JAAPA Magazine
Home In this issue Past Issues About us Contact us Subscribe to us Advertise with us
Quick Search
Using the search form

The pathophysiology, diagnosis, and treatment of IBS

   If you prefer to view this article in PDF form, click here.

The pathophysiology, diagnosis, and treatment of IBS

A thorough history and examination, with appropriate testing, are vital to establish rapport with the patient, identify any comorbid conditions, and exclude organic causes of symptoms.

Lauren Kolfenbach, MPAS, PA-C

The author practices at the Swedish Family Medicine Center, Littleton, Colo. She has indicated no relationships to disclose relating to the content of this article.

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 hyperalgesiais mediated by the CNS, local GI innervation, or a combination of the two.

Nervous system dysfunction Many experts argue that IBS is due to a neuralgic dysfunction of the gut and 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 brain-gut 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 corticotrophin-releasing 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 disorders14 (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 sleep16,18 (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 for directing treatment, many patients have fluctuating symptoms or do not classically fit into one of the three groups. IBS is best characterized by changes in bowel 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

Laboratory testing The history and physical examination allow the practitioner to glean information useful in determining the need for further studies. The AGA recommends a routine CBC and fecal occult blood testing. If alarm symptoms are present, a full workup and referral to a gastroenterologist are warranted.14 If there are no alarm symptoms and the Rome criteria are met, the patient may be evaluated based on age. Those older than 50 years should be referred to a gastroenterologist for a colonoscopy; those younger than 50 years may be evaluated based on their predominant symptom. Further tests may include a chemistry panel, ESR, thyroid-stimulating hormone level, stool analysis for ova and parasites, and tests for antiendomysial and antigliadin antibodies.20 Additional testing may be indicated but is more often performed after referral to a gastroenterologist.

Treatment

Once the diagnosis of IBS has been made, the treatment plan is based on the nature and severity of the symptoms, the degree of functional impairment, and the presence of psychosocial factors. A therapeutic relationship is essential for effective management and decreases the number of follow-up visits.21 The provider must be nonjudgmental, give a thorough explanation of the disorder and its chronicity, provide reassurance that IBS is not dangerous or life threatening, and involve the patient in the treatment plan.22 Despite the benign nature of IBS, studies show that it significantly affects quality of life; therefore, providers must actively listen and communicate understanding and compassion to these patients.

Diet While patients are more likely to have generalized postprandial symptoms than reactions to specific types of food, symptom diaries can sometimes identify social and dietary triggers. Problematic dietary substances often include coffee, alcohol, carbonated drinks, disaccharides, beans, and leafy vegetables.20

Increased fiber intake has long been recommended for treatment of IBS, but studies are not conclusive as to its benefit. Fiber is thought to increase stool bulk, to bind to agents such as bile, to enhance the stool’s water-holding properties, and to promote gel formation to provide lubrication.23 Safety and low cost make a trial of fiber, 20 to 25 g daily, either dietary or in supplements, reasonable in all patients.24 The dosage may require titration over several weeks to reduce abdominal pain and bloating.

For patients with mild symptoms, reassurance and education may be sufficient, but those with moderate to severe symptoms may require pharmacologic therapy (see Table 4). This decision is based on the predominant symptom and presence of comorbid psychiatric conditions.

Medication Antispasmodic agents relax smooth muscle in the gut and reduce propulsive contractions, decreasing postprandial abdominal pain, gas, bloating, and fecal urgency.21,23,25 Dicyclomine, hyoscyamine, and clidinium bromide/chlordiazepoxide work through anticholinergic or antimuscarinic properties and may be used in an as-needed or in an anticipatory fashion.25,26 Higher dosages are more effective, but anticholinergic side effects may be a limiting factor.

At low dosages, tricyclic antidepressants (TCAs) and, potentially, selective serotonin reuptake inhibitors (SSRIs) have analgesic properties independent of their effect on mood.26,27 The proposed mechanism is a facilitation of endogenous endorphin release and blockade of norepinephrine reuptake, which leads to an enhancement of descending inhibitory pain pathways and blockade of the pain neuromodulator serotonin.28 Additionally, the anticholinergic properties of TCAs may slow intestinal transit time, making them effective in the treatment of diarrhea. Studies have shown improvement in global symptoms, abdominal pain, and diarrhea in patients taking low-dose TCAs. One in three patients treated with TCAs experiences an improvement in symptoms.29 TCAs such as amitriptyline, nortriptyline, imipramine, and desipramine should be started at lower dosages than those used for treatment of depression, and then they should be slowly titrated until pain control or tolerance is achieved. Allow 3 to 4 weeks before reassessment.26 TCAs should be used with caution in the elderly and in patients with constipation, conduction abnormalities, and impaired ventricular function. SSRIs such as paroxetine, fluoxetine, and sertraline may also be beneficial, but supporting studies are limited and these agents are currently recommended only for patients with concomitant depression or anxiety.30,31 Because of the high rate of coexisting anxiety and its role in IBS exacerbations, benzodiazepines are sometimes prescribed. Their use should be limited, however, because of the risks of drug interactions, habituation, and rebound withdrawal.26,30

