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appear as raised pink, purple, or flesh-colored skin papules and are often diagnosed late.Diagnosis and Staging. Workup should begin with a his-tory and physical exam. The entire skin should be checked for synchronous primaries, satellite lesions, and in-transit metas-tases, and all nodal basins should be examined for lymphade-nopathy. Suspicious lesions should undergo excisional biopsy with 1to 3-mm margins; however, tumors that are large or are in a cosmetically or anatomically challenging area can be approached by incisional biopsy, including punch biopsy.136 Brunicardi_Ch16_p0511-p0540.indd 53019/02/19 3:09 PM 531THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16ABCFigure 16-12. A. AP view of advanced melanoma in a 59-year-old male. B. Lateral view C. After resection and reconstruction with skin grafting.Tissue specimen should include full thickness of the lesion and a small section of normal adjacent skin to aid the pathologist in diagnosis. Clinically suspicious lymph nodes should
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Surgery_Schwartz. appear as raised pink, purple, or flesh-colored skin papules and are often diagnosed late.Diagnosis and Staging. Workup should begin with a his-tory and physical exam. The entire skin should be checked for synchronous primaries, satellite lesions, and in-transit metas-tases, and all nodal basins should be examined for lymphade-nopathy. Suspicious lesions should undergo excisional biopsy with 1to 3-mm margins; however, tumors that are large or are in a cosmetically or anatomically challenging area can be approached by incisional biopsy, including punch biopsy.136 Brunicardi_Ch16_p0511-p0540.indd 53019/02/19 3:09 PM 531THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16ABCFigure 16-12. A. AP view of advanced melanoma in a 59-year-old male. B. Lateral view C. After resection and reconstruction with skin grafting.Tissue specimen should include full thickness of the lesion and a small section of normal adjacent skin to aid the pathologist in diagnosis. Clinically suspicious lymph nodes should
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skin grafting.Tissue specimen should include full thickness of the lesion and a small section of normal adjacent skin to aid the pathologist in diagnosis. Clinically suspicious lymph nodes should undergo fine-needle aspiration (FNA), as this has been shown to have a high sensitivity and specificity for detection of melanoma in large lymph nodes.136-139Melanoma is characterized according to the American Joint Committee on Cancer (AJCC) as localized disease (stage I and II), regional disease (stage III), or distant metastatic disease (stage IV). The Breslow tumor thickness replaced the Clark’s level as the most important prognostic indicator for melanoma stag-ing.132,140 The Breslow tumor thickness measures the depth of penetration of the lesions from the top of the granular layer of the epidermis into the dermal layer and is directly related to the risk of disease progression. Tumor ulceration, mitotic rate ≥1 per mm2, and metastasis are all also associated with worse prognosis. In the
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Surgery_Schwartz. skin grafting.Tissue specimen should include full thickness of the lesion and a small section of normal adjacent skin to aid the pathologist in diagnosis. Clinically suspicious lymph nodes should undergo fine-needle aspiration (FNA), as this has been shown to have a high sensitivity and specificity for detection of melanoma in large lymph nodes.136-139Melanoma is characterized according to the American Joint Committee on Cancer (AJCC) as localized disease (stage I and II), regional disease (stage III), or distant metastatic disease (stage IV). The Breslow tumor thickness replaced the Clark’s level as the most important prognostic indicator for melanoma stag-ing.132,140 The Breslow tumor thickness measures the depth of penetration of the lesions from the top of the granular layer of the epidermis into the dermal layer and is directly related to the risk of disease progression. Tumor ulceration, mitotic rate ≥1 per mm2, and metastasis are all also associated with worse prognosis. In the
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into the dermal layer and is directly related to the risk of disease progression. Tumor ulceration, mitotic rate ≥1 per mm2, and metastasis are all also associated with worse prognosis. In the presence of regional node metastasis, the num-ber of nodes affected is the most important prognostic indicator. For stage IV disease, the site of metastasis is strongly associated with prognosis, and elevated lactate dehydrogenase (LDH) is associated with a worse prognosis.141There is no supportive evidence for chest X-ray or com-puted tomography (CT) in the staging of patients unless there is positive regional lymph node disease, although it can be used to work up specific signs and symptoms when metastatic disease is suspected.136 In patients with stage III or greater disease, there is a high risk for distant metastasis, and imaging is recommended for baseline staging. These patients should receive additional imaging that includes CT of the chest, abdomen, and pelvis; whole-body positon
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Surgery_Schwartz. into the dermal layer and is directly related to the risk of disease progression. Tumor ulceration, mitotic rate ≥1 per mm2, and metastasis are all also associated with worse prognosis. In the presence of regional node metastasis, the num-ber of nodes affected is the most important prognostic indicator. For stage IV disease, the site of metastasis is strongly associated with prognosis, and elevated lactate dehydrogenase (LDH) is associated with a worse prognosis.141There is no supportive evidence for chest X-ray or com-puted tomography (CT) in the staging of patients unless there is positive regional lymph node disease, although it can be used to work up specific signs and symptoms when metastatic disease is suspected.136 In patients with stage III or greater disease, there is a high risk for distant metastasis, and imaging is recommended for baseline staging. These patients should receive additional imaging that includes CT of the chest, abdomen, and pelvis; whole-body positon
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Surgery_Schwartz_3605
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risk for distant metastasis, and imaging is recommended for baseline staging. These patients should receive additional imaging that includes CT of the chest, abdomen, and pelvis; whole-body positon emission tomography (PET)-CT; or brain magnetic resonance imaging (MRI).136The sentinel lymph node biopsy (SLNB) technique for melanoma was introduced in 1992 and has become a corner-stone in the management of melanoma, although its role in man-agement continues to be refined. SLNB is a standard staging procedure to evaluate the regional nodes for patients with clini-cally node-negative malignant melanoma. Detecting subclinical nodal metastasis in may benefit from lymphadenectomy or adju-vant therapy. This technique identifies the first draining lymph node from the primary lesion and has shown excellent accuracy and significantly less morbidity compared to complete resection of nodal basins. It is almost always performed at the time of initial wide excision, as SLN mapping after lymphatic
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Surgery_Schwartz. risk for distant metastasis, and imaging is recommended for baseline staging. These patients should receive additional imaging that includes CT of the chest, abdomen, and pelvis; whole-body positon emission tomography (PET)-CT; or brain magnetic resonance imaging (MRI).136The sentinel lymph node biopsy (SLNB) technique for melanoma was introduced in 1992 and has become a corner-stone in the management of melanoma, although its role in man-agement continues to be refined. SLNB is a standard staging procedure to evaluate the regional nodes for patients with clini-cally node-negative malignant melanoma. Detecting subclinical nodal metastasis in may benefit from lymphadenectomy or adju-vant therapy. This technique identifies the first draining lymph node from the primary lesion and has shown excellent accuracy and significantly less morbidity compared to complete resection of nodal basins. It is almost always performed at the time of initial wide excision, as SLN mapping after lymphatic
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excellent accuracy and significantly less morbidity compared to complete resection of nodal basins. It is almost always performed at the time of initial wide excision, as SLN mapping after lymphatic violation from surgical excision could decrease the accuracy of the test. Recently, the results of MSLT-1, an international, multicenter, phase III trial were published. This study randomized clinically node negative patients to either SLNB at the time of primary melanoma excision (and completion lymphadenectomy if posi-tive) or nodal basin monitoring (and delayed complete lymph-adenectomy for recurrent lymph node disease).142 The results of this study demonstrated that SLNB, with immediate lymphad-enectomy if positive, improved disease-free survival by 7% and 10% in patients with intermediate thickness (1.2–3.5 mm) and thick (>3.5 mm) lesions respectively. The use of SLNB in lesions <1.2 mm thick did not affect disease-free survival. SLNB should also be offered to thin lesions with
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Surgery_Schwartz. excellent accuracy and significantly less morbidity compared to complete resection of nodal basins. It is almost always performed at the time of initial wide excision, as SLN mapping after lymphatic violation from surgical excision could decrease the accuracy of the test. Recently, the results of MSLT-1, an international, multicenter, phase III trial were published. This study randomized clinically node negative patients to either SLNB at the time of primary melanoma excision (and completion lymphadenectomy if posi-tive) or nodal basin monitoring (and delayed complete lymph-adenectomy for recurrent lymph node disease).142 The results of this study demonstrated that SLNB, with immediate lymphad-enectomy if positive, improved disease-free survival by 7% and 10% in patients with intermediate thickness (1.2–3.5 mm) and thick (>3.5 mm) lesions respectively. The use of SLNB in lesions <1.2 mm thick did not affect disease-free survival. SLNB should also be offered to thin lesions with
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Surgery_Schwartz_3607
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thickness (1.2–3.5 mm) and thick (>3.5 mm) lesions respectively. The use of SLNB in lesions <1.2 mm thick did not affect disease-free survival. SLNB should also be offered to thin lesions with high-risk features (thickness >0.75, ulceration, mitoses ≥1 per mm2.136 The SLNB involves preoperative lymphoscintigraphy with intradermal injections of technetium-sulfur colloid to delineate lymphatic drainage and intraoperative intradermal injection of 1 mL of isosulfan or methylene blue dye near the tumor or biopsy site. (Figs. 16-13 and 16-14). The radioactive tracer-dye combination allows the sentinel node to be identified in 98% of cases. An incision over the lymph node basin of interest allows nodes to be excised and studied with hematoxylin and eosin and immunohistochemistry (S100, HMB45, and MART-1/Melan-A) staining (Fig. 16-15). 10Brunicardi_Ch16_p0511-p0540.indd 53119/02/19 3:09 PM 532SPECIFIC CONSIDERATIONSPART IIABSentinellymph nodeInjection siteSurgical exposure of sentinel
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Surgery_Schwartz. thickness (1.2–3.5 mm) and thick (>3.5 mm) lesions respectively. The use of SLNB in lesions <1.2 mm thick did not affect disease-free survival. SLNB should also be offered to thin lesions with high-risk features (thickness >0.75, ulceration, mitoses ≥1 per mm2.136 The SLNB involves preoperative lymphoscintigraphy with intradermal injections of technetium-sulfur colloid to delineate lymphatic drainage and intraoperative intradermal injection of 1 mL of isosulfan or methylene blue dye near the tumor or biopsy site. (Figs. 16-13 and 16-14). The radioactive tracer-dye combination allows the sentinel node to be identified in 98% of cases. An incision over the lymph node basin of interest allows nodes to be excised and studied with hematoxylin and eosin and immunohistochemistry (S100, HMB45, and MART-1/Melan-A) staining (Fig. 16-15). 10Brunicardi_Ch16_p0511-p0540.indd 53119/02/19 3:09 PM 532SPECIFIC CONSIDERATIONSPART IIABSentinellymph nodeInjection siteSurgical exposure of sentinel
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Surgery_Schwartz_3608
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and MART-1/Melan-A) staining (Fig. 16-15). 10Brunicardi_Ch16_p0511-p0540.indd 53119/02/19 3:09 PM 532SPECIFIC CONSIDERATIONSPART IIABSentinellymph nodeInjection siteSurgical exposure of sentinel lymph nodeAfferent lymphaticchannelsSentinellymph nodePrimary melanomaSentinellymphnodeInguinal nodesABCFLOWINJ SITEAxillaryNODEANTFLOWPOSTTymphoMelanoma Primary Injection SiteSubmanibular Lymph nodesPopliteal nodesFigure 16-13. After injection of radioactive technetium-99–labeled sulfur colloid tracer at the primary cutaneous melanoma site, sentinel lymph node basins are identified. A. Lymphoscintig-raphy of 67-year-old male with a malignant melanoma of the right heel; sentinel lymph nodes in both the right popliteal fossa and inguinal region. B. Lymphoscintigraphy of 52-year-old male with a malignant melanoma of the posterior right upper arm; sentinel lymph node in the right axillary region. C. Lymphoscintigraphy of 69-year-old male with a facial melanoma; sentinel lymph nodes in the
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Surgery_Schwartz. and MART-1/Melan-A) staining (Fig. 16-15). 10Brunicardi_Ch16_p0511-p0540.indd 53119/02/19 3:09 PM 532SPECIFIC CONSIDERATIONSPART IIABSentinellymph nodeInjection siteSurgical exposure of sentinel lymph nodeAfferent lymphaticchannelsSentinellymph nodePrimary melanomaSentinellymphnodeInguinal nodesABCFLOWINJ SITEAxillaryNODEANTFLOWPOSTTymphoMelanoma Primary Injection SiteSubmanibular Lymph nodesPopliteal nodesFigure 16-13. After injection of radioactive technetium-99–labeled sulfur colloid tracer at the primary cutaneous melanoma site, sentinel lymph node basins are identified. A. Lymphoscintig-raphy of 67-year-old male with a malignant melanoma of the right heel; sentinel lymph nodes in both the right popliteal fossa and inguinal region. B. Lymphoscintigraphy of 52-year-old male with a malignant melanoma of the posterior right upper arm; sentinel lymph node in the right axillary region. C. Lymphoscintigraphy of 69-year-old male with a facial melanoma; sentinel lymph nodes in the
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a malignant melanoma of the posterior right upper arm; sentinel lymph node in the right axillary region. C. Lymphoscintigraphy of 69-year-old male with a facial melanoma; sentinel lymph nodes in the submandibular region. ANT = anterior; INJ = injection; POST = posterior.Risks of this technique are uncommon but include skin necrosis near the site of injection, anaphylactic shock, lymphedema, sur-gical site infections, seromas, and hematomas.Surgical Management of the Primary Tumors and Lymph Nodes. The appropriate excision margin is based on primary tumor thickness. Several retrospective studies suggest that for melanoma in situ, 0.5 to 1 cm margins are sufficient.143-145 We believe that 1-cm margins should be obtained in anatomically fea-sible areas given the possibility of an incidental finding of a small invasive component in permanent sections. Several studies com-pared 1to 3-cm margins and 2to 5-cm margins in melanoma <2 mm thick, and 2to 4-cm margins in melanoma lesions 1 to
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Surgery_Schwartz. a malignant melanoma of the posterior right upper arm; sentinel lymph node in the right axillary region. C. Lymphoscintigraphy of 69-year-old male with a facial melanoma; sentinel lymph nodes in the submandibular region. ANT = anterior; INJ = injection; POST = posterior.Risks of this technique are uncommon but include skin necrosis near the site of injection, anaphylactic shock, lymphedema, sur-gical site infections, seromas, and hematomas.Surgical Management of the Primary Tumors and Lymph Nodes. The appropriate excision margin is based on primary tumor thickness. Several retrospective studies suggest that for melanoma in situ, 0.5 to 1 cm margins are sufficient.143-145 We believe that 1-cm margins should be obtained in anatomically fea-sible areas given the possibility of an incidental finding of a small invasive component in permanent sections. Several studies com-pared 1to 3-cm margins and 2to 5-cm margins in melanoma <2 mm thick, and 2to 4-cm margins in melanoma lesions 1 to
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Surgery_Schwartz_3610
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finding of a small invasive component in permanent sections. Several studies com-pared 1to 3-cm margins and 2to 5-cm margins in melanoma <2 mm thick, and 2to 4-cm margins in melanoma lesions 1 to 4 mm thick and found no difference. 146-149 A British trial suggested that there is a limit to how narrow margins can be for melanomas >2 mm thick by showing that 1-cm margins provide worse outcomes compared to 3-cm margins.150 Tumors <1 mm thick require 0.5 to 1 cm margins. Tumors 1 to 2 mm thick require 1 to 2 cm margins, and tumors >2 mm thick require 2-cm margins.Completion lymphadenectomy is commonly performed in cases of sentinel nodes with metastatic disease, but it has been shown that most of these nodal basins do not have addi-tional disease. Thus, many surgeons do not perform routine completion lymphadenectomy for positive nodes, and data from the MSLT-2 may provide guidance. It has been shown that those patients with nonsentinel lymph node positivity found on completion lymph
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Surgery_Schwartz. finding of a small invasive component in permanent sections. Several studies com-pared 1to 3-cm margins and 2to 5-cm margins in melanoma <2 mm thick, and 2to 4-cm margins in melanoma lesions 1 to 4 mm thick and found no difference. 146-149 A British trial suggested that there is a limit to how narrow margins can be for melanomas >2 mm thick by showing that 1-cm margins provide worse outcomes compared to 3-cm margins.150 Tumors <1 mm thick require 0.5 to 1 cm margins. Tumors 1 to 2 mm thick require 1 to 2 cm margins, and tumors >2 mm thick require 2-cm margins.Completion lymphadenectomy is commonly performed in cases of sentinel nodes with metastatic disease, but it has been shown that most of these nodal basins do not have addi-tional disease. Thus, many surgeons do not perform routine completion lymphadenectomy for positive nodes, and data from the MSLT-2 may provide guidance. It has been shown that those patients with nonsentinel lymph node positivity found on completion lymph
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Surgery_Schwartz_3611
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completion lymphadenectomy for positive nodes, and data from the MSLT-2 may provide guidance. It has been shown that those patients with nonsentinel lymph node positivity found on completion lymph node dissection after a positive SLN have higher rates of recurrence and lower rates of sur-vival. The therapeutic value, however, has not been clearly demonstrated. In patients with clinically positive lymph nodes but absent signs of distant metastasis on PET-CT, therapeu-tic lymph node dissection is associated with 5-year survival rates of 30% to 50%. In these cases, resection of the primary melanoma lesion and a completion lymphadenectomy should be performed.Individuals with face, anterior scalp, and ear prima-ries who have a positive SLNB should undergo a superficial parotidectomy in addition to a modified radical neck dissection. Figure 16-14. Technique of sentinel lymph node biopsy for cutaneous melanoma. A. After injection of radioactive technetium-99–labeled sulfur colloid tracer at
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Surgery_Schwartz. completion lymphadenectomy for positive nodes, and data from the MSLT-2 may provide guidance. It has been shown that those patients with nonsentinel lymph node positivity found on completion lymph node dissection after a positive SLN have higher rates of recurrence and lower rates of sur-vival. The therapeutic value, however, has not been clearly demonstrated. In patients with clinically positive lymph nodes but absent signs of distant metastasis on PET-CT, therapeu-tic lymph node dissection is associated with 5-year survival rates of 30% to 50%. In these cases, resection of the primary melanoma lesion and a completion lymphadenectomy should be performed.Individuals with face, anterior scalp, and ear prima-ries who have a positive SLNB should undergo a superficial parotidectomy in addition to a modified radical neck dissection. Figure 16-14. Technique of sentinel lymph node biopsy for cutaneous melanoma. A. After injection of radioactive technetium-99–labeled sulfur colloid tracer at
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to a modified radical neck dissection. Figure 16-14. Technique of sentinel lymph node biopsy for cutaneous melanoma. A. After injection of radioactive technetium-99–labeled sulfur colloid tracer at a lower abdominal wall primary cutaneous melanoma site, B. sentinel lymph node basins are identified. (Reproduced with permission from Gershenwald JE, Ross MI: Sentinel-lymph-node biopsy for cutane-ous melanoma, N Engl J Med. 2011 May 5;364(18):1738-1745.)Brunicardi_Ch16_p0511-p0540.indd 53219/02/19 3:09 PM 533THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16ABFigure 16-15. Operation of sentinel lymph node biopsy for cutaneous melanoma. After preoperative injection of radioactive technetium-99–labeled sulfur colloid tracer and intraoperative injection of Lymphazurin blue dye around the primary melanoma excision site, the nodal basin of interest is identified. An incision is made directly overlying the lymph node basin in the posterior axillary space. The sentinel lymph nodes are identified and
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Surgery_Schwartz. to a modified radical neck dissection. Figure 16-14. Technique of sentinel lymph node biopsy for cutaneous melanoma. A. After injection of radioactive technetium-99–labeled sulfur colloid tracer at a lower abdominal wall primary cutaneous melanoma site, B. sentinel lymph node basins are identified. (Reproduced with permission from Gershenwald JE, Ross MI: Sentinel-lymph-node biopsy for cutane-ous melanoma, N Engl J Med. 2011 May 5;364(18):1738-1745.)Brunicardi_Ch16_p0511-p0540.indd 53219/02/19 3:09 PM 533THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16ABFigure 16-15. Operation of sentinel lymph node biopsy for cutaneous melanoma. After preoperative injection of radioactive technetium-99–labeled sulfur colloid tracer and intraoperative injection of Lymphazurin blue dye around the primary melanoma excision site, the nodal basin of interest is identified. An incision is made directly overlying the lymph node basin in the posterior axillary space. The sentinel lymph nodes are identified and
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Surgery_Schwartz_3613
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excision site, the nodal basin of interest is identified. An incision is made directly overlying the lymph node basin in the posterior axillary space. The sentinel lymph nodes are identified and excised.Patients with positive sentinel nodes in the inguino-femoral nodal basin should undergo an inguino-femoral lymphadenec-tomy that includes removal of Cloquet’s node. If Cloquet’s node is positive or the patient has three or more nodes that contain melanoma metastases the probability of clinically occult posi-tive pelvic nodes is increased. The effect of ileo-obturator lymph node dissection on the survival of these patients is unknown.Surgery for Regional and Distant Metastasis. Nonmeta-static, in-transit disease should undergo excision to clear mar-gins when feasible. However, disease not amenable to complete excision derives benefit from isolated limb perfusion (ILP) and isolated limb infusion (ILI) (Fig. 16-16). These two modali-ties are used to treat regional disease, and their
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Surgery_Schwartz. excision site, the nodal basin of interest is identified. An incision is made directly overlying the lymph node basin in the posterior axillary space. The sentinel lymph nodes are identified and excised.Patients with positive sentinel nodes in the inguino-femoral nodal basin should undergo an inguino-femoral lymphadenec-tomy that includes removal of Cloquet’s node. If Cloquet’s node is positive or the patient has three or more nodes that contain melanoma metastases the probability of clinically occult posi-tive pelvic nodes is increased. The effect of ileo-obturator lymph node dissection on the survival of these patients is unknown.Surgery for Regional and Distant Metastasis. Nonmeta-static, in-transit disease should undergo excision to clear mar-gins when feasible. However, disease not amenable to complete excision derives benefit from isolated limb perfusion (ILP) and isolated limb infusion (ILI) (Fig. 16-16). These two modali-ties are used to treat regional disease, and their
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Surgery_Schwartz_3614
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not amenable to complete excision derives benefit from isolated limb perfusion (ILP) and isolated limb infusion (ILI) (Fig. 16-16). These two modali-ties are used to treat regional disease, and their purpose is to administer high doses of chemotherapy, commonly melphalan, to an affected limb while avoiding systemic drug toxicity. ILI was shown to provide a 31% response rate in one study, while hyperthermic ILP provided a 63% complete response rate in an independent study.151-154The most common sites of metastasis of melanoma are the lung and liver. These are followed by the brain, gastroin-testinal tract, distant skin, and subcutaneous tissue. A limited subset of patients with small-volume, limited distant metastases to the brain, gastrointestinal tract, or distant skin can be treated with surgical resection or directed radiation. Liver metastases are better dealt without surgical resection unless they arise from an ocular primary. Adjuvant therapy after resection of meta-static
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Surgery_Schwartz. not amenable to complete excision derives benefit from isolated limb perfusion (ILP) and isolated limb infusion (ILI) (Fig. 16-16). These two modali-ties are used to treat regional disease, and their purpose is to administer high doses of chemotherapy, commonly melphalan, to an affected limb while avoiding systemic drug toxicity. ILI was shown to provide a 31% response rate in one study, while hyperthermic ILP provided a 63% complete response rate in an independent study.151-154The most common sites of metastasis of melanoma are the lung and liver. These are followed by the brain, gastroin-testinal tract, distant skin, and subcutaneous tissue. A limited subset of patients with small-volume, limited distant metastases to the brain, gastrointestinal tract, or distant skin can be treated with surgical resection or directed radiation. Liver metastases are better dealt without surgical resection unless they arise from an ocular primary. Adjuvant therapy after resection of meta-static
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with surgical resection or directed radiation. Liver metastases are better dealt without surgical resection unless they arise from an ocular primary. Adjuvant therapy after resection of meta-static lesions is not standard of care. However, there are ongo-ing clinical trials addressing whether drugs and vaccines will be beneficial in this setting.115 Surgery may provide palliation for patients with gastrointestinal obstruction, gastrointestinal hem-orrhage, and nongastrointestinal hemorrhage. Radiotherapy for symptomatic bony or brain metastases provides palliation in dif-fuse disease.Adjuvant and Palliative Therapies. Eastern Cooperative Oncology Group (ECOG) Trials 1684, 1690, and 1694 were prospective randomized controlled trials that demonstrated Overhead heaterHot air blanketVenouscatheterArterialcatheterPneumatictourniquetPumpchamber25cc SyringeWarmingcoilEsmarchbandageDrug inpre-warmedsalineFigure 16-16. Isolated limb infusion. Schematic of isolated limb infusion of lower
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Surgery_Schwartz. with surgical resection or directed radiation. Liver metastases are better dealt without surgical resection unless they arise from an ocular primary. Adjuvant therapy after resection of meta-static lesions is not standard of care. However, there are ongo-ing clinical trials addressing whether drugs and vaccines will be beneficial in this setting.115 Surgery may provide palliation for patients with gastrointestinal obstruction, gastrointestinal hem-orrhage, and nongastrointestinal hemorrhage. Radiotherapy for symptomatic bony or brain metastases provides palliation in dif-fuse disease.Adjuvant and Palliative Therapies. Eastern Cooperative Oncology Group (ECOG) Trials 1684, 1690, and 1694 were prospective randomized controlled trials that demonstrated Overhead heaterHot air blanketVenouscatheterArterialcatheterPneumatictourniquetPumpchamber25cc SyringeWarmingcoilEsmarchbandageDrug inpre-warmedsalineFigure 16-16. Isolated limb infusion. Schematic of isolated limb infusion of lower
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SyringeWarmingcoilEsmarchbandageDrug inpre-warmedsalineFigure 16-16. Isolated limb infusion. Schematic of isolated limb infusion of lower extremity. (Adapted with permis-sion from Testori A, Verhoef C, Kroon HM, et al: Treatment of melanoma metas-tases in a limb by isolated limb perfusion and isolated limb infusion, J Surg Oncol. 2011 Sep;104(4):397-404.)Brunicardi_Ch16_p0511-p0540.indd 53319/02/19 3:09 PM 534SPECIFIC CONSIDERATIONSPART IIdisease-free survival advantages in patients with melanoma >4 mm in thickness with or without lymph node involvement if they received adjuvant treatment with high-dose interferon (IFN).155-157 A European Organization for Research and Treat-ment of Cancer (EORTC) trial also showed recurrence-free survival benefit with pegylated IFN.158 It is important to note that IFN therapy is not well tolerated and the pooled analysis of these trials did not show an improvement in overall survival benefit.Most patients with melanoma will not be surgical
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Surgery_Schwartz. SyringeWarmingcoilEsmarchbandageDrug inpre-warmedsalineFigure 16-16. Isolated limb infusion. Schematic of isolated limb infusion of lower extremity. (Adapted with permis-sion from Testori A, Verhoef C, Kroon HM, et al: Treatment of melanoma metas-tases in a limb by isolated limb perfusion and isolated limb infusion, J Surg Oncol. 2011 Sep;104(4):397-404.)Brunicardi_Ch16_p0511-p0540.indd 53319/02/19 3:09 PM 534SPECIFIC CONSIDERATIONSPART IIdisease-free survival advantages in patients with melanoma >4 mm in thickness with or without lymph node involvement if they received adjuvant treatment with high-dose interferon (IFN).155-157 A European Organization for Research and Treat-ment of Cancer (EORTC) trial also showed recurrence-free survival benefit with pegylated IFN.158 It is important to note that IFN therapy is not well tolerated and the pooled analysis of these trials did not show an improvement in overall survival benefit.Most patients with melanoma will not be surgical
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to note that IFN therapy is not well tolerated and the pooled analysis of these trials did not show an improvement in overall survival benefit.Most patients with melanoma will not be surgical candi-dates. Although medical options for melanoma have historically been poor, several recent studies have shown promise in drug therapy for metastatic melanoma. BRAF inhibitors (sorafenib), anti-PD1 antibodies, CTLA antibodies (ipilimumab), and high-dose interleukin-2 (IL-2) with and without vaccines have been shown in randomized studies to provide survival benefit in metastatic disease.159-165 Despite the excitement of recent drugs, surgery will likely play an adjunct role in treating individuals who develop resistance to these drugs over time.Special Circumstances. Special circumstances of note are melanoma in pregnant women, melanoma of unknown prima-ries, and noncutaneous melanomas. The prognosis of pregnant patients is similar to women who are not pregnant. Extrapo-lation of studies
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Surgery_Schwartz. to note that IFN therapy is not well tolerated and the pooled analysis of these trials did not show an improvement in overall survival benefit.Most patients with melanoma will not be surgical candi-dates. Although medical options for melanoma have historically been poor, several recent studies have shown promise in drug therapy for metastatic melanoma. BRAF inhibitors (sorafenib), anti-PD1 antibodies, CTLA antibodies (ipilimumab), and high-dose interleukin-2 (IL-2) with and without vaccines have been shown in randomized studies to provide survival benefit in metastatic disease.159-165 Despite the excitement of recent drugs, surgery will likely play an adjunct role in treating individuals who develop resistance to these drugs over time.Special Circumstances. Special circumstances of note are melanoma in pregnant women, melanoma of unknown prima-ries, and noncutaneous melanomas. The prognosis of pregnant patients is similar to women who are not pregnant. Extrapo-lation of studies
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Surgery_Schwartz_3618
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note are melanoma in pregnant women, melanoma of unknown prima-ries, and noncutaneous melanomas. The prognosis of pregnant patients is similar to women who are not pregnant. Extrapo-lation of studies examining the SLNB technique in pregnant women with breast cancer suggests lymphoscintigraphy may be done safely during pregnancy without risk to the fetus (blue dye is contraindicated). General anesthesia should be avoided during the first trimester, and local anesthetics should be used during this time. It has been suggested by some that after excising the primary tumor during pregnancy, the SLNB may be performed after delivery.Unknown primary melanoma occurs in 2% to 5% of cases and most commonly occurs in the lymph nodes. In these cases, a thorough search for the primary lesion should be sought, includ-ing eliciting a history about prior skin lesions, skin procedures (e.g., curettage and electrodessication, excision, laser), and review of any prior “benign” pathology. The surgeon
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Surgery_Schwartz. note are melanoma in pregnant women, melanoma of unknown prima-ries, and noncutaneous melanomas. The prognosis of pregnant patients is similar to women who are not pregnant. Extrapo-lation of studies examining the SLNB technique in pregnant women with breast cancer suggests lymphoscintigraphy may be done safely during pregnancy without risk to the fetus (blue dye is contraindicated). General anesthesia should be avoided during the first trimester, and local anesthetics should be used during this time. It has been suggested by some that after excising the primary tumor during pregnancy, the SLNB may be performed after delivery.Unknown primary melanoma occurs in 2% to 5% of cases and most commonly occurs in the lymph nodes. In these cases, a thorough search for the primary lesion should be sought, includ-ing eliciting a history about prior skin lesions, skin procedures (e.g., curettage and electrodessication, excision, laser), and review of any prior “benign” pathology. The surgeon
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Surgery_Schwartz_3619
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be sought, includ-ing eliciting a history about prior skin lesions, skin procedures (e.g., curettage and electrodessication, excision, laser), and review of any prior “benign” pathology. The surgeon should be aware that melanoma is known to spontaneously regress because of an immune response. Melanoma of unknown pri-mary has survival rates comparable to melanoma diagnosed with a known primary of the same stage.The most common noncutaneous disease site is ocular melanoma, and treatment of this condition includes photocoag-ulation, partial resection, radiation, or enucleation.166-168 Ocular melanomas exclusively metastasize to the liver and not regional lymph nodes, and some patients benefit from liver resection. Melanoma of the mucous membranes most commonly presents in the oral cavity, oropharynx, nasopharynx, paranasal sinus, anus, rectum, and female genitalia. Patients with this presenta-tion have a worse prognosis (10% 5-year survival) than patients with cutaneous melanomas.
