Defecatory Dysfunction
Mark R. Ellerkmann
CONSTIPATION
Various subjective and objective definitions exist for constipation. Commonly they address frequency of bowel movements, stool consistency, and degree of difficulty with evacuation. Typically, less than three bowel movements per week, straining more than 25% of the time, sensation of incomplete evacuation, hard, inspissated stools (scybala), daily stool weights less than 35 g, and prolonged colonic transit have all been used to subjectively and objectively define constipation.
Differential Diagnosis
Although diet and stool bulk play an important role in the transit time of fecal material, constipation may be thought of as a disorder of gastrointestinal motility. Any number of etiologies can affect the motor function of the large intestine or its outlet from the pelvic floor (Table 23.1). These conditions range from underlying systemic diseases that directly impair bowel motor and sensory activity to secondary metabolic, endocrine, and neurologic disorders that affect motility and absorption. Functional disorders, such as irritable bowel syndrome (IBS), ileus, and colonic inertia, may contribute to symptoms of constipation. In contrast, mechanical obstruction with pelvic organ prolapse (POP), rectal prolapse, and neoplasm can lead to constipation from obstructed defecation. Dementia and limitations in a patient’s physical ability to get to a bathroom can play a role in the pathogenesis of constipation and fecal impaction as well. Poor nutrition and certain medications can also lead to constipation (Table 23.2).
Etiology
Systemic, Endocrine, and Neurologic Disorders
Diabetes mellitus, thyroid disease, and pregnancy are the most common underlying systemic causes of constipation. Symptoms tend to improve and become less severe after diabetic control is achieved or thyroid disease is corrected. Constipation in pregnancy has a reported prevalence of 11% to 38% (1). Etiologies include reduction in colonic motility and gut transit times because of the muscle-relaxing effects of progesterone, increased colonic water absorption related to increased aldosterone levels (2), and mechanical obstruction by the uterus. Less common but equally important systemic diseases known to cause constipation include collagen, vascular, and muscle disorders, such as systemic sclerosis, amyloidosis, dermatomyositis, and myotonic dystrophy. Metabolic disorders leading to electrolyte imbalances, such as hypercalcemia and hypokalemia, may also promote constipation, as may endocrinopathies such as porphyria, panhypopituitarism, pheochromocytoma, and glucagonoma.
Neural control of intestinal function is coordinated by the interrelationship of the enteric, sympathetic, and parasympathetic systems. Central nervous system lesions or injury involving the sacral nerves or spinal cord can compromise parasympathetic innervation of the bowel. Examples include trauma to the pelvic floor, lesions of the sacral cauda equina, injury to the lumbosacral spine, and meningomyelocele (3,4). Constipation can be associated with central neuropathies, such as multiple sclerosis, Parkinson’s disease, and Shy-Drager syndrome. Multiple sclerosis, for example, has been shown to compromise bowel motility both directly (prolonged transit time, possible rectosphincteric dyssynergia) and indirectly (physical inactivity, medication side effects) (5). High spinal cord lesions may also be associated with constipation, even though lower colonic reflexes remain intact.
Peripheral neuropathies responsible for constipation may be either acquired or congenital. Patients who acquire Chagas’ disease commonly
present with progressively worsening symptoms of constipation and abdominal distention caused by segmental megacolon secondary to enteric neuronal degeneration. Nongastrointestinal neoplasms, such as carcinoid tumors and small cell carcinoma of the lung, have been associated with paraneoplastic visceral neuropathy, which can result in chronic constipation. The pathogenesis of this disorder is not entirely clear but may be related to either myenteric plexus inflammation or neuronal degeneration.
present with progressively worsening symptoms of constipation and abdominal distention caused by segmental megacolon secondary to enteric neuronal degeneration. Nongastrointestinal neoplasms, such as carcinoid tumors and small cell carcinoma of the lung, have been associated with paraneoplastic visceral neuropathy, which can result in chronic constipation. The pathogenesis of this disorder is not entirely clear but may be related to either myenteric plexus inflammation or neuronal degeneration.
