Version July 2025
INTRODUCTION —
Because the risk for colorectal cancer (CRC) is increased in patients with inflammatory bowel disease (IBD), the goal of surveillance colonoscopy is to detect dysplasia, the precursor of colorectal cancer. We recommend surveillance for dysplasia and colorectal cancer in patients with IBD, and our approach is generally consistent with multiple societies worldwide [1-7].
The epidemiology, risk factors, and pathology of colon cancer in IBD and the evidence supporting a role for surveillance will be reviewed here. Methods for cancer surveillance will also be discussed. The risk factors, clinical manifestations, and diagnosis of IBD are discussed separately.
●(See "Definitions, epidemiology, and risk factors for inflammatory bowel disease".)
●(See "Clinical manifestations, diagnosis, and prognosis of ulcerative colitis in adults".)
●(See "Clinical manifestations, diagnosis, and prognosis of Crohn disease in adults".)
EPIDEMIOLOGY —
The risk of colorectal cancer (CRC) in patients with inflammatory bowel disease (IBD) is increased compared with the general population. In a population-based study of over 96,000 patients with IBD, the overall risk of CRC was 1.29 cases per 1000 person-years [8].
The mean age of developing CRC in the setting of IBD is lower than for sporadic CRC (40 to 50 years versus 60 years) [9,10]. (See "Epidemiology and risk factors for colorectal cancer", section on 'Epidemiology'.)
Male sex may be a risk factor for colorectal cancer in IBD patients. In one population-based study of more than 7000 patients with IBD, males had a 60 percent higher risk of CRC (RR 1.6 95% CI 1.2-2.2) compared with females [11]. The effect of sex was seen only after ten years of follow-up and limited to patients diagnosed before age 45. This difference may be explained by variation in the extent of inflammation, or by factors related to patient behaviors that affect compliance with medication and surveillance [12].
Ulcerative colitis — The association of ulcerative colitis (UC) and colorectal cancer depends mainly upon the duration, extent, and activity of disease [8,13-18]. In a population-based cohort study including over 96,000 patients with IBD (with >10 years follow up in >50 percent of the cohort), patients with extensive colitis (defined by the Montreal classification as disease extending proximal to the splenic flexure) had an increased risk of CRC compared with individuals from the general population who were matched for age, sex, year of birth, and place of residence (521 versus 343 cases of CRC of per 1000 person-year follow up; adjusted hazard ratio [aHR] 1.88, 95% CI 1.72-2.07) [8]. In contrast, the risk of CRC in patients with ulcerative proctitis or left-sided colitis was not significantly higher compared with the general population (aHR 0.97, 95% CI 0.76-1.25 and aHR 0.90, 95% CI 0.72-1.14, respectively).
The risk factors for CRC in patients with UC are [19]:
●Presence and severity of inflammation – The presence and severity of inflammation appear to be important markers of risk [20-22]. In a meta-analysis of four studies including 1025 patients with ulcerative colitis, mucosal inflammation (including both histologic and endoscopic inflammation) was associated with an increased risk of colorectal neoplasia (OR 3.5, 95% CI 2.6-4.8) [22].
In a case-control study, endoscopic features of severe inflammation, such as pseudopolyps and strictures, were associated with an increased risk of colorectal neoplasia (OR 2.29, 95% CI 1.28-4.11 and OR 4.62, 95% CI 1.03-20.8, respectively) [23]. However, data on pseudopolyps as a risk factor for dysplasia have been mixed [24,25]. A case-control study (in which cases and controls were matched for the extent and duration of UC) also found that the risk of CRC was increased in patients with a history of inflammatory pseudopolyps [24]. In a subsequent study of 462 patients with IBD, pseudopolyps were not associated with increased risk of CRC after a median follow up of nearly five years [25]. (See 'Inflammatory pseudopolyps' below.)
●Age at disease onset/disease duration – Younger age at disease onset/duration of disease appears to be a risk factor in patients with extensive colitis [8,26]. In one series, the absolute risk of CRC in patients with extensive colitis was 30 percent after 35 years of disease [26]. The risk was increased in those with the onset of symptoms prior to age 15 years. However, in other reports, the age of onset of colitis did not increase the risk of CRC after adjusting for the longer period of time that young patients were at risk and the extent of the disease [27].
●Ileitis – One study suggested that ileitis (in which mucosal inflammation involves the terminal ileum) may be an independent risk factor for CRC [28]. However, other studies have not confirmed this association [29,30]. (See "Endoscopic diagnosis of inflammatory bowel disease in adults", section on 'Direct visualization'.)
Extensive colitis — Patients with extensive colitis, defined by the Montreal Classification as disease extending proximal to the splenic flexure, have the greatest risk of CRC. Compared to an age-matched population, the risk begins to increase 8 to 10 years following the onset of symptoms [8,31,32]. In a meta-analysis, cumulative risks of CRC after 10, 20, and greater than 20 years of disease were 1, 2, and 5 percent, respectively. High-risk groups were patients with extensive colitis and an IBD diagnosis before age 30 (SIR 6.4, 95% CI 2.4-17.5 and 7.2, 95% CI 2.9-17.8, respectively) [33]. In older epidemiologic studies, the incidence was higher than in recent decades [26,31,34-36].
