Aamir M. Ali MD
Brian E. Lacy MD, PhD
Gastrointestinal (GI) complaints are common in the elderly and range from mild self-limited episodes of acid reflux to life-threatening episodes of bowel ischemia. Some diseases, such as diverticulitis and colon cancer, are more common in the elderly, whereas other conditions, such as acid reflux disease, may present differently. Comorbid illnesses and polypharmacy may also contribute to, and modify the presentations and outcomes of, various GI disorders in the elderly. For instance, there is an increased prevalence of peptic ulcer disease in the elderly as a result of increased nonsteroidal anti-inflammatory drug (NSAID) use, which often masks ulcer-related pain. The increased use of anticoagulation therapy leads to worse outcomes in elderly patients with ulcer-related bleeding. It is important to understand GI disorders in the context of the elderly patient, realizing that common illnesses may present and progress differently than in the younger patient and thus are often diagnosed late in their course.
DISORDERS OF THE ESOPHAGUS
ESSENTIALS OF DIAGNOSIS
GASTROESOPHAGEAL REFLUX DISEASE
Gastroesophageal reflux disease (GERD) is the most common GI disorder affecting the elderly. Symptoms affect at least 40% of the elderly U.S. population on a monthly basis and approximately 7–10% on a daily basis. Persistent symptoms can dramatically affect quality of daily life. Once symptoms develop, at least 50% of patients will have persistent symptoms or require ongoing medical therapy. Persistent, untreated, or undertreated symptoms may lead to complications of acid reflux disease, including esophagitis, peptic strictures, esophageal ulcers with bleeding, and Barrett's esophagus. These complications are more likely to occur in the elderly.
The diagnosis of GERD can be readily made if patients complain of typical symptoms of pyrosis (substernal burning with radiation to the mouth and throat) and sour regurgitation, and if these symptoms improve with treatment. Many elderly patients with GERD have reduced symptoms because of decreased visceral sensation or the use of medications that may blunt or reduce sensation. Quite commonly, however, patients have atypical symptoms, such as a chronic cough, difficult-to-control asthma, laryngitis, or recurrent chest pain.
Upper endoscopy (esophagogastroduodenoscopy; EGD) should be performed in all patients with persistent
symptoms of reflux despite medical therapy, patients with a history of acid reflux longer than 5 years, and those with possible complications from acid reflux. EGD is safe to perform, even in the very elderly. Unlike a barium swallow or upper GI series, EGD directly visualizes the esophagus and stomach and allows the endoscopist to perform biopsies. Patients thought to have extraintestinal manifestations of GERD should undergo ambulatory evaluation with a 24-h pH probe. Esophageal manometry is not routinely of benefit in the evaluation of patients with GERD, unless antireflux surgery is being considered.
Many physicians advocate a step-up approach to the treatment of GERD (Table 23-1). Lifestyle modifications are suggested first. If symptoms resolve, no further treatment is required. If symptoms fail to improve, then a histamine-type 2 receptor antagonist (H2RA) should be used either once or twice daily. Cimetidine is generally not recommended because of potential drug interactions and a higher incidence of adverse side effects compared with other H2RAs. Persistent symptoms, or incomplete resolution of symptoms with H2RA, warrant treatment with a proton pump inhibitor (PPI) and evaluation with upper endoscopy.
Table 23-1. Treatment of gastroesophageal reflux disease: A step-up approach.
An alternative approach to the treatment of GERD is to use step-in therapy. Patients with chronic symptoms of GERD, evidence of esophagitis on EGD, or extraesophageal manifestations of GERD are prescribed lifestyle modifications and started on a PPI at the first visit. This approach leads to fewer office visits, a reduction in procedures, improved patient satisfaction, and reduced overall costs. Antireflux surgery is rarely a viable option for the elderly given the presence of comorbid conditions, increased risks of surgery, and recent data showing that ~50% of patients who undergo antireflux surgery still require the routine use of acid suppressants years later. There are no data on the utility or safety of endoscopic therapies for GERD in the elderly; thus, these procedures cannot be recommended.
Odynophagia, or painful swallowing, is an uncommon complaint in the elderly, accounting for < 5% of all visits to a gastroenterologist. Common causes are listed in Table 23-2. Precipitating factors include diminished esophageal peristalsis, erosive esophagitis, presence of
an esophageal stricture, poor fluid intake while taking pills, or taking multiple pills at once. Evaluation should begin with an EGD to permit direct inspection of the esophagus and allow biopsies, if necessary. Treatment begins with removing the offending medication (if applicable) and treating the underlying disorder, such as acid reflux disease. Patients should take pills one at a time, with adequate amounts of water, to ensure that each pill is adequately cleared from the esophagus. Fungal infections of the esophagus may be treated with either nystatin swish-and-swallow or fluconazole. Viral infections should be treated with acyclovir or famciclovir.
Table 23-2. Causes of odynophagia.
Dysphagia, or difficulty swallowing, is a common complaint in the elderly. Dysphagia is classified as oropharyngeal (transfer) or esophageal (transit). Oropharyngeal dysphagia refers to impaired movement of liquids or solids from the oral cavity to the upper esophagus. Painful or diseased teeth, xerostomia, poorly fitting dentures, and mandibular destruction are common causes of transfer dysphagia. Neuromuscular disorders affecting the tongue, soft palate, oropharynx, and upper esophageal sphincter may produce disturbances in normal oroesophageal movement. Neurological causes of oropharyngeal dysphagia predominate and include cerebrovascular disease, Parkinson's disease, multiple sclerosis, Alzheimer's disease, and upper motor neuron diseases. Muscular disorders such as myasthenia gravis, polymyositis, and amyloidosis may also produce dysphagia. Finally, patients with a history of surgery or radiation to the oral cavity or neck are at risk for transfer dysphagia.
Figure 23-1. Evaluation of dysphagia.
Patients with oropharyngeal dysphagia typically cough, gag, choke, or aspirate their food during the initiation of a swallow. Those with transit dysphagia often complain of solid foods or liquids “sticking,” “catching,” or “hanging up” in their esophagus, and they may point to their substernal area. Using a series of questions and the algorithm outlined in Figure 23-1, the cause of esophageal (transit) dysphagia can be identified in nearly 90% of cases. Dysphagia to solids usually reflects an underlying mechanical obstruction, whereas dysphagia to both liquids and solids reflects an underlying neuromuscular disorder. Patients should be questioned to ensure they do not have either odynophagia or globus (a persistent sensation of fullness in the throat that usually improves with eating), because the evaluation and treatment of these 2 conditions is different. The physician should look for evidence of anemia and unintentional weight loss, either of which could indicate a serious disorder. The nature of the dysphagia (solids or both solids and liquids) and the temporal nature of the swallowing disorder (intermittent or progressive in nature) should be determined. Finally, associated
symptoms of chest pain or acid reflux should be elicited.
In the elderly a barium swallow is often ordered as the initial test to evaluate dysphagia. Patients should be evaluated by a speech language pathologist who can coordinate a swallowing study (modified barium swallow or videofluoroscopy) using thin, thick, and solid food materials. Upper endoscopy as the initial test has the advantage of directly inspecting the mucosa, taking biopsies if necessary, and dilating the esophagus, if a stricture or mass is present. If upper endoscopy is normal and complaints of dysphagia persist, then esophageal manometry should be performed. This is a safe and readily performed procedure that can accurately identify neuromuscular disorders that cause dysphagia.
Treatment is directed toward the underlying disorder in addition to ensuring adequate nutrition and preventing aspiration. Patients are taught which consistency of foods can be safely swallowed, proper swallowing techniques, and how to modify their posture to improve their swallowing. Medical therapy is not effective. If aspiration occurs or the nutritional status of the patient suffers, a feeding jejunostomy or gastrostomy should be considered.
