The stomach and duodenum are anatomically contiguous structures, share an interrelated physiology, and have similar disease processes. Peptic ulceration is the most common inflammatory disorder of the gastrointestinal tract and is responsible for significant disability. The stomach and duodenum are principally affected by peptic ulceration.
ANATOMY
The stomach is divided into the fundus, body, and antrum (Fig. 3-1). The fundus is the superior dome of the stomach; the body extends from the fundus to the angle of the stomach (incisura angularis), located on the lesser curvature; and the antrum extends from the body to the pylorus. Hydrochloric acid—secreting parietal cells are found in the fundus, pepsinogen-secreting chief cells are found in the proximal stomach, and gastrin-secreting G cells are found in the antrum.
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Figure 3-1 • Anatomy of the stomach. |
Six arterial sources supply blood to the stomach: the left and right gastric arteries to the lesser curvature; the left and right gastroepiploic arteries to the greater curvature; the short gastric arteries, branching from the splenic artery to supply the fundus; and the gastroduodenal artery, branching to the pylorus (Fig. 3-2). The vagus nerve supplies parasympathetic innervation via the anterior left and posterior right trunks. These nerves stimulate gastric motility and the secretion of pepsinogen and hydrochloric acid.
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Figure 3-2 • Arteries and veins of the stomach and spleen. A. Arterial supply. Observe that the stomach receives its main blood supply from branches of the celiac trunk. The fundus of the stomach is supplied by short gastric arteries arising from the splenic artery. The spleen is supplied by the splenic artery, the largest branch of the celiac trunk, which runs a tortuous course to the hilum of the spleen and breaks up into its terminal (splenic) branches. |
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Figure 3-2 • B. Venous drainage. The drainage of the stomach is directly or indirectly into the portal vein. The splenic vein usually receives the inferior mesenteric vein and then unites with the superior mesenteric vein to form the portal vein as shown here. From Moore KL, Dalley AF II. Clinically Oriented Anatomy. 4th ed. Baltimore: Lippincott Williams & Wilkins, 1999. |
The duodenum is divided into four portions(Fig. 3-3). The first portion begins at the pylorus and includes the duodenal bulb. The ampulla of Vater, through which the common bile duct and pancreatic duct drain, is located in the medial wall of the descending second portion of the duodenum. The transverse third portion is traversed anteriorly by the superior mesenteric vessels. The ascending fourth portion terminates at the ligament of Treitz, which defines the duodenal–jejunal junction. The arterial supply to the duodenum is via the superior pancreaticoduodenal artery, which arises from the gastroduodenal artery, and via the inferior pancreaticoduodenal artery, which arises from the superior mesenteric artery.
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Figure 3-3 • Anatomy of the duodenum. |
GASTRIC AND DUODENAL ULCERATION
PATHOGENESIS
The etiology of benign peptic gastric and duodenal ulceration involves a compromised mucosal surface undergoing acid-peptic digestion. Substances that alter mucosal defenses include nonsteroidal anti-inflammatory drugs, alcohol, and tobacco. Alcohol directly attacks the mucosa, nonsteroidal anti-inflammatory drugs alter prostaglandin synthesis, and tobacco restricts mucosal vascular perfusion. However, the most important and remarkable advancement in understanding the pathogenesis of peptic ulceration was the radical idea that infestation with the organism Helicobacter pylori was the causative factor in gastric and duodenal ulceration. This discovery destroyed prevailing dogma and profoundly altered the medical and surgical treatment for this disease process. So profound was this discovery that the 2005 Nobel Prize in Medicine was awarded to Drs. Marshall and Warren, two iconoclastic Australian researchers, "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease."
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HISTORY
Patients typically present with epigastric pain relieved by antacids. Sensations of fullness and mild nausea are common, but vomiting is rare unless pyloric obstruction is present secondary to scarring. Physical examination is often benign except for occasional epigastric tenderness.
DIAGNOSTIC EVALUATION
The radiographic evaluation of peptic ulcers entails barium studies that reveal evidence of crater deformities at areas of ulceration. Serum testing determines whether there are antibodies to H. pylori, and breath testing confirms infection.
Definitive diagnosis is made by direct visualization of the ulcer using endoscopy (see Color Plate 1). For nonhealing gastric ulcers refractory to medical therapy, it is extremely important that biopsy of the ulcer be performed to rule out gastric carcinoma. Duodenal ulcers are rarely malignant.
TREATMENT
Medical treatment is similar for gastric and duodenal ulceration. The goals of medical therapy are to decrease production of or neutralize stomach acid and to enhance mucosal protection against acid attack. Medications include antacids (CaCO3), H2-blockers (cimetidine, ranitidine), mucosal coating agents (sucralfate), and proton-pump inhibitors (omeprazole). If H. pylori is present, treatment with oral antibiotics is associated with a 90% eradication rate. Treatment regimens may consist of tetracycline/metronidazole/bismuth subsalicylate, amoxicillin/metronidazole/ranitidine, or other combinations.
