Updated: Jan 04, 2019
Author: David A Piccoli, MD; Chief Editor: Carmen Cuffari, MD 



The term colitis refers to inflammation of the colon. It may be associated with enteritis (inflammation of the small intestine), proctitis (inflammation of the rectum), or both. Inflammatory bowel disease (IBD) is a generic term used to describe 3 idiopathic disorders that are associated with gastrointestinal (GI) inflammation:

  • Crohn disease (CD)

  • Ulcerative colitis (UC)

  • Indeterminate colitis

IBD affects approximately 1.5 million Americans and worldwide, the incidence seems to be increasing. In 2012, a systematic review of all population-based studies describing the incidence and/or prevalence of IBD was performed. The review demonstrated that the incidence of IBD (both CD and UC) is increasing in many regions of the world. However, the incidence and prevalence of IBD remained highest in industrialized nations. Less data were available from developing countries, but the evidence suggests that IBD is emerging as a global disease.[1]

In addition, numerous different conditions can cause colitis, each of which has its own pathophysiology. These include the following:

  • Necrotizing enterocolitis (NEC)

  • Allergic colitis

  • Pseudomembranous colitis

  • Infectious colitis (bacterial, parasitic, or viral)

  • Ischemic colitis

  • Colitis secondary to immune deficiency disorders


Necrotizing enterocolitis

NEC is a common cause of colitis in newborns (see the image below). Very small and ill preterm infants are particularly susceptible to NEC. NEC is multifactorial, but prematurity and the presence of bacteria in the GI tract are significant risk factors associated with NEC.

Necrotizing enterocolitis totalis. Necrotizing enterocolitis totalis.

NEC appears to involve an inappropriate inflammatory response in an immature intestine. The final common pathway seems to include the endogenous production of inflammatory mediators, such as endotoxin lipopolysaccharide, platelet-activating factor, tumor necrosis factor, and other cytokines, decreased epidermal growth factor, and progressive mucosal damage by free radical production.[2]

Hypoxic ischemia and aggressive enteral feedings are also associated with the pathogenesis of NEC. Varying degrees of mucosal 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.[3] 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. Immunologic responses may range 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 (PMNs).

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, cephalosporin and beta-lactam antibiotics are most frequently implicated in children. Cases in children with underlying comorbid conditions, IBD in particular, are also common.[4]

Inflammatory bowel disease

The etiology of IBD is poorly understood. Genetic and environmental influences are involved in the pathogenesis. IBD may present either as UC or as CD. Indeterminate colitis is a term to describe a chronic idiopathic colitis that cannot be separated based on conventional diagnostic modalities to either Crohn colitis or ulcerative colitis.

A study by Starr et al sought to identify proteins that enable differentiation between CD and UC in children with new onset IBD. The study found two panels of candidate biomarkers for the diagnosis of IBD and the differentiation of IBD subtypes to guide appropriate therapeutic interventions in pediatric patients.[5]

Inflammatory bowel disease. Severe colitis noted d 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, whereas CD is manifested by transmural inflammation and granulomas that may affect 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, with the ileum being the most commonly affected segment.

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, and reactive oxygen metabolites) entering and subsequently being deposited in various tissues and organs, such as the eyes (uveitis), skin (erythema nodosum), liver (cholangitis, hepatitis), and joints (arthritis).

Infectious colitis

Infectious colitis is the most common cause of pediatric colitis, particularly beyond the first year of life. It can be caused by bacterial, viral, and parasitic pathogens.

Bacterial colitis

The most common bacterial causes of colitis in children are Escherichia coli (including both enterohemorrhagic E coli [EHEC] and enteroinvasive E coli [EIEC]) and species of Shigella, Salmonella, Campylobacter, and Yersinia.

