Background
Colitis is an inflammation of the colon. It may be associated with enteritis (inflammation of the intestine) and/or proctitis (inflammation of the rectum). Inflammatory bowel disease (IBD) is a generic term used to describe 2 idiopathic disorders that are associated with GI inflammation: Crohn disease (CD) and ulcerative colitis (UC). A study from Scotland reported a 3-fold rise in newly diagnosed CD from 1968-1983 and a 4.4-fold rise from 1968-1988. However, a consistent upward trend in cases of UC in the same period did not occur.
Pathophysiology
The pathophysiology of colitis differs because of various etiologies.
Necrotizing enterocolitis
Necrotizing enterocolitis (NEC) is common cause of colitis in newborns.
Necrotizing enterocolitis totalis. Very small and ill preterm infants are particularly susceptible to NEC. Prematurity and the presence of bacteria in the GI tract are significant risk factors associated with NEC.
NEC appears to involve a final common pathway that includes the endogenous production of inflammatory mediators, such as endotoxin lipopolysaccharide, platelet-activating factor, tumor necrosis factor, and other cytokines,[1] that are involved in intestinal injury.
Hypoxic ischemia and aggressive enteral feedings are also associated in the pathogenesis of NEC. Varying degrees of mucosal and/or transmural necrosis of the intestine and colon are recognized. The distal ileum and proximal colon are most frequently involved; in severe cases, gangrene may involve the whole bowel from the rectum to the stomach. NEC presents with the gas accumulation in the submucosa of the bowel wall and progresses to necrosis leading to perforation of the bowel, peritonitis, and sepsis. Histological changes in NEC include mucosal edema, hemorrhage, coagulation necrosis, and mucosal ulceration.
Allergic colitis
In children aged 2 weeks to 1 year, the most common form of colitis is allergic colitis, which results from hypersensitivity commonly to cow's milk and soy milk. The so-called breast milk allergy is a status of food allergy induced in breastfed babies by heterologous proteins (typically cow's milk proteins) ingested by their mothers and appearing in their breast milk. The immunologic responses may vary from classic allergic mast cell activation to immune complex formation.
Pseudomembranous colitis
Pseudomembranous colitis is a form of inflammatory colitis characterized by the pathologic presence of pseudomembranes consisting of mucin, fibrin, necrotic cells, and polymorphonuclear leukocytes. This form of colitis is pathognomonic of infection by toxin-producing Clostridium difficile and develops as a result of altered normal microflora (usually by antibiotic therapy) that favors overgrowth and colonization of the intestine by Clostridium difficile and production of its toxins. Although every antibiotic has been reported to be associated with pseudomembranous colitis, clindamycin and amoxicillin are the antibiotics most frequently implicated in children.
Inflammatory bowel disease
IBD is an uncommon cause of chronic colitis in children but is becoming more frequent. The etiology is poorly understood.
Inflammatory bowel disease. Severe colitis noted during colonoscopy. The mucosa is grossly denuded, with active bleeding noted. This patient had her colon resected very shortly after this view was obtained. Genetic and environmental influences are involved in the pathogenesis of IBD. It can present in 2 different forms: UC and CD.
UC is characterized by inflammation and ulceration confined to colonic mucosa. CD is manifested by transmural inflammation and granulomas affecting any segment of the GI tract, including the colon. UC invariably involves the rectum and extends proximally without skipping segments. In contrast, CD has discontinuous patchy involvement of the GI tract, involving the small bowel, ileum, and colon. Growth failure results from malabsorption and loss of proteins from inflammation and damage to the mucosa; it is 3 times more likely to occur in children with CD than in children with UC.
The diarrhea also results from mucosal damage, bile acid malabsorption, bacterial overgrowth, and protein exudation from mucosa. Extraintestinal manifestations, which are slightly more common in CD than in UC, result from bacterial products and inflammatory mediators (eg, cytokines, prostaglandins, reactive oxygen metabolites) entering and subsequently being deposited in various tissues and organs, such as eye (uveitis), skin (erythema nodosum), liver (cholangitis, hepatitis), and joints (arthritis).
