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an easy and practical approach. BJU Int. 2005;96(3):330-333. 47. Lee BC, Rodin DM, Shah KK, Dahl DM. Laparoscopic inguinal hernia repair during laparoscopic radical prostatectomy. BJU Int. 2007;99(3):637-639. 48. Bittner R, Arregui ME, Bisgaard T, et al. Guidelines for laparoscopic (TAPP) and endoscopic (TEP) treatment of inguinal hernia (International Endohernia Society [IEHS]). Surg Endosc. 2011;25(9):2773-2843. 49. Bittner R, Montgomery MA, Arregui E, et al. Update of guidelines on laparoscopic (TAPP) and endoscopic (TEP) treatment of inguinal hernia (International Endohernia Society). Surg Endosc. 2015;29(2):289-321. 50. Waite KE, Herman MA, Doyle PJ. Comparison of robotic versus laparoscopic transabdominal preperitoneal (TAPP) inguinal hernia repair. J Robot Surg. 2016;10(3):239-244. 51. Higgins RM, Frelich MJ, Bosler ME, Gould JC. Cost analysis of robotic versus laparoscopic general surgery procedures. Surg Endosc. 2017;31(1):185-192. 52. Kolachalam R, Dickens E, D’Amico L, et
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Surgery_Schwartz. an easy and practical approach. BJU Int. 2005;96(3):330-333. 47. Lee BC, Rodin DM, Shah KK, Dahl DM. Laparoscopic inguinal hernia repair during laparoscopic radical prostatectomy. BJU Int. 2007;99(3):637-639. 48. Bittner R, Arregui ME, Bisgaard T, et al. Guidelines for laparoscopic (TAPP) and endoscopic (TEP) treatment of inguinal hernia (International Endohernia Society [IEHS]). Surg Endosc. 2011;25(9):2773-2843. 49. Bittner R, Montgomery MA, Arregui E, et al. Update of guidelines on laparoscopic (TAPP) and endoscopic (TEP) treatment of inguinal hernia (International Endohernia Society). Surg Endosc. 2015;29(2):289-321. 50. Waite KE, Herman MA, Doyle PJ. Comparison of robotic versus laparoscopic transabdominal preperitoneal (TAPP) inguinal hernia repair. J Robot Surg. 2016;10(3):239-244. 51. Higgins RM, Frelich MJ, Bosler ME, Gould JC. Cost analysis of robotic versus laparoscopic general surgery procedures. Surg Endosc. 2017;31(1):185-192. 52. Kolachalam R, Dickens E, D’Amico L, et
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Surgery_Schwartz_10703
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RM, Frelich MJ, Bosler ME, Gould JC. Cost analysis of robotic versus laparoscopic general surgery procedures. Surg Endosc. 2017;31(1):185-192. 52. Kolachalam R, Dickens E, D’Amico L, et al. Early outcomes of robotic-assisted inguinal hernia repair in obese patients: a multi-institutional, retrospective study. Surg Endosc. 2018;32(1):229-235. 53. Iraniha A, Peloquin J. Long-term quality of life and outcomes following robotic assisted TAPP inguinal hernia repair. J Robot Surg. 2018;12(2):261-269. 54. Pickett LC. Prosthetic choice in open inguinal hernia repair. In: Jacob BP, Ramshaw B, eds. The SAGES Manual of Hernia Repair. New York: Springer; 2013:19-26. 55. Sajid MS, Leaver C, Baig MK, Sains P. Systematic review and meta-analysis of the use of lightweight versus heavy-weight mesh in open inguinal hernia repair. Br J Surg. 2012;99(1):29-37. 56. Sorensen CG, Rosenberg J. The use of sterilized mosquito nets for hernioplasty: a systematic review. Hernia. 2012;16(6): 621-625. 57. Luboga
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Surgery_Schwartz. RM, Frelich MJ, Bosler ME, Gould JC. Cost analysis of robotic versus laparoscopic general surgery procedures. Surg Endosc. 2017;31(1):185-192. 52. Kolachalam R, Dickens E, D’Amico L, et al. Early outcomes of robotic-assisted inguinal hernia repair in obese patients: a multi-institutional, retrospective study. Surg Endosc. 2018;32(1):229-235. 53. Iraniha A, Peloquin J. Long-term quality of life and outcomes following robotic assisted TAPP inguinal hernia repair. J Robot Surg. 2018;12(2):261-269. 54. Pickett LC. Prosthetic choice in open inguinal hernia repair. In: Jacob BP, Ramshaw B, eds. The SAGES Manual of Hernia Repair. New York: Springer; 2013:19-26. 55. Sajid MS, Leaver C, Baig MK, Sains P. Systematic review and meta-analysis of the use of lightweight versus heavy-weight mesh in open inguinal hernia repair. Br J Surg. 2012;99(1):29-37. 56. Sorensen CG, Rosenberg J. The use of sterilized mosquito nets for hernioplasty: a systematic review. Hernia. 2012;16(6): 621-625. 57. Luboga
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Surgery_Schwartz_10704
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Surgery_Schwartz
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inguinal hernia repair. Br J Surg. 2012;99(1):29-37. 56. Sorensen CG, Rosenberg J. The use of sterilized mosquito nets for hernioplasty: a systematic review. Hernia. 2012;16(6): 621-625. 57. Luboga S, Macfarlane SB, von Schreeb J, et al. Increasing access to surgical services in sub-saharan Africa: priorities for national and international agencies recommended by the Bellagio Essential Surgery Group. PLoS Med. 2009;6(12):e1000200. 58. Jacobs DO. Improving surgical services in developing nations: getting to go. World J Surg. 2010;34(11):2509-2510. 59. Earle DB, Mark LA. Prosthetic material in inguinal hernia repair: how do I choose? Surg Clin North Am. 2008;88(1):179-201. 60. Beale EW, Hoxworth RE, Livingston EH, Trussler AP. The role of biologic mesh in abdominal wall reconstruction: a systematic review of the current literature. Am J Surg. 2012;204(4):510-517. 61. Smart NJ, Bloor S. Durability of biologic implants for use in hernia repair: a review. Surg Innov.
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Surgery_Schwartz. inguinal hernia repair. Br J Surg. 2012;99(1):29-37. 56. Sorensen CG, Rosenberg J. The use of sterilized mosquito nets for hernioplasty: a systematic review. Hernia. 2012;16(6): 621-625. 57. Luboga S, Macfarlane SB, von Schreeb J, et al. Increasing access to surgical services in sub-saharan Africa: priorities for national and international agencies recommended by the Bellagio Essential Surgery Group. PLoS Med. 2009;6(12):e1000200. 58. Jacobs DO. Improving surgical services in developing nations: getting to go. World J Surg. 2010;34(11):2509-2510. 59. Earle DB, Mark LA. Prosthetic material in inguinal hernia repair: how do I choose? Surg Clin North Am. 2008;88(1):179-201. 60. Beale EW, Hoxworth RE, Livingston EH, Trussler AP. The role of biologic mesh in abdominal wall reconstruction: a systematic review of the current literature. Am J Surg. 2012;204(4):510-517. 61. Smart NJ, Bloor S. Durability of biologic implants for use in hernia repair: a review. Surg Innov.
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Surgery_Schwartz_10705
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Surgery_Schwartz
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reconstruction: a systematic review of the current literature. Am J Surg. 2012;204(4):510-517. 61. Smart NJ, Bloor S. Durability of biologic implants for use in hernia repair: a review. Surg Innov. 2012;19(3):221-229. 62. Campanelli G, Sfeclan C, Cavalli M, Biondi A. Reducing postoperative pain: the use of Tisseel for mesh fixation in inguinal hernia repair. Surg Technol Int. 2012;22:134-139. 63. Fortelny RH, Petter-Puchner AH, Glaser KS, Redl H. Use of fibrin sealant (Tisseel/Tissucol) in hernia repair: a systematic review. Surg Endosc. 2012;26(7):1803-1812. 64. Taylor C, Layani L, Liew V, Ghusn M, Crampton N, White S. Laparoscopic inguinal hernia repair without mesh fixation, early results of a large randomised clinical trial. Surg Endosc. 2008;22(3):757-762. 65. Sajid MS, Ladwa N, Kalra L, McFall M, Baig MK, Sains P. A meta-analysis examining the use of tacker mesh fixation versus glue mesh fixation in laparoscopic inguinal hernia repair. Am J Surg.
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Surgery_Schwartz. reconstruction: a systematic review of the current literature. Am J Surg. 2012;204(4):510-517. 61. Smart NJ, Bloor S. Durability of biologic implants for use in hernia repair: a review. Surg Innov. 2012;19(3):221-229. 62. Campanelli G, Sfeclan C, Cavalli M, Biondi A. Reducing postoperative pain: the use of Tisseel for mesh fixation in inguinal hernia repair. Surg Technol Int. 2012;22:134-139. 63. Fortelny RH, Petter-Puchner AH, Glaser KS, Redl H. Use of fibrin sealant (Tisseel/Tissucol) in hernia repair: a systematic review. Surg Endosc. 2012;26(7):1803-1812. 64. Taylor C, Layani L, Liew V, Ghusn M, Crampton N, White S. Laparoscopic inguinal hernia repair without mesh fixation, early results of a large randomised clinical trial. Surg Endosc. 2008;22(3):757-762. 65. Sajid MS, Ladwa N, Kalra L, McFall M, Baig MK, Sains P. A meta-analysis examining the use of tacker mesh fixation versus glue mesh fixation in laparoscopic inguinal hernia repair. Am J Surg.
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Surgery_Schwartz_10706
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Surgery_Schwartz
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MS, Ladwa N, Kalra L, McFall M, Baig MK, Sains P. A meta-analysis examining the use of tacker mesh fixation versus glue mesh fixation in laparoscopic inguinal hernia repair. Am J Surg. 2013;206(1):103-111. 66. Morrison JE, Jr, Jacobs VR. Laparoscopic preperitoneal inguinal hernia repair using preformed polyester mesh without fixation: prospective study with 1-year follow-up results in a rural setting. Surg Laparosc Endosc Percutan Tech. 2008;18(1):33-39. 67. Aasvang E, Kehlet H. Surgical management of chronic pain after inguinal hernia repair. Br J Surg. 2005;92(7):795-801. 68. Kehlet H. Chronic pain after groin hernia repair. Br J Surg. 2008;95(2):135-136. 69. Reinpold WM, Nehls J, Eggert A. Nerve management and chronic pain after open inguinal hernia repair: a prospective two phase study. Ann Surg. 2011;254(1):163-168. 70. Alfieri S, Amid PK, Campanelli G, et al. International guide-lines for prevention and management of post-operative chronic pain following inguinal hernia surgery.
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Surgery_Schwartz. MS, Ladwa N, Kalra L, McFall M, Baig MK, Sains P. A meta-analysis examining the use of tacker mesh fixation versus glue mesh fixation in laparoscopic inguinal hernia repair. Am J Surg. 2013;206(1):103-111. 66. Morrison JE, Jr, Jacobs VR. Laparoscopic preperitoneal inguinal hernia repair using preformed polyester mesh without fixation: prospective study with 1-year follow-up results in a rural setting. Surg Laparosc Endosc Percutan Tech. 2008;18(1):33-39. 67. Aasvang E, Kehlet H. Surgical management of chronic pain after inguinal hernia repair. Br J Surg. 2005;92(7):795-801. 68. Kehlet H. Chronic pain after groin hernia repair. Br J Surg. 2008;95(2):135-136. 69. Reinpold WM, Nehls J, Eggert A. Nerve management and chronic pain after open inguinal hernia repair: a prospective two phase study. Ann Surg. 2011;254(1):163-168. 70. Alfieri S, Amid PK, Campanelli G, et al. International guide-lines for prevention and management of post-operative chronic pain following inguinal hernia surgery.
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Surgery_Schwartz_10707
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Surgery_Schwartz
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Ann Surg. 2011;254(1):163-168. 70. Alfieri S, Amid PK, Campanelli G, et al. International guide-lines for prevention and management of post-operative chronic pain following inguinal hernia surgery. Hernia. 2011; 15(3):239-249. 71. Callesen T, Beck K, Kehlet H. Prospective study of chronic pain after groin hernia repair. Br J Surg. 1999;86(12):1528-1531. 72. Bay-Nielsen M, Perkins FM, Kehlet H; Danish Hernia Database. Pain and functional impairment 1 year after inguinal herniorrhaphy: a nationwide questionnaire study. Ann Surg. 2001;233(1):1-7. 73. Aasvang EK, Bay-Nielsen M, Kehlet H. Pain and functional impairment 6 years after inguinal herniorrhaphy. Hernia. 2006;10(4):316-321. 74. Aasvang EK, Kehlet H. The effect of mesh removal and selective neurectomy on persistent postherniotomy pain. Ann Surg. 2009;249(2):327-334. 75. Rab M, Ebmer J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications for the treatment of groin pain. Plast Reconstr Surg.
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Surgery_Schwartz. Ann Surg. 2011;254(1):163-168. 70. Alfieri S, Amid PK, Campanelli G, et al. International guide-lines for prevention and management of post-operative chronic pain following inguinal hernia surgery. Hernia. 2011; 15(3):239-249. 71. Callesen T, Beck K, Kehlet H. Prospective study of chronic pain after groin hernia repair. Br J Surg. 1999;86(12):1528-1531. 72. Bay-Nielsen M, Perkins FM, Kehlet H; Danish Hernia Database. Pain and functional impairment 1 year after inguinal herniorrhaphy: a nationwide questionnaire study. Ann Surg. 2001;233(1):1-7. 73. Aasvang EK, Bay-Nielsen M, Kehlet H. Pain and functional impairment 6 years after inguinal herniorrhaphy. Hernia. 2006;10(4):316-321. 74. Aasvang EK, Kehlet H. The effect of mesh removal and selective neurectomy on persistent postherniotomy pain. Ann Surg. 2009;249(2):327-334. 75. Rab M, Ebmer J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications for the treatment of groin pain. Plast Reconstr Surg.
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Surgery_Schwartz_10708
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Surgery_Schwartz
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Ann Surg. 2009;249(2):327-334. 75. Rab M, Ebmer J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications for the treatment of groin pain. Plast Reconstr Surg. 2001; 108(6):1618-1623. 76. Loos MJ, Scheltinga MR, Roumen RM. Tailored neurectomy for treatment of postherniorrhaphy inguinal neuralgia. Surgery. 2010;147(2):275-281. 77. Zacest AC, Magill ST, Anderson VC, Burchiel KJ. Long-term outcome following ilioinguinal neurectomy for chronic pain. J Neurosurg. 2010;112(4):784-789. 78. Klaassen Z, Marshall E, Tubbs RS, Louis RG, Jr, Wartmann CT, Loukas M. Anatomy of the ilioinguinal and iliohypogastric Brunicardi_Ch37_p1599-p1624.indd 162329/01/19 2:04 PM 1624SPECIFIC CONSIDERATIONSPART IInerves with observations of their spinal nerve contributions. Clin Anat. 2011;24(4):454-461. 79. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis and treatment of genitofemoral and ilioinguinal entrapment neuralgia. Surgery.
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Surgery_Schwartz. Ann Surg. 2009;249(2):327-334. 75. Rab M, Ebmer J, Dellon AL. Anatomic variability of the ilioinguinal and genitofemoral nerve: implications for the treatment of groin pain. Plast Reconstr Surg. 2001; 108(6):1618-1623. 76. Loos MJ, Scheltinga MR, Roumen RM. Tailored neurectomy for treatment of postherniorrhaphy inguinal neuralgia. Surgery. 2010;147(2):275-281. 77. Zacest AC, Magill ST, Anderson VC, Burchiel KJ. Long-term outcome following ilioinguinal neurectomy for chronic pain. J Neurosurg. 2010;112(4):784-789. 78. Klaassen Z, Marshall E, Tubbs RS, Louis RG, Jr, Wartmann CT, Loukas M. Anatomy of the ilioinguinal and iliohypogastric Brunicardi_Ch37_p1599-p1624.indd 162329/01/19 2:04 PM 1624SPECIFIC CONSIDERATIONSPART IInerves with observations of their spinal nerve contributions. Clin Anat. 2011;24(4):454-461. 79. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis and treatment of genitofemoral and ilioinguinal entrapment neuralgia. Surgery.
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Surgery_Schwartz_10709
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nerve contributions. Clin Anat. 2011;24(4):454-461. 79. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis and treatment of genitofemoral and ilioinguinal entrapment neuralgia. Surgery. 1987;102(4):581-586. 80. Starling JR, Harms BA. Ilioinguinal, iliohypogastric, and genitofemoral neuralgia. In: Bendavid R, ed. Prostheses and Abdominal Wall Hernia. Austin, TX: RG Landes Co; 1994: 351-356. 81. Amid PK. A 1-stage surgical treatment for postherniorrhaphy neuropathic pain: triple neurectomy and proximal end implantation without mobilization of the cord. Arch Surg. 2002;137(1):100-104. 82. Kim DH, Murovic JA, Tiel RL, Kline DG. Surgical management of 33 ilioinguinal and iliohypogastric neuralgias at Louisiana State University Health Sciences Center. Neurosurgery. 2005;56(5):1013-1020; discussion 1013-1020. 83. Madura JA, Madura JA 2nd, Copper CM, Worth RM. Inguinal neurectomy for inguinal nerve entrapment: an experience with 100 patients. Am J Surg. 2005;189(3):283-287. 84. Amid
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Surgery_Schwartz. nerve contributions. Clin Anat. 2011;24(4):454-461. 79. Starling JR, Harms BA, Schroeder ME, Eichman PL. Diagnosis and treatment of genitofemoral and ilioinguinal entrapment neuralgia. Surgery. 1987;102(4):581-586. 80. Starling JR, Harms BA. Ilioinguinal, iliohypogastric, and genitofemoral neuralgia. In: Bendavid R, ed. Prostheses and Abdominal Wall Hernia. Austin, TX: RG Landes Co; 1994: 351-356. 81. Amid PK. A 1-stage surgical treatment for postherniorrhaphy neuropathic pain: triple neurectomy and proximal end implantation without mobilization of the cord. Arch Surg. 2002;137(1):100-104. 82. Kim DH, Murovic JA, Tiel RL, Kline DG. Surgical management of 33 ilioinguinal and iliohypogastric neuralgias at Louisiana State University Health Sciences Center. Neurosurgery. 2005;56(5):1013-1020; discussion 1013-1020. 83. Madura JA, Madura JA 2nd, Copper CM, Worth RM. Inguinal neurectomy for inguinal nerve entrapment: an experience with 100 patients. Am J Surg. 2005;189(3):283-287. 84. Amid
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Surgery_Schwartz_10710
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Surgery_Schwartz
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discussion 1013-1020. 83. Madura JA, Madura JA 2nd, Copper CM, Worth RM. Inguinal neurectomy for inguinal nerve entrapment: an experience with 100 patients. Am J Surg. 2005;189(3):283-287. 84. Amid PK, Chen DC. Surgical treatment of chronic groin and testicular pain after laparoscopic and open preperitoneal inguinal hernia repair. J Am Coll Surg. 2011;213(4):531-536. 85. Chen DC, Hiatt JR, Amid PK. Operative management of refractory neuropathic inguinodynia by a laparoscopic ret-roperitoneal approach. JAMA Surg. 2013;148(10):962-967. 86. Benito-Leon J, Picardo A, Garrido A, Cuberes R. Gabapentin therapy for genitofemoral and ilioinguinal neuralgia. J Neurol. 2001;248(10):907-908. 87. LeBlanc KE, LeBlanc KA. Groin pain in athletes. Hernia. 2003;7(2):68-71. 88. Fong Y, Wantz GE. Prevention of ischemic orchitis during inguinal hernioplasty. Surg Gynecol Obstet. 1992;174(5):399-402. 89. Shin D, Lipshultz LI, Goldstein M, et al. Herniorrhaphy with polypropylene mesh causing inguinal vasal
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Surgery_Schwartz. discussion 1013-1020. 83. Madura JA, Madura JA 2nd, Copper CM, Worth RM. Inguinal neurectomy for inguinal nerve entrapment: an experience with 100 patients. Am J Surg. 2005;189(3):283-287. 84. Amid PK, Chen DC. Surgical treatment of chronic groin and testicular pain after laparoscopic and open preperitoneal inguinal hernia repair. J Am Coll Surg. 2011;213(4):531-536. 85. Chen DC, Hiatt JR, Amid PK. Operative management of refractory neuropathic inguinodynia by a laparoscopic ret-roperitoneal approach. JAMA Surg. 2013;148(10):962-967. 86. Benito-Leon J, Picardo A, Garrido A, Cuberes R. Gabapentin therapy for genitofemoral and ilioinguinal neuralgia. J Neurol. 2001;248(10):907-908. 87. LeBlanc KE, LeBlanc KA. Groin pain in athletes. Hernia. 2003;7(2):68-71. 88. Fong Y, Wantz GE. Prevention of ischemic orchitis during inguinal hernioplasty. Surg Gynecol Obstet. 1992;174(5):399-402. 89. Shin D, Lipshultz LI, Goldstein M, et al. Herniorrhaphy with polypropylene mesh causing inguinal vasal
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Surgery_Schwartz_10711
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Surgery_Schwartz
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ischemic orchitis during inguinal hernioplasty. Surg Gynecol Obstet. 1992;174(5):399-402. 89. Shin D, Lipshultz LI, Goldstein M, et al. Herniorrhaphy with polypropylene mesh causing inguinal vasal obstruction: a preventable cause of obstructive azoospermia. Ann Surg. 2005;241(4):553-558. 90. Hallén M, Sandblom G, Nordin P, et al. Male infertility after mesh hernia repair: a prospective study. Surgery. 2011; 149(2):179-184. 91. Finley RK, Jr, Miller SF, Jones LM. Elimination of urinary retention following inguinal herniorrhaphy. Am Surg. 1991;57(8):486-488; discussion 488-489. 92. Aeberhard P, Klaiber C, Meyenberg A, Osterwalder A, Tschudi J. Prospective audit of laparoscopic totally extraperitoneal inguinal hernia repair: a multicenter study of the Swiss Association for Laparoscopic and Thoracoscopic Surgery (SALTC). Surg Endosc. 1999;13(11):1115-1120. 93. Dulucq JL, Wintringer P, Mahajna A. Laparoscopic totally extraperitoneal inguinal hernia repair: lessons learned from 3,100
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Surgery_Schwartz. ischemic orchitis during inguinal hernioplasty. Surg Gynecol Obstet. 1992;174(5):399-402. 89. Shin D, Lipshultz LI, Goldstein M, et al. Herniorrhaphy with polypropylene mesh causing inguinal vasal obstruction: a preventable cause of obstructive azoospermia. Ann Surg. 2005;241(4):553-558. 90. Hallén M, Sandblom G, Nordin P, et al. Male infertility after mesh hernia repair: a prospective study. Surgery. 2011; 149(2):179-184. 91. Finley RK, Jr, Miller SF, Jones LM. Elimination of urinary retention following inguinal herniorrhaphy. Am Surg. 1991;57(8):486-488; discussion 488-489. 92. Aeberhard P, Klaiber C, Meyenberg A, Osterwalder A, Tschudi J. Prospective audit of laparoscopic totally extraperitoneal inguinal hernia repair: a multicenter study of the Swiss Association for Laparoscopic and Thoracoscopic Surgery (SALTC). Surg Endosc. 1999;13(11):1115-1120. 93. Dulucq JL, Wintringer P, Mahajna A. Laparoscopic totally extraperitoneal inguinal hernia repair: lessons learned from 3,100
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Surgery_Schwartz_10712
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Surgery_Schwartz
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and Thoracoscopic Surgery (SALTC). Surg Endosc. 1999;13(11):1115-1120. 93. Dulucq JL, Wintringer P, Mahajna A. Laparoscopic totally extraperitoneal inguinal hernia repair: lessons learned from 3,100 hernia repairs over 15 years. Surg Endosc. 2009;23(3):482-486. 94. Kapiris S, Mavromatis T, Andrikopoulos S, Georgiades C, Floros D, Diamantopoulos G. Laparoscopic transabdominal preperitoneal hernia repair (TAPP): stapling the mesh is not mandatory. J Laparoendosc Adv Surg Tech A. 2009;19(3):419-422. 95. Swadia ND. Laparoscopic totally extra-peritoneal inguinal hernia repair: 9 year’s experience. Hernia. 2011;15(3):273-279. 96. Petros JG, Rimm EB, Robillard RJ, Argy O. Factors influencing postoperative urinary retention in patients undergoing elective inguinal herniorrhaphy. Am J Surg. 1991;161(4):431-433; discussion 434. 97. Amato B, Moja L, Panico S, et al. Shouldice technique versus other open techniques for inguinal hernia repair. Cochrane Database Syst Rev.
