PELVIC FLOOR DISORDERS : a multidisciplinary textbook. [2 ed.] 9783030408619, 3030408612

Table of contents :
Foreword
Preface
Contents
Contributors
Part I: State of the Art Pelvic Floor Anatomy
1: Pelvic Floor Anatomy
1.1 Introduction
1.1.1 Support of the Pelvic Organs: Conceptual Overview
1.2 Anatomy and Prolapse
1.2.1 Overview
1.2.2 Apical Segment
1.2.3 Anterior Compartment
1.2.4 Perineal Membrane (Urogenital Diaphragm)
1.2.5 Posterior Compartment and Perineal Membrane
1.2.6 Lateral Segment Comprising of the Levator Ani Muscle Support
1.2.7 Endopelvic Fascia and Levator Ani Interactions
1.2.8 The Levator Plate
1.2.9 Interaction Between Different Compartments
1.2.10 Nerves
1.3 Summary
References
2: Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues
2.1 Introduction: How Complicated Is That?
2.1.1 The Role of Reproductive Hormones on the Pelvic Floor Function During the Life Span
2.1.2 Hormonal Changes and Pelvic Floor Symptoms
2.2 The Role of Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues in Epidemiology of Pelvic Floor Function
2.2.1 Sexual Hormone Receptors
2.2.2 Biochemical Properties of Pelvic Floor Tissues
2.2.2.1 Collagen of Pelvic Floor Tissues
Anterior Vaginal Wall
Periurethral Tissue
Cardinal Ligaments
Uterosacral Ligament
Endopelvic Fascia
The Arcus Tendineus Fasciae Pelvis (ATFP)
Elastin
2.2.3 The Role of Matrix Metalloproteinases (MMPs) on Pelvic Floor Tissue Remodeling
2.3 The Recent Investigations and Possibilities for Future Research
2.4 Hormonal Impact on Vaginal Atrophy, the Role on Pelvic Floor Dysfunction, and Treatment
2.4.1 Conclusion: Hormone Therapy
2.5 Summary and Recommendations for Practice
References
3: The Integral System of Pelvic Floor Function and Dysfunction
3.1 Introduction
3.2 The Integral Theory of Pelvic Floor Function
3.3 The Integral System
3.4 Part 1: Pubourethral Ligament: How the Midurethral Sling Was Discovered
3.4.1 Development of the Artificial Collagenous Neoligament for PUL Repair
3.4.2 Application of the Neoligament Surgical Principle to PUL and Other Ligaments
3.4.3 Clinical Relevance of Some Initial MUS Operation Findings (1988–1989)
3.4.4 Closure of the Urethra
3.4.5 Role of PUL and Subsidiary Structures in Normal Urethral Closure and Incontinence
3.4.6 Role of Lax PUL in the Causation of Urinary Stress Incontinence
3.4.7 External Urethral Ligament Laxity: A Rarely Recognized Cause of Nonstress Urine Leakage
3.4.8 Anorectal Closure
3.4.9 Serendipity: Cure of Fecal Incontinence (FI) Following PUL and USL Sling Repair
3.4.10 Surgical Repair of PUL by MUS
3.4.11 Surgical Results for PUL Repair (Midurethral Sling)
3.4.12 Zone of Critical Elasticity: Tethered Vagina Syndrome and Role of Fibrosis in Incontinence After Post-obstetric Fistula Repair
3.5 Part 2: The Uterosacral Ligament “USL”: Cure of Uterine Prolapse with Posterior Sling
3.5.1 Role of USL in Micturition
3.5.2 Role of USL in Normal Defecation
3.5.3 Lax USLs: Anatomical Pathways to Pain, Bladder, and Bowel Dysfunction
3.5.4 Lax USLs: Role in “Obstructive Micturition and Defecation” (Organ Emptying Problems)
3.5.5 Lax USL: Pathways from Ligament Laxity to Symptoms of Urge, Frequency, and Nocturia
3.5.6 Lax USL: Anatomical Pathway to Chronic Pelvic Pain
3.6 Part 3: Cardinal Ligament (CL): Its Role in Cystocele Causation
3.7 Part 4: ATFP: Role in Lateral Cystocele and Urinary Stream Diversion
3.8 Part 5: Deep Transversus Perinei (DTP): Role in Rectocele and Descending Perineal Syndrome
3.8.1 Anatomical and Surgical Significance of DTP Ligaments
3.8.2 PB Function Is Linked to USL Function
3.8.3 Surgical Principles Derived from the Integral System
3.8.4 Complications of Total Ligament Repair Surgery Using the TFS Tensioned Mini Sling
3.8.5 Role of Muscle in Continence Control
3.8.6 Muscle, Ligament, or Both?
3.8.7 The Three-Muscle, 3-Month Pelvic Floor Muscle Strengthening Study
3.8.8 Is Rectopexy or Sacrocolpopexy (SCP) an Anatomically Correct Method for Restoration of Rectal Intussusception and Rectal Prolapse?
3.9 Conclusion
References
4: The Pelvic Floor: Neurocontrol and Functional Concepts
4.1 Introduction
4.2 The Urinary and Recto-Anal Systems
4.3 Urinary and Faecal Storage and Voiding
4.3.1 Bladder Equilibrium
4.3.2 The Lumbosacral Loop
4.3.3 The Pontine Loop
4.3.4 The Cortical System
4.3.5 Central Representation of Afferent Information from Bladder and Bowel
4.3.6 Universal Organisation of CNS Control Systems
4.4 The Pelvic Floor and Its Innervation
4.5 Pelvic Floor Dysfunction in Incontinence
4.6 Investigation of the Pelvic Floor
4.7 Urinary Storage: The Default Mode
4.8 Urethral Opening: Voiding
4.9 The Bladder Trigone During Micturition
4.10 Neurological Feedback Control of Anorectal Function
4.11 When Things Go Wrong: Urge, Frequency, and Nocturia
4.12 Overactive Bladder Syndrome (OAB)
4.13 How Does Detrusor Overactivity Relate to Feedback Control?
4.14 Events Occurring in Detrusor Overactivity and Overactive Bladder Syndrome
4.15 Non-linear Flow Mechanics Enhance the Storage and Voiding Responses
4.16 Why Urodynamic Urethral Pressure Measurements Correlate Poorly with Clinical States
4.17 How Repeatable Are Urine Flow Measurements in an Individual?
4.18 Detrusor Underactivity
4.19 Low Bladder Compliance
4.20 Clinical Variations in Bladder Symptoms Are Consistent with the Chaos Theory Feedback Equation
4.21 Concluding Remarks
References
Part II: Pelvic Floor Imaging
5: Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound
5.1 Introduction
5.2 Principles of Pelvic Floor Ultrasound
5.3 Two-Dimensional Transperineal Ultrasound (2D TPUS)
5.3.1 Convex Transducers
5.3.2 Linear/Microconvex Transducers
5.4 Three-Dimensional/Four-Dimensional Transperineal Ultrasound (3D/4D TPUS)
5.4.1 Volumetric Transducers
5.5 Two-Dimensional Endovaginal Ultrasound (2D EVUS)
5.6 Three-Dimensional Endovaginal Ultrasound (3D EVUS)
5.7 Two-Dimensional Endoanal Ultrasound (2D EAUS)
5.8 Three-Dimensional Endoanal Ultrasound (3D EAUS)
5.9 Conclusions
References
6: Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy
6.1 Introduction
6.2 Basic Technique
6.3 The Anterior Compartment: Urethra and Bladder Base
6.3.1 The Urethra
6.3.2 Paraurethral Tissues
6.3.3 The Bladder Neck and Trigone
6.4 The Fornices
6.5 The Central Compartment: Uterus and Vault
6.6 The Posterior Compartment
6.6.1 Normal Anatomy in the Midsagittal Plane
6.6.2 The Perineal Body/Transversus Perinei
6.6.3 The Rectovaginal Septum
6.6.4 The Anal Canal on Tomographic Imaging
6.7 The Levator Ani Muscle
6.7.1 2D Imaging
6.7.2 Axial Plane
6.7.3 Multislice Imaging
6.8 Static Versus Dynamic “Normality”
6.9 Urethral Mobility and Bladder Neck Configuration
6.10 Pelvic Organ Descent
6.11 Hiatal Dimensions
6.12 Conclusions
References
7: Endovaginal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy
7.1 Introduction
7.2 Technical Aspects of 3D Endovaginal Ultrasound
7.3 Ultrasonographic Anatomy of the Pelvic Floor
7.4 Assessment of the Anterior Compartment
7.5 Assessment of the Posterior Compartment
7.6 Discussion
7.7 Conclusion
References
8: Endoanal and Endorectal Ultrasonography: Methodology and Normal Anorectal Anatomy
8.1 Introduction
8.2 Ultrasonographic Technique
8.3 Endosonographic Anatomy of the Anal Canal
8.4 Endosonographic Anatomy of the Rectum
8.5 Normal Values
8.6 Conclusions
References
9: Technical Innovations in Pelvic Floor Ultrasonography
9.1 Introduction
9.2 Volume Render Mode
9.3 Maximum Intensity Projection
9.4 Brush Options: Segmentation—Sculpting
9.5 Fusion Imaging
9.6 PixelFlux
9.7 Framing
9.8 Motion Tracking and Color Vector Mapping
9.9 Elastography
9.9.1 Endovaginal Elastography
9.9.2 Endoanal Elastography
9.10 Contrast-Enhanced Ultrasound (CEUS)
9.10.1 Rectal Cancer
9.10.2 Contrast-Enhanced Voiding Urosonography (ceVUS)
9.10.3 Contrast-Enhanced Ultrasound Genitography
9.11 Automatic Ultrasound Calculation Systems
9.12 Conclusions
References
10: Magnetic Resonance Imaging: Methodology and Normal Pelvic Floor Anatomy
10.1 Introduction
10.2 The Anatomy of the Female Pelvic Floor
10.3 The Anterior Compartment
10.4 The Middle Compartment
10.5 The Posterior Compartment
10.5.1 The Posterior Compartment Contains the Rectum and Anal Sphincter
10.5.1.1 The Internal Anal Sphincter
10.5.1.2 The Intersphincteric Space and Longitudinal Layer
10.5.1.3 The Outer Striated Layer: External Anal Sphincter
10.5.1.4 The Outer Striated Layer: Puborectal Muscle
10.5.1.5 Anal Sphincter Support
10.6 The Endopelvic Fascia
10.7 The Pelvic Diaphragm
10.7.1 The Levator Ani Muscle
10.7.2 The Ischiococcygeus Muscle
10.8 The Perineal Membrane (Urogenital Diaphragm)
10.9 Conclusion
References
11: Dynamic Magnetic Resonance Imaging of the Pelvic Floor: Technique and Methodology
11.1 Introduction
11.2 Patient Positioning
11.3 Patient Preparation
11.4 Imaging Protocol
11.5 Image Analysis
11.5.1 Three-Compartment Model
11.5.2 Reference Systems
11.5.3 Anorectal Angle
11.5.4 Evacuation Ability
11.6 Normal Findings
11.7 Conclusion
References
Part III: Obstetric Pelvic Floor and Anal Sphincter Trauma
12: Mechanisms of Pelvic Floor Trauma During Vaginal Delivery
12.1 Biomechanics of the Second Stage of Labor
12.2 Injury from Vaginal Birth
12.3 Mechanisms of Levator Muscle Injury
12.4 Effect of Pregnancy on Pelvic Floor Tissue Properties
12.5 Finite Element Models of Vaginal Birth
12.6 Other Approaches to Modeling Vaginal Birth
12.7 Pudendal Nerve Stretch During Vaginal Birth
12.8 Effect of Forceps on Cephalolevator Disproportion
12.9 Effect of Maternal Pushing Styles During the Second Stage
12.10 Conclusions
References
13: Posterior Compartment Trauma and Management of Acute Obstetric Anal Sphincter Injuries
13.1 Introduction
13.2 Rectoceles
13.3 Obstetric Anal Sphincter Injuries (OASIS)
13.3.1 Applied Anatomy and Physiology
13.3.2 Diagnosis of OASIS
13.3.3 Repair of OASIS
13.3.4 Timing of Repair
13.3.5 Technique of Repair
13.3.6 Repair of Rectal Buttonhole Tear
13.3.7 Suture Material
13.3.8 Role of Antibiotics
13.3.9 Stool Softeners
13.3.10 Postoperative Catheterization
13.3.11 Postoperative Analgesia
13.3.12 Follow-Up
13.3.13 Anal Incontinence Symptoms After Primary Repair
13.3.14 Management of Subsequent Pregnancies
13.3.15 Training Issues
13.4 Conclusions
References
14: Neurogenic Trauma During Delivery
14.1 Introduction
14.2 Neural Anatomy
14.3 Pudendal Neuropathy
14.4 Mechanism of Nerve Injury
14.5 Measuring Nerve Injury
14.6 Striated Urethral Sphincter
14.7 External Anal Sphincter
14.8 Levator Ani Musculature
14.9 Conclusions
References
15: Prevention of Perineal Trauma
15.1 Introduction
15.2 Interventions in the Antenatal Period
15.2.1 Antepartum Perineal Massage
15.2.2 Pelvic Floor Muscle Training
15.3 Interventions During Labor and Birth
15.3.1 Water Birth
15.3.2 Position During Labor and Birth
15.3.3 Application of Warm Perineal Compresses in the Second Stage of Labor
15.3.4 Manual Perineal Protection (MPP)
15.3.5 Second Stage Perineal Massage
15.3.6 Episiotomy
15.3.7 Instrumental Delivery
15.3.8 Epidural Analgesia
15.3.9 Interventions to Correct or Deliver with an Occipito-Posterior Position
15.4 Conclusions
References
Part IV: Urinary Incontinence and Voiding Dysfunction
16: Overview: Epidemiology and Etiology of Urinary Incontinence and Voiding Dysfunction
16.1 General Comments and Definitions
16.2 Prevalence of Urinary Incontinence
16.3 Factors Influencing the Prevalence of Urinary Incontinence
16.4 OAB and Other LUTS
16.5 Public Health Consequences of UI and LUTS on a Global Scale
16.6 Voiding Dysfunction
16.7 Overall Conclusion
References
17: Urinary Incontinence and Voiding Dysfunction: Patient-Reported Outcome Assessment
17.1 Introduction
17.2 Development of a PRO
17.3 Linguistic and Cultural Validation
17.4 Types of PROs
17.4.1 Symptom Frequency and Bother
17.4.2 Discomfort and ADL
17.4.3 Treatment Satisfaction
17.4.4 Productivity
17.4.5 QALY
17.4.6 Types for Urinary Problems
17.4.7 Health-Related Quality of Life (HRQL) PRO
17.4.8 PROs for LUTS in Women: Symptom Bother and Urgency
17.4.9 Screening Questionnaires
17.5 International Consultation on Incontinence Modular Questionnaire (ICIQ)
17.6 Voiding Dysfunction
17.7 Limitations of PRO
17.8 Future of PRO
17.9 Conclusion
References
18: Urodynamics Techniques and Clinical Applications
18.1 Introduction
18.2 Urodynamic Techniques
18.2.1 Free Uroflowmetry and Measurement of Post-void Residual Volume
18.2.2 Evaluation of Storage Function: Filling Cystometry
18.2.3 Evaluation of Voiding Function: Pressure-Flow Studies or Voiding Cystometry
18.2.4 Video-Urodynamics
18.2.5 Ambulatory Urodynamics
18.2.6 Urethral Pressure Profilometry
18.3 Clinical Applications
18.3.1 Overactive Bladder
18.3.1.1 Free Uroflowmetry and Measurement of Post-void Residual Volume
18.3.1.2 Filling Cystometry
Detrusor Overactivity
Reduced Bladder Compliance
18.3.2 Stress Urinary Incontinence
18.3.2.1 Free Uroflowmetry and Measurement of Post-void Residual Volume
18.3.2.2 Assessment of Urethral Function
Urethral Pressure Profilometry
Abdominal Leak Point Pressure
18.3.2.3 Pelvic Organ Prolapse
18.3.3 Underactive Bladder and Detrusor Underactivity
18.3.3.1 Free Uroflowmetry and Measurement of Post-void Residual Volume
18.3.3.2 Pressure-Flow Studies
18.3.4 Bladder Outlet Obstruction
18.4 Future Perspectives
18.5 Conclusions
References
19: Ultrasonographic Techniques and Clinical Applications
19.1 Introduction
19.2 External Ultrasound
19.2.1 Examination Technique
19.3 Endoluminal Ultrasound
19.3.1 Examination Technique
19.4 Discussion
19.5 Conclusions
References
20: Biofeedback
20.1 Introduction
20.2 Purpose of Using Biofeedback
20.3 Effect of Biofeedback Training
20.4 Clinical Recommendations for the Use of Biofeedback
20.5 Conclusion
References
21: Selection of Midurethral Slings for Women with Stress Urinary Incontinence
21.1 Introduction
21.2 Other Types of Retropubic Midurethral Slings
21.2.1 Top-Down Systems
21.2.2 Intravaginal Slingplasty (IVS)
21.2.3 Self-Made Slings
21.2.4 Overview
21.3 Other Approaches for Sling Placement
21.3.1 The Transobturator Route
21.3.2 Outside-In Versus Inside-Out
21.3.3 Retropubic Versus Obturator
21.4 Predictors of Failure
21.4.1 Intrinsic Sphincter Deficiency
21.4.2 Effect of MUS on Lower Urinary Tract Function
21.4.3 The Elderly
21.4.4 The Obese
21.5 Biological Slings and Exitless Slings
21.5.1 Exitless Mini-Sling
21.6 Surgeon-Related Factors
21.7 Summary
21.8 Conclusions
References
22: Tape Positioning: Does It Matter?
22.1 Introduction
22.2 The Theoretical Basis for Midurethral Sling Placement
22.3 Proposed Mechanism of Action of the Midurethral Tape
22.3.1 The Controversy Regarding Sling Location and the Evidence on the Importance of Sling Location
22.3.2 Evidence in Favor of Primacy of Location in the Continence Mechanism of Midurethral Slings
22.3.3 The Benefits of Determining the Location of a Failed Sling
22.4 Does the Position of the Sling Change After Implantation?
22.5 If Location of the Sling Is Important, Does Suture Fixation of the Sling upon Implantation Help?
22.6 What Explains Successful Outcomes Following Sling Surgery in Patients in Whom the Sling Is Not Located Midurethrally? Dynamic Functional Assessment of Slings and Its Correlation with Outcome
22.7 Tape Position and Postoperative Complications
22.8 Future Directions
22.9 Conclusion
References
23: Colposuspension and Fascial Sling
23.1 Introduction
23.2 Colposuspension
23.2.1 Historical Background
23.2.2 Mechanism Action
23.2.3 Surgical Technique of the Modern Colposuspension
23.2.4 Indications
23.2.5 Contraindications
23.2.6 Complications
23.3 Fascial Sling
23.3.1 Historical Background
23.3.2 Mechanism of Action
23.3.3 Variation in Surgical Technique of the Autologous Fascial Sling
23.3.3.1 The Original Aldridge Sling
23.3.4 Indications for a Fascial Sling
23.3.5 Contraindications
23.4 Outcomes of Colposuspension and Fascial Sling
23.5 Is Laparoscopic Colposuspension as Effective as Open?
23.6 Do the Sutures Used for a Colposuspension Affect Outcome?
23.7 Is Colposuspension as Effective as an Autologous Fascial Sling?
23.8 Is the Sling on a String as Effective as the Traditional Aldridge Sling?
23.9 Is a Shorter Sling on a String as Effective as a Full Length Detached Sling?
23.10 Is an Autologous Sling Better at the Mid-Urethra or the Bladder Neck?
23.11 Is Fascia Lata as Effective as Rectus Sheath Fascia?
23.12 Are Allografts as Effective as Autologous Slings?
23.13 Are Xenograft Slings as Effective as Autologous Slings?
23.14 Conclusion
References
24: Injectable Biomaterials
24.1 Introduction
24.2 Safety of Urethral Bulking Agents
24.3 Efficacy of Urethral Bulking Agents
24.4 Future Directions
24.5 Conclusions
References
25: Artificial Urinary Sphincter in Women
25.1 Introduction
25.2 Artificial Urinary Sphincter
25.3 Indications
25.4 Contraindications
25.5 Operation
25.5.1 Preoperative Counselling and Preparation
25.5.2 Open Procedure for Insertion of AUS
25.5.2.1 Abdominal Approach
25.5.2.2 Vaginal Approach
25.5.2.3 Laparoscopic Extra-Peritoneal Approach for Insertion of AUS in Women
Patient Preparation
25.6 Complications
25.6.1 Per-operative Complications
25.6.1.1 During Trocar Placement
25.6.2 Early Post-operative Complications
25.6.2.1 Urinary Retention
25.6.2.2 Infection and Extrusion of the Prosthesis
25.6.3 Late Post-operative Complications
25.6.3.1 Urethral Atrophy, Erosion or Extrusion
25.6.3.2 Mechanical Failure
25.6.3.3 Recurrent/Persistent Urinary Incontinence
25.7 Brief Review of the Literature About AUS Implantation in Women
25.7.1 Open Procedure
25.7.2 Laparoscopic Procedure
25.7.3 Robot-Assisted Artificial Urinary Sphincter Insertion
25.8 Conclusion
References
26: Pharmacological Treatment of Urinary Incontinence and Overactive Bladder: The Evidence
26.1 Introduction
26.2 Pathophysiology
26.2.1 Muscarinic Receptors
26.3 Detrusor Overactivity
26.3.1 Outflow Obstruction Hypothesis
26.3.2 Neurogenic Hypothesis
26.3.3 Urethral Reflex
26.3.4 Myogenic Hypothesis
26.3.5 Urothelial Afferent Hypothesis
26.4 Clinical Presentation
26.5 Investigation
26.5.1 Urodynamic Investigations
26.5.2 Cystourethroscopy
26.6 Conservative Management
26.6.1 Bladder Retraining
26.7 Medical Management
26.8 Antimuscarinics
26.8.1 Oxybutynin
26.8.2 Tolterodine
26.8.3 Trospium Chloride
26.8.4 Solifenacin
26.8.5 Darifenacin
26.8.6 Fesoterodine
26.8.7 Propiverine
26.9 Anticholinergic Burden
26.10 β-Adrenoceptors and OAB
26.10.1 Mirabegron
26.10.2 Combination Therapy: Mirabegron and Solifenacin
26.10.3 Desmopressin
26.11 Oestrogens in the Management of Overactive Bladder
26.11.1 Combination Therapy: Oestrogens and Antimuscarinics
26.12 Conclusions
References
27: Intravesical Botulinum Toxin for the Treatment of Overactive Bladder
27.1 Introduction
27.2 Recommendation for Practice
27.2.1 Injection Procedure
27.2.2 Neurogenic Detrusor Overactivity (NDO) Treatment with OnabotulinumtoxinA
27.2.3 Overactive Bladder Treatment with OnabotulinumtoxinA
27.3 Future Directions
27.4 Conclusion
References
28: Sacral Nerve Stimulation for Overactive Bladder and Voiding Dysfunction
28.1 Historical Overview
28.2 Mode of Action
28.3 Indications
28.4 Selection Criteria
28.5 Implant Technique
28.6 Results
28.7 Predictive Factors
28.8 Complications
28.9 Newer and Investigational (Experimental) Neuromodulation Techniques
28.10 Conclusions
References
Part V: Anal Incontinence
29: Overview: Epidemiology and Aetiology of Anal Incontinence
29.1 Introduction
29.2 Epidemiology of Anal Incontinence
29.2.1 Prevalence
29.2.2 How Future Estimates of Prevalence May Be Affected
29.2.3 Incidence
29.2.4 Risk Factors
29.2.5 Future Directions
29.3 Aetiology of Anal Incontinence
29.3.1 Continence
29.3.2 Incontinence
29.3.3 Risk Factors for Incontinence
29.3.3.1 Age
29.3.3.2 Nursing Home Residence
29.3.3.3 Gender
29.3.3.4 Childbirth
Mechanisms for Anal Incontinence After Childbirth
Epidemiology of Anal Incontinence After Childbirth
29.3.3.5 Urinary Incontinence
29.3.3.6 Diabetes
29.3.3.7 Gastrointestinal Disorders and Stool Consistency
Diarrhoea
Rectal Urgency
Constipation/Faecal Impaction
Irritable Bowel Syndrome
29.3.3.8 Neurological/Psychiatric Disorders
Dementia
Depression
29.3.3.9 Nutrition
Obesity
Vitamin D
29.3.3.10 Physical Mobility
29.3.3.11 Radiation
29.3.3.12 Prolapse
29.3.3.13 Surgery
Anorectal Surgery
Rectal Resection
Other Surgeries
Ureterosigmoidostomy
Hysterectomy
Cholecystectomy
29.3.3.14 Smoking
29.3.4 Future Directions
References
30: Patient-Reported Outcome Assessment in Anal Incontinence
30.1 Introduction
30.2 Development of PROMs
30.3 Evaluation of Reliability, Validity, and Responsiveness of PROMs
30.4 Anal or Fecal Incontinence Symptom Severity Scales
30.5 Anal or Fecal Incontinence-Specific Quality of Life Questionnaire
30.6 Combined Questionnaire of Anal Incontinence Severity Scale and Anal Incontinence-Specific Quality of Life Questionnaire
30.7 Recommendation for Practice in Choosing Appropriate PROMs for Anal Incontinence
30.8 Future Directions
References
31: Anorectal Manometry
31.1 Introduction
31.2 Manometric Data
31.3 Anorectal Manometry and Fecal Incontinence
31.4 Anorectal Manometry and Pelvic Floor Rehabilitation
31.5 High-Resolution Manometry and High-Definition Three-Dimensional Anorectal Manometry
References
32: Endoanal Ultrasonography in Anal Incontinence
32.1 Introduction
32.2 Internal Anal Sphincter Abnormalities
32.3 External Anal Sphincter Abnormalities
32.4 Puborectalis Muscle Abnormalities
32.5 Accuracy and Reliability
32.6 EAUS Versus EVUS and TPUS
32.7 EAUS Versus MRI
32.8 Current Recommendations for Research for EAUS
32.9 Conclusions
References
33: Transperineal Ultrasonography in the Assessment of Anal Incontinence and Obstetric Anal Sphincter Injuries
33.1 Introduction
33.2 Recommendations for Practice
33.2.1 Endovaginal Ultrasound (EVUS)
33.2.2 Transperineal Ultrasound (TPUS)
33.2.2.1 2D-TPUS
33.2.2.2 3D-TPUS
33.3 Conclusions
References
34: Magnetic Resonance Imaging
34.1 Introduction
34.2 Technique
34.2.1 MRI Coil
34.2.2 Preparation
34.2.3 Imaging Protocol
34.3 MRI Findings
34.4 Accuracy for Sphincter Defects
34.5 Accuracy for Sphincter Atrophy
34.6 MRI in the Management of Fecal-Incontinent Patients
34.7 Conclusions
References
35: Neurophysiological Evaluation: Techniques and Clinical Evaluation
35.1 Introduction
35.2 Neural Control of Colorectal Motility
35.3 Nerve Conduction Studies
35.4 Pudendal Nerve Terminal Motor Latency (PNTML)
35.5 Electromyography (EMG)
35.6 Developments Neurophysiological Investigations
35.7 Cortical Evoked Potentials (CEP)
35.8 Motor Evoked Potentials
35.9 Mucosal Blood Flow: Laser Doppler Flowmetry (LDF)
35.10 Sacral Nerve Stimulators
35.11 Conclusion
References
36: Behavioral Therapies and Biofeedback for Anal Incontinence
36.1 Introduction
36.2 Etiological Factors
36.3 Factors Predicting Response to Pelvic Physiotherapy
36.4 Diagnostic Process
36.4.1 Measurement Instruments
36.4.2 Physical Examination
36.5 Physiotherapy Analysis/Diagnosis
36.6 Therapeutic Process
36.7 Evaluation
36.8 Updating the Evidence After Publication of the Dutch Evidence Statement
36.8.1 Prior (2013) Assessment of Electrical Stimulation of the Anal Mucosa or Perineum
36.8.2 Prior (2013) Assessment of Pelvic Floor Muscle Exercises
36.8.3 Prior (2013) Assessment of Biofeedback Therapy
36.9 Update: Review of Evidence from January 2012 to May 2016
36.10 Conclusions
36.11 Spin Off
36.12 Recommendations for Practice
36.13 Future Directions
References
37: Sphincter Repair and Postanal Repair
37.1 Introduction
37.2 Diagnostic Workup
37.3 Indications
37.4 Surgical Technique
37.5 Technical Considerations at Surgery
37.5.1 Overlapping vs. End-to-End Repair
37.5.2 Separate Suturing of External and Internal Sphincters
37.5.3 Scar Tissue
37.5.4 Suture Material
37.5.5 Diverting Stoma
37.6 Other Considerations
37.6.1 Primary Repair vs. Sphincteroplasty
37.6.2 Failed Primary Repair
37.6.3 Age
37.6.4 Pudendal Neuropathy
37.6.5 Biofeedback
37.6.6 Concomitant Perineal Operations
37.6.7 Alternative Surgical Options
37.6.8 Financial Aspects
37.7 Measurement of Outcomes After Sphincteroplasty
37.7.1 Descriptive Measures
37.7.2 Severity Measures
37.7.3 Impact Measures
37.8 Results of Sphincteroplasty
37.8.1 Short-Term Results
37.8.2 Long-Term Results
37.9 Sexual Function After Sphincteroplasty
37.10 Postanal Repair
References
38: Dynamic Graciloplasty
38.1 Introduction
38.2 Perioperative Assessment
38.2.1 Indications for Graciloplasty
38.2.2 Contraindications to Graciloplasty
38.3 Technique
38.4 Outcomes and Complications of Dynamic Graciloplasty
38.5 Adynamic Graciloplasty
38.6 Total Anorectal Reconstruction (TAR)
38.7 Conclusion
References
39: Injectable and Implantable Biomaterials for Anal Incontinence
39.1 Introduction
39.2 Types of Agents Used
39.3 Technique
39.4 Safety and Adverse Events
39.5 Efficacy
39.6 Anorectal Physiology and Endoanal Ultrasound
39.7 Discussion
39.8 Conclusions
References
40: Sacral Neuromodulation for Fecal Incontinence
40.1 Introduction
40.2 Technique and Its Evolution
40.3 Mechanism of Action
40.4 Indications
40.5 Prognostic Factors of Outcome
40.6 Outcome
40.7 Future Directions
References
41: Posterior Tibial Nerve Stimulation for Faecal Incontinence
41.1 Introduction
41.2 Percutaneous PTNS
41.3 Transcutaneous PTNS
41.4 Mechanism of Action
41.5 Percutaneous PTNS vs. Sacral Nerve Stimulation
41.6 Percutaneous PTNS vs. Transcutaneous PTNS
41.7 PTNS vs. Sham
References
42: Radiofrequency
42.1 Introduction
42.2 Recommendations for Practice
42.2.1 Technique (Fig. 42.1)
42.2.2 Complications
42.2.3 Results
42.3 Future Directions
References
43: Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell
43.1 Introduction
43.2 Sphincter Replacing Procedures
43.3 Muscle Transposition Techniques
43.4 Gluteoplasty (Gluteus Maximus Plasty)
43.5 Dynamic Gluteoplasty
43.6 Graciloplasty
43.7 Dynamic Graciloplasty
43.8 Artificial Bowel Sphincter (ABS)
43.9 Magnetic Anal Ring
43.10 Stem Cell Transposition
43.11 Anal Plugs
43.12 Colostomy
43.13 Conclusion
References
44: Treatment of Anal Incontinence: Which Outcome Should We Measure?
44.1 Introduction
44.2 Symptom Assessment
44.2.1 Symptom Severity Questionnaires
44.2.1.1 The Jorge-Wexner Score
44.2.1.2 The St Mark’s Incontinence Score
44.2.1.3 The Revised Faecal Incontinence Scale
44.2.1.4 The Faecal Incontinence Severity Index (FISI)
44.2.2 Symptom Severity Questionnaires Designed to Assess Outcomes for Rectal Cancer Treatment
44.2.2.1 The Low Anterior Resection Syndrome Score (LARS Score)
44.2.2.2 The Memorial Sloan Kettering Cancer Center (MSKCC) Bowel Function Instrument
44.2.3 Diary Monitoring
44.2.4 Quality of Life Questionnaires
44.2.4.1 The Rockwood Scale (FIQL)
44.2.5 The Combined Assessment of Symptom Severity and Quality of Life
44.2.5.1 The Rapid Assessment Faecal Incontinence Score (RAFIS)
44.2.5.2 ICIQ-BS
44.2.6 Visual Analogue Scores
44.2.7 Interview Assessment
44.3 Anorectal Structure and Function
44.3.1 Anorectal Physiology
44.3.1.1 Anorectal Manometry
44.3.1.2 Sensory Measurements
44.3.1.3 Neurophysiology
44.3.2 Saline Continence Tests or Porridge Enema
44.3.3 Imaging
44.3.3.1 Endoanal Ultrasound
44.3.3.2 MRI
44.4 Future Directions
References
Part VI: Pelvic Organ Prolapse
45: Epidemiology and Etiology of Pelvic Organ Prolapse
45.1 Definition and Classification
45.2 Prevalence and Incidence
45.3 Risk Factors and Pathophysiological Mechanisms
45.3.1 Ethnicity
45.3.2 Familiarity and Other Genetic Risk Factors
45.3.3 Obstetric Factors
45.3.4 Age and Hormonal Status
45.3.5 Socioeconomic Factors
45.3.6 General Medical Conditions
45.3.7 Previous Pelvic Surgery
References
46: Patient-Reported Outcomes and Pelvic Organ Prolapse
46.1 Introduction
46.2 Recommendations for Practice
46.2.1 POP Symptomatology
46.2.2 Patient-Reported Outcome Questionnaires
46.2.3 Selecting PRO Instruments
46.2.4 Categories of PROs
46.3 PRO Instruments for POP
46.3.1 Screeners
46.3.2 Symptom Questionnaires
46.3.3 Quality of Life Questionnaires or Health-Related Quality of Life Questionnaires
46.3.4 Sexual Function
46.3.5 Patients’ Expectations and Satisfaction
46.4 Future Directions
Further Reading
Screeners
Detection of Patients with POP Symptoms Before a Clinical Examination
Detection of Patients with LUTS
Detection of Patients with Sexual Dysfunction
Symptom Questionnaires
PROs with Wide Coverage of POP Symptoms
PROs Focusing on LUTS
PROs Focusing on Bowel Function
Quality of Life Questionnaires
Generic Questionnaires
Condition Specific
Sexual Function
Generic PROs
Condition-Specific PROs
Patients’ Expectations PROs
Patients’ Satisfaction PROs
References
47: Integrated Imaging Approach to Pelvic Organ Prolapse
47.1 Introduction
47.2 Review of Imaging Techniques
47.2.1 Evacuation Proctography (EP)
47.2.2 Ultrasonography (US)
47.2.2.1 Two-Dimensional Transperineal Ultrasound (2D TPUS)
47.2.2.2 Three-Dimensional Transperineal Ultrasound (3D TPUS)
47.2.2.3 Four-Dimensional Transperineal Ultrasound (4D TPUS)
47.2.2.4 Three-Dimensional Endoanal Ultrasound (3D EAUS)
47.2.2.5 Three-Dimensional Endovaginal Ultrasound (3D EVUS)
47.2.2.6 Dynamic Endovaginal Ultrasound
47.2.3 Magnetic Resonance Imaging (MRI)
47.3 Review of the Literature and Recommendations
47.4 Summary and Conclusions
References
48: Transperineal Ultrasound: Practical Applications
48.1 Introduction
48.2 Instrumentation and Indications
48.3 Anterior Compartment Pathology
48.3.1 Residual Urine and Bladder Wall
48.3.1.1 The Anatomy of Stress Urinary Incontinence
48.3.1.2 Anterior Compartment Prolapse
48.3.1.3 Central Compartment
48.3.1.4 Posterior Compartment
48.3.1.5 The Anal Sphincter
48.3.1.6 Synthetic Implants
48.3.2 The Levator Ani
48.4 Conclusions
References
49: Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage
49.1 Introduction
49.1.1 Imaging Modalities for Endovaginal Imaging
49.1.2 3D EVUS Technique for Levator Ani Imaging
49.2 Clinical Applications
49.2.1 Prevalence of Pelvic Floor Injury Following Vaginal Delivery
49.2.2 Levator Ani Injury and Hematomas
49.2.3 Levator Ani Avulsion
49.2.4 LAD: Levator Ani Deficiency Score as a Measure of Levator Ani Atrophy
49.2.5 Scoring System
49.2.6 Changes of Levator Ani with Aging
49.2.6.1 Levator Plate Descent Angle and Minimal Levator Hiatus
49.3 Future Research
References
50: Magnetic Resonance Imaging, Levator Ani Damage, and Pelvic Organ Prolapse
50.1 Introduction
50.2 Functional Anatomy: Levator Ani Muscle and Connective Tissue Work Together to Provide Pelvic Organ Support
50.2.1 Levator Ani Muscle Anatomy
50.2.2 Levator Ani Muscle Lines of Action
50.2.3 What Type of Injury Occurs to Lead to These Visible Abnormalities?
50.2.4 Location and Types of Levator Injury
50.2.5 Injury Distorts the Pelvic Sidewall Supports
50.2.6 The Amount of Injured Muscle Matters
50.2.7 Levator Failure and Surgical Outcome
50.2.8 Muscle Injury Reduces Force
50.2.9 Levator Ani Injury and Fascial Failure
50.2.10 Exposed Vaginal Length, Pressure Differentials, and Symptomatic Prolapse
50.3 Concluding Message and Future Directions
References
51: Dynamic Magnetic Resonance Imaging of Pelvic Floor Pathologies
51.1 Introduction and Definitions of Pelvic Floor Dysfunction
51.2 Indications of Dynamic Pelvic Floor MRI
51.3 Anterior Compartment
51.4 Middle Compartment
51.5 Posterior Compartment
51.5.1 Anorectal Descent
51.5.2 Rectocele
51.5.3 Intussusception and Rectal Prolapse
51.5.3.1 Intussusception
51.5.3.2 External Rectal Prolapse
51.5.4 Enterocele
51.6 Pelvic Floor Relaxation
51.7 Dyssynergic Defecation
51.8 Conclusion
References
52: Pelvic Floor Muscle Training in Prevention and Treatment of Pelvic Organ Prolapse
52.1 Introduction
52.2 Methods
52.3 Results
52.3.1 In the General Population
52.3.1.1 Hypopressive Technique
52.3.2 FMT to Prevent and Treat POP in the Peripartum Period
52.3.3 Prevention
52.3.4 PFMT in Combination with Surgery
52.3.5 Long-Term Effect
52.4 Discussion
52.4.1 Conscious Contraction (Bracing or “Performing the Knack”) to Prevent and Treat POP
52.4.2 Strength Training
52.5 Conclusions
References
53: Use of Pessaries for Pelvic Organ Prolapse
53.1 Introduction
53.2 Types of Pessaries
53.2.1 Support Pessaries
53.2.2 Space-Filling Pessaries
53.2.3 Incontinence Pessaries
53.3 Pessary Selection
53.3.1 Assessment and Insertion
53.3.2 Follow-Up Pessary Care
53.4 Complications of Pessary Treatment
53.5 Evidence of Effectiveness
53.6 Training of Pessary Practitioners
53.7 Future Directions
References
54: Anterior and Posterior Colporrhaphy: Native Tissue Versus Mesh
54.1 Introduction
54.2 Vaginal Defects: What Needs to Be Fixed?
54.3 Vaginal Vault Fixation: Importance to More Effective Colporrhaphies
54.4 Anterior (Level II) Repair [11]
54.5 Posterior (Level II) Repair [11]
54.6 Posterior (Level III) Repair [11, 19]
54.7 Posterior (Level I) Repair
54.8 Efficacy of Outcomes of Native Tissue and Mesh Colporrhaphies
54.9 Conclusion
Appendix
Pelvic Organ Prolapse Quantification (POP-Q) [11, 16]
Posterior Repair Quantification (PR-Q) [11, 15, 17]
References
55: Apical Prolapse Surgery
55.1 Uterine Prolapse
55.1.1 Uterine Preservation
55.1.2 Uterine Prolapse: Hysterectomy or Uterine Preservation
55.1.3 Vault Prolapse
55.2 Route of Sacral Colpopexy
55.3 Conclusion
References
56: Laparoscopic Pelvic Floor Surgery
56.1 Introduction
56.2 Laparoscopic Colposuspension
56.2.1 Management of Stress Urinary Incontinence
56.2.2 The Rise and Fall of Laparoscopic Colposuspension
56.2.3 Technique of Laparoscopic Colposuspension
56.2.3.1 Preperitoneal or Transperitoneal Approach
56.2.3.2 Operative Technique
56.2.3.3 Outcomes
56.2.4 Conclusion
56.3 Laparoscopic Sacrocolpopexy
56.3.1 Management of Level I Defects
56.3.2 Laparoscopic Versus Open Sacrocolpopexy
56.3.3 Technique of Laparoscopic Sacrocolpopexy
56.3.4 Outcomes
56.3.5 Outcomes in the Elderly
56.3.6 Learning Curve
56.3.7 Conclusion
56.4 Associated Ventral Rectopexy
56.4.1 Concurrence with Posterior Pelvic Floor Dysfunctions (PFD)
56.4.2 Associating Anterior Rectopexy in Combined Middle and Posterior Compartment Problems
56.4.3 Technique and Outcomes of an Associated Anterior Rectopexy
56.5 Future Directions
References
57: The Robotic Approach to Urogenital Prolapse
57.1 Introduction
57.2 Robot-Assisted Surgery: The Context
57.2.1 History of Robot-Assisted Surgery
57.2.2 Components of Robotic Surgery System
57.2.3 Use of Robotic Surgery in Other Sub-specialties of Gynaecology and Surgical Specialties
57.2.4 Laparoscopic Versus Robot-Assisted Surgery
57.3 Robotic Approach to Apical Prolapse
57.3.1 Robot-Assisted Sacrocolpopexy (RASC)
57.3.2 Robot-Assisted Sacrohysteropexy (RASH)
57.3.3 Other Procedures Amenable to Urogynaecological Robot-Assisted Procedures
57.4 Considerations with Robotic Surgery
57.4.1 Preoperative Evaluation and Risk Assessment
57.4.2 Education and Learning
57.4.3 Cosmesis
57.4.4 Safety
57.4.5 Economical Cost
57.5 Summary of Pros and Cons of Robotic Surgery
57.6 Future Directions
57.7 Conclusion
References
Further Reading
58: Concurrent Prolapse and Incontinence Surgery
58.1 Introduction
58.2 Diagnostic Tests to Unmask Occult SUI
58.3 Patients with Concomitant POP and SUI (Overt Incontinence)
58.4 Patients with POP and Masked (Occult) Incontinence
58.5 Patients Who Suffer from POP Only Without Overt or Masked Incontinence
58.6 Side Effects of Additional Incontinence Surgery in Patients Who Undergo Prolapse Operations
58.7 Recommendations for Practice
58.8 Future Directions
References
59: Management of Pelvic Organ Prolapse: A Unitary or Multidisciplinary Approach?
59.1 Introduction
59.2 Epidemiological Basis for Coexistence of Pelvic Floor Disorders
59.3 Why the Multidisciplinary Approach
59.4 The Use of Quality of Life Questionnaires
59.5 Improved Treatment Rates with Pelvic Floor Rehabilitative Therapy
59.6 Models for Multidisciplinary Approach
59.7 Combined Surgical Cases
59.8 Barriers to Multidisciplinary Management of Pelvic Floor Prolapse
59.9 Future of Multidisciplinary Approach
59.10 Conclusion
References
Part VII: Constipation and Obstructed Defecation
60: Epidemiology and Etiology of Constipation and Obstructed Defecation: An Overview
60.1 Introduction
60.2 Definition
60.3 Epidemiology
60.4 Etiology and Pathophysiology
60.4.1 Secondary Constipation
60.4.2 Primary Constipation
60.4.2.1 Normal Transit Constipation and Irritable Bowel Syndrome (IBS)
60.4.2.2 Slow Transit Constipation
60.4.2.3 Outlet Obstruction
60.5 Future Directions
References
61: Patient-Reported Outcome Assessment in Constipation and Obstructed Defecation
61.1 Introduction
61.1.1 Constipation Symptom Severity Scales
61.1.2 Constipation-Specific Quality-of-Life Questionnaire
61.1.3 Recommendation for Practice in Choosing Appropriate PROMs for Constipation
61.2 Future Directions
References
62: Anorectal Manometry, Rectal Sensory Testing and Evacuation Tests
62.1 Introduction
62.2 Anal Manometry
62.3 Vector Manometry
62.4 High-Resolution Anal Manometry (HR-ARM)
62.4.1 Rectal Sensory Testing
62.4.2 Rectal Sensation to Electrical Stimulation
62.5 Balloon Expulsion Test (BET)
62.6 Recommendation for Practice
62.7 Future Direction
References
63: Ultrasonography in the Assessment of Obstructive Defecation Syndrome
63.1 Introduction
63.2 Transperineal/Translabial/Introital Ultrasound
63.2.1 Dynamic Transperineal Ultrasound
63.2.2 Dynamic Translabial Ultrasound
63.2.3 Dynamic Endovaginal Ultrasound
63.2.4 Endoanal Ultrasound and Echodefecography
63.3 Ultrasonographic Assessment of Obstructive Defecation Syndrome
63.4 Ultrasound vs. X-ray Defecography (DEF) vs. MR Defecography (MR-DEF) in the Assessment of ODS
63.5 Ultrasound Assessment After Pelvic Floor Surgery
63.6 Conclusions
References
64: Echodefecography: Technique and Clinical Application
64.1 Introduction
64.2 Echodefecography (EDF) Technique
64.3 3D Transvaginal and Transrectal Ultrasonography (TTUS)
64.3.1 Technique
64.3.2 Transvaginal Approach
64.3.3 Transrectal Approach
References
65: Evacuation Proctography
65.1 Introduction
65.2 Patient Preparation
65.3 Examination Technique
65.3.1 Small Bowel, Rectal and Vaginal Opacification, and Defecation
65.4 Image Analysis
65.4.1 Parameters
65.4.1.1 Anorectal Angle (ARA)
65.4.1.2 Anorectal Junction (ARJ)
65.4.1.3 Pubococcygeal Line (PCL)
65.4.2 Normal Findings
65.4.2.1 Rest
65.4.2.2 Squeeze/Strain (Push)
65.4.2.3 Evacuation
65.4.2.4 Recovery
65.4.3 Pathological Findings
65.4.3.1 Abnormal Pelvic Floor Descent
65.4.3.2 Anismus (Dyssynergic Defecation)
65.4.3.3 Intussusception and Rectal Prolapse
65.4.3.4 Rectocele
65.4.3.5 Enterocele and Sigmoidocele
65.5 Conclusions
References
66: The Abdominal Approach to Rectal Prolapse
66.1 Introduction
66.2 Etiology
66.3 Assessment of Patients with Rectal Prolapse and Associated Symptoms
66.4 Selection of Patients for Abdominal Procedures
66.5 Abdominal Procedures
66.5.1 Ripstein Procedure (Anterior Sling Rectopexy)
66.5.2 Posterior Mesh Rectopexy
66.5.3 Suture Rectopexy
66.5.4 Sigmoid Resection Associated with Rectopexy
66.6 Abdominal Surgical Techniques
66.7 Minimally Invasive Approach
66.7.1 Ventral Mesh Rectopexy
66.7.2 Robotic Ventral Mesh Retopexy
66.7.3 Combined Rectopexy and Pelvic Organ Prolapse Approach
66.8 Incontinence Improvements and Mechanisms
66.9 Management of Recurrent Rectal Prolapse
66.10 Conclusions
References
67: The Perineal Approach to Rectal Prolapse
67.1 Introduction
67.2 Delorme Procedure
67.3 Perineal Rectosigmoidectomy (Altemeier Procedure)
67.4 Anal Encirclement (Thiersch Wire)
67.5 Management of Recurrent Rectal Prolapse
67.6 Management of Incarcerated or Strangulated Rectal Prolapse
67.7 Conclusion
References
68: The Laparoscopic Approach to Rectal Prolapse
68.1 Introduction
68.2 Epidemiology
68.3 Etiology
68.4 Pelvic Floor Anatomy and (Patho) Physiology
68.5 Symptoms
68.6 Investigations
68.7 Indications
68.8 Surgical Techniques
68.8.1 Laparoscopic Ventral Mesh Rectopexy
68.9 What Are the Results of Rectopexy?
68.10 Role of Lateral Ligaments?
68.11 Choice of Operation?
68.12 Need for Colonic Resection?
68.13 Robotic Approach
68.14 Preoperative Considerations: Urinary Incontinence
68.15 Postoperative Considerations: Mesh-Related Complications
68.16 Conclusion
References
69: The Role of Robotic Surgery in Rectal Prolapse
69.1 Introduction
69.2 Preoperative Assessment
69.3 Surgical Approaches to Rectal Prolapse
69.4 Perineal Operations
69.4.1 Delorme’s Operation
69.4.2 Altemeier’s Operation
69.5 Abdominal Operations
69.5.1 Abdominal Suture Rectopexy
69.5.2 Abdominal Resection Rectopexy
69.5.3 Laparoscopic Ventral Mesh Rectopexy
69.6 Robotic Approach to Rectal Prolapse
69.7 Technique
69.8 Complications
69.9 Recurrence Rates and Functional Outcomes
69.10 Other Aspects
69.11 Conclusions
References
70: Sacral Neuromodulation for Constipation
70.1 Introduction
70.2 Technique and Its Evolution
70.3 Mechanism of Action
70.4 Indications
70.5 Prognostic Factors of Outcome
70.6 Outcome
References
Part VIII: Pelvic Pain and Sexual Dysfunction
71: Bladder Pain Syndrome/Interstitial Cystitis
71.1 Introduction
71.2 Definition
71.3 Epidemiology
71.4 Nonbladder Syndromes (NBS)
71.5 Etiology and Pathogenesis
71.5.1 Infection
71.5.2 Mastocytosis
71.5.3 Dysfunctional Bladder Epithelium
71.5.4 Neurogenic Inflammation
71.5.5 Reduced Vascularization
71.5.6 Pelvic Floor Dysfunction
71.5.7 Autoimmunity
71.6 Diagnosis
71.6.1 Gynecological Associated/Confusable Disease
71.7 Treatment
71.7.1 Conservative Therapy
71.7.2 Medical Therapy
71.7.2.1 Oral Therapy
Protection of the Mucosal Surface
Antihistamines
Immunosuppressant
Other Oral Medications
71.7.3 Intravesical Instillation
71.7.4 Pain Modulators
71.7.4.1 Analgesics
(Grade of Recommendation: C—Level of Evidence: 4)
71.7.5 Multimodal Medical Therapy
71.7.5.1 Procedural Intervention
71.8 Conclusions
References
72: Pelvic Pain Associated with a Gynecologic Etiology
72.1 Introduction
72.2 Evaluation of Pelvic Pain of Gynecologic Origin
72.2.1 History
72.2.2 Physical Exam
72.3 Etiologies and Treatments of Pelvic Pain by Site
72.3.1 Perineum and Vulva
72.3.2 Vagina
72.3.3 Cervix
72.3.4 Uterus
72.3.5 Adnexa
72.3.6 Musculoskeletal Considerations
72.3.7 Extragynecologic Considerations
72.4 Multidisciplinary Approach to Chronic Pelvic Pain
72.5 Summary
References
73: Chronic Idiopathic Anorectal Pain Disorders
73.1 Introduction
73.2 Definition
73.3 Topographic Sensitive Innervation of the Perineum
73.4 History and Physical Examination of the Perineum
73.4.1 History
73.4.2 Associated Signs
73.4.3 Physical Examination
73.5 Psychologic Aspects and Somatization of Pain
73.6 Proctalgia Fugax
73.6.1 Definition
73.6.2 Epidemiology
73.6.3 Pathophysiology
73.6.4 Physical Examination
73.6.5 Treatment
73.7 Levator Ani Syndromes (Chronic Proctalgia)
73.7.1 Definition
73.7.2 Epidemiology
73.7.3 Pathophysiology
73.7.4 Physical Examination
73.7.5 Treatment
73.8 Unspecified Anorectal Pain
73.8.1 Myofascial and Coccygeal Pain Syndromes
73.8.1.1 History
73.8.1.2 Physical Examination
73.8.1.3 Treatment
73.8.2 Postoperative Anorectal Neuralgias
73.8.3 Nerve Compression Anorectal Neuralgias
73.8.3.1 Pudendal Neuralgia
Symptoms of Pudendal Neuralgia
Physical Examination
Diagnostic Workup
Electrophysiological Diagnosis
Pelvic Radiography
Magnetic Resonance Imaging of the Pelvis
Magnetic Resonance Imaging of the Medullary Cone
Treatment
Pudendal Canal Injections
Decompression Surgery
73.8.3.2 Cluneal Neuralgia
Physical Examination
Treatment
73.8.4 Pain of Central Origin
73.9 Conclusions
References
74: Female Sexual Dysfunction
74.1 Female Sexual Function
74.2 Female Sexual Dysfunction
74.3 Assessment
74.4 Sexual Function Questionnaires
74.5 Treatment
74.6 Pelvic Floor Disorders and Sexual Function
References
75: A Myofascial Perspective on Chronic Urogenital Pain in Women
75.1 Introduction
75.2 Bladder Pain Syndrome and Vulvodynia
75.3 Pain Mapping
75.4 Exploring Mechanisms of Pain
75.5 Structure and Function of Fascia
75.6 Continuity of Pelvic Fascia
75.7 Role of Fascia in Chronic Urogenital Pain
75.8 Fascial Tonicity and Organ Function
75.9 Role of Non-relaxing Muscles
75.10 Surface Electromyography in Studies of Pelvic Floor Muscles
75.11 SEMG Studies of Chronic Urogenital Pain Disorders
75.12 Conclusion
References
76: Pharmacological Treatment of Chronic Pelvic Pain
76.1 Introduction
76.2 Traditional Analgesics
76.3 Hormonal Treatment
76.4 Local Anaesthetics
76.5 Antidepressants
76.6 Membrane Stabilisers
76.7 Anxiolytics
76.8 Conclusion
References
77: Idiopathic Chronic Pelvic Pain: A Different Perspective
77.1 Introduction
77.2 The Present Scope of ICPP: Presence of Other Symptoms
77.3 Anatomical Pathway to ICCP
77.4 USL Laxity as a Cause of CPP
77.5 Pretreatment Diagnosis That USL Laxity Is the Cause of ICPP
77.5.1 Confirmation of USL Origin of Pain by Vaginal Examination
77.5.2 Confirmation of USL Origin of Pain with “Simulated Operations”
77.5.3 Confirmation of USL Origin of Pain by the Bornstein Test
77.6 Improvement of CPP by Squatting-Based PFR
77.6.1 How the Skilling Squatting-Based PFR Method Evolved
77.6.2 The Simplified Skilling PFR Method
77.7 Surgical Repair Option
77.7.1 USL Native Tissue Repair Technique
77.7.2 Posterior Sling Repair of USL
77.7.3 USL Tensioned TFS Sling
77.8 Discussion
77.9 Conclusions
References
Part IX: Fistulae
78: Urogenital Fistulae
78.1 Introduction
78.2 Aetiology and Epidemiology
78.3 Associated Conditions
78.4 Diagnosis
78.5 Classification
78.6 Treatment
78.7 Post-operative Management and Results
78.8 Ongoing Incontinence
78.9 The Future
78.10 Conclusion
References
79: Rectovaginal Fistulae
79.1 Definition
79.2 Etiology
79.3 Classification
79.4 Presentation
79.5 Assessment and Investigations
79.6 Treatment
79.6.1 Surgical Techniques
79.6.1.1 Endorectal Advancement Flap
79.6.1.2 Transvaginal Flap
79.6.1.3 Excision of Fistula and Layered Closure
79.6.1.4 Rectal Sleeve Advancement Flap
79.6.1.5 Episio/Perineoproctotomy
79.6.1.6 Tissue Interposition
79.6.1.7 Use of Biomaterials
Surgisis™ Mesh Repair
Surgisis™ Fistula Plug
79.6.1.8 Abdominal Operations
Direct Closure with Interposed Omental Graft
Rectal Excision (Anterior Resection) with Colorectal/Coloanal Anastomosis
Proctectomy
Diversion Ileostomy/Colostomy
79.6.1.9 Other Techniques
79.6.2 Choice of Surgery
79.6.2.1 Peripartum Rectovaginal Fistula
79.6.2.2 Crohn’s Disease
79.6.2.3 RVF Due to Radiation
79.6.2.4 RVF Due to Malignancy
79.6.2.5 Postoperative (Iatrogenic) RVF
79.6.2.6 Recurrent RVF
79.6.3 Suggested Algorithm
79.7 Conclusions
References
80: Emerging Concepts in Classification of Anal Fistulae
80.1 Introduction
80.2 Anatomy
80.2.1 The Anogenital Muscles
80.2.2 The Anogenital Spaces (Fig. 80.2)
80.2.3 The Fasciae (Fig. 80.3)
80.3 Pathogenesis
80.3.1 Natural Anal Abscess Patterns (Table 80.1 and Fig. 80.4)
80.3.2 Natural Anal Fistula Patterns (Fig. 80.6)
80.4 A Proposed Anal Fistula Classification (Table 80.2)
80.4.1 Characteristics and Benefits of the New Classification
80.5 Anal Fistula Map
80.5.1 Abbreviations, Pathway and Recording Format Used in Anal Fistula Map
80.5.1.1 Abbreviations
80.5.1.2 Recording Pathway
80.6 Discussion
80.6.1 Limitations of Current Classifications
80.7 Conclusion
References
81: Ultrasonographic Assessment of Anorectal Fistulae
81.1 Introduction
81.2 Assessment of Anorectal Fistulae
81.2.1 Physical Examination
81.2.2 Fistulography
81.2.3 Endoanal Ultrasonography
81.2.3.1 Endoanal Ultrasonography in Crohn’s Disease
81.2.3.2 EAUS Vs. MRI
81.2.4 Transperineal Ultrasonography
81.3 Conclusion
References
82: MR Imaging of Fistula-in-Ano
82.1 Introduction
82.2 Aetiology, Classification, and Treatment of Fistula-in-Ano Relevant to Imaging
82.3 Imaging Fistula-in-Ano: Which Technique to Use?
82.3.1 MRI Technique
82.3.2 MRI Interpretation and Reporting
82.3.3 Extensions
82.3.4 The Radiological Report
82.4 Effect of Pre-Operative MRI on Surgery and Clinical Outcome
82.5 Differential Diagnosis of Perianal Sepsis
82.6 Which Patients Should be Imaged?
82.7 Conclusion
82.7.1 Future Directions
References
83: Surgical Treatment of Anorectal Sepsis
83.1 Introduction
83.1.1 Cryptoglandular Theory and the Spectrum of Anorectal Sepsis Comprising the Acute Abscess and Chronic Fistula
83.1.2 Principles of Treatment: Drainage of Sepsis, Eradication of Fistula Tracts, Preservation of Continence
83.1.3 The Ideal Operation
83.2 Pre-operative Evaluation
83.2.1 Endoanal Ultrasound
83.2.2 MRI
83.2.3 Anorectal Physiology and Continence Assessment
83.3 Management of Acute Anorectal Sepsis (Abscess)
83.3.1 Simple Drainage (Simple Recommendations for Practice)
83.3.2 Drainage and Loose Seton
83.3.3 Modified LIFT Approach
83.4 Management of Chronic Anorectal Sepsis (Fistula)
83.4.1 Fistulotomy With or Without Repair of Sphincter Complex
83.4.2 Cutting Seton
83.4.3 Endorectal and Anodermal Advancement Flaps
83.4.4 LIFT
83.4.5 VAAFT
83.4.6 Fibrin Glue
83.4.7 Anal Fistula Plugs
83.4.8 FiLaC
83.4.9 OTSC (Over-The-Scope-Clip)
83.5 Discussion
83.6 Future Directions
83.6.1 Stem Cell
83.6.2 3D Modeling
83.7 Conclusion
References
84: Management of Anorectal Fistulae in Crohn’s Disease
84.1 Introduction
84.2 Classification
84.3 Diagnosis
84.4 Treatment
84.4.1 Observation
84.4.2 Antibiotics and Immunomodulators
84.4.3 Biologic Medications
84.4.4 Fistulotomy
84.4.5 Seton Placement
84.4.6 Mucosal Advancement Flap
84.4.7 Ligation of the Intersphincteric Fistula Tract (LIFT)
84.4.8 Fibrin Glue Injection and Fistula Plug
84.4.9 Mesenchymal Stem Cell Injection
84.4.10 Rectovaginal Fistula
84.4.11 Stoma Diversion
84.5 Future Directions
References
Part X: Failure or Recurrence After Surgical Treatment: What to Do When It All Goes Wrong
85: Imaging and Management of Complications of Urogynecologic Surgery
85.1 Introduction
85.2 Intra-Operative Complications Involving Anti-Incontinence Procedures
85.2.1 Overview
85.2.2 Slings and Urethral Bulking Agents
85.2.3 Retropubic Procedures
85.3 Complications of Pelvic Organ Prolapse Surgery
85.3.1 Overview
85.3.2 Apical Segment Complications
85.3.3 Lateral Vaginal Complications
85.3.4 Anterior Compartment Complications
85.3.5 Posterior Compartment Complications
85.3.6 Introital Vaginal Complications
85.4 Conclusions
References
86: Surgical Management of Complications After Urogynaecological Surgery
86.1 Introduction
86.1.1 Classification
86.2 Complications Following Incontinence Surgery
86.2.1 Introduction
86.2.2 Mid-urethral Tape Operations
86.2.2.1 Intraoperative Injuries
Urinary Tract Injury
Bowel Injury
Vascular Injury
86.2.2.2 Post-operative Complications
Immediate
Voiding Dysfunction, Retention
Infections
Urinary Tract Infections (UTIs)
Surgical Site Infections
Remote Complications
Mesh-Related Complications
Chronic Pain
Management of Chronic Pain with Surgery
86.2.3 Para-urethral Bulking
86.2.3.1 Introduction
86.2.4 Burch Colposuspension: Open and Laparoscopic
86.2.4.1 Introduction
86.2.4.2 Intraoperative Injury at the Time of Surgery
Urinary Tract Injury
Bowel Injury (Laparoscopic Route)
Vascular Injury
86.2.4.3 Post-operative Complications
Immediate
Wound Complications
Haematoma
Infection
Voiding Dysfunction
Remote Complications
Posterior Compartment Prolapse
Chronic Pain
Bladder Dysfunction
86.2.5 Autologous Fascial Sling (AFS)
86.2.5.1 Introduction
86.2.5.2 Intraoperative Complications
Visceral and Vascular Injuries
86.2.5.3 Postoperative Complications
Voiding Dysfunction
Bladder Dysfunction
86.3 Complications Following Prolapse Surgery
86.3.1 Introduction
86.3.2 Anterior Colporrhaphy
86.3.2.1 Introduction
86.3.2.2 Intraoperative Complications
86.3.2.3 Post-operative Complications
86.3.3 Posterior Colporrhaphy
86.3.3.1 Introduction
86.3.3.2 Intraoperative Complications
86.3.3.3 Post-operative Complications
86.3.4 Sacrospinous Colopopexy/Hysteropexy
86.3.4.1 Introduction
86.3.4.2 Intraoperative Complications
Nerve Damage
Vascular Damage
Visceral Damage
86.3.4.3 Post-operative Complications
Dyspareunia
Prolapse Recurrence
Voiding Dysfunction
Bladder Dysfunction
86.3.5 Vaginal Mesh Surgery
86.3.5.1 Introduction
86.3.5.2 Post-operative Complications
86.3.5.3 Management of Complications
86.3.6 Abdominal Prolapse Surgery
86.3.6.1 Mesh Complications
86.3.6.2 Vascular Injuries
86.3.6.3 Spondylodiscitis
86.3.6.4 Ureteric Injury
86.3.6.5 De Novo Stress Urinary Incontinence
86.4 Conclusion
References
87: Endosonographic Investigation of Anorectal Surgery Complications
87.1 Introduction
87.2 Early Complications
87.2.1 Postoperative Anorectal Pain
87.2.2 Postoperative Hemorrhage/Hematoma
87.2.3 Infection/Sepsis
87.3 Late Complications
87.3.1 Chronic Anal Pain
87.3.2 Anal Stenosis/Stricture
87.3.3 Anorectal/Rectovaginal Fistula
87.3.4 Fecal Incontinence
87.4 Conclusions
References
88: Investigation and Management of Complications After Coloproctological Surgery
88.1 Introduction
88.2 Infection-Related Complications
88.2.1 Anastomotic Leak
88.2.2 Abscesses
88.2.2.1 Small Perianastomotic Abscess (3 cm)
88.2.2.3 Abscess in Continuity with Leak
88.2.3 Low Rectal Anastomotic Sinus
88.2.4 Anastomotic Stricture
88.2.4.1 Colonic
88.2.4.2 Rectal
88.2.5 Fistula
88.2.6 Wound Infection
88.3 Intraoperative Organ Injury
88.3.1 Ureteric Injury
88.3.2 Splenic Injury
88.4 Stomal Complications
88.4.1 Stoma Retraction and Stenosis
88.4.2 Peristomal Skin Complications
88.5 Thromboembolic Complications
88.6 Sexual Dysfunction
88.6.1 Sympathetic Damage
88.6.2 Parasympathetic Damage
88.6.3 Treatment of Postoperative Sexual Dysfunction
88.7 Defecatory Dysfunction
88.8 Complications After Surgery for Functional Disorders
88.8.1 Fecal Incontinence
88.8.2 Rectal Prolapse
88.8.3 Obstructed Defecation
88.9 Conclusions
References
Part XI: Miscellaneous
89: Congenital Abnormalities of the Pelvic Floor: Assessment and Management
89.1 Introduction
89.2 Incidence
89.3 Classification
89.4 Embryology
89.5 Associated Malformation
89.6 Anorectal Anatomy
89.7 Clinical Investigation and Surgery of ARM
89.7.1 Assessment of Male Neonate with ARM
89.7.2 Surgery of ARM
89.7.3 Definitive Treatment
89.7.4 Assessment of the Female Neonate
89.7.5 Surgery of ARM
89.7.6 Definitive Treatment
89.8 Rectal Atresia
89.9 Results of Treatment
89.9.1 Operative Complications
89.9.2 Long-Term Results
89.10 Rare and Casuistic Malformations
89.11 Diagnostic Imaging of Anorectal Malformations and Other Pelvic Floor Abnormalities in Pediatric Patients
89.11.1 Invertogram (Lateral Horizontal-Beam-Prone Radiograph)
89.11.2 Transperineal Ultrasound (TPUS)
89.11.3 Colostogram
89.11.4 Magnetic Resonance Imaging (MRI)
89.11.5 Computed Tomography Imaging (CT)
89.12 Conclusions
References
90: Male Urinary Incontinence: Assessment and Management
90.1 Introduction
90.2 Assessment
90.2.1 History
90.2.2 Examination
90.2.3 Urinalysis
90.2.4 Uroflometry and Bladder Ultrasound
90.2.5 Bladder Diary
90.2.6 Pad Testing
90.2.7 Urodynamics
90.2.8 Cystoscopy
90.3 Management
90.3.1 Conservative
90.3.2 Pelvic Floor Muscle Training
90.3.3 Pharmacotherapy
90.3.4 Bulking Agents
90.3.5 Surgical Treatment
90.3.5.1 Artificial Urinary Sphincter
90.3.5.2 Male Slings
Bone Anchored Slings (BAS)
Trans-obturator Slings (TS)
Quadratic Sling
Adjustable Slings
90.3.5.3 Decision Making
90.4 Conclusions
90.5 Future Directions
References
Appendix: Management Consensus Statement
A.1 Management of Urinary Incontinence in Women From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.2 Assessment and Conservative Management of Faecal Incontinence From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.3 Surgical Management of Faecal Incontinence From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.4 Management of Pelvic Organ Prolapse From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.5 Surgical Management of Pelvic Organ Prolapse (POP) From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.6 Management of Constipation From “An International Urogynecological Association (IUGA)/International Continence Society (ICS) Joint Report on the Terminology for Female Anorectal Dysfunction” in Neurourology and Urodynamics 2017;36:10–34
A.7 Bladder Pain Syndrome (BPS) From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.8 Management of Vesicovaginal Fistula (VVF) From “Incontinence, 6th Edition 2017”. Abrams P, Cardozo L, Wagg A, Wein A, Editors. ICUD-ICS 2016 (with permission)
A.9 Management of Anorectal Fistulae From “The ASCRS Textbook of Colon and Rectal Surgery, 3rd Edition 2015”. Steele SR, Hull TL, Read TE, Saclarides TJ, Senagore AJ, Whitlow CB, Editors. Springer International Publishing 2016 (modified with permis
Index

Citation preview

Giulio A. Santoro Andrzej P. Wieczorek Abdul H. Sultan Editors

Pelvic Floor Disorders A Multidisciplinary Textbook Second Edition

123

Pelvic Floor Disorders

Giulio A. Santoro  •  Andrzej P. Wieczorek Abdul H. Sultan Editors

Pelvic Floor Disorders A Multidisciplinary Textbook Second Edition

Editors Giulio A. Santoro Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery Regional Hospital, Treviso University of Padua Padua Italy

Andrzej P. Wieczorek Department of Pediatric Radiology Medical University of Lublin Children’s University Hospital Lublin Poland

Abdul H. Sultan Urogynaecology and Pelvic Floor Reconstruction Unit Croydon University Hospital St George’s University of London London UK

ISBN 978-3-030-40861-9    ISBN 978-3-030-40862-6 (eBook) https://doi.org/10.1007/978-3-030-40862-6 © Springer Nature Switzerland AG 2021 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

This book is dedicated to all the patients, some of whom have suffered whilst allowing us to learn and improve our skills

Learn from yesterday, live for today, hope for tomorrow. The important thing is not to stop questioning Education is not the learning of facts, but the training of the mind to think Albert Einstein

Foreword

It is indeed a deep honor to be asked to provide a foreword to this comprehensive book on pelvic floor disorders. The editors Santoro, Wieczorek, and Sultan—a colorectal surgeon, a radiologist, and urogynecologist—form a unique multidisciplinary team. Together they have successfully unraveled the complexities of the pelvic floor by holistically dealing with every aspect: urogynecology, urology, colorectal surgery, radiology, physical therapy, gynecology, and oncology. The authors are carefully selected experts in the different subspecialties. The book starts off with basic pelvic floor anatomy and physiology, thus providing a basis to understand the pathophysiology of pelvic floor disorders. For each disorder, namely urinary and anal incontinence, pelvic organ prolapse, constipation, and obstructed defecation, the epidemiology, diagnosis, conservative and surgical approach are discussed for both primary and recurrent conditions. Furthermore, other associated conditions such as obstetric anal sphincter injury, pelvic pain, and female sexual dysfunction are covered in detail. The section on ultrasound and magnetic resonance imaging contains outstanding quality of reproduced images. This inclusion is important as with improved technology, our understanding of the functioning of the pelvic floor has improved. The book is well referenced and up to date. This book is a must-read for every clinician, medical or allied health professions, looking after patients with pelvic floor dysfunction not only in females but also in men and children. It should hopefully promote a multidisciplinary approach to care, thus reducing anxiety, cost, and hospital appointments for patients. I would like to congratulate the editors on this masterpiece, which hopefully will bridge the gaps in knowledge and improve the care we provide to women with pelvic floor disorders. August 2020

Ranee Thakar President of the International Urogynecological Association Consultant Obstetrician and Urogynecologist Croydon University Hospital, Croydon, UK David Castro Diaz General Secretary of the International Continence Society Functional Urology Unit University Hospital of Canary Islands Tenerife, Spain

