Health Articles

Occult GI bleeding may occur secondary loangiodysplasia in the mucosa of the slomach or duodenum. These lesions occur more frequently with age and arc more common in the colon (see Ch. 55); Ihcy often cause upper Gl bleeding in patients with chronic renal failure. Occasionally, Ihey can be identified on endoscopy, bul often angiographic confirmation is needed. Choosing appropriate therapy can be difficult. If bleeding is severe enough k> require transfusion, endoscopy wilh electrocoagulation is Ihe treatment of choice. Refractory bleeding requires surgery. In patients at increased surgical risk, a trial of hormonal therapy with a combination of 0.05 mg ethinyl estradiol and I mg noret hind rone daily may be warranted, bul whether hormonal Iherapy is truly ef’feclive remains controversial.

This relatively rare condition is more common in Ihe elderly because the ligaments supporting the stomach are relaxed. A complete Jwisl of the organ can result in strangulation of the blood supply, which can lead lo gangrene. Patients often present with severe epigastric pain of abrupt onsel followed by retching with an inability lo vomit or belch.
Two types of gastric volvulus occur. The more common organoaxial volvulus involves a rotation of the slomach on ils longitudinal axis (from cardia to pylorus); an x-ray oflen shows an “upside-down stomach”and double air-fluid levels (fundus and antrum). The less common mesenteroaxial volvulus results from rotation around a vertical axis passing through the center of I he lesser and greater curvatures. Patients usually presenl with a distended upper abdomen, which hampers passage of a nasogastric tube. The combination of an inability lo vomit, upper abdominal pain and distention, and an impediment to nasogastric lube insertion is known as Borchardt’s triad. Diagnostic clues are usually obtained on x-ray examination, cither with a plain film of Hie abdomen or wilh contrast material added. Acute gastric volvulus reauires emergency surgery.

Intragastric masses consisting of extrinsic substances such as hair, fruit and vegetable fibers, or a mixture of such substances. Bezoars are seen wilh increased frequency in (he elderly, especially after vagotomy or sublolal gastrectomy, and may be related to reduced gastric motility. They occur often in elderly diabetic patients because of severely abnormal gastric emptying. An edentulous patient may be at risk because food fibers arc insufficiently broken up. Pulpy fruits or vegetables— especially citrus fruits but also figs, coconuts, apples, green beans, sauerkraut, berries, potato peels, and brussels sprouts—most commonly lead to bezoars.
Diagnosis begins by ruling oul mechanical obstruction. Barium x-ray studies may indicate a mass lesion in the stomach, which may mimic a cancer. Treatment with endoscopy, including attempts to break up Ihe lesion with a biopsy forceps or a jet spray of water, is often successful.

Zoliinger-Ellison syndrome was initially described as a triad of recurring peptic ulcer disease, marked gastric hypersecretion of acid, and a pancreatic adenoma. Later, the adenoma was found to produce a high gastrin output, resulting in continuous stimulation of the parietal cells to produce excessive acid. Because about 33% of patients with this syndrome are over age 60, it should be considered in any patient with persistent or recurring peptic ulcer disease. If Zoliinger-Ellison syndrome remains a possibility after a serum gastrin determination, gastric secretory studies should be performed. Traditionally, patients with this syndrome have a basal acid output > 15 mPq/L, and maximal stimulation docs no( double the output. Provocative testing with IV secretin is definitive. In normal subjects, IV secretin slightly increases, slightly decreases, or has no effeel on serum gastrin levels. In patients with gastrinoma, within 10 min after Ihe secretin injection, serum gastrin levels increase by at least 200 pg/mL and then gradually decrease to baseline levels. Once (he diagnosis of /.ollinger-Ellison syndrome is made, all candidates for surgery need evaluation wilh abdominal ultrasonography, computed tomography, and selective arteriography to localize tumors and to exclude metastases.
Treatment
Surgery is the treatment of choice, with cure rates approaching 40% in patients who have undergone successful resections. Contraindications to surgery include unresectable metastatic disease.
Omeprazole is the medical treatment of choice because of its potency, long duration of action, and favorable side effect profile. Ini-lially, the dose is usually 60 mg/day orally; gastric acid secretion is monitored, and the dose is adjusted as necessary. Goals for gastric acid suppression are basal acid output < 10 niF.q/h in patients who are not operative candidates, < 5 mEq/h in patients with gastric resection, and < 1 mEq/h in patients with severe reflux.