Salmonella infections can be divided into those that cause typhoid (enteric) fever and those that do not. In more industrialized countries, infection with nontyphoid Salmonella accounts for a significant proportion of cases of food poisoning. Salmonella infections are typically spread via the fecal-oral route; outbreaks are commonly 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 after gastrectomy, 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. They cause diarrhea by producing several toxins and prostaglandins, which stimulate 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 in several different ways, depending on their specific pathologic characteristics. Pathologic strains of E coli have been classified as follows:

  • Enteropathogenic

  • Enterotoxic

  • Enteroinvasive

  • Enteroaggregative

  • Enteroadherent

  • Enterohemorrhagic

EHEC, including O157:H7 and O26:H11, causes 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 PMNs. EIEC, on the other hand, exhibits almost exactly the same pathogenetic mechanisms as Shigella.

Parasitic colitis

Entamoeba histolytica is the most common cause of parasitic colitis in the world. Transmission takes place through ingestion of trophozoites (usually from water contamination) and person-to-person transmission (typically because of poor sanitation). Balantidium coli is a large ciliated protozoan that also causes colitis; balantidiasis manifests in much the same way as amebiasis.

Viral colitis

Colitis caused by cytomegalovirus (CMV) infection is a rare form that typically is found in immunocompromised patients (eg, organ recipients who are receiving immunosuppressive treatment). It results in deep round ulcerations that have a tendency to bleed easily and profusely. Adenovirus infection can also cause a severe colitis in immunocompromised patients, especially those with AIDS, although patients with solid organ and bone marrow transplants are also at risk.

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.

Congenital immune deficiency

Several primary immunodeficiency syndromes, including common variable immunodeficiency, chronic granulomatous disease, Wiskott-Aldrich syndrome, and IPEX (immunodysregulation, polyendocrinopathy, enteropathy, X-linked) syndrome, have all been associated with an IBD-like clinical and histopathological presentation. Patients may present with clinical signs and symptoms indistinguishable from patients with IBD, including chronic abdominal pain, diarrhea, and colitis-like symptoms. Indeed, extraintestinal manifestations such as failure to thrive, developmental delay and perianal diseases are common presenting complaints.


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 the available evidence suggests that IBD involves an abnormal immune response, likely to environmental factors, in a genetically susceptible host. The observation that IBD is occurs more frequently in industrialized, as opposed to developing, countries has led to the “hygiene hypothesis.” The hygiene hypothesis suggests that in parts of the world where humans are exposed to fewer microbes, the intestinal immune system might not be as prepared to respond to antigens. Like bacteria, diet is thought to be a potential environmental factor as the bacteria and diet are two of the most common environmental factors to which the gut is exposed.

Evidence also suggests a genetic predisposition to IBD, including ethnic differences, family aggregation, concordance rates in twins, chromosomal linkage, and genetic syndromes associated with IBD. However, the lack of total concordance of disease among monozygotic twins, along with other differences, supports a role for environmental 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.


United States statistics

Approximately 25% of cases of IBD occur during childhood and adolescence.[6] The risk of IBD in family members of an affected individual is 5-30%; children born to a parent with IBD develop IBD approximately 6-9% of the time, and, in the rare instance that both parents have IBD, studies estimate that their children have a 33% chance of developing IBD by age 28 years.[7]

The prevalence of CD and UC in the United States is estimated to be 400 per 100,000 persons. NEC affects 1-5% of patients admitting to neonatal intensive care units (ICUs). NEC may occur in 2-5% of infants with birth weights lower than 1500 g and up to 10% of infants with birth weights lower than 1000 g. In the United States, the prevalence of amebiasis in high-risk groups is reported to be 1-4%.

International statistics

IBD is most prevalent in northern Europe and North America and is less common in the Asia-Pacific region, with the exception of Australia.[8] Dramatic increases in incidence of IBD have occurred in many parts of the world, typically occurring in more industrialized countries.[1] A north-to-south gradient also appears to be present, with higher incidences of both UC and CD in northern locations. The prevalence of amebic infections worldwide varies from 5-81%, with the highest frequencies occurring in tropical climates.

