Surgery_Schwartz

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Surgery_Schwartz. 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. 2007;14:2263-2269. 58. Girvent M, Carlson GL, Anderson I, et al. Intestinal failure after surgery for complicated radiation enteritis. Ann R Coll Surg Engl. 2000;82:198-201. 59. Kiliç D, Egehan I, Ozenirler S, Dursun A. Double-blinded, randomized, placebo-controlled study to evaluate the effectiveness of sulphasalazine in preventing acute gastrointestinal complications due to radiotherapy. Radiother Oncol. 2000;57:125-129. 60. Waddell BE, Lee RJ, Rodriguez-Bigas MA, Weber TK, Petrelli NJ. Absorbable mesh sling prevents radiation-induced bowel injury during “sandwich” chemoradiation for rectal cancer. Arch Surg. 2000;135:1212-1217. 61. Yahchouchy EK, Marano AF, Etienne JC, et al. Meckel’s diverticulum. J Am Coll Surg. 2001;192(5):654-662. 62. Cullen JJ, Kelly KA, Moir CR, et al. Surgical


Surgery_Schwartz

Surgery_Schwartz. cancer. Arch Surg. 2000;135:1212-1217. 61. Yahchouchy EK, Marano AF, Etienne JC, et al. Meckel’s diverticulum. J Am Coll Surg. 2001;192(5):654-662. 62. Cullen JJ, Kelly KA, Moir CR, et al. Surgical management of Meckel’s diverticulum. An epidemiologic, population-based study. Ann Surg. 1994;220(4):564-568. 63. Zani A, Eaton S, Rees CM, et al. Incidentally detected Meckel diverticulum: to resect or not to resect? Ann Surg. 2008;247:276-281. 64. Park JJ, Wolff BG, Tollefson MK, Walsh EE, Larson DR. Meckel diverticulum: the Mayo Clinic experience with 1476 patients (1950-2002). Ann Surg. 2005;241(3):529-533. 65. Lobo DN, Balfour TW, Iftikhar SY, et al. Periampullary diverticula and pancreaticobiliary disease. Br J Surg. 1999; 86:588-597. 66. Chow DC, Babaian M, Taubin HL. Jejunoileal diverticula. Gastroenterologist. 1997;5:78-84. 67. Kumar S, Sarr MG, Kamath PS: Mesenteric venous thrombosis. N Engl J Med. 2001;345:1683-1688. 68. Gralnek IM. Obscure-overt gastrointestinal bleeding.


Surgery_Schwartz

Surgery_Schwartz. Gastroenterologist. 1997;5:78-84. 67. Kumar S, Sarr MG, Kamath PS: Mesenteric venous thrombosis. N Engl J Med. 2001;345:1683-1688. 68. Gralnek IM. Obscure-overt gastrointestinal bleeding. Gastroenterology. 2005;128:1424-1430. 69. Laine L, Sahota A, Shah A. Does capsule endoscopy improve outcomes in obscure gastrointestinal bleeding? Randomized trial versus dedicated small bowel radiography. Gastroenterology. 2010;138(5):1673-1680. 70. Andriulli A, Loperfido S, Napolitano G, et al. Incidence rates of post-ERCP complications: a systematic survey of prospective studies. Am J Gastroenterol. 2007;102(8):1781-1788. 71. Genzlinger JL, McPhee MS, Fisher JK, et al. Significance of retroperitoneal air after endoscopic retrograde cholangiopancreatography with sphincterotomy. Am J Gastroenterol. 1999;94(5):1267-1270. 72. Varban O, Ardestani A, Azagury D, Kis B, Brooks DC, Tavakkoli A. Contemporary management of adult intussusception: who needs a resection? World J Surg.


Surgery_Schwartz

Surgery_Schwartz. Am J Gastroenterol. 1999;94(5):1267-1270. 72. Varban O, Ardestani A, Azagury D, Kis B, Brooks DC, Tavakkoli A. Contemporary management of adult intussusception: who needs a resection? World J Surg. 2013;37(8):1872-1877. 73. Varban O, Ardestani A, Azagury D, et al. Resection or reduction? The dilemma of managing retrograde intussusception after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2013;9(5): 725-730. 74. Buchman AL, Solapio J, Fryer J. AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterology. 2003;124(4):1111-1134. 75. Bianchi A. Intestinal loop lengthening—a technique for increasing small-intestinal length. J Pediatr Surg. 1980;15(2): 145-151. 76. Jones BA, Hull MA, Potanos KM, et al. Report of 111 consecutive patients enrolled in the International Serial Transverse Enteroplasty (STEP) data registry: a retrospective observational study. J Am Coll Surg. 2013;216(3):438-446. 77. Messing B, Crenn P, Beau P, Boutron-Ruault MC, Rambaud JC,


