eMedicine Specialties > Emergency Medicine > Gastrointestinal

Inflammatory Bowel Disease

Author: Sarvotham Kini, MD, Associate Professor of Emergency Medicine, Medical University of South Carolina, Charleston.
Contributor Information and Disclosures

Updated: Nov 20, 2009

Introduction

Background

The term inflammatory bowel disease (IBD) refers to primarily ulcerative colitis (UC) and Crohn's disease (CD). These are chronic conditions of uncertain etiology, characterized by recurrent episodes of abdominal pain, often with diarrhea. Although both ulcerative colitis and Crohn's disease have distinct pathologic findings, a significant percentage of patients with inflammatory bowel disease (IBD) have indeterminate findings. Crohn's disease is also referred to a regional enteritis, terminal ileitis, or granulomatous ileocolitis.

Pathophysiology

Multiple etiologies have been proposed for inflammatory bowel disease (IBD), but the precise cause is unknown. However, considerable evidence suggests that inflammatory mediators play an important role in the pathologic and clinical characteristic of these disorders. Cytokines, released by macrophages in response to various antigenic stimuli, bind to different receptors and produce autocrine, paracrine, and endocrine effects. Cytokines differentiate lymphocytes into different types of T cells. Helper T cells, type 1 (Th-1), are associated principally with Crohn's disease, whereas Th-2 cells are associated principally with ulcerative colitis. The immune response disrupts the intestinal mucosa and leads to a chronic inflammatory process.1

In ulcerative colitis (UC), inflammation begins in the rectum and extends proximally in an uninterrupted fashion to the proximal colon, eventually involving the entire length of the large intestine. The rectum is always involved in ulcerative colitis, and no "skip areas" (ie, normal areas of the bowel interspersed with diseased areas) are present. Ulcerative colitis primarily involves the mucosa and the submucosa, with formation of crypt abscesses and mucosal ulceration. The mucosa typically appears granular and friable. In more severe cases, pseudopolyps form, consisting of areas of hyperplastic growth with swollen mucosa surrounded by inflamed mucosa with shallow ulcers. In severe ulcerative colitis, inflammation and necrosis can extend below the lamina propria to involve the submucosa and the circular and longitudinal muscles, although this is very unusual.

Ulcerative colitis remains confined to the rectum in approximately 25% of cases. In the remainder of cases, ulcerative colitis spreads proximally and contiguously. Pancolitis occurs in 10% of patients. The small intestine is never involved, except when the distal terminal ileum is inflamed in a superficial manner, referred to as backwash ileitis. Even with less than total colonic involvement, the disease is strikingly and uniformly continuous. As the disease becomes chronic, the colon becomes a rigid foreshortened tube that lacks its usual haustral markings, leading to the lead pipe appearance observed on barium enema. The skip areas observed in the colon in Crohn's disease do not occur in ulcerative colitis.

Crohn's disease, on the other hand, consists of segmental involvement by a nonspecific granulomatous inflammatory process. The most important pathologic feature is that Crohn's disease is transmural, involving all layers of the bowel, not just the mucosa and the submucosa, which is characteristic of ulcerative colitis. Crohn's disease can affect any portion of the gastrointestinal tract from the mouth to the anus. Furthermore, Crohn's disease is discontinuous, with skip areas interspersed between one or more involved areas.

Late in the disease, the mucosa develops a cobblestone appearance, which results from deep longitudinal ulcerations interlaced with intervening normal mucosa. The 3 major patterns of involvement in Crohn's disease are (1) disease in the ileum and cecum (occurring in 40% of patients), (2) disease confined to the small intestine (occurring in 30% of patients), and (3) disease confined to the colon (occurring in 25% of patients). Rectal sparing is a typical but not constant feature of Crohn's disease. However, anorectal complications (eg, fistulas, abscesses) are common. Much less commonly, Crohn's disease involves the more proximal parts of the gastrointestinal (GI) tract, including the mouth, tongue, esophagus, stomach, and duodenum. Crohn's disease causes 3 patterns of involvement: inflammatory disease, strictures, and fistulas.

Ulcerative colitis and Crohn's disease are generally diagnosed using clinical, endoscopic, and histologic criteria. Histologically, transmural non-necrotizing lymphoid granulomas are characteristic of Crohn's disease. However, they may not be found in a given case of Crohn's disease, and no single finding is absolutely diagnostic for one disease or the other. Furthermore, approximately 20% of patients have a clinical picture that falls between Crohn's disease and ulcerative colitis; they are said to have indeterminate colitis.