Left-sided colitis — Most studies have found that the risk of CRC increases after 15 to 20 years (approximately one decade later than in extensive colitis) in patients with colitis confined to the left colon (ie, distal to the splenic flexure) [37,38].
Proctitis — Patients with ulcerative proctitis and distal proctosigmoiditis are probably not at increased risk for CRC and do not need to be followed with endoscopic surveillance [26].
Crohn disease — The risk of CRC in longstanding Crohn disease (CD) involving the colon is probably comparable to UC [27,39,40]. However, not all studies reached these conclusions and thus the magnitude of risk in patients with CD remains unsettled. In a population-based study, the relative risk of colon cancer was 2.5 in patients with CD and 5.6 in those with disease restricted to the colon [27]. The relative risk was even greater in patients who were less than 30 years of age at the time of diagnosis (RR 21, compared with those diagnosed after age 30). Similar findings have been reported in other studies [41].
CRC in CD is observed in a similar time frame as in UC [42,43]. This was illustrated in one series that included 80 patients with CRC complicating UC or CD [42]. The median duration of disease prior to the diagnosis of CRC was comparable for CD and UC (15 and 18 years, respectively). The median age at diagnosis of CRC was 55 years in CD and 43 years in UC. One series found that CD patients undergoing surgery for cancer had more advanced CRC than patients with UC [44].
Ileal pouch anal anastomosis — The incidence of CRC in patients with IBD who have undergone restorative proctocolectomy with an ileal pouch anal anastomosis (IPAA) is low [45]. In a case-control study that included 1200 patients with IBD (1053 with UC, 46 with CD, and 101 with indeterminate colitis) and IPAA, the cumulative incidence for pouch carcinoma at 5, 10, 15, and 20 years was 0.6, 1.4, 2.1, and 3.3 percent, respectively. The only risk factors for pouch neoplasia were a prior history of colorectal dysplasia and carcinoma (HR 3.8, 95% CI, 1.4-10.2 and HR 24.7 95% CI, 9.6-63.4, respectively). (See "Restorative proctocolectomy with ileal pouch-anal anastomosis: Laparoscopic approach", section on 'Patient selection criteria for laparoscopic RPC-IPAA'.)
Primary sclerosing cholangitis — An increased risk of CRC has been observed in patients with UC complicated by primary sclerosing cholangitis (PSC) [8,14]. CRC in patients with PSC was more likely to occur in the right colon, suggesting a possible role of bile acids in oncogenesis (a hypothesis supported by studies showing a protective effect of ursodeoxycholic acid) [46,47]. (See "Primary sclerosing cholangitis: Inflammatory bowel disease and colorectal cancer".)
MOLECULAR PATHOGENESIS —
The pathogenesis of colon cancer in inflammatory bowel disease (IBD) differs from sporadic colorectal cancer (CRC), and distinct genetic features are present in colorectal tumors in IBD patients [48-50]. (See "Molecular genetics of colorectal cancer".)
The genetic features of IBD-associated tumors represent potential therapeutic targets and could be used to develop disease-specific diagnostic markers [48,50,51]. In genomic analyses of IBD-associated cancers, there were lower rates of APC and KRAS mutations compared with sporadic cancers while alterations in TP53, IDH1, and MYC were more frequent [48,50].
Loss of heterozygosity for the p53 gene and src activation occur earlier in cancers associated with IBD than in sporadic CRC [52-54]. Src activity in UC correlates with the degree of dysplasia [55].
ENDOSCOPIC AND HISTOLOGIC FINDINGS
Colorectal cancer — Colorectal cancer (CRC) complicating inflammatory bowel disease (IBD) may appear mass-like, nodular, ulcerated, or plaque-like [56]. Diffusely infiltrative cancer may be difficult to detect. As in sporadic colorectal cancer, most lesions in the colon are adenocarcinomas [57]. (See "Pathology and prognostic determinants of colorectal cancer".)
IBD-related cancer occurs in areas with presently or previously active endoscopic and/or histologic inflammation [58].
Dysplasia — Dysplastic epithelium is one of the most important biomarkers for malignancy and provides the rationale for surveillance. Dysplasia is a precursor to IBD-associated colorectal cancer.
Synchronous tumors are more common in IBD than in sporadic CRC and can be found in the colon, rectum, anus, and internal or external fistulous tracts [55,57].
Endoscopic description — Most dysplasia in IBD is endoscopically visible [59-61]. Terms such as dysplasia-associated lesion or mass (DALM) and adenoma-like or non-adenoma-like DALM, should be abandoned in favor of describing lesions using the Paris classification, modified by the Surveillance for Colorectal Endoscopic Neoplasia Detection and Management in Inflammatory Bowel Disease Patients International Consensus (SCENIC) group to incorporate features specific to IBD [1,4,62]. Lesion location should be identified as within or outside an area of known colitis and lesion description should include the following (table 1):
●Morphology – Polypoid (pedunculated or sessile) or nonpolypoid (slightly elevated, flat, or depressed).
