General Surgery (Board Review Series) 1st Edition

12

Stomach and Duodenum

Stewart Long

1. Anatomy and Histology
2. Topographic anatomy of the stomach (Figure 12-1)
3. The anterior surface

• is adjacent to the left hemidiaphragm and the left hepatic lobe.

2. The posterior surface

• is adjacent to the left hemidiaphragm, left kidney, left adrenal, and the pancreas.

3. The greater curvature

• is adjacent to the transverse colon inferiorly and the spleen laterally.

4. Risks of percutaneous placement of gastrostomy tubesinclude hemorrhage or perforation given the proximity of the liver and colon, respectively.

• Gastrostomy tubes pass through the anterior abdominal wall to the stomach lumen to provide enteral nutrition or allow for decompression of the stomach.

1. Topographic anatomy of the duodenum

• The duodenum spans 20 to 30 cm from the pyloric sphincter to the ligament of Treitzand is divided into four parts.

1. The first portion [i.e., the duodenal bulb (cap)]overlies the common bile duct and is the site of over 90% of duodenal ulcers.
2. The second (i.e., descending) portionis attached to the pancreas and is retroperitoneal. The common bile duct and main pancreatic duct merge to form the ampulla of Vater, which enters this portion of the duodenum.
3. The third (i.e., transverse) portionis attached to the uncinate process of the pancreas and is wedged between the superior mesenteric artery anteriorly and the aorta posteriorly.

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4. The fourth (i.e., ascending) portionenters the jejunum at the ligament of Treitz.

Figure 12-1. The major topographic areas of the stomach and major arteries supplying the stomach and duodenum. (Adapted with permission from Lawrence P: Essentials of General Surgery. Baltimore, Williams & Wilkins, 1992, p 176.)

1. Arterial and venous supply
2. Gastric arterial blood supplyis primarily from the celiac trunk.
3. The lesser curve

• is supplied by the rightand left gastric arteries.

1. The greater curve

• is supplied by the rightand left gastroepiploic arteries.

1. The fundus

• is also supplied by the short gastric arteriesbranching from the distal splenic artery.

1. The pylorus

• is supplied by direct branches of the gastroduodenal artery.

1. Ligation

• of all but one of these major vessels may be performed without necrosis of the stomach wall.

2. Duodenal arterial blood supplystems primarily from the gastroduodenal artery and the superior mesenteric artery.
3. The superior pancreaticoduodenal branch

• of the gastroduodenal arterysupplies the duodenal bulb and the descending portion.

1. The inferior pancreaticoduodenal branch

• of the superior mesenteric arterysupplies the third and fourth portions of the duodenum.

1. These branches may communicateto provide collateral flow between the celiac trunk and the superior mesenteric artery.

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3. Venous and lymphatic drainage parallel each other.
4. Venous drainage

• is predominantly through the splenic and superior mesenteric veins.

1. Lymphatic drainage

• Frequent communications between lymph channelsallow for easy spread of neoplastic disease through local lymph nodes.

1. Innervation
2. The vagus nervesare the major nerve supply.
3. The left (anterior) vagus branches intothe

• hepatic division.
• anterior gastric wall branch.

3. The right (posterior) vagus branches intothe

• celiac branch.
• posterior gastric wall branch.

4. Gastroduodenal pain

• is sensed via afferent sympathetic fibers from T5–T10.

1. Histology
2. The stomach comprises

• an external serosa.
• muscle layers.
• submucosa.
• muscularis mucosa.
• a mucosa.

2. The proximal third of the stomachcontains three layers of smooth muscle: the outer longitudinal, the middle circular, and the inner oblique.
3. The distal two thirds of the stomachcontains a single longitudinal layer. This layer demonstrates spontaneous, repeated electrical discharges for peristalsis.
4. The mucosais lined by simple columnar epithelium with surface mucous cells.
5. The proximal cardiac glands

• secrete mucus.

1. The fundus and body

• contain oxyntic glands with parietal and chief cells.

2. Parietal cells secrete

• HClfor digestion.
• intrinsic factorfor vitamin B₁₂ absorption in the terminal ileum.

3. Chief cells secrete

• pepsinogenfor protein digestion.

1. The antrum contains

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• mucus-secreting cells.
• gastrin-producing G cells.

1. The pyloric sphincter

• is a thick circumferential layer of smooth muscle.

5. The duodenum consists of

• mucosal layers.
• submucosal layers.
• muscular layers.
• serosal layers.
• Brunner's glandsunique to the duodenum secrete an alkaline mucus.

1. Surgical anatomy of the stomach and duodenum
2. Vagotomy and pyloroplasty
3. Division of the main vagal trunks at the esophageal hiatus (truncal vagotomy)

• ablates the cephalic phase of gastric acid secretion.
• desensitizes the parietal cells to gastrin.

1. Denervation of the pylorus

• also results in discordant gastric emptying, which causes rapid emptying of liquids and abnormal solid emptying.

1. Division and reconstruction of the pylorus (pyloroplasty)

• is performed with this procedure to facilitate gastric emptying (Figure 12-2).

1. Diarrhea may occur after vagotomy

• but generally resolves with time.

Figure 12-2. A Heineke-Mikulicz pyloroplasty. A longitudinal incision is made through the pyloric sphincter and then the duodenum is closed in a transverse manner. (Adapted with permission from Lawrence P: Essentials of General Surgery. Baltimore, Williams & Wilkins, 1992, p 195.)

2. Other types of vagotomy procedures(Figure 12-3)

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1. Selective vagotomy

• denervates the entire stomach, but preserves innervation to the hepatobiliary system and celiac ganglia.

1. Proximal gastric vagotomy (parietal cell vagotomy or highly selective vagotomy)

• denervates fibers to the acid-secreting fundic mucosa, preserving pyloric vagal innervation.

1. These procedures are associated with a lower complication rate, but have a higher recurrence rateof ulcer disease versus truncal vagotomy.
2. Gastric resection and reconstruction
3. Antrectomy

• consists of removing the gastric antrum for ulcer disease.

1. Reconstruction

• may be performed by a Billroth I gastroduodenostomyor a Billroth II gastrojejunostomy (Figure 12-4).

1. Total gastrectomy

• involves removing the entire stomach.
• may be performed for curative resection of gastric neoplasms, massive diffuse gastric bleeding, or palliation in Zollinger-Ellison syndrome.

Figure 12-3. The truncal vagotomy and the proximal gastric vagotomy. (A) The main nerve trunks are both divided at the esophageal hiatus, denervating the entire abdomen of vagal innervation after truncal vagotomy. (B) A proximal gastric vagotomy or highly selective vagotomy only denervated the acid-producing parietal cell mass in the fundic region.

