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Official Journal of the American Society of Abdominal Surgeons, Inc.

This article originally appeared in the Winter 2013 / Spring 2014 issue of the Journal.

Diverticulum in Small Bowel with Foreign Object

Steven Behrends, M.D.1
John R. Dobson, III M.D.2
Stephen Larsen, Ph.D.3
Frederick Larsen, B.S.4
Ferris Buhler, B.A.5

Address for correspondence:
Stephen Larsen, Ph.D.
Department of Pre-Clinical Sciences
Cleveland University
10850 Lowell Ave.
Overland Park, KS 66210
Tel: 913-234-0763
Fax: 913-234-0904

1 General Surgery, private practice, Kansas City, Missouri
2 Pathology, Saint Luke's South Hospital, Overland Park, Kansas
3 Professor, Pre-Clinical Sciences, Cleveland University, Overland Park, Kansas
4 Analytical Chemist, Independence Police Forensic Laboratory, Independence, Missouri
5 Intern, Cleveland University, Overland Park, Kansas


This case involves surgical removal of a foreign object sequestered in a jejunal diverticulum. The object was determined to be silicone rubber. Subsequent surgery revealed multiple jejunal diverticuli with chronic diverticulitis, which may have masked long-standing symptoms of celiac disease.


Acute abdominal emergencies may prove to be a diagnostic conundrum. Imaging can identify regional anatomy; however, anatomic variations can confound the specific diagnosis. Surgical intervention revealed a jejunal diverticulum containing a foreign object with the potential for perforation. Histological studies provided information regarding tissue alterations due to the presence of the foreign object and for classification of diverticulum type. Chemical analysis of the foreign object was determined to be polydimethylsiloxane. A possible link between the patient's long-standing symptoms from previously diagnosed celiac disease and the presence of a biologically inert foreign object is discussed. Literature related to the ingestion of foreign objects is reviewed.

KEY WORDS: jejunum, diverticulosis, perforation, polydimethylsiloxane, celiac sprue, enteropathy

ABBREVIATIONS: FO, foreign object; GI, gastrointestinal; EGD, esophagogastroduo-denoscopy; SI, small intestine; CT, computed tomography; H&E, hematoxylin & eosin stain; FTIR, Fourier Transform Attenuated Total Reflection Infrared Spectroscopy; PDMS, polydimethylsiloxane; NG, nasogastric; TURP, transurethral resection of prostate


The discovery of an FO lodged in a jejunal diverticulum prompted study of the anatomy, histology, and embryology of this case. Diverticula can form in the GI tract from esophagus to rectum, with the most common occurrence being in the colon. The incidence of diverticula in the small bowel is low, falling within a range from 0.2% to 6%, as found in upper GI radiographs and observed at autopsy.1,2 Two types of diverticula occur and can be classified as true (congenital) or false (acquired). True diverticula possess three wall layers: mucosa, submucosa, and muscularis externa (propria), present in normal SI. False diverticula possess the two innermost layers, with the muscularis externa being attenuated or absent.3,4 A fourth, thin serosal layer is also present on the outer intestinal surface. Most diverticula are found on the antimesenteric border of the SI.2 It has been reported that the frequency of occurrence of diverticula increases with age and is more often found in males than females.5,6Most ingested foreign bodies will pass spontaneously; however, approximately 1% will require surgical removal of the FO.7 We present a surgical case, physical and chemical analysis of the FO, and histology of the tissues involved.


In 1995, a sixty-two-year-old, physically active, mentally alert male presented with mild to acute gastric discomfort and weight loss, resulting in orders for a diagnostic EGD. Duodenal tissue sections indicated blunted villi and lymphocyte infiltration in the mucosal epithelium. Based on the histopathology and clinical symptoms, celiac disease was reported as probable diagnosis.8 A gluten-free diet was recommended and complied with by the patient. Major symptoms diminished with time, and weight gain followed; however, the patient continued to experience recurring episodes of GI distress.

Axial CT Scan (Figure 1A) and coronal CT Scan (Figure 1B) showing radiopaque FO in lower left abdomen.

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In 2010, the patient suffered moderate to acute pain in left upper and left lower abdominal quadrants and suprapubic region. Symptoms persisted and were severe enough to require a visit to the emergency room. A CT scan revealed an FO in the lower left abdomen, with possible perforation of the bowel (Figures 1A & 1B).

