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111
Colonic Dysplasia inPatients
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withUlcerative Colitis: Endoscopic
10
orSurgical Management?
LindaFerrari andAlessandroFichera
Introduction
Colectomy rates for acute indications in ulcerative colitis (UC) have been decreasing during the last two decades [1–4]. This is due in part to more effective medical
therapy, resulting in higher remission rates. On the other hand, operative management of ulcerative colitis appears to be slowly increasing for oncological indications, as a consequence of a more chronic course of the disease [5]. Risks factors for
CRC development in patients with UC are extent and duration of the disease especially with early age at diagnosis [6, 7]. As a consequence, with improved medical
therapy resulting in a prolonged duration of chronic disease, the incidence of dysplasia and malignancy in UC is expected to increase [5].
Historically, the treatment UC dysplasia has been surgical. Proctocolectomy has
been the traditional approach, due to the high risk of multifocality. However, in the
last decade, endoscopic management has been shown to be a treatment option for
early and limited dysplasia in high volume centres [8, 9]. The aim of this chapter is
to present the scientic evidence in support of endoscopic and surgical approaches
for UC associated colonic dysplasia.
L. Ferrari
Guy’s and St Thomas’ NHS Foundation Trust, London, UK
A. Fichera (*)
Division of Colon and Rectal Surgery, Baylor University Medical Center, Dallas, TX, USA
e-mail: alessandro.chera@bswhealth.org
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
K. Umanskiy, N. Hyman (eds.), Difcult Decisions in Colorectal Surgery,
Difcult Decisions in Surgery: An Evidence-Based Approach,
https://doi.org/10.1007/978-3-031-42303-1_10
113
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L. Ferrari and A. Fichera
Search Strategy (PICO Table)
A comprehensive literature search of all English-language publications was done on
PubMed using the following terms “dysplasia, ulcerative colitis, neoplasia, dysplasia associated mass lesion (DALM), adenoma like lesion (ALM), endoscopic submucosal dissection, inammatory bowel disease (IBD)”. The search was limited to
manuscripts published between January 1st, 1980 and December 31st, 2022. All
references in each manuscript identied from the PubMed search were then individually reviewed and examined for potential inclusion if appropriate.
PICO Table
Patients
Patients with UC and
mucosal dysplasia
Intervention Comparator
Endoscopic
resection
Colectomy Progression to malignancy.
Outcome of interest
Disease-free and overall survival
Results
Risk Factors forDysplasia andCancer inPatients
withUlcerative Colitis
In contrast with sporadic colorectal cancer, colitis associated CRCs do not follow
the adenoma-carcinoma sequence. Chronic inammation is the main driver of
tumorigenesis [10]. Histologic inammation, extent and duration of disease, presence of inammatory polyps and colonic strictures are well-known independent risk
factors for colorectal dysplasia and cancer [11, 12]. Furthermore, primary sclerosing cholangitis (PSC) is a very strong risk factor for high grade dysplasia and CRC
[13] in patients with UC.
Surveillance Strategies andTechniques
Surveillance colonoscopy should be routinely performed in patients with
UC.European and British guidelines stratify patients in one of three risk categories
(high, intermediate, or low risk group) with surveillance intervals ranging from
annually to every ve years [14, 15] (Fig.10.1). American guidelines recommend
surveillance every 1–3years considering the presence of risk factors when planning
the next surveillance interval [16]. Across the board all guidelines recommend
annual surveillance in patients with PSC, due to the high neoplastic risk [14–16].
