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Artigo de Atualização • Rev. Col. Bras. Cir. 26 (3) • Jun 1999 • https://doi.org/10.1590/S0100-69911999000300012   copiar

Colite de derivação fecal

Diversion colitis

Autoria SCIMAGO INSTITUTIONS RANKINGS

Resumos

A colite de derivação fecal (CD) é um processo inflamatório que ocorre no segmento colorretal desfuncionalizado, após uma cirurgia de desvio do trânsito intestinal. As principais características dessa entidade clínica são: apresenta-se na desfuncionalização do cólon ou reto; não há doença inflamatória intestinal preexistente; nunca acomete o sítio proximal à colostomia e ocorre resolução do processo após a restauração do trânsito intestinal. Diversas são as hipóteses postuladas para explicar o seu aparecimento; todavia, a deficiência nutricional do epitélio colônico, pela ausência dos ácidos graxos de cadeia curta (AGCC), no segmento desfuncionalizado, é a mais aceita na atualidade. Os autores fazem uma revisão da literatura enfocando os aspectos clínicos, histopatológicos e terapêuticos desta doença.

Colite de derivação; Ácidos graxos de cadeia curta; Mucosa intestinal; Colostomia

The authors present a revision of diversion colitis. It is an inflammatory disorder that occurs in the colorectum segment after a diverting colostomy. The main features of this disease are: colon or rectum disfunction; no previous intestinal inflammatory disorder; it never attacks the colon upper colostomy; after intestinal transit restoration, the inflammatory process is solved. Many hypothesis are postulated to explain its occurrance. They include: fecal stasis; changes in the bacterial population of colon; nutritional deficiency of colonic epithelium due to the absence of short chain fatty acids in the defunctionalized segment is the most accepted nowadays. The absence of fatty acids produces energetic defficiency in colon mucosa, reduced electrolite absorption and secretion, and reduced mucus production. The patients have abdominal pain, mucus diarrhoea and bleeding. Histopathological features include chronical inflamation of colon wall, vascular congestion and changes in mucosa cripts. Lynphoid hiperplasy of mucosa and submucosa are common. The diagnosis is done by endoscopy, radiology, pathology and laboratory data. Surgery is considered the best treatment and when the intestinal continuity is restored the patients get cured. The topical use of short chain fatty acids by enema have had good results in some cases. As diversion colitis results in many assimptomatic patients, its incidence is understimated and more attention is needed always when a colostomy is done.

Derivation colitis; Short-chain fatty acids; Intestinal mucosa

ARTIGO DE ATUALIZAÇÃO

Colite de derivação fecal

Diversion colitis

Francisco Edilson Leite Pinto Júnior, ACBC-RNI; Ariano José Freitas de Oliveira, RCBC-RNII; Kallyandre Ferreira de MedeirosII; Ana Maria de Oliveira RamosIII; Aldo da Cunha Medeiros, TCBC-RNIV

IProfessor Assistente I da Disciplina de Técnica Operatória - Cirurgia Experimental. Coordenador da Residência Médica em Cirurgia Geral da UFRN. Mestre pela UFPE

IIResidente de Cirurgia Geral da UFRN

IIIProfessora de Patologia da UFRN

IVDoutor em Cirurgia. Professor Adjunto IV e Chefe da Disciplina de Técnica Operatória e Cirurgia Experimental da UFRN. Pesquisador 1b do CNPq

Endereço para correspondência Endereço para correspondência: Dr. Francisco Edilson Leite Pinto Júnior Av. Brigadeiro Gomes Ribeiro, 1025 59056-520 - Natal-RN E-mail: edilsonpinto@uol.com.br

RESUMO

A colite de derivação fecal (CD) é um processo inflamatório que ocorre no segmento colorretal desfuncionalizado, após uma cirurgia de desvio do trânsito intestinal. As principais características dessa entidade clínica são: apresenta-se na desfuncionalização do cólon ou reto; não há doença inflamatória intestinal preexistente; nunca acomete o sítio proximal à colostomia e ocorre resolução do processo após a restauração do trânsito intestinal. Diversas são as hipóteses postuladas para explicar o seu aparecimento; todavia, a deficiência nutricional do epitélio colônico, pela ausência dos ácidos graxos de cadeia curta (AGCC), no segmento desfuncionalizado, é a mais aceita na atualidade. Os autores fazem uma revisão da literatura enfocando os aspectos clínicos, histopatológicos e terapêuticos desta doença.

Unitermos: Colite de derivação; Ácidos graxos de cadeia curta; Mucosa intestinal; Colostomia.

