Stricture and pouchitis after ileal pouch-anal anastomosis

QSTQMY CARE SECTION EDITOR: Kathy Cafitri Brown, RN, MN, CETN

Stricture and Pouchitis After Ileal Pouch-Anal Anastomosis Therese Jacobson, RN, MSN, C E T N

Ileal pouch-anal anastomosis is a surgical procedure used for the treatment of people with chronic ulcerative colitis and familial adenomatous polyposis. The surgery is intended to preserve anal sphincter function, but it carries a risk for certain complications, including pouchitis and anastomotic stricture. The purpose of this article is to review the clinical manifestations, causes, and treatment of anastomotic stricture and pouchitis after ileal pouchanal anastomosis. (J WOCN 1997;24:295-301)

he ileal p o u c h - a n a l a n a s t o m o s i s (IPAA) procedure was initially described by Parks and Nicholls in 1978. I When this procedure is performed, the colon and proximal rectum are removed, and the mucosa is stripped from the distal rectum and proximal anal canal. 2 Some surgeons perform a mucosectomy, whereas others p u r p o s e l y avoid this procedure. Those surgeons who avoid performing a mucosectomy do so because they believe that continence preservation is enhanced when the mucosa is left intact; those who do perform the procedure believe that the threat of cancer developing in the remaining mucosa outweighs any benefit to continence. 3 After resection of the colon and proximal rectum, a length of terminal ileum is reconstructed into an ileal pouch. 4 Construction of a J-shaped ileal pouch requires a 30- to 40-cm segment of ileum. As an alternative, anS-shaped ileal pouch can be constructed that requires 36 to 45 cm of bowel, or a W-shaped pouch may be created that requires 40 to 54 cm of ileum? The method of performing the anastomosis varies: some surgeons hand sew the pouch at the dentate line, whereas others staple at the dentate line, or staple above the anal columns. 6 In most patients, a temporary ileostomy is created.

T

Complications of the IPAA The IPAA p r o c e d u r e has a r e p o r t e d overall morbidity rate of 39% to 58% from the time of surgery to the twelfth postoperative year. 5,7-~°When morbidity is differentiated according to the patient's diagnosis, the complication rate is reported to be 6% to 28% for patients with familial adenomatous polyposis (FAP), and 60% to 79% for those with chronic ulcerative colitis (CUC). 9,11These complications include sepsis, obstruction, fistula, sexual problems, anastomotic stricture, and pouchitis (Table). 1,s,7-1°,12This article will focus on anastomotic stricture and pouchitis after IPAA.

Stricture Strictures may form at the ileoanal anastomosis after surgery. These areas of narrowing v a r y - - f r o m a weblike stricture that is easily dilated with a gloved finger, ~,1°to a recurring stenosis that requires repeated dilations under general anesthesia to relieve obstruction, is Reports of the incidence of strictures that occur within 12 years of surgery vary from 9% to 100%. 1'7'1° A lack of uniformity in defining stricture and differences in exclusion criteria may account for this wide

Ms. Jacobson is an Enterostomal Therapy Nurse, Mayo Medical Center, Rochester Methodist Hospital, Rochester. Reprint requests: Therese Jacobson, RN, MSN, CETN,Mayo Medical Center, Rochester Methodist Hospital, 201 West Center, Rochester, MN 55902.

Cop yright © 1997by the Wound, Ostomy and Continence Nurses Society. I071-5754/97/$5.00 + 0

21/I/86207

295

JWOCN 296 Jacobson

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/ Anus

I~igure !. Anal dilation technique. (Illustration by permission of Mayo Foundation.)