TABLE 23.1 Differential Diagnosis of Constipation | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Congenital neuropathies may lead to functional obstruction and chronic constipation. Hirschsprung’s disease, the best-known of these disorders, is characterized by a congenital absence of intramural ganglion cells of both the submucosal and myenteric plexuses. The variability of clinical symptoms and poor correlation between symptoms and aganglionic segment length may result in delayed diagnosis in adulthood (6). Hallmark findings in adults include absence of the rectosphincteric inhibitory reflex, failure of the internal anal sphincter to relax after manometric distention, and absence of neurons on rectal wall biopsy (7). Other disorders of the enteric nervous system can include abnormally functioning or diminished concentration of enteric neurons (zonal colonic aganglionosis) (8) or loss or malfunction of inhibitory motor neurons, which serves as the pathophysiologic basis for disinhibitory motor disease (intestinal pseudo-obstruction and sphincteric achalasia) (9).
Functional Constipation
Constipation has been traditionally defined as three or fewer bowel movements per week. However, patients may refer to other symptoms of defecatory dysfunction, including dyschezia, excessive straining, digital manipulation to facilitate defecation, abnormal variations in stool consistency, or sensations
of incomplete emptying. In one study, only one third of patients complaining of constipation related this complaint to infrequent defecation. More common complaints included the inability to defecate when desired (34%), the passage of hard stools (44%), and straining associated with defecation (52%) (10). Given the range of symptoms related to constipation as well as the subjectivity of self-reporting, attempts have been made over the years to classify bowel dysfunction in terms of functional gastrointestinal disorders (FGIDs) that are identified only by symptoms. To this end, the recently revised Rome III criteria are proposed to classify the functional bowel disorders, including functional diarrhea. The FGIDs will be discussed in more detail later in this chapter.
of incomplete emptying. In one study, only one third of patients complaining of constipation related this complaint to infrequent defecation. More common complaints included the inability to defecate when desired (34%), the passage of hard stools (44%), and straining associated with defecation (52%) (10). Given the range of symptoms related to constipation as well as the subjectivity of self-reporting, attempts have been made over the years to classify bowel dysfunction in terms of functional gastrointestinal disorders (FGIDs) that are identified only by symptoms. To this end, the recently revised Rome III criteria are proposed to classify the functional bowel disorders, including functional diarrhea. The FGIDs will be discussed in more detail later in this chapter.
TABLE 23.2 Drugs Associated with Constipation | ||||||||||||||||||||||||||||||||||||||||||||||||||
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Idiopathic Constipation
In approaching the differential diagnosis of constipation, it is necessary to consider and exclude conditions that could contribute to the symptom. When concurrent disease processes, diet, medications, and psychological factors cannot be identified, attempts to classify constipation as idiopathic may be based on age of presentation, colonic transit times, or anorectal sensory and motor dysfunction. Commonly, colonic transit times are used based on the presumption that there is some underlying colonic or anorectal motor dysfunction responsible for the disorder. To characterize constipation on this basis, four subtypes have been classified: (a) normal colonic and rectal transit time; (b) slow colonic transit time only; (c) slow rectal transit time only; (d) slow colonic and rectal transit times (11) (Table 23.3).
Age and Constipation
In children, chronic constipation may involve both physiologic and psychological factors. Children may present with symptoms of abdominal pain and distention when constipation is associated with fecal impaction with or without rectal (megarectum) and sigmoid (megacolon) dilation. Affected children may report the absence of a defecatory urge. Alternatively, they may demonstrate a conscious inhibitory or withholding reflex (learned response) related to previous experiences with dyschezia (possibly related to anal fissures or attempts to evacuate large stools) (7). Although decreased transit times localized to the distal colon and rectum have been demonstrated in many children with chronic constipation (12), manometric thresholds for rectal sensation and resting anal sphincter pressures are often normal (13,14). With the exception of children with Hirschsprung’s disease, manometry usually demonstrates normal relaxation of the internal anal sphincter. Conversely, studies suggest that roughly two thirds of constipated children with encopresis suffer from anismus or rectosphincteric dyssynergia (failure to relax the puborectalis and external anal sphincter) (7,15) (Fig. 23.1). The role of dietary fiber appears to be important; several studies have demonstrated that fiber alone is independently negatively correlated with chronic constipation and that an inadequate daily intake of fiber is a risk factor for chronic constipation in children (16,17).