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Surgery_Schwartz. and Thoracoscopic Surgery (SALTC). Surg Endosc. 1999;13(11):1115-1120. 93. Dulucq JL, Wintringer P, Mahajna A. Laparoscopic totally extraperitoneal inguinal hernia repair: lessons learned from 3,100 hernia repairs over 15 years. Surg Endosc. 2009;23(3):482-486. 94. Kapiris S, Mavromatis T, Andrikopoulos S, Georgiades C, Floros D, Diamantopoulos G. Laparoscopic transabdominal preperitoneal hernia repair (TAPP): stapling the mesh is not mandatory. J Laparoendosc Adv Surg Tech A. 2009;19(3):419-422. 95. Swadia ND. Laparoscopic totally extra-peritoneal inguinal hernia repair: 9 year’s experience. Hernia. 2011;15(3):273-279. 96. Petros JG, Rimm EB, Robillard RJ, Argy O. Factors influencing postoperative urinary retention in patients undergoing elective inguinal herniorrhaphy. Am J Surg. 1991;161(4):431-433; discussion 434. 97. Amato B, Moja L, Panico S, et al. Shouldice technique versus other open techniques for inguinal hernia repair. Cochrane Database Syst Rev.
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Surgery_Schwartz_10713
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Surgery_Schwartz
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Am J Surg. 1991;161(4):431-433; discussion 434. 97. Amato B, Moja L, Panico S, et al. Shouldice technique versus other open techniques for inguinal hernia repair. Cochrane Database Syst Rev. 2012;(4):CD001543. 98. Glassow F. The Shouldice Hospital technique. Int Surg. 1986;71(3):148-153. 99. Kingsnorth AN, Britton BJ, Morris PJ. Recurrent inguinal hernia after local anaesthetic repair. Br J Surg. 1991;68(4):273-275. 100. Lichtenstein IL, Shulman AG, Amid PK. Use of mesh to prevent recurrence of hernias. Postgrad Med. 1990;87(1):155-158, 160. 101. Scott NW, McCormack K, Graham P, Go PM, Ross SJ, Grant AM. Open mesh versus non-mesh for repair of femoral and inguinal hernia. Cochrane Database Syst Rev. 2002;(4):CD002197. 102. Simons MP, Aufenacker T, Bay-Nielsen M, et al. European Hernia Society guidelines on the treatment of inguinal her-nia in adult patients. Hernia. 2009;13(4):343-403. 103. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias:
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Surgery_Schwartz. Am J Surg. 1991;161(4):431-433; discussion 434. 97. Amato B, Moja L, Panico S, et al. Shouldice technique versus other open techniques for inguinal hernia repair. Cochrane Database Syst Rev. 2012;(4):CD001543. 98. Glassow F. The Shouldice Hospital technique. Int Surg. 1986;71(3):148-153. 99. Kingsnorth AN, Britton BJ, Morris PJ. Recurrent inguinal hernia after local anaesthetic repair. Br J Surg. 1991;68(4):273-275. 100. Lichtenstein IL, Shulman AG, Amid PK. Use of mesh to prevent recurrence of hernias. Postgrad Med. 1990;87(1):155-158, 160. 101. Scott NW, McCormack K, Graham P, Go PM, Ross SJ, Grant AM. Open mesh versus non-mesh for repair of femoral and inguinal hernia. Cochrane Database Syst Rev. 2002;(4):CD002197. 102. Simons MP, Aufenacker T, Bay-Nielsen M, et al. European Hernia Society guidelines on the treatment of inguinal her-nia in adult patients. Hernia. 2009;13(4):343-403. 103. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias:
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Surgery_Schwartz_10714
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guidelines on the treatment of inguinal her-nia in adult patients. Hernia. 2009;13(4):343-403. 103. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias: results of 3,019 operations from five diverse surgical sources. Am Surg. 1992;58(4):255-257. 104. Kingsnorth AN, Porter CS, Bennett DH, Walker AJ, Hyland ME, Sodergren S. Lichtenstein patch or Perfix plug-and-patch in inguinal hernia: a prospective double-blind randomized controlled trial of short-term outcome. Surgery. 2000;127(3):276-283. 105. Li J, Ji Z, Li Y. Comparison of mesh-plug and Lichtenstein for inguinal hernia repair: a meta-analysis of randomized controlled trials. Hernia. 2012;16(5):541-548. 106. Willaert W, De Bacquer D, Rogiers X, Troisi R, Berrevoet F. Open preperitoneal techniques versus lichtenstein repair for elective inguinal hernias. Cochrane Database Syst Rev. 2012;(7):CD008034. 107. McCormack K, Scott NW, Go PM, Ross S, Grant AM; EU Hernia Trialists Collaboration.
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Surgery_Schwartz. guidelines on the treatment of inguinal her-nia in adult patients. Hernia. 2009;13(4):343-403. 103. Shulman AG, Amid PK, Lichtenstein IL. The safety of mesh repair for primary inguinal hernias: results of 3,019 operations from five diverse surgical sources. Am Surg. 1992;58(4):255-257. 104. Kingsnorth AN, Porter CS, Bennett DH, Walker AJ, Hyland ME, Sodergren S. Lichtenstein patch or Perfix plug-and-patch in inguinal hernia: a prospective double-blind randomized controlled trial of short-term outcome. Surgery. 2000;127(3):276-283. 105. Li J, Ji Z, Li Y. Comparison of mesh-plug and Lichtenstein for inguinal hernia repair: a meta-analysis of randomized controlled trials. Hernia. 2012;16(5):541-548. 106. Willaert W, De Bacquer D, Rogiers X, Troisi R, Berrevoet F. Open preperitoneal techniques versus lichtenstein repair for elective inguinal hernias. Cochrane Database Syst Rev. 2012;(7):CD008034. 107. McCormack K, Scott NW, Go PM, Ross S, Grant AM; EU Hernia Trialists Collaboration.
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versus lichtenstein repair for elective inguinal hernias. Cochrane Database Syst Rev. 2012;(7):CD008034. 107. McCormack K, Scott NW, Go PM, Ross S, Grant AM; EU Hernia Trialists Collaboration. Laparoscopic tech-niques versus open techniques for inguinal hernia repair. Cochrane Database Syst Rev. 2003;(1):CD001785. 108. Andersson B, Hallén M, Leveau P, Bergenfelz A, Westerdahl J. Laparoscopic extraperitoneal inguinal hernia repair versus open mesh repair: a prospective randomized controlled trial. Surgery. 2003;133(5):464-472. 109. Hallén M, Bergenfelz A, Westerdahl J. Laparoscopic extraperitoneal inguinal hernia repair versus open mesh repair: long-term follow-up of a randomized controlled trial. Surgery. 2008;143(3):313-317. 110. Lau H, Patil NG, Yuen WK. Day-case endoscopic totally extraperitoneal inguinal hernioplasty versus open Lichtenstein hernioplasty for unilateral primary inguinal hernia in males: a randomized trial. Surg Endosc. 2006;20(1):76-81. 111. Neumayer L,
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Surgery_Schwartz. versus lichtenstein repair for elective inguinal hernias. Cochrane Database Syst Rev. 2012;(7):CD008034. 107. McCormack K, Scott NW, Go PM, Ross S, Grant AM; EU Hernia Trialists Collaboration. Laparoscopic tech-niques versus open techniques for inguinal hernia repair. Cochrane Database Syst Rev. 2003;(1):CD001785. 108. Andersson B, Hallén M, Leveau P, Bergenfelz A, Westerdahl J. Laparoscopic extraperitoneal inguinal hernia repair versus open mesh repair: a prospective randomized controlled trial. Surgery. 2003;133(5):464-472. 109. Hallén M, Bergenfelz A, Westerdahl J. Laparoscopic extraperitoneal inguinal hernia repair versus open mesh repair: long-term follow-up of a randomized controlled trial. Surgery. 2008;143(3):313-317. 110. Lau H, Patil NG, Yuen WK. Day-case endoscopic totally extraperitoneal inguinal hernioplasty versus open Lichtenstein hernioplasty for unilateral primary inguinal hernia in males: a randomized trial. Surg Endosc. 2006;20(1):76-81. 111. Neumayer L,
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extraperitoneal inguinal hernioplasty versus open Lichtenstein hernioplasty for unilateral primary inguinal hernia in males: a randomized trial. Surg Endosc. 2006;20(1):76-81. 111. Neumayer L, Giobbie-Hurder A, Jonasson O, et al. Open mesh versus laparoscopic mesh repair of inguinal hernia. N Engl J Med. 2004;350(18):1819-1827. 112. Lal P, Kajla RK, Chander J, Ramteke VK. Laparoscopic total extraperitoneal (TEP) inguinal hernia repair: overcoming the learning curve. Surg Endosc. 2004;18(4):642-645. 113. Katkhouda N, Campos GM, Mavor E, Trussler A, Khalil M, Stoppa R. Laparoscopic extraperitoneal inguinal hernia repair. A safe approach based on the understanding of rectus sheath anatomy. Surg Endosc. 1999;13(12):1243-1246. 114. Wake BL, McCormack K, Fraser C, Vale L, Perez J, Grant AM. Transabdominal pre-peritoneal (TAPP) vs totally extraperitoneal (TEP) laparoscopic techniques for ingui-nal hernia repair. Cochrane Database Syst Rev. 2005;(1): CD004703.Brunicardi_Ch37_p1599-p1624.indd
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Surgery_Schwartz. extraperitoneal inguinal hernioplasty versus open Lichtenstein hernioplasty for unilateral primary inguinal hernia in males: a randomized trial. Surg Endosc. 2006;20(1):76-81. 111. Neumayer L, Giobbie-Hurder A, Jonasson O, et al. Open mesh versus laparoscopic mesh repair of inguinal hernia. N Engl J Med. 2004;350(18):1819-1827. 112. Lal P, Kajla RK, Chander J, Ramteke VK. Laparoscopic total extraperitoneal (TEP) inguinal hernia repair: overcoming the learning curve. Surg Endosc. 2004;18(4):642-645. 113. Katkhouda N, Campos GM, Mavor E, Trussler A, Khalil M, Stoppa R. Laparoscopic extraperitoneal inguinal hernia repair. A safe approach based on the understanding of rectus sheath anatomy. Surg Endosc. 1999;13(12):1243-1246. 114. Wake BL, McCormack K, Fraser C, Vale L, Perez J, Grant AM. Transabdominal pre-peritoneal (TAPP) vs totally extraperitoneal (TEP) laparoscopic techniques for ingui-nal hernia repair. Cochrane Database Syst Rev. 2005;(1): CD004703.Brunicardi_Ch37_p1599-p1624.indd
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pre-peritoneal (TAPP) vs totally extraperitoneal (TEP) laparoscopic techniques for ingui-nal hernia repair. Cochrane Database Syst Rev. 2005;(1): CD004703.Brunicardi_Ch37_p1599-p1624.indd 162429/01/19 2:04 PM
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Surgery_Schwartz. pre-peritoneal (TAPP) vs totally extraperitoneal (TEP) laparoscopic techniques for ingui-nal hernia repair. Cochrane Database Syst Rev. 2005;(1): CD004703.Brunicardi_Ch37_p1599-p1624.indd 162429/01/19 2:04 PM
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Thyroid, Parathyroid, and AdrenalGeeta Lal and Orlo H. Clark 38chapterTHYROIDHistorical BackgroundGoiters (from the Latin guttur, throat), defined as an enlarge-ment of the thyroid, have been recognized since 2700 b.c. even though the thyroid gland was not documented as such until the Renaissance period. In 1619, Hieronymus Fabricius ab Aqua-pendente recognized that goiters arose from the thyroid gland. The term thyroid gland (Greek thyreoeides, shield-shaped) is, however, attributed to Thomas Wharton in his Adenographia (1656). In 1776, the thyroid was classified as a ductless gland by Albrecht von Haller and was thought to have numerous func-tions ranging from lubrication of the larynx to acting as a res-ervoir for blood to provide continuous flow to the brain, and to beautifying women’s necks. Burnt seaweed was considered to be the most effective treatment for goiters.The first accounts of thyroid surgery for the treatment of goiters were given by Roger Frugardi in 1170. In
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Surgery_Schwartz. Thyroid, Parathyroid, and AdrenalGeeta Lal and Orlo H. Clark 38chapterTHYROIDHistorical BackgroundGoiters (from the Latin guttur, throat), defined as an enlarge-ment of the thyroid, have been recognized since 2700 b.c. even though the thyroid gland was not documented as such until the Renaissance period. In 1619, Hieronymus Fabricius ab Aqua-pendente recognized that goiters arose from the thyroid gland. The term thyroid gland (Greek thyreoeides, shield-shaped) is, however, attributed to Thomas Wharton in his Adenographia (1656). In 1776, the thyroid was classified as a ductless gland by Albrecht von Haller and was thought to have numerous func-tions ranging from lubrication of the larynx to acting as a res-ervoir for blood to provide continuous flow to the brain, and to beautifying women’s necks. Burnt seaweed was considered to be the most effective treatment for goiters.The first accounts of thyroid surgery for the treatment of goiters were given by Roger Frugardi in 1170. In
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women’s necks. Burnt seaweed was considered to be the most effective treatment for goiters.The first accounts of thyroid surgery for the treatment of goiters were given by Roger Frugardi in 1170. In response to failure of medical treatment, two setons were inserted at right angles into the goiter and tightened twice daily until the goiter separated. The open wound was treated with caustic powder and left to heal. However, thyroid surgery continued to be hazardous with prohibitive mortality rates (>40%) until the latter half of the 19th century, when advances in general anesthesia, antisep-sis, and hemostasis enabled surgeons to perform thyroid sur-gery with significantly reduced mortality and morbidity rates. The most notable thyroid surgeons were Emil Theodor Kocher (1841–1917) and C.A. Theodor Billroth (1829–1894), who per-formed thousands of operations with increasingly successful results. However, as more patients survived thyroid operations, new problems and issues became
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Surgery_Schwartz. women’s necks. Burnt seaweed was considered to be the most effective treatment for goiters.The first accounts of thyroid surgery for the treatment of goiters were given by Roger Frugardi in 1170. In response to failure of medical treatment, two setons were inserted at right angles into the goiter and tightened twice daily until the goiter separated. The open wound was treated with caustic powder and left to heal. However, thyroid surgery continued to be hazardous with prohibitive mortality rates (>40%) until the latter half of the 19th century, when advances in general anesthesia, antisep-sis, and hemostasis enabled surgeons to perform thyroid sur-gery with significantly reduced mortality and morbidity rates. The most notable thyroid surgeons were Emil Theodor Kocher (1841–1917) and C.A. Theodor Billroth (1829–1894), who per-formed thousands of operations with increasingly successful results. However, as more patients survived thyroid operations, new problems and issues became
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C.A. Theodor Billroth (1829–1894), who per-formed thousands of operations with increasingly successful results. However, as more patients survived thyroid operations, new problems and issues became apparent. After total thyroid-ectomy, patients (particularly children) became myxedematous with cretinous features. Myxedema was first effectively treated in 1891 by George Murray using a subcutaneous injection of an extract of sheep’s thyroid, and later, Edward Fox demonstrated that oral therapy was equally effective. In 1909, Kocher was awarded the Nobel Prize for medicine in recognition “for his works on the physiology, pathology, and surgery of the thyroid gland.”EmbryologyThe thyroid gland arises as an outpouching of the primitive foregut around the third week of gestation. It originates at the base of the tongue at the foramen cecum. Endoderm cells in the floor of the pharyngeal anlage thicken to form the medial thyroid anlage (Fig. 38-1) that descends in the neck anterior to
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Surgery_Schwartz. C.A. Theodor Billroth (1829–1894), who per-formed thousands of operations with increasingly successful results. However, as more patients survived thyroid operations, new problems and issues became apparent. After total thyroid-ectomy, patients (particularly children) became myxedematous with cretinous features. Myxedema was first effectively treated in 1891 by George Murray using a subcutaneous injection of an extract of sheep’s thyroid, and later, Edward Fox demonstrated that oral therapy was equally effective. In 1909, Kocher was awarded the Nobel Prize for medicine in recognition “for his works on the physiology, pathology, and surgery of the thyroid gland.”EmbryologyThe thyroid gland arises as an outpouching of the primitive foregut around the third week of gestation. It originates at the base of the tongue at the foramen cecum. Endoderm cells in the floor of the pharyngeal anlage thicken to form the medial thyroid anlage (Fig. 38-1) that descends in the neck anterior to
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at the base of the tongue at the foramen cecum. Endoderm cells in the floor of the pharyngeal anlage thicken to form the medial thyroid anlage (Fig. 38-1) that descends in the neck anterior to structures that form the hyoid bone and larynx. During its descent, the anlage remains connected to the foramen cecum via an epithelial-lined tube known as the thyroglossal duct. The epithelial cells making up the anlage give rise to the thyroid fol-licular cells. The paired lateral anlages originate from the fourth branchial pouch and fuse with the median anlage at approxi-mately the fifth week of gestation. The lateral anlages are neu-roectodermal in origin (ultimobranchial bodies) and provide the calcitonin producing parafollicular or C cells, which thus come to lie in the superoposterior region of the gland. Thyroid fol-licles are initially apparent by 8 weeks, and colloid formation begins by the 11th week of gestation.Developmental AbnormalitiesThyroglossal Duct Cyst and Sinus. Thyroglossal
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Surgery_Schwartz. at the base of the tongue at the foramen cecum. Endoderm cells in the floor of the pharyngeal anlage thicken to form the medial thyroid anlage (Fig. 38-1) that descends in the neck anterior to structures that form the hyoid bone and larynx. During its descent, the anlage remains connected to the foramen cecum via an epithelial-lined tube known as the thyroglossal duct. The epithelial cells making up the anlage give rise to the thyroid fol-licular cells. The paired lateral anlages originate from the fourth branchial pouch and fuse with the median anlage at approxi-mately the fifth week of gestation. The lateral anlages are neu-roectodermal in origin (ultimobranchial bodies) and provide the calcitonin producing parafollicular or C cells, which thus come to lie in the superoposterior region of the gland. Thyroid fol-licles are initially apparent by 8 weeks, and colloid formation begins by the 11th week of gestation.Developmental AbnormalitiesThyroglossal Duct Cyst and Sinus. Thyroglossal
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the gland. Thyroid fol-licles are initially apparent by 8 weeks, and colloid formation begins by the 11th week of gestation.Developmental AbnormalitiesThyroglossal Duct Cyst and Sinus. Thyroglossal duct cysts are the most commonly encountered congenital cervical anoma-lies. During the fifth week of gestation, the thyroglossal duct lumen starts to obliterate, and the duct disappears by the eighth week of gestation. Rarely, the thyroglossal duct may persist in whole or in part. Thyroglossal duct cysts may occur anywhere along the migratory path of the thyroid, although 80% are found in juxtaposition to the hyoid bone. They are usually asymptom-atic but occasionally become infected by oral bacteria, prompt-ing the patient to seek medical advice. Thyroglossal duct sinuses Thyroid 1625Historical Background / 1625Embryology / 1625Developmental Abnormalities / 1625Thyroid Anatomy / 1627Thyroid Histology / 1629Thyroid Physiology / 1629Evaluation of Patients With Thyroid Disease / 1633Benign
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Surgery_Schwartz. the gland. Thyroid fol-licles are initially apparent by 8 weeks, and colloid formation begins by the 11th week of gestation.Developmental AbnormalitiesThyroglossal Duct Cyst and Sinus. Thyroglossal duct cysts are the most commonly encountered congenital cervical anoma-lies. During the fifth week of gestation, the thyroglossal duct lumen starts to obliterate, and the duct disappears by the eighth week of gestation. Rarely, the thyroglossal duct may persist in whole or in part. Thyroglossal duct cysts may occur anywhere along the migratory path of the thyroid, although 80% are found in juxtaposition to the hyoid bone. They are usually asymptom-atic but occasionally become infected by oral bacteria, prompt-ing the patient to seek medical advice. Thyroglossal duct sinuses Thyroid 1625Historical Background / 1625Embryology / 1625Developmental Abnormalities / 1625Thyroid Anatomy / 1627Thyroid Histology / 1629Thyroid Physiology / 1629Evaluation of Patients With Thyroid Disease / 1633Benign
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Background / 1625Embryology / 1625Developmental Abnormalities / 1625Thyroid Anatomy / 1627Thyroid Histology / 1629Thyroid Physiology / 1629Evaluation of Patients With Thyroid Disease / 1633Benign Thyroid Disorders / 1634Solitary Thyroid Nodule / 1641Malignant Thyroid Disease / 1645Parathyroid 1663Historical Background / 1663Embryology / 1663Anatomy and Histology / 1664Parathyroid Physiology and Calcium Homeostasis / 1664Hyperparathyroidism / 1665Hypoparathyroidism / 1681Adrenal 1681Historical Background / 1681Embryology / 1681Anatomy / 1682Adrenal Physiology / 1682Disorders of the Adrenal Cortex / 1685Disorders of the Adrenal Medulla / 1693The Adrenal Incidentaloma / 1695Adrenal Insufficiency / 1697Adrenal Surgery / 1698Brunicardi_Ch38_p1625-p1704.indd 162501/03/19 11:20 AM 1626result from infection of the cyst secondary to spontaneous or surgical drainage of the cyst and are accompanied by minor inflammation of the surrounding skin. Histologically, thyroglos-sal duct cysts are
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Surgery_Schwartz. Background / 1625Embryology / 1625Developmental Abnormalities / 1625Thyroid Anatomy / 1627Thyroid Histology / 1629Thyroid Physiology / 1629Evaluation of Patients With Thyroid Disease / 1633Benign Thyroid Disorders / 1634Solitary Thyroid Nodule / 1641Malignant Thyroid Disease / 1645Parathyroid 1663Historical Background / 1663Embryology / 1663Anatomy and Histology / 1664Parathyroid Physiology and Calcium Homeostasis / 1664Hyperparathyroidism / 1665Hypoparathyroidism / 1681Adrenal 1681Historical Background / 1681Embryology / 1681Anatomy / 1682Adrenal Physiology / 1682Disorders of the Adrenal Cortex / 1685Disorders of the Adrenal Medulla / 1693The Adrenal Incidentaloma / 1695Adrenal Insufficiency / 1697Adrenal Surgery / 1698Brunicardi_Ch38_p1625-p1704.indd 162501/03/19 11:20 AM 1626result from infection of the cyst secondary to spontaneous or surgical drainage of the cyst and are accompanied by minor inflammation of the surrounding skin. Histologically, thyroglos-sal duct cysts are
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from infection of the cyst secondary to spontaneous or surgical drainage of the cyst and are accompanied by minor inflammation of the surrounding skin. Histologically, thyroglos-sal duct cysts are lined by pseudostratified ciliated columnar epithelium and squamous epithelium, with heterotopic thyroid tissue present in 20% of cases.The diagnosis usually is established by observing a 1to 2-cm, smooth, well-defined midline neck mass that moves upward with protrusion of the tongue. Routine thyroid imaging is not necessary, although thyroid scintigraphy and ultrasound have been performed to document the presence of normal thy-roid tissue in the neck. Treatment involves the “Sistrunk opera-tion,” which consists of en bloc cystectomy and excision of the central hyoid bone to minimize recurrence. Approximately 1% of thyroglossal duct cysts are found to contain cancer, which is usually papillary (85%). The role of total thyroidectomy in this setting is debated, but it is advised in patients
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Surgery_Schwartz. from infection of the cyst secondary to spontaneous or surgical drainage of the cyst and are accompanied by minor inflammation of the surrounding skin. Histologically, thyroglos-sal duct cysts are lined by pseudostratified ciliated columnar epithelium and squamous epithelium, with heterotopic thyroid tissue present in 20% of cases.The diagnosis usually is established by observing a 1to 2-cm, smooth, well-defined midline neck mass that moves upward with protrusion of the tongue. Routine thyroid imaging is not necessary, although thyroid scintigraphy and ultrasound have been performed to document the presence of normal thy-roid tissue in the neck. Treatment involves the “Sistrunk opera-tion,” which consists of en bloc cystectomy and excision of the central hyoid bone to minimize recurrence. Approximately 1% of thyroglossal duct cysts are found to contain cancer, which is usually papillary (85%). The role of total thyroidectomy in this setting is debated, but it is advised in patients
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Approximately 1% of thyroglossal duct cysts are found to contain cancer, which is usually papillary (85%). The role of total thyroidectomy in this setting is debated, but it is advised in patients with large tumors, particularly if there are additional thyroid nodules and evidence of cyst wall invasion or lymph node metastases.1 Squamous, Hürthle cell, and anaplastic cancers also have been reported but are rare. Medullary thyroid cancers (MTCs) are, however, not found in thyroglossal duct cysts.Lingual Thyroid. A lingual thyroid represents a failure of the median thyroid anlage to descend normally and may be the only thyroid tissue present. Intervention becomes necessary for obstructive symptoms such as choking, dysphagia, airway obstruction, or hemorrhage. Many of these patients develop hypothyroidism. Medical treatment options include administra-tion of exogenous thyroid hormone to suppress thyroid-stim-ulating hormone (TSH) and radioactive iodine (RAI) ablation followed by hormone
