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Surgery_Schwartz. free flap: a radiologic comparison of 3D morphology. Head Neck. 2012;34(10):1377-1382. 124. Shipchandler TZ, Waters HH, Knott PD, Fritz MA. Orbito-maxillary reconstruction using the layered fibula osteocutane-ous flap. Arch Facial Plast Surg. 2012;14(2):110-115. 125. Shiboski CH, Schmidt BL, Jordan RC. Tongue and tonsil car-cinoma: increasing trends in the U.S. population ages 20-44 years. Cancer. 2005;103(9):1843-1849. 126. Gillison ML, Shah KV. Chapter 9: role of mucosal human papillomavirus in nongenital cancers. J Natl Cancer Inst Monogr. 2003;(31)(31):57-65. 127. Fakhry C, Westra WH, Li S, et al. Improved survival of patients with human papillomavirus-positive head and neck squamous cell carcinoma in a prospective clinical trial. J Natl Cancer Inst. 2008;100(4):261-269. 128. Parsons JT, Mendenhall WM, Stringer SP, et al. Squamous cell carcinoma of the oropharynx: surgery, radiation ther-apy, or both. Cancer. 2002;94(11):2967-2980. 129. Huang SH, Hansen A, Rathod S, O’Sullivan B.


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Surgery_Schwartz. JT, Mendenhall WM, Stringer SP, et al. Squamous cell carcinoma of the oropharynx: surgery, radiation ther-apy, or both. Cancer. 2002;94(11):2967-2980. 129. Huang SH, Hansen A, Rathod S, O’Sullivan B. Primary surgery versus (chemo)radiotherapy in oropharyngeal can-cer: the radiation oncologist’s and medical oncologist’s perspectives. Curr Opin Otolaryngol Head Neck Surg. 2015;23(2):139-147. 130. de Almeida JR, Byrd JK, Wu R, et al. A systematic review of transoral robotic surgery and radiotherapy for early oropharynx cancer: a systematic review. Laryngoscope. 2014;124(9):2096-2102. 131. de Almeida JR, Li R, Magnuson JS, et al. Oncologic outcomes after transoral robotic surgery: a multi-institutional study. JAMA Otolaryngol Head Neck Surg. 2015;141(12):1043-1051. 132. de Almeida JR, Moskowitz AJ, Miles BA, et al. Cost-effec-tiveness of transoral robotic surgery versus (chemo)radio-therapy for early T classification oropharyngeal carcinoma: a cost-utility analysis. Head Neck.


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Surgery_Schwartz. JR, Moskowitz AJ, Miles BA, et al. Cost-effec-tiveness of transoral robotic surgery versus (chemo)radio-therapy for early T classification oropharyngeal carcinoma: a cost-utility analysis. Head Neck. 2016;38(4):589-600. 133. Howard J, Masterson L, Dwivedi RC, et al. Minimally inva-sive surgery versus radiotherapy/chemoradiotherapy for small-volume primary oropharyngeal carcinoma. Cochrane Database Syst Rev. 2016;12:CD010963. 134. Vega C, Leon X, Cervelli D, et al. Total or subtotal glossec-tomy with microsurgical reconstruction: functional and onco-logical results. Microsurgery. 2011;31(7):517-523.Brunicardi_Ch18_p0613-p0660.indd 65701/03/19 5:25 PM 658SPECIFIC CONSIDERATIONSPART II 135. Cohen WA, Albornoz CR, Cordeiro PG, et al. Health-related quality of life following reconstruction for com-mon head and neck surgical defects. Plast Reconstr Surg. 2016;138(6):1312-1320. 136. Lin DT, Yarlagadda BB, Sethi RK, et al. Long-term func-tional outcomes of total glossectomy with or


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Surgery_Schwartz. for com-mon head and neck surgical defects. Plast Reconstr Surg. 2016;138(6):1312-1320. 136. Lin DT, Yarlagadda BB, Sethi RK, et al. Long-term func-tional outcomes of total glossectomy with or without total laryngectomy. JAMA Otolaryngol Head Neck Surg. 2015;141(9):797-803. 137. Sinclair CF, Carroll WR, Desmond RA, Rosenthal EL. Func-tional and survival outcomes in patients undergoing total glossectomy compared with total laryngoglossectomy. Oto-laryngol Head Neck Surg. 2011;145(5):755-758. 138. Chepeha DB, Sacco AG, Erickson VR, et al. Oropha-ryngoplasty with template-based reconstruction of oro-pharynx defects. Arch Otolaryngol Head Neck Surg. 2009;135(9):887-894. 139. Kimata Y, Uchiyama K, Sakuraba M, et al. Velopharyn-geal function after microsurgical reconstruction of lat-eral and superior oropharyngeal defects. Laryngoscope. 2002;112(6):1037-1042. 140. Hall SF, Groome PA, Irish J, O’Sullivan B. Towards further understanding of prognostic factors for head and neck cancer


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Surgery_Schwartz. and superior oropharyngeal defects. Laryngoscope. 2002;112(6):1037-1042. 140. Hall SF, Groome PA, Irish J, O’Sullivan B. Towards further understanding of prognostic factors for head and neck cancer patients: the example of hypopharyngeal cancer. Laryngo-scope. 2009;119(4):696-702. 141. Hall SF, Groome PA, Irish J, O’Sullivan B. Radiotherapy or surgery for head and neck squamous cell cancer: establish-ing the baseline for hypopharyngeal carcinoma? Cancer. 2009;115(24):5711-5722. 142. Dirven R, Swinson BD, Gao K, Clark JR. The assessment of pharyngocutaneous fistula rate in patients treated pri-marily with definitive radiotherapy followed by salvage surgery of the larynx and hypopharynx. Laryngoscope. 2009;119(9):1691-1695. 143. Burke MS, Kaplan SE, Kaplowitz LJ, et al. Pectoralis major myocutaneous flap for reconstruction of circumferential pha-ryngeal defects. Ann Plast Surg. 2013;71(6):649-651. 144. Patel RS, Goldstein DP, Brown D, Irish J, Gullane PJ, Gilbert RW. Circumferential


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Surgery_Schwartz. myocutaneous flap for reconstruction of circumferential pha-ryngeal defects. Ann Plast Surg. 2013;71(6):649-651. 144. Patel RS, Goldstein DP, Brown D, Irish J, Gullane PJ, Gilbert RW. Circumferential pharyngeal reconstruction: history, critical analy-sis of techniques, and current therapeutic recommendations. Head Neck. 2010;32(1):109-120. 145. Murray DJ, Gilbert RW, Vesely MJ, et al. Functional outcomes and donor site morbidity following circumferential pharyn-goesophageal reconstruction using an anterolateral thigh flap and salivary bypass tube. Head Neck. 2007;29(2):147-154. 146. Durmus K, Kakarala K, Old MO, Teknos TN, Ozer E. Antero-lateral thigh butterfly free flap reconstruction for peristomal recurrence following laryngectomy: our experience in six patients. Clin Otolaryngol. 2013;38(4):339-342. 147. Induction chemotherapy plus radiation compared with sur-gery plus radiation in patients with advanced laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study


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Surgery_Schwartz. chemotherapy plus radiation compared with sur-gery plus radiation in patients with advanced laryngeal cancer. The Department of Veterans Affairs Laryngeal Cancer Study Group. N Engl J Med. 1991;324(24):1685-1690. 148. Weber RS, Berkey BA, Forastiere A, et al. Outcome of salvage total laryngectomy following organ preservation therapy: the radiation therapy oncology group trial 91-11. Arch Otolaryn-gol Head Neck Surg. 2003;129(1):44-49. 149. Harris BN, Bhuskute AA, Rao S, Farwell DG, Bewley AF. Primary surgery for advanced-stage laryngeal cancer: a stage and subsite-specific survival analysis. Head Neck. 2016;38(9):1380-1386. 150. Vengalil S, Giuliani ME, Huang SH, et al. Clinical outcomes in patients with T4 laryngeal cancer treated with primary radiotherapy versus primary laryngectomy. Head Neck. 2016;38 Suppl 1:E2035-E2040. 151. Day AT, Sinha P, Nussenbaum B, Kallogjeri D, Haughey BH. Management of primary T1-T4 glottic squamous cell carcinoma by transoral laser microsurgery.


