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Intestinal polyps are intraluminal protuberant tumors characterized by their gross morphological appearance, location(s), number, size, and presence (pedunculated) or absence (sessile) of a stalk. Additional salient features include specific histological features used to discriminate between types and to aid in predicting malignant potential. Extraintestinal manifestations are also associated with specific poly-posis syndromes.

Age of occurrence is important with respect to clinical significance and malignant potential. Family history of polyps or polyposis syndromes can also be predictive of disease evolution and aid in screening and surveillance of family members.

In children, juvenile polyps account for approximately 90% of colonic polyps. They can be classified as hamartomatous or inflammatory and are also commonly referred to as retention polyps. Grossly, they are large (up to 3 cm), mostly pedunculated, erythematous, and friable. Fluid-filled cysts on the surface can be appreciated endoscopically; microscopically, this corresponds to dilated, mucous-laden cystic glands and some inflammatory cells (Figure 2).

This type of polyp is not in itself neoplastic; however, focal areas of adenomatous and epithelial changes indicate a risk of carcinoma. The presence of these findings in an index case also confers increased risk of carcinoma in first-degree relatives. The age of the subject, family history and inheritance patterns, number and location of polyps, and histology guide the frequency of surveillance colono-scopy. Symptoms of rectal bleeding usually bring these children to the attention of a physician. Polyps can cause clinically significant, but often painless, bleeding so as to cause anemia, and they can be linked to abdominal pain, rectal prolapse, or lead points associated with intussusceptions.

Syndromes associated with juvenile polyps are summarized in Table 4. Other intestinal polyposis syndromes are outlined in Table 5.

Adenomas are composed by immature cells, with the growth rate exceeding regenerative/replacement needs of the colonic crypt. Three features of these polyps aid in detecting malignant potential. Regarding size, adenomatous polyps less than 1 cm have a 2% incidence of being malignant; larger ones have a risk more than 2.5 times that of colorectal carcinoma for the general population. Regarding histology, the degree of cellular atypia defines the degree of irregularity; this can vary from region to region even within a single polyp. Villous structures are associated with the highest risk group, followed by tubulovillous types ( Figure 3), with simple tubular types conferring the lowest risk of dysplasia. Smaller polyps tend to display a tubular nature.

Adenomatous polyps are much more common in adults than in children and bear significant malignant potential. They are usually inherited in an autosomally dominant manner. When they occur in children, it is usually in the context of familial adenomatous poly-posis-neoplastic polyps that appear gradually, rarely in the first decade of life. Adenomatous polyps may be singular and isolated, multiple, limited to the colon or spread throughout the gastrointestinal tract, or occur in a syndromic manner. Gardner's syndrome, Turcot's syndrome, and Cronkhite-Canada syndrome are all adenomatous in nature.

Lymphoid hyperplasia may be mistaken for polyps and consists of sessile projections. Histologically,

Table 1 Bacterial pathogens grouped by pathogenic mechanism





Enteropathogenic Escherichia coli Enterohemorrhagic E. coli Enteroaggregative E. coli Diffuse-adherent E. coli

Shigella Salmonella Yersinia enterocolitica Campylobacter jejuni Vibrio parahemolyticus


Enterotoxigenic E. coli Yersinia enterocolitica Aeromonas Vibrio cholerae


Enteropathogenic E. coli Enterohemorrhagic E. coli Clostridium difficile

Table 2 Bacterial enteric infections


Epidemiology and pathogenesis Clinical features

Diagnosis and treatment

Shigella S. dysentriae S. sonnei S. flexneri S. boydii

Salmonella S. typhi S. paratyphi S. enteritidis


Clostridium C. difficile


Y. enterolytica

Acute infection

Highly contagious; low infective dose (10-100 organisms)

Infective load: 103-105 organisms Reservoirs: poultry and eggs, lizards, amphibians Raw/undercooked foods Mucosal invasion (jejunum and colon Inflammatory response with active secretion

Transmission by contaminated foods (poultry, eggs, milk; water; domestic animals) Initial site(s): jejunum colon

Enteric flora

Toxin A (enterotoxin: alters permeability; inflammation mediator) Toxin B (cytotoxin) Pseudomembranes

Transmission Contaminated pork, Enterotoxin elaboration

Bacterial dysentery Crampy abdominal pain and watery stools Progressive to bloody, mucoid, pus-laden stools Tenesmus Fever

Meningismus Febrile seizures in younger patients Hemolytic uremic syndrome (HUS) possible Five clinical syndromes Acute gastroenteritis

(12- to 72-h incubation) Focal, nonintestinal infection Bacteremia

Asymptomatic carrier state Enteric fever Abdominal cramping, nausea Vomiting

Bloody, mucoid stools Rose spots on the trunk Leucopenia

Prolonged excretion possible, variable by age Carrier state not uncommon Incubation period of

2-11 days Fever prodrome Severe diarrhea Tenesmus Abdominal pain

Antibiotic-associated diarrhea May be restricted to the right colon

Diagnosis Crypt abscesses Lymphatic hypertrophy Necrosis

Elevated WBC count Stool culture Treatment

Fluid and electrolyte replacement Hand washing to prevent transmission Limited role of antibiotics Diagnosis