Disorders of esophageal motility occur in the elderly, although age alone does not lead to a decrease in esophageal peristalsis. Presenting symptoms are usually dysphagia, chest pain, or persistent acid reflux disease. Achalasia is the most well-recognized motility disorder of the esophagus. Its prevalence increases with age; 7-12 in 100,000 elderly patients are affected. Treatment options include pneumatic dilatation, botulinum toxin injection of the lower esophageal sphincter, and surgery. Medical therapy (eg, nitrates, calcium channel blockers) is rarely effective. Surgery is an option, although it should be approached cautiously. Pneumatic dilatation produces significant relief of symptoms in many patients but is associated with a 3–10% risk of perforation. For many elderly patients, initial treatment of achalasia is best approached using botulinum toxin injection. It is safe and effective and provides symptom relief in the majority of patients for up to 9-12 mo. A second injection is often required. Side effects are uncommon and include transient chest or abdominal pain, rash, or low-grade fever.
Other common motility disorders that can occur in the elderly population include diffuse esophageal spasm, nutcracker esophagus, hypertensive lower esophageal sphincter, and ineffective esophageal motility. These conditions are diagnosed by esophageal manometry.
Esophageal cancer is one of the most lethal types of cancer known; 5-year survival is ~5%. Both types of esophageal cancer, squamous cell and adenocarcinoma, are found predominantly in patients older than 60. Risk factors for squamous cell carcinoma include ethnicity (4-5 times more common in blacks than in whites), tobacco and alcohol use, previous radiation to the head or neck, achalasia, and chronic esophagitis. Barrett's esophagus, which develops in the setting of chronic acid reflux disease, is the major risk factor for adenocarcinoma of the esophagus.
The presenting symptom for both types of cancer is the same: progressive dysphagia, first to solids and then to liquids. This is usually associated with weight loss and anemia. Odynophagia, cough, hoarseness, and recurrent pneumonia may also be present.
Although a barium swallow may reveal evidence of a mass, the diagnosis is made during upper endoscopy. Endoscopic ultrasonography has been shown to be more accurate than computed tomography (CT) for assessing tumor invasion.
Surgery (esophagectomy) is recommended if the tumor is localized to the esophagus without metastasis (a T1 or T2 lesion). For patients who are poor surgical candidates or who have invasive disease, chemotherapy (5-fluorouracil, cisplatin, mitomycin C) and local irradiation may provide palliation or even cure in a select group of patients. Metallic stents are often deployed in the esophagus to improve dysphagia and minimize aspiration in those patients who are not surgical candidates. Endoscopic therapy using lasers may provide temporary relief of dysphagia by decreasing the tumor burden. In patients with nutritional compromise, endoscopically
placed gastrostomy or jejunostomy tubes may be required.
DISORDERS OF THE STOMACH
ESSENTIALS OF DIAGNOSIS
PEPTIC ULCER DISEASE
Peptic ulcer disease (PUD) refers to both gastric ulcers (GUs) and duodenal ulcers (DUs). Approximately 5 million cases of PUD will occur this year in the United States. The elderly are more likely to suffer complications of PUD, including hospitalization, need for blood transfusions, emergency surgery, and death. The 2 most common causes of PUD are NSAIDs and H. pylori.
More than 40% of elderly patients are prescribed NSAIDs, and up to 8% will be hospitalized because of a complication of NSAID use within the first year of initiating treatment. All NSAIDs increase the risk of PUD, although some appear to carry a lower risk of inducing an ulcer than others. A meta-analysis revealed that ibuprofen, at doses < 1200 mg/day, was the NSAID least likely to induce serious GI injury, with a relative risk of inducing PUD 2.1 times greater than for controls. In contrast, the relative risk of serious GI injury when using ketoprofen was 7 times higher than ibuprofen. Overall, 25% of chronic NSAID users will experience either a GU or a DU at some point in their lifetime. Cyclo-oxygenase-2 (COX-2) inhibitors have been shown to have less overall GI toxicity. However, no data exist regarding the complications of chronic use of COX-2 inhibitors in elderly patients. Aspirin may increase the risk of PUD by 1.5-3.9-fold above average. Low-dose aspirin (75 mg/day) is generally safer than high-dose aspirin (> 300 mg/day).
Acute infection with H. pylori leads to a localized mucosal inflammatory response, reducing the normal gastroduodenal mechanisms that protect the mucosa from ulceration. H. pylori is thought to be responsible for nearly 70% of GUs and 80–90% of DUs not related to NSAID use.
Patients may have hematemesis or coffee-ground emesis. Elderly patients with PUD may have epigastric pain; however, as many as 50% of patients will not have pain from either a GU or a DU, and suspicion of PUD is raised because of anemia or blood in the stools.
In patients suspected of having PUD, a complete blood cell count (CBC), prothrombin time, blood urea nitrogen (BUN), and creatinine should be obtained and stool checked for occult blood loss. Patients should be asked about a history of PUD; their use of aspirin, NSAIDs, and warfarin; and previous diagnostic studies (upper GI series, testing for H. pylori). Upper endoscopy should be performed in older patients suspected of having PUD to identify the lesion, perform a biopsy in the stomach for H. pylori, rule out a malignancy, and initiate endoscopic therapy for a bleeding ulcer, if necessary.
Hemorrhage and perforation are the most common complications of PUD and have been reported to occur in ~50% of patients older than 70.
If an ulcer is found, therapy should be initiated with a PPI for at least 8 weeks to ensure healing. NSAIDs and aspirin should be stopped. If the patient is found to be H. pylori positive, double or triple antibiotic therapy should be started. In the case of a GU, healing should be documented 8-12 weeks later with follow-up EGD. Patients who require chronic NSAID or aspirin use should be treated concurrently with a PPI or misoprostol. Both agents are effective in reducing the risk of PUD in chronic NSAID users, although, as a group, the PPIs are generally better tolerated than misoprostol.
infected, and the majority are asymptomatic. Acute H. pylori infection may lead to ulceration of the stomach or duodenum, whereas chronic H. pylori infection may lead to atrophic gastritis, gastric adenocarcinoma, or development of a mucosa-associated lymphoid tumor (MALT lymphoma). H. pylori is now considered a class I carcinogen by the World Health Organization. Testing for H. pylori should be performed in all individuals with a history of peptic ulcer disease or evidence of gastritis, duodenitis, or gastric atrophy or when an ulcer or erosion is identified during endoscopic or fluoroscopic examination. The diagnosis of H. pylori infection can be made from biopsies obtained during upper endoscopy or by detecting antibodies in the serum. Breath hydrogen tests are most useful in documenting eradication. Multiple treatment regimens have been shown to be effective in eradicating H. pylori. A twice-daily PPI for 10-14 days in conjunction with 2 different antibiotics (clarithromycin with either metronidazole or amoxicillin are the most effective) is the most common therapy. Eradication rates range from 75–95%, depending on the treatment regimen. The recurrence of PUD and complications of PUD are markedly reduced with H. pylori eradication.
Dyspepsia is defined as chronic or recurrent pain or discomfort in the upper abdomen, which is thought to arise in the upper GI tract. It is exceedingly common in clinical practice, affecting an estimated 20–30% of older adults.
Patients may complain of upper abdominal pain, nausea, bloating, early satiety, or reflux symptoms. Dyspepsia traditionally has been classified as ulcer-like, reflux-like, or dysmotility-like; however, this classification has not been satisfactorily shown to improve either the evaluation or the treatment of patients with dyspepsia. However, it is important to distinguish patients with organic problems such as an ulcer from those with functional or nonulcer dyspepsia because the treatment and further evaluation are dramatically different.
