Acute and chronic diarrheal disorders are common problems at all ages. It has been estimated that 5% to 7% of the population has an episode of acute diarrhea each year and that 3% to 5% have chronic diarrhea that lasts more than 4 weeks. It is likely that the prevalence of diarrhea is similar in older individuals. This article reviews the impact of diarrhea in the elderly, many of whom are less fit physiologically to withstand the effect of diarrhea on fluid balance and nutritional balance.
Scope of the problem
Acute and chronic diarrheal disorders are common problems at all ages. It has been estimated that 5% to 7% of the population has an episode of acute diarrhea each year and that 3% to 5% have chronic diarrhea that lasts more than 4 weeks. It is likely that the prevalence of diarrhea is similar in older individuals. The impact of diarrhea may be disproportionate in the elderly, many of whom are less fit physiologically to withstand the effect of diarrhea on fluid balance and nutritional balance.
Some of the impairment of physiologic fitness may be due to the effects of aging itself (eg, senescence of the immune system, age-related reduction in renal function, or nutritional status) and some is due to concomitant illnesses that cause or are complicated by diarrhea and that are more common in the elderly. For example, diabetes mellitus is more common as people grow older and diabetic neuropathy is more prevalent in diabetics with longer durations of disease. It is not unexpected that a complication of longstanding diabetic neuropathy, such as chronic diarrhea, might be seen frequently in older patients.
Keen observers have noted that some diarrheal diseases may present differently in the elderly than in younger patients. For example, celiac disease may present with extraintestinal symptoms such as cognitive decline or neuropathy that could be confused with other conditions. It is essential that clinicians caring for older patients consider a broad differential diagnosis when investigating symptoms.
Diarrhea and malabsorption may have devastating effects on quality of life in the elderly. Fecal incontinence is a likely outcome when continence mechanisms that are “good enough” with formed stool are stressed by trying to hold back fluid stools (see the article by Leung and Rao in this issue). Malabsorption may tip the scales in elders with marginal nutritional status due to poor intake. Older patients are more likely to be hospitalized with diarrhea, more likely to stay in the hospital longer, and more likely to die with diarrhea than younger patients.
Changes in intestinal structure and function with normal aging
Histologic studies of the intestinal mucosa published 30 years ago concluded that villous height and surface area declined in old age. More recent investigation suggests that this is not the case and that there is no difference in jejunal mucosal biopsy specimens from old and young healthy subjects. This is more in keeping with modern notions of epithelial biology in which epithelial cells are continuously replaced, turning over every 5 to 6 days. As in the bone marrow, stem cells that produce enterocytes do not seem to wear out or become exhausted in the absence of disease over the course of a lifetime. Regardless of the age of the body housing the gut, the epithelium is eternally young.
This translates into maintenance of excellent epithelial function. In general, absorptive function is well preserved into old age. Absorption of d -xylose (when corrected for declines in renal function) is well maintained in a patient aged 80 years and declines only modestly thereafter. The ability to absorb lactose in adult life (due to a gene-regulator mutation that is prevalent among individuals from the northern European gene pool) may decline with time but the mechanism for this is not clear. There is no evidence that fat or protein absorption decreases with increasing age. Most micronutrients are absorbed well; the exceptions are calcium, folic acid, and vitamin B 12 .
Calcium malabsorption may be more of a problem with inadequate vitamin D effect due to reduced sun exposure, vitamin D intake, or renal processing of vitamin D to active forms than an epithelial defect, although some evidence points to reduced epithelial sensitivity to vitamin D. Folate malabsorption has been attributed to impaired luminal hydrolysis accentuated by achlorhydria or reduced folate conjugase activity. Vitamin B 12 levels tend to be lower in older subjects than in younger individuals, but this too may be multifactorial because direct measurement of radiolabeled cyanocobalamin absorption is normal.
Salivary, gastric, biliary, and pancreatic secretory capacities are not diminished in healthy elders, although there is some evidence that physiologic stimulation of secretion may be reduced. Changes in secretion may be related to changes in the regulatory systems of the gastrointestinal tract: the mucosal regulatory cell system, the enteric nervous system, or the immune system.
The mucosal regulatory system includes about a dozen types of enteroendocrine cells and so-called “brush cells” located in the epithelium. These cells comprise about 10% of the epithelial cells in the gut and seem to be renewed along with the rest of the enterocytes from stem cells in the crypts. They have access to the lumen by the apical microvillar membrane and can sense physical and chemical characteristics of chyme within the lumen. In addition, these cells can respond to neurotransmitters released by nearby nerves. The enteroendocrine cells respond by release of regulatory substances, such as serotonin and various peptides, into the subepithelial space and lumen. The brush cells respond by manufacture of nitric oxide which also has regulatory effects on nearby cells. These regulatory substances can interact with local elements of the enteric nervous system, local effector cells by paracrine effects, and more distantly through hormone effects on other parts of the gut. Although some diseases have been associated with depletion of these cells, there is no evidence that aging impairs their function.