Age-, sex-, and race-related demographics

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. It 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. It is common in males.

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 2-3% of all infants.[9]


Diarrheal diseases are among the leading causes of morbidity and mortality in children worldwide, causing 1 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. The mortality of NEC is higher than 50% in infants with birth weights lower than 1000 g.

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 in UC are the duration and extent of disease. After the first decade of disease, the risk of development of colon cancer increases rapidly; thus, surveillance colonoscopy should be performed annually or biannually after 8-10 years of colonic disease. Colectomy should be performed if there is finding of high-grade dysplasia.[10]

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-aminosalicylic acid (5-ASA). Despite complications, most children with CD lead active lives, despite intermittent symptom flare-ups.

Patient Education

Psychosocial support and education for the family are important in achieving long-term goals in the treatment of IBD. Counseling and peer support for the adolescent who has growth and pubertal delays are helpful.

For patient education resources, see Crohn Disease in Children and Teens.




Patients with necrotizing enterocolitis (NEC) may exhibit a wide spectrum of illness, ranging from mild disease with only guaiac-positive stools to severe disease 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 mucus in the stool, vomiting, and diarrhea after introduction of milk when they are aged approximately 1 week to 3 months. The symptoms may also be mild and may be indistinguishable from esophageal reflux. The syndrome is also known to occur in exclusively breastfed 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.

Patients with pseudomembranous colitis typically present with profuse watery or mucoid diarrhea, tenesmus, fever, abdominal cramps, and tenderness, usually within 1 week of antibiotic therapy. The stools may be frankly bloody or guaiac-positive.

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 those 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 severe 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 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 common extraintestinal complaints in UC. The presence of ankylosing spondylitis is more consistent with CD than with UC. Pubertal development may be delayed or arrested in active UC. Aphthous stomatitis is often present during the initial attack or relapse of UC. Renal calculi develop in 6% of patients, mainly as uric acid in UC and as oxalate in CD. Ophthalmic complications (eg, uveitis, iritis, and episcleritis) may be a sign of IBD or secondary to corticosteroid therapy in patients treated for IBD.

IBD 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 following ingestion 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. Stools are frequent (10-12/day, on average) and contain mucus and blood; tenesmus is common. Fever is noted, often in the range of 102-104°F (39-40°C). Shigella infection occasionally produces central nervous system (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 may be as high as 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. Infection is acquired through ingestion of raw meat, poultry, fish, and water.

Yersinia enterocolitica infection presents with the 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 temperatures ranging from 99° to 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 symptoms similar to those of 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 symmetric purpuric rash that is most noticeable over the extensor surfaces of the arms, legs, and buttocks.

Physical Examination

NEC may present with abdominal distention, tenderness, and guarding. Hypotension, tachycardia, tachypnea, hypoxia, shock, disseminated intravascular coagulation (DIC), and cardiopulmonary arrest may be noted. The stool may have frank blood or may be heme-guaiac positive.

Allergic colitis presents with blood and mucus in the stool. Children are usually well-appearing; however, in rare cases, in patients with allergic enterocolitis, 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 and may require an emergent colectomy.

IBD may present with pallor, tachycardia, abdominal tenderness, and blood in the stool. An elevated temperature, weight loss, and dehydration may be noted. The presence of abdominal distention with decreased or absent bowel sounds is indicative of actual or impending obstruction or 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. It is a medical and surgical emergency.

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 the 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.


The most serious acute complication of UC is toxic megacolon with the risk of perforation. It is reported to occur in up to 5% of all patients with UC but is a relatively uncommon entity in pediatric patients. Toxic megacolon is more common in UC than in CD. In a single-center case-controlled study of toxic megacolon in children, only 2/10 patients had a CD phenotype; the remainder had UC.[11]

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. The complications of colitis caused by IBD are addressed in greater detail in the articles on Crohn disease and ulcerative colitis.