Octreotide, a synlhetic analog of somatostatin, decreases scrum gastrin levels and gastric acid produclion in patients wilh Zoliinger-Ellison syndrome but can be given only parenterally. Furthermore, long-lerm studies have not shown any increased benefit of octreotide over omeprazole. Chemotherapy with streptozocin and 5-FU has been shown to decrease serum gastrin levels in patients with metastatic disease but is usually reserved for patients with liver metastases lo provide symplomatic relief from mass effects of the tumor.

An ulceration of the mucous membrane penetrating the imtscularis mucosa and occurring in the areas bathed in acid and pepsin. In younger persons, duodena! ulcer is the predominant form of peptic ulceration, but in the elderly, (he proportion of gastric ulcer increases. Peptic ulcer presentation later in life may be more acute, including severe hemorrhage, perforation, and obstruction. Aggressive therapy is often needed in older patients, and surgery should not be delayed or withheld solely because of age. All gastric ulcers should be evaluated endoscopicalfy to differentiate benign ulcers from carcinoma. Furthermore, multiple biopsies of benign-appearing gastric ulcers are needed to rule oul malignancy (4 to 6 biopsies at the ulcer margins and biopsy of the ulcer base); endoscopy should be repeated in 2 to 3 mo to ensure healing and to exclude gastric carcinoma.
Giant duodenal ulcers in some elderly men cause upper abdominal pain, often radiating (o the back. These ulcers may exceed 2 cm in diameter and may involve most of the surface of the duodenal bulba.s well as contiguous organs such as the pancreas, gallbladder, and liver. Fre-quently. (if bleeding occurs. A giant duodenal ulcer is diagnosed using barium x-ray studies or endoscopy. Surgery is usually preferable to medical treatment.
Treatment
Therapy for peptic ulcer in the elderly is similar to that in younger palients. However, certain principles require closer attention when treating older palienls. For treatment of complications (hemorrhage. perforation, obstruction), see Ch. 62.
Antacids: Although these medications are used frequently for symptoms of peptic ulcer disease, their high sodium content can cause sodium overload in the elderly. Tilralac Plus Liquid is the antacid with the lowest sodium content. Other possible side effects are diarrhea (predominantly with antacids containing magnesium), constipation (predominantly with antacids containing calcium), and altered absorption of other drugs, including digoxin, quinidine, isoniazid, anil broad-spectrum antibiotics.
Histamine Hz-receptor blockers: The primary drugs currently used to treat peptic ulcer disease are the histamine H:-receptor blockers. These drugs may produce menial confusion in the elderly patient, particularly when given parcntcrally. Also, cimetidinc is associated with several important drug interactions and may increase blood levels of diazepam, warfarin, theophylline, and phenytoin.
Sticrsilate: By enhancing the protective mechanisms of the gastric mucosa, sucralfate provides an effective alternative therapy for acute peptic ulcer. In the elderly, this drug offers the advantage of being potentially free of the systemic side effects produced by histamine Hs-receptor blockers. The recommended dosage of sucralfate for duodenal ulcer is I gm orally qid for 4 (o 6 wk; for gastric ulcer. I gm orally qid for 12 wk.
Omeprazole: This proton-pump inhibitor is Ihe treatment of choice lor patients wilh ulcer refractory to high-dose histamine H^-receptor blockers. All hough the side effeel profile has been favorable in humans, more long-term studies are needed before chronic acid suppressive therapy can be recommended.
Misoprostol: This prostaglandin Ei analog has both antisecretory and mucosal protective properties that may preveni gastric ulcer formation caused by nonsteroidal anti-inflammatory drugs (NSAIDs). Adverse effects of misoprostol include diarrhea and abdominal pain, which may interfere with compliance in the elderly population.

Enlarged gastric rugae involving part or all of the stomach characterize Menetrier’s disease, a relatively unusual condition that is not unique (o the elderly. A number of conditions mimicking Menetrier’s disease arc more likely to occur in older persons, including gastric lymphoma, infiltrative carcinoma, granulomatous disorders such as tuberculosis, and other infiltrative conditions such as amyloidosis. These conditions may be associated with vague epigastric pain and weight loss. More important, however, may be the frequent finding of hy-poalbuminemia secondary to protein loss across the gastric mucosa.
