id
stringlengths 14
28
| title
stringclasses 18
values | content
stringlengths 2
999
| contents
stringlengths 19
1.02k
|
|---|---|---|---|
Surgery_Schwartz_7502
|
Surgery_Schwartz
|
>24 hours * In all patients, test and treat for H pylori, and if vagotomy not performed (most patients today) consider lifelong PPI. ** Avoid truncal vagotomy and avoid gastrectomy if BMI<21 *** Consider adding vagotomy for type II and type III gastric ulcerNoNoYes**Figure 26-44. Algorithm for operation for perforated peptic ulcer. ASA = acetylsalicylic acid; BMI = body mass index; Bx = biopsy; HSV = highly selective vagotomy; Hx = history; PPI = proton pump inhibitor; Rx = treatment; TV/D = truncal vagotomy and drainage.Brunicardi_Ch26_p1099-p1166.indd 113501/03/19 7:12 PM 1136SPECIFIC CONSIDERATIONS PART IImarginal ulcer can be life-threatening. In the United States and Western Europe, there is clearly a trend away from definitive operation for perforated duodenal ulcer.92,121In the stable patient without multiple operative risk fac-tors, perforated gastric ulcers are best treated by distal gastric resection. Vagotomy is usually added for type II and III gastric ulcers.
|
Surgery_Schwartz. >24 hours * In all patients, test and treat for H pylori, and if vagotomy not performed (most patients today) consider lifelong PPI. ** Avoid truncal vagotomy and avoid gastrectomy if BMI<21 *** Consider adding vagotomy for type II and type III gastric ulcerNoNoYes**Figure 26-44. Algorithm for operation for perforated peptic ulcer. ASA = acetylsalicylic acid; BMI = body mass index; Bx = biopsy; HSV = highly selective vagotomy; Hx = history; PPI = proton pump inhibitor; Rx = treatment; TV/D = truncal vagotomy and drainage.Brunicardi_Ch26_p1099-p1166.indd 113501/03/19 7:12 PM 1136SPECIFIC CONSIDERATIONS PART IImarginal ulcer can be life-threatening. In the United States and Western Europe, there is clearly a trend away from definitive operation for perforated duodenal ulcer.92,121In the stable patient without multiple operative risk fac-tors, perforated gastric ulcers are best treated by distal gastric resection. Vagotomy is usually added for type II and III gastric ulcers.
|
Surgery_Schwartz_7503
|
Surgery_Schwartz
|
the stable patient without multiple operative risk fac-tors, perforated gastric ulcers are best treated by distal gastric resection. Vagotomy is usually added for type II and III gastric ulcers. Patch closure with biopsy; or local excision and closure; or biopsy, closure, truncal vagotomy, and drainage are alter-native operations in the unstable or high-risk patient, or in the patient with a perforation in an inopportune location. All perfo-rated gastric ulcers, even those in the prepyloric position, should be biopsied if they are not removed at surgery.Obstructing Peptic UlcerAcute ulcers associated with obstruction due to edema and/or motor dysfunction may respond to intensive antisecretory ther-apy and nasogastric suction. But most patients with significant obstruction from chronic ulceration will require some sort of more substantial intervention. Endoscopic balloon dilation can often transiently improve obstructive symptoms, but many of these patients ultimately fail and come to
|
Surgery_Schwartz. the stable patient without multiple operative risk fac-tors, perforated gastric ulcers are best treated by distal gastric resection. Vagotomy is usually added for type II and III gastric ulcers. Patch closure with biopsy; or local excision and closure; or biopsy, closure, truncal vagotomy, and drainage are alter-native operations in the unstable or high-risk patient, or in the patient with a perforation in an inopportune location. All perfo-rated gastric ulcers, even those in the prepyloric position, should be biopsied if they are not removed at surgery.Obstructing Peptic UlcerAcute ulcers associated with obstruction due to edema and/or motor dysfunction may respond to intensive antisecretory ther-apy and nasogastric suction. But most patients with significant obstruction from chronic ulceration will require some sort of more substantial intervention. Endoscopic balloon dilation can often transiently improve obstructive symptoms, but many of these patients ultimately fail and come to
|
Surgery_Schwartz_7504
|
Surgery_Schwartz
|
will require some sort of more substantial intervention. Endoscopic balloon dilation can often transiently improve obstructive symptoms, but many of these patients ultimately fail and come to operation.123The standard operation for obstructing PUD is vagotomy and antrectomy. Alternatively, vagotomy and gastrojejunos-tomy should be considered if a difficult duodenal stump is anticipated with resection. HSV and gastrojejunostomy may be comparable to V + A for obstructing ulcer disease,124 and this procedure is appealing because it can be done laparoscopically and does not complicate future resection, if needed. However, potentially curable gastric or duodenal cancers can be missed with this approach.Intractable or Nonhealing Peptic UlcerIntractability should be an unusual indication for peptic ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the sur-geon: Maybe the patient has a missed cancer; maybe the patient
|
Surgery_Schwartz. will require some sort of more substantial intervention. Endoscopic balloon dilation can often transiently improve obstructive symptoms, but many of these patients ultimately fail and come to operation.123The standard operation for obstructing PUD is vagotomy and antrectomy. Alternatively, vagotomy and gastrojejunos-tomy should be considered if a difficult duodenal stump is anticipated with resection. HSV and gastrojejunostomy may be comparable to V + A for obstructing ulcer disease,124 and this procedure is appealing because it can be done laparoscopically and does not complicate future resection, if needed. However, potentially curable gastric or duodenal cancers can be missed with this approach.Intractable or Nonhealing Peptic UlcerIntractability should be an unusual indication for peptic ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the sur-geon: Maybe the patient has a missed cancer; maybe the patient
|
Surgery_Schwartz_7505
|
Surgery_Schwartz
|
ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the sur-geon: Maybe the patient has a missed cancer; maybe the patient is noncompliant (not taking prescribed PPI, still taking NSAIDs, still smoking); maybe the patient has Helicobacter despite the presence of a negative test or previous treatment. Because acid secretion can be totally blocked and H pylori eradicated with modern medication, the question remains: “Why does the patient have a persistent ulcer diathesis?” The surgeon should review the differential diagnosis of nonhealing ulcer before any consideration of operative treatment (Table 26-13).Surgical treatment should be considered in patients with nonhealing or intractable PUD who have multiple recurrences, large ulcers (>2 cm), complications (obstruction, perforation, or hemorrhage), or suspected malignancy. Definitive operation, particularly gastric resection, should be considered most cau-tiously
|
Surgery_Schwartz. ulcer operation nowadays. The patient referred for surgical evaluation because of intractable PUD should raise red flags for the sur-geon: Maybe the patient has a missed cancer; maybe the patient is noncompliant (not taking prescribed PPI, still taking NSAIDs, still smoking); maybe the patient has Helicobacter despite the presence of a negative test or previous treatment. Because acid secretion can be totally blocked and H pylori eradicated with modern medication, the question remains: “Why does the patient have a persistent ulcer diathesis?” The surgeon should review the differential diagnosis of nonhealing ulcer before any consideration of operative treatment (Table 26-13).Surgical treatment should be considered in patients with nonhealing or intractable PUD who have multiple recurrences, large ulcers (>2 cm), complications (obstruction, perforation, or hemorrhage), or suspected malignancy. Definitive operation, particularly gastric resection, should be considered most cau-tiously
|
Surgery_Schwartz_7506
|
Surgery_Schwartz
|
large ulcers (>2 cm), complications (obstruction, perforation, or hemorrhage), or suspected malignancy. Definitive operation, particularly gastric resection, should be considered most cau-tiously in the thin or marginally nourished individual.It is important that the surgeon not fall into the trap of per-forming a large, irreversible operation on these patients, based on the unproven theory that if all other methods have failed to heal the ulcer, a large operation is required. Although there are good data in the surgical literature suggesting that the major-ity of patients do well after the larger elective ulcer operations, most of these data are several decades old and may not be par-ticularly relevant to the modern patient.114 Candidates for ulcer operation today are different than those of 30 to 50 years ago. One might argue that current medical care has healed the typical peptic ulcers, and that patients presenting with true intractabil-ity or nonhealing will be more difficult to
|
Surgery_Schwartz. large ulcers (>2 cm), complications (obstruction, perforation, or hemorrhage), or suspected malignancy. Definitive operation, particularly gastric resection, should be considered most cau-tiously in the thin or marginally nourished individual.It is important that the surgeon not fall into the trap of per-forming a large, irreversible operation on these patients, based on the unproven theory that if all other methods have failed to heal the ulcer, a large operation is required. Although there are good data in the surgical literature suggesting that the major-ity of patients do well after the larger elective ulcer operations, most of these data are several decades old and may not be par-ticularly relevant to the modern patient.114 Candidates for ulcer operation today are different than those of 30 to 50 years ago. One might argue that current medical care has healed the typical peptic ulcers, and that patients presenting with true intractabil-ity or nonhealing will be more difficult to
|
Surgery_Schwartz_7507
|
Surgery_Schwartz
|
of 30 to 50 years ago. One might argue that current medical care has healed the typical peptic ulcers, and that patients presenting with true intractabil-ity or nonhealing will be more difficult to treat and are likely to have chronic problems after a major ulcer operation.If surgery is necessary, a lesser operation may be preferable. It is prudent to avoid truncal vagotomy and/or distal gastrectomy as the initial elective operation for intractable peptic ulcer in the thin or asthenic patient. Alternatives for intractable duo-denal ulcer include HSV with or without gastrojejunostomy (reversible drainage operation). In patients with nonhealing gas-tric ulcer, wedge resection with HSV should be considered in thin or frail patients. Otherwise, distal gastrectomy (to include the ulcer) is recommended. It is unnecessary to add a vagotomy in patients with type I or type IV (juxta-esophageal) gastric ulcers because they are usually associated with acid hyposecretion. Type IV gastric ulcers
|
Surgery_Schwartz. of 30 to 50 years ago. One might argue that current medical care has healed the typical peptic ulcers, and that patients presenting with true intractabil-ity or nonhealing will be more difficult to treat and are likely to have chronic problems after a major ulcer operation.If surgery is necessary, a lesser operation may be preferable. It is prudent to avoid truncal vagotomy and/or distal gastrectomy as the initial elective operation for intractable peptic ulcer in the thin or asthenic patient. Alternatives for intractable duo-denal ulcer include HSV with or without gastrojejunostomy (reversible drainage operation). In patients with nonhealing gas-tric ulcer, wedge resection with HSV should be considered in thin or frail patients. Otherwise, distal gastrectomy (to include the ulcer) is recommended. It is unnecessary to add a vagotomy in patients with type I or type IV (juxta-esophageal) gastric ulcers because they are usually associated with acid hyposecretion. Type IV gastric ulcers
|
Surgery_Schwartz_7508
|
Surgery_Schwartz
|
It is unnecessary to add a vagotomy in patients with type I or type IV (juxta-esophageal) gastric ulcers because they are usually associated with acid hyposecretion. Type IV gastric ulcers may be difficult to resect as part of a distal gas-trectomy, and a variety of surgical techniques have been described to treat these more proximal lesions (Fig. 26-45).Zollinger-Ellison Syndrome127-129ZES is caused by the hypersecretion of gastrin, typically by a duodenal or pancreatic neuroendocrine tumor (i.e., gastrinoma). Most cases (80%) are sporadic, but 20% are inherited. The inherited or familial form of gastrinoma is associated with mul-tiple endocrine neoplasia type I (MEN I), which is characterized by parathyroid, pituitary, and pancreatic (or duodenal) tumors. Gastrinoma is the most common islet cell tumor in patients with MEN I. Patients with MEN I usually have multiple gastrinomas, and surgical cure is usually not achievable; sporadic gastrino-mas are more often solitary and are more
|
Surgery_Schwartz. It is unnecessary to add a vagotomy in patients with type I or type IV (juxta-esophageal) gastric ulcers because they are usually associated with acid hyposecretion. Type IV gastric ulcers may be difficult to resect as part of a distal gas-trectomy, and a variety of surgical techniques have been described to treat these more proximal lesions (Fig. 26-45).Zollinger-Ellison Syndrome127-129ZES is caused by the hypersecretion of gastrin, typically by a duodenal or pancreatic neuroendocrine tumor (i.e., gastrinoma). Most cases (80%) are sporadic, but 20% are inherited. The inherited or familial form of gastrinoma is associated with mul-tiple endocrine neoplasia type I (MEN I), which is characterized by parathyroid, pituitary, and pancreatic (or duodenal) tumors. Gastrinoma is the most common islet cell tumor in patients with MEN I. Patients with MEN I usually have multiple gastrinomas, and surgical cure is usually not achievable; sporadic gastrino-mas are more often solitary and are more
|
Surgery_Schwartz_7509
|
Surgery_Schwartz
|
islet cell tumor in patients with MEN I. Patients with MEN I usually have multiple gastrinomas, and surgical cure is usually not achievable; sporadic gastrino-mas are more often solitary and are more often amenable to surgical cure. About 50% to 60% of gastrinomas are malignant, with lymph node, liver, or other distant metastases at operation. Five-year survival in patients presenting with metastatic disease is approximately 40%. More than 90% of patients with sporadic, completely resected gastrinoma will be cured.The most common symptoms of ZES are epigastric pain, GERD, and diarrhea. More than 90% of patients with gastri-noma have peptic ulcers. Most ulcers are in a typical location (proximal duodenum), but atypical ulcer location (distal duo-denum, jejunum, or multiple ulcers) should prompt an evalu-ation for gastrinoma. Gastrinoma also should be considered in the differential diagnosis of recurrent or refractory peptic ulcer, secretory diarrhea, gastric rugal hypertrophy,
|
Surgery_Schwartz. islet cell tumor in patients with MEN I. Patients with MEN I usually have multiple gastrinomas, and surgical cure is usually not achievable; sporadic gastrino-mas are more often solitary and are more often amenable to surgical cure. About 50% to 60% of gastrinomas are malignant, with lymph node, liver, or other distant metastases at operation. Five-year survival in patients presenting with metastatic disease is approximately 40%. More than 90% of patients with sporadic, completely resected gastrinoma will be cured.The most common symptoms of ZES are epigastric pain, GERD, and diarrhea. More than 90% of patients with gastri-noma have peptic ulcers. Most ulcers are in a typical location (proximal duodenum), but atypical ulcer location (distal duo-denum, jejunum, or multiple ulcers) should prompt an evalu-ation for gastrinoma. Gastrinoma also should be considered in the differential diagnosis of recurrent or refractory peptic ulcer, secretory diarrhea, gastric rugal hypertrophy,
|
Surgery_Schwartz_7510
|
Surgery_Schwartz
|
should prompt an evalu-ation for gastrinoma. Gastrinoma also should be considered in the differential diagnosis of recurrent or refractory peptic ulcer, secretory diarrhea, gastric rugal hypertrophy, esophagi-tis with stricture, bleeding or perforated ulcer, familial ulcer, peptic ulcer with hypercalcemia, and gastric neuroendocrine tumor (carcinoid). The majority of patients with ZES have been symptomatic for several years before definitive diagnosis and, 3Table 26-13Differential diagnosis of intractability or nonhealing peptic ulcer diseaseCancer Gastric Pancreatic DuodenalPersistent Helicobacter pylori infection Tests may be false-negative Consider empiric treatmentNoncompliant patient Failure to take prescribed medication Surreptitious use of NSAIDsMotility disorderZollinger-Ellison syndromeBrunicardi_Ch26_p1099-p1166.indd 113601/03/19 7:12 PM 1137STOMACHCHAPTER 26in general, patients with ZES and MEN1 are diagnosed in their 20s and 30s, while those with sporadic ZES more
|
Surgery_Schwartz. should prompt an evalu-ation for gastrinoma. Gastrinoma also should be considered in the differential diagnosis of recurrent or refractory peptic ulcer, secretory diarrhea, gastric rugal hypertrophy, esophagi-tis with stricture, bleeding or perforated ulcer, familial ulcer, peptic ulcer with hypercalcemia, and gastric neuroendocrine tumor (carcinoid). The majority of patients with ZES have been symptomatic for several years before definitive diagnosis and, 3Table 26-13Differential diagnosis of intractability or nonhealing peptic ulcer diseaseCancer Gastric Pancreatic DuodenalPersistent Helicobacter pylori infection Tests may be false-negative Consider empiric treatmentNoncompliant patient Failure to take prescribed medication Surreptitious use of NSAIDsMotility disorderZollinger-Ellison syndromeBrunicardi_Ch26_p1099-p1166.indd 113601/03/19 7:12 PM 1137STOMACHCHAPTER 26in general, patients with ZES and MEN1 are diagnosed in their 20s and 30s, while those with sporadic ZES more
|
Surgery_Schwartz_7511
|
Surgery_Schwartz
|
syndromeBrunicardi_Ch26_p1099-p1166.indd 113601/03/19 7:12 PM 1137STOMACHCHAPTER 26in general, patients with ZES and MEN1 are diagnosed in their 20s and 30s, while those with sporadic ZES more typically are diagnosed in their 40s and 50s.ZES is an important element in the differential diagnosis of hypergastrinemia (Fig. 26-46). All patients with gastrinoma have an elevated gastrin level, and hypergastrinemia in the pres-ence of elevated BAO strongly suggests gastrinoma. Patients with gastrinoma usually have a BAO >15 mEq/h or >5 mEq/h if they have had a previous procedure for peptic ulcer. Acid secre-tory medications should be held for several days before gastrin measurement, because acid suppression may falsely elevate gas-trin levels. Causes of hypergastrinemia can be divided into those associated with hyperacidity and those associated with hypo-acidity (see Fig. 26-46). The diagnosis of ZES is confirmed by the secretin stimulation test. An IV bolus of secretin (2 U/kg) is
|
Surgery_Schwartz. syndromeBrunicardi_Ch26_p1099-p1166.indd 113601/03/19 7:12 PM 1137STOMACHCHAPTER 26in general, patients with ZES and MEN1 are diagnosed in their 20s and 30s, while those with sporadic ZES more typically are diagnosed in their 40s and 50s.ZES is an important element in the differential diagnosis of hypergastrinemia (Fig. 26-46). All patients with gastrinoma have an elevated gastrin level, and hypergastrinemia in the pres-ence of elevated BAO strongly suggests gastrinoma. Patients with gastrinoma usually have a BAO >15 mEq/h or >5 mEq/h if they have had a previous procedure for peptic ulcer. Acid secre-tory medications should be held for several days before gastrin measurement, because acid suppression may falsely elevate gas-trin levels. Causes of hypergastrinemia can be divided into those associated with hyperacidity and those associated with hypo-acidity (see Fig. 26-46). The diagnosis of ZES is confirmed by the secretin stimulation test. An IV bolus of secretin (2 U/kg) is
|
Surgery_Schwartz_7512
|
Surgery_Schwartz
|
those associated with hyperacidity and those associated with hypo-acidity (see Fig. 26-46). The diagnosis of ZES is confirmed by the secretin stimulation test. An IV bolus of secretin (2 U/kg) is given, and gastrin levels are checked before and after injection. An increase in serum gastrin of 200 pg/mL or greater suggests the presence of gastrinoma. Patients with gastrinoma should have serum calcium and parathyroid hormone levels determined to rule out MEN1 and, if present, parathyroidectomy should be considered before resection of gastrinoma.About 80% of primary tumors are found in the gastrinoma triangle (Fig. 26-47), and many tumors are small (<1 cm), mak-ing preoperative localization difficult. Transabdominal ultra-sound is quite specific, but not very sensitive. CT will detect most lesions >2 cm in size, and MRI is comparable. EUS is more sensitive than noninvasive imaging tests, but it still misses many smaller lesions or lesions in inaccessible locations (e.g., the pan-creatic
|
Surgery_Schwartz. those associated with hyperacidity and those associated with hypo-acidity (see Fig. 26-46). The diagnosis of ZES is confirmed by the secretin stimulation test. An IV bolus of secretin (2 U/kg) is given, and gastrin levels are checked before and after injection. An increase in serum gastrin of 200 pg/mL or greater suggests the presence of gastrinoma. Patients with gastrinoma should have serum calcium and parathyroid hormone levels determined to rule out MEN1 and, if present, parathyroidectomy should be considered before resection of gastrinoma.About 80% of primary tumors are found in the gastrinoma triangle (Fig. 26-47), and many tumors are small (<1 cm), mak-ing preoperative localization difficult. Transabdominal ultra-sound is quite specific, but not very sensitive. CT will detect most lesions >2 cm in size, and MRI is comparable. EUS is more sensitive than noninvasive imaging tests, but it still misses many smaller lesions or lesions in inaccessible locations (e.g., the pan-creatic
|
Surgery_Schwartz_7513
|
Surgery_Schwartz
|
>2 cm in size, and MRI is comparable. EUS is more sensitive than noninvasive imaging tests, but it still misses many smaller lesions or lesions in inaccessible locations (e.g., the pan-creatic tail). Somatostatin receptor scintigraphy (the octreotide scan) or Gallium-68 dotatate PET/CT are sensitive and specific when the pretest probability of gastrinoma is high and may iden-tify sites of regional or distant metastatic disease (Fig. 26-48). Angiographic localization studies are infrequently performed for gastrinoma. Both diagnostic angiography and transhepatic selective venous sampling of the portal system have been sup-planted by selective arterial secretin infusion, which helps to localize the tumor as inside or outside the gastrinoma triangle. This study too, is rarely performed given increasing availability of endoscopic ultrasonography and accurate nuclear medicine imaging.All patients with sporadic (nonfamilial) gastrinoma should be considered for surgical exploration. The
|
Surgery_Schwartz. >2 cm in size, and MRI is comparable. EUS is more sensitive than noninvasive imaging tests, but it still misses many smaller lesions or lesions in inaccessible locations (e.g., the pan-creatic tail). Somatostatin receptor scintigraphy (the octreotide scan) or Gallium-68 dotatate PET/CT are sensitive and specific when the pretest probability of gastrinoma is high and may iden-tify sites of regional or distant metastatic disease (Fig. 26-48). Angiographic localization studies are infrequently performed for gastrinoma. Both diagnostic angiography and transhepatic selective venous sampling of the portal system have been sup-planted by selective arterial secretin infusion, which helps to localize the tumor as inside or outside the gastrinoma triangle. This study too, is rarely performed given increasing availability of endoscopic ultrasonography and accurate nuclear medicine imaging.All patients with sporadic (nonfamilial) gastrinoma should be considered for surgical exploration. The
|
Surgery_Schwartz_7514
|
Surgery_Schwartz
|
