eMedicine Specialties > Pediatrics: General Medicine > Gastroenterology

Colitis

Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge

Updated: Jun 17, 2009

Introduction

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.

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.

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.

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

• 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

Clinical

History

The following may be observed in patients with colitis:

• Necrotizing enterocolitis (NEC) occurs with wide spectrum of illness, from mild with only guaiac-positive stools to severe with peritonitis, perforation, shock, coagulopathy, and death. The onset is usually insidious, but illness may rapidly progress. The first sign is abdominal distention with gastric retention, emesis, and discomfort. Illness may progress to hemodynamic compromise. A plain film radiograph of the abdomen can assist in the diagnosis.
• Infants with allergic colitis present with blood and mucous in the stool, vomiting, and diarrhea after introduction of milk when they are aged approximately 1 week to 3 months. The syndrome is also known to occur in exclusively breast-fed infants, as a reaction to food allergens present in the mother's diet and appearing in the breast milk. The typical presentation of milk-protein sensitivity colitis is the acute onset of blood-streaked mucoid diarrheal stool in a well-appearing infant younger than 6 months. The infants do not appear sick or dehydrated, and weight gain is typically within normal limits.
• Pseudomembranous colitis usually presents with profuse watery or mucoid diarrhea, tenesmus, fever, abdominal cramps, and tenderness usually within one week of antibiotic therapy. The stools may be frankly bloody or guaiac-positive.
• Inflammatory bowel disease (IBD) is generally diagnosed in children aged 5-16 years. The onset of IBD, with Crohn disease (CD) or ulcerative colitis (UC), is usually insidious, consisting of growth failure, weight loss, diarrhea, and occult rectal bleeding.
  • Growth failure is more common in children with CD (35-88%) than in children with UC (6-12%). Weight loss has been reported in as many as 68% of children who are diagnosed with IBD.
  • UC tends to run a more complicated course in children than in adults. Abdominal pain and diarrhea, with or without occult blood, are the most common symptoms at presentation. The pain is frequently colicky and, in CD, may localize to the right lower quadrant or periumbilical area. Frank rectal bleeding occurs in fewer than 25% of all cases but is more common in UC than CD. Perianal disease, including fissures, skin tags, fistulae, and abscesses, occurs in 15% of children with CD and may precede the intestinal manifestations by several years, leading to a misdiagnosis that may include infectious colitis, iron deficiency anemia, juvenile rheumatoid arthritis, and growth disorders.
  • Arthralgias and arthritis are among the most frequent extraintestinal complaints of children with UC. The presence of ankylosing spondylitis is more consistent with a diagnosis of CD than UC. Pubertal development may be delayed or arrested in patients with active UC. Aphthous stomatitis is frequently present during the initial attack or relapse of UC. Renal calculi develop in 6% of patients, predominantly as uric acid in UC and as oxalate in CD. Ophthalmic complications (eg, uveitis, iritis, episcleritis) may be a sign of IBD or secondary to corticosteroid therapy in patients treated for IBD.
  • The disease is characterized as mild, moderate, or severe, depending on stool frequency, amount of abdominal tenderness, fever, and hemoglobin and albumin concentrations.
• Salmonellae may cause food-borne outbreaks, often in summer and fall. The child experiences abdominal cramps and nausea after an incubation period of 8-48 hours postingestion of a contaminated source, food or water. The stools are watery and may contain blood. Fever is noted in most children.
• Shigellae may cause asymptomatic infection, mild gastroenteritis, or bacillary dysentery. Bacillary dysentery begins suddenly with fever and abdominal pain, and diarrhea begins shortly thereafter. The stools are frequent, averaging of 10-12 daily, and they contain mucous and blood; tenesmus is common. The child has a fever, often in the range of 102-104°F (39-40°C). A shigellae infection occasionally produces CNS irritation and presents as seizure, even before other manifestations of the illness arise.
• Campylobacter enteritis is characterized by the abrupt onset of fever and abdominal pain, shortly followed by diarrhea. Temperature often remains normal in children younger than 3 months, but ranges up to 40°C in older children. Vomiting is uncommon. Two thirds of the children may have severe abdominal pain. The stools are watery and occur 2-20 times daily; they contain blood in 50-95% of cases.
• Yersinia enterocolitica infection presents with an abrupt onset of watery diarrhea that may contain blood. Most of the patients experience severe abdominal pain, which may be mistaken for appendicitis. Older children have a febrile response with a temperature from 99-104°F. Joint pain secondary to arthritis and rashes occur in 5-10% of patients with yersiniosis.
• Amebiasis is manifested clinically as dysenteric colitis, commonly presenting with bloody diarrhea, abdominal pain, and fever. B coli causes similar symptoms to amebiasis.
• Henoch-Schönlein purpura (HSP) is preceded by upper respiratory infection in one third to three fourths of patients. The patient presents with colicky abdominal pain, migratory arthritis affecting the larger joints, and a purpuric rash that is symmetrical and most noticeable over the extensor surfaces of the arms, legs, and buttocks.