On barium x-ray studies, all these conditions, including Menetrier’s disease, may show large gastric folds appearing as polypoid filling defects along the greater curvature of the stomach. Endoscopy with adequate biopsy helps the differential diagnosis. Treatment depends on the diagnosis. Sometimes, anticholinergics decrease the gastric protein loss in Menetrier’s disease. Occasionally, gastrectomy is required.

Atrophic gastritis is characterized by an increased number of inflammatory cells in the stomach wall and varying degrees of atrophy of the gastric mucosa. This gastritis appears (o be progressive and may eventually develop into gastric atrophy—a more diffuse disorder characterized by a decreased number of secretory cells (both chief and parietal) in the mucosa of the gastric body and fundus. Generally, these age-related gastric mucosal changes correlate with decreased gastric secretion.
Two types of atrophic gastritis exist. Type A, a more diffuse gastritis, is antral sparing and usually associated with decreased acid output, elevated serum gastrin levels, and circulating antibodies to parietal cells. This type of gastritis may evolve into characteristic pernicious anemia. Type B is a more focal, antral gastritis caused by Helicobacter pylori infection. This type is associated with a smaller reduction in acid secretion, normal serum gastrin levels, and an absence of antibodies to parietal cells.
Patients with these conditions arc usually asymptomatic, although benign gastric ulcer may develop. Both atrophic gastritis and gastric-atrophy, which share the prematignant stains of pernicious anemia, have the potential for malignancy. Managing patients with these conditions, therefore, usually includes periodic endoscopic cytologic evaluation and biopsy for carcinoma. Although the optimal interval for these examinations has not been determined, they are generally performed every year or two.
Pernicious anemia is the end-stage condition in type A chronic gastritis. It usually presents as a hematologic abnormality in the elderly, and Gl symptoms are unusual. The diagnosis, however, is strongly supported by the finding of characteristic achlorhydria, an absence of gastric acid secretion in response to maxima! stimulation. Up to 10% of patients with pernicious anemia eventually are found to have carcinoma of the stomach, which occurs (hree to five times more often in these patienls than in the general population of similar age.

Gastric and duodenal acid peptic disorders frequently occur in Ihe elderly. With age, the incidence of duodenal ulcers appears lo decrease; this may be relaled lo diminishing gastric acid secretion. Secretory sludies have repeatedly demonstraled decreased acid oulpul and a relative increase in achlorhydria with aging. In association with decreased acid output, basal serum gastrin concentrations tend to increase with age. The incidence of gastric ulcers may actually increase in the elderly, particularly in those chronically taking nonsteroidal anti-inflammatory drugs (NSAII)s). Both duodenal and gastric ulcers tend to develop more complications in older palients, making surgery more likely.
Other disorders of Ihe stomach and duodenum affecting the elderly include atrophic gastritis, gastric atrophy, hypertrophic gastropathy, bezoars, gaslric volvulus, and gastric tumors. For a discussion of gastric tumors, sec Ch. 60.

Neuromuscular (motility) defects or mechanical obstructing lesions can cause esophageal dysphagia by interfering with the transport of ingested material down the esophagus. These two types of disorders can usually be differentiated by taking a detailed history. Motility disorders are more likely to cause dysphagia for solids and liquids; obstructing lesions usually produce dysphagia for solids only, but sometimes dysphagia for liquids develops late in the course of the disease if the esophageal lumen becomes subtotally occluded (see TABU-. 54-2).
Obstructive dysphagia can also result when a foreign object lodges in the esophagus. Many elderly persons are susceptible to this problem because they have poor vision and wear dentures, which decrease their ability to feel objects in the mouth (especially bones in meat). Sometimes, (he foreign object is ihe dentures.
Motility Disorders
Achalasia: Most patients with achalasia present between ages 20 and 40, but a second peak occurs in the elderly. Neurologic in origin.
achalasia results from defects of the ganglion cells in Auerbach’s plexus of the esophageal wall. The disorder causes slowly progressive dysphagia for solids and liquids and insidious weight loss. Regurgitation of undigested foods may cause nocturnal coughing and aspiration. An elderly palienl may have had symptoms for months or years before diagnosis.
