25. | Principles of Surgery, Companion Handbook

Chapter 24 Stomach

Principles of Surgery Companion Handbook

CHAPTER

24
STOMACH

Anatomy
Physiology
Diagnosis of Gastric Disease
	Symptoms
	Signs
	Diagnostic Studies
	Other Conditions
Acid-Peptic Disease
	Classification
	Clinical Manifestations and Diagnosis
	Complications
	Treatment of Peptic Ulcer Disease
	Acute Erosive Gastritis
Gastric Neoplasms
	Malignant Tumors
Surgery of the Stomach
	Vagotomy
	Resection
	Reconstruction
	Postgastrectomy Syndromes
Treatment of Morbid Obesity

ANATOMY

Functional Relationships The fundus is located in the upper abdomen; it is thin walled and freely distensible and stores and partially digests food. Capacity is 1.5–2.0 L. The cardia is immediately adjacent to the gastroesophageal (GE) junction. The fundus is to the left of and superior to the cardia. The body extends from the fundus to the incisura. The antrum is the thick-walled, distal portion of the stomach; it mixes and grinds food and then releases it slowly through the pyloric sphincter. The pancreas is dorsal (inflammation delays gastric emptying, masses cause satiety). The liver is to the right and ventral, whereas the spleen is directly to the left and lateral. Enlargement of either also interferes with gastric capacity. Likewise, gastric disease (e.g., peptic ulceration) may affect adjacent organs. The biliary tree runs posterior to the duodenum.

Blood Supply and Lymphatics There are four major nutrient arteries (e.g., right/left gastric, right/left gastroepiploic) and an extensive submucosal arteriole plexus. See Fig. 24-1 for complete details. Short gastric veins arise from splenic veins and connect the fundus and spleen. The stomach can survive on only one major artery. Lymphatic drainage follows the vascular supply.

FIGURE 24-1 Blood supply of the stomach.

Innervation The major autonomic supply is vagal. The hepatic branch arises from the left anterior vagus and the celiac branch from the right posterior vagus. Each main vagus terminates in a nerve of Laterjet, which gives off small branches to the lesser curvature (secretory innervation to parietal cells). The distal-most branches are the “crow's feet,” innervating the motor activity of the antrum. Splanchnic (sympathetic) branches follow arteries and modulate blood flow and muscular function.

Morphology External serosa, outer longitudinal, middle circular, inner oblique smooth muscle, then submucosa, muscularis mucosa, and mucosa. Small submucosal arterioles feed a rich mucosal capillary network.

Fundic Mucosa (Proximal Two-Thirds) Composed of deep glands that open into pits. Glands have surface epithelial (protect surface with mucus, alkaline secretions), mucous neck (line glands), progenitor (at base of gland), chief (secrete pepsinogen), parietal (secrete HCl), and endocrine cells (serotonin).

Antral Mucosa (Distal One-Third) Surface epithelial, mucous neck, and G cells (produce gastrin).

Sphincters Lower esophageal sphincter (LES) constitutes the distal 5 cm of esophagus-stomach junction. Relaxes with swallowing and then contracts to prevent reflux of gastric contents. Pyloric sphincter minimizes duodenogastric reflux and meters movement of food into duodenum, rejecting particles larger than 2 mm.

PHYSIOLOGY

Storage The stomach stores food for up to 4 h. Receptive relaxation is muscular relaxation with ingestion. Solid food settles on the greater curvature; liquids pass freely along the lesser curvature. The antrum grinds and recirculates food. The pylorus regulates emptying.

Digestion Salivary amylase acts on starches, only in center of gastric bolus (remains alkaline). Peptic digestion reduces the size of meat particles. Gastric lipase assists with early fat digestion. Most digestion, however, occurs in the small intestine.

