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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1267_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword
- •Foreword
- •Contents
- •References
- •2.1 Introduction
- •2.2.1 Crohn’s Disease
- •2.2.2 Ulcerative Colitis
- •References
- •3.2.1 Bacterial Sensing
- •3.2.1.2 Toll-Like Receptors, TLRs
- •3.2.2 Autophagy: Autophagy-Related 16-like 1, ATG16L1
- •3.1 Introduction
- •3.2.4.1 Interleukin-23 Receptor, IL-23R
- •3.2.4.2 Fractalkine Receptor 1, CX3CR1
- •3.2.4.3 Transforming Growth Factor Beta (TGF-β)
- •3.2.4.4 Angiotensinogen
- •3.2.4.5 Tumour Necrosis Factor Alpha (TNFα)
- •3.2.6 Cell Signalling: Janus Kinase 2 (JAK2)
- •3.2.8 Other Processes
- •References
- •4.1 Introduction
- •4.2 Genetics
- •4.3 Epigenetics
- •4.5 DNA Methylation
- •4.9 MicroRNA
- •4.12 Summary
- •References
- •5.1 Introduction
- •5.2.1 TNFα
- •5.2.2 Th1 Cytokines
- •5.2.3 IL-1 Cytokines
- •5.2.4 Th2 Cytokines
- •5.2.5 Th17 Cytokines
- •5.2.6 TL1A
- •5.3 “Regulatory” Cytokines
- •5.3.1 TGFβ
- •5.3.2 IL-10
- •5.4 Concluding Remarks
- •References
- •6.1.1.1 Collagens
- •6.1.1.3 Glycoproteins
- •6.2.1 Integrins
- •6.3.1 Extracellular Matrix Stiffness
- •6.3.1.1 Modeling Extracellular Matrix Stiffness
- •References
- •7.1 Introduction
- •7.5 Future Outlook
- •References
- •8.1 Introduction
- •8.2.1 Smoking
- •8.3 Conclusion
- •References
- •9.4 Conclusions
- •References
- •10.1 Ulcerative Colitis
- •10.1.1 Epidemiology
- •10.1.2 Etiology
- •10.2.1 Pathogenesis
- •References
- •11.4 Conclusion
- •References
- •12.1 Introduction
- •12.2 Clinical Biomarkers
- •12.3 Cellular Biomarkers
- •12.4 Serologic Biomarkers
- •12.5 Other Factors
- •12.6 Conclusions
- •References
- •13.1 Introduction
- •13.3 Bowel Ultrasound
- •13.4 Computed Tomography Enterography
- •13.5 Magnetic Resonance Imaging
- •13.5.2 Functional MR Imaging Techniques
- •13.5.3 Hybrid Imaging Techniques
- •13.6 Conclusion
- •References
- •14.1.1 Ultrasound Stiffness Imaging
- •14.1.2 Shear Wave Elastography
- •14.5 Conclusion
- •References
- •15.1 Introduction
- •15.2.1 Stricturing IBD
- •15.2.2 Stricturing CD
- •15.2.3 Stricturing UC
- •15.4.1 Steroids
- •15.4.2 5-ASA
- •15.4.3 Purine Analogs
- •15.4.4 Methotrexate
- •15.4.5 Anti-TNFs
- •15.4.6 Other Biologics
- •15.5 Other Measures
- •15.6 Conclusion
- •References
- •16.1 Introduction
- •17.2.4 Abscess
- •17.3 Stricturoplasty or Resection
- •17.4 Approach
- •16.6 Conclusion
- •References
- •17.1 Introduction
- •17.2.2 Fibrotic Phenotype
- •17.2.3 Fistulising Disease
- •17.4.1 Open
- •17.4.2 Handassisted
- •17.4.3 Multi-Port
- •17.4.4 Single-Port
- •17.4.5 Single Port versus Multi-Port
- •17.4.6 Decision Making
- •17.5 Anastomosis
- •17.7 Conclusion
- •References
- •18.1 Introduction
- •18.4.1 Initial Evaluation
- •18.5.1 Pre-IPAA (Afferent Limb/Ileostomy Closure Site)
- •18.5.2 The Fibrotic IPAA Body
- •18.5.3 Post-IPAA (Efferent Limb, Anal Canal)
- •18.6 Conclusion
- •References
- •19.2 Pathophysiology
- •19.3 Diagnosis
- •19.4 Surgical Approach
- •19.4.1 Resections
