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Surgery_Schwartz_10502 | Surgery_Schwartz | novel targets for therapeutic approaches.Extent of disease is the strongest predictor of long-term outcome. Several staging systems for rhabdomyosarcoma are available. The Intergroup Rhabdomyosarcoma Study Group system is based on surgical-pathologic groupings. Multidis-ciplinary evaluation including pediatric oncologists, surgical subspecialists, and radiation oncologists is critical to plan the best treatment approach to maximize local tumor control while minimizing long-term treatment effects.Complete surgical resection is the treatment of choice for rhabdomyosarcoma when function and cosmesis can be preserved. Patients who are able to undergo a complete tumor resection with negative (group I) or microscopic surgical mar-gins (group II) are able to undergo less intensive systemic ther-apy and still have overall survival rates approaching 90%.258 At some anatomic sites, in particular the head and neck and genito-urinary system, surgery is often avoided because the associated | Surgery_Schwartz. novel targets for therapeutic approaches.Extent of disease is the strongest predictor of long-term outcome. Several staging systems for rhabdomyosarcoma are available. The Intergroup Rhabdomyosarcoma Study Group system is based on surgical-pathologic groupings. Multidis-ciplinary evaluation including pediatric oncologists, surgical subspecialists, and radiation oncologists is critical to plan the best treatment approach to maximize local tumor control while minimizing long-term treatment effects.Complete surgical resection is the treatment of choice for rhabdomyosarcoma when function and cosmesis can be preserved. Patients who are able to undergo a complete tumor resection with negative (group I) or microscopic surgical mar-gins (group II) are able to undergo less intensive systemic ther-apy and still have overall survival rates approaching 90%.258 At some anatomic sites, in particular the head and neck and genito-urinary system, surgery is often avoided because the associated |
Surgery_Schwartz_10503 | Surgery_Schwartz | ther-apy and still have overall survival rates approaching 90%.258 At some anatomic sites, in particular the head and neck and genito-urinary system, surgery is often avoided because the associated morbidity would be substantial. Recent findings suggest that chemotherapy alone can adequately control many such tumors. In the second International Society of Paediatric Oncology study of rhabdomyosarcoma (MMT84), the choice of local treatment was based on response to initial chemotherapy such that radical surgery and radiation therapy were avoided in 66% of patients. Among the patients who subsequently developed local relapse, the 5-year overall survival rate after salvage therapy was 46%.258Unlike other soft tissue sarcomas, rhabdomyosarcomas have a high propensity for lymph node metastasis, with rates up to 20% to 30% for sites such as the extremities, parates-ticular nodes, and prostate. Lymph node sampling and, more recently, sentinel lymph node mapping have been used to evalu-ate | Surgery_Schwartz. ther-apy and still have overall survival rates approaching 90%.258 At some anatomic sites, in particular the head and neck and genito-urinary system, surgery is often avoided because the associated morbidity would be substantial. Recent findings suggest that chemotherapy alone can adequately control many such tumors. In the second International Society of Paediatric Oncology study of rhabdomyosarcoma (MMT84), the choice of local treatment was based on response to initial chemotherapy such that radical surgery and radiation therapy were avoided in 66% of patients. Among the patients who subsequently developed local relapse, the 5-year overall survival rate after salvage therapy was 46%.258Unlike other soft tissue sarcomas, rhabdomyosarcomas have a high propensity for lymph node metastasis, with rates up to 20% to 30% for sites such as the extremities, parates-ticular nodes, and prostate. Lymph node sampling and, more recently, sentinel lymph node mapping have been used to evalu-ate |
Surgery_Schwartz_10504 | Surgery_Schwartz | with rates up to 20% to 30% for sites such as the extremities, parates-ticular nodes, and prostate. Lymph node sampling and, more recently, sentinel lymph node mapping have been used to evalu-ate regional node status in children with rhabdomyosarcoma.About 15% to 20% of patients with rhabdomyosarcoma have distant metastasis at presentation, most commonly (40–50% of cases) to the lungs, followed by bone marrow and bone. However, all patients with rhabdomyosarcoma are assumed to have micrometastatic disease at presentation. Therefore, multia-gent chemotherapy is recommended for all patients with rhab-domyosarcoma. Combination regimens including vincristine, dactinomycin, and cyclophosphamide continue to be the basis of effective curative therapy.254 Although various combinations including doxorubicin, ifosfamide, cisplatin, and etoposide have been shown to be active against rhabdomyosarcoma, they have not improved outcomes.258,259 Radiation therapy is given to most patients with | Surgery_Schwartz. with rates up to 20% to 30% for sites such as the extremities, parates-ticular nodes, and prostate. Lymph node sampling and, more recently, sentinel lymph node mapping have been used to evalu-ate regional node status in children with rhabdomyosarcoma.About 15% to 20% of patients with rhabdomyosarcoma have distant metastasis at presentation, most commonly (40–50% of cases) to the lungs, followed by bone marrow and bone. However, all patients with rhabdomyosarcoma are assumed to have micrometastatic disease at presentation. Therefore, multia-gent chemotherapy is recommended for all patients with rhab-domyosarcoma. Combination regimens including vincristine, dactinomycin, and cyclophosphamide continue to be the basis of effective curative therapy.254 Although various combinations including doxorubicin, ifosfamide, cisplatin, and etoposide have been shown to be active against rhabdomyosarcoma, they have not improved outcomes.258,259 Radiation therapy is given to most patients with |
Surgery_Schwartz_10505 | Surgery_Schwartz | doxorubicin, ifosfamide, cisplatin, and etoposide have been shown to be active against rhabdomyosarcoma, they have not improved outcomes.258,259 Radiation therapy is given to most patients with microscopic residual disease (group II) after resection.The prognosis for children with rhabdomyosarcomas is related to tumor site, surgical-pathologic grouping, and tumor histology. The 5-year disease-free survival rate for all patients has been reported to be 65%. Five-year disease-free survival rates for patients in groups I, II, III, and IV have been reported to be 84%, 74%, 62%, and 23%, respectively (see Table 36-3).260Nonrhabdomyosarcoma Soft Tissue SarcomasApproximately 60% of soft tissue sarcomas in children are nonrhabdomyosarcomas. These include numerous histologic subtypes, which are generally categorized into four groups: (a) fibrosarcoma, (b) Kaposi’s sarcoma, (c) other “specified” soft tissue sarcomas (e.g., synovial, angiosarcoma, hemangiopericy-toma, leiomyosarcoma, | Surgery_Schwartz. doxorubicin, ifosfamide, cisplatin, and etoposide have been shown to be active against rhabdomyosarcoma, they have not improved outcomes.258,259 Radiation therapy is given to most patients with microscopic residual disease (group II) after resection.The prognosis for children with rhabdomyosarcomas is related to tumor site, surgical-pathologic grouping, and tumor histology. The 5-year disease-free survival rate for all patients has been reported to be 65%. Five-year disease-free survival rates for patients in groups I, II, III, and IV have been reported to be 84%, 74%, 62%, and 23%, respectively (see Table 36-3).260Nonrhabdomyosarcoma Soft Tissue SarcomasApproximately 60% of soft tissue sarcomas in children are nonrhabdomyosarcomas. These include numerous histologic subtypes, which are generally categorized into four groups: (a) fibrosarcoma, (b) Kaposi’s sarcoma, (c) other “specified” soft tissue sarcomas (e.g., synovial, angiosarcoma, hemangiopericy-toma, leiomyosarcoma, |
Surgery_Schwartz_10506 | Surgery_Schwartz | are generally categorized into four groups: (a) fibrosarcoma, (b) Kaposi’s sarcoma, (c) other “specified” soft tissue sarcomas (e.g., synovial, angiosarcoma, hemangiopericy-toma, leiomyosarcoma, liposarcoma, and extraosseous Ewing’s sarcoma), and (d) “unspecified” soft tissue sarcoma.261 The most common subtypes are synovial sarcoma, MPNST, and fibro-sarcoma. No single histology accounts for more than 15% of all cases.As with adult tumors, the evaluation of the soft tissue mass begins with a history and physical examination followed by imaging, which usually includes MRI. A CT scan of the chest is important for evaluation of metastatic disease. A core needle biopsy is generally required to establish a diagnosis. Surgery remains the primary treatment of nonrhabdomyosarcoma, and Brunicardi_Ch36_p1567-p1598.indd 158901/03/19 6:38 PM 1590SPECIFIC CONSIDERATIONSPART IIlocal control of large, high-grade tumors is improved with radia-tion therapy. The prognostic factors for children with | Surgery_Schwartz. are generally categorized into four groups: (a) fibrosarcoma, (b) Kaposi’s sarcoma, (c) other “specified” soft tissue sarcomas (e.g., synovial, angiosarcoma, hemangiopericy-toma, leiomyosarcoma, liposarcoma, and extraosseous Ewing’s sarcoma), and (d) “unspecified” soft tissue sarcoma.261 The most common subtypes are synovial sarcoma, MPNST, and fibro-sarcoma. No single histology accounts for more than 15% of all cases.As with adult tumors, the evaluation of the soft tissue mass begins with a history and physical examination followed by imaging, which usually includes MRI. A CT scan of the chest is important for evaluation of metastatic disease. A core needle biopsy is generally required to establish a diagnosis. Surgery remains the primary treatment of nonrhabdomyosarcoma, and Brunicardi_Ch36_p1567-p1598.indd 158901/03/19 6:38 PM 1590SPECIFIC CONSIDERATIONSPART IIlocal control of large, high-grade tumors is improved with radia-tion therapy. The prognostic factors for children with |
Surgery_Schwartz_10507 | Surgery_Schwartz | 158901/03/19 6:38 PM 1590SPECIFIC CONSIDERATIONSPART IIlocal control of large, high-grade tumors is improved with radia-tion therapy. The prognostic factors for children with nonrhab-domyosarcoma are similar to those for adults, and the role of chemotherapy for high-risk tumors is unclear, as for adults.RESEARCH PERSPECTIVESAs the molecular alterations associated with various sar-coma subtypes are elucidated, many new potential targets for therapeutic intervention will be identified. A wide variety of DNA alterations have been observed in sarcomas that result in mutated genes encoding proteins ranging from transcription fac-tors to tyrosine kinases to cytokines. The challenge in identify-ing therapeutic targets in sarcoma is to identify those that are specifically important to cellular function. The ideal therapeutic target has been described as a single molecule that is critical for pathogenesis, is expressed and active, is involved in a single pathway amenable to blockade (i.e., | Surgery_Schwartz. 158901/03/19 6:38 PM 1590SPECIFIC CONSIDERATIONSPART IIlocal control of large, high-grade tumors is improved with radia-tion therapy. The prognostic factors for children with nonrhab-domyosarcoma are similar to those for adults, and the role of chemotherapy for high-risk tumors is unclear, as for adults.RESEARCH PERSPECTIVESAs the molecular alterations associated with various sar-coma subtypes are elucidated, many new potential targets for therapeutic intervention will be identified. A wide variety of DNA alterations have been observed in sarcomas that result in mutated genes encoding proteins ranging from transcription fac-tors to tyrosine kinases to cytokines. The challenge in identify-ing therapeutic targets in sarcoma is to identify those that are specifically important to cellular function. The ideal therapeutic target has been described as a single molecule that is critical for pathogenesis, is expressed and active, is involved in a single pathway amenable to blockade (i.e., |
Surgery_Schwartz_10508 | Surgery_Schwartz | function. The ideal therapeutic target has been described as a single molecule that is critical for pathogenesis, is expressed and active, is involved in a single pathway amenable to blockade (i.e., no alternative bypass path-ways exist), and is critical for sarcoma cell survival.25CONCLUSIONSSoft tissue sarcomas are a heterogeneous family of rare tumors, accounting for approximately 1% of malignancies in adults. The etiology in the vast majority of patients is sporadic, and the man-agement of such diverse tumors is complex. Diagnosis by light microscopy is inexact, but molecular diagnosis, although still in its infancy, holds great promise. The natural history of soft tissue sarcomas is well established. Approximately two-thirds of cases arise in the extremities, and the remaining one-third are distrib-uted between the retroperitoneum, trunk, abdomen, and head and neck. The management algorithm for soft tissue sarcomas is complex and depends on tumor stage, site, and histology. The | Surgery_Schwartz. function. The ideal therapeutic target has been described as a single molecule that is critical for pathogenesis, is expressed and active, is involved in a single pathway amenable to blockade (i.e., no alternative bypass path-ways exist), and is critical for sarcoma cell survival.25CONCLUSIONSSoft tissue sarcomas are a heterogeneous family of rare tumors, accounting for approximately 1% of malignancies in adults. The etiology in the vast majority of patients is sporadic, and the man-agement of such diverse tumors is complex. Diagnosis by light microscopy is inexact, but molecular diagnosis, although still in its infancy, holds great promise. The natural history of soft tissue sarcomas is well established. Approximately two-thirds of cases arise in the extremities, and the remaining one-third are distrib-uted between the retroperitoneum, trunk, abdomen, and head and neck. The management algorithm for soft tissue sarcomas is complex and depends on tumor stage, site, and histology. The |
