eMedicine Specialties > Gastroenterology > Colon

Irritable Bowel Syndrome

Author: Jenifer K Lehrer, MD, Attending Physician, Jefferson Health System, Frankford-Torresdale Campus
Coauthor(s): Gary R Lichtenstein, MD, Director of Inflammatory Bowel Disease Center, Professor, Department of Internal Medicine, University of Pennsylvania
Contributor Information and Disclosures

Updated: Aug 9, 2009

Introduction

Background

Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and altered bowel habits in the absence of specific and unique organic pathology. Osler coined the term mucous colitis in 1892 when he wrote of a disorder of mucorrhea and abdominal colic with a high incidence in patients with coincident psychopathology. Since that time, the syndrome has been referred to by sundry terms, including spastic colon, irritable colon, and nervous colon.

Traditionally, irritable bowel syndrome is a diagnosis of exclusion. No specific motility or structural correlates have been consistently demonstrated, so irritable bowel syndrome remains a clinically defined illness.

Manning and associates established 6 criteria to distinguish irritable bowel syndrome from organic bowel disease.¹ Although historically important, these criteria are insensitive (58%), nonspecific (74%), and less reliable in men. The Manning criteria to distinguish irritable bowel syndrome from organic disease are as follows:

• Onset of pain associated with more frequent bowel movements
• Onset of pain associated with looser bowel movements
• Pain relieved by defecation
• Visible abdominal bloating
• Subjective sensation of incomplete evacuation more than 25% of the time
• Mucorrhea more than 25% of the time

More recently, a consensus panel created and then updated the Rome criteria to provide a standardized diagnosis for research and clinical practice. The Rome III criteria (2006) for the diagnosis of irritable bowel syndrome require that patients must have recurrent abdominal pain or discomfort at least 3 days per month during the previous 3 months that is associated with 2 or more of the following:

• Relieved by defecation
• Onset associated with a change in stool frequency
• Onset associated with a change in stool form or appearance

Supporting symptoms include the following:

• Altered stool frequency
• Altered stool form
• Altered stool passage (straining and/or urgency)
• Mucorrhea
• Abdominal bloating or subjective distention

Four bowel patterns may be seen with irritable bowel syndrome. These patterns include IBS-D (diarrhea predominant), IBS-C (constipation predominant), IBS-M (mixed diarrhea and constipation), and IBS-A (alternating diarrhea and constipation). The usefulness of these subtypes is debatable. Notably, within 1 year, 75% of patients change subtypes, and 29% switch between constipation-predominant IBS and diarrhea-predominant IBS.

Pathophysiology

• Altered GI motility includes distinct aberrations in small and large bowel motility.
  • The myoelectric activity of the colon is composed of background slow waves with superimposed spike potentials. Colonic dysmotility in irritable bowel syndrome manifests as variations in slow-wave frequency and a blunted, late-peaking, postprandial response of spike potentials. Patients who are prone to diarrhea demonstrate this disparity to a greater degree than patients who are prone to constipation.
  • Small bowel dysmotility manifests in delayed meal transit in patients prone to constipation and in accelerated meal transit in patients prone to diarrhea. In addition, patients exhibit shorter intervals between migratory motor complexes (the predominant interdigestive small bowel motor patterns). 
  • Current theories integrate these widespread motility aberrations and hypothesize a generalized smooth muscle hyperresponsiveness. They describe increased urinary symptoms, including frequency, urgency, nocturia, and hyperresponsiveness to methacholine challenge.
• Visceral hyperalgesia is the second part of the traditional 3-part complex that characterizes irritable bowel syndrome.
  • Enhanced perception of normal motility and visceral pain characterizes irritable bowel syndrome. Rectosigmoid and small bowel balloon inflation produces pain at lower volumes in patients than in controls. Notably, hypersensitivity appears with rapid but not gradual distention.
  • Patients who are affected describe widened dermatomal distributions of referred pain. 
  • Sensitization of the intestinal afferent nociceptive pathways that synapse in the dorsal horn of the spinal cord provides a unifying mechanism.
• Psychopathology is the third aspect.
  • Associations between psychiatric disturbances and irritable bowel syndrome pathogenesis are not clearly defined. 
  • Patients with psychological disturbances relate more frequent and debilitating illness than control populations. 
  • Patients who seek medical care have a higher incidence of panic disorder, major depression, anxiety disorder, and hypochondriasis than control populations. 
  • An Axis I disorder coincides with the onset of GI symptoms in as many as 77% of patients. 
  • A higher prevalence of physical and sexual abuse has been demonstrated in patients with irritable bowel syndrome. 
  • Whether psychopathology incites development of irritable bowel syndrome or vice versa remains unclear.
• Microscopic inflammation has been documented in some patients. This concept is groundbreaking in that irritable bowel syndrome had previously been considered to have no demonstrable pathologic alterations.
  • Both colonic inflammation and small bowel inflammation have been discovered in a subset of patients with irritable bowel syndrome as well as in patients with inception of irritable bowel syndrome after infectious enteritis (postinfectious irritable bowel syndrome). Risk factors for developing postinfectious irritable bowel syndrome include female gender, longer duration of illness, the type of pathogen involved, an absence of vomiting during the infectious illness, and young age.
  • Laparoscopic full-thickness jejunal biopsy samples revealed infiltration of lymphocytes into the myenteric plexus and intraepithelial lymphocytes in a subset of patients. Neuronal degeneration of the myenteric plexus was also present in some patients.
  • Patients with postinfectious irritable bowel syndrome may have increased numbers of colonic mucosal lymphocytes and enteroendocrine cells.
  • Enteroendocrine cells in postinfectious irritable bowel syndrome appear to secrete high levels of serotonin, increasing colonic secretion and possibly leading to diarrhea.
• Small bowel bacterial overgrowth has been heralded as a unifying mechanism for the symptoms of bloating and distention common to patients with irritable bowel syndrome. This has led to proposed treatments with probiotics and antibiotics.
• The fecal microflora also differs among patients with irritable bowel syndrome versus controls. A sophisticated molecular analysis suggested an alteration in the patterns and the contents of gut bacteria.²

