id
stringlengths 14
28
| title
stringclasses 18
values | content
stringlengths 2
999
| contents
stringlengths 19
1.02k
|
|---|---|---|---|
Surgery_Schwartz_8202 | Surgery_Schwartz | database (SEER) between 1992 and 2006, of a total number of 10,945 small intestine cancers, 4315 were neuroendocrine in origin, 3412 were carcinomas, 2023 were lymphomas, and 1084 were sarcomas.54 Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors arising in the small intestine and comprise the vast majority of tumors that were formerly classified as leiomyomas, leiomyosarcomas, and smooth muscle tumors of the intestine. The small intestine is frequently affected by metastases from or local invasion by cancers originating at other sites. Melanoma, in particular, is associated with a propensity for metastasis to the small intestine.Most patients with small-intestinal cancers are in their fifth or sixth decade of life. Reported risk factors for developing small-intestinal cancers include consumption of red meat, inges-tion of smoked or cured foods, Crohn’s disease, celiac sprue, hereditary nonpolyposis colorectal cancer (HNPCC), familial adenomatous polyposis | Surgery_Schwartz. database (SEER) between 1992 and 2006, of a total number of 10,945 small intestine cancers, 4315 were neuroendocrine in origin, 3412 were carcinomas, 2023 were lymphomas, and 1084 were sarcomas.54 Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors arising in the small intestine and comprise the vast majority of tumors that were formerly classified as leiomyomas, leiomyosarcomas, and smooth muscle tumors of the intestine. The small intestine is frequently affected by metastases from or local invasion by cancers originating at other sites. Melanoma, in particular, is associated with a propensity for metastasis to the small intestine.Most patients with small-intestinal cancers are in their fifth or sixth decade of life. Reported risk factors for developing small-intestinal cancers include consumption of red meat, inges-tion of smoked or cured foods, Crohn’s disease, celiac sprue, hereditary nonpolyposis colorectal cancer (HNPCC), familial adenomatous polyposis |
Surgery_Schwartz_8203 | Surgery_Schwartz | cancers include consumption of red meat, inges-tion of smoked or cured foods, Crohn’s disease, celiac sprue, hereditary nonpolyposis colorectal cancer (HNPCC), familial adenomatous polyposis (FAP), and Peutz-Jeghers syndrome.PathophysiologyThe small intestine contains over 90% of the mucosal surface area of the gastrointestinal tract but only 1.1% to 2.4% of all gastrointestinal malignancies. Proposed explanations for the low frequency of small-intestinal neoplasms include (a) dilu-tion of environmental carcinogens in the liquid chyme present in the small-intestinal lumen; (b) rapid transit of chyme, limiting the contact time between carcinogens and the intestinal mucosa; (c) a relatively low concentration of bacteria in small-intestinal chyme and, therefore, a relatively low concentration of carcino-genic products of bacterial metabolism; (d) mucosal protection by secretory IgA and hydrolases such as benzpyrene hydroxy-lase that may render carcinogens less active; and (e) efficient | Surgery_Schwartz. cancers include consumption of red meat, inges-tion of smoked or cured foods, Crohn’s disease, celiac sprue, hereditary nonpolyposis colorectal cancer (HNPCC), familial adenomatous polyposis (FAP), and Peutz-Jeghers syndrome.PathophysiologyThe small intestine contains over 90% of the mucosal surface area of the gastrointestinal tract but only 1.1% to 2.4% of all gastrointestinal malignancies. Proposed explanations for the low frequency of small-intestinal neoplasms include (a) dilu-tion of environmental carcinogens in the liquid chyme present in the small-intestinal lumen; (b) rapid transit of chyme, limiting the contact time between carcinogens and the intestinal mucosa; (c) a relatively low concentration of bacteria in small-intestinal chyme and, therefore, a relatively low concentration of carcino-genic products of bacterial metabolism; (d) mucosal protection by secretory IgA and hydrolases such as benzpyrene hydroxy-lase that may render carcinogens less active; and (e) efficient |
Surgery_Schwartz_8204 | Surgery_Schwartz | of carcino-genic products of bacterial metabolism; (d) mucosal protection by secretory IgA and hydrolases such as benzpyrene hydroxy-lase that may render carcinogens less active; and (e) efficient epithelial cellular apoptotic mechanisms that serve to eliminate clones harboring genetic mutations.Recent advances have begun to clarify the molecular pathogenesis of small-intestinal adenocarcinomas and GISTs; there has been less progress with respect to the pathogen-esis of the other small-intestinal malignancies (Table 28-10). Small-intestinal adenocarcinomas are believed to arise from Table 28-10Features of small intestinal malignanciesTUMOR TYPECELL OF ORIGINFREQUENCYaPREDOMINANT SITEAdenocarcinomaEpithelial cell35–50%DuodenumCarcinoidEnterochromaffin cell20–40%IleumLymphomaLymphocyte10–15%IleumGISTInterstitial cell of Cajal10–15%–aFrequencies given as percentages of small intestinal malignancies comprised by each of the tumor types. Gastrointestinal stromal tumors (GISTs) display no | Surgery_Schwartz. of carcino-genic products of bacterial metabolism; (d) mucosal protection by secretory IgA and hydrolases such as benzpyrene hydroxy-lase that may render carcinogens less active; and (e) efficient epithelial cellular apoptotic mechanisms that serve to eliminate clones harboring genetic mutations.Recent advances have begun to clarify the molecular pathogenesis of small-intestinal adenocarcinomas and GISTs; there has been less progress with respect to the pathogen-esis of the other small-intestinal malignancies (Table 28-10). Small-intestinal adenocarcinomas are believed to arise from Table 28-10Features of small intestinal malignanciesTUMOR TYPECELL OF ORIGINFREQUENCYaPREDOMINANT SITEAdenocarcinomaEpithelial cell35–50%DuodenumCarcinoidEnterochromaffin cell20–40%IleumLymphomaLymphocyte10–15%IleumGISTInterstitial cell of Cajal10–15%–aFrequencies given as percentages of small intestinal malignancies comprised by each of the tumor types. Gastrointestinal stromal tumors (GISTs) display no |
Surgery_Schwartz_8205 | Surgery_Schwartz | cell of Cajal10–15%–aFrequencies given as percentages of small intestinal malignancies comprised by each of the tumor types. Gastrointestinal stromal tumors (GISTs) display no regional variation in prevalence within the small intestine.preexisting adenomas through a sequential accumulation of genetic abnormalities in a model like that described for the pathogenesis of colorectal cancer. Adenomas are histologi-cally classified as tubular, villous, and tubulovillous. Tubular adenomas have the least aggressive features. Villous adenomas have the most aggressive features and tend to be large, sessile, and located in the second portion of the duodenum. Malignant degeneration has been reported to be present in up to 45% of vil-lous adenomas by the time of diagnosis. Patients with FAP have a nearly 100% cumulative lifetime risk of developing duodenal adenomas that have the potential to undergo malignant trans-formation. The risk of duodenal cancer in these patients is over 100-fold greater | Surgery_Schwartz. cell of Cajal10–15%–aFrequencies given as percentages of small intestinal malignancies comprised by each of the tumor types. Gastrointestinal stromal tumors (GISTs) display no regional variation in prevalence within the small intestine.preexisting adenomas through a sequential accumulation of genetic abnormalities in a model like that described for the pathogenesis of colorectal cancer. Adenomas are histologi-cally classified as tubular, villous, and tubulovillous. Tubular adenomas have the least aggressive features. Villous adenomas have the most aggressive features and tend to be large, sessile, and located in the second portion of the duodenum. Malignant degeneration has been reported to be present in up to 45% of vil-lous adenomas by the time of diagnosis. Patients with FAP have a nearly 100% cumulative lifetime risk of developing duodenal adenomas that have the potential to undergo malignant trans-formation. The risk of duodenal cancer in these patients is over 100-fold greater |
Surgery_Schwartz_8206 | Surgery_Schwartz | 100% cumulative lifetime risk of developing duodenal adenomas that have the potential to undergo malignant trans-formation. The risk of duodenal cancer in these patients is over 100-fold greater than in the general population. Indeed, duode-nal cancer is the leading cause of cancer-related death among patients with FAP who have undergone colectomy. Patients with Peutz-Jeghers syndrome develop hamartomatous polyps; however, these polyps can contain adenomatous foci that can undergo malignant transformation (Fig. 28-21).A defining feature of GISTs is their gain of function mutation of proto-oncogene KIT, a receptor tyrosine kinase. Figure 28-21. Small bowel polyp in Peutz-Jeghers syndrome. This image was captured by a wireless capsule endoscope as it was traveling through the small intestine. (Used with permission from Anne T. Wolf, M.D., Department of Medicine, Brigham and Women’s Hospital, Boston, MA.)Brunicardi_Ch28_p1219-p1258.indd 124223/02/19 2:24 PM 1243SMALL INTESTINECHAPTER | Surgery_Schwartz. 100% cumulative lifetime risk of developing duodenal adenomas that have the potential to undergo malignant trans-formation. The risk of duodenal cancer in these patients is over 100-fold greater than in the general population. Indeed, duode-nal cancer is the leading cause of cancer-related death among patients with FAP who have undergone colectomy. Patients with Peutz-Jeghers syndrome develop hamartomatous polyps; however, these polyps can contain adenomatous foci that can undergo malignant transformation (Fig. 28-21).A defining feature of GISTs is their gain of function mutation of proto-oncogene KIT, a receptor tyrosine kinase. Figure 28-21. Small bowel polyp in Peutz-Jeghers syndrome. This image was captured by a wireless capsule endoscope as it was traveling through the small intestine. (Used with permission from Anne T. Wolf, M.D., Department of Medicine, Brigham and Women’s Hospital, Boston, MA.)Brunicardi_Ch28_p1219-p1258.indd 124223/02/19 2:24 PM 1243SMALL INTESTINECHAPTER |
Surgery_Schwartz_8207 | Surgery_Schwartz | (Used with permission from Anne T. Wolf, M.D., Department of Medicine, Brigham and Women’s Hospital, Boston, MA.)Brunicardi_Ch28_p1219-p1258.indd 124223/02/19 2:24 PM 1243SMALL INTESTINECHAPTER 28Pathological KIT signal transduction is believed to be a cen-tral event in GIST pathogenesis. The majority of GISTs have activating mutations in the c-kit proto-oncogene, which cause KIT to become constitutively activated, presumably leading to persistence of cellular growth or survival signals. Because the interstitial cells of Cajal normally express KIT, these cells have been implicated as the cell of origin for GISTs. KIT expression is assessed by staining the tissues for CD117 antigen, which is part of the KIT receptor and is present in 95% of GISTs.Clinical PresentationMost small-intestinal neoplasms are asymptomatic until they become large. Partial small bowel obstruction, with associ-ated symptoms of crampy abdominal pain and distention, nau-sea, and vomiting, is the most common | Surgery_Schwartz. (Used with permission from Anne T. Wolf, M.D., Department of Medicine, Brigham and Women’s Hospital, Boston, MA.)Brunicardi_Ch28_p1219-p1258.indd 124223/02/19 2:24 PM 1243SMALL INTESTINECHAPTER 28Pathological KIT signal transduction is believed to be a cen-tral event in GIST pathogenesis. The majority of GISTs have activating mutations in the c-kit proto-oncogene, which cause KIT to become constitutively activated, presumably leading to persistence of cellular growth or survival signals. Because the interstitial cells of Cajal normally express KIT, these cells have been implicated as the cell of origin for GISTs. KIT expression is assessed by staining the tissues for CD117 antigen, which is part of the KIT receptor and is present in 95% of GISTs.Clinical PresentationMost small-intestinal neoplasms are asymptomatic until they become large. Partial small bowel obstruction, with associ-ated symptoms of crampy abdominal pain and distention, nau-sea, and vomiting, is the most common |
Surgery_Schwartz_8208 | Surgery_Schwartz | neoplasms are asymptomatic until they become large. Partial small bowel obstruction, with associ-ated symptoms of crampy abdominal pain and distention, nau-sea, and vomiting, is the most common mode of presentation. Obstruction can be the result of either luminal narrowing by the tumor itself or intussusception, with the tumor serving as the lead point. Hemorrhage, usually indolent, is the second most common mode of presentation.Physical examination may be unrevealing, but it also may reveal a palpable abdominal mass in those with large tumors. Findings of intestinal obstruction may be present in some patients. A fecal occult blood test may be positive. Jaundice secondary to biliary obstruction or hepatic metastasis may be present. Cachexia, hepatomegaly, and ascites may be present with advanced disease.Although the clinical presentation is usually not specific for tumor type, some general comments are appropriate. Adeno-carcinomas, as well as adenomas (from which most are believed to | Surgery_Schwartz. neoplasms are asymptomatic until they become large. Partial small bowel obstruction, with associ-ated symptoms of crampy abdominal pain and distention, nau-sea, and vomiting, is the most common mode of presentation. Obstruction can be the result of either luminal narrowing by the tumor itself or intussusception, with the tumor serving as the lead point. Hemorrhage, usually indolent, is the second most common mode of presentation.Physical examination may be unrevealing, but it also may reveal a palpable abdominal mass in those with large tumors. Findings of intestinal obstruction may be present in some patients. A fecal occult blood test may be positive. Jaundice secondary to biliary obstruction or hepatic metastasis may be present. Cachexia, hepatomegaly, and ascites may be present with advanced disease.Although the clinical presentation is usually not specific for tumor type, some general comments are appropriate. Adeno-carcinomas, as well as adenomas (from which most are believed to |
Surgery_Schwartz_8209 | Surgery_Schwartz | disease.Although the clinical presentation is usually not specific for tumor type, some general comments are appropriate. Adeno-carcinomas, as well as adenomas (from which most are believed to arise), are most commonly found in the duodenum, except in patients with Crohn’s disease, in whom most are found in the ileum. Lesions in the periampullary location can cause obstruc-tive jaundice or pancreatitis. Adenocarcinomas located in the duodenum tend to be diagnosed earlier in their progression than those located in the jejunum or ileum, which are rarely diagnosed prior to the onset of locally advanced or metastatic disease.Carcinoid tumors of the small intestine are also usually diagnosed after the development of metastatic disease. These tumors are associated with a more aggressive behavior than the more common appendiceal carcinoid tumors. Approximately 25% to 50% of patients with carcinoid tumor-derived liver metastases will develop manifestations of the carcinoid syn-drome. These | Surgery_Schwartz. disease.Although the clinical presentation is usually not specific for tumor type, some general comments are appropriate. Adeno-carcinomas, as well as adenomas (from which most are believed to arise), are most commonly found in the duodenum, except in patients with Crohn’s disease, in whom most are found in the ileum. Lesions in the periampullary location can cause obstruc-tive jaundice or pancreatitis. Adenocarcinomas located in the duodenum tend to be diagnosed earlier in their progression than those located in the jejunum or ileum, which are rarely diagnosed prior to the onset of locally advanced or metastatic disease.Carcinoid tumors of the small intestine are also usually diagnosed after the development of metastatic disease. These tumors are associated with a more aggressive behavior than the more common appendiceal carcinoid tumors. Approximately 25% to 50% of patients with carcinoid tumor-derived liver metastases will develop manifestations of the carcinoid syn-drome. These |
Surgery_Schwartz_8210 | Surgery_Schwartz | than the more common appendiceal carcinoid tumors. Approximately 25% to 50% of patients with carcinoid tumor-derived liver metastases will develop manifestations of the carcinoid syn-drome. These manifestations include diarrhea, flushing, hypo-tension, tachycardia, and fibrosis of the endocardium and valves the right heart. Candidate tumor-derived mediators of the car-cinoid syndrome such as serotonin, bradykinin, and substance P undergo nearly complete metabolism during the first passage through the liver. As a result, symptoms of carcinoid syndrome are rare in the absence of liver metastases.Lymphoma may involve the small intestine primarily or as a manifestation of disseminated systemic disease. Primary small-intestinal lymphomas are most commonly located in the ileum, which contains the highest concentration of lymphoid tissue in the intestine. Although partial small bowel obstruction is the most common mode of presentation, 10% of patients with small-intestinal lymphoma present | Surgery_Schwartz. than the more common appendiceal carcinoid tumors. Approximately 25% to 50% of patients with carcinoid tumor-derived liver metastases will develop manifestations of the carcinoid syn-drome. These manifestations include diarrhea, flushing, hypo-tension, tachycardia, and fibrosis of the endocardium and valves the right heart. Candidate tumor-derived mediators of the car-cinoid syndrome such as serotonin, bradykinin, and substance P undergo nearly complete metabolism during the first passage through the liver. As a result, symptoms of carcinoid syndrome are rare in the absence of liver metastases.Lymphoma may involve the small intestine primarily or as a manifestation of disseminated systemic disease. Primary small-intestinal lymphomas are most commonly located in the ileum, which contains the highest concentration of lymphoid tissue in the intestine. Although partial small bowel obstruction is the most common mode of presentation, 10% of patients with small-intestinal lymphoma present |
Surgery_Schwartz_8211 | Surgery_Schwartz | the highest concentration of lymphoid tissue in the intestine. Although partial small bowel obstruction is the most common mode of presentation, 10% of patients with small-intestinal lymphoma present with bowel perforation.The small intestine is the second most common site of GIST tumors after the stomach, containing 25% to 35% of GISTs. There appears to be no regional variation in the preva-lence of GISTs within the small intestine. GISTs have a greater propensity to be associated with overt hemorrhage than the other small-intestinal malignancies (Fig. 28-22).Metastatic tumors involving the small intestine can induce intestinal obstruction and bleeding.DiagnosisBecause of the absent or nonspecific symptoms associated with most small-intestinal neoplasms, these lesions are rarely diagnosed preoperatively. Laboratory tests are nonspecific, except for elevated urinary 5-hydroxyindole acetic acid (5-HIAA) and serum chromogranin A (CgA) levels in patients with carcinoid syndrome, both of | Surgery_Schwartz. the highest concentration of lymphoid tissue in the intestine. Although partial small bowel obstruction is the most common mode of presentation, 10% of patients with small-intestinal lymphoma present with bowel perforation.The small intestine is the second most common site of GIST tumors after the stomach, containing 25% to 35% of GISTs. There appears to be no regional variation in the preva-lence of GISTs within the small intestine. GISTs have a greater propensity to be associated with overt hemorrhage than the other small-intestinal malignancies (Fig. 28-22).Metastatic tumors involving the small intestine can induce intestinal obstruction and bleeding.DiagnosisBecause of the absent or nonspecific symptoms associated with most small-intestinal neoplasms, these lesions are rarely diagnosed preoperatively. Laboratory tests are nonspecific, except for elevated urinary 5-hydroxyindole acetic acid (5-HIAA) and serum chromogranin A (CgA) levels in patients with carcinoid syndrome, both of |
Surgery_Schwartz_8212 | Surgery_Schwartz | preoperatively. Laboratory tests are nonspecific, except for elevated urinary 5-hydroxyindole acetic acid (5-HIAA) and serum chromogranin A (CgA) levels in patients with carcinoid syndrome, both of which have low sensitivity. Elevated carcinoembryonic antigen (CEA) levels are associated with small-intestinal adenocarcinomas, but only in the presence of liver metastases.Contrast radiography of the small intestine may demon-strate benign and malignant lesions. Enterocolysis is reported to have a sensitivity of over 90% in the detection of small bowel tumors and is the test of choice, particularly for tumors located in the distal small bowel. Upper GI with small bowel follow-through examinations have reported sensitivities ranging from only 30% to 44% (Fig. 28-23). CT scanning can detect abnor-malities in 70% to 80% of cases with small bowel tumor and assess for metastatic spread. Tumors associated with significant bleeding can be localized with angiography or radioisotope-tagged red | Surgery_Schwartz. preoperatively. Laboratory tests are nonspecific, except for elevated urinary 5-hydroxyindole acetic acid (5-HIAA) and serum chromogranin A (CgA) levels in patients with carcinoid syndrome, both of which have low sensitivity. Elevated carcinoembryonic antigen (CEA) levels are associated with small-intestinal adenocarcinomas, but only in the presence of liver metastases.Contrast radiography of the small intestine may demon-strate benign and malignant lesions. Enterocolysis is reported to have a sensitivity of over 90% in the detection of small bowel tumors and is the test of choice, particularly for tumors located in the distal small bowel. Upper GI with small bowel follow-through examinations have reported sensitivities ranging from only 30% to 44% (Fig. 28-23). CT scanning can detect abnor-malities in 70% to 80% of cases with small bowel tumor and assess for metastatic spread. Tumors associated with significant bleeding can be localized with angiography or radioisotope-tagged red |
Surgery_Schwartz_8213 | Surgery_Schwartz | abnor-malities in 70% to 80% of cases with small bowel tumor and assess for metastatic spread. Tumors associated with significant bleeding can be localized with angiography or radioisotope-tagged red blood cell (RBC) scans.Tumors located in the duodenum can be visualized and biopsied on EGD. In addition, endoscopic ultrasonography (EUS) can offer additional information such as the layers of the intestinal wall involved by the lesion. Occasionally, the distal ileum can suc-cessfully be visualized during colonoscopy. Intraoperative enter-oscopy can be used to directly visualize small-intestinal tumors beyond the reach of standard endoscopic techniques. For more distal small bowel lesions, capsule endoscopy and double-balloon Figure 28-22. Jejunal gastrointestinal stromal tumor (GIST). This patient presented with overt obscure GI bleeding and was found to have a 7-cm jejunal GIST. The picture represents the laparo-scopic view of the mass (black arrow), arising from the antimesenteric | Surgery_Schwartz. abnor-malities in 70% to 80% of cases with small bowel tumor and assess for metastatic spread. Tumors associated with significant bleeding can be localized with angiography or radioisotope-tagged red blood cell (RBC) scans.Tumors located in the duodenum can be visualized and biopsied on EGD. In addition, endoscopic ultrasonography (EUS) can offer additional information such as the layers of the intestinal wall involved by the lesion. Occasionally, the distal ileum can suc-cessfully be visualized during colonoscopy. Intraoperative enter-oscopy can be used to directly visualize small-intestinal tumors beyond the reach of standard endoscopic techniques. For more distal small bowel lesions, capsule endoscopy and double-balloon Figure 28-22. Jejunal gastrointestinal stromal tumor (GIST). This patient presented with overt obscure GI bleeding and was found to have a 7-cm jejunal GIST. The picture represents the laparo-scopic view of the mass (black arrow), arising from the antimesenteric |
