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COLON
181
hese medications only for patients with severe disease who are neither
t toxic nor show signs of impending perforation. A rapid response within 3 to 5 days of starting treatment is expected; otherwise, patients should have surgery. ese patients require very close observation, both clini­cally and with a daily plain lm of the abdomen. Intravenous antibiotics are oen used but have been shown to be ineective and, in fact, could exacerbate symptoms if an antibiotic-associated colitis develops. 
General Recommendations f
or Patients with Severe
Ulcerative Colitis
est for C. difficile Toxin A and B
T
All patients with a severe exacerbation of UC should be tested for C. dicile cytotoxin A and B. A supine and decubitus plain lm of the
abdomen are obtained upon admission. If thumbprinting, pneuma­tosis intestinalis, or megacolon is observed, surgery should be con­sidered. If surgery is not undertaken, then daily imaging should be performed until clear improvement in the patient’s condition occurs. 
Flexible Sigmoidoscopy with Biopsies
In most patients with severe UC, a exible sigmoidoscopy is adequate to determine disease severity and to obtain biopsy specimens for CMV testing. e appearance of the mucosa alone is not adequate to exclude C. dicile infection because 50% do not have pseudomem­branes upon endoscopic examinations. erefore, performing biop­sies is very important because the histologic features characteristic of pseudomembranous colitis may be present. 
Deep Vein Thrombosis Prophylaxis
Patients with active UC have a threefold risk of venous thromboem­bolism. Some of factors that contribute to this risk include thrombo­cytosis, inammatory cytokines, and bed rest. Bloody diarrhea is not a contraindication for prophylaxis with heparin. 
Evaluate for Tuberculosis and Hepatitis B
Initial treatment for the patient with severe ulcerative colitis is with intra­venous steroids. It is important to evaluate for tuberculosis and hepatitis B because if the patient does not respond to intravenous steroids, the treatment options are iniximab, cyclosporine, or surgery. e preferred test to evaluate for tuberculosis is QuantiFERON because patients may have false-negative results related to nutritional status or treatment. 
Avoid Narcotics and Antidiarrheal Medications
e use of narcotics and antidiarrheal medications increases the risk of toxic megacolon. Unfortunately for patients who have abdominal pain, no good alternatives are available. If any of these medications are used, patients should have a daily kidney-ureter-bladder radio­graph in the upright position to assess the diameter of the colon. 
Do Not Use Antibiotics
Unless evidence of bacterial infection is noted, antibiotics do not have a role in the treatment of patients with severe UC. Small clinical tri­als have compared metronidazole, metronidazole + tobramycin, and ciprooxacin with placebo as adjuvant treatments in patients treated with intravenous steroids and have not shown benet. 
Diet as Tolerated
Except for patients in whom urgent surgery is indicated, diet should be as tolerated. Nutrition is a predictor of postsurgical complications, and there is no role for total parenteral nutrition as primary treat­ment in patients with severe UC. 
Perform Close Observation and Consult Colorectal Surgery upon Admission
Patients should be evaluated on an ongoing basis, and a surgical con­sultation should be obtained when the patient is admitted to the hospi­tal. Keep in mind the dierent predictors of colectomy (Table 35-7) and do not delay surgery in patients who are not responding to treatment. 
Vaccinations
e approach to vaccinations in patients with UC is described in
Table 35-8. 
Pregnancy
Treating the mother is the most important watchword of medical therapy in patients with UC. If the mother’s disease is under control, the chance for premature labor or spontaneous abortion is no dif­ferent from that for an unaected mother. e activity of IBD in the mother during pregnancy is dependent on the disease activity at the time of conception. If the disease is inactive at conception, the prob­ability that a serious are will develop during pregnancy is low. Con­versely, if conception occurs during a relapse, there is a 30% chance of further worsening of symptoms during pregnancy.
Prednisone, 5-ASA agents, thiopurines, anti-TNF-α agents, and anti­adhesion molecules are safe to use during pregnancy and should be used if the mother requires these medications to maintain remission or control symptoms. However, it is recommended that use of biologic agents be discontinued during the third trimester of pregnancy. Low birth weight, once believed to be a result of corticosteroid use during pregnancy, is more likely related to disease activity and nutritional deciencies. Even though sulfasalazine has a sulfa moiety, sulfasalazine does not cause ker­nicterus. Azathioprine and 6-MP are considered by the Food and Drug Administration to be class D drugs and are not recommended during pregnancy, and studies show an increased risk of congenital malforma­tions when azathioprine or 6-MP were used during pregnancy in patients with IBD. However, these studies are small and have limited power, and these medications have been used oen in uneventful pregnancies. In a systematic review and meta-analysis by Akbari etal, ve quality studies of female patients with IBD who received thiopurines during pregnancy (total: 3045 women) and three studies of male patients taking thiopu­rines (total: 217 men) were analyzed. e pooled analysis showed that the risk of congenital malformations in babies of pregnant women was not statistically signicant (OR, 1.45; 95% CI, 0.99 to 2.13); neither was
he incidence of congenital defects in infants born of fathers taking thio-
t purines (OR, 1.87; 95% CI, 0.67 to 5.25, P = .236). A similar British study published in 2014 by Ban etal compared 1703 children born to moth­ers with IBD from 1990-2010 with 384,811 children of mothers without IBD. Major congenital abnormalities were seen in 2.7% of children born to mothers with IBD and in 2.8% of children born to mothers without IBD. e adjusted OR of major congenital malformations according to drug use was 0.82 (95% CI, 0.42 to 1.61) for 5-ASA, 0.48 (95% CI, 0.15 to
1.15) for corticosteroids, and 1.27 (95% CI, 0.48 to 3.39) for thiopurines. A multicenter national prospective study of pregnancy and neonatal out­comes in women with IBD (PIANO) in the United States was initiated in
2007. In a preliminary report in 2013, information was available on 279 patients exposed to thiopurines. No observed increase in the risk of con­genital malformations or other complications was observed in infants exposed to thiopurines compared with infants who were not exposed to thiopurines during pregnancy.
Methotrexate is class X and thus is contraindicated during pregnancy. 
Cancer Risk
D
uring the course of the disease, colorectal cancer will occur in
approximately 6% of patients with UC and will be the cause of
182
Medic
al Trea
TMenT of UlceraTive coliTis
and oT
her coliTides
TABLE 35-7: Predictors of Colectomy in Patients with Ulcerative Colitis
er Oxford Criteria (Travis et
Mark
Clinical
ospitalization at diagnosis
H Stool frequency >12/d Fever >38°C Tachycardia >100 Albumin <30 g/L on day 4 Attack lasting >6 wk ESR >30 mm/hr, or CRP >25 mg/L Need for anti-TNF-α
Evaluation aer 72 hr of IV steroids 8 bowel movements/24 hr or 3-8 bowel
movements + CRP >45 mg/L
Aer 7 days of treatment, patients with >3
stools/day or visible blood have a 60% chance of continuous symptoms and a 40% chance of requiring a colectomy in 3-30 wk
Need for early use of immunomodulators
Endoscopic
xtensive deep ulceration
E Mucosal detachment at edge of ulcer Large mucosal abrasions “Well-like” ulcers
Histologic
requent crypt abscesses
F Focal and segmental mononuclear cell inltration Paucity of eosinophils
al,
1996
) T
ruelove and Witts
≥3 criteria = 50% likelihood of urgent
colectomy
Bloody stool frequency of 6 or more per
day Tachycardia (90 bpm) Temperature >37.8°C Anemia (hemoglobin <10.5 g/dL) ESR >30 mm/hr
Radiologic
olonic dilatation
C Small bowel dilatation
, C-reactive protein; ESR, erythrocyte sedimentation rate; IV, intravenous; TNF, tumor necrosis factor.
