Colitis following fecal diversion: still a challenge

Diagnóstico diferencial entre colite relacionada à derivação fecal e as doenças inflamatórias intestinais: o desafio persiste

2 - ORIGINAL ARTICLE

COLITIS FOLLOWING FECAL DIVERSION: STILL A CHALLENGE¹

Leonaldson dos Santos Castro²

Alberto Schanaider³

Bettina Wolff Castro²

Castro LS, Schanaider A, Castro BW. Colitis following fecal diversion: still a challenge. Acta Cir Bras [serial online] 2000 Oct-Dec;15(4). Available from: URL: http://www.scielo.br/acb.

ABSTRACT: After fecal diversion, nonspecific colitis may be seen in the defunctionalized colon. The purpose of this prospective study is to identify specific findings that could help in the differential diagnosis between diversion colitis and other inflammatory bowel diseases in order to avoid inappropriate diagnosis and therapy. It was studied, prospectively, thirteen consecutive patients from two public hospitals of Rio de Janeiro who had undergone temporary colostomy for indications other than inflammatory bowel disease. They were submitted to endoscopy with biopsy of both proximal and distal colorectal segments, and prospectively evaluated before and after restoration of intestinal continuity. Endoscopy with biopsy of both proximal and distal excluded colorectal segments showed a nonspecific mucosal and submucosal inflammation, resembling ulcerative colitis ( p < 0.01). There was endoscopic resolution in all patients once restoration of intestinal continuity was established (p < 0.01) and also histologic improvement after the stoma closure. In conclusion there are no specific findings that make possible an unequivocal distinction between diversion colitis and other nonspecific inflammatory diseases. Diagnosis should be achieved if after stoma closure occur remission of endoscopic large bowel inflammatory signs with improvement in mucosal histologic appearance and prompt relief of clinical complaints.

SUBJECT HEADINGS: Colitis. Colostomy. Inflammatory bowel diseases. Diagnosis differential.

INTRODUCTION

Inflammatory findings have been described in defunctioned segments of the colon and rectum after surgical diversion by Jackman¹, Morson² and Glotzer³ who called them ‘diversion colitis’. This condition is usually asymptomatic, but it may be manifested by rectal discharge of mucus or blood and tenesmus.^4-12 Its endoscopic and histologic appearances can include erythema, friability, exudate, chronic and acute infiltrates in the lamina propria, ulceration, crypt abscess and lymphoid follicular hiperplasia.^4,8,9,13-20 . Besides there are focal areas of leukocyte congregation.²¹ It can occur within a few weeks or can be discovered after years postdiversion. It is noteworthy that physician must be familiarized with this type of iatrogenic entity in order to prevent a misleading diagnosis or an unsuitable therapy.

METHODS

Thirteen consecutive patients who underwent temporary colostomy were studied. They derived from University Hospital Clementino Fraga Filho of the Federal University of Rio de Janeiro and Hospital of Ipanema, where all of them were evaluated. Eight patients had acute abdominal conditions (obstruction, perforation and peritonitis) and were submitted to emergency surgery. The remainder were treated with two stage elective surgery (Table 1).

All were waiting for colostomy closure and agreed to participate in this study. Every patient underwent endoscopy of both proximal colon and excluded colorectum without preparatory cleansing. The endoscopic findings were noted by a single author. Five abnormalities - erythema, edema, friability, granularity and ulcerations - were scored as absent (grade 0), mild (1) or severe (2). The sum of the scores was considered to be an endoscopic index of the proximal nonexcluded colon (EI1-p), which served as endoscopic control, or of the distal excluded colorectum (EI1-d), both with a range of 0 to 10. Three mucosal specimens were obtained by forceps biopsy of both nonexcluded and defunctionalized bowel. The biopsy specimens were fixed in Bouin's solution and stained with hematoxylin and eosin. Like endoscopic appearances, each histologic findings - inflammation, erosions, edema, exsudate and crypt abscess - were noted and graded from 0 to 2 by a single pathologist. The sum these scores was considered to be a histologic index of the proximal colon (HI1-p), which served as histologic control, or of the distal colorectum (HI1-d). Between 25 to 79 days after restoration of intestinal continuity, these studies were repeated in the distal refunctionalized segment, originating the postoperative endoscopic and histologic indices (EI-2 and HI-2 respectively). The preoperative indices of the proximal segment were compared with the preoperative indices of the excluded segment (EI1-p versus EI1-d, HI1-p versus HI1-d), and all the preoperative indices were also compared with the postoperative indices (EI1-p versus EI2/ EI1-d versus EI2; HI1-p versus HI2/ HI1-d versus HI2). Statistical analysis was performed using the Wilcoxon test. Significance was assigned to any P value of less than 0.05.