Surgery_Schwartz_8214 | Surgery_Schwartz | patient presented with overt obscure GI bleeding and was found to have a 7-cm jejunal GIST. The picture represents the laparo-scopic view of the mass (black arrow), arising from the antimesenteric side of the small bowel (*). He underwent a successful laparoscopic resection.Brunicardi_Ch28_p1219-p1258.indd 124323/02/19 2:24 PM 1244SPECIFIC CONSIDERATIONSPART IIFigure 28-23. Small bowel lesion identified during a small bowel follow-through (arrow). This patient had previously had a metastatic renal lesion to his duodenum requiring a Whipple procedure. During follow-up imaging 3 years later, he was found to have this new lesion in his jejunum. He underwent a laparoscopic small bowel resection. Pathology revealed a benign jejunal sessile polyp.endoscopy have been used to evaluate small bowel. CT and MR enterography are also increasing utilized as noninvasive tests to look for small bowel masses. PET scans can also help assess metabolic activity of lesions and risk of | Surgery_Schwartz. patient presented with overt obscure GI bleeding and was found to have a 7-cm jejunal GIST. The picture represents the laparo-scopic view of the mass (black arrow), arising from the antimesenteric side of the small bowel (*). He underwent a successful laparoscopic resection.Brunicardi_Ch28_p1219-p1258.indd 124323/02/19 2:24 PM 1244SPECIFIC CONSIDERATIONSPART IIFigure 28-23. Small bowel lesion identified during a small bowel follow-through (arrow). This patient had previously had a metastatic renal lesion to his duodenum requiring a Whipple procedure. During follow-up imaging 3 years later, he was found to have this new lesion in his jejunum. He underwent a laparoscopic small bowel resection. Pathology revealed a benign jejunal sessile polyp.endoscopy have been used to evaluate small bowel. CT and MR enterography are also increasing utilized as noninvasive tests to look for small bowel masses. PET scans can also help assess metabolic activity of lesions and risk of |
Surgery_Schwartz_8215 | Surgery_Schwartz | evaluate small bowel. CT and MR enterography are also increasing utilized as noninvasive tests to look for small bowel masses. PET scans can also help assess metabolic activity of lesions and risk of malignancy.TherapyBenign neoplasms of the small intestine that are symptomatic should be surgically resected or removed endoscopically, if fea-sible. Tumors located in the duodenum, including asymptomatic lesions incidentally found during EGD, can pose the great-est therapeutic challenges. These lesions should be biopsied; symptomatic tumors and adenomas, because of their malignant potential, should be removed. In general, duodenal tumors less than 1 cm in diameter are amenable to endoscopic polypectomy. Lesions greater than 2 cm in diameter are technically difficult to remove endoscopically and may need to be removed surgi-cally. Surgical options include transduodenal polypectomy and segmental duodenal resection. Tumors located in the second portion of the duodenum near the ampulla of | Surgery_Schwartz. evaluate small bowel. CT and MR enterography are also increasing utilized as noninvasive tests to look for small bowel masses. PET scans can also help assess metabolic activity of lesions and risk of malignancy.TherapyBenign neoplasms of the small intestine that are symptomatic should be surgically resected or removed endoscopically, if fea-sible. Tumors located in the duodenum, including asymptomatic lesions incidentally found during EGD, can pose the great-est therapeutic challenges. These lesions should be biopsied; symptomatic tumors and adenomas, because of their malignant potential, should be removed. In general, duodenal tumors less than 1 cm in diameter are amenable to endoscopic polypectomy. Lesions greater than 2 cm in diameter are technically difficult to remove endoscopically and may need to be removed surgi-cally. Surgical options include transduodenal polypectomy and segmental duodenal resection. Tumors located in the second portion of the duodenum near the ampulla of |
Surgery_Schwartz_8216 | Surgery_Schwartz | and may need to be removed surgi-cally. Surgical options include transduodenal polypectomy and segmental duodenal resection. Tumors located in the second portion of the duodenum near the ampulla of Vater may require pancreaticoduodenectomy. EUS may offer utility for duodenal tumors ranging in size between 1 and 2 cm in diameter, with those limited to the mucosa being amenable to endoscopic pol-ypectomy. Endoscopic resection of biopsy-proven benign duo-denal periampullary adenomas leads to equivalent efficacy to surgery but with lower morbidity. Adenomas can recur; there-fore, surveillance endoscopy is required after these procedures.55Duodenal adenomas occurring in the setting of FAP require an especially aggressive approach to management. Patients with FAP should undergo screening EGD starting sometime during their second or third decade of life. Adenomas detected should be removed endoscopically, if possible, followed by surveillance endoscopy in 6 months and yearly thereafter, in | Surgery_Schwartz. and may need to be removed surgi-cally. Surgical options include transduodenal polypectomy and segmental duodenal resection. Tumors located in the second portion of the duodenum near the ampulla of Vater may require pancreaticoduodenectomy. EUS may offer utility for duodenal tumors ranging in size between 1 and 2 cm in diameter, with those limited to the mucosa being amenable to endoscopic pol-ypectomy. Endoscopic resection of biopsy-proven benign duo-denal periampullary adenomas leads to equivalent efficacy to surgery but with lower morbidity. Adenomas can recur; there-fore, surveillance endoscopy is required after these procedures.55Duodenal adenomas occurring in the setting of FAP require an especially aggressive approach to management. Patients with FAP should undergo screening EGD starting sometime during their second or third decade of life. Adenomas detected should be removed endoscopically, if possible, followed by surveillance endoscopy in 6 months and yearly thereafter, in |
Surgery_Schwartz_8217 | Surgery_Schwartz | sometime during their second or third decade of life. Adenomas detected should be removed endoscopically, if possible, followed by surveillance endoscopy in 6 months and yearly thereafter, in the absence of recurrence. If surgery is required, pancreaticoduodenectomy is generally necessary because adenomas in patients with FAP tend to be multiple and sessile, with a predilection for the peri-ampullary region. Further, localized resections are complicated by high recurrence rates. Given the potential for recurrences in the duodenal remnant following pylorus-preserving pancreati-coduodenectomy, there is rationale for recommending the appli-cation of standard pancreaticoduodenectomy in these patients. However, recurrences have been reported even following this procedure; therefore, continuing surveillance is necessary. For most adenocarcinomas of the duodenum, except those in the third or fourth portion of the duodenum where a local resection could be considered, pancreaticoduodenectomy | Surgery_Schwartz. sometime during their second or third decade of life. Adenomas detected should be removed endoscopically, if possible, followed by surveillance endoscopy in 6 months and yearly thereafter, in the absence of recurrence. If surgery is required, pancreaticoduodenectomy is generally necessary because adenomas in patients with FAP tend to be multiple and sessile, with a predilection for the peri-ampullary region. Further, localized resections are complicated by high recurrence rates. Given the potential for recurrences in the duodenal remnant following pylorus-preserving pancreati-coduodenectomy, there is rationale for recommending the appli-cation of standard pancreaticoduodenectomy in these patients. However, recurrences have been reported even following this procedure; therefore, continuing surveillance is necessary. For most adenocarcinomas of the duodenum, except those in the third or fourth portion of the duodenum where a local resection could be considered, pancreaticoduodenectomy |
Surgery_Schwartz_8218 | Surgery_Schwartz | surveillance is necessary. For most adenocarcinomas of the duodenum, except those in the third or fourth portion of the duodenum where a local resection could be considered, pancreaticoduodenectomy is required.The surgical therapy of jejunal and ileal malignancies usually consists of wide-local resection of the intestine harboring the lesion. For adenocarcinomas, a wide excision of corresponding mesentery is done to achieve regional lymphadenectomy, as is done for adenocarcinomas of the colon. In the presence of locally-advanced or metastatic disease, palliative intestinal resection or bypass is performed. Chemotherapy has no proven efficacy in the adjuvant or palliative treatment of small-intestinal adenocarcinomas.The goal of surgical therapy for carcinoids is resection of all visible disease. Localized small-intestinal carcinoid tumors should be treated with segmental intestinal resection and regional lymphadenectomy. Nodal metastases are unusual with tumors less than 1 cm in | Surgery_Schwartz. surveillance is necessary. For most adenocarcinomas of the duodenum, except those in the third or fourth portion of the duodenum where a local resection could be considered, pancreaticoduodenectomy is required.The surgical therapy of jejunal and ileal malignancies usually consists of wide-local resection of the intestine harboring the lesion. For adenocarcinomas, a wide excision of corresponding mesentery is done to achieve regional lymphadenectomy, as is done for adenocarcinomas of the colon. In the presence of locally-advanced or metastatic disease, palliative intestinal resection or bypass is performed. Chemotherapy has no proven efficacy in the adjuvant or palliative treatment of small-intestinal adenocarcinomas.The goal of surgical therapy for carcinoids is resection of all visible disease. Localized small-intestinal carcinoid tumors should be treated with segmental intestinal resection and regional lymphadenectomy. Nodal metastases are unusual with tumors less than 1 cm in |
Surgery_Schwartz_8219 | Surgery_Schwartz | disease. Localized small-intestinal carcinoid tumors should be treated with segmental intestinal resection and regional lymphadenectomy. Nodal metastases are unusual with tumors less than 1 cm in diameter, but they are present with 75% to 90% of tumors larger than 3 cm in diameter. In approximately 30% of cases, multiple small-intestinal carcinoid tumors are present (Fig. 28-24). Therefore, the entire small intestine should Figure 28-24. Small bowel carcinoid tumor. This patient pre-sented with history of abdominal pain and on CT was found to have a circumferentially thickened loop of distal small bowel with associated mesenteric stranding and lymphadenopathy. An octreotide scan demonstrated abnormal activity in the area, concerning for a carcinoid tumor. He underwent an open small bowel resection. Pathology revealed a multifocal carcinoid tumor with 50 distinct nodules and metastasis to mesenteric lymph nodes.Brunicardi_Ch28_p1219-p1258.indd 124423/02/19 2:24 PM 1245SMALL | Surgery_Schwartz. disease. Localized small-intestinal carcinoid tumors should be treated with segmental intestinal resection and regional lymphadenectomy. Nodal metastases are unusual with tumors less than 1 cm in diameter, but they are present with 75% to 90% of tumors larger than 3 cm in diameter. In approximately 30% of cases, multiple small-intestinal carcinoid tumors are present (Fig. 28-24). Therefore, the entire small intestine should Figure 28-24. Small bowel carcinoid tumor. This patient pre-sented with history of abdominal pain and on CT was found to have a circumferentially thickened loop of distal small bowel with associated mesenteric stranding and lymphadenopathy. An octreotide scan demonstrated abnormal activity in the area, concerning for a carcinoid tumor. He underwent an open small bowel resection. Pathology revealed a multifocal carcinoid tumor with 50 distinct nodules and metastasis to mesenteric lymph nodes.Brunicardi_Ch28_p1219-p1258.indd 124423/02/19 2:24 PM 1245SMALL |
Surgery_Schwartz_8220 | Surgery_Schwartz | bowel resection. Pathology revealed a multifocal carcinoid tumor with 50 distinct nodules and metastasis to mesenteric lymph nodes.Brunicardi_Ch28_p1219-p1258.indd 124423/02/19 2:24 PM 1245SMALL INTESTINECHAPTER 28be examined before planning extent of resection. In the presence of metastatic disease, tumor debulking should be conducted as it can be associated with long-term survival and amelioration of symptoms of the carcinoid syndrome. Response rates of 30% to 50% have been reported to chemotherapy regimens based on agents such as doxorubicin, 5-fluorouracil, and streptozocin. However, none of these regimens is associated with a clearly demonstrable impact on the natural history of disease. Octreo-tide is the most effective pharmacologic agent for management of symptoms of carcinoid syndrome.Localized small-intestinal lymphoma should be treated with segmental resection of the involved intestine and adjacent mesentery. If the small intestine is diffusely affected by lym-phoma, | Surgery_Schwartz. bowel resection. Pathology revealed a multifocal carcinoid tumor with 50 distinct nodules and metastasis to mesenteric lymph nodes.Brunicardi_Ch28_p1219-p1258.indd 124423/02/19 2:24 PM 1245SMALL INTESTINECHAPTER 28be examined before planning extent of resection. In the presence of metastatic disease, tumor debulking should be conducted as it can be associated with long-term survival and amelioration of symptoms of the carcinoid syndrome. Response rates of 30% to 50% have been reported to chemotherapy regimens based on agents such as doxorubicin, 5-fluorouracil, and streptozocin. However, none of these regimens is associated with a clearly demonstrable impact on the natural history of disease. Octreo-tide is the most effective pharmacologic agent for management of symptoms of carcinoid syndrome.Localized small-intestinal lymphoma should be treated with segmental resection of the involved intestine and adjacent mesentery. If the small intestine is diffusely affected by lym-phoma, |
Surgery_Schwartz_8221 | Surgery_Schwartz | syndrome.Localized small-intestinal lymphoma should be treated with segmental resection of the involved intestine and adjacent mesentery. If the small intestine is diffusely affected by lym-phoma, chemotherapy rather than surgical resection should be the primary therapy. The value to adjuvant chemotherapy after resection of localized lymphoma is controversial.Small-intestinal GISTs should be treated with segmental intestinal resection. If the diagnosis is known prior to resec-tion, wide lymphadenectomy can be avoided as GISTs are rarely associated with lymph node metastases. GISTs are resistant to conventional chemotherapy agents. Imatinib (Gleevec) is a tyrosine kinase inhibitor with potent activity against tyrosine kinase KIT, and it is used in those with metastatic disease. Clini-cal trials have shown that 80% of patients with unresectable or metastatic GISTs derive clinical benefit from the administra-tion of Imatinib, with 50% to 60% having objective evidence of reduction in | Surgery_Schwartz. syndrome.Localized small-intestinal lymphoma should be treated with segmental resection of the involved intestine and adjacent mesentery. If the small intestine is diffusely affected by lym-phoma, chemotherapy rather than surgical resection should be the primary therapy. The value to adjuvant chemotherapy after resection of localized lymphoma is controversial.Small-intestinal GISTs should be treated with segmental intestinal resection. If the diagnosis is known prior to resec-tion, wide lymphadenectomy can be avoided as GISTs are rarely associated with lymph node metastases. GISTs are resistant to conventional chemotherapy agents. Imatinib (Gleevec) is a tyrosine kinase inhibitor with potent activity against tyrosine kinase KIT, and it is used in those with metastatic disease. Clini-cal trials have shown that 80% of patients with unresectable or metastatic GISTs derive clinical benefit from the administra-tion of Imatinib, with 50% to 60% having objective evidence of reduction in |
Surgery_Schwartz_8222 | Surgery_Schwartz | trials have shown that 80% of patients with unresectable or metastatic GISTs derive clinical benefit from the administra-tion of Imatinib, with 50% to 60% having objective evidence of reduction in tumor volume.56 Imatinib has shown great promise as a neoadjuvant and adjuvant therapy for GISTs. Studies have emphasized the potential for development of tumor resistance to this agent. In this setting, an alternative tyrosine kinas inhibitor, sunitinib, has been used with good results.Metastatic cancers affecting the small intestine that are symptomatic should be treated with palliative resection or bypass except in the most advanced cases. Systemic therapy may be offered if effective chemotherapy exists for the primary cancer.OutcomesComplete resection of duodenal adenocarcinomas is associ-ated with postoperative 5-year survival rates ranging from 50% to 60%. Complete resection of adenocarcinomas located in the jejunum or ileum is associated with 5-year survival rates of 20% to 30%.57 | Surgery_Schwartz. trials have shown that 80% of patients with unresectable or metastatic GISTs derive clinical benefit from the administra-tion of Imatinib, with 50% to 60% having objective evidence of reduction in tumor volume.56 Imatinib has shown great promise as a neoadjuvant and adjuvant therapy for GISTs. Studies have emphasized the potential for development of tumor resistance to this agent. In this setting, an alternative tyrosine kinas inhibitor, sunitinib, has been used with good results.Metastatic cancers affecting the small intestine that are symptomatic should be treated with palliative resection or bypass except in the most advanced cases. Systemic therapy may be offered if effective chemotherapy exists for the primary cancer.OutcomesComplete resection of duodenal adenocarcinomas is associ-ated with postoperative 5-year survival rates ranging from 50% to 60%. Complete resection of adenocarcinomas located in the jejunum or ileum is associated with 5-year survival rates of 20% to 30%.57 |
Surgery_Schwartz_8223 | Surgery_Schwartz | with postoperative 5-year survival rates ranging from 50% to 60%. Complete resection of adenocarcinomas located in the jejunum or ileum is associated with 5-year survival rates of 20% to 30%.57 Five-year survival rates of 75% to 95% fol-lowing resection of localized small-intestinal carcinoid tumors have been reported. In the presence of carcinoid tumor-derived liver metastases, 5-year survival rates of 19% to 54% have been reported. The overall 5-year survival rate for patients diagnosed with intestinal lymphoma ranges from 20% to 40%. For patients with localized lymphoma amenable to surgical resection, the 5-year survival rate is 60%.The recurrence rate following resection of GISTs aver-ages 35%. The 5-year survival rate following surgical resection has been reported to range from 35% to 60%. Both tumor size and mitotic index are independently correlated with prognosis. Low-grade tumors (mitotic index <10 per high-power field) measuring less than 5 cm in diameter are associated with | Surgery_Schwartz. with postoperative 5-year survival rates ranging from 50% to 60%. Complete resection of adenocarcinomas located in the jejunum or ileum is associated with 5-year survival rates of 20% to 30%.57 Five-year survival rates of 75% to 95% fol-lowing resection of localized small-intestinal carcinoid tumors have been reported. In the presence of carcinoid tumor-derived liver metastases, 5-year survival rates of 19% to 54% have been reported. The overall 5-year survival rate for patients diagnosed with intestinal lymphoma ranges from 20% to 40%. For patients with localized lymphoma amenable to surgical resection, the 5-year survival rate is 60%.The recurrence rate following resection of GISTs aver-ages 35%. The 5-year survival rate following surgical resection has been reported to range from 35% to 60%. Both tumor size and mitotic index are independently correlated with prognosis. Low-grade tumors (mitotic index <10 per high-power field) measuring less than 5 cm in diameter are associated with |
Surgery_Schwartz_8224 | Surgery_Schwartz | 60%. Both tumor size and mitotic index are independently correlated with prognosis. Low-grade tumors (mitotic index <10 per high-power field) measuring less than 5 cm in diameter are associated with excel-lent prognosis.RADIATION ENTERITISRadiation therapy is a component of multi-modality therapy for many intra-abdominal and pelvic cancers such as those of the cervix, endometrium, ovary, bladder, prostate, and rectum. An undesired side effect of radiation therapy is radiation-induced injury to the small intestine, which can present clinically as two distinct syndromes: acute and chronic radiation enteritis. Acute radiation enteritis is a transient condition that occurs in approximately 75% of patients undergoing radiation therapy for abdominal and pelvic cancers. Chronic radiation is enteritis is inexorable and develops in approximately 5% to 15% of these patients.PathophysiologyRadiation induces cellular injury directly and through the gen-eration of free radicals. The principal | Surgery_Schwartz. 60%. Both tumor size and mitotic index are independently correlated with prognosis. Low-grade tumors (mitotic index <10 per high-power field) measuring less than 5 cm in diameter are associated with excel-lent prognosis.RADIATION ENTERITISRadiation therapy is a component of multi-modality therapy for many intra-abdominal and pelvic cancers such as those of the cervix, endometrium, ovary, bladder, prostate, and rectum. An undesired side effect of radiation therapy is radiation-induced injury to the small intestine, which can present clinically as two distinct syndromes: acute and chronic radiation enteritis. Acute radiation enteritis is a transient condition that occurs in approximately 75% of patients undergoing radiation therapy for abdominal and pelvic cancers. Chronic radiation is enteritis is inexorable and develops in approximately 5% to 15% of these patients.PathophysiologyRadiation induces cellular injury directly and through the gen-eration of free radicals. The principal |
Surgery_Schwartz_8225 | Surgery_Schwartz | enteritis is inexorable and develops in approximately 5% to 15% of these patients.PathophysiologyRadiation induces cellular injury directly and through the gen-eration of free radicals. The principal mechanism of radiation-induced cell death is believed to be apoptosis resulting from free-radical–induced breaks in double-stranded DNA. Because radiation has its greatest impact on rapidly proliferating cells, the small-intestinal epithelium is acutely susceptible to radiationinduced injury. Pathological correlates of this acute injury include villus blunting and a dense infiltrate of leukocytes and plasma cells within the crypts. With severe cases, mucosal sloughing, ulceration, and hemorrhage are observed. The inten-sity of injury is related to the dose of radiation administered, with most cases occurring in patients who have received at least 4500 cGy. Risk factors for acute radiation enteritis include con-ditions that may limit splanchnic perfusion such as hyperten-sion, diabetes | Surgery_Schwartz. enteritis is inexorable and develops in approximately 5% to 15% of these patients.PathophysiologyRadiation induces cellular injury directly and through the gen-eration of free radicals. The principal mechanism of radiation-induced cell death is believed to be apoptosis resulting from free-radical–induced breaks in double-stranded DNA. Because radiation has its greatest impact on rapidly proliferating cells, the small-intestinal epithelium is acutely susceptible to radiationinduced injury. Pathological correlates of this acute injury include villus blunting and a dense infiltrate of leukocytes and plasma cells within the crypts. With severe cases, mucosal sloughing, ulceration, and hemorrhage are observed. The inten-sity of injury is related to the dose of radiation administered, with most cases occurring in patients who have received at least 4500 cGy. Risk factors for acute radiation enteritis include con-ditions that may limit splanchnic perfusion such as hyperten-sion, diabetes |
Surgery_Schwartz_8226 | Surgery_Schwartz | cases occurring in patients who have received at least 4500 cGy. Risk factors for acute radiation enteritis include con-ditions that may limit splanchnic perfusion such as hyperten-sion, diabetes mellitus, coronary artery disease, and restricted mobility of the small intestine due to adhesions. Injury is potentiated by concomitant administration of chemotherapeutic agents, such as doxorubicin, 5-fluorouracil, actinomycin D, and methotrexate, that act as radiation-sensitizers. Because of the intestinal epithelium’s capacity for regeneration, the mucosal injury that is characteristic of acute radiation enteritis resolves after the cessation of radiation therapy.In contrast, chronic radiation enteritis is characterized by a progressive occlusive vasculitis that leads to chronic ischemia and fibrosis that affects all layers of the intestinal wall, rather than the mucosa alone. These changes can lead to strictures, abscesses, and fistulas, which are responsible for the clinical | Surgery_Schwartz. cases occurring in patients who have received at least 4500 cGy. Risk factors for acute radiation enteritis include con-ditions that may limit splanchnic perfusion such as hyperten-sion, diabetes mellitus, coronary artery disease, and restricted mobility of the small intestine due to adhesions. Injury is potentiated by concomitant administration of chemotherapeutic agents, such as doxorubicin, 5-fluorouracil, actinomycin D, and methotrexate, that act as radiation-sensitizers. Because of the intestinal epithelium’s capacity for regeneration, the mucosal injury that is characteristic of acute radiation enteritis resolves after the cessation of radiation therapy.In contrast, chronic radiation enteritis is characterized by a progressive occlusive vasculitis that leads to chronic ischemia and fibrosis that affects all layers of the intestinal wall, rather than the mucosa alone. These changes can lead to strictures, abscesses, and fistulas, which are responsible for the clinical |