Multiple factors predispose the individual with IPAA to stricture

formation.

variation in reported incidence. In particular, mild strictures that respond to gentle digital dilation have been reported as occurring in almost all patients. 1,~° Multiple factors predispose the individual with an IPAA to stricture formation. Patients with CUC have been observed to experience stricture more frequently than those with FAP. 11 Smalldiameter stapling devices, pelvic sepsis, use of a temporary ileostomy, and construction of aW-shaped pouch have been associated with an increased risk of stricture formation. ~3 Ischemia, anastomotic tension, and secondary healing of a partial separation of the anastomosis also have been suggested as possible contributing factors. 14 Keighley and colleagues 8 reported that anastomotic strictures occurred in 8% of a group of 99 patients who had a stapled anastomosis, as compared with 22% of a group of 69 patients with handsewn anastomoses. Pena and associates 1 p o s t u l a t e d that the rectal mucosectomy may increase the occurrence of anastomotic stricture. The risk of severe strictures increases when the ileal pouch retracts under anastomotic tension, TM or when the rectal mucosa is resected above the dentate line. 13Strictures occurring after anastomotic dehis-

cence and sepsis also have been found to be long and dense, and to require multiple dilations. ~3 Anastomotic strictures are typically diagnosed when they produce obstructive symptoms, including straining, anal pain, the passage of frequent watery stools, urgency, abdominal cramps, sensation of incomplete emptying, and leakage. ~,13 Galandiuk and colleagues 11reported that more than half of the anastomotic strictures requiring dilation under anesthesia were not diagnosed until after ileostomy closure, and 29% of patients with anatomic evidence of outlet obstruction remained asymptomatic. Minor strictures can be gently dilated with a gloved finger. ~5 Milder strictures typically resolve after one to two dilations. ~3In contrast, between 10%~and 56%15 of the patients with more severe anastomotic strictures require more vigorous dilation. 15After an initial dilation under anesthesia, the patient can be taught to continue dilation at home (Figure 1).16The patient is taught to gently insert a lubricated bougie dilator into the anus through the anastomosis, and to hold the dilator in place for 10 seconds. 16The size of the dilator, the frequency of dilation, and the duration should be determined by the physician. 16When strictures continue to recur, even after vigorous and repeated dilations, surgical resection may become necessary. In one series of 463 patients, anastomotic stricture developed in 43, and three experienced pouch failure due to persistent obstruction, diarrhea, and incontinence. ~sAll three required a permanent ileostomy, and two underwent ex~ cision of the pouch. 15 The risk of recurrent stricture formation after IPAA is significant. Once a patient has had a stricture dilated under anesthesia, the possibility of recurrent stricture has been reported to be 52%21 Dilation is the current medical treatment for anastomotic stricture. The WOC nurse should provide patient education regarding symptoms of stricture and the rationale and technique for anal dilation. Patients can be taught to perform self-dilation. Initially, the patient is given a schedule of dilations prescribed by the physician. However, the interval between dilations can gradually increase as symptoms decrease. In addition to teaching patients to adjust their dilation schedule, education concerning the symp-

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Volume 24, Number 6

toms of stricture formation allows early identification of a stricture that is not responding to home dilation and requires more invasive management. Further research is needed to refine the management of anastomotic stricture after 1PAA. Pertinent questions in the area of WOC nursing management include: (1) What are the current dilation techniques used by patients at home? (2) What is the optimal frequency and duration of dilation? (3) Does the technique of selfdilation prevent or reduce the need for more invasive dilation in the clinic or hospital setting? (4) Do patients comply with home dilation regimens? In addition to these questions, research is needed to define other interventions designed to increase the interval between surgical dilLations, and to assess the impact of symptomatic anastomotic stricture on the patient's overall satisfaction with the IPAA and other aspects of his or her quality of life.