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Surgery_Schwartz. be sought, includ-ing eliciting a history about prior skin lesions, skin procedures (e.g., curettage and electrodessication, excision, laser), and review of any prior “benign” pathology. The surgeon should be aware that melanoma is known to spontaneously regress because of an immune response. Melanoma of unknown pri-mary has survival rates comparable to melanoma diagnosed with a known primary of the same stage.The most common noncutaneous disease site is ocular melanoma, and treatment of this condition includes photocoag-ulation, partial resection, radiation, or enucleation.166-168 Ocular melanomas exclusively metastasize to the liver and not regional lymph nodes, and some patients benefit from liver resection. Melanoma of the mucous membranes most commonly presents in the oral cavity, oropharynx, nasopharynx, paranasal sinus, anus, rectum, and female genitalia. Patients with this presenta-tion have a worse prognosis (10% 5-year survival) than patients with cutaneous melanomas.
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oropharynx, nasopharynx, paranasal sinus, anus, rectum, and female genitalia. Patients with this presenta-tion have a worse prognosis (10% 5-year survival) than patients with cutaneous melanomas. Management should be excision to negative margins, and radical resections should be avoided because the role of surgery is locoregional control, not cure. Generally speaking, lymph node dissection should be avoided because the benefit is unclear.Merkel Cell CarcinomaMerkel cell carcinoma (MCC) is an aggressive neuroendocrine tumor of the skin whose incidence has been rapidly increas-ing. Although it is a much rarer malignancy than melanoma, the prognosis is much worse, with a 5-year survival of 46%.169 Merkel cells are epidermal appendages involved in the sensation Figure 16-17. Merkel cell carcinoma seen just above the left knee in a 44-year-old female.of light touch, and along with Merkel cell carcinoma, are cyto-keratin-20 positive. This stain is now used to confirm the diag-nosis. Other
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Surgery_Schwartz. oropharynx, nasopharynx, paranasal sinus, anus, rectum, and female genitalia. Patients with this presenta-tion have a worse prognosis (10% 5-year survival) than patients with cutaneous melanomas. Management should be excision to negative margins, and radical resections should be avoided because the role of surgery is locoregional control, not cure. Generally speaking, lymph node dissection should be avoided because the benefit is unclear.Merkel Cell CarcinomaMerkel cell carcinoma (MCC) is an aggressive neuroendocrine tumor of the skin whose incidence has been rapidly increas-ing. Although it is a much rarer malignancy than melanoma, the prognosis is much worse, with a 5-year survival of 46%.169 Merkel cells are epidermal appendages involved in the sensation Figure 16-17. Merkel cell carcinoma seen just above the left knee in a 44-year-old female.of light touch, and along with Merkel cell carcinoma, are cyto-keratin-20 positive. This stain is now used to confirm the diag-nosis. Other
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seen just above the left knee in a 44-year-old female.of light touch, and along with Merkel cell carcinoma, are cyto-keratin-20 positive. This stain is now used to confirm the diag-nosis. Other risk factors include age >65 years (the median age of diagnosis is 70 years), UV exposure, Merkel cell polyoma virus, and immunosuppression. MCC typically presents as a rapidly growing, flesh-colored to red or purple papule or plaque (Fig. 16-17). Regional nodes are involved in 30% of patients at diagnosis, and 50% will develop systemic disease (skin, lymph nodes, liver, lung, bone, and brain).170,171 There are no standard-ized diagnostic imaging studies for staging, but CT of the chest, abdomen, pelvis and octreotide scans may provide useful infor-mation when clinically indicated.After a thorough skin examination, treatment should begin by evaluating nodal basins. Patients without clinical nodal dis-ease should undergo an SLNB prior to wide local excision because studies suggest a benefit.172
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Surgery_Schwartz. seen just above the left knee in a 44-year-old female.of light touch, and along with Merkel cell carcinoma, are cyto-keratin-20 positive. This stain is now used to confirm the diag-nosis. Other risk factors include age >65 years (the median age of diagnosis is 70 years), UV exposure, Merkel cell polyoma virus, and immunosuppression. MCC typically presents as a rapidly growing, flesh-colored to red or purple papule or plaque (Fig. 16-17). Regional nodes are involved in 30% of patients at diagnosis, and 50% will develop systemic disease (skin, lymph nodes, liver, lung, bone, and brain).170,171 There are no standard-ized diagnostic imaging studies for staging, but CT of the chest, abdomen, pelvis and octreotide scans may provide useful infor-mation when clinically indicated.After a thorough skin examination, treatment should begin by evaluating nodal basins. Patients without clinical nodal dis-ease should undergo an SLNB prior to wide local excision because studies suggest a benefit.172
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skin examination, treatment should begin by evaluating nodal basins. Patients without clinical nodal dis-ease should undergo an SLNB prior to wide local excision because studies suggest a benefit.172 In patients with sentinel lymph nodes with metastatic disease, completion lymphad-enectomy and/or radiation therapy may follow, and in patients with node-negative disease, observation or radiation therapy should be considered.172 SLNB is important for staging and treatment, and the literature suggests that it predicts recurrenceand relapse-free survival. Elective lymph node dissection may decrease regional nodal recurrence and in-transit metastases. Patients with clinically positive nodes should have an FNA to confirm disease. If positive, a metastatic staging workup should follow, and, if negative, treatment of the primary and nodal basin as managed for sentinel lymph node-positive disease should be considered. A negative FNA and open biopsy-negative disease should be managed by
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Surgery_Schwartz. skin examination, treatment should begin by evaluating nodal basins. Patients without clinical nodal dis-ease should undergo an SLNB prior to wide local excision because studies suggest a benefit.172 In patients with sentinel lymph nodes with metastatic disease, completion lymphad-enectomy and/or radiation therapy may follow, and in patients with node-negative disease, observation or radiation therapy should be considered.172 SLNB is important for staging and treatment, and the literature suggests that it predicts recurrenceand relapse-free survival. Elective lymph node dissection may decrease regional nodal recurrence and in-transit metastases. Patients with clinically positive nodes should have an FNA to confirm disease. If positive, a metastatic staging workup should follow, and, if negative, treatment of the primary and nodal basin as managed for sentinel lymph node-positive disease should be considered. A negative FNA and open biopsy-negative disease should be managed by
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if negative, treatment of the primary and nodal basin as managed for sentinel lymph node-positive disease should be considered. A negative FNA and open biopsy-negative disease should be managed by treatment of the primary disease alone. Brunicardi_Ch16_p0511-p0540.indd 53419/02/19 3:09 PM 535THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16Patients with metastatic disease should be managed according to consensus from a multidisciplinary tumor board.Important surgical principles for excision of the primary lesion are to excise with wide margins down to fascia and com-plete circumferential and peripheral deep-margin assessment. Recommended management for margins is 1 to 3 cm, but there are no randomized trials defining these margins. Chemotherapy and adjuvant radiation are commonly used, but there are no data to support a specific regimen or that demonstrate a definitive survival benefit.Recurrence of MCC is common. One study of 95 patients showed a 47% recurrence, with 80% of recurrences
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Surgery_Schwartz. if negative, treatment of the primary and nodal basin as managed for sentinel lymph node-positive disease should be considered. A negative FNA and open biopsy-negative disease should be managed by treatment of the primary disease alone. Brunicardi_Ch16_p0511-p0540.indd 53419/02/19 3:09 PM 535THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16Patients with metastatic disease should be managed according to consensus from a multidisciplinary tumor board.Important surgical principles for excision of the primary lesion are to excise with wide margins down to fascia and com-plete circumferential and peripheral deep-margin assessment. Recommended management for margins is 1 to 3 cm, but there are no randomized trials defining these margins. Chemotherapy and adjuvant radiation are commonly used, but there are no data to support a specific regimen or that demonstrate a definitive survival benefit.Recurrence of MCC is common. One study of 95 patients showed a 47% recurrence, with 80% of recurrences
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are no data to support a specific regimen or that demonstrate a definitive survival benefit.Recurrence of MCC is common. One study of 95 patients showed a 47% recurrence, with 80% of recurrences occurring within 2 years and 96% occurring within 5 years.173,174 Regional lymph node disease is common, and 70% of patients will have nodal spread within 2 years of disease presentation. Five-year overall survival of head and neck disease in surgically treated patients is between 40% and 68%.Kaposi’s SarcomaKaposi’s sarcoma is characterized by the proliferation and inflammation of endothelial-derived spindle cell lesions. There are five major forms of this angioproliferative disorder: classic (Mediterranean), African endemic, HIV-negative men having sex with men (MSM)-associated, and immunosuppression-associated. They are all driven by the human herpesvirus (HHV-8).175 Kaposi’s sarcoma is diagnosed after the fifth decade of life and predominantly found on the skin but can occur anywhere in
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Surgery_Schwartz. are no data to support a specific regimen or that demonstrate a definitive survival benefit.Recurrence of MCC is common. One study of 95 patients showed a 47% recurrence, with 80% of recurrences occurring within 2 years and 96% occurring within 5 years.173,174 Regional lymph node disease is common, and 70% of patients will have nodal spread within 2 years of disease presentation. Five-year overall survival of head and neck disease in surgically treated patients is between 40% and 68%.Kaposi’s SarcomaKaposi’s sarcoma is characterized by the proliferation and inflammation of endothelial-derived spindle cell lesions. There are five major forms of this angioproliferative disorder: classic (Mediterranean), African endemic, HIV-negative men having sex with men (MSM)-associated, and immunosuppression-associated. They are all driven by the human herpesvirus (HHV-8).175 Kaposi’s sarcoma is diagnosed after the fifth decade of life and predominantly found on the skin but can occur anywhere in
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They are all driven by the human herpesvirus (HHV-8).175 Kaposi’s sarcoma is diagnosed after the fifth decade of life and predominantly found on the skin but can occur anywhere in the body. In North America, the Kaposi’s sarcoma herpes virus is transmitted via sexual and nonsexual routes and predominantly affects individuals with compromised immune systems such as those with HIV and transplant recipients on immune-suppressing medications. Clinically, Kaposi’s sarcoma appears as multifocal, rubbery blue-red nodules. Treatment of AIDS-associated Kaposi’s sarcoma is with antiviral therapy, and many patients experience a dramatic treatment response.176,177 Those individuals who do not respond and have limited muco-cutaneous disease may benefit from cryotherapy, photodynamic therapy, radiation therapy, intralesional injections, and topical therapy. Surgical biopsy is important for disease diagnosis, but given the high local recurrence and the fact that Kaposi’s sar-coma represents more
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Surgery_Schwartz. They are all driven by the human herpesvirus (HHV-8).175 Kaposi’s sarcoma is diagnosed after the fifth decade of life and predominantly found on the skin but can occur anywhere in the body. In North America, the Kaposi’s sarcoma herpes virus is transmitted via sexual and nonsexual routes and predominantly affects individuals with compromised immune systems such as those with HIV and transplant recipients on immune-suppressing medications. Clinically, Kaposi’s sarcoma appears as multifocal, rubbery blue-red nodules. Treatment of AIDS-associated Kaposi’s sarcoma is with antiviral therapy, and many patients experience a dramatic treatment response.176,177 Those individuals who do not respond and have limited muco-cutaneous disease may benefit from cryotherapy, photodynamic therapy, radiation therapy, intralesional injections, and topical therapy. Surgical biopsy is important for disease diagnosis, but given the high local recurrence and the fact that Kaposi’s sar-coma represents more
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therapy, intralesional injections, and topical therapy. Surgical biopsy is important for disease diagnosis, but given the high local recurrence and the fact that Kaposi’s sar-coma represents more of a systemic rather than local disease, the benefit of surgery is limited and generally should not be pursued except for palliation.Dermatofibrosarcoma ProtuberansThis rare, low-grade sarcoma of fibroblast origin commonly afflicts individuals during their third decade of life. It has low distant metastatic potential, but it behaves aggressively locally with finger-like extensions. Tumor depth is the most important prognostic variable. Presentation is characteristically a slow-growing, asymptomatic, violaceous plaque involving the trunk, head, neck, or extremities (Fig. 16-18). Nearly all cases are posi-tive for CD34 and negative for factor XIIIa.178,179 Treatment is wide local excision with 3-cm margins down to deep underly-ing fascia or Mohs microsurgery in cosmetically sensitive areas
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Surgery_Schwartz. therapy, intralesional injections, and topical therapy. Surgical biopsy is important for disease diagnosis, but given the high local recurrence and the fact that Kaposi’s sar-coma represents more of a systemic rather than local disease, the benefit of surgery is limited and generally should not be pursued except for palliation.Dermatofibrosarcoma ProtuberansThis rare, low-grade sarcoma of fibroblast origin commonly afflicts individuals during their third decade of life. It has low distant metastatic potential, but it behaves aggressively locally with finger-like extensions. Tumor depth is the most important prognostic variable. Presentation is characteristically a slow-growing, asymptomatic, violaceous plaque involving the trunk, head, neck, or extremities (Fig. 16-18). Nearly all cases are posi-tive for CD34 and negative for factor XIIIa.178,179 Treatment is wide local excision with 3-cm margins down to deep underly-ing fascia or Mohs microsurgery in cosmetically sensitive areas
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are posi-tive for CD34 and negative for factor XIIIa.178,179 Treatment is wide local excision with 3-cm margins down to deep underly-ing fascia or Mohs microsurgery in cosmetically sensitive areas where maximum tissue preservation will benefit.180 No nodal dissection is needed, and both approaches provide similar local control.181 Some clinicians have used radiation therapy and bio-logic agents (imatinib) as adjuvant therapy with some success in patients with advanced disease. Local recurrence occurs in 50% to 75% of cases, usually within 3 years of treatment. Thus, clini-cal follow-up is important. Recurrent tumors should be resected whenever possible.Figure 16-18. Dermatofibrosarcoma protuberans of the left flank.Malignant Fibrous Histiocytoma (Undifferentiated Pleomorphic Sarcoma and Myxofibrosarcoma)This uncommon, cutaneous, spindle-cell, soft tissue sarcoma occurs in the extremities, head, and neck of elderly patients. They present as solitary, soft to firm, skin-colored
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Surgery_Schwartz. are posi-tive for CD34 and negative for factor XIIIa.178,179 Treatment is wide local excision with 3-cm margins down to deep underly-ing fascia or Mohs microsurgery in cosmetically sensitive areas where maximum tissue preservation will benefit.180 No nodal dissection is needed, and both approaches provide similar local control.181 Some clinicians have used radiation therapy and bio-logic agents (imatinib) as adjuvant therapy with some success in patients with advanced disease. Local recurrence occurs in 50% to 75% of cases, usually within 3 years of treatment. Thus, clini-cal follow-up is important. Recurrent tumors should be resected whenever possible.Figure 16-18. Dermatofibrosarcoma protuberans of the left flank.Malignant Fibrous Histiocytoma (Undifferentiated Pleomorphic Sarcoma and Myxofibrosarcoma)This uncommon, cutaneous, spindle-cell, soft tissue sarcoma occurs in the extremities, head, and neck of elderly patients. They present as solitary, soft to firm, skin-colored
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and Myxofibrosarcoma)This uncommon, cutaneous, spindle-cell, soft tissue sarcoma occurs in the extremities, head, and neck of elderly patients. They present as solitary, soft to firm, skin-colored subcutane-ous nodules. Complete surgical resection is the treatment of choice, and adjuvant radiation therapy provides local control; patients with positive margins benefit most from this combina-tion. Nevertheless, patients undergoing complete gross resection will experience recurrence in 30% to 35% of cases.135 Up to 50% of patients may present with distant metastasis, and this is a contraindication to surgical resection.AngiosarcomaAngiosarcoma is an uncommon, aggressive cancer that arises from vascular endothelial cells and occurs in four variants, all of which have a poor prognosis.182 The 5-year survival estimate is 15%.183 The head and neck variant presents in individuals older than 40 years as an ill-defined red patch on the face or scalp, often with satellite lesions and distant
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Surgery_Schwartz. and Myxofibrosarcoma)This uncommon, cutaneous, spindle-cell, soft tissue sarcoma occurs in the extremities, head, and neck of elderly patients. They present as solitary, soft to firm, skin-colored subcutane-ous nodules. Complete surgical resection is the treatment of choice, and adjuvant radiation therapy provides local control; patients with positive margins benefit most from this combina-tion. Nevertheless, patients undergoing complete gross resection will experience recurrence in 30% to 35% of cases.135 Up to 50% of patients may present with distant metastasis, and this is a contraindication to surgical resection.AngiosarcomaAngiosarcoma is an uncommon, aggressive cancer that arises from vascular endothelial cells and occurs in four variants, all of which have a poor prognosis.182 The 5-year survival estimate is 15%.183 The head and neck variant presents in individuals older than 40 years as an ill-defined red patch on the face or scalp, often with satellite lesions and distant