Surgery_Schwartz_8227 | Surgery_Schwartz | and fibrosis that affects all layers of the intestinal wall, rather than the mucosa alone. These changes can lead to strictures, abscesses, and fistulas, which are responsible for the clinical manifestations of chronic radiation enteritis.Clinical PresentationThe most common manifestations of acute radiation enteritis are nausea, vomiting, diarrhea, and crampy abdominal pain. Symptoms are generally transient and subside after the discon-tinuation of radiation therapy. Because the diagnosis is usually obvious, given the clinical context, no specific diagnostic tests are required. However, if patients develop signs suggestive of peritonitis, CT scanning should be performed to rule out the presence of other conditions capable of causing acute abdominal syndromes.The clinical manifestations of chronic radiation enteritis usually become evident within 2 years of radiation administra-tion, although they can begin as early as several months or as late as decades afterwards. The most common | Surgery_Schwartz. and fibrosis that affects all layers of the intestinal wall, rather than the mucosa alone. These changes can lead to strictures, abscesses, and fistulas, which are responsible for the clinical manifestations of chronic radiation enteritis.Clinical PresentationThe most common manifestations of acute radiation enteritis are nausea, vomiting, diarrhea, and crampy abdominal pain. Symptoms are generally transient and subside after the discon-tinuation of radiation therapy. Because the diagnosis is usually obvious, given the clinical context, no specific diagnostic tests are required. However, if patients develop signs suggestive of peritonitis, CT scanning should be performed to rule out the presence of other conditions capable of causing acute abdominal syndromes.The clinical manifestations of chronic radiation enteritis usually become evident within 2 years of radiation administra-tion, although they can begin as early as several months or as late as decades afterwards. The most common |
Surgery_Schwartz_8228 | Surgery_Schwartz | of chronic radiation enteritis usually become evident within 2 years of radiation administra-tion, although they can begin as early as several months or as late as decades afterwards. The most common clinical presenta-tions are diarrhea or one of partial small bowel obstruction with nausea, vomiting, intermittent abdominal distention, crampy abdominal pain, and weight loss. The terminal ileum is the most frequently affected segment. Other manifestations of chronic radiation enteritis include complete bowel obstruction, acute or chronic intestinal hemorrhage, and abscess or fistula formation.DiagnosisEvaluation of patients suspected of having chronic radia-tion enteritis should include review of the records of their Brunicardi_Ch28_p1219-p1258.indd 124523/02/19 2:24 PM 1246SPECIFIC CONSIDERATIONSPART IIradiation treatments for information on total radiation dose administered, fractionation, and volume of treatment. Areas that received high doses should be noted, as lesions | Surgery_Schwartz. of chronic radiation enteritis usually become evident within 2 years of radiation administra-tion, although they can begin as early as several months or as late as decades afterwards. The most common clinical presenta-tions are diarrhea or one of partial small bowel obstruction with nausea, vomiting, intermittent abdominal distention, crampy abdominal pain, and weight loss. The terminal ileum is the most frequently affected segment. Other manifestations of chronic radiation enteritis include complete bowel obstruction, acute or chronic intestinal hemorrhage, and abscess or fistula formation.DiagnosisEvaluation of patients suspected of having chronic radia-tion enteritis should include review of the records of their Brunicardi_Ch28_p1219-p1258.indd 124523/02/19 2:24 PM 1246SPECIFIC CONSIDERATIONSPART IIradiation treatments for information on total radiation dose administered, fractionation, and volume of treatment. Areas that received high doses should be noted, as lesions |
Surgery_Schwartz_8229 | Surgery_Schwartz | CONSIDERATIONSPART IIradiation treatments for information on total radiation dose administered, fractionation, and volume of treatment. Areas that received high doses should be noted, as lesions subse-quently found in imaging studies usually localize to areas that had received high radiation doses. Enterocolysis is the most accurate imaging test for diagnosing chronic radiation enteri-tis, with reported sensitivities and specificities of over 90% (Fig. 28-25). CT scan findings are neither very sensitive nor specific for chronic radiation enteritis. However, CT scanning should be obtained to rule out the presence of recurrent can-cer since its clinical manifestations may overlap with those of chronic radiation enteritis.TherapyMost cases of acute radiation enteritis are self-limited. Support-ive therapy, including the administration of antiemetics, is usu-ally sufficient. Patients with diarrhea-induced dehydration may require hospital admission and parenteral fluid administration. | Surgery_Schwartz. CONSIDERATIONSPART IIradiation treatments for information on total radiation dose administered, fractionation, and volume of treatment. Areas that received high doses should be noted, as lesions subse-quently found in imaging studies usually localize to areas that had received high radiation doses. Enterocolysis is the most accurate imaging test for diagnosing chronic radiation enteri-tis, with reported sensitivities and specificities of over 90% (Fig. 28-25). CT scan findings are neither very sensitive nor specific for chronic radiation enteritis. However, CT scanning should be obtained to rule out the presence of recurrent can-cer since its clinical manifestations may overlap with those of chronic radiation enteritis.TherapyMost cases of acute radiation enteritis are self-limited. Support-ive therapy, including the administration of antiemetics, is usu-ally sufficient. Patients with diarrhea-induced dehydration may require hospital admission and parenteral fluid administration. |
Surgery_Schwartz_8230 | Surgery_Schwartz | therapy, including the administration of antiemetics, is usu-ally sufficient. Patients with diarrhea-induced dehydration may require hospital admission and parenteral fluid administration. Rarely are symptoms severe enough to necessitate reduction in or cessation of radiation therapy.In contrast, the treatment of chronic radiation enteritis represents a formidable challenge. Antidiarrheal agents may have a role in the management of diarrhea while, in those with obstructive symptoms, a low residue diet may be tried. Surgery for this condition is difficult, is associated with high morbidity rates, and should be avoided in the absence of specific indica-tions such as high-grade obstruction, perforation, hemorrhage, intra-abdominal abscesses, and fistulas. The goal of surgery is limited resection of diseased intestine with primary anastomosis Figure 28-25. Radiation enteritis. This contrast radiograph reveals widely separated loops of small bowel with luminal narrowing, loss of mucosal | Surgery_Schwartz. therapy, including the administration of antiemetics, is usu-ally sufficient. Patients with diarrhea-induced dehydration may require hospital admission and parenteral fluid administration. Rarely are symptoms severe enough to necessitate reduction in or cessation of radiation therapy.In contrast, the treatment of chronic radiation enteritis represents a formidable challenge. Antidiarrheal agents may have a role in the management of diarrhea while, in those with obstructive symptoms, a low residue diet may be tried. Surgery for this condition is difficult, is associated with high morbidity rates, and should be avoided in the absence of specific indica-tions such as high-grade obstruction, perforation, hemorrhage, intra-abdominal abscesses, and fistulas. The goal of surgery is limited resection of diseased intestine with primary anastomosis Figure 28-25. Radiation enteritis. This contrast radiograph reveals widely separated loops of small bowel with luminal narrowing, loss of mucosal |
Surgery_Schwartz_8231 | Surgery_Schwartz | of diseased intestine with primary anastomosis Figure 28-25. Radiation enteritis. This contrast radiograph reveals widely separated loops of small bowel with luminal narrowing, loss of mucosal folds, and ulceration. This patient had received radiation therapy for a pelvic malignancy 8 years before this examination.between healthy bowel segments. However, the characteristi-cally diffuse nature of fibrosis and dense adhesions among bowel segments can make limited resection difficult to achieve. Further, it is difficult to distinguish between normal and irra-diated intestine intraoperatively by either gross inspection or even frozen section analysis. This distinction is important as anastomoses between irradiated segments of intestine have been associated with leak rates as high as 50%.58 If limited resec-tion is not achievable, an intestinal bypass procedure may be an option, except in cases for which hemorrhage is the surgical indication. There remain cases in which resections | Surgery_Schwartz. of diseased intestine with primary anastomosis Figure 28-25. Radiation enteritis. This contrast radiograph reveals widely separated loops of small bowel with luminal narrowing, loss of mucosal folds, and ulceration. This patient had received radiation therapy for a pelvic malignancy 8 years before this examination.between healthy bowel segments. However, the characteristi-cally diffuse nature of fibrosis and dense adhesions among bowel segments can make limited resection difficult to achieve. Further, it is difficult to distinguish between normal and irra-diated intestine intraoperatively by either gross inspection or even frozen section analysis. This distinction is important as anastomoses between irradiated segments of intestine have been associated with leak rates as high as 50%.58 If limited resec-tion is not achievable, an intestinal bypass procedure may be an option, except in cases for which hemorrhage is the surgical indication. There remain cases in which resections |
Surgery_Schwartz_8232 | Surgery_Schwartz | If limited resec-tion is not achievable, an intestinal bypass procedure may be an option, except in cases for which hemorrhage is the surgical indication. There remain cases in which resections extensive enough to cause short bowel syndrome are unavoidable. This condition is discussed in detail below in the “Short Bowel Syn-drome” section.OutcomesAcute radiation injury to the intestine is self-limited; its sever-ity is not correlated with the probability of chronic radiation enteritis developing. Surgery for chronic radiation enteritis is associated with high morbidity rates and reported mortality rates averaging 10%.PreventionIn view of significant morbidity associated with radiation enteri-tis, groups have studies possible measures to reduce or prevent such side effects. Keeping radiation exposure to below 5000 cGy is associated with minimal long-term side effects and is recom-mended where clinically possible.Uses of multibeam radiation techniques to minimize the area of maximal | Surgery_Schwartz. If limited resec-tion is not achievable, an intestinal bypass procedure may be an option, except in cases for which hemorrhage is the surgical indication. There remain cases in which resections extensive enough to cause short bowel syndrome are unavoidable. This condition is discussed in detail below in the “Short Bowel Syn-drome” section.OutcomesAcute radiation injury to the intestine is self-limited; its sever-ity is not correlated with the probability of chronic radiation enteritis developing. Surgery for chronic radiation enteritis is associated with high morbidity rates and reported mortality rates averaging 10%.PreventionIn view of significant morbidity associated with radiation enteri-tis, groups have studies possible measures to reduce or prevent such side effects. Keeping radiation exposure to below 5000 cGy is associated with minimal long-term side effects and is recom-mended where clinically possible.Uses of multibeam radiation techniques to minimize the area of maximal |
Surgery_Schwartz_8233 | Surgery_Schwartz | exposure to below 5000 cGy is associated with minimal long-term side effects and is recom-mended where clinically possible.Uses of multibeam radiation techniques to minimize the area of maximal radiation exposure, as well as tilt tables to move the bowel out of the pelvic during radiation, are increasingly utilized. Few small studies have suggested that oral sulphasala-zine may help reduce the incidence of acute radiation-induced enteritis.59In patients undergoing pelvic surgery that are likely to require postoperative radiation therapy, surgical techniques that keep the small bowel out of the pelvic have been recommended. These measures include use of absorbable mesh sling to sepa-rate the pelvic from the true abdominal cavity and prevent the small bowel from being exposed to pelvic radiation.60MECKEL’S DIVERTICULAMeckel’s diverticulum is the most prevalent congenital anom-aly of the gastrointestinal tract, affecting approximately 2% of the general population. Meckel’s diverticuli | Surgery_Schwartz. exposure to below 5000 cGy is associated with minimal long-term side effects and is recom-mended where clinically possible.Uses of multibeam radiation techniques to minimize the area of maximal radiation exposure, as well as tilt tables to move the bowel out of the pelvic during radiation, are increasingly utilized. Few small studies have suggested that oral sulphasala-zine may help reduce the incidence of acute radiation-induced enteritis.59In patients undergoing pelvic surgery that are likely to require postoperative radiation therapy, surgical techniques that keep the small bowel out of the pelvic have been recommended. These measures include use of absorbable mesh sling to sepa-rate the pelvic from the true abdominal cavity and prevent the small bowel from being exposed to pelvic radiation.60MECKEL’S DIVERTICULAMeckel’s diverticulum is the most prevalent congenital anom-aly of the gastrointestinal tract, affecting approximately 2% of the general population. Meckel’s diverticuli |
Surgery_Schwartz_8234 | Surgery_Schwartz | DIVERTICULAMeckel’s diverticulum is the most prevalent congenital anom-aly of the gastrointestinal tract, affecting approximately 2% of the general population. Meckel’s diverticuli are designated true diverticuli because their walls contain all the layers found in normal small intestine. Their location varies among individual patients, but they are usually found in the ileum within 100 cm of the ileocecal valve (Fig. 28-26). Approximately 60% of Meckel’s diverticuli contain heterotopic mucosa, of which over 60% consist of gastric mucosa. Pancreatic acini are the next most common; others include Brunner’s glands, pancre-atic islets, colonic mucosa, endometriosis, and hepatobiliary tissues. A useful, although crude, mnemonic describing Meck-el’s diverticuli is the “rule of twos”: 2% prevalence, 2:1 male predominance, location 2 feet proximal to the ileocecal valve in adults, and half of those who are symptomatic are under 2 years of age.PathophysiologyDuring the eighth week of | Surgery_Schwartz. DIVERTICULAMeckel’s diverticulum is the most prevalent congenital anom-aly of the gastrointestinal tract, affecting approximately 2% of the general population. Meckel’s diverticuli are designated true diverticuli because their walls contain all the layers found in normal small intestine. Their location varies among individual patients, but they are usually found in the ileum within 100 cm of the ileocecal valve (Fig. 28-26). Approximately 60% of Meckel’s diverticuli contain heterotopic mucosa, of which over 60% consist of gastric mucosa. Pancreatic acini are the next most common; others include Brunner’s glands, pancre-atic islets, colonic mucosa, endometriosis, and hepatobiliary tissues. A useful, although crude, mnemonic describing Meck-el’s diverticuli is the “rule of twos”: 2% prevalence, 2:1 male predominance, location 2 feet proximal to the ileocecal valve in adults, and half of those who are symptomatic are under 2 years of age.PathophysiologyDuring the eighth week of |
Surgery_Schwartz_8235 | Surgery_Schwartz | prevalence, 2:1 male predominance, location 2 feet proximal to the ileocecal valve in adults, and half of those who are symptomatic are under 2 years of age.PathophysiologyDuring the eighth week of gestation, the omphalomesenteric (vitelline) duct normally undergoes obliteration. Failure or Brunicardi_Ch28_p1219-p1258.indd 124623/02/19 2:24 PM 1247SMALL INTESTINECHAPTER 28Figure 28-26. Meckel’s diverticulum. This intraoperative photograph shows Meckel’s diverticulum in ileum that has been eviscerated.incomplete vitelline duct obliteration results in a spectrum of abnormalities, the most common of which is Meckel’s divertic-ulum. Other abnormalities include omphalomesenteric fistula, enterocyst, and a fibrous band connecting the intestine to the umbilicus. A remnant of the left vitelline artery can persist to form a mesodiverticular band tethering a Meckel’s diverticulum to the ileal mesentery.Bleeding associated with Meckel’s diverticulum is usu-ally the result of ileal mucosal | Surgery_Schwartz. prevalence, 2:1 male predominance, location 2 feet proximal to the ileocecal valve in adults, and half of those who are symptomatic are under 2 years of age.PathophysiologyDuring the eighth week of gestation, the omphalomesenteric (vitelline) duct normally undergoes obliteration. Failure or Brunicardi_Ch28_p1219-p1258.indd 124623/02/19 2:24 PM 1247SMALL INTESTINECHAPTER 28Figure 28-26. Meckel’s diverticulum. This intraoperative photograph shows Meckel’s diverticulum in ileum that has been eviscerated.incomplete vitelline duct obliteration results in a spectrum of abnormalities, the most common of which is Meckel’s divertic-ulum. Other abnormalities include omphalomesenteric fistula, enterocyst, and a fibrous band connecting the intestine to the umbilicus. A remnant of the left vitelline artery can persist to form a mesodiverticular band tethering a Meckel’s diverticulum to the ileal mesentery.Bleeding associated with Meckel’s diverticulum is usu-ally the result of ileal mucosal |
Surgery_Schwartz_8236 | Surgery_Schwartz | artery can persist to form a mesodiverticular band tethering a Meckel’s diverticulum to the ileal mesentery.Bleeding associated with Meckel’s diverticulum is usu-ally the result of ileal mucosal ulceration that occurs adjacent to acid-producing, heterotopic gastric mucosa located within the diverticulum. Intestinal obstruction associated with Meckel’s diverticulum can result from several mechanisms:1. Volvulus of the intestine around the fibrous band attaching the diverticulum to the umbilicus2. Entrapment of intestine by a mesodiverticular band (Fig. 28-27)3. Intussusception with the diverticulum acting as a lead point4. Stricture secondary to chronic diverticulitisMeckel’s diverticuli can be found in inguinal or femoral hernia sacs (known as Littre’s hernia). These hernias, when incarcerated, can cause intestinal obstruction.Figure 28-27. Meckel’s diverticulum with mesodiverticular band (A). One mechanism by which Meckel’s diverticuli can cause small bowel obstruction is entrapment | Surgery_Schwartz. artery can persist to form a mesodiverticular band tethering a Meckel’s diverticulum to the ileal mesentery.Bleeding associated with Meckel’s diverticulum is usu-ally the result of ileal mucosal ulceration that occurs adjacent to acid-producing, heterotopic gastric mucosa located within the diverticulum. Intestinal obstruction associated with Meckel’s diverticulum can result from several mechanisms:1. Volvulus of the intestine around the fibrous band attaching the diverticulum to the umbilicus2. Entrapment of intestine by a mesodiverticular band (Fig. 28-27)3. Intussusception with the diverticulum acting as a lead point4. Stricture secondary to chronic diverticulitisMeckel’s diverticuli can be found in inguinal or femoral hernia sacs (known as Littre’s hernia). These hernias, when incarcerated, can cause intestinal obstruction.Figure 28-27. Meckel’s diverticulum with mesodiverticular band (A). One mechanism by which Meckel’s diverticuli can cause small bowel obstruction is entrapment |
Surgery_Schwartz_8237 | Surgery_Schwartz | can cause intestinal obstruction.Figure 28-27. Meckel’s diverticulum with mesodiverticular band (A). One mechanism by which Meckel’s diverticuli can cause small bowel obstruction is entrapment of the intestine by a mesodiverticular band (B).Clinical PresentationMeckel’s diverticuli are asymptomatic unless associated com-plications arise. The lifetime incidence rate of complications arising in patients with Meckel’s diverticuli has been estimated to be approximately 4% to 6%.61,62 Although initial data had suggested that the risk of developing a complication related to Meckel’s diverticulum decreases with age, this has been ques-tioned. In a population-based reviews at Olmsted County, Cullen and colleagues suggested that the risk of developing Meckel’s diverticulum–related complications does not change with age.62The most common presentations associated with symp-tomatic Meckel’s diverticuli are bleeding, intestinal obstruction, and diverticulitis. Bleeding is the most common | Surgery_Schwartz. can cause intestinal obstruction.Figure 28-27. Meckel’s diverticulum with mesodiverticular band (A). One mechanism by which Meckel’s diverticuli can cause small bowel obstruction is entrapment of the intestine by a mesodiverticular band (B).Clinical PresentationMeckel’s diverticuli are asymptomatic unless associated com-plications arise. The lifetime incidence rate of complications arising in patients with Meckel’s diverticuli has been estimated to be approximately 4% to 6%.61,62 Although initial data had suggested that the risk of developing a complication related to Meckel’s diverticulum decreases with age, this has been ques-tioned. In a population-based reviews at Olmsted County, Cullen and colleagues suggested that the risk of developing Meckel’s diverticulum–related complications does not change with age.62The most common presentations associated with symp-tomatic Meckel’s diverticuli are bleeding, intestinal obstruction, and diverticulitis. Bleeding is the most common |
Surgery_Schwartz_8238 | Surgery_Schwartz | does not change with age.62The most common presentations associated with symp-tomatic Meckel’s diverticuli are bleeding, intestinal obstruction, and diverticulitis. Bleeding is the most common presentation in children with Meckel’s diverticuli, representing over 50% of Meckel’s diverticulum-related complications among patients less than 18 years of age. Bleeding associated with Meckel’s diverticuli is rare among patients older than 30 years of age.Intestinal obstruction is the most common presentation in adults with Meckel’s diverticuli. Diverticulitis, present in 20% of patients with symptomatic Meckel’s diverticuli, is associated with a clinical syndrome that is indistinguishable from acute appendicitis. Neoplasms, most commonly carcinoid tumors, are present in 0.5% to 3.2% of symptomatic Meckel’s diverticuli that are resected.DiagnosisMost Meckel’s diverticuli are discovered incidentally on radio-graphic imaging, during endoscopy, or at the time of surgery. In the absence of | Surgery_Schwartz. does not change with age.62The most common presentations associated with symp-tomatic Meckel’s diverticuli are bleeding, intestinal obstruction, and diverticulitis. Bleeding is the most common presentation in children with Meckel’s diverticuli, representing over 50% of Meckel’s diverticulum-related complications among patients less than 18 years of age. Bleeding associated with Meckel’s diverticuli is rare among patients older than 30 years of age.Intestinal obstruction is the most common presentation in adults with Meckel’s diverticuli. Diverticulitis, present in 20% of patients with symptomatic Meckel’s diverticuli, is associated with a clinical syndrome that is indistinguishable from acute appendicitis. Neoplasms, most commonly carcinoid tumors, are present in 0.5% to 3.2% of symptomatic Meckel’s diverticuli that are resected.DiagnosisMost Meckel’s diverticuli are discovered incidentally on radio-graphic imaging, during endoscopy, or at the time of surgery. In the absence of |