The enteric nervous system is affected by aging, because like other neural networks, replacement of neurons is slow or nonexistent. Loss of neurons from the enteric nervous system begins in childhood and seems to accelerate as we grow older. It has been estimated that 40% to 60% of the enteric neurons are lost over a lifetime. The wonder may be that gastrointestinal function is as well preserved as it is. There may be greater loss of cholinergic neurons than nitrergic neurons, accounting for some of the motility changes that are observed as we age.
Another regulatory system that may be affected by aging is the immune system. It is now known that immune cells release substances that affect gut function as well as modulate gut responses to infection. Although evidence is scanty, the immune system may be less capable in the elderly, a concept known as “immunosenescence.” Immunosenescence may reflect an overall reduction in the ability to respond to infection with cellular and humoral effectors or a misdirection of the immune system against autoantigens, which may have something to do with the changes in the gut microbiota that have been observed with aging. Old people tended to have reduced populations of bifidobacteria and increased bacteroides. The impact of these changes on susceptibility to enteric infection or on the occurrence of gastrointestinal symptoms has not been worked out. Potentially the bacterial flora of the gut might be manipulated to alter the mucosal immune response.
Changes in intestinal structure and function with normal aging
Histologic studies of the intestinal mucosa published 30 years ago concluded that villous height and surface area declined in old age. More recent investigation suggests that this is not the case and that there is no difference in jejunal mucosal biopsy specimens from old and young healthy subjects. This is more in keeping with modern notions of epithelial biology in which epithelial cells are continuously replaced, turning over every 5 to 6 days. As in the bone marrow, stem cells that produce enterocytes do not seem to wear out or become exhausted in the absence of disease over the course of a lifetime. Regardless of the age of the body housing the gut, the epithelium is eternally young.
This translates into maintenance of excellent epithelial function. In general, absorptive function is well preserved into old age. Absorption of d -xylose (when corrected for declines in renal function) is well maintained in a patient aged 80 years and declines only modestly thereafter. The ability to absorb lactose in adult life (due to a gene-regulator mutation that is prevalent among individuals from the northern European gene pool) may decline with time but the mechanism for this is not clear. There is no evidence that fat or protein absorption decreases with increasing age. Most micronutrients are absorbed well; the exceptions are calcium, folic acid, and vitamin B 12 .
Calcium malabsorption may be more of a problem with inadequate vitamin D effect due to reduced sun exposure, vitamin D intake, or renal processing of vitamin D to active forms than an epithelial defect, although some evidence points to reduced epithelial sensitivity to vitamin D. Folate malabsorption has been attributed to impaired luminal hydrolysis accentuated by achlorhydria or reduced folate conjugase activity. Vitamin B 12 levels tend to be lower in older subjects than in younger individuals, but this too may be multifactorial because direct measurement of radiolabeled cyanocobalamin absorption is normal.
Salivary, gastric, biliary, and pancreatic secretory capacities are not diminished in healthy elders, although there is some evidence that physiologic stimulation of secretion may be reduced. Changes in secretion may be related to changes in the regulatory systems of the gastrointestinal tract: the mucosal regulatory cell system, the enteric nervous system, or the immune system.
The mucosal regulatory system includes about a dozen types of enteroendocrine cells and so-called “brush cells” located in the epithelium. These cells comprise about 10% of the epithelial cells in the gut and seem to be renewed along with the rest of the enterocytes from stem cells in the crypts. They have access to the lumen by the apical microvillar membrane and can sense physical and chemical characteristics of chyme within the lumen. In addition, these cells can respond to neurotransmitters released by nearby nerves. The enteroendocrine cells respond by release of regulatory substances, such as serotonin and various peptides, into the subepithelial space and lumen. The brush cells respond by manufacture of nitric oxide which also has regulatory effects on nearby cells. These regulatory substances can interact with local elements of the enteric nervous system, local effector cells by paracrine effects, and more distantly through hormone effects on other parts of the gut. Although some diseases have been associated with depletion of these cells, there is no evidence that aging impairs their function.
The enteric nervous system is affected by aging, because like other neural networks, replacement of neurons is slow or nonexistent. Loss of neurons from the enteric nervous system begins in childhood and seems to accelerate as we grow older. It has been estimated that 40% to 60% of the enteric neurons are lost over a lifetime. The wonder may be that gastrointestinal function is as well preserved as it is. There may be greater loss of cholinergic neurons than nitrergic neurons, accounting for some of the motility changes that are observed as we age.
