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Surgery_Schwartz. it has been argued that a “normal” fasting gastrin level in these patients is inappropriately high, and that there is an impaired feedback mechanism, especially in light of the apparently increased sensitivity of the parietal cell mass to gastrin. Many of these long-standing observations now seem reasonable in light of recently gained understanding of the perturbations in acid and gastrin secretion associated with H pylori infection. Some patients with duodenal ulcer also have increased rates of gastric emptying that deliver an increased acid load per unit of time to the duodenum. Finally, the buffering capacity of the duodenum in many patients with duodenal ulcer is compromised due to decreased duodenal bicarbonate secretion and duodenal gastric metaplasia.In patients with gastric ulcer, acid secretion is vari-able. Currently, five types of gastric ulcer are described, although the original Johnson classification contained three types (Fig. 26-30).96 The most common, Johnson type I


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Surgery_Schwartz. acid secretion is vari-able. Currently, five types of gastric ulcer are described, although the original Johnson classification contained three types (Fig. 26-30).96 The most common, Johnson type I gas-tric ulcer, is typically located near the angularis incisura on the lesser curvature, close to the border between antral and corpus mucosa. Patients with type I gastric ulcer usually have normal or decreased acid secretion. Type II gastric ulcer is associ-ated with active or quiescent duodenal ulcer disease, and type III gastric ulcer is prepyloric ulcer disease. Both type II and type III gastric ulcers are associated with normal or increased gastric acid secretion and surgically are treated similar to duode-nal ulcer. Type IV gastric ulcers occur near the GE junction, and acid secretion is normal or below normal. Type V gastric ulcers are medication induced and may occur anywhere in the stomach. Patients with gastric ulcers may have weak mucosal defenses that permit an abnormal amount


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Surgery_Schwartz. normal or below normal. Type V gastric ulcers are medication induced and may occur anywhere in the stomach. Patients with gastric ulcers may have weak mucosal defenses that permit an abnormal amount of injurious acid back-diffusion into the mucosa. Duodenogastric reflux may play a role in weakening the gastric mucosal defenses, and a variety of components in duodenal juice, including bile, lysolecithin, and pancreatic juice, have been shown to cause injury and inflam-mation in the gastric mucosa. NSAIDs and aspirin have similar effects. Although chronic gastric ulcer usually is associated with surrounding gastritis, it is unproven that the latter leads to the former.Nonsteroidal Anti-Inflammatory Drugs in Peptic Ulcer Disease. Chronic use of NSAIDs (including aspirin) increases the risk of peptic ulcer disease about fivefold and upper GI bleeding at least twofold.97-100 Complications of PUD (specifi-cally hemorrhage and perforation) are much more common in patients taking NSAIDs. More


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Surgery_Schwartz. peptic ulcer disease about fivefold and upper GI bleeding at least twofold.97-100 Complications of PUD (specifi-cally hemorrhage and perforation) are much more common in patients taking NSAIDs. More than half of patients who present with peptic ulcer hemorrhage or perforation report the recent use of NSAIDs, including aspirin. Many of these patients remain asymptomatic until they develop these life-threatening complications.Figure 26-29. Frequency of physiologic abnormali-ties in patients with duodenal ulcer (DU). HCO3 = bicarbonate; MAO = maximal acid output. (Reproduced with permission from Yamada T, Alpers DH, Laine L, et al: Textbook of Gastroenterology, 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)2550751000Approximate % of DU patientsPathophysiologic abnormalities in DUvary in frequencyNocturnal acid secretionpH inhibition of gastrin releaseGastric emptyingPentagastrin-stimulated MAODaytime acid secretionDuodenal acid loadDuodenal HCO3 secretionFigure


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Surgery_Schwartz. in DUvary in frequencyNocturnal acid secretionpH inhibition of gastrin releaseGastric emptyingPentagastrin-stimulated MAODaytime acid secretionDuodenal acid loadDuodenal HCO3 secretionFigure 26-28. “Causes” of peptic ulcer disease. Z.E. = Zollinger-Ellison syndrome. (Data from Graham DY, Lew GM, Klein PD, et al. Effect of treatment of Helicobacter pylori infec-tion on the long-term recurrence of gas-tric or duodenal ulcer. A randomized, controlled study, Ann Intern Med. 1992 May 1;116(9):705-708.)Conditions associated with peptic ulcerNSAIDuseNone knownZ.E., otherH. pyloriinfectionNSAIDuseNone knownZ.E., otherH. pyloriinfectionDuodenalGastricBrunicardi_Ch26_p1099-p1166.indd 112201/03/19 7:12 PM 1123STOMACHCHAPTER 26The overall risk of significant serious adverse GI events in patients taking NSAIDs is more than three times that of con-trols (Table 26-6). This risk increases to five times in patients more than age 60 years old. In elderly patients taking NSAIDs, the likelihood that


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Surgery_Schwartz. taking NSAIDs is more than three times that of con-trols (Table 26-6). This risk increases to five times in patients more than age 60 years old. In elderly patients taking NSAIDs, the likelihood that they will require an operation related to a GI complication is 10 times that of the control group, and the risk that they will die from a GI cause is about four and one-half times higher. This problem is put into perspective when one realizes that approximately 20 million patients in the United States take NSAIDs on a regular basis; perhaps even more regularly take aspirin. Persons who take NSAIDs also have a higher hospitalization rate for serious GI events than those who do not.Factors that clearly put patients at increased risk for NSAID-induced GI complications include age >60, prior GI event, high NSAID dose, concurrent steroid intake, and con-current anticoagulant intake. Proton pump inhibitors have been shown to significantly decrease upper GI bleeding risk in patients on chronic


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Surgery_Schwartz. event, high NSAID dose, concurrent steroid intake, and con-current anticoagulant intake. Proton pump inhibitors have been shown to significantly decrease upper GI bleeding risk in patients on chronic warfarin, low dose aspirin, and/or antiplate-let agents.101-103 ANY patient taking NSAIDs or aspirin who has one or more of these risk factors should receive concomitant acid suppressive medication,104 preferably PPI (Table 26-7). High-dose H2 blockers have been shown to be somewhat less effective than PPIs in preventing GI complications in these high-risk patients on antiplatelet therapy, but clearly, they are better than no acid suppression.105Smoking, Stress, and Other Factors. Epidemiologic studies suggest that smokers are about twice as likely to develop PUD as nonsmokers. Smoking increases gastric acid secretion and duodenogastric reflux. Smoking decreases both gastroduodenal prostaglandin production and pancreaticoduodenal bicarbonate production. These observations may be related,


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Surgery_Schwartz. gastric acid secretion and duodenogastric reflux. Smoking decreases both gastroduodenal prostaglandin production and pancreaticoduodenal bicarbonate production. These observations may be related, and any or all could explain the observed association between smoking and PUD.Although difficult to measure, both physiologic and psy-chologic stress undoubtedly play a role in the development of peptic ulcer in some patients.106 In 1842, Curling described duodenal ulcer and/or duodenitis in burn patients. Decades later, Cushing described the appearance of acute peptic ulcer-ation in patients with head trauma (Cushing’s ulcer). Even the ancients recognized the undeniable links between PUD and stress. Patients still present with ulcer complications (bleeding, perforation, and obstruction) that are seemingly exacerbated by stressful life events. The use of crack cocaine has been linked to juxtapyloric peptic ulcers with a propensity to perforate. Alco-hol is commonly mentioned as a risk factor


