment of any residual acute infection.Chronic inflammatory changes from otitis media intersect with and share common etiological factors with cholesteatoma. Cholesteatoma is an epidermoid cyst of the middle ear and/or mastoid cavity that develops as result of Eustachian tube dysfunction. While several theories exist regarding causes of cholesteatoma, most cholesteatoma arises from squamous epi-thelium drawn into the middle ear via retraction pockets, most commonly in the pars flaccida.9 Squamous epithelium may also migrate into the middle ear via a perforation. Chronic mastoid-itis that fails medical management or is associated
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pockets, most commonly in the pars flaccida.9 Squamous epithelium may also migrate into the middle ear via a perforation. Chronic mastoid-itis that fails medical management or is associated with cho-lesteatoma is treated by mastoidectomy. Chronic inflammation and destruction of middle ear structures by osteolytic enzymes of cholesteatoma matrix may also be associated with erosion of the ossicular chain, which can be reconstructed with various prostheses or autologous ossicular replacement techniques.Complications of otitis media with or without cholestea-toma may be grouped into two categories: intratemporal (oto-logic) and intracranial.10 Fortunately, complications are rare in the antibiotic era, but mounting antibiotic resistance necessitates an increased awareness of these conditions. Intratemporal com-plications include acute coalescent mastoiditis, petrositis, facial nerve paralysis, and labyrinthitis. In acute coalescing mastoid-itis, destruction of the bony lamellae by an acute
Surgery_Schwartz. pockets, most commonly in the pars flaccida.9 Squamous epithelium may also migrate into the middle ear via a perforation. Chronic mastoid-itis that fails medical management or is associated with cho-lesteatoma is treated by mastoidectomy. Chronic inflammation and destruction of middle ear structures by osteolytic enzymes of cholesteatoma matrix may also be associated with erosion of the ossicular chain, which can be reconstructed with various prostheses or autologous ossicular replacement techniques.Complications of otitis media with or without cholestea-toma may be grouped into two categories: intratemporal (oto-logic) and intracranial.10 Fortunately, complications are rare in the antibiotic era, but mounting antibiotic resistance necessitates an increased awareness of these conditions. Intratemporal com-plications include acute coalescent mastoiditis, petrositis, facial nerve paralysis, and labyrinthitis. In acute coalescing mastoid-itis, destruction of the bony lamellae by an acute
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com-plications include acute coalescent mastoiditis, petrositis, facial nerve paralysis, and labyrinthitis. In acute coalescing mastoid-itis, destruction of the bony lamellae by an acute purulent pro-cess results in severe pain, fever, and fluctuance behind the ear. The mastoid air cells coalesce into one common space filled with pus. Mastoid infection may also spread to the petrous apex, causing retro-orbital pain and sixth-nerve palsy. These diagno-ses are confirmed by computed tomographic scan. Facial nerve paralysis may also occur secondary to an acute inflammatory process in the middle ear or mastoid.11Intratemporal complications of otitis media are managed by myringotomy tube placement in addition to appropriate IV antibiotics. In acute coalescent mastoiditis and petrositis, mas-toidectomy is also performed as necessary to drain purulent foci. Labyrinthitis refers to inflammation of the inner ear. Most cases are idiopathic or are secondary to viral infections of the
Surgery_Schwartz. com-plications include acute coalescent mastoiditis, petrositis, facial nerve paralysis, and labyrinthitis. In acute coalescing mastoid-itis, destruction of the bony lamellae by an acute purulent pro-cess results in severe pain, fever, and fluctuance behind the ear. The mastoid air cells coalesce into one common space filled with pus. Mastoid infection may also spread to the petrous apex, causing retro-orbital pain and sixth-nerve palsy. These diagno-ses are confirmed by computed tomographic scan. Facial nerve paralysis may also occur secondary to an acute inflammatory process in the middle ear or mastoid.11Intratemporal complications of otitis media are managed by myringotomy tube placement in addition to appropriate IV antibiotics. In acute coalescent mastoiditis and petrositis, mas-toidectomy is also performed as necessary to drain purulent foci. Labyrinthitis refers to inflammation of the inner ear. Most cases are idiopathic or are secondary to viral infections of the
Surgery_Schwartz_4199
Surgery_Schwartz
mas-toidectomy is also performed as necessary to drain purulent foci. Labyrinthitis refers to inflammation of the inner ear. Most cases are idiopathic or are secondary to viral infections of the endolymphatic space. The patient experiences vertigo together with sensorineural hearing loss, and symptoms may smolder over several weeks. Labyrinthitis associated with middle ear infection may be serous or suppurative. In the former case, bac-terial products and/or inflammatory mediators transudate into the inner ear via the round window membrane, establishing an inflammatory process therein. Total recovery is eventually pos-sible after the middle ear is adequately treated.Suppurative labyrinthitis, however, is a much more toxic condition in which the acute purulent bacterial infection extends into the inner ear and causes marked destruction of the sensory hair cells and neurons of the eighth-nerve ganglion. This con-dition may be a harbinger for meningitis and must be treated rapidly. The