Following general surgical consultation, a laparotomy was recommended to remove the FO. Open abdominal surgery revealed the presence of a jejunal diverticulum with an FO projecting through the wall to the outer serosal layer. A 4- cm length of bowel was resected (Figures 2A & 2B), and a side-to-side anastomotic bowel repair was performed. The surgical pathology report disclosed an intestinal specimen with deep outpouchings consistent with diverticulosis. The report further revealed a 1.2 x 0.7 x 0.3 cm orange-yellow, grossly apparent foreign body protruding from a 2.7 x 2.2 cm bulge in the intestinal wall. Internal inspection of the diverticulum disclosed tan-brown mucosa enclosing a 3.7 x 1.0 x 0.6 cm orange-yellow, rubbery FO (Figures 3A & 3B). Serial sections of the FO were obtained and stained with H&E. Tissue sections were obtained from the wall of the diverticulum (Di-1).

The patient experienced an uneventful recovery and reported being symptom-free at his 6-month follow-up examination. As a result of general well-being and the absence of GI complaints previously attributed to celiac disease, the patient discontinued his gluten-free diet. This behavior is understandable, as the literature indicates compliance with this diet is difficult, due to its personal and social inconvenience, expense, lower palatability, and lack of availability.9,10

In 2011, a subsequent acute abdominal episode resulted in exploratory surgery of the intraperitoneal SI, which revealed a 30-cm section of jejunum with multiple communicating diverticula varying in size from 5-30 mm (Figure 4). This segment was resected, and successful bowel repair was completed. The patient continues to ignore a gluten-free diet and remains symptom-free. A series of tissue sections was obtained along the anti-mesenteric length of this section to identify histologic signs of celiac disease.

SI presented at surgical site with FO projecting from diverticulum (Di-1). A second, smaller diverticululm (Di-2) is also shown.

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Resected bowel with affected diverticulum (Di-1), adjacent diverticulum (Di-2), and small intestine (SI).

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Front and rear surface of FO.

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Cross section of FO.

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30-cm resection with communicating diverticula that have been surgically opened.

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FO slide with amorphous matrix and crystalloid aggregates, 400x.

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Brownish stained external margin of FO, 100x. No biological cells are observed in either slide.

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Tissue from Di-1 showing attenuated villi, extensive fibrosis of SM and ME, and serositis caused by FO, 11x.

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Fibrotic tissue and inflammatory cells in SM & ME, 400x.

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Normal villi, 40x.

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Physical examination of the FO revealed a pink-pigmented, elastomeric compound with surface vesicles. These vesicles suggest a bio-film layer stained brown-green as a result of bile salt adsorption/absorption. The inability to grossly identify the FO prompted use of microscopic and analyticalchemical techniques to determine if the material was biological or synthetic and to differentiate between ingestion of a foreign material and in situ formation.11

Histological examination of FO serial sections with light microscopy revealed a homogenous matrix with 7-50 μm crystalloid aggregates present throughout the specimen (Figures 5A & 5B). No cellular elements were observed, ruling out a biological origin. Samples from the FO were analyzed by infrared spectrometry and the data compared to the spectra of a known sample of medical-grade PDMS and chemical library spectra.12,13 The unknown sample was determined to be composed of silicone rubber.14,15

An attempt was made to identify the source of the FO, and a patient interview ruled out his being a "deliberate ingester" of bizarre objects.16,17 Materials usually found in enteroliths and lacto-, phyto-, pharmaco-, or trichobezoars were absent, ruling out in situ formation.18,19,20,21,22 The route of FO placement in the diverticulum must either have been per os23,24 or retrograde via the rectum (per podicem), the latter being highly unlikely.

It is beyond the scope of this paper to identify the source of the FO, however, it was of interest to determine how long the FO was present in the digestive tract. The ability of PDMS to resist bio-degradation is well documented25,26,27 and is generally stable within the ranges of 2-8 pH and 34.4-37.8oC normally found in the digestive tract.28 The presence of vesicles and slight adsorption/absorption of surface bile pigments indicates prolonged exposure to digestive juices. Also, the rounded ends of the FO suggest it was subjected to mechanical ablation and shaping by peristalsis over a significant period of time.

