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Surgery_Schwartz_7402 | Surgery_Schwartz | same pathway as CCK (which also has properties of a satiety hormone). The orexigenic hormone ghrelin has the opposite effect.Liquid Emptying. The gastric emptying of water or isotonic saline follows first-order kinetics, with a half emptying time around 12 minutes. Thus, if one drinks 200 mL of water, about 100 mL enters the duodenum by 12 minutes, whereas if one drinks 400 mL of water, about 200 mL enters the duodenum by 12 minutes. This emptying pattern of liquids is modified consid-erably as the caloric density, osmolarity, and nutrient composi-tion of the liquid changes (Fig. 26-20). Up to an osmolarity of about 1 M, liquid emptying occurs at a rate of about 200 kcal per hour. Duodenal osmoreceptors and hormones (e.g., secretin and VIP) are important modulators of liquid gastric emptying. Generally, liquid emptying is delayed in the supine position.Traditionally, liquid emptying has been attributed to the activity of the proximal stomach, but it is probably more complicated than | Surgery_Schwartz. same pathway as CCK (which also has properties of a satiety hormone). The orexigenic hormone ghrelin has the opposite effect.Liquid Emptying. The gastric emptying of water or isotonic saline follows first-order kinetics, with a half emptying time around 12 minutes. Thus, if one drinks 200 mL of water, about 100 mL enters the duodenum by 12 minutes, whereas if one drinks 400 mL of water, about 200 mL enters the duodenum by 12 minutes. This emptying pattern of liquids is modified consid-erably as the caloric density, osmolarity, and nutrient composi-tion of the liquid changes (Fig. 26-20). Up to an osmolarity of about 1 M, liquid emptying occurs at a rate of about 200 kcal per hour. Duodenal osmoreceptors and hormones (e.g., secretin and VIP) are important modulators of liquid gastric emptying. Generally, liquid emptying is delayed in the supine position.Traditionally, liquid emptying has been attributed to the activity of the proximal stomach, but it is probably more complicated than |
Surgery_Schwartz_7403 | Surgery_Schwartz | Generally, liquid emptying is delayed in the supine position.Traditionally, liquid emptying has been attributed to the activity of the proximal stomach, but it is probably more complicated than previously thought. Clearly, receptive relax-ation and gastric accommodation play a role in gastric empty-ing of liquids. Patients with a denervated (e.g., vagotomized), resected, or plicated (e.g., fundoplication) proximal stomach have decreased gastric compliance and may show accelerated gastric emptying of liquids.Some observations suggest an active role for the distal stomach in liquid emptying. For instance, even if the proximal intragastric pressure is lower than duodenal pressure, normal gastric emptying of liquids can occur. Also, diabetic patients CCK (µg/kg)0.25Low-fat dietHight-fat diet0102030405060700.51.02.0% Suppression of gastric emptyingFigure 26-19. Cholecystokinin (CCK) inhibits gastric emptying. (Reproduced with permission from Covasa M, Ritter RC: Adapta-tion to high-fat | Surgery_Schwartz. Generally, liquid emptying is delayed in the supine position.Traditionally, liquid emptying has been attributed to the activity of the proximal stomach, but it is probably more complicated than previously thought. Clearly, receptive relax-ation and gastric accommodation play a role in gastric empty-ing of liquids. Patients with a denervated (e.g., vagotomized), resected, or plicated (e.g., fundoplication) proximal stomach have decreased gastric compliance and may show accelerated gastric emptying of liquids.Some observations suggest an active role for the distal stomach in liquid emptying. For instance, even if the proximal intragastric pressure is lower than duodenal pressure, normal gastric emptying of liquids can occur. Also, diabetic patients CCK (µg/kg)0.25Low-fat dietHight-fat diet0102030405060700.51.02.0% Suppression of gastric emptyingFigure 26-19. Cholecystokinin (CCK) inhibits gastric emptying. (Reproduced with permission from Covasa M, Ritter RC: Adapta-tion to high-fat |
Surgery_Schwartz_7404 | Surgery_Schwartz | Suppression of gastric emptyingFigure 26-19. Cholecystokinin (CCK) inhibits gastric emptying. (Reproduced with permission from Covasa M, Ritter RC: Adapta-tion to high-fat diet reduces inhibition of gastric emptying by CCK and intestinal oleate, Am J Physiol Regul Integr Comp Physiol. 2000 Jan;278(1):R166-R170.)7006005004003001002000Residual gastric volume (mL)Time (min)806040200Figure 26-20. Nutrient composition and caloric density affect liquid gastric emptying. Glucose solution (purple circles), the least calorically dense, emptied the fastest. Other more calorically dense solutions, such as milk protein (green triangles) and pep-tide hydrolysates (red circles and blue triangles), emptied slower. (Reproduced with permission from Calbet JA, MacLean DA. Role of caloric content on gastric emptying in humans, J Physiol. 1997 Jan 15;498 (Pt 2):553-559.)Brunicardi_Ch26_p1099-p1166.indd 111401/03/19 7:11 PM 1115STOMACHCHAPTER 26may have normal proximal gastric motor function and | Surgery_Schwartz. Suppression of gastric emptyingFigure 26-19. Cholecystokinin (CCK) inhibits gastric emptying. (Reproduced with permission from Covasa M, Ritter RC: Adapta-tion to high-fat diet reduces inhibition of gastric emptying by CCK and intestinal oleate, Am J Physiol Regul Integr Comp Physiol. 2000 Jan;278(1):R166-R170.)7006005004003001002000Residual gastric volume (mL)Time (min)806040200Figure 26-20. Nutrient composition and caloric density affect liquid gastric emptying. Glucose solution (purple circles), the least calorically dense, emptied the fastest. Other more calorically dense solutions, such as milk protein (green triangles) and pep-tide hydrolysates (red circles and blue triangles), emptied slower. (Reproduced with permission from Calbet JA, MacLean DA. Role of caloric content on gastric emptying in humans, J Physiol. 1997 Jan 15;498 (Pt 2):553-559.)Brunicardi_Ch26_p1099-p1166.indd 111401/03/19 7:11 PM 1115STOMACHCHAPTER 26may have normal proximal gastric motor function and |
Surgery_Schwartz_7405 | Surgery_Schwartz | emptying in humans, J Physiol. 1997 Jan 15;498 (Pt 2):553-559.)Brunicardi_Ch26_p1099-p1166.indd 111401/03/19 7:11 PM 1115STOMACHCHAPTER 26may have normal proximal gastric motor function and pro-foundly delayed gastric emptying of liquids. Indeed, antral contractile activity does correlate with liquid gastric emptying, and this distal gastric activity appears to vary with the nutrient composition and caloric content of the liquid meal. Depend-ing on the circumstances, distal gastric motor activity can pro-mote or inhibit gastric emptying of liquids. Distal gastrectomy and pyloric stenting both obviously interfere with distal gastric motor activity, and both accelerate the initial rapid phase of liq-uid gastric emptying.Solid Emptying. Normally, the half-time of solid gastric emp-tying is less than 2 hours. Unlike liquids, which display an initial rapid phase followed by a slower linear phase of emptying, sol-ids have an initial lag phase during which little emptying of sol-ids | Surgery_Schwartz. emptying in humans, J Physiol. 1997 Jan 15;498 (Pt 2):553-559.)Brunicardi_Ch26_p1099-p1166.indd 111401/03/19 7:11 PM 1115STOMACHCHAPTER 26may have normal proximal gastric motor function and pro-foundly delayed gastric emptying of liquids. Indeed, antral contractile activity does correlate with liquid gastric emptying, and this distal gastric activity appears to vary with the nutrient composition and caloric content of the liquid meal. Depend-ing on the circumstances, distal gastric motor activity can pro-mote or inhibit gastric emptying of liquids. Distal gastrectomy and pyloric stenting both obviously interfere with distal gastric motor activity, and both accelerate the initial rapid phase of liq-uid gastric emptying.Solid Emptying. Normally, the half-time of solid gastric emp-tying is less than 2 hours. Unlike liquids, which display an initial rapid phase followed by a slower linear phase of emptying, sol-ids have an initial lag phase during which little emptying of sol-ids |
Surgery_Schwartz_7406 | Surgery_Schwartz | is less than 2 hours. Unlike liquids, which display an initial rapid phase followed by a slower linear phase of emptying, sol-ids have an initial lag phase during which little emptying of sol-ids occurs. It is during this phase that much of the grinding and mixing occurs. A linear emptying phase follows, during which the smaller particles are metered out to the duodenum. Solid gastric emptying is a function of meal particle size, caloric con-tent, and composition (especially fat). When liquids and solids are ingested together, the liquids empty first. Solids are stored in the fundus and delivered to the distal stomach at constant rates for grinding. Liquids also are sequestered in the fundus, but they appear to be readily delivered to the distal stomach for early emptying. The larger the solid component of the meal, the slower the liquid emptying. Patients bothered by dumping syn-drome are advised to limit the amount of liquid consumed with the solid meal, taking advantage of this | Surgery_Schwartz. is less than 2 hours. Unlike liquids, which display an initial rapid phase followed by a slower linear phase of emptying, sol-ids have an initial lag phase during which little emptying of sol-ids occurs. It is during this phase that much of the grinding and mixing occurs. A linear emptying phase follows, during which the smaller particles are metered out to the duodenum. Solid gastric emptying is a function of meal particle size, caloric con-tent, and composition (especially fat). When liquids and solids are ingested together, the liquids empty first. Solids are stored in the fundus and delivered to the distal stomach at constant rates for grinding. Liquids also are sequestered in the fundus, but they appear to be readily delivered to the distal stomach for early emptying. The larger the solid component of the meal, the slower the liquid emptying. Patients bothered by dumping syn-drome are advised to limit the amount of liquid consumed with the solid meal, taking advantage of this |
Surgery_Schwartz_7407 | Surgery_Schwartz | solid component of the meal, the slower the liquid emptying. Patients bothered by dumping syn-drome are advised to limit the amount of liquid consumed with the solid meal, taking advantage of this effect. Three prokinetic (metoclopramide, erythromycin, domperidone) may be used to treat delayed gastric emptying. Typical doses and mechanism of action are shown in Table 26-4.DIAGNOSIS OF GASTRIC DISEASESigns and SymptomsThe most common symptoms of gastric disease are pain, weight loss, early satiety, and anorexia. Nausea, vomiting, bloating, and anemia also are frequent complaints. Several of these symptoms (pain, bloating, nausea, and early satiety) are often described by physicians as dyspepsia, synonymous with the common nonmedical term indigestion. Common causes of dyspepsia include gastroesophageal reflux disease (GERD), helicobacter gastritis, and other disorders of the stomach, gallbladder, and pancreas. Although none of the aforementioned symptoms alone is specific for gastric | Surgery_Schwartz. solid component of the meal, the slower the liquid emptying. Patients bothered by dumping syn-drome are advised to limit the amount of liquid consumed with the solid meal, taking advantage of this effect. Three prokinetic (metoclopramide, erythromycin, domperidone) may be used to treat delayed gastric emptying. Typical doses and mechanism of action are shown in Table 26-4.DIAGNOSIS OF GASTRIC DISEASESigns and SymptomsThe most common symptoms of gastric disease are pain, weight loss, early satiety, and anorexia. Nausea, vomiting, bloating, and anemia also are frequent complaints. Several of these symptoms (pain, bloating, nausea, and early satiety) are often described by physicians as dyspepsia, synonymous with the common nonmedical term indigestion. Common causes of dyspepsia include gastroesophageal reflux disease (GERD), helicobacter gastritis, and other disorders of the stomach, gallbladder, and pancreas. Although none of the aforementioned symptoms alone is specific for gastric |