increasing availability of endoscopic ultrasonography and accurate nuclear medicine imaging.All patients with sporadic (nonfamilial) gastrinoma should be considered for surgical exploration. The lesions can be located in over 90% of patients, and a majority are cured by extirpation of the gastrinoma.130,131 A thorough intraoperative exploration of the gastrinoma triangle and pancreas is essential, but other sites (i.e., liver, stomach, small bowel, mesentery, and pelvis) should be evaluated as part of a thorough intra-abdom-inal evaluation to find the primary tumor, which is most often solitary and often in the duodenal wall. The duodenum and pan-creatic head should be extensively mobilized and intraoperative ultrasound should be utilized. Intraoperative EGD with transil-lumination may be considered. If the tumor cannot be located, longitudinal duodenotomy with inspection and palpation of the duodenal wall is performed. Lymph nodes from the portal, peri-pancreatic, and celiac drainage
|
Surgery_Schwartz. increasing availability of endoscopic ultrasonography and accurate nuclear medicine imaging.All patients with sporadic (nonfamilial) gastrinoma should be considered for surgical exploration. The lesions can be located in over 90% of patients, and a majority are cured by extirpation of the gastrinoma.130,131 A thorough intraoperative exploration of the gastrinoma triangle and pancreas is essential, but other sites (i.e., liver, stomach, small bowel, mesentery, and pelvis) should be evaluated as part of a thorough intra-abdom-inal evaluation to find the primary tumor, which is most often solitary and often in the duodenal wall. The duodenum and pan-creatic head should be extensively mobilized and intraoperative ultrasound should be utilized. Intraoperative EGD with transil-lumination may be considered. If the tumor cannot be located, longitudinal duodenotomy with inspection and palpation of the duodenal wall is performed. Lymph nodes from the portal, peri-pancreatic, and celiac drainage
|
Surgery_Schwartz_7515
|
Surgery_Schwartz
|
considered. If the tumor cannot be located, longitudinal duodenotomy with inspection and palpation of the duodenal wall is performed. Lymph nodes from the portal, peri-pancreatic, and celiac drainage basins should be removed. Abla-tion or resection of hepatic metastases when identified should be considered.The management of gastrinoma in patients with MEN I is controversial because patients are infrequently cured by opera-tion. Acid hypersecretion in patients with gastrinoma can always be managed with high-dose PPIs. Highly selective vagotomy may make management easier in some patients and should be considered in those with surgically untreatable or unresectable gastrinoma. Gastrectomy for ZES is not indicated.STRESS GASTRITIS AND STRESS ULCERStress gastritis is a peculiar entity that has all but disappeared from the clinical (if not endoscopic) lexicon, largely due to bet-ter critical care and acid suppression or cytoprotective agents (e.g., sucralfate) in the intensive care unit
|
Surgery_Schwartz. considered. If the tumor cannot be located, longitudinal duodenotomy with inspection and palpation of the duodenal wall is performed. Lymph nodes from the portal, peri-pancreatic, and celiac drainage basins should be removed. Abla-tion or resection of hepatic metastases when identified should be considered.The management of gastrinoma in patients with MEN I is controversial because patients are infrequently cured by opera-tion. Acid hypersecretion in patients with gastrinoma can always be managed with high-dose PPIs. Highly selective vagotomy may make management easier in some patients and should be considered in those with surgically untreatable or unresectable gastrinoma. Gastrectomy for ZES is not indicated.STRESS GASTRITIS AND STRESS ULCERStress gastritis is a peculiar entity that has all but disappeared from the clinical (if not endoscopic) lexicon, largely due to bet-ter critical care and acid suppression or cytoprotective agents (e.g., sucralfate) in the intensive care unit
|
Surgery_Schwartz_7516
|
Surgery_Schwartz
|
has all but disappeared from the clinical (if not endoscopic) lexicon, largely due to bet-ter critical care and acid suppression or cytoprotective agents (e.g., sucralfate) in the intensive care unit (ICU). Stress gastritis and stress ulcer are probably due to inadequate gastric mucosal Figure 26-45. Operations for gastric ulcer. (Reproduced with permission from Feldman M, Sharschmidt BF, Sleisenger MH: Slei-senger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/ Management 6th ed. Philadelphia, PA: Elsevier/Saunders; 1998.)Ulcer excisionAntrectomyPauchet procedureKelling-MadlenerprocedureCsendes procedure(Roux reconstruction)Csendes procedureBrunicardi_Ch26_p1099-p1166.indd 113701/03/19 7:12 PM 1138SPECIFIC CONSIDERATIONS PART IIblood flow during periods of intense physiologic stress. Ade-quate mucosal blood flow is important to maintain the mucosal barrier and to buffer any back-diffused hydrogen ions. When blood flow is inadequate, these
|
Surgery_Schwartz. has all but disappeared from the clinical (if not endoscopic) lexicon, largely due to bet-ter critical care and acid suppression or cytoprotective agents (e.g., sucralfate) in the intensive care unit (ICU). Stress gastritis and stress ulcer are probably due to inadequate gastric mucosal Figure 26-45. Operations for gastric ulcer. (Reproduced with permission from Feldman M, Sharschmidt BF, Sleisenger MH: Slei-senger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology/Diagnosis/ Management 6th ed. Philadelphia, PA: Elsevier/Saunders; 1998.)Ulcer excisionAntrectomyPauchet procedureKelling-MadlenerprocedureCsendes procedure(Roux reconstruction)Csendes procedureBrunicardi_Ch26_p1099-p1166.indd 113701/03/19 7:12 PM 1138SPECIFIC CONSIDERATIONS PART IIblood flow during periods of intense physiologic stress. Ade-quate mucosal blood flow is important to maintain the mucosal barrier and to buffer any back-diffused hydrogen ions. When blood flow is inadequate, these
|
Surgery_Schwartz_7517
|
Surgery_Schwartz
|
periods of intense physiologic stress. Ade-quate mucosal blood flow is important to maintain the mucosal barrier and to buffer any back-diffused hydrogen ions. When blood flow is inadequate, these processes fail and mucosal breakdown occurs. Modern intensive care, with emphasis on adequate tissue perfusion and oxygenation, has undoubtedly decreased the severity of gastric mucosal injury seen in the ICU today. Although it is still common to see small mucosal ero-sions when performing upper endoscopy in the ICU, it is rare for these lesions to coalesce into the larger bleeding erosions that plagued the ICU patient 30 to 50 years ago. The rationale for routine acid suppression in the ICU, supported by excellent data from clinical trials and the laboratory, is that less mucosal injury will be caused in the potentially weakened gastric mucosa if there is less luminal acid.132 There are some studies suggest-ing that routine acid suppression leads to overgrowth of gastric bacteria, which
|
Surgery_Schwartz. periods of intense physiologic stress. Ade-quate mucosal blood flow is important to maintain the mucosal barrier and to buffer any back-diffused hydrogen ions. When blood flow is inadequate, these processes fail and mucosal breakdown occurs. Modern intensive care, with emphasis on adequate tissue perfusion and oxygenation, has undoubtedly decreased the severity of gastric mucosal injury seen in the ICU today. Although it is still common to see small mucosal ero-sions when performing upper endoscopy in the ICU, it is rare for these lesions to coalesce into the larger bleeding erosions that plagued the ICU patient 30 to 50 years ago. The rationale for routine acid suppression in the ICU, supported by excellent data from clinical trials and the laboratory, is that less mucosal injury will be caused in the potentially weakened gastric mucosa if there is less luminal acid.132 There are some studies suggest-ing that routine acid suppression leads to overgrowth of gastric bacteria, which
|
Surgery_Schwartz_7518
|
Surgery_Schwartz
|
be caused in the potentially weakened gastric mucosa if there is less luminal acid.132 There are some studies suggest-ing that routine acid suppression leads to overgrowth of gastric bacteria, which increases the incidence and/or severity of aspira-tion pneumonia in the ICU.133,134 Nevertheless, acid suppression, particularly in the severely ill patient, remains an important part of clinical pathways in most ICUs.135 In the extraordinarily rare patient requiring operation today for hemorrhagic stress gastri-tis, the surgical options include V + D with oversewing of the major bleeding lesions, or near total gastrectomy. Angiographic embolization and endoscopic hemostatic treatment should be considered as well.ATROPHIC GASTRITISAtrophic gastritis is characterized by atrophy or disappearance of gastric glands and loss of parietal and chief cells. The most common cause is chronic H pylori infection, particularly in the corporal distribution (as opposed to the antral distribution which is
|
Surgery_Schwartz. be caused in the potentially weakened gastric mucosa if there is less luminal acid.132 There are some studies suggest-ing that routine acid suppression leads to overgrowth of gastric bacteria, which increases the incidence and/or severity of aspira-tion pneumonia in the ICU.133,134 Nevertheless, acid suppression, particularly in the severely ill patient, remains an important part of clinical pathways in most ICUs.135 In the extraordinarily rare patient requiring operation today for hemorrhagic stress gastri-tis, the surgical options include V + D with oversewing of the major bleeding lesions, or near total gastrectomy. Angiographic embolization and endoscopic hemostatic treatment should be considered as well.ATROPHIC GASTRITISAtrophic gastritis is characterized by atrophy or disappearance of gastric glands and loss of parietal and chief cells. The most common cause is chronic H pylori infection, particularly in the corporal distribution (as opposed to the antral distribution which is
|
Surgery_Schwartz_7519
|
Surgery_Schwartz
|
of gastric glands and loss of parietal and chief cells. The most common cause is chronic H pylori infection, particularly in the corporal distribution (as opposed to the antral distribution which is more typically associated with peptic ulcer disease). Auto-immune destruction of cells (pernicious anemia) and chemical irritation (e.g., bile reflux) can also result in atrophic gastritis. Some patients with atrophic gastritis develop intestinal meta-plasia in the gastric mucosa that may progress to dysplasia and then to gastric cancer. Numerous cofactors have been impli-cated, including diet, altered gastric microbiome, genetics, and hypergastrinemia. Patients with atrophic gastritis are at risk for Elevated serum gastrin(off PPI + H2RA)Measure BAO and gastric pHSecretin stimulation testBAO > 10 mEq/hpH <2BAO lowpH > 2Previous GI surgery• Vagotomy?• Massive SB resectionAtrophicgastritisPerniciousanemiaRenal insuffNoYesConfirm with EGD/Bxtest/treat H pylorigive B12Significant elevation
|
Surgery_Schwartz. of gastric glands and loss of parietal and chief cells. The most common cause is chronic H pylori infection, particularly in the corporal distribution (as opposed to the antral distribution which is more typically associated with peptic ulcer disease). Auto-immune destruction of cells (pernicious anemia) and chemical irritation (e.g., bile reflux) can also result in atrophic gastritis. Some patients with atrophic gastritis develop intestinal meta-plasia in the gastric mucosa that may progress to dysplasia and then to gastric cancer. Numerous cofactors have been impli-cated, including diet, altered gastric microbiome, genetics, and hypergastrinemia. Patients with atrophic gastritis are at risk for Elevated serum gastrin(off PPI + H2RA)Measure BAO and gastric pHSecretin stimulation testBAO > 10 mEq/hpH <2BAO lowpH > 2Previous GI surgery• Vagotomy?• Massive SB resectionAtrophicgastritisPerniciousanemiaRenal insuffNoYesConfirm with EGD/Bxtest/treat H pylorigive B12Significant elevation
|
Surgery_Schwartz_7520
|
Surgery_Schwartz
|
> 10 mEq/hpH <2BAO lowpH > 2Previous GI surgery• Vagotomy?• Massive SB resectionAtrophicgastritisPerniciousanemiaRenal insuffNoYesConfirm with EGD/Bxtest/treat H pylorigive B12Significant elevation in serumgastrin in response to IV secretin?G-cell +/or ECLcell hyperplasiaLoop GJ with antralalkalinizationTakedown GJOrTV and AConsider TV+ antrectomyRetained antrum on“duodenal stump”Resect retained antrumOrConvert B2 to B1AntralstasisS/P gastrectomy B2Confirm with EGD + BxConsider resectionZollinger-EllisonsyndromeOctreotide scanR/O MEN-1Figure 26-46. Algorithm for diagnosis and management of hypergastrinemia. BAO = basal acid output; B1 = Billroth 1; B2 = Billroth 2; Bx = biopsy; ECL = enterochromaffin-like; EGD = esophagogastroduodenoscopy; GJ = gastrojejunostomy; H2RA = histamine 2 receptor antagonist; insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status post; TV = truncal vagotomy; TV and A
|
Surgery_Schwartz. > 10 mEq/hpH <2BAO lowpH > 2Previous GI surgery• Vagotomy?• Massive SB resectionAtrophicgastritisPerniciousanemiaRenal insuffNoYesConfirm with EGD/Bxtest/treat H pylorigive B12Significant elevation in serumgastrin in response to IV secretin?G-cell +/or ECLcell hyperplasiaLoop GJ with antralalkalinizationTakedown GJOrTV and AConsider TV+ antrectomyRetained antrum on“duodenal stump”Resect retained antrumOrConvert B2 to B1AntralstasisS/P gastrectomy B2Confirm with EGD + BxConsider resectionZollinger-EllisonsyndromeOctreotide scanR/O MEN-1Figure 26-46. Algorithm for diagnosis and management of hypergastrinemia. BAO = basal acid output; B1 = Billroth 1; B2 = Billroth 2; Bx = biopsy; ECL = enterochromaffin-like; EGD = esophagogastroduodenoscopy; GJ = gastrojejunostomy; H2RA = histamine 2 receptor antagonist; insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status post; TV = truncal vagotomy; TV and A
|
Surgery_Schwartz_7521
|
Surgery_Schwartz
|
antagonist; insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status post; TV = truncal vagotomy; TV and A = truncal vagotomy and antrectomy.Brunicardi_Ch26_p1099-p1166.indd 113801/03/19 7:12 PM 1139STOMACHCHAPTER 26gastric cancer and should undergo periodic endoscopic surveil-lance. Metaplastic atrophic gastritis and dysplastic atrophic gastritis in particular, are markers of increased risk for gastric cancer. Patients with high grade dysplasia may benefit from gas-trectomy. Cancer risk is related to the extent of the atrophic gas-tritis and intestinal metaplasia, and grading systems have been developed to stratify cancer risk based on endoscopic findings. Two such systems are the operative link on gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia (OLGIM) assessment.136,137 These systems define the severity (“stage”) of atrophic gastritis based on the
|
Surgery_Schwartz. antagonist; insuff = insufficiency; MEN1 = multiple endocrine neoplasia type I; PPI = proton pump inhibitor; R/O = rule out; SB = small bowel; S/P = status post; TV = truncal vagotomy; TV and A = truncal vagotomy and antrectomy.Brunicardi_Ch26_p1099-p1166.indd 113801/03/19 7:12 PM 1139STOMACHCHAPTER 26gastric cancer and should undergo periodic endoscopic surveil-lance. Metaplastic atrophic gastritis and dysplastic atrophic gastritis in particular, are markers of increased risk for gastric cancer. Patients with high grade dysplasia may benefit from gas-trectomy. Cancer risk is related to the extent of the atrophic gas-tritis and intestinal metaplasia, and grading systems have been developed to stratify cancer risk based on endoscopic findings. Two such systems are the operative link on gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia (OLGIM) assessment.136,137 These systems define the severity (“stage”) of atrophic gastritis based on the
|
Surgery_Schwartz_7522
|
Surgery_Schwartz
|
link on gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia (OLGIM) assessment.136,137 These systems define the severity (“stage”) of atrophic gastritis based on the histologic grading of at least five gastric biopsies (lesser and greater curve antrum; Figure 26-47. Gastrinoma triangle. (Reproduced with permission from Ritchie WP, Steele G, Dean RH: General Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 1995.)Figure 26-48. Positive gallium-68 dotatate scan in patient with gastrinoma.Table 26-14Types of gastric tumorsMalignant tumors Carcinoma Lymphoma Gastrointestinal stromal tumor (GIST) Neuroendocrine tumorBenign tumors Hyperplastic polyp Adenomatous polyp Leiomyoma Lipoma Schwannoma Hetrotopic pancreaslesser and greater curve corpus; angularis incisura). Since pathol-ogists are more likely to agree on the histological diagnosis of intestinal metaplasia than they are on atrophic gastritis, the latter tool (OLGIM) may be more useful in
|
Surgery_Schwartz. link on gastritis assessment (OLGA) and the operative link on gastric intestinal metaplasia (OLGIM) assessment.136,137 These systems define the severity (“stage”) of atrophic gastritis based on the histologic grading of at least five gastric biopsies (lesser and greater curve antrum; Figure 26-47. Gastrinoma triangle. (Reproduced with permission from Ritchie WP, Steele G, Dean RH: General Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 1995.)Figure 26-48. Positive gallium-68 dotatate scan in patient with gastrinoma.Table 26-14Types of gastric tumorsMalignant tumors Carcinoma Lymphoma Gastrointestinal stromal tumor (GIST) Neuroendocrine tumorBenign tumors Hyperplastic polyp Adenomatous polyp Leiomyoma Lipoma Schwannoma Hetrotopic pancreaslesser and greater curve corpus; angularis incisura). Since pathol-ogists are more likely to agree on the histological diagnosis of intestinal metaplasia than they are on atrophic gastritis, the latter tool (OLGIM) may be more useful in
|
Surgery_Schwartz_7523
|
Surgery_Schwartz
|
incisura). Since pathol-ogists are more likely to agree on the histological diagnosis of intestinal metaplasia than they are on atrophic gastritis, the latter tool (OLGIM) may be more useful in stratifying gastric cancer risk. Patients stratified as stage 3 or 4 gastritis and those with pernicious anemia may benefit from surveillance endoscopy every 3 years. Serum markers are also useful in helping to iden-tify patients with atrophic gastritis who usually have increased serum gastrin and iron deficiency due to parietal cell loss and hypochlorhydria or achlorhydria; decreased pepsinogen I levels due to chief cell loss; and B12 deficiency due to parietal cell loss and concomitant loss of intrinsic factor.MALIGNANT NEOPLASMS OF THE STOMACHThe most common primary malignant gastric neoplasm is adeno-carcinoma (95%); lymphoma and GIST account for most of the remaining cases (Table 26-14). Other rare primary malignancies include neuroendocrine tumor, angiosarcoma, carcinosarcoma, and
|
Surgery_Schwartz. incisura). Since pathol-ogists are more likely to agree on the histological diagnosis of intestinal metaplasia than they are on atrophic gastritis, the latter tool (OLGIM) may be more useful in stratifying gastric cancer risk. Patients stratified as stage 3 or 4 gastritis and those with pernicious anemia may benefit from surveillance endoscopy every 3 years. Serum markers are also useful in helping to iden-tify patients with atrophic gastritis who usually have increased serum gastrin and iron deficiency due to parietal cell loss and hypochlorhydria or achlorhydria; decreased pepsinogen I levels due to chief cell loss; and B12 deficiency due to parietal cell loss and concomitant loss of intrinsic factor.MALIGNANT NEOPLASMS OF THE STOMACHThe most common primary malignant gastric neoplasm is adeno-carcinoma (95%); lymphoma and GIST account for most of the remaining cases (Table 26-14). Other rare primary malignancies include neuroendocrine tumor, angiosarcoma, carcinosarcoma, and
|
Surgery_Schwartz_7524
|
Surgery_Schwartz
|
is adeno-carcinoma (95%); lymphoma and GIST account for most of the remaining cases (Table 26-14). Other rare primary malignancies include neuroendocrine tumor, angiosarcoma, carcinosarcoma, and squamous cell carcinoma. Occasionally the stomach is a site of hematogenous metastasis from other sites (e.g., melanoma or breast cancer). Malignant tumors from adjacent organs may also invade the stomach by direct extension (e.g., colon or pancreas) or by peritoneal dissemination (e.g., ovary or appendiceal).AdenocarcinomaEpidemiology. Gastric cancer is the fourth most common can-cer type and the second leading cause of cancer death world-wide. Over the past century, there has been a dramatic decrease in the incidence of gastric cancer in most Western industrialized countries (Fig. 26-49). This decrease has been largely in the so-called intestinal form rather than in the diffuse form of gastric cancer. In Asia and Eastern Europe, gastric cancer remains a leading cause of cancer death. In 2017
|
Surgery_Schwartz. is adeno-carcinoma (95%); lymphoma and GIST account for most of the remaining cases (Table 26-14). Other rare primary malignancies include neuroendocrine tumor, angiosarcoma, carcinosarcoma, and squamous cell carcinoma. Occasionally the stomach is a site of hematogenous metastasis from other sites (e.g., melanoma or breast cancer). Malignant tumors from adjacent organs may also invade the stomach by direct extension (e.g., colon or pancreas) or by peritoneal dissemination (e.g., ovary or appendiceal).AdenocarcinomaEpidemiology. Gastric cancer is the fourth most common can-cer type and the second leading cause of cancer death world-wide. Over the past century, there has been a dramatic decrease in the incidence of gastric cancer in most Western industrialized countries (Fig. 26-49). This decrease has been largely in the so-called intestinal form rather than in the diffuse form of gastric cancer. In Asia and Eastern Europe, gastric cancer remains a leading cause of cancer death. In 2017
|
Surgery_Schwartz_7525
|
Surgery_Schwartz
|
has been largely in the so-called intestinal form rather than in the diffuse form of gastric cancer. In Asia and Eastern Europe, gastric cancer remains a leading cause of cancer death. In 2017 in the United States, approximately 28,000 new cases of stomach cancer were diagnosed (17,750 in men and 10,250 in women), and 10,960 deaths will be attributed to this disease (6720 in men and 4240 in women).138 The estimated 5-year survival rate is 27%, up from about 15% in 1975.In general, gastric cancer is a disease of the elderly, and it is twice as common in blacks as in whites. In younger patients, tumors are more often of the diffuse variety and tend to be large, aggressive, and poorly differentiated, sometimes involving the entire stomach (linitis plastic). Gastric cancer has a higher inci-dence in groups of lower socioeconomic status.4Brunicardi_Ch26_p1099-p1166.indd 113901/03/19 7:12 PM 1140SPECIFIC CONSIDERATIONS PART IIEtiology. Gastric cancer is more common in patients with
|
Surgery_Schwartz. has been largely in the so-called intestinal form rather than in the diffuse form of gastric cancer. In Asia and Eastern Europe, gastric cancer remains a leading cause of cancer death. In 2017 in the United States, approximately 28,000 new cases of stomach cancer were diagnosed (17,750 in men and 10,250 in women), and 10,960 deaths will be attributed to this disease (6720 in men and 4240 in women).138 The estimated 5-year survival rate is 27%, up from about 15% in 1975.In general, gastric cancer is a disease of the elderly, and it is twice as common in blacks as in whites. In younger patients, tumors are more often of the diffuse variety and tend to be large, aggressive, and poorly differentiated, sometimes involving the entire stomach (linitis plastic). Gastric cancer has a higher inci-dence in groups of lower socioeconomic status.4Brunicardi_Ch26_p1099-p1166.indd 113901/03/19 7:12 PM 1140SPECIFIC CONSIDERATIONS PART IIEtiology. Gastric cancer is more common in patients with
|
Surgery_Schwartz_7526
|
Surgery_Schwartz
|
in groups of lower socioeconomic status.4Brunicardi_Ch26_p1099-p1166.indd 113901/03/19 7:12 PM 1140SPECIFIC CONSIDERATIONS PART IIEtiology. Gastric cancer is more common in patients with per-nicious anemia, blood group A, or a family history of gastric cancer. When patients migrate from a high-incidence region to a low-incidence region, the risk of gastric cancer decreases in the subsequent generations born in the new region. This strongly suggests an environmental influence on the development of gas-tric cancer. Environmental factors appear to be more important in the pathogenesis of the intestinal form of gastric cancer com-pared to the diffuse form. The commonly accepted risk factors for gastric cancer are listed in Table 26-15.Diet and Drugs A diet high in pickled, salted, or smoked food is found in many regions of high gastric cancer risk. Dietary nitrates have been implicated as a possible cause of gastric cancer. Gastric bacteria (more abundant in the achlorhydric
|
