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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1199_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Foreword for Benign Anorectal Disorders
- •Preface 1
- •Preface 2
- •1.5 Nerve Supply of Anal Canal and Rectum
- •1.6 Anorectal Spaces
- •Bibliography
- •2: Physiology of Defecation
- •2.1 Normal Defecation
- •2.1.2 Reservoir
- •Contents
- •1: Surgical Anatomy of Anal Canal and Rectum
- •1.1 Rectum
- •1.1.1 Relations
- •1.2 Anal Canal
- •1.2.1 Inner Lining
- •Bibliography
- •3: Hemorrhoids
- •3.1 Introduction
- •3.3.1 Vascular Hemorrhoids
- •3.3.2 Mucosal Hemorrhoids
- •3.3.3 Internal Hemorrhoids
- •3.3.4 External Hemorrhoids
- •3.4 Symptoms
- •3.4.1 Bleeding
- •3.4.2 Protrusion
- •3.4.3 Pain
- •3.4.4 Discharge and Irritation
- •3.4.5 Anemia
- •3.4.6 Painful Mass in the Anal Region
- •3.5 Clinical Examination
- •3.5.1 Digital Rectal Examination
- •3.5.2 Endoscopic Examination
- •3.6 Treatment
- •3.6.2 Medical Treatment
- •3.6.3.1 Injection Sclerotherapy
- •3.6.3.2 Rubber Band Ligation
- •3.6.3.3 Cryotherapy
- •3.6.3.4 Infrared Coagulation (IRC)
- •3.6.3.4.1 Complications
- •3.6.3.6 Direct Current Therapy
- •3.6.4 Surgical Treatment
- •3.6.4.2 Closed Hemorrhoidectomy (Ferguson)
- •3.6.4.3 White Head (Submucosal) Hemorrhoidectomy
- •3.6.4.4 Laser Hemorrhoidectomy
- •3.6.4.5 LigaSure Hemorrhoidectomy
- •3.6.4.6 Hemorrhoidectomy by Ultrasonic Scalpel (HUS)
- •3.6.4.6.1 Mechanism
- •3.6.4.6.2 Coaptive Coagulation
- •3.6.4.6.3 Cavitation Effect
- •3.6.4.6.4 Technique
- •3.6.4.8 Doppler-Guided Hemorrhoidal Artery Ligation (DGHAL)
- •3.6.4.8.1 Procedure
- •3.6.4.8.2 Postoperative Complications
- •3.6.4.8.3 Results
- •3.7.1 Pain
- •3.7.2 Urinary Retention
- •3.7.3 Postoperative Bleeding
- •3.7.4 Wound Infection
- •3.7.5 Fecal Impaction
- •3.7.6 Stenosis
- •3.7.7 Recurrence
- •3.7.8 Incontinence
- •3.7.9 Other Late Complications
- •3.8 Special Situations
- •3.8.1 Thrombosed Hemorrhoids
- •3.8.2 Strangulated Hemorrhoids
- •3.8.3 Anorectal Varices and Portal Hypertension
- •3.8.4 Pregnancy
- •3.8.5 Crohn’s Disease and Ulcerative Colitis
- •3.8.6 Immunocompromised Patients
- •3.8.7 Coagulation Disorders
- •3.8.8 Fissure
- •3.8.9 Sepsis
- •Conclusion
- •Bibliography
- •4: Anal Fissure
- •4.1 Introduction
- •4.2 Epidemiology
- •4.4 Pathology
- •4.5 Etiopathogenesis
- •4.5.1 Microtrauma to Anal Canal Mucosa
- •4.5.2 Anal Sphincteric Spasm
- •4.5.3 Anal Mucosal Ischemia
- •4.5.4 Trauma During Childbirth
- •4.5.5 Other Causes of Secondary Anal Fissure
- •4.6 Clinical Features
- •4.7 Differential Diagnosis
- •4.8 Management
- •4.8.2.1 Medical Management
- •4.8.2.2.3 Fissurectomy
- •4.8.2.2.4 Anal Dilatation or Stretch (Lord’s Procedure)
- •4.8.2.2.5 V-Y Mucosal Advancement Flap
- •4.8.2.2.6 Internal Anal Sphincterolysis
- •4.8.2.2.7 Direct Current Treatment
- •4.8.3 Recurrence
- •4.8.4 Special Situations
- •4.9 Prevention
- •Conclusion
- •Bibliography
- •5: Perianal Sepsis and Fistula
- •5.1 Introduction
- •5.2 Anatomy
- •5.3 Epidemiology and Etiology
- •5.4.1 Anorectal Abscess
- •5.4.2 Anal Fistula
- •5.5 Diagnosis
- •5.5.1 Anorectal Abscess
- •4.8.2.1.1 Chemical Sphincterotomy
- •4.8.2.1.2 Topical Nitroglycerine
- •4.8.2.1.3 Topical Diltiazem (2 %)
- •4.8.2.1.4 Topical Nifedipine (0.3 %)
- •4.8.2.1.5 Topical Bethanechol
- •4.8.2.1.6 Botulinum Toxin
- •4.8.2.1.8 Minoxidil
- •4.8.2.2 Surgical Management
- •4.8.2.2.1 Internal Sphincterotomy
- •4.8.2.2.2 Fissurotomy and Posterior Sphincterotomy
- •5.5.2 Anal Fistulas
- •5.5.3 Special Studies
- •5.5.3.1 Sigmoidoscopy and Colonoscopy
- •5.5.3.2 Fistulography
- •5.5.3.3 Endoanal Ultrasonography
- •5.5.3.4 Computed Tomography (CT) Scan
- •5.5.3.5 Magnetic Resonance Imaging (MRI)
- •5.5.3.6 Anorectal Manometry
- •5.5.3.7 Fistuloscopy
- •5.6 Treatment
- •5.6.1 Anorectal Abscess
- •5.6.2 Horseshoe Abscess
