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Practice of Geriatrics
Reza Shaker, M.D., Kulwinder S. Dua, M.D., M.B., B.S., M.R.C.P., DNB, and Timothy R. Koch, M.D.
Pharyngeal and Esophageal Disorders
Disorders of the Stomach, Duodenum, Pancreas, and Liver
Disorders of the Small and Large Intestines
Swallowing is a highly coordinated event that involves sequential and overlapping contractions of the facial, cervical, oral, pharyngeal, laryngeal, and esophageal muscular apparatus. It results in transit of ingested material and saliva from the mouth into the stomach. For descriptive purposes, swallowing can be divided into four consecutive phases: (1) preparatory, (2) oral, (3) pharyngeal, and (4) esophageal phases. These phases merely represent the anatomic regions traversed by the bolus.
During the preparatory phase, the bolus remains for the most part in the oral cavity, undergoing physical and some chemical changes. Through the act of mastication and mixing with saliva it develops suitable physical qualities that prepare it for transit through the aerodigestive tract. During the oral phase, sequential squeezing of the tongue against the hard and soft palates generates a peristalic pressure wave that propels the bolus from the oral cavity into the pharynx. During the pharyngeal phase, the pharynx, upper esophageal sphincter (UES), and larynx are elevated, and three of the four routes connected to the pharynx—namely, the nasal cavity, oral cavity, and larynx—are sealed off while the fourth route, the UES, opens and the bolus is transported into the esophagus by rapid forceful posterior tongue movements as well as by peristaltic contractions of the pharyngeal constrictors. During oropharyngeal swallowing, the nasopharynx is sealed by the contraction of the superior pharyngeal constrictor and elevation of the soft palate and its contact with the posterior pharyngeal wall. During oropharyngeal swallowing, the UES transiently relaxes and subsequently is pulled upward and forward by the contraction of the same suprahyoid muscles that displace the larynx. Oropharyngeal swallowing begins with the closure of the vocal cords,1 signifying the activation of airway protection, and ends when the cords return to their resting positions. During this time respiration is reflexively inhibited. During the esophageal phase of swallowing the bolus is transported further into the esophagus and stomach.
Oropharyngeal dysphagia (OPD) may develop when either the efficacy or the coordination of either the transport or protective aspects of oropharyngeal swallowing are compromised. The true prevalence of OPD is not known. However, studies have shown that it has a 50% to 60% prevalence in nursing homes and a 10% to 30% prevalence in general medical wards.1,2
Except for silent aspiration, which presents with frequent episodes of pneumonia, most patients with OPD seek help because of symptoms. These symptoms reflect abnormalities in the transport or protective functions of oropharyngeal swallowing (Table 46-1). Dysphagia symptoms are highly specific and should not be labeled psychogenic. A frequently reported symptom is a sensation of inadequate clearance of the bolus from the pharynx: “food sticks in the throat.” This sensation, although it may be caused by the presence of a large residue in the piriform sinus or valleculae, may also be a referred sensation resulting from obstruction of the distal esophagus. Strictures of the proximal esophagus may also present with cervical symptoms. For this reason, in patients with complaints of cervical symptoms evaluation of the esophagus must be part of the dysphagia work-up. Because inflammation, abrasion, or tumors of the hypopharyngeal area may produce the same sensation, a careful examination by direct visualization of this area must be included in the work-up. Swallow-related coughing or choking due to misdirection of the bolus into the airway is another common complaint. Predeglutitive aspiration occurs when the bolus is lost from the mouth into the hypopharynx prematurely when swallowing has not yet been triggered and the airway is still open. This condition is commonly seen in post-cerebrovascular accident (CVA) dysphagic patients. Deglutitive aspiration results from incompetent or absent closure of the glottis during the swallowing sequence, allowing the bolus to invade the airway while being transported through the hypopharynx. Postdeglutitive aspiration occurs when bolus transport is incomplete and a large residue remains behind in the piriform sinus or valleculae at the end of the swallowing sequence; it is seen in patients with parkinsonism, postcerebrovascular accident, myasthenia gravis, and multiple sclerosis.