Evaluation of dyspepsia begins with a thorough history and physical examination to determine whether the pain or discomfort arises in the GI tract or elsewhere (heart, lungs, musculoskeletal system). Patients should be asked about unintentional weight loss, odynophagia, dysphagia, a family history of GI tract cancer, and evidence of blood loss or jaundice.
Laboratory tests, including a CBC, erythrocyte sedimentation rate (ESR), liver function tests (LFTs), electrolytes, amylase, and lipase, should be performed. Patients should be evaluated by upper endoscopy to rule out an ulcer or cancer. Initial testing with upper endoscopy has been shown to improve quality of life and lead to a reduction in dyspeptic symptoms. If endoscopy is normal and symptoms persist, a right upper quadrant (RUQ) ultrasonogram should be performed. If this is normal and complaints persist, a solid-phase gastric emptying scan should be performed. In an older patient with persistent symptoms, concerns about occult malignancy should prompt a CT scan of the abdomen with both oral and intravenous contrast.
Patients with persistent dyspeptic symptoms and a normal evaluation are categorized as having nonulcer dyspepsia (NUD). Treating this group of patients can be quite challenging. Few data support the routine use of antacids, antimuscarinic agents, or sucralfate. Routine treatment with H2RAs has shown a slight benefit, but better results have been obtained with the use of once- or twice-daily PPIs. It is possible that some of the benefits of these trials occurred because patients with GERD were included in the dyspepsia category. Empiric treatment for suspected H. pylori does not improve patient outcomes. However, eradicating H. pylori, if present, does lead to a reduction in symptoms and an improvement in quality of life. Prokinetic agents (metoclopramide and erythromycin) are generally ineffective in treating patients with dyspepsia. Finally, the use of low-dose tricyclic antidepressants may improve symptoms of dyspepsia, although the mechanism of action in those patients who respond is unclear. There are no controlled, published studies to date on the use of selective serotonin reuptake inhibitors in the treatment of dyspepsia.
Each year gastric cancer affects approximately 25,000 Americans, the vast majority of whom are older than 60. The overall 5-year survival rate is estimated at 16%. Nearly 95% of gastric cancers are adenocarcinomas. Carcinoids, sarcomas, and lymphomas make up the remaining 5%. Risk factors for gastric cancer include chronic atrophic gastritis, H. pylori, pernicious anemia, family history of gastric cancer, partial gastrectomy, tobacco use, and consumption of large quantities of salted or smoked foods.
Presenting symptoms of gastric cancer are usually vague, and this inevitably leads to a delay in diagnosis. Patients may complain of nausea, early satiety, epigastric fullness, weight loss, and abdominal pain. Physical examination may reveal a mass, a succussion splash from gastric outlet obstruction, or evidence of peripheral lymphadenopathy. Unfortunately, by the time symptoms are severe or physical examination findings are apparent, patients usually have widespread disease.
Gastric cancer is best detected by upper endoscopy because barium studies may miss early cancers or lesions in the antrum. CT scanning is useful to assess the depth of tumor invasion and the presence of lymphadenopathy. Both endoscopic ultrasonography and positron emission tomography scans are evolving technologies that may improve tumor staging.
Surgical therapy offers the only cure for gastric cancer; however, the overall 5-year survival is poor (20–40%) and operative mortality high (15–25%). Endoscopic resection of large masses, laser therapy, and stent placement may provide palliation for some patients with obstructive symptoms. Chemotherapy and radiation do not provide any survival benefits.
DISORDERS OF THE COLON
ESSENTIALS OF DIAGNOSIS
Constipation can be defined as infrequent bowel movements (< 3/week), straining at stool, hard consistency, pain with defecation, or the need to digitally assist evacuation. Using all these definitions, the prevalence of constipation in the elderly in the community setting is estimated at 40%, nearly twice that of middle-aged patients. Forty-five percent of elderly patients take laxatives regularly. Interestingly, infrequent bowel movements (< 3/week) are not a common complaint in the elderly, occurring in < 5% of the community-based elderly. More commonly, elderly patients complain of straining at stool (25.6%), hard stools (27%), incomplete evacuation (22.7%), and the need to digitally assist evacuation (20%). Abdominal bloating and distention may occur, and patients may complain of rectal fullness, rectal pressure, back pain, left lower quadrant pain, or generalized abdominal discomfort. These symptoms increase in intensity as the frequency of bowel movements declines.
Constipation is most often divided into 3 general categories: slow transit constipation, pelvic floor dysfunction, and irritable bowel syndrome. However, there is often overlap between these groups. Up to 25% of patients with persistent constipation unresponsive to fiber therapy have apparently normal physiology, even after extensive evaluation. These patients are best categorized as having functional constipation.
Both over-the-counter and prescription medications should be reviewed in the history and questions asked about daily fluid and fiber intake as well as exercise. The clinician should look for coexisting neurological disorders (Parkinson's disease), systemic disorders (hypothyroidism), and musculoskeletal disorders (severe arthritis requiring narcotics), any of which could contribute to constipation (Table 23-3). One of the most important aspects of the evaluation should be to identify the patient with mechanical obstruction secondary to cancer, rectal prolapse, stricture, or a large polyp. Signs of these disorders may include unintentional weight loss, anemia, or evidence of GI bleeding.
Simple screening laboratory tests (CBC, thyroid-stimulating hormone [TSH], ESR, electrolytes) should be performed to look for evidence of anemia, hypothyroidism, or a systemic inflammatory disorder. Colon
cancer is more common in the elderly and often presents with constipation. Therefore, in patients with chronic constipation who fail to respond to simple remedies such as increasing fluid and fiber intake, colonoscopy should be performed to exclude a mechanical cause of constipation. The combination of flexible sigmoidoscopy and barium enema (BE) is an alternative approach, although smaller lesions may be missed by BE.
Table 23-3. Common causes of constipation.
In the elderly patient, constipation may reflect an underlying malignancy; this is often the patient's primary concern. Other mechanical causes of constipation include rectal prolapse, rectal intussusception, recurrent sigmoid volvulus, extrinsic compression of the colon, and colonic strictures secondary to previous episodes of diverticulitis. In addition, medications, neurological disorders, systemic diseases, metabolic disorders, poor fluid intake, and immobility can cause constipation (see Table 23-3).
After mechanical causes of constipation have been ruled out, treatment should be initiated based on the primary complaint. Patients with straining and incomplete evacuation usually respond best to fluids, routinely scheduled bathroom time, and bulk-forming agents (Table 23-4). Patients with infrequent bowel movements typically respond best to osmotic agents or polyethylene glycol (PEG) solutions. These can be used safely in the elderly and do not generally interfere with the absorption of medications.
Patients with diarrhea most often complain of frequent stools (> 3/day) or loose stools. However, other patients use the term diarrhea to describe fecal incontinence or fecal urgency. The etiology of acute diarrhea (lasting < 2 weeks) in the elderly is similar to that of younger
adults, with a few exceptions. Most cases of acute diarrhea are related to viral or bacterial infections, but it can also be caused by medications, medication interactions, or dietary supplements. Clostridium difficile colitis is more prevalent in the elderly because of more frequent hospitalizations, increased antibiotic use, and increased numbers of patients in institutional settings. Chronic diarrhea, lasting > 2 weeks, may result from fecal impaction, medications, irritable bowel syndrome, IBD, obstruction from colon cancer, malabsorption, thyrotoxicosis, or lymphoma. Lactase deficiency is common worldwide and is present in most individuals to some degree as they age, although it is less common in northern Europeans, North American Indians, and certain groups in Africa. Symptoms of bloating, abdominal distention, and loose stools usually begin in early adulthood, often worsening with age. Uncommon causes of diarrhea include Whipple's disease, jejunal diverticulosis, bowel ischemia, amyloidosis, lymphoma, and scleroderma with bacterial overgrowth.