Frequency

United States

Population-based studies estimate the prevalence of irritable bowel syndrome at 10-20% and the incidence of irritable bowel syndrome at 1-2% per year. Of people with irritable bowel syndrome, approximately 10-20% seek medical care. An estimated 20-50% of gastroenterology referrals relate to this symptom complex.

International

The incidence is markedly different among countries.

Mortality/Morbidity

• Irritable bowel syndrome is a chronic relapsing condition. Clinicians must be forthcoming with patients because knowledge may help allay undue fears as their disease waxes and wanes. Irritable bowel syndrome does not increase the mortality or the risk of inflammatory bowel disease or cancer.
• The principal associated physical morbidities of irritable bowel syndrome include abdominal pain and lifestyle modifications secondary to altered bowel habits.
• Work absenteeism resulting in lost wages is more frequent in patients with irritable bowel syndrome.

Race

• American and European cultures demonstrate similar frequencies of irritable bowel syndrome across racial and ethnic lines. However, within the United States, survey questionnaires indicate a lower prevalence of irritable bowel syndrome in Hispanics in Texas and Asians in California.
• Populations of Asia and Africa may have a lower prevalence of irritable bowel syndrome.
• The role of different cultural influences and varying health care–seeking behaviors is unclear.

Sex

In Western countries, women are 2-3 times more likely to develop irritable bowel syndrome than men, although males represent 70-80% of patients with irritable bowel syndrome in the Indian subcontinent. Women seek health care more often, but the irritable bowel syndrome-specific influence of this occurrence remains unknown. Other factors, such as a probably greater incidence of abuse in women, may confound interpretation of this statistic.

Age

• Patients often retrospectively note the onset of abdominal pain and altered bowel habits in childhood.
• Approximately 50% of people with irritable bowel syndrome report symptoms beginning before they were aged 35 years.
• The development of symptoms in people older than 40 years does not exclude irritable bowel syndrome but should prompt a closer search for an underlying organic etiology.

Clinical

History

A meticulous history is the key to establish a diagnosis of irritable bowel syndrome. The Rome criteria provide the construct upon which questions are based (see Background). 