1. Physiology
2. Secretory factors of the upper gastrointestinal tract (Table 12-1)
3. Gastric acid secretion

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Figure 12-4. Billroth I and Billroth II. Both reconstructions follow vagotomy and antrectomy, which involves resection of the distal stomach. (A) In a Billroth I or gastroduodenostomy, the duodenum is reanastomosed to the stomach in physiologic continuity. (B) In the Billroth II or gastrojejunostomy, the duodenal stump is closed with a suture and a jejunal loop is reanastomosed to the remaining stomach. (Adapted with permission from Lawrence P: Essentials of General Surgery. Baltimore, Williams & Wilkins, 1992, p 193.)

1. The basolateral membrane of parietal cells contains receptors forhistamine, gastrin, and acetylcholine.

• These receptors decrease gastric pH through alterations in ion transport.

2. During the cephalic phase

• acid secretion increases in response to the thought, sight, or smell of food via vagal stimulation.

3. During the gastric phase

• acid secretion increases as food enters the stomach via gastrin-mediatedstimulation.

4. During the intestinal phase

• a decrease in stomach acidity is seen when acidified chymeenters the duodenum.

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1. Gastric motility
2. Increases in gastric volume

• lead to vagally mediated receptive relaxationof the stomach.

2. Meal ingestion

• stimulates proximal contraction and distal peristalsis.

3. The pylorus

• then closes 2–3 seconds before antral contraction, producing churning of chyme.

Table 12-1. Characteristics of Several Gastric and Duodenal Secretory Factors

Factor Source Stimulus Action Gastrin G cells in antrum and duodenum Meals, amino acids, gastric distension Stimulates acid secretion and mucosal growth Somatostatin Pancreatic D cell Intraluminal fat, PGE2 Inhibits acid secretion and gastrin release Histamine Mast cells Adrenergic stimuli Stimulates acid secretion Acetylcholine Vagus nerve terminus Vagal stimulation Acid stimulation Pepsin Chief cells Meals Initiate protein digestion Bicarbonate Mucous cells, pancreatic ductal cells Low mucosal pH, cholinergic stimuli Neutralize acid Intrinsic factor Parietal cells Meals, gastrin, histamine, acetylcholine Bind vitamin B12 for terminal ileum absorption Cholecystokinin Duodenum and jejunum Luminal fats and proteins Gallbladder contraction, stimulates exocrine pancreatic secretion Secretin S cells of duodenum and jejunum Duodenal acidification Stimulates pancreatic secretion Gastric inhibitory peptide Duodenum and jejunum Meals Augments insulin response to enteral feedings Motilin Enterochromaffin cells of small intestine Fasting state, erythromycin stimulates motilin receptors Regulates migrating motor complex PGE2 = prostaglandin E2.

III. Upper Gastrointestinal Hemorrhage

• is defined as bleeding proximalto the ligament of Treitz.

1. Risk factors include

• previous upper gastrointestinal bleed.
• peptic ulcer disease.
• nonsteroidal anti-inflammatory drug (NSAID) use.
• alcohol abuse.
• smoking.
• liver disease.

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• trauma or burn history.
• esophageal varices.
• sepsis.
• vomiting.
• splenic vein thrombosis.

1. Potential causes are characterized in Table 12-2

• Peptic ulcer diseaseis the leading cause of upper gastrointestinal bleeding.

1. Signs and symptoms may include

• hypotension/syncope/shock.
• hematemesis/coffee ground emesis.
• melena/guaiac-positive stools.
• epigastric pain.
• fatigue.

1. Diagnosis
2. Examination of the nasogastric (N/G) tube aspirate

• can rapidly confirm the presence of upper gastrointestinal bleeding.

2. Endoscopic esophagogastroduodenoscopy (EGD)

• localizes most sources of upper gastrointestinal bleeding.

1. Treatment
2. Initial treatmentinvolves

• protection of the airwayif necessary (i.e., intubation).
• adequate volume resuscitation.

2. Subsequent managementinvolves

• appropriate treatment of the specific cause of bleeding.

1. Mostcauses can be treated endoscopically, with surgery reserved for severe bleeding refractory to initial measures.
2. Angiographic embolizationis used in some situations when the patient is a poor surgical candidate.
3. Gastritis
4. Overview
5. Gastritis consists of inflammatory changes in the mucosasecondary to epithelial damage from decreased mucosal defenses.
6. Clinically, gastritis is differentiatedas acute or chronic gastritis.
7. Acute gastritis

• is classified according to the cause (i.e., stress, Helicobacter pyloriinfection, NSAIDs).

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1. Chronic gastritis

• is classified as Type A (fundal) or Type B (antral).

Table 12-2. Causes of Upper Gastrointestinal Bleeding

Disease Risks Diagnosis Treatment Miscellaneous PUD H. pylori infection, alcohol abuse, smoking EGD EGD, medical therapy, surgery as indicated Posterior duodenal ulcer erodes into gastroduodenal artery Acute gastritis Sepsis, CNS injury (Cushing's ulcer), trauma, severe burns (Curling's ulcer) EGD EGD, medical therapy Mucosal superficial erosions in proximal stomach Esophageal varices Portal hypertension, alcohol abuse EGD Sclerotherapy, vasopressin infusion Portal venous system is valveless Mallory-Weiss tear Severe retching, alcohol abuse EGD Majority spontaneously resolve Linear mucosal tear at esophageal hiatus Aorto-duodenal fistula Abdominal aortic aneurysm, previous aortic surgery Angiography Emergent resection, repair hole in duodenum Most present with a “sentinel bleed” before massive hemorrhage Gastric neoplasm Adenocarcinoma, lymphoma EGD with biopsy Resection May mimic PUD Hemobilia/hemosuccus pancreaticus Prior history of hepatic/biliary trauma or chronic pancreatitis EGD, selective angiography Angiographic embolization Arterial erosion into biliary or pancreatic ducts CNS = central nervous system; EGD = esophagogastroduodenoscopy; H. pylori = Helicobacter pylori; PUD = peptic ulcer disease.

1. Risk factors
2. Predisposing factors for acute erosive gastritisinclude

• NSAID use.
• cigarette smoking.
• alcohol abuse.

2. Predisposing factors for acute stress gastritisinclude

• multiple trauma.
• major burns.
• sepsis.
• brain injury.
• renal failure.
• adult respiratory distress syndrome (ARDS).
• hypotension.
• an extended stay in the intensive care unit.

3. Chronic gastritis
4. Type A (fundal) is associated with

• pernicious anemia.
• parietal cell antibodies.
• achlorhydria.
• autoimmune diseases.

1. Type B (antral) is associated with

• H. pyloriinfection in almost 100% of cases.

1. Pathology
2. Acute erosive gastritis is characterized by

• a friable edematous mucosa with erosions and sites of bleeding that may be localized or diffuse.
• Mucosal ischemiais generally the inciting pathologic event.

2. Chronic gastritis typically is manifest

• by a patchy and irregular distribution of mucosal erosions.

