Abstract
Irritable bowel syndrome (IBS) is another condition of the “evil quadruplets.” It often coexists with endometriosis and adds to the pain of this condition. The mainstay is pain that is worsened by food and improved by defecation. It is also important to remember that IBS is diagnosed based on symptoms, and endoscopy is often performed in those patients is done to rule out any other bowel disease. This condition is best managed by a gastroenterologist but it is important to note that quite a large number of patients with this condition have spasm of pelvic floor muscles and treatment of that spasm may improve some of the IBS symptoms.
Irritable bowel syndrome (IBS) is another condition of the “evil quadruplets.” It often coexists with endometriosis and adds to the pain of this condition. The mainstay is pain associated with change in bowel habit. It is also important to remember that IBS is diagnosed based on symptoms, and endoscopy is often performed in those patients is done to rule out any other bowel disease. This condition is best managed by a gastroenterologist but it is important to note that quite a large number of patients with this condition have spasm of pelvic floor muscles and treatment of that spasm may improve some of the IBS symptoms.
Introduction
Irritable bowel syndrome (IBS) is an important member of disorders of gut–brain interaction. It is a chronic disease with recurring periods of exacerbation. It is defined by the presence of abdominal pain in association with change in bowel habits in the absence of detectable organic disease. As the most commonly diagnosed gastrointestinal (GI) condition, it is often part of the differential diagnosis in the evaluation of chronic pelvic pain. Globally, the prevalence of IBS varies greatly, with South America having the highest prevalence (21%) and Southeast Asia the lowest (7%). The prevalence of IBS in North America is 12% [1]. It is most commonly found in women, and prevalence seems to decline with age, decreasing by 25% in patients older than age 50 [1, 2. In a survey of 1,924 patients with a history of GI symptoms, 56.9% met criteria for IBS; however, 43.1% of these had not been formally diagnosed. Still, the impact on quality of life is significant [3]. In some studies, up to 70% of patients with IBS symptoms do not consult a physician; nevertheless, the disease accounts for $20 billion annually in total direct and indirect costs, including medications [41, 4].
Pathophysiology
The pathogenesis of IBS is heterogeneous, complex, and, likely, multifactorial. Traditionally, the focus has been on GI motility, visceral hypersensitivity, and psychosocial factors. More recently, studies have focused on alternate potential causes of IBS, including inflammation, alterations in microbiota, bacterial overgrowth, and food sensitivity. Studies evaluating the role of genetics are being pursued.
Gastrointestinal Dysmotility
Normally after meals, increase in colonic motility occurs by an irregular alternation of quiescence, sporadic nonpropagating contractions, and progression of intestinal contents by propagating movements. In IBS, however, there is increased frequency and irregularity of luminal contractions. In constipation-dominant IBS, transit time is prolonged, whereas in diarrhea-dominant IBS, there is exaggerated motor response to cholecystokinin and meal ingestion, leading to decreased bowel transit time. Recent data show that pelvic floor dyssynergia can mimic non-diarrhea predominant IBS symptoms, suggesting anorectal function tests should be considered in these patients [5]. Serotonin (5-hydroxytryptamine [5-HT]) plays a central role in GI motility, secretion, and pain modulation. Patients with IBS-C have been shown to have decreased levels of 5-HT, while patients with IBS-D have been found to have increased levels. Serotonin activity is modulated through 5-HT3 and 5-HT4 receptors, which have been a focus for some therapeutic initiatives [6].
Visceral Hypersensitivity
Visceral hypersensitivity has been postulated to be linked with various issues, including psychosocial events, prior history of abuse, and small and large bowel permeability. The interaction may be through the brain–gut axis and/or mucosal immunity [1]. Increased intestinal sensitivity in IBS causes abdominal pain and GI motor disorder, which provokes alterations in defecation patterns; that is, diarrhea or constipation. Several studies suggest that this selective hypersensitization of visceral afferent nerves in the gut are triggered by bowel distention or bloating. Abnormal visceral perception is suggested by excessive sensitivity to balloon distention documented at the rectosigmoid and the anorectum [7].
Intestinal Inflammation (Including Postinfectious IBS)
Postinfectious IBS (IBS-PI) has been reported to occur in 3%–36% of patients with enteric infections. Up to 10% of IBS patients report that their symptoms began with an acute infectious process. Intestinal mucosa from IBS patients have demonstrated activation of the immune system. An increased number of activated immunocompetent cells, such as T-lymphocytes, neutrophils, and mast cells, were seen in immunohistological assessment of intestinal mucosa, suggesting persistent inflammation in mucosa and enteric nerves, possibly contributing to the pathogenesis of IBS. IBS-PI attributed to viral infections seem to have only short-term effects; however, those attributed to bacterial, protozoan, or helminth infections seem to have a prolonged course. Some studies report that half of IBS-PI patients develop spontaneous recovery within 6 to 8 years [1]. IBS-PI is often associated with female gender, younger age, prolonged duration of infection, use of antibiotics, smoking, anxiety, and depression. The bowel symptoms following this acute infectious enteritis could be due to malabsorption, increased colonic mucosal lymphocytes, and enteroendocrine cells secreting high levels of serotonin [61, 6].