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Surgery_Schwartz. seemingly exacerbated by stressful life events. The use of crack cocaine has been linked to juxtapyloric peptic ulcers with a propensity to perforate. Alco-hol is commonly mentioned as a risk factor for PUD, but con-firmatory data are lacking.Clinical ManifestationsMore than 90% of patients with PUD complain of abdominal pain. The pain is typically nonradiating, burning in quality, and located in the epigastrium. The mechanism of the pain is unclear. Patients with duodenal ulcer often experience pain 2 to 3 hours after a meal and at night. Two-thirds of patients with duodenal ulcers will complain of pain that awakens them from sleep. The pain of gastric ulcer more commonly occurs with eating and is less likely to awaken the patient at night. A history of PUD, use of NSAIDs, over-the-counter antacids, or antisecretory drugs is suggestive of the diagnosis. Other signs and symptoms include nausea, bloating, weight loss, stool positive for occult blood, and anemia. Duodenal ulcer is about


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Surgery_Schwartz. antacids, or antisecretory drugs is suggestive of the diagnosis. Other signs and symptoms include nausea, bloating, weight loss, stool positive for occult blood, and anemia. Duodenal ulcer is about twice as common in men compared to women, but the incidence of gastric ulcer is similar in men and women. On average, gastric ulcer patients are older than duodenal ulcer patients, and the incidence is increasing in the elderly, perhaps because of increasing NSAID and aspirin.DiagnosisIn the young patient with dyspepsia and without alarm symp-toms, it may be appropriate to initiate empirical PPI therapy for PUD without upper endoscopy or upper GI series. NSAIDs and aspirin should be stopped if the patient is taking these drugs, and Helicobacter should be ruled out with testing and treated if pres-ent. It is prudent to discuss with the patient the small possibility of an alternative diagnosis, including malignancy, even if symp-toms improve with the initiation of empiric therapy. Patients


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Surgery_Schwartz. pres-ent. It is prudent to discuss with the patient the small possibility of an alternative diagnosis, including malignancy, even if symp-toms improve with the initiation of empiric therapy. Patients with persistent dyspepsia, and those who cannot stop NSAIDs or aspirin for health reasons should have an upper endoscopy, and all patients, regardless of age, should have this study if any alarm symptoms (see Table 26-5) are present. A double-contrast upper GI X-ray study may be useful. Once an ulcer has been confirmed endoscopically or radiologically, obvious possible causes (Helicobacter, NSAIDs, gastrinoma, cancer) should always be considered. All gastric ulcers should be adequately biopsied, and any sites of gastritis should be biopsied to rule out H pylori, and for histologic evaluation. Additional testing for H pylori may be indicated. It is reasonable to test all peptic IIIIIIIVVNSAID-inducedAcid hypersecretionFigure 26-30. Modified Johnson classification for gastric ulcer. I.


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Surgery_Schwartz. Additional testing for H pylori may be indicated. It is reasonable to test all peptic IIIIIIIVVNSAID-inducedAcid hypersecretionFigure 26-30. Modified Johnson classification for gastric ulcer. I. Lesser curve, incisura. II. Body of stomach, incisura + duodenal ulcer (active or healed). III. Prepyloric. IV. High on lesser curve, near gastroesophageal junction. V. Medication-induced (NSAID/acetylsalicylic acid), anywhere in stomach. (Reproduced with permission from Cameron JL: Current Surgical Therapy, 9th ed. Philadelphia, PA: Elsevier/Mosby; 2008.)Brunicardi_Ch26_p1099-p1166.indd 112301/03/19 7:12 PM 1124SPECIFIC CONSIDERATIONS PART IIulcer patients and those with nonulcer dyspepsia for H pylori (Table 26-8). A baseline serum gastrin level to rule out gastri-noma should be considered if the peptic ulcer is unusual (distal duodenal or jejunal) or if the patient is Helicobacter and NSAID negative.ComplicationsThe three most common complications of PUD, in decreas-ing order of


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Surgery_Schwartz. if the peptic ulcer is unusual (distal duodenal or jejunal) or if the patient is Helicobacter and NSAID negative.ComplicationsThe three most common complications of PUD, in decreas-ing order of frequency, are bleeding, perforation, and obstruction.92,94,107 Most peptic ulcer–related deaths in the United States are due to bleeding. Inhospital mortality and length of stay can be predicted by the AIMS65 score,108 with a score of 0 predicting negligible mortality and a score of 5 predicting a 30% inhospital mortality. Bleeding peptic ulcers are by far the most common cause of upper GI bleeding in patients admitted to a hospital (Fig. 26-31).109,110 Patients with a bleeding peptic ulcer typically present with melena and/or hematemesis. Naso-gastric aspiration is usually confirmatory of upper GI bleeding. Abdominal pain is quite uncommon. Shock may be present, necessitating aggressive resuscitation and blood transfusion. Table 26-7Patients taking NSAIDs or aspirin need concomitant acid


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Surgery_Schwartz. GI bleeding. Abdominal pain is quite uncommon. Shock may be present, necessitating aggressive resuscitation and blood transfusion. Table 26-7Patients taking NSAIDs or aspirin need concomitant acid suppressing medication if any of the following risk factors are present• Age over 60 years• History of acid/peptic disease• Concurrent steroid intake• Concurrent anticoagulant intake• High-dose or chronic NSAID use• High-dose or chronic aspirin use >325 mg/dayTable 26-8Indications for diagnosis and treatment of Helicobacter pyloriEstablished• Active peptic ulcer disease (gastric or duodenal ulcer)• Confirmed history of peptic ulcer disease (not previously treated for H pylori)• Gastric mucosa-associated lymphoid tissue lymphoma (low grade)• After endoscopic resection of early gastric cancer• Uninvestigated dyspepsia (depending on H pylori prevalence)Controversial• Nonulcer dyspepsia• Gastroesophageal reflux disease• Persons using NSAIDs• Unexplained iron deficiency anemia• Populations at


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Surgery_Schwartz. dyspepsia (depending on H pylori prevalence)Controversial• Nonulcer dyspepsia• Gastroesophageal reflux disease• Persons using NSAIDs• Unexplained iron deficiency anemia• Populations at higher risk for gastric cancerReproduced with permission from Chey WD, Wong BC; Practice Parameters Committee of the American College of Gastroenterology: American College of Gastroenterology guideline on the management of Helicobacter pylori infection, Am J Gastroenterol. 2007 Aug;102(8):1808-1825.Table 26-6Hospitalization rates for GI events with and without NSAID use in selected large populationsANNUALIZED INCIDENCEb THERAPIES USEDCLINICAL UPPER GI EVENTScCOMPLICATED UPPER GI EVENTSdSTUDYaNSAID CONTROLSTUDY DRUGSCONTROLSTUDY DRUGCONTROLSTUDY DRUGMUCOSANSAIDs (n = 4439)Misoprostol 200 μg four times a day + NSAID (n = 4404)3.1%1.6%1.5%0.7%CLASSIbuprofen 800 mg three times a day, diclofenac 75 mg twice a day (n = 3987)Celecoxib 400 mg twice a day (n = 3995)3.5%2.1%1.5%0.8% (No aspirine:


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Surgery_Schwartz. times a day + NSAID (n = 4404)3.1%1.6%1.5%0.7%CLASSIbuprofen 800 mg three times a day, diclofenac 75 mg twice a day (n = 3987)Celecoxib 400 mg twice a day (n = 3995)3.5%2.1%1.5%0.8% (No aspirine: 2.9%)1.4%1.3%0.4%VIGORNaproxen 500 mg twice a day (n = 4047)Rofecoxib 50 mg four times a day (n = 4029)4.5%2.1%1.4%0.6%aMUCOSA and VIGOR trials included only rheumatoid arthritis patients; CLASS trial included osteoarthritis (73%) and rheumatoid arthritis (27%).bIncidence for MUCOSA trial represents doubling of results provided at 6 months (although median follow-up was <6 months). Incidences for VIGOR and CLASS trials represent rates per 100 patient-years, although VIGOR median follow-up was 9 months, and CLASS data include only the first 6 months of the study.cIncludes perforations, obstructions, bleeding, and uncomplicated ulcers discovered on clinically indicated work-up.dIncludes perforation, obstruction, bleeding (documented due to ulcer or erosions in MUCOSA and CLASS; major


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Surgery_Schwartz. bleeding, and uncomplicated ulcers discovered on clinically indicated work-up.dIncludes perforation, obstruction, bleeding (documented due to ulcer or erosions in MUCOSA and CLASS; major bleeding in VIGOR).e21% of patients in CLASS study were taking low-dose aspirin.Note: All differences between controls and study drugs were significant except clinical upper GI events in overall CLASS study (P = .09).Reproduced with permission from Laine L: Approaches to nonsteroidal anti-inflammatory drug use in the high-risk patient, Gastroenterology 2001 Feb;120(3):594-606.Brunicardi_Ch26_p1099-p1166.indd 112401/03/19 7:12 PM 1125STOMACHCHAPTER 26Early endoscopy is important to diagnose the cause of the bleed-ing and to assess the need for hemostatic therapy.Three-fourths of the patients who come to the hospital with bleeding peptic ulcer will stop bleeding if given acid sup-pression and nothing by mouth. However, one fourth will con-tinue to bleed or will rebleed after an initial quiescent


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Surgery_Schwartz. to the hospital with bleeding peptic ulcer will stop bleeding if given acid sup-pression and nothing by mouth. However, one fourth will con-tinue to bleed or will rebleed after an initial quiescent period, and virtually all the mortalities (and all the operations for bleeding) occur in this group. This group can be fairly well delineated based on clinical factors related to the magnitude of the hemorrhage, comorbidities, age, and endoscopic find-ings. Shock, hematemesis, transfusion requirement exceeding four units in 24 hours, and certain endoscopic stigmata (active bleeding or visible vessel) define this high-risk group. Risk stratification tools have proven useful in predicting rebleed-ing and death, and in identifying a low risk cohort. As can be seen in Table 26-9, the maximal Blatchford score is 23, and the maximal Rockall score is 11. The former does not use endoscopic criteria and may be better in identifying the low-risk cohort. Studies have shown that a Blatchford score of 1


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Surgery_Schwartz. score is 23, and the maximal Rockall score is 11. The former does not use endoscopic criteria and may be better in identifying the low-risk cohort. Studies have shown that a Blatchford score of 1 or less, or a Rockall score of 2 or less, identifies patients who are very unlikely to be suffering from life-threatening upper GI bleeding. The shorter modified Blatchford score may be just as useful (BUN, Hgb, pulse, BP; maximal score 16).111 High-risk patients benefit from endoscopic therapy to stop the bleeding, while low-risk patients with low-risk lesions can be promptly discharged and treated as outpatients. The most common endoscopic hemostatic modalities used are injection with epinephrine and electrocautery. In a case with exposed vessel, mechanical hemostasis using clips is useful to control the bleeding.112 Biopsy should be performed to evaluate for H pylori infection. Persistent bleeding or rebleeding after endo-scopic therapy is an indication for repeat endoscopic treatment.


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Surgery_Schwartz. control the bleeding.112 Biopsy should be performed to evaluate for H pylori infection. Persistent bleeding or rebleeding after endo-scopic therapy is an indication for repeat endoscopic treatment. Surgery should be considered after two endoscopic failures. Elderly patients and patients with multiple comorbidities do not tolerate repeated episodes of hemodynamically significant hemorrhage, and they may benefit from early elective opera-tion after initially successful endoscopic treatment, especially if they have a high-risk ulcer.Planned surgery under controlled circumstances often yields better outcomes than emergent surgery. Deep bleeding ulcers on the posterior duodenal bulb or lesser gastric curvature are high-risk lesions because they often erode large arteries less amenable to nonoperative treatment, and early operation should be considered.Perforated peptic ulcer usually presents as an acute abdo-men. The patient can often give the exact time of onset of the excruciating


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Surgery_Schwartz. nonoperative treatment, and early operation should be considered.Perforated peptic ulcer usually presents as an acute abdo-men. The patient can often give the exact time of onset of the excruciating abdominal pain. Initially, a chemical peritonitis develops from the gastric and/or duodenal secretions, but within hours a bacterial peritonitis supervenes. The patient is in obvi-ous distress, and the abdominal examination shows peritoneal signs. Usually, marked involuntary guarding and rebound ten-derness is evoked by a gentle examination. Upright chest X-ray shows free air in about 80% of patients (Fig. 26-32). Once the diagnosis has been made, the patient is given analgesia and antibiotics, resuscitated with isotonic fluid, and taken to the operating room. Fluid sequestration into the third space of the inflamed peritoneum can be impressive, so preoperative fluid resuscitation is mandatory. Sometimes, the perforation has sealed spontaneously by the time of presentation, and surgery can


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Surgery_Schwartz. space of the inflamed peritoneum can be impressive, so preoperative fluid resuscitation is mandatory. Sometimes, the perforation has sealed spontaneously by the time of presentation, and surgery can be avoided if the patient is doing well. Nonoperative man-agement is appropriate only if there is objective evidence that the leak has sealed (i.e., radiologic contrast study), and in the absence of clinical peritonitis.Gastric outlet obstruction occurs in no more than 5% of patients with PUD. It is usually due to duodenal or prepyloric ulcer disease, and it may be acute (from inflammatory swelling and peristaltic dysfunction) or chronic (from cicatrix). Patients typically present with nonbilious vomiting and may have pro-found hypokalemic hypochloremic metabolic alkalosis and dehydration. Pain or discomfort is common. Weight loss may be prominent, depending on the duration of symptoms. A succus-sion splash may be audible with stethoscope placed in the epi-gastrium. Initial treatment is