The incidence of gallstones and kidney stones is increased in Crohn's disease because of malabsorption of fat and bile salts. Gallstones are formed because of increased cholesterol concentration in the bile, caused by a reduced bile salt pool. Patients who have Crohn's disease with ileal disease or resection also are likely to form calcium oxalate kidney stones. With the fat malabsorption, unabsorbed long-chain fatty acids bind calcium in the lumen. Oxalate in the lumen normally is bound to calcium. Calcium oxalate is poorly soluble and poorly absorbed; however, if calcium is bound to malabsorbed fatty acids, oxalate combines with sodium to form sodium oxalate, which is soluble and is absorbed in the colon (enteric hyperoxaluria). The development of calcium oxalate stones in Crohn's disease requires an intact colon to absorb oxalate. Patients with ileostomies do not develop calcium oxalate stones.

Extraintestinal manifestations of inflammatory bowel disease (IBD) include iritis, episcleritis, arthritis, and skin involvement, as well as pericholangitis and sclerosing cholangitis. These extraintestinal manifestations (EIM) are observed in up to 20-40% of patients with IBD.2

Frequency

United States

The incidence is 70-150 cases per 100,000 individuals.

The incidence of inflammatory bowel disease (IBD) varies within different geographic areas. Crohn's disease (CD) and ulcerative colitis (UC) both occur at the highest incidence in Europe, the United Kingdom, and North America.

International

The incidence of inflammatory bowel disease (IBD) ranges from 2.2-14.3 cases per 100,000 person-years for ulcerative colitis and from 3.1-14.6 cases per 100,000 person-years for Crohn's disease. Overall, the combined incidence for inflammatory bowel disease is 10 cases per 100,000 annually.3,4

Mortality/Morbidity

The quality of life generally is lower in those with Crohn's disease than in those with ulcerative colitis, in part because of recurrences after surgery performed for Crohn's disease.

  • The most common causes of death in inflammatory bowel disease (IBD) are peritonitis with sepsis, malignancy, thromboembolic disease, and complications of surgery.
  • Toxic megacolon, one of the most dreaded complications of ulcerative colitis, can lead to perforation, sepsis, and death.
  • Malnutrition and chronic anemia are observed in long-standing Crohn's disease.
  • Children with Crohn's disease or ulcerative colitis can exhibit growth retardation.

Race

  • Incidence among whites is approximately 4 times that of other races.
  • IBD is observed most commonly in Northern Europe and North America. It is a disease of industrialized nations.
  • Incidence is higher in Ashkenazi Jews (ie, those who have immigrated from Northern Europe) than in other groups.

Sex

  • Incidence is slightly greater in females than in males.

Age

  • Incidence peaks in the second and third decades of life.
  • A second smaller peak occurs in patients aged 55-65 years.
  • Crohn's disease and ulcerative colitis can occur in childhood, although the incidence is much lower in children younger than 15 years.

Clinical

History

  • Patients with ulcerative colitis (UC) most commonly present with bloody diarrhea, whereas patients with Crohn's disease (CD) usually present with nonbloody diarrhea.
    • Abdominal pain and cramping, fever, and weight loss occur in more severe cases.
    • The greater the extent of colon involvement, the more likely the patient is to have diarrhea.
    • Rectal urgency or tenesmus reflects reduced compliance of the inflamed rectum.
    • Patients might have formed stools if their disease is confined to the rectum.
    • As the degree of inflammation increases, systemic symptoms develop, including low-grade fever, malaise, nausea, vomiting, sweats, and arthralgias.
    • Fever, dehydration, and abdominal tenderness develop in severe ulcerative colitis, reflecting progressive inflammation into deeper layers of the colon.
  • The presentation of Crohn's disease is generally more insidious than that of ulcerative colitis, with ongoing abdominal pain, anorexia, diarrhea, weight loss, and fatigue.
    • Grossly bloody stools, while typical of ulcerative colitis, are less common in Crohn's disease.
    • Stools may be formed, but loose stools predominate if the colon or the terminal ileum is involved extensively.
    • One half of patients with Crohn's disease present with perianal disease (eg, fistulas, abscesses).
    • Occasionally, acute right lower quadrant pain and fever, mimicking appendicitis, may be noted.
    • Commonly, the diagnosis is established only after several years of recurrent abdominal pain, fever, and diarrhea.
  • Crohn's disease with gastroduodenal involvement may mimic peptic ulcer disease and can progress to gastric outlet obstruction.
  • Many patients with inflammatory bowel disease (IBD) have irritable bowel syndrome, which can produce occasional cramping, irregular bowel habits, and passage of mucus without blood or pus.
  • Weight loss is observed more commonly in Crohn's disease than in ulcerative colitis because of the malabsorption associated with small bowel disease. Patients may reduce their food intake in an effort to control their symptoms.
  • Systemic symptoms are common and include fever, sweats, malaise, and arthralgias. A low-grade fever may be the first warning sign of a flare.
  • Recurrences may occur with emotional stress, infections or other acute illnesses, pregnancy, dietary indiscretions, use of cathartics or antibiotics, or withdrawal of anti-inflammatory or steroid medications.
  • Children may present with growth retardation and delayed or failed sexual maturation.
  • In 10-20% of cases, patients present with extraintestinal manifestations, including arthritis, uveitis, or liver disease.