CRP
ath in 3% of patients with extensive disease. These rates are
de much higher than for the general population. The risk for colorec­tal cancer is known to increase with increasing extent and dura­tion of disease, with younger age at symptom onset, with chronic active disease, and with primary sclerosing cholangitis. High-risk patients should be advised to enroll in surveillance programs.
TABLE 35-8: Vaccinations in Patients with
Ulcerative Colitis
ariable Instructions
V
General Check vaccination history and check im-
The magnitude of the risk in these patients is controversial, and recently a case series has suggested that the risk of colon cancer has decreased. The American College of Gastroenterology (ACG),
At diagnosis Check hepatitis B serology, vaccinate if
American Gastroenterological Association (AGA), European Crohn’s and Colitis Organization, the British Society of Gastroen­terology, and the National Institute for Clinical Excellence recom­mend performing the first screening colonoscopy 8 to 10 years after diagnosis in patients with both universal and left-sided coli­tis (Table 35-9). In patients with primary sclerosing cholangitis, the risk of colon cancer is greatly increased, and screening starts at the time of diagnosis. If dysplasia is not found, some variability exists in the recommendations regarding the frequency of sub­sequent screening colonoscopic examinations, with the suggested interval varying from yearly to every 5 years. From a practical standpoint it is easier to follow the AGA and ACG recommenda­tions, which are that screening colonoscopic examinations should be performed every 1 to 3 years. With longer duration of disease, the interval between screenings is shorter. European societies rec­ommend screening with chromoendoscopy and use of targeted biopsies, and if chromoendoscopy is not available, they recom­mend that a colonoscopy be performed with at least 33 random
Ye a rl y Inuenza
Every 5 yr Pneumococcal
Every 10 yr In adults, tetanus and diphtheria
Trav e l Refer to travel clinic 3 mo before traveling
Contraindicated
while taking an immunosuppressant
biopsies. U.S. societies recommend chromoendoscopy only in special cases; otherwise, the recommendation is to perform high­definition colonoscopy with white light and a minimum of 33 biopsies.
e goal of colonoscopic screening is to decrease death from colon cancer in patients with IBD. erefore, if either conrmed low­grade dysplasia is found on consecutive colonoscopies or if conrmed
high-grade dysplasia is found, or if multifocal dysplasia or an asymp­tomatic cancer is detected, the patient should have a total procto­colectomy. Additional indications for colectomy include a stricture or extensive pseudopolyposis that prevent adequate screening. Although these recommendations have not been shown to reduce the
mune status
negative
Check hepatitis A serology, vaccinate if
negative Pneumonia vaccine Inuenza Human papillomavirus
Herpes zoster or varicella, yellow fever,
rabies, triple viral vaccine, bacillus
Calmette–Guérin, polio (Sabin)
COLON
183
TABLE 35-9: Screening Guidelines of International Societies for Neoplasia in Persons with Ulcerative Colitis
ariable ECCO 2008 BSG 2010 (and NICE) AGA 2010 ACG 2010
V
st screening 8-10 yr 10 yr Maximum 8 yr 8-10 yr
Fir
Surveillance interval Extensive: 2 yearly to 20 yr then annually
Le sided: 2 yearly starting at 15 yr PSC: 1 yearly
Chromoendoscopy 1-3 y
More oen at high risk (e.g., PSC)
Biopsies 33+ if no chromoendoscopy 33+ if no chromoendoscopy 33+ 33+
G, American College of Gastroenterology; AGA, American Gastroenterological Association; BSG, British Society of Gastroenterology; ECCO, European
AC
Crohn’s and Colitis Organization; NICE, National Institute for Clinical Excellence; PSC, primary sclerosing cholangitis.
ancer-related mortality rate compared with an unscreened popula-
c tion, cancer surveillance for patients with UC has become the stan­dard of care and must be oered to those who are eligible. 
ectal Cancer Prevention
Color
In patients with IBD, the only medication that appears to decrease the risk of colon cancer is 5-ASA. Folic acid supplementation may decrease the risk of colon cancer in patients who do not have dys­plasia. However, if dysplasia is present, folic acid supplementation should be discontinued because it increases the risk of progression to colon cancer. 
THER COLITIDES
O
oscopic Colitis
Micr
icroscopic colitis (MC) includes collagenous and lymphocytic
M colitis. Previously considered a rare disease, the prevalence of MC has increased since the term was coined in 1980. For example, in the years 1993-1995, the annual incidence of collagenous colitis per 100,000 inhabitants in Sweden was 3.7, and for lymphocytic colitis it was 3.1. In the years 2004-2008, the incidence of collagenous colitis in Sweden had increased to 5.8 per 100,000 inhabitants, and for lym­phocytic colitis it increased to 4.5. In Olmstead County, Minnesota, the incidence of MC increased from 0.8/100,000 inhabitants in 1985­1989 to 19.1/100,000 in 1998-2001.
MC is a signicant cause of chronic diarrhea. It accounts for approximately 10% of cases of chronic nonbloody diarrhea, and at least 20% of these patients are older than 70 years. It aects per­sons of all ages but is rare in children. At least 25% of patients are younger than 45 years. Patients with MC are typically women older than 65 years. Previous or current cigarette smoking is a risk factor for both lymphocytic and collagenous colitis. Some medications such as NSAIDs have been implicated as triggers of the disease, and in some cases may cause the disease. Other drugs such as proton pump inhibitors cause an increase in intraepithelial lymphocytes in the colon, but they do not cause diarrhea in all the patients. e range of drugs that have been associated with MC also include ticlopidine, serotonin reuptake inhibitors, and simvastatin. Patients commonly present with the sudden onset of liquid diarrhea. More than 20% of patients have at least 10 bowel movements per day, and more than 25% have nocturnal bowel movements.
MC is often associated with other immune diseases includ­ing rheumatoid arthritis, scleroderma, atrophic gastritis, chronic active hepatitis, primary biliary cirrhosis, hypothyroidism, and celiac disease. The diagnosis can be confirmed by documenting
By risk: low, 5 yr; intermediate,
3 yr; high, 1 yr
Recommended Special cases Not yet
a secretory diarrhea, normal-appearing colonic mucosa at colo­noscopy, and an abnormal histologic appearance. The histologic abnormality in collagenous colitis is a thickened apical subepithe­lial collagen layer and irregular collagen deposition with a ragged, spiculated deep edge. The collagen band is composed of type III collagen and fibronectin, and it measures between 7 and 100 μm in thickness. Other findings include a thickened basement mem­brane and an excess of lymphocytes, plasma cells, eosinophils, and mast cells in the lamina propria. Patients with lymphocytic colitis do not have subepithelial eosinophilic deposits. Histologic abnormalities may be limited to the proximal colon, spare the rec­tum, and be discontinuous, and thus a colonoscopy and biopsies of the right and left side are necessary to confirm or exclude the diagnosis. 
ersion Colitis
Div
version colitis, bypass colitis, exclusion colitis, and disuse colitis
Di are synonyms for the colonic inammatory process that invariably occurs when the fecal stream is diverted from a colonic segment. If the patient did not have inammation prior to the surgery that diverted the fecal stream, symptoms resolve with reanastomosis. Examples of patients who experience diversion colitis are those who have undergone diversion for diverticulitis, cancer, or anastomotic leaks. Hematochezia and mucus discharge from the rectum or mucous stula are the primary symptoms, and these symptoms can present from 1 month to 3 years aer the diversion is performed. However, some patients with diverted colons are asymptomatic, with only pathologic or endoscopic ndings. Typical histologic ndings include mucin depletion, mucosal edema, a decreased number and depth of crypts, supercial ulcerations, expansion of cellular elements of the lamina propria, granulocyte inltration, and brosis of the lamina propria. e colonoscopic appearance of a diverted segment may show typical features of colitis such as narrowing, erythema, ulceration, friability, exudate, or a distorted mucosal vascular pattern.
