The worldwide prevalence of IBS is estimated to be 7%-10% with wide geographic variability[3]. In the United States the prevalence of IBS is estimated to be approximately 10% to 15%[4] and one large European prospective, population-based cohort study estimated prevalence of 15.4%[5]. IBS is less common in people older than 50 compared with those younger than 50 (OR 0.75)[6] and is more common in women compared with men (OR 1.67)[7]. IBS may be associated with a number of other disorders including fibromyalgia, depression, chronic fatigue syndrome, non-cardiac chest pain and anxiety[4]. There is conflicting evidence regarding IBS prevalence and socioeconomic status[6,8,9] and this relationship remains unproven.

That the diagnosis and management of IBS relies on clinical symptoms highlights that the pathophysiology remains incompletely understood. Initial research in the early 20^th century utilizing direct visualization of the gastric mucosa in patients with gastrocutaneous fistulae provided the first scientific evidence that the gut is physiologically responsive to stressful emotional and environmental stimuli. Later studies showed that patients with IBS-type symptoms had an enhanced gastrointestinal motor response to various stimuli such as fatty meals, peptide hormones and psychological stressors and increased motility was sometimes associated with pain[10]. Recent advances in knowledge have, however, facilitated an increased understanding of the underlying disease processes, but it remains likely that there are multiple etiological factors involved. Those currently implicated in IBS symptom presentation include altered gastrointestinal motility, visceral hypersensitivity, post-infectious gastroenteritis, intestinal inflammation, altered gut microbiota, food sensitivity and interactions of the brain-gut axis[11]. IBS linked to brain-gut interactions is suggested by the association of IBS with anxiety, depression and other psychiatric conditions[1]. Furthermore, it is recognized that psychological stress exacerbates and exaggerates the symptoms of IBS and associated psychological and psychiatric co-morbidity negatively influence the patient experience of the condition[12]. Persistent post infectious gastroenteritis IBS-type symptoms are common in up to 20% of cases[1], and this is linked to an intestinal inflammatory etiology indicating an alternate pathogenesis to brain-gut interactions[13]. Further etiological factors for IBS development include alterations in gut microbiota and associated predisposing influences on both the microbiome and IBS symptoms including host genetics, stress, diet, antibiotic use and early life experiences[14]. Gut microbiota and their metabolites have notable influences on recognised IBS associations including the brain-gut axis, visceral hypersensitivity, gastrointestinal motility, intestinal barrier function and immune regulation[14]. Though causation is not established, the expanding science of the human gut microbiome and microbe-host interactions suggest gut microbial alterations play a key role in IBS pathophysiology[14]. These various pathophysiological factors may co-exist in the same patient, adding to the heterogeneity and complexity of understanding IBS and may, in part, explain the varying response to current symptom based treatments[15].

The Rome criteria are criteria that were devised by expert consensus for the diagnosis of FGIDs; these criteria define multiple different FGID including IBS. The most recent iteration of these criteria is the Rome IV, released in 2016. The diagnostic criteria for IBS by the Rome IV criteria are as follows[16]: Recurrent abdominal pain, on average, at least one day per week in the last 3 mo associated with two or more of the following: Pain related to defecation; Associated with a change in frequency of stool; Associated with a change in form (appearance) of stool. The criteria should be fulfilled for the last 3 mo with symptom onset at least 6 mo before diagnosis.

By the Rome IV criteria, the IBS subtype is classified based on the predominant symptom of constipation or diarrhea as follows[16]: IBS with predominant constipation (IBS-C); IBS with predominant diarrhea (IBS-D); IBS with mixed bowel habits (IBS-M); IBS unclassified (IBS-U).

This classification is based upon the percentage of different stool types as defined by the Bristol stool scale. IBS-C is diagnosed if > 25% are stool type 1 and 2 and < 25% are stool type 6 and 7; IBS-D is diagnosed if < 25% are stool type 1 and 2 and > 25% are stool type 6 and 7; and IBS-M is diagnosed if > 25% are stool type 1 and 2 and > 25% are stool type 6 and 7. IBS-U is diagnosed if the patient meets diagnostic criteria for IBS but stool type cannot be accurately categorized into one of the other subtypes.

Assessment for alarm features should be performed in all patients that meet the diagnostic criteria for IBS[17]. The aim of identifying alarm features is to allow consideration of further investigations in patients with signs/symptoms of other possible underlying conditions such as colorectal/ovarian cancer and inflammatory bowel disease. Alarm features include the following[16,18,19]: New onset, or overt, rectal bleeding or melena; Nocturnal pain or diarrhea; Iron-deficiency anemia; Unexplained weight loss; Family history of colon cancer, ovarian cancer, celiac disease, IBD; Fever; Age of onset > 50 years; Severe or progressively worsening symptoms; Abdominal/pelvic/rectal mass or lymphadenopathy; Recent change in bowel habits.

Although the prevalence of alarm features is high in IBS patients[18] the sensitivity of alarm features in predicting organic disease in patients with typical symptoms of IBS is low. This may be due to the fact that besides celiac disease, which a large systematic review demonstrated is four times as prevalent in patients with IBS compared with the general population[20], the prevalence of underlying organic disease is the same in patients with IBS as in the general population[3]. However, certain alarm features such as weight loss and anemia do offer high specificity for organic disease and the American College of Gastroenterology (ACG) state that the absence of alarm features should reassure the clinician that the diagnosis of IBS is correct[3].

IBS is a disease that is associated with significantly reduced health-related quality of life and impaired work productivity[3]. IBS patients utilize 50% more healthcare resources than matched controls without IBS and overall direct and indirect annual healthcare costs in these patients are estimated at $20 billion[3]. This increased cost can be attributed not only to increased medication use but also increased diagnostic testing and lost wages. In 1995, Talley et al[21] estimated the excess yearly direct healthcare cost of IBS in the United States to be $8 billion and extrapolating from that study, excess cost of approximately $800 million was estimated for radiology services in these patients. This highlights the importance of accurately defining the role of radiologic imaging in the investigation of patients presenting with IBS-type symptoms in order to rationalize the use of this expensive and, in certain jurisdictions, limited resource.

As well as increased costs, another concern regarding the over-utilization of radiologic diagnostic testing is the radiation exposure imparted as a result of plain radiography, nuclear medicine and CT imaging. Although there is evidence of significant costs associated with radiologic imaging in these patients there is a paucity of studies assessing radiation exposure in this patient group. Englund et al[22] demonstrated that over a 10-year period in Sweden, 149 IBS patients had a radiation exposure similar to that of a subgroup of patients with ulcerative colitis. A direct comparison of radiation exposure in IBS patients with that of the general population was not performed in this study so it is difficult to draw conclusions from these results. This result does, however, again demonstrate that radiologic imaging is still being used frequently in the investigation of patients with IBS.