Idiopathic constipation is twice as common in females as males in the young to middle-aged population (10). Of the patients who remain refractory to therapeutic intervention, 30% have normal colonic transit studies (18). Several studies have suggested that this subset of individuals has more psychopathology, including depression, than those individuals with delayed transit times (19,20), but there appears to be little efficacy in using psychological
factors to characterize subtypes of idiopathic constipation (21).
factors to characterize subtypes of idiopathic constipation (21).
TABLE 23.3 Diagnostic Algorithm for Idiopathic Constipation | |
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 FIGURE 23.1 ● Colonic transit study of a patient with rectosphincteric dyssynergia or colonic stricture on day 5 after ingestion of one Sitzmark capsule. The progression of markers to the rectum was normal. |
There is an exponentially increased prevalence of constipation after the age of 65 years (10). Although it is generally accepted that age does not significantly affect colonic motor function in healthy individuals, this increase in prevalence could result from chronic stress to the enteric nervous system resulting in denervation and neuronal loss. This may be secondary to underlying systemic or colonic disorders or side effects from medications (7). Conditions affecting elderly patients, such as changes in mental status (dementia, Alzheimer’s disease, confusion) and factors associated with mobility and bathroom access, may contribute to delayed defecation, which, in turn, may contribute to fecal impaction, a significant problem in elderly patients (22). Longstanding dilation of the rectum and rectosigmoid may contribute to denervation, diminished sensation, and worsening constipation.
Evaluation
The evaluation of the constipated patient begins with a careful history, with special consideration to the age of onset and duration of symptoms. Symptoms present since birth or childhood suggest
an underlying congenital etiology. In contrast, constipation occurring later in life tends to be an acquired disorder. A sudden or recent change in bowel habits suggests an underlying organic lesion, whereas chronic symptoms usually represent a functional bowel disorder. A review of symptoms with respect to defecatory dysfunction must include questions regarding frequency and consistency of bowel movements, the presence of melena or hematochezia, the time required for a bowel movement, and the need to strain or digitally facilitate evacuation. Associated symptoms of dyschezia, obstipation, encopresis, incomplete defecation, anismus, fecal incontinence, abdominopelvic pain, or bloating must also be reviewed.
an underlying congenital etiology. In contrast, constipation occurring later in life tends to be an acquired disorder. A sudden or recent change in bowel habits suggests an underlying organic lesion, whereas chronic symptoms usually represent a functional bowel disorder. A review of symptoms with respect to defecatory dysfunction must include questions regarding frequency and consistency of bowel movements, the presence of melena or hematochezia, the time required for a bowel movement, and the need to strain or digitally facilitate evacuation. Associated symptoms of dyschezia, obstipation, encopresis, incomplete defecation, anismus, fecal incontinence, abdominopelvic pain, or bloating must also be reviewed.
Medications (prescription, nonprescription, and alternative) should be reviewed in detail because many have constipating side effects (see Table 23.2). Chronic laxative use or abuse is a common precipitating factor contributing to chronic constipation. Stimulant laxatives such as the anthraquinones (aloe, senna, cascara), bisacodyl/castor oil, and the polyphenolic derivatives can cause degeneration of Meissner’s and Auerbach’s plexuses through neurotoxicity (10,23).
Patients should be questioned regarding a family history of both benign and malignant intestinal disorders. Psychosocial issues must also be addressed to detect any concurrent psychological diagnoses, history of emotional disorders, physical or sexual abuse, familial dysfunction, and other life stressors. A careful review of past medical, surgical, gynecologic, and obstetric history is essential.