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Surgery_Schwartz. Approximately 1% of thyroglossal duct cysts are found to contain cancer, which is usually papillary (85%). The role of total thyroidectomy in this setting is debated, but it is advised in patients with large tumors, particularly if there are additional thyroid nodules and evidence of cyst wall invasion or lymph node metastases.1 Squamous, Hürthle cell, and anaplastic cancers also have been reported but are rare. Medullary thyroid cancers (MTCs) are, however, not found in thyroglossal duct cysts.Lingual Thyroid. A lingual thyroid represents a failure of the median thyroid anlage to descend normally and may be the only thyroid tissue present. Intervention becomes necessary for obstructive symptoms such as choking, dysphagia, airway obstruction, or hemorrhage. Many of these patients develop hypothyroidism. Medical treatment options include administra-tion of exogenous thyroid hormone to suppress thyroid-stim-ulating hormone (TSH) and radioactive iodine (RAI) ablation followed by hormone
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hypothyroidism. Medical treatment options include administra-tion of exogenous thyroid hormone to suppress thyroid-stim-ulating hormone (TSH) and radioactive iodine (RAI) ablation followed by hormone replacement. Surgical excision is rarely needed but, if required, should be preceded by an evaluation of normal thyroid tissue in the neck to avoid inadvertently render-ing the patient hypothyroid.Ectopic Thyroid. Normal thyroid tissue may be found any-where in the central neck compartment, including the esopha-gus, trachea, and anterior mediastinum. Thyroid tissue has been observed adjacent to the aortic arch, in the aortopulmonary win-dow, within the upper pericardium, or in the interventricular septum. Often, “tongues” of thyroid tissue are seen to extend off the inferior poles of the gland and are particularly appar-ent in large goiters. Thyroid tissue situated lateral to the carotid sheath and jugular vein, previously termed lateral aberrant thyroid, almost always represents
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Surgery_Schwartz. hypothyroidism. Medical treatment options include administra-tion of exogenous thyroid hormone to suppress thyroid-stim-ulating hormone (TSH) and radioactive iodine (RAI) ablation followed by hormone replacement. Surgical excision is rarely needed but, if required, should be preceded by an evaluation of normal thyroid tissue in the neck to avoid inadvertently render-ing the patient hypothyroid.Ectopic Thyroid. Normal thyroid tissue may be found any-where in the central neck compartment, including the esopha-gus, trachea, and anterior mediastinum. Thyroid tissue has been observed adjacent to the aortic arch, in the aortopulmonary win-dow, within the upper pericardium, or in the interventricular septum. Often, “tongues” of thyroid tissue are seen to extend off the inferior poles of the gland and are particularly appar-ent in large goiters. Thyroid tissue situated lateral to the carotid sheath and jugular vein, previously termed lateral aberrant thyroid, almost always represents
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the gland and are particularly appar-ent in large goiters. Thyroid tissue situated lateral to the carotid sheath and jugular vein, previously termed lateral aberrant thyroid, almost always represents metastatic thyroid cancer in lymph nodes, and not remnants of the lateral anlage that had Buccalcavity1234EndodermMedian thyroiddiverticulumTracheo-esophageal tube1stpharyngealpouch2nd pouch 3rd pouch 4th pouch Figure 38-1. Thyroid embryology—early development of the median thyroid anlage as a pharyngeal pouch. (Reproduced with permission from Cady B, Rossi R: Surgery of the Thyroid and Para-thyroid Glands. Philadelphia, PA: WB Saunders; 1991.)Key Points1 There has been a paradigm shift in the surgical manage-ment of Graves’ disease with increased use of total or near-total thyroidectomy, rather than subtotal thyroidectomy.2 Familial nonmedullary thyroid cancer is increasingly being recognized as a separate entity. Surgeons must be aware of the potential for false-negative fine-needle
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Surgery_Schwartz. the gland and are particularly appar-ent in large goiters. Thyroid tissue situated lateral to the carotid sheath and jugular vein, previously termed lateral aberrant thyroid, almost always represents metastatic thyroid cancer in lymph nodes, and not remnants of the lateral anlage that had Buccalcavity1234EndodermMedian thyroiddiverticulumTracheo-esophageal tube1stpharyngealpouch2nd pouch 3rd pouch 4th pouch Figure 38-1. Thyroid embryology—early development of the median thyroid anlage as a pharyngeal pouch. (Reproduced with permission from Cady B, Rossi R: Surgery of the Thyroid and Para-thyroid Glands. Philadelphia, PA: WB Saunders; 1991.)Key Points1 There has been a paradigm shift in the surgical manage-ment of Graves’ disease with increased use of total or near-total thyroidectomy, rather than subtotal thyroidectomy.2 Familial nonmedullary thyroid cancer is increasingly being recognized as a separate entity. Surgeons must be aware of the potential for false-negative fine-needle
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rather than subtotal thyroidectomy.2 Familial nonmedullary thyroid cancer is increasingly being recognized as a separate entity. Surgeons must be aware of the potential for false-negative fine-needle aspi-ration biopsy in this setting.3 Fine-needle aspiration biopsies are now classified into six groups based on the risk of malignancy associated with each group (Bethesda criteria).4 Encapsulated follicular variants of papillary thyroid can-cers are now designated noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP).5 Lobectomy or total/near-total thyroidectomy are consid-ered appropriate treatments for low-risk thyroid cancers. Some small papillary thyroid cancers (<1 cm) can be fol-lowed with active surveillance.6 Focused mini-incision parathyroidectomy, after appropri-ate localization, has become the procedure of choice for the treatment of sporadic primary hyperparathyroidism.7 Parathyroidectomy has been shown to improve the clas-sic and the so-called
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Surgery_Schwartz. rather than subtotal thyroidectomy.2 Familial nonmedullary thyroid cancer is increasingly being recognized as a separate entity. Surgeons must be aware of the potential for false-negative fine-needle aspi-ration biopsy in this setting.3 Fine-needle aspiration biopsies are now classified into six groups based on the risk of malignancy associated with each group (Bethesda criteria).4 Encapsulated follicular variants of papillary thyroid can-cers are now designated noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP).5 Lobectomy or total/near-total thyroidectomy are consid-ered appropriate treatments for low-risk thyroid cancers. Some small papillary thyroid cancers (<1 cm) can be fol-lowed with active surveillance.6 Focused mini-incision parathyroidectomy, after appropri-ate localization, has become the procedure of choice for the treatment of sporadic primary hyperparathyroidism.7 Parathyroidectomy has been shown to improve the clas-sic and the so-called
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appropri-ate localization, has become the procedure of choice for the treatment of sporadic primary hyperparathyroidism.7 Parathyroidectomy has been shown to improve the clas-sic and the so-called nonspecific symptoms and metabolic complications of primary hyperparathyroidism.8 Normocalcemic hyperparathyroidism is being increasingly recognized; however, there are no definitive guidelines for management.9 Very high calcium and parathyroid hormone levels in a patient with primary hyperparathyroidism should alert the surgeon to the presence of a possible parathyroid carcinoma.10 Subclinical Cushing’s syndrome is characterized by subtle abnormalities in corticosteroid synthesis, and many of its manifestations appear to be treated by adrenalectomy.11 Fine-needle aspiration biopsy has a very limited role in the evaluation of adrenal incidentalomas unless the patient has previously had a cancer and should only be performed after appropriate biochemical studies have been performed to rule out
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Surgery_Schwartz. appropri-ate localization, has become the procedure of choice for the treatment of sporadic primary hyperparathyroidism.7 Parathyroidectomy has been shown to improve the clas-sic and the so-called nonspecific symptoms and metabolic complications of primary hyperparathyroidism.8 Normocalcemic hyperparathyroidism is being increasingly recognized; however, there are no definitive guidelines for management.9 Very high calcium and parathyroid hormone levels in a patient with primary hyperparathyroidism should alert the surgeon to the presence of a possible parathyroid carcinoma.10 Subclinical Cushing’s syndrome is characterized by subtle abnormalities in corticosteroid synthesis, and many of its manifestations appear to be treated by adrenalectomy.11 Fine-needle aspiration biopsy has a very limited role in the evaluation of adrenal incidentalomas unless the patient has previously had a cancer and should only be performed after appropriate biochemical studies have been performed to rule out
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role in the evaluation of adrenal incidentalomas unless the patient has previously had a cancer and should only be performed after appropriate biochemical studies have been performed to rule out pheochromocytoma.12 Laparoscopic adrenalectomy has become the procedure of choice for excision of most adrenal lesions, except known or suspected cancers.Brunicardi_Ch38_p1625-p1704.indd 162601/03/19 11:20 AM 1627THYROID, PARATHYROID, AND ADRENALCHAPTER 38failed to fuse with the main thyroid, as previously suggested by Crile. Even if not readily apparent on physical examination or ultrasound imaging, the ipsilateral thyroid lobe contains a focus of papillary thyroid cancer (PTC), which may be microscopic.Pyramidal Lobe. Normally the thyroglossal duct atrophies, although it may remain as a fibrous band. In about 50% of indi-viduals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting up from the isthmus, lying just to the left or right of the midline. In the
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Surgery_Schwartz. role in the evaluation of adrenal incidentalomas unless the patient has previously had a cancer and should only be performed after appropriate biochemical studies have been performed to rule out pheochromocytoma.12 Laparoscopic adrenalectomy has become the procedure of choice for excision of most adrenal lesions, except known or suspected cancers.Brunicardi_Ch38_p1625-p1704.indd 162601/03/19 11:20 AM 1627THYROID, PARATHYROID, AND ADRENALCHAPTER 38failed to fuse with the main thyroid, as previously suggested by Crile. Even if not readily apparent on physical examination or ultrasound imaging, the ipsilateral thyroid lobe contains a focus of papillary thyroid cancer (PTC), which may be microscopic.Pyramidal Lobe. Normally the thyroglossal duct atrophies, although it may remain as a fibrous band. In about 50% of indi-viduals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting up from the isthmus, lying just to the left or right of the midline. In the
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band. In about 50% of indi-viduals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting up from the isthmus, lying just to the left or right of the midline. In the normal individual, the pyra-midal lobe is not palpable, but in disorders resulting in thyroid hypertrophy (e.g., Graves’ disease, diffuse nodular goiter, or lymphocytic thyroiditis), the pyramidal lobe usually is enlarged and palpable.Thyroid AnatomyThe anatomic relations of the thyroid gland and surrounding structures are depicted in Fig. 38-2. The adult thyroid gland is brown in color and firm in consistency and is located posterior to the strap muscles. The normal thyroid gland weighs approx-imately 20 g, but gland weight varies with body weight and iodine intake. The thyroid lobes are located adjacent to the thy-roid cartilage and connected in the midline by an isthmus that is located just inferior to the cricoid cartilage. A pyramidal lobe is present in about 50% of patients. The thyroid
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Surgery_Schwartz. band. In about 50% of indi-viduals, the distal end that connects to the thyroid persists as a pyramidal lobe projecting up from the isthmus, lying just to the left or right of the midline. In the normal individual, the pyra-midal lobe is not palpable, but in disorders resulting in thyroid hypertrophy (e.g., Graves’ disease, diffuse nodular goiter, or lymphocytic thyroiditis), the pyramidal lobe usually is enlarged and palpable.Thyroid AnatomyThe anatomic relations of the thyroid gland and surrounding structures are depicted in Fig. 38-2. The adult thyroid gland is brown in color and firm in consistency and is located posterior to the strap muscles. The normal thyroid gland weighs approx-imately 20 g, but gland weight varies with body weight and iodine intake. The thyroid lobes are located adjacent to the thy-roid cartilage and connected in the midline by an isthmus that is located just inferior to the cricoid cartilage. A pyramidal lobe is present in about 50% of patients. The thyroid
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adjacent to the thy-roid cartilage and connected in the midline by an isthmus that is located just inferior to the cricoid cartilage. A pyramidal lobe is present in about 50% of patients. The thyroid lobes extend to the midthyroid cartilage superiorly and lie adjacent to the carotid sheaths and sternocleidomastoid muscles laterally. The strap muscles (sternohyoid, sternothyroid, and superior belly of the omohyoid) are located anteriorly and are innervated by the ansa cervicalis (ansa hypoglossi). The thyroid gland is enveloped by a loosely connecting fascia that is formed from the parti-tion of the deep cervical fascia into anterior and posterior divi-sions. The true capsule of the thyroid is a thin, densely adherent fibrous layer that sends out septa that invaginate into the gland, forming pseudolobules. The thyroid capsule is condensed into the posterior suspensory or Berry’s ligament near the cricoid cartilage and upper tracheal rings.Sup. thyroid a. and v.PyramidallobeCommon
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Surgery_Schwartz. adjacent to the thy-roid cartilage and connected in the midline by an isthmus that is located just inferior to the cricoid cartilage. A pyramidal lobe is present in about 50% of patients. The thyroid lobes extend to the midthyroid cartilage superiorly and lie adjacent to the carotid sheaths and sternocleidomastoid muscles laterally. The strap muscles (sternohyoid, sternothyroid, and superior belly of the omohyoid) are located anteriorly and are innervated by the ansa cervicalis (ansa hypoglossi). The thyroid gland is enveloped by a loosely connecting fascia that is formed from the parti-tion of the deep cervical fascia into anterior and posterior divi-sions. The true capsule of the thyroid is a thin, densely adherent fibrous layer that sends out septa that invaginate into the gland, forming pseudolobules. The thyroid capsule is condensed into the posterior suspensory or Berry’s ligament near the cricoid cartilage and upper tracheal rings.Sup. thyroid a. and v.PyramidallobeCommon
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forming pseudolobules. The thyroid capsule is condensed into the posterior suspensory or Berry’s ligament near the cricoid cartilage and upper tracheal rings.Sup. thyroid a. and v.PyramidallobeCommon carotid a.Common carotid a.Thyroid cartilageInt. jugular v.Int. jugular v.Recurrent laryngeal n.Recurrentlaryngeal n.Vagus n.Vagus n.Vagus n.Arch of aortaThyrocervical trunkInf. thyroid v.Middle thyroid v.Ext. carotid a.Thyroidea ima a.(variable)TracheaSternocleido-mastoid m.Inf. thyroid a.Vertebralv. and a. Thyroid glandStrap musclesABFigure 38-2. Anatomy of the thyroid gland and surrounding structures, viewed anteriorly (A) and in cross-section (B). a. = artery; m. = muscle; n. = nerve; v. = vein.Brunicardi_Ch38_p1625-p1704.indd 162701/03/19 11:20 AM 1628SPECIFIC CONSIDERATIONSPART IIBlood Supply. The superior thyroid arteries arise from the ipsilateral external carotid arteries and divide into anterior and posterior branches at the apices of the thyroid lobes. The infe-rior
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Surgery_Schwartz. forming pseudolobules. The thyroid capsule is condensed into the posterior suspensory or Berry’s ligament near the cricoid cartilage and upper tracheal rings.Sup. thyroid a. and v.PyramidallobeCommon carotid a.Common carotid a.Thyroid cartilageInt. jugular v.Int. jugular v.Recurrent laryngeal n.Recurrentlaryngeal n.Vagus n.Vagus n.Vagus n.Arch of aortaThyrocervical trunkInf. thyroid v.Middle thyroid v.Ext. carotid a.Thyroidea ima a.(variable)TracheaSternocleido-mastoid m.Inf. thyroid a.Vertebralv. and a. Thyroid glandStrap musclesABFigure 38-2. Anatomy of the thyroid gland and surrounding structures, viewed anteriorly (A) and in cross-section (B). a. = artery; m. = muscle; n. = nerve; v. = vein.Brunicardi_Ch38_p1625-p1704.indd 162701/03/19 11:20 AM 1628SPECIFIC CONSIDERATIONSPART IIBlood Supply. The superior thyroid arteries arise from the ipsilateral external carotid arteries and divide into anterior and posterior branches at the apices of the thyroid lobes. The infe-rior
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Supply. The superior thyroid arteries arise from the ipsilateral external carotid arteries and divide into anterior and posterior branches at the apices of the thyroid lobes. The infe-rior thyroid arteries arise from the thyrocervical trunk shortly after their origin from the subclavian arteries. The inferior thy-roid arteries travel upward in the neck posterior to the carotid sheath to enter the thyroid lobes at their midpoint. A thyroidea ima artery arises directly from the aorta or innominate in 1% to 4% of individuals to enter the isthmus or replace a missing inferior thyroid artery. The inferior thyroid artery crosses the recurrent laryngeal nerve (RLN), necessitating identification of the RLN before the arterial branches can be ligated. The venous drainage of the thyroid gland occurs via multiple small surface veins, which coalesce to form three sets of veins—the supe-rior, middle, and inferior thyroid veins. The superior thyroid veins run with the superior thyroid arteries
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Surgery_Schwartz. Supply. The superior thyroid arteries arise from the ipsilateral external carotid arteries and divide into anterior and posterior branches at the apices of the thyroid lobes. The infe-rior thyroid arteries arise from the thyrocervical trunk shortly after their origin from the subclavian arteries. The inferior thy-roid arteries travel upward in the neck posterior to the carotid sheath to enter the thyroid lobes at their midpoint. A thyroidea ima artery arises directly from the aorta or innominate in 1% to 4% of individuals to enter the isthmus or replace a missing inferior thyroid artery. The inferior thyroid artery crosses the recurrent laryngeal nerve (RLN), necessitating identification of the RLN before the arterial branches can be ligated. The venous drainage of the thyroid gland occurs via multiple small surface veins, which coalesce to form three sets of veins—the supe-rior, middle, and inferior thyroid veins. The superior thyroid veins run with the superior thyroid arteries
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via multiple small surface veins, which coalesce to form three sets of veins—the supe-rior, middle, and inferior thyroid veins. The superior thyroid veins run with the superior thyroid arteries bilaterally. The middle vein or veins are the least consistent. The superior and middle veins drain directly into the internal jugular veins. The inferior veins often form a plexus, which drains into the bra-chiocephalic veins.Nerves. The left RLN arises from the vagus nerve where it crosses the aortic arch, loops around the ligamentum arteriosum, and ascends medially in the neck within the tracheoesophageal groove. The right RLN arises from the vagus at its crossing with the right subclavian artery. The nerve usually passes posterior to the artery before ascending in the neck, its course being more oblique than the left RLN. Along their course in the neck, the RLNs may branch, and pass anterior, posterior, or interdigitate with branches of the inferior thyroid artery (Fig. 38-3). The right
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Surgery_Schwartz. via multiple small surface veins, which coalesce to form three sets of veins—the supe-rior, middle, and inferior thyroid veins. The superior thyroid veins run with the superior thyroid arteries bilaterally. The middle vein or veins are the least consistent. The superior and middle veins drain directly into the internal jugular veins. The inferior veins often form a plexus, which drains into the bra-chiocephalic veins.Nerves. The left RLN arises from the vagus nerve where it crosses the aortic arch, loops around the ligamentum arteriosum, and ascends medially in the neck within the tracheoesophageal groove. The right RLN arises from the vagus at its crossing with the right subclavian artery. The nerve usually passes posterior to the artery before ascending in the neck, its course being more oblique than the left RLN. Along their course in the neck, the RLNs may branch, and pass anterior, posterior, or interdigitate with branches of the inferior thyroid artery (Fig. 38-3). The right
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more oblique than the left RLN. Along their course in the neck, the RLNs may branch, and pass anterior, posterior, or interdigitate with branches of the inferior thyroid artery (Fig. 38-3). The right RLN may be nonrecurrent in 0.5% to 1% of individuals and often is associated with a vascular anomaly. Nonrecurrent left RLNs are rare but have been reported in patients with situs inversus and a right-sided aortic arch. The RLN may branch in its course in the neck, and identification of a small nerve should alert the surgeon to this possibility. Identification of the nerves or their branches often necessitates mobilization of the most lateral and posterior extent of the thyroid gland, the tubercle of Zucker-kandl, at the level of the cricoid cartilage. The last segments of the nerves often course below the tubercle and are closely approximated to the ligament of Berry. Branches of the nerve may traverse the ligament in 25% of individuals and are particu-larly vulnerable to injury at this
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Surgery_Schwartz. more oblique than the left RLN. Along their course in the neck, the RLNs may branch, and pass anterior, posterior, or interdigitate with branches of the inferior thyroid artery (Fig. 38-3). The right RLN may be nonrecurrent in 0.5% to 1% of individuals and often is associated with a vascular anomaly. Nonrecurrent left RLNs are rare but have been reported in patients with situs inversus and a right-sided aortic arch. The RLN may branch in its course in the neck, and identification of a small nerve should alert the surgeon to this possibility. Identification of the nerves or their branches often necessitates mobilization of the most lateral and posterior extent of the thyroid gland, the tubercle of Zucker-kandl, at the level of the cricoid cartilage. The last segments of the nerves often course below the tubercle and are closely approximated to the ligament of Berry. Branches of the nerve may traverse the ligament in 25% of individuals and are particu-larly vulnerable to injury at this
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below the tubercle and are closely approximated to the ligament of Berry. Branches of the nerve may traverse the ligament in 25% of individuals and are particu-larly vulnerable to injury at this junction. The RLNs terminate by entering the larynx posterior to the cricothyroid muscle.The RLNs innervate all the intrinsic muscles of the larynx, except the cricothyroid muscles, which are innervated by the external laryngeal nerves. Injury to one RLN leads to paralysis of the ipsilateral vocal cord, which comes to lie in the parame-dian or the abducted position. The paramedian position results in a normal but weak voice, whereas the abducted position leads to a hoarse voice and an ineffective cough. Bilateral RLN injury may lead to airway obstruction, necessitating emergency trache-ostomy, or loss of voice. If both cords come to lie in an abducted position, air movement can occur, but the patient has an ineffec-tive cough and is at increased risk of repeated respiratory tract infections
