improved outcomes in colon and rectal surgery
12. Carter FM, McLoed, Cohen Z. Subtotal colectomy for ulcer-ative colitis: complications related to the rectal remnant. Dis Colon Rectum 1991; 34: 1005–9.
13. Karch LA, Bauer JJ, Gorfine SR et al. Subtotal colectomy with Hartmann’s pouch for inflammatory bowel disease.Dis Colon Rectum 1995; 38: 635–9.
14. Boushey RP, Marcello PW, Martel G et al. Laparoscopic total colectomy: an evolutionary experience. Dis Colon Rectum 2007; 50: 1512–19.
15. Eaden JA, Abrams K, Mayberry JF. The risk of colorectal cancer in ulcerative colitis: a meta-analysis. Gut 2001; 48: 526–35.
16. Hata K, Watanabe T, Kazama S et al. Earlier surveillance colonoscopy programme improves survival in patients with ulcerative colitis associated colorectal cancer: results of a 23-year surveillance programme in the Japanese population. Br J Cancer 2003; 89: 1232–6.
17. MpofuC,WatsonAJ,RhodesJM.Strategiesfordetectingcolon cancer and/or dysplasia in patients with inflammatory bowel disease. Cochrane Database Syst Rev 2004; 2: CD000279.
18. Bernstein CN, Shanahan F, Weinstein WM. Are we telling patients the truth about surveillance colonoscopy in ulcer-ative colitis? Lancet 1994; 343: 71–4.
19. Connell WR, Lennard-Jones JE, Williams CB et al. Factors affecting the outcome of endoscopic surveillance for cancer in ulcerative colitis. Gastroenterology 1994; 107: 934–44.
20. Befrits R, Ljung T, Jaramillo E et al. Low-grade dysplasia in extensive, long-standing inflammatory bowel disease: a fol-low-up study. Dis Colon Rectum 2002; 45: 615–20.
21. Gumaste V,Sachar DB,Greenstein AJ.Benign and malignant strictures in ulcerative colitis. Gut 1992; 33: 938–41.
22. Camilleri-Brennan J, Munro A, Steele FJ. Does an ileostomy pouch offer a better quality of life than a permanent ileos-tomy for patients with ulcerative colitis. J Gastrointest Surg 2003; 7: 814–9.
23. Carlsen E, Bergan A. Technical aspects and complications of end ileostomies.World J Surg 1995; 19: 632–5.
24. Berry AR, Campos RDE, Lee ECG. Perineal and pelvic mor-bidity following perimuscular excision of the rectum for inflammatory bowel disease. Br J Surg 1986; 73: 675–7.
25. Rivadeneira DE, Schoetz DJ, Marcello PW et al. Vacuum-assisted closure of complex wounds of the perineum; a new paradigm in perineal wound care (abstract). Dis Colon Rectum 2003; 46:A67.
26. Dozois E.Proctocolectomy and Brooke ileostomy for chronic ulcerative colitis. Clin Colon Rectal Surg 2004; 17: 65–70.
27. Wickland M, Jansson I, Asztely M et al. Gynaecological problems related to anatomical changes after conventional proctocolectomy and ileostomy. Int J Colorect Dis 1990; 5: 49–52.
28. Camillari-Brennan J,Steele RJ.Objective assessment of qual-ity of life following panproctocolectomy and ileostomy for ulcerative colitis.Ann R Coll Surg 2001; 83(5): 321–4.
29. Pemberton JH, Phillips SF, Ready RR et al. Quality of life after Brooke ileostomy and ileal pouch-anal anastomosis for chronic ulcerataive colitis. Comparison of performance sta-tus.Ann Surg 1989; 209: 620–8.
30. Kock NG. Intra-abdominal “reservoir” in patients with per-manent ileostomy. Preliminary observations on a procedure resulting in fecal “continence”in five ileostomy patients.Arch Surg 1969; 99: 223–31.
31. Nessar G, Fazio VW, Tekkis P et al. Long-term outcome and quality of life after continent ileostomy. Dis Colon Rectum 2006; 49: 336–44.
32. Castillo E, Thomassie LM, Whitlow CB et al. Continent ileostomy: current experience. Dis Colon Rectum 2005; 48: 1263–8.