Because of the variety of organs involved in oropharyngeal swallowing, dysphagia results from a large number of causes that may affect the muscular apparatus of the oropharynx or their related neuromuscular plates and the peripheral as well as the central nervous systems. These diseases may affect oropharyngeal transport, deglutitive airway closure, or both (Table 46-2). Neuromuscular diseases are responsible for approximately 80% of cases, while local structural lesions of the oropharynx account for the rest. OPD has been reported in approximately 25% of adults following head injury, of which 94% have been reported to recover in about 3 months. OPD also poses a significant clinical problem in post-CVA patients. Malignancies of the head and neck account for approximately 10% of all the cancers occurring in North America. The total number of newly diagnosed cases of head and neck cancer in the United States, excluding skin cancer, is estimated at 78,000. The age-specific incidence increases markedly after age 50, and the male-to-female ratio is 3:1. Surgical resection or radiation therapy in these patients can result in OPD, leading to difficult management problems.


Primary neurogenic cricopharyngeal (CP) muscle dysfunction includes cricopharyngeal achalasia and discoordination of UES relaxation and opening, with pharyngeal peristalsis due to neurogenic causes such as cerebrovascular hemorrhage and Parkinson’s disease. Primary myogenic CP dysfunction is due to loss of elasticity as well as fibrotic changes of the UES. A variety of causes, including gastroesophageal reflux and aging, have been suggested. Causes of laryngeal paralysis include insults to the recurrent or superior laryngeal nerve due to a variety of surgical, inflammatory, or central nervous system diseases.
Because of the proximity to the pharynx, structural abnormalities of the most proximal portion of the esophagus may present with symptoms of cervical dysphagia. These abnormalities include proximal esophageal rings, which are usually reflux induced. Dysphagia usually is associated with solid food. Cervical symptoms and choking develop when bolus impaction occurs. Reflux symptoms such as heartburn may be minimal. Proximal esophageal webs, as seen in the Plummer-Vinson or the Paterson-Brown-Kelly syndrome, occur in the upper 2 to 4 cm of the esophagus and are associated with iron deficiency anemia. Proximal esophageal strictures may develop from lye ingestion, nasogastric tube placement, or reflux disease. However, isolated involvement of the proximal esophagus is rare. Malignant strictures of the proximal esophagus induced by squamous cell carcinoma or adenocarcinoma in the presence of Barrett’s esophagus present with symptoms of cervical dysphagia and should be included in the differential diagnosis of an esophageal stricture.
Diagnostic modalities in the majority of cases will identify a specific derangement in the oral or pharyngeal phase of swallowing, although they rarely help in determining causative factors. The approach to the dysphagic patient must be systematic, starting with a detailed history of the problem and followed by physical and neurologic examinations. Special attention should be given to concomitant disorders that may be responsible for OPD. A history of recurrent pneumonia, weight loss, water and sour brash, regurgitation, and heartburn must be sought, and a careful account of the use of medications, including tranquilizers and ulcer and cancer agents, must be taken. Because some symptoms of OPD such as hoarseness may be due to either unilateral paralysis of the cords or inflammation of the glottis resulting from frequent aspiration of food, correct diagnosis requires a thorough laryngologic examination.
Until recently, barium studies were the only modality used for evaluation of OPD patients. During the past decade, several other modalities such as manometry, endoscopy, ultrasonography, and scintigraphy have been introduced to this field. Intense research in various disciplines is ongoing, making the approach to the OPD patient a dynamic and improving phenomenon. Currently, videofluoroscopic recording of a modified barium swallow is the diagnostic modality of choice. During this study, recordings of a variety of boluses with different consistencies and volumes are made for subsequent analysis, and these recordings are also used for future comparisons to evaluate progress. Although the use of intraluminal strain gauges for pharyngeal manometry has resulted in a significant increase in our knowledge of pharyngeal pressure phenomena, this modality remains mainly a research tool.