- •5.6.3 Abscess and Primary Fistulotomy
- •5.6.4 Fistula-in-Ano
- •5.6.4.1 Advancement Flap
- •5.6.4.2 Fibrin Glue
- •5.6.4.3 Seton
- •5.6.4.4 Anal Fistula Plug
- •5.6.4.5 Ligation of Intersphincteric Fistula Tract (LIFT)
- •5.6.4.6 Video-Assisted Anal Fistula Treatment (VAAFT)
- •5.6.4.7 Autologous Adipose-Derived Stem Cell
- •5.6.4.8 Fistulectomy and Fistulotomy
- •5.6.4.9 Fistulectomy with Primary Sphincter Reconstruction
- •5.6.5 Intersphincteric Fistula-in-Ano
- •Conclusion
- •Bibliography
- •6: Pilonidal Disease
- •6.1 Introduction
- •6.2 Etiology
- •6.2.1 Theory of Acquired Origin
- •6.3 Clinical Features
- •6.4 Differential Diagnosis
- •6.5 Investigations
- •6.6 Treatment
- •6.6.1 Conservative Treatment
- •6.6.2 Operative Procedures
- •6.6.2.1 Simple Incision of Abscess
- •6.6.2.3 Excision With or Without Wound Closure
- •6.6.2.4 Bascom I Technique
- •6.6.2.6 Vacuum-Assisted Closure (VAC)
- •6.7 Prevention of Recurrence
- •6.8 Summary
- •Bibliography
- •7: Rectovaginal Fistulas
- •7.1 Introduction
- •7.2 Etiology
- •7.2.1 Congenital
- •7.2.2 Acquired
- •7.2.2.1 Child Birth
- •7.2.2.2 Diverticular Disease
- •7.2.2.4 Malignancies
- •7.2.2.5 Radiation Therapy
- •7.2.2.6 Operative Trauma
- •7.3.1 Size
- •7.3.2 Location and Etiology
- •7.3.3 Anatomy
- •7.3.3.1 Pelvic Enterovaginal Fistula
- •7.3.3.2 High Rectovaginal Fistula
- •7.3.3.3 Midzone Rectovaginal Fistula
- •7.3.3.4 Low Rectovaginal Fistula
- •7.3.3.5 Suprasphincteric and Transsphincteric Anovaginal Fistula
- •7.4 Clinical Presentation
- •7.5 Diagnosis
- •7.5.2 Anorectal Manometry
- •7.5.3 Neurophysiologic Testing
- •7.5.4 Vaginography
- •7.5.5 Barium Enema
- •7.5.6 Computed Tomography (CT) Scan
- •7.5.7 Endoanal Ultrasonography (EAUS)
- •7.5.8 Magnetic Resonance Imaging (MRI)
- •7.5.9 Endoanal MRI
- •7.6 Management
- •7.6.1 Medical Management
- •7.6.2 Surgical Treatment
- •7.6.2.1 Transanal Approaches
- •7.6.2.1.1 Mucosal Advancement Flap Repair
- •7.6.2.1.2 Transanal Sleeve Advancement Flap (TSAF)
- •7.6.2.2 Transvaginal Approaches
- •7.6.2.2.1 Transvaginal Inversion Repair
- •7.6.2.3 Transperineal Approaches
- •7.6.2.3.1 Simple Fistulotomy
- •7.6.2.3.2 Fistulotomy with Perineoproctotomy with Layered Closure
- •7.6.2.3.3 Perineal Repair with Levatoroplasty
- •7.6.2.4 Transsphincteric Approach
- •7.6.2.5 Repair with Biological Agents
- •7.6.2.6 Tissue Transfer Procedures
- •7.6.2.6.1 Gracilis Transfer
- •7.6.2.6.2 Martius Flap Repair
- •7.6.2.7 Transabdominal Approaches
- •7.6.2.8 Fistula Division
- •7.6.2.8.1 Coloanal Sleeve Reconstruction
- •7.6.2.8.2 Bricker Patch
- •7.6.2.8.3 Stoma
- •7.6.2.9 Laparoscopic Repair
- •7.7 Complications
- •7.7.1 Complications of Local Repairs
- •7.7.1.1 Bleeding
- •7.7.1.2 Infection
- •7.7.1.3 Urinary Retention
- •7.7.1.4 Recurrence
- •7.7.2 Complications of Abdominal Repairs
- •7.7.2.1 Bleeding
- •7.7.2.2 Infection
- •7.7.2.3 Enterocutaneous Fistula
- •7.7.2.4 Recurrence
- •Bibliography
- •8: Anorectal Injuries
- •8.1 Introduction
- •8.2 Etiology
- •8.2.1 Trauma
- •8.2.1.1 Blunt Anorectal Trauma
- •8.2.1.2 Penetrating Anorectal Trauma
- •8.2.1.3 Blast Injury
- •8.2.2 Anorectal Foreign Bodies
- •8.2.3 Obstetric Injury
- •8.2.4 Iatrogenic Injuries
- •8.2.5 Sexual Assault
- •8.3 Diagnosis of Anorectal Trauma
- •8.3.1 Unstable Patient
- •8.3.2 Stable Patient
- •8.4 Grade of Injury
- •8.5 Surgical Strategy
- •8.5.1 Technical Points in Surgery
- •8.5.2 Anorectal Foreign Bodies
- •8.5.4 Iatrogenic Anorectal Injuries
- •8.5.5 Closure of Colostomy
- •8.6 Outcome
- •8.6.1 Complications
- •8.6.2 Mortality
- •Conclusion
- •Bibliography
- •9: Anal Incontinence
- •9.1 Introduction
- •9.2 Anatomy of the Anal Sphincter Complex
- •9.3 Causes of Incontinence
- •9.3.1 Trauma
- •9.3.2 Neurological Conditions
- •9.3.3 Diarrheal States
- •9.3.4 Congenital Disease
- •9.3.5 Pelvic Floor Denervation
- •9.3.6 Aging