●Borders – Distinct or indistinct.
●Features of submucosal invasion (if present) – Depressions, overlying ulceration or failure to lift with attempted submucosal injection.
Using these descriptors, lesions can be classified as endoscopically resectable or endoscopically unresectable. Endoscopically resectable lesions have the following characteristics:
•Distinct margins (when viewed with chromoendoscopy) [63].
•The lesion appears to be completely removed on visual inspection after endoscopic resection.
•Histologic examination of the resected specimen is consistent with complete removal (figure 1).
Kudo pit pattern classification has not routinely been applied to lesion characterization in colitis surveillance, since regenerative mucosa can demonstrate pit pattern III and IV without any associated dysplasia (figure 2) [64]. Identifying a Kudo pit pattern I or II may have role in ruling out neoplasia [65,66].
Histologic classification — In the United States, dysplasia is classified as either intestinal- or gastric-type based on the histologic characteristics of cell differentiation. In each of these two categories, there are sub-categories that include serrated lesions, goblet cell deficient and crypt cell types. Some cases may show a mixture of both intestinal and gastric differentiation. The grade of dysplasia is qualified as [67,68]:
●Negative
●Indefinite
●Positive (with subgroups of low-grade and high-grade dysplasia)
In other parts of the world, but particularly in parts of Europe and Asia, pathologists prefer the Modified Vienna Classification [69].
Distinguishing dysplasia from reactive changes — Histologically, dysplasia may be difficult to distinguish from epithelial regeneration in the setting of mucosal inflammation or ulceration [70]; as such, IBD surveillance is ideally performed when the patient is in endoscopic remission. Dysplasia should be confirmed by a pathologist with expertise in IBD since interobserver variability is substantial, especially for discriminating highly reactive changes from true dysplasia. Common architectural and cytologic abnormalities seen in dysplastic epithelium include [67,71-73]:
●Increased mitoses (typical and atypical)
●Increased nuclear size
●Variation in the size and shape of nuclei (pleomorphism)
●Altered nuclear polarity
●Hyperchromaticity
●Lack of surface maturation
●Stratification of nuclei
●Abrupt transition
●Back-to-back gland pattern, cribriform
Regenerative changes are usually most prominent at the bases of the crypts, show evidence of surface maturation, and do not exhibit architectural disturbances [67]. One study found that immunostaining for alpha-methylacyl-Coa-racemase, a mitochondrial and peroxisomal enzyme overexpressed in many types of cancers, was highly specific for detecting dysplasia and distinguishing regenerating epithelium from true dysplasia [74].
GOAL OF SURVEILLANCE —
The goal of surveillance for patients with inflammatory bowel disease (IBD) is to detect dysplasia, which is associated with a high risk of colorectal cancer (CRC) and to reduce mortality in those who develop colon cancer. Despite the lack of randomized controlled trials, screening colonoscopy is recommended by multiple societies and is the standard of care [5,6,75-80]. In a large cohort study of IBD patients, the incidence of colon cancer was higher in those who did not have a colonoscopy within 6 to 36 months of the cancer diagnosis compared with those who did have surveillance (2.7 versus 1.6 percent). This study also demonstrated improved survival in patients with IBD undergoing colonoscopy compared to those without surveillance (OR 0.34, 95% CI 0.12-0.95) [81].
The body of literature supporting the role of colonoscopy for surveillance in IBD patients is mainly derived from case series, case-control studies, and population-based cohort studies, which suggest that surveillance results in an earlier cancer stage at diagnosis and improved CRC-related survival [81-84]. In a systematic review of four observational studies of patients with IBD, the surveillance group had fewer deaths from CRC compared with no surveillance (8 versus 22 percent; OR 0.36, 95% CI 0.19-0.69) [85].
Strategies to improve detection of dysplasia are warranted to reduce the risk of interval cancer in IBD because advanced CRC can occur despite surveillance [15,86]. In one study of over 1200 patients with UC or Crohn disease enrolled in a surveillance colonoscopy program, 1.3 percent were diagnosed with CRC; 30 percent of CRC cases were determined to be interval cancers [87]. An analysis of a prospectively collected surveillance database demonstrated that over 50 percent of the cancers were interval cancers [15]. These studies were based on a variety of surveillance methods, some of which are no longer commonly used.
APPROACH TO SURVEILLANCE
Patient selection and timing for initial surveillance — Timing of initial endoscopic surveillance is informed by disease extent, disease duration, comorbid conditions (eg, primary sclerosing cholangitis), and surgical history:
●Disease involving more than one-third of the colon – For patients with ulcerative colitis (UC) and Crohn disease (CD) involving more than one-third of the colon, we perform screening colonoscopy eight years after disease or symptom onset to initiate surveillance for colorectal neoplasia. Surveillance remains the standard of care, although reduction in mortality due to surveillance has not been clearly established. (See 'Goal of surveillance' above.)