Gastric Acid Secretion Interdigestive acid production is 2–5 mEq/h (BAO = basal acid output). The sight and smell of food stimulate acid and pepsinogen secretion (cephalic phase). Response is vagally mediated, and this also enhances the action of gastrin. Gastrin is elaborated by G cells in response to gastric distention and vagal stimulation. Gastrin, in turn, stimulates acid secretion from parietal cells. Luminal acid then suppresses gastrin secretion (negative feedback). Acidification of the duodenum causes secretin release, which inhibits gastrin and acid production and stimulates pancreatic bicarbonate release. Duodenum and upper jejunum also secrete small amounts of gastrin.

Parietal Cell Function Parietal cells secrete HCl. This occurs via H⁺/K⁺ exchange pump, which requires ATP. Acetylcholine (vagal release), gastrin, and histamine stimulate and cimetidine, ranitidine, and famotidine (H₂ blockers), omeprazole (H⁺/K⁺-ATPase inhibitor), and prostaglandins (Cytotec) inhibit acid secretion. Vagotomy profoundly diminishes response to gastrin and histamine; however, anticholinergics only partially inhibit the response.

Surface Cell Function Impervious to H⁺. Secrete protective layer of mucus and bicarbonate.

Gastric Emptying Meal anticipation causes vagal gastrin release, acid secretion, and together with ingestion, receptive relaxation, antral contractions, and relaxation of the pylorus. Liquids empty continuously, at a rate dependent on osmolarity. Solids are reduced to millimeter-sized particles and then traverse the pylorus. Osmolality of chyme is diluted by recirculation (trituration), preventing dumping. Fats empty slowest. The gastric pacemaker is on the greater curvature; action potentials travel toward the pylorus. Gastric emptying may be assessed with saline instillation, barium radiographs, or bimodal radiolabeled meals. With instillation of 750 mL of saline, less than 400 mL should be left by 30 min.

Sphincters Proximally is the LES, a high pressure zone at the GE junction. The LES relaxes with esophageal peristalsis. Distally is the true pyloric sphincter, which functions as above.

Other Gastric Function Intrinsic factor, produced by parietal cells, is essential for ileal vitamin B₁₂ absorption. Gastric acid helps maintain foregut sterility. Gastric mucosa may participate in immunosurveillance and disposal of toxic substances. The stomach also rapidly warms (or cools) ingested contents. Gastric acid facilitates duodenal iron absorption.

DIAGNOSIS OF GASTRIC DISEASE

Symptoms

Anorexia Lack of appetite, frequently associated with physiologic stress. Common cause of weight loss with GI neoplasms.

Nausea and Vomiting See Chap. 22.

Pain Gastric mucosa devoid of pain endings. Gastritis, neoplasms, distention, and even gastric ulcers are relatively painless. Duodenal disease (i.e., ulceration) has characteristic pain patterns: gnawing midepigastric pain that is relieved when acid is buffered (meals, antacids) and worse with unopposed acid (early morning). Gastric ulcers have subtle, diffuse pain during or after meals unless perforated; then the pain is generalized.

Reflux Gastric contents into esophagus. May cause (1) heartburn, (2) expectoration of chyme, and (3) cough from aspiration. Caused by loss of LES pressure zone. Vagal tone, intraabdominal pressure, drugs, and GI hormones may influence LES pressure. May be surgically corrected by Nissen fundoplication.

Signs

Bleeding Hematemesis is the vomiting of blood. Coffee-ground emesis reflects slow bleeding (acid-hematin); bright-red emesis implies rapid bleeding (varix, ulcer, tears, severe gastritis). Stools are usually black (melena) but may be red with rapid bleeds. Neoplasms can cause slow, chronic blood loss.

Weight Loss Neoplasia and gastric ulcer usually cause weight loss. Duodenal ulcer is associated with weight gain; food neutralizes acid, relieving duodenal ulcer pain.

Gastric Distention Produces autonomic-mediated pallor, tachypnea, bradycardia, and hypotension. Diagnosed by inspection/percussion; remedied by nasogastric aspiration.

Tenderness Duodenal ulcers may have associated deep midepigastric tenderness. Gastric ulcers and neoplasms are usually nontender. Perforated ulcers cause generalized peritonitis with abdominal rigidity.