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Preface

The pelvic floor is one of the most complex anatomical and functional areas of the human body and to this day has remained an enigma. Although it is still empirically divided in anterior, middle, and posterior compartments, the pelvic floor components act in unison to maintain bowel, bladder, and sexual function. Pelvic floor disorders represent a significant physical, social, and economic problem that often poses a challenge to specialists dealing with them. The reason for this is that the functional mechanisms are so complex and poorly understood that patient’s symptoms do not always correspond to physical examination findings, because various co-existing occult conditions are often underestimated. In order to achieve the optimal treatment, it is mandatory to overcome the fractured uni-disciplinary approach to the pelvic floor with multidisciplinary teams of experts (colorectal surgeons, urologists, urogynecologists, gastroenterologists, radiologists, physiatrists) having a unitary vision. In 2010 we published the book Pelvic Floor Disorders: Imaging and Multidisciplinary Approach to Management. Since then there have been more than 180,000 downloads of the online version of the chapters, confirming the huge interest and demand in this field. Major developments in diagnostics and treatments of pelvic floor disorders over the last few years led us to work on a new edition: Pelvic Floor Disorders: A Multidisciplinary Textbook. The result is not simply an update of the previous book, but to a considerable extent providing a comprehensive overview of pelvic floor anatomy and physiology, principles and technical aspects of imaging modalities, mechanisms of pelvic floor trauma during vaginal delivery, epidemiology, etiology, assessment and management of urinary incontinence and voiding dysfunction, anal incontinence, pelvic organ prolapse, constipation and obstructed defecation, pelvic pain and sexual dysfunctions, perineal and perianal fistula, and management of failures or recurrences after surgery. This textbook was also produced to meet the needs of education. It is a manual of practical instructions that we hope could be of great value to both medical students and specialists in the field. In particular, the various ultrasonographic techniques for the imaging of the pelvic floor (transperineal, endovaginal, endoanal, endorectal, 2D/3D/4D) are presented in a systematic way. Hundreds of images and anatomical illustrations have been included to help the reader to learn how to visualize and interpret ultrasound images but also provide more experienced examiners with an opportunity to review and re-appraise their techniques. Standardization of the methodology is fundamental to increase accuracy, reliability, and repeatability, leading to a wider acceptance of these modalities in the daily practice. Surgical procedures described in every detail in the text are accomplished by videos on the e-book version. In the Appendix Section, the algorithms for the treatment of pelvic floor disorders, according to the 6th International Consultation on Incontinence, summarize step-by-step the approach to these different pathological conditions. These algorithms should be considered for adoption into routine clinical practice to standardize management in accordance with the best available evidence-based medicine. This would enable consistent management with a view to reducing unnecessary surgeries, thereby minimizing the risk of failure, as well as faster and more effective treatment of postoperative complications. Our sincere gratitude goes to Springer for supporting the idea of publishing the new edition as a textbook and, in particular, to Subramaniam Vinodhini, Hemalatha Gunasekaran, Donatella xi

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Preface

Rizza and Elisa Geranio for their constant assistance throughout the development of the project, organizing every stage of the editorial work. Our deep appreciation to all international authors who have contributed to many chapters, sharing their knowledge and expertise. Without their invaluable help, this book would not have been possible. Further, thanks must go to our hospitals and institutions (Prof. Giacomo Zanus, Chief of IV°Division of General Surgery, Regional Hospital Treviso, Dr. Francesco Benazzi, CEO of AULSS 2 Marca Trevigiana, Italy; Medical University of Lublin, Children’s Teaching Hospital, Department of Pediatric Radiology, Lublin, Poland; Department of Obstetrics and UroGynaecology, Croydon University Hospital, Croydon, Surrey, UK) whose advanced technological support made it possible to accomplish this new project. We hope that this textbook would be a necessary companion to all clinicians involved in the care of our patients suffering from pelvic floor disorders. Treviso, Italy Lublin, Poland  Croydon, UK  August 2020

Giulio A. Santoro Andrzej P. Wieczorek Abdul H. Sultan

Contents

Part I State of the Art Pelvic Floor Anatomy 1 Pelvic Floor Anatomy�����������������������������������������������������������������������������������������������    3 S. Abbas Shobeiri and John O. L. DeLancey 2 Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues���������   25 Heinz Koelbl and Ksenia Halpern-Elenskaia 3 The Integral System of Pelvic Floor Function and Dysfunction���������������������������   31 Peter Petros, Michael Swash, and Darren Gold 4 The Pelvic Floor: Neurocontrol and Functional Concepts�����������������������������������   57 Michael Swash and Peter Petros Part II Pelvic Floor Imaging 5 Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound�����������   73 Andrzej P. Wieczorek, Magdalena Maria Woźniak, Jacek Piłat, and Giulio A. Santoro 6 Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy�����������������������������������������������������������������������������������������������   89 Hans Peter Dietz 7 Endovaginal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy�����������������������������������������������������������������������������������������������  111 Giulio A. Santoro, Andrzej P. Wieczorek, S. Abbas Shobeiri, and Aleksandra Stankiewicz 8 Endoanal and Endorectal Ultrasonography: Methodology and Normal Anorectal Anatomy �����������������������������������������������������  133 Giulio A. Santoro, Luigi Brusciano, and Abdul H. Sultan 9 Technical Innovations in Pelvic Floor Ultrasonography���������������������������������������  147 Magdalena Maria Woźniak, Andrzej P. Wieczorek, Giulio Aniello Santoro, Aleksandra Stankiewicz, Jakob Scholbach, and Michał Chlebiej 10 Magnetic Resonance Imaging: Methodology and Normal Pelvic Floor Anatomy�����������������������������������������������������������������������������������������������  171 Jeroen A. W. Tielbeek and Jaap Stoker 11 Dynamic Magnetic Resonance Imaging of the Pelvic Floor: Technique and Methodology �����������������������������������������������������������������������������������  179 Khoschy Schawkat and Cäcilia S. Reiner

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Part III Obstetric Pelvic Floor and Anal Sphincter Trauma 12 Mechanisms of Pelvic Floor Trauma During Vaginal Delivery ���������������������������  189 James A. Ashton-Miller and John O. L. DeLancey 13 Posterior Compartment Trauma and Management of Acute Obstetric Anal Sphincter Injuries���������������������������������������������������������������������������  211 Abdul H. Sultan and Ranee Thakar 14 Neurogenic Trauma During Delivery���������������������������������������������������������������������  223 Kimberly Kenton and Julia Geynisman-Tan 15 Prevention of Perineal Trauma �������������������������������������������������������������������������������  229 Ranee Thakar and Abdul H. Sultan Part IV Urinary Incontinence and Voiding Dysfunction 16 Overview: Epidemiology and Etiology of Urinary Incontinence and Voiding Dysfunction �����������������������������������������������������������������������������������������  239 Ian Milsom and Maria Gyhagen 17 Urinary Incontinence and Voiding Dysfunction: Patient-Reported Outcome Assessment �����������������������������������������������������������������  249 Eduardo Cortes and Linda Cardozo 18 Urodynamics Techniques and Clinical Applications���������������������������������������������  263 Michel Wyndaele and Paul Abrams 19 Ultrasonographic Techniques and Clinical Applications �������������������������������������  277 Andrzej P. Wieczorek, Magdalena Maria Woźniak, and Aleksandra Stankiewicz 20 Biofeedback���������������������������������������������������������������������������������������������������������������  301 Kari Bø and Paolo Di Benedetto 21 Selection of Midurethral Slings for Women with Stress Urinary Incontinence�������������������������������������������������������������������������������������  305 Joseph K.-S. Lee and Peter L. Dwyer 22 Tape Positioning: Does It Matter?���������������������������������������������������������������������������  317 Aparna Hegde and G. Willy Davila 23 Colposuspension and Fascial Sling�������������������������������������������������������������������������  329 Fiona Reid 24 Injectable Biomaterials���������������������������������������������������������������������������������������������  339 Tomi S. Mikkola 25 Artificial Urinary Sphincter in Women �����������������������������������������������������������������  343 Amrith Raj Rao and Philippe Grange 26 Pharmacological Treatment of Urinary Incontinence and Overactive Bladder: The Evidence�������������������������������������������������������������������������  351 Dudley Robinson and Linda Cardozo 27 Intravesical Botulinum Toxin for the Treatment of Overactive Bladder�������������  365 Pawel Miotla and Tomasz Rechberger 28 Sacral Nerve Stimulation for Overactive Bladder and Voiding Dysfunction �����  375 Philip E. V. Van Kerrebroeck

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Part V Anal Incontinence 29 Overview: Epidemiology and Aetiology of Anal Incontinence�����������������������������  387 Alison J. Hainsworth, Andrew B. Williams, and Alexis M. P. Schizas 30 Patient-Reported Outcome Assessment in Anal Incontinence�����������������������������  399 Toshiki Mimura 31 Anorectal Manometry����������������������������������������������������������������������������������������������  411 Filippo Pucciani and Iacopo Giani 32 Endoanal Ultrasonography in Anal Incontinence�������������������������������������������������  417 Giulio Aniello Santoro, Luigi Brusciano, and Abdul H. Sultan 33 Transperineal Ultrasonography in the Assessment of Anal Incontinence and Obstetric Anal Sphincter Injuries���������������������������������������������  437 Cristina Ros-Cerro, Eva Maria Martínez-Franco, and Montserrat Espuña-Pons 34 Magnetic Resonance Imaging ���������������������������������������������������������������������������������  445 Jeroen A. W. Tielbeek and Jaap Stoker 35 Neurophysiological Evaluation: Techniques and Clinical Evaluation�����������������  451 Mitul Patel, Kumaran Thiruppathy, and Anton Emmanuel 36 Behavioral Therapies and Biofeedback for Anal Incontinence ���������������������������  459 Bary Berghmans, Esther Bols, Maura Seleme, Silvana Uchôa, Donna Bliss, and Toshiki Mimura 37 Sphincter Repair and Postanal Repair�������������������������������������������������������������������  473 Adam Studniarek, Johan Nordenstam, and Anders Mellgren 38 Dynamic Graciloplasty���������������������������������������������������������������������������������������������  483 Piotr Walega and Maciej Walega 39 Injectable and Implantable Biomaterials for Anal Incontinence�������������������������  491 Alex Hotouras and Pasquale Giordano 40 Sacral Neuromodulation for Fecal Incontinence���������������������������������������������������  503 Klaus E. Matzel and Birgit Bittorf 41 Posterior Tibial Nerve Stimulation for Faecal Incontinence���������������������������������  511 Gregory P. Thomas, Carolynne J. Vaizey, and Yasuko Maeda 42 Radiofrequency���������������������������������������������������������������������������������������������������������  517 Luanne Force, Mariana Berho, and Steven D. Wexner 43 Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell���������������������������������������������������������������������������������  521 Zoran Krivokapić and Barišić Goran 44 Treatment of Anal Incontinence: Which Outcome Should We Measure?�����������  533 Alison J. Hainsworth, Alexis M. P. Schizas, and Andrew B. Williams Part VI Pelvic Organ Prolapse 45 Epidemiology and Etiology of Pelvic Organ Prolapse�������������������������������������������  547 Stefano Salvatore, Sarah De Bastiani, and Fabio Del Deo 46 Patient-Reported Outcomes and Pelvic Organ Prolapse �������������������������������������  555 Stavros Athanasiou

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47 Integrated Imaging Approach to Pelvic Organ Prolapse �������������������������������������  577 Giulio A. Santoro, Andrzej P. Wieczorek, Magdalena Maria Woźniak, Jonia Alshiek, Abbas Shoebeiri, and Abdul H. Sultan 48 Transperineal Ultrasound: Practical Applications �����������������������������������������������  587 Hans Peter Dietz 49 Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage���������������������������������������������  619 Jonia Alshiek, Ghazaleh Rostaminia, Lieschen H. Quiroz, and S. Abbas Shobeiri 50 Magnetic Resonance Imaging, Levator Ani Damage, and Pelvic Organ Prolapse���������������������������������������������������������������������������������������������������������  639 John O. L. DeLancey 51 Dynamic Magnetic Resonance Imaging of Pelvic Floor Pathologies�������������������  653 Cäcilia S. Reiner and Khoschy Schawkat 52 Pelvic Floor Muscle Training in Prevention and Treatment of Pelvic Organ Prolapse����������������������������������������������������������������������������������������������  661 Kari Bø and Ingeborg H. Brækken 53 Use of Pessaries for Pelvic Organ Prolapse �����������������������������������������������������������  667 Dimos Sioutis and Rohna Kearney 54 Anterior and Posterior Colporrhaphy: Native Tissue Versus Mesh���������������������  675 Bernard T. Haylen 55 Apical Prolapse Surgery�������������������������������������������������������������������������������������������  687 Christopher Maher 56 Laparoscopic Pelvic Floor Surgery�������������������������������������������������������������������������  695 Jan Deprest, Ann-Sophie Page, Albert Wolthuis, and Susanne Housmans 57 The Robotic Approach to Urogenital Prolapse������������������������������������������������������  709 Claire M. McCarthy, Orfhlaith E. O’Sullivan, and Barry A. O’Reilly 58 Concurrent Prolapse and Incontinence Surgery���������������������������������������������������  723 Annette Kuhn 59 Management of Pelvic Organ Prolapse: A Unitary or Multidisciplinary Approach? �����������������������������������������������������������  729 David Ossin and G. Willy Davila Part VII Constipation and Obstructed Defecation 60 Epidemiology and Etiology of Constipation and Obstructed Defecation: An Overview�����������������������������������������������������������������������������������������  737 Mahmoud Abu Gazala and Steven D. Wexner 61 Patient-Reported Outcome Assessment in Constipation and Obstructed Defecation ���������������������������������������������������������������������������������������������  741 Toshiki Mimura 62 Anorectal Manometry, Rectal Sensory Testing and Evacuation Tests�����������������  753 Mitul Patel, Kumaran Thiruppathy, and Anton Emmanuel 63 Ultrasonography in the Assessment of Obstructive Defecation Syndrome���������  761 Marc Beer-Gabel, Ugo Grossi, Christian Raymond S. Magbojos, and Giulio A. Santoro

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64 Echodefecography: Technique and Clinical Application��������������������������������������  781 Sthela M. Murad-Regadas, Francisco Sérgio P. Regadas, and Steven D. Wexner 65 Evacuation Proctography�����������������������������������������������������������������������������������������  801 Magdalena Maria Woźniak, Aleksandra Stankiewicz, Alexander Clark, and Andrzej P. Wieczorek 66 The Abdominal Approach to Rectal Prolapse �������������������������������������������������������  811 Sthela M. Murad-Regadas, Rodrigo A. Pinto, and Steven D. Wexner 67 The Perineal Approach to Rectal Prolapse�������������������������������������������������������������  827 Alison Althans, Anuradha Bhama, and Scott R. Steele 68 The Laparoscopic Approach to Rectal Prolapse ���������������������������������������������������  835 Bart Van Geluwe and Andrè D’Hoore 69 The Role of Robotic Surgery in Rectal Prolapse���������������������������������������������������  847 Adam Studniarek, Anders Mellgren, and Johan Nordenstam 70 Sacral Neuromodulation for Constipation�������������������������������������������������������������  855 Klaus E. Matzel and Birgit Bittorf Part VIII Pelvic Pain and Sexual Dysfunction 71 Bladder Pain Syndrome/Interstitial Cystitis ���������������������������������������������������������  861 Mauro Cervigni 72 Pelvic Pain Associated with a Gynecologic Etiology ���������������������������������������������  879 Megan B. Shannon and Elizabeth R. Mueller 73 Chronic Idiopathic Anorectal Pain Disorders �������������������������������������������������������  891 Bruno Roche and Cosimo Riccardo Scarpa 74 Female Sexual Dysfunction �������������������������������������������������������������������������������������  909 Dorothy Kammerer-Doak and Rebecca Rogers 75 A Myofascial Perspective on Chronic Urogenital Pain in Women�����������������������  923 Marek Jantos 76 Pharmacological Treatment of Chronic Pelvic Pain ���������������������������������������������  945 Ashish Shetty, Oscar Morice, and Sohier Elneil 77 Idiopathic Chronic Pelvic Pain: A Different Perspective �������������������������������������  951 Peter Petros and Yuki Sekiguchi Part IX  Fistulae 78 Urogenital Fistulae���������������������������������������������������������������������������������������������������  965 Andrew Browning 79 Rectovaginal Fistulae�����������������������������������������������������������������������������������������������  975 A. Muti Abulafi and Abdul H. Sultan 80 Emerging Concepts in Classification of Anal Fistulae�������������������������������������������  995 Arun Rojanasakul and Charles B. Tsang 81 Ultrasonographic Assessment of Anorectal Fistulae��������������������������������������������� 1003 Giulio Aniello Santoro, Christian Raymond S. Magbojos, Giovanni Maconi, and Iwona Sudoł-Szopińska

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82 MR Imaging of Fistula-in-Ano ������������������������������������������������������������������������������� 1029 Steve Halligan 83 Surgical Treatment of Anorectal Sepsis ����������������������������������������������������������������� 1041 Charles B. Tsang 84 Management of Anorectal Fistulae in Crohn’s Disease����������������������������������������� 1059 Jeanie Ashburn and Luca Stocchi Part X Failure or Recurrence After Surgical Treatment: What to Do When It All Goes Wrong 85 Imaging and Management of Complications of Urogynecologic Surgery����������� 1075 Jonia Alshiek and S. Abbas Shobeiri 86 Surgical Management of Complications After Urogynaecological Surgery������� 1097 Ivilina Pandeva and Mark Slack 87 Endosonographic Investigation of Anorectal Surgery Complications����������������� 1115 Christian Raymond S. Magbojos and Giulio Aniello Santoro 88 Investigation and Management of Complications After Coloproctological Surgery��������������������������������������������������������������������������������������� 1125 Tim W. Eglinton and Frank A. Frizelle Part XI Miscellaneous 89 Congenital Abnormalities of the Pelvic Floor: Assessment and Management������ 1139 Paweł Nachulewicz, Magdalena Maria Woźniak, and Agnieszka Brodzisz 90 Male Urinary Incontinence: Assessment and Management��������������������������������� 1159 Nadir I. Osman and Christopher R. Chapple Appendix: Management Consensus Statement������������������������������������������������������������� 1169 Index����������������������������������������������������������������������������������������������������������������������������������� 1179

Contents

Contributors

Paul Abrams  Bristol Urological Institute, Southmead Hospital, Bristol, UK A. Muti Abulafi  Department of Colorectal Surgery, Croydon University Hospital, Surrey, UK Jonia  Alshiek  Department of Obstetrics and Gynecology, INOVA Health, Inova Women’s Hospital, Virginia Commonwealth University, Falls Church, VA, USA Technion Medical School, Hillel Yaffe Hospital, Hadera, Israel Alison Althans  Case Western Reserve University School of Medicine, Cleveland, OH, USA Jeanie Ashburn  Wake Forest University, Baptist Medical Center, Winston-Salem, NC, USA James A. Ashton-Miller  Pelvic Floor Research Group, Biomechanics Research Laboratory, Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI, USA Stavros Athanasiou  National and Kapodistrian University of Athens, Athens, Greece Marc  Beer-Gabel  Neurogastroenterology and Pelvic Floor Unit, Laniado Medical Center, Natanya, Israel Bary  Berghmans Pelvic Care Center Maastricht, Maastricht University Medical Centre, Maastricht, The Netherlands Mariana  Berho Department of Pathology and Laboratory Medicine, Cleveland Clinic Florida, Weston, FL, USA Anuradha  Bhama Department of Colorectal Surgery, Cleveland Clinic Foundation, Cleveland, OH, USA Birgit  Bittorf Sektion Koloproktologie, Chirurgische Klinik der Universität ErlangenNürnberg, Erlangen, Germany Donna Bliss  University of Minnesota School of Nursing, Minneapolis, MN, USA Kari Bø  Department of Sports Medicine, Norwegian School of Sport Sciences, Oslo, Norway Esther Bols  Department of Epidemiology, Maastricht University, Maastricht, The Netherlands Ingeborg H. Brækken  Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway Agnieszka  Brodzisz Department of Pediatric Radiology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland Andrew Browning  Barbara May Foundation, Bowral, NSW, Australia Luigi Brusciano  XI Divisione di Chirurgia Generale e dell’Obesità, Università degli Studi della Campania “Luigi Vanvitelli”, Caserta, Italy Linda Cardozo  Department of Urogynaecology, Kings College Hospital, London, UK

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Mauro Cervigni  Female Pelvic Medicine and Reconstructive Surgery Center, “La Sapienza” University, ICOT-Polo Pontino, Latina, Italy Christopher  R.  Chapple Department of Urology, Sheffield Teaching Hospitals NHS Foundation, Trust, Sheffield, UK Michał  Chlebiej Faculty of Mathematics and Computer Science, Nicolaus Copernicus University in Toruń, Toruń, Poland Alexander Clark  Imaging Department, University Hospitals of North Midlands NHS Trust, Keele University, Stoke-on-Trent, UK Eduardo Cortes  Kingston Hospital, London, UK Andrè  D’Hoore Department of Abdominal Surgery, University Hospitals Gasthuisberg Leuven, Leuven, Belgium G. Willy Davila  Department of Gynecology, Section in Female Pelvic Medicine Reconstructive Surgery, Cleveland Clinic Florida, Weston, FL, USA Dorothy Mangurian Comprehensive Women’s Center, Holy Cross Medical Group, Fort Lauderdale, FL, USA Sarah De Bastiani  IRCCS San Raffaele Scientific Institute, Milan, Italy John O. L. DeLancey  Norman F. Miller Professor of Gynecology, Female Pelvic Medicine and Reconstructive Surgery, Department of Obstetrics and Gynecology, University of Michigan Medical School, Ann Arbor, MI, USA Fabio Del Deo  IRCCS San Raffaele Scientific Institute, Milan, Italy Jan Deprest  Pelvic Floor Unit, University Hospitals Leuven, Leuven, Belgium Paolo Di Benedetto  Department of Rehabilitation Medicine, Institute of Physical Medicine and Rehabilitation, University of Udine, Udine, Italy Hans  Peter  Dietz Sydney Medical School-Nepean, University of Sydney, Sydney, NSW, Australia Peter  L.  Dwyer  Department of Urogynaecology, Mercy Hospital for Women, Melbourne, VIC, Australia Tim  W.  Eglinton Division of Colorectal Surgery, Department of Academic Surgery, University of Otago, Christchurch, New Zealand Sohier Elneil  Division of Pain Medicine, University College London Hospitals, London, UK Anton Emmanuel  Gastrointestinal Physiology Unit, University College Hospital, London, UK Montserrat  Espuña-Pons Pelvic Floor Unit, Institut Clínic de Ginecologia, Obstetrícia i Neonatologia (ICGON), Hospital Clínic de Barcelona, Universitat de Barcelona, Barcelona, Spain Luanne Force  Department of Colorectal Surgery, Digestive Disease Center, Cleveland Clinic Florida, Weston, FL, USA Frank  A.  Frizelle Division of Colorectal Surgery, Department of Academic Surgery, University of Otago, Christchurch, New Zealand Mahmoud  Abu Gazala Department of Colorectal Surgery, Digestive Disease Center, Cleveland Clinic Florida, Weston, FL, USA Julia Geynisman-Tan  Department of Obstetrics and Gynecology, Female Pelvic Medicine and Reconstructive Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA

Contributors

Contributors

xxi

Iacopo Giani  Proctology Unit, USL Toscana Centro, Firenze, Italy Pasquale Giordano  Royal London Hospitals, Barts Health NHS Trust, London, UK Darren Gold  UNSW Professorial Surgical Unit, St Vincent’s Hospital Sydney, Sydney, NSW, Australia Barišić Goran  Clinical Center of Serbia, Clinic for Digestive Surgery, First Surgical Clinic, Belgrade School of Medicine, University of Belgrade, Belgrade, Serbia Philippe Grange  King’s College Hospital, London, UK Ugo Grossi  Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery, Regional Hospital, Treviso, Italy and University of Padua, Padua, Italy Maria  Gyhagen Department of Obstetrics & Gynaecology, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden Alison J. Hainsworth  Colorectal Surgery, Guy’s and St Thomas’ Hospital, London, UK Steve Halligan  Centre for Medical Imaging, University College London, London, UK Ksenia Halpern-Elenskaia  Department of Obstetrics and Gynecology, Medical University Vienna, Vienna, Austria Bernard T. Haylen  University of New South Wales, Sydney, NSW, Australia Aparna Hegde  Tata Center for Urogynecology and Pelvic Health, Mumbai and the Center for Urogynecology and Pelvic Health, New Delhi, India Alex Hotouras  Royal London Hospitals, Barts Health NHS Trust, London, UK Susanne Housmans  Pelvic Floor Unit, University Hospitals Leuven, Leuven, Belgium Marek Jantos  Behavioural Medicine Institute of Australia, Adelaide, SA, Australia Dorothy  Kammerer-Doak  Women’s Pelvic Specialty Care of New Mexico, Albuquerque, NM, USA Rohna  Kearney Warrell Unit, St Mary’s Hospital, Manchester University Hospitals NHS Trust, Manchester Academic Health Science Centre, Manchester, UK School of Medical Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, UK Kimberly Kenton  Department of Obstetrics and Gynecology, Female Pelvic Medicine and Reconstructive Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA Heinz Koelbl  Department of Obstetrics and Gynecology, Medical University Vienna, Vienna, Austria Zoran  Krivokapić Clinical Center of Serbia, Clinic for Digestive Surgery, First Surgical Clinic, Belgrade School of Medicine, University of Belgrade, Belgrade, Serbia Annette Kuhn  Department of Urogynaecology, University of Bern, Frauenklinik, Inselspital, Bern, Switzerland Joseph K.-S. Lee  St Vincents Clinic University of NSW, Sydney, NSW, Australia Giovanni Maconi  Diagnostica e Fisiopatologia Gastroenterologica, Ospedale Luigi Sacco, Milan, Italy Yasuko  Maeda  Western General Hospital, King’s College London, University of London, Harrow, UK

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Christian Raymond S. Magbojos  Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery, Regional Hospital, Treviso, Italy and University of Padua, Padua, Italy Christopher Maher  Urogynaecologist Wesley and Royal Brisbane and Women’s Hospital, University of QLD, Brisbane, QLD, Australia Eva  Maria  Martínez-Franco Parc Sanitari Sant Joan de Déu, Sant Boi del Llobregat, Barcelona, Spain Klaus  E.  Matzel Sektion Koloproktologie, Chirurgische Klinik der Universität ErlangenNürnberg, Erlangen, Germany Claire M. McCarthy  Department of Obstetrics and Gynaecology, Cork University Maternity Hospital, Cork, Ireland Anders Mellgren  Division of Colon and Rectal Surgery, University of Illinois at Chicago, Chicago, IL, USA Tomi  S.  Mikkola Department of Obstetrics and Gynecology, Helsinki University Central Hospital, Helsinki, Finland Ian Milsom  Department of Obstetrics & Gynaecology, Sahlgrenska Academy at Gothenburg University, Gothenburg, Sweden Toshiki  Mimura Division of Gastroenterological, General and Transplant Surgery, Jichi Medical University, Tochigi, Japan Pawel Miotla  2nd Department of Gynaecology, Medical University of Lublin, Lublin, Poland Oscar Morice  University College London Medical School, London, UK Elizabeth R. Mueller  Female Pelvic Medicine and Reconstructive Surgery, Departments of Urology, Obstetrics and Gynecology, Loyola University Stritch School of Medicine, Chicago, IL, USA Sthela M. Murad-Regadas  Colorectal Surgery at University Hospital, School of Medicine, Federal University of Ceara, Fortaleza, Ceara, Brazil Anorectal Physiology and Pelvic Floor Unit, Sao Carlos Hospital, Fortaleza, Ceara, Brazil Paweł  Nachulewicz  Clinic of Pediatric Surgery and Traumatology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland Johan Nordenstam  Division of Colon and Rectal Surgery, University of Illinois at Chicago, Chicago, IL, USA Barry A. O’Reilly  Department of Obstetrics and Gynaecology, University College Dublin, Dublin, Ireland Department of Urogynaecology, Cork University Maternity Hospital, Cork, Ireland ASSERT Centre, University College Cork, Cork, Ireland Orfhlaith  E.  O’Sullivan Department of Obstetrics and Gynaecology, Cork University Maternity Hospital, Cork, Ireland Nadir  I.  Osman Department of Urology, Sheffield Teaching Hospitals NHS Foundation, Trust, Sheffield, UK David Ossin  Department of Gynecology, Section in Female Pelvic Medicine Reconstructive Surgery, Cleveland Clinic Florida, Weston, FL, USA Holy Cross Medical Group, Dorothy Mangurian Comprehensive Women’s Center, Boca Raton, FL, USA

Contributors

Contributors

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Ann-Sophie Page  Pelvic Floor Unit, University Hospitals Leuven, Leuven, Belgium Ivilina  Pandeva Department of Gynaecology, Addenbrooke’s Hospital, University of Cambridge Teaching Hospital, Cambridge, UK Mitul Patel  Gastrointestinal Physiology Unit, University College Hospital, London, UK Peter Petros  University of NSW Professorial Department of Surgery, St Vincent’s Hospital, Sydney, NSW, Australia School of Mechanical and Chemical Engineering, University of Western Australia, Perth, WA, Australia Jacek  Piłat Department of General and Transplant Surgery and Nutritional Treatment, Medical University of Lublin, Lublin, Poland Rodrigo A. Pinto  Department of Gastroenterology, Service of Colorectal Surgery, Hospital das Clínicas, University of São Paulo School of Medicine, São Paulo, Brazil Filippo Pucciani  Department of Surgery and Translational Medicine, University of Florence, Firenze, Italy Lieschen H. Quiroz  The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA Amrith Raj Rao  Manipal Hospital, Bangalore, India Tomasz Rechberger  2nd Department of Gynaecology, Medical University of Lublin, Lublin, Poland Francisco Sérgio P. Regadas  Department of Surgery, School of Medicine, Federal University of Ceara, Fortaleza, Ceara, Brazil Fiona  Reid The Warrell Unit, Manchester University Hospitals NHS Foundation Trust, Manchester, UK Cäcilia S. Reiner  Institute of Diagnostic and Interventional Radiology, University Hospital Zurich, Zurich, Switzerland Dudley Robinson  Department of Urogynaecology, King’s College Hospital, London, UK Bruno  Roche Proctology Unit, School of Medicine, University of Geneva, Clinique Hirslanden Grangettes, Geneva, Switzerland Rebecca Rogers  Department of Obstetrics and Gynecology, Albany Medical School, Albany, NY, USA Arun Rojanasakul  King Chulalongkorn Memorial Hospital, Bangkok, Thailand Cristina  Ros-Cerro Pelvic Floor Unit, Institut Clínic de Ginecologia, Obstetrícia i Neonatologia (ICGON), Hospital Clínic de Barcelona, Universitat de Barcelona, Barcelona, Spain Ghazaleh Rostaminia  The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA Stefano Salvatore  IRCCS San Raffaele Scientific Institute, Milan, Italy Giulio  A.  Santoro  Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery, Regional Hospital, Treviso, Italy and University of Padua, Padua, Italy Cosimo Riccardo Scarpa  Visceral Surgery Division, Yverdon Hospital, University Hospital of Geneva, Yverdon les Bains, Switzerland Khoschy Schawkat  Institute of Diagnostic and Interventional Radiology, University Hospital Zurich, Zurich, Switzerland

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Alexis M. P. Schizas  Colorectal Surgery, Guy’s and St Thomas’ Hospital, London, UK Jakob  Scholbach Mathematisches Institut, Westfälische Wilhelms-Universität Münster, Münster, Germany Yuki Sekiguchi   Women’s Clinic LUNA, Yokohama, Japan Yokohama City University Graduate School of Medicine, Yokohama, Japan Maura Seleme  abafi-HOLLAND, Maastricht, The Netherlands Faculdade Inspirar, Curitiba, Brazil Megan B. Shannon  Female Pelvic Medicine and Reconstructive Surgery, Virginia Women’s Center, Richmond, VA, USA Ashish Shetty  Division of Pain Medicine, University College London Hospitals, London, UK S.  Abbas  Shobeiri University of Virgina INOVA Campus, Department of Obstetrics and Gynecology, INOVA Women’s Hospital, Falls Church, VA, USA Dimos Sioutis  Third Department of Obstetrics and Gynaecology, Attikon Hospital, National and Kapapodistrian University of Athens, Athens, Greece Mark Slack  Department of Gynaecology, Addenbrooke’s Hospital, University of Cambridge Teaching Hospital, Cambridge, UK Aleksandra Stankiewicz  Imaging Department, University Hospitals of North Midlands NHS Trust, Keele University, Stoke-on-Trent, UK Scott R. Steele  Department of Colorectal Surgery, Cleveland Clinic Foundation, Cleveland, OH, USA Luca Stocchi  Mayo Clinic Florida, Jacksonville, FL, USA Jaap  Stoker  Department of Radiology and Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Adam Studniarek  Division of Colon and Rectal Surgery, University of Illinois at Chicago, Chicago, IL, USA Iwona  Sudoł-Szopińska Department of Radiology, National Institute of Geriatrics, Rheumatology and Rehabilitation, Warsaw, Poland Department of Diagnostic Imaging, Warsaw Medical University, Warsaw, Poland Abdul H. Sultan  Urogynaecology and Pelvic Floor Reconstruction Unit, Croydon University Hospital, St George’s University of London, London, UK Michael Swash  The Royal London Hospital, London, UK Ranee  Thakar Department of Obstetrics and Gynecology, Croydon University Hospital, Croydon, Surrey, UK Kumaran Thiruppathy  Division of Colorectal Surgery, Royal Berkshire Hospital, Reading, UK Gregory P. Thomas  Ashford and St Peter’s NHS Trust, Surrey, UK Jeroen A. W. Tielbeek  Department of Radiology and Nuclear Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands Charles  B.  Tsang Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore Silvana Uchôa  Universidade Católica de Pernambuco, Recife, Pernambuco, Brazil

Contributors

Contributors

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Carolynne J. Vaizey  St Mark’s Hospital Foundation, Harrow, UK Bart  Van Geluwe Department of Abdominal Surgery, University Hospitals Gasthuisberg Leuven, Leuven, Belgium Philip  E.  V.  Van Kerrebroeck Department of Urology, Maastricht University Medical Center, Maastricht, The Netherlands Maciej Walega  Department of Anaesthesiology, University Hospital Düsseldorf, Düsseldorf, Germany Piotr  Walega 3rd Department of Surgery, Jagiellonian University Collegium Medicum, Krakow, Poland Steven D. Wexner  Digestive Disease Center, Department of Colorectal Surgery, Cleveland Clinic Florida, Weston, FL, USA Andrzej  P.  Wieczorek  Department of Pediatric Radiology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland Andrew B. Williams  Colorectal Surgery, Guy’s and St Thomas’ Hospital, London, UK Albert Wolthuis  Pelvic Floor Unit, University Hospitals Leuven, Leuven, Belgium Magdalena  Maria  Woźniak Department of Pediatric Radiology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland Michel Wyndaele  Division of Urology, UMC Utrecht, Utrecht, The Netherlands

Part I State of the Art Pelvic Floor Anatomy

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Pelvic Floor Anatomy S. Abbas Shobeiri and John O. L. DeLancey

Learning Objectives

• To conceptualize pelvic organ support. • To become familiarize with room analogy and suspension bridge analogy of pelvic organ support. • To understand the intricate anatomy of the levator ani subdivisions. • To understand the role of endopelvic fascia and connective tissue for pelvic organ support.

1.1

Introduction

Pelvic floor disorders are a spectrum of diseases that include urinary incontinence (UI), fecal incontinence, and pelvic organ prolapse (POP) which represent a public health issue in the United States and around the world [1]. Pelvic floor disorders are debilitating conditions with 24% of adult women having at least one of the pelvic floor disorders [2]. This epidemic results in surgery in one of nine women [3]. In the United States, the National Center for Health Statistics estimates 400,000 operations per year which are performed for pelvic floor dysfunction, with 300,000 occurring in the inpatient setting [4]. Among the Australian women, the lifetime risk of surgery for POP in the general female population was 19% [5]. In an Austrian study, an estimation of the frequency for post-hysterectomy vault prolapse requiring surgical repair was between 6% and 8% [6]. A single vaginal birth S. A. Shobeiri (*) University of Virgina INOVA Campus, Department of Obstetrics and Gynecology, INOVA Women’s Hospital, Falls Church, VA, USA e-mail: [email protected] J. O. L. DeLancey Pelvic Floor Research Group, Department of Obstetrics and Gynecology, University of Michigan Medical School, Ann Arbor, MI, USA e-mail: [email protected]

has been shown to significantly increase the odds of prolapse (OR 9.73, 95% CI 2.68–35.35) with subsequent vaginal births not shown to be associated with a significant increase in the odds of prolapse [7]. It is forecasted that the number of American women with at least one pelvic floor disorder will increase from 28.1 million in 2010 to 43.8 million in 2050. During this time period, the number of women with UI will increase 55% from 18.3 million to 28.4 million. For fecal incontinence, the number of affected women will increase 59% from 10.6 to 16.8 million, and the number of women with POP will increase 46% from 3.3 to 4.9 million. The highest projections is that in 2050, 58.2 million women in the United States will have at least one pelvic floor disorder, 41.3 million with UI, 25.3 million with fecal incontinence, and 9.2 million with POP. All these forecasts, although varied, point the direction to increased prevalence of pelvic floor disorders which has important public health implications. Understanding the causes of pelvic floor disorders is in its infancy. What is known is that prolapse arises because of injuries and deterioration of the muscles, nerves, and connective tissue that support and control normal pelvic function. This chapter focuses on the anatomy of the pelvic floor in women and how the anterior, posterior compartments are supported by apical and lateral segments.

1.1.1 S  upport of the Pelvic Organs: Conceptual Overview The pelvic organs rely on (1) their connective tissue attachments to the pelvic walls and (2) support from the levator ani muscles that are under neuronal control from the peripheral and central nervous systems. In this chapter, the term “pelvic floor” is used broadly to include all the structures supporting the pelvic floor with special emphasis on the levator ani group of muscles. To convey the pelvic floor supportive structures’ 3D architecture to the reader, we use the “room analogy.” Using this analogy, the reader can conceptualize the pelvic floor

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_1

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ANTERIOR

LATERAL

MIDDLE

POSTERIOR

Fig. 1.1  Room analogy. © Shobeiri 2013

Fig. 1.3  Room analogy with anterior, middle, and posterior compartments and the lateral walls marked. © Shobeiri 2013

Pubic Bone

Pubocervical Fascia

Rectovaginal Fascia

Levator Ani Muscle

Fig. 1.2  Room analogy with three compartments separated. © Shobeiri 2013

hiatus as the door out of the pelvis (Fig. 1.1). Using this very simplified analogy, if one views the pelvic floor hiatus from the S1 location on the sacrum, the door frame for this room is the perineal membrane, the walls and the floor the levator ani muscle, and the ceiling the pubic bone. Pelvic floor contains three viscus hollows (Fig. 1.2). We arbitrarily call these anterior and posterior compartments with lateral and apical support segments (Fig. 1.3). The tissue separating the anterior compartment and vagina is pubocervical fibromuscularis or pubocervical fascia or fibromuscularis. The tissue ­separating the vaginal canal from the posterior compartment has been called several names: the rectovaginal fibromuscularis or rectovaginal fascia or septum (Fig. 1.4). Some have even argued that this tissue doesn’t exist which may be due to its complex anatomy. The term “fascia” is often used by surgeons to refer to the strong tissue that they sew together during anterior repairs. This has led to confusion and misun-

Fig. 1.4  Room analogy: pubocervical fibromuscularis and rectovaginal fascia separating the three compartments. © Shobeiri 2013

derstanding of the anatomy. The pubocervical fibromuscularis and the rectovaginal fibromuscularis are attached laterally to the levator ani muscle with thickening of adventitia in this area. Anatomically, the endopelvic fascia refers to the areolar connective tissue that surrounds the vagina. It continues down the length of the vagina as loose areolar tissue surrounding the pelvic viscera. Histologic examination has shown that the vagina is made up of three layers—epithelium, muscularis, and adventitia [8, 9]. The adventitial layer is loose areolar connective tissue made up of collagen and elastin, forming the vaginal tube. Therefore, the tissue that surgeons call fascia at the time of surgery is best described as fibromuscularis, since it is a mixture of muscularis and adventitia. Anteriorly, pubocervical fibromuscularis is attached to the levator ani using arcus tendineus fascia pelvis (Fig. 1.5).

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Bladder outlet

Vaginal canal

Anal canal

Fig. 1.5  Retropubic anatomy showing points of attachments of the arcus tendineus levator ani (ATLA) and the arcus tendineus fascia pelvis (ATFP). The urethra (U) sits on the hammock like pubocervical fibromuscularis. # denotes the levator ani attachment to the obturator internus muscle Pubic symphysis (PS). © Shobeiri 2013

Fig. 1.7  Room analogy: three compartments separation. © Shobeiri 2013

Perineal Membrane Arcus Tendineus

Posterior Arcus

Levator Ani

Fig. 1.6  Room analogy: the line of attachment of the pubocervical fascia to the levator ani is arcus tendineus fascia pelvis. The line of attachment of the rectovaginal fascia to the levator ani is the posterior arcus. Both are shown as red lines. © Shobeiri 2013

Posterior attachment of rectovaginal fibromuscularis to the levator ani is poorly understood, but we will refer to it as the posterior arcus (Fig. 1.6) [10]. The anterior compartment is home to the urethra and the lower part of the bladder. The vaginal canal is in the middle, and the posterior compartment is home to anorectum (Fig. 1.7). This analogy is not far from reality. When one looks at the pelvic floor structures, the anterior and posterior compartments are clearly separated as described (Fig.  1.8). Compartmentalization of the pelvic floor has led to different medical specialties looking at that specific compartment and paying less attention to the whole pelvic floor (Fig. 1.9).

Fig. 1.8  Midsagittal anatomy of an intact cadaveric specimen demonstrating the three different compartments. Pubocervical fibromuscularis (PCFM), rectovaginal fibromuscularis (RVF). © Shobeiri 2013

If one looks at the vaginal canal from the side, he or she can appreciate different levels of support as described by DeLancey and colleagues [11] (Fig. 1.10). Looking at these supportive structures from the sagittal view exposes the connective tissue elements that keep the room standing. Generally, a “suspension bridge” analogy is useful for describing these structures (Fig. 1.11). Although in the room analogy, the anterior and posterior compartments house the pelvic organs, in reality, the pelvic organs are part of the whole pelvic biomechanical system and play an important supportive role through their connections with structures, such as the cardinal and uterosacral ligaments. Adapting this suspension bridge to the human body and the perineal body and the sacrum become the two anchoring points of the bridge. The perineal membrane (Level III) and the uterosacral ligaments (Level I) form the two masts of the suspension

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Fig. 1.11  Suspension bridge analogy; the depiction of a normal bridge. © Shobeiri 2013 P

Fig. 1.9  Room analogy: each area or compartment may be managed by a different specialist. There is a great need for one specialty that understands the interaction between different compartments and manages them concurrently as much as possible. © Shobeiri 2013

ATLA

IS

Post-Arcus Perineal Membrane

Uterosacral support

Sacrum

Anococcygeal ligament

PB

Fig. 1.12  Suspension bridge analogy; the depiction of a suspension bridge adapted to human female pelvic floor structures. The red masts are the ischial spine (IS) and the pubis (P). The blue lines are the levator ani fibers. The green line is the uterosacral ligaments (USL) continuous with the posterior arcus line. The anococcygeal ligament provides anchoring point for the posterior structures. Arcus tendineus levator ani (ATLA), perineal body (PB). © Shobeiri 2013

Lateral Attachments

III

USL

II

I PR

Fig. 1.10 Room analogy: Level I supports are provided by the uterosacral-­cardinal ligament complex (yellow arrows), which keep the “room” upright. Level II supports are provided by the lateral tendineus attachments (red lines). The support is provided by perineal membrane (green area). © Shobeiri 2013

bridge (Fig. 1.12). The lateral wires are the levator ani muscles of the lateral wall (Fig. 1.13), and the attachments of the vagina to the levator ani muscles laterally in the mid part of the vagina form Level II support. The levator ani muscles and the interconnecting fibromuscular structures support the bladder and urethra anteriorly, the vaginal canal in the middle, and the anorectal structures posteriorly (Fig. 1.14). Like a room or a suspension bridge, the pelvic floor is subjected to loads that should be appropriate for its design.

PV PA

LP

Fig. 1.13  Suspension bridge analogy; the depiction of a suspension bridge adapted to human female pelvic floor structures. The levator ani fibers have intricate and overlapping paths. The puboanalis (PA) and puboperinealis form some of the supportive structures of the perineum. The puborectalis (PR) fibers form the sling behind the rectum. Pubovisceralis (PV) is a collective term we have applied here to the iliococcygeus and pubococcygeus fibers. The levator plate (LP) is formed by overlapping of the PV and PR fibers. © Shobeiri 2013

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P Bladder

IS

Vagina Rectum Sacrum Anus PB

Fig. 1.14  Suspension bridge analogy; the depiction of different compartments of pelvic floor. Ischial spine (IS), pubis (P), perineal body (PB). © Shobeiri 2013

Should these loads exceed what the pelvic floor is capable of handling, there would be failure in one or multiple supportive elements. The pelvic floor is not a static structure. The levator ani works in concert with the ligamentous structures to withstand intra-abdominal pressure that could predispose to POP and urinary or fecal incontinence during daily activities (Fig.  1.15). The lower end of the pelvic floor is held closed by the pelvic floor muscles, preventing prolapse by constricting the base. The spatial relationship of the organs and the pelvic floor is important. Pelvic support is a combination of constriction, suspension, and structural geometry. The levator ani muscle has puboperinealis, puboanalis, pubovaginalis, puborectalis, pubococcygeus, and iliococcygeus subdivisions (Fig. 1.16). The pubococcygeus is a functional unit of the iliococcygeus, and these two collectively are known as the pubovisceralis muscle in some literature. We will avoid this term as it can be confusing. The relationship of these muscles to each other is intricate, as they crisscross in different angles to each other (Figs. 1.17 and 1.18).

1.2

Anatomy and Prolapse

1.2.1 Overview Level I support is composed of the uterosacral and cardinal ligaments that form the support of the uterus and upper one third of the vagina. Stretching and failure of Level I can result in pure apical prolapse of the uterus or an enterocele formation. At Level II, there are direct lateral attachments of the pubocervical fibromuscularis and rectovaginal fibromuscularis to the lateral support segment formed by the levator ani muscles. The variations of defect in this level will be described in the following sections. In Level III the vaginal wall is anteriorly fused with the urethra, posteriorly with the

Fig. 1.15  Right lateral standing anatomic depiction of the three compartments exposed to intra-abdominal pressure, which results in activation of the muscles to prevent prolapse or urinary and fecal incontinence. Anus (A), bladder (B), cervix (Cx), levator ani (LA), rectum (R), urethra (U), vagina (V). © Shobeiri 2013

perineal body. Levator ani muscles in this area are poorly described, but mostly consist of fibrous sheets that envelop the lateral aspects of the vaginal introitus.

1.2.2 Apical Segment While Level I cardinal and uterosacral ligaments can be surgically identified supporting the cervix and the upper third of the vagina [12, 13], as they fan out toward the sacrum and laterally, they become a mixture of connective tissue, blood vessels, nerves, smooth muscle, and adipose tissue. The uterosacral ligaments act like rubber bands in that they may lengthen with initial Valsalva, but resist any further lengthening at a critical point in which they have to return to their comfortable length or break (Fig. 1.19). Level I and levator ani muscles are interdependent. Intact levator ani muscles moderate the tension placed on the Level I support structures, and intact Level I support lessens the pressure imposed from above on the pelvic floor.

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a

b

c

Fig. 1.16 (a) The relative position of levator ani subdivisions during ultrasound imaging. Iliococcygeus (IC), puboperinealis (PP), superficial transverse perinei (STP), puboanalis (PA). Illustration: John Yanson. From Shobeiri et al. [25], with permission. (b) The levator ani muscle is color coded: from left to right, light brown = coccygeus muscle (CG), brown = iliococcygeus muscle (IC), magenta = ATLA/ATFP, red = pubovisceralis muscle (PV), green = puborectalis muscle (PR),

pink = puboperinealis muscle (PP), orange = puboanalis muscle (PA). The labels are placed to orient the viewer to the relative position of the other structures in the pelvis. Copyright © Shobeiri 2009. (c) The left lateral view of the left hemi-pelvis. Arcus tendineus levator ani (ATLA), bladder (B), external anal sphincter (EAS), iliococcygeus (IC), pubococcygeus (PC), puborectalis (PR), pubic symphysis (PS), urethra (U). © Shobeiri 2013

1.2.3 Anterior Compartment

tendineus from the levator ani is associated with stress incontinence and anterior prolapse. The detachment can be unilateral (Fig. 1.21) or bilateral (Fig. 1.22), causing a displacement cystocele. In addition, the defect can be complete or incomplete. The surgeon who performs an anterior repair (Fig.  1.22) in reality worsens the underlying disease process. The upper portions of the anterior vaginal wall can prolapse due to lack of Level I support and failure of uterosacral-cardinal complex. Over time this failure may lead to increased load in the paravaginal area and failure of Level II paravaginal support. A study of 71 women with anterior compartment prolapse has shown that paravaginal defect usually results from a detachment of the arcus tendineus fas-

Anterior compartment support depends on the integrity of vaginal muscularis and adventitia and their connections to the arcus tendineus fascia pelvis. The arcus tendineus fascia pelvis is at one end connected to the lower sixth of the pubic bone, 1–2 cm lateral to the midline, and at the other end to the ischial spine. A simple case of a distension cystocele could result from a defect in pubocervical fibromuscularis (Fig. 1.20). The anterior wall fascial attachments to the arcus tendineus fascia pelvis have been called the paravaginal fascial attachments by Richardson et al. [14]. Detachment of arcus

1  Pelvic Floor Anatomy

cia pelvis from the ischial spine, and rarely from the pubic bone [15]. Resuspension of the vaginal apex at the time of surgery, in addition to paravaginal or anterior colporrhaphy, may help to return the anterior wall to a more normal position or at least to prevent future failures. Another scenario that the surgeon faces is the lack of any tangible fibromuscular tissue in the anterior compartment (Fig. 1.23). Plication of the available tissue may cause vaginal narrowing and dyspareunia. The knowledge of this condition is essential,

Fig. 1.17  Right hemipelvis of a fresh frozen pelvis showing the overlapping of the levator ani subdivisions fibers. Orange arrows: puborectalis; blue arrows: iliococcygeus; white arrows: pubococcygeus. Note the relationship between the iliococcygeus and pubococcygeus fibers. © Shobeiri 2013

a

Fig. 1.18 (a) Right hemipelvis of a fresh frozen pelvis with the organs removed. The puborectalis (PR), iliococcygeus (IC), and pubococcygeus (PC) form the lateral sidewall. Note the relationship between the iliococcygeus and pubococcygeus fibers. Coccyx (C), pubic symphysis

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as it will require bridging of the anterior compartment with autologous fascia lata graft [16]. The commercially available biologic tissue has had high failure rates for the anterior compartment and no improvement in the posterior compartment. Various grading systems such as Pelvic Organ Prolapse Quantification (POPQ) system [17] used to describe prolapse do not take into account the underlying cause of the prolapse. Site of care pelvic floor imaging augments the physical examination to delineate the pathophysiology of pelvic organ prolapse.

Fig. 1.19  Right hemipelvis of a fresh frozen pelvis showing the uterosacral fibers. The borders of the ligament are shown in dotted line. Cervix (Cx), coccyx (C), pubic symphysis (PS). © Shobeiri 2013

b

(PS). © Shobeiri 2013. (b) The same right hemipelvis of a fresh frozen pelvis with the organs removed. The puboanalis and the puboperinealis are outlined. These fibers are involved in the stabilization of the anus and the perineum, respectively. © Shobeiri 2013

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b

Fig. 1.22  Room analogy: bilateral detachment of the pubocervical fibromuscularis can result in a cystocele. © Shobeiri 2013

Fig. 1.20  Room analogy: (a) an occult pubocervical fibromuscularis defect can result in an overt cystocele (b). © Shobeiri 2013 Fig. 1.23  Room analogy: absence or severe deficiency of the pubocervical fibromuscularis can result in a cystocele. © Shobeiri 2013

1.2.4 P  erineal Membrane (Urogenital Diaphragm)

Fig. 1.21  Right hemipelvis of a fresh frozen pelvis showing a paravaginal defect repair outlined in green. Arcus tendineus fascia pelvis (ATFP), arcus tendineus levator ani (ATLS), pubic symphysis (PS), urethra (U). © Shobeiri 2013

A critical but perhaps underappreciated part of pelvic floor support is the perineal membrane as it forms the Level III support (Fig.  1.24) and one of the anchoring points in the suspension bridge analogy. On the anterior part caudad to the levator ani muscles, there is a dense triangular membrane called the urogenital diaphragm. However, this layer is not a single muscle layer with a double layer of fascia (“diaphragm”), but rather a set of connective tissues that surround the urethra; the term perineal membrane has been used more recently to reflect its true nature [18]. The perineal membrane is a single connective tissue membrane, with muscle lying immediately above. The perineal membrane lies at the

1  Pelvic Floor Anatomy

a

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b

c

Fig. 1.24  Three levels of support. (a) Attachments of the cervix and vagina to the pelvic walls demonstrating different regions of support with the uterus in situ. Note that the uterine corpus and the bladder have been removed. (b) Levels of vaginal support after hysterectomy. Level I (suspension) and Level II (attachment). In level I the paracolpium suspends the vagina from the lateral pelvic walls. Fibers of Level I extend both vertically and also posteriorly toward the sacrum. In Level II the

vagina is attached to the arcus tendineus fasciae pelvis and the superior fascia of levator ani. (c) Close up of the lower margin of Level II after a wedge of vagina has been removed (inset). Note how the anterior vaginal wall, through its connections to the arcus tendineus fascia pelvis, forms a supportive layer clinically referred to as the pubocervical fascia (From DeLancey [11], with permission)

level of the hymen and attaches the urethra, vagina, and perineal body to the ischiopubic rami.

that can be unilateral (Fig. 1.26) or bilateral (Fig. 1.27). Such defects need to be differentiated from total loss of rectovaginal fibromuscularis that may require augmentation of the compartment with autologous or cadaveric tissue. Most often, the separation of the posterior arcus may be apical and may require reattachment of the posterior arcus to the uterosacral ligament or the iliococcygeal muscle. The fibers of the perineal membrane connect through the perineal body, thereby providing a layer that resists downward descent of the rectum. A separate Level I support does not exist for anterior and posterior compartments. In the room analogy used here, the perineal membrane is analogous to the door frame. If the bottom of the door frame is missing (Fig. 1.28), then the resistance to downward descent is lost and a perineocele develops. This situation can be elusive, as

1.2.5 P  osterior Compartment and Perineal Membrane The posterior compartment is bound to perineal body and the perineal membrane caudad (Level III), paracolpium and the uterosacral ligaments cephalad (level I), and the posterior arcus connected to the levator ani laterally (Level II). As in the anterior compartment, a simple defect in rectovaginal fibromuscularis (Fig. 1.25) can cause a distention rectocele. A defect in the posterior arcus also called arcus tendineus rectovaginalis (ATRV) is associated with a pararectal defect

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a

b

Fig. 1.25  Room analogy: (a) an occult rectovaginal defect can result in an overt rectocele (b). © Shobeiri 2013

the clinical diagnosis is made by realizing the patient’s need to splint very close to the vaginal opening in order to have a bowel movement, and the physical examination may reveal an elongated or “empty” perineal body (Fig.  1.29). Reattachment of the separated structures during perineorrhaphy corrects this defect and is a mainstay of reconstructive surgery. Because the puboperinealis muscles are intimately connected with the cranial surface of the perineal membranes, this reattachment also restores the muscles to a more normal position under the pelvic organs in a location where they can provide support. Two-dimensional magnetic resonance imaging (MRI) of posterior vaginal prolapse has elucidated further how the posterior vaginal wall fail by studying different 3D characteristics of models of rectocele-type posterior vaginal prolapse (PVPR) in women [19]. Increased folding (kneeling) of

S. A. Shobeiri and J. O. L. DeLancey

a

b

Fig. 1.26 (a) Room analogy: right lateral detachment of the rectovaginal septum can result in a rectocele. © Shobeiri 2013. (b) The surgical view of the posterior compartment showing the relationship between the levator ani muscle (LAM), the rectovaginal fibromuscularis (RVF), and the arcus tendineus fasciae rectovaginalis (ATRV). © Shobeiri 2013

Fig. 1.27  Room analogy: bilateral detachment of the rectovaginal septum can result in a rectocele. © Shobeiri 2013

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a

Fig. 1.28  Room analogy: absence or severe deficiency of rectovaginal fascia can result in a rectocele. © Shobeiri 2013

b

the vagina and an overall downward displacement are consistently present in rectocele. Forward protrusion, perineal descent, and distal widening are sometimes seen as well (Fig. 1.30). Three anal canal muscular structures that contribute to fecal continence are the internal anal sphincter (IAS), the external anal sphincter (EAS), and the levator plate. The EAS is made up of voluntary muscle that encompasses the anal canal. It is described as having three parts: 1. The deep part is integral with the puborectalis. Posteriorly there is some ligamentous attachment. Anteriorly some fibers are circular. 2. The superficial part has a very broad attachment to the underside of the coccyx via the anococcygeal ligament. Anteriorly there is a division into circular fibers and a decussation to the superficial transverse perinei. 3. The subcutaneous part lies below the IAS. The IAS always extends cephalad to the EAS for a distance of more than 1–2 cm. The internal sphincter lies consistently between the external sphincter and the anal mucosa, extending below the dentate line by 1 cm. Normally, the EAS begins below the IAS [20]. The muscle fibers from the puboanalis portion of the levator ani become fibroelastic as they extend caudally to merge with the conjoined longitudinal layer also known as the longitudinal muscle (CLL) that is inserted between the EAS and IAS (see Figs. 1.29b and 1.31a, b) [21]. The CLL fibers and the puboanalis fibers cannot be palpated clinically. However,

Fig. 1.29 (a) A perineocele in a patient with need to splint to have a bowel movement. © Shobeiri 2013. (b) This drawing demonstrates the right sagittal hemipelvis view of the perineal support structures. The perineum, a small seemingly insignificant part of the female body, is packed with muscles and fascial layers that interconnect in an intricate manner. External anal sphincter (EAS), internal anal sphincter (IAS), ischiopubic rami (IPR), puboanalis (PA), puboanalis insertion (PAI), perineal body (PB), puboperinealis (PP), puboperineal insertion (PPI), pubic symphysis (PS), rectum (R), rectovaginal septum, (RVS), superficial transverse perinei (STP), urethra (U), vagina (V). © Shobeiri 2013

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S. A. Shobeiri and J. O. L. DeLancey

a

b Normal

c

d Posterior Prolapse Downward Displacement

“Kneeling”

Forward Protrusion

Distal Widening

Perineal Descent

Fig. 1.30  Characteristics of posterior prolapse. Comparison of control (a, b) and case (c, d) in lateral view (a, c) and oblique view (b, d) showing five characteristic features (c, d) during rest (blue) and Valsalva (pink): (1) increased folding (kneeling), (2) downward displacement in

the upper two thirds part of the vagina, (3) forward protrusion, (4) perineal descent, and (5) distal widening in the lower third part of the vagina. Pubis and sacrum are shown in white. The P-IS line is shown in turquoise. © DeLancey 2011

the puboperinealis fibers, which are medially located, can be palpated as a distinct band of fibers joining the perineal body (see Figs. 1.29b and 1.32). Per MRI studies done by Hsu and colleagues, the EAS includes a subcutaneous portion (EAS-SQ) (see Fig. 1.32), a visibly separate deeper portion (EAS-M), and a lateral portion that has lateral winged projections (EAS-W). The EAS-SQ is the distinct part of the EAS (Fig. 1.33). A clear

separation does not exist between concentric portion of EAS-M and the winged EAS-W. The EAS-W fibers have differing fiber directions than the other portions, forming an open “U-shaped” configuration that cannot be visualized in midsagittal view except in the posterior anus. These fibers are contiguous with the EAS but visibly separate from the levator plate muscles, whose fibers they parallel [22].

1  Pelvic Floor Anatomy

a

15

b

Fig. 1.31 (a) Perineal dissection in a fresh frozen pelvis shows the relationship of the external anal sphincter (EAS) to the perineal body (PB) and the puboanalis/puboperinealis complex (PA). Ischiorectal fat (IRF), Vagina (V). © Shobeiri 2013. (b) Perineal dissection in a fresh frozen pelvis shows the relationship of the superficial transverse perinei

(STP) to the other puboanalis fibers that start inserting at the perineal level at Fig (a) and then wrap around the anal canal. The ischiocavernosus (ISC) and the bulbospongiosus muscle (BS) are depicted here. Levator ani muscle (LAM). © Shobeiri 2013

1.2.6 L  ateral Segment Comprising of the Levator Ani Muscle Support

from one pelvic sidewall to the other; the pubococcygeus muscle, which travels from the tip of the coccyx to the pubic bone (see Fig.  1.17); the puborectalis muscle, originating from the anterior portion of the perineal membrane and the pubic bone to form a sling behind the rectum; and the puboperinealis and puboanalis, which are thin broad fibromuscular poorly described structures that attach to the perineal body and anus to stabilize the perineal region. Margulies and colleagues showed excellent reliability and reproducibility in visualizing major portions of the levator ani with magnetic resonance imaging (MRI) in nulliparous volunteers [25]. Because puboanalis, pubovaginalis, and puboperinealis are small, they are proven hard to visualize with conventional MRI. However, these muscles are easily seen with three-dimensional (3D) endovaginal ultrasonography (EVUS) [26]. The shortest distance between the pubic symphysis and the levator plate is the minimal levator hiatus. This is d­ ifferent from the urogenital hiatus, which is bounded anteriorly by the pubic bones, laterally by levator ani muscles, and posteriorly by the perineal body and EAS.  The baseline tonic activity of the levator ani muscle keeps the minimal levator hiatus closed by compressing the urethra, vagina, and rectum against the pubic bone as they exit through this opening [27]. The levator ani fibers converge behind the rectum to form the levator plate. With contraction, the levator plate elevates to form a horizontal shelf over which pelvic organs rest. The deficiency of any portion of the levator ani results in weakening of the levator plate and descensus of pelvic organs [28].

It is generally accepted that the levator ani muscles and the associated fascial layer surround pelvic organs like a funnel to form the pelvic diaphragm [23]. Given that we employ concepts such as pelvic floor spasm, levator spasm, and pelvic floor weakness, understanding the basic concepts of pelvic floor musculature is essential to formulate a clinical opinion. The area posterior to the pubic bone is dense with bands of intertwined levator ani muscles; this defies conventional description of the levator ani as comprising the puborectalis, pubococcygeus, and iliococcygeus. The anatomy of distal subdivisions of the levator ani muscle was further described in a study by Kearney et al. [24]. The origins and insertions of these muscles as well as their characteristic anatomical relations are shown in Table 1.1 and Fig. 1.16. Using a nomenclature based on the attachment points, the lesser known subdivisions of the levator ani muscles, the muscles posterior to the pubic bone are identified as pubovaginalis, puboanalis, and puboperinealis [21]. The pubovaginalis is poorly described but may be analogous to the urethrovaginal ligaments. The puboanalis originates from behind the pubic bone as a thin band and inserts around the anus into the longitudinal ligaments. The puboperinealis, which is most often 0.5 cm in diameter, originates from the pubic bone and inserts into the perineal body. The four major components of the levator ani muscle are the iliococcygeus, which forms a thin, relatively flat, horizontal shelf that spans the potential gap

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(Fig. 1.35a, b). In such cases the ligaments and the endopelvic fascia will assume the majority of the pelvic floor load until they fail as well. Different varieties of levator ani injury EAS-M can cause different interesting types of clinical defects. A partial defect and separation of the levator ani muscles will Rectum result in a displacement cystocele (Fig. 1.36). However, the clinician may not be able to distinguish if this is a displacement cystocele due to paravaginal defect and arcus tendineus separation or due to muscle loss. The consequences of this EAS-W lack of recognition can be that the surgeon may elect to do an anterior repair and, by placating the pubocervical fibromusSQ-EAS cularis, make the lateral defect worse. The lack of basic information about the levator ani status may account for varied results in the anterior repair studies. Additionally, in an b attempted paravaginal repair, the surgeon may realize that (C)Shobeiri there is no muscle to attach the arcus tendineus to. A visual analogy is that of the pubocervical fibromuscularis Vaginal epithelium which is a swinging trapezoid (Fig.  1.37a). The mechanical effect of this detachment allows the trapezoid to rotate downRectovaginal ward. When this happens, the anterior vaginal wall protrudes Septum through the introitus. Upward support of the trapezoid is also (Peach) provided by the cardinal and uterosacral ligaments in Level I. For this reason, resuspension of the vaginal apex at the time Bulbospongiosus of surgery in addition to paravaginal or anterior colporrhaphy (Yellow) helps to return the anterior wall to a more normal position. External anal sphincter (Purple) A partial defect (see Fig. 1.37a) is subjected to excessive forces and may progress over time to involve the apical and Superficial transverse posterior compartments as well (see Fig.  1.37b). How fast perinei (Green) this occurs depends on the strength of the patient’s connective Internal anal sphincter tissue. One woman with injured muscles may have strong (Blue) connective tissue that compensates and never develops proAnal mucosa lapse, while another woman with even less muscle injury but (Brown) weaker connective tissue may develop prolapse with aging. Fig. 1.32 (a) Drawing of external anal sphincter (EAS) subdivisions. There are instances of catastrophic injury during childbirth Anterior portion of model is to the left, posterior to the right. Notice decussation of fibers toward the coccyx posteriorly. The main body of during which complete muscle loss occurs and the patient the EAS also has a concentric portion posteriorly that is not shown in presents with a displacement cystocele, rectocele, and varied this view. Main body of EAS (EAS-M), winged portion of EAS (EAS-­ types of incontinence (Fig.  1.38). This scenario is different W), subcutaneous EAS (SQ-EAS). (b) Drawing of perineal region as with patients who have a defect in pubocervical and rectomay be seen after a clean midline episiotomy. The drawing depicts the vaginal fibromuscularis (Fig.  1.39), which develops into a relationship of muscles to the rectovaginal septum. © Shobeiri 2013 distention cystocele and rectocele over time. A cystocele and rectocele repair that can be used for the latter case will worsen 1.2.7 Endopelvic Fascia and Levator Ani the condition of the first patient with levator damage. a

Interactions

The levator ani muscles and the endopelvic fascia work as a unit to provide pelvic organ support. Under normal conditions, the actions of the levator ani muscles hold the pelvic floor closed and provide a lifting force to prevent pelvic floor descent. If the muscles maintain normal tone, the ligaments of the endopelvic fascia will have little tension on them even with increases in abdominal pressure (Fig. 1.34a–c). If the muscles are damaged by a tear or complete separation from their attachments, the pelvic floor sags downward overtime, and the organs are pushed through the urogenital hiatus

1.2.8 The Levator Plate The levator plate has varied definitions and is viewed differently by different sources. In MRI, Hsu and colleagues’ modeling views it as a flap valve that requires the dorsal traction of the uterosacral ligaments and, to some extent, of the cardinal ligaments, to hold the cervix back in the hollow of the sacrum. The measurement obtained is called the levator plate angle (LPA). It also requires the ventral

1  Pelvic Floor Anatomy

17

a

Vaginal anal

b

PB

EAS-M

Perineal Skin

c EAS-SQ

Anal Canal

Vagina

IAS BS

(C)Shobeiri RVF

Perineum

STP

d

IAS

Anal Canal

Shobeiri©

EAS

Fig. 1.33 (a) Perineal dissection in a cadaveric specimen shows the relationship of the subcutaneous external anal sphincter (EAS-SQ) to the main portion of EAS, the winged portion of EAS, and the superficial transverse perinei (STP). The internal anal sphincter is marked with the dotted line. Anal canal (A), main body of EAS (EAS-M), winged portion of EAS (EAS-W), rectum (R), rectovaginal fascia (RVF), urethra (U), vagina (V). © Shobeiri 2013. (b) Histological slide showing relationship of the subcutaneous external anal sphincter (EAS-SQ) to the main portion of EAS (EAS-M) and the internal anal sphincter (IAS). © Shobeiri 2013. (c) Drawing of the mid left sagittal section as seen in Fig. 1.32a. Bulbospongiosus (BS), external anal sphincter (EAS), internal anal sphincter (IAS), rectovaginal fibromuscularis (RVF), superficial transTable 1.1  Divisions of the levator ani muscles—international standardized terminology Origin/insertion Puboperinealis (PP) Pubis/perineal body Pubovaginalis (PV) Pubis/vaginal wall at the level of the mid-urethra Puboanalis (PA) Pubis/intersphincteric groove between internal and external anal sphincter to end in the anal skin Puborectalis (PR) Pubis/forms sling behind the rectum Iliococcygeus (IC) Tendineus arch of the levator ani/the two sides fuse in the iliococcygeal raphe Pubococcygeus Pubic symphysis to superficial part of (PC) anococcygeal ligament

IRF

EAS-W PR (C)Shobeiri PA

EAS-M

EAS-SQ

LMF V

IAS

verse perinei (STP). © Shobeiri 2013. (d) Histologic slide of the left coronal view of the anal canal showing the relationship of the anal sphincter subdivisions to the puboanalis fibers (PA lined with small arrows pointing downward). The small arrows on the bottom line the course of the longitudinal muscle fibers (LMF), which is an extension of the iliococcygeus fibers that become progressively fibrous until they insert into the anal sphincter complex. The puboanalis and the puboperinealis muscle fibers stabilize the perineum, while the puborectalis (PR) closes the levator hiatus. External anal sphincter-subq (EAS-Q), external anal sphincter-main portion (EAS-M), external anal sphincter-winged portion (EAS-W), internal anal sphincter (IAS), ischiorectal fat (IRF), vagina (V). © Shobeiri 2013

pull of the pubococcygeal portions of the levator ani muscle to swing the levator plate more horizontally to close the urogenital hiatus. From another point of view, the levator plate is the point where the pubococcygeus, iliococcygeus, and the puborectalis come together under the rectum to create the anorectal angle (see Figs. 1.13, 1.17, and 1.18). In e­ ndovaginal ultrasound the movement of the levator plate relative to the transducer can be measured as levator plate descent angle (LPDA) [28]. LPA and LPDA likely measure different functions. LPDA change has been correlated with levator ani deficiency (Fig.  1.40). The location of the levator plate depends on the integrity of the

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a

USL

b ATLA PS

CX

IC

IS PAM RVF V

ATRV

R (C)Shobeiri

c CL ↑Ligament Tension

USL Unbalanced Pressures

Balanced Pressures

Pulls on Uterus

A. Normal

Hiatus Open B. Levator Injury

Fig. 1.34 (a) Right lateral standing anatomic depiction of the levator ani muscle and uterosacral-cardinal complex interaction. © Shobeiri 2013. (b) Drawing of the interaction between the rectovaginal fibromuscularis and the uterosacral ligaments. The levator ani muscle and uterosacral-cardinal complex give cephalad static support, while the iliococcygeus fibers give lateral support to the posterior compartment. The puboanalis and the puboperinealis muscles stabilize the perineum, while the puborectalis closes the levator hiatus. Arcus tendineus levator ani (ATLA), arcus tendineus fascia rectovaginalis (ATRV), cervix (CX), iliococcygeus (IC), ischial spine (IS), puboanalis muscle (PAM), pubic

Pressure Differential C. Exposed Vagina

© DeLancey

Hiatus Closed

symphysis (PS), rectum (R), rectovaginal fibromuscularis (RVF), uterosacral ligament (USL), vagina (V). © Shobeiri 2013. (c) Diagrammatic representation of interactions between levator ani muscle, anterior vaginal prolapse, and cardinal/uterosacral ligament suspension. With normal levator function (A), the vaginal walls are in apposition, and anterior and posterior pressures are balanced. Levator damage (B) results in hiatal opening, and the vagina becomes exposed to a pressure differential between abdominal and atmospheric pressures. This pressure differential (C) creates a traction force on the cardinal ligament (CL) and uterosacral ligament (USL). From © DeLancey [32] with permission

1  Pelvic Floor Anatomy

19

a

a

b

b

a

Fig. 1.36  Room analogy: (a) unilateral levator ani tears may or may not result in prolapse or incontinence initially, but over time the other supportive structures will decompensate resulting in pelvic floor laxity (b). © Shobeiri 2013

levator ani muscles and the integrity of the anococcygeal ligament (Fig. 1.41a, b).

