Understanding the Effects of Colostomy-induced Alterations on Cutaneous Immunity
- Thu, 7/16/09 - 11:48am
- 0 Comments
- 3203 reads
Abstract: Objective. This study describes the immunological response in the dermal layer of the peri-colostomic region, and identifies and quantifies the cellular elements present. Methods. Forty-one patients with colostomies present for more than 8 weeks were included. Thirty-one patients were men (75.6%) and 10 were women (24.4%) with an average age of 49.9 years. Thirty-four patients (82.9%) were classified as surgical risk class I and 7 patients (17.1%) were classified as class II. The data were analyzed statistically using the Mann-Whitney, Kruskal-Wallis, and Dunn tests using 0.05 or 5%. Results. Analysis of the immuno-cellular response regarding the time of permanence of the colostomy showed a significant frequency of T lymphocytes (pan T-CD3) in all the time periods in a significantly superior number (P < 0.001) than the B lymphocytes (CD20) and the T lymphocytes-natural killer (CD57). T-helper cells (CD4) were present in larger numbers in the first three periods. Conclusion. The presence of a colostomy for more than 8 weeks promotes the development of a chronic inflammation and an immuno-cellular response in the dermal layer of the peri-colostomy region. However, its intensity did not demonstrate a statistically significant difference based on time of colostomy existence. The immuno-cellular response in the peri-colostomic dermal area is composed of a major number of T lymphocytes (pan T-CD3) and T lymphocytes-helper (CD4), and is more numerous between the 16th and 20th weeks, whereas, less cellular activity was noted between the 30th and 50th weeks.
Address correspondence to:
Prof. Valdemir J. Salles, MD
University of Taubaté
José Bonani 199
Taubaté, São Paulo
Brazil 12031-260
Phone: 55 12 36316061
E-mail: valiris@vivax.com.br
The rate of complications that occur at a colostomy site range from 15% to 34%1 and therefore, the massive presence of bacteria secondary to local exposure to the intestinal content may lead to cellulitis, abscess, ulceration, and fistula.1–4 Reported rates of septic complications of the pericolostomic region range from 2.2% to 30%.4–9
A morpho-functional difference is present between the skin tissue of the abdominal wall and that of the anal region.10 The skin of the anal canal region has specific traits that allow frequent contact with the enteric bacterial content with little or no clinical effect. Nevertheless, this condition occurring in the abdominal wall in the presence of a colostomy or an entero-cutaneous fistula is still not completely clarified, since there are no studies demonstrating the changes in the local immunological system determined by the ectopic bacterial colonization.
An initial prospective study11 was conducted in order to determine the prevalence and type of bacteria in the peristomal skin of patients with a colostomy. It demonstrated that the most frequently cultured bacteria were Escherichia coli (91.2%), followed by Bacteroides spp and Peptococcus spp (38.2%), Klebsiella spp (32.3%), and Bacteroides fragilis (29.4%). When the frequency of cultured bacteria was compared to the duration of the colostomy, E coli was present during all the study periods, while Peptococcus spp increased over time; Bacteroides fragilis and Klebsiella spp were not found in the period after 20 weeks.11
The objective of the present study was to characterize the immunological response in the dermal layer of the pericolostomic region by quantifying the role of T- and B-lymphocytes and macrophages in the pericolostomic immunocompetent tissue.
1. Park JJ, Del Pino A, Orsay CP, et al. Stoma complications: the Cook County Hospital experience. Dis Colon Rectum. 1999;42(12):1575–1580.
2. Smith LE, Geraldine, MH. Manejo de las ostomías. In: Zuidema GD, ed. Cirugía del aparato digestivo IV. 3rd ed. Buenos Aires, Argentina: Editora Panamericana; 1993:200–214.
3. Londono-Schimmer EE, Leong AP, Phillips RK. Life table analysis of stomal complications following colostomy. Dis Colon Rectum. 1994;37(9):916–920.
4. Nour S, Beck J, Stringer MD. Colostomy complications: infants and children. Ann R Coll Surg Engl. 1996;78(6):526–530.
5. Leenen LP, Kuypers JH. Some factors influencing the outcome of stoma surgery. Dis Colon Rectum. 1989;32(6):500–504.
6. Hoffman MS, Barton DP, Gates J, et al. Complications of colostomy performed on gynecologic cancer patients. Gynecol Oncol. 1992;44(3):231–234.