- •19.4.2 Strictureplasties
- •19.4.2.1 History
- •19.4.2.2 Indications
- •19.4.2.3 General Technique
- •19.4.2.4 Conventional Strictureplasties
- •Judd Strictureplasty
- •Moskel-Walske-Neumayer Strictureplasty
- •Jaboulay Strictureplasty
- •Poggioli Strictureplasty
- •19.4.2.6 Results
- •Short-Term Results
- •Long-Term Results
- •19.5 Future Perspectives
- •References
- •20.1 Introduction
- •20.6 Summary
- •References
- •21.1 Introduction
- •21.2 Wound Healing
- •21.3 Crohn’s Disease Fistula
- •21.7 Summary
- •References
- •22.1 Introduction
- •22.3 The Transforming Growth Factor-β (TGF-β) Pathways
- •22.4.1 Connective Tissue Growth Factor (CTGF/CCN2)
- •22.4.2 Platelet Derived Growth Factor
- •22.4.3 Wnt-Signaling
- •22.4.4 Hedgehog Signaling
- •22.4.5 Notch Signaling
- •22.6.1 Coagulation Stage
- •22.6.3 Fibrous Adhesion Stage
- •22.7.4 Material Barriers
- •22.7.5 Pharmaceutical Approaches
- •22.8.4 Smooth Muscle Cells
- •22.12 Conclusions
- •References
- •23.1 Introduction
- •23.2 Liver
- •23.2.1 Farnesoid X Receptor (FXR)
- •23.2.2 Lysyl Oxidase (LOXL2)
- •23.2.3 Statins
- •23.2.4 5-Hydroxytryptamine (5HT)
- •23.2.5 Caspase Inhibition
- •23.2.6 Chemokine Receptors CCR2/5
- •23.2.7 GR-MD-02
- •23.2.8 PPAR Gamma
- •23.3 Lung
- •23.3.1 Pirfenidone
- •23.3.2 Nintedanib/Tyrosine Kinase Inhibitors
- •23.3.3 Lysophospholipids
- •23.3.4 mTOR
- •23.3.5 Prostacyclin
- •23.3.6 Integrin αvβ6
- •23.3.7 Endothelin Receptor Antagonism
- •23.3.8 Interleukin (IL)-13
- •23.3.9 Connective Tissue Growth Factor
- •23.3.10 Serum Amyloid P
- •23.4 Kidney
- •23.4.2 Pyridoxamine
- •23.4.3 Janus Kinase (JAK)1/2
- •23.4.4 Bindarit-CCL (MCP) Inhibitor
- •23.4.5 Phosphodiesterase Inhibition
- •23.5 Skin
- •23.5.1 TGFβ Targeted Therapies
- •23.5.2 Thalidomide/Pomalidomide
- •23.5.3 Paquinimod
- •23.6 Heart
- •23.6.1 Renin Angiotensin Aldosterone System (RAAS)
- •23.6.2 Transforming Growth Factor (TGF)-β
- •23.7 Conclusion
- •References
- •Index

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Chapter 18
Management ofIleal Pouch Strictures
andAnal Stricturing Disease:
AClinical Challenge
JeanH.Ashburn andTracyL.Hull
Abstract Restorative proctocolectomy with an ileal pouch-anal anastomosis
(IPAA) has been an ideal surgical option for patients with chronic ulcerative colitis
(UC), familial adenomatous polyposis, and selected patients with colorectal cancer
and Crohn’s disease for nearly four decades. In most cases, patients enjoy excellent
quality of life with a durable surgical and functional result, avoiding the need for a
permanent conventional ileostomy.
Despite great success, patients with IPAA may suffer from several pouch-related
complications that are a challenge for the patient and clinician. IPAA-associated
brotic stricturing disease is one such challenging complication that requires
thoughtful judgment for successful management. Treatment of brotic strictures of
the IPAA requires a multidisciplinary approach involving medical, endoscopic and
surgical input for accurate diagnosis, effective treatment, and improvement of quality of life.