- •9.3.7 Miscellaneous
- •9.4 Clinical Evaluation
- •9.4.1 Medical History
- •9.4.2 Examination
- •9.4.3 Investigations
- •9.4.3.1 Manometry
- •9.4.3.2 Measurement of Sphincter Strength
- •9.4.3.3 Anal Sphincter Electromyography (EMG)
- •9.4.3.4 Anal Ultrasound
- •9.4.3.5 Balloon Proctography and Defecography
- •9.4.3.7 Endoscopy
- •9.4.3.8 Pudendal Nerve Motor Latency (PNML)
- •9.5.1 Conservative Treatment
- •9.5.1.1 Diet
- •9.5.1.2 Pharmacological Treatment
- •9.5.1.3 Bowel Management
- •9.5.1.4 Physical Treatment
- •9.5.1.5 Biofeedback
- •9.5.1.6 Faradic Stimulation
- •9.5.2 Surgical Treatment
- •9.5.2.1 Thiersch Operation
- •9.5.2.2 Repair of Obstetrical Injuries
- •9.5.2.4 Restoration of the Anorectal Angle
- •9.5.2.5 Muscular Graft
- •9.5.2.5.1 Gluteoplasty
- •9.5.2.5.2 Graciloplasty
- •9.5.2.5.2.1 Adynamic Graciloplasty
- •9.5.2.5.2.2 Dynamic Graciloplasty
- •9.5.2.6 Sacral Nerve Stimulation (SNS)
- •9.5.2.8 The FENIX™ Continence Restoration System
- •9.5.2.9 Miscellaneous Procedures
- •9.5.2.9.1 Smooth Muscle Plasty
- •9.5.2.9.2 Reinforcement of the Occlusion Mechanism
- •9.5.2.9.3 Secca Procedure
- •9.5.2.9.4 Injectable Agents
- •9.5.2.9.5 Colostomy
- •Bibliography
- •10: Complete Rectal Prolapse in Adults
- •10.1 Introduction
- •10.2 Etiology
- •10.3 Clinical Features
- •10.4 Diagnosis
- •10.5 Treatment
- •10.5.1 Abdominal Procedure
- •10.5.1.1 Suture Rectopexy
- •10.5.1.2 Prosthetic or Mesh Rectopexy
- •10.5.1.3 Posterior Mesh Rectopexy
- •10.5.1.4 Ripstein Procedure (Anterior Sling Rectopexy)
- •10.5.1.5 Rectopexy with Resection
- •10.5.1.6 Ventral Rectopexy
- •10.5.1.7 Laparoscopic Rectopexy
- •10.5.2 Perineal Procedure
- •10.5.2.1 Thiersch Procedure
- •10.5.2.2 Delorme Operation
- •10.5.2.3 Perineal Rectosigmoidectomy (Altemeier’s Procedure)
- •10.6 Comparison of Different Procedures and Approaches
- •10.7 Choice of Operation
- •10.8 Recurrent Prolapse
- •10.9 Summary
- •Bibliography
- •11: Pelvic Floor Dysfunction
- •11.1 Introduction
- •11.2 Anatomical Footprint for Pelvic Floor Surgical Navigation
- •11.3 Clinical Features
- •11.3.1 Urinary Continence
- •11.3.2 Bladder Storage/Sensation Symptoms
- •11.3.3 Voiding/Micturition Symptoms
- •11.3.4 Pelvic Organ Prolapse Symptoms
- •11.3.5 Sexual Dysfunction Symptoms
- •11.3.6 Anorectal Dysfunction Symptoms
- •11.3.7 Pelvic Pain Syndrome/Pudendal Neuralgia (Nantes Criteria)
- •11.3.8 Erectile Tissue Denervation (S2–S4) Symptoms
- •11.4 Evaluation for Pelvic Floor Dysfunction
- •11.4.1 Examination for Pelvic Organ Prolapse
- •11.4.2 Evaluation for Anorectal Dysfunction
- •11.4.3 Evaluation for Anorectal Incontinence
- •11.4.4 Evaluation for Functional Defecation Syndromes
- •11.4.4.4 Rule Out Slow-Transit Constipation
- •11.4.4.5 Imaging for Pelvic Floor Dysfunction with ODS
- •11.4.4.5.1 Dynamic Fluoroscopic Defecography
- •11.4.4.5.2 Anal Endosonography
- •11.4.4.5.3 Dynamic MRI Defecography
- •11.5 Causes of Anorectal Outlet Obstruction
- •11.5.1 Paradoxical Puborectalis Syndrome (PPR) or Anismus
- •11.5.2 Rectal Intussusception
- •11.5.3 Rectocele
- •11.5.4 Idiopathic Megarectum
- •11.6 Management of Pelvic Floor Dysfunction
- •11.6.1 Surgery for ODS: Stapled Transanal Resection Rectopexy (STARR)
- •11.6.1.1 Operative Procedure
- •11.6.2 Pelvic Organ Prolapse Surgery with STARR (POPSTARR)
- •11.7 Descending Perineum Syndrome
- •11.8 Functional Pelvic Pain Disorders
- •11.8.1 Levator Ani Syndrome
- •11.8.2 Proctalgia Fugax
- •Bibliography
- •12: Perianal Dermatology
- •12.1 Introduction
- •12.3.1 Contact Dermatitis
- •12.3.2 Danthron Contact Dermatitis
- •12.3.4 Seborrheic Dermatitis
- •12.3.5 Atopic Dermatitis
- •12.3.6 Psoriasis
- •12.3.7 Lichen Simplex Chronicus
- •12.3.9 Hidradenitis Suppurativa
- •12.3.10 Crohn’s Disease (Synonym: Regional Ileitis)
- •12.3.12.1 Anal Fissures
- •12.3.12.2 Anal Fistula