Table 23-4. Treatment of constipation.
A complete history and physical examination, including a rectal examination, may provide information on cause and direct further evaluation. Medication history may reveal a causative agent for the diarrhea, and recent antibiotic use may suggest C. difficile. A history of recent weight loss raises the concern for malignancy, IBD, microcytic colitis, malabsorption, or thyrotoxicosis. Fluid status should be assessed in all elderly patients with diarrhea because they are particularly susceptible to dehydration.
Stool cultures should be obtained to exclude infection in patients with acute diarrhea. C. difficile toxin assay should be obtained if there is a history of recent antibiotic use. Qualitative or quantitative stool fat should be checked in patients with steatorrhea. A TSH should also be checked as part of the initial workup of diarrhea.
In patients with C. difficile who fail sequential therapy with metronidazole first and then oral vancomycin, the presence of pseudomembranes should be confirmed by sigmoidoscopy or colonoscopy. Colonoscopy is also appropriate in patients with a history of weight loss, bloody diarrhea, and diarrhea lasting > 4 weeks (Table 23-5). If the colonoscopy appears grossly normal, biopsies should be obtained to rule out microscopic colitis.
Treatment of diarrhea is based on the underlying cause. In those with no evidence of acute infection, loperamide (≤ 8/day) is generally effective in treating symptoms. Care must be exercised in the elderly with commonly used antimotility products, such as Lomotil, which contain atropine. In microscopic colitis, treatment is generally aimed at slowing colonic transit with the use of loperamide. Other alternatives include bismuth subsalicylate, prednisone, cholestyramine, or the 5-ASA products. Deodorized tincture of opium often improves symptoms in patients who fail to respond to other treatments.
Table 23-5. Indications for colonoscopy.
Diverticular disease is a disorder of industrialized nations. Diverticulosis is found in > 60% of those older than 70 and nearly 80% of those older than 80. Diverticula are outpouchings of the mucosa and submucosa that develop because of increased colonic luminal pressures. Diverticula are most commonly found on the left side of the colon; they are less common on the right side of the colon and are rarely, if ever, found in the cecum or rectum. The majority of patients who have diverticula are asymptomatic. A BE, colonoscopy, or CT scan performed for some other reason commonly identifies diverticula. Approximately 15–20% of older adults who have diverticulosis will have a complication, among them diverticular bleeding or diverticulitis.
Diverticular bleeding is characterized by the sudden onset of painless hematochezia, sometimes in large volume. Although most diverticula are present on the left side of the colon, 70% of diverticular bleeding occurs on the right side. If an episode occurs and the patient is hemodynamically stable, colonoscopy can be scheduled urgently as an outpatient. Eighty percent of diverticular bleeding will stop spontaneously. Patients should be hospitalized if bleeding persists, if they are hemodynamically unstable, or if blood loss compromises other organ systems. Evaluation includes colonoscopy to exclude
sources of bleeding such as arteriovenous malformations (AVMs), ischemia, IBD, and cancer. If bleeding persists, a bleeding scan should be performed followed by angiography, if necessary. Surgical resection of the bleeding area may be required.
In uncomplicated diverticulitis, patients have lower abdominal pain (usually on the left), fever, and an elevated white blood cell count. On physical examination, the patient does not appear toxic, and there are no palpable abdominal masses or peritoneal signs. An abdominal radiograph should be performed to look for pneumoperitoneum. Treatment can be initiated in the outpatient setting with clear liquids for 2-3 days and oral antibiotics that should cover both anaerobes and gram-negative organisms. Metronidazole and a fluoroquinolone or third-generation cephalosporin for 2 weeks is generally well tolerated and very effective. The patient should call the office in 24 h and be seen 48- 72 h after the initial evaluation. If no improvement occurs, the patient should be hospitalized and a CT scan of the abdomen performed.
Diverticulitis becomes complicated if an abscess, stricture, or fistula develops. Patients often have an elevated pulse or are hypotensive. Some elderly patients have lethargy or confusion. Abdominal examination may reveal a mass in the left lower quadrant or evidence of a draining fistula to the bladder, uterus, or skin. Peritoneal signs may be present. Patients with complicated diverticulitis require hospitalization. Patients should be given nothing by mouth and provided intravenous fluids. Blood cultures and an abdominal CT scan should be performed. Intravenous antibiotics should be initiated rapidly to cover both gram-negative organisms and anaerobes. If no improvement is seen within 48-72 h, an abdominal CT scan should be repeated.
Patients with an episode of diverticulitis have approximately a 35% chance of a second episode occurring within the next 5 years. Patients with > 2 episodes of diverticulitis in the same segment of colon should be referred to a surgeon for possible resection.
INFLAMMATORY BOWEL DISEASE
A second peak of IBD occurs in the U.S. population after age 65. Approximately 10–15% of all newly diagnosed cases of Crohn's disease and ulcerative colitis occur in this age group. Symptoms of Crohn's disease are similar to those in a younger population, although older patients with Crohn's disease may have fewer complaints of abdominal pain or cramps possibly because of reduced sensory thresholds or the concurrent use of multiple medications. Patients typically have a history of nonbloody diarrhea, unintentional weight loss, and fatigue. Evidence of anemia may be present (pallor, shortness of breath, reduced exercise tolerance). Extraintestinal manifestations of Crohn's disease, including joint effusions, oral ulcers, painful nodular lesions on the extremities (erythema nodosum), uveitis, and back pain secondary to sacroileitis, commonly occur. Although Crohn's disease may develop anywhere from the mouth to the anus, in elderly patients it is less likely than in younger patients to involve large portions of the GI tract. The correct diagnosis is often delayed in the older patient because symptoms of Crohn's disease may mimic other diseases, including infectious diarrhea, ischemic colitis, lactose intolerance, medication-induced diarrhea, diverticulitis, celiac disease, microscopic colitis, or bacterial overgrowth.
Ulcerative colitis (UC) usually presents with tenesmus and frequent bloody bowel movements. Extraintestinal manifestations of UC are similar to those of Crohn's disease and also include dermatological manifestations such as pyoderma gangrenosum. Pyoderma ulcers typically appear as round or oval lesions on the shins and forearms. Elderly patients with UC are more likely to have limited left-sided disease or proctitis compared with younger patients, who often have pancolitis. The first attack of UC in an older patient is generally more severe and more likely to require steroids than that in a younger patient. Of elderly patients with UC, approximately 15% will eventually require surgery. The diagnosis of either UC or Crohn's is made based on a thoughtful physical examination and history supplemented by appropriate laboratory studies and colonoscopy. Treatment should be undertaken with gastroenterology consultation.
(See Chapter 30)
For many older patients, fecal incontinence can lead to a decline in physical activity, loss of social contacts, and, eventually, isolation. The scope of the problem is impressive. Fecal incontinence is now the second leading cause of nursing home placement in the United States. Up to 7% of the elderly population have incontinence of solid or liquid stool at least once each week, and up to 50% of nursing home residents suffer from fecal incontinence. Most patients never report this problem to their clinician. Elderly men are more likely to suffer from incontinence than women. Patients are
more likely to be incontinent of liquid, than solid, stool. Precipitating factors include prior surgery to the anorectal area (sphincterotomy for anal fissure, hemorrhoidectomy, episiotomy); difficult or prolonged childbirth with injury to the pudendal nerve; complete rectal prolapse; diabetic neuropathy; radiation injury to the anorectal area; IBD; and lumbosacral disease with resultant injury to L5-S4 nerve roots.