Masses Distal gastric neoplasms may show anterior, movable masses. Pancreatic masses are fixed; liver masses descend with inspiration. Virchow's node is left supraclavicular metastasis.

Diagnostic Studies

Radiography Barium studies miss some duodenal lesions and most superficial gastric erosions; however, endoscopy is preferred for mucosal lesions, especially bleeding.

Endoscopy Essential for hemorrhage, gastric ulceration, and most duodenal ulcerations. Lesions may be biopsied for histology as well as for H. pylori. Therapeutic techniques may be used for control of duodenal bleeding (e.g., electrocautery, epinephrine injection).

Gastric Analysis Saline lavages before/after a histalogue (2µg/kg) or pentagastrin (6µg/kg) dose. Maximal acid output (MAO) is 10–15 mEq/h; BAO is 2–3 mEq/h. Duodenal ulcer patients may have higher values; gastric ulcer patients may have lower values. However, significant overlap exists. Zollinger-Ellison (ZE) syndrome shows a high BAO (>50 mEq/h) with the BAO/MAO ratio at 0.6.

Other Conditions

Acid-reducing procedures may lead to anemia, and there is a question of gastric remnant cancer due to the resulting achlorhydria. Diarrhea may be due to dumping or postvagotomy syndrome.

ACID-PEPTIC DISEASE

Classification

Includes erosive gastritis and peptic ulcer. Reflux affects esophagus (see Chap. 23). True ulcers extend through the mucosa into the submucosa, in contrast with gastritis. Ulcers usually are chronic and include an inflammatory reaction.

PEPTIC ULCER

Duodenal ulcers are usually within 1–2 cm of the pylorus. They are often associated with acid hypersecretion. Gastric ulcers are as follows: Type I (most common)—proximal antrum or corpus (often acid hyposecretion); Type II—secondary to duodenal ulcer with pyloric stenosis; Type III—prepyloric/pyloric channel ulcer, similar etiology to duodenal ulceration.

Pathogenesis Three basic etiologies: acid hypersecretion, H. pylori, and nonsteroidal anti-inflammatory drugs (NSAIDs). H. pylori is found in 95 percent of duodenal ulcer disease and 80 percent of gastric ulcer disease. Eradicating H. pylori almost eliminates peptic ulcer disease. H. pylori may decrease acid resistance of mucous layer. Cause and effect, however, are difficult to prove. NSAIDs suppress prostaglandin synthesis and weaken the mucosal barrier. Between 10 and 30 percent of chronic NSAID users may develop peptic ulcer disease. Zollinger-Ellison (ZE) syndrome occurs in 0.1–1.0 percent of all peptic ulcer disease patients, and in about 20 percent of these patients, there is associated multiple endocrine neoplasia Type I (MEN-I).

Duodenal Ulcer Pathogenesis Overall, patients with duodenal ulcers secrete more acid compared with controls due to an increase in parietal cells, chief cells, or trophic factors (gastrin). H. pylori increases gastrin output and causes duodenitis. Some patients also have motility disorders, with rapid gastric emptying of liquids, exposing the duodenum to more acid than normal. The most prevalent physiologic abnormality may be decreased duodenal bicarbonate secretion.

Gastric Ulcer Pathogenesis Overall, basic defect is in gastric mucosal defense against acid-pepsin. Acid output is normal to nearly undetectable. Contrast with duodenal ulcer disease (some acid is required). Most basic abnormality may be reflux of duodenal contents. May be pyloric dysfunction; also caused by smoking. Reflux of bile acids, lysolethicin, and pancreatic secretions has a negative effect and damages the mucosa. Aspirin has a similar effect.

Clinical Manifestations and Diagnosis

Pain is the most common feature, gnawing or sharp midepigastric pain. Duodenal ulcer pain develops many hours after a meal when the bulb is empty. Relieved by food and alkali. In contrast, gastric ulcer pain is exacerbated with eating. Pain is usually chronic and recurrent. Other symptoms include nausea, weight loss, and mild tenderness. The peak incidence of gastric ulcers is at 50–65 years; most duodenal ulcers occur in the fourth decade.