Chest x-ray may show a dilated esophagus with an air-fluid level from retained food and saliva. About 50% of patients do not have the normal gastric air bubble. Barium swallow studies reveal a dilated, sometimes tortuous esophagus with a smooth, “bird-beak” narrowing at the gastroesophageal junction. Esophageal manometry usually provides the diagnostic findings of increased lower esophageal sphincter pressure with incomplete sphincteric relaxation during swallowing and an aperistaltic esophagus. These delects result in a major functional obstruction of food passing from the esophagus.
In the elderly, differentiating between idiopathic achalasia and secondary achalasia from cancer (which rarely produces identical radiographic and manomctric findings) is particularly important. Gastric, pancreatic, or lung cancer or lymphoma may be associated with such findings. Therefore, endoscopy with biopsy of any suspicious area is mandatory in all patients with achalasia. The clinical triad that suggests secondary achalasia is age > 50 yr, dysphagia for < 1 yr, and weight loss > 15 Ib.
Treatment for achalasia may be medical or surgical. Generally, good results can be obtained with either approach, and the choice should be based on the physicians skills, the patient’s health, and the patient’s preference alter being informed about the techniques, risks, and expected outcomes. Medical management may be more suitable for older patients in poor health.
Initial medical treatment usually consists of pneumatic dilation of the lower esophageal sphincter. Although such dilation is not quite as effective as Heller myotomy (80% vs. 95% success rate), it is associated with less morbidity (particularly gastroesophageal reflux), does not require general anesthesia, and is a same-day procedure.
Surgery is indicated when several balloon dilations over a relatively short period are needed (o maintain lower esophageal sphincter patency. Surgical intervention is also indicated when pneumatic dilation causes esophageal perforation. This complication occurs in about 5% of cases and requires surgical closure of the perforated area along with myotomy.
Occasionally, dysphagia can be sufficiently relieved by giving a smooth-muscle-relaxing drug just before meals. Either nitroglycerin tablets 0.4 mg sublinguals 5 min before meals or nifedipine capsules 10 mg bitten and held subfingually 15 min before meals may be effective. The rapid action of these drugs enhances lower esophageal sphincter relaxation and may improve dysphagia during the meal. However, most achalasia patients require the more definitive procedures discussed above to open the esophagogastric junction. Because the elderly patient with other serious medical problems may not be a candidate for pneumatic dilation or surgery, treatment with smooth-muscle-relax ing drugs should be considered definitive therapy. These drugs may cause transient symptomatic hypotension: patienls should be lold that lightheadedness, weakness, and other manifestations ol’poslural hypotension occasionally develop after taking them.
Scleroderma (progressive systemic sclerosis): Esophageal involvement occurs in > 80% of scleroderma cases and seems to correlate with Raynaud’s phenomenon. Scleroderma produces a slowly progressive dysphagia for liquids and solids, as in achalasia; heartburn is also a prominent symptom. Up to 40% of these patienls develop a peptic esophageal stricture. Manomctric findings include decreased peristalsis in the lower esophagus (smooth muscle) and normal peristalsis in the upper esophagus (striated muscle). Also, lower esophageal sphincter pressure is very low.
Treatment consists of acid suppression with omeprazole 20 mg/day orally. In patients with severe reflux, 24-h pH monitoring can be used to ascertain the effectiveness of treatment, and the omeprazole dosage can be increased as needed to control reflux.
Diffuse esophageal spasm and related disorders: Diffuse esophageal spasm is an esophageal motility disorder manifested by dysphagia, chest pain, or in some cases, both. Dysphagia usually occurs intermittently for liquids and solids. Both symptoms may be induced by stress and may be exacerbated by hot or cold foods or drinks.
This disorder may be related to several nonspecific esophageal motility disorders that can progress to achalasia. One such disorder, nutcracker esophagus, is characterized by high-amplitude peristaltic contractions (> 180 mm Hg) and associated symptoms of dysphagia, chest pain, or both.