1.2.9 I nteraction Between Different Compartments

b

Fig. 1.35  Room analogy: the clinical presentation of a combined cystocele/rectocele may have varied pathophysiologies. Depicted to the left is a cystocele/rectocele due to pubocervical and rectovaginal fibromuscularis defects. (a) Bilateral levator ani tears may or may not result in prolapse or incontinence initially, but over time the other supportive structures will decompensate resulting in pelvic floor laxity (b). © Shobeiri 2013

Understanding the direction and magnitude of vaginal movement is important to overall quantitative understanding of the prolapse. In a study that developed and tested a method for measuring the relationship between the rise in intra-­ abdominal pressure and sagittal plane movements of the anterior and posterior vaginal walls during Valsalva in a pilot sample of women with and without prolapse, the authors found that movement of the vaginal wall and compliance of its support was quantifiable and was found to vary along the

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a

b

c

d

Fig. 1.37  Conceptual diagram showing the mechanical effect of detachment of the arcus tendineus fascia pelvis from the ischial spine. (a) The trapezoidal plane of the pubocervical fascia. The attachments to the pubis and the ischial spines are intact. (b) The connection to the

spine has been lost, allowing the fascial plane to swing downward. (c) Normal anterior vaginal wall as seen with a weighted speculum in place. (d) The effect of dorsal detachment of the arcus from the ischial spine. © DeLancey 2002

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a

b

Fig. 1.39  Room analogy: multicompartmental defect—pubocervical fibromuscularis and rectovaginal septum defects. © Shobeiri 2013

length of the vagina. Compliance was greatest in the upper vagina of all groups [29]. Women with cystocele demonstrated the most compliant vaginal wall support (Fig. 1.42). The direction of movement differs between rectocele and cystocele. In rectocele, the posterior vaginal wall generally moves in the direction of the vaginal orifice. In cystocele, the upper anterior vaginal wall movement is directed toward the vaginal orifice, and the lower anterior vaginal wall movement is directed toward ventral direction [29].

1.2.10 Nerves There are three main nerves that supply the pelvic floor:

Fig. 1.38  Room analogy: obstetric injuries can be catastrophic or subtle. A complete right unilateral levator ani detachment (avulsion) (a). Injury to the perineal support (the missing green part of the door frame), which may result in sliding of the rectovaginal fascia and a clinical perineocele (b). © Shobeiri 2013

1. The pudendal nerve supplies the urethral and anal sphincters and the perineal muscles. The pudendal nerve originates from S2 to S4 foramina and runs through the Alcock canal, which is caudal to the levator ani muscles. The pudendal nerve has three branches, the clitoral, perineal, and inferior hemorrhoidal, which innervate the clitoris, the perineal musculature, inner perineal skin, and the EAS, respectively [21]. The blockade of the pudendal nerve decreases resting and squeeze pressures in the vagina and rectum, increases the length of the urogenital hiatus, and decreases electromyography activity of the puborectalis muscle [30]. 2. The levator ani nerve innervates the major musculature that supports the pelvic floor. The levator ani nerve originates from S3 to S5 foramina, runs inside of the pelvis on

22 Fig. 1.40 (a) Drawing of the levator plate angle (LPA) measured by magnetic resonance imaging (MRI) vs. the levator plate descent angle (LPDA) obtained by 3D endovaginal ultrasound. The levator plate position relative to the pubic levator plate ultrasound reference assessment line (PLURAL) is shown. A normal LPDA relative to the reference line (PLURAL) is normally 0° to −15°. Bladder (B), levator plate (LP), levator plate angle (LPA) obtained by MRI, levator plate descent angle (LPDA) obtained by 3D endovaginal ultrasound, pubic symphysis (PS), sacrum/ coccyx (S). © Shobeiri 2013. (b) Drawing of the levator plate angle (LPDA) vs. the perineal body descent angle (PBDA) obtained by 3D endovaginal ultrasound. The PBDA is a useful objective measurement of perineal descensus in otherwise normal individuals. External anal sphincter (EAS), perineal body (PB). © Shobeiri 2013

S. A. Shobeiri and J. O. L. DeLancey

a

S

MRI Horizontal Reference line

LPA

B

PS LPDA Pubic Levator Ultrasound Reference Line LP

b

S

MRI Horizontal Reference line

LPA

B

PS

LPDA LP

PBDA EAS PB

a

Fig. 1.41 (a) The mid-sagittal view of the right hemi-pelvis with the red box highlighting the levator plate region. Anus (A), anococcygeal ligament (ACL) bladder (B), external anal sphincter muscle (EAS), internal anal sphincter (IAS), levator plate (LP), pubic symphysis (PS), rectum (R), rectovaginal fibromuscularis (RVS), sacrum/coccyx (S), superficial

Pubic Levator Ultrasound Reference Line Shobeiri©

b

transverse perinei muscle (STP), urethra (U), uterus (UT), vagina (V). © Shobeiri 2013. (b) The mid-sagittal view of the right hemi-pelvis with the red box highlighting the levator plate region zoomed in from Fig 1.39a. Anococcygeal ligament (ACL), pubococcygeus (PC), puborectalis (PR), rectum (R), sacrum/coccyx (S). © Shobeiri 2013

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Movement Angle and Distance Anterior

Posterior 0°

0° 10

J

J

10

Normal Cystocele Rectocele

1

1 -90°

A

A

-90°

Movement Angle 2

3

4

5

6

7

8

9

10 0

-20

-20

Angle of Movement

Angle of Movement

1 0

-40 -60 -80 -100 -120 -140

A

B

C

D

E

F

G

H

I

J

-40 -60 -80 -100 -120

Location

Fig. 1.42  Top Direction and magnitude (mm) of vaginal wall displacement of the anterior and posterior support system. Bottom Angle of displacement (degrees from the horizontal) in normal women, women with

the cranial surface of the levator ani muscle, and provides the innervation to all the subdivisions of the muscle. 3. Motor nerves to the IAS are derived from 1. L5-presacral plexus sympathetic fibers and 2. S2–4 parasympathetic fibers of the pelvic splanchnic nerve. The levator ani muscle often has a dual somatic innervation, with the levator ani nerve (Fig.  1.43) as its constant and main neuronal supply [21, 31].

-140

Location

cystocele, and women with rectocele. From D.M. Spahlinger et al. [29] with permission

ATLA LAN

PB ATFP

V

CG

PP

1.3

Summary

The knowledge of pelvic floor anatomy and function is essential for effective ultrasound imaging of pelvic floor pathologies. With advancing ultrasound technology, new ultrasound techniques have increased our ability to detect pelvic floor defects and have helped us to gain insight into pathophysiology of pelvic floor disorders.

C IC PV

PA PR A

Fig. 1.43  The levator ani nerve in relation to the levator ani muscle complex and pelvic structures. Anal canal (A), arcus tendineus fascia pelvis (ATFP), arcus tendineus levator ani (ATLA), coccyx (C), coccygeus (CG), iliococcygeus (IC), levator ani nerve (LAN), puboanalis (PA), perineal body (PB), puboperinealis (PP), puborectalis (PR), pubovisceralis (PV), vagina (V). © Shobeiri 2013

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References 1. NIH.  State-of-the-science conference statement on prevention of fecal and urinary incontinence in adults. NIH Consens State Sci Statements. 2007;24(1):1–37. 2. Nygaard I, Barber MD, Burgio KL, Kenton K, Meikle S, Schaffer J, et  al. Prevalence of symptomatic pelvic floor disorders in US women. JAMA. 2008;300(11):1311–6. 3. Olsen ALSV, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol. 1997;89(4):501–6. 4. Boyles SH, Weber AM, Meyn L.  Procedures for pelvic organ prolapse in the United States, 1979-1997. Am J Obstet Gynecol. 2003;188(1):108–15. 5. Smith FJ, Holman CD, Moorin RE, Tsokos N.  Lifetime risk of undergoing surgery for pelvic organ prolapse. Obstet Gynecol. 2010;116(5):1096–100. 6. Aigmueller T, Dungl A, Hinterholzer S, Geiss I, Riss P. An estimation of the frequency of surgery for posthysterectomy vault prolapse. Int Urogynecol J. 2010;21(3):299–302. 7. Quiroz LH, Munoz A, Shippey SH, Gutman RE, Handa VL.  Vaginal parity and pelvic organ prolapse. J Reprod Med. 2010;55(3–4):93–8. 8. Ricci JV, Thom CH. The myth of a surgically useful fascia in vaginal plastic reconstructions. Q Rev Surg. 1954;11:253. 9. Gitsch E, Palmrich AH.  Operative anatomie. Berlin: De Gruyter; 1977. 10. Albright T, Gehrich A, Davis G, Sabi F, Buller J.  Arcus tendineus fascia pelvis: a further understanding. Am J Obstet Gynecol. 2005;193(3):677–81. 11. DeLancey JO. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol. 1992;166:1717–28. 12. Campbell RM. The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol. 1950;59(1):1–12. 13. Range RL, Woodburne RT.  The gross and microscopic anat omy of the transverse cervical ligaments. Am J Obstet Gynecol. 1964;90:460. 14. Richardson AC, Edmonds PB, Williams NL.  Treatment of stress urinary incontinence due to paravaginal fascial defect. Obstet Gynecol. 1981;57(3):357–62. 15. DeLancey J.  Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol. 2002;187(1):93–8. 16. Chesson RR, Schlossberg SM, Elkins TE, Menefee S, McCammon K, Franco N, et  al. The use of fascia lata graft for correction of severe or recurrent anterior vaginal wall defects. J Pelvic Surg. 1999;5(2):96–103. 17. Bump RC, Mattiasson A, Bo K, Brubaker LP, DeLancey JO, Klarskov P, et  al. The standardization of terminology of female

S. A. Shobeiri and J. O. L. DeLancey pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol. 1996;175(1):10–7. 18. Oelrich T. The striated urogenital sphincter muscle in the female. Anat Rec. 1983;205:223–32. 19. Luo J, Larson KA, Fenner DE, Ashton-Miller JA, DeLancey JO. Posterior vaginal prolapse shape and position changes at maximal Valsalva seen in 3-D MRI-based models. Int Urogynecol J. 2012;23(9):1301–6. 20. DeLancey JO, Toglia MR, Perucchini D. Internal and external anal sphincter anatomy as it relates to midline obstetric lacerations. Obstet Gynecol. 1997;90:924. 21. Shobeiri SA, Chesson RR, Gasser RF. The internal innervation and morphology of the human female levator ani muscle. Am J Obstet Gynecol. 2008;199(6):686.e1–6. 22. Hsu Y, Fenner DE, Weadock WJ, DeLancey JOL. Magnetic resonance imaging and 3-dimensional analysis of external anal sphincter anatomy. Obstet Gynecol. 2005;106(6):1259–65. 23. Lawson JO.  Pelvic anatomy. I.  Pelvic floor muscles. Ann R Coll Surg Engl. 1974;54:244. 24. Kearney R, Sawhney R, DeLancey JO.  Levator ani muscle anatomy evaluated by origin-insertion pairs. Obstet Gynecol. 2004;104(1):168–73. 25. Margulies RU, Hsu Y, Kearney R, Stein T, Umek WH, DeLancey JOL.  Appearance of the levator ani muscle subdivisions in magnetic resonance images. Obstet Gynecol. 2006;107(5):1064–9. 26. Shobeiri SA, Leclaire E, Nihira MA, Quiroz LH, O’Donoghue D.  Appearance of the levator ani muscle subdivisions in endovaginal three-dimensional ultrasonography. Obstet Gynecol. 2009;114:66–72. 27. Taverner D.  An electromyographic study of the normal function of the external anal sphincter and pelvic diaphragm. Dis Colon Rectum. 1959;2:153. 28. Shobeiri SA, Rostaminia G, White D, Quiroz LH. The determinants of minimal levator hiatus and their relationship to the puborectalis muscle and the levator plate. BJOG. 2013;120(2):205–11. 29. Spahlinger DM, Newcomb L, Ashton-Miller JA, DeLancey JOL, Chen L. Relationship between intra-abdominal pressure and vaginal wall movements during Valsalva in women with and without pelvic organ prolapse: technique development and early observations. Int Urogynecol J. 2014;25(7):873–81. 30. Guaderrama NM, Liu J, Nager CW, Pretorius DH, Sheean G, Kassab G, et al. Evidence for the innervation of pelvic floor muscles by the pudendal nerve. Obstet Gynecol. 2005;106(4):774–81. 31. Wallner C, van Wissen J, Maas CP, Dabhoiwala N, DeRuiter MC, Lamers WH.  The contribution of the levator ani nerve and the pudendal nerve to the innervation of the levator ani muscles; a study in human fetuses. Eur Urol. 2008;54:1136. 32. JOL DL.  Chapter two—pelvic floor anatomy and pathology. In: Hoyte L, Damaser M, editors. Biomechanics of the female pelvic floor. New York: Academic; 2016. p. 13–51.

2

Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues Heinz Koelbl and Ksenia Halpern-Elenskaia

Learning Objectives

• Thus, the goals of this chapter are to (1) discuss the ultrastructural components of the pelvic floor and to review the biochemical processes of pelvic floor remodeling and (2) to discuss the influence of sexual hormones on pelvic floor function and to give the advices for the clinical practice.

2.1

I ntroduction: How Complicated Is That?

Pelvic floor function is very complex and depends on many factors as anatomical modifications and mechanical strength. These depend also on many other factors as injury of the muscles, connective tissue remodeling, and degradation, pelvic enervation, and vascularization. Numerous other predisposing conditions may lead to abnormalities in pelvic floor tissues, including lifestyle factors, such as heavy lifting, smoking, and adverse working environment, and chronic medical conditions, such as obesity, anemia, malnutrition, or pulmonary disease. The impact of gene polymorphisms and genetically predisposed susceptibility on the occurrence of the pelvic floor function has been proven as well. The aim of this chapter is to clarify how all these factors affect the biomechanical properties and hormonal changes of the pelvic floor.

2.1.1 T  he Role of Reproductive Hormones on the Pelvic Floor Function During the Life Span Reproductive hormones, especially estrogen, have a significant impact on the pelvic floor. Due to the natural hypoestrogenic state, some girls before the onset of menarche present various voiding dysfunctions and vaginal problems. Between the age of 9 and 12, estrogen levels rise. Cyclic changes in estrogen and hormonal changes during pregnancy markedly bring into focus what estrogen means to the pelvic floor function [1]. However, pelvic floor is mostly affected in perimenopause and menopause. Menopause, as one example of prolonged duration of estrogen deprivation, leads to well-known consequences such as urogenital atrophy [2]. Women who never leaked urine before may develop urinary leakage. Although the bladder neck and the proximal urethra form the continence mechanism, the folds in the submucosal tissues of the urethra can offer an additional seal affect. If the urethral tissues are thinner and drier from estrogen deficiency, they cannot make as tight a closure to prevent leakage. Sexual intercourse may also become uncomfortable because of thinner and drier vaginal tissues [3]. Nevertheless, the role of menopause on pelvic floor dysfunctions is unclear. Neither menopausal status nor the length of hormone deficiency has been clearly associated with the risk or severity of pelvic floor disorders [4]. As many as 50% of postmenopausal women complain of urogenital symptoms [5].

2.1.2 H  ormonal Changes and Pelvic Floor Symptoms H. Koelbl (*) · K. Halpern-Elenskaia Department of Obstetrics and Gynecology, Medical University Vienna, Vienna, Austria e-mail: [email protected]; ksenia.halpern@ meduniwien.ac.at

Hormonal changes that occur during a woman’s life span impact many aspects of female physiology. The lower urinary and female genital tracts are closely related and both derive embryologically from the urogenital sinus.

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_2

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The mutual embryology of the urethra and vagina (from the urogenital sinus and the Mueller’s ducts), together with the hormone receptors known to be present in the urethra and the bladder neck, explains the hormone-dependent cyclical and trophic changes in the urogenital region that have an onset shortly after. As age has been clearly shown to affect the prevalence and progression of both stress urinary incontinence (SUI) and pelvic organ prolapse (POP) [6], it is intuitive to believe that declining sexual hormone levels may contribute to biochemical changes observed within tissues. A loss of estrogen results in urogenital aging. Dyspareunia, dysuria, urinary frequency and urgency, nocturia, incontinence, and thinning of tissues make it susceptible to trauma, and recurrent infections are all facilitated by estrogen withdrawal. In addition to vulvo-vaginal symptoms, lower acid pH of the estrogen-deficient vagina increases the likelihood of urinary tract infections. It has been noticed that progesterone has adverse effects on the female urinary tract function since it is linked to an increase in the adrenergic tone, provoking a decreased tone in the ureters, urethra, and bladder [7]. This could be the reason why urinary symptoms worsen during the secretory phase of the menstrual cycle, and progesterone may be responsible for the increase in urgency during pregnancy, although the precise mechanism is not fully figured out.

2.2

 he Role of Biochemical Properties T and Hormonal Receptors of Pelvic Floor Tissues in Epidemiology of Pelvic Floor Function

2.2.1 Sexual Hormone Receptors Estrogen receptors (ERs) are a group of proteins found inside cells. They are different from peptide hormones, which tend to be cell surface receptors built into the plasma membrane of cells. However, some ERs associate with the cell surface membrane and can be rapidly activated by exposure of the cells to estrogen. Upon hormone binding, the receptor can initiate multiple signaling pathways which ultimately lead to changes in the behavior of the target cells. ERs are present in the epithelial tissues of the urethra, bladder, and vaginal mucosa and also in diverse structures of the pelvic floor as uterosacral ligaments, levator ani muscles, and pubocervical fascia [8]. ERs are activated by the hormone estrogen (17β-estradiol). Two classes of ERs exist: nuclear estrogen receptors (ERα and ERβ), which are members of the nuclear receptor family of intracellular receptors, and membrane estrogen receptors

(mERs) (GPER (GPR30), ER-X, and Gq-mER), which are mostly G protein-coupled receptors. Once activated by estrogen, the ER is able to translocate into the nucleus and bind to DNA to regulate the activity of different genes. There are two different forms of the estrogen receptor, usually referred to as α and β, each encoded by a separate gene (ESR1 and ESR2, respectively). Hormone-­ activated ERs form dimers, and, since the two forms are coexpressed in many cell types, the receptors may form ERα (αα) or ERβ (ββ) homodimers or ERαβ (αβ) heterodimers. Estrogen is involved in the increase of the cell maturation index of epithelial structures. It has been demonstrated that alterations in the ratio of the estrogen receptor α (ERα) to ERβ may be related to the development of SUI [9]. Progesterone receptors (PR) are also expressed in the lower urinary tract, even if with less density than ER [10].

2.2.2 B  iochemical Properties of Pelvic Floor Tissues The female pelvic floor is an anatomically complex structure made of smooth and skeletal muscles, ligaments, and fascia. Structurally, the female pelvic organs are supported by pelvic floor muscles, cardinal and uterosacral ligaments, and the endopelvic fascia. The ligaments and fascia are primarily composed of extracellular matrix (ECM). The latter is made of a ground substance of proteoglycans and glycoproteins with collagen, along with elastin, which confers the extraordinary compliance and elasticity required for vaginal childbirth. The integrity of the pelvic floor is maintained mostly by fibrillary ECM components, collagen and elastin. It has been well described that women suffering from connective tissue diseases such as Ehlers–Danlos syndrome or Marfan’s disease have a higher risk of POP and SUI, suggesting that connective tissue disorder is an etiological factor [11].

2.2.2.1 Collagen of Pelvic Floor Tissues As mentioned above, collagen is playing a major role in the pelvic floor’s supportive structures. ECM is in constant rearrangement with synthesis and breakdown of collagen through a process of remodeling. There are 28 types of collagen described in the body, but the most abundant in the pelvic floor are types I and III. Type I collagen is considered the strongest, being highly prevalent in fascia, ligaments, and fibrous tissues. Type III, reticulate collagen, is also found in the same tissues but tends to be located on the surface of the fibril. The arrangement of the different types of collagen into fibrils of variable sizes confers strength or laxity depending on the ratio, density, and degree of cross-linking that are

2  Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues

important for the maintenance of the mechanical properties of the extracellular matrix, which is tissue-specific. Several studies have taken a closer look at tissue properties through the use of human pelvic floor biopsies of women with either POP or SUI. Here is the small overview on the distribution of collagen in pelvic floor function and its influence on the pelvic floor disorders. Anterior Vaginal Wall It was found that women with POP have statistically significantly less dense staining of collagen type III than women in the control group after controlling for age, weight, parity, urodynamic stress incontinence, and menopause [12]. Periurethral Tissue Weakened pelvic floor support may result from lower collagen content, but also from alterations within the distribution of collagen fibers. Much more disordered collagen fiber distribution within periurethral specimens of women with SUI compared with unaffected controls were detected [13]. Collagen type III is significantly reduced in patients with SUI and POP.  Some findings are pointing out that women with SUI have less collagen type III around the urethra regardless of the degree of pelvic relaxation. So it appears that collagen has a significant role in the maintenance of urinary continence (Table 2.1) [14, 15]. Cardinal Ligaments In women with POP, loosely arranged connective tissue fibers and less dense ECM as well as smaller collagen fibers were seen under the electron microscope [16]. Uterosacral Ligament Recent research is going even deeper and analyzes the molecular mechanisms of the POP development. One exciting example is the transcriptional regulator genes as homeobox (HOX). HOX genes are involved in embryonic development of the urogenital tract. It could be demonstrated that HOXA11 is essential for organogenesis of the uterosacral ligament. A decreased expression of collagen types I and Table 2.1  Periurethral connective tissue status, Goepel et al. [14] Extracellular matrix proteins Collagen type 1 Collagen type III Collagen type IV Collagen type V Collagen type VI Fibronectin Laminin Vitronectin

Continent women +++ +++ + + +++ + + ++

Incontinent women ++ ++ + + + + + −(+)

−  =  negative; +  =  weak; ++  =  moderate and +++  =  strong immuno-reactivity

27

III in uterosacral ligaments is correlated with a decrease in function of this homeobox gene, HOXA11, involved in the development of the lower uterine segment and cervix and can be also associated with POP [17]. Endopelvic Fascia Diminished collagen levels have been found in multiple pelvic tissues of women with SUI, including the endopelvic fasciae [18]. The Arcus Tendineus Fasciae Pelvis (ATFP) ATFP which provides support to the anterior vagina is comprised primarily of parallel bundles of type III collagen fibers (84%), an intermediate amount of elastin (13%), and very little smooth muscle. It was shown that menopause in the absence of hormone therapy is associated with a decrease in quantity of collagen I in the ATFP, resulting in a decrease in the ratio of collagen I/(III + V). This may compromise the tensile strength and an increase susceptibility to anterior vaginal wall prolapse [19]. Elastin Another important mechanical component of ECM is elastin, which affords resiliency through its ability to recoil, returning the collagen fibers to their original configuration post-loading. The length and amount of elastin could also change the mechanics of the vagina and are associated with changes in the phenotype of smooth muscle, which synthesizes the elastin. For example, elastin fibers are smaller and less expressed in vaginal tissue of women with POP [20]. Tissue strength relies on cross-linkages between elastin and collagen fibers formed by the enzyme lysyl oxidase (LOX). A lower elastin content and decreased mRNA expression of LOX were found in uterosacral ligaments of women with POP compared with normal controls [21]. Elastin is synthesized and broken down in the female genital tract and allows for tremendous accommodation and regeneration after childbirth. A loss of vaginal elastin can result in widening of the vaginal opening, which, in turn, could alter the loading conditions of the attached connective tissues and in turn pelvic organ support.

2.2.3 T  he Role of Matrix Metalloproteinases (MMPs) on Pelvic Floor Tissue Remodeling Since Jackson et al. described the increased MMP activity in women with POP, there has been increasing interest in examining the relationship between collagen degradation and pelvic floor disorders (PFD) [22].

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Collagen breakdown is regulated by matrix metalloproteinases (MMPs). These enzymes are secreted as proenzymes and require activation. There are 23 different types identified as being involved in different tissue types. The interstitial and neutrophil collagenases (MMP-1, MMP-8, MMP-13) cleave fibrillar collagen, while the denatured peptides are degraded by the gelatinases (MMP-2 and MMP-9). These enzymes’ actions are further regulated by tissue-­ derived inhibitors of metalloproteinases (TIMPs) that bind to them and regulate their activity. The recent findings indicate that women who suffer from POP have a higher expression level of MMP-1 than women without POP. Therefore, enhanced activity of MMPs may explain the reason for the reduced collagen content in the pelvic connective tissues, which eventually causes POP. Also a concurrent decrease in the expression of tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) is one of the hypotheses of elevated MMP-1 activity [23]. The role of an overactive degradation mechanism can be an interesting linkage, as helical peptide α1, a collagen breakdown product, is excreted in higher amounts in the urine of women with SUI [24]. Recent studies show consistent results of the impact of higher MMP activity in the development of SUI and POP. The contribution of TIMP to this process remains to be established [25].

2.3

 he Recent Investigations T and Possibilities for Future Research

The extracellular matrix content of the pelvic floor is the major focus of recent investigations and pointed for potential molecular markers of the dysfunction. The identification of women predisposed to develop PFD would help in the patients’ management and care. However, it is important to highlight that the techniques used to measure collagen and elastin content vary between the abovementioned studies. Different structures and biopsy sites of the pelvic floor (vagina wall, arcus tendineus fasciae pelvis, paraurethral tissue, parametrium, and uterosacral ligaments) have been examined, and further studies are needed to understand the real process of pelvic floor remodeling. Future research will deal with the discovery of the genetic contribution to PFD.  Genetic mutations or polymorphisms affect the transcription of mRNA coding for a wide variety of proteins responsible for ECM metabolism. Polymorphisms have been identified in genes of ECM component proteins, proteolytic enzymes, regulatory proteins, and receptors. These mutations may therefore downregulate the synthesis of collagen and elastin or upregulate their breakdown. Single nucleotide polymorphisms (SNPs) are the most abundant type of DNA sequence variation in the human genome and are also in focus of research. A specific haplo-

type for the ER β gene is probably associated with an increased risk of POP [26]. SNPs are present in the progesterone receptor gene that can alter its expression. Similarly, the estrogen receptor β gene also contains multiple SNPs affecting its expression.

2.4

 ormonal Impact on Vaginal Atrophy, H the Role on Pelvic Floor Dysfunction, and Treatment

Synthesis and metabolism of collagen in the genital and urinary tract are under the control of estrogens [27]. It also increases the number of muscle fibers in the detrusor muscle and in the urethral muscles [28]. With an average life expectancy of 75–80 years, women spend about 25–30 years of their life in menopause, i. e., in a state of hormone deficiency. Within the scope of menopause syndrome, signs of degeneration in the urinary and genital organs caused by estrogen deficiency play a significant role [29]. Studies have shown lower serum estradiol (E2) levels in premenopausal women with SUI, with and without concurrent POP [9, 30]. The proof of steroid hormone receptors in the female urethra and the associated ability of tissue containing estrogen receptors to respond to estrogens are the real rationale for providing hormone replacement. In addition to improving the degree of proliferation in the vagina and urethra, the blood flow in the periurethral venous plexus is increased, and the collagen content in the periurethral connective tissue is raised, thus improving elasticity [29]. The intensity of the effect of estrogen replacement on the urethra, for example, depends on the receptor density and the binding affinity of the estrogen to the receptor. Estriol has a lower binding capacity on the estrogen receptor complex and thus a shorter retention time in the cell nucleus. At low doses, estriol only demonstrates the early estrogen effects, e.g., epithelium proliferation in the vagina and urethra, but not the late estrogen effects such as proliferation in the endometrium. Epithelium proliferation leads to a significant improvement of subjective complaints, and presumably to a quantitative decrease in urinary leakage due to a “sealing effect” [31], without any measurable effect on pressure. In order to achieve an influence on the urethral pressure components, a higher estradiol dose or the use of estrogens with greater receptor binding affinity (estradiol, conjugated estrogens), a longer duration of substitution, and possibly even adjuvant therapy measures such as pelvic floor training are probably necessary. The impact of estrogen on tissue may be related to its systemic or local levels, or altered sensitivity from a decreased amount of receptors noted in genitourinary tissues [9, 32]. Sex hormones may exert their effect through pathways other than ECM metabolism. An increase in periurethral

2  Biochemical Properties and Hormonal Receptors of Pelvic Floor Tissues

vasculature in postmenopausal women treated with exogenous estrogens possibly improves the periurethral blood flow, urethral adaptation, and periurethral stability and thereby increases maximum urethral pressure [33]. Recent studies also indicate that a low estradiol level might have a negative impact on the lower urinary tract and continence mechanism and work as a possible risk factor for female SUI [34]. Interestingly, the WHI study reported that hormone therapy (HT) users ran a higher risk of developing SUI and that hormonal supplementation with estrogen alone led to a higher risk for developing UI than an estrogen/progestin combination [35]. The effect of HT on urinary incontinence symptoms is still a matter of debate. Some studies conclude that the route of therapy has different effects, as oral systemic estrogen worsened incontinence, while vaginal estrogen improved incontinence [36]. However, this raises the question why exogenous estrogens seem to be bad and endogenous estrogens seem to be good for lower urinary tract symptoms (LUTS). One possible explanation for the different clinical results could be that the distribution of estrogen receptors in the bladder and pelvic floor changes during the different menopausal stages with different response to exogenous estrogen therapy.

2.4.1 Conclusion: Hormone Therapy By increasing skin collagen content, mucopolysaccharides and hyaluronic acid, estrogen therapy encourages the growth and development of vaginal epithelial cells which make up the thick layers of the vaginal wall and condone a moist, supple, and elastic environment [37]. Therefore, locally administered vaginal estrogens are effective in the treatment of menopause-related vulval and vaginal symptoms, and a Cochrane review reported equal efficiency across all products tested: creams, pessaries, tablets, and vaginal rings.

2.5

Summary and Recommendations for Practice

Both POP and SUI have negative effects on body image, and consequently only 17% of women are completely positive about their sex life [38]. Doubtless intensive research should be continued to improve women’s quality of life. To date, much effort has been directed toward understanding the mechanism of pathogenesis of PFD based on remodeling of ECM and how its turnover is influenced by sexual hormones. Current research supports the hypothesis that the ECM turnover plays an important role in pathophysiology of

29

PFD. Current data also indicates that sex hormones may alter ECM metabolism by having variable interactions with their corresponding receptors. Comprehension of the pathophysiology responsible for PFD is clinically relevant on various levels. First, identifying the patient population at risk can lead to preventive strategies. Second, it may allow the development of interventional therapies that could modify ECM maturation and turnover. Future research will focus on understanding what processes control ECM remodeling and aging to offer each single patient the appropriate therapy. Future studies addressing the genetic basis of pelvic floor dysfunction are required, and investigations of biomechanical properties of pelvic floor support should be performed together with identification of candidate genes for pelvic dysfunctions to determine the relationship between genetics and biomechanics in the pelvic floor.

References 1. Bump RC, Norton PA.  Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clinics North Amer. 1998;4:723–46. 2. Robinson KM, McCance KL, Gray P.  Structure and function of the reproductive systems. In: KL MC, Huether SE, editors. Pathophysiology: the biologic basis for disease in adults and children. 2nd ed. St. Louis: Mosby-Year Book; 1994. p. 711–44. 3. Sherburn M, Guthrie JR, Dudley EC, O’Conell HE, Dennerstein L.  Is incontinence associated with menopause? Obstet Gynecol. 2001;98:628–33. 4. Lawrence JM, Lukacz ES, Nager CW, Hsu JW, Luber KM. Prevalence and co-occurrence of pelvic floor disorders in community-­ dwelling women. Obstet Gynecol. 2008;111(3):678–85. 5. Bruce D, Rymer J.  Symptoms of the menopause. Best Pract Res Clin Obstet Gynaecol. 2009;23(1):25–32. 6. Nygaard I, Barber M, Burgio K, Kenton K, Meikle S, Schaffer J, et  al. Prevalence of symptomatic pelvic floor disorders in US women. JAMA. 2008;300:1311–6. 7. Hextall A, Bidmead J, Cardozo L, Hooper R.  The impact of the menstrual cycle on urinary symptoms and the results of urodynamic investigation. Br J Obstet Gynaecol. 2001;108(11):1193–6. 8. Gebhart JB, Rickard DJ, Barrett TJ, Lesnick TG, Webb MJ, Podratz KC, et al. Expression of estrogen receptor isoforms alpha and beta messenger RNA in vaginal tissue of premenopausal and postmenopausal women. Am J Obstet Gynecol. 2001;185(6):1325–30. discussion 1330–1331 9. Xie Z, Shi H, Zhou C, Dong M, Hong L, Jin H.  Alterations of estrogen receptor-alpha and -beta in the anterior vaginal wall of women with urinary incontinence. Eur J Obstet Gynecol Reprod Biol. 2007;134(2):254–8. 10. Blakeman PJ, Hilton P, Bulmer JN.  Oestrogen and progesterone receptor expression in the female lower urinary tract, with reference to estrogen status. BJU Int. 2000;86(1):32–8. 11. Carley M, Schaffer J. Urinary incontinence and pelvic organ prolapse in women with Marfan or Ehlers Danlos syndrome. Am J Obstet Gynecol. 2000;182:1021–3. 12. Lin S-Y, Tee Y-T, Ng S-C, Chang H, Lin P, Chen G-D.  Changes in the extracellular matrix in the anterior vagina of women with or without prolapse. Int Urogynecol J Pelvic Floor Dysfunct. 2007;18:43–8.

30 13. Trabucco E, Soderberg M, Cobellis L, Torella M, Bystrom B, Ekman-Ordeberg G, et al. Role of proteoglycans in the ­organization of periurethral connective tissue in women with stress urinary incontinence. Maturitas. 2007;58:395–405. 14. Goepel C, Hefler L, Methfessel HD, Koelbl H. Periurethral connective tissue status of postmenopausal women with genital prolapse with and without stress incontinence. Acta Obstet Gynecol Scand. 2003;82(7):659–64. 15. Liapis A, Bakas P, Pafiti A, Frangos-Plemenos M, Arnoyannaki N, Creatsas G.  Changes of collagen type III in female patients with genuine stress incontinence and pelvic floor prolapse. Eur J Obstet Gynecol Reprod Biol. 2001;97(1):76–9. 16. Salman M, Ozyuncu O, Sargon M, Kucukali T, Durukan T. Light and electron microscopic evaluation of cardinal ligaments in women with or without uterine prolapse. Int Urogynecol J Pelvic Floor Dysfunct. 2010;21:235–9. 17. Connell K, Guess M, Chen H, Andikyan V, Bercik R, Taylor H. HOXA11 is critical for development and maintenance of uterosacral ligaments and deficient in pelvic prolapse. J Clin Invest. 2008;118:1050–5. 18. Chen Y, DeSautel M, Anderson A, Badlani G, Kushner L. Collagen synthesis is not altered in women with stress urinary incontinence. Neurourol Urodyn. 2004;23:367–73. 19. Moalli PA, Talarico LC, Sung VW, Klingensmith WL, Shand SH, Meyn LA, et  al. Impact of menopause on collagen subtypes in the arcus tendineous fasciae pelvis. Am J Obstet Gynecol. 2004 Mar;190(3):620–7. 20. Karam J, Vazquez D, Lin V, Zimmern P.  Elastin expression and elastic fiber width in the anterior vaginal wall of postmenopausal women with and without prolapse. BJU Int. 2007;100:346–50. 21. Klutke J, Ji Q, Campeau J, Starcher B, Felix JC, Stanczyk FZ, et al. Decreased endopelvic fascia elastin content in uterine prolapse. Acta Obstet Gynecol Scand. 2008;87:111–5. 22. Jackson S, Avery N, Tarlton J, Eckford S, Abrams P, Bailey A.  Changes in metabolism of collagen in genitourinary prolapse. Lancet. 1996;347:1658–61. 23. Chen B, Wen Y, Wang H, Polan ML.  Differences in estrogen modulation of tissue inhibitor of matrix metalloproteinase-1 and matrix metalloproteinase-1 expression in cultured fibroblasts from continent and incontinent women. Am J Obstet Gynecol. 2003;189:59–65. 24. Kushner L, Mathrubutham M, Burney T, Greenwald R, Badlani G. Excretion of collagen derived peptides is increased in women with stress urinary incontinence. Neurourol Urodyn. 2004;23:198–203. 25. Feng Y, Wang Y, Yan B, Li L, Deng Y.  Matrix metalloproteinase-­1 expression in women with and without pelvic organ pro-

H. Koelbl and K. Halpern-Elenskaia lapse: a systematic review and meta-analysis. Clin Transl Sci. 2016;9(5):267–73. 26. Chen H-Y, Wan L, Chung Y-W, Chen W-C, Tsai F-J, Tsai C-H.  Estrogen receptor beta gene haplotype is associated with pelvic organ prolapse. Eur J Obstet Gynecol Reprod Biol. 2008;138:105–9. 27. Robinson D, Cardozo LD. The role of estrogens in female lower urinary tract dysfunction. Urology. 2003;62(4 Suppl 1):45–51. 28. Aikawa K, Sugino T, Matsumoto S, Chichester P, Whitbeck C, Levin RM. The effect of ovariectomy and estradiol on rabbit bladder smooth muscle contraction and morphology. J Urol. 2003;170(2 Pt 1):634–7. 29. Petri E, Koelbl H. Hormone replacement therapy through the ages: new cognition and therapy concepts. http://www.kup.at/cd-buch/8inhalt.html 30. Lang JH, Zhu L, Sun ZJ, Chen J.  Estrogen levels and estrogen receptors in patients with stress urinary incontinence and pelvic organ prolapse. Int J Gynaecol Obstet. 2003;80:35–9. 31. Chung AK, Peters KM, Diokno AC. Epidemiology of the dysfunctional urinary sphincter. In: Corcos J, Schick E, editors. The urinary sphincter. New York: Marcel Decker; 2001. p. 183–6. 32. Bodner-Adler B, Bodner K, Kimberger O, Halpern K, Koelbl H, Umek W.  Association of endogenous circulating sex steroids and condition-specific quality of life domains in postmenopausal women with pelvic floor disorders. Arch Gynecol Obstet. 2018;297(3):725–30. 33. Klutke J, Bergman A. Hormonal influence on the urinary tract. Urol Clin North Am. 1995;22:629–39. 34. Bodner-Adler B, Bodner K, Kimberger O, Halpern K, Rieken M, Koelbl H, Umek W.  Role of serum steroid hormones in women with stress urinary incontinence: a case-control study. BJU Int. 2017;120(3):416–21. 35. Capobianco G, Wenger JM, Meloni GB, Dessole M, Cherchi PL, Dessole S.  Triple therapy with Lactobacilli acidophili, estriol plus pelvic floor rehabilitation for symptoms of urogenital aging in postmenopausal women. Arch Gynecol Obstet. 2014;289:601–8. 36. Hendrix SL, Cochrane BB, Nygaard IE, Handa VL, Barnabei VM, Iglesia C, et al. Effects of estrogen with and without progestin on urinary incontinence. JAMA. 2005;293:935–48. 37. Lethaby A, Ayeleke RO, Roberts H.  Local estrogen for vaginal atrophy in postmenopausal women. Cochrane Database Syst Rev. 2016;31(8). 38. Roos AM, Thakar R, Sultan AH, Burger CW, Paulus AT.  Pelvic floor dysfunction: women’s sexual concerns unraveled. J Sex Med. 2014;11(3):743–52.

3

The Integral System of Pelvic Floor Function and Dysfunction Peter Petros, Michael Swash, and Darren Gold

Learning Objectives

3.1

• To understand how five main ligaments cause bladder, uterine, and rectal prolapses; how two main ligaments, pubourethral and uterosacral, cause bladder, bowel, and pain symptoms. • To understand the dynamic anatomy of the ligaments, connective tissue structures, and muscles involved in organ support and function. • To apply an anatomically based diagnostic system which accurately diagnoses which ligaments are causing which prolapse and which bladder, bowel, and pain symptoms. • To understand the anatomical pathway to pelvic organ prolapse and bladder, bowel, and pain dysfunctions. • To introduce a squatting-based pelvic floor regime which uniquely strengthen the three involuntary muscle forces which close and open the urethra and anus. • To understand the surgical principles deriving from the Integral System, in particular, conservation of uterus, vaginal elasticity, and the importance of ligament reinforcement.

The Integral Theory states that pelvic organ symptoms and prolapse are both mainly caused by looseness in the vagina and/or its suspensory ligaments, a consequence of altered collagen/elastin [1]. The Theory explains how nerves, ligaments, and muscles work interactively for organ support and function, all, in turn, directed by a binary cortical feedback system (Fig. 3.1). The Integral Theory System (ITS) is a management system, entirely anatomical, based on the Theory [2–5]. Ligament laxity due to collagen defect is the weak point in the system. It is the basis of the ITS diagnostic and management system. The ITS surgical system differs considerably from traditional vaginal surgery methods which either excise the vagina or, more recently, place mesh sheets behind it [6], with very poor results, >80% failure at 6 months [6]. In contrast, the ITS surgical methods are entirely ligament based. The vagina is conserved. No mesh is placed behind the vagina. Using special applicators, strips of tape are applied in the precise position of the damaged ligaments. These create a wound reaction and within 6  weeks, new collagen is created to reinforce the ligament [5].

3.2

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-40862-6_3) contains supplementary material, which is available to authorized users. P. Petros (*) · D. Gold UNSW Professorial Surgical Unit, St Vincent’s Hospital Sydney, Sydney, NSW, Australia e-mail: [email protected]; [email protected] M. Swash The Royal London Hospital, London, UK e-mail: [email protected]

Introduction

 he Integral Theory of Pelvic Floor T Function

In its present form, the Integral Theory states that pelvic organ prolapse (POP), chronic pelvic pain, and bladder and bowel dysfunction are mainly caused by collagen/elastin deterioration in five main suspensory ligaments and their vaginal attachments [6]. The ligaments are listed and shown in Fig.  3.2a, b. The Integral Theory explains cure for POP and bladder and bowel dysfunction via the dual function of the ligaments: i.e., their role in pelvic organ suspension and as insertion points for three oppositely acting muscle forces. Lax ligament insertion points weaken muscle forces so they cannot adequately close the urethral or anal tubes (inconti-

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_3

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central inhibitory or acceleratory instructions SPINAL CORD

efferent afferent

PUL

USL

BLADDER N

CX

N

MUSCLES MUSCLES

ATFP PELVIC RIM

CL

Fig. 3.1  Binary control of bladder and bowel. Schematic 3D sagittal view. The system is in normal closed mode. The pelvic floor works like a trampoline which is suspended by PUL (pubourethral ligaments) anteriorly, ATFP (arcus tendineus fascia pelvis) and CL (cardinal ligaments) laterally, and USL (uterosacral ligaments) posteriorly. The organs are stretched and balanced by three opposite vector forces (arrows), contracting against PUL and USL (uterosacral ligament). Afferent impulses from stretch receptors “N” are reflexly suppressed cortically (white arrow). When required, the cortex activates the defecation and micturition reflexes: the forward muscles relax, pubococ-

cygeus for urethra (broken circle) and puborectalis for anus (not shown); this allows the posterior muscles (posterior arrows) to unrestrictedly open out the posterior wall of anus and urethra (broken lines) just prior to bladder/rectal evacuation by smooth muscle contraction (spasm). If PUL or USL is loose, the muscles contracting against them (arrows) weaken. Urethra/anus cannot be closed (incontinence) and opened (emptying problems); neither can the organs be bidirectionally stretched sufficiently to support “N” and to prevent activation of the evacuation reflexes (“urge incontinence”). CX cervix

nence), evacuate them (constipation, bladder emptying problems), or tension the bladder and rectum sufficiently to prevent inappropriate activation of the micturition and defecation reflexes by peripheral stretch receptors (urinary and fecal urge incontinence). The pelvic muscles are themselves often damaged during childbirth, both by direct injury and by damage to their nerve supply, causing primary weakness of these muscles, in addition to ligamentous stretch injury. Symptoms from the pictorial diagnostic algorithm (Fig. 3.2b) accurately indicate which ligaments are damaged. Due to childbirth and ageing, all five ligaments may be stretched and weakened (Fig. 3.3). Each damaged ligament is linked to a specific prolapse (Fig.  3.2a) and specific symptoms (Fig. 3.2b).

3.3

The Integral System

The Integral System [1, 2] applies the Theory toward a practical, everyday system for management of female pelvic floor disorders. Diagnosis of ligament damage is guided by a validated ligament-specific questionnaire “ITSQ” [7] or other questionnaire capable of detailing the symptoms in Fig. 3.2b. The symptoms are transcribed to the pictorial algorithm shown in Fig. 3.2b. This indicates the sites of ligament damage which should be confirmed by vaginal examination. Surgery shortens and reinforces the damaged ligaments, so that the pelvic floor muscles, even though weakened, can act more efficiently against them. Surgical treatment consists of precise insertion of thin strips of tape along the line in any of the five damaged

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tail bone

a

public bone

tail bone

b

public bone

bladder

bladder

uterus 3

2

1

uterus

4

bowel

4

vagina

bowel

vagina

Anterior ligaments (PUL & EUL)

Middle ligments (ATFP & CL) cystocoele

1

3

2

1

Posterior ligaments (USL & PB) rectocoele

4

uterine/apical prolapse

3

2

stress incontinence

Front ligaments (PUL)

Middle ligments (ATFP & CL)

2

cystocoele

Back ligaments (USL & PB)

4

rectocoele

3 uterine/apical prolapse 1

stress incontinence acnormal emptying

S

frequency and urgency

B

UT

nocturia

PS USL

2 ATFP PUL EUL

CL 3

faecal incontinence

faecal incontinence

1

obstructed defecation

pelvic pain

4 PB

tethered vagina

Fig. 3.2 (a) How birth damage creates ligament damage to cause pelvic organ prolapse (POP). Lower figure—The circles represent damage to six ligaments and vagina by the fetal head as it descends down the vaginal canal. The positions of the ligaments create three natural zones, anterior, middle, and posterior. Upper figure—correlations of damaged ligaments with a specific prolapse. “1”: damaged PUL (pubourethral ligament) causes bladder neck opening and stress incontinence. “2”: damaged CL (cardinal ligament) causes transverse defect; dislocation of vagina from ATFP (arcus tendineus fascia pelvis) causes lateral/central defect. “3”: damaged USL (uterosacral ligaments) uterine prolapse. “4”: damaged PB (perineal body) causes rectocele. The main ligaments are indicated in capital letters, two in each zone: PUL, EUL external

urethal ligament (anterior ligaments); ATFP, CL (middle ligaments); USL, PB perineal body (posterior ligaments). ∗EUL attaches the external meatus to the anterior surface of pubic bone. (b) The pictorial diagnostic algorithm—prolapse and symptoms are related. 3D sagittal view sitting position. The three zones contain two ligaments each, and these may cause specific prolapse or symptoms as indicated. The size of the bar correlates broadly with the site and probability of symptom causation. Labelling as in Fig.  3.2a. Tethered vagina is caused by anterior vaginal scarring in middle zone. The main symptom is unstoppable urine loss on getting out of bed in the morning. B bladder, PS pubic symphysis, S sacrum, UT uterus

ligaments (Fig. 3.4) so as to reinforce them, plus reattachment of stretched or displaced vaginal fascia. Up to 90% cure for POP and up to 80% for pelvic pain and for bladder and bowel dysfunction can be achieved by reconstruction of these five ligaments [8] (Fig. 3.4). Properly taught and administered, this

method has the capacity to reduce care costs due to incontinence, to improve quality of life for older women, and, potentially, to reduce admissions to nursing homes. Data from the Kamakura group in Japan (Table 3.1) and others confirms that the functional disorders that commonly present to each of the

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three relevant surgical specialties (Fig. 3.1) can be improved or cured with hospital stays of 80% failure rate with level 2 vaginal repair at 6 months [7]. Only a tape insertion procedure can create the new collagen needed to strengthen weak ligaments for high POP and symptom cure (Table 3.1).

S USL CX

USL CL

ATFP ATFP

VAG CL

Fig. 3.3  Head stretches ligaments at birth. 3D view from above of inlet. Cervical ring at full dilatation (10 cm). The uterosacral ligaments (USL), cardinal ligaments (CL), and vaginal attachments (VAG) to cervical ring (CX) may be overstretched or torn to cause uterine/apical prolapse, cystocele anteriorly, high rectocele, and enterocele posteriorly. As the head exits the birth canal, the perineal body may be damaged and separated to cause low rectocele (perineocele), descending perineal syndrome, internal and external sphincter damage. ATFP arcus tendineus fascia pelvis, S sacrum

3.4

 art 1: Pubourethral Ligament: How P the Midurethral Sling Was Discovered

The Integral System paradigm had its origins in an endeavor to create a new operation for repair of USI, the midurethral sling (MUS). Development of the MUS procedure began with two unrelated observations in the mid-

Fig. 3.4  The TFS shortens and reinforces all five damaged ligaments. The tape is applied along the length of the ligaments to tension and shorten them: PUL pubourethral, ATFP arcus tendineus fascia pelvis, CL cardinal, USL uterosacral; deep transversus perinei part of PB (perineal body). The tape creates a collagenous reaction which strengthens the damaged ligament. Insert: TFS tool A polypropylene anchor 11 × 4 mm sits on a stainless steel applicator. A lightweight macropore monofilament tape passes through a one-way system at the anchor base which shortens and tensions the damaged ligament

USL

PUL CL

ATFP PB

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Table 3.1  Data from Inoue et al. (mean age 70 years) [8]

Variable Prolapse Urgency Nocturia Day time frequency Dragging pain Fecal incontinence

N 278 133 86 132

Observed No of cure rate cured (%) 257 92.10 124 93.20 62 72.10 120 90.10

95%lower CI 0.891 0.879 0.597 0.935

96%upper CI 0.952 0.971 0.809 0.999

Test results H0: p ≤ p0 vs. H1: p > p0 ∗ ∗ / ∗

56

52

92.90

0.862

0.998

∗

52

46

88.50

0.798

0.977

#

Lower and upper 95% confidence intervals for the observed relative frequencies of prolapse, urgency, nocturia, daytime frequency, dragging pain, and fecal incontinence. Parallelly the results of testing the hypothesis. H0: p  p0 have entered. ∗, #, and / mean significant p values when p0 is setting equal to 0.80, 0.75, and 0.60, respectively. In other words these symbols depict that the observed cure rates are significant (p 90% cure in patients with “double procedure for urinary stress incontinence. Later, in the mid-­ incontinence,” both USI and FI, following a single MUS procedure [23] and Abendstein and Liedl reported cure of FI with posterior sling procedures [24–26]. FI may be caused equally by PUL and USL laxity. This section deals with PUL causation. USL causation is dealt with under the USL section. PUL

EUL

3.4.10 Surgical Repair of PUL by MUS H

Fig. 3.9  Mechanism of leakage with external urethral ligament (EUL) laxity. Suburethral vagina “H” and the forward vector PCM (pubococcygeus muscle, red arrow) constitute the distal closure mechanism. If EUL is loose, the slow-twitch fibers of PCM (arrow) cannot seal the distal urethra; urine may be lost, usually as a seepage

MUS cures USI by insertion of a tape in the position of the middle part of the urethra to shorten and reinforce the damaged PUL (Fig. 3.12). Whatever the type of instrument used to insert the tape, optimal methodology requires prior insertion of an 18-gauge Foley catheter, use of a non-stretch tape which is inserted so as to touch but not indent the urethra, cystoscopic checking for inadvertent bladder perforation,

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a

b

Fig. 3.11 (a) Role of pubourethral ligament (PUL) and uterosacral ligament (USL) in anorectal closure. Resting closed (right figure): slow-twitch muscle fibers “S” close urethral and anal tubes. Active closed (continence) (left figure): fast-twitch fibers exaggerate the actions of “resting closed.” Forward pubococcygeus muscle (PCM) contraction against PUL (forward arrow) stabilizes the anterior rectal wall; backward contraction by levator plate (LP) against PUL (backward arrow) stretches the rectum backward. The longitudinal muscle

ani (LMA) (downward arrow) pulls the anterior margin of down against USL to rotate the rectum (R) around a contracted puborectalis muscle (PRM) (yellow) to “kink” the rectum and close the anorectal angle “Ra.” (b) Anorectal closure (schematic). PRM contracts forward to stabilize the posterior wall of anorectum. LP inserts into the posterior wall of the rectum. LP contracts backward against PUL to stretch the rectum backward. LMA contracts downward to rotate the rectum around PRM to close it. B bladder, CX cervix, PB perineal body, V vagina

and testing either by cough or suprapubic pressure for urine loss during the procedure. To minimize postoperative urinary retention, it is recommended that the surgeon always tighten the tape over a No. 8 Hegar dilator or a No. 18 Foley catheter. If further tightening is required, it should also be done over a Hegar dilator or catheter. EUL/hammock laxity repair (Fig.  3.13) should be carried out at the same time as the midurethral sling repair (Video 4).

3.4.11 Surgical Results for PUL Repair (Midurethral Sling) More than 2000 papers have been published on the standard retropubic and TOT midurethral sling procedures, reporting cure rates for both between 80 and 90%. TFS was the first mini sling for USI, performed in September 2003. A randomized clinical trial by Sivaslioglu et al. [27] gave 5-year

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3.4.12 Zone of Critical Elasticity: Tethered Vagina Syndrome and Role of Fibrosis in Incontinence After Post-obstetric Fistula Repair

cure rates for TFS of 89% against 78% for TOT. Nakamura from the Yokohama Clinic reported a 91% cure rate for ISD (MUP 80% failure rate at 6  months. In contrast, using TFS ligament repair, the Kamakura [8] and Yokohama [31] units reported >90% surgical cure rate for third- and fourth-degree POP at 12  months, with minimal deterioration (79% cured at 60 months) [15] and minimal tape erosions. The Yokohama units reported no tape erosions. It was the view of the Yokohama unit [28, 31] that the lightweight purpose-knitted tape, or prevention of tape slippage by the anchor, and precise mm by mm tensioning of the tape all contributed to their report of no tape rejections.

3.5.1 Role of USL in Micturition The mechanisms for micturition and defecation are similar. With reference to Fig. 3.16, relaxation of the PCM forward vector (insert) allows the posterior vectors LP/LMA to pull open the posterior urethral wall. Opening out the urethral tube as in Fig. 3.16, lower figure, lowers the internal resistance to urine flow inversely by the fourth power of the radius. For example, if the radius is doubled, resistance to flow decreases 16 times (2 × 2 × 2 × 2). If USL is loose, the muscle forces weaken; the urethra cannot be fully opened; and the detrusor has to empty against a narrower tube (Fig. 3.17). The detrusor has to work harder to empty the bladder, and the patient experiences this as “obstructed micturition” (Video 6).

An overtight SCP or rectopexy mesh will counteract the downward vectors; urethra and anus cannot be adequately opened; the patient presents with obstructive defecation or micturition. It has been demonstrated that correction of a lax USL can improve symptoms of “obstructive micturition,” reduce residual urine, and, in some cases, restore normal micturition in women who needed to self-catheterize [32].

3.5.2 Role of USL in Normal Defecation The mechanisms of defecation and micturition are almost identical, except that it is PRM, not PCM which relaxes for defecation. PCM actually contracts to pull forward the anterior anorectal wall during defecation. The pressure of PRM on the posterior rectal wall is released (Fig. 3.18). The posterior vectors LP/LMA pull against USL to stretch open the posterior rectal wall (Fig.  3.18) [33]. This decreases the internal resistance to evacuation inversely by the third power of the anal radius [34]; the rectum contracts to empty. Abendstein cured obstructive defecation syndrome (ODS) and intussusception with a posterior sling which lifted the prolapsed vagina and rectum “like the apex of a tent” [25]. This was validated by pre- and postoperative defecating proctograms. The anatomical rationale was that the USLs not only suspend the uterus; they also attach to the lateral walls of the rectum (Video 7).

bladder

arc PVL

PU

L

E

ZC

PCM

LP LMA

vagina

Fig. 3.16 Micturition. Upper XR. Resting closed Directional slow-­ twitch muscle fibers maintain urethral closure distally and at bladder neck (2). Lower XR. Micturition The forward vector (insert) relaxes. The backward vectors stretch the vagina (V) backward and downward against USL to open out the posterior urethral wall. The pubovesical ligament attach-

ment to the arc of Gilvernert (PVL, insert figure) prevents the anterior bladder wall prolapsing into the outflow tract. B bladder, CX cervix, LMA longitudinal muscle ani, LP levator plate, PCM pubococcygeus muscle, PUL pubourethral ligament, R rectum, S sacrum, U urethra, USL uterosacral ligament, ZCE zone of critical elasticity

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Fig. 3.17  “Obstructive” micturition is consistent with muscle inability to open urethral tube. The electromyography (EMG) in the posterior fornix of vagina shows muscle activity preceding detrusor contraction.

The weak muscles cannot “grip” sufficiently to pull open the urethral tube, and so they have to continually contract to force the urine through an insufficiently opened tube

3.5.3 L  ax USLs: Anatomical Pathways to Pain, Bladder, and Bowel Dysfunction

posteriorly acting muscle forces, LP/LMA, which contract against USLs. A loose USL (Fig. 3.20) will cause weakening of the urethral or anorectal LP/LMA opening forces [32–35]. The bladder detrusor or rectum then contracts against an unopened tube. This is perceived by the patient as “obstructed micturition” or “obstructed defecation,” with symptoms such as “feeling bladder has not emptied, “stopping and starting,” multiple emptying, post-micturition dribble, raised residual urine [32], and, for bowel, constipation or obstructive defecation (ODS) [25]. Shortening and reinforcing CL/USL by a posterior sling restores prolapse and the external opening mechanisms with improvement of “obstructive” symptoms and reduced residual urine volume for bladder [32] and improved bowel emptying [25].

The USLs are the anchoring point for the backward/downward vectors which are critical for control of bladder and bowel function. A fundamental tenet of the Integral System is that even minor laxity in the USL may cause major symptoms of: • • • • •

Micturition difficulty and obstructive defecation “ODS”. Bladder and bowel urgency and frequency. Nocturia. Bladder and bowel incontinence. Chronic pelvic pain.

The reason a minor change in USL length can cause such major symptoms is the exponential nature of the control mechanisms: Poiseuille’s Law governing urine flow (inversely by the fourth power of the radius) and Gordon’s Law which governs muscle contractile strength. A striated muscle contracts efficiently only over a limited length [35] (Fig. 3.19). If the insertion point is loose (Figs. 3.19 and 3.20), the muscle effectively lengthens and loses contractile force. When a muscle is already inherently damaged, for example, by partial denervation, this deleterious effect is magnified.

3.5.4 L  ax USLs: Role in “Obstructive Micturition and Defecation” (Organ Emptying Problems) X-ray video studies presented here demonstrate that both bladder and anorectum are actively opened out by the same

3.5.5 L  ax USL: Pathways from Ligament Laxity to Symptoms of Urge, Frequency, and Nocturia The Integral Theory interprets urgency to micturate or defecate as an inappropriate activation of the micturition or defecation reflexes. One important cause is lax PUL or USL (Fig. 3.21). The directional muscles which contract against PUL or USL will suffer reduced contractile strength. The weakened LP/LMA muscles (Fig. 3.21) cannot stretch the vagina or anorectum sufficiently to support the stretch receptors “N,” so they now fire off at a lower volume to activate the micturition or defecation reflexes. The cortex perceives these impulses as frequency and urgency symptoms and if this happens at night, nocturia (Fig. 3.22).

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a

b

Fig. 3.18  Anorectal opening (defecation) X-ray defecating procto-­ myogram sitting position. (a) At rest The anorectal angle (ARA) to the upper left of the green square is angled. The anus is closed. The superior surface of the levator plate (LP) muscle is almost horizontal. Defecation mode ARA is opened out by backward and downward vectors LP/LMA (arrows). Note the insertion of levator plate into the posterior wall of

Fig. 3.19  Gordon’s Law—A striated muscle contracts efficiently over a limited length. If a ligament which is the insertion point of a muscle lengthens, say by “L,” so does the muscle. Muscle lengthening say by “L” results in a rapid decrease in muscle force, shortening more so

rectum. The conjoint longitudinal muscle of the anus (downward vector, LMA) pulls down the anterior margin of the contracted LP. This is identical with what happens during micturition [21]. (b) The resultant diagonal vector (arrow) opens out the ARA. The anterior wall of anus is pulled forward by pubococcygeus (arrow) further opening out the anal canal [33]. LMA longitudinal muscle ani, PRM puborectalis muscle

3

2

Maximal muscle force [%]

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Shortened muscle

80 60 40 20

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Fig. 3.20 Potential consequences of loose uterosacral ligaments (USL) as interpreted by Gordon’s Law. View from above. The uterus has prolapsed to first degree. The USLs have elongated by “L.” The rectum (R) also has descended, by virtue of its attachments laterally to the elongated USL. The rectum loses tension. LP (levator plate) inserts into the posterior wall of R, so LP also lengthens. LMA (longitudinal muscle ani) now has to pull against a lax LP and USLs. The contractile force and resulting movement of the anorectal angle will be diminished. The large wavy arrows signify diminished contractile strength. ATFP arcus tendineus fascia pelvis, EAS external anal sphincter, PB perineal body, PCM pubococcygeus muscle, PS pubic symphysis, PUL pubourethral ligament, S sacrum

Fig. 3.21  Urge incontinence of urine and feces as interpreted by Gordon’s Law. If the uterosacral ligaments (USL) lengthen by “L,” so do the directional muscles (arrows) (the wavy form and pink color of the arrows denote weakened muscle contractile force) lengthen by “L” and their contractile force weakens. The tissues cannot be stretched sufficiently to maintain a constant supporting tension for the stretch receptors “N.” “N” fire off increased afferent impulses at a low bladder or rectal volume, and this is perceived by the cortex as urgency to evacuate. If the quantum of afferents is sufficient to stimulate the micturition or defecation reflexes, the mechanical dimension of the reflexes is activated: the forward muscles relax; the backward muscles open out urethra or anus; bladder and rectum contract; the patient may uncontrollably lose urine or feces (“urge incontinence”). ATFP arcus tendineus fascia pelvis, CL cardinal ligament, CX cervix, PUL pubourethral ligament

CORTEX

PONS

increased efferent increased afferent PUL BLADDER

USL cx

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N MUSCLES

MUSCLES

ATFP

CL PELVIC RIM

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3  The Integral System of Pelvic Floor Function and Dysfunction

47

PCM

C

LMA

CORTEX N

C 0

USL

G

afferent impulses

PONS

inhibitory centre

LP

Fig. 3.22  Mechanical origin of nocturia—patients asleep. Pelvic muscles (large arrows) are relaxed. As the bladder (broken line outline) fills, it is distended downward by gravity “G.” If the uterosacral ligaments (USL) are weak, the bladder base continues to descend; at a critical point, the cortical closure reflex “C” is overcome; the stretch receptors “N” now activate the micturition reflex “O” which accelerates the pro-

cess of evacuation: the patients is awakened by a feeling of urgency (nocturia); PCM (pubococcygeus muscle) is actively relaxed by the cortex. If the micturition reflex is not adequately controlled, LP/LMA contracts to open the urethra and the detrusor contracts; the patient may lose urine on the way to toilet. LMA longitudinal muscle ani, LP levator plate

3.5.6 L  ax USL: Anatomical Pathway to Chronic Pelvic Pain

anesthetic injection into the cervical part of the USLs [39] as did Petros in three patients with interstitial cystitis, abdominal pain, and suburethral tenderness [41]. Gunnemann reversed anterior rectal wall intussusception with a cylindrical vaginal pessary, inserted under ultrasound control [42].

The role of USLs in producing chronic pelvic pain was described in detail by Heinrich Martius in 1938 [36] but was rediscovered only in 1996 [37]. Chronic pelvic pain is perceived in the visceral nerve distributions T12-L1 and S2–4, causing pain in the lower abdomen, groin, lower sacrum [38], introitus [39], paraurethral tissues [40], the pain of interstitial cystitis [41], and deep dyspareunia [37]. Inability of the weakened pelvic muscles to tension the uterosacral ligaments may cause unsupported nerve plexuses within the USLs to fire (Fig. 3.23). Objective proof of USLs as the pathway to chronic pelvic pain origin was obtained by different types of “simulated operations.” Simulated operations mechanically support pelvic ligaments, while the physician directly observes changes in symptoms. Digital support of PUL can control USI (Video 1). USL support with the lower blade of a speculum or by a tampon can relieve chronic pain and urge symptoms. Speaking clinically, the stretch receptors are very sensitive. Digital or mechanical support of the bladder base stretch receptors N, PUL and USL, will usually relieve urge symptoms in a clinical situation by inhibiting the micturition reflex (Video 8). However, excess pressure may cause urge or even urine loss (Video 9). Wu et al. reported relief of pelvic pain and suburethral tenderness by insertion of the lower part of a bivalve speculum to support the posterior fornix [40]. Bornstein relieved vulvodynia pain by local

3.6

 art 3: Cardinal Ligament (CL): Its P Role in Cystocele Causation

Dislocation of CL and anterior vaginal wall from their attachments to the anterior cervical ring is the principal cause of cystocele (Fig.  3.24). Surgical cure for POP is best performed vaginally, ideally repairing both CL and USL with a tape (Fig. 3.25) [8, 31, 43]. CL/USL reconstruction will also improve urinary hesitancy and residual urine [32]. The cervical TFS tape will reattach the insertion point of ATFP if it is dislocated from the ischial spine (Fig. 3.25) and so reconstitute the depth of the sulcus on that side.

3.7

 art 4: ATFP: Role in Lateral Cystocele P and Urinary Stream Diversion

The role of ATFP (arcus tendineus fascia pelvis) is to support the paracolpium of the vagina in the manner of a sheet strung across two washing lines. Birth-related dislocation of the ATFP is almost invariably at the ischial spine. This is

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we believe maybe dislocation of the “pubovisceral” muscle. “Pubovisceral” muscle dislocations have been “rediscovered” in the past 10  years. “Pubovisceral” combines PCM and PRM. This term is not anatomically accurate. PCM and PRM are entirely separate muscles with different functions. Studies by Dietz et al. showed that women with levator avulsion defects were twice as likely to show pelvic organ prolapse of stage II or higher, mainly due to an increased risk of cystocele and uterine prolapse [44]. There was little correlation with incontinence, urinary or fecal. Scheffler et al. [45] reported a case of diverted urinary stream with response to a TFS “U-sling” operation. This operation attaches a prolapsed distal vagina to the ATFP ligamentous origins behind the symphysis. In the Scheffler case [45], the TFS sling most probably reattached a unilateral PCM dislocation.

3.8

Ganglion Frankenhäuser

L

 art 5: Deep Transversus Perinei P (DTP): Role in Rectocele and Descending Perineal Syndrome

The perineal body is an essential inferior supporting structure for the vagina and anorectum. It is approximately 4 cm in length. It supports 50% of the posterior vaginal wall [46] and a significant part of the anterior wall of rectum. In its distal 2 cm, the PB is densely adherent to vagina and anus. The PB is attached to the descending ramus by deep transversus perinei (DTP) ligaments (Fig. 3.26). At surgical dissection, DTP is distinctively whitish in its macroscopic appearance, and its structure is similar to the other pelvic ligaments, consisting of collagen, elastin, smooth muscle, nerve, and blood vessels. It contains small amounts of striated muscle [47].

3.8.1 A  natomical and Surgical Significance of DTP Ligaments

Fig. 3.23  Pathogenesis of chronic pelvic pain. The Ganglions of the Frankenhauser and the sacral plexuses are supported by uterosacral ligaments (USL) at their uterine end. “L” indicates ligament laxity. The posterior directional forces are weakened and cannot stretch the USLs sufficiently for them to support the nerves. The unsupported nerves may be stimulated by gravity or by the prolapse or by intercourse to fire off and be perceived as pain by the cortex

uniquely corrected by the TFS CL operation [8] (Fig. 3.25). Stretching of the paracolpium attachment to ATFP is considered to be the main cause of the more distally located cystocele (“lateral/central defect”). Another cause of this defect

It is not well known that the key structural components of the perineal bodies are the deep transversus perinei ligaments which attach PB to the skeleton [47]. The deep transversus perinei (DTP) ligament is attached to the posterior surface of the descending ramus, exactly at the junction of the upper 2/3 and lower 1/3. During the second stage of delivery, DTP can elongate to cause low rectocele (“perineocele”) and “descending perineal syndrome” (Figs.  3.26 and 3.27). The perineal body can only be repaired by insertion of a tensioned tape which penetrates the DTP behind the descending ramus to repair and elevate the DTPs (Fig. 3.26) [48]. It is not unusual for one DTP to be destroyed as a result of childbirth.

3  The Integral System of Pelvic Floor Function and Dysfunction

a

49

b

Uterus

r

r PCF

CL vagina

Fig. 3.24  Pathogenesis of “high cystocele” (transverse defect). (a) Dislocation of cardinal ligament (CL) and the pubocervical fascial (PCF) layer of the anterior vaginal wall from their attachments to the

anterior cervical ring allow PCF to rotate down as a cystocele. (b) Appearance on vaginal examination. The prolapsed CL and the overlying vagina (V) are located on the lateral side of the cervix (CX)

b

a

IS

Fig. 3.25 (a) TFS cardinal (CL) and uterosacral (ULS) ligaments repair. Ligaments are shortened and reinforced by a thin tape placed along their length. (b) Posterior IVS with a tape on the anterior cervical ring. IS ischial spine (with permission from [43])

3.8.2 PB Function Is Linked to USL Function The perineal bodies and uterosacral ligaments work as a unit. The extension of rectovaginal fascia (RVF) from PB to cervix (Fig. 3.28) helps anchor the PBs when the backward acting vector (LP) contracts. Tensioning the RVF by LP “smooths out” the rectal mucosa, and this helps to facilitate

rectal evacuation by reducing frictional resistance to fecal flow. Structural damage to PB and its RVF attachment may result in a patient having to splint her perineum to adequately evacuate feces or mitigate anal mucosal prolapse or hemorrhoidal descent during defecation. In a normal patient, slow-­twitch levator plate contractions at rest stretch RVF backward. This helps to prevent mucosal in folding

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OF

OF

Vagina

A

DTP PB

TP 2

PB

DTP

Rectocoele

Fig. 3.26  Surgical cure of descending perineal syndrome. Left figure. Stretched and laterally displaced deep transversus perinei (DTP) ligaments. The attachment to perineal body (PB) is also stretched. This allows protrusion of rectocele into the vagina. Right figure. TP1 is the

TP 1 Tape

downward displaced position of DTP. TP2 shows how a tensioned tape inserted into the body of DTP and tensioned will elevate and restore the position of DTP, also curing descending perineal syndrome. A anal canal, OF obturator foramen

rectum to prolapse downward (Fig. 3.28). This may cause rectal intussusception and symptoms of obstructive defecation. Inability to stretch the loose rectovaginal fascia and the attached distal part of rectum upward may contribute to tissue back pressure. This may cause prolapsed rectal mucosa, hemorrhoids, and, if the backward pressure is sufficient, possibly contribute to formation of a solitary rectal ulcer. DTPs have been erroneously called deep transversus perinei muscles. Histology demonstrates a typical ligament structure: smooth muscle, collagen, elastin, blood vessels, and nerves. Anatomically they are in the same position of “puboperinei muscles.”

Fig. 3.27  Model pathogenesis of deep transverse perinei (DTP) ligaments and their causation of the descending perineal syndrome. The perineal body (PB) is attached behind the upper 2/3 and lower 1/3 of the descending ramus by DTP ligaments. The PBs are connected in the midline by fibromuscular tissue (CT). Childbirth may stretch PB and CT, elongate it, and push DTP laterally. The rectum may protrude as a rectocele (fingers). The angulated and lengthened DTPs are the ultimate cause of “descending perineal syndrome”. CT is known in some parts of Europe as the “central tendon of the perineal body”

and back pressure on the rectal veins which may otherwise manifest as hemorrhoids or anal mucosal prolapse. The deep transversus perinei (DTP) ligaments (Figs.  3.26 and 3.27) attach PB to the descending ramus and thus stabilize it. Loose DTPs may cause the descending perineal syndrome. Damage to USL will cause both the vagina and the

3.8.3 S  urgical Principles Derived from the Integral System The implications of differential strength of ligaments and vagina for pelvic surgery technique are important. Interpretation of the experimental work of Yamada on tissue strength is the key to understanding the ligament-based rules for surgical reconstruction according to the Integral Theory System [1]. Yamada demonstrated that the breaking strain of ligaments was approximately 300  mg/mm2 and that of vagina, 60 mg/mm2 [49]. This means ligaments are primarily structural, but the vagina is not. X-ray video studies during straining and micturition confirmed that ligaments do not stretch significantly during effort or evacuation; only the

3  The Integral System of Pelvic Floor Function and Dysfunction

UT USL CX

P of D

RVF

The Japanese TFS surgeons [8, 31] have found that following these rules greatly diminishes postoperative pain and urinary retention and allows the TFS to be performed as a day procedure under local anesthesia. Once the ligaments have been shortened and reinforced, the directional muscle forces act immediately to restore all the functions dependent on the competent ligaments.