Colonocytes are nourished from the bloodstream and from luminal contents by short-chain fatty acids (SCFAs) that are a byproduct of the metabolism of carbohydrates by colonic bacteria. In an intact colon in patients with a normal diet, a concentration of 100 to 200 mmol/L of SCFAs is recovered in stool, whereas a diverted segment has less than 5 mmol/L. Treatment with twice­daily 60-mL SCFA enemas delivered into the diverted segment effectively improves symptoms and resolves endoscopic and his­tologic inflammation. One formulation that typically works well is a combination of 60-mmol acetate, 30-mmol propionate, and 40-mmol butyrate with sufficient sodium chloride and sodium hydroxide to bring the osmolality to 280 mOsm and the pH to 7.0; 100-mmol butyrate enemas at the same osmolality and pH also
1-3 yr More oen at high risk
(e.g., PSC)
1-2 yr
184
hould be successful. Responses also have been seen with 5-ASA
s
Medic
al Trea
TMenT of UlceraTive coliTis
enemas. The best therapy for diversion colitis is reanastomosis. However, enemas given daily or even every other day can be used to maintain remission until reanastomosis becomes feasible. 
Radiation Colopath
hen organs adjacent to the rectum are treated with radiation ther-
W
y
apy, a radiation colopathy develops in 5% to 10% of patients. With newer concentrating techniques, the organ with dose-limiting toler­ance of ionizing radiation has changed from the skin to the gastroin­testinal tract. e most common malignancies that are usually treated with radiation therapy that cause radiation colitis are transitional cell carcinoma of the bladder, squamous cell carcinoma of the cervix, endometrial cancer, and adenocarcinoma of the prostate or rectum.
Early radiation injury is caused by direct damage to the crypt cells of the epithelium, and late injury is caused by damage to the vascular endothelium and connective tissue. Half the patients who have 6000 cGy delivered to a region of the colon or 8000 cGy delivered to the rectum will experience early or late radiation colopathy. Apparently, the margin of safety is very narrow, because these doses are close to those required for treatment of the tumor.
Early radiation colopathy oen occurs within the rst month of therapy. With epithelial disruption, symptoms of diarrhea, hema­tochezia, tenesmus, and mucus discharge occur. Upon endoscopy, the mucosal abnormalities are similar to those seen in UC. e mucosa is edematous and friable, with supercial ulcerations, and the mucosal vascular pattern is decreased. However, the mucosal abnormalities are conned to the radiated part and are not con­tinuous as in UC. Histologic ndings include a decrease in the height of the epithelial cells, mucin depletion, ulceration, and crypt abscesses. Anterior rectal ulcerations, luminal narrowing, radio­logic “thumbprinting,” and loss of haustrations are additional signs of early toxicity.
erapy of early radiation toxicity includes symptomatic treat­ment such as antispasmodic agents, antidiarrheal medications, bulk­ing agents, and topical anesthetics. Steroid enemas may help, but 5-ASA agents are not eective. Attempts to minimize the risk of developing early radiation injury include surgical xation of bowel away from the anticipated port, administration of free radical scaven­gers such as diallyl sulde (garlic), use of cyclooxygenase inhibitors such as aspirin, hyperbaric oxygen, and glutamine-supplemented diets.
Late injury from radiation therapy often occurs within 5 years but may present several decades after therapy. Symptoms are slowly progressive and are related to changes in the submu­cosal layers of the bowel. Common presenting symptoms include abdominal pain and diarrhea related to the development of fibrous strictures and partial obstruction. Fistulas, perforation, and impaired motility also may occur. The symptoms in patients with late radiation proctopathy are tenesmus, mucous discharge, change in stool caliber, and hematochezia. Endoscopically, the usual findings include telangiectasias, granularity, friability, dis­crete ulcers in the anterior rectum, and strictures. Late radiation injury resembles ischemia with submucosal fibrosis, telangiecta­sias of small vessels, hyalinized endothelium of larger blood vessel walls, fistulas, and fissures.
Treatment of late complications of radiation therapy is rarely eective. Steroid enemas or other medical therapies are of marginal benet; use of a neodymium:yttrium-aluminum-garnet laser or bipo­lar electrocoagulation of bleeding telangiectasia may help decrease hematochezia. Occasionally, strictures can be dilated manually or with endoscopically placed balloon dilators. Because of the brittle nature of radiated bowel, perforation is a frequent complication of bowel dilation. Surgery for obstruction, bleeding, stulas, or perfora­tion is high risk because of frequent delayed healing of the wound and surgical anastomosis. 
and oT
her coliTides
Drug-Induced Colitis
ertain drugs may cause inammation of the colon that is endoscopi-
C cally indistinguishable from IBD. e distinction, though, is most important because drug-induced colitis is best treated by withdrawal of the medication, and IBD oen requires the institution of potentially toxic medications. Mucosal inammation of the colon is a rare adverse eect from some commonly used medications such as NSAIDs and contraceptives. Even if the incidence of colitis is exceedingly low, the common use of these medications makes drug-induced colitis poten­tially a more important problem than IBD. Other medications that may cause a drug-induced colitis include methyldopa, penicillamine, potas­sium supplements, 5-uorouracil, oral gold, and isotretinoin.
The colitis that can occur as a result of oral contraceptive use can be indistinguishable from Crohn colitis, with patients presenting with chronic diarrhea and aphthoid ulcers through­out the colon. Symptoms and signs of oral contraceptive colitis completely resolve without sequelae upon discontinuation of the hormone. The pathogenesis is believed to be due to an occlusive vascular phenomenon.
e symptoms and endoscopic ndings of NSAID-induced coli­tis usually mimic UC. e inammation is diuse with supercial ulcerations. e pathogenesis of NSAID-induced colitis involves cyclooxygenase inhibition and the loss of cytoprotective prosta­glandins. e dierentiation between IBD and NSAID-induced colitis is further complicated because arthritis, a condition oen treated with NSAIDs, may or may not be related to IBD. A patient with arthritis who takes NSAIDs and experiences symptoms and signs suggestive of UC should stop taking these medications. Other eects of NSAIDs on the gastrointestinal tract include complicated ulcer disease, stricture from submucosal brosis, perforation from deep ulceration, and diaphragmatic-like narrowing in the small bowel or colon.
u
S
Adler DJ, Korelitz BI. e therapeutic ecacy of 6-mercaptopurine in refrac-
Akbari M, Shah S, Velayos FS, etal. Systematic review and meta-analysis on
Ban L, Tata LJ, Fiaschi L, Card T. Limited risks of major congenital anomalies
Bernstein CN, Shanahan F, Weinstein WM, et al. Are we telling patients
Bjarnason I, Zanelli G, Smith T, et al. Nonsteroidal anti-inammatory
Boyko EJ, Koepsell TD, Perera DR, etal. Risk of ulcerative colitis among for-
Breuer RI, Soergel KH, Lashner BA, etal. Short chain fatty acid rectal irri-
Brzezinski A, Rankin GB, Seidner DL, etal. Use of old and new oral 5-ami-
Calkins BM. A meta-analysis of the role of smoking in inammatory bowel
Chang KH, Burke JP, Coey JC. Iniximab versus cyclosporine as rescue ther-
Connell WR, Lennard-Jones JE, Williams CB, etal. Factors aecting the out-
Dwarakanath AD, Yu LG, Brooks C, etal. “Sticky” neutrophils, pathergic ar-
East JE. Colonoscopic cancer surveillance in inammatory bowel disease:
S t
g g e
tory ulcerative colitis. Am J Gastroenterol. 1990;85:717–722.
the eects of thiopurines on birth outcomes from female and male patients
with inammatory bowel disease. Inamm Bowel Dis. 2013;19:15–22.
in children of mothers with IBD and eects of medications. Gastroenterol-
ogy. 2014;146:76–84.
the truth about surveillance colonoscopy in ulcerative colitis? Lancet.