33. Beck DE. Clinical aspects of continent ileostomy. Clinics in colon and rectal surgery 2004; 17: 57–63.
34. Kaiser AM, Stein JP, Beart RW Jr. T-pouch: a new valve design for a continent ileostomy. Dis Colon Rectum 2002; 45: 411–5.
35. Fazio VS, Church JM. Complications and function of the continent ileostomy at the Cleveland Clinic. World J Surg 1988; 12: 148–54.
36. Lepisto AH,Jarvinen HJ.Durability of Kock continent ileos-tomy. Dis Colon Rectum 2003; 46: 925–8.
37. Pastore RLO,Wolff BG,Hodge D.Total abdominal colectomy and ileorectal anastomosis for inflammatory bowel disease. Dis Colon rectum 1997; 40: 1455–64.
38. Elton C, Makin G, Hitos K et al. Mortality, morbidity and functional outcome after ileorectal anastomosis. Br J Surg 2003; 90: 59–65.
39. Khubchandani IT, Sandfort MR, Rosen L et al. Current sta-tus of ileorectal anastomosis for inflammatory bowel disease. Dis Colon rectum 1989; 32: 400–3.
40. Lofberg R,Leijonmarck CE,Bronstrom O.Mucosal dysplasia and DNA content in ulcerative colitis patients with ileorectal anastomosis.Follow-up study in a definite patient group.Dis Colon Rectum 1991; 34: 566–71.
41. Gruner OP, FLatmark A, Naas R et al. Ileorectal anasto-mosis in ulcerative colitis. Results in 57 patients. Scand J Gastroenterol 1975; 10: 641–6.
42. Paoluzi OA, Dipaolo MC, Ricci F et al. Ileo-rectal anasto-mosis in ulcerative colitis: results of a long-term follow-up study. Ital J Gastroenertol 1994; 26: 392–7.
43. Marcello PW, Milsom JW, Wong SK et al. Laparoscopic restorative proctocolectomy: case-matched comparative study with open restorative proctocolectomy. Dis Colon Rectum 2000; 43: 604–8.
44. Tilney HS, Lovegrove RE, Heriot AG et al. Comparison of short-term outcomes of laparoscopic vs.open approaches to ileal pouch surgery. Int J Colorectal Dis 2007; 22: 531–42.
45. Larson DW, Davies MA, Dozois EJ et al. Sexual function, body image and quality of life after laparoscopic and open ileal pouch-anal anastomosis. Dis Colon Rectum 2007; 51: 392–6.
46. Browning SM,Nivatvongs S.Intraoperative abandonment of ileal pouch to anal anastomosis-the Mayo Clinic experience. J Am Coll Surg 1998; 186: 441–6.
47. Smith L, Friend WG, Medwell SJ. The superior mesenteric artery. The critical factor in the pouch pull-through proce-dure. Dis Colon Rectum 1984; 27: 741–4.
surgery for ulcerative colitis
48. Burnstein MJ, Schoetz DJ, Coller JA, Veidenheimer MC. Technique of mesenteric lengthening in ileal reservoir-anal anastomosis. Dis Colon Rectum 1987; 30: 863–6.
49. Metcalf DR, Nivatvongs S, Sullivan TM et al. A technique of extending small-bowel mesentery for ileal pouch-anal anasto-mosis: report of a case.Dis Colon Rectum 2008; 51(3): 363–4.
50. Hueting WE,Buskens E,Tweel IVD et al.Results and compli-cations after ileal pouch anal anastomosis:a meta-analysis of 43 observational studies comprising 9,317 patients.Dig Surg 2005; 22: 69–79.
51. Bullard KM, Madoff RD, Gemlo BT. Is ileoanal pouch func-tion stable with time/ Results of a prospective audit. Dis Colon Rectum 2002; 45(3): 299–304.
52. Cornish JA,tan E,Teare J,Teoh TG et al.The effect of restor-ative proctocolectomy on sexual function, urinary function, fertility, pregnancy and delivery: a systematic review. Dis Colon Rectum 2007; 50: 1128–38.
53. Counihan TC,Roberts PL,Schoetz DJ et al.Fertility and sex-ual and gynecological function after ileal pouch anal anasto-mosis. Dis Colon Rectum 1994; 37: 1126–9.