1. Signs and symptoms of acute gastritis
2. Painless upper gastrointestinal bleeding

• is the hallmark of gastritis.
• is usually slow and intermittent, but can be profuse.

2. Other symptomsmay include

• epigastric pain.
• nausea.
• vomiting.

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3. Other signsinclude

• blood in the N/G tube aspirate.
• guaiac-positive stools.
• unexplained anemia.
• a drop in the hematocrit.

1. The diagnosis of acute gastritis

• is confirmed by EGD.

1. Treatment of acute gastritis
2. Resuscitation

• with crystalloid and appropriate blood products is essential.

2. Antacids, H₂-blockers, and proton pump inhibitors (e.g., omeprazole)

• are used to decrease gastric pH.

3. Endoscopic electrocautery

• may occasionally be used to treat a localized source of bleeding.

4. Surgery for acute gastritis

• is associated with a high mortality.
• is rarely necessary.

1. Vagotomy and pyloroplasty

• with oversewing of obvious bleeding points is recommended in most patients who require an operation.

1. Total gastric resection

• is reserved for diffuse bleeding not amenable to any other therapy.

1. Peptic Ulcer Disease
2. Ulcers are classified according to location.

• Common locations include the stomach, duodenum, esophagus, and jejunum (i.e., after gastrojejunostomy).

1. Duodenal ulcers

most commonly occur in middle-aged men.

• Ninety-five percent occur within 2 cm of the pylorusin the first portion of the duodenum.

1. Risk factors
2. The primary risk factor

• is the presence ofH. pylori in the upper gastrointestinal tract.

2. Other risk factorsinclude

• cigarette smoking.
• NSAID use.
• delayed gastric emptying.
• uremia.

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• Zollinger-Ellison syndrome.

2. Pathogenesis
3. H. pyloriinfection

• plays a major role in the weakening of mucosal defenses and subsequent ulcer development.

1. Gastric acid secretion

• is usually elevatedin patients with duodenal ulcers, in contrast to gastric ulcers.

3. Signs and symptoms

. Epigastric pain

• is a cardinal feature.
• is typically burning, stabbing, and gnawing.
• may be relieved by food or antacids.

1. Other possible symptomsinclude

• nausea.
• vomiting.
• anorexia.
• hematemesis.
• melena.

1. Patients can present with

• guaiac-positive stools.
• symptoms of hypotension secondary to hemorrhage (e.g., syncope).

4. Diagnosis

. EGD is the preferred diagnostic method

• because it allows for visualization, biopsy, and possible treatment.

1. H. pyloriinfection can be confirmed with

• biopsy.
• noninvasive techniques (e.g., breath test).

1. Contrast radiographs

• may demonstrate retention of contrast in the ulcer.

5. Treatment

. Medical therapy is primary in the treatment of uncomplicated duodenal ulcer disease.

1. Frequently used agentsinclude

• H₂-blockers(e.g., famotidine).
• proton pump inhibitors(e.g., omeprazole).

2. Antibiotic therapy (when H. pylori is present)in addition to these agents heals more than 90% of ulcers.
3. Surgeryis required in a small minority of patients with ulcer disease.

• Indications for surgery are listed in Table 12-3.

1. Gastric ulcers have many characteristics similar to duodenal ulcers.
2. Clinical presentation

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• Gastric adenocarcinoma may mimic gastric ulcer disease;therefore, care must be taken to rule out malignancy.

Table 12-3. Indications for Surgical Therapy of a Duodenal Ulcer

Indication Definition Clinical Findings Procedure Perforation Full-thickness erosion of ulcer through deuodenal wall Severe epigastric pain, peritonitis, free air, 90% occur on anterior duodenal bulb (first portion) Oversewing piece of omentum over perforation (Graham patch); may perform definitive ulcer operation depending on patient status Hemorrhage Blood transfusion (≥ 6 units), recurrent bleeding after endoscopic therapy Severe hypotension or shock, hematemesis, blood from rectum (frequently associated with a posterior duodenal ulcer with erosion into the gastroduodenal artery) Duodentomy and direct vessel oversewing followed by vagotomy and pyloroplasty Obstruction Obstructive symptoms secondary to scarring and edema Nausea, vomiting, anorexia, pyloric channel ulcers Vagotomy and antrectomy with Billroth II or vagotomy and drainage Intractability Recurrent or persistent ulceration despite ≥ 8 weeks of H2-blockers or ≥ 6 weeks of proton pump inhibitors as well as adequate treatment forHelicobacter pylori Persistent pain refractory to medical therapy; symptoms significantly interfere with daily activities Parietal cell vagotomy

2. Risk factors

• The risk factors for gastric ulcer disease are generally the same as those for duodenal ulcer disease.

3. Location
4. The location of the gastric ulcers plays an important role in determining the pathogenesis and treatment.
5. Classification of gastric ulcersis based on their location (Figure 12-5).

• Gastric ulcers most commonly occur on the lesser curveof the stomach.

1. Acid secretionmay not be elevated, unlike in duodenal ulcer disease.
2. Signs and symptoms

. Epigastric pain is generally gnawing, dull, and burning.

• Food may aggravate or precipitate painin contrast to duodenal ulcers.

1. Other possible symptomsinclude nausea, vomiting, and anorexia.

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1. Perforation and severe hemorrhage

• may also occur, as with duodenal ulcers.

Figure 12-5. The location of the four types of gastric ulcer. (A) Type I occurs along the lesser curvature and is associated with large volumes of secretion. (B) Type II occurs in the body of the stomach and in combination with a duodenal ulcer. (C) Type III is simply a prepyloric ulcer. (D) Type IV is rare and occurs in close proximity to the gastroesophageal junction. (Adapted with permission from Blackbourne LH: Advanced Surgical Recall. Baltimore, Williams & Wilkins, 1997, p 375.)

5. Diagnosis

. Endoscopy

• is the most reliablediagnostic tool.
• allows for biopsy of the ulcerto evaluate for carcinoma.
• Indications for early endoscopyinclude weight loss, obstructive symptoms, a palpable mass, guaiac-positive stools, and anemia.

1. Barium contrast radiographs

• may be useful if endoscopic evaluation is incomplete or contraindicated.

6. Treatment

. Medical therapy

• is the primary treatment, like in duodenal ulcers.
• involves administration of acid-reducing agents with antibiotics when H. pyloriis present.

1. Indications for surgeryinclude

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• intractability.
• severe hemorrhage.
• perforation.
• obstruction.
• These indications are identical to those for duodenal ulcers (see Table 12-3).

1. Definitive surgical treatment

• may vary depending on the site and pathogenesis of the gastric ulcer (Table 12-4).

1. Gastric versus duodenal ulcers

• A key difference in the approach to patients is the appropriate recognitionand management of malignancy in patients with gastric ulcers.