Surgery_Schwartz. in groups of lower socioeconomic status.4Brunicardi_Ch26_p1099-p1166.indd 113901/03/19 7:12 PM 1140SPECIFIC CONSIDERATIONS PART IIEtiology. Gastric cancer is more common in patients with per-nicious anemia, blood group A, or a family history of gastric cancer. When patients migrate from a high-incidence region to a low-incidence region, the risk of gastric cancer decreases in the subsequent generations born in the new region. This strongly suggests an environmental influence on the development of gas-tric cancer. Environmental factors appear to be more important in the pathogenesis of the intestinal form of gastric cancer com-pared to the diffuse form. The commonly accepted risk factors for gastric cancer are listed in Table 26-15.Diet and Drugs A diet high in pickled, salted, or smoked food is found in many regions of high gastric cancer risk. Dietary nitrates have been implicated as a possible cause of gastric cancer. Gastric bacteria (more abundant in the achlorhydric
|
Surgery_Schwartz_7527
|
Surgery_Schwartz
|
or smoked food is found in many regions of high gastric cancer risk. Dietary nitrates have been implicated as a possible cause of gastric cancer. Gastric bacteria (more abundant in the achlorhydric stomach of patients with atrophic gastritis, a risk factor for gastric cancer) convert nitrate into nitrite, a known carcinogen. A diet high in fresh fruits and vegetables and rich in vitamin C and E has been shown to decrease the risk of gastric cancer. The reduced consumption of nitrate-rich preserved foods seen with the widespread availability of refrigeration has been sug-gested as a cause of the dramatic decrease in gastric cancer seen in North America and Western Europe over the last century. Eastern AsiaCentral and Eastern EuropeLess developed regionsWorldMore developed regionsSouth AmericaWestern AsiaCentral AmericaSouthern EuropePolynesiaSouth-Central AsiaCaribbeanWestern EuropeMelanesiaSouth-Eastern AsiaNorthern EuropeSouthern AfricaAustralia/New ZealandEastern AfricaNorthern
|
Surgery_Schwartz. or smoked food is found in many regions of high gastric cancer risk. Dietary nitrates have been implicated as a possible cause of gastric cancer. Gastric bacteria (more abundant in the achlorhydric stomach of patients with atrophic gastritis, a risk factor for gastric cancer) convert nitrate into nitrite, a known carcinogen. A diet high in fresh fruits and vegetables and rich in vitamin C and E has been shown to decrease the risk of gastric cancer. The reduced consumption of nitrate-rich preserved foods seen with the widespread availability of refrigeration has been sug-gested as a cause of the dramatic decrease in gastric cancer seen in North America and Western Europe over the last century. Eastern AsiaCentral and Eastern EuropeLess developed regionsWorldMore developed regionsSouth AmericaWestern AsiaCentral AmericaSouthern EuropePolynesiaSouth-Central AsiaCaribbeanWestern EuropeMelanesiaSouth-Eastern AsiaNorthern EuropeSouthern AfricaAustralia/New ZealandEastern AfricaNorthern
|
Surgery_Schwartz_7528
|
Surgery_Schwartz
|
AmericaWestern AsiaCentral AmericaSouthern EuropePolynesiaSouth-Central AsiaCaribbeanWestern EuropeMelanesiaSouth-Eastern AsiaNorthern EuropeSouthern AfricaAustralia/New ZealandEastern AfricaNorthern AmericaMiddle AfricaNorthern AfricaWestern AfricaMicronesia40302010010203040FemaleMaleIncidenceMortalityFigure 26-49. Gastric cancer incidence and death rates per 100,000 population in men and women, in different regions and countries. (Reproduced with permission from The Global Cancer Observatory All Rights Reserved, September, 2018.)Table 26-15Factors increasing or decreasing the risk of gastric cancerIncrease risk Family history Diet (high in nitrates, salt, fat) Familial polyposis Gastric adenomas Hereditary nonpolyposis colorectal cancer Helicobacter pylori infection Atrophic gastritis, intestinal metaplasia, dysplasia Previous gastrectomy or gastrojejunostomy (>10 y ago) Tobacco use Ménétrier’s diseaseDecrease risk Aspirin Diet (high fresh fruit and vegetable intake) Vitamin
|
Surgery_Schwartz. AmericaWestern AsiaCentral AmericaSouthern EuropePolynesiaSouth-Central AsiaCaribbeanWestern EuropeMelanesiaSouth-Eastern AsiaNorthern EuropeSouthern AfricaAustralia/New ZealandEastern AfricaNorthern AmericaMiddle AfricaNorthern AfricaWestern AfricaMicronesia40302010010203040FemaleMaleIncidenceMortalityFigure 26-49. Gastric cancer incidence and death rates per 100,000 population in men and women, in different regions and countries. (Reproduced with permission from The Global Cancer Observatory All Rights Reserved, September, 2018.)Table 26-15Factors increasing or decreasing the risk of gastric cancerIncrease risk Family history Diet (high in nitrates, salt, fat) Familial polyposis Gastric adenomas Hereditary nonpolyposis colorectal cancer Helicobacter pylori infection Atrophic gastritis, intestinal metaplasia, dysplasia Previous gastrectomy or gastrojejunostomy (>10 y ago) Tobacco use Ménétrier’s diseaseDecrease risk Aspirin Diet (high fresh fruit and vegetable intake) Vitamin
|
Surgery_Schwartz_7529
|
Surgery_Schwartz
|
intestinal metaplasia, dysplasia Previous gastrectomy or gastrojejunostomy (>10 y ago) Tobacco use Ménétrier’s diseaseDecrease risk Aspirin Diet (high fresh fruit and vegetable intake) Vitamin CBrunicardi_Ch26_p1099-p1166.indd 114001/03/19 7:12 PM 1141STOMACHCHAPTER 26Tobacco use probably increases the risk of stomach cancer, and alcohol use probably has no effect. Regular aspirin use may be protective.Helicobacter pylori80,139 The risk of gastric cancer in patients with chronic H pylori infection is increased about threefold. Compared to uninfected patients, patients with a history of gas-tric ulcers are more likely to develop gastric cancer (incidence ratio 1.8, 95% confidence interval 1.6–2.0), and patients with a history of duodenal ulcers are at decreased risk for gastric can-cer (incidence ratio 0.6, 95% confidence interval 0.4–0.7). This may be due to the fact that some patients develop antral-pre-dominant disease (predisposing to duodenal ulcer and somehow protecting
|
Surgery_Schwartz. intestinal metaplasia, dysplasia Previous gastrectomy or gastrojejunostomy (>10 y ago) Tobacco use Ménétrier’s diseaseDecrease risk Aspirin Diet (high fresh fruit and vegetable intake) Vitamin CBrunicardi_Ch26_p1099-p1166.indd 114001/03/19 7:12 PM 1141STOMACHCHAPTER 26Tobacco use probably increases the risk of stomach cancer, and alcohol use probably has no effect. Regular aspirin use may be protective.Helicobacter pylori80,139 The risk of gastric cancer in patients with chronic H pylori infection is increased about threefold. Compared to uninfected patients, patients with a history of gas-tric ulcers are more likely to develop gastric cancer (incidence ratio 1.8, 95% confidence interval 1.6–2.0), and patients with a history of duodenal ulcers are at decreased risk for gastric can-cer (incidence ratio 0.6, 95% confidence interval 0.4–0.7). This may be due to the fact that some patients develop antral-pre-dominant disease (predisposing to duodenal ulcer and somehow protecting
|
Surgery_Schwartz_7530
|
Surgery_Schwartz
|
(incidence ratio 0.6, 95% confidence interval 0.4–0.7). This may be due to the fact that some patients develop antral-pre-dominant disease (predisposing to duodenal ulcer and somehow protecting against gastric cancer), while other patients develop corpus-predominant gastritis, resulting in hypochlorhydria and somehow predisposing to gastric ulcer and gastric cancer (Fig. 26-50).10 The theoretical sequence for development of gas-tric adenocarcinoma is diagrammed in Fig. 26-51.10,80 Recently, it has been demonstrated that bone marrow-derived stem cells play a key role in the pathogenesis of gastric adenocarcinoma in patients with chronic H pylori infection.80 However, it must be recognized that gastric adenocarcinoma is a multifactorial dis-ease. Not all patients with gastric cancer have H pylori, and there are some geographic areas with a high prevalence of chronic H pylori infection and a low prevalence of gastric cancer (the “African enigma”). Finally, H pylori–infected patients seem
|
Surgery_Schwartz. (incidence ratio 0.6, 95% confidence interval 0.4–0.7). This may be due to the fact that some patients develop antral-pre-dominant disease (predisposing to duodenal ulcer and somehow protecting against gastric cancer), while other patients develop corpus-predominant gastritis, resulting in hypochlorhydria and somehow predisposing to gastric ulcer and gastric cancer (Fig. 26-50).10 The theoretical sequence for development of gas-tric adenocarcinoma is diagrammed in Fig. 26-51.10,80 Recently, it has been demonstrated that bone marrow-derived stem cells play a key role in the pathogenesis of gastric adenocarcinoma in patients with chronic H pylori infection.80 However, it must be recognized that gastric adenocarcinoma is a multifactorial dis-ease. Not all patients with gastric cancer have H pylori, and there are some geographic areas with a high prevalence of chronic H pylori infection and a low prevalence of gastric cancer (the “African enigma”). Finally, H pylori–infected patients seem
|
Surgery_Schwartz_7531
|
Surgery_Schwartz
|
and there are some geographic areas with a high prevalence of chronic H pylori infection and a low prevalence of gastric cancer (the “African enigma”). Finally, H pylori–infected patients seem to be at decreased risk for the development of adenocarcinoma of the distal esophagus and cardia region.140 Perhaps corporeal gas-tritis decreases acid secretion, creating a less damaging refluxate and thus reducing the risk for Barrett’s esophagus, the precursor lesion for these tumors.Epstein-Barr Virus About 10% of gastric adenocarcinomas carry the EBV virus. Recently it has been suggested that EBV infection is a late step in gastric carcinogenesis, since EBV tran-scripts are present in cancer cells but not in the metaplastic cells of precursor epithelium.141Genetic Factors A variety of genetic abnormalities have been described in gastric cancer (Table 26-16). Most gastric can-cers are aneuploid. The most common genetic abnormalities in sporadic gastric cancer affect the p53 and COX-2 genes.
|
Surgery_Schwartz. and there are some geographic areas with a high prevalence of chronic H pylori infection and a low prevalence of gastric cancer (the “African enigma”). Finally, H pylori–infected patients seem to be at decreased risk for the development of adenocarcinoma of the distal esophagus and cardia region.140 Perhaps corporeal gas-tritis decreases acid secretion, creating a less damaging refluxate and thus reducing the risk for Barrett’s esophagus, the precursor lesion for these tumors.Epstein-Barr Virus About 10% of gastric adenocarcinomas carry the EBV virus. Recently it has been suggested that EBV infection is a late step in gastric carcinogenesis, since EBV tran-scripts are present in cancer cells but not in the metaplastic cells of precursor epithelium.141Genetic Factors A variety of genetic abnormalities have been described in gastric cancer (Table 26-16). Most gastric can-cers are aneuploid. The most common genetic abnormalities in sporadic gastric cancer affect the p53 and COX-2 genes.
|
Surgery_Schwartz_7532
|
Surgery_Schwartz
|
have been described in gastric cancer (Table 26-16). Most gastric can-cers are aneuploid. The most common genetic abnormalities in sporadic gastric cancer affect the p53 and COX-2 genes. Over two-thirds of gastric cancers have deletion or suppression of the important tumor-suppressor gene p53. Additionally, approxi-mately the same proportion have overexpression of COX-2. In the colon, tumors with upregulation of this gene have suppressed apoptosis, more angiogenesis, and higher metastatic potential. Gastric tumors that overexpress COX-2 are more aggressive. Recently, a germline mutation in the CDH1 gene encoding E-cadherin was shown to be associated with hereditary diffuse gastric cancer. Prophylactic total gastrectomy should be consid-ered in patients with these mutations.142Premalignant Conditions of the Stomach Figure 26-52 shows the prevalence of some premalignant conditions associated with the development of early gastric cancer in a series of 1900 cases from Tokyo. By far the
|
Surgery_Schwartz. have been described in gastric cancer (Table 26-16). Most gastric can-cers are aneuploid. The most common genetic abnormalities in sporadic gastric cancer affect the p53 and COX-2 genes. Over two-thirds of gastric cancers have deletion or suppression of the important tumor-suppressor gene p53. Additionally, approxi-mately the same proportion have overexpression of COX-2. In the colon, tumors with upregulation of this gene have suppressed apoptosis, more angiogenesis, and higher metastatic potential. Gastric tumors that overexpress COX-2 are more aggressive. Recently, a germline mutation in the CDH1 gene encoding E-cadherin was shown to be associated with hereditary diffuse gastric cancer. Prophylactic total gastrectomy should be consid-ered in patients with these mutations.142Premalignant Conditions of the Stomach Figure 26-52 shows the prevalence of some premalignant conditions associated with the development of early gastric cancer in a series of 1900 cases from Tokyo. By far the
|
Surgery_Schwartz_7533
|
Surgery_Schwartz
|
Conditions of the Stomach Figure 26-52 shows the prevalence of some premalignant conditions associated with the development of early gastric cancer in a series of 1900 cases from Tokyo. By far the most common precancerous lesion is atrophic gastritis. There is a growing appreciation of the impor-tant influence of the chronic inflammatory milieu on the genome of mucosal cells. Chronic inflammation leads to both genetic Acute pangastritisChronic pangastritisDecreased acidGastric cancerChronic antral gastritisDecreased SSTIncreased gastrinIncreased acidDUFigure 26-50. Helicobacter, gastritis, and the pathogenesis of duo-denal ulcer (DU) or gastric cancer.Figure 26-51. Gastric carcinogenesis. (Reproduced with permission from Yamada T, Alpers DH, Laine L, et al: Textbook of Gastroenterology, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)NormalDysplasiaCancerIntestinal metaplasiaAtrophic gastritisChronic superficial gastritisH pyloriDiet low in vitamin C, EHigh-salt
|
Surgery_Schwartz. Conditions of the Stomach Figure 26-52 shows the prevalence of some premalignant conditions associated with the development of early gastric cancer in a series of 1900 cases from Tokyo. By far the most common precancerous lesion is atrophic gastritis. There is a growing appreciation of the impor-tant influence of the chronic inflammatory milieu on the genome of mucosal cells. Chronic inflammation leads to both genetic Acute pangastritisChronic pangastritisDecreased acidGastric cancerChronic antral gastritisDecreased SSTIncreased gastrinIncreased acidDUFigure 26-50. Helicobacter, gastritis, and the pathogenesis of duo-denal ulcer (DU) or gastric cancer.Figure 26-51. Gastric carcinogenesis. (Reproduced with permission from Yamada T, Alpers DH, Laine L, et al: Textbook of Gastroenterology, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)NormalDysplasiaCancerIntestinal metaplasiaAtrophic gastritisChronic superficial gastritisH pyloriDiet low in vitamin C, EHigh-salt
|
Surgery_Schwartz_7534
|
Surgery_Schwartz
|
4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)NormalDysplasiaCancerIntestinal metaplasiaAtrophic gastritisChronic superficial gastritisH pyloriDiet low in vitamin C, EHigh-salt dietBrunicardi_Ch26_p1099-p1166.indd 114101/03/19 7:12 PM 1142SPECIFIC CONSIDERATIONS PART IIand epigenetic changes in mucosal cells, which in the stomach leads to the development of gastritis-associated cancer.143,144Polyps Benign gastric polyps are classified as neoplastic (ade-noma and fundic gland polyps) or nonneoplastic (hyperplastic polyp, inflammatory polyp, hamartomatous polyp).145 In general, inflammatory and hamartomatous polyps have little or no malig-nant potential. Fundic gland polyps, commonly seen in patients on long-term PPI therapy, are not premalignant, but in patients with familial adenomatous polyposis (FAP), dysplasia in these lesions is not uncommon, and there are numerous reports of gas-tric cancer arising in a background of fundic gland polyposis in this
|
Surgery_Schwartz. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)NormalDysplasiaCancerIntestinal metaplasiaAtrophic gastritisChronic superficial gastritisH pyloriDiet low in vitamin C, EHigh-salt dietBrunicardi_Ch26_p1099-p1166.indd 114101/03/19 7:12 PM 1142SPECIFIC CONSIDERATIONS PART IIand epigenetic changes in mucosal cells, which in the stomach leads to the development of gastritis-associated cancer.143,144Polyps Benign gastric polyps are classified as neoplastic (ade-noma and fundic gland polyps) or nonneoplastic (hyperplastic polyp, inflammatory polyp, hamartomatous polyp).145 In general, inflammatory and hamartomatous polyps have little or no malig-nant potential. Fundic gland polyps, commonly seen in patients on long-term PPI therapy, are not premalignant, but in patients with familial adenomatous polyposis (FAP), dysplasia in these lesions is not uncommon, and there are numerous reports of gas-tric cancer arising in a background of fundic gland polyposis in this
|
Surgery_Schwartz_7535
|
Surgery_Schwartz
|
with familial adenomatous polyposis (FAP), dysplasia in these lesions is not uncommon, and there are numerous reports of gas-tric cancer arising in a background of fundic gland polyposis in this setting. Hyperplastic polyps usually occur in the setting of chronic inflammation. Large hyperplastic polyps (>2 cm) may harbor dysplasia or carcinoma in situ, and gastric cancer may develop remote from the hyperplastic polyp in an area of associ-ated chronic inflammation. Gastric adenomas are premalignant. Patients with familial adenomatous polyposis (FAP) have a high prevalence of gastric adenomatous polyps (about 50%), and are 10 times more likely to develop adenocarcinoma of the stomach than the general population.146 Screening EGD is indicated in these families. Patients with hereditary nonpolyposis colorectal cancer may also be at risk for gastric cancer.147Atrophic Gastritis Chronic atrophic gastritis (Fig. 26-53) is by far the most common precursor for gastric cancer, particularly the
|
Surgery_Schwartz. with familial adenomatous polyposis (FAP), dysplasia in these lesions is not uncommon, and there are numerous reports of gas-tric cancer arising in a background of fundic gland polyposis in this setting. Hyperplastic polyps usually occur in the setting of chronic inflammation. Large hyperplastic polyps (>2 cm) may harbor dysplasia or carcinoma in situ, and gastric cancer may develop remote from the hyperplastic polyp in an area of associ-ated chronic inflammation. Gastric adenomas are premalignant. Patients with familial adenomatous polyposis (FAP) have a high prevalence of gastric adenomatous polyps (about 50%), and are 10 times more likely to develop adenocarcinoma of the stomach than the general population.146 Screening EGD is indicated in these families. Patients with hereditary nonpolyposis colorectal cancer may also be at risk for gastric cancer.147Atrophic Gastritis Chronic atrophic gastritis (Fig. 26-53) is by far the most common precursor for gastric cancer, particularly the
|
Surgery_Schwartz_7536
|
Surgery_Schwartz
|
colorectal cancer may also be at risk for gastric cancer.147Atrophic Gastritis Chronic atrophic gastritis (Fig. 26-53) is by far the most common precursor for gastric cancer, particularly the intestinal subtype (see Fig. 26-52). The prevalence of atro-phic gastritis is higher in older age groups, but it is also com-mon in younger people in areas with a high incidence of gastric cancer. In many patients, H pylori is critical in the pathogenesis of atrophic gastritis. Correa described three distinct patterns of chronic atrophic gastritis: autoimmune (involves the acid-secreting proximal stomach), hypersecretory (involving the distal stomach), and environmental (involving multiple random areas at the junction of the oxyntic and antral mucosa).139Intestinal Metaplasia Gastric carcinoma often occurs in an area of intestinal metaplasia, and the risk of gastric cancer is proportional to the extent of intestinal metaplasia of the gastric mucosa. These observations suggest that intestinal
|
Surgery_Schwartz. colorectal cancer may also be at risk for gastric cancer.147Atrophic Gastritis Chronic atrophic gastritis (Fig. 26-53) is by far the most common precursor for gastric cancer, particularly the intestinal subtype (see Fig. 26-52). The prevalence of atro-phic gastritis is higher in older age groups, but it is also com-mon in younger people in areas with a high incidence of gastric cancer. In many patients, H pylori is critical in the pathogenesis of atrophic gastritis. Correa described three distinct patterns of chronic atrophic gastritis: autoimmune (involves the acid-secreting proximal stomach), hypersecretory (involving the distal stomach), and environmental (involving multiple random areas at the junction of the oxyntic and antral mucosa).139Intestinal Metaplasia Gastric carcinoma often occurs in an area of intestinal metaplasia, and the risk of gastric cancer is proportional to the extent of intestinal metaplasia of the gastric mucosa. These observations suggest that intestinal
|
Surgery_Schwartz_7537
|
Surgery_Schwartz
|
occurs in an area of intestinal metaplasia, and the risk of gastric cancer is proportional to the extent of intestinal metaplasia of the gastric mucosa. These observations suggest that intestinal metaplasia is a precursor lesion to gastric cancer. There are different pathologic subtypes of intestinal metaplasia in the stomach, based upon the histologic and biochemical characteristics of the changed muco-sal glands. In the complete type of intestinal metaplasia, the glands are lined with goblet cells and intestinal absorptive cells Table 26-16Genetic abnormalities in gastric cancerABNORMALITIESGENEAPPROXIMATE FREQUENCY %Deletion/suppressionp53FHITAPCDCCE-cadherin60–70605050<5Amplification/overexpressionCOX-2HGF/SFVEGFc-metAIB-1β-catenink-samrasc-erb B-27060504540252010–155–7Microsatellite instability 25–40DNA aneuploidy 60–75Reproduced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia,
|
Surgery_Schwartz. occurs in an area of intestinal metaplasia, and the risk of gastric cancer is proportional to the extent of intestinal metaplasia of the gastric mucosa. These observations suggest that intestinal metaplasia is a precursor lesion to gastric cancer. There are different pathologic subtypes of intestinal metaplasia in the stomach, based upon the histologic and biochemical characteristics of the changed muco-sal glands. In the complete type of intestinal metaplasia, the glands are lined with goblet cells and intestinal absorptive cells Table 26-16Genetic abnormalities in gastric cancerABNORMALITIESGENEAPPROXIMATE FREQUENCY %Deletion/suppressionp53FHITAPCDCCE-cadherin60–70605050<5Amplification/overexpressionCOX-2HGF/SFVEGFc-metAIB-1β-catenink-samrasc-erb B-27060504540252010–155–7Microsatellite instability 25–40DNA aneuploidy 60–75Reproduced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia,
|
Surgery_Schwartz_7538
|
Surgery_Schwartz
|
instability 25–40DNA aneuploidy 60–75Reproduced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.1900 CasesPrecancerouslesionNumber of casesHyperplasticpolypAdenomaChronic ulcerAtrophicgastritisVerrucousgastritisStomachremnantAberrantpancreas10471318022620Total 19000.532.470.6894.841.370.110100%Figure 26-52. Precancerous lesions of the stomach.Figure 26-53. Chronic atrophic gastritis. (Used with permission from Kristen Stashek, MD.)Brunicardi_Ch26_p1099-p1166.indd 114201/03/19 7:12 PM 1143STOMACHCHAPTER 26(Fig. 26-54). These cells are indistinguishable histologically and biochemically from their small bowel counterparts. There is evi-dence that eradication of H pylori infection leads to significant regression of intestinal metaplasia and improvement in atrophic gastritis. Treatment of H pylori is mandatory for patients with these pathologic findings and
|
Surgery_Schwartz. instability 25–40DNA aneuploidy 60–75Reproduced with permission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.1900 CasesPrecancerouslesionNumber of casesHyperplasticpolypAdenomaChronic ulcerAtrophicgastritisVerrucousgastritisStomachremnantAberrantpancreas10471318022620Total 19000.532.470.6894.841.370.110100%Figure 26-52. Precancerous lesions of the stomach.Figure 26-53. Chronic atrophic gastritis. (Used with permission from Kristen Stashek, MD.)Brunicardi_Ch26_p1099-p1166.indd 114201/03/19 7:12 PM 1143STOMACHCHAPTER 26(Fig. 26-54). These cells are indistinguishable histologically and biochemically from their small bowel counterparts. There is evi-dence that eradication of H pylori infection leads to significant regression of intestinal metaplasia and improvement in atrophic gastritis. Treatment of H pylori is mandatory for patients with these pathologic findings and
|
Surgery_Schwartz_7539
|
Surgery_Schwartz
|