Another regulatory system that may be affected by aging is the immune system. It is now known that immune cells release substances that affect gut function as well as modulate gut responses to infection. Although evidence is scanty, the immune system may be less capable in the elderly, a concept known as “immunosenescence.” Immunosenescence may reflect an overall reduction in the ability to respond to infection with cellular and humoral effectors or a misdirection of the immune system against autoantigens, which may have something to do with the changes in the gut microbiota that have been observed with aging. Old people tended to have reduced populations of bifidobacteria and increased bacteroides. The impact of these changes on susceptibility to enteric infection or on the occurrence of gastrointestinal symptoms has not been worked out. Potentially the bacterial flora of the gut might be manipulated to alter the mucosal immune response.
Acute diarrhea in the elderly
Infections
Acute diarrhea remains a common disorder in the general population with 6% of persons in 1 large sample having diarrhea in the 4 weeks preceding the survey (an annualized rate of 0.72 episodes per person-year). Persons aged 65 years or older had a lower than average incidence (0.32 episodes per person-year). Older data suggest that the risk of hospitalization for gastroenteritis is twice as high for individuals aged 65 to 74 years and 4 times as high for individuals aged 75 years and older than in patients less than 50 years old.
The usual bacterial, viral, and protozoal pathogens account for most of the identified cases of acute diarrhea. These include Salmonella , Shigella , Campylobacter , Clostridium difficile , Escherichia coli , Norovirus, Rotovirus, Giardia , Cryptosporidium , and Entameba histolytica . In individuals with immunodeficiencies due to AIDS or immunosuppressive drug treatment (eg, corticosteroids, methotrexate, thiopurines, or antitumor necrosis factor biologicals) opportunistic infections with cytomegalovirus or herpesvirus should be considered. Older patients also travel more than in the past and so travelers’ diarrhea may occur. In general, the presentations of these usual pathogens are similar to those seen in younger patients, and the course, treatment, and prognosis are similar to those of younger individuals.
Many older individuals reside in communal residences or nursing homes rather than in single family homes. This type of accommodation increases the opportunities for spread of infections if strict regimes to limit common source and person-to-person spread of infections are not in place. An excellent example of this phenomenon is pseudomembranous colitis due to C difficile . Older individuals are more likely than younger adults to be hospitalized and to receive antibiotics for infections. They may become ill or be colonized with C difficile which they can bring into their residential institutions where it can spread widely in the environment.
Older individuals are not only more likely to contract C difficile infection, but they are more likely to contract fulminant disease that may be fatal. This may be due to impaired immune competence, comorbid illnesses, increased exposure to drugs that may predispose to infection (such as proton pump inhibitors), or to drugs that predispose to more toxic strains of C difficile (such as fluoroquinolones). Fulminant disease can be managed medically, but colectomy may be needed for unresponsive cases.
Relapse of C difficile colitis also is more common in the elderly and seems to be increasing. Risk factors for relapse include fecal incontinence, longer duration of fever, and treatment with H 2 receptor antagonists. The proper management of relapsing disease is still undefined; in general, longer periods of antibiotic therapy are recommended, but novel therapies that replete the normal fecal flora or stimulate immunity are under development.
Drugs
Because of the sheer number and variety of drugs consumed by people as they grow older, drug-induced diarrhea is a prominent cause of loose stools in the elderly. If diarrhea begins soon after instituting a new drug, it is not too difficult to assign blame. To do this the physician must take a good drug history, not merely review a list of drugs that are being consumed. This history should include not only the drug and dose but also the timing of doses and any dose adjustments made over time.
Nearly half of the drugs listed in the pharmacopeia have diarrhea as one of their common side effects. Common categories of drugs associated with diarrhea are presented in List 1.
List 1. Medications associated with diarrhea
Acid-reducing agents (eg, histamine H 2 receptor antagonists, proton pump inhibitors)
Antacids (eg, those that contain magnesium)
Antiarrhythmics (eg, quinidine)
Antibiotics (most)
Anti-inflammatory agents (eg, nonsteroidal anti-inflammatory drugs [NSAIDs], gold salts, 5-aminosalicylates)
Antihypertensives (eg, β-adrenergic receptor blocking drugs)
Antineoplastic agents (many)
Antiretroviral agents
Colchicine
Herbal products
Heavy metals
Prostaglandin (eg, misoprostol)
Theophylline
Vitamin and mineral supplements (eg, vitamin C, magnesium)
Tube Feedings
Another form of iatrogenic diarrhea that is common in the elderly is as a result of tube feeding. This is most likely to occur with calorie-dense formulas infused directly into the small bowel and represents a variant of dumping syndrome. It may also occur with intragastric feeding, but this is less likely if normal regulatory mechanisms of duodenal control of gastric emptying are intact. Postulated mechanisms for tube feeding-associated diarrhea include hypertonicity-induced increases in intraluminal volume and motility, stimulation of gastrointestinal peptide release, and bacterial overgrowth. Slowing the rate of infusion, modifying the formula to increase fiber, or giving an antidiarrheal such as loperamide or diphenoxylate may mitigate the problem.
