Deborah Allen Irritable bowel syndrome (IBS) is the most common gastrointestinal (GI) complaint seen in primary care offices and is the most common diagnosis for gastroenterologists.1 It is classified as a “functional” GI disorder because there are problems with normal gut function; however, no identifiable organic or structural causes explain its development.1–3 A correlation appears to exist among abnormalities in GI tract motility, alterations in autonomic regulation, sensitivity in abdominal viscera, brain-gut interaction abnormalities, and changes within the GI flora.4–7 IBS is characterized by abdominal bloating, flatulence, abdominal pain, and bowel dysfunction.6 IBS has been defined by the American College of Gastroenterology as abdominal discomfort associated with altered bowel habits and symptoms of constipation, including infrequent stools, straining, passage of hard stools, and feelings of incomplete or difficult evacuation.7 The 1998 Rome II diagnostic criteria for IBS were updated in 2006 to Rome III, and these criteria are currently still being used for the diagnosis of IBS (Box 139-1).2,7,8 Additional features that support the diagnosis of IBS include abnormal stool passage (i.e., straining, urgency, or feeling of incomplete evacuation), changes in the form of feces, effort needed to defecate, passage of mucus, and bloating or sensation of abdominal distention.1,9 It is recommended that health care professionals also consider IBS if a patient reports abdominal pain or discomfort, bloating, or a change in bowel habit consistently for 6 months.1 In the past, IBS was described as spastic colon, mucous colitis, nervous bowel, spastic colitis, and functional bowel.5,10 Functional disorders are often characterized by intestine movement or intestine sensitivity because no known structural disorder is identified. Therefore the diagnosis is based on patient symptoms and the diagnostic criteria for each disorder.11 The lack of sensitive diagnostic criteria, a reluctance to seek care for fluctuating symptoms, faulty perceptions, ambiguities in defining the condition, absence of specific and reproducible examinations and markers, and potentially demeaning connotations of IBS sometimes cause health care providers, patients, and others to feel ill at ease with the diagnosis of IBS. These influences make accurate estimates of worldwide IBS prevalence difficult.1,2,9,12–14 Reports of prevalence vary widely from 2.5% to 37% worldwide,2,6,9,12–15 yet only 5% to 7% percent are diagnosed with the condition.5,10 Most epidemiologic studies demonstrate that IBS is up to 50% more common in females than in males, appears to be familial, and is estimated to affect 10% to 30% of the adult population in Western countries.1,5,9,10,16,17 Some studies show that the prevalence of IBS appears to be similar among racial groups.18 Other studies show an increase in whites and African Americans, but a lesser prevalence among Asians.17 The influence of socioeconomic status is also controversial. Zhu and colleagues found no difference in socioeconomic classes2; others reported low socioeconomic class as a risk factor for IBS.18,19 Although IBS symptoms can been seen in childhood, symptoms typically have their onset in late adolescence to early adulthood; peak prevalence occurs in the third and fourth decades of life, and the condition is usually diagnosed before age 50. However, IBS symptoms often persist into the seventh and eight decades of life.1,2,18,19 Annually, IBS accounts for approximately 3.5 million physician visits in the United States, affecting 10% to 15% of Western populations, and is the most common condition referred by primary care providers to gastroenterology specialists.1,3,9,13 The number of office visits for patients with IBS has been estimated to comprise 25% to 28% of all gastroenterology consultation office visits.9,15 Persons with IBS miss three times as many work days as do healthy individuals, see health care providers more often for GI and non-GI complaints, and consume 50% more health care resources than similar groups. The costs associated with IBS are an estimated $20 billion in direct and indirect expenses in the United States.9,15,19 Impairments to quality of life are often higher in patients with IBS, which affects personal and social relationships and overall well-being.2,14,15,17,18,20 The goals of clinical management are twofold: (1) to exclude the presence of underlying organic disease while considering the risk and expense of a thorough diagnostic evaluation; and (2) to provide support, education, and reassurance to optimize the quality of life of those for whom IBS has become a chronic condition. Research during the past decade has dramatically improved our understanding of the etiology of IBS as a complex, multifactorial disorder involving a number of physiologic processes including altered GI motility, microscopic inflammation, bacterial overgrowth, increased gut sensitivity, mental health problems, and brain-gut signal problems, with suspected genetic linkage; however, no specific physiologic reason has been identified.1,3–5,18 Studies have demonstrated that patients with