Surgery_Schwartz_10509 | Surgery_Schwartz | are distrib-uted between the retroperitoneum, trunk, abdomen, and head and neck. The management algorithm for soft tissue sarcomas is complex and depends on tumor stage, site, and histology. The most common site of metastasis is the lungs, and metastasis generally occurs within 3 years of diagnosis.Soft tissue sarcomas have unique molecular profiles that contribute to varying responses to systemic therapy. Doxorubicinbased regimens have been the mainstay of treatment for the past two decades; however, it is now clear that specific histologic subtypes have increased sensitivity to specific agents. For exam-ple, angiosarcomas are more sensitive to paclitaxel, while leio-myosarcoma is sensitive to gemcitabine and docetaxel. Progress in understanding of soft tissue sarcoma biology is crucial for the development of additional therapeutic targets. Drug engineering will enable molecular-based therapies to become increasingly incorporated into clinical trials and, with success, into standard | Surgery_Schwartz. are distrib-uted between the retroperitoneum, trunk, abdomen, and head and neck. The management algorithm for soft tissue sarcomas is complex and depends on tumor stage, site, and histology. The most common site of metastasis is the lungs, and metastasis generally occurs within 3 years of diagnosis.Soft tissue sarcomas have unique molecular profiles that contribute to varying responses to systemic therapy. Doxorubicinbased regimens have been the mainstay of treatment for the past two decades; however, it is now clear that specific histologic subtypes have increased sensitivity to specific agents. For exam-ple, angiosarcomas are more sensitive to paclitaxel, while leio-myosarcoma is sensitive to gemcitabine and docetaxel. Progress in understanding of soft tissue sarcoma biology is crucial for the development of additional therapeutic targets. Drug engineering will enable molecular-based therapies to become increasingly incorporated into clinical trials and, with success, into standard |
Surgery_Schwartz_10510 | Surgery_Schwartz | for the development of additional therapeutic targets. Drug engineering will enable molecular-based therapies to become increasingly incorporated into clinical trials and, with success, into standard treatment strategies for soft tissue sarco-mas in the near future.REFERENCESEntries highlighted in bright blue are key references. 1. Demetri GD, Benjamin RS, Blanke CD, et al. NCCN Task Force report: management of patients with gastrointestinal stromal tumor (GIST)—update of the NCCN clinical practice guidelines. J Natl Compr Canc Netw. 2007;5(suppl 2):S1-S29; quiz S30. 2. Coindre JM, Terrier P, Guillou L, et al. Predictive value of grade for metastasis development in the main histologic types of adult soft tissue sarcomas: a study of 1240 patients from the French Federation of Cancer Centers Sarcoma Group. Cancer. 2001;91:1914-1926. 3. Gronchi A, Miceli R, Colombo C, et al. Primary extremity soft tissue sarcomas: outcome improvement over time at a single institution. Ann Oncol. | Surgery_Schwartz. for the development of additional therapeutic targets. Drug engineering will enable molecular-based therapies to become increasingly incorporated into clinical trials and, with success, into standard treatment strategies for soft tissue sarco-mas in the near future.REFERENCESEntries highlighted in bright blue are key references. 1. Demetri GD, Benjamin RS, Blanke CD, et al. NCCN Task Force report: management of patients with gastrointestinal stromal tumor (GIST)—update of the NCCN clinical practice guidelines. J Natl Compr Canc Netw. 2007;5(suppl 2):S1-S29; quiz S30. 2. Coindre JM, Terrier P, Guillou L, et al. Predictive value of grade for metastasis development in the main histologic types of adult soft tissue sarcomas: a study of 1240 patients from the French Federation of Cancer Centers Sarcoma Group. Cancer. 2001;91:1914-1926. 3. Gronchi A, Miceli R, Colombo C, et al. Primary extremity soft tissue sarcomas: outcome improvement over time at a single institution. Ann Oncol. |
Surgery_Schwartz_10511 | Surgery_Schwartz | Centers Sarcoma Group. Cancer. 2001;91:1914-1926. 3. Gronchi A, Miceli R, Colombo C, et al. Primary extremity soft tissue sarcomas: outcome improvement over time at a single institution. Ann Oncol. 2011;22:1675-1681. 4. Gronchi A, Pollock R. Surgery in retroperitoneal soft tissue sarcoma: a call for a consensus between Europe and North America. Ann Surg Oncol. 2011;18:2107-2110. 5. American Cancer Society. Cancer Facts and Figures 2017. Available at: https://www.cancer.org/research/cancer-facts-statistics/all-cancer-facts-figures/cancer-facts-figures-2017 .html. Accessed August 3, 2018. 6. Gatta G, Van Der Zwan JM, Casali PG, et al. Rare cancers are not so rare: the rare cancer burden in Europe. Eur J Cancer. 2011;47:2493-2511. 7. Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012. CA Cancer J Clin. 2012;62:10-29. 8. Gonin-Laurent N, Hadj-Hamou N, Vogt N, et al. RB1 and TP53 pathways in radiation-induced sarcomas. Oncogene. 2007;26:6106-6112. 9. Brady MS, Gaynor JJ, Brennan MF. | Surgery_Schwartz. Centers Sarcoma Group. Cancer. 2001;91:1914-1926. 3. Gronchi A, Miceli R, Colombo C, et al. Primary extremity soft tissue sarcomas: outcome improvement over time at a single institution. Ann Oncol. 2011;22:1675-1681. 4. Gronchi A, Pollock R. Surgery in retroperitoneal soft tissue sarcoma: a call for a consensus between Europe and North America. Ann Surg Oncol. 2011;18:2107-2110. 5. American Cancer Society. Cancer Facts and Figures 2017. Available at: https://www.cancer.org/research/cancer-facts-statistics/all-cancer-facts-figures/cancer-facts-figures-2017 .html. Accessed August 3, 2018. 6. Gatta G, Van Der Zwan JM, Casali PG, et al. Rare cancers are not so rare: the rare cancer burden in Europe. Eur J Cancer. 2011;47:2493-2511. 7. Siegel R, Naishadham D, Jemal A. Cancer statistics, 2012. CA Cancer J Clin. 2012;62:10-29. 8. Gonin-Laurent N, Hadj-Hamou N, Vogt N, et al. RB1 and TP53 pathways in radiation-induced sarcomas. Oncogene. 2007;26:6106-6112. 9. Brady MS, Gaynor JJ, Brennan MF. |
Surgery_Schwartz_10512 | Surgery_Schwartz | CA Cancer J Clin. 2012;62:10-29. 8. Gonin-Laurent N, Hadj-Hamou N, Vogt N, et al. RB1 and TP53 pathways in radiation-induced sarcomas. Oncogene. 2007;26:6106-6112. 9. Brady MS, Gaynor JJ, Brennan MF. Radiation-associated sarcoma of bone and soft tissue. Arch Surg. 1992;127: 1379-1385. 10. Vorburger SA, Xing Y, Hunt KK, et al. Angiosarcoma of the breast. Cancer. 2005;104:2682-2688. 11. Riad S, Biau D, Holt GE, et al. The clinical and functional outcome for patients with radiation-induced soft tissue sarcoma. Cancer. 2012;118:2682-2692. 12. Dineen SP, Roland CL, Feig R, et al. Radiation-associated undifferentiated pleomorphic sarcoma is associated with worse clinical outcomes than sporadic lesions. Ann Surg Oncol. 2015;22(12):3913-3920. 13. Smith AH, Pearce NE, Fisher DO, et al. Soft tissue sarcoma and exposure to phenoxyherbicides and chlorophenols in New Zealand. J Natl Cancer Inst. 1984;73:1111-1117. 14. Huang HY, Li CF, Huang WW, et al. A modification of NIH consensus criteria to | Surgery_Schwartz. CA Cancer J Clin. 2012;62:10-29. 8. Gonin-Laurent N, Hadj-Hamou N, Vogt N, et al. RB1 and TP53 pathways in radiation-induced sarcomas. Oncogene. 2007;26:6106-6112. 9. Brady MS, Gaynor JJ, Brennan MF. Radiation-associated sarcoma of bone and soft tissue. Arch Surg. 1992;127: 1379-1385. 10. Vorburger SA, Xing Y, Hunt KK, et al. Angiosarcoma of the breast. Cancer. 2005;104:2682-2688. 11. Riad S, Biau D, Holt GE, et al. The clinical and functional outcome for patients with radiation-induced soft tissue sarcoma. Cancer. 2012;118:2682-2692. 12. Dineen SP, Roland CL, Feig R, et al. Radiation-associated undifferentiated pleomorphic sarcoma is associated with worse clinical outcomes than sporadic lesions. Ann Surg Oncol. 2015;22(12):3913-3920. 13. Smith AH, Pearce NE, Fisher DO, et al. Soft tissue sarcoma and exposure to phenoxyherbicides and chlorophenols in New Zealand. J Natl Cancer Inst. 1984;73:1111-1117. 14. Huang HY, Li CF, Huang WW, et al. A modification of NIH consensus criteria to |
Surgery_Schwartz_10513 | Surgery_Schwartz | sarcoma and exposure to phenoxyherbicides and chlorophenols in New Zealand. J Natl Cancer Inst. 1984;73:1111-1117. 14. Huang HY, Li CF, Huang WW, et al. A modification of NIH consensus criteria to better distinguish the highly lethal subset of primary localized gastrointestinal stromal tumors: a subdi-vision of the original high-risk group on the basis of outcome. Surgery. 2007;141:748-756. 15. Stewart FW. Lymphangiosarcoma in post-mastectomy lymphedema; a report of six cases in elephantiasis chirurgica. Cancer. 1948;1(1):64-81. 16. Stewart NJ, Pritchard DJ, Nascimento AG, et al. Lymphan-giosarcoma following mastectomy. Clin Orthop Relat Res. 1995;320:135-141. 17. Kelly-Hope LA, Thomas BC, Bockarie MJ, et al. Lymphatic filariasis in the Democratic Republic of Congo; micro-stratification overlap mapping (MOM) as a prerequisite for control and surveillance. Parasit Vectors. 2011;4:178. 18. Pardini M, Bonzano L, Roccatagliata L, et al. Functional mag-netic resonance evidence of cortical | Surgery_Schwartz. sarcoma and exposure to phenoxyherbicides and chlorophenols in New Zealand. J Natl Cancer Inst. 1984;73:1111-1117. 14. Huang HY, Li CF, Huang WW, et al. A modification of NIH consensus criteria to better distinguish the highly lethal subset of primary localized gastrointestinal stromal tumors: a subdi-vision of the original high-risk group on the basis of outcome. Surgery. 2007;141:748-756. 15. Stewart FW. Lymphangiosarcoma in post-mastectomy lymphedema; a report of six cases in elephantiasis chirurgica. Cancer. 1948;1(1):64-81. 16. Stewart NJ, Pritchard DJ, Nascimento AG, et al. Lymphan-giosarcoma following mastectomy. Clin Orthop Relat Res. 1995;320:135-141. 17. Kelly-Hope LA, Thomas BC, Bockarie MJ, et al. Lymphatic filariasis in the Democratic Republic of Congo; micro-stratification overlap mapping (MOM) as a prerequisite for control and surveillance. Parasit Vectors. 2011;4:178. 18. Pardini M, Bonzano L, Roccatagliata L, et al. Functional mag-netic resonance evidence of cortical |
Surgery_Schwartz_10514 | Surgery_Schwartz | mapping (MOM) as a prerequisite for control and surveillance. Parasit Vectors. 2011;4:178. 18. Pardini M, Bonzano L, Roccatagliata L, et al. Functional mag-netic resonance evidence of cortical alterations in a case of reversible congenital lymphedema of the lower limb: a pilot study. Lymphology. 2007;40:19-25. 19. Schiffman S, Berger A. Stewart-Treves syndrome. J Am Coll Surg. 2007;204:328. 20. Demicco EG, Maki RG, Lev DC, et al. New therapeutic targets in soft tissue sarcoma. Adv Anat Pathol. 2012;19: 170-180. 21. Wunder JS, Nielsen TO, Maki RG, et al. Opportunities for improving the therapeutic ratio for patients with sarcoma. Lancet Oncol. 2007;8:513-524. 22. Guillou L, Benhattar J, Gengler C, et al. Translocation-positive low-grade fibromyxoid sarcoma: clinicopathologic and molec-ular analysis of a series expanding the morphologic spectrum and suggesting potential relationship to sclerosing epithelioid fibrosarcoma: a study from the French Sarcoma Group. Am J Surg Pathol. | Surgery_Schwartz. mapping (MOM) as a prerequisite for control and surveillance. Parasit Vectors. 2011;4:178. 18. Pardini M, Bonzano L, Roccatagliata L, et al. Functional mag-netic resonance evidence of cortical alterations in a case of reversible congenital lymphedema of the lower limb: a pilot study. Lymphology. 2007;40:19-25. 19. Schiffman S, Berger A. Stewart-Treves syndrome. J Am Coll Surg. 2007;204:328. 20. Demicco EG, Maki RG, Lev DC, et al. New therapeutic targets in soft tissue sarcoma. Adv Anat Pathol. 2012;19: 170-180. 21. Wunder JS, Nielsen TO, Maki RG, et al. Opportunities for improving the therapeutic ratio for patients with sarcoma. Lancet Oncol. 2007;8:513-524. 22. Guillou L, Benhattar J, Gengler C, et al. Translocation-positive low-grade fibromyxoid sarcoma: clinicopathologic and molec-ular analysis of a series expanding the morphologic spectrum and suggesting potential relationship to sclerosing epithelioid fibrosarcoma: a study from the French Sarcoma Group. Am J Surg Pathol. |
Surgery_Schwartz_10515 | Surgery_Schwartz | analysis of a series expanding the morphologic spectrum and suggesting potential relationship to sclerosing epithelioid fibrosarcoma: a study from the French Sarcoma Group. Am J Surg Pathol. 2007;31:1387-1402. 23. Levine EA. Prognostic factors in soft tissue sarcoma. Semin Surg Oncol. 1999;17:23-32.678Brunicardi_Ch36_p1567-p1598.indd 159001/03/19 6:38 PM 1591SOFT TISSUE SARCOMASCHAPTER 36 24. Sorensen PH, Triche TJ. Gene fusions encoding chimaeric transcription factors in solid tumours. Semin Cancer Biol. 1996;7:3-14. 25. Borden EC, Baker LH, Bell RS, et al. Soft tissue sarcomas of adults: state of the translational science. Clin Cancer Res. 2003;9:1941-1956. 26. Oda Y, Tsuneyoshi M. Recent advances in the molecular pathology of soft tissue sarcoma: implications for diagnosis, patient prognosis, and molecular target therapy in the future. Cancer Sci. 2009;100:200-208. 27. Karnes PS. Neurofibromatosis: a common neurocutaneous disorder. Mayo Clin Proc. 1998;73:1071-1076. 28. Fong Y, | Surgery_Schwartz. analysis of a series expanding the morphologic spectrum and suggesting potential relationship to sclerosing epithelioid fibrosarcoma: a study from the French Sarcoma Group. Am J Surg Pathol. 2007;31:1387-1402. 23. Levine EA. Prognostic factors in soft tissue sarcoma. Semin Surg Oncol. 1999;17:23-32.678Brunicardi_Ch36_p1567-p1598.indd 159001/03/19 6:38 PM 1591SOFT TISSUE SARCOMASCHAPTER 36 24. Sorensen PH, Triche TJ. Gene fusions encoding chimaeric transcription factors in solid tumours. Semin Cancer Biol. 1996;7:3-14. 25. Borden EC, Baker LH, Bell RS, et al. Soft tissue sarcomas of adults: state of the translational science. Clin Cancer Res. 2003;9:1941-1956. 26. Oda Y, Tsuneyoshi M. Recent advances in the molecular pathology of soft tissue sarcoma: implications for diagnosis, patient prognosis, and molecular target therapy in the future. Cancer Sci. 2009;100:200-208. 27. Karnes PS. Neurofibromatosis: a common neurocutaneous disorder. Mayo Clin Proc. 1998;73:1071-1076. 28. Fong Y, |
