Meckel diverticulum is a remnant of the fetal omphalomesenteric duct and is an outpouching of the distal ileumpresent in 1% to 2% of the population. Although most diverticula are asymptomatic throughout life, some cause massive, painless GI bleeding. Ectopic gastric tissue within thediverticulum causes ulceration of mucosa in the adjacentileum. Meckel diverticulum may be a lead point for intussusception or may enable twisting (volvulus) of neighboring bowel around its vascular supply. Diverticulitis mimicsappendicitis. Diagnosis may be made in most cases by technetium scan (Meckel scan), which labels the acid-producingmucosa. Because not all diverticula are seen, ultrasound, barium enteroclysis, or video capsule endoscopy may beuseful. When the level of suspicion is high, surgical or laparoscopic investigation is warranted. The treatment is surgical excision.
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The peak incidence of IBD in children is in the second decadeof life. IBD includes Crohn’s disease (CD), which can involve any part of the gut, and ulcerative colitis (UC), which affects only the colon. The incidence of IBD is increasing, especiallyin industrialized countries, for reasons that are unclear. IBD is uncommon in tropical and Third World countries. It is more common in Jewish than in other ethnic populations. Geneticfactors play a role in susceptibility, with significantly higher riskif there is a family history of IBD. Having a first-degree relative with IBD increases the risk about 30-fold. Susceptibilityhas been linked to some HLA subtypes, and linkage analysishas identified multiple other susceptibility loci on several chromosomes. Environmental factors (not yet identified) also seemto play a role because there is often nonconcordance amongmonozygotic twins. It is possible that viral infections can initiate the inflammatory process. Dietary triggers are unproven.Smoking doubles the risk of CD and halves the risk for UC.
Clinical manifestations depend on the region of involvement. UC involves only the colon, whereas CD can include the entire gut from mouth to anus. Colitis from either condition results in diarrhea, blood, and mucus in the stool; urgency; and tenesmus, a sensation of incomplete emptying after defecation. When colitis is severe, the child often awakens from sleep to pass stool. Toxic megacolon is a life-threatening complication characterized by fever, abdominal distention and pain, massively dilated colon, anemia, and low serum albumin owing to fecal protein losses. Symptoms of colitis always are present in UC and usually suggest the diagnosis early in its course. Extraintestinal manifestations of UC occur in a few patients and may include primary sclerosing cholangitis, arthritis, uveitis, and pyoderma gangrenosum (Table 129-1).
Symptoms can be subtle in CD. Small bowel involvement in CD is associated with loss of appetite, crampy postprandial pain, poor growth, delayed puberty, fever, anemia, and lethargy. Some symptoms may be present for some time before the diagnosis is made. Severe CD with fibrosis may cause partial or complete small bowel obstruction. Perineal abnormalities, including skin tags and fistulas, are another feature distinguishing CD from UC. Other extraintestinal manifestations of CD include arthritis, erythema nodosum, and uveitis or iritis.
Blood tests should include complete blood count, albumin,erythrocyte sedimentation rate, and C-reactive protein(Table 129-2). Anemia and elevated platelet counts are typical. Testing for abnormal serum antibodies can be helpfulin diagnosing IBD and in discriminating between the colitis of CD and UC. Antineutrophil cytoplasmic antibody is found in about 66% of UC patients and in only a few CD