Only a minority of patients with OPD are amenable to medical or surgical therapy. The majority, however, require retraining and practice in the use of various swallowing maneuvers and techniques to achieve an adequate and safe swallow. Cricopharyngeal dilatation and myotomy have been performed for a variety of neurogenic and myogenic causes of OPD with variable results. In general, myotomy yields good results in CP achalasia owing to primary CP muscle involvement. The results are less predictable for disease due to primary neurogenic causes if other parts of the swallowing apparatus are also involved. Recently, endoscopic transmucosal botulinum toxin injection into the CP muscle has been tried in patients with CP achalasia. However, the close proximity of the injection area to the vocal cords raises special concern about possible respiratory complications. Surgical treatment of Zenker’s diverticulum has evolved with advances in the understanding of its pathophysiology. Transcutaneous extramucosal cricopharyngeal myotomy with or without diverticulectomy or diverticulopexy traditionally has been the treatment of choice depending on the size of the diverticulum; it yields excellent results in over 90% of cases.
In patients with an inadequate deglutitive glottal closure mechanism such as that seen after partial laryngectomy due to malignancy or in patients with Parkinson’s disease or amyotrophic lateral sclerosis, the deglutitive airway closure could be improved by injecting a nonabsorbable material such as Teflon into the posthemilaryngectomy pseudo–vocal cords or lateral thyroarytenoid muscle. Injection of Teflon results in bulk formation in the injection site and displaces the true cord or surgically constructed pseudo-cord toward the midline. The majority of OPD patients, however, require specialized rehabilitation of their swallowing function. Maintaining adequate nutrition during this period is essential; otherwise, the vicious cycle of malnutrition, OPD complications, and further malnutrition will become self-perpetuating.
Several therapeutic maneuvers have been used to improve oropharyngeal bolus transport and airway safety. A change in bolus size or consistency is helpful in some patients, while in others swallowing with the head in a specific position may help to ensure safe passage of the bolus through the hypopharynx. Flexion of the head by displacing the larynx under the epiglottis reduces the chances of aspiration, and rotating the head toward the weaker side causes relative closure of this side and improves pharyngeal transit. Similarly, tilting the head toward the weaker side directs the bolus laterally and may improve pharyngeal bolus transit and prevent aspiration. In summary, a multidisciplinary approach is needed, not only to identify the cause or causes of OPD but also to direct its management. The disciplines involved may include gastroenterology, otolaryngology, neurology, and speech-language pathology. Speech therapists with a special interest in swallowing problems are needed to participate in the treatment of these patients.
Gastroesophageal Reflux
Entry of the gastric contents into the esophagus (i.e., gastroesophageal reflux) occurs in varying degrees in symptomatic as well as asymptomatic individuals. Depending on a variety of factors including but not limited to the frequency of reflux episodes and the composition of the refluxed material, the effectiveness of the esophageal clearance mechanism, and the esophageal mucosal resistance and regeneration capability, gastroesophageal reflux events may lead to inflammation, mucosal disruption, ulceration, stricture, bleeding, and a premalignant condition marked by gastric metaplasia of the esophageal mucosa (Barrett’s esophagus). The term gastroesophageal reflux disease (GERD) is commonly used to describe any symptomatic clinical condition or histologic changes that result from a backward flow of the gastric contents into the esophagus. Symptomatic GERD is the most common disease of the esophagus. Heartburn (pyrosis) is the cardial symptom of GERD and is reported to occur in 10% to 20% of the population. Four to seven percent of the population are reported to experience heartburn daily.
A multitude of airway and aerodigestive disorders have been attributed to GERD. The most common clinical symptom of GERD, however, is heartburn or pyrosis, described as a retrosternal burning sensation or discomfort. Heartburn may be absent in a substantial percentage of GERD patients with esophageal injury as well as in those with supraesophageal complications of GERD. Severe heartburn may not be accompanied by any detectable macroscopic changes. Therefore, the severity of various symptoms of reflux disease varies widely among patients and may not correlate closely with the degree of severity of esophageal injury. There is wide variation in the clinical course of reflux symptoms; in some patients they undergo spontaneous remission, whereas in others they become intractable and are accompanied by complications.