Surgery_Schwartz_8239 | Surgery_Schwartz | Meckel’s diverticuli that are resected.DiagnosisMost Meckel’s diverticuli are discovered incidentally on radio-graphic imaging, during endoscopy, or at the time of surgery. In the absence of bleeding, Meckel’s diverticuli rarely are diag-nosed prior to the time of surgical intervention. For those pre-senting with symptoms suggestive of a Meckel’s diverticulum, confirmatory imaging can be challenging. The sensitivity of CT scanning for the detection of Meckel’s diverticuli is too low to be clinically useful. Enterocolysis is associated with an accuracy of 75% but is usually not applicable during acute presentations of complications related to Meckel’s diverticuli. Radionuclide scans (99MTc–pertechnetate) can be helpful in the diagnosis of Meckel’s diverticulum; this test is, however, positive only when the diverticulum contains associated ectopic gastric mucosa that is capable of uptake of the tracer (Fig. 28-28). The accuracy of radionuclide scanning is reported to be 90% in pediatric | Surgery_Schwartz. Meckel’s diverticuli that are resected.DiagnosisMost Meckel’s diverticuli are discovered incidentally on radio-graphic imaging, during endoscopy, or at the time of surgery. In the absence of bleeding, Meckel’s diverticuli rarely are diag-nosed prior to the time of surgical intervention. For those pre-senting with symptoms suggestive of a Meckel’s diverticulum, confirmatory imaging can be challenging. The sensitivity of CT scanning for the detection of Meckel’s diverticuli is too low to be clinically useful. Enterocolysis is associated with an accuracy of 75% but is usually not applicable during acute presentations of complications related to Meckel’s diverticuli. Radionuclide scans (99MTc–pertechnetate) can be helpful in the diagnosis of Meckel’s diverticulum; this test is, however, positive only when the diverticulum contains associated ectopic gastric mucosa that is capable of uptake of the tracer (Fig. 28-28). The accuracy of radionuclide scanning is reported to be 90% in pediatric |
Surgery_Schwartz_8240 | Surgery_Schwartz | only when the diverticulum contains associated ectopic gastric mucosa that is capable of uptake of the tracer (Fig. 28-28). The accuracy of radionuclide scanning is reported to be 90% in pediatric patients but less than 50% in adults. Angiography can localize the site of bleeding during acute hemorrhage related to Meckel’s diverticuli.Brunicardi_Ch28_p1219-p1258.indd 124723/02/19 2:24 PM 1248SPECIFIC CONSIDERATIONSPART IIFigure 28-28. Meckel’s diverticulum with ectopic gastric tissue. The diagnosis was made in this patient using 99MTc–pertechnetate scintig-raphy. The study revealed an abnormal focus of radiotracer accumulation in the right lower quadrant (arrow).TherapyThe surgical treatment of symptomatic Meckel’s diverticuli should consist of diverticulectomy with removal of associated bands connecting the diverticulum to the abdominal wall or intestinal mesentery. If the indication for diverticulectomy is bleeding, segmental resection of ileum that includes both the | Surgery_Schwartz. only when the diverticulum contains associated ectopic gastric mucosa that is capable of uptake of the tracer (Fig. 28-28). The accuracy of radionuclide scanning is reported to be 90% in pediatric patients but less than 50% in adults. Angiography can localize the site of bleeding during acute hemorrhage related to Meckel’s diverticuli.Brunicardi_Ch28_p1219-p1258.indd 124723/02/19 2:24 PM 1248SPECIFIC CONSIDERATIONSPART IIFigure 28-28. Meckel’s diverticulum with ectopic gastric tissue. The diagnosis was made in this patient using 99MTc–pertechnetate scintig-raphy. The study revealed an abnormal focus of radiotracer accumulation in the right lower quadrant (arrow).TherapyThe surgical treatment of symptomatic Meckel’s diverticuli should consist of diverticulectomy with removal of associated bands connecting the diverticulum to the abdominal wall or intestinal mesentery. If the indication for diverticulectomy is bleeding, segmental resection of ileum that includes both the |
Surgery_Schwartz_8241 | Surgery_Schwartz | of associated bands connecting the diverticulum to the abdominal wall or intestinal mesentery. If the indication for diverticulectomy is bleeding, segmental resection of ileum that includes both the diverticulum and the adjacent ileal peptic ulcer should be per-formed. Segmental ileal resection may also be necessary if the diverticulum contains a tumor or if the base of the diverticulum is inflamed or perforated.The management of incidentally found (asymptomatic) Meckel’s diverticuli is controversial. Until recently, most authors recommended against prophylactic removal of asymptomatic Meckel’s diverticuli, given the low lifetime incidence of com-plications. Supporting this approach, a meta-analysis has shown that 758 prophylactic diverticulectomies needed to be performed to prevent one Meckel’s-related death.63 Others have had greater enthusiasm for prophylactic diverticulectomy has appeared in the literature.64 Proponents of this approach cite the minimal mor-bidity associated with | Surgery_Schwartz. of associated bands connecting the diverticulum to the abdominal wall or intestinal mesentery. If the indication for diverticulectomy is bleeding, segmental resection of ileum that includes both the diverticulum and the adjacent ileal peptic ulcer should be per-formed. Segmental ileal resection may also be necessary if the diverticulum contains a tumor or if the base of the diverticulum is inflamed or perforated.The management of incidentally found (asymptomatic) Meckel’s diverticuli is controversial. Until recently, most authors recommended against prophylactic removal of asymptomatic Meckel’s diverticuli, given the low lifetime incidence of com-plications. Supporting this approach, a meta-analysis has shown that 758 prophylactic diverticulectomies needed to be performed to prevent one Meckel’s-related death.63 Others have had greater enthusiasm for prophylactic diverticulectomy has appeared in the literature.64 Proponents of this approach cite the minimal mor-bidity associated with |
Surgery_Schwartz_8242 | Surgery_Schwartz | death.63 Others have had greater enthusiasm for prophylactic diverticulectomy has appeared in the literature.64 Proponents of this approach cite the minimal mor-bidity associated with removing Meckel’s diverticuli and the possibility that previous estimates of the lifetime incidence of complications related to Meckel’s diverticuli may be erroneously low. Many have advocated a selective approach, with a recom-mendation to remove diverticuli in patients younger than 50 years of age, or those with band attachments, those with ectopic tissue, or those >2 cm in length on the assumption that these diverticuli are more likely to develop complications. No controlled data sup-porting or refuting these recommendations exist.ACQUIRED DIVERTICULAAcquired diverticuli are designated false diverticuli because their walls consist of mucosa and submucosa but lack a com-plete muscularis. Acquired diverticuli are more common in the duodenum, and tend to be located near the ampulla; such diverticuli are | Surgery_Schwartz. death.63 Others have had greater enthusiasm for prophylactic diverticulectomy has appeared in the literature.64 Proponents of this approach cite the minimal mor-bidity associated with removing Meckel’s diverticuli and the possibility that previous estimates of the lifetime incidence of complications related to Meckel’s diverticuli may be erroneously low. Many have advocated a selective approach, with a recom-mendation to remove diverticuli in patients younger than 50 years of age, or those with band attachments, those with ectopic tissue, or those >2 cm in length on the assumption that these diverticuli are more likely to develop complications. No controlled data sup-porting or refuting these recommendations exist.ACQUIRED DIVERTICULAAcquired diverticuli are designated false diverticuli because their walls consist of mucosa and submucosa but lack a com-plete muscularis. Acquired diverticuli are more common in the duodenum, and tend to be located near the ampulla; such diverticuli are |
Surgery_Schwartz_8243 | Surgery_Schwartz | their walls consist of mucosa and submucosa but lack a com-plete muscularis. Acquired diverticuli are more common in the duodenum, and tend to be located near the ampulla; such diverticuli are known as periampullary, juxtapapillary, and perivaterian diverticuli. Approximately 75% of juxtapapillary diverticuli arise on the medial wall of the duodenum. Acquired diverticuli in the jejunum or ileum are known as jejunoileal diverticuli. Eighty percent of jejunoileal diverticuli are localized to the jejunum, 15% to the ileum, and 5% to both jejunum and ileum. Diverticuli in the jejunum tend to be large and accom-panied by multiple other diverticuli, whereas those in the ileum tend to be small and solitary.The prevalence of duodenal diverticuli, as detected on upper GI examinations (Fig. 28-29), has been reported to range from 0.16% to 6%.65 Their prevalence, as detected during ERCP examinations, has been reported to range from 5% to 27%. A 23% prevalence rate has been reported in an autopsy | Surgery_Schwartz. their walls consist of mucosa and submucosa but lack a com-plete muscularis. Acquired diverticuli are more common in the duodenum, and tend to be located near the ampulla; such diverticuli are known as periampullary, juxtapapillary, and perivaterian diverticuli. Approximately 75% of juxtapapillary diverticuli arise on the medial wall of the duodenum. Acquired diverticuli in the jejunum or ileum are known as jejunoileal diverticuli. Eighty percent of jejunoileal diverticuli are localized to the jejunum, 15% to the ileum, and 5% to both jejunum and ileum. Diverticuli in the jejunum tend to be large and accom-panied by multiple other diverticuli, whereas those in the ileum tend to be small and solitary.The prevalence of duodenal diverticuli, as detected on upper GI examinations (Fig. 28-29), has been reported to range from 0.16% to 6%.65 Their prevalence, as detected during ERCP examinations, has been reported to range from 5% to 27%. A 23% prevalence rate has been reported in an autopsy |
Surgery_Schwartz_8244 | Surgery_Schwartz | has been reported to range from 0.16% to 6%.65 Their prevalence, as detected during ERCP examinations, has been reported to range from 5% to 27%. A 23% prevalence rate has been reported in an autopsy series. The prevalence of duodenal diverticuli increases with age; they are Brunicardi_Ch28_p1219-p1258.indd 124823/02/19 2:24 PM 1249SMALL INTESTINECHAPTER 28Figure 28-29. Duodenal diverticulum. This contrast radiograph demonstrates a duodenal diverticulum (arrows) that extends medially into the substance of the head of the pancreas.Figure 28-30. Jejunoileal diverticuli. This picture demonstrates incidental jejunal diverticuli identified during a laparoscopic cholecystectomy. The diverticuli are typically located on the mesenteric aspect of the jejunum. Resection was not indicated as the diverticuli were asymptomatic.rare in patients under the age of 40 years. The mean age of diagnosis ranges from 56 to 76 years.The prevalence of jejunoileal diverticuli (Fig. 28-30) has been | Surgery_Schwartz. has been reported to range from 0.16% to 6%.65 Their prevalence, as detected during ERCP examinations, has been reported to range from 5% to 27%. A 23% prevalence rate has been reported in an autopsy series. The prevalence of duodenal diverticuli increases with age; they are Brunicardi_Ch28_p1219-p1258.indd 124823/02/19 2:24 PM 1249SMALL INTESTINECHAPTER 28Figure 28-29. Duodenal diverticulum. This contrast radiograph demonstrates a duodenal diverticulum (arrows) that extends medially into the substance of the head of the pancreas.Figure 28-30. Jejunoileal diverticuli. This picture demonstrates incidental jejunal diverticuli identified during a laparoscopic cholecystectomy. The diverticuli are typically located on the mesenteric aspect of the jejunum. Resection was not indicated as the diverticuli were asymptomatic.rare in patients under the age of 40 years. The mean age of diagnosis ranges from 56 to 76 years.The prevalence of jejunoileal diverticuli (Fig. 28-30) has been |
Surgery_Schwartz_8245 | Surgery_Schwartz | as the diverticuli were asymptomatic.rare in patients under the age of 40 years. The mean age of diagnosis ranges from 56 to 76 years.The prevalence of jejunoileal diverticuli (Fig. 28-30) has been estimated to range from 1% to 5%.66 Their prevalence increases with age; most patients diagnosed with these diver-ticuli are in the sixth and seventh decades of life.PathophysiologyThe pathogenesis of acquired diverticuli is hypothesized to be related to acquired abnormalities of intestinal smooth muscle or dysregulated motility, leading to herniation of mucosa and submucosa through weakened areas of muscularis.Acquired diverticuli can be associated with bacterial over-growth, leading to vitamin B12 deficiency, megaloblastic anemia, malabsorption, and steatorrhea. Periampullary duodenal diver-ticuli have been described to become distended with intralumi-nal debris and to compress the common bile duct or pancreatic duct, thus causing obstructive jaundice or pancreatitis, respec-tively. | Surgery_Schwartz. as the diverticuli were asymptomatic.rare in patients under the age of 40 years. The mean age of diagnosis ranges from 56 to 76 years.The prevalence of jejunoileal diverticuli (Fig. 28-30) has been estimated to range from 1% to 5%.66 Their prevalence increases with age; most patients diagnosed with these diver-ticuli are in the sixth and seventh decades of life.PathophysiologyThe pathogenesis of acquired diverticuli is hypothesized to be related to acquired abnormalities of intestinal smooth muscle or dysregulated motility, leading to herniation of mucosa and submucosa through weakened areas of muscularis.Acquired diverticuli can be associated with bacterial over-growth, leading to vitamin B12 deficiency, megaloblastic anemia, malabsorption, and steatorrhea. Periampullary duodenal diver-ticuli have been described to become distended with intralumi-nal debris and to compress the common bile duct or pancreatic duct, thus causing obstructive jaundice or pancreatitis, respec-tively. |
Surgery_Schwartz_8246 | Surgery_Schwartz | have been described to become distended with intralumi-nal debris and to compress the common bile duct or pancreatic duct, thus causing obstructive jaundice or pancreatitis, respec-tively. Jejunoileal diverticuli can also cause intestinal obstruction through intussusception or compression of adjacent bowel.Brunicardi_Ch28_p1219-p1258.indd 124923/02/19 2:25 PM 1250SPECIFIC CONSIDERATIONSPART IIClinical PresentationAcquired diverticuli are asymptomatic unless associated com-plications arise. Such complications are estimated to occur in 6% to 10% of patients with acquired diverticuli and include intestinal obstruction, diverticulitis, hemorrhage, perforation, and malabsorption. Periampullary duodenal diverticuli may be associated with choledocholithiasis, cholangitis, recurrent pan-creatitis, and sphincter of Oddi dysfunction. However, a clear link between the presence of the diverticuli and the development of these conditions has not been demonstrated. Symptoms such as intermittent | Surgery_Schwartz. have been described to become distended with intralumi-nal debris and to compress the common bile duct or pancreatic duct, thus causing obstructive jaundice or pancreatitis, respec-tively. Jejunoileal diverticuli can also cause intestinal obstruction through intussusception or compression of adjacent bowel.Brunicardi_Ch28_p1219-p1258.indd 124923/02/19 2:25 PM 1250SPECIFIC CONSIDERATIONSPART IIClinical PresentationAcquired diverticuli are asymptomatic unless associated com-plications arise. Such complications are estimated to occur in 6% to 10% of patients with acquired diverticuli and include intestinal obstruction, diverticulitis, hemorrhage, perforation, and malabsorption. Periampullary duodenal diverticuli may be associated with choledocholithiasis, cholangitis, recurrent pan-creatitis, and sphincter of Oddi dysfunction. However, a clear link between the presence of the diverticuli and the development of these conditions has not been demonstrated. Symptoms such as intermittent |
Surgery_Schwartz_8247 | Surgery_Schwartz | and sphincter of Oddi dysfunction. However, a clear link between the presence of the diverticuli and the development of these conditions has not been demonstrated. Symptoms such as intermittent abdominal pain, flatulence, diarrhea, and consti-pation are reported to be present in 10% to 30% of patients with jejunoileal diverticuli. The relationship between these symp-toms and the presence of the diverticuli is similarly unclear.DiagnosisMost acquired diverticuli are discovered incidentally on radiographic imaging, during endoscopy, or at the time of surgery. On ultrasound and CT scanning, duodenal diverticuli may be mistaken for pancreatic pseudocysts and fluid collections, biliary cysts, and periampullary neoplasms. These lesions can be missed on endoscopy, particularly with forward-viewing endoscopes, and are best diagnosed on upper gastrointestinal radiographs. Enterocolysis is the most sensitive test for detecting jejunoileal diverticuli.TherapyAsymptomatic-acquired diverticuli | Surgery_Schwartz. and sphincter of Oddi dysfunction. However, a clear link between the presence of the diverticuli and the development of these conditions has not been demonstrated. Symptoms such as intermittent abdominal pain, flatulence, diarrhea, and consti-pation are reported to be present in 10% to 30% of patients with jejunoileal diverticuli. The relationship between these symp-toms and the presence of the diverticuli is similarly unclear.DiagnosisMost acquired diverticuli are discovered incidentally on radiographic imaging, during endoscopy, or at the time of surgery. On ultrasound and CT scanning, duodenal diverticuli may be mistaken for pancreatic pseudocysts and fluid collections, biliary cysts, and periampullary neoplasms. These lesions can be missed on endoscopy, particularly with forward-viewing endoscopes, and are best diagnosed on upper gastrointestinal radiographs. Enterocolysis is the most sensitive test for detecting jejunoileal diverticuli.TherapyAsymptomatic-acquired diverticuli |
Surgery_Schwartz_8248 | Surgery_Schwartz | endoscopes, and are best diagnosed on upper gastrointestinal radiographs. Enterocolysis is the most sensitive test for detecting jejunoileal diverticuli.TherapyAsymptomatic-acquired diverticuli should be left alone. Bacte-rial overgrowth associated with acquired diverticuli is treated with antibiotics. Other complications, such as bleeding and diverticulitis, are treated with segmental intestinal resection for diverticuli located in the jejunum or ileum.Bleeding and obstruction related to lateral duodenal diverticuli are generally treated with diverticulectomy alone. Treatment of such complications in medial duodenal diverticuli that penetrate the substance of the pancreas can be very challenging. Complications related to these medial duodenal diverticuli should be managed nonoperatively if possible, using endoscopy. In emergent situations, bleeding related to medial duodenal diverticuli can be controlled using a lateral duodenotomy and oversewing of the bleeding vessel. Similarly, | Surgery_Schwartz. endoscopes, and are best diagnosed on upper gastrointestinal radiographs. Enterocolysis is the most sensitive test for detecting jejunoileal diverticuli.TherapyAsymptomatic-acquired diverticuli should be left alone. Bacte-rial overgrowth associated with acquired diverticuli is treated with antibiotics. Other complications, such as bleeding and diverticulitis, are treated with segmental intestinal resection for diverticuli located in the jejunum or ileum.Bleeding and obstruction related to lateral duodenal diverticuli are generally treated with diverticulectomy alone. Treatment of such complications in medial duodenal diverticuli that penetrate the substance of the pancreas can be very challenging. Complications related to these medial duodenal diverticuli should be managed nonoperatively if possible, using endoscopy. In emergent situations, bleeding related to medial duodenal diverticuli can be controlled using a lateral duodenotomy and oversewing of the bleeding vessel. Similarly, |
Surgery_Schwartz_8249 | Surgery_Schwartz | if possible, using endoscopy. In emergent situations, bleeding related to medial duodenal diverticuli can be controlled using a lateral duodenotomy and oversewing of the bleeding vessel. Similarly, perforation can be managed with wide drainage rather than complex surgery. Whether diverticulectomy should be done in patients with biliary or pancreatic symptoms is controversial and is not routinely recommended.MESENTERIC ISCHEMIAMesenteric ischemia can present as one of two distinct clinical syndromes: acute mesenteric ischemia and chronic mesenteric ischemia.Four distinct pathophysiologic mechanisms can lead to acute mesenteric ischemia:1. Arterial embolus2. Arterial thrombosis3. Vasospasm (also known as nonocclusive mesenteric isch-emia or NOMI)4. Venous thrombosisEmbolus is the most common cause of acute mesen-teric ischemia and is responsible for over 50% of cases. The embolic source is usually in the heart, most often the left atrial or ventricular thrombi or valvular lesions. | Surgery_Schwartz. if possible, using endoscopy. In emergent situations, bleeding related to medial duodenal diverticuli can be controlled using a lateral duodenotomy and oversewing of the bleeding vessel. Similarly, perforation can be managed with wide drainage rather than complex surgery. Whether diverticulectomy should be done in patients with biliary or pancreatic symptoms is controversial and is not routinely recommended.MESENTERIC ISCHEMIAMesenteric ischemia can present as one of two distinct clinical syndromes: acute mesenteric ischemia and chronic mesenteric ischemia.Four distinct pathophysiologic mechanisms can lead to acute mesenteric ischemia:1. Arterial embolus2. Arterial thrombosis3. Vasospasm (also known as nonocclusive mesenteric isch-emia or NOMI)4. Venous thrombosisEmbolus is the most common cause of acute mesen-teric ischemia and is responsible for over 50% of cases. The embolic source is usually in the heart, most often the left atrial or ventricular thrombi or valvular lesions. |
Surgery_Schwartz_8250 | Surgery_Schwartz | common cause of acute mesen-teric ischemia and is responsible for over 50% of cases. The embolic source is usually in the heart, most often the left atrial or ventricular thrombi or valvular lesions. Indeed, up to 95% of patients with acute mesenteric ischemia due to emboli will have a documented history of cardiac disease. Embolism to the superior mesenteric artery accounts for 50% of cases; most of these emboli become wedged and cause occlusion at branch points in the midto distal superior mesenteric artery, usually distal to the origin of the middle colic artery. In contrast, acute occlusions due to thrombosis tend to occur in the proximal mes-enteric arteries, near their origins. Acute thrombosis is usually superimposed on preexisting atherosclerotic lesions at these sites. NOMI is the result of vasospasm and is usually diagnosed in critically ill patients receiving vasopressor agents.Mesenteric venous thrombosis accounts for 5% to 15% of cases of acute mesenteric ischemia and | Surgery_Schwartz. common cause of acute mesen-teric ischemia and is responsible for over 50% of cases. The embolic source is usually in the heart, most often the left atrial or ventricular thrombi or valvular lesions. Indeed, up to 95% of patients with acute mesenteric ischemia due to emboli will have a documented history of cardiac disease. Embolism to the superior mesenteric artery accounts for 50% of cases; most of these emboli become wedged and cause occlusion at branch points in the midto distal superior mesenteric artery, usually distal to the origin of the middle colic artery. In contrast, acute occlusions due to thrombosis tend to occur in the proximal mes-enteric arteries, near their origins. Acute thrombosis is usually superimposed on preexisting atherosclerotic lesions at these sites. NOMI is the result of vasospasm and is usually diagnosed in critically ill patients receiving vasopressor agents.Mesenteric venous thrombosis accounts for 5% to 15% of cases of acute mesenteric ischemia and |
Surgery_Schwartz_8251 | Surgery_Schwartz | the result of vasospasm and is usually diagnosed in critically ill patients receiving vasopressor agents.Mesenteric venous thrombosis accounts for 5% to 15% of cases of acute mesenteric ischemia and involves the supe-rior mesenteric vein in 95% of cases.67 The inferior mesenteric vein is only rarely involved. Mesenteric venous thrombosis is classified as primary if no etiologic factor is identifiable, or as secondary if an etiologic factor, such as heritable or acquired coagulation disorders, is identified.Regardless of the pathophysiologic mechanism, acute mes-enteric ischemia can lead to intestinal mucosal sloughing within 3 hours of onset and full-thickness intestinal infarction by 6 hours.In contrast, chronic mesenteric ischemia develops insidi-ously, allowing for development of collateral circulation, and, therefore, rarely leads to intestinal infarction. Chronic mesen-teric arterial ischemia results from atherosclerotic lesions in the main splanchnic arteries (celiac, superior | Surgery_Schwartz. the result of vasospasm and is usually diagnosed in critically ill patients receiving vasopressor agents.Mesenteric venous thrombosis accounts for 5% to 15% of cases of acute mesenteric ischemia and involves the supe-rior mesenteric vein in 95% of cases.67 The inferior mesenteric vein is only rarely involved. Mesenteric venous thrombosis is classified as primary if no etiologic factor is identifiable, or as secondary if an etiologic factor, such as heritable or acquired coagulation disorders, is identified.Regardless of the pathophysiologic mechanism, acute mes-enteric ischemia can lead to intestinal mucosal sloughing within 3 hours of onset and full-thickness intestinal infarction by 6 hours.In contrast, chronic mesenteric ischemia develops insidi-ously, allowing for development of collateral circulation, and, therefore, rarely leads to intestinal infarction. Chronic mesen-teric arterial ischemia results from atherosclerotic lesions in the main splanchnic arteries (celiac, superior |