Ideally, surveillance colonoscopy is performed when the patient has achieved clinical and endoscopic remission. We document endoscopic disease activity using an endoscopic scoring system [88,89] (see "Endoscopic diagnosis of inflammatory bowel disease in adults"):
•For UC, the Mayo endoscopic subscore is commonly used as a target for treatment with a proposed remission score of 0 to 1 (calculator 1) [90,91]. The Ulcerative Colitis Endoscopic Index of Severity (UCEIS) and Ulcerative Colitis Colonoscopic Index of Severity (UCCIS) are validated endoscopic scores; UCEIS has a proposed remission score of ≤1.
•For CD, the Simple Endoscopic Score for Crohn Disease (SES-CD) has been used with a proposed remission score of ≤3 [90,92].
At the time of surveillance colonoscopy, we also obtain histologic staging biopsies to assess mucosal healing and the extent of disease activity.
●Disease involving one-third of the colon or less – We initiate surveillance colonoscopy at eight years after disease onset for patients with isolated proctitis or disease involving one-third of the colon or less to reassess disease extent as colitis may progress over time. In a study of a pathology database, the diagnosis of colorectal cancer (CRC) was delayed or missed in 17 to 35 percent of inflammatory bowel disease patients when screening was delayed until 8 to 10 or even 15 years, prompting many societies to adopt a shorter duration of disease at which to recommend starting surveillance [93,94].
●History of primary sclerosing cholangitis – We initiate surveillance at the time of diagnosis in patients with a history of primary sclerosing cholangitis.
●Family history of colon cancer – We discuss screening with patients with a strong family history of CRC (ie, first-degree relative diagnosed before age 50 years) and offer colonoscopy depending on the age and preference of the patient [1,2,95]. (See "Screening for colorectal cancer in patients with a family history of colorectal cancer or advanced polyp".)
●History of colorectal surgery – Patients who had proctocolectomy and ileal pouch anal anastomosis (IPAA) for the indication of dysplasia or colon cancer should undergo surveillance pouchoscopy beginning one year after surgery because of the risk of developing dysplasia of the pouch [7,96]. Pouch surveillance is continued annually for such patients. (See "Surgical management of ulcerative colitis", section on 'Pouch dysplasia/cancer' and "Management of acute and chronic pouchitis".)
For patients with ileoanal pouch but without a history of dysplasia or CRC, the approach to pouch surveillance is informed by the presence of other risk factors for dysplasia. Patients with any of the following risk factors should undergo pouch surveillance every one to three years [7]:
•History of primary sclerosing cholangitis
•Chronic pouchitis or chronic cuffitis
•CD of the pouch
•Greater than eight-year history of UC
•Family history of colon cancer in a first-degree relative
For patients without a history of or risk factors for dysplasia, we perform surveillance pouchoscopy every three years [97].
Data have suggested that dysplasia or cancer of the pouch is uncommon in patients at average risk. In a systematic review of 33 studies including 8403 patients who had IPAA with variable duration of follow-up, the pooled prevalence of colon cancer or dysplasia in the ileoanal pouch was 0.5 percent and 0.8 percent, respectively [97].
Surveillance for and management of anal transitional zone (ATZ) dysplasia after stapled IPAA is discussed separately. (See "Restorative proctocolectomy with ileal pouch-anal anastomosis: Laparoscopic approach", section on 'Anal transitional zone dysplasia'.)
Follow-up for patients without dysplasia — For patients without dysplasia on initial surveillance colonoscopy, the timing of subsequent surveillance is informed by the following [89]:
●Disease activity – We use disease activity to guide timing of the next surveillance examination:
•Moderately to severely active inflammation – One year
•Mildly active inflammation – Two to three years
•Mucosal healing (ie, no significant inflammation) – For patients with mucosal healing who have had ≥2 surveillance examinations, we extend the surveillance interval to three to five years.
●Disease extent – For patients with disease involving one-third of the colon or less, we perform surveillance colonoscopy in three to five years. For patients with disease involving more than one-third of the colon, we perform surveillance colonoscopy in two to three years, unless there are indications for earlier follow-up (eg, moderately to severely active inflammation).
●Family history of colon cancer – For patients with family history of colon cancer in a first-degree relative at an age younger than 50 years, we perform surveillance colonoscopy in one year. For patients with family history of colon cancer in a relative who is not first-degree and not younger than 50 years of age, we perform surveillance colonoscopy in two to three years.
●Pseudopolyps – For patients with innumerable pseudopolyps carpeting the colon, we perform colonoscopy in one year. For patients with scattered pseudopolyps, we perform surveillance colonoscopy in two to three years. (See 'Inflammatory pseudopolyps' below.)
METHODS FOR SURVEILLANCE
General measures — For patients with inflammatory bowel disease (IBD), high-quality surveillance colonoscopy optimizes dysplasia detection and requires quiescent disease activity and adequate bowel preparation [6,77,98,99]. Examination with high-definition white light should be standard, and data have supported using an adjunctive method such as dye-based or virtual chromoendoscopy, in addition to a possible role for segmental re-inspection. (See 'Chromoendoscopy' below.)
Endoscopists should be adequately trained to detect and characterize lesions in IBD [100]. Programs to train endoscopists to identify and characterize dysplasia are being developed and validated [101].
Chromoendoscopy — Society guidelines advocate for high-definition colonoscopy with chromoendoscopy and targeted biopsies as the strategy that optimizes dysplasia detection [1,2,4,77,102].