Stool culture Treatment Supportive Very limited role for antibiotics


Incubation for culture Treatment Supportive

Role for antibiotics for limiting excretion period and duration of illness Diagnosis Stool C. difficile toxins


Endoscopy and histology Pseudomembranes (mucin, fibrin, polymorphonuclear lymphocytes, necrotic debris) Erythema Edema Friability Apthous ulcers Treatment Supportive therapy Cessation of offending antibiotic Metronidazole as first-line agent Vancomycin secondary agent Probiotics useful in relapse prevention Diagnosis Cultures not very accurate

Table 2 Continued


Epidemiology and pathogenesis Clinical features

Diagnosis and treatment

Aeromonas A. hydrophila

Escherichia coli Enteropathogenic E. coli (EPEC)

Enterotoxigenic E. coli (ETEC)

Enteroinvasive E. coli (EIEC)

Enterohemorrhagic E. coli (EHEC)

Enteroaggregative E. coli (EAEC)

Diffuse adherent E. coli (DAEC)

Water contaminants

Localized adherence to enterocytes Signal transduction Intimate adherence and effacement

Enterotoxin elaboration Heat labile (LT) toxin Heat stabile (ST) toxin Fimbriae-based attachment Stimulate adenylate cyclase (LT) and guanylate cyclase (ST) to secrete fluid

Colonize colon Invade tissue Replicate within cells Secretory enterotoxins

Part of normal enteric flora in healthy animals Cytotoxin similar to Shiga toxin Adherence O157:H7 prototypical Transmission Contaminated, undercooked meat

Unpasteurized apple cider Children and the elderly more prone to HUS

Localized adherence likely

(HEp-2 or HeLa cells) Enterotoxin

Increased intestinal mucus secretion Diffuse adherence likely (HEp-2 or HeLa cells)

Three syndromes Mild watery diarrhea Bloody diarrhea Persistent diarrhea

Diarrhea Vomiting Malaise Fever

Mucoid, nonbloody stools Two-week duration Nausea

Abdominal pain Watery diarrhea Traveler's diarrhea

Shigella-like Watery diarrhea Then, bloody mucoid, pus-laden diarrhea Tenesmus and fever possible

Hemorrhagic colitis Crampy abdominal pain Watery diarrhea progressing to bloody stools Absence of fever HUS

Diarrhea Watery Mucoid Persistent


Endoscopy Mucosal ulcerations, friability throughout colon, and terminal ileum possible Histology Lamina propria infiltration of inflammatory cells Ulcerative and necrotic areas Dilated crypts Treatment

Antibiotics Diagnosis

Stool culture Treatment Antibiotics

Diagnosis Presence of adherent organisms on small intestinal/rectal biopsy Treatment

Antibiotics Diagnosis Bioassays Immunoassays Gene probes for ST or LT Treatment Supportive

Antibiotics decrease duration of excretion; not recommended for children Diagnosis Bioassays Serotyping ELISA Treatment Supportive Limited antibiotic role Diagnosis Serotyping

Serum antibody tests Cytotoxin bioassays DNA hybridization PCR-based tests ELISA Treatment No effective therapy Supportive care Dehydration correction Management of electrolyte abnormalities Blood transfusions as necessary Diagnosis DNA probes

Diagnosis DNA probes

Table 3 Additional colonic pathogens



Clinical symptoms

Diagnosis and treatment

Amoeba Entamoeba histolytica

Helminths Trichuris trichura (whipworm)

Schistosomiasis S. mansoni

Travel to endemic areas a risk factor Large intestinal commensal organism Transmission Person-to-person contact Contaminated food/water (cysts)

Cysts transform into trophozoytes at the terminal ileum Invade mucosa and submucosa

Primarily colonic

Snail as pathogen Contaminates fresh water

Acute onset Fulminant colitis Bloody, mucoid diarrhea Abdominal distention Abdominal pain Perforation possible Hepatic abscesses possible

Heavy infestations associated with (bloody) diarrhea Rectal prolapse

Dysenteric-like illness Bloody diarrhea Perianal fistulas

Diagnosis Histopathology: Hyperemia and edema Acute inflammation Microulceration Flask ulcer formation (Fresh) stool examination for cysts or trophozoites Treatment lodoquinol Metronidazole


Stool assays Treatment Thiabendazole Mebendazole Diagnosis Endoscopic Focal and diffuse fibrosis Intraluminal

Granulamatous masses (bilharziomas) Stool exam for viable eggs Treatment Praziquantal hyperplastic lymphoid follicles are present; it is not uncommon for ulcerations to overlie these areas.

Inflammatory polyps (also referred to as pseudo-polyps) can be seen during the recovery phase from inflammation or in inflammatory diseases, and they are often seen in the context of IBD. They can be

Juvenile Polyp And Inflammatory Polyp
Figure 2 Endoscopic view of colonic polyps in a patient with juvenile polyposis col. (Reproduced with permission from Kleinman RE, Gilger MA, Braverman RM, Finegold MS, Hawkins EP, and Klish WJ (eds.) (1998) Atlas of Pediatric Gastrointestinal Disease. Hamilton Ontario: Decker.)

associated with phases of regeneration and are plei-morphic in nature.

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