- •12.3.12.3 Pilonidal Cyst/Sinus
- •12.3.12.4 Pruritus Ani
- •12.4 Infections
- •12.4.1 Folliculitis and Furunculosis
- •12.4.2 Streptococcal Dermatitis/Perianal Cellulitis
- •12.4.3 Perianal Abscess
- •12.4.4 Ecthyma Gangrenosum
- •12.4.5 Necrotizing Infections
- •12.4.6 Common Mycoses
- •12.4.7 Thread/Pinworms
- •12.4.8 Sexually Transmitted Diseases (STDs)
- •12.4.9 Miscellaneous Infections
- •12.5 Benign Tumors
- •12.5.1 Hemorrhoids
- •12.6 Premalignant Dermatoses and Frank Malignancies
- •12.6.1 Porokeratosis
- •12.6.2 Anal Intraepithelial Neoplasia
- •12.6.3 Carcinoma of the Anus
- •12.6.5 Miscellaneous Malignancies
- •12.8 Trauma in the Perianal Area
- •Conclusion
- •References
- •13: Benign Ulcers of the Anorectum
- •13.1 Introduction
- •13.2 Etiology
- •13.3 Signs and Symptoms
- •13.3.1 Diarrhea
- •13.3.2 Pain
- •13.3.3 Hemorrhage
- •13.3.4 Discharges
- •13.3.5 Pruritis or Itching
- •13.4 Diagnosis and Investigation
- •13.4.1 Endoscopy (Macroscopic and Microscopic Appearance)
- •13.4.2 Anorectal Function Tests
- •13.4.3 Radiological Investigation
- •13.4.3.1 Defecography
- •13.4.3.2 Barium Enema
- •13.4.3.3 Transrectal Ultrasound
- •13.4.4 Differential Diagnosis
- •13.5 Special Anorectal Ulcers
- •13.5.1 Anal Fissure
- •13.5.2 Hemorrhoidal Ulcer
- •13.5.3 Varicose Ulcer
- •13.5.4 Tubercular Ulcer
- •13.5.5 Syphilitic Ulcers
- •13.5.6 Dysenteric Ulceration
- •13.5.7 AIDS-Associated Anorectal Ulcers
- •13.5.8.1 Introduction
- •13.5.8.2 Clinical Features
- •13.5.8.4 Investigations
- •13.5.8.4.1 Sigmoidoscopy
- •13.5.8.4.2 Defecography
- •13.5.8.4.3 Barium Enema
- •13.5.8.4.4 Transrectal Ultrasonography (TRUS)
- •13.5.8.4.5 Anorectal Manometry
- •13.5.8.5 Differential Diagnosis
- •13.5.8.6 Management of SRUS
- •13.5.8.6.1 Conservative Treatment
- •13.5.8.6.2 Surgery
- •13.5.9 Suppository-Related Ulcers
- •13.5.10 Nicorandil-Induced Ulcers
- •13.6 Radiation-Induced Anorectal Ulcers
- •Bibliography
- •14: Benign Strictures of Anorectum
- •14.1 Introduction
- •14.2 Diagnosis
- •14.3 Etiology
- •14.3.1 Amoebic Proctocolitis
- •14.3.2 Tuberculous Stricture
- •14.3.3 Lymphogranuloma Venereum
- •14.3.4 Actinomycosis
- •14.3.6 Ischemic Colitis
- •14.3.7 Stricture Following Bowel Anastomosis
- •14.3.8 Stricture Following Anorectal Surgery
- •14.3.9 Strictures Following Traumatic Injuries
- •14.3.10 Postradiation Stricture
- •14.3.11 Endometriosis
- •14.4 Treatment Options
- •14.4.1 Diet and Medical Treatment
- •14.4.2 Dilatations
- •14.4.3 Surgical Treatment
- •14.4.3.1 Sphincterotomy
- •14.4.3.2 Anoplasty (Stricturoplasty)
- •14.4.3.3 Surgery for Rectal Strictures
- •14.4.3.4 Colostomy
- •14.5 Summary
- •Bibliography
- •15: Benign Tumors of the Anorectum
- •15.1 Introduction
- •15.2 Benign Tumors of Epithelial Origin
- •15.2.2 Keratoacanthoma
- •15.2.3.1 Etiopathogenesis
- •15.2.3.2 Epidemiological Facts
- •15.2.3.4 Investigations
- •15.2.3.5 Treatment
- •15.2.4 Preventive Measures
- •15.2.5.1 Serrated Polyps and Adenoma
- •15.2.6 Nonneoplastic Adenomas
- •15.2.6.1 Hyperplastic Polyp
- •15.2.6.3 Hamartomatous Polyps, Juvenile Polyp, and Retention Polyp
- •15.2.6.4 Lymphoid Hyperplasia and Lymphoid Polyp
- •15.3 Benign Mesenchymal Tumors
- •15.3.1 Lipoma
- •15.3.2 Fibroma
- •15.3.4 Leiomyoma
- •15.3.7 Hemangioma
- •15.3.8 Lymphangioma
- •15.4 Benign Exogenous, Extrinsic, and Miscellaneous Tumors
- •15.4.1 Barium Granuloma
- •15.4.2 Endometriosis
- •15.4.4 Sarcoidosis
- •15.4.5 Tuberculosis
- •Conclusion
- •Bibliography

9 Anal Incontinence
113
Fig. 9.3 Saline perfusion system showing the anorectal pressures. There are 16 sensors at a distance of 1 cm, each
which tracks the pressure changes in the anorectum (Diagram courtesy of Dr. Uday C. Ghoshal)
a
bcd
Fig. 9.4 EMG study

114
P.N. Joshi et al.
to the repair of anorectal malformations and for
biofeedback therapy for nonrelaxing puborectalis
syndrome.
