In the elderly, gastrointestinal (GI) disorders, especially those of the large intestine, account for a significant portion of physician visits, inpatient hospitalizations, and health care expenditure in the United States. Not only are large intestinal disorders common, but in the elderly their presentations, complications, and treatment may be different than in the young. This chapter focuses on diagnosis and treatment of a variety of diseases of the large intestine, including diverticular disease, Clostridium difficile-associated diarrhea, microscopic colitis, inflammatory bowel disease, colonic ischemia, colonic obstruction, and lower GI bleeding.
Diagnosis of GI disorders in an elderly patient poses several additional challenges to the physician on top of those present for all patients. First, comorbid illnesses are frequent and often numerous, and some such as dementia and depression may impair adequate communication between patient and caregiver. Second, medications and their side effects may cloud the clinical picture; polypharmacy is common in the elderly. Lastly, symptoms attributable to the large intestine may be manifestations of different diseases in the elderly than they would in the young. The astute geriatrician must take these factors into consideration when treating all patients.
Symptoms of digestive diseases may be misinterpreted or atypical in the aged. For example, constipation may be a symptom of irritable bowel syndrome in a young patient, whereas it might herald an obstructing lesion in an older patient. Rectal bleeding in a young person is most commonly from hemorrhoids or inflammatory bowel disease. In the elderly, diverticulosis or colon cancer more commonly cause rectal bleeding. A complete and thorough history is imperative in patients, especially the elderly. Subtle clues to the diagnosis are sometimes dismissed as physiologic aspects of aging. Physical examination and some laboratory tests including tests of liver function are unaffected by aging, and any abnormality should be evaluated for the presence of a disease state and not dismissed as an age-related change (Table 92-1).
Table 92-1 Influence of Age on Likely Diagnosis of Lower Gastrointestinal Symptoms ||Download (.pdf)
Table 92-1 Influence of Age on Likely Diagnosis of Lower Gastrointestinal Symptoms
Inflammatory bowel disease
Irritable bowel syndrome
Inflammatory bowel disease
Colonoscopy in the elderly is safe and well tolerated. Several studies of indications and outcomes of patients older than 80 years having elective and emergency endoscopic procedures found those tests to be safe; advanced age is not a contraindication to endoscopy. Moreover, the yield for diagnostic testing with colonoscopy in the elderly is relatively high.
Adequate bowel preparation is critical to a successful colonoscopic examination. Bowel cleansing in the elderly should be performed with care. Preparation with standard doses of polyethylene glycol based lavage solutions (PEG-ELS) in the elderly is well tolerated and produces satisfactory bowel cleansing in more than 95% of all cases. Sodium phosphate osmotic laxative preparation may also be used for bowel preparation, but causes significant fluid shifts and may cause electrolyte abnormalities or renal failure in this subset of patients. Sodium phosphate laxatives should be used with caution in the elderly and those with kidney or heart disease.
Most colonoscopies are performed under conscious sedation. Sedation for colonoscopy usually includes a combination of a benzodiazepine (midazolam or diazepam) and a narcotic (meperidine or fentanyl), or may include a short-acting anesthetic agent such as propofol. The elderly may be more sensitive to the agents used for sedation in GI endoscopy; small incremental doses should be given and the patient monitored closely for signs of cardiopulmonary compromise. Nevertheless, age alone is not a major determinant of morbidity; rapid or excessive dosing contributes more to complications from sedation than does age itself.
Endoscopic ultrasound (EUS) can be used to diagnose and manage disease of the anorectum. EUS utilizes high frequency ultrasound waves emitted from a probe attached to an endoscope to delineate the layers of the rectal wall, the internal and external anal sphincters, and the pelvic floor muscles. EUS may be helpful in evaluating these structures in patients with fecal incontinence. EUS also is frequently used to stage rectal malignancy, providing information about the depth of tumor invasion and the status of regional lymph nodes. Direct tissue sampling is available through fine needle aspiration at the time of the EUS.
Contrast studies of the large intestine involve coating the colonic mucosa with a contrast medium, usually barium sulfate, following thorough colonic preparation. Barium enemas may be performed by either single- or double-contrast method; in the latter, air is insufflated as well as barium. The single-contrast technique often is used to diagnose colonic strictures, fistula, obstruction, or diverticulitis. Double-contrast barium enema more commonly is used to detect polyps or mucosal abnormalities.
There exists some controversy concerning whether double-contrast barium enema is effective as a screening tool for colon cancer. Many experts consider colonoscopy to be the gold standard screening test. Colonoscopy is safe in the elderly and is widely available. However, contrast studies may be reasonable as a first-line test when colonic strictures are suspected or the presence of likely or known obstruction might make colonoscopy unsafe.
CT colonography (virtual colonoscopy) is a radiographic technique that combines helical CT and graphics software to create a three-dimensional view of the colonic lumen. This technology was developed to detect colonic polyps. In preliminary trials of CT colonography, detection rates for polyps greater than 5 mm were similar to those for optical colonoscopy. Debate remains about the significance of finding polyps of different sizes; comparisons of CT colonography with optical colonoscopy rest on what the investigators deem to be a “significant” polyp, with much disagreement about the significance of polyps less than 5 mm. Nonetheless, CT colonography will likely play an increasingly important role in colon cancer screening in the coming years.
There are several limitations of CT colonography. First, the procedure requires formal bowel preparation, similar to that required for optical colonoscopy. Moreover, polyps and other abnormalities found at CT colonography, detected in 10% to 30% of all examinations, require conventional colonoscopy for removal. Lastly, in addition to colonic lesions, incidental extracolonic findings on CT colonography such as gall bladder, liver, and renal/adrenal abnormalities may require evaluation and possibly further invasive testing.