Treatment of diffuse esophageal spasm and related conditions includes administering nitrates (isosorbide dinilrate 10 to 30 mg orally tid) or calcium channel blockers (preferably nifedipine 10 to 30 mg orally lid or diltiazcm 30 to 90 mg orally qid). Use of longer-acting nitrates or sustained-release calcium channel blockers may increase patient compliance because of decreased dosing frequency. Esophageal dilation may also be helpful, and in severe, refractory cases, esophageal myotomy may be considered. Many patients benefit from learning that their pain originates in the esophagus, not in ihe hear!, and from learning how to cope better wilh stress.
Obstructing Lesions
Esophageal carcinoma (see also Ch. f>0): Palients with esophageal carcinoma are generally > 50 yr and present with rapidly progressive dysphagia (solids first, then liquids) and weight loss. Typically, they have no history of heartburn, although it may occur. A history of heavy alcohol and tobacco use is common. Barium x-ray studies often suggest the diagnosis, but endoscopy (with biopsy and cytologic evaluation) is necessary for a more definitive diagnosis.
Treatment depends on the extent of the disease. When possible, surgical resection is the treatment of choice. CT scanning may help determine resectability. Radiation therapy, chemotherapy, or both may be palliative. The prognosis is grim, with a 5-yr survival rate of < 5%,
Peptic Stricture: This condition is characterized by progressive dysphagia lor solids and usually follows a long history of heartburn or other reflux symptoms. The diagnosis is made by barium radiography, but endoscopy is needed to rule out carcinoma. The strictures are smooth, tapered, and of varying lengths. If they are located above (he distal esophagus, Barrett’s esophagus (metaplastic columnar epithelium I in ing the distal esophagus) may be present. Palients with this condition, which is related to chronic gastroesophageal reflux, have an increased risk of cancer.
Treatment for patients with peptic stricture consists of long-term antireflux therapy. Intermittent esophageal dilation is often necessary as well, and occasionally surgery is required.
Rings and webs: These disorders, associated with intermittent dysphagia for solids, are best diagnosed by barium swallow. Endoscopic evaluation is indicated if the diagnosis is in doubt. Because the first episode frequently occurs while the patient is eating steak and bread, these disorders have been termed steakhouse syndrome. The bolus is usually forced down by drinking liquids but occasionally must be regurgitated, and then Ihe meal can usually be finished without difficulty.
The most common structural lesion is Schatzki’s ring, composed of invaginaled mucosa. The ring, located at the gastroesophageal mucosal junction, is seen on barium swallow about 3 to 4 cm above the diaphragm. It most often produces symptoms when the lumen is narrowed to ^ 12 mm.
Treatment consists of a single esophageal dilation with a large-caliber bougie. If the symptoms occur infrequently, more careful eating habits may suffice.
Vascular causes: Esophageal dysphagia may also he caused by vascular anomalies that compress the esophagus. The more common lesions are congenital aortic-arch abnormalities associated wilh dysphagia presenting in early childhood, such as dysphagia lusoria (dysphagia caused by a retroesophageal aberrant right subclavian artery and an anomalous left pulmonary artery). Occasionally, symptoms present in adulthood. Dysphagia aortica is a disorder of ihe elderly resulting from esophageal compression by either a large thoracic aortic aneurysm or an atherosclerotic, rigid aorta posteriorly and the heart or esophageal hiatus anteriorly.

Etiology
In the elderly, five types of abnormalities may cause oropharyngeal dysphagia: cerebrovascular accidents, other neuromuscular disorders, oropharyngeal tumors. Zenker’s diverticulum, and cervical hypertrophic osteoarthropathy (see TABLE 54-1).
Cerebrovascular accidents: Patients who have had a major stroke often have dysphagia, particularly if the lesion involves critical areas in the brain stem that affect the swallowing center. Dysphagia may occur in Wallenberg’s syndrome (occlusion of the posterior inferior cerebellar artery, which supplies blood to the lateral area of the medulla thai in-nervales the homolateral palatal muscles) or in pseudobulbar palsy (impairment of Ihe muscles supplied by the medulla oblongata caused by bilateral multiple cerebral infarctions). Dysphagia may also occur in bulbar palsy (paralysis or weakness of the muscles supplied hy the medulla oblongata not caused by cerebral infarctions). In patients with Ihese syndromes, dysphagia may be the primary symptom, making the specific diagnosis difficult. Patienls with poststroke dysphagia occasionally respond to retraining of the physical aspects of swallowing. Such rehabilitation is best performed in conjunction wilh a videotaped barium swallow to assess ihe effects of difficult foods (ie, semisolid, solid) on swallowing and lo evaluate for aspiration.