Surgery_Schwartz_10516 | Surgery_Schwartz | prognosis, and molecular target therapy in the future. Cancer Sci. 2009;100:200-208. 27. Karnes PS. Neurofibromatosis: a common neurocutaneous disorder. Mayo Clin Proc. 1998;73:1071-1076. 28. Fong Y, Coit DG, Woodruff JM, et al. Lymph node metasta-sis from soft tissue sarcoma in adults. Analysis of data from a prospective database of 1772 sarcoma patients. Ann Surg. 1993;217:72-77. 29. Benns M, Dalsing M, Sawchuck A, et al. Soft tissue sarcomas may present with deep vein thrombosis. J Vasc Surg. 2006;43:788-793. 30. Grimer R, Judson I, Peake D, et al. Guidelines for the manage-ment of soft tissue sarcomas. Sarcoma. 2010;2010:506182. 31. Heslin MJ, Smith JK. Imaging of soft tissue sarcomas. Surg Oncol Clin N Am. 1999;8:91-107. 32. Pearlstone DB, Pisters PW, Bold RJ, et al. Patterns of recur-rence in extremity liposarcoma: implications for staging and follow-up. Cancer. 1999;85:85-92. 33. Roberge D, Hickeson M, Charest M, et al. Initial McGill expe-rience with fluorodeoxyglucose | Surgery_Schwartz. prognosis, and molecular target therapy in the future. Cancer Sci. 2009;100:200-208. 27. Karnes PS. Neurofibromatosis: a common neurocutaneous disorder. Mayo Clin Proc. 1998;73:1071-1076. 28. Fong Y, Coit DG, Woodruff JM, et al. Lymph node metasta-sis from soft tissue sarcoma in adults. Analysis of data from a prospective database of 1772 sarcoma patients. Ann Surg. 1993;217:72-77. 29. Benns M, Dalsing M, Sawchuck A, et al. Soft tissue sarcomas may present with deep vein thrombosis. J Vasc Surg. 2006;43:788-793. 30. Grimer R, Judson I, Peake D, et al. Guidelines for the manage-ment of soft tissue sarcomas. Sarcoma. 2010;2010:506182. 31. Heslin MJ, Smith JK. Imaging of soft tissue sarcomas. Surg Oncol Clin N Am. 1999;8:91-107. 32. Pearlstone DB, Pisters PW, Bold RJ, et al. Patterns of recur-rence in extremity liposarcoma: implications for staging and follow-up. Cancer. 1999;85:85-92. 33. Roberge D, Hickeson M, Charest M, et al. Initial McGill expe-rience with fluorodeoxyglucose |
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Surgery_Schwartz_10521 | Surgery_Schwartz | S, Davis A, Kandel R, et al. Residual disease following unplanned excision of a soft-tissue sarcoma of an extremity. J Bone Joint Surg Am. 1996;78:650-655. 52. Presant CA, Russell WO, Alexander RW, et al. Soft-tissue and bone sarcoma histopathology peer review: the frequency of disagreement in diagnosis and the need for second pathology opinions. The Southeastern Cancer Study Group experience. J Clin Oncol. 1986;4:1658-1661. 53. Pfeifer J, Hill D, O’Sullivan M, et al. Diagnostic gold standard for soft tissue tumours: morphology or molecular genetics? Histopathology. 2002;37:485-500. 54. Fletcher CD, Gustafson P, Rydholm A, et al. Clinicopatho-logic re-evaluation of 100 malignant fibrous histiocytomas: prognostic relevance of subclassification. J Clin Oncol. 2001;19:3045-3050. 55. Tschoep K, Kohlmann A, Schlemmer M, et al. Gene expression profiling in sarcomas. Crit Rev Oncol Hematol. 2007;63:111-124. 56. Coindre JM, Hostein I, Maire G, et al. Inflammatory malig-nant fibrous | Surgery_Schwartz. S, Davis A, Kandel R, et al. Residual disease following unplanned excision of a soft-tissue sarcoma of an extremity. J Bone Joint Surg Am. 1996;78:650-655. 52. Presant CA, Russell WO, Alexander RW, et al. Soft-tissue and bone sarcoma histopathology peer review: the frequency of disagreement in diagnosis and the need for second pathology opinions. The Southeastern Cancer Study Group experience. J Clin Oncol. 1986;4:1658-1661. 53. Pfeifer J, Hill D, O’Sullivan M, et al. Diagnostic gold standard for soft tissue tumours: morphology or molecular genetics? Histopathology. 2002;37:485-500. 54. Fletcher CD, Gustafson P, Rydholm A, et al. Clinicopatho-logic re-evaluation of 100 malignant fibrous histiocytomas: prognostic relevance of subclassification. J Clin Oncol. 2001;19:3045-3050. 55. Tschoep K, Kohlmann A, Schlemmer M, et al. Gene expression profiling in sarcomas. Crit Rev Oncol Hematol. 2007;63:111-124. 56. Coindre JM, Hostein I, Maire G, et al. Inflammatory malig-nant fibrous |
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Surgery_Schwartz_10525 | Surgery_Schwartz | in a series of patients treated at a single institution: local control directly impacts survival. Ann Surg. 2010;251:506. 69. Heslin MJ, Cordon-Cardo C, Lewis JJ, et al. Ki-67 detected by MIB-1 predicts distant metastasis and tumor mortality in primary, high grade extremity soft tissue sarcoma. Cancer. 1998;83:490-497. 70. Ch’ng E, Tomita Y, Zhang B, et al. Prognostic signifi-cance of CD100 expression in soft tissue sarcoma. Cancer. 2007;110:164-172. 71. Kattan MW, Leung DH, Brennan MF. Postoperative nomo-gram for 12-year sarcoma-specific death. J Clin Oncol. 2002;20:791-796. 72. Eilber FC, Kattan MW. Sarcoma nomogram: validation and a model to evaluate impact of therapy. J Am Coll Surg. 2007;205:S90-S95. 73. Dalal KM, Kattan MW, Antonescu CR, et al. Subtype spe-cific prognostic nomogram for patients with primary liposar-coma of the retroperitoneum, extremity, or trunk. Ann Surg. 2006;244:381-391. 74. Gronchi A, Miceli R, Shurell E, et al. Outcome prediction in primary resected | Surgery_Schwartz. in a series of patients treated at a single institution: local control directly impacts survival. Ann Surg. 2010;251:506. 69. Heslin MJ, Cordon-Cardo C, Lewis JJ, et al. Ki-67 detected by MIB-1 predicts distant metastasis and tumor mortality in primary, high grade extremity soft tissue sarcoma. Cancer. 1998;83:490-497. 70. Ch’ng E, Tomita Y, Zhang B, et al. Prognostic signifi-cance of CD100 expression in soft tissue sarcoma. Cancer. 2007;110:164-172. 71. Kattan MW, Leung DH, Brennan MF. Postoperative nomo-gram for 12-year sarcoma-specific death. J Clin Oncol. 2002;20:791-796. 72. Eilber FC, Kattan MW. Sarcoma nomogram: validation and a model to evaluate impact of therapy. J Am Coll Surg. 2007;205:S90-S95. 73. Dalal KM, Kattan MW, Antonescu CR, et al. Subtype spe-cific prognostic nomogram for patients with primary liposar-coma of the retroperitoneum, extremity, or trunk. Ann Surg. 2006;244:381-391. 74. Gronchi A, Miceli R, Shurell E, et al. Outcome prediction in primary resected |
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Surgery_Schwartz_10561 | Surgery_Schwartz | tumors comparing interruption versus continuation of treatment beyond 1 year: the French Sarcoma Group. J Clin Oncol. 2007;25: 1107-1113. 216. Benjamin RS, Debiec-Rychter M, Le Cesne A, et al. Gastrointestinal stromal tumors II: medical oncology and tumor response assessment. Semin Oncol. 2009;4:302-311. 217. Maleddu A, Pantaleo MA, Nannini M, et al. Mechanisms of secondary resistance to tyrosine kinase inhibitors in gastrointestinal stromal tumours (review). Oncol Rep. 2009;21:1359-1366.Brunicardi_Ch36_p1567-p1598.indd 159501/03/19 6:38 PM 1596SPECIFIC CONSIDERATIONSPART II 218. Chu D, Lacouture ME, Weiner E, et al. Risk of hand-foot skin reaction with the multitargeted kinase inhibitor sunitinib in patients with renal cell and non–renal cell carcinoma: a meta-analysis. Clin Genitourin Cancer. 2009;7:11-19. 219. Zhu X, Stergiopoulos K, Wu S. Risk of hypertension and renal dysfunction with an angiogenesis inhibitor sunitinib: systematic review and meta-analysis. Acta Oncol. | Surgery_Schwartz. tumors comparing interruption versus continuation of treatment beyond 1 year: the French Sarcoma Group. J Clin Oncol. 2007;25: 1107-1113. 216. Benjamin RS, Debiec-Rychter M, Le Cesne A, et al. Gastrointestinal stromal tumors II: medical oncology and tumor response assessment. Semin Oncol. 2009;4:302-311. 217. Maleddu A, Pantaleo MA, Nannini M, et al. Mechanisms of secondary resistance to tyrosine kinase inhibitors in gastrointestinal stromal tumours (review). Oncol Rep. 2009;21:1359-1366.Brunicardi_Ch36_p1567-p1598.indd 159501/03/19 6:38 PM 1596SPECIFIC CONSIDERATIONSPART II 218. Chu D, Lacouture ME, Weiner E, et al. Risk of hand-foot skin reaction with the multitargeted kinase inhibitor sunitinib in patients with renal cell and non–renal cell carcinoma: a meta-analysis. Clin Genitourin Cancer. 2009;7:11-19. 219. Zhu X, Stergiopoulos K, Wu S. Risk of hypertension and renal dysfunction with an angiogenesis inhibitor sunitinib: systematic review and meta-analysis. Acta Oncol. |
Surgery_Schwartz_10562 | Surgery_Schwartz | Cancer. 2009;7:11-19. 219. Zhu X, Stergiopoulos K, Wu S. Risk of hypertension and renal dysfunction with an angiogenesis inhibitor sunitinib: systematic review and meta-analysis. Acta Oncol. 2009;48:9-17. 220. Chu TF, Rupnick MA, Kerkela R, et al. Cardiotoxicity asso-ciated with the tyrosine kinase inhibitor sunitinib. Lancet. 2007;370(9604):2011-2009. 221. George S, Wang Q, Heinrich MC, et al. Efficacy and safety of regorafenib in patients with metastatic and/or unresectable GI stromal tumor after failure of imatinib and sunitinib: a multicenter phase II trial. J Clin Oncol. 2012;30(19):2401-2407. 222. Demetri GD, Reichardt P, Kang YK, et al. Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumours after failure of imatinib and sunitinib (GRID): an international, multicentre, randomised, placebo-controlled, phase 3 trial. Lancet. 2013;381(9863):295-302. 223. Boyar MS, Taub RN. New strategies for treating GIST when imatinib fails. Cancer Invest. | Surgery_Schwartz. Cancer. 2009;7:11-19. 219. Zhu X, Stergiopoulos K, Wu S. Risk of hypertension and renal dysfunction with an angiogenesis inhibitor sunitinib: systematic review and meta-analysis. Acta Oncol. 2009;48:9-17. 220. Chu TF, Rupnick MA, Kerkela R, et al. Cardiotoxicity asso-ciated with the tyrosine kinase inhibitor sunitinib. Lancet. 2007;370(9604):2011-2009. 221. George S, Wang Q, Heinrich MC, et al. Efficacy and safety of regorafenib in patients with metastatic and/or unresectable GI stromal tumor after failure of imatinib and sunitinib: a multicenter phase II trial. J Clin Oncol. 2012;30(19):2401-2407. 222. Demetri GD, Reichardt P, Kang YK, et al. Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumours after failure of imatinib and sunitinib (GRID): an international, multicentre, randomised, placebo-controlled, phase 3 trial. Lancet. 2013;381(9863):295-302. 223. Boyar MS, Taub RN. New strategies for treating GIST when imatinib fails. Cancer Invest. |
Surgery_Schwartz_10563 | Surgery_Schwartz | international, multicentre, randomised, placebo-controlled, phase 3 trial. Lancet. 2013;381(9863):295-302. 223. Boyar MS, Taub RN. New strategies for treating GIST when imatinib fails. Cancer Invest. 2007;25:328-335. 224. Cassier PA, Dufresne A, Fayette J, et al. Emerging drugs for the treatment of soft tissue sarcomas. Expert Opin Emerg Drugs. 2007;12:139-153. 225. Andtbacka RH, Ng CS, Scaife CL, et al. Surgical resection of gastrointestinal stromal tumors after treatment with imatinib. Ann Surg Oncol. 2007;14:14-24. 226. Desai J, Shankar S, Heinrich MC, et al. Clonal evolution of resistance to imatinib in patients with metastatic gastrointesti-nal stromal tumors. Clin Cancer Res. 2007;13:5398-5405. 227. DeMatteo RP, Maki RG, Singer S, et al. Results of tyrosine kinase inhibitor therapy followed by surgical resection for metastatic gastrointestinal stromal tumor. Ann Surg. 2007;245:347-352. 228. Raut CP, Posner M, Desai J, et al. Surgical management of advanced gastrointestinal | Surgery_Schwartz. international, multicentre, randomised, placebo-controlled, phase 3 trial. Lancet. 2013;381(9863):295-302. 223. Boyar MS, Taub RN. New strategies for treating GIST when imatinib fails. Cancer Invest. 2007;25:328-335. 224. Cassier PA, Dufresne A, Fayette J, et al. Emerging drugs for the treatment of soft tissue sarcomas. Expert Opin Emerg Drugs. 2007;12:139-153. 225. Andtbacka RH, Ng CS, Scaife CL, et al. Surgical resection of gastrointestinal stromal tumors after treatment with imatinib. Ann Surg Oncol. 2007;14:14-24. 226. Desai J, Shankar S, Heinrich MC, et al. Clonal evolution of resistance to imatinib in patients with metastatic gastrointesti-nal stromal tumors. Clin Cancer Res. 2007;13:5398-5405. 227. DeMatteo RP, Maki RG, Singer S, et al. Results of tyrosine kinase inhibitor therapy followed by surgical resection for metastatic gastrointestinal stromal tumor. Ann Surg. 2007;245:347-352. 228. Raut CP, Posner M, Desai J, et al. Surgical management of advanced gastrointestinal |
Surgery_Schwartz_10564 | Surgery_Schwartz | followed by surgical resection for metastatic gastrointestinal stromal tumor. Ann Surg. 2007;245:347-352. 228. Raut CP, Posner M, Desai J, et al. Surgical management of advanced gastrointestinal stromal tumors after treatment with targeted systemic therapy using kinase inhibitors. J Clin Oncol. 2006;24:2325-2331. 229. Gronchi A, Fiore M, Miselli F, et al. Surgery of residual disease following molecular-targeted therapy with imatinib mesylate in advanced/metastatic GIST. Ann Surg. 2007;245:341-346. 230. DeMatteo RP, Ballman KV, Antonescu CR, et al. Placebocontrolled randomized trial of adjuvant imatinib mesylate following the resection of localized, primary gastrointestinal stromal tumor (GIST). Lancet. 2009;373(9669):1097-1104. 231. Joensuu H, Eriksson M, Sundby Hall K, et al. One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307(12):1265-1272. 232. The ESMO/European Sarcoma Network Working Group. Gastrointestinal | Surgery_Schwartz. followed by surgical resection for metastatic gastrointestinal stromal tumor. Ann Surg. 2007;245:347-352. 228. Raut CP, Posner M, Desai J, et al. Surgical management of advanced gastrointestinal stromal tumors after treatment with targeted systemic therapy using kinase inhibitors. J Clin Oncol. 2006;24:2325-2331. 229. Gronchi A, Fiore M, Miselli F, et al. Surgery of residual disease following molecular-targeted therapy with imatinib mesylate in advanced/metastatic GIST. Ann Surg. 2007;245:341-346. 230. DeMatteo RP, Ballman KV, Antonescu CR, et al. Placebocontrolled randomized trial of adjuvant imatinib mesylate following the resection of localized, primary gastrointestinal stromal tumor (GIST). Lancet. 2009;373(9669):1097-1104. 231. Joensuu H, Eriksson M, Sundby Hall K, et al. One vs three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307(12):1265-1272. 232. The ESMO/European Sarcoma Network Working Group. Gastrointestinal |