Colonic diverticula are herniations of colonic mucosa through the smooth muscle layers of the colon. Strictly speaking, because colonic diverticula do not involve the muscle layer but rather are herniations of the mucosa and submucosa, they are actually pseudodiverticula. Diverticulosis has been increasingly recognized in western society and is thought to be a disorder of older individuals. Diverticula are present in approximately one-third of persons by age 50 and in approximately two-thirds by age 80. In western society, the predominance of diverticula occurs on the left side of the colon, specifically the sigmoid colon, although diverticula can occur anywhere in the colon.
There are three factors implicated in the pathogenesis of colonic diverticulosis. First, altered colonic motility results in increased luminal pressure along segments of the colon, and the resulting high-pressure areas cause out-pouchings at areas of weakness. Second, low intake of dietary fiber predisposes to diverticular disease, because low stool weights and slower stool transit times allow for relative increases in colonic intraluminal pressure. Third, with age the structural integrity of the colonic muscular wall decreases, and diverticula are more likely to form as a result.
Diverticulosis is usually an incidental finding in patients undergoing radiographic studies or colonoscopy for other reasons. There is no clear indication for therapy or follow-up in such patients. Large cohort studies suggest that complications of diverticular disease may be prevented by intake of a high-fiber diet. Although prospective, randomized studies are lacking, a diet high in fiber and low in fat appears to be reasonable, and one that likely provides other health benefits as well as potentially decreasing the risk of complications from diverticulosis.
Painful Diverticular Disease
Some patients with diverticulosis have left lower quadrant pain, and when examined, do not have evidence of inflammation. These patients may have painful diverticular disease. Pain often is described as crampy, located in the left lower abdomen, and may be associated with diarrhea or constipation as well as tenderness over the affected area. The pain is often exacerbated by eating and diminished by defecation or the passage of flatus. The symptoms of painful diverticular disease often overlap with those of irritable bowel syndrome, and therefore painful diverticular disease is considered part of the spectrum of functional bowel disorders. It is important to consider other causes of left lower quadrant pain such as diverticulitis, colonic obstruction, and incarcerated hernias in such patients.
Diverticulitis, defined as having diverticulosis in association with inflammation, infection, or both, is probably the most common clinical manifestation of diverticular disease. Diverticulitis develops in approximately 10% to 25% of individuals with diverticulosis who are followed for 10 years or more; however, less than 20% of these patients require hospitalization.
The process by which a diverticulum becomes inflamed has been compared to appendicitis, in which the diverticulum becomes obstructed by stool in its neck. The resulting obstruction eventually leads to micro- or macroperforation of the diverticulum. Fever, leukocytosis, and rebound tenderness often ensue. In an elderly patient, absence of these findings unfortunately does not rule out diverticulitis, and an aggressive evaluation is indicated if this diagnosis is suspected.
An abdominal and pelvic CT scan often confirms the diagnosis when the clinical suspicion is for diverticulitis, and the radiographic finding may or may not include evidence of a pericolic abscess. Colonoscopy or barium enema should be delayed until inflammation has improved because of an increased risk of colonic perforation with these studies. Patients with severe pain, nausea, and vomiting often require hospitalization and benefit from intravenous antibiotics. Most patients with diverticulitis will improve within 48 to 72 hours, and then a 5 to 7 day course of oral antibiotics with gradual introduction of oral intake is adequate therapy. Selected patients with relatively mild symptoms and who are able to tolerate oral intake may be managed with close outpatient monitoring including oral antibiotics and bowel rest. Given the high incidence of complicated disease, there should be a low threshold for hospitalization in elderly patients with diverticulitis.
Patients with complicated disease including those with abscesses may need drainage by surgery or interventional radiology. Surgery is recommended for patients with diverticulitis who fail to respond to medical therapy within 72 hours, those with two or more attacks, and those with one attack complicated by abscess, obstruction, or when the inflammatory process involves the bladder. The operation can usually be done in one stage with a primary bowel anastomosis. Sometimes, however, a two-stage procedure with a temporary colostomy may be necessary.
Three to five percent of patients with diverticulosis have hemorrhage from a diverticulum. Diverticular hemorrhage is the most common identifiable cause of significant lower GI bleeding, accounting for 30% to 40% of cases with confirmed sources.
Bleeding associated with diverticula is typically brisk, and painless. While the majority of diverticula are located in the left colon, bleeding from diverticular disease usually arises from the right colon. Bleeding is said to arise from arterial rupture of the vasa recta as it courses over the dome of a diverticulum. Bleeding ceases spontaneously in 70% to 80% of patients, and re-bleeding rates range from 22% to 38%. Re-bleeding is more likely when the initial bleed is severe.
The initial step in the management of patients with hemodynamically significant bleeding from diverticulosis is stabilization with intravenous fluid and blood products as necessary. Stable patients with suspected diverticular hemorrhage may undergo colonoscopy following rapid colonic purge. Colonoscopy in this setting allows for the ability to identify a diverticular source, to exclude alternative diagnoses, and to provide therapy of actively bleeding lesions.
In patients with recurrent bleeding, nuclear tagged red blood cell scans (scintigraphy) may localize the bleeding site. A positive bleeding scan may lead to angiography, which may allow for nonsurgical management of diverticular hemorrhage. Patients who require more than three units of packed red cell transfusions over 24 hours, have bleeding refractory to treatment, or are hemodynamically unstable may require surgical management. Preoperative nuclear red blood cell scans or angiography often help localize the diseased segment and allow for limited bowel resections. Blind total colectomy is rarely indicated.
Clostridium difficile, an anaerobic gram-positive, spore forming toxigenic bacillus was first isolated in 1935. It was not until 1978 when the association between the toxin elaborated by this bacteria and antibiotic-associated psedudomembranous colitis was made. The organism is now recognized as the single most important cause of nosocomial infectious diarrhea in the United States.
The pathogenesis of C. difficile colitis involves several steps. Patients must first be exposed to antibiotics. While the most common antibiotics associated with C. difficile colitis are ampicillin, amoxicillin, cephalosporins, and clindamycin, virtually all antibiotics (including those used to treat C. difficile colitis) have been implicated in causing disease (Table 92-2).