Surgery_Schwartz_7408 | Surgery_Schwartz | reflux disease (GERD), helicobacter gastritis, and other disorders of the stomach, gallbladder, and pancreas. Although none of the aforementioned symptoms alone is specific for gastric disease, when elicited in the con-text of a careful history and physical examination, they point to a differential diagnosis, which can be refined with certain tests. Early endoscopy should be considered in patients present-ing with recent onset of alarm symptoms (weight loss, anemia, dysphagia, vomiting) particularly those over 55 years of age (Table 26-5).Diagnostic TestsEsophagogastroduodenoscopy. Esophagogastroduodenos-copy (EGD) is a safe and accurate outpatient procedure per-formed under conscious sedation.64 Smaller flexible scopes with excellent optics and a working channel are easily passed trans-nasally in the unsedated patient. Following an 8-hour fast, the flexible scope is advanced under direct vision into the esopha-gus, stomach, and duodenum. The fundus and GE junction are inspected by | Surgery_Schwartz. reflux disease (GERD), helicobacter gastritis, and other disorders of the stomach, gallbladder, and pancreas. Although none of the aforementioned symptoms alone is specific for gastric disease, when elicited in the con-text of a careful history and physical examination, they point to a differential diagnosis, which can be refined with certain tests. Early endoscopy should be considered in patients present-ing with recent onset of alarm symptoms (weight loss, anemia, dysphagia, vomiting) particularly those over 55 years of age (Table 26-5).Diagnostic TestsEsophagogastroduodenoscopy. Esophagogastroduodenos-copy (EGD) is a safe and accurate outpatient procedure per-formed under conscious sedation.64 Smaller flexible scopes with excellent optics and a working channel are easily passed trans-nasally in the unsedated patient. Following an 8-hour fast, the flexible scope is advanced under direct vision into the esopha-gus, stomach, and duodenum. The fundus and GE junction are inspected by |
Surgery_Schwartz_7409 | Surgery_Schwartz | in the unsedated patient. Following an 8-hour fast, the flexible scope is advanced under direct vision into the esopha-gus, stomach, and duodenum. The fundus and GE junction are inspected by retroflexing the scope. To rule out cancer with a high degree of accuracy, all patients with gastric ulcer diag-nosed on upper GI series or found at EGD should have multiple biopsy specimens of the base and rim of the lesion. Brush cytol-ogy also should be considered. Gastritis should be biopsied both for histologic examination and assessment (see discussion on gastritis in “Helicobacter Pylori Infection”) and for a tissue ure-ase test and histologic evaluation to rule out the presence of H pylori. If Helicobacter infection is detected, it should be treated because of the etiologic association with peptic ulcers, mucosa-associated lymphoid tissue (MALT), and gastric cancer; in addition, eradication may ameliorate symp-toms. The most serious complications of EGD are perforation (which is rare, but | Surgery_Schwartz. in the unsedated patient. Following an 8-hour fast, the flexible scope is advanced under direct vision into the esopha-gus, stomach, and duodenum. The fundus and GE junction are inspected by retroflexing the scope. To rule out cancer with a high degree of accuracy, all patients with gastric ulcer diag-nosed on upper GI series or found at EGD should have multiple biopsy specimens of the base and rim of the lesion. Brush cytol-ogy also should be considered. Gastritis should be biopsied both for histologic examination and assessment (see discussion on gastritis in “Helicobacter Pylori Infection”) and for a tissue ure-ase test and histologic evaluation to rule out the presence of H pylori. If Helicobacter infection is detected, it should be treated because of the etiologic association with peptic ulcers, mucosa-associated lymphoid tissue (MALT), and gastric cancer; in addition, eradication may ameliorate symp-toms. The most serious complications of EGD are perforation (which is rare, but |
Surgery_Schwartz_7410 | Surgery_Schwartz | ulcers, mucosa-associated lymphoid tissue (MALT), and gastric cancer; in addition, eradication may ameliorate symp-toms. The most serious complications of EGD are perforation (which is rare, but can occur anywhere from the cervical esoph-agus to the duodenum), aspiration, and respiratory depression from excessive sedation. Although EGD is a more sensitive test than double-contrast upper GI series, these modalities should be considered complementary rather than mutually exclusive.Barium Upper GI Study. Plain abdominal X-rays may be helpful in the diagnosis of gastric perforation (pneumoperi-toneum) or delayed gastric emptying (large air-fluid level). Double-contrast upper GI series may be better than EGD at elucidating gastric diverticula, fistula, tortuosity, stricture loca-tion, and size or morphology of hiatal hernia.65 Although there are radiologic characteristics of ulcers that suggest the pres-ence or absence of malignancy, gastric ulcers always require adequate biopsy.Computed | Surgery_Schwartz. ulcers, mucosa-associated lymphoid tissue (MALT), and gastric cancer; in addition, eradication may ameliorate symp-toms. The most serious complications of EGD are perforation (which is rare, but can occur anywhere from the cervical esoph-agus to the duodenum), aspiration, and respiratory depression from excessive sedation. Although EGD is a more sensitive test than double-contrast upper GI series, these modalities should be considered complementary rather than mutually exclusive.Barium Upper GI Study. Plain abdominal X-rays may be helpful in the diagnosis of gastric perforation (pneumoperi-toneum) or delayed gastric emptying (large air-fluid level). Double-contrast upper GI series may be better than EGD at elucidating gastric diverticula, fistula, tortuosity, stricture loca-tion, and size or morphology of hiatal hernia.65 Although there are radiologic characteristics of ulcers that suggest the pres-ence or absence of malignancy, gastric ulcers always require adequate biopsy.Computed |
Surgery_Schwartz_7411 | Surgery_Schwartz | or morphology of hiatal hernia.65 Although there are radiologic characteristics of ulcers that suggest the pres-ence or absence of malignancy, gastric ulcers always require adequate biopsy.Computed Tomographic Scanning and Magnetic Resonance Imaging. Usually, significant gastric disease can be diag-nosed without these sophisticated imaging studies. However, one or the other should be part of the routine staging work-up for patients with a malignant gastric tumor. Magnetic resonance imaging (MRI) may prove clinically useful as a quantitative test for gastric emptying, and it may even hold some promise for the 1Table 26-4Drugs that accelerate gastric emptyingAGENTTYPICAL ADULT DOSEMECHANISM OF ACTIONMetoclopramide10 mg PO four times a dayDopamine antagonistErythromycin250 mg PO four times a dayMotilin agonistDomperidone10 mg PO four times a dayDopamine antagonistTable 26-5Alarm symptoms that indicate the need for upper endoscopyAge >55 years with new onset dyspepsiaUnintentional weight | Surgery_Schwartz. or morphology of hiatal hernia.65 Although there are radiologic characteristics of ulcers that suggest the pres-ence or absence of malignancy, gastric ulcers always require adequate biopsy.Computed Tomographic Scanning and Magnetic Resonance Imaging. Usually, significant gastric disease can be diag-nosed without these sophisticated imaging studies. However, one or the other should be part of the routine staging work-up for patients with a malignant gastric tumor. Magnetic resonance imaging (MRI) may prove clinically useful as a quantitative test for gastric emptying, and it may even hold some promise for the 1Table 26-4Drugs that accelerate gastric emptyingAGENTTYPICAL ADULT DOSEMECHANISM OF ACTIONMetoclopramide10 mg PO four times a dayDopamine antagonistErythromycin250 mg PO four times a dayMotilin agonistDomperidone10 mg PO four times a dayDopamine antagonistTable 26-5Alarm symptoms that indicate the need for upper endoscopyAge >55 years with new onset dyspepsiaUnintentional weight |
Surgery_Schwartz_7412 | Surgery_Schwartz | dayMotilin agonistDomperidone10 mg PO four times a dayDopamine antagonistTable 26-5Alarm symptoms that indicate the need for upper endoscopyAge >55 years with new onset dyspepsiaUnintentional weight lossPersistent or recurrent vomitingProgressive dysphagiaRecent onset odynophagiaUnexplained iron deficiency anemia or GI bleedingPalpable abdominal mass or lymphadenopathyFamily history of upper gastrointestinal cancerBrunicardi_Ch26_p1099-p1166.indd 111501/03/19 7:11 PM 1116SPECIFIC CONSIDERATIONS PART IIanalysis of myoelectric derangements in patients with gastropa-resis. Virtual gastroscopy using multi detector CT scan or MRI is not yet widely used, but these techniques may prove useful for screening and staging of gastric disease66-68 (Fig. 26-21). CTA or MRA is useful in evaluating the blood supply to the stomach after endovascular treatment of aortic and/or visceral arterial disease or in patients with previous upper abdominal operation in whom gastric conduit construction | Surgery_Schwartz. dayMotilin agonistDomperidone10 mg PO four times a dayDopamine antagonistTable 26-5Alarm symptoms that indicate the need for upper endoscopyAge >55 years with new onset dyspepsiaUnintentional weight lossPersistent or recurrent vomitingProgressive dysphagiaRecent onset odynophagiaUnexplained iron deficiency anemia or GI bleedingPalpable abdominal mass or lymphadenopathyFamily history of upper gastrointestinal cancerBrunicardi_Ch26_p1099-p1166.indd 111501/03/19 7:11 PM 1116SPECIFIC CONSIDERATIONS PART IIanalysis of myoelectric derangements in patients with gastropa-resis. Virtual gastroscopy using multi detector CT scan or MRI is not yet widely used, but these techniques may prove useful for screening and staging of gastric disease66-68 (Fig. 26-21). CTA or MRA is useful in evaluating the blood supply to the stomach after endovascular treatment of aortic and/or visceral arterial disease or in patients with previous upper abdominal operation in whom gastric conduit construction |
Surgery_Schwartz_7413 | Surgery_Schwartz | the blood supply to the stomach after endovascular treatment of aortic and/or visceral arterial disease or in patients with previous upper abdominal operation in whom gastric conduit construction is contemplated, e.g., with esophagectomy.Arteriography can be helpful in the occasional poor-risk patient with exsanguinating gastric hemorrhage, in the patient with occult gastric bleeding, or when CTA or MRA is inconclu-sive in delineating vascular anatomy.Endoscopic Ultrasound. Endoscopic ultrasound (EUS) is useful in the evaluation and management of gastric mass lesions.69-71 Local staging of gastric adenocarcinoma with EUS is quite accurate, and this modality can be used to plan therapy. At many centers, patients with transmural and/or node positive adenocarcinoma of the stomach are considered for preoperative (neoadjuvant) chemoradiation therapy. EUS is the best way to clinically stage these patients locoregion-ally. Suspicious nodes can be sampled with EUS-guided endoscopic needle | Surgery_Schwartz. the blood supply to the stomach after endovascular treatment of aortic and/or visceral arterial disease or in patients with previous upper abdominal operation in whom gastric conduit construction is contemplated, e.g., with esophagectomy.Arteriography can be helpful in the occasional poor-risk patient with exsanguinating gastric hemorrhage, in the patient with occult gastric bleeding, or when CTA or MRA is inconclu-sive in delineating vascular anatomy.Endoscopic Ultrasound. Endoscopic ultrasound (EUS) is useful in the evaluation and management of gastric mass lesions.69-71 Local staging of gastric adenocarcinoma with EUS is quite accurate, and this modality can be used to plan therapy. At many centers, patients with transmural and/or node positive adenocarcinoma of the stomach are considered for preoperative (neoadjuvant) chemoradiation therapy. EUS is the best way to clinically stage these patients locoregion-ally. Suspicious nodes can be sampled with EUS-guided endoscopic needle |