Current guidelines [14–16] advocate the use of chromoendoscopy for surveillance. Superiority of high-denition chromoendoscopy to high-denition whitelight endoscopy has been reported in a recent randomised controlled trial from
Sweden [17]. However, high denition endoscopy is considered a less time
European surveillance guideline: indicaon for surveillance colonoscopies
10 Colonic Dysplasia in Patients with Ulcerative Colitis: Endoscopic or Surgical…
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˃30% involvement and
8-10 years aer disease onset symptoms
at disease onset for paents with PSC
OR
115
Low risk
5 years
No high or intermediate
factors present
Intermediate risk
2-3 years
Post-inflammatory polyps
First degree relaves CRC age
≥ 50 years
Extensive colis with midmoderate inflammaon*
High risk
annually
PSC
First degree relaves CRC age
≤ 50 years
Dysplasia ≤ 5 years
Extensive colis with severe
inflammaon*
Stricture with ≤ 5 years
Fig. 10.1 Surveillance strategy adapted from of the European Crohn’s and Colitis Organisation
(ECCO) [14]. *Presence of inammation is based on endoscopic or histologic inammation. CRC
Colorectal cancer, PSC Primary sclerosing cholangitis
consuming and a good alternative to chromoendoscopy [16] with similar dysplasia
detection rates. As a consequence, the utility of random biopsies, four quadrant
every ten centimetres, has been questioned with the use of high denition endoscopy systems [8]. Non-inferiority in neoplastic detection was reported for surveillance using only targeted biopsies vs targeted and random biopsies in a randomised
controlled trail [18]. The added value of random biopsies is higher in patients with
concomitant PSC (3.7% per colonoscopy and 0.3% per biopsy) [17–19], previous
dysplasia or tubular appearing colon [19].
Classification ofUC Associated Dysplasia
Diagnosis of colorectal dysplasia and cancer in patients with UC should be conrmed by two pathologists, with expertise in the eld of inammatory bowel disease [8, 14–16] due to the high level of interobserver variability for low grade
dysplasia and indenite dysplasia, especially when inammation is present.
Dysplasia, in patients with UC, can be visible or invisible. Invisible is detected
on random biopsies. According to the Scenic Consensus statement [8], visible dysplasia can be polypoid (pedunculated or sessile), non polypoid (supercial elevated,
at or depressed). Other general descriptors are presence of ulceration and assessment of borders (distinct or indistinct) [8]. Microscopically, dysplasia is also graded
and ranges between mild or low grade dysplasia (LGD) to high grade dysplasia
(HGD) based on the cellular and nuclear orientation changes.
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According to SCENIC consensus, and endoscopically resectable lesion indicates
that (1) distinct margins of the lesion could be identied, (2) the lesion appears to be
completely removed on visual inspection after endoscopic resection, (3) histologic
examination of the resected specimen is consistent with complete removal, and (4)
biopsy specimens taken from mucosa immediately adjacent to the resection site are
free of dysplasia on histologic examination.
L. Ferrari and A. Fichera
Management ofColonic Dysplasia
Until recently, international guidelines recommended total proctocolectomy for UC
patients with colorectal dysplasia [8, 14–16]. Reason behind this is the possible risk
of synchronous dysplasia in the setting of long-standing extensive disease. However,
there is increased evidence supporting the use of endoscopic treatment of these
lesions [21–28].
For invisible dysplasia detected in random biopsies, current guidelines recommend strict surveillance by IBD endoscopists [8]. For visible dysplasia, different
endoscopic and surgical options are currently available, and nal decision should be
made weighting grade of dysplasia, unifocal or multifocal lesions and also patient
characteristics (age, comorbidities, etc.) and preferences. If visible lesions are considered suitable for endoscopic resection, rst decision to be made is which technique to used. This depends on several factors: lesion size, shape, site, surface and
surrounding area (known as Five “s”), risk of invasion and endoscopic accessibility
[8, 29].
Small polypoid or at lesions can be removed with simple endoscopic snare
technique. For larger lesions, endoscopic mucosal resection (EMR) should be considered. This involves lifting the lesion from the muscularis propria using submucosal injection with saline to perform complete excision of the lesion. Furthermore,
endoscopic submucosal dissection (ESD) should be considered for lesions larger
than 20mm, especially if they are non-polypoid or if high grade dysplasia is present. ESD allows the lesion to be lifted deeper, at the level of muscularis propria,
where the lesion can be dissected. ESD has several advantages: high en block resection rate and radical (R0) resections with a relatively low risk of adverse events such
as bleeding or perforation [27].