Table 92-2 Antibiotics Associated with Clostridium difficile Colitis
Next, exposure to antibiotics leads to altered colonic microflora, which in turn changes the protective barrier typically present in the colon against C difficile. Colonization of the organism in the colon is then possible. C difficile infection may result in an asymptomatic carrier state, or patients may develop diarrhea and colitis. Patients with intact immune systems and an ability to mount an early antibody response to C difficile toxin usually become asymptomatic carriers of the organism. On the other hand, patients lacking sufficient ability to mount an adequate immune response develop diarrhea and colitis.
Risk factors for the development of C difficile colitis include advanced age, multiple comorbid illnesses, intensive care unit stay, use of a nasogastric tube, acid antisecretory medications, and length of hospital stay (Table 92-3).
Table 92-3 Risk Factors for Clostridium difficile Infection ||Download (.pdf)
Table 92-3 Risk Factors for Clostridium difficile Infection
Use of nasogastric tube
Acid antisecretory medications
Intensive care unit stay
Length of hospitalization
Clinical manifestations of C difficile infection range from asymptomatic carriage to mild to moderate diarrhea to life-threatening pseudomembranous colitis (Figure 92-1). Asymptomatic carriage of C difficile is common in hospitalized patients, and in fact, studies have shown that 10% to 16% of hospitalized patients receiving antibiotics are carriers of C difficile. Asymptomatic carriers should not be treated. In patients who develop diarrhea with C difficile, symptoms often develop soon after colonization. Fever, abdominal pain, and leukocytosis accompany the watery, nonbloody diarrhea. Mucus or occult blood may be present, but hematochezia should prompt an evaluation for other disease states. Patients with more severe disease may develop colonic ileus or toxic dilation without diarrhea. Abdominal radiographs will often reveal the colonic dilation.
Clinical Manifestations of Clostridium difficle infection.
There are several tests for diagnosing C difficile colitis. The most widely used is an enzyme linked immunoassay. This assay detects either one of the two C difficile toxins. While the main advantages are speed, cost, ease of testing, and high specificity, this immunoassay has relatively low sensitivity. Other diagnostic tests including C difficile culture, tissue culture cytotoxic assay, and PCR for detection of toxin genes are rarely used because of their high cost, need for specialized laboratory techniques, and length of time to make the diagnosis.
Colonoscopy, or more often flexible sigmoidoscopy, may be helpful in making the diagnosis of C difficile colitis but is not necessary. Endoscopy is most useful when the diagnosis is in doubt or when disease severity demands rapid diagnosis. The finding of colonic pseudomembranes in a patient with antibiotic-associated diarrhea is almost pathognomonic for C difficile colitis (Figure 92-2).
Therapy for C difficile colitis begins with withdrawal of the precipitating antibiotics if possible. Metronidazole and vancomycin are both effective in the treatment of C difficile-associated disease. (Note that the only FDA-approved drug for treating C difficile colitis in the United States is vancomycin). Metronidazole is by far less expensive, and the use of vancomycin carries with it a concern for the induction of vancomycin-resistant enterococci; therefore, the usual initial therapy is with a 10 to 14 day course of oral metronidazole. This is effective in treating the majority of patients. In patients who are too ill or cannot take oral medication, IV metronidazole can be substituted. Patients who do not respond to metronidazole can be switched to oral vancomycin. Because intravenous vancomycin does not penetrate the colonic lumen, this formulation is not effective in treating C difficile colitis. Probiotic agents such as Lactobacillus GG and Saccharomyces boulardii have been used to reconstitute the colonic microflora, and are occasionally added to metronidazole or vancomycin to treat C difficile colitis, but their effectiveness has not been demonstrated in well-designed trials.
Unfortunately, recurrent C difficile infection is a common problem and particularly prevalent in older adults. Symptomatic recurrence may result from reinfection with either the same or a different strain of C difficile. Resistance to metronidazole or vancomycin is seldom if ever an important factor in recurrence. Therefore, patients with recurrent C difficile colitis generally are given another trial with the antibiotic used to treat the initial infection. In some patients, a prolonged taper of vancomycin as well as the addition of cholestyramine over many months may be needed to prevent further recurrence (Table 92-4). A variety of other strategies, including the use of some nonabsorbable antibiotics and fecal transplantation, have been used in the treatment of recurrent C difficile infection.
Table 92-4 Vancomycin Taper for Second Relapse of Clostridium difficile Colitis
The term “microscopic colitis” refers to two distinct but similar clinical entities, lymphocytic and collagenous colitis. Combined, they are characterized by chronic watery diarrhea and feature histologic evidence of chronic mucosal inflammation in the absence of endoscopic or radiological abnormalities of the large intestine. They differ principally by the presence or absence of a thickened collagenous band, which when present in collagenous colitis is located in the colonic subepithelium.
Both lymphocytic and collagenous colitis occur most commonly in people in their sixth to eighth decade. There is a strong female predominance. Most patients present with chronic watery stools for months to years. The pattern of symptoms in patients with microscopic colitis fluctuates and consists of exacerbations and remissions over years. Crampy abdominal pain is common, and symptoms often improve with fasting. Physical examination in patients with microscopic colitis is usually unremarkable, and occult blood in the stool is uncommon. Colonoscopic examinations are usually normal. It is important to exclude infectious causes of diarrhea by testing the stool for ova and parasites, bacterial pathogens, and C. difficile toxin prior to making the diagnosis of microscopic colitis. The diagnosis relies on histopathologic evaluation of biopsied material from the diseased colon.