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Surgery_Schwartz. Head Neck. 2016;38 Suppl 1:E2035-E2040. 151. Day AT, Sinha P, Nussenbaum B, Kallogjeri D, Haughey BH. Management of primary T1-T4 glottic squamous cell carcinoma by transoral laser microsurgery. Laryngoscope. 2017;127(3):597-604. 152. Suarez C, Rodrigo JP, Silver CE, et al. Laser surgery for early to moderately advanced glottic, supraglottic, and hypopharyn-geal cancers. Head Neck. 2012;34(7):1028-1035. 153. Gilbert RW, Goldstein DP, Guillemaud JP, Patel RS, Higgins KM, Enepekides DJ. Vertical partial laryngectomy with temporoparietal free flap reconstruction for recurrent laryngeal squamous cell carcinoma: technique and long-term outcomes. Arch Otolaryngol Head Neck Surg. 2012;138(5): 484-491. 154. Leone CA, Capasso P, Topazio D, Russo G. Supracricoid laryngectomy for recurrent laryngeal cancer after chemora-diotherapy: a systematic review and meta-analysis. Acta Oto-rhinolaryngol Ital. 2016;36(6):439-449. 155. Starmer HM, Quon H, Simpson M, et al. Speech-language pathology care and


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Surgery_Schwartz. cancer after chemora-diotherapy: a systematic review and meta-analysis. Acta Oto-rhinolaryngol Ital. 2016;36(6):439-449. 155. Starmer HM, Quon H, Simpson M, et al. Speech-language pathology care and shortand long-term outcomes of laryngeal cancer treatment in the elderly. Laryngoscope. 2015;125(12):2756-2763. 156. Gitomer SA, Hutcheson KA, Christianson BL, et al. Influ-ence of timing, radiation, and reconstruction on complications and speech outcomes with tracheoesophageal puncture. Head Neck. 2016;38(12):1765-1771. 157. de Braud F, al-Sarraf M. Diagnosis and management of squa-mous cell carcinoma of unknown primary tumor site of the neck. Semin Oncol. 1993;20(3):273-278. 158. Grau C, Johansen LV, Jakobsen J, Geertsen P, Andersen E, Jensen BB. Cervical lymph node metastases from unknown primary tumours. Results from a national survey by the Dan-ish Society for Head and Neck Oncology. Radiother Oncol. 2000;55(2):121-129. 159. Jereczek-Fossa BA, Jassem J, Orecchia R. Cervical lymph node


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Surgery_Schwartz. tumours. Results from a national survey by the Dan-ish Society for Head and Neck Oncology. Radiother Oncol. 2000;55(2):121-129. 159. Jereczek-Fossa BA, Jassem J, Orecchia R. Cervical lymph node metastases of squamous cell carcinoma from an unknown primary. Cancer Treat Rev. 2004;30(2):153-164. 160. Motz K, Qualliotine JR, Rettig E, Richmon JD, Eisele DW, Fakhry C. Changes in unknown primary squamous cell carci-noma of the head and neck at initial presentation in the era of human papillomavirus. JAMA Otolaryngol Head Neck Surg. 2016;142(3):223-228. 161. McGuirt WF, McCabe BF. Significance of node biopsy before definitive treatment of cervical metastatic carcinoma. Laryn-goscope. 1978;88(4):594-597. 162. Zhu L, Wang N. 18F-fluorodeoxyglucose positron emission tomography-computed tomography as a diagnostic tool in patients with cervical nodal metastases of unknown primary site: a meta-analysis. Surg Oncol. 2013;22(3):190-194. 163. Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A.


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Surgery_Schwartz. as a diagnostic tool in patients with cervical nodal metastases of unknown primary site: a meta-analysis. Surg Oncol. 2013;22(3):190-194. 163. Waltonen JD, Ozer E, Hall NC, Schuller DE, Agrawal A. Metastatic carcinoma of the neck of unknown primary origin: evolution and efficacy of the modern workup. Arch Otolaryn-gol Head Neck Surg. 2009;135(10):1024-1029. 164. Chai RL, Rath TJ, Johnson JT, et al. Accuracy of com-puted tomography in the prediction of extracapsular spread of lymph node metastases in squamous cell carcinoma of the head and neck. JAMA Otolaryngol Head Neck Surg. 2013;139(11):1187-1194. 165. Robbins KT, Ferlito A, Silver CE, et al. Contemporary management of sinonasal cancer. Head Neck. 2011;33(9): 1352-1365. 166. Ganly I, Patel SG, Singh B, et al. Craniofacial resection for malignant paranasal sinus tumors: report of an international collaborative study. Head Neck. 2005;27(7):575-584. 167. Ganly I, Patel SG, Singh B, et al. Complications of cra-niofacial resection for


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Surgery_Schwartz. malignant paranasal sinus tumors: report of an international collaborative study. Head Neck. 2005;27(7):575-584. 167. Ganly I, Patel SG, Singh B, et al. Complications of cra-niofacial resection for malignant tumors of the skull base: report of an international collaborative study. Head Neck. 2005;27(6):445-451. 168. Fu TS, Monteiro E, Muhanna N, Goldstein DP, de Almeida JR. Comparison of outcomes for open versus endoscopic approaches for olfactory neuroblastoma: a systematic review and individual participant data meta-analysis. Head Neck. 2016;38 Suppl 1:E2306-E2316.Brunicardi_Ch18_p0613-p0660.indd 65801/03/19 5:25 PM 659DISORDERS OF THE HEAD AND NECKCHAPTER 18 169. Al-Sarraf M, LeBlanc M, Giri PG, et al. Chemoradiotherapy versus radiotherapy in patients with advanced nasopharyngeal cancer: phase III randomized intergroup study 0099. J Clin Oncol. 1998;16(4):1310-1317. 170. Vlantis AC, Tsang RK, Yu BK, et al. Nasopharyngectomy and surgical margin status: a survival analysis. Arch


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Surgery_Schwartz. phase III randomized intergroup study 0099. J Clin Oncol. 1998;16(4):1310-1317. 170. Vlantis AC, Tsang RK, Yu BK, et al. Nasopharyngectomy and surgical margin status: a survival analysis. Arch Otolaryngol Head Neck Surg. 2007;133(12):1296-1301. 171. Sinha S, Dedmon MM, Naunheim MR, Fuller JC, Gray ST, Lin DT. Update on surgical outcomes of lateral temporal bone resection for ear and temporal bone malignancies. J Neurol Surg B Skull Base. 2017;78(1):37-42. 172. Beyea JA, Moberly AC. Squamous cell carcinoma of the temporal bone. Otolaryngol Clin North Am. 2015;48(2): 281-292. 173. Mazzoni A, Zanoletti E, Marioni G, Martini A. En bloc temporal bone resections in squamous cell carcinoma of the ear. technique, principles, and limits. Acta Otolaryngol. 2016;136(5):425-432. 174. Gurgel RK, Karnell LH, Hansen MR. Middle ear cancer: a population-based study. Laryngoscope. 2009;119(10): 1913-1917. 175. Rosenthal EL, King T, McGrew BM, Carroll W, Magnuson JS, Wax MK. Evolution of a paradigm for


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Surgery_Schwartz. LH, Hansen MR. Middle ear cancer: a population-based study. Laryngoscope. 2009;119(10): 1913-1917. 175. Rosenthal EL, King T, McGrew BM, Carroll W, Magnuson JS, Wax MK. Evolution of a paradigm for free tissue transfer reconstruction of lateral temporal bone defects. Head Neck. 2008;30(5):589-594. 176. Ferris R, Goldenberg D, Haymart MR, et al. American Thyroid Association consensus review of the anatomy, ter-minology and rationale for lateral neck dissection in dif-ferentiated thyroid cancer. Thyroid. 2012;22(5):501-508. 177. Robbins KT, Clayman G, Levine PA, et al. Neck dissection classification update:revisions proposed by the American Head and Neck Society and the American Academy of Otolar-yngology—Head and Neck Surgery. Arch Otolaryngol Head Neck Surg. 2002;128(7):751-758. 178. Wang Y, Ow TJ, Myers JN. Pathways for cervical metasta-sis in malignant neoplasms of the head and neck region. Clin Anat. 2012;25(1):54-71. 179. Weiss MH, Harrison LB, Isaacs RS. Use of decision analy-sis


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Surgery_Schwartz. Y, Ow TJ, Myers JN. Pathways for cervical metasta-sis in malignant neoplasms of the head and neck region. Clin Anat. 2012;25(1):54-71. 179. Weiss MH, Harrison LB, Isaacs RS. Use of decision analy-sis in planning a management strategy for the stage N0 neck. Arch Otolaryngol Head Neck Surg. 1994;120(7):699-702. 180. Bocca E, Pignataro O, Oldini C, Cappa C. Functional neck dissection: an evaluation and review of 843 cases. Laryngo-scope. 1984;94(7):942-945. 181. Medina JE, Byers RM. Supraomohyoid neck dissection: rationale, indications, and surgical technique. Head Neck. 1989;11(2):111-122. 182. Shah JP. Patterns of cervical lymph node metastasis from squamous carcinomas of the upper aerodigestive tract. Am J Surg. 1990;160(4):405-409. 183. Huang SH, Hwang D, Lockwood G, Goldstein DP, O’Sullivan B. Predictive value of tumor thickness for cervi-cal lymph-node involvement in squamous cell carcinoma of the oral cavity: a meta-analysis of reported studies. Cancer.