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Surgery_Schwartz. below the tubercle and are closely approximated to the ligament of Berry. Branches of the nerve may traverse the ligament in 25% of individuals and are particu-larly vulnerable to injury at this junction. The RLNs terminate by entering the larynx posterior to the cricothyroid muscle.The RLNs innervate all the intrinsic muscles of the larynx, except the cricothyroid muscles, which are innervated by the external laryngeal nerves. Injury to one RLN leads to paralysis of the ipsilateral vocal cord, which comes to lie in the parame-dian or the abducted position. The paramedian position results in a normal but weak voice, whereas the abducted position leads to a hoarse voice and an ineffective cough. Bilateral RLN injury may lead to airway obstruction, necessitating emergency trache-ostomy, or loss of voice. If both cords come to lie in an abducted position, air movement can occur, but the patient has an ineffec-tive cough and is at increased risk of repeated respiratory tract infections
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loss of voice. If both cords come to lie in an abducted position, air movement can occur, but the patient has an ineffec-tive cough and is at increased risk of repeated respiratory tract infections from aspiration.The superior laryngeal nerves also arise from the vagus nerves. After their origin at the base of the skull, these nerves 1) Nerve in tracheoesophageal groove R: 64% L: 77% 4) Nerve between branches of inferior thyroid artery R: 7% L: 67% 2) Nerve lateral to trachea R: 28% L: 17% R: 8% L: 6%5) Nerve posterior to artery R: 53% L: 69% R: 37% L: 24%3) Nerve far anterior6) Nerve anterior to artery7) Artery absent R: 3% L: 1%Figure 38-3. Relationship of recurrent laryngeal nerve to the inferior thyroid artery—the superior parathyroid is characteristically dorsal to the plane of the nerve, whereas the inferior gland is ventral to the nerve.Brunicardi_Ch38_p1625-p1704.indd 162801/03/19 11:20 AM 1629THYROID, PARATHYROID, AND ADRENALCHAPTER
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Surgery_Schwartz. loss of voice. If both cords come to lie in an abducted position, air movement can occur, but the patient has an ineffec-tive cough and is at increased risk of repeated respiratory tract infections from aspiration.The superior laryngeal nerves also arise from the vagus nerves. After their origin at the base of the skull, these nerves 1) Nerve in tracheoesophageal groove R: 64% L: 77% 4) Nerve between branches of inferior thyroid artery R: 7% L: 67% 2) Nerve lateral to trachea R: 28% L: 17% R: 8% L: 6%5) Nerve posterior to artery R: 53% L: 69% R: 37% L: 24%3) Nerve far anterior6) Nerve anterior to artery7) Artery absent R: 3% L: 1%Figure 38-3. Relationship of recurrent laryngeal nerve to the inferior thyroid artery—the superior parathyroid is characteristically dorsal to the plane of the nerve, whereas the inferior gland is ventral to the nerve.Brunicardi_Ch38_p1625-p1704.indd 162801/03/19 11:20 AM 1629THYROID, PARATHYROID, AND ADRENALCHAPTER
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dorsal to the plane of the nerve, whereas the inferior gland is ventral to the nerve.Brunicardi_Ch38_p1625-p1704.indd 162801/03/19 11:20 AM 1629THYROID, PARATHYROID, AND ADRENALCHAPTER 38travel along the internal carotid artery and divide into two branches at the level of the hyoid bone. The internal branch of the superior laryngeal nerve is sensory to the supraglottic larynx. Injury to this nerve is rare in thyroid surgery, but its occurrence may result in aspiration. The external branch of the superior laryngeal nerve lies on the inferior pharyngeal constric-tor muscle and descends alongside the superior thyroid vessels before innervating the cricothyroid muscle. Cernea and col-leagues2 proposed a classification system to describe the rela-tionship of this nerve to the superior thyroid vessels (Fig. 38-4). The type 2a variant, in which the nerve crosses below the tip of the thyroid superior pole, occurs in up to 20% of individuals and places the nerve at a greater risk of
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Surgery_Schwartz. dorsal to the plane of the nerve, whereas the inferior gland is ventral to the nerve.Brunicardi_Ch38_p1625-p1704.indd 162801/03/19 11:20 AM 1629THYROID, PARATHYROID, AND ADRENALCHAPTER 38travel along the internal carotid artery and divide into two branches at the level of the hyoid bone. The internal branch of the superior laryngeal nerve is sensory to the supraglottic larynx. Injury to this nerve is rare in thyroid surgery, but its occurrence may result in aspiration. The external branch of the superior laryngeal nerve lies on the inferior pharyngeal constric-tor muscle and descends alongside the superior thyroid vessels before innervating the cricothyroid muscle. Cernea and col-leagues2 proposed a classification system to describe the rela-tionship of this nerve to the superior thyroid vessels (Fig. 38-4). The type 2a variant, in which the nerve crosses below the tip of the thyroid superior pole, occurs in up to 20% of individuals and places the nerve at a greater risk of
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thyroid vessels (Fig. 38-4). The type 2a variant, in which the nerve crosses below the tip of the thyroid superior pole, occurs in up to 20% of individuals and places the nerve at a greater risk of injury. Therefore, the superior pole vessels should not be ligated en masse, but should be individually divided, low on the thyroid gland and dissected lateral to the cricothyroid muscle. Injury to this nerve leads to inability to tense the ipsilateral vocal cord and hence difficulty “hitting high notes,” difficulty projecting the voice, and voice fatigue during prolonged speech.Sympathetic innervation of the thyroid gland is provided by fibers from the superior and middle cervical sympathetic ganglia. The fibers enter the gland with the blood vessels and are vasomotor in action. Parasympathetic fibers are derived from the vagus nerve and reach the gland via branches of the laryngeal nerves.Parathyroid Glands. The embryology and anatomy of the parathyroid glands are discussed in detail in
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Surgery_Schwartz. thyroid vessels (Fig. 38-4). The type 2a variant, in which the nerve crosses below the tip of the thyroid superior pole, occurs in up to 20% of individuals and places the nerve at a greater risk of injury. Therefore, the superior pole vessels should not be ligated en masse, but should be individually divided, low on the thyroid gland and dissected lateral to the cricothyroid muscle. Injury to this nerve leads to inability to tense the ipsilateral vocal cord and hence difficulty “hitting high notes,” difficulty projecting the voice, and voice fatigue during prolonged speech.Sympathetic innervation of the thyroid gland is provided by fibers from the superior and middle cervical sympathetic ganglia. The fibers enter the gland with the blood vessels and are vasomotor in action. Parasympathetic fibers are derived from the vagus nerve and reach the gland via branches of the laryngeal nerves.Parathyroid Glands. The embryology and anatomy of the parathyroid glands are discussed in detail in
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fibers are derived from the vagus nerve and reach the gland via branches of the laryngeal nerves.Parathyroid Glands. The embryology and anatomy of the parathyroid glands are discussed in detail in the “Parathyroid Gland” section of this chapter. About 85% of individuals have four parathyroid glands that can be found within 1 cm of the junction of the inferior thyroid artery and the RLN. The supe-rior glands are usually located dorsal to the RLN, whereas the inferior glands are usually found ventral to the RLN (Fig. 38-5).Lymphatic System. The thyroid gland is endowed with an extensive network of lymphatics. Intraglandular lymphatic ves-sels connect both thyroid lobes through the isthmus and also drain to perithyroidal structures and lymph nodes. Regional lymph nodes include pretracheal, paratracheal, perithyroidal, RLN, superior mediastinal, retropharyngeal, esophageal, and upper, middle, and lower jugular chain nodes. These lymph nodes can be classified into seven levels as depicted
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Surgery_Schwartz. fibers are derived from the vagus nerve and reach the gland via branches of the laryngeal nerves.Parathyroid Glands. The embryology and anatomy of the parathyroid glands are discussed in detail in the “Parathyroid Gland” section of this chapter. About 85% of individuals have four parathyroid glands that can be found within 1 cm of the junction of the inferior thyroid artery and the RLN. The supe-rior glands are usually located dorsal to the RLN, whereas the inferior glands are usually found ventral to the RLN (Fig. 38-5).Lymphatic System. The thyroid gland is endowed with an extensive network of lymphatics. Intraglandular lymphatic ves-sels connect both thyroid lobes through the isthmus and also drain to perithyroidal structures and lymph nodes. Regional lymph nodes include pretracheal, paratracheal, perithyroidal, RLN, superior mediastinal, retropharyngeal, esophageal, and upper, middle, and lower jugular chain nodes. These lymph nodes can be classified into seven levels as depicted
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perithyroidal, RLN, superior mediastinal, retropharyngeal, esophageal, and upper, middle, and lower jugular chain nodes. These lymph nodes can be classified into seven levels as depicted in Fig. 38-6. The central compartment includes nodes located in the area between the two carotid sheaths, whereas nodes lateral to the vessels are present in the lateral compartment. Thyroid can-cers may metastasize to any of these regions, although metas-tases to submaxillary nodes (level I) are rare (<1%). There also can be “skip” metastases to nodes in the lateral ipsilateral neck without central neck nodes.Thyroid HistologyMicroscopically, the thyroid is divided into lobules that contain 20 to 40 follicles (Fig. 38-7). There are about 3 × 106 follicles in the adult male thyroid gland. The follicles are spherical and average 30 μm in diameter. Each follicle is lined by cuboidal epithelial cells and contains a central store of colloid secreted from the epithelial cells under the influence of the
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Surgery_Schwartz. perithyroidal, RLN, superior mediastinal, retropharyngeal, esophageal, and upper, middle, and lower jugular chain nodes. These lymph nodes can be classified into seven levels as depicted in Fig. 38-6. The central compartment includes nodes located in the area between the two carotid sheaths, whereas nodes lateral to the vessels are present in the lateral compartment. Thyroid can-cers may metastasize to any of these regions, although metas-tases to submaxillary nodes (level I) are rare (<1%). There also can be “skip” metastases to nodes in the lateral ipsilateral neck without central neck nodes.Thyroid HistologyMicroscopically, the thyroid is divided into lobules that contain 20 to 40 follicles (Fig. 38-7). There are about 3 × 106 follicles in the adult male thyroid gland. The follicles are spherical and average 30 μm in diameter. Each follicle is lined by cuboidal epithelial cells and contains a central store of colloid secreted from the epithelial cells under the influence of the
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are spherical and average 30 μm in diameter. Each follicle is lined by cuboidal epithelial cells and contains a central store of colloid secreted from the epithelial cells under the influence of the pituitary hor-mone TSH. The second group of thyroid secretory cells is the C cells or parafollicular cells, which contain and secrete the hor-mone calcitonin. They are found as individual cells or clumped in small groups in the interfollicular stroma and located in the upper poles of the thyroid lobes.Thyroid PhysiologyIodine Metabolism. The average daily iodine requirement is 0.1 mg, which can be derived from foods such as fish, milk, and eggs or as additives in bread or salt. In the stomach and jeju-num, iodine is rapidly converted to iodide and absorbed into the bloodstream, and from there it is distributed uniformly through-out the extracellular space. Iodide is actively transported into the thyroid follicular cells by an adenosine triphosphate (ATP)–dependent process. The thyroid is
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Surgery_Schwartz. are spherical and average 30 μm in diameter. Each follicle is lined by cuboidal epithelial cells and contains a central store of colloid secreted from the epithelial cells under the influence of the pituitary hor-mone TSH. The second group of thyroid secretory cells is the C cells or parafollicular cells, which contain and secrete the hor-mone calcitonin. They are found as individual cells or clumped in small groups in the interfollicular stroma and located in the upper poles of the thyroid lobes.Thyroid PhysiologyIodine Metabolism. The average daily iodine requirement is 0.1 mg, which can be derived from foods such as fish, milk, and eggs or as additives in bread or salt. In the stomach and jeju-num, iodine is rapidly converted to iodide and absorbed into the bloodstream, and from there it is distributed uniformly through-out the extracellular space. Iodide is actively transported into the thyroid follicular cells by an adenosine triphosphate (ATP)–dependent process. The thyroid is
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it is distributed uniformly through-out the extracellular space. Iodide is actively transported into the thyroid follicular cells by an adenosine triphosphate (ATP)–dependent process. The thyroid is the storage site of >90% of the body’s iodine content and accounts for one-third of the plasma iodine loss. The remaining plasma iodine is cleared via renal excretion.Thyroid Hormone Synthesis, Secretion, and Transport. The synthesis of thyroid hormone consists of several steps 1cmType 1Type 2aType 2bFigure 38-4. Relationship of the external branch of the superior laryngeal nerve and superior thyroid artery originally described by Cernea and colleagues.2 In type 1 anatomy, the nerve crosses the artery ≥1 cm above the superior aspect of the thyroid lobe. In type 2 anatomy, the nerve crosses the artery <1 cm above the thyroid pole (2a) or below (2b) it. (Reproduced with permission from Bliss RD, Gauger PG, Delbridge LW:Surgeon’s approach to the thyroid gland: surgical anatomy and the
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Surgery_Schwartz. it is distributed uniformly through-out the extracellular space. Iodide is actively transported into the thyroid follicular cells by an adenosine triphosphate (ATP)–dependent process. The thyroid is the storage site of >90% of the body’s iodine content and accounts for one-third of the plasma iodine loss. The remaining plasma iodine is cleared via renal excretion.Thyroid Hormone Synthesis, Secretion, and Transport. The synthesis of thyroid hormone consists of several steps 1cmType 1Type 2aType 2bFigure 38-4. Relationship of the external branch of the superior laryngeal nerve and superior thyroid artery originally described by Cernea and colleagues.2 In type 1 anatomy, the nerve crosses the artery ≥1 cm above the superior aspect of the thyroid lobe. In type 2 anatomy, the nerve crosses the artery <1 cm above the thyroid pole (2a) or below (2b) it. (Reproduced with permission from Bliss RD, Gauger PG, Delbridge LW:Surgeon’s approach to the thyroid gland: surgical anatomy and the
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the artery <1 cm above the thyroid pole (2a) or below (2b) it. (Reproduced with permission from Bliss RD, Gauger PG, Delbridge LW:Surgeon’s approach to the thyroid gland: surgical anatomy and the importance of technique, World J Surg. 2000 Aug;24(8):891-897.)Brunicardi_Ch38_p1625-p1704.indd 162901/03/19 11:20 AM 1630SPECIFIC CONSIDERATIONSPART II(Fig. 38-8). The first, iodide trapping, involves active (ATP-dependent) transport of iodide across the basement mem-brane of the thyrocyte via an intrinsic membrane protein, the sodium/iodine (Na+/I–) symporter. Thyroglobulin (Tg) is a large (660 kDa) glycoprotein, which is present in thyroid follicles and has four tyrosyl residues. The second step in thyroid hormone synthesis involves oxidation of iodide to iodine and iodination of tyrosine residues on Tg, to form monoiodotyrosines (MIT) and diiodotyrosines (DIT). Both processes are catalyzed by thyroid peroxidase (TPO). A recently identified protein, pen-drin, is thought to mediate
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Surgery_Schwartz. the artery <1 cm above the thyroid pole (2a) or below (2b) it. (Reproduced with permission from Bliss RD, Gauger PG, Delbridge LW:Surgeon’s approach to the thyroid gland: surgical anatomy and the importance of technique, World J Surg. 2000 Aug;24(8):891-897.)Brunicardi_Ch38_p1625-p1704.indd 162901/03/19 11:20 AM 1630SPECIFIC CONSIDERATIONSPART II(Fig. 38-8). The first, iodide trapping, involves active (ATP-dependent) transport of iodide across the basement mem-brane of the thyrocyte via an intrinsic membrane protein, the sodium/iodine (Na+/I–) symporter. Thyroglobulin (Tg) is a large (660 kDa) glycoprotein, which is present in thyroid follicles and has four tyrosyl residues. The second step in thyroid hormone synthesis involves oxidation of iodide to iodine and iodination of tyrosine residues on Tg, to form monoiodotyrosines (MIT) and diiodotyrosines (DIT). Both processes are catalyzed by thyroid peroxidase (TPO). A recently identified protein, pen-drin, is thought to mediate
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residues on Tg, to form monoiodotyrosines (MIT) and diiodotyrosines (DIT). Both processes are catalyzed by thyroid peroxidase (TPO). A recently identified protein, pen-drin, is thought to mediate iodine efflux at the apical membrane. The third step leads to coupling of two DIT molecules to form tetra-iodothyronine or thyroxine (T4), and one DIT molecule with one MIT molecule to form 3,5,3′-triiodothyronine (T3) or 3,3′,5′-triiodothyronine reverse (rT3). When stimulated by TSH, thyrocytes form pseudopodia, which encircle portions of cell membrane containing Tg, which in turn, fuse with enzymecontaining lysosomes. In the fourth step, Tg is hydrolyzed to release free iodothyronines (T3 and T4) and monoand diiodo-tyrosines. The latter are deiodinated in the fifth step to yield iodide, which is reused in the thyrocyte. In the euthyroid state, T4 is produced and released entirely by the thyroid gland, whereas only 20% of the total T3 is produced by the thyroid. Most of the T3 is produced by
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Surgery_Schwartz. residues on Tg, to form monoiodotyrosines (MIT) and diiodotyrosines (DIT). Both processes are catalyzed by thyroid peroxidase (TPO). A recently identified protein, pen-drin, is thought to mediate iodine efflux at the apical membrane. The third step leads to coupling of two DIT molecules to form tetra-iodothyronine or thyroxine (T4), and one DIT molecule with one MIT molecule to form 3,5,3′-triiodothyronine (T3) or 3,3′,5′-triiodothyronine reverse (rT3). When stimulated by TSH, thyrocytes form pseudopodia, which encircle portions of cell membrane containing Tg, which in turn, fuse with enzymecontaining lysosomes. In the fourth step, Tg is hydrolyzed to release free iodothyronines (T3 and T4) and monoand diiodo-tyrosines. The latter are deiodinated in the fifth step to yield iodide, which is reused in the thyrocyte. In the euthyroid state, T4 is produced and released entirely by the thyroid gland, whereas only 20% of the total T3 is produced by the thyroid. Most of the T3 is produced by
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reused in the thyrocyte. In the euthyroid state, T4 is produced and released entirely by the thyroid gland, whereas only 20% of the total T3 is produced by the thyroid. Most of the T3 is produced by peripheral deiodination (removal of 5′-iodine from the outer ring) of T4 in the liver, muscles, kidney, and anterior pituitary, a reaction that is catalyzed by 5′-mono-deiodinase. Some T4 is converted to rT3, the metaboli-cally inactive compound, by deiodination of the inner ring of T4. In conditions such as Graves’ disease, toxic multinodular goi-ter, or a stimulated thyroid gland, the proportion of T3 released from the thyroid may be dramatically elevated. Thyroid hor-mones are transported in serum bound to carrier proteins such as T4-binding globulin, T4-binding prealbumin, and albumin. Only a small fraction (0.02%) of thyroid hormone (T3 and T4) is free (unbound) and is the physiologically active component. T3 is the more potent of the two thyroid hormones, although its circulating
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Surgery_Schwartz. reused in the thyrocyte. In the euthyroid state, T4 is produced and released entirely by the thyroid gland, whereas only 20% of the total T3 is produced by the thyroid. Most of the T3 is produced by peripheral deiodination (removal of 5′-iodine from the outer ring) of T4 in the liver, muscles, kidney, and anterior pituitary, a reaction that is catalyzed by 5′-mono-deiodinase. Some T4 is converted to rT3, the metaboli-cally inactive compound, by deiodination of the inner ring of T4. In conditions such as Graves’ disease, toxic multinodular goi-ter, or a stimulated thyroid gland, the proportion of T3 released from the thyroid may be dramatically elevated. Thyroid hor-mones are transported in serum bound to carrier proteins such as T4-binding globulin, T4-binding prealbumin, and albumin. Only a small fraction (0.02%) of thyroid hormone (T3 and T4) is free (unbound) and is the physiologically active component. T3 is the more potent of the two thyroid hormones, although its circulating
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Only a small fraction (0.02%) of thyroid hormone (T3 and T4) is free (unbound) and is the physiologically active component. T3 is the more potent of the two thyroid hormones, although its circulating plasma level is much lower than that of T4. T3 is less tightly bound to protein in the plasma than T4, and so it enters tissues more readily. T3 is three to four times more active than T4 per unit weight, with a half-life of about 1 day, compared to approximately 7 days for T4.The secretion of thyroid hormone is controlled by the hypothalamic-pituitary-thyroid axis (Fig. 38-9). The hypo-thalamus produces a peptide, the thyrotropin-releasing hor-mone (TRH), which stimulates the pituitary to release TSH or thyrotropin. TRH reaches the pituitary via the portovenous circulation. TSH, a 28-kDa glycopeptide, mediates iodide trap-ping, secretion, and release of thyroid hormones, in addition to increasing the cellularity and vascularity of the thyroid gland. The TSH receptor (TSH-R) belongs to a
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Surgery_Schwartz. Only a small fraction (0.02%) of thyroid hormone (T3 and T4) is free (unbound) and is the physiologically active component. T3 is the more potent of the two thyroid hormones, although its circulating plasma level is much lower than that of T4. T3 is less tightly bound to protein in the plasma than T4, and so it enters tissues more readily. T3 is three to four times more active than T4 per unit weight, with a half-life of about 1 day, compared to approximately 7 days for T4.The secretion of thyroid hormone is controlled by the hypothalamic-pituitary-thyroid axis (Fig. 38-9). The hypo-thalamus produces a peptide, the thyrotropin-releasing hor-mone (TRH), which stimulates the pituitary to release TSH or thyrotropin. TRH reaches the pituitary via the portovenous circulation. TSH, a 28-kDa glycopeptide, mediates iodide trap-ping, secretion, and release of thyroid hormones, in addition to increasing the cellularity and vascularity of the thyroid gland. The TSH receptor (TSH-R) belongs to a
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mediates iodide trap-ping, secretion, and release of thyroid hormones, in addition to increasing the cellularity and vascularity of the thyroid gland. The TSH receptor (TSH-R) belongs to a family of G-protein–coupled receptors that have seven transmembrane-spanning domains and use cyclic adenosine monophosphate in the signal-transduction pathway. TSH secretion by the anterior pituitary is also regulated via a negative feedback loop by T4 and T3. Because the pituitary has the ability to convert T4 to T3, the latter is thought to be more important in this feedback control. T3 also inhibits the release of TRH.The thyroid gland also is capable of autoregulation, which allows it to modify its function independent of TSH. As an adap-tation to low iodide intake, the gland preferentially synthesizes Lower parathyroidUpper parathyroidInt. jugular v.Recurrent laryngeal n.ThyroidInferior thyroid a.Common carotid a. Figure 38-5. Relationship of the parathyroids to the recurrent laryngeal nerve.
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Surgery_Schwartz. mediates iodide trap-ping, secretion, and release of thyroid hormones, in addition to increasing the cellularity and vascularity of the thyroid gland. The TSH receptor (TSH-R) belongs to a family of G-protein–coupled receptors that have seven transmembrane-spanning domains and use cyclic adenosine monophosphate in the signal-transduction pathway. TSH secretion by the anterior pituitary is also regulated via a negative feedback loop by T4 and T3. Because the pituitary has the ability to convert T4 to T3, the latter is thought to be more important in this feedback control. T3 also inhibits the release of TRH.The thyroid gland also is capable of autoregulation, which allows it to modify its function independent of TSH. As an adap-tation to low iodide intake, the gland preferentially synthesizes Lower parathyroidUpper parathyroidInt. jugular v.Recurrent laryngeal n.ThyroidInferior thyroid a.Common carotid a. Figure 38-5. Relationship of the parathyroids to the recurrent laryngeal nerve.