Surgery_Schwartz_10565 | Surgery_Schwartz | three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307(12):1265-1272. 232. The ESMO/European Sarcoma Network Working Group. Gastrointestinal stromal tumors: ESMO clinical recommen-dations for diagnosis, treatment and follow-up. Ann Oncol. 2012;23:49-55. 233. Gold JS, Gönen M, Gutiérrez A, et al. Development and validation of a prognostic nomogram for recurrence-free sur-vival after complete surgical resection of localised primary gastrointestinal stromal tumour: a retrospective analysis. Lancet Oncol. 2009;10:1045-1052. 232. Joensuu H, Vehtari A, Riihimäki J, et al. Risk of recur-rence of gastrointestinal stromal tumour after surgery: an analysis of pooled population-based cohorts. Lancet Oncol. 2012;13(3):265-274. 234. Demetri GD, Antonia S, Benjamin RS, et al. Soft tissue sarcoma. J Natl Compr Canc Netw. 2010;8:630-674. 235. van der Zwan SM, DeMatteo RP. Gastrointestinal stromal tumor: 5 years later. Cancer. | Surgery_Schwartz. three years of adjuvant imatinib for operable gastrointestinal stromal tumor: a randomized trial. JAMA. 2012;307(12):1265-1272. 232. The ESMO/European Sarcoma Network Working Group. Gastrointestinal stromal tumors: ESMO clinical recommen-dations for diagnosis, treatment and follow-up. Ann Oncol. 2012;23:49-55. 233. Gold JS, Gönen M, Gutiérrez A, et al. Development and validation of a prognostic nomogram for recurrence-free sur-vival after complete surgical resection of localised primary gastrointestinal stromal tumour: a retrospective analysis. Lancet Oncol. 2009;10:1045-1052. 232. Joensuu H, Vehtari A, Riihimäki J, et al. Risk of recur-rence of gastrointestinal stromal tumour after surgery: an analysis of pooled population-based cohorts. Lancet Oncol. 2012;13(3):265-274. 234. Demetri GD, Antonia S, Benjamin RS, et al. Soft tissue sarcoma. J Natl Compr Canc Netw. 2010;8:630-674. 235. van der Zwan SM, DeMatteo RP. Gastrointestinal stromal tumor: 5 years later. Cancer. |
Surgery_Schwartz_10566 | Surgery_Schwartz | GD, Antonia S, Benjamin RS, et al. Soft tissue sarcoma. J Natl Compr Canc Netw. 2010;8:630-674. 235. van der Zwan SM, DeMatteo RP. Gastrointestinal stromal tumor: 5 years later. Cancer. 2005;104:1781-1788. 236. Eisenberg BL, Harris J, Blanke CD, et al. Phase II trial of neoadjuvant/adjuvant imatinib mesylate (IM) for advanced primary and metastatic/recurrent operable gastrointestinal stromal tumor (GIST): early results of RTOG 0132/ACRIN 6665. J Surg Oncol. 2008;99:42-47. 237. McAuliffe JC, Hunt KK, Lazar AJF, et al. A randomized, phase II study of preoperative plus postoperative imatinib in GIST: evidence of rapid radiographic response and tem-poral induction of tumor cell apoptosis. Ann Surg Oncol. 2009;16:910-919. 238. Fiore M, Palassini E, Fumagalli E, et al. Preoperative ima-tinib mesylate for unresectable or locally advanced primary gastrointestinal stromal tumors (GIST). Eur J Surg Oncol. 2009;35:739-745. 239. Emile J, Brahimi S, Coindre J, et al. Frequencies of KIT and PDGFRA | Surgery_Schwartz. GD, Antonia S, Benjamin RS, et al. Soft tissue sarcoma. J Natl Compr Canc Netw. 2010;8:630-674. 235. van der Zwan SM, DeMatteo RP. Gastrointestinal stromal tumor: 5 years later. Cancer. 2005;104:1781-1788. 236. Eisenberg BL, Harris J, Blanke CD, et al. Phase II trial of neoadjuvant/adjuvant imatinib mesylate (IM) for advanced primary and metastatic/recurrent operable gastrointestinal stromal tumor (GIST): early results of RTOG 0132/ACRIN 6665. J Surg Oncol. 2008;99:42-47. 237. McAuliffe JC, Hunt KK, Lazar AJF, et al. A randomized, phase II study of preoperative plus postoperative imatinib in GIST: evidence of rapid radiographic response and tem-poral induction of tumor cell apoptosis. Ann Surg Oncol. 2009;16:910-919. 238. Fiore M, Palassini E, Fumagalli E, et al. Preoperative ima-tinib mesylate for unresectable or locally advanced primary gastrointestinal stromal tumors (GIST). Eur J Surg Oncol. 2009;35:739-745. 239. Emile J, Brahimi S, Coindre J, et al. Frequencies of KIT and PDGFRA |
Surgery_Schwartz_10567 | Surgery_Schwartz | for unresectable or locally advanced primary gastrointestinal stromal tumors (GIST). Eur J Surg Oncol. 2009;35:739-745. 239. Emile J, Brahimi S, Coindre J, et al. Frequencies of KIT and PDGFRA mutations in the MolecGIST prospective population-based study differ from those of advanced GISTs. Med Oncol. 2012;29:1765-1772. 240. Gronchi A, Casali P, Mariani L, et al. Quality of surgery and outcome in extra-abdominal aggressive fibromatosis: a series of patients surgically treated at a single institution. J Clin Oncol. 2003;21:1390-1397. 241. Lev D, Kotilingam D, Wei C, et al. Optimizing treatment of desmoid tumors. J Clin Oncol. 2007;25:1785-1791. 242. Salas S, Dufresne A, Bui B, et al. Prognostic factors influencing progression-free survival determined from a series of sporadic desmoid tumors: a wait-and-see policy according to tumor presentation. J Clin Oncol. 2011;29: 3553-3558. 243. Bonvalot S, Eldweny H, Haddad V, et al. Extra-abdominal primary fibromatosis: aggressive management | Surgery_Schwartz. for unresectable or locally advanced primary gastrointestinal stromal tumors (GIST). Eur J Surg Oncol. 2009;35:739-745. 239. Emile J, Brahimi S, Coindre J, et al. Frequencies of KIT and PDGFRA mutations in the MolecGIST prospective population-based study differ from those of advanced GISTs. Med Oncol. 2012;29:1765-1772. 240. Gronchi A, Casali P, Mariani L, et al. Quality of surgery and outcome in extra-abdominal aggressive fibromatosis: a series of patients surgically treated at a single institution. J Clin Oncol. 2003;21:1390-1397. 241. Lev D, Kotilingam D, Wei C, et al. Optimizing treatment of desmoid tumors. J Clin Oncol. 2007;25:1785-1791. 242. Salas S, Dufresne A, Bui B, et al. Prognostic factors influencing progression-free survival determined from a series of sporadic desmoid tumors: a wait-and-see policy according to tumor presentation. J Clin Oncol. 2011;29: 3553-3558. 243. Bonvalot S, Eldweny H, Haddad V, et al. Extra-abdominal primary fibromatosis: aggressive management |
Surgery_Schwartz_10568 | Surgery_Schwartz | a wait-and-see policy according to tumor presentation. J Clin Oncol. 2011;29: 3553-3558. 243. Bonvalot S, Eldweny H, Haddad V, et al. Extra-abdominal primary fibromatosis: aggressive management could be avoided in a subgroup of patients. Eur J Surg Oncol. 2008;34: 462-468. 244. Fiore M, Rimareix F, Mariani L, et al. Desmoid-type fibromatosis: a front-line conservative approach to select patients for surgical treatment. Ann Surg Oncol. 2009;16: 2587-2593. 245. Constantinidou A, Scurr M, Jones R, et al. Treatment of aggressive fibromatosis with pegylated liposomal doxorubi-cin: The Royal Marsden Hospital experience. J Clin Oncol. (Meeting Abstracts), Abstract 10519, 2009. 246. Gounder MM, Lefkowitz RA, Keohan ML, et al. Activity of sorafenib against desmoid tumor/deep fibromatosis. Clin Cancer Res. 2011;17:4082-4090. 247. Dufresne A, Penel N, Salas S, et al. Updated outcome with long term follow-up of imatinib for the treatment of progres-sive or recurrent aggressive fibromatosis | Surgery_Schwartz. a wait-and-see policy according to tumor presentation. J Clin Oncol. 2011;29: 3553-3558. 243. Bonvalot S, Eldweny H, Haddad V, et al. Extra-abdominal primary fibromatosis: aggressive management could be avoided in a subgroup of patients. Eur J Surg Oncol. 2008;34: 462-468. 244. Fiore M, Rimareix F, Mariani L, et al. Desmoid-type fibromatosis: a front-line conservative approach to select patients for surgical treatment. Ann Surg Oncol. 2009;16: 2587-2593. 245. Constantinidou A, Scurr M, Jones R, et al. Treatment of aggressive fibromatosis with pegylated liposomal doxorubi-cin: The Royal Marsden Hospital experience. J Clin Oncol. (Meeting Abstracts), Abstract 10519, 2009. 246. Gounder MM, Lefkowitz RA, Keohan ML, et al. Activity of sorafenib against desmoid tumor/deep fibromatosis. Clin Cancer Res. 2011;17:4082-4090. 247. Dufresne A, Penel N, Salas S, et al. Updated outcome with long term follow-up of imatinib for the treatment of progres-sive or recurrent aggressive fibromatosis |
Surgery_Schwartz_10569 | Surgery_Schwartz | Cancer Res. 2011;17:4082-4090. 247. Dufresne A, Penel N, Salas S, et al. Updated outcome with long term follow-up of imatinib for the treatment of progres-sive or recurrent aggressive fibromatosis (desmoid tumor): a FNCLCC/French Sarcoma Group phase II trial. Age. 2009;40:59. 248. Chugh R, Wathen JK, Patel SR, et al. Efficacy of imatinib in aggressive fibromatosis: results of a phase II multicenter Sarcoma Alliance for Research through Collaboration (SARC) trial. Clin Cancer Res. 2010;16:4884-4891. 249. Penel N, Le Cesne A, Bui B, et al. Imatinib for progressive and recurrent aggressive fibromatosis (desmoid tumors): an FNCLCC/French Sarcoma Group phase II trial with a long-term follow-up. Ann Oncol. 2011;22:452-457. 250. Criscione VD, Weinstock MA. Descriptive epidemiology of dermatofibrosarcoma protuberans in the United States, 1973 to 2002. J Am Acad Dermatol. 2007;56:968-973. 251. Fiore M, Miceli R, Mussi C, et al. Dermatofibrosarcoma protuberans treated at a single | Surgery_Schwartz. Cancer Res. 2011;17:4082-4090. 247. Dufresne A, Penel N, Salas S, et al. Updated outcome with long term follow-up of imatinib for the treatment of progres-sive or recurrent aggressive fibromatosis (desmoid tumor): a FNCLCC/French Sarcoma Group phase II trial. Age. 2009;40:59. 248. Chugh R, Wathen JK, Patel SR, et al. Efficacy of imatinib in aggressive fibromatosis: results of a phase II multicenter Sarcoma Alliance for Research through Collaboration (SARC) trial. Clin Cancer Res. 2010;16:4884-4891. 249. Penel N, Le Cesne A, Bui B, et al. Imatinib for progressive and recurrent aggressive fibromatosis (desmoid tumors): an FNCLCC/French Sarcoma Group phase II trial with a long-term follow-up. Ann Oncol. 2011;22:452-457. 250. Criscione VD, Weinstock MA. Descriptive epidemiology of dermatofibrosarcoma protuberans in the United States, 1973 to 2002. J Am Acad Dermatol. 2007;56:968-973. 251. Fiore M, Miceli R, Mussi C, et al. Dermatofibrosarcoma protuberans treated at a single |
Surgery_Schwartz_10570 | Surgery_Schwartz | dermatofibrosarcoma protuberans in the United States, 1973 to 2002. J Am Acad Dermatol. 2007;56:968-973. 251. Fiore M, Miceli R, Mussi C, et al. Dermatofibrosarcoma protuberans treated at a single institution: a surgical disease with a high cure rate. J Clin Oncol. 2005;23:7669-7675. 252. McArthur GA. Molecular targeting of dermatofibrosarcoma protuberans: a new approach to a surgical disease. J Natl Compr Canc Netw. 2007;5:557-562.Brunicardi_Ch36_p1567-p1598.indd 159601/03/19 6:38 PM 1597SOFT TISSUE SARCOMASCHAPTER 36 253. Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80:2321-2332. 254. Meyer WH, Spunt SL. Soft tissue sarcomas of childhood. Cancer Treat Rev. 2004;30:269-280. 255. Barr FG, Chatten J, D’Cruz CM, et al. Molecular assays for chromosomal translocations in the diagnosis of pediatric soft tissue sarcomas. JAMA. 1995;273:553-557. 256. Xia SJ, Pressey JG, Barr FG. Molecular | Surgery_Schwartz. dermatofibrosarcoma protuberans in the United States, 1973 to 2002. J Am Acad Dermatol. 2007;56:968-973. 251. Fiore M, Miceli R, Mussi C, et al. Dermatofibrosarcoma protuberans treated at a single institution: a surgical disease with a high cure rate. J Clin Oncol. 2005;23:7669-7675. 252. McArthur GA. Molecular targeting of dermatofibrosarcoma protuberans: a new approach to a surgical disease. J Natl Compr Canc Netw. 2007;5:557-562.Brunicardi_Ch36_p1567-p1598.indd 159601/03/19 6:38 PM 1597SOFT TISSUE SARCOMASCHAPTER 36 253. Grovas A, Fremgen A, Rauck A, et al. The National Cancer Data Base report on patterns of childhood cancers in the United States. Cancer. 1997;80:2321-2332. 254. Meyer WH, Spunt SL. Soft tissue sarcomas of childhood. Cancer Treat Rev. 2004;30:269-280. 255. Barr FG, Chatten J, D’Cruz CM, et al. Molecular assays for chromosomal translocations in the diagnosis of pediatric soft tissue sarcomas. JAMA. 1995;273:553-557. 256. Xia SJ, Pressey JG, Barr FG. Molecular |
Surgery_Schwartz_10571 | Surgery_Schwartz | Chatten J, D’Cruz CM, et al. Molecular assays for chromosomal translocations in the diagnosis of pediatric soft tissue sarcomas. JAMA. 1995;273:553-557. 256. Xia SJ, Pressey JG, Barr FG. Molecular pathogenesis of rhabdomyosarcoma. Cancer Biol Ther. 2002;1:97-104. 257. Scrable H, Witte D, Shimada H, et al. Molecular differential pathology of rhabdomyosarcoma. Genes Chromosomes Cancer. 1989;1:23-35. 258. Flamant F, Rodary C, Rey A, et al. Treatment of non-metastatic rhabdomyosarcomas in childhood and adolescence. Results of the second study of the International Society of Paediatric Oncology: MMT84. Eur J Cancer. 1998;34:1050-1062. 259. Crist WM, Anderson JR, Meza JL, et al. Intergroup rhabdomyosarcoma study-IV: results for patients with nonmetastatic disease. J Clin Oncol. 2001;19:3091-3102. 260. Crist WM, Garnsey L, Beltangady MS, et al. Prognosis in children with rhabdomyosarcoma: a report of the intergroup rhabdomyosarcoma studies I and II. Intergroup Rhabdomyo-sarcoma Committee. | Surgery_Schwartz. Chatten J, D’Cruz CM, et al. Molecular assays for chromosomal translocations in the diagnosis of pediatric soft tissue sarcomas. JAMA. 1995;273:553-557. 256. Xia SJ, Pressey JG, Barr FG. Molecular pathogenesis of rhabdomyosarcoma. Cancer Biol Ther. 2002;1:97-104. 257. Scrable H, Witte D, Shimada H, et al. Molecular differential pathology of rhabdomyosarcoma. Genes Chromosomes Cancer. 1989;1:23-35. 258. Flamant F, Rodary C, Rey A, et al. Treatment of non-metastatic rhabdomyosarcomas in childhood and adolescence. Results of the second study of the International Society of Paediatric Oncology: MMT84. Eur J Cancer. 1998;34:1050-1062. 259. Crist WM, Anderson JR, Meza JL, et al. Intergroup rhabdomyosarcoma study-IV: results for patients with nonmetastatic disease. J Clin Oncol. 2001;19:3091-3102. 260. Crist WM, Garnsey L, Beltangady MS, et al. Prognosis in children with rhabdomyosarcoma: a report of the intergroup rhabdomyosarcoma studies I and II. Intergroup Rhabdomyo-sarcoma Committee. |
Surgery_Schwartz_10572 | Surgery_Schwartz | WM, Garnsey L, Beltangady MS, et al. Prognosis in children with rhabdomyosarcoma: a report of the intergroup rhabdomyosarcoma studies I and II. Intergroup Rhabdomyo-sarcoma Committee. J Clin Oncol. 1990;8:443-452. 261. Loeb DM, Thornton K, Shokek O. Pediatric soft tissue sarcomas. Surg Clin North Am. 2008;88:615-627, vii.Brunicardi_Ch36_p1567-p1598.indd 159701/03/19 6:38 PM | Surgery_Schwartz. WM, Garnsey L, Beltangady MS, et al. Prognosis in children with rhabdomyosarcoma: a report of the intergroup rhabdomyosarcoma studies I and II. Intergroup Rhabdomyo-sarcoma Committee. J Clin Oncol. 1990;8:443-452. 261. Loeb DM, Thornton K, Shokek O. Pediatric soft tissue sarcomas. Surg Clin North Am. 2008;88:615-627, vii.Brunicardi_Ch36_p1567-p1598.indd 159701/03/19 6:38 PM |