Surgery_Schwartz_8252 | Surgery_Schwartz | circulation, and, therefore, rarely leads to intestinal infarction. Chronic mesen-teric arterial ischemia results from atherosclerotic lesions in the main splanchnic arteries (celiac, superior mesenteric, and inferior mesenteric arteries). In most patients with symptoms attributable to chronic mesenteric ischemia, at least two of these arteries are either occluded or severely stenosed. A chronic form of mesenteric venous thrombosis can involve the portal or splenic veins and may lead to portal hypertension, with result-ing esophagogastric varices, splenomegaly, and hypersplenism.Severe abdominal pain, out of proportion to the degree of tenderness on examination is the hallmark of acute mesenteric ischemia, regardless of the pathophysiologic mechanism. The pain is typically perceived to be colicky and most severe in the mid-abdomen. Associated symptoms can include nausea, vomiting, and diarrhea. Physical findings are characteristically absent early in the course of ischemia. With the | Surgery_Schwartz. circulation, and, therefore, rarely leads to intestinal infarction. Chronic mesen-teric arterial ischemia results from atherosclerotic lesions in the main splanchnic arteries (celiac, superior mesenteric, and inferior mesenteric arteries). In most patients with symptoms attributable to chronic mesenteric ischemia, at least two of these arteries are either occluded or severely stenosed. A chronic form of mesenteric venous thrombosis can involve the portal or splenic veins and may lead to portal hypertension, with result-ing esophagogastric varices, splenomegaly, and hypersplenism.Severe abdominal pain, out of proportion to the degree of tenderness on examination is the hallmark of acute mesenteric ischemia, regardless of the pathophysiologic mechanism. The pain is typically perceived to be colicky and most severe in the mid-abdomen. Associated symptoms can include nausea, vomiting, and diarrhea. Physical findings are characteristically absent early in the course of ischemia. With the |
Surgery_Schwartz_8253 | Surgery_Schwartz | colicky and most severe in the mid-abdomen. Associated symptoms can include nausea, vomiting, and diarrhea. Physical findings are characteristically absent early in the course of ischemia. With the onset of bowel infarction, abdominal distension, peritonitis, and passage of bloody stools occur.Chronic mesenteric ischemia presents insidiously. Post-prandial abdominal pain is the most prevalent symptom, produc-ing a characteristic aversion to food (“food fear”) and weight loss. These patients are often thought to have a malignancy and suffer a prolonged period of symptoms before the correct diag-nosis is made.Most patients with chronic mesenteric venous thrombosis are asymptomatic because of the presence of extensive collat-eral venous drainage routes; this condition is usually discovered as an incidental finding on imaging studies. However, some patients with chronic mesenteric venous thrombosis present with bleeding from esophagogastric varices.The diagnosis and management of these | Surgery_Schwartz. colicky and most severe in the mid-abdomen. Associated symptoms can include nausea, vomiting, and diarrhea. Physical findings are characteristically absent early in the course of ischemia. With the onset of bowel infarction, abdominal distension, peritonitis, and passage of bloody stools occur.Chronic mesenteric ischemia presents insidiously. Post-prandial abdominal pain is the most prevalent symptom, produc-ing a characteristic aversion to food (“food fear”) and weight loss. These patients are often thought to have a malignancy and suffer a prolonged period of symptoms before the correct diag-nosis is made.Most patients with chronic mesenteric venous thrombosis are asymptomatic because of the presence of extensive collat-eral venous drainage routes; this condition is usually discovered as an incidental finding on imaging studies. However, some patients with chronic mesenteric venous thrombosis present with bleeding from esophagogastric varices.The diagnosis and management of these |
Surgery_Schwartz_8254 | Surgery_Schwartz | as an incidental finding on imaging studies. However, some patients with chronic mesenteric venous thrombosis present with bleeding from esophagogastric varices.The diagnosis and management of these disorders, which are of primary vascular origin, are discussed in the section on “Mesen-teric Artery Occlusive Disease” in Chapter 23 “Arterial Disease.”MISCELLANEOUS CONDITIONSObscure GI BleedingUp to 90% of lesions responsible for GI bleeding are within the reach of EGD and colonoscopy. Obscure GI bleeding refers to gastrointestinal bleeding for which no source has been identified by routine endoscopic studies (EGD and colonoscopy). Overt Brunicardi_Ch28_p1219-p1258.indd 125023/02/19 2:25 PM 1251SMALL INTESTINECHAPTER 28GI bleeding refers to the presence of hematemesis, melena, or hematochezia. In contrast, occult GI bleeding occurs in the absence of overt bleeding and is identified on laboratory tests (e.g., iron-deficiency anemia) or examination of the stool (e.g., positive guaiac | Surgery_Schwartz. as an incidental finding on imaging studies. However, some patients with chronic mesenteric venous thrombosis present with bleeding from esophagogastric varices.The diagnosis and management of these disorders, which are of primary vascular origin, are discussed in the section on “Mesen-teric Artery Occlusive Disease” in Chapter 23 “Arterial Disease.”MISCELLANEOUS CONDITIONSObscure GI BleedingUp to 90% of lesions responsible for GI bleeding are within the reach of EGD and colonoscopy. Obscure GI bleeding refers to gastrointestinal bleeding for which no source has been identified by routine endoscopic studies (EGD and colonoscopy). Overt Brunicardi_Ch28_p1219-p1258.indd 125023/02/19 2:25 PM 1251SMALL INTESTINECHAPTER 28GI bleeding refers to the presence of hematemesis, melena, or hematochezia. In contrast, occult GI bleeding occurs in the absence of overt bleeding and is identified on laboratory tests (e.g., iron-deficiency anemia) or examination of the stool (e.g., positive guaiac |
Surgery_Schwartz_8255 | Surgery_Schwartz | In contrast, occult GI bleeding occurs in the absence of overt bleeding and is identified on laboratory tests (e.g., iron-deficiency anemia) or examination of the stool (e.g., positive guaiac test). Obscure GI bleeding is occult in 20% of cases.68Obscure bleeding can be frustrating for both the patient and the clinician, and this is particularly true for obscure-overt bleeding, which cannot be localized despite aggressive diag-nostic measures. Most of the small bowel is beyond the reach of these examinations and, hence, contains most lesions respon-sible for obscure GI bleeding. Small intestinal angiodysplasias account for approximately 75% of cases in adults, and neo-plasms account for approximately 10%. Meckel’s diverticulum is the most common etiology of obscure GI bleeding in children. Other etiologies of obscure GI bleeding include Crohn’s dis-ease, infectious enteritides, nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers and erosions, vasculitis, ischemia, var-ices, | Surgery_Schwartz. In contrast, occult GI bleeding occurs in the absence of overt bleeding and is identified on laboratory tests (e.g., iron-deficiency anemia) or examination of the stool (e.g., positive guaiac test). Obscure GI bleeding is occult in 20% of cases.68Obscure bleeding can be frustrating for both the patient and the clinician, and this is particularly true for obscure-overt bleeding, which cannot be localized despite aggressive diag-nostic measures. Most of the small bowel is beyond the reach of these examinations and, hence, contains most lesions respon-sible for obscure GI bleeding. Small intestinal angiodysplasias account for approximately 75% of cases in adults, and neo-plasms account for approximately 10%. Meckel’s diverticulum is the most common etiology of obscure GI bleeding in children. Other etiologies of obscure GI bleeding include Crohn’s dis-ease, infectious enteritides, nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers and erosions, vasculitis, ischemia, var-ices, |
Surgery_Schwartz_8256 | Surgery_Schwartz | Other etiologies of obscure GI bleeding include Crohn’s dis-ease, infectious enteritides, nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers and erosions, vasculitis, ischemia, var-ices, diverticuli, and intussusception.The diagnostic evaluation of patients with obscure GI bleeding should be tailored to the severity to bleeding and to the availability of technology and expertise. Enteroscopy is playing an increasingly important role. Several endoscopic techniques for visualizing the small intestine are available: push enteros-copy, sonde enteroscopy, intraoperative enteroscopy, double balloon endoscopy, and wireless capsule enteroscopy.Push enteroscopy entails advancing a long endoscope (such as a pediatric or adult colonoscope or a specialized instru-ment) beyond the ligament of Treitz into the proximal jejunum. This procedure can allow for visualization of approximately 60 cm of the proximal jejunum. Diagnostic yield in patients with obscure GI bleeding ranges from 3% to | Surgery_Schwartz. Other etiologies of obscure GI bleeding include Crohn’s dis-ease, infectious enteritides, nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers and erosions, vasculitis, ischemia, var-ices, diverticuli, and intussusception.The diagnostic evaluation of patients with obscure GI bleeding should be tailored to the severity to bleeding and to the availability of technology and expertise. Enteroscopy is playing an increasingly important role. Several endoscopic techniques for visualizing the small intestine are available: push enteros-copy, sonde enteroscopy, intraoperative enteroscopy, double balloon endoscopy, and wireless capsule enteroscopy.Push enteroscopy entails advancing a long endoscope (such as a pediatric or adult colonoscope or a specialized instru-ment) beyond the ligament of Treitz into the proximal jejunum. This procedure can allow for visualization of approximately 60 cm of the proximal jejunum. Diagnostic yield in patients with obscure GI bleeding ranges from 3% to |
Surgery_Schwartz_8257 | Surgery_Schwartz | Treitz into the proximal jejunum. This procedure can allow for visualization of approximately 60 cm of the proximal jejunum. Diagnostic yield in patients with obscure GI bleeding ranges from 3% to 65%. In addition to diagnosis, push enteroscopy allows for cauterization of bleed-ing sites.In Sonde enteroscopy, a long, thin fiberoptic instrument is propelled through the intestine by peristalsis following infla-tion of a balloon at the instrument’s tip. Visualization is done during instrument withdrawal; approximately 50% to 75% of the small intestinal mucosa can be examined. However, this instrument lacks biopsy or therapeutic capability. Further, it lacks tip deflection capability, limiting complete mucosal visu-alization, and has therefore been abandoned in favor of capsule endoscopy.Wireless capsule enteroscopy is an excellent tool in the patient who is hemodynamically stable but continues to bleed. This technique has reported success rates as high as 90% in identifying a small | Surgery_Schwartz. Treitz into the proximal jejunum. This procedure can allow for visualization of approximately 60 cm of the proximal jejunum. Diagnostic yield in patients with obscure GI bleeding ranges from 3% to 65%. In addition to diagnosis, push enteroscopy allows for cauterization of bleed-ing sites.In Sonde enteroscopy, a long, thin fiberoptic instrument is propelled through the intestine by peristalsis following infla-tion of a balloon at the instrument’s tip. Visualization is done during instrument withdrawal; approximately 50% to 75% of the small intestinal mucosa can be examined. However, this instrument lacks biopsy or therapeutic capability. Further, it lacks tip deflection capability, limiting complete mucosal visu-alization, and has therefore been abandoned in favor of capsule endoscopy.Wireless capsule enteroscopy is an excellent tool in the patient who is hemodynamically stable but continues to bleed. This technique has reported success rates as high as 90% in identifying a small |
Surgery_Schwartz_8258 | Surgery_Schwartz | capsule enteroscopy is an excellent tool in the patient who is hemodynamically stable but continues to bleed. This technique has reported success rates as high as 90% in identifying a small bowel pathology. In a randomized study of patients with obscure GI bleeding, evaluation with capsule endoscopy vs. small bowel contrast study had a much higher diagnostic yield (30% vs. 7%, respectively); however, this did not translate into an improvement in outcomes. The rates of rebleeding, hospitalization, need for blood transfusion, and therapeutic interventions were similar between the two arms.The inability to perform biopsies or carry out any thera-peutic interventions of capsule endoscope likely prevents the improved diagnostic yield of the test from translating into improved patient outcomes and highlights the continuing chal-lenge with evaluation of the small bowel.69For patients in whom bleeding from an obscure GI source has apparently stopped, push enteroscopy or capsule enteroscopy is | Surgery_Schwartz. capsule enteroscopy is an excellent tool in the patient who is hemodynamically stable but continues to bleed. This technique has reported success rates as high as 90% in identifying a small bowel pathology. In a randomized study of patients with obscure GI bleeding, evaluation with capsule endoscopy vs. small bowel contrast study had a much higher diagnostic yield (30% vs. 7%, respectively); however, this did not translate into an improvement in outcomes. The rates of rebleeding, hospitalization, need for blood transfusion, and therapeutic interventions were similar between the two arms.The inability to perform biopsies or carry out any thera-peutic interventions of capsule endoscope likely prevents the improved diagnostic yield of the test from translating into improved patient outcomes and highlights the continuing chal-lenge with evaluation of the small bowel.69For patients in whom bleeding from an obscure GI source has apparently stopped, push enteroscopy or capsule enteroscopy is |
Surgery_Schwartz_8259 | Surgery_Schwartz | highlights the continuing chal-lenge with evaluation of the small bowel.69For patients in whom bleeding from an obscure GI source has apparently stopped, push enteroscopy or capsule enteroscopy is a reasonable initial study. If these examinations do not reveal a potential source of bleeding, then enterocolysis should be performed. Standard small bowel follow-through examinations are associated with a low diagnostic yield in this setting and should be avoided. 99MTc–pertechnetate scintigraphy to diagnose Meckel’s diverticulum should be considered, although its yield in patients older than 40 years of age is extremely low. If still no diagnosis has been made, a “watch-and-wait” approach is reasonable, although angiography should be considered if the episode of bleeding was overt. Angiography can reveal angiodysplasia and vascular tumors in the small intestine even in the absence of ongoing bleeding. In many instances, however, angiography is done in patients with persistent bleeding | Surgery_Schwartz. highlights the continuing chal-lenge with evaluation of the small bowel.69For patients in whom bleeding from an obscure GI source has apparently stopped, push enteroscopy or capsule enteroscopy is a reasonable initial study. If these examinations do not reveal a potential source of bleeding, then enterocolysis should be performed. Standard small bowel follow-through examinations are associated with a low diagnostic yield in this setting and should be avoided. 99MTc–pertechnetate scintigraphy to diagnose Meckel’s diverticulum should be considered, although its yield in patients older than 40 years of age is extremely low. If still no diagnosis has been made, a “watch-and-wait” approach is reasonable, although angiography should be considered if the episode of bleeding was overt. Angiography can reveal angiodysplasia and vascular tumors in the small intestine even in the absence of ongoing bleeding. In many instances, however, angiography is done in patients with persistent bleeding |
Surgery_Schwartz_8260 | Surgery_Schwartz | can reveal angiodysplasia and vascular tumors in the small intestine even in the absence of ongoing bleeding. In many instances, however, angiography is done in patients with persistent bleeding from an obscure GI source, and it is also often performed after a 99MTc-labeled RBC scan, which, if positive, is followed by angiography to localize the source of bleeding. Patients who remain undiagnosed but continue to bleed and those with recurrent episodic bleeding significant enough to require blood transfusions should then undergo exploratory laparoscopy or laparotomy with intraoperative enteroscopy. An endoscope (usually a colonoscope) is inserted into the small bowel through peroral intubation or through an enterotomy made in the small bowel or cecum. The endoscope is advanced by successively telescoping short segments of intestine onto the end to the instrument. In addition to the endoscopic image, the transilluminated bowel should be examined externally with the operating room | Surgery_Schwartz. can reveal angiodysplasia and vascular tumors in the small intestine even in the absence of ongoing bleeding. In many instances, however, angiography is done in patients with persistent bleeding from an obscure GI source, and it is also often performed after a 99MTc-labeled RBC scan, which, if positive, is followed by angiography to localize the source of bleeding. Patients who remain undiagnosed but continue to bleed and those with recurrent episodic bleeding significant enough to require blood transfusions should then undergo exploratory laparoscopy or laparotomy with intraoperative enteroscopy. An endoscope (usually a colonoscope) is inserted into the small bowel through peroral intubation or through an enterotomy made in the small bowel or cecum. The endoscope is advanced by successively telescoping short segments of intestine onto the end to the instrument. In addition to the endoscopic image, the transilluminated bowel should be examined externally with the operating room |
Surgery_Schwartz_8261 | Surgery_Schwartz | telescoping short segments of intestine onto the end to the instrument. In addition to the endoscopic image, the transilluminated bowel should be examined externally with the operating room lights dimmed, as this maneuver may facilitate the identification of angiodysplasias. Identified lesions should be marked with a suture placed on the serosal surface of the bowel; these lesions can be resected after completion of endoscopy. Examination should be performed during instrument insertion rather than withdrawal because instrument-induced mucosal trauma can be confused with angiodysplasias.Figure 28-31 provides a diagnostic and management algo-rithm for patients with obscure GI bleeding.Small Bowel PerforationPrior to the 1980s, duodenal perforation due to peptic ulcer dis-ease was the most common form of small bowel perforation. Today, iatrogenic injury incurred during gastrointestinal endos-copy is the most common cause of small bowel perforation. Other etiologies of small bowel | Surgery_Schwartz. telescoping short segments of intestine onto the end to the instrument. In addition to the endoscopic image, the transilluminated bowel should be examined externally with the operating room lights dimmed, as this maneuver may facilitate the identification of angiodysplasias. Identified lesions should be marked with a suture placed on the serosal surface of the bowel; these lesions can be resected after completion of endoscopy. Examination should be performed during instrument insertion rather than withdrawal because instrument-induced mucosal trauma can be confused with angiodysplasias.Figure 28-31 provides a diagnostic and management algo-rithm for patients with obscure GI bleeding.Small Bowel PerforationPrior to the 1980s, duodenal perforation due to peptic ulcer dis-ease was the most common form of small bowel perforation. Today, iatrogenic injury incurred during gastrointestinal endos-copy is the most common cause of small bowel perforation. Other etiologies of small bowel |
Surgery_Schwartz_8262 | Surgery_Schwartz | most common form of small bowel perforation. Today, iatrogenic injury incurred during gastrointestinal endos-copy is the most common cause of small bowel perforation. Other etiologies of small bowel perforation include infections (especially tuberculosis, typhoid, and CMV), Crohn’s disease, ischemia, drugs (e.g., potassiumand NSAID-induced ulcers), radiation-induced injury, Meckel’s and acquired diverticuli, neoplasms (especially lymphoma, adenocarcinoma, and mela-noma), and foreign bodies.Among iatrogenic injuries, duodenal perforation dur-ing endoscopic retrograde cholangiography (ERCP) with endoscopic sphincterotomy (ES) is the most common. With improved technique and technology, the incidence of this is decreasing but remains at around 0.5%.70 The Stapfer classifi-cation is commonly used to categorize different types of ERCP-related perforations. These are:• Type I: Free bowel wall perforation• Type II: Retroperitoneal duodenal perforation secondary to periampullary injury• Type | Surgery_Schwartz. most common form of small bowel perforation. Today, iatrogenic injury incurred during gastrointestinal endos-copy is the most common cause of small bowel perforation. Other etiologies of small bowel perforation include infections (especially tuberculosis, typhoid, and CMV), Crohn’s disease, ischemia, drugs (e.g., potassiumand NSAID-induced ulcers), radiation-induced injury, Meckel’s and acquired diverticuli, neoplasms (especially lymphoma, adenocarcinoma, and mela-noma), and foreign bodies.Among iatrogenic injuries, duodenal perforation dur-ing endoscopic retrograde cholangiography (ERCP) with endoscopic sphincterotomy (ES) is the most common. With improved technique and technology, the incidence of this is decreasing but remains at around 0.5%.70 The Stapfer classifi-cation is commonly used to categorize different types of ERCP-related perforations. These are:• Type I: Free bowel wall perforation• Type II: Retroperitoneal duodenal perforation secondary to periampullary injury• Type |
Surgery_Schwartz_8263 | Surgery_Schwartz | used to categorize different types of ERCP-related perforations. These are:• Type I: Free bowel wall perforation• Type II: Retroperitoneal duodenal perforation secondary to periampullary injury• Type III: Perforation of the pancreatic or bile duct• Type IV: Retroperitoneal air aloneType II (retroperitoneal duodenal injuries) are the most common and can often be managed nonsurgically. Manifesta-tions of such contained duodenal perforation following ERCP can resemble those of ERCP-induced pancreatitis, including hyperamylasemia.Brunicardi_Ch28_p1219-p1258.indd 125123/02/19 2:25 PM 1252SPECIFIC CONSIDERATIONSPART IICT scanning is the most sensitive test for diagnosing duo-denal perforations; positive findings include pneumoperitoneum for free perforations, but more commonly retroperitoneal air, contrast extravasation, and paraduodenal fluid collections. If all patients undergoing a therapeutic ERCP are imaged with a CT scan following the procedure, up to 30% will have evidence of | Surgery_Schwartz. used to categorize different types of ERCP-related perforations. These are:• Type I: Free bowel wall perforation• Type II: Retroperitoneal duodenal perforation secondary to periampullary injury• Type III: Perforation of the pancreatic or bile duct• Type IV: Retroperitoneal air aloneType II (retroperitoneal duodenal injuries) are the most common and can often be managed nonsurgically. Manifesta-tions of such contained duodenal perforation following ERCP can resemble those of ERCP-induced pancreatitis, including hyperamylasemia.Brunicardi_Ch28_p1219-p1258.indd 125123/02/19 2:25 PM 1252SPECIFIC CONSIDERATIONSPART IICT scanning is the most sensitive test for diagnosing duo-denal perforations; positive findings include pneumoperitoneum for free perforations, but more commonly retroperitoneal air, contrast extravasation, and paraduodenal fluid collections. If all patients undergoing a therapeutic ERCP are imaged with a CT scan following the procedure, up to 30% will have evidence of |