Surgery_Schwartz

Surgery_Schwartz. Serial Transverse Enteroplasty (STEP) data registry: a retrospective observational study. J Am Coll Surg. 2013;216(3):438-446. 77. Messing B, Crenn P, Beau P, Boutron-Ruault MC, Rambaud JC, Matuchansky C. Long-term survival and parenteral nutrition dependence in adult patients with short bowel syndrome. Gastroenterology. 1999;117(5):1043-1050. 78. Cai J. Intestine and multivisceral transplantation in the United States: a report of 20-year national registry data (1990-2009). Clin Transpl. 2009;83-101.Brunicardi_Ch28_p1219-p1258.indd 125723/02/19 2:25 PM


Surgery_Schwartz

Surgery_Schwartz. Brunicardi_Ch28_p1219-p1258.indd 125823/02/19 2:25 PMThis page intentionally left blank


Surgery_Schwartz

Surgery_Schwartz. Colon, Rectum, and AnusMary R. Kwaan, David B. Stewart Sr, and Kelli Bullard Dunn 29chapterEMBRYOLOGY AND ANATOMYEmbryologyThe embryonic gastrointestinal tract begins developing during the fourth week of gestation. The primitive gut is derived from the endoderm and divided into three segments: foregut, midgut, and hindgut. Both midgut and hindgut contribute to the colon, rec-tum, and anus.The midgut develops into the small intestine, ascending colon, and proximal transverse colon, and receives blood supply from the superior mesenteric artery. During the sixth week of gestation, the midgut herniates out of the abdominal cavity and then rotates 270° counterclockwise around the superior mesen-teric artery to return to its final position inside the abdominal cavity during the tenth week of gestation. The hindgut develops into the distal transverse colon, descending colon, rectum, and Embryology and Anatomy 1259Embryology / 1259Anatomy / 1260Congenital Anomalies / 1263Normal


Surgery_Schwartz

Surgery_Schwartz. week of gestation. The hindgut develops into the distal transverse colon, descending colon, rectum, and Embryology and Anatomy 1259Embryology / 1259Anatomy / 1260Congenital Anomalies / 1263Normal Physiology 1263Fluid and Electrolyte Exchanges / 1263Short-Chain Fatty Acids / 1263Colonic Microflora and Intestinal Gas / 1263Motility, Defecation, and Continence / 1263Clinical Evaluation 1264Clinical Assessment / 1264Endoscopy / 1264Imaging / 1265Physiologic and Pelvic Floor Investigations / 1266Laboratory Studies / 1266Evaluation of Common Symptoms / 1267General Surgical Considerations 1270Resections / 1270Anastomoses / 1274Ostomies and Preoperative Stoma Planning / 1275Functional Results / 1278Anesthesia Considerations / 1278Operative Preliminaries / 1279Inflammatory Bowel Disease 1279General Considerations / 1279Ulcerative Colitis / 1282Operative Management / 1283Crohn’s Disease / 1283Indeterminate Colitis / 1286Diverticular Disease 1286Inflammatory Complications (Diverticulitis) /


Surgery_Schwartz

Surgery_Schwartz. Considerations / 1279Ulcerative Colitis / 1282Operative Management / 1283Crohn’s Disease / 1283Indeterminate Colitis / 1286Diverticular Disease 1286Inflammatory Complications (Diverticulitis) / 1286Hemorrhage / 1288Giant Colonic Diverticulum / 1288Right-Sided Diverticula / 1288Adenocarcinoma and Polyps 1288Incidence / 1288Epidemiology (Risk Factors) / 1288Pathogenesis of Colorectal Cancer / 1289Polyps / 1290Inherited Colorectal Carcinoma / 1291Prevention: Screening and Surveillance / 1293Routes of Spread and Natural History / 1295Staging and Preoperative Evaluation / 1295Therapy for Colonic Carcinoma / 1296Therapy for Rectal Carcinoma / 1299Follow-Up and Surveillance / 1302Treatment of Recurrent Colorectal Carcinoma / 1302Minimally Invasive Techniques for Resection / 1302Other Neoplasms 1303Rare Colorectal Tumors / 1303Retrorectal/Presacral Tumors / 1304Anal Canal and Perianal Tumors / 1304Other Benign Colorectal Conditions 1305Rectal Prolapse and Solitary Rectal Ulcer