LP

AVF

3.8.4 C  omplications of Total Ligament Repair Surgery Using the TFS Tensioned Mini Sling

R

V

51

Venous return obstructed PB

Fig. 3.28  Structural effect of loose uterosacral ligaments (USL). The rectum is held up by USLs like the apex of a tent. Loose USLs may cause rectal prolapse and anterior rectal wall intussusception (“R,” downward arrows). The prolapsed rectal mucosa may cause back pressure in the rectal veins to cause hemorrhoids. CX cervix, LP levator plate, PB perineal body, R rectum, RVF rectovaginal fascia, UT uterus, V vagina

vagina stretched, very significantly. It follows that any reconstructive surgery has to reinforce the structural part of the ligaments, which consist mostly of Type 1 collagen and elastic tissue. Only an implanted tape can do this [9]. The vagina is an elastic organ which plays an important role in transmitting the vector forces to close and open the bladder [2]. Because healing is by scarring and not regeneration, elasticity cannot be surgically reproduced in the vagina. Therefore the vagina must be conserved. Excision of vagina reduces the quantum of elastin and Type 3 collagen available for proper function. Finally, the uterus is the direct or indirect insertion point for all the ligaments. Mesh sheets create dense collagen which may shrink to cause pain and the Tethered Vagina Syndrome. Hysterectomy should therefore be avoided where possible. As well as dividing the cardinal and uterosacral ligaments, hysterectomy severs the descending uterine artery, which is the main blood supply of the proximal ends of the cardinal and uterosacral ligaments. This may cause ligament atrophy even with cervical preservation. Three rules of surgery evolve from this discussion: 1. A loose ligament must be shortened and reinforced with thin strips of tensioned tape to create a collagenous neoligament [9]. This was the surgical principle applied in the original midurethral sling procedure. 2. The vagina must be conserved, not excised. 3. The uterus must not be removed without good cause.

The minimal nature of the TFS tensioned mini sling and its universal applicability allow surgeons to repair even all five ligaments at the same time. This method was followed by the Kamakura and Yokohama units in Japan. Approximately 3600 TFS tapes were inserted into 1495 Japanese patients between 2007 and 2016 by two units, Kamakura [8] and Yokohama [31]. Almost all patients were discharged within 24  h. This indicates, in general, that short-term complications were minimal. However, from a total of 700 patients, the Kamakura unit had three cases of ileus which presented some months after the initial surgery and required surgical intervention. The cause was attributed to inadvertent intraperitoneal placement of the tape. In these 700 patients, 6 reported postoperative pain after a 4-ligament TFS repair (ATFP, cardinal, uterosacral, perineal body ligaments). All pain settled by 6 weeks except for a patient with hip pain, which settled by 24 months (Inoue personal communication). In 989 TFS tape implants for PB, ATFP, CL, and USL, the Kamakura unit reported a 1.1% erosion rate for TFS repair PUL, USL, ATFP, and CL ligaments [8]. However, initial tape erosion rate for PB TFS was 25%; wrong placement of the TFS was identified as the cause. Following modification of the insertion technique, the erosion rate fell to 2.5%. The Kamakura unit’s experience with TFS PB repair emphasized that the TFS ligament repair method is technique and operator dependent. In 60 POP patients [31], the Yokohama unit reported one case of hemorrhage requiring hospitalization for several days, but no transfusion. There was one case of urinary retention which settled by 2 weeks, two cervical protrusions requiring cervical amputation. There were no erosions; five patients had postoperative pain which settled by 3 months. In 100 USI cases [28], Nakamura et  al. reported no erosions, 1 bladder perforation (recognized at the time of implant), 6 cases with de novo urgency, and 2 with postoperative pain; 1 settled in 2 weeks and 1 in 3 months.

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3.8.5 Role of Muscle in Continence Control

3.8.6 Muscle, Ligament, or Both? The question is “at what point of damage does this happen?” Results from a blinded experiment carried out by PP and MS in 47 women with a mean age of 47 years (range 18–78) emphasized the importance of ligaments. A group of 47 women had muscle biopsies of the PCM at the same time as a midurethral sling. Almost all biopsies showed evidence of severe muscle damage; 89% were cured the next day after a midurethral sling (MUS) [57]. It was concluded that correction of ligamentous laxity can cure incontinence, even when there is muscle weakness. Clearly more research is needed to more fully evaluate the role of damaged muscles in those patients who were not cured by ligament repair.

3.8.7 T  he Three-Muscle, 3-Month Pelvic Floor Muscle Strengthening Study Further insights into this question may be deduced from Patricia Skilling’s squatting-based pelvic floor study. This

SCP MESH

tail bone

x

bo we l

USL

rvi

ce

SSL

sto

ce

le

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pubic bone

urethra cy

It is evident that firm ligaments are required to enable the directional forces which open and close the urethra and anal tubes. Earlier work on pelvic floor function in post-delivery and prospective studies [50–56], led by Swash at St. Mark’s Hospital, delineated direct muscle during delivery and coincidental damage to the innervation of the pelvic floor musculature as being associated with incontinence. The latter was consequent to nerve stretch damage and was shown to be progressive in association with ageing and especially with perineal descent, itself a marker for ligamentous damage, although the latter was not fully recognized at that time. These findings gave rise to a Unifying Theory by Swash et al. [51]. The Unifying Theory postulated that bladder and bowel symptoms were caused by neurological and muscle damage occasioned at childbirth. The Integral System is complementary to these findings and expands our understanding. It emphasizes the role of ligaments, which act as force transducers of muscle contraction. The latter occur in carefully modulated sequence in the various pelvic floor functions of continence and evacuation of bladder and bowel. There are critical roles for muscles pulling against competent ligaments for all pelvic floor functions. It follows that at some point a damaged muscle must affect bladder and bowel functions. The Swash theory taken together with the Integral System therefore provides a cogent explanation for the range of failed symptoms following successful ligament surgery for prolapse.

r

e

el

oc

t ec

Fig. 3.29  The anatomy of sacrocolpopexy (SCP) or rectopexy mesh. Schematic sagittal view. Patient standing. SCP mesh is attached to the sacral promontory. Uterosacral ligaments (USL) are attached at S3-4. SSL sacrospinous ligament

3-month regime showed very significant improvement in all pelvic floor symptoms [58, 59], although mainly in younger women. This regime was oriented mainly toward strengthening the three-directional muscle forces which close the urethra. The regime was home-based. It ran over 3 months with only four visits. It included electrical stimulation in the posterior vaginal fornix using a 50 Hz cylindrical probe. Of 147 patients (mean age 52.5 years), 53% completed the program. Median QoL improvement reported was 66%, mean cough stress test urine loss reduced from 2.2 g to 0.2 g; 24-h pad loss reduced from a mean of 3.7 g to a mean of 0.76 g frequency; nocturia and pelvic pain were significantly improved. Residual urine reduced from mean 202  ml to mean 71 ml. Approximately 3% of patients reported worsening of their stress incontinence, and these were referred for surgery [58].

3.8.8 I s Rectopexy or Sacrocolpopexy (SCP) an Anatomically Correct Method for Restoration of Rectal Intussusception and Rectal Prolapse? Using pre- and postoperative X-ray proctography, Abendstein demonstrated high rates of cure for rectal intussusception with a posterior sling which was inserted

3  The Integral System of Pelvic Floor Function and Dysfunction

in the position of the uterosacral ligaments [25]. Abendstein’s study confirmed the Integral Theory’s prediction that rectal intussusception in women was mainly caused by USL prolapse. Because USL is attached to the lateral walls of the rectum, the rectal wall would also prolapse (Fig.  3.28). Figure  3.29 demonstrates that a mesh used for rectopexy or sacrocolpopexy is far more vertical than the natural attachments of rectum to USL. It follows that if the mesh is too tight, it may impede the downward acting LMA opening vector for urethra and anorectum to cause obstructive evacuation symptoms. Alternatively, if it is too loose, it may not fully restore the intussusception and mucosal prolapse.

3.9

Conclusion

These and other data presented in the main body of this chapter are consistent with both the Unifying and Integral Theories. The Skilling study confirmed that pelvic floor muscles play an important role in all the mechanisms outlined in this chapter. Why the exercises do not work so well in older women may have several explanations, in particular, postmenopausal collagen loss and more marked muscle weakness. However, the high cure rates attained by TFS CL/ USL tapes in 70-year-old women plus the muscle biopsy data tend to indicate that muscle function, though critically important, is ultimately reliant on a firm ligamentous insertion point.

Take-Home Messages

1. Ligaments suspend organs. Collagen is their main structural component. Collagen weakens at childbirth, menopause to cause prolapse, symptoms. Vagina needs elasticity to function. 2. Opening/closure on anus/urethra is exponentially controlled. Accurate restoration of tension in PUL and USL is mandatory to achieve reliable symptom cure. 3. Longer-term surgical cure for POP/symptoms is not possible if ligaments are weak. Collagenous neoligaments (MUS, posterior sling, SCP) can only be created using mesh tapes.

References 1. Petros PE.  DSc thesis University of Western Australia 2012. The Integral Theory System. A management system based on the Integral Theory: a universal theory of pelvic floor function and dysfunction in the female.

53 2. Petros PE, Ulmsten U. An Integral Theory of female urinary incontinence. Acta Obst Gynecol Scand. 1990;69(Suppl. 153):1–79. 3. Holm-Larsen T.  The economic impact of nocturia. Neurourol Urodyn. 2014;33:S10–4. 4. Abrams P, Andersson KE, Birder L, 4th International Consultation on Incontinence Recommendations of the International Scientific Committee. 4th International Consultation on Incontinence Recommendations of the International Scientific Committee. Evaluation and treatment of urinary incontinence, pelvic organ prolapse and faecal incontinence. Neurourol Urodyn. 2010;29(1):1767–820. 5. Cathryn MA Breeman S, Elders A, et al. (for the PROSPECT study group). Mesh, graft, or standard repair for women having primary transvaginal anterior or posterior compartment prolapse surgery: two parallel-group, multicentre, randomised, controlled trials (PROSPECT). Lancet 2017;389(10067):381–392. 6. Liedla B, Inoue H, Sekiguchic Y, Gold D, Wagenlehner F, Haverfieldf M, Petros P. Update of the integral theory and system for management of pelvic floor dysfunction in females. Eur J Urol. 2018;17(3):100–8. 7. Wagenlehner FM, Frohlich O, Bschleipfer T, Weidner W, Perletti G.  The integral theory system questionnaire: an anatomically directed questionnaire to determine pelvic floor dysfunctions in women. World J Urol. 2014;32:769. 8. Inoue H, Kohata Y, Sekiguchi Y, Kusaka T, Fukuda T, Monnma M.  The TFS minisling restores major pelvic organ prolapse and symptoms in aged Japanese women by repairing damaged suspensory ligaments—12-48 month data. Pelviperineology. 2015;34:79–83. 9. Petros PE, Ulmsten U, Papadimitriou J.  The autogenic neoligament procedure: a technique for planned formation of an artificial neo-­ ligament. Acta Obstet Gynecol Scand Suppl. 1990;69(153):43–51. 10. Petros PE, Ulmsten U. The combined intravaginal sling and tuck operation. An ambulatory procedure for stress and urge incontinence. Acta Obstet Gynecol Scand Suppl. 1990;153:53–9. 11. Ulmsten U, Petros P. Intravaginal slingplasty (IVS): an ambulatory surgical procedure for treatment of female urinary incontinence. Scand J Urol Nephrol. 1995;1:75–82. 12. Ulmsten U, Henriksson L, Johnson P, Varhos G.  An ambulatory surgical procedure under local anesthesia for treatment of female urinary incontinence. Int Urogynecol J. 1996;7:81–6. 13. Petros PE.  New ambulatory surgical methods using an anatomical classification of urinary dysfunction improve stress, urge, and abnormal emptying. Int J Urogynecol. 1997;8(5):270–8. 14. Liedl B, Inoue H, Sekiguchi Y, et  al. Is overactive bladder in the female surgically curable by ligament repair? Cent Eur J Urol. 2017;70:51–7. 15. Inoue H, Kohata Y, Fukuda T, Monma M, et  al. Repair of damaged ligaments with tissue fixation system minisling is sufficient to cure major prolapse in all three compartments: 5-year data. J Obstet Gynaecol Res. 2017;43(10):1570–7. 16. Enhorning G. Simultaneous recording of intravesical and intraurethral pressure. Acta Chir Scandinavica. 1961;27(276):61–8. 17. Constantinou CE, Govan DE.  Contribution and timing of transmitted and generated pressure components in female urethra. In: Zimmer NR, Sterling AM, editors. Progression in clinical and biological research, vol. 78. New York: Alan R. Liss; 1981. p. 113–20. 18. Petros PE, Ulmsten U.  Role of the pelvic floor in bladder neck opening and closure: I muscle forces. Int J Urogynecol Pelvic Floor. 1997;8:74–80. 19. Petros PE, Ulmsten U.  Role of the pelvic floor in bladder neck opening and closure: II vagina. Int J Urogynecol Pelvic Floor. 1997;8:69–73.

54 20. Courtney H. Anatomy of the pelvic diaphragm and anorectal musculature as related to sphincter preservation in anorectal surgery. Am J Surg. 1950;79:155–73. 21. Petros PE, Von Konsky B. Anchoring the midurethra restores bladder neck anatomy and continence. Lancet. 1999;354:997–8. 22. Petros PE. Cure of urinary and fecal incontinence by pelvic ligament reconstruction suggests a connective tissue etiology for both. Int J Urogynecol. 1999;10:356. 23. Petros PE, Swash MA.  Musculoelastic theory of anorec tal function and dysfunction in the female. J Pelviperineol. 2008;27:89–121. 24. Hocking IJ.  Double incontinence, stress urinary and faecal, cured by surgical reinforcement of the pubourethral ligaments. J Pelviperineol. 2008;27:110. 25. Abendstein B, Petros PE, Richardson PA. Ligamentous repair using the Tissue Fixation System confirms a causal link between damaged suspensory ligaments and urinary and fecal incontinence. J Pelviperineol. 2008;27:114–7. 26. Abendstein B, Brugger BA, Furtschegger A, Rieger M, Petros PE.  Role of the uterosacral ligaments in the causation of rectal intussusception, abnormal bowel emptying, and fecal incontinence—a prospective study. J Pelviperineol. 2008;27:118–21. 27. Sivaslioglu AA, Eylem U, Serpi A, et al. A prospective randomized controlled trial of the transobturator tape and tissue fixation minisling in patients with stress urinary incontinence: 5-year results. J Urol. 2012;188:194–9. 28. Nakamura R, Yao M, Maeda Y, Fujisaki A, Sekiguchi Y. Retropubic tissue fixation system tensioned mini-sling carried out under local anesthesia cures stress urinary incontinence and intrinsic sphincter deficiency: 1-year data. Int J Urol. 2017;24(7):532–7. 29. Petros PE, Ulmsten U.  The free graft procedure for cure of the tethered vagina syndrome. Scand J Urol Nephr. 1993;27(Suppl 153):85–7. 30. Browning A, Williams G, Petros P.  Skin flap vaginal augmentation helps prevent and cure post obstetric fistula repair urine leakage: a critical anatomical analysis. Br J Obstet Gynaecol. 2017;125(6):745–9. 31. Sekiguchi Y, Kinjo M, Maeda Y, Kubota Y. Reinforcement of suspensory ligaments under local anesthesia cures pelvic organ prolapse: 12-month results. Int Urogynecol J. 2014;25(6):783–9. 32. Petros P, Lynch W, Bush M.  Surgical repair of uterosacral/cardinal ligaments in the older female using the tissue Fixation system improves symptoms of obstructed micturition and residual urine. Pelviperineology. 2015;34:112–6. 33. Petros P, Swash M, Bush M, Fernandez M, Gunnemann A, Zimmer M.  Defecation 1: testing a hypothesis for pelvic striated muscle action to open the anorectum. Tech Coloproctol. 2012;16(6):437–43. 34. Bush M, Petros P, Swash M, Fernandez M, Gunnemann A. Defecation 2: internal anorectal resistance is a critical factor in defecatory disorders. Tech Coloproctol. 2012;16(6):445–50. 35. Gordon AM, Huxley AF, Julian FJ. The variation in isometric tension with sarcomere length in vertebrate muscle fibres. J Physiol. 1966;184(1):170–92. 36. Weintraub A, Petros P.  Editorial dedicated to Professor Heinrich Martius, pioneer in the ligamentous origin of chronic pelvic pain in the female. Pelviperineology. 2017;36:66. 37. Petros PE.  Severe chronic pelvic pain in women may be caused by ligamentous laxity in the posterior fornix of the vagina. Pelviperineology. 2017;36:71–3.

P. Petros et al. 38. Sekiguchi Y, Inoue H, Liedl B, Haverfield M, Richardson P, Yassouridis A, Pinango-Luna S, Wagenlehner F, Gold D. Is Chronic Pelvic Pain in the female surgically curable by uterosacral/cardinal ligament repair? Pelviperineology. 2017;36:74–8. 39. Zarfati D, Petros PE. The Bornstein Test—a local anaesthetic technique for testing uterosacral nerve plexus origins of chronic pelvic pain. Pelviperineology. 2017;36:89–91. 40. Wu Q, Luo L, Petros PE. Case report: mechanical support of the posterior fornix relieved urgency and suburethral tenderness. Pelviperineology. 2013;32:55–6. 41. Petros PE.  Interstitial cystitis (painful bladder syndrome) may, in some cases, be a referred pain from the uterosacral ligaments. Pelviperineology. 2010;29:56–9. 42. Gunnemann A, Petros PE.  The role of vaginal apical support in the genesis of anterior rectal wall prolapse. Tech Coloproctol. 2014;18(5):517–8. 43. Shkarupa D, Kubin N, Pisarev A, Zaytseva A, Shapovalova E.  The hybrid technique of pelvic organ prolapse treatment: apical sling and subfascial colporrhaphy. Int Urogynecol J. 2017;28(9):1407–13. 44. Dietz H, Simpson J. Levator trauma is associated with pelvic organ prolapse. Br J Obstet Gynaecol. 2008;115:979–84. 45. Scheffler KU, Petros PE, Oliver W, Hakenberg OW. A hypothesis for urinary stream divergence in the female: unilateral dislocation of the pubovisceral muscle. Pelviperineology. 2014;33:10–3. 46. Abendstein B, Petros PE, Richardson PA, Goeschen K, Dodero D. The surgical anatomy of rectocele and anterior rectal wall intussusception. Int Urogynecol J. 2008;19(5):513–7. 47. Wagenlehner FM, Del Amo E, Santoro GA, Petros P.  Live anatomy of the perineal body in patients with third-degree rectocele. Colorectal Dis. 2013;15:1416–22. 48. Wagenlehner FM, Del Amo E, Santoro GA, Petros P.  Perineal body repair in patients with third degree rectocele: a critical analysis of the tissue fixation system. Colorectal Dis. 2013;15:e760–5. 49. Yamada H. Aging rate for the strength of human organs and tissues. In: Evans FG, editor. Strength of biological materials. Baltimore: Williams & Wilkins Co; 1970. p. 272–80. 50. Swash M, Henry MM, Snooks SJ.  A unifying concept of pelvic floor disorders and incontinence. J Royal Soc Med. 1985;78:906–8. 51. Snooks SJ, Swash M. Abnormalities in the innervation of the urethral striated sphincter musculature in incontinence. Br J Urol. 1984;56:401–5. 52. Snooks SJ, Badenoch D, Tiptaft R, Swash M. Perineal nerve damage in genuine stress urinary incontinence: an electrophysiological study. Br J Urol. 1985;57:422–6. 53. Snooks SJ, Barnes RPH, Swash M.  Damage to the voluntary anal and urinary sphincter musculature in incontinence. J Neurol Neurosurg Psychiatry. 1984;47:1269–73. 54. Beersieck F, Parks AG, Swash M. Pathogenesis of idiopathic ano-­ rectal incontinence; a histometric study of the anal sphincter musculature. J Neurol Sci. 1979;42:111–27. 55. Snooks SJ, Henry MM, Swash M. Faecal incontinence due to external anal sphincter division in childbirth is associated with damage to the innervation of the pelvic floor musculature: a double pathology. Br J Obstet Gynaecol. 1985;92:824–8. 56. Snooks SJ, Swash M, Henry MM, Setchell M. Risk factors in childbirth causing damage to the pelvic floor innervation. Br J Surg. 1985;72(Suppl):S15–7.

3  The Integral System of Pelvic Floor Function and Dysfunction 57. Petros PE, Swash M, Kakulas B. Stress urinary incontinence results from muscle weakness and ligamentous laxity in the pelvic floor. J Pelviperineol. 2008;27:107–9. 58. Skilling PM, Petros PE.  Synergistic non-surgical management of pelvic floor dysfunction: second report. Int Urogynecol J. 2004;15:106–10.

55 59. Petros PE, Skilling PM. Pelvic floor rehabilitation according to the Integral Theory of Female Urinary Incontinence—first report. Eur J Obstet Gynecol. 2001;94:264–9.

4

The Pelvic Floor: Neurocontrol and Functional Concepts Michael Swash and Peter Petros

Learning Objectives

• The pelvic floor is a musculo-elastic structure that, in women, includes the vagina as a central elastic structure. • Impaired pelvic floor elasticity prevents normal muscle anchoring, causing muscle weakness and functional disorder, such as pain, urgency, and incontinence of urine or faeces. • The motor and sensory innervation of the pelvic floor is critically important for continence and evacuation, through its connexions to spinal cord and brainstem neural control systems. • In healthy adults higher-level control systems override these reflex systems to establish voluntary evacuation. • Pelvic floor dysfunction in women is often initiated by obstetric damage to the pelvic floor muscles and ligaments. In extreme cases, direct anal sphincter tears are a marker of pelvic floor damage. When the pelvic floor is incompetent, its motor and sensory innervation is often progressively damaged by recurrent stretching during straining at stool. • Pelvic floor repair procedures should be designed to improve functional ligamentous elasticity: this can be effective even when there is established muscle and nerve damage.

Electronic Supplementary Material The online version of this chapter (https://doi.org/10.1007/978-3-030-40862-6_4) contains supplementary material, which is available to authorized users. M. Swash Department of Neurology and Neuroscience, Royal London Hospital and Barts and the London School of Medicine, QMUL, London, UK e-mail: [email protected] P. Petros (*) UNSW Professorial Surgical Unit, St Vincent’s Hospital Sydney, Sydney, NSW, Australia e-mail: [email protected]

4.1

Introduction

The pelvic floor is a holistic functional entity, concerned with urinary and faecal continence and voiding, and sexual function. In women there are specialised features allowing childbirth, always a natural process but nonetheless a function that is associated with risk for damage to both the anterior and posterior components of the pelvic floor [1–4], including its nerve supply [5]. Sometimes childbirth leads to urinary or faecal incontinence and organ prolapse as delayed, chronic problems [6]. In everyday life urinary and faecal storage (continence) and voiding (micturition and defaecation) are under voluntary control, although subject to stimulus in relation to sensory input to the central nervous system. The central nervous system (CNS) control systems for these functions mature during childhood in relation to the imposed norms of society that require voiding at appropriate times and places [7]. It is therefore necessary for the bladder and rectum to act as storage receptacles until voiding is appropriate and possible. Consequently, for most of the time, the pelvic floor maintains bladder and bowel in a continent, storage mode [7]. As in most neurocontrol systems, there are several levels of control circuits, following a Jacksonian system of progressively higher levels of awareness and control. All of these levels in the control system are modulated by sensory afferent and descending motor neural command systems [8]. The systems controlling bowel and bladder are analogous to each other although separately ‘wired’.

4.2

The Urinary and Recto-Anal Systems

The bladder wall consists of smooth muscle innervated by parasympathetic motor nerve fibres. This parasympathetic innervation of the detrusor muscle is cholinergic, dependent on muscarinic motor endings on smooth muscle fibres [9]. These parasympathetic nerve fibres are postganglionic, derived from pelvic parasympathetic ganglia that are themselves innervated by preganglionic fibres originating

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in the intermediolateral columns of the lumbosacral cord. Muscle fibres in the bladder base and in the internal urethral sphincter are innervated by sympathetic nerve fibres, also originating in the intermediolateral cell columns of the spinal cord, but using norepinephrine as transmitter [6]. Relaxation of the internal urethral sphincter is dependent, in part, on sympathetic innervation of the muscle, utilising beta-adrenergic parasympathetic efferents that release nitric oxide as transmitter. Although it is widely believed that urinary continence is achieved by low resting tone in the bladder detrusor muscle, and tonic contraction of the internal urethral sphincter, this concept is an oversimplification. Circumferential contraction around a narrow tube, such as the urethra, is not, in general, an effective sphincteric mechanism. A more effective mechanism utilises kinking of the urethra, due to a backward muscular vector pulling the urethra posteriorly and causing a kink, thus obstructing any urine flow. This is achieved by contraction of the posterior muscle vectors in a backward/ downward direction, i.e. by the levator plate and the conjoint longitudinal muscle of the anus (Fig. 4.1), a muscle grouping that has been shown to be in a state of continuous mild tonic contractile activity in the default storage mode [10]. The pubococcygeus muscle provides an opposing force, centered on the urethra. Mild resting contraction of the puborectalis muscle is a major factor in the mainteFig. 4.1  Central and peripheral control of bladder and bowel. Schematic 3D sagittal view. System in default storage mode. Three directional muscle forces PCM (pubococcygeus), LP (levator plate), and conjoint longitudinal muscle of the anus (LMA) tense the organs bidirectionally against the suspensory ligaments PUL (pubourethral), CL (cardinal), and USL (uterosacral) to prevent activation of micturition and defaecation responses. Green arrows, neurological pathways; white arrow, central cortical control via the closure reflex. ATFP arcus tendineus fascia pelvis, CX cervix. N, sensory receptors in bladder trigone

nance of faecal continence, generating tension and kinking of the recto-anal junction by opposing muscle forces [11]. In addition to sympathetic motor innervation of the base of the bladder and internal urinary sphincter muscle, there is an extensive sensory innervation of the bladder wall and mucosa [6]. This consists of mechanoreceptors, sensitive to stretch and distension, and other receptors that signal inflammatory change, including pain. The receptors responsible for these sensations are complex and interdependent. The main sensitive area in the bladder is at the bladder base in the trigone region and in the immediately adjacent proximal urethra, in the urinary sphincter region. There are similar anatomical specialisations in the anal canal [12]. Slight relaxation of the internal anal sphincter allows fractional extrusion of faecal content into the proximal anal canal, inducing the ‘sampling reflex’ [13], that acts as a potent stimulus which, unless voluntarily suppressed, leads to the initiation of defaecation. Similarly, the increasing sense of urinary urgency felt when the bladder is full, particularly in response to a change of posture, such as standing, or coughing, reflects the passage of small quantities of urine into the proximal urethra within the urinary sphincter pressure zone, initiating an urgent voiding response. The external urinary sphincter is innervated by somatic efferent motor fibres from the S2/S3 spinal segments. This voluntary striated sphincter muscle does not totally encircle the urethra

efferent afferent

PUL

BLADDER N

USL CX

N

MUSCLES MUSCLES

ATFP PELVIC RIM

CL

4  The Pelvic Floor: Neurocontrol and Functional Concepts

and so is incapable of completely occluding it when contracted [14]. Like the external anal sphincter in faecal continence, the striated external urinary sphincter, or its smooth muscle counterpart, is not the major muscle of urinary continence.

4.3

 rinary and Faecal Storage U and Voiding

Voluntary urinary voiding occurs in response to increasing pressure and volume within the bladder, causing excitation of afferents from bladder trigone sensory receptors, and also in response to subtle passage of urine into the upper urethra—the equivalent to the sampling reflex within the anal canal [15]. In babies and young children, or in spinal cord injury above the sacral level, the response to this afferent information, signalling the immediate need to void urine, is a switch in equilibrium from storage to voiding.

4.3.1 Bladder Equilibrium At the most caudal, and unconscious, level, the change in command from default storage to voiding occurs at the Onuf urinary and faecal sphincter spinal nucleus at S2/S3 leading to bladder detrusor contraction, internal and external urethral sphincter relaxation, and relaxation of the tonic pubococcygeus contraction [16]. Urine can then flow through the urethra. In health, however, this switch between storage and voiding is itself controlled by more rostral circuits. These are the storage and voiding components of the pontine micturition centre, located in the periaqueductal grey matter of the pons [6, 16]. This pontine system is itself managed by higher-level thalamic and cortical mechanisms (see below and Fig. 4.1). The pressure within the urethra during voiding varies, non-linearly, according to the urethral resistance. Urethral resistance is inversely proportional to the fourth power of the radius of the urethra, as described by Poiseuille’s Law for flow of a liquid in a narrow tube [17] (see below). Thus, a widely open urethra requires much less detrusor pressure to void urine than does a less widely open urethra, and a focal narrow urethral diameter, as in prostatic enlargement, may be so resistant to urine flow as to cause difficulty voiding [18].

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injury, the reflex relationship between the Onuf nucleus and the bladder and bowel is intact, and urinary voiding and defaecation are therefore then under strictly lower-level reflex control, without the possibility of voluntary modulation. Voluntary control of these functions requires supraspinal mechanisms [16].

4.3.3 The Pontine Loop The first of these supraspinal systems depends on another ‘switch mechanism’ involving the periaqueductal grey (PAG) matter of the midbrain and the pontine micturition centre (PMC), first described by Barrington in 1933 [19]. Two groups of neurons have been recognised in this region, subserving storage (PAG activity) and voiding (PMC activity), respectively [12]. Sensory information from the bladder projects from the Onuf system in the sacral cord to this cluster of neurons adjacent to the periaqueductal grey matter in the midbrain [16].

4.3.4 The Cortical System The pontine storage and voiding systems also receive descending input from higher centres including frontal lobe, insular cortex, and hypothalamus [12, 16]. Neural output from the pontine PAG projects caudally, initiating motor commands to the Onuf nucleus and modulating bladder detrusor contraction in the coordinated response necessary for voiding. The equilibrium between these two functions is determined by the balance between sensory input and descending activity from the brain itself, reflecting information regarding timing, and determinations based on learned social and behavioural rules, thus requiring predominantly frontal cortical control of the peripheral opening mechanism (see Figs. 4.1 and 4.2) for both defaecation and micturition. These concepts have been investigated in some detail using functional MRI and PET scanning [8]. This work has also shown activity in a lateral pontine region (the L region) adjacent to the PMC that has been found to be to be active during suppression of the voiding response and therefore in the maintenance of storage (continence) until a suitable opportunity arises.

4.3.2 The Lumbosacral Loop

4.3.5 C  entral Representation of Afferent Information from Bladder and Bowel

In the normal human, the simple spinal mechanism limited to the sacral spinal cord for urinary voiding and defaecation described above is subject to modulation from higher CNS centres. After spinal transection, for example, due to spinal

Processing of afferent information from the bladder and bowel therefore involves relaying this information, most of it carried in autonomic afferents, to the thalamus, and thence to the insular cortex, a region of the brain concerned with infor-

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4.3.6 U  niversal Organisation of CNS Control Systems

PONS C C

inhibitory centre

0 afferent impulses

LP

C PCM

N

LMA

Fig. 4.2  Storage is dominant (C). Micturition is suppressed (green broken lines). The closed trapdoor represents inactive inhibitory centres. ‘N’, stretch receptors. Arrows, the three-directional vectors (PCM, LP, LMA). O open (voiding) response (inhibited in this sequence). LMA levator muscle ani, LP levator plate, PCM pubococcygeus muscle

mation management from internal organs, and therefore in homeostasis [8, 12, 16]. This region is linked to affective and social context-driven aspects of brain function in concert with the anterior cingulate cortex. Prefrontal cortical connexions to the limbic system, including the suprachiasmatic nucleus, important in timing cyclic tasks, are dominant in normal humans in managing both continence and voiding. During voiding in normal subjects, there is activation of the medial prefrontal area [20], suggesting that this region is important in conscious decision-making about voiding. Lesions in prefrontal cortex or its deep white matter are classically associated with uncontrolled micturition in socially inappropriate circumstances [21, 22]. Such behaviour is characteristically a feature of prefrontal traumatic brain injury, deep white matter anterior cerebral infarcts, gliomas, and certain neurodegenerative conditions, especially frontal dementia syndromes.

This successive layering of control systems built on a simple lower-level reflex system is a characteristic common to the organisation of all mammalian motor systems [23]. Such a system allows modulation of various control points within the layered systems. Thus the afferent-efferent system located in the sacral spinal cord at the Onuf nucleus is modulated by the ponto-mesencephalic storage and voiding neurons, which intercede in the balanced storage equilibrium that maintains urinary and faecal continence. This system is itself modulated by time-dependent neuronal systems, probably mainly of hypothalamic origin, based on the suprachiasmatic nucleus, which subserves time modulatory functions in many functional domains, and is also influenced by prefrontal cortical ‘decision-making’ neuronal circuits and by emotional input from insular and callosal neuronal systems. Voluntary control of sympathetic and parasympathetic neuronal systems, in the context of bladder and recto-anal and bowel detrusor and sphincteric muscular systems, is perhaps more precise and overt than control systems involving other autonomic neuronal pathways, but it is not unique; for example, smooth muscle peristalsis in the oesophagus links seamlessly to swallowing itself and to striated muscle activity in the upper oesophagus as well as control of the cardiac sphincter at the lower end of the oesophagus. Like other striated muscles in the body, the local muscular systems in the pelvic floor contain muscle spindles and other sensory endings [24], including tendon organs at the points of insertion of muscles into tendon, and smaller myelinated and unmyelinated fibres responsible for the sensation of pain and other nociceptive functions. In addition Pacinian corpuscles, which signal pressure, are distributed in fascial planes within the muscles and in the tissue, especially peritoneum, surrounding the bladder and bowel. The system thus receives signals not only from the smooth muscle systems of the bladder and rectum but also from the mucosa of these organs and from the muscles of the pelvic floor. The signals include pressure, tension, stretch, and rate of change of stretch, the letter two types of sensation representing spindle activity. There is a complex sensory system intrinsic to receptors on epithelial sensory cells in the bladder and bowel walls, conferring spatial and temporal information about bladder and bowel contents, respectively [6]. Clearly, not all these sensations are perceived in consciousness, but all are important afferent systems that integrate with central neural pathways in storage and voiding of urine and faeces.

4  The Pelvic Floor: Neurocontrol and Functional Concepts

4.4

The Pelvic Floor and Its Innervation

The basic structure of the pelvic floor consists of muscular and fascial planes positioned in relation to the anorectal, vaginal, and urethral openings. The perineal musculature within the pelvic floor functions as a whole during urinary and faecal storage, which should be regarded as the default mode, but the anterior and posterior components are capable of distinct, separate function during micturition and defaecation, respectively. These functions are under separate but analogous control within the central nervous system, as described above. The innervation of the pelvic floor musculature is largely from somatic efferent and afferent nerve fibres travelling within the lumbosacral plexus, and therefore entering these muscles superiorly, but the external anal sphincter and external urethral sphincter muscles, and the puborectalis and pubococcygeus muscles, are innervated by branches of the pudendal nerve, the external urethral and inferior rectal nerves, that supply these muscles from a caudal aspect. All these nerves are derived from sacral spinal segments via the lumbosacral plexus [25].

4.5

 elvic Floor Dysfunction P in Incontinence

When there is damage to the pelvic floor, for example, from stretch injury to ligaments, muscles, and pelvic nerves during a difficult childbirth, or in multipara, the pelvic floor musculature is functionally at a mechanical disadvantage [26]. If a muscle tendon is stretched and has lost its normal elasticity, the force applied during contraction of its muscle will be reduced, and it will reach its maximum more slowly as the lax ligaments are tightened more slowly than normal [27]. Since it is likely that damage to pelvic floor ligaments during a difficult childbirth will not be equally distributed across all the pelvic ligaments (see illustrations) within the pelvic floor, the muscle force vectors resulting from contraction of the pelvic floor muscles will then be distributed in an abnormal pattern. This results in voiding dysfunction and difficulty in maintaining urinary and/or faecal storage. There may also be associated pelvic pain, and, since the anatomy is distorted, there will be a degree of visible perineal descent on coughing or straining and, in the extreme case, organ prolapse [14]. These functional and structural abnormalities usually slowly progress over time [4]. Very difficult deliveries, especially those requiring forceps assistance, are frequently associated with more severe abnormalities in the pelvic floor postpartum, sometimes with anal sphincter tears. The latter are particularly likely to be associated with ligamentous damage and

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with damage to the innervation of the pelvic floor musculature, a combination of abnormality especially associated with disorders of continence. In the presence of weakness of the pelvic floor due to lax ligaments, tearing of muscle fibres, and damage to the somatic innervation of pelvic floor muscles and sphincters, the central nervous system will adapt and modify descending motor commands, insofar as it is capable of doing so, to prevent urinary or faecal leakage. Similarly, adaptations in CNS function occur in relation to other pelvic floor disorders, for example, urgency. These natural adaptations form the functional basis for the use of conditioning therapy, or other neuromodulation procedures, usually based on methods to facilitate increased sensory awareness [28]. These management strategies reinforce the process of maintaining storage at rest but are unlikely to have any biological effect on the already damaged system, particularly regarding its multifactorial nature. When the innervation of some of the muscles of the pelvic floor is damaged, there is less capacity for resetting of control systems.

4.6

Investigation of the Pelvic Floor

The clinical features of pelvic floor disorders and the use of investigations such as video cystometry and anorectal manometry are described elsewhere in this book. Video cystometrograms provide information about pressure/flow relationships within the urinary system, together with bladder volumes before and after voiding. This information is essentially descriptive and does not, of itself, provide insight into the underlying pathophysiology of pelvic floor dysfunction. Anorectal manometry, similarly, is essentially a descriptive account of pressures generated within the anal canal, the anal sphincter region, and the rectum at rest and during attempted straining at stool. Voluntary straining at stool is not the same process as normal defaecation. These investigative data must therefore be interpreted in relation to the historical pathogenesis of the pelvic floor dysfunction and the results of quantitative clinical assessment of pelvic floor function made by careful clinical examination. Neurophysiological investigation of the pelvic floor musculature and its innervation has been important in defining clinically relevant abnormalities, but it does not necessarily guide the surgeon or physician in designing therapy. For example, pudendal and perineal nerve terminal motor latency determinations showed that there was damage to the pelvic floor nerves in women with pelvic floor prolapse, people with urinary incontinence, and even those with a history of difficult childbirth without overt pelvic floor symptoms [2, 24, 29]. However, best management of these disorders, when

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necessary, requires supporting the lax ligaments that accompany damage to the nerve supply of the pelvic floor, thus at least partially alleviating muscular weakness and resolving the clinical disorder.

4.7

Urinary Storage: The Default Mode

During urinary storage [14] in women (Figs.  4.2 and 4.3), three muscle vectors stretch the vagina, like a membrane, in opposite directions. The voiding response is quiescent, and afferent sensory activity is reduced (green broken lines). Tonic activity in the pubococcygeus muscle (PCM) has stretched the suburethral vaginal hammock forwards against the pubourethral ligament (PUL) to close the distal urethra. The levator plate (LP) stretches the proximal vagina and bladder base backwards against the PUL, further tensioning the vagina. The longitudinal muscle of the anus (LMA) contracts against the uterosacral ligament (USL) to rotate the bladder and kink the urethral tube at the bladder neck, maintaining continence (see Fig. 4.4).

4.8

Urethral Opening: Voiding

The bladder is a highly distensile receptacle which can hold large amounts of urine, even in excess of 1000 ml. Voiding via the urethra follows activation of the micturition response [5, 6] (Fig. 4.5). For urine evacuation to occur, storage must be suppressed and voiding activated. Normal voiding is defined as the controlled emptying of the bladder on demand and rapid recovery to the closed state on completion. Voiding is activated by both stretch and surface receptors at the bladder base that vary in sensitivity from person to person. Voiding is a neurological feedback system, requiring coordination by the central nervous system. There are four main components (Fig. 4.5): 1. The hydrostatic pressure of a full bladder activates bladder stretch and mucosal surface receptors (N) that signal to the cortex via the spinal cord and brainstem (see above). 2. The anterior striated PCM muscles relax. 3. The posterior striated muscles (LP/LMA) stretch open the outflow tract (Figs. 4.5 and 4.6) reducing internal urethral resistance to flow. 4. Parasympathetic activation causes bladder detrusor muscle contraction. The bladder contracts as a whole due to electrical transmission fibre to fibre [30] to expel urine.

Fig. 4.3  Changes in bladder and anorectum when storage is dominant. Note the change in vaginal shape (V) and the positions of bladder (B), rectum (R), and levator plate (LP) relative to the vertical and horizontal bony coordinates (white broken lines) during straining. Vaginal elasticity is critical for transmission of muscle forces by directional vectors (arrows). Upper XR. Resting closed (storage) phase PUL pubourethral ligament, USL uterosacral ligament. CX cervix, U urethra, Ra anorectal angle, Bv ligamentous attachment of bladder base to upper vagina. Lower XR. On effort (straining down) Directional vector forces (arrows) stretch the distal vagina and urethra forwards against PUL. The bladder base and rectum are tensed backwards against PUL by the backward vector LP (backward arrow). The downward vector (white arrow) pulls bladder base and rectum downwards against USL to close the bladder neck (BN) and Ra. Adequate elasticity is required in the anterior vaginal wall ‘ZCE’, a zone of critical elasticity (see insert), for this to occur. Arc precervical arc of Gilvernet, PB perineal body, PCM pubococcygeus ligaments, PVL pubovesical ligament, S sacrum

4  The Pelvic Floor: Neurocontrol and Functional Concepts

63

inhibitory centre efferents relax PCM

0 afferent impulses 0

LP N

LMA

Fig. 4.4  Opening (micturition) reflex is dominant. The brain is in “voiding” (micturition) mode ‘O’. The storage mode is suppressed and does not appear in the figure. Afferent impulses are upregulated (black dots). Relaxation of PCM (forward arrow) allows LP/LMA to stretch the vagina (blue) backwards. This stretches open (funnels) the posterior urethral wall decreasing resistance to urine flow and reducing the detrusor pressure required to void urine. The small black arrow indicates a slight downward excursion of PUL to facilitate backward stretching of the vagina. LMA longitudinal muscle ani, LP levator plate, PCM pubococcygeus muscle, PUL pubourethral ligament

In Fig. 4.4, the lower urinary tract is in voiding mode (O) due to afferent input to the central nervous system. The inhibitory pontine L centre is inactivated (open trapdoor in Fig.  4.4); the forward vector PCM relaxes (faint broken lines); LP/LMA vectors stretch the vagina and open the urethra; this action decreases the urethral resistance to flow

Fig. 4.5  Anatomical changes in bladder and anorectum when voiding is active. Upper XR Resting storage mode. Tonic muscle contraction (forward vector) maintains urethral closure distally and at bladder neck. Lower XR Voiding. The forward vector (insert) relaxes. Backward vectors stretch the vagina backwards and downwards against USL to open out the posterior urethral wall. The pubovesical ligament attachment to the arc of Gilvernet (PVL, insert figure) prevents the anterior bladder wall prolapsing into the outflow tract. B bladder, CX cervix, LMA longitudinal muscle ani, LP levator plate, PCM pubococcygeus muscle, PUL pubourethral ligament, R rectum, S sacrum, USL uterosacral ligament, V vagina

(Poiseuille’s Law, see Fig. 4.10). Urine entering the proximal urethra further enhances afferent sensory impulses [7], and the posterior urethral wall is opened out by flattening the trigone, accelerating micturition (Video 1).

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4.11 W  hen Things Go Wrong: Urge, Frequency, and Nocturia

PS PCM PUL PUL BLADDER

trigone

H C

LP

0

Urgency to micturate or defecate represents inappropriate activation of the micturition or defaecation reflexes. PUL or USL ligaments (Fig. 4.1) are the effective insertion points of the three-directional muscle vectors (arrows). If PUL or USL is lax, their attached muscles (arrows) lose contractile efficacy. The weakened PCM and LP/LMA muscles then cannot tense the vagina or anorectum sufficiently to modulate sensory input. Micturition or defaecation responses may be then activated leading to urge urinary or faecal incontinence.

LMA

Fig. 4.6  The trigone. The trigone extends to the external urethral meatus. Pubococcygeus muscle (PCM) relaxation is indicated by a broken line pink arrow. When the upward and forward contracting PCM relaxes, levator plate (LP) stretches the vagina and trigone backwards into a semirigid structure. Longitudinal mascle ani (LMA) pulls down the trigone. C closed diameter of urethra (storage reflex dominant), O open diameter of urethra (voiding reflex dominant). H hammock, PS pubic symphysis, PUL pubourethral ligaments

4.9

 he Bladder Trigone During T Micturition

The trigone (Fig. 4.6) extends from the bladder base to the tip of the external meatus. Its intrinsic stiffness resembles that of the anterior vaginal wall. The posterior muscular vector, the levator plate muscle, stretches the trigone posteriorly. This reduces urethral resistance to urine flow because the posterior urethral wall becomes semi-rigid, creating a funnel, as seen in the micturition X-ray.

4.10 N  eurological Feedback Control of Anorectal Function A system similar to that for bladder control operates for anorectal closure and evacuation (Fig. 4.1) (see also Video 2). As the rectum fills, the stretch and surface receptors (N) send signals to the cord that are relayed to the frontal cortex. These can be suppressed voluntarily by the storage response (white arrow), which activates contraction of the opposed directional musculoligamentous forces (arrows) that support the anorectum from below. A further temporary control mechanism for both bladder and rectum is voluntary upward contraction of the puborectalis muscle. This counteracts the downward mechanical pressure of the bladder or faecal contents and diminishes sensory activation (green arrows).

4.12 Overactive Bladder Syndrome (OAB) In 1993, it was shown that prematurely activated, but otherwise normal micturition [31, 32], usually termed urge incontinence but also known as ‘detrusor instability’ or more recently ‘detrusor overactivity’ (DO), followed the same activation sequence as normal micturition (Fig. 4.4): first, a feeling of urgency, then a decrease in urethral pressure (X), followed detrusor contraction causing increased detrusor pressure, and urine flow (Fig. 4.7). At the onset of the syndrome, there is a strong afferent phase of urethral sensory activation, due to urine entering the upper urethra, as the trigone opens out slightly. Conflict between a natural desire to inhibit this unwanted signal for micturition and the urge to void produces physiological uncertainty between the storage (C) and voiding responses, which can be recognised urodynamically (Fig. 4.8).

4.13 H  ow Does Detrusor Overactivity Relate to Feedback Control? Detrusor overactivity represents a prematurely activated micturition sequence. Close examination of the urodynamic patterns in Fig.  4.7 indicates that the micturition reflex has been activated and bladder (B) and urethra (U) show identical wave patterns. When the micturition response is activated, excitation of smooth muscle fibres by parasympathetic nerve endings in the detrusor muscle causes the bladder to contract as a whole [30], as seen in the video X-ray voiding study (see Video 1). However, the detrusor muscle spasms. It does not relax and contracts like a striated muscle. What the bladder pressure transducer is measuring is the repeated striated muscle contractions of the rhabdosphincter as it tries to close the urethra at the base of the bladder.

4  The Pelvic Floor: Neurocontrol and Functional Concepts

65

U O

X

CLOSED

C C

OPEN

O

feeling of urgency CP

Ou

1.0gm urine loss

Od

Om Cm

B

Y

Fig. 4.7  Detrusor overactivity ‘DO’—premature activation of a normal micturition reflex. Urodynamic graph of a patient with a full bladder undergoing a handwashing test. The binary control system becomes unstable. ‘C’ indicates the storage mode is dominant—the striated muscles are acting to close the urethra and trigone, causing a rise in urethral pressure (UP). ‘O’ indicates the muscles are relaxing, causing a fall in urethral pressure and leading to voiding. The sequence of events in a patient with urge incontinence and DO is: (1) A feeling of urgency, (2) A fall in urethral pressure at X (graph ‘U’), (3) A rise in bladder pressure at Y (graph ‘B’), (4) 1.0 g urine loss arrow, (graph ‘CP’). U urethral pressure graph, B bladder pressure graph, CP closure pressure graph (U − B), C closure (continence) reflex, O opening (micturition) reflex, with its components being: Ou urethral relaxation, Od detrusor contraction, Om opening out of the outflow tract by the posterior muscle forces before voiding

CLOSED

OPEN after Glieck

4.14 E  vents Occurring in Detrusor Overactivity and Overactive Bladder Syndrome These are both manifestations of abnormal neurocontrol of the voiding response. When voiding is activated, there is a sensation of urgency associated with bladder contraction, beginning with slow waves of contraction, before the bladder contracts as a whole during voiding. If it is inconvenient to pass urine, the urethral closure response intervenes so that urine storage continues. Urethral closure increases the pressure in the urethra as well as in the bladder (see ‘C’, Fig. 4.9). However, if there is sufficient sensory input from bladder and trigone and from the urinary sampling response in the proximal urethra, urgency

Fig. 4.8  Bladder instability. Bladder control swings between storage and voiding. Lax ligaments prevent maintenance of the closed storage position; the bladder now oscillates between storage (continence) and voiding phases. Because there is a short-time delay in switching between these two modes, the pressure curves are sinusoidal. This is clearly illustrated in both ‘U’ and ‘B’ in Fig. 4.7. The process resembles the feedback systems described in Chaos Theory (see text)

intensifies and micturition resurges. The forward vector PCM relaxes, and the urethral pressure falls (see ‘O’, Fig.  4.9). Urodynamically (Fig.  4.8), the switch between storage and micturition is manifested as a wave pattern (Figs. 4.8 and 4.9). When the closure response ‘C’ is dominant, the urethra narrows, and the urethral pressure rises. When the opening

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(voiding) response ‘O’ is dominant, the striated muscles acting on the urethra relax and the urethral pressure falls. Because there is a brief delay between the afferent signals from the bladder reaching brainstem and higher centres causing this switch to the voiding response via the pontine micturition centre, the system may ‘hunt’ between the two states of storage and voiding, thus creating a ‘wave pattern’ (Fig. 4.9).

4.15 N  on-linear Flow Mechanics Enhance the Storage and Voiding Responses

Fig. 4.10  The pressure/flow relationship as measured during bench experiments (unbroken lines) and by computer simulation (broken lines). Note that a 0.75 mm decrease in tube diameter from 4 mm to 3.25 mm (a 19% decrease) increases the expulsion pressure by 250% (red lines), consistent with Poiseuille’s Law. After Bush et al. [17, 18]

C

C

C

C

O

O

O

TIME

70

60

measured

50

Pressure

Fig. 4.9  Unstable phasic urodynamic bladder pattern ‘DO’. The micturition reflex has been activated. The bladder swings between ‘open’ and ‘closed’ attractors (see Fig. 4.8). Intravesical pressure rises, while the ‘storage’ mode ‘C’ is dominant; the pressure falls, while the ‘voiding’ mode ‘O’ is dominant. Delay in switching from closure mode to open mode produces the phasic pattern

PRESSURE

Bladder and rectum are elastic and expansile receptacles. The urethral and anal diameters are narrowed during storage and widened during voiding or evacuation by exter-

nally acting striated muscle forces (Fig.  4.10). This external mechanism causes a non-linear change in resistance to flow that is inversely proportional to the fourth power of the radius (Poiseuille’s Law; see Fig. 4.10) [17, 18]. Therefore, in the urinary system, the flow response to narrowing or opening the urethral diameter is very rapid. For example, young people empty their bladders in just a few seconds. This concept of internal resistance to flow within the urethra is key to understanding normal storage (continence) and voiding (micturition) and abnormal bladder states, e.g. incontinence, ‘obstructive’ micturition, and obstructive defaecation. This interpretation is also important in understanding data from urodynamics, especially its wide variance, and the results of corrective surgery.

40 straight tube 3.25mm diam

30

20 straight tube 4mm diam

10

0 0

5

10

15 Flow Rate (cc/s)

20

25

30

4  The Pelvic Floor: Neurocontrol and Functional Concepts

4.16 W  hy Urodynamic Urethral Pressure Measurements Correlate Poorly with Clinical States During passage of urine, including incontinent leakage, urine flows from the bladder to the exterior. Bench testing [17] and mathematical modelling [18] indicate that the key factor Fig. 4.11  Normal micturition in the female. Upper image: Voiding X-ray (broken lines, subscript m) superimposed on resting X-ray. Clips have been applied to the midurethra ‘1’, bladder neck ‘2’, and bladder base ‘3’. Note downward/ backward displacement of the clips indicating stretching open of the posterior urethral wall. Lower image Note electromyography (EMG) activity (arrows) mainly at the start of micturition—the urine occupying the urethral tube is incompressible and helps to hold the urethra open as long as it is flowing. LP levator plate

67

controlling the rate of urine outflow is the diameter of the urethra (Figs. 4.9, 4.10, and 4.11) which, in turn, regulates the resistance to flow against the pressure (P) of detrusor contraction. Whether urine leaks or not depends on the resistance to flow within the urethra (see above). Urodynamic studies are limited to measurement of intravesical and intra-­ urethral pressures ‘P’ and flow rates. Pressure is derived

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Fig. 4.12 ‘Outflow obstruction’ in the female— Lax ligament insertions for the LP/LMA opening vectors cannot open the urethra sufficiently against its elastic forces. Even with constant activation of the pelvic muscles, the stream is slow and prolonged with electromyography (EMG) activity seen throughout the micturition cycle

from the relation between applied force and transverse urethral area (πr2). Intra-urethral pressure ‘P’, being proportionate to r2, is not what prevents urine loss. Pressure at any point on the urethral diameter is not a sufficiently sensitive measurement index of incontinence, because it is the resistance to urine flow, which is proportionate to r2, which prevents urine loss, not external urethral pressure. Conversely, for urine to flow easily, there must be adequate external opening of the urethra, by opening out its posterior wall, as shown in the micturition X-ray (Figs. 4.5 and 4.11). If the urethra cannot be opened out adequately, there is a sensation of obstruction to flow. In Fig. 4.11, the urethra has been rapidly opened out by prior external muscle contraction, so micturition is rapid and effective. Continued external striated muscle contraction is not required as urine is incompressible and itself maintains urethral opening. In contrast, in Fig.  4.12, the urethra cannot be adequately opened. The posterior muscles LP and LMA (Fig. 4.6) have to contract repeatedly, and urine flow is slow.

4.17 H  ow Repeatable Are Urine Flow Measurements in an Individual? Urine flow studies measure the volume of urine flowing through the urethra at a defined diameter expressed as ml/ second. Urine flow is determined by the internal resistance to flow [17, 18] as discussed above. Individual repeat flow measurements [18] are remarkably variable, because the opening mechanism assisting micturition is activated by pelvic floor striated muscle vectors (see EMGs in Fig. 4.12) and detrusor contractile power may vary from void to void. A very minor change in urethral diameter causes a profound change in flow rate.

4.18 Detrusor Underactivity Detrusor underactivity (DU) is an ill-defined entity. Osman et al. [33] noted that:

DU is present in 9–48% of men and 12–45% of older women undergoing urodynamic evaluation for non-neurogenic lower urinary tract symptoms (LUTS). Multiple aetiologies are implicated, affecting myogenic function and neural control mechanisms, as well as the efferent and afferent innervations. Diagnostic criteria are based on urodynamic approximations relating to bladder contractility such as maximum flow rate and detrusor pressure at maximum flow. Other estimates rely on mathematical formulas to calculate isovolumetric contractility indexes or urodynamic "stop tests." Most methods have major disadvantages or are as yet poorly validated. Contraction strength is only one aspect of bladder voiding function. The others are the speed and persistence of the contraction.

The ‘myogenic function and neural control mechanisms’ mentioned by Osman et  al. [33] are relevant but undefined concepts, as they are at present impossible to quantify. We present here an alternative mechanism based on research by Bush et al. [17] which is consistent with Osman’s conceptual analysis [33]. If the urethra can be opened by the external muscle forces to 4 mm diameter (Fig. 4.11), urine could flow at a rate of 7 ml/second with no recordable detrusor pressure. This does not mean that the bladder is ‘underactive’. The bladder smooth muscle will contract sufficiently that the bladder can empty fully. Demonstrable urinary flow indicates that the urethra has been opened sufficiently to lower the internal resistance to a point at which the detrusor force enables flow to occur. For example, at a flow rate of 20  ml/s (Fig.  4.10), a 50 cm head of pressure from the detrusor is needed to overcome the internal resistance to flow in a 3.25  mm tube, but only a 20 cm head of pressure is required for a 4 mm tube. The graph (Fig. 4.10) illustrates the difference in voiding patterns in Fig. 4.11 (rapid flow) and Fig. 4.12 (slow flow).

4.19 Low Bladder Compliance In a study of detrusor instability (now termed detrusor overactivity) and low compliance [34], the low compliance data could only be reconciled by considering ‘low compliance’ as a partially activated micturition reflex. Bladder ‘stiffness’ is a consequence of smooth muscle contraction by an activated but modulated micturition reflex.

4  The Pelvic Floor: Neurocontrol and Functional Concepts

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4.20 Clinical Variations in Bladder Symptoms Are Consistent with the Chaos Theory Feedback Equation

OPEN unstable CLOSED unstable

XNEXT

c stabled closed

CHAOTICZONE

One of the mysteries of clinical urology is the marked variability of symptoms such as urgency and nocturia. This variability is consistent with the classic Chaos Theory [35] feedback equation Xnext = Xc (1 − X). In Fig. 4.13 the feedback control system [34] was tested for compatibility with the Chaos Theory graph derived from the Chaos Theory feedback equation Xnext = Xc (1 − X). Calculations were made (see below) in three functional modes: low afferent activity (normal mode), increased afferent activity from a micturition reflex activated but controlled (low compliance mode), and excessive afferent activity exceeding the ability of the closure reflex to inhibit the afferent impulses ‘overactive bladder’ mode (see Fig. 4.1). An excess of afferent signals brings the system into the ‘chaotic zone’ in which equilibrium oscillates between voiding (open) and storage (closed): in this zone the closure reflex is in unstable competition with the micturition reflex (see Figs. 4.8 and 4.9). These three func-

tional modes conform with classic Chaos Theory feedback calculations. As long as the closure reflex mechanisms, both central and peripheral, can control the increasing sensory input ‘X’ (X = no of afferent impulses), the patient’s bladder remains in ‘stable closed’ mode, and the patient is dry. At the peak of the curve, the reflex closure mechanisms are overcome by the excessive number of afferent impulses (X) arriving at the pontine micturition centre and cortex; the micturition response begins to be activated. The system becomes unstable and oscillates between ‘open’ and ‘closed’ (Figs. 4.8 and 4.9). Patients may therefore report complete dryness on some days, yet they may wet four to five times on other days.

4.21 Concluding Remarks The neurocontrol systems responsible for appropriate voiding of urine and faeces are linked to the default position of continent storage. The control system is organised on a layered sequence of neural systems that consist of local pelvic floor and bladder and anorectal structures—the end-organs— and spinal, brainstem, and higher-level cortical circuits. These circuits are integrated and responsive to each other. When the pelvic floor and its sphincteric systems are damaged, for example, by a difficult childbirth, or prostatic obstruction, a measure of adaptation in these neural systems is possible, although little is known about their adaptive capacity. It is essential that any corrective pelvic floor surgical procedures should retain the inherent musculo-elasticity of this system, since this determines the musculotendinous function necessary for normal function of the pelvic floor and its sphincteric systems.

retention after Glieck

Fig. 4.13  (after Gleick 1987). The graph is that of a classic Chaos Theory feedback equation Xnext = Xc (1 − X) applied to normal bladder, low compliance bladder, and unstable bladder (see text). The line ‘c’ represents the sum of cortical and peripheral inhibition via the musculo-­ elastic system (two variables). Xnext can be equated to the number of afferent impulses. x axis, time; y axis, Xnext. If the control mechanisms are all working properly, the system is in storage mode. Along line ‘c’, the voiding response is activated. However, while the peripheral and central mechanisms remain sufficiently supportive, the feedback system maintains the patient dry. Further along ‘c’, there is a bifurcation. The quantum of afferents is now excessive and exceeds the ability of the cortex to retain the closed phase; the bladder begins to swing between the ‘storage’ and ‘void’ attractors. This is ‘detrusor instability’ (DI) ‘overactivity’. The system in the Chaotic Zone is very finely balanced. Any minor factor, for example, perimenstrual relaxation of the cervix, will loosen USLs, and the muscle vectors cannot maintain equilibrium. Afferent activity XNEXT increases, and the system may enter the Chaotic Zone. The patient is then sometimes dry, sometimes wet

References 1. Snooks SJ, Barnes RPH, Swash M.  Damage to the voluntary anal and urinary sphincter musculature in incontinence. J Neurol Neurosurg Psychiatry. 1984;47:1269–73. 2. Swash M, Snooks SJ, Henry MM.  A unifying concept of pelvic floor disorders and incontinence. J Roy Soc Med. 1985;78: 906–11. 3. Snooks SJ, Swash M, Setchell M, Henry MM.  Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet. 1984;2:546–50. 4. Snooks SJ, Swash M, Henry MM, Setchell M. Risk factors in childbirth causing damage to the pelvic floor innervation: a precursor of stress incontinence. Int J Colorect Dis. 1986;1:20–4. 5. Sultan AH, Kamm MA, Hudson CN, et al. Anal sphincter disruption during vaginal delivery. N Engl J Med. 1993;329:1905–11. 6. Smith ARB, Hosker GL, Warrell DW. The role of partial denervation of the pelvic floor in the aetiology of genitourinary prolapse and stress incontinence of urine: a neurophysiological study. J Obstet Gynaecol. 1989;96:244–8.

70 7. Fowler CJ, Griffiths D, de Groat WC. The neural control of micturition. Nat Rev Neurosci. 2008;9:453–6. 8. Holstege G, Sie JAML. The central control of the pelvic floor, chapter 8. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor: its function and disorders. London: WB Saunders; 2001. p. 94–101. 9. Abrams P, Andersson KE, Buccafusco JJ, et  al. Muscarinic receptors, their distribution and function in body systems, and the implications for treating overactive bladder. Br J Pharmacol. 2006;148:565–78. 10. Neill ME, Parks AG, Swash M.  Physiological studies of the anal sphincter muscle in faecal incontinence and rectal prolapse. Br J Surg. 1981;68:531–6. 11. Parks AG.  Anorectal incontinence. Proc Roy Soc Med. 1975;68:681–90. 12. Trivedi PM, Griffiths DJ. Neurological control of the bowel in health and disease, chapter 2. In: Fowler CJ, Panicker JN, Emmanuel A, editors. Pelvic organ dysfunction in neurological disease: clinical management and rehabilitation. Cambridge: Cambridge University Press (Medicine); 2010. p. 25–39. 13. Miller R, Bartolo D, Cerveto F, Mortensen NJ.  Anorectal sampling: comparison of normal and incontinent subjects. Br J Surg. 1985;75:44–7. 14. Petros PE, Ulmsten U.  Role of the pelvic floor in bladder neck opening and closure: 1. Muscle forces. Int J Urogynecol Pelvic Floor. 1997;8:74–80. 15. Oliver S, Fowler CJ, Mundy A, Craggs M.  Measuring the sensations of urge and bladder filling during cystometry in urge incontinence and the effects of neuromodulation. Neurourol Urodyn. 2003;22:7–16. 16. Griffiths DJ, Apostolidis A.  Neurological control of the blad der in health and disease, chapter 1. In: Fowler CJ, Panicker JN, Emmanuel A, editors. Pelvic organ dysfunction in neurological disease: clinical management and rehabilitation. Cambridge: Cambridge University Press (Medicine); 2010. p. 1–24. 17. Bush MB, Petros PEP, Barrett-Lennard B. On the flow through the human urethra. Biomechanics. 1997;30:967–9. 18. Petros PE, Bush MB.  A mathematical model of micturition gives new insights into pressure measurement and function. Int J Urogynecol. 1998;9:103–7. 19. Barrington FJ. The relation of the hind-brain to micturition. Brain. 1921;44:23–53. 20. Blok BFM, Sturms LM, Holstege G. Brain activation during micturition in women. Brain. 1998;121:2033–41.

M. Swash and P. Petros 21. Ueki K. Disturbance of micturition observed in some patients with brain tumour. Neurol Med Chir. 1960;2:25–33. 22. Andrew J, Nathan PW. Lesions of the anterior frontal lobes and disturbances of micturition and defaecation. Brain. 1964;87:233–62. 23. Porter R, Lemon RL. Corticospinal function and voluntary movement. Monographs of the physiological society 45. Oxford: Clarendon Press; 1995. 24. Swash M. Electrophysiological investigation of the posterior pelvic floor and anal sphincters, chapter 16. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor: its function and disorders. London: WB Saunders; 2001. p. 213–34. 25. Kerremans R.  Morphological and physiological aspects of anal continence and defaecation. Brussels: Editions Arscia; 1969. 26. Petros PE, Swash M. The musculo-elastic theory of anorectal function and dysfunction. Pelviperineology. 2008;27:89–93. 27. Petros PE, Kakulas B, Swash M.  Stress urinary incontinence results from muscle weakness and laxity in the pelvic floor. Pelviperineology. 2008;27:107–9. 28. Enck P, Musial F.  Biofeedback in pelvic floor disorders, chapter 27. In: Pemberton JH, Swash M, Henry MM, editors. The pelvic floor: its function and disorders. London: WB Saunders; 2001. p. 393–402. 29. Jones PN, Luboiwski DZ, Swash M, Henry MM. Relation between perineal descent and pudendal nerve damage in idiopathic faecal incontinence. Int J Colorectal Dis. 1987;2:93–5. 30. Creed K.  Functional diversity of smooth muscle. Br Med Bull. 1979;3:243–7. 31. Petros PE, Ulmsten U.  Tests for detrusor instability in women. These mainly measure the urethral resistance created by pelvic floor contraction acting against a premature activation of the micturition reflex. Acta Obstet Gynecol Scand. 1993;72:661–7. 32. Petros PE, Ulmsten U.  Bladder instability in women: a premature activation of the micturition reflex. Neurourol Urodynam. 1993;12:235–9. 33. Osman NI, Chapple CR, Abrams P, et  al. Detrusor underactivity and the underactive bladder: a new clinical entity? A review of current terminology, definitions, epidemiology, aetiology and diagnosis. Eur Urol. 2014;65:389–98. 34. Petros PE. Detrusor instability and low compliance may represent different levels of disturbance in peripheral feedback control of the micturition reflex. Neurourol Urodynamics. 1999;18:81–91. 35. Gleick J. “Inner Rhythms” in chaos—making a new science. London: Cardinal Penguin; 1987. p. 275–300.

Part II Pelvic Floor Imaging

5

Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound Andrzej P. Wieczorek, Magdalena Maria Woźniak, Jacek Piłat, and Giulio A. Santoro

Learning Objectives

• To learn basic principles of physics of ultrasonography and their influence on obtained images. • To familiarize with types of pelvic floor ultrasound including 2D/3D transperineal ultrasound (TPUS), 2D/3D endovaginal ultrasound (EVUS), and 2D/3D endoanal ultrasound (EAUS) and their advantages and limitations. • To identify various types of transducers and anatomical approaches which can be applied for pelvic floor ultrasound and distinguish different imaging possibilities with each type of transducer. • To learn about existing more advanced ultrasound options such as Doppler ultrasound, elastography, three- and four-dimensional US, and tomographic ultrasound imaging (TUI) and recognize their possibilities.

5.1

Introduction

Female pelvic floor is one of the most complex regions in the human body. Pelvic organs with different functionality are supported by numerous muscular fibers (levator musculature and perineal musculature) and connective tissue forming ligaments A. P. Wieczorek (*) · M. M. Woźniak Department of Pediatric Radiology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland e-mail: [email protected] J. Piłat Department of General and Transplant Surgery and Nutritional Treatment, Medical University of Lublin, Lublin, Poland G. A. Santoro Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery, Regional Hospital, Treviso, University of Padua, Padua, Italy e-mail: [email protected]

and fascia (endopelvic fascia, pubocervical fascia, rectovaginal septum, perineal membrane, perineal body, uterosacral ligaments, cardinal ligaments) and interconnected to somatic and autonomic nerves and vascular structures. The simplistic division in three compartments should be replaced by the current concept of considering the pelvic floor as a mechanical threedimensional apparatus that acts as unit, influencing urinary and anal continence, sexual satisfaction, and vaginal delivery [1, 2]. Viewing the pelvic floor as a horizontal model rather than as a set of vertical compartments helps to understand why disorders observed in one compartment may have their origin in dysfunction of another compartment or why most females present multicompartmental damages. As a consequence, there is a need of an integrated approach to the management of the pelvic floor disorders involving a multidisciplinary team of clinicians that address these problems (urologists, gynecologists, colorectal surgeons, gastroenterologists, radiologists, physiotherapists) [1, 2]. The aim of pelvic floor evaluation is to explain the symptoms, identify the causative mechanism and its risk factors, and finally propose treatment. A thorough history and physical examination will often provide ample evidence to make a diagnosis and develop an effective treatment plan. Patients unresponsive to the initial therapy or with recurrence of symptoms or candidate to surgery should however further be investigated using sophisticated tests. Imaging techniques play a fundamental role in the diagnosis of pelvic floor disorders and are included in the pathways of urinary and anal incontinence, obstructed defecation, voiding dysfunction, and pelvic organ prolapse proposed by various scientific societies (ICS, International Continence Society; IUGA, International Urogynecological Association; ICI, International Consultation on Incontinence) [3–5]. Ultrasound, X-ray (evacuation proctography, cystography, videourodynamics, barium enema, transit time) and MRI techniques can help to identify the anatomical or functional abnormalities of the pelvic floor. Radiological findings can confirm clinical findings or discriminate damages that were misled or underestimated by physical examination alone. Due to costs, access and availability, and patient compliance, most guidelines recommend

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_5

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to perform pelvic floor ultrasound as the first-line or screening tool modality [3–5]. “Pelvic floor ultrasound” is a synonymous of a large variety of techniques (translabial, transperineal, endovaginal, endoanal, 3D/4D acquisitions, dynamic US, assessment of vascularity patterns, and tissue stiffness—elastography), having different advantages and limitations [6, 7]. Understanding the physics of ultrasound, the mechanism of interactions of ultrasound beam with tissues, the process of image formation, the choice of imaging parameters, the optimization of quality of image (gain, focus, resolution), the identification of artifacts, the characteristics of transducers (mechanical and electronic frequencies, field of view, convex, end-fire, linear) and scanners, and the different anatomical approaches that can be used is therefore of utmost importance [8–11]. Despite ultrasound is considered operator-­dependent, an adequate training and use of standardized methodology have demonstrated a very good intra- and interobserver reproducibility of this modality [12–14]. Great advance has been made in developing a very sophisticated ultrasound technology; however the vertical model for care of disease has limited a clinician’s understanding to the vertical unit in which the clinician (urologist, gynecologist, and colorectal surgeon) has an expertise. The emerging concept of horizontal integration of pelvic floor dysfunction evaluation and management is expanding to ultrasound approach that must be integrated and multicompartmental [6, 15]. Global or total ultrasound addresses all pelvic floor anatomy and functionality in one setting, allowing identification of coexisting dysfunctions of the three compartments [6].