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Surgery_Schwartz_10574 | Surgery_Schwartz | Inguinal HerniasChandan Das, Tahir Jamil, Stephen Stanek, Ziya Baghmanli, James R. Macho, Joseph Sferra, and F. Charles Brunicardi 37chapterINTRODUCTIONInguinal herniorrhaphy is one of the most commonly performed operations in the United States.1 Based on estimates made by the National Center for Health Statistics, in 2010 nearly 515,000 inguinal hernia operations were performed in hospitals, and an additional 450,000 were performed in ambulatory surgery centers.1Approximately 75% of abdominal wall hernias occur in the groin. Of inguinal hernia repairs, 90% are performed in men, and 10% are performed in women. This is thought to be because the lifetime risk of inguinal hernia is 27% in men and 3% in women.2 The incidence of inguinal hernia in men has a bimodal distribution, with peaks before the first year of age and after age 40. Abramson demonstrated the age-dependence of inguinal hernias in 1978. Those age 25 to 34 years had a life-time prevalence rate of 15%, whereas those age | Surgery_Schwartz. Inguinal HerniasChandan Das, Tahir Jamil, Stephen Stanek, Ziya Baghmanli, James R. Macho, Joseph Sferra, and F. Charles Brunicardi 37chapterINTRODUCTIONInguinal herniorrhaphy is one of the most commonly performed operations in the United States.1 Based on estimates made by the National Center for Health Statistics, in 2010 nearly 515,000 inguinal hernia operations were performed in hospitals, and an additional 450,000 were performed in ambulatory surgery centers.1Approximately 75% of abdominal wall hernias occur in the groin. Of inguinal hernia repairs, 90% are performed in men, and 10% are performed in women. This is thought to be because the lifetime risk of inguinal hernia is 27% in men and 3% in women.2 The incidence of inguinal hernia in men has a bimodal distribution, with peaks before the first year of age and after age 40. Abramson demonstrated the age-dependence of inguinal hernias in 1978. Those age 25 to 34 years had a life-time prevalence rate of 15%, whereas those age |
Surgery_Schwartz_10575 | Surgery_Schwartz | before the first year of age and after age 40. Abramson demonstrated the age-dependence of inguinal hernias in 1978. Those age 25 to 34 years had a life-time prevalence rate of 15%, whereas those age 75 years and over had a rate of 47% (Table 37-1).3 Approximately 70% of femoral hernia repairs are performed in women; however, the most common subtype of groin hernia in men and women is still the indirect inguinal hernia. Inguinal hernias are five times more common than femoral hernias.4Globally, the inguinal hernia repair has become one of the most important procedures in improving quality of life and preventing disability. In one study, an international coopera-tive organization performed over 1033 hernia repairs on 926 patients, and their impact was measured in disability adjusted life years (DALYs). They were able to avoid 5014 DALYs or 5.41 DALYs per patient.5HistorySurgical repair of hernias has been documented as far back as in ancient Egyptian and Greek civilizations.4 In the | Surgery_Schwartz. before the first year of age and after age 40. Abramson demonstrated the age-dependence of inguinal hernias in 1978. Those age 25 to 34 years had a life-time prevalence rate of 15%, whereas those age 75 years and over had a rate of 47% (Table 37-1).3 Approximately 70% of femoral hernia repairs are performed in women; however, the most common subtype of groin hernia in men and women is still the indirect inguinal hernia. Inguinal hernias are five times more common than femoral hernias.4Globally, the inguinal hernia repair has become one of the most important procedures in improving quality of life and preventing disability. In one study, an international coopera-tive organization performed over 1033 hernia repairs on 926 patients, and their impact was measured in disability adjusted life years (DALYs). They were able to avoid 5014 DALYs or 5.41 DALYs per patient.5HistorySurgical repair of hernias has been documented as far back as in ancient Egyptian and Greek civilizations.4 In the |
Surgery_Schwartz_10576 | Surgery_Schwartz | years (DALYs). They were able to avoid 5014 DALYs or 5.41 DALYs per patient.5HistorySurgical repair of hernias has been documented as far back as in ancient Egyptian and Greek civilizations.4 In the past, early management of inguinal hernias often involved a conservative approach with operative management reserved only for compli-cations. Surgery often involved routine excision of the testicle, and wounds were closed with cauterization or allowed to close by secondary intention. These procedures were 1performed without aseptic technique, and infection and recur-rence rates were high.From the late 1700s to the early 1800s, physicians including Hesselbach, Cooper, Camper, Scarpa, Richter, and Gimbernat identified vital components of the inguinal region from cadaveric dissection. This improved understanding of the anatomy and pathophysiology of inguinal hernias. These findings, coupled with the development of aseptic technique, led surgeons such as Marcy, Kocher, and Lucas-Championnière | Surgery_Schwartz. years (DALYs). They were able to avoid 5014 DALYs or 5.41 DALYs per patient.5HistorySurgical repair of hernias has been documented as far back as in ancient Egyptian and Greek civilizations.4 In the past, early management of inguinal hernias often involved a conservative approach with operative management reserved only for compli-cations. Surgery often involved routine excision of the testicle, and wounds were closed with cauterization or allowed to close by secondary intention. These procedures were 1performed without aseptic technique, and infection and recur-rence rates were high.From the late 1700s to the early 1800s, physicians including Hesselbach, Cooper, Camper, Scarpa, Richter, and Gimbernat identified vital components of the inguinal region from cadaveric dissection. This improved understanding of the anatomy and pathophysiology of inguinal hernias. These findings, coupled with the development of aseptic technique, led surgeons such as Marcy, Kocher, and Lucas-Championnière |
Surgery_Schwartz_10577 | Surgery_Schwartz | understanding of the anatomy and pathophysiology of inguinal hernias. These findings, coupled with the development of aseptic technique, led surgeons such as Marcy, Kocher, and Lucas-Championnière to perform sac dissection, high ligation, and closure of the internal ring. This led to improved outcomes, but recurrence rates remained unacceptably high.At around this time, Bassini (1844–1924) pioneered a new method that transformed inguinal hernia repair into a success-ful venture with minimal morbidity. The success of the Bassini repair over its predecessors ushered in an era of tissue-based repairs. The Bassini repair was then modified into the McVay and Shouldice repairs. All three of these techniques, as well as modern variations such as the Desarda operation, are currently practiced.6The next major advancement in inguinal hernia repair was in the 1980s. At this time, Lichtenstein applied a piece of mesh to the floor of the inguinal canal, allowing for a truly tension-free repair. | Surgery_Schwartz. understanding of the anatomy and pathophysiology of inguinal hernias. These findings, coupled with the development of aseptic technique, led surgeons such as Marcy, Kocher, and Lucas-Championnière to perform sac dissection, high ligation, and closure of the internal ring. This led to improved outcomes, but recurrence rates remained unacceptably high.At around this time, Bassini (1844–1924) pioneered a new method that transformed inguinal hernia repair into a success-ful venture with minimal morbidity. The success of the Bassini repair over its predecessors ushered in an era of tissue-based repairs. The Bassini repair was then modified into the McVay and Shouldice repairs. All three of these techniques, as well as modern variations such as the Desarda operation, are currently practiced.6The next major advancement in inguinal hernia repair was in the 1980s. At this time, Lichtenstein applied a piece of mesh to the floor of the inguinal canal, allowing for a truly tension-free repair. |
Surgery_Schwartz_10578 | Surgery_Schwartz | next major advancement in inguinal hernia repair was in the 1980s. At this time, Lichtenstein applied a piece of mesh to the floor of the inguinal canal, allowing for a truly tension-free repair. This technique demonstrated superior outcomes compared to previous tissue-based repairs. There were several other advantages of this process. In addition to being truly tension-free, the mesh could restore the strength of the transversalis fascia, and importantly, the technique had a very short learning curve. The superior outcomes have been widely reproduced regardless of hernia size and type, and they were achievable among both expert and nonexpert hernia surgeons.7With the advent of minimally invasive surgery, inguinal hernia repair underwent its most recent transformation. Laparo-scopic inguinal hernia repair offers an alternative approach, minimizes postoperative pain,8 and improves recovery. Since the initial description by Ger, the laparoscopic method has become more sophisticated. | Surgery_Schwartz. next major advancement in inguinal hernia repair was in the 1980s. At this time, Lichtenstein applied a piece of mesh to the floor of the inguinal canal, allowing for a truly tension-free repair. This technique demonstrated superior outcomes compared to previous tissue-based repairs. There were several other advantages of this process. In addition to being truly tension-free, the mesh could restore the strength of the transversalis fascia, and importantly, the technique had a very short learning curve. The superior outcomes have been widely reproduced regardless of hernia size and type, and they were achievable among both expert and nonexpert hernia surgeons.7With the advent of minimally invasive surgery, inguinal hernia repair underwent its most recent transformation. Laparo-scopic inguinal hernia repair offers an alternative approach, minimizes postoperative pain,8 and improves recovery. Since the initial description by Ger, the laparoscopic method has become more sophisticated. |
Surgery_Schwartz_10579 | Surgery_Schwartz | hernia repair offers an alternative approach, minimizes postoperative pain,8 and improves recovery. Since the initial description by Ger, the laparoscopic method has become more sophisticated. Refinements in approach and technique have Introduction1599History / 1599Anatomy / 1600Pathophysiology / 1604Diagnosis1606History / 1606Physical Examination / 1607Imaging / 1607Treatment1608Prophylactic Antibiotics / 1609Open Approach / 1609Laparoscopic Approach / 1613Robot-Assisted Inguinal Hernia Repair / 1616Prosthesis Considerations / 1616Complications1618Hernia Recurrence / 1618Pain / 1619Cord and Testes Injury / 1620Laparoscopic Complications / 1620Hematomas and Seromas / 1621Outcomes1621Brunicardi_Ch37_p1599-p1624.indd 159929/01/19 2:02 PM 1600Key Points1 Conservative management of asymptomatic inguinal hernias is recommended.2 A thorough understanding of groin anatomy is essential to successful surgical treatment of inguinal hernias.3 Elective repair of inguinal hernias can be | Surgery_Schwartz. hernia repair offers an alternative approach, minimizes postoperative pain,8 and improves recovery. Since the initial description by Ger, the laparoscopic method has become more sophisticated. Refinements in approach and technique have Introduction1599History / 1599Anatomy / 1600Pathophysiology / 1604Diagnosis1606History / 1606Physical Examination / 1607Imaging / 1607Treatment1608Prophylactic Antibiotics / 1609Open Approach / 1609Laparoscopic Approach / 1613Robot-Assisted Inguinal Hernia Repair / 1616Prosthesis Considerations / 1616Complications1618Hernia Recurrence / 1618Pain / 1619Cord and Testes Injury / 1620Laparoscopic Complications / 1620Hematomas and Seromas / 1621Outcomes1621Brunicardi_Ch37_p1599-p1624.indd 159929/01/19 2:02 PM 1600Key Points1 Conservative management of asymptomatic inguinal hernias is recommended.2 A thorough understanding of groin anatomy is essential to successful surgical treatment of inguinal hernias.3 Elective repair of inguinal hernias can be |
Surgery_Schwartz_10580 | Surgery_Schwartz | asymptomatic inguinal hernias is recommended.2 A thorough understanding of groin anatomy is essential to successful surgical treatment of inguinal hernias.3 Elective repair of inguinal hernias can be undertaken using a laparoscopic, robotic, or open approach.4 Robotic-assisted hernia surgery is quickly becoming adopted by general surgeons because of its better ergonomics and visualization.5 The use of prosthetic mesh as a reinforcement significantly improves recurrence rates, whether the repair is open or laparoscopic.6 Recurrence, pain, and quality of life are the metrics by which hernia repair outcomes are measured.7 Laparoscopic inguinal hernia repair results in less pain; how-ever, mastery of this technique has a longer learning curve.led to the development of the intraperitoneal onlay mesh,9,10 the transabdominal preperitoneal (TAPP) repair,11 and the totally extraperitoneal (TEP) repair.12 Irrespective of the approach, suc-cessful surgical treatment of inguinal hernias depends | Surgery_Schwartz. asymptomatic inguinal hernias is recommended.2 A thorough understanding of groin anatomy is essential to successful surgical treatment of inguinal hernias.3 Elective repair of inguinal hernias can be undertaken using a laparoscopic, robotic, or open approach.4 Robotic-assisted hernia surgery is quickly becoming adopted by general surgeons because of its better ergonomics and visualization.5 The use of prosthetic mesh as a reinforcement significantly improves recurrence rates, whether the repair is open or laparoscopic.6 Recurrence, pain, and quality of life are the metrics by which hernia repair outcomes are measured.7 Laparoscopic inguinal hernia repair results in less pain; how-ever, mastery of this technique has a longer learning curve.led to the development of the intraperitoneal onlay mesh,9,10 the transabdominal preperitoneal (TAPP) repair,11 and the totally extraperitoneal (TEP) repair.12 Irrespective of the approach, suc-cessful surgical treatment of inguinal hernias depends |