Most diagnoses are by upper endoscopy or an upper GI series. In young patients, treatment is often based on symptoms alone, without diagnostic imaging. In elderly patients, imaging must be used because of the risk of malignancy. A double-contrast GI series detects 90 percent of gastric and duodenal ulcers, similar to endoscopy. Endoscopy is needed for all gastric ulcers because of the risk of malignancy. Endoscopy also provides material for H. pylori testing.

Complications

There are three main complications: bleeding, perforation, and obstruction. They usually follow previous symptoms. Between 15 and 20 percent of peptic ulcer disease develops gross bleeding. Patients present with melena (duodenal and gastric ulcers) or hematemesis (gastric ulcers). Bleeding peptic ulcer disease is only one-third of all massive upper GI bleeding. Between 5 and 10 percent of peptic ulcers will perforate, which produces peritonitis, fever, leukocytosis, ileus, and marked abdominal pain. Pneumoperitoneum occurs in 75 percent. Occasionally, perforations seal or lead to abscess, or they may track to right lower quadrant. Obstruction occurs in less than 5 percent, most often in chronic duodenal ulcer disease. Vomiting can cause contraction alkalosis. Diagnosis is by GI series, endoscopy, and the saline load test.

ZOLLINGER-ELLISON SYNDROME

Symptoms include hypergastrinemia and severe peptic ulceration from a gastrinoma. Ulcers may be more distal and multiple. BAO is markedly elevated (BAO/MAO ratio >0.6); the gastrin level may be greater than 1000 pg/mL. Equivocal gastrin levels may be stimulated with intravenous calcium or secretin administration. Gastrinomas are neoplasms, and they are overwhelmingly malignant (>90 percent) but slow growing; 50 percent have nodal or liver metastases at the time of diagnosis.

Treatment of Peptic Ulcer Disease

Medical Therapy (Table 24-1) Nonoperative treatment aims at (1) neutralizing gastric acid, (2) inhibiting secretion, and (3) protecting the gastric mucosa from injury. Antacids work by buffering gastric acid. H₂-receptor antagonists block receptors on parietal cells. Most potent are the substituted benzimidazoles, which block H⁺/K⁺-ATPase (omeprazole) and which work even in gastrinoma patients. Gastric mucosa can be protected with PgE₂ analogues (e.g., Misoprostol, Cytotec) that increase mucosal blood flow and bicarbonate and mucus production. Sucralfate binds to proteins in ulcer craters, promoting healing. Bismuth coats exposed protein and has activity against H. pylori (requires combined therapy).

TABLE 24-1 DRUGS FOR THE TREATMENT OF GASTRITIS AND PEPTIC ULCER

H. pylori eradication is via combined therapy: (1) bismuth-tetracycline-metronidazole or (2) omeprazole plus two of clarithromycin, amoxicillin, and metronidazole. Eradication of H. pylori is very effective in preventing ulcer recurrence.

Operative Therapy, Duodenal Ulcer Disease Today, surgery is most often performed for complications of peptic ulcer disease or emergently, due to effectiveness of medical treatment. Indications are bleeding, obstruction, perforation, or intractability. Today, for duodenal ulcer disease, medically refractory pain is most often treated with highly selective vagotomy, reducing infectious complications and side effects.

Bleeding is main cause of death from duodenal ulcer disease. Upper endoscopy is essential for diagnosis and initial treatment (cautery, epinephrine injection). Follow this with H₂ blockers. Operation is indicated for a 6-unit bleed after initial control. Operative approach is via a pyloromyotomy, with undersewing of the bleeding ulcer base, incorporating the gastroduodenal artery. After control, highly selective vagotomy can be performed or, in a poor-risk patient, vagotomy and pyloroplasty.

Perforation can be treated with simple closure and omental patch (Graham patch) in the poor-risk patient. Before H. pylori treatment, 80 percent recurred. In better-risk patients, a definitive procedure is preferred. Obstruction most often is treated with vagotomy and antrectomy, removing the scarred pyloris.

