Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by altered bowel habits and chronic abdominal pain. Population-based studies estimate its prevalence at between 10% and 15%, with a female-to-male predominance of 2:1 and an initial presentation at between 30 and 50 years old.1 The most commonly diagnosed GI disorder, IBS constitutes 25% to 50% of referrals to gastroenterologists. Even though only 15% of those affected seek medical attention, IBS has significant economic and social effects; it is the second leading cause of work absenteeism in the United States, after the common cold, and was estimated to cost $1.7 billion in 2000.2 Total health care expenditures for patients with IBS are noted to be 49% higher than those for control populations, with the majority of excess health care costs attributable to medical care unrelated to lower GI problems.3
Although 10% to 15% of Americans report symptoms of IBS, providers often feel ill-equipped to deal with these patients.4 Limited knowledge of the syndrome's pathophysiology and a lack of effective treatment options leave both clinicians and patients frustrated. PAs need the tools to better assess, diagnose, and treat patients with IBS.
Pathophysiology
The etiology of IBS remains unclear. Several studies show that affected persons have abnormal GI motility in response to a number of stimuli, including meals, distention, stress, and certain chemicals; however, no one predominant pattern of motor activity has emerged as a marker.5
Visceral hypersensitivity has also been reported. While 50% to 70% of patients with IBS have visceral pain thresholds below the normal range, they show normal— in some studies, elevated—somatic pain thresholds. 6 It remains unclear whether visceral hyperalgesia is mediated by the CNS, local GI innervation, or a combination of the two.
Nervous system dysfunction Many experts argue a breakdown in the interaction between the GI tract and the brain. Bidirectional communication between the CNS and the gut is essential in both health and disease. The autonomic nervous system communicates emotional changes to the gut, while the CNS is involved in the perception of events in the gut. A dysfunction in this communication may contribute to the dysfunction seen in IBS. Studies using positron emission tomography and functional MRI show abnormal CNS processing of noxious visceral stimuli.4,7 Potential markers include serotonin, calcitonin gene-related peptide, substance P, bradykinin, tachykinins, and neurotrophins.2,8 A number of the new medications marketed for IBS target serotonin. This neurotransmitter plays a role in the stimulation of intestinal secretion, peristalsis, and the function of visceral pain receptors through the 5-hydroxytryptamine3 (5-HT3) and 5-HT4 pathways.9
Role of the psyche The dysregulation of the braingut axis may also help explain the role of psychosocial factors and the high rate of psychiatric comorbidity in persons with IBS. Clinical observations show that patients often suffer exacerbations during times of elevated stress. Furthermore, patients with IBS who do not seek medical attention are psychologically indistinguishable from healthy controls; however, those who do seek care exhibit increased anxiety, depression, phobias, and somatization.10 Patients who seek care are also more likely to have a history of physical or sexual abuse.11 Recent studies suggest that corticotrophinreleasing factor (CRF) may play a role. In a normal GI tract, reaction to stress may be mediated by CRF, a peptide released from the paraventricular nucleus. The overactivity of brain CRF and the CRF-receptor signaling system contributes to anxiety disorders and depression. In patients with IBS, IV administration of CRF increases abdominal pain and colonic motility to a higher degree than in normal controls.12
Other theories include microscopic inflammation, small bowel bacterial overgrowth, and a postinfectious etiology. There is a 20% to 30% incidence of persistent IBS symptoms 1 year after bacterial gastroenteritis.13 Heredity may also play a role, but the relationship between genetic factors and learned behavior is still unclear.
Diagnosis
Because IBS is a functional disorder for which no specific diagnostic test exists, many providers view it as a diagnosis of exclusion. The American College of Gastroenterology and the American Gastroenterological Association (AGA) encourage a cost-effective approach with a limited work-up for patients without alarm features.
Differential diagnosis In the workup of patients with possible IBS, conditions such as inflammatory bowel disease, infection, celiac sprue, adenocarcinoma of the colon, and lactose intolerance must be considered, as must various non-GI diseases and functional disorders 14 (see Table 1). Symptom details such as volume, frequency, and consistency of stool are important. Commonly seen upper GI symptoms that are associated with IBS include reflux, dysphagia, early satiety, intermittent dyspepsia, nausea, and noncardiac chest pain.15 Patients also commonly complain of a wide variety of extraintestinal symptoms, including bronchospasm, dysmenorrhea, dyspareunia, polyuria, and low back pain. They are also more likely to suffer from fibromyalgia, temporomandibular disorder, and chronic pelvic pain, and they are three times as likely to undergo hysterectomy and other surgical procedures.16,17 Be alert to symptoms that are not consistent with IBS, such as anorexia, malnutrition, weight loss, or pain that is progressive and affects sleep 16,18 (see Table 2). Other important aspects of the history include medications and social, family, travel, and dietary histories.
The clinical manifestations of IBS vary widely. Patient subgroups are described as constipation-predominant, diarrhea-predominant, and pain-predominant. While classifying patients into subgroups may be helpful fordirecting treatment, many patients have fluctuating symptoms or do not classically fit into one of the three groups. IBS is best characterized by changes in bowelthat IBS is due to a neuralgic dysfunction of the gut and movement frequency or appearance and abdominal pain that is relieved by defecation. Some patients report bloating, distention, urgency, a feeling of incomplete evacuation, and the presence of mucus in the stool.14
Physical examination A detailed physical examination serves to screen for findings inconsistent with IBS and to provide reassurance that the patient's concerns are being seriously considered. The abdominal examination may reveal mild diffuse or left lower quadrant tenderness, but findings such as organomegaly, a mass, or ascites are inconsistent with the diagnosis. In women, a pelvic examination is often indicated, and for patients with complaints of incontinence or dyschezia, a rectal examination can help identify a lax sphincter or paradoxical pelvic floor muscle contraction.
Diagnostic criteria To standardize the diagnosis of IBS based on positive symptoms, the Manning criteria were formulated in 1978.19 In 1992, in an effort to standardize clinical research protocols, an international working team designed the Rome criteria, which were revised in 1999 and again in 200618 (see Table 3). The AGA recommends a diagnosis based on identifying positive symptoms with the Rome criteria and excluding, in a cost-effective manner, other conditions with similar presentations. 20 In the absence of alarm features, the specificity of the Rome I criteria for IBS is greater than 98%.21