1994;343:71–74.
drug-induced intestinal inammation in humans. Gastroenterology.
1987;93:480–489.
mer and current cigarette smokers. N Engl J Med. 1987;316:707–710.
gation for le-sided ulcerative colitis: a randomized, placebo-controlled
trial. Gut. 1997;40:485–491.
nosalicylic acid formulations in inammatory bowel disease. Cleve Clin J
Med. 1995;62:317–323.
disease. Dig Dis Sci. 1989;34:1841–1854.
apy in acute severe steroid-refractory ulcerative colitis: a systematic review
and meta-analysis. Int J Colorectal Dis. 2013;28:287–293.
come of endoscopic surveillance for cancer in ulcerative colitis. Gastroen-
terology. 1994;107:934–944.
thritis, and response to heparin in pyoderma gangrenosum complicating
ulcerative colitis. Gut. 1995;37:585–588.
what’s new beyond random biopsy? Clin Endosc. 2012;45:274–277.
e d
R
e
a d i n g
COLON
185
Ernest DL, Trier JS. Radiation enteritis and colitis. In: Sleisenger MH, Fordtran
JS, eds. Gastrointestinal Disease. Philadelphia: WB Saunders; 1993.
Farmer RG, Easley KA, Rankin GB, etal. Clinical patterns, natural history,
and progression of ulcerative colitis: a long-term follow-up of 1,116 pa­tients. Dig Dis Sci. 1993;38:1137–1146.
Fernandez-Banares F, Bertran X, Esteve-Comas M, etal. Azathioprine is use-
ful in maintaining long-term remission induced by intravenous cyclo­sporine in steroid-refractory severe ulcerative colitis. Am J Gastroenterol. 1996;91:2498–2499.
Gies N, Kroeker KI, Wong K, Fedorak RN. Treatment of ulcerative colitis with
adalimumab or iniximab: long- term follow-up of a single-centre cohort. Aliment Pharmacol er. 2010;32:522–528.
Harig JM, Soergel KH, Komorowski RA, etal. Treatment of diversion colitis
with short-chain fatty acid irrigation. N Engl J Med. 1989;320:23–28.
Hawthorne AB, Logan RFA, Hawkey CJ, etal. Randomized controlled trial
of azathioprine withdrawal in ulcerative colitis. Br Med J. 1992;305:20–22.
Järnerot G, Hertervig E, Friis-Liby I, etal. Iniximab as rescue therapy in se-
vere to moderately severe ulcerative colitis: a randomized, placebo- con­trolled study. Gastroenterology. 2005;128:1805–1811.
Kornbluth A, Sachar BD, etal. Ulcerative colitis practice guidelines in adults:
American College of Gastroenterology, Practice Parameters Committee. Am J Gastroenterol. 2010;105:501–523.
Kozarek R, Bedard C, Patterson D, etal. Cyclosporine use in the precolectomy
chronic ulcerative colitis patient: a community experience and its rela­tionship to prospective and controlled clinical trials. Am J Gastroenterol. 1995;90:2093–2096.
Lashner BA. Recommendations for colorectal cancer screening in ulcerative
colitis: a review of research from a single university-based surveillance program. Am J Gastroenterol. 1992;87(2):168–175.
Lashner BA, Hanauer SB, Silverstein MD, etal. Testing nicotine gum for ul-
cerative colitis patients: experience with single patient trials. Dig Dis Sci. 1990;35:827–832.
Lashner BA, Kirsner JB. Inammatory bowel disease in older people. Clin
Geriatr Med. 1991;7:287–299.
Lashner BA, Shaheen MJ, Hanauer SB, etal. Passive smoking is associated
with an increased risk of developing inammatory bowel disease in chil­dren. Am J Gastroenterol. 1993;88:336–359.
Lawson MM, omas AG, Akobeng AK. Tumour necrosis factor alpha block-
ing agents for induction of remission in ulcerative colitis. Cochrane Data- base Syst Rev. 2006;(3). CD005112.
Lemann M, Galian A, Rutgeerts P, et al. Comparison of budesonide and
5-aminosalicylic acid enemas in active distal ulcerative colitis. Aliment Pharmacol er. 1995;9:557–562.
Lichtiger S, Present DH, Kornbluth A, etal. Cyclosporine in severe ulcerative
colitis refractory to steroid therapy. N Engl J Med. 1994;330:1841–1845.
Loerg R, Danielsson A, Suhr O, etal. Oral budesonide versus prednisolone
in patients with active extensive and le-sided ulcerative colitis. Gastroen- terology. 1996;110:1713–1718.
Loerg R, Ostergaard omsen O. Budesonide versus prednisolone reten-
tion enemas in active distal ulcerative colitis. Aliment Pharmacol er. 1994;8:623–629.
Lv R, Qiao W, Wu Z, et al. Tumor necrosis factor alpha blocking agents as
treatment for ulcerative colitis intolerant or refractory to conventional medical therapy: a meta-analysis. PLoS One. 2014;9(1):e86692.
Manz M, Nichetti P, Seibold F, etal. Treatment algorithm for moderate to
severe ulcerative colitis. Practical consensus recommendations. Swiss Med Wkly. 2014;141:w13235.
Marteau P, Probert CS, Lindgren S, etal. Combined oral and enema treatment
with Pentasa (mesalazine) is superior to oral therapy alone in patients with extensive mild/moderate active ulcerative colitis: a randomised, double blind, placebo controlled study. Gut. 2005;54(7):960–965.
Meyers S, Sachar DB, Present DH, etal. Olsalazine sodium in the treatment of
ulcerative colitis among patients intolerant of sulfasalazine: a prospective, randomized, placebo-controlled, double-blind, dose-ranging clinical trial. Gastroenterology. 1987;93:1255–1262.
Nakada T, Kubota Y, Sasagawa I, et al. erapeutic experience of hyper-
baric oxygenation in radiation colitis: report of a case. Dis Colon Rectum. 1993;36:962–965.
Nguyen GC, Kaplan GG, Harris ML, Brant SR. A national survey of the preva-
lence and impact of Clostridium dicile infection among hospitalized inammatory bowel disease patients. Am J Gastroenterol. 2008;103:1443–
1450.
Present DH, Meltzer SJ, Krumholz MP, etal. 6-Mercaptopurine in the man-
agement of inammatory bowel disease: short- and long-term toxicity. Ann Intern Med. 1989;111:641–649.
Retsky JE, Kra SC. e extraintestinal manifestations of inammatory bowel
disease. In: Kirsner JB, Shorter RG, eds. Inammatory Bowel Disease. Bal- timore: Williams & Wilkins; 1995.
Riddell RH, Goldman H, Ransoho DF, et al. Dysplasia in inammatory
bowel disease: standardized classication with provisional clinical appli­cations. Hum Pathol. 1983;14(11):931–68.
Samuelsson S. Ulceros Colit och Proktit [dissertation]. Uppsala, Sweden: De-
partment of Social Medicine, University of Uppsala; 1976.
Sandborn WJ, Feagan BG, Marano C, etal. Subcutaneous golimumab induces
clinical response and remission in patients with moderate to severe ulcera­tive colitis. Gastroenterology. 2014;146:85–95.
Sandborn WJ, Feagan BG, Marano C, etal. Subcutaneous golimumab main-
tains clinical response in patients with moderate to severe ulcerative coli­tis. Gastroenterology. 2014;146:96–109.
