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Solitary Rectal Ulcer Syndrome

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Solitary Rectal Ulcer Syndrome A Rare and Often Unrecognized Cause of Hematochezia and Tenesmus in Childhood: Solitary Rectal Ulcer Syndrome Deniz Ertem*; Yesim Acar§; Esin Kotiloglu Karaa‡; and Ender Pehlivanoglu, MD* ABSTRACT. Solitary rectal ulcer syndrome (SRUS) is for rectal prolapse in most cases seems to be exces- an unusual disorder of childhood, which usually pre- sive straining efforts during which high intra-ab- sents with rectal bleeding, mucous discharge, prolonged dominal pressure forces the anterior rectal mucosa straining, tenesmus, and localized pain in the perineal firmly into the contracting puborectalis muscle.9–12 area. After the first description by Cruveilhier, Madigan and Morson further detailed the clinical and pathologic The anterior rectal mucosa is frequently forced into features of SRUS in 1969. The pathogenesis of the syn- the anal canal and as a consequence becomes stran- drome is not well-understood. The postulated mecha- gulated, causing congestion, edema, and ulcer- nism responsible for rectal prolapse in most cases seems ation.1–3 to be excessive straining efforts during which high intra- Histologically, the presence of fibromuscular oblit- abdominal pressure forces the anterior rectal mucosa eration of the lamina propria with disorientation of firmly into the contracting puborectalis muscle. The an- muscle fibers is characteristic, which could be sec- terior rectal mucosa is frequently forced into the anal ondary to chronic mechanical and ischemic trauma canal and as a consequence becomes strangulated, caus- ing congestion, edema, and ulceration. and inflammation by hard stools, and intussuscep- 2,3,12–17 Histologically, the presence of fibromuscular oblitera- tion of the rectal mucosa. Although the syn- tion of the lamina propria with disorientation of muscle drome is well-recognized in adults, the pediatric fibers is characteristic, which could be secondary to experience with this condition is limited and often chronic mechanical and ischemic trauma and inflamma- remains unrecognized or misdiagnosed.1–6,13,14 A tion by hard stools, and intussusception of the rectal misdiagnosis has been reported in one fourth of mucosa. Although the syndrome is well-recognized in adult cases, and the correct diagnosis usually de- adults, the pediatric experience with this condition is layed approximately 5 to 7 years.2,3,15 There are few limited and often remains unrecognized or misdiag- 1–6 nosed. A misdiagnosis has been reported in one fourth of pediatric case reports in English literature. Here, adult cases, and the correct diagnosis usually delayed we describe 2 children with SRUS, aged 11 and 14 approximately 5 to 7 years. There are few pediatric case years, whose SRUS was diagnosed 2 and 6 years, reports in English literature. Here, we describe 2 children respectively, after the onset of the first signs and with SRUS, aged 11 and 14 years, whose SRUS was symptoms. diagnosed 2 and 6 years, respectively, after the onset of the first signs and symptoms. Pediatrics 2002;110(6). URL: http://www.pediatrics.org/cgi/content/full/110/6/ CASE REPORTS e79; rectal bleeding, solitary rectal ulcer syndrome. Case 1 An 11-year-old girl was referred to our outpatient clinic with a ABBREVIATION. SRUS, solitary rectal ulcer syndrome. 2-year history of rectal bleeding, digital extraction of feces, and intermittent rectal prolapse during defecation. She had hard stools every other day, containing fresh blood on the surface of it. There olitary rectal ulcer syndrome (SRUS) is an un- was a history of regular laxative use, but the hematochezia had not usual disorder of childhood, which usually pre- been resolved despite treatment. There was no history of weight sents with rectal bleeding, mucous discharge, loss, fever, arthralgia, skin rash, abdominal pain, change in appe- S tite or daily activity, intake of antibiotics, or bleeding tendency. prolonged straining, tenesmus, and localized pain 1–6 The physical examination, including digital rectal examination, in the perineal area. After the first description by was normal. Her anthropometric measurements were at the 7 8 Cruveilhier, Madigan and Morson further detailed 50th percentile for both height and weight. The laboratory find- the clinical and pathologic features of SRUS in 1969. ings revealed hypochromic and microcytic anemia (hemoglobin The pathogenesis of the syndrome is not well- 10.7 g/dL, hematocrit 33.8%, mean corpuscular volume 62.7 fl, ϫ 3 3 understood. The postulated mechanism responsible platelet count 343 10 /mm ), normal erythrocyte sedimentation rate (10 mm/h), and normal coagulation profile. White blood cell count was 6800/mm3; liver function tests, and serum proteins were within normal ranges. Stool examination