Chronic diarrhea in the elderly
Secretory Diarrhea
As in younger individuals, secretory diarrhea is the most common type of chronic diarrhea encountered. Secretory diarrhea is almost always a result of reduced fluid and electrolyte absorption (rather than net secretion by the gut) related to inhibition of mucosal absorption rate or rapid motility that limits the contact time needed for complete absorption. The result of this is stools in which most of the osmolality is due to electrolytes (small osmotic gap, see later discussion).
There are many causes of chronic secretory diarrhea (List 2). Particularly in older patients, the thoughtful clinician first needs to consider systemic disorders that might be causing diarrhea before targeting primary gastrointestinal problems.
List 2. Differential diagnosis of secretory diarrhea in the elderly
Ileal bile acid malabsorption
Microscopic colitis
Collagenous colitis
Lymphocytic colitis
Diverticulitis
Drugs (see List 1)
Disordered motility/regulation
Diabetic autonomic neuropathy
Irritable bowel syndrome (IBS)
Postsympathectomy diarrhea
Postvagotomy diarrhea
Endocrinopathies
Addison disease
Carcinoid syndrome
Gastrinoma
Hyperthyroidism
Mastocytosis
Medullary carcinoma of the thyroid
Pheochromocytoma
Somatostatinoma
VIPoma
Idiopathic secretory diarrhea
Epidemic secretory (Brainerd) diarrhea
Sporadic idiopathic secretory diarrhea
Laxative abuse (stimulant laxatives)
Neoplasia
Colon carcinoma
Lymphoma
Villous adenoma
Vasculitis
Endocrine diseases
Diabetes is a prevalent problem for older patients. Diarrhea complicates the lives of about 20% of diabetics, making diabetes the most common systemic disease causing diarrhea. The term, “diabetic diarrhea,” should be restricted to diabetics with chronic secretory diarrhea. Steatorrhea can occur in diabetics, but is usually due to coexisting celiac disease, pancreatic exocrine insufficiency, or small bowel bacterial overgrowth. Diabetic diarrhea is considered to be a manifestation of autonomic neuropathy with decreased function of the adrenergic system and enteric nervous system. Coexisting fecal incontinence can make diabetic diarrhea a nightmare for patients. Clonidine can be effective in diabetics with chronic secretory diarrhea, but opiate antidiarrheals work well also.
Addison disease is less common than diabetes among the elderly, but it is an important condition to consider in a differential diagnosis of chronic diarrhea because its systemic effects can be subtle. The lassitude, fatigue, and weight loss characteristic of Addison disease may be ascribed to “old age” in the elderly, and electrolyte changes may be masked by concomitant use of diuretics for other medications. A cosyntropin stimulation test should be part of a second tier of investigations in patients with chronic diarrhea.
Hyperthyroidism also may not produce its full range of symptoms in the elderly. Patients may present with weight loss and diarrhea, but the adrenergic symptoms, such as tachycardia and tremor, may be absent. It is good practice to check the levels of thyroid hormone and thyroid stimulating hormone (TSH) in elderly patients with chronic diarrhea.
A group of endocrine problems that is rare at any age includes tumors secreting autocoids or gastrointestinal peptides. Although carcinoid tumors, gastrointestinal, and pancreatic endocrine neoplasms need to be considered in the differential diagnosis, they are so rare that measurement of plasma peptides and metabolites should only be done when the characteristic syndromes (eg, Zollinger-Ellison syndrome or carcinoid syndrome) are present, tumor is identified, or all other diagnostic tests have been negative. Especially in the last situation, abnormal results are more likely to be false-positives rather than true-positives due to the rarity of these tumors.
Drugs and iatrogenic diarrhea
As with acute diarrhea, drug therapy can cause chronic diarrhea. Because older patients are treated with a bevy of drugs for therapeutic and preventative purposes, such complications can be common. Chronic diarrhea may result if drug interactions or declining renal function result in higher blood levels. Diarrhea may be due to a drug that the patient has taken for a while and the clear relationship between drug ingestion and initiation of diarrhea, as seen with acute drug-induced diarrhea, may be missing.
