IRRITABLE BOWEL SYNDROME
1. DEFINITION
Irritable bowel syndrome (IBS) is a functional bowel disorder for which no structural or biochemical explanations have been found. It has also been called mucous colitis, spastic colon and irritable colon. The ICD 10AM Code is K58.
2. DIAGNOSIS
Diagnosis can be made by using either the Manning (validated) or Rome II criteria (recommended but not validated). The term is often misused, partly because, in practice, its definition defies ready precision.
2.1 Manning Criteria for IBS (1) 1. Pain eased after bowel movement
2. More frequent bowel movements at onset of pain 3. Looser stools at onset of pain
4. Visible (abdominal) distention 5. Feeling of incomplete evacuation 6. Passage of mucus
2.2 Rome II criteria for IBS (2)
• At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has two of three features;
• Relieved with defecation; and/or
• Onset associated with a change in frequency of stool; and/or
• Onset associated with a change in form (appearance) of stool
• Symptoms cumulatively supporting IBS diagnosis
• Abnormal stool frequency
• Abnormal stool form (lumpy/hard or loose/watery stool)
• Abnormal stool passage (straining, urgency, or feeling of incomplete evacuation)
• Passage of mucus
• Bloating or feeling of abdominal distension
In all cases, the diagnosis is contingent upon the exclusion of other and organic conditions; it is essential that bleeding, overt and occult and other possibly sinister findings be excluded. Symptom subtypes - constipation predominant, diarrhoea predominant and alternating type symptomatology have limited value as patient and doctor view may differ (3). IBS is. associated with substantial morbidity but no mortality. Compared with the population, IBS sufferers report a poorer general state of health and higher absenteeism (4). In the U.S. IBS is the most common cause for referral to a gastroenterologist and accounts for 3.5 million physician visits, 2.2 million prescriptions and 35,000 hospitalizations p.a. with similar figures reported for Europe and the U.K. (5).
3. PREVALENCE
Most community based studies report a population prevalence of 10-20%
in developed countries using the different definitions. It has been reported in less developed countries but the data are sparse (4, 6, 7).
4. NATURAL HISTORY
IBS is a chronic disorder with fluctuating symptoms. Longitudinal studies show a turnover of those affected, with similar proportion reporting loss of symptoms and new symptomatology (8). It is not associated with any known complications or shortening of life expectancy.
5. ASSOCIATIONS AND POSSIBLE CAUSAL FACTORS
More than 80% of patients with IBS have dyspepsia; in the majority of these the dyspepsia is functional. Psychological vulnerability and the experience of having problems have been strongly associated with the prevalence and incidence of IBS (9). Psychological morbidity has been associated in many studies with consulting behavior in general and IBS in particular (7, 10).
6. AGE
Prevalence may decline with age but this may be due to reporting bias (4). In a population-based cohort of 2956 newly diagnosed irritable bowel syndrome patients aged 20-79 years, Ruigomez found only 12% were 60 years or older (11) .
7. GENDER
IBS predominantly affects women (4, 11). Clinic based studies have a female to male ratio of 3-4 to 1, higher than the ratios of 2:1 seen in community studies.
8. GENETIC FACTORS
There is limited evidence for a genetic role in IBS (12). Twin studies show IBS is twice as frequent in monozygotic compared with dizygotic twins (13). Environmental factors more than genes may be important in pathogenesis although genes may determine susceptibility to post infective IBS (13).
9. EFFECTS OF INTERVENTION
Surprisingly few drugs have demonstrated effectiveness in IBS. The antidiarrhoeal loperamide and opoids have been shown to be effective in those with diarrhoea. Tricyclic antidepressants have been shown to be effective in one meta-analysis (NNT=3) (14). Serotonin receptor agonists
and antagonists are currently being trialed however their effectiveness may be outweighed by their side-effect profile.
10. CAUSES
The main contenders for causing IBS are visceral hypersensitivity, motor abnormalities, psychosocial distress and infection and inflammation.