The focus of this review is to provide a structured approach to the challenges that
the clinician encounters when faced with a patient with IPAA-associated brosis
and stricturing disease and to discuss the surgical options that alleviate the morbidity caused by ileal pouch brosis when medical treatments fail.
Keywords Ileal pouch · Surgery for IPAA stricture · Ileostomy · Multidisciplinary
ileal pouch team · Ileal pouch failure · Pouch disorders · Pouch stricture
Ileal pouch brosis
J. H. Ashburn · T. L. Hull (*)
Department of Colorectal Surgery, Digestive Diseases and Surgery Institute,
Cleveland Clinic Foundation, Cleveland, OH, USA
e-mail: jashburn@wakehealth.edu; HULLT@ccf.org
F. Rieder (ed.), Fibrostenotic Inammatory Bowel Disease,
https://doi.org/10.1007/978-3-319-90578-5_18
253© Springer International Publishing AG, part of Springer Nature 2018

254
J. H. Ashburn and T. L. Hull
18.1 Introduction
Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) has been an
ideal surgical option for patients with ulcerative colitis and familial adenomatous
polyposis, and very selected patient with colorectal cancer and Crohn’s disease, for
over three decades [1, 2]. In most cases, patients report excellent quality of life with
a durable surgical and functional result, and are able to avoid a lifelong ileostomy
[3]. IPAA has undergone several modications in its approach since it was popularized in the early 1980s. Over this time, innovative approaches have been applied to
IPAA surgery, functional outcomes have improved, and pouch survival has remained
high when performed in high-volume centers with surgeons experienced in these
types of surgery [4, 5].
When surgery goes according to plan and recovery proceeds without event,
patients enjoy excellent quality of life with manageable bowel function and are
without major lifestyle limitations [3]. However, circumstances may occur in which
patients suffer from immediate or eventual IPAA dysfunction with compromised
bowel function and quality of life [1, 6, 7]. One cause of a poorly functioning IPAA
that poses great challenges to the patient and clinician alike is development of
brotic stricturing disease in or adjacent to the IPAA.A proposed etiology, diagnostic approach, and management strategies often employed to address this challenge
will be discussed at length in the following text.
18.2 Construction oftheIleoanal Pouch
IPAA surgery consists of removal of the colorectum and creation of an ileal reservoir, which is constructed from the distal ileum (Fig.18.1). The reservoir is joined,
using varying methods, to the anorectal ring to restore intestinal continuity. In
patients with severe fulminant colitis or who have poor health, the procedure is
performed over an extended time period in multiple stages. This usually involves
performing a colectomy with end ileostomy, followed by proctectomy with
diverted IPAA when health is restored, usually after a waiting period >6months.
In very carefully selected patients who are otherwise t and have no risk factors
for poor healing, a single-stage IPAA may be a safe option, but this should be a
rare occurrence [8].
The rst reports of IPAA decades ago described construction of an S-shaped ileal
pouch that was secured to the anal canal using a hand-sewn anastomosis [9]. A variety of congurations have been considered over time, including the S, J, W and H
congurations (Fig.18.2) [10]. The J pouch is the most popular conguration presently, as it is the easiest and most expeditious to construct and its construction may
be assisted by stapling devices [11]. The S and W pouches necessitate a lengthier
segment of distal ileum and typically require a hand-sewn approach to construct the

18 Management ofIleal Pouch Strictures andAnal Stricturing Disease: AClinical Challenge
Fig. 18.1 Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA)
255
Fig. 18.2 Ileal J pouch
(left) and S pouch (right)

256
Fig. 18.3 Mesenteric reach with J (left) and S (right) pouch congurations
J. H. Ashburn and T. L. Hull
actual pouch, and thus are more time-consuming and technically challenging to
create. The J pouch conguration is most commonly used unless adequate mesenteric length is not available, as creating a tension-free pouch-anal anastomosis is the
most critical step to successful pouch surgery. In the case where a J pouch will not
reach without tension, an S pouch may be helpful as its conguration allows for a
longer reach (2–4cm longer than J pouch) into the pelvis (Fig.18.3). A pouch-anal
anastomosis created under tension is destined to result in anastomotic leak and pelvic sepsis in the short term, and leads to pelvic brosis or chronic pouch ischemia
with poor pouch function over time [1].