IBS process sensory information from the gut differently than do persons without IBS.14 The signs and symptoms of IBS appear to be predominantly related to changes in central nervous system processing of sensory information; exaggerated normal intestinal motility patterns; or sensory abnormalities in the colon, rectum, or small intestine.6,9,10 A number of theories of the mechanisms for altered intestinal motility and sensitivity have recently evolved. Although altered motility is often mentioned as a cause of IBS, controversy remains about the exact electrical and contractile activity of the colon in IBS. Normal bowel motility predominantly consists of segmenting contractions that function to inhibit the transit of bowel contents. Any increase in segmenting contractions with decreased transit time results in constipation, whereas a decrease in contractions with increased transit time results in more frequent stools.10 In patients who have IBS, the colon delays the movement of feces, allowing an increase in absorption of the feces.5,9 This altered motility leads to changes in stool consistency. The increase in intestinal peristalsis and motility that usually follows the ingestion of a meal is thought to be increased in patients with IBS.3,19 More consistently demonstrated in IBS is an exaggeration of normal colonic motility in response to external and enteric stimuli, such as psychological stress, anxiety, anger, various drugs, acute intestinal infection, and (more recently discovered) small bowel bacterial overgrowth.1,2,5,6,10,13 Postinfectious IBS has been the topic of recent research; a few studies have demonstrated that as many as 10% to 30% of post–acute gastroenteritis patients with previously normal bowel function develop long-term symptoms suggestive of IBS.5,10,18 The exact cause of postinfectious IBS is unknown but could involve injury to the enteric nervous system, immune hypersensitivity, or chronic mucosal inflammation that results in an alteration of gut motility.1,5 Proponents of the postinfectious theory speculated that IBS patients are postinfectious and that efforts should be directed toward measures to prevent and treat severe cases of acute gastroenteritis.5,10,18 Research has also shown that the the use of antibiotics in acute gastroenteritis for the purpose of preventing IBS may reduce symptoms.3,5,9,10 Another factor possibly affecting the development of IBS is the role of small bowel bacterial overgrowth.3 Intestinal flora provides nutrition to the host, keeps the mucosal immune system in check, and regulates epithelial growth and function. However, it has been reported that a large portion of patients with IBS have small bowel bacterial overgrowth.3 Therefore treatment of IBS symptoms may be improved with the use of probiotics.3–5,9,10 Balloon distention studies used to determine the pathogenesis of IBS in the sigmoid, ileum, and colorectum demonstrate that painful symptoms at significantly lower pressures and higher pain frequency and severity are often seen in persons with IBS compared with healthy individuals. This concept, known as hyperalgesia, suggests that altered visceral sensation plays a role in the pathogenesis of IBS.6,16 Other diagnostic tests include endoscopy, radiology, stool samples (fecal calprotectin measurements, fecal ova and parasites, fecal occult blood), thyroid function tests, flexible sigmoidoscopy, and colonoscopy.5,10,15 However, there are no biochemical, histopathologic diagnostic tests that can determine all causes of IBS.1 Research suggests that with IBS there is increased sensitivity to mechanical stimulation in the small bowel and colon, increased or unusual somatic referral of visceral pain, and increased sensitivity to normal intestinal functions. Several possible mechanisms of visceral afferent dysfunction have been suggested to explain the increased visceral sensitivity in IBS. These mechanisms include altered receptor sensitivity at the viscus, increased excitability neurons of the spinal cord, and altered central modulation of sensation.3,9,16,18 Evidence suggests that abnormalities in extrinsic autonomic innervation of the viscera occur with functional bowel disorders and that neuroimmune interactions may mediate stress-induced GI responses.16,18 Research has focused on the role of enteric nervous system neurotransmitters, such as serotonin, in controlling intestinal motility and visceral afferent (sensory) responses to normal stimuli (gas, sugars, bile acids, fatty acids) and noxious stimuli (allergens, infectious agents, balloon distention).18 Eighty percent of the body’s serotonin is located in the gut, manufactured and released from enterochromaffin cells located in the mucosa. Increases in intraluminal pressures result in the release of serotonin.9 These neurotransmitters stimulate afferent fibers in the mucosa and initiate a peristaltic reflex, enhancing GI motility and mediating visceral pain.18 A preliminary study demonstrated increased plasma levels of postprandial serotonin in women with IBS compared with healthy controls.3 Serotonin, along with corticotropin-releasing hormone (CRH), may also play a role in mediating