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Surgery_Schwartz. G, Goldstein DP, O’Sullivan B. Predictive value of tumor thickness for cervi-cal lymph-node involvement in squamous cell carcinoma of the oral cavity: a meta-analysis of reported studies. Cancer. 2009;115(7):1489-1497. 184. D’Cruz AK, Vaish R, Kapre N, et al. Elective versus thera-peutic neck dissection in node-negative oral cancer. N Engl J Med. 2015;373(6):521-529. 185. Farrag T, Lin F, Brownlee N, Kim M, Sheth S, Tufano RP. Is routine dissection of level II-B and V-A necessary in patients with papillary thyroid cancer undergoing lateral neck dissec-tion for FNA-confirmed metastases in other levels. World J Surg. 2009;33(8):1680-1683. 186. Eskander A, Merdad M, Freeman JL, Witterick IJ. Pattern of spread to the lateral neck in metastatic well-differenti-ated thyroid cancer: a systematic review and meta-analy-sis. Thyroid. 2013;23(5):583-592. 187. Cooper JS, Zhang Q, Pajak TF, et al. Long-term follow-up of the RTOG 9501/intergroup phase III trial: postoperative concurrent radiation


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Surgery_Schwartz. review and meta-analy-sis. Thyroid. 2013;23(5):583-592. 187. Cooper JS, Zhang Q, Pajak TF, et al. Long-term follow-up of the RTOG 9501/intergroup phase III trial: postoperative concurrent radiation therapy and chemotherapy in high-risk squamous cell carcinoma of the head and neck. Int J Radiat Oncol Biol Phys. 2012;84(5):1198-1205. 188. Bernier J, Cooper JS, Pajak TF, et al. Defining risk levels in locally advanced head and neck cancers: a comparative analysis of concurrent postoperative radiation plus chemo-therapy trials of the EORTC (#22931) and RTOG (# 9501). Head Neck. 2005;27(10):843-850. 189. Patil VM, Prabhash K, Noronha V, et al. Neoadjuvant che-motherapy followed by surgery in very locally advanced technically unresectable oral cavity cancers. Oral Oncol. 2014;50(10):1000-1004. 190. Zafereo M. Surgical salvage of recurrent cancer of the head and neck. Curr Oncol Rep. 2014;16(5):386-014-0386-0. 191. James A, Stewart C, Warrick P, Tzifa C, Forte V. Branchial sinus of the


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Surgery_Schwartz. M. Surgical salvage of recurrent cancer of the head and neck. Curr Oncol Rep. 2014;16(5):386-014-0386-0. 191. James A, Stewart C, Warrick P, Tzifa C, Forte V. Branchial sinus of the piriform fossa: reappraisal of third and fourth bran-chial anomalies. Laryngoscope. 2007;117(11):1920-1924. 192. Oyewumi M, Inarejos E, Greer ML, et al. Ultrasound to differ-entiate thyroglossal duct cysts and dermoid cysts in children. Laryngoscope. 2015;125(4):998-1003. 193. Stodulski D, Mikaszewski B, Majewska H, Wisniewski P, Stankiewicz C. Probability and pattern of occult cervical lymph node metastases in primary parotid carcinoma. Eur Arch Otorhinolaryngol. 2017;274(3):1659-1664. 194. Seethala RR. An update on grading of salivary gland carcino-mas. Head Neck Pathol. 2009;3(1):69-77. 195. Colella G, Cannavale R, Chiodini P. Meta-analysis of sur-gical approaches to the treatment of parotid pleomorphic adenomas and recurrence rates. J Craniomaxillofac Surg. 2015;43(6):738-745. 196. Ariyan S. The


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Surgery_Schwartz. Cannavale R, Chiodini P. Meta-analysis of sur-gical approaches to the treatment of parotid pleomorphic adenomas and recurrence rates. J Craniomaxillofac Surg. 2015;43(6):738-745. 196. Ariyan S. The functional pectoralis major musculocutaneous island flap for head and neck reconstruction. Plast Reconstr Surg. 1990;86(4):807-808. 197. Howard BE, Nagel TH, Barrs DM, Donald CB, Hayden RE. Reconstruction of lateral skull base defects: a comparison of the submental flap to free and regional flaps. Otolaryngol Head Neck Surg. 2016;154(6):1014-1018. 198. Herr MW, Emerick KS, Deschler DG. The supraclavicular artery flap for head and neck reconstruction. JAMA Facial Plast Surg. 2014;16(2):127-132. 199. Chepeha DB, Annich G, Pynnonen MA, et al. Pectoralis major myocutaneous flap vs revascularized free tissue trans-fer: complications, gastrostomy tube dependence, and hospi-talization. Arch Otolaryngol Head Neck Surg. 2004;130(2): 181-186. 200. Kang SY, Old MO, Teknos TN. Lateral arm free tissue


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Surgery_Schwartz. tissue trans-fer: complications, gastrostomy tube dependence, and hospi-talization. Arch Otolaryngol Head Neck Surg. 2004;130(2): 181-186. 200. Kang SY, Old MO, Teknos TN. Lateral arm free tissue transfer for parotid reconstruction: a pictorial essay. Head Neck. 2017. 201. Chepeha DB, Teknos TN, Fung K, et al. Lateral oroman-dibular defect: when is it appropriate to use a bridging reconstruction plate combined with a soft tissue revascu-larized flap? Head Neck. 2008;30(6):709-717. 202. Chepeha DB, Khariwala SS, Chanowski EJ, et al. Thoracodor-sal artery scapular tip autogenous transplant: vascularized bone with a long pedicle and flexible soft tissue. Arch Otolaryngol Head Neck Surg. 2010;136(10):958-964. 203. Chepeha DB, Teknos TN, Shargorodsky J, et al. Rectangle tongue template for reconstruction of the hemiglossectomy defect. Arch Otolaryngol Head Neck Surg. 2008;134(9):993-998. 204. Kang SY, Old MO, Teknos TN. Contour and osteotomy of free fibula transplant using a ruler


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Surgery_Schwartz. for reconstruction of the hemiglossectomy defect. Arch Otolaryngol Head Neck Surg. 2008;134(9):993-998. 204. Kang SY, Old MO, Teknos TN. Contour and osteotomy of free fibula transplant using a ruler template. Laryngoscope. 2016;126(10):2288-2290. 205. Young D, Harrison DA, Cuthbertson BH, Rowan K, Trac-Man Collaborators. Effect of early vs late tracheostomy placement on survival in patients receiving mechani-cal ventilation: the TracMan randomized trial. JAMA. 2013;309(20):2121-2129. 206. Szakmany T, Russell P, Wilkes AR, Hall JE. Effect of early tracheostomy on resource utilization and clinical outcomes in Brunicardi_Ch18_p0613-p0660.indd 65901/03/19 5:25 PM 660SPECIFIC CONSIDERATIONSPART IIcritically ill patients: meta-analysis of randomized controlled trials. Br J Anaesth. 2015;114(3):396-405. 207. Higgins KM, Punthakee X. Meta-analysis comparison of open versus percutaneous tracheostomy. Laryngoscope. 2007;117(3):447-454. 208. Brass P, Hellmich M, Ladra A, Ladra J, Wrzosek A.