Older individuals are more likely than younger patients to have had surgeries or radiation therapy that may cause chronic diarrhea. The therapeutic intervention may predate the onset of diarrhea by decades, but will have set the stage for chronic diarrhea. For example, gastrectomy may not cause diarrhea until the bacterial overgrowth that it encourages actually develops. Radiation enteritis likewise is a condition that may produce symptoms years after the treatment was completed.
IBS
IBS is the most common diagnosis made by clinicians in patients with chronic diarrhea, but it is an unlikely diagnosis for chronic diarrhea at any age, especially in diarrhea presenting for the first time in older patients. The salient symptom of IBS is abdominal pain; the diagnosis should not be made in patients without substantial abdominal pain or discomfort. A category of “functional diarrhea” includes patients with painless diarrhea, but that diagnosis should be applied cautiously in the elderly, because most functional syndromes first present earlier in life and an alternate diagnosis can be made in most patients with continuous diarrhea. In the author’s opinion functional diarrhea should be limited to those individuals with episodic or variable diarrhea in whom no alternative diagnosis can be reached.
Microscopic colitis
Lymphocytic colitis and collagenous colitis, the two varieties of microscopic colitis, are common in older patients. In the general population, they are as common as Crohn disease, but the age distribution of microscopic colitis skews older, with a median age of onset of 68 years, making it much more likely than Crohn disease as a cause of diarrhea in the elderly.
Although these diseases are inflammatory processes in the mucosa, the mucosa does not ulcerate, hence the typical findings of inflammatory diarrhea (blood and pus) are absent. Microscopic colitis patients have the same HLA-D subtypes as celiac disease (DQ2, 8). Presumably microscopic colitis is due to some luminal antigen, either dietary or microbial, that induces an increase in intraepithelial lymphocytes and in inflammatory cells in the lamina propria. The antigen is almost certainly not gluten. The only histologic difference between lymphocytic colitis and collagenous colitis is thickening of the subepithelial collagen band in the latter, the cause of which remains obscure.
The clinical history of microscopic colitis is characteristic: the gradual onset of watery, loose stools which can become moderately voluminous (typically 500–1000 g/24 h). Stools are not bloody, pus and mucus are not typically present, and weight loss is gradual and minimal. In older individuals fecal incontinence is common, so much so that elderly patients with this presentation should have microscopic colitis at the top of their differential diagnoses.
The diagnosis of microscopic colitis depends on obtaining enough biopsies from the colon to allow the pathologist to make the diagnosis. Most gastrointestinal pathologists are aware of the criteria for this diagnosis and so it should be missed rarely if biopsies are obtained. The trick is to remember to do this when the gross findings at colonoscopy are normal. One study suggested that this only happens about 80% of the time.
Treatment of microscopic colitis is straightforward. The best evidence is that budesonide is effective in collagenous colitis and probably lymphocytic colitis. Treatment should continue for 1 to 2 months at a dose of 9 mg daily. It can then be tapered off, but patients should be warned that the disease often relapses and further courses of treatment may be needed. Budesonide is not approved by the US Food and Drug Administration for this indication. Glucocorticoid side effects can occur in patients given budesonide, especially if they are receiving concomitant therapy with drugs that inhibit cytochrome P450 3A4. Weaker evidence supports the use of bismuth subsalicylate and cholestyramine in microscopic colitis. Response rates with mesalamine or sulfasalazine are so low (∼30%) that they should not be used for this indication. Diarrhea due to microscopic colitis usually can be controlled with opiate antidiarrheals and such therapy may be sufficient for some patients.
Bile acid diarrhea
It is well recognized that chronic diarrhea occurs when ileal dysfunction or resection results in delivery of a critically high concentration of bile acids into the colon (3–5 mmol/L). Reaching this concentration depends on two offsetting trends: the extent of reduction of bile acid absorption by the ileum and not flooding the colon with fluid that tends to dilute bile acid concentrations. Patients with extensive ileal resections (>100 cm) deliver so much excess fluid to the colon that the critical concentration cannot be reached and diarrhea will not occur through a bile acid-mediated mechanism. Such patients may have diarrhea due to loss of surface area, but using bile acid-binding resins will not help.
Although this mechanism has been well worked out, the importance of bile acid malabsorption as a cause for chronic diarrhea is debated. In Europe, where a test for bile acid malabsorption (SeHCAT retention) is readily available, bile acid malabsorption is believed to be prevalent in chronic diarrhea and bile acid-binding resins are felt to be helpful in otherwise idiopathic diarrhea. In the United States, research studies show that bile acid malabsorption is a common phenomenon in patients with chronic diarrhea, but therapeutic trials of cholestyramine have been unhelpful, with the results on stool weight not predicted by the extent of bile acid malabsorption.