Surgery_Schwartz_7414 | Surgery_Schwartz | for preoperative (neoadjuvant) chemoradiation therapy. EUS is the best way to clinically stage these patients locoregion-ally. Suspicious nodes can be sampled with EUS-guided endoscopic needle biopsy. Malignant tumors that are confined to the mucosa on EUS may be amenable to endoscopic muco-sal resection (EMR). EUS also can be used to assess tumor response to chemotherapy. Submucosal masses are commonly discovered during routine EGD. Large submucosal masses should be resected unless benign pathology is a certainty, but observation may be appropriate for some small submucosal masses (e.g., lipoma or leiomyoma). There are endoscopic characteristics of benign and malignant mesenchymal tumors, and thus, EUS can provide reassurance, but no guarantee, that small lesions under observation are probably benign. Thus, EUS-guided needle biopsy should be considered. Submucosal varices also can be assessed by EUS.Gastric Secretory Analysis. Analysis of gastric acid output requires gastric | Surgery_Schwartz. for preoperative (neoadjuvant) chemoradiation therapy. EUS is the best way to clinically stage these patients locoregion-ally. Suspicious nodes can be sampled with EUS-guided endoscopic needle biopsy. Malignant tumors that are confined to the mucosa on EUS may be amenable to endoscopic muco-sal resection (EMR). EUS also can be used to assess tumor response to chemotherapy. Submucosal masses are commonly discovered during routine EGD. Large submucosal masses should be resected unless benign pathology is a certainty, but observation may be appropriate for some small submucosal masses (e.g., lipoma or leiomyoma). There are endoscopic characteristics of benign and malignant mesenchymal tumors, and thus, EUS can provide reassurance, but no guarantee, that small lesions under observation are probably benign. Thus, EUS-guided needle biopsy should be considered. Submucosal varices also can be assessed by EUS.Gastric Secretory Analysis. Analysis of gastric acid output requires gastric |
Surgery_Schwartz_7415 | Surgery_Schwartz | are probably benign. Thus, EUS-guided needle biopsy should be considered. Submucosal varices also can be assessed by EUS.Gastric Secretory Analysis. Analysis of gastric acid output requires gastric intubation, and it is performed infrequently nowadays. This test may be useful in the evaluation of patients with hypergastrinemia, including the Zollinger-Ellison syn-drome (ZES), patients with refractory ulcer or GERD, and patients with recurrent ulcer after operation. Historically, gas-tric analysis was performed most commonly to test for the ade-quacy of vagotomy in postoperative patients with recurrent or persistent ulcer. Now this can be done by assessing peripheral ABCDFigure 26-21. Conventional double-contrast barium study (A) shows a focal protruding mass (arrow) on the gastric fundus. Axial com-puted tomographic scan (B) also shows a protruding polyp (arrow). The three-dimensional computed tomographic gastrographic images in the transparent (C) mode shows an elevated lesion on the | Surgery_Schwartz. are probably benign. Thus, EUS-guided needle biopsy should be considered. Submucosal varices also can be assessed by EUS.Gastric Secretory Analysis. Analysis of gastric acid output requires gastric intubation, and it is performed infrequently nowadays. This test may be useful in the evaluation of patients with hypergastrinemia, including the Zollinger-Ellison syn-drome (ZES), patients with refractory ulcer or GERD, and patients with recurrent ulcer after operation. Historically, gas-tric analysis was performed most commonly to test for the ade-quacy of vagotomy in postoperative patients with recurrent or persistent ulcer. Now this can be done by assessing peripheral ABCDFigure 26-21. Conventional double-contrast barium study (A) shows a focal protruding mass (arrow) on the gastric fundus. Axial com-puted tomographic scan (B) also shows a protruding polyp (arrow). The three-dimensional computed tomographic gastrographic images in the transparent (C) mode shows an elevated lesion on the |
Surgery_Schwartz_7416 | Surgery_Schwartz | Axial com-puted tomographic scan (B) also shows a protruding polyp (arrow). The three-dimensional computed tomographic gastrographic images in the transparent (C) mode shows an elevated lesion on the gastric fundus (arrow). Photograph of the total gastrectomy specimen (D) shows a well-demarcated polypoid mass (arrow); this lesion was confirmed as early gastric carcinoma type I on microscopic examination (not shown). (Reproduced with permission from Shin KS, Kim SH, Han JK, et al: Three-dimensional MDCT gastrography compared with axial CT for the detection of early gastric cancer, J Comput Assist Tomogr. 2007 Sep-Oct;31(5):741-749.)Brunicardi_Ch26_p1099-p1166.indd 111601/03/19 7:11 PM 1117STOMACHCHAPTER 26pancreatic polypeptide levels in response to sham feeding.72 A 50% increase in pancreatic polypeptide within 30 minutes of sham feeding suggests intact vagal function.Normal basal acid output (BAO) is greater than 5 mEq/h. MAO is the average of the two final stimulated 15-minute | Surgery_Schwartz. Axial com-puted tomographic scan (B) also shows a protruding polyp (arrow). The three-dimensional computed tomographic gastrographic images in the transparent (C) mode shows an elevated lesion on the gastric fundus (arrow). Photograph of the total gastrectomy specimen (D) shows a well-demarcated polypoid mass (arrow); this lesion was confirmed as early gastric carcinoma type I on microscopic examination (not shown). (Reproduced with permission from Shin KS, Kim SH, Han JK, et al: Three-dimensional MDCT gastrography compared with axial CT for the detection of early gastric cancer, J Comput Assist Tomogr. 2007 Sep-Oct;31(5):741-749.)Brunicardi_Ch26_p1099-p1166.indd 111601/03/19 7:11 PM 1117STOMACHCHAPTER 26pancreatic polypeptide levels in response to sham feeding.72 A 50% increase in pancreatic polypeptide within 30 minutes of sham feeding suggests intact vagal function.Normal basal acid output (BAO) is greater than 5 mEq/h. MAO is the average of the two final stimulated 15-minute |
Surgery_Schwartz_7417 | Surgery_Schwartz | polypeptide within 30 minutes of sham feeding suggests intact vagal function.Normal basal acid output (BAO) is greater than 5 mEq/h. MAO is the average of the two final stimulated 15-minute periods and is usually 10 to 15 mEq/h. Peak acid output is defined as the highest of the four stimulated periods. Patients with a gastrinoma commonly have a high BAO, often above 30 mEq/h, but consistently above 15 mEq/h unless there has been previous vagotomy or gastric resection. In patients with gastrinoma, the ratio of BAO to MAO exceeds 0.6. Normal acid output in the patient prescribed acid-suppressive medica-tion usually means that the patient is noncompliant. To assess acid-secretory capacity in the absence of medication effect, H2 blockers and PPIs should be withheld for several days before gastric analysis.Scintigraphy. The standard scintigraphic evaluation of gastric emptying involves the ingestion of a test meal with one or two isotopes and scanning the patient under a gamma camera. A | Surgery_Schwartz. polypeptide within 30 minutes of sham feeding suggests intact vagal function.Normal basal acid output (BAO) is greater than 5 mEq/h. MAO is the average of the two final stimulated 15-minute periods and is usually 10 to 15 mEq/h. Peak acid output is defined as the highest of the four stimulated periods. Patients with a gastrinoma commonly have a high BAO, often above 30 mEq/h, but consistently above 15 mEq/h unless there has been previous vagotomy or gastric resection. In patients with gastrinoma, the ratio of BAO to MAO exceeds 0.6. Normal acid output in the patient prescribed acid-suppressive medica-tion usually means that the patient is noncompliant. To assess acid-secretory capacity in the absence of medication effect, H2 blockers and PPIs should be withheld for several days before gastric analysis.Scintigraphy. The standard scintigraphic evaluation of gastric emptying involves the ingestion of a test meal with one or two isotopes and scanning the patient under a gamma camera. A |
Surgery_Schwartz_7418 | Surgery_Schwartz | analysis.Scintigraphy. The standard scintigraphic evaluation of gastric emptying involves the ingestion of a test meal with one or two isotopes and scanning the patient under a gamma camera. A curve for gastric emptying is plotted, and the half-time is calcu-lated. Normal standards exist at each facility. Duodenogastric reflux can be quantitated by the IV administration of hepato-biliary iminodiacetic acid (HIDA scan), which is concentrated and excreted by the liver into the duodenum. Software allows a semiquantitative assessment of how much of the isotope refluxes into the stomach. Positron emission tomography (PET) scan or CT/PET scan is useful in staging certain patients with gastric malignancy.Tests for Helicobacter pylori. A variety of tests can help the clinician to determine whether the patient has active H pylori infection.73 The predictive value (positive and negative) of any of these tests when used as a screening tool depends on the prevalence of H pylori infection in the | Surgery_Schwartz. analysis.Scintigraphy. The standard scintigraphic evaluation of gastric emptying involves the ingestion of a test meal with one or two isotopes and scanning the patient under a gamma camera. A curve for gastric emptying is plotted, and the half-time is calcu-lated. Normal standards exist at each facility. Duodenogastric reflux can be quantitated by the IV administration of hepato-biliary iminodiacetic acid (HIDA scan), which is concentrated and excreted by the liver into the duodenum. Software allows a semiquantitative assessment of how much of the isotope refluxes into the stomach. Positron emission tomography (PET) scan or CT/PET scan is useful in staging certain patients with gastric malignancy.Tests for Helicobacter pylori. A variety of tests can help the clinician to determine whether the patient has active H pylori infection.73 The predictive value (positive and negative) of any of these tests when used as a screening tool depends on the prevalence of H pylori infection in the |
Surgery_Schwartz_7419 | Surgery_Schwartz | the patient has active H pylori infection.73 The predictive value (positive and negative) of any of these tests when used as a screening tool depends on the prevalence of H pylori infection in the screened population. A positive test is quite accurate in predicting H pylori infection, but a negative test can be unreliable. Thus, in the appropriate clinical setting, treatment for H pylori should be initiated on the basis of a positive test, but not necessarily withheld if the test is negative. Helicobacter infection should be treated when the diagnosis is made and eradication is confirmed.A positive serologic test is presumptive evidence of active infection if the patient has never been treated for H pylori. Histologic examination of gastric mucosal biopsy using special stains is the gold standard test for helicobacter infection. Other sensitive tests include commercially available rapid urease tests, which assay for the presence of urease in mucosal biopsy speci-mens (strong | Surgery_Schwartz. the patient has active H pylori infection.73 The predictive value (positive and negative) of any of these tests when used as a screening tool depends on the prevalence of H pylori infection in the screened population. A positive test is quite accurate in predicting H pylori infection, but a negative test can be unreliable. Thus, in the appropriate clinical setting, treatment for H pylori should be initiated on the basis of a positive test, but not necessarily withheld if the test is negative. Helicobacter infection should be treated when the diagnosis is made and eradication is confirmed.A positive serologic test is presumptive evidence of active infection if the patient has never been treated for H pylori. Histologic examination of gastric mucosal biopsy using special stains is the gold standard test for helicobacter infection. Other sensitive tests include commercially available rapid urease tests, which assay for the presence of urease in mucosal biopsy speci-mens (strong |