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5-year survival estimate is 15%.183 The head and neck variant presents in individuals older than 40 years as an ill-defined red patch on the face or scalp, often with satellite lesions and distant metastasis, and has a median survival of 18 to 28 months. Lymphedema-associated angiosarcoma (Stewart-Treves) develops on an extremity ipsi-lateral to an axillary lymphadenectomy. It appears on the upper, medial arm as a violaceous plaque in an individual with nonpit-ting edema and has a poor survival. Radiation-induced angio-sarcoma occurs 4 to 25 years after radiation therapy for benign and malignant conditions. Finally, the epithelioid variant of angiosarcoma involves the lower extremities and also has a poor prognosis. Surgical excision with wide margins is the treatment Brunicardi_Ch16_p0511-p0540.indd 53519/02/19 3:09 PM 536SPECIFIC CONSIDERATIONSPART IIof choice for localized disease, but the rate of recurrence is high. Adjuvant radiation therapy can be considered in a
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Surgery_Schwartz. 5-year survival estimate is 15%.183 The head and neck variant presents in individuals older than 40 years as an ill-defined red patch on the face or scalp, often with satellite lesions and distant metastasis, and has a median survival of 18 to 28 months. Lymphedema-associated angiosarcoma (Stewart-Treves) develops on an extremity ipsi-lateral to an axillary lymphadenectomy. It appears on the upper, medial arm as a violaceous plaque in an individual with nonpit-ting edema and has a poor survival. Radiation-induced angio-sarcoma occurs 4 to 25 years after radiation therapy for benign and malignant conditions. Finally, the epithelioid variant of angiosarcoma involves the lower extremities and also has a poor prognosis. Surgical excision with wide margins is the treatment Brunicardi_Ch16_p0511-p0540.indd 53519/02/19 3:09 PM 536SPECIFIC CONSIDERATIONSPART IIof choice for localized disease, but the rate of recurrence is high. Adjuvant radiation therapy can be considered in a
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53519/02/19 3:09 PM 536SPECIFIC CONSIDERATIONSPART IIof choice for localized disease, but the rate of recurrence is high. Adjuvant radiation therapy can be considered in a multidisci-plinary fashion. Cases of extremity disease can be considered for amputation. For widely metastatic disease, chemotherapy and radiation may provide palliation, but these modalities do not prolong overall survival.115Extramammary Paget’s DiseaseThis rare adenocarcinoma of apocrine glands arises in axillary, perianal, and genital regions of men and women.184 Clinical pre-sentation is that of erythematous or nonpigmented plaques with an eczema-like appearance that often persist after failed treat-ment from other therapies. An important characteristic and one that the surgeon must be acutely aware of is the high incidence of concomitant other malignancies with this cutaneous disease. Forty percent of cases are associated with primary gastrointesti-nal and genitourinary malignancies, and a diligent search
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Surgery_Schwartz. 53519/02/19 3:09 PM 536SPECIFIC CONSIDERATIONSPART IIof choice for localized disease, but the rate of recurrence is high. Adjuvant radiation therapy can be considered in a multidisci-plinary fashion. Cases of extremity disease can be considered for amputation. For widely metastatic disease, chemotherapy and radiation may provide palliation, but these modalities do not prolong overall survival.115Extramammary Paget’s DiseaseThis rare adenocarcinoma of apocrine glands arises in axillary, perianal, and genital regions of men and women.184 Clinical pre-sentation is that of erythematous or nonpigmented plaques with an eczema-like appearance that often persist after failed treat-ment from other therapies. An important characteristic and one that the surgeon must be acutely aware of is the high incidence of concomitant other malignancies with this cutaneous disease. Forty percent of cases are associated with primary gastrointesti-nal and genitourinary malignancies, and a diligent search
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incidence of concomitant other malignancies with this cutaneous disease. Forty percent of cases are associated with primary gastrointesti-nal and genitourinary malignancies, and a diligent search should be made after a diagnosis of extramammary Paget’s disease is made. Treatment is surgical resection with negative microscopic margins, and adjuvant radiation may provide additional locore-gional control.CONCLUSIONThe skin is the largest organ in the human body and is com-posed of three organized layers that are the source of numer-ous pathologies. Recognition and management of cutaneous and subcutaneous diseases require an astute clinician to opti-mize clinical outcomes. Improvements in drugs, therapies, and healthcare practices have helped recovery from skin injuries. Skin and subcutaneous diseases are often managed medically, although surgery frequently complements treatment. Benign tumors are surgical diseases, while malignant tumors are pri-marily treated surgically, and additional
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Surgery_Schwartz. incidence of concomitant other malignancies with this cutaneous disease. Forty percent of cases are associated with primary gastrointesti-nal and genitourinary malignancies, and a diligent search should be made after a diagnosis of extramammary Paget’s disease is made. Treatment is surgical resection with negative microscopic margins, and adjuvant radiation may provide additional locore-gional control.CONCLUSIONThe skin is the largest organ in the human body and is com-posed of three organized layers that are the source of numer-ous pathologies. Recognition and management of cutaneous and subcutaneous diseases require an astute clinician to opti-mize clinical outcomes. Improvements in drugs, therapies, and healthcare practices have helped recovery from skin injuries. Skin and subcutaneous diseases are often managed medically, although surgery frequently complements treatment. Benign tumors are surgical diseases, while malignant tumors are pri-marily treated surgically, and additional
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diseases are often managed medically, although surgery frequently complements treatment. Benign tumors are surgical diseases, while malignant tumors are pri-marily treated surgically, and additional modalities including chemotherapy and radiation therapy are sometimes required. The management of melanoma is at an exciting phase, requiring the coordinated multidisciplinary care of medical oncologists, surgical oncologists, radiation oncologists, der-matopathologists, and plastic and reconstructive surgeons. The advent of new drug therapies will redefine the role of surgery in this disease in the coming years.REFERENCESEntries highlighted in bright blue are key references. 1. Kanitakis J. Anatomy, histology and immunohistochemistry of normal human skin. Eur J Dermatology. 2002;12(4):390-401. 2. Chug D, Hake A, Holbrook K. The structure and development of skin. In: Freedberg I, Eisen A, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill;
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Surgery_Schwartz. diseases are often managed medically, although surgery frequently complements treatment. Benign tumors are surgical diseases, while malignant tumors are pri-marily treated surgically, and additional modalities including chemotherapy and radiation therapy are sometimes required. The management of melanoma is at an exciting phase, requiring the coordinated multidisciplinary care of medical oncologists, surgical oncologists, radiation oncologists, der-matopathologists, and plastic and reconstructive surgeons. The advent of new drug therapies will redefine the role of surgery in this disease in the coming years.REFERENCESEntries highlighted in bright blue are key references. 1. Kanitakis J. Anatomy, histology and immunohistochemistry of normal human skin. Eur J Dermatology. 2002;12(4):390-401. 2. Chug D, Hake A, Holbrook K. The structure and development of skin. In: Freedberg I, Eisen A, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill;
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D, Hake A, Holbrook K. The structure and development of skin. In: Freedberg I, Eisen A, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; 2003:47-88. 3. Michael Weitz, Brian Kearns, eds. Skin. In: Junqueira’s Basic Histology. 14th ed. New York: McGraw-Hill Education; 2016. 4. Segre JA. Epidermal barrier formation and recovery in skin disorders. J Clin Invest. 2006;116(5):1150-1158. 5. Elias PM. Stratum corneum defensive functions: an integrated view. J Invest Dermatol. 2005;125(2):183-200. 6. Girolomoni G, Caux C, Dezutter-Dambuyant C, Dezutter-Dambuyant C, Ricciardi-Castagnoli P. Langerhans cells: still a fundamental paradigm for studying the immunobiology of dendritic cells. Trends Immunol. 2002;23(1):6-8. 7. Mutyambizi K, Berger CL, Edelson RL. The balance between immunity and tolerance: the role of Langerhans cells. Cell Mol Life Sci. 2009;66(5):831-840. 8. Lori F, Kelly LM, Lisziewicz J. APC-targeted immuniza-tion for the treatment of
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Surgery_Schwartz. D, Hake A, Holbrook K. The structure and development of skin. In: Freedberg I, Eisen A, Wolff K, eds. Fitzpatrick’s Dermatology in General Medicine. 6th ed. New York: McGraw-Hill; 2003:47-88. 3. Michael Weitz, Brian Kearns, eds. Skin. In: Junqueira’s Basic Histology. 14th ed. New York: McGraw-Hill Education; 2016. 4. Segre JA. Epidermal barrier formation and recovery in skin disorders. J Clin Invest. 2006;116(5):1150-1158. 5. Elias PM. Stratum corneum defensive functions: an integrated view. J Invest Dermatol. 2005;125(2):183-200. 6. Girolomoni G, Caux C, Dezutter-Dambuyant C, Dezutter-Dambuyant C, Ricciardi-Castagnoli P. Langerhans cells: still a fundamental paradigm for studying the immunobiology of dendritic cells. Trends Immunol. 2002;23(1):6-8. 7. Mutyambizi K, Berger CL, Edelson RL. The balance between immunity and tolerance: the role of Langerhans cells. Cell Mol Life Sci. 2009;66(5):831-840. 8. Lori F, Kelly LM, Lisziewicz J. APC-targeted immuniza-tion for the treatment of
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RL. The balance between immunity and tolerance: the role of Langerhans cells. Cell Mol Life Sci. 2009;66(5):831-840. 8. Lori F, Kelly LM, Lisziewicz J. APC-targeted immuniza-tion for the treatment of HIV-1. Expert Rev Vaccines. 2004;3 (4 suppl):S189-S198. 9. Yu SH, Bordeaux JS, Baron ED. The immune system and skin cancer. Adv Exp Med Biol. 2014;810:182-191. 10. Lens MB, Dawes M. Global perspectives of contemporary epi-demiological trends of cutaneous malignant melanoma. Br J Dermatol. 2004;150(2):179-185. 11. Lock-Andersen J, Drzewiecki KT, Wulf HC. Eye and hair colour, skin type and constitutive skin pigmentation as risk factors for basal cell carcinoma and cutaneous malignant melanoma. A Danish case-control study. Acta Derm Venereol. 1999;79(1):74-80. 12. Tachibana T. The Merkel cell: recent findings and unresolved problems. Arch Histol Cytol. 1995;58(4):379-396. 13. Munde PB, Khandekar SP, Dive AM, Aparna Sharmal. Pathophysiology of merkel cell. J Oral Maxillofac Pathol.
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Surgery_Schwartz. RL. The balance between immunity and tolerance: the role of Langerhans cells. Cell Mol Life Sci. 2009;66(5):831-840. 8. Lori F, Kelly LM, Lisziewicz J. APC-targeted immuniza-tion for the treatment of HIV-1. Expert Rev Vaccines. 2004;3 (4 suppl):S189-S198. 9. Yu SH, Bordeaux JS, Baron ED. The immune system and skin cancer. Adv Exp Med Biol. 2014;810:182-191. 10. Lens MB, Dawes M. Global perspectives of contemporary epi-demiological trends of cutaneous malignant melanoma. Br J Dermatol. 2004;150(2):179-185. 11. Lock-Andersen J, Drzewiecki KT, Wulf HC. Eye and hair colour, skin type and constitutive skin pigmentation as risk factors for basal cell carcinoma and cutaneous malignant melanoma. A Danish case-control study. Acta Derm Venereol. 1999;79(1):74-80. 12. Tachibana T. The Merkel cell: recent findings and unresolved problems. Arch Histol Cytol. 1995;58(4):379-396. 13. Munde PB, Khandekar SP, Dive AM, Aparna Sharmal. Pathophysiology of merkel cell. J Oral Maxillofac Pathol.
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cell: recent findings and unresolved problems. Arch Histol Cytol. 1995;58(4):379-396. 13. Munde PB, Khandekar SP, Dive AM, Aparna Sharmal. Pathophysiology of merkel cell. J Oral Maxillofac Pathol. 2013;17(3):408-412. 14. Ogawa H. The Merkel cell as a possible mechanoreceptor cell. Prog Neurobiol. 1996;49(4):317-334. 15. Bos JD, Zonneveld I, Das PK, Krieg SR, van der Loos CM, Kapsenberg ML. The skin immune system (SIS): distribution and immunophenotype of lymphocyte subpopulations in nor-mal human skin. J Invest Dermatol. 1987;88(5):569-573. 16. Spetz AL, Strominger J, Groh-Spies V. T cell subsets in normal human epidermis. Am J Pathol. 1996;149(2):665-674. 17. Toker C. Clear cells of the nipple epidermis. Cancer. 1970;25(3):601-610. 18. Garijo MF, Val D, Val-Bernal JF. An overview of the pale and clear cells of the nipple epidermis. Histol Histopathol. 2009;24(3):367-376. 19. Dillon DA, Lester SC. Lesions of the nipple. Surg Pathol Clin. 2009;2(2):391-412. 20. Lundquist K, Kohler S,
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Surgery_Schwartz. cell: recent findings and unresolved problems. Arch Histol Cytol. 1995;58(4):379-396. 13. Munde PB, Khandekar SP, Dive AM, Aparna Sharmal. Pathophysiology of merkel cell. J Oral Maxillofac Pathol. 2013;17(3):408-412. 14. Ogawa H. The Merkel cell as a possible mechanoreceptor cell. Prog Neurobiol. 1996;49(4):317-334. 15. Bos JD, Zonneveld I, Das PK, Krieg SR, van der Loos CM, Kapsenberg ML. The skin immune system (SIS): distribution and immunophenotype of lymphocyte subpopulations in nor-mal human skin. J Invest Dermatol. 1987;88(5):569-573. 16. Spetz AL, Strominger J, Groh-Spies V. T cell subsets in normal human epidermis. Am J Pathol. 1996;149(2):665-674. 17. Toker C. Clear cells of the nipple epidermis. Cancer. 1970;25(3):601-610. 18. Garijo MF, Val D, Val-Bernal JF. An overview of the pale and clear cells of the nipple epidermis. Histol Histopathol. 2009;24(3):367-376. 19. Dillon DA, Lester SC. Lesions of the nipple. Surg Pathol Clin. 2009;2(2):391-412. 20. Lundquist K, Kohler S,
|
Surgery_Schwartz_3636
|
Surgery_Schwartz
|
pale and clear cells of the nipple epidermis. Histol Histopathol. 2009;24(3):367-376. 19. Dillon DA, Lester SC. Lesions of the nipple. Surg Pathol Clin. 2009;2(2):391-412. 20. Lundquist K, Kohler S, Rouse R V. Intraepidermal cytoker-atin 7 expression is not restricted to Paget cells but is also seen in Toker cells and Merkel cells. Am J Surg Pathol. 1999;23(2):212-219. 21. Sato K, Leidal R, Sato F. Morphology and development of an apoeccrine sweat gland in human axillae. Am J Physiol. 1987;252(1 Pt 2):R166-80. 22. Burgeson RE, Nimni ME. Collagen types. Molecular structure and tissue distribution. Clin Orthop Relat Res. 1992;(282):250-272. 23. Eyden B. The myofibroblast: an assessment of controversial issues and a definition useful in diagnosis and research. Ultra-struct Pathol. 25(1):39-50. 24. Braverman IM. The cutaneous microcirculation. J Investig Dermatology Symp Proc. 2000;5:3-9. 25. Johansson O. The innervation of the human epidermis. J Neurol Sci. 1995;130(2):228. 26. Avram
|
Surgery_Schwartz. pale and clear cells of the nipple epidermis. Histol Histopathol. 2009;24(3):367-376. 19. Dillon DA, Lester SC. Lesions of the nipple. Surg Pathol Clin. 2009;2(2):391-412. 20. Lundquist K, Kohler S, Rouse R V. Intraepidermal cytoker-atin 7 expression is not restricted to Paget cells but is also seen in Toker cells and Merkel cells. Am J Surg Pathol. 1999;23(2):212-219. 21. Sato K, Leidal R, Sato F. Morphology and development of an apoeccrine sweat gland in human axillae. Am J Physiol. 1987;252(1 Pt 2):R166-80. 22. Burgeson RE, Nimni ME. Collagen types. Molecular structure and tissue distribution. Clin Orthop Relat Res. 1992;(282):250-272. 23. Eyden B. The myofibroblast: an assessment of controversial issues and a definition useful in diagnosis and research. Ultra-struct Pathol. 25(1):39-50. 24. Braverman IM. The cutaneous microcirculation. J Investig Dermatology Symp Proc. 2000;5:3-9. 25. Johansson O. The innervation of the human epidermis. J Neurol Sci. 1995;130(2):228. 26. Avram
|
Surgery_Schwartz_3637
|
Surgery_Schwartz
|
IM. The cutaneous microcirculation. J Investig Dermatology Symp Proc. 2000;5:3-9. 25. Johansson O. The innervation of the human epidermis. J Neurol Sci. 1995;130(2):228. 26. Avram AS, Avram MM, James WD. Subcutaneous fat in normal and diseased states: 2. Anatomy and physiology of white and brown adipose tissue. J Am Acad Dermatol. 2005;53(4):671-683. 27. König A, Lehmann C, Rompel R, Happle R. Cigarette smok-ing as a triggering factor of hidradenitis suppurativa. Derma-tology. 1999;198(3):261-264. 28. Pink AE, Simpson MA, Desai N, Trembath RC, Barker JNW. γ-Secretase mutations in hidradenitis suppurativa: new insights into disease pathogenesis. J Invest Dermatol. 2013;133(3):601-607. 29. Jemec GBE. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012;366(2):158-164. 30. Matusiak L, Bieniek A, Szepietowski JC. Increased serum tumour necrosis factor-alpha in hidradenitis sup-purativa patients: is there a basis for treatment with anti-tumour necrosis factor-alpha agents?
|
Surgery_Schwartz. IM. The cutaneous microcirculation. J Investig Dermatology Symp Proc. 2000;5:3-9. 25. Johansson O. The innervation of the human epidermis. J Neurol Sci. 1995;130(2):228. 26. Avram AS, Avram MM, James WD. Subcutaneous fat in normal and diseased states: 2. Anatomy and physiology of white and brown adipose tissue. J Am Acad Dermatol. 2005;53(4):671-683. 27. König A, Lehmann C, Rompel R, Happle R. Cigarette smok-ing as a triggering factor of hidradenitis suppurativa. Derma-tology. 1999;198(3):261-264. 28. Pink AE, Simpson MA, Desai N, Trembath RC, Barker JNW. γ-Secretase mutations in hidradenitis suppurativa: new insights into disease pathogenesis. J Invest Dermatol. 2013;133(3):601-607. 29. Jemec GBE. Clinical practice. Hidradenitis suppurativa. N Engl J Med. 2012;366(2):158-164. 30. Matusiak L, Bieniek A, Szepietowski JC. Increased serum tumour necrosis factor-alpha in hidradenitis sup-purativa patients: is there a basis for treatment with anti-tumour necrosis factor-alpha agents?
|
Surgery_Schwartz_3638
|
Surgery_Schwartz
|
L, Bieniek A, Szepietowski JC. Increased serum tumour necrosis factor-alpha in hidradenitis sup-purativa patients: is there a basis for treatment with anti-tumour necrosis factor-alpha agents? Acta Derm Venereol. 2009;89(6):601-603.Brunicardi_Ch16_p0511-p0540.indd 53619/02/19 3:09 PM 537THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16 31. Schlapbach C, Hänni T, Yawalkar N, Hunger RE. Expression of the IL-23/Th17 pathway in lesions of hidradenitis suppura-tiva. J Am Acad Dermatol. 2011;65(4):790-798. 32. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol. 1983;22(5):325-328. 33. Mandal A, Watson J. Experience with different treatment mod-ules in hidradenitis suppuritiva: a study of 106 cases. Surgeon. 2005;3(1):23-26. 34. Tierney E, Mahmoud BH, Hexsel C, Ozog ND, Hamzavi I. Randomized control trial for the treatment of hidradenitis sup-purativa with a neodymium-doped yttrium aluminium garnet laser. Dermatologic Surg.
|
Surgery_Schwartz. L, Bieniek A, Szepietowski JC. Increased serum tumour necrosis factor-alpha in hidradenitis sup-purativa patients: is there a basis for treatment with anti-tumour necrosis factor-alpha agents? Acta Derm Venereol. 2009;89(6):601-603.Brunicardi_Ch16_p0511-p0540.indd 53619/02/19 3:09 PM 537THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16 31. Schlapbach C, Hänni T, Yawalkar N, Hunger RE. Expression of the IL-23/Th17 pathway in lesions of hidradenitis suppura-tiva. J Am Acad Dermatol. 2011;65(4):790-798. 32. Clemmensen OJ. Topical treatment of hidradenitis suppurativa with clindamycin. Int J Dermatol. 1983;22(5):325-328. 33. Mandal A, Watson J. Experience with different treatment mod-ules in hidradenitis suppuritiva: a study of 106 cases. Surgeon. 2005;3(1):23-26. 34. Tierney E, Mahmoud BH, Hexsel C, Ozog ND, Hamzavi I. Randomized control trial for the treatment of hidradenitis sup-purativa with a neodymium-doped yttrium aluminium garnet laser. Dermatologic Surg.