Pre and postoperative barium examination of the large bowel was performed in all cases.

RESULTS

Six men and seven women of a mean age of 57 years (range from 25 to 69) were evaluated. It was performed 9 loop colostomy. 3 end colostomy with mucous fistula and 1 Hartmann's procedure (Table 1).

Fecal diversion period was a mean of 7 (3 to 19) months. Rectal bleeding, mucous discharge and tenesmus were the most frequent symptoms. Six patients had mild symptoms and other two, occasionally, moderate symptoms related to diversion. Preoperative barium enema was generally displayed a shortened, narrowed and tubular colon (Figure 1).

Figure 1
- Barium enema demonstrating lack of distensibility, rigidity and shortening of excluded colon.

As observed in Table 2, no significant abnormalities were seen in the control indices (EI1-p and HI1-p).

However, the defunctionalized bowel indices (EI1-d and HI1-d) showed remarkable inflammatory features (p < 0.01). Endoscopic changes of excluded segments demonstrated erythema, edema, granularity and friability of the colorectal mucosa. In four patients (31%) it was also observed aphthous ulcers ranging from 1 to 5 mm in diameter. Intestinal surface was often covered by mucous exsudate although sometimes pus was present. The most common histologic finding included lymphoplasmacytic infiltrates in the lamina propria associated with edema and vascular congestion. Cryptitis and crypt abscesses were seen in four patients (31%), almost exclusively in cases with severe inflammation. In addition, there were loss of mucin secretion and submucosal involvement associated with the higher degrees of inflammation (Figure 2).

Figure 2
- Photomicorgraph demonstrating marked architectural alteration of the crypts with crypt abscesses, mucosal ulceration, dense lymphoplasmacytic infiltrates and luminal exsudate. Hematoxylin and eosin stain. Original magnification X300.

After reanastomosis, complete remission of the abnormal endoscopic findings was observed. In such circumstances all patients showed marked improvement in the histologic findings. Statistical analysis of EI1-d versus EI2 and of HI1-d versus HI2 revealed differences highly significant (p < 0.01). There were no statistical differences when EI1-p was compared with EI2 (p > 0.05). Notwithstanding, the comparison between HI1-p and HI2 presented a significant difference (p < 0.01), indicating that there was histologic improvement but it was not complete.

After restoration of intestinal continuity, barium contrast X-ray study had normal appearance.

DISCUSSION

Diversion colitis is a nonspecific inflammatory and iatrogenic process that develops in bypassed colonic segment after surgical diversion of the fecal stream. It was first defined by Glotzer3, in 1981. Because of its recently description the natural history of this entity is still unclear and attempts to identify a specific etiologic agent have been unsuccessful¹⁷. Therefore clinical recognition remain a challenge and unfortunately it is not uncommon to mislead the diagnosis and postpone the suitable treatment. Most of the times, a prospective evaluation of the patient clinical course after the intestinal closure surgery is the only way to achieve a correct diagnosis.