Surgery_Schwartz_7420 | Surgery_Schwartz | the gold standard test for helicobacter infection. Other sensitive tests include commercially available rapid urease tests, which assay for the presence of urease in mucosal biopsy speci-mens (strong presumptive evidence of infection). Urease is an omnipresent enzyme in H pylori strains that colonize the gas-tric mucosa. The carbon labeled urea breath test has become the standard test to confirm eradication of H pylori following appropriate treatment.74 In this test, the patient ingests urea labeled with nonradioactive 13C or 14C. The labeled urea is acted upon by the urease present in the H pylori and converted into ammonia and carbon dioxide. The radiolabeled carbon dioxide is excreted from the lungs and can be detected in the expired air (Fig. 26-22). It also can be detected in a blood sample. The fecal antigen test also is quite sensitive and specific for active H pylori infection and may also be used to confirm cure after treatment. Helicobacter culture may be useful to assess | Surgery_Schwartz. the gold standard test for helicobacter infection. Other sensitive tests include commercially available rapid urease tests, which assay for the presence of urease in mucosal biopsy speci-mens (strong presumptive evidence of infection). Urease is an omnipresent enzyme in H pylori strains that colonize the gas-tric mucosa. The carbon labeled urea breath test has become the standard test to confirm eradication of H pylori following appropriate treatment.74 In this test, the patient ingests urea labeled with nonradioactive 13C or 14C. The labeled urea is acted upon by the urease present in the H pylori and converted into ammonia and carbon dioxide. The radiolabeled carbon dioxide is excreted from the lungs and can be detected in the expired air (Fig. 26-22). It also can be detected in a blood sample. The fecal antigen test also is quite sensitive and specific for active H pylori infection and may also be used to confirm cure after treatment. Helicobacter culture may be useful to assess |
Surgery_Schwartz_7421 | Surgery_Schwartz | sample. The fecal antigen test also is quite sensitive and specific for active H pylori infection and may also be used to confirm cure after treatment. Helicobacter culture may be useful to assess antimi-crobial resistance in persistently recalcitrant cases.Antroduodenal Motility Testing and Electrogastrography. Antroduodenal motility testing and electrogastrography (EGG) are performed in specialized centers and may be useful in the evaluation of the occasional patient with dyspeptic symptoms. EGG consists of the transcutaneous recording of gastric myo-electric activity. Antroduodenal motility testing is done with a tube placed transnasally or transorally into the distal duodenum. There are pressure-recording sensors extending from the stom-ach to the distal duodenum. The combination of these two tests together with scintigraphy provides a thorough assessment of gastric motility.HELICOBACTER PYLORI INFECTIONOver 50% of people worldwide are infected with Helicobacter pylori.75,76 | Surgery_Schwartz. sample. The fecal antigen test also is quite sensitive and specific for active H pylori infection and may also be used to confirm cure after treatment. Helicobacter culture may be useful to assess antimi-crobial resistance in persistently recalcitrant cases.Antroduodenal Motility Testing and Electrogastrography. Antroduodenal motility testing and electrogastrography (EGG) are performed in specialized centers and may be useful in the evaluation of the occasional patient with dyspeptic symptoms. EGG consists of the transcutaneous recording of gastric myo-electric activity. Antroduodenal motility testing is done with a tube placed transnasally or transorally into the distal duodenum. There are pressure-recording sensors extending from the stom-ach to the distal duodenum. The combination of these two tests together with scintigraphy provides a thorough assessment of gastric motility.HELICOBACTER PYLORI INFECTIONOver 50% of people worldwide are infected with Helicobacter pylori.75,76 |
Surgery_Schwartz_7422 | Surgery_Schwartz | of these two tests together with scintigraphy provides a thorough assessment of gastric motility.HELICOBACTER PYLORI INFECTIONOver 50% of people worldwide are infected with Helicobacter pylori.75,76 Infection with H pylori is a chronic disease and does not resolve spontaneously without specific treatment. World-wide, H pylori–induced gastritis accounts for 80% to 90% of all gastritis. Chronic gastritis associated with H pylori is the most important risk factor for peptic ulcer and gastric adeno-carcinoma. Successful H pylori treatment largely eliminates recurrent peptic ulcer in infected patients, and eradication of H pylori worldwide would eliminate most cases of gastric Figure 26-22. Labeled urea breath test to detect Helicobacter infection. (Repro-duced with permission from Walsh JH, Peterson WL. The treatment of Helico-bacter pylori infection in the management of peptic ulcer disease, N Engl J Med. 1995 Oct 12;333(15):984-991.)[13C] urea13CO2 (µmol)Positive breathurea | Surgery_Schwartz. of these two tests together with scintigraphy provides a thorough assessment of gastric motility.HELICOBACTER PYLORI INFECTIONOver 50% of people worldwide are infected with Helicobacter pylori.75,76 Infection with H pylori is a chronic disease and does not resolve spontaneously without specific treatment. World-wide, H pylori–induced gastritis accounts for 80% to 90% of all gastritis. Chronic gastritis associated with H pylori is the most important risk factor for peptic ulcer and gastric adeno-carcinoma. Successful H pylori treatment largely eliminates recurrent peptic ulcer in infected patients, and eradication of H pylori worldwide would eliminate most cases of gastric Figure 26-22. Labeled urea breath test to detect Helicobacter infection. (Repro-duced with permission from Walsh JH, Peterson WL. The treatment of Helico-bacter pylori infection in the management of peptic ulcer disease, N Engl J Med. 1995 Oct 12;333(15):984-991.)[13C] urea13CO2 (µmol)Positive breathurea |
Surgery_Schwartz_7423 | Surgery_Schwartz | Walsh JH, Peterson WL. The treatment of Helico-bacter pylori infection in the management of peptic ulcer disease, N Engl J Med. 1995 Oct 12;333(15):984-991.)[13C] urea13CO2 (µmol)Positive breathurea testUreaseBloodHours1213CO2 in breathNH2NH22NH3+CO2H2O + 13C = 0Negative breathurea testBrunicardi_Ch26_p1099-p1166.indd 111701/03/19 7:11 PM 1118SPECIFIC CONSIDERATIONS PART IIadenocarcinoma, a major cause of cancer death worldwide.77 Helicobacter pylori infection is also associated with MALT lymphoma, dyspepsia, hyperplastic gastric polyps, and even immune thrombocytopenic purpura.Human beings are the only reservoir for H pylori. Infection is presumed to occur by oral ingestion of the bacterium, which dramatically alters the gastric microbiome.78 In helicobacter-infected individuals, 90% of gastric bacteria are helicobacter, whereas in helicobacter-negative patients 90% of gastric bac-teria are a combination of firmicutes, actinobacteria, bacte-roidetes, proteobacteria, and | Surgery_Schwartz. Walsh JH, Peterson WL. The treatment of Helico-bacter pylori infection in the management of peptic ulcer disease, N Engl J Med. 1995 Oct 12;333(15):984-991.)[13C] urea13CO2 (µmol)Positive breathurea testUreaseBloodHours1213CO2 in breathNH2NH22NH3+CO2H2O + 13C = 0Negative breathurea testBrunicardi_Ch26_p1099-p1166.indd 111701/03/19 7:11 PM 1118SPECIFIC CONSIDERATIONS PART IIadenocarcinoma, a major cause of cancer death worldwide.77 Helicobacter pylori infection is also associated with MALT lymphoma, dyspepsia, hyperplastic gastric polyps, and even immune thrombocytopenic purpura.Human beings are the only reservoir for H pylori. Infection is presumed to occur by oral ingestion of the bacterium, which dramatically alters the gastric microbiome.78 In helicobacter-infected individuals, 90% of gastric bacteria are helicobacter, whereas in helicobacter-negative patients 90% of gastric bac-teria are a combination of firmicutes, actinobacteria, bacte-roidetes, proteobacteria, and |
Surgery_Schwartz_7424 | Surgery_Schwartz | 90% of gastric bacteria are helicobacter, whereas in helicobacter-negative patients 90% of gastric bac-teria are a combination of firmicutes, actinobacteria, bacte-roidetes, proteobacteria, and fusobacteria. The prevalence of H pylori infection varies among populations and is strongly cor-related with socioeconomic conditions. In developing countries, H pylori infection usually occurs in childhood, and over 80% of adults are infected. Reinfection after curative treatment is common. Infection rates are lower in industrialized countries, and the prevalence of infection in the United States has been declining since the second half of the 19th century as hygiene and sanitation have improved. Nonetheless, H pylori infection is predicted to remain endemic in the United States for the next century. Family members of infected individuals and healthcare workers are at increased risk of infection.With specialized flagella and a rich supply of urease, H pylori is uniquely equipped for survival | Surgery_Schwartz. 90% of gastric bacteria are helicobacter, whereas in helicobacter-negative patients 90% of gastric bac-teria are a combination of firmicutes, actinobacteria, bacte-roidetes, proteobacteria, and fusobacteria. The prevalence of H pylori infection varies among populations and is strongly cor-related with socioeconomic conditions. In developing countries, H pylori infection usually occurs in childhood, and over 80% of adults are infected. Reinfection after curative treatment is common. Infection rates are lower in industrialized countries, and the prevalence of infection in the United States has been declining since the second half of the 19th century as hygiene and sanitation have improved. Nonetheless, H pylori infection is predicted to remain endemic in the United States for the next century. Family members of infected individuals and healthcare workers are at increased risk of infection.With specialized flagella and a rich supply of urease, H pylori is uniquely equipped for survival |
Surgery_Schwartz_7425 | Surgery_Schwartz | Family members of infected individuals and healthcare workers are at increased risk of infection.With specialized flagella and a rich supply of urease, H pylori is uniquely equipped for survival in the hostile envi-ronment of the stomach.[79-81] Helicobacter strains that lack either flagella or urease are nonpathogenic. The pathogenesis of helicobacter infection involves survival in the acidic gastric lumen, flagellated movement from the lumen across the mucus layer to the surface epithelial cell, adhesion to the surface epi-thelial cell, and toxin production. Up to 15% of the protein in a Helicobacter organism is composed of cytoplasmic urease that converts periplasmic urea into CO2 and ammonia. This buffers the surrounding acid, allowing the bacteria to survive the inimical luminal environment until it can burrow deeply into the surface mucus, propelled by its flagella (Fig. 26-23). H pylori typically does not invade the surface epithelial cell layer. Rather, it triggers a host | Surgery_Schwartz. Family members of infected individuals and healthcare workers are at increased risk of infection.With specialized flagella and a rich supply of urease, H pylori is uniquely equipped for survival in the hostile envi-ronment of the stomach.[79-81] Helicobacter strains that lack either flagella or urease are nonpathogenic. The pathogenesis of helicobacter infection involves survival in the acidic gastric lumen, flagellated movement from the lumen across the mucus layer to the surface epithelial cell, adhesion to the surface epi-thelial cell, and toxin production. Up to 15% of the protein in a Helicobacter organism is composed of cytoplasmic urease that converts periplasmic urea into CO2 and ammonia. This buffers the surrounding acid, allowing the bacteria to survive the inimical luminal environment until it can burrow deeply into the surface mucus, propelled by its flagella (Fig. 26-23). H pylori typically does not invade the surface epithelial cell layer. Rather, it triggers a host |