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Surgery_Schwartz. or discomfort is common. Weight loss may be prominent, depending on the duration of symptoms. A succus-sion splash may be audible with stethoscope placed in the epi-gastrium. Initial treatment is nasogastric suction, IV hydration and electrolyte repletion, and acid suppression. The diagnosis is confirmed by endoscopy. Most patients admitted to the hospital nowadays with obstructing ulcer disease require intervention, either balloon dilation or operation. Cancer must be ruled out because most patients who present with the symptoms of gastric outlet obstruction will have a pancreatic, gastric, or duodenal malignancy.Medical Treatment of Peptic Ulcer DiseasePPIs are the mainstay of medical therapy for PUD, but high-dose H2RAs and sucralfate are also quite effective. Patients hospitalized for ulcer complications should receive high-dose intravenous PPI and, when discharged, should be considered for lifelong PPIs unless the definitive cause is eliminated or a definitive operation


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Surgery_Schwartz. for ulcer complications should receive high-dose intravenous PPI and, when discharged, should be considered for lifelong PPIs unless the definitive cause is eliminated or a definitive operation performed. Peptic ulcer patients should stop smoking and avoid alcohol and NSAIDs (including aspirin). Patients who require NSAIDs or aspirin to treat other medical conditions should always take concomi-tant PPIs or high dose H2 receptor blockers. Testing for H pylori infection is performed, and if it is found, it should be treated with one of several acceptable regimens (Table 26-10).113 If initial H pylori testing is negative and ulcer symptoms per-sist, an empirical trial of anti–H pylori therapy is reasonable since false-negative H pylori tests are not uncommon. Gener-ally, acid suppression can be stopped after 3 months if the ulcerogenic stimulus (e.g., H pylori, NSAIDs, or aspirin) has been removed. However, long-term maintenance PPI therapy should be considered in all patients admitted


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Surgery_Schwartz. be stopped after 3 months if the ulcerogenic stimulus (e.g., H pylori, NSAIDs, or aspirin) has been removed. However, long-term maintenance PPI therapy should be considered in all patients admitted to hospital with ulcer complications, all high-risk patients on NSAIDs or aspi-rin (the elderly or debilitated), and all patients requiring anti-coagulation or antiplatelet agents or those with a history of recurrent ulcer or bleeding. Consideration should also be given to maintenance PPI therapy in refractory smokers with a history of peptic ulcer. Sucralfate acts locally on mucosal defects and is well tolerated, and occasionally it is useful as a supplement to acid suppression.2Peptic ulcer40%24%6%4%6%5%10%5%No obvious causeOtherNeoplasmErosive diseaseMallory-Weiss syndromeOesophagitisVaricesFigure 26-31. Causes of upper GI bleeding. (Reproduced with permission from Dallal HJ, Palmer KR: ABC of the upper gastro-intestinal tract: Upper gastrointestinal haemorrhage, BMJ. 2001 Nov


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Surgery_Schwartz. 26-31. Causes of upper GI bleeding. (Reproduced with permission from Dallal HJ, Palmer KR: ABC of the upper gastro-intestinal tract: Upper gastrointestinal haemorrhage, BMJ. 2001 Nov 10;323(7321):1115-1117.)Brunicardi_Ch26_p1099-p1166.indd 112501/03/19 7:12 PM 1126SPECIFIC CONSIDERATIONS PART IITable 26-9Risk-stratification tools for upper gastrointestinal hemorrhageaA. BLATCHFORD SCORE AT PRESENTATIONPOINTS Systolic blood pressure 100–109 mmHg1 90–99 mmHg2 <90 mmHg3 Blood urea nitrogen 6.5–7.9 mmol/L2 8.0–9.9 mmol/L3 10.0–24.9 mmol/L4 ≥25 mmol/L6 Hemoglobin for men 12.0–12.9 g/dL1 10.0–11.9 g/dL3 <10.0 g/dL6 Hemoglobin for women 10.0–11.9 g/dL1 <10.0 g/dL6 Other variables at presentation Pulse ≥100 beats/min1 Melena1 Syncope2 Hepatic disease2 Cardiac failure2 B. ROCKALL SCOREVARIABLEPOINTSAge <60 y 60–79 y ≥80 y012Shock Heart rate >100 beats/min Systolic blood pressure <100 mmHg12Coexisting illness Ischemic heart disease, congestive heart failure, other


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Surgery_Schwartz. ROCKALL SCOREVARIABLEPOINTSAge <60 y 60–79 y ≥80 y012Shock Heart rate >100 beats/min Systolic blood pressure <100 mmHg12Coexisting illness Ischemic heart disease, congestive heart failure, other major illness Renal failure, hepatic failure, metastatic cancer23Endoscopic diagnosis No lesions observed, Mallory-Weiss syndrome Peptic ulcer, erosive disease, esophagitis Cancer of the upper GI tract012Endoscopic stigmata of recent hemorrhage Clean base ulcer, flat pigmented spot Blood in upper GI tract, active bleeding, visible vessel, clot02aPanel A shows the values used in the Blatchford risk-stratification score, which ranges from 0 to 23, with higher scores indicating higher risk. Panel B shows the Rockall score, with point values assigned for each of three clinical variables (age and the presence of shock and coexisting illnesses) and two endoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating


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Surgery_Schwartz. presence of shock and coexisting illnesses) and two endoscopic variables (diagnosis and stigmata of recent hemorrhage). The complete Rockall score ranges from 0 to 11, with higher scores indicating higher risk. Patients with a clinical Rockall score (Age + Shock + Coexisting illness) of 0 or a complete Rockall score of 2 or less are considered to be at low risk for rebleeding or death.Reproduced with permission from Gralnek IM, Barkun AN, Bardou M: Management of acute bleeding from a peptic ulcer, N Engl J Med. 2008 Aug 28;359(9):928-937.COMPLETE ROCKALL SCORECLINICAL ROCKALL SCOREBrunicardi_Ch26_p1099-p1166.indd 112601/03/19 7:12 PM 1127STOMACHCHAPTER 26Surgical Treatment of Peptic Ulcer DiseaseThe indications for surgery in PUD are (in order of decreasing frequency) perforation, obstruction, bleeding, and intractabil-ity or nonhealing.114,115 Gastric cancer must always be consid-ered in patients with gastric ulcer or gastric outlet obstruction. Today, most patients undergoing


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Surgery_Schwartz. bleeding, and intractabil-ity or nonhealing.114,115 Gastric cancer must always be consid-ered in patients with gastric ulcer or gastric outlet obstruction. Today, most patients undergoing emergent operation have simple patch of a perforated ulcer or oversewing of a bleed-ing ulcer.[92] Simultaneous performance of vagotomy either truncal or highly selective is increasingly uncommon, probably due to surgeon unfamiliarity with the procedure and reliance on postoperative PPIs to decrease acid secretion. But even in the current era, vagotomy may improve outcomes in emergency ulcer surgery.116-118 Before denying the stable low-risk patient a highly selective vagotomy or truncal vagotomy and drainage as an adjunct to simple patch or oversew, the surgeon should con-sider that many patients having emergency operation for peptic ulcer will not take long-term PPI, do not have Helicobacter, or will continue to smoke or take NSAIDs.Unfortunately, the data from many excellent randomized clinical