Post infective IBS accounts for 6-17% of IBS (15). Up to 33% of bacterial gastroenteritis will result in IBS, however, there are few case control studies to indicate relative risk (16). Reported risk factors for post infective IBS include psychological vulnerability (RR=2, 95% CI1.7-2.4), female gender (RR=3.4, 95%CI 1.1-9.8), duration of infective illness (RR=11.4, 95%CI 2.2-5.8) and bacterial toxin (RR=10.5, 95%CI 1.4-7.6) (17, 18). A case review of over 500,000 general practice records found the incidence of new cases of IBS amongst those with a reported history of gastroenteritis to be 0.3% and 4% giving an adjusted relative risk of 11.9%
(95% confidence interval 6.7 to 21.0).
The role of visceral hypersensitivity and motor dysfunction is controversial.
Only a minority of patients with IBS seek medical attention. Even so, IBS patients represent up to half of those presenting in gastroenterological practice. Whilst those who do not seek help do not differ from their normal community controls in their psychological profile, those seeking help are, in general, different. Many have clear evidence of depression, anxiety, personality disorder, somatization. In some, their psychological problems go back to childhood and a history of abuse, physical or sexual, adult or in childhood can be elicited by gentle empathic questioning. There is also good evidence of a lowered pain threshold in the gut of these patients. IBS patients characteristically report pain at lower levels of distension than normal when subjected to balloon inflation in the small bowel or rectum. In addition a variety of changes in motility pattern have been seen in this order;
none are specific and their significance is yet to be determined.
References
1. Manning AP, Thompson WG, Heaton KW et al. Towards positive diagnosis of the irritable bowel. Br. Med. J. 2,653-4 (1978).
2. Thompson WG, Longstreth GF, Drossman DA, et al. Functional bowel disorders and 7 (1999).
3. Mearin F, Balboa A, Badia X, Baro E, Caldwell E, Cucala M et al. Irritable bowel syndrome subtypes according to bowel habit: revisiting the alternating subtype. Eur. J.
Gastroenterol. Hepatol. 15(2),165-72 (2003).
functional abdominal pain. Gut 45, 43-
4. Hungin AP, Whorwell PJ, Tack J, Mearin F. The prevalence, patterns and impact of irritable bowel syndrome: an international survey of 40,000 subjects. Aliment.
Pharmacol. Ther. 17,643-50 (2003).
5. Everhart JE, Renault PF. Irritable bowel syndrome in office-based practice in the United States. Gastroenterology. 100,998-1005 (1991).
6. Thompson WG. Irritable bowel syndrome: prevalence, prognosis and consequences.
CMAJ 134,111-3 (1986).
7. Drossman DA, Sandler RS, McKee DC, Lovitz AJ. Bowel patterns among subjects not seeking health care. Use of a questionnaire to identify a population with bowel dysfunction. Gastroenterology. 83,529-34 (1982).
8. Talley NJ, Weaver AL, Zinsmeister AR, Melton LJ 3rd. Onset and disappearance of gastrointestinal symptoms and functional gastrointestinal disorders. Am. J. Epidemiol.
136,165-77 (1992).
9. Kay L, Jorgensen T, Jensen KH. The epidemiology of irritable bowel syndrome in a random population: prevalence, incidence, natural history and risk factors. J. Intern. Med.
236,23-30 (1994).
10. Sandler RS, Drossman DA, Nathan HP, McKee DC. Symptom complaints and health care seeking behavior in subjects with bowel dysfunction. Gastroenterology. 87,314-8 (1984).
11. Ruigomez A, Wallander MA, Johansson S, Garcia Rodriguez LA. One-year follow-up of newly diagnosed irritable bowel syndrome patients. Aliment. Pharmacol. Ther. 13,1097- 1102 (1999).
12. Woodman CL, Breen K, Noyes R Jr et al. The relationship between irritable bowel syndrome and psychiatric illness : a family study. Psychosomatics. 39,45-54 (1998).