Pouchitis Pouchitis is a nonspecific inflammation of the reservoir.~° For some, pouchitis occurs as an isolated or recurrent event, but for others it is a chronic condition. ~The typical symptoms of pouchitis include abdominal cramping, urgency, bleeding, increase in number of stools, incontinence, fever, malaise, and extraintestinal manifestations of inflammatory bowel disease.l,~7-~9Because there are no definitive endoscopic or histologic criteria for pouchitis, its diagnosis is typically based on the presence of suggestive clinical symptoms. 19In an effort to provide objective criteria for the diagnosis of pouchitis, Sandborn and associates 2° have developed the Pouchitis Disease Activity Index (PDAI). The PDAI consist~s of three categories of findings: clinical, endoscopic, and histologic. The clinical signs of pouchitis are stool frequency, rectal bleeding, urgency--with abdominal cramping, and fever. 2° The endoscopic findings are edema, granularity, friability, loss of vascular pattern, mucus exudate, and ulceration. 2° The histologic findings are polymorphonucleocyte infiltration and ulceration. 2° In a study of 25 patients, the investigators compared the PDAI to other pouchitis scoring systems and concluded that the PDAI had greater sensitivity. 2°With use of the PDAI rating scale, a score of 7 or more is indicative of pouchitis. 2°

j

/

Ileal pouch-anal

reservoir

.

/

"

297

;,

•

-:~

/

/ Catheter -tip syringe

Figure 2. Irrigation of reservoir. (Illustration by permission of Mayo Foundation.)

Other methods to diagnose pouchitis are being investigated. In one study, higher concentrations of fecal alphal-antitrypsin , an indicator of protein leaking into the intestine, reliably identified active pouchitisY The leakage of the alpha 1- antitrypsin protein into the intestine was postulated to be the result of histologic changes that occur with pouchitis. 2IIn another study, perinuclear antineutrophil cytoplasmic antibodies were found in 100% of a group of 19 patients with chronic pouchitis. 22The presence of the antibodies was significantly higher in patients with chronic pouchitis when compared with 33 patients without pouchitis or those with ileostomies. = Nonetheless, the value of perinuclear antineutrophil cytoplasmic antibodies in predicting the possibility of developing chronic pouchitis requires further study before it gains widespread clinical use. 22 Based on current methods of diagnosis, pouchitis is reported to occur in 15% to 34% of patients after IPAA. 5,7q°,I2Symptoms have been reported as early as 2 days after ileostomy closure, and as late as 95 months after surgery. ~9The incidence of pouchitis is significantly higher among patients with CUC as compared with those with FAp4,19; and in two series, the condition was completely absent a m o n g patients with an IPAA because of FAP. 5,9 The risk of pouchitis is even higher when CUC coexists with primary sclerosing cholangitis. 23Additionally, the incidence of pouchitis is higher in patients who exhibit extraintestinal manifestations of IBD such as arthritis and skin and eye changes. I9 The risk of pouchitis developing increases

Pouchitis is a nonspecific inflammation of the reservoir.

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Jacobson

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Table. IPAA o u t c o m e s

Diagnosis (%) Authors

Type of pouch (%)

n

CUC

FAP

J

Marcello et al. 19937 Keighley et al. 1993~

460 168

83 61

9 15

94

de Silva et al. 1991s

61

92

7

38

24

McMullen et a1.19919

73

66

34

52

48

Grotz and Pember~on 1993l°

1400

88

Gemlo et al. 199212

196

W

Mortality rate (%) 0.4 0

38

0 0 0.14

90

0.4

and Penna et al, 19911

over time. 24Penna and associates23reported that the prevalence of pouchitis among a group of 1043 patients was 15% at I year, 36% at 5 years, and 46% at 10 years. Once a patient experiences a single episode of pouchitis, the risk of recurrence is approximately 61%. 6 The cause of pouchitis remains unknown. 1,4,174sFecal stasis, CUC recurrence, Crohn's disease, and ischemia of the pouch mucosa have been suggested as possible causes, a4Because stool is stored in the ileal pouch, bacterial overgrowth may occur. The prompt relief of symptoms of pouchitis after antibiotic therapy lends further support to this hypothesis, ls,24To further evaluate this theory, the stool of subjects with IPAA was compared with samples from subjects with a Brooke ileostomy, and the ratio of anaerobic to aerobic bacteria was found to be higher among the IPAA groupY However, patients with and without pouchitis were not found to have significant differences inbacterial concentrations, asInadequate emptying of the pouch caused by stricture also has been postulated as a contributing factor to pouchitis. ~ In one study of 102 patients, 39 had a stricture, 17 had pouchitis; however, only 4 patients with pouchitis also had a stricture. ~3There was no significant difference in incidence of pouchitis between patients with and without stricture. 13 The predisposition to ulcerative colitis and the transformation of ileal mucosa to a more colonlike mucosa also have been postulated as contributing factors