Microscopic colitis is characterized by increased mononuclear cells in the lamina propria and between crypt epithelial cells, while collagenous colitis features a thickened subepithelial collagen layer. Contrasted to the normal colon where the collagen layer typically is 4 to 5 micrometers thick, in collagenous colitis the collagen layer is greater than 10 micrometers thick and averages 20 to 60 micrometers. The thickened layer is predominantly made up of type VI collagen, and it is this thickened collagen band that distinguishes collagenous colitis from lymphocytic colitis. Although inflammatory changes may be found diffusely throughout the colon in microscopic colitis, multiple biopsies of the left colon proximal to the rectosigmoid usually are sufficient to make the diagnosis.
There have been few controlled trials regarding treatment for microscopic colitis, and therapy is largely empiric. Most reports suggest that no single agent works. The pattern of the diarrhea in microscopic colitis often is relapsing; patients sometimes find relief with one agent, but unfortunately symptom improvement may not be permanent. Almost one-third of patients respond to antidiarrheal agents like loperamide as well as stool bulking agents like psyllium or methylcellulose; however, these agents do not improve the subepithelial inflammation or reduce the thickness of the collagen band.
Other treatment trials in microscopic colitis have examined the effect of aminosalicylates, corticosteroids, and bile acid absorbing resins. Alone or in combination, these agents reduce subepithelial inflammation and collagen thickness. Budesonide, an orally administered, topically active synthetic corticosteroid with significant first-pass metabolism has shown considerable promise in the treatment of microscopic colitis. Budesonide is an attractive agent here because of limited systemic side-effects and improvement of symptoms with once daily dosing, but unfortunately relapse after stopping the drug is common. In severe refractory cases, diverting ileostomy or proctocolectomy is a treatment of last resort.
Crohn's disease and ulcerative colitis comprise the vast majority of inflammatory bowel disease (IBD) (Table 92-5). They are characterized by a tendency for immune activation and inflammation within the GI tract. IBD commonly has its onset in the young adult population, but is found with increasing frequency in the elderly as well.
Table 92-5 Differentiating Crohn's Disease and Ulcerative Colitis ||Download (.pdf)
Table 92-5 Differentiating Crohn's Disease and Ulcerative Colitis
Throughout the GI tract, with skipped segments
Continuous disease from the rectum involving only the colon
Aphthous ulcers, cobblestoning
Micro ulcers, linear ulcers
Depth of inflammation
The age of diagnosis may range from early childhood through the entire lifespan. Epidemiological studies suggest there is a bimodal distribution of the age of onset, with the peak incidence of IBD occurring in the second and third decades, and a second smaller peak in the elderly between the ages of 60 and 70 years. “Late-onset” IBD accounts for approximately 12% cases of ulcerative colitis and 16% cases of Crohn's disease. However, in the elderly, presenting symptoms of IBD often are presumed to be attributable to another cause, and initially the correct diagnosis is sometimes overlooked. On the other hand, many experts believe that much of what was previously considered to be IBD in the elderly is actually attributable to other causes, and in particular, to ischemic colitis.
Crohn's disease is a chronic inflammatory process of unknown etiology, which most often affects the distal ileum, but can affect any segment of the GI tract including the colon. It is characterized by transmural inflammation of the bowel wall, the presence of apthae and ulcers, and the interspersing of segments of involved bowel with uninvolved bowel, i.e. skip lesions. Fissures, fistulas, and strictures are common in Crohn's disease. According to most published series, Crohn's disease of the colon, also known as Crohn's colitis, is more common in the elderly than in the young.
The presentation of Crohn's disease may be subtle and varies considerably. The clinical picture of Crohn's disease in the elderly as compared to the young has its roots in the propensity for Crohn's disease in the elderly to involve the colon. Consequently, intestinal obstruction, perforation, and fistula—features often associated with small bowel disease are less common. The majority of elderly patients with Crohn's disease manifest their disease with abdominal pain, weight loss, fever, and diarrhea. The diarrhea, typically watery in Crohn's disease can be bloody when the colon is involved.
Common laboratory abnormalities such as anemia, leukocytosis, thrombocytosis, hypoalbuminemia, and elevated erythrocyte sedimentation rate, as well as C-reactive protein levels vary with the severity of the illness. Interestingly, anemia in Crohn's disease can be because of either iron deficiency from chronic GI blood loss or from vitamin B-12 deficiency if the Crohn's disease involves a large enough segment of the distal ileum, the site for B-12 absorption in the small bowel.
Unfortunately, no single symptom, sign, or diagnostic test definitively establishes the diagnosis of Crohn's disease, and prolonged delays in diagnosis probably occur more frequently in elderly patients. Ultimately, a constellation of suggestive symptoms and laboratory abnormalities should prompt further evaluation. Common intestinal infections should be excluded, and tests may include stool cultures, stool examination for ova and parasites, and assays for C. difficile toxin.
Ultimately, the diagnosis of Crohn's disease is confirmed by findings on barium studies, colonoscopy, and histopathology. Colonoscopy and barium studies can identify the characteristic linear ulcers, skip lesions, and mucosal edema in Crohn's disease. Barium studies are superior for finding fistulas and defining the anatomic location of disease. CT and MR enterography may play an increasing role in the diagnosis of Crohn's disease. Because of its ability to see the mucosa directly and sample it for histopathologic examination, colonoscopy complements radiologic studies in making the diagnosis of Crohn's disease.
Computed tomography studies provide superior definition of the colon wall, can identify pyogenic complications like abscesses and perforations, and also can detect other intra-abdominal pathology that might mimic the presentation of Crohn's disease, such as appendicitis or nephrolithiasis. On the other hand, CT does not demonstrate fine mucosal detail and often appears normal early in the course of disease.
The principles of IBD management are the same regardless of the age of the patient. Nonetheless, there are several important considerations when treating elderly patients with IBD. The most commonly used medications in the treatment of Crohn's disease include sulfasalazine, mesalamine (5-aminosalicylic acid), and corticosteroids; all of these are well tolerated in the elderly population. However, corticosteroid use confers a higher risk of complications in the elderly, including accelerated bone loss and fractures, hypertension, and glucose intolerance (Table 92-6).