Physical

• NEC may present with abdominal distention, tenderness, and guarding. The infant may develop hypotension, tachycardia, tachypnea, hypoxia, shock, disseminated intravascular coagulation (DIC), and cardiopulmonary arrest. The stool may have frank blood or may be heme-guaiac positive.
• Allergic colitis presents with blood and mucous in the stool. Children are usually well appearing; however, uncommonly, the colitis is severe, and the children may become anemic and present with failure to thrive.
• Pseudomembranous colitis presents with diarrhea with frank blood or a guaiac-positive stool. An abdominal examination may elicit tenderness. Signs of perforation, peritonitis, and toxic megacolon may be present.
• IBD may present with pallor, tachycardia, abdominal tenderness, and blood in the stool. The child may present with an elevated temperature, weight loss, and dehydration. The presence of abdominal distention with decreased or absent bowel sounds is indicative of actual or impending perforation. Rarely, CD causes intestinal obstruction. Toxic megacolon is a life-threatening complication of UC and CD. Toxic megacolon almost always involves the transverse colon and may present with ileus, peritonitis secondary to perforation, and sepsis.
• Amebiasis may present with temperature elevation, hematochezia, abdominal tenderness, or complications such as liver abscess, colonic perforation, and peritonitis.
• HSP presents with a purpuric symmetric rash commonly over legs, buttocks, and arms. Asymptomatic microhematuria occurs in 80% of affected patients. The child may have hypertension, proteinuria, and hematochezia. Joint swelling may be present.

Causes

• Inflammation of the colon can be caused by infection, hypersensitivity to various allergens, ischemia, vasculitis, or several drugs.
• The cause of colitis in IBD is unknown, but recent studies have identified a gene (NOD2) involved in at least 20% of cases of Crohn disease. This gene is involved in the regulation of the epithelial response to bacterial antigens, thus stressing the role of bacteria in the pathogenesis of IBD. Evidence suggests a genetic predisposition to IBD, including ethnic differences, family aggregation, concordance rates in twins, chromosomal linkage, and genetic syndromes associated with IBD. The lack of total concordance of disease among monozygotic twins and other differences support a role for cofactors in the development of IBD.
• In the United States, bacterial and viral infections are very common causes of colitis, whereas in developing countries, parasitic infections are very common causes.

Differential Diagnoses

Workup

Laboratory Studies

The following studies may be indicated in patients with colitis:

• For newborns with necrotizing enterocolitis (NEC), obtain an ABG, WBC count, hemoglobin, platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), electrolytes, and disseminated intravascular coagulation (DIC) profile as indicated.
• A child with allergic colitis may have an elevated WBC count, low hemoglobin, often (but not invariably) an increase in eosinophils, and hypoalbuminemia (if a condition of protein-losing enteropathy coexists). In the search for fecal leucocytes, stools are positive for neutrophils and eosinophils.
• In patients with pseudomembranous colitis, WBC counts are usually higher than 15,000/mcL. An etiologic diagnosis requires the identification for C difficile toxin in the stool.
• When bacterial etiology (eg, Salmonella species, Shigella species, Campylobacter species, Yersinia species, E coli, C difficile) is suspected, stools need to be tested for cultures, and Gram and methylene blue staining of the stool is recommended. The WBC counts can be elevated or normal.
  • Most of the organisms may be cultured from the stool by using appropriate media, but enrichment techniques for Y enterocolitica may be required. Infectious agents, such as Clostridium perfringens, E coli, and S epidermidis species, have been recovered from stool cultures in patients with colitis. Nonetheless, in most cases, no pathogen is identified.
  • Failure to isolate pathogenic organisms may be because of possible clearance of the organisms at time of isolation, failure to identify an organism, lack of suitable culture techniques, or laboratories not routinely testing for all pathogens.
  • Enterohemorrhagic E Coli (EHEC), including O157:H7 and O26:H11, causes hemorrhagic colitis and systemic complications, including hemolytic uremic syndrome (HUS).
  • In typical infectious colitis, the lamina propria of the large intestine is infiltrated by polymorphonuclear leukocytes.
• If a parasitic cause (E histolytica, B coli) is suspected, consider a stool examination, serology, or scrapings of mucosal ulcerations to identify the organism.
• In a child with suspected inflammatory bowel disease (IBD), colonoscopy is the test of choice and never should be avoided if the patient's condition is stable enough to allow the test to be performed. If Crohn disease (CD) is being considered, an upper GI endoscopy and radiography with barium swallow and small bowel follow-through also need to be done.
• Blood studies should include CBC count, serum electrolyte level, BUN level, creatinine level, C-reactive protein (CRP) level, and liver function test results (eg, transaminases, total protein, serum albumin, PT). CRP is elevated in as many as 90% of patients with CD and in more than 50% of those with ulcerative colitis (UC). Thrombocytosis and hypoalbuminemia correlate best with histologic inflammation of the colon in UC. Acute phase reactants are more likely to be elevated in patients with CD than in those with UC. If the differential diagnosis between Crohn colitis and UC is unclear, measuring serum levels of Anti-Saccharomyces cerevisiae antibody (ASCA) and perinuclear antineutrophilic cytoplasmic antibody (p-ANCA) antibody may be very useful: the former is found almost exclusively in Crohn colitis, whereas the latter are more indicative of UC. Stool blood and fecal leukocytes may indicate the presence of active inflammation.
• Assessment of skeletal age is indicated in children with short stature.
• In patients with Henoch-Schönlein purpura (HSP), findings from routine laboratory studies, including CBC count, electrolyte levels, serum protein levels, and C3 complement levels, are usually normal. The erythrocyte sedimentation rate (ESR) may be elevated. The diagnosis is based on clinical findings.