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Surgery_Schwartz. KM, Punthakee X. Meta-analysis comparison of open versus percutaneous tracheostomy. Laryngoscope. 2007;117(3):447-454. 208. Brass P, Hellmich M, Ladra A, Ladra J, Wrzosek A. Percuta-neous techniques versus surgical techniques for tracheostomy. Cochrane Database Syst Rev. 2016;7:CD008045. 209. Ferris RL, Blumenschein G, Jr, Fayette J, et al. Nivolumab for recurrent squamous-cell carcinoma of the head and neck. N Engl J Med. 2016. 210. Eskander A, Monteiro E, Irish J, et al. Adherence to guideline-recommended process measures for squamous cell carcinoma of the head and neck in ontario: impact of surgeon and hospi-tal volume. Head Neck. 2016;38 Suppl 1:E1987-E1992.Brunicardi_Ch18_p0613-p0660.indd 66001/03/19 5:25 PM


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Surgery_Schwartz. Chest Wall, Lung, Mediastinum, and PleuraKatie S. Nason, Rose B. Ganim, and James D. Luketich 19chapterTRACHEAAnatomyThe trachea is composed of cartilaginous and membranous por-tions, beginning with the cricoid cartilage, the first complete cartilaginous ring of the airway. The cricoid cartilage consists of an anterior arch and a posterior broad-based plate. Articulat-ing with the posterior cricoid plate are the arytenoid cartilages. The vocal cords originate from the arytenoid cartilages and then attach to the thyroid cartilage. The subglottic space, the nar-rowest part of the trachea with an internal diameter of approxi-mately 2 cm, begins at the inferior surface of the vocal cords and extends to the first tracheal ring. The remainder of the distal trachea is 10.0 to 13.0 cm long, consists of 18 to 22 rings, and has an internal diameter of 2.3 cm (Fig. 19-1).1Bronchoscopically, the tracheal rings are visible as C-shaped hyaline cartilaginous structures that provide rigid-ity to the


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Surgery_Schwartz. of 18 to 22 rings, and has an internal diameter of 2.3 cm (Fig. 19-1).1Bronchoscopically, the tracheal rings are visible as C-shaped hyaline cartilaginous structures that provide rigid-ity to the anterior and lateral tracheal walls. The open ends of the C-rings are connected by the trachealis smooth muscle and encased in a dense band of connective tissue called perichon-drium. The first tracheal ring is attached directly to the cricoid cartilage; there are approximately two rings for every 1 cm of tracheal length.The tracheal blood supply, which includes the inferior thy-roid, subclavian, supreme intercostal, internal thoracic, innomi-nate, and superior and middle bronchial arteries, enters the airway near the junction of the membranous and cartilaginous portions (Fig. 19-2). Each arterial branch supplies a segment of 1.0 to 2.0 cm, thereby limiting circumferential mobilization to that same distance. The vessels are interconnected along the lat-eral surface of the trachea by an


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Surgery_Schwartz. branch supplies a segment of 1.0 to 2.0 cm, thereby limiting circumferential mobilization to that same distance. The vessels are interconnected along the lat-eral surface of the trachea by an important longitudinal vascular anastomosis that feeds transverse segmental vessels to the soft tissues between the cartilages.Tracheal InjuryTracheal injury can result from a variety of causes, includ-ing inhalation of smoke or toxic fumes, aspiration of liquids or solid objects, endotracheal intubation, blunt and penetrating trauma, and iatrogenic injury during operative procedures. Early diagnosis is critical to avoid subsequent complications, includ-ing respiratory infection and tracheal stenosis. Management of smoke or toxic fume inhalation and liquid aspiration is com-monly supportive; use of antibiotics, respiratory support, and airway clearance with flexible bronchoscopy is dictated by the patient’s condition. In rare circumstances, extracorporeal mem-brane oxygenation is required if


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Surgery_Schwartz. of antibiotics, respiratory support, and airway clearance with flexible bronchoscopy is dictated by the patient’s condition. In rare circumstances, extracorporeal mem-brane oxygenation is required if there is associated injury to the more distal airways and lung parenchyma.Despite ubiquitous use of high-volume–low-pressure cuffs, overinflation of the endotracheal cuff is the most common cause of injury secondary to endotracheal intubation. High cuff pressures can cause ischemia of the contiguous airway wall in as short as 4 hours. Prolonged overinflation can lead to scarring Trachea661Anatomy / 661Tracheal Injury / 661Tracheal Fistulas / 664Tracheal Neoplasms / 665Lung667Anatomy / 667Normal Lung Histology / 668Preinvasive Lesions / 669Invasive or Malignant Lesions / 670Lung Cancer Epidemiology / 673Screening for Lung Cancer in High-Risk Populations / 675Solitary Pulmonary Nodule / 677Metastatic Lesions to the Lung / 678Primary Lung Cancer-Associated Signs and Symptoms / 680Lung


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Surgery_Schwartz. / 673Screening for Lung Cancer in High-Risk Populations / 675Solitary Pulmonary Nodule / 677Metastatic Lesions to the Lung / 678Primary Lung Cancer-Associated Signs and Symptoms / 680Lung Cancer Management / 683Lung Cancer Treatment / 693Options for Thoracic Surgical Approaches / 701Postoperative Care / 703Postoperative Complications / 705Spontaneous Pneumothorax / 705Pulmonary Infections / 706Massive Hemoptysis / 717End-Stage Lung Disease / 719Chest Wall720Chest Wall Mass / 720Benign Chest Wall Neoplasms / 722Primary Malignant Chest Wall Tumors / 723Other Tumors of the Chest Wall / 725Chest Wall Reconstruction / 726Mediastinum726Anatomy and Pathologic Entities / 726History and Physical Examination / 727Imaging and Serum Markers / 727Diagnostic Nonsurgical Biopsies of the Mediastinum / 729Surgical Biopsies and Resection of Mediastinal Masses / 730Mediastinal Neoplasms / 730Mediastinal Cysts / 735Mediastinitis / 735Pleura and Pleural Space736Anatomy / 736Pleural Effusion /


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Surgery_Schwartz. / 729Surgical Biopsies and Resection of Mediastinal Masses / 730Mediastinal Neoplasms / 730Mediastinal Cysts / 735Mediastinitis / 735Pleura and Pleural Space736Anatomy / 736Pleural Effusion / 736Access and Drainage of Pleural Fluid Collections / 736Malignant Pleural Effusion / 739Empyema / 740Chylothorax / 741Tumors of the Pleura / 743Brunicardi_Ch19_p0661-p0750.indd 66101/03/19 7:00 PM 662Key Points1 Lung cancer continues to be a highly lethal and extremely common cancer, with 57% of patients presenting with dis-tant metastasis and 5-year survival of 18%. Lung cancer incidence is second only to the incidence of prostate cancer in men and breast cancer in women, with 222,500 esti-mated new cases in 2017. Squamous cell carcinoma and adenocarcinoma of the lung are the most common sub-types and are rarely found in the absence of a smoking history. Nonsmokers who live with smokers have a 24% increased risk of lung cancer compared to nonsmokers who do not live with smokers.2 A


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Surgery_Schwartz. sub-types and are rarely found in the absence of a smoking history. Nonsmokers who live with smokers have a 24% increased risk of lung cancer compared to nonsmokers who do not live with smokers.2 A multidisciplinary approach to evaluation of NSCLC, with standardized criteria and terminology for diagnosis in cytologic and small biopsy specimens, and routine molec-ular testing for known mutations, such as EGFR mutations and EML4-ALK fusion oncogenes is now recommended for the evaluation and management of lung nodules due to major advances in targeted therapy. Adequate tissue acquisition at the time of diagnostic workup is critical and facilitates patient care while minimizing the number of procedures to which the patient is subjected.3 The terms bronchioloalveolar carcinoma and mixed subtype adenocarcinoma have been eliminated from the classification of lung adenocarcinoma as a result of increased understanding of important clinical, radiologic, pathologic, and genetic differences


Surgery_Schwartz

Surgery_Schwartz. adenocarcinoma have been eliminated from the classification of lung adenocarcinoma as a result of increased understanding of important clinical, radiologic, pathologic, and genetic differences between mucinous and nonmucinous adenocarcinomas. The classification system delineates a stepwise pathologic progression, from AAH to invasive adenocarcinoma based on the predominant histo-logic growth patterns.4 The U.S. Preventive Services Task Force now recommends annual screening for lung cancer with low-dose computed tomography screening in high risk patients. Annual screen-ing averted 14% of lung cancer deaths when applied to a population of asymptomatic adults age 55 to 80 years who have a 30 pack-year smoking history and are either currently smoking or have quit within the past 15 years. Patients should be healthy enough to tolerate curative treat-ment, specifically surgery per guidelines, and screening should be discontinued once the patient has not smoked for 15 years or develops a