5.2

Principles of Pelvic Floor Ultrasound

Ultrasound imaging is a technique of generating images using a very high-frequency sound. Sound is a mechanical, vibration form of energy. Ultrasound for medical imaging is generated in special crystalline materials which, when electrically excited, are capable of vibrating at frequencies of millions of vibrations per second [8]. Operating frequencies for medical ultrasound are in the 1–40  MHz range, with external imaging machines typically using frequencies of 1–20 MHz. Higher frequencies are in principle more desirable, since they provide higher resolution, but tissue attenuation limits how high the frequency can be for a given penetration distance. However, one cannot arbitrarily increase the ultrasound frequency to get finer resolution, since the signal experiences an attenuation of about 1 dB/cm/ MHz [9]. The velocity of propagation of ultrasonic longitudinal waves in soft tissues varies depending on the type of tissue, in single collagen fibers (tendons) equals c  =  1700  m/s, in

lung tissue 650 m/s, in bone tissue from 1500 to 4300 m/s [3]. The speed of ultrasound wave c is determined by the formula: c=

C p

c—speed of sound, C—coefficient of stiffness, p—density. Different materials respond differently to interrogation by ultrasound, depending on the extent to which their medium particles will resist change due to mechanical disturbance. This medium property is referred to as the characteristic acoustic impedance of a medium. It is a measure of the resistance of the particles of the medium to mechanical vibrations. This resistance increases in proportion to the density of the medium and the velocity of ultrasound in the medium. Acoustic impedance, Z, may be defined as the product of medium density and ultrasound velocity in the medium [8]:

Z = density ´ velocity

Ultrasound waves are generated by piezoelectric crystals in the transducers. The number of piezoelectric crystals in the transducers and the range of frequencies they can operate in are very important features. In case of 2D technology, the number usually exceeds 190 elements; in 3D and 4D technologies, the transducer may be designed as a matrix array, where the number of piezoelectric elements may be multiplied to more than a 1000 elements. The signals generated in the transducer are subsequently sent to the tissue and received back by transmit channels. The number of physical active channels can reach a few hundred (over 500), whereas transmit channels used in post-processing may reach even a few millions. Ultrasound imaging is based on the signals generated by the returning echoes at the transducer that are electronically processed to increase their sizes and organized in computer memory before being displayed to the user. The echoes returning from different tissue depths must be subjected to compensation for attenuation differences. Time gain compensation (TGC) is a process of applying differential amplification to signals received from different tissue depths, with echoes originating from longer distances being amplified to a greater extent than those from shorter distances in such a way that similar tissue boundaries give equal-sized signals regardless of their depth in tissue. The latest generations of scanners have automatic adjustment of TGC independent from the operator. The difference between the maximum and minimum values of the displayed signal is defined as dynamic range, and it is one of the most essential parameters that determine its image quality [11]. Nowadays dynamic range may vary from 70 Db to over 300 Db. Because the dynamic range of signal sizes may be very wide, the range of signal sizes is

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound

compressed by using logarithmic amplifiers. Pulses with identical waveforms are repeated each time the crystal is excited, at a rate known as the pulse repetition frequency (PRF). The PRF represents the number of pulses or bursts of ultrasonic energy, released by the transducer in one second, and is different from the vibration frequency of the transducer [8]. The most basic but at the same time a crucial mode in pelvic floor ultrasound is the brightness mode (B-mode). In B-mode the signals from returning echoes are displayed as dots of varying intensities (gain). The intensity of a dot (the brightness) is a relative measure of echo size, with large echoes appearing as very bright dots, while at the other extreme non-reflectors, they appear totally dark. It is important to notice that an ultrasound pulse consists of a range of frequencies, not a single frequency. For example, a pulse from a 5 MHz transducer could be composed of a range of frequencies from 4 MHz to 6 MHz. This range of frequencies is called the bandwidth [5]. Another important feature is use of harmonics imaging. The ultrasound pulse starts out with a sinusoidal waveform. As the wave passes through tissue, the wave speeds up very slightly during the compression phase, and during the refraction phase, the wave slows slightly. This causes a distortion of the wave and creates the harmonic frequencies. Harmonics are frequencies at multiples above the fundamental frequency—the frequency that was emitted from the transducer. The fundamental frequency is also known as the first harmonic [5]. The main advantage of the harmonic imaging is increasing the resolution of the image obtained. More advanced techniques in pelvic floor ultrasound include the use of multidimensional imaging—three-­ dimensional (3D) and four-dimensional (4D). The main prerequisite for construction of three-dimensional (3D) ultrasound images is very fast data acquisition. Transducers for real-time imaging may be classified broadly into two categories: mechanical transducers and electronic transducers. In mechanical transducers, the beam sweep is achieved through physical movement of some part of the transducer, usually the crystal element(s), whereas in electronic transducers the beam is swept by electronic activation of crystal elements, without causing the transducer to move physically. The collected data are processed at high speed, so that real-­ time presentation on the screen is possible. This is called the four-dimensional (4D) technique (4D = 3D + real time) [8]. The 3D image can be displayed in various ways, such as transparent views of the entire volume of interest (render mode), images of surfaces (surface mode), images in three perpendicular sections (axial, sagittal, coronal) called multiplanar reconstruction (MPR), or as a volume 3D box accessible from every side and section. Post-processing options of 3D and 4D images enable numerous manipulations of the

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image such as zooming, rotating, contrasting, sharpening, changing the transparency, removing artifacts in order to present the volumetric image in the most diagnostic manner. In order to produce high-quality images, it is crucial to understand the nature of artifacts in pelvic floor imaging. The major causes of artifacts include multiple reflections across acoustic boundaries, acoustic shadowing due to strong reflectors or absorbers of ultrasound, and poor physical condition of the transducer. Other artifacts may be caused by refraction of ultrasound, scattering, wave interference phenomena, or less than perfect mechanical and electrical isolation of crystal elements. Lastly important features influencing the diagnostic value of pelvic floor ultrasound are the environmental conditions such as proper room lightning, proper monitor settings (Fig. 5.1), and the ability of the user to operate the scanner accordingly. Summarizing, a variety of factors contributes to the overall quality of the ultrasound image. These include the design of equipment components, especially the transducer; the choice of imaging parameters, particularly the beam frequency; and the skilled use of the equipment by the operator. A good-quality image should contain information that is associated with high spatial resolution (ability to distinguish between objects in space), high contrast resolution (ability to distinguish between signals of different size), and high temporal resolution (ability to separate between events in time). In addition, the image should be free of any avoidable artifacts [8].

5.3

Two-Dimensional Transperineal Ultrasound (2D TPUS)

2D TPUS is performed with the patient placed in the dorsal lithotomy position, with hips flexed and abducted and a convex transducer positioned on the perineum between the mons pubis and the anal margin (perineal approach). The dimension of the transducer should be large enough to cover in the midsagittal plane all anatomical structures between posterior margin of the symphysis pubis and anterior margin of the coccyx/posterior part of the levator ani, e.g., bladder, urethra, vaginal walls, anal canal, and rectum. TPUS is a term that should be regarded as being synonymous with “translabial ultrasound” (transducer placed on one of the labia majora) or “perineal ultrasound” (transducer placed between the posterior vaginal wall and anal canal), while “introital ultrasound” is usually assumed to imply placement of transducers with smaller footprints (such as endfire transvaginal probes or hokey-stick intraoperative transducers) within the introitus. The general term of “TPUS” is often adopted for all these techniques. Imaging is usually performed

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Fig. 5.1  Influence of monitor setting for the quality image

with the patient at rest, during maximal Valsalva maneuver and during pelvic floor muscle contraction (squeeze test) to dynamically define the position and anatomical relationship between urethra and bladder, vaginal walls, and the anorectal region anal canal. In order to avoid false-negative results, transducer pressure on the perineum must be as small as possible, while still m ­ aintaining good tissue contact, in order to allow full pelvic organ descent [16, 17].

5.3.1 Convex Transducers Two-dimensional transperineal ultrasound (2D TPUS) in B-mode represents the most frequently used modality providing 2D imaging of the pelvic floor in the midsagittal section [6, 16, 17]. It is performed with convex transducers that may differ depending on frequency and surface of contact (Table 5.1). The higher is the frequency, the smaller is the shape of convex surface. The conventional “large” convex transducers usually used for abdominal and obstetrical scanning have low resolution due to low frequencies, because they must have high penetration to image deep organs in the patient’s body. They work at frequen-

cies ranging from 2 to 6–8 MHz, with a field of view at least 70° (Fig. 5.2a). The number of crystals/piezoelectric elements in large convex transducers may differ depending on manufacturers; however it is around 192 elements placed on a surface of approx. 50–62 mm length and 8–13 mm width (acoustic aperture). Another type of transducer also used for 2D TPUS scanning is a “small” convex transducer designed primarily for pediatric or early pregnancy examinations. It is characterized by higher frequency (from 5 to 9–10 MHz) in comparison to “large” convex transducers and smaller sizes of acoustic aperture (Table 5.1, Fig. 5.2b). A third type of transducer also suitable for 2D TPUS scanning is an endocavitary end-­ fire microconvex probe used for gynecological/urological purposes. It is characterized by frequency ranging from 5–6 to 8–9 MHz and smallest acoustic aperture (Table 5.1, Fig. 5.2c). Some scanners have dedicated protocol for urogynecology; however the operator can adjust the setting to get good-quality images. The focal zone should be concentrated at the level of the bladder neck, which is approx. 30–40 mm deep, whereas the field of view and the ultrasound angle can be regulated to focus on a certain anatomical structure to obtain better image. A limitation of the 2D TPUS technique is its sensitivity in

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound Table 5.1  Types and characteristic of convex transducers used in 2D TPUS examinations Type of probe Example transducer “Large” 6C2 convex BK-Medical

4

27

10

Example ultrasound 2D TPUS image Fig. 5.2  Two-dimensional transperineal ultrasound performed with different types of transducer. Pelvic floor structures are visualized in the midsagittal section. Differentiation of the external and internal sphincters and the lumen of anal canal are visible better with higher-frequency (small convex and end-fire) transducer than with lower-frequency (large convex) transducer. (a) Large convex

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Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

Abdominal Obstetrical 2–6 MHz 192 62°/71° 62.5 × 13 mm

a “Small” convex

9C2 BK-Medical

(b) Small convex 1,5

30,7

10

56

Fig.2 Technical drawing and dimensions (mm)

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture End-fire

Pediatric Early pregnancy 2–9 MHz 192 74°/104° 52 × 8 mm

b

8819 BK-Medical

(c) End-fire. A anal canal, B bladder, SP symphysis pubis, U urethra 319

22,1

18,2

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

Gynecology Urology 6–9 MHz 128 150° 26 × 5 mm

c

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Fig. 5.3  Sagittal section of pelvic floor structures by two-dimensional transperineal ultrasound. During Valsalva maneuver, air trapped into rectocele (R) produces typical reverberation artifact. B bladder, SP symphysis pubis, U urethra

dynamic studies when the image may be distorted by artifacts caused by the reflections from gases in the anal canal in patients with rectocele/enterocele (Fig. 5.3).

5.3.2 Linear/Microconvex Transducers For introintal use in adult patients and in case of children and newborns to find out the anatomical disorder in pelvic floor, higher-frequency transducers (linear, microconvex, or end-­fire gynecological/obstetrical or urological) can be used (Table 5.2, Fig. 5.4). Linear transducers provide visualization of superficial pelvic anatomical structures or subcutaneous fluid collections/fistulas and anorectal malformations that can be missed by low-frequency transduc-

ers. Frequency of linear transducers is higher than large convex transducers and may range from 5–7 MHz even up to 20–22 MHz. The most common range of frequency varies from 8 to 10–12 MHZ for the transducers dedicated to small part imaging, breast imaging, and musculoskeletal scanning. “Hokey-stick” intraoperative linear transducers are also appropriate for this purpose due to small size, angulated shape, and high frequency, delivering high-resolution image. These transducers can be introduced endovaginally/endoanally with a finger guidance to the suspected area. Microconvex and end-fire gynecological/ obstetrical or urological transducers have higher frequencies starting from 5 up to 9–12 MHz, with better resolution than large convex transducers, but are limited by a small surface of contact (Table 5.2, Fig. 5.4).

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound Table 5.2  Types and characteristic of linear transducers used in 2D TPUS examinations Type of probe Example transducer 13 L5 “Lower-­ frequency” BK-Medical linear

Example ultrasound 2D TPUS image Fig. 5.4  Pelvic floor structures by transperineal ultrasound visualized with different types of transducers. (a) “Lowerfrequency” linear transducer— sagittal section (A anal canal, B bladder, U urethra)

0

10

a 22

66

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

Small parts MSK (large joints) 5–13 MHz 192 49.9 + 2 × 15° 50 × 4 mm

18L5 “Higher-­ frequency” BK-Medical linear

(b) “Higher-­frequency” linear transducer—sagittal section showing intraurethral tumor (T)

b 30,5

97

57

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

Pediatric small parts MSK (small joints) 5–18 MHz 192 38.4 + 2 × 15° 38.4 × 3.5 mm

Foot-print/ X18 L5s hokey-stick BK-Medical

24 3

17

14

9,5

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

Intraoperative MSK (finger/toe joints) 5–18 MHz 150 Trapezoidal: 24.0 mm wide + expansion angle 2 × 15° 3.5 × 24 mm

(c) Foot-print/hokey-stick transducer—the lumen of an ectopic ureter (EU) having the orifice in the urethra

c

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5.4

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T  hree-Dimensional/Four-Dimensional Transperineal Ultrasound (3D/4D TPUS)

5.4.1 Volumetric Transducers Volumetric transabdominal probes developed for obstetric imaging (RAB 8–4, GE Healthcare Ultrasound, Milwaukee, WI, USA; AVV 531, Hitachi Medical Systems, Tokyo, Japan; V 8–4, Philips Ultrasound, Bothell, WA, USA; 3D 4–7 EK, Medison, Seoul, South Korea) and other may be used for 3D/4DTPUS. These transducers combine an electronic curved array of 4–8 MHz with mechanical sector technology, allowing fast motorized sweeps through the field of view, a technology that was pioneered in the Voluson systems manufactured by Kretztechnik, now GE Healthcare Ultrasound [18]. For the “pelvic floor” assessment, the suggested set is maximum aperture and acquisition angles (70° and 85°, respectively), depth of 8  cm, two focal zones at 1.5  cm and 4.5  cm, low or medium harmonics, speckle reduction 5, and crossbeam 2 [18] (Table 5.3, Fig. 5.5). An advantage of 3D TPUS compared with 2D mode is the opportunity to obtain tomographic or multislice imaging (TUI), for example, in the axial plane, in order to assess the entire puborectalis muscle and its attachment to the pubic rami, as described by Dietz et al. [19, 20]. It is also possible to measure the diameter and area of the levator hiatus and to determine the degree of hiatal distension on Valsalva maneuver. 4D TPUS imaging involves real-time acquisition of volume ultrasound data, which can then be visualized instantly in orthogonal planes or rendered volumes. This simplifies the assessment of functional anatomy since 3D data can be archived as a cine loop, encompassing maneuvers such as squeeze test or Valsalva maneuver [6]. Similar to DICOM viewer software used in radiology, offline analysis is possible on the actual system or on a personal computer (PC) with the help of dedicated software. Similarly as in 2D TPUS, particularly on prolapse assessment, pressure on the perineum must be kept to a minimum to allow full development of the prolapse [18]. The limitation of 3D/4D TPUS is a small region of interest (acquisition angle) not able to cover all pelvic floor organs in patients with high-grade prolapse and in patients with high BMI.

5.5

T  wo-Dimensional Endovaginal Ultrasound (2D EVUS)

EVUS is performed with the patient placed in the same position as that adopted for TPUS.  It may be performed with electronic linear transducer, frequency 4–14  MHz (type 8838, X14L4 BK-Medical, Herlev, Denmark); with electronic biplane transducer (linear and transverse perpendicular arrays), frequency 5–12 MHz (type 8848, BK-Medical)

[21]; with high-multifrequency (9–16 MHz), 360° rotational mechanical transducer (type 2052, 20R3 BK-Medical) [21]; or with radial electronic probe (type AR 54 AW, 5–10 MHz, Hitachi Medical Systems) (Table 5.4, Fig. 5.6 and 5.7). It is important to keep the transducer inserted into the vagina in a neutral position and to avoid excessive pressure on surrounding structures, which might distort the anatomy [6, 21]. The biplane electronic probe provides 2D sagittal (linear array) and axial (transverse array) sectional imaging of the anterior and posterior compartments. Imaging is usually performed with the patient at rest, during maximal Valsalva maneuver and during squeeze test. The vascular pattern of the pelvic floor structures may also be assessed using color Doppler mode [21, 22]. Dressler et al. [13] reported from good to excellent repeatability and reproducibility of the measurements of the suburethral tape location obtained by pelvic ultrasound performed with transvaginal end-fire probe. This demonstrates that for experienced operators which have no access to dedicated pelvic floor equipment, conventional gynecological transducers provide adequate results.

5.6

T  hree-Dimensional Endovaginal Ultrasound (3D EVUS)

Radial electronic transducer, electronic linear transducer, and rotational mechanical transducer provide a 360° view of the pelvic floor [6, 21]. However with the radial electronic transducer, the 3D acquisition is freehand, whereas with the linear electronic transducer and the mechanical transducer, the 3D acquisition is automatic. The mechanical probe has an internal motorized system that allows an acquisition of 300 aligned transaxial 2D images over a distance of 60 mm in 60 s, without any movement of the probe within the tissue. The set of 2D images is reconstructed instantaneously into a high-resolution 3D image for real-time manipulation and volume rendering. However the operator may individually adjust the distance of acquisition, slice thickness, and time of acquisition which is subsequently reflected in the image quality obtained (shorter time and thicker slice thickness are related to lower quality of the image). An advantage of 3D compared with 2D mode is the opportunity to obtain sagittal, axial, coronal, and any desired oblique sectional image. The 3D volume can also be archived and further post-processed for offline analysis on the ultrasonographic system or on a PC with the help of dedicated software. The methodology of 2D and 3D EVUS was described by Santoro and Wieczorek [6, 7, 14, 21]. Detailed ultrasound morphology of the urethra and its vasculature was described by Wieczorek et al. [7, 12, 22–24] and Lone et al. [25, 26]. Shobeiri et al. [27] described the ultrasonographic anatomy of levator ani subdivisions, whereas Santoro et  al. [28] described the perineal body anatomy.

“Small” volumetric

Range of frequencies Number of elements Image field Acoustic aperture

Primary purpose

Range of frequencies Number of elements Image field Acoustic aperture RAB6-D GE Medical

Primary purpose

Type of probe Example transducer “Large” RAB 4–8 volumetric GE Medical

Abdominal Obstetrics, urology, and pediatrics 2–8 MHz 192 90° × 85° 62.2 × 34.0 mm

Abdomen, Pediatric, obstetric, and gynecology 2–8 MHz 192 70° × 85° 63.6 × 37.8 mm

b

(b) Volumetric “abdominal/obstetrical” transducer—tomographic imaging

a

(continued)

Example ultrasound 2D TPUS image Fig. 5.5  Three-dimensional image of pelvic floor structures by 3D TPUS visualized with different types of transducers. (a) Volumetric “abdominal/obstetrical” transducer—multiplanar reconstruction and surface mode (A anal canal, B bladder, SP symphysis pubis, U urethra)

Table 5.3  Types and characteristic of volumetric transducers used in 3D/4D TPUS examinations 5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound 81

Matrix

Endovaginal volumetric

Range of frequencies Number of elements Image field Acoustic aperture

Primary purpose

RSM 5-14 GE Medical

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

RIC5-9-D GE Medical

Table 5.3 (continued)

Gynecology and urology Small parts, pediatrics, MSK Peripheral vascular 5–13 MHz 960 37.5 mm (B) × 30° (Volume scan) 54.3 mm × 50.5 mm

Obstetrics, gynecology, and urology 4–9 MHz 192 179° × 120° 22.4 × 22.6 mm

c

(c) Volumetric endovaginal transducer—multiplanar reconstruction and surface mode

82 A. P. Wieczorek et al.

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound

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Table 5.4  Types and characteristic of transducers used in 2D/3D EVUS and 2D/3D EAUS examinations Type of probe Example transducer 20R3 High-­ BK-Medical resolution 360°

Example ultrasound 3D EVUS/EAUS image 38

,4

2

54

Fig. 5.6  Three-dimensional image of pelvic floor structures by endovaginal (3D EVUS) and endoanal (3D EAUS) approaches visualized with different types of transducers. High-resolution 360° transducer: (a) 3D EVUS, (b, c) 3D EAUS. A anus, ES external sphincter, IS internal sphincter, R rectum, SP symphysis pubis, U urethra, V vagina

17

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

EVUS EAUS 9–16 MHz 1 360° NA

a

b

c (continued)

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Table 5.4 (continued) Type of probe Example transducer Linear X14L4 360° BK-Medical

Example ultrasound 3D EVUS/EAUS image (d, e) 3D EVUS with linear 360° transducer 2

36

5 55

15

36

θ16.4

Primary purpose Range of frequencies Number of elements Image field Acoustic aperture

EVUS EAUS 4–14 MHz 192 360° 65 × 5.5 mm

d

e (f) 3D EAUS with linear 360° transducer. A anal canal, B bladder, ES external sphincter, IS internal sphincter, PB perineal body, R rectum, SP symphysis pubis, U urethra, V transducer into vagina

f (continued)

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound

85

Table 5.4 (continued) Type of probe Example transducer Linear E14CL4b biplane BK-Medical 2,5

35

F 20

Primary purpose Range of frequencies Number of elements Image field

Acoustic aperture

5.7

F 32,4

Example ultrasound 3D EVUS/EAUS image Fig. 5.7  Axial section of the urethra visualized with linear biplane transducer. (a) Elastographic image of the urethra during Valsalva maneuver; (b) compare B-mode gray scale of the urethra image shown simultaneously to the elastographic image. U urethra; white arrow, rhabdosphincter muscle at rest (blue, soft); yellow arrow, longitudinal smooth muscle during contraction/bladder neck opening (red, hard)

Urology/prostate Prostate elastography 4–14 MHz 128 transverse 192 sagittal 138°/178° transverse 65 mm + 2 × 15° sagittal 23 × 5.5 mm transverse 65 × 5.5 sagittal

T  wo-Dimensional Endoanal Ultrasound (2D EAUS)

Endoanal ultrasound (EAUS) includes examination of the anal canal (endoanal ultrasound—EAUS) and of rectal region (endorectal ultrasound—ERUS). EAUS is performed with high-multifrequency, 360° rotational mechanical transducer, linear electronic transducer, or a radial electronic transducer, as described above for EVUS (2052, 20R3, 8838; E14CL4b BK-Medical). During examination, the patient may be placed in a dorsal lithotomy, left lateral or prone position. However, irrespective of patient position, the transducer should be rotated so that the anterior aspect of the anal canal is superior (12 o’clock position) on the screen: the right lateral aspect is to the left (9 o’clock), the left lateral aspect is to the right (3 o’clock), and the posterior aspect is inferior (6 o’clock) [6]. The recording of data should extend from the upper aspect of the puborectalis muscle to the anal verge [6, 29] (Table 5.4, Fig. 5.6). The high-resolution 360° transducers provide minimal slice thickness of 1  mm. The rotating crystal moves mechanically, and the operator can decide individually and adjust the distance scanned up from a minimum of 0 mm to a maximum of 60  mm using two buttons on the probe. The number and the depth of the focal zone/zones can be also manually adjusted by the user. The location of the buttons directly on the probe enables manipulation of the image without the need of changing the position of the transducer introduced endoanally, which is mostly important in rectal examination performed with a distension of rectal ampulla by a water-filled balloon. For such type of examination, a special

ring is applied to the probe handle, sealing the probe cover. The cover is filled with a variable amount of degassed water (approx. 60–100  ml) depending on the compliance of the examined section of the bowel. Using a dedicated rectoscope (slightly wider than the standard one), the probe can be inserted to a depth of 20  cm enabling examination of the deeply located lesions and precise assessment of the depth/ extend of the infiltration of tumors (Fig. 5.8) as well as precise

Fig. 5.8  3D ERUS. High-resolution 360° transducer. Examination performed with degassed water-filled balloon. A ampulla recti, B water balloon, T tumor

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assessment of very high fistulas. In the evaluations of fistulas, it is helpful to use hydrogen peroxide (approx. 2–5 ml) as a contrast medium that is injected through the external opening. Hydrogen peroxide allows precise visualization of the anatomy of the fistulas and helps to differentiate active tract from scar tissue. Similar technical solution with the opportunity of examining the anorectal region is offered with the transrectum composite probe type UST-678 (Hitachi, Japan). This probe enables scanning with the field of view of 120° (convex array), on the length of 60 mm (linear array). The frequency of the transducer can be adjusted from 3 to 9 MHz (convex array) and from 4 to 10 MHz (linear array). A balloon cover filled with water and fixed by the dedicated rubber band to the transducer allows examination of the rectal ampulla. Compared to the transducers previously described, the new linear electronic probe (type 8838, BK-Medical), frequency of 4–4 MHz, or its recent version X14L4 offers similar imaging opportunities (only in sagittal section) (360°, length of scanning from 0 to 60 mm length, 1 mm minimal slice thickness, manual adjustment of focal zones) with full measurement capabilities as the probes above but with higher resolution. The limitation of this probe is lack of a system for the distension of rectal ampulla by a water-filled balloon.

5.8

Three-Dimensional Endoanal Ultrasound (3D EAUS)

The methodology of 2D and 3D EAUS was described by Santoro et al. [6, 29]. The mechanical rotational transducer or the electronic linear transducer allows automatic 3D acquisition without movement of the probe relative to the tissue under investigation. After the dataset has been recorded, it is possible to interrogate the dataset in 3D, with multiplanar imaging [6]. The 3D image may be rotated, tilted, and sliced to allow the operator to vary infinitely the different section parameters and to visualize and measure distance, area, angle, and volume in any plane [29]. There are also tools to change the transparency of the dataset (volume rendering) [29].

5.9

Conclusions

Ultrasound technology provides a variety of transducers with high range of frequencies, different acoustic aperture, shape, size, and philosophy of beam formation. Pelvic floor ultrasound can be performed both with relatively simple ultrasound equipment used for abdominal or obstetrical purposes and with high-end scanners dedicated for urology or proctology. Technical achievements together with Doppler modes,

elastography, as well as the opportunity of ultrasound/MR fusion allow for assessment of female pelvic floor structures of all three compartments in 2D, 3D, and 4D techniques. Different anatomical approaches such as TPUS, EVUS, EAUS, and abilities of post-processing give the clinicians diagnostic power to understand the anatomy and anatomical abnormalities. Ultrasound can be used as an extension for clinically obtained dose of information and its better understanding but can be also employed for qualification for certain surgical procedures. Another advantage of using ultrasound is the opportunity of detailed diagnosis of postsurgical complications and explanation of the causes of surgical failure. All these factors make ultrasound the modality which should be considered as the first choice imaging technique in diagnostics of female pelvic floor disorders.

Take-Home Messages

• Pelvic floor ultrasound can be performed with a variety of transducers and anatomical approaches. • The knowledge of capabilities and limitations of each type of transducer, anatomical access, and post-processing options is crucial for performing pelvic floor ultrasound in a proper way and making reliable diagnosis. • Modern ultrasound technologies such as Doppler ultrasound, elastography, three- and four-­ dimensional ultrasound, and tomographic ultrasound imaging (TUI) can enhance significantly the quality of information obtained; however good knowledge of the technical aspects of the techniques and their pros and cons is essential.

References 1. Davila GW. Concept of the pelvic floor as a unit. In: Davila GW, Ghoniem GM, Wexner SD, editors. Pelvic floor dysfunction. A multidisciplinary approach. London: Springer-Verlag; 2006. p. 3–6. 2. DeLancey JOL. The hidden epidemic of pelvic floor dysfunction: achievable goals for improved prevention and treatment. Am J Obstet Gynecol. 2005;192:1488–95. 3. Haylen BT, de Ridder D, Freeman RM, Swift SE, Berghmans B, Lee J, Monga A, Petri E, Rizk DE, Sand PK, Schaer GN.  An International Urogynecological Association (IUGA)/ International Continence Society (ICS) joint report on the terminology for female pelvic floor dysfunction. Int Urogynecol J. 2010;21:5–26. 4. Bliss D, Mimura T, Berghmans B, Bharucha A, Chiarioni G, Emmanuel A, Maeda Y, Northwood M, Peden-Mcalpine C, Rafiee H, Rock-Wood T, Santoro GA, Taylor S, Whitehead W. Assessment

5  Principles and Technical Aspects of Integrated Pelvic Floor Ultrasound and conservative management of faecal incontinence and quality of life in adults. In: Abrams P, Cardozo L, Wagg A, Wein A, editors. Incontinence. 6th ed. Bristol: ICUD-ICS; 2017. p. 1993–2085. 5. Sultan AH, Monga A, Lee J, Emmanuel A, Norton C, Santoro G, Hull T, Berghmans B, Brody S, Haylen BT.  An International Urogynecological Association (IUGA)/International Continence Society (ICS) joint report on the terminology for female anorectal dysfunction. Int Urogynecol J. 2017;28:5–31. 6. Santoro GA, Wieczorek AP, Dietz HP, Mellgren A, Sultan AH, Shobeiri SA, Stankiewicz A, Bartram C. State of the art: an integrated approach to pelvic floor ultrasonography. Ultrasound Obstet Gynecol. 2011;37:381–96. 7. Wieczorek AP, Stankiewicz A, Santoro GA, Wozniak MM, Bogusiewicz M, Rechberger T. Pelvic floor disorders: role of new ultrasonographic techniques. World J Urol. 2011;29:615–23. 8. Tole NM, Ostensen H, World Health Organization. Diagnostic Imaging and Laboratory Technology Team. Basic physics of ultrasonic imaging. In: Tole NM; editor. Ostensen,Harald: World Health Organization. 2005. P. 95. 9. Brunner E. How ultrasound system considerations influence front-­ end component choice. Analog Dialogue. 2002;36:1–3. 10. Lee Y, Kang J, Yoo Y.  Automatic dynamic range adjustment for ultrasound B-mode imaging. Ultrasonics. 2015;56:435–43. 11. Starkoff B.  Ultrasound physical principles in today’s technology. Australas J Ultrasound Med. 2014;17:4–10. 12. Wieczorek AP, Wozniak MM, Stankiewicz A, Santoro GA, Bogusiewicz M, Rechberger T. 3-D high-frequency endovaginal ultrasound of female urethral complex and assessment of inter-­ observer reliability. Eur J Rad. 2012;81:e7–e12. 13. Dresler MM, Kociszewski J, Wlazlak E, Pedraszewski P, Trzeciak A, Surkont G. Repeatability and reproducibility of measurements of the suburethral tape location obtained in pelvic floor ultrasound performed with a transvaginal probe. J Ultrasonograph. 2017;17:101–5. 14. Santoro GA, Wieczorek AP, Shobeiri SA, Mueller ER, Pilat J, Stankiewicz A, Battistella G.  Interobserver and interdisciplinary reproducibility of 3D endovaginal ultrasound assessment of pelvic floor anatomy. Int Urogynec J Pelvic Floor Dysfunct. 2011;22:53–9. 15. Hainsworth AJ, Solanki D, Hamad A, Morris SJ, Schizas AM, Williams AB. Integrated total pelvic floor ultrasound in pelvic floor defaecatory dysfunction. Colorectal Dis. 2017;19:O54–65. 16. Dietz HP.  Ultrasound imaging of the pelvic floor. Part I: two-­ dimensional aspects. Ultrasound Obst Gynecol. 2004;23:80–92. 17. Shek KL, Dietz HP. Assessment of pelvic organ prolapse: a review. Ultrasound Obstet Gynecol. 2016;48:681–92.

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18. Dietz HP, Severino M, Kamisan Atan I, Shek KL, Guzman RR. Warping of the levator hiatus: how significant is it? Ultrasound Obstet Gynecol. 2016;48:239–42. 19. Dietz HP, Bernardo MJ, Kirby A, Shek KL. Minimal criteria for the diagnosis of avulsion of the puborectalis muscle by tomographic ultrasound. Internat Urogynecol J. 2011;22:699–704. 20. Dietz HP.  Ultrasound imaging of the pelvic floor. Part II: three-­ dimensional or volume imaging. Ultrasound Obstet Gynecol. 2004;23:615–25. 21. Santoro GA, Wieczorek AP, Stankiewicz A, Wozniak MM, Bogusiewicz M, Rechberger T. High-resolution three-dimensional endovaginal ultrasonography in the assessment of pelvic floor anatomy: a preliminary study. Internat Urogynecol J Pelvic Floor Dysfunct. 2009;20:1213–22. 22. Wieczorek AP, Wozniak MM, Stankiewicz A, Bogusiewicz M, Santoro G, Rechberger T, Scholbach J. The assessment of normal female urethral vascularity with Color Doppler endovaginal ultrasonography: preliminary report. Pelviperineology. 2009;28:59–61. 23. Wieczorek AP, Wozniak MM, Stankiewicz A, Santoro GA, Bogusiewicz M, Rechberger T, Scholbach J. Quantitative assessment of urethral vascularity in nulliparous females using high-frequency endovaginal ultrasonography. World J Urol. 2011;29:625–32. 24. Wieczorek AP, Wozniak MM.  Endovaginal urethra and bladder imaging. In: Shobeiri SA, editor. Practical pelvic floor ultrasonography. A multicompartmental approach to 2D/3D/4D ultrasonography of pelvic floor. New York: Springer-Verlag; 2014. p. 91–113. 25. Lone F, Thakar R, Wieczorek AP, Sultan AH, Stankiewicz A.  Assessment of urethral vascularity using 2D color Doppler high-frequency endovaginal ultrasonography in women treated for symptomatic stress urinary incontinence: 1-year prospective follow-up study. Int Urogynecol J. 2016;27:85–92. 26. Lone F, Sultan AH, Stankiewicz A, Thakar R, Wieczorek AP.  Vascularity of the urethra in continent women using colour Doppler high-frequency endovaginal ultrasonography. Springerplus. 2014;3:619. 27. Shobeiri SA, Leclaire E, Nihira MA, Quiroz LH, O’Donoghue D.  Appearance of the levator ani muscle subdivisions in endovaginal three-dimensional ultrasonography. Obstet Gynecol. 2009;114:66–72. 28. Santoro GA, Shobeiri SA, Petros PP, Zapater P, Wieczorek AP.  Perineal body anatomy seen by three-dimensional endovaginal ultrasound of asymptomatic nulliparae. Colorectal Dis. 2016;18:400–9. 29. Santoro GA, Fortling B.  The advantages of volume rendering in three-dimensional endosonography of the anorectum. Dis Colon Rectum. 2007;50:359–68.

6

Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy Hans Peter Dietz

Learning Objectives

• To appreciate the basic methodology of translabial/ perineal ultrasound using 2D and 3D/4D systems. • To understand the basic functional anatomy of the female pelvic floor. • To recognize normal anatomical structures both in the midsagittal and the axial plane. • To identify the levator ani and the anal sphincter in tomographic imaging.

6.1

Introduction

Ultrasound is the primary imaging method in gynecology and commonly used in urology and colorectal surgery. Hence it is not surprising that it is increasingly popular in the imaging assessment of pelvic floor anatomy. This development is long overdue, seeing that pathophysiology and etiology of many pelvic floor conditions are still poorly understood at present. The evaluation of urethral and paraurethral anatomy and pelvic organ mobility has become easier due to recent technological developments [1]. The same applies to the assessment of defecatory dysfunction [2]. The advent of 3D ultrasound now allows access to the axial plane, and 4D ultrasound enables the observation of function in the form of maneuvers such as cough, Valsalva, and pelvic floor muscle contraction [3]. Tomographic techniques are increasingly used for the assessment of birth trauma to levator ani [4] and anal sphincter muscles [5] which will become a key performance indicator of obstetric services and change maternity services delivery worldwide [6]. Other techniques such as endovaginal and endo-anal ultrasound have been used in the investigation of pelvic floor H. P. Dietz (*) Sydney Medical School Nepean, University of Sydney, Sydney, NSW, Australia e-mail: [email protected]

disorders, but this chapter will exclusively cover translabial or transperineal ultrasound which, for the sake of simplicity, the author calls “pelvic floor ultrasound.” This modality is unique in that it allows a comprehensive assessment of pelvic floor structures in one single, noninvasive investigation of at most 10  min duration. It can replace video cystourethrography, magnetic resonance imaging, defecation proctography, and endo-anal ultrasound in women suffering from symptoms of lower urinary tract dysfunction, prolapse, obstructed defecation, and fecal incontinence, using systems almost universally available. Chapter 48 will cover pathological findings, while this chapter deals with normal anatomy. The definition of “normal” is fundamental to the practice of medicine. Without “normal” there is no “abnormal” and no basis for therapeutic intervention. This is particularly true in a newly developed diagnostic field such as pelvic floor ultrasound. Overdiagnosis, that is, the risk of misinterpreting findings as abnormal that are in fact within the normal range, is always a danger. Hence I will try to define “normal,” both in terms of static anatomy and in terms of “dynamic anatomy,” i.e., function, as far as it applies to urogynecological conditions.

6.2

Basic Technique

The basic requirements for pelvic floor imaging include a B-mode capable two-dimensional (2D) ultrasound system with cine-loop function, a 3.5–6  MHz curved array transducer, and a videoprinter. However, to allow for the full scope of diagnostic capabilities, 3D/4D imaging is indispensable. For over 20 years, Voluson-type systems have been the market leaders in the field of 3D/4D ultrasound. Consequently most of the literature on 3D pelvic floor ultrasound is based on the utilization of such systems, even if most manufacturers now offer equipment that can be employed usefully. Any 4D capable ultrasound system with abdominal 4D transducers in an obstetric imaging unit

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_6

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should be suitable for pelvic floor ultrasound, provided the aperture angle is 70° or better and provided the acquisition angle can be set to at least 70°. For severe prolapse and hiatal ballooning, aperture and acquisition angles of 80–90° can become necessary. The examination is performed in dorsal lithotomy with the hips flexed and slightly abducted or alternatively in the standing position. Asking the patient to place her heels close to the buttocks will result in an improved pelvic tilt. A full bladder or bowel may prevent full development of pelvic organ prolapse [7]. Therefore, imaging is best performed after bladder emptying; otherwise bladder filling should be specified. Occasionally, catheterization will be necessary. For preparation of the probe, it is covered with either a powder-free glove, condom, or thin plastic wrap for hygienic purposes, after covering the transducer surface with ultrasound gel and while avoiding air bubbles between transducer surface and glove. The probe is then placed on the perineum after parting the labia, producing a midsagittal view showing urethra and anal canal at the same time (see Fig. 6.1). Tissue hydration and scar tissue can affect visibility, but obesity is virtually never a problem. Conditions are best in pregnancy and poorest in the senium. The probe can be placed firmly without causing significant discomfort, unless there is marked atrophy or vulvitis. During a Valsalva it is essential, however, not to exert undue pressure to allow full development of pelvic organ descent. After scanning the probe is mechanically cleaned, followed by disinfection with alcoholic wipes. Sterilization as for intracavitary transducers is usually considered unnecessary. On translabial ultrasound, pelvic floor structures are initially shown in the midsagittal plane [1]. This orientation, shown in Fig. 6.1, allows imaging of the urethra, the bladder neck and trigone, the cervix, the rectal ampulla, and the anal canal. While there is no universal consensus on image orien-

H. P. Dietz

tation, the first published translabial images had the perineum at the top and the symphysis pubis on the left [7], and this is still the most commonly used orientation. It is particularly convenient when using three-dimensional (3D)/four-­ dimensional (4D) systems as shown in Fig. 6.2. The top left image represents the midsagittal plane, with the bottom right showing a rendered volume of the levator hiatus. The advent of 3D/4D imaging has given easy, noninvasive access to the axial plane allowing imaging of the caudal part of the levator ani muscle and the opening in this muscular plate, the levator hiatus (Fig. 6.2). The levator hiatus is an important part of the birth canal and the largest potential hernial portal in the human body. It is of central importance in the pathophysiology of female pelvic organ prolapse (POP), a highly prevalent condition that may require surgery at least once during the lifetime of 10–20% of the female population [8, 9]. POP is best understood as a hernia through the levator hiatus. In childbirth the hiatus is distended massively [10], and the limiting structure, the puborectalis muscle, runs a substantial risk of permanent damage, either due to irreversible overdistension or due to actual disruption in the shape of avulsion, i.e., disconnection from its insertion on the os pubis [11, 12]. Both forms of trauma seem to be risk factors for POP and POP recurrence after reconstructive surgery [13– 16]. Hence, imaging of the levator hiatus and puborectalis muscle in axial plane images is becoming increasingly popular. Most recently, the coronal plane has attracted increasing interest as it provides excellent views of the anal canal, especially the anal sphincter complex, and volume acquisition is optimally performed in the coronal plane, as shown in Fig. 6.3. The increasing prevalence of anal sphincter trauma, especially in jurisdictions with rising forceps rates such as in the UK and Australia [17], makes the development of this method particularly timely and important.

Urethra

vagina and canal

symphysis

bladder

Fig. 6.1  Transducer placement on the perineum (left) with schematic representation of the resulting midsagittal field of vision. Right image adapted from [1], with permission

6  Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy

Fig. 6.2  Standard representation of female pelvic floor structures on translabial/perineal ultrasound. The midsagittal plane is shown in (a), the coronal in (b), the axial in (c). A rendered volume (i.e., the semitransparent representation of all pixels in the “region of interest,” the box seen in

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a–c) in the axial plane is given in (d). Often, a and d are of the most interest and are combined, leaving out b and c. In d the patient’s right-hand side is represented on the left, as if the pelvic floor was viewed from below. L levator ani, S symphysis pubis. From [74], with permission

transversus perinei

perineum

IAS EAS

ischiorectal fossa

a

b

anal mucosa

Fig. 6.3  Transducer placement for exo-anal sphincter imaging (left), and schematic illustration of imaged structures in the resulting coronal or transverse plane (right). EAS external anal sphincter, IAS internal anal sphincter. From [32], with permission

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Live anatomy of pelvic floor structures as observed on real-time imaging commonly bears only limited resemblance to textbook illustrations. The “urogenital diaphragm” is a figment of the imagination to those performing translabial ultrasound. The levator plate appears very different from textbook illustrations derived from cadaver dissection, and the anal canal is longer and slimmer in reality than in drawings derived from endo-anal ultrasound which necessarily dilates and shortens this structure. Common forms of prolapse such as cystocele and rectocele appear rather different from textbook illustrations when imaged live. Given that cadaver dissection and illustrations derived from dissection are frequently misleading, it seems a­ ppropriate to use this chapter to describe the normal anatomy of the pelvic floor as seen on 3D/4D pelvic floor ultrasound.

6.3

 he Anterior Compartment: Urethra T and Bladder Base

6.3.1 The Urethra The female urethra is a muscular tube of about 3–3.5 cm in length, made up principally of a smooth muscle layer (the longitudinal smooth muscle of the urethra) and the striated urethral sphincter, which surrounds the smooth muscle like an elongated, spindle-shaped torus. At rest the smooth muscle is hypoechoic, and the striated muscle hyperechogenic, as seen in Fig. 6.4. The rhabdosphincter is better appreciated in the axial plane where it is apparent as a hyperechoic ring

a

Fig. 6.4  The urethra as seen on translabial 4D ultrasound. The midsagittal plane is on the left (a). Small arrows show the external meatus at the top, and the internal urethral meatus at the bottom. Large arrows

shape; in the midsagittal plane, it is harder to see due to the echogenicity of retropubic fibrofatty tissue. Echogenicity of smooth and striated urethral muscle changes with the angle of the incident beam, i.e., the angle between urethra and transducer. On Valsalva the urethra frequently rotates around the symphysis pubis, changing the angle between urethral structures and the incident beam; and the hypoechogenic stripe of urethral smooth muscle seems to disappear (Fig. 6.5). If the urethra rotates more than 90°, it may “reappear” once the smooth muscle of the proximal urethra is again more parallel with the incident beam, which often occurs in severe cystocele.

6.3.2 Paraurethral Tissues This muscular tube is anchored to the pelvic sidewall or, rather, the os pubis. This anchoring is highly variable, with anywhere between 1 and 7 distinct structures [18] made up of varying amounts of connective tissue and smooth muscle fibers. These structures are generally termed the “pubourethral ligaments” and can be visualized in the coronal plane (Fig. 6.6). The functional effect of those ligaments is commonly observed in the form of urethral kinking and a demonstration of the concept of pressure, or rather, force transmission at times of increased intra-abdominal pressure. Tethering of the urethra to the os pubis is clearly important for urinary stress continence [19]. Figure 6.7 shows marked urethral kinking, which is common in anterior compartment prolapse.

b

indicate the urethral rhabdosphincter which appears as two hyperechoic stripes on the left and as a hyperechoic ring shape on the right (b)

6  Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy

a

Fig. 6.5  Determination of bladder neck descent and retrovesical angle: Ultrasound images show the midsagittal plane at rest (a) and on Valsalva (b). A anal canal, B bladder, L levator ani, R rectal ampulla, S symphysis pubis, U urethra, Ut uterus, V vagina. The images demonstrate the

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b

measurement of distances between interior symphyseal margin and bladder neck (vertical, x; horizontal, y) and the retrovesical angle at rest (rva-r) and on Valsalva (rva-s). From [53], with permission

which can be followed laterally to reach the ureteric orifices. The “trigone” or bladder base is formed by thickened smooth muscle between the internal meatus and the two ureteric orifices. If desired, color Doppler can be used to demonstrate ureteric patency. The detrusor muscle (Fig. 6.8) is usually thinner than the trigone itself. Its thickness is associated with symptoms of the overactive bladder and with urodynamic detrusor overactivity. Under 50  ml bladder filling, 5  mm is regarded as the limit of normal [20–22], but DWT has poor test characteristics for urge urinary incontinence and detrusor overactivity [22, 23].

6.4

Fig. 6.6  Coronal plane imaging showing the length of the urethra (large arrow to large arrow) and multiple linear structures (small arrows) investing the urethral rhabdosphincter surrounding the hypoechogenic longitudinal smooth muscle/vascular plexus/mucosa of the urethra

6.3.3 The Bladder Neck and Trigone The bladder neck, i.e., the urethrovesical junction or internal meatus of the urethra, is visible as a “notch” or a slight dimple on translabial imaging. Approximately 1–2 cm dorsal to this dimple one will find the inter-ureteric ridge,

The Fornices

The anterior vaginal fornices have been of interest as they are clinically easily accessible for the assessment of paravaginal or bladder fascia, although clinical examination seems of limited validity and reproducibility [24, 25]. Often, an abnormal fornix means not just fascial damage, but rather much more severe trauma in the shape of levator avulsion. However, there may be a subset of women in whom the levator is intact but the paravaginal fascia is detached from the arcus tendineus fasciae pelvis, and this may be evident as a loss of forniceal definition [26]. On axial plane imaging, the fornices are plainly visible, especially in their lower reaches (Fig. 6.9). Tomographic imaging on Valsalva seems to be useful in assessing the fornices more cranially (Fig. 6.10).

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Fig. 6.7  Midsagittal imaging at rest (left) and on Valsalva (right) in patient with grade II cystocele. There is marked urethral kinking at mid-­ urethral level, i.e., at the location of urethral tethering to the pelvic sidewall. The small arrows indicate external and internal urethral meatus,

and the large arrow the location of urethral kinking. The variability of urethral echogenicity relative to the angle between urethra and incident beam is also clearly apparent

a

b

c

d

Fig. 6.8  Measurement of bladder wall thickness at the dome in four women with non-neuropathic bladder dysfunction. In all cases shown in images (a–d) residual urine is well below 50 ml. The limit of normality is usually taken to be 5 mm. From [74], with permission

6  Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy

6.6

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The Posterior Compartment

6.6.1 N  ormal Anatomy in the Midsagittal Plane The standard midsagittal orientation is defined by both anal canal and urethra being visible in one plane which shows the rectal ampulla, often stool-filled, the anorectal angle, and the anal canal, a tubular structure about 4.5  cm in length. The anorectal junction is easy to identify, either due to the hyperechoic nature of stool or bowel gas in the rectal ampulla or due to the iso-echoic anal mucosal folds occupying the space between the two hypoechogenic linear strips of the internal anal sphincter (IAS).

6.6.2 The Perineal Body/Transversus Perinei

Fig. 6.9  The appearance of puborectalis muscle and lateral vaginal fornices in a rendered volume in the axial plane. The two arrows indicate the fornices. From [75], with permission

6.5

 he Central Compartment: Uterus T and Vault

The anteverted uterus is visible above the bladder roof, with the endometrial stripe identifiable as a near-horizontal line that can be followed to the cervical canal (Fig. 6.11). In retroversion the cervix may be harder to identify, and small bowel covers the bladder roof. The cervix may be shadowed by rectal ampulla, if it is filled with stool and/or gas. A small, atrophic uterus is sometimes very difficult to locate, especially if high. As the myometrium is iso-echoic and very similar in echogenicity to the vaginal walls, identifying the uterus can be a challenge for the beginner, but often nabothian follicles help in identifying the cervix. In general, ­moving images are easier to interpret, and this is especially true for the uterus. In older women and in an axial uterus, the myometrium can cause acoustic shadowing due to scattering of ultrasonic energy, and this may also be the case with fibroids, especially if calcified. After hysterectomy, the space usually occupied by the uterus is filled by peristalsing small bowel. The vault itself may at times be easy to locate (Fig.  6.12); at other times it will be hidden by a full rectum unless the vault descends beyond the hymen.

Ventrocaudal to the anal canal, one can locate the triangular iso-echoic structure of the perineal body, which is highly variable in dimensions even in nulliparous women [27]. It is bounded by the vagina ventrally (outlined more clearly after a vaginal examination due to bubbles caught in the vaginal rugae) and the external anal sphincter dorsally. Its most distinct structure, the transversus perinei muscle, is also very variable but often identified in the coronal plane (Fig. 6.13) where, on imaging of the anal sphincter, it often appears as a linear or wing-like structure, the fibers of which may contribute to the more cranial aspects of the external anal sphincter (EAS), occasionally causing a hose clamp-like appearance.

6.6.3 The Rectovaginal Septum The rectovaginal septum (RVS) is the cranial continuation and condensation of the fibromuscular perineal body and sometimes visible on perineal imaging; see Fig. 6.14. It is a fascia that prevents herniation of the rectal ampulla into the lower vagina, given that there is a substantial pressure differential between the former (intra-abdominal pressure) and the latter (atmospheric pressure) [28]. Dynamic testing with a Valsalva maneuver is required to detect RVS defects as static appearances do not seem to be predictive of function [29]. Such defects are very common, even in nulliparae [30], and represent the only form of prolapse that is clearly associated with obesity [31].

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Fig. 6.10  Fornices are assessed by tomographic ultrasound, with eight slices obtained from the plane of minimal hiatal dimensions to 12.5 mm above this plane. In the figure, the fornices are all intact (i.e., showing a

Fig. 6.11  Anteverted uterus as seen in the midsagittal plane, with the corpus resting on the roof of the empty bladder. The cervix is just visible cranial to the rectal ampulla which often obscures a normally situated cervix. B  bladder, POD  pouch of Douglas, R  rectal ampulla, S symphysis pubis, V vagina. The uterus is outlined by dots; both cervix and endometrial echo are clearly visible

H. P. Dietz

triangular appearance, with the apex aiming toward the os pubis) and indicated with (∗). From [26], with permission

Fig. 6.12  Appearance of a normal, well-supported vaginal vault in patient with stage 2 cystocele. The position of bladder (B), vault (V), and rectal ampulla (R) are measured against the inferoposterior margin of the symphysis pubis (S)

6  Transperineal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy

Fig. 6.13  The echogenicity and appearance of the perineum vary greatly even in vaginally nulliparous women. However, in the latter it is often possible to identify a hyperechoic transverse structure superficial to the external anal sphincter (EAS); see those tomographic transverse

a

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slices of the perineum. Sometimes fibers seem to be completely separate from the EAS (top row; fat oblique arrows); at other times some fibers clearly merge with the EAS (bottom row; thin vertical arrows)

b

c

Fig. 6.14  Appearance of a presumably intact rectovaginal septum on 3D pelvic floor imaging in orthogonal planes (a–c). Arrow indicates the location of the septum which appears as a linear hyperechogenic structure in the midsagittal (a) and axial (c) plane

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6.6.4 T  he Anal Canal on Tomographic Imaging The anal canal and rectal ampulla are conveniently imaged in the midsagittal plane, but this is not the case for the anal sphincters. Traditionally, sphincter imaging is undertaken by endo-anal probes which provide a coronal plane view of the sphincters, visualizing them as donut- or target-shaped structures. On pelvic floor ultrasound, this requires rotation of the transducer to the coronal plane (see Fig. 6.3). Volume acquisition at 60–70° aperture and acquisition angle, with harmonics set to “high” and focal zones adjusted to sit at the depth of the area of interest, provides optimal imaging. A pelvic floor muscle contraction and adjustment of transducer pressure may also help to optimize resolutions. The distance between external anal sphincter and transducer surface is highly variable, not the least due to the state of the perineum, but is easily adjusted by holding the transducer at a rather steep angle

a

(more vertical than horizontal) and by varying the position of the transducer relative to the fourchette and anus. A view of the three sectional planes allows centering of the sphincter in the volume (Fig. 6.15). The anal canal should be horizontal in the B (midsagittal) plane and vertical in the C (transverse) plane, an orientation that helps identify the cranial extent of the EAS (Fig. 6.16) by locating the fascial plane between EAS and levator ani. The EAS is then imaged in tomographic slices, from above the EAS cranially to the subcutaneous EAS below the termination of the IAS caudally (Fig. 6.17) [32]. Depending on EAS length, which can vary from 8 to 35 mm in healthy individuals [33], the interslice interval may have to be set to anywhere from 1.5 to 5 mm. The cranial termination of the EAS is of importance for the reproducibility of slice location, and several factors may impact on the identification of this structure. Commonly, the ventral and dorsal aspects of the EAS show “rotational asymmetry,” that is, on average the EAS is slightly longer venb

c

Fig. 6.15  Imaging of the anal sphincters in cross-sectional planes. The a plane shows the typical donut appearance of the external anal sphincter (EAS, hyperechogenic) and the internal anal sphincter (IAS, hypoechoic) in the coronal plane. The standard midsagittal orientation is given in the

b plane, providing proof that the entire EAS is included in the volume. An oblique axial view is represented in the c plane and demonstrates that the anal canal is properly centered in the volume, i.e., seen as vertical in c. Reproduced with permission from [74]

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Fig. 6.16  A crucial step in translabial 4D sphincter imaging is the identification of the cranial limit of the external anal sphincter (EAS). This has to be obtained dorsally, at least in parous women, as the ventral aspect of the EAS may have been altered by birth trauma. The midsagit-

tal plane (usually given in the plane of an orthogonal representation as in Figure 6.16) allows the identification of the fascial plane between EAS and levator ani (arrows)

Fig. 6.17  Tomographic imaging of normal external and internal anal sphincters. The reference plane at the top left shows the midsagittal plane. Vertical lines indicate the location of eight coronal slices given in this figure. The most cranial slice (center top) is located above the external anal

sphincter (EAS) (left thick line in the reference image); the most caudad (bottom right) is placed below the internal anal sphincter (right thick line) in the reference image. As a result, the entire EAS should be covered in this tomographic representation. From [32], with permission

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Fig. 6.18  Occasionally, a prominent LMA (longitudinal muscle of the anus, indicated by arrows) may interfere with locating the cranial margin of the external anal sphincter (EAS), as evident in the midsagittal reference plane (slice 0) given on the top left of this tomographic repre-

sentation of the EAS. In such cases, the presumed “drop” shape of the EAS allows an estimation of its cranial limit, as given here. A small incidental hemorrhoid in slices 6–8 is indicated by (∗)

trally than dorsally, but the o­ pposite may also occur. Such asymmetry however does not seem to affect diagnostic performance [33]. Occasionally, it is possible to distinguish separate components of the EAS, with the most distal component often being more echogenic than the more proximal component of the muscle. This can lead to ambiguity in the identification of the cranial EAS margin, since two fascial planes rather than one may be identified. In this situation one needs to use the more proximal of the two planes. Another source of inter-­individual variation is the longitudinal muscle of the anus (LMA) which can be so thick as to resemble a cranial continuation of the EAS (Fig.  6.18). Sometimes the cranial termination of the EAS has to be extrapolated assuming a teardrop-shaped EAS. In practice, fortunately, these variations in anatomical appearance are of minor importance and unlikely to interfere with the diagnosis of sphincter trauma. Finally, it has to be mentioned that hemorrhoids can adversely affect imaging of the caudal aspects of the internal anal sphincter.

6.7

The Levator Ani Muscle

6.7.1 2D Imaging The puborectalis muscle can be seen on 2D translabial ultrasound in a parasagittal plane, with the transducer tilted from dorsomedially to ventrolaterally as in Fig.  6.19 [34]. The fibers of the puborectalis muscle may be followed from the os pubis to the anal canal; more cranial aspects of the levator usually show a different fiber direction.

6.7.2 Axial Plane Except when using obsolete side-firing vaginal transducers, access to the axial plane requires 3D/4D transducers, and this is the main reason why 4D imaging using abdominal volume probes has become such an asset to pelvic floor medicine over the last 10 years. Noninvasive, easy access to the

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c

caudal

dorsal

Symphysis pubis

Puborectalis muscle Pelvic sidewall

Fig. 6.19  Transducer orientation for imaging of the puborectalis muscle by translabial 2D ultrasound (left image), the resulting parasagittal view in a schematic drawing (center), and a normal muscle insertion on

a

b

ultrasound, with the hyperechogenic muscle fibers clearly visible (right). Adapted from [34], with permission

c

d

Fig. 6.20  Measuring hiatal dimensions as shown in a rendered volume (a, b) and in an oblique single axial plane (c, d). The region of interest (ROI) box in (a) (approx. 1.8 cm deep) is located between the symphysis pubis and the levator ani posterior to the anorectal angle. Image (b) represents a semitransparent view of all pixels in the ROI box on the left. The determination of hiatal dimensions using a single oblique axial

plane is shown in (c) and (d). The midsagittal plane on the left (c) demonstrates a line indicating the minimal sagittal diameter of the hiatus, i.e., the location of the oblique axial plane shown in (d). The dotted line in (b) and (d) represents hiatal area measurements (21.77 cm2 in (b), 23.05 cm2 in (d)). A anal canal, B bladder, L levator ani, R rectum, S symphysis pubis. From [36], with permission

axial plane has led to this method largely replacing MRI for imaging of levator trauma, especially in the form of tomographic imaging. In addition, the levator hiatus, the largest potential hernial portal in the human body, can be imaged either as a single plane [35] or with the help of a “rendered volume” [36], i.e., a semitransparent representation of all volume pixels in a given space, a technology that was originally developed for fetal imaging (see Fig. 6.20). Both methods are equally valid and repeatable and allow quantification of the “levator hiatus,” through which all forms of uterovaginal and anorectal prolapse can be seen to herniate out of the abdominal space. Due to the requirements of childbirth, the hiatus is much larger in women than in men and constitutes a structural and functional compromise. The levator ani may be congenitally overdistensible [35] and vary between individuals and also between ethnic groups [35, 37], but “ballooning” [38] is clearly more likely in vaginally parous women due to the fact that childbirth enlarges hiatal dimensions [39]. Hiatal area is strongly associated with pelvic organ descent [41] and moderately with prolapse recurrence after pelvic reconstructive surgery [16, 40, 41], which makes it potentially useful in the investigation of women with pelvic floor disorders (see Chap. 48).

6.7.3 Multislice Imaging Contrary to tomographic imaging with computed tomography (CT) and MRI, volume ultrasound produces not just a series of predetermined slices but rather a volume of information that allows us to alter slice orientation arbitrarily, after completion of an examination that takes only a few minutes. This has already been mentioned in the context of sphincter imaging, and it is equally useful in the assessment of the levator ani, the second major muscular structure to suffer permanent, clinically relevant damage in childbirth. The primary component of the levator ani complex, both in childbirth and for pelvic organ support, is the puborectalis muscle, a V-shaped structure that inserts on the inferior pubic ramus and the body of the os pubis bilaterally, coursing around the anorectal junction posteriorly where it defines the anorectal angle. Dorsally the anococcygeal raphe anchors it to the coccyx, which explains the commonly used alternative anatomical term, pubococcygeus [42]. Figure 6.21 shows a comparison of graphic representation, dissection, and sonographic representation of the intact puborectalis muscle. As opposed to the anal canal, we are unable to identify the cranial termination of the puborectalis muscle since it is in continuity with iliococcygeus and coccygeus muscles.

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Symphysis pubis

Symphysis pubis Pubic ramus

Pubic ramus Urethra Puborectalis Ischiorectal fossa Anus

Urethra Puborectalis Ischiorectal fossa Anus

Fig. 6.21  Representation of the puborectalis muscle in a drawing (left), on cadaver dissection (middle), and in a rendered volume, axial plane (right)

Fig. 6.22  Tomographic imaging of the puborectalis muscle in a nulliparous patient. The interstice interval is standardized to 2.5 mm. The central slice should show the most inferior aspect of the symphyseal gap, with the pubic rami appearing hyperechoic. The left central slice

2.5 mm caudad shows the pubic rami further apart. In the right central slice, the pubic rami are usually invisible due to acoustic shadowing. The arrows indicate the location of the pubic rami/the os pubis in the three central slices

Hence, we use the symphysis pubis as a reference structure, with the central slice placed approximately at the plane of minimal hiatal dimensions showing the symphysis pubis closing (Fig. 6.22). On tomographic representation, a 2.5 mm interslice interval allows coverage of the entire muscle [43].

While imaging on pelvic floor muscle contraction results in clearer images, assessment at rest may be equally valid [44, 45]. Using the minimum criterion of three central positive slices for the diagnosis of avulsion (see Chap. 48) [46], a false-positive diagnosis of avulsion seems unlikely [47]. In

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Fig. 6.23  Measurement of the levator-urethra gap (LUG) between the center of the urethra and the insertion of the puborectalis can be helpful in difficult cases. The limits of normal for this measurement have been defined as 25 mm in Caucasians and 23.6 mm in East Asians

difficult cases, measurement of the “levator-urethra gap” or LUG (Fig. 6.23) is useful [48–50]. An equivalent measurement, the levator-symphysis gap or LSG, has been described on MRI [51]. Cutoffs of 25  mm in Caucasians [48] and 23.6 mm in East Asians [49] have been defined as limits of normality. Function of the levator muscle can be ascertained by measuring muscle thickening and shortening on contraction, but indirect measures such as bladder neck lift or a reduction in hiatal dimensions are more practicable (see Fig.  6.24) and associated with other parameters of pelvic floor function [52, 53]. However, excellent pelvic floor functionality may not be evident in high-displacement measurements due to high resting tone and low tissue elasticity; sonographic measures of pelvic floor function may therefore not be superior to other measures of “strength” such as digital palpation or perineometry.

6.8

Static Versus Dynamic “Normality”

In clinical medicine, we commonly describe “static” normality which is quite often all there is to see and assess. An ovary looks “normal” or “not” – it has no “dynamic” normality. The pelvic floor is very different in this regard however. Most pelvic floor dysfunction is due to abnormalities of dynamic anatomy or function. Female pelvic organ prolapse, obstructed defecation, and stress urinary incontinence are disorders of functional anatomy—problems usually only become apparent once support structures are put under strain. The degree of strain is essential when it comes to measuring organ descent. Assessment of organ descent during a Valsalva maneuver performed in the supine position after bladder emptying [54] shows good test characteristics even if Valsalva pressure is not controlled [55], provided it is performed over a time period of at least 6 s [56] and provided levator co-activation is avoided [57]. Figure  6.25 demonstrates the importance of an optimal Valsalva maneuver. Assessment in the standing position will result in lower

organ location, but test characteristics are not improved compared to the supine position [58]. Normality of a quantitative measure such as organ descent can be defined in at least two ways: mathematically as the mean plus/minus two standard deviations and against symptoms arising from abnormal anatomy, i.e., symptoms of stress urinary incontinence in the case of urethral mobility and bladder neck configuration and symptoms of prolapse in the case of pelvic organ mobility. The mathematical approach to defining normality requires assessment of nulliparae, since pregnancy and childbirth are clearly the main environmental confounder. The second approach is appropriate in a population in which symptoms are common, e.g., in women who seek assessment or treatment for manifestations of pelvic floor dysfunction.

6.9

 rethral Mobility and Bladder Neck U Configuration

Excessive bladder neck descent or “hypermobility” has been commonly thought to be responsible for stress urinary incontinence (SUI) and urodynamic stress incontinence (USI), but “hypermobility” of the bladder neck is usually not defined numerically. Bladder neck descent as shown in Fig. 6.26 varies greatly in young, healthy, asymptomatic women [59] and is likely to be genetically determined [60]. It varies between ethnic groups [61–63] and is associated with stress urinary incontinence [64, 65]. This association between stress continence and bladder neck mobility is consistent with the concept of force or pressure transmission through “pubourethral ligaments” (see above): the more mobile the urethra, the greater the likelihood of poor function of these ligaments, and the poorer may be pressure transmission. This concept is supported by the observation that mobility at the locus of urethral tethering by pubourethral structures, the mid-urethra, is more strongly associated with continence than bladder neck mobility [19]. Recent work suggests a cutoff of 25 mm for the definition of “bladder neck hypermobility” [66]. However, its associa-

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Fig. 6.24  Three methods of determining the effect of a pelvic floor muscle contraction (PFMC) in the midsagittal plane, using 2D translabial ultrasound. The left-hand images in each pair (a, c, e) represent the resting state; the right-hand images show findings on PFMC. The top pair illustrates measurement of the levator plate angle (angle between symphyseal axis and levator hiatus in the midsagittal plane), the middle

H. P. Dietz

pair shows reduction of the anteroposterior diameter of the levator hiatus (LH (ap)), and the bottom pair illustrates bladder neck (BN) displacement on PFMC, analogous to the way BN descent is measured on Valsalva. LA levator ani, SP symphysis pubis. From [53], with permission

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Fig. 6.25  Levator co-activation as a confounder of Valsalva effort. The top row of images shows the midsagittal, and the bottom row the axial plane. a and d demonstrate findings at rest, b and e a suboptimal Valsalva confounded by pelvic floor muscle (PFM) activation, and c

and f a full, appropriate Valsalva. It is evident that, while there is some bladder neck descent on Valsalva in (b), the levator hiatus in e is in fact smaller than in (d), indicating a confounding PFM contraction. LA levator ani. Adapted from [57] with permission

tion with stress urinary incontinence is barely strong enough to use the “symptoms” approach to determining normality, with an area under the curve of 0.61 on ROC statistics, and the mathematical approach (mean + 2SD) in young Caucasian nulliparae would yield 35 mm [59]. The association between proximal urethral rotation and retrovesical angle on the one hand and stress continence on the other hand is even weaker, with AUCs below 0.6 [66]. However, an “open” retrovesical angle (RVA) of 140° or higher and proximal urethral rotation of >45° have been identified as the “anatomical correlate” of stress urinary incontinence since the 1960s [67, 68]. This has been confirmed on translabial ultrasound [66]; hence, it seems reasonable to define an RVA of  0.8) and good reliability for rhabdosphincter measurements (ICC > 0.6) in a group of 24 asymptomatic nulliparous females. The urethra is surrounded by connective tissue containing numerous ves-

sels. In the reconstructed longitudinal plane, these vessels appear to form three levels (Fig. 7.24). The first level, situated cranially, is seen below the urinary bladder neck. The second level is situated in the middle region of the urethra penetrating from the ventral side to reach the RS. The vessels penetrating here, on transverse section, have a typical “V” shape (Fig. 7.24). The third and lowest level is situated below the lower margin of the SP, in the area of the external ostium. Using 3D color Doppler imaging, we can observe the global vascularization of the urethra (Fig. 7.25). It is possible to visualize the spatial distribution of blood flow, to demonstrate vessel continuity and vessel branching in different planes, and to evaluate the pattern of vascularization (density of vessels, branching, caliber

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changes, and tortuosity). Using special software (Pixel Flux), it is possible a quantitative assessment of the urethra vascularity, measuring velocity (V), perfused area (A), perfusion intensity (I), pulsatility index (PI), and resistance index (RI). Wieczorek et al. [24] reported that the midurethra had the highest value of V and lowest value of A.  The intramural part had the lowest

value of I and the highest values of RI and PI. The distal urethra presented the highest value of I and the lowest value of RI. The values of V, A, and I were significantly higher in the external part of the midurethra compared with the internal part. Excellent interobserver and intraobserver reproducibility was shown in the majority of parameters for the entire urethra.

7.5

Assessment of the Posterior Compartment

The posterior compartment is evaluated by using the axial, sagittal, and coronal planes of the 3D volume acquired by 2052 transducers or by using the biplane (type 8848) or the linear array (type 8838) transducers (Fig.  7.26) [9]. Assessment includes measurements of the internal (IAS) and external anal sphincters (EAS). In the axial plane the IAS appears as a concentric hypoechoic ring surrounding a more echogenic central mucosa, and the EAS appears as a concentric band of mixed echogenicity surrounding the IAS (Fig. 7.27). The thickness of the internal and external sphincters is taken in the coronal plane at the 3 o’clock and 9 o’clock positions. An echogenic disruption is defined as a gap. The location of any defect is described using a Fig. 7.25  Three-dimensional color Doppler imaging. Spatial distribu- clock-­face notation. The longitudinal plane allows examition of the urethral vessels. Image obtained by 8848 transducer (BK nation of the perineal body, appearing as a pyramidalMedical). U urethra. Reproduced with permission from: Santoro GA, shaped, slightly hyperechoic structure anterior to the anal Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-­ sphincter and of the rectovaginal septum (RVS), visualized Verlag Italy, 2010

a

b

Fig. 7.26  Schematic illustrations of endovaginal ultrasonography performed by 8848 (a) and 8838 (b) transducers (BK Medical) for the assessment of the posterior compartment

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a

Fig. 7.27  Axial view of the anal complex obtained by 8848 transducer (BK Medical) using the transverse array. The external anal sphincter (EAS) appears as a hyperechoic ring surrounding the hypoechoic ring of the internal anal sphincter (IAS); PVM pubovisceral muscle. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

Perineal body

Cranial Anorectal Junction

Rectum

as a three-layer-­structure (hyperechoic, hypoechoic, and hyperechoic layers) between the external margin of the vagina and the external part of the rectal wall (Fig. 7.28). An RVS defect is defined as a discontinuity in this echographic pattern. In the mid-­sagittal plane, the anorectal angle (ARA), formed by the longitudinal axis of the anal canal and the posterior rectal wall, can also be measured at rest and during maximal pelvic floor contraction and Valsalva maneuver. Dynamic EVUS is particularly useful in the evaluation of posterior compartment disorders, prolapse, and obstructed defecation syndrome (see Chaps. 49 and 63).