Surgery_Schwartz_7426 | Surgery_Schwartz | environment until it can burrow deeply into the surface mucus, propelled by its flagella (Fig. 26-23). H pylori typically does not invade the surface epithelial cell layer. Rather, it triggers a host immune response by attach-ing to gastric epithelial cells. Important Helicobacter adhesins mediating surface cell injury include neutrophil activating pro-tein A, heat shock protein 60, and sialic acid–binding adhesin. Helicobacter-produced toxins include vacuolating cytotoxin A and cag A (cytotoxin-associated gene A). The initial inflammatory response to Helicobacter infection is characterized by recruit-ment of neutrophils, followed sequentially by T and B lympho-cytes, plasma cells, and macrophages (Fig. 26-24). The resultant chronic gastric inflammation in affected individuals is charac-terized by enhanced mucosal expression of multiple cytokines and the presence of reactive oxygen and nitrogen species, and long-term infection is associated with mucosal cell DNA damage and | Surgery_Schwartz. environment until it can burrow deeply into the surface mucus, propelled by its flagella (Fig. 26-23). H pylori typically does not invade the surface epithelial cell layer. Rather, it triggers a host immune response by attach-ing to gastric epithelial cells. Important Helicobacter adhesins mediating surface cell injury include neutrophil activating pro-tein A, heat shock protein 60, and sialic acid–binding adhesin. Helicobacter-produced toxins include vacuolating cytotoxin A and cag A (cytotoxin-associated gene A). The initial inflammatory response to Helicobacter infection is characterized by recruit-ment of neutrophils, followed sequentially by T and B lympho-cytes, plasma cells, and macrophages (Fig. 26-24). The resultant chronic gastric inflammation in affected individuals is charac-terized by enhanced mucosal expression of multiple cytokines and the presence of reactive oxygen and nitrogen species, and long-term infection is associated with mucosal cell DNA damage and |
Surgery_Schwartz_7427 | Surgery_Schwartz | charac-terized by enhanced mucosal expression of multiple cytokines and the presence of reactive oxygen and nitrogen species, and long-term infection is associated with mucosal cell DNA damage and chromosomal instability and increased apopto-sis (Fig. 26-25).80,81 The net effect is a weakening of mucosal defenses. The mechanism by which the helicobacter organism avoids recognition and destruction by the mucosal immune sys-tem is a topic of interest and active research.82Acute H pylori infection causes a nonerosive pangastritis that is invariably followed by the development of chronic gastritis. Chronic antral gastritis with sparing of the proximal stomach occurs in about 10% of infected patients, and this pre-disposes to peptic ulcer disease (PUD). The other 90% of Heli-cobacter-infected patients develop chronic inflammation of the proximal stomach (corpus dominant gastritis), which can lead to gastric cancer in about 1% to 3% of this group.Figure 26-23. Helicobacter pylori closely | Surgery_Schwartz. charac-terized by enhanced mucosal expression of multiple cytokines and the presence of reactive oxygen and nitrogen species, and long-term infection is associated with mucosal cell DNA damage and chromosomal instability and increased apopto-sis (Fig. 26-25).80,81 The net effect is a weakening of mucosal defenses. The mechanism by which the helicobacter organism avoids recognition and destruction by the mucosal immune sys-tem is a topic of interest and active research.82Acute H pylori infection causes a nonerosive pangastritis that is invariably followed by the development of chronic gastritis. Chronic antral gastritis with sparing of the proximal stomach occurs in about 10% of infected patients, and this pre-disposes to peptic ulcer disease (PUD). The other 90% of Heli-cobacter-infected patients develop chronic inflammation of the proximal stomach (corpus dominant gastritis), which can lead to gastric cancer in about 1% to 3% of this group.Figure 26-23. Helicobacter pylori closely |
Surgery_Schwartz_7428 | Surgery_Schwartz | patients develop chronic inflammation of the proximal stomach (corpus dominant gastritis), which can lead to gastric cancer in about 1% to 3% of this group.Figure 26-23. Helicobacter pylori closely adherent to the cell membrane (top), and spiral-shaped H pylori attached to epithelial surface and surrounding microvilli (bottom). In the image on the bottom, the bacterial flagella can be seen arising from the upper pole of the bacterium. (Reproduced with permission from Mertz HR, Walsh JH: Peptic ulcer pathophysiology, Med Clin North Am. 1991 Jul;75(4):799-814.)H pylori infection is the major cause of peptic ulceration. Patients with H pylori infection and antral gastritis are three and one-half times more likely to develop PUD than patients without H pylori infection. Up to 90% of patients with duode-nal ulcers, and at least 70% of patients with gastric ulcers, have H pylori infection. It is clear from multiple randomized prospec-tive studies that curing H pylori infection dramatically | Surgery_Schwartz. patients develop chronic inflammation of the proximal stomach (corpus dominant gastritis), which can lead to gastric cancer in about 1% to 3% of this group.Figure 26-23. Helicobacter pylori closely adherent to the cell membrane (top), and spiral-shaped H pylori attached to epithelial surface and surrounding microvilli (bottom). In the image on the bottom, the bacterial flagella can be seen arising from the upper pole of the bacterium. (Reproduced with permission from Mertz HR, Walsh JH: Peptic ulcer pathophysiology, Med Clin North Am. 1991 Jul;75(4):799-814.)H pylori infection is the major cause of peptic ulceration. Patients with H pylori infection and antral gastritis are three and one-half times more likely to develop PUD than patients without H pylori infection. Up to 90% of patients with duode-nal ulcers, and at least 70% of patients with gastric ulcers, have H pylori infection. It is clear from multiple randomized prospec-tive studies that curing H pylori infection dramatically |
Surgery_Schwartz_7429 | Surgery_Schwartz | with duode-nal ulcers, and at least 70% of patients with gastric ulcers, have H pylori infection. It is clear from multiple randomized prospec-tive studies that curing H pylori infection dramatically alters the natural history of PUD, decreasing the recurrent ulcer rate from more than 75% in patients treated with a course of acid-suppressive therapy alone (in whom H pylori is not eradicated) to less than 20% in patients treated with a course of antibacterial therapy (Fig. 26-26).83In patients with duodenal ulcer caused by helicobacter, the associated antral gastritis leads to relative hypergastrinemia by depleting antral somatostatin, the primary inhibitor of antral gastrin release. H pylori infection is associated with decreased Brunicardi_Ch26_p1099-p1166.indd 111801/03/19 7:11 PM 1119STOMACHCHAPTER 26levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. The mechanism of decreased antral somatostatin synthesis and | Surgery_Schwartz. with duode-nal ulcers, and at least 70% of patients with gastric ulcers, have H pylori infection. It is clear from multiple randomized prospec-tive studies that curing H pylori infection dramatically alters the natural history of PUD, decreasing the recurrent ulcer rate from more than 75% in patients treated with a course of acid-suppressive therapy alone (in whom H pylori is not eradicated) to less than 20% in patients treated with a course of antibacterial therapy (Fig. 26-26).83In patients with duodenal ulcer caused by helicobacter, the associated antral gastritis leads to relative hypergastrinemia by depleting antral somatostatin, the primary inhibitor of antral gastrin release. H pylori infection is associated with decreased Brunicardi_Ch26_p1099-p1166.indd 111801/03/19 7:11 PM 1119STOMACHCHAPTER 26levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. The mechanism of decreased antral somatostatin synthesis and |
Surgery_Schwartz_7430 | Surgery_Schwartz | PM 1119STOMACHCHAPTER 26levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. The mechanism of decreased antral somatostatin synthesis and release may be related to (a) antral alkalinization due to heli-cobacter urease (acid in the antrum releases somatostatin); (b) toxic cytokine effect on antral D cells; and/or (c) Helicobacter production of N-α-methylhistamine, an H3 receptor agonist, which binds H3 receptors on the antral D cell and decreases somatostatin release.84 Since the gastritis does not involve the oxcyntic mucosa, hypergastrinemia leads to hyperacidity and parietal cell hyperplasia. The acid hypersecretion and the antral gastritis are thought to lead to antral epithelial metaplasia in the postpyloric duodenum. This duodenal metaplasia allows H pylori to colonize the duodenal mucosa, and this is where the duodenal ulcer occurs. In fact, in patients with gastric metapla-sia of the duodenum, the risk of developing | Surgery_Schwartz. PM 1119STOMACHCHAPTER 26levels of somatostatin, decreased somatostatin messenger RNA production, and fewer somatostatin-producing D cells. The mechanism of decreased antral somatostatin synthesis and release may be related to (a) antral alkalinization due to heli-cobacter urease (acid in the antrum releases somatostatin); (b) toxic cytokine effect on antral D cells; and/or (c) Helicobacter production of N-α-methylhistamine, an H3 receptor agonist, which binds H3 receptors on the antral D cell and decreases somatostatin release.84 Since the gastritis does not involve the oxcyntic mucosa, hypergastrinemia leads to hyperacidity and parietal cell hyperplasia. The acid hypersecretion and the antral gastritis are thought to lead to antral epithelial metaplasia in the postpyloric duodenum. This duodenal metaplasia allows H pylori to colonize the duodenal mucosa, and this is where the duodenal ulcer occurs. In fact, in patients with gastric metapla-sia of the duodenum, the risk of developing |
Surgery_Schwartz_7431 | Surgery_Schwartz | duodenal metaplasia allows H pylori to colonize the duodenal mucosa, and this is where the duodenal ulcer occurs. In fact, in patients with gastric metapla-sia of the duodenum, the risk of developing a duodenal ulcer increases 50-fold. When H pylori colonizes the duodenum, there is a significant decrease in acid-stimulated duodenal bicarbonate release. When H pylori infection is successfully treated, acid secretory physiology tends to normalize. Relapse of duodenal ulcer after eradication of H pylori may signal reinfection of the gastric mucosa by the organism.Many patients with antral dominant helicobacter gastritis never develop duodenal ulcer, and some patients with peptic ulcer do not have Helicobacter. This obviously suggests that there are other important pathogenetic factors involved in peptic ulcer. And even in the presence of active H pylori infection, strong acid suppression usually heals peptic ulcer, an observa-tion consistent with the old dictum “no acid, no ulcer.” But | Surgery_Schwartz. duodenal metaplasia allows H pylori to colonize the duodenal mucosa, and this is where the duodenal ulcer occurs. In fact, in patients with gastric metapla-sia of the duodenum, the risk of developing a duodenal ulcer increases 50-fold. When H pylori colonizes the duodenum, there is a significant decrease in acid-stimulated duodenal bicarbonate release. When H pylori infection is successfully treated, acid secretory physiology tends to normalize. Relapse of duodenal ulcer after eradication of H pylori may signal reinfection of the gastric mucosa by the organism.Many patients with antral dominant helicobacter gastritis never develop duodenal ulcer, and some patients with peptic ulcer do not have Helicobacter. This obviously suggests that there are other important pathogenetic factors involved in peptic ulcer. And even in the presence of active H pylori infection, strong acid suppression usually heals peptic ulcer, an observa-tion consistent with the old dictum “no acid, no ulcer.” But |