Operative Therapy, Gastric Ulcer Disease Medical therapy for gastric ulcer disease is not as effective as for duodenal ulcer disease. Surgery for gastric ulcer disease is needed earlier than for duodenal ulcer disease due to the higher incidence of malignancy. Gastric ulcer disease that recurs after medical therapy or that fails to heal needs operative intervention. Prepyloric gastric ulcers are treated as duodenal ulcers. Standard Type I gastric ulcers are treated with distal gastrectomy, including the ulcer. Vagotomy is not required.

Operative Therapy, Zollinger-Ellison Syndrome Since imaging studies are becoming more accurate, surgery is indicated for patients without metastatic disease. In patients with metastatic disease, omeprazole is very effective. Intraoperative ultrasound is useful for localized duodenal and pancreatic lesions, which should be resected.

Acute Erosive Gastritis

Acute erosive gastritis is the most common cause of upper GI bleeding. It accompanies severe, stressful illnesses.

Pathogenesis Includes acid secretion, back-diffusion of H⁺ ions, decreased gastric mucosal blood flow, decreased mucus and alkaline secretion, and submucosal buffers. May be initiated by a disruption in the H⁺ barrier. Aspirin, NSAIDs, alcohol, and bile salts may contribute.

Diagnosis Painless upper GI bleeding implies acute erosive gastritis. Endoscopy is critical; barium studies are not useful.

Therapy Directed at (1) repletion of losses from bleeding, (2) gastric rest with lavage of retained blood and clots (80 percent will stop bleeding spontaneously), and (3) neutralizing gastric acid with H₂ blockers and antacid pH titration to greater than 5. Omeprazole is as effective as antacids. Sucralfate may decrease pulmonary infections (decreased gastric bacterial colonization). Other adjuncts include transendoscopic cautery, pitressin, and intraarterial embolization. Persistent bleeding (> 4–6 units, massive exsanguination) may be treated initially endoscopically with cautery or arterio-graphically, but persistence requires operation with gastrotomy and oversewing of bleeding sites accompanied by vagotomy and pyloroplasty. Gastrectomy may be needed if all other therapies fail.

GASTRIC NEOPLASMS

Malignant Tumors

GASTRIC CANCER

Over 90 percent of gastric tumors are malignant. Adenocarcinoma comprises 95 percent, lymphoma 4 percent, and leiomyosarcoma 1 percent. The highest incidence is in Chile, Japan, and Iceland. The United States has had a rapid decline in rate.

Etiology Foods high in nitrates (smoked foods) increase risk. Pernicious anemia and achlorhydria predispose. H. pylori may increase the risk sixfold. Other risk factions include smoking, gastric ulcer, and previous partial gastrectomy.

Pathologic Features Types include (1) superficial spreading (most favorable prognosis; does not penetrate through muscularis mucosae; no ulceration; early detection has 75 percent 10-year survival; detected only by endoscopy/screening) and infiltrating carcinoma, which may include (2) polypoid, (3) ulcerative, or (4) scirrhous (linitis plastica), which involves extensive wall infiltration without ulceration, giving a “leather-bottle” appearance to the upper GI series. Spread may be via lymphatics, hematogenous, by peritoneal seeding, or by direct extension. Fifty percent or more patients have tumor spread at the time of diagnosis.

Signs and Symptoms Anorexia, weight loss (> 95 percent). Symptoms usually occur late. Slow bleeding leads to hemorrhage. Nausea, vomiting, and dysphagia are common. Pain is infrequent and late. Examination reveals a mass (50 percent), but tenderness is rare. Hepatomegaly (liver metastasis), ovarian involvement (Krukenberg tumor), and pelvic seeding (Blumer's shelf) may be detected. Advanced malignancy may show an involved left supraclavicular node (Virchow's node).

Diagnosis and Staging Upper endoscopy with biopsy is essential. A GI series often is complementary. CT scanning is used for preoperative staging. The TNM staging is shown in Table 24-2. Early gastric cancer is confined to the mucosa/submucosa. First found in Japan. Most are well differentiated. There is an excellent 5-year survival when disease is confined to the mucosa (99 percent) or submucosa (93 percent).