Although relatively inert from a chemical and biochemical perspective, siloxanes can provoke inflammation and immunologic responses.29,30 The Di-1 wall sample shows attenuation of the mucosa, extensive fibrosis of submucosa and muscularis externa, and the presence of serositis (Figure 6A). Areas with an increased presence of eosinophils, lymphocytosis, and extensive fibrosis observed in Di-1 (Figure 6B) are likely due to mechanical irritation from the presence of the FO and the physiologic action of peristalsis.

Histopathology observations of chronic inflammation and fibrosis in the diverticulum, along with the known chemical stability of the FO, suggest that the FO was not recently sequestered in the small bowel. Inflammation in the diverticulum could account for chronic GI distress over a significant period of time. Although coincidental remission of celiac disease must be considered, it seems reasonable that the FO and presence of multiple diverticula created "mischief " in the GI tract, mimicking symptoms of celiac disease. Serial non-diverticula wall tissue samples from the subsequent acute abdominal surgery's 30-cm resected bowel were examined. The H&E slide shown in Figure 7 indicates a normal structure. The lack of blunted villi and an acceptable number of lymphocytes in the epithelial layer suggest no frank celiac disease.8


Emergency surgery revealed an FO in the process of perforating the wall of a jejunal diverticulum. The impending perforation appears to have been provoked by blunt trauma injury to the lower left abdominal wall. The FO was composed of synthetic PDMS silicone rubber, a non-biological compound used in manufacturing of biomedical devices.31 The FO entered the GI tract per os and either created a new diverticulum or entered a pre-existing cavity.32 The diverticulum containing the FO exhibited chronic inflammation and extensive wall fibrosis, which apparently resisted perforation for a substantial period of time. Multiple SI wall tissue sections from regions devoid of diverticula did not show histopathology associated with celiac disease. The GI symptoms suffered by this patient and ascribed to celiac disease may have been caused by the presence of an FO and multiple jejunal diverticula. FIGURE 7. Normal villi, 40x.


1. Floch M, Floch N, Kowdley K, et al., eds. Netter's Gastroenterology. 2nd ed. Philadelphia: Saunders; 2010.

2. Clarke R, Ferraro R, Ozick L, el al. Small intestinal diverticulosis. Medscape. 2010. Available at: Accessed February 2, 2011

3. Gray S, Akin J, Skandalakis J. Three varieties of congenital diverticulum of the intestine. Surg Clin North Am. 1974; 54(6):1371-7.

4. Noffsinger A, Fenoglio-Preiser CM, Maru D, et al. Gastrointestinal Diseases: Atlas of Nontumor Pathology. 1st Ed. Washington, D.C.: American Registry of Pathology; 2007:831.

5. Jeyarajah R, Harford W. Diverticula of the hypopharynx, esophagus, stomach, jejunum, and ileum. In: Feldman M, Friedman L, Sleisenger M, eds. Sleisenger's and Fordtran's Gastrointestinal and Liver Disease. 7th Ed. Philadelphia: Saunders; 2002:359.

6. Kumar V, Cotran R, Robbins S, eds. Robbins Basic Pathology. 7th Ed. Philadelphia: Saunders; 2003:854.

7. Eisen GM, Baron TH, Dominitz JA, et al. Guideline for management of ingested foreign bodies. Gastrointest Endosc. 2002; 55(7):802-6.

8. Forbes A, Misiewicz JJ, Compton CC, et al., eds. Atlas of Clinical Gastroenterology. 3rd Ed. Philadelphia: Elsevier Mosby; 2005:82.

9. Ljungman G, Myrdal U. Compliance in teenagers with coeliac disease – a Swedish follow-up study. Acta Paediatr. 1993; 82:235-238.

10. Lerner A. New therapeutic strategies for celiac disease. Autoimmun Rev. 2010; 9:144-147.

11. Byrd-Bredbenner C, Beshgetoor D, Moe G, et al., eds. Wardlaw's Perspectives in Nutrition. New York: McGraw-Hill; 2007:562.

12. Sidwell JA. Rapra Collection of Infrared Spectroscopy of Rubbers, Plastics, and Thermoplastic Elastomers. 2nd Ed. [no city]: Smithers Rapra Technology; 1997:315.

13. Smith B. Infrared Spectral Interpretation: a Systematic Approach. Boca Raton: CRC Press; 1999:265.

14. Larsen FN. Gel permeation chromatography of silicones. J Chromatogr A. 1971; 55(1):220.

15. Larsen FN. Molecular characterization of silicones by gel permeation chromatography. American Laboratory. 1969;1:10-16.