Surgery_Schwartz_8264 | Surgery_Schwartz | air, contrast extravasation, and paraduodenal fluid collections. If all patients undergoing a therapeutic ERCP are imaged with a CT scan following the procedure, up to 30% will have evidence of air in the retroperitoneum, but the majority are asymptomatic. These patients do not require any specific therapy.71True cases of retroperitoneal perforations of the duodenum can be managed nonoperatively in the absence of progression and sepsis. However, intraoperitoneal duodenal perforations require surgical repair with pyloric exclusion and gastrojeju-nostomy or tube duodenostomy. Iatrogenic small bowel perfora-tion incurred during endoscopy, if immediately recognized, can sometimes be repaired using endoscopic techniques.Perforation of the jejunum and ileum occurs into the peri-toneal cavity and usually causes overt symptoms and signs, such as abdominal pain, tenderness, and distention accompa-nied by fever and tachycardia. Plain abdominal radiographs may reveal free intraperitoneal air if | Surgery_Schwartz. air, contrast extravasation, and paraduodenal fluid collections. If all patients undergoing a therapeutic ERCP are imaged with a CT scan following the procedure, up to 30% will have evidence of air in the retroperitoneum, but the majority are asymptomatic. These patients do not require any specific therapy.71True cases of retroperitoneal perforations of the duodenum can be managed nonoperatively in the absence of progression and sepsis. However, intraoperitoneal duodenal perforations require surgical repair with pyloric exclusion and gastrojeju-nostomy or tube duodenostomy. Iatrogenic small bowel perfora-tion incurred during endoscopy, if immediately recognized, can sometimes be repaired using endoscopic techniques.Perforation of the jejunum and ileum occurs into the peri-toneal cavity and usually causes overt symptoms and signs, such as abdominal pain, tenderness, and distention accompa-nied by fever and tachycardia. Plain abdominal radiographs may reveal free intraperitoneal air if |
Surgery_Schwartz_8265 | Surgery_Schwartz | usually causes overt symptoms and signs, such as abdominal pain, tenderness, and distention accompa-nied by fever and tachycardia. Plain abdominal radiographs may reveal free intraperitoneal air if intraperitoneal perforation has occurred. If perforation is suspected but not clinically obvious, CT scanning should be performed. Jejunal and ileal perforations require surgical repair or segmental resection.Chylous AscitesChylous ascites refers to the accumulation of triglyceride-rich peritoneal fluid with a milky or creamy appearing, caused by the presence of intestinal lymph in the peritoneal cavity. Chy-lomicrons, produced by the intestine and secreted into lymph during the absorption of long-chain fatty acids, account for the characteristic appearance and triglyceride content of chyle.The most common etiologies of chylous ascites in Western countries are abdominal malignancies and cirrhosis. In Eastern and developing countries, infectious etiologies, such as tuber-culosis and | Surgery_Schwartz. usually causes overt symptoms and signs, such as abdominal pain, tenderness, and distention accompa-nied by fever and tachycardia. Plain abdominal radiographs may reveal free intraperitoneal air if intraperitoneal perforation has occurred. If perforation is suspected but not clinically obvious, CT scanning should be performed. Jejunal and ileal perforations require surgical repair or segmental resection.Chylous AscitesChylous ascites refers to the accumulation of triglyceride-rich peritoneal fluid with a milky or creamy appearing, caused by the presence of intestinal lymph in the peritoneal cavity. Chy-lomicrons, produced by the intestine and secreted into lymph during the absorption of long-chain fatty acids, account for the characteristic appearance and triglyceride content of chyle.The most common etiologies of chylous ascites in Western countries are abdominal malignancies and cirrhosis. In Eastern and developing countries, infectious etiologies, such as tuber-culosis and |
Surgery_Schwartz_8266 | Surgery_Schwartz | most common etiologies of chylous ascites in Western countries are abdominal malignancies and cirrhosis. In Eastern and developing countries, infectious etiologies, such as tuber-culosis and filariasis, account for most cases. Chylous ascites can also develop as a complication of abdominal and thoracic operations and trauma. Operations particularly associated with this complication include abdominal aortic aneurysm repair, retroperitoneal lymph node dissection, inferior vena cava resec-tion, and liver transplantation. Other etiologies of chylous asci-tes include congenital lymphatic abnormalities (e.g., primary lymphatic hypoplasia), radiation, pancreatitis, and right-sided heart failure.Three mechanisms have been postulated to cause chylous ascites: (a) exudation of chyle from dilated lymphatics on the wall of the bowel and in the mesentery caused by obstruction of lymphatic vessels at the base of the mesentery or the cisterna chili (e.g., by malignancies), (b) direct leakage of | Surgery_Schwartz. most common etiologies of chylous ascites in Western countries are abdominal malignancies and cirrhosis. In Eastern and developing countries, infectious etiologies, such as tuber-culosis and filariasis, account for most cases. Chylous ascites can also develop as a complication of abdominal and thoracic operations and trauma. Operations particularly associated with this complication include abdominal aortic aneurysm repair, retroperitoneal lymph node dissection, inferior vena cava resec-tion, and liver transplantation. Other etiologies of chylous asci-tes include congenital lymphatic abnormalities (e.g., primary lymphatic hypoplasia), radiation, pancreatitis, and right-sided heart failure.Three mechanisms have been postulated to cause chylous ascites: (a) exudation of chyle from dilated lymphatics on the wall of the bowel and in the mesentery caused by obstruction of lymphatic vessels at the base of the mesentery or the cisterna chili (e.g., by malignancies), (b) direct leakage of |
Surgery_Schwartz_8267 | Surgery_Schwartz | lymphatics on the wall of the bowel and in the mesentery caused by obstruction of lymphatic vessels at the base of the mesentery or the cisterna chili (e.g., by malignancies), (b) direct leakage of chyle through a lymphoperitoneal fistula (e.g., those that develop as a result of trauma or surgery), and (c) exudation of chyle through the wall of dilated retroperitoneal lymphatic vessels (e.g., in congenital lymphangiectasia or thoracic duct obstruction).Patients with chylous ascites develop abdominal distention over a period of weeks to months. Postoperative chylous ascites can present acutely during the first postoperative week. Delayed presentations following surgery can occur if the mechanism of ascites formation is adhesion-induced lymphatic obstruction rather than lymphatic vessel disruption.Obscure gastrointestinal bleedingRule out upper and lower GIbleeding;EGD and colonoscopyMinor bleeding(intermittent)Major bleeding(persistent)Initiate appropriatetherapyRepeat EGD/Colonoscopy | Surgery_Schwartz. lymphatics on the wall of the bowel and in the mesentery caused by obstruction of lymphatic vessels at the base of the mesentery or the cisterna chili (e.g., by malignancies), (b) direct leakage of chyle through a lymphoperitoneal fistula (e.g., those that develop as a result of trauma or surgery), and (c) exudation of chyle through the wall of dilated retroperitoneal lymphatic vessels (e.g., in congenital lymphangiectasia or thoracic duct obstruction).Patients with chylous ascites develop abdominal distention over a period of weeks to months. Postoperative chylous ascites can present acutely during the first postoperative week. Delayed presentations following surgery can occur if the mechanism of ascites formation is adhesion-induced lymphatic obstruction rather than lymphatic vessel disruption.Obscure gastrointestinal bleedingRule out upper and lower GIbleeding;EGD and colonoscopyMinor bleeding(intermittent)Major bleeding(persistent)Initiate appropriatetherapyRepeat EGD/Colonoscopy |
Surgery_Schwartz_8268 | Surgery_Schwartz | gastrointestinal bleedingRule out upper and lower GIbleeding;EGD and colonoscopyMinor bleeding(intermittent)Major bleeding(persistent)Initiate appropriatetherapyRepeat EGD/Colonoscopy ifrebleedsTreat source, e.g.,small bowelresectionLocalize bleeding:Serial clamping or intraoperativeenteroscopy followed by resectionPositivePositiveNegativeUnstableStableTaggedRBC scanNegativeandpatient stableSource ofbleeding identifiedSourceuncertainAngiographyand treatmentOperatingroomEnteroclysisEnteroscopyCapsuleendoscopyFigure 28-31. Diagnostic and management algorithm for obscure gastrointestinal bleeding.Brunicardi_Ch28_p1219-p1258.indd 125223/02/19 2:25 PM 1253SMALL INTESTINECHAPTER 28Paracentesis is the most important diagnostic test. Chyle typically has a cloudy and turbid appearance; however, it may be clear in fasting patients (such as those in the immediate postoperative period). Fluid triglyceride concentrations above 110 mg/dL are diagnostic. CT scanning may be useful in identifying | Surgery_Schwartz. gastrointestinal bleedingRule out upper and lower GIbleeding;EGD and colonoscopyMinor bleeding(intermittent)Major bleeding(persistent)Initiate appropriatetherapyRepeat EGD/Colonoscopy ifrebleedsTreat source, e.g.,small bowelresectionLocalize bleeding:Serial clamping or intraoperativeenteroscopy followed by resectionPositivePositiveNegativeUnstableStableTaggedRBC scanNegativeandpatient stableSource ofbleeding identifiedSourceuncertainAngiographyand treatmentOperatingroomEnteroclysisEnteroscopyCapsuleendoscopyFigure 28-31. Diagnostic and management algorithm for obscure gastrointestinal bleeding.Brunicardi_Ch28_p1219-p1258.indd 125223/02/19 2:25 PM 1253SMALL INTESTINECHAPTER 28Paracentesis is the most important diagnostic test. Chyle typically has a cloudy and turbid appearance; however, it may be clear in fasting patients (such as those in the immediate postoperative period). Fluid triglyceride concentrations above 110 mg/dL are diagnostic. CT scanning may be useful in identifying |
Surgery_Schwartz_8269 | Surgery_Schwartz | it may be clear in fasting patients (such as those in the immediate postoperative period). Fluid triglyceride concentrations above 110 mg/dL are diagnostic. CT scanning may be useful in identifying pathological intraabdominal lymph nodes and masses and in identifying extent and localization of fluid. Lymphangiography and lymphoscintigraphy may help localize lymph leaks and obstruction; this information is particularly useful for surgical planning.There is little data on optimal management of patients with chylous ascites. The general approach is to focus on evaluating and treating the underlying causes, especially for patients with infec-tious, inflammatory, or hemodynamic etiologies for this condition.Most patients respond to administration of a high-protein and low-fat diet supplemented with medium-chain triglycerides. This regimen is designed to minimize chyle production and flow. Medium-chain triglycerides are absorbed by the intestinal epithelium and are transported to liver | Surgery_Schwartz. it may be clear in fasting patients (such as those in the immediate postoperative period). Fluid triglyceride concentrations above 110 mg/dL are diagnostic. CT scanning may be useful in identifying pathological intraabdominal lymph nodes and masses and in identifying extent and localization of fluid. Lymphangiography and lymphoscintigraphy may help localize lymph leaks and obstruction; this information is particularly useful for surgical planning.There is little data on optimal management of patients with chylous ascites. The general approach is to focus on evaluating and treating the underlying causes, especially for patients with infec-tious, inflammatory, or hemodynamic etiologies for this condition.Most patients respond to administration of a high-protein and low-fat diet supplemented with medium-chain triglycerides. This regimen is designed to minimize chyle production and flow. Medium-chain triglycerides are absorbed by the intestinal epithelium and are transported to liver |
Surgery_Schwartz_8270 | Surgery_Schwartz | with medium-chain triglycerides. This regimen is designed to minimize chyle production and flow. Medium-chain triglycerides are absorbed by the intestinal epithelium and are transported to liver through the portal vein; they do not contribute to chylomicron formation.Patients who do not respond to this approach should be fasted and placed on TPN. Octreotide can further decrease lymph flow. Paracentesis is indicated for respiratory difficul-ties related to abdominal distention. Overall, two-thirds of patients will respond to conservative therapy. However, one-third of patients will require surgical therapy for chylous ascites. In general, postoperative and trauma-related cases that fail to respond to initial nonoperative therapy are best managed by surgical repair. Lymphatic leaks are localized and repaired with fine nonabsorbable sutures. If extravasation of chyle is localized to the periphery of the small bowel mesentery, then a limited small bowel resection can be performed | Surgery_Schwartz. with medium-chain triglycerides. This regimen is designed to minimize chyle production and flow. Medium-chain triglycerides are absorbed by the intestinal epithelium and are transported to liver through the portal vein; they do not contribute to chylomicron formation.Patients who do not respond to this approach should be fasted and placed on TPN. Octreotide can further decrease lymph flow. Paracentesis is indicated for respiratory difficul-ties related to abdominal distention. Overall, two-thirds of patients will respond to conservative therapy. However, one-third of patients will require surgical therapy for chylous ascites. In general, postoperative and trauma-related cases that fail to respond to initial nonoperative therapy are best managed by surgical repair. Lymphatic leaks are localized and repaired with fine nonabsorbable sutures. If extravasation of chyle is localized to the periphery of the small bowel mesentery, then a limited small bowel resection can be performed |
Surgery_Schwartz_8271 | Surgery_Schwartz | are localized and repaired with fine nonabsorbable sutures. If extravasation of chyle is localized to the periphery of the small bowel mesentery, then a limited small bowel resection can be performed instead. For patients who are poor surgical candidates and who do not respond to prolonged conservative therapy, peritoneovenous shunting may be an option. However, these shunts are associated with high rates of complications, including sepsis and disseminated intra-vascular coagulation. Because of the viscosity of chyle, these shunts are associated with a high occlusion rate.IntussusceptionIntussusception refers to a condition where one segment of the intestine becomes drawn in to the lumen of the distal segment of the bowel. It is usually seen in the pediatric population, where the ileum intussuscepts into the cecum (ileocolic intussuscep-tion). In children, it is often an idiopathic condition and treated nonsurgically by radiological reduction.Intussusceptions are far less common and | Surgery_Schwartz. are localized and repaired with fine nonabsorbable sutures. If extravasation of chyle is localized to the periphery of the small bowel mesentery, then a limited small bowel resection can be performed instead. For patients who are poor surgical candidates and who do not respond to prolonged conservative therapy, peritoneovenous shunting may be an option. However, these shunts are associated with high rates of complications, including sepsis and disseminated intra-vascular coagulation. Because of the viscosity of chyle, these shunts are associated with a high occlusion rate.IntussusceptionIntussusception refers to a condition where one segment of the intestine becomes drawn in to the lumen of the distal segment of the bowel. It is usually seen in the pediatric population, where the ileum intussuscepts into the cecum (ileocolic intussuscep-tion). In children, it is often an idiopathic condition and treated nonsurgically by radiological reduction.Intussusceptions are far less common and |
Surgery_Schwartz_8272 | Surgery_Schwartz | into the cecum (ileocolic intussuscep-tion). In children, it is often an idiopathic condition and treated nonsurgically by radiological reduction.Intussusceptions are far less common and usually have a distinct pathologic lead point, which can be malignant in up to one-half of cases.72 They commonly present with a history of intermittent abdominal pain and signs and symptoms of bowel obstruction. CT scan is the investigation of choice, where a “tar-get sign” may be seen (Fig. 28-32). Treatment is surgical resec-tion of the involved segment and the lead point, which needs to undergo pathological evaluation to rule out an underlying malignancy.With increasing use of CT imaging, target signs are some-times seen on CT scans of patients who do not have a clinical presentation indicative of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.In patients who have undergone a Roux-en-Y gastric bypass surgery, an | Surgery_Schwartz. into the cecum (ileocolic intussuscep-tion). In children, it is often an idiopathic condition and treated nonsurgically by radiological reduction.Intussusceptions are far less common and usually have a distinct pathologic lead point, which can be malignant in up to one-half of cases.72 They commonly present with a history of intermittent abdominal pain and signs and symptoms of bowel obstruction. CT scan is the investigation of choice, where a “tar-get sign” may be seen (Fig. 28-32). Treatment is surgical resec-tion of the involved segment and the lead point, which needs to undergo pathological evaluation to rule out an underlying malignancy.With increasing use of CT imaging, target signs are some-times seen on CT scans of patients who do not have a clinical presentation indicative of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.In patients who have undergone a Roux-en-Y gastric bypass surgery, an |
Surgery_Schwartz_8273 | Surgery_Schwartz | of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.In patients who have undergone a Roux-en-Y gastric bypass surgery, an atypical form of intussusception has been increasingly described. In these cases, the distal bowel is drawn in to the lumen of the proximal bowel (retrograde intussuscep-tion). These intussusceptions are usually not associated with a lead point and may represent a motility disorder of the bowel following the Roux-en-Y reconstruction. Surgical reductions without resection have been successfully reported in these patients.73Pneumatosis IntestinalisPneumatosis intestinalis indicates the presence of gas within the bowel wall. It may affect any region of the GI tract, but it is most commonly seen in the jejunum. Pneumatosis intestinalis is not a disease but merely a sign that can be idiopathic or associated with many intestinal or nonintestinal disorders, such as obstruc-tive pulmonary disease | Surgery_Schwartz. of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.In patients who have undergone a Roux-en-Y gastric bypass surgery, an atypical form of intussusception has been increasingly described. In these cases, the distal bowel is drawn in to the lumen of the proximal bowel (retrograde intussuscep-tion). These intussusceptions are usually not associated with a lead point and may represent a motility disorder of the bowel following the Roux-en-Y reconstruction. Surgical reductions without resection have been successfully reported in these patients.73Pneumatosis IntestinalisPneumatosis intestinalis indicates the presence of gas within the bowel wall. It may affect any region of the GI tract, but it is most commonly seen in the jejunum. Pneumatosis intestinalis is not a disease but merely a sign that can be idiopathic or associated with many intestinal or nonintestinal disorders, such as obstruc-tive pulmonary disease |
Surgery_Schwartz_8274 | Surgery_Schwartz | the jejunum. Pneumatosis intestinalis is not a disease but merely a sign that can be idiopathic or associated with many intestinal or nonintestinal disorders, such as obstruc-tive pulmonary disease and asthma. Most cases of pneumatosis intestinalis are secondary to an identifiable cause, and 15% are idiopathic. The pathogenesis of pneumatosis intestinalis is not fully understood.The surgical interest in this finding is the association of it with bowel ischemia and infarction, both of which necessitate emergent surgical intervention (Fig. 28-33). Thus, patients with this radiological finding need to be fully evaluated and moni-tored closely to rule out such intraabdominal catastrophes.ABFigure 28-32. Small bowel intussusception. A. Target sign seen on CT scans in patients with small bowel intussusception (arrow). B. The distal bowel is clearly within the lumen of the proximal bowel (arrow).Brunicardi_Ch28_p1219-p1258.indd 125323/02/19 2:25 PM 1254SPECIFIC | Surgery_Schwartz. the jejunum. Pneumatosis intestinalis is not a disease but merely a sign that can be idiopathic or associated with many intestinal or nonintestinal disorders, such as obstruc-tive pulmonary disease and asthma. Most cases of pneumatosis intestinalis are secondary to an identifiable cause, and 15% are idiopathic. The pathogenesis of pneumatosis intestinalis is not fully understood.The surgical interest in this finding is the association of it with bowel ischemia and infarction, both of which necessitate emergent surgical intervention (Fig. 28-33). Thus, patients with this radiological finding need to be fully evaluated and moni-tored closely to rule out such intraabdominal catastrophes.ABFigure 28-32. Small bowel intussusception. A. Target sign seen on CT scans in patients with small bowel intussusception (arrow). B. The distal bowel is clearly within the lumen of the proximal bowel (arrow).Brunicardi_Ch28_p1219-p1258.indd 125323/02/19 2:25 PM 1254SPECIFIC |
Surgery_Schwartz_8275 | Surgery_Schwartz | with small bowel intussusception (arrow). B. The distal bowel is clearly within the lumen of the proximal bowel (arrow).Brunicardi_Ch28_p1219-p1258.indd 125323/02/19 2:25 PM 1254SPECIFIC CONSIDERATIONSPART IISHORT BOWEL SYNDROMEIntestinal resection is performed for many of the diseases dis-cussed in this chapter and generally is associated with minimal morbidity. However, when extent of resection is great enough, a devastating condition known as short bowel syndrome may result. Although the best definition of short bowel syndrome is likely a functional one, reflecting a state of significant malabsorption of both macronutrients and micronutrients, some have used a more anatomical definition with it being arbi-trarily defined as the presence of less than 200 cm of residual small bowel in adult patients.74In adults, the most common etiologies of short bowel syn-drome are acute mesenteric ischemia, malignancy, and Crohn’s disease. Seventy-five percent of cases result from resection | Surgery_Schwartz. with small bowel intussusception (arrow). B. The distal bowel is clearly within the lumen of the proximal bowel (arrow).Brunicardi_Ch28_p1219-p1258.indd 125323/02/19 2:25 PM 1254SPECIFIC CONSIDERATIONSPART IISHORT BOWEL SYNDROMEIntestinal resection is performed for many of the diseases dis-cussed in this chapter and generally is associated with minimal morbidity. However, when extent of resection is great enough, a devastating condition known as short bowel syndrome may result. Although the best definition of short bowel syndrome is likely a functional one, reflecting a state of significant malabsorption of both macronutrients and micronutrients, some have used a more anatomical definition with it being arbi-trarily defined as the presence of less than 200 cm of residual small bowel in adult patients.74In adults, the most common etiologies of short bowel syn-drome are acute mesenteric ischemia, malignancy, and Crohn’s disease. Seventy-five percent of cases result from resection |
Surgery_Schwartz_8276 | Surgery_Schwartz | in adult patients.74In adults, the most common etiologies of short bowel syn-drome are acute mesenteric ischemia, malignancy, and Crohn’s disease. Seventy-five percent of cases result from resection of a large amount of small bowel at a single operation. Twenty-five percent of cases result from the cumulative effects of multiple operations during which small intestine is resected. This latter pattern is typical of patients with Crohn’s disease who develop short bowel syndrome; the former is typical of patients with acute mesenteric ischemia who develop intestinal infarction. In pediat-ric patients, intestinal atresias, volvulus, and necrotizing entero-colitis are the most common etiologies of short bowel syndrome.The prevalence of short bowel syndrome is hard to esti-mate due to its multifactorial nature and wide spectrum of presentation and treatment, which may include home total par-enteral nutrition (TPN).PathophysiologyResection of less than 50% of the small intestine is generally | Surgery_Schwartz. in adult patients.74In adults, the most common etiologies of short bowel syn-drome are acute mesenteric ischemia, malignancy, and Crohn’s disease. Seventy-five percent of cases result from resection of a large amount of small bowel at a single operation. Twenty-five percent of cases result from the cumulative effects of multiple operations during which small intestine is resected. This latter pattern is typical of patients with Crohn’s disease who develop short bowel syndrome; the former is typical of patients with acute mesenteric ischemia who develop intestinal infarction. In pediat-ric patients, intestinal atresias, volvulus, and necrotizing entero-colitis are the most common etiologies of short bowel syndrome.The prevalence of short bowel syndrome is hard to esti-mate due to its multifactorial nature and wide spectrum of presentation and treatment, which may include home total par-enteral nutrition (TPN).PathophysiologyResection of less than 50% of the small intestine is generally |