ABSTRACT

The authors present a revision of diversion colitis. It is an inflammatory disorder that occurs in the colorectum segment after a diverting colostomy. The main features of this disease are: colon or rectum disfunction; no previous intestinal inflammatory disorder; it never attacks the colon upper colostomy; after intestinal transit restoration, the inflammatory process is solved. Many hypothesis are postulated to explain its occurrance. They include: fecal stasis; changes in the bacterial population of colon; nutritional deficiency of colonic epithelium due to the absence of short chain fatty acids in the defunctionalized segment is the most accepted nowadays. The absence of fatty acids produces energetic defficiency in colon mucosa, reduced electrolite absorption and secretion, and reduced mucus production. The patients have abdominal pain, mucus diarrhoea and bleeding. Histopathological features include chronical inflamation of colon wall, vascular congestion and changes in mucosa cripts. Lynphoid hiperplasy of mucosa and submucosa are common. The diagnosis is done by endoscopy, radiology, pathology and laboratory data. Surgery is considered the best treatment and when the intestinal continuity is restored the patients get cured. The topical use of short chain fatty acids by enema have had good results in some cases. As diversion colitis results in many assimptomatic patients, its incidence is understimated and more attention is needed always when a colostomy is done.

Key words: Derivation colitis; Short-chain fatty acids; Intestinal mucosa.

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Full text available only in PDF format.

REFERÊNCIAS

1. Morson BC, Dawson IMP.Gastrointestinal Pathology. 1a ed. Londres: Blackwell Scientific Publications, 1972, pp. 485.

2. Glotzer DJ, Glick ME, Goldman H. Proctitis and colitis following diversion of the fecal stream. Gastroenterology 1981 ;80(3):438-441.

3. Murray FE, O'Brein MJ, Birkett DH, et al. Diversion colitis. Gastroenterology 1987;93(6): 1.404-1.408.

4. Agarwal VP, Schimmel EM. Diversion colitis: a nutritional deficiency syndrome? Nutr Rev 1989;47(9):257-261.

5. Bories C, Miazza B, Galian A, et al. Idiopathic chronic watery diarrhea from excluded rectosigmoid with goblet cell hyperplasia cured by restoration of large bowel continuity. Dig Dis Sci 1986; 31(7): 769-772.

6. Bosshardt RT, Abel ME. Proctitis following fecal diversion. Dis Colon Rectum 1984;27:605-607.

7. Ferguson CM, Siegel RJ. A prospective evaluation of diversion colitis. Am Surg 1991;57(1):46-49.

8. Passaro E, Drenick E, Wilson SE. Bypass enteritis - A new complication of jejunoileaI bypass for obesity. Am J Surg 1976; 131: 169-174.

9. Collin DP, McCormick PG, Schmith MG. Quantitative gas-chromatographic determination of short-chain fatty acids in aqueous samples. Clin Chem 1974;20(9):1.235-1.237.

10. Ma CK, Glottlieb C, Haas PA. Diversion colitis: a clinicopathologic study of 21 cases. Human Pathol 1990;21(4):429-436.

11. Haas PA;Fox TA; Szilagy EJ. Endoscopic examination of the colon and rectum distal to a colostomy. Am J Gastroenterol. 1990; 85(7): 850-854.

12. MacPherson B, Pfeiffer CJ - Experimental colitis. Digestion 1976; 14 (5):424-452.

13. Harig JM, Soergel KH, Komorowski RA, et al. Treatment of diversion colitis with short-chain-fatty acid irrigation. New Engl J Med 1989; 320( 1 ):23-28.

14. Roediger WEW. What sequence of pathogenetic events leads to acute ulcerative colitis? Dis Colon Rectum 1988;31(6):482-487.

15. Roediger WEW. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 1980;21(9):793-798.

16. Roediger WEW. The colonic epithelium in ulcerative colitis: Na energy- deficiency diseases? The Lancet 1980;4(2):712-715.

17. Tripodi J, Gordey S, Burakoff R. A case of diversion colitis treated with 5-aminosalicylic acid enemas. Am J Gastroenterol 1992; 87(5): 645-647.

18. Ordein JJ, Lorenzo CD, Flores A, et al. Diversion colitis in children with severe gastrointestinal motility disorders. Am J Gastroenterol 1992; 87( I ):88-90.

19. O!say CP, Kim DO, Pearl RK, et al. Diversion colitis in patients scheduled for colostomy closure. Dis Colon Rectum 1993;36(4); 366-367.