Table 12-4. Types of Gastric Ulcers

Type Pathogenesis Definitive Treatment I Decreased mucosal defense, low acid status Distal gastrectomy with ulcer excision II High acid secretory status Antrectomy with truncal vagotomy, vagotomy and pyloroplasty, or vagotomy and drainage III High acid secretory status Vagotomy and antrectomy with ulcer excision in specimen IV High acid secretory status Excision of ulcer or distal gastroectomy with vertical extension to include ulcer V Associated with nonsteroidal anti-inflammatory drugs Usually responds to withdrawal of agent and medical treatment; surgery is rarely indicated

1. Gastric Neoplasms
2. Benign gastric neoplasms
3. Leiomyomas

• are the most common benign gastric neoplasms.
• are usually asymptomatic, but hemorrhage or obstruction can occur.
• are submucosal lesionsthat are well-encapsulated.
• Treatment involves resectionof the lesion with margins of normal tissue.

2. Hyperplastic polyps

• account for 70%–80% of all gastric polyps.
• consist of histologically normal gastric epithelium.
• have no malignant potential.

3. Adenomatous polyps

• carry a 10%–20% risk of carcinoma, with an increased risk associated with increasing polyp size (e.g., > 2 cm).

1. Treatment

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• consists of endoscopic resection of pedunculated lesions.

1. Operative excision may be required for

• sessile lesions larger than 2 cm.
• polyps with foci of invasive carcinoma.
• polyps complicated by pain or bleeding.

1. Malignant gastric neoplasms
2. Adenocarcinoma of the stomach

• is the most common malignant lesion of the stomach.
• occurs more frequently in malesthan females.
• is rare in the United States, although it is more common in Japan.

1. Risk factorsinclude

• dietary nitrates.
• the presence of adenomatous polyps.
• exposure to H. pylori.
• chronic gastritis.
• pernicious anemia.
• achlorhydria.

1. Signs and symptoms
2. The clinical presentation

• may be indistinguishable from peptic ulcer disease.

2. Symptomsinclude

• weight loss.
• pain.
• nausea and vomiting.
• anorexia.
• dysphagia.

3. Signs of advanced diseaseinclude

• supraclavicular adenopathy (Virchow's node).
• ovarian metastases (Krukenberg's tumor).

1. Diagnosis
2. Endoscopyis the definitive diagnostic method with an accuracy of more than 95% when multiple biopsy specimens are obtained.

• Approximately 75% of patients have metastatic disease at the time of diagnosis.

1. To characterize the extent of the diseaseuse

• barium contrast studies.
• computed tomography (CT) scan.
• endoscopic ultrasound.

1. Staging and prognosis(Table 12-5)
2. Treatment
3. Surgical resection

• Surgical resection may be curative, although most tumors are at an advanced stage at the time of diagnosis.

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• Procedures include a subtotal or total gastrectomyplus lymph node dissection for tumors amenable to curative resection.

1. Surgical palliation with gastric resection

• is also frequently performed for incurable disease to provide relief of symptoms (e.g., dysphagia).

2. Radiation therapy and chemotherapy

• play a minor role in the management of gastric cancer.

Table 12-5. Staging and Prognosis of Adenocarcinoma of the Stomach

Stage Description 5-Year Survival Rate I Mucosal involvement 66% II Through muscularis propria without lymph node involvement 33% III Any lymph node involvement without distant metastases 10% IV Distant metastases or extension of primary tumor into adjacent structures (e.g., liver) 0%

2. Gastric lymphoma
3. Overview
4. Non-Hodgkin lymphomas

• account for 5% of malignant gastric tumors.
• occur most frequently in patients 60–70 years old.

1. A subset of lymphomas associated with mucosal-associated lymphoid tissue (MALT)have a strong association with H. pylori infection.
2. Signs and symptomsinclude

• epigastric pain.
• weight loss.
• anorexia.
• nausea.
• vomiting.
• occult bleeding and anemia(50% of patients).

2. Diagnosis
3. Endoscopic biopsy

• with brush cytology and ultrasound are 90% accurate.

1. Chest and abdominal CT scan and bone marrow biopsy

• are used to identify systemic disease.

3. Staging of gastric lymphomas(Table 12-6)
4. Treatmentis controversial.
5. The role of gastric resection

• is controversial, with many advocating the use of chemoradiation therapy alone.

1. Gastrectomy allows for

• accurate histological diagnosis.
• local cure.

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• elimination of the risk of hemorrhage or perforation.

2. Combination chemoradiation therapy

• with or without surgical resectionis generally used to treat gastric lymphomas.

3. MALT-associated lymphomas

• may regress with treatment of H. pylori.

5. Overall survivalfor all stages of gastric lymphoma is greater than or equal to 50%.
6. Gastric leiomyosarcomas

• require wide excision, although local recurrence and peritoneal involvement are common.

4. Gastric carcinoids

• are extremely rare.

Table 12-6. Gastric Lymphoma Staging

Stage Definition I Tumor confined to stomach only II Spread to perigastric lymph nodes III Nodal spread beyond perigastric nodes (e.g., para-aortic nodes) IV Spread to other abdominal organs (e.g., liver, spleen)

VII. Surgical Treatment of Morbid Obesity

1. Overview
2. Morbid (severe) obesity

• is defined as more than 100 lb above ideal body weight, or a body mass index greater than or equal to 35.
• is also associated with an increasein overall mortality.

2. Associated morbidityincludes

• cardiac and pulmonary dysfunction.
• diabetes mellitus.
• degenerative joint disease.
• sexual dysfunction.

3. Dietary management

• has not achieved uniform, long-term success for the treatment of morbid obesity.
• Ninety-five percent of patients will regain all weight lost through diets.

1. Results of surgical treatment
2. The average weight loss is 50%–67% of excess weightwithin 1.5 years.
3. Most patients requiring insulin

• for non–insulin-dependent diabetes mellitus (NIDDM) preoperatively will not require insulin after surgery.

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3. Hypertensionresolves or improves in 80% of patients.
4. Obstructive sleep apneausually resolves.
5. The patient's self imageoften improves.
6. Surgical options
7. Gastroplasty

• provides slightly less weight loss than gastric bypass.

1. Meshused in the procedure may erode into the stomach.
2. Gastroesophageal refluxmay also occur, which generally requires conversion to a gastric bypass.
3. Gastric bypass(Figure 12-6)

• involves formation of a small stomach pouch and a gastrojejunostomyto drain the pouch.

1. Weight loss is regained

• in 10%–15% of patients from excessive, constant nibbling of high-calorie foods.

1. Operative mortality

• with surgery is 0.5%.