Imaging Studies

• The diagnostic yield of plain film radiographs is relatively low. Nevertheless, the diagnosis of NEC can be assisted by a plain film radiograph of the abdomen, demonstrating pneumatosis intestinalis (ie, gas accumulation in the submucosa of the bowel wall) in 50-75% of patients, gas in the portal vein in severe cases, and pneumoperitoneum in patients with perforation of the bowel.
• Plain film radiography also can be useful in establishing a diagnosis of toxic megacolon, bowel obstruction, or perforation, and they should be performed as initial studies.

Treatment

Medical Care

• Treatment of allergic colitis consists of elimination of the offending protein from the infant's diet. Infants should receive a formula containing casein-hydrolysate as the protein source (eg, Nutramigen, Pregestimil, Alimentum). Mothers of exclusively breastfed infants with allergic colitis should eliminate the offending proteins (typically milk) from their diets. Persistence of gross bleeding after 14 days following a formula change is an indication for proctosigmoidoscopy. Infants with response to diet change should be challenged around their first birthday.
• Treatment of a child with pseudomembranous colitis depends on the severity of disease. Mild cases require cessation of antibiotics and supportive therapy with fluids and electrolytes. Evaluate patients with severe or persistent antibiotic-associated colitis for C difficile toxin in the stool. The patient should be treated with oral metronidazole (30 mg/kg/d in 4 divided doses) or oral vancomycin (40 mg/kg/d in 4 divided doses).
• Management of bacterial colitis is somewhat controversial. Shigellosis stands alone as the only form of bacterial colitis for which antibiotics have proved efficacious.
  • Antimicrobial therapy shortens the course of the illness and the duration of excretion of the organisms in the stool by alleviating the signs and symptoms and limiting the transmission of the disease. Trimethoprim-sulfamethoxazole (TMP-SMZ) is the initial drug of choice; fluoroquinolones and ceftriaxone are the alternatives.
  • If Salmonella bacteremia is suspected, intravenous cefotaxime (200 mg/kg/d in 4 divided doses) or ceftriaxone (100 mg/kg/d in 2 divided doses) should be initiated. Alternative treatments include chloramphenicol (100 mg/kg/d in 4 divided doses) or, in adolescents, fluoroquinolones. TMP-SMZ is the drug of choice when oral treatment is indicated.
  • In Yersinia enterocolitica, antibiotic therapy of intravenous gentamicin (5-7.5 mg/kg/d in 3 divided doses) is indicated in patients with persistent diarrhea or suspected sepsis. Alternative antibiotics may include chloramphenicol, colistin, and kanamycin.
  • Campylobacter enteritis is usually self-limited. The organism is sensitive to erythromycin and ciprofloxacin, but antibiotic treatment has not been proved to decrease the duration of diarrhea.
  • Treatment of amebic colitis includes metronidazole and iodoquinol or paromomycin.
  • Please see the eMedicine articles, Crohn Disease and Ulcerative Colitis.
• Management of inflammatory bowel disease (IBD) depends on the severity of the disease at presentation and is intended to decrease the bowel inflammation, with the goal of eventual healing, managing complications, and preventing recurrence or worsening disease.
  • The therapy includes pharmacotherapy, surgery, nutrition,⁵ supportive therapy, psychotherapy, and cancer screening.
  • Medications used to treat IBD can be classified into six categories, as follows:
    • Aminosalicylates (sulfasalazine, mesalamine)
    • Corticosteroids (prednisone, budesonide)
    • Immunomodulators (eg, azathioprine, 6-mercaptopurine)
    • Antibiotics (eg, metronidazole, ciprofloxacin)
    • Probiotics (Lactobacillus GG, Saccharomyces boulardii)
    • Biological agents (eg, infliximab)⁶
  • Children with mild manifestations can be treated as outpatients with arrangement for follow-up treatment with a gastroenterologist.
• The initial therapy for children with mild ulcerative colitis (UC) or Crohn disease (CD) is usually sulfasalazine, a 5-aminosalicylate drug (5-ASA) that is given alone or in combination with topical enemas (ie, corticosteroid, mesalamine) or corticosteroid foam. Adolescents may prefer the foam because of its ease of administration and reduced sensation of rectal distention and urgency.
• Patients with moderate and severe disease (fever, bloody stools, severe abdominal pains, anemia, hypoalbuminemia) require supportive treatment, often with intravenous hydration.
• Hospitalization is often indicated for management of acute disease with corticosteroids and or immunosuppressive agents.
• Intravenous methylprednisolone or hydrocortisone at a dose equivalent to 1-2 mg/kg/d of prednisone is recommended. The goal is to use steroids for a short period and change to a maintenance therapy as soon as possible.
• Maintenance therapy may require administration of 5-ASA or an immunomodulator, such as azathioprine or 6-mercaptopurine.
• Refractory patients with CD may need infliximab as a maintenance agent. Infliximab has been used in the treatment of severe CD, but experience with its use in severe UC is limited.
• If toxic megacolon is suspected, aggressive resuscitation with fluids and electrolytes is required.
• Begin a combination of broad-spectrum intravenous antibiotics, such as ampicillin (200 mg/kg/d), gentamicin (5-7.5 mg/kg/d), and clindamycin (40 mg/kg/d). Alternate therapy may include either ampicillin/sulbactam (Unasyn) or cefoxitin in combination with gentamicin.
• Medical treatment includes adequate nutritional intake and social and emotional support.
• Nutrition therapy may be primary or adjunctive in CD but is only adjunctive in UC. Elemental or polymeric formulas may affect remission in as many as 80% of patients with CD.
• No specific therapy is indicated for Henoch-Schönlein purpura (HSP). Steroids are used to treat severe abdominal pain or arthritis in selected patients.