20. Haas PA, Hass GP. A critical evaluation of the hartmann's procedure. Am Surg 1988;54(6):380-385.

21. Komorowski RA. Histologic spectrum of diversion colitis. Am J Surg Pathol 1990;14(6):548-554.

22. Haque S, Eisen RS, West AB. The morphologic features of diversion colitis. Human Pathol 1993;24(2): 211-219.

23. Yeong ML, Bethwaite PB, Prasad J, et al. Lymphoid follicular hyperplasia- A distinctive feature of diversion colitis. Histopathology 1991;19:55-61.

24. Roe AM, Warren BF, Brodribb AJM, et al. Diversion colitis and involution of the defunctioned anorectum. Gut 1993;34(3): 382-385.

25. Korelitz BI, Cheskin LJ, Sohn N, et al. The fate of the rectal segment after diversion of the fecal stream in crohn's diseases: Its implications for surgical management. J Clin Gastroenterol1985;7(1):37-43.

26. Lechner GL, Frank W; Jantsch H, et al. Lymphoid follicular hyperplasia in excluded colonic segments: A radiologic sign of diversion colitis. Radiology 1990;176(1):135-136.

27. Neut C, Colombel JF, Guillemot F, et al. Impaired bacterial flora in human excluded colon. Gut 1989;30(8): 1.094-1.098.

28. Korelitz BI, Cheskin LJ, Sohn N, et al. Proctitis after fecal diversion in crohn 's disease and its elimination with reanastomosis: implications for surgical management. Gastroenterology 1984;87(3):710-713.

29. Surawicz CM, Belic L. Rectal biopsy helps to distinguish acute self-limited colitis from idiopathic inflammatory bowel disease. Gastroenterology 1984;86(1): 104-113.

30. Geraghty JM, Talbot IC. Diversion colitis: histological features in the colon and rectum after defunctioning colostomy. Gut 1991 ;32 (9):1.020-1.023.

31. Roediger WEW. The starved colon. Diminished mucosal nutrition, diminished absorption, and colitis. Dis Colon Rectum 1990; 33( I O): 858-862.

32. Roediger WEW, Nance S. Metabolic induction of experimental ulcerative colitis by inhibition of fatty acid oxidation. Br J Exp Pathol 1986; 67(6):773-782.

33. Lu ES, Lin T, Harms BL, et al. A severe case of diversion colitis with large ulcerations. Am J Gastroenterol 1995;90(9);1.508-1510.

34. Haque S, West AB. Editorial: Diversion colitis- 20 years a-growing. J Cl Gastroenterol 1992;15(4):281-283.

35. Guillemot F, Colombel JF, Neut C, et al. Treatment of diversion colitis by short-chain fatty acids. Dis Colon Rectum 1991 ;34 (10): 861-864.

Recebido em 23/11/98

Aceito para pub1icaçãob em 19/4/99

Trabalho realizado no Departamento de Cirurgia da Universidade Federal do Rio Grande do Norte - UFRN.