1. Complications of gastric operations include

Figure 12-6. Surgical procedure for bariatric surgery. (A) Vertical banded gastroplasty consists of placing a Silastic ring near the incisura, creating an in-flow obstruction and limiting the volume of food consumed. Erosion of mesh into the stomach is a potential problem. (B) The proximal Roux-en-Y gastric bypass consists of the formation of a small gastric pouch anastomosed to a long jejunal limb. Typically, the staple line is divided. (Adapted with permission from Greenfield L: Surgery: Scientific Principles and Practice, 2nd ed. Philadelphia, Lippincott Williams & Wilkins, 1997, pp 791–792.)

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• perforation or leak at anastomosis sites.
• necrosis of the distal stomach.
• ulcer formation at anastomosis sites (often responds to medical therapy).
• obstruction or stenosis (may be treated with endoscopic balloon dilation).
• vitamin B₁₂deficiency or anemia.
• gallstone formation with rapid weight loss(cholecystectomy may be performed at the time of operation).

VIII. Miscellaneous Disorders of the Stomach and Duodenum

1. Mallory-Weiss tear

• is a potential cause of upper gastrointestinal bleeding that results from a longitudinal tearof the mucosa and submucosa near the gastroesophageal junction.

1. Risk factorsinclude

• severe retching or coughing.
• alcohol abuse.
• presence of a hiatal hernia.

2. Symptomsmay include

• epigastric pain.
• substernal pain.
• classically, hematemesis after an episode of forceful retching.

3. Endoscopic evaluation

• can confirm the presence of a tear.

4. Treatment
5. Bleeding stops spontaneously

• in 90% of patients.

1. Persistent bleeding

• is managed with endoscopic electrocautery.

1. Refractory bleeding

• may require surgical repair of the laceration.

1. Dumping syndrome
2. Symptoms

• generally occur after rapid entry of a carbohydrate loadinto the small bowel secondary to bypass of the pylorus (e.g., Billroth II).

1. Characteristic gastrointestinal and vasomotor symptomsinclude

• nausea.
• vomiting.
• abdominal pain.

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• flatus.
• palpitations.
• dizziness.
• diaphoresis.

1. Early symptoms

• occur immediately after a meal.
• may occur 1–3 hours after a meal, secondary to reactive hypoglycemia (i.e., late dumping syndrome).

2. Treatment

. Most cases resolve with time

• although dietary changes (i.e., small, low-carbohydrate meals) and somatostatin may be beneficial.

1. Severe cases

• may require conversion to a Roux-en-Y gastrojejunostomy (Figure 12-7).

Figure 12-7. Truncal vagotomy with antrectomy and Roux-en-Y anastomosis. This anastomosis is particularly useful to correct many of the problems associated with vagotomy and Billroth I reanastomosis. It is particularly useful for alkaline reflux gastritis because reflux of small bowel contents into the stomach is reduced. (Adapted with permission from Lawrence P: Essentials of General Surgery. Baltimore, Williams & Wilkins, 1992, p 194.)

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1. Afferent loop syndrome

• results from obstruction of the afferent limbafter a Billroth II procedure (see Figure 12-6) with accumulation of biliary secretions.

1. Over 66% present in the first postoperative week with

• postprandial right upper quadrant (RUQ) pain.
• nonbilious vomiting.
• fever.
• steatorrhea.

2. Diagnosis

• Contrast radiographs, CT scan, and endoscopy may be useful.

3. Treatment consists of

• surgical reconstruction with a Roux-en-Y gastrojejunostomy or balloon dilation.

1. Alkaline reflux gastritis

• results from bile reflux into the stomach.

1. Symptomsinclude

• postprandial epigastric pain.
• nausea.
• vomiting.

2. Diagnosis

• is made with endoscopic confirmation of bile reflux and biopsy-proven gastritis.

3. Treatment

• Sucralfatemay be used to bind bile.
• Surgery is rarely required.

1. Gastric volvulus

• is very rare.
• results from torsion of the stomach secondary to laxity of the ligamentous support to the stomach.
• is frequently associated witha diaphragmatic hernia.
• Treatment involves emergent detorsionand fixation of the stomach.

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Review Test

Directions: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case.

1. A 63-year-old woman underwent placement of a percutaneous endoscopic gastrostomy tube 1 day ago. Today she is tachycardic with a heart rate of 135 beats/min and a blood pressure of 95/45 mm Hg. Her abdomen is distended and notably tender. Abdominal plain film radiograph reveals a large amount of free air. A small amount of contrast added to the gastrostomy tube confirms appropriate placement within the stomach. Her hematocrit is 37% and her white blood cell count is within normal limits. Her calcium is 7.8 mg/dL. Which of the following is the most likely cause of this patient's symptoms?

(A) Injury to the esophagus during endoscope placement

(B) Injury to the liver during placement of the gastrostomy tube

(C) Injury to the transverse colon during placement of the gastrostomy tube

(D) Traumatic injury to the spleen during placement of the gastrostomy tube

(E) Acute pancreatitis caused by retrograde flow of gastric contents into the ampulla of Vater

1–C. Although rare, major complications associated with gastrostomy tube placement may occur, given the proximity of several major organs. Hemorrhage secondary to inadvertent placement of the percutaneous needle may be secondary to lacerations of the liver (superomedial), spleen (lateral), or major vessels along the greater or lesser curvature of the stomach. In addition, the proximity of the colon inferiorly makes colon perforation a significant risk factor. Given the scenario of an acute abdomen associated with free air on the abdominal film, injury to the transverse colon is most likely. Although simultaneous injury to other organs with associated hemorrhage is possible, the most likely primary origin of this patient's clinical findings is perforation of the transverse colon. Acute pancreatitis may occur with endoscopic manipulation of the biliary tree, but is rarely a complication of gastrostomy tube placement.

2. A 35-year-old trauma victim with a severe closed head injury is post-trauma day 14. After surviving an eventful intensive care unit stay, he has recently undergone elective tracheostomy and percutaneous gastrostomy tube placement. Today he is febrile to 39°C (102.2°F) and tachycardic to 125 beats/min. He is comatose secondary to his head injury, but his abdomen is quiet and rigid to palpation. Which of the following is the most appropriate next step in the management of this patient?

(A) Esophagogastroduodenoscopy (EGD)

(B) Emergent laparotomy

(C) Barium swallow

(D) A barium enema to identify any source of colonic injury

(E) Immediate removal of the gastrostomy tube with observation

2–B. Given this patient's scenario with severe diffuse abdominal pain and a suspected bowel perforation, an exploratory laparotomy with appropriate surgical management of the injury is indicated. Other potential life-threatening injuries associated with an acute abdomen may also be identified at the time of operation. Endoscopy, barium swallow, or a barium enema would simply delay therapy for potential life-threatening intra-abdominal injuries that may exist in this patient and are therefore not indicated in this situation. Barium studies may actually worsen the situation by introducing barium into the peritoneal cavity.