Surgical Care

• Surgery is indicated in UC or CD if uncontrolled GI bleeding, bowel perforation, bowel obstruction, failure to respond to medical therapy, and unacceptable medical toxicity are present.
• Total colectomy may be indicated in UC when the patient has toxic megacolon or acute fulminant colitis or in selected severe forms when medical therapy (including the newest immunosuppressive agents, eg, tacrolimus, infliximab) has failed.⁷ In UC, colectomy usually is performed with the creation of a "pouch" from the distal ileum and is curative (see Ulcerative Colitis). As many as 40% of the children may develop the so-called "pouchitis" (inflammation of the pouch) within 1 year. This entity is of unclear origin, but typically responds quickly to a course of antimicrobial treatment. Recent evidence in adults suggests that prophylaxis with probiotics may be an effective preventative tool.
• In CD, surgery is not curative because recurrent disease at the site of surgery is common. In CD, segmental bowel resection is the most common procedure and usually involves the diseased terminal ileum and adjacent inflamed colon. Stricturoplasty should be considered if there is stenosed bowel segment without active inflammation.
• At times surgical resection is used to treat growth failure.

Consultations

• A surgical consultation is required in patients with suspected toxic megacolon, appendicitis, intestinal obstruction, fulminant colitis, or significant GI bleeding.

Diet

• See Medical Care.

Medication

Because the causes of colitis are multiple and quite diverse, medical treatment of colitis is based on the underlying diagnosis.

Anti-inflammatory agents

Corticosteroids and 5-aminosalicylic acid (5-ASA) derivatives are used to treat ulcerative colitis (UC). See the corresponding eMedicine articles for the specific underlying diagnoses.

Sulfasalazine (Azulfidine, EN-tabs)

Sulfonamide derivative conjugate of 5-ASA. Serves as a carrier for 5-ASA. Useful in the management of UC and acts locally in colon to decrease inflammatory response and systemically inhibit prostaglandin synthesis.