Surgery_Schwartz. mas-toidectomy is also performed as necessary to drain purulent foci. Labyrinthitis refers to inflammation of the inner ear. Most cases are idiopathic or are secondary to viral infections of the endolymphatic space. The patient experiences vertigo together with sensorineural hearing loss, and symptoms may smolder over several weeks. Labyrinthitis associated with middle ear infection may be serous or suppurative. In the former case, bac-terial products and/or inflammatory mediators transudate into the inner ear via the round window membrane, establishing an inflammatory process therein. Total recovery is eventually pos-sible after the middle ear is adequately treated.Suppurative labyrinthitis, however, is a much more toxic condition in which the acute purulent bacterial infection extends into the inner ear and causes marked destruction of the sensory hair cells and neurons of the eighth-nerve ganglion. This con-dition may be a harbinger for meningitis and must be treated rapidly. The
Surgery_Schwartz_4200
Surgery_Schwartz
into the inner ear and causes marked destruction of the sensory hair cells and neurons of the eighth-nerve ganglion. This con-dition may be a harbinger for meningitis and must be treated rapidly. The goal of management of inner ear infection, which occurs secondary to middle ear infection, is to “sterilize” the middle ear space with antibiotics and the placement of a myr-ingotomy tube.The most common intracranial complication of otitis media is meningitis. Otologic meningitis in children is most commonly associated with an H. influenzae type B infection. Other intra-cranial complications include epidural abscess, subdural abscess, brain abscess, otitic hydrocephalus, and sigmoid sinus thrombo-phlebitis. In these cases, the otogenic source must be urgently treated with antibiotics and myringotomy tube placement. Mas-toidectomy and neurosurgical consultation may be necessary.Facial Nerve Disorders. Bell’s palsy is the most common etiology of facial nerve weakness/paralysis and is
Surgery_Schwartz. into the inner ear and causes marked destruction of the sensory hair cells and neurons of the eighth-nerve ganglion. This con-dition may be a harbinger for meningitis and must be treated rapidly. The goal of management of inner ear infection, which occurs secondary to middle ear infection, is to “sterilize” the middle ear space with antibiotics and the placement of a myr-ingotomy tube.The most common intracranial complication of otitis media is meningitis. Otologic meningitis in children is most commonly associated with an H. influenzae type B infection. Other intra-cranial complications include epidural abscess, subdural abscess, brain abscess, otitic hydrocephalus, and sigmoid sinus thrombo-phlebitis. In these cases, the otogenic source must be urgently treated with antibiotics and myringotomy tube placement. Mas-toidectomy and neurosurgical consultation may be necessary.Facial Nerve Disorders. Bell’s palsy is the most common etiology of facial nerve weakness/paralysis and is
Surgery_Schwartz_4201
Surgery_Schwartz
myringotomy tube placement. Mas-toidectomy and neurosurgical consultation may be necessary.Facial Nerve Disorders. Bell’s palsy is the most common etiology of facial nerve weakness/paralysis and is clinically dis-tinct from that occurring as a complication of otitis media in that the otologic exam is normal.12 Bell’s palsy is rapid, unilat-eral and, historically, considered idiopathic. It is now accepted, however, that the majority of these cases represent a viral neu-ropathy caused by herpes simplex. It is critical that clinicians distinguish Bell’s palsy from other causes of facial weakness/palsy. Alternative diagnoses are suggested by weakness/paraly-sis that arise gradually (rather than <72 hours), is bilateral, is accompanied by other neurological deficits, or does not show some recovery within 2 to 3 weeks and complete recovery at 3 to 4 months. Treatment includes oral steroids plus antiviral ther-apy (i.e., valacyclovir). Complete recovery is the norm, but it does not occur
Surgery_Schwartz. myringotomy tube placement. Mas-toidectomy and neurosurgical consultation may be necessary.Facial Nerve Disorders. Bell’s palsy is the most common etiology of facial nerve weakness/paralysis and is clinically dis-tinct from that occurring as a complication of otitis media in that the otologic exam is normal.12 Bell’s palsy is rapid, unilat-eral and, historically, considered idiopathic. It is now accepted, however, that the majority of these cases represent a viral neu-ropathy caused by herpes simplex. It is critical that clinicians distinguish Bell’s palsy from other causes of facial weakness/palsy. Alternative diagnoses are suggested by weakness/paraly-sis that arise gradually (rather than <72 hours), is bilateral, is accompanied by other neurological deficits, or does not show some recovery within 2 to 3 weeks and complete recovery at 3 to 4 months. Treatment includes oral steroids plus antiviral ther-apy (i.e., valacyclovir). Complete recovery is the norm, but it does not occur