Sandborn WJ, Tremaine WJ, Oord KP, et al. Transdermal nicotine
for mildly to moderately active ulcerative colitis. Ann Intern Med. 1997;126:364–371.
Sandborn WJ, Tremaine WJ, Schroeder KW, etal. A placebo-controlled trial
of cyclosporine enemas for mildly to moderately active le-sided ulcera­tive colitis. Gastroenterology. 1994;106:1429–1435.
Selhub J, Dhar GJ, Rosenberg IH, etal. Inhibition of folate enzymes by sul-
fasalazine. J Clin Invest. 1978;61:221–224.
Sheppach W, Sommer H, Kirchner T, etal. Eect of butyrate enemas on the
colonic mucosa in distal ulcerative colitis. Gastroenterology. 1992;103:51–
56.
Shetty K, Rybicki L, Brzezinski A, etal. e risk of cancer or dysplasia in ul-
cerative colitis patients with primary sclerosing cholangitis. Am J Gastro- enterol. 1999;94:1643–1649.
Silverberg MS, Satsangi J, Ahmad T, et al. Toward an integrated clinical,
molecular and serological classication of inammatory bowel disease: report of a Working Party of the 2005 Montreal World Congress of Gas­troenterology. Can J Gastroenterol. 2005;19(suppl A):5–36.
Sloth H, Bisgaard C, Grove A, etal. Collagenous colitis: a prospective trial of
prednisolone in six patients. J Intern Med. 1991;229:443–446.
Stenson WF, Cort D, Rodgers J, etal. Dietary supplementation with sh oil in
ulcerative colitis. Ann Intern Med. 1992;116:609–614.
Tedesco FJ, Volpicelli NA, Moore FS, etal. Estrogen- and progesterone-asso-
ciated colitis: a disorder with clinical and endoscopic features mimicking Crohn’s colitis. Gastrointest Endosc. 1982;28:247–249.
omas GA, Rhodes J, Ragunath K, et al. Transdermal nicotine compared
with oral prednisolone therapy for active ulcerative colitis. Eur J Gastroen- terol Hepatol. 1996;8:769–776.
omas GAO, Rhodes J, Mani V, etal. Transdermal nicotine as maintenance
therapy for ulcerative colitis. N Engl J Med. 1995;332:988–992.
Travis SPL, Danese S, Kupcinskas L, etal. Once-daily budesonide MMX in
active, mild-to-moderate ulcerative colitis: results from the randomised CORE II study. Gut. 2014;63:433–441.
Travis SPL, Farrant JM, Ricketts C, etal. Predicting outcome in severe ulcera-
tive colitis. Gut. 1996;38:905–910.
Tripodi J, Gorcey S, Burakoff R, etal. A case of diversion colitis treated
with 5-aminosalicylic acid enemas. Am J Gastroenterol. 1992;87:645–
647.
Truelove SC, Witts LJ. Cortisone in ulcerative colitis: nal report on a thera-
peutic trial. BMJ. 1955;2:1041–1048.
C U C: S

O
vi P. Kiran
Ra
INTR
ODUCTION
D
espite major advances in the medical treatment of ulcerative colitis (UC), surgery is still frequently required. Because the aim of surgery is to cure the disease, elimination of all colorectal mucosa is ideal. is operative strategy may need to be modied depending upon patient-, disease-, and treatment-related factors, which may have an impact on short- and long-term outcomes, as well as quality of life. 
EV
OLUTION OF SURGERY FOR
ULCERATIVE COLITIS
Surgery for UC evolved from the initial description of a colos­tomy in the late nineteenth century, through appendicostomy or cecostomy, to ileostomy with or without a blowhole colostomy, especially for toxic megacolon. Total abdominal colectomy with an ileorectal anastomosis subsequently developed as a technique that allowed resection of diseased colon without a stoma. However, patients who undergo this procedure have ongoing symptoms from proctitis, function is unpredictable, and there is an increasing risk of cancer in the rectum. ese disadvantages precluded widespread adoption of the ileorectal anastomosis and raised questions about its durability. Total proctocolectomy with end ileostomy allows the elimination of all diseased mucosa, but it includes a perma­nent external appliance. e continent ileostomy developed as an alternative. is procedure involves construction of an ileal pouch, made continent by a valve in the eerent limb, and anastomosed to the abdominal skin. It was not too much of a leap to use the anal sphincters instead of a valve and to anastomose the pouch to the anus instead of the abdominal skin. Construction of this ileoanal pouch allows removal of all diseased mucosa but maintains per anal defecation. It has become the standard surgical procedure for the treatment of UC. 
INDIC PERSONS WITH ULCERATIVE COLITIS
1. F
ailure of medical treatment: e presence of intractable symp
t
oms despite maximal medical therapy is a common indication for surgery. Failure of medical treatment also may be due to an inability to tolerate a reasonable maintenance dose of antiinam­matory medications that help patients avoid the development of drug-related adverse eects or an overall poor quality of life.
omplications: Emergency surgery may be required for acute
2. C co acolon, perforation, and hemorrhage. Stricture, dysplasia, and cancer are long-term complications that also may require surgery.
3. C
ancer: e risk of colon cancer in a patient with chronic UC has
een estimated to range from 2% at 20 years aer onset of disease
b
186
ATIONS FOR SURGERY IN
mplications such as severe acute or fulminant colitis, toxic meg-
o 43% at 35 years. e ndings of a meta-analysis suggested a
t cumulative incidence of colorectal cancer of 8.5% at 20 years and
17.8% at 30 years. Patients begin colonoscopic surveillance with biopsies at about 8 years aer the onset of their disease. When dysplasia is detected and conrmed by pathologic review, factors such as the location, type, and degree of dysplasia, its extent, and the severity of associated background colitis determine the cancer risk. Adenomatous dysplasia such as that found in a discrete ad­enoma is not necessarily an indication for colectomy as long as the adenoma can be treated endoscopically.
ther: Extraintestinal manifestations of ulcerative colitis and
4. O g
rowth retardation in children are other occasional indications
for surgery. 
OPERA
TIONS FOR ULCERATIVE
COLITIS
Ileostom
A
n ileostomy may be temporary or permanent. Temporary fecal diversion may protect a distal anastomosis, be part of the rst stage of a proctocolectomy in a sick patient, or be part of the treatment of a pouch complication. A permanent ileostomy may be needed when an insoluble distal pouch problem exists, when a patient is not t to undergo a staged proctectomy and creation of a pouch, or most com­monly aer a total proctocolectomy (TPC). 
Straight
A straight ileoanal anastomosis, which was initially performed in the 1940s, was associated with high rates of fecal urgency and fre­quency, leading to low overall satisfaction and problems with conti­nence. ese outcomes, which are expected in the absence of a fecal reservoir, along with the anastomotic complications of the proce­dure, led to the creation of an ileostomy in a signicant proportion of patients. A variation of the straight ileoanal anastomosis in which multiple 3- to 4-cm longitudinal myotomies are performed at three
­circumferential sites has been reported to have comparable function to the ileal pouch–anal anastomosis (IPAA) except for nocturnal soiling. 
Subtotal Colectom
A s toxic colitis or megacolon. It is less extensive than a proctocolec­tomy but avoids the risks associated with pelvic dissection and the creation of an anastomosis. It is therefore suitable for a rst-step
y
Ileoanal Anastomosis
y
ubtotal colectomy and ileostomy is the procedure of choice for
COLON
187
rocedure in malnourished or moribund patients and in those
p receiving large doses of steroids or immunosuppression, as well as when potential problems with sexual dysfunction or fertility need to be minimized. Performing a subtotal colectomy rather than a one-stage restorative proctocolectomy is safer when a diagnosis of Crohn disease cannot be excluded because it provides a large speci­men for histologic evaluation and preserves options for denitive treatment.