Dosing

Adult

1 g PO tid/qid initially; followed by maintenance dose of 1.5-2 g/d PO divided q6h

Pediatric

<2 years: Contraindicated
>2 years:
Initial: 6.7-10 mg/kg PO q4h; alternatively, 10-15 mg/kg PO q6h or 13.3-20 mg/kg q8h; not to exceed 6 g/d
Maintenance: 50-75 mg/kg/d PO in 3-4 divided doses; not to exceed 2 g/d

Interactions

Decreases effects of iron, digoxin, cyclosporine, and folic acid; conversely, increases effects of PO anticoagulants, PO hypoglycemic agents, and methotrexate; may alter platelets, caution with coadministration of drugs affecting coagulation

Contraindications

Documented hypersensitivity; hypersensitivity to drugs containing sulfa moiety (eg, thiazides, furosemide, sulfonylureas, salicylate) or any component; GI or GU obstruction; porphyria

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Pregnancy category D near term; caution in patients with renal (adjust dose) or hepatic impairment, blood dyscrasias, G-6-PD deficiency, fragile X chromosome associated with mental retardation, or urinary obstruction

Mesalamine (5-ASA, Asacol, Pentasa, Rowasa)

Used for mild-to-moderate UC. The active component of sulfasalazine used for IBD. Effects chemical mediators of inflammatory response, particularly prostaglandins and leukotrienes. Usual course of therapy in adults is 3-6 wk. Some patients may need concurrent rectal and PO therapy. PO products are formulated to release slowly throughout GI tract.

Dosing

Adult

Capsules: 1 g PO qid
Tablets: 800 mg PO tid
Rectal suppository: Insert 1 PR bid, retain for 1-3 h
Retention enema: 60 mL (4 g) PR hs

Pediatric

Capsules: 50 mg/kg/d PO divided q6-12h
Tablets: 50 mg/kg/d PO divided q8-12h
Rectal: Not established

Interactions

May decrease effect of digoxin; may alter platelets, caution with coadministration of drugs affecting coagulation

Contraindications

Documented hypersensitivity; hypersensitivity to salicylates

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Elderly persons may have difficulty administering and retaining rectal suppositories; caution in patients with renal or hepatic impairment

Hydrocortisone (Hydrocortone, Cortef)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Dosing

Adult

15-240 mg PO q12h

Pediatric

1-5 mg/kg/d or 100 mg/m²/d PO divided q12-24h

Interactions

Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific UC, diabetes, and myasthenia gravis

Methylprednisolone (Adlone, Medrol, Solu-Medrol, Depo-Medrol, Depopred)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Dosing

Adult

2-60 mg/d PO/IV/IM in 1-4 divided doses followed by gradual reduction to lowest level that can maintain clinical response

Pediatric

0.5-1.7 mg/kg/d or 5-25 mg/m²/d PO/IV/IM divided q6-12h

Interactions

Coadministration with digoxin, may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics

Contraindications

Documented hypersensitivity; viral, fungal, or tubercular skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Antidiarrheal agents

These agents are used in the treatment of diarrhea adjunctly with rehydration therapy to correct fluid and electrolyte depletion. Note that inhibition of peristaltic activity induced by opioidlike agents (eg, loperamide) is contraindicated in established infectious colitis.

Loperamide (Imodium)

Acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. Prolongs movement of electrolytes and fluid through bowel and increases viscosity and loss of fluids and electrolytes. Also has a mild proabsorptive effect on Na and Cl on the epithelial cells.

Dosing

Adult

4 mg PO initially; followed by 2 mg after each loose stool; not to exceed 16 mg/d

Pediatric

Initial:
2-6 years: 1 mg PO tid
6-8 years: 2 mg PO bid
8-12 years: 2 mg PO tid
Maintenance: 0.1 mg/kg PO after each loose stool; not to exceed initial dose
Chronic diarrhea: 0.08-0.24 mg/kg/d divided bid/tid; not to exceed 2 mg/dose

Interactions

Phenothiazines, tricyclic antidepressants, and CNS depressants may increase toxicity

Contraindications

Documented hypersensitivity; diarrhea resulting from infections; pseudomembranous colitis

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Discontinue use if no clinical improvement in 48 h; because primarily metabolized in liver, monitor for CNS toxicity in patients with hepatic insufficiency; do not use if high fever or blood in stool coincides with diarrhea; caution in infectious diarrhea caused by organism penetrating intestinal wall

Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Trimethoprim

sulfamethoxazole (TMP-SMZ, Bactrim, Bactrim DS, Septra, Septra DS, Cotrim, Cotrim DS) - Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. Dose is based on trimethoprim component.

Dosing

Adult

Mild-to-moderate infections: 6-10 mg/kg/d PO/IV divided q12h
Severe infections: 15-20 mg/kg/d PO/IV divided q8-12h for 14 d

Pediatric

<2 months: Contraindicated
>2 months: Mild-to-moderate infections: 6-10 mg/kg/d PO/IV divided q12h
Severe infections: 15-20 mg/kg/d PO/IV divided q8-12h for 14 d

Interactions

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly persons; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Contraindications

Documented hypersensitivity; megaloblastic anemia caused byfolate deficiency; age <2 mo

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not use during last trimester of pregnancy due to potential toxicity to newborn (eg, jaundice, hemolytic anemia, kernicterus); discontinue at first appearance of rash or sign of adverse reaction; frequently obtain CBC counts; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, long-term alcoholism, elderly persons, those receiving anticonvulsant therapy, individuals with malabsorption syndrome); hemolysis may occur in G-6-PDdeficiency; persons with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses adrenal function tests during therapy); give fluids to prevent crystalluria and stone formation

Ampicillin (Marcillin, Omnipen, Polycillin, Principen, Totacillin)

Bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication PO.