TABLE 24-2 TNM STAGING OF GASTRIC CANCER

Treatment Primarily surgical. Subtotal gastrectomy, even if palliative, is useful except in most severe circumstances. Include 50–85 percent of stomach, gastrocolic omentum, nodes and mesentery, and proximal duodenum. Margins must be free of tumor. Reestablish continuity via gastrojejunostomy. Adjuvant therapy, especially for recurrence, is poor. Overall 5-year survival is less than 10 percent. Early diagnosis can lead to increased survival (Japan).

OTHER GASTRIC MALIGNANCIES

Lymphoma/Lymphosarcoma May be isolated to stomach or from widespread disease. Thickened rugal folds. Anorexia, weight loss, and early satiety are common. Diagnosis is made by biopsy. May be treated by radiation therapy alone (preferred) or radiation with resection for bleeding and obstruction. Survival may approach 85 percent at 5 years.

Leiomyosarcoma Least common. Smooth muscle malignancy. Hemorrhage common. Resection is preferred treatment. Distal spread occurs late, and survival is favorable. Prognosis is related to tumor grade, size, and margins.

Benign Gastric Neoplasms Polyps Most common benign tumors of stomach. (1) Adenomatous polyps occur with pernicious anemia, Peutz-Jeghers syndrome, and Gardner's syndrome. These do have a malignant potential and should be biopsied via endoscopy with a snare. Malignant polyps are treated as gastric adenocarcinoma. (2) Inflammatory polyps are sessile and asymptomatic and may be seen with hypertrophic gastritis (Ménétrier's disease) or multiple inflammatory gastric polyps. They must be biopsied endoscopically but do not require formal resection.

Leiomyomas Common smooth muscle benign neoplasms. At more than 4 cm they ulcerate and may have massive hemorrhage, requiring emergency operation with formal resection. Smaller lesions may be wedged or shelled out.

Miscellaneous Lesions Submucosal lipomas are detected radiographically and are of little consequence. Ectopic pancreas may present as a mucosal dimple.

OTHER GASTRIC PATHOLOGY

Hypertrophic Gastritis (Ménétrier's Disease) Rare gastric epithelial inflammation with massive gastric folds and eventually multiple polyps. There is submucosal edema with inflammatory cells and glandular hypertrophy. Plasma proteins may be lost through this epithelium. Rarely, kwashiorkor may develop. Initially managed nutritionally. Must follow serially to assess for development of cancer.

Mallory-Weiss Tear Gastric mucosal disruption at esophagogastric junction after violent retching. Massive bleeding in only 10 percent. Bleeding stops spontaneously in 80–90 percent. Confirm by endoscopy. Operation uncommonly indicated. Massive hemorrhage may require operation with high gastrotomy and deep oversewing without acid reduction.

MISCELLANEOUS CONDITIONS

Acute gastric dilatation is followed by vasovagal symptoms. Usually occurs intra- or postoperatively. Gastric volvulus is uncommon and associated with paraesophageal hiatal hernia. Gangrene and perforation will develop. Therefore, even asymptomatic paraesophageal hernias should have operative repair. Foreign bodies occur in children, and sharp objects should be retrieved endoscopically. Bezoars are nondigestible conglomerates that occur in postgastrectomy patients or with ingestion of hair or persimmons. Treatment is with papain or endoscopic fragmentation. Atrophic gastritis, or pernicious anemia, shows parietal cell loss, achlorhydria, and loss of intrinsic factor and, subsequently, B₁₂ depletion. There is a high risk for malignancy. Corrosive gastritis may be caused by caustic ingestion (alkali cause esophageal strictures), and strong acid may lead to gastric perforation. Dieulafoy's lesion is a bleeding mucosal end artery with mucosal erosion.

SURGERY OF THE STOMACH

Antiulcer surgery is aimed at reducing acid secretion via vagotomy, antrectomy, and/or removing a parietal cell mass. Following resection, reconstruction is required.