Nevertheless, bile acid-binders are of help in some patients with chronic secretory diarrhea and should be tried empirically when no diagnosis has been reached after study or when a bile acid-mediated diarrhea seems likely (eg, previous ileal resection or disease, previous cholecystectomy with predominantly morning diarrhea). The majority of the dose of bile acid-binder should be given at bedtime. Typically 4 g of colestipol, 4.5 g of cholestyramine, or 2.5 g of colesevelam should be tried initially at bedtime. Care must be taken to avoid coadministration with drugs that might be adsorbed by the resin.
Osmotic Diarrhea
Osmotic diarrhea is due to ingestion of some substance that is poorly absorbed and therefore results in retention of water within the lumen of the intestine. The malabsorbed substances are either dietary components, such as disaccharides, or poorly absorbable ions, such as magnesium.
Lactose malabsorption is a true age-related condition. Lactose is the universal carbohydrate found in mammalian milk. Most babies are born with lactose phlorizin hydrolase (LPH, “lactase”) in the brush border of small bowel enterocytes that has a high capacity to split lactose into its component monosaccharides, glucose, and galactose. These monosaccharides are then rapidly absorbed by the glucose-sodium cotransporter and are removed from the lumen. Some infants are born without active LPH and suffer with primary lactose intolerance. Like most mammals, most humans lose LPH activity after weaning, typically by the age of 20 years in humans. Some people maintain LPH activity into adult life as a result of a mutation in the gene regulator. This results in the ability to digest and absorb lactose in adult life. This mutation is prevalent in the northern European gene pool and so the expectation in this population is that milk and dairy products can be consumed for a lifetime. Even in this population, however, the capacity for lactose hydrolysis declines with age and eventually may not be sufficient to hydrolyze all the lactose that is consumed. Those individuals then may develop symptoms, depending on the amount of lactose consumed.
Symptoms of lactose intolerance include excessive flatus and diarrhea. The severity of these symptoms depends on the load of lactose consumed and the residual capacity for lactose hydrolysis. For every 10 g of carbohydrate that enters the colon, about 1 L of hydrogen gas and about 60 mmol of short chain fatty acids are produced by fermentation by enteric bacteria. Excessive flatus production can be seen with ingestion of relative small amounts of lactose in a lactose-intolerant person. Diarrhea depends on the absorbability of short chain fatty acids and their effects on colonic fluid absorption. The capacity of the colonic flora for fermentation of carbohydrate is about 80 g in the average adult and so unabsorbed lactose does not drive diarrhea directly until this threshold is exceeded.
Older individuals may have always tolerated lactose and may not recognize that it is now causing their diarrhea. Clues to the diagnosis are the intermittency of symptoms (which depend on the amount of lactose ingested, which may vary from day-to-day) and the presence of flatus. Stool pH with carbohydrate malabsorption is acid (pH <6) and an osmotic gap may be present (typically >50 mOsm/kg). Other carbohydrates, such as fructose, have limited capacity for absorption, and fiber is by definition not absorbable; concurrent ingestion of these substances may amplify symptoms in patients with lactose intolerance.
Other substances causing osmotic diarrhea are poorly absorbed ions, such as magnesium, sulfate, or phosphate. Magnesium is the prototype for this category. In addition to a small component of active absorption, 7% of the ingested load is absorbed passively, leaving 93% behind in the lumen to obligate water retention. Thus stool output is directly proportional to load, accounting for magnesium’s effectiveness as a laxative.
Patients with diarrhea may be taking poorly absorbed ions for therapeutic reasons or may ingest them inadvertently. For example, some calcium supplements or antacids contain magnesium and may induce diarrhea as a side effect. Other individuals may be taking laxatives to produce a factitious illness. Stools from patients with magnesium-induced diarrhea will have low concentrations of sodium and potassium, a high stool osmotic gap (>50 mOsm/kg), and high concentrations of magnesium.
Inflammatory Diarrhea
Conditions that result in inflammation of the wall of the intestine and ulceration of the mucosa can cause blood and pus to appear in the stools, the fundamental characteristics of an inflammatory diarrhea (List 3). A brief differential diagnosis of this includes idiopathic inflammatory bowel disease, diverticular disease and diverticular colitis, ischemia, and neoplasia.