Surgery_Schwartz_8277 | Surgery_Schwartz | nature and wide spectrum of presentation and treatment, which may include home total par-enteral nutrition (TPN).PathophysiologyResection of less than 50% of the small intestine is generally well tolerated. However, clinically significant malabsorption occurs when greater than 50% to 80% of the small intestine has been resected. Among adult patients who lack a functional colon, lifelong TPN dependence is likely to persist if there is less than 100 cm of residual small intestine. Among adult patients who have an intact and functional colon, lifelong TPN dependence is likely to persist if there is less than 60 cm of residual small intestine. Among infants with short bowel syn-drome, weaning from TPN-dependence has been achieved with as little as 10 cm of residual small intestine.Residual bowel length is not the only factor predictive of achieving independence from TPN (enteral autonomy), 5Figure 28-33. STEP procedure. This illustration depicts the serial transverse enteroplasty (STEP) | Surgery_Schwartz. nature and wide spectrum of presentation and treatment, which may include home total par-enteral nutrition (TPN).PathophysiologyResection of less than 50% of the small intestine is generally well tolerated. However, clinically significant malabsorption occurs when greater than 50% to 80% of the small intestine has been resected. Among adult patients who lack a functional colon, lifelong TPN dependence is likely to persist if there is less than 100 cm of residual small intestine. Among adult patients who have an intact and functional colon, lifelong TPN dependence is likely to persist if there is less than 60 cm of residual small intestine. Among infants with short bowel syn-drome, weaning from TPN-dependence has been achieved with as little as 10 cm of residual small intestine.Residual bowel length is not the only factor predictive of achieving independence from TPN (enteral autonomy), 5Figure 28-33. STEP procedure. This illustration depicts the serial transverse enteroplasty (STEP) |
Surgery_Schwartz_8278 | Surgery_Schwartz | length is not the only factor predictive of achieving independence from TPN (enteral autonomy), 5Figure 28-33. STEP procedure. This illustration depicts the serial transverse enteroplasty (STEP) procedure. Lengthening of dilated small intestine is accomplished by serial applications of an intestinal stapling device, with firings oriented perpendicular to the long axis of the intestine. (Used with permission from Patrick Javid, M.D. and Tom Jaksic, M.D., Department of Surgery, Children’s Hospital, Boston, MA.)Table 28-11Risk factors for development of short bowel syndrome after massive small bowel resectionSmall bowel length <200 cmAbsence of ileocecal valveAbsence of colonDiseased remaining bowel (e.g., Crohn’s disease)Ileal resectionhowever. Other determinants of the severity of malabsorption include the presence or absence of an intact colon, as indicated previously. The colon has the capacity to absorb large fluid and electrolyte loads. In addition, the colon can play an important, | Surgery_Schwartz. length is not the only factor predictive of achieving independence from TPN (enteral autonomy), 5Figure 28-33. STEP procedure. This illustration depicts the serial transverse enteroplasty (STEP) procedure. Lengthening of dilated small intestine is accomplished by serial applications of an intestinal stapling device, with firings oriented perpendicular to the long axis of the intestine. (Used with permission from Patrick Javid, M.D. and Tom Jaksic, M.D., Department of Surgery, Children’s Hospital, Boston, MA.)Table 28-11Risk factors for development of short bowel syndrome after massive small bowel resectionSmall bowel length <200 cmAbsence of ileocecal valveAbsence of colonDiseased remaining bowel (e.g., Crohn’s disease)Ileal resectionhowever. Other determinants of the severity of malabsorption include the presence or absence of an intact colon, as indicated previously. The colon has the capacity to absorb large fluid and electrolyte loads. In addition, the colon can play an important, |
Surgery_Schwartz_8279 | Surgery_Schwartz | include the presence or absence of an intact colon, as indicated previously. The colon has the capacity to absorb large fluid and electrolyte loads. In addition, the colon can play an important, albeit small, role in nutrient assimilation by absorbing short chain fatty acids. Second, an intact ileocecal valve is believed to be associated with decreased malabsorption. The ileocecal valve delays transit of chyme from the small intestine into the colon, thereby prolonging the contact time between nutrients and the small-intestinal absorptive mucosa. Third, healthy, rather than diseased, residual small intestine is associated with decreased severity of malabsorption. Fourth, resection of jejunum is better tolerated than resection of ileum, as the capacity for bile salt and vitamin B12 absorption is specific to the ileum (Table 28-11).During the first 1 to 2 years following massive small bowel resection, the remaining intestine undergoes compensa-tory adaptation, as discussed previously. | Surgery_Schwartz. include the presence or absence of an intact colon, as indicated previously. The colon has the capacity to absorb large fluid and electrolyte loads. In addition, the colon can play an important, albeit small, role in nutrient assimilation by absorbing short chain fatty acids. Second, an intact ileocecal valve is believed to be associated with decreased malabsorption. The ileocecal valve delays transit of chyme from the small intestine into the colon, thereby prolonging the contact time between nutrients and the small-intestinal absorptive mucosa. Third, healthy, rather than diseased, residual small intestine is associated with decreased severity of malabsorption. Fourth, resection of jejunum is better tolerated than resection of ileum, as the capacity for bile salt and vitamin B12 absorption is specific to the ileum (Table 28-11).During the first 1 to 2 years following massive small bowel resection, the remaining intestine undergoes compensa-tory adaptation, as discussed previously. |
Surgery_Schwartz_8280 | Surgery_Schwartz | is specific to the ileum (Table 28-11).During the first 1 to 2 years following massive small bowel resection, the remaining intestine undergoes compensa-tory adaptation, as discussed previously. Clinically, the period of adaptation is associated with reductions in volume and fre-quency of bowel movements, increases in the capacity for enteral nutrient assimilation, and reductions in TPN requirements. As this process completes, some patients are successfully weaned off TPN. Understanding the mechanisms mediating intestinal adaptation may suggest strategies for enhancing adaptation in patients with short bowel syndrome who are unable to achieve independence from TPN. To date, the phenomenon of intestinal adaptation in patients remains poorly understood.13Malabsorption in patients who have undergone mas-sive small bowel resection is exacerbated by a characteristic hypergastrinemia-associated gastric acid hypersecretion that persists for 1 to 2 years postoperatively. The increased acid | Surgery_Schwartz. is specific to the ileum (Table 28-11).During the first 1 to 2 years following massive small bowel resection, the remaining intestine undergoes compensa-tory adaptation, as discussed previously. Clinically, the period of adaptation is associated with reductions in volume and fre-quency of bowel movements, increases in the capacity for enteral nutrient assimilation, and reductions in TPN requirements. As this process completes, some patients are successfully weaned off TPN. Understanding the mechanisms mediating intestinal adaptation may suggest strategies for enhancing adaptation in patients with short bowel syndrome who are unable to achieve independence from TPN. To date, the phenomenon of intestinal adaptation in patients remains poorly understood.13Malabsorption in patients who have undergone mas-sive small bowel resection is exacerbated by a characteristic hypergastrinemia-associated gastric acid hypersecretion that persists for 1 to 2 years postoperatively. The increased acid |
Surgery_Schwartz_8281 | Surgery_Schwartz | undergone mas-sive small bowel resection is exacerbated by a characteristic hypergastrinemia-associated gastric acid hypersecretion that persists for 1 to 2 years postoperatively. The increased acid Brunicardi_Ch28_p1219-p1258.indd 125423/02/19 2:25 PM 1255SMALL INTESTINECHAPTER 28load delivered to the duodenum inhibits absorption by a variety of mechanisms, including the inhibition of digestive enzymes, most of which function optimally under alkaline conditions.TherapyMedical Therapy. For patients after massive small bowel resection, the initial treatment priorities include management of the primary condition precipitating the intestinal resection and the repletion of fluid and electrolytes lost in the severe diarrhea that characteristically occurs. Most patients will require TPN, at least initially. Enteral nutrition should be gradually introduced, once ileus has resolved. High-dose histamine-2 receptor antago-nists or proton pump inhibitors should be administered to reduce | Surgery_Schwartz. undergone mas-sive small bowel resection is exacerbated by a characteristic hypergastrinemia-associated gastric acid hypersecretion that persists for 1 to 2 years postoperatively. The increased acid Brunicardi_Ch28_p1219-p1258.indd 125423/02/19 2:25 PM 1255SMALL INTESTINECHAPTER 28load delivered to the duodenum inhibits absorption by a variety of mechanisms, including the inhibition of digestive enzymes, most of which function optimally under alkaline conditions.TherapyMedical Therapy. For patients after massive small bowel resection, the initial treatment priorities include management of the primary condition precipitating the intestinal resection and the repletion of fluid and electrolytes lost in the severe diarrhea that characteristically occurs. Most patients will require TPN, at least initially. Enteral nutrition should be gradually introduced, once ileus has resolved. High-dose histamine-2 receptor antago-nists or proton pump inhibitors should be administered to reduce |
Surgery_Schwartz_8282 | Surgery_Schwartz | at least initially. Enteral nutrition should be gradually introduced, once ileus has resolved. High-dose histamine-2 receptor antago-nists or proton pump inhibitors should be administered to reduce gastric acid secretion. Antimotility agents, such as loperamide hydrochloride or diphenoxylate, may be administered to delay small-intestinal transit. Octreotide can be administered to reduce the volume of gastrointestinal secretions, although, in animal models, its use is associated with an inhibition of intestinal adaptation.During the period of adaptation, generally lasting 1 to 2 years postoperatively, TPN and enteral nutrition are titrated to allow for independence from TPN. Patients who remain dependent on TPN face substantial TPN-associated morbidities including catheter sepsis, venous thrombosis, liver and kidney failure, and osteoporosis. Liver failure is a significant source of morbidity and often leads to liver transplantation (always in combination with small bowel | Surgery_Schwartz. at least initially. Enteral nutrition should be gradually introduced, once ileus has resolved. High-dose histamine-2 receptor antago-nists or proton pump inhibitors should be administered to reduce gastric acid secretion. Antimotility agents, such as loperamide hydrochloride or diphenoxylate, may be administered to delay small-intestinal transit. Octreotide can be administered to reduce the volume of gastrointestinal secretions, although, in animal models, its use is associated with an inhibition of intestinal adaptation.During the period of adaptation, generally lasting 1 to 2 years postoperatively, TPN and enteral nutrition are titrated to allow for independence from TPN. Patients who remain dependent on TPN face substantial TPN-associated morbidities including catheter sepsis, venous thrombosis, liver and kidney failure, and osteoporosis. Liver failure is a significant source of morbidity and often leads to liver transplantation (always in combination with small bowel |
Surgery_Schwartz_8283 | Surgery_Schwartz | venous thrombosis, liver and kidney failure, and osteoporosis. Liver failure is a significant source of morbidity and often leads to liver transplantation (always in combination with small bowel transplantation). Due to these complications, patients with short bowel syndrome on TPN have a reduced life expectancy, with 5-year survival rates of 50% to 75%.Nontransplant Surgical Therapy. Among patients with sto-mas, restoration of intestinal continuity should be performed whenever possible, to capitalize on the absorptive capacity of all residual intestine. Other forms of nontransplant surgery designed to improve intestinal absorption are associated with unclear efficacy and/or substantial morbidities and therefore should not be applied routinely.The goal of these operations is to increase nutrient and fluid absorption by either slowing intestinal transit or increasing intestinal length. Operations designed to slow intestinal transit include segmental reversal of the small bowel, | Surgery_Schwartz. venous thrombosis, liver and kidney failure, and osteoporosis. Liver failure is a significant source of morbidity and often leads to liver transplantation (always in combination with small bowel transplantation). Due to these complications, patients with short bowel syndrome on TPN have a reduced life expectancy, with 5-year survival rates of 50% to 75%.Nontransplant Surgical Therapy. Among patients with sto-mas, restoration of intestinal continuity should be performed whenever possible, to capitalize on the absorptive capacity of all residual intestine. Other forms of nontransplant surgery designed to improve intestinal absorption are associated with unclear efficacy and/or substantial morbidities and therefore should not be applied routinely.The goal of these operations is to increase nutrient and fluid absorption by either slowing intestinal transit or increasing intestinal length. Operations designed to slow intestinal transit include segmental reversal of the small bowel, |
Surgery_Schwartz_8284 | Surgery_Schwartz | nutrient and fluid absorption by either slowing intestinal transit or increasing intestinal length. Operations designed to slow intestinal transit include segmental reversal of the small bowel, interposition of a segment of colon between segments of small bowel, construc-tion of small-intestinal valves, and electrical pacing of the small intestine. Reported experience with these procedures is limited to case reports or series of a few cases. Objective evidence of increased absorption is lacking; further, these procedures are frequently associated with intestinal obstruction.The intestinal lengthening operation for which has the lon-gest history is the longitudinal intestinal lengthening and tailor-ing (LILT) procedure, first described by Bianchi in 1980.75 The procedure entails separation of the dual vasculature of the small intestine, followed by longitudinal division of the bowel with subsequent isoperistaltic end-to-end anastomosis. This proce-dure has the potential to double the | Surgery_Schwartz. nutrient and fluid absorption by either slowing intestinal transit or increasing intestinal length. Operations designed to slow intestinal transit include segmental reversal of the small bowel, interposition of a segment of colon between segments of small bowel, construc-tion of small-intestinal valves, and electrical pacing of the small intestine. Reported experience with these procedures is limited to case reports or series of a few cases. Objective evidence of increased absorption is lacking; further, these procedures are frequently associated with intestinal obstruction.The intestinal lengthening operation for which has the lon-gest history is the longitudinal intestinal lengthening and tailor-ing (LILT) procedure, first described by Bianchi in 1980.75 The procedure entails separation of the dual vasculature of the small intestine, followed by longitudinal division of the bowel with subsequent isoperistaltic end-to-end anastomosis. This proce-dure has the potential to double the |
Surgery_Schwartz_8285 | Surgery_Schwartz | of the dual vasculature of the small intestine, followed by longitudinal division of the bowel with subsequent isoperistaltic end-to-end anastomosis. This proce-dure has the potential to double the length of small intestine to which it is applied. This procedure has generally been used for pediatric patients with dilated residual small bowel.An alternative surgical approach to lengthening the small bowel is the serial transverse enteroplasty procedure (STEP) has been described. This procedure is designed to accom-plish lengthening of dilated small intestine without the need for separating its dual vasculature (Fig. 28-33). A report from an international registry of 111 patients showed that 47% of patients achieved enteral autonomy at a median follow-up of 21 months.76Intestinal Transplantation. This complex procedure is being increasingly performed to treat patients with short bowel syn-drome. The currently accepted indication for intestinal trans-plantation is the presence of | Surgery_Schwartz. of the dual vasculature of the small intestine, followed by longitudinal division of the bowel with subsequent isoperistaltic end-to-end anastomosis. This proce-dure has the potential to double the length of small intestine to which it is applied. This procedure has generally been used for pediatric patients with dilated residual small bowel.An alternative surgical approach to lengthening the small bowel is the serial transverse enteroplasty procedure (STEP) has been described. This procedure is designed to accom-plish lengthening of dilated small intestine without the need for separating its dual vasculature (Fig. 28-33). A report from an international registry of 111 patients showed that 47% of patients achieved enteral autonomy at a median follow-up of 21 months.76Intestinal Transplantation. This complex procedure is being increasingly performed to treat patients with short bowel syn-drome. The currently accepted indication for intestinal trans-plantation is the presence of |
Surgery_Schwartz_8286 | Surgery_Schwartz | complex procedure is being increasingly performed to treat patients with short bowel syn-drome. The currently accepted indication for intestinal trans-plantation is the presence of life-threatening complications attributable to intestinal failure and/or long-term TPN therapy. Specific complications for which intestinal transplantation is indicated include (a) impending or overt liver failure, (b) throm-bosis of major central veins, (c) frequent episodes of catheter-related sepsis, and (d) frequent episodes of severe dehydration.Of the transplants involving the intestine, 37% were intestine-alone transplants, 30% included intestine, liver, and pancreas, and 24% were intestine and liver.77Isolated intestinal transplantation is used for patients with intestinal failure who have no significant liver disease or failure of other organs. Combined intestine/liver transplantation is used for patients with both intestinal and liver failure. Multivisceral transplantation has been used for | Surgery_Schwartz. complex procedure is being increasingly performed to treat patients with short bowel syn-drome. The currently accepted indication for intestinal trans-plantation is the presence of life-threatening complications attributable to intestinal failure and/or long-term TPN therapy. Specific complications for which intestinal transplantation is indicated include (a) impending or overt liver failure, (b) throm-bosis of major central veins, (c) frequent episodes of catheter-related sepsis, and (d) frequent episodes of severe dehydration.Of the transplants involving the intestine, 37% were intestine-alone transplants, 30% included intestine, liver, and pancreas, and 24% were intestine and liver.77Isolated intestinal transplantation is used for patients with intestinal failure who have no significant liver disease or failure of other organs. Combined intestine/liver transplantation is used for patients with both intestinal and liver failure. Multivisceral transplantation has been used for |
Surgery_Schwartz_8287 | Surgery_Schwartz | liver disease or failure of other organs. Combined intestine/liver transplantation is used for patients with both intestinal and liver failure. Multivisceral transplantation has been used for patients with giant desmoid tumors involving the vascular supply of the liver and pancreas as well as that of the intestine, for diffuse gastrointestinal motil-ity disturbances, and for diffuse splanchnic thrombosis.Nearly 80% of survivors have full intestinal graft function with no need for TPN. However, morbidities associated with intestinal transplantation are substantial and include acute and chronic rejection, CMV infection, and posttransplant lymphop-roliferative disease.Alternative Therapies. Pharmacologic and biologic thera-pies designed to expand intestinal mucosal surface area or to enhance the efficiency of intestinal absorption are beginning to undergo clinical evaluation. Promising regimens include GLP-2 and the combination of glutamine and growth hormone with a modified, | Surgery_Schwartz. liver disease or failure of other organs. Combined intestine/liver transplantation is used for patients with both intestinal and liver failure. Multivisceral transplantation has been used for patients with giant desmoid tumors involving the vascular supply of the liver and pancreas as well as that of the intestine, for diffuse gastrointestinal motil-ity disturbances, and for diffuse splanchnic thrombosis.Nearly 80% of survivors have full intestinal graft function with no need for TPN. However, morbidities associated with intestinal transplantation are substantial and include acute and chronic rejection, CMV infection, and posttransplant lymphop-roliferative disease.Alternative Therapies. Pharmacologic and biologic thera-pies designed to expand intestinal mucosal surface area or to enhance the efficiency of intestinal absorption are beginning to undergo clinical evaluation. Promising regimens include GLP-2 and the combination of glutamine and growth hormone with a modified, |
Surgery_Schwartz_8288 | Surgery_Schwartz | to enhance the efficiency of intestinal absorption are beginning to undergo clinical evaluation. Promising regimens include GLP-2 and the combination of glutamine and growth hormone with a modified, high-carbohydrate diet.OutcomesApproximately 50% to 70% of patients with short bowel syn-drome who initially require TPN are ultimately able to achieve independence from TPN.73 Prognosis for achieving enteral autonomy is better among pediatric patients than among adults.Information on survival among patients with short bowel syndrome is limited. In a recently reported study of 124 adults with short bowel syndrome due to nonmalignant etiologies, the survival rates at 2 and 5 years of follow up were 86% and 45%, respectively.77 Patients with end-enterostomies and those hav-ing less than 50 cm of residual small intestine had significantly worse survivals than those without these features.No randomized trials comparing intestinal transplanta-tion to chronic TPN administration among patients | Surgery_Schwartz. to enhance the efficiency of intestinal absorption are beginning to undergo clinical evaluation. Promising regimens include GLP-2 and the combination of glutamine and growth hormone with a modified, high-carbohydrate diet.OutcomesApproximately 50% to 70% of patients with short bowel syn-drome who initially require TPN are ultimately able to achieve independence from TPN.73 Prognosis for achieving enteral autonomy is better among pediatric patients than among adults.Information on survival among patients with short bowel syndrome is limited. In a recently reported study of 124 adults with short bowel syndrome due to nonmalignant etiologies, the survival rates at 2 and 5 years of follow up were 86% and 45%, respectively.77 Patients with end-enterostomies and those hav-ing less than 50 cm of residual small intestine had significantly worse survivals than those without these features.No randomized trials comparing intestinal transplanta-tion to chronic TPN administration among patients |