Dosing

Adult

250-500 mg PO q6h
0.5-1.5 g IM q4-6h
0.5-3 g IV q4-6h

Pediatric

50-100 mg/kg/d PO divided q4-6h; not to exceed 3 g/d
100-400 mg/kg/d IM/IV divided q4-6h; not to exceed 12 g/d

Interactions

Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction

Ampicillin and sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.

Dosing

Adult

1.5 (1 g ampicillin plus 0.5 g sulbactam) to 3 g (2 g ampicillin plus 1 g sulbactam) IV/IM q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin

Pediatric

3 months-12 years: 100-200 mg ampicillin/kg/d (150-300 mg Unasyn) IV divided q6h
>12 years: Administer as in adults; not to exceed 4 g/d sulbactam or 8 g/d ampicillin

Interactions

Probenecid and disulfiram elevate levels; allopurinol decreases effects and has additive effects on ampicillin rash; may decrease effects of oral contraceptives

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal failure; evaluate rash and differentiate from hypersensitivity reaction

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with an agent against gram-positive organisms and one that covers anaerobes.

Dosing

Adult

3-6 mg/kg/d IV qd or divided; dosing regimens vary; adjust dose according to CrCl and changes in volume of distribution

Pediatric

<5 years: 2.5 mg/kg/dose IV/IM q8h
>5 years: 5-7.5 mg/kg/d divided q8h; not to exceed 300 mg/d; monitor as in adults

Interactions

Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis) and adjust dose, myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; monitor each regimen by at least a trough level drawn 30 min before the fourth dose; may draw a peak level 30 min after 30 min infusion

Metronidazole (Flagyl, Protostat)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for C difficile enterocolitis).

Dosing

Adult

250-500 mg PO tid/qid
Loading dose: 15 mg/kg or 1 g for 70-kg adult IV over 1 h
Maintenance dose: 6 h following loading dose; infuse 7.5 mg/kg or 500 mg IV for 70-kg adult over 1 h q6-8h; not to exceed 4 g/d

Pediatric

Infants and children:
Oral: 30 mg/kg/d PO divided q6-8h
Intravenous: Administer as in adults using body weight

Interactions

May increase toxicity of anticoagulants, lithium, and phenytoin; cimetidine may increase toxicity; disulfiramlike reaction may occur with PO ingested ethanol

Contraindications

Documented hypersensitivity; first trimester of pregnancy

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in hepatic disease and severe renal dysfunction; monitor for seizures and development of peripheral neuropathy

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections.

Dosing

Adult

1-2 g IV q6-8h

Pediatric

Infants and children: 80-160 mg/kg/d IV divided q4-6h; higher doses for severe or serious infections; not to exceed 12 g/d

Interactions

Probenecid may increase effects; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins.

Dosing

Adult

1-2 g IV q12-24h; not to exceed 4 g/d

Pediatric

Neonates > 7 d: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d

Interactions

Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; caution in breastfeeding women and allergy to penicillin

Cefotaxime (Claforan)

For septicemia and treatment of susceptible organisms. Arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.

Dosing

Adult

1-2 g IV/IM q4-8h; not to exceed 12 g/d

Pediatric

Infants and children: 200 mg/kg/d IV/IM divided q6-8h
>12 years or >50 kg: Administer as in adults

Interactions

Probenecid may increase levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe renal impairment; has been associated with severe colitis

Chloramphenicol (Chloromycetin)

Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Dosing

Adult

50-100 mg/kg/d PO/IV divided q6h for 10 d; not to exceed 4 g/d

Pediatric

>3 months: 50-75 mg/kg/d PO/IV divided q6h; not to exceed 4 g/d

Interactions

When administered concurrently with barbiturates, chloramphenicol serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; levels may be increased or decreased

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Pregnancy category D near term; use only for indicated infections, or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (ie, gray baby syndrome)

Vancomycin (Lyphocin, Vancocin, Vancoled)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients unable to receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal penetrating injuries, is combined with an agent active against enteric flora and/or anaerobes. To avoid toxicity, current recommendation is to assay vancomycin trough levels 30 min before fourth dose. Use CrCl to adjust dose in patients with renal impairment.