Endoscopic Submucosal Dissection (ESD)
UC patients are at increased risk of developing colorectal cancer (CRC) through the
inammation-dysplasia-carcinoma sequence. For this reason, early identication
and treatment of dysplastic lesions can potentially reduce the risk of CRC.Data to
support the use of endoscopic submucosal dissection (ESD) for UC associated dysplastic lesions have been collected mainly during the last eight years [22–28]
(Table10.1). Manta etal. [27] pulled together data from seven independent international research collaborations [21–27]. By cumulative analysis, there were a total of
10 Colonic Dysplasia in Patients with Ulcerative Colitis: Endoscopic or Surgical…
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Table 10.1 ESD to treat dysplasia in patients with ulcerative colitis
Study, year
and country
Smith LA
(2008) [21]
UK
Iacopini F
(2015) [22]
Italy/Japan
Suzuki N
(2017) [23]
UK/Japan
Kinoshita S
(2018) [24]
Japan
Yang DH
etal. (2019)
[25]
Korea
Matsumoto
K (2019)
[26]
Japan
Manta R
etal. (2021)
[27]
Italy
Kasuga K
(2021) [28]
Japan
UC patients Outcomes
69 UC patients En bloc
resection 78%.
R0 resection
94% after en
bloc resection.
9 UC patients En block
resection 80%.
R0 resection
70%.
32 UC patients En bloc
resection 91%.
R0 resection
72%.
25 UC patients in
clinical remission
(Mayo total
score<2)
15 UC patients. En block
17 UC patients.
7 underwent ESD and
10 total
proctocolectomy.
53 UC patients En block
17 UC patients. 9
underwent ESD.
8 subtotal colectomy.
En block
resection 100%.
R0 resection
76%.
resection
93.3%.
R0 resection
80%.
En block
resection 100%.
R0 resection
86%
resection 100%.
R0 resection
96.2%.
En bloc
resection 91%.
R0 resections
82%.
Dysplasia during
follow-up assessment
Median follow-up
18months.
0 metachronous
lesions or cancer. 98%
cure for ESD-assisted
EMR
Median follow-up
24months.
0 local recurrence
0 metachronous
dysplasia.
Median follow-up
33months.
4% local recurrence.
9% metachronous
dysplasia.
Median follow-up
21months.
0 local recurrence.
4% metachronous
HGD.
Patient underwent a
proctocolectomy. No
cancer progression.
Median follow-up
24.7months.
14% local recurrence.
14% metachronous
recurrence.
No cancer progression.
Median follow-up
21months.
0 local recurrence.
71% metachronous
recurrence
Median follow-up
27months.
0 local recurrence.
3.7% metachronous
recurrence.
Both patients
underwent surgery.
No cancer progression.
Median follow-up
25months.
0 local recurrence.
22% metachronous
recurrence.
Both patients
underwent denitive
ESD.
117
Quality of
evidence
Moderate
Moderate
Moderate
Moderate
Moderate
Moderate
Moderate
Moderate
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208 patients with 216 treated lesions. There was a slight prevalence of males
[M/F=1.39] with a median age of >60years, and there was a 59.6% prevalence of
extensive colitis. The median duration disease ranged from 7 to 20years [27].
In total, en bloc resection was successfully performed in 191 ESD procedures,
corresponding to 88.4% of 216 lesions and 91.8% of 208 patients. R0 resection was
achieved in 169 ESDs, equivalent to a 78.2% of lesions and 81.3% of patients.
According to the operator, en bloc resection and R0, respectively, were achieved in
113 (86.9%) and 107 (82.3%) of 130 lesions treated by European endoscopists, and
in 78 (92.9%) and 62 (73.8%) of 84 lesions treated by Asian endoscopists, without
a statistically signicant difference between groups. The median diameter of
removed lesions in the different studies varied from 15 to 35mm (range: 8–73).