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Lower parathyroidUpper parathyroidInt. jugular v.Recurrent laryngeal n.ThyroidInferior thyroid a.Common carotid a. Figure 38-5. Relationship of the parathyroids to the recurrent laryngeal nerve. a. = artery; v. = vein.Brunicardi_Ch38_p1625-p1704.indd 163001/03/19 11:20 AM 1631THYROID, PARATHYROID, AND ADRENALCHAPTER 38T3 rather than T4, thereby increasing the efficiency of secreted hormone. In situations of iodine excess, iodide transport, per-oxide generation, and synthesis and secretion of thyroid hor-mones are inhibited. Excessively large doses of iodide may lead to initial increased organification, followed by suppression, a phenomenon called the Wolff-Chaikoff effect. Epinephrine and human chorionic gonadotropin hormones stimulate thyroid hormone production. Thus, elevated thyroid hormone levels are found in pregnancy and gynecologic malignancies such as hydatidiform mole. In contrast, glucocorticoids inhibit thyroid hormone production. In severely ill patients, peripheral
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Surgery_Schwartz. Lower parathyroidUpper parathyroidInt. jugular v.Recurrent laryngeal n.ThyroidInferior thyroid a.Common carotid a. Figure 38-5. Relationship of the parathyroids to the recurrent laryngeal nerve. a. = artery; v. = vein.Brunicardi_Ch38_p1625-p1704.indd 163001/03/19 11:20 AM 1631THYROID, PARATHYROID, AND ADRENALCHAPTER 38T3 rather than T4, thereby increasing the efficiency of secreted hormone. In situations of iodine excess, iodide transport, per-oxide generation, and synthesis and secretion of thyroid hor-mones are inhibited. Excessively large doses of iodide may lead to initial increased organification, followed by suppression, a phenomenon called the Wolff-Chaikoff effect. Epinephrine and human chorionic gonadotropin hormones stimulate thyroid hormone production. Thus, elevated thyroid hormone levels are found in pregnancy and gynecologic malignancies such as hydatidiform mole. In contrast, glucocorticoids inhibit thyroid hormone production. In severely ill patients, peripheral
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hormone levels are found in pregnancy and gynecologic malignancies such as hydatidiform mole. In contrast, glucocorticoids inhibit thyroid hormone production. In severely ill patients, peripheral thyroid hormones may be reduced, without a compensatory increase in TSH levels, giving rise to the euthyroid sick syndrome.Thyroid Hormone Function. Free thyroid hormone enters the cell membrane by diffusion or by specific carriers and is car-ried to the nuclear membrane by binding to specific proteins. T4 is deiodinated to T3 and enters the nucleus via active trans-port, where it binds to the thyroid hormone receptor. The T3 receptor is similar to the nuclear receptors for glucocorticoids, mineralocorticoids, estrogens, vitamin D, and retinoic acid. In humans, two types of T3 receptor genes (α and β) are located on chromosomes 3 and 17. Thyroid receptor expression depends on peripheral concentrations of thyroid hormones and is tissue specific—the α form is abundant in the central nervous
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Surgery_Schwartz. hormone levels are found in pregnancy and gynecologic malignancies such as hydatidiform mole. In contrast, glucocorticoids inhibit thyroid hormone production. In severely ill patients, peripheral thyroid hormones may be reduced, without a compensatory increase in TSH levels, giving rise to the euthyroid sick syndrome.Thyroid Hormone Function. Free thyroid hormone enters the cell membrane by diffusion or by specific carriers and is car-ried to the nuclear membrane by binding to specific proteins. T4 is deiodinated to T3 and enters the nucleus via active trans-port, where it binds to the thyroid hormone receptor. The T3 receptor is similar to the nuclear receptors for glucocorticoids, mineralocorticoids, estrogens, vitamin D, and retinoic acid. In humans, two types of T3 receptor genes (α and β) are located on chromosomes 3 and 17. Thyroid receptor expression depends on peripheral concentrations of thyroid hormones and is tissue specific—the α form is abundant in the central nervous
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and β) are located on chromosomes 3 and 17. Thyroid receptor expression depends on peripheral concentrations of thyroid hormones and is tissue specific—the α form is abundant in the central nervous sys-tem, whereas the β form predominates in the liver. Each gene product has a ligand-independent, amino-terminal domain; IIVVIIIIIIIVVITrapezius m.Sternocleidomastoid m.Central neck nodesUpper jugular nodesSubmaxillary nodesParotidMiddle jugular nodesAnterior mediastinalnodesPosteriortriangleLower jugular nodesExternaljugularnodeSternocleido-mastoid m.Spinal accessory n.Jugulodigastric nodeDeep lateral nodesIntercalatednodeTransversecervical chainof nodesDigastric m.Mandibular &submandibularnodesSubmental nodeHyoidInternal jugularchain of nodesStrap muscleSuperior thyroid nodesAnterior superficialcervical nodesSupra-clavicular nodes ABFigure 38-6. A and B. Lymph nodes in the neck can be divided into six regions. Upper mediastinal nodes constitute level VII. m. = muscle; n. =
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Surgery_Schwartz. and β) are located on chromosomes 3 and 17. Thyroid receptor expression depends on peripheral concentrations of thyroid hormones and is tissue specific—the α form is abundant in the central nervous sys-tem, whereas the β form predominates in the liver. Each gene product has a ligand-independent, amino-terminal domain; IIVVIIIIIIIVVITrapezius m.Sternocleidomastoid m.Central neck nodesUpper jugular nodesSubmaxillary nodesParotidMiddle jugular nodesAnterior mediastinalnodesPosteriortriangleLower jugular nodesExternaljugularnodeSternocleido-mastoid m.Spinal accessory n.Jugulodigastric nodeDeep lateral nodesIntercalatednodeTransversecervical chainof nodesDigastric m.Mandibular &submandibularnodesSubmental nodeHyoidInternal jugularchain of nodesStrap muscleSuperior thyroid nodesAnterior superficialcervical nodesSupra-clavicular nodes ABFigure 38-6. A and B. Lymph nodes in the neck can be divided into six regions. Upper mediastinal nodes constitute level VII. m. = muscle; n. =
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superficialcervical nodesSupra-clavicular nodes ABFigure 38-6. A and B. Lymph nodes in the neck can be divided into six regions. Upper mediastinal nodes constitute level VII. m. = muscle; n. = nerve.Brunicardi_Ch38_p1625-p1704.indd 163101/03/19 11:20 AM 1632SPECIFIC CONSIDERATIONSPART IIa ligand-binding, carboxy-terminal domain; and centrally located DNA-binding regions. Binding of thyroid hormone leads to the transcription and translation of specific hormone-responsive genes.Thyroid hormones affect almost every system in the body. They are important for fetal brain development and skeletal mat-uration. T3 increases oxygen consumption, basal metabolic rate, and heat production by stimulation of Na+/K+ ATPase in various tissues. It also has positive inotropic and chronotropic effects on the heart by increasing transcription of the Ca2+ ATPase in the sarcoplasmic reticulum and increasing levels of β-adrenergic receptors and concentration of G proteins. Myocardial α recep-tors are
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Surgery_Schwartz. superficialcervical nodesSupra-clavicular nodes ABFigure 38-6. A and B. Lymph nodes in the neck can be divided into six regions. Upper mediastinal nodes constitute level VII. m. = muscle; n. = nerve.Brunicardi_Ch38_p1625-p1704.indd 163101/03/19 11:20 AM 1632SPECIFIC CONSIDERATIONSPART IIa ligand-binding, carboxy-terminal domain; and centrally located DNA-binding regions. Binding of thyroid hormone leads to the transcription and translation of specific hormone-responsive genes.Thyroid hormones affect almost every system in the body. They are important for fetal brain development and skeletal mat-uration. T3 increases oxygen consumption, basal metabolic rate, and heat production by stimulation of Na+/K+ ATPase in various tissues. It also has positive inotropic and chronotropic effects on the heart by increasing transcription of the Ca2+ ATPase in the sarcoplasmic reticulum and increasing levels of β-adrenergic receptors and concentration of G proteins. Myocardial α recep-tors are
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Surgery_Schwartz_10754
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on the heart by increasing transcription of the Ca2+ ATPase in the sarcoplasmic reticulum and increasing levels of β-adrenergic receptors and concentration of G proteins. Myocardial α recep-tors are decreased, and actions of catecholamines are amplified. Thyroid hormones are responsible for maintaining the normal hypoxic and hypercapnic drive in the respiratory center of the brain. They also increase gastrointestinal (GI) motility, leading to diarrhea in hyperthyroidism and constipation in hypothyroid-ism. Thyroid hormones also increase bone and protein turnover H2O2 GenerationIodinationDifferentiationGrowthHormone synthesisCREBCREMPAX-8TTF-1TTF-2XXXXXIP3PKCDAGPKAPIP2ATPcAMPPLCGqGSGIACTSHRTSHIGF-1 RIGF-1 NISIodide uptakeMITDITT3T4T3T4HydrolysisNADP+NADPHH2O2H2O22O2TPOTgTgTPOI or HOICouplingOrganificationMITDITMITDITT3T4DehalogenaseI–I–Figure 38-8. Thyroid follicular cell showing the major signaling pathways involved in thyroid cell growth and function and key steps in thy-roid hormone
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Surgery_Schwartz. on the heart by increasing transcription of the Ca2+ ATPase in the sarcoplasmic reticulum and increasing levels of β-adrenergic receptors and concentration of G proteins. Myocardial α recep-tors are decreased, and actions of catecholamines are amplified. Thyroid hormones are responsible for maintaining the normal hypoxic and hypercapnic drive in the respiratory center of the brain. They also increase gastrointestinal (GI) motility, leading to diarrhea in hyperthyroidism and constipation in hypothyroid-ism. Thyroid hormones also increase bone and protein turnover H2O2 GenerationIodinationDifferentiationGrowthHormone synthesisCREBCREMPAX-8TTF-1TTF-2XXXXXIP3PKCDAGPKAPIP2ATPcAMPPLCGqGSGIACTSHRTSHIGF-1 RIGF-1 NISIodide uptakeMITDITT3T4T3T4HydrolysisNADP+NADPHH2O2H2O22O2TPOTgTgTPOI or HOICouplingOrganificationMITDITMITDITT3T4DehalogenaseI–I–Figure 38-8. Thyroid follicular cell showing the major signaling pathways involved in thyroid cell growth and function and key steps in thy-roid hormone
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38-8. Thyroid follicular cell showing the major signaling pathways involved in thyroid cell growth and function and key steps in thy-roid hormone synthesis. The basal membrane of the cell in contact with the circulation and its apical surface contact the thyroid follicle. Thy-roid hormone synthesis is initiated by the binding of thyroid-stimulating hormone (TSH) to the TSH receptor (TSHR), a G-protein–coupled transmembrane receptor, on the basal membrane. Activation leads to an increase in cyclic adenosine monophosphate (cAMP), phosphorylation of protein kinase A (PKA), and activation of target cytosolic and nuclear proteins. The protein kinase C (PKC) pathway is stimulated at higher doses of TSH. Iodide is actively transported into the cell via the Na/I symporter (NIS) and flows down an electrical gradient to the apical membrane. There, thyroid peroxidase (TPO) oxidizes iodide and iodinated tyrosyl residues on thyroglobulin (Tg) in the presence of peroxide (H2O2). Monoand
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Surgery_Schwartz. 38-8. Thyroid follicular cell showing the major signaling pathways involved in thyroid cell growth and function and key steps in thy-roid hormone synthesis. The basal membrane of the cell in contact with the circulation and its apical surface contact the thyroid follicle. Thy-roid hormone synthesis is initiated by the binding of thyroid-stimulating hormone (TSH) to the TSH receptor (TSHR), a G-protein–coupled transmembrane receptor, on the basal membrane. Activation leads to an increase in cyclic adenosine monophosphate (cAMP), phosphorylation of protein kinase A (PKA), and activation of target cytosolic and nuclear proteins. The protein kinase C (PKC) pathway is stimulated at higher doses of TSH. Iodide is actively transported into the cell via the Na/I symporter (NIS) and flows down an electrical gradient to the apical membrane. There, thyroid peroxidase (TPO) oxidizes iodide and iodinated tyrosyl residues on thyroglobulin (Tg) in the presence of peroxide (H2O2). Monoand
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Surgery_Schwartz_10756
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down an electrical gradient to the apical membrane. There, thyroid peroxidase (TPO) oxidizes iodide and iodinated tyrosyl residues on thyroglobulin (Tg) in the presence of peroxide (H2O2). Monoand diiodotyrosyl (MIT, DIT) residues are also coupled to form T4 and T3 by TPO. Thyroglobulin carrying T4 and T3 is then internalized by pinocytosis and digested in lysosomes. Thyroid hormone is released into the circulation, while MIT and DIT are deiodinated and recycled. ATP = adenosine triphosphate; CREB = cAMP response element binding protein; CREM = cAMP response element modulator; DAG = diacylglycerol; IGF-1 = insulin-like growth factor 1; IP3 = inositol-3-phosphate; NADP+ = nicotinamide adenine dinucleotide phosphate, oxidized form; NADPH = nicotinamide adenine dinucleotide phosphate; PIP2 = phosphatidylinositol; PLC = phospholipase C; T3 = 3,5′,3-triiodothyronine; T4 = thyroxine. (Reproduced with permission from Kopp P: Pendred’s syndrome and genetic defects in thyroid hormone
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Surgery_Schwartz. down an electrical gradient to the apical membrane. There, thyroid peroxidase (TPO) oxidizes iodide and iodinated tyrosyl residues on thyroglobulin (Tg) in the presence of peroxide (H2O2). Monoand diiodotyrosyl (MIT, DIT) residues are also coupled to form T4 and T3 by TPO. Thyroglobulin carrying T4 and T3 is then internalized by pinocytosis and digested in lysosomes. Thyroid hormone is released into the circulation, while MIT and DIT are deiodinated and recycled. ATP = adenosine triphosphate; CREB = cAMP response element binding protein; CREM = cAMP response element modulator; DAG = diacylglycerol; IGF-1 = insulin-like growth factor 1; IP3 = inositol-3-phosphate; NADP+ = nicotinamide adenine dinucleotide phosphate, oxidized form; NADPH = nicotinamide adenine dinucleotide phosphate; PIP2 = phosphatidylinositol; PLC = phospholipase C; T3 = 3,5′,3-triiodothyronine; T4 = thyroxine. (Reproduced with permission from Kopp P: Pendred’s syndrome and genetic defects in thyroid hormone
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PIP2 = phosphatidylinositol; PLC = phospholipase C; T3 = 3,5′,3-triiodothyronine; T4 = thyroxine. (Reproduced with permission from Kopp P: Pendred’s syndrome and genetic defects in thyroid hormone synthesis, Rev Endocr Metab Disord. 2000 Jan;1(1-2):109-121.)Figure 38-7. Normal thyroid histology—follicular cells surround colloid.Brunicardi_Ch38_p1625-p1704.indd 163201/03/19 11:20 AM 1633THYROID, PARATHYROID, AND ADRENALCHAPTER 38and the speed of muscle contraction and relaxation. They also increase glycogenolysis, hepatic gluconeogenesis, intestinal glucose absorption, and cholesterol synthesis and degradation.Evaluation of Patients With Thyroid DiseaseTests of Thyroid Function. A multitude of different tests are available to evaluate thyroid function. No single test is sufficient to assess thyroid function in all situations, and the results must be interpreted in the context of the patient’s clinical condition. TSH is the only test necessary in most patients with thyroid nodules
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Surgery_Schwartz. PIP2 = phosphatidylinositol; PLC = phospholipase C; T3 = 3,5′,3-triiodothyronine; T4 = thyroxine. (Reproduced with permission from Kopp P: Pendred’s syndrome and genetic defects in thyroid hormone synthesis, Rev Endocr Metab Disord. 2000 Jan;1(1-2):109-121.)Figure 38-7. Normal thyroid histology—follicular cells surround colloid.Brunicardi_Ch38_p1625-p1704.indd 163201/03/19 11:20 AM 1633THYROID, PARATHYROID, AND ADRENALCHAPTER 38and the speed of muscle contraction and relaxation. They also increase glycogenolysis, hepatic gluconeogenesis, intestinal glucose absorption, and cholesterol synthesis and degradation.Evaluation of Patients With Thyroid DiseaseTests of Thyroid Function. A multitude of different tests are available to evaluate thyroid function. No single test is sufficient to assess thyroid function in all situations, and the results must be interpreted in the context of the patient’s clinical condition. TSH is the only test necessary in most patients with thyroid nodules
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Surgery_Schwartz_10758
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assess thyroid function in all situations, and the results must be interpreted in the context of the patient’s clinical condition. TSH is the only test necessary in most patients with thyroid nodules that clinically appear to be euthyroid.Serum Thyroid-Stimulating Hormone (Normal 0.5–5 μU/mL) The tests for serum TSH are based on the following principle: monoclonal TSH antibodies are bound to a solid matrix and bind serum TSH. A second monoclonal antibody binds to a separate epitope on TSH and is labeled with radioisotope, enzyme, or fluorescent tag. Therefore, the amount of serum TSH is propor-tional to the amount of bound secondary antibody (immunomet-ric assay). Serum TSH levels reflect the ability of the anterior pituitary to detect free T4 levels. There is an inverse relation-ship between the free T4 level and the logarithm of the TSH concentration—small changes in free T4 lead to a large shift in TSH levels. The ultrasensitive TSH assay has become the most sensitive and specific
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Surgery_Schwartz. assess thyroid function in all situations, and the results must be interpreted in the context of the patient’s clinical condition. TSH is the only test necessary in most patients with thyroid nodules that clinically appear to be euthyroid.Serum Thyroid-Stimulating Hormone (Normal 0.5–5 μU/mL) The tests for serum TSH are based on the following principle: monoclonal TSH antibodies are bound to a solid matrix and bind serum TSH. A second monoclonal antibody binds to a separate epitope on TSH and is labeled with radioisotope, enzyme, or fluorescent tag. Therefore, the amount of serum TSH is propor-tional to the amount of bound secondary antibody (immunomet-ric assay). Serum TSH levels reflect the ability of the anterior pituitary to detect free T4 levels. There is an inverse relation-ship between the free T4 level and the logarithm of the TSH concentration—small changes in free T4 lead to a large shift in TSH levels. The ultrasensitive TSH assay has become the most sensitive and specific
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the free T4 level and the logarithm of the TSH concentration—small changes in free T4 lead to a large shift in TSH levels. The ultrasensitive TSH assay has become the most sensitive and specific test for the diagnosis of hyperand hypo-thyroidism and for optimizing T4 therapy.Total T4 (Reference Range 55–150 nmol/L) and T3 (Reference Range 1.5–3.5 nmol/L) Total T4 and T3 levels are measured by radioimmunoassay and measure both the free and bound components of the hormones. Total T4 levels reflect the output from the thyroid gland, whereas T3 levels in the nonstimulated thyroid gland are more indicative of peripheral thyroid hor-mone metabolism, and are, therefore, not generally suitable as a general screening test. Total T4 levels are increased not only in hyperthyroid patients, but also in those with elevated Tg levels secondary to pregnancy, estrogen/progesterone use, or congeni-tal diseases. Similarly, total T4 levels decrease in hypothyroidism and in patients with decreased Tg
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Surgery_Schwartz. the free T4 level and the logarithm of the TSH concentration—small changes in free T4 lead to a large shift in TSH levels. The ultrasensitive TSH assay has become the most sensitive and specific test for the diagnosis of hyperand hypo-thyroidism and for optimizing T4 therapy.Total T4 (Reference Range 55–150 nmol/L) and T3 (Reference Range 1.5–3.5 nmol/L) Total T4 and T3 levels are measured by radioimmunoassay and measure both the free and bound components of the hormones. Total T4 levels reflect the output from the thyroid gland, whereas T3 levels in the nonstimulated thyroid gland are more indicative of peripheral thyroid hor-mone metabolism, and are, therefore, not generally suitable as a general screening test. Total T4 levels are increased not only in hyperthyroid patients, but also in those with elevated Tg levels secondary to pregnancy, estrogen/progesterone use, or congeni-tal diseases. Similarly, total T4 levels decrease in hypothyroidism and in patients with decreased Tg
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in those with elevated Tg levels secondary to pregnancy, estrogen/progesterone use, or congeni-tal diseases. Similarly, total T4 levels decrease in hypothyroidism and in patients with decreased Tg levels due to anabolic steroid use and protein-losing disorders like nephrotic syndrome. Indi-viduals with these latter disorders may be euthyroid if their free T4 levels are normal. Measurement of total T3 levels is impor-tant in clinically hyperthyroid patients with normal T4 levels, who may have T3 thyrotoxicosis. As discussed previously in “Thyroid Hormone Synthesis, Secretion, and Transport,” total T3 levels often are increased in early hypothyroidism.Free T4 (Reference Range 12–28 pmol/L) and Free T3 (3–9 pmol/L) These radioimmunoassay-based tests are a sensitive and accurate measurement of biologically active thy-roid hormone. Free T4 estimates are not performed as a routine screening tool in thyroid disease. Use of this test is confined to cases of early hyperthyroidism in which
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Surgery_Schwartz. in those with elevated Tg levels secondary to pregnancy, estrogen/progesterone use, or congeni-tal diseases. Similarly, total T4 levels decrease in hypothyroidism and in patients with decreased Tg levels due to anabolic steroid use and protein-losing disorders like nephrotic syndrome. Indi-viduals with these latter disorders may be euthyroid if their free T4 levels are normal. Measurement of total T3 levels is impor-tant in clinically hyperthyroid patients with normal T4 levels, who may have T3 thyrotoxicosis. As discussed previously in “Thyroid Hormone Synthesis, Secretion, and Transport,” total T3 levels often are increased in early hypothyroidism.Free T4 (Reference Range 12–28 pmol/L) and Free T3 (3–9 pmol/L) These radioimmunoassay-based tests are a sensitive and accurate measurement of biologically active thy-roid hormone. Free T4 estimates are not performed as a routine screening tool in thyroid disease. Use of this test is confined to cases of early hyperthyroidism in which
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of biologically active thy-roid hormone. Free T4 estimates are not performed as a routine screening tool in thyroid disease. Use of this test is confined to cases of early hyperthyroidism in which total T4 levels may be normal but free T4 levels are raised. In patients with end-organ resistance to T4 (Refetoff’s syndrome), T4 levels are increased, but TSH levels usually are normal. Free T3 is most useful in con-firming the diagnosis of early hyperthyroidism, in which levels of free T4 and free T3 rise before total T4 and T3. Free T4 levels may also be measured indirectly using the T3-resin uptake test. If free T4 levels are increased, fewer hormone binding sites are available for binding radiolabeled T3 that has been added to the patient’s serum. Therefore, more T3 binds with an ion-exchange resin, and the T3-resin uptake is increased.Thyrotropin-Releasing Hormone This test is useful to evalu-ate pituitary TSH secretory function and is performed by admin-istering 500 μg of TRH
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Surgery_Schwartz. of biologically active thy-roid hormone. Free T4 estimates are not performed as a routine screening tool in thyroid disease. Use of this test is confined to cases of early hyperthyroidism in which total T4 levels may be normal but free T4 levels are raised. In patients with end-organ resistance to T4 (Refetoff’s syndrome), T4 levels are increased, but TSH levels usually are normal. Free T3 is most useful in con-firming the diagnosis of early hyperthyroidism, in which levels of free T4 and free T3 rise before total T4 and T3. Free T4 levels may also be measured indirectly using the T3-resin uptake test. If free T4 levels are increased, fewer hormone binding sites are available for binding radiolabeled T3 that has been added to the patient’s serum. Therefore, more T3 binds with an ion-exchange resin, and the T3-resin uptake is increased.Thyrotropin-Releasing Hormone This test is useful to evalu-ate pituitary TSH secretory function and is performed by admin-istering 500 μg of TRH
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resin, and the T3-resin uptake is increased.Thyrotropin-Releasing Hormone This test is useful to evalu-ate pituitary TSH secretory function and is performed by admin-istering 500 μg of TRH intravenously and measuring TSH levels after 30 and 60 minutes. In a normal individual, TSH levels should increase at least 6 μIU/mL from the baseline. This test also was previously used to assess patients with borderline hyperthyroidism but has largely been replaced by sensitive TSH assays for this purpose.Thyroid Antibodies Thyroid antibodies include anti-Tg, anti-microsomal, or anti-TPO and thyroid-stimulating immuno-globulin (TSI). Anti-Tg and anti-TPO antibody levels do not determine thyroid function, but rather indicate the underlying disorder, usually an autoimmune thyroiditis. About 80% of patients with Hashimoto’s thyroiditis have elevated thyroid anti-body levels; however, levels may also be increased in patients with Graves’ disease, multinodular goiter, and occasionally, thyroid
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Surgery_Schwartz. resin, and the T3-resin uptake is increased.Thyrotropin-Releasing Hormone This test is useful to evalu-ate pituitary TSH secretory function and is performed by admin-istering 500 μg of TRH intravenously and measuring TSH levels after 30 and 60 minutes. In a normal individual, TSH levels should increase at least 6 μIU/mL from the baseline. This test also was previously used to assess patients with borderline hyperthyroidism but has largely been replaced by sensitive TSH assays for this purpose.Thyroid Antibodies Thyroid antibodies include anti-Tg, anti-microsomal, or anti-TPO and thyroid-stimulating immuno-globulin (TSI). Anti-Tg and anti-TPO antibody levels do not determine thyroid function, but rather indicate the underlying disorder, usually an autoimmune thyroiditis. About 80% of patients with Hashimoto’s thyroiditis have elevated thyroid anti-body levels; however, levels may also be increased in patients with Graves’ disease, multinodular goiter, and occasionally, thyroid