54. Marcello PW, Roberts PL. Cystic pelvic masses. Seminars in colon and rectal surgery 1997; 8; 190–7.
55. Francois Y, Dozois RR, Kelly KA et al. Small intestinal obstruction complicating ileal-pouch-anal anastomotis.Ann Surg 1989; 209: 46–50.
56. Marcello PW, Roberts PL, Schoetz JD Jr et al. Obstruction after ileal pouch-anal anastomosis: a preventable complica-tion? Dis Colon Rectum 1994; 37: 1176–7.
57. MacLean AR,Cohen Z,MacRae HM et al.Risk ofsmall bowel obstruction after the ileal pouch-anal anastomosis.Ann Surg 2002; 235: 200–6.
58. Becker JM,Dayton MT,Fazio VW et al.Prevention of postop-erative abdominal adhesions by a sodium hyaluronate-based bioresorbable membrane: a prospective,randomized,double-blind multicenter study. J Am Coll Surg 1996; 183: 297–306.
59. Fazio VW, Ziv Y, Church JM et al. Ileal pouch-anal anasto-moses complications and function in 1005 patients. Ann Surg 1995; 222: 120–7.
60. Scott NA, Dozois RR, Beart RW et al. Postoperative intra-abdominal and pelvic sepsis complicating ileal pouch anal anastomosis. Int J Colorectal Dis 1988; 3: 149–52.
61. Weston-Petrides GK, Lovegrove RE, Tilney HS et al. Comparison of outcomes after restorative proctocolectomy with or without defunctioning ileostomy. Arch Surg 2008; 143(4): 406–12.
62. Ziv Y, Fazio VW, Church JM et al. Stapled ileal pouch-anal anastomoses are safer than handsewn anastomosis in patients with ulcerative colitis.Am J Surg 1996; 171: 320–3.
63. Gorgun E, Remzi FH. Complications of ileoanal pouches. Clin Colon Rectal Surg 2004; 17: 43–55.
64. Raval MJ, Schnitzler M, O’Connor BI et al. Improved out-come due to increased experience and individualized man-agement of leaks after ileal pouch-anal anastomosis. Ann Surg 2007; 246: 763–70.
65. Prudhome M, Dozois RR, Godlewski G et al. Anal can-cal strictures after ileal pouch-anal anastomosis. Dis Colon Rectum 2003; 46: 20–3.
66. Marcello PW, Roberts PL, Schoetz DJ Jr et al. Long-term results of the ileoanal pouch procedure.Arch Surg 1993;128: 500–4.
67. Fazio VW, Tjandra JJ. Pouch advancement and neoileoa-nal anastomosis for anastomotic stricture and anovaginal fistula complicating restorative proctocolectomy. Br J Surg 1992; 79: 694–6.
68. Fleshner PR, Schoetz DJ Jr. Surgical management of ulcer-ative colitis in the ASCRS textbook of colon and rectal sur-gery, 2007: 567–83.
69. Fazio VW, Ziv Y, Church JW et al. Ileal pouch-anal anas-tomosis complications and function in 1005 patients. Ann Surg 1995; 222: 120–7.
70. Shah NS,Remzi FH,Massman A et al.Management and treat-ment outcome of pouch-vaginal fistulas following restorative proctocolectomy. Dis Colon Rectum 2000; 46: 911–7.
71. Lohmuller JL, Pemberton JH, Dozois R et al. Pouchitis and extraintestinal manifestations of inflammatory bowel dis-ease after ileal pouch-anal anastomosis.Ann Surg 1990; 211: 622–7.
72. Penna C, Dozois R, Tremaine W et al. Pouchitis after ileal pouch-anal anastomosis for ulcerative colitis occurs with increased frequency in patients with associated primary scle-rosing cholangitis. Gut 1996; 38: 234–9.
73. Sanborn WJ,Tremaine WJ,Batts KP et al.Pouchitis after ileal pouch-anal anastomosis: a pouchitis disease activity index. Mayo Clin Proc 1994; 69: 409–15.
74. Fazio VW, Wu JS, Lavery IC. Repeat ileal pouch-anal anas-tomosis to salvage septic complications of pelvic pouches: clinical outcome and quality of life assessment. Ann Surg 1998; 228: 588–97.