Table 92-6 Doses and Adverse Reactions with Commonly Used Medications to Treat Inflammatory Bowel Disease ||Download (.pdf)
Table 92-6 Doses and Adverse Reactions with Commonly Used Medications to Treat Inflammatory Bowel Disease
Nausea, folate deficiency, hemolytic anemia with glucose-6-phosphatase dehydrogenase deficiency
Up to 4.8 g/d
Up to 60 mg/day
Cushingoid appearance, glucose intolerance, osteoporosis, avascular necrosis, proximal myopathy, irritability, hypertension, cataract, glaucoma
6-MP 1.5 mg/kg
AZA 3 mg/kg
Pancreatitis, pancytopenia, hepatitis
Up to 1 g/d
Anorexia, nausea/vomiting, disulfiram-like effect, peripheral neuropathy
Up to 1 g/d
Nausea/vomiting, rash, hepatitis, spontaneous tendon rupture
Immunomodulators like azathioprine, 6-mercaptopurine, and methotrexate are used effectively in the young to maintain remission of Crohn's disease. These agents are usually well tolerated in the elderly as well; however, some authorities argue against their use in older patients on the theoretical grounds that they may further impair the immune dysfunction associated with aging and result in increased risk of infection or possibly malignancy.
Finally, some antibiotics such as metronidazole and ciprofloxacin have been shown to be effective in inducing and maintaining remission, as well as healing perineal fistulas, in patients with Crohn's disease. The long-term use of antibiotics typically is limited by the occurrence of significant side effects. Specifically, irreversible peripheral neuropathy can occur with the use of metronidazole, while antibiotic-associated diarrhea may be a complication of prolonged ciprofloxacin use.
Elderly patients with ileal or ileal–colonic Crohn's disease occasionally require intestinal resection, but generally tolerate surgery well and appear to have low rates of postoperative recurrence. Proctocolectomy with ileostomy is a common surgical option for patients with extensive Crohn's colitis. In elderly patients who are debilitated or malnourished, an initial subtotal colectomy with ileostomy is less debilitating and permits weight gain and improved physical well-being. If proctocolectomy is subsequently required, it can be done with a low complication rate, but may not be necessary at all if rectal disease is absent. A conventional ileostomy is generally favored in elderly patients following colectomy, because anal sphincter sparing surgical procedures, such as an ileal pouch–anal anastomosis, often have poor functional results in older patients.
Ulcerative colitis (UC) is a chronic inflammatory disorder of the GI tract of unknown etiology that affects the mucosa and submucosa of the large intestine in a continuous fashion. The inflammatory process invariably involves the rectum and extends proximally to variable distances, but does not involve the GI tract proximal to the colon. For many elderly patients, UC is a relatively mild illness, because colonic inflammation often is limited to the rectum or sigmoid colon. This distribution of disease is generally associated with less systemic manifestations, better response to medical therapy, and less need for surgery than more extensive UC.
The severity of UC may be subjectively classified as mild, moderate, or severe and is generally proportional to the extent of colonic inflammation. Symptoms in elderly patients are similar to those seen in young patients, and include bloody diarrhea, rectal pain, tenesmus, urgency, and abdominal pain. In comparison to Crohn's disease, the diarrhea in UC almost always is bloody. Fecal urgency, a sensation of incomplete evacuation, and fecal incontinence also are common. Unfortunately, older patients appear to be more likely than younger patients to present with a severe initial attack, and that first severe manifestation is associated with a relatively high fatality rate.
Laboratory findings in UC are nonspecific and reflect the severity of the underlying disease. In patients with limited distal disease, laboratory abnormalities may be absent except perhaps for mild anemia. In patients with extensive disease, severe iron deficiency anemia, hypoalbuminemia, leukocytosis, and thrombocytosis are common.
Toxic megacolon is a feared complication of UC, and it occurs more frequently in older patients. One should be suspicious of toxic megacolon in a patient whose diarrhea improves but whose abdomen is distended and tympanic. Other markers of worsening systemic inflammation, such as fever and leukocytosis, will also be present. The diagnosis is usually made by abdominal radiography. Colonoscopy should not be attempted when there is a suspicion for toxic megacolon, as perforation may ensue.
Similar to the situation in Crohn's disease, there is no single test that can definitively diagnose UC with acceptable sensitivity and specificity. In elderly people, it is important to exclude other diseases that may mimic UC, like ischemic colitis, radiation proctocolitis, diverticulitis, malignancy, and infectious colitis.
Again, the constellation of characteristic signs and symptoms often prompts an endoscopic examination, which may show the classic findings of diffuse erythema, mucosal edema, granular mucosa, and ulcerations starting in the rectum without intervening areas of normal mucosa (Figure 92-3). In the proper clinical setting, flexible sigmoidoscopy with biopsy is usually sufficient to establish a diagnosis of UC. Complete colonoscopy with ileoscopy is necessary to determine the extent of disease and to exclude Crohn's disease. However, complete colonoscopy is not recommended in patients with active UC for fear of perforation; the procedure can be safely performed once active disease has been controlled.
Ulcerative colitis as seen on colonoscopy.
Most elderly patients with UC respond favorably to medical management. Once in remission, relapse occurs less frequently in the elderly regardless of the severity of the initial attack. A range of agents is available for medical therapy of UC, and these may be administered orally, rectally, or parenterally depending on the site and severity of disease. Pharmacologic agents used to treat UC in the elderly are similar to the ones used to treat Crohn's disease and include sulfasalazine, mesalamine, corticosteroids, and immunomodulators.
The mainstays of treatment for UC are aminosalicylates, and they may be administered orally or rectally. Formulations designed either for enema or suppositories are reasonable choices when treating distal disease. Unfortunately, distal disease in elderly patients is more refractory to topical therapy than in the young, and so often elderly subjects with distal disease will require oral formulations of aminosalicylates to achieve and maintain remission.