Physical examination should include a focused abdominal, pelvic, and neurologic evaluation to rule out extraintestinal causes of constipation. Abdominal examination should include an assessment of previous incision sites and a search for ventral and inguinal hernias. Distention, tympany, and the presence of masses or hepatosplenomegaly should be documented. The presence of bowel sounds and any abdominal discomfort should be quantified and the location and quality described.
Rectal and pelvic examinations are essential. Typically performed in the dorsal or semi-Fowler’s lithotomy position, a careful systematic evaluation of pelvic organ support is undertaken using the Pelvic Organ Prolapse Quantification (POPQ) method. An overall stage of prolapse and compartment-specific stages are assigned. If present, attempts should be made to qualify and describe site-specific defects, especially with respect to anterior and posterior compartments. An assessment for perineal descent and rectal prolapse should be done, and when present the type of rectal prolapse should be documented. Perineal examination should also look for any deformity, presence of surgical or traumatic scarring, ongoing sepsis, “dovetail sign” or flattening of the bilateral gluteal creases, or atrophy of the gluteal or perineal muscles. Rectal examination may reveal a stricture from previous anorectal surgery or trauma or may detect a neoplasm. The texture and amount of stool in the rectal vault should be noted. A large, hard mass of feces suggests impaction. Sphincter tone and symmetry should be assessed. With the patient straining, the presence of a paradoxical contraction of the puborectalis may indicate rectosphincteric dyssynergia. Neurologic examination should include an assessment of autonomic function and reflexes, including lower extremity deep tendon reflexes as well as pelvic and perineal sensation and bulbocavernosus and clitoral-anal reflexes.
In the patient with acute complaints of altered bowel habits, with a family history of colorectal cancer, or in the age group appropriate for colorectal cancer screening, colonoscopy, double-contrast barium enema, or computed tomographic colonography should be performed.
If there is no evidence suggesting an underlying systemic or organic etiology, conservative therapy may be pursued. For patients failing to respond to initial therapy, a 1- to 2-week bowel diary and a measurement of colonic transit time with either radiopaque markers or scintigraphic techniques are the most useful diagnostic investigations (24). Further testing and diagnostic studies should be tailored to the specific complaint (see Table 23.3).
Treatment
Most patients presenting with uncomplicated idiopathic constipation may be treated conservatively with modifications in diet and toileting behavior, fiber supplementation, and laxatives. If fecal impaction was diagnosed on initial evaluation, the patient must first be disimpacted. Twice-daily enemas or oral polyethylene glycol may be used to facilitate this. For severe constipation, biofeedback and other pharmacologic agents may be used. If symptoms persist after failure of escalating medical therapy, diagnostic studies evaluating colonic and anorectal function should be undertaken.
Conservative Behavioral Therapy
Conservative therapy begins with patient education. Most patients require reassurance that their condition is not life-threatening and can be successfully managed. Regular toileting strategies to
prevent impaction are often used with children as well as with patients suffering from dementia, physical handicaps, and neurogenic constipation. Postprandial colonic motility can be enhanced, with behavior modification aimed at encouraging morning and postprandial defecation. Other initial recommendations include reducing excessive use of laxatives or cathartics, increasing daily fluid and fiber intake, and behavioral modification, including daily exercise. Biofeedback using visible or audible signal recordings from rectal manometric or electromyographic monitoring may be useful in treating chronic constipation related to pelvic floor dyssynergia (25).
prevent impaction are often used with children as well as with patients suffering from dementia, physical handicaps, and neurogenic constipation. Postprandial colonic motility can be enhanced, with behavior modification aimed at encouraging morning and postprandial defecation. Other initial recommendations include reducing excessive use of laxatives or cathartics, increasing daily fluid and fiber intake, and behavioral modification, including daily exercise. Biofeedback using visible or audible signal recordings from rectal manometric or electromyographic monitoring may be useful in treating chronic constipation related to pelvic floor dyssynergia (25).