in the development of pouchitis. 24However, colonic metaplasia has been noted in patients with and without pouchitis76 The higher incidence of pouchitis in patients with CUC compared with those with FAP raises the question whether pouchitis represents a recurrence of CUC.24Increased cytokine levels have been reported in pouchitis and active CUC77 Nonetheless, it is possible that pouchitis represents distinctive clinical conditions, and that these differences may account for differences in the clinical manifestations of recurrent versus chronic cases. 17 Still other theories regarding the cause of pouchitis have been postulated. Levels of short-chain fatty acids (SCFA) have been studied to determine possible changes in bacterial fermentation during pouchitis. 26 In one study, SCFA were similar for patients with and without pouchitisY However, other investigators have reported that SCFA concentrations are lower in the stool of patients with pouchitis. 26'2s'29 Oxygen free radical production by xanthine oxidase occurs when the mucosa becomes ischemic; and allopurinol, a xanthine oxidase inhibitor, was found to prevent or alleviate the symptoms of pouchitis in 50% of a group of 22 patients, leading to speculation that the production of oxygen free radicals in the pouch may account for the subsequent inflammation and associated symptoms.3° Dehydroxylation of bile acids caused by bacterial overgrowth may damage the mucosa of the ileal pouch and lead to pouchitis. 31The increased incidence

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299

Complications (%) Morbidity (%)

Sepsis

Obstruction

Fistula

58

5

20

6

9

18

41

12

18

16

15

18

51

20

25

10

16

21

5

47

5

16

3

15

1

39

6

17

5

Mild:

31

4 Male 7 Female

6

almost all Mild: almost all

34

4

30

of pouchitis in patients with both CUC and primary sclerosing cholangitis suggests a link between the inflammatory changes in the pouch and those in the liver and biliary system. 23 Surgical technique also may act as a risk factor for pouchitis. In one study of 88 patients, pouchitis occurred more often in patients with handsewn anastomoses when compared with those with stapled anastomoses. 32The one difference cited by the authors was in the vascular manipulation necessary to lengthen the ileum to facilitate a tension-free anastomosis with the handsewn technique. However, the significance to the incidence of pouchitis remains unclear. Additionally, incidence of pouchitis was 31.8% for patients with an anastomosis less than 0.5 cm from the dentate line, compared with 0% for an anastomosis more than 0.5 cm from the dentate line. 32 Treatment options for pouchitis include antibiotics, a n t i - i n f l a m m a t o r y drugs, i m m u n o s u p p r e s s i v e drugs, nutritional agents--such as SCFA enemas or glutamine suppositories, oxygen free radical inhibition with use of allopurinol, and surgery. 24A 7- to 10-day course of metronidazole is the most commonly prescribed treatment for pouchitis. 24 Generally, patients report an improvement within I to 2 days. Because chron;Lc pouchitis may be related to incomplete emptying of the reservoir with resulting fecal stasis, some patients may be taught to intermittently intubate and irrigate the reservoir (Figure 2). 33`34One tech-

Stricture

Pouchitis

nique involves inserting a lubricated, size 30 French catheter into the anus about 3 inches, slowly instilling 60 to 120 ml of water, removing the catheter, and having the patient expel the water. 34 Surgical excision of the ileal pouch may be considered for those with intractable pouchitis. In one series, 2% of patients with pouchitis ultimately required pouch excision because of intractable and debilitating symptoms. 24 Further research is needed to refine the nursing m a n a g e m e n t of pouchitis after IPAA. Currently, the WOC nurse provides education regarding s y m p t o m identification and irrigation technique. However, there is a dearth of information regarding optimal irrigation procedures and the impact of irrigation.