EMG is used to record electrical activity in the
muscle of continence during anorectal function. It
is used to determine whether there is evidence of
inappropriate puborectalis contraction during defecation. It is also used for sphincter mapping, especially in patients with ectopic anus and congenital
anomalies and after severe disruption. Needle
EMG either with concentric needle or with singlefi ber electrodes had in the past an important role in
the clinical mapping of the EAS. The result of needle EMG agrees well with endoanal USG and with
surgical or histological methods to identify the
sphincter damage. Surface EMG with an anal plug
within the anal canal is without pain and with less
risk of infection and has a defi nite role in indicating
and applying biofeedback training.
9.4.3.4 Anal Ultrasound
Endoscopic ultrasound (EUS) is one of the latest
additions to the armamentarium for the evaluation of the anal sphincter. EUS maps the defects
of the internal and external sphincters. It is the
single most important investigation in the management of sphincter injuries. The internal and
external anal sphincters are seen as hypoechoic
and hyperechoic structures, respectively, in the
EUS. The puborectalis muscle is seen as a hyperechoic U-shaped structure. The defect in the
sphincter could be demonstrated preoperatively,
which helps in planning the incision and repair.
EUS cannot be performed if there is anal stenosis. The lack of widespread availability and training is also a limiting factor (Fig.
9.5 ).
When performed by experienced clinician,
endoanal USG approaches 100 % sensitivity and
specifi city in identifying the sphincter defects. A
15 mm diameter probe with 360° rotation
10 MHz transducer are used to image the sphincter at several levels in the anal canal. The IAS is
imaged as a hypoechoic ring close to the transducer, surrounded by a hyperechoic ring representing the EAS. Sphincter defect is measured as
a lateral breaks in the sphincter. Endo USG
sphincter abnormalities are seen in 90 % of the
women whose sole risk factor for fecal incontinence is obstetric trauma.
Fig. 9.5 Anorectal USG endoscopic ultrasonogram
showing the defect in external anal sphincter (Diagram
courtesy of Dr. Preveer Rai)
9.4.3.5 Balloon Proctography and Defecography
This study is useful in establishing any alteration
in the anatomical structures and mechanisms of
defecation (Macleod 1979 ; Mahieu et al. 1984 ;
Pichrell et al 1959 ). It shows how well the person
can hold and evacuate stool. It also identifi es
structural changes in the rectum and anus such as
rectoceles and rectal prolapse.
Defecography or the dynamic proctogram is
used to defi ne the anatomy and changes of the
pelvic fl oor muscle position with defecation. It
can identify abnormalities such as prolapse, perineal descent, and intussusception. This procedure
utilizes the paste of barium and potato powder to
stimulate the fecal material. Video recording of
straining, squeezing, and defecation into a radiolucent commode allows real-time assessment of
anatomic changes during defecation.
9.4.3.6 Magnetic Resonance
Imaging (MRI)
It is an alternative to anal ultrasound and provides
more detailed information about the anatomy
especially about the external sphincter (Fig. 9.6 ).
9.4.3.7 Endoscopy
Flexible or rigid sigmoidoscopy and fl exible
colonoscopy may be useful to exclude colonic
pathology.

9 Anal Incontinence
115
Fig. 9.6 MRI pictures of the pelvic fl oor and anorectum
9.4.3.8 Pudendal Nerve Motor Latency (PNML)
The pudendal nerve, containing fi bers from sacral
nerves S2–S4, provides motor innervation to the
external sphincter and receives sensory information from the perineum. PNML measures the
conduction time to external sphincter contraction
after the nerve stimulation at the level of the
ischial spine. This is easily performed using a
digitally mounted device with a stimulating electrode mounted at the fi ngertip and recording electrode mounted at the base of the fi nger. The mass
production of a self-adhesive disposable electrode, which can easily be mounted on a gloved
fi nger, has enabled this assessment to become
routine in most centers.
The normal latency is 2.1 ± 0.2 ms. Prolonged
latency may be associated with obstetric injury, perineal descent, prolapse, and medical neuropathies
The success rate after sphincter repair decreases
from about 90 % with intact pudendal nerve to 50 %
in the presence of pudendal neuropathy.
9.5 Treatment of Anal
Incontinence
9.5.1 Conservative Treatment
9.5.1.1 Diet
Dietary modifi cation is important for successful management. Both diarrhea and constipation
can contribute to incontinence. So dietary advice
must be tailored to address the underlying cause,
or it may be ineffective or counterproductive.
In persons with disease aggravated by diarrhea
or those with rectal loading by soft stools, the
patients must be advised to increase dietary fi ber
and reduce intake of wholegrain cereals/bread,
fruit, and vegetables which contain natural laxative compounds (rhubarb, fi gs, prunes/plums);
beans, pulses, cabbage, sprouts, and spices (especially chili); artifi cial sweeteners (e.g., sugar-free
chewing gum); alcohol (especially stout, beer,
and ale); lactose if there is some degree of lactase
defi ciency; and caffeine. Caffeine lowers the resting tone of the anal canal and also causes diarrhea. Excessive doses of vitamin C, magnesium,
phosphorus, and/or calcium supplements may
increase fecal incontinence. Reducing olestra fat
substitute, which can cause diarrhea, may also
help (Norton et al.
2007 ).
9.5.1.2 Pharmacological Treatment
Patients with minor degree of incontinence or
patients who are unfi t for surgery may be
treated conservatively (Brocklehurst 1978 ;
Marti and Noethiger 1981 ). Stool thickeners,
bulk-forming agents, and high fi ber intake
should be routinely prescribed to obtain fi rm
stools. Evacuation can be stimulated by glycerin suppositories used at predictable time of
the day. The suppositories produce rectal distention. Through repeated applications, rectal
volume may increase and the sensations of rectal distention are stimulated. The patient will
then be continent until the next artifi cially
induced bowel movement. Various pharmacological agents are:
(a) Adsorbents :
Kaopectate – useful for mild degree of
incontinence and acts by absorbing excess
fl uid in the stool.