A systematic review found that loperamide improved diarrhea symptoms in patients with IBS; in some small studies, it was found to improve global symptoms.26,30 This agent is an opioid that does not cross the blood-brain barrier and works to slow intestinal transit and increase both intestinal water absorption and resting sphincter tone.24

Alosetron is a 5-HT3 receptor antagonist that has been shown to alleviate abdominal pain and improve quality of life in women with diarrhea-predominant IBS.32 Due to risks of ischemic colitis and serious complications related to constipation, the FDA removed it from the market in 2000. Currently, its use is restricted to those in whom traditional treatments have failed and whose providers are enrolled in the prescribing program for alosetron.24,26,30

Tegaserod, a partial 5-HT4 receptor agonist, is approved by the FDA for those with constipation-predominant IBS. It stimulates the release of neurotransmitters, increases colonic motility, and inhibits visceral sensitivity to rectal distention. A dosage of 6 mg twice daily has been shown to improve global symptoms and constipation. Tegaserod is approved for short-term use and is contraindicated in those with severe renal impairment, moderate or severe hepatic impairment, or a history of bowel obstruction, symptomatic gallbladder disease, suspected sphincter of Oddi dysfunction, or abdominal adhesions.30,33,34

Antibiotics have been reported to be helpful in those with refractory diarrhea but should be used only when a bacterial source is suspected.30,35 Other agents, such as peppermint oil, ginger, Chinese herbals, aloe vera, fennel, and probiotics, may have some role in the treatment of IBS, but more studies of these agents are needed before strong recommendations can be made.30,35

Psychological and behavioral therapies Significant methodologic limitations accompany the study of these modalities; however, cognitive behavior therapy, dynamic (interpersonal) therapy, and stress management or relaxation techniques including hypnosis, biofeedback training, meditation, and yoga may be useful tools. Patients with an associated psychological diagnosis, maladaptive coping styles, intermittent bowel symptoms of short duration, and exacerbations occurring at times of stress are most likely to benefit from psychological treatment.22

Conclusion

While the pathophysiology of IBS remains something of a mystery, this condition is one of the most common seen in primary care and has a significant effect on quality of life. A thorough history and physical examination accompanied by appropriate testing help to rule out other conditions and establish trust and rapport. Treatments are intended to control symptoms and should be chosen based on their severity and character. When diagnostic and therapeutic tools are used appropriately, IBS can be less challenging and frustrating to both patient and provider.

References

1. Talley NJ, Zinsmeister AR, Van Dyke C, Melton LJ 3rd. Epidemiology of colonic symptoms and the irritable bowel syndrome. Gastroenterology. 1991;101(4):927-934. Erratum in: Gastroenterology. 1992;102(2):746.

2. American Gastroenterological Association. The burden of gastrointestinal diseases report. 2001. Available at: www.gastro.org/wmspage.cfm?parm1. Accessed December 7, 2006.

3. Levy RL, Von Korff M, Whitehead WE, et al. Costs of care for irritable bowel syndrome patients in a health maintenance organization. Am J Gastroenterol. 2001;96(11):3122-3129.

4. Mertz H, Morgan V, Tanner G, et al. Regional cerebral activation in irritable bowel syndrome and control subjects with painful and nonpainful rectal distention. Gastroenterology. 2000;118(5):842-848.

5. Mayer EA. Emerging disease model for functional gastrointestinal disorders. Am J Med. 1999;107(5A):12S-19S.

6. Naliboff BD, Munakata J, Fullerton S, et al. Evidence for two distinct perceptual alterations in irritable bowel syndrome. Gut. 1997;41(4):505-512.

7. Hobday DI, Aziz Q, Thacker N, et al. A study of the cortical processing of anorectal sensation using functional MRI. Brain. 2001;124(pt 2):361-368.

8. Bueno L, Fioramonti J, Garcia-Villar R. Pathobiology of visceral pain: molecular mechanisms and therapeutic implications, III. visceral afferent pathways: a source of new therapeutic targets for abdominal pain. Am J Physiol Gastrointest Liver Physiol. 2000;278(5):G670-G676.

9. Crowell MD. Role of serotonin in the pathophysiology of the irritable bowel syndrome. Br J Pharmacol. 2004;141(8):1285-1293.

10. Folks DG. The interface of psychiatry and irritable bowel syndrome. Curr Psychiatry Rep. 2004;6(3):210-215.

11. Salmon P, Skaife K, Rhodes J. Abuse, dissociation, and somatization in irritable bowel syndrome: towards an explanatory model. J Behav Med. 2003;26(1):1-18.