7. Cubertafond P, Gainant A, Barbier J, Coste G. Colostomies: indications and complications. Apropos of an analysis of 1142 cases [in French]. Chirurgie. 1985;111(4):331–341.
8. Bartlett SP, Burton RC. Effects of prophylactic antibiotics on wound infection after elective colon and rectal surgery:1960 to 1980. Am J Surg. 1983;145(2):300–309.
9. Simon GL, Gorbach SL. The human intestinal microflora. Dig Dis Sci. 1986;31(9 Suppl):147S–162S.
10. Stoutenbeek CP, van Saene HK, Miranda DR, Zandstra DF. The effect of selective decontamination of the digestive tract on colonization and infection rate in multiple trauma patients. Intensive Care Med. 1984;10(4):185–192.
11. Salles VJA, Saad SS, Matos D. Chronic wound infection: bacterial colonization in the dermal pericolostomic region. WOUNDS. 2008;20(4):107–109.
12. Bouillot JL, Aouad K. Traitement chirurgical des complications des colostomies. In: Encyclopedie Médico Chirurgicale. Techniques chirurgicales. Appareil digestif. Paris, France: Elsevier; 2002:2.
13. Pastore RL, Bigalli D, Azcoitia IF, Ciaponi GP, Bilenca OL, Griffero REH. Complicaciones de las colostomies. Rev Argent Cir. 1990;59:263–264.
14. Gervaz E, Dauge-Geffroy MD, Sobhani I, et al. Quantitative analysis of the immune cells in the anal mucosa. Pathol Res Pract. 1995;191(11):1067–1071.
15. Geller M. Current immunologic mechanisms in antigenic cutaneous presentation. Ann Acad Nac Med. 1994;154:234–235.
16. Zaitz C. Immunology of dermatophytosis [in Portuguese]. Ann Bras Dermatol. 1994;69(3):217–222.
17. Abbas AK, Lichtman AH, Pober JS, eds. Cellular and Molecular Immunology. 4th ed. Philadelphia, PA: W.B. Saunders; 2000.
18. Torre LF, Nicolai AP. Amikacin gel administration in the treatment of peristomal dermatitis. Drugs Exp Clin Res. 1998;24(3):153–157.
19. Salles VJA, Sarhan SS, Matos D. Bacteriologia da região dérmica em área peri-colostômica. Rev Bras Coloproct. 2004;24(4):345–353.
20. Wilhelm KP, Maibach HI. Factors predisposing to cutaneous irritation. Dermatol Clin. 1990;8(1):17–22.
21. Hachem JP, Crumrine D, Fluhr J, Brown BE, Feingold KR, Elias PM. pH directly regulates epidermal permeability barrier homeostasis, and stratum corneum integrity/cohesion. J Invest Dermatol. 2003;121(2):345–353.
22. Johnson FE. An improved technique for skin graft placement using a suction drain. Surg Gynecol Obstet.1984;159(6):584–585.
23. Demling RH, DeSanti L. Scar management strategies in wound care. Rehab Manag. 2001;14(6):26–30.
24. Sahl WJ Jr, Clever H. Cutaneous scars: Part II. Int J Dermatol. 1994;33(11):763–769.
25. Scharffetter K, Kulozik M, Stolz W, et al. Localization of collagen alpha 1(1) gene expression during wound healing by in situ hybridization. J Invest Dermatol. 1989;93(3):405–412.
26. Miles AA. The inflammatory response in relation to local infections. Surg Clin North Am. 1980;60(1):93–105.
27. Zitelli JA. Synthetic skin. Adv Dermatol. 1989;4:325–342.
28. Celada A, Nathan C. Macrophage activation revisited. Immunol Today. 1994;15(3):100–102.
29. Becknell B, Caligiuri MA. Interleukin-2, interleukin-15, and their roles in human natural killer cells. Adv Immunol. 2005;86:209–239.
30. Kirwan SE, Burshtyn DN. Regulation of natural killer cell activity. Curr Opin Immunol. 2007;19(1):46–54.
31. Madison KC. Barrier function of the skin: “la raison d’être” of the epidermis. J Invest Dermatol. 2003;121(2):231–241.