As a result of the advent of proton pump inhibitors (PPIs) and the increased understanding of the role H. pylori plays in peptic ulceration, operations for ulcer disease have become infrequent. Indications for surgical treatment in the acute setting are either perforation or massive bleeding. Indications for elective operation are a chronic nonhealing ulcer after medical therapy or gastric outlet obstruction. The operation chosen must address the indication for which the procedure is performed. Historically, before the era of PPIs and H. pylori, the goal of surgery was to permanently reduce acid secretion by removing the entire antrum. In most instances, vagotomy and distal gastrectomy (antrectomy), with Billroth I or II anastomosis, fulfilled these criteria (Figs. 3-4 and 3-5). Because denervation of the
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stomach by truncal vagotomy alters normal patterns of gastric motility and causes gastric atony, surgical drainage procedures are required afterward to ensure satisfactory gastric emptying. Today, most cases of perforation are treated with closure of the defect with omental patch, and cases of bleeding are treated with suture ligation of the bleeding vessel.
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Figure 3-4 • Vagotomy and antrectomy with Billroth I anastomosis. |
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Figure 3-5 • Vagotomy and antrectomy with Billroth II anastomosis. |
STRESS GASTRITIS AND ULCERATION
PATHOGENESIS
Critically ill patients subjected to severe physiologic stress, often in the intensive care unit setting, are at risk for developing gastroduodenal mucosal erosion that can progress to ulceration. The commonly accepted etiology of stress gastritis and ulceration is mucosal ischemia induced by an episode of hypotension from hemorrhage, sepsis, hypovolemia, or cardiac dysfunction. Ischemia disrupts cellular mechanisms of mucosal protection, resulting in mucosal acidification and superficial erosion. Areas of erosion may coalesce and form superficial ulcers. Stress ulcers may be seen throughout the stomach and proximal duodenum.
HISTORY
Patients are usually critically ill and have a recent history of hypotension. Massive upper gastrointestinal bleeding is the usual finding.
DIAGNOSTIC EVALUATION
Sites of hemorrhage can be identified by endoscopy.
TREATMENT
Endoscopy can often control bleeding by either electrocoagulation or photocoagulation. Persistent or recurrent bleeding unresponsive to endoscopic techniques requires surgical intervention. Depending on the circumstances, operations for control of bleeding stress gastritis or ulcer require oversewing of the bleeding vessel. Usually, vagotomy is also performed to reduce acid secretion. In many cases, because bleeding is often diffuse and cannot be controlled by simple suture ligation, partial or total gastrectomy is performed.
PREVENTION
Prevention of stress ulceration involves maintaining blood pressure, tissue perfusion, and acid–base stability, as well as decreasing acid production while bolstering mucosal protection. The incidence of life-threatening hemorrhagic gastritis has decreased as intravenous H2-blocker therapy and oral cytoprotectants have been introduced to the intensive care setting.
CUSHING'S ULCER
Distinct from stress gastritis, Cushing's ulcers are seen in patients with intracranial pathology (e.g., tumors, head injury). Ulcers are single and deep and may involve the esophagus, stomach, and duodenum. Because of the depth of ulceration, perforation is a common complication. Neuronally mediated acid hypersecretion is thought to be the main cause of Cushing's ulcer.
ZOLLINGER-ELLISON SYNDROME AND GASTRINOMAS
PATHOGENESIS
Zollinger-Ellison syndrome occurs in patients with severe peptic ulceration and evidence of a gastrinoma (non–B-cell pancreatic tumor). Peptic ulceration results from the production of large volumes of highly acidic gastric secretions owing to elevated serum gastrin levels. Ninety percent of gastrinomas are found in the "gastrinoma triangle," defined by the junction of the cystic duct and the common bile duct, the junction of the second and third portions of the duodenum, and the junction of the neck and body of the pancreas.
HISTORY
Gastrin-secreting tumors produce a clinical picture of epigastric pain, weight loss, vomiting, and severe diarrhea.
DIAGNOSTIC EVALUATION
Diagnosis is confirmed by the secretin-stimulation test, in which the injection of intravenous secretin elevates serum gastrin levels to at least 200 pg/mL. Once diagnosed, tumor localization is performed by magnetic resonance imaging, abdominal ultrasound,
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computed tomography, selective abdominal angiography, or selective venous sampling.
TREATMENT
Acid hypersecretion can be controlled medically with H2 blockade and PPI. Somatostatin analogs (octreotide) have been found to be effective in decreasing tumor secretion of gastrin and in controlling the growth of tumor metastases.
Gastrinoma is a curable disease, despite the malignant nature of most tumors. Complete resection of tumors results in a near 100% 10-year survival rate. Incomplete resection or unresectability carries <50% 10-year survival rate. When simple excision or enucleation for cure is not feasible, an attempt is made to prolong survival by debulking and performing lymph node dissection to reduce tumor burden and acid hypersecretion.
STOMACH CANCER
Despite the decreasing incidence of gastric carcinoma in Western populations during the past decades, patient survival has not improved. In the United States, fewer than 10% of patients with stomach cancer survive 5 years. Illustrative of geographic variation, stomach cancer is endemic in Japan. Because of the high incidence of disease, mass screening programs are able to detect early-stage lesions, which accounts for a 50% overall survival rate at 5 years.