During a subtotal colectomy, preservation of the main trunk of the inferior mesenteric artery with division of the mesenteric branches minimizes damage to the autonomic nerves and allows easier identi­cation of the stump when a subsequent proctectomy is performed. Having a longer distal stump also allows the stapled end to reach the anterior abdominal wall for subcutaneous placement. Subcutaneous rather than intraperitoneal stump placement avoids the possibility of rectal stump blowout, which can cause peritonitis or a pelvic abscess and necessitates a repeat laparotomy. If the rectosigmoid stump is very friable, it is matured primarily as a mucus stula or secondarily aer 10 days of hanging out of the wound as a “tail” that is 10 cm in length and wrapped in gauze. If a repeat anastomosis is not intended, it is best to complete a proctectomy soon because the development of a stricture in the rectal stump as a result of persistent inammation may prevent adequate surveillance. 
Abdominal Colectom
lectomy with ileorectal anastomosis (IRA) is technically simple
A co and leads to rapid recovery, but bowel function is dependent upon the distensibility of the rectum, the severity of residual disease, and the adequacy of the anal sphincters. Transection of the rectum should be performed at the level of the sacral promontory to pre­serve the full length of the rectum for optimal capacity. An ileosig­moid anastomosis is an alternative when the distal sigmoid is spared from active disease. e risk of cancer in the rectum is 3% to 8% over long-term follow-up, and the overall failure rate for an IRA reaches 54% over 20 years. e main advantage of an IRA is that it avoids the hazards of pelvic dissection and thus merits consideration in specic circumstances. It allows restoration of health, completion of educa­tion and pregnancy in some young patients prior to a subsequent restorative proctocolectomy, and may be the denitive procedure in elderly patients who do not want to undergo an ileostomy. One-stage surgery is usually performed unless the patient has toxic colitis, intra­abdominal sepsis, and signicant malnutrition or unless doubt exists with regard to the normality of the rectal mucosa. In some circum­stances, resection of diseased colon at an initial subtotal colectomy may allow recovery of function and compliance of the rectum, which then becomes usable. Favorable results have been reported aer primary or secondary IRA, even when proctitis is present. e key aspect of functionality is rectal compliance, which is best judged by rigid proctoscopy. Anastomotic complications are similar whether the ileum is anastomosed to diseased or macroscopically normal rec­tum, and a routine proximal ileostomy is not indicated. Equivalent results have also been reported with both sutured and stapled anas­tomoses. e rectum needs to be monitored with yearly surveillance because cancer has been reported to occur in both nonfunctioning and functioning rectums. 
Ileostom
e Turnbull blowhole colostomy and loop ileostomy described in
 the 1960s has a role in extremely ill patients and in situations in which colonic mobilization is hazardous, such as a contained perforation, pregnancy, or a high-lying splenic exure. e main advantage of the procedure is that the colon is not disturbed; the main disadvantage is that the diseased colon is le behind and may lead to persistent toxic­ity. e procedure is contraindicated in patients with free perforation
y and Blowhole Colostomy
y with Ileorectal Anastomosis
or bleeding. A denitive procedure is performed aer the patient has recovered. 
otal Proctocolectomy and Ileostomy
T
with a Brooke ileostomy is curative and is reported to be asso-
A TPC ciated with good quality of life. However, the need for an external appliance, with the complications of leakage around the bag, skin rashes and infections, potential psychosocial issues, and problems with healing of the perineal wound, are disadvantages. Quality of life may be better aer an IPAA than with an ileostomy. A TPC and ileostomy is undoubtedly the best option for patients with poor anal sphincter function and for patients who want to address their dis­ease in the least complicated manner with one operation and a mini­mal chance of needing another operation. A single-stage procedure is avoided in patients with fulminant disease, toxic megacolon, and severe malnutrition or perianal sepsis. Although a subtotal colectomy is the procedure usually performed for severe colonic hemorrhage, a total proctocolectomy occasionally may be indicated for patients with signicant rectal hemorrhage.
Proctectomy Surgical Technique
Aer the colectomy is completed, the rectum may be dissected within the mesorectum to avoid damage to autonomic nerves, but this dis­section is associated with greater blood loss. Dissection in the avas­cular plane between the investing layer of fascia of the rectum and the presacral fascia to the lower border of the third sacral vertebra followed by dissection close to the rectal wall results in less loss of blood and still preserves the pelvic nerves. e lateral rectal dissec­tion is kept close to the rectal wall at the level of the lateral ligament. Anteriorly, the rectal dissection is carried out on the rectal side of the fascia of Denonvilliers, exposing the vertical muscle bers of the rectum but not the seminal vesicles, and the perineal proctectomy is completed with use of the endoanal technique. An intersphincteric dissection is performed, preserving the anal skin, external sphinc­ter, and levator muscles, because this approach has been reported to be associated with a lower incidence of impotence and a low rate of unhealed perineal wound. Primary closure of the perineal wound is then performed. Alternatively, the anus may be removed completely or not at all. e rectum can be transected at the level of the leva­tors, closing the rectal stump by sutures or staples and thus avoiding a perianal wound altogether. A mucosal proctectomy with or without closure of the anorectal stump has also been proposed.
Up to 11% of patients may have an unhealed perianal wound that is managed by serial wound curettage and cautery, resurfac­ing with skin graing, or lling of cavities with vascularized pedicle muscle gras such as gracilis, semimembranosus, rectus abdominis, or omentum. An inferior gluteal myocutaneous gra has also been used. When a proctocolectomy is performed in the acute setting, it is associated with high mortality and morbidity rates. Pelvic dissection may lead to a pelvic abscess, an enteric stula, or autonomic nerve damage. 
Continent Ileostom
Developed by Nils Kock, the continent ileostomy procedure provides freedom from the need for an external appliance. It consists of the creation of an ileal reservoir (pouch), which is connected to the skin of the abdominal wall by a spout. By intussuscepting the bowel, a nipple valve is created at the exit of the spout from the pouch; it is stabilized by sutures or staples. is valve prevents leakage of stool. Stool is evacuated by the intermittent insertion of a drainage catheter though the ush ileostomy into the pouch. e pouch consists of an S-shaped reservoir made of three 15-cm limbs of small bowel and an exit conduit containing the valve. Patients with UC who are not
y
188
Chr
C UlCera
oni
tive Colitis:
sUrgiCal options
c
andidates for an IPAA, who prefer to avoid an IPAA, or whose IPAA fails are potential candidates for the procedure. In the latter case, the initial pouch can be modied for use as the continent ileostomy pouch. Although most patients who undergo the continent ileostomy procedure have a good quality of life, long-term pouch revision and excision rates are high, predominantly because of slippage of the nip­ple valve. Various modications have been described to help anchor
of patients still require a repeat operation for valve slippage, prolapse, and incontinence. 
Restorativ
e restorative proctocolectomy procedure, developed in the 1970s,
e Proctocolectomy
is currently the gold standard operation for patients with UC who are undergoing surgery. e components of this procedure are total col­ectomy, proctectomy, and construction of an ileal reservoir with the creation of an IPAA. A compliant sac made up of loops of small bowel constitutes the reservoir. e procedure may be performed in one, two, or three stages, and the pouch-anal anastomosis is either stapled or hand sewn. In the stapled procedure, the anal transitional zone is preserved and anastomosis is performed 1 cm above the dentate line. Annual biopsy surveillance of the anal transitional zone is then performed. Patients who are poorly compliant at follow-up and those with marked extraintestinal manifestations of UC are best treated with an anal mucosectomy and a hand-sewn anastomosis.