16. Webb WA. Management of foreign bodies of the upper gastrointestinal tract. Gastroenterology. 1988; 94:204-16.

17. Lyons MF, Tsuchida AM. Foreign bodies of the gastrointestinal tract. Med Clin North Am. 1993; 77(5):1101-1113.

18. Salim AS. Small bowel obstruction with multiple perforations due to enterolith (bezoar) formed without gastrointestinal pathology. Postgrad Med J. 1990; 66:872-873.

19. Hayee B, Khan HN, Al-Mishlab T, et al. A case of enterolith small bowel obstruction and jejunal diverticulosis. World J Gastroenterol. 2003; 9(4):883-884.

20. Lough E, Richmond B, Maxwell D, et al. Obstructing phytobezoar arising from proximal jejunal diverticulum. Am J Surg. 2008; 195(1):106-107.

21. Malhotra A, Jones L, Drugas G. Simultaneous gastric and small intestinal trichobezoars. Pediatr Emerg Care. 2008; 24(11):774-776.

22. Monchal T, Hornez E, Bourgouin S, et al. Enterolith ileus due to jejunal diverticulosis. Am J Surg. 2010; 199(4):e45-47.

23. Dawwas MF, Jah A, Griffiths WJ, et al. Image of the month, jejunal diverticular peforation secondary to delayed distal migration of biliary endoprosthesis. Arch Surg. 2011; 146(4):483-484.

24. Volcani BE. In: Bendz G, Lindquist I (eds.) Biochemistry of Silicon and Related Problems. London: Plenum Press; 1978:591.

25. Colas A, Curtis J. Silicone biomaterials: history and chemistry & medical applications of silicones. In: Ratner BD, Hoffman AS, Schoen FJ, et al. Biomaterials Science: an Introduction to Materials in Medicine. [no city]: Elsevier Academic Press; 2004:697-706.

26. Östman M. Siloxanes. KEMI Swedish Chemicals Agency. 2005. Available at: floden/kemamne_eng/siloxaner_eng.htm. Accessed February 23, 2011.

27. Blocksma R, Braley S. The silicones in plastic surgery. Plast Reconstr Surg. 1965; 35(4):366-370.

28. Guyton A, Hall J, eds. Textbook of Medical Physiology. 11th Ed. Philadelphia: Elsevier; 2006:794.

29. Kossovsky N, Heggers JP. The bioreactivity of silicone. Crit Rev Biocompat. 1987; 3(1):53-85.

30. Bradley SG, White KL, McCay JA, et al. Immunotoxicity of 180 day exposure to polydimethylsiloxane (silicone) fluid, gel and elastomer and polyurethane disks in female b6c3f1 mice. Drug Chem Toxicol. 1994; 17(3):221-269.

31. Rowe VK, Spencer SC, Bass SL. Toxicological studies on certain commercial silicones. J Ind Hyg Toxicol. 1948; 30(6):332-352.

32. Fintelmann F, Levine MS, Rubesin SE. Jejunal diverticulosis: findings on CT in 28 patients. AJR Am J Roentgenol. 2008; 190(5):1286-1290.

The American Board of Abdominal Surgery
The American Society of Abdominal Surgeons, Inc.
Foundation for Abdominal Surgery

Louis F. Alfano, Jr., M.D., Editor-in-Chief
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Director of Continuing Medical Education

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Axial CT Scan (Figure 1A) and coronal CT Scan
(Figure 1B) showing radiopaque FO in lower left abdomen.
SI presented at surgical site with FO projecting from diverticulum (Di-1). A second, smaller diverticululm (Di-2) is also shown.
Resected bowel with affected diverticulum (Di-1), adjacent diverticulum (Di-2), and small intestine (SI).
30-cm resection with communicating diverticula that have been surgically opened. FIGURE 3 A. Front and rear surface of FO.
Cross section of FO.
30-cm resection with communicating diverticula that have been surgically opened.
FO slide with amorphous matrix and crystalloid aggregates, 400x.
Brownish stained external margin of FO, 100x. No biological cells are observed in either slide.
Tissue from Di-1 showing attenuated villi, extensive fibrosis of SM and ME, and serositis caused by FO, 11x.
Fibrotic tissue and inflammatory cells in SM & ME, 400x.
Normal villi, 40x..