H pylori infection leads to significant regression of intestinal metaplasia and improvement in atrophic gastritis. Treatment of H pylori is mandatory for patients with these pathologic findings and H pylori infection.Benign Gastric Ulcer Although once considered a premalig-nant condition, it is likely that the older literature addressing gastric ulcers was confounded by the inclusion of inadequately biopsied ulcers s as “benign,” when, in fact, they were malig-nant. Regardless, all gastric ulcers should be viewed as malig-nant until proven otherwise with adequate biopsy and follow-up.Gastric Remnant Cancer It has long been recognized that stomach cancer can develop in the gastric remnant following subtotal gastrectomy. The extent of risk is controversial, but the phenomenon is real. Most tumors develop >10 years follow-ing the initial operation, and they usually arise in an area of chronic gastritis, metaplasia, and dysplasia. This is often near the anastomosis, but many of these
|
Surgery_Schwartz. H pylori infection leads to significant regression of intestinal metaplasia and improvement in atrophic gastritis. Treatment of H pylori is mandatory for patients with these pathologic findings and H pylori infection.Benign Gastric Ulcer Although once considered a premalig-nant condition, it is likely that the older literature addressing gastric ulcers was confounded by the inclusion of inadequately biopsied ulcers s as “benign,” when, in fact, they were malig-nant. Regardless, all gastric ulcers should be viewed as malig-nant until proven otherwise with adequate biopsy and follow-up.Gastric Remnant Cancer It has long been recognized that stomach cancer can develop in the gastric remnant following subtotal gastrectomy. The extent of risk is controversial, but the phenomenon is real. Most tumors develop >10 years follow-ing the initial operation, and they usually arise in an area of chronic gastritis, metaplasia, and dysplasia. This is often near the anastomosis, but many of these
|
Surgery_Schwartz_7540
|
Surgery_Schwartz
|
tumors develop >10 years follow-ing the initial operation, and they usually arise in an area of chronic gastritis, metaplasia, and dysplasia. This is often near the anastomosis, but many of these tumors are quite large at pre-sentation. Bile or alkali reflux gastritis has been implicated as a precursor, and the greatest number of cases have been reported following Billroth II gastroenterostomy where some transit of pancreatic and biliary secretions through the stomach is obli-gate. Although Roux-en-Y anastomosis has been suggested to be protective, this hypothesis remains unproven. Stage for stage, the prognosis for gastric stump cancer is similar to that of other proximal gastric cancers.148Other Premalignant States Mutations in the E-cadherin gene (CDH1) are associated with hereditary diffuse gastric cancer (HDGC). HDGC is an autosomal dominant trait with a high degree of penetrance. Indeed, the lifetime risk of gastric cancer in individuals with pathogenic germline mutations is 70%
|
Surgery_Schwartz. tumors develop >10 years follow-ing the initial operation, and they usually arise in an area of chronic gastritis, metaplasia, and dysplasia. This is often near the anastomosis, but many of these tumors are quite large at pre-sentation. Bile or alkali reflux gastritis has been implicated as a precursor, and the greatest number of cases have been reported following Billroth II gastroenterostomy where some transit of pancreatic and biliary secretions through the stomach is obli-gate. Although Roux-en-Y anastomosis has been suggested to be protective, this hypothesis remains unproven. Stage for stage, the prognosis for gastric stump cancer is similar to that of other proximal gastric cancers.148Other Premalignant States Mutations in the E-cadherin gene (CDH1) are associated with hereditary diffuse gastric cancer (HDGC). HDGC is an autosomal dominant trait with a high degree of penetrance. Indeed, the lifetime risk of gastric cancer in individuals with pathogenic germline mutations is 70%
|
Surgery_Schwartz_7541
|
Surgery_Schwartz
|
gastric cancer (HDGC). HDGC is an autosomal dominant trait with a high degree of penetrance. Indeed, the lifetime risk of gastric cancer in individuals with pathogenic germline mutations is 70% (in men) and 56% (in women).149 CDH1 is a tumor-suppressor gene and a second somatic hit is required for tumorigenesis. The median age at diagnosis of gastric cancer is 38 years. Presentation with clini-cally significant gastric cancer in this setting is associated with a grave prognosis. Increasing recognition of HDGC has afforded the opportunity for early recognition of pathogenic mutations in relatives of individuals with index cases and utilization of prophy-lactic or early total gastrectomy.142 Multifocal intramucosal carci-noma is a frequent finding on putative prophylactic gastrectomy specimens, even in patients without a preoperative diagnosis of carcinoma, affirming the role of early intervention. Surgery should be conducted with the aim of complete extirpation of the stomach to
|
Surgery_Schwartz. gastric cancer (HDGC). HDGC is an autosomal dominant trait with a high degree of penetrance. Indeed, the lifetime risk of gastric cancer in individuals with pathogenic germline mutations is 70% (in men) and 56% (in women).149 CDH1 is a tumor-suppressor gene and a second somatic hit is required for tumorigenesis. The median age at diagnosis of gastric cancer is 38 years. Presentation with clini-cally significant gastric cancer in this setting is associated with a grave prognosis. Increasing recognition of HDGC has afforded the opportunity for early recognition of pathogenic mutations in relatives of individuals with index cases and utilization of prophy-lactic or early total gastrectomy.142 Multifocal intramucosal carci-noma is a frequent finding on putative prophylactic gastrectomy specimens, even in patients without a preoperative diagnosis of carcinoma, affirming the role of early intervention. Surgery should be conducted with the aim of complete extirpation of the stomach to
|
Surgery_Schwartz_7542
|
Surgery_Schwartz
|
specimens, even in patients without a preoperative diagnosis of carcinoma, affirming the role of early intervention. Surgery should be conducted with the aim of complete extirpation of the stomach to squamous lined esophagus proximally and normal duodenal mucosa distally. Mutation-carrying females are also at increased risk of breast cancer, most often lobular carcinomas, and should be carefully monitored.Up to 10% of gastric cancer cases appear to be familial without a clear-cut genetic diagnosis. First-degree relatives of patients with gastric cancer have a twoto threefold increased risk of developing the disease. Patients with hereditary nonpol-yposis colorectal cancer have a 10% risk of developing gastric cancer, predominantly the intestinal subtype. The mucous cell hyperplasia of Ménétrier’s disease is generally considered to carry a 5% to 10% risk of adenocarcinoma. Periodic surveil-lance EGD is prudent in all the aforementioned conditions. The glandular hyperplasia associated
|
Surgery_Schwartz. specimens, even in patients without a preoperative diagnosis of carcinoma, affirming the role of early intervention. Surgery should be conducted with the aim of complete extirpation of the stomach to squamous lined esophagus proximally and normal duodenal mucosa distally. Mutation-carrying females are also at increased risk of breast cancer, most often lobular carcinomas, and should be carefully monitored.Up to 10% of gastric cancer cases appear to be familial without a clear-cut genetic diagnosis. First-degree relatives of patients with gastric cancer have a twoto threefold increased risk of developing the disease. Patients with hereditary nonpol-yposis colorectal cancer have a 10% risk of developing gastric cancer, predominantly the intestinal subtype. The mucous cell hyperplasia of Ménétrier’s disease is generally considered to carry a 5% to 10% risk of adenocarcinoma. Periodic surveil-lance EGD is prudent in all the aforementioned conditions. The glandular hyperplasia associated
|
Surgery_Schwartz_7543
|
Surgery_Schwartz
|
disease is generally considered to carry a 5% to 10% risk of adenocarcinoma. Periodic surveil-lance EGD is prudent in all the aforementioned conditions. The glandular hyperplasia associated with gastrinoma is not prema-lignant, but ECL hyperplasia and/or carcinoid tumors can occur.PathologyDysplasia It is generally accepted that gastric dysplasia is the universal precursor to gastric adenocarcinoma. Patients with severe dysplasia should be considered for gastric resection if the abnormality is widespread or multifocal, or EMR if the severe dysplasia is localized. Patients with mild dysplasia should be followed with endoscopic biopsy surveillance, and Helicobacter eradication.Early Gastric Cancer Early gastric cancer is defined as adeno-carcinoma limited to the mucosa (T1a) and submucosa (T1b) of the stomach. The entity is common in Asia, where the higher frequency of gastric cancer justified adoption of aggressive surveillance programs. Approximately 10% of patients clini-cally staged
|
Surgery_Schwartz. disease is generally considered to carry a 5% to 10% risk of adenocarcinoma. Periodic surveil-lance EGD is prudent in all the aforementioned conditions. The glandular hyperplasia associated with gastrinoma is not prema-lignant, but ECL hyperplasia and/or carcinoid tumors can occur.PathologyDysplasia It is generally accepted that gastric dysplasia is the universal precursor to gastric adenocarcinoma. Patients with severe dysplasia should be considered for gastric resection if the abnormality is widespread or multifocal, or EMR if the severe dysplasia is localized. Patients with mild dysplasia should be followed with endoscopic biopsy surveillance, and Helicobacter eradication.Early Gastric Cancer Early gastric cancer is defined as adeno-carcinoma limited to the mucosa (T1a) and submucosa (T1b) of the stomach. The entity is common in Asia, where the higher frequency of gastric cancer justified adoption of aggressive surveillance programs. Approximately 10% of patients clini-cally staged
|
Surgery_Schwartz_7544
|
Surgery_Schwartz
|
of the stomach. The entity is common in Asia, where the higher frequency of gastric cancer justified adoption of aggressive surveillance programs. Approximately 10% of patients clini-cally staged with early gastric cancer will have lymph node metastases. There are several subtypes of early gastric cancer (Table 26-17 and Fig. 26-55). Approximately 70% of early gas-tric cancers are well differentiated, and 30% are poorly differen-tiated. The overall cure rate with adequate gastric resection and lymphadenectomy is 95%. In some Japanese centers, 50% of the gastric cancers treated are early stage (compared to less than 20% of resected gastric adenocarcinomas in the United States). Selected patients with early gastric cancer can be treated with endoscopic resection.150Table 26-17Macroscopic types of superficial gastric cancerType 0-I (protruding)aPolypoid tumorsType 0-II (superficial)Tumors with or without minimal elevation or depression relative to the surrounding mucosa Type
|
Surgery_Schwartz. of the stomach. The entity is common in Asia, where the higher frequency of gastric cancer justified adoption of aggressive surveillance programs. Approximately 10% of patients clini-cally staged with early gastric cancer will have lymph node metastases. There are several subtypes of early gastric cancer (Table 26-17 and Fig. 26-55). Approximately 70% of early gas-tric cancers are well differentiated, and 30% are poorly differen-tiated. The overall cure rate with adequate gastric resection and lymphadenectomy is 95%. In some Japanese centers, 50% of the gastric cancers treated are early stage (compared to less than 20% of resected gastric adenocarcinomas in the United States). Selected patients with early gastric cancer can be treated with endoscopic resection.150Table 26-17Macroscopic types of superficial gastric cancerType 0-I (protruding)aPolypoid tumorsType 0-II (superficial)Tumors with or without minimal elevation or depression relative to the surrounding mucosa Type
|
Surgery_Schwartz_7545
|
Surgery_Schwartz
|
types of superficial gastric cancerType 0-I (protruding)aPolypoid tumorsType 0-II (superficial)Tumors with or without minimal elevation or depression relative to the surrounding mucosa Type 0-IIaSlightly elevated tumors (superficial elevated) Type 0-IIbTumors without elevation or depression (superficial flat) Type 0-IIcSlightly depressed tumors (superficial depressed)Type 0-III (excavated)Tumors with deep depressionaTumors with less than 3-mm elevation are usually classified as–IIa, with more elevated tumors being classified as 0-I.Figure 26-54. Complete intestinal metaplasia of the stomach. Note intestinal type crypts lined with goblet cells and intestinal absorptive cells. (Used with permission from Kristen Stashek, MD.)Brunicardi_Ch26_p1099-p1166.indd 114301/03/19 7:12 PM 1144SPECIFIC CONSIDERATIONS PART IIGross Morphology and Histologic Subtypes Gastric cancer has been subdivided into four morphologic subtypes: polypoid, fungating, ulcerative, and scirrhous. The first two
|
Surgery_Schwartz. types of superficial gastric cancerType 0-I (protruding)aPolypoid tumorsType 0-II (superficial)Tumors with or without minimal elevation or depression relative to the surrounding mucosa Type 0-IIaSlightly elevated tumors (superficial elevated) Type 0-IIbTumors without elevation or depression (superficial flat) Type 0-IIcSlightly depressed tumors (superficial depressed)Type 0-III (excavated)Tumors with deep depressionaTumors with less than 3-mm elevation are usually classified as–IIa, with more elevated tumors being classified as 0-I.Figure 26-54. Complete intestinal metaplasia of the stomach. Note intestinal type crypts lined with goblet cells and intestinal absorptive cells. (Used with permission from Kristen Stashek, MD.)Brunicardi_Ch26_p1099-p1166.indd 114301/03/19 7:12 PM 1144SPECIFIC CONSIDERATIONS PART IIGross Morphology and Histologic Subtypes Gastric cancer has been subdivided into four morphologic subtypes: polypoid, fungating, ulcerative, and scirrhous. The first two
|
Surgery_Schwartz_7546
|
Surgery_Schwartz
|
CONSIDERATIONS PART IIGross Morphology and Histologic Subtypes Gastric cancer has been subdivided into four morphologic subtypes: polypoid, fungating, ulcerative, and scirrhous. The first two are character-ized by a largely intraluminal mass. Polypoid tumors are not ulcerated; fungating tumors are predominantly intraluminal with ulceration. In the latter two gross subtypes, the bulk of the tumor mass is confined to the wall of the stomach. Ulcerative tumors are self-descriptive. Scirrhous tumors infiltrate the entire thickness of the stomach and cover a very large surface area, commonly involve the entire stomach and have a particularly poor prognosis. Although these latter lesions may be technically resectable with total gastrectomy, it is common for both the esophageal and duodenal margins of resection to show micro-scopic evidence of tumor infiltration; distant metastasis, overt or occult, is frequent and death from recurrent disease within 6 months is common. Palliative
|
Surgery_Schwartz. CONSIDERATIONS PART IIGross Morphology and Histologic Subtypes Gastric cancer has been subdivided into four morphologic subtypes: polypoid, fungating, ulcerative, and scirrhous. The first two are character-ized by a largely intraluminal mass. Polypoid tumors are not ulcerated; fungating tumors are predominantly intraluminal with ulceration. In the latter two gross subtypes, the bulk of the tumor mass is confined to the wall of the stomach. Ulcerative tumors are self-descriptive. Scirrhous tumors infiltrate the entire thickness of the stomach and cover a very large surface area, commonly involve the entire stomach and have a particularly poor prognosis. Although these latter lesions may be technically resectable with total gastrectomy, it is common for both the esophageal and duodenal margins of resection to show micro-scopic evidence of tumor infiltration; distant metastasis, overt or occult, is frequent and death from recurrent disease within 6 months is common. Palliative
|
Surgery_Schwartz_7547
|
Surgery_Schwartz
|
margins of resection to show micro-scopic evidence of tumor infiltration; distant metastasis, overt or occult, is frequent and death from recurrent disease within 6 months is common. Palliative chemotherapy may prolong median survival.151The location of the primary tumor in the stomach is essen-tial in planning an operation. Several decades ago, the large majority of gastric cancers were in the distal stomach. Recently, there has been a proximal migration of tumors, so currently, the distribution is closer to 40% distal, 30% middle, and 30% proximal.Histology The most important prognostic indicators in gastric cancer are both histologic: lymph node involvement and depth of tumor invasion. Tumor grade (degree of differentiation: well, moderately, or poorly) is also important prognostically.There are several histologic classifications of gastric cancer. The World Health Organization recognizes several histologic types (Table 26-18). The Japanese classification is similar but more
|
Surgery_Schwartz. margins of resection to show micro-scopic evidence of tumor infiltration; distant metastasis, overt or occult, is frequent and death from recurrent disease within 6 months is common. Palliative chemotherapy may prolong median survival.151The location of the primary tumor in the stomach is essen-tial in planning an operation. Several decades ago, the large majority of gastric cancers were in the distal stomach. Recently, there has been a proximal migration of tumors, so currently, the distribution is closer to 40% distal, 30% middle, and 30% proximal.Histology The most important prognostic indicators in gastric cancer are both histologic: lymph node involvement and depth of tumor invasion. Tumor grade (degree of differentiation: well, moderately, or poorly) is also important prognostically.There are several histologic classifications of gastric cancer. The World Health Organization recognizes several histologic types (Table 26-18). The Japanese classification is similar but more
|
Surgery_Schwartz_7548
|
Surgery_Schwartz
|
are several histologic classifications of gastric cancer. The World Health Organization recognizes several histologic types (Table 26-18). The Japanese classification is similar but more detailed. The commonly used Lauren classifi-cation separates gastric cancers into intestinal type (53%), dif-fuse type (33%), and unclassified (14%). The intestinal type is associated with chronic atrophic gastritis, severe intestinal meta-plasia, and dysplasia, and tends to be less aggressive than the diffuse type. The diffuse type of gastric cancer is more likely to be poorly differentiated and is associated with younger patients and proximal tumors. The Ming classification also is useful and easy to remember, with only two types—expanding (67%) and infiltrative (33%).Recently, the significance of human epidermal growth factor receptor-2 (HER2) was reported in patients with gastric cancer. In breast cancer, overexpression of HER2 has been reported in 15% to 25% of cases, and it is well recognized as
|
Surgery_Schwartz. are several histologic classifications of gastric cancer. The World Health Organization recognizes several histologic types (Table 26-18). The Japanese classification is similar but more detailed. The commonly used Lauren classifi-cation separates gastric cancers into intestinal type (53%), dif-fuse type (33%), and unclassified (14%). The intestinal type is associated with chronic atrophic gastritis, severe intestinal meta-plasia, and dysplasia, and tends to be less aggressive than the diffuse type. The diffuse type of gastric cancer is more likely to be poorly differentiated and is associated with younger patients and proximal tumors. The Ming classification also is useful and easy to remember, with only two types—expanding (67%) and infiltrative (33%).Recently, the significance of human epidermal growth factor receptor-2 (HER2) was reported in patients with gastric cancer. In breast cancer, overexpression of HER2 has been reported in 15% to 25% of cases, and it is well recognized as
|
Surgery_Schwartz_7549
|
Surgery_Schwartz
|
epidermal growth factor receptor-2 (HER2) was reported in patients with gastric cancer. In breast cancer, overexpression of HER2 has been reported in 15% to 25% of cases, and it is well recognized as an unfavorable prognostic factor. The development of molecular targeted agents such as trastuzumab has improved the survival of HER2-positive patients. Likewise, in gastric cancer, HER2 overexpression has been reported in 13% to 30% of patients. HER2 targeting with trastuzumab resulted in improved survival in patients with stage IV gastric cancer, and immunohistochem-istry (IHC) staining for HER2 should be performed in recurrent or metastatic cases.152 Expression of other growth receptors in gastric cancer have been characterized as well, including HER1 (epidermal growth factor rector) and HER3. The latter is associ-ated with poor prognosis, but efforts to target these receptors for therapeutic benefit are still exploratory.153Pathologic Staging Ultimately, prognosis is related to
|
Surgery_Schwartz. epidermal growth factor receptor-2 (HER2) was reported in patients with gastric cancer. In breast cancer, overexpression of HER2 has been reported in 15% to 25% of cases, and it is well recognized as an unfavorable prognostic factor. The development of molecular targeted agents such as trastuzumab has improved the survival of HER2-positive patients. Likewise, in gastric cancer, HER2 overexpression has been reported in 13% to 30% of patients. HER2 targeting with trastuzumab resulted in improved survival in patients with stage IV gastric cancer, and immunohistochem-istry (IHC) staining for HER2 should be performed in recurrent or metastatic cases.152 Expression of other growth receptors in gastric cancer have been characterized as well, including HER1 (epidermal growth factor rector) and HER3. The latter is associ-ated with poor prognosis, but efforts to target these receptors for therapeutic benefit are still exploratory.153Pathologic Staging Ultimately, prognosis is related to
|
Surgery_Schwartz_7550
|
Surgery_Schwartz
|
and HER3. The latter is associ-ated with poor prognosis, but efforts to target these receptors for therapeutic benefit are still exploratory.153Pathologic Staging Ultimately, prognosis is related to patho-logic stage. The most widespread system for staging of gastric cancer is the tumor-node-metastasis (TNM) staging system based on depth of tumor invasion, extent of lymph node metastases, and presence of distant metastases. This system was developed by the American Joint Committee on Cancer and the International Union Against Cancer, and it has under gone several modifications since it was originally conceived (Table 26-19).Clinical Manifestations. Most patients who are diagnosed with gastric cancer in the United States have advanced stage III or IV disease at the time of diagnosis. The most common symp-toms are weight loss and decreased food intake due to anorexia and early satiety. Abdominal pain (usually not severe and often ignored) is also common. Other symptoms include nausea,
|
Surgery_Schwartz. and HER3. The latter is associ-ated with poor prognosis, but efforts to target these receptors for therapeutic benefit are still exploratory.153Pathologic Staging Ultimately, prognosis is related to patho-logic stage. The most widespread system for staging of gastric cancer is the tumor-node-metastasis (TNM) staging system based on depth of tumor invasion, extent of lymph node metastases, and presence of distant metastases. This system was developed by the American Joint Committee on Cancer and the International Union Against Cancer, and it has under gone several modifications since it was originally conceived (Table 26-19).Clinical Manifestations. Most patients who are diagnosed with gastric cancer in the United States have advanced stage III or IV disease at the time of diagnosis. The most common symp-toms are weight loss and decreased food intake due to anorexia and early satiety. Abdominal pain (usually not severe and often ignored) is also common. Other symptoms include nausea,
|
Surgery_Schwartz_7551
|
Surgery_Schwartz
|
most common symp-toms are weight loss and decreased food intake due to anorexia and early satiety. Abdominal pain (usually not severe and often ignored) is also common. Other symptoms include nausea, vomit-ing, and bloating. Acute GI bleeding is somewhat unusual (5%), but chronic occult blood loss is common and manifests as iron Type IIaType IType IIBType IIcType IIIExcavatedDepressedFlatElevatedProtrudedFigure 26-55. Pathologic types of early gastric cancer. (Repro-duced with permission from Fenoglio-Preiser CM, Noffsinger AE, Belli J, et al: Pathologic and phenotypic features of gastric cancer, Semin Oncol. 1996 Jun;23(3):292-306.)Table 26-18World Health Organization histologic typing of gastric cancerAdenocarcinoma Papillary adenocarcinoma Tubular adenocarcinoma Mucinous adenocarcinoma Signet-ring cell carcinomaAdenosquamous carcinomaSquamous cell carcinomaSmall cell carcinomaUndifferentiated carcinomaOthersReproduced with permission from Ming S-C, Goldman H: Pathology of the