Examination of the anorectal area can be performed with the patient in either a recumbent or a prone position. Perirectal erythema may be seen because of leakage of liquid stool. Local reflexes can be assessed by evaluating whether an anal wink is present. The external anal sphincter (EAS; striated muscle) should be assessed for evidence of mechanical injury, scar tissue, and strength during voluntary contraction. The internal anal sphincter (IAS; smooth muscle) provides most of the resting tone of the anal canal and should be assessed for resting tone. Examination should also include looking for evidence of fecal impaction, a rectal mass, hemorrhoids, rectocele, and the presence of rectal prolapse during straining.
Flexible sigmoidoscopy or colonoscopy should be performed to look for a mechanical cause of incontinence (eg, large mass, fistula). Anorectal manometry can objectively measure the resting pressure of the anal canal (predominantly from the IAS), tone and contractile pressures of the EAS, and sensation within the anorectal area. Pudendal nerve testing may be required in some patients.
In the absence of a surgically correctable cause, fecal incontinence can often be improved with behavioral interventions such as routine bathroom time 30-40 min after each meal to take advantage of the natural gastrocolic reflex. This allows emptying of the rectosigmoid colon and minimizes the chance of an accident occurring later. Bulk-forming agents should be used to create more firm stool and increase evacuation. Kegel exercises should be performed several times each day to strengthen the EAS. Loperamide may be used routinely in small doses to slow colonic transit and increase anal canal pressures. In patients with severe incontinence, a diverting colostomy or ileostomy may be required to improve quality of life.
Anal fissures may develop because of excessive straining or from the passage of rocky, hard stools. Patients typically complain of significant anal pain after defecation and report small amounts of bright red blood per rectum. Patients are often fearful of having another bowel movement because of persistent pain, and spasm of the anal sphincter can make examination of the area very difficult. Conservative therapy with sitz baths, stool softeners, and fiber products usually leads to healing of an acute anal fissure over 1-2 weeks. Topical nitroglycerin, calcium channel blockers, or botulinum toxin injection can be used to treat nonhealing or chronic fissures. Surgical therapy, using lateral internal sphincterotomy, may be necessary in some patients; however, fecal incontinence may develop in 3–30% of patients.
Although commonly thought to develop as a result of straining and constipation, hemorrhoids may actually develop because of sliding of the lining of the anal canal. There are multiple nonsurgical treatments for hemorrhoids that do not prolapse (grade 1) or that prolapse and reduce spontaneously (grade 2). Bulking agents are commonly used to help minimize straining and the development of shear forces, although their efficacy has not been documented. Injection sclerotherapy, electrocoagulation, photocoagulation, cryotherapy, and laser therapy have proven beneficial. Rubber banding may lead to better healing and a lower rate of recurrence; however, it is more uncomfortable for the patient than the other procedures mentioned, is more difficult to perform, and is not recommended in immunocompromised patients because of an increased risk of sepsis. Surgery should be reserved for those patients with persistent symptoms who have failed nonoperative techniques.
ESSENTIALS OF DIAGNOSIS
UPPER GASTROINTESTINAL BLEEDING
Peptic ulcer disease accounts for > 50% of upper GI bleeding in the elderly. Esophagitis and gastritis are other common causes. Variceal bleeding, Mallory-Weiss tears, gastric cancer, vascular ectasias, AVMs, and aortoenteric fistulas are less common causes of upper GI (UGI) bleeding in the elderly (Table 23-6).
UGI bleeding may present with hematemesis (vomiting bright red blood), coffee-ground emesis, or melena. Chronic, slow UGI bleeding may present only with iron-deficiency anemia and a positive fecal occult blood test. Pain is an uncommon feature of UGI bleeding in the elderly. Large-volume blood loss may result in circulatory collapse, syncope, or confusion. A careful medical history provides valuable information in identifying the source of UGI bleeding and in planning management. Any history of ulcer disease or liver disease, a list of all recent and current medications, including NSAIDs and anticoagulants, and patterns of alcohol use should be elicited. Physical examination includes orthostatic blood pressure and pulse measurement and evaluation for rebound tenderness and guarding. Orthostatic changes in pulse are more reliable indicators of hypovolemia than changes in blood pressure. Signs of chronic liver disease should be noted.
Table 23-6. Causes of GI bleeding in the elderly.
Laboratory evaluation includes a CBC and coagulation and chemistry profiles. The hematocrit at presentation may not accurately reflect the amount of blood lost because plasma and red cell volumes are reduced proportionally. It usually takes 24 h for extravascular fluid to restore vascular volume and reduce the hematocrit. Although a positive nasogastric lavage supports a UGI source of bleeding, a nonbloody aspirate is seen in 16% of patients with documented UGI bleeding. An elevated BUN-creatinine ratio (eg, > 35) also supports a UGI source of bleeding.
Assessment of hemodynamic status followed, if necessary, by resuscitation of the unstable patient should precede any workup of UGI bleeding. Patients with ongoing acute UGI hemorrhage should be admitted to the intensive care unit. Anticoagulation should be stopped and reversal with fresh-frozen plasma initiated. After initial hemodynamic stabilization of the patient, upper endoscopy is performed to identify and treat the source of bleeding. If the history or physical examination suggests a variceal source, an octreotide infusion must be initiated and urgent endoscopy performed. Acid suppression with an intravenous or oral PPI has been shown to improve outcomes in patients with bleeding related to peptic ulcer disease. Patients infected with H. pylori should be treated.
The hospital course of the elderly patient with UGI bleeding is more likely to be prolonged by cardiac, neurological, or renal complications. Significant blood loss may unmask underlying coronary artery disease by increasing myocardial oxygen demand. UGI bleeding is associated with a mortality rate ranging from 6–44%.
Surgery for acute UGI bleeding is associated with mortality rates as high as 25%.
LOWER GASTROINTESTINAL BLEEDING
Colonic diverticuli and AVMs are the most frequent causes of lower GI (LGI) bleeding. IBD, bowel ischemia, NSAID-induced colitis, radiation colitis or proctitis, infections, cancer, recent polypectomy, and hemorrhoids should also be considered in the differential diagnosis (see Table 23-6).
A positive fecal occult blood test may be the only indication of LGI bleeding. Acute LGI bleeding presents as hematochezia. Painless, large-volume hematochezia suggests a diverticular source. Abdominal pain coupled with hematochezia, especially in a patient with a history of vascular disease, suggests bowel ischemia. Loose bloody stools may occur in infections, IBD, and bowel ischemia.
Although anemia is a consistent feature of chronic LGI bleeding, the hematocrit in patients with acute LGI bleeding may be normal until equilibrium with extravascular fluid is reached.
Stabilization of any existing hemodynamic instability is critical before proceeding with the workup of LGI bleeding. Because hematochezia may represent a briskly bleeding upper GI source in up to 10% of cases, upper endoscopy should be performed in patients with hematochezia and hemodynamic instability before proceeding with colonoscopy. Prompt colonoscopic identification and treatment of the source of bleeding should be attempted, although endoscopic treatment of diverticular bleeding is not very successful. Patients with significant bleeding despite attempted endoscopic treatment should undergo angiography with intra-arterial vasopressin infusion or angiographic embolic therapy. Surgery may benefit patients with recurrent bleeding or high transfusion requirements despite endoscopic or angiographic therapy.
LGI bleeding in the elderly is associated with a better clinical outcome than UGI bleeding. However, acute blood loss in the elderly may lead to myocardial or cerebral ischemia and renal failure.