The ideal method of constructing the pouch-anal anastomosis has long been
debated, with the stapled IPAA as the preferred method over hand-sewn IPAA in
most instances. The introduction of stapling devices several decades ago made it
possible for the stapled IPAA to be less-time consuming and associated with better outcomes than hand-sewn IPAA [12]. In addition, patients with UC undergoing a stapled IPAA rarely develop cancer in the preserved anal transition zone
(ATZ) [13]. The stapled IPAA is carried out with either a single or double-stapled approach and the IPAA is joined to the ATZ, thus preserving anal sensory
epithelium (Fig. 18.4). Conversely, a hand-sewn IPAA is performed by rst
removing all anorectal mucosa from the dentate line cranially to the anorectal
transection (Fig.18.5). The IPAA is then delivered into the pelvis and sutured to
the internal sphincter at the neo dentate line in a radial fashion. If properly performed, the anal sensory epithelium and all rectal mucosa is removed in this
method. However, this method is more likely to exhibit stricture formation at the
anastomosis.

18 Management ofIleal Pouch Strictures andAnal Stricturing Disease: AClinical Challenge
257
Fig. 18.4 Stapled IPAA
Fig. 18.5 Mucosectomy with hand-sewn IPAA

258
J. H. Ashburn and T. L. Hull
18.3 Etiology ofFibrotic IPAA Dysfunction
Although many factors may underlie stricture formation, patients who undergo pelvic
pouch surgery most commonly develop brosis due to the presence of chronic pelvic
sepsis. This persistent inammation in the pelvis and/or anoperineum, if not controlled
early, leads to brotic changes in the pre-pouch small bowel (afferent limb), pouch
body, pouch outlet (efferent limb) or anoperineum [14, 15]. Chronic pelvic sepsis that
develops in the months following IPAA surgery is likely the result of technical complications leading to pouch-anal anastomotic leak. Conversely, pelvic sepsis which develops many months to years after IPAA surgery is more likely to be untoward sequelae
of Crohn’s disease. Regardless of etiology, all pouch- related sepsis necessitates expeditious diagnosis and drainage in order to reduce the risk of stricture development.
Other etiologies have been proposed as causes of IPAA brosis and stricture,
including weight gain and increased abdominal girth after pouch surgery resulting
in excessive mesenteric tension and chronic pouch ischemia [16–18]. In addition,
pelvic radiation in the setting of IPAA surgery is associated with pouch brosis and
subsequent high risk for failure [19].
Regardless of etiology, clinical symptoms from IPAA-related brosis depends
upon location and severity of inammation. Fibrotic strictures upstream of the IPAA
in the pre-pouch ileum (afferent limb) cause patients to suffer from obstructive symptoms like abdominal pain, cramping, and limited dietary intake of brous foods.
Bowel motions may be primarily watery or loose, as more bulky components of stool
do not pass easily and are detained upstream of the stricture. Fibrosis around or involving the pouch body restricts the ability of the pouch to accommodate and distend, thus
reducing its volume and leads to frequent bowel motions. Strictures of the efferent
limb (rectal cuff) or anal canal may make pouch emptying difcult, leading to excessive straining, feelings of incomplete emptying, chronic pouch dilation and stretch,
and overow incontinence [20]. Often, a careful and meticulous history can elicit
these telltale symptoms from the patient, allowing the clinician to predict the location
of stricture even before radiographic or endoscopic evaluation is complete.
An additional site of concern after IPAA surgery is the ileostomy closure site,
which may develop stricturing disease due to a subclinical anastomotic leak or ischemia at the time of ileostomy closure, or excessive scar formation after closure
(Fig.18.6). This site must always be interrogated and considered as a part of the
Fig. 18.6 Fibrotic stricture
at stapled ileostomy
closure site (reuse by
permission only JA CCF)
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