|
Surgery_Schwartz. most common symp-toms are weight loss and decreased food intake due to anorexia and early satiety. Abdominal pain (usually not severe and often ignored) is also common. Other symptoms include nausea, vomit-ing, and bloating. Acute GI bleeding is somewhat unusual (5%), but chronic occult blood loss is common and manifests as iron Type IIaType IType IIBType IIcType IIIExcavatedDepressedFlatElevatedProtrudedFigure 26-55. Pathologic types of early gastric cancer. (Repro-duced with permission from Fenoglio-Preiser CM, Noffsinger AE, Belli J, et al: Pathologic and phenotypic features of gastric cancer, Semin Oncol. 1996 Jun;23(3):292-306.)Table 26-18World Health Organization histologic typing of gastric cancerAdenocarcinoma Papillary adenocarcinoma Tubular adenocarcinoma Mucinous adenocarcinoma Signet-ring cell carcinomaAdenosquamous carcinomaSquamous cell carcinomaSmall cell carcinomaUndifferentiated carcinomaOthersReproduced with permission from Ming S-C, Goldman H: Pathology of the
|
Surgery_Schwartz_7552
|
Surgery_Schwartz
|
cell carcinomaAdenosquamous carcinomaSquamous cell carcinomaSmall cell carcinomaUndifferentiated carcinomaOthersReproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.Brunicardi_Ch26_p1099-p1166.indd 114401/03/19 7:12 PM 1145STOMACHCHAPTER 26deficiency anemia and heme-positive stool. Dysphagia is com-mon if the tumor involves the cardia of the stomach. Paraneoplas-tic syndromes such as Trousseau’s syndrome (thrombophlebitis), acanthosis nigricans (hyperpigmentation of the axilla and groin), or peripheral neuropathy are rarely present.Physical examination typically is normal. Other than signs of weight loss, specific positive physical findings usually indi-cate incurability. A focused examination in a patient in whom gastric cancer is a likely part of the differential diagnosis should include an examination of the neck, chest, abdomen, and rectum. Cervical, supraclavicular (on the left referred
|
Surgery_Schwartz. cell carcinomaAdenosquamous carcinomaSquamous cell carcinomaSmall cell carcinomaUndifferentiated carcinomaOthersReproduced with permission from Ming S-C, Goldman H: Pathology of the Gastrointestinal Tract, 2nd ed. Baltimore, MD: Williams & Wilkins; 1998.Brunicardi_Ch26_p1099-p1166.indd 114401/03/19 7:12 PM 1145STOMACHCHAPTER 26deficiency anemia and heme-positive stool. Dysphagia is com-mon if the tumor involves the cardia of the stomach. Paraneoplas-tic syndromes such as Trousseau’s syndrome (thrombophlebitis), acanthosis nigricans (hyperpigmentation of the axilla and groin), or peripheral neuropathy are rarely present.Physical examination typically is normal. Other than signs of weight loss, specific positive physical findings usually indi-cate incurability. A focused examination in a patient in whom gastric cancer is a likely part of the differential diagnosis should include an examination of the neck, chest, abdomen, and rectum. Cervical, supraclavicular (on the left referred
|
Surgery_Schwartz_7553
|
Surgery_Schwartz
|
a patient in whom gastric cancer is a likely part of the differential diagnosis should include an examination of the neck, chest, abdomen, and rectum. Cervical, supraclavicular (on the left referred to as Virchow’s node), and axillary lymph nodes may be enlarged, and can be sampled with fine-needle aspiration cytology. Malignant pleural effusions or ascites, or aspiration pneumonitis may be present. An abdominal mass may indicate a large (usually T4) primary tumor, liver metastases, or carcinomatosis (including Kruken-berg’s tumor of the ovary). A palpable umbilical nodule (Sister Joseph’s nodule) is pathognomonic of advanced disease. Rec-tal exam may reveal heme-positive stool and hard nodularity extraluminally and anteriorly, indicating so-called drop metas-tases, or rectal shelf of Blumer in the pouch of Douglas.Diagnostic Evaluation. Distinguishing between peptic ulcer and gastric cancer on clinical grounds alone can be difficult. Patients over the age of 55 years who have
|
Surgery_Schwartz. a patient in whom gastric cancer is a likely part of the differential diagnosis should include an examination of the neck, chest, abdomen, and rectum. Cervical, supraclavicular (on the left referred to as Virchow’s node), and axillary lymph nodes may be enlarged, and can be sampled with fine-needle aspiration cytology. Malignant pleural effusions or ascites, or aspiration pneumonitis may be present. An abdominal mass may indicate a large (usually T4) primary tumor, liver metastases, or carcinomatosis (including Kruken-berg’s tumor of the ovary). A palpable umbilical nodule (Sister Joseph’s nodule) is pathognomonic of advanced disease. Rec-tal exam may reveal heme-positive stool and hard nodularity extraluminally and anteriorly, indicating so-called drop metas-tases, or rectal shelf of Blumer in the pouch of Douglas.Diagnostic Evaluation. Distinguishing between peptic ulcer and gastric cancer on clinical grounds alone can be difficult. Patients over the age of 55 years who have
|
Surgery_Schwartz_7554
|
Surgery_Schwartz
|
of Blumer in the pouch of Douglas.Diagnostic Evaluation. Distinguishing between peptic ulcer and gastric cancer on clinical grounds alone can be difficult. Patients over the age of 55 years who have new-onset dyspep-sia as well as all patients with dyspepsia and alarm symptoms (weight loss, recurrent vomiting, dysphagia, evidence of GI bleeding, or anemia) or with a family history of gastric cancer should undergo prompt upper endoscopy and biopsy if a muco-sal lesion is noted. Essentially, all patients in whom gastric can-cer is part of the differential diagnosis should have endoscopy and biopsy. If suspicion for cancer is high and the biopsy is negative, the patient should be reendoscoped and more aggres-sively biopsied. In some patients with gastric tumors, upper GI series can be helpful in planning treatment. Although a good double-contrast barium upper GI examination is sensitive for gastric tumors (up to 75% sensitive), in most centers, endos-copy has become the gold standard for
|
Surgery_Schwartz. of Blumer in the pouch of Douglas.Diagnostic Evaluation. Distinguishing between peptic ulcer and gastric cancer on clinical grounds alone can be difficult. Patients over the age of 55 years who have new-onset dyspep-sia as well as all patients with dyspepsia and alarm symptoms (weight loss, recurrent vomiting, dysphagia, evidence of GI bleeding, or anemia) or with a family history of gastric cancer should undergo prompt upper endoscopy and biopsy if a muco-sal lesion is noted. Essentially, all patients in whom gastric can-cer is part of the differential diagnosis should have endoscopy and biopsy. If suspicion for cancer is high and the biopsy is negative, the patient should be reendoscoped and more aggres-sively biopsied. In some patients with gastric tumors, upper GI series can be helpful in planning treatment. Although a good double-contrast barium upper GI examination is sensitive for gastric tumors (up to 75% sensitive), in most centers, endos-copy has become the gold standard for
|
Surgery_Schwartz_7555
|
Surgery_Schwartz
|
in planning treatment. Although a good double-contrast barium upper GI examination is sensitive for gastric tumors (up to 75% sensitive), in most centers, endos-copy has become the gold standard for the diagnosis of gastric malignancy. In addition, recent advances in endoscopy have contributed to the earlier diagnosis of gastric cancer. Magnify-ing endoscopy with narrow-band imaging (NBI) has undergone technological improvements and can observe the microvascu-lar architecture of the mucosa and microsurface pattern of the lesion. Magnifying endoscopy with NBI has been reported to be accurate and reliable in the diagnosis of early gastric cancer.154Preoperative staging of gastric cancer is best accomplished with abdominal/pelvic CT scanning with IV and oral contrast. MRI is probably comparable. The best way to stage the tumor locally is via EUS, which gives fairly accurate (80%) informa-tion about the depth of tumor penetration into the gastric wall, and can usually show enlarged (>5
|
Surgery_Schwartz. in planning treatment. Although a good double-contrast barium upper GI examination is sensitive for gastric tumors (up to 75% sensitive), in most centers, endos-copy has become the gold standard for the diagnosis of gastric malignancy. In addition, recent advances in endoscopy have contributed to the earlier diagnosis of gastric cancer. Magnify-ing endoscopy with narrow-band imaging (NBI) has undergone technological improvements and can observe the microvascu-lar architecture of the mucosa and microsurface pattern of the lesion. Magnifying endoscopy with NBI has been reported to be accurate and reliable in the diagnosis of early gastric cancer.154Preoperative staging of gastric cancer is best accomplished with abdominal/pelvic CT scanning with IV and oral contrast. MRI is probably comparable. The best way to stage the tumor locally is via EUS, which gives fairly accurate (80%) informa-tion about the depth of tumor penetration into the gastric wall, and can usually show enlarged (>5
|
Surgery_Schwartz_7556
|
Surgery_Schwartz
|
The best way to stage the tumor locally is via EUS, which gives fairly accurate (80%) informa-tion about the depth of tumor penetration into the gastric wall, and can usually show enlarged (>5 mm) perigastric and celiac lymph nodes. However, there are limitations to tumor staging with EUS. It is highly operator dependent and may underes-timate lymph node involvement because normal-sized nodes (<5 mm) can harbor metastases. EUS is most accurate in distin-guishing early gastric cancer (T1) from more advanced tumors.Positron Emission Tomography Scanning Whole-body PET scanning derives its power from the preferential accumulation of positron-emitting 18F-fluorodeoxy glucose in tumor com-pared to nontumor cells. It is most useful in the evaluation of distant metastasis in gastric cancer, but it can also be useful in locoregional staging. PET scan is accurate when combined with spiral CT (PET-CT)155 and should be considered before major surgery in patients with particularly high-risk or
|
Surgery_Schwartz. The best way to stage the tumor locally is via EUS, which gives fairly accurate (80%) informa-tion about the depth of tumor penetration into the gastric wall, and can usually show enlarged (>5 mm) perigastric and celiac lymph nodes. However, there are limitations to tumor staging with EUS. It is highly operator dependent and may underes-timate lymph node involvement because normal-sized nodes (<5 mm) can harbor metastases. EUS is most accurate in distin-guishing early gastric cancer (T1) from more advanced tumors.Positron Emission Tomography Scanning Whole-body PET scanning derives its power from the preferential accumulation of positron-emitting 18F-fluorodeoxy glucose in tumor com-pared to nontumor cells. It is most useful in the evaluation of distant metastasis in gastric cancer, but it can also be useful in locoregional staging. PET scan is accurate when combined with spiral CT (PET-CT)155 and should be considered before major surgery in patients with particularly high-risk or
|
Surgery_Schwartz_7557
|
Surgery_Schwartz
|
it can also be useful in locoregional staging. PET scan is accurate when combined with spiral CT (PET-CT)155 and should be considered before major surgery in patients with particularly high-risk or locally advanced tumors.Staging Laparoscopy and Peritoneal Cytology Laparoscopy has emerged as a valuable adjunct to gastric cancer staging, par-ticularly in patients with more substantial tumors. This modality allows for rapid identification of macrosopic peritoneal metas-tases. Peritoneal lavage identifies an additional subset of patients with microscopic dissemination. The prognostic 5Table 26-19AJCC Staging Classification for 8th EditionsAJCC 8TH EDITIONSTAGETNMIAT1N0M0IBT2N0M0T1N1M0IIAT3N0M0T2N1M0T1N2M0IIBT4aN0M0T3N1M0T2N2M0T1N3aM0IIIAT4bN1M0T4aN1M0T4aN2M0T3N2M0T2N3aM0IIIBT4bN1M0T4bN2M0T4aN3aM0T3N3aM0T2N3bM0T1N3bM0IIICT4bN3aM0T4bN3bM0T4aN3bM0T3N3bM0IVAny TAny NM1T1 Tumor invades lamina propria, muscularis mucosa, or submucosa, T2 Tumor invades muscularis propria, T3 Tumor penetrates
|
Surgery_Schwartz. it can also be useful in locoregional staging. PET scan is accurate when combined with spiral CT (PET-CT)155 and should be considered before major surgery in patients with particularly high-risk or locally advanced tumors.Staging Laparoscopy and Peritoneal Cytology Laparoscopy has emerged as a valuable adjunct to gastric cancer staging, par-ticularly in patients with more substantial tumors. This modality allows for rapid identification of macrosopic peritoneal metas-tases. Peritoneal lavage identifies an additional subset of patients with microscopic dissemination. The prognostic 5Table 26-19AJCC Staging Classification for 8th EditionsAJCC 8TH EDITIONSTAGETNMIAT1N0M0IBT2N0M0T1N1M0IIAT3N0M0T2N1M0T1N2M0IIBT4aN0M0T3N1M0T2N2M0T1N3aM0IIIAT4bN1M0T4aN1M0T4aN2M0T3N2M0T2N3aM0IIIBT4bN1M0T4bN2M0T4aN3aM0T3N3aM0T2N3bM0T1N3bM0IIICT4bN3aM0T4bN3bM0T4aN3bM0T3N3bM0IVAny TAny NM1T1 Tumor invades lamina propria, muscularis mucosa, or submucosa, T2 Tumor invades muscularis propria, T3 Tumor penetrates
|
Surgery_Schwartz_7558
|
Surgery_Schwartz
|
TAny NM1T1 Tumor invades lamina propria, muscularis mucosa, or submucosa, T2 Tumor invades muscularis propria, T3 Tumor penetrates subserosal connective tissue without invasion of visceral peritoneum or adjacent structures, T4a Tumor invades serosa (visceral peritoneum), T4b: Tumor invades adjacent structures, N0 No regional lymph node metastasis, N1 Metastasis in 1-2 regional lymph nodes, N2: Metastasis in 3-6 regional lymph nodes, N3: Metastasis in 7 or more regional lymph nodes, N3a: Metastasis in 7-15 regional lymph nodes N3b: Metastasis in 16 or more regional lymph nodes, M0 No distant metastasis, M1 Distant metastasis.Used with the permission of the American College of Surgeons. Amin MB, Edge SB, Greene FL, et al. (Eds.) AJCC Cancer Staging Manual, 8th Ed. Springer New York, 2017.Brunicardi_Ch26_p1099-p1166.indd 114501/03/19 7:12 PM 1146SPECIFIC CONSIDERATIONS PART IIsignificance of the latter has been established by several investigators.156,157 Gastrectomy should be
|
Surgery_Schwartz. TAny NM1T1 Tumor invades lamina propria, muscularis mucosa, or submucosa, T2 Tumor invades muscularis propria, T3 Tumor penetrates subserosal connective tissue without invasion of visceral peritoneum or adjacent structures, T4a Tumor invades serosa (visceral peritoneum), T4b: Tumor invades adjacent structures, N0 No regional lymph node metastasis, N1 Metastasis in 1-2 regional lymph nodes, N2: Metastasis in 3-6 regional lymph nodes, N3: Metastasis in 7 or more regional lymph nodes, N3a: Metastasis in 7-15 regional lymph nodes N3b: Metastasis in 16 or more regional lymph nodes, M0 No distant metastasis, M1 Distant metastasis.Used with the permission of the American College of Surgeons. Amin MB, Edge SB, Greene FL, et al. (Eds.) AJCC Cancer Staging Manual, 8th Ed. Springer New York, 2017.Brunicardi_Ch26_p1099-p1166.indd 114501/03/19 7:12 PM 1146SPECIFIC CONSIDERATIONS PART IIsignificance of the latter has been established by several investigators.156,157 Gastrectomy should be
|
Surgery_Schwartz_7559
|
Surgery_Schwartz
|
114501/03/19 7:12 PM 1146SPECIFIC CONSIDERATIONS PART IIsignificance of the latter has been established by several investigators.156,157 Gastrectomy should be deferred in patients with positive peritoneal cytology without obvious peritoneal metastases. Patients with gastric cancer who undergo R0 resec-tion (i.e., no gross residual disease) and are found to have posi-tive peritoneal cytology (no gross carcinomatosis) have a much poorer prognosis than those with negative cytology (median survival 14.8 months vs. 98.5 months).156 Stand-alone laparos-copy may influence management in up to 36% of cases and is increasingly advocated to allow appropriate initial treatment selection. The yield is likely highest in patients with T3 or T4 tumors, proximal tumors, or evidence of regional nodal involve-ment158; such patients may benefit from neoadjuvant therapy, and laparoscopy should be offered prior to initiation of treat-ment. Systemic therapy is the cornerstone of therapy for patients
|
Surgery_Schwartz. 114501/03/19 7:12 PM 1146SPECIFIC CONSIDERATIONS PART IIsignificance of the latter has been established by several investigators.156,157 Gastrectomy should be deferred in patients with positive peritoneal cytology without obvious peritoneal metastases. Patients with gastric cancer who undergo R0 resec-tion (i.e., no gross residual disease) and are found to have posi-tive peritoneal cytology (no gross carcinomatosis) have a much poorer prognosis than those with negative cytology (median survival 14.8 months vs. 98.5 months).156 Stand-alone laparos-copy may influence management in up to 36% of cases and is increasingly advocated to allow appropriate initial treatment selection. The yield is likely highest in patients with T3 or T4 tumors, proximal tumors, or evidence of regional nodal involve-ment158; such patients may benefit from neoadjuvant therapy, and laparoscopy should be offered prior to initiation of treat-ment. Systemic therapy is the cornerstone of therapy for patients
|
Surgery_Schwartz_7560
|
Surgery_Schwartz
|
involve-ment158; such patients may benefit from neoadjuvant therapy, and laparoscopy should be offered prior to initiation of treat-ment. Systemic therapy is the cornerstone of therapy for patients with Stage IV disease and surgery is generally reserved for pal-liation of symptoms (e.g., an obstructing distal tumor) in patients with metastases identified during laparoscopy.Treatment. Surgical resection is the only potentially curative treatment for gastric cancer,159 and most patients with clini-cally resectable locoregional disease should undergo gastrec-tomy. The goals of curative surgical treatment are resection of all tumor (i.e., R0 resection and adequate lymphadenectomy to afford accurate staging and provide locoregional control. Gener-ally, the surgeon strives for a grossly negative margin of at least 5 cm, although an evidence base for this is lacking and recent retrospective analyses have suggested that more conservative resections may be adequate.160 Conversely, complete
|
Surgery_Schwartz. involve-ment158; such patients may benefit from neoadjuvant therapy, and laparoscopy should be offered prior to initiation of treat-ment. Systemic therapy is the cornerstone of therapy for patients with Stage IV disease and surgery is generally reserved for pal-liation of symptoms (e.g., an obstructing distal tumor) in patients with metastases identified during laparoscopy.Treatment. Surgical resection is the only potentially curative treatment for gastric cancer,159 and most patients with clini-cally resectable locoregional disease should undergo gastrec-tomy. The goals of curative surgical treatment are resection of all tumor (i.e., R0 resection and adequate lymphadenectomy to afford accurate staging and provide locoregional control. Gener-ally, the surgeon strives for a grossly negative margin of at least 5 cm, although an evidence base for this is lacking and recent retrospective analyses have suggested that more conservative resections may be adequate.160 Conversely, complete
|
Surgery_Schwartz_7561
|
Surgery_Schwartz
|
margin of at least 5 cm, although an evidence base for this is lacking and recent retrospective analyses have suggested that more conservative resections may be adequate.160 Conversely, complete resection of diffuse tumors sometimes proves challenging, and wider gross margins guided by frozen section are sometimes appro-priate. Prior to extending the resection on the basis of a positive frozen section margin, the surgeon should determine whether the microscopic tumor cells are within the wall or on the serosal. The latter may indicate incurable disseminated disease, render-ing additional resection proximally or distally moot, particularly when it makes the anastomosis or stump closure more difficult or hazardous.More than 15 resected lymph nodes are required for ade-quate staging, a relevant marker of quality of care.161,162 Thera-peutic nihilism should be avoided, and in the low-risk patient, an aggressive attempt to resect all tumor should be made. The primary tumor may be resected
|
Surgery_Schwartz. margin of at least 5 cm, although an evidence base for this is lacking and recent retrospective analyses have suggested that more conservative resections may be adequate.160 Conversely, complete resection of diffuse tumors sometimes proves challenging, and wider gross margins guided by frozen section are sometimes appro-priate. Prior to extending the resection on the basis of a positive frozen section margin, the surgeon should determine whether the microscopic tumor cells are within the wall or on the serosal. The latter may indicate incurable disseminated disease, render-ing additional resection proximally or distally moot, particularly when it makes the anastomosis or stump closure more difficult or hazardous.More than 15 resected lymph nodes are required for ade-quate staging, a relevant marker of quality of care.161,162 Thera-peutic nihilism should be avoided, and in the low-risk patient, an aggressive attempt to resect all tumor should be made. The primary tumor may be resected
|
Surgery_Schwartz_7562
|
Surgery_Schwartz
|
marker of quality of care.161,162 Thera-peutic nihilism should be avoided, and in the low-risk patient, an aggressive attempt to resect all tumor should be made. The primary tumor may be resected en bloc with adjacent involved organs (e.g., distal pancreas, transverse colon, or spleen) during the course of curative gastrectomy. Palliative gastrectomy may be indicated in the rare patient with incurable disease, but most patients presenting with stage IV gastric cancer can be managed without major operation.163Extent of Gastrectomy The standard operation for gastric cancer is radical subtotal gastrectomy. Unless required for R0 resection, total gastrectomy confers no additional survival ben-efit and may have adverse nutritional or quality-of-life conse-quences and higher perioperative morbidity and mortality.164 Subtotal gastric resection typically entails ligation of the left and right gastric and gastroepiploic arteries at their origins, as well as the en bloc removal of the distal
|
Surgery_Schwartz. marker of quality of care.161,162 Thera-peutic nihilism should be avoided, and in the low-risk patient, an aggressive attempt to resect all tumor should be made. The primary tumor may be resected en bloc with adjacent involved organs (e.g., distal pancreas, transverse colon, or spleen) during the course of curative gastrectomy. Palliative gastrectomy may be indicated in the rare patient with incurable disease, but most patients presenting with stage IV gastric cancer can be managed without major operation.163Extent of Gastrectomy The standard operation for gastric cancer is radical subtotal gastrectomy. Unless required for R0 resection, total gastrectomy confers no additional survival ben-efit and may have adverse nutritional or quality-of-life conse-quences and higher perioperative morbidity and mortality.164 Subtotal gastric resection typically entails ligation of the left and right gastric and gastroepiploic arteries at their origins, as well as the en bloc removal of the distal
|
Surgery_Schwartz_7563
|
Surgery_Schwartz
|
and mortality.164 Subtotal gastric resection typically entails ligation of the left and right gastric and gastroepiploic arteries at their origins, as well as the en bloc removal of the distal 2/3 of the stomach, includ-ing the pylorus and 2 cm of duodenum, the greater and lesser omentum, and all associated lymphatic tissue (Fig. 26-56). In the absence of involvement by direct extension, the spleen and pancreatic tail are not removed.Reconstruction is usually by Billroth II gastrojejunostomy or Roux-en-Y gastrojejunostomy. The former is associated with shorter operative time and precludes roux limb stasis. The lat-ter mitigates bile reflux and, therefore, may be associated with better quality of life long term. In East Asia, especially Japan, Billroth-I gastroduodenostomy is frequently performed after distal gastrectomy. Billroth-I gastroduodenostomy consists of one anastomosis (which is usually straightforward and keeps the duodenum in the food stream). In the United States,
|