The Surveillance for Colorectal Endoscopic Neoplasia Detection and Management in Inflammatory Bowel Disease Patients International Consensus (SCENIC) panel established the benefit of dye-based chromoendoscopy over standard-definition white light endoscopy and suggested a benefit of dye-based chromoendoscopy over high-definition white light (HDWL) colonoscopy, based primarily on one observational study of 75 patients with IBD that showed higher rates of dysplasia detection with chromoendoscopy compared with HDWL colonoscopy (21 versus 9 percent) [4,103-109]. Subsequent studies have demonstrated the yield of dye-based and virtual chromoendoscopy [77].
●Dye-based chromoendoscopy – Studies suggested that dye-based chromoendoscopy was superior to standard-definition white light colonoscopy, but its superiority over HDWL colonoscopy has been less clear [66,110-114]. In a meta-analysis of six randomized trials including 978 patients with IBD undergoing surveillance colonoscopy, use of dye-based chromoendoscopy resulted in higher rates of detecting dysplasia of any severity compared with HDWL (18.8 versus 9.4 percent, OR 1.94, 95% CI 1.21-3.11) [113]. However, rates for detecting high grade dysplasia were not statistically different between the groups (2.8 versus 1.1 percent, OR 2.21, 95% CI 0.64-7.62).
●Virtual chromoendoscopy – Virtual chromoendoscopy (utilizing narrow band imaging [NBI], i-SCAN, or autofluorescence imaging [AFI]) has been evaluated in IBD surveillance and compared with dye-based chromoendoscopy. While the study results have been mixed, virtual chromoendoscopy has been endorsed by society guidelines based on data suggesting a comparable yield for detecting dysplasia but with shorter procedure times [77].
Data from randomized trials have supported using virtual chromoendoscopy for IBD surveillance. In a trial comparing dye-based chromoendoscopy with virtual chromoendoscopy using NBI in 131 patients with ulcerative colitis, the number of neoplastic lesions detected per colonoscopy was not significantly different between groups (0.47 versus 0.32 lesions per colonoscopy) [115]. In addition, rates of overall neoplasia detection were not significantly different between groups, whereas the average withdrawal time was seven minutes longer with dye-based chromoendoscopy. In a trial comparing colonoscopy surveillance methods in 270 patients with IBD, there were no significant differences in neoplasia detection rates with use of i-SCAN, HDWL, or dye-based chromoendoscopy [66]. In a study comparing virtual chromoendoscopy using i-SCAN with dye-based chromoendoscopy in 129 patients with IBD, there were no significant differences in overall rates of neoplasia detection. However, virtual chromoendoscopy resulted in shorter median total examination times and withdrawal times (15 versus 20 minutes, and 10 versus 14 minutes, respectively) [116].
Multiple quality indicators have been proposed to ensure high quality surveillance colonoscopy in patients with IBD. Key performance measures include adequate bowel preparation, use of high-definition colonoscopy, use of chromoendoscopy, and tracking neoplasia detection rates [77]. (See 'Society guideline links' below.)
Role of random biopsies — Our practice is to take only targeted biopsies during surveillance examination using chromoendoscopy, except in patients who are at high risk for dysplasia, as described below.
At the time of surveillance colonoscopy, we take several random biopsies to assess mucosal healing or the extent of inflammation (ie, histologic staging biopsies) to inform surveillance intervals because chronic mucosal inflammation is a key risk factor for IBD-associated neoplasia. (See 'Patient selection and timing for initial surveillance' above.)
Data have demonstrated negligible additional yield of random biopsies for surveillance during high quality colonoscopy [60,117].The SCENIC panelists, however, did not reach consensus on this issue: 60 percent voted to abandon random biopsy when using chromoendoscopy, and 25 percent voted to perform random biopsies given the concern for missing dysplasia in a small proportion of patients [4]. In the SCENIC analysis, dysplasia was detected with random biopsies in approximately 10 percent of patients undergoing either chromoendoscopy or high-definition white light colonoscopy, and on targeted biopsies in the other 90 percent, resulting in approximately 0.1 percent of random biopsies detecting dysplasia [4]. Society guidelines have also supported abandoning random biopsies in patients at average risk, provided that disease is in remission, bowel preparation is adequate, and a high quality examination was performed [118]. Of note, histologic staging biopsies are distinct from random surveillance biopsies and are performed to assess disease activity and guide surveillance intervals.