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Surgery_Schwartz. Patients should be healthy enough to tolerate curative treat-ment, specifically surgery per guidelines, and screening should be discontinued once the patient has not smoked for 15 years or develops a life-limiting health condition, becomes unable to tolerate lung surgery, or is unwilling to undergo curative lung resection. With this approach, it is expected that 50% of diagnosed cancers will be early stage. Screening of patients age 50 years or older with a 20 pack-year or greater history and additional risk factors (as determined by the Tammemagi lung cancer risk calculator or other validated risk scores) that increase the risk of lung cancer to 1.3% or greater should also be considered as part of lung cancer screening programs. In all cases, patient–physician shared decision-making should be undertaken, with a discussion of the risks and benefits of screening.5 Assessment of patient risk before thoracic resection is based on clinical judgment and systematic assessment of


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Surgery_Schwartz. should be undertaken, with a discussion of the risks and benefits of screening.5 Assessment of patient risk before thoracic resection is based on clinical judgment and systematic assessment of cardiopulmonary status using established algorithms.6 Maximum oxygen consumption (v. o2max) values provide important additional information in those patients with severely impaired Dlco and forced expiratory volume in 1 second. Values of <10 mL/kg per minute generally pro-hibit any major pulmonary resection because the mortality in patients with these levels is 26% compared with only 8.3% in patients whose v. o2max is ≥10 mL/kg per minute; values of >15 mL/kg per minute generally indicate the patient’s ability to tolerate pneumonectomy.7 Tumor ablative strategies are viable alternatives to surgical resection for early stage lung cancer in inoperable patients. While premature, ablative techniques may ultimately be shown to have efficacy equivalent to lobectomy for the pri-mary treatment of very


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Surgery_Schwartz. resection for early stage lung cancer in inoperable patients. While premature, ablative techniques may ultimately be shown to have efficacy equivalent to lobectomy for the pri-mary treatment of very small peripheral early-stage lung cancers and become primary therapy, even in operable patients, although limited resection with wedge (at least 2 cm margin and at least 1:1 tumor/margin ratio) and seg-mentectomy provide better margins of treatment and nodal sampling ensures occult nodal metastasis are identified. Multidisciplinary collaboration among thoracic surgery, interventional radiology/pulmonology, and radiation oncol-ogy is required to ensure that development of these ablative techniques occurs through properly designed and well-con-trolled prospective studies and will ensure that patients receive the best available therapy, regardless of whether it is surgical resection or ablative therapy.8 The term non–small cell lung carcinoma (NSCLC) includes many tumor cell types, including


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Surgery_Schwartz. receive the best available therapy, regardless of whether it is surgical resection or ablative therapy.8 The term non–small cell lung carcinoma (NSCLC) includes many tumor cell types, including large cell, squa-mous cell, and adenocarcinoma. The approach to diagno-sis and management and the terminology used in describing these tumors are evolving rapidly. In particular, the evaluation and management of adenocarcinoma of the lung has shifted dramatically and firm establishment of NSCLC cell type prior to chemotherapy for advanced stage lung cancer is essential.9 Increasing evidence suggests a significant role for gastro-esophageal reflux disease in the pathogenesis of chronic lung diseases such as bronchiectasis and idiopathic pulmo-nary fibrosis, and it may also contribute to bronchiolitis obliterans syndrome in lung transplant patients.10 Treatment of pulmonary aspergillosis/aspergilloma is indi-vidualized. Following colonization of a lung cavity or area of bronchiectasis, fungal


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Surgery_Schwartz. obliterans syndrome in lung transplant patients.10 Treatment of pulmonary aspergillosis/aspergilloma is indi-vidualized. Following colonization of a lung cavity or area of bronchiectasis, fungal growth within the cavity appears as an irregular cavitary lining, progressing over time as a late finding in chronic pulmonary aspergillosis to a fungal ball called an aspergilloma. Asymptomatic patients can be observed without any additional therapy. Similarly, mild hemoptysis, which is not life-threatening, can be managed with medical therapy, including antifungals and cough suppressants. Oral triazole therapy is now considered the standard of care for chronic, cavitary pulmonary aspergil-losis. Massive hemoptysis had traditionally been an indi-cation for urgent or emergent operative intervention. However, with the advancement of endovascular tech-niques, bronchial artery embolization in select centers with experience in these techniques has been effective.11 In patients with malignant


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Surgery_Schwartz. However, with the advancement of endovascular tech-niques, bronchial artery embolization in select centers with experience in these techniques has been effective.11 In patients with malignant pleural effusion, poor expan-sion of the lung (because of entrapment by tumor or adhe-sions) generally predicts a poor result with pleurodesis and is the primary indication for placement of indwelling pleu-ral catheters. These catheters have dramatically changed the management of end-stage cancer treatment because they substantially shorten the amount of time patients spend in the hospital during their final weeks of life.Brunicardi_Ch19_p0661-p0750.indd 66201/03/19 7:00 PM


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Surgery_Schwartz. CHAPTER 19663CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAEpiglottisAryepiglottic m.Transverse, obliquearytenoid mm.Lateralcricoarytenoid m.Posteriorcricoarytenoid m.Thyroid cartilage facetRecurrentlaryngeal n.Internallaryngeal n.Thyroepiglottic m.Thyroarytenoid m.Cricothyroid m.(cut)Inferiorthyroid a.Branch from internal thoracic a. Superior bronchial a.Middle bronchial a.1Lateral longitudinalanastomosis32Figure 19-2. Arterial blood supply to the larynx and upper trachea. a. = artery.Figure 19-1. Anatomy of the larynx and upper trachea. m. = muscle; n. = nerve.and stenosis; full-thickness injury can result in fistulae between the innominate artery anteriorly and the esophagus posteriorly. Avoidance requires careful cuff management to keep pressures as low as possible; in circumstances of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after


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Surgery_Schwartz. of prolonged ventilatory support and high airway pressure, cuff pressure monitoring (to maintain pressures <20 mmHg) is advisable.Historically, clinically significant tracheal stenosis after tracheostomy occurred in 3% to 12% of cases, with severe stenosis in 1% to 2%.2 With the use of low-pressure cuffs, the estimated incidence has decreased to 4.9 cases per million patients per year. Intubation-related risk factors include pro-longed intubation; high tracheostomy through the first tracheal ring or cricothyroid membrane; transverse rather than vertical incision on the trachea; oversized tracheostomy tube; prior tra-cheostomy or intubation; and traumatic intubation. Stenosis is also more common in older patients, in women, after radiation, or after excessive corticosteroid therapy, and in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed


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Surgery_Schwartz. in the setting of concomitant diseases such as autoimmune disorders, severe reflux disease, or obstructive sleep apnea and the setting of severe respiratory failure. However, even a properly placed tra-cheostomy can lead to tracheal stenosis because of scarring and local injury. Mild ulceration and stenosis are frequently seen after tracheostomy removal. Use of the smallest tracheostomy tube possible, rapid downsizing, and a vertical tracheal incision minimize the risk for posttracheostomy stenosis.Stridor and dyspnea on exertion are the primary symp-toms of tracheal stenosis. In the setting of postintubation injury, a significant portion of the cartilaginous structural support to the airway is destroyed by regional ischemic necrosis; during healing, a weblike fibrous growth develops and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of


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Surgery_Schwartz. and narrows the airway (Fig. 19-3). In contrast, stenosis caused by tracheostomy is most commonly due to an excess of granulation tissue forma-tion around the tracheal stoma site. Time to onset of symptoms after extubation or tracheostomy decannulation usually ranges from 2 to 12 weeks, but symptoms can appear immediately or as long as 1 to 2 years later. Frequently, patients are misdiag-nosed as having asthma or bronchitis, and treatment for such illnesses can persist for some time before the correct diagnosis is discovered. Generally, symptom intensity is related to the degree of stenosis and to the patient’s underlying pulmonary disease.Brunicardi_Ch19_p0661-p0750.indd 66301/03/19 7:00 PM 664SPECIFIC CONSIDERATIONSPART IIFigure 19-3. Diagram of the principal postintubation lesions. A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level.