Other symptoms of GERD include regurgitation, hypersalivation (water brash), sour taste (sour brash), frequent belching, and epigastric pain. GERD-induced odynophagia is uncommon, and the presence of this symptom should prompt investigation for infectious esophagitis such as that induced by Candida, herpes simplex, or cytomegalovirus infection of the esophagus. Gastrointestinal blood loss due to esophagitis generally presents as occult gastrointestinal blood loss, but occasionally esophagitis may induce frank upper gastrointestinal bleeding.
Distal esophageal stricture presents with gradually developing solid food dysphagia. With formation of a stricture, reflux symptoms may abate. In severe cases, liquid dysphagia may be present. In reflux patients without heartburn, solid food dysphagia due to stricture formation may be the presenting symptom. Although peptic esophageal strictures are nearly always located in the distal esophagus, they may occur in the proximal esophagus and present as cervical dysphagia.
The pathogenesis of GERD is believed to be multifactorial. These factors include (1) those affecting the antireflux mechanism (such as lower esophageal sphincter tone, frequency of inappropriate lower esophageal sphincter [LES] relaxation, angle of the esophagogastric junction, and presence or absence of hiatal hernia), (2) volume of gastric content (balance between intake and gastric secretion against gastric emptying), (3) composition and potency of refluxed material (presence of acid, pepsin, bile salts, pancreatic enzyme, byproducts of digestion, and so on), (4) efficiency of the esophageal clearance mechanism (primary and secondary esophageal peristalsis, saliva and its bicarbonate content), and (5) esophageal mucosal resistance to injury and its reparative abilities. Each of these factors or a combination of them may play a predominant role in inducing reflux injury in a given patient. Other conditions that may predispose a patient to reflux by reducing LES tone, provoking LES relaxation, or impairing the esophageal clearance mechanism include unconsciousness, head injury, mental retardation, and nasogastric intubation. Systemic sclerosis especially predisposes the patient to reflux injury and its complication of stricture because of the negligible LES tone, impaired esophageal peristalsis, and decreased salivary production associated with this disease. Pill-induced esophageal lesions (due to potassium tablets, tetracycline, vitamin C, or quinidine) must be considered.
Recent clinical observations indicate that the extent of reflux injury is not limited to the esophagus, and supraesophageal complications of reflux disease are more prevalent than was previously thought. GERD is becoming a disease attended by physicians of various disciplines. About 10% of patients with severe reflux esophagitis develop peptic stricture during the course of their disease. About 40% of all peptic strictures are accompanied by Barrett’s esophagus.
Barrett’s esophagus is defined as replacement of the esophageal squamous cell epithelium by metaplastic columnar-type epithelium due to reflux injury. Because of its malignant potential, development of Barrett’s esophagus is clinically significant and must be followed closely. About 10% to 20% of patients with reflux esophagitis develop Barrett’s epithelium. The true incidence of adenocarcinoma arising from Barrett’s esophagus is unclear. The risk has been reported to be between 5% and 10%, and it is commonly seen in patients older than 40 years of age. Barrett’s ulcer develops most often on the posterior or posterolateral esophageal wall and may result in significant bleeding or perforation. Stricture may also develop in patients with Barrett’s esophagus. Transformation of the columnar epithelium in Barrett’s esophagus into the stages of mild dysplasia, then severe dysplasia, and eventually frank adenocarcinoma is a time-dependent process. An estimated 5% to 10% of all esophageal malignancies are thought to be due to adenocarcinoma developed in Barrett’s esophagus. Adenocarcinoma in Barrett’s epithelium may be multifocal and is well advanced at diagnosis.
Extreme caution must be exercised in attributing chest pain to reflux disease even when the results of a conventional cardiac work-up such as angiography are reported normal because abnormalities of the microvascular cardiac circulation that escape detection by conventional methods may exist.