Fiber
Fiber is a bulking agent that increases fecal volume and density. Fiber consists of insoluble and soluble components that vary depending on the source. The cell wall in fiber resists digestion and contributes to the physical bulking property. It may also serve as a substrate for bacterial proliferation and gas production, which may stimulate colonic motility. It is hypothesized that the therapeutic effect of fiber on large bowel function is multifactorial. First, through enhancing bacterial metabolism and fermentation, fiber may enhance the absorption of bacterial metabolites, such as secondary bile acids. Second, gas production leads to colonic distention and increases in intraluminal pressures, which triggers peristaltic activity. Third, the presence of fiber promotes intraluminal water absorption, increasing fecal bulk and consistency (26).
Burkitt et al first advocated the efficacy of dietary fiber in the early 1970s (27). Bowel frequency, stool weight, and intestinal transit times were compared between African and British cohorts. The authors concluded that the high prevalence of constipation in Western societies was associated with a diminished intake of dietary fiber. The role of fiber in the pathogenesis and prevention of constipation has been difficult to ascertain. Several studies have failed to detect a difference in dietary fiber intake in constipated patients versus healthy controls (28, 29, 30). Most studies demonstrate a beneficial effect of bran in treating constipation in patients with IBS (31, 32, 33) and diverticular disease (34, 35, 36). A meta-analysis of 27 studies investigating the relationship between dietary fiber and bowel function found that constipated patients continued to have lower stool weights and longer transit times despite being maintained on high-fiber diets (37). In another meta-analysis of 36 separate trials evaluating laxative and fiber therapy for the treatment of chronic constipation, Tramonte et al found improved stool consistency, decreased abdominal pain, and an increase in weekly bowel movement frequency in patients treated with both daily fiber supplements and laxatives (38). The data could not determine, however, whether fiber was superior to laxatives or whether one type of laxative was better than another.
The accurate assessment of fiber intake is often difficult. Although the recommended daily intake of fiber is 25 to 35 g, or 10 to 13 g per 1,000 kcal (39), the average American typically consumes only 14 to 15 g daily. Fiber therapy may be recommended for patients who have constipation without evidence of impaction, megacolon or megarectum, or obstructing gastrointestinal lesions (Table 23.4). Patients may be started on a high-fiber cereal and should be encouraged to continue daily fiber consumption, increasing the amount to 25 to 35 g/d. Intake of six to eight 8-oz glasses of water per day is recommended with this fiber load. Bloating can be a side effect that typically resolves
over weeks. If bloating persists, a different type of fiber supplement or type of cereal may be substituted.
over weeks. If bloating persists, a different type of fiber supplement or type of cereal may be substituted.
TABLE 23.4 Fiber Content | |||||||||||||||||||||||||||||||||||||||||||||||||
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Laxatives
The use of laxatives is widespread in Western society, especially in the elderly population (40). Laxatives may be classified by their mechanism of action and content (Table 23.5). Bulk-forming laxatives include both natural (psyllium) and synthetic (methylcellulose, polycarbophil) components, which increase the water content and bulk volume of stool. The mechanism of action is similar to that of fiber, and the net effect of bulk-forming laxatives is demonstrated by decreased colonic transit times, increased stool mass and density, and improved stool consistency (11).
TABLE 23.5 Laxatives: Mechanism of Action and Content | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Emollient laxatives include docusate salts and mineral oil. The anionic action of docusate salts decreases stool surface tension, thereby enhancing the penetration and absorption of intestinal fluids, which results in softened stools. Docusate salts may also alter intestinal mucosal permeability, promoting absorption of other laxatives. Their overall efficacy in the treatment of chronic idiopathic constipation has been questioned because studies have failed to demonstrate objective improvement in defecatory frequency, colonic transit
times, and stool weights (7). Mineral oil, administered orally or rectally as an enema, also works as an emollient to penetrate and soften stool.
times, and stool weights (7). Mineral oil, administered orally or rectally as an enema, also works as an emollient to penetrate and soften stool.
