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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
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
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.
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,
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,
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 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 types (6) : (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 13 C 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.
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
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.
Mortality from upper gastrointestinal bleeding has remained at around 10% for the past 45 to 50 years despite advances in endoscopy, surgery, and intensive care units. This constant rate may be related to the fact that high-risk patients like the elderly are now living longer and constitute the 10% of patients who die from bleeding. (7) , (8) In one study, of 1098 cases admitted to a specialized bleeding unit, 52% had severe upper gastrointestinal bleeding, of which two thirds were over 60 years of age. (9) Thirty-day bleeding-related mortality was around 4%, and all these were elderly patients. The National American Society of Gastrointestinal Endoscopy survey on upper gastrointestinal bleeding revealed that the mortality rate was 13.4% in those over 60 years, whereas it was 8.7% in those below 60 years. (10) Preexisting congestive heart failure and arrhythmias, stroke, encephalopathy, liver disease, neoplasms, COPD, pneumonia, and renal disease all were associated with higher mortality rates. A recent study showed that age, shock, co-morbidity, major endoscopic stigmata of recent hemorrhage, and rebleeding were all independent predictors of mortality. (11)
General principles of management of gastrointestinal bleeding are similar in the young and the old. The need for blood transfusion is largely dictated by the presence of ongoing bleeding, hemodynamic instability, and the presence of preexisting conditions that decrease the patient s tolerance to blood loss. Those without volume depletion but requiring transfusion (e.g., severe anemia precipitating congestive heart failure) can be given packed red cells and monitored closely for volume overload. The timing of diagnostic procedures depends on the urgency of the need for therapeutic intervention. Endoscopy is accurate, rapid, and relatively safe and allows therapeutic intervention. Endoscopic evidence of active bleeding, visible blood vessels, and fresh clots on an ulcer base indicate a high risk of continued or recurrent bleeding. These features in an elderly patient merit active therapeutic intervention including early surgery, because rebleeding significantly increases mortality in the elderly. In 5% to 10% of cases, endoscopy does not identify the bleeding site. In these patients, angiography can be considered if bleeding is ongoing or recurrent. Elderly patients with variceal bleeding should be treated aggressively because the survival rate in patients with variceal bleeding is similar in the young and the old.
Several structural and functional changes occur
in the pancreas with increasing age. The diameter
Alcohol use and gallstones account for 80% of cases of acute pancreatitis observed in the general population. About 10% to 15% of cases are idiopathic. When causes of pancreatitis are stratified by age, ischemia is seen to be an important cause of acute pancreatitis in the elderly. In one study, 27% of patients developed pancreatitis following coronary bypass. (15) The incidence of gallstone pancreatitis is significantly higher in older people than in younger ones. As much as 55% of all cases of pancreatitis in those over 60 years of age are due to biliary tract disease, whereas alcohol accounts for only 20% of cases. (16) There is also a higher incidence of idiopathic pancreatitis in the elderly. Some of these cases may be secondary to biliary microlithiasis. Drugs such as diuretics and steroids can also cause pancreatitis. Pancreatic cancer should be suspected in all elderly patients presenting with pancreatitis for the first time.
Acute pancreatitis frequently presents atypically in those over 60 years of age. Absence of typical abdominal pain and the presence of multiorgan failure, shock, hypothermia, and hyperglycemia are some of the clinical presentations. Unfortunately, in many cases the diagnosis is made at autopsy. Pancreatic necrosis is frequently observed in these cases. Acute pancreatitis should be strongly considered in elderly patients who present with unexplained systemic complications, especially during the postoperative period. Diagnostic investigations, including amylase-lipase levels, computed tomography (CT) of the abdomen, and, when appropriate, endoscopic retrograde cholangiopancreatography (ERCP) should be done.
Treatment guidelines in the elderly are similar to those used in younger individuals. However, patients presenting with acute severe nonresolving gallstone pancreatitis should undergo urgent ERCP and sphincterotomy for stone removal. (17) , (18) Those with idiopathic pancreatitis should be evaluated for biliary microlithiasis, and, if these are present, these patients should also undergo sphincterotomy. Another option includes the use of ursodeoxycholic acid. Rarely, manometry of the sphincter of Oddi may be required to diagnose papillary stenosis as a cause of idiopathic pancreatitis requiring sphincterotomy. Other obstructive causes, such as adenomas and carcinomas, should also be considered in these cases.