Opium derivative – loperamide (Imodium),
commonly used. Others agents are diphenoxylate hydrochloride (Lomotil), diphenoxylate
hydrochloride + atropine, codeine, and tincture of opium.
(b) Tricyclic antidepressant :
Like amitriptyline (20 mg, daily). It has
anticholinergic and serotoninergic properties.
(c) Bulking agents :

116
P.N. Joshi et al.
Better used for patients of diarrheal vari-
ety of irritable bowel syndrome
(d) Bile salt binders:
Cholestyramine and colestipol. These resins treat bile acid diarrhea by binding with
bile salts in the small intestine.
(e) Topical agents :
Act on the internal sphincter and increases
the resting tone, e.g., 10 % phenylephrine
9.5.1.3 Bowel Management
The aim is to allow the patients to produce a complete bowel movement at a schedule time by
using an individualized combination of dietary
measures, laxatives, suppositories, enemas, and
digitization. This method is useful for patients
with neurological problems, diabetes, and congenital anorectal malformation. This is also useful for patients with overfl ow incontinence and
pediatric patients with encopresis having symptoms of seepage of stool from full rectum. The
aim is complete cleansing of the colon by the use
of various combinations. Later, the use of the
daily formulation of polyethylene glycol/laxative
is better.
9.5.1.4 Physical Treatment
Muscular training is very important to stimulate
muscles and to increase the muscular activity by
regular sphincter exercise. Training may be voluntary, with or without biofeedback control of
the increased endoanal pressure level, or may be
performed by electrical stimulation using
implanted electrodes or externally activated plugs
(Bleijenberg and Kuijpers
1987 ; Loygue and
Dubois 1964 ).
Electrical stimulation seems not to result in an
increase of anal tone but regression of muscular
fatigability. If contractions can be sustained for
50–60 s, rectal compliance will increase and then
continence can be achieved.
9.5.1.5 Biofeedback
Biofeedback has a broad acceptance as a useful
treatment of fecal incontinence. The term “biofeedback” describes a therapeutic instrument that
derives from psychologic “theory of learning.”
This type of learning is also called instrumental
learning or operant conditioning. A body function that cannot or can only be perceived poorly
by the subject under normal condition is measured by a technical device and demonstrated
(feedback) to the subject. There are two methods
of biofeedback training:
(1) Response to rectal distension using mano-
metric techniques
(2) Unrelated to rectal distension, muscle
strengthening using EMG or manometric
technique
Biofeedback may result in a better coordination of sphincter activity in carefully selected
(without any obvious cause on defecography but
abnormal manometry) and motivated patients
(Corman
1985 ; Denis et al 1983 ). A balloon
placed within the anal canal is connected to a
transducer, and a graph on the monitor will show
the pressure readings at different stages of
attempted defecation. The patient observes the
anal pressure peak reached by sphincter contraction with or without rectal distention. He is
trained accordingly as when and how to relax the
sphincters. Improvement usually occurs within
three to fi ve training sessions.
The treatment is supervised by a biofeedback
therapist who evaluates patients during 6–8
weeks. Both methods are effective, although
some patients may respond better to one system
than the other. Biofeedback therapy is best
applied to motivated patients with some ability to
voluntarily contract the external anal sphincter
(even if the muscle is partially disrupted) and an
intact rectal sensation. Biofeedback is benefi cial
in patients with incontinence of variable etiologies such as diabetes, after childbirth, and after
anorectal surgery; however, the best results can
be seen in patients who have primarily a sensory
problem in the anal canal leading to insensible
loss of feces. The results of biofeedback training
in different patient groups suffering from incontinence vary from 64 to 89 %, with an overall success rate of approximately 70 %. Symptom
improvement may sustain several years after
treatment. The exact mechanism of success is
unclear. Nevertheless, it is safe and effective and

9 Anal Incontinence
117
does not preclude other treatments. Biofeedback
may result in a better coordination of sphincter
activity in carefully selected (without any obvious cause on defecography but abnormal manometry) and motivated patients (Corman 1985 ;
Denis et al 1983 ).
9.5.1.6 Faradic Stimulation
The goals of this treatment are to increase the
strength of the pelvic fl oor muscles and normalize
the refl ex activity of the muscles via stimulation of
the afferent and efferent fi bers of the anorectal
sphincters. An electric muscle stimulator with
sinusoidal, faradic, and interrupted direct current
outputs is used. It has been suggested that electrical stimulation can transform type II (fast twitch)
motor units to mainly type I (slow twitch) units
(Sokunbi and Okunsanya 2002 ). Type I motor
units have been observed to generate more tension,
thereby increasing the tone of the pelvic fl oor muscles, resulting in decrease in the symptoms of
incontinence. Modifying sensations around the
anorectal region can inhibit fecal incontinence by
stimulating the afferent fi bers, whereas stimulation
of efferent fi bers can induce voiding by stimulating the contraction of the region.
The patient lies in a prone position with pillows under the abdomen and the ankle. The
patient should be adequately draped to allow
minimal exposure of the area being treated. A
four-pole electrode (6 cm by 8 cm) application is
utilized with two electrodes placed medial to the
ischial tuberosities on either side of the anus, and
the remaining two are placed along an imaginary
line joining the posterior inferior iliac spine, 5 cm
each from the midline (Continence Foundation
2001; Sokunbi and Okunsanya
The duration of the stimulation is between
20 min and an hour per day for about 20 days. The
treatment may be needed for a period ranging
from a few weeks to several months (Continence
Foundation 2001; Sokunbi and Okunsanya 2002 ).
2002 ).
9.5.1.7 Percutaneous Tibial Nerve
Stimulation (PTNS)
There is extensive evidence regarding the effi cacy of PTNS in urinary incontinence. Data on
the effi cacy of PTNS for fecal incontinence (FI)
are limited to a small case series with short follow- up. However, in a recently cited study, it was
found to improve the FI score after 12 sessions of
treatment and further after top-up sessions.