Vagotomy

Eliminates cholinergic stimulus to parietal cells. BAO and MAO are reduced by 80 and 50 percent, respectively. Gastrin levels increase. May be truncal vagotomy (next to esophagus), selective (just after celiac/hepatic branches), or highly selective (parietal cell branches). Truncal vagotomy alters motility by denervating antral pump (“crow's feet”). Requires concomitant emptying procedure (pyloroplasty or gastrojejunostomy). Avoid pyloroplasty if there is significant scarring. Highly selective vagotomy denervates parietal cells and preserves the gastric emptying mechanism; pyloroplasty is not necessary.

Resection

Required for malignant disease. Subtotal gastrectomy now uncommon for ulcer disease. Removes antrum and major portion of parietal cells. Reconstruction is described below. Antrectomy with vagotomy has the lowest recurrence if surgery is needed for ulcer disease.

Reconstruction

Following resection, the gastric remnant must be anastomosed to the small intestine. Either a gastroduodenostomy is done (to the stump of the duodenum, distal to resection, Billroth I) or a gastrojejunostomy is done (to the proximal jejunum, immediately distal to the ligament of Treitz, Billroth II). Gastroduodenostomy is preferred if technically possible. For total gastrectomy, a roux-en-Y esophagojejunostomy is needed to prevent alkaline reflux.

CHOICE OF OPERATION

First, consider the disease process; then look at morbidly, recurrence, and side effects. Table 24-3 provides a summary for duodenal ulcer disease. These data, however, do not reflect the factor of H. pylori eradication. Laparoscopic approaches to gastric surgery are evolving and are currently only applied in elective settings.

TABLE 24-3 MORTALITY, SIDE EFFECTS, AND RECURRENCE RATES FOR THE THREE MOST COMMON ACID-REDUCING OPERATIONS

Postgastrectomy Syndromes

Procedures that destroy or bypass the pylorus or sever the vagal trunks may cause a wide range of disturbances. About 20 percent of patients have transient symptoms, 5 percent have permanent, nondisabling symptoms, but 1 percent may become “gastric cripples.” Therefore, lesser, pyloric-sparing procedures (i.e., parietal cell vagotomy) are being used more frequently.

Dumping Syndrome Related to ingestion of carbohydrates after pyloric ablation and their rapid movement into the small intestine. Characterized by light-headedness, palpitations, cramps, and diarrhea. Frequent small meals with few carbohydrates help. Octreotide is used in refractory cases.

Small-Capacity Syndrome Associated with extensive resections. Early satiety.

Postvagotomy Diarrhea May cause explosive diarrhea unrelated to meals, and gallstones. Occurs most often with truncal vagotomy (up to 30 percent), least with parietal cell vagotomy. Pathogenesis unclear; may be bile salts.

Bile Gastritis Erosive gastritis with reflux of bile through incompetent or bypassed pylorus. Low-grade pain, nausea, bilious vomiting. Roux-en-Y diversion may give relief. Only significant in 2 percent.

Afferent-Loop Syndrome Severe postprandial pain relieved by massive bilious vomiting. From obstruction at junction of afferent limb and gastric remnant. Treated by conversion to roux-en-Y.

Gastric Stump Carcinoma May develop in up to 3 percent of gastrectomy patients.

TREATMENT OF MORBID OBESITY

Morbid obesity constitutes weight 100 lb over ideal body weight. Ultimately hypertension, non-insulin-dependent diabetes mellitus, arthritis, gallstones, and cardiopulmonary dysfunction develop. Almost always refractory to medical therapy. Previously, jejunoileal bypass was successful, but complications (e.g., malabsorption, liver disease, renal calculi, gallstones) have led to its abandonment. Currently, operations aim to limit daily intake to about 800 kcal. Gastric bypass with a roux-en-Y jejunal limb to a 30–60-mL gastric pouch has been successful. Alternatively, gastric partitioning (vertical banded gastroplasty) is also used. Results show average of 50–67 percent loss of excess weight at 1.5 years.

For a more detailed discussion, see Ashley SW, Evoy D, and Daly JM: Stomach, chap. 24 in Principles of Surgery, 7th ed.