OCCULT GASTROINTESTINAL BLEEDING
Iron deficiency anemia or a positive fecal occult blood test in the elderly patient may reflect chronic blood loss from cancer, AVMs, ulcers, or erosions in the GI tract. Evaluation should begin with a colonoscopy. If this is negative, upper endoscopy should be performed, followed, if necessary, by a small bowel follow-through to identify a source of bleeding in the small intestine.
GASTROINTESTINAL BLEEDING OF OBSCURE ORIGIN
Recurrent acute or chronic GI bleeding without an identifiable source after appropriate endoscopic and barium contrast studies is considered to be of obscure origin. Visualization of the small intestine identifies a source in many patients and may be achieved through push or sonde enteroscopy. Capsule enteroscopy is a promising new technique that, like sonde enteroscopy, allows visualization of the small bowel, although it lacks therapeutic capability. Patients requiring transfusion or hospitalization may benefit from radioisotope-tagged red blood cell scintigraphy or mesenteric angiography. Exploratory laparotomy with intraoperative enteroscopy should be reserved for patients with severe, persistent, or recurrent bleeding who do not have a diagnosis despite having undergone appropriate diagnostic testing.
ESSENTIALS OF DIAGNOSIS
ACUTE MESENTERIC ISCHEMIA
Emboli to the superior mesenteric artery (SMA) cause nearly 50% of acute mesenteric ischemia (AMI) cases, and this often occurs in the setting of underlying cardiac hypokinesis, arrhythmias, or atheromatous involvement of the aorta. SMA thrombosis causes 18–25% of AMI cases and usually occurs in patients with diffuse atherosclerotic disease. Nonobstructive mesenteric ischemia (NOMI) accounts for ~20% of AMI cases and is often seen in patients with underlying atherosclerosis who experience a low-flow state and in those taking vasoconstrictive agents or digitalis. The frequency of NOMI has been decreasing in recent years, presumably because of increased long-term use of vasodilating agents and the decreased use of digitalis. Mesenteric vein thrombosis (MVT) accounts for 5% of AMI cases and, in elderly patients, is associated with hypercoagulability from malignancy or recent abdominal surgery. Regardless of cause, AMI should be treated as an emergency and should be sought aggressively in at-risk patients.
Abdominal pain is reported in nearly 80% of patients with AMI. Patients with NOMI are less likely to report pain than those with AMI from other causes. Often the abdominal pain is disproportional to the physical findings, which may be normal. However, as bowel necrosis develops, fever, nausea, vomiting, and hematochezia may arise, and physical findings of abdominal distension and rebound tenderness may occur. Mental confusion develops in 33% of elderly patients with AMI.
Laboratory abnormalities in patients with AMI include leukocytosis, metabolic acidosis, and hyperamylasemia. An abdominal plain film should be obtained, not to diagnose AMI but to exclude other causes of abdominal pain. CT scanning is useful only in the diagnosis of MVT. Magnetic resonance angiography detects proximal occlusions but often fails to detect more distal occlusion or NOMI. The test of choice to confirm the diagnosis of AMI is selective SMA angiography. This modality is both diagnostic and therapeutic because infusion of the vasodilator papaverine may be initiated if evidence of occlusion is noted on angiography.
The differential diagnosis in a patient with AMI includes peptic ulcer disease, acute pancreatitis, small bowel obstruction, gallstone disease, and diverticulitis.
Early diagnosis is the key to improving outcomes in AMI. Surgical and gastroenterological consultations should be obtained soon after presentation. Management of AMI should be aggressive and begins by treating any precipitating conditions such as hypovolemia, congestive heart failure (CHF), or cardiac arrhythmias. Vasoconstrictors should be avoided in hypotensive patients. Angiography should be performed early if hypotension or hypovolemia are not present, and papaverine infusion should be initiated once vaso-occlusion or vasoconstriction is documented. Even in patients with signs of an acute abdomen, angiographic data are often helpful in the subsequent surgical management.
In the absence of peritoneal signs, proximal or major embolic occlusions are managed by papaverine infusion followed by embolectomy or thrombolysis. Distal or minor embolic occlusions or NOMI are managed expectantly with papaverine infusion and repeat angiography. Thrombotic occlusion in the patient without peritoneal signs can be managed expectantly if adequate collateralization with acceptable filling of the SMA is seen on angiography. Absence of collateralization with poor filling of the SMA warrants papaverine infusion followed by surgical revascularization. MVT discovered incidentally on a CT scan ordered for an unrelated indication can be observed or treated with a short course of anticoagulation. MVT in the patient without peritoneal signs should be treated with anticoagulation and close medical observation.
Intestinal infarction resulting in intestinal perforation and intra-abdominal sepsis is a frequent complication of AMI. Patients with AMI who present with an acute abdomen should be placed on broad-spectrum antibiotics and undergo emergency laparotomy with resection of necrotic bowel followed by a second-look operation within 24-48 h.
The average mortality rate for patients with AMI is 71%. The outcome is improved significantly if the diagnosis is made before intestinal infarction occurs.
CHRONIC MESENTERIC ISCHEMIA
Intestinal angina results from inability of atherosclerotic mesenteric vessels to meet the increased metabolic demands of digestion.
Patients with chronic mesenteric ischemia (CMI) have abdominal pain that begins shortly after eating and resolves over 1-3 h. Symptoms may initially occur only with large meals, but with progression of the disease even small meals can trigger pain. Bloating, constipation, or diarrhea may accompany abdominal pain. Significant weight loss often results because patients develop a fear of eating. Nearly 50% of patients have an abdominal bruit, which is not specific to CMI. Intestinal infarction with bowel perforation and abdominal sepsis may occur.
It is important to exclude other causes of postprandial pain such as peptic ulcer disease, gastric outlet obstruction, and gallstone and pancreatic disease. Measurements of serum alkaline phosphatase, bilirubin, amylase, and lipase and performance of abdominal ultrasonography and EGD are indicated. If this initial evaluation is unrevealing, selective SMA angiography should be performed. Diagnosis based solely on angiography is problematic because patients with occlusion of even 3 splanchnic vessels can be asymptomatic.
Occlusion of at least 2 of the 3 splanchnic vessels in a patient with CMI symptoms warrants revascularization. Surgical revascularization is the treatment of choice for CMI, with a success rate of > 90% of patients and recurrence in < 10%. In patients who are poor surgical candidates, percutaneous transluminal mesenteric angioplasty (PTMA), with or without stenting, is an option with initial success rates comparable to surgical revascularization. Higher recurrence rates have been reported among patients treated with PTMA.
The causes of colonic ischemia (CI) include IMA thrombus or embolus, CHF, cardiac arrhythmias, shock, vasculitis, hematological disorders, infections, medications (NSAIDs, digitalis, vasopressin, pseudoephedrine, sumatriptan, cocaine, amphetamines, gold), constipation, surgery, and trauma. No cause can be established unequivocally in most cases of CI. The extent of injury can range from mild reversible colopathy to gangrene or fulminant colitis. “A recent study demonstrated the presence of a congenital or acquired thrombophilic state in 72% of ambulatory patients presenting with colonic ischemia.”
Patients with CI usually present with crampy lower left quadrant pain and loose, bloody stools. Blood loss significant enough to lead to hemodynamic instability is atypical of CI and suggests other diagnoses. Physical examination often reveals abdominal tenderness of variable severity over the location of the affected portion of bowel. Peritoneal signs may be transiently present in reversible CI; the persistence of these signs for several hours suggests transmural infarction and mandates surgical exploration. Strictures, chronic colitis, gangrene resulting in perforation, and intra-abdominal sepsis are complications of CI.