|
Surgery_Schwartz_3639
|
Surgery_Schwartz
|
E, Mahmoud BH, Hexsel C, Ozog ND, Hamzavi I. Randomized control trial for the treatment of hidradenitis sup-purativa with a neodymium-doped yttrium aluminium garnet laser. Dermatologic Surg. 2009;35(8):1188-1198. 35. Shuja F, Chan CS, Rosen T. Biologic drugs for the treatment of hidradenitis suppurativa: an evidence-based review. Dermatol Clin. 2010;28(3):511-521, 523-524. 36. Falola RA, DeFazio MV, Anghel EL, Mitnick CD, Attinger CE, Evans KK. What heals hidradenitis suppurativa: surgery, immunosuppression, or both? Plast Reconstr Surg. 2016;138 (3 suppl):219S-229S. 37. Marzano A V, Cugno M, Trevisan V, et al. Role of inflam-matory cells, cytokines and matrix metalloproteinases in neutrophil-mediated skin diseases. Clin Exp Immunol. 2010;162(1):100-107. 38. Bister V, Mäkitalo L, Jeskanen L, Saarialho-Kere U. Expres-sion of MMP-9, MMP-10 and TNF-alpha and lack of epithelial MMP-1 and MMP-26 characterize pyoderma gangrenosum. J Cutan Pathol. 2007;34(12):889-898. 39. Shore RN. Pyoderma
|
Surgery_Schwartz. E, Mahmoud BH, Hexsel C, Ozog ND, Hamzavi I. Randomized control trial for the treatment of hidradenitis sup-purativa with a neodymium-doped yttrium aluminium garnet laser. Dermatologic Surg. 2009;35(8):1188-1198. 35. Shuja F, Chan CS, Rosen T. Biologic drugs for the treatment of hidradenitis suppurativa: an evidence-based review. Dermatol Clin. 2010;28(3):511-521, 523-524. 36. Falola RA, DeFazio MV, Anghel EL, Mitnick CD, Attinger CE, Evans KK. What heals hidradenitis suppurativa: surgery, immunosuppression, or both? Plast Reconstr Surg. 2016;138 (3 suppl):219S-229S. 37. Marzano A V, Cugno M, Trevisan V, et al. Role of inflam-matory cells, cytokines and matrix metalloproteinases in neutrophil-mediated skin diseases. Clin Exp Immunol. 2010;162(1):100-107. 38. Bister V, Mäkitalo L, Jeskanen L, Saarialho-Kere U. Expres-sion of MMP-9, MMP-10 and TNF-alpha and lack of epithelial MMP-1 and MMP-26 characterize pyoderma gangrenosum. J Cutan Pathol. 2007;34(12):889-898. 39. Shore RN. Pyoderma
|
Surgery_Schwartz_3640
|
Surgery_Schwartz
|
L, Saarialho-Kere U. Expres-sion of MMP-9, MMP-10 and TNF-alpha and lack of epithelial MMP-1 and MMP-26 characterize pyoderma gangrenosum. J Cutan Pathol. 2007;34(12):889-898. 39. Shore RN. Pyoderma gangrenosum, defective neutrophil chemo-taxis, and leukemia. Arch Dermatol. 1976;112(12):1792-1793. 40. Hommes DW, Oldenburg B, van Bodegraven AA, et al. Guide-lines for treatment with infliximab for Crohn’s disease. Neth J Med. 64(7):219-229. 41. Roy DB, Conte ET, Cohen DJ. The treatment of pyoderma gangrenosum using etanercept. J Am Acad Dermatol. 2006;54 (3 suppl 2):S128-S134. 42. Khurrum Baig M, Marquez H, Nogueras JJ, Weiss EG, Wexner SD. Topical tacrolimus (FK506) in the treatment of recalcitrant parastomal pyoderma gangrenosum associated with Crohn’s disease: report of two cases. Color Dis. 2004;6(4):250-253. 43. Lyell A. Toxic epidermal necrolysis (the scalded skin syn-drome): a reappraisal. Br J Dermatol. 1979;100(1):69-86. 44. Stern RS, Chan HL. Usefulness of case report
|
Surgery_Schwartz. L, Saarialho-Kere U. Expres-sion of MMP-9, MMP-10 and TNF-alpha and lack of epithelial MMP-1 and MMP-26 characterize pyoderma gangrenosum. J Cutan Pathol. 2007;34(12):889-898. 39. Shore RN. Pyoderma gangrenosum, defective neutrophil chemo-taxis, and leukemia. Arch Dermatol. 1976;112(12):1792-1793. 40. Hommes DW, Oldenburg B, van Bodegraven AA, et al. Guide-lines for treatment with infliximab for Crohn’s disease. Neth J Med. 64(7):219-229. 41. Roy DB, Conte ET, Cohen DJ. The treatment of pyoderma gangrenosum using etanercept. J Am Acad Dermatol. 2006;54 (3 suppl 2):S128-S134. 42. Khurrum Baig M, Marquez H, Nogueras JJ, Weiss EG, Wexner SD. Topical tacrolimus (FK506) in the treatment of recalcitrant parastomal pyoderma gangrenosum associated with Crohn’s disease: report of two cases. Color Dis. 2004;6(4):250-253. 43. Lyell A. Toxic epidermal necrolysis (the scalded skin syn-drome): a reappraisal. Br J Dermatol. 1979;100(1):69-86. 44. Stern RS, Chan HL. Usefulness of case report
|
Surgery_Schwartz_3641
|
Surgery_Schwartz
|
Color Dis. 2004;6(4):250-253. 43. Lyell A. Toxic epidermal necrolysis (the scalded skin syn-drome): a reappraisal. Br J Dermatol. 1979;100(1):69-86. 44. Stern RS, Chan HL. Usefulness of case report literature in determining drugs responsible for toxic epidermal necrolysis. J Am Acad Dermatol. 1989;21(2 pt 1):317-322. 45. Valeyrie-Allanore L, Roujeau J-C. Epidermal necrolysis. In: Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York: McGraw-Hill; 2012. 46. Chung W-H, Hung S-I, Yang J-Y, et al. Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis. Nat Med. 2008;14(12):1343-1350. 47. Chung W-H, Hung S-I, Hong H-S, et al. Medical genet-ics: a marker for Stevens–Johnson syndrome. Nature. 2004;428(6982):486-486. 48. Downey A, Jackson C, Harun N, et al. Toxic epidermal necrol-ysis: review of pathogenesis and management. J Am Acad Dermatol. 2012;66(6):995-1003. 49. Garcia-Doval I, LeCleach L, Bocquet H, Otero
|
Surgery_Schwartz. Color Dis. 2004;6(4):250-253. 43. Lyell A. Toxic epidermal necrolysis (the scalded skin syn-drome): a reappraisal. Br J Dermatol. 1979;100(1):69-86. 44. Stern RS, Chan HL. Usefulness of case report literature in determining drugs responsible for toxic epidermal necrolysis. J Am Acad Dermatol. 1989;21(2 pt 1):317-322. 45. Valeyrie-Allanore L, Roujeau J-C. Epidermal necrolysis. In: Fitzpatrick’s Dermatology in General Medicine. 8th ed. New York: McGraw-Hill; 2012. 46. Chung W-H, Hung S-I, Yang J-Y, et al. Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis. Nat Med. 2008;14(12):1343-1350. 47. Chung W-H, Hung S-I, Hong H-S, et al. Medical genet-ics: a marker for Stevens–Johnson syndrome. Nature. 2004;428(6982):486-486. 48. Downey A, Jackson C, Harun N, et al. Toxic epidermal necrol-ysis: review of pathogenesis and management. J Am Acad Dermatol. 2012;66(6):995-1003. 49. Garcia-Doval I, LeCleach L, Bocquet H, Otero
|
Surgery_Schwartz_3642
|
Surgery_Schwartz
|
A, Jackson C, Harun N, et al. Toxic epidermal necrol-ysis: review of pathogenesis and management. J Am Acad Dermatol. 2012;66(6):995-1003. 49. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syn-drome: does early withdrawal of causative drugs decrease the risk of death? Arch Dermatol. 2000;136(3):323-327. 50. Kardaun S, Jonkman M. Dexamethasone pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis. Acta Derm Venereol. 2007;87(2):144-148. 51. French LE, Trent JT, Kerdel FA. Use of intravenous immuno-globulin in toxic epidermal necrolysis and Stevens–Johnson syndrome: Our current understanding. Int Immunopharmacol. 2006;6(4):543-549. 52. Lee HY, Lim YL, Thirumoorthy T, Pang SM. The role of intravenous immunoglobulin in toxic epidermal necrolysis: a retrospective analysis of 64 patients managed in a specialized centre. Br J Dermatol. 2013;169(6):1304-1309. 53. Creamer D, Walsh SA, Dziewulski P, et al. UK
|
Surgery_Schwartz. A, Jackson C, Harun N, et al. Toxic epidermal necrol-ysis: review of pathogenesis and management. J Am Acad Dermatol. 2012;66(6):995-1003. 49. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syn-drome: does early withdrawal of causative drugs decrease the risk of death? Arch Dermatol. 2000;136(3):323-327. 50. Kardaun S, Jonkman M. Dexamethasone pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis. Acta Derm Venereol. 2007;87(2):144-148. 51. French LE, Trent JT, Kerdel FA. Use of intravenous immuno-globulin in toxic epidermal necrolysis and Stevens–Johnson syndrome: Our current understanding. Int Immunopharmacol. 2006;6(4):543-549. 52. Lee HY, Lim YL, Thirumoorthy T, Pang SM. The role of intravenous immunoglobulin in toxic epidermal necrolysis: a retrospective analysis of 64 patients managed in a specialized centre. Br J Dermatol. 2013;169(6):1304-1309. 53. Creamer D, Walsh SA, Dziewulski P, et al. UK
|
Surgery_Schwartz_3643
|
Surgery_Schwartz
|
in toxic epidermal necrolysis: a retrospective analysis of 64 patients managed in a specialized centre. Br J Dermatol. 2013;169(6):1304-1309. 53. Creamer D, Walsh SA, Dziewulski P, et al. UK guidelines for the management of Stevens–Johnson syndrome/toxic epider-mal necrolysis in adults 2016. J Plast Reconstr Aesthetic Surg. 2016;69(6):e119-e153. 54. Battie C, Verschoore M. Cutaneous solar ultraviolet exposure and clinical aspects of photodamage. Indian J Dermatol Venereol Leprol. 2012;78 suppl 1(7):S9-S14. 55. Eliya-Masamba MC, Banda GW. Primary closure versus delayed closure for non bite traumatic wounds within 24 hours post injury. In: Eliya-Masamba MC, ed. Cochrane Database of Sys-tematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2013. 56. Presutti RJ. Bite wounds. Postgrad Med. 1997;101(4):243-254. 57. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical expe-rience. Ann Plast Surg. 1997;38(6):563-576; discussion 577.
|
Surgery_Schwartz. in toxic epidermal necrolysis: a retrospective analysis of 64 patients managed in a specialized centre. Br J Dermatol. 2013;169(6):1304-1309. 53. Creamer D, Walsh SA, Dziewulski P, et al. UK guidelines for the management of Stevens–Johnson syndrome/toxic epider-mal necrolysis in adults 2016. J Plast Reconstr Aesthetic Surg. 2016;69(6):e119-e153. 54. Battie C, Verschoore M. Cutaneous solar ultraviolet exposure and clinical aspects of photodamage. Indian J Dermatol Venereol Leprol. 2012;78 suppl 1(7):S9-S14. 55. Eliya-Masamba MC, Banda GW. Primary closure versus delayed closure for non bite traumatic wounds within 24 hours post injury. In: Eliya-Masamba MC, ed. Cochrane Database of Sys-tematic Reviews. Chichester, UK: John Wiley & Sons, Ltd; 2013. 56. Presutti RJ. Bite wounds. Postgrad Med. 1997;101(4):243-254. 57. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical expe-rience. Ann Plast Surg. 1997;38(6):563-576; discussion 577.
|
Surgery_Schwartz_3644
|
Surgery_Schwartz
|
1997;101(4):243-254. 57. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical expe-rience. Ann Plast Surg. 1997;38(6):563-576; discussion 577. This seminal paper laid the foundation for the use of nega-tive pressure wound therapy devices for open wounds. 58. Abrahamian FM, Goldstein EJC. Microbiology of animal bite wound infections. Clin Microbiol Rev. 2011;24(2):231-246. 59. Kennedy SA, Stoll LE, Lauder AS. Human and other mam-malian bite injuries of the hand. J Am Acad Orthop Surg. 2015;23(1):47-57. 60. Robson MC, Krizek TJ, Heggers JP. Biology of surgical infec-tion. Curr Probl Surg. March 1973:1-62. 61. Cummings P. Antibiotics to prevent infection in patients with dog bite wounds: a meta-analysis of randomized trials. Ann Emerg Med. 1994;23(3):535-540. A meta-analysis of eight randomized trials demonstrated the reduced risk of infec-tion after dog bites with the use of prophylactic antibiotics. 62. Paschos NK, Makris EA, Gantsos
|
Surgery_Schwartz. 1997;101(4):243-254. 57. Argenta LC, Morykwas MJ. Vacuum-assisted closure: a new method for wound control and treatment: clinical expe-rience. Ann Plast Surg. 1997;38(6):563-576; discussion 577. This seminal paper laid the foundation for the use of nega-tive pressure wound therapy devices for open wounds. 58. Abrahamian FM, Goldstein EJC. Microbiology of animal bite wound infections. Clin Microbiol Rev. 2011;24(2):231-246. 59. Kennedy SA, Stoll LE, Lauder AS. Human and other mam-malian bite injuries of the hand. J Am Acad Orthop Surg. 2015;23(1):47-57. 60. Robson MC, Krizek TJ, Heggers JP. Biology of surgical infec-tion. Curr Probl Surg. March 1973:1-62. 61. Cummings P. Antibiotics to prevent infection in patients with dog bite wounds: a meta-analysis of randomized trials. Ann Emerg Med. 1994;23(3):535-540. A meta-analysis of eight randomized trials demonstrated the reduced risk of infec-tion after dog bites with the use of prophylactic antibiotics. 62. Paschos NK, Makris EA, Gantsos
|
Surgery_Schwartz_3645
|
Surgery_Schwartz
|
1994;23(3):535-540. A meta-analysis of eight randomized trials demonstrated the reduced risk of infec-tion after dog bites with the use of prophylactic antibiotics. 62. Paschos NK, Makris EA, Gantsos A, Georgoulis AD. Primary closure versus non-closure of dog bite wounds. A randomised controlled trial. Injury. 2014;45(1):237-240. 63. Hardwicke J, Hunter T, Staruch R, Moiemen N. Chemical burns—an historical comparison and review of the literature. Burns. 2012;38(3):383-387. 64. Vandeweyer E, Heymans O, Deraemaecker R. Extravasation injuries and emergency suction as treatment. Plast Reconstr Surg. 2000;105(1):109-110. 65. Kumar RJ, Pegg SP, Kimble RM. Management of extravasa-tion injuries. ANZ J Surg. 2001;71(5):285-289. 66. Harrold K, Gould D, Drey N. The management of cytotoxic chemotherapy extravasation: a systematic review of the lit-erature to evaluate the evidence underpinning contemporary practice. Eur J Cancer Care (Engl). 2015;24(6):771-800. 67. Frye K, Luterman A. Thermal
|
Surgery_Schwartz. 1994;23(3):535-540. A meta-analysis of eight randomized trials demonstrated the reduced risk of infec-tion after dog bites with the use of prophylactic antibiotics. 62. Paschos NK, Makris EA, Gantsos A, Georgoulis AD. Primary closure versus non-closure of dog bite wounds. A randomised controlled trial. Injury. 2014;45(1):237-240. 63. Hardwicke J, Hunter T, Staruch R, Moiemen N. Chemical burns—an historical comparison and review of the literature. Burns. 2012;38(3):383-387. 64. Vandeweyer E, Heymans O, Deraemaecker R. Extravasation injuries and emergency suction as treatment. Plast Reconstr Surg. 2000;105(1):109-110. 65. Kumar RJ, Pegg SP, Kimble RM. Management of extravasa-tion injuries. ANZ J Surg. 2001;71(5):285-289. 66. Harrold K, Gould D, Drey N. The management of cytotoxic chemotherapy extravasation: a systematic review of the lit-erature to evaluate the evidence underpinning contemporary practice. Eur J Cancer Care (Engl). 2015;24(6):771-800. 67. Frye K, Luterman A. Thermal
|
Surgery_Schwartz_3646
|
Surgery_Schwartz
|
extravasation: a systematic review of the lit-erature to evaluate the evidence underpinning contemporary practice. Eur J Cancer Care (Engl). 2015;24(6):771-800. 67. Frye K, Luterman A. Thermal burns. In: Plastic Surgery Secrets Plus. 2nd ed. Mosby, Inc; 2010:643-647. 68. Britt LD, Dascombe WH, Rodriguez A. New horizons in man-agement of hypothermia and frostbite injury. Surg Clin North Am. 1991;71(2):345-370. 69. Lindan O, Greenway RM, Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and sitting positions using a “bed of springs and nails.” Arch Phys Med Rehabil. 1965;46:378-385. 70. Tayyib N, Coyer F. Effectiveness of pressure ulcer preven-tion strategies for adult patients in intensive care units: a systematic review. Worldviews Evidence-Based Nurs. 2016;13(6):432-444. 71. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223. 72. Cannon BC, Cannon JP. Management of pressure ulcers. Am J Health Syst Pharm.
|
Surgery_Schwartz. extravasation: a systematic review of the lit-erature to evaluate the evidence underpinning contemporary practice. Eur J Cancer Care (Engl). 2015;24(6):771-800. 67. Frye K, Luterman A. Thermal burns. In: Plastic Surgery Secrets Plus. 2nd ed. Mosby, Inc; 2010:643-647. 68. Britt LD, Dascombe WH, Rodriguez A. New horizons in man-agement of hypothermia and frostbite injury. Surg Clin North Am. 1991;71(2):345-370. 69. Lindan O, Greenway RM, Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and sitting positions using a “bed of springs and nails.” Arch Phys Med Rehabil. 1965;46:378-385. 70. Tayyib N, Coyer F. Effectiveness of pressure ulcer preven-tion strategies for adult patients in intensive care units: a systematic review. Worldviews Evidence-Based Nurs. 2016;13(6):432-444. 71. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223. 72. Cannon BC, Cannon JP. Management of pressure ulcers. Am J Health Syst Pharm.
|
Surgery_Schwartz_3647
|
Surgery_Schwartz
|
Nurs. 2016;13(6):432-444. 71. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223. 72. Cannon BC, Cannon JP. Management of pressure ulcers. Am J Health Syst Pharm. 2004;61(18):1895-1905. 73. Larson JD, Altman AM, Bentz ML, Larson DL. Pressure ulcers and perineal reconstruction. Plast Reconstr Surg. 2014;133(1):39e-48e.Brunicardi_Ch16_p0511-p0540.indd 53719/02/19 3:09 PM 538SPECIFIC CONSIDERATIONSPART II 74. Waites KB, Canupp KC, Chen Y, DeVivo MJ, Moser SA. Bac-teremia after spinal cord injury in initial versus subsequent hospitalizations. J Spinal Cord Med. 2001;24(2):96-100. 75. Siroky MB. Pathogenesis of bacteriuria and infection in the spinal cord injured patient. Am J Med. July 2002:67S-79S. 76. Límová M. Active wound coverings: bioengineered skin and dermal substitutes. Surg Clin North Am. 2010;90(6):1237-1255. 77. Nahabedian MY. Acellular dermal matrices in primary breast reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 44S-53S. 78. Ellis CV,
|
Surgery_Schwartz. Nurs. 2016;13(6):432-444. 71. Lyder CH. Pressure ulcer prevention and management. JAMA. 2003;289(2):223. 72. Cannon BC, Cannon JP. Management of pressure ulcers. Am J Health Syst Pharm. 2004;61(18):1895-1905. 73. Larson JD, Altman AM, Bentz ML, Larson DL. Pressure ulcers and perineal reconstruction. Plast Reconstr Surg. 2014;133(1):39e-48e.Brunicardi_Ch16_p0511-p0540.indd 53719/02/19 3:09 PM 538SPECIFIC CONSIDERATIONSPART II 74. Waites KB, Canupp KC, Chen Y, DeVivo MJ, Moser SA. Bac-teremia after spinal cord injury in initial versus subsequent hospitalizations. J Spinal Cord Med. 2001;24(2):96-100. 75. Siroky MB. Pathogenesis of bacteriuria and infection in the spinal cord injured patient. Am J Med. July 2002:67S-79S. 76. Límová M. Active wound coverings: bioengineered skin and dermal substitutes. Surg Clin North Am. 2010;90(6):1237-1255. 77. Nahabedian MY. Acellular dermal matrices in primary breast reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 44S-53S. 78. Ellis CV,
|
Surgery_Schwartz_3648
|
Surgery_Schwartz
|
substitutes. Surg Clin North Am. 2010;90(6):1237-1255. 77. Nahabedian MY. Acellular dermal matrices in primary breast reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 44S-53S. 78. Ellis CV, Kulber DA. Acellular dermal matrices in hand reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 256S-269S. 79. Rajan S. Skin and soft-tissue infections: classifying and treat-ing a spectrum. Cleve Clin J Med. 2012;79(1):57-66. 80. Moet GJ, Jones RN, Biedenbach DJ, Stilwell MG, Fritsche TR. Contemporary causes of skin and soft tissue infections in North America, Latin America, and Europe: report from the SENTRY Antimicrobial Surveillance Program (1998–2004). Diagn Microbiol Infect Dis. 2007;57(1):7-13. 81. Stevens DL, Bisno AL, Chambers HF, et al. Executive sum-mary: practice guidelines for the diagnosis and manage-ment of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):147-159. 82. Goldstein EJC, Anaya DA,
|
Surgery_Schwartz. substitutes. Surg Clin North Am. 2010;90(6):1237-1255. 77. Nahabedian MY. Acellular dermal matrices in primary breast reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 44S-53S. 78. Ellis CV, Kulber DA. Acellular dermal matrices in hand reconstruction. Plast Reconstr Surg. 2012;130(5 suppl 2): 256S-269S. 79. Rajan S. Skin and soft-tissue infections: classifying and treat-ing a spectrum. Cleve Clin J Med. 2012;79(1):57-66. 80. Moet GJ, Jones RN, Biedenbach DJ, Stilwell MG, Fritsche TR. Contemporary causes of skin and soft tissue infections in North America, Latin America, and Europe: report from the SENTRY Antimicrobial Surveillance Program (1998–2004). Diagn Microbiol Infect Dis. 2007;57(1):7-13. 81. Stevens DL, Bisno AL, Chambers HF, et al. Executive sum-mary: practice guidelines for the diagnosis and manage-ment of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):147-159. 82. Goldstein EJC, Anaya DA,
|
Surgery_Schwartz_3649
|
Surgery_Schwartz
|
for the diagnosis and manage-ment of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):147-159. 82. Goldstein EJC, Anaya DA, Dellinger EP. Necrotizing soft-tissue infection: diagnosis and management. Clin Infect Dis. 2007;44(5):705-710. 83. Bosshardt TL, Henderson VJ, Organ CH. Necrotizing soft-tissue infections. Arch Surg. 1996;131(8):846-854. 84. Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resis-tant Staphylococcus aureus in Los Angeles. N Engl J Med. 2005;352(14):1445-1453. 85. Wall DB, Klein SR, Black S, et al. A simple model to help distinguish necrotizing fasciitis from nonnecrotizing soft tis-sue infection. J Am Coll Surg. 2000;191(3):227-231. 86. Wong C-H, Khin L-W, Heng K-S, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue
|
Surgery_Schwartz. for the diagnosis and manage-ment of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):147-159. 82. Goldstein EJC, Anaya DA, Dellinger EP. Necrotizing soft-tissue infection: diagnosis and management. Clin Infect Dis. 2007;44(5):705-710. 83. Bosshardt TL, Henderson VJ, Organ CH. Necrotizing soft-tissue infections. Arch Surg. 1996;131(8):846-854. 84. Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resis-tant Staphylococcus aureus in Los Angeles. N Engl J Med. 2005;352(14):1445-1453. 85. Wall DB, Klein SR, Black S, et al. A simple model to help distinguish necrotizing fasciitis from nonnecrotizing soft tis-sue infection. J Am Coll Surg. 2000;191(3):227-231. 86. Wong C-H, Khin L-W, Heng K-S, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue
|
Surgery_Schwartz_3650
|
Surgery_Schwartz
|
C-H, Khin L-W, Heng K-S, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7): 1535-1541. 87. Willy C, Rieger H, Vogt D. Hyperbare Oxygenation bei nekrotisierenden Weichteilinfektionen: Kontra. Der Chir. 2012;83(11):960-972. 88. Moghimi M, Salentijn E, Debets-Ossenkop Y, Karagozoglu KH, Forouzanfar T. Treatment of cervicofacial actinomycosis: a report of 19 cases and review of literature. Med Oral Patol Oral Cir Bucal. 2013;18(4):e627-32. 89. Wong VK, Turmezei TD, Weston VC. Actinomycosis. BMJ. 2011;343:d6099. 90. de Villiers E-M. Cross-roads in the classification of papilloma-viruses. Virology. 2013;445(1-2):2-10. 91. Cardoso JC, Calonje E. Cutaneous manifestations of human papillomaviruses: a review. Acta dermatovenerologica Alpina, Pannonica, Adriat. 2011;20(3):145-154. 92. Majewski S, Jablonska S. Human papillomavirus-associ-ated tumors of
|
Surgery_Schwartz. C-H, Khin L-W, Heng K-S, Tan KC, Low CO. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7): 1535-1541. 87. Willy C, Rieger H, Vogt D. Hyperbare Oxygenation bei nekrotisierenden Weichteilinfektionen: Kontra. Der Chir. 2012;83(11):960-972. 88. Moghimi M, Salentijn E, Debets-Ossenkop Y, Karagozoglu KH, Forouzanfar T. Treatment of cervicofacial actinomycosis: a report of 19 cases and review of literature. Med Oral Patol Oral Cir Bucal. 2013;18(4):e627-32. 89. Wong VK, Turmezei TD, Weston VC. Actinomycosis. BMJ. 2011;343:d6099. 90. de Villiers E-M. Cross-roads in the classification of papilloma-viruses. Virology. 2013;445(1-2):2-10. 91. Cardoso JC, Calonje E. Cutaneous manifestations of human papillomaviruses: a review. Acta dermatovenerologica Alpina, Pannonica, Adriat. 2011;20(3):145-154. 92. Majewski S, Jablonska S. Human papillomavirus-associ-ated tumors of
|
Surgery_Schwartz_3651
|
Surgery_Schwartz
|
manifestations of human papillomaviruses: a review. Acta dermatovenerologica Alpina, Pannonica, Adriat. 2011;20(3):145-154. 92. Majewski S, Jablonska S. Human papillomavirus-associ-ated tumors of the skin and mucosa. J Am Acad Dermatol. 1997;36(5 pt 1):659-685. 93. Rogers HD, Macgregor JL, Nord KM, et al. Acquired epidermodysplasia verruciformis. J Am Acad Dermatol. 2009;60(2):315-320. 94. Jacobelli S, Laude H, Carlotti A, et al. Epidermodysplasia verruciformis in human immunodeficiency virus-infected patients: a marker of human papillomavirus-related disor-ders not affected by antiretroviral therapy. Arch Dermatol. 2011;147(5):590-596. 95. Garland SM, Kjaer SK, Muñoz N, et al. Impact and effec-tiveness of the quadrivalent human papillomavirus vaccine: a systematic review of 10 years of real-world experience. Clin Infect Dis. 2016;63(4):519-527. 96. Connolly M, Bazmi K, O’Connell M, Lyons JF, Bourke JF. Cryotherapy of viral warts: a sustained 10-s freeze is more effective than the
|
Surgery_Schwartz. manifestations of human papillomaviruses: a review. Acta dermatovenerologica Alpina, Pannonica, Adriat. 2011;20(3):145-154. 92. Majewski S, Jablonska S. Human papillomavirus-associ-ated tumors of the skin and mucosa. J Am Acad Dermatol. 1997;36(5 pt 1):659-685. 93. Rogers HD, Macgregor JL, Nord KM, et al. Acquired epidermodysplasia verruciformis. J Am Acad Dermatol. 2009;60(2):315-320. 94. Jacobelli S, Laude H, Carlotti A, et al. Epidermodysplasia verruciformis in human immunodeficiency virus-infected patients: a marker of human papillomavirus-related disor-ders not affected by antiretroviral therapy. Arch Dermatol. 2011;147(5):590-596. 95. Garland SM, Kjaer SK, Muñoz N, et al. Impact and effec-tiveness of the quadrivalent human papillomavirus vaccine: a systematic review of 10 years of real-world experience. Clin Infect Dis. 2016;63(4):519-527. 96. Connolly M, Bazmi K, O’Connell M, Lyons JF, Bourke JF. Cryotherapy of viral warts: a sustained 10-s freeze is more effective than the
|
Surgery_Schwartz_3652
|
Surgery_Schwartz
|
real-world experience. Clin Infect Dis. 2016;63(4):519-527. 96. Connolly M, Bazmi K, O’Connell M, Lyons JF, Bourke JF. Cryotherapy of viral warts: a sustained 10-s freeze is more effective than the traditional method. Br J Dermatol. 2001;145(4):554-557. 97. Coopman SA, Johnson RA, Platt R, Stern RS. Cutaneous disease and drug reactions in HIV infection. N Engl J Med. 1993;328(23):1670-1674. 98. Khambaty MM, Hsu SS. Dermatology of the patient with HIV. Emerg Med Clin North Am. 2010;28(2):355-368. 99. Severson JL, Tyring SK. Relation between herpes simplex viruses and human immunodeficiency virus infections. Arch Dermatol. 1999;135(11):1393-1397. 100. Crum-Cianflone N, Hullsiek KH, Satter E, et al. Cutaneous malignancies among HIV-infected persons. Arch Intern Med. 2009;169(12):1130. 101. Davis PA, Wastell C. A comparison of biomechanical proper-ties of excised mature scars from HIV patients and non-HIV controls. Am J Surg. 2000;180(3):217-222. 102. North PE, Waner M, Mizeracki A, Mihm
|
Surgery_Schwartz. real-world experience. Clin Infect Dis. 2016;63(4):519-527. 96. Connolly M, Bazmi K, O’Connell M, Lyons JF, Bourke JF. Cryotherapy of viral warts: a sustained 10-s freeze is more effective than the traditional method. Br J Dermatol. 2001;145(4):554-557. 97. Coopman SA, Johnson RA, Platt R, Stern RS. Cutaneous disease and drug reactions in HIV infection. N Engl J Med. 1993;328(23):1670-1674. 98. Khambaty MM, Hsu SS. Dermatology of the patient with HIV. Emerg Med Clin North Am. 2010;28(2):355-368. 99. Severson JL, Tyring SK. Relation between herpes simplex viruses and human immunodeficiency virus infections. Arch Dermatol. 1999;135(11):1393-1397. 100. Crum-Cianflone N, Hullsiek KH, Satter E, et al. Cutaneous malignancies among HIV-infected persons. Arch Intern Med. 2009;169(12):1130. 101. Davis PA, Wastell C. A comparison of biomechanical proper-ties of excised mature scars from HIV patients and non-HIV controls. Am J Surg. 2000;180(3):217-222. 102. North PE, Waner M, Mizeracki A, Mihm
|
Surgery_Schwartz_3653
|
Surgery_Schwartz
|
PA, Wastell C. A comparison of biomechanical proper-ties of excised mature scars from HIV patients and non-HIV controls. Am J Surg. 2000;180(3):217-222. 102. North PE, Waner M, Mizeracki A, Mihm MC Jr. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31(1):11-22. 103. Léauté-Labrèze C, Dumas de la Roque E, Hubiche T, Boralevi F, Thambo JB, Taïeb A. Propranolol for severe hemangiomas of infancy. N Engl J Med. 2008;358(24):2649-2651. 104. Léauté-Labrèze C, Hoeger P, Mazereeuw-Hautier J, et al. A randomized, controlled trial of oral propranolol in infantile hemangioma. N Engl J Med. 2015;372(8):735-746. A multi-center, randomized, double-blind, adaptive, phase 2 and 3 trial that showed propranolol is a very effective treatment for infantile hemangioma. 105. Kelly JW, Rivers JK, MacLennan R, Harrison S, Lewis AE, Tate BJ. Sunlight: a major factor associated with the develop-ment of melanocytic nevi in Australian schoolchildren. J Am Acad
|
Surgery_Schwartz. PA, Wastell C. A comparison of biomechanical proper-ties of excised mature scars from HIV patients and non-HIV controls. Am J Surg. 2000;180(3):217-222. 102. North PE, Waner M, Mizeracki A, Mihm MC Jr. GLUT1: a newly discovered immunohistochemical marker for juvenile hemangiomas. Hum Pathol. 2000;31(1):11-22. 103. Léauté-Labrèze C, Dumas de la Roque E, Hubiche T, Boralevi F, Thambo JB, Taïeb A. Propranolol for severe hemangiomas of infancy. N Engl J Med. 2008;358(24):2649-2651. 104. Léauté-Labrèze C, Hoeger P, Mazereeuw-Hautier J, et al. A randomized, controlled trial of oral propranolol in infantile hemangioma. N Engl J Med. 2015;372(8):735-746. A multi-center, randomized, double-blind, adaptive, phase 2 and 3 trial that showed propranolol is a very effective treatment for infantile hemangioma. 105. Kelly JW, Rivers JK, MacLennan R, Harrison S, Lewis AE, Tate BJ. Sunlight: a major factor associated with the develop-ment of melanocytic nevi in Australian schoolchildren. J Am Acad
|
Surgery_Schwartz_3654
|
Surgery_Schwartz
|
hemangioma. 105. Kelly JW, Rivers JK, MacLennan R, Harrison S, Lewis AE, Tate BJ. Sunlight: a major factor associated with the develop-ment of melanocytic nevi in Australian schoolchildren. J Am Acad Dermatol. 1994;30(1):40-48. 106. Krengel S, Hauschild A, Schafer T. Melanoma risk in con-genital melanocytic naevi: a systematic review. Br J Dermatol. 2006;155(1):1-8. 107. Schaffer J V. Pigmented lesions in children: when to worry. Curr Opin Pediatr. 2007;19(4):430-440. 108. Fuchs A, Marmur E. The kinetics of skin cancer: progression of actinic keratosis to squamous cell carcinoma. Dermatol Surg. 2007;33(9):1099-1101. 109. Marks R, Rennie G, Selwood T. The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol. 1988;124(7):1039-1042. 110. Robins P, Gupta AK. The use of topical fluorouracil to treat actinic keratosis. Cutis. 2002;70(2 suppl):4-7. 111. Fu W, Cockerell CJ. The actinic (solar) keratosis: a 21st-century perspective. Arch
|
Surgery_Schwartz. hemangioma. 105. Kelly JW, Rivers JK, MacLennan R, Harrison S, Lewis AE, Tate BJ. Sunlight: a major factor associated with the develop-ment of melanocytic nevi in Australian schoolchildren. J Am Acad Dermatol. 1994;30(1):40-48. 106. Krengel S, Hauschild A, Schafer T. Melanoma risk in con-genital melanocytic naevi: a systematic review. Br J Dermatol. 2006;155(1):1-8. 107. Schaffer J V. Pigmented lesions in children: when to worry. Curr Opin Pediatr. 2007;19(4):430-440. 108. Fuchs A, Marmur E. The kinetics of skin cancer: progression of actinic keratosis to squamous cell carcinoma. Dermatol Surg. 2007;33(9):1099-1101. 109. Marks R, Rennie G, Selwood T. The relationship of basal cell carcinomas and squamous cell carcinomas to solar keratoses. Arch Dermatol. 1988;124(7):1039-1042. 110. Robins P, Gupta AK. The use of topical fluorouracil to treat actinic keratosis. Cutis. 2002;70(2 suppl):4-7. 111. Fu W, Cockerell CJ. The actinic (solar) keratosis: a 21st-century perspective. Arch
|
Surgery_Schwartz_3655
|
Surgery_Schwartz
|
P, Gupta AK. The use of topical fluorouracil to treat actinic keratosis. Cutis. 2002;70(2 suppl):4-7. 111. Fu W, Cockerell CJ. The actinic (solar) keratosis: a 21st-century perspective. Arch Dermatol. 2003;139(1):66-70. 112. Pariser RJ. Benign neoplasms of the skin. Med Clin North Am. 1998;82(6):1285-307, v-vi. 113. Lee EH, Nehal KS, Disa JJ. Benign and premalignant skin lesions. Plast Reconstr Surg. 2010;125(5):188e-198e. 114. Mentzel T. Cutaneous lipomatous neoplasms. Semin Diagn Pathol. 2001;18(4):250-257. 115. Reszko A, Wilson L, Leffell D. Devita, Hellman, Rosenberg’s Cancer: Principles and Practice. 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011. 116. Benjamin CL, Ananthaswamy HN. p53 and the pathogenesis of skin cancer. Toxicol Appl Pharmacol. 2007;224(3):241-248. 117. Netscher DT, Leong M, Orengo I, Yang D, Berg C, Krishnan B. Cutaneous malignancies: melanoma and nonmelanoma types. Plast Reconstr Surg. 2011;127(3):37e-56e.Brunicardi_Ch16_p0511-p0540.indd
|
Surgery_Schwartz. P, Gupta AK. The use of topical fluorouracil to treat actinic keratosis. Cutis. 2002;70(2 suppl):4-7. 111. Fu W, Cockerell CJ. The actinic (solar) keratosis: a 21st-century perspective. Arch Dermatol. 2003;139(1):66-70. 112. Pariser RJ. Benign neoplasms of the skin. Med Clin North Am. 1998;82(6):1285-307, v-vi. 113. Lee EH, Nehal KS, Disa JJ. Benign and premalignant skin lesions. Plast Reconstr Surg. 2010;125(5):188e-198e. 114. Mentzel T. Cutaneous lipomatous neoplasms. Semin Diagn Pathol. 2001;18(4):250-257. 115. Reszko A, Wilson L, Leffell D. Devita, Hellman, Rosenberg’s Cancer: Principles and Practice. 9th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011. 116. Benjamin CL, Ananthaswamy HN. p53 and the pathogenesis of skin cancer. Toxicol Appl Pharmacol. 2007;224(3):241-248. 117. Netscher DT, Leong M, Orengo I, Yang D, Berg C, Krishnan B. Cutaneous malignancies: melanoma and nonmelanoma types. Plast Reconstr Surg. 2011;127(3):37e-56e.Brunicardi_Ch16_p0511-p0540.indd
|
Surgery_Schwartz_3656
|
Surgery_Schwartz
|
DT, Leong M, Orengo I, Yang D, Berg C, Krishnan B. Cutaneous malignancies: melanoma and nonmelanoma types. Plast Reconstr Surg. 2011;127(3):37e-56e.Brunicardi_Ch16_p0511-p0540.indd 53819/02/19 3:09 PM 539THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16 118. Siegle RJ, MacMillan J, Pollack S V. Infiltrative basal cell carcinoma: a nonsclerosing subtype. J Dermatol Surg Oncol. 1986;12(8):830-836. 119. Kimyai-Asadi A, Alam M, Goldberg LH, et al. Efficacy of narrowmargin excision of well-demarcated primary facial basal cell carcinomas. J Am Acad Dermatol. 2005;53(3):464-468. 120. Rowe DE, Carroll RJ, Day CL. Mohs surgery is the treat-ment of choice for recurrent (previously treated) basal cell carcinoma. J Dermatol Surg Oncol. 1989;15(4):424-431. A heavily referenced paper from 1989 demonstrating the effectiveness of Mohs micrographic surgery in local control of recurrent basal cell carcinoma. 121. Rowe DE, Carroll RJ, Day CL. Long-term recurrence rates in previously untreated (primary)
|
Surgery_Schwartz. DT, Leong M, Orengo I, Yang D, Berg C, Krishnan B. Cutaneous malignancies: melanoma and nonmelanoma types. Plast Reconstr Surg. 2011;127(3):37e-56e.Brunicardi_Ch16_p0511-p0540.indd 53819/02/19 3:09 PM 539THE SKIN AND SUBCUTANEOUS TISSUECHAPTER 16 118. Siegle RJ, MacMillan J, Pollack S V. Infiltrative basal cell carcinoma: a nonsclerosing subtype. J Dermatol Surg Oncol. 1986;12(8):830-836. 119. Kimyai-Asadi A, Alam M, Goldberg LH, et al. Efficacy of narrowmargin excision of well-demarcated primary facial basal cell carcinomas. J Am Acad Dermatol. 2005;53(3):464-468. 120. Rowe DE, Carroll RJ, Day CL. Mohs surgery is the treat-ment of choice for recurrent (previously treated) basal cell carcinoma. J Dermatol Surg Oncol. 1989;15(4):424-431. A heavily referenced paper from 1989 demonstrating the effectiveness of Mohs micrographic surgery in local control of recurrent basal cell carcinoma. 121. Rowe DE, Carroll RJ, Day CL. Long-term recurrence rates in previously untreated (primary)
|
Surgery_Schwartz_3657
|
Surgery_Schwartz
|
the effectiveness of Mohs micrographic surgery in local control of recurrent basal cell carcinoma. 121. Rowe DE, Carroll RJ, Day CL. Long-term recurrence rates in previously untreated (primary) basal cell carcinoma: implications for patient follow-up. J Dermatol Surg Oncol. 1989;15(3):315-328. 122. Geisse J, Caro I, Lindholm J, Golitz L, Stampone P, Owens M. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, random-ized, vehicle-controlled studies. J Am Acad Dermatol. 2004;50(5):722-733. A multicenter, randomized, parallel, vehicle-controlled, double-blind, phase III clinical study which showed that 5% imiquimod cream was an effective treatment for superficial BCC. 123. Marks R, Gebauer K, Shumack S, et al. Imiquimod 5% cream in the treatment of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial. J Am Acad Dermatol. 2001;44(5):807-813. 124. Schulze HJ, Cribier B, Requena L, et al. Imiquimod 5% cream
|
Surgery_Schwartz. the effectiveness of Mohs micrographic surgery in local control of recurrent basal cell carcinoma. 121. Rowe DE, Carroll RJ, Day CL. Long-term recurrence rates in previously untreated (primary) basal cell carcinoma: implications for patient follow-up. J Dermatol Surg Oncol. 1989;15(3):315-328. 122. Geisse J, Caro I, Lindholm J, Golitz L, Stampone P, Owens M. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from two phase III, random-ized, vehicle-controlled studies. J Am Acad Dermatol. 2004;50(5):722-733. A multicenter, randomized, parallel, vehicle-controlled, double-blind, phase III clinical study which showed that 5% imiquimod cream was an effective treatment for superficial BCC. 123. Marks R, Gebauer K, Shumack S, et al. Imiquimod 5% cream in the treatment of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial. J Am Acad Dermatol. 2001;44(5):807-813. 124. Schulze HJ, Cribier B, Requena L, et al. Imiquimod 5% cream
|
Surgery_Schwartz_3658
|
Surgery_Schwartz
|
of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial. J Am Acad Dermatol. 2001;44(5):807-813. 124. Schulze HJ, Cribier B, Requena L, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from a randomized vehicle-controlled phase III study in Europe. Br J Dermatol. 2005;152(5):939-947. 125. Shumack S, Robinson J, Kossard S, et al. Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens. Arch Dermatol. 2002;138(9):1165-1171. 126. Vidal D, Matías-Guiu X, Alomar A. Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma. Clin Exp Dermatol. 2004;29(5):518-525. 127. Rowe DE, Carroll RJ, Day CL. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992;26(6):976-990. 128. National
|
Surgery_Schwartz. of superficial basal cell carcinoma: results of a multicenter 6-week dose-response trial. J Am Acad Dermatol. 2001;44(5):807-813. 124. Schulze HJ, Cribier B, Requena L, et al. Imiquimod 5% cream for the treatment of superficial basal cell carcinoma: results from a randomized vehicle-controlled phase III study in Europe. Br J Dermatol. 2005;152(5):939-947. 125. Shumack S, Robinson J, Kossard S, et al. Efficacy of topical 5% imiquimod cream for the treatment of nodular basal cell carcinoma: comparison of dosing regimens. Arch Dermatol. 2002;138(9):1165-1171. 126. Vidal D, Matías-Guiu X, Alomar A. Open study of the efficacy and mechanism of action of topical imiquimod in basal cell carcinoma. Clin Exp Dermatol. 2004;29(5):518-525. 127. Rowe DE, Carroll RJ, Day CL. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992;26(6):976-990. 128. National
|
Surgery_Schwartz_3659
|
Surgery_Schwartz
|
recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992;26(6):976-990. 128. National Comprehensive Cancer Network. Squamous cell carcinoma, National Comprehensive Cancer Network clini-cal practice guidelines in oncology, squamous cell carcinoma, version 1.2018. In: National Comprehensive Cancer Network. Fort Washington, PA; 2017. 129. Kao GF. Carcinoma arising in Bowen’s disease. Arch Derma-tol. 1986;122(10):1124-1126. 130. Cassarino DS, Derienzo DP, Barr RJ. Cutaneous squamous cell carcinoma: a comprehensive clinicopathologic classifica-tion. Part one. J Cutan Pathol. 2006;33(3):191-206. 131. Schwartz RA. Keratoacanthoma. J Am Acad Dermatol. 1994;30(1):1-19. 132. Balch CM, Soong SJ, Gershenwald JE, et al. Prognostic factors analysis of 17,600 melanoma patients: validation of the American Joint Committee on Cancer melanoma staging system. J Clin Oncol.
|
Surgery_Schwartz. recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992;26(6):976-990. 128. National Comprehensive Cancer Network. Squamous cell carcinoma, National Comprehensive Cancer Network clini-cal practice guidelines in oncology, squamous cell carcinoma, version 1.2018. In: National Comprehensive Cancer Network. Fort Washington, PA; 2017. 129. Kao GF. Carcinoma arising in Bowen’s disease. Arch Derma-tol. 1986;122(10):1124-1126. 130. Cassarino DS, Derienzo DP, Barr RJ. Cutaneous squamous cell carcinoma: a comprehensive clinicopathologic classifica-tion. Part one. J Cutan Pathol. 2006;33(3):191-206. 131. Schwartz RA. Keratoacanthoma. J Am Acad Dermatol. 1994;30(1):1-19. 132. Balch CM, Soong SJ, Gershenwald JE, et al. Prognostic factors analysis of 17,600 melanoma patients: validation of the American Joint Committee on Cancer melanoma staging system. J Clin Oncol.