7.6

Internal sphincter

b

Anal Canal

Puborectalis Longitudinal Fibres

Discussion

The pelvic floor is a 3D mechanical apparatus with a complex job description [25]. It involves specialized striated and smooth muscles, which together with ligaments, fascia, and nerves provide support for and assist in the function of the urogenital organs and the anorectum [25]. The pelvic floor can be described as a musculotendinous sheet that spans the pelvic outlet and consists mainly of the symmetrical paired LA muscle, which is like a funnel and not a flat, 2D structure. Therefore it is important to use 3D imaging to precisely visu-

c Fig. 7.28  Longitudinal view of the posterior compartment. (a, b) Schematic illustrations. (c) Ultrasonographic image obtained by 8848 transducer (BK Medical) using the linear array (PR: puborectalis)

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alize it. When we display a normal 2D-US cross-sectional view, there are many elements of the image that will not be correctly recognized as components of a 3D structure, or at least not perceived in their true spatial relationships. With conventional ultrasound we are usually looking at a 3D structure that contains a solid volume of echoes and which therefore does not readily translate onto a 2D projection. In routine clinical scanning, the operator forms a mental representation of the 3D anatomic or pathological structure while viewing a large series of 2D slices interactively. In this case the operator is using manual sense information about the physical location of the individual slices in building up 3D subjective impressions. 3D- and indeed 4D-US have been promoted by different ultrasound companies for several years. The acquisition of a 3D data volume and the underlying techniques are, however, different from application to application. The pelvic floor requires extremely high-­ resolution 3D volumes of data for adequate and precise diagnostic evaluation. An advantage of working with high-resolution 3D-US is that the 3D image does not remain fixed; rather, it can be freely rotated, rendered, tilted, and sliced to allow the operator to infinitely vary the different section parameters and visualize the different structures at different angles to obtain the most information from the data. After data are acquired, it is possible to select coronal anterior–posterior or posterior–anterior as well as sagittal right– left views, together with any oblique image plane. The multiview function allows the reader to see up to six different and specialized views at once with multiplanar reconstruction [3, 7, 8]. These functions were only available in computed tomography scan and magnetic resonance imaging and are deemed very helpful for clinicians in visualizing pathologies, allowing for precise surgery planning and appropriate patient management. Three-dimensional US allows us to assess directly the different planes in which anatomic structures of the pelvic floor are located. It has been shown to be reliably used in visualization of the pelvic floor structures of the anterior and posterior compartments in nullipara [4, 22]. The most extensively evaluated pelvic floor structures are the LH and the LA muscle, because significant correlations have been reported between LA defects and increased LH size and pelvic organ descent [26, 27] (see Chaps. 48 and 49). Tilting the axial plane in the acquired 3D data volume provides a maximal transverse section of the PVM, not otherwise obtainable with conventional 2D-EVUS, thus avoiding the artifacts due to its oblique shape. Our measurements [9] of PVM thickness (6.0 mm on both sides) in nulliparous volunteers were consistent with measurements taken on MRI, which is regarded a gold standard in the assessment of LA muscle. Tunn et al. [28] found 6.3 mm muscle thickness bilaterally, and Alt et al. [29] reported similar values (6.4 mm) on 3 Tesla MR scanner. 3D-EVUS shows excellent interobserver agreement for identification of LA and moderate to

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substantial agreement for identification of its subdivisions, and it is not affected by women’s age [30]. As the lateral attachments of the PVM to the pubic bone are also clearly visualized, 3D-EVUS can be utilized to document major levator ani trauma, in a similar way to 3D translabial ultrasound (TLUS) [31] and MRI [13, 27, 32]. Javadian et al. [32] found no difference between 3D-EVUS and MRI when comparing “normal” versus “abnormal” LA appearance. Similar results were reported by van Gruting et al. [33] who found that ultrasound is as good as MRI for the detection of major LA avulsion, while MRI still remain gold standard when minor avulsion is suspected. Moreover, LA avulsion seen on EVUS correlated better with patient’s symptoms than MRI or 3D-TPUS [33]. Interesting conclusions on LA avulsions were drawn from the recent multicenter study on correlation between ultrasound findings and anatomical dissection in the same cadaver [34]. 3D-TPUS performed in 30 cadavers identified avulsions in 11 cases (36.7%; one bilateral and ten unilateral), while anatomical dissection did not confirm any LA avulsion. However, the perineal ultrasound approach could represent the major limit in this study. Van Delft et al. [35] reported a good correlation (ICC 0.72) between 3D-EVUS and 3D-TPUS to analyze hiatus area and anteroposterior diameter with the patient at rest and to diagnose levator avulsion. However, palpation correlates only fair with both methods. Further studies in this field are required. 3D-EVUS allows a detailed evaluation of the LA muscle subdivisions [15] which are not visualized by TLUS [31]. Although it may be argued that these subdivisions of the LA muscle are not important, knowing exactly which muscles are damaged may not be inconsequential in clinical practice. Many of the functions of the pelvic floor governing micturition, defecation, and intercourse are only recently understood by describing the LA anatomy. Subdivisions are important because the muscles exert their action by contraction. For example, a patient with defecatory dysfunction due to a detached puboperinealis will not benefit from a posterior repair. Also, reattachment of the puboperinealis does not address defecatory dysfunction due to loss of anorectal angle from a damaged puborectalis. Biometric indices of the LH determined in the axial tilted plane in our study on 20 nulliparous females (AP diameter 4.84 cm, LL diameter 3.28 cm, hiatal area 12 cm2) [9] were consistent to the results published by Dietz et al. [11] in 49 nulliparous females with 3D-TLUS (AP diameter 4.52 cm, LL diameter 3.75 cm, hiatal area 11.25 cm2) and Tunn et al. [28] in 20 nulliparous females with MRI (AP diameter 4.1  cm, LL diameter 3.3  cm, hiatal area 12.8  cm2). In the same tilted axial plane, the paravaginal spaces and urethral symmetry can be assessed [9]. This deems clinically relevant as a lateral paravaginal defect can be suspected when a wider paravaginal space or an asymmetry of the urethra is observed. It has been hypothesized that paravaginal defects, due to

7  Endovaginal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy

separation of the endopelvic fascia from the arcus tendineus fascia pelvis, are the underlying anatomical abnormalities in anterior vaginal wall descent [36, 37] (see Chap. 49). Understanding the anatomy of the pelvic diaphragm is important for urogynecologists and proctologists. Damage to the perineal muscles and/or perineal body, frequently occurring during vaginal childbirth, is associated with pelvic organ prolapse [14]. As reported by Orno et al. [38], these muscles cannot be visualized in their entirety by using 2D-EVUS because they originate from the walls of the pelvis and converge at the perineal body from different angles. 3D-EVUS could overcome this limitation. Tilting the reconstructed axial plane from the SP, anteriorly, to the ischiopubic rami laterally, we are able to evaluate the different insertion points and to determine the dimensions of the superficial perineal muscles. In contrast with these findings, 3D-TLUS cannot properly assess the perineal structures due to the shape of the transducer, its position on the introital area, and a limited field of view of the acquired volume [37]. In the same scan, the AP diameter of the UGH can also be measured. Our study confirmed that this diameter had a positive correlation with LH area [9]. In the diagnostics of the anterior compartment dysfunctions, it is very important to assess the morphology and ­location of the urethra and to evaluate its supportive structures [28]. High-resolution 3D-EVUS gives the opportunity to assess the urethral position in three different planes and allows the anatomy and morphology of the bladder neck and urethral complex to be quantified [9] (see Chap. 19). Biometric indices of the urethral complex determined in our study [9] were comparable to the results reported by Umek et al. [6] with 3D transrectal US, with regard to both urethral thickness (11 mm on vaginal vs. 11.5 mm on rectal scans) and width (14 mm on vaginal vs. 15 mm on rectal scans) and to RS thickness (3.0  mm on vaginal vs. 2.7  mm on rectal scans) and volume (0.46 cm3 on vaginal vs. 0.5 cm3 on rectal scans). Additionally, the mean bladder neck–RS distance determined in our study (9.1  mm) was consistent with the measurement reported by using MRI (10  mm) [39]. Moreover, recent study from Xuan et  al. [40] showed that 3D-EVUS has excellent intra- and interobserver repeatability for urethral measurements and higher than 2D ultrasound. Urethral measurements are important indices in diagnostics of urinary incontinence. Females with urinary incontinence have smaller RS as compared to continent patients [41]. Santiago et al. [42] have compared ultrasound urethral measurements in patients with radiological diagnosis of bladder neck funneling and found that smaller RS length and area are associated with X-ray funneling. They have postulated a cutoff of 3.5 cm3 urethral volume on ultrasound as reliable as X-ray funneling in the diagnosis of intrinsic sphincter deficiency. The current gold standard for assessment of the posterior compartment is considered to be endoanal US (EAUS)

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[3, 7]. EVUS offers an alternative imaging modality of the anal sphincter complex and has proven to be as accurate as EAUS [2]. We found that measurements of anal sphincter thickness by 3D-EVUS were consistent with measurements reported by using EAUS, TLUS, or MRI [43–45]. However, regardless of the absolute dimensions of the anal sphincters, the most relevant utility of US modalities applies in the detection of localized EAS defects in patients with idiopathic fecal incontinence, passive fecal incontinence, or obstructive defecation disorders. In a recent study by Ros et al. [46], designed to compare sensitivity and specificity of 2D/3D-­ TPUS and 3D-EVUS with the gold standard 3D-EAUS in detecting residual defects after primary repair of obstetric anal sphincter injuries, 2D-TPUS and 3D-EVUS were found not accurate. 3D-TPUS showed good agreement with 3D-EAUS and high sensitivity in detecting residual defects. The most important advantage of EVUS compared to EAUS is the access to the longitudinal plane that allows assessment of the ARA, rectovaginal septum, and perineal body [9, 20].

7.7

Conclusion

High-resolution 3D-EVUS provides a detailed assessment of the pelvic floor for both identifying and measuring specific anatomic structures and for understanding their complex spatial arrangements. It is relatively easy and fast to perform, correlates well with other imaging modalities, and delivers additional information on the urethral complex and superficial perineal structures at the same time.

Take-Home Messages

• High-resolution 3D allows real-time manipulation, volume rendering, and offline analysis. • Both static and dynamic anatomy of the pelvic floor muscles and pelvic organs can reliably visualized by 3D and dynamic endovaginal ultrasonography. • Levator ani muscle subdivisions can be visualized in the proper planes in which they are located by 3D endovaginal ultrasonography.

References 1. Tunn R, Petri E. Introital and transvaginal ultrasound as the main tool in the assessment of urogenital and pelvic floor dysfunction: an imaging panel and practical approach. Ultrasound Obstet Gynecol. 2003;22:205–13. 2. Sultan AH, Loder PB, Bartram CI, et al. Vaginal endosonography. New approach to image the undisturbed anal sphincter. Dis Colon Rectum. 1994;37:1296–9.

130 3. Santoro GA, Fortling B.  New technical developments in endoanal and endorectal ultrasonography. In: Santoro GA, Di Falco G, editors. Benign anorectal diseases. Diagnosis with endoanal and endorectal ultrasonography and new treatment options. Milan: Springer-Verlag; 2006. p. 13–26. 4. Dietz HP, Steensma AB. Posterior compartment prolapse on two-­ dimensional and three-dimensional pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynecol. 2005;26:73–7. 5. Mitterberger M, Pinggera GM, Mueller T, et  al. Dynamic transurethral sonography and 3-dimensional reconstruction of the rhabdosphincter and urethra: initial experience in continent and incontinent women. J Ultrasound Med. 2006;25:315–20. 6. Umek WH, Lami T, Stutterecker D, et al. The urethra during pelvic floor contraction: observations on three-dimensional ultrasound. Obstet Gynecol. 2002;100:796–800. 7. Santoro GA, Fortling B.  The advantages of volume rendering in three-dimensional endosonography of the anorectum. Dis Colon Rectum. 2007;50:359–68. 8. Santoro GA, Wieczorek AP, Dietz HP, et al. State of the art: an integrated approach to pelvic floor ultrasonography. Ultrasound Obstet Gynecol. 2011;37:381–96. 9. Santoro GA, Wieczorek AP, Stankiewicz A, et al. High-resolution three-dimensional endovaginal ultrasonography in the assessment of pelvic floor anatomy: a preliminary study. Int Urogynecol J. 2009;20:1213–22. 10. Shobeiri SA, Chesson RR, Gasser RF. The internal innervation and morphology of the human female levator ani muscle. Am J Obst Gynecol. 2008;199:686.e1–6. 11. Dietz HP, Shek C, Clarke B. Biometry of the pubovisceral muscle and levator hiatus by three-dimensional pelvic floor ultrasound. Ultrasound Obstet Gynecol. 2005;25:580–5. 12. Ashton-Miller JA, DeLancey JO. Functional anatomy of the female pelvic floor. Ann N Y Acad Sci. 2007;1101:266–96. 13. Kearney R, Sawhney R, DeLancey JO.  Levator ani muscle anatomy evaluated by origin-insertion pairs. Obstet Gynecol. 2004;104:168–73. 14. Margulies RU, Hsu Y, Kearney R, et  al. Appearance of the levator ani muscle subdivisions in magnetic resonance images. Obstet Gynecol. 2006;107:1064–9. 15. Shobeiri SA, Leclaire E, Nihira MA, Quiroz LH, O'Donoghue D.  Appearance of the levator ani muscle subdivisions in endovaginal three-dimensional ultrasonography. Obstet Gynecol. 2009;114:66–72. 16. Shobeiri SA, Rostaminia G, White D, Quiroz LH. The determinants of minimal levator hiatus and their relationship to the puborectalis muscle and the levator plate. BJOG. 2013;120:205–11. 17. van Delft K, Schwertner-Tiepelmann N, Thakar R, Sultan AH. Inter-­ rater reliability of assessment of levator ani muscle strength and attachment to the pubic bone in nulliparous women. Ultrasound Obstet Gynecol. 2013;42:341–6. 18. van Delft K, Shobeiri SA, Thakar R, Schwertner-Tiepelmann N, Sultan AH.  Intra- and inter-rater reliability of levator ani muscle biometry and avulsion using three-dimensional endovaginal sonography. Ultrasound Obstet Gynecol. 2014;43:202–9. 19. Santoro GA, Wieczorek AP, Shobeiri SA, et al. Interobserver and interdisciplinary reproducibility of 3D endovaginal ultrasound assessment of pelvic floor anatomy. Int Urogynecol J Pelvic Floor Dysfunct. 2011;22:53–9. 20. Santoro GA, Shobeiri SA, Petros PP, Zapater P, Wieczorek AP. Perineal body anatomy seen by three-dimensional endovaginal ultrasound of asymptomatic nulliparae. Colorectal Dis. 2016;18: 400–9. 21. DeLancey JOL, Hurd WW. Size of the urogenital hiatus in the levator ani muscles in normal women and women with pelvic organ prolapse. Obstet Gynecol. 1998;91:364–8.

G. A. Santoro et al. 22. Shobeiri SA, White D, Quiroz LH, Nihira MA. Anterior and posterior compartment 3D endovaginal ultrasound anatomy based on direct histologic comparison. Int Urogynecol J. 2012;23:1047–53. 23. Wieczorek AP, Wozniak MM, Stankiewicz A, Santoro GA, Bogusiewicz M, Rechberger T. 3-D high-frequency endovaginal ultrasound of female urethral complex and assessment of inter-­ observer reliability. Eur J Radiol. 2012;81:e7–e12. 24. Wieczorek AP, Woźniak MM, Stankiewicz A, et  al. Quantitative assessment of urethral vascularity in nulliparous females using high-frequency endovaginal ultrasonography. World J Urol. 2011;29:625–32. 25. DeLancey JO.  The hidden epidemic of pelvic floor dysfunction: achievable goals for improved prevention and treatment. Am J Obstet Gynecol. 2005;192:1488–95. 26. Lien KC, Mooney B, DeLancey JO, et  al. Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol. 2004;103:31–40. 27. DeLancey JO, Morgan DM, Fenner DE, et al. Comparison of levator ani muscle defects and function in women with and without pelvic organ prolapse. Obstet Gynecol. 2007;109:295–302. 28. Tunn R, DeLancey JOL, Howard D, et al. Anatomic variations in the levator ani muscle, endopelvic fascia and urethra in nulliparas evaluated by magnetic resonance imaging. Am J Obstet Gynecol. 2003;188:116–21. 29. Alt CD, Hampel F, Hallscheidt P, Sohn C, Schlehe B, Brocker KA. 3T MRI-based measurements for the integrity of the female pelvic floor in 25 healthy nulliparous women. Neurourol Urodyn. 2016;35:218–23. 30. Quiroz LH, Shobeiri SA, White D, Wild RA. Does age affect visualization of the levator ani in nulliparous women? Int Urogynecol J. 2013;24:1507–13. 31. Dietz HP. Quantification of major morphological abnormalities of the levator ani. Ultrasound Obstet Gynecol. 2007;29:329–34. 32. Javadian P, O'Leary D, Rostaminia G, et al. How does 3D endovaginal ultrasound compare to magnetic resonance imaging in the evaluation of levator ani anatomy? Neurourol Urodyn. 2017;36:409–13. 33. van Gruting IMA, Stankiewicz A, Sultan AH, Thakar R.  Is MRI the gold standard imaging technique to diagnose levator ani muscle avulsion? abstract - IUJ. 2016;27, suppl 1 S54–55. 34. Da Silva AS, Digesu GA, Dell'Utri C, Fritsch H, Piffarotti P, Khullar V. Do ultrasound findings of levator ani “avulsion” correlate with anatomical findings: a multicenter cadaveric study. Neurourol Urodyn. 2016;35:683–8. 35. van Delft KW, Sultan AH, Thakar R, Shobeiri SA, Kluivers KB.  Agreement between palpation and transperineal and endovaginal ultrasound in the diagnosis of levator ani avulsion. Int Urogynecol J. 2015;26:33–9. 36. DeLancey JO. Fascial and muscular abnormalities in women with urethral hypermobility and anterior vaginal wall prolapse. Am J Obstet Gynecol. 2002;187:93–8. 37. Dietz HP, Steensma AB, Hastings R. Three-dimensional ultrasound imaging of the pelvic floor: the effect of parturition on paravaginal support structures. Ultrasound Obstet Gynecol. 2003;21:589–95. 38. Orno AK, Marsal K, Herbst A. Ultrasonographic anatomy of perineal structures during pregnancy and immediately following obstetric injury. Ultrasound Obstet Gynecol. 2008;32:527–34. 39. Umek WH, Kearney R, Morgan DM. The axial location of structural regions in the urethra: a magnetic resonance study in nulliparous women. Obstet Gynecol. 2003;102:1039–45. 40. Xuan Y, Yue S, Sun L.  Repeatability of female midurethral measurement using high-frequency 3-dimensional transvaginal ultrasonography. J Ultrasound Med. 2018;37:1389–95. 41. Zacharakis D, Grigoriadis T, Pitsouni E. Ultrasonographic evaluation of the urethral rhabdosphincter morphology in female patients with urodynamic stress incontinence. Fem Pelv Med Reconstr Surg. 2017;23:267–71.

7  Endovaginal Ultrasonography: Methodology and Normal Pelvic Floor Anatomy 42. Santiago A, Quiroz L, Shobeiri SA. Decreased urethral volume is comparable to funneling as a predictor of intrinsic sphincter deficiency. Fem Pelv Med Reconstr Surg. 2017;23:336–42. 43. Williams AB, Cheetham MJ, Bartram CI, et al. Gender differences in the longitudinal pressure profile of the anal canal related to anatomical structure as demonstrated on three-dimensional anal endosonography. Br J Surg. 2000;87:1674–9. 44. Hall RJ, Rogers RG, Saiz L, Qualls C.  Translabial ultrasound assessment of the anal sphincter complex: normal measurements

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of the internal and external anal sphincters at the proximal, mid and distal levels. Int Urogynecol J. 2007;18:881–8. 45. Schaefer A, Enck P, Furst G, et al. Anatomy of the anal sphincters. Comparison of anal endosonography to magnetic resonance imaging. Dis Colon Rectum. 1994;37:777–81. 46. Ros C, Martinez-Franco E, Wozniak MM, et al. Postpartum twoand three-dimensional ultrasound evaluation of anal sphincter complex in women with obstetric anal sphincter injury. Ultrasound Obstet Gynecol. 2017;49:08–514.

8

Endoanal and Endorectal Ultrasonography: Methodology and Normal Anorectal Anatomy Giulio A. Santoro, Luigi Brusciano, and Abdul H. Sultan

Learning Objectives

• To understand the technical aspects of high-­resolution three-dimensional endoanal and endorectal ultrasound. • To understand the normal ultrasound anatomy of the anal canal and the rectal wall.

8.1

Introduction

The anal canal is surrounded by the internal sphincter (IAS), the longitudinal muscle layer (LM), and the external sphincter (EAS) [1–3] (Fig.  8.1). The anatomy of the anorectal region is currently of clinical interest. An intact anal sphincter complex has a decisive role for continence [4]. It is very important for gynecologists to know where birth damage may occur, leading to rupture of the IAS or EAS as well as the puborectalis muscle (PR) [4]. Knowledge of the correct anatomy helps to identify defects and to reconstruct them in a meticulous way to achieve as good a functional result as possible [4]. With the help of endoanal (EAUS) and endorectal ultrasonography (ERUS), it has become possible to demonstrate clearly the morphology of the anal sphincter complex and to detect sphincter disruptions or defects. The

G. A. Santoro (*) Tertiary Referral Pelvic Floor and Incontinence Center, IV°Division of General Surgery, Regional Hospital, Treviso, University of Padua, Padua, Italy e-mail: [email protected] L. Brusciano Division of General and Obesity Surgery, Master of Coloproctology, University of Campania “Luigi Vanvitelli”, Napoli, Italy e-mail: [email protected] A. H. Sultan

Urogynaecology and Pelvic Floor Reconstruction Unit Croydon University Hospital, St George’s University of London, London, UK e-mail: [email protected]

results of ultrasound studies have also demonstrated the sexual differences in the ventral part of the EAS [5–11]. The purpose of this chapter is to present the techniques of EAUS and ERUS and to revise the ultrasonographic anatomy of the anal sphincter complex in axial, longitudinal, and coronal planes with the use of high-resolution three-dimensional reconstruction.

8.2

Ultrasonographic Technique

Endoanal ultrasound, as previously reported in Chap. 5 is commonly performed with high multifrequency, 360° rotational mechanical transducer, linear electronic transducer, or radial electronic transducer (2052, 20R3, 8838; E14CL4b BK Medical). During examination the patient is placed in dorsal lithotomy or in the left lateral decubitus position. Before the probe is inserted into the anus, a digital rectal examination should be performed. If there is an anal stenosis, the inserted finger can be used to check whether easy passage of the probe will be possible. A gel-containing condom is placed over the probe, and a thin layer of water-­soluble lubricant is placed on the exterior of the condom. Any air interface will cause a major interference pattern. The patient should be instructed before the examination that no pain should be experienced. Under no circumstances should force be used to advance the probe. By convention, the transducer is positioned to provide the following image: the anterior aspect of the anal canal will be superior (12 o’clock) on the screen, right lateral will be left (9 o’clock), left lateral will be right (3 o’clock), and posterior will be inferior (6 o’clock). Some adjustments may be necessary in the gain of the ultrasound unit to provide optimal imaging. It is always possible to perfectly depict all layers of the anal canal circumferentially. This is very important when assessing the canal at different levels. At the origin of the anal canal, the “U”-shaped sling of the puborectalis is the main landmark and should be used for final adjustment. Three-dimensional ultrasound (3D-US) is constructed from a synthesis of a high number of parallel transaxial two-­

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_8

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134 Fig. 8.1  Normal anatomy of the anal canal. The muscularis propria of the rectal wall consists of both circular and longitudinal smooth muscle fibers. The circular layer is continuous with the circular internal anal sphincter muscle. The longitudinal layer extends into the intersphincteric space of the anal canal. The external sphincter extends further down than the internal sphincter. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

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Longitudinal muscle

Circular muscle Puborectalis

Internal hemorrhoidal vein Deep external sphincter

Internal sphincter Superficial external sphincter

Subcutaneous external sphincter

External hemorrhoidal vein

its recent version X14L4 offers similar imaging opportunities (only in sagittal section) (360°, length of scanning from 0 to 60 mm length, 1 mm minimal slice thickness, manual adjustment of focal zones) with full measurement capabilities as the probe above, but with higher resolution (Fig. 8.3). After a 3D dataset has been acquired, it is immediately possible to select coronal anterior–posterior or posterior–anterior as well as sagittal right–left views, together with any oblique image plane. The 3D image can be rotated, tilted, and sliced to allow the operator to infinitely vary the different section parameters, visualize the assessed region at different angles, and measure accurately distance, area, angle, and volume [12].

8.3 Fig. 8.2  Schematic illustrations of the technique of three-dimensional endoanal ultrasonography performed by 2052 transducer (BK Medical) for the assessment of the anorectal region. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

dimensional (2D) images. The 2052 transducer has a built-in 3D automatic motorized system that allows an acquisition of 300 transaxial images over a distance of 60 mm in 60 s, without requiring any movement relative to the investigated tissue (see Chap. 5) [12] (Fig. 8.2). The new linear electronic probe (type 8838, BK Medical), frequency of 4–14 MHz, or

Endosonographic Anatomy of the Anal Canal

The normal anatomy of anal sphincters is complex but has a basic five-layer pattern with subepithelial tissues of moderate reflectivity, the IAS of low reflectivity, and the LM and the EAS of mixed reflectivity [13, 14]. The ultrasonographer must have a clear understanding of what each of these five layers represents anatomically (Fig. 8.3): 1. The first hyperechoic layer, from inner to outer, corresponds to the interface of the transducer with the anal mucosal surface.

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External anal sphincter

Internal anal sphincter

Probe

Subepithelial tissue

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Fig. 8.3  Normal ultrasonographic five-layer structure of the mid-anal canal. (a) Axial image obtained by 2050 transducer (BK Medical); (b) axial image obtained by 8838 transducer (BK Medical); (c) schematic

representation. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. SpringerVerlag Italy, 2010

2. The second layer represents the subepithelial tissues and appears moderately reflective. The mucosa as well the level of dentate line is not visualized. The muscularis submucosae ani can be sonographically identified in the upper part of the anal canal as a low reflective band. 3. The third hypoechoic layer corresponds to the IAS. The sphincter is not completely symmetric, either in thickness or termination. It can be traced superiorly into the circular muscle of the rectum, extending from the anorectal junction to approximately 1  cm below the dentate line. In older age groups, the IAS loses its uniform low echogenicity, which is characteristic of smooth muscle throughout the gut, to become more echogenic and inhomogeneous in texture [15]. 4. The fourth hyperechoic layer represents the LM. It presents a wide variability in thickness and is not always distinctly visible along the entire anal canal. The LM appears moderately echogenic, which is surprising as it is mainly

smooth muscle; however, an increased fibrous stroma may account for this. In the intersphincteric space, the LM conjoins with striated muscle fibers from the levator ani, particularly the puboanalis, and a large fibroelastic element derived from the endopelvic fascia to form the “conjoined longitudinal layer” (CLL) (Fig. 8.4) [14]. Its fibroelastic component, permeating through the subcutaneous part of the EAS, terminates in the perianal skin. According to the “Integral Theory” proposed by Papa Petros, the CLL creates the downward force for bladder neck closure during effort and stretches open the outflow tract during micturition [16]. 5. The fifth mixed echogenic layer corresponds to the EAS.  The EAS is made up of voluntary muscle that encompasses the anal canal. It is described as having three parts [17]: (1) The deep part is integral with the PR.  Posteriorly there is some ligamentous attachment. Anteriorly some fibers are circular and some decussate

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PC CLL

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Fig. 8.4 (a) The puboanalis (PA) rises from the medial border of the pubococcygeus muscle (PC); SP symphysis pubis. (b) Schematic representation. Fibers from the longitudinal muscle run through the internal anal sphincter to form the muscularis submucosae ani (MSA). (c) Coronal image of the anal canal obtained by 2052 transducer (BK

Medical). The PA joins the longitudinal muscle layer (LL) of the rectum to form the conjoined longitudinal layer (CLL). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

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PR

Level I

IAS

EAS

Level II

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Fig. 8.5  Three levels of assessment of the anal canal in the axial plane. Scan obtained by 2052 transducer (BK Medical) (see text). Right side of the image is left side of the patient. EAS external anal sphincter, IAS

internal anal sphincter, PR puborectalis. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-­Verlag Italy, 2010

into the deep transverse perinei. (2) The superficial part has a very broad attachment to the underside of the coccyx via the anococcygeal ligament. Anteriorly there is a division into circular fibers and a decussation to the superficial transverse perinei. (3) The subcutaneous part lies below the IAS.

• Upper level: the sling of the PR, the deep part of the EAS, and the complete ring of IAS. • Middle level: the superficial part of the EAS (complete ring), the CLL, the IAS (complete ring), and the transverse perinei muscles. • Lower level: the subcutaneous part of the EAS.

Ultrasound imaging of the anal canal can be divided into three levels of assessment in the axial plane (upper, middle, and lower levels), referring to the following anatomical structures (Figs. 8.5 and 8.6) [18, 19–21]:

The muscles of the lower and the upper part of the anal canal are different. The first ultrasonographic image recorded is normally the PR muscle and is labeled “Upper level.” The PR slings the anal canal instead of completely surrounding it.

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a

Level I

Level II

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IAS

EAS

Level III

c

Fig. 8.6  Three levels of assessment of the anal canal. (a) Schematic representation; (b) coronal image and (c) sagittal image obtained by 2052 transducer (BK Medical). The internal sphincter (IAS) ends at the

level of the junction between the superficial external sphincter (EAS sp) (Md middle level) and subcutaneous external sphincter (EAS sc) (Lo lower level). PR puborectalis, Up upper level

At its upper end, the PR is attached to the funnel-shaped levator ani muscle, and the levator ani anchors the sphincter complex to the inner side of the pelvis. The deep part of the EAS is similar in echogenicity to the PR and cannot be differentiated from it posteriorly. Anteriorly, the circular fibers of the deep part of the EAS are not recognizable in females, whereas in males thin arcs of muscle from the deeper part of the sphincter may be seen extending anteriorly. Moving the probe a few millimeters in the distal direction will show an intact anterior EAS forming just below the superficial transverse perinei muscles, imaged at 11 o’clock and 1 o’clock (Fig. 8.7). This image, labeled “Middle level,” is a mid-anal projection where

the IAS, CLL, and superficial EAS are all identified. The anterior part of the EAS differs between genders, and anatomic studies have shown that this difference is already present in the fetus. In males, the EAS is symmetrical at all levels; in females, it is shorter anteriorly, and there is no evidence of an anterior ring high in the canal (Fig. 8.8). In females, fibers between the transverse perinei fuse with the EAS, so that there is no plane of dissection between these two structures. In males a plane of fat persists between the transverse perinei and the EAS.  In examining a female subject, the ultrasonographic differences between the natural gap (hypoechoic areas with smooth, regular edges) and sphincter ruptures (mixed echogenicity due to

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b

Fig. 8.7  Images of the transverse perinei muscles (TP) in the axial plane in male (a) and female (b). The anococcygeal ligament (ACL) is seen as a posterior hypoechoic triangle. Scan obtained by 2052 trans-

ducer (BK Medical). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. SpringerVerlag Italy, 2010

scarring, with irregular edges) occurring at the upper anterior part of the anal canal must be kept in mind. Three-dimensional longitudinal images are particularly useful to assess these anatomic characteristics of the EAS [22–26] (Figs. 8.8 and 8.9). EAUS is not able to precisely assess the perineal body because of the lack of clear limits. Also the proposed use of a finger introduced into the vagina as a landmark seems to be of poor benefit, altering its normal configuration due to the digital compression on the central perineum [27, 28]. At this level, the anococcygeal raphe is seen as a posterior hypoechoic triangle (Fig. 8.7). When the probe is pulled further out, the image of the IAS will disappear, and only the subepithelium and the subcutaneous segment of the LM + EAS will be seen. This last image is labeled “Lower level” (Fig. 8.6). The perianal anatomic spaces are also visualized by EUAS.  The submucosal (subepithelial) space is defined as the layer between the external cone surface and the inner border of the IAS. The intersphincteric space, containing the longitudinal layer, is located between the IAS and EAS. The ischioanal space, which surrounds the anal canal, is pyramid shaped and is located outside the EAS.  The supralevator space is located superior to the levator ani muscle.

inferiorly along the curve of the sacrum to pass through the pelvic diaphragm and become the anal canal. It is surrounded by fibrofatty tissue that contains blood vessels, nerves, lymphatics, and small lymph nodes. The superior one-third is covered anteriorly and laterally by the pelvic peritoneum. The middle one-third is only covered with peritoneum anteriorly, where it curves anteriorly onto the bladder in the male and onto the uterus in the female. The lower one-third of the rectum is below the peritoneal reflection and is related anteriorly to the bladder base, ureters, seminal vesicles, and prostate in the male and to the lower uterus, cervix, and vagina in the female. The rectal wall consists of five layers surrounded by perirectal fat or serosa (Fig. 8.10). On ultrasound the normal rectal wall is 2–3 mm thick and is composed of a five-­ layer structure [28]. There is some debate as to what the actual layers represent anatomically. Hildebrandt et al. [29] believe that three layers are anatomical, while the other layers represent interfaces between the anatomical layers. Beynon et  al. [30], however, have produced both experimental and clinical evidence that the five anatomic layers are recognizable. Good visualization depends on maintaining the probe in the center lumen of the rectum and having adequate distension of a water-filled latex balloon covering the transducer to achieve good acoustic contact with the rectal wall. It is important to eliminate all bubbles within the balloon to avoid artifacts that limit the overall utility of the study. The rectum can be of varying diameters, and therefore the volume of water in the balloon may have to be adjusted intermittently. The five layers represent (Fig. 8.11):

8.4

Endosonographic Anatomy of the Rectum

The normal rectum is 11–15 cm long and has a maximum diameter of 4 cm. It is continuous with the sigmoid colon superiorly at the level of the third sacral segment and courses

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a

b

c

d

e

f

Fig. 8.8  The ventral part of the external sphincter differs between males (a, c, e) and females (b, d, f) (see text). (a, b) Schematic representation. (c–f) Three-dimensional endosonographic reconstructions in the longitudinal plane. The distance between the anterior anorectal junction and the external sphincter is called the gap (arrows). EAS

external anal sphincter, IAS internal anal sphincter, MD middle level, PR puborectalis muscle, UP upper level. Scans obtained by 2052 transducer (BK Medical) (c, e, f) and 8838 transducer (BK Medical) (d). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

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Fig. 8.9  External sphincter at three levels of the anal canal in male and female. (a, b) Schematic representation; (c) Ultrasonographic images in the axial plane. Male on the left, female on the right. LM longitudinal muscle, EAS external anal sphincter, d deep external sphincter,

s superficial external sphincter, sc subcutaneous external sphincter. Scans obtained by 2052 transducer (BK Medical). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

a

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5 4

3

Fig. 8.10  Diagrammatic representation of the five-layer structure of the normal rectal wall. (a, b): 1, mucosa; 2, submucosa; 3, muscularis propria/circular layer; 4, muscularis propria/longitudinal layer; 5,

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serosa/perirectal fat interface. Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

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Interface: hyperechoic Mucosa/MM: hypoechoic Submucosa: hypoechoic Muscularis propria: hypoechoic Serosa/mesorectal fat; hyperechoic

d

Fig. 8.11 (a) Schematic and ultrasound representation of the five layers of the rectal wall in the axial plane: 1, acoustic interface with mucosal surfaces; 2, mucosa; 3, submucosa; 4, muscularis propria; 5, serosa/ perirectal fat interface. (b) Ultrasound magnification. (c) Three-­ dimensional reconstruction of the rectal wall in the coronal plane (nor-

mal mode). (d) Three-dimensional reconstruction of the rectal wall in the coronal plane (volume render mode). Scans obtained by 2052 transducer (T) (BK Medical). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. SpringerVerlag Italy, 2010

8  Endoanal and Endorectal Ultrasonography: Methodology and Normal Anorectal Anatomy

1. The first hyperechoic layer: the interface of the balloon with the rectal mucosal surface. 2. The second hypoechoic layer: the mucosa and muscularis mucosae. 3. The third hyperechoic layer: the submucosa. 4. The fourth hypoechoic layer: the muscularis propria (in rare cases seen as two layers: inner circular and outer longitudinal layer). 5. The fifth hyperechoic layer: the serosa or the interface with the fibrofatty tissue surrounding the rectum (mesorectum). The mesorectum contains blood vessels, nerves, and lymphatics and has an inhomogeneous echo pattern. Very small, round to oval, hypoechoic lymph nodes should be distinguished from blood vessels which also appear as circular hypoechoic structures. Endorectal ultrasound allows an accurate visualization of all pelvic organs adjacent to the rectum: the bladder, seminal vesicles, and prostate in males (Fig. 8.12) and the uterus, cervix, vagina, and urethra in females (Fig. 8.13). Intestinal loops can also be easily identified as elongated structures (Fig. 8.14). Three-dimensional ERUS is also used to visualize the endopelvic fascia. This echogenic layer is a well-determined structure reaching from the pelvic wall from one side to the other [31]. Using post-processing volume render mode (see Chap. 5), it is also possible to analyze the information inside the 3D volume and visualize the internal mucosal surface (Fig. 8.11).

8.5

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Fig. 8.13  Longitudinal view of the vagina. Scans obtained by 2052 transducer (BK Medical)

Normal Values

The anal canal length is the distance measured between the proximal canal, where the PR is identified, and the lower border of the subcutaneous EAS. It is significantly longer in

Fig. 8.14  Sonographic view of the intestinal loops (IL). Scans obtained by 2052 transducer (BK Medical). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-­Verlag Italy, 2010

Fig. 8.12  Coronal view of the bladder (B), seminal vesicles (SV), prostate gland (P), urethra (U), and obturator foramen (OF). Scans obtained by 2052 transducer (BK Medical). Reproduced with permission from: Santoro GA, Wieczorek AP, Bartram CI (eds) Pelvic Floor Disorders. Springer-Verlag Italy, 2010

males than in females, as a result of a longer EAS, whereas there is no difference in PR length [32]. In males the anterior part of the EAS is present along the entire length of the canal (Figs. 8.9 and 8.10). In females the anterior ring of the EAS is shorter. Williams et  al. [23] reported that the anterior EAS occupied 58% of the male anal canal compared with 38% of the female canal (P   4 mm thick should be considered abnormal whatever the patient’s age; conversely an IAS of 2 mm is normal in a young patient but abnormal in an elderly one. The LM is 2.5 ± 0.6 mm in males and 2.9 ± 0.6 mm in females. The average thickness of the EAS is 8.6 ± 1.1 mm in males and 7.7 ± 1.1 mm in females. However, EAUS largely overestimates the size of the EAS due to its failure to recognize and separate the LM.  By using the reconstructed 3D coronal plane, the anterior longitudinal extent of the EAS can also be measured (Fig. 8.15). Many studies have specifically addressed the problems of the reproducibility of EAUS sphincter measurements [11, 33–36]. Enck et al. [35] examined a small group of healthy volunteers and concluded that EAUS did not provide reliable measurements of IAS and EAS thicknesses. Gold et al. [36] examined 51 patients and found that measurements of the IAS were more reproducible than those of the EAS.  These findings are consistent with results from Beets-Tan et  al. [33], which compared EAUS, endoanal magnetic resonance imaging (MRI), and phased-­ array MRI for anal sphincter measurement in healthy volunteers. EAUS enabled reliable measurement of IAS thickness only, whereas both MRI modalities enabled reliable measure-

Fig. 8.15  Measurement of the anterior length of the external sphincter in the coronal plane (arrows). Scans obtained by 8838 transducer 16 MHz frequency (BK Medical)

G. A. Santoro et al.

ment of all sphincter components. Measurement errors of the LM and EAS are related to the ultrasonographic features of these muscles, which show low contrast with the surrounding hyperechoic fatty tissue. Both the inner and outer borders of the EAS are more difficult to define, leading to less reliable measurement. In contrast, the IAS is easy to define because it is a hypoechoic structure that is highlighted against hyperechoic fatty tissues. Williams et  al. [23] reported different results. They found an excellent correlation for the interobserver measurement of the EAS, IAS, and submucosal width on endosonography and poor correlation only for the LM. Frudinger et al. [11] also reported that the EAS thickness was difficult to define in only 2% of patients at all three levels examined and in 3% at the subcutaneous level only. A significant negative correlation with the patients’ age was also demonstrated in this study, at all anal canal levels. In particular, the anterior EAS region was found to be significantly thinner in older subjects. The high inherent soft tissue contrast makes MRI a more reliable imaging method to measure anal sphincter components [37–43]. Multiplanar EAUS, however, has enabled detailed longitudinal measurement of the components of the anal canal [8, 12, 44]. Williams et al. [23] reported that the anterior EAS was significantly longer in men than women (30.1 mm vs. 16.9 mm; P  1 indicates that the target lesion compresses less than the normal reference tissue, indicating lower strain and greater stiffness [36]. In shear-wave elastography (SWE), measurement of the shear-­ wave speed results in qualitative and quantitative estimates of tissue elasticity [37]. The elasticity measurements, using SWE or 2D SWE, may be expressed as either shear-wave velocity (m/s) or Young’s modulus (kPa) [38].

9.9.1 Endovaginal Elastography Strain elastography (SE) is a technique of parametric imaging that allows quantification of the elasticity of tissue. Kreutzkamp et al. [39] attempted to determine if the elasticity of paraurethral tissue correlates with urethral mobility and urinary incontinence (UI). One region of interest was placed in the tissue between the urethra and vagina at midlevel of the urethra bordering the urethral wall. The second ROI was set at the level of the os urethra internum in the tissue of the bladder neck in one line to the first ROI. The authors measured elasticity in both ROIs with TDI-Q (Tissue Doppler ImagingQuantification Software) and calculated the ratio between ROIs. Mobility of the urethra was quantified by measuring the angle between a line parallel to the urethra and a line parallel to the bladder neck during stress and rest. SE analysis was feasible in all cases. A correlation between urethral mobility and elasticity of the paraurethral tissue was found. In case of increasing urethral mobility, the paraurethral tissue close to the bladder neck seems to be more elastic, and the patients reported about more symptoms of UI. No noticeable correlation between UI and urethral elasticity was shown. SE may be a useful technique for direct quantification of tissue elasticity and assessment of pelvic floor biomechanics [39]. Female striated urogenital sphincter contraction measured by shear-wave elastography during pelvic floor muscle activation was described by Aljuraifani et  al. [40]. The authors used ultrasound shear-wave elastography (SWE), a noninvasive real-time technique to estimate tissue stiffness. As muscle stiffness can be used as an estimate of muscle force, SWE provides an opportunity to study contraction of the periurethral musculature. Stiffness in a region expected to contain the striated urogenital sphincter (SUS) was quantified using SWE at rest and during a pelvic floor muscle contractions performed at 10%, 25%, and 50% of maximal voluntary contraction (MVC). Two repetitions were performed for 10 s. The authors showed that during contraction, stiffness increased in the region of the SUS in all participants

M. M. Woźniak et al.

and at all contraction intensities. Multiple regions of increased stiffness were detected, with 95.8% of regions situated ventral to the mid-urethra within the anatomical area of the SUS.  The increase in stiffness was greater for 50% MVC than both 10% and 25% MVC contraction intensities (P  50% improvement in Wexner incontinence scores from an average of 13.5 to 8.26 on 5-year follow-up [10]. These promising results were not reproduced in subsequent series. Two early series by Efron et al. also demonstrated some improvement in Wexner incontinence scores, from an average of 14 to 11  in 46 patients [9, 11]. They also found significant improvement in quality of life scores, but they did not demonstrate any measurable effects on physiologic testing such as ultrasound or manometry [9, 11]. Later series have not shown the same promising results as early series. One study by Felt-Bersma et al. in 2007 of 11 patients showed a modest improvement of the Vaizey incontinence score from 18 to 15 [7]. Another small series of 15 patients in 2008 showed an improvement of the Wexner incontinence score of 14–11, with minimal improvement of quality of life [8]. Kim et al. failed to demonstrate any benefit from radiofrequency treatment in eight patients after 8 months [12]. A multicenter study in 2010 of 24 patients showed a modest improvement in fecal incontinence score of 15.6–12 after 1 year [12]. One study evaluating 3-year outcomes in 31 patients demonstrated that efficacy of the procedure diminished over the course of the study, with only 6% of patients maintaining a clinical response [13]. Abbas et al. were able to demonstrate a better 3-year response, with 22% of the patients in that series having a sustained clinical effect over 3 years [14]. A recent sham-controlled clinical trial of 40 patients demonstrated a mild improvement of the Vaizey incontinence score by 2.5 points, but did not in quality of life scores when compared to the sham group [15]. Finally, a recent analysis of ten studies concluded that radiofrequency treatment of the anal canal provided a modest improvement in patients with mild fecal incontinence, with minimal complications [16]. No study was able to demonstrate any change in physiologic testing such as ultrasound or manometry [16]. A recent guideline for the treatment of fecal incontinence from 2014 stated the efficacy of radiofrequency augmentation is low to intermediate based on some quality evidence [17].

42.3 Future Directions Further study should be done to identify patients who may have potentially benefit from radiofrequency treatment to the anal canal for fecal incontinence.

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Take-Home Messages

Radiofrequency augmentation of the anal sphincter muscles can be moderately effective for mild-tomoderate fecal incontinence. A discussion should be had with the patient regarding expectations after this procedure, since improvements are at best modest. After other treatable causes for fecal incontinence have been excluded, radiofrequency may be attempted.

References 1. Takahashi T, Garcia-Osogobio S, Valdovinos MA, Mass W, Jimenez R, Jauregui LA, et al. Radio-frequency energy delivery to the anal canal for the treatment of fecal incontinence. Dis Colon Rectum. 2002;45(7):915–22. 2. Paquette IM, Bordeianou L.  Evaluation and treatment of FI.  In: Steele SR, Hull TL, Read TE, Saclarides TJ, Senagore AJ, Whitlow CB, editors. The ASCRS textbook. 3rd ed. New York, NY: Springer; 2017. p. 1091–105. 3. Frascio M, Mandolfino F, Imperatore M, Stabilini C, Fornaro R, Gianetta E, et al. The SECCA procedure for faecal incontinence: a review. Colorectal Dis. 2014;16(3):167–72. 4. Brown HW, Wexner SD, Segall MM, Brezoczky KL, Lukacz ES. Accidental bowel leakage in the mature women’s health study: prevalence and predictors. Int J Clin Pract. 2012;66(11):1101–8. 5. Arts J, Bisschops R, Blondeau K, Farré R, Vos R, Holvoet L, et al. A double-blind sham-controlled study of the effect of radiofrequency energy on symptoms and distensibility of the gastro-esophageal junction in GERD. Am J Gastroenterol. 2012;107(2):222–30. 6. Herman RM, Berho M, Murawski M, Nowakowski M, Ryś J, Schwarz T, et  al. Defining the histopathological changes induced by nonablative radiofrequency treatment of faecal incontinence – a blinded assessment in an animal model. Colorectal Dis. 2015;17(5):433–40. 7. Felt-Bersma RJ, Szojda MM, Mulder CJ. Temperature-controlled radiofrequency energy (SECCA) to the anal canal for the treatment of faecal incontinence offers moderate improvement. Eur J Gastroenterol Hepatol. 2007;19(7):575–80. 8. Lefebure B, Tuech JJ, Bridoux V, Gallas S, Leroi AM, Denis P, et  al. Temperature-controlled radio frequency energy delivery (Secca procedure) for the treatment of fecal incontinence: results of a prospective study. Int J Colorectal Dis. 2008;23(10):993–7. 9. Efron JE, Corman ML, Fleshman J, Barnett J, Nagle D, Birnbaum E, et  al. Safety and effectiveness of temperature-controlled radio-frequency energy delivery to the anal canal (Secca procedure) for the treatment of fecal incontinence. Dis Colon Rectum. 2003;46(12):1606–16. 10. Takahashi-Monroy T, Morales M, Garcia-Osogobio S, Valdovinos MA, Belmonte C, Barreto C, et al. SECCA procedure for the treatment of fecal incontinence: results of five-year follow-up. Dis Colon Rectum. 2008;51(3):355–9.

520 11. Efron JE. The SECCA procedure: a new therapy for treatment of fecal incontinence. Surg Technol Int. 2004;13:107–10. 12. Kim DW, Yoon HM, Park JS, Kim YH, Kang SB. Radiofrequency energy delivery to the anal canal: is it a promising new approach to the treatment of fecal incontinence? Am J Surg. 2009;197(1):14–8. 13. Lam TJ, Visscher AP, Meurs-Szojda MM, Felt-Bersma RJ. Clinical response and sustainability of treatment with temperature-­controlled radiofrequency energy (Secca) in patients with faecal incontinence: 3 years follow-up. Int J Colorectal Dis. 2014;29(6):755–61. 14. Abbas MA, Tam MS, Chun LJ.  Radiofrequency treatment for fecal incontinence: is it effective long-term? Dis Colon Rectum. 2012;55(5):605–10.

L. Force et al. 15. Visscher AP, Lam TJ, Meurs-Szojda MM, Felt-Bersma RJF. Temperature-controlled delivery of radiofrequency energy in fecal incontinence: a randomized sham-controlled clinical trial. Dis Colon Rectum. 2017;60(8):860–5. 16. Felt-Bersma RJ. Temperature-controlled radiofrequency energy in patients with anal incontinence: an interim analysis of worldwide data. Gastroenterol Rep (Oxf). 2014;2(2):121–5. 17. Kaiser AM, Orangio GR, Zutshi M, Alva S, Hull TL, Marcello PW, et al. Current status: new technologies for the treatment of patients with fecal incontinence. Surg Endosc. 2014;28(8):2277–301.

Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell

43

Zoran Krivokapić and Barišić Goran

Learning Objectives

• In this chapter, less frequently used and novel techniques under investigation for the treatment of fecal incontinence will be discussed.

43.1 Introduction Fecal incontinence is a socially incapacitating condition. It is quite distressing for patients and has negative effects on social interactions and mental health and severely affects quality of life. It seems that the incidence of fecal incontinence has been rising by time. A study published at the end of the last century reported that fecal incontinence affected 2% of the general population [1]. Meta-analysis published 10 years later reported quite higher rates, ranging from 11% to 15% [2]. A more recent study reported the prevalence of fecal incontinence of 6% in women younger than 40 years old, 15% in women older than 40 years, and 6–10% in men [3]. However, these differences may be the consequence of various definitions of fecal incontinence used in studies performed in diverse time periods and may not reflect the accurate increase. The most common cause of fecal incontinence is injury of the anal sphincter during vaginal delivery, followed by iatrogenic injuries caused by surgical procedures such as fistulotomy, hemorrhoidectomy, and sphincterotomy. Direct perineal trauma as a consequence of traffic accidents as well as war injuries and/or post-pelvic irradiation may also play

Z. Krivokapić (*) · B. Goran Clinical Center of Serbia, Clinic for Digestive Surgery, First Surgical Clinic, Belgrade School of Medicine, University of Belgrade, Belgrade, Serbia e-mail: [email protected]

an important role. Conservative treatment is usually a first choice but is ineffective in most cases, especially in traumatic fecal incontinence. In these cases, only surgical treatment may give satisfactory results. In most cases, the decision as to which surgical procedure should be used depends on the severity of anal sphincter injury, experience of surgical team, and funds, because some procedures are quite expensive. Patients who have limited sphincter defects (less than 50% of the circumference revealed by endorectal ultrasound) may be offered sphincteroplasty as a first choice, because this is a relatively cheap procedure with satisfactory results in around 50% of patients in the long term. At the same time, perineal anatomy can be restored with excellent aesthetic results. Patients with more extensive injuries, not amenable to sphincteroplasty, may be offered artificial sphincter implantation, muscle transposition, etc. Patients with anatomically intact, but not functional sphincters, may benefit from sacral nerve stimulation, biofeedback, bulking agents, etc., but these procedures may be beneficial even in patients with sphincter defects. In some cases multiple procedures may be combined. New and emerging techniques such as stem cell therapy may change the treatment algorithm in the near future. However, in cases when all treatments fail, the only reasonable solution may be the permanent stoma. In this chapter, we will focus on less frequent and investigational techniques for fecal incontinence treatment.

43.2 Sphincter Replacing Procedures Sphincter replacing therapy is indicated in patients with large sphincter defects, more than 50% of the muscle missing, or completely destroyed sphincters. It may also be indicated in case of sacral nerve stimulation (SNS) failure in patients who would like to avoid colostomy. In practice, the sphincter replacement procedures are divided in muscle transposition techniques or the artificial bowel sphincter (ABS) implantation. Although frequently used in the past, the indications for sphincter replacement surgery are decreas-

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_43

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ing since the introduction of SNS. In modern surgery indications include end stage severe fecal incontinence associated with extensive anal sphincter loss or congenital anorectal malformation, as imperforate anus or spina bifida, or perianal colostomy after abdominoperineal resection where the only other option is a stoma [4, 5].

43.3 Muscle Transposition Techniques Muscle transposition techniques are usually used in the management of end-stage incontinence where previous, less aggressive treatments have failed. Various skeletal muscles were used in the past as neosphincters in order to maintain fecal continence [6]. These muscles were typically in close proximity to the anus and were harvested and encircled around the anus in order to substitute anal sphincters [6]. The earliest successful report ensued when Chetwood [7] performed transposition of the gluteus muscle to restore continence in a patient who developed fecal incontinence after trauma. Gracilis muscle transposition (without electrical stimulation) was first described by Pickrell et al. in 1952 [8] in order to restore continence in four children. Fedorov et al. [9] used adductor longus muscle, while Hakelius et al. [10] utilized free autogenous muscle transplant for the treatment of anal incontinence in children. Some advocated smooth muscle transplants [11], while Hallan [12] used electrically stimulated sartorius neosphincter in a canine model. Sartorius neosphincter showed excellent results in animal model but was not successful in humans. The main downside of all passive muscle transposition techniques was the inability of patients to voluntarily contract the transposed muscle in an effective manner to maintain continence. Another problem was the inability of the transposed muscle to maintain tonic contraction over prolonged periods of time. In practice, only two muscles were used for this purpose: the gluteus and the gracilis muscle.

43.4 G  luteoplasty (Gluteus Maximus Plasty) Since Chetwood reported the first transposition of the gluteus maximus muscle in order to treat fecal incontinence, various modifications of the original technique were described. In 1930, Chittenden [13] used gluteal muscle flaps for anal reconstruction after abdominoperineal resection, while Bistrom [14] transposed gluteus muscle and pulled the rectal stump through a previously created hole in the muscle for treatment of fecal incontinence. After the

Z. Krivokapić and B. Goran

World War II, this technique was almost abandoned until in 1981 Bruining [15] reported modified technique of gluteus muscle transposition in a 17-year-old female injured in a traffic accident. He detached gluteus muscles from the femur and wrapped them around the anus to create a “scissorlike” mechanism. In 1982 Hentz [16] modified the technique by detaching gluteus muscles from the sacral and coccygeal origin and wrapped them around the anus in order to stabilize spitted muscle slings at a proper resting tension and fiber length. In order to minimize donor site morbidity (hip destabilization), Orgel [17] proposed the technique of a double-­ split gluteus maximus muscle flap, where he mobilized only the inferior part of one muscle (usually the right side) at its insertion at the iliotibial band and femur. A number of case reports or small series were reported since 1980, using different techniques with a proximally or distally based muscle flaps [18–23]. In 1996, Guelinckx et al. [24], encouraged by reported results of dynamic cardiomyoplasty and dynamic graciloplasty, presented results in seven patients treated by conventional and four patients treated by dynamic gluteoplasty. Theoretically, the use of the gluteus maximus muscle as a substitute for anal sphincters has advantages because it is normally used as an auxiliary muscle to maintain fecal continence and patients can be easily trained to use it. At the same time, it is a well-vascularized, large, and powerful muscle, supplied by the superior and inferior gluteal artery, capable for forceful contraction. It is innervated by the inferior gluteal nerve originating from the L5 and S1 nerve roots which makes it functional even in cases of fecal incontinence due to the pudendal neuropathy. Active contraction and high tonus of the muscle can be maintained for longer periods compared to the gracilis muscle which is of paramount importance for maintaining continence. Furthermore, its neurovascular structures can easily be preserved during dissection and detachment from the sacrum, and neurovascular pedicle has less traction compared to graciloplasty. In most cases muscle wraps have sufficient length to reach the anal canal without excessive tension. Several wrap configurations are possible because the amount of the transferred muscle far exceeds the amount of muscle tissue of a normal anal sphincter. It enables enough of healthy and contractile muscle to completely encircle the anus and form a muscle cuff even in cases when muscle atrophy occur, which is not uncommon after transposition. The best functional results were obtained with a technique that uses caudal parts of both gluteus muscles to encircle the anus [25]. Unfortunately, there are important drawbacks regarding to this technique. Gluteus maximus contains predominantly type II striated muscle fibers which make it prone to fatigue. It is not capable to sustain continuous contraction for a longer period of time. Furthermore, the

43  Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell

muscle after dissection is bulky, making it technically demanding to tunnel and wrap around the anus especially in patients with deficient perineal body or excessive scarring of the rectovaginal septum. There is also a problem with a higher donor site morbidity compared to gracilis muscle transposition. In gluteoplasty, in most cases, muscles from both sides should be harvested, while in graciloplasty only one muscle is taken. Gluteus maximus is a hip extensor, important for walking, running, standing up from sitting position, and walking upstairs, so patient may experience some difficulties in everyday life. In most cases, sport ­activities are dramatically reduced after muscle transposition. At the same time, this natural function of the muscle can make continence difficult to maintain when patient is running or climbing stairs [26]. Finally, surgical technique for gluteoplasty is more complex and challenging because the access to its neurovascular bundle is less familiar compared to graciloplasty. Those may be the reasons why it never gained the same popularity as the graciloplasty, even though results of non-stimulated gluteoplasty were shown to be superior [27] or at least equal [21] to the results of non-stimulated graciloplasty. The best candidate for this procedure is a young patient with severe sphincter defects or destroyed sphincters not amenable to sphincteroplasty. It may be a good option for patients who may benefit from transposition of substantial muscle bulk but without excessive rectovaginal scarring. The primary contraindication for this procedure is the presence of injured or nonfunctioning gluteus maximus muscles. Patients with fecal incontinence secondary to a spina bifida or myelomeningocele should not be treated with gluteoplasty because the nerve supply of the muscle is derived from the inferior gluteal nerve, originating from L5 to S1. Conversely, patients with Leriche syndrome are not candidates for this procedure, since vascular supply for the muscle originates from the superior and inferior gluteal artery. Complications after gluteoplasty are not uncommon. The most frequent complication is wound infection occurring in almost one quarter of patients [28]. Other, less frequent complications include skin necrosis, anal canal necrosis, anal canal stricture, fecal impaction, obstructive defecation, chronic pain, and donor site morbidity such as posterior thigh numbness, dysesthesia, and severe chronic pain. Christiansen [21] reported wound infection in three out of seven patients after bilateral gluteoplasty. Hultman [23] reported donor site morbidity and perirectal complications in 64% of patients in a retrospective analysis of 25 consecutive patients undergoing gluteoplasty for fecal incontinence. Puerta [29] reported a success rate of 70% using the gluteus transposition technique in 22 patients with fecal incontinence. Madoff [30] reported wound infection in 27% and anal stricture in 9% out of 11 patients treated with dynamic

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gluteoplasty. In most reports, continence improved after gluteoplasty. There are a limited number of studies with objective assessment of long-term results. Guelinckx reported continence for stool in 9 out of the 11 patients, while seven patients were also continent for liquids [24]. Christiansen found improvement in continence in three out of seven patients, while in four it remained unchanged [21]. Hultman found that gluteoplasty was successful in restoring fecal continence in 72% and partially successful in 16% of patients [23]. According to a review of the literature by Fleshner, complete continence was achieved in 60% and partial continence in 36%, while total failure was observed in 4% of patients [28]. Combined data from 17 studies including 149 patients with gluteoplasty showed successful or partially successful outcome in 73% of patients with an overall complication rate of 38%. Since the first report by Chittenden, anorectal reconstruction after abdominoperineal resection (APR) by gluteoplasty has received little attention, so only few reports were published [20, 29, 31] (Fig. 43.1).

43.5 Dynamic Gluteoplasty Madoff [30] reported results of the prospective multicenter study where electrostimulation of the transposed gluteus muscle was performed in order to improve results. He achieved good results in all patients initially but maintained successful outcome in only 5 (45%) out of the 11 patients and concluded that this procedure should be limited to investigational purposes. Guelinckx [24] treated 11 patients, 7 with conventional and 4 patients with dynamic gluteoplasty. All patients who had satisfactory results and were continent for both solid and liquid stool were in dynamic gluteoplasty group. However, dynamic gluteoplasty newer gained such a popularity as dynamic graciloplasty. It was probably because the gracilis was technically easier to use, had less variations in the nerve and blood supply, and had less donor site morbidity. Finally, electrostimulation threshold is much higher in gluteoplasty resulting in shorter device battery life.

43.6 Graciloplasty Passive gracilis muscle transposition (without electrical stimulation) was first described by Pickrell et al. in 1952 [8] after an attempt to restore continence function in four children. More than 30 years after, Corman [32] reported good results with this technique, while Faucheron et  al. [33] confirmed that significant proportion of patients may have satisfactory continence after passive gracilis transposition.

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b

c

Fig. 43.1 (a–c) Gluteoplasty. (a) Marks in the operative field. (b) Identifying the inferior gluteal nerve and vascular pedicle. (c) Transposition of the muscle. (Reprinted with permission from McPhail

L.E., Hultman C.S. Gluteoplasty for the Treatment of Fecal Incontinence. In: Ratto C., Doglietto G.B., Lowry A.C., Påhlman L., Romano G. (eds) Fecal Incontinence. Springer, Milano 2007)

The gracilis muscle is the most superficial adductor of the thigh and has little impact on motion of the lower extremity. Its natural function is to assist the legs in adduction and internal rotation, so when this muscle is used for a neosphincter procedure, adjacent muscles take over its function. As a result, there is minimal donor site morbidity, and patients can perform most of everyday activities including sports [34]. This superficial muscle has constant and proximal neurovascular supply, which enables effortless dissection and in most cases sufficient muscle length to overlap around the anus. Unfortunately, like all skeletal muscles, gracilis has a majority of type II, fatigue prone, fast-twitch muscle fibers and is incapable to sustain prolonged, forceful contraction. At the same time, natural function of this muscle has nothing in common with muscles responsible for

continence making it very difficult for a patient to learn how to contract and use the gracilis muscle as a neosphincter. Muscle fatigue and the inability of patients to voluntarily contract the transposed muscle were the main reasons why successful results of non-­ stimulated graciloplasty were achieved in less than 50% of patients. Moreover, most of the patients had severe constipation due to outlet obstruction produced by overtightening of the anus with the transposed muscle [35]. Finally, in many cases of fecal incontinence, there is an adjacent pudendal nerve damage, which precludes this technique. Results of non-stimulated graciloplasty were successful in less than 50% of cases, although some claimed that continence rate was improved in more than 80% [32, 35–37] (Fig. 43.2).

43  Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell

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b

c d

Fig. 43.2 (a) Dissection of the gracilis muscle. (b) Preserving of the neurovascular bundle. (c) Muscle transposition. (d) Muscle wrapped around the anal canal

43.7 Dynamic Graciloplasty

prone muscle fibers to a slow, fatigue-resistant fibers by continuous electrical stimulation. In Italy, Cavina [43] et al. used A physiologic base for dynamic graciloplasty was the results graciloplasty for anal sphincter reconstruction after abdomifrom experimental studies in muscle physiology in animals. noperineal resection. In England, group around N. Williams They found that low-frequency electrical stimulation of the stimulated directly the nerve trunk using external device muscle can change normal muscle fiber pattern and trans- periodically. In Maastricht, Beaten et  al. used permanent form fiber type II, fatigue prone muscles into fiber I, fatigue-­ implantable stimulator for electrostimulation of the muscle. resistant muscles [12, 38]. This process can change skeletal Direct nerve stimulation is more physiological and requires muscle-like gracilis into a muscle with properties of a lower stimulation level thus maximizing battery life, while sphincter muscle. muscle electrodes are more secure, and there is less chance Introduction of muscle electrostimulation techniques, of lead displacement. This procedure became the most popubased on research in using the latissimus dorsi muscle to lar form of a muscle neosphincter because of its simplicity, assist a failing heart in dynamic cardiomyoplasty [39], the nature of neurovascular supply of the gracilis muscle, renewed the interest in the gracilis muscle transposition. and minor donor site morbidity. Although the first electrical stimulation for treatment of fecal Dynamic graciloplasty is a major procedure, and many incontinence after operation for anorectal agenesis was complications have been reported. The most frequent were reported by Dickson in 1968 [40], it was C.  Beaten from wound complications. In a prospective multicenter study Maastricht who in 1986 implanted the first neurostimulator including 139 patients from 12 centers, Madoff [30] reported in a patient who already had conventional graciloplasty major wound complications in 32% of patients and minor 10 years earlier for anal atresia. wound complications in 29%. Tendon detachment was The new technique, named dynamic graciloplasty, was recorded in 3%, pain in 22%, and device/stimulation probattributed to Beaten [41] and Williams [42] who indepen- lems in 11% of patients. Necrosis of the neoanus as well as dently developed the concept of transforming fast, fatigue the gracilis muscle was also reported. Moreover, 48% of the

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138 reported complications in this study required one or more reoperations [30]. Functional failure, which was not related to some specific complication, was recorded in 40% of all failures [30]. Constipation was reported after graciloplasty in approximately 16% of patients, and in some cases it was due to overtightening of the anus with the gracilis. Insufficient contraction of the gracilis muscle is complication caused by muscular or stimulation problems. Dynamic graciloplasty is a very complex procedure, and experience is very important in order to reduce complication rate and improve results. It should be performed only in high-volume centers. Madoff [30] reported significant differences in complication rate and outcome comparing high- and low-volume centers. The overall major wound complication rate was 17.4% in high-volume centers compared to 33.1% in low-­volume centers. In the literature, the success rates of dynamic graciloplasty in treatment of fecal incontinence vary from 45% to 80% [44–49]. Most studies reported a small number of patients with an overall improvement of continence in about 50% of cases with follow-up ranging from 7  months to 4  years. Again, high-volume centers did better than inexperienced ones. The reported overall success rate was 80% in experienced centers compared to only 47% in inexperienced centers [30]. Large differences in success rates may be related to the learning curve associated with this complex procedure. It may also be related to the length of the follow-­up and different tools and definitions used to measure outcomes. Although the results of dynamic graciloplasty are satisfactory in general, the problem is very high complication rate, mostly wound infections, high rates of reoperation, and complications related to the implanted devices. There are also issues with obstructive defecation. In addition, the long-­ term consequences of chronic electrostimulation may cause the problem because there are concerns that chronic electrostimulation may decrease muscle fiber diameter and lead to muscle degeneration and atrophy by affecting the collateral blood supply [50, 51]. Another important disadvantage is the high cost of the procedure. However, studies showed that there is a considerable cost benefit of graciloplasty compared to the costs of the colostomy in the long term [52]. Muscle transposition techniques continue to have its role in treatment of fecal incontinence although results are not always predictable. Since they are major surgical procedures with lots of complications, they should be reserved only for selected cases, when all other options are not possible and when permanent colostomy is the only alternative.

43.8 Artificial Bowel Sphincter (ABS) The ABS manages incontinence by imitating the natural action of the sphincter muscle. The device consists of an

Z. Krivokapić and B. Goran

inflatable cuff that occludes the anal canal, a pressure-­ regulating balloon located in the retroperitoneal space, and a control pump placed in the scrotum or labia. It was designed as a sphincter replacement procedure for treatment of an end-stage fecal incontinence in cases when all previous treatments failed in patients who wanted to avoid colostomy. The first artificial bowel sphincter for fecal incontinence was implanted by Christiansen in 1987 [53]. He used urinary sphincter (AMS 800), while Lehur [54] designed it specifically for fecal incontinence treatment in 1996. Since that time, the artificial bowel sphincter has been used mostly in specialized centers. However, most studies had a small number of patients, and it was difficult to assess the effectiveness of this device. One meta-analysis included 21 studies with 541 patients and revealed that ABS was implanted only in patients with severe end-stage fecal incontinence [55]. The most common indication was sphincter destruction followed by congenital malformations, while one study included perineal colostomy after abdominoperineal resection. There was no mortality, but complication rate was high. The pooled rate of surgical revision was 49%, and the most common reason was device malfunction, such as cuff rupture or balloon and pump leak and cuff unbuttoning. However, device malfunction did not appear to be a major cause of definite failure. The pooled rate of permanent device removal was 24%. The most common reasons were device infection and erosion (pooled rates 56%). The pooled rate of retaining a functional device was 69%. Evacuatory difficulty was common, but it was severe in only 8% of patients. In cases when the artificial bowel sphincter is operational, without serious complications, patients might experience a significant improvement in continence and even in quality of life. The pooled improvement rate of continence was between 55% and 75% depending on the method/scale used for evaluating continence function. All studies revealed significant improvements in QOL after implantation, including at long-term follow-up. ABS is successful method for treating severe fecal incontinence, but at the price of a very high complication rate, frequently leading to subsequent explantation of the device. The most frequent complication is infection which was reported to be around 26% (in some series up to 76%) [56], followed by constipation that occurs in approximately 29% of patients. Pain and technical failure are also common complications, in some cases necessitating device removal. Patients should be well informed about the high rate of complications before accepting this procedure. As a result of technical challenges, device malfunctions and high infection rates, followed by high rates of further surgery for complications, this device never became widely accepted (Fig. 43.3).

43  Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell

43.9 Magnetic Anal Ring Magnetic anal ring was first used for anal incontinence treatment by Lehur and colleagues in 2010 [57] although it was originally developed for the treatment of gastroesophageal reflux disease (LINX® Reflux Management System, Torax

“Sphincter” Balloon

Pump

Fig. 43.3  Artificial bowel sphincter (Reprinted with permission from Herold A. Incontinence. In: Herold A, Lehur PA, Matzel KE, O Connell PR.  European manual of medicine, Coloproctology. Springer-­Verlag Berlin Heidelberg 2008)

a

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Medical). This device was considered to add support of a weakened anal sphincter through the magnetism of beads placed around the anal canal (FENIX® Continence Restoration System, Torax Medical). Several small studies revealed that surgical procedure is straightforward, and the safety profile is acceptable. They reported promising short-­ term outcomes with this technique, but long-term outcomes still remain unknown. In general, therapeutic success rates ranged between 53% and 66% at short-term follow-up. In one study, long-term results with the median follow-up of 5 years were published [58]. This study included 35 patients with severe fecal incontinence for ≥6 months, who had previously failed conservative therapy. During follow-up, device had to be removed in seven patients due to complications. Therapeutic success rates, including treatment failures (device explantation or stoma creation), were 63% at year 1, 66% at year 3, and 53% at year 5 [58]. The most frequent adverse events included defecatory dysfunction (20%), implant site pain (14%), device erosion (11%), implant site infection (11%), and bleeding (9%) [58]. Authors concluded that magnetic anal sphincter augmentation may provide excellent outcomes in patients with functioning device. This technique may develop into a promising new treatment option for fecal incontinence. The perfect indication has yet to be determined, and more studies with larger numbers of patients with a longer follow-up are necessary to determine the role of magnetic anal ring in surgical treatment of fecal incontinence. However, in 2017, Torax Medical announced the discontinuation of sales and clinical studies of the FENIX® Continence Restoration System (Fig. 43.4). b

Fig. 43.4 (a, b) FENIX® Continence Restoration System. (a) Fenix glamor closed. (b) Fenix glamor opened (Reprinted with permission from Torax Medical)

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43.10 Stem Cell Transposition The concept of full regeneration of the damaged tissue is not a new one, but, until recently, it was mostly seen in futuristic movies and revealed human aspiration and thoughts toward noninvasive and perfect healing. Today, we are able to investigate these processes in vitro and in vivo thus making regeneration of the tissue possible. Mesenchymal stem cells have remarkable pluripotent abilities to differentiate into different types of cells like myocytes, osteocytes, adipocytes, etc. In addition, in many tissues, they serve as internal repair system, dividing essentially without limit to replenish other cells during the whole life. They are regarded to have potential to improve muscle contractile function by replacing fibrous tissue of the injured muscle with a new muscle cells. There are two kinds of stem cells: embryonic stem cells and somatic or “adult” stem cells (present in blood, bone marrow, and fat tissue). The adipose tissue is the richest source of adult stem and other regenerative cells, so-called adipose-­ derived regenerative cells (ADRCs). It is estimated that ADRC accounts to approximately 1% of all nucleated cells in the lipoaspirate, which is more than 100-fold the yield obtained from bone marrow aspiration and much easier to harvest [59, 60].The reparative mechanism of ADRCs includes the modulation of inflammation and trophic factors to improve engraftment. It also improves the endogenous regenerative potential without risks of rejection. Most authors agree that many different growth factors and other mediators are involved in this process of tissue regeneration. Furthermore, secretion of high levels of angiogenic factors and production of multiple growth factors make them a suitable option for muscle repair [61, 62]. The ability of ADRCs to differentiate into muscle cells has been clearly shown in both in vitro [63, 64] and in vivo [65, 66] studies. Thus, the concept of regeneration of the injured anal sphincter muscle tissue and improvement of its function using stem cells might be promising alternative treatment strategy. So far, stem cell transplantation is mostly an experimental method, studied mainly in animal models, but there are also studies performed in humans. These studies have confirmed the long-­ term safety of application of mesenchyme and muscle-derived stem cells in treatment of urinary and fecal incontinence, perianal fistula repair, and graft material enhancement [67– 72]. Others reported satisfactory results in chronic anal fissure treatment with ADRCs [73] (Figs. 43.5 and 43.6). According to the results of an experimental model in rats [74], bone marrow-derived mesenchymal stem cell injection improved muscle regeneration and contractility function of the anal sphincter. Kang [75] reported that autologous muscle-­ derived stem cells enhanced contractility of the anal sphincter and differentiation of muscle masses at the stem cell injection sites. Recently, randomized double-blind clinical trial was performed in humans in order to evaluate the efficacy of allogeneic transplantation of ADSCs for relieving fecal inconti-

Fig. 43.5 Liposuction

Fig. 43.6  Injection of adipose-derived regenerative cells into the external anal sphincter

nence in patients with external anal sphincter defects treated with sphincteroplasty. Although the number of patients was small and follow-up was short, this study showed that injection of ADSCs in the anal sphincter during sphincter repair surgery may cause replacement of fibrous tissue with muscle tissue, which exhibits contractile function [76]. Another randomized, prospective, placebo-controlled trial in humans is

43  Other Surgical Options for Anal Incontinence: From End Stoma to Stem Cell

ongoing in order to assess the safety of adipose-derived mesenchymal stem cells after the injection into the anal sphincter. The secondary end point is to compare the efficacy of ADRCs in patients with fecal incontinence [77]. Another strategy is to harvest stem cells directly from the striated skeletal muscle and culture them in  vitro into the myoblasts. The advantage of this procedure is that after implantation these cells only differentiate into muscle cell lines, regardless of the type of tissues in the vicinity. Skeletal muscles have the capability to regenerate (at least partially) and to repair damage. Special stem cells, called satellite cells, located among the muscle fibers, became activated in response to muscle damage and transform into myoblasts, which are then capable of intense proliferation in order to repair damage. The technology of in vitro myoblast culturing is already available and is continuously improving. The first study, involving ten women with obstetric external anal sphincter disruption treated by injection of adult stem cells, autologous myoblasts (AM), was published by Frudinger [78]. No adverse events were observed. At 12  months the Wexner incontinence score had decreased by a mean of 13.7  units, anal squeeze pressures were unchanged, and overall quality of life scores improved by a median of 30 points. Authors concluded that treatment with autologous myoblasts was safe and well tolerated and significantly improved symptoms of anal incontinence due to obstetric anal sphincter trauma. Recently, first randomized, placebo-­controlled study of intrasphincteric injections of autologous myoblasts in 24 patients with fecal incontinence was published [79]. This was a phase 2, double-blind, placebo-­controlled study where administration of AM or placebo was performed with eight injections in the existing residual external anal sphincter under endoanal ultrasound guidance. At follow-up visits (6 and 12 months), CCI and FIQL scores, anorectal manometry, perineal electrophysiological tests, anal ultrasound, and MRI were performed. Myoblast injection resulted in a significant reduction in CCI scores and improvement in quality of life. The CCI score at 6 and 12 months decreased from a median of 15 at baseline to 9 and 6.5, respectively. After 12 months there was a >30% reduction in the CCI score in 58% of patients in the AM arm compared with 8% in the placebo arm. Excellent results obtained in this and two other studies [78, 80] revealed that the injection of AM in the anal sphincter may become a standard treatment for FI and may change the treatment paradigm of fecal incontinence in the near future.

ble of reducing fecal incontinence-related problems. Different types of anal plugs are commercially available. Plugs are made of different materials (polyurethane, polyvinyl alcohol) and come in different designs, shapes, and sizes. First they were used in patients with fecal incontinence due to major neurological problems, such as spina bifida. A limited data regarding this procedure exist in the literature. One prospective, randomized, controlled study evaluated the use of the anal plugs in children and adults with fecal incontinence [81]. This study showed that the majority of patients gained some benefits, reflected in reduced soiling, and the small but quantifiable improvements in the quality of life. The conclusion of this study was that anal plug may be a good solution for selected patients. In a Cochrane review that included four studies with a total of 136 patients, they found that plugs may be helpful in alleviating problems caused by incontinence [82]. However, the available data suggest that anal plugs can be difficult to tolerate because 48 participants (35%) were excluded before the end of the study, suggesting poor compliance. Satisfying results were obtained in 77% of users that achieved a ≥50% reduction in incontinence frequency [82]. Selection of the type of plug can be very important for its performance. Intolerance of the device and failure of retention are the most frequently reported adverse events. So far, anal plugs can be considered as relatively efficient, cheap, and acceptable symptomatic fecal incontinence treatment option in a selected group of people, either as a substitute for other forms of management or as an adjuvant treatment option (Fig. 43.7).