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of patients with Hashimoto’s thyroiditis have elevated thyroid anti-body levels; however, levels may also be increased in patients with Graves’ disease, multinodular goiter, and occasionally, thyroid neoplasms.Serum Thyroglobulin Tg is only made by normal or abnormal thyroid tissue. It normally is not released into the circulation in large amounts but increases dramatically in destructive pro-cesses of the thyroid gland, such as thyroiditis, or overactive states such as Graves’ disease and toxic multinodular goiter. The most important use for serum Tg levels is in monitoring patients with differentiated thyroid cancer for recurrence, partic-ularly after total thyroidectomy and RAI ablation. Elevated anti-Tg antibodies can interfere with the accuracy of serum Tg levels and should always be measured when interpreting Tg levels.ThyroidPortalsystemHypothalamusTRHTissueTSH++T4T4T4T3T3T3––II“Free”Figure 38-9. Hypothalamic-pituitary-thyroid hormone axis. In both the hypothalamus and
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Surgery_Schwartz. of patients with Hashimoto’s thyroiditis have elevated thyroid anti-body levels; however, levels may also be increased in patients with Graves’ disease, multinodular goiter, and occasionally, thyroid neoplasms.Serum Thyroglobulin Tg is only made by normal or abnormal thyroid tissue. It normally is not released into the circulation in large amounts but increases dramatically in destructive pro-cesses of the thyroid gland, such as thyroiditis, or overactive states such as Graves’ disease and toxic multinodular goiter. The most important use for serum Tg levels is in monitoring patients with differentiated thyroid cancer for recurrence, partic-ularly after total thyroidectomy and RAI ablation. Elevated anti-Tg antibodies can interfere with the accuracy of serum Tg levels and should always be measured when interpreting Tg levels.ThyroidPortalsystemHypothalamusTRHTissueTSH++T4T4T4T3T3T3––II“Free”Figure 38-9. Hypothalamic-pituitary-thyroid hormone axis. In both the hypothalamus and
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be measured when interpreting Tg levels.ThyroidPortalsystemHypothalamusTRHTissueTSH++T4T4T4T3T3T3––II“Free”Figure 38-9. Hypothalamic-pituitary-thyroid hormone axis. In both the hypothalamus and pituitary, 3,5′,3-triiodothyronine (T3) is primarily responsible for inhibition of thyrotropin-releasing hor-mone (TRH) and thyroid-stimulating hormone (TSH) secretion. T4 = thyroxine. (Reproduced with permission from Greenspan FS, Gardner D: Basic and Clinical Endocrinology, 6th ed. New York, NY: McGraw-Hill Education; 2001.)Brunicardi_Ch38_p1625-p1704.indd 163301/03/19 11:20 AM 1634SPECIFIC CONSIDERATIONSPART IISerum Calcitonin (0–4 pg/mL Basal) This 32-amino-acid polypeptide is secreted by the C cells and functions to lower serum calcium levels, although in humans, it has only minimal physiologic effects. It is also a sensitive marker of MTC.Thyroid Imaging Radionuclide Imaging Both iodine-123 (123I) and iodine-131 (131I) are used to image the thyroid gland. The former emits low-dose
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Surgery_Schwartz. be measured when interpreting Tg levels.ThyroidPortalsystemHypothalamusTRHTissueTSH++T4T4T4T3T3T3––II“Free”Figure 38-9. Hypothalamic-pituitary-thyroid hormone axis. In both the hypothalamus and pituitary, 3,5′,3-triiodothyronine (T3) is primarily responsible for inhibition of thyrotropin-releasing hor-mone (TRH) and thyroid-stimulating hormone (TSH) secretion. T4 = thyroxine. (Reproduced with permission from Greenspan FS, Gardner D: Basic and Clinical Endocrinology, 6th ed. New York, NY: McGraw-Hill Education; 2001.)Brunicardi_Ch38_p1625-p1704.indd 163301/03/19 11:20 AM 1634SPECIFIC CONSIDERATIONSPART IISerum Calcitonin (0–4 pg/mL Basal) This 32-amino-acid polypeptide is secreted by the C cells and functions to lower serum calcium levels, although in humans, it has only minimal physiologic effects. It is also a sensitive marker of MTC.Thyroid Imaging Radionuclide Imaging Both iodine-123 (123I) and iodine-131 (131I) are used to image the thyroid gland. The former emits low-dose
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effects. It is also a sensitive marker of MTC.Thyroid Imaging Radionuclide Imaging Both iodine-123 (123I) and iodine-131 (131I) are used to image the thyroid gland. The former emits low-dose radiation, has a half-life of 12 to 14 hours, and is used to image lingual thyroids or goiters. In contrast, 131I has a half-life of 8 to 10 days and leads to higher-dose radiation expo-sure. Therefore, this isotope is used to screen and treat patients with differentiated thyroid cancers for metastatic disease. The images obtained by these studies provide information not only about the size and shape of the gland, but also the distribution of functional activity. Areas that trap less radioactivity than the surrounding gland are termed cold (Fig. 38-10), whereas areas that demonstrate increased activity are termed hot. The risk of malignancy is higher in “cold” lesions (20%) compared to “hot” or “warm” lesions (<5%). Technetium Tc 99m pertech-netate (99mTc) is taken up by the thyroid gland and is
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Surgery_Schwartz. effects. It is also a sensitive marker of MTC.Thyroid Imaging Radionuclide Imaging Both iodine-123 (123I) and iodine-131 (131I) are used to image the thyroid gland. The former emits low-dose radiation, has a half-life of 12 to 14 hours, and is used to image lingual thyroids or goiters. In contrast, 131I has a half-life of 8 to 10 days and leads to higher-dose radiation expo-sure. Therefore, this isotope is used to screen and treat patients with differentiated thyroid cancers for metastatic disease. The images obtained by these studies provide information not only about the size and shape of the gland, but also the distribution of functional activity. Areas that trap less radioactivity than the surrounding gland are termed cold (Fig. 38-10), whereas areas that demonstrate increased activity are termed hot. The risk of malignancy is higher in “cold” lesions (20%) compared to “hot” or “warm” lesions (<5%). Technetium Tc 99m pertech-netate (99mTc) is taken up by the thyroid gland and is
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are termed hot. The risk of malignancy is higher in “cold” lesions (20%) compared to “hot” or “warm” lesions (<5%). Technetium Tc 99m pertech-netate (99mTc) is taken up by the thyroid gland and is increas-ingly being used for thyroid evaluation. This isotope is taken up by the mitochondria, but is not organified. It also has the advantage of having a shorter half-life and minimizes radiation exposure. It is particularly sensitive for nodal metastases. More recently, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) combined with computed tomography (CT) is being increasingly used to screen for metastases in patients with thyroid cancer in whom other imaging studies are nega-tive. PET scans are not routinely used in the evaluation of thy-roid nodules; however, they may show clinically occult thyroid lesions. There are several recent reports of rates of malignancy in these lesions ranging from 14% to 63%. These incidentally Figure 38-10. Radioactive iodine scan of the
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Surgery_Schwartz. are termed hot. The risk of malignancy is higher in “cold” lesions (20%) compared to “hot” or “warm” lesions (<5%). Technetium Tc 99m pertech-netate (99mTc) is taken up by the thyroid gland and is increas-ingly being used for thyroid evaluation. This isotope is taken up by the mitochondria, but is not organified. It also has the advantage of having a shorter half-life and minimizes radiation exposure. It is particularly sensitive for nodal metastases. More recently, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) combined with computed tomography (CT) is being increasingly used to screen for metastases in patients with thyroid cancer in whom other imaging studies are nega-tive. PET scans are not routinely used in the evaluation of thy-roid nodules; however, they may show clinically occult thyroid lesions. There are several recent reports of rates of malignancy in these lesions ranging from 14% to 63%. These incidentally Figure 38-10. Radioactive iodine scan of the
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clinically occult thyroid lesions. There are several recent reports of rates of malignancy in these lesions ranging from 14% to 63%. These incidentally Figure 38-10. Radioactive iodine scan of the thyroid, with the arrow showing an area of decreased uptake, a cold nodule.discovered nodules should be worked up by ultrasound and fine-needle aspiration biopsy (FNAB).Ultrasound Ultrasound is an excellent noninvasive and por-table imaging study of the thyroid gland with the added advan-tage of no radiation exposure. It is helpful in the evaluation of thyroid nodules, distinguishing solid from cystic ones, and pro-viding information about size and multicentricity. In addition, characteristics such as echotexture, shape, borders and presence of calcifications, and vascularity can provide useful information regarding risk of malignancy. Ultrasound is also especially help-ful for assessing cervical lymphadenopathy (Fig. 38-11) and to guide FNAB. An experienced ultrasonographer is necessary for
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Surgery_Schwartz. clinically occult thyroid lesions. There are several recent reports of rates of malignancy in these lesions ranging from 14% to 63%. These incidentally Figure 38-10. Radioactive iodine scan of the thyroid, with the arrow showing an area of decreased uptake, a cold nodule.discovered nodules should be worked up by ultrasound and fine-needle aspiration biopsy (FNAB).Ultrasound Ultrasound is an excellent noninvasive and por-table imaging study of the thyroid gland with the added advan-tage of no radiation exposure. It is helpful in the evaluation of thyroid nodules, distinguishing solid from cystic ones, and pro-viding information about size and multicentricity. In addition, characteristics such as echotexture, shape, borders and presence of calcifications, and vascularity can provide useful information regarding risk of malignancy. Ultrasound is also especially help-ful for assessing cervical lymphadenopathy (Fig. 38-11) and to guide FNAB. An experienced ultrasonographer is necessary for
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regarding risk of malignancy. Ultrasound is also especially help-ful for assessing cervical lymphadenopathy (Fig. 38-11) and to guide FNAB. An experienced ultrasonographer is necessary for the best results.Computed Tomography/Magnetic Resonance Imaging Scan CT and magnetic resonance imaging (MRI) studies provide excellent imaging of the thyroid gland and adjacent nodes and are particularly useful in evaluating the extent of large, fixed, or substernal goiters (which cannot be evaluated by ultrasound) and their relationship to the airway and vascular structures. Noncontrast CT scans should be obtained for patients who are likely to require subsequent RAI therapy. If contrast is necessary, therapy needs to be delayed by several months. Combined PET-CT scans are increasingly being used for Tg-positive, RAI-negative tumors.Benign Thyroid DisordersHyperthyroidism. The clinical manifestations of hyperthy-roidism result from an excess of circulating thyroid hormone. Hyperthyroidism may arise
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Surgery_Schwartz. regarding risk of malignancy. Ultrasound is also especially help-ful for assessing cervical lymphadenopathy (Fig. 38-11) and to guide FNAB. An experienced ultrasonographer is necessary for the best results.Computed Tomography/Magnetic Resonance Imaging Scan CT and magnetic resonance imaging (MRI) studies provide excellent imaging of the thyroid gland and adjacent nodes and are particularly useful in evaluating the extent of large, fixed, or substernal goiters (which cannot be evaluated by ultrasound) and their relationship to the airway and vascular structures. Noncontrast CT scans should be obtained for patients who are likely to require subsequent RAI therapy. If contrast is necessary, therapy needs to be delayed by several months. Combined PET-CT scans are increasingly being used for Tg-positive, RAI-negative tumors.Benign Thyroid DisordersHyperthyroidism. The clinical manifestations of hyperthy-roidism result from an excess of circulating thyroid hormone. Hyperthyroidism may arise
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RAI-negative tumors.Benign Thyroid DisordersHyperthyroidism. The clinical manifestations of hyperthy-roidism result from an excess of circulating thyroid hormone. Hyperthyroidism may arise from a number of conditions that are listed in Table 38-1. It is important to distinguish disorders such as Graves’ disease and toxic nodular goiters that result from increased production of thyroid hormone from those dis-orders that lead to a release of stored hormone from injury to the thyroid gland (thyroiditis) or from other nonthyroid gland–related conditions. The former disorders lead to an increase in RAI uptake (RAIU), whereas the latter group is characterized by low RAIU. Of these disorders, Graves’ disease, toxic mul-tinodular goiter, and solitary toxic nodule are most relevant to the surgeon.Diffuse Toxic Goiter (Graves’ Disease) Although originally described by the Welsh physician Caleb Parry in a posthumous article in 1825, this disorder is known as Graves’ disease after Robert Graves,
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Surgery_Schwartz. RAI-negative tumors.Benign Thyroid DisordersHyperthyroidism. The clinical manifestations of hyperthy-roidism result from an excess of circulating thyroid hormone. Hyperthyroidism may arise from a number of conditions that are listed in Table 38-1. It is important to distinguish disorders such as Graves’ disease and toxic nodular goiters that result from increased production of thyroid hormone from those dis-orders that lead to a release of stored hormone from injury to the thyroid gland (thyroiditis) or from other nonthyroid gland–related conditions. The former disorders lead to an increase in RAI uptake (RAIU), whereas the latter group is characterized by low RAIU. Of these disorders, Graves’ disease, toxic mul-tinodular goiter, and solitary toxic nodule are most relevant to the surgeon.Diffuse Toxic Goiter (Graves’ Disease) Although originally described by the Welsh physician Caleb Parry in a posthumous article in 1825, this disorder is known as Graves’ disease after Robert Graves,
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Toxic Goiter (Graves’ Disease) Although originally described by the Welsh physician Caleb Parry in a posthumous article in 1825, this disorder is known as Graves’ disease after Robert Graves, an Irish physician who described three patients in 1835. Graves’ disease is by far the most common cause of hyperthyroidism in North America, accounting for 60% to 80% of cases. It is an autoimmune disease with a strong famil-ial predisposition, female preponderance (5:1), and peak inci-dence between the ages of 40 and 60 years. Graves’ disease is characterized by thyrotoxicosis, diffuse goiter, and extrathy-roidal conditions including ophthalmopathy, dermopathy (pre-tibial myxedema), thyroid acropachy, gynecomastia, and other manifestations.Etiology, Pathogenesis, and Pathology. The exact etiology of the initiation of the autoimmune process in Graves’ disease is not known. However, conditions such as the postpartum state, iodine excess, lithium therapy, and bacterial and viral infections have
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Surgery_Schwartz. Toxic Goiter (Graves’ Disease) Although originally described by the Welsh physician Caleb Parry in a posthumous article in 1825, this disorder is known as Graves’ disease after Robert Graves, an Irish physician who described three patients in 1835. Graves’ disease is by far the most common cause of hyperthyroidism in North America, accounting for 60% to 80% of cases. It is an autoimmune disease with a strong famil-ial predisposition, female preponderance (5:1), and peak inci-dence between the ages of 40 and 60 years. Graves’ disease is characterized by thyrotoxicosis, diffuse goiter, and extrathy-roidal conditions including ophthalmopathy, dermopathy (pre-tibial myxedema), thyroid acropachy, gynecomastia, and other manifestations.Etiology, Pathogenesis, and Pathology. The exact etiology of the initiation of the autoimmune process in Graves’ disease is not known. However, conditions such as the postpartum state, iodine excess, lithium therapy, and bacterial and viral infections have
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of the initiation of the autoimmune process in Graves’ disease is not known. However, conditions such as the postpartum state, iodine excess, lithium therapy, and bacterial and viral infections have been suggested as possible triggers. Genetic factors also play a role, as haplotyping studies indicate that Graves’ disease is associated with certain human leukocyte antigen (HLA) hap-lotypes, including HLA-B8, HLA-DR3, and HLADQA1*0501 in Caucasian patients, whereas HLA-DRB1*0701 is protective Brunicardi_Ch38_p1625-p1704.indd 163401/03/19 11:20 AM 1635THYROID, PARATHYROID, AND ADRENALCHAPTER 38against it. Polymorphisms of the cytotoxic T-lymphocyte anti-gen 4 (CTLA-4) gene also have been associated with Graves’ disease development. CD40 has also been recognized as a Graves’ susceptibility gene. It has an important role in B-cell function and its upregulation leads to a lower threshold for B-cell activation. It can also lead to enhanced IL-6 secretion and activation of T-cells in
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Surgery_Schwartz. of the initiation of the autoimmune process in Graves’ disease is not known. However, conditions such as the postpartum state, iodine excess, lithium therapy, and bacterial and viral infections have been suggested as possible triggers. Genetic factors also play a role, as haplotyping studies indicate that Graves’ disease is associated with certain human leukocyte antigen (HLA) hap-lotypes, including HLA-B8, HLA-DR3, and HLADQA1*0501 in Caucasian patients, whereas HLA-DRB1*0701 is protective Brunicardi_Ch38_p1625-p1704.indd 163401/03/19 11:20 AM 1635THYROID, PARATHYROID, AND ADRENALCHAPTER 38against it. Polymorphisms of the cytotoxic T-lymphocyte anti-gen 4 (CTLA-4) gene also have been associated with Graves’ disease development. CD40 has also been recognized as a Graves’ susceptibility gene. It has an important role in B-cell function and its upregulation leads to a lower threshold for B-cell activation. It can also lead to enhanced IL-6 secretion and activation of T-cells in
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gene. It has an important role in B-cell function and its upregulation leads to a lower threshold for B-cell activation. It can also lead to enhanced IL-6 secretion and activation of T-cells in thyrocytes leading to a local inflam-matory response. Other susceptibility genes include PTPN22 (encodes the lymphoid tyrosine phosphatase) and CD25, which encodes for the interleukin-2 receptor α-chain (IL-2Rα).3 Once initiated, the inflammatory process causes sensitized T-helper lymphocytes to stimulate B lymphocytes, which produce anti-bodies directed against the thyroid hormone receptor. TSIs or antibodies that stimulate the TSH-R, as well as TSH-binding inhibiting immunoglobulins or antibodies, have been described. The thyroid-stimulating antibodies stimulate the thyrocytes to grow and synthesize excess thyroid hormone, which is a hall-mark of Graves’ disease. Graves’ disease also is associated with other autoimmune conditions such as type 1 diabetes mellitus, Addison’s disease, pernicious
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Surgery_Schwartz. gene. It has an important role in B-cell function and its upregulation leads to a lower threshold for B-cell activation. It can also lead to enhanced IL-6 secretion and activation of T-cells in thyrocytes leading to a local inflam-matory response. Other susceptibility genes include PTPN22 (encodes the lymphoid tyrosine phosphatase) and CD25, which encodes for the interleukin-2 receptor α-chain (IL-2Rα).3 Once initiated, the inflammatory process causes sensitized T-helper lymphocytes to stimulate B lymphocytes, which produce anti-bodies directed against the thyroid hormone receptor. TSIs or antibodies that stimulate the TSH-R, as well as TSH-binding inhibiting immunoglobulins or antibodies, have been described. The thyroid-stimulating antibodies stimulate the thyrocytes to grow and synthesize excess thyroid hormone, which is a hall-mark of Graves’ disease. Graves’ disease also is associated with other autoimmune conditions such as type 1 diabetes mellitus, Addison’s disease, pernicious
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excess thyroid hormone, which is a hall-mark of Graves’ disease. Graves’ disease also is associated with other autoimmune conditions such as type 1 diabetes mellitus, Addison’s disease, pernicious anemia, and myasthenia gravis.Macroscopically, the thyroid gland in patients with Graves’ disease is diffusely and smoothly enlarged, with a concomitant increase in vascularity. Microscopically, the gland is hyperplastic, and the epithelium is columnar with minimal colloid present. The nuclei exhibit mitosis, and papillary pro-jections of hyperplastic epithelium are common. There may be aggregates of lymphoid tissue, and vascularity is markedly increased.Clinical Features. The clinical manifestations of Graves’ disease can be divided into those related to hyperthyroidism and those specific to Graves’ disease. Hyperthyroid symp-toms include heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake. Symptoms of increased adrenergic stimulation include
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Surgery_Schwartz. excess thyroid hormone, which is a hall-mark of Graves’ disease. Graves’ disease also is associated with other autoimmune conditions such as type 1 diabetes mellitus, Addison’s disease, pernicious anemia, and myasthenia gravis.Macroscopically, the thyroid gland in patients with Graves’ disease is diffusely and smoothly enlarged, with a concomitant increase in vascularity. Microscopically, the gland is hyperplastic, and the epithelium is columnar with minimal colloid present. The nuclei exhibit mitosis, and papillary pro-jections of hyperplastic epithelium are common. There may be aggregates of lymphoid tissue, and vascularity is markedly increased.Clinical Features. The clinical manifestations of Graves’ disease can be divided into those related to hyperthyroidism and those specific to Graves’ disease. Hyperthyroid symp-toms include heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake. Symptoms of increased adrenergic stimulation include
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Graves’ disease. Hyperthyroid symp-toms include heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake. Symptoms of increased adrenergic stimulation include palpitations, nervous-ness, fatigue, emotional lability, hyperkinesis, and tremors. The most common GI symptoms include increased frequency of bowel movements and diarrhea. Female patients often develop amenorrhea, decreased fertility, and an increased incidence of miscarriages. Children experience rapid growth with early bone maturation, whereas older patients may present with cardiovas-cular complications such as atrial fibrillation and congestive heart failure.On physical examination, weight loss and facial flush-ing may be evident. The skin is warm and moist, and African American patients often note darkening of their skin. Tachycar-dia or atrial fibrillation is present, with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse
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Surgery_Schwartz. Graves’ disease. Hyperthyroid symp-toms include heat intolerance, increased sweating and thirst, and weight loss despite adequate caloric intake. Symptoms of increased adrenergic stimulation include palpitations, nervous-ness, fatigue, emotional lability, hyperkinesis, and tremors. The most common GI symptoms include increased frequency of bowel movements and diarrhea. Female patients often develop amenorrhea, decreased fertility, and an increased incidence of miscarriages. Children experience rapid growth with early bone maturation, whereas older patients may present with cardiovas-cular complications such as atrial fibrillation and congestive heart failure.On physical examination, weight loss and facial flush-ing may be evident. The skin is warm and moist, and African American patients often note darkening of their skin. Tachycar-dia or atrial fibrillation is present, with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse
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note darkening of their skin. Tachycar-dia or atrial fibrillation is present, with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse wave (collapsing pulse). A fine tremor, muscle wasting, and proximal muscle group weakness with hyperactive tendon reflexes often are present.Approximately 50% of patients with Graves’ disease also develop clinically evident ophthalmopathy, and dermopathy occurs in 1% to 2% of patients. It is characterized by deposi-tion of glycosaminoglycans, leading to thickened skin in the pretibial region and dorsum of the foot (Fig. 38-12). Eye symp-toms include lid lag (von Graefe’s sign), spasm of the upper eyelid revealing the sclera above the corneoscleral limbus (Dal-rymple’s sign), and a prominent stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion (chemosis), proptosis, limitation of upward and lateral gaze (from
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Surgery_Schwartz. note darkening of their skin. Tachycar-dia or atrial fibrillation is present, with cutaneous vasodilation leading to a widening of the pulse pressure and a rapid falloff in the transmitted pulse wave (collapsing pulse). A fine tremor, muscle wasting, and proximal muscle group weakness with hyperactive tendon reflexes often are present.Approximately 50% of patients with Graves’ disease also develop clinically evident ophthalmopathy, and dermopathy occurs in 1% to 2% of patients. It is characterized by deposi-tion of glycosaminoglycans, leading to thickened skin in the pretibial region and dorsum of the foot (Fig. 38-12). Eye symp-toms include lid lag (von Graefe’s sign), spasm of the upper eyelid revealing the sclera above the corneoscleral limbus (Dal-rymple’s sign), and a prominent stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion (chemosis), proptosis, limitation of upward and lateral gaze (from