|
Surgery_Schwartz_3660
|
Surgery_Schwartz
|
CM, Soong SJ, Gershenwald JE, et al. Prognostic factors analysis of 17,600 melanoma patients: validation of the American Joint Committee on Cancer melanoma staging system. J Clin Oncol. 2001;19(16):3622-3634. This paper looked at over 17,000 melanoma patients in 2001, validating the AJCC TNM staging system for melanoma. 133. Cust AE, Armstrong BK, Goumas C, et al. Sunbed use dur-ing adolescence and early adulthood is associated with increased risk of early-onset melanoma. Int J Cancer. 2011;128(10):2425-2435. 134. Elwood JM, Jopson J. Melanoma and sun exposure: an over-view of published studies. Int J Cancer. 1997;73(2):198-203. 135. Chudnovsky Y, Khavari PA, Adams AE. Melanoma genetics and the development of rational therapeutics. J Clin Invest. 2005;115(4):813-824. 136. National Comprehensive Cancer Network. Melanoma, National Comprehensive Cancer Network clinical practice guidelines in oncology, melanoma, Version 1.2017. In: National Compre-hensive Cancer Network. Fort Washington,
|
Surgery_Schwartz. CM, Soong SJ, Gershenwald JE, et al. Prognostic factors analysis of 17,600 melanoma patients: validation of the American Joint Committee on Cancer melanoma staging system. J Clin Oncol. 2001;19(16):3622-3634. This paper looked at over 17,000 melanoma patients in 2001, validating the AJCC TNM staging system for melanoma. 133. Cust AE, Armstrong BK, Goumas C, et al. Sunbed use dur-ing adolescence and early adulthood is associated with increased risk of early-onset melanoma. Int J Cancer. 2011;128(10):2425-2435. 134. Elwood JM, Jopson J. Melanoma and sun exposure: an over-view of published studies. Int J Cancer. 1997;73(2):198-203. 135. Chudnovsky Y, Khavari PA, Adams AE. Melanoma genetics and the development of rational therapeutics. J Clin Invest. 2005;115(4):813-824. 136. National Comprehensive Cancer Network. Melanoma, National Comprehensive Cancer Network clinical practice guidelines in oncology, melanoma, Version 1.2017. In: National Compre-hensive Cancer Network. Fort Washington,
|
Surgery_Schwartz_3661
|
Surgery_Schwartz
|
Cancer Network. Melanoma, National Comprehensive Cancer Network clinical practice guidelines in oncology, melanoma, Version 1.2017. In: National Compre-hensive Cancer Network. Fort Washington, PA; 2016. 137. Basler GC, Fader DJ, Yahanda A, Sondak VK, Johnson TM. The utility of fine needle aspiration in the diagnosis of melanoma metastatic to lymph nodes. J Am Acad Dermatol. 1997;36(3 pt 1):403-408. 138. Hall BJ, Schmidt RL, Sharma RR, Layfield LJ. Fine-needle aspiration cytology for the diagnosis of metastatic melanoma: systematic review and meta-analysis. Am J Clin Pathol. 2013;140(5):635-642. 139. Cangiarella J, Symmans WF, Shapiro RL, et al. Aspiration biopsy and the clinical management of patients with malig-nant melanoma and palpable regional lymph nodes. Cancer. 2000;90(3):162-166. 140. Balch CM, Gershenwald JE, Soong S, et al. Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol. 2009;27(36):6199-6206. 141. Weide B, Elsässer M, Büttner P, et al. Serum
|
Surgery_Schwartz. Cancer Network. Melanoma, National Comprehensive Cancer Network clinical practice guidelines in oncology, melanoma, Version 1.2017. In: National Compre-hensive Cancer Network. Fort Washington, PA; 2016. 137. Basler GC, Fader DJ, Yahanda A, Sondak VK, Johnson TM. The utility of fine needle aspiration in the diagnosis of melanoma metastatic to lymph nodes. J Am Acad Dermatol. 1997;36(3 pt 1):403-408. 138. Hall BJ, Schmidt RL, Sharma RR, Layfield LJ. Fine-needle aspiration cytology for the diagnosis of metastatic melanoma: systematic review and meta-analysis. Am J Clin Pathol. 2013;140(5):635-642. 139. Cangiarella J, Symmans WF, Shapiro RL, et al. Aspiration biopsy and the clinical management of patients with malig-nant melanoma and palpable regional lymph nodes. Cancer. 2000;90(3):162-166. 140. Balch CM, Gershenwald JE, Soong S, et al. Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol. 2009;27(36):6199-6206. 141. Weide B, Elsässer M, Büttner P, et al. Serum
|
Surgery_Schwartz_3662
|
Surgery_Schwartz
|
CM, Gershenwald JE, Soong S, et al. Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol. 2009;27(36):6199-6206. 141. Weide B, Elsässer M, Büttner P, et al. Serum markers lactate dehydrogenase and S100B predict independently disease outcome in melanoma patients with distant metastasis. Br J Cancer. 2012;107(3):422-428. 142. Morton DL, Thompson JF, Cochran AJ, et al. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. N Engl J Med. 2014;370(7):599-609. This was a phase 3 trial evaluating outcomes in 2001 patients with primary cutaneous melanoma that demonstrated the use-fulness of SLN biopsy in patients with thick and interme-diate-thickness melanoma. 143. Duffy KL, Truong A, Bowen GM, et al. Adequacy of 5-mm surgical excision margins for non-lentiginous melanoma in situ. J Am Acad Dermatol. 2014;71(4):835-838. 144. Akhtar S, Bhat W, Magdum A, Stanley PR. Surgical excision margins for melanoma in situ. J Plast Reconstr Aesthetic
|
Surgery_Schwartz. CM, Gershenwald JE, Soong S, et al. Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol. 2009;27(36):6199-6206. 141. Weide B, Elsässer M, Büttner P, et al. Serum markers lactate dehydrogenase and S100B predict independently disease outcome in melanoma patients with distant metastasis. Br J Cancer. 2012;107(3):422-428. 142. Morton DL, Thompson JF, Cochran AJ, et al. Final trial report of sentinel-node biopsy versus nodal observation in melanoma. N Engl J Med. 2014;370(7):599-609. This was a phase 3 trial evaluating outcomes in 2001 patients with primary cutaneous melanoma that demonstrated the use-fulness of SLN biopsy in patients with thick and interme-diate-thickness melanoma. 143. Duffy KL, Truong A, Bowen GM, et al. Adequacy of 5-mm surgical excision margins for non-lentiginous melanoma in situ. J Am Acad Dermatol. 2014;71(4):835-838. 144. Akhtar S, Bhat W, Magdum A, Stanley PR. Surgical excision margins for melanoma in situ. J Plast Reconstr Aesthetic
|
Surgery_Schwartz_3663
|
Surgery_Schwartz
|
for non-lentiginous melanoma in situ. J Am Acad Dermatol. 2014;71(4):835-838. 144. Akhtar S, Bhat W, Magdum A, Stanley PR. Surgical excision margins for melanoma in situ. J Plast Reconstr Aesthetic Surg. 2014;67(3):320-323. 145. Felton S, Taylor RS, Srivastava D. Excision margins for melanoma in situ on the head and neck. Dermatologic Surg. 2016;42(3):327-334. 146. Veronesi U, Cascinelli N, Adamus J, et al. Thin stage I primary cutaneous malignant melanoma. N Engl J Med. 1988;318(18):1159-1162. 147. Cohn-Cedermark G, Rutqvist LE, Andersson R, et al. Long term results of a randomized study by the Swedish Melanoma Study Group on 2-cm versus 5-cm resection margins for patients with cutaneous melanoma with a tumor thickness of 0.8-2.0 mm. Cancer. 2000;89(7):1495-1501. 148. Balch CM, Soong SJ, Smith T, et al. Long-term results of a prospective surgical trial comparing 2 cm vs. 4 cm excision margins for 740 patients with 1-4 mm melanomas. Ann Surg Oncol. 2001;8(2):101-108. 149. Balch CM,
|
Surgery_Schwartz. for non-lentiginous melanoma in situ. J Am Acad Dermatol. 2014;71(4):835-838. 144. Akhtar S, Bhat W, Magdum A, Stanley PR. Surgical excision margins for melanoma in situ. J Plast Reconstr Aesthetic Surg. 2014;67(3):320-323. 145. Felton S, Taylor RS, Srivastava D. Excision margins for melanoma in situ on the head and neck. Dermatologic Surg. 2016;42(3):327-334. 146. Veronesi U, Cascinelli N, Adamus J, et al. Thin stage I primary cutaneous malignant melanoma. N Engl J Med. 1988;318(18):1159-1162. 147. Cohn-Cedermark G, Rutqvist LE, Andersson R, et al. Long term results of a randomized study by the Swedish Melanoma Study Group on 2-cm versus 5-cm resection margins for patients with cutaneous melanoma with a tumor thickness of 0.8-2.0 mm. Cancer. 2000;89(7):1495-1501. 148. Balch CM, Soong SJ, Smith T, et al. Long-term results of a prospective surgical trial comparing 2 cm vs. 4 cm excision margins for 740 patients with 1-4 mm melanomas. Ann Surg Oncol. 2001;8(2):101-108. 149. Balch CM,
|
Surgery_Schwartz_3664
|
Surgery_Schwartz
|
Smith T, et al. Long-term results of a prospective surgical trial comparing 2 cm vs. 4 cm excision margins for 740 patients with 1-4 mm melanomas. Ann Surg Oncol. 2001;8(2):101-108. 149. Balch CM, Urist MM, Karakousis CP, et al. Efficacy of 2-cm surgical margins for intermediate-thickness melanomas (1 to 4 mm). Results of a multi-institutional randomized surgical trial. Ann Surg. 1993;218(3):262-269. 150. Hayes AJ, Maynard L, Coombes G, et al. Wide versus nar-row excision margins for high-risk, primary cutaneous mela-nomas: long-term follow-up of survival in a randomised trial. Lancet Oncol. 2016;17(2):184-192. A multicenter random-ized trial that demonstrated superiority of 3 cm margins over 1 cm margins for cutaneous melanoma >2 mm in thickness. 151. Beasley GM, Caudle A, Petersen RP, et al. A multi-institu-tional experience of isolated limb infusion: defining response and toxicity in the US. J Am Coll Surg. 2009;208(5):706-715.Brunicardi_Ch16_p0511-p0540.indd 53919/02/19 3:09
|
Surgery_Schwartz. Smith T, et al. Long-term results of a prospective surgical trial comparing 2 cm vs. 4 cm excision margins for 740 patients with 1-4 mm melanomas. Ann Surg Oncol. 2001;8(2):101-108. 149. Balch CM, Urist MM, Karakousis CP, et al. Efficacy of 2-cm surgical margins for intermediate-thickness melanomas (1 to 4 mm). Results of a multi-institutional randomized surgical trial. Ann Surg. 1993;218(3):262-269. 150. Hayes AJ, Maynard L, Coombes G, et al. Wide versus nar-row excision margins for high-risk, primary cutaneous mela-nomas: long-term follow-up of survival in a randomised trial. Lancet Oncol. 2016;17(2):184-192. A multicenter random-ized trial that demonstrated superiority of 3 cm margins over 1 cm margins for cutaneous melanoma >2 mm in thickness. 151. Beasley GM, Caudle A, Petersen RP, et al. A multi-institu-tional experience of isolated limb infusion: defining response and toxicity in the US. J Am Coll Surg. 2009;208(5):706-715.Brunicardi_Ch16_p0511-p0540.indd 53919/02/19 3:09
|
Surgery_Schwartz_3665
|
Surgery_Schwartz
|
et al. A multi-institu-tional experience of isolated limb infusion: defining response and toxicity in the US. J Am Coll Surg. 2009;208(5):706-715.Brunicardi_Ch16_p0511-p0540.indd 53919/02/19 3:09 PM 540SPECIFIC CONSIDERATIONSPART II 152. Boesch CE, Meyer T, Waschke L, et al. Long-term outcome of hyperthermic isolated limb perfusion (HILP) in the treat-ment of locoregionally metastasised malignant melanoma of the extremities. Int J Hyperthermia. 2010;26(1):16-20. 153. Lindnér P, Doubrovsky A, Kam PCA, Thompson JF. Prognos-tic factors after isolated limb infusion with cytotoxic agents for melanoma. Ann Surg Oncol. 2002;9(2):127-136. 154. Lens MB, Dawes M. Isolated limb perfusion with melphalan in the treatment of malignant melanoma of the extremities: a systematic review of randomised controlled trials. Lancet Oncol. 2003;4(6):359-364. 155. Kirkwood JM, Manola J, Ibrahim J, et al. A pooled analy-sis of eastern cooperative oncology group and intergroup trials of adjuvant high-dose
|
Surgery_Schwartz. et al. A multi-institu-tional experience of isolated limb infusion: defining response and toxicity in the US. J Am Coll Surg. 2009;208(5):706-715.Brunicardi_Ch16_p0511-p0540.indd 53919/02/19 3:09 PM 540SPECIFIC CONSIDERATIONSPART II 152. Boesch CE, Meyer T, Waschke L, et al. Long-term outcome of hyperthermic isolated limb perfusion (HILP) in the treat-ment of locoregionally metastasised malignant melanoma of the extremities. Int J Hyperthermia. 2010;26(1):16-20. 153. Lindnér P, Doubrovsky A, Kam PCA, Thompson JF. Prognos-tic factors after isolated limb infusion with cytotoxic agents for melanoma. Ann Surg Oncol. 2002;9(2):127-136. 154. Lens MB, Dawes M. Isolated limb perfusion with melphalan in the treatment of malignant melanoma of the extremities: a systematic review of randomised controlled trials. Lancet Oncol. 2003;4(6):359-364. 155. Kirkwood JM, Manola J, Ibrahim J, et al. A pooled analy-sis of eastern cooperative oncology group and intergroup trials of adjuvant high-dose
|
Surgery_Schwartz_3666
|
Surgery_Schwartz
|
controlled trials. Lancet Oncol. 2003;4(6):359-364. 155. Kirkwood JM, Manola J, Ibrahim J, et al. A pooled analy-sis of eastern cooperative oncology group and intergroup trials of adjuvant high-dose interferon for melanoma. Clin Cancer Res. 2004;10(5):1670-1677. A multicenter, random-ized trial that demonstrated high-dose interferon may be effective as an adjuvant treatment for melanoma. 156. Kirkwood JM, Strawderman MH, Ernstoff MS, Smith TJ, Borden EC, Blum RH. Interferon alfa-2b adjuvant therapy of high-risk resected cutaneous melanoma: the Eastern Cooperative Oncology Group Trial EST 1684. J Clin Oncol. 1996;14(1):7-17. 157. Kirkwood JM, Ibrahim JG, Sondak VK, et al. Highand low-dose interferon alfa-2b in high-risk melanoma: first analy-sis of intergroup trial E1690/S9111/C9190. J Clin Oncol. 2000;18(12):2444-2458. 158. Eggermont AMM, Suciu S, Santinami M, et al. Adjuvant ther-apy with pegylated interferon alfa-2b versus observation alone in resected stage III melanoma: final
|
Surgery_Schwartz. controlled trials. Lancet Oncol. 2003;4(6):359-364. 155. Kirkwood JM, Manola J, Ibrahim J, et al. A pooled analy-sis of eastern cooperative oncology group and intergroup trials of adjuvant high-dose interferon for melanoma. Clin Cancer Res. 2004;10(5):1670-1677. A multicenter, random-ized trial that demonstrated high-dose interferon may be effective as an adjuvant treatment for melanoma. 156. Kirkwood JM, Strawderman MH, Ernstoff MS, Smith TJ, Borden EC, Blum RH. Interferon alfa-2b adjuvant therapy of high-risk resected cutaneous melanoma: the Eastern Cooperative Oncology Group Trial EST 1684. J Clin Oncol. 1996;14(1):7-17. 157. Kirkwood JM, Ibrahim JG, Sondak VK, et al. Highand low-dose interferon alfa-2b in high-risk melanoma: first analy-sis of intergroup trial E1690/S9111/C9190. J Clin Oncol. 2000;18(12):2444-2458. 158. Eggermont AMM, Suciu S, Santinami M, et al. Adjuvant ther-apy with pegylated interferon alfa-2b versus observation alone in resected stage III melanoma: final
|
Surgery_Schwartz_3667
|
Surgery_Schwartz
|
Clin Oncol. 2000;18(12):2444-2458. 158. Eggermont AMM, Suciu S, Santinami M, et al. Adjuvant ther-apy with pegylated interferon alfa-2b versus observation alone in resected stage III melanoma: final results of EORTC 18991, a randomised phase III trial. Lancet (London, England). 2008;372(9633):117-126. 159. Flaherty LE, Othus M, Atkins MB, et al. Southwest Oncology Group S0008: A phase III trial of high-dose interferon alfa-2b versus cisplatin, vinblastine, and dacarbazine, plus interleu-kin-2 and interferon in patients with high-risk melanoma— an Intergroup Study of Cancer and Leukemia Group B, Children’s Oncology Group, Eastern Cooperative Oncology Group, and Southwest Oncology Group. J Clin Oncol. 2014; 32(33):3771-3778. 160. Eggermont AMM, Chiarion-Sileni V, Grob J-J, et al. Adjuvant ipilimumab versus placebo after complete resection of high-risk stage III melanoma (EORTC 18071): a randomised, doubleblind, phase 3 trial. Lancet Oncol. 2015;16(5):522-530. 161. Atkins MB, Lotze MT,
|
Surgery_Schwartz. Clin Oncol. 2000;18(12):2444-2458. 158. Eggermont AMM, Suciu S, Santinami M, et al. Adjuvant ther-apy with pegylated interferon alfa-2b versus observation alone in resected stage III melanoma: final results of EORTC 18991, a randomised phase III trial. Lancet (London, England). 2008;372(9633):117-126. 159. Flaherty LE, Othus M, Atkins MB, et al. Southwest Oncology Group S0008: A phase III trial of high-dose interferon alfa-2b versus cisplatin, vinblastine, and dacarbazine, plus interleu-kin-2 and interferon in patients with high-risk melanoma— an Intergroup Study of Cancer and Leukemia Group B, Children’s Oncology Group, Eastern Cooperative Oncology Group, and Southwest Oncology Group. J Clin Oncol. 2014; 32(33):3771-3778. 160. Eggermont AMM, Chiarion-Sileni V, Grob J-J, et al. Adjuvant ipilimumab versus placebo after complete resection of high-risk stage III melanoma (EORTC 18071): a randomised, doubleblind, phase 3 trial. Lancet Oncol. 2015;16(5):522-530. 161. Atkins MB, Lotze MT,
|
Surgery_Schwartz_3668
|
Surgery_Schwartz
|
ipilimumab versus placebo after complete resection of high-risk stage III melanoma (EORTC 18071): a randomised, doubleblind, phase 3 trial. Lancet Oncol. 2015;16(5):522-530. 161. Atkins MB, Lotze MT, Dutcher JP, et al. High-dose recombi-nant interleukin 2 therapy for patients with metastatic mela-noma: analysis of 270 patients treated between 1985 and 1993. J Clin Oncol. 1999;17(7):2105-2116. 162. Chapman PB, Hauschild A, Robert C, et al. Improved sur-vival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-2516. A phase 3 clinical trial demonstrating effectiveness of vemurafenib in melanoma patients with BRAF V600E mutations. 163. Hodi FS, O’Day SJ, McDermott DF, et al. Improved survival with ipilimumab in patients with metastatic melanoma. N Engl J Med. 2010;363(8):711-723. A phase III clinical trial demonstrating some improvement in survival with the use of ipilimumab in the treatment of recalcitrant metastatic melanoma. 164. Smith FO, Downey
|
Surgery_Schwartz. ipilimumab versus placebo after complete resection of high-risk stage III melanoma (EORTC 18071): a randomised, doubleblind, phase 3 trial. Lancet Oncol. 2015;16(5):522-530. 161. Atkins MB, Lotze MT, Dutcher JP, et al. High-dose recombi-nant interleukin 2 therapy for patients with metastatic mela-noma: analysis of 270 patients treated between 1985 and 1993. J Clin Oncol. 1999;17(7):2105-2116. 162. Chapman PB, Hauschild A, Robert C, et al. Improved sur-vival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-2516. A phase 3 clinical trial demonstrating effectiveness of vemurafenib in melanoma patients with BRAF V600E mutations. 163. Hodi FS, O’Day SJ, McDermott DF, et al. Improved survival with ipilimumab in patients with metastatic melanoma. N Engl J Med. 2010;363(8):711-723. A phase III clinical trial demonstrating some improvement in survival with the use of ipilimumab in the treatment of recalcitrant metastatic melanoma. 164. Smith FO, Downey
|
Surgery_Schwartz_3669
|
Surgery_Schwartz
|
Med. 2010;363(8):711-723. A phase III clinical trial demonstrating some improvement in survival with the use of ipilimumab in the treatment of recalcitrant metastatic melanoma. 164. Smith FO, Downey SG, Klapper JA, et al. Treatment of meta-static melanoma using interleukin-2 alone or in conjunction with vaccines. Clin Cancer Res. 2008;14(17):5610-5618. 165. Rosenberg SA, Yang JC, Topalian SL, et al. Treatment of 283 consecutive patients with metastatic melanoma or renal cell cancer using high-dose bolus interleukin 2. JAMA. 271(12):907-913. 166. Albert DM, Ryan LM, Borden EC. Metastatic ocular and cutaneous melanoma: a comparison of patient characteris-tics and prognosis. Arch Ophthalmol (Chicago, Ill 1960). 1996;114(1):107-108. 167. Inskip PD, Devesa SS, Fraumeni JF. Trends in the incidence of ocular melanoma in the United States, 1974-1998. Cancer Causes Control. 2003;14(3):251-257. 168. Starr OD, Patel D V, Allen JP, McGhee CN. Iris melanoma: pathology, prognosis and surgical
|
Surgery_Schwartz. Med. 2010;363(8):711-723. A phase III clinical trial demonstrating some improvement in survival with the use of ipilimumab in the treatment of recalcitrant metastatic melanoma. 164. Smith FO, Downey SG, Klapper JA, et al. Treatment of meta-static melanoma using interleukin-2 alone or in conjunction with vaccines. Clin Cancer Res. 2008;14(17):5610-5618. 165. Rosenberg SA, Yang JC, Topalian SL, et al. Treatment of 283 consecutive patients with metastatic melanoma or renal cell cancer using high-dose bolus interleukin 2. JAMA. 271(12):907-913. 166. Albert DM, Ryan LM, Borden EC. Metastatic ocular and cutaneous melanoma: a comparison of patient characteris-tics and prognosis. Arch Ophthalmol (Chicago, Ill 1960). 1996;114(1):107-108. 167. Inskip PD, Devesa SS, Fraumeni JF. Trends in the incidence of ocular melanoma in the United States, 1974-1998. Cancer Causes Control. 2003;14(3):251-257. 168. Starr OD, Patel D V, Allen JP, McGhee CN. Iris melanoma: pathology, prognosis and surgical
|
Surgery_Schwartz_3670
|
Surgery_Schwartz
|
of ocular melanoma in the United States, 1974-1998. Cancer Causes Control. 2003;14(3):251-257. 168. Starr OD, Patel D V, Allen JP, McGhee CN. Iris melanoma: pathology, prognosis and surgical intervention. Clin Exp Ophthalmol. 2004;32(3):294-296. 169. Lemos BD, Storer BE, Iyer JG, et al. Pathologic nodal evalu-ation improves prognostic accuracy in Merkel cell carcinoma: analysis of 5823 cases as the basis of the first consensus stag-ing system. J Am Acad Dermatol. 2010;63(5):751-761. 170. Akhtar S, Oza KK, Wright J. Merkel cell carcinoma: report of 10 cases and review of the literature. J Am Acad Dermatol. 2000;43(5):755-767. 171. Medina-Franco H, Urist MM, Fiveash J, Heslin MJ, Bland KI, Beenken SW. Multimodality treatment of Merkel cell carci-noma: case series and literature review of 1024 cases. Ann Surg Oncol. 2001;8(3):204-208. 172. National Comprehensive Cancer Network. Merkel cell carcinoma. In: National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology,
|
Surgery_Schwartz. of ocular melanoma in the United States, 1974-1998. Cancer Causes Control. 2003;14(3):251-257. 168. Starr OD, Patel D V, Allen JP, McGhee CN. Iris melanoma: pathology, prognosis and surgical intervention. Clin Exp Ophthalmol. 2004;32(3):294-296. 169. Lemos BD, Storer BE, Iyer JG, et al. Pathologic nodal evalu-ation improves prognostic accuracy in Merkel cell carcinoma: analysis of 5823 cases as the basis of the first consensus stag-ing system. J Am Acad Dermatol. 2010;63(5):751-761. 170. Akhtar S, Oza KK, Wright J. Merkel cell carcinoma: report of 10 cases and review of the literature. J Am Acad Dermatol. 2000;43(5):755-767. 171. Medina-Franco H, Urist MM, Fiveash J, Heslin MJ, Bland KI, Beenken SW. Multimodality treatment of Merkel cell carci-noma: case series and literature review of 1024 cases. Ann Surg Oncol. 2001;8(3):204-208. 172. National Comprehensive Cancer Network. Merkel cell carcinoma. In: National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology,
|
Surgery_Schwartz_3671
|
Surgery_Schwartz
|
1024 cases. Ann Surg Oncol. 2001;8(3):204-208. 172. National Comprehensive Cancer Network. Merkel cell carcinoma. In: National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology, Merkel Cell Carcinoma Version 1.2018. Fort Washington, PA; 2017. 173. Bichakjian CK, Lowe L, Lao CD, et al. Merkel cell carcinoma: critical review with guidelines for multidisciplinary manage-ment. Cancer. 2007;110(1):1-12. 174. Ott MJ, Tanabe KK, Gadd MA, et al. Multimodal-ity management of Merkel cell carcinoma. Arch Surg. 1999;134(4):388-393. 175. Ramírez-Amador V, Anaya-Saavedra G, Martínez-Mata G. Kaposi’s sarcoma of the head and neck: a review. Oral Oncol. 2010;46(3):135-145. 176. Bower M, Weir J, Francis N, et al. The effect of HAART in 254 consecutive patients with AIDS-related Kaposi’s sarcoma. AIDS. 2009;23(13):1701-1706. 177. Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi’s sarcoma on HAART is associated with suppression of HIV replication and is independent of
|
Surgery_Schwartz. 1024 cases. Ann Surg Oncol. 2001;8(3):204-208. 172. National Comprehensive Cancer Network. Merkel cell carcinoma. In: National Comprehensive Cancer Network Clinical Practice Guidelines in Oncology, Merkel Cell Carcinoma Version 1.2018. Fort Washington, PA; 2017. 173. Bichakjian CK, Lowe L, Lao CD, et al. Merkel cell carcinoma: critical review with guidelines for multidisciplinary manage-ment. Cancer. 2007;110(1):1-12. 174. Ott MJ, Tanabe KK, Gadd MA, et al. Multimodal-ity management of Merkel cell carcinoma. Arch Surg. 1999;134(4):388-393. 175. Ramírez-Amador V, Anaya-Saavedra G, Martínez-Mata G. Kaposi’s sarcoma of the head and neck: a review. Oral Oncol. 2010;46(3):135-145. 176. Bower M, Weir J, Francis N, et al. The effect of HAART in 254 consecutive patients with AIDS-related Kaposi’s sarcoma. AIDS. 2009;23(13):1701-1706. 177. Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi’s sarcoma on HAART is associated with suppression of HIV replication and is independent of
|
Surgery_Schwartz_3672
|
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sarcoma. AIDS. 2009;23(13):1701-1706. 177. Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi’s sarcoma on HAART is associated with suppression of HIV replication and is independent of protease inhibitor therapy. Br J Cancer. 2006;94(7):1000-1006. 178. Aiba S, Tabata N, Ishii H, Ootani H, Tagami H. Dermatofi-brosarcoma protuberans is a unique fibrohistiocytic tumour expressing CD34. Br J Dermatol. 1992;127(2):79-84. 179. Abenoza P, Lillemoe T. CD34 and factor XIIIa in the differ-ential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans. Am J Dermatopathol. 1993;15(5):429-434. 180. Fields RC, Hameed M, Qin L-X, et al. Dermatofibrosarcoma protuberans (DFSP): predictors of recurrence and the use of systemic therapy. Ann Surg Oncol. 2011;18(2):328-336. 181. Meguerditchian A-N, Wang J, Lema B, Kraybill WG, Zeitouni NC, Kane JM 3rd. Wide excision or Mohs micrographic sur-gery for the treatment of primary dermatofibrosarcoma protu-berans. Am J Clin Oncol.
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Surgery_Schwartz. sarcoma. AIDS. 2009;23(13):1701-1706. 177. Martinez V, Caumes E, Gambotti L, et al. Remission from Kaposi’s sarcoma on HAART is associated with suppression of HIV replication and is independent of protease inhibitor therapy. Br J Cancer. 2006;94(7):1000-1006. 178. Aiba S, Tabata N, Ishii H, Ootani H, Tagami H. Dermatofi-brosarcoma protuberans is a unique fibrohistiocytic tumour expressing CD34. Br J Dermatol. 1992;127(2):79-84. 179. Abenoza P, Lillemoe T. CD34 and factor XIIIa in the differ-ential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans. Am J Dermatopathol. 1993;15(5):429-434. 180. Fields RC, Hameed M, Qin L-X, et al. Dermatofibrosarcoma protuberans (DFSP): predictors of recurrence and the use of systemic therapy. Ann Surg Oncol. 2011;18(2):328-336. 181. Meguerditchian A-N, Wang J, Lema B, Kraybill WG, Zeitouni NC, Kane JM 3rd. Wide excision or Mohs micrographic sur-gery for the treatment of primary dermatofibrosarcoma protu-berans. Am J Clin Oncol.
