Laboratory Studies
For newborns with necrotizing enterocolitis (NEC), the following studies should be obtained as indicated:
- White blood cell (WBC) count
- Hemoglobin concentration
- Platelet count
- Prothrombin time (PT)
- Activated partial thromboplastin time (aPTT)
- Electrolyte levels
- Disseminated intravascular coagulation (DIC) profile
A child with allergic colitis may have an elevated WBC count, a low hemoglobin level, often (but not invariably) eosinophilia, and hypoalbuminemia (if a condition of protein-losing enteropathy coexists). In the search for fecal leukocytes, stools are positive for neutrophils and eosinophils.
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.
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 radiography with barium swallow and small-bowel follow-through must also be done.
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.
If differentiating between Crohn colitis and UC proves difficult, measuring serum levels of anti-Saccharomyces cerevisiae antibody (ASCA) and perinuclear antineutrophilic cytoplasmic antibody (pANCA) antibody may be very useful: the former is found almost exclusively in Crohn colitis, whereas the latter is 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, 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.
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.
[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].
Higuchi LM. Epidemiology and diagnosis of inflammatory bowel disease in children and adolescents. UpToDate. 2005;12.3.
Hou JK, El-Serag H, Thirumurthi S. Distribution and Manifestations of Inflammatory Bowel Disease in Asians, Hispanics, and African Americans: A Systematic Review. Am J Gastroenterol. May 26 2009;[Medline].
Karwowski CA, Keljo D, Szigethy E. Strategies to improve quality of life in adolescents with inflammatory bowel disease. Inflamm Bowel Dis. May 26 2009;[Medline].
Watanabe C, Sumioka M, Hiramoto T, et al. Magnifying colonoscopy used to predict disease relapse in patients with quiescent ulcerative colitis. Inflamm Bowel Dis. Jun 5 2009;[Medline].
[Guideline] 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.
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].
[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].
Floch MH, Madsen KK, Jenkins DJ, et al. Recommendations for probiotic use. J Clin Gastroenterol. Mar 2006;40(3):275-8. [Medline].
Eshuis EJ, Bemelman WA, Stokkers PC. Infliximab for the treatment of ulcerative colitis. Expert Rev Gastroenterol Hepatol. Jun 2009;3(3):219-29. [Medline].
Turner D, Mack D, Leleiko N, et al. Severe pediatric ulcerative colitis: a prospective multicenter study of outcomes and predictors of response. Gastroenterology. Feb 26 2010;[Medline].
Bousvaros A. Overview of the management of Crohn's disease in children and adolescents. UpToDate. 2005;13.2.
Hyams JS. Inflammatory bowel disease. Pediatr Rev. Sep 2005;26(9):314-20. [Medline].
Murray K. Ulcerative colitis in children and adolescents. UpToDate. 2005;13.2.
Komati JT, Sdepanian VL. Effectiveness of Infliximab in Brazilian Children and Adolescents With Crohn Disease and Ulcerative Colitis According to Clinical Manifestations, Activity Indices of Inflammatory Bowel Disease, and Corticosteroid Use. J Pediatr Gastroenterol Nutr. Apr 7 2010;[Medline].
[Best Evidence] Baldassarre ME, Laforgia N, Fanelli M, Laneve A, Grosso R, Lifschitz C. Lactobacillus GG improves recovery in infants with blood in the stools and presumptive allergic colitis compared with extensively hydrolyzed formula alone. J Pediatr. Mar 2010;156(3):397-401. [Medline].
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].
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].
[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].