Dosing

Adult

0.5-2 g/d PO divided q6-8h for 7-10 d

Pediatric

40 mg/kg/d PO divided q6-8h for 7-10 d; not to exceed 2 g/d

Interactions

Erythema, histaminelike flushing and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced, when coadministered with nondepolarizing muscle relaxants

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal failure; neutropenia; red man syndrome is caused by too rapid IV infusion (not an allergic reaction) but rarely occurs when dose is given over 2 h or as PO or IP administration

Follow-up

Complications

• For colitis caused by inflammatory bowel disease (IBD), please refer to Crohn Disease (CD) and Ulcerative Colitis (UC).
• The most serious acute complication of UC is toxic megacolon with the risk of perforation. The risk of colon cancer increases after 8-10 years of having UC.
• The complications of CD tend to increase with time and include bowel strictures, fistulas, abscess, and intestinal obstruction. After surgery, patients may develop short bowel syndrome and malabsorption.
• Hemolytic uremic syndrome (HUS) is the best-known and most important complication of colitis caused by enterohemorrhagic E coli (EHEC).

Prognosis

• About 70% children with UC enter remission within 3 months of initial therapy, and 50% remain in remission over the next year. Colectomy within 5 years is required in as many as 26% of children who present with severe disease compared with less than 10% of those who present with mild disease.
• Approximately 70% of children with CD require surgery within 10-20 years after the diagnosis.
• The risk factors for developing adenocarcinoma are duration and the extent of disease.
• Colonoscopy should be performed annually or biannually after 10 years of colonic disease and colectomy should be performed if there is finding of dysplasia.⁸
• The course of UC is marked by remissions and exacerbations. Most patients respond initially to medical treatment, and many children with mild manifestations stay in remission on prophylactic therapy with 5-aminosalicylate drug (5-ASA).
• After the first decade of disease, the risk of development of colon cancer increases rapidly; thus, surveillance colonoscopies should be performed routinely after 8-10 years of disease.
• Despite complications, most children with CD lead active lives, despite intermittent flare-up of symptoms.
• Please see Crohn Disease and Ulcerative Colitis for a more detailed description of prognosis in these conditions.

Patient Education

• Psychosocial support and education for the family is important in achieving long-term goals in the treatment of IBD. Counseling and peer support for the adolescent who has growth and pubertal delays is helpful.
• For excellent patient education resources, visit eMedicine's patient education articles Crohn Disease in Children and Teens and Inflammatory Bowel Disease.

Miscellaneous

Medicolegal Pitfalls

• Failure to make an early diagnosis of necrotizing enterocolitis (NEC) may lead to catastrophic course. Early suspicion and intervention, including abdominal obstructive series, lab studies, and treatment, are indicated.
• Failure to recognize complications of colitis (eg, toxic megacolon, hemolytic uremic syndrome [HUS], disseminated intravascular coagulation [DIC]) may result in mortality and require early diagnosis and intervention to prevent a catastrophe.

Multimedia

Media file 1: Necrotizing enterocolitis totalis.

Media file 2: 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.

References

1. [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].

2. 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].

3. 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].

4. 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].

5. 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].

6. Eshuis EJ, Bemelman WA, Stokkers PC. Infliximab for the treatment of ulcerative colitis. Expert Rev Gastroenterol Hepatol. Jun 2009;3(3):219-29. [Medline].

7. 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].

8. 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].

9. [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].

10. [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.

11. [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].

12. Afghani B, Stutman HR. Toxin-related diarrheas. Pediatr Ann. Oct 1994;23(10):549-50, 553-5. [Medline].

13. 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].

14. Baldassano RN, Piccoli DA. Inflammatory bowel disease in pediatric and adolescent patients. Gastroenterol Clin North Am. Jun 1999;28(2):445-58. [Medline].

15. Becker JM. Surgical therapy for ulcerative colitis and Crohn's disease. Gastroenterol Clin North Am. Jun 1999;28(2):371-90, viii-ix. [Medline].

16. Bousvaros A. Overview of the management of Crohn's disease in children and adolescents. UpToDate. 2005;13.2.

17. Floch MH, Madsen KK, Jenkins DJ, et al. Recommendations for probiotic use. J Clin Gastroenterol. Mar 2006;40(3):275-8. [Medline].

18. 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].

19. Higuchi LM. Epidemiology and diagnosis of inflammatory bowel disease in children and adolescents. UpToDate. 2005;12.3.

20. Hoshiko M. Laboratory diagnosis of infectious diarrhea. Pediatr Ann. Oct 1994;23(10):570-4. [Medline].

21. Hyams JS. Crohn's disease in children. Pediatr Clin North Am. Feb 1996;43(1):255-77. [Medline].

22. Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2000;21(9):291-5. [Medline].

23. Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2005;26(9):314-20. [Medline].