12. Sagami Y, Shimada Y, Tayama J, et al. Effect of a corticotropin releasing hormone receptor antagonist on colonic sensory and motor function in patients with irritable bowel syndrome. Gut. 2004;53(7):958-964.

13. Park H. The pathophysiology of irritable bowel syndrome: inflammation and motor disorder [in Korean]. Korean J Gastroenterol. 2006;47(2):101-110.

14. Holten KB, Wetherington A, Bankston L. Diagnosing the patient with abdominal pain and altered bowel habits: is it irritable bowel syndrome? Am Fam Physician. 2003;67(10):2157-2162.

15. Lynn RB, Friedman LS. Irritable bowel syndrome. N Engl J Med. 1993;329(26):1940-1945.

16. Paterson WG, Thompson WG, Vanner SJ, et al. Recommendations for the management of irritable bowel syndrome in family practice. CMAJ. 1999;161(2):154-160.

17. Smith RP. Lower gastrointestinal disease in women. Obstet Gynecol Clin North Am. 2001;28(2):351-361, viii.

18. Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and functional abdominal pain. Gut. 1999;45(suppl 2):II43-II47.

19. Manning AP, Thompson WG, Heaton KW, Morris AF. Towards positive diagnosis of the irritable bowel. Br Med J. 1978;2(6138):653-654.

20. Drossman DA, Camilleri M, Mayer EA, Whitehead WE. AGA technical review on irritable bowel syndrome. Gastroenterology. 2002;123(6):2108-2131.

21. Vanner SJ, Depew WT, Paterson WG, et al. Predictive value of the Rome criteria for diagnosing the irritable bowel syndrome. Am J Gastroenterol. 1999;94(10):2912-2917.

22. Mertz HR. Irritable bowel syndrome. N Engl J Med. 2003;349(22):2136-2146.

23. Mearin F. Pharmacological treatment of the irritable bowel syndrome and other functional bowel disorders. Digestion. 2006;73(suppl 1):28-37.

24. Viera AJ, Hoag S, Shaughnessy J. Management of irritable bowel syndrome. Am Fam Physician. 2002;66(10):1867-1874.

25. Brandt LJ, Bjorkman D, Fennerty MB, et al. Systematic review on the management of irritable bowel syndrome in North America. Am J Gastroenterol. 2002;97(11 suppl):S7-S26.

26. Chun AB, Desautels S, Wald A. Clinical manifestations and diagnosis of irritable bowel syndrome. In: Rose BD, ed. UpToDate. Waltham, Mass: UpToDate; 2005.

27. Clouse RE. Antidepressants for irritable bowel syndrome. Gut. 2003;52(4):598-599.

28. Gorard DA, Libby GW, Farthing MJ. Treating functional gastrointestinal disorders with antidepressants. Am J Med. 2000;108(9):756.

29. Jackson JL, O’Malley PG, Tomkins G, et al. Treatment of functional gastrointestinal disorders with antidepressant medications: a meta-analysis. Am J Med. 2000;108(1):65-72.

30. Hadley SK, Gaarder SM. Treatment of irritable bowel syndrome. Am Fam Physician. 2005;72(12):2501-2506.

31. Tabas G, Beaves M, Wang J, et al. Paroxetine to treat irritable bowel syndrome not responding to high-fiber diet: a double-blind, placebo-controlled trial. Am J Gastroenterol. 2004;99(5):914-920.

32. Cremonini F, Delgado-Aros S, Camilleri M. Efficacy of alosetron in irritable bowel syndrome: a meta-analysis of randomized controlled trials. Neurogastroenterol Motil. 2003;15(1):79-86.

33. Camilleri M. Tegaserod in the treatment of irritable bowel syndrome and chronic constipation. 2006. Available at: http://patients.uptodate.com/topic.asp?file=gi_dis/22332. Accessed December 7, 2006.

34. Evans BW, Clark WK, Moore DJ, Whorwell PJ. Tegaserod for the treatment of irritable bowel syndrome (Cochrane Review). The Cochrane Database of Systematic Reviews 2004, Issue 1. Art. No.: CD003960. DOI:10.1002/14651858.CD003960.

35. Spanier JA, Howden CW, Jones MP. A systematic review of alternative therapies in the irritable bowel syndrome. Arch Intern Med. 2003;163(3):265-274.







JAAPA: Home | In This Issue | Past Issues | About Us | Contact Us | Subscribe To Us | Advertise With Us


© 2007 Haymarket Media, Inc. and the American Academy of Physician Assistants. All rights reserved.
Use of jaapa.com subject to License agreement. Please read our Disclaimer and Privacy policy.