Stool cultures should be obtained to exclude infectious colitis. The patient with suspected CI who does not have peritoneal signs should undergo a nonprepared colonoscopy or BE within 48 h of symptom onset. Colonoscopy offers higher sensitivity and the capability to obtain biopsy specimens. Patients with peritoneal signs should undergo urgent surgical exploration. CT scans are normal in up to 66% of patients with established CI.
The patient with CI who does not have peritoneal signs should be treated with fluids, bowel rest, and broad-spectrum antibiotics. Underlying CHF or cardiac arrhythmias should be treated and vasoconstricting medications withdrawn. The patients should be monitored closely for fever, leukocytosis, or peritoneal signs. The persistence of peritoneal signs should prompt surgical exploration. Recurrence of CI occurs in only 5% of patients.
LIVER & PANCREAS
Hepatitis A occurs less frequently in the elderly than in the younger population, but the elderly may have a
more severe course, with a higher risk of fulminant liver failure and death. Comorbidities and a decreased likelihood of liver transplantation contribute to the lower survival of older patients with fulminant disease.
Acute hepatitis B virus (HBV) infection is uncommon in the older population and often runs a mild and subclinical course. Symptoms, when present, include fever, malaise, arthralgias, myalgias, nausea, vomiting, abdominal pain, and jaundice. PEG interferon-α, used to treat chronic HBV in patients with decompensated liver disease, may cause increased side effects in the elderly.
Hepatitis C (HCV) is most commonly diagnosed after routine laboratory studies reveal elevated aminotransferase levels. Acute symptoms are rare and are similar to those seen in acute HBV. Older age at HCV infection is associated with increased rates of cirrhosis and mortality. Daily alcohol use worsens the prognosis. PEG interferon-α with ribavirin is the standard treatment for chronic HCV infection. Heart disease, a common affliction in the elderly, is a relative contraindication to ribavirin therapy. Despite concerns about increased side effects in the elderly, several small studies have demonstrated the safety and efficacy of interferon treatment in older patients.
Polypharmacy coupled with altered pharmacodynamics accounts for the increased incidence of drug-related hepatotoxicity in the elderly. NSAIDs, amiodarone, hepatic hydroxymethylglutaryl coenzyme A reductase inhibitors, and antituberculosis medications have been associated with hepatotoxicity in the elderly. LFTs should be monitored in patients receiving these medications.
Steep elevations in aminotransferase levels after a hemodynamic insult are typical of hepatic ischemia. Risk factors include acute myocardial infarction, CHF, valvular heart disease, cardiac arrhythmias, cardiomyopathy, sepsis, trauma, and burns. The magnitude of the aminotransferase elevation does not correlate with the extent of liver injury and does not predict outcome. Correction of hemodynamic instability leads to normalization of aminotransferase levels within 10 days.
Up to 40% of patients with primary biliary cirrhosis are elderly. Patients present with fatigue, pruritus, and elevated alkaline phosphatase levels. Diagnosis is suggested by the presence of antimitochondrial antibody (AMA) in the appropriate clinical setting and is confirmed by liver biopsy. Treatment with ursodeoxycholic acid improves survival and delays the need for liver transplantation.
More than 50% of patients with hepatocellular carcinoma (HCC) in the United States are elderly. Survival rates are significantly lower in patients diagnosed with HCC after the age of 65. Cirrhosis secondary to chronic HCV or HBV infection and alcoholic liver disease is the most frequent cause of HCC. Diagnosis is suggested by elevated alpha-fetoprotein (AFP) levels and imaging studies. Surgical resection in selected patients is the treatment of choice. Patients who are poor surgical candidates may be treated with transarterial chemoembolization. Patients with hepatic cirrhosis should be screened with liver ultrasonography and serum AFP levels every 6 mo for early detection of HCC. A CT scan of the abdomen is recommended every 1-2 years.
Age alone is not a contraindication for liver transplantation. Elderly recipients of liver transplants have the same rates of postoperative mortality and survival as younger recipients. Five-year survival, however, is lower among elderly recipients of liver transplantation. Carefully selected elderly patients with end-stage liver disease should be considered for liver transplantation.
Age-related increases in cholesterol secretion in bile, combined with decreased bile acid secretion, leads to increased cholesterol saturation and, therefore, increased bile lithogenicity. Cholelithiasis is twice as common in women as in men. Cholelithiasis is often asymptomatic and is discovered during radiological studies of the abdomen performed for unrelated reasons. Ten to 25% of patients with asymptomatic gallstones will become symptomatic each decade. Symptomatic gallstone disease typically presents with RUQ pain, nausea, and vomiting. Diagnosis is suggested in the appropriate clinical setting by elevated alkaline phosphatase and bilirubin levels and is confirmed by ultrasonography.
Laparoscopic cholecystectomy is the treatment of choice for symptomatic cholelithiasis in the elderly; postoperative mortality and morbidity in selected elderly patients are comparable to that for younger patients. Poor surgical candidates may be treated with endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy, extracorporeal shock wave lithotripsy, or ursodeoxycholic acid. Asymptomatic cholelithiasis should not be treated.
Common symptoms of cholecystitis are often blunted in older patients or are mistaken for other disease processes; thus, delays in diagnosis are common. An acute attack frequently follows a large fatty meal or awakens a patient from sleep. Symptoms consist of epigastric or RUQ pain, nausea, and vomiting. Fever and RUQ tenderness are present on physical examination. Elevations in serum bilirubin, alkaline phosphatase, aminotransferases, and white blood cell counts are characteristic. The diagnosis is made clinically and confirmed ultrasonographically. Gangrene and necrosis of the gallbladder are more common in the elderly population
and are associated with increased morbidity and mortality. Cholangitis or chronic cholecystitis are other frequent complications.
Treatment of cholecystitis consists of stabilization with intravenous fluids, bowel rest, pain control, and broad-spectrum antibiotics followed by cholecystectomy. However, because older patients with acute cholecystitis frequently have significant comorbidities and hemodynamic or respiratory instability, emergent cholecystectomy often carries a high risk of complications and death. In such patients, immediate percutaneous cholecystostomy followed, after stabilization, with surgery alone or in combination with ERCP has been shown to result in favorable outcomes.
Gallbladder carcinoma is rare in the United States. Gallstone disease, female gender, and smoking are significant risk factors. The diagnosis is often made incidentally at surgery. The prognosis is poor.
BILIARY TRACT DISEASE
Choledocholithiasis may occur in as many as 50% of all elderly patients with gallstones. Common bile duct stones remain asymptomatic until they cause obstruction. Choledocholithiasis presents with recurrent attacks of RUQ pain, fever, and jaundice (Charcot's triad), often accompanied by nausea and vomiting. Hepatomegaly and RUQ tenderness may be noted on physical examination. Elevated serum and urine bilirubin levels, accompanied by elevations in serum alkaline phosphatase and aminotransferase levels, occur typically. Although ERCP was used frequently in the past for diagnosis, the demonstrated high sensitivity and specificity and the low risk associated with magnetic resonance cholangiopancreatography and endoscopic ultrasonography mandate the use of these modalities for diagnosis. Choledocholithiasis demonstrated on these studies warrants therapeutic ERCP.
Symptomatic common bile duct stones are treated with papillotomy and stone extraction during ERCP, followed by laparoscopic cholecystectomy in patients with an intact gallbladder. Fever, mental status changes, or leukocytosis accompanying the symptoms of choledocholithiasis suggest cholangitis. Such patients should be managed aggressively with broad-spectrum antibiotics and therapeutic ERCP.