The technique of chromoendoscopy plus random biopsies likely maximizes dysplasia detection, and may be considered for a selected, higher risk group [119-121]. A study evaluating the role of random biopsy after chromoendoscopy in 1000 patients demonstrated the following yields for dysplasia detection: 0.2 percent per biopsy, 1.2 percent per colonoscopy, and 12.8 percent per patient [120]. On multivariate analysis, random biopsy-only detected dysplasia was associated with a personal history of dysplasia (OR 12.7, 95% CI 4.9-33.3), concomitant primary sclerosing cholangitis (PSC) (OR 4.1, 95% CI 1.3-12.9), or a tubular appearing colon (OR 7.0, 95% CI 2.2-22.5). In a trial of 305 patients who had a total of 9760 random biopsies during chromoendoscopy or high definition-white light colonoscopy, dysplasia was detected in biopsy specimens from nine patients (yield of dysplasia: 0.092 percent), but detection rates were not significantly different between groups [119]. In a cohort study of 300 patients with dysplasia, risk factors for detecting dysplasia in random biopsies included longer disease duration (OR 1.04, 95% CI, 1.01-1.07), active inflammation (OR 2.89, 95% CI, 1.26-6.67), and history of PSC (OR 3.66, 95% CI, 1.21-11.08) [121]. These data support obtaining random biopsies during surveillance colonoscopy in high-risk groups (eg, patients with PSC) [117].
In addition to high-risk patients, random surveillance biopsies (ie, four quadrant biopsies taken every 10 cm) may be used during colonoscopy with standard-definition white light endoscopy [117], from areas of prior dysplasia, or in areas of limited mucosal visibility [6].
MANAGEMENT OF ENDOSCOPIC FINDINGS
Patients with dysplasia
Polypoid dysplasia — For endoscopically resectable dysplastic polyps that are not associated with dysplastic changes in flat mucosa elsewhere in the colon, we suggest removing the polyp endoscopically and close surveillance to ensure complete resection [4,6,122-124].
Polypoid lesions <20 mm typically undergo endoscopic resection with subsequent surveillance intervals informed by resection technique, lesion morphology, and histology [6]:
•Any lesion with high-grade dysplasia or incomplete resection: Colonoscopy in three to six months
•Sessile lesion 10 mm to 19 mm with low-grade dysplasia: Colonoscopy in 12 months
•Sessile lesions <10 mm or pedunculated lesion with low-grade dysplasia: Colonoscopy in 24 months
Larger lesions (≥20 mm) usually undergo endoscopic resection with intensive surveillance or may be referred for surgery. For patients who undergo endoscopic resection, we perform colonoscopy every three to six months for the first year following lesion resection.
This approach to polypoid dysplasia is informed by follow-up studies demonstrating that polypectomy with complete excision and continued surveillance provides adequate treatment of patients with endoscopically resectable polypoid dysplasia [4,125-127]. The Surveillance for Colorectal Endoscopic Neoplasia Detection and Management in Inflammatory Bowel Disease Patients International Consensus (SCENIC) panel pooled data from six studies found that during mean follow-up periods between 36 and 82 months, the incidence of CRC was 19 of 311 patients (6 percent, range 2 to 13 percent) [4]. In a meta-analysis of 10 studies that included 376 patients with ulcerative colitis (UC) who underwent resection of polypoid dysplasia prior to the advent of chromoendoscopy with a combined 1704 years of follow-up, the pooled incidence of cancer and dysplasia were 5.3 (95% CI 2.7-10.1) and 65 (95% CI 54-78) per 1000 patient-years, respectively [127].
If the follow-up surveillance examination reveals that polyp resection was incomplete and high-grade dysplasia or cancer is histologically confirmed, surgical consultation is obtained for further management.
Some guidelines had recommended taking biopsies from the mucosa immediately adjacent to the resection site to ensure that the lateral margins are free of dysplasia on histologic examination [1,4]. This practice is based on expert opinion. Visual inspection by trained endoscopists is likely sufficient, with a yield of 0 to 5 percent for unsuspected dysplasia [128,129].
We do not routinely take biopsies from the lateral resection margin unless there are concerns about the adequacy of the resection. As endoscopists performing inflammatory bowel disease (IBD) surveillance exams become familiar with optical diagnosis and treatment of IBD-associated dysplastic lesions, biopsies of the lateral margins can initially aid in their assessment of the completeness of resection.
Nonpolypoid dysplasia — Endoscopic management and surveillance of nonpolypoid, endoscopically resectable dysplasia is suggested after complete endoscopic resection, although data on long-term dysplasia and colorectal cancer (CRC) risk after endoscopic resection of nonpolypoid dysplastic lesions are not available [4]. Nonpolypoid lesions can be technically more difficult to remove, especially in the presence of fibrosis from prior or ongoing inflammation.
Patients with nonpolypoid dysplasia should be managed by an endoscopist with expertise in advanced endoscopic resection techniques. We perform surveillance colonoscopy within one to six months and repeat the exam in 12 months after the index resection. We obtain biopsy specimens of the resection site to document eradication of dysplastic tissue. Annual surveillance colonoscopy should be performed thereafter [1,4].
Invisible dysplasia — Invisible dysplasia is dysplasia detected on random (ie, non-targeted) biopsies of colonic mucosa without an associated visible lesion in patients undergoing high-definition white light colonoscopy or chromoendoscopy. Patients found to have invisible dysplasia on random biopsy should be referred to an IBD center that offers high-definition chromoendoscopy. A discussion of risks and benefits of management strategies should be discussed with the patient.