Bacterial colitis
Bacterial colitis is the most common cause of colitis, particularly beyond the first year of life. It can be caused by bacterial, viral, and parasitic agents. The most common bacterial agents are Escherichia coli (enterohemorrhagic E coli [EHEC] and enteroinvasive E coli [EIEC]) and species of Shigella, Salmonella, Campylobacter, and Yersinia.
Salmonella infections are typically spread by the fecal-oral route; the outbreaks commonly are associated with contaminated eggs, dairy products, and meats. Gastric acid is usually lethal to the organism, but susceptibility to infection is increased with decreased GI motility, rapid emptying of the stomach postgastrectomy, a large quantity of ingested bacteria, malnutrition, antibiotic use, and achlorhydria. Salmonellae can penetrate the epithelial layer to the level of the lamina propria and evoke a leukocyte response. Salmonellae cause diarrhea by producing several toxins and prostaglandins, stimulating the active secretion of fluids and electrolytes.
Shigella species attach to binding sites on the surface of the intestinal mucosal cells. The organism penetrates and proliferates in the cell, which leads to cell destruction, produces mucosal ulcerations, and causes bleeding. Shigellae also elaborate the exotoxins that produce diarrhea.
E coli may produce diarrhea because of several characteristics. Pathologic strains have been classified as enteropathogenic, enterotoxic, enteroinvasive, enteroaggregative, enteroadherent, and enterohemorrhagic. EHEC, including O157:H7 and O26:H11, cause hemorrhagic colitis and systemic complications (eg, hemolytic uremic syndrome [HUS]). The risk of developing HUS after infection with E coli O157 is estimated to be 10-15% in children. In typical infectious colitis, the lamina propria of the large intestine is infiltrated by polymorphonuclear leukocytes. On the other hand, EIEC share almost identical pathogenetic mechanisms with Shigella.
Parasitic colitis
Entamoeba histolytica is the most common cause of parasitic colitis in the world. Transmission is through ingestion of trophozoites, usually from water contamination, and person-to-person transmission because of poor sanitation. Balantidium coli is a large ciliated protozoan that manifests very similar to amebiasis.
Viral colitis caused by cytomegalovirus infection
Colitis caused by cytomegalovirus (CMV) infection is a rare form of colitis that typically is found in immunocompromised patients, such as organ recipients who are receiving immunosuppressive treatment. It results in deep round ulcerations that have a tendency to bleed easily and profusely.
Ischemic colitis
Ischemic colitis is a form of vasculitis that results from inflammation and ischemia of colonic mucosa, which causes rectal bleeding and abdominal pain. This form of colitis is common in Henoch-Schönlein purpura (HSP), which is considered one of the collagen vascular diseases.
Epidemiology
Frequency
United States
The onset of IBD commonly occurs during adolescence and young adulthood. The risk of IBD in family members of an affected individual is 7-22%; a child's risk of acquiring the disease is more than 35% if both parents have the disease.
- The prevalence of UC in the United States is 100-200 per 100,000 population.
- The incidence of CD is approximately 3-4 per 100,000 population, and the prevalence is 30-100 per 100,000 population.
- NEC affects 1-5% of patients admitting to neonatal ICUs.
- NEC may occur in 2-5% of infants with birthweights less than 1500 g.
- In the United States, the prevalence of amebiasis in high-risk groups is reported to be 1-4%.
International
The incidence UC is highest in northern European countries and the United States (15/100,000); incidence is lowest in Japan and South Africa (1/100,000).[2]
- A north-to-south gradient appears to be present, with higher incidence of both UC and CD in northern locations.
- The prevalence of amebic infections worldwide varies from 5-81%, with the highest frequency occurring in tropical climates.
Mortality/Morbidity
Morbidity and mortality are as follows:
- Diarrheal diseases are some of the leading causes of morbidity and mortality in children worldwide, causing one billion episodes of illness and 3-5 million deaths annually.