Acute pancreatitis occurs more frequently and runs a more severe course in the elderly compared with younger patients. Gallstones, medications, and cancer account for a higher proportion of acute pancreatitis in the elderly compared with younger patients. Alcohol is a common precipitating factor in both age groups. Typical presenting symptoms include epigastric pain radiating to the back along with nausea and vomiting. The diagnosis is made by elevations in amylase and lipase levels. Elevated alkaline phosphatase and bilirubin levels suggest gallstone pancreatitis, which can be confirmed by abdominal ultrasonography or CT. Patients with altered mental status or hemodynamic instability or those meeting 3 or more of Ranson's criteria (Table 23-7) should undergo a dynamic CT scan to rule out pancreatic necrosis. Bowel rest, intravenous hydration, and pain control are the cornerstones of therapy for mild acute pancreatitis. Patients with pancreatic necrosis should be placed on broad-spectrum antibiotics, and CT-guided aspiration of necrotic areas should be considered if symptoms do not improve after 5-7 days.
Endoscopic treatment of elderly patients with gallstone pancreatitis yields better outcomes than conservative treatment followed by elective cholecystectomy. Laparoscopic cholecystectomy with preoperative ERCP or intraoperative cholangiography can be performed with a postoperative risk profile comparable to that for younger individuals. In patients who are poor surgical candidates, ERCP with sphincterotomy decreases the risk for recurrent gallstone pancreatitis.
Polypharmacy places elderly patients at risk for drug-induced pancreatitis. Azathioprine, 6-mercaptopurine, estrogen, mesalamine, furosemide, and angiotensin-converting enzyme inhibitors are commonly implicated. Suspected medications should be stopped when pancreatitis is diagnosed. Other causes of pancreatitis,
such as hyperlipidemia or hypercalcemia, should be sought and treated if no other cause is found.
Table 23-7. Ranson's criteria.
The diagnosis of chronic pancreatitis in elderly patients poses several difficulties. The structural changes commonly associated with chronic pancreatitis (ductal irregularity or dilation, calcification, abnormal echogenicity) are also observed in aging patients without pancreatitis. Because pancreatic function is maintained in the elderly, functional testing may help in establishing the diagnosis. Treatment consists of hydration, pain management, pancreatic enzyme replacement, and avoidance of alcohol.
Pancreatic cancer accounts for 5% of all cancer deaths in the United States. Painless jaundice, pruritus, and weight loss are common presenting symptoms. Elevated CA 19-9 levels suggest the diagnosis, which is confirmed by abdominal imaging or demonstration of extrinsic compression of the bile duct during ERCP. Pancreaticoduodenectomy is the only treatment with any demonstrated benefit and should be offered to selected elderly patients with high overall fitness and low comorbidity. The prognosis of pancreatic cancer remains grim.
GI MANAGEMENT OF MALNUTRITION (also see Chapter 39)
Patients who are unable to swallow or who cannot eat sufficiently to maintain adequate nutrition may be candidates for tube feeding. Nasogastric tubes are a short-term alternative. Gastrostomy or jejunostomy tubes are appropriate for patients requiring longer term tube feeding. Gastrostomy tubes allow bolus feeding and are preferable to jejunostomy tubes, which usually require continuous infusion. However, patients with gastric outlet obstruction or poor gastric emptying are not candidates for gastrostomy tubes and should receive jejunostomy tubes. Aspiration precautions (elevating the head of the bed, checking residuals) should be carefully observed because gastrostomy tube feeding does not prevent aspiration.
Chronic parenteral nutrition is appropriate only in carefully selected patients whose GI tract cannot be used. This includes patients with a nonfunctioning or obstructed GI tract, prolonged ileus, massive GI bleeding, severe malabsorption, persistent vomiting, high-output fistulas, severe pancreatitis or enterocolitis, peritonitis, and mesenteric ischemia. Complications of parenteral feeding include catheter-related thrombosis and sepsis.
Obtaining a complete and accurate history may be difficult in elderly patients with abdominal pain because of cognitive impairment or sensory deficits that limit communication. At the same time, the classical presentations of many diseases are less common in the elderly. The ability to mount a febrile response and the sensation of pain are limited in older patients in part because of increased use of medications such as steroids and NSAIDs. Similarly, laboratory values may be normal in older patients despite the presence of considerable underlying disease. To prevent these factors from delaying diagnosis and treatment in elderly patients, the physician must use great skill in the medical interview, physical examination, and diagnostic testing.
The history should assess the chronology, character, location, and severity of the pain along with precipitating and alleviating factors. Chronology includes the onset, progression, and duration of pain. Pain of abrupt onset with rapid progression suggests a more aggressive cause. Characterization of the pain may help in diagnosis. Pain may be described as aching (appendicitis, diverticulitis, pelvic inflammatory disease), burning (GERD, perforated peptic ulcer), cramping (small bowel obstruction, biliary colic), boring (pancreatitis), excruciating (acute mesenteric ischemia), or tearing (ruptured abdominal aortic aneurysm). However, older patients may have limited pain or atypical presentations.
Location of the pain can also offer clues to the diagnosis. Epigastric pain and upper abdominal pain suggest a gastric, hepatobiliary, or pancreatic process. Midabdominal pain may represent an ileocecal process, whereas hypogastric pain suggests involvement of the colon or genitourinary structures. Shifting location of the pain may represent appendicitis or the development of peritonitis after visceral rupture. Subdiaphragmatic irritation is often referred to the shoulder. Because cardiac disease presents atypically in the elderly, any complaints of upper abdominal discomfort by patients with appropriate risk factors should raise the suspicion of coronary disease.
Severity of pain is a subjective parameter, and its usefulness is reduced further in elderly patients, whose experience of pain may be blunted because of diabetes or the use of anti-inflammatory medications. Severe pain in the absence of commensurate physical findings should raise the suspicion of acute mesenteric ischemia. Postprandial pain suggests gastric ulcers, mesenteric ischemia,
pancreatitis, or biliary colic. Relief of pain with food may be reported by patients with duodenal ulcers.
A thorough medication history should be obtained. The use of NSAIDs, steroids, and anticoagulants should be noted. The possibility of drug-induced pancreatitis or hepatotoxicity should be considered.
The differential diagnosis generated during the medical history should guide the physical examination. Absence of fever in older patients should not diminish the suspicion for infection because older patients frequently do not mount an appropriate febrile response to infectious agents. The abdomen should be examined for distension, ecchymoses, abnormal masses, enlarged organs, hernias, and abnormal peristalsis. Hyperperistalsis suggests obstruction or enteritis, whereas hypoperistalsis supports the diagnosis of peritonitis. An abdominal bruit, although neither sensitive nor specific, supports the diagnosis of mesenteric ischemia. The absence of rebound tenderness in the elderly should not exclude the possibility of peritonitis. Rectal and genital/pelvic examinations are an essential component of the evaluation.
The diagnostic hypotheses generated during the history and physical examination should guide the laboratory tests that are ordered. A urinalysis and CBC with differential should be ordered with the caveat that elderly patients may have significant underlying infection with normal white blood cell counts. Serum chemistry analysis provides information regarding fluid status. Amylase, lipase, and a liver chemistry profile are appropriate in the setting of upper abdominal pain.
Diagnostic tests should be ordered based on the findings of the history, physical examination, and laboratory evaluation. A set of supine and upright plain abdominal films is useful in identifying obstruction, radio-opaque gallstones, or a calcified pancreas. An upright chest x-ray film should be obtained to check for air under the diaphragm. Suspected hepatobiliary or pancreatic disease should be investigated by ultrasonography or CT scan. CT scanning is useful in demonstrating appendicitis, diverticulitis, bowel obstruction, retroperitoneal hemorrhage, and mesenteric lymph node enlargement as well as hepatobiliary and pancreatic disease. Patients suspected of having acute mesenteric ischemia should have prompt selective mesenteric angiography.
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