AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 gastrointestinal 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. 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, 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 exist. The distal ileum and proximal colon are involved most frequently, but, 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 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. 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 typically are 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 prevalence is 30-100 per 100,000 population.
• NEC affects 1-5% of patients admitting to neonatal intensive care units.
• 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).

• 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 generally is diagnosed in children aged 5-16 years. IBD has a bimodal distribution with an early onset at ages 15-25 years and a second smaller peak at ages 50-80 years.
• HSP occurs in school-aged children and young adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• 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 progress rapidly. 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 typically is 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.
• IBD generally is diagnosed in children aged 5-16 years. The onset of IBD, with CD or 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.
• 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.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• For newborns with NEC, obtain an ABG, WBC count, hemoglobin, platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), electrolytes, and 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 usually are higher than 15,000/mm³. 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 Yersinia 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.

    EHEC, including O157:H7 and O26:H11, causes hemorrhagic colitis and systemic complications, including the 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 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 is being considered, an upper GI endoscopy and an x-ray with barium swallow and small bowel follow-through also need to be done.
• Blood studies should include CBC, serum electrolytes, BUN, creatinine, C-reactive protein (CRP), and liver function tests (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 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 HSP, findings from routine lab studies, including CBC, electrolytes, serum proteins, and C3 complement, are usually normal. The 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 radiographs also can be useful in establishing a diagnosis of toxic megacolon, bowel obstruction, or perforation, and they should be performed as initial studies.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The treatment of NEC includes cessation of feedings, nasogastric decompression, and intravenous fluid resuscitation with attention to electrolytes and acid-base balance. Antibiotics should be started as soon as cultures are obtained. Close monitoring with cardiorespiratory support is provided as required. Exploratory laparotomy with resection of bowel and external ostomy diversion is indicated if there is failure of medical management, erythema of abdominal wall, a single fixed loop, a palpable mass, and/or evidence of perforation (eg, pneumoperitoneum, brown paracentesis). Central venous access is needed after bowel resection for total parenteral nutrition. Closely monitor the child for complications of short bowel syndrome and central catheters.

• 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, IV 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 IV 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 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, 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)
  • 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 UC or 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 (IV) hydration.
• Hospitalization is often indicated for management of acute disease with corticosteroids and or immunosuppressive agents.
• IV 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 IV 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 Unasyn (ampicillin/sulbactam) 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 up to 80% of patients with CD.
• No specific therapy is indicated for 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. In UC, colectomy usually is performed with the creation of a "pouch" from the distal ileum and is curative (see Ulcerative Colitis). Up to 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

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Because the causes of colitis are multiple and quite diverse, it is evident that the medical treatment of this condition is based on the underlying diagnosis.

Drug Category: Anti-inflammatory agents

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

Drug Category: 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.

Drug Category: Antibiotics

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

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Complications

• For colitis caused by inflammatory bowel diseases, please refer to Crohn Disease and Ulcerative Colitis.
• 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.
• HUS is the best-known and most important complication of colitis caused by 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 up to 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.
• 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-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

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to make an early diagnosis of 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, HUS, DIC) may result in mortality and require early diagnosis and intervention to prevent a catastrophe.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• 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].
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Article Last Updated: Jun 13, 2006