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Surgery_Schwartz. emergency operation for peptic ulcer will not take long-term PPI, do not have Helicobacter, or will continue to smoke or take NSAIDs.Unfortunately, the data from many excellent randomized clinical trials evaluating elective operation for peptic ulcer over the last several decades may be irrelevant to most patients pre-senting for ulcer surgery today.114 The large majority of these excellent studies were done in the pre-PPI, pre-Helicobacter, pre-NSAID era, and focused on elective operation for intracta-ble disease, an unusual indication for operation nowadays. Thus, today’s surgeon should take great care in applying this literature to inform surgical decision making.Traditionally, the vast majority of peptic ulcers were treated by a variant of one of the three basic operations: parietal cell vagotomy, also called highly selective vagotomy (HSV) or proximal gastric vagotomy, vagotomy and drainage (V+D), and vagotomy and distal gastrectomy. Recurrence rates are lowest but morbidity


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Surgery_Schwartz. cell vagotomy, also called highly selective vagotomy (HSV) or proximal gastric vagotomy, vagotomy and drainage (V+D), and vagotomy and distal gastrectomy. Recurrence rates are lowest but morbidity highest with the latter procedure, while the oppo-site is true for HSV (Table 26-11).114,115HSV severs the vagal nerve supply to the proximal two-thirds of the stomach, where essentially all the parietal cells are located, and preserves the vagal innervation to the antrum and pylorus and the remaining abdominal viscera (Fig. 26-33). Thus, the operation decreases total gastric acid secretion by about 75%, and GI side effects are rare. Elective HSV has largely been supplanted by long-term PPI treatment, but the operation, which has a learning curve, may still be useful in the patient (elective or emergent) who is noncompliant with, intolerant of, or cannot afford medical treatment. Historically, HSV has not performed particularly well for type II (gastric and duodenal) and type III


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Surgery_Schwartz. or emergent) who is noncompliant with, intolerant of, or cannot afford medical treatment. Historically, HSV has not performed particularly well for type II (gastric and duodenal) and type III (prepyloric) gastric ulcer, perhaps because of hypergastrinemia caused by gastric outlet obstruction and persistent antral stasis. Figure 26-32. Pneumoperitoneum on upright chest X-ray in patient with perforated ulcer.Table 26-10Helicobacter pylori therapies (10–14 days)Clarithromycin triple therapy standard or double dose PPI twice a day clarithromycin 500 mg twice a day amoxicillin 1 g twice a day; or metronidazole 500 mg three times a dayMetronidazole triple therapy standard or double dose PPI twice a day metronidazole 500 mg twice a day amoxicillin 1 g twice a dayLevofloxacin triple therapy standard dose PPI twice a day amoxicillin 1 g twice a day levofloxacin 500 mg dailySequential therapy standard or double dose PPI (10–14 days) amoxicillin 1 g twice a day (5–7 days); then clarithromycin


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Surgery_Schwartz. dose PPI twice a day amoxicillin 1 g twice a day levofloxacin 500 mg dailySequential therapy standard or double dose PPI (10–14 days) amoxicillin 1 g twice a day (5–7 days); then clarithromycin 500 mg twice a day and metronidazole 500 mg twice a day (5–7 days)Bismuth quadruple therapy (commonly used when above regimens fail to eradicate H pylori) standard dose PPI twice a day bismuth subsalicylate 300 mg four times a day tetracycline 500 mg four times a day metronidazole 250 mg four times a dayPPI = proton pump inhibitor.Table 26-11Clinical results of surgery for duodenal ulcer PARIETAL CELL VAGOTOMYTRUNCAL VAGOTOMY AND PYLOROPLASTYTRUNCAL VAGOTOMY AND ANTRECTOMYOperative mortality rate (%)0<11Ulcer recurrence rate (%)5–155–15<2Dumping (%) Mild<51010–15 Severe011–2Diarrhea (%) Mild<52520 Severe021–2Reproduced with permission from Mulholland MW, Debas HT: Chronic duodenal and gastric ulcer, Surg Clin North Am. 1987 Jun;67(3):489-507.Brunicardi_Ch26_p1099-p1166.indd 112701/03/19


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Surgery_Schwartz. with permission from Mulholland MW, Debas HT: Chronic duodenal and gastric ulcer, Surg Clin North Am. 1987 Jun;67(3):489-507.Brunicardi_Ch26_p1099-p1166.indd 112701/03/19 7:12 PM 1128SPECIFIC CONSIDERATIONS PART IIThe Taylor procedure, a straightforward laparoscopic operation, consists of a posterior truncal vagotomy and anterior seromy-otomy (but anterior HSV is probably equivalent), and it is an attractive and simple alternative to HSV with similar results.Truncal vagotomy and pyloroplasty, and truncal vagot-omy and gastrojejunostomy are the paradigmatic vagotomy and drainage procedures. HSV may be substituted for truncal vagotomy. The advantage of V + D is that it can be performed safely and quickly by the experienced surgeon. The main dis-advantages are the side effect profile (10% of patients have significant dumping and/or diarrhea). During truncal vagotomy (Fig. 26-34), care must be taken not to perforate the esophagus, a potentially lethal complication. Intraoperative


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Surgery_Schwartz. (10% of patients have significant dumping and/or diarrhea). During truncal vagotomy (Fig. 26-34), care must be taken not to perforate the esophagus, a potentially lethal complication. Intraoperative frozen sec-tion confirmation of at least two vagal trunks is prudent; addi-tional vagal trunks are common. Unlike HSV, V + D is widely accepted as a successful definitive operation for complicated PUD. It has been described as a useful part of the operative treatment for bleeding duodenal and gastric ulcer, perforated duodenal and gastric ulcer, and obstructing duodenal and gastric (types II and III) ulcer. When applied to gastric ulcer, the ulcer should be excised or biopsied.Truncal vagotomy denervates the antropyloric mechanism, and therefore, some sort of procedure is necessary to ablate or bypass the pylorus. Gastrojejunostomy is a good choice in patients with gastric outlet obstruction or a severely diseased proximal duodenum. The anastomosis is done between the proximal jejunum and