43.11 Anal Plugs The anal plug is a special intra-anal device that acts as a physical barrier and prevents fecal leakage, thus enabling continence. This is a simple and low-cost treatment, capa-

529

Fig. 43.7  Anal plug

530

43.12 Colostomy Although fecal diversion is usually the last choice in treatment of severe fecal incontinence, it has a 100% cure rate, but it is still unknown whether it truly improves QOL in these patients in whom all previous treatments have failed. The first study that addressed this issue was published by Colquhoun [83]. It was a cross-sectional postal survey of 110 patients with fecal incontinence or an end colostomy. QOL measures used in this study included the Short Form 36 General Quality of Life Assessment (SF-36) and the Fecal Incontinence Quality of Life (FIQOL) score. Analysis of the SF-36 revealed higher social function score in the colostomy group, and analysis of the FIQOL revealed higher scores in the coping, embarrassment, lifestyle, and depression scales in the colostomy group compared to the FI group. The conclusion of this study was that colostomy improves QOL in patients who suffer moderate-to-severe fecal incontinence. Finally, colostomy formation has acceptable complication rate, offers 100% cure with no relapse, results in better QOL, and may be a good option when all previous treatments fail. However, creation of a permanent stoma is a radical option and has a distinctive form of physical impairment and QOL adjustment. One retrospective study [84] has examined patients’ views of a colostomy in fecal incontinence and included 11 males and 58 females with a median age of 64 years. The majority of patients had experienced a variety of problems with the stoma, while only ten patients reported no problems with their stoma. On the other hand, the majority (83%) felt that the stoma did not restrict their life, and nearly all felt that the stoma had improved their quality of life. The overwhelming majority of patients in this study were positive about the stoma and the difference it had made to their life. Although the literature is sparse regarding colostomy in fecal incontinence treatment, based on available studies, we can conclude that colostomy may be a viable option in patients with an endstage, severe fecal incontinence, where all previous treatment attempts have failed.

Z. Krivokapić and B. Goran

ter, when a permanent colostomy is the only other viable alternative. ABS is successful method for treating severe fecal incontinence, but at the price of a very high complication rate, frequently leading to subsequent explantation of the device. Magnetic anal sphincter augmentation may provide satisfactory outcomes in patients with functioning device, but Torax Medical announced the discontinuation of sales of the FENIX® Continence Restoration System. Promising initial results with different cell therapy options may change the treatment paradigm of fecal incontinence in the near future, but further research is needed in this area. Anal plugs can be considered as a relatively efficient, cheap, and acceptable symptomatic fecal incontinence treatment option in a selected group of patients, either as a substitute for other forms of management or as an adjuvant treatment option. At the end, colostomy may be a decent option in patients with an end-stage, severe fecal incontinence, where all previous treatment attempts have failed.

Take-Home Messages

• Surgical treatment of fecal incontinence is often complex and should be performed only in specialized centers. • Patients with limited sphincter defects (less than 50% of the circumference) may be offered sphincteroplasty as a first choice. • Sphincter replacing therapy is indicated in patients with large sphincter defects or completely destroyed sphincters but with a price of high morbidity, complications, high rates of reoperation, and frequently unpredictable results. • New and under investigation techniques such as stem cell therapy may change the treatment paradigm of fecal incontinence in the near future, but further research is needed.

References 43.13 Conclusion In summary, surgical treatment of fecal incontinence is often quite challenging. In most cases, the decision regarding surgical procedure depends on severity of anal sphincter injury, experience of surgical team, and funds, because some procedures are quite expensive. Muscle transposition techniques still have a role in the treatment of fecal incontinence, but with a price of high morbidity, complications, wound infections, high rates of reoperation, and frequently unpredictable results. Graciloplasty appears to be superior to gluteoplasty, as it has less donor site morbidity. These techniques should only be considered in cases with a severely deficient sphinc-

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532 electrically stimulated canine rectus abdominis muscle island-flap stomal sphincters. Plast Reconstr Surg. 2003;111(1):189–98. 51. Bouamrire’ne D, Micallef JP, Rouanet P, Bacou F.  Electrical stimulation-­ induced changes in double-wrapped muscles for dynamic graciloplasty. Arch Surg. 2000;135(10):1161–7. 52. Adang EM, Engel GL, Rutten FF, Geerdes BP, Baeten CG. Cost-­ effectiveness of dynamic graciloplasty in patients with fecal incontinence. Dis Colon Rectum. 1998;41(6):725–33. 53. Christiansen J, Ronholt Hansen C, Rasmussen O. Implantation of artificial sphincter for anal incontinence. Lancet. 1987;2:244–5. 54. Lehur PA, Glemain P, Bruley des Varannes S, Buzelin JM, Leborgne J, Lehur PA, Glemain P.  Outcome of patients with an implanted artificial anal sphincter for severe faecal incontinence. A single institution report. Int J Colorect Dis. 1998;13(2):88–92. 55. Hong KD, Dasilva G, Kalaskar SN, Chong Y, Wexner SD. Long-­ term outcomes of artificial bowel sphincter for fecal incontinence: a systematic review and meta-analysis. J Am Coll Surg. 2013;217(4):718–25. 56. Darnis B, FaucheronJl F-D, Henri Damon H, Fau-Barth XBX.  Technical and functional results of the artificial bowel sphincter for treatment of severe fecal incontinence: is there any benefit for the patient? Dis Colon Rectum. 2013;56(1530-0358 (Electronic)):505–10. 57. Lehur PA, McNevin S, Buntzen S, Mellgren AF, Laurberg S, Madoff RD.  Magnetic anal sphincter augmentation for the treatment of fecal incontinence: a preliminary report from a feasibility study. Dis Colon Rectum. 2010;53(12):1604–10. 58. Sugrue J, Lehur PA, Madoff RD, et  al. Long-term experience of magnetic anal sphincter augmentation in patients with fecal incontinence. Dis Colon Rectum. 2017;60(1):87–95. 59. Lin KMY, Masuda Y, Togashi K, Ohno T, Tamura T, Toyoshima Y, Sugimachi K, Toyoda M, Marc H, Douglas A. Characterization of adipose tissue-derived cells isolated with the Celution system. Cytotherapy. 2008;10(4):417–26. 60. Strem BM, Hicok KC, Zhu M, Wulur I, Alfonso Z, Schreiber RE, Fraser JK, Hedrick MH.  Multipotential differentiation of adipose tissue-derived stem cells. Keio J Med. 2005;54(3):132–41. 61. Kalbermatten DF, Schaakxs D, Kingham PJ, Wiberg M.  Neurotrophic activity of human adipose stem cells isolated from deep and superficial layers of abdominal fat. Cell Tissue Res. 2011;344:251–60. 62. Kim Y, Kim H, Cho H, Bae Y, Suh K, Jung J. Direct comparison of human mesenchymal stem cells derived from adipose tissues and bone marrow in mediating neovascularization in response to vascular ischemia. Cell Physiol Biochem. 2007;20:867–76. 63. Zuk PA, Zhu M, Ashjian P, De Ugarte DA, Huang JI, Mizuno H, Alfonso ZC, Fraser JK, Benhaim P, Hedrick MH.  Human adipose tissue is a source of multipotent stem cells. Mol Biol Cell. 2002;13:4279–95. 64. Eom YW, Lee JE, Yang MS, Jang IK, Kim HE, Lee DH, Kim YJ, Park WJ, Kong JH, Shim KY, et al. Effective myotube formation in human adipose tissue-derived stem cells expressing dystrophin and myosin heavy chain by cellular fusion with mouse C2C12 myoblasts. Biochem Biophys Res Commun. 2011;408:167–73. 65. de la Garza-Rodea AS, van der Velde-van Dijke I, Boersma H, Goncalves MA, van Bekkum DW, de Vries AA, KnaanShanzer S.  Myogenic properties of human mesenchymal stem cells derived from three different sources. Cell Transplant. 2012;21:153–73. 66. Vieira NM, Bueno CR Jr, Brandalise V, Moraes LV, Zucconi E, Secco M, Suzuki MF, Camargo MM, Bartolini P, Brum PC, et al. SJL dystrophic mice express a significant amount of human muscle proteins following systemic delivery of human adipose-­ derived stromal cells without immunosuppression. Stem Cells. 2008;26:2391–8. 67. Voswinkel J, Francois S, Simon JM, Benderitter M, Gorin NC, Mohty M, Fouillard L, Chapel A.  Use of mesenchymal stem cells (MSC) in chronic inflammatory fistulizing and fibrotic dis-

Z. Krivokapić and B. Goran eases: a comprehensive review. Clin Rev Allergy Immunol. 2013;45(2):180–92. 68. Guadalajara H, Herreros D, De-La-Quintana P, Trebol J, Garcia-­ Arranz M, Garcia-Olmo D.  Long-term follow-up of patients undergoing adipose-derived adult stem cell administration to treat complex perianal fistulas. Int J Colorectal Dis. 2012;27(5):595–600. 69. García-Olmo D, García-Arranz M, Herreros D, Pascual I, Peiro C, Rodríguez-Montes JA. A phase I clinical trial of the treatment of Crohn’s fistula by adipose mesenchymal stem cell transplantation. Dis Colon Rectum. 2005;48(7):1416–23. 70. Lee WY, Park KJ, Cho YB, Yoon SN, Song KH, Kim-do S, Jung SH, Kim M, Yoo HW, Kim I, Ha H, Yu CS.  Autologous adipose tissue-derived stem cells treatment demonstrated favorable and sustainable therapeutic effect for Crohn’s fistula. Stem Cells. 2013;31(11):2575–81. 71. Sanz-Baro R, García-Arranz M, Guadalajara H, de la Quintana P, Herreros MD, García-Olmo D.  First-in-human case study: pregnancy in women With Crohn’s perianal fistula treated with adipose-­derived stem cells: a safety study. Stem Cells Transl Med. 2015;4(6):598–602. 72. Lane FL, Jacobs S. Stem cells in gynecology. Am J Obstet Gynecol. 2012;207(3):149–56. 73. Andjelkov K, Sforza M, Barisic G, Soldatovic I, Hiranyakas A, Krivokapic Z. A novel method for treatment of chronic anal fissure: adipose-derived regenerative cells – a pilot study. Colorectal Dis. 2016;19:570–5. 74. Lorenzi B, Pessina F, Lorenzoni P, Urbani S, Vernillo R, Sgaragli G, Gerli R, Mazzanti B, Bosi A, Saccardi R, Lorenzi M. Treatment of experimental injury of anal sphincters with primary surgical repair and injection of bone marrow-derived mesenchymal stem cells. Dis Colon Rectum. 2008;51(4):411–20. 75. Kang SB, Lee HN, Lee JY, Park JS, Lee HS, Lee JY. Sphincter contractility after muscle-derived stem cells autograft into the cryoinjured anal sphincters of rats. Dis Colon Rectum. 2008;51:1367–73. 76. Sarveazad A, Newstead GL, Mirzaei R, Taghi M, Joghataei MB, Babahajian A, Mahjoubi B. A new method for treating fecal incontinence by implanting stem cells derived from human adipose tissue: preliminary findings of a randomized double-blind clinical trial. Stem Cell Res Therapy. 2017;8:40. 77. Park EJ, Kang J, Baik SH. Treatment of faecal incontinence using allogeneic-adipose-derived mesenchymal stem cells: a study protocol for a pilot randomised controlled trial. BMJ Open. 2016;17(6):2. 78. Frudinger A, Kölle D, Schwaiger W, Pfeifer J, Paede J, Halligan S.  Muscle-derived cell injection to treat anal incontinence due to obstetric trauma: pilot study with 1 year follow-up. Gut. 2010;59(1):55–61. 79. Boyer O, Bridoux V, Giverne C, Bisson A, Koning E, Leroi AM, Chambon P, Déhayes J, Le Corre S, Jacquot S, Bastit D, Martinet J, Houivet E, Tuech JJ, Benichou J, Michot F, Study Group of Myoblast Therapy for Faecal Incontinence. Autologous myoblasts for the treatment of fecal incontinence results of a phase 2 randomized placebo-controlled study (MIAS). Ann Surg. 2018;267(3):443–50. 80. Romaniszyn M, Rozwadowska N, Malcher A, Kolanowski T, Walega P, Kurpisz M. Implantation of autologous muscle-derived stem cells in treatment of fecal incontinence: results of an experimental pilot study. Tech Coloproctol. 2015;19:685–96. 81. Bond C, Youngson G, MacPherson I, Garrett A, Bain N, Donald S, Macfarlane TV. Anal plugs for the management of fecal incontinence in children and adults a randomized control trial. J Clin Gastroenterol. 2007;41(1):45–53. 82. Deutekom M, Dobben AC.  Plugs for containing faecal incontinence. Cochrane Database Syst Rev. 2015;7:CD005086. 83. Colquhoun P, Kaiser R Jr, Efron J, Weiss EG, Nogueras JJ, Vernava AM, Wexner SD.  Is the quality of life better in patients with colostomy than patients with fecal incontience? World J Surg. 2006;10:1925–8. 84. Norton C, Burch J, Kamm MA. Patients’ views of a colostomy for fecal incontinence. Dis Colon Rectum. 2005;48(5):1062–9.

Treatment of Anal Incontinence: Which Outcome Should We Measure?

44

Alison J. Hainsworth, Alexis M. P. Schizas, and Andrew B. Williams

Learning Objectives

• To understand symptom assessment with patient questionnaires, stool diaries and patient interviews. • To understand which questionnaires can be used for assessment of severity, bother of symptoms and quality of life. To understand the advantages and drawbacks of difference questionnaires and that a combination of tools may be required for a thorough and complete evaluation. • To understand why and when is it also useful to assess anorectal structure and function. • To understand why and how to assess outcomes after treatment for anal incontinence.

44.1 Introduction Faecal incontinence is a common condition which adversely affects quality of life and has substantial economic costs worldwide [1]. Outcome measures may be subjective measurements (i.e. symptom assessment) or objective measurements (i.e. assessment of the structure and function of the anorectum). The impact of faecal incontinence is dependent upon patient perception as well as cultural and psychosocial factors. Subjective assessment of symptoms includes how symptoms have changed following an intervention, impact upon quality of life and patient satisfaction. This can be achieved with patient questionnaires (Table  44.1), stool diaries and patient interviews. Objective assessment of the anorectal structure and anorectal function includes how measurements

A. J. Hainsworth (*) · A. M. P. Schizas · A. B. Williams Colorectal Surgery, Guy’s and St Thomas’ Hospital, London, UK e-mail: [email protected]; [email protected]

have changed following treatment and the identification of persistent abnormalities in patients whose symptoms have failed to improve despite treatment (e.g. a persistent sphincter defect following attempted surgical repair). This can be achieved with anorectal physiology, saline or porridge continence tests or imaging with endoanal ultrasound or MRI. (Tables 44.2 and 44.3 summarise the outcome measures which can be used.)

44.2 Symptom Assessment The underlying pathophysiology of faecal incontinence is multifactorial and so symptoms alone cannot be used to determine treatment [2]. However, the assessment of symptoms and how they have changed following treatment is an important indicator of how ‘successful’ any interventions are. The aim of any intervention should be to reduce severity of symptoms and improve a patient’s quality of life. Patient questionnaires aim to assess faecal incontinence in terms of: • The severity of symptoms (four main aspects (the frequency and type of incontinence, faecal leakage, faecal urgency) and reliance upon behaviour such as avoidance techniques and the use of adjuncts such as pads, plugs and antidiarrhoeal medications to control symptoms). • The amount of bother inflicted upon the patient. • The effects on quality of life (impact on factors such as self-esteem, confidence, anxiety and depression). Bowel function diaries can also be used to assess severity. Qualitative analysis with interview data can be used to assess patients’ perception, their satisfaction with treatments and the acceptability of treatments [3]. There may be difficulty in comparing the results from questionnaires between different populations as the concepts of faecal incontinence are affected by different cultural and

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Table 44.1  The questionnaires which can be used to assess faecal incontinence Questionnaire (authors) Type Symptom severity scores Self-­assessment Pescatori score (frequency to (Pescatori et al.) flatus/mucous, [57] liquid or solid stool) American Medical Self-­assessment Systems score [58] (retrospective review of symptoms over past 4 weeks) Designed to be Jorge and Wexner Faecal Incontinence filled in by physicians but score/Cleveland Clinic Score (Jorge also used as self-assessment and Wexner) [5] (type and frequency, pad usage, lifestyle alteration) Interview-based or St Mark’s faecal incontinence score/ self-administered questionnaire Vaizey score (about past (Vaizey et al.) [6] 4 weeks) The Revised Faecal Short 5-item Incontinence Scale assessment tool (Sansoni et al.) [9]

Faecal Incontinence Severity Index (FISI) (Rockwood et al.) [10]

Cancer specific LARS score (Emmersten et al). [15] MSKCC bowel function instrument (Temple et al.) [12]

Quality of life scores The Rockwood scale (FIQL) (Rockwood et al.) [24]

Purpose Diagnostic tool for frequency and type of anal incontinence

Quality of Life (QoL)

Validation

No

Pros

Cons

Simple to use. Sensitive to frequency

Limited to a score of only 6 points. Does not take amount in account

Includes stool lost, Complex frequency and effect on lifestyle

Designed to assess No outcomes after artificial bowel sphincter Diagnostic tool, grade severity

Yes

Valid, responsive, reproducible [26]

Simple to use, easily understood by patients [6]

Subtle assessment of QoL. Does not include urgency, leakage amount or volume

Diagnostic tool, grade severity

Yes

Responsive [26], Includes urgency, reproducible, high antidiarrhoeal medication clinical validity and utility [6]

Subtle assessment of QoL

For use in outcome and epidemiological research and clinical practice Diagnostic tool

No

Responsive, reliable

Short, reliable

No

Criterion validity, test-retest reliability and responsiveness to change have been partly or adequately validated [7]

Simple tool to assess severity

Does not include urgency, leakage amount or volume

Self-­assessment

Diagnostic tool

No

Valid, reliable

Simple, quick evaluation

Correlates to QoL

Self-­assessment survey (41 points) which can be used via email/paper/by interview in the phone [16]

Diagnostic tool to prospectively evaluate symptoms after sphincter preserving cancer surgery

No

Reliable, valid

Not routinely used Broad scope (length and scoring influence its practicality)

Self-­assessment (29 items in 4 domains: lifestyle behaviour, depression, embarrassment)

Assessment of QoL specific to anal incontinence

Yes

Reliable, valid, responsive [25, 26]

Self-­assessment (weighted scores for four types of leakage and five frequencies)

Does not measure leakage. No single summary measure

44  Treatment of Anal Incontinence: Which Outcome Should We Measure?

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Table 44.1 (continued) Questionnaire (authors) Type Combined severity and quality of life ICIQ-BS [29, 31] Self-­assessment (17 questions in 3 scored domains: bowel pattern, bowel control and quality of life)

Rapid assessment faecal incontinence score (RAFIS) (De La Portilla et al.) [27]

Self-­assessment (includes visual analogue scale)

Visual analogue scores Self-­assessment Visual analogue score severity (Devesa et al.) [33] Self-­assessment Visual analogue score QoL (Devesa et al.) [33]

Purpose

Quality of Life (QoL)

Yes Assessment of symptom severity, the bother of symptoms and QoL

Rapid assessment of both severity and QoL

Yes

Rapid assessment of severity

No

Rapid assessment of QoL

Yes

Validation

Pros

Cons

Robust, valid, reliable, reasonable response to changes in symptoms and QoL following intervention Significant correlation between RAFIS and Jorge-Wexner score and Rockwood scale. Reliable

Assessment of the severity, the bother and QoL. Can be applied across international populations

Does not report on leakage amount or volume. More work needed to assess responsiveness to change [7]

Not concordant with Jorge-Wexner Only correlation with Rockwood scale was for embarrassment subscale

Fast assessment of Superficial both severity and assessment of both aspects. QoL Sensitivity to change in symptoms/QoL after treatment and test-retest has not been assessed Fast assessment

Fast assessment

Cannot replace other questionnaires Cannot replace other questionnaires

Table 44.2  Possible outcome measures for the treatment of anal incontinence Outcome measure Symptom severity

Assessment tools Questionnaires Bowel diaries Patient interviews

Bother

Questionnaires Patient interviews

Quality of life

Questionnaires Patient interviews

Patients’ perception and acceptability of treatment Anal sphincter function Anal sphincter structure

Patient interviews

Anorectal physiology Endoanal ultrasound MRI Volume vector manometry

Importance The aim of treatment is to improve symptoms and so these should be assessed

Limitations – There may be poor correlation between symptom severity and quality of life – As anal incontinence is multifactorial symptoms may persist despite an intervention which has solved one aspect; this will not be apparent on assessment of symptoms only The aim of treatment is to improve the – As above bother of anal incontinence and so this should be assessed – Multiple contributing factors which are The aim of treatment is to improve complex to assess quality of life and so this should be assessed Treatments must be acceptable to patients Objective parameters useful to assess – Changes in function may not be change for research reflected in patient symptoms – Changes in structure may not be Useful in research Useful in clinical practice if symptoms reflected in patient symptoms have failed to improve despite treatment or if symptoms deteriorate despite an initial improvement

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Table 44.3  A summary of the tools which can be used to measure outcomes after treatment of anal incontinence Tool Questionnaires

Advantages Disadvantages – Not all are responsive to change after intervention – Assess the patients’ symptoms, amount of bother inflicted and quality of life which are the main outcome – Severity may be underestimated by patients due to avoidance behaviour or recall bias measures for any intervention – Few questionnaires assess all aspects of severity and quality of life; multiple questionnaires may be required Bowel diaries – Avoid recall bias for symptom severity – Although recommended by some societies, there are few published examples of those which can be used in clinical practice Patient interviews – Allow qualitative assessment (e.g. patient perception – Time consuming and the acceptability of treatments) Anorectal physiology – Objective measure of change in anorectal function after – May not correlate with change in symptoms treatment Imaging (endoanal – Objective measure of change in anorectal structure after – May not correlate with change in symptoms ultrasound/MRI) treatment

psychosocial factors [4]. There are also few questionnaires which are used to evaluate severity and treatment outcomes that address all four aspects of severity simultaneously. Moreover, some assess severity of symptoms of anal incontinence and others assess quality of life in relation to anal incontinence, but few assess both. There have also been questionnaires designed to assess cancer-specific outcomes following the surgical treatment of rectal cancer.

44.2.1 Symptom Severity Questionnaires Table 44.1 summarises the symptom questionnaires which assess faecal incontinence. The International Consultation on Incontinence (ICI) has recommended the Jorge-Wexner, St Mark’s incontinence score and Revised Faecal Incontinence Scale for use in both research and clinical practice and the Faecal Incontinence Severity Index (FISI) for use in research (optional in clinical practice).

44.2.1.1  The Jorge-Wexner Score The Jorge-Wexner score (also known as the Wexner score or the Cleveland Clinic Score) may be filled in by physicians or patients as a self-assessment tool [5]. It is simple to use and easily understood by patients [6]. It is used to grade severity of faecal incontinence and to assess its impact upon lifestyle; it was the first score to include usage of pads and lifestyle alteration as well as frequency and severity of episodes. However, it only allows a subtle assessment of quality of life and does not include urgency, leakage or volume. The International Consultation on Continence (ICI) has examined the score and found that construct and criterion validity, internal consistency, test-retest reliability and responsiveness are partly or adequately validated [7].

44.2.1.2  The St Mark’s Incontinence Score The St Mark’s incontinence score (also known as the Vaizey score) is widely used to assess severity of anal incontinence [6]. It combines elements of the Pescatori score, the Wexner score and the American Medical Systems score with the addition of questions about urgency and the use of antidiarrhoeal medications. (The Pescatori score was one of the first scores designed to assess anal incontinence and simply diagnoses the frequency and type of anal incontinence. The American Medical Systems score was designed to assess outcomes after an artificial bowel sphincter.) The St Mark’s incontinence score was developed after clinicians noticed that patients used avoidance behaviour (remaining close to the toilet) to control their symptoms such that severity may be underestimated if urgency is not accounted for. It also reduces the emphasis placed on pad usage (compared to the Jorge-Wexner score) as pad usage may simply reflect the fastidiousness of the patient or co-­ existing urinary incontinence rather than anal incontinence severity. The St Mark’s incontinence score has shown the greatest change after treatment compared to the Pescatori score, the Jorge-Wexner and the American Medical Systems score and is a useful score for comparison of patients and treatments. A recent study of 390 patients by the team at St Mark’s hospital compared patients’ subjective perception of bowel control (scale 0–10) with the St Mark’s incontinence score (a change in the score was documented in 131 patients who underwent biofeedback). The St Mark’s incontinence score correlated moderately well with patients’ subjective perception of their symptoms and was reliable regardless of type of incontinence, age and gender. The authors reaffirmed that the St Mark’s score is suitable for the evaluation of treatment outcomes [8].

44  Treatment of Anal Incontinence: Which Outcome Should We Measure?

44.2.1.3  The Revised Faecal Incontinence Scale The Revised Faecal Incontinence Scale was developed to provide a short, psychometrically sound tool to assess severity of faecal incontinence before and after treatment [9]. The authors examined 61 people with faecal incontinence at baseline and 38 at follow-up and found the score was able to discriminate between different levels of incontinence severity, had superior internal consistency and test-retest ­ reliability to the Wexner and St Mark’s scores and was at least as responsive to detecting a change in incontinence after treatment as the Wexner and St Mark’s scores. 44.2.1.4  T  he Faecal Incontinence Severity Index (FISI) The Faecal Incontinence Severity Index is a diagnostic tool based on a type x frequency matrix which includes four types of leakage (gas, mucus, liquid and solid) and five frequencies (1–3 times per month, once per week, twice per week, once per day and twice per day). It was developed by surgeons (who suggested which aspects to include) and patients (who ranked each aspect) to assess severity of symptoms [10]. It can be used to assess treatment outcomes in research; for example, Zutshi used it to assess 10-year outcomes after anal sphincter repair for faecal incontinence and found that continence deteriorates in the long term following surgical repair [11]. Further work is needed for evaluating construct validity and internal consistency [7].

44.2.2 Symptom Severity Questionnaires Designed to Assess Outcomes for Rectal Cancer Treatment Sphincter preserving surgery for rectal cancer is often possible, but functional results are not well understood [12], and many patients suffer with low anterior resection syndrome (LARS). Questionnaires have been developed to assess symptoms and their contributing factors and to consolidate the treatment of LARS and assess treatment outcomes [13]. The LARS score and MSKCC bowel function instrument (both discussed below) are suitable for the comprehensive and in-depth assessment of LARS although focused assessment with the Wexner score, St Mark’s score or FISI may also be used. Experts recommend that the consistent use of the same questionnaires in order that different institutions can compare outcomes and interventions [13]. A systematic review in 2017 found that there is still substantial variation in reporting of functional outcomes following low anterior resection and a consensus is still needed to improve and standardise research into low anterior resection syndrome and its treatment [14].

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44.2.2.1  T  he Low Anterior Resection Syndrome Score (LARS Score) The low anterior resection syndrome (LARS) score has been specifically developed to assess bowel dysfunction after low anterior resection and is the most useful tool for rapid assessment. It is a simple tool for quick evaluation, and the results can be categorised as no LARS (score 0–20), minor LARS (score 21–29) and major LARS (score 30–42). It is highly sensitive and specific to ‘major’ LARS [15]. The authors who developed this questionnaire invited all 1143 low anterior resection patients identified in a national Colorectal Cancer Database to complete the questionnaire, 961 participated. There were significant differences in groups with and without radiotherapy, tumour height above or below 5  cm and total mesorectal excision/partial mesorectal excision. The LARS score correlates with quality of life though quality of life is not assessed by the questionnaire. 44.2.2.2  T  he Memorial Sloan Kettering Cancer Center (MSKCC) Bowel Function Instrument The MSKCC instrument was developed to prospectively evaluate bowel function following sphincter preserving surgery for rectal cancer [12]. The authors developed a 41-point bowel function survey after a literature review, expert opinion and patient interviews. They asked 184 patients to complete the survey (70.1% response rate) and found that the instrument was reliable and valid (radiation, coloanal anastomoses and handsewn anastomoses had significantly worse function). This bowel function instrument can be used via the web/ email, with paper or on the phone via interview [16]. The scope of the MSKCC bowel function instrument is broader than the LARS score as it covers the consequences of the symptoms as well as their severity reliable and is valid for assessment of outcomes after rectal cancer surgery. However, it is not routinely used as it is lengthy and its’ scoring system (which involves re-coding, three subscale scores, a global score and a total score) may make it less practical [13].

44.2.3 Diary Monitoring Symptom questionnaires may be misleading, only provide a snapshot of bowel habits and fail to reflect day-to-day variations or the relationship between bowel symptoms and stool form [17]. Bowel diaries are recordings of bowel habits which are widely used in diagnostic and interventional studies [18]. They may be more accurate than interviews or questionnaires with less recall bias [17, 19, 20]. For example,

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Manning examined 150 patients and found a discrepancy between recalled and recorded figures for bowel frequency of three or more bowel actions per week in 16% of patients [20]. Diary monitoring provides an objective assessment of severity if filled out correctly by patients. Although some societies advocate bowel diaries to assess bowel dysfunction and guide treatment, there are few published examples which can be used in clinical practice. The International Continence Society suggests the following are included: urgency, flatus and faecal incontinence (amount, consistency), passive staining/ soiling, pads (changes, degree of soiling), straining/difficulty/time in the toilet, unsuccessful attempts to defecate, assistive measures (e.g. digital stimulation, manual evacuation, irrigation, laxative or rectal evacuant use), diet and fluids (type and/or timing) [18]. Daily stool diaries have been frequently used to assess outcomes after treatment of faecal incontinence with sacral nerve stimulation. Improvements in both the number of episodes of faecal incontinence per week (as recorded in the diary) and summative symptom scores (Cleveland score, St Mark’s score) have been seen in both the short and the long term [21].

44.2.4 Quality of Life Questionnaires There may be poor correlation between symptom severity and quality of life [22, 23]. Symptom scores alone do not allow satisfactory evaluation of the impact of faecal incontinence on quality of life, and therefore both aspects of faecal incontinence should be assessed [22]. Quality of life can be assessed using generic scales such as the SF36 questionnaire or specific scales such as the Rockwood scale.

44.2.4.1  The Rockwood Scale (FIQL) The Rockwood scale (the Rockwood faecal incontinence quality of life scale (FIQL)) is a widely used tool to specifically assess the impact of faecal incontinence on quality of life [24] (it has also been translated into Spanish) [25]. It contains 29 different items to form four scales for the assessment of lifestyle, coping/behaviour, depression/ self-­perception and embarrassment, but there is no single summary measure. It was suggested by experts and then proposed to patients for ranking. Psychometric evaluation has shown that this is a reliable and valid measurement with significant correlations with the subscales in the SF-36 [24]. The International Consultation on Continence recommend its use in research but as an optional tool in clinical practice [18].

A. J. Hainsworth et al.

44.2.5 The Combined Assessment of Symptom Severity and Quality of Life There are different scores to measure the severity of and impact on quality of life, of faecal incontinence but often not together, and some authors recommend a combination of scores to allow thorough assessment [26]. Minguez (who translated the Rockwood scale into Spanish) compared the Rockwood scale to the Jorge-Wexner score and found a strong correlation between the two [25]. They also found that pad usage is an independent factor which worsens quality of life scores. Bols examined the Vaizey score (St Mark’s faecal incontinence score), the Jorge-Wexner score and Rockwood scale and concluded that although all total scores had adequate to excellent responsiveness and longitudinal construct validity, there were psychometric limitations for each. They also found a strong correlation between some items (particularly between embarrassment and coping/behaviour subscales). However, they still suggested a combination of the Wexner score for severity assessment with the Rockwood score for quality of life is required to enable a thorough and complete evaluation [26]. Bordeianou performed a prospective analysis in 502 consecutive patients to examine the relationship between the Faecal Incontinence Severity Index (FISI) and the Rockwood scale and SF-36. There was only moderate correlation with embarrassment and coping/behaviour and no correlation with lifestyle/depression, stressing the need to measure both variables (severity and quality of life) to determine the true impact of treatment [23].

44.2.5.1  T  he Rapid Assessment Faecal Incontinence Score (RAFIS) The rapid assessment faecal incontinence score (RAFIS) was developed to quickly assess faecal incontinence in both its severity and impact upon quality of life. It consists of a visual analogue scale combined with the frequency of episodes of faecal incontinence within the last month. The authors examined 261 consecutive subjects and found a significant correlation between RAFIS and the Jorge-Wexner score and the Rockwood scale. They concluded that RAFIS is a valid and reliable tool to assess both aspects of faecal incontinence [27] (severity and quality of life) although only superficially and has not been routinely adopted for clinical or research practice. 44.2.5.2  ICIQ-BS The modular international consultation on incontinence questionnaire for bowel symptoms (ICIQ-BS) has been developed as a comprehensive, robust, condition-specific self-completion questionnaire to assess bowel symptoms, the amount of bother they cause and their impact on quality of

44  Treatment of Anal Incontinence: Which Outcome Should We Measure?

life [28, 29]. It is the top-rated questionnaire for evaluation of symptoms severity and impact on health-related quality of life [30]. It can be applied across international populations in clinical practice and research and enables comparison of findings from different settings and studies [31]. Online versions are also psychometrically robust, in men and women, including Veterans [32]. It shows a reasonable response to changes in symptoms and quality of life following an intervention [29], but more work is needed in this domain [7].

44.2.6 Visual Analogue Scores Visual analogue scores have also been developed to assess the severity of faecal incontinence and its impact upon quality of life but have not been shown to be a suitable substitute for other scoring systems. Devesa examined 103 consecutive patients affected by faecal incontinence to determine if a single score represented in a visual analogue scale (VAS) could replace the Jorge-Wexner score and Rockwood faecal incontinence quality of life scale. A VAS for quality of life could not substitute all four subscales of the Rockwood score. A VAS for severity was not concordant with the Jorge-­ Wexner score. The authors concluded that a VAS does not assess the same issues for severity of symptoms and impact upon quality of life for faecal incontinence as the Jorge-­ Wexner score and Rockwood scale. The only significant correlation was between the VAS for faecal incontinence and the embarrassment subscale of the Rockwood scale [33].

44.2.7 Interview Assessment Interviews can be used for qualitative assessment and to assess patient acceptability of treatments and patient perception of their symptoms and how they have changed following an intervention. For example, Thin performed a randomised clinical trial of sacral versus percutaneous tibial nerve stimulation in patients with faecal incontinence and qualitative interview data suggested both treatments had high acceptability amongst patients [3]. Symptom severity questionnaires can also be used in an interview scenario. For example, the St Mark’s score can be used as both an interview-based and a self-administered incontinence score [34].

44.3 Anorectal Structure and Function Patients’ symptoms, the amount of bother experienced by the symptoms and their impact upon quality of life may be considered the most important and relevant outcome mea-

539

sures in the treatment of anal incontinence. However, anorectal structure and function are also useful outcome measures, particularly in the context of therapeutic trials for faecal incontinence. This is because: 1. Symptom severity may be underestimated by day-to-day variation in symptoms and patient avoidance of certain activities to reduce incontinent episodes. 2. The pathophysiology of faecal incontinence is multifactorial, and therefore there may be several contributing factors towards symptoms which may not all be solved with a single intervention. 3. Objective parameters may be useful to determine outcomes in uncontrolled studies. 4. If faecal incontinence initially responds to treatment and then symptoms deteriorate, there may be failure of treatment or another contributing factor (e.g. recurrent incontinence after sacral nerve stimulation due to device malfunction) [35]. Tests of anorectal structure and function include anal manometry, rectal compliance and sensation with either balloon studies or Barostat, saline continence tests, porridge enema, pudendal nerve terminal motor latency, needle EMG of the external sphincter, endoanal ultrasound and endoanal MRI. Tests of anorectal structure and function in a research context can help to strengthen the argument for implementation of certain therapies and ensure treatments are more widely available. Previously, although biofeedback treatment was known to ameliorate symptoms in patients with faecal incontinence, it was not known if it also caused an improvement in anorectal function. Rao examined anorectal manometry, saline continence tests, prospective stool diaries and bowel satisfaction scores before and after biofeedback for faecal incontinence and found a significant improvement in all parameters in both the short and long term [36, 37]. The examination of anorectal function as well as patient symptoms in these studies helped to highlight the effectiveness of biofeedback therapy for faecal incontinence. Norton performed a randomised control study which examined conservative treatment in 171 patients. All versions of conservative treatment (from standard advice to hospital biofeedback plus a home electromyogram biofeedback device) improved continence, quality of life, psychological well-being and anal sphincter function (measured with a diary, symptom questionnaire, continence score, patient’s rating of change, quality of life, hospital anxiety and depression score and anorectal manometry). The assessment of anorectal manometry showed subjective and objective improvement in faecal incontinence following all types of conservative measures.

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44.3.1 Anorectal Physiology Anorectal physiology includes anorectal manometry, sensory measurements and neurophysiology.

44.3.1.1  Anorectal Manometry Anorectal manometry includes conventional anal manometry, high-resolution manometry, high-definition manometry, vector volume manometry and ambulatory manometry. Anorectal manometry measurements include functional anal canal length, maximum resting pressure, maximum squeeze pressure, involuntary squeeze pressure, endurance squeeze pressure and resting pressures. Manometry may be useful to evaluate treatment outcomes [38]. For example, in patients with low anterior resection syndrome (LARS), there is reduced anal pressure after surgery which can be treated with biofeedback. The level of incontinence correlates with reduced resting pressure levels [39, 40], and a recovery in anorectal function can be monitored with anorectal manometry [41]. Improvements in faecal incontinence and quality of life are also associated with a significant increase in maximal anal resting pressure following artificial sphincter reimplantation for faecal incontinence [42], and some have observed reduced anal pressures in patients with persistent incontinence despite surgical repair obstetric anal sphincter injury [43]. However, some have found no association between improvement of symptoms and anal manometry pressures following treatment of faecal incontinence. Sorensen found no correlation between anal pressures and severity of symptoms after primary obstetric injury repair [44]. Grey examined 85 patients following anal sphincter repair, and whilst there were significant improvements in quality of life, there were no changes in anal manometry [45]. This may be explained by a systematic review of long-term outcomes after anal sphincter repair for faecal incontinence which analysed data from 16 studies comprising nearly 900 repairs. There was poor correlation between severity of symptoms and quality of life, and the authors concluded that despite worsening results over time, most patients remain satisfied with their sphincteroplasty [46]. This may be due to the variety of techniques used; as more advanced manometric techniques are used more widely (e.g. high-definition anal manometry) and as a consensus emerges regarding normal values, changes in anal manometry may reflect changes in symptoms more frequently. 44.3.1.2  Sensory Measurements Sensory measurements are made with rectal balloon distention, Barostat and rectal impedance studies. Measurements include rectal sensation (first and urge sensation and maximal tolerated

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volume) and compliance. Progress after treatment with either pelvic floor rehabilitation or rectal sensitivity training with balloon distension (the subject is trained to feel the distension and to tolerate progressively lower or larger volumes depending on if there is rectal hyper- or hyposensitivity present) can be documented according to the volumes tolerated. However, although there may be an improvement in rectal capacity, this may not be reflected by patients’ symptoms. For example, Terra examined 281 patients and found a moderate improvement in maximal tolerated volume and severity of faecal incontinence, but only a few patients had a substantial improvement in the St Mark’s faecal incontinence score [47]. The authors have done further work which concludes that additional tests (including anal sensitivity testing, anal manometry and endoanal ultrasound) only have a limited role in assessing treatment outcomes after pelvic floor retraining and will not necessarily predict any improvement in symptoms [48].

44.3.1.3  Neurophysiology Neurophysiology includes EMG (electromyography) and pudendal nerve terminal motor latency. Measurements include assessment of activity in the external sphincter and puborectalis. EMG can be used for strength training during biofeedback and be used to quantify the reinnervation of the external anal sphincter by detecting a prolongation in the motor unit potential [18].

44.3.2 Saline Continence Tests or Porridge Enema Following a sphincter repair with defunctioning colostomy or low anterior resection with a defunctioning loop ileostomy, a water holding procedure provides a simple examination for the evaluation of the anal sphincter function prior to stoma reversal. Saline or another liquid (e.g. porridge) is inserted into the rectum via a catheter and the patient asked to walk around with a pad in for 20 min to assess continence [38, 49].

44.3.3 Imaging 44.3.3.1  Endoanal Ultrasound Endoanal ultrasound may be used pre- and post-surgical sphincter repair to assess the effect of the operation on the sphincter defect and to investigate unsatisfactory results after surgery [50] (Fig. 44.1). Some have found a good correlation between patient symptoms and post-operative appearances on endoanal ultrasound. Felt-Bersma examined 18 patients before and after anal sphincter repair. There was not only good correlation between the clinical effect of sphincter repair and changes on endoanal ultrasound and anal manome-

44  Treatment of Anal Incontinence: Which Outcome Should We Measure?

541

44.4 Future Directions Questionnaires which incorporate both severity of symptoms and quality of life should be further developed and routinely used [57]. A consensus on assessment of low anterior resection syndrome and which tool used to assess how patient symptoms change after treatment is needed. More work is needed to assess and improve responsiveness to change after treatment for symptom questionnaires. Further work will be done on how changes in anorectal structure and function relate to patient symptoms.

Take-Home Messages

Fig. 44.1  Endoanal ultrasound. A sagittal view of the anal sphincter complex. The white arrow shows the internal anal sphincter, the dashed arrow shows the longitudinal muscle and the black arrow the external sphincter

try, but post-operative persistent incontinence could be attributed to remaining sphincter defects [51]. Norderval found improved St Mark’s scores correlated with the length of the external anal sphincter defect following primary repair of obstetric anal sphincter tears in 63 women (61 controls) (the integrity of the internal anal sphincter did not differ) [52]. Sorensen examined 59 women (29 cases after primary obstetric injury repair and 30 controls) and found that anterior sphincter length correlated with severity of incontinence (though there was no correlation between anal pressures and severity of incontinence) [44]. Endoanal ultrasound can also be used to assess the safety of new treatments, for example, to ensure that there is no migration of an artificial bowel sphincter [53] or inter-­ sphincteric bulking agents such as the Gatekeeper™ [54].

44.3.3.2  MRI MRI is equivalent to endoanal ultrasound for the assessment of external sphincter defects but not internal sphincter defects [55]. Research has shown that external anal sphincter atrophy following sphincteroplasty (for obstetric injury causing incontinence) can only be visualised on endoanal MRI but not ultrasound and that atrophy affects continence post-­ operatively [56]. However, the quality of ultrasound has improved since this study, and although imaging the sphincter post-operatively may be useful for research purposes, it is often not available for routine post-operative assessment in clinical practice.

1. Treatment of anal incontinence may be assessed by subjective or objective outcomes. 2. It is important to assess outcomes to: –– Check that treatments are successful in the short, medium and long term. –– Understand why a treatment has or has not worked. –– Allow improvement in treatments. –– Increase the adoption of treatments by multiple units. –– Check patient acceptability of treatments. 3. Subjective outcomes: Symptoms (severity, bother and quality of life) may be assessed with patient questionnaires, stool diaries and patient interviews. Often a combination of questionnaires is required for the complete evaluation of both symptom severity and impact upon quality of life. The ICIQ-BS is the only questionnaire at present which assesses symptoms, quality of life and bother of symptoms simultaneously. Patients may use avoidance behaviour which leads to underestimation by the clinician of symptom severity. 4. Objective outcomes: Anorectal structure and function may be assessed with anorectal physiology, saline or porridge continence tests, endoanal ultrasound and endoanal MRI. The pathophysiology of anal incontinence is multifactorial and so the assessment of the anorectal structure and function may explain why symptoms are not solved with a single intervention. Assessment of anorectal structure and function may explain a recurrence of symptoms despite initial success (e.g. recurrent incontinence after sacral nerve stimulation due to device malfunction) and may be useful to determine outcomes in uncontrolled studies.

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44  Treatment of Anal Incontinence: Which Outcome Should We Measure? 37. Ozturk R, Niazi S, Stessman M, Rao SSC. Long-term outcome and objective changes of anorectal function after biofeedback therapy for faecal incontinence. Aliment Pharmacol Ther. 2004;20(6):667–74. 38. Witte M, Schwandner F, Klar E. Before and after anorectal surgery: which information is needed from the functional laboratory? Visc Med. 2018;34(2):128–33. 39. Rasmussen OO, Petersen IK, Christiansen J.  Anorectal function following low anterior resection. Colorectal Dis. 2003;5(3):258–61. 40. Lee SJ, Park YS.  Serial evaluation of anorectal function following low anterior resection of the rectum. Int J Colorectal Dis. 1998;13(5–6):241–6. 41. van Duijvendijk P, Slors JFM, Taat CW, van Tets WF, van Tienhoven G, Obertop H, et al. Prospective evaluation of anorectal function after total mesorectal excision for rectal carcinoma with or without preoperative radiotherapy. Am J Gastroenterol. 2002;97(9):2282–9. 42. Lehur P-A, Zerbib F, Neunlist M, Glemain P, Bruley-des-Varannes S. Comparison of quality of life and anorectal function after artificial sphincter implantation. Dis Colon Rectum. 2002;45(4):508–13. 43. Dickinson KJ, Pickersgill P, Anwar S. Functional and physiological outcomes following repair of obstetrics anal sphincter injury. A case. Int J Surg Lond Engl. 2013;11(10):1137–40. 44. Soerensen MM, Pedersen BG, Santoro GA, Buntzen S, Bek K, Laurberg S.  Long-term function and morphology of the anal sphincters and the pelvic floor after primary repair of obstetric anal sphincter injury. Colorectal Dis. 2014;16(10):O347–55. 45. Grey BR, Sheldon RR, Telford KJ, Kiff ES. Anterior anal sphincter repair can be of long term benefit: a 12-year case cohort from a single surgeon. BMC Surg. 2007;7(1):1. 46. Glasgow SC, Lowry AC.  Long-term outcomes of anal sphinc ter repair for fecal incontinence: a systematic review. Dis Colon Rectum. 2012;55(4):482–90. 47. Terra MP, Dobben AC, Berghmans B, Deutekom M, Baeten CGMI, Janssen LWM, et  al. Electrical stimulation and pelvic floor muscle training with biofeedback in patients with fecal incontinence: a cohort study of 281 patients. Dis Colon Rectum. 2006;49(8):1149–59.

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Part VI Pelvic Organ Prolapse

Epidemiology and Etiology of Pelvic Organ Prolapse

45

Stefano Salvatore, Sarah De Bastiani, and Fabio Del Deo

Learning Objectives

• This chapter aims to provide to the reader the actual knowledge on epidemiological data based on different classification systems, different definitions, and the concomitance of symptoms related to POP with or without functional disorders. • This chapter also illustrates the evidence of risk factors and pathophysiological mechanisms based on the most recent literature, making the reader aware regarding all the multifactorial elements related to POP.

45.1 Definition and Classification Prolapse (Latin: Prolapsus—“a slipping forth”) refers to a falling, slipping, or downward displacement of a part or organ. Pelvic organ refers most commonly to the uterus and/ or the different vaginal compartments and their neighboring organs such as bladder, rectum, or bowel. Different sites of female genital prolapse are described according to the organ involved. The anterior compartment prolapse is characterized by herniation of anterior vaginal wall often associated with descent of the bladder (also called cystocele). Hernia of the posterior vaginal segment, or posterior compartment prolapse, is often associated with descent of the rectum (or rectocele). Apical compartment prolapse (uterine prolapse, vaginal vault prolapse) is characterized by the descent of the

apex of the vagina into the lower vagina, to the hymen, or beyond the vaginal introitus. The apex can be either the uterus and cervix, cervix alone, or vaginal vault, depending upon whether the woman has undergone hysterectomy. Apical prolapse is often associated with enterocele, the herniation of the intestines to or through the vaginal wall. The uterine procidentia is instead, the herniation of all three compartments through the vaginal introitus. Division of the vagina into separate compartments is somewhat arbitrary, because the vagina is a continuous organ, and prolapse of one compartment is often associated with prolapse of another [1]. About 50% of parous women are affected. Prolapse of pelvic organ (POPs) can cause pelvic, urinary, bowel, and sexual symptoms [2]. A system of three integrated levels of vaginal support has been described by DeLancey [3]. All levels of vaginal support are connected through a continuous endopelvic fascia support network: –– Level 1—Uterosacral/cardinal ligament complex, which suspends the uterus and upper vagina to the sacrum and lateral pelvic side wall. Level 1 support represents vertical fibers of the paracolpium that are a continuation of the uterosacral/cardinal ligament complex which inserts variably into the cervix and vagina. Loss of level 1 support contributes to the prolapse of the uterus and/or vaginal apex. –– Level 2—Paravaginal attachments along the length of the vagina to the superior fascia of the levator ani muscle and the arcus tendineus fascia pelvis (also referred to as the “white line”). Loss of level 2 support contributes to anterior vaginal wall prolapse (cystocele).

S. Salvatore (*) · S. De Bastiani · F. Del Deo IRCCS San Raffaele Scientific Institute, Milan, Italy e-mail: [email protected] © Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_45

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A second classification system was introduced in 1996, the Pelvic Organ Prolapse Quantification (POP-Q) system, and it has become the standard classification system [6]. The POP-Q system is the POP classification system of choice of the International Continence Society (ICS), the American Urogynecologic Society (AUGS), and the Society of Gynecologic Surgeons (SGS) [6]. The American College of Obstetricians and Gynecologists has also recommended its use [7]. It has proven interobserver and intraobserver reliability [8] and is the system used most commonly in the medical literature [9]. The POP-Q is an objective, site-­specific system for describing and staging POP in women [10]. In the POP-Q system, the topography of the vagina is described using six points (two on the anterior vaginal wall, two on the superior vagina, and two on the posterior vaginal wall) and several other measurements [10]. Taken together, these measurements can be used to produce a sagittal ­diagram of the prolapse and a detailed description of vaginal anatomy. For the purposes of simple clinical communication or grouping patients for research purposes, an ordinal staging system using the POP-Q measurements was developed: –– Stage 0—No prolapse. –– Stage I—The requirements for stage 0 are not met, but the most distal portion of the prolapse is >1 cm distal to the level of the hymenal plane. –– Stage II—The most distal portion of the prolapse is between ≤1 cm proximal to the hymenal plane and ≥1 cm distal to the hymenal plane. –– Stage III—The most distal portion of the prolapse is between >1 cm distal to the hymenal plane, but no further than 2  cm less than the total vaginal length in. In other words, the maximum prolapse is more than 1 cm outside the hymenal plane, but it is 2 cm less than the maximum possible protrusion. –– Stage IV—Eversion of the total length of the vagina.

D

C

Ba

3 cm

Aa Bp Ap tvl

–– Level 3—Perineal body, perineal membrane, and superficial and deep perineal muscles, which support the distal one third of the vagina. Anteriorly, loss of level 3 support can result in urethral hypermobility. Posteriorly, loss of level 3 support can result in a distal rectocele or perineal descent [4, 5].

S. Salvatore et al.

gh

pb

POP-Q PROLAPSED ORGAN COMPARTMENT SITE Anterior

Aa Ab

Middle

C D

Posterior

Ap Bp

Urethra (urethrocele) Bladder (cystocele) Cervix Small bowel (enterocele) Small bowel (enterocele) Rectum (rectocele) Perineal body

VAGINAL WALL SITE Distal anterior vaginal wall Proximal and distal anterior vaginal wall Cervix Uterosacral scar Proximal posterior vaginal wall Proximal and distal posterior vaginal wall Perineal body

A simplified version of the POP-Q system, which was developed by an international group of investigators, has been proposed [11, 12]. Like the standard POP-Q examination, the Simple POPQ (S-POPQ) measures the anterior, posterior, and up to two measurements of the apex, including both the cervix and posterior cul-de-sac. The S-POPQ records the ordinal stage of the four measurements by estimating the distances involved. While not recommended by leading societies, the Baden-­ Walker Halfway Scoring System is another commonly used POP staging system. The degree, or grade, of each prolapsed structure is described individually (e.g., grade 1 anterior vaginal wall prolapse or grade 3 uterine prolapse). The grade/degree is defined as the extent of prolapse for each structure noted on examination while the patient is strain-

45  Epidemiology and Etiology of Pelvic Organ Prolapse

ing. Because there are no clear demarcations among the cutoff stages, the Baden-Walker system lacks the precision and reproducibility of the POP-Q system. The system has five degrees/grades [13].

45.2 Prevalence and Incidence Pelvic organ prolapse is one of the most frequent disorders connected with age that makes women visit their gynecologist. The worldwide prevalence of POP has recently been reported to be around 9% [14]. If the diagnosis is based on clinical evaluation, the prevalence ranges from 41% to 56% as compared to 3–7% when the diagnosis is based on symptoms or complaints from women [15, 16]. In a study done in the United States, the prevalence of POP was lower in African American women 1.9% as compared to Caucasian women 2.8% and Hispanic women 5.1% [17]. The difference in prevalence of POP between Africans residing in the United States and those living in Africa could be explained by a comparatively higher number of deliveries, difficult access to skilled delivery attendance, and heavier physical workload among African living in sub-Saharan Africa. In the United States, this problem may affect even 24% of the women’s population, whereby the percentage depends mainly on age. Among women between 20 and 39 years of age, it concerns 10% of the population, whereas it involves up to 50% of women in their 80s [18]. With regard to the aging process of the society, this problem will involve a higher rate of the total women’s population. One estimates that in 2050 it will concern over 30% of women over 20 years old [19]. In the United States, the incidence of women submitted to surgical procedures connected with one of the types of prolapse is 11.8%, which constitutes the most common indication for surgical procedure. There are approximately 300,000 POP surgeries each year in the United States [20, 21]. In developed countries, approximately 20% of surgical procedures among women are carried out due to pelvic organ prolapse [22–24]. It is also worth mentioning that the problem is probably more frequent, because only 10% of the population struggling with pelvic organ prolapse in their everyday life seeks help from a gynecologist and the majority never ask for it [25]. Population-based studies report an 11–19% lifetime risk in women undergoing surgery for prolapse or incontinence [26, 27]. The exact prevalence of POP is difficult to ascertain, for several reasons: (1) different classification systems have been used for diagnosis; (2) studies vary by whether the rate of prolapse reported is for women who are symptomatic or asymptomatic; and (3) it is unknown how many women with

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POP do not seek medical attention. The distinction between symptomatic and asymptomatic POP is clinically relevant, since treatment is generally indicated only for women with symptoms. However, there are few high-quality data regarding the prevalence of symptomatic POP. Rates of asymptomatic POP are probably even higher. Several studies have used clinical examination to assess the prevalence of POP in a community-based setting. One study included 497 women who were seen in an outpatient clinic for routine gynecologic care and were assessed using the Pelvic Organ Prolapse Quantification (POP-Q) system. The overall distribution of POP-Q system stages was as follows: stage 0, 6.4%; stage 1, 43.3%; stage 2, 47.7%; and stage 3, 2.6%. No subjects examined had POP-Q system stage 4 prolapse. The distribution of the POP-Q system stages in the population revealed a bell-shaped curve, with most subjects having stage 1 or 2 support. Few subjects had either stage 0 (excellent support) or stage 3 (moderate to severe pelvic support defects) [28]. If we analyze a Sliwa et al. work, we found that the most frequent pelvic disorder reported in their group of patients was the defect connected with both cystocele and rectocele. This may lead to the conclusion that cystocele is the most common type of dysfunction throughout the whole group of women with pelvic organ disorders [24]. Similar results were obtained by Hendrix et al. on a large group where the most frequently observed disorder was also cystocele [29].

45.3 R  isk Factors and Pathophysiological Mechanisms 45.3.1 Ethnicity Several studies showed that Hispanic and European women seem to have a higher risk of developing POP compared to Asian or African women [30–34]. In Zacharin’s cadaveric study, pubourethral ligaments, endopelvic fascia, and endopelvic attachment to the obturator fascia were reported to be stronger and thicker in Chinese compared to Caucasian women [35]. A significantly less pelvic organ mobility in Asian women was shown also by Dietz et al. using perineal ultrasound [34]. The reasons for these ethnic discrepancies are still unclear.

45.3.2 Familiarity and Other Genetic Risk Factors It is generally recognized that POP has an inheritable predisposition. In a case-control study, Chiaffarino et  al. showed

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that the risk of urogenital prolapse was higher in women with mother or sister reporting this condition: the odds ratios (ORs) were 3.2 (95% CI 1.1–7.6) and 2.4 (95% CI 1.0–5.6), respectively, in comparison with women whose mother or sisters reported no prolapse [36]. The reason why some females with little to no risk factors develop POP while other females with multiple risk factors do not is clearly that some women have a genetic predisposition to prolapse. Analyzing young women with stage III and IV POP, Jack et al. showed that the risk of prolapse among their siblings was five times higher than that of the risk for the general population [37]. The authors concluded that POP has a dominant pattern of inheritance with incomplete penetrance. Buchsbaum et al. found a high concordance in the POP stage between nulliparous women and their parous sisters, thus supporting the hypothesis of a familial basis for this condition [38]. Nevertheless, they highlighted the importance of vaginal delivery that appeared to confer a risk for more advanced prolapse. Some genetic variants have been found in families with an increased incidence of POP. In the genome-wide association study conducted by Allen-Brady et al., results from association analysis identified five single-nucleotide polymorphisms significantly associated with POP [39]. More recently the same authors performed a genome-wide linkage analysis using a resource of high-risk POP pedigrees and results showed that loci on chromosomes 10q and 17q may predispose to POP development [40]. Further studies investigated the role of specific genetic polymorphisms in increasing the susceptibility to early onset of POP, such as polymorphism in the promoter of LAMC1 gene or of COL1A1 gene [41, 42]. Although results were encouraging, their clinical application cannot be recommended based on current evidence. Women with genetic disorders of the connective tissue, such as Marfan or Ehlers-Danlos syndrome, have high rates of POP [43–47]. It is well-known that the vaginal wall is composed of connective tissue in its subepithelial layer and adventitia and also vaginal and uterine supportive tissues are mainly made of collagen and elastin. Therefore in these women, the connective tissue disorder may occur also in terms of pelvic organ descent. Apart from these genetic diseases, numerous data show that women with POP have an abnormal pelvic extracellular matrix metabolism with an increased collagen turnover. Connective tissue remodeling throughout the body is controlled by matrix metalloproteinases (MMP), a family of calcium-dependent zinc-containing endopeptidases. An overexpression of MMP-1 and 2 has been observed in women with prolapse with a concurrent decrease in their inhibitor TIMPs [48, 49]. The consequences are an excessive tendency toward connective tissue degradation and a decrease in the amount of collagen in pelvic tissue that has been reported from women with POP.

S. Salvatore et al.

45.3.3 Obstetric Factors Pelvic floor tissue trauma that occurs during childbirth is universally considered the main risk factor for developing POP later in life [50–56]. Pregnancy itself has been widely accepted as a risk factor for pelvic floor dysfunction. This association is strongest for stress urinary incontinence (SUI), whereas for POP it has been less well established. In the study by O’Boyle et al., all 21 nulliparous nonpregnant women had a POP-Q stage 0–I, while out of 21 nulliparous pregnant women, 47.6% had a stage II POP (p  = 5 mm (detrusor hypertrophy) seems associated with urge urinary incontinence and detrusor overactivity [13]. Detrusor hypertrophy can be variable depending on location, with the dome often thicker than the posterior bladder base beyond the trigone, especially in women with cystocele (Fig. 48.3). As a result, DWT is not in fact a good test [14, 15]. Unlike the situation in the male bladder, DWT may not be predictive of voiding difficulty in women [16, 17]. Occasionally, a trigonal cystic structure may be observed, the differential diagnosis being ureterocele and Nabothian follicle (Fig. 48.4).

48.3.1.1 T  he Anatomy of Stress Urinary Incontinence In women suffering from stress urinary incontinence or urodynamic stress incontinence, the proximal urethra commonly rotates postero-inferiorly on Valsalva manoeuvre as the urethra and anterior vaginal wall are tethered to the symphysis pubis and the pelvic sidewall. In essence, the symphysis acts as a fulcrum around which the entire anterior compartment rotates. Points of reference for measurements of bladder neck mobility are either the central axis of the symphysis pubis [18] or its inferior-posterior margin [19]. The former may be more accurate, providing measurements that are independent of transducer position or movement. However, obtaining the central axis of the pubis can be difficult in postmenopausal women due to calcification of the interpubic disc, and visualization of the entire interpubic disc makes inclusion of the posterior compartment and anorectal angle in the resulting image or volume difficult to impossible.

48  Transperineal Ultrasound: Practical Applications

a

589

b

Fig. 48.2  Bladder stone (long arrow, left) and transitional cell carcinoma (TCC; short arrow, right). (a) The stone is hyperechogenic and shows distal acoustic shadowing; (b) the TCC is iso-echoic and produces no shadowing

these measures have good test characteristics for the diagnosis of urodynamic stress incontinence [23, 24], similar to DWT and the diagnosis of detrusor overactivity, underscoring the continuing need for urodynamic testing in the assessment of urinary incontinence. Funnelling of the internal urethral meatus (Figs. 48.1 and 48.6) is often observed on Valsalva in women suffering from stress urinary incontinence. Funnelling is commonly, but not necessarily, seen at the time of urine leakage. Marked funnelling as shown in Fig. 48.6 is associated with poor maximum urethral closure pressures [25, 26]. Other (indirect) signs of urine leakage on Valsalva are greyscale echoes (‘streaming’) within the usually invisible urethral lumen and the appearance of two linear or ‘specular’ echoes indicating the lumen of a fluid-filled urethra. Fig. 48.3  Asymmetrical detrusor hypertrophy in a patient with symptoms of the overactive bladder and urodynamic detrusor overactivity

Bladder neck mobility can be determined in a highly repeatable fashion (Fig. 48.5) [20]. The difference between values at rest and on maximal Valsalva yields a numerical value for bladder neck descent (BND). The same method can be used for the mobility of any given point, which is especially useful for quantifying segmental urethral mobility. It is the mobility of the mid-urethra rather than that of the bladder neck which is most strongly associated with stress incontinence [21]. In addition, urethral rotation may be quantified by comparing the angle of inclination between proximal urethra and any other fixed axis. Another parameter commonly obtained is the urethrovesical (or retrovesical) angle between proximal urethra and trigone and/or the angle γ between the central symphyseal axis and a line from the inferior symphyseal margin to the bladder neck [22]. Unfortunately, none of

48.3.1.2 Anterior Compartment Prolapse Clinicians use the word ‘cystocele’ and ‘anterior vaginal wall descent’ interchangeably, and descent of the anterior vaginal wall does indeed usually mean ‘cystocele’, that is, descent or ‘prolapse’ of the bladder. However, such clinical appearances may occasionally be due to a urethral diverticulum or other cystic structures of the anterior vaginal wall such as Gartner’s duct cysts, remnants of the Wolffian ducts of embryological development (Fig.  48.7). Urethral diverticula are commonly overlooked in women with lower urinary tract symptoms and are a correctable cause of lower urinary tract symptoms. Small diverticula may appear as a mostly hyperechogenic irregularity of the urethra, although they show a clearly cystic or solid-cystic appearance. Any spatially circumscribed para-urethral abnormality is better appreciated in the sectional planes, which are useful in differentiating other cystic or mixed solid-cystic structures from a urethral diverticulum. Figure 48.8 shows typical appearances of four very different, urethroscopically con-

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H. P. Dietz

a

Fig. 48.4  Cystic structures in the anterior compartment, seen in the midsagittal or parasagittal planes. (a) Ureterocele, i.e. a sacculation of the intravesical part of the ureter, which is due to a stenosis of the

b

vesico-ureteric junction. Ureteroceles fill and empty with ureteric peristalsis. (b) Nabothian follicle which is part of the cervix and moves with it on Valsalva

a

b

c

d

Fig. 48.5  Determination of bladder neck descent and retrovesical angle: ultrasound images show the midsagittal plane at rest (a, c) and on Valsalva (b, d). A anal canal, B bladder, L levator ani, R rectal ampulla, S symphysis pubis, U urethra, Ut uterus, V vagina. The lower images

demonstrate the measurement of distances between inferior symphyseal margin and bladder neck (vertical, x and horizontal, y) and the retrovesical angle at rest (rva-r) and on Valsalva (From [19], with permission)

48  Transperineal Ultrasound: Practical Applications

591

a

b

Fig. 48.6  Marked funnelling of the bladder neck (arrows) on Valsalva in the midsagittal plane (a) and a rendered volume (b). Such appearances are suggestive of a low-pressure urethra (‘intrinsic sphincter deficiency’) and urodynamic stress incontinence

a

c

Fig. 48.7  Gartner cyst (Mullerian remnant; large arrows) as seen in the midsagittal plane (a), coronal plane (b), axial plane (c) and axial rendered volume (d). The small arrows in the bottom right panel indicate

b

d

the circular urethral rhabdosphincter, confirming the diagnosis. The primary differential diagnosis, a urethral diverticulum, grows from inside the rhabdosphincter and tends to destroy its ring structure

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H. P. Dietz

a

b

d c

e

g

Fig. 48.8  Varying appearances of urethral diverticula. Images of the midsagitta (a, c, e, g) and coronal plane (b, d, f, h) obtained from 4 different patients with a confirmed urethral diverticulum on urethroscopy are shown.

f

h

(a, b) Hyperechogenic foci and distortion; (c, d) Small cystic structure; (e, f) Simple posterior urethral diverticulum; (g, h) Circumferential complex urethral diverticulum. Arrows indicate the diverticulum

48  Transperineal Ultrasound: Practical Applications

a

593

b

c

Aa Ba C D

Bp Ap

tvl

Fig. 48.9  Cystocele on clinical examination (a). ICS POPQ diagram and coordinates (b) and pelvic floor ultrasound in the midsagittal plane (c). A anus, B bladder, L levator ani, S symphysis pubis, U uterus

a

b

Fig. 48.10  Cystocele types as seen on maximal Valsalva in the midsagittal plane. (a) Cystocele with open retrovesical angle of over 180° (RVA, indicated by lines placed through the trigone and the proximal urethra). (b) Typical large cystocele with intact retrovesical angle of about 110°. A anus, B bladder, L levator ani, S symphysis pubis

firmed urethral diverticula. A urethral diverticulum usually arises dorsal to the urethra and may develop by surrounding the organ, initially within the confines of the fascia of the urethral rhabdosphincter, explaining the horseshoe shape of larger diverticula (Fig. 48.8d). Occasionally, they may also be found ventral to the urethra, i.e. in the space of Retzius. Most often, however, excessive descent of the anterior vaginal wall is indeed a ‘cystocele’ or prolapse of the bladder as shown in Fig. 48.9. Historically, two types of cystoceles have been described, and they seem to have rather different functional implications (Fig. 48.10) [27]. A cystourethrocele or Green type II cystocele is associated with stress urinary incontinence and normal voiding, while a cystocele with intact retrovesical angle or Green type III cystocele tends to be found in women with voiding dysfunction and symptoms of prolapse rather than stress incontinence. The former is not associated with avulsion of the levator ani, as opposed to the Green type III cystocele, which argues against a traumatic

pathogenesis for cystourethrocele [28]. Occasionally, a severe cystocele may result in inversion of the bladder neck, that is, rotation of the bladder neck up to 180° on Valsalva and marked urethral kinking. Fig. 48.11 shows quantification of pelvic organ descent in a patient with three-compartment prolapse.

48.3.1.3 Central Compartment The uterus can be difficult to identify because of its iso-­ echoic nature, similar in echotexture to the vagina, especially in women with small, atrophic uteri. In women with significant uterine descent, a specular (mirror-like) echo indicates the leading edge of the cervix. Nabothian follicles may help distinguish the cervix from vaginal wall (Figs.  48.4 and 48.12). Occasionally, imaging will show a retroverted uterus compressing the urethra and/or bladder neck, explaining symptoms of voiding difficulties. Even more impressively, a low anteverted uterus may result in rectal intussusception in

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women with symptoms of obstructed defecation, which is termed a ‘colpocele’ on defecation proctography (Fig. 48.13).

