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97
Surgical treatment options include pouch excision, stricturoplasty, reconstruc-
tion, or a proximal diverting stoma [31, 32, 62]. All but stricturoplasty can be con-
sidered as pouch failure. Wu et al. [63] is the only study comparing both
stricturoplasty with balloon dilatation and found survival rates of 83.1 and 82.0%
for patients with stricturoplasty and endoscopic dilation, respectively (log-rank test:
p= 0.752). They also found that CD on univariate analysis was associated with a
stricture free survival (p=0.02). This study recommended the use of balloon dilata-
tion in the rst instance for pouch strictures with surgical stricturoplasty reserved
for refractory cases. All other management strategies have not been compared for
efcacy and safety.
8.6.3 Small Bowel Obstruction
The management of small bowel obstruction in a CD pouch has been poorly studied
but these should be managed in a similar fashion to any small bowel obstruction.
MacLean etal. [34] suggested that these rarely require any operative form of treat-
ment and can be managed conservatively [34].
We suggest that patients with suspected small bowel obstruction need urgent
investigations. Whilst awaiting investigations early surgical opinion is impor-
tant. Early investigations include bloods, abdominal and erect chest x-rays to
rule out perforation. Early cross sectional imaging will also be vital to help the
diagnosis.
Initial treatment may include making the patient nil by mouth, intravenous
uids and decompression of the stomach with a nasogastric tube. In CD of the
pouch, an underlying inammatory process may be the underlying cause of
intestinal obstruction. In this situation, a trial of medical therapy to include ste-
roids, antibiotics or biologics may help reduce inammation and resolve the
obstruction. Endoscopic therapy can include endoscopic dilatation and stenting.
Surgical techniques such as stricturoplasties and bowel resection can also be
considered.
8.6.4 Fistulae
The treatment of stulae in CD of the pouch is based on small case series. Ricart
etal. [64] reported that four of the ve patients (80%) with stulae had a complete
response with sustained closure of all stulae with iniximab [64].This was further
supported by Viazis [65] who reported a 66.7% complete stulae closure in patients
given 1 year of iniximab. Gaertner etal. [66] whilst they could not compare ef-
cacy of each management strategy, found that seton insertion and lay-open stu-
lotomy were associated with high healing rates in stulae [66].
8 Crohn’s Disease intheIleal Pouch Anal Anastomosis: Management Strategies
98
8.6.5 Pouch Vaginal Fistulae
Pouch vaginal stulae can be managed using medical and surgical approaches.
Ricart et al. [64] found that iniximab caused complete remission in a third of
patients who had pouch vaginal stulae [64]. A case series by Koroos [67] high-
lighted that CD paediatric pouch vaginal stulae could be healed with iniximab.
Surgical options include primary repair of the transvaginal stula with healing rates
reported as 55% when done as a primary procedure and 40% when performed sec-
ondarily [68]. Shah etal. [50] supported local repair following pouch vaginal stu-
lae, they achieved pouch vaginal stula closure using local repairs in addition to
medical therapy, setons, and stomas [50] with an overall healing rate of 52% at
49-month mean follow-up. Heriot etal. [49] supported these ndings, reporting
outcomes in 37 patients (54%) who underwent local transvaginal repair, they found
primary healing rate was 40% at a median follow-up of 19months, with an overall
pouch failure rate of 35% at a median of 4.2years [49].
Mallick etal. [68] reported that local repair with pouch advancement ap was
associated with a healing rate of 55% when done as a primary procedure and 40%
when performed secondarily after a different procedure, which included ileal
pouch advancement ap and transvaginal approach to repair [68]. They high-
lighted that pouch failure was higher in patients with CD who underwent primary
surgical repair compared with non-CD patients with pouch vaginal stulae.
Despite seemingly good results, the authors strongly recommended faecal diver-
sion in the management of pouch vaginal stula as the authors felt that this gave
the best chance of resolution of sepsis and inammation [68]. In this study, a
delayed diagnosis of CD was made in 24 patients, and these patients had lower
success rates following ileal advancement aps compared with the non-Crohn’s
group (25 vs. 48%). Other studies have used EUA, setons and glue successfully in
pouch vaginal stulae [69].
Based on their experience, Gaertner etal. [66] proposed the following treatment
algorithm for management of ileal pouch stulae [66] (Fig.8.1).
8.6.6 Pouch Failure
Despite attempts to salvage a CD pouch, it has been estimated that pouch excision
rates are 45–55% in patients with pre-operative CD [5, 9]. Whilst there is no abso-
lute indication for pouch excision in CD of the pouch, we suggest that a joint
decision with the patient and the multi-disciplinary team to include physicians,
surgeons and nurses are essential. Reasons to consider pouch failure include;
symptoms which are not tolerable to the patient, medically refractory disease,
signs of persistent metabolic disease, failure to thrive, malnourishment, and over-
all poor quality of life. In this instance, pouch excision or an ileostomy should be
offered.