Surgery_Schwartz_10581 | Surgery_Schwartz | mesh,9,10 the transabdominal preperitoneal (TAPP) repair,11 and the totally extraperitoneal (TEP) repair.12 Irrespective of the approach, suc-cessful surgical treatment of inguinal hernias depends on a sound grasp of inguinal anatomy.AnatomyThe inguinal canal is an approximately 4to 6-cm long cone-shaped region situated in the anterior portion of the pelvic basin (Fig. 37-1). The canal begins on the posterior abdominal wall, where the spermatic cord passes through a hiatus in the transver-salis fascia also known as the deep (internal) inguinal ring. The canal concludes medially at the superficial (external) inguinal ring, the point at which the spermatic cord crosses a defect in the external oblique aponeurosis. The boundaries of the ingui-nal canal are the external oblique aponeurosis anteriorly, the internal oblique muscle laterally, the transversalis fascia and transversus abdominis muscle posteriorly, the internal oblique and transversus abdominis muscle superiorly, and the | Surgery_Schwartz. mesh,9,10 the transabdominal preperitoneal (TAPP) repair,11 and the totally extraperitoneal (TEP) repair.12 Irrespective of the approach, suc-cessful surgical treatment of inguinal hernias depends on a sound grasp of inguinal anatomy.AnatomyThe inguinal canal is an approximately 4to 6-cm long cone-shaped region situated in the anterior portion of the pelvic basin (Fig. 37-1). The canal begins on the posterior abdominal wall, where the spermatic cord passes through a hiatus in the transver-salis fascia also known as the deep (internal) inguinal ring. The canal concludes medially at the superficial (external) inguinal ring, the point at which the spermatic cord crosses a defect in the external oblique aponeurosis. The boundaries of the ingui-nal canal are the external oblique aponeurosis anteriorly, the internal oblique muscle laterally, the transversalis fascia and transversus abdominis muscle posteriorly, the internal oblique and transversus abdominis muscle superiorly, and the |
Surgery_Schwartz_10582 | Surgery_Schwartz | anteriorly, the internal oblique muscle laterally, the transversalis fascia and transversus abdominis muscle posteriorly, the internal oblique and transversus abdominis muscle superiorly, and the inguinal (Poupart’s) ligament inferiorly. The spermatic cord traverses the inguinal canal, and it contains three arteries, three veins, two nerves, the pampiniform venous plexus, and the vas deferens. It is enveloped in three layers of spermatic fascia.Additional important structures surrounding the inguinal canal include the iliopubic tract, the lacunar ligament, Cooper’s ligament, and the conjoined tendon (Fig. 37-2). The iliopubic tract is an aponeurotic band that begins at the anterior superior iliac spine and inserts into Cooper’s ligament from above. It forms on the deep inferior margin of the transversus abdominis and transversalis fascia. The shelving edge of the inguinal ligament is a structure that connects the iliopubic tract to the inguinal ligament. The iliopubic tract helps form | Surgery_Schwartz. anteriorly, the internal oblique muscle laterally, the transversalis fascia and transversus abdominis muscle posteriorly, the internal oblique and transversus abdominis muscle superiorly, and the inguinal (Poupart’s) ligament inferiorly. The spermatic cord traverses the inguinal canal, and it contains three arteries, three veins, two nerves, the pampiniform venous plexus, and the vas deferens. It is enveloped in three layers of spermatic fascia.Additional important structures surrounding the inguinal canal include the iliopubic tract, the lacunar ligament, Cooper’s ligament, and the conjoined tendon (Fig. 37-2). The iliopubic tract is an aponeurotic band that begins at the anterior superior iliac spine and inserts into Cooper’s ligament from above. It forms on the deep inferior margin of the transversus abdominis and transversalis fascia. The shelving edge of the inguinal ligament is a structure that connects the iliopubic tract to the inguinal ligament. The iliopubic tract helps form |
Surgery_Schwartz_10583 | Surgery_Schwartz | transversus abdominis and transversalis fascia. The shelving edge of the inguinal ligament is a structure that connects the iliopubic tract to the inguinal ligament. The iliopubic tract helps form the inferior margin of the internal inguinal ring as it courses medially, where it continues as the anteromedial border of the femoral canal. The lacunar ligament, or ligament of Gimbernat, is the triangular fanning of the inguinal ligament as it joins the pubic 2tubercle. Cooper’s (pectineal) ligament is the lateral portion of the lacunar ligament that is fused to the periosteum of the pubic tubercle. The conjoined tendon is commonly described as the fusion of the inferior fibers of the internal oblique and transversus abdominis aponeurosis at the point where they insert on the pubic tubercle.Inguinal hernias are generally classified as direct, indirect, or femoral based upon the site of herniation relative to surround-ing structures. Indirect hernias protrude lateral to the inferior | Surgery_Schwartz. transversus abdominis and transversalis fascia. The shelving edge of the inguinal ligament is a structure that connects the iliopubic tract to the inguinal ligament. The iliopubic tract helps form the inferior margin of the internal inguinal ring as it courses medially, where it continues as the anteromedial border of the femoral canal. The lacunar ligament, or ligament of Gimbernat, is the triangular fanning of the inguinal ligament as it joins the pubic 2tubercle. Cooper’s (pectineal) ligament is the lateral portion of the lacunar ligament that is fused to the periosteum of the pubic tubercle. The conjoined tendon is commonly described as the fusion of the inferior fibers of the internal oblique and transversus abdominis aponeurosis at the point where they insert on the pubic tubercle.Inguinal hernias are generally classified as direct, indirect, or femoral based upon the site of herniation relative to surround-ing structures. Indirect hernias protrude lateral to the inferior |
Surgery_Schwartz_10584 | Surgery_Schwartz | hernias are generally classified as direct, indirect, or femoral based upon the site of herniation relative to surround-ing structures. Indirect hernias protrude lateral to the inferior epigastric vessels, through the deep inguinal ring. Direct hernias protrude medial to the inferior epigastric vessels, within Hesselbach’s triangle. The borders of the triangle are the ingui-nal ligament inferiorly, the lateral edge of rectus sheath medi-ally, and the inferior epigastric vessels superolaterally. Femoral hernias protrude through the small and inflexible femoral ring. They traverse the empty space between the femoral vein and the lymphatic channels. The borders of the femoral ring include the iliopubic tract and inguinal ligament anteriorly, Cooper’s liga-ment posteriorly, the lacunar ligament medially, and the femoral vein laterally. The Nyhus classification categorizes hernia defects by location, size, and type (Table 37-2).Laparoscopic inguinal hernia repair requires a thorough | Surgery_Schwartz. hernias are generally classified as direct, indirect, or femoral based upon the site of herniation relative to surround-ing structures. Indirect hernias protrude lateral to the inferior epigastric vessels, through the deep inguinal ring. Direct hernias protrude medial to the inferior epigastric vessels, within Hesselbach’s triangle. The borders of the triangle are the ingui-nal ligament inferiorly, the lateral edge of rectus sheath medi-ally, and the inferior epigastric vessels superolaterally. Femoral hernias protrude through the small and inflexible femoral ring. They traverse the empty space between the femoral vein and the lymphatic channels. The borders of the femoral ring include the iliopubic tract and inguinal ligament anteriorly, Cooper’s liga-ment posteriorly, the lacunar ligament medially, and the femoral vein laterally. The Nyhus classification categorizes hernia defects by location, size, and type (Table 37-2).Laparoscopic inguinal hernia repair requires a thorough |
Surgery_Schwartz_10585 | Surgery_Schwartz | medially, and the femoral vein laterally. The Nyhus classification categorizes hernia defects by location, size, and type (Table 37-2).Laparoscopic inguinal hernia repair requires a thorough knowledge of inguinal anatomy from a posterior perspective (Fig. 37-3). Intraperitoneal points of reference are the five peritoneal folds, bladder, inferior epigastric vessels, and psoas muscle (Fig. 37-4). Two potential spaces exist within the pre-peritoneum. Between the peritoneum and the posterior lamina of the transversalis fascia is Bogros’s (preperitoneal) space. This area contains preperitoneal fat and areolar tissue. The most medial aspect of the preperitoneal space, that which lies superior to the bladder, is known as the space of Retzius. The posterior perspective also allows visualization of the myopectineal orifice of Fruchaud, a relatively weak portion of the abdominal wall that is divided by the inguinal ligament (Fig. 37-5).The vascular space is situated between the posterior and | Surgery_Schwartz. medially, and the femoral vein laterally. The Nyhus classification categorizes hernia defects by location, size, and type (Table 37-2).Laparoscopic inguinal hernia repair requires a thorough knowledge of inguinal anatomy from a posterior perspective (Fig. 37-3). Intraperitoneal points of reference are the five peritoneal folds, bladder, inferior epigastric vessels, and psoas muscle (Fig. 37-4). Two potential spaces exist within the pre-peritoneum. Between the peritoneum and the posterior lamina of the transversalis fascia is Bogros’s (preperitoneal) space. This area contains preperitoneal fat and areolar tissue. The most medial aspect of the preperitoneal space, that which lies superior to the bladder, is known as the space of Retzius. The posterior perspective also allows visualization of the myopectineal orifice of Fruchaud, a relatively weak portion of the abdominal wall that is divided by the inguinal ligament (Fig. 37-5).The vascular space is situated between the posterior and |
Surgery_Schwartz_10586 | Surgery_Schwartz | of the myopectineal orifice of Fruchaud, a relatively weak portion of the abdominal wall that is divided by the inguinal ligament (Fig. 37-5).The vascular space is situated between the posterior and anterior laminae of the transversalis fascia, and it houses the Table 37-1Inguinal hernia prevalence by ageAGE (Y)25–3435–4445–5455–6465–7475+Current prevalence (%)121520262934Lifetime prevalence (%)151928344047Current = repaired hernias excluded; lifetime = repaired hernias included.Brunicardi_Ch37_p1599-p1624.indd 160029/01/19 2:02 PM 1601INGUINAL HERNIASCHAPTER 37Abdominal ringLateral leafPubic tubercleSpermatic cordInterrupted sutures taken to suture the medial leaf to the inguinal ligament Interrupted sutures between the upper border of the strip and conjoined muscle and internal oblique muscleInternal oblique muscle seen through the splitting incision made in the medial leafReflected medial leaf after a strip has been separatedFigure 37-2. Ligaments that contribute to the | Surgery_Schwartz. of the myopectineal orifice of Fruchaud, a relatively weak portion of the abdominal wall that is divided by the inguinal ligament (Fig. 37-5).The vascular space is situated between the posterior and anterior laminae of the transversalis fascia, and it houses the Table 37-1Inguinal hernia prevalence by ageAGE (Y)25–3435–4445–5455–6465–7475+Current prevalence (%)121520262934Lifetime prevalence (%)151928344047Current = repaired hernias excluded; lifetime = repaired hernias included.Brunicardi_Ch37_p1599-p1624.indd 160029/01/19 2:02 PM 1601INGUINAL HERNIASCHAPTER 37Abdominal ringLateral leafPubic tubercleSpermatic cordInterrupted sutures taken to suture the medial leaf to the inguinal ligament Interrupted sutures between the upper border of the strip and conjoined muscle and internal oblique muscleInternal oblique muscle seen through the splitting incision made in the medial leafReflected medial leaf after a strip has been separatedFigure 37-2. Ligaments that contribute to the |
Surgery_Schwartz_10587 | Surgery_Schwartz | oblique muscleInternal oblique muscle seen through the splitting incision made in the medial leafReflected medial leaf after a strip has been separatedFigure 37-2. Ligaments that contribute to the inguinal canal include the inguinal ligament, Cooper’s ligament, and the lacunar ligament. The iliopubic tract originates and inserts in a similar fashion to the inguinal ligament, but in a deeper position. m. = muscle.Abdominal ringLateral leafMedial leafPubic tubercleSpermatic cordInterrupted sutures taken to suture the medial leaf to the inguinal ligament Figure 37-1. Location and orientation of the inguinal canal within the pelvic basin. Boundaries of the canal include: transversus abdominus and transversalis fascia posterior; internal oblique muscle superior; external oblique aponeurosis anterior; inguinal ligament inferior. m. = muscle.inferior epigastric vessels. The inferior epigastric artery supplies the rectus abdominis. It is derived from the external iliac artery, and it | Surgery_Schwartz. oblique muscleInternal oblique muscle seen through the splitting incision made in the medial leafReflected medial leaf after a strip has been separatedFigure 37-2. Ligaments that contribute to the inguinal canal include the inguinal ligament, Cooper’s ligament, and the lacunar ligament. The iliopubic tract originates and inserts in a similar fashion to the inguinal ligament, but in a deeper position. m. = muscle.Abdominal ringLateral leafMedial leafPubic tubercleSpermatic cordInterrupted sutures taken to suture the medial leaf to the inguinal ligament Figure 37-1. Location and orientation of the inguinal canal within the pelvic basin. Boundaries of the canal include: transversus abdominus and transversalis fascia posterior; internal oblique muscle superior; external oblique aponeurosis anterior; inguinal ligament inferior. m. = muscle.inferior epigastric vessels. The inferior epigastric artery supplies the rectus abdominis. It is derived from the external iliac artery, and it |