Although some cases of chronic pancreatitis are idiopathic, most are secondary to alcohol consumption. Obstructive chronic pancreatitis should always raise the suspicion of an ampullary neoplasm or pancreatic carcinoma. These patients usually have a dilated pancreatic duct and do not show the typical pancreatic calcification seen in those with alcohol or idiopathic pancreatitis. Rarely, pancreatic stones are noted in the pancreatic duct in asymptomatic elderly subjects. (19)
Pain is less severe in older patients with chronic pancreatitis, and many may never experience any pain. Disease progression is also slower in the elderly than in the young, and therefore few, if any, show evidence of endocrine or exocrine insufficiency or require intervention for complications.
Most patients with ductal adenocarcinoma of the pancreas are over the age of 60 years. Patients with chronic pancreatitis from any cause have a higher risk of developing pancreatic carcinoma. (20) , (21) The chances of developing pancreatic carcinoma in patients with chronic pancreatitis are directly related to increasing age.
Brushings for cytologic examination obtained during ERCP, endoscopic ultrasonography with fine-needle aspiration, and analysis of cystic fluid may provide further help in diagnosis. In selected cases, angiography and laparoscopy may be required.
The only hope for cure in patients with pancreatic adenocarcinoma is surgery. Surgery is also the preferred treatment for mucinous ductal ectasia and cystic neoplasms because some of these tumors may be either malignant or premalignant. Evidence of biliary obstruction in patients with pancreatic carcinoma generally implies advanced disease except in those with ampullary carcinoma, in whom biliary obstruction can occur early. Palliative therapy includes modalities such as placement of biliary endoprostheses to relieve biliary obstruction, radiotherapy, and pain control, which may involve celiac ganglion block.
Several age-related changes have been described in liver structure and function. With aging, there
The mortality rate from chronic liver disease is highest among patients over 65 years. Some of these diseases develop in the young who survive to older age, whereas others develop in old age. In one national study, the incidence of toxic hepatitis, primary biliary cirrhosis, and nonalcoholic cirrhosis peaked in patients between 70 and 79 years, whereas alcoholic cirrhosis peaked at 50 to 59 years. (25) Liver can be affected by systemic conditions such as cardiac failure. Some rare diseases such as the Budd-Chiari syndrome and idiopathic hemochromatosis can also present in the elderly.
Decreased bile acid production, increased cholesterol saturation of bile, reduced gallbladder sensitivity to cholecystokinin, and increased prevalence of duodenal diverticula are some of the factors that predispose to formation of gallstones in the elderly. By 70 years of age, about 35% of women and 20% of men have gallstones. Although many are asymptomatic, some may present with biliary pain, cholecystitis, pancreatitis, cholangitis, or obstructive jaundice. Gallbladder cancer, also found predominantly in the elderly, can present with several of the same clinical features. As in younger patients, diagnostic investigations include liver function tests, ultrasound or CT scans of the abdomen (or both), and ERCP examination. In interpreting abnormal liver function test results, one should keep in mind that an isolated rise in alkaline phosphatase levels in the elderly can be secondary to bone disease. With advances in anesthesia and surgical techniques, urgent cholecystectomy in elderly patients presenting with acute cholecystitis has a mortality rate similar to that seen in the young. Laparoscopic cholecystectomy is becoming increasingly popular and is particularly useful in treating symptomatic cholelithiasis in the frail elderly. If clinical and biochemical test results raise a suspicion of common bile duct stones, patients scheduled for laparoscopic cholecystectomy should undergo ERCP evaluation prior to surgery. Extremely ill elderly patients considered to be at high risk for surgery and not responding to conservative treatment can be treated by ultrasound-guided percutaneous cholecystostomy. Patients with gallstones in the common bile duct and those with gallstone pancreatitis require ERCP with sphincterotomy and stone extraction using a basket or a balloon. Larger stones can be removed by crushing them with a lithotriptor. In a subset of cases, biliary endoprostheses with regular exchanges can be used for long-term management of nonretrievable common bile duct stones.
Obstructive jaundice in the elderly is more commonly secondary to malignancy than to choledocholithiasis. Adenocarcinoma of the pancreas accounts for most of these cases. Other malignancies include ampullary, gallbladder, bile duct, duodenal, and metastatic cancers. Most of these patients present with painless jaundice with or without a palpably enlarged gallbladder. Benign biliary strictures can result from cholangitis, bile duct injuries, or radiotherapy. Primary sclerosing cholangitis is rare in persons over 65 years of age.