Hemolytic uremic syndrome (HUS) is the best-known and most important complication of colitis caused by enterohemorrhagic E coli (EHEC).



Diagnostic Considerations

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

Differential Diagnoses



Laboratory Studies

For newborns with necrotizing enterocolitis (NEC), the following studies should be obtained as indicated:

  • Arterial blood gas (ABG) values

  • White blood cell (WBC) count

  • Hemoglobin concentration

  • Platelet count

  • Prothrombin time (PT)

  • Activated partial thromboplastin time (aPTT)

  • Electrolyte levels

  • Disseminated intravascular coagulation (DIC) profile

  • Inflammatory markers, such as C-reactive protein (CRP)

A child with allergic colitis may have an elevated WBC count, a low hemoglobin level, often (but not invariably) peripheral eosinophilia, and hypoalbuminemia (if a condition of protein-losing enteropathy coexists). The stool findings are often heme positive.

In patients with pseudomembranous colitis, WBC counts are usually higher than 15,000/µL. An etiologic diagnosis requires identification of C difficile toxin in the stool. PCR, however, is being utilized more commonly.

When a bacterial cause (eg, Salmonella species, Shigella species, Campylobacter species, Yersinia species, E coli, or C difficile) is suspected, stool samples must be cultured, and Gram staining and methylene blue staining of the stool are recommended. WBC counts may be elevated or normal.

Most of the organisms may be cultured from the stool by using appropriate media, but enrichment techniques may be required for Y enterocolitica. 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 attributable to possible clearance of the organisms at time of isolation, inability to identify an organism, lack of suitable culture techniques, or laboratories that do not routinely test 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 (PMNs).

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 should never be omitted if the patient’s condition is stable enough to allow the test to be performed. If Crohn disease (CD) is being considered, upper gastrointestinal (GI) endoscopy and small bowel imaging with upper GI small-bowel follow-through or MR enterography must also be done. Some centers are starting to use more small bowel ultrasound to evaluate the small bowel.

Blood studies should include a complete blood count (CBC); levels of serum electrolytes, blood urea nitrogen (BUN), creatinine, and C-reactive protein (CRP); and liver function test results (eg, transaminases, total protein, serum albumin, and 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.

Stool calprotectin and lactoferrin are useful measures of intestinal inflammation. In UC, the concentration of fecal calprotectin has been shown to correlate well with the gold standard, colonoscopy.[38]

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, 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.

Serologic markers may be helpful to discriminate Crohn's disease from ulcerative colitis. However, serologic markers are generally not helpful to distinguish between inflammatory bowel disease from non- inflammatory bowel disease controls. However, more scientific evidence is needed and studies are ongoing.[12, 13]  

Plain Radiography

The diagnostic yield of plain radiography is relatively low. Nevertheless, the diagnosis of NEC can be facilitated by obtaining 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 can also be useful in establishing a diagnosis of toxic megacolon, bowel obstruction, or perforation; consequently, it should be performed as an initial study.



Pharmacologic and Supportive Therapy

The treatment of one cause of colitis, necrotizing enterocolitis (NEC), includes cessation of feedings, nasogastric decompression, and intravenous (IV) 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. Surgical therapy (see below) is initiated if medical therapy fails.

Treatment of allergic colitis primarily involves dietary measures (see below).

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/day in 4 divided doses) or oral vancomycin (40 mg/kg/day in 4 divided doses). Fidaxomicin was approved in 2011 by the US Food and Drug Administration for the treatment of C difficile associated disease in adults. Fecal Microbiota Transplantation is now a well-established therapy for refractory/recurrent disease.

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/day in 4 divided doses) or ceftriaxone (100 mg/kg/day in 2 divided doses) should be initiated. Alternative treatments include chloramphenicol (100 mg/kg/day in 4 divided doses) or, in adolescents, fluoroquinolones. TMP-SMZ is the drug of choice when oral treatment is indicated.