Surgery_Schwartz_7432 | Surgery_Schwartz | in peptic ulcer. And even in the presence of active H pylori infection, strong acid suppression usually heals peptic ulcer, an observa-tion consistent with the old dictum “no acid, no ulcer.” But suc-cessful helicobacter treatment eliminates ulcer recurrence and the need for long-term PPI. And long-term PPI in patients with active Helicobacter infection may lead to corpus predominant gastritis, which leads to atrophic gastritis and increases the risk of gastric cancer. Thus, Helicobacter infection should be treated and eradication confirmed.Testing for H pylori infection should be performed in patients with peptic ulcer, gastritis, significant dyspepsia, MALT lymphoma, and early gastric cancer.85 Noninvasive methods for diagnosis of H pylori infection include the urea breath test, serology, and detection of stool antigen. The urea breath test has a sensitivity and specificity of greater than 90% and is useful for initial diagnosis of infection and for follow-up after eradication | Surgery_Schwartz. in peptic ulcer. And even in the presence of active H pylori infection, strong acid suppression usually heals peptic ulcer, an observa-tion consistent with the old dictum “no acid, no ulcer.” But suc-cessful helicobacter treatment eliminates ulcer recurrence and the need for long-term PPI. And long-term PPI in patients with active Helicobacter infection may lead to corpus predominant gastritis, which leads to atrophic gastritis and increases the risk of gastric cancer. Thus, Helicobacter infection should be treated and eradication confirmed.Testing for H pylori infection should be performed in patients with peptic ulcer, gastritis, significant dyspepsia, MALT lymphoma, and early gastric cancer.85 Noninvasive methods for diagnosis of H pylori infection include the urea breath test, serology, and detection of stool antigen. The urea breath test has a sensitivity and specificity of greater than 90% and is useful for initial diagnosis of infection and for follow-up after eradication |
Surgery_Schwartz_7433 | Surgery_Schwartz | and detection of stool antigen. The urea breath test has a sensitivity and specificity of greater than 90% and is useful for initial diagnosis of infection and for follow-up after eradication therapy since it is positive only in the presence of active infection. The stool antigen test is another noninvasive test to detect active H pylori infection, but it is recommended that only locally validated tests be used.86 Because H pylori induces a strong immunologic response, serological testing is useful but may not be as accurate as the urea breath test or the stool antigen test, and a positive serology persists after eradica-tion of H pylori infection, so serology is not useful to confirm successful treatment of Helicobacter infection. H pylori infec-tion can also be diagnosed by histologic evaluation of gastric biopsies and/or the rapid urease test on fresh biopsies. Culture of H pylori is not routine and is usually reserved for recurrent infection and for antibiotic sensitivity testing | Surgery_Schwartz. and detection of stool antigen. The urea breath test has a sensitivity and specificity of greater than 90% and is useful for initial diagnosis of infection and for follow-up after eradication therapy since it is positive only in the presence of active infection. The stool antigen test is another noninvasive test to detect active H pylori infection, but it is recommended that only locally validated tests be used.86 Because H pylori induces a strong immunologic response, serological testing is useful but may not be as accurate as the urea breath test or the stool antigen test, and a positive serology persists after eradica-tion of H pylori infection, so serology is not useful to confirm successful treatment of Helicobacter infection. H pylori infec-tion can also be diagnosed by histologic evaluation of gastric biopsies and/or the rapid urease test on fresh biopsies. Culture of H pylori is not routine and is usually reserved for recurrent infection and for antibiotic sensitivity testing |
Surgery_Schwartz_7434 | Surgery_Schwartz | of gastric biopsies and/or the rapid urease test on fresh biopsies. Culture of H pylori is not routine and is usually reserved for recurrent infection and for antibiotic sensitivity testing when second-line therapy has failed. All tests for H pylori have a false negative rate. Empiric Helicobacter treatment can be considered despite negative tests if clinical likelihood of infection is high, e.g., a compliant nonsmoking, non–NSAID-consuming patient facing operation for nonhealing peptic ulcer or a patient with unex-plained gastritis.Patients with a positive test should be treated and eradi-cation confirmed. Spontaneous cure without treatment is very rare. It is important to note that none of the therapeutic regimens reported to date cure H pylori infection in 100% of patients. To be effective, antimicrobial drugs must be combined with gas-tric acid secretion inhibitors or bismuth salts. The Maastricht V/Florence Consensus Report87 provides current recommenda-tions for diagnosis and | Surgery_Schwartz. of gastric biopsies and/or the rapid urease test on fresh biopsies. Culture of H pylori is not routine and is usually reserved for recurrent infection and for antibiotic sensitivity testing when second-line therapy has failed. All tests for H pylori have a false negative rate. Empiric Helicobacter treatment can be considered despite negative tests if clinical likelihood of infection is high, e.g., a compliant nonsmoking, non–NSAID-consuming patient facing operation for nonhealing peptic ulcer or a patient with unex-plained gastritis.Patients with a positive test should be treated and eradi-cation confirmed. Spontaneous cure without treatment is very rare. It is important to note that none of the therapeutic regimens reported to date cure H pylori infection in 100% of patients. To be effective, antimicrobial drugs must be combined with gas-tric acid secretion inhibitors or bismuth salts. The Maastricht V/Florence Consensus Report87 provides current recommenda-tions for diagnosis and |
Surgery_Schwartz_7435 | Surgery_Schwartz | antimicrobial drugs must be combined with gas-tric acid secretion inhibitors or bismuth salts. The Maastricht V/Florence Consensus Report87 provides current recommenda-tions for diagnosis and treatment of H pylori infection in various clinical scenarios, including recommendations for areas with high metronidazole and clarithromycin resistance.87,88 Ideally, a treatment regimen is chosen with 90% effectiveness. Treat-ment failure requires an alternative course of therapy. Failure to eradicate infection after two tries should prompt Helicobacter culture and sensitivity testing and referral to a specialist. With assiduous treatment, Helicobacter eradication can be achieved in nearly every patient. Patients with atrophic gastritis require endoscopic surveillance (see discussion of gastritis later in this Figure 26-24. Model of Helico-bacter effects on duodenal ulcer pathogenesis. (Reproduced with per-mission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s | Surgery_Schwartz. antimicrobial drugs must be combined with gas-tric acid secretion inhibitors or bismuth salts. The Maastricht V/Florence Consensus Report87 provides current recommenda-tions for diagnosis and treatment of H pylori infection in various clinical scenarios, including recommendations for areas with high metronidazole and clarithromycin resistance.87,88 Ideally, a treatment regimen is chosen with 90% effectiveness. Treat-ment failure requires an alternative course of therapy. Failure to eradicate infection after two tries should prompt Helicobacter culture and sensitivity testing and referral to a specialist. With assiduous treatment, Helicobacter eradication can be achieved in nearly every patient. Patients with atrophic gastritis require endoscopic surveillance (see discussion of gastritis later in this Figure 26-24. Model of Helico-bacter effects on duodenal ulcer pathogenesis. (Reproduced with per-mission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s |
Surgery_Schwartz_7436 | Surgery_Schwartz | later in this Figure 26-24. Model of Helico-bacter effects on duodenal ulcer pathogenesis. (Reproduced with per-mission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.)Multiple factors (smoking, ageat acquisition of infection)Somatostatin/gastrindysregulationAcquisition of H pyloriDuodenum ulcerationIncreased acidsecretionGastric metaplasiain duodenumDuodenum bicarbonate secretionInflammation (Duodenitis)Chronic H pyloriinfection in stomachH pylori colonization in duodenumBrunicardi_Ch26_p1099-p1166.indd 111901/03/19 7:11 PM 1120SPECIFIC CONSIDERATIONS PART IIchapter) because the same sequence of inflammation to meta-plasia to dysplasia to carcinoma, that is well known to occur in the esophagus from reflux-induced inflammation (and in the colon from inflammatory bowel disease), is now increasingly well recognized to occur in the stomach with Helicobacter-induced | Surgery_Schwartz. later in this Figure 26-24. Model of Helico-bacter effects on duodenal ulcer pathogenesis. (Reproduced with per-mission from Feldman M, Friedman LS, Sleisenger MH, et al: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 7th ed. Philadelphia, PA: Elsevier/Saunders; 2002.)Multiple factors (smoking, ageat acquisition of infection)Somatostatin/gastrindysregulationAcquisition of H pyloriDuodenum ulcerationIncreased acidsecretionGastric metaplasiain duodenumDuodenum bicarbonate secretionInflammation (Duodenitis)Chronic H pyloriinfection in stomachH pylori colonization in duodenumBrunicardi_Ch26_p1099-p1166.indd 111901/03/19 7:11 PM 1120SPECIFIC CONSIDERATIONS PART IIchapter) because the same sequence of inflammation to meta-plasia to dysplasia to carcinoma, that is well known to occur in the esophagus from reflux-induced inflammation (and in the colon from inflammatory bowel disease), is now increasingly well recognized to occur in the stomach with Helicobacter-induced |
Surgery_Schwartz_7437 | Surgery_Schwartz | to occur in the esophagus from reflux-induced inflammation (and in the colon from inflammatory bowel disease), is now increasingly well recognized to occur in the stomach with Helicobacter-induced gastritis. Helicobacter also clearly has an etiologic role in the development of gastric lymphoma.PEPTIC ULCER DISEASEPeptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper. They may be acute or chronic and, ultimately, are caused by an imbalance between mucosal defenses and acid/peptic injury (Fig. 26-27).89,90 Peptic ulcer remains a common outpatient diagnosis, but the number of Figure 26-25. Pathogen-host interactions in the pathogenesis of Helicobacter pylori infection. ICAM = intercellular adhesion molecule-1; IFN-γ = interferon-γ; LPS = lipopolysaccharide; NF-κB = nuclear factor κB; PAI = pathogenicity island; PMN = polymorphonuclear neutrophil; TNF-α = tumor necrosis factor-α; VCAM = vascular cell adhesion molecule. (Used with | Surgery_Schwartz. to occur in the esophagus from reflux-induced inflammation (and in the colon from inflammatory bowel disease), is now increasingly well recognized to occur in the stomach with Helicobacter-induced gastritis. Helicobacter also clearly has an etiologic role in the development of gastric lymphoma.PEPTIC ULCER DISEASEPeptic ulcers are focal defects in the gastric or duodenal mucosa that extend into the submucosa or deeper. They may be acute or chronic and, ultimately, are caused by an imbalance between mucosal defenses and acid/peptic injury (Fig. 26-27).89,90 Peptic ulcer remains a common outpatient diagnosis, but the number of Figure 26-25. Pathogen-host interactions in the pathogenesis of Helicobacter pylori infection. ICAM = intercellular adhesion molecule-1; IFN-γ = interferon-γ; LPS = lipopolysaccharide; NF-κB = nuclear factor κB; PAI = pathogenicity island; PMN = polymorphonuclear neutrophil; TNF-α = tumor necrosis factor-α; VCAM = vascular cell adhesion molecule. (Used with |