for ova, parasites, From the *Division of Pediatric Gastroenterology and Nutrition, ‡Depart- and cultures were negative 3 times. Autoimmune markers (pe- ment of Pathology, §Okmeydani Social Security Teaching Hospital, Mar- rinuclear antineutrophil cytoplasmic antibody and antineutrophil mara University School of Medicine, Istanbul, Turkey, cytoplasmic antibody) were negative. Colonoscopy revealed 2 Received for publication Mar 7, 2002; accepted Aug 14, 2002. ulcers 15 and 20 mm in diameter surrounded by a hyperemic halo Reprint requests to (E.P.) Division of Pediatric Gastroenterology and Nu- and covered with fibrinous exudates on the anterior rectal wall 4 trition, Marmara University School of Medicine, Tophanelioglu Cd. 13-15, to 5 cm from the anus. Several biopsies were obtained from both 81190, Altunizade-Istanbul, Turkey. E-mail: [email protected] the center and the margin of the ulcers. The rest of the colono- PEDIATRICS (ISSN 0031 4005). Copyright © 2002 by the American Acad- scopic examination up to the caecum was normal. Histopatholog- emy of Pediatrics. ical examination revealed erosion and superficial ulceration with http://www.pediatrics.org/cgi/content/full/110/6/Downloaded from www.aappublications.org/newse79 PEDIATRICS by guest on September Vol. 110 26, 2021 No. 6 December 2002 1of4 Fig 1. Superficial rectal mucosa showing erosion and ulceration Fig 2. Fibrous enlargement of lamina propria by extension of covered with inflammatory exudates (arrows) and regenerative muscle fibers (arrows) and muscle bundles intermingled around changes in glandular epithelium (hematoxylin-eosin stain, ϫ10). the crypts (hematoxylin-eosin stain, ϫ20). inflammatory cell infiltration in the lamina propria, distortion of history of abdominal pain, constipation, weight loss, change in crypts, and regenerative changes in crypt epithelium (Fig 1). There daily activity or appetite, recent use of antibiotics, arthralgia, was expansion of the lamina propria with the extension of fibro- aphthous skin, or oral lesions. Physical assessment, including blasts around the crypts (Fig 2). Biopsy samples obtained from the digital rectal examination, was normal. The laboratory investiga- normal-looking colonic segments were also normal histologically, tion revealed a normal complete blood count and blood coagula- and no parasite or granuloma or inclusion bodies were detected in tion profile. The erythrocyte sedimentation rate was 5 mm/h, the biopsy samples. The macroscopic involvement of the distal autoimmune markers (perinuclear antineutrophil cytoplasmic an- part of the rectum and microscopic examination of the macro- tibody and antineutrophil cytoplasmic antibody) both were neg- scopic lesions led us to the diagnosis of SRUS. An increase in ative. Microscopic examination of stool showed 4 to 5 leukocytes, dietary fiber and regular use of laxatives were advised, and she and 10 to 15 erythrocytes but negative for ova and parasites 3 was treated with sulfasalazine enema for 6 months. The symptoms times. Stool cultures were also negative for pathogenic microor- resolved for a few months but then recurred despite the passage of ganisms. Flexible colonoscopy revealed a circumferential ulcer 3 soft stool with easy defecation. Detrimental effects of the worsen- to 4 cm in length 5 to 6 cm distal to the anal verge. The surface of ing of symptoms in lifestyle of both the child and her parents led the ulcer was covered with grayish exudates, and the ulcer was us to refer the patient to a pediatric surgeon for surgical interven- well demarcated from the surrounding normal mucosa. The mu- tion. Because the SRUS in this patient was associated with mucosal cosal and vascular structures beyond this ulcer up to the caecum rectal prolapse, Ekehorn sacrorectopexy was performed at the end were completely normal. Multiple biopsies were obtained from of 1.5 years of conservative treatment. Her signs and symptoms both ulcer center and ulcer margin and from normal-looking parts (rectal bleeding, rectal prolapse, feeling of incomplete defecation, of the total colonic segments. Histopathological examination of the digital extraction of feces) resolved gradually during the 18 mucosa from the ulcer showed epithelial hyperplasia with goblet months of follow-up after the surgical procedure. A repeat cell depletion, regenerative crypt epithelium, and fibrous enlarge- colonoscopy performed 12 months after the rectopexy revealed ment of the lamina propria. Biopsy samples obtained from the healing of the rectal ulcers. normal-looking colonic segments all were normal histologically. and no parasite or granuloma or inclusion bodies were detected in Case 2 the biopsy samples. After the exclusion of infective and inflam- A 14-year-old boy was admitted to our outpatient clinic with matory causes of rectal ulcer, clinical history
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