Malignant biliary obstruction usually requires palliative treatment because most of these obstructions are secondary to advanced diseases or the frail elderly patient is too ill to undergo extensive surgical resection. Diagnosis can be made by obtaining samples from ERCP brushings or biopsies or by CT-guided or endoscopic ultrasound-guided fine-needle aspiration. Biliary decompression is generally achieved by ERCP sphincterotomy or placement of an endoprosthesis. In tumors involving the hepatic hilum, multiple endoprostheses may be required to decompress the right and left hepatic systems. Endoscopic biliary decompression is as successful in relieving obstruction as surgery is, but it requires a shorter hospital stay and is less expensive. It should therefore be the preferred treatment modality, especially in the elderly. Percutaneous biliary decompression (external or internal) is another alternative. Complications of this method include hemorrhage, infection, peritonitis, and catheter displacement. It should therefore be considered if the ERCP technique fails.
Alcohol liver disease should always be considered in the differential diagnosis when an elderly person presents with hepatic dysfunction. In one study from the United States, presentation with alcohol liver cirrhosis peaked in the seventh decade. (26) Clinical features of alcohol liver disease in the elderly are similar to those seen in younger patients. However, older patients are more likely to present with severe disease than younger subjects. (27) Elderly patients with alcohol liver disease also have a higher mortality rate. (28)
Decreased hepatic volume and decreased blood flow with increasing age may result in altered pharmacokinetics and predispose the elderly to drug-related diseases. Unfortunately, many old patients are taking multiple medications. Not surprisingly, adverse drug reactions have an increased prevalence in the elderly. In a Danish study, the incidence of toxic hepatitis reached 50 per million person-years in 70- to 79-year-old people compared to an overall incidence of 20 per million person-years. (25) Elderly patients are particularly likely to develop toxic hepatitis with certain drugs. For example, isoniazid-induced hepatitis occurs in more than 2% of patients over 50 years old but is virtually unknown under the age of 20 years. An anti-inflammatory drug, benoxaprofen, had to be withdrawn from use following fatal hepatotoxicity that occurred predominantly in elderly women. Halothane reexposure in patients with previously known halothane-induced injury results in more severe hepatotoxicity in elderly patients than in young ones. Whereas several drug-related hepatic injuries are idiosyncratic reactions and therefore are unpredictable, many are dose-related and require dose adjustments. For example, amiodarone toxicity requires dose adjustment in the elderly. Drug-induced liver disease may present like hepatitis with increased transaminase levels (acetaminophen, isoniazid, methyldopa), or like cholestatic hepatitis with raised transaminases and alkaline phosphatase levels, mimicking cholangitis (phenytoin, quinidine, nitrofurantoin, erythromycin), or with a primarily cholestatic picture (estrogens, chlorpromazine, chlorpropamide, anabolic steroids).
Although the peak incidence of hepatocellular carcinoma worldwide occurs in early to middle adulthood, this cancer is predominantly a disease of the elderly in Europe and North America. Some of the common predisposing factors are liver cirrhosis, previous hepatitis B infection, and hemochromatosis.
Metastases to the liver, especially from the gastrointestinal tract, form another important group of hepatic malignancies seen in the elderly. Anorexia, weight loss, malaise, abdominal pain, jaundice, hepatomegaly, and ascites are some of the clinical features. These patients usually have raised alkaline phosphatase levels, and those with hepatocellular carcinoma may have raised alphafetoprotein levels. Diagnosis generally requires liver biopsy, usually CT-guided. Surgical resection, regional chemotherapy, cryoablation, and alcohol injection into the tumor are some of the treatment options.
More than 50% of cases of liver abscess in the developed countries occur in those over 60 years of age. Most of these cases are secondary to ascending cholangitis. High fever, rigors, and other classic features of sepsis are generally lacking in the elderly, most of whom present with nonspecific symptoms such as epigastric pain, weight loss, or confusion. Alkaline phosphatase levels are usually raised in these patients. Due to the potential lethal nature of this condition, especially in the elderly, early intervention by percutaneous or surgical drainage may be necessary.
Viral hepatitis should always be considered in the differential diagnosis of any elderly patient presenting with anorexia, jaundice, and elevated transaminase concentrations. In patients who are admitted with episodes of hypotension and grossly elevated transaminase levels, one should consider ischemic hepatitis. Fluctuating liver function test results are seen in patients with heart failure. Mild increases in transaminase levels may be associated with alcoholism, chronic hepatitis, and fatty liver in patients with obesity, hyperlipidemia, and diabetes mellitus. Primary biliary cirrhosis and chronic active hepatitis may also occur in the elderly. Although with the availability of serologic markers for hepatitis C, the diagnosis of cryptogenic cirrhosis had to be revised in several cases, a study from the Mayo Clinic reported that a higher incidence of cryptogenic cirrhosis occurs in the elderly, raising the possibility that there may be a specific form of senile cirrhosis. (29) Variceal bleeding secondary to portal hypertension should be treated aggressively
Advances in surgery and immunosuppressive treatment have greatly improved the results of liver transplantation. In a retrospective analysis, Pirsch and colleagues found excellent graft and patient survival in liver transplant recipients over 60 years of age compared to those under 60 years. (30) Old age alone, therefore, should not be a contraindication to liver transplantation.