Most patients with simple heartburn, especially that of a mild nature and transient or short duration, do not require any diagnostic tests and are easily managed medically. However, patients with severe or long-standing heartburn, dysphagia, atypical symptoms such as chest pain, GI bleeding, and supraesophageal complaints require one or more diagnostic tests to determine the extent and severity of the disease and to tailor their therapy. Endoscopy with or without biopsy is the diagnostic modality of choice. It helps to determine the presence or absence of Barrett’s mucosa, significant stricture, and the extent and severity of the mucosal injury.
A barium esophagram is helpful in selected patients with dysphagia in whom it is possible that a distal esophageal ring exists as well as for preoperative evaluation. Atypical symptoms of GERD, such as chest pain and pressure and wheezing, can be elicited by the Bernstein test (intraesophageal acid-saline infusion, with patient unaware of sequence of infusion). Manometry can help in the evaluation of reflux-associated dysphagia, since dysphagia may be caused by abnormal esophageal motor function induced by gastroesophageal reflux disease. Manometry is also useful in preoperative evaluation of esophageal peristaltic function. Concurrent ambulatory pH monitoring of the esophagus and pharynx aids in the detection of pharyngeal acid reflux. It also helps in evaluating the correlation between reflux episodes and the patient’s atypical symptoms and has been used to assess the efficacy of acid suppressive or surgical therapy.
Treatment must be tailored to the disease of each patient. In most patients, reflux symptoms respond favorably to aggressive therapy but recur soon after therapy is stopped. In a minority of patients, reflux symptoms are refractory to treatment and may require surgical therapy.
General precautionary measures include elevating the head of the bed (6 to 8 inches) and dietary measures such as avoidance of fatty foods, chocolate, alcohol, cigarettes, peppermint, and caffeine, which are known to decrease the LES resting pressure. Another measure is weight loss. Since reflux episodes occur most frequently 1 to 3 hours after a meal, refraining from eating for 2 to 3 hours prior to retiring will be helpful. However, these measures are not usually sufficient by themselves to remedy moderate to severe reflux symptoms. Although dietary discretion may reduce the frequency of symptoms, it is ineffective in treating esophagitis.
Antacid and algenic acid work primarily by their capacity to neutralize acids, but this effect is temporary. Large doses of antacid (½ and 3 hours after meals and at bedtime) have been used to treat GERD. Algenic acid, which is present in some aluminum hydroxide antacids, acts as a mechanical barrier by forming a highly viscous solution that floats over the gastric contents and may reduce the number of reflux episodes. Acid-suppressive agents, either H2 receptor antagonists such as ranitidine, nizatidine, or famotidine, or proton pump inhibitors such as omeprazole or lansoprazole comprise the mainstay of the medical management of gastroesophageal reflux disease. Mild to moderate esophagitis responds favorably to H2 receptor antagonists in 75% to 90% of cases. In patients with severe disease, H2 receptor antagonists tend to be less effective. Proton pump inhibitors have been shown consistently to be superior to H2 receptor antagonists in healing reflux esophagitis and relieving symptoms. In patients with severe reflux esophagitis, a proton pump inhibitor such as omeprazole (20 to 40 mg po bid for 8 to 12 weeks) is frequently needed for efficacy.
One of the characteristics of moderate to severe reflux disease is its tendency to recur. More than 80% of esophageal mucosal lesions recur within 6 months of the termination of pharmacologic antireflux therapy. For this reason, maintenance therapy is needed to sustain healing. Maintenance therapy requires full doses of therapeutic agents. Prokinetic agents such as cisapride (Propulsid), 10 mg po qid or 20 mg po bid, in combination with acid-suppressive therapy may improve results in selected cases by enhancing esophageal motility, LES tone, and gastric emptying.
Surgical therapy (conventional or laparoscopic fundoplication) is reserved for patients who fail to respond to medical management such as young patients in whom lifetime therapy is undesirable or patients with supraesophageal manifestation of reflux disease such as asthma and laryngitis that do not respond adequately to acid-suppressive therapy.