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Surgery_Schwartz. A. A circumferential lesion at the cuff site after the use of an endotracheal tube. B. Potential lesions after the use of tracheostomy tubes. Anterolateral stenosis can be seen at the stomal level. Circumferential stenosis can be seen at the cuff level (lower than with an endotracheal tube). The segment in between is often inflamed and malacotic. C. Damage to the subglottic larynx. D. Tracheoesophageal fistula occurring at the level of the tracheostomy cuff; circumferential damage is usual at this level. E. Tracheoinnominate artery fistula. (Adapted with permission from Grillo H. Surgical treatment of postintubation tracheal injuries. J Thorac Cardiovasc Surg. 1979 Dec;78(6):860-875.)Acute Management. A comprehensive bronchoscopic evalua-tion is critical in the initial phase of evaluation. Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and


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Surgery_Schwartz. Stenosis length, location, distance between the vocal cords and proximal steno-sis, and distance from the distal aspect to the major carina must be documented. In patients with severe stenosis and respiratory compromise, rigid bronchoscopy can be used to dilate the steno-sis; this provides immediate relief of the airway obstruction and facilitates thorough evaluation of the stenosis. Rarely, if ever, is tracheostomy necessary.Most intubation injuries are located in the upper third of the trachea and can be accessed for resection through a col-lar incision. Resection typically involves 2 to 4 cm of trachea for benign stenosis. It is critical to fully resect all inflamed and scarred tissue. However, a primary anastomosis can still be per-formed without undue tension, even if up to one half of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with


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Surgery_Schwartz. of the tra-chea requires resection.2 Ideally, the patient is extubated in the operating room or shortly thereafter. For patients in whom tra-cheal resection is not possible, such as patients with significant comorbidities or with an excessively long stenosis, endotracheal stenting, typically silicone T-tubes, can provide palliation. Wire mesh stents should not be used, given their known propensity to erode through the wall of the airway. Balloon dilation, laser ablation, and tracheoplasty have also been described, although the efficacy is marginal.Tracheal replacement is evolving as an option for manage-ment of tracheal stenosis as bioengineering techniques for decel-lularizing donor trachea have been developed. This removes all antigens against which the recipient immune system might react and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal


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Surgery_Schwartz. and enables use of the donor trachea scaffolding without risk of rejection. Following decellularization, the donor tracheal scaf-folding is seeded with recipient chondrocytes, to restore tracheal rigidity, and with recipient epithelial cells, to recreate the inner epithelial lining. Several case reports of successful allogeneic tracheal transplantation have been published. The technique continues to be limited to a few highly specialized centers, due, in part, to the scarcity of donor trachea and the need for tissue bioengineering expertise as well as the lack of established effi-cacy for the approach. Current efforts are focused on creation of biosynthetic scaffolding that can be used instead of donor trachea. This would substantially increase the availability of the tracheal replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and


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Surgery_Schwartz. replacement material and enable widespread use of the technique, but early results have been contested, including three case reports called into question as containing multiple data fab-rications and omissions.Tracheal FistulasTracheoinnominate Artery Fistula. Tracheoinnominate artery fistula has two main causes: low placement of a trache-ostomy and hyperinflation of the tracheal cuff. Tracheostomy placement should be through the second to fourth tracheal rings without reference to the location of the sternal notch. When placed below the fourth tracheal ring, the inner curve of the tracheostomy cannula will be positioned to exert pressure on the posterior aspect of the innominate artery, leading to arterial ero-sion. Similarly, the tracheal cuff, when hyperinflated, will cause ischemic injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery


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Surgery_Schwartz. injury to the anterior airway and subsequent erosion into the artery. Most cuff-induced fistulas will develop within 2 weeks after placement of the tracheostomy.Clinically, tracheoinnominate artery fistulas present with bleeding. A premonitory hemorrhage often occurs and, although it is usually not massive, must not be ignored or simply attrib-uted to general airway irritation or wound bleeding. With sig-nificant bleeding, the tracheostomy cuff can be hyperinflated to temporarily occlude the arterial injury. If such an effort is unsuccessful, the tracheostomy incision should be immediately opened widely and a finger inserted to compress the artery Brunicardi_Ch19_p0661-p0750.indd 66401/03/19 7:00 PM


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Surgery_Schwartz. CHAPTER 19665CHEST WALL, LUNG, MEDIASTINUM, AND PLEURA1Cuffhyperinflation2Digital control3 BronchoscopiccompressionOrotracheal tubeready in place if neededOrotrachealtube replacingtracheostomytubeForward pressureapplied withbronchoscopeFigure 19-4. Steps in the emergency management of a tracheoinnominate artery fistula.against the manubrium (Fig. 19-4). The patient can then be orally intubated, and the airway suctioned free of blood. Emer-gent surgical resection of the involved segment of artery is per-formed, usually without reconstruction.Tracheoesophageal Fistula. Tracheoesophageal fistu-las (TEFs) occur primarily in patients receiving prolonged mechanical ventilator support concomitant with an indwelling nasogastric tube.4 Cuff compression of the membranous trachea against the nasogastric tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive


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Surgery_Schwartz. tube leads to airway and esophageal injury and fistula development. Clinically, airway suctioning reveals saliva, gastric contents, or tube feedings. Gastric insuf-flation, secondary to positive pressure ventilation, can occur. Bronchoscopy is diagnostic; with the bronchoscope inserted, the endotracheal tube is withdrawn, and the fistula at the cuff site is exposed. Alternatively, esophagoscopy demonstrates the cuff of the endotracheal tube in the esophagus.Treatment, first and foremost, requires removing tubes from the esophagus and weaning the patient from the ventila-tor. The cuff of the endotracheal tube should be placed below the fistula, avoiding overinflation. To minimize aspiration, a gastrostomy tube should be placed for gastric decompression (to prevent reflux) and a jejunostomy tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of


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Surgery_Schwartz. tube for feeding. If aspira-tion persists, esophageal diversion with cervical esophagostomy can be performed. Once weaned from the ventilator, tracheal resection and primary anastomosis, repair of the esophageal defect, and interposition of a muscle flap between the trachea and esophagus can be performed (Fig. 19-5).5Tracheal NeoplasmsAlthough extremely rare, the most common primary tracheal neoplasms are squamous cell carcinomas (related to smoking) and adenoid cystic carcinomas. Clinically, tracheal tumors pres-ent with cough, dyspnea, hemoptysis, stridor, or symptoms of invasion of contiguous structures (such as the recurrent laryn-geal nerve or the esophagus). The most common radiologic finding of tracheal malignancy is tracheal stenosis, but it is found in only 50% of cases. With tumors other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage


Surgery_Schwartz

Surgery_Schwartz. other than squamous cell carcinomas, symptoms may persist for months because of slow tumor growth rates. Stage of presentation is advanced, with approximately 50% of patients presenting with stage IV disease. Five-year survival for all tracheal neoplasms is 40% but falls to 15% for those with stage IV disease.6Squamous cell carcinomas often present with regional lymph node metastases and are frequently unresectable at pre-sentation. Their biologic behavior is similar to that of squamous cell carcinoma of the lung. Adenoid cystic carcinomas, a type of Brunicardi_Ch19_p0661-p0750.indd 66501/03/19 7:00 PM 666SPECIFIC CONSIDERATIONSPART IIACBDCricoidSternohyoid m.EsophagusFigure 19-5. Single-stage operation for clo-sure of a tracheoesophageal fistula and tra-cheal resection. A. The fistula is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea


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Surgery_Schwartz. is divided, and the trachea is transected below the level of damage. B. The fistula is closed on the tra-cheal side in a single layer and the esopha-geal side in a double layer. The damaged trachea segment is resected. C. A pedicled muscle flap, such as the sternohyoid muscle, is used to buttress the esophageal repair. D. View of completed tracheal anastomosis. m. = muscle.salivary gland tumor, are generally slow growing, spread sub-mucosally, and tend to infiltrate along nerve sheaths and within the tracheal wall. Although indolent in nature, adenoid cystic carcinomas are malignant and can spread to regional lymph nodes, lung, and bone. Squamous cell carcinoma and adenoid cystic carcinomas represent approximately 65% of all tracheal neoplasms. The remaining 35% is comprised of small cell car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography


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Surgery_Schwartz. car-cinomas, mucoepidermoid carcinomas, adenocarcinomas, lym-phomas, and others.7Therapy. Evaluation and treatment of patients with tracheal tumors should include neck and chest computed tomography (CT) and rigid bronchoscopy. Rigid bronchoscopy permits gen-eral assessment of the airway and tumor; it also allows debride-ment or laser ablation of the tumor to provide relief of dyspnea. If the tumor is judged to be completely resectable, primary resection and anastomosis is the treatment of choice for these tumors (Fig. 19-6). Up to 50% of the length of the trachea can be resected with primary anastomosis. In most tracheal resections, anterolateral tracheal mobilization and suturing of the chin to the sternum for 7 days are done routinely. Use of laryngeal and hilar release is determined at the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to