There is little evidence that a generalized age-related loss of absorptive function occurs in the small intestine. Age-related declines in specific enzymes such as lactase have been reported. There has been more interest in studies of intestinal motor activity in the elderly. Abnormal motility could be related to the aging process or to underlying diseases that are increasingly prevalent in older patients.
Small intestinal motility, as measured by manometric tubes passed into the intestine, does not appear to change with age, showing only minor changes in amplitude of contractions. Studies have consistently shown that fasting and postprandial small intestinal contractions are similar in young and elderly subjects. Individuals who have symptoms consistent with abnormal small intestinal transit, such as abdominal distention or diarrhea, should be evaluated to exclude an underlying disease as an explanation. A small intestinal barium x-ray study is a useful screening test for evaluating symptoms related to small intestinal transit. Findings of abnormal small intestinal transit, dilatation, or diverticulosis may suggest a reason for the patient s symptoms. Small intestinal transit can be altered by autonomic neuropathic disorders. Rapid small bowel transit can induce diarrhea. Dilatation of the small bowel may be due to malabsorption syndromes, and small intestinal diverticulosis and slow intestinal transit can result in small bowel bacterial overgrowth that causes diarrhea.
Many studies have been designed to define the prevalence of intestinal symptoms in young and old patients. These studies have included inpatient and outpatient diagnoses in individuals seeking medical care as well as surveys of defined populations of individuals who have not necessarily consulted a physician. One of the proposed gastrointestinal motility disorders is irritable bowel syndrome (IBS), which can be defined by the presence of three or more Manning criteria (briefly summarized as follows: (1) pain relieved by defecation, (2) looser stools during pain, (3) more frequent stooling during pain, (4) abdominal distention, (5) a feeling of incomplete evacuation, and (6) passing mucus through the rectum). The prevalence of IBS in a population of individuals not necessarily seen by a physician has been estimated as 11% among individuals 65 years old or older. (31)
Chronic constipation is another common chronic gastrointestinal disorder in the United States. (32) The prevalence of constipation is 4.5% among individuals 65 to 74 years old and 10.2% among individuals 75 years old or older. Constipation affects three times as many women as men. An estimated 4.5 million individuals in the United States have constipation, and they visit a physician an estimated 2.5 million times yearly for evaluation of this symptom.
The development of fecal incontinence is an important factor in considering future requirements for nursing home care of elderly individuals. Incontinence of liquid fecal material is most common. Fecal incontinence is more common in men than in women.
The effects of aging on neural and intrinsic muscular control of gastrointestinal smooth muscle are poorly understood. Principal theories of the process of senescence include two main hypotheses: (1) chronic exposure to toxins results in an age-related neuropathic or myopathic process, or (2) genes involved in the normal functioning of neurons or smooth muscle undergo gradual changes in expression that eventually result in "aging." In the first proposed mechanism, potential exposures include chronic ingestion of exogenous neurotoxins or chronic production of endogenous neurotoxins such as tissue free radicals. In examination of the second mechanism, studies of gene expression in senescence have led to the concept of genetic instability, in which changes in DNA and chromatin occur with aging. It is not yet known whether genetic instability results in changes in intestinal function.
Motility of the intestine is regulated by endocrine and neural systems. Extrinsic nerve fibers (preganglionic parasympathetic and postganglionic sympathetic fibers) communicate with nerve cell bodies in intestinal nerve plexuses. Disruption of extrinsic innervation (due to central nervous system damage or spinal cord injury) alters enteric nervous system function and results in altered motility. There is little evidence to support
Intrinsic intestinal nerves provide both excitatory and inhibitory input to smooth muscle cells. Age-related changes may include a loss of nerve input (either inhibitory or excitatory) from enteric neurons that innervate the intestinal smooth muscle cells. Multiple studies have supported the concept of an age-related loss of enteric neurons, and recent work using human colon has revealed that an age-related loss of inhibitory nerve input to colonic circular smooth muscle may occur. Loss of inhibitory nerve input could change colonic motility by diminishing the normal descending relaxation of the colon or by decreasing the normal inhibition of nonpropagating colonic contractions. Opiates, for example, induce constipation by increasing the occurrence of nonpropagating contractions in the distal gut.