J. Segal and A. Hart
99
8.7 Prognosis ofCD ofthePouch
In a cohort of 32 patients with CD of the pouch, 93% of patients developed compli-
cations including abscesses, pouchitis, and strictures and 29% of these patients had
pouch failure [70] secondary to these complications. Of those patients who retained
their pouch 60% had leakage, with 45% using pads. Gu etal. [71] reported a 5 and
10year pouch retention rate of 58% and 50%, respectively [71]. This included 17
patients who had inammatory CD, 7 had who brostenotic disease, and 41 had
stulising phenotype.
In a small study comparing RPC for UC vs RPC for CD, the CD group experienced
signicantly fewer median daily bowel movements (p=0.02), with less episodes of
Ileal pouch fistula
Define fistula tract anatomy and
review initial pathology
(peivic MRI +/– endoanal US & review slides with GI
pathologist)
Control sepsis
(consider EUA with seton
placement and treat pouchitis)
Crohn’s disease
Medical treatment
(consider anti-TNF therapy)
Cryptoglandular
Definitive repair
according to fistula
tract anatomy
Anastomotic failure
High
fistula
Low
fistula
Definitive repair
according to
fistula tract
anatomy
Can be
repeated
Can be
repeated
Can be
repeated
Failure
Definitive repair
according to fistula
tract anatomy
Observation with
quiescent fistulas
Pouch
revision or
excision
Failure to medical
treatment, severe
pelvic fibrosis,
poor pouch
function
Fig. 8.1 Treatment algorithm for management of ileal pouch stulae (Gaertner et al. [66])
8 Crohn’s Disease intheIleal Pouch Anal Anastomosis: Management Strategies
100
incontinence for liquids (p<0.01) and less episodes of pouchitis (p<0.01). However,
pouch excision rates are signicantly higher in the CD group (2 vs 0%, p<0.01) [72].
Overall, understanding CD in restorative proctocolectomy in terms of its bene-
ts, risks and treatment options remains very limited. A consensus denition of CD
of the pouch will be benecial to future study designs in addition to being able to
understand and separate CD complications of the pouch from other non-CD compli-
cations. This will allow future trials to specically address CD complications and
assess treatment affect for that specic complication. Further randomized control
trials are likely to require multi-centre approach due to relatively small numbers.
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8 Crohn’s Disease intheIleal Pouch Anal Anastomosis: Management Strategies
105© Springer International Publishing AG, part of Springer Nature 2019
J. Warusavitarne, Z. Perry-Woodford (eds.), The Ileoanal Pouch,
https://doi.org/10.1007/978-3-319-94385-5_9
Chapter 9
Microbiology oftheIleoanal Pouch
andManaging Pouchitis
SimonMcLaughlin
Abstract Pouchitis is the most common cause of pouch dysfunction occurring in
20–50% of patients following restorative proctocolectomy for ulcerative colits
(UC). In 6% of patients the inammation extends proximal to the pouch; pre-pouch
ileitis. The inammation that occurs in patients with pouchitis is likely secondary to
the combination of a dysregulated immune system that exists in all patients with UC
and a stimulus from the gut microbiota.
The mainstay of treatment is antibiotic therapy which is likely to be effective by
reducing total gut microbial load and therefore stimulus to the immune system. In
those who do not respond or lose response to this treatment there is evidence for the
development of antibiotic resistant bacteria and changing antibiotic class is often
effective. In those refractory to antibiotics biologic therapy can be effective.
Keywords Pouchitis · Pre-pouch ileitis · Restorative proctocoelctomy · Biologics
Probiotics
9.1 Introduction
Restorative proctolectomy (RPC) with ileal-pouch anal anastomosis is the operation
of choice for patients who require surgery for ulcerative colitis (UC). Following
surgery expected bowel frequency is 4–8 times per day and 0–2 overnight. This
frequency increases in patients with pouch dysfunction. Pouchitis is the most com-
mon cause of pouch dysfunction occurring in 20–50% of patients [1–3]. It usually
presents with an increase in stool frequency and urgency, some patients will also
develop abdominal cramping, fever and per-anal bleeding. To correctly diagnose
S. McLaughlin
The Royal Bournemouth and Christchurch Hospitals NHS foundation trust,
Bournemouth, UK
Centre of Postgraduate Research and Medical Education, Bournemouth University,
Poole, UK
e-mail: simon.mclaughlin@nhs.net
106
pouchitis and exclude other conditions baseline tests should include stool tests to
exclude common pathogens including C. difcile.
A exible pouchoscopy with intubation of the pre-pouch ileum is essential. In
some patients the inammation will be found to extend proximal to the pouch; pre-
pouch ileitis.
9.2 Microbiological Aetiology
Whether a dysbiosis (altered gut microbiota composition) or an abnormal host
immune response to normal commensal microbiota is the cause of inammatory
bowel disease has been the subject of a large number of studies. Considerable evi-
dence from clinical practice implicate bacteria in the pathogenesis of pouchitis;
pouchitis occurs in the area of the small bowel with the highest concentration of
bacteria, antibiotics are effective treatment for treating pouchitis and probiotics can
prevent the onset of pouchitis and reduce disease relapse.