An erosion is a break in the mucosa that appears as a whitish lesion with an erythematous halo on endoscopy. Hemorrhagic gastritis, on the other hand, appears as red streaks, patches, or petechiae. Because of the high use of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) in the geriatric population, erosive and hemorrhagic gastritis should always be considered in old patients presenting with nausea, abdominal discomfort or symptoms of anemia secondary to chronic blood loss. Some may present with acute upper gastrointestinal bleeding. Therapy with synthetic prostaglandins (e.g., misoprostol) reduces NSAID-induced mucosal injury. Enteric-coated NSAIDs have also been shown to reduce the incidence of gastritis. These patients may also benefit by using a newer generation of prostaglandin-sparing NSAIDs (e.g., nabumetone).
In patients with atrophic gastritis, there is variable gland loss, often accompanied by intestinal metaplasia. The gastric antrum may show an increase in the number of gastrin cells when hypochlorhydria or achlorhydria is associated with gastric atrophy. Serum gastrin levels are raised. Hyperplasia of the enterochromaffin-like cells may also occur. Many studies have shown that a high proportion of asymptomatic people over the age of 60 years have atrophic gastritis. However, there is no relation between age and degree of atrophy.3 In one study, no one over the age of 60 with an initially normal gastric mucosa developed gastric atrophy during follow-up for 10 years.4 Thus, gastric atrophy is not a normal part of aging but rather is the result of some specific abnormal mechanisms. Basal and peak gastric acid output appear to decrease with increasing age; however, if one corrects for the presence of Helicobacter pylori and atrophic gastritis, there may be no change in acid production with aging. Pepsin secretion does not change with age. Severe atrophic gastritis can result in diminished production of intrinsic factor leading to vitamin B12 malabsorption.
Helicobacter pylori is a gram-negative, wavy-shaped rod. In the developed countries, H. pylori infection is uncommon before the third decade of life; thereafter, it shows an age-related rise in prevalence. Seropositivity peaks at around 40% to 50% after the age of 50 years. Although H. pylori is a frequent cause of nonerosive nonspecific gastritis, its role in the pathogenesis of gastric atrophy and hypochlorhydria is also now well established. More than 80% of patients with pernicious anemia have antibodies to H. pylori. Because the prevalence of H. pylori rises with age, it is possible that age-related changes in the histology and function of the stomach could be secondary to H. pylori infection.5
Peptic Ulcer Disease
Peptic ulcers can develop in the esophagus, stomach, duodenum, and jejunum (after gastrojejunostomy) and in areas with ectopic gastric mucosa. Although there is an implied pathogenic association with acid and pepsin, present data suggest that there are two common types of peptic ulcers: ulcers associated with NSAIDs and those associated with the H. pylori organism. The incidence of peptic ulcer has risen with age, possibly because of the increased use of NSAIDs and the increased prevalence of H. pylori in the elderly.
NSAID therapy is associated with a three- to fivefold increased risk of hospitalization for ulcers or their complications. Gastric ulcers are more common than duodenal ulcers, and rarely, NSAIDs can also induce small bowel or esophageal ulcers. Ulcers related to NSAIDs can be categorized into three types6: (1) small mucosal ulcers that develop acutely, probably secondary to topical contact and involving the fundus more than the antrum. These ulcers heal rapidly and can be prevented by using prostaglandin cytoprotection or enteric-coated NSAIDs; (2) 3- to 5- mm ulcers that develop over days to months of NSAID use and involve the antrum more than the fundus. These ulcers probably develop secondary to topical or systemic effects of NSAIDs and therefore may or may not be prevented by using enteric-coated pills, but they can be prevented by using prostaglandin cytoprotection; and (3) chronic, large, deep ulcers, mainly in the antrum and probably related to the systemic effects of NSAIDs. These ulcers may cause complications such as bleeding and perforation and may not be prevented by taking enteric-coated pills or by using prostaglandin cytoprotection.