48.3.1.4 Posterior Compartment Descent of the posterior vaginal wall can be due to a number of different anatomical abnormalities with different patho-

Fig. 48.11  On Valsalva in the midsagittal plane, prolapse is quantified against a horizontal line placed through the inferoposterior symphyseal margin, as in this patient with three-compartment prolapse. There is descent of the bladder neck to 16 mm below the symphysis, of the bladder to 19 mm below, of the uterus to 21 mm below, of an enterocoele to 26 mm below and of the rectal ampulla to 31 mm below the reference line. B bladder, E enterocoele, R rectal ampulla, S symphysis pubis, U uterus

a

Fig. 48.12  A Nabothian follicle (arrow) can provide a convenient marker of the cervix, as in this patient with third-degree cystocele and second-degree uterine prolapse. The green line of the region of interest (the ‘box’ in a) serves as the line of reference here; however, the result-

H. P. Dietz

physiological and therapeutic implications, even if, on clinical assessment of surface anatomy, those conditions are generally subsumed under the term ‘rectocele’. Many gynaecologists are unaware of this fact since they never see anything but surface anatomy. Even digital rectal examination (which needs to be performed on Valsalva to demonstrate true rectocele and intussusception) is not routinely employed. The link between anatomical abnormalities and defecatory dysfunction, mostly in the sense of obstructed defecation (incomplete bowel emptying, straining at stool and digitation) [29], is frequently not fully appreciated by both gynaecologists and colorectal surgeons. The ‘gold standard’ diagnostic method, defecation proctography, is invasive, expensive and not commonly available. Pelvic floor ultrasound is cheaper, non-invasive and much better accepted by the patient and seems to yield similar findings [30–32], even without 3D/4D imaging. It is poised to replace defecation proctography for the initial investigation for women with posterior compartment prolapse and obstructed defecation [33]. Clinical posterior compartment descent is most commonly found to be due to a ‘true’ or radiological rectocele on imaging: a defect of the rectovaginal septum that results in herniation of the anterior wall of the rectal ampulla into the vagina [34]. On translabial ultrasound the rectovaginal septum (RVS) is often not easy to visualize (see Fig. 6.15, for an exception) unless one uses endovaginal imaging, but direct assessment of the RVS on static ultrasound seems to be of very limited clinical utility [35].

b

ing axial plane rendered volume in (b) is not suitable for hiatal measurement since the line of minimal dimensions (oblique line in a) lies partly outside the box. This manifests in an overestimate of hiatal depth posteriorly. A anal canal, B bladder, S symphysis pubis, U uterus

48  Transperineal Ultrasound: Practical Applications

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a

b

Fig. 48.13  A colpocele, i.e. a rectal intussusception propelled by the cervix of a prolapsing uterus. This usually is due to the cervix (as in this patient), but very occasionally an acutely retroverted uterus can result in a colpocele caused by the fundus. The anal canal and anterior rectal

a

wall are shown by the dotted line, (a) with the cervix inverting the anterior wall of the rectal ampulla. A anal canal, B bladder, Cx cervix, S symphysis pubis, Ut uterus. The dotted line in (b) shows hiatal area

b

c

Aa Ba C D

Bp Ap

tvl

Fig. 48.14  Rectocele on clinical photograph (a), representation on POP-Q (b; Ba = −3, C = −4, Bp = +1) and appearances on imaging (c; A anal canal, B bladder, L levator ani, R rectocele, S symphysis pubis) (From [109], with permission)

Diagnosis of a ‘true’ rectocele does not rely on identification of the RVS itself but rather on demonstration of a pocket or diverticulum, i.e. a discontinuity of the anterior anal muscularis on Valsalva (Fig. 48.14). A rectocele is defined by its depth and descent relative to the symphysis pubis (Fig. 48.15). Another manifestation of posterior compartment descent is perineal hypermobility where the RVS is intact but may be abnormally distensible (Fig.  48.16), synonymous with ‘descending perineum syndrome’ and associated with excessive distensibility of the levator hiatus [36]. The latter is not surprising since the levator plate distends not just laterally but downwards as well.

Both rectocele and perineal hypermobility are associated with symptoms of prolapse, i.e. of a vaginal lump or a dragging sensation, but obstructed defecation is more likely with a true, radiological rectocele, that is, a defect of the RVS [37]. Other causes of posterior compartment prolapse include a combined rectoenterocele, an isolated enterocele, rectal intussusception or a deficient perineum giving the impression of a ‘bulge’ [38, 39]. Rectal intussusception is an early stage of rectal prolapse where rectal mucosa and muscularis enter the proximal anal canal, changing it to a ‘martini glass’ configuration. This condition, not uncommon but rarely diagnosed by gynaecologists, is strongly

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a

b

c

d

Fig. 48.15  Translabial ultrasound images in the midsagittal plane. (a) and (c) are images at rest; (b) and (d) are obtained on maximal Valsalva. (b) Rectocele descent against a reference line placed through the inferoposterior symphyseal margin; (d) Rectocele depth measured against a

a

b

Fig. 48.16  Anatomical abnormalities of the posterior vaginal compartment associated with symptoms of obstructed defecation, showing a ‘true rectocoele’, i.e. (a) defect of the rectovaginal septum, (b) descent

reference line placed through the ventral aspect of the internal anal sphincter. A anal canal, B bladder, R rectal ampulla, S symphysis pubis, V vagina (From [110], with permission)

c

of the rectal ampulla without rectocoele (‘perineal hypermobility’) and (c) rectal intussusception (From [111], with permission)

48  Transperineal Ultrasound: Practical Applications

597

associated with abnormalities of the levator ani muscle and hiatus [40]. Current ultrasound data do not support the ­classification of defects originally described by Cullen Richardson [34], suggesting that some of the defects described were artefactual, i.e. produced on dissection. This is plausible given the technical challenges inherent in separating the vaginal muscularis from the RVS proper. A competent assessment of posterior compartment prolapse by imaging can have substantial therapeutic consequences. The overwhelming majority of women with posterior compartment descent are treated with a simple posterior colporrhaphy, a procedure that creates a scar plate

a

b

Fig. 48.17  Posterior mesh repair (a, small arrows) usually ‘cures’ the vaginal manifestation of rectocele. However, sometimes the rectocele itself, i.e. the diverticulum of the rectal ampulla, is still sufficiently

a

between the vagina and anorectum, distorting and compressing a true rectocele, enterocoele or intussusception, without addressing the actual underlying abnormality. Even the use of posterior compartment mesh may not be truly curative as shown in Fig. 48.17 where a true rectocele is prevented from developing into the vagina by an Apogee mesh. While the posterior vagina now looks normal, neither the patient’s symptoms of obstructed defecation nor the anatomical abnormality are cured, since her rectocele now develops into the perineum. If a patient suffers from a symptomatic true rectocele, then clearly a defect-specific rectocele repair should be the surgical treatment of choice [41]. Figure 48.18 shows find-

large to cause symptoms, developing into the perineum rather than the vagina (b, big arrow outlined by dots)

b

Fig. 48.18  Sonographic appearances on Valsalva, before (a) and 6  months after (b) defect-specific rectocele repair. A anal canal, B bladder, R rectocele/rectal ampulla, S symphysis pubis (From [112], with permission)

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H. P. Dietz

ings before and 3  months after repair of a transverse RVS defect. On the other hand, if posterior compartment descent is due to a hyper-distensible fascia or perineal descent, plication of this fascia or even a levatorplasty may be a better surgical option. Needless to say, it seems to make little sense to remove portions of rectal wall as in the STARR (stapled transanal rectal resection) procedure in someone who has a herniation of the rectal wall due to a defect of the RVS, since one would expect neither the rectocele nor the patient’s symptoms to be cured. Figure 48.19 demonstrates typical appearances of an isolated enterocoele which tends to manifest clinically as post-­ hysterectomy vault prolapse. This is less common than a combination of recto- and enterocoele. Both may also occur in women with intact uterus. The contents of an enterocoele are usually the small bowel and/or omentum which appears iso-echoic and homogeneous, less often the sigmoid colon which tends to be more inhomogeneous with hypo-­echogenic

a

aspects indicating bowel wall. Peristalsis is commonly observed on real-time scanning. The treatment of rectal intussusception (Fig. 48.20) is even more controversial, although this is a controversy that gynaecologists are rarely exposed to since they are unlikely to diagnose the condition. Intussusception is even more strongly associated with symptoms of obstructed defecation than rectocele [42] and is often associated with other manifestations of prolapse. In the author’s unit, it has a prevalence of about 1:25. A further complication may be the development of a lateral or posterior rectocele due to severe damage to the levator plate; this may also be considered a buttock hernia and is palpable on digital rectal examination during Valsalva manoeuvre. The standard approach to rectal intussusception is a rectopexy, either via a laparotomy or laparoscopically. This usually involves mesh and can be combined with a vault suspension procedure. Another approach implemented in the unit of the author is to utilize the RVS for an anterior vaginal

b

c

Aa Ba C D

Bp Ap

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Fig. 48.19  Vault prolapse/enterocele on clinical photograph (a), representation on POP-Q (b; Ba = −3, D = +2.5, Bp = −1) and appearances on imaging (c; B bladder, E enterocele, R rectal ampulla, S symphysis pubis) (From [109], with permission)

a

b

Fig. 48.20  Intussusception with unusual posterior rectocele (arrow) in patient with severe obstructed defecation, bilateral avulsion and severe ballooning. The distended ampulla with posterior sacculation is outlined in all three orthogonal planes in the midsagittal plane (a) and a rendered volume showing the axial plane (b)

48  Transperineal Ultrasound: Practical Applications

rectopexy to the sacrospinous ligaments. This can conveniently be combined with a vault suspension and avoids denervation of the rectum, a common consequence of open or laparoscopic rectopexy procedures.

48.3.1.5 The Anal Sphincter The external and internal anal sphincters are usually imaged with endo-anal ultrasound [43] and MRI [44], which is particularly useful in women with faecal incontinence and after obstetric anal sphincter injury (OASI). These techniques are intrusive, involving endo-anal placement of an ultrasound probe or endocoil. Distortion of the anatomy is inevitable, which may be one explanation why our textbook illustrations often seem so different from observed anatomy on real-time ultrasound. For different reasons, neither MRI nor endo-anal ultrasound allow dynamic assessment on manoeuvres, e.g. on sphincter contraction. Exo-anal ultrasound imaging on the other hand does not have these disadvantages. It was first described by Peschers et al. in 1997 [44] and is now widely used to image the anal sphincter using either endo-­vaginal or transabdominal probe [45–48]. This method has been shown to have good correlation with 2D endo-anal imaging [48] and recently has been developed further using modern 4D transducers [49–53]. For a detailed overview of this novel technique, see [52]. For imaging of the anal canal, we use a standard curved array volume transducer in the transverse or coronal plane, i.e. perpendicular to the anal canal. The probe is inclined quite steeply from ventrocaudal to dorsocranial to obtain a coronal view of the anal canal (Fig. 6.3). Additional application of gel in the midline is often beneficial to fill the ­gluteal fold. Imaging is performed on sphincter contraction which seems to enhance the definition of muscular defects. Figures 6.15–6.18 describe the basic methodology.

599

Figure 48.21 contrasts tomographic imaging (TUI) of a normal anal sphincter on the left with the same sphincter 3 months after a vaginal delivery when it showed a significant defect that had been overlooked immediately postpartum; in the delivery suite, a second-degree perineal tear had been diagnosed by the attending midwife. Even after accurate diagnosis and primary repair of a major perineal tear, a significant defect of the external anal sphincter remains visible in 30–40% of patients [50], both in the short term and many years later when over 50% of patients are symptomatic [53]. Sonographically detected defects are associated with anal incontinence, both after OASI repair [50, 53] and later in life [51]. To quantify the extent of trauma, we determine the number of abnormal slices, with > = 4/6 slices required for the diagnosis of a ‘residual defect’ [52]. Another method is to measure the defect angle as in Fig.  48.22; a cut-off has empirically been set at 30°, although attempts at validating defect angle have not been successful to date [54]. Translabial ultrasound of the anal sphincter is increasingly used in research. Its simplicity and superior acceptance by patients [55] will, much more so than in the case of more intrusive methods, allow incorporation into clinical practice. While pain, oedema and the presence of suture material make imaging difficult shortly after childbirth, exo-anal imaging is eminently feasible within a very few days. Follow-up after 2–3 months, once the effect of potential neuropathy has subsided, allows a final assessment of the quality of both diagnosis and treatment in the delivery suite. Establishment of postnatal imaging services in the context of ‘perineal clinics’ is overdue as third-degree tears are ­frequently overlooked after childbirth, with the experience of the personnel involved being one of the main factors in the diagnosis [56], and as primary repair is clearly insufficient in many cases [50, 53].

Fig. 48.21  Tomographic imaging of the anal sphincters. This is a comparison of (a) antenatal and (b) postnatal imaging, showing a 3b perineal tear (asterisk) that was overlooked in the delivery suite

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Fig. 48.22  Overlooked, unrepaired 3b tear with well-repaired episiotomy. The angle measurements illustrate quantification of this tear which measures well over 30° in 5/6 slices

Figures 48.21–48.25 show different forms of residual anal sphincter defects after vaginal delivery. In Fig. 48.22 there is evidence of a 3b tear that was not recognized at the time of postnatal suturing of an episiotomy (see arrow). Figure  48.23 demonstrates a poor result after end-to-end repair, while Fig. 48.24 shows equally poorly reconstructive results after an overlap repair. Even worse, Fig. 48.25 represents a rectovaginal fistula after a poorly repaired fourthdegree tear. Due to increasing medicolegal and public pressure, maternal trauma will likely become a key performance indicator of obstetric services [57]. As regards antenatal and intrapartum research, future perinatal intervention trials should include imaging of maternal trauma as an outcome measure since maternal trauma is a common adverse consequence of vaginal childbirth. On a final note, occasionally one will encounter other abnormalities which may at times interfere with identification of the caudal margin of the internal anal sphincter. The latter is, as mentioned in Chap. 6, important for reproducible slice placement. Figure 48.26 is an inflamed, symptomatic haemorrhoid, while Fig. 48.27 shows what is likely an iatrogenic defect of the internal anal sphincter after haemorrhoidectomy repair, a not uncommon cause of post- haemorrhoidectomy

anal incontinence. However, it has to be mentioned that such abnormalities of the internal anal sphincter can at times be observed in women without a history of surgical intervention.

48.3.1.6 Synthetic Implants Synthetic implants have become popular for the surgical treatment of stress urinary incontinence and since the mid-­2000s also for POP. Over the last 5 years. There has been a backlash due to novel complications such as chronic pain and erosion, with substantial adverse publicity on social media and in the lay press. This is increasingly leading to referrals for imaging of slings and meshes, a task for which few imaging services are equipped or trained. While biological materials such as Surgisis or Permacol tend to degrade over time and may not remain visible on any imaging modality, this is not the case for implants made of polypropylene and similar synthetic materials. Synthetic sling and mesh implants are virtually invisible on MR, CT and conventional X-ray but highly echogenic on sonographic imaging. Ultrasound can confirm the presence of suburethral slings (Figs. 48.28–48.34) and distinguish different types of implants (see Fig.  48.29 for a transobturator sling) [58].

48  Transperineal Ultrasound: Practical Applications

601

Fig. 48.23  Poor reconstructive result after end-to-end repair of a 3c tear after forceps delivery

Fig. 48.24  Status after unsuccessful overlap repair of a 3c tear, showing substantial distortion and a marked perineal scar (arrows). The patient was faecally incontinent

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Fig. 48.25  Small rectovaginal fistula 3 months after insufficiently repaired 3c tear. The fistula is a small filiform echogenic line, indicated by arrows in two central slices. The two arrows in the top left-hand image indicate the longitudinal extent of the internal anal sphincter defect

Fig. 48.26  Inflamed haemorrhoid on tomographic imaging, indicated by arrows. Haemorrhoids can obscure the distal aspect of the internal anal sphincter and sometimes even the external anal sphincter, interfering with the assessment

48  Transperineal Ultrasound: Practical Applications

603

Fig. 48.27  Status after haemorrhoidectomy in a 60-year-old patient with mild anal incontinence. The internal anal sphincter is invisible between 4 and 7 o’clock in most slices and thickened over the remaining circumference, possible iatrogenic trauma

a

b

Fig. 48.28  Appearance of a typical suburethral sling (arrow) in the midsagittal plane at rest (a) and on maximal Valsalva (b). The line in (b) demonstrates measurement of the sling- pubis gap. B bladder, R rectum, S symphysis pubis

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a

Fig. 48.29  Suburethral slings are generally hyperechoic and easily identified posterior to the urethra. On this image a Monarc transobturator tape is shown in the midsagittal plane (a) and in an axial rendered volume (b). In the axial plane, the course of mesh from one pelvic side-

a

b

wall to the other is clearly shown, demonstrating that the mesh remains well outside the donut-shaped urethral rhabdosphincter (From [113], with permission)

b

Fig. 48.30  TFS (tissue fixation system) slings as seen in the midsagittal plane in two different patients. The TFS has been used not just for urinary incontinence as a suburethral sling, which appears highly echogenic and nondeformable (as seen in both a and b), but also for pro-

lapse. In (a) there is an implant under the trigone, and in (b) another is found in the perineum. The latter is the most prone to erode and cause chronic pain

Standard ­polypropylene slings have a rather typical sonographic appearance that changes under load as the implant is deformed by interaction with surrounding tissues. More densely woven tapes such as the IVS may be smaller and harder to visualize or wider and less deformable, such as the TFS (Fig. 48.31).

Suburethral slings all seem to act by direct, dynamic compression under load, which is apparent on imaging, with the sling changing from a linear to a c-shape [59]. Complications due to excessive tensioning such as voiding dysfunction or de novo symptoms of urgency and/or urge incontinence commonly have a sonographic correlate in a tightly rolled-up

48  Transperineal Ultrasound: Practical Applications

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a

b

c

Fig. 48.31  ‘Tethered’ suburethral sling (TVT) in the midsagittal plane (a), the coronal plane (b) and the axial plane (c). The tape (arrows) seems unremarkable in (a), but in (b) it is apparent that it does not run symmetrically. In (c) it becomes obvious that the cause of this asym-

a

c

metry is perforation of the urehral rhabdosphincter on the patient’s left. The longitudinal smooth muscle does not seem to be affected. Such placement is due to surgical error and may be asymptomatic. Its natural history is unclear

b

d

Fig. 48.32  A TVT that has perforated the urethra as imaged in the midsagittal plane (a), the coronal plane (b), the axial plane (c) and a rendered volume in the axial plane (d). Part of the tape on the patient’s right hand side has been removed

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a

b

c

d

Fig. 48.33  Patient after TVT division due to de novo urgency, urge incontinence and chronic mild obstruction. (a) shows the midsagittal plane (A anal canal, B bladder, R rectal ampulla, S symphysis pubis, U urethra). The arrow indicates the most likely location for a TVT, but the tape is invisible in the midsagittal plane. (b) and (c) shows coronal

and axial views, with the two free tape ends indicated by arrows. The gap between the two tape ends is also evident in the axial plane rendered volume (d), with a gap between the cut ends of about 5–7 mm at rest (Adapted from [114], with permission)

band that leaves only a small gap between the implant and symphysis pubis, especially on Valsalva. This ‘sling-pubis gap’ (Fig.  48.28) seems to be the most consistently useful measure of ‘sling tightness’, with a gap of 8–14 mm on maximal Valsalva being rated as ‘normal’ [60]. An implant that is seen as too close to the urethra, rigid and compressive, with a low sling-pubis gap of less than 8 mm, will prompt the surgeon either to attempt dilatation/stretching of the sling if identified within the first week or 10 days, or to undertake sling division at a later stage. In some instances slings are shown to be ‘tethered’, i.e. placed deep to the fascia of the urethral rhabdosphincter and therefore through the muscle rather than outside it, as shown in Fig. 48.31. Occasionally, imaging will suggest perforation and/or stenosis (Fig. 48.32). Sling division, a minor procedure that may be performed under local anaesthetic, tends to result in a 5–10 mm gap between mesh arms documenting successful division as shown in Fig.  48.33. Rarely, faulty sling placement will result in perforation and even transection of the urethra, and ultimately the implant may be found in the space of Retzius (Fig. 48.34). Injectables are not used

widely, but some materials such as Macroplastique (TM) are echogenic and easily identified para-urethrally or under the bladder neck (Fig. 48.35). However, appearances on imaging are not predictive of treatment success. Mesh implants used in prolapse surgery are another o­ bvious indication for translabial ultrasound, and 3D/4D imaging with sectional plane and rendering capabilities is particularly useful in identifying polypropylene mesh implants (Figs.  48.36– 48.42) [61–63]. In the anterior compartment, mesh is commonly situated posterior to the bladder neck, caudal to the trigone and the posterior bladder wall, visible as an echogenic linear or curvilinear structure. Mesh can be identified in the three orthogonal planes (Fig. 48.36) and also in rendered volumes (Fig. 48.37). A Valsalva manoeuvre often helps visualization and shows mesh rotating around the fulcrum of the symphysis pubis. More caudally placed transobturator meshes can act like an oversized trigonal sling, rotating dorsocaudally. Persistent prolapse of the central or posterior compartment and distance from the transducer can impair visualization by translabial imaging. While mesh shrinkage, contraction or

48  Transperineal Ultrasound: Practical Applications

Fig. 48.34  The final outcome of urethral tape erosion may not necessarily be surgical removal. Occasionally the tape may erode through the entire urethra to eventually be found in the space of Retzius, as in this patient who had symptoms of the overactive bladder, voiding dysfunction and recurrent UTIs for years without being assessed or treated. (a)

a

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This transobturator tape (arrow), 7 years after implantation, is now situated in the space of Retzius. (b–c) An orthogonal representation of imaging shown here is particularly useful to define the spatial extent of unusual para-urethral findings

b

c

Fig. 48.35  Macroplastique silicone macroparticles used in incontinence surgery are very echogenic and found surrounding the urethra both anteriorly and posteriorly, as shown both in the orthogonal views

d

(a–c) and in a rendered volume (d). The implant is visible as a donut shape in c and d

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a

b

Fig. 48.36  Identification of anterior compartment mesh on Valsalva (a, midsagittal plane; b, coronal plane; and c, axial plane). Arrows show mesh length in the midsagittal (a) and the coronal plane (b–c). B blad-

a

c

der, L levator ani, R rectum, S symphysis pubis (Modified from [59], with permission)

b

Fig. 48.37  Ultrasound images showing anterior mesh failure: (a) at rest; (b) on submaximal Valsalva manoeuvre; (c) on maximum Valsalva. Cystocele recurrence ventral and caudal to a well-supported mesh suggests that the caudal aspect of the implant was insufficiently secured to

a

c

the bladder neck, leading to dislodgement of the mesh from the bladder base. B bladder; BN bladder neck, L levator ani muscle, R rectum, S symphysis pubis, U urethra (From [60], with permission)

b

Fig. 48.38  Translabial imaging of a transobturator anterior compartment mesh. The mesh (arrows) is seen posterior to proximal urethra and bladder neck in the midsagittal plane (a) and in a rendered volume in an oblique axial plane (b) (From [115], with permission)

48  Transperineal Ultrasound: Practical Applications

a

b

Fig. 48.39  Ultrasound images showing apical mesh failure: (a) at rest; (b) on submaximal Valsalva manoeuvre; (c) on maximum Valsalva. Cystocele recurrence dorsal to the mesh with high mobility of the cra-

a

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c

nial mesh aspect suggests dislodgement of apical attachment. B bladder, S symphysis pubis, U urethra (From [60], with permission)

b

Fig. 48.40  Ultrasound images showing global mesh failure: (a) at rest; (b) on submaximal Valsalva manoeuvre; (c) on maximum Valsalva. Cystocele recurrence behind the mesh is associated with high mobility

a

c

of the entire mesh on Valsalva, suggesting dislodgement of both lateral and apical attachments. B bladder, L levator ani muscle, R rectum, S symphysis pubis (From [60], with permission)

b

Fig. 48.41  Midsagittal view (a) and axial plane rendered volume (b) in a patient after successful Perigee (P) and Apogee (A) implantation. The midsagittal plane (a) demonstrates absence of prolapse on Valsalva,

despite severe levator ballooning evident in the axial plane (b) in this patient with bilateral avulsion injury (Modified from [59], with permission)

retraction is often considered as one of the causes of pelvic pain after mesh repairs [64], this has been refuted by longitudinal studies [62, 65]. The so-called mesh shrinkage is very

likely due to poor surgical technique and/or an excess of material, resulting in mesh folds during implantation or immediately after closure [65].

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b

Fig. 48.42 (a) Suburethral sling (‘Monarc’) and posterior compartment mesh repair (‘Apogee’) in a patient with clinical prolapse cure and symptoms of obstructed defecation 6 months postoperatively. (b) A rec-

tal intussusception (I), which is due to an enterocele barred from developing into the vagina (A anal canal, L levator ani, R Rectum, S symphysis pubis)

Prolapse recurrence after mesh use can be a particularly vexing problem. In a recent study of recurrence after anterior mesh repair [63], we identified three distinct anatomical situations: (1) anterior failure, cystocele ventral and caudal to a mesh with intact anchoring; (2) apical failure, cystocele/ anterior enterocele/uterine prolapse dorsal and caudal to a mesh with failure of apical anchoring and finally (3) global failure, cystocele with high mesh mobility due to failure of both apical and lateral anchoring mechanisms (Figs. 48.38–48.40). Most prolapse recurrence in this series was global or apical (i.e. failure of apical and lateral anchoring). Only a small minority showed anterior failures which suggest dislodgment of the mesh from the bladder base, likely due to faulty surgical technique [63]. This implies that most cases of cystocele recurrence are ‘engineering’ problems rather than issues of surgical technique. This is supported by the observation that dislodgment of mesh-anchoring structures is associated with hiatal area on Valsalva [63]; the larger the hiatus, the higher the loads placed on anchoring structures such as transobturator arms and the higher the probability of mechanical failure of load-bearing structures [66]. It should not be difficult to come up with engineering solutions to the problem of anchor dislodgment; unfortunately, research and development in this field seems to have come to a halt due to poor patient selection and unscrupulous marketing which has provoked widespread medicolegal action. As a result, many women have suffered complications such as chronic pain and erosion without any conceivable benefit. Unfortunately, ultrasound is largely useless in the evaluation of these two main mesh complications. Anterior compartment meshes, as long as they are anchored effectively, result in superior anatomical outcomes, especially in women with major levator tears [67, 68]. On the

other hand, the evidence suggests that they are no more effective and clearly more likely to lead to complications than native tissue repair in the posterior compartment. They may be encountered sonographically as hyperechogenic curvilinear structures in the posterior vaginal wall (Figs. 48.41 and 48.42). Figure 48.42 shows an unusual complication in a patient with post-­ hysterectomy vault prolapse who was ‘cured’ by a posterior compartment mesh. Postoperatively she developed de novo obstructed defecation which on imaging turned out to be an intussusception. Her enterocoele, prevented from passing through and everting the vagina, now inverts the rectal ampulla, trying to pass through the alternate passage of the anal canal.

48.3.2 The Levator Ani Axial plane imaging 3D/4D ultrasound has allowed the introduction of axial plane imaging into clinical practice. This is particularly useful for the assessment of the pelvic floor in the narrower sense: the levator ani muscle and hiatus. Translabial ultrasound has confirmed 60-year old, forgotten clinical data [69, 70] and recent MRI studies [71] showing that major structural abnormalities of the levator ani muscle are common in women who have given birth vaginally [3]. Most recent studies use the methodology described in this chapter for the assessment of such trauma and show a prevalence of 10–15% after normal vaginal delivery, 10–20% after vacuum and 40–60% after forceps delivery, with the highest prevalence after rotational forceps; for an overview of prevalence, see [72]. Reproducible assessment of the levator ani muscle on translabial 3D/4D ultrasound requires identification of the plane of minimal dimensions, i.e. the minimal distance between the interpubic disc ventrally and the anorectal angle

48  Transperineal Ultrasound: Practical Applications

dorsally (Fig. 48.43). This provides the reference plane for standardized assessment both of the levator hiatus, the largest hernia portal in the human body, and of the insertions of the puborectalis muscle on the inferior pubic ramus, the commonest location of major maternal birth trauma. A defect of this muscle insertion is defined as ‘avulsion’, due to the caudal aspects of the levator ani muscle, the ‘puborectalis’ or ‘pubococcygeus/pubovisceralis’ muscle, being separated from the bone on which it inserts in a direct muscle-bone ‘enthesis’. The only known mechanism for such trauma is excessive distension of the muscle during vaginal delivery at the time of crowning of the foetal head. This trauma is most commonly occult as the vaginal skin and muscularis layer tend to fail in a different location, together with the perineal body. This frequently leaves the site of avulsion covered by intact vagina, preventing discovery of an avulsion, even if a vaginal haematoma may at times signal major hidden trauma. It is not surprising therefore that it has a

b

taken clinical obstetrics so long to realize how common major maternal trauma truly is, and how important for the future life of the affected mother: avulsion is the primary modifiable etiological factor in the pathogenesis of female pelvic organ prolapse [72]. Figure 48.44 illustrates a comparison of clinical examination, axial plane rendered volume and MR imaging in a patient with unilateral right-sided levator avulsion after a normal vaginal delivery at term. The levator can in fact be imaged with a 2D ultrasound—either with the help of a side-­ firing endocavitary probe or with an abdominal curved array placed in a parasagittal orientation (Fig.  48.45) [73]. However, it is more convenient and much more reproducible to use standard 3D/4D abdominal/obstetric probes placed on the perineum in the midsagittal plane (Fig. 6.1). Using settings similar to those for imaging a baby’s face, a rendered volume, with the rendering direction set from distally to proximally, results in images that rival MRI (Fig. 48.46). c

Fig. 48.43  Measuring hiatal dimensions as shown in an oblique single axial plane (a, b) and in a rendered volume (c, d). The determination of hiatal dimensions using a single oblique axial plane is shown in (a) and (b). The midsagittal plane on the left (a) demonstrates a line indicating the minimal sagittal diameter of the hiatus, i.e. the location of the oblique axial plane shown in (b). The region of interest (ROI) box in (c)

a

611

b

Fig. 48.44  Typical right-sided levator avulsion injury was diagnosed in the delivery suite after a normal vaginal delivery at term, (a) on 3D ultrasound (b) and on magnetic resonance imaging (c) 3 months post-

d

(approx. 1.8 cm deep) is located between the symphysis pubis and the levator ani posterior to the anorectal angle. Image (d) represents a semi-­ transparent view of all pixels in the ROI box on the left. The dotted line in (b) and (d) represents hiatal area measurements (23.05 cm2 in (b), 21.77 cm2 in (d)) (From [115], with permission)

c

partum. This patient was asymptomatic apart from deep dyspareunia (From [115], with permission)

612

a

H. P. Dietz

b caudal

dorsal

Symphysis pubis Puborectalis muscle Pelvic sidewall

c

Fig. 48.45  Parasagittal view of the insertion of the puborectalis muscle on the pelvic sidewall. The image in (c) shows a normal insertion of the muscle, with the hyperechogenic muscle fibres clearly visible. (a)

transducer placement; (b) schematic line drawing of the principal structures seen in (c) (From [74], with permission)

Fig. 48.46  Right-sided avulsion in a patient with third-degree cystocele and first-degree uterine prolapse. The midsagittal plane (a) shows descent of bladder and uterus on Valsalva. (b) Tomographic representation of the puborectalis muscle in the patient obtained on pelvic floor

muscle contraction, showing a right-sided complete avulsion (asterisk). A anal canal, B bladder, L levator ani, S symphysis pubis, U uterus. The patient’s right side is represented on the left side of the slices

Standardized evaluation of the levator ani is made possible (and very simple) by the acquisition of volume data, i.e. fan-shaped blocks of volume pixels or ‘voxels’, which is cur-

rently near impossible with other diagnostic modalities. Avulsion can be diagnosed in several different ways including palpation [74], but multislice or tomographic imaging

48  Transperineal Ultrasound: Practical Applications

613

(TUI) is probably the most reproducible and valid, [75–78], and it correlates well with MR for the diagnosis of levator trauma [79]. Figure 48.46 shows a typical right-sided complete avulsion of the puborectalis on tomographic imaging in a patient with cystocele and stage 1 uterine descent, while Fig. 48.47 demonstrates a bilateral defect on TUI, complete on the right and partial on the left. Incomplete defects do not seem to be associated with prolapse or prolapse recurrence [80], which means that the distinction between incomplete and complete trauma, i.e. the definition of a ‘full avulsion’, is crucial. Given the generally accepted 2.5 mm interslice interval for pelvic floor tomography, the minimal criterion for a full avulsion requires the three central slices in Figs. 48.46 and 48.47 to be abnormal [76]. This implies that slice location is of the essence, and it is fortunate that the appearance of the symphysis pubis allows standardization of slice location to within 1  mm (Fig.  48.47). Care has to be taken, however, with identification of the plane of minimal dimensions, as

omission of this step in the generation of a set of TUI slices may result in false-positive findings in caudal slices. This particularly affects women with a strong levator contraction in whom warping of the levator plate from ventrocaudal to dorsocranial may be quite marked. If the appearance of muscle insertions on TUI is equivocal due to partial trauma, scar tissue, limited image quality or artefact, the ‘levator-urethra gap’ (LUG) (Fig.  48.48) can be very useful in establishing a diagnosis, even if any biometric measurement is of course subject to interethnic and interindividual variation. It is therefore not surprising that different cut-offs for a ‘normal’ LUG have been established for Caucasians (2.5  cm) [81] and East Asians (2.36 cm) [79]. The LUG has an equivalent on MRI [82] and can be used as the only criterion for the diagnosis of avulsion [83]. Usually, imaging for levator assessment is performed on pelvic floor muscle contraction as this enhances tissue discrimination, but TUI at rest seems to be equally valid [84, 85].

Fig. 48.47  Tomographic imaging of the puborectalis, showing a complete right-sided and partial left-sided avulsion. The required appearance of the symphysis pubis (open on the left-central slice, closing on

the central slice and closed (invisible) on the right-central slice) is shown by the arrows

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Fig. 48.48  Illustration of the measurement of the levator-urethra gap (LUG) in the three central slices of a tomographic representation of the puborectalis muscle. All measurements on the left (the patient’s right) are clearly abnormal, indicating a complete right-sided avulsion

Major delivery-related levator injury plays a substantial role in the aetiology of female pelvic organ prolapse. Very likely there are other factors, such as altered biomechanics of intact muscle, fascial trauma and neuropathy. However, it is clear that avulsion enlarges the levator hiatus [86], reduces contractile strength [87] and is associated with prolapse, especially in the anterior and central compartments [72, 88]. Levator defects seem to be the single strongest risk factor for prolapse recurrence after reconstructive surgery [89–91], which is not surprising since enlargement of the levator hiatus through whatever mechanism will necessarily result in increased strain on any load-bearing structure [66]. Axial plane imaging of the levator ani muscle has not just led to a rediscovery of avulsion as a central factor in the pathogenesis of pelvic floor disorders; it has also made us realize that prolapse is truly a hernia: a hernia of pelvic organs through the largest potential hernia portal in the human body, the levator hiatus. This triangular structure is the most complex ‘defect’ in the abdominal wall as it is crucial for the function of three vital organ systems: the reproductive tract (intercourse and childbirth), the lower urinary tract (elimination of liquid waste) and the lower gastrointestinal tract (elimination of solid waste). Not surprisingly, the pelvic floor in women is a compromise between competing priorities. From an evolutionary point of view, reproduction is of course the top priority, and it is not surprising that pelvic floor disorders are common and sometimes very difficult to treat. The current functional anatomy of the female pelvic floor is the result of rapid evolutionary change, with major differences in bony and soft tissue anatomy between our nearest relatives, the simian primates and Homo sapiens. Over the last 15 years, it has become evident that there are major interindividual and interethnic variations in dimensions and biomechanical properties of the levator hiatus [92–94]. Such international comparisons have become possible due to the standardization of the assessment of hiatal dimensions by axial plane pelvic floor ultrasound, first described in 2005

[95] and since extensively validated against MRI [96] and clinical examination [97, 98]. Repeatability is clearly excellent [78, 99, 100]. In childbirth, the levator hiatus has to undergo a very substantial degree of distension [102, 103], which may result in macroscopic trauma (avulsion) (see above) or irreversible over-distension of the puborectalis muscle, i.e. ‘microtrauma’ [72]. Hiatal enlargement to 25  cm2 on Valsalva or higher is defined as ‘ballooning’ on the basis of receiver operator characteristics statistics [105] and normative data in young nulliparous women [95]. Hiatal area can be assessed both in axial plane slices at the plane of minimal hiatal dimensions or in rendered volumes (see Fig. 48.43 for a comparison of the two methods). Since the hiatal plane is non-Euclidean (warped rather than flat), hiatal area measurements obtained in rendered volumes may be more valid and more reproducible as well as easier to obtain [105]. The degree of distension is strongly associated with prolapse and symptoms of prolapse [106], and both avulsion and ‘ballooning’ seem to be independent risk factors of female POP and POP recurrence after reconstructive surgery [107, 108]. Most recently, it has become clear that hiatal distensibility is the pathophysiological correlate of ‘vaginal laxity’ [109], a common and often misunderstood complaint that can result in substantial bother, mainly through its impact on sexual function [110].

48.4 Conclusions Pelvic floor ultrasound imaging is a highly useful diagnostic tool for physicians and researchers dealing with pelvic floor disorders, especially since the introduction of 3D/4D ultrasound which allows simple, cheap and highly reproducible assessment of the axial plane, and multislice or tomographic imaging. The increasing ubiquity of such systems, new software options, and the increasing availability of training will likely lead to a more general acceptance of imaging as an

48  Transperineal Ultrasound: Practical Applications

integral part of the investigation of women with pelvic floor disorders. The issue of levator trauma, one of the most significant developments in pelvic floor medicine, is taking pelvic floor ultrasound into the mainstream of urogynaecology and will enhance communication between the different clinical specialties dealing with such patients, such as urologists, gynaecologists, colorectal surgeons, physiotherapists and imaging specialists. The method has great potential to improve not just diagnostic but also therapeutic skills, and this is becoming increasingly obvious. Tomographic imaging of the anal sphincter and levator ani will enable obstetricians to assess maternal birth trauma with unprecedented ease and accuracy and at a minimal cost. This will likely result in the establishment of maternal trauma as a key performance indicator of obstetric services, a development that is long overdue and likely to substantially change obstetric practice.

Take-Home Messages

• Translabial ultrasound is the imaging method of choice in the evaluation of pelvic floor disorders such as urinary incontinence, defecation disorders, anal incontinence and pelvic organ prolapse. • 3D/4D imaging using volume transducers allows the assessment of distinct abnormalities such as implants or urethral diverticula in the orthogonal planes. • Tomographic or multislice imaging has revolutionized the assessment of maternal birth trauma in the form of levator avulsion and anal sphincter tears.

References 1. Olsen AL, Smith VJ, Bergstrom JO, Colling JC, Clark AL. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol. 1997;89(4):501–6. 2. Smith F, Holman CD, Moorin RE, Tsokos N. Lifetime risk of undergoing surgery for pelvic organ prolapse. Obstet Gynecol. 2010;116:1096–100. 3. Dietz HP, Lanzarone V.  Levator trauma after vaginal delivery. Obstet Gynecol. 2005;106(4):707–12. 4. Kearney R, Miller JM, Ashton-Miller JA, DeLancey JO. Obstetric factors associated with levator ani muscle injury after vaginal birth. Obstet Gynecol. 2006;107(1):144–9. 5. Dietz H, Simpson J.  Levator trauma is associated with pelvic organ prolapse. Br J Obstet Gynaecol. 2008;115:979–84. 6. Shek K, Chantarasorn V, Langer S, Phipps H, Dietz HP. Does the epi-no device reduce levator trauma? A randomised controlled trial. Int Urogynecol J. 2011;22(12):1521–8. 7. Dietz H.  Forceps: towards obsolescence or revival? Acta Obstet Gynecol Scand. 2015;94(4):347–51. 8. Dietz HP. Pelvic floor ultrasound in prolapse: what's in it for the surgeon? Int Urogynecol J. 2011;22:1221–32.

615 9. Dietz HP, Wilson PD. The influence of bladder volume on the position and mobility of the urethrovesical junction. Int Urogynecol J. 1999;10(1):3–6. 10. Oerno A, Dietz H.  Levator co-activation is a significant confounder of pelvic organ descent on Valsalva maneuver. Ultrasound Obstet Gynecol. 2007;30:346–50. 11. Orejuela F, Shek K, Dietz H.  The time factor in the assessment of prolapse and levator ballooning. Int Urogynecol J. 2012;23:175–8. 12. Dietz HP, Velez D, Shek KL, Martin A. Determination of postvoid residual by translabial ultrasound. Int Urogynecol J. 2012;23:1749–52. 13. Khullar V, Cardozo LD, Salvatore S, Hill S. Ultrasound: a noninvasive screening test for detrusor instability. Br J Obstet Gynaecol. 1996;103(9):904–8. 14. Yang JM, Huang WC. Bladder wall thickness on ultrasonographic cystourethrography: affecting factors and their implications. J Ultrasound Med. 2003;22(8):777–82. 15. Lekskulchai O, Dietz H.  Detrusor wall thickness as a test for detrusor overactivity in women. Ultrasound Obstet Gynecol. 2008;32:535–9. 16. Lekskulchai O, Dietz H. Is detrusor hypertrophy in women associated with symptoms and signs of voiding dysfunction? Aust NZ J Obstet Gynaecol. 2009;49:653–6. 17. Titus J, Blatt A, Chan L.  Ultrasound measurement of bladder wall thickness in the assessment of voiding dysfunction. J Urol. 2008;179:2275–9. 18. Schaer G. The clinical value of sonographic imaging of the urethrovesical anatomy. Scand J Urol Nephrol. 2001;207:80–6. 19. Dietz HP. Pelvic floor ultrasound in incontinence: What’s in it for the surgeon? Int Urogynecol J. 2011;22(9):1085–97. 20. Dietz HP.  Ultrasound imaging of the pelvic floor. Part I: two-­ dimensional aspects. [Review] [86 refs]. Ultrasound Obstet Gynecol. 2004;23(1):80–92. 21. Pirpiris A, Shek KL, Dietz HP. Urethral mobility and urinary incontinence. Ultrasound Obstet Gynecol. 2010;36:507–11. 22. Masata J, Martan A, Svabik K, Drahoradova O, Pavlikova M. Ultrasound imaging of the lower urinary tract after successful tension- free vaginal tape (TVT) procedure. Ultrasound Obstet Gynecol. 2006;2006:221–8. 23. Dietz H, Nazemian K, Shek KL, Martin A. Can urodynamic stress incontinence be diagnosed by ultrasound? Int Urogynecol J. 2012;23(24):1399–403. 24. Naranjo-Ortiz C, Shek K, Dietz H. What is normal bladder neck anatomy? Int Urogynecol J. 2016;27(6):945–50. 25. Dietz HP, Clarke B. The urethral pressure profile and ultrasound imaging of the lower urinary tract. Int Urogynecol J Pelvic Floor Dysfunct. 2001;12(1):38–41. 26. Masata J, et al. Ultrasound imaging of urethral funneling. Ginecol Gen Salud Mujer. 1999;10(S1):S62. 27. Green TH.  Urinary stress incontinence: differential diagnosis, pathophysiology, and management. Am J Obstet Gynecol. 1975;122(3):378–400. 28. Eisenberg V, Chantarasorn V, Shek KL, Dietz HP. Does levator ani injury affect cystocele type? Ultrasound Obstet Gynecol. 2010;36:618–23. 29. Dietz H, Cartmill J. Imaging in patients with obstructed defecation. Tech Coloproctol. 2013;17:473–4. 30. Perniola G, Shek C, Chong CCW, Chew S, Cartmill J, Dietz HP. Defecation proctography and translabial ultrasound in the investigation of defecatory disorders. Ultrasound Obstet Gynecol. 2008;31:567–71. 31. Steensma AB, Oom DM, Burger CW, Schouten WR. Assessment of posterior compartment prolapse: a comparison of evacuation proctography and 3D transperineal ultrasound. Colorectal Dis. 2010;12(6):533–9.

616 32. Beer-Gabel M, Assoulin Y, Amitai M, Bardan E. A comparison of dynamic transperineal ultrasound (DTP-US) with dynamic evacuation proctography (DEP) in the diagnosis of cul de sac hernia (enterocele) in patients with evacuatory dysfunction. Int J Colorectal Dis. 2008;23:513–9. 33. Dietz HP, Beer-Gabel M. Ultrasound in the investigation of posterior compartment vaginal prolapse and obstructed defecation. Ultrasound Obstet Gynecol. 2012;40:14–27. 34. Richardson AC.  The rectovaginal septum revisited: its relationship to rectocele and its importance in rectocele repair. Clin Obstet Gynecol. 1993;36(4):976–83. 35. Dietz HP.  Can the rectovaginal septum be visualised on ultrasound? Ultrasound Obstet Gynecol. 2011;37(4):348–52. 36. Chantarasorn V, Shek K, Dietz HP.  Sonographic appearance of the perineal body and changes in mobility after childbirth. Int Urogynecol J. 2012;23(6):729–33. 37. Dietz HP, Korda A.  Which bowel symptoms are most strongly associated with a true rectocele? Aust NZ J Obstet Gynaecol. 2005;45:505–8. 38. Dietz HP, Steensma AB. Posterior compartment prolapse on twodimensional and three-dimensional pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynecol. 2005;26:73–7. 39. Guzman Rojas R, Kamisan Atan I, Shek KL, Dietz HP. The prevalence of abnormal posterior compartment anatomy in urogynecological patients. Int Urogynecol J. 2016;27(6):939–44. 40. Rodrigo N, Shek K, Dietz H.  Rectal intussusception is associated with abnormal levator structure and morphometry. Tech Coloproctol. 2011;15:39–43. 41. Richardson AC. The anatomic defects in rectocele and enterocele. J Pelvic Surg. 1996;1:214–21. 42. Thakar R, Sultan A. Anal endosonography and its role in assessing the incontinent patient. Best Pract Res Clin Obstet Gynaecol. 2004;18:157–73. 43. Stoker J, Rociu E, Wiersma TG, Lameris JS. Imaging of anorectal disease. Br J Surg. 2000;87(1):10–27. 44. Peschers UM, DeLancey JO, Schaer GN, Schuessler B. Exoanal ultrasound of the anal sphincter: normal anatomy and sphincter defects. Br J Obstet Gynaecol. 1997;104(9):999–1003. 45. Wisser J, Schar G, Kurmanavicius J, Huch R, Huch A. Use of 3D ultrasound as a new approach to assess obstetrical trauma to the pelvic floor. Ultraschall Med. 1999;20(1):15–8. 46. Timor-Tritsch IE, Monteagudo A, Smilen SW, Porges RF, Avizova E. Simple ultrasound evaluation of the anal sphincter in female patients using a transvaginal transducer. Ultrasound Obstet Gynecol. 2005;25(2):177–83. 47. Valsky DV, Messing B, Petkova R, et al. Postpartum evaluation of the anal sphincter by transperineal three-dimensional ultrasound in primiparous women after vaginal delivery and following surgical repair of third-degree tears by the overlapping technique. Ultrasound Obstet Gynecol. 2007;29(2):195–204. 48. Oom DMJ, West RL, Schouten WR, Steensma AB. Detection of anal sphincter defects in female patients with fecal incontinence: a comparison of 3-dimensional transperineal ultrasound and 2-dimensional endoanal ultrasound. Dis Colon Rectum. 2012;55:646–52. 49. Guzman Rojas R, Shek KL, Langer SM, Dietz HP. Prevalence of anal sphincter injury in primiparous women. Ultrasound Obstet Gynecol. 2013;42(4):461–6. 50. Shek KL, Guzman Rojas R, Dietz HP.  Residual defects of the external anal sphincter following primary repair: an observational study using transperineal ultrasound. Ultrasound Obstet Gynecol. 2014;44:704–9. 51. Guzman Rojas R, Shek KL, Kamisan Atan I, Dietz HP.  Anal sphincter trauma and anal incontinence in urogynecological patients. Ultrasound Obstet Gynecol. 2015;46:363–6.

H. P. Dietz 52. Dietz HP.  Exo-anal imaging of the anal sphincters: a pictorial introduction. J Ultrasound Med. 2018;37:263–80. 53. Turel F, Langer S, Shek KL, Dietz HP.  Long-term follow-up of obstetric anal sphincter injury. Dis Colon Rectum. 2018;62(3):1. 54. Subramaniam N, Brown C, Dietz HP.  EAS defect size: does it matter? Int Urogynecol J. 2017;28(S1):S33–4. 55. Van Gruting I, Arendsen L, Naiu M, Thakar R, Sultan A. Can transperineal ultrasound replace endoanal ultrasound for the detection of anal sphincter defects? Int Urogynecol J. 2016;27(S1):S51–2. 56. Andrews V, Sultan AH, Thakar R, Jones PW. Occult anal sphincter injuries- myth or reality? BJOG. 2006;113:195–200. 57. Dietz H, Pardey J, Murray H.  Pelvic floor and anal sphincter trauma should be key performance indicators of maternity services. Int Urogynecol J. 2015;26:29–32. 58. Dietz HP, Barry C, Lim YN, Rane A. Two-dimensional and threedimensional ultrasound imaging of suburethral slings. Ultrasound Obstet Gynecol. 2005;26(2):175–9. 59. Dietz H, Wilson P. The Iris effect: how 2D and 3D volume ultrasound can help us understand anti- incontinence procedures. Ultrasound Obstet Gynecol. 2004;23:267–71. 60. Chantarasorn V, Shek K, Dietz H.  Sonographic appearance of transobturator slings: implications for function and dysfunction. Int Urogynecol J. 2011;22:493–8. 61. Shek C, et  al. Imaging of the perigee transobturator mesh and its effect on stress incontinence. Ultrasound Obstet Gynecol. 2007;30(4):446. 62. Dietz H, Erdmann M, Shek K. Mesh contraction: myth or reality? Am J Obstet Gynecol. 2011;204(2):173.e1–4. 63. Shek KL, Wong V, Lee J, et al. Anterior compartment mesh: a descriptive study of mesh anchoring failure. Ultrasound Obstet Gynecol. 2013;42:699–704. 64. Feiner B, Maher C. Vaginal mesh contraction: definition, clinical presentation, and management. Obstet Gynecol. 2010;115:325–30. 65. Svabik K, Martan A, Masata JL, El-Haddad R, Hubka P, Pavlikova M. Ultrasound appearances after mesh implantation- evidence of mesh contraction or folding? Int Urogynecol J. 2011;22(5):529–33. 66. Dietz H.  Mesh in prolapse surgery: an imaging perspective. Ultrasound Obstet Gynecol. 2012;40:495–503. 67. Svabik K, Martan A, Masata J, El-Haddad R, Hubka P. Comparison of vaginal mesh repair with sacrospinous vaginal colpopexy in the management of vaginal vault prolapse after hysterectomy in patients with levator ani avulsion: a randomized controlled trial. Ultrasound Obstet Gynecol. 2014;43:365–71. 68. Wong V, Shek KL, Goh J, Krause H, Martin A, Dietz HP. Cystocele recurrence after anterior colporrhaphy with and without mesh use. Eur J Obstet Gynecol Reprod Biol. 2014;172:131–5. 69. Gainey HL. Post-partum observation of pelvic tissue damage. Am J Obstet Gynecol. 1943;46:457–66. 70. Gainey HL. Postpartum observation of pelvic tissue damage: further studies. Am J Obstet Gynecol. 1955;70(4):800–7. 71. DeLancey J, et  al. Levator ani muscle structure and function in women with prolapse compared to women with normal support. Neurourol Urodyn. 2003;22(5):542–3. 72. Dietz HP, Wilson PD, Milsom I.  Maternal birth trauma: why should it matter to urogynaecologists? Curr Opin Obstet Gynecol. 2016;28(5):441–8. 73. Dietz H, Shek K. Can 2D translabial ultrasound be used to diagnose levator avulsion? Int Urogynecol J. 2008;19(S1):S163–4. 74. Dietz H, Moegni F, Shek K. Diagnosis of Levator avulsion injury: a comparison of three methods. Ultrasound Obstet Gynecol. 2012;40(6):693–8. 75. Dietz H. Quantification of major morphological abnormalities of the levator ani. Ultrasound Obstet Gynecol. 2007;29:329–34. 76. Dietz HP, Bernardo MJ, Kirby A, Shek Kl. Minimal criteria for the diagnosis of avulsion of the puborectalis muscle by tomographic ultrasound. Int Urogynecol J. 2011;22(6):699–704.

48  Transperineal Ultrasound: Practical Applications 77. Adisuroso T, Shek K, Dietz H. Tomographic imaging of the pelvic floor in nulliparous women: limits of normality. Ultrasound Obstet Gynecol. 2012;39(6):698–703. 78. Tan L, Shek KL, Kamisan Atan I, Guzman Rojas R, Dietz HP. The repeatability of sonographic measures of functional pelvic floor anatomy. Int Urogynecol J. 2015;26:1667–72. 79. Zhuang R, Song YF, Chen ZQ, et al. Levator avulsion using a tomographic ultrasound and magnetic resonance-based model. Am J Obstet Gynecol. 2011;205:232.e1–8. 80. Pilzek A, et  al. Recurrence after prolapse surgery: does partial avulsion matter? Ultrasound Obstet Gynecol. 2013;42(S1):37–8. 81. Dietz H, Abbu A, Shek K.  The Levator urethral gap measurement: a more objective means of determining levator avulsion? Ultrasound Obstet Gynecol. 2008;32:941–5. 82. Singh K, Jakab M, Reid WM, Berger LA, Hoyte L. Three-dimensional magnetic resonance imaging  assessment of levator ani morphologic features in different  grades of prolapse. Am J Obstet Gynecol. 2003;188(4): 910–5. 83. Dietz HP, Pattillo Garnham A, Guzman RR. Is the levator-­urethra gap helpful for the diagnosis of avulsion? Int Urogynecol J. 2016;27(6):909–13. 84. Dietz HP, Pattillo Garnham A, Guzmán Rojas R.  Diagnosis of levator avulsion: is it necessary to perform TUI on pelvic floor muscle contraction? Ultrasound Obstet Gynecol. 2017;49:252–6. 85. van Delft K, Thakar R, Sultan AH, Kluivers KB. Does the prevalence of levator ani muscle avulsion differ when assessed using tomographic ultrasound imaging at rest vs on maximum pelvic floor muscle contraction? Ultrasound Obstet Gynecol. 2015;46(1):99–103. 86. Shek K, Dietz H.  The effect of childbirth on hiatal dimensions: a prospective observational study. Obstet Gynecol. 2009;113:1272–8. 87. Dietz HP, Shek C.  Levator avulsion and grading of pelvic floor muscle strength. Int Urogynecol J. 2008;19(5):633–6. 88. Dietz HP, Steensma AB. The prevalence of major abnormalities of the levator ani in urogynaecological patients. BJOG Int J Obstet Gynaecol. 2006;113(2):225–30. 89. Dietz HP, Chantarasorn V, Shek KL.  Levator avulsion is a risk factor for cystocele recurrence. Ultrasound Obstet Gynecol. 2010;36:76–80. 90. Weemhoff M, Vergeldt TF, Notten K, Serroyen J, Kampschoer PH, Roumen FJ. Avulsion of puborectalis muscle and other risk factors for cystocele recurrence: a 2-year follow-up study. Int Urogynecol J. 2012;23(1):65–71. 91. Friedman T, Eslick G, Dietz HP.  Risk factors for prolapse recurrence-­systematic review and meta-analysis. Int Urogynecol J. 2018;29(1):13–21. 92. Abdool Z, Dietz HP, Lindeque G. Pelvic floor biometry: are there ethnic differences? Ultrasound Obstet Gynecol. 2017;50:242. 93. Shek KL, Krause H, Wong V, Goh J, Dietz HP.  Is pelvic organ support different between young nulliparous Africans and Caucasians? Ultrasound Obstet Gynecol. 2016 Jun;47(6):774–8. 94. Cheung RYK, Shek KL, Chan SSC, Chung TKH, Dietz HP.  Pelvic floor muscle biometry and pelvic organ mobility in Asian and Caucasian nulliparae. Ultrasound Obstet Gynecol. 2015;45(5):599–604. 95. Dietz H, Shek K, Clarke B. Biometry of the pubovisceral muscle and levator hiatus by three-dimensional pelvic floor ultrasound. Ultrasound Obstet Gynecol. 2005;25:580–5.

617 96. Kruger J, Heap SW, Murphy BA, Dietz HP. Pelvic floor function in nulliparous women using 3-dimensional ultrasound and magnetic resonance imaging. Obstet Gynecol. 2008;111:631–8. 97. Khunda A, Shek KL, Dietz HP.  Can ballooning of the levator hiatus be determined clinically? Am J Obstet Gynecol. 2012;206(3):e241–4. 98. Gerges B, Kamisan Atan I, Shek KL, Dietz HP.  How to determine ‘ballooning’ of the levator hiatus on clinical examination. Int Urogynecol J. 2013;24:1933–7. 99. Yang J, Yang S, Huang W. Biometry of the pubovisceral muscle and levator hiatus in nulliparous Chinese women. Ultrsound Obstet Gynecol. 2006;26:710–6. 100. Majida M, Braekken IH, Umek W, Bo K, Saltyte Benth J, Ellstrom Engh M. Interobserver repeatability of three- and four-­ dimensional transperineal ultrasound assessment of pelvic floor muscle anatomy and function. Ultrasound Obstet Gynecol. 2010;33(5):567–73. 101. Lien KC, Mooney B, DeLancey JO, Ashton-Miller JA. Levator ani muscle stretch induced by simulated vaginal birth. Obstetrics and gynecology. 2004;103(1):31–40. 102. Svabik K, Shek KL, Dietz HP. How much does the puborectalis muscle have to stretch in childbirth? Br J Obstet Gynaecol. 2009;116:1657–62. 103. Dietz H, De Leon J, Shek K. Ballooning of the levator hiatus. Ultrasound Obstet Gynecol. 2008;31:676–80. 104. Kruger J, Heap S, Murphy B, Dietz H. How best to measure the levator hiatus: evidence for the non-Euclidean nature of the ‘plane of minimal dimensions’. Ultrasound Obstet Gynecol. 2010;36:755–8. 105. Rodrigo N, Shek K, Wong V, Martin A, Dietz H. The Use of 3-Dimensional Ultrasound of the Pelvic Floor to Predict Recurrence Risk after Pelvic Reconstructive Surgery. Aust NZ J Obstet Gynaecol. 2014;54(3):206–11. 106. Friedman T, Eslick G, Dietz HP. Risk factors for prolapse recurrence- systematic review and meta- analysis. Int Urogynecol J. 2018;29(1):13–21. 107. Dietz HP, Stankiewicz M, Kamisan Atan I, Ferreira CWS, Socha M. Vaginal Laxity: What does this symptom mean? Int Urogynecol J. 2018;29(5):723–28. 108. Manzini L, Friedman T, Turel F, Dietz HP. Vaginal laxity: What measure of levator ani distensibility is most predictive? Ultrasound Obstet Gynecol. 2020;55(5):683–687. 109. Dietz HP. Female Pelvic Organ Prolapse- a review. Australian Family Physician. 2015;44(7):446–52. 110. Zhang X, Shek K, Dietz H. How large does a rectocele have to be to cause symptoms? Int Urogynecol J. 2015;26(9):1355–9. 111. Dietz HP. Pelvic floor ultrasound, chapter 4.5. In: Stoker J, Taylor SA, DeLancey JOL, editors. Imaging pelvic floor disorders. London: Springer Verlag; 2008. 112. Guzman Rojas R, Kamisan Atan I, Shek K, Dietz H. Defect-specific rectocele repair: medium-term anatomical, functional and subjective outcomes. Aust NZ J Obstet Gynaecol. 2015;55(5):487–92. 113. Dietz HP. Pelvic floor ultrasound. In: Fleischer AC et al (eds) Sonography in obstetrics and gynecology: principles and practice, 7th edn. Mc-Graw Hill, New York 2010. 114. Dietz HP. Pelvic floor ultrasound: a review. Am J Obstet Gynecol. 2010;202:321–34. 115. Dietz HP. Pelvic floor ultrasound. Australasian Society for Ultrasound in Medicine Bulletin. 2007;10:17–23.

Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage

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Jonia Alshiek, Ghazaleh Rostaminia, Lieschen H. Quiroz, and S. Abbas Shobeiri

Learning Objectives

• To describe three-dimensional (3D) endovaginal sonographic anatomy of the pelvic floor structures. • To understand the 3D endovaginal ultrasound (EVUS) technique with transducer position and image orientation and optimization. • To provide overview of angles and measurements in 3D endovaginal pelvic floor ultrasound.

49.1 Introduction 49.1.1 Imaging Modalities for Endovaginal Imaging The pelvic floor is a complex three-dimensional structure, with a variety of functional and anatomical areas. It consists of a musculotendinous sheet that spans the pelvic outlet and consists of paired levator ani muscle (LAM). It is broadly accepted that the LAM consists of subdivisions that have been characterized according to the origin and insertion points, consisting of the pubococcygeal/iliococcygeal, puborectal, and puboanal/puboperineal portions. Although magnetic resonance imaging (MRI) descriptions of the pubo-

J. Alshiek Department of Obstetrics and Gynecology, INOVA Health, Falls Church, VA, USA G. Rostaminia · L. H. Quiroz The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA S. A. Shobeiri (*) University of Virgina INOVA Campus, Department of Obstetrics and Gynecology, INOVA Women’s Hospital, Falls Church, VA, USA e-mail: [email protected]

visceral included the puboperinealis, pubovaginalis, and puboanalis (Fig. 49.1), more recent 3D EVUS literature uses the term pubovisceralis to group iliococcygeus and pubococcygeus together [1, 2]. Even though we use the term pubovisceralis in this book, the term has caused much confusion, and, where imaging allows, the terms pubococcygeus and iliococcygeus should be used. The term pubovisceralis was originally used because MRI could not delineate LAM subdivisions. Lateral to the pubovisceral muscle group is the puborectal division, which forms a sling around and behind the rectum, just cephalad to the external anal sphincter. Lastly, the iliococcygeus division forms a flat, horizontal shelf, spanning both pelvic side walls (Fig.  49.1) [3]. The complex relationship of the LAM subdivisions could be demonstrated to the learner by using one’s hands as a teaching model (Fig. 49.2). The validity of 3D EVUS to visualize LAM subdivisions has been established by meticulous anatomic studies [2]. These subdivisions were localized in cadaveric dissections (Figs. 49.3 and 49.4), then correlated with images seen in nulliparous women, based on origin and insertion points, and were shown to have excellent interobserver reliability.

49.1.2 3D EVUS Technique for Levator Ani Imaging All the endovaginal and endoanal images in this chapter are obtained from a Flex Focus scanner (BK Medical, Analogic, Peabody, MA, USA) (Fig.  49.5). EVUS has been found a valid method for visualization of the pelvic floor [4]. We recommend that the operator have a clear understanding of the technique, as well as familiarity with the controls of the machine. Most importantly, improper settings of the equipment can lead to artifact. Two 360° probes can be used interchangeably for endovaginal levator ani imaging. The 2052 transducer (Fig. 49.6),

© Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_49

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J. Alshiek et al. A B C D E

F G H

I

J

PV

PR

IC

PP STP PA

1a 1b 2a 2b 2c 2d 3a 3b 3c 3d

Fig. 49.1  The relative position of levator ani subdivisions during ultrasound imaging. Levels 1–3 are identified below the figure. The A–J markings on top of the figure correspond to the ultrasound images shown in Fig.  49.5.5. Iliococcygeus (IC), puboanalis (PA), puboperinealis (PP), superficial transverse perinei (STP) (Illustration: John Yanson; From Shobeiri et al. [2], with permission)

which the probe originally introduced for colorectal imaging, has a built-in 3D automatic motorized system (proximal-­ distal actuation mechanism is enclosed within the shield of the probe). This equipment allows for the acquisition of 300 images in 60 s for a distance of 60 mm. The 8838 probe is a 60  mm 360° rotational transducer and obtains an image every 0.55° for a total of 720 images (Fig. 49.7). The images are acquired automatically with the touch of the 3D button on the equipment console. The data from the closely spaced 2D images are combined as a 3D volume displayed as a data volume that can then be stored and analyzed separately. No special patient preparation is required and no vaginal or rectal contrast is necessary. The patient is asked to keep a comfortable amount of urine in the bladder. The patient is placed on the dorsal lithotomy position, and the probe is inserted in a neutral position, with care not to press on the upper or lower vaginal areas so as not to distort anatomy.

Fig. 49.2 The relative position of levator ani subdivisions using the hand model. Although one’s hand works as a unit, each finger has a distinct function. Just as with the hand, levator ani muscle (LAM) subdivisions have distinct functions. Using this analogy, losing one’s hand is akin to LAM avulsion where muscles are torn from the pubic bone attachment; losing one’s finger(s) is akin to LAM deficiency and dysfunction in individual LAM subdivisions. The thumbs form the anorectum (AR), iliococcygeus (IC), perineal body (PB), pubic symphysis (PS), puboanalis (PA), puboperinealis (PP), vagina (V). Anterior (A), left (L), posterior (P), right (R). (© Shobeiri)

The probe should create a horizontal line with the body’s axis. When placing the ultrasound gel in the probe cover, we recommend for air bubbles to be gently squeezed out of the probe cover, so as to minimize the potential for artifact. Once 3D endovaginal imaging is selected on the console, the rotating crystal will begin to rotate, signaling that the probe is ready for insertion. Based on our anatomic studies, we recommend placing the probe 6 cm inside the vagina, just 2 cm above the level of the urethrovesical junction. If using the 2052 probe, the two buttons that move the crystal cephalad and caudad should be facing the 12 o’clock position. Once the acquisition is started, it is important that the operator minimize movement by stabilizing the probe during the full length of the scan. This will help optimize image quality in obtaining the 3D volume (Fig. 49.8). We have characterized three levels for assessment of the axial plane [2] (Fig.  49.1). Notice that these levels are different from

49  Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage

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Fig. 49.3  Subgrouping of the pubococcygeus/iliococcygeus (PC), puborectalis (PR), and the puboanalis/puboperinealis (PA) muscle groups. The lines of actions of these muscle groups and their relative contributions to the levator plate are shown. Anococcygeal ligaments (ACL) and arcus tendineus fascia pelvis (ATFP) are shown. The blue line is the puboperinealis; red, puboanalis; green, puborectalis; purple, pubococcygeus/iliococcygeus Pubic symphysis (PS). (© Shobeiri) Fig. 49.5  BK Flex Focus ultrasound machine with a 2052 probe (BK Medical, Analogic, Peabody, MA, USA)

(STP), puboperinealis, and puboanalis. The STP serves as the reference point. • Level 2: Contains the attachment of the pubovaginalis, puboperinealis, puboanalis, puborectalis, and iliococcygeus to the pubic bone. • Level 3: Contains the subdivisions cephalad to the inferior pubic ramus, namely, the pubococcygeus and iliococcygeus, which wing out toward the ischial spine.

Fig. 49.4  Gross cadaveric dissection. A needle is seen inserted into the puboperinealis. Arcus tendineus fascia pelvis (ATFP), iliococcygeus (IC), perineum (P), pubic bone insertion (PB), puboanalis (PA), puboperinealis (PP), superficial transverse perinei (STP) (From Shobeiri et al. [2], with permission)

DeLancey’s three levels of pelvic floor support [5] and are used purely as reference points for looking at the levator ani subdivisions in the axial plane. • Level 1: Contains all the muscles that insert into the perineal body, namely, the superficial transverse perinei

Functionally, and based on the levator ani volume measurements, we divide the muscles into (1) puboperinealis + puboanalis [PA], (2) puborectalis [PR], and (3) pubococcygeus  +  iliococcygeus [PC] (Fig.  49.3). By 3D EVUS reconstruction of nulliparous subjects, PA, PR, and PC groups had the volume of 4.4  cm3 (range 2.1–6.7  cm3), 4.2  cm3 (range 1.9–6.5  cm3), and 4.5 (range 2.2–6.8  cm3), respectively. Although they have a wide range in volumes, the proportions remain constant within the individual [6]. When analyzing a 3D volume caudad to cephalad, the first structure to visualize as a landmark is the STP muscle (Fig.  49.9). Visualization of this structure will consistently point to the most caudad structure seen by the probe in the vaginal canal. In normal nulliparous individuals, the external anal sphincter may be visualized just below the STP. If using the 2052 probe, there are two buttons located on the dorsal portion of the probe handle used to move the rotating crystal caudal or cephalad. By pressing the cephalad button, the rotating

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Fig. 49.7  BK 8838 transducer (BK Medical, Analogic, Peabody, MA, USA)

Fig. 49.6  BK 2052 transducer (BK Medical, Analogic, Peabody, MA, USA)

crystal can be slowly moved cephalad, and the p­ erineal body and puboperinealis muscle come into view (Fig. 49.10). The puboperinealis is hard to find consistently for the untrained eyes, because it has perhaps less than 30 muscle fibers and lies very close to the vaginal epithelium. At the same level but more laterally are the fibers of the puboanalis that travel at a 45° to surround the anal canal and insert into longitudinal fibers of the anus at the level of the external anal sphincter (Fig.  49.11). Continuing to move the crystal cephalad will show the puborectalis forming a sling around the rectum, and it can be followed to its insertion into the inferior margin of the pubic symphysis and the perineal membrane. Moving further cephalad will show the medial relationship of the iliococcygeus muscle in its medial relationship to the puborectalis (Fig. 49.12). The reliability of visualization of levator ani subdivisions has been reported in nulliparous patients. The levator ani

Fig. 49.8  An endovaginal 3D volume at the level of puborectalis muscle hiatus in axial plane (© Shobeiri)

subdivisions in these scans were examined at levels 1, 2, and 3 (Fig.  49.1). The visibility was scored by two blinded observers. Interrater reliability was calculated by taking the number of agreements and dividing by the number of obser-

49  Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage

Fig. 49.9  The most caudad muscle seen by 3D endovaginal ultrasound imaging is the superficial transverse perinei muscle, which is highlighted. Anus (A), external anal sphincter (EAS), pubic symphysis (PS), transducer (T) (© Shobeiri)

a

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Fig. 49.11  The puboanalis (PA) lies just lateral to the puboperinealis (PP), and they are part of the same functional groups. Anus (A), pubic symphysis (PS), transducer (T) (© Shobeiri)

b

Fig. 49.10 (a) The scant fibers of the puboperinealis muscles (PP) are highlighted. (b) The perineal body (PB) is highlighted in the same axial view as (a). Anus (A), perineal body (PB), puboperinealis (PP), pubic symphysis (PS), transducer (T) (© Shobeiri)

vations in the total number of subjects. There was 98%, 96%, and 92% agreement for level 1, 2, and 3 muscles, respectively. Cohen’s kappa index/standard error were calculated for individual muscles as follows: STP and puborectalis were seen by both raters 100%, puboperinealis 65%, pubovaginalis, and puboanalis 65% (95% confidence interval 0.1–1), and iliococcygeus 90% (95% confidence interval 0.6–1).

In addition to visualization of the muscle subdivisions, the interobserver and the interdisciplinary repeatability of (1) levator hiatus length; (2) levator hiatus width; (3) levator hiatus area; (4) LAM attachment to the pubic rami, on both sides; (5) anorectal angle (ARA); and (6) urethral thickness measurements using 3D EVUS have been established [7]. A team of six investigators in three different specialties (urogynecology (UGN), radiology (RAD), colorectal surgery

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(CRS)) was formed. Each discipline included two investigators: UGN #1 and UGN #2; RAD #1 and RAD #2; and CRS #1 and CRS #2. Prior to study initiation, a dedicated training session was completed, and preliminary trial measurements

were performed. For the training session, an expert 3D reader demonstrated to each of the readers the technique to be used for measurements, including bony and soft tissue landmarks. Readers discussed and refined the measurement technique for each parameter until all readers were in agreement regarding measurement methodology. In order to minimize the effect of imaging variations on the final measurements, a standardized protocol for review of the study data sets was strictly defined and jointly approved by all investigators. Each ultrasound volume was displayed in a symmetrical orientation in the coronal, sagittal, and transverse planes and assessed in standardized sequences. The overall interobserver repeatability for levator hiatus dimensions was good to excellent (ICC, 0.655–0.889), for urethral thickness was good (ICC, 0.624), and for ARA was moderate (ICC, 0472) (Table 49.1). The interdisciplinary repeatability for levator hiatus indices was good to excellent (ICC, 0.639–0.915), for urethral thickness was moderate to good (ICC, 0.565–0.671), and for ARA was fair to moderate (ICC, 0.204–0.434) (Table 49.2) [7].

49.2 Clinical Applications

Fig. 49.12  The puborectalis (PR) is shown at its cephalad insertion point to the pubic symphysis (PS). Note that PR has a wide insertion area that includes the PS, and the perineal membrane, which is more caudad. The iliococcygeus muscle (IC) fibers are seen medial to the puborectalis fibers. Anus (A), transducer (T) (© Shobeiri)

Pelvic floor disorders are common, costly, and distressing conditions for women, resulting in greater than 300,000 operations per year, and leading