If Yersinia enterocolitica infection is likely, antibiotic therapy with IV gentamicin (5-7.5 mg/kg/day 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 proven to decrease the duration of diarrhea.

Treatment of amebic colitis includes metronidazole and iodoquinol or paromomycin.

Management of inflammatory bowel disease (IBD) depends on the disease location, the disease behavior, and the severity of the disease at presentation. The general goals for managing IBD are to eliminate symptoms of disease, improve quality of life, and avoid hospitalization and surgery. One of the primary aims is to promote and allow normal, unrestricted activity. Although clinical improvement is imperatives, in order to increase the chance of lasting remission and decrease the potential for adverse effects of long-standing inflammation, mucosal healing is important.[14]

Therapy for IBD includes pharmacotherapy, surgery (see below), nutrition and bone health (see below), supportive therapy, psychotherapy, and cancer screening.[15] (See Crohn Disease and Ulcerative Colitis.)

Medications used to treat IBD can be classified into 6 categories, as follows:

  • Aminosalicylates (eg, sulfasalazine and mesalamine)[16, 17]

  • Corticosteroids (eg, prednisone and budesonide)[18]

  • Immunomodulators (eg, azathioprine, 6-mercaptopurine [6-MP])[19]

  • Antibiotics (eg, metronidazole and ciprofloxacin)[20]

  • Probiotics (eg, Lactobacillus GG and Saccharomyces boulardii)[21]

  • Biologic agents (eg, infliximab)[22, 23]

Children with mild manifestations can be treated as outpatients, with arrangements made 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 (5-ASA) drug that is given alone or in combination with topical enemas (eg, corticosteroid or mesalamine) or corticosteroid foam.[24] Adolescents may prefer the foam because of its ease of administration and the reduced sensation of rectal distention and urgency.

Patients with moderate and severe disease (eg, fever, bloody stools, severe abdominal pains, anemia, or hypoalbuminemia) require supportive treatment, often with IV hydration. Hospitalization is often indicated for management of acute disease with corticosteroids or immunosuppressive agents.[22]

IV methylprednisolone or hydrocortisone at a dosage equivalent to 1-2 mg/kg/day of prednisone is recommended. The goal is to use steroids for a short period and then switch to maintenance therapy as soon as possible. Maintenance therapy may require administration of 5-ASA or an immunomodulator, such as azathioprine or 6-MP.

Patients with refractory IBD or patients who present in a moderate to severe fashion may need a biologic agent, such as infliximab.[23, 25, 26]  Additionally, studies in adult patients have demonstrated that for moderate-to-severe CD, combination therapy with a biologic plus an immunomodulator may be more effective than using a medication from either class alone.[27]

If toxic megacolon is suspected, aggressive resuscitation with fluids and electrolytes is required. A surgical consultation is required in patients with suspected toxic megacolon, appendicitis, intestinal obstruction, fulminant colitis, or significant GI bleeding.

Begin a combination of broad-spectrum IV antibiotics, such as ampicillin (200 mg/kg/day), gentamicin (5-7.5 mg/kg/day), and clindamycin (40 mg/kg/day). Alternate therapy may include either ampicillin-sulbactam or cefoxitin in combination with gentamicin.

No specific therapy is indicated for Henoch-Schönlein purpura (HSP). Steroids are used to treat severe abdominal pain or arthritis in selected patients.