Surgery_Schwartz. and mortality.164 Subtotal gastric resection typically entails ligation of the left and right gastric and gastroepiploic arteries at their origins, as well as the en bloc removal of the distal 2/3 of the stomach, includ-ing the pylorus and 2 cm of duodenum, the greater and lesser omentum, and all associated lymphatic tissue (Fig. 26-56). In the absence of involvement by direct extension, the spleen and pancreatic tail are not removed.Reconstruction is usually by Billroth II gastrojejunostomy or Roux-en-Y gastrojejunostomy. The former is associated with shorter operative time and precludes roux limb stasis. The lat-ter mitigates bile reflux and, therefore, may be associated with better quality of life long term. In East Asia, especially Japan, Billroth-I gastroduodenostomy is frequently performed after distal gastrectomy. Billroth-I gastroduodenostomy consists of one anastomosis (which is usually straightforward and keeps the duodenum in the food stream). In the United States,
|
Surgery_Schwartz_7564
|
Surgery_Schwartz
|
performed after distal gastrectomy. Billroth-I gastroduodenostomy consists of one anastomosis (which is usually straightforward and keeps the duodenum in the food stream). In the United States, traditional surgical teaching eschews gastroduodenostomy following gas-tric cancer resection because of the possibility of anastomotic recurrence and obstruction. A risk of remnant carcinoma attrib-uted to bile reflux has been invoked in support of Roux-en-Y reconstruction over Billroth II or I. Strong evidence linking reconstruction approach to long-term oncologic outcome is lacking.Total gastrectomy with Roux-en-Y esophagojejunostomy may be required for R0 resection (Fig. 26-57) and is frequently the optimal operation for patients with proximal gastric adeno-carcinoma. The construction of a jejunal pouch is associated with superior nutritional recovery in some but not all reports, and is a consideration.102 Proximal subtotal gastric resection, Gastroepiploicvs.ABDuodenumTransverse
|
Surgery_Schwartz. performed after distal gastrectomy. Billroth-I gastroduodenostomy consists of one anastomosis (which is usually straightforward and keeps the duodenum in the food stream). In the United States, traditional surgical teaching eschews gastroduodenostomy following gas-tric cancer resection because of the possibility of anastomotic recurrence and obstruction. A risk of remnant carcinoma attrib-uted to bile reflux has been invoked in support of Roux-en-Y reconstruction over Billroth II or I. Strong evidence linking reconstruction approach to long-term oncologic outcome is lacking.Total gastrectomy with Roux-en-Y esophagojejunostomy may be required for R0 resection (Fig. 26-57) and is frequently the optimal operation for patients with proximal gastric adeno-carcinoma. The construction of a jejunal pouch is associated with superior nutritional recovery in some but not all reports, and is a consideration.102 Proximal subtotal gastric resection, Gastroepiploicvs.ABDuodenumTransverse
|
Surgery_Schwartz_7565
|
Surgery_Schwartz
|
of a jejunal pouch is associated with superior nutritional recovery in some but not all reports, and is a consideration.102 Proximal subtotal gastric resection, Gastroepiploicvs.ABDuodenumTransverse colonTumorLiverStomachStomachJejunumTransverse colonPancreasFigure 26-56. A and B. Radical subtotal gastrectomy. vs. = vessels. (Reproduced with permission from Daly JM, Cady B, Low DW: Atlas of Surgical Oncology. St. Louis, MO: Elsevier/Mosby-Year Book; 1993.)Brunicardi_Ch26_p1099-p1166.indd 114601/03/19 7:13 PM 1147STOMACHCHAPTER 26a technically feasible alternative to total gastrectomy for some proximal gastric tumors, requires esophagogastrostomy to a denervated distal gastric remnant, and functional outcomes are generally poor.165 Pyloroplasty in this setting virtually guar-antees bile esophagitis, and if the pylorus is left intact, gastric emptying may be problematic. An isoperistaltic jejunal intero-sition (Henley loop) between the esophagus and antrum may mitigate some of the
|
Surgery_Schwartz. of a jejunal pouch is associated with superior nutritional recovery in some but not all reports, and is a consideration.102 Proximal subtotal gastric resection, Gastroepiploicvs.ABDuodenumTransverse colonTumorLiverStomachStomachJejunumTransverse colonPancreasFigure 26-56. A and B. Radical subtotal gastrectomy. vs. = vessels. (Reproduced with permission from Daly JM, Cady B, Low DW: Atlas of Surgical Oncology. St. Louis, MO: Elsevier/Mosby-Year Book; 1993.)Brunicardi_Ch26_p1099-p1166.indd 114601/03/19 7:13 PM 1147STOMACHCHAPTER 26a technically feasible alternative to total gastrectomy for some proximal gastric tumors, requires esophagogastrostomy to a denervated distal gastric remnant, and functional outcomes are generally poor.165 Pyloroplasty in this setting virtually guar-antees bile esophagitis, and if the pylorus is left intact, gastric emptying may be problematic. An isoperistaltic jejunal intero-sition (Henley loop) between the esophagus and antrum may mitigate some of the
|
Surgery_Schwartz_7566
|
Surgery_Schwartz
|
esophagitis, and if the pylorus is left intact, gastric emptying may be problematic. An isoperistaltic jejunal intero-sition (Henley loop) between the esophagus and antrum may mitigate some of the adverse symptoms associated with this operation but adds additional complexity.Extent of Lymphadenectomy The 3rd edition of Japanese classification of gastric carcinoma defines lymph node sta-tions on the basis of anatomic landmarks. Lymph node stations 1 to 12 and 14V are classified as regional and metastasis to any other lymph nodal stations constitute distant disease (M1) (see Fig. 26-4). So-called D1 lymphadenectomy in distal gastrec-tomy requires the dissection of stations 1, 3, 4sb, 4d, 5, 6, and 7. Additional resection of stations 8a, 9, 11p, and 12a constitute D2 lymphadenectomy. D1 lymphadenectomy in total gastrec-tomy requires dissection of stations 1 through 7; D2 lymph-adenectomy includes stations 8a to 12a as well. The operation most commonly performed in the United States for
|
Surgery_Schwartz. esophagitis, and if the pylorus is left intact, gastric emptying may be problematic. An isoperistaltic jejunal intero-sition (Henley loop) between the esophagus and antrum may mitigate some of the adverse symptoms associated with this operation but adds additional complexity.Extent of Lymphadenectomy The 3rd edition of Japanese classification of gastric carcinoma defines lymph node sta-tions on the basis of anatomic landmarks. Lymph node stations 1 to 12 and 14V are classified as regional and metastasis to any other lymph nodal stations constitute distant disease (M1) (see Fig. 26-4). So-called D1 lymphadenectomy in distal gastrec-tomy requires the dissection of stations 1, 3, 4sb, 4d, 5, 6, and 7. Additional resection of stations 8a, 9, 11p, and 12a constitute D2 lymphadenectomy. D1 lymphadenectomy in total gastrec-tomy requires dissection of stations 1 through 7; D2 lymph-adenectomy includes stations 8a to 12a as well. The operation most commonly performed in the United States for
|
Surgery_Schwartz_7567
|
Surgery_Schwartz
|
in total gastrec-tomy requires dissection of stations 1 through 7; D2 lymph-adenectomy includes stations 8a to 12a as well. The operation most commonly performed in the United States for gastric cancer is a D1 resection and involves removal of the primary tumor with perigastric nodes. The standard operation for gastric cancer in Asia and specialized U.S. centers is D2 gastrectomy, which involves a more extensive lymphadenectomy (removal of the D1 and D2 nodes). In addition to the tissue removed in a D1 resection, D2 gastrectomy includes the superior peritoneum overlying the mesocolon and, selectively, the pancreas, as well as nodes along the common hepatic and splenic arteries, and the celiac axis. Splenectomy and distal pancreatectomy are not routinely performed because this has been shown to increase the morbidity and mortality of the operation.166,167The purported survival advantage of D2 gastrectomy in gastric cancer is illustrated in Table 26-20, which shows the 5-year survival
|
Surgery_Schwartz. in total gastrec-tomy requires dissection of stations 1 through 7; D2 lymph-adenectomy includes stations 8a to 12a as well. The operation most commonly performed in the United States for gastric cancer is a D1 resection and involves removal of the primary tumor with perigastric nodes. The standard operation for gastric cancer in Asia and specialized U.S. centers is D2 gastrectomy, which involves a more extensive lymphadenectomy (removal of the D1 and D2 nodes). In addition to the tissue removed in a D1 resection, D2 gastrectomy includes the superior peritoneum overlying the mesocolon and, selectively, the pancreas, as well as nodes along the common hepatic and splenic arteries, and the celiac axis. Splenectomy and distal pancreatectomy are not routinely performed because this has been shown to increase the morbidity and mortality of the operation.166,167The purported survival advantage of D2 gastrectomy in gastric cancer is illustrated in Table 26-20, which shows the 5-year survival
|
Surgery_Schwartz_7568
|
Surgery_Schwartz
|
to increase the morbidity and mortality of the operation.166,167The purported survival advantage of D2 gastrectomy in gastric cancer is illustrated in Table 26-20, which shows the 5-year survival rates for gastric cancer stratified by pathologic stage for the United States and Japan. Randomized prospective trials have not confirmed this survival advantage. Two stud-ies showed increased operative mortality with D2 gastrectomy, but the most recent study did not (Table 26-21).166,168,169 With extended lymphadenectomy, much of the morbidity and mor-tality is attributable to performance of splenectomy and distal pancreatectomy, which are no longer routinely included as part of the D2 gastrectomy. Because D2 lymphadenectomy in total gastrectomy requires the dissection of station 10 (i.e., splenic hilar lymph nodes) splenectomy is still selectively performed, particularly for locally advanced fundic tumors.Longer-term follow-up from the Dutch lymphdenectomy trial demonstrating a
|
Surgery_Schwartz. to increase the morbidity and mortality of the operation.166,167The purported survival advantage of D2 gastrectomy in gastric cancer is illustrated in Table 26-20, which shows the 5-year survival rates for gastric cancer stratified by pathologic stage for the United States and Japan. Randomized prospective trials have not confirmed this survival advantage. Two stud-ies showed increased operative mortality with D2 gastrectomy, but the most recent study did not (Table 26-21).166,168,169 With extended lymphadenectomy, much of the morbidity and mor-tality is attributable to performance of splenectomy and distal pancreatectomy, which are no longer routinely included as part of the D2 gastrectomy. Because D2 lymphadenectomy in total gastrectomy requires the dissection of station 10 (i.e., splenic hilar lymph nodes) splenectomy is still selectively performed, particularly for locally advanced fundic tumors.Longer-term follow-up from the Dutch lymphdenectomy trial demonstrating a
|
Surgery_Schwartz_7569
|
Surgery_Schwartz
|
(i.e., splenic hilar lymph nodes) splenectomy is still selectively performed, particularly for locally advanced fundic tumors.Longer-term follow-up from the Dutch lymphdenectomy trial demonstrating a disease-specific survival advantage with D2 dissection170 as well as recognition that pancreas and spleen preserving dissection can be performed with low morbidity169 have provided momentum for increased utilization of D2 gas-trectomy at high-volume centers in the United States and Europe. Some experts have argued that the D2 operation affords better staging and informs more rational decision-making regarding multimodality therapy. Without question, D2 provides a bet-ter yield of evaluable nodes. Given the frequent inadequacy of lymph node evaluation with gastrectomy in the United States and the association with poorer outcomes, greater attention to the conduct of the operation and pathologic specimen evaluation is clearly desirable. Whether better outcomes after more exten-sive
|
Surgery_Schwartz. (i.e., splenic hilar lymph nodes) splenectomy is still selectively performed, particularly for locally advanced fundic tumors.Longer-term follow-up from the Dutch lymphdenectomy trial demonstrating a disease-specific survival advantage with D2 dissection170 as well as recognition that pancreas and spleen preserving dissection can be performed with low morbidity169 have provided momentum for increased utilization of D2 gas-trectomy at high-volume centers in the United States and Europe. Some experts have argued that the D2 operation affords better staging and informs more rational decision-making regarding multimodality therapy. Without question, D2 provides a bet-ter yield of evaluable nodes. Given the frequent inadequacy of lymph node evaluation with gastrectomy in the United States and the association with poorer outcomes, greater attention to the conduct of the operation and pathologic specimen evaluation is clearly desirable. Whether better outcomes after more exten-sive
|
Surgery_Schwartz_7570
|
Surgery_Schwartz
|
and the association with poorer outcomes, greater attention to the conduct of the operation and pathologic specimen evaluation is clearly desirable. Whether better outcomes after more exten-sive dissection are an epiphenomenon of improved pathologic staging, or a function of therapeutic benefit, remains unclear.Chemotherapy and Radiation for Gastric Cancer The actu-arial 5-year survival rates for resected gastric adenocarcinoma stages I, II, and III in the United States are approximately 75%, 50%, and 25%, respectively. Because most surgical patients have stage II disease or greater, adjuvant therapy is indicated in the majority of patients who undergo initial resection. Adjuvant chemotherapy alone has not proven effective, at least in studies from Europe and the United States.171 Several studies from Table 26-20Gastric cancer 5-year survival and operative mortality in the United States and Japan MARUYAMA (JAPAN), 1971–1985AMERICAN COLLEGE OF SURGEONS, 1982–1987MEMORIAL SLOAN
|
Surgery_Schwartz. and the association with poorer outcomes, greater attention to the conduct of the operation and pathologic specimen evaluation is clearly desirable. Whether better outcomes after more exten-sive dissection are an epiphenomenon of improved pathologic staging, or a function of therapeutic benefit, remains unclear.Chemotherapy and Radiation for Gastric Cancer The actu-arial 5-year survival rates for resected gastric adenocarcinoma stages I, II, and III in the United States are approximately 75%, 50%, and 25%, respectively. Because most surgical patients have stage II disease or greater, adjuvant therapy is indicated in the majority of patients who undergo initial resection. Adjuvant chemotherapy alone has not proven effective, at least in studies from Europe and the United States.171 Several studies from Table 26-20Gastric cancer 5-year survival and operative mortality in the United States and Japan MARUYAMA (JAPAN), 1971–1985AMERICAN COLLEGE OF SURGEONS, 1982–1987MEMORIAL SLOAN
|
Surgery_Schwartz_7571
|
Surgery_Schwartz
|
Several studies from Table 26-20Gastric cancer 5-year survival and operative mortality in the United States and Japan MARUYAMA (JAPAN), 1971–1985AMERICAN COLLEGE OF SURGEONS, 1982–1987MEMORIAL SLOAN KETTERING, 1985–1994No. patients317618,365675Stage I91%50%84%Stage II72%29%61%Stage III44%13%29%Stage IV9%3%25%Operative mortality1%7%3%60 cmFigure 26-57. Reconstruction after total gastrectomy. Jejunal pouch (not shown here) should be considered. (Reproduced with permission from Zinner MJ: Atlas of Gastric Surgery. New York, NY: Elsevier/Churchill Livingstone; 1992.)Brunicardi_Ch26_p1099-p1166.indd 114701/03/19 7:13 PM 1148SPECIFIC CONSIDERATIONS PART IIJapan and Korea have indicated a survival advantage with adju-vant chemotherapy after D2 gastrectomy.172-174 The discordance between outcomes in Asia and those from the United States and Europe have been attributed to differences in disease biology or treatment approaches. Proponents of the latter suggest that D2 lymphadenectomy
|
Surgery_Schwartz. Several studies from Table 26-20Gastric cancer 5-year survival and operative mortality in the United States and Japan MARUYAMA (JAPAN), 1971–1985AMERICAN COLLEGE OF SURGEONS, 1982–1987MEMORIAL SLOAN KETTERING, 1985–1994No. patients317618,365675Stage I91%50%84%Stage II72%29%61%Stage III44%13%29%Stage IV9%3%25%Operative mortality1%7%3%60 cmFigure 26-57. Reconstruction after total gastrectomy. Jejunal pouch (not shown here) should be considered. (Reproduced with permission from Zinner MJ: Atlas of Gastric Surgery. New York, NY: Elsevier/Churchill Livingstone; 1992.)Brunicardi_Ch26_p1099-p1166.indd 114701/03/19 7:13 PM 1148SPECIFIC CONSIDERATIONS PART IIJapan and Korea have indicated a survival advantage with adju-vant chemotherapy after D2 gastrectomy.172-174 The discordance between outcomes in Asia and those from the United States and Europe have been attributed to differences in disease biology or treatment approaches. Proponents of the latter suggest that D2 lymphadenectomy
|
Surgery_Schwartz_7572
|
Surgery_Schwartz
|
outcomes in Asia and those from the United States and Europe have been attributed to differences in disease biology or treatment approaches. Proponents of the latter suggest that D2 lymphadenectomy provides sufficient locoregional control and that chemotherapy alone has efficacy after optimal surgery. A preferred adjuvant approach in the United States incorpo-rates chemotherapy and radiation based on the results of the Intergroup trial. This prospective randomized study of adju-vant treatment with chemotherapy (5-fluorouracil and leucovo-rin) and radiation (4500 cGy) demonstrated a survival benefit in resected patients with stage II and III adenocarcinoma of the stomach.175 Only 10% of patients entered in the study actually had D2 gastrectomy, and most (54%) had less than an adequate D1 gastrectomy. Because adequacy of lymphadenectomy has been correlated with survival, particularly in patients with stage III gastric cancer, it has been suggested that the benefits of adjuvant
|
Surgery_Schwartz. outcomes in Asia and those from the United States and Europe have been attributed to differences in disease biology or treatment approaches. Proponents of the latter suggest that D2 lymphadenectomy provides sufficient locoregional control and that chemotherapy alone has efficacy after optimal surgery. A preferred adjuvant approach in the United States incorpo-rates chemotherapy and radiation based on the results of the Intergroup trial. This prospective randomized study of adju-vant treatment with chemotherapy (5-fluorouracil and leucovo-rin) and radiation (4500 cGy) demonstrated a survival benefit in resected patients with stage II and III adenocarcinoma of the stomach.175 Only 10% of patients entered in the study actually had D2 gastrectomy, and most (54%) had less than an adequate D1 gastrectomy. Because adequacy of lymphadenectomy has been correlated with survival, particularly in patients with stage III gastric cancer, it has been suggested that the benefits of adjuvant
|
Surgery_Schwartz_7573
|
Surgery_Schwartz
|
D1 gastrectomy. Because adequacy of lymphadenectomy has been correlated with survival, particularly in patients with stage III gastric cancer, it has been suggested that the benefits of adjuvant chemoradiation shown in this study would be vitiated by a more extensive operation.Neoadjuvant chemotherapy has emerged as a viable alter-native to adjuvant chemoradiotherapy in Europe and the United States. Theoretical advantages of this approach include more consistent completion of multimodality therapy, downstaging, earlier treatment of micrometastatic disease, and the ability to gauge response at the in situ tumor. The MAGIC trial, a random-ized controlled trial comparing perioperative epirubicin, cispla-tin, and 5-flourouracil to surgery alone demonstrated a survival advantage and supported this approach in patients with at least stage II disease.176 A subset of patients with very symptomatic tumors may not be eligible for this approach, and the perception that systemic therapy is an
|
Surgery_Schwartz. D1 gastrectomy. Because adequacy of lymphadenectomy has been correlated with survival, particularly in patients with stage III gastric cancer, it has been suggested that the benefits of adjuvant chemoradiation shown in this study would be vitiated by a more extensive operation.Neoadjuvant chemotherapy has emerged as a viable alter-native to adjuvant chemoradiotherapy in Europe and the United States. Theoretical advantages of this approach include more consistent completion of multimodality therapy, downstaging, earlier treatment of micrometastatic disease, and the ability to gauge response at the in situ tumor. The MAGIC trial, a random-ized controlled trial comparing perioperative epirubicin, cispla-tin, and 5-flourouracil to surgery alone demonstrated a survival advantage and supported this approach in patients with at least stage II disease.176 A subset of patients with very symptomatic tumors may not be eligible for this approach, and the perception that systemic therapy is an
|
Surgery_Schwartz_7574
|
Surgery_Schwartz
|
this approach in patients with at least stage II disease.176 A subset of patients with very symptomatic tumors may not be eligible for this approach, and the perception that systemic therapy is an ineffective detour for patients who require locoregional control with surgery is sometimes hard to overcome. Regardless, neoadjuvant approaches are increasingly utilized, and even more rigorous regimens incorporating radio-therapy or targeted agents have been explored, sometimes with promising outcomes.177Recent clinical trials from Asia suggest the potential ben-efit of adjuvant chemotherapy after D2 lymphadenectomy in patients with advanced gastric cancer. These trials compared surgery alone and surgery plus adjuvant chemotherapy including oral fluoropyrimidines in resected advanced gastric cancer.172,173 A study from the Japan Clinical Oncology Group showed a 69% overall 5-year survival rate in patients with clinically curable T2b, T3, and T4 gastric cancer, treated with D2 gastrectomy
|
Surgery_Schwartz. this approach in patients with at least stage II disease.176 A subset of patients with very symptomatic tumors may not be eligible for this approach, and the perception that systemic therapy is an ineffective detour for patients who require locoregional control with surgery is sometimes hard to overcome. Regardless, neoadjuvant approaches are increasingly utilized, and even more rigorous regimens incorporating radio-therapy or targeted agents have been explored, sometimes with promising outcomes.177Recent clinical trials from Asia suggest the potential ben-efit of adjuvant chemotherapy after D2 lymphadenectomy in patients with advanced gastric cancer. These trials compared surgery alone and surgery plus adjuvant chemotherapy including oral fluoropyrimidines in resected advanced gastric cancer.172,173 A study from the Japan Clinical Oncology Group showed a 69% overall 5-year survival rate in patients with clinically curable T2b, T3, and T4 gastric cancer, treated with D2 gastrectomy
|
Surgery_Schwartz_7575
|
Surgery_Schwartz
|
cancer.172,173 A study from the Japan Clinical Oncology Group showed a 69% overall 5-year survival rate in patients with clinically curable T2b, T3, and T4 gastric cancer, treated with D2 gastrectomy alone.178 A subsequent trial from Korea demonstrated a survival advantage with adjuvant capecitabine and oxaliplatin after D2 gastrectomy compared to D2 gastrectomy alone.173 It is uncer-tain whether this approach can be translated to patients in the United States.Although the prognosis of metastatic or recurrent gastric cancer is poor, systemic chemotherapy provides a significant survival benefit over the best supportive care.179,180 Agents that have shown activity against gastric cancer include 5-fluorouracil (5-FU), cisplatin, doxorubicin, methotrexate, taxanes, and camptothecin. Until recently, 5-FU–based chemotherapy, especially in combination with platinums, played a key role in the treatment for the unresectable gastric cancer as well as several types of cancer, such as colon and
|