In addition to aminosalicylates, corticosteroids are effective in achieving remission, but steroid use is associated with frequent side effects. Therefore, corticosteroids should only be used temporarily in UC as a means to induce remission. They should not be used long-term as they have not been shown to be effective at preventing relapses, and their side effect profile makes prolonged use unsatisfactory.
In patients who do not respond to aminosalicylates, immunomodulators such as azathioprine or 6-mercaptopurine can be introduced. These drugs are purine analogues, interfere with nucleic acid metabolism and cell growth, and exert their cytotoxic effects on lymphoid cells. Azathioprine and 6-mercaptopurine use is subject to a delayed response; patients may require up to 6 to 12 weeks to see an effect from these agents. Fortunately, they are effective at maintaining remission, once a response is achieved.
Surgery for UC is indicated in patients who fail medical therapy, have acute fulminant disease, are steroid dependent, or develop a dysplastic lesion or cancer. UC is cured following total proctocolectomy. In the elderly, total proctocolectomy with ileostomy remains a popular choice, because restorative procedures like ileo–anal anastomosis are limited by functional morbidity. An alternative surgical procedure is a subtotal colectomy. In patients who have a subcolectomy, a rectal stump is left that provides the patient with an improved chance for fecal continence. Such patients, however, continue to have colonic mucosa, as such have an ongoing increased risk for colon cancer to develop in the diseased segment, and require periodic surveillance of the retained rectum.
The risk of colon cancer in patients with long-standing IBD is a significant complication of the disease. Colon cancer rates generally are higher in patients with UC than those with Crohn's disease; it appears to be the degree of ongoing inflammation in the colon that confers an increased risk of colon cancer. As such, patients with Crohn's colitis are believed to have an equally high risk of developing colon cancer as their UC peers. In patients with long-standing UC, surveillance for colon cancer includes annual colonoscopy with random mucosal biopsies of the entire colon looking for evidence of early or advanced dysplasia. Areas that appear suspicious are also targeted. The risk of colon cancer increases substantially after 8 to 10 years of disease, and after many years approaches nine times the risk of the general population in patients of the same age group. During surveillance, patients found to have low- or high-grade dysplasia or carcinoma generally are offered proctocolectomy.
Colon ischemia (CI) is the most common intestinal vascular disorder in the elderly. Until the 1950s, the only well-described form of CI was gangrene. During the 1950s, however, a variety of ischemic manifestations other than gangrene were noted after ligation of the inferior mesenteric artery during abdominal surgery. Careful review of these cases revealed a spectrum of diseases in addition to infarction that included healed ulcers, strictures, pseudotumors, and ischemic UC.
The colon receives its blood supply from branches of the superior mesenteric artery and inferior mesenteric artery. The colon is protected from ischemia by an abundant collateral circulation formed by the marginal arterial complex of Drummond, central anastomotic artery, and arc of Riolan. Occlusion of a major vessel results in opening of collateral pathways in response to arterial hypotension distal to the occlusion. Increased blood flow through collateral pathways maintains adequate perfusion for a variable but brief period of time. If blood flow is diminished for a prolonged period, vasoconstriction develops in the affected bed and may persist after the primary cause of the mesenteric ischemia is reversed.
In most cases, the cause of an episode of CI cannot be established with certainty, and no vascular occlusion can be identified. The causes of CI are vast and include thrombosis, embolus, shock, volvulus, hematologic disorders, infections, trauma, surgery, and medications (Table 92-7). The colon is particularly susceptible to ischemia, perhaps owing to its relatively low blood flow during periods of functional activity, and its sensitivity to autonomic stimulation. What triggers a specific episode of CI, however, usually is not known.
Table 92-7 Causes of Colonic Ischemia ||Download (.pdf)
Table 92-7 Causes of Colonic Ischemia
Inferior mesenteric artery thrombosis
Inherited and/or acquired hypercoagulable states
CI encompasses a spectrum of injury. The specific conditions resulting from ischemic injury to the colon are classified as reversible or irreversible, and then can be characterized further as reversible ischemic colonopathy, reversible or transient ischemic colitis, chronic ulcerative ischemic colitis, ischemic colonic stricture, colonic gangrene, and fulminant universal ischemic colitis.
Despite a growing understanding of the pathophysiology of CI and its disparate clinical presentations, many cases of transient or reversible ischemia still are missed because diagnostic studies are not performed early enough in the course of disease. This is because patients may not seek medical advice for a disease that is self-limited or the initial symptoms may be confused with other conditions such as IBD.
Approximately 90% of persons with CI are older than age 60 and have widespread evidence of atherosclerosis. Up to 10% of patients may have a potentially obstructing lesion of the colon, including carcinoma, benign stricture, and diverticulitis. Patients with CI usually are not critically ill at the time of diagnosis, and their abdominal pain typically is mild. Mesenteric angiography plays little role in the diagnosis and management of this condition; since colonic blood flow usually has normalized by the time of presentation, the prognosis is excellent.
Typically, CI presents with the sudden onset of mild crampy left lower quadrant abdominal pain. The pain frequently is accompanied, or followed within 24 hours, by bloody diarrhea or bright red blood per rectum. In most cases, blood loss is minimal; hemodynamically significant bleeding should prompt consideration of other diagnoses, such as diverticular bleeding. Severe pain is unusual and may indicate irreversible transmural necrosis.
The differential diagnosis of CI includes infectious colitis, IBD, pseudomembranous colitis, diverticulitis, and colon carcinoma. In all patients suspected of having colonic ischemia, infection with organisms such as Salmonella, Shigella, Campylobacter, and E. coli O157:H7 should be excluded. In fact, E. coli O157:H7 infection induces a colitis that mimics or may even cause CI. Many commonly used medications are associated with CI, and include digitalis, nonsteroidal anti-inflammatory drugs, imipramine, danazol, and sumatriptan (Table 92-8).