3. A 69-year-old, white woman with a history of chronic mesenteric ischemia has recently undergone superior mesenteric artery (SMA) saphenous vein bypass grafting after presenting with acute SMA occlusion. On postoperative day 3 she was returned to the operating room and underwent small bowel resection and reanastomosis with duodenojejunostomy. Now, 48 hours after her second surgery, she is passing large melanotic stools and her hematocrit has fallen from 32% to 20%. Despite aggressive resuscitation with crystalloid and 2 units of packed red blood cells (PRBCs), her hematocrit remains 21%. If an upper gastrointestinal source of bleeding is suspected, which of the following would be the most appropriate next step?

(A) Esophagogastroduodenoscopy (EGD)

(B) Emergent laparotomy

(C) Mesenteric vessel arteriography

(D) Vasopressin administration

(E) Placement of a Sengstaken-Blakemore tube

3–A. After initial resuscitative efforts, esophagogastroduodenoscopy (EGD) would be the most appropriate diagnostic, and frequently therapeutic measure for this patient. Most causes of upper gastrointestinal bleeding can be diagnosed by endoscopy. In addition, several therapeutic techniques for upper gastrointestinal bleeding can also be performed endoscopically (e.g., electrocautery, banding of varices). Given this presentation, exploratory laparotomy or angiography are not indicated at this point in the work-up. Angiography may be indicated when a gastrointestinal source of bleeding is suspected but not confirmed by endoscopic techniques. Both administering vasopressin and placing a Sengstaken-Blakemore tube are useful for variceal bleeding; however, without confirming variceal bleeding as the source of hemorrhage, these techniques would not be indicated.

4. A 63-year-old man with no significant past medical history is admitted with an acute abdomen secondary to gastric perforation. If a definitive ulcer procedure is performed on this patient, which of the following procedures is associated with the lowest ulcer recurrence rate?

(A) Truncal vagotomy

(B) Truncal vagotomy and pyloroplasty

(C) Vagotomy and antrectomy

(D) Parietal cell vagotomy

(E) Gastric bypass

4–C. Among the choices provided, vagotomy with a simultaneous antrectomy has the lowest ulcer recurrence rate. However, this procedure is associated with a higher morbidity secondary to anastomotic complications (e.g., leak or stricture) or problems associated with denervation of the proximal stomach and distal bowel. Complications include postvagotomy diarrhea, dumping syndrome, delayed gastric emptying, and alkaline reflux gastritis.

5. A thin, cachectic, 61-year-old woman presents to the office requesting a prescription for a “strong heartburn medicine.” She complains of gnawing abdominal pain after meals. Upon further questioning she admits to an unwanted 25-pound weight loss over the previous 3 months. She is a nonsmoker. Physical examination is unremarkable except for some mild epigastric tenderness. Rectal examination is heme-negative. Which of the following would be the most appropriate definitive diagnostic test for this patient?

(A) Esophagogastroduodenoscopy (EGD) with biopsy

(B) Esophageal manometry

(C) Magnetic resonance image (MRI) of the abdomen

(D) Upper gastrointestinal barium swallow

(E) Angiography of mesenteric vessels

5–A. A recent 25-lb unintended weight loss should raise suspicion for a possible malignancy in any patient. This patient's symptoms of epigastric pain in association with the weight loss should raise suspicion for an upper gastrointestinal malignancy such as gastric carcinoma. Among the choices above, endoscopy with biopsy of any suspicious lesions would be the most appropriate definitive diagnostic examination.

Findings on upper gastrointestinal barium swallow may be suggestive of ulcerative disease or malignancy, but endoscopic biopsy would allow for histologic verification of suspicious lesions. Angiography would not provide adequate information for definitive diagnosis. Esophageal manometry is useful for diagnosis of esophageal dysmotility disorders but would not be useful in this situation. Magnetic resonance imaging (MRI) would not allow for biopsy and tissue diagnosis.

6. An obese, 45-year-old businessman comes to the office for a routine physical examination. He states that his father and grandfather have died from stomach cancer. He admits to smoking one pack of unfiltered cigarettes a day and to moderate alcohol consumption only on weekends. He also states that he takes an antacid pill after meals for heartburn. All of the following are considered risk factors for gastric adenocarcinoma EXCEPT:

(A) Helicobacter pylori infection

(B) Smoking

(C) High-fat diet

(D) Previous gastric surgery

(E) Alkaline reflux gastritis

6–C. A diet high in saturated fats is associated with a relative increased risk for developing colon adenocarcinoma but has not been shown to be associated with gastric adenocarcinoma. A diet that includes nitrates is a significant risk factor for gastric adenocarcinoma. Other significant risk factors include H. pylori infection, smoking, previous gastric surgery, and chronic alkaline reflux gastritis.

7. A 42-year-old woman presents to the office with a 2-month history of increasing nausea and nonbilious vomiting associated with a 15-lb weight loss. Upon upper gastrointestinal endoscopy, biopsy reveals Helicobacter pyloriand a low-grade lymphoma. Which of the following is the most appropriate statement regarding the management of gastric lymphoma?

(A) Treatment is limited to radiation therapy alone

(B) Treatment consists of surgery alone

(C) Some lymphomas may regress with treatment of H. pylori

(D) Overall 5-year survival is less than 20%

(E) Obstructive symptoms are a contraindication to surgery

7–C. There is a small subset of lymphomas that are specifically associated with the presence of Helicobacter pylori. These lesions arise from mucosal-associated lymphoid tissue (MALT). There is evidence suggesting that many of these lesions may regress with eradication of H. pylori. Overall management of gastric lymphomas remains controversial. Treatment generally involves a combination of chemotherapy, radiation therapy, and surgery, although recent studies have suggested that chemoradiation therapy alone may be adequate. Overall survival for all stages of gastric lymphoma is greater than or equal to 50%. Obstructive symptoms may frequently be an indication for surgery, rather than a contraindication.

8. A 62-year-old man with a history of alcoholic cirrhosis presents to the emergency room with a 4-hour history of hematemesis. His abdomen is soft. He is tachycardic with a heart rate of 121 beats/min and has a blood pressure of 98/58 mm Hg. Which of the following is the most appropriate step in the immediate management of this patient?

(A) Airway control and resuscitation

(B) Intravenous vasopressin infusion

(C) Placement of a Sengstaken-Blakemore tube

(D) Performance of a barium swallow

(E) Upright chest radiograph to evaluate for free air

8–A. Whatever the cause of bleeding in this patient, the first and foremost important step in his management is securing a functional airway (e.g., endotracheal intubation) and adequate volume resuscitation (e.g., crystalloid and blood products when necessary). Administering intravenous vasopressin or placing a Sengstaken-Blakemore tube are appropriate in the management of esophageal varices but should not precede initial resuscitative measures. Although a chest radiograph should be performed early in the course of management to rule out potential pulmonary pathology and to identify a pulmonary source of hemorrhage, it should not precede resuscitation. A barium swallow is not indicated in this situation.