RISK FACTORS
Environmental and dietary factors are thought to influence the development of gastric cancer. Smoked fish and meats contain benzopyrene, a probable carcinogen to gastric mucosa. Nitrosamines are known carcinogens that are formed by the conversion of dietary nitrogen to nitrosamines in the gastrointestinal tract by bacterial metabolism. Atrophic gastritis, as seen in patients with hypogammaglobulinemia and pernicious anemia, is considered to be a premalignant condition for developing gastric cancer, because high gastric pH encourages bacterial growth. Chronic atrophic gastritis results in achlorhydria, and 75% of patients with gastric cancer are achlorhydric.
PATHOLOGY
Most tumors are adenocarcinomas, and spread is via lymphatics, venous drainage, and direct extension. Most tumors are located in the antral prepyloric region.
Gastric tumors can be typed according to gross appearance. Polypoid fungating nodular tumors are usually well differentiated and carry a relatively good prognosis after surgery. Ulcerating or penetrating tumors are the most common and are often mistaken for benign peptic ulcers because of their sessile nature. Superficial spreading lesions diffusely infiltrate through mucosa and submucosa and have a poor prognosis because most are metastatic at the time of diagnosis.
The pathologic staging of gastric cancer is based on depth of tumor invasion and lymph node status. Survival is closely correlated with the pathologic stage of a specific tumor (Fig. 3-6).
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Figure 3-6 • Staging system for gastric carcinoma. |
HISTORY
Patients with gastric cancer usually give a history of vague and nonspecific symptoms. Upper abdominal discomfort, dyspepsia, early satiety, belching, weight loss, anorexia, nausea, vomiting, hematemesis, or melena is common. Definite symptoms do not occur until tumor growth causes luminal obstruction, tumor infiltration results in gastric dysmotility, or erosion causes bleeding. By the time of diagnosis, tumors are usually unresectable. Later symptoms indicative of metastatic disease are abdominal distention owing to ascites, resulting from hepatic or peritoneal metastases, and dyspnea and pleural effusions, resulting from pulmonary metastases.
PHYSICAL EXAMINATION
Few findings are noted on physical examination, except in advanced disease. A firm, nontender, mobile epigastric mass can be palpated, and hepatomegaly with ascites may be present. Other distant signs of metastatic disease include Virchow supraclavicular sentinel node, Sister Joseph umbilical node, and Blumer shelf on rectal examination.
DIAGNOSTIC EVALUATION
Anemia is often found on routine blood studies. The anemia is usually hypochromic and microcytic secondary to iron deficiency. Stool is often positive for occult blood.
In recent years, upper endoscopy has replaced the barium-contrast upper gastrointestinal study as the imaging modality of choice. Endoscopy allows direct visualization and biopsy of the tumor.
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At least four biopsies should be made of the lesion. With 10 biopsies, the diagnostic accuracy approaches 100%. In Japan, the double-contrast air/barium study is used extensively for screening. Once diagnosis is made, computed tomography is performed to evaluate local extension and to look for evidence of ascites or metastatic disease.
STAGING
Staging for stomach cancer is according to TNM classification (Table 3-1).
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TABLE 3-1 American Joint Committee on Cancer (AJCC) TNM Classification of Carcinoma of the Stomach |
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TREATMENT
The theory behind curative resection involves en bloc primary tumor resection with wide disease-free margins and disease-free lymph nodes. Tumors are located either in the proximal, middle, or distal stomach. The type of operation performed for cure depends on tumor location. Distal lesions located in the antral or prepyloric area are treated with subtotal gastrectomy and Billroth II or Roux-en-Y anastomosis (Fig. 3-7).
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Figure 3-7 • Billroth II reconstruction after antral gastric cancer resection. |
Midgastric and proximal lesions are treated with total gastrectomy, with extensive lymph node dissection. The lesser and greater omentum are removed, along with the spleen. If the body or tail of the pancreas is involved, distal pancreatectomy can be performed. Reconstruction is achieved via Roux-en-Y anastomosis (Fig. 3-8).
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Figure 3-8 • Roux-en-Y esophagojejunostomy reconstruction after total gastrectomy. |
Proximal lesions carry a poor prognosis, and surgical intervention is usually palliative. If there is extension into the distal esophagus, it is resected, along with the cardia and lesser curvature. The remaining stomach tube is closed, and the proximal aspect is anastomosed to the midesophagus through a right thoracotomy. If extensive esophageal involvement is discovered, radical near-total gastrectomy and a near-complete esophagectomy are performed, with continuity restored using a distal transverse colon and proximal left colon interposition (Fig. 3-9).
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Figure 3-9 • Colonic interposition after near-total esophagectomy and near-total gastrectomy. |
PROGNOSIS
The overall 5-year survival rate for gastric cancer in the United States is approximately 10%. Based on pathologic staging of tumors, the survival rate for stage I is 70%; stage II, 30%; stage III, 10%; and stage IV, 0%.
KEY POINTS