Submucosal brosis was detected in 104 (77.1%) of 135 lesions. The overall rate of
complications was 9.6%, including 6.7% bleedings and 2.9% perforations, all managed endoscopically. At follow-up, recurrence was observed in only eight (3.8%)
patients, and a metachronous lesion developed in 13 (6.2%) cases.
Data from the above studies [21–28] shows that ESD is a safe technique to
remove non-invasive lesions in UC patients. It should be performed in selected
high-volume centers, where appropriate long-term follow-up can be offered.
L. Ferrari and A. Fichera
Surgical management ofColonic Dysplasia
Historically, surgery has been the treatment of choice for low and high grade dysplasia in patients with UC [20, 31–44]. Several series have been published, most of
them retrospective, single institution and with limited numbers. Summary of the
existing evidence from the literature is presented in Table10.2.
With the recent data on ESD, surgery should be reserved for endoscopically
unresectable lesions, invisible high grade dysplasia and high-risk colons, when
strictures are present and surveillance might be difcult [8, 30]. When surgery is
indicated, a total proctocolectomy is indicated in case of HGD or CRC to reduce
overall risk of dysplasia and cancer.
Although patients with LGD have been considered at limited risk for cancer
development, there are evidence that certain endoscopic characteristics are associated with increased risk of progression. Choi etal. [44] looked at risk factors for
progression of LGD to HGD or CRC. In 172 patients that were followed for a
median of 48 months, 21 had immediate colectomy and 152 only surveillance
endoscopy. On multivariate analysis, factors associated with signicant risk of
HGD and CRC were: macroscopically non-polypoid dysplasia (P<0.001) or invisible dysplasia (P=0.02), dysplastic lesions ≥1cm in size (P=0.01), and a previous
history of “indenite for dysplasia” (P=0.01). The cumulative incidence of HGD
or CRC at 1 and 5years after detection of LGD was 0% and 1.8% in patients with
no risk factors, 9.6% and 17.7% with one risk factor and 29.0% and 53.4% for two
risk factors. For those with three risk factors, cumulative risk of HGD or CRC
development was 61.6% and 80.7% at 1 and 2years, respectively. This important
study identied endoscopic ndings as prognostic factors that should be considered
10 Colonic Dysplasia in Patients with Ulcerative Colitis: Endoscopic or Surgical…
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119
Table 10.2
Study and year
of publication
Blackstone
MO (1981)
[20]
Woolrich AJ
(1992) [31]
Provenzale D
(1995) [32]
Befrits R
(2002) [33]
Ulmann T
(2002) [34]
Ullman T
(2003) [35]
Jess T (2006)
[36]
Lim CH
(2003) [37]
Rutter MD
(2006) [38]
Pekow JR
(2010) [39]
Goldstone R
(2011) [40]
Surgical management for colonic dysplasia
Sample size Dysplasia during FU
112 long-standing UC
patients
FU: 4years
121 UC patients
FU >7years
Computer generated
population of 10,000,
30year old UC patients
with pancolitis for over
10years
60 UC patients with at
LGD
FU: 10years
18 UC patients with at
LGD
Median FU:32months
46 UC patients with at
LGD
Median FU: 15months.
11 colectomy.
21 surveillance
29 IBD patients including
Crohn’s disease.
Median FU:17.8years
128 UC patients >8years 29 patients had LGD, and 97 no
600 UC patients.
Median FU: 8.5years
28 UC patients with LGD
Median FU: 50months
121 UC patients with
extensive disease >7years
and LGH
Median FU: 37months
Dysplasia in 12 patients.
7 developed CRC.
Only 2 patients with CRC had HGD
Dysplasia or CRC in 27 patients
(22%)
Mean FU: 16years.
Prophylactic colectomy increased
life expectancy by 2–10months vs
surveillance and 1.1–1.4years vs no
surveillance.
Yearly surveillance for LGD
increased life expectancy by up to
1.2years vs no surveillance.
LGD at index colonoscopy in 16
(26%) patients.
73% had LGD in subsequent
colonoscopies.
