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