PTNS was well tolerated with high acceptability in the majority of patients. The effect of PTNS
diminishes with time (usually after 42 months),
and additional therapy sessions at 6 months’
intervals may result in greater improvement
(Hotouras et al.
2014 ).
9.5.2 Surgical Treatment
The main indication for surgical intervention is
major incontinence refractory to biofeedback and
sacral nerve stimulation. This is the fi rst line of treatment option in cases of obstetric injury with isolated
sphincter defect and has an excellent outcome.
The choice of surgical techniques depends
mainly on the nature and the level of the lesion
responsible for incontinence. Bowel preparation
and sterilization are mandatory.
The aims of the various surgical techniques
used are reduction of anal canal diameter, sphincter construction, reinforcement of the occlusion
mechanism, increase of muscular mass, decrease
in the size of the anorectal angle at rest, substitutive sphincteroplasty, and artifi cial sphincter
implantation.
9.5.2.1 Thiersch Operation
Encirclement of the anal orifi ce with wire or nonabsorbable suture material, fascia lata, or Tefl on
has been used to prevent rectal prolapse (Goebell
1927 ). This procedure creates a static barrier to
passage of rectal content, especially solid feces,
but not liquids or fl atus. It does not contribute
anything to voluntary control and maintenance of
continence. This procedure is frequently complicated by secondary infection and extrusion of the
suture material as a foreign body and is offered to
old and debilitated patients and children (Fig. 9.7 ).
9.5.2.2 Repair of Obstetrical Injuries
In this type of injury, the posterior vaginal wall,
muscles of the perineum, the external anal
sphincter, the internal anal sphincter, and the wall

118
Fig. 9.7 Thiersch
operation
P.N. Joshi et al.
of the rectum are torn. Hence it is necessary to
stitch back all these components to regain the full
continence. An attempt at repair should be made
at the time of delivery. If this fails, at least 6
months should elapse before an attempt at repair
is made which gives the tissue suffi cient time to
return to normal. The operation at this time will
be easier to perform and chances of success are
enhanced.
Layer method of repair is done for old obstetric tears (Fig. 9.8a–e ). An inverted semilunar inci-
sion is made at the junction of the posterior
vaginal wall and the rectal mucosa, and the lateral
end of the incision should reach the stumps of the
sphincters. The vaginal fl ap is dissected upward
keeping close to the vaginal wall. The dissection
is carried out till the puborectalis is demonstrated
on either side. The dissection is then carried out to
demonstrate and mobilize the stump of the sphincter muscle, which is then grasped by Babcock forceps. The defi cient seromuscular layer of the
rectum is repaired by taking interrupted sutures
with atraumatic 2-0 PDS. The puborectalis part of
levator is stitched in front by two–three interrupted stitches. The stumps of mobilized sphincter ends are then stitched together in front with
same suture material or Prolene. Excessive vaginal mucosa is excised and the wound is closed
with a drain, if necessary. An indwelling urethral
catheter is passed into the bladder and retained for
4–5 days; the drain is removed after 48 h and skin
suture after 7 or 8 days. It is not necessary to constipate the patient in immediate postoperative
period. Stool softeners are given from the third
day of operation to have an easy passage of soft
stool. The addition of an antibiotic is essential for
the prevention of infection.
Repair of the defi ciency following fi stula
operation is done by double bracing the sphincter
muscles. This type of repair is feasible if twothirds of the sphincter muscle is intact (Figs.
9.9
and 9.10 ).
9.5.2.3 Sphincter Reconstruction
(Sphincteroplasty
with Levatorplasty)
Direct reconstruction is the procedure of choice
for tears, traumatic and obstetrical laceration, or
iatrogenic sphincter trauma. For old, established
lesion, secondary sphincteroplasty gives good
results (Blaisdell 1940 ; Blaisdell 1956 ; Engel
et al 1974 ).
In fresh lesion, reconstruction with end-toend sphincter sutures should always be tried.
U-shaped deep stitches should be placed using
slowly absorbable synthetic monofi laments.

9 Anal Incontinence
a
119
b
c
d
e
Fig. 9.8 ( a – e ) Steps of layered repair of obstetric perineal tear
Knot should be tied carefully to avoid further
muscular lacerations as healthy muscles are not
able to hold a simple suture. Vaginal and anal
wound edges are closed, whereas skin edges are
approximated to allow drainage and to prevent
infection.
In old lesion, repair is performed through a
curvilinear incision parallel to the external
sphincter, extending to at least 180–200°.
Anoderm and anal mucosa are mobilized from
the scar and the sphincter. The sphincter is dissected free with wide margin. The muscle ends
are overlapped to reduce anal margin. Mattress
sutures are placed with a 2.0 absorbable suture
material. The skin wound is closed partially to
prevent infection. Electrical stimulation may be

120
P.N. Joshi et al.
Figs. 9.9 and 9.10 Overlapping sphincteroplasty
(Courtesy of S. Mantoo, Singapore)
helpful for the identifi cation of the sphincter.
Nerve branches should be preserved, and fi brotic
edges of the sphincter should not be excised. The
use of nerve stimulator has been found to be useful in diffi cult situation.
When dealing with obstetric tears or a complicated episiotomy, it is necessary to repair not
only the sphincter but also the rectovaginal septum (Corman 1980 ; Mille et al. 1988 ).