Surgery_Schwartz_10588 | Surgery_Schwartz | anterior; inguinal ligament inferior. m. = muscle.inferior epigastric vessels. The inferior epigastric artery supplies the rectus abdominis. It is derived from the external iliac artery, and it anastomoses with the superior epigastric, a continuation of the internal thoracic artery. The epigastric veins course paral-lel to the arteries within the rectus sheath, posterior to the rectus muscles. Inspection of the internal inguinal ring will reveal the deep location of the inferior epigastric vessels.Nerves of interest in the inguinal region are the ilioin-guinal, iliohypogastric, genitofemoral, and lateral femoral cutaneous nerves (Figs. 37-6 and 37-7). The ilioinguinal and iliohypogastric nerves arise together from the first lumbar nerve (L1). The ilioinguinal nerve emerges from the lateral border of the psoas major and passes obliquely across the quadratus lumborum. At a point just medial to the anterior Brunicardi_Ch37_p1599-p1624.indd 160129/01/19 2:02 PM 1602SPECIFIC | Surgery_Schwartz. anterior; inguinal ligament inferior. m. = muscle.inferior epigastric vessels. The inferior epigastric artery supplies the rectus abdominis. It is derived from the external iliac artery, and it anastomoses with the superior epigastric, a continuation of the internal thoracic artery. The epigastric veins course paral-lel to the arteries within the rectus sheath, posterior to the rectus muscles. Inspection of the internal inguinal ring will reveal the deep location of the inferior epigastric vessels.Nerves of interest in the inguinal region are the ilioin-guinal, iliohypogastric, genitofemoral, and lateral femoral cutaneous nerves (Figs. 37-6 and 37-7). The ilioinguinal and iliohypogastric nerves arise together from the first lumbar nerve (L1). The ilioinguinal nerve emerges from the lateral border of the psoas major and passes obliquely across the quadratus lumborum. At a point just medial to the anterior Brunicardi_Ch37_p1599-p1624.indd 160129/01/19 2:02 PM 1602SPECIFIC |
Surgery_Schwartz_10589 | Surgery_Schwartz | the lateral border of the psoas major and passes obliquely across the quadratus lumborum. At a point just medial to the anterior Brunicardi_Ch37_p1599-p1624.indd 160129/01/19 2:02 PM 1602SPECIFIC CONSIDERATIONSPART IIInferior epigastric vesselsCooper’s ligamentPubic tubercleArcuate lineUmbilicusLinea albaRectus muscleDeepinguinalringIliopubictractExternal iliacvesselsIndirecthernia siteDirecthernia siteObturatorvesselsTransversusabdominismusclearchSuperioranteriorcrusSpermatic cordSpermatic vesselsFemoral canalFigure 37-3. Anatomy of the groin region from the posterior perspective.AA UmbilicusB Median umbilical ligament (urachus)C Medial umbilical ligament (obliterated umbilical vein)D Lateral umbilical ligament (inferior epigastric vessels)E Lateral fossa (indirect hernia)F Medial fossa (direct hernia)G Supravesical fossaBEFBladderGCDFigure 37-4. Posterior view of intraperitoneal folds and associated fossa: A. Umbilicus. B. Median umbilical ligament. C. Medial | Surgery_Schwartz. the lateral border of the psoas major and passes obliquely across the quadratus lumborum. At a point just medial to the anterior Brunicardi_Ch37_p1599-p1624.indd 160129/01/19 2:02 PM 1602SPECIFIC CONSIDERATIONSPART IIInferior epigastric vesselsCooper’s ligamentPubic tubercleArcuate lineUmbilicusLinea albaRectus muscleDeepinguinalringIliopubictractExternal iliacvesselsIndirecthernia siteDirecthernia siteObturatorvesselsTransversusabdominismusclearchSuperioranteriorcrusSpermatic cordSpermatic vesselsFemoral canalFigure 37-3. Anatomy of the groin region from the posterior perspective.AA UmbilicusB Median umbilical ligament (urachus)C Medial umbilical ligament (obliterated umbilical vein)D Lateral umbilical ligament (inferior epigastric vessels)E Lateral fossa (indirect hernia)F Medial fossa (direct hernia)G Supravesical fossaBEFBladderGCDFigure 37-4. Posterior view of intraperitoneal folds and associated fossa: A. Umbilicus. B. Median umbilical ligament. C. Medial |
Surgery_Schwartz_10590 | Surgery_Schwartz | hernia)F Medial fossa (direct hernia)G Supravesical fossaBEFBladderGCDFigure 37-4. Posterior view of intraperitoneal folds and associated fossa: A. Umbilicus. B. Median umbilical ligament. C. Medial umbilical ligament (obliterated umbilical vein). D. Lateral umbilical ligament (inferior epigastric vessels). E. Lateral fossa (indirect hernia). F. Medial fossa (direct hernia). G. Supravesical fossa. (Modified with permission from Rowe JS, Skandalakis JE, Gray SW: Multiple bilateral inguinal hernias, Am Surg. 1973 May;39(5):269-270.)Table 37-2Nyhus classification systemType IIndirect hernia; internal abdominal ring normal; typically in infants, children, small adultsType IIIndirect hernia; internal ring enlarged without impingement on the floor of the inguinal canal; does not extend to the scrotumType IIIADirect hernia; size is not taken into accountType IIIBIndirect hernia that has enlarged enough to encroach upon the posterior inguinal wall; indirect sliding or scrotal hernias are | Surgery_Schwartz. hernia)F Medial fossa (direct hernia)G Supravesical fossaBEFBladderGCDFigure 37-4. Posterior view of intraperitoneal folds and associated fossa: A. Umbilicus. B. Median umbilical ligament. C. Medial umbilical ligament (obliterated umbilical vein). D. Lateral umbilical ligament (inferior epigastric vessels). E. Lateral fossa (indirect hernia). F. Medial fossa (direct hernia). G. Supravesical fossa. (Modified with permission from Rowe JS, Skandalakis JE, Gray SW: Multiple bilateral inguinal hernias, Am Surg. 1973 May;39(5):269-270.)Table 37-2Nyhus classification systemType IIndirect hernia; internal abdominal ring normal; typically in infants, children, small adultsType IIIndirect hernia; internal ring enlarged without impingement on the floor of the inguinal canal; does not extend to the scrotumType IIIADirect hernia; size is not taken into accountType IIIBIndirect hernia that has enlarged enough to encroach upon the posterior inguinal wall; indirect sliding or scrotal hernias are |
Surgery_Schwartz_10591 | Surgery_Schwartz | scrotumType IIIADirect hernia; size is not taken into accountType IIIBIndirect hernia that has enlarged enough to encroach upon the posterior inguinal wall; indirect sliding or scrotal hernias are usually placed in this category because they are commonly associated with extension to the direct space; also includes pantaloon herniasType IIICFemoral herniaType IVRecurrent hernia; modifiers A–D are sometimes added, which correspond to indirect, direct, femoral, and mixed, respectivelysuperior iliac spine, it pierces the transversus and internal oblique muscles to enter the inguinal canal and exits through the superficial inguinal ring. It supplies somatic sensation to the skin of the upper and medial thigh. In males, it also inner-vates the base of the penis and upper scrotum. In females, it innervates the mons pubis and labium majus. The iliohypo-gastric nerve arises from T12–L1. After it pierces the deep abdominal wall, it courses between the internal oblique and transversus abdominis, | Surgery_Schwartz. scrotumType IIIADirect hernia; size is not taken into accountType IIIBIndirect hernia that has enlarged enough to encroach upon the posterior inguinal wall; indirect sliding or scrotal hernias are usually placed in this category because they are commonly associated with extension to the direct space; also includes pantaloon herniasType IIICFemoral herniaType IVRecurrent hernia; modifiers A–D are sometimes added, which correspond to indirect, direct, femoral, and mixed, respectivelysuperior iliac spine, it pierces the transversus and internal oblique muscles to enter the inguinal canal and exits through the superficial inguinal ring. It supplies somatic sensation to the skin of the upper and medial thigh. In males, it also inner-vates the base of the penis and upper scrotum. In females, it innervates the mons pubis and labium majus. The iliohypo-gastric nerve arises from T12–L1. After it pierces the deep abdominal wall, it courses between the internal oblique and transversus abdominis, |
Surgery_Schwartz_10592 | Surgery_Schwartz | innervates the mons pubis and labium majus. The iliohypo-gastric nerve arises from T12–L1. After it pierces the deep abdominal wall, it courses between the internal oblique and transversus abdominis, supplying both. It then divides into lat-eral and anterior cutaneous branches. A common variant is for the iliohypogastric and ilioinguinal nerves to exit around the superficial inguinal ring as a single entity. The genitofemoral nerve arises from L1 to L2, courses along the retroperitoneum, and emerges on the anterior aspect of the psoas. It then divides into genital and femoral branches. The genital branch enters the inguinal canal lateral to the inferior epigastric vessels, and it courses ventral to the iliac vessels and iliopubic tract. In males, it travels through the superficial inguinal ring and sup-plies the ipsilateral scrotum and cremaster muscle. In females, it supplies the ipsilateral mons pubis and labium majus. The Brunicardi_Ch37_p1599-p1624.indd 160229/01/19 2:02 PM | Surgery_Schwartz. innervates the mons pubis and labium majus. The iliohypo-gastric nerve arises from T12–L1. After it pierces the deep abdominal wall, it courses between the internal oblique and transversus abdominis, supplying both. It then divides into lat-eral and anterior cutaneous branches. A common variant is for the iliohypogastric and ilioinguinal nerves to exit around the superficial inguinal ring as a single entity. The genitofemoral nerve arises from L1 to L2, courses along the retroperitoneum, and emerges on the anterior aspect of the psoas. It then divides into genital and femoral branches. The genital branch enters the inguinal canal lateral to the inferior epigastric vessels, and it courses ventral to the iliac vessels and iliopubic tract. In males, it travels through the superficial inguinal ring and sup-plies the ipsilateral scrotum and cremaster muscle. In females, it supplies the ipsilateral mons pubis and labium majus. The Brunicardi_Ch37_p1599-p1624.indd 160229/01/19 2:02 PM |
Surgery_Schwartz_10593 | Surgery_Schwartz | ring and sup-plies the ipsilateral scrotum and cremaster muscle. In females, it supplies the ipsilateral mons pubis and labium majus. The Brunicardi_Ch37_p1599-p1624.indd 160229/01/19 2:02 PM 1603INGUINAL HERNIASCHAPTER 37Epigastric vesselsInternal spermaticvesselsIliopsoas muscleIliopubictractMyopectinealorificeExternal iliac a. and v.Vas deferensObturator n.Obturator vesselsLacunar ligamentCooper's ligamentFigure 37-5. Posterior view of the myopectineal orifice of Fruchaud. a. = artery; n. = nerve; v. = vein.Ilioinguinal n.Iliohypogastric n.Iliac m.Lateral femoralcutaneous n.Femoral n.Inguinal ligamentGenitofemoral n.(femoral branch)(genital branch)Iliopectinal archPectineal ligamentIliopubic tractLacunar ligamentFigure 37-6. Retroperitoneal view of major inguinal nerves and their courses. m. = muscle; n. = nerve.femoral branch courses along the femoral sheath, supply-ing the skin of the upper anterior thigh. The lateral femoral cutaneous nerve arises from L2 to L3, emerges | Surgery_Schwartz. ring and sup-plies the ipsilateral scrotum and cremaster muscle. In females, it supplies the ipsilateral mons pubis and labium majus. The Brunicardi_Ch37_p1599-p1624.indd 160229/01/19 2:02 PM 1603INGUINAL HERNIASCHAPTER 37Epigastric vesselsInternal spermaticvesselsIliopsoas muscleIliopubictractMyopectinealorificeExternal iliac a. and v.Vas deferensObturator n.Obturator vesselsLacunar ligamentCooper's ligamentFigure 37-5. Posterior view of the myopectineal orifice of Fruchaud. a. = artery; n. = nerve; v. = vein.Ilioinguinal n.Iliohypogastric n.Iliac m.Lateral femoralcutaneous n.Femoral n.Inguinal ligamentGenitofemoral n.(femoral branch)(genital branch)Iliopectinal archPectineal ligamentIliopubic tractLacunar ligamentFigure 37-6. Retroperitoneal view of major inguinal nerves and their courses. m. = muscle; n. = nerve.femoral branch courses along the femoral sheath, supply-ing the skin of the upper anterior thigh. The lateral femoral cutaneous nerve arises from L2 to L3, emerges |
Surgery_Schwartz_10594 | Surgery_Schwartz | courses. m. = muscle; n. = nerve.femoral branch courses along the femoral sheath, supply-ing the skin of the upper anterior thigh. The lateral femoral cutaneous nerve arises from L2 to L3, emerges lateral to the psoas muscle at the level of L4, and crosses the iliacus mus-cle obliquely toward the anterior superior iliac spine. It then passes inferiorly to the inguinal ligament where it divides to supply the lateral thigh (Fig. 37-8).The preperitoneal anatomy seen in laparoscopic hernia repair led to characterization of important anatomic areas of interest, known as the triangle of doom, the triangle of pain, and the circle of death (Fig. 37-9).7 The triangle of doom is bordered medially by the vas deferens and laterally by the vessels of the spermatic cord. The contents of the space include the external iliac vessels, deep circumflex iliac vein, femoral nerve, and gen-ital branch of the genitofemoral nerve. The triangle of pain is a region bordered by the iliopubic tract and gonadal | Surgery_Schwartz. courses. m. = muscle; n. = nerve.femoral branch courses along the femoral sheath, supply-ing the skin of the upper anterior thigh. The lateral femoral cutaneous nerve arises from L2 to L3, emerges lateral to the psoas muscle at the level of L4, and crosses the iliacus mus-cle obliquely toward the anterior superior iliac spine. It then passes inferiorly to the inguinal ligament where it divides to supply the lateral thigh (Fig. 37-8).The preperitoneal anatomy seen in laparoscopic hernia repair led to characterization of important anatomic areas of interest, known as the triangle of doom, the triangle of pain, and the circle of death (Fig. 37-9).7 The triangle of doom is bordered medially by the vas deferens and laterally by the vessels of the spermatic cord. The contents of the space include the external iliac vessels, deep circumflex iliac vein, femoral nerve, and gen-ital branch of the genitofemoral nerve. The triangle of pain is a region bordered by the iliopubic tract and gonadal |