A study by Hyams et al that evaluated 416 children 12 weeks after they were treated for ulcerative colitis with mesalazine (132 children), oral corticosteroids (141), or intravenous corticosteroids (143) reported that at week 12, corticosteroid-free remission was achieved by 64 (48%) patients in the mesalazine group, 47 (33%) in the oral corticosteroid group, and 30 (21%) in the intravenous corticosteroid group (p< 0·0001). Seven percent of patients in the mesalazine group, 15% in the oral corticosteroid group, and 36% in the intravenous corticosteroid group required treatment escalation. Eight patients who were first treated with intravenous corticosteroids underwent colectomy. Factors that predicted remission at 12 weeks included a Pediatric Ulcerative Colitis Activity Index score of less than 35, higher baseline albumin by 1 g/dL increments among children younger than 12 years, and week 4 remission. The study also reported that predictors of treatment escalation by week 12 in patients initially treated with intravenous corticosteroids included baseline total Mayo score of 11 or higher, rectal biopsy eosinophil count less than or equal to 32 cells per high power field, rectal biopsy surface villiform changes, and not achieving week 4 remission.[28]

Nutritional Therapy

Treatment of allergic colitis consists of eliminating the offending protein from the infant’s diet. Infants should receive a formula containing casein-hydrolysate as the protein source. Mothers of exclusively breastfed infants with allergic colitis should eliminate the offending proteins (typically milk or milk and soy) from their diets. Persistence of gross bleeding after 14 days after a formula change is an indication for proctosigmoidoscopy. Infants who respond to diet change should be challenged around 12-14 months of age.

A study by Baldassarre et al found that the addition of Lactobacillus rhamnosus GG (LGG) to extensively hydrolyzed casein formula (EHCF) significantly improved hematochezia and fecal calprotectin in comparison with the results noted with EHCF alone.[29]  However, the long-term effects of treating infants with probiotics are unknown.

The treatment of IBD includes adequate nutritional intake and social and emotional support. Nutrition therapy may be primary or adjunctive in CD but is generally only adjunctive in UC. Defined formula diets with polymeric, semi-elemental, or elemental formulas may induce remission in as many as 80% of patients with CD.[30] The mechanism of action is unknown but may be secondary to excluding potentially harmful components in the usual diet or through changes in the composition of the gut microbiome and/or metabolome.[39]

Bowel Resection and Strictureplasty

In patients with NEC, surgical intervention is required in 30-35% of babies.[31] Exploratory laparotomy with resection of bowel and external ostomy diversion is indicated if there is failure of medical management, erythema of the abdominal wall, a single fixed loop, a palpable mass, or evidence of perforation (eg, pneumoperitoneum or brown paracentesis). Central venous access is needed after bowel resection to permit total parenteral nutrition. Closely monitor the child for complications of short bowel syndrome and central catheters.

Surgery is indicated in patients with UC or CD if uncontrolled gastrointestinal (GI) bleeding, bowel perforation, bowel obstruction, failure to respond to medical therapy, and unacceptable medical toxicity are present.[32]

Total colectomy may be indicated to treat UC when the patient has toxic megacolon or acute fulminant colitis or in selected severe forms of the disease for which medical therapy (including rescue immunosuppressive agents such as infliximab) has failed.[33]

In UC, colectomy usually involves the creation of a pouch from the distal ileum and typically is curative (see Ulcerative Colitis). As many as 70% of the children develop at least one episode of so-called pouchitis (inflammation of the pouch) following proctocolectomy.[34] This entity is of unclear origin but typically responds quickly to a course of antimicrobial treatment. Evidence from studies of adults suggests that prophylaxis with probiotics may be an effective preventative tool.[35]

In CD, surgery is not curative, because recurrent disease at the site of surgery is common. Segmental bowel resection is the most common procedure for treating CD and usually involves the diseased terminal ileum and adjacent inflamed colon. Strictureplasty should be considered if there is stenosed bowel segment without active inflammation. At times, surgical resection is used to treat growth failure. Adult studies suggest a role for biologics in prevention of postoperative recurrence of the disease, particularly prevention of endoscopic recurrence of disease.[36, 37]



Medication Summary

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

Anti-inflammatory Agents

Class Summary

Corticosteroids and 5-aminosalicylic acid (5-ASA) derivatives are used to treat ulcerative colitis (UC).