To induce normal relaxation or contraction of smooth muscle cells, receptors for specific excitatory or inhibitory neurotransmitters must be present on the smooth muscle cell, and the contractile apparatus of the myocyte must be functional. There is little evidence in humans at present to support the idea that an age-related myopathic disorder may cause abnormalities in intestinal motility.
Bleeding from the lower gut may present as outlet bleeding (bright red blood during or after defecation), suspicious bleeding (blood mixed with or streaked on stool), acute hemorrhage, or occult bleeding (anemia, iron deficiency, or positive results on stool occult blood test).
The differential diagnosis remains complex. Outlet bleeding is commonly thought to be due to an anal fissure, hemorrhoids, distal colorectal neoplasia, or proctitis. It has been suggested that a flexible sigmoidoscopy should be performed for simple uncomplicated outlet bleeding.
The available studies support a recommendation for total colonoscopy for evaluation of suspicious bleeding, acute hemorrhage (when the patient is stable), and occult bleeding. (33) Causes of acute hemorrhage, in descending order of occurrence, include diverticular bleeding (often from right-sided diverticula), angiodysplasia, inflammatory bowel disease, ischemic colitis, and, less likely, infectious colitis, colorectal neoplasia, solitary rectal ulcer syndrome, and radiation colitis. There are many unusual origins of acute lower intestinal hemorrhage. Poor visualization of the colon during an acute hemorrhage may lead to performance of visceral angiography as an additional diagnostic study. In patients with occult bleeding, a common finding is colorectal neoplasia; angiodysplasia is less likely, and ischemic colitis and occult inflammatory bowel disease are unlikely.
Epidemiologic studies of inflammatory bowel disease (IBD) have shown a second peak in occurrence in patients over the age of 60. The etiology of colitis can be complex in elderly patients. Several other conditions must be considered during evaluation of an elderly patient who presents with a colitis-like disorder.
Two types of infectious colitis may be overlooked in elderly patients. Because of the use of many antibiotics, patients can develop a pseudo-membranous colitis that can mimic the picture of toxic megacolon. Overgrowth of Clostridium difficile is thought to be the main pathogenic factor, and a stool test may show the presence of a C. difficile toxin. On endoscopy of the lower intestine, patchy but multiple cream-yellow plaques or membranes may be seen in the left colon more commonly than in the right colon. Treatment regimens include oral metronidazole or oral vancomycin. Recurrent pseudomembranous colitis can be treated by changing the oral antibiotic regimen, treating for a longer period (4 weeks), or adding therapy to potentially bind the bacterial toxin (cholestyramine). In a second type of atypical infectious colitis, cancer chemotherapy is associated with development of a cytomegalovirus-induced colitis. At colonoscopy, discrete ulcers are seen in the colon, and colonic mucosal biopsies will aid in the diagnosis.
Three types of noninfectious colitis should be considered in evaluating elderly patients. Colitis induced by the use of NSAIDs can mimic the signs of mild ulcerative colitis. Following radiation therapy, especially in men with adenocarcinoma of the prostate, lower endoscopy may reveal rectal telangiectasias consistent with a diagnosis of radiation proctitis. Medical therapies are often ineffective in this condition, but laser therapy has been useful in selected patients to reduce blood loss. Ischemic colitis is more common in elderly patients, and it has been reported especially often following aortoiliac reconstructive surgery. At colonoscopy, findings include deep linear ulcers, edema, diffuse petechiae, and a sharp demarcation proximal to the splenic flexure of the colon; the finding of necrotic colon requires rapid surgical intervention.
When no specific cause of colitis can be identified after tests that include appropriate stool cultures for pathogenic bacteria and stool examinations to exclude ova and parasites, treatment is designed to improve symptoms. Medical therapy for idiopathic IBD should begin with the safest and most cost-effective treatment, and progression to increasingly complex treatments should be based on the patient s response. Medical treatment of idiopathic IBD is summarized in Table 46-5 . Distal colitis or proctitis may respond initially to treatment with enemas (containing a corticosteroid or a 5-aminosalicylic acid compound).
Mildly or moderately active colitis is often treated with sulfasalazine. The lowest effective dose should be used, and folic acid should be given simultaneously as a supplement. In patients who cannot tolerate the side effects of sulfasalazine and in selected patients who are allergic to sulfa drugs, compounds derived from the active moiety of sulfasalazine (Azulfidine), 5-aminosalicylic acid, are now available. 5-Aminosalicylic acid compounds are no more effective than sulfasalazine.