SUMMARY Stricture and pouchitis are two of the complications that patients may experience after IPAA. Medical research has focused on the cause of these complications, treatment options, evaluation of risk factors including surgical technique, and scoring systems to standardize diagnosis. It is clear that our knowledge of anastomotic stricture and pouchitis is incomplete. Our patients often ask questions such as "Will I get pouchitis?" and "Will I ever be rid of this stricture?" To answer these questions WOC nurses must not only review current information, we also m u s t s y s t e m a t i c a l l y s t u d y these complications to further clarify options

Sexual problems 1.2 Male 8.6 Female 4 Male 8 Female

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to manage these significant complications. REFERENCES 1. Nicholls RJ, Parks AG. Cited by: Penna JP, Gemlo BT, Rothenberger DA. Ileal pouch-anal anastomosis. Bailliere's Clin Gastroenterol 1992;6:113-28. 2. Lohmuller JL, Pemberton JH, Dozois RR, Ilstrup D, van Heerclen J. Pouchitis and extraintestinal manifestations of inflammatory bowel disease after ileal pouch-anal anastomosis. Ann Surg 1990;211:622-9. 3. Dozois RR, Kelly KA, Welling DR, Gordon H, Beart RW Jr, Wolff BG, et al. Ileal pouch-anal anastomosis: comparison of results in familial adenomatous polyposis and chronic ulcerative colitis. Ann Surg 1989;210:268-73. 4. Kelly K. Anal sphincter-saving operations for chronic ulcerative colitis. Am J Surg 1992;163:5-11. 5. de Silva HJ, de Angelis CP, Soper N, Kettlewell MGW, Modensen NJ, Jewell DP. Clinical and functional outcome after restorative proctocolectomy. Br J Surg 1991;78:1039-44. 6. Pemberton JH. Surgical approaches to proctocolectomy for inflammatory bowel disease. In: Phillips SF, Pemberton JH, Shorter RG, editors. The large intestine: physiology, pathophysiology, and disease. New York: Raven Press; 1991.p.629-55. 7. Marcello PW, Roberts PL, Schoet-z DJ, Caller JA, Murray JJ, Veidenheimer MC. Long-term results of the ileoanal procedure. Arch Surg 1993;128:500-4. 8. Keighley MR, Grobler S, Bain I. An audit of restorative proctocolectomy. Gut 1993;34:680-4. 9. McMullen K, Hicks TC, Ray JE, Gathright JB, Timmcke AE. Complications associated with ileal pouch-anal anastomosis. World J Surg 1991;15:763-7. 10. Grotz RL, Pembedon JH. The ileal pouch operation for ulcerative colitis. Surg Clin North Am 1993;73:909-32. 11. Galandiuk S, Scott NA, Dozois RR, Kelly KA, Ilstrup DM, Bead RW Jr, et al. Ileal pouch-anal anastomosis: reoperation for pouch-related complications. Ann Surg 1990;212:446-54. 12. Gemlo BT, Wang WD, Rothenberger DA, Goldberg SM. Ileal pouch-anal anastomosis: patterns of failure. Arch Surg 1992;127:784-7. 13. Lewis WG, Kuzu A, Sagar PM, Holdsworth PJ, Johnston D. Stricture at the pouch-anal anastomosis after restorative proctocolectomy. Dis Colon Rectum 1994;37:120-5. 14. Dozois RR. In discussion: Galandiuk S, Scoff NA, Dozois RR, Kelly KA, Ilstrup DM, Bead RW Jr. et al. ileal pouch-anal anastomosis: reoperation for pouch-related complications. Ann Surg 1990;212:446-54. 15. Tsao JI, Galandiuk S, Pemberton JH. Pouchogram: predictor of clinical outcome following ileal pouch-anal anastomosis. Dis Colon Rectum 1992;35:547-51. 16. Mayo Foundation. Anal dilation following ileal pouch-anal anastomosis or cola-anal