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Surgery_Schwartz. the time of surgery, based on the surgeon’s judgment of the degree of tension present. For longer resections, specialized maneuvers are necessary such as laryn-geal release and right hilar release to minimize tension on the anastomosis.Postoperative mortality, which occurs in up to 10% of patients, is associated with the length of tracheal resection, use of laryngeal release, the type of resection, and the histologic type of the cancer. Factors associated with improved long-term survival include complete resection and use of radiation as adjuvant therapy in the setting of incomplete resection.8 Due to their radiosensitivity, radiotherapy is frequently given postop-eratively after resection of both adenoid cystic carcinomas and squamous cell carcinomas.9 A dose of 50 Gy or greater is usual. Nodal positivity does not seem to be associated with worse sur-vival. Survival at 5 and 10 years is much better for adenoid Brunicardi_Ch19_p0661-p0750.indd 66601/03/19 7:00 PM


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Surgery_Schwartz. CHAPTER 19667CHEST WALL, LUNG, MEDIASTINUM, AND PLEURAHigh-index of suspicion(cough, dyspnea, hemoptysis,stridor, and hoarseness)Complete staging: computedtomography/PETscan/mediastinoscopyFlexible/rigid bronchoscopyTumor resectablePerformance statusadequate for surgeryDebridement and/orlaser ablationPrinciples of tracheal resection• May resect up to 50% of tracheal length• Anterolateral mobilization only• Suture head in forward flexion for 7 days• Laryngeal and hilar release as needed for relief of tensionRadiotherapy 50 Gy (±chemotherapy)(primary treatment or postoperatively)Tumor unresectable1) Probable grossly positive tracheal resection margin2) Metastatic disease3) Length of resection precludes safe reconstruction4) Invasion of unresectable adjacent organsPoor performancestatuscystic (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local


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Surgery_Schwartz. (73% and 57%, respectively) than for tracheal cancers (47% and 36%, respectively; P <.05). For patients with unre-sectable tumors, radiation may be given as the primary therapy to improve local control, but it is rarely curative. For recurrent airway compromise, stenting or laser therapies should be con-sidered as part of the treatment algorithm.LUNGAnatomySegmental Anatomy. The segmental bronchial and vascular anatomy of the lungs allows subsegmental and segmental resec-tions, if the clinical situation requires or if lung tissue can be preserved10 (Fig. 19-7). Note the continuity of the pulmonary parenchyma between adjacent segments of each lobe.Lymphatic Drainage. Lymph nodes that drain the lungs are divided into two groups according to the tumor-node-metastasis (TNM) staging system for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of


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Surgery_Schwartz. for lung cancer: the pulmonary lymph nodes (N1) and the mediastinal nodes (N2) (Fig. 19-8).The N1 lymph nodes constitute the following: (a) intrapul-monary or segmental nodes that lie at points of division of seg-mental bronchi or in the bifurcations of the pulmonary artery; (b) lobar nodes that lie along the upper, middle, and lower lobe bronchi; (c) interlobar nodes located in the angles formed by the main bronchi bifurcating into the lobar bronchi; and (d) hilar nodes along the main bronchi. The interlobar lymph nodes lie in the depths of the interlobar fissure on each side and constitute a lymphatic sump for each lung, referred to as the lymphatic sump of Borrie; all of the pulmonary lobes of the corresponding lung drain into this group of nodes (Fig. 19-9). On the right, the nodes of the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump


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Surgery_Schwartz. the lymphatic sump lie around the bronchus inter-medius (bounded above by the right upper lobe bronchus and below by the middle lobe and superior segmental bronchi). On the left, the lymphatic sump is confined to the interlobar fis-sure, with the lymph nodes in the angle between the lingular and lower lobe bronchi. These nodes are always in close proximity to pulmonary arterial branches and typically must be carefully dissected to identify the pulmonary arterial segments for divi-sion during lung resection.The N2 lymph nodes consist of four main groups. (a) The anterior mediastinal nodes are located in association with the upper surface of the pericardium, the phrenic nerves, the liga-mentum arteriosum, and the left aspect of the innominate vein. (b) The posterior mediastinal group includes paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are


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Surgery_Schwartz. paraesophageal lymph nodes within the inferior pulmonary ligament and, more superiorly, between the esophagus and trachea near the arch of the azygos vein. (c) The tracheobronchial lymph nodes are made up of three subgroups that are located near the bifurcation of the trachea. These include the subcarinal nodes, which lie in the obtuse angle between the trachea and each main stem bronchus, and the nodes that lay anterior to the lower end of the trachea. (d) Paratracheal lymph nodes are located in proximity to the trachea in the superior mediastinum. Those on the right side form a chain with the tracheobronchial nodes inferiorly and with some of the deep cervical nodes above (scalene lymph nodes).Lymphatic drainage to the mediastinal lymph nodes from the right lung is ipsilateral, except for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and


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Surgery_Schwartz. for occasional bilateral drain-age to the superior mediastinum. In contrast, in the left lung, particularly the left lower lobe, lymphatic drainage occurs with equal frequency to ipsilateral and contralateral superior medi-astinal nodes.Figure 19-6. Algorithm for eval-uation and treatment of tracheal neoplasm. PET = positron emis-sion tomography.Brunicardi_Ch19_p0661-p0750.indd 66701/03/19 7:00 PM 668SPECIFIC CONSIDERATIONSPART IIRight lung and bronchiLeft lung and bronchi11112222333333444445555556666668888888999999101010101010107771+21+2Segments 1. Apical2. Posterior3. Anterior4. Lateral5. Medial6. Superior7. Medial Basal *8. Anterior Basal9. Lateral Basal10. Posterior Basal * Medial basal (7) not present in left lungFigure 19-7. Segmental anatomy of the lungs and bronchi.3p3a6AoPA512LBrachiocephalicartery2R4RAo4LAzygos vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of


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Surgery_Schwartz. vein10R711R12,13,14R8R9R9L8LPA11L10L12,13,14LFigure 19-8. The location of regional lymph node stations for lung cancer.Figure 19-9. The lymphatic sump of Borrie includes the groups of lymph nodes that receive lymphatic drainage from all pulmonary lobes of the corresponding lung.Normal Lung HistologyThe lung can be conveniently viewed as two linked compo-nents: the tracheobronchial tree (or conducting airways com-ponent) and the alveolar spaces (or gas exchange component). The tracheobronchial tree consists of approximately 23 airway divisions to the level of the alveoli. It includes the main bronchi, lobar bronchi, segmental bronchi (to designated bronchopulmo-nary segments), and terminal bronchioles (i.e., the smallest air-ways still lined by bronchial epithelium and without alveoli). The tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet


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Surgery_Schwartz. tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, which both derive from basal cells (Fig. 19-10). Ciliated cells predominate. Goblet cells, which release mucus, can significantly increase in number in acute bronchial injury, such as exposure to cigarette smoke. The normal bronchial epithelium also contains bron-chial submucosal glands, which are mixed salivary-type glands Brunicardi_Ch19_p0661-p0750.indd 66801/03/19 7:00 PM


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Surgery_Schwartz. CHAPTER 19669CHEST WALL, LUNG, MEDIASTINUM, AND PLEURABAFigure 19-10. Normal lung histology. A. Pseudostratified ciliated columnar cells and mucous cells normally line the tracheobronchial tree. B. A Kulchitsky cell is depicted (arrow).containing mucous cells, serous cells, and neuroendocrine cells called Kulchitsky cells, which are also found within the surface epithelium. The bronchial submucosal glands can give rise to salivary gland–type tumors, including mucoepidermoid carci-nomas and adenoid cystic carcinomas.Two cell types, called type I and type II pneumocytes, make up the alveolar epithelium. Type I pneumocytes com-prise 40% of the total number of alveolar epithelial cells, but cover 95% of the surface area of the alveolar wall. These cells are not capable of regeneration because they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen


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Surgery_Schwartz. they have no mitotic potential. Type II pneumocytes cover only 3% of the alveo-lar surface, but comprise 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen in the alveolar spaces.Preinvasive LesionsThe term “precancerous” does not mean that an inevitable pro-gression to invasive carcinoma will occur, but such lesions, particularly those with high-grade dysplasia,11,12 do constitute a clear marker for potential development of invasive cancer. Three precancerous lesions of the respiratory tract are currently recognized.1. Squamous dysplasia and carcinoma in situ. Cigarette smoke can induce a transformation of the tracheobron-chial pseudostratified epithelium to metaplastic squamous mucosa, with subsequent evolution to dysplasia as cellu-lar abnormalities accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered


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Surgery_Schwartz. accumulate. Dysplastic changes include altered cellular polarity and increased cell size, number of cell layers, nuclear-to-cytoplasmic ratio, and number of mitoses. Gradations are considered mild, moderate, or severe. Carcinoma in situ represents carcinoma still con-fined by the basement membrane.2. Atypical adenomatous hyperplasia (AAH). AAH is a lesion smaller than 5.0 mm, comprising epithelial cells lining the alveoli that are similar to type II pneumocytes. Histologically, AAH is similar to adenocarcinoma in situ; it represents the beginning stage of a stepwise evolution to adenocarcinoma in situ and then to adenocarcinoma. With the availability of thin-section CT, it is possible to detect Brunicardi_Ch19_p0661-p0750.indd 66901/03/19 7:00 PM 670SPECIFIC CONSIDERATIONSPART IIpreinvasive adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell


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Surgery_Schwartz. adenocarcinoma lesions as early as AAH. These lesions can be multiple, are typically small (5 mm or less), and have a ground-glass appearance.3. Diffuse idiopathic pulmonary neuroendocrine cell hyper-plasia. This rare lesion represents a diffuse proliferation of neuroendocrine cells, but without invasion of the basement membrane. It can exist as a diffuse increase in the number of single neuroendocrine cells, or as small lesions less than 5.0 mm in diameter. Lesions over 5.0 mm in size or that breach the basement membrane are carcinoid tumors.Invasive or Malignant LesionsThe pathologic diagnosis of lung cancer is currently based on light microscopic criteria and is broadly divided into two main groups: non–small cell lung carcinoma and neuroendocrine tumors.13 Immunohistochemical staining and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma


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Surgery_Schwartz. and electron micros-copy are used as adjuncts in diagnosis, particularly in the assess-ment of potential neuroendocrine tumors.Non–Small Cell Lung Carcinoma. The term non–small cell lung carcinoma (NSCLC) includes many tumor cell types, including large cell, squamous cell, and adenocarcinoma. His-torically, these subtypes were considered to be a uniform group based on limited understanding of the distinct clinical behaviors of the subtypes as well as the fact that there were few treat-ment options available. With increasing understanding of the molecular biology underlying these tumor subtypes, however, the approach to diagnosis and management and the terminology used in describing these tumors are evolving rapidly.Adenocarcinoma The incidence of adenocarcinoma has increased over the last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in


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Surgery_Schwartz. last several decades, and it is now the most common lung cancer, accounting for 30% of lung cancers in Table 19-1Difference between invasive mucinous adenocarcinoma and nonmucinous adenocarcinoma in situ/minimally invasive adenocarcinoma/lepidic predominant adenocarcinoma INVASIVE MUCINOUS ADENOCARCINOMA (FORMERLY MUCINOUS BAC)NONMUCINOUS AIS/MIA/LPA (FORMERLY NONMUCINOUS BAC)Female49/84 (58%)52,120-123101/140 (72%)52,120-123Smoker39/87 (45%)52,120-122,12475/164 (46%)52,120-122,124Radiographic appearanceMajority consolidation; air bronchogram125Majority ground-glass attenuation23,56,58,103,129-134 Frequent multifocal and multilobar presentation56,125-128 Cell typeMucin-filled, columnar, and/or goblet50-52,125,135Type II pneumocyte and/or Clara cell50-52,125,135Phenotype CK7Mostly positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive


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Surgery_Schwartz. positive (∼88%)a54,55,136-139Positive (∼98%)a54,55,136-139 CK20Positive (∼54%)a54,55,136-139Negative (∼5%)a54,55,136-139 TTF-1Mostly negative (∼17%)a54,55,120,137-139Positive (∼67%)a54,55,120,137-139Genotype KRAS mutationFrequent (∼76%)a55,94,121,127,140-144Some (∼13%)a55,121,127,140-144 EGFR mutationAlmost none (∼3)a55,121,127,140-142Frequent (∼45%)a55,121,127,140-142Note: aNumbers represent the percentage of cases that are reported to be positive.Abbreviations: BAC = bronchioloalveolar carcinoma; AIS = adenocarcinoma in situ; MIA = minimally invasive adenocarcinoma; LPA = lepidic predominant adenocarcinoma; EGFR = epidermal growth factor receptor; TTF = thyroid transcription factor.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male


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Surgery_Schwartz. for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.male smokers and 40% of lung cancers in female smokers. Adenocarcinoma is the histologic subtype for 80% and 60% of lung cancers in nonsmoking females and males, respectively. It occurs more frequently in females than in males. It is the most frequent histologic subtype in women, patients who are under 45 years of age, and Asian populations.14Histologic Subtyping of Adenocarcinoma. Increasing under-standing of lung adenocarcinoma, such as important clinical, radiologic, pathologic, and genetic differences between mucinous and nonmucinous adenocarcinomas, prompted multiple changes in the classification system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy


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Surgery_Schwartz. system in 2011.15 Based on consensus, the international working group proposed a multidisciplinary approach, with standardized criteria and terminology for diagno-sis in cytologic and small biopsy specimens, and routine molecu-lar testing for known mutations, such as EGFR and KRAS mutations (Table 19-1). The new classification system delineated a stepwise pathologic progression, from AAH to invasive adenocarcinoma based on the predominant histologic growth patterns; the terms bronchioloalveolar carcinoma and mixed subtype adenocarcinoma were eliminated in favor of more biologically driven classification (Table 19-2).1. Adenocarcinoma in situ (AIS). AISs are small (≤3 cm) sol-itary adenocarcinomas that have pure lepidic growth; lepidic growth is characterized by tumor growth within the alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely


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Surgery_Schwartz. alveolar spaces. These lesions are not invasive into the stroma, vas-cular system, or pleura and do not have papillary or micro-papillary patterns or intra-alveolar tumor cells. They are very rarely mucinous, consisting of type II pneumocytes or Clara cells. These patients are expected to have 100% dis-ease-specific survival with complete surgical resection. On CT scan, AIS can appear as a pure ground-glass neoplasm, 123Brunicardi_Ch19_p0661-p0750.indd 67001/03/19 7:00 PM


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Surgery_Schwartz. CHAPTER 19671CHEST WALL, LUNG, MEDIASTINUM, AND PLEURATable 19-2New classification system for lung adenocarcinomaPreinvasive lesions Atypical adenomatous hyperplasia Adenocarcinoma in situ (≤3 cm formerly BAC) Nonmucinous Mucinous Mixed mucinous/nonmucinousMinimally invasive adenocarcinoma (≤3 cm lepidic predominant tumor with ≤5 mm invasion) Nonmucinous Mucinous Mixed mucinous/nonmucinousInvasive adenocarcinoma Lepidic predominant (formerly nonmucinous BAC pattern, with >5 mm invasion) Acinar predominant Papillary predominant Micropapillary predominant Solid predominant with mucin productionVariants of invasive adenocarcinoma Invasive mucinous adenocarcinoma (formerly mucinous BAC) Colloid Fetal (low and high grade) EntericAbbreviations: BAC = bronchioloalveolar carcinoma; IASLC = International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al:


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Surgery_Schwartz. International Association for the Study of Lung Cancer; ATS = American Thoracic Society; ERS = European Respiratory Society.Reproduced with permission from Travis WD, Brambilla E, Noguchi M, et al: International association for the study of lung cancer/american thoracic society/european respiratory society international multidisciplinary classification of lung adenocarcinoma, J Thorac Oncol. 2011 Feb;6(2):244-285.but occasionally it will present as part of a solid or part-solid nodule. Mucinous AIS is more likely to appear solid or to have the appearance of consolidation. As with AAH, the lesions can be single or multiple; the ground-glass changes in AIS, however, tend to have a higher attenuation com-pared to AAH. The 8th edition American Joint Committee on Cancer (AJCC) staging manual t-stage for AIS is tumor in situ (Tis).2. Minimally invasive adenocarcinoma (MIA). In the same size solitary lesion, if less than 5 mm of invasion are noted within a predominantly lepidic growth