- In the United States, 20-35 million episodes of diarrhea occur each year in the 16.5 million children who are younger than 5 years, resulting in 300-400 deaths.
- Medical treatment fails in 20% of patients who have NEC with pneumatosis intestinalis at diagnosis, resulting in a 9-25% mortality rate. The mortality rate of NEC is greater than 50% in infants with birthweights less than 1000 g.
Race
The prevalence of IBD is increased among Jewish people of European Ashkenazi descent. A positive family history is the most consistent risk factor for children with IBD. HSP is common in white people. Food-allergic colitis is believed to be present in approximately 0.5% of all infants.
Sex
HSP is common in males.
Age
NEC is a disease of newborns, with low and very low birth weight preterm infants being particularly susceptible.
Allergic colitis is the most common form of colitis during the first year of life.
IBD is generally diagnosed in children aged 5-16 years. IBD has a bimodal distribution with an early onset at age 15-25 years and a second smaller peak at age 50-80 years.
HSP occurs in school-aged children and young adults.[3]
[Best Evidence] Henderson G, Craig S, Baier RJ, Helps N, Brocklehurst P, McGuire W. Cytokine gene polymorphisms in preterm infants with necrotising enterocolitis: genetic association study. Arch Dis Child Fetal Neonatal Ed. Mar 2009;94(2):F124-8. [Medline].
Hou JK, El-Serag H, Thirumurthi S. Distribution and Manifestations of Inflammatory Bowel Disease in Asians, Hispanics, and African Americans: A Systematic Review. Am J Gastroenterol. May 26 2009;[Medline].
Karwowski CA, Keljo D, Szigethy E. Strategies to improve quality of life in adolescents with inflammatory bowel disease. Inflamm Bowel Dis. May 26 2009;[Medline].
Wiskin AE, Wootton SA, Culliford DJ, Afzal NA, Jackson AA, Beattie RM. Impact of disease activity on resting energy expenditure in children with inflammatory bowel disease. Clin Nutr. Jun 8 2009;[Medline].
Hartman C, Eliakim R, Shamir R. Nutritional status and nutritional therapy in inflammatory bowel diseases. World J Gastroenterol. Jun 7 2009;15(21):2570-8. [Medline].
Eshuis EJ, Bemelman WA, Stokkers PC. Infliximab for the treatment of ulcerative colitis. Expert Rev Gastroenterol Hepatol. Jun 2009;3(3):219-29. [Medline].
Turner D, Mack D, Leleiko N, et al. Severe pediatric ulcerative colitis: a prospective multicenter study of outcomes and predictors of response. Gastroenterology. Feb 26 2010;[Medline].
Komati JT, Sdepanian VL. Effectiveness of Infliximab in Brazilian Children and Adolescents With Crohn Disease and Ulcerative Colitis According to Clinical Manifestations, Activity Indices of Inflammatory Bowel Disease, and Corticosteroid Use. J Pediatr Gastroenterol Nutr. Apr 7 2010;[Medline].
Karoui S, Serghini M, Chaieb M, et al. [Frequency and predictive factors of colectomy and coloproctectomy in ulcerative colitis]. Tunis Med. Feb 2009;87(2):115-9. [Medline].
Watanabe C, Sumioka M, Hiramoto T, et al. Magnifying colonoscopy used to predict disease relapse in patients with quiescent ulcerative colitis. Inflamm Bowel Dis. Jun 5 2009;[Medline].
[Guideline] Cohen JL, Strong SA, Hyman NH, et al. Practice parameters for the surgical treatment of ulcerative colitis. Dis Colon Rectum. Nov 2005;48(11):1997-2009. [Medline].
[Guideline] IBD Guideline Team, Cincinnati Children's Hospital Medical Center. Evidence-based care guideline for the management of pediatric moderate/severe inflammatory bowel disease (IBD). Apr 5 2007.
[Guideline] Lichtenstein GR, Abreu MT, Cohen R, Tremaine W. American Gastroenterological Association Institute medical position statement on corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease. Gastroenterology. Mar 2006;130(3):935-9. [Medline].