List 3. Causes of inflammatory diarrhea in the elderly
Diverticulitis
Infectious diseases
Invasive bacterial infections (eg, tuberculosis, yersinosis)
Invasive parasitic infections (eg, amebiasis, strongyloides)
Pseudomembranous colitis
Ulcerating viral infections (eg, cytomegalovirus, herpes simplex virus)
Inflammatory bowel disease
Crohn disease
Ulcerative colitis
Ulcerative jejunoileitis
Ischemic colitis
Neoplasia
Colon cancer
Lymphoma
Radiation colitis
Idiopathic inflammatory bowel disease
Ulcerative colitis and Crohn disease are often believed to be diseases of young people. Although this is usually true, epidemiologic research shows that ulcerative colitis and Crohn disease occur with some frequency in older patients. Although this was believed to be due to misdiagnosis, subsequent work has borne out this observation. The presentations and courses of inflammatory bowel diseases in the elderly are somewhat different than in younger individuals, but there is an overall similarity that makes them familiar. A detailed review of this subject may be found elsewhere in this issue.
Diverticular disease and diverticular colitis
Diverticulosis is an age-related phenomenon that reaches epidemic proportions among the elderly. Up to 65% of people ≥65 years have diverticula. This condition is asymptomatic in most patients. Five percent to 10% of people with diverticulosis may develop symptoms of diverticulitis or diverticular hemorrhage in their lifetime.
Recently it has been recognized that some patients with diverticulosis develop a segmental colitis in the diverticula-bearing parts of their colons that may produce chronic pain and diarrhea. The diagnosis depends on obtaining biopsies from the colon that show typical histopathologic findings. Treatment is undefined; most clinicians use mesalamine, but there is little direct evidence of benefit.
Ischemia
Ischemic colitis is an acute condition that produces bloody diarrhea and abdominal pain, usually in the left lower quadrant. It seems to be due to low flow conditions in the inferior mesenteric artery and can be seen following circulatory compromise and as a side effect of certain drugs. It usually is self-limited, and in contrast to small intestinal ischemia, does not go on to produce necrosis and death. Diagnosis is made on the basis of sigmoidoscopy or colonoscopy.
Neoplasia
Colon cancer and lymphoma occasionally present with diarrhea. Stools may have blood and pus in them due to mucosal ulceration proximal to an obstructing lesion. Large villous adenomas in the rectum may produce diarrhea due to excessive secretion of mucus from their surface.
Fatty Diarrhea
The presence of steatorrhea implies problems with the solubilization of dietary fat by bile acids or malabsorption by the small intestine (List 4). Isolated colonic pathology cannot produce steatorrhea. Certain conditions, such as small intestinal bacterial overgrowth, may be more common in the elderly. Others that produce fatty diarrhea, such as celiac disease, may present atypically.
List 4. Causes of fatty diarrhea in the elderly
Malabsorption syndromes
Mesenteric ischemia
Mucosal diseases (eg, celiac disease, Whipple disease)
Short bowel syndrome
Small intestinal bacterial overgrowth
Maldigestion
Inadequate luminal bile acid concentration
Pancreatic exocrine insufficiency
Celiac disease
The spectrum of celiac disease has expanded in recent years as criteria for the diagnosis have liberalized. Once considered only a disease of young people, celiac disease is now being diagnosed for the first time in some older adults. The presentation of celiac disease may be more subtle, with accelerated osteopenia, hypoprothrombinemia, overshadowing diarrhea and weight loss. A full treatment of this condition in the elderly can be found in the article by Rashtak and Murray in this issue.
Other mucosal diseases
Whipple disease, lymphangectasia, and other mucosal diseases do not seem to be especially prevalent in the elderly, but are sometimes diagnosed in older patients. With its wide variety of extraintestinal symptoms, Whipple disease can masquerade as decline in the elderly.
Pancreatic exocrine insufficiency
Malabsorption in older patients may be due to pancreatic exocrine insufficiency. In young adults it has been claimed that the pancreas secretes more than 10 times the necessary amount of enzymes to avoid steatorrhea. This margin may narrow in old age, but most cases of pancreatic exocrine insufficiency in the elderly seem to be due to chronic pancreatitis, although the cause of this may not be recognized. Alcohol-related pancreatitis is less common in the elderly than in younger adults. Late onset chronic pancreatitis produces less pain and progresses more rapidly to endocrine and exocrine pancreatic insufficiency. Because pancreatic cancer may present with pancreatic exocrine insufficiency, patients with this diagnosis need a structural evaluation of the pancreas.
Bile acid deficiency
Patients who do not deliver sufficient bile acid to the duodenum to solubilize fat develop steatorrhea due to incomplete fat digestion. This can be seen with primary biliary cirrhosis or other causes of severe cholestasis and in patients with extensive ileal resections who cannot reabsorb bile acid. This cause of maldigestion is not always considered, but can be managed with bile acid supplements.