Table 92-8 Medications Associated with Colon Ischemia
An elderly patient who presents with the sudden onset of abdominal pain and rectal bleeding or bloody diarrhea may benefit from a gentle barium enema or colonoscopy within 48 hours, once other more serious life threatening diagnoses are excluded. Colonoscopy is preferable because it is more sensitive in demonstrating mucosal abnormalities and permits histopathologic evaluation of the colon mucosa. Conventional sigmoidoscopy is of value only if the segment of involved bowel is within reach of the sigmoidoscope; CI involves the sigmoid in 50% to 60% of patients and the rectum in less than 10% of cases. Findings vary greatly depending on the stage at which sigmoidoscopy or colonoscopy is performed. At the outset, purplish blebs representing mucosal and submucosal hemorrhage may be seen. As hemorrhage is absorbed, varying degrees of necrosis, inflammation, ulceration, and mucosal sloughing occur, resembling UC or Crohn's disease.
Thumbprinting is the major radiologic finding in the acute presentation of CI. Thumbprints represent submucosal hemorrhage and edema. A barium enema repeated 1 week after an initial study should reflect evolution of the injury; either the areas of hemorrhage resorb and the study returns to normal or the thumbprints are replaced by a segmental pattern of colitis as the mucosa ulcerates.
The treatment of CI is based on early diagnosis and continued monitoring, with special attention to the radiologic or colonoscopic appearance of the colon. This form of surveillance is essential in that it establishes the diagnosis and verifies its reversibility or shows progression to chronic ischemic colitis or stricture. Management includes stabilization of the patient, optimization of cardiac function, and bowel rest. Systemic antibiotics are administered routinely in most cases. Systemic glucocorticoids are of no proven value and increase the risk of perforation. If abdominal examination, fever, and leukocytosis suggest deterioration or if the patient experiences diarrhea or bleeding for more than 2 weeks, irreversible damage is likely, and surgical resection is usually indicated.
Colonic obstruction results in dilation of the colon, abdominal distention and in some cases, colonic perforation. The majority of colonic obstructions are the result of mechanical obstruction from cancer, volvulus, stricture, impacted stool, surgical adhesion, or bowel intussusception. Patients with acute colonic obstruction can develop megacolon, the diagnosis of which is based on a cecal diameter of 12 centimeters or greater. Cecal distension is critical, because the cecum is the part of the colon that is most susceptible to ischemia and perforation based on LaPlace's law:
where T is wall tension, P is pressure, and R is the radius. With obstruction, as fluid and gas accumulate in the colon and intraluminal pressure increases, the radius of the colon increases. Wall tension is the greatest, and hence the risk for perforation most acute, at the area of greatest radius, which is generally in the cecum.
Acute Colonic Pseudo-Obstruction
Acute colonic pseudo-obstruction, also known as Ogilve syndrome, usually presents as intestinal ileus with massive bowel dilation postoperatively or in the setting of a severe intercurrent illness.
The colon is innervated extrinsically via the sympathetic and parasympathetic nervous systems and locally via the enteric neurons. The sympathetic nervous system, by inhibition of acetylcholine release, inhibits colonic motility. On the other hand, the parasympathetic nervous system, via acetylcholine release from the vagus and sacral nerves, stimulates colonic motility. An imbalance of these two systems favoring colonic inhibitory motor input results in colonic ileus and acute colonic pseudo-obstruction.
Acute colonic pseudo-obstruction usually presents in patients with severe underlying illness like stroke, myocardial infarction, or sepsis, or after surgical procedures. It is most common after orthopedic procedures of the pelvis, hips or knees, abdominal surgery, or obstetric procedures.
The presentation of acute colonic pseudo-obstruction may be subtle and variable, although the most characteristic clinical feature is severe abdominal distention and failure to pass flatus or stool. Some patients report only mild distention and minimal pain. Indeed, a high level of suspicion is necessary to make the diagnosis, because patients often present after surgery with perioperative bowel cleansing and so early passage of stool is not expected.
The hallmark of the disease is colonic dilation on standard abdominal radiography. The entire colon can be affected, although in some cases just the right sided segments can be dilated. The presence of air in the rectum implies that there is no mechanical obstruction, and is therefore important to note before making a diagnosis of acute colonic pseudo-obstruction.
Initial management of acute colonic pseudo-obstruction involves correcting reversible causes of colonic ileus such as electrolyte imbalances, hypoxemia, hypovolemia, and removal of medications that can exacerbate the problem. The vast majority of patients are successfully treated with these relatively simple measures. Bowel rest and intravenous hydration is imperative. Colonoscopic decompression, with or without placement of a decompression tube, is an option in patients with prolonged pseudo-obstruction. In fact, through the 1990s, the primary therapeutic approach for patients with acute colonic pseudo-obstruction who had not responded to conservative measures was endoscopic decompression of the colon.
Recently, a placebo-controlled study confirmed the efficacy of the cholinesterase inhibitor neostigmine (1–2 mg IV or SQ) in patients with acute colonic pseudo-obstruction. Relative contraindications to the use of neostigmine include a heart rate <50 beats per minute or systolic blood pressure <90 mm Hg; sick sinus syndrome or history of second- or third-degree arteriovenous block without a pacemaker; serum creatinine greater than 3 mg/dL; or active bronchospasm requiring medication (Table 92-9). Following neostigmine administration, patients should be monitored closely. A second administration of neostigmine can be attempted if there is partial or no response to the first trial.
Table 92-9 Contraindications to Use of Neostigmine ||Download (.pdf)
Table 92-9 Contraindications to Use of Neostigmine
Hypersensitivity to neostigmine
Recent myocardial infarction
Mechanical urinary or intestinal obstruction
Peptic ulcer disease
Therapy with beta-blockers
In selected patients who fail conservative and medical management, colonoscopic decompression of the unprepped bowel can be attempted. However, care is required since during colonoscopy air is insufflated into an already dilated colon. Recalling the principles of LaPlace's law, by increasing intraluminal pressure, wall tension increases in proportion to the radius of the colon, and therefore additional air insufflation carries with it an increased risk of colonic perforation. Surgical decompression, sometimes via placement of a cecostomy tube, remains another option for patients who do not respond to medical and endoscopic interventions.