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Surgery_Schwartz. bypass the pylorus. Gastrojejunostomy is a good choice in patients with gastric outlet obstruction or a severely diseased proximal duodenum. The anastomosis is done between the proximal jejunum and the most dependent portion of the greater gastric curvature, in either an antecolic or retrocolic fashion (Fig. 26-35). Marginal ulceration is a potential complication. 6–8cm 7cmFigure 26-33. Highly selective vagotomy. (Reproduced with per-mission from Zinner MJ Schwartz SI, Ellis H: Maingot’s Abdominal Operations, 10th ed. Vol. I. Stamford, CT: Appleton & Lange; 1997.)Resected segmentResected segmentCeliac branchHepatic branchFigure 26-34. Truncal vagotomy. (Reproduced with permission from Zollinger RM Jr, Zollinger RM Sr: Zollinger’s Atlas of Surgi-cal Operations, 8th ed. New York, NY: McGraw-Hill Education; 2003.)Figure 26-35. Retrocolic gastrojejunostomy. Note meso-colon sutured to stomach (b, c, d). (Reproduced with per-mission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the


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Surgery_Schwartz. Education; 2003.)Figure 26-35. Retrocolic gastrojejunostomy. Note meso-colon sutured to stomach (b, c, d). (Reproduced with per-mission from Zuidema GD, Yeo CJ: Shackelford’s Surgery of the Alimentary Tract, 5th ed. Vol. II. Philadelphia, PA: Elsevier/Saunders; 2002.)Suture reinforcing the angleMesocolonbcdStomachJejunumBrunicardi_Ch26_p1099-p1166.indd 112801/03/19 7:12 PM 1129STOMACHCHAPTER 26Mechanical complications are also possible such as afferent or efferent loop obstruction, internal hernia, and intussusception. Pyloroplasty is useful in patients who require a pyloroduo-denotomy to deal with the ulcer complication (e.g., posterior bleeding duodenal ulcer), in those with limited or focal scarring in the pyloric region, or when gastrojejunostomy is technically difficult. The most commonly performed pyloroplasty is the Heineke-Mikulicz type (Fig. 26-36). Other occasionally use-ful techniques include the Finney (Fig. 26-37) and the Jaboulay pyloroplasties (Fig. 26-38). These


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Surgery_Schwartz. commonly performed pyloroplasty is the Heineke-Mikulicz type (Fig. 26-36). Other occasionally use-ful techniques include the Finney (Fig. 26-37) and the Jaboulay pyloroplasties (Fig. 26-38). These more extensive pyloroplasty techniques may make subsequent distal gastric resection more difficult and/or hazardous.Although vagotomy and antrectomy (V + A) is associated with a very low ulcer recurrence rate and is applicable to many patients with complicated PUD (e.g., bleeding duodenal and gastric ulcer, obstructing peptic ulcer, nonhealing gastric ulcer, and recurrent ulcer), V + A has a higher operative mortality risk (compared with HSV or V + D), and is irreversible. Fol-lowing antrectomy, GI continuity may be reestablished with a Billroth I gastroduodenostomy (Fig. 26-39) or a Billroth II loop gastrojejunostomy (Fig. 26-40). Since antrectomy routinely leaves a 60% to 70% gastric remnant, routine reconstruction as a Roux-en-Y gastrojejunostomy should be avoided (Fig. 26-41). Although


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Surgery_Schwartz. loop gastrojejunostomy (Fig. 26-40). Since antrectomy routinely leaves a 60% to 70% gastric remnant, routine reconstruction as a Roux-en-Y gastrojejunostomy should be avoided (Fig. 26-41). Although the Roux-en-Y operation is an excellent procedure for keeping duodenal contents out of the stomach and esophagus, in the presence of a large gastric remnant, this reconstruction will predispose to marginal ulceration and/or gastric stasis.V + A should be avoided in hemodynamically unsta-ble patients, and in patients with extensive inflammation and/or scarring of the proximal duodenum, because secure MucosaPylorusAntrumGambee stitchCBDAFigure 26-36. A through D. Heineke-Mikulicz pyloroplasty. (Reproduced with permission from Zinner MJ: Atlas of Gastric Surgery. New York, NY: Elsevier/Churchill Livingstone; 1992.)Brunicardi_Ch26_p1099-p1166.indd 112901/03/19 7:12 PM 1130SPECIFIC CONSIDERATIONS PART IIanastomosis (Billroth I) or duodenal closure (Billroth II) may be difficult.Distal


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Surgery_Schwartz. Livingstone; 1992.)Brunicardi_Ch26_p1099-p1166.indd 112901/03/19 7:12 PM 1130SPECIFIC CONSIDERATIONS PART IIanastomosis (Billroth I) or duodenal closure (Billroth II) may be difficult.Distal gastrectomy without vagotomy (usually about a 50% gastrectomy to include the ulcer) has traditionally been the procedure of choice for type I gastric ulcer. The addition of vagotomy should be considered for type II and III gastric ulcers (because the pathophysiology is more analogous to duodenal ulcer), or if the patient is believed to be at increased risk for recurrent ulcer, or perhaps even if Billroth II reconstruction is contemplated (to decrease the chance of marginal ulcer). Subto-tal gastrectomy (75% distal gastrectomy) without vagotomy is rarely used to treat PUD today, although it was the most popular ulcer operation at the middle of the last century.Pylorus preserving gastrectomy (PPG) was first reported as a surgical option for gastric ulcer that could minimize both dumping and


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Surgery_Schwartz. the most popular ulcer operation at the middle of the last century.Pylorus preserving gastrectomy (PPG) was first reported as a surgical option for gastric ulcer that could minimize both dumping and duodenogastric reflux. Though not widely adopted for this indication, in some centers PPG is considered a good minimally invasive surgical option for early gastric cancer.119,120Choice of Operation for Peptic Ulcer. The choice of opera-tion for the individual patient with PUD depends on a variety of factors, including the type of ulcer (duodenal, gastric, recurrent, or marginal), the indication for operation, and the condition of the patient. Other important considerations are intra-abdominal factors (duodenal scarring/inflammation, adhesions, or difficult exposure), the ulcer diathesis status of the patient, the surgeon’s experience and personal preference, whether H pylori infection is present, the need for NSAID therapy, previous treatment, and the likelihood of future compliance with


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Surgery_Schwartz. of the patient, the surgeon’s experience and personal preference, whether H pylori infection is present, the need for NSAID therapy, previous treatment, and the likelihood of future compliance with treatment. Table 26-12 shows the surgical options for managing various aspects of PUD. Stomach Stom.AB DC Approximation suture PylorusInvertedincisionGallbladderDuodenumConnellthrough & throughsuture (1st ant. tier)Duod.Cushingseromuscularsuture (2nd ant. tier)Posteriorthrough &through sutureFigure 26-37. A through D. Finney pyloroplasty. ant. = anterior; Duod. = duodenum; Stom. = stomach. (Reproduced with permission from Zuidema GD: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, PA: Elsevier/Saunders; 1996.)Brunicardi_Ch26_p1099-p1166.indd 113001/03/19 7:12 PM 1131STOMACHCHAPTER 26In general, resective procedures have a lower ulcer recurrence rate, but a higher morbidity and mortality rate (see Table 26-11) compared to nonresective ulcer operations. Because