75. Lovegrove RE, Herior AG, Constantinides V et al. Meta-analysis of short-term and long-term outcomes of J, W, and S ileal reservoirs for restorative proctocolectomy. Colorectal Dis 2006; 9: 310–20.
76. Seow-Choen F,Tsunoda A,Nicholls RJ.Prospective randomized trial comparing anal function after hand-sewn ileoanal anasto-mosisvs.stapledileoanalanastomosiswithoutmucosectomyin restorative proctocolectomy. Br J Surg 1991; 78: 430–4.
77. Luukkonen P, Jarvinen H. Stapled vs. hand sutured ileoanal anastomosis in restorative proctocolectomy: a prospective randomized trial.Arch Surg 1993; 128: 437–40.
78. Reilly WT, Pemberton JH, Wolff BG et al. Randomized prospective trial comparing ileal pouch-anal anastomosis performed by excising the anal mucosa to ileal pouch-anal anastomosis.Ann Surg 1997; 225: 666–76.
79. Lovegrove RE, Constantinides VA, Heriot AG et al. A com-parison of hand-sewn vs. stapled ileal pouch anal anasto-mosis (IPAA) following proctocolectomy-a meta-analysis of 4183 patients.Ann Surg 2006; 244: 18–26.
80. O’Riordain MG, Fazio VW, Lavery IC et al. Incidence and natural history of dysplasia of the anal transitional zone after ileal pouch-anal anastomosis: results of a five-year to ten-year follow-up. Dis Colon Rectum 2000; 43: 1660–5.
81. Herline AJ, Meisinger LL, Rusin LC et al. Is routine pouch surveillance for dysplasia indicated for ileoanal pouches? Dis Colon Rectum 2003; 46: 156–9.
improved outcomes in colon and rectal surgery
82. Hyman NH,Fazio VW,Tuckson WB,Lavery IC.Consequences of ileal pouch-anal anastomosis for Crohn’s colitis.Dis Colon Rectum 1991; 34: 653–7.
83. Sagar PM, Dozois RR, Wolff BG. Long-term results of ileal pouch-anal anastomosis in patients with Crohn’s disease.Dis Colon Rectum 1996; 39: 893–8.
84. Keighley MR. The final diagnosis in pouch patients for presumed ulcerative colitis may change to Crohn’s disease;
patients should be warned of the consequence. Acta Chir Iugosl 2000; 47: 27–31.
85. Braveman JM,Schoetz DJ,Marcello PW et al.The fate of the ileal pouch in patients developing Crohn’s disease.Dis Colon Rectum 2004; 47: 1613–20.
86. Melmed GY, Fleshner PR, Bardakcioglu O et al. Family history and serology predict Crohn’s disease after ileal-pouch-anal anas-tomosis for ulcerative colitis. Dis Colon Rectum 2008; 51: 100–8.
2 Surgery for Crohn’s disease
Jorge Canedo, Tolga Erim, and Steven D Wexner
Crohn’s Disease (CD) is a lifelong disorder of unknown etiology characterized by chronic focal, transmural, and granulomatosos inflammation that can affect any portion of the gastrointesti-nal tract. The transmural inflammation often leads to fibrosis and to obstructive clinical presentations. Crohn’s disease was first described by B. Crohn, L.Ginzburg, and G.Oppenheimer in 1932 as an inflammatory condition limited to the terminal ileum.(1) Later, Lockhart-Mummery and Morson (2) described granulomatous colitis, and the disease process was understood to potentially affect the large bowel.It can occur from the mouth through the anus.
The clinical symptoms are related to the site of the disease. As it is more prevalent among the terminal ileum and right colon, the most frequently symptoms are: diarrhea, weight loss, abdominal pain, and perineal disease. But the clinical features indicate the site of the disease.(3)
a) Oral: Aphthous ulceration on the background of a mucosal edema is the most common oral manifestation of CD. Additional lesions described include: granulomatous masses, chelitis,and granulomatous sialadenitis.Lesions usually coex-ist with an intestinal disease.
b) Esophagus: Although more rare, lesions here may cause dysphagia or pain.
c) Stomach and duodenum: Less than 5% of the patients pres-ent with gastroduodenal Crohn’s disease; the distal antrum and the duodenum are the most commonly affected areas. Both sites can present as a peptic ulcer disease. In addition, outlet gastric obstruction may occur after a healing stricture in the antrum.
d) Small bowel: Some findings of extended involvement include malabsorption,protein-losing enteropathy,diarrhea,anemia, and steatorrhea.If segmental thickening or structuring devel-ops, the patient may present with obstructive symptoms.
e) Ileocecal: Symptoms of obstruction are more frequently due to inflammatory swelling or structuring. Transmural inflam-mation and local sepsis often result in a palpable inflamma-tory mass in the right lower quadrant.
f) Colon: involvement often includes the symptoms of diar-rhea, associated with pain.
g) Perianal disease:Is common and may precede other manifesta-tions; as a fistula, an abscess, or one or more fissures and tags.