A restorative proctocolectomy can be performed with accept­able complication rates, functional outcomes, and quality of life and is applicable to several subgroups of patients. Satisfactory function has been reported in children younger than 10 years and also in elderly persons as long as they have reasonable sphincter function. In indeterminate colitis, the short- and long-term results are similar to those with UC; however, such patients who are then diagnosed with Crohn disease have worse outcomes. IPAA has also been performed in patients in whom colorectal carcinoma complicates inammatory bowel disease, although deterioration in the function of the pouch occurs when such patients undergo radiotherapy.
Pouch Configuration and Anastomosis
It is generally agreed that functional results of IPAA are the same regardless of the pouch congurations (J, S, or W). Evacuation disor­ders are more common with the S pouch if the exit conduit is longer than 2 cm because this conguration may lead to obstructive def­ecation. e J pouch conguration is the most popular because of the simplicity of its construction. Some controversy exists regarding the inuence of anastomotic technique on pouch function. A stapled IPAA is associated with a lower incidence of sepsis and stretch­induced sphincter trauma and preserves the anal transitional zone. e stapled anastomosis functions better, has fewer complications, and is associated with a lower pouch excision rate. 
Staging the Procedure
For carefully selected patients in whom the risk of anastomotic leak is likely minimal, the procedure can be performed without a diverting stoma (in one stage). However, an anastomotic leak can lead to sig­nicant morbidity and potentially aects long-term pouch function, predisposing to pouch failure. us, in the majority of instances, a two-stage procedure is preferable in which the ileoanal pouch is pro­tected with a temporary loop ileostomy because the ileostomy reduces the consequences of an anastomotic leak. Patients with inactive or mild colitis and those for whom steroids have either been discon­tinued or tapered to a low dose are candidates for such an approach. For patients with more orid colitis and those taking high-dose steroids or potent immunosuppressive medication and anti–tumor necrosis factor agents (which may predispose to post-IPAA septic
complications), a three-stage approach is safest. An initial subtotal colectomy minimizes disease and allows the withdrawal of medica­tion and improvement of nutrition before a subsequent completion proctectomy and IPAA. is approach has reduced surgical risks and improved long-term pouch retention. 
Technique of Creation of an Ileoanal J Pouch
Standard oral and mechanical bowel preparation is undertaken before creation of an ileoanal J pouch. e operation begins with a midline incision for open surgery or port placement for laparoscopy, aer which the colon is mobilized from the pelvic brim proximal to the middle colic vessels, which are preserved. High ligation of the inferior mesenteric vessels is then performed. Dissection is contin­ued into the pelvis using electrocautery in the plane between the pre­sacral fascia and the investing fascia propria of the rectum. Dissection in this plane is then carried down to the pelvic oor, aer which the distal rectum is stapled across 1 cm above the dentate line. A J pouch 20 cm in length is fashioned from the distal ileum through the use of staples and is anastomosed to the anal canal proximal to the dentate line. In some circumstances in which problems may exist with reach of the pouch to the anal canal, the S-shaped design allows the pouch to reach an extra 2 cm. e pouch-anal anastomosis is completed with the use of circular stapling device for a stapled anastomosis. When a hand-sewn anastomosis is performed, mucosectomy of the anorectal remnant is completed prior to anastomosis. 
Problems with Reach of the Pouch
Minimal information is available on the rate of abandonment of IPAA as a result of technical diculties; in two reported series, this rate has been suggested to be 4.1% and 6%. e reach of the pouch is inu­enced by the length of the superior mesenteric artery, the orienta­tion of the small bowel, and the anatomy of the pelvis and mesentery. Problems with pouch reach are traditionally considered to aect tall patients and those with a high body mass index, especially when they are men. Weight loss before surgery may be helpful. Some maneuvers at the time of surgery may facilitate reach of the pouch to the anal canal. ese maneuvers include high ligation of the ileocolic ves­sels, release of the small bowel mesentery from the retroperitoneum, mobilization of the duodenum, excision of the redundant mesenteric tissue lateral to the superior mesenteric vessels (“gib-sail”), and the creation of peritoneal-releasing incisions along the mesenteric edge of the small intestine. Although ligation of some of the branches or of the main trunk of the superior mesenteric artery itself have also been described, this maneuver is associated with a risk for compromise of blood supply to the entire small intestine.
Diculty with reach of the pouch to the anal canal needs to be anticipated prior to rectal transection so the operation may be modi­ed accordingly to facilitate an ileal pouch rectal anastomosis. Prior to transection of the rectum, a pouch is simulated and the most dependent portion eventually destined to connect to the anal canal is held in a Babcock forceps and delivered into the pelvis. e simulta­neous passage of a gloved nger into the anal canal allows conrma­tion of reach of the Babcock forceps to the intended level of rectal t
ransection. Alternatively, if the apex of the small bowel reaches below the symphysis pubis, then an IPAA is likely to be feasible. If the signs point to a problem with reach, the rectal stump may be intentionally le slightly long to minimize tension on the IPAA. Orientation of the pouch in such a way as to direct the pouch mesentery anteriorly may produce less tension on the anastomosis. When preliminary assess­ment suggests that these eorts will fail, consideration may be given to the creation of an “S” instead of a “J” pouch. In the rare circumstance in which the pouch has been created but cannot then be mobilized adequately for anastomosis to the anal canal, the end of the pouch may be closed o. e pouch is then sewn in the pelvis and diverted with a proximal ileostomy. Aer 2 years, an IPAA may be attempted again in the hope that mesenteric lengthening has occurred. 
COLON
189
OUTCOMES OF ILEAL POUCH–ANAL ANAST
F
azio etal recently reported outcomes for a large number of patients with prolonged follow-up aer IPAA, suggesting that excellent long­term functional outcomes and quality of life can be expected.
Complications after Ileal Pouch–Anal Anastomosis
P
ouch-related complications occur postoperatively in the interme­diate and long term. Immediate postoperative sepsis occurs in 5% to 20% of all cases, and the most common early complications are anastomotic leak or stricture, abdominal wound infections, and small bowel obstructions. Ileostomy-related complications include small bowel obstruction, high output, prolapse, retraction, dehydra­tion, electrolyte imbalance, stenosis, parastomal hernia, and leakage. Ileostomy closure is associated with a 5% to 25% incidence of small bowel obstruction and anastomotic complications. Other complica­tions specic to restorative proctocolectomy include pouchitis, stu­lae (pouch-vaginal, pouch-cutaneous, or pouch-perineal), ischemia of the pouch, water and electrolyte imbalance, and obstruction. Sex­ual disturbances as a result of damage to the autonomic nerves dur­ing rectal dissection and reactionary or secondary bleeding also may occur. Pouchitis is discussed specically in Chapter 39. 
Overall Quality of Life
e majority of patients are satised with their quality of life aer surgery for ulcerative colitis, with good functional results expected in the majority of patients even upon long-term follow-up. Quality of life also continues to be excellent with minimal deterioration in pouch function with time. 
Function of the Pouch
e median daily stool frequency varies from 7.5 at 1 month post­operatively to 5.4 at 1 year postoperatively. When function stabilizes, the stool frequency is expected to be ve during the day, whereas the range of nighttime defecation is zero to three, depending on the time of the evening meal. Although 18% to 40% of patients may experi­ence some element of urgency, seepage, incontinence, or the use of pads on prolonged follow-up, a similar proportion may be incon­tinent preoperatively. Regardless, most patients report satisfaction with their medical situation. Similar long-term function results can be expected aer creation of an IPAA in pediatric patients. 
Pouchitis
e cumulative risk of pouchitis increases with increased duration
 of follow-up. A signicantly lower incidence of pouchitis occurs in nonsmokers and in patients with primary sclerosing cholangitis compared with matched control subjects. Patients with extraintesti­nal manifestations of UC may be more prone to pouchitis than those without such manifestations. Anastomotic strictures and excessively large pouches that empty poorly may be predisposed to pouchitis. Frequent attacks and attacks refractory to treatment may be due to previously unrecognized Crohn disease. 