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Surgery_Schwartz. 26In general, resective procedures have a lower ulcer recurrence rate, but a higher morbidity and mortality rate (see Table 26-11) compared to nonresective ulcer operations. Because ulcer recur-rence often is related to H pylori and/or NSAIDs, it is usually managed adequately without reoperation. Thus, gastric resection to minimize recurrence in duodenal ulcer disease is usually not justified; resection for gastric ulcer remains the standard because of the risk of cancer. Clearly, the modern trend in peptic ulcer operation could be described as “less is more.”121,122Bleeding Peptic UlcerBleeding is the most common cause of ulcer-related death, but only rarely do patients with bleeding gastric or duodenal ulcer require operation today. The success of endoscopic treatment and medical therapy for bleeding PUD has resulted in the selec-tion of a small subgroup of high-risk patients for today’s sur-geon. It is likely that patients currently coming to operation for bleeding PUD are at


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Surgery_Schwartz. for bleeding PUD has resulted in the selec-tion of a small subgroup of high-risk patients for today’s sur-geon. It is likely that patients currently coming to operation for bleeding PUD are at higher risk for a poor outcome than ever before. The surgical options for treating bleeding PUD include suture ligation of the bleeder; suture ligation and definitive non-resective ulcer operation (HSV or V + D); and gastric resection (usually, including vagotomy and ulcer excision). Gastric ulcer requires biopsy if not resected.The management of bleeding peptic ulcer is summarized in the algorithm provided in Fig. 26-42. All patients admitted to the hospital with bleeding peptic ulcer should be adequately Stomach Stom.AB DCPylorusInvertedincisionGallbladderDuodenumConnellthrough & throughsuture (1st ant. tier)Duod.Cushingseromuscularsuture (2nd ant. tier)Posteriorthrough &through sutureFigure 26-38. A through D. Jaboulay pyloroplasty. ant. = anterior; Duod. = duodenum; Stom. = stomach.


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Surgery_Schwartz. (1st ant. tier)Duod.Cushingseromuscularsuture (2nd ant. tier)Posteriorthrough &through sutureFigure 26-38. A through D. Jaboulay pyloroplasty. ant. = anterior; Duod. = duodenum; Stom. = stomach. (Reproduced with permission from Zuidema GD: Shackelford’s Surgery of the Alimentary Tract, 4th ed. Philadelphia, PA: Elsevier/Saunders; 1996.)Brunicardi_Ch26_p1099-p1166.indd 113101/03/19 7:12 PM 1132SPECIFIC CONSIDERATIONS PART IIresuscitated and started on IV PPI.125 Most patients will stop bleeding with these measures alone, but about 25% will continue to bleed or will rebleed in hospital. It is important to identify this high-risk group early with clinical and endoscopic parameters because, essentially, all the deaths from bleeding ulcer occur in this group. Surgical consultation is mandatory, and endoscopic hemostatic therapy (cautery, epinephrine injection, clipping) is indicated and usually successful in these high-risk patients.126 Indications for operation include massive


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Surgery_Schwartz. mandatory, and endoscopic hemostatic therapy (cautery, epinephrine injection, clipping) is indicated and usually successful in these high-risk patients.126 Indications for operation include massive hemorrhage unre-sponsive to initial endoscopic control, recurrent hemorrhage ABCFigure 26-40. A through C. Billroth II antecolic gastrojejunostomy. (Reproduced with permission from Zinner MJ Schwartz SI, Ellis H: Maingot’s Abdominal Operations, 10th ed. Vol. I. Stamford, CT: Appleton & Lange; 1997.)Figure 26-39. A and B. Billroth I gastroduo-denostomy. (Reproduced with permission from Zinner MJ: Atlas of Gastric Surgery. New York, NY: Elsevier/Churchill Livingstone; 1992.)ABBrunicardi_Ch26_p1099-p1166.indd 113201/03/19 7:12 PM 1133STOMACHCHAPTER 26requiring multiple transfusions after two attempts at endoscopic control, ongoing hemorrhage and transfusion with limited availability of blood for transfusion or lack of availability of a therapeutic endoscopist, early rehospitalization for


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Surgery_Schwartz. attempts at endoscopic control, ongoing hemorrhage and transfusion with limited availability of blood for transfusion or lack of availability of a therapeutic endoscopist, early rehospitalization for bleeding ulcer, and concurrent indications for surgery such as perforation or obstruction. Patients with massive bleeding from high-risk lesions (e.g., posterior duodenal ulcer with erosion of gastroduo-denalartery, or lesser curvature gastric ulcer with erosion of left gastric artery or branch) should be considered for operation as should those presenting in shock, those requiring more than four units of blood in 24 hours or eight units of blood in 48 hours, and those with ulcers >2 cm in diameter. The mortality rate for surgery for bleeding peptic ulcer is around 20%. Angiography and embolization may be useful in some patients.Operation for Bleeding Peptic Ulcer (Fig. 26-43)The two operations most commonly used for bleeding duode-nal ulcer are oversewing of the ulcer with or without


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Surgery_Schwartz. may be useful in some patients.Operation for Bleeding Peptic Ulcer (Fig. 26-43)The two operations most commonly used for bleeding duode-nal ulcer are oversewing of the ulcer with or without vagotomy and drainage,121 or V + A. Oversewing alone results in a higher rebleeding rate but a lower operative mortality rate than defini-tive operation. When the mortality for reoperation for rebleed-ing is considered, the overall mortality is probably comparable for the two approaches. Patients who are in shock or medically unstable should not have gastric resection.An initial pyloromyotomy incision allows access to the bleeding posterior duodenal ulcer, and an expeditious Kocher maneuver allows the surgeon to control the hemorrhage with the left hand if necessary. Heavy suture material on a stout needle is used to place figure-of-eight sutures or a U-stitch to secure the bleeding vessel at the base of the posterior duodenal ulcer. Multiple sutures are usually necessary. Once the surgeon is


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Surgery_Schwartz. needle is used to place figure-of-eight sutures or a U-stitch to secure the bleeding vessel at the base of the posterior duodenal ulcer. Multiple sutures are usually necessary. Once the surgeon is unequivocally convinced that hemostasis is secure, a pyloro-plasty can be performed. If the patient is stable, vagotomy may be considered if the surgeon is experienced and the vagotomy straightforward. If the patient is not a high operative risk and V + A is selected, smaller duodenal ulcers are resected with the specimen; larger bleeding duodenal ulcers must often be left behind in the duodenal stump. In this situation, suture hemo-stasis must be attained and a secure duodenal closure accom-plished. The anterior wall of the open duodenum can be sutured to either the proximal or distal lip of the posterior ulcer once the bleeding vessel has been sutured. The duodenal closure can be buttressed with omentum and the duodenum should be decompressed, either with a lateral duodenostomy or


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Surgery_Schwartz. of the posterior ulcer once the bleeding vessel has been sutured. The duodenal closure can be buttressed with omentum and the duodenum should be decompressed, either with a lateral duodenostomy or retrograde tube via the proximal jejunum or well secured nasogastric tube secured with tip well into afferent limb. Right upper quadrant closed suction peritoneal drainage is important. Use of a feed-ing jejunostomy is also considered. A Billroth II anastomosis reestablishes gastrointestinal continuity.The initial management of bleeding gastric ulcers and the indications for operation are similar to those for bleeding duodenal ulcer. These lesions tend to occur in older and/or medically complicated patients, and this fact may increase the operative risk. However, experience shows that planned surgery in a resuscitated patient results in a better operative survival rate than emergent operation in a patient who has rebled and is in shock. Distal gastric resection to include the bleeding ulcer