●Unifocal, low-grade dysplasia – Although the management of invisible, low-grade dysplasia remains controversial, we agree with most societies that the diagnosis of invisible dysplasia should be confirmed by a second pathologist with expertise in interpretation of biopsies in patients with IBD and a repeat colonoscopy with high-definition chromoendoscopy should be performed by an experienced endoscopist. In addition to targeted biopsies, we also obtain additional random biopsies at the follow-up colonoscopy to maximize the yield of dysplasia.
The rates of progression from low-grade dysplasia to high-grade dysplasia and cancer range from 0 to greater than 50 percent [130,131]. Studies performed in the era of chromoendoscopy demonstrate that the majority of patients with low-grade dysplasia will not progress to higher grades of dysplasia during three to four years of follow-up [132-135]. A meta-analysis of studies using white light colonoscopy for surveillance demonstrated a positive predictive value of flat (invisible) low-grade dysplasia of 22 percent for concurrent CRC and 36 percent for concurrent high-grade dysplasia and/or CRC [136].
●Multifocal, low-grade dysplasia – For patients with multifocal, invisible, low-grade dysplasia that is detected on random biopsy during surveillance colonoscopy and confirmed by a second pathologist, we recommend colonoscopy with chromoendoscopy by an experienced endoscopist [1,2,4]. Chromoendoscopy in patients with invisible dysplasia may identify a visible lesion that may be amenable to endoscopic removal. Variable rates of progression from low-grade dysplasia (identified by random biopsies using standard-definition colonoscopies) to high-grade dysplasia or CRC have been reported.
●High-grade dysplasia – Patients with invisible high-grade dysplasia confirmed by a second pathologist should be managed by an endoscopist with expertise in IBD surveillance with high-definition chromoendoscopy. This approach was also advocated by the SCENIC panel, although they did not endorse either endoscopic surveillance or colectomy for these patients, as much of the literature predates the video-endoscopic era [4].
An endoscopically resectable lesion may be managed with intensive surveillance [4] as studies demonstrate that curative resection of circumscribed lateral spreading lesions with high-grade dysplasia can be achieved [61,137]. For most patients, the first surveillance colonoscopy is performed in three to six months after the index examination, and then annually thereafter. However, this can vary depending on findings at endoscopy and the judgment of the expert endoscopist.
We agree with the SCENIC consensus statement that if dysplasia is not detected on the follow-up colonoscopy, a decision regarding surveillance versus colectomy should be individualized after a discussion of risks and benefits of the different management strategies [4]. Alternatively, the European Crohn's and Colitis Organization and The American Society for Gastrointestinal Endoscopy state that high-grade dysplasia without an associated endoscopically visible lesion is an indication for surgery [1,2].
Inflammatory pseudopolyps — Inflammatory pseudopolyps are irregularly shaped islands of residual intact colonic mucosa that are the result of the mucosal ulceration and regeneration that occurs in IBD (picture 1 and picture 2). (See "Overview of colon polyps", section on 'Inflammatory pseudopolyps'.)
When typical features are present, inflammatory pseudopolyps do not require excision unless they cause symptoms (eg, bleeding, obstruction). While not dysplastic, they are a marker of prior severe inflammation, which is a risk factor for colon cancer in UC [24,29]. However, their presence can also complicate the recognition of dysplastic lesions. Inflammatory pseudopolyps can be recognized by their histologic features; thus, a biopsy can help make the distinction in unclear cases. In a study of 1582 patients with IBD who underwent surveillance colonoscopy, the presence of pseudopolyps was not a risk factor for developing colorectal neoplasia during a median follow up of 4.8 years [25].
Strictures — For patients with IBD and colonic stricture(s) that can be traversed during surveillance colonoscopy and evaluated with multiple biopsies that are negative for colorectal neoplasia, we perform the next surveillance colonoscopy in one year [89].
Patients with IBD with a colorectal stricture that cannot be passed or adequately biopsied should be referred for surgical consultation for consideration of resection [1]. Strictures can complicate both colonic Crohn disease (CD) and UC, and their presence requires close surveillance due to an increased risk of CRC that has been reported in most but not all studies [23,138-140]. In one retrospective study of 293 IBD patients with colorectal strictures requiring surgery, dysplasia or cancer was found in 3.5 percent of strictures [141]. In a population-based study of 640 CD patients, the risk of developing colon cancer was higher in patients with colonic stenosis compared with those without stenosis (HR 18.8 95% CI 3.45-102.7). The probability of developing CRC for these patients was 5.5 and 7.5 percent after 5 and 10 years, respectively [142].
CHEMOPREVENTION —
Although several agents have been evaluated for prevention of CRC in patients with inflammatory bowel disease (IBD), none have conclusively been shown to decrease the risk of CRC. In IBD, cancer risk is thought to be related to chronic inflammation. A drug that reduces inflammation may lead to a reduction in colitis-associated neoplasia. Data are mixed and recommendations are based upon mainly observational studies [143].
Several drugs have been studied in the non-IBD population (particularly nonsteroidal antiinflammatory drugs and calcium) and some have also been evaluated in IBD and in the aggregate have not been found to be effective. (See "Epidemiology and risk factors for colorectal cancer" and "NSAIDs (including aspirin): Role in prevention of colorectal cancer".)