Sulfasalazine (Azulfidine, Azulfidine EN-tabs)

Sulfasalazine is a sulfonamide derivative conjugate of 5-ASA. It serves as a carrier for 5-ASA. Sulfasalazine is useful in the management of UC and acts locally in the colon to decrease the inflammatory response and systemically inhibit prostaglandin synthesis.

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

Mesalamine is used for mild-to-moderate UC. It is the active component of sulfasalazine. Mesalamine affects chemical mediators of the inflammatory response, particularly prostaglandins and leukotrienes. The usual course of therapy in adults lasts 3-6 weeks. Some patients may need concurrent rectal and oral therapy. Oral products are formulated to release slowly throughout the gastrointestinal (GI) tract.

Hydrocortisone (Solu-Cortef, Cortef)

Hydrocortisone decreases inflammation by suppressing the migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability.

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

Methylprednisolone decreases inflammation by suppressing the migration of PMNs and reversing increased capillary permeability.

Antidiarrheal agents

Class Summary

Antidiarrheal agents are used to treat diarrhea in conjunction 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)

Loperamide acts on intestinal muscles to inhibit peristalsis and slow intestinal motility. It prolongs the movement of electrolytes and fluid through the bowel and increases viscosity and loss of fluids and electrolytes. It also has a mild proabsorptive effect on sodium and chlorine in the epithelial cells.


Class Summary

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

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

Trimethoprim-sulfamethoxazole (TMP-SMZ) inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. The antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except for Pseudomonas aeruginosa. The dose is based on the trimethoprim component.


Ampicillin has bactericidal activity against susceptible organisms. It is an alternative to amoxicillin when the patient is unable to take medication orally.

Ampicillin-sulbactam (Unasyn)

Ampicillin-sulbactam is a combination of a beta-lactamase inhibitor with ampicillin. It covers skin organisms, enteric flora, and anaerobes. It is not ideal for nosocomial pathogens.


Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. It is used in combination with an agent that covers gram-positive organisms and one that covers anaerobes.

Metronidazole (Flagyl, Flagyl ER)

Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (except for C difficile enterocolitis).

Cefoxitin (Mefoxin)

Cefoxitin is a second-generation cephalosporin that is indicated for gram-positive cocci and gram-negative rod infections.

Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity; it has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. Ceftriaxone arrests bacterial growth by binding to 1 or more penicillin-binding proteins.

Cefotaxime (Claforan)

Cefotaxime is used for septicemia and treatment of susceptible organisms. It arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. Cefotaxime is a third-generation cephalosporin with a gram-negative spectrum of activity; it has lower efficacy against gram-positive organisms.

Chloramphenicol (Chloromycetin)

Chloramphenicol binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is effective against gram-negative and gram-positive bacteria.

Vancomycin (Vancocin)

Vancomycin is a potent antibiotic that is directed against gram-positive organisms and is active against Enterococcus species. It is useful in the treatment of septicemia and skin-structure infections. Vancomycin is indicated for patients who are unable to receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora or anaerobes.

To prevent toxicity, the current recommendation is to assay vancomycin trough levels 30 minutes before the fourth dose. Use the creatinine clearance to adjust the dose in patients with renal impairment.


Questions & Answers


What is colitis?

Which conditions can cause colitis?

What is the pathophysiology of necrotizing enterocolitis (NEC)?

What is the pathophysiology of allergic colitis?

What is the pathophysiology of pseudomembranous colitis?

What is the pathophysiology of colitis in inflammatory bowel disease (IBD)?

What is the pathophysiology of infectious colitis?

What is the pathophysiology of bacterial colitis?

What is the pathophysiology of parasitic colitis?

What is the pathophysiology of viral colitis?

What is the pathophysiology of ischemic colitis?

In which primary immunodeficiency syndromes is colitis a manifestation?

What causes colitis?

What is the prevalence of colitis in the US?

What is the global prevalence of colitis?