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Surgery_Schwartz. in a resuscitated patient results in a better operative survival rate than emergent operation in a patient who has rebled and is in shock. Distal gastric resection to include the bleeding ulcer is the procedure of choice for bleeding gastric ulcer. Second best is V + D with oversewing and biopsy of the ulcer to rule out cancer. Oversewing of the bleeder and biopsy followed by long-term acid suppression is a reasonable alternative in high-risk or unstable patients.50 to 60 cm< 50% gastricremnantFigure 26-41. Roux-en-Y gastrojejunostomy. (Reproduced with permission from Ritchie WP, Steele G, Dean RH: General Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 1995.)Table 26-12Surgical options in the treatment of duodenal and gastric ulcerINDICATIONDUODENALGASTRICBleeding1. Oversewa2. Oversew, V + D3. V + A1. Oversew and biopsya2. Oversew, biopsy, V + D3. Distal gastrectomybPerforation1. Patcha2. Patch, HSV3. Patch, V + D1. Biopsy and patcha2. Wedge excision, V + D3. Distal


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Surgery_Schwartz. V + D3. V + A1. Oversew and biopsya2. Oversew, biopsy, V + D3. Distal gastrectomybPerforation1. Patcha2. Patch, HSV3. Patch, V + D1. Biopsy and patcha2. Wedge excision, V + D3. Distal gastrectomybObstruction1. HSV + GJ2. V + A1. Biopsy; HSV + GJ2. Distal gastrectomybIntractability/nonhealing1. HSVb2. V + D3. V + A1. HSV and wedge excision2. Distal gastrectomyaUnless the patient is in shock or moribund, a definitive procedure should be considered.bOperation of choice in low-risk patient.GJ = gastrojejunostomy; HSV = highly selective vagotomy; V + A = vagotomy and antrectomy; V + D = vagotomy and drainage.Brunicardi_Ch26_p1099-p1166.indd 113301/03/19 7:12 PM 1134SPECIFIC CONSIDERATIONS PART IIPerforated Peptic Ulcer (Fig. 26-44)Perforation is the second most common complication of peptic ulcer, but nowadays it is a much more common indication for operation than bleeding. As with bleeding ulcer, NSAID and/or aspirin use have been inextricably linked with perforated PUD,


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Surgery_Schwartz. of peptic ulcer, but nowadays it is a much more common indication for operation than bleeding. As with bleeding ulcer, NSAID and/or aspirin use have been inextricably linked with perforated PUD, especially in the elderly population.61 Surgery is almost always indicated for ulcer perforation, although occasionally nonsurgi-cal treatment can be used in the stable patient without peritoni-tis in whom radiologic studies document a sealed perforation. Patients with acute perforation and GI blood loss (either chronic or acute) should be suspected of having a second ulcer or a GI cancer.The options for surgical treatment of perforated duode-nal ulcer are simple patch closure, patch closure and HSV, or patch closure and V + D. Simple patch closure, currently the most commonly performed operation for perforated peptic ulcer, is the procedure of choice in patients with hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old. In stable patients without


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Surgery_Schwartz. for perforated peptic ulcer, is the procedure of choice in patients with hemodynamic instability and/or exudative peritonitis signifying a perforation >24 hours old. In stable patients without longstanding perfo-ration, particularly those with chronic symptoms or failure of medical treatment, the addition of HSV should be considered. Vagotomy and drainage is also an acceptable definitive opera-tion for perforated duodenal ulcer, but occasionally side effects are disabling, and if gastrojejunostomy has been performed, Hospital admissionBleeding peptic ulcerBleeding recursin hospitalO.R.20% high risk80% Low riskBleeding stopsDischargeBleeding recursBleeding persists>4 PRBC transfused/24hDeep ulcer eroding big vesselHemodynamic instabilityHemostatic Rx unavailableEndoscopic hemostatic RxConsult surgeonResuscitateContinuous IV PPI dripEGDLifelong acid suppressionTest + Rx H. pyloriAvoid NSAIDs/ASA if possibleYesShock?NoYesTransfusion?NoYesActive bleeding on EGD?NoYesVisible vessel on


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Surgery_Schwartz. surgeonResuscitateContinuous IV PPI dripEGDLifelong acid suppressionTest + Rx H. pyloriAvoid NSAIDs/ASA if possibleYesShock?NoYesTransfusion?NoYesActive bleeding on EGD?NoYesVisible vessel on EGD?NoYesAbnormal PT, PTT, or platelets?NoFigure 26-42. Algorithm for the treatment of bleeding peptic ulcer. ASA = acetylsalicylic acid; EGD = esophagogastroduodenoscopy; O.R. = operating room; PPI = proton pump inhibitor; PRBC = unit of packed red blood cells; PT = prothrombin time; PTT = partial throm-boplastin time; Rx = treatment.Brunicardi_Ch26_p1099-p1166.indd 113401/03/19 7:12 PM 1135STOMACHCHAPTER 26Operation for bleeding peptic ulcerYesYesNoGastric ulcerDuodenal ulcerType 1,2,3Distal gastrectomy**Hemodynamically unstable?OrHigh operative risk?Csendes procPauchet procKelling-Madlener proc(see text)*Add lifelong PPI**Add TV for type 2 + 3Oversew + TV/DOversew + TV/ABMI < 21? ordifficult duodenum?Type 4RebleedRebleedDuodenal ulcer*Gastric ulcer*1) Bx and oversew2) Wedge


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Surgery_Schwartz. proc(see text)*Add lifelong PPI**Add TV for type 2 + 3Oversew + TV/DOversew + TV/ABMI < 21? ordifficult duodenum?Type 4RebleedRebleedDuodenal ulcer*Gastric ulcer*1) Bx and oversew2) Wedge resectionOversewNoFigure 26-43. Algorithm for operation for bleeding peptic ulcer. BMI = body mass index; Bx = biopsy; PPI = proton pump inhibitor; proc = procedure; TV = truncal vagotomy; TV/A = truncal vagotomy and antrectomy; TV/D = truncal vagotomy and drainage.Operation for Perforated Peptic UlcerYesPatch + HSV,orPatch + TV/DWedge resection and TV/D or HSVOrDistal gastrectomy including perforation*** Duodenal ulcer* Gastric ulcer* PatchBx + PatchOrWedge resectionChronic ulcer HX?OrPerforation on RX?OrNSAIDs/ASA necessary? Gastric ulcer* Duodenal ulcer* Hemodynamically unstable?OrHigh operative risk?OrPerforation >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


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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.


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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


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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


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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


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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


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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


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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


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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,


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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.


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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


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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


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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


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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


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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


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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,


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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


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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


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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%


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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