The pathogenesis of this disorder has been attributed to the deficiency of short-chain fatty acids (SCFAs) in the excluded colon^22,30 and also to bacterial overgrowth.^23,24 although it have not been widely accepted.^25,26 Roediger²⁷ demonstrated that SCFAs are the major energy source for human colonocytes and are associated with a trophic effect.^25,28 Probably the depletion of this energy source, as seen in segments of the colon and rectum after surgical fecal diversion^23,25, may contribute to homeostatic imbalance of the colonic epithelium determining functional and structural injury of the colonocyte. However, many systemic and local factors such as free oxygen radicals and acid arachidonic may induce the inflammatory response and the tissue damage.²⁹

This prospective study showed an incidence of 100% of diversion colitis in patients that underwent fecal diversion, unrelated to age and period of diversion. However, its incidence in the literature is lower because it tends to be underestimated.^8,14 Onset typically occurs 3-36 months after fecal diversion, although it can be observed even up to 35 years.³¹ Patients are usually asymtomatic but may complain of mucous or bloody rectal discharge, tenesmus, anorectal pain or can develop stricture formation, in most severe cases.¹¹ The inflammatory process may compromise the entire diverted segment or be confined to the rectum. It seems that the type of colostomy doesn’t interfere with the clinical features.^7,32 Accurate diagnosis is based on thorough clinical history, histologic and endoscopic findings. Nevertheless, distinction between diversion colitis and active idiopathic inflammatory bowel disease it is not easy and most of the times virtually unfeasible. Some authors even suggest that diversion colitis may play a role as a risk factor for ulcerative colitis.³³

The natural history, the clinical features before the first surgery, and also the surgical procedure chosen provide some clues for the suspicion of diversion colitis. We emphasize that failure to recognize this condition may results in unnecessary proctocolectomy⁵ or other inappropriate therapy.

Colonoscopy in the excluded segments of colon or rectum may show mucosal erythema, hyperemia, edema, friability, as well as granularity, nodularity and aphtous ulcerations. The remarkable point is that these abnormalities usually subside after the re-establishment of large bowel continuity. Ours endoscopic and histologic findings after stoma closure were similar to those observed in the mucosa of the nonexcluded colon (control), although the histologic remission was incomplete. As reported by others authors^16,22, the most common findings were lymphoplasmacytic infiltrates in the lamina propria (100%). Superficial ulcerations and crypt abscesses associated with submucosa involvement were seen in cases with moderate to severe inflammation. We could not find granulomas although they have been reported^5,22,36, but if they are present it should raise the suspicion of Crohn's disease. Nevertheless in most instances it is virtually impossible to establish a precise diagnosis strictly on the basis of endoscopic and histologic presentations.

Therefore differential diagnosis between primary idiopathic inflammatory bowel disease and diversion colitis could only be supported by a global analysis including clinical picture, X-rays studies of the bowel, endoscopic features and biopsy findings. The absence of previous clinical history of Crohn's disease or ulcerative colitis may be helpful for establishing the proper diagnosis. Frequently we receive patients which required an emergency colostomy outward our surveillance and without an accurate history and clinical settings. In that circumstances we could lost essential data since we don’t know the characteristics of the distal colorectum before diversion and neither the previous diagnosis.

CONCLUSIONS

Diversion colitis is a nonspecific inflammatory and iatrogenic process that develops in bypassed colonic segment after surgical diversion of the fecal stream. No pathognomonic features were identified and this condition may mimic both ulcerative colitis and Crohn’s disease. Despite of the complementary exams, the remission of clinical complains and improvement of inflammatory signs after stoma closure were the most confident features able to help in the differential diagnosis.

ACKNOWLEDGMENTS

The authors are grateful to Leopoldo Jotha Lopes, M.D., for histologic study and Pedro Carvalho Rodrigues for statistical analysis.

Castro LS, Schanaider A, Castro BW. Diagnóstico diferencial entre colite relacionada à derivação fecal e as doenças inflamatórias intestinais: o desafio persiste. Acta Cir Bras [serial online] 2000 Oct-Dec;15(4). Available from: URL:http://www.scielo.br/acb.