How does the prevalence of colitis vary among patient groups?

What is the prognosis of colitis?

What are the risks factors for developing adenocarcinoma in ulcerative colitis (UC)?

What is included in patient education about colitis?


What are the signs and symptoms of Henoch-Schönlein purpura (HSP)?

What are the signs and symptoms of necrotizing enterocolitis (NEC)?

What are the signs and symptoms of allergic colitis?

What are the signs and symptoms of pseudomembranous colitis?

What are the signs and symptoms of inflammatory bowel disease (IBD)?

What are the signs and symptoms of ulcerative colitis (UC)?

What are the initial signs and symptoms of Crohn disease (CD)?

What are common extraintestinal complaints in ulcerative colitis?

How is inflammatory bowel disease (IBD) characterized?

What are the signs and symptoms of salmonellae infection in colitis?

What are the signs and symptoms of Shigella infection in colitis?

What are the signs and symptoms of Campylobacter enteritis infection in colitis?

What is the signs and symptoms of yersinia enterocolitica infection in colitis?

What are the signs and symptoms of amebiasis infection in colitis?

Which physical findings suggest necrotizing enterocolitis (NEC)?

Which physical findings suggest allergic colitis?

Which physical findings suggest pseudomembranous colitis?

Which physical findings suggest inflammatory bowel disease (IBD)?

Which physical findings suggest amebiasis?

Which physical findings suggest Henoch-Schönlein purpura (HSP)?

What are potential complications of colitis?


What can result from a failure to diagnosis colitis?

What are the differential diagnoses for Colitis?


Which lab result is characteristic of Henoch-Schönlein purpura (HSP)?

Which lab studies are performed in the evaluation of necrotizing enterocolitis (NEC)?

Which lab results suggest allergic colitis?

Which lab results suggest pseudomembranous colitis?

What is included in the evaluation of colitis with a suspected bacterial etiology?

Which lab result is characteristic of infectious colitis?

What is included in the evaluation of colitis with a suspected parasitic etiology?

How is suspected inflammatory bowel disease (IBD) evaluated in children?

What is the role of blood studies in the workup of colitis?

Which stool studies are performed in the workup of colitis?

When is assessment of skeletal age indicated in the evaluation of colitis?

What is the role of serologic markers in the workup of colitis?

What is the role of plain radiography in the workup of colitis?


How is necrotizing enterocolitis (NEC) treated?

What is the primary treatment for allergic colitis?

What are the treatment options for pseudomembranous colitis?

What is the role of antibiotics in the treatment of bacterial colitis?

What is the efficacy for antimicrobial therapy for the treatment of bacterial colitis?

What are the treatment options for salmonella bacteremia in colitis?

What is the treatment options for Yersinia enterocolitica infection in colitis?

What are the treatment options for Campylobacter enteritis in colitis?

What is the treatment options for amebic colitis?

What are the goals of treatment for inflammatory bowel disease (IBD)?

What are the treatment options for inflammatory bowel disease (IBD)?

What is the initial therapy for children with ulcerative colitis (UC)?

When is hospitalization indicated in the treatment of ulcerative colitis (UC)?

What is the inpatient treatment for ulcerative colitis (UC)?

What are the treatment options for refractory inflammatory bowel disease (IBD)?

How is toxic megacolon in colitis treated?

Which medications are used in the treatment toxic megacolon in colitis?

How is Henoch-Schönlein purpura (HSP) treated?

What is the efficacy of treatments for ulcerative colitis (UC)?

What is the role of nutritional therapy in the treatment of colitis?

What is the role of surgery in the treatment of colitis?


What is the basis for selection of medical treatment for colitis?

Which medications in the drug class Antibiotics are used in the treatment of Colitis?

Which medications in the drug class Antidiarrheal agents are used in the treatment of Colitis?

Which medications in the drug class Anti-inflammatory Agents are used in the treatment of Colitis?