The overall prognosis of patients with acute colonic pseudo-obstruction is poor, with an in-hospital mortality approaching 30%, attributable primarily to the severity of the underlying illness. The most significant complication of acute dilatation is colonic perforation, which occurred in 3% of cases in one retrospective series.
Lower GI bleeding is defined as that which arises distal to the ligament of Treitz. Lower GI bleeding occurs less frequently and is less severe than upper GI bleeding.
The incidence of lower GI bleeding increases significantly with age. The majority of lower GI bleeding in the elderly is the result of diverticula, vascular ectasias, and CI (Table 92-10). This section will focus on the approach to the patient with lower GI bleeding and bleeding from vascular ectasias. Diverticular hemorrhage and CI were discussed previously.
Table 92-10 Causes of Lower GI Hemorrhage ||Download (.pdf)
Table 92-10 Causes of Lower GI Hemorrhage
Inflammatory bowel disease
Acute lower GI bleeding presents with bright red blood per rectum, hematochezia, or melena depending on the location of the bleeding. Bright red blood per rectum usually indicates a distal colonic source or rapidly bleeding upper source. Melena usually indicates a right sided colonic lesion or upper source.
The first goal in the management of a patient with lower GI bleeding is resuscitation and hemodynamic stabilization. This may include administration of crystalloid intravenous fluids and blood products. Initial testing usually includes complete blood count, blood chemistry, coagulation profile, and blood type and cross-match, and the results help guide further management. For example, a low mean corpuscle volume often is a sign of chronic blood loss; a BUN-to-creatinine ratio of greater than 20:1 usually indicates an upper GI source; an elevated INR requires consideration of reversal in the face of hemodynamically significant bleeding.
Approximately 12% of patients thought to have lower GI bleeding have an upper GI bleeding source. It is important to exclude upper GI bleeding in patients with presumed lower GI bleeding, and often this can be accomplished with passage of a nasogastric tube and analysis of the gastric aspirate. Bilious fluid without blood in the nasogastric tube aspirate usually confirms the suspicion of lower GI bleeding. If an upper GI source is still in question, urgent upper endoscopy may be performed.
Although urgent upper endoscopy for the diagnosis and treatment of upper GI bleeding is predicated on sound data, urgent colonoscopy in lower GI bleeding has been practiced less consistently. Colonoscopy has the advantage of allowing for the diagnosis and immediate treatment of actively bleeding lesions. A number of reports have shown that “urgent colonoscopy” is safe and yields a specific diagnosis in a high proportion of elderly patients with lower GI bleeding. On the basis of a high diagnostic yield, low rate of complications, and theoretical therapeutic potential, urgent colonoscopy following a rapid colonic purge has been recommended as the diagnostic procedure of choice in most patients with hemodynamically significant lower GI bleeding.
Other diagnostic tests in patients with active lower GI bleeding include scintigraphy (nuclear tagged red blood cell scans) and angiography. Approximately 45% of patients with lower GI bleeding have positive red blood cell scintigraphy. Tagged red blood cell scans can detect bleeding at a rate greater than 0.1 mL/min and are useful to localize the site of bleeding, but unfortunately offer no option for therapy. If a patient has a positive bleeding scan, angiography with selective embolization can be performed to attempt to stop the bleeding. In order to detect active bleeding, angiography requires a higher rate of bleeding than scintigraphy, 0.5 mL/min compared to 0.1 mL/min. Transcatheter embolization of a lower GI bleeding source is usually effective in 70% to 90% of patients. If bleeding cannot be stopped with angiography, surgery to remove the bleeding colonic segment may be necessary. If a specific bleeding site can be localized with the above studies, a limited surgical resection can be performed rather than a subtotal colectomy.
Vascular ectasias, which arise from an age-related degeneration of previously normal blood vessels, typically occur in the cecum and proximal ascending colon. Along with diverticular bleeding, they are responsible for the majority of significant lower GI bleeding episodes in the elderly. Ectasias are found in up to 25% of persons older than 60 years who do not have symptoms; they typically are multiple and less than 5 mm in diameter. Despite a long standing belief to the contrary, there is no etiologic connection between vascular ectasias and aortic stenosis. Vascular ectasias probably arise as a result of repeated episodes of incomplete, low-grade obstruction of submucosal veins caused by increased tension in the colonic wall. The ultimate result is tortuosity and dilation of the venules and the arteriolar–capillary unit that feeds it, resulting in a small arteriovenous communication (Figure 92-4).
Proposed concept of the development of cecal vascular ectasias. A, Normal state of vein perforating muscular layers. B, With muscle contraction or increased intraluminal pressure, the vein is partially obstructed. C, After repeated episodes over many years, the submucosal vein becomes dilated and tortuous. D, Later, the veins and venules draining into the abnormal submucosal vein become similarly dilated and tortuous. E, Ultimately, the capillary ring becomes dilated, the precapillary sphincter becomes incompetent, and a small arteriovenous communication is present through the ectasia.
Lower GI bleeding caused by a vascular ectasia may be clinically indistinguishable from diverticular bleeding and is characterized by painless hematochezia. Bleeding from vascular ectasias may be hemodynamically significant, and a variety of treatment options exists including electrocoagulation, injection therapy, heater probe application, or argon plasma coagulation.
Diseases of the large intestine that occur in the elderly are a heterogeneous group of disorders, which are a major cause of morbidity and mortality in this population. The fundamental principle of thorough history and physical examination skills will aid the clinician at arriving at these diagnoses. With the help of modern therapeutic modalities, we can alleviate the pain and suffering associated with many of these diseases.