Moderately active to severely active colitis may require oral corticosteroid therapy, usually for periods of at least 2 to 3 months. Low doses of corticosteroids are no more effective than placebo for maintenance. Long-term high-dose corticosteroid therapy is associated with significant complications. Antibiotic therapy appears to be more effective in patients with Crohn s disease, especially for fistulous disease or treatment of perineal Crohn s disease. Nutritional therapy is not effective for primary therapy of ulcerative colitis, and nutritional treatment of Crohn s disease requires a liquid diet that many patients do not find acceptable. Although a polymeric diet or an elemental diet may diminish the corticosteroid dose needed in Crohn s disease, its benefit is lost after it has been discontinued.
Immunosuppressive therapy should not be considered simply a substitute for surgical therapy and should be used by physicians with the appropriate experience. 6-Mercaptopurine does not appear to be effective as a single agent but can diminish the corticosteroid dose needed. Cyclosporine and methotrexate are both toxic medications and should probably be reserved for treatment of Crohn s disease. Long-term maintenance therapy of IBD includes use of sulfasalazine, 5-aminosalicylic acid compounds, metronidazole, or 6-mercaptopurine (in combination with low-dose corticosteroid therapy).
Constipation, a subjective term describing the symptom of unsatisfactory defecation, is a common chronic digestive disorder. (32) Most patients with a complaint of constipation are seen by general practitioners and general internists. Constipation represents different problems to different individuals. It may be described as infrequent defecation or straining, passage of firm or small-volume fecal material, pain with defecation, or a discrepancy between expected output and actual results.
The cause of age-related constipation is presently incompletely understood. Conventional proposals of causation include chronic disease processes (e.g., diabetes mellitus), intake of opiates or medications that have anticholinergic side effects, or insufficient exercise or water-fiber intake. None of these proposals has been convincingly supported by available studies. Colon transit studies have repeatedly shown an increase in the number of retained markers in the rectosigmoid region, suggesting that constipated elderly individuals have slow left-sided colorectal transit.
To understand the causes of constipation it is important to consider the mechanisms of defecation. The process of defecation requires four major mechanisms: (1) an anorectal sensation of an urge to defecate following rectal distention, (2) reflex relaxation of the internal anal sphincter, (3) colorectal motility, chiefly manifested by propagating contractions, and (4) an increase in intra-abdominal pressure by Valsalva s maneuver to produce perineal descent.
Constipation can be caused by many different diseases (Table 46-6) . Known causes of constipation include neuropathic disorders such as Hirschsprung s disease and Chagas disease, myopathic disorders such as scleroderma and amyloidosis, and mechanical or functional obstruction, such as that due to adenocarcinoma of the
At the initial visit, evaluation of a complaint of constipation begins with a proper history and physical examination. This includes an estimate of the frequency of stooling, length of time symptoms have been present, and associated symptoms such as straining, abdominal pain, abdominal distention, and fullness or bloating. Recent onset of constipation, especially in older patients, suggests a need to exclude mechanical obstruction. Imaging of the colon and rectum by endoscopy or barium colon radiography should then be performed. To exclude endocrine causes of colonic dysmotility, fasting serum glucose, serum calcium, potassium, creatinine, and thyroid-stimulating hormone levels should be measured. Constipation may be associated with beginning a new medication or increasing the dosage of an existing medication, especially calcium channel antagonists, opiate agonists, anticholinergic medications, and aluminum-containing antacids. Other historical factors that must be addressed are the possible habitual use of laxatives for the purpose of purgation and an onset of constipation following an episode of anal pain.
In many patients, the cause of the symptoms may remain unclear. A primary differentiation that must be made is whether the patient has normal transit constipation (probably irritable bowel syndrome) or abnormal colorectal transit. A simple test to distinguish these two categories is a Sitzmarks colonic transit study. Commercially prepared gelatin capsules containing 24 radiopaque rings are available (Sitzmarks, Lafayette Pharmacal, Inc., Fort Worth, Texas). The movement of nonabsorbable markers through the colon is followed by exposing flat plate abdominal radiographs. Before performing this test, it may be necessary to evacuate the patient s colon. It is necessary during the study for patients to refrain from taking laxatives, enemas, suppositories, and medications that cause constipation. The presence of retained markers (defined as greater than 20% of the total ingested) throughout the colon at day 5 is consistent with constipation due to so-called colonic inertia, while markers retained within the rectosigmoid region are consistent with constipation due to rectosigmoid dysmotility or a rectal outlet obstruction. The term spastic pelvic floor syndrome should be reserved for patients who have difficulty in initiating defecation and in whom insufficient relaxation of the levator ani muscle can be demonstrated.