Sphincteroplasty is successful in more than
90 % of the patients with fecal incontinence due
Table 9.2 Results of direct sphincter repair
% With complete
References n
Manning and Pratt (
Fang et al. (
Corman (
Cterceko et al. (
Table 9.3 Overall results of anterior overlapping
sphincteroplasty
References No. Excellent/good (%)
Fang et al. (
Hawley (
Fleshman et al. (
Oliveira et al. (
Gilliland et al. (
Buie (
1985 ) 28 100
1985 ) 100 52
2001 ) 158 62
1964 ) 102 74
1984 ) 79 58
1988 ) 44 54
1984 ) 76 58
1991 ) 55 72
1996 ) 55 71
1998 ) 100 60
response
to sphincter injury, restoring most of them almost
completely to normal. Results of various series
have been shown in Tables
9.2 and 9.3 .
9.5.2.4 Restoration of the Anorectal Angle
An adequate fl ap-valve mechanism can be
achieved by the restoration of the anorectal angle.
A postanal repair devised by Parks ( 1975 ) is the
most effective operation especially in patients
with sphincter denervation as in descending
perineum syndrome and idiopathic anorectal
incontinence with internal and external sphincter
dysfunction (loss of the normal anorectal angle
as after abdominal rectopexy or short anal canal).
Adequate muscle mass must be present for this
operation to be successful.
A V-shaped incision posterior to the anus,
with its apex at the level of the tip of the coccyx,
is made. The intersphincteric plane is opened and
bluntly dissected. The anal canal and the internal
sphincter are separated from the external sphincter up to the level of the puborectalis sling. The
dissection is continued upward in the retrorectal
fatty space after the division of Waldeyer’s fascia
to expose the upper surface of the levator ani
muscles. The presacral fascia should not be
opened so as to avoid massive venous bleeding.
A lattice is constructed as high as possible
with polypropylene, size 0 from one limb of the

9 Anal Incontinence
121
Table 9.4 Results of postanal repair
Good/excellent
Reference no.
Browning, Parks 140 (
Henry, Simson 129 (
Yoshioka, Keighley 116 (
1983 ) 86
1985 ) 70
1988 ) 57
results (%)
levator ani to the other at the level of the
iliococcygeal muscle. A second lattice is inserted
at the level of the pubococcygeal muscle. A third
one is inserted in order to approximate the
puborectalis muscle. Finally, the external sphincter is approximated and the skin sutured in the
shape of a Y after insertion of suction drainage.
The knots should not be tied too tightly to prevent
ischemia and necrosis. Results of post anal repair
have been depicted in Table 9.4 .
9.5.2.5 Muscular Graft
To supplement the sphincter muscular mass, several muscular grafts have been used. In the fi rst
half of the century, the gluteus maximus muscle
was the most commonly used muscle as a transposition fl ap. Chetwood fi rst described the operation in 1902 involving the gluteus maximus
muscle and fascial slings to reinforce the sphincter muscles in children. In 1929, the procedure
was revised in which free ends of the fascia were
used to encircle the anus and anchored to the gluteus maximus muscle on each side. In this technique, the anal canal was enclosed in a fascial
ring so that the sphincter could be tightened by
contracting the gluteus muscle (Wreden
1929 ).
Since that time, multiple case reports have
reported the gluteus maximus muscle as an effective replacement of the anal sphincter. However,
enthusiasm for the gluteoplasty diminished after
the introduction of the gracilis procedures.
In 1981, Salmons reported on the transformation of skeletal muscle from fast-twitch fatigueprone (type II) muscle fi bers to slow-twitch
fatigue-resistant (type I) muscle fi bers by the
application of low-frequency electrical stimulation. Expanding on this idea in 1988, Baeten and
associates ( 1988 ) connected a pulse generator to
a patient with suboptimal function of the gracilis
muscle transplant. The result was a neosphincter with involuntary resting tone. Widespread
adoption of this technique improved the success
of gracilis transpositions. However, the procedure
involves many components and requires technical
expertise, predisposing it to an array of complications that proved to undermine its advantages.
Consequently, the focus shifted back to its static
counterpart with modifi cations of the original
technique to improve outcome. Graciloplasty
continues to be performed to replace sphincter
muscle loss and as an adjunct to the artifi cial
bowel sphincter. Advances in the technique of
stimulated graciloplasty have led to its application
in total anorectal reconstruction for anal atresia
and following abdominoperineal resection (APR).
Gluteus myocutaneous fl ap is used for large skin
and muscle defects such as after extralevator APR.
9.5.2.5.1 Gluteoplasty
The advantages of the gluteus maximus muscle
include its large muscle bulk, single proximal
innervation, and proximity to the anal canal.
In addition, buttock contraction is a standard
response to impending incontinence. In the
prone-jackknife position, the lower 10 % of both
gluteus maximus muscles and fascia are mobilized from their origins on the ileum and sacrum
and distally freed in two strips. The neurovascular bundle is preserved which arises near the
ischial tuberosity. The two strips on each side are
tunnelled beneath the skin and secured to their
contralateral counterparts through lateral incisions on the contralateral sides of the anus
(Fig. 9.11 ).
9.5.2.5.2 Graciloplasty
9.5.2.5.2.1 Adynamic Graciloplasty
Two or three 3- to 5-cm longitudinal incisions
along the length of the medial thigh allow the
identifi cation and mobilization of the gracilis.
The neurovascular supply arises in the proximal
portion of the muscle and allows the division of
the tendon at its attachment to the tibia without
compromising viability. The muscle is then
tunneled through either the anterior or the posterior perianal incision. Through an additional contralateral perianal incision, the muscle is wrapped
around the anus using one of three confi gurations: α, gamma, or epsilon. The tendon is

122
Fig. 9.11 Gluteoplasty
a
P.N. Joshi et al.
b
c
Fig. 9.12 ( a – c ) Adynamic graciloplasty
anchored to the contralateral ischial tuberiosity
with a nonabsorbable suture. However, the muscle, not the tendon, is meant to encircle the anus,
as the operation aims to achieve a dynamic result
as opposed to Thiersch-type wrap of a fi brotic
band of tendon. At completion, the wrap should
allow the snug insertion of one fi nger (Fig. 9.12a–c ).
The patient relaxes the sphincter by assuming a
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