50% developed advanced neoplasia.
Incidences of progression was 13%
at 1year, 26% at 2years and 33% at
5years.
19 had LGD and 2 HGD at study
end 14 of the 46 progressed to
advanced neoplasia (median time
progression 25months)
Among 6 patients with at LGD,
who did not undergo colectomy,
none progressed to CRC.
Median FU:17.8years.
dysplasia (controls).
FU: 10years.
HGD or CRC in 3/29 (10%) LGD
patients vs 4/97 controls (4.0%).
74 patients (12.3%) developed
neoplasia, including 30 CRC.
Incidence of CRC was 2.5% at
20years, 7.6% at 30years, and
10.8% at 40years.
1 at LGD progressed to HGD and 1
polypoid LGD progressed to CRC
In total, 7 patients who progressed to
CRC and 6 of 8 who progressed to
HGD had distal LGD initially.
Interval for progression was shorter
for patients with distal vs proximal
LGD.
Quality of
evidence
Low
Moderate
Poor
Moderate
Mod-low
High-mod
Mod-low
Low
Moderate
Moderate
Moderate
(continued)
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Table 10.2 (continued)
Study and year
of publication
Stolwijk JA
(2013) [41]
Zisman TL
(2012) [42]
Wanders LK
(2014) [43]
Choi CH
(2015) [44]
UK
Fumery M
(2017) [45]
UC ulcerative colitis, FU follow up, LGD low grade dysplasia, CRC colorectal cancer, HGD high
grade dysplasia
Sample size Dysplasia during FU
293 UC patients with UC
>8years.
FU at 10 and 15years
42 UC patients with
pancolitis ≥8years and
LGD
Mean FU: 3.9years
Meta-analysis
376 UC patients with
polypoid dysplasia, FU:
1000years
172 UC patients with
extensive disease and
LGD
21 colectomy
152 surveillance
Meta-analysis.
671 UC patients with
LGD
FU 10years.
Incidence of any dysplasia was
23.5%, and of CRC 4.0%.
FU 15years.
33.3% and 6.8% respectively.
19% (8/42) of patients progressed to
advanced neoplasia (two cancer, six
HGD) while 17% (7/42) had
persistent LGD and 64% (27/42)
indenite dysplasia or no dysplasia
Pooled CRC and HGD rates were
6.7 and 9 per thousand years of
patient follow-up.
Longer study duration did not
correlate with advanced neoplasia
rates.
FU: 48months
13% and 8.6% of patients developed
HGD and CRC respectively.
Annual incidence of advanced
neoplasia 1.8%.
Annual incidence of CRC 0.8%.
High risk features associated with
dysplasia progression: PSC, invisible
dysplasia, distal location, and
multifocal LGD.
L. Ferrari and A. Fichera
Quality of
evidence
Moderate
Highmoderate
High
Highmoderate
High
to properly select patients for surgical intervention rather than just using the degree
for dysplasia.
A meta-analysis including 14 surveillance cohort studies collected data on 671
patients with UC-LGD (52 developed CRC) [45]. The pooled annual incidence of
CRC was 0.8% (95% CI, 0.4–1.3); the pooled annual incidence of advanced neoplasia was 1.8% (95% CI, 0.9–2.7). Factors signicantly associated with dysplasia
progression were concomitant primary sclerosing cholangitis (OR, 3.4; 95% CI,
1.5–7.8), invisible dysplasia (vs visible dysplasia; OR, 1.9; 95% CI, 1.0–3.4), distal
location (vs proximal location; OR, 2.0; 95% CI, 1.1–3.7) and multifocal dysplasia
(vs unifocal dysplasia; OR, 3.5; 95% CI, 1.5–8.5). In 12 surgical cohort studies of
450 patients who underwent colectomy for UC-LGD, 34 patients had synchronous
CRC (pooled prevalence, 17%; 95% CI, 8–33) [45].
Although LGD has been considered not an absolute indications for surgical management, different endoscopic parameters should be considered to identify
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