As summarized in
Table 46-7
, optimal treatment
of constipation would be a specific therapy
designed to correct an underlying condition. In
many patients no specific cause can be identified,
and instruction about a high-fiber diet remains
If these initial measures are not helpful, patients with constipation and documented abnormal results on a marker study may experience symptomatic improvement by consuming a low-fiber diet. A small group of patients with severe colorectal dysmotility obtain relief from abdominal pain through colonic cleansing, but they cannot maintain colonic evacuation. If additional medical therapy is required, there are three major categories of laxatives that may be used. Irritant or stimulant laxatives include anthraquinone compounds, which are active ingredients in extracts of senna, aloe, cascara, or rhubarb. Many available herbal tea preparations include an anthraquinone compound. Other over-the-counter stimulant chemicals include phenolphthalein and bisacodyl. These agents generally should not be prescribed for the long term because increasing doses will be necessary over time to initiate defecation, and older patients may develop fecal incontinence as well as potential colonic nerve toxicity.
Osmotic agents tend to increase the water content of fecal material. The use of mineral oil is not recommended because reflux of this material can cause lipid pneumonia. Magnesium salts such as citrate of magnesia have been extensively used and are relatively safe. Patients receiving these agents should have periodic screening of renal function and serum magnesium level. In patients with decreased renal function, poorly absorbed sugars such as lactulose and sorbitol may be beneficial. The use of sorbitol 70% syrup may be preferable because it is less expensive. (34) Among other similar agents, available studies have found that wetting agents or surfactants such as docusate calcium or docusate sodium produce no consistent benefit.
The third major class of laxatives includes drugs that function as neurotransmitter agonists. In general, use of these compounds has been disappointing. Bethanechol chloride is a cholinergic agonist that increases phasic contractions in human colon. Neostigmine bromide can decrease metabolism of endogenous acetylcholine, which in normal individuals increases phasic contractions. Its use may induce severe side effects. Cisapride releases acetylcholine at the level of the nerve plexus and seems to be helpful in inducing phasic colonic contractions. Cisapride may be ineffective in long-term therapy and has been associated with development of prolonged QT syndrome.
Regular use of suppositories (two to three mornings a week) may be beneficial in maintaining rectal evacuation in patients with constipation due to a rectal outlet obstruction. Carbon dioxide-producing suppositories distend the rectum and may initiate descending relaxation of the circular smooth muscle. In selected patients with the spastic pelvic floor syndrome and in patients with neurologic diseases affecting the external anal sphincter, biofeedback techniques designed to teach the patient to relax the external anal sphincter may be helpful. (35) These methods require good patient compliance, are time-consuming, and require a specialist for instruction.
Among potential complications, there is evidence that chronic constipation can lead to fecal impaction, overflow fecal incontinence, sigmoid volvulus, and stercoral (pressure) colonic ulcerations. Chronic therapy may be helpful in preventing these problems. There is little evidence that hemorrhoids, melanosis coli, or colon cancer are caused by constipation. Identification of melanosis coli is not helpful because there is no correlation between the occurrence of melanosis coli and the presence of abnormal colorectal transit or the frequency of bowel movements.
Acute dilatation of the colon (Ogilvie s syndrome) can be related to multiple causes including surgery or trauma (spinal surgery, hip fracture), use of medications (narcotic analgesics, anticholinergic medications), endocrine disorders (hypothyroidism), or electrolyte imbalance (hypokalemia or hypercalcemia). An increased risk of colonic perforation is thought to be associated with a transverse colonic or cecal diameter of more than 9 cm on an abdominal flat plate radiograph. Management is often hotly debated. If a specific cause is identified, it should be corrected. If an endocrine origin, electrolyte imbalance, or medication-induced origin cannot be rapidly reversed, a decision must be made about whether the patient needs lower endoscopy to decompress the colon or a conservative management plan that includes repositioning the patient and passing a short-term nasogastric decompression tube and a soft rectal decompression tube. Cautious
Sigmoid volvulus is a poorly studied colonic disorder. Development of megacolon is believed to be a major risk factor for the formation of a sigmoid volvulus. Patients in the United States with sigmoid volvulus have a mean age of approximately 70, whereas in African nations in which a high-fiber diet is consumed, the mean age of patients with sigmoid volvulus is at least 20 years younger. Symptoms may be very poorly localized in patients who present with sigmoid volvulus. Physicians must maintain a high level of suspicion, especially in older individuals who present with abdominal distention, a change in bowel habits, or poorly localized abdominal discomfort. On an abdominal flat plate radiograph, classically there are multiple dilated loops of ahaustral bowel that stop abruptly at the pelvic inlet. Colonic perforation is a major complication that is to be feared in this disorder. Initial management includes acute decompression of the volvulus by lower endoscopy or, less commonly, radiologically through use of a gentle Gastrografin enema. If the situation recurs, the surgical literature supports sigmoid colon resection before the patient is discharged from the hospital.