Hyperosmolar laxatives include nonabsorbable sugars, such as lactulose and sorbitol, as well as glycerine and polyethylene glycol (GoLYTELY). These agents work by increasing intracolonic osmolarity, which promotes water absorption by stool with subsequent softening. Sorbitol and lactulose are poorly absorbed and are ultimately hydrolyzed by colonic coliform bacteria. Through hydrolysis, lactic, acetic, and formic acids are created and increase intracolonic osmolarity. Side effects include abdominal bloating and flatulence. Polyethylene glycol is not hydrolyzed and is typically associated with fewer symptoms of bloating and flatulence. Polyethylene glycol is usually used for preoperative bowel preparation; however, it may also be used in cases of severe constipation (11).
Saline laxatives include magnesium-containing solutions such as magnesium sulfate, phosphate, and citrate. Saline laxatives increase colonic osmolarity, which, in turn, results in increased water absorption and subsequent stool softening. Administered by enema or suppository, saline laxatives can give rise to mineral and metabolic imbalances and, in patients with renal insufficiency, magnesium toxicity (11).
Stimulant laxatives are typically indicated if bulk or osmotic laxatives are not effective. They include castor oil, the diphenylmethanes (phenolphthaleins, bisacodyl), and the anthraquinones (senna, aloe, cascara sagrada, and danthron). Castor oil, after intestinal conversion to ricinoleic acid, stimulates intestinal secretion and motility. The diphenylmethanes act directly to stimulate colonic motility and small intestine water absorption. The anthraquinones, in contrast, are catalyzed by intestinal microorganisms and promote colonic peristalsis by altering intraluminal fluid and electrolyte composition (7). Stimulant laxatives may be abused, and chronic daily use may lead to diarrhea, electrolyte abnormalities, and dehydration. However, use up to two or three times per week may be undertaken for longer periods.
Prokinetic agents include drugs that directly stimulate gastrointestinal motor activity. The efficacy of metoclopramide, cisapride, cholinergic agonists such as bethanechol, cholinesterase inhibitors such as neostigmine, and serotonin agonists in the treatment of chronic idiopathic constipation is questionable. Metoclopramide, for example, appears to be more effective in treating upper gastrointestinal motor disorders, whereas studies addressing the efficacy of cisapride report conflicting results. Current research is examining the facilitatory role of serotonin agonists on enteric cholinergic transmission and opioid receptor antagonist therapy in the treatment of chronic constipation (7).
MOTILITY DISORDERS
Megacolon and Megarectum
Megacolon and megarectum may occur separately or together and may be divided into either primary or secondary entities (7). Primary megacolon or megarectum is usually present from birth and is associated with an underlying neurologic pathology. Although Hirschsprung’s disease is the most classic example, other possibilities include meningomyelocele and other lumbosacral spinal cord lesions. Secondary megacolon or megarectum is an acquired disease state usually found in children and elderly people. It may follow bowel surgery resulting in an anastomotic stricture (see Fig. 23.1) and is usually associated with constipation or defecatory dysfunction. Diagnostic criteria are based on radiographic (Fig. 23.2) and manometric findings, including increased rectal compliance and elasticity, decreased rectal sensation, increased sensory thresholds, and diminished internal anal sphincter relaxation (41).
 FIGURE 23.2 ● Contrast enema showing megacolon above an anastomotic stricture. |
Functional Gastrointestinal Disorders
Attempts to characterize IBS date back to 1820, when Powell first described a triad of pain, bowel dysfunction, and flatulence (42). It was not until 1962 that the syndrome was described in more detail (43), with the first classification of all the FGIDs appearing in 1979 (44). The Manning criteria (45) and the Kruis criteria (46) formed the basis for the first internationally recognized classification system for IBS, the Rome criteria. Since their introduction in 1988, the Rome criteria have become the gold standard for the diagnosis of FGIDs (47). The FGIDs are identified only by symptoms. Rome I criteria recommended that the diagnosis of IBS be based on the presence of abdominal pain or discomfort associated with a chronic change in bowel habit and two or more supporting criteria. Rome II criteria recommend that the diagnosis of IBS be based on the presence of two of the three main diagnostic criteria alone and provide consensus statements for each of the 25 FGIDs located throughout five anatomic regions (48). In 2006, a further revision of the Rome II criteria was published (Rome III) that further refined the diagnostic criteria for the FGIDs and their respective treatment options (49).