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stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion (chemosis), proptosis, limitation of upward and lateral gaze (from involvement of the inferior and medial rectus muscles, respectively), keratitis, and even blindness due to optic nerve involvement. The etiology of Graves’ ophthalmopathy is not completely known; however, Figure 38-11. Thyroid ultrasound showing a lymph node (arrow) along the carotid artery.Table 38-1Differential diagnosis of hyperthyroidismINCREASED HORMONE SYNTHESIS (INCREASED RAIU)RELEASE OF PREFORMED HORMONE (DECREASED RAIU)Graves’ disease (diffuse toxic goiter)Toxic multinodular goiterToxic adenomaDrug induced—amiodarone, iodineThyroid cancerStruma ovariiHydatidiform moleTSH-secreting pituitary adenomaThyroiditis—acute phase of Hashimoto’s thyroiditis, subacute thyroiditisFactitious (iatrogenic) thyrotoxicosis“Hamburger thyrotoxicosis”RAIU = radioactive iodine uptake; TSH =
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Surgery_Schwartz. stare, due to catecholamine excess. True infiltrative eye disease results in periorbital edema, conjunctival swelling and congestion (chemosis), proptosis, limitation of upward and lateral gaze (from involvement of the inferior and medial rectus muscles, respectively), keratitis, and even blindness due to optic nerve involvement. The etiology of Graves’ ophthalmopathy is not completely known; however, Figure 38-11. Thyroid ultrasound showing a lymph node (arrow) along the carotid artery.Table 38-1Differential diagnosis of hyperthyroidismINCREASED HORMONE SYNTHESIS (INCREASED RAIU)RELEASE OF PREFORMED HORMONE (DECREASED RAIU)Graves’ disease (diffuse toxic goiter)Toxic multinodular goiterToxic adenomaDrug induced—amiodarone, iodineThyroid cancerStruma ovariiHydatidiform moleTSH-secreting pituitary adenomaThyroiditis—acute phase of Hashimoto’s thyroiditis, subacute thyroiditisFactitious (iatrogenic) thyrotoxicosis“Hamburger thyrotoxicosis”RAIU = radioactive iodine uptake; TSH =
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pituitary adenomaThyroiditis—acute phase of Hashimoto’s thyroiditis, subacute thyroiditisFactitious (iatrogenic) thyrotoxicosis“Hamburger thyrotoxicosis”RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163501/03/19 11:20 AM 1636SPECIFIC CONSIDERATIONSPART IIorbital fibroblasts and muscles are thought to share a common antigen, the TSH-R. Ophthalmopathy is thought to result from inflammation caused by cytokines released from sensitized killer T lymphocytes and cytotoxic antibodies. Gynecomas-tia is common in young men. Rare bony involvement leads to subperiosteal bone formation and swelling in the metacarpals (thyroid acropachy). Onycholysis, or separation of fingernails from their beds, is a commonly observed finding. On physical examination, the thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. There may be an overlying bruit or thrill over the thyroid gland and a loud venous
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Surgery_Schwartz. pituitary adenomaThyroiditis—acute phase of Hashimoto’s thyroiditis, subacute thyroiditisFactitious (iatrogenic) thyrotoxicosis“Hamburger thyrotoxicosis”RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163501/03/19 11:20 AM 1636SPECIFIC CONSIDERATIONSPART IIorbital fibroblasts and muscles are thought to share a common antigen, the TSH-R. Ophthalmopathy is thought to result from inflammation caused by cytokines released from sensitized killer T lymphocytes and cytotoxic antibodies. Gynecomas-tia is common in young men. Rare bony involvement leads to subperiosteal bone formation and swelling in the metacarpals (thyroid acropachy). Onycholysis, or separation of fingernails from their beds, is a commonly observed finding. On physical examination, the thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. There may be an overlying bruit or thrill over the thyroid gland and a loud venous
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the thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. There may be an overlying bruit or thrill over the thyroid gland and a loud venous hum in the supraclavicular space.Diagnostic Tests. The diagnosis of hyperthyroidism is made by a suppressed TSH with or without an elevated free T4 or T3 level. If eye signs are present, other tests are generally not needed. However, in the absence of eye findings, an 123I uptake and scan should be performed. An elevated uptake, with a dif-fusely enlarged gland, confirms the diagnosis of Graves’ disease and helps to differentiate it from other causes of hyperthyroid-ism. Technetium scintigraphy (using pertechnetate, which is trapped by the thyroid, but not organified) can also be used to determine etiology. While technetium scans result in low range of normal uptake and high background activity, total-body radi-ation exposure is less than that of 123I scans. If free T4 levels are normal, free T3
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Surgery_Schwartz. the thyroid usually is diffusely and symmetrically enlarged, as evidenced by an enlarged pyramidal lobe. There may be an overlying bruit or thrill over the thyroid gland and a loud venous hum in the supraclavicular space.Diagnostic Tests. The diagnosis of hyperthyroidism is made by a suppressed TSH with or without an elevated free T4 or T3 level. If eye signs are present, other tests are generally not needed. However, in the absence of eye findings, an 123I uptake and scan should be performed. An elevated uptake, with a dif-fusely enlarged gland, confirms the diagnosis of Graves’ disease and helps to differentiate it from other causes of hyperthyroid-ism. Technetium scintigraphy (using pertechnetate, which is trapped by the thyroid, but not organified) can also be used to determine etiology. While technetium scans result in low range of normal uptake and high background activity, total-body radi-ation exposure is less than that of 123I scans. If free T4 levels are normal, free T3
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While technetium scans result in low range of normal uptake and high background activity, total-body radi-ation exposure is less than that of 123I scans. If free T4 levels are normal, free T3 levels should be determined, as they often are elevated in early Graves’ disease or toxic nodules (T3 toxi-cosis). Anti-Tg and anti-TPO antibodies are elevated in up to 75% of patients but are not specific. Elevated TSH-R or thyroidstimulating antibodies (TSAb) are diagnostic of Graves’ disease and are increased in about 90% of patients. CT or MRI scans of the orbits are useful in evaluating Graves’ ophthalmopathy.Treatment. Graves’ disease may be treated by any of three treatment modalities: antithyroid drugs, thyroid ablation with radioactive 131I, and thyroidectomy. The choice of treatment depends on several factors, as discussed in the following sections.Antithyroid Drugs Antithyroid medications generally are administered in preparation for RAI ablation or surgery. The drugs commonly used are
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Surgery_Schwartz. While technetium scans result in low range of normal uptake and high background activity, total-body radi-ation exposure is less than that of 123I scans. If free T4 levels are normal, free T3 levels should be determined, as they often are elevated in early Graves’ disease or toxic nodules (T3 toxi-cosis). Anti-Tg and anti-TPO antibodies are elevated in up to 75% of patients but are not specific. Elevated TSH-R or thyroidstimulating antibodies (TSAb) are diagnostic of Graves’ disease and are increased in about 90% of patients. CT or MRI scans of the orbits are useful in evaluating Graves’ ophthalmopathy.Treatment. Graves’ disease may be treated by any of three treatment modalities: antithyroid drugs, thyroid ablation with radioactive 131I, and thyroidectomy. The choice of treatment depends on several factors, as discussed in the following sections.Antithyroid Drugs Antithyroid medications generally are administered in preparation for RAI ablation or surgery. The drugs commonly used are
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on several factors, as discussed in the following sections.Antithyroid Drugs Antithyroid medications generally are administered in preparation for RAI ablation or surgery. The drugs commonly used are propylthiouracil (PTU, 100 to 300 mg three times daily) and methimazole (10 to 30 mg three times daily, then once daily). Methimazole has a longer half-life and can be dosed once daily. Both drugs reduce thyroid hormone production by inhibiting the organic binding of iodine and the coupling of iodotyrosines (mediated by TPO). In addition, PTU also inhibits the peripheral conversion of T4 to T3, making it useful for the treatment of thyroid storm. Both drugs can cross the placenta, inhibiting fetal thyroid function, and are excreted in breast milk, although PTU has a lower risk of transplacental transfer. Methimazole also has been associated with congeni-tal aplasia; therefore, PTU is preferred in pregnant and breast-feeding women. Side effects of treatment include reversible
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Surgery_Schwartz. on several factors, as discussed in the following sections.Antithyroid Drugs Antithyroid medications generally are administered in preparation for RAI ablation or surgery. The drugs commonly used are propylthiouracil (PTU, 100 to 300 mg three times daily) and methimazole (10 to 30 mg three times daily, then once daily). Methimazole has a longer half-life and can be dosed once daily. Both drugs reduce thyroid hormone production by inhibiting the organic binding of iodine and the coupling of iodotyrosines (mediated by TPO). In addition, PTU also inhibits the peripheral conversion of T4 to T3, making it useful for the treatment of thyroid storm. Both drugs can cross the placenta, inhibiting fetal thyroid function, and are excreted in breast milk, although PTU has a lower risk of transplacental transfer. Methimazole also has been associated with congeni-tal aplasia; therefore, PTU is preferred in pregnant and breast-feeding women. Side effects of treatment include reversible
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transplacental transfer. Methimazole also has been associated with congeni-tal aplasia; therefore, PTU is preferred in pregnant and breast-feeding women. Side effects of treatment include reversible granulocytopenia, skin rashes, fever, peripheral neuritis, poly-arteritis, vasculitis, hepatitis, and, rarely, agranulocytosis and aplastic anemia. Patients should be monitored for these pos-sible complications and should always be warned to stop PTU or methimazole immediately and seek medical advice should they develop a sore throat or fever. Treatment of agranulocy-tosis involves admission to the hospital, discontinuation of the drug, and broad-spectrum antibiotic therapy. Surgery should be postponed until the granulocyte count reaches 1000 cells/mm3.The dose of antithyroid medication is titrated as needed in accordance with TSH and T4 levels. Most patients have improved symptoms in 2 weeks and become euthyroid in about 6 weeks. Some physicians use the block-replace regimen, by adding T4
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Surgery_Schwartz. transplacental transfer. Methimazole also has been associated with congeni-tal aplasia; therefore, PTU is preferred in pregnant and breast-feeding women. Side effects of treatment include reversible granulocytopenia, skin rashes, fever, peripheral neuritis, poly-arteritis, vasculitis, hepatitis, and, rarely, agranulocytosis and aplastic anemia. Patients should be monitored for these pos-sible complications and should always be warned to stop PTU or methimazole immediately and seek medical advice should they develop a sore throat or fever. Treatment of agranulocy-tosis involves admission to the hospital, discontinuation of the drug, and broad-spectrum antibiotic therapy. Surgery should be postponed until the granulocyte count reaches 1000 cells/mm3.The dose of antithyroid medication is titrated as needed in accordance with TSH and T4 levels. Most patients have improved symptoms in 2 weeks and become euthyroid in about 6 weeks. Some physicians use the block-replace regimen, by adding T4
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as needed in accordance with TSH and T4 levels. Most patients have improved symptoms in 2 weeks and become euthyroid in about 6 weeks. Some physicians use the block-replace regimen, by adding T4 (0.05 to 0.10 mg) to prevent hypothyroidism and suppress TSH secretion, because some, but not all, studies sug-gest that this reduces recurrence rates. The length of therapy is debated. Treatment with antithyroid medications is associated ABFigure 38-12. A. Graves’ ophthalmopathy and (B) pretibial myx-edema. This patient demonstrates exophthalmos, proptosis, perior-bital swelling, congestion, and edema of the conjunctiva.Brunicardi_Ch38_p1625-p1704.indd 163601/03/19 11:20 AM 1637THYROID, PARATHYROID, AND ADRENALCHAPTER 38with a high relapse rate when these drugs are discontinued, with 40% to 80% of patients developing recurrent disease after a 1to 2-year course. Patients with small glands are less likely to recur, so that treatment for curative intent is reserved for patients with (a)
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Surgery_Schwartz. as needed in accordance with TSH and T4 levels. Most patients have improved symptoms in 2 weeks and become euthyroid in about 6 weeks. Some physicians use the block-replace regimen, by adding T4 (0.05 to 0.10 mg) to prevent hypothyroidism and suppress TSH secretion, because some, but not all, studies sug-gest that this reduces recurrence rates. The length of therapy is debated. Treatment with antithyroid medications is associated ABFigure 38-12. A. Graves’ ophthalmopathy and (B) pretibial myx-edema. This patient demonstrates exophthalmos, proptosis, perior-bital swelling, congestion, and edema of the conjunctiva.Brunicardi_Ch38_p1625-p1704.indd 163601/03/19 11:20 AM 1637THYROID, PARATHYROID, AND ADRENALCHAPTER 38with a high relapse rate when these drugs are discontinued, with 40% to 80% of patients developing recurrent disease after a 1to 2-year course. Patients with small glands are less likely to recur, so that treatment for curative intent is reserved for patients with (a)
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to 80% of patients developing recurrent disease after a 1to 2-year course. Patients with small glands are less likely to recur, so that treatment for curative intent is reserved for patients with (a) small, nontoxic goiters less than 40 g; (b) mildly elevated thyroid hormone levels; (c) negative or low or titers of thyroid hormone receptor antibodies; and (d) rapid decrease in gland size with antithyroid medications. The catecholamine response of thyrotoxicosis can be alleviated by administering β-blocking agents. β-Blockade should be considered in all patients with symptomatic thyrotoxicosis and is recommended for elderly patients, those with coexistent cardiac disease, and patients with resting heart rates >90 bpm. These drugs have the added effect of decreasing the peripheral conversion of T4 to T3. Pro-pranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily. Higher doses are some-times required due to increased clearance of the
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Surgery_Schwartz. to 80% of patients developing recurrent disease after a 1to 2-year course. Patients with small glands are less likely to recur, so that treatment for curative intent is reserved for patients with (a) small, nontoxic goiters less than 40 g; (b) mildly elevated thyroid hormone levels; (c) negative or low or titers of thyroid hormone receptor antibodies; and (d) rapid decrease in gland size with antithyroid medications. The catecholamine response of thyrotoxicosis can be alleviated by administering β-blocking agents. β-Blockade should be considered in all patients with symptomatic thyrotoxicosis and is recommended for elderly patients, those with coexistent cardiac disease, and patients with resting heart rates >90 bpm. These drugs have the added effect of decreasing the peripheral conversion of T4 to T3. Pro-pranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily. Higher doses are some-times required due to increased clearance of the
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conversion of T4 to T3. Pro-pranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily. Higher doses are some-times required due to increased clearance of the medication. Caution should be exercised in patients with asthma. Calcium channel blockers are useful for rate control in patients in whom β-blockers are contraindicated.Radioactive Iodine Therapy (131I) RAI forms the mainstay of Graves’ disease treatment in North America. The major advan-tages of this treatment are the avoidance of a surgical procedure and its concomitant risks, reduced overall treatment costs, and ease of treatment. Antithyroid drugs are given until the patient is euthyroid and then discontinued to maximize drug uptake. The 131I dose is calculated after a preliminary scan and usu-ally consists of 8 to 12 mCi administered orally. After standard treatment with RAI, most patients become euthyroid within 2 months. However, only about 50% of patients treated with RAI are
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Surgery_Schwartz. conversion of T4 to T3. Pro-pranolol is the most commonly prescribed medication in doses of about 20 to 40 mg four times daily. Higher doses are some-times required due to increased clearance of the medication. Caution should be exercised in patients with asthma. Calcium channel blockers are useful for rate control in patients in whom β-blockers are contraindicated.Radioactive Iodine Therapy (131I) RAI forms the mainstay of Graves’ disease treatment in North America. The major advan-tages of this treatment are the avoidance of a surgical procedure and its concomitant risks, reduced overall treatment costs, and ease of treatment. Antithyroid drugs are given until the patient is euthyroid and then discontinued to maximize drug uptake. The 131I dose is calculated after a preliminary scan and usu-ally consists of 8 to 12 mCi administered orally. After standard treatment with RAI, most patients become euthyroid within 2 months. However, only about 50% of patients treated with RAI are
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and usu-ally consists of 8 to 12 mCi administered orally. After standard treatment with RAI, most patients become euthyroid within 2 months. However, only about 50% of patients treated with RAI are euthyroid 6 months after treatment, and the remain-ing are still hyperthyroid or already hypothyroid.4 After 1 year, about 2.5% of patients develop hypothyroidism each year. RAI also has been documented to lead to progression of Graves’ oph-thalmopathy (33% after RAI compared to 16% after surgery), and ophthalmopathy is more common in smokers. Although there is no evidence of long-term problems with infertility, and overall cancer incidence rates are unchanged, there is a small increased risk of nodular goiter, thyroid cancer,5 and hyperpara-thyroidism (HPT)6 in patients who have been treated with RAI. Patients treated with RAI have an unexplained increase in their overall and cardiovascular mortality rates when compared to the general population.RAI therapy is therefore most often used in
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Surgery_Schwartz. and usu-ally consists of 8 to 12 mCi administered orally. After standard treatment with RAI, most patients become euthyroid within 2 months. However, only about 50% of patients treated with RAI are euthyroid 6 months after treatment, and the remain-ing are still hyperthyroid or already hypothyroid.4 After 1 year, about 2.5% of patients develop hypothyroidism each year. RAI also has been documented to lead to progression of Graves’ oph-thalmopathy (33% after RAI compared to 16% after surgery), and ophthalmopathy is more common in smokers. Although there is no evidence of long-term problems with infertility, and overall cancer incidence rates are unchanged, there is a small increased risk of nodular goiter, thyroid cancer,5 and hyperpara-thyroidism (HPT)6 in patients who have been treated with RAI. Patients treated with RAI have an unexplained increase in their overall and cardiovascular mortality rates when compared to the general population.RAI therapy is therefore most often used in
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RAI. Patients treated with RAI have an unexplained increase in their overall and cardiovascular mortality rates when compared to the general population.RAI therapy is therefore most often used in older patients with small or moderate-sized goiters, those who have relapsed after medical or surgical therapy, and those in whom antithyroid drugs or surgery are contraindicated. Absolute contraindications to RAI include women who are pregnant (or planning pregnancy within 6 months of treatment) or breastfeeding. Relative contra-indications include young patients (i.e., especially children and adolescents), those with thyroid nodules, and those with oph-thalmopathy. Lack of access to a high-volume thyroid surgeon is also a consideration. The higher the initial dose of 131I, the earlier the onset and the higher the incidence of hypothyroidism.Surgical Treatment In North America, surgery is recom-mended when RAI is contraindicated as in patients who (a) have confirmed cancer or suspicious
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Surgery_Schwartz. RAI. Patients treated with RAI have an unexplained increase in their overall and cardiovascular mortality rates when compared to the general population.RAI therapy is therefore most often used in older patients with small or moderate-sized goiters, those who have relapsed after medical or surgical therapy, and those in whom antithyroid drugs or surgery are contraindicated. Absolute contraindications to RAI include women who are pregnant (or planning pregnancy within 6 months of treatment) or breastfeeding. Relative contra-indications include young patients (i.e., especially children and adolescents), those with thyroid nodules, and those with oph-thalmopathy. Lack of access to a high-volume thyroid surgeon is also a consideration. The higher the initial dose of 131I, the earlier the onset and the higher the incidence of hypothyroidism.Surgical Treatment In North America, surgery is recom-mended when RAI is contraindicated as in patients who (a) have confirmed cancer or suspicious
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and the higher the incidence of hypothyroidism.Surgical Treatment In North America, surgery is recom-mended when RAI is contraindicated as in patients who (a) have confirmed cancer or suspicious thyroid nodules, (b) are young, (c) desire to conceive soon (<6 months) after treatment, (d) have had severe reactions to antithyroid medications, (e) have large goiters (>80 g) causing compressive symptoms, and (f) are reluctant to undergo RAI therapy. Relative indications for thyroidectomy include patients, particularly smokers, with mod-erate to severe Graves’ ophthalmopathy, those desiring rapid control of hyperthyroidism with a chance of being euthyroid, and those demonstrating poor compliance to antithyroid medica-tions. Pregnancy is also a relative contraindication, and surgery should be used only when rapid control is needed and antithy-roid medications cannot be used. Surgery is best performed in the second trimester. The goal of thyroidectomy for Graves’ disease should be the
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Surgery_Schwartz. and the higher the incidence of hypothyroidism.Surgical Treatment In North America, surgery is recom-mended when RAI is contraindicated as in patients who (a) have confirmed cancer or suspicious thyroid nodules, (b) are young, (c) desire to conceive soon (<6 months) after treatment, (d) have had severe reactions to antithyroid medications, (e) have large goiters (>80 g) causing compressive symptoms, and (f) are reluctant to undergo RAI therapy. Relative indications for thyroidectomy include patients, particularly smokers, with mod-erate to severe Graves’ ophthalmopathy, those desiring rapid control of hyperthyroidism with a chance of being euthyroid, and those demonstrating poor compliance to antithyroid medica-tions. Pregnancy is also a relative contraindication, and surgery should be used only when rapid control is needed and antithy-roid medications cannot be used. Surgery is best performed in the second trimester. The goal of thyroidectomy for Graves’ disease should be the
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be used only when rapid control is needed and antithy-roid medications cannot be used. Surgery is best performed in the second trimester. The goal of thyroidectomy for Graves’ disease should be the complete and permanent control of the disease with minimal morbidity. Patients should be rendered euthyroid before operation with antithyroid drugs that should be continued up to the day of surgery. Lugol’s iodide solution or saturated potassium iodide generally is administered beginning 7 to 10 days preoperatively (three drops twice daily) to reduce vascularity of the gland and decrease the risk of precipitating thyroid storm. The major action of iodine in this situation is to inhibit release of thyroid hormone. If it is not possible to render the patient euthyroid prior to surgery (if the surgery is urgent or the patient is allergic to antithyroid medications), the patient can be prepared with β-blockade and potassium iodide alone. Steroids can be a useful adjunct in this situation.The
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Surgery_Schwartz. be used only when rapid control is needed and antithy-roid medications cannot be used. Surgery is best performed in the second trimester. The goal of thyroidectomy for Graves’ disease should be the complete and permanent control of the disease with minimal morbidity. Patients should be rendered euthyroid before operation with antithyroid drugs that should be continued up to the day of surgery. Lugol’s iodide solution or saturated potassium iodide generally is administered beginning 7 to 10 days preoperatively (three drops twice daily) to reduce vascularity of the gland and decrease the risk of precipitating thyroid storm. The major action of iodine in this situation is to inhibit release of thyroid hormone. If it is not possible to render the patient euthyroid prior to surgery (if the surgery is urgent or the patient is allergic to antithyroid medications), the patient can be prepared with β-blockade and potassium iodide alone. Steroids can be a useful adjunct in this situation.The
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is urgent or the patient is allergic to antithyroid medications), the patient can be prepared with β-blockade and potassium iodide alone. Steroids can be a useful adjunct in this situation.The extent of thyroidectomy to be performed used to be determined by the desired outcome (risk of recurrence vs. euthy-roidism) and surgeon experience. In patients with coexistent thyroid cancer and those who refused RAI therapy or had severe ophthalmopathy or life-threatening reactions to antithyroid medications (vasculitis, agranulocytosis, or liver failure), total or near-total thyroidectomy was recommended. Ophthalmopa-thy has been demonstrated to stabilize or improve in most patients after total thyroidectomy, presumably from removal of the antigenic stimulus. A subtotal thyroidectomy, leaving a 4to 7-g remnant, was recommended for all remaining patients. Dur-ing subtotal thyroidectomy, remnant tissue may be left on each side (bilateral subtotal thyroidectomy), or a total lobectomy can be