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A-N, Wang J, Lema B, Kraybill WG, Zeitouni NC, Kane JM 3rd. Wide excision or Mohs micrographic sur-gery for the treatment of primary dermatofibrosarcoma protu-berans. Am J Clin Oncol. 2009;33(3):1. 182. Requena L, Sangueza OP. Cutaneous vascular proliferations. Part III. Malignant neoplasms, other cutaneous neoplasms with significant vascular component, and disorders errone-ously considered as vascular neoplasms. J Am Acad Dermatol. 1998;38(2 pt 1):143-175. 183. Holden CA, Spittle MF, Jones EW. Angiosarcoma of the face and scalp, prognosis and treatment. Cancer. 1987;59(5):1046-1057. 184. Wagner G, Sachse MM. Extramammary Paget disease— clinical appearance, pathogenesis, management. JDDG J der Dtsch Dermatologischen Gesellschaft. 2011;9(6):448-454.Brunicardi_Ch16_p0511-p0540.indd 54019/02/19 3:09 PM
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Surgery_Schwartz. A-N, Wang J, Lema B, Kraybill WG, Zeitouni NC, Kane JM 3rd. Wide excision or Mohs micrographic sur-gery for the treatment of primary dermatofibrosarcoma protu-berans. Am J Clin Oncol. 2009;33(3):1. 182. Requena L, Sangueza OP. Cutaneous vascular proliferations. Part III. Malignant neoplasms, other cutaneous neoplasms with significant vascular component, and disorders errone-ously considered as vascular neoplasms. J Am Acad Dermatol. 1998;38(2 pt 1):143-175. 183. Holden CA, Spittle MF, Jones EW. Angiosarcoma of the face and scalp, prognosis and treatment. Cancer. 1987;59(5):1046-1057. 184. Wagner G, Sachse MM. Extramammary Paget disease— clinical appearance, pathogenesis, management. JDDG J der Dtsch Dermatologischen Gesellschaft. 2011;9(6):448-454.Brunicardi_Ch16_p0511-p0540.indd 54019/02/19 3:09 PM
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The BreastCatherine C. Parker, Senthil Damodaran, Kirby I. Bland, and Kelly K. Hunt 17chapterA BRIEF HISTORY OF BREAST CANCER THERAPYBreast cancer has captured the attention of surgeons throughout the ages. The Smith Surgical Papyrus (3000–2500 b.c.) is the earliest known document to refer to breast cancer. The cancer was in a man, but the description encompassed most of the common clinical features. In reference to this cancer, the author concluded, “There is no treatment.”1 There were few other historical references to breast cancer until the first century. In De Medicina, Celsus commented on the value of operations for early breast cancer: “None of these may be removed but the cacoethes (early cancer), the rest are irritated by every method of cure. The more violent the operations are, the more angry they grow.”2 In the second century, Galen inscribed his classical clinical observation: “We have often seen in the breast a tumor exactly resembling the animal the crab. Just as the
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Surgery_Schwartz. The BreastCatherine C. Parker, Senthil Damodaran, Kirby I. Bland, and Kelly K. Hunt 17chapterA BRIEF HISTORY OF BREAST CANCER THERAPYBreast cancer has captured the attention of surgeons throughout the ages. The Smith Surgical Papyrus (3000–2500 b.c.) is the earliest known document to refer to breast cancer. The cancer was in a man, but the description encompassed most of the common clinical features. In reference to this cancer, the author concluded, “There is no treatment.”1 There were few other historical references to breast cancer until the first century. In De Medicina, Celsus commented on the value of operations for early breast cancer: “None of these may be removed but the cacoethes (early cancer), the rest are irritated by every method of cure. The more violent the operations are, the more angry they grow.”2 In the second century, Galen inscribed his classical clinical observation: “We have often seen in the breast a tumor exactly resembling the animal the crab. Just as the
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the more angry they grow.”2 In the second century, Galen inscribed his classical clinical observation: “We have often seen in the breast a tumor exactly resembling the animal the crab. Just as the crab has legs on both sides of his body, so in this disease the veins extending out from the unnatural growth take the shape of a crab’s legs. We have often cured this disease in its early stages, but after it has reached a large size, no one has cured it. In all operations we attempt to excise the tumor in a circle where it borders on the healthy tissue.”3The Galenic system of medicine ascribed cancers to an excess of black bile and concluded that excision of a local bodily outbreak could not cure the systemic imbalance. Theories espoused by Galen dominated medicine until the Renaissance. In 1652, Tulp introduced the idea that cancer was contagious when he reported an elderly woman and her housemaid who both developed breast cancer (N. Tulp, Observationes medi-cae 1652). This single
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Surgery_Schwartz. the more angry they grow.”2 In the second century, Galen inscribed his classical clinical observation: “We have often seen in the breast a tumor exactly resembling the animal the crab. Just as the crab has legs on both sides of his body, so in this disease the veins extending out from the unnatural growth take the shape of a crab’s legs. We have often cured this disease in its early stages, but after it has reached a large size, no one has cured it. In all operations we attempt to excise the tumor in a circle where it borders on the healthy tissue.”3The Galenic system of medicine ascribed cancers to an excess of black bile and concluded that excision of a local bodily outbreak could not cure the systemic imbalance. Theories espoused by Galen dominated medicine until the Renaissance. In 1652, Tulp introduced the idea that cancer was contagious when he reported an elderly woman and her housemaid who both developed breast cancer (N. Tulp, Observationes medi-cae 1652). This single
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In 1652, Tulp introduced the idea that cancer was contagious when he reported an elderly woman and her housemaid who both developed breast cancer (N. Tulp, Observationes medi-cae 1652). This single incidence was accepted as conclusive A Brief History of Breast Cancer Therapy541Embryology and Functional Anatomy of the Breast543Embryology / 543Functional Anatomy / 544Physiology of the Breast547Breast Development and Function / 547Pregnancy, Lactation, and Senescence / 548Gynecomastia / 549Infectious and Inflammatory Disorders of the Breast550Bacterial Infection / 550Mycotic Infections / 550Hidradenitis Suppurativa / 550Mondor’s Disease / 550Common Benign Disorders and Diseases of the Breast551Aberrations of Normal Development and Involution / 551Pathology of Nonproliferative Disorders / 552Pathology of Proliferative Disorders Without Atypia / 553Pathology of Atypical Proliferative Diseases / 553Treatment of Selected Benign Breast Disorders and Diseases / 554Risk Factors for Breast
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Surgery_Schwartz. In 1652, Tulp introduced the idea that cancer was contagious when he reported an elderly woman and her housemaid who both developed breast cancer (N. Tulp, Observationes medi-cae 1652). This single incidence was accepted as conclusive A Brief History of Breast Cancer Therapy541Embryology and Functional Anatomy of the Breast543Embryology / 543Functional Anatomy / 544Physiology of the Breast547Breast Development and Function / 547Pregnancy, Lactation, and Senescence / 548Gynecomastia / 549Infectious and Inflammatory Disorders of the Breast550Bacterial Infection / 550Mycotic Infections / 550Hidradenitis Suppurativa / 550Mondor’s Disease / 550Common Benign Disorders and Diseases of the Breast551Aberrations of Normal Development and Involution / 551Pathology of Nonproliferative Disorders / 552Pathology of Proliferative Disorders Without Atypia / 553Pathology of Atypical Proliferative Diseases / 553Treatment of Selected Benign Breast Disorders and Diseases / 554Risk Factors for Breast
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/ 552Pathology of Proliferative Disorders Without Atypia / 553Pathology of Atypical Proliferative Diseases / 553Treatment of Selected Benign Breast Disorders and Diseases / 554Risk Factors for Breast Cancer555Hormonal and Nonhormonal Risk Factors / 555Risk Assessment Models / 555Risk Management / 556BRCA Mutations / 558Epidemiology and Natural History of Breast Cancer561Epidemiology / 561Natural History / 562Histopathology of Breast Cancer563Carcinoma In Situ / 563Invasive Breast Carcinoma / 565Diagnosis of Breast Cancer567Examination / 567Imaging Techniques / 567Breast Biopsy / 574Breast Cancer Staging and Biomarkers575Breast Cancer Staging / 575Biomarkers / 575Overview of Breast Cancer Therapy580In Situ Breast Cancer (Stage 0) / 580Early Invasive Breast Cancer (Stage I, IIA, or IIB) / 582Advanced Local-Regional Breast Cancer (Stage IIIA or IIIB) / 585Internal Mammary Lymph Nodes / 587Distant Metastases (Stage IV) / 587Local-Regional Recurrence / 587Breast Cancer Prognosis /
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Surgery_Schwartz. / 552Pathology of Proliferative Disorders Without Atypia / 553Pathology of Atypical Proliferative Diseases / 553Treatment of Selected Benign Breast Disorders and Diseases / 554Risk Factors for Breast Cancer555Hormonal and Nonhormonal Risk Factors / 555Risk Assessment Models / 555Risk Management / 556BRCA Mutations / 558Epidemiology and Natural History of Breast Cancer561Epidemiology / 561Natural History / 562Histopathology of Breast Cancer563Carcinoma In Situ / 563Invasive Breast Carcinoma / 565Diagnosis of Breast Cancer567Examination / 567Imaging Techniques / 567Breast Biopsy / 574Breast Cancer Staging and Biomarkers575Breast Cancer Staging / 575Biomarkers / 575Overview of Breast Cancer Therapy580In Situ Breast Cancer (Stage 0) / 580Early Invasive Breast Cancer (Stage I, IIA, or IIB) / 582Advanced Local-Regional Breast Cancer (Stage IIIA or IIIB) / 585Internal Mammary Lymph Nodes / 587Distant Metastases (Stage IV) / 587Local-Regional Recurrence / 587Breast Cancer Prognosis /
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IIB) / 582Advanced Local-Regional Breast Cancer (Stage IIIA or IIIB) / 585Internal Mammary Lymph Nodes / 587Distant Metastases (Stage IV) / 587Local-Regional Recurrence / 587Breast Cancer Prognosis / 587Surgical Techniques in Breast Cancer Therapy588Excisional Biopsy With Needle Localization / 588Sentinel Lymph Node Dissection / 590Breast Conservation / 591Mastectomy and Axillary Dissection / 591Modified Radical Mastectomy / 592Reconstruction of the Breast and Chest Wall / 593Nonsurgical Breast Cancer Therapies594Radiation Therapy / 594Chemotherapy Adjuvant / 594Antiestrogen Therapy / 597Ablative Endocrine Therapy / 598Anti-HER2 Therapy / 598Special Clinical Situations599Nipple Discharge / 599Axillary Lymph Node Metastases in the Setting of an Unknown Primary Cancer / 600Breast Cancer During Pregnancy / 600Male Breast Cancer / 600Phyllodes Tumors / 600Inflammatory Breast Carcinoma / 601Rare Breast Cancers / 602Brunicardi_Ch17_p0541-p0612.indd 54101/03/19 5:04 PM 542evidence
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Surgery_Schwartz. IIB) / 582Advanced Local-Regional Breast Cancer (Stage IIIA or IIIB) / 585Internal Mammary Lymph Nodes / 587Distant Metastases (Stage IV) / 587Local-Regional Recurrence / 587Breast Cancer Prognosis / 587Surgical Techniques in Breast Cancer Therapy588Excisional Biopsy With Needle Localization / 588Sentinel Lymph Node Dissection / 590Breast Conservation / 591Mastectomy and Axillary Dissection / 591Modified Radical Mastectomy / 592Reconstruction of the Breast and Chest Wall / 593Nonsurgical Breast Cancer Therapies594Radiation Therapy / 594Chemotherapy Adjuvant / 594Antiestrogen Therapy / 597Ablative Endocrine Therapy / 598Anti-HER2 Therapy / 598Special Clinical Situations599Nipple Discharge / 599Axillary Lymph Node Metastases in the Setting of an Unknown Primary Cancer / 600Breast Cancer During Pregnancy / 600Male Breast Cancer / 600Phyllodes Tumors / 600Inflammatory Breast Carcinoma / 601Rare Breast Cancers / 602Brunicardi_Ch17_p0541-p0612.indd 54101/03/19 5:04 PM 542evidence
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During Pregnancy / 600Male Breast Cancer / 600Phyllodes Tumors / 600Inflammatory Breast Carcinoma / 601Rare Breast Cancers / 602Brunicardi_Ch17_p0541-p0612.indd 54101/03/19 5:04 PM 542evidence and started an idea which persisted into the 20th century among some lay people. The majority of respected sur-geons considered operative intervention to be a futile and ill-advised endeavor. The Renaissance and the wars of the 16th and 17th centuries brought developments in surgery, particularly in anatomical understanding. However, there were no new theories espoused in relation to cancer. Beginning with Morgagni, surgi-cal resections were more frequently undertaken, including some early attempts at mastectomy and axillary dissection. The 17th century saw the start of the Age of Enlightenment, which lasted until the 19th century. In terms of medicine, this resulted in the abandonment of Galen’s humoral pathology, which was repudi-ated by Le Dran, and the subsequent rise in cellular
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Surgery_Schwartz. During Pregnancy / 600Male Breast Cancer / 600Phyllodes Tumors / 600Inflammatory Breast Carcinoma / 601Rare Breast Cancers / 602Brunicardi_Ch17_p0541-p0612.indd 54101/03/19 5:04 PM 542evidence and started an idea which persisted into the 20th century among some lay people. The majority of respected sur-geons considered operative intervention to be a futile and ill-advised endeavor. The Renaissance and the wars of the 16th and 17th centuries brought developments in surgery, particularly in anatomical understanding. However, there were no new theories espoused in relation to cancer. Beginning with Morgagni, surgi-cal resections were more frequently undertaken, including some early attempts at mastectomy and axillary dissection. The 17th century saw the start of the Age of Enlightenment, which lasted until the 19th century. In terms of medicine, this resulted in the abandonment of Galen’s humoral pathology, which was repudi-ated by Le Dran, and the subsequent rise in cellular
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which lasted until the 19th century. In terms of medicine, this resulted in the abandonment of Galen’s humoral pathology, which was repudi-ated by Le Dran, and the subsequent rise in cellular pathology as espoused by Virchow. Le Dran stated that breast cancer was a local disease that spread by way of lymph vessels to axillary lymph nodes. When operating on a woman with breast cancer, he routinely removed any enlarged axillary lymph nodes.4In the 19th century, Moore, of the Middlesex Hospital, London, emphasized complete resection of the breast for cancer and stated that palpable axillary lymph nodes also should be removed.5 In a presentation before the British Medical Asso-ciation in 1877, Banks supported Moore’s concepts and advo-cated the resection of axillary lymph nodes even when palpable lymphadenopathy was not evident, recognizing that occult involvement of axillary lymph nodes was frequently present. In 1894, Halsted and Meyer reported their operations for treatment of breast
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Surgery_Schwartz. which lasted until the 19th century. In terms of medicine, this resulted in the abandonment of Galen’s humoral pathology, which was repudi-ated by Le Dran, and the subsequent rise in cellular pathology as espoused by Virchow. Le Dran stated that breast cancer was a local disease that spread by way of lymph vessels to axillary lymph nodes. When operating on a woman with breast cancer, he routinely removed any enlarged axillary lymph nodes.4In the 19th century, Moore, of the Middlesex Hospital, London, emphasized complete resection of the breast for cancer and stated that palpable axillary lymph nodes also should be removed.5 In a presentation before the British Medical Asso-ciation in 1877, Banks supported Moore’s concepts and advo-cated the resection of axillary lymph nodes even when palpable lymphadenopathy was not evident, recognizing that occult involvement of axillary lymph nodes was frequently present. In 1894, Halsted and Meyer reported their operations for treatment of breast
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lymphadenopathy was not evident, recognizing that occult involvement of axillary lymph nodes was frequently present. In 1894, Halsted and Meyer reported their operations for treatment of breast cancer.6 By demonstrating superior local-regional con-trol rates after radical resection, these surgeons established radi-cal mastectomy as state-of-the-art treatment for that era. Halsted and Meyer advocated complete dissection of axillary lymph node levels I to III. Both routinely resected the long thoracic nerve and the thoracodorsal neurovascular bundle with the axil-lary contents. In 1943, Haagensen and Stout described the grave signs of breast cancer, which included: (a) edema of the skin of the breast, (b) skin ulceration, (c) chest wall fixation, (d) an axillary lymph node >2.5 cm in diameter, and (e) fixed axillary lymph nodes. Women with two or more signs had a 42% local recurrence rate and only a 2% 5-year disease-free survival rate.7 Based on these findings, they declared that women
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Surgery_Schwartz. lymphadenopathy was not evident, recognizing that occult involvement of axillary lymph nodes was frequently present. In 1894, Halsted and Meyer reported their operations for treatment of breast cancer.6 By demonstrating superior local-regional con-trol rates after radical resection, these surgeons established radi-cal mastectomy as state-of-the-art treatment for that era. Halsted and Meyer advocated complete dissection of axillary lymph node levels I to III. Both routinely resected the long thoracic nerve and the thoracodorsal neurovascular bundle with the axil-lary contents. In 1943, Haagensen and Stout described the grave signs of breast cancer, which included: (a) edema of the skin of the breast, (b) skin ulceration, (c) chest wall fixation, (d) an axillary lymph node >2.5 cm in diameter, and (e) fixed axillary lymph nodes. Women with two or more signs had a 42% local recurrence rate and only a 2% 5-year disease-free survival rate.7 Based on these findings, they declared that women
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and (e) fixed axillary lymph nodes. Women with two or more signs had a 42% local recurrence rate and only a 2% 5-year disease-free survival rate.7 Based on these findings, they declared that women with grave signs were beyond cure by radical surgery. In 1948, Patey and Dyson of the Middlesex Hospital, London, advocated a modi-fied radical mastectomy for the management of advanced oper-able breast cancer, explaining, “Until an effective general agent for treatment of carcinoma of the breast is developed, a high proportion of these cases are doomed to die.”8 Their technique included removal of the breast and axillary lymph nodes with preservation of the pectoralis major muscle. They showed that removal of the pectoralis minor muscle allowed access to and clearance of axillary lymph node levels I to III.During the 1970s, there was a transition from the Halsted radical mastectomy to the modified radical mastectomy as the surgical procedure most frequently used by American surgeons to
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Surgery_Schwartz. and (e) fixed axillary lymph nodes. Women with two or more signs had a 42% local recurrence rate and only a 2% 5-year disease-free survival rate.7 Based on these findings, they declared that women with grave signs were beyond cure by radical surgery. In 1948, Patey and Dyson of the Middlesex Hospital, London, advocated a modi-fied radical mastectomy for the management of advanced oper-able breast cancer, explaining, “Until an effective general agent for treatment of carcinoma of the breast is developed, a high proportion of these cases are doomed to die.”8 Their technique included removal of the breast and axillary lymph nodes with preservation of the pectoralis major muscle. They showed that removal of the pectoralis minor muscle allowed access to and clearance of axillary lymph node levels I to III.During the 1970s, there was a transition from the Halsted radical mastectomy to the modified radical mastectomy as the surgical procedure most frequently used by American surgeons to
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levels I to III.During the 1970s, there was a transition from the Halsted radical mastectomy to the modified radical mastectomy as the surgical procedure most frequently used by American surgeons to treat breast cancer. This transition acknowledged that: (a) fewer patients were presenting with advanced local disease with or without the grave signs described by Haagensen, (b) extirpation of the pectoralis major muscle was not essential for local-regional control in stages I and II breast cancer, and (c) neither the modified radical mastectomy nor the Halsted radi-cal mastectomy consistently achieved local-regional control of stage III breast cancer. Radiation therapy was incorporated into the management of advanced breast cancer and demonstrated improvements in local-regional control. The National Surgical Key Points1 The breast receives its principal blood supply from per-forating branches of the internal mammary artery, lateral branches of the posterior intercostal arteries, and
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Surgery_Schwartz. levels I to III.During the 1970s, there was a transition from the Halsted radical mastectomy to the modified radical mastectomy as the surgical procedure most frequently used by American surgeons to treat breast cancer. This transition acknowledged that: (a) fewer patients were presenting with advanced local disease with or without the grave signs described by Haagensen, (b) extirpation of the pectoralis major muscle was not essential for local-regional control in stages I and II breast cancer, and (c) neither the modified radical mastectomy nor the Halsted radi-cal mastectomy consistently achieved local-regional control of stage III breast cancer. Radiation therapy was incorporated into the management of advanced breast cancer and demonstrated improvements in local-regional control. The National Surgical Key Points1 The breast receives its principal blood supply from per-forating branches of the internal mammary artery, lateral branches of the posterior intercostal arteries, and
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The National Surgical Key Points1 The breast receives its principal blood supply from per-forating branches of the internal mammary artery, lateral branches of the posterior intercostal arteries, and branches from the axillary artery, including the highest thoracic, lat-eral thoracic, and pectoral branches of the thoracoacromial artery.2 The axillary lymph nodes usually receive >75% of the lymph drainage from the breast, and the rest flows through the lymph vessels that accompany the perforating branches of the internal mammary artery and enters the parasternal (internal mammary) group of lymph nodes.3 Breast development and function are initiated by a variety of hormonal stimuli, with the major trophic effects being modulated by estrogen, progesterone, and prolactin.4 Benign breast disorders and diseases are related to the nor-mal processes of reproductive life and to involution, and there is a spectrum of breast conditions that ranges from normal to disorder to disease (aberrations
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Surgery_Schwartz. The National Surgical Key Points1 The breast receives its principal blood supply from per-forating branches of the internal mammary artery, lateral branches of the posterior intercostal arteries, and branches from the axillary artery, including the highest thoracic, lat-eral thoracic, and pectoral branches of the thoracoacromial artery.2 The axillary lymph nodes usually receive >75% of the lymph drainage from the breast, and the rest flows through the lymph vessels that accompany the perforating branches of the internal mammary artery and enters the parasternal (internal mammary) group of lymph nodes.3 Breast development and function are initiated by a variety of hormonal stimuli, with the major trophic effects being modulated by estrogen, progesterone, and prolactin.4 Benign breast disorders and diseases are related to the nor-mal processes of reproductive life and to involution, and there is a spectrum of breast conditions that ranges from normal to disorder to disease (aberrations
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and diseases are related to the nor-mal processes of reproductive life and to involution, and there is a spectrum of breast conditions that ranges from normal to disorder to disease (aberrations of normal devel-opment and involution classification).5 To calculate breast cancer risk using the Gail model, a woman’s risk factors are translated into an overall risk score by multiplying her relative risks from several cat-egories. This risk score is then compared with an adjusted population risk of breast cancer to determine the wom-an’s individual risk. This model is not appropriate for use in women with a known BRCA1 or BRCA2 mutation or women with lobular or ductal carcinoma in situ.6 Routine use of screening mammography in women ≥50 years of age reduces mortality from breast cancer by 25%. Magnetic resonance imaging (MRI) screening is recom-mended in women with BRCA mutations and may be con-sidered in women with a greater than 20% to 25% lifetime risk of developing breast
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Surgery_Schwartz. and diseases are related to the nor-mal processes of reproductive life and to involution, and there is a spectrum of breast conditions that ranges from normal to disorder to disease (aberrations of normal devel-opment and involution classification).5 To calculate breast cancer risk using the Gail model, a woman’s risk factors are translated into an overall risk score by multiplying her relative risks from several cat-egories. This risk score is then compared with an adjusted population risk of breast cancer to determine the wom-an’s individual risk. This model is not appropriate for use in women with a known BRCA1 or BRCA2 mutation or women with lobular or ductal carcinoma in situ.6 Routine use of screening mammography in women ≥50 years of age reduces mortality from breast cancer by 25%. Magnetic resonance imaging (MRI) screening is recom-mended in women with BRCA mutations and may be con-sidered in women with a greater than 20% to 25% lifetime risk of developing breast
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by 25%. Magnetic resonance imaging (MRI) screening is recom-mended in women with BRCA mutations and may be con-sidered in women with a greater than 20% to 25% lifetime risk of developing breast cancer.7 Core-needle biopsy is the preferred method for diagnosis of palpable or nonpalpable breast abnormalities.8 When a diagnosis of breast cancer is made, the surgeon should determine the clinical stage, histologic characteris-tics, and appropriate biomarker levels before initiating local therapy.9 Sentinel node dissection is the preferred method for stag-ing of the regional lymph nodes in women with clinically node-negative invasive breast cancer. Axillary dissection may be avoided in women with one to two positive senti-nel nodes who are treated with breast conserving surgery, whole breast radiation, and systemic therapy.10 Local-regional and systemic therapy decisions for an indi-vidual patient with breast cancer are best made using a multidisciplinary treatment approach. The sequencing
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Surgery_Schwartz. by 25%. Magnetic resonance imaging (MRI) screening is recom-mended in women with BRCA mutations and may be con-sidered in women with a greater than 20% to 25% lifetime risk of developing breast cancer.7 Core-needle biopsy is the preferred method for diagnosis of palpable or nonpalpable breast abnormalities.8 When a diagnosis of breast cancer is made, the surgeon should determine the clinical stage, histologic characteris-tics, and appropriate biomarker levels before initiating local therapy.9 Sentinel node dissection is the preferred method for stag-ing of the regional lymph nodes in women with clinically node-negative invasive breast cancer. Axillary dissection may be avoided in women with one to two positive senti-nel nodes who are treated with breast conserving surgery, whole breast radiation, and systemic therapy.10 Local-regional and systemic therapy decisions for an indi-vidual patient with breast cancer are best made using a multidisciplinary treatment approach. The sequencing
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and systemic therapy.10 Local-regional and systemic therapy decisions for an indi-vidual patient with breast cancer are best made using a multidisciplinary treatment approach. The sequencing of therapies is dependent on patient and tumor related factors including breast cancer subtype.Brunicardi_Ch17_p0541-p0612.indd 54201/03/19 5:04 PM 543THE BREASTCHAPTER 17Adjuvant Breast and Bowel Project (NSABP) conducted a ran-domized trial in the early 1970s to determine the impact of local and regional treatments on survival in operable breast cancer. In the B-04 trial, 1665 women were enrolled and stratified by clinical assessment of the axillary lymph nodes. The clinically node-negative women were randomized into three treatment groups: (a) Halsted radical mastectomy; (b) total mastectomy plus radiation therapy; and (c) total mastectomy alone. Clini-cally node-positive women were randomized to Halsted radical mastectomy or total mastectomy plus radiation therapy. This trial accrued
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Surgery_Schwartz. and systemic therapy.10 Local-regional and systemic therapy decisions for an indi-vidual patient with breast cancer are best made using a multidisciplinary treatment approach. The sequencing of therapies is dependent on patient and tumor related factors including breast cancer subtype.Brunicardi_Ch17_p0541-p0612.indd 54201/03/19 5:04 PM 543THE BREASTCHAPTER 17Adjuvant Breast and Bowel Project (NSABP) conducted a ran-domized trial in the early 1970s to determine the impact of local and regional treatments on survival in operable breast cancer. In the B-04 trial, 1665 women were enrolled and stratified by clinical assessment of the axillary lymph nodes. The clinically node-negative women were randomized into three treatment groups: (a) Halsted radical mastectomy; (b) total mastectomy plus radiation therapy; and (c) total mastectomy alone. Clini-cally node-positive women were randomized to Halsted radical mastectomy or total mastectomy plus radiation therapy. This trial accrued