Physical

  • Fever, tachycardia, dehydration, and toxicity may occur. Pallor may be noted, reflecting anemia. The magnitude of these factors is related directly to the severity of the attack.
  • Evaluate for signs of localized peritonitis, although abdominal tenderness is common. Patients with toxic megacolon appear septic. They have high fever; lethargy; chills; tachycardia; and increasing abdominal pain, tenderness, and distention.
  • Patients with Crohn's disease may develop a mass in the right lower quadrant.
  • The rectal examination often reveals bloody stool on gross or Hemoccult examination.
  • Complications (eg, perianal fissures or fistulas, abscesses, rectal prolapse) may be observed in up to 90% of patients with Crohn's disease.
  • The physical examination should include a search for extraintestinal manifestations, such as iritis, episcleritis, arthritis, and dermatologic involvement.

Distinguishing Features of Crohn's Disease Versus Ulcerative Colitis

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Table
FeaturesCrohn’s DiseaseUlcerative Colitis
Skip areasCommonNever
Cobblestone mucosaCommonRare
Transmural involvementCommonOccasional
Rectal sparingCommonNever
Perianal involvementCommonNever
FistulasCommonNever
StricturesCommonOccasional
GranulomasCommonOccasional
FeaturesCrohn’s DiseaseUlcerative Colitis
Skip areasCommonNever
Cobblestone mucosaCommonRare
Transmural involvementCommonOccasional
Rectal sparingCommonNever
Perianal involvementCommonNever
FistulasCommonNever
StricturesCommonOccasional
GranulomasCommonOccasional

Causes

  • The etiology of inflammatory bowel disease (IBD) is unknown. Environmental, infectious, genetic, autoimmune, and host factors have been suspected. Interactions among these factors may be more important.
    • Inflammatory mediators
      • Interleukin-1
      • Tumor necrosis factor–alpha (TNF-alpha)
    • Aggravation by bacterial infection and inflammatory cascade
    • Positive family history: The most important risk factor for developing IBD is a positive family history.
  • The risk of developing ulcerative colitis is higher in nonsmokers and former smokers than in current smokers. The onset of ulcerative colitis occasionally appears to coincide with smoking cessation. This does not imply that smoking would improve the symptoms of ulcerative colitis. Interestingly, some success in the use of nicotine patches has been reported. On the contrary, patients with Crohn's disease have a higher incidence of smoking than the general population, and those patients with Crohn's disease who continue to smoke appear to be less likely to respond to medical therapy.

More on Inflammatory Bowel Disease

Overview: Inflammatory Bowel Disease
Differential Diagnoses & Workup: Inflammatory Bowel Disease
Treatment & Medication: Inflammatory Bowel Disease
Follow-up: Inflammatory Bowel Disease
Multimedia: Inflammatory Bowel Disease
References
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Further Reading

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Keywords

IBD, inflammatory bowel disease, IBD symptoms, IBD diagnosis, IBD treatment, ulcerative colitis, Crohns, Crohn disease, Crohn's disease, regional enteritis, terminal ileitis, granulomatous ileocolitis, inflammation of the colon, colitis, irritable bowel syndrome, mucous colitis, spastic colon

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Contributor Information and Disclosures

Author

Sarvotham Kini, MD, Associate Professor of Emergency Medicine, Medical University of South Carolina, Charleston.
Sarvotham Kini, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, and South Carolina Medical Association
Disclosure: Nothing to disclose.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eugene Hardin, MD, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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