Surgery_Schwartz_7438 | Surgery_Schwartz | = lipopolysaccharide; NF-κB = nuclear factor κB; PAI = pathogenicity island; PMN = polymorphonuclear neutrophil; TNF-α = tumor necrosis factor-α; VCAM = vascular cell adhesion molecule. (Used with permission from Manuel Amieva, Stanford University.)cag+H pyloristraincag-PAI-encodedsecretoryapparatusMultiple adhesions:BabA (binds tolewis B), AIpA,AlpB, HopZPhospholipaseA2Alterationsin mucousglycoproteinsGastricepithelialcellFlagellaMucusActinpolymerizationCagAphosphorylationVacAApoptosisDisruption of epithelialbarrierFasexpressionUreaseLPSPorinsInterleukin-8CagAMacrophageInterleukin-12Th 1 cellTh 2 cellB cellCytokine-inducedchanges in gastric physiologyTh 0 cellICAM and VCAMexpressionPMN recruitmentInterleukin-8Chemotacticinterleukin-8 gradienton proteoglycanscaffoldingNeutrophilT cellB cellBlood vesselNF-˜ B AP-1 GRO-°ENA-78T-cell and B-cellextravasationINF-˛ TNF-°Interleukin-1˙MHC II, B7-1,and | Surgery_Schwartz. = lipopolysaccharide; NF-κB = nuclear factor κB; PAI = pathogenicity island; PMN = polymorphonuclear neutrophil; TNF-α = tumor necrosis factor-α; VCAM = vascular cell adhesion molecule. (Used with permission from Manuel Amieva, Stanford University.)cag+H pyloristraincag-PAI-encodedsecretoryapparatusMultiple adhesions:BabA (binds tolewis B), AIpA,AlpB, HopZPhospholipaseA2Alterationsin mucousglycoproteinsGastricepithelialcellFlagellaMucusActinpolymerizationCagAphosphorylationVacAApoptosisDisruption of epithelialbarrierFasexpressionUreaseLPSPorinsInterleukin-8CagAMacrophageInterleukin-12Th 1 cellTh 2 cellB cellCytokine-inducedchanges in gastric physiologyTh 0 cellICAM and VCAMexpressionPMN recruitmentInterleukin-8Chemotacticinterleukin-8 gradienton proteoglycanscaffoldingNeutrophilT cellB cellBlood vesselNF-˜ B AP-1 GRO-°ENA-78T-cell and B-cellextravasationINF-˛ TNF-°Interleukin-1˙MHC II, B7-1,and |
Surgery_Schwartz_7439 | Surgery_Schwartz | gradienton proteoglycanscaffoldingNeutrophilT cellB cellBlood vesselNF-˜ B AP-1 GRO-°ENA-78T-cell and B-cellextravasationINF-˛ TNF-°Interleukin-1˙MHC II, B7-1,and B7-2expressionAnti-H+/K+-ATPaseantibodiesBrunicardi_Ch26_p1099-p1166.indd 112001/03/19 7:11 PM 1121STOMACHCHAPTER 26physician visits, hospital admissions, and elective operations for PUD has decreased steadily and dramatically over the past four decades. Interestingly, the start of these trends all predated the widespread use of acid suppression, or highly selective vagot-omy. The incidence of emergency surgery and the death rate associated with peptic ulcers has not decreased nearly so dra-matically. These epidemiologic changes probably represent the net effect of several factors, including (beneficially) decreased prevalence of H pylori infection, better medical therapy, and increased outpatient management and (detrimentally) the use of NSAIDs and aspirin (with and without ulcer prophylaxis) | Surgery_Schwartz. gradienton proteoglycanscaffoldingNeutrophilT cellB cellBlood vesselNF-˜ B AP-1 GRO-°ENA-78T-cell and B-cellextravasationINF-˛ TNF-°Interleukin-1˙MHC II, B7-1,and B7-2expressionAnti-H+/K+-ATPaseantibodiesBrunicardi_Ch26_p1099-p1166.indd 112001/03/19 7:11 PM 1121STOMACHCHAPTER 26physician visits, hospital admissions, and elective operations for PUD has decreased steadily and dramatically over the past four decades. Interestingly, the start of these trends all predated the widespread use of acid suppression, or highly selective vagot-omy. The incidence of emergency surgery and the death rate associated with peptic ulcers has not decreased nearly so dra-matically. These epidemiologic changes probably represent the net effect of several factors, including (beneficially) decreased prevalence of H pylori infection, better medical therapy, and increased outpatient management and (detrimentally) the use of NSAIDs and aspirin (with and without ulcer prophylaxis) |
Surgery_Schwartz_7440 | Surgery_Schwartz | decreased prevalence of H pylori infection, better medical therapy, and increased outpatient management and (detrimentally) the use of NSAIDs and aspirin (with and without ulcer prophylaxis) in an aging population with multiple risk factors.Figure 26-26. Helicobacter treatment dramatically decreases the recurrence rate of duodenal and gastric ulcer. (Reproduced with permission from Peek RM, Blaser MJL: Pathophysiology of Helico-bacter pylori-induced gastritis and peptic ulcer disease, Am J Med. 1997 Feb;102(2):200-207.)Figure 26-27. Balance of aggressive and defensive factors in the gastric mucosa. (Reproduced with permission from Suerbaum S, Michetti P: Helicobacter pylori infection, N Engl J Med. 2002 Oct 10;347(15):1175-1186.)PUD is one of the most common GI disorders in the United States with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years.91 The costs of PUD, including lost work time and productivity, are estimated to be | Surgery_Schwartz. decreased prevalence of H pylori infection, better medical therapy, and increased outpatient management and (detrimentally) the use of NSAIDs and aspirin (with and without ulcer prophylaxis) in an aging population with multiple risk factors.Figure 26-26. Helicobacter treatment dramatically decreases the recurrence rate of duodenal and gastric ulcer. (Reproduced with permission from Peek RM, Blaser MJL: Pathophysiology of Helico-bacter pylori-induced gastritis and peptic ulcer disease, Am J Med. 1997 Feb;102(2):200-207.)Figure 26-27. Balance of aggressive and defensive factors in the gastric mucosa. (Reproduced with permission from Suerbaum S, Michetti P: Helicobacter pylori infection, N Engl J Med. 2002 Oct 10;347(15):1175-1186.)PUD is one of the most common GI disorders in the United States with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years.91 The costs of PUD, including lost work time and productivity, are estimated to be |
Surgery_Schwartz_7441 | Surgery_Schwartz | with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years.91 The costs of PUD, including lost work time and productivity, are estimated to be above $8 billion per year in the United States. In 1998, approximately 1.5% of all Medicare hospital costs were spent treating PUD, and the crude mortal-ity rate for peptic ulcer was 1.7 per 100,000 individuals. Using the National Inpatient Sample, it can be estimated that the mortality rate in patients hospitalized in 2006 with duodenal ulcer was 3.7% compared to 2.1% for gastric ulcer,92 and the age adjusted hospitalization rate was 56.5 per 100,000, down 21% from the previous decade. Recent studies have shown an increase in the rates of hospitalization and mortality in elderly patients for the peptic ulcer complications of bleeding and perforation.93 This may be due in part to the increasingly com-mon use of NSAIDs and aspirin in this elderly cohort, many of whom also have H pylori | Surgery_Schwartz. with a prevalence of about 2%, and a lifetime cumulative prevalence of about 10%, peaking around age 70 years.91 The costs of PUD, including lost work time and productivity, are estimated to be above $8 billion per year in the United States. In 1998, approximately 1.5% of all Medicare hospital costs were spent treating PUD, and the crude mortal-ity rate for peptic ulcer was 1.7 per 100,000 individuals. Using the National Inpatient Sample, it can be estimated that the mortality rate in patients hospitalized in 2006 with duodenal ulcer was 3.7% compared to 2.1% for gastric ulcer,92 and the age adjusted hospitalization rate was 56.5 per 100,000, down 21% from the previous decade. Recent studies have shown an increase in the rates of hospitalization and mortality in elderly patients for the peptic ulcer complications of bleeding and perforation.93 This may be due in part to the increasingly com-mon use of NSAIDs and aspirin in this elderly cohort, many of whom also have H pylori |
Surgery_Schwartz_7442 | Surgery_Schwartz | for the peptic ulcer complications of bleeding and perforation.93 This may be due in part to the increasingly com-mon use of NSAIDs and aspirin in this elderly cohort, many of whom also have H pylori infection.Pathophysiology and EtiologyA variety of factors may contribute to the development of PUD. Although it is now recognized that the large majority of duode-nal and gastric ulcers are caused by H pylori infection (see previ-ous discussion on H pylori) and/or NSAID use20,94 (Fig. 26-28), the final common pathway to ulcer formation is acid-peptic injury of the gastroduodenal mucosal barrier. Acid suppression heals both duodenal and gastric ulcers and prevents recurrence if continued. In general, H pylori predisposes to ulceration, both by acid hypersecretion and by compromise of mucosal defense mechanisms. NSAID use causes ulcers predominantly by com-promise of mucosal defenses. Duodenal ulcer was traditionally viewed as a disease of increased acid-peptic action on the duo-denal | Surgery_Schwartz. for the peptic ulcer complications of bleeding and perforation.93 This may be due in part to the increasingly com-mon use of NSAIDs and aspirin in this elderly cohort, many of whom also have H pylori infection.Pathophysiology and EtiologyA variety of factors may contribute to the development of PUD. Although it is now recognized that the large majority of duode-nal and gastric ulcers are caused by H pylori infection (see previ-ous discussion on H pylori) and/or NSAID use20,94 (Fig. 26-28), the final common pathway to ulcer formation is acid-peptic injury of the gastroduodenal mucosal barrier. Acid suppression heals both duodenal and gastric ulcers and prevents recurrence if continued. In general, H pylori predisposes to ulceration, both by acid hypersecretion and by compromise of mucosal defense mechanisms. NSAID use causes ulcers predominantly by com-promise of mucosal defenses. Duodenal ulcer was traditionally viewed as a disease of increased acid-peptic action on the duo-denal |
Surgery_Schwartz_7443 | Surgery_Schwartz | defense mechanisms. NSAID use causes ulcers predominantly by com-promise of mucosal defenses. Duodenal ulcer was traditionally viewed as a disease of increased acid-peptic action on the duo-denal mucosa, whereas gastric ulcer was viewed as a disease of weakened mucosal defenses. An increased understanding of peptic ulcer pathophysiology has blurred this overly simplistic distinction. Clearly, weakened mucosal defenses play a role in both duodenal and gastric ulcers, and acid hypersecretion may result in a duodenal or gastric ulcer in the setting of normal mucosal defenses.Elimination of H pylori infection or NSAID use is important for optimal ulcer healing, and perhaps is even more important in preventing ulcer recurrence and/or complications. A variety of other diseases are known to cause peptic ulcer, including ZES (gastrinoma), antral G-cell hyperfunction and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic stress. Other causative agents include drugs | Surgery_Schwartz. defense mechanisms. NSAID use causes ulcers predominantly by com-promise of mucosal defenses. Duodenal ulcer was traditionally viewed as a disease of increased acid-peptic action on the duo-denal mucosa, whereas gastric ulcer was viewed as a disease of weakened mucosal defenses. An increased understanding of peptic ulcer pathophysiology has blurred this overly simplistic distinction. Clearly, weakened mucosal defenses play a role in both duodenal and gastric ulcers, and acid hypersecretion may result in a duodenal or gastric ulcer in the setting of normal mucosal defenses.Elimination of H pylori infection or NSAID use is important for optimal ulcer healing, and perhaps is even more important in preventing ulcer recurrence and/or complications. A variety of other diseases are known to cause peptic ulcer, including ZES (gastrinoma), antral G-cell hyperfunction and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic stress. Other causative agents include drugs |