9. A 68-year-old man presents to the emergency room complaining of severe intense abdominal pain that came on suddenly and quickly reached peak intensity. Upon evaluation, the patient is lying completely still, is tachycardic, and has an ashen-gray appearance. Upon further questioning he reveals that the pain began in his epigastric region and then moved down to the right quadrants. His abdomen is rigid and extremely tender. Laboratory investigation reveals a white blood cell count of 30,000 and a hematocrit of 44%. Which of the following is the most likely cause of this patient's clinical presentation?

(A) Mallory-Weiss tear

(B) Bleeding duodenal ulcer

(C) Acute gastritis

(D) Perforated peptic ulcer

(E) Gastric lymphoma

9–D. Gnawing epigastric pain that suddenly progresses to severe intense epigastric pain is frequently associated with perforated peptic ulcer disease. Patients may rapidly develop peritonitis and tend to lie very still to prevent further peritoneal irritation. A Mallory-Weiss tear is generally precipitated by forceful retching or coughing before development of pain. Although pain associated with acute gastritis may come on rapidly, it is generally not associated with rupture and peritoneal irritation. Gastric lymphoma may present with a perforation but is a rare occurrence relative to perforated peptic ulcer disease. Although a bleeding duodenal ulcer is a possibility despite a normal hematocrit, perforation and hemorrhage from peptic ulcer disease rarely occur simultaneously and bleeding ulcers are unlikely to cause peritonitis unless bleeding is directly into the peritoneum.

10. An 85-year-old man presents with a 3-day history of severe abdominal pain. The patient's temperature is 39.4°C (103°F), he is tachycardic with 130 beats/min, and he has a blood pressure of 80/40 mm Hg. The patient is becoming more tachypneic, and upon placement of a Foley catheter no urine is produced. His abdomen is rigid and plain abdominal film demonstrates free air under the right hemidiaphragm. His past medical history is significant for coronary artery disease, emphysema, chronic renal insufficiency secondary to insulin-dependent diabetes mellitus, as well as manic depression. Which of the following is the most appropriate operation to perform on this patient?

(A) Pyloromyotomy

(B) Omental patching with or without a vagotomy

(C) Gastrectomy

(D) Billroth II

(E) Vagotomy and antrectomy

10–B. Given this patient's other comorbidities and the persistence of severe hypotension, the most appropriate operation would be one that effectively treats the perforation and minimizes the time the patient is in the operating room. Omental patching of a perforated ulcer involves oversewing the greater omentum directly over the perforated intestine. Additionally, a vagotomy may be done quickly as an acid-reducing procedure. If Helicobacter pylori is identified, appropriate treatment is also important to prevent recurrence postoperatively. A gastrectomy or antrectomy with a Billroth I, Billroth II, or Roux-en-Y gastrojejunostomy are effective in the treatment of this disease but would likely significantly increase the operative time and would not be the best choice given this scenario.

Directions: Each set of matching questions in this section consists of a list of four to twenty-six lettered options followed by several numbered items. For each numbered item, select the appropriate lettered option(s). Each lettered option may be selected once, more than once, or not at all.

Questions 11–21

1. Alkaline reflux gastritis
2. Dumping syndrome
3. Gastric volvulus
4. Mallory-Weiss tear
5. Hemobilia
6. Duodenal ulcer
7. Gastric ulcer
8. Afferent loop syndrome
9. Aortoduodenal fistula
10. Cushing's ulcer
11. Curling's ulcer

For each clinical scenario, select the most appropriate upper gastrointestinal disorder(s).

11. An elderly man with a history of an abdominal aortic aneurysm repair 10 years ago presents with a history of one episode of hematemesis. He is currently hemodynamically stable, but appears very anxious and scared. Upon endoscopy, there is no evidence of bleeding to the level of the pylorus. (SELECT 2 DISORDERS)

11–F, I. Despite the history of a previous abdominal aortic aneurysm repair, this patient could still potentially have a duodenal ulcer, which remains one of the most frequent causes of upper gastrointestinal bleeding in this population. Although rare (0.05%), one must always suspect aortoenteric fistula in any patient with a history of an abdominal aortic aneurysm repair or a history of aortic surgery. This patient may have experienced what is known as a “sentinel bleed,” which is usually followed by massive hemorrhage within 48 hours. The most accurate means of diagnosis is angiography, although preparations for emergent surgery should be made immediately upon diagnosis in case rebleeding occurs during the evaluation. Treatment involves closure of the duodenum and reconstruction of the aortic graft.

12. A 30-year-old woman presents with a 3–4-day history of bloody bilious emesis. The patient has no medical illnesses but did sustain a significant liver laceration treated with several weeks of bedrest after a high-speed motor vehicle accident 3 months earlier. Upper endoscopy does not reveal any evidence of gastric ulceration or gastritis. There is noted to be minimal blood-tinged bile around the region of the ampulla of Vater without obvious signs of duodenal ulceration or inflammation. (SELECT 1 DISORDER)

12–E. Hemobilia is another rare cause of massive upper gastrointestinal bleeding that must be considered when the source cannot be localized to the stomach or duodenum. Pseudoaneurysms resulting from blunt trauma to the liver may erode into the lumen of the biliary tract, leading to bilious bloody emesis. This may also be seen with chronic pancreatitis, which may cause erosion of a peripancreatic artery into the pancreatic duct. Endoscopy may demonstrate arterial blood from the ampulla of Vater. Angiography is frequently used for diagnosis and embolization therapy.

13. A 45-year-old motorcyclist suffered a severe closed head injury 2 days ago. Today he has an unexplained drop in his hematocrit from 43% to 25%, and his guaiac stool test is positive. Aspiration of the nasogastric tube contents are grossly positive for blood. (SELECT 3 DISORDERS)

13–F, G, J. The most likely diagnosis would be Cushing's ulcer, which is the eponym for acute gastritis associated with severe neurologic injury. Classically, Cushing's ulcer is solitary and can be located anywhere from the distal esophagus to the fourth portion of the duodenum. Perforation is the most common complication. The pathogenesis may be related to centrally mediated gastric hypersecretion. Cushing's ulcers generally occur in the stomach but can also occur in the duodenum. Additionally, the patient could have had peptic ulcer disease previously with the presentation of gastric or duodenal ulcers at this time.

14. A 56-year-old woman was caught in a house fire started by a kerosene heater. She was immediately brought to the surgical intensive care unit and resuscitated and débrided. Her total body surface area (TBSA) burn estimate is 40% partial and full thickness burns. Thirty-six hours after admission the patient's nasogastric tube drains 1 L of bright red blood over a 1-hour period. Endoscopy reveals diffuse mucosal bleeding. (SELECT 1 DISORDER)

14–K. Curling's ulcer is a variant of acute gastritis associated with a thermal burn injury of greater than 35% of total body surface area (TBSA). Curling's ulcer is usually found in the duodenum and also has the tendency to perforate. Endoscopy may be both diagnostic and therapeutic.