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Surgery_Schwartz. is urgent or the patient is allergic to antithyroid medications), the patient can be prepared with β-blockade and potassium iodide alone. Steroids can be a useful adjunct in this situation.The extent of thyroidectomy to be performed used to be determined by the desired outcome (risk of recurrence vs. euthy-roidism) and surgeon experience. In patients with coexistent thyroid cancer and those who refused RAI therapy or had severe ophthalmopathy or life-threatening reactions to antithyroid medications (vasculitis, agranulocytosis, or liver failure), total or near-total thyroidectomy was recommended. Ophthalmopa-thy has been demonstrated to stabilize or improve in most patients after total thyroidectomy, presumably from removal of the antigenic stimulus. A subtotal thyroidectomy, leaving a 4to 7-g remnant, was recommended for all remaining patients. Dur-ing subtotal thyroidectomy, remnant tissue may be left on each side (bilateral subtotal thyroidectomy), or a total lobectomy can be
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a 4to 7-g remnant, was recommended for all remaining patients. Dur-ing subtotal thyroidectomy, remnant tissue may be left on each side (bilateral subtotal thyroidectomy), or a total lobectomy can be performed on one side with a subtotal thyroidectomy on the other side (Hartley-Dunhill procedure). Results were similar with either procedure, but the latter procedure was theoretically associated with fewer complications and requires reentering only one side of the neck should recurrence require reoperation. Most studies, however, show no difference in the rates of com-plications with either approach, although patients undergoing a total resection had higher rates of temporary hypoparathyroid-ism. However, patients treated with subtotal thyroidectomy are prone to recurrence, the rates of which are dependent on rem-nant size. Based on the current evidence, recently revised guide-lines from the American Thyroid Association (ATA) recommend total or near-total thyroidectomy as the procedure
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Surgery_Schwartz. a 4to 7-g remnant, was recommended for all remaining patients. Dur-ing subtotal thyroidectomy, remnant tissue may be left on each side (bilateral subtotal thyroidectomy), or a total lobectomy can be performed on one side with a subtotal thyroidectomy on the other side (Hartley-Dunhill procedure). Results were similar with either procedure, but the latter procedure was theoretically associated with fewer complications and requires reentering only one side of the neck should recurrence require reoperation. Most studies, however, show no difference in the rates of com-plications with either approach, although patients undergoing a total resection had higher rates of temporary hypoparathyroid-ism. However, patients treated with subtotal thyroidectomy are prone to recurrence, the rates of which are dependent on rem-nant size. Based on the current evidence, recently revised guide-lines from the American Thyroid Association (ATA) recommend total or near-total thyroidectomy as the procedure
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are dependent on rem-nant size. Based on the current evidence, recently revised guide-lines from the American Thyroid Association (ATA) recommend total or near-total thyroidectomy as the procedure of choice for the surgical management of Graves’ disease.7 Recurrent thyrotoxicosis usually is managed by radioiodine treatment.Toxic Multinodular Goiter Toxic multinodular goiters usu-ally occur in older individuals, who often have a prior history of a nontoxic multinodular goiter. Over several years, enough thyroid nodules become autonomous to cause hyperthyroidism. The presentation often is insidious in that hyperthyroidism may only become apparent when patients are placed on low doses of thyroid hormone suppression for the goiter. Some patients have T3 toxicosis, whereas others may present only with atrial fibrillation or congestive heart failure. Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the antiarrhythmic agent amiodarone
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Surgery_Schwartz. are dependent on rem-nant size. Based on the current evidence, recently revised guide-lines from the American Thyroid Association (ATA) recommend total or near-total thyroidectomy as the procedure of choice for the surgical management of Graves’ disease.7 Recurrent thyrotoxicosis usually is managed by radioiodine treatment.Toxic Multinodular Goiter Toxic multinodular goiters usu-ally occur in older individuals, who often have a prior history of a nontoxic multinodular goiter. Over several years, enough thyroid nodules become autonomous to cause hyperthyroidism. The presentation often is insidious in that hyperthyroidism may only become apparent when patients are placed on low doses of thyroid hormone suppression for the goiter. Some patients have T3 toxicosis, whereas others may present only with atrial fibrillation or congestive heart failure. Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the antiarrhythmic agent amiodarone
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present only with atrial fibrillation or congestive heart failure. Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the antiarrhythmic agent amiodarone (Jod-Basedow 1Brunicardi_Ch38_p1625-p1704.indd 163701/03/19 11:20 AM 1638SPECIFIC CONSIDERATIONSPART IIhyperthyroidism). Symptoms and signs of hyperthyroidism are similar to Graves’ disease, but extrathyroidal manifestations are absent.Diagnostic Studies. Blood tests are similar to Graves’ disease with a suppressed TSH level and elevated free T4 or T3 levels. RAI uptake also is increased, showing multiple nodules with increased uptake and suppression of the remaining gland.Treatment. Hyperthyroidism must be adequately controlled. Both RAI and surgical resection may be used for treatment. When surgery is performed, near-total or total thyroidectomy is recommended to avoid recurrence and the consequent increased complication rates with repeat surgery. Care must be taken in identifying the
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Surgery_Schwartz. present only with atrial fibrillation or congestive heart failure. Hyperthyroidism also can be precipitated by iodide-containing drugs such as contrast media and the antiarrhythmic agent amiodarone (Jod-Basedow 1Brunicardi_Ch38_p1625-p1704.indd 163701/03/19 11:20 AM 1638SPECIFIC CONSIDERATIONSPART IIhyperthyroidism). Symptoms and signs of hyperthyroidism are similar to Graves’ disease, but extrathyroidal manifestations are absent.Diagnostic Studies. Blood tests are similar to Graves’ disease with a suppressed TSH level and elevated free T4 or T3 levels. RAI uptake also is increased, showing multiple nodules with increased uptake and suppression of the remaining gland.Treatment. Hyperthyroidism must be adequately controlled. Both RAI and surgical resection may be used for treatment. When surgery is performed, near-total or total thyroidectomy is recommended to avoid recurrence and the consequent increased complication rates with repeat surgery. Care must be taken in identifying the
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surgery is performed, near-total or total thyroidectomy is recommended to avoid recurrence and the consequent increased complication rates with repeat surgery. Care must be taken in identifying the RLN, which may be found laterally on the thy-roid (rather than posterior) or stretched anteriorly over a nodule. RAI therapy is reserved for elderly patients who represent very poor operative risks, provided there is no airway compression from the goiter and thyroid cancer is not a concern. However, because uptake is less than in Graves’ disease, larger doses of RAI often are needed to treat the hyperthyroidism. Furthermore, RAI-induced thyroiditis has the potential to cause swelling and acute airway compromise and leaves the goiter intact, with the possibility of recurrent hyperthyroidism.Toxic Adenoma Hyperthyroidism from a single hyperfunction-ing nodule typically occurs in younger patients who note recent growth of a long-standing nodule along with the symptoms of hyperthyroidism. Toxic
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Surgery_Schwartz. surgery is performed, near-total or total thyroidectomy is recommended to avoid recurrence and the consequent increased complication rates with repeat surgery. Care must be taken in identifying the RLN, which may be found laterally on the thy-roid (rather than posterior) or stretched anteriorly over a nodule. RAI therapy is reserved for elderly patients who represent very poor operative risks, provided there is no airway compression from the goiter and thyroid cancer is not a concern. However, because uptake is less than in Graves’ disease, larger doses of RAI often are needed to treat the hyperthyroidism. Furthermore, RAI-induced thyroiditis has the potential to cause swelling and acute airway compromise and leaves the goiter intact, with the possibility of recurrent hyperthyroidism.Toxic Adenoma Hyperthyroidism from a single hyperfunction-ing nodule typically occurs in younger patients who note recent growth of a long-standing nodule along with the symptoms of hyperthyroidism. Toxic
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Adenoma Hyperthyroidism from a single hyperfunction-ing nodule typically occurs in younger patients who note recent growth of a long-standing nodule along with the symptoms of hyperthyroidism. Toxic adenomas are characterized by somatic mutations in the TSH-R gene, although G-protein–stimulating gene (gsp) mutations may occur also.8 Most hyperfunctioning or autonomous thyroid nodules have attained a size of at least 3 cm before hyperthyroidism occurs. Physical examination usu-ally reveals a solitary thyroid nodule without palpable thyroid tissue on the contralateral side. RAI scanning shows a “hot” nodule with suppression of the rest of the thyroid gland. These nodules are rarely malignant. Smaller nodules may be man-aged with antithyroid medications and RAI. Larger nodules can require higher doses, which can lead to hypothyroidism. Sur-gery (lobectomy and isthmusectomy) is preferred to treat young patients and those with larger nodules. Percutaneous ethanol injection (PEI) has been
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Surgery_Schwartz. Adenoma Hyperthyroidism from a single hyperfunction-ing nodule typically occurs in younger patients who note recent growth of a long-standing nodule along with the symptoms of hyperthyroidism. Toxic adenomas are characterized by somatic mutations in the TSH-R gene, although G-protein–stimulating gene (gsp) mutations may occur also.8 Most hyperfunctioning or autonomous thyroid nodules have attained a size of at least 3 cm before hyperthyroidism occurs. Physical examination usu-ally reveals a solitary thyroid nodule without palpable thyroid tissue on the contralateral side. RAI scanning shows a “hot” nodule with suppression of the rest of the thyroid gland. These nodules are rarely malignant. Smaller nodules may be man-aged with antithyroid medications and RAI. Larger nodules can require higher doses, which can lead to hypothyroidism. Sur-gery (lobectomy and isthmusectomy) is preferred to treat young patients and those with larger nodules. Percutaneous ethanol injection (PEI) has been
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Surgery_Schwartz_10795
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Surgery_Schwartz
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doses, which can lead to hypothyroidism. Sur-gery (lobectomy and isthmusectomy) is preferred to treat young patients and those with larger nodules. Percutaneous ethanol injection (PEI) has been reported to have reasonable success rates but has not been directly compared with surgery.Thyroid Storm Thyroid storm is a condition of hyperthyroid-ism accompanied by fever, central nervous system agitation or depression, and cardiovascular and GI dysfunction, including hepatic failure. The condition may be precipitated by abrupt cessation of antithyroid medications, infection, thyroid or non-thyroid surgery, and trauma in patients with untreated thyrotoxi-cosis. Occasionally, thyroid storm may result from amiodarone administration or exposure to iodinated contrast agents or fol-lowing RAI therapy. This condition was previously associated with high mortality rates but can be appropriately managed in an intensive care unit setting. β-Blockers are given to reduce peripheral T4 to T3 conversion
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Surgery_Schwartz. doses, which can lead to hypothyroidism. Sur-gery (lobectomy and isthmusectomy) is preferred to treat young patients and those with larger nodules. Percutaneous ethanol injection (PEI) has been reported to have reasonable success rates but has not been directly compared with surgery.Thyroid Storm Thyroid storm is a condition of hyperthyroid-ism accompanied by fever, central nervous system agitation or depression, and cardiovascular and GI dysfunction, including hepatic failure. The condition may be precipitated by abrupt cessation of antithyroid medications, infection, thyroid or non-thyroid surgery, and trauma in patients with untreated thyrotoxi-cosis. Occasionally, thyroid storm may result from amiodarone administration or exposure to iodinated contrast agents or fol-lowing RAI therapy. This condition was previously associated with high mortality rates but can be appropriately managed in an intensive care unit setting. β-Blockers are given to reduce peripheral T4 to T3 conversion
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Surgery_Schwartz_10796
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Surgery_Schwartz
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This condition was previously associated with high mortality rates but can be appropriately managed in an intensive care unit setting. β-Blockers are given to reduce peripheral T4 to T3 conversion and decrease the hyperthyroid symptoms. Oxygen supplementation and hemodynamic support should be instituted. Nonaspirin compounds can be used to treat pyrexia, and Lugol’s iodine or sodium ipodate (intravenously) should be administered to decrease iodine uptake and thyroid hormone secretion. PTU therapy blocks the formation of new thyroid hormone and reduces peripheral conversion of T4 to T3. Corticosteroids often are helpful to prevent adrenal exhaustion and block hepatic thyroid hormone conversion.Hypothyroidism. Deficiency in circulating levels of thyroid hormone leads to hypothyroidism and, in neonates, to cretin-ism, which is characterized by neurologic impairment and men-tal retardation. Hypothyroidism also may occur in Pendred’s syndrome (associated with deafness) and Turner’s
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Surgery_Schwartz. This condition was previously associated with high mortality rates but can be appropriately managed in an intensive care unit setting. β-Blockers are given to reduce peripheral T4 to T3 conversion and decrease the hyperthyroid symptoms. Oxygen supplementation and hemodynamic support should be instituted. Nonaspirin compounds can be used to treat pyrexia, and Lugol’s iodine or sodium ipodate (intravenously) should be administered to decrease iodine uptake and thyroid hormone secretion. PTU therapy blocks the formation of new thyroid hormone and reduces peripheral conversion of T4 to T3. Corticosteroids often are helpful to prevent adrenal exhaustion and block hepatic thyroid hormone conversion.Hypothyroidism. Deficiency in circulating levels of thyroid hormone leads to hypothyroidism and, in neonates, to cretin-ism, which is characterized by neurologic impairment and men-tal retardation. Hypothyroidism also may occur in Pendred’s syndrome (associated with deafness) and Turner’s
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Surgery_Schwartz_10797
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Surgery_Schwartz
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and, in neonates, to cretin-ism, which is characterized by neurologic impairment and men-tal retardation. Hypothyroidism also may occur in Pendred’s syndrome (associated with deafness) and Turner’s syndrome. Conditions that cause hypothyroidism are listed in Table 38-2.Clinical Features Failure of thyroid gland development or function in utero leads to cretinism and characteristic facies similar to those of children with Down syndrome and dwarfism. Failure to thrive and severe mental retardation often are present. Immediate testing and treatment with thyroid hormone at birth can lessen the neurologic and intellectual deficits. Hypothyroid-ism developing in childhood or adolescence results in delayed development and may also lead to abdominal distention, umbili-cal hernia, and rectal prolapse. In adults, symptoms in general are nonspecific, including tiredness, weight gain, cold intoler-ance, constipation, and menorrhagia. Patients with severe hypo-thyroidism or myxedema develop
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Surgery_Schwartz. and, in neonates, to cretin-ism, which is characterized by neurologic impairment and men-tal retardation. Hypothyroidism also may occur in Pendred’s syndrome (associated with deafness) and Turner’s syndrome. Conditions that cause hypothyroidism are listed in Table 38-2.Clinical Features Failure of thyroid gland development or function in utero leads to cretinism and characteristic facies similar to those of children with Down syndrome and dwarfism. Failure to thrive and severe mental retardation often are present. Immediate testing and treatment with thyroid hormone at birth can lessen the neurologic and intellectual deficits. Hypothyroid-ism developing in childhood or adolescence results in delayed development and may also lead to abdominal distention, umbili-cal hernia, and rectal prolapse. In adults, symptoms in general are nonspecific, including tiredness, weight gain, cold intoler-ance, constipation, and menorrhagia. Patients with severe hypo-thyroidism or myxedema develop
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Surgery_Schwartz_10798
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Surgery_Schwartz
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prolapse. In adults, symptoms in general are nonspecific, including tiredness, weight gain, cold intoler-ance, constipation, and menorrhagia. Patients with severe hypo-thyroidism or myxedema develop characteristic facial features due to the deposition of glycosaminoglycans in the subcutane-ous tissues, leading to facial and periorbital puffiness. The skin becomes rough and dry and often develops a yellowish hue from reduced conversion of carotene to vitamin A. Hair becomes dry and brittle, and severe hair loss may occur. There is also a characteristic loss of the outer two thirds of the eyebrows. An enlarged tongue may impair speech, which is already slowed, in keeping with the impairment of mental processes. Patients may also have nonspecific abdominal pain accompanied by disten-tion and constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include bra-dycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary
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Surgery_Schwartz. prolapse. In adults, symptoms in general are nonspecific, including tiredness, weight gain, cold intoler-ance, constipation, and menorrhagia. Patients with severe hypo-thyroidism or myxedema develop characteristic facial features due to the deposition of glycosaminoglycans in the subcutane-ous tissues, leading to facial and periorbital puffiness. The skin becomes rough and dry and often develops a yellowish hue from reduced conversion of carotene to vitamin A. Hair becomes dry and brittle, and severe hair loss may occur. There is also a characteristic loss of the outer two thirds of the eyebrows. An enlarged tongue may impair speech, which is already slowed, in keeping with the impairment of mental processes. Patients may also have nonspecific abdominal pain accompanied by disten-tion and constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include bra-dycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary
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Surgery_Schwartz_10799
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Surgery_Schwartz
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constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include bra-dycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary effusions. When hypothyroidism occurs as a result of pituitary failure, other features of hypopituitarism, such as pale, waxy skin; loss of body hair; and atrophic genita-lia, may be present.Table 38-2Causes of hypothyroidismPRIMARY (INCREASED TSH LEVELS)SECONDARY (DECREASED TSH LEVELS)TERTIARYHashimoto’s thyroiditisPituitary tumorHypothalamic insufficiencyRAI therapy for Graves’ diseasePituitary resection or ablationResistance to thyroid hormonePostthyroidectomy Excessive iodine intake Subacute thyroiditis Medications: antithyroid drugs, lithium Rare: iodine deficiency, dyshormogenesis RAI = radioactive iodine; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163801/03/19 11:20 AM 1639THYROID, PARATHYROID, AND ADRENALCHAPTER 38Laboratory Findings Hypothyroidism
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Surgery_Schwartz. constipation. Libido and fertility are impaired in both sexes. Cardiovascular changes in hypothyroidism include bra-dycardia, cardiomegaly, pericardial effusion, reduced cardiac output, and pulmonary effusions. When hypothyroidism occurs as a result of pituitary failure, other features of hypopituitarism, such as pale, waxy skin; loss of body hair; and atrophic genita-lia, may be present.Table 38-2Causes of hypothyroidismPRIMARY (INCREASED TSH LEVELS)SECONDARY (DECREASED TSH LEVELS)TERTIARYHashimoto’s thyroiditisPituitary tumorHypothalamic insufficiencyRAI therapy for Graves’ diseasePituitary resection or ablationResistance to thyroid hormonePostthyroidectomy Excessive iodine intake Subacute thyroiditis Medications: antithyroid drugs, lithium Rare: iodine deficiency, dyshormogenesis RAI = radioactive iodine; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163801/03/19 11:20 AM 1639THYROID, PARATHYROID, AND ADRENALCHAPTER 38Laboratory Findings Hypothyroidism
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Surgery_Schwartz_10800
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Surgery_Schwartz
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= radioactive iodine; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163801/03/19 11:20 AM 1639THYROID, PARATHYROID, AND ADRENALCHAPTER 38Laboratory Findings Hypothyroidism is characterized by low circulating levels of T4 and T3. Raised TSH levels are found in primary thyroid failure, whereas secondary hypothyroidism is characterized by low TSH levels that do not increase following TRH stimulation. Thyroid autoantibodies are highest in patients with autoimmune disease (Hashimoto’s thyroiditis, Graves’ dis-ease) and may also be elevated in patients with nodular goiter and thyroid neoplasms. An electrocardiogram demonstrates decreased voltage with flattening or inversion of T waves.Treatment T4 is the treatment of choice and is administered in dosages varying from 50 to 200 μg per day, depending on the patient’s size and condition. Starting doses of 100 μg of T4 daily are well tolerated; however, elderly patients and those with coexisting heart disease and
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Surgery_Schwartz. = radioactive iodine; TSH = thyroid-stimulating hormone.Brunicardi_Ch38_p1625-p1704.indd 163801/03/19 11:20 AM 1639THYROID, PARATHYROID, AND ADRENALCHAPTER 38Laboratory Findings Hypothyroidism is characterized by low circulating levels of T4 and T3. Raised TSH levels are found in primary thyroid failure, whereas secondary hypothyroidism is characterized by low TSH levels that do not increase following TRH stimulation. Thyroid autoantibodies are highest in patients with autoimmune disease (Hashimoto’s thyroiditis, Graves’ dis-ease) and may also be elevated in patients with nodular goiter and thyroid neoplasms. An electrocardiogram demonstrates decreased voltage with flattening or inversion of T waves.Treatment T4 is the treatment of choice and is administered in dosages varying from 50 to 200 μg per day, depending on the patient’s size and condition. Starting doses of 100 μg of T4 daily are well tolerated; however, elderly patients and those with coexisting heart disease and
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Surgery_Schwartz_10801
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Surgery_Schwartz
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50 to 200 μg per day, depending on the patient’s size and condition. Starting doses of 100 μg of T4 daily are well tolerated; however, elderly patients and those with coexisting heart disease and profound hypothyroidism should be started on a considerably lower dose such as 25 to 50 μg daily because of associated hypercholesterolemia and atherosclerosis. The dose can be slowly increased over weeks to months to attain a euthyroid state. A baseline electrocardiogram should always be obtained in patients with severe hypothyroidism before treat-ment. T4 dosage is titrated against clinical response and TSH levels, which should return to normal. The management of patients with subclinical hypothyroidism (normal T4, slightly raised TSH) is controversial. Some evidence suggests that patients with subclinical hypothyroidism and increased antithy-roid antibody levels should be treated because they will sub-sequently develop hypothyroidism. Patients who present with myxedema coma may require
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Surgery_Schwartz. 50 to 200 μg per day, depending on the patient’s size and condition. Starting doses of 100 μg of T4 daily are well tolerated; however, elderly patients and those with coexisting heart disease and profound hypothyroidism should be started on a considerably lower dose such as 25 to 50 μg daily because of associated hypercholesterolemia and atherosclerosis. The dose can be slowly increased over weeks to months to attain a euthyroid state. A baseline electrocardiogram should always be obtained in patients with severe hypothyroidism before treat-ment. T4 dosage is titrated against clinical response and TSH levels, which should return to normal. The management of patients with subclinical hypothyroidism (normal T4, slightly raised TSH) is controversial. Some evidence suggests that patients with subclinical hypothyroidism and increased antithy-roid antibody levels should be treated because they will sub-sequently develop hypothyroidism. Patients who present with myxedema coma may require
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