Altered Microbiota and Bacterial Overgrowth
A range of host factors may account for the differences in fecal microbiota of IBS patients compared to controls. These factors may include diet, genetics, and recent antibiotic use. Luminal- and mucosa-associated microbiota can affect the host via immunomicrobial interactions contributing to IBS symptoms. Emerging data suggest that the fecal microbiota in individuals with IBS differ from those of healthy controls and vary with their predominant symptom. In some studies, small intestinal bacterial overgrowth (SIBO) is more prevalent in IBS patients and its eradication with antibiotics may alleviate some symptoms. SIBO is typically diagnosed by indirect methods with diagnostic limitations. Reports on the prevalence of SIBO in IBS patients vary quite largely, ranging from 10% to 84%. Due to significant inconsistencies among studies, the relationship between IBS and SIBO remain unclear [61, 6, 8, 9].
Food Sensitivity
Many patients identify certain food items as triggers for their IBS symptoms. As such, food is a central issue for some patients. As many as 70% of patients report that IBS symptoms are associated with or exacerbated by certain foods in their diet. Although true food allergies play a small part in IBS symptomatology, food intolerances are quite common. Multiple studies have shown that poorly absorbed carbohydrates can have osmotic effects and lead to fermentation and gas production, contributing to various symptoms [1, 10].
More recent studies have explored the role of several other mechanisms, including genetic predisposition, altered intestinal permeability, disordered bile salt metabolism, and abnormalities in 5-HT metabolism. A better understanding of the pathophysiology of IBS will pave the way for novel therapies.
Diagnosis
Diagnosis of IBS rests heavily on a symptom-based criteria. Ensuring the absence of GI alarm signs is an important step in distinguishing between a chronic IBS issue and an acute problem, which may require more urgent evaluation. Alarm signs include evidence of GI bleeding, anemia, and weight loss. Patients often have several GI symptoms simultaneously. It is important to validate their concerns by ensuring them that all of their symptoms will be evaluated; however, it is sometimes best to explore each separately.
Understanding when a patient’s pain began is important in determining if the issue is acute or chronic. The location of the pain is helpful for similar reasons. A diffuse pain, or one with a migratory pattern, may be more consistent with IBS than a focal pain. Pain that is constant is likely not IBS, which is usually intermittent. Severity of pain can vary significantly in IBS and may range from mild to quite severe. Frequency of pain is a helpful indicator for the care provider, as it helps one understand how often this issue is disruptive to the patient. Treatment for a patient whose pain occurs only two or three times per year will vary quite significantly from that for a patient whose discomfort is daily. With this same concept in mind, the length of time that the pain lasts is quite important, as well. Pain that lasts only seconds will likely not benefit from medications as needed (prn) basis because it is likely gone by the time the patient finds his or her medication bottle. Determining if certain factors, such as food and bowel movement, exacerbate or alleviate the abdominal pain can be significant. Lastly, associated factors may be helpful, such as nausea and vomiting, fever and chills, diarrhea and constipation, and evidence of GI bleeding.
Rome IV criteria were developed in 2016 to assist in the diagnosis of IBS in clinical practice and to ensure consistency in patient selection for clinical trials. The Rome IV criteria define IBS as recurrent abdominal pain at least once per week in the prior 3 months with symptom onset at least 6 months before diagnosis. Abdominal pain must be associated with at least two of the following: defecation, change in stool frequency, and change in stool form.
Physical exam is helpful to elicit pain that is focal and to rule out rebound tenderness, which may indicate appendicitis. Patients with IBS range from benign, nontender abdomen to diffuse tenderness on exam. As IBS is a functional disorder, there are no laboratory or radiological findings to help with diagnosis. Laboratory evaluation may be used to help exclude conditions such as inflammatory bowel disease (IBD) and celiac disease, which may mimic IBS [11]. Radiological evaluation may be used to exclude structural issues that may be in the provider’s differential diagnosis. We often use an abdominal radiograph to evaluate retained stool burden, which may be contributing to patient symptoms. In the same manner, there are no specific endoscopic signs for IBS. Endoscopic evaluation may be used only to exclude processes, such as peptic ulcer disease, celiac disease, and IBD.
Rome III criteria for diagnosing IBSa |
Recurrent abdominal pain or discomfortb at least 3 days/month in the prior 3 months associated with two or more of the following:
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Rome IV criteria for diagnosing IBSc |
Recurrent abdominal pain, on average, at least 1 day/week in the prior 3 months, associated with two or more of the following criteria:
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a Criterion fulfilled for the prior 3 months with symptom onset at least 6 months before diagnosis.
b “Discomfort” means an uncomfortable sensation not described as pain.
c Criteria fulfilled for the prior 3 months with symptom onset at least 6 months before diagnosis.