24. Kirschner BS. Ulcerative colitis in children. Pediatr Clin North Am. Feb 1996;43(1):235-54. [Medline].

25. La Via WV. Parasitic gastroenteritis. Pediatr Ann. Oct 1994;23(10):556-60. [Medline].

26. Markowitz JF. Inflammatory bowel disease: the pediatrician's role. Contemporary Pediatrics. May 1996;13(5):25-46.

27. Motil KJ, Grand RJ. Ulcerative colitis and Crohn disease in children. Pediatr Rev. Oct 1987;9(4):109-20. [Medline].

28. Murray K. Ulcerative colitis in children and adolescents. UpToDate. 2005;13.2.

29. 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].

30. Papadakis KA, Targan SR. Current theories on the causes of inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):283-96. [Medline].

31. SanJoaquin VH. Aeromonas, Yersinia, and Miscellaneous Bacterial Enteropathogens. Pediatric Annals. 1994;23(10):544-548. [Medline].

32. Scotiniotis I, Rubesin SE, Ginsberg GG. Imaging modalities in inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):391-421, ix. [Medline].

33. 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].

34. Stein RB, Hanauer SB. Medical therapy for inflammatory bowel disease. Gastroenterol Clin North Am. Jun 1999;28(2):297-321. [Medline].

35. Stutman HR. Salmonella, Shigella, and Campylobacter: common bacterial causes of infectious diarrhea. Pediatr Ann. Oct 1994;23(10):538-43. [Medline].

36. 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].

37. Ulshen M. Inflammatory bowel disease. In: Nelson Textbook of Pediatrics. 16^th ed. 2000:1150-7.

Keywords

colitis, inflammatory bowel disease, IBD, Crohn disease, CD, ulcerative colitis, UC, necrotizing enterocolitis, NEC, allergic colitis, pseudomembranous colitis, infectious colitis, parasitic colitis, ischemic colitis, bowel perforation, sepsis, diarrhea, uveitis, erythema nodosum, cholangitis, hepatitis, arthritis, abdominal distention, emesis, growth failure, weight loss, abdominal pain, iron deficiency anemia, juvenile rheumatoid arthritis, dysentery, disseminated intravascular coagulation, toxic megacolon, liver abscess, colonic perforation, proteinuria, hypertension, treatment, diagnosis

Contributor Information and Disclosures

Author

Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge
Jagvir Singh, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

Robert Baldassano, MD, Director, Center for Pediatric Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Associate Professor, Department of Pediatrics, The Children's Hospital of Philadelphia, University of Pennsylvania
Robert Baldassano, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Gastroenterological Association, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Stefano Guandalini, MD, Director, University of Chicago Celiac Disease Program, Section Chief of Gastroenterology, Hepatology and Nutrition; Professor, Department of Pediatrics, University of Chicago Comer Children's Hospital
Stefano Guandalini, MD is a member of the following medical societies: American Gastroenterological Association, European Society for Paediatric Gastroenterology, Hepatology & Nutrition, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.

CME Editor

Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, SUNY-Downstate Medical Center
Steven M Schwarz, MD, FAAP, FACN, AGAF is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, American Gastroenterological Association, American Pediatric Society, Gastroenterology Research Group, New York Academy of Medicine, North American Society for Pediatric Gastroenterology and Nutrition, and Society for Pediatric Research
Disclosure: TAP Pharmaceuticals Honoraria Speaking and teaching; Curemark, LLC Consulting fee Board membership; Centocor, Inc. Grant/research funds Independent contractor

Chief Editor

Carmen Cuffari, MD, Associate Professor, Department of Pediatrics, Division of Gastroenterology/Nutrition, Johns Hopkins University School of Medicine
Carmen Cuffari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

• Relevant clinical guidelines include the following:
  • Practice parameters for the surgical treatment of ulcerative colitis. ⁹
  • Evidence-based care guideline for management of pediatric moderate/severe inflammatory bowel disease (IBD) ¹⁰
  • American Gastroenterological Association Institute medical position statement on corticosteroids, immunomodulators, and infliximab in inflammatory bowel disease ¹¹
• Relevant clinical trials include the following
  • Efficacy Study of Granulocytapheresis Plus Steroids vs Steroids Alone in Active Steroid Dependent Ulcerative Colitis (ATICCA)
  • (CB-01-02/01) Randomized Placebo Controlled Trial of Budesonide-MMX™ (CB-01-02) 6 mg and 9 mg in Patients With Ulcerative Colitis
  • Immune Regulation in Ulcerative Colitis or Crohn's Disease
• Related eMedicine topics include the following
  • Ulcerative Colitis (Pediatrics: General Medicine)
  • Ulcerative Colitis (Radiology)
  • Necrotizing Enterocolitis (Radiology)
  • Colitis, Ischemic (Radiology)
  • Ulcerative Colitis, Surgical Treatment (Pediatrics: Surgery)
  • Necrotizing Enterocolitis, Surgical Treatment (Pediatrics: Surgery)

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