Patients may also have systemic symptoms; fatigue, weight loss, and fever are the primary systemic symptoms in Crohn’s disease. Postprandial obstructed symptoms from narrowed intestinal segments make the patient avoid eating. Weight loss may also be related to malabsorption and, in children, may be the presenting sign before any obvious intestinal manifestations of the disease.
Fever is common in patients with Crohn’s disease and may be due to other chronic inflammation or due to a perforation with associated fistula or abscess. Crohn’s disease is diagnosed most frequently among people aged 15 to 30 years, with no differences in prevalence between males and females. However, there is a second peak between the sixth and seventh decades of life (4) and diagnosis may also be made during early childhood.
Since its discovery in the Mount Sinai Hospital in New York City almost 76 years ago, the exact cause of Crohn’s disease remains unknown. Among many theories are genetic, immunologic, bacterial, and bacterial antigens. The current theory about the pathophysiology is that the intestinal flora, in conjunction with unidentified environmental factors trigger and drives an exaggera-dated immunologic response in a genetically susceptible host.(5) Theresultisachronicinflammationthattypicallyextendsbeyond the mucosa and throughout to the serosa.Potential risk factors to develop CD are smoking and having first degree relatives with the disease.(6)
Symptoms of CD are heterogeneous,but most of the time include diarrhea for more than 6 weeks, abdominal pain, and weight loss. In most cases,the patient will have a clinic,radiologic,endoscopic, and histological evaluation to have its diagnosis.
Crohn’s disease most often involves the distal small bowel and proximal large bowel. Almost one half of all patients have dis-ease that involves both the ileum and the colon. While another one-third have disease confined to the small bowel, primarily the terminal ileum. The clinical presentation might be divided according to the main symptoms into:
1. Intestinal Symptoms
2. Extraintestinal symptoms
3. Biliary and Liver Manifestations
The patient with CD should undergo complete evaluation. In most cases, the leading symptom that precipitates evaluation is diarrhea. Eighty-five percent of patients with CD report more than 5 bowel movements (BM) per day and weight loss as part of the initial diagnosis.(7) The history and physical examina-tion might uncover general complaints including weakness and fatigue. In addition, as mentioned above, there are the specific symptoms according to disease site.
On physical examination,paleness of the mucosa could indicate anemia.Iron deficiency anemia occurs in up to 30% ofthe patients. (8) Typically, the abdominal examination reveals abnormal bowel sounds, detection of an abdominal mass, and pain to palpation. Inspection of the perianal regional can provide evidence of fistula, fissure,abscess,orskintap.Rectaldigitalexaminationmightdetect a stenosis or blood.
improved outcomes in colon and rectal surgery
The initial complementary evaluation starts with blood tests and stool examination.
Blood tests can either provide specific or nonspecific diagnosis, as well the general health status of the patient. The introduction of biological therapies in IBD has renewed interest in inflamma-tory markers (especially C reactive protein (CRP)), given their potential to select responders to these treatments. Controversy exists as to whether or not CRP is a useful marker, and should be preferred in CD as it correlates well with disease activity.(9) But a more recent study showed that neither CRP nor other biological markers were associated with the endoscopic lesions. (10) Elevated leukocytes and thrombocyte time can also indicate active inflammation.
Serologic response to various microbes and autoantigens can develop into CD. In addition to the well-established atypi-cal perinuclear antineutrophil cytoplasmic antibodies (atypical P-ANCA) and anti-Saccharomyces cerevisiae mannan antibodies (ASCA), a number of new antibodies have recently been dis-covered and data on their clinical significance has been rapidly increasing. The combination of atypical P-ANCA and ASCA, may be of help in patients in whom distinction between CD and Ulcerative Colitis is not obvious with the classic diagnostic tools (patient history, radiologic examination, endoscopy and biopsy).