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plus radiation therapy; and (c) total mastectomy alone. Clini-cally node-positive women were randomized to Halsted radical mastectomy or total mastectomy plus radiation therapy. This trial accrued patients between 1971 and 1974, an era that pre-dated widespread availability of effective systemic therapy for breast cancer and therefore reflect survival associated with local-regional therapy alone. There were no differences in survival between the three groups of node-negative women or between the two groups of node-positive women. These overall survival equivalence patterns persisted at 25 years of follow-up.9The next major advance in the surgical management of breast cancer was the development of breast conserving surgery. Breast conserving surgery and radium treatment was first reported by Geoffrey Keynes of St Bartholomew’s Hospital, London in the British Medical Journal in 1937.10 Several decades later, the NSABP launched the B-06 trial, a phase 3 study that randomized 1851
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Surgery_Schwartz. plus radiation therapy; and (c) total mastectomy alone. Clini-cally node-positive women were randomized to Halsted radical mastectomy or total mastectomy plus radiation therapy. This trial accrued patients between 1971 and 1974, an era that pre-dated widespread availability of effective systemic therapy for breast cancer and therefore reflect survival associated with local-regional therapy alone. There were no differences in survival between the three groups of node-negative women or between the two groups of node-positive women. These overall survival equivalence patterns persisted at 25 years of follow-up.9The next major advance in the surgical management of breast cancer was the development of breast conserving surgery. Breast conserving surgery and radium treatment was first reported by Geoffrey Keynes of St Bartholomew’s Hospital, London in the British Medical Journal in 1937.10 Several decades later, the NSABP launched the B-06 trial, a phase 3 study that randomized 1851
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Surgery_Schwartz_3689
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Surgery_Schwartz
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by Geoffrey Keynes of St Bartholomew’s Hospital, London in the British Medical Journal in 1937.10 Several decades later, the NSABP launched the B-06 trial, a phase 3 study that randomized 1851 patients to total mastec-tomy, lumpectomy alone, or lumpectomy with breast irradia-tion. The results showed no difference in disease-free, distant disease-free, and overall survival among the three groups; how-ever, the omission of radiation therapy resulted in significantly higher rates of ipsilateral breast tumor recurrence in those who received lumpectomy alone.11 The B-06 trial excluded patients who had palpable axillary lymph nodes, and those patients randomized to breast conserving surgery had frozen sections performed. If on frozen section the margins were involved, the surgeon proceeded to perform a mastectomy, but the patient was included in the analysis as having had a breast conserv-ing operation. Furthermore, in B-06, local in-breast recurrences were regarded as “nonevents” in terms
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Surgery_Schwartz. by Geoffrey Keynes of St Bartholomew’s Hospital, London in the British Medical Journal in 1937.10 Several decades later, the NSABP launched the B-06 trial, a phase 3 study that randomized 1851 patients to total mastec-tomy, lumpectomy alone, or lumpectomy with breast irradia-tion. The results showed no difference in disease-free, distant disease-free, and overall survival among the three groups; how-ever, the omission of radiation therapy resulted in significantly higher rates of ipsilateral breast tumor recurrence in those who received lumpectomy alone.11 The B-06 trial excluded patients who had palpable axillary lymph nodes, and those patients randomized to breast conserving surgery had frozen sections performed. If on frozen section the margins were involved, the surgeon proceeded to perform a mastectomy, but the patient was included in the analysis as having had a breast conserv-ing operation. Furthermore, in B-06, local in-breast recurrences were regarded as “nonevents” in terms
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Surgery_Schwartz_3690
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Surgery_Schwartz
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a mastectomy, but the patient was included in the analysis as having had a breast conserv-ing operation. Furthermore, in B-06, local in-breast recurrences were regarded as “nonevents” in terms of disease-free survival. Both the NSABP B-04 and B-06 trials were taken to refute the Halstedian concept that cancer spread throughout a region of the breast to lymphatics and then on to distant sites. Bernard Fisher proposed the “alternative hypothesis” that breast cancer was a systemic disease at diagnosis and that tumor cells had access to both the blood and lymphatic systems and that regional lymph nodes were a marker of systemic disease and not a barrier to the dissemination of cancer cells. He proposed that host factors were important in the development of metastasis and that varia-tions in the local-regional approach to breast cancer treatment were not likely to substantially impact survival. This idea was dominant for a number of years but has been challenged by the Early Breast Cancer
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Surgery_Schwartz. a mastectomy, but the patient was included in the analysis as having had a breast conserv-ing operation. Furthermore, in B-06, local in-breast recurrences were regarded as “nonevents” in terms of disease-free survival. Both the NSABP B-04 and B-06 trials were taken to refute the Halstedian concept that cancer spread throughout a region of the breast to lymphatics and then on to distant sites. Bernard Fisher proposed the “alternative hypothesis” that breast cancer was a systemic disease at diagnosis and that tumor cells had access to both the blood and lymphatic systems and that regional lymph nodes were a marker of systemic disease and not a barrier to the dissemination of cancer cells. He proposed that host factors were important in the development of metastasis and that varia-tions in the local-regional approach to breast cancer treatment were not likely to substantially impact survival. This idea was dominant for a number of years but has been challenged by the Early Breast Cancer
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Surgery_Schwartz_3691
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Surgery_Schwartz
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local-regional approach to breast cancer treatment were not likely to substantially impact survival. This idea was dominant for a number of years but has been challenged by the Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) overview analysis, which reported that “the avoidance of recur-rence in a conserved breast . . . avoids about one breast cancer death over the next 15 years for every four such recurrences avoided,”12 indicating that not all breast cancer is a systemic disease at presentation.During the 1970s, clinical trials were initiated to determine the value of systemic therapy in the postoperative setting as an adjuvant to surgery. The EBCTCG was established in 1985 to coordinate the meta-analysis of data from randomized clinical trials in order to examine the impact of adjuvant treatments for breast cancer on recurrence and mortality. The EBCTCG overview has demonstrated that anthracycline containing regimens are superior to cyclophosphamide, methotrexate, and
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Surgery_Schwartz. local-regional approach to breast cancer treatment were not likely to substantially impact survival. This idea was dominant for a number of years but has been challenged by the Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) overview analysis, which reported that “the avoidance of recur-rence in a conserved breast . . . avoids about one breast cancer death over the next 15 years for every four such recurrences avoided,”12 indicating that not all breast cancer is a systemic disease at presentation.During the 1970s, clinical trials were initiated to determine the value of systemic therapy in the postoperative setting as an adjuvant to surgery. The EBCTCG was established in 1985 to coordinate the meta-analysis of data from randomized clinical trials in order to examine the impact of adjuvant treatments for breast cancer on recurrence and mortality. The EBCTCG overview has demonstrated that anthracycline containing regimens are superior to cyclophosphamide, methotrexate, and
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Surgery_Schwartz_3692
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Surgery_Schwartz
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of adjuvant treatments for breast cancer on recurrence and mortality. The EBCTCG overview has demonstrated that anthracycline containing regimens are superior to cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), and more recently, that the addition of a taxane to an anthracycline-based regimen reduces breast cancer mortality by one-third.11 The overview has also demonstrated that tamoxifen is of benefit only in patients with estrogen recep-tor (ER) positive breast cancer and that tamoxifen may decrease mortality from breast cancer by as much as 30%.13 Importantly, the EBCTCG data have shown that proportional reduction in risk was not significantly affected by standard clinical and pathologic factors such as tumor size, ER status, and nodal status.14 This underscores the importance of stratification of risk in determining adjuvant therapy decisions in order to minimize the toxicities of therapies in those unlikely to benefit, yet real-ize the substantial benefits gained in
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Surgery_Schwartz. of adjuvant treatments for breast cancer on recurrence and mortality. The EBCTCG overview has demonstrated that anthracycline containing regimens are superior to cyclophosphamide, methotrexate, and 5-fluorouracil (CMF), and more recently, that the addition of a taxane to an anthracycline-based regimen reduces breast cancer mortality by one-third.11 The overview has also demonstrated that tamoxifen is of benefit only in patients with estrogen recep-tor (ER) positive breast cancer and that tamoxifen may decrease mortality from breast cancer by as much as 30%.13 Importantly, the EBCTCG data have shown that proportional reduction in risk was not significantly affected by standard clinical and pathologic factors such as tumor size, ER status, and nodal status.14 This underscores the importance of stratification of risk in determining adjuvant therapy decisions in order to minimize the toxicities of therapies in those unlikely to benefit, yet real-ize the substantial benefits gained in
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Surgery_Schwartz_3693
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Surgery_Schwartz
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of stratification of risk in determining adjuvant therapy decisions in order to minimize the toxicities of therapies in those unlikely to benefit, yet real-ize the substantial benefits gained in local-regional control and survival in those at higher risk.Many early randomized clinical trials considered all patients similarly in terms of treatment viewing breast cancer as more of a homogeneous disease. Breast cancer has traditionally been defined by pathologic determinants using conventional light microscopy and basic histologic techniques. In the 1980s, immunohistochemistry allowed assessment of the expression of individual tumor markers (most commonly proteins) while DNA was initially assessed in terms of its ploidy status. Sub-sequently, breast cancer specimens have been interrogated at the level of the DNA by labeling genes of interest and allow-ing fluorescent dyes to quantify the abundance of a particular gene and comparing a large number of genes simultaneously in a single
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Surgery_Schwartz. of stratification of risk in determining adjuvant therapy decisions in order to minimize the toxicities of therapies in those unlikely to benefit, yet real-ize the substantial benefits gained in local-regional control and survival in those at higher risk.Many early randomized clinical trials considered all patients similarly in terms of treatment viewing breast cancer as more of a homogeneous disease. Breast cancer has traditionally been defined by pathologic determinants using conventional light microscopy and basic histologic techniques. In the 1980s, immunohistochemistry allowed assessment of the expression of individual tumor markers (most commonly proteins) while DNA was initially assessed in terms of its ploidy status. Sub-sequently, breast cancer specimens have been interrogated at the level of the DNA by labeling genes of interest and allow-ing fluorescent dyes to quantify the abundance of a particular gene and comparing a large number of genes simultaneously in a single
|
Surgery_Schwartz_3694
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Surgery_Schwartz
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at the level of the DNA by labeling genes of interest and allow-ing fluorescent dyes to quantify the abundance of a particular gene and comparing a large number of genes simultaneously in a single breast cancer specimen. Gene expression arrays have shown that breast cancers cluster according to their intrinsic gene expression patterns into at least five intrinsic subtypes and these intrinsic subtypes correlate with breast cancer outcomes.15 Breast cancers are now classified by molecular subtypes and these are being used for risk stratification and decision making in terms of local-regional and systemic therapies.Currently, 50% of American women will consult a sur-geon regarding breast disease, 25% will undergo breast biopsy for diagnosis of an abnormality, and 12% will develop some variant of breast cancer. Considerable progress has been made in the integration of surgery, radiation therapy, and systemic therapy to control local-regional disease, enhance survival, and improve the
|
Surgery_Schwartz. at the level of the DNA by labeling genes of interest and allow-ing fluorescent dyes to quantify the abundance of a particular gene and comparing a large number of genes simultaneously in a single breast cancer specimen. Gene expression arrays have shown that breast cancers cluster according to their intrinsic gene expression patterns into at least five intrinsic subtypes and these intrinsic subtypes correlate with breast cancer outcomes.15 Breast cancers are now classified by molecular subtypes and these are being used for risk stratification and decision making in terms of local-regional and systemic therapies.Currently, 50% of American women will consult a sur-geon regarding breast disease, 25% will undergo breast biopsy for diagnosis of an abnormality, and 12% will develop some variant of breast cancer. Considerable progress has been made in the integration of surgery, radiation therapy, and systemic therapy to control local-regional disease, enhance survival, and improve the
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Surgery_Schwartz_3695
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Surgery_Schwartz
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of breast cancer. Considerable progress has been made in the integration of surgery, radiation therapy, and systemic therapy to control local-regional disease, enhance survival, and improve the quality of life of breast cancer survivors. Surgeons are traditionally the first physician consulted for breast care, and it is critical for them to be well trained in all aspects of the breast from embryologic development, to growth and development, to benign and malignant disease processes. This will allow the greatest opportunity to achieve optimal outcomes for patients and their families.EMBRYOLOGY AND FUNCTIONAL ANATOMY OF THE BREASTEmbryologyAt the fifth or sixth week of fetal development, two ventral bands of thickened ectoderm (mammary ridges, milk lines) are evident in the embryo.16 In most mammals, paired breasts develop along these ridges, which extend from the base of the forelimb (future axilla) to the region of the hind limb (inguinal area). These ridges are not prominent in the
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Surgery_Schwartz. of breast cancer. Considerable progress has been made in the integration of surgery, radiation therapy, and systemic therapy to control local-regional disease, enhance survival, and improve the quality of life of breast cancer survivors. Surgeons are traditionally the first physician consulted for breast care, and it is critical for them to be well trained in all aspects of the breast from embryologic development, to growth and development, to benign and malignant disease processes. This will allow the greatest opportunity to achieve optimal outcomes for patients and their families.EMBRYOLOGY AND FUNCTIONAL ANATOMY OF THE BREASTEmbryologyAt the fifth or sixth week of fetal development, two ventral bands of thickened ectoderm (mammary ridges, milk lines) are evident in the embryo.16 In most mammals, paired breasts develop along these ridges, which extend from the base of the forelimb (future axilla) to the region of the hind limb (inguinal area). These ridges are not prominent in the
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Surgery_Schwartz_3696
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Surgery_Schwartz
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mammals, paired breasts develop along these ridges, which extend from the base of the forelimb (future axilla) to the region of the hind limb (inguinal area). These ridges are not prominent in the human embryo and disappear after a short time, except for small portions that may persist in the pectoral region. Accessory breasts (polymastia) or accessory nipples (polythelia) may Brunicardi_Ch17_p0541-p0612.indd 54301/03/19 5:04 PM 544SPECIFIC CONSIDERATIONSPART IIFigure 17-1. The mammary milk line. (Visual Art: © 2013. The University of Texas MD Anderson Cancer Center.)Figure 17-2. Anatomy of the breast. Tangential and cross-sectional (sagittal) views of the breast and associated chest wall. (Reproduced with permission from Bland KI, Copeland EMI: The Breast: Comprehensive Management of Benign and Malignant Diseases, 4th ed. Philadelphia, PA: Elsevier/Saunders; 2009.)occur along the milk line (Fig. 17-1) when normal regression fails. Each breast develops when an ingrowth of
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Surgery_Schwartz. mammals, paired breasts develop along these ridges, which extend from the base of the forelimb (future axilla) to the region of the hind limb (inguinal area). These ridges are not prominent in the human embryo and disappear after a short time, except for small portions that may persist in the pectoral region. Accessory breasts (polymastia) or accessory nipples (polythelia) may Brunicardi_Ch17_p0541-p0612.indd 54301/03/19 5:04 PM 544SPECIFIC CONSIDERATIONSPART IIFigure 17-1. The mammary milk line. (Visual Art: © 2013. The University of Texas MD Anderson Cancer Center.)Figure 17-2. Anatomy of the breast. Tangential and cross-sectional (sagittal) views of the breast and associated chest wall. (Reproduced with permission from Bland KI, Copeland EMI: The Breast: Comprehensive Management of Benign and Malignant Diseases, 4th ed. Philadelphia, PA: Elsevier/Saunders; 2009.)occur along the milk line (Fig. 17-1) when normal regression fails. Each breast develops when an ingrowth of
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Surgery_Schwartz_3697
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Surgery_Schwartz
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of Benign and Malignant Diseases, 4th ed. Philadelphia, PA: Elsevier/Saunders; 2009.)occur along the milk line (Fig. 17-1) when normal regression fails. Each breast develops when an ingrowth of ectoderm forms a primary tissue bud in the mesenchyme. The primary bud, in turn, initiates the development of 15 to 20 secondary buds. Epithelial cords develop from the secondary buds and extend into the surrounding mesenchyme. Major (lactiferous) ducts develop, which open into a shallow mammary pit. Dur-ing infancy, a proliferation of mesenchyme transforms the mammary pit into a nipple. If there is failure of a pit to elevate above skin level, an inverted nipple results. This congenital malformation occurs in 4% of infants. At birth, the breasts are identical in males and females, demonstrating only the pres-ence of major ducts. Enlargement of the breast may be evi-dent, and a secretion, historically referred to as witch’s milk, may be produced. These transitory events occur in response to
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Surgery_Schwartz. of Benign and Malignant Diseases, 4th ed. Philadelphia, PA: Elsevier/Saunders; 2009.)occur along the milk line (Fig. 17-1) when normal regression fails. Each breast develops when an ingrowth of ectoderm forms a primary tissue bud in the mesenchyme. The primary bud, in turn, initiates the development of 15 to 20 secondary buds. Epithelial cords develop from the secondary buds and extend into the surrounding mesenchyme. Major (lactiferous) ducts develop, which open into a shallow mammary pit. Dur-ing infancy, a proliferation of mesenchyme transforms the mammary pit into a nipple. If there is failure of a pit to elevate above skin level, an inverted nipple results. This congenital malformation occurs in 4% of infants. At birth, the breasts are identical in males and females, demonstrating only the pres-ence of major ducts. Enlargement of the breast may be evi-dent, and a secretion, historically referred to as witch’s milk, may be produced. These transitory events occur in response to
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Surgery_Schwartz_3698
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Surgery_Schwartz
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only the pres-ence of major ducts. Enlargement of the breast may be evi-dent, and a secretion, historically referred to as witch’s milk, may be produced. These transitory events occur in response to maternal hormones that cross the placenta.The breast remains undeveloped in the female until puberty, when it enlarges in response to ovarian estrogen and progesterone, which initiate proliferation of the epithelial and connective tissue elements. However, the breasts remain incompletely developed until pregnancy occurs. Absence of the breast (amastia) is rare and results from an arrest in mam-mary ridge development that occurs during the sixth fetal week. Poland’s syndrome consists of hypoplasia or complete absence of the breast, costal cartilage and rib defects, hypoplasia of the subcutaneous tissues of the chest wall, and brachysyndactyly. Breast hypoplasia also may be iatrogenically induced before puberty by trauma, infection, or radiation therapy. Symmastia is a rare anomaly
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Surgery_Schwartz. only the pres-ence of major ducts. Enlargement of the breast may be evi-dent, and a secretion, historically referred to as witch’s milk, may be produced. These transitory events occur in response to maternal hormones that cross the placenta.The breast remains undeveloped in the female until puberty, when it enlarges in response to ovarian estrogen and progesterone, which initiate proliferation of the epithelial and connective tissue elements. However, the breasts remain incompletely developed until pregnancy occurs. Absence of the breast (amastia) is rare and results from an arrest in mam-mary ridge development that occurs during the sixth fetal week. Poland’s syndrome consists of hypoplasia or complete absence of the breast, costal cartilage and rib defects, hypoplasia of the subcutaneous tissues of the chest wall, and brachysyndactyly. Breast hypoplasia also may be iatrogenically induced before puberty by trauma, infection, or radiation therapy. Symmastia is a rare anomaly
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Surgery_Schwartz_3699
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Surgery_Schwartz
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tissues of the chest wall, and brachysyndactyly. Breast hypoplasia also may be iatrogenically induced before puberty by trauma, infection, or radiation therapy. Symmastia is a rare anomaly recognized as webbing between the breasts across the midline. Accessory nipples (polythelia) occur in <1% of infants and may be associated with abnormalities of the urinary and cardiovascular systems. Supernumerary breasts may occur in any configuration along the mammary milk line but most frequently occur between the normal nipple location and the symphysis pubis. Turner’s syndrome (ovarian agenesis and dysgenesis) and Fleischer’s syndrome (displacement of the nipples and bilateral renal hypoplasia) may have polymastia as a component. Accessory axillary breast tissue is uncommon and usually is bilateral.Functional AnatomyThe breast is composed of 15 to 20 lobes (Fig. 17-2), which are each composed of several lobules.17 Fibrous bands of con-nective tissue travel through the breast (Cooper’s
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Surgery_Schwartz. tissues of the chest wall, and brachysyndactyly. Breast hypoplasia also may be iatrogenically induced before puberty by trauma, infection, or radiation therapy. Symmastia is a rare anomaly recognized as webbing between the breasts across the midline. Accessory nipples (polythelia) occur in <1% of infants and may be associated with abnormalities of the urinary and cardiovascular systems. Supernumerary breasts may occur in any configuration along the mammary milk line but most frequently occur between the normal nipple location and the symphysis pubis. Turner’s syndrome (ovarian agenesis and dysgenesis) and Fleischer’s syndrome (displacement of the nipples and bilateral renal hypoplasia) may have polymastia as a component. Accessory axillary breast tissue is uncommon and usually is bilateral.Functional AnatomyThe breast is composed of 15 to 20 lobes (Fig. 17-2), which are each composed of several lobules.17 Fibrous bands of con-nective tissue travel through the breast (Cooper’s
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Surgery_Schwartz_3700
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Surgery_Schwartz
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bilateral.Functional AnatomyThe breast is composed of 15 to 20 lobes (Fig. 17-2), which are each composed of several lobules.17 Fibrous bands of con-nective tissue travel through the breast (Cooper’s suspensory ligaments), insert perpendicularly into the dermis, and provide structural support. The mature female breast extends from the level of the second or third rib to the inframammary fold at the sixth or seventh rib. It extends transversely from the lateral border of the sternum to the anterior axillary line. The deep or posterior surface of the breast rests on the fascia of the pecto-ralis major, serratus anterior, and external oblique abdominal muscles, and the upper extent of the rectus sheath. The retro-mammary bursa may be identified on the posterior aspect of the breast between the investing fascia of the breast and the fascia of the pectoralis major muscles. The axillary tail of Spence extends laterally across the anterior axillary fold. The upper outer quad-rant of the
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Surgery_Schwartz. bilateral.Functional AnatomyThe breast is composed of 15 to 20 lobes (Fig. 17-2), which are each composed of several lobules.17 Fibrous bands of con-nective tissue travel through the breast (Cooper’s suspensory ligaments), insert perpendicularly into the dermis, and provide structural support. The mature female breast extends from the level of the second or third rib to the inframammary fold at the sixth or seventh rib. It extends transversely from the lateral border of the sternum to the anterior axillary line. The deep or posterior surface of the breast rests on the fascia of the pecto-ralis major, serratus anterior, and external oblique abdominal muscles, and the upper extent of the rectus sheath. The retro-mammary bursa may be identified on the posterior aspect of the breast between the investing fascia of the breast and the fascia of the pectoralis major muscles. The axillary tail of Spence extends laterally across the anterior axillary fold. The upper outer quad-rant of the
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Surgery_Schwartz_3701
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Surgery_Schwartz
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the investing fascia of the breast and the fascia of the pectoralis major muscles. The axillary tail of Spence extends laterally across the anterior axillary fold. The upper outer quad-rant of the breast contains a greater volume of tissue than do the other quadrants. The breast has a protuberant conical form. The base of the cone is roughly circular, measuring 10 to 12 cm in diameter. Considerable variations in the size, contour, and den-sity of the breast are evident among individuals. The nulliparous breast has a hemispheric configuration with distinct flattening above the nipple. With the hormonal stimulation that accom-panies pregnancy and lactation, the breast becomes larger and increases in volume and density, whereas with senescence, it assumes a flattened, flaccid, and more pendulous configuration with decreased volume.Nipple-Areola Complex. The epidermis of the nipple-are-ola complex is pigmented and is variably corrugated. During puberty, the pigment becomes darker and the
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Surgery_Schwartz. the investing fascia of the breast and the fascia of the pectoralis major muscles. The axillary tail of Spence extends laterally across the anterior axillary fold. The upper outer quad-rant of the breast contains a greater volume of tissue than do the other quadrants. The breast has a protuberant conical form. The base of the cone is roughly circular, measuring 10 to 12 cm in diameter. Considerable variations in the size, contour, and den-sity of the breast are evident among individuals. The nulliparous breast has a hemispheric configuration with distinct flattening above the nipple. With the hormonal stimulation that accom-panies pregnancy and lactation, the breast becomes larger and increases in volume and density, whereas with senescence, it assumes a flattened, flaccid, and more pendulous configuration with decreased volume.Nipple-Areola Complex. The epidermis of the nipple-are-ola complex is pigmented and is variably corrugated. During puberty, the pigment becomes darker and the
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