The hypothesis that an abnormal immune response is fundamental to the disease
process that occurs in all forms of IBD is well established [4]. In pouchitis this is
demonstrated by the knowledge that the incidence of pouchitis in familial adenoma-
tous polyposis (FAP) patients is about 10 times less common than in patients with a
history of ulcerative colitis suggesting that the increased risk in UC patients may be
due to an abnormal immune system.
Around 99% of gut microbiota are contained in four phyla; Firmicutes,
Bacteroidetes, Proteobacteria and Actinobacteria [5, 6]. At the species level how-
ever, each individual has his or her own unique gut microbiota, It has been appreci-
ated for about 10 years that 90% of gut microbiota cannot be cultured [5] and
therefore molecular biology techniques (16s ribosomal RNA polymerase chain
reaction) are required to accurately identify the composition of gut microbiota. Data
from early culture-based techniques must therefore be disregarded and will not be
discussed here.
Following closure of ileostomy the pouch microbiota evolve over at least the rst
year and differ between patients. In a study by Falk etal. two patients underwent
repeated pouch mucosal biopsy [7]. The microbiota were identied using terminal
restriction fragment length polymorphism (T-RFLP), cloning and sequencing, the
microbiotal composition evolved over time and at 1 year was broadly similar to that
found in the normal colon.
A reduction in bacterial diversity is thought to be fundamental to the pathogen-
esis of all forms of IBD.Kubacher etal. identied a reduction in diversity in patients
with a history of chronic pouchitis who had a relapse of pouchitis following an
antibiotic induced remission when compared to patients maintained on the probiotic
VSL#3 who remained in remission [8].
In the probiotic treated patients increases in the diversity of Lactobacilli and
Bidobacteria were identied.
It is recognised that gastroenteritis secondary to pathogenic bacteria such as cam-
pylobacter and C.difcile can mimic a new presentation of IBD and also cause a
S. McLaughlin
107
are of symptoms in patients with known IBD.CMV infection is unusual in patients
not immunosuppressed but silent carriage is not uncommon. One group identied
CMV in biopsies taken from both pouchitis and non-pouchitis pouch patients using
a polymerase chain reaction (PCR) and sequencing technique. No signicant differ-
ence was found in the incidence of CMV in each group when classied using the
modied pouch disease activity index suggesting that CMV is unlikely to be impli-
cated in the pathogenesis of pouchitis [9].
Six studies have compared the differences in the microbiota in pouchitis and
non-pouchitis RPC patients using molecular biology techniques with differing
results.
The earliest study by Komanduri etal. paradoxically reported an increase in the
bacterial diversity in pouch biopsy samples from pouchitis patients compared to
biopsies from the ileum of non IBD controls with an intact colon. There was an
increase in the proportion of proteobacteria and a reduction in rmicutes as well as
a difference in the Rumicoccus species associated with pouchitis (R. obeum) and
non-pouchitis (R. gnavus) [10].
These ndings are at odds to other IBD studies and should be interpreted with
caution as there were signicant limitations to this study. Bacterial analysis was
undertaken by grouping biopsy samples together by disease type rather than by
analysing each patient sample individually. It therefore remains possible that the
identied differences could have been from single patient samples within each
group. Furthermore according to the authors’ the technique at most identied 73%
of the microbial population.
An early study from the St. Mark’s group used a hybrid culture and molecular
biology technique where mucosal biopsies were rst cultured on agar before bacte-
ria were extracted and amplied using PCR and proles were generated using
TRFLP [11]. No differences between pouchitis and non-pouchitis groups or FAP
and UC groups were identied. It should however be appreciated that the culturing
of biopsies before PCR would favour growth of bacteria supported by the culture
medium and inuence the results of PCR.In addition, the TRFLP technique can
only identify dominant species groups and cannot identify individual bacterial
species.
A further study by Lim etal. utilised the TRFLP technique to compare pouchitis
(5 UC patients) and non-pouchitis (15 UC patients). No differences in diversity or
TRFLP prole were identied between groups [12].
In 2008 the St. Mark’s group reported the results of the rst study that identied
the microbiota in pouchitis and non pouchitis UC patients and compared this to
pouchitis and non pouchitis FAP patients using a 16s rRNA sequencing technique
[13]. In total 24 patients were studied (patients with antibiotic resistant pouchitis
were excluded) the results identied a signicant increase in Proteobacteria and a
signicant reduction in Bacteroidetes and Faecalibacterium prausnitzii in the total
UC compared with the total FAP group. Similar ndings have been reported in a
study which compared the microbiota in IBD and non-IBD surgical specimens [5],
suggesting that a similar dysbiosis exists in all types of IBD.This study also dem-
onstrated that the ileal pouch microbiota differed from those expected in the normal
colon; Proteobacteria usually account for a small proportion of colonic microbiota
9 Microbiology oftheIleoanal Pouch andManaging Pouchitis