psychological, stress-induced GI responses through the brain-gut axis.13,16 Although defecating often relieves pain, stress and food increase it.5,19 Studies of the relationship between psychosocial factors and IBS suggest that although emotional responses to stress affect GI function and produce symptoms in all persons, these symptoms are believed to play a role in the development and pathogenesis of IBS symptoms to a greater extent in persons with IBS.1 Several studies have reported that persons with IBS have a greater incidence of psychosocial stressors and abuse than healthy individuals. It has also been shown that patients with IBS have increased incidences of psychiatric illnesses such as depression, anxiety, or other abnormal illness behaviors.1,10,13,16 In addition, patients diagnosed with IBS seek more professional medical advice, have increased absences from work, and request to be seen by a gastroenterologist more frequently than controls.3,9,19,20 People with IBS often believe that stress triggers their symptoms5; however, many physicians are reluctant to refer patients for psychological treatment.20 Abdominal pain must be present for an IBS diagnosis.1,6,8,13,18 The pain associated with IBS is often described as nonradiating, intermittent, and crampy; pain can occur anywhere but is usually located in the left lower abdominal quadrant.10,15,19,20 Symptoms frequently occur after food or alcohol consumption.10 Because IBS is a functional chronic disorder in which symptoms fluctuate over time, it is critical to establish the absence of nocturnal symptoms to diagnosis IBS.16,19 Diarrhea, constipation, or a pattern of alternating diarrhea and constipation may be reported in conjunction with abdominal pain.4,6,8,18 It is necessary to clarify what is meant by these complaints because normal patterns of defecation can range from three bowel movements per week to three bowel movements per day, so this needs to be defined by the individual patient’s norm. Mucus in the stool is sometimes reported. Complaints of abdominal distention, bloating, nausea, lethargy, and backache are common1,10,18,19 and most likely reflect increased sensitivity to normal amounts of intestinal gas rather than an actual increase in gas. The likelihood of organic disease is indicated by an acute onset of GI symptoms or an onset of symptoms in patients older than 50 years. Nocturnal symptoms, bloody or greasy stool, weight loss, malnutrition, evidence of GI bleeding, anemia, recurrent nausea, vomiting, and fever are incompatible with a diagnosis of IBS and require immediate diagnostic evaluation or referral.10,18,19 Although bleeding is not associated with IBS, it may occur secondary to an anal fissure or hemorrhoids aggravated by an alteration in bowel habits associated with IBS. However, careful diagnostic evaluation is required before rectal bleeding can be ascribed to distal benign causes. A complete health history should be elicited in the presence of abdominal pain with an alteration in bowel habits.10 The history should include a thorough investigation of the presenting symptoms, the associated symptoms, and the presence of nocturnal symptoms. The patient should be questioned about previous diagnostic evaluations for similar symptoms. A past medical history and family history of GI problems, such as colon cancer, inflammatory bowel disease, and celiac disease, should be obtained. These are often associated with other disease processes and need further evaluation. The patient should be asked about recent travel, GI infections, and the use of any prescription or over-the-counter medications that could cause diarrhea or constipation. A thorough review of diet, with particular emphasis on any food allergies or sensitivities such as lactose or fructose intolerance, should be undertaken.19 The review of symptoms should focus on the differential diagnoses for abdominal pain with an alteration in bowel habits. A menstrual history and gynecologic review of symptoms are essential in women to exclude urogenital sources of abdominal pain, such as pelvic inflammatory disease (PID), ovarian cysts, uterine fibroids, or endometriosis. A sensitive psychosocial history should be elicited to determine sources of stress, coping mechanisms, support systems, reactions to stress in the past, and the use of psychological counseling services to cope with past stressors. A history of physical or sexual abuse as a child or an adult should also be explored at some point. Patients with IBS often have symptoms consistent with other disease processes. Most patients with IBS have comorbidities including other functional gastrointestinal disorders (FGIDs); gastroesophageal reflux disease (GERD); psychiatric disorders such as depression, anxiety, and obsessive-compulsive disorders; chronic fatigue syndrome; fibromyalgia; gynecologic disorders; and asthma.1,16,18
Irritable Bowel Syndrome
Definition and Epidemiology
Pathophysiology
Altered Motility
Enhanced Visceral Sensation
Role of Enteric Neurotransmitters
Psychosocial Factors
Clinical Presentation
Comorbidities
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Irritable Bowel Syndrome
Chapter 139