Surgery_Schwartz. cancer.172,173 A study from the Japan Clinical Oncology Group showed a 69% overall 5-year survival rate in patients with clinically curable T2b, T3, and T4 gastric cancer, treated with D2 gastrectomy alone.178 A subsequent trial from Korea demonstrated a survival advantage with adjuvant capecitabine and oxaliplatin after D2 gastrectomy compared to D2 gastrectomy alone.173 It is uncer-tain whether this approach can be translated to patients in the United States.Although the prognosis of metastatic or recurrent gastric cancer is poor, systemic chemotherapy provides a significant survival benefit over the best supportive care.179,180 Agents that have shown activity against gastric cancer include 5-fluorouracil (5-FU), cisplatin, doxorubicin, methotrexate, taxanes, and camptothecin. Until recently, 5-FU–based chemotherapy, especially in combination with platinums, played a key role in the treatment for the unresectable gastric cancer as well as several types of cancer, such as colon and
|
Surgery_Schwartz_7576
|
Surgery_Schwartz
|
5-FU–based chemotherapy, especially in combination with platinums, played a key role in the treatment for the unresectable gastric cancer as well as several types of cancer, such as colon and lung. In the 1990s, the introduction of novel anticancer agents such as camptoth-ecin, taxanes, third-generation platinums, and new oral fluo-ropyrimidines, improved the prognosis of unresectable gastric cancer.179,180It is likely that targeted molecular agents will have an increasing role in treating gastric cancer. Recently, Trastu-zumab, a humanized molecular antibody reactive against the extracellular domain of HER2, increased the effectiveness of cytotoxic chemotherapy in patients with HER2 over-expressing advanced gastric cancer.152 Other large trials are ongoing. Deter-mination of HER2 gene amplification status may have prognos-tic significance.181Endoscopic Resection182 The shortand long-term morbidity associated with gastrectomy and the relatively infrequent dis-semination of superficial
|
Surgery_Schwartz. 5-FU–based chemotherapy, especially in combination with platinums, played a key role in the treatment for the unresectable gastric cancer as well as several types of cancer, such as colon and lung. In the 1990s, the introduction of novel anticancer agents such as camptoth-ecin, taxanes, third-generation platinums, and new oral fluo-ropyrimidines, improved the prognosis of unresectable gastric cancer.179,180It is likely that targeted molecular agents will have an increasing role in treating gastric cancer. Recently, Trastu-zumab, a humanized molecular antibody reactive against the extracellular domain of HER2, increased the effectiveness of cytotoxic chemotherapy in patients with HER2 over-expressing advanced gastric cancer.152 Other large trials are ongoing. Deter-mination of HER2 gene amplification status may have prognos-tic significance.181Endoscopic Resection182 The shortand long-term morbidity associated with gastrectomy and the relatively infrequent dis-semination of superficial
|
Surgery_Schwartz_7577
|
Surgery_Schwartz
|
status may have prognos-tic significance.181Endoscopic Resection182 The shortand long-term morbidity associated with gastrectomy and the relatively infrequent dis-semination of superficial (i.e., T1) tumors to regional nodes have compelled exploration of endoscopic resection for selected lesions. Numerous East Asian centers have demonstrated that some patients with early gastric cancer are adequately treated with endoscopic mucosal resection (EMR). EMR is most appro-priate for patients in whom the probability of lymph node metas-tasis is low. According to the Japanese treatment guidelines for gastric cancer, EMR is a standard treatment for well differenti-ated gastric cancer confined to the mucosa (T1a), measuring less than 2 cm and without signs of ulceration. Such lesions are associated with a negligible risk of lymph node metastasis. 6Table 26-21Randomized trials comparing D1 and D2 gastrectomy for gastric cancerAUTHORSNUMBER OF PATIENTSTYPE OF SURGERYPOSTOPERATIVE
|
Surgery_Schwartz. status may have prognos-tic significance.181Endoscopic Resection182 The shortand long-term morbidity associated with gastrectomy and the relatively infrequent dis-semination of superficial (i.e., T1) tumors to regional nodes have compelled exploration of endoscopic resection for selected lesions. Numerous East Asian centers have demonstrated that some patients with early gastric cancer are adequately treated with endoscopic mucosal resection (EMR). EMR is most appro-priate for patients in whom the probability of lymph node metas-tasis is low. According to the Japanese treatment guidelines for gastric cancer, EMR is a standard treatment for well differenti-ated gastric cancer confined to the mucosa (T1a), measuring less than 2 cm and without signs of ulceration. Such lesions are associated with a negligible risk of lymph node metastasis. 6Table 26-21Randomized trials comparing D1 and D2 gastrectomy for gastric cancerAUTHORSNUMBER OF PATIENTSTYPE OF SURGERYPOSTOPERATIVE
|
Surgery_Schwartz_7578
|
Surgery_Schwartz
|
are associated with a negligible risk of lymph node metastasis. 6Table 26-21Randomized trials comparing D1 and D2 gastrectomy for gastric cancerAUTHORSNUMBER OF PATIENTSTYPE OF SURGERYPOSTOPERATIVE COMPLICATIONSPOSTOPERATIVE MORTALITY5 YEAR SURVIVALBonenkamp et al.711D125445 D2431047Cuschieri et al.400D1286.535 D2461333Degiuli et al.267D1123 D217.92.2 Data from Bonenkamp JJ, Hermans J, Sasako M, et al. Extended lymph node dissection for gastric cancer. N Engl J Med. 1999;340:908; Cuschieri A, Fayers P, Fielding J, et al. Postoperative morbidity and mortality after D1 and D2 resections for gastric cancer: preliminary results of the MRC randomized controlled surgical trial. The Surgical Cooperative Group. Lancet. 1996;347:995; and Degiuli M, Sasako M, Ponti A, et al. Morbidity and mortality in the Italian Gastric Cancer Study Group randomized clinical trial of D1 versus D2 resection for gastric cancer. Br J Surg. 2010;97:5.Brunicardi_Ch26_p1099-p1166.indd 114801/03/19 7:13 PM
|
Surgery_Schwartz. are associated with a negligible risk of lymph node metastasis. 6Table 26-21Randomized trials comparing D1 and D2 gastrectomy for gastric cancerAUTHORSNUMBER OF PATIENTSTYPE OF SURGERYPOSTOPERATIVE COMPLICATIONSPOSTOPERATIVE MORTALITY5 YEAR SURVIVALBonenkamp et al.711D125445 D2431047Cuschieri et al.400D1286.535 D2461333Degiuli et al.267D1123 D217.92.2 Data from Bonenkamp JJ, Hermans J, Sasako M, et al. Extended lymph node dissection for gastric cancer. N Engl J Med. 1999;340:908; Cuschieri A, Fayers P, Fielding J, et al. Postoperative morbidity and mortality after D1 and D2 resections for gastric cancer: preliminary results of the MRC randomized controlled surgical trial. The Surgical Cooperative Group. Lancet. 1996;347:995; and Degiuli M, Sasako M, Ponti A, et al. Morbidity and mortality in the Italian Gastric Cancer Study Group randomized clinical trial of D1 versus D2 resection for gastric cancer. Br J Surg. 2010;97:5.Brunicardi_Ch26_p1099-p1166.indd 114801/03/19 7:13 PM
|
Surgery_Schwartz_7579
|
Surgery_Schwartz
|
in the Italian Gastric Cancer Study Group randomized clinical trial of D1 versus D2 resection for gastric cancer. Br J Surg. 2010;97:5.Brunicardi_Ch26_p1099-p1166.indd 114801/03/19 7:13 PM 1149STOMACHCHAPTER 26En bloc resection is required to evaluate margins for confirma-tion of complete resection. The development of endoscopic submucosal dissection (ESD) allows en bloc resection of larger tumors. This has increased the feasibility of endoscopic resec-tion of larger lesions (<3 cm) at experienced centers. If patho-logic evaluation of the resected specimen does not demonstrate ulceration, penetration of the muscularis mucosae, or lymphatic invasion, the risk of lymph node metastases is less than 1%. Even the occasional patient with higher risk stigmata may be managed endoscopically, particularly in the presence of comor-bidities that preclude safe operation.Screening for Gastric Cancer. In Japan, it clearly has been shown that patients participating in gastric cancer screening
|
Surgery_Schwartz. in the Italian Gastric Cancer Study Group randomized clinical trial of D1 versus D2 resection for gastric cancer. Br J Surg. 2010;97:5.Brunicardi_Ch26_p1099-p1166.indd 114801/03/19 7:13 PM 1149STOMACHCHAPTER 26En bloc resection is required to evaluate margins for confirma-tion of complete resection. The development of endoscopic submucosal dissection (ESD) allows en bloc resection of larger tumors. This has increased the feasibility of endoscopic resec-tion of larger lesions (<3 cm) at experienced centers. If patho-logic evaluation of the resected specimen does not demonstrate ulceration, penetration of the muscularis mucosae, or lymphatic invasion, the risk of lymph node metastases is less than 1%. Even the occasional patient with higher risk stigmata may be managed endoscopically, particularly in the presence of comor-bidities that preclude safe operation.Screening for Gastric Cancer. In Japan, it clearly has been shown that patients participating in gastric cancer screening
|
Surgery_Schwartz_7580
|
Surgery_Schwartz
|
particularly in the presence of comor-bidities that preclude safe operation.Screening for Gastric Cancer. In Japan, it clearly has been shown that patients participating in gastric cancer screening pro-grams have a significantly decreased risk of dying from gastric cancer. Thus, screening is effective in a high-risk population. Screening the general population in the United States (a low-risk country) is probably not justified, but patients clearly at risk for gastric cancer probably should have periodic endoscopy and biopsy. This includes patients with familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, gastric adenomas, Ménétrier’s disease, intestinal metaplasia or dyspla-sia, and remote gastrectomy or gastrojejunostomy.Gastric LymphomaGastric lymphomas generally account for about 4% of gastric malignancies. Over half of patients with non-Hodgkin’s lym-phoma have involvement of the GI tract. The stomach is the most common site of primary GI lymphoma, and over
|
Surgery_Schwartz. particularly in the presence of comor-bidities that preclude safe operation.Screening for Gastric Cancer. In Japan, it clearly has been shown that patients participating in gastric cancer screening pro-grams have a significantly decreased risk of dying from gastric cancer. Thus, screening is effective in a high-risk population. Screening the general population in the United States (a low-risk country) is probably not justified, but patients clearly at risk for gastric cancer probably should have periodic endoscopy and biopsy. This includes patients with familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer, gastric adenomas, Ménétrier’s disease, intestinal metaplasia or dyspla-sia, and remote gastrectomy or gastrojejunostomy.Gastric LymphomaGastric lymphomas generally account for about 4% of gastric malignancies. Over half of patients with non-Hodgkin’s lym-phoma have involvement of the GI tract. The stomach is the most common site of primary GI lymphoma, and over
|
Surgery_Schwartz_7581
|
Surgery_Schwartz
|
account for about 4% of gastric malignancies. Over half of patients with non-Hodgkin’s lym-phoma have involvement of the GI tract. The stomach is the most common site of primary GI lymphoma, and over 95% are non-Hodgkin’s type. Most are B-cell type, thought to arise in mucosa associated lymphoid tissue (MALT), although most high-grade gastric lymphomas are without any characteristics of the low-grade MALT neoplasm.183 About half of gastric lym-phomas are histologically low grade, and about half are high grade. Interestingly, the normal stomach is relatively devoid of lymphoid tissue. However, in the setting of chronic gastritis, the stomach acquires MALT, which can undergo malignant degen-eration. Again, H pylori is thought to be the culprit. In popula-tions with a high incidence of gastric lymphoma, there is a high incidence of H pylori infection; patients with gastric lymphoma also usually have H pylori infection.184Low-grade MALT lymphoma, essentially a monoclonal proliferation of
|
Surgery_Schwartz. account for about 4% of gastric malignancies. Over half of patients with non-Hodgkin’s lym-phoma have involvement of the GI tract. The stomach is the most common site of primary GI lymphoma, and over 95% are non-Hodgkin’s type. Most are B-cell type, thought to arise in mucosa associated lymphoid tissue (MALT), although most high-grade gastric lymphomas are without any characteristics of the low-grade MALT neoplasm.183 About half of gastric lym-phomas are histologically low grade, and about half are high grade. Interestingly, the normal stomach is relatively devoid of lymphoid tissue. However, in the setting of chronic gastritis, the stomach acquires MALT, which can undergo malignant degen-eration. Again, H pylori is thought to be the culprit. In popula-tions with a high incidence of gastric lymphoma, there is a high incidence of H pylori infection; patients with gastric lymphoma also usually have H pylori infection.184Low-grade MALT lymphoma, essentially a monoclonal proliferation of
|
Surgery_Schwartz_7582
|
Surgery_Schwartz
|
lymphoma, there is a high incidence of H pylori infection; patients with gastric lymphoma also usually have H pylori infection.184Low-grade MALT lymphoma, essentially a monoclonal proliferation of B cells, presumably arises from a background of chronic gastritis associated with H pylori. These relatively innocuous tumors then undergo degeneration to high-grade lymphoma, which is the usual variety seen by the surgeon. Remarkably, when the H pylori is eradicated and the gastritis improves, the low-grade MALT lymphoma often disappears. Thus, low-grade MALT lymphoma is not a surgical lesion. Careful follow-up is necessary particularly in those lesions with a t(11:18) translocation, thought to be a risk factor for a more aggressive MALT lesion. If low-grade lymphoma per-sists after H pylori eradication, radiation should be consid-ered for disease clinically confined to the stomach (stage I), while chemotherapy with or without radiation is used for more advanced lesions (Fig.
|
Surgery_Schwartz. lymphoma, there is a high incidence of H pylori infection; patients with gastric lymphoma also usually have H pylori infection.184Low-grade MALT lymphoma, essentially a monoclonal proliferation of B cells, presumably arises from a background of chronic gastritis associated with H pylori. These relatively innocuous tumors then undergo degeneration to high-grade lymphoma, which is the usual variety seen by the surgeon. Remarkably, when the H pylori is eradicated and the gastritis improves, the low-grade MALT lymphoma often disappears. Thus, low-grade MALT lymphoma is not a surgical lesion. Careful follow-up is necessary particularly in those lesions with a t(11:18) translocation, thought to be a risk factor for a more aggressive MALT lesion. If low-grade lymphoma per-sists after H pylori eradication, radiation should be consid-ered for disease clinically confined to the stomach (stage I), while chemotherapy with or without radiation is used for more advanced lesions (Fig.
|
Surgery_Schwartz_7583
|
Surgery_Schwartz
|
H pylori eradication, radiation should be consid-ered for disease clinically confined to the stomach (stage I), while chemotherapy with or without radiation is used for more advanced lesions (Fig. 26-58).Patients with high-grade gastric lymphoma require aggres-sive oncologic treatment for cure and present with many of the same symptoms as gastric cancer patients. However, systemic symptoms such as fever, weight loss, and night sweats occur in about 50% of patients with gastric lymphoma. The tumors may bleed and/or obstruct. Lymphadenopathy and/or organomegaly suggest systemic disease. Diagnosis is by endoscopy and biopsy. Much of the tumor may be submucosal, and an assiduous attempt at biopsy is necessary. Primary lymphoma is usually nodular with enlarged gastric folds. A diffusely infiltrative pro-cess akin to linitis plastica is more suggestive of secondary gas-tric involvement by lymphoma. A diligent search for extragastric disease is necessary before the diagnosis of localized
|
Surgery_Schwartz. H pylori eradication, radiation should be consid-ered for disease clinically confined to the stomach (stage I), while chemotherapy with or without radiation is used for more advanced lesions (Fig. 26-58).Patients with high-grade gastric lymphoma require aggres-sive oncologic treatment for cure and present with many of the same symptoms as gastric cancer patients. However, systemic symptoms such as fever, weight loss, and night sweats occur in about 50% of patients with gastric lymphoma. The tumors may bleed and/or obstruct. Lymphadenopathy and/or organomegaly suggest systemic disease. Diagnosis is by endoscopy and biopsy. Much of the tumor may be submucosal, and an assiduous attempt at biopsy is necessary. Primary lymphoma is usually nodular with enlarged gastric folds. A diffusely infiltrative pro-cess akin to linitis plastica is more suggestive of secondary gas-tric involvement by lymphoma. A diligent search for extragastric disease is necessary before the diagnosis of localized
|
Surgery_Schwartz_7584
|
Surgery_Schwartz
|
pro-cess akin to linitis plastica is more suggestive of secondary gas-tric involvement by lymphoma. A diligent search for extragastric disease is necessary before the diagnosis of localized primary gastric lymphoma is made. This includes EUS; CT scanning of the chest, abdomen, and pelvis; and bone marrow biopsy. Most patients with high-grade gastric lymphoma are currently treated with chemotherapy and radiation, without surgical resection. Treatment-related perforation or bleeding is an unusual but recognized complication. For disease limited to the stomach and regional nodes, radical subtotal D2 gastrectomy may be performed, especially for bulky tumors with bleeding and/or obstruction. Palliative gastrectomy for tumor complica-tions also has a role. Certainly, a multidisciplinary team should be involved in managing patients with primary gastric lymphoma.Gastrointestinal Stromal TumorGISTs arise from interstitial cells of Cajal (ICC) and are dis-tinct from leiomyoma and
|
Surgery_Schwartz. pro-cess akin to linitis plastica is more suggestive of secondary gas-tric involvement by lymphoma. A diligent search for extragastric disease is necessary before the diagnosis of localized primary gastric lymphoma is made. This includes EUS; CT scanning of the chest, abdomen, and pelvis; and bone marrow biopsy. Most patients with high-grade gastric lymphoma are currently treated with chemotherapy and radiation, without surgical resection. Treatment-related perforation or bleeding is an unusual but recognized complication. For disease limited to the stomach and regional nodes, radical subtotal D2 gastrectomy may be performed, especially for bulky tumors with bleeding and/or obstruction. Palliative gastrectomy for tumor complica-tions also has a role. Certainly, a multidisciplinary team should be involved in managing patients with primary gastric lymphoma.Gastrointestinal Stromal TumorGISTs arise from interstitial cells of Cajal (ICC) and are dis-tinct from leiomyoma and
|
Surgery_Schwartz_7585
|
Surgery_Schwartz
|
team should be involved in managing patients with primary gastric lymphoma.Gastrointestinal Stromal TumorGISTs arise from interstitial cells of Cajal (ICC) and are dis-tinct from leiomyoma and leiomyosarcoma, which arise from smooth muscle.185,186 Prognosis in patients with GIST tumors depends on tumor size, location, and mitotic count. Metasta-sis, when it occurs, is typically by the hematogenous route. Virtually all GISTs should be resected along with a margin of normal tissue. Most GISTs (and almost no smooth muscle tumors) express c-KIT (CD117) or the related PDGF receptor A, as well as CD34; almost all smooth muscle tumors (and almost no GISTs) express actin and desmin. These markers can often be detected on specimens obtained by fine-needle aspiration187 and are useful in differentiating between GIST and smooth muscle tumor histopathologically. Lesions that are definitively leiomyoma by histopathologic criteria can be observed if small and asymptomatic. Larger or symptomatic
|
Surgery_Schwartz. team should be involved in managing patients with primary gastric lymphoma.Gastrointestinal Stromal TumorGISTs arise from interstitial cells of Cajal (ICC) and are dis-tinct from leiomyoma and leiomyosarcoma, which arise from smooth muscle.185,186 Prognosis in patients with GIST tumors depends on tumor size, location, and mitotic count. Metasta-sis, when it occurs, is typically by the hematogenous route. Virtually all GISTs should be resected along with a margin of normal tissue. Most GISTs (and almost no smooth muscle tumors) express c-KIT (CD117) or the related PDGF receptor A, as well as CD34; almost all smooth muscle tumors (and almost no GISTs) express actin and desmin. These markers can often be detected on specimens obtained by fine-needle aspiration187 and are useful in differentiating between GIST and smooth muscle tumor histopathologically. Lesions that are definitively leiomyoma by histopathologic criteria can be observed if small and asymptomatic. Larger or symptomatic
|
Surgery_Schwartz_7586
|
Surgery_Schwartz
|
between GIST and smooth muscle tumor histopathologically. Lesions that are definitively leiomyoma by histopathologic criteria can be observed if small and asymptomatic. Larger or symptomatic gastric leiomyomas are adequately treated by enucleation or wedge resection. Lesions that are definitively GIST or leio-myosarcoma are best treated by resection with negative mar-gins. Most equivocal lesions should be resected provided that the patient has a reasonable operative risk.Two-thirds of all GISTs occur in the stomach and have a more favorable prognosis than do GISTs occurring in other locations. Epithelial cell stromal GIST is the most common cell type arising in the stomach, and cellular spindle type is the next most common. The glomus tumor type is seen only in the stom-ach. Smaller lesions are usually found incidentally, although they occasionally may ulcerate and cause bleeding. Larger lesions may produce symptoms of weight loss, abdominal pain, fullness, early satiety, and
|
Surgery_Schwartz. between GIST and smooth muscle tumor histopathologically. Lesions that are definitively leiomyoma by histopathologic criteria can be observed if small and asymptomatic. Larger or symptomatic gastric leiomyomas are adequately treated by enucleation or wedge resection. Lesions that are definitively GIST or leio-myosarcoma are best treated by resection with negative mar-gins. Most equivocal lesions should be resected provided that the patient has a reasonable operative risk.Two-thirds of all GISTs occur in the stomach and have a more favorable prognosis than do GISTs occurring in other locations. Epithelial cell stromal GIST is the most common cell type arising in the stomach, and cellular spindle type is the next most common. The glomus tumor type is seen only in the stom-ach. Smaller lesions are usually found incidentally, although they occasionally may ulcerate and cause bleeding. Larger lesions may produce symptoms of weight loss, abdominal pain, fullness, early satiety, and
|
Surgery_Schwartz_7587
|
Surgery_Schwartz
|
lesions are usually found incidentally, although they occasionally may ulcerate and cause bleeding. Larger lesions may produce symptoms of weight loss, abdominal pain, fullness, early satiety, and bleeding. An abdominal mass may be palpable. Metastasis is by the hematogenous route, most often to liver.Diagnosis is by endoscopy and biopsy, although the inter-pretation of the latter may be problematic. When performed, a transluminal (i.e., endoscopic) approach to biopsy is preferred to a percutaneous one, to avoid to the potential for fragmenta-tion and peritoneal seeding. A nondiagnostic biopsy does not preclude resection of a suspicious appearing lesion. Metastatic workup entails CT of the abdomen, and pelvis (chest X-ray suf-fices in lieu of CT of the chest for most patients). Most GISTs are solitary. Local resection with clear margins is adequate sur-gical treatment but is sometimes impractical for larger prepy-loric or pyloric channel tumors, or those near the GE junction.
|
Surgery_Schwartz. lesions are usually found incidentally, although they occasionally may ulcerate and cause bleeding. Larger lesions may produce symptoms of weight loss, abdominal pain, fullness, early satiety, and bleeding. An abdominal mass may be palpable. Metastasis is by the hematogenous route, most often to liver.Diagnosis is by endoscopy and biopsy, although the inter-pretation of the latter may be problematic. When performed, a transluminal (i.e., endoscopic) approach to biopsy is preferred to a percutaneous one, to avoid to the potential for fragmenta-tion and peritoneal seeding. A nondiagnostic biopsy does not preclude resection of a suspicious appearing lesion. Metastatic workup entails CT of the abdomen, and pelvis (chest X-ray suf-fices in lieu of CT of the chest for most patients). Most GISTs are solitary. Local resection with clear margins is adequate sur-gical treatment but is sometimes impractical for larger prepy-loric or pyloric channel tumors, or those near the GE junction.
