Radiol Oncol 1993; 27 : 39-43. Letter to the editor Postirradiation intraabdominal adhesions Marko Snoj Department of Surgery, Institute of Oncology, Ljubljana, Slovenia Introduction Intraabdominal adhesions are most frequent cause of small bowel obstruction1 and female infertility.2 They can be localised in any part of the bowel, but most usually they are found in the small bowel.1 They occur most frequently after surgery in the abdominal cavity, seldom they are caused by peritoneal infection and even more rarely they follow irradiation of this 3 region. Various experiments have been conducted for intraabdominal adhesion prevention in the past, but none gave satisfactory result.4 Recently, two new, more physiologically oriented approaches were introduced. The first is based on local administration of recombinant tissue plasminogen activator5 and the second on the use of surface active material.6 In the present article we would like to discuss the problem of postirradiation intraabdominal adhesions in the light of the use of surface active materials. Postirradiation intraabdominal adhesions Chronic postirradiation enteritis is most often a disease of middle aged women treated by irradiation for gynecologic carcinoma.7 Less fre- Correspondence to: Marko Snoj MD, PhD, Institute of Oncology, Department of Surgery, Zaloska 2, 61105 Ljubljana, Slovenia. quently it is observed in older men treated for prostatic cancer8 and in younger men treated for malignant testicular tumors.9 The latent period between irradiation and appearance of the first symptoms of irradiation enteritis is very variable: it ranges form half a year to 31 years, being about 6 years on average.10 In the past, little attention was devoted to the problem of postirradiation adhesions. The bulk of the research on chronic postirradiation enteritis was centred on the mucosa or the bowel wall. Thus, chronic postirradiation enteritis was found to appear as a mucosal damage (ulcerations and fissures), or as a generalised fibrosis of the bowel wall with special emphasis on the submucous layer, and as a damage of the vessels resembling those at atherosclero-sis.10 The injury is frequently localised as jeju-nitis, ileitis or proctitis, but most often it is a combination of all previously mentioned localisations. It is expressed clinically as malabsorption, or bowel obstruction, which is mainly due to intraabdominal adhesions, or as bleeding on the stool. At operation, the surgeon is faced by a difficult situation. At the beginning of surgery, slow and meticulous adhesiolysis is done; afterwards, resection and anastomosis of the bowel are performed if necessary. After this first intervention there are frequently recurrences of adhesive ileus. In these cases, subsequent sur- 50 Snoj M gery is even more difficult than the first one and carries significant mortality. Therefore it would be highly warranted to prevent the recurrence of adhesive ileus. Recently, it was realised that the studying of bowel serosa is the key to the solution of the problem of adhesive obstruction after irradia-tion.3 Thus, it was observed in a rat model that intraabdominal adhesions began to from two months after abdominal irradiation with a single-dose of 13.5 - 17.5 Gy. They were associated with a concurrent serosal destruction. Postirradiation adhesions were even more expressed when there was inflammation present, or after a surgical procedure in this region.11 Surface active materials Surface active materials are present in the peritoneal fluid in a concentration from 11 to 25 mg/L. Its relative concentration is: 81 % phos-phatidylcholine, 5 % lysophosphatidylcholines, 6.5 % sphyngomyelines, 3.5 % phosphatidylino-sitols and 4 % phosphatidyletanolamines.12 It was postulated that phospholipid adheres to both parietal and visceral peritoneal surfaces and is held in place by the attraction of the positive charge of choline head to the negative charge of peritoneal surface. To the cavity long-chain fatty acids are presented and interacting with their counterparts from opposing side provide lubrication.12 We have found out in animal experiments that the surface active materials effectively prevent adhesions after surgery,6 adhesions after intestinal anastomosis13 and those after bacterial peritonitis. 14 Therefore they could be instilled in the peritoneal cavity after the adhesiolysis in postirradiation adhesive ileus. Postirradiation adhesions prevention by surface active materials Surface active materials efficiently prevent intraabdominal adhesion formation only when instilled intraperitoneal^, but not when applied intravenously.6 When applied intraperitoneal^, special attention should be paid to possible formation of intestinal anastomosis, since too high a dosis could lead to anastomotic dehis-cence and peritonitis.13 The next question applies to the appropriate timing of surface active material application. Thus, application after irradiation does not seem wise since only about 5 % of patients Jater develop chronic irradiation enteritis. It seems much more possible to use them after the adhesiolysis for adhesive obstruction. In this case they could be instilled intraperitoneally at the end of the operation. This would be in line with experimental evidence that single dose of surface active material at the end of operation is as efficient as three doses in three consecutive days.13 It seems that surface active materials could play an important role in postirradiation adhesion prevention. Therefore, they bring the new light of hope for patients with this grave and often fatal disease. References 1. Bizer LS, Leibling RW, Delany HM, Gliedman ML Small bowel obstruction: The role of nonoperative treatment in simple intestinal obstruction and predictive criteria for strangulation obstruction. Surgery 1981; 89: 407-13, 2. Holtz G. Prevention of postoperative adhesions. Rep Med 1980; 24: 141-45. 3. McBride WH, Mason KA, Davis C, Withers HR, Smathers JB. Adhesion formation in experimental chronic radiation enteropathy. Int J Rad Oncol Biol Phys 1989; 16: 737-43. 4. Ellis H. The causes and prevention of intestinal adhesions. Br J Surg 1982; 69: 241-3. 5. Menzies D, Ellis H. Intraabdominal adhesions and their prevention by topical tissue plasminogen activator. J Lab Clin Med 1989; 101: 921-9. 6. Ar'Rajab A, Ahren B, Rozga J, Bengmark S. Phosphatidylcholine prevents postoperative peritoneal adhesions. J Surg Res 1991; 50: 212-5. 7. De Cosse JJ, Rhodes RS, Wentz WB, et al. The natural history and management of radiation induced injury of the gastrointestinal tract. Ann Surg 1969; 170: 369-84. 8. Duggan FJ, Sanford EJ, Rohner TJ. Radiation enteritis following radiotherapy for prostatic carcinoma. Br J Urol 1975; 47: 441-4. Postirradiation intraabdominal adhesions .51 9. Roswit B, Malsky JJ, Reid CB. Severe radiation injuries of the stomach, small intestine, colon and rectum. Am J Roentgenol 1972; 114: 460-75. 10. Galland RB, Spencer J. Radiation enteritis. Edward Arnold 1990. 11. McBride WH, Mason K, Withers R, Davis C. Effect of interleukin 1, inflammation, and surgery on the incidence of adhesion formation after abdominal irradiation in mice. Cancer Res 1989; 49: 169-73. 12. Grahame GR, Torchia MG, Dankewich KA, Ferguson 1A. Surface activc material in peritoneal effluent of CAPD patients. Bull Periton Dial 198.5; 5: 109-11. 13. Snoj M, Ar'Rajab A, Arhen B, Bengmark S. Effect of phosphatidylcholine on postoperative adhesions after small bowel anastomosis in thc rat. Br J Surg 1992; 79: 427 9. 14. Snoj M, Ar'Rajab A, Arhen B, Larson K, Bengmark S. Phospholipase resistant phosphatidylcho-line reduces intraabdominal adhesions induced by bacterial peritonitis. Res Exp Med 1993 in press.