Symptoms consistent with irritable bowel syndrome include the following:

• Altered bowel habits
• Constipation variably results in complaints of hard stools of narrow caliber, painful or infrequent defecation, and intractability to laxatives.
• Diarrhea usually is described as small volumes of loose stool, with evacuation preceded by urgency or frequent defecation.
• Postprandial urgency is common.
• Alternating habits are common. Characteristically, one feature predominates in a single patient, but significant variability exists among patients.
• Abdominal pain
• Descriptions are protean. Pain frequently is diffuse without radiation. Common sites of pain include the lower abdomen, specifically the left lower quadrant.
• Acute episodes of sharp pain are often superimposed on a more constant dull ache.
• Meals may precipitate pain, and defecation commonly improves pain. Defecation may not fully relieve pain.
• Pain from presumed gas pockets in the splenic flexure may masquerade as anterior chest pain or left upper quadrant abdominal pain. This splenic flexure syndrome is demonstrable by balloon inflation in the splenic flexure and should be considered in the differential of chest or left upper quadrant abdominal pain.
• Abdominal distention
• Patients frequently report increased amounts of bloating and gas. Quantitative measurements fail to support this claim.
• People with irritable bowel syndrome may manifest increasing abdominal circumference throughout the day, as assessed by CT scan. They may also demonstrate intolerance to otherwise normal amounts of abdominal distention.
• Clear or white mucorrhea of a noninflammatory etiology is commonly reported.
• Noncolonic and extraintestinal symptoms
• Epidemiologic associations with dyspepsia, heartburn, nausea, vomiting, sexual dysfunction (including dyspareunia and poor libido), and urinary frequency and urgency have been noted.
• Symptoms may worsen in the perimenstrual period.
• Fibromyalgia is a common comorbidity.
• Stressor-related symptoms
• These symptoms may be revealed with careful questioning.
• Emphasize avoidance of stressors.
• Inconsistent symptoms are an alert to the possibility of an organic pathology. Symptoms not consistent with irritable bowel syndrome include the following:
• Onset in middle age or older
• Acute symptoms: Irritable bowel syndrome is defined by chronicity.
• Progressive symptoms
• Nocturnal symptoms
• Anorexia or weight loss
• Fever
• Rectal bleeding
• Painless diarrhea
• Steatorrhea
• Lactose and/or fructose intolerance
• Gluten intolerance

Physical

• The patient has an overall healthy appearance.
• The patient may be tense or anxious.
• The patient may present with sigmoid tenderness or a palpable sigmoid cord.

Causes

The causes of irritable bowel syndrome remain poorly defined, but they are being avidly researched.

• Postulated etiologies of irritable bowel syndrome
  • Abnormal transit profiles and an enhanced perception of normal motility may exist.
  • Up to one third of patients with irritable bowel syndrome may have altered colonic transit. Delayed colonic motility may be more common in IBS-C versus healthy controls. Similarly, accelerated colonic transit may be more common in IBS-D versus healthy controls.³
  • Local histamine sensitization of the afferent neuron causing earlier depolarization may occur.
• Causes related to enteric infection (see Pathophysiology) 
  • Colonic muscle hyperreactivity and neural and immunologic alterations of the colon and small bowel may persist after gastroenteritis.
  • Psychological comorbidity independently predisposes the patient to the development of postinfectious irritable bowel syndrome.
  • Psychological illness may create a proinflammatory cytokine milieu, leading to irritable bowel syndrome through an undefined mechanism after acute infection.
• Central neurohormonal mechanisms
  • Abnormal glutamate activation of N- methyl-D- aspartate (NMDA) receptors, activation of nitric oxide synthetase, activation of neurokinin receptors, and induction of calcitonin gene-related peptide have been observed.
  • The limbic system mediation of emotion and autonomic response enhances bowel motility and reduces gastric motility to a greater degree in patients who are affected than in controls. Limbic system abnormalities, as demonstrated by positron emission tomography, have been described in patients with irritable bowel syndrome and in those with major depression.
  • The hypothalamic-pituitary axis may be intimately involved in the origin. Motility disturbances correspond to an increase in hypothalamic corticotropin-releasing factor (CRF) production in response to stress. CRF antagonists eliminate these changes.
• As discussed in Pathophysiology, Pimentel and colleagues have proposed that small bowel bacterial overgrowth provides a unifying mechanism for the common symptoms of bloating and gaseous distention in patients with irritable bowel syndrome.⁴
• Bloating and distention may also occur from intolerance to dietary fats. Reflex-mediated small bowel gas clearance is more impaired by lipids (fat) ingestion in patients with irritable bowel syndrome versus patients without irritable bowel syndrome.
• Recent elimination and challenge diets have suggested that poorly absorbed short-chain carbohydrates, in the form of fructose and fructans, may create symptoms among patients with irritable bowel syndrome, as measured by a visual analogue scale.⁵

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