Surgery_Schwartz_7444 | Surgery_Schwartz | peptic ulcer, including ZES (gastrinoma), antral G-cell hyperfunction and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic stress. Other causative agents include drugs (all NSAIDs, aspirin, and cocaine), smoking, and psychologic stress. In the United States, probably more than 90% of serious peptic ulcer complications can be attributed to H pylori infec-tion, NSAID use, and/or cigarette smoking.Acid Secretion and Peptic Ulcer. A variety of abnormalities related to mucosal acid exposure have been described in patients with duodenal ulcer (Fig. 26-29).95 Although duodenal ulcer patients as a group have a higher mean BAO and mean MAO compared to normal controls, many duodenal ulcer patients have basal and peak acid outputs in the normal range, and there is no correlation between acid secretion and the severity of the ulcer disease. As a group, duodenal ulcer patients produce more acid than normal controls in response to any known acid secre-tory stimulus. | Surgery_Schwartz. peptic ulcer, including ZES (gastrinoma), antral G-cell hyperfunction and/or hyperplasia, systemic mastocytosis, trauma, burns, and major physiologic stress. Other causative agents include drugs (all NSAIDs, aspirin, and cocaine), smoking, and psychologic stress. In the United States, probably more than 90% of serious peptic ulcer complications can be attributed to H pylori infec-tion, NSAID use, and/or cigarette smoking.Acid Secretion and Peptic Ulcer. A variety of abnormalities related to mucosal acid exposure have been described in patients with duodenal ulcer (Fig. 26-29).95 Although duodenal ulcer patients as a group have a higher mean BAO and mean MAO compared to normal controls, many duodenal ulcer patients have basal and peak acid outputs in the normal range, and there is no correlation between acid secretion and the severity of the ulcer disease. As a group, duodenal ulcer patients produce more acid than normal controls in response to any known acid secre-tory stimulus. |
Surgery_Schwartz_7445 | Surgery_Schwartz | correlation between acid secretion and the severity of the ulcer disease. As a group, duodenal ulcer patients produce more acid than normal controls in response to any known acid secre-tory stimulus. Although they usually have normal fasting serum gastrin levels, DU patients often produce more gastric acid at AcidPepsinNSAIDsH pyloriAggressionDefenseRepairBicarbonateBlood flowMucusCell junctionsApical resistanceRestitutionMucoid capProliferationGrowth factors0%10%20%30%40%50%60%70%80%90%100%Duodenal ulcerrecurrenceGastric ulcerrecurrenceRanitidine +antibioticsRanitidine aloneBrunicardi_Ch26_p1099-p1166.indd 112101/03/19 7:11 PM 1122SPECIFIC CONSIDERATIONS PART IIany given dose of gastrin than controls. Considering that many duodenal ulcer patients do produce excessive gastric acid, 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 | Surgery_Schwartz. correlation between acid secretion and the severity of the ulcer disease. As a group, duodenal ulcer patients produce more acid than normal controls in response to any known acid secre-tory stimulus. Although they usually have normal fasting serum gastrin levels, DU patients often produce more gastric acid at AcidPepsinNSAIDsH pyloriAggressionDefenseRepairBicarbonateBlood flowMucusCell junctionsApical resistanceRestitutionMucoid capProliferationGrowth factors0%10%20%30%40%50%60%70%80%90%100%Duodenal ulcerrecurrenceGastric ulcerrecurrenceRanitidine +antibioticsRanitidine aloneBrunicardi_Ch26_p1099-p1166.indd 112101/03/19 7:11 PM 1122SPECIFIC CONSIDERATIONS PART IIany given dose of gastrin than controls. Considering that many duodenal ulcer patients do produce excessive gastric acid, 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 |
Surgery_Schwartz_7446 | 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 | 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 |
Surgery_Schwartz_7447 | 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 | 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 |
Surgery_Schwartz_7448 | 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 | 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 |
Surgery_Schwartz_7449 | 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 | 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 |
Surgery_Schwartz_7450 | 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 | 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 |
Surgery_Schwartz_7451 | 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 | 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 |
Surgery_Schwartz_7452 | 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, | 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, |
Surgery_Schwartz_7453 | 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 | 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 |
Surgery_Schwartz_7454 | 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 | 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 |
Surgery_Schwartz_7455 | 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 | 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 |
Surgery_Schwartz_7456 | 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. | 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. |
Surgery_Schwartz_7457 | 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 | 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 |
Surgery_Schwartz_7458 | 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 | 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 |
Surgery_Schwartz_7459 | 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 | 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 |
Surgery_Schwartz_7460 | 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: | 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: |
Surgery_Schwartz_7461 | 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 | 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 |
Surgery_Schwartz_7462 | 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 | 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 |
Surgery_Schwartz_7463 | 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 | 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 |
Surgery_Schwartz_7464 | 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. | 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. |
Surgery_Schwartz_7465 | 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 | 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 |
Surgery_Schwartz_7466 | 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 | 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 |
Surgery_Schwartz_7467 | 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 | 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 |
Surgery_Schwartz_7468 | 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 | 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 |
Surgery_Schwartz_7469 | 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 | 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 |
Surgery_Schwartz_7470 | 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 | 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 |
Surgery_Schwartz_7471 | 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 | 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 |
Surgery_Schwartz_7472 | 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 | 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 |
Surgery_Schwartz_7473 | 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 | 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 |
Surgery_Schwartz_7474 | 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 | 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 |
Surgery_Schwartz_7475 | 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 | 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 |
Surgery_Schwartz_7476 | 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 | 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 |
Surgery_Schwartz_7477 | 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 | 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 |
Surgery_Schwartz_7478 | 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 | 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 |
Surgery_Schwartz_7479 | 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 | 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 |
Surgery_Schwartz_7480 | 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 | 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 |
Surgery_Schwartz_7481 | 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 | 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 |
Surgery_Schwartz_7482 | 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 | 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 |
Surgery_Schwartz_7483 | 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 | 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 |
Surgery_Schwartz_7484 | 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 | 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 |
Surgery_Schwartz_7485 | 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 | 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 |
Surgery_Schwartz_7486 | 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 | 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 |
Surgery_Schwartz_7487 | 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 | 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 |
Surgery_Schwartz_7488 | 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 | 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 |
Surgery_Schwartz_7489 | 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. | 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. |
Surgery_Schwartz_7490 | 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 | 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 |
Surgery_Schwartz_7491 | 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 | 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 |
Surgery_Schwartz_7492 | 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 | 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 |
Surgery_Schwartz_7493 | 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 | 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 |
Surgery_Schwartz_7494 | 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 | 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 |
Surgery_Schwartz_7495 | 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 | 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 |
Surgery_Schwartz_7496 | 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 | 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 |
Surgery_Schwartz_7497 | 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, | 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, |
Surgery_Schwartz_7498 | 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 | 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 |
Surgery_Schwartz_7499 | 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 | 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 |
Surgery_Schwartz_7500 | 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 | 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 |
Surgery_Schwartz_7501 | 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 | 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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