RESUMO: Uma forma de colite relacionada à derivação fecal pode ser identificada nos segmentos colônicos excluídos do trânsito fecal. Esta condição inflamatória, ao mimetizar a doença de Crohn e a colite ulcerativa, pode resultar em diagnóstico e tratamento inapropriados. Este estudo prospectivo objetivou rever os efeitos da derivação fecal e caracterizar a evolução após a restauração do trânsito intestinal. Foram avaliados treze pacientes sem doença inflamatória intestinal e submetidos previamente à uma colostomia. Os achados da endoscopia com biópsia colo-retal, dos segmentos proximal e distal desfuncionalizados, evidenciaram uma inflamação inespecífica da mucosa e da submucosa, muito semelhante aquela da colite ulcerativa (p<0.01). Depois do fechamento da colostomia observou-se a regressão das alterações endoscópicas e histopatológicas. Em conclusão, enfatiza-se que na presença de uma colostomia, a colite relacionada à derivação fecal deve ser aventada no diagnóstico diferencial das doenças inflamatórias inespecíficas intestinais. O restabelecimento da continuidade intestinal é o único tratamento garantido para a obtenção da remissão clínica.

DESCRITORES: Colite. Colostomia. Enteropatias inflamatórias. Diagnóstico diferencial.

Address for correspondence:

Alberto Schanaider

Rua Eurico Cruz 33/603

Rio de Janeiro - RJ

22461-200

Data do recebimento: 02/07/2000

Data da revisão: 15/08/2000

Data da aprovação: 21/09/2000

• 1. Jackman RJ. Lesions of the lower bowel. Springfield: C. C. Thomas; 1958.
• 2. Morson BC, Dawson I MP. Gastrointestinal pathology. London: Blackwell Scientific; 1972.
• 3. Glotzer, DJ, Glick ME., Goldman H. Proctitis and colitis following diversion of the fecal stream. Gastroenterology 1981;80:438-41.
• 4. Bosshardt RT, Abel ME. Proctitis following fecal diversion. Dis Colon Rectum 1984;27:605-7.
• 5. Murray FE, OBrien MJ, Birkett DH, Kennedy SM; Lamont T. Diversion colitis: pathologic findings in a resected sigmoid colon and rectum. Gastroenterology 1987;93:1404-8.
• 6. Guillemot F, Colombel JF, Neut C; Verplanck N; Lecomte M; Romond C; et al. Treatment of diversion colitis by short-chain fatty acids: prospective and double-blind study. Dis Colon Rectum 1991;34: 861-4.
• 7. Haas PA, Fox TA. The fate of the forgotten rectal pouch after Hartmanns procedure without reconstruction. Am J Surg 1990;159:106-11.
• 8. Haas PA, Fox TA, Szilagy E.J. Endoscopic examination of the colon and rectum distal to a colostomy. Am J Gastroenterol 1990;85:850-4.
• 9. Ma CK, Gottlieb C, Haas PA. Diversion colitis: a clinicopathologic study of 21 cases. Hum Pathol 1990;21:429-36.
• 10. Nobels F, Colemont L, Van Moer E. A case of diversion rectitis. Acta Clin Belg 1989;44:202-4.
• 11. Ona FV, Boger JN. Rectal bleeding due to diversion colitis. Am J Gastroenterol 1985;80:40-1.
• 12. Ordein JJ, Di Lorenzo C, Flores A, Hyman PE. Diversion colitis in children with severe gastrointestinal motility disorders. Am J Gastroenterol 1992;1:88-90.
• 13. Diversion colitis (editorial). Lancet 1989,1:764 .
• 14. Fergunson CM, Siegel RJ. A prospective evaluation of diversion colitis. Am Surg 1991;57:46-9.
• 15. Goldman H. Other inflammatory disorders of the intestines. In: Ming SC, Goldman H. Pathology of the gastrointestinal tract. Philadelphia: WB Saunders; 1992. p 689-724.
• 16. Komorowski RA. Histologic spectrum of diversion colitis. Am J Surg Pathol 1990;14:548-54.
• 17. Edwards CM, George B, Warren B. Diversion colitis: new light through old windows. Histopathology 1999;34:1-5.
• 18. Tanaka M, Riddel RH. The pathological diagnosis and differential diagnosis of Crohns disease. Hepatogastroenterol 1990;37:18-31.
• 19. Waye JD. Differentiation of inflammatory bowel conditions by endoscopy and biopsy. Endoscopy 1992;24:551-4.
• 20. Yeong ML, Bethwaite PB, Prasad J, Isbister WH. Limphoid follicular hyperplasia: a distinctive feature of diversion colitis. Histopathology 1991;19:55-61.
• 21. Stein DT, Paldi JH., Goodwin DA. In-111 leukocyte scan in diversion colitis. Clin Nuc Med 1983;8:1-2.
• 22. Harig JM, Soergel K, Komorowski RA, Wood CM. Treatment of diversion colitis with short-chain fatty acid irrigation. N Eng J Med 1989;320:23-8.
• 23. Neut C, Colombel JF, Guillemot F, Cortot A, Gower P, Quandalle P, et al. Impaired bacterial flora in human excluded colon. Gut 1989;30:1094-8.
• 24. Scheppach W; Christl SU; Bartram HP; Richter F; Kasper H. Effects of short-cahin fatty acids on the inflamed colonic mucosa. Scand J Gastroenterol Suppl 1997;222:53-7.
• 25. Harig JM, Soergel KK. Treatment of diversion colitis with short-chain fatty acid irrigation. Gastroenterology 1987;92:1425.
• 26. Winslet MC, Poxon V, Youngs J et al. A pathophysiologic study of diversion proctitis. Surg Gynecol Obstet 1993;177:57-60.
• 27. Roediger WE. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 1980;21:793-8.
• 28. Kripke SA, Fox AD, Berman JM, Settle RG, Rombeau JL. Stimulation of intestinal growth with intracolonic infusion of short-chain fatty acids. J P E N 1989;13:109-15.
• 29. Triantafillidis JK, Nicolakis D, Mountaneas G, Pomonis E. Treatment of diversion colitis with 5-aminosalicylic acid enemas: comparison with betamethasone enemas. Am J Gastroenterol 1991;86:1552-3.
• 30. Rolandeli RH, Settle G, Saul S, Jacobs D, Mattei P, Rombeau JL. A comparision of parenteral nutrition and enteral feeding with pectin in experimental colitis. Clin Res 1985;33:708A.
• 31. Giardiello FM; Lazenby AJ. The atypical colitides. Gastroenterol Clin North Am 1999;28:479-90
• 32. Vujanic GM; Dojcinov SD. Diversion colitis in children: an iatrogenic appendix vermiformis? Histopathology 2000;36:41-6.
• 33. Shaw-Dunn J, Wrigth R. Changes in the large intestine after 35 years of defunctioning by ileostomy. Roy Col Surg Engl 1981;63:210-21.
• 34. Korelitz BI, Heskin LJ, Sohn N, Sommers SC. Proctitis after diversion in Crohns disease and its elimination with reanastomosis: implications for surgical management. Gastroenterology 1984;87:710-3.
• 35. Lim AG, Langmead FL, Feakins RM, Rampton DS. Diversion colitis: a trigger for ulcerative colitis in the in-stream colon? Gut 1999;44:279-82.
• 36. Lavoine E, Vissuzaine C, Cardiot G, Sobhani I, Benhamou G, Mignon M, et al. Proctitis of diversion on an excluded rectum in patients with hemorrhagic rectocolitis. Gastroenterol Clin Biol 1996;20:243-7.

1. From the National Institute of Cancer, University Hospital Clementino Fraga Filho and Department of Surgery of the Faculty of Medicine of the Federal University of Rio de Janeiro.

. From the National Institute of Cancer, University Hospital Clementino Fraga Filho and Department of Surgery of the Faculty of Medicine of the Federal University of Rio de Janeiro.

2. CNPq Researcher

3. Associate Professor.

Publication Dates

• Publication in this collection
  08 Nov 2000
• Date of issue
  Dec 2000

History

• Accepted
  21 Sept 2000
• Reviewed
  15 Aug 2000
• Received
  02 July 2000