Surgery_Schwartz_10595 | Surgery_Schwartz | the external iliac vessels, deep circumflex iliac vein, femoral nerve, and gen-ital branch of the genitofemoral nerve. The triangle of pain is a region bordered by the iliopubic tract and gonadal vessels, and it encompasses the lateral femoral cutaneous, femoral branch of the genitofemoral and femoral nerves. The circle of death is a vascular continuation formed by the common iliac, internal iliac, obturator, inferior epigastric, and external iliac vessels.Brunicardi_Ch37_p1599-p1624.indd 160329/01/19 2:03 PM 1604SPECIFIC CONSIDERATIONSPART IIFigure 37-7. Anterior view of the five major nerves of the inguinal region.Femoral branch ofgenitofemoral n.Ilioinguinal n.Lateral femoralcutaneous n.Medial and intermediatefemoral cutaneous nn.Saphenous n.Iliohypogastric n.Genital branch ofgenitofemoral n.Figure 37-8. Sensory dermatomes of the major nerves in the groin area. n. = nerve.PathophysiologyInguinal hernias may be congenital or acquired. Most adult inguinal hernias are considered | Surgery_Schwartz. the external iliac vessels, deep circumflex iliac vein, femoral nerve, and gen-ital branch of the genitofemoral nerve. The triangle of pain is a region bordered by the iliopubic tract and gonadal vessels, and it encompasses the lateral femoral cutaneous, femoral branch of the genitofemoral and femoral nerves. The circle of death is a vascular continuation formed by the common iliac, internal iliac, obturator, inferior epigastric, and external iliac vessels.Brunicardi_Ch37_p1599-p1624.indd 160329/01/19 2:03 PM 1604SPECIFIC CONSIDERATIONSPART IIFigure 37-7. Anterior view of the five major nerves of the inguinal region.Femoral branch ofgenitofemoral n.Ilioinguinal n.Lateral femoralcutaneous n.Medial and intermediatefemoral cutaneous nn.Saphenous n.Iliohypogastric n.Genital branch ofgenitofemoral n.Figure 37-8. Sensory dermatomes of the major nerves in the groin area. n. = nerve.PathophysiologyInguinal hernias may be congenital or acquired. Most adult inguinal hernias are considered |
Surgery_Schwartz_10596 | Surgery_Schwartz | n.Figure 37-8. Sensory dermatomes of the major nerves in the groin area. n. = nerve.PathophysiologyInguinal hernias may be congenital or acquired. Most adult inguinal hernias are considered acquired defects in the abdomi-nal wall. There is however, a known hereditary association that is not well understood.13 The most likely risk factor for inguinal hernia is weakness in the abdominal wall musculature; how-ever, there are several other risk-factors that have been studied (Table 37-3). Congenital hernias, which make up the majority of pediatric hernias, can be considered a developmental defect rather than an acquired weakness. During the normal course of development, the testes descend from the intra-abdominal space into the scrotum in the third trimester. Their descent is guided by the gubernaculum through an evagination of the peritoneum, which protrudes through the inguinal canal and becomes the processus vaginalis. Between 36 and 40 weeks’ gestation, the processus vaginalis closes | Surgery_Schwartz. n.Figure 37-8. Sensory dermatomes of the major nerves in the groin area. n. = nerve.PathophysiologyInguinal hernias may be congenital or acquired. Most adult inguinal hernias are considered acquired defects in the abdomi-nal wall. There is however, a known hereditary association that is not well understood.13 The most likely risk factor for inguinal hernia is weakness in the abdominal wall musculature; how-ever, there are several other risk-factors that have been studied (Table 37-3). Congenital hernias, which make up the majority of pediatric hernias, can be considered a developmental defect rather than an acquired weakness. During the normal course of development, the testes descend from the intra-abdominal space into the scrotum in the third trimester. Their descent is guided by the gubernaculum through an evagination of the peritoneum, which protrudes through the inguinal canal and becomes the processus vaginalis. Between 36 and 40 weeks’ gestation, the processus vaginalis closes |
Surgery_Schwartz_10597 | Surgery_Schwartz | through an evagination of the peritoneum, which protrudes through the inguinal canal and becomes the processus vaginalis. Between 36 and 40 weeks’ gestation, the processus vaginalis closes and eliminates the peritoneal open-ing at the internal inguinal ring.14 Failure of the peritoneum to close results in a patent processus vaginalis (PPV). In preterm babies, indirect inguinal hernias as a result of PPV is very high (Fig. 37-10). However, overall, the risk of developing a symp-tomatic hernia during childhood in the presence of a known PPV is relatively low.15Overall, there is limited data regarding the etiology of inguinal hernia development. Several studies have documented strenuous physical activity as a risk factor for acquired inguinal hernia.16 A case-controlled study of over 1400 male patients with inguinal hernia revealed that a positive family history was associated with an eightfold lifetime incidence of Brunicardi_Ch37_p1599-p1624.indd 160429/01/19 2:03 PM 1605INGUINAL | Surgery_Schwartz. through an evagination of the peritoneum, which protrudes through the inguinal canal and becomes the processus vaginalis. Between 36 and 40 weeks’ gestation, the processus vaginalis closes and eliminates the peritoneal open-ing at the internal inguinal ring.14 Failure of the peritoneum to close results in a patent processus vaginalis (PPV). In preterm babies, indirect inguinal hernias as a result of PPV is very high (Fig. 37-10). However, overall, the risk of developing a symp-tomatic hernia during childhood in the presence of a known PPV is relatively low.15Overall, there is limited data regarding the etiology of inguinal hernia development. Several studies have documented strenuous physical activity as a risk factor for acquired inguinal hernia.16 A case-controlled study of over 1400 male patients with inguinal hernia revealed that a positive family history was associated with an eightfold lifetime incidence of Brunicardi_Ch37_p1599-p1624.indd 160429/01/19 2:03 PM 1605INGUINAL |
Surgery_Schwartz_10598 | Surgery_Schwartz | patients with inguinal hernia revealed that a positive family history was associated with an eightfold lifetime incidence of Brunicardi_Ch37_p1599-p1624.indd 160429/01/19 2:03 PM 1605INGUINAL HERNIASCHAPTER 37Inferolateral border:iliopubic tractDeep circumflexiliac a. & v.Lateral border:reflected peritoneumLat. femoral cutaneous n.Ant. femoral cutaneous n. or other variable branchesFemoral br. of genitofemoral n.Femoral n.Superomedial border:gonadal vesselsLateral border:gonadal vesselsGenital branch ofgenitofemoral nerveIliac veinIliac arteryMedial border:ductus deferensPosterior border:peritoneal edgeDeep ringABFigure 37-9. Borders and contents of the (A) triangle of doom and (B) triangle of pain. a. = artery; Ant. = anterior; br. = branch; Lat. = lateral; n. = nerve; v. = vein. (Modified with permission from Colborn GL, Skandalakis JE: Laparoscopic cadaveric anatomy of the inguinal area, Probl Gen Surg. 1995;12(1):13-20.)inguinal hernia.17 Chronic obstructive pulmonary disease | Surgery_Schwartz. patients with inguinal hernia revealed that a positive family history was associated with an eightfold lifetime incidence of Brunicardi_Ch37_p1599-p1624.indd 160429/01/19 2:03 PM 1605INGUINAL HERNIASCHAPTER 37Inferolateral border:iliopubic tractDeep circumflexiliac a. & v.Lateral border:reflected peritoneumLat. femoral cutaneous n.Ant. femoral cutaneous n. or other variable branchesFemoral br. of genitofemoral n.Femoral n.Superomedial border:gonadal vesselsLateral border:gonadal vesselsGenital branch ofgenitofemoral nerveIliac veinIliac arteryMedial border:ductus deferensPosterior border:peritoneal edgeDeep ringABFigure 37-9. Borders and contents of the (A) triangle of doom and (B) triangle of pain. a. = artery; Ant. = anterior; br. = branch; Lat. = lateral; n. = nerve; v. = vein. (Modified with permission from Colborn GL, Skandalakis JE: Laparoscopic cadaveric anatomy of the inguinal area, Probl Gen Surg. 1995;12(1):13-20.)inguinal hernia.17 Chronic obstructive pulmonary disease |
Surgery_Schwartz_10599 | Surgery_Schwartz | with permission from Colborn GL, Skandalakis JE: Laparoscopic cadaveric anatomy of the inguinal area, Probl Gen Surg. 1995;12(1):13-20.)inguinal hernia.17 Chronic obstructive pulmonary disease also significantly increases the risk of direct inguinal hernias, thought to be due to repeated instances of intra-abdominal pressure during coughing.18 Several studies have suggested a protective effect of obesity. In a large, population-based prospective study of American individuals (First National Health and Nutrition Examination Survey), the risk of inguinal hernia development in obese men was only 50% that of normal-weight men, while the risk in overweight men was 80% that of nonobese men. A possible explanation is the increased difficulty in detecting inguinal hernias in obese individuals.18Epidemiologic studies have identified risk factors that may predispose to a hernia. Microscopic examination of skin of inguinal hernia patients demonstrated significantly decreased ratios of type I to | Surgery_Schwartz. with permission from Colborn GL, Skandalakis JE: Laparoscopic cadaveric anatomy of the inguinal area, Probl Gen Surg. 1995;12(1):13-20.)inguinal hernia.17 Chronic obstructive pulmonary disease also significantly increases the risk of direct inguinal hernias, thought to be due to repeated instances of intra-abdominal pressure during coughing.18 Several studies have suggested a protective effect of obesity. In a large, population-based prospective study of American individuals (First National Health and Nutrition Examination Survey), the risk of inguinal hernia development in obese men was only 50% that of normal-weight men, while the risk in overweight men was 80% that of nonobese men. A possible explanation is the increased difficulty in detecting inguinal hernias in obese individuals.18Epidemiologic studies have identified risk factors that may predispose to a hernia. Microscopic examination of skin of inguinal hernia patients demonstrated significantly decreased ratios of type I to |
Surgery_Schwartz_10600 | Surgery_Schwartz | studies have identified risk factors that may predispose to a hernia. Microscopic examination of skin of inguinal hernia patients demonstrated significantly decreased ratios of type I to type III collagen. Type III collagen does not contribute to wound tensile strength as significantly as type I collagen. Additional analyses of similar skin revealed disaggregated collagen tracts with decreased collagen fiber density.19 Collagen disorders such as Ehlers-Danlos syndrome are also associated with an increased incidence of hernia formation (Table 37-4). Recent studies have found an association between concentrations of extracellular matrix Brunicardi_Ch37_p1599-p1624.indd 160529/01/19 2:03 PM 1606SPECIFIC CONSIDERATIONSPART IITable 37-3Presumed causes of groin herniationCoughingChronic obstructive pulmonary diseaseObesityStraining Constipation ProstatismPregnancyBirthweight <1500 gFamily history of a herniaValsalva’s maneuverAscitesUpright positionCongenital connective tissue | Surgery_Schwartz. studies have identified risk factors that may predispose to a hernia. Microscopic examination of skin of inguinal hernia patients demonstrated significantly decreased ratios of type I to type III collagen. Type III collagen does not contribute to wound tensile strength as significantly as type I collagen. Additional analyses of similar skin revealed disaggregated collagen tracts with decreased collagen fiber density.19 Collagen disorders such as Ehlers-Danlos syndrome are also associated with an increased incidence of hernia formation (Table 37-4). Recent studies have found an association between concentrations of extracellular matrix Brunicardi_Ch37_p1599-p1624.indd 160529/01/19 2:03 PM 1606SPECIFIC CONSIDERATIONSPART IITable 37-3Presumed causes of groin herniationCoughingChronic obstructive pulmonary diseaseObesityStraining Constipation ProstatismPregnancyBirthweight <1500 gFamily history of a herniaValsalva’s maneuverAscitesUpright positionCongenital connective tissue |
Surgery_Schwartz_10601 | Surgery_Schwartz | obstructive pulmonary diseaseObesityStraining Constipation ProstatismPregnancyBirthweight <1500 gFamily history of a herniaValsalva’s maneuverAscitesUpright positionCongenital connective tissue disordersDefective collagen synthesisPrevious right lower quadrant incisionArterial aneurysmsCigarette smokingHeavy liftingPhysical exertionFigure 37-10. Varying degrees of closure of the processus vagi-nalis (PV). A. Closed PV. B. Minimally patent PV. C. Moderately patent PV. D. Scrotal hernia.Table 37-4Connective tissue disorders associated with groin herniationOsteogenesis imperfectaCutis laxa (congenital elastolysis)Ehlers-Danlos syndromeHurler-Hunter syndromeMarfan’s syndromeCongenital hip dislocation in childrenPolycystic kidney diseaseα1-Antitrypsin deficiencyWilliams syndromeAndrogen insensitivity syndromeRobinow’s syndromeSerpentine fibula syndromeAlport’s syndromeTel Hashomer camptodactyly syndromeLeriche’s syndromeTesticular feminization syndromeRokitansky-Mayer-Küster | Surgery_Schwartz. obstructive pulmonary diseaseObesityStraining Constipation ProstatismPregnancyBirthweight <1500 gFamily history of a herniaValsalva’s maneuverAscitesUpright positionCongenital connective tissue disordersDefective collagen synthesisPrevious right lower quadrant incisionArterial aneurysmsCigarette smokingHeavy liftingPhysical exertionFigure 37-10. Varying degrees of closure of the processus vagi-nalis (PV). A. Closed PV. B. Minimally patent PV. C. Moderately patent PV. D. Scrotal hernia.Table 37-4Connective tissue disorders associated with groin herniationOsteogenesis imperfectaCutis laxa (congenital elastolysis)Ehlers-Danlos syndromeHurler-Hunter syndromeMarfan’s syndromeCongenital hip dislocation in childrenPolycystic kidney diseaseα1-Antitrypsin deficiencyWilliams syndromeAndrogen insensitivity syndromeRobinow’s syndromeSerpentine fibula syndromeAlport’s syndromeTel Hashomer camptodactyly syndromeLeriche’s syndromeTesticular feminization syndromeRokitansky-Mayer-Küster |
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