15. A 48-year-old woman with severe rheumatoid arthritis reports dull epigastric pain aggravated by food. She ingests 2400 mg of ibuprofen daily. Her vital signs are stable. She is guaiac-negative. Abdominal examination reveals moderate epigastric pain, but no rebound tenderness. You empirically discontinue her nonsteroidal anti-inflammatory drug (NSAID) therapy and the symptoms resolve within 6 weeks. (SELECT 2 DISORDERS)

15–F, G. This patient most likely has a gastric ulcer as a result of her nonsteroidal anti-inflammatory drug (NSAID) use, although she could still potentially have a duodenal ulcer. Only endoscopy or barium swallow would differentiate these two possible diagnoses. Gastric ulcers typically present with dull, gnawing epigastric pain that may be precipitated or aggravated by food. Type V gastric ulcers can be located anywhere in the stomach and are usually associated with the use of NSAIDs. Treatment is medical therapy and withdrawal of the offending agent if possible. Surgery is rarely indicated, however one should be suspicious for carcinoma should the ulcer persist.

16. A 50-year-old man complains of epigastric pain relieved by antacids. Endoscopic biopsy of the antral mucosa is positive for Helicobacter pylori. A barium swallow shows enlarged gastric mucosa and evidence of duodenal bulb spasm. (SELECT 1 DISORDER)

16–F. This patient has a classic presentation of a duodenal ulcer. Over 90% of duodenal ulcers are associated with Helicobacter pylori. Eradication of H. pylori heals the ulcer in over 90% of patients. Characteristic radiographic findings include demonstration of an ulcer crater and associated duodenal spasm. Typically, duodenal ulcer pain is relieved by ingestion of antacids or food.

17. An elderly man who has been debilitated in a nursing home for the past 6 years and who has a history of paraesophageal hernia presents to the emergency room complaining of sudden, severe, substernal chest pain. The patient is febrile with a temperature of 39°C (102.2°F) and his white blood cell count is 25,000. After proper placement of a nasogastric tube, the tip is noted to be in the left hemithorax upon chest radiograph. (SELECT 1 DISORDER)

17–C. Although rare, gastric volvulus typically occurs in patients who have herniation of the stomach through the diaphragm (e.g., paraesophageal hernia, traumatic diaphragmatic hernia). Gastric volvulus results from spontaneous torsion of the stomach compromising tissue perfusion, which may lead to necrosis, as suggested by this patient's elevated temperature and white blood cell count. Patients often present with chest pain, although cardiac evaluation is generally unremarkable. The diagnosis should be suspected when the chest radiograph reveals a retrocardiac air bubble or demonstrates the presence of the tip of the nasogastric tube in the hemithorax above the level of the diaphragm. Treatment involves emergent laparotomy and resection or detorsion of the affected stomach, depending on the presence or absence of necrosis.

18. A 43-year-old, previously healthy woman presents to the emergency room with a 3-hour history of hematemesis. The patient states that she has had the “stomach flu” for 3 days and has been vomiting bilious emesis during her illness. She notes that the emesis became bloody after an episode of “dry heaves” this morning. (SELECT 1 DISORDER)

18–D. Mallory-Weiss syndrome is the result of a linear tear in the mucosa of the gastric cardia, which typically results from violent retching or vomiting. Often a history of alcohol abuse or recent binge drinking is obtained, although this syndrome may occur in other clinical settings as well (e.g., severe coughing). The typical presentation involves initial nonbloody emesis followed later by hematemesis. Usually, the bleeding is painless. Evaluation with endoscopy allows for accurate diagnosis and rules out other sources of hematemesis. The majority of patients heal spontaneously without surgical intervention.

19. A 52-year-old woman with a recent Billroth I reconstruction (gastroduodenostomy) after ulcer surgery reports that within minutes after eating a meal she experiences weakness, palpitations, dizziness, diaphoresis, and a strong desire to lie down. You advise her to eat smaller meals and to avoid liquids with her meals. She returns in 4 weeks reporting improvement in her symptoms. You reassure her that most likely all of her symptoms will resolve with time. (SELECT 1 DISORDER)

19–B. Dumping syndrome is divided into early and late dumping. This patient is experiencing the more common early dumping syndrome often termed “early vasomotor dumping,” which is caused by the rapid onset of cardiovascular symptoms. Typical symptoms include nausea, vomiting, abdominal pain, excessive flatus, palpitations, dizziness, and diaphoresis. Symptoms can follow any meal, but worst offenders are foods high in carbohydrates and sugars. Over 90% of patients are successfully treated with dietary manipulation and time. Somatostatin analogs such as octreotide may be used before meals if dietary manipulations fail. Surgery is rarely indicated. When necessary, surgical reconstruction to a Roux-en-Y gastrojejunostomy may provide excellent relief of symptoms.

20. A 59-year-old man is 1 week postoperative from a Billroth II reconstruction (gastrojejunostomy) performed after antrectomy and vagotomy for chronic gastric outlet obstruction secondary to duodenal ulcer disease. He has been eating regular food for 1 day, although he now reports intermittent colicky right upper quadrant (RUQ) pain relieved by bilious vomiting. His abdomen is distended. Plain abdominal film reveals a single dilated segment of bowel in the RUQ. (SELECT 1 DISORDER)

20–H. Afferent loop syndrome is present only after Billroth II reconstructions and is caused by intermittent obstruction of the afferent limb. The classic symptoms are intermittent right upper quadrant (RUQ) or epigastric pain that is relieved by bilious vomiting. Evaluation consists of radionucleotide scanning, which may demonstrate a massively dilated afferent limb. Severe dilation of the afferent loop can result in rupture and peritonitis, thus urgent surgical intervention is generally required. Conversion to a Roux-en-Y gastrojejunostomy is an appropriate surgical option.

21. A 46-year-old woman is 2 months postoperative from a gastroduodenostomy (Billroth I) performed to treat her ulcer disease. She complains of severe upper abdominal pain that is burning in nature. She reports that the pain usually occurs just after eating a large meal. Endoscopic examination reveals a “beefy red” gastric mucosa. Biopsy demonstrates both acute and chronic inflammation. (SELECT 1 DISORDER)

21–A. Alkaline reflux gastritis is largely a diagnosis of exclusion. Patients complain of severe upper abdominal burning and often bilious vomiting. One must exclude marginal ulceration, afferent loop syndrome, chronic gastroparesis, and anastomotic stricture first. Endoscopy typically reveals marked gastritis and a “beefy red” appearance in the presence of bile reflux into the stomach. Radionucleotide scanning may demonstrate this bile reflux. Diagnosis is often made with biopsy that demonstrates acute and chronic inflammation of the mucosa. There is no specific medical treatment, although there has been some success with the use of sucralfate. Surgery is rarely necessary.