Surgery_Schwartz_8289 | Surgery_Schwartz | of residual small intestine had significantly worse survivals than those without these features.No randomized trials comparing intestinal transplanta-tion to chronic TPN administration among patients with short bowel syndrome have been reported. One-, 5-, and 10-year graft survival rates of intestine-alone recipients were 80%, 44%, and 26%; while those for intestine and liver and intestine, liver, and pancreas were 62%, 45%, 36% and 69%, 48%, 33%, respectively.78REFERENCESEntries highlighted in bright blue are key references. 1. Tavakkolizadeh A, Whang EE, Ashley SW, Zinner MJ. Small intestine. In: Brunicardi F, Andersen D, Billiar T, et al, eds. Principles of Surgery. 9th ed. New York: McGraw-Hill; 2004:28-1 to 28-32. 2. McMinn RMH. Last’s Anatomy: Regional and Applied. 9th ed. Singapore: Churchill Livingstone; 1994:337.Brunicardi_Ch28_p1219-p1258.indd 125523/02/19 2:25 PM 1256SPECIFIC CONSIDERATIONSPART II 3. Yan KS, Chia LA, Li X, et al. The intestinal stem cell markers Bmi1 | Surgery_Schwartz. of residual small intestine had significantly worse survivals than those without these features.No randomized trials comparing intestinal transplanta-tion to chronic TPN administration among patients with short bowel syndrome have been reported. One-, 5-, and 10-year graft survival rates of intestine-alone recipients were 80%, 44%, and 26%; while those for intestine and liver and intestine, liver, and pancreas were 62%, 45%, 36% and 69%, 48%, 33%, respectively.78REFERENCESEntries highlighted in bright blue are key references. 1. Tavakkolizadeh A, Whang EE, Ashley SW, Zinner MJ. Small intestine. In: Brunicardi F, Andersen D, Billiar T, et al, eds. Principles of Surgery. 9th ed. New York: McGraw-Hill; 2004:28-1 to 28-32. 2. McMinn RMH. Last’s Anatomy: Regional and Applied. 9th ed. Singapore: Churchill Livingstone; 1994:337.Brunicardi_Ch28_p1219-p1258.indd 125523/02/19 2:25 PM 1256SPECIFIC CONSIDERATIONSPART II 3. Yan KS, Chia LA, Li X, et al. The intestinal stem cell markers Bmi1 |
Surgery_Schwartz_8290 | Surgery_Schwartz | Churchill Livingstone; 1994:337.Brunicardi_Ch28_p1219-p1258.indd 125523/02/19 2:25 PM 1256SPECIFIC CONSIDERATIONSPART II 3. Yan KS, Chia LA, Li X, et al. The intestinal stem cell markers Bmi1 and Lgr5 identify two functionally distinct populations. Proc Natl Acad Sci U S A. 2012;109:466-471. 4. Thomson ABR, Keelan M, Thiesen A, et al. Small bowel review: normal physiology part 2. Dig Dis Sci. 2001;46: 2567-2587. 5. Laforenza U. Water channel proteins in the gastrointestinal tract. Mol Aspects Med. 2012;33:642-650. 6. Dyer J, Wood IS, Palejwala A, Ellis A, Shirazi-Beechy SP. Expression of monosaccharide transporters in intestine of diabetic humans. Am J Physiol. 2002;282:G241-G248. 7. Rubino F, Nathan DM, Eckel RH, et al; Delegates of the 2nd Diabetes Surgery Summit. Metabolic surgery in the treatment algorithm for type 2 diabetes: a joint statement by international diabetes organizations. Diabetes Care. 2016; 39(6):861-877. 8. Rolfs A, Hediger MA. Intestinal metal ion absorption: | Surgery_Schwartz. Churchill Livingstone; 1994:337.Brunicardi_Ch28_p1219-p1258.indd 125523/02/19 2:25 PM 1256SPECIFIC CONSIDERATIONSPART II 3. Yan KS, Chia LA, Li X, et al. The intestinal stem cell markers Bmi1 and Lgr5 identify two functionally distinct populations. Proc Natl Acad Sci U S A. 2012;109:466-471. 4. Thomson ABR, Keelan M, Thiesen A, et al. Small bowel review: normal physiology part 2. Dig Dis Sci. 2001;46: 2567-2587. 5. Laforenza U. Water channel proteins in the gastrointestinal tract. Mol Aspects Med. 2012;33:642-650. 6. Dyer J, Wood IS, Palejwala A, Ellis A, Shirazi-Beechy SP. Expression of monosaccharide transporters in intestine of diabetic humans. Am J Physiol. 2002;282:G241-G248. 7. Rubino F, Nathan DM, Eckel RH, et al; Delegates of the 2nd Diabetes Surgery Summit. Metabolic surgery in the treatment algorithm for type 2 diabetes: a joint statement by international diabetes organizations. Diabetes Care. 2016; 39(6):861-877. 8. Rolfs A, Hediger MA. Intestinal metal ion absorption: |
Surgery_Schwartz_8291 | Surgery_Schwartz | in the treatment algorithm for type 2 diabetes: a joint statement by international diabetes organizations. Diabetes Care. 2016; 39(6):861-877. 8. Rolfs A, Hediger MA. Intestinal metal ion absorption: an update. Curr Opin Gastroenterol. 2001;17:177-183. 9. Nagler-Anderson C. Man the barrier! Strategic defenses in the intestinal mucosa. Nat Rev Immunol. 2001;1:59-67. 10. Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol. 2003;3:331-341. 11. Jarchum I, Pamer EG. Regulation of innate and adaptive immunity by the commensal microbiota. Curr Opin Immunol. 2011;23:353-360. 12. Rehfeld JF. The new biology of gastrointestinal hormones. Physiol Rev. 1998;78(4):1087-1108. 13. Tavakkolizadeh A, Whang EE. Understanding and augmenting human intestinal adaptation: a call for more clinical research. JPEN J Parenter Enteral Nutr. 2002;26:251-255. 14. Scott FI, Osterman MT, Mahmoud NN, Lewis JD. Secular trends in small-bowel obstruction and adhesiolysis in the | Surgery_Schwartz. in the treatment algorithm for type 2 diabetes: a joint statement by international diabetes organizations. Diabetes Care. 2016; 39(6):861-877. 8. Rolfs A, Hediger MA. Intestinal metal ion absorption: an update. Curr Opin Gastroenterol. 2001;17:177-183. 9. Nagler-Anderson C. Man the barrier! Strategic defenses in the intestinal mucosa. Nat Rev Immunol. 2001;1:59-67. 10. Mowat AM. Anatomical basis of tolerance and immunity to intestinal antigens. Nat Rev Immunol. 2003;3:331-341. 11. Jarchum I, Pamer EG. Regulation of innate and adaptive immunity by the commensal microbiota. Curr Opin Immunol. 2011;23:353-360. 12. Rehfeld JF. The new biology of gastrointestinal hormones. Physiol Rev. 1998;78(4):1087-1108. 13. Tavakkolizadeh A, Whang EE. Understanding and augmenting human intestinal adaptation: a call for more clinical research. JPEN J Parenter Enteral Nutr. 2002;26:251-255. 14. Scott FI, Osterman MT, Mahmoud NN, Lewis JD. Secular trends in small-bowel obstruction and adhesiolysis in the |
Surgery_Schwartz_8292 | Surgery_Schwartz | a call for more clinical research. JPEN J Parenter Enteral Nutr. 2002;26:251-255. 14. Scott FI, Osterman MT, Mahmoud NN, Lewis JD. Secular trends in small-bowel obstruction and adhesiolysis in the United States: 1988-2007. Am J Surg. 2012;204(3):315-320. 15. Scott JW, Olufajo OA, Brat GA, et al. Use of national burden to define operative emergency general surgery. JAMA Surg. 2016;151(6):e160480. 16. Ceresoli M, Coccolini F, Catena F, et al. Water-soluble contrast agent in adhesive small bowel obstruction: a systematic review and meta-analysis of diagnostic and therapeutic value. Am J Surg. 2016;211(6):1114-1125. 17. Rocha FG, Theman TA, Matros E, Ledbetter SM, Zinner MJ, Ferzoco SJ. Nonoperative management of patients with a diagnosis of high-grade small bowel obstruction by computed tomography. Arch Surg. 2009;144(11):1000-1004. 18. Chu DI, Gainsbury ML, Howard LA, Stucchi AF, Becker JM. Early versus late adhesiolysis for adhesive-related intestinal obstruction: a nationwide analysis | Surgery_Schwartz. a call for more clinical research. JPEN J Parenter Enteral Nutr. 2002;26:251-255. 14. Scott FI, Osterman MT, Mahmoud NN, Lewis JD. Secular trends in small-bowel obstruction and adhesiolysis in the United States: 1988-2007. Am J Surg. 2012;204(3):315-320. 15. Scott JW, Olufajo OA, Brat GA, et al. Use of national burden to define operative emergency general surgery. JAMA Surg. 2016;151(6):e160480. 16. Ceresoli M, Coccolini F, Catena F, et al. Water-soluble contrast agent in adhesive small bowel obstruction: a systematic review and meta-analysis of diagnostic and therapeutic value. Am J Surg. 2016;211(6):1114-1125. 17. Rocha FG, Theman TA, Matros E, Ledbetter SM, Zinner MJ, Ferzoco SJ. Nonoperative management of patients with a diagnosis of high-grade small bowel obstruction by computed tomography. Arch Surg. 2009;144(11):1000-1004. 18. Chu DI, Gainsbury ML, Howard LA, Stucchi AF, Becker JM. Early versus late adhesiolysis for adhesive-related intestinal obstruction: a nationwide analysis |
Surgery_Schwartz_8293 | Surgery_Schwartz | Arch Surg. 2009;144(11):1000-1004. 18. Chu DI, Gainsbury ML, Howard LA, Stucchi AF, Becker JM. Early versus late adhesiolysis for adhesive-related intestinal obstruction: a nationwide analysis of inpatient outcomes. J Gastrointest Surg. 2013;17:288-297. 19. Lombardo S, Baum K, Filho JD, Nirula R. Should adhesive small bowel obstruction be managed laparoscopically? A National Surgical Quality Improvement Program propensity score analysis. J Trauma Acute Care Surg. 2014;76(3):696-703. 20. Wiggins T, Markar SR, Harris A. Laparoscopic adhesiolysis for acute small bowel obstruction: systematic review and pooled analysis. Surg Endosc. 2015;29(12):3432-3442. 21. Duron J, Jourdan-Da Silva N, Tezenas du Montcel S, et al. Adhesive postoperative small bowel obstruction: incidence and risk factors of recurrence after surgical treatment: a multicenter prospective study. Ann Surg. 2006;244(5):750-757. 22. Wahl WL, Wong SL, Sonnenday CJ, et al. Implementation of a small bowel obstruction guideline | Surgery_Schwartz. Arch Surg. 2009;144(11):1000-1004. 18. Chu DI, Gainsbury ML, Howard LA, Stucchi AF, Becker JM. Early versus late adhesiolysis for adhesive-related intestinal obstruction: a nationwide analysis of inpatient outcomes. J Gastrointest Surg. 2013;17:288-297. 19. Lombardo S, Baum K, Filho JD, Nirula R. Should adhesive small bowel obstruction be managed laparoscopically? A National Surgical Quality Improvement Program propensity score analysis. J Trauma Acute Care Surg. 2014;76(3):696-703. 20. Wiggins T, Markar SR, Harris A. Laparoscopic adhesiolysis for acute small bowel obstruction: systematic review and pooled analysis. Surg Endosc. 2015;29(12):3432-3442. 21. Duron J, Jourdan-Da Silva N, Tezenas du Montcel S, et al. Adhesive postoperative small bowel obstruction: incidence and risk factors of recurrence after surgical treatment: a multicenter prospective study. Ann Surg. 2006;244(5):750-757. 22. Wahl WL, Wong SL, Sonnenday CJ, et al. Implementation of a small bowel obstruction guideline |
Surgery_Schwartz_8294 | Surgery_Schwartz | recurrence after surgical treatment: a multicenter prospective study. Ann Surg. 2006;244(5):750-757. 22. Wahl WL, Wong SL, Sonnenday CJ, et al. Implementation of a small bowel obstruction guideline improves hospital efficiency. Surgery. 2012;152:626-632. 23. Ellis H, Moran BJ, Thompson JN, et al. Adhesion-related hospital readmissions after abdominal and pelvic surgery: a retrospective cohort study. Lancet. 1999;353:1476-1480. 24. Angenete E, Jacobsson A, Gellerstedt M, Haglind E. Effect of laparoscopy on the risk of small-bowel obstruction: a population-based register study. Arch Surg. 2012;147(4):359-365. 25. Fazio VW, Cohen Z, Fleshman JW, et al. Reduction in adhesive small-bowel obstruction by Seprafilm adhesion barrier after intestinal resection. Dis Colon Rectum. 2006; 49(1):1-11. 26. Kumar S, Wong PF, Leaper DJ. Intra-peritoneal prophylactic agents for preventing adhesions and adhesive intestinal obstruction after non-gynaecological abdominal surgery. Cochrane Database Syst | Surgery_Schwartz. recurrence after surgical treatment: a multicenter prospective study. Ann Surg. 2006;244(5):750-757. 22. Wahl WL, Wong SL, Sonnenday CJ, et al. Implementation of a small bowel obstruction guideline improves hospital efficiency. Surgery. 2012;152:626-632. 23. Ellis H, Moran BJ, Thompson JN, et al. Adhesion-related hospital readmissions after abdominal and pelvic surgery: a retrospective cohort study. Lancet. 1999;353:1476-1480. 24. Angenete E, Jacobsson A, Gellerstedt M, Haglind E. Effect of laparoscopy on the risk of small-bowel obstruction: a population-based register study. Arch Surg. 2012;147(4):359-365. 25. Fazio VW, Cohen Z, Fleshman JW, et al. Reduction in adhesive small-bowel obstruction by Seprafilm adhesion barrier after intestinal resection. Dis Colon Rectum. 2006; 49(1):1-11. 26. Kumar S, Wong PF, Leaper DJ. Intra-peritoneal prophylactic agents for preventing adhesions and adhesive intestinal obstruction after non-gynaecological abdominal surgery. Cochrane Database Syst |
Surgery_Schwartz_8295 | Surgery_Schwartz | S, Wong PF, Leaper DJ. Intra-peritoneal prophylactic agents for preventing adhesions and adhesive intestinal obstruction after non-gynaecological abdominal surgery. Cochrane Database Syst Rev. 2009;(1):CD005080. 27. Suwa K, Ushigome T, Ohtsu M, et al. Risk factors for early postoperative small bowel obstruction after anterior resection for rectal cancer. World J Surg. 2018;42(1):233-238. 28. Dalal KM, Gollub MJ, Miner TJ, et al. Management of patients with malignant bowel obstruction and stage IV colorectal cancer. J Palliat Med. 2011;14(7):822-828. 29. Doorly MG, Senagore AJ. Pathogenesis and clinical and economic consequences of postoperative ileus. Surg Clin North Am. 2012;92(2):259-272. 30. Vather R, Trivedi S, Bissett I. Defining postoperative ileus: results of a systematic review and global survey. J Gastrointest Surg. 2013;17(5):962-972. 31. Wolff BG, Viscusi ER, Delaney CP, Du W, Techner L. Patterns of gastrointestinal recovery after bowel resection and total abdominal | Surgery_Schwartz. S, Wong PF, Leaper DJ. Intra-peritoneal prophylactic agents for preventing adhesions and adhesive intestinal obstruction after non-gynaecological abdominal surgery. Cochrane Database Syst Rev. 2009;(1):CD005080. 27. Suwa K, Ushigome T, Ohtsu M, et al. Risk factors for early postoperative small bowel obstruction after anterior resection for rectal cancer. World J Surg. 2018;42(1):233-238. 28. Dalal KM, Gollub MJ, Miner TJ, et al. Management of patients with malignant bowel obstruction and stage IV colorectal cancer. J Palliat Med. 2011;14(7):822-828. 29. Doorly MG, Senagore AJ. Pathogenesis and clinical and economic consequences of postoperative ileus. Surg Clin North Am. 2012;92(2):259-272. 30. Vather R, Trivedi S, Bissett I. Defining postoperative ileus: results of a systematic review and global survey. J Gastrointest Surg. 2013;17(5):962-972. 31. Wolff BG, Viscusi ER, Delaney CP, Du W, Techner L. Patterns of gastrointestinal recovery after bowel resection and total abdominal |
Surgery_Schwartz_8296 | Surgery_Schwartz | and global survey. J Gastrointest Surg. 2013;17(5):962-972. 31. Wolff BG, Viscusi ER, Delaney CP, Du W, Techner L. Patterns of gastrointestinal recovery after bowel resection and total abdominal hysterectomy: pooled results from the placebo arms of alvimopan phase III North American clinical trials. Am Coll Surg. 2007;205(1):43-51. 32. Gendall KA, Kennedy RR, Watson AJ, Frizelle FA. The effect of epidural analgesia on postoperative outcome after colorectal surgery. Colorectal Dis. 2007;9(7):584-598. 33. Noblett SE, Snowden CP, Shenton BK, Horgan AF. Randomized clinical trial assessing the effect of Doppler-optimized fluid management on outcome after elective colorectal resection. Br J Surg. 2006;93:1069-1076. 34. Tan EK, Cornish J, Darzi AW, Tekkis PP. Meta-analysis: alvimopan vs. placebo in the treatment of post-operative ileus. Aliment Pharmacol Ther. 2007;25(1):47-57. 35. Gaines SL, Giroux K, Thomas S, Gregory JS. Real world efficacy of alvimopan on elective bowel resection | Surgery_Schwartz. and global survey. J Gastrointest Surg. 2013;17(5):962-972. 31. Wolff BG, Viscusi ER, Delaney CP, Du W, Techner L. Patterns of gastrointestinal recovery after bowel resection and total abdominal hysterectomy: pooled results from the placebo arms of alvimopan phase III North American clinical trials. Am Coll Surg. 2007;205(1):43-51. 32. Gendall KA, Kennedy RR, Watson AJ, Frizelle FA. The effect of epidural analgesia on postoperative outcome after colorectal surgery. Colorectal Dis. 2007;9(7):584-598. 33. Noblett SE, Snowden CP, Shenton BK, Horgan AF. Randomized clinical trial assessing the effect of Doppler-optimized fluid management on outcome after elective colorectal resection. Br J Surg. 2006;93:1069-1076. 34. Tan EK, Cornish J, Darzi AW, Tekkis PP. Meta-analysis: alvimopan vs. placebo in the treatment of post-operative ileus. Aliment Pharmacol Ther. 2007;25(1):47-57. 35. Gaines SL, Giroux K, Thomas S, Gregory JS. Real world efficacy of alvimopan on elective bowel resection |
Surgery_Schwartz_8297 | Surgery_Schwartz | in the treatment of post-operative ileus. Aliment Pharmacol Ther. 2007;25(1):47-57. 35. Gaines SL, Giroux K, Thomas S, Gregory JS. Real world efficacy of alvimopan on elective bowel resection patients: an analysis of statistical versus clinical significance. Am J Surg. 2012;203(3):308-311. 36. Kappelman MD, Moore KR, Allen JK, Cook SF. Recent trends in the prevalence of Crohn’s disease and ulcerative colitis in a commercially insured US population. Dig Dis Sci. 2013;58(2):519-525. 37. Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142(1):46-54. 38. Zheng JJ, Zhu XS, Huangfu Z, Gao ZX, Guo ZR, Wang Z. Crohn’s disease in mainland China: a systematic analysis of 50 years of research. Chin J Dig Dis. 2005;6(4):175-181. 39. Kaplan GG, Jackson T, Sands BE, Frisch M, Andersson RE, Korzenik J. The risk of developing Crohn’s disease after an appendectomy: a | Surgery_Schwartz. in the treatment of post-operative ileus. Aliment Pharmacol Ther. 2007;25(1):47-57. 35. Gaines SL, Giroux K, Thomas S, Gregory JS. Real world efficacy of alvimopan on elective bowel resection patients: an analysis of statistical versus clinical significance. Am J Surg. 2012;203(3):308-311. 36. Kappelman MD, Moore KR, Allen JK, Cook SF. Recent trends in the prevalence of Crohn’s disease and ulcerative colitis in a commercially insured US population. Dig Dis Sci. 2013;58(2):519-525. 37. Molodecky NA, Soon IS, Rabi DM, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology. 2012;142(1):46-54. 38. Zheng JJ, Zhu XS, Huangfu Z, Gao ZX, Guo ZR, Wang Z. Crohn’s disease in mainland China: a systematic analysis of 50 years of research. Chin J Dig Dis. 2005;6(4):175-181. 39. Kaplan GG, Jackson T, Sands BE, Frisch M, Andersson RE, Korzenik J. The risk of developing Crohn’s disease after an appendectomy: a |
Surgery_Schwartz_8298 | Surgery_Schwartz | of 50 years of research. Chin J Dig Dis. 2005;6(4):175-181. 39. Kaplan GG, Jackson T, Sands BE, Frisch M, Andersson RE, Korzenik J. The risk of developing Crohn’s disease after an appendectomy: a meta-analysis. Am J Gastroenterol. 2008;103(11):2925-2931. 40. Nikolaaus S, Schreiber S. Diagnosis of inflammatory bowel disease. Gastroenterology. 2007;133(5):1670-1689. 41. Frolkis AD, Dykeman J, Negrón ME, et al. Risk of surgery for inflammatory bowel diseases has decreased over time: a systematic review and meta-analysis of population-based studies. Gastroenterology. 2013;145(5):996-1006. 42. Fazio VW, Marchetti F, Church JM, et al. Effect of resection margins on the recurrence of Crohn’s disease of the small bowel. Ann Surg. 1996;224(4):563-571. 43. McLeod RS, Wolff BG, Ross S, Parkes R, McKenzie M. Recurrence of Crohn’s disease after ileocolic resection is not affected by anastomotic type: results of a multicenter, randomized, controlled trial. Dis Colon Rectum. 2009;52(5): | Surgery_Schwartz. of 50 years of research. Chin J Dig Dis. 2005;6(4):175-181. 39. Kaplan GG, Jackson T, Sands BE, Frisch M, Andersson RE, Korzenik J. The risk of developing Crohn’s disease after an appendectomy: a meta-analysis. Am J Gastroenterol. 2008;103(11):2925-2931. 40. Nikolaaus S, Schreiber S. Diagnosis of inflammatory bowel disease. Gastroenterology. 2007;133(5):1670-1689. 41. Frolkis AD, Dykeman J, Negrón ME, et al. Risk of surgery for inflammatory bowel diseases has decreased over time: a systematic review and meta-analysis of population-based studies. Gastroenterology. 2013;145(5):996-1006. 42. Fazio VW, Marchetti F, Church JM, et al. Effect of resection margins on the recurrence of Crohn’s disease of the small bowel. Ann Surg. 1996;224(4):563-571. 43. McLeod RS, Wolff BG, Ross S, Parkes R, McKenzie M. Recurrence of Crohn’s disease after ileocolic resection is not affected by anastomotic type: results of a multicenter, randomized, controlled trial. Dis Colon Rectum. 2009;52(5): |
Surgery_Schwartz_8299 | Surgery_Schwartz | R, McKenzie M. Recurrence of Crohn’s disease after ileocolic resection is not affected by anastomotic type: results of a multicenter, randomized, controlled trial. Dis Colon Rectum. 2009;52(5): 919-927.Brunicardi_Ch28_p1219-p1258.indd 125623/02/19 2:25 PM 1257SMALL INTESTINECHAPTER 28 44. Michelassi F, Upadhyay GA. Side-to-side isoperistaltic strictureplasty in the treatment of extensive Crohn’s disease. J Surg Res. 2004;117(1):71-78. 45. Tan JJ, Tjandra JJ. Laparoscopic surgery for Crohn’s disease: a meta-analysis. Dis Colon Rectum. 2007;50(5):576-585. 46. Delaney CP, Fazio VW. Crohn’s disease of the small bowel. Surg Clin North Am. 2001;81:137-158. 47. Penner RM, Madsen KL, Fedorak RN. Postoperative Crohn’s disease. Inflamm Bowel Dis. 2005;11:765-777. 48. Evenson AR, Shrikhande G, Fischer JE. Abdominal abscess and enteric fistula. In: Zinner MJ, Ashley SW, eds. Maingot’s Abdominal Operations. 11th ed. New York: McGraw Hill; 2007:184. 49. Coughlin S, Roth L, Lurati G, Faulhaber | Surgery_Schwartz. R, McKenzie M. Recurrence of Crohn’s disease after ileocolic resection is not affected by anastomotic type: results of a multicenter, randomized, controlled trial. Dis Colon Rectum. 2009;52(5): 919-927.Brunicardi_Ch28_p1219-p1258.indd 125623/02/19 2:25 PM 1257SMALL INTESTINECHAPTER 28 44. Michelassi F, Upadhyay GA. Side-to-side isoperistaltic strictureplasty in the treatment of extensive Crohn’s disease. J Surg Res. 2004;117(1):71-78. 45. Tan JJ, Tjandra JJ. Laparoscopic surgery for Crohn’s disease: a meta-analysis. Dis Colon Rectum. 2007;50(5):576-585. 46. Delaney CP, Fazio VW. Crohn’s disease of the small bowel. Surg Clin North Am. 2001;81:137-158. 47. Penner RM, Madsen KL, Fedorak RN. Postoperative Crohn’s disease. Inflamm Bowel Dis. 2005;11:765-777. 48. Evenson AR, Shrikhande G, Fischer JE. Abdominal abscess and enteric fistula. In: Zinner MJ, Ashley SW, eds. Maingot’s Abdominal Operations. 11th ed. New York: McGraw Hill; 2007:184. 49. Coughlin S, Roth L, Lurati G, Faulhaber |
Surgery_Schwartz_8300 | Surgery_Schwartz | Fischer JE. Abdominal abscess and enteric fistula. In: Zinner MJ, Ashley SW, eds. Maingot’s Abdominal Operations. 11th ed. New York: McGraw Hill; 2007:184. 49. Coughlin S, Roth L, Lurati G, Faulhaber M. Somatostatin analogues for the treatment of enterocutaneous fistulas: a systematic review and meta-analysis. World J Surg. 2012;36(5):1016-1029. 50. Wainstein DE, Fernandez E, Gonzalez D, Chara O, Berkowski D. Treatment of high-output enterocutaneous fistulas with a vacuum-compaction device. A ten-year experience. World J Surg. 2008;32(3):430-435. 51. Fazio VW, Coutsoftides T, Steiger E. Factors influencing the outcome of treatment of small bowel cutaneous fistula. World J Surg. 1983;7:481-488. 52. Owen RM, Love TP, Perez SD, et al. Definitive surgical treatment of enterocutaneous fistula: outcomes of a 23-year experience. JAMA Surg. 2013;148(2):118-126. 53. Martinez JL, Luque-de-Leon E, Ballinas-Oseguera G, Mendez JD, Juarez-Oropeza MA, Roman-Ramos R. Factors predictive of | Surgery_Schwartz. Fischer JE. Abdominal abscess and enteric fistula. In: Zinner MJ, Ashley SW, eds. Maingot’s Abdominal Operations. 11th ed. New York: McGraw Hill; 2007:184. 49. Coughlin S, Roth L, Lurati G, Faulhaber M. Somatostatin analogues for the treatment of enterocutaneous fistulas: a systematic review and meta-analysis. World J Surg. 2012;36(5):1016-1029. 50. Wainstein DE, Fernandez E, Gonzalez D, Chara O, Berkowski D. Treatment of high-output enterocutaneous fistulas with a vacuum-compaction device. A ten-year experience. World J Surg. 2008;32(3):430-435. 51. Fazio VW, Coutsoftides T, Steiger E. Factors influencing the outcome of treatment of small bowel cutaneous fistula. World J Surg. 1983;7:481-488. 52. Owen RM, Love TP, Perez SD, et al. Definitive surgical treatment of enterocutaneous fistula: outcomes of a 23-year experience. JAMA Surg. 2013;148(2):118-126. 53. Martinez JL, Luque-de-Leon E, Ballinas-Oseguera G, Mendez JD, Juarez-Oropeza MA, Roman-Ramos R. Factors predictive of |
Surgery_Schwartz_8301 | Surgery_Schwartz | fistula: outcomes of a 23-year experience. JAMA Surg. 2013;148(2):118-126. 53. Martinez JL, Luque-de-Leon E, Ballinas-Oseguera G, Mendez JD, Juarez-Oropeza MA, Roman-Ramos R. Factors predictive of recurrence and mortality after surgical repair of enterocutaneous fistula. J Gastrointest Surg. 2012;16(1):156-163. 54. Qubaiah O, Devesa SS, Platz CE, Huycke MM, Dores GM. Small intestinal cancer: a population-based study of incidence and survival patterns in the United States, 1992 to 2006. Cancer Epidemiol Biomarkers Prev. 2010;19:1908-1918. 55. Ceppa EP, Burbridge RA, Rialon KL, et al. Endoscopic versus surgical ampullectomy: an algorithm to treat disease of the ampulla of Vater. Ann Surg. 2013;257(2):315-322. 56. Judson I, Demetri G. Advances in the treatment of gastrointestinal stromal tumors. Ann Oncol. 2007;18:S20-S24. 57. Agrawal S, McCarron EC, Gibbs JF, Nava HR, Wilding GE, Rajput A. Surgical management and outcome in primary adenocarcinoma of the small bowel. Ann Surg Onc. | Surgery_Schwartz. fistula: outcomes of a 23-year experience. JAMA Surg. 2013;148(2):118-126. 53. Martinez JL, Luque-de-Leon E, Ballinas-Oseguera G, Mendez JD, Juarez-Oropeza MA, Roman-Ramos R. Factors predictive of recurrence and mortality after surgical repair of enterocutaneous fistula. J Gastrointest Surg. 2012;16(1):156-163. 54. Qubaiah O, Devesa SS, Platz CE, Huycke MM, Dores GM. Small intestinal cancer: a population-based study of incidence and survival patterns in the United States, 1992 to 2006. Cancer Epidemiol Biomarkers Prev. 2010;19:1908-1918. 55. Ceppa EP, Burbridge RA, Rialon KL, et al. Endoscopic versus surgical ampullectomy: an algorithm to treat disease of the ampulla of Vater. Ann Surg. 2013;257(2):315-322. 56. Judson I, Demetri G. Advances in the treatment of gastrointestinal stromal tumors. Ann Oncol. 2007;18:S20-S24. 57. Agrawal S, McCarron EC, Gibbs JF, Nava HR, Wilding GE, Rajput A. Surgical management and outcome in primary adenocarcinoma of the small bowel. Ann Surg Onc. |
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.