Diverticulosis is an interesting but very poorly understood colonic disorder. There is good evidence that the prevalence of diverticulosis increases with age. In Western countries, diverticulosis is more common in the sigmoid colon, while in East Asian countries it is more common in the right colon. Radiologic studies have initiated an understanding that diverticulosis is often a clinically insignificant finding. Theories of formation have focused on diverticula as hernias related to a combination of high intracolonic pressure or an inherent weakening of the colonic wall. In the older literature there was speculation that this disorder was caused by constipation, straining at stool, or flatulence (all discounted at this time). It has been proposed more recently that a low-fiber diet leads to increased intracolonic pressure. Simultaneously, classic advice had focused on avoiding certain high-fiber foods (containing seeds and similar fiber-rich items) in the hope that this could prevent episodes of diverticulitis.
Among complications of diverticulosis, it is commonly believed that right-sided colonic diverticula are more likely to present as hematochezia, whereas left-sided colonic diverticula are more likely to present as diverticulitis. Diverticulitis as a clinical diagnosis remains a concern in patients who present with a change in bowel habits, a new onset of lower abdominal pain, fever, or leukocytosis. Many unusual fistulas have been reported in patients with diverticulitis. If there is a suspicion of an intra-abdominal abscess, a CT scan of the abdomen may be helpful. Uncomplicated diverticulitis has been treated with oral antibiotic therapy designed to provide coverage for anaerobic bacteria and coliform bacteria. Patients require a follow-up study to image the colon and rectum to exclude a neoplasm. The surgical literature has proposed segmental sigmoid colonic resection for patients who have had two documented episodes of diverticulitis.
Incontinence of liquid or solid stool has been called the "unvoiced symptom" because many individuals with this disorder have not discussed their problem with a physician. (36) This suggests that physicians must specifically inquire about this disorder. Maintenance of fecal continence involves coordination of the internal and external anal sphincters. Incontinence occurs when rectal pressure exceeds the combined anal canal pressure. There are few controlled studies of the epidemiology of fecal incontinence. There does appear to be an age-related increase in the prevalence of this disorder, although different studies provide conflicting evidence about potential gender differences. Evidence in many studies shows that the overall prevalence of fecal incontinence in individuals over age 65 appears to range from 3% to 18%.
It is not entirely clear whether the increased prevalence of incontinence in the elderly is due to age-related changes in anal sphincter function or to an increased prevalence in the elderly of diseases that affect the anal sphincter. Physiologic studies of the anal sphincteric muscles demonstrate age-related declines in resting anal canal pressure (associated with internal anal sphincter pressure) as well as maximal squeeze pressure (associated with external anal sphincter pressure). It has been proposed from histologic studies that sclerosis of the internal anal sphincter is an age-related process. However, among patients with fecal incontinence, 40% have normal anal canal pressures, and it has been estimated that 80% of patients with fecal incontinence have a neurologic disease, diabetes mellitus, cognitive
In the individual patient with fecal incontinence, the physician must consider these possible explanations: presence of liquid stool in the rectum (diarrhea-related such as diabetic diarrhea), an inadequate rectal reservoir (poor rectal compliance), poor rectal sensation (a common problem in spinal cord injury patients), or anal sphincteric dysfunction related to pelvic muscle or nerve damage (common after childbirth). History and physical examination should be useful in distinguishing patients with fecal incontinence related to a neurologic disorder, such as a spinal cord lesion or cerebral infarction, or to previous trauma such as anal surgery or vaginal delivery. A major differentiation that must be made in patients with fecal incontinence is whether there is overflow incontinence induced by a rectal impaction or loss of anal sphincter function. Patients with overflow incontinence often present with diarrhea and should respond to rectal evacuation. A commonly used method of examination of fecal incontinence is anorectal manometry. This test allows measurement of anal canal pressure, rectal sensation, and rectal compliance. During the test, perianal sensation is examined to exclude the presence of a spinal cord lesion.
Treatment options include intermittent fecal disimpaction, a trial of nonflatus-producing fiber supplements (calcium polycarbophil or methylcellulose), loperamide hydrochloride (interferes with propagating contractions and increases anal sphincter pressure), or a trial of a bile acid-binding agent (such as cholestyramine). Recently reported successes in the use of anorectal neuromuscular retraining by biofeedback for treatment of fecal incontinence encourage the performance of anorectal manometry in patients with fecal incontinence that is potentially related to loss of anal sphincter function.
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