anastomosis. Rochester (MN):Mayo Clinic; 1994. 17. Rauh SM, Schoetz DJ Jr, Roberts PL, Murray JJ, Caller JA, Veidenheimer MC. Pouchitis--is it a wastebasket diagnosis? Dis Colon Rectum 1991;34;685-9. 18. Mignon M, Steffler C, Phillips SF. Pouchitis--a poorly understood entity. Dis Colon Rectum 1995;38:100-3. 19. Fozard BJ, Pemberton JH. Results of pouch surgery after ileo-anal anastomosis: the implications of pouchitis. World J Surg 1992;16:8804. 20. Sandborn WJ, Tremaine WJ, Baffs KP, Pemberton JH, Phillips SF. Pouchitis after ileal pouch-anal anastomosis: a pouchitis disease activity index. Mayo Clin Proc 1994;69:409-15. 21. Boerr LA, Sambuelli AM, Sugai E, Graziano A, Valero J, Kogan Z, et al. Faecal alpha~-antitrypsin concentration in the diagnosis and management of patients with pouchitis. Eur J Gastroenterol Hepato11995;7:129-33. 22. Sandborn WJ, Landers C J, Tremaine WJ, Tartan SR. Antineutrophil cytoplasmic antibody correlates with chronic pouchitis after ileal pouch-anal anastomosis. Am J Gastoenterol 1995;90:740-7. 23. Penna C, Dozois RR, LaRusso NF, Tremaine WJ. Pouchitis after ileal pouch anal anastomosis for chronic ulcerative colitis occurs with increased frequency in patients with associated primary sclerosing cholangitis (abstract). Gastroenterology 1994; 106:A751. 24. Sandborn WJ. Pouchitis following ileal pouchanal anastomosis: definition, pathogenesis, and treatment. Gastroenterology 1994;107:1856-60. 25. Sandborn WJ, Tremaine WJ, Barfs KP, Pemberton JH, Rossi SS, Hofmann AF, et al. Fecal bile acids, short-chain taffy acids, and bacteria after ileal pouch-anal anastomosis do not differ in patients with pouchitis. Dig Dis Sci 1995;40:1474-83. 26. Clausen MR, Tvede M, Mortensen PB. Short-chain fatty acids in pouch contents from patients with and without pouchitis after ileal pouch-anal anastomosis. Gastroenterology 1992;103:1144-53. 27. Patel RT, Bain I, Youngs D, Keighley MR. Cytokine production in pouchitis is similar to that in ulcerative colitis. Dis Colon Rectum 1995;38:831-7. 28. Sagar PM, Taylor BA, Godwin P, Holdsworth PJ, Johnston D, Lewis W, et al. Acute pouchitis and deficiencies of fuel. Dis Colon Rectum 1995;38:488-93. 29. Wischmeyer P, Pemberton JH, Phillips SF. Chronic pouchitis after ileal pouch-anal anastomosis: responses to butyrate and glutamine suppositories in a pilot study. Mayo Clin Proc 1993;68:978-81. 30. Levin KE, Pemberton JH, Phillips SF,Zinsmeister AR, Pezim ME. Role of oxygen free radicals in the etiology of pouchitis. Dis Colon Rectum 1992;35:452-6. 31. Salemans JM, Nagengast FM, Lubbers EJC, Kuijpers JH. Postoperative and long-term results of ileal pouch-anal anastomosis for ulcerative

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colitis and familial polyposis coll. Dig Dis Sci 1992;37:1882-9. 32. Gozzetti G, Poggioli G. Marchelti F, Laureti S. Grazi GL Mastrorilli M, et al. Functional outcome in handsewn versus stapled ileal pouch-anal anastomosis. Am J Surg 1994;168:325-9. 33. Davis C, Alexander F, Lavery I, Fazio MW.

301

Resultsof mucosal proctectomy versusextrarectal dissection for ulcerative colitis and familial polyposis in children and young adults. J Pediatr Surg 1994;29:305-9. 34. Mayo Foundation. Irrigation of reservoir following ileal pouch-anal anastomosis surgery. Rochester (MN):Mayo Clinic; 1994.

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