Papp et.al (11) analyzed several studies, and found that these combinations had sensitivities of 30% to 64%, specificity more than 90%, and PPV from 77% to 96%. Newer markers derived from various microbial inhabitants of the gut, such as Omp, I2, and CBir1 offer new ways to stratify patients into serologic subgroups. Also, glycan markers including antilaminaribioside carbohydrate antibody (ALCA) (18–38%),antichitobioside car-bohydrate antibody (ACCA) (21–36%), and antimannobioside carbohydrate antibody (AMCA) (28%) may play an important role in making a CD diagnosis or prognosis.(12) More impor-tantly, 24–44% of the CD patients found ASCA negative in one study were positive for one or more of the antiglycan anti-bodies. The combination of several serological markers, such as gASCA, pANCA, and ALCA, had the best accuracy. Their increased amounts and levels of antibody responses against gASCA, ALCA, ACCA, AMCA and Omp were associated with more complicated disease behaviour (44.7% vs.53.6% vs.71.1% vs. 82.0%) and a higher frequency of Crohn’s disease-related abdominal surgery (38.5% vs. 48.8% vs. 60.7% vs. 75.4%).(12) Although the prevalence of antibodies is also higher in healthy relatives of IBD patients than in the control population, their role as subclinical markers is yet to be established.
One example of a stool marker is neutrophil determination. However, neutrophil determination in the stool is inefficient because of its brief lifetime. This means that the sample should be examined within a few hours of its collection. Other exam-ples of stool markers include calprotectin and lactoferrin. They are produced in significant amounts in white blood cells. The mucosal barrier is altered in CD, allowing white cells to cross
the intestinal wall. Activated leukocytes infiltrate the mucosa and can be detected in feces. Lactoferrin is an iron-binding glycoprotein found concentrated in the secondary granules of the neutrophils. Granule proteins can be released from living cells, while cell death does not appear to increase this phenom-enon. Calprotectin is a cytoplasmic antimicrobial component in granulocytes, monocytes, and macrophages. But besides its promises, D’Incà et al. (13) observed that calprotectin and lac-toferrin determination appears to reflect endoscopic and his-tological disease activity in ulcerative colitis but not in Crohn’s disease.
In clinical practice,imaging techniques are used at initial presenta-tion to establish a diagnosis and to assess exact location, extent, and severity of disease at the time. These methods are also used as follow-up during and after treatment to direct treatment strategies and determine optimal choice and dose of medication. Patients with established CD typically undergo many investigations over a lifetime.
Small bowel series
The small bowel has been defined for many years as the “black box” of the gastrointestinal system, due to its lack of endoscopic acces-sibility. Therefore, the conventional radiological methods (small bowel enteroclysis (SBE) (Figure 32.1a,Figure 32.1b,Figure 32.1c) and small bowel follow through (SBFT)) were the only imaging methods that could provide information on the morphological features of the small bowel valuable in the diagnosis and manage-ment of CD.Both SBE and SBFT,when performed by experienced examiners, appear to be characterized by similar sensitivity (85– 95%)andspecificity(89–94%)indetectingtheradiologicallesions typical of Crohn’s disease.(14) Preference for one technique or the other largely depends on institutional standards. Both procedures are able to evaluate small bowel peristalsis, including the presence of strictures and/or dilations, the distensibility of the intestinal loops, the presence of fistulae, the morphology of circular folds, and morphology of the mucosal surface.
For primary evaluation, endoscopy has widely replaced the bar-ium enema (BE) as diagnostic method. However, BE can provide important additional information in the differential diagnosis of chronic inflammatory colonic diseases or if intestinal intubation is not achieved at colonoscopy.The advantage of a BE over endos-copy is a clear and reproducible demonstration of the patterns of distribution and character of the disease as well as the detection of fistulae.(15) With the advance of CT and MRI images, and wireless endoscopic capsule,barium examinations not only of the stomach but also of the colon are decreasing in frequency.
The disadvantage of the enema is the same as the one for SBE: limited information about transmural and extraintestinal abnormalities.
Lemberg et al. (16) concluded the need to include EGD in the evaluation of children suspected of having IBD.The current study