Afghani B, Stutman HR. Toxin-related diarrheas. Pediatr Ann. Oct 1994;23(10):549-50, 553-5. [Medline].
Andres PG, Friedman LS. Epidemiology and the natural course of inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):255-81, vii. [Medline].
Baldassano RN, Piccoli DA. Inflammatory bowel disease in pediatric and adolescent patients. Gastroenterol Clin North Am. Jun 1999;28(2):445-58. [Medline].
Becker JM. Surgical therapy for ulcerative colitis and Crohn's disease. Gastroenterol Clin North Am. Jun 1999;28(2):371-90, viii-ix. [Medline].
Bousvaros A. Overview of the management of Crohn's disease in children and adolescents. UpToDate. 2005;13.2.
Floch MH, Madsen KK, Jenkins DJ, et al. Recommendations for probiotic use. J Clin Gastroenterol. Mar 2006;40(3):275-8. [Medline].
Han PD, Burke A, Baldassano RN, et al. Nutrition and inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):423-43, ix. [Medline].
Higuchi LM. Epidemiology and diagnosis of inflammatory bowel disease in children and adolescents. UpToDate. 2005;12.3.
Hoshiko M. Laboratory diagnosis of infectious diarrhea. Pediatr Ann. Oct 1994;23(10):570-4. [Medline].
Hyams JS. Crohn's disease in children. Pediatr Clin North Am. Feb 1996;43(1):255-77. [Medline].
Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2000;21(9):291-5. [Medline].
Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2005;26(9):314-20. [Medline].
Kirschner BS. Ulcerative colitis in children. Pediatr Clin North Am. Feb 1996;43(1):235-54. [Medline].
La Via WV. Parasitic gastroenteritis. Pediatr Ann. Oct 1994;23(10):556-60. [Medline].
Markowitz JF. Inflammatory bowel disease: the pediatrician's role. Contemporary Pediatrics. May 1996;13(5):25-46.
Motil KJ, Grand RJ. Ulcerative colitis and Crohn disease in children. Pediatr Rev. Oct 1987;9(4):109-20. [Medline].
Murray K. Ulcerative colitis in children and adolescents. UpToDate. 2005;13.2.
Neu J. Necrotizing enterocolitis: the search for a unifying pathogenic theory leading to prevention. Pediatr Clin North Am. Apr 1996;43(2):409-32. [Medline].
Papadakis KA, Targan SR. Current theories on the causes of inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):283-96. [Medline].
SanJoaquin VH. Aeromonas, Yersinia, and Miscellaneous Bacterial Enteropathogens. Pediatric Annals. 1994;23(10):544-548. [Medline].
Scotiniotis I, Rubesin SE, Ginsberg GG. Imaging modalities in inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):391-421, ix. [Medline].
Sherman PM, Petric M, Cohen MB. Infectious gastroenterocolitides in children: an update on emerging pathogens. Pediatr Clin North Am. Apr 1996;43(2):391-407. [Medline].
Stein RB, Hanauer SB. Medical therapy for inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):297-321. [Medline].
Stutman HR. Salmonella, Shigella, and Campylobacter: common bacterial causes of infectious diarrhea. Pediatr Ann. Oct 1994;23(10):538-43. [Medline].
Udall JN Jr. Secretory diarrhea in children: newly recognized toxins and hormone- secreting tumors. Pediatr Clin North Am. Apr 1996;43(2):333-53. [Medline].
Ulshen M. Inflammatory bowel disease. In: Nelson Textbook of Pediatrics. 16th ed. 2000:1150-7.
[Best Evidence] Baldassarre ME, Laforgia N, Fanelli M, Laneve A, Grosso R, Lifschitz C. Lactobacillus GG improves recovery in infants with blood in the stools and presumptive allergic colitis compared with extensively hydrolyzed formula alone. J Pediatr. Mar 2010;156(3):397-401. [Medline].
Print