Pouch Failure
P
ermanent pouch failure, dened as pouch excision or permanent diversion, occurs in 5% to 20% of cases. e most common reasons for pouch excision include pelvic sepsis, with or without a stula,
OMOSIS
and poor function. Most pouch failures occur in the rst 2 years aer surgery, and dehiscence of IPAA, poor function, pouchitis, and peri­anal disease are the major causes of pouch failure. Ischemia of the pouch, diagnosis of Crohn disease, chronic pouch sepsis, and refrac­tory pouchitis are also causes of pouch failure. ere appears to be no increased incidence in pediatric patients. 
ouch Fistula
P
Fi
stulas involving the pouch occur in 3% to 17% of patients. Fistulae may be pouch vaginal, pouch perineal, pouch cutaneous, and pouch perianal. e most common is the pouch-vaginal stula. Successful repair can be achieved in 60% of patients, although multiple proce­dures are oen required. Procedures that can be performed include stulotomy, debridement, transanal closures, seton, vaginal ap repairs, and endoanal ileal advancement aps with or without sphinc­teroplasty. Nonlocal treatment options include temporary diversion, transabdominal closures, revision of the pouch, bulbocavernosus ap repairs, vulval fat interpositions, and gracilis muscle ap repairs. 
Risk of Car
ysplasia of the pouch remains a concern for patients with UC under-
D going IPAA, and an association of villous atrophy with pouch dysplasia has been reported. Carcinoma in the anal transition zone aer IPAA is another potential concern. Data from long-term follow-up suggests that dysplasia is infrequent, is most common in the rst 2 to 3 years aer surgery, and may disappear on a repeat biopsy. When persistent dysplasia develops in the anal transition zone, it can be managed by removal of the diseased mucosa, with a transanal pouch–anal reanasto­mosis. Patients who are at a high risk of developing dysplasia or cancer in the anal canal include those with colorectal cancer at index surgery, rectal dysplasia, and any dysplasia in the colon identied preopera­tively. A mucosectomy should be performed in these patients. Cancer also may develop in patients who undergo a mucosectomy because of incomplete stripping of the mucosa, with up to 21% of patients having retained mucosal epithelial cells in the anal transitional zone. Pouch and anal transition zone surveillance are indicated for every patient with an IPAA and should be performed every 1 to 2 years depending on circumstances and length of follow-up. 
ertility, Sexual Problems, and Obstetric Outcome
F
IP
AA is associated with reduced fertility. Although some patients report sexual dysfunction aer the procedure, the incidence of seri­ous sexual dysfunction such as impotence (<1%) and retrograde ejaculation (<5%) is low. In female patients, a signicant increase in vaginal dryness and dyspareunia may occur postoperatively without any change in sexual desire, arousal, or frequency of inter­course, whereas the majority of male patients report no change or an improvement in their sexual relationship with their partner. Some controversy exists with regard to whether pregnant patients with a pouch should undergo vaginal delivery or cesarean section, but vagi­nal delivery appears to be safe and associated with good quality of life even when some deterioration of pouch function has occurred. 
Extraintestinal Manif
lthough some extraintestinal manifestations disappear aer col-
A
ctomy, others may continue to progress despite the elimination of
e intestinal disease. romboembolic events and erythema nodosum are commonly cured or improved aer proctocolectomy, whereas ocular manifestations and primary sclerosing cholangitis are unaected. 
cinoma
estations
190
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tive Colitis:
sUrgiCal options
Quantification of Risk for Pouch Failure after Ileal Pouch Anal Anastomosis Surgery
e Cleveland Clinic ileal pouch failure model was developed to predict the risk of ileal pouch failure in clinical practice on a longitudinal basis. Patient diagnosis, prior anal disease, abnormal anal manometry, patient comorbidity, pouch-perineal or pouch-vaginal stulae, pelvic sepsis, anastomotic stricture, and separation were found to be independent pre­dictors of pouch survival and were used in the nal multivariate model. 
Salvage of the Failed Pelvic Pouch
Pouch salvage may be possible in 50% to 95% of patients. e incidence of early and late complications aer pouch salvage is high, and delayed healing of the perineal wound is one of the common complications. Indications for salvage surgery or major revision of the pouch include a long eerent limb, a pouch or anastomotic-associated stula, peri­pouch sepsis, an anastomotic stricture, and previous pouch excision (provided the anal sphincter function continues to be good). Salvage by abdominoanal disconnection and repeat IPAA has been reported to result in good function in patients with nonseptic complications, and redo pouch is the procedure of choice for pouch dysfunction result­ing from a long exit conduit and long strictures. Revision of the pouch can also be performed with good results for septic complications, but a worse outcome may be expected compared with salvage aer nonseptic complications, and these patients should be warned of the possibility of a permanent stoma when undergoing IPAA. In the absence of gross sepsis or edema, local repairs are attempted rst, with stulas that are close to the anal verge and for short strictures that are unresponsive to dilation. A transabdominal redo pouch is indicated aer failure of multiple local treatment procedures, presence of a long exit conduit, long stricture, or chronic presacral sinus.
S
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S t
g g e
C
ornish JA, Tan E, Teare J, et al. e eect of restorative proctocolectomy
on sexual function, urinary function, fertility, pregnancy and delivery: a systematic review. Dis Colon Rectum. 2007;50(8):1128–1138.
da Luz Moreira A, Kiran RP, Lavery I. Clinical outcomes of ileorectal anasto-
mosis for ulcerative colitis. Br J Surg. 2010;97(1):65–69.
Fazio VW, Kiran RP, Remzi FH, etal. Ileal pouch anal anastomosis: analysis of
outcome and quality of life in 3707 patients. Ann Surg. 2013;257(4):679–
685.
Gu J, Remzi FH, Shen B, etal. Operative strategy modies risk of pouch-relat-
ed outcomes in patients with ulcerative colitis on preoperative anti-tumor necrosis factor-α therapy. Dis Colon Rectum. 2013;56(11):1243–1252.
Gullberg K, Stahlberg D, Liljeqvist L, etal. Neoplastic transformation of the
pelvic pouch mucosa in patients with ulcerative colitis. Gastroenterology. 1997;112(5):1487–1492.
Kiran RP. e ideal design of the ileoanal pouch: one for each patient? Dis
Colon Rectum. 2012;55(12):1201–1202.
Kiran RP, Ahmed Ali U, Nisar PJ, etal. Risk and location of cancer in patients
with preoperative colitis-associated dysplasia undergoing proctocolec­to my. Ann Surg. 2014;259(2):302–309.
McLeod RS, Lavery IC, Leatherman JR, etal. Factors aecting quality of life
with a conventional ileostomy. World J Surg. 1986;10(3):474–480.
Nicholls RJ. Restorative proctocolectomy with various types of reservoir.
World J Surg. 1987;11(6):751–762.
O’Riordain MG, Fazio VW, Lavery IC, et al. Incidence and natural history
of dysplasia of the anal transitional zone aer ileal pouch-anal anas­tomosis: results of a ve-year to ten-year follow-up. Dis Colon Rectum. 2000;43(12):1660–1665.
Reilly WT, Pemberton JH, Wol BG, et al. Randomized prospective trial
comparing ileal pouch-anal anastomosis performed by excising the anal mucosa to ileal pouch-anal anastomosis performed by preserving the anal mucosa. Ann Surg. 1997;225(6):666–676. discussion 676–677.
Sjodahl R, Lemon E, Nystrom PO, Olaison G. Complications, surgical re-
vision and quality of life with conventional and continent ileostomy. Acta Chir Scand. 1990;156(5):403–407.
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