Surgery_Schwartz

Surgery_Schwartz. Neoplasms 1303Rare Colorectal Tumors / 1303Retrorectal/Presacral Tumors / 1304Anal Canal and Perianal Tumors / 1304Other Benign Colorectal Conditions 1305Rectal Prolapse and Solitary Rectal Ulcer Syndrome / 1305Volvulus / 1306Megacolon / 1308Colonic Pseudo-Obstruction (Ogilvie’s Syndrome) / 1308Ischemic Colitis / 1309Infectious Colitis / 1309Anorectal Diseases 1310Hemorrhoids / 1310Anal Fissure / 1313Anorectal Sepsis and Cryptoglandular Abscess / 1313Perianal Abscess / 1314Ischiorectal Abscess / 1314Intersphincteric Abscess / 1314Supralevator Abscess / 1316Perianal Sepsis in the Immunocompromised Patient / 1316Necrotizing Soft Tissue Infection of the Perineum / 1316Fistula In Ano / 1317Rectovaginal Fistula / 1317Perianal Dermatitis / 1319Sexually Transmitted Diseases / 1320Pilonidal Disease / 1320Hidradenitis Suppurativa / 1320Trauma 1321Penetrating Colorectal Injury / 1321Blunt Colorectal Injury / 1321Iatrogenic Injury / 1321Anal Sphincter Injury and Incontinence / 1322Foreign


Surgery_Schwartz

Surgery_Schwartz. Disease / 1320Hidradenitis Suppurativa / 1320Trauma 1321Penetrating Colorectal Injury / 1321Blunt Colorectal Injury / 1321Iatrogenic Injury / 1321Anal Sphincter Injury and Incontinence / 1322Foreign Body / 1323The Immunocompromised Patient 1323Human Immunodeficiency Virus / 1323Immunosuppression for Transplantation 1323The Neutropenic Patient 1323Brunicardi_Ch29_p1259-p1330.indd 125923/02/19 2:28 PM 1260proximal anus, all of which receive their blood supply from the inferior mesenteric artery. During the sixth week of gestation, the distal-most end of the hindgut, the cloaca, is divided by the urorectal septum into the urogenital sinus and the rectum.The distal anal canal is derived from ectoderm and receives its blood supply from the internal pudendal artery. The dentate line divides the endodermal hindgut from the ectodermal distal anal canal.AnatomyThe large intestine extends from the ileocecal valve to the anus. It is divided anatomically and functionally into the colon,


Surgery_Schwartz

Surgery_Schwartz. the endodermal hindgut from the ectodermal distal anal canal.AnatomyThe large intestine extends from the ileocecal valve to the anus. It is divided anatomically and functionally into the colon, rectum, and anal canal. The wall of the colon and rectum comprise four distinct layers: mucosa, submucosa, muscularis propria (inner circular muscle, outer longitudinal muscle), and serosa. In the colon, the outer longitudinal muscle is separated into three teniae coli, which converge proximally at the appendix and dis-tally at the rectum, where the outer longitudinal muscle layer is circumferential. In the distal rectum, the inner smooth muscle layer coalesces to form the internal anal sphincter. The intraperi-toneal colon and proximal one-third of the rectum are covered by serosa; the mid and lower rectum lack serosa.Colon Landmarks. The colon begins at the junction of the terminal ileum and cecum and extends approximately 150 cm (3 to 5 feet) to the rectum. The rectosigmoid junction is found


Surgery_Schwartz

Surgery_Schwartz. rectum lack serosa.Colon Landmarks. The colon begins at the junction of the terminal ileum and cecum and extends approximately 150 cm (3 to 5 feet) to the rectum. The rectosigmoid junction is found at approximately the level of the sacral promontory and is arbitrarily described as the point at which the three teniae coli coalesce to form the outer longitudinal smooth muscle layer of the rectum. The cecum is the widest diameter portion of the colon (normally 7.5–8.5 cm) and has the thinnest muscular wall. As a result, the cecum is most vulnerable to perforation and least vulnerable to obstruction. The ascending colon is usu-ally fixed to the retroperitoneum. The hepatic flexure marks the transition to the transverse colon. The transverse colon is relatively mobile, but it is tethered by the gastrocolic ligament and colonic mesentery. The greater omentum is attached to the anterior/superior edge of the transverse colon. These attach-ments explain the characteristic triangular appearance