The category of functional bowel disorders includes symptoms related to the middle and lower gastrointestinal tract. This group is further subclassified by Rome II and III criteria into the following categories:
IBS
Functional abdominal bloating
Functional constipation
Functional diarrhea
Unspecified functional bowel disorders
By definition, these diagnoses presume the absence of biochemical or structural etiologies, and symptoms must have occurred for the first time at least 6 months before the patient presents and their presence on at least 3 days per month during the past 3 months would indicate current activity (49).
IBS is a poorly understood, chronic disorder characterized by episodic abdominal pain and changes in bowel habits. In addition to gastrointestinal and defecatory dysfunction, individuals with IBS may also suffer from sleep disturbances, sexual and lower urinary tract dysfunction, and other nongastrointestinal pain syndromes (50). About 60% of patients report abdominal pain or discomfort as their primary complaint. Symptoms characterizing defecatory dysfunction appear to be equally divided between diarrhea-predominant IBS, constipation-predominant IBS, and a variation of the two (51).
Similar to other chronic functional syndromes, a conceptual model involving the interplay of cognitive, behavioral, psychological, genetic, infectious, dietary, and physiologic components has been developed to serve as a framework for understanding the multiple possible factors that may contribute to IBS symptoms. Because there is no single biochemical, physiologic, neurologic, or psychological marker for IBS, researchers have stressed the interrelationship of these multiple components.
Cognitive factors, including abnormal coping mechanisms; misconceptions regarding disease, nutrition, and medications; and illness behavior are common in patients with IBS. Behavioral factors, such as traumatic or stressful events, are often correlated to the first onset of IBS symptoms and have been associated with changes in stool pattern, abdominal pain, and defecation frequency (52,53). IBS is diagnosed more frequently in patients with a history of prior psychological trauma or physical or sexual abuse, especially if incurred during childhood (54,55). Concurrent psychological disorders have been diagnosed in 42% to 61% of patients and include depression, anxiety, panic, and somatization disorders (50,56). Genetic factors may also play a role in the development of IBS because symptoms also appear to be more common in first-degree relatives (57). Infectious disease may in some way be responsible for triggering IBS because several studies have shown an increased risk for IBS symptoms after gastrointestinal infection (58,59). Histologic and biochemical studies have demonstrated evidence of long-term, persistent mucosal inflammation and changes in mucosal permeability in predisposed individuals suffering from IBS symptoms following an initial infectious insult.
There is little evidence to support a causal relationship between specific diet and the development of IBS. Patients intolerant or allergic to specific foods do not necessarily experience improvement of IBS symptoms when these food types are removed from their diets (50,60).
Many symptoms of IBS are consistent with dysfunction of the sensory and motor function of the enteric nervous system. These include dysfunction of neuroenteric regulation resulting in altered intestinal motility, myoelectrical activity, tone and compliance, sensation, and fluid and electrolyte absorption. Unfortunately, correlations between these alterations and IBS symptoms remain weak, raising the question of clinical relevance.
Diagnostic Criteria
Irritable Bowel Syndrome
IBS is characterized by abdominal pain or discomfort associated with defecation or a change in bowel habit. Often having a chronic, relapsing course, symptoms of IBS often overlap with those of other FGIDs, and the diagnostic criteria are listed in Table 23.6 (49). Supporting symptoms may help to classify patients, according to Rome II criteria, further into diarrhea- or constipation-predominant IBS. These include the following (61):
TABLE 23.6 Functional Gastrointestinal Disorders | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Fewer than three bowel movements per week
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