Small intestinal bacterial overgrowth
Proper digestion and absorption in the small intestine depends on a germ-free environment. If bacterial counts build up, bile acid becomes deconjugated and can be absorbed from the lumen, lowering bile acid concentration and reducing fat absorption. Bacteria may disrupt the absorption of other nutrients, such as vitamin B 12 , or may ferment carbohydrate substrates. Patients may develop abdominal bloating, pain, diarrhea, and weight loss.
Bacteria can build up when stasis of luminal contents is due to structural problems such as jejunal diverticulosis or strictures, gastrocolic fistula, or upper tract surgeries. Small intestinal bacterial overgrowth (SIBO) also may develop with motility problems, such as seen with scleroderma, achlorhydria, or hypochlorhydria as seen with pernicious anemia or prolonged proton pump inhibitor therapy.
The frequency with which SIBO develops in older people is not clearly defined. Quantitative culture of luminal contents is deemed to be the gold standard test for SIBO with positive culture yielding greater than 10 5 bacteria/mL. Several different kinds of breath tests have been developed as “noninvasive” alternates, but technical issues mar performance statistics. Abnormal tests seem to occur more frequently in the older population, but the clinical significance of this observation is not clear.
Patients with symptoms and positive tests for SIBO should be given a trial of antibiotic therapy. A broad range of antibiotics has been used for this purpose, including trimethoprim/sulfamethoxazole, tetracycline, metronidazole, fluoroquinolones, and rifaxamin. When steatorrhea is prominent, antibiotics that kill the anaerobic bacteria that deconjugate bile acids are recommended. Patients should receive a short course of therapy (10–14 days) and the impact of therapy on symptoms should then be assessed. If results are favorable, no therapy is needed until relapse occurs (as is likely because antibiotics do not treat the underlying problem predisposing to SIBO). If relapses are frequent, long-term suppressive therapy may be required. If there is no response to the initial course of therapy, an alternative antibiotic should be selected, based on sensitivity studies.
Mesenteric vascular insufficiency
Acute loss of blood flow to the small intestine is a life-threatening medical emergency. Chronic reduction of blood flow as seen with progressive atherosclerosis of the mesenteric arteries can produce a syndrome of pain and weight loss. The pain is termed “intestinal angina” and occurs 1 to 3 hours postprandially. It is located in the periumbilical area and can be severe. Weight loss may be due to malabsorption, but is more likely due to sitophobia, avoidance of eating in an effort to limit pain. Diarrhea does occur sometimes. Diagnosis of this syndrome depends on recognizing the symptoms and their relation to meals in the setting of a patient with advanced atherosclerosis. Doppler sonography, magnetic resonance or CT angiography, or standard mesenteric angiography can be used for further evaluation. Revascularization or stenting can be used to treat this syndrome.
Diabetic steatorrhea
Diabetes can produce a watery diarrhea (see earlier discussion) or a fatty diarrhea. Three causes should be sought if steatorrhea is identified in a diabetic: celiac disease, SIBO, and pancreatic exocrine insufficiency.
Post-surgical steatorrhea
Many different surgeries can predispose to the development of diarrhea or steatorrhea. Gastrectomy can result in dumping syndrome and often causes a 10% to 15% loss of body weight attributed to maldigestion. Extensive small bowel resection will produce steatorrhea as a matter of course as the absorptive surface area is reduced. The onset of diarrhea may be delayed as it may depend on development of aggravating factors, such as bacterial overgrowth.
Miscellaneous Diarrheas
Sometimes patients will report “diarrhea” when other processes are present that they cannot describe adequately. Identification of these processes is important because their management is different from the management of diarrhea.
Fecal impaction
Patients with constipation may develop a fecal impaction, a mass of stool that is too large to be passed through the anus. Rectal distention causes relaxation of the internal anal sphincter and obstruction induces secretion proximal to the obstructing bolus. Liquid stool can flow around the impaction and may leak or be passed. The patient experiences loose stools that they report as diarrhea. A thoughtful digital rectal examination can identify impaction and should lead to effective treatment. Once the impaction is removed, the problem with loose stools should abate.
Fecal incontinence
Another condition that may be reported as “diarrhea” is fecal incontinence. Many patients will not report accidental passage of stool without prompting and it is essential to ask patients about incontinence. Fecal incontinence is not due to voluminous diarrhea alone; there must be compromise of the sensory or muscle function that ordinarily preserves continence (see the article by Leung and Rao, elsewhere in this issue).
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