|
Surgery_Schwartz_7588
|
Surgery_Schwartz
|
GISTs are solitary. Local resection with clear margins is adequate sur-gical treatment but is sometimes impractical for larger prepy-loric or pyloric channel tumors, or those near the GE junction. 7Brunicardi_Ch26_p1099-p1166.indd 114901/03/19 7:13 PM 1150SPECIFIC CONSIDERATIONS PART IITrue invasion of adjacent structures by the primary tumor is occasionally seen with larger more aggressive lesions. If safe, en bloc resection of involved surrounding organs is appropriate to remove all tumor.The risk of tumor recurrence or metastasis behavior has been stratified into four groups according to the tumor size and mitotic count.110 Very low risk is defined by size <2 cm and <5 mitoses/50 HPF (high-power field). Low risk is defined by size 2 to 5 cm and <5 mitoses/50 cm. Intermediate risk is defined by size <5 cm and 6 to 10 mitoses/50 HPF or size 5 to 10 cm and >5 mitoses/50 HPF. High risk is defined by size >5 cm and >5 mitoses/50HPF, size >10 cm regardless of mitotic rate or >10
|
Surgery_Schwartz. GISTs are solitary. Local resection with clear margins is adequate sur-gical treatment but is sometimes impractical for larger prepy-loric or pyloric channel tumors, or those near the GE junction. 7Brunicardi_Ch26_p1099-p1166.indd 114901/03/19 7:13 PM 1150SPECIFIC CONSIDERATIONS PART IITrue invasion of adjacent structures by the primary tumor is occasionally seen with larger more aggressive lesions. If safe, en bloc resection of involved surrounding organs is appropriate to remove all tumor.The risk of tumor recurrence or metastasis behavior has been stratified into four groups according to the tumor size and mitotic count.110 Very low risk is defined by size <2 cm and <5 mitoses/50 HPF (high-power field). Low risk is defined by size 2 to 5 cm and <5 mitoses/50 cm. Intermediate risk is defined by size <5 cm and 6 to 10 mitoses/50 HPF or size 5 to 10 cm and >5 mitoses/50 HPF. High risk is defined by size >5 cm and >5 mitoses/50HPF, size >10 cm regardless of mitotic rate or >10
|
Surgery_Schwartz_7589
|
Surgery_Schwartz
|
is defined by size <5 cm and 6 to 10 mitoses/50 HPF or size 5 to 10 cm and >5 mitoses/50 HPF. High risk is defined by size >5 cm and >5 mitoses/50HPF, size >10 cm regardless of mitotic rate or >10 mitoses/50 HPF regardless of size. As mentioned, stomach lesions are associated with lower risk than are tumors in other locations. Classification based on tumor location, size, and mitotic rate have been proposed to evaluate the risk of recurrence and metastasis and role for adjuvant therapy.188 In an effort to further refine risk stratification, a number of nomo-grams have been introduced incorporating tumor features. These tools draw upon and are subject to the limitations of the institu-tional data from which they are derived, but they are sometimes helpful in counseling patients.Mutations in the oncodriver c-kit and PDGFRA are pres-ent in a majority of GISTs. This has been exploited through the use of imatinib (Gleevec), a tyrosine kinase inhibitor. Sev-eral clinical trials in a
|
Surgery_Schwartz. is defined by size <5 cm and 6 to 10 mitoses/50 HPF or size 5 to 10 cm and >5 mitoses/50 HPF. High risk is defined by size >5 cm and >5 mitoses/50HPF, size >10 cm regardless of mitotic rate or >10 mitoses/50 HPF regardless of size. As mentioned, stomach lesions are associated with lower risk than are tumors in other locations. Classification based on tumor location, size, and mitotic rate have been proposed to evaluate the risk of recurrence and metastasis and role for adjuvant therapy.188 In an effort to further refine risk stratification, a number of nomo-grams have been introduced incorporating tumor features. These tools draw upon and are subject to the limitations of the institu-tional data from which they are derived, but they are sometimes helpful in counseling patients.Mutations in the oncodriver c-kit and PDGFRA are pres-ent in a majority of GISTs. This has been exploited through the use of imatinib (Gleevec), a tyrosine kinase inhibitor. Sev-eral clinical trials in a
|
Surgery_Schwartz_7590
|
Surgery_Schwartz
|
in the oncodriver c-kit and PDGFRA are pres-ent in a majority of GISTs. This has been exploited through the use of imatinib (Gleevec), a tyrosine kinase inhibitor. Sev-eral clinical trials in a metastatic disease setting demonstrated marked improvements in median survival from 9 months to greater than 5 years.189 These striking results not only estab-lished imatinib as the primary therapy for metastatic GIST, but they also compelled broader efforts to target solid tumors with small molecule inhibitors. Notably, up to 50% of treated patients develop resistance to imatinib by 2 years, and several Low-grade (indolent) MALTLymphoma persistsStage IIChemo** + XRT*Stage IXRT**XRT: external beam radiation therapy, approximately 30 Gy with 10 Gy boost**Chemo: chemotherapy regimens include chlorambucil, fludarabinel,and cyclosphosphamide, vincristine, prednisone (COP) +/– rituximabClose follow-upNo residual diseaseResidual diseaseFurther chemotherapy*Chemo: chemotherapy regimen usually
|
Surgery_Schwartz. in the oncodriver c-kit and PDGFRA are pres-ent in a majority of GISTs. This has been exploited through the use of imatinib (Gleevec), a tyrosine kinase inhibitor. Sev-eral clinical trials in a metastatic disease setting demonstrated marked improvements in median survival from 9 months to greater than 5 years.189 These striking results not only estab-lished imatinib as the primary therapy for metastatic GIST, but they also compelled broader efforts to target solid tumors with small molecule inhibitors. Notably, up to 50% of treated patients develop resistance to imatinib by 2 years, and several Low-grade (indolent) MALTLymphoma persistsStage IIChemo** + XRT*Stage IXRT**XRT: external beam radiation therapy, approximately 30 Gy with 10 Gy boost**Chemo: chemotherapy regimens include chlorambucil, fludarabinel,and cyclosphosphamide, vincristine, prednisone (COP) +/– rituximabClose follow-upNo residual diseaseResidual diseaseFurther chemotherapy*Chemo: chemotherapy regimen usually
|
Surgery_Schwartz_7591
|
Surgery_Schwartz
|
chlorambucil, fludarabinel,and cyclosphosphamide, vincristine, prednisone (COP) +/– rituximabClose follow-upNo residual diseaseResidual diseaseFurther chemotherapy*Chemo: chemotherapy regimen usually cyclophosphamide,doxorobicin, vincristine, prednisone (CHOP) +/– rituximab**XRT: external beam radiation, approximately 30 Gy with 10 Gy boostFollow-upLymphoma regressionHigh-grade (aggressive)SurgeryStage IVChemo* +/– XRT**Stage I, II, IIIChemo* + XRT**Stage III or IVLymph node involvementt(11:18) translocationConfined to gastric wallNo t(11:18) translocationH pylori eradication therapyand chemo** +/– XRT*H pylori eradication therapyRe-evaluate at 3–6 monthsH pylori eradication therapyRe-evaluate at 12 monthsFigure 26-58. Algorithm for the treatment of gastric lymphoma. MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma, Ann Surg. 2004
|
Surgery_Schwartz. chlorambucil, fludarabinel,and cyclosphosphamide, vincristine, prednisone (COP) +/– rituximabClose follow-upNo residual diseaseResidual diseaseFurther chemotherapy*Chemo: chemotherapy regimen usually cyclophosphamide,doxorobicin, vincristine, prednisone (CHOP) +/– rituximab**XRT: external beam radiation, approximately 30 Gy with 10 Gy boostFollow-upLymphoma regressionHigh-grade (aggressive)SurgeryStage IVChemo* +/– XRT**Stage I, II, IIIChemo* + XRT**Stage III or IVLymph node involvementt(11:18) translocationConfined to gastric wallNo t(11:18) translocationH pylori eradication therapyand chemo** +/– XRT*H pylori eradication therapyRe-evaluate at 3–6 monthsH pylori eradication therapyRe-evaluate at 12 monthsFigure 26-58. Algorithm for the treatment of gastric lymphoma. MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma, Ann Surg. 2004
|
Surgery_Schwartz_7592
|
Surgery_Schwartz
|
MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma, Ann Surg. 2004 Jul;240(1):28-37.)Brunicardi_Ch26_p1099-p1166.indd 115001/03/19 7:13 PM 1151STOMACHCHAPTER 26second-line agents have been utilized for patients with refrac-tory disease, most notable sunitinib.The efficacy of imatinib as adjuvant therapy for high risk GIST has been demonstrated in two randomized clinical trials, ACOSOG Z9001 and SSG XVIII.190,191 The former trial randomized patients to 1 year of adjuvant imatinib or pla-cebo and showed an improvement in recurrence-free survival with imatinib. The latter trial demonstrated an overall survival advantage with 3 years compared to 1 year of therapy. Imatinib is now recommended in high risk groups as an adjuvant therapy, for three years or longer. Preoperative therapy with imatinib may be indicated in selected patients with larger lesions
|
Surgery_Schwartz. MALT = mucosa-associated lymphoid tissue. (Reproduced with permission from Yoon SS, Coit DG, Portlock CS, et al. The diminishing role of surgery in the treatment of gastric lymphoma, Ann Surg. 2004 Jul;240(1):28-37.)Brunicardi_Ch26_p1099-p1166.indd 115001/03/19 7:13 PM 1151STOMACHCHAPTER 26second-line agents have been utilized for patients with refrac-tory disease, most notable sunitinib.The efficacy of imatinib as adjuvant therapy for high risk GIST has been demonstrated in two randomized clinical trials, ACOSOG Z9001 and SSG XVIII.190,191 The former trial randomized patients to 1 year of adjuvant imatinib or pla-cebo and showed an improvement in recurrence-free survival with imatinib. The latter trial demonstrated an overall survival advantage with 3 years compared to 1 year of therapy. Imatinib is now recommended in high risk groups as an adjuvant therapy, for three years or longer. Preoperative therapy with imatinib may be indicated in selected patients with larger lesions
|
Surgery_Schwartz_7593
|
Surgery_Schwartz
|
Imatinib is now recommended in high risk groups as an adjuvant therapy, for three years or longer. Preoperative therapy with imatinib may be indicated in selected patients with larger lesions that may be more difficult to completely resect or require multivis-ceral resection.Molecular profiling has been embraced with growing rec-ognition that specific tumor subtypes are insensitive to imatinib. Patients with PDGFRA D842V mutations, for example, do not respond to imatinib.192 Management of metastatic GIST is prin-cipally medical, but surgery has a selected role. An algorithm for the treatment of patients with metastatic GIST is shown in Fig. 26-59.Gastric Neuroendocrine Tumors193,194Compared to neuroendocrine tumors of the midgut and hind-gut, neuroendcorine tumors of the stomach are rare. Gastric neuroendocrine tumors comprise about 1% of all neuroen-docrine tumors and less than 2% of gastric neoplasms. They arise from gastric enterochromaffin-like (ECL) cells and may have malignant
|
Surgery_Schwartz. Imatinib is now recommended in high risk groups as an adjuvant therapy, for three years or longer. Preoperative therapy with imatinib may be indicated in selected patients with larger lesions that may be more difficult to completely resect or require multivis-ceral resection.Molecular profiling has been embraced with growing rec-ognition that specific tumor subtypes are insensitive to imatinib. Patients with PDGFRA D842V mutations, for example, do not respond to imatinib.192 Management of metastatic GIST is prin-cipally medical, but surgery has a selected role. An algorithm for the treatment of patients with metastatic GIST is shown in Fig. 26-59.Gastric Neuroendocrine Tumors193,194Compared to neuroendocrine tumors of the midgut and hind-gut, neuroendcorine tumors of the stomach are rare. Gastric neuroendocrine tumors comprise about 1% of all neuroen-docrine tumors and less than 2% of gastric neoplasms. They arise from gastric enterochromaffin-like (ECL) cells and may have malignant
|
Surgery_Schwartz_7594
|
Surgery_Schwartz
|
Gastric neuroendocrine tumors comprise about 1% of all neuroen-docrine tumors and less than 2% of gastric neoplasms. They arise from gastric enterochromaffin-like (ECL) cells and may have malignant potential. The apparent incidence of gastric neuroendocrine tumors is increasing, perhaps related to increased detection or the increasing use of acid suppres-sive medication. The latter may cause hypergastrinemia, and gastrin has a recognized trophic effect on gastric ECL cells. Nomenclature remains a point of confusion; carcinoid and well-differentiated neuroendocrine tumor (NET) are synony-mous according to WHO classification.Gastric neuroendocrine tumors are classified into one of three different types. Type I is the most common, account-ing for about 75% of cases. Type I lesions occur in patients with chronic hypergastrinemia secondary to pernicious anemia or atrophic gastritis. These lesions occur more frequently in women, are often multiple and small, and have low malignant potential
|
Surgery_Schwartz. Gastric neuroendocrine tumors comprise about 1% of all neuroen-docrine tumors and less than 2% of gastric neoplasms. They arise from gastric enterochromaffin-like (ECL) cells and may have malignant potential. The apparent incidence of gastric neuroendocrine tumors is increasing, perhaps related to increased detection or the increasing use of acid suppres-sive medication. The latter may cause hypergastrinemia, and gastrin has a recognized trophic effect on gastric ECL cells. Nomenclature remains a point of confusion; carcinoid and well-differentiated neuroendocrine tumor (NET) are synony-mous according to WHO classification.Gastric neuroendocrine tumors are classified into one of three different types. Type I is the most common, account-ing for about 75% of cases. Type I lesions occur in patients with chronic hypergastrinemia secondary to pernicious anemia or atrophic gastritis. These lesions occur more frequently in women, are often multiple and small, and have low malignant potential
|
Surgery_Schwartz_7595
|
Surgery_Schwartz
|
with chronic hypergastrinemia secondary to pernicious anemia or atrophic gastritis. These lesions occur more frequently in women, are often multiple and small, and have low malignant potential (<5% metastasize). The role of long-term acid sup-pression with resultant hypergastrinemia in the pathogenesis of type I gastric carcinoids is unclear. Type II gastric neuroendo-crine tumors are associated with MEN1 and ZES. These lesions also tend to be small and multiple, but they have a somewhat higher malignant potential than type I lesions (10% metasta-size). Type II lesions are more common in the setting of MEN1; they are quite uncommon in patients with sporadic ZES. The constellation of gastric acidity, hypergastrinemia, and gastric neuroendocrine tumors suggests gastrinoma until proven other-wise. Type III gastric neuroendocrine tumors are sporadic. They are most often solitary (usually >2 cm) and occur more com-monly in men. They are not associated with hypergastrinemia. Most patients
|
Surgery_Schwartz. with chronic hypergastrinemia secondary to pernicious anemia or atrophic gastritis. These lesions occur more frequently in women, are often multiple and small, and have low malignant potential (<5% metastasize). The role of long-term acid sup-pression with resultant hypergastrinemia in the pathogenesis of type I gastric carcinoids is unclear. Type II gastric neuroendo-crine tumors are associated with MEN1 and ZES. These lesions also tend to be small and multiple, but they have a somewhat higher malignant potential than type I lesions (10% metasta-size). Type II lesions are more common in the setting of MEN1; they are quite uncommon in patients with sporadic ZES. The constellation of gastric acidity, hypergastrinemia, and gastric neuroendocrine tumors suggests gastrinoma until proven other-wise. Type III gastric neuroendocrine tumors are sporadic. They are most often solitary (usually >2 cm) and occur more com-monly in men. They are not associated with hypergastrinemia. Most patients
|
Surgery_Schwartz_7596
|
Surgery_Schwartz
|
Type III gastric neuroendocrine tumors are sporadic. They are most often solitary (usually >2 cm) and occur more com-monly in men. They are not associated with hypergastrinemia. Most patients have regional nodal or distant metastases at the time of diagnosis, and some present with symptoms of carcinoid syndrome.Gastric neuroendocrine tumors are usually diagnosed with endoscopy and biopsy. The type can be determined based upon clinical context, patient history, the presence or absence of atro-phic gastric mucosa, gastric pH and gastrin level. Some tumors are submucosal and may be quite small. They are often confused with heterotopic pancreas or small leiomyomas. Biopsy may be difficult because of the submucosal location, and EUS can be helpful in defining the size and depth of the lesion. Plasma 8Metastatic or recurrent GISTRepeat imaging in 1 to 3 monthsResponsive/Stable diseaseResectableConsidersurgeryContinueimatinibUnresectableConsidersurgeryDose escalation toimatinib 400 mg
|
Surgery_Schwartz. Type III gastric neuroendocrine tumors are sporadic. They are most often solitary (usually >2 cm) and occur more com-monly in men. They are not associated with hypergastrinemia. Most patients have regional nodal or distant metastases at the time of diagnosis, and some present with symptoms of carcinoid syndrome.Gastric neuroendocrine tumors are usually diagnosed with endoscopy and biopsy. The type can be determined based upon clinical context, patient history, the presence or absence of atro-phic gastric mucosa, gastric pH and gastrin level. Some tumors are submucosal and may be quite small. They are often confused with heterotopic pancreas or small leiomyomas. Biopsy may be difficult because of the submucosal location, and EUS can be helpful in defining the size and depth of the lesion. Plasma 8Metastatic or recurrent GISTRepeat imaging in 1 to 3 monthsResponsive/Stable diseaseResectableConsidersurgeryContinueimatinibUnresectableConsidersurgeryDose escalation toimatinib 400 mg
|
Surgery_Schwartz_7597
|
Surgery_Schwartz
|
Plasma 8Metastatic or recurrent GISTRepeat imaging in 1 to 3 monthsResponsive/Stable diseaseResectableConsidersurgeryContinueimatinibUnresectableConsidersurgeryDose escalation toimatinib 400 mg bidSunitinibRegorafenibClinical trialUnifocalMultifocalProgressive diseaseImatinib 400 mg four times a day in all KIT, non-D842V PDGFRA mutations,and WT GIST Consider 400 mg twice a day in exon 9 KIT mutationsConsider clinical trial in PDGFRA D842V mutationsFigure 26-59. Algorithm for the treatment of malignant gastrointestinal stromal tumor. (Reproduced with permission from Balachandran VP, DeMatteo RP: Gastrointestinal stromal tumors: who should get imatinib and for how long? Adv Surg. 2014;48:165-183.)Brunicardi_Ch26_p1099-p1166.indd 115101/03/19 7:13 PM 1152SPECIFIC CONSIDERATIONS PART IIchromogranin A levels are frequently elevated. CT scan and octreotide or gallium dotatate scans are useful for staging.Type I and II patients with numerous diminutive lesions can be followed with
|
Surgery_Schwartz. Plasma 8Metastatic or recurrent GISTRepeat imaging in 1 to 3 monthsResponsive/Stable diseaseResectableConsidersurgeryContinueimatinibUnresectableConsidersurgeryDose escalation toimatinib 400 mg bidSunitinibRegorafenibClinical trialUnifocalMultifocalProgressive diseaseImatinib 400 mg four times a day in all KIT, non-D842V PDGFRA mutations,and WT GIST Consider 400 mg twice a day in exon 9 KIT mutationsConsider clinical trial in PDGFRA D842V mutationsFigure 26-59. Algorithm for the treatment of malignant gastrointestinal stromal tumor. (Reproduced with permission from Balachandran VP, DeMatteo RP: Gastrointestinal stromal tumors: who should get imatinib and for how long? Adv Surg. 2014;48:165-183.)Brunicardi_Ch26_p1099-p1166.indd 115101/03/19 7:13 PM 1152SPECIFIC CONSIDERATIONS PART IIchromogranin A levels are frequently elevated. CT scan and octreotide or gallium dotatate scans are useful for staging.Type I and II patients with numerous diminutive lesions can be followed with
|
Surgery_Schwartz_7598
|
Surgery_Schwartz
|
A levels are frequently elevated. CT scan and octreotide or gallium dotatate scans are useful for staging.Type I and II patients with numerous diminutive lesions can be followed with serial endoscopy. Small lesions con-fined to the mucosa (typically type I or type II lesions) less than 1 cm may be treated endoscopically with EMR if there are only a few lesions (<5). Occasionally a slightly larger lesion (1–2 cm) necessitate local surgical excision. Larger lesions and type III lesions should be removed by D1 or D2 gastrectomy. Antrectomy to mitigate gastric secretion in type I patients with refractory growing lesions was invoked as a viable treatment strategy in the past, but it is rarely indicated.Survival is excellent for node-negative patients (>90% 5-year survival); node-positive patients have a 50% 5-year sur-vival. Gastrinoma should be resected if located in patients with type II carcinoid. The 5-year survival for patients with type I gastric carcinoid is close to 100%; for
|
Surgery_Schwartz. A levels are frequently elevated. CT scan and octreotide or gallium dotatate scans are useful for staging.Type I and II patients with numerous diminutive lesions can be followed with serial endoscopy. Small lesions con-fined to the mucosa (typically type I or type II lesions) less than 1 cm may be treated endoscopically with EMR if there are only a few lesions (<5). Occasionally a slightly larger lesion (1–2 cm) necessitate local surgical excision. Larger lesions and type III lesions should be removed by D1 or D2 gastrectomy. Antrectomy to mitigate gastric secretion in type I patients with refractory growing lesions was invoked as a viable treatment strategy in the past, but it is rarely indicated.Survival is excellent for node-negative patients (>90% 5-year survival); node-positive patients have a 50% 5-year sur-vival. Gastrinoma should be resected if located in patients with type II carcinoid. The 5-year survival for patients with type I gastric carcinoid is close to 100%; for
|
Surgery_Schwartz_7599
|
Surgery_Schwartz
|
patients have a 50% 5-year sur-vival. Gastrinoma should be resected if located in patients with type II carcinoid. The 5-year survival for patients with type I gastric carcinoid is close to 100%; for patients with type III lesions, the 5-year survival is less than 50%. Somatostatin ana-logue therapy may delay progression of metastatic disease. Sur-gical debulking may have a role in selected patients with limited metastatic disease.BENIGN GASTRIC NEOPLASMSLeiomyomaThe typical leiomyoma is submucosal and firm. If ulcerated, it has an umbilicated appearance and may bleed. Histologically, these lesions appear to be of smooth muscle origin. Lesions <2 cm are usually asymptomatic and benign. Larger lesions may cause symptoms such as bleeding, obstruction, or pain. Asymp-tomatic lesions <2 cm may be carefully observed or enucleated if fine-needle aspiration and immune markers confirm smooth muscle tumor; larger lesions and symptomatic lesions should be removed by wedge resection (often
|
Surgery_Schwartz. patients have a 50% 5-year sur-vival. Gastrinoma should be resected if located in patients with type II carcinoid. The 5-year survival for patients with type I gastric carcinoid is close to 100%; for patients with type III lesions, the 5-year survival is less than 50%. Somatostatin ana-logue therapy may delay progression of metastatic disease. Sur-gical debulking may have a role in selected patients with limited metastatic disease.BENIGN GASTRIC NEOPLASMSLeiomyomaThe typical leiomyoma is submucosal and firm. If ulcerated, it has an umbilicated appearance and may bleed. Histologically, these lesions appear to be of smooth muscle origin. Lesions <2 cm are usually asymptomatic and benign. Larger lesions may cause symptoms such as bleeding, obstruction, or pain. Asymp-tomatic lesions <2 cm may be carefully observed or enucleated if fine-needle aspiration and immune markers confirm smooth muscle tumor; larger lesions and symptomatic lesions should be removed by wedge resection (often
|
Surgery_Schwartz_7600
|
Surgery_Schwartz
|
cm may be carefully observed or enucleated if fine-needle aspiration and immune markers confirm smooth muscle tumor; larger lesions and symptomatic lesions should be removed by wedge resection (often possible laparoscopically). When lesions thought to be leiomyoma are observed rather than resected, the patient should be made aware of their presence and the small possibility for malignancy.LipomaLipomas are benign submucosal fatty tumors that are usually asymptomatic, found incidentally on upper GI series or EGD. Endoscopically, they have a characteristic appearance; there also is a characteristic appearance on EUS. Excision is unnec-essary unless the patient is symptomatic.GastroparesisGastric motility disorders include delayed gastric emptying (gastroparesis), rapid gastric emptying, and motor and sensory abnormalities (e.g., functional dyspepsia). Surgically relevant secondary disorders of gastric motility (e.g., dumping, gastric stasis, and Roux syndrome) are discussed under
|
Surgery_Schwartz. cm may be carefully observed or enucleated if fine-needle aspiration and immune markers confirm smooth muscle tumor; larger lesions and symptomatic lesions should be removed by wedge resection (often possible laparoscopically). When lesions thought to be leiomyoma are observed rather than resected, the patient should be made aware of their presence and the small possibility for malignancy.LipomaLipomas are benign submucosal fatty tumors that are usually asymptomatic, found incidentally on upper GI series or EGD. Endoscopically, they have a characteristic appearance; there also is a characteristic appearance on EUS. Excision is unnec-essary unless the patient is symptomatic.GastroparesisGastric motility disorders include delayed gastric emptying (gastroparesis), rapid gastric emptying, and motor and sensory abnormalities (e.g., functional dyspepsia). Surgically relevant secondary disorders of gastric motility (e.g., dumping, gastric stasis, and Roux syndrome) are discussed under
|
Surgery_Schwartz_7601
|
Surgery_Schwartz
|
and motor and sensory abnormalities (e.g., functional dyspepsia). Surgically relevant secondary disorders of gastric motility (e.g., dumping, gastric stasis, and Roux syndrome) are discussed under Postgastrec-tomy Problems. Gastroparesis is the most surgically relevant primary disorder of gastric motility.195,196Most patients with primary gastroparesis present with nausea, vomiting, bloating, early satiety, and/or abdominal pain. Eighty percent of these patients are women; some are diabetic. Postprandial vomiting significantly complicates the management of blood glucose in the latter group, predispos-ing to hypoglycemia following preprandial insulin. In patients with gastroparesis, it is important to rule out mechanical gastric outlet obstruction, and small-bowel obstruction. An upper GI series may suggest slow gastric emptying and relative atony, 9or it may be normal. EGD may show bezoars or retained food but is frequently normal. Gastric emptying scintigraphy shows delayed solid
|
Surgery_Schwartz. and motor and sensory abnormalities (e.g., functional dyspepsia). Surgically relevant secondary disorders of gastric motility (e.g., dumping, gastric stasis, and Roux syndrome) are discussed under Postgastrec-tomy Problems. Gastroparesis is the most surgically relevant primary disorder of gastric motility.195,196Most patients with primary gastroparesis present with nausea, vomiting, bloating, early satiety, and/or abdominal pain. Eighty percent of these patients are women; some are diabetic. Postprandial vomiting significantly complicates the management of blood glucose in the latter group, predispos-ing to hypoglycemia following preprandial insulin. In patients with gastroparesis, it is important to rule out mechanical gastric outlet obstruction, and small-bowel obstruction. An upper GI series may suggest slow gastric emptying and relative atony, 9or it may be normal. EGD may show bezoars or retained food but is frequently normal. Gastric emptying scintigraphy shows delayed solid
|
Subsets and Splits
No community queries yet
The top public SQL queries from the community will appear here once available.