  • 1. Morson BC, Dawson IMP.Gastrointestinal Pathology. 1a ed. Londres: Blackwell Scientific Publications, 1972, pp. 485.
  • 2. Glotzer DJ, Glick ME, Goldman H. Proctitis and colitis following diversion of the fecal stream. Gastroenterology 1981 ;80(3):438-441.
  • 3. Murray FE, O'Brein MJ, Birkett DH, et al. Diversion colitis. Gastroenterology 1987;93(6): 1.404-1.408.
  • 4. Agarwal VP, Schimmel EM. Diversion colitis: a nutritional deficiency syndrome? Nutr Rev 1989;47(9):257-261.
  • 5. Bories C, Miazza B, Galian A, et al. Idiopathic chronic watery diarrhea from excluded rectosigmoid with goblet cell hyperplasia cured by restoration of large bowel continuity. Dig Dis Sci 1986; 31(7): 769-772.
  • 6. Bosshardt RT, Abel ME. Proctitis following fecal diversion. Dis Colon Rectum 1984;27:605-607.
  • 7. Ferguson CM, Siegel RJ. A prospective evaluation of diversion colitis. Am Surg 1991;57(1):46-49.
  • 8. Passaro E, Drenick E, Wilson SE. Bypass enteritis - A new complication of jejunoileaI bypass for obesity. Am J Surg 1976; 131: 169-174.
  • 9. Collin DP, McCormick PG, Schmith MG. Quantitative gas-chromatographic determination of short-chain fatty acids in aqueous samples. Clin Chem 1974;20(9):1.235-1.237.
  • 10. Ma CK, Glottlieb C, Haas PA. Diversion colitis: a clinicopathologic study of 21 cases. Human Pathol 1990;21(4):429-436.
  • 11. Haas PA;Fox TA; Szilagy EJ. Endoscopic examination of the colon and rectum distal to a colostomy. Am J Gastroenterol. 1990; 85(7): 850-854.
  • 12. MacPherson B, Pfeiffer CJ - Experimental colitis. Digestion 1976; 14 (5):424-452.
  • 13. Harig JM, Soergel KH, Komorowski RA, et al. Treatment of diversion colitis with short-chain-fatty acid irrigation. New Engl J Med 1989; 320( 1 ):23-28.
  • 14. Roediger WEW. What sequence of pathogenetic events leads to acute ulcerative colitis? Dis Colon  Rectum 1988;31(6):482-487.
  • 15. Roediger WEW. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 1980;21(9):793-798.
  • 16. Roediger WEW. The colonic epithelium in ulcerative colitis: Na energy- deficiency diseases? The Lancet 1980;4(2):712-715.
  • 17. Tripodi J, Gordey S, Burakoff R. A case of diversion colitis treated with 5-aminosalicylic acid enemas. Am J Gastroenterol 1992; 87(5): 645-647.
  • 18. Ordein JJ, Lorenzo CD, Flores A, et al. Diversion colitis in children with severe gastrointestinal motility disorders. Am J Gastroenterol 1992; 87( I ):88-90.
  • 19. O!say CP, Kim DO, Pearl RK, et al. Diversion colitis in patients scheduled for colostomy closure. Dis Colon Rectum 1993;36(4); 366-367.
  • 20. Haas PA, Hass GP. A critical evaluation of the hartmann's procedure. Am Surg 1988;54(6):380-385.
  • 21. Komorowski RA. Histologic spectrum of diversion colitis. Am J Surg Pathol 1990;14(6):548-554.
  • 22. Haque S, Eisen RS, West AB. The morphologic features of diversion colitis. Human Pathol 1993;24(2): 211-219.
  • 23. Yeong ML, Bethwaite PB, Prasad J, et al. Lymphoid follicular hyperplasia- A distinctive feature of diversion colitis. Histopathology 1991;19:55-61.
  • 24. Roe AM, Warren BF, Brodribb AJM, et al. Diversion colitis and involution of the defunctioned anorectum. Gut 1993;34(3): 382-385.
  • 25. Korelitz BI, Cheskin LJ, Sohn N, et al. The fate of the rectal segment after diversion of the fecal stream in crohn's diseases: Its implications for surgical management. J Clin Gastroenterol1985;7(1):37-43.
  • 26. Lechner GL, Frank W; Jantsch H, et al. Lymphoid follicular hyperplasia in excluded colonic segments: A radiologic sign of diversion colitis. Radiology 1990;176(1):135-136.
  • 27. Neut C, Colombel JF, Guillemot F, et al. Impaired bacterial flora in human excluded colon. Gut 1989;30(8): 1.094-1.098.
  • 28. Korelitz BI, Cheskin LJ, Sohn N, et al. Proctitis after fecal diversion in crohn 's disease and its elimination with reanastomosis: implications for surgical management. Gastroenterology 1984;87(3):710-713.
  • 29. Surawicz CM, Belic L. Rectal biopsy helps to distinguish acute self-limited colitis from idiopathic inflammatory bowel disease. Gastroenterology 1984;86(1): 104-113.
  • 30. Geraghty JM, Talbot IC. Diversion colitis: histological features in the colon and rectum after defunctioning colostomy. Gut 1991 ;32 (9):1.020-1.023.
  • 31. Roediger WEW. The starved colon. Diminished mucosal nutrition, diminished absorption, and colitis. Dis Colon Rectum 1990; 33( I O): 858-862.
  • 32. Roediger WEW, Nance S. Metabolic induction of experimental ulcerative colitis by inhibition of fatty acid oxidation. Br J Exp Pathol 1986; 67(6):773-782.
  • 33. Lu ES, Lin T, Harms BL, et al. A severe case of diversion colitis with large ulcerations. Am J Gastroenterol 1995;90(9);1.508-1510.
  • 34. Haque S, West AB. Editorial: Diversion colitis- 20 years a-growing. J Cl Gastroenterol 1992;15(4):281-283.
  • 35. Guillemot F, Colombel JF, Neut C, et al. Treatment of diversion colitis by short-chain fatty acids. Dis  Colon  Rectum 1991 ;34 (10): 861-864.
  • Endereço para correspondência:
    Dr. Francisco Edilson Leite Pinto Júnior
    Av. Brigadeiro Gomes Ribeiro, 1025
    59056-520 - Natal-RN
    E-mail:

    • Datas de Publicação

    • Publicação nesta coleção
      26 Jan 2010
    • Data do Fascículo
      Jun 1999

    Histórico

    • Recebido
      23 Nov 1998
    • Aceito
      19 Abr 1999
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