Other neuromuscular disorders: Several neurologic and muscular disorders thai affect movement of the tongue, pharynx, or upper esophageal sphincter may produce oropharyngeal dysphagia. In the elderly patient, likely candidates include Parkinson’s disease, myasthenia gravis, hypothyroidism or hyperthyroidism, and amyotrophic lateral sclerosis. With these disorders, dysphagia may be the only symptom. Diagnosis may be difficult, particularly with hyperthyroidism, which may not have typical manifestations in the elderly.
Oropharyngeal tumors: Head and neck tumors may cause oropharyngeal dysphagia, particularly in the elderly. If such a tumor is sus-peeled after a thorough history and examination, direct laryngoscopy complemented by CT should be performed.
Zenker’s diverticulum: Transient prc-esophageal dysphagia may be the earliest symptom of this outpouching of one or more layers of the esophageal wall immediately above the upper esophageal sphincter. When the sac becomes large enough lo retain food, patients develop the typical symptoms of persistent cough, fullness in the neck, gurgling in the throat, postprandial regurgitation, aspiration, and an offensive odor and tasle. Some diverticula become so large that palienls must perform various maneuvers, such as applying pressure to the neck and coughing repeatedly, to empty them. These sacs can become large enough l<) produce a visible mass in the neck or to obstruct ihe esophagus by compression.
Much controversy surrounds ihe pathogenesis of these diverticula. Diminished opening of the upper esophageal sphincter because of decreased elasticity is currently thought to play a major role. If symptoms become disabling or repeated tracheal aspiration occurs, surgical diver-ticulectomy and cricopharyngeal myotomy is the treatment.
Cervical hypertrophic osteoarthropathy: Although asymptomatic cervical osteophytes (spurs) may occur in 20% to 30% of the population, only about 75 cases of osteophyte-indueed dysphagia have been reported. Mosl are secondary to diffuse idiopathic skeletal hyperostosis, in which flowing calcification occurs within at least four contiguous vertebrae in conjunction with minimal degeneralive disk disease and an absence of apophyseal joint ankylosis. In the elderly, cervical osteophytes may be relaled to dysphagia when they arc extraordinarily large, when they occur in the cricoid cartilage region (C6) where the esophagus is relatively immobile, or when periesophagitis occurs secondary to rapid expansion of the osteophyte.
Diagnostic studies should include plain cervical spine films with lateral views, as well as barium videofluoroscopy with food bolus to determine the degree of compression during swallowing. Most patients can be managed with reassurance and support: if Ihe dysphagia is unremitting, surgical removal of the osteophyte may be necessary.
Diagnosis
Identifying the cause of oropharyngeal dysphagia requires close attention to the history, physical examination, and appropriate diagnostic tests. Barium x-ray studies of Ihe pharynx and upper esophageal sphincter are little help without videofluoroscopy. Because the sequence of muscular changes needed to transfer ingested material from mouth to upper esophagus occurs in about I sec, rapid-sequence pictures must be obtained. Manometric studies of the pharynx and upper esophageal sphincter are only occasionally helpful, but as manometric techniques continue to improve, these studies should provide better diagnostic information.
Treatment
Treatment depends on the underlying cause. Treatable disorders, including Parkinson’s disease, myasthenia gravis, and thyroid abnormalities, should receive Ihe appropriate therapy. Depending on the degree of dysphagia, medical treatment for parkinsonism and myasthenia gravis may not completely restore swallowing. Tumors should be resected, if possible, or should be treated with chemotherapy or radiation therapy. However, surgical resection or radiation therapy for a tumor can cause a subsequent stricture that may precipitate dysphagia.
For a patient with an otherwise unbeatable neuromuscular disorder, such as a stroke, rehabilitation techniques are often effective (eg, altering the diet or eating with the head held in different positions). These approaches should be determined after consultation with a speech pathologist that includes radiographic assessment of the patient’s ability to swallow various types of food (liquid, semisolid, solid) while maintaining different head positions.