The risk of NSAID-induced ulcer complications increases in patients over the age of 60 years who have cardiovascular disease, take high or multiple doses of NSAIDs, and take concomitant corticosteroid therapy. Prostaglandin analogs (misoprostol) significantly reduce the incidence of gastric as well as duodenal ulcers induced by NSAIDs. NSAID-induced ulcers can heal with the use of proton pump inhibitors despite the continuous use of NSAIDs.
Helicobacter pylori shows an age-related rise in prevalence. About 40% to 50% of individuals are H. pylori seropositive by the age of 50 years. H. pylori prevalence reaches 95% in those with duodenal ulcers and 65% in those with gastric ulcers. The mechanism by which this bacteria leads to ulceration is not known. The organism, or factors released by it, might weaken mucosal defenses. Infected individuals also show elevated levels of gastrin and pepsinogen. Several tests are available for diagnosing H. pylori infection. Tests using the urease activity of the bacteria are the 13C breath test (90% to 95% sensitivity) and the Campylobacter-like organism (CLO) test (90% to 98% sensitivity) on gastric biopsy specimen. Serum antibodies against H. pylori (95% sensitivity) cannot differentiate present from past infection unless follow-up titers show a rise. Other methods to diagnose H. pylori infection include histology or culture (70% to 95% sensitivity).
Elderly patients with peptic ulcer disease usually present with nonspecific abdominal discomfort or marked weight loss, or they may be asymptomatic. Many present for the first time with complications such as bleeding, perforation, or symptoms of obstruction. Some with chronic blood loss present with cardiac symptoms such as angina or cardiac failure. The presence of systemic diseases like chronic obstructive pulmonary disease (COPD), cardiopulmonary diseases requiring aspirin or anticoagulation for therapy, chronic renal failure, or chronic liver diseases predispose the elderly to peptic ulcer disease and its complications. Complications are seen in about 50% of patients over 70 years. Bleeding is most common and has a higher mortality rate than it does in young patients.
Esophageal and gastric cancers also present frequently in the elderly, and therefore all esophageal and gastric ulcers need endoscopic evaluation, including biopsies and follow-up documentation of healing.
Peptic ulcer disease in the elderly patient is treated using the same guidelines as for the young. However, because many old patients receive drugs for other systemic conditions, one should also be aware of drug interactions and side effects. For example, inhibition of hepatic microsomal cytochrome P450 by cimetidine will raise serum levels of drugs like warfarin, theophylline, and phenytoin. Almost all H2-receptor antagonists can cause nondose-related central nervous system (CNS) effects such as confusion, disorientation, lethargy, and somnolence. Eradication of H. pylori requires combination therapy (Table 46-3). Frail elderly people with multiorgan diseases who are high surgical risks, those who have had complications, those who have had ulcer disease and need anticoagulation, and those who have frequent recurrences of ulcers despite avoiding NSAIDs or eradicating H. pylori can be given a H2-receptor antagonist at bedtime for prophylaxis. Patients requiring NSAIDs can be given enteric-coated ones, or concurrent administration of misoprostol can be tried. A new generation of prostaglandin-sparing NSAIDs (e.g., nabumetone) is also being tried in some of these patients.


Upper Gastrointestinal Bleeding
Table 46-4 lists some of the causes of upper gastrointestinal bleeding. More than 90% of upper gastrointestinal bleeds are secondary to peptic ulcer disease, erosions, varices, and Mallory-Weiss tears. In the elderly, one should also consider upper gastrointestinal malignancies, vascular anomalies like Dieulafoy’s anomaly, and aortoenteric fistulas. Increasing use of NSAIDs and systemic conditions like COPD, chronic renal failure, and chronic liver disease predispose the elderly to bleeding from ulcer disease.


Upper gastrointestinal bleeding can be overt (e.g., hematemesis or melena), or it can be occult. If severe, it can present as hematochezia. Because of associated systemic disease, acute bleeding may not be as well tolerated by the elderly as by the young. Similarly, chronic occult bleeding leading to anemia may present as worsening cardiac failure or exacerbation of angina.

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