●5-aminosalicylates – We continue mesalamine in patients with ulcerative colitis to maintain remission and for potential chemoprevention. We do not continue mesalamine in patients on biologic therapies who have endoscopic remission. The European Crohn's and Colitis Organization states that 5-aminosalicylates (5-ASAs) may reduce the incidence of colorectal cancer in ulcerative colitis [80]. While the data for the chemopreventive effect of 5-ASAs are conflicting, 5-ASAs are generally considered to be low risk with a good safety profile, with both an anti-inflammatory effect and potential molecular anticarcinogenic effect [13,143]. (See "Medical management of low-risk adult patients with mild to moderate ulcerative colitis", section on 'Induction of remission'.)
●Ursodeoxycholic acid – (See "Primary sclerosing cholangitis: Inflammatory bowel disease and colorectal cancer".)
●Folic acid – (See "Primary sclerosing cholangitis: Inflammatory bowel disease and colorectal cancer".)
●Other agents – While some studies have suggested that thiopurine use may decrease the risk of CRC, there are insufficient data to recommend thiopurines for chemoprevention in patients with IBD [2,17,80,144-146]. Data supporting use of other advanced therapies is accumulating [13,147].
A retrospective cohort study suggested that statin use was associated with lower risk of CRC in patients with IBD, but prospective studies are need to confirm these findings [148].
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Ulcerative colitis in adults" and "Society guideline links: Crohn disease in adults" and "Society guideline links: Colorectal cancer".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Colon and rectal cancer screening (The Basics)" and "Patient education: Ulcerative colitis in adults (The Basics)" and "Patient education: Crohn disease in adults (The Basics)" and "Patient education: Colonoscopy (The Basics)")
●Beyond the Basics topics (see "Patient education: Screening for colorectal cancer (Beyond the Basics)" and "Patient education: Ulcerative colitis (Beyond the Basics)" and "Patient education: Crohn disease (Beyond the Basics)" and "Patient education: Colonoscopy (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Epidemiology – The risk of colorectal cancer (CRC) in patients with inflammatory bowel disease is related to the type, severity, duration, and anatomic extent of the disease. Patients with extensive colitis, defined as disease extending proximal to the splenic flexure, have the greatest risk of CRC. (See 'Epidemiology' above.)
●Endoscopic methods for surveillance – For surveillance, we typically perform chromoendoscopy using a high-definition colonoscope with targeted biopsies because this technique has shown the highest yield for overall dysplasia detection. Dye-based chromoendoscopy involves the topical application of indigo carmine or methylene blue to enhance mucosal irregularities and facilitate targeted biopsies. Virtual chromoendoscopy is an alternative for endoscopists with training in this modality. In addition, we obtain biopsies from the colon to assess histologic disease activity. (See 'Chromoendoscopy' above.)
Surveillance with high-definition white light colonoscopy with targeted and random biopsies is an acceptable alternative to chromoendoscopy, and multiple biopsies are required to adequately sample the colon. We obtain four biopsies every 10 cm from the cecum to the rectum. Additional biopsies should be taken in the sigmoid colon and rectum. Alternatively, six biopsies from the right colon, transverse colon, descending colon, sigmoid, and proximal and distal rectum can be taken in patients with ulcerative colitis (UC). (See 'Role of random biopsies' above.)
In addition, areas of mucosal irregularity should be biopsied.
●Patient selection and timing – For most patients with left-sided or extensive UC, or Crohn colitis involving more than one-third of the colon, we perform colonoscopy at eight years after disease onset to initiate surveillance for dysplasia, and we generally continue surveillance examinations every one to three years. (See 'Approach to surveillance' above.)
For patients who have undergone a subtotal colectomy with an ileostomy and have a rectum left in place (ie, a Hartmann's pouch), surveillance examination of the remaining rectum is performed every one to three years.
For patients with an ileal pouch anal anastomosis (IPAA), surveillance pouchoscopy is performed at time intervals that are guided by the patient’s risk for dysplasia:
•For patients with a history of CRC or dysplasia, we perform pouchoscopy yearly.
•For patients without a history of CRC or dysplasia but with other risk factors (eg, chronic pouchitis, primary sclerosing cholangitis), we perform pouchoscopy every one to three years.
•For patients without risk factors, we perform pouchoscopy every three years.
●Management of dysplasia – For endoscopically resectable dysplastic lesions that are not associated with dysplastic changes in flat mucosa elsewhere in the colon, we remove the dysplastic polyp endoscopically and follow up with close surveillance. If the follow-up examination reveals that polyp resection was incomplete and dysplasia or cancer is histologically confirmed, surgical consultation is obtained for further management. (See 'Polypoid dysplasia' above.)
Patients found to have invisible dysplasia on random biopsy only should be referred for high-definition dye-based or virtual chromoendoscopy at an expert inflammatory bowel disease center. (See 'Invisible dysplasia' above.)
ACKNOWLEDGMENT —
The UpToDate editorial staff thank Dr. Mark A. Peppercorn for his past contributions as an author to prior versions of this topic review.
The UpToDate editorial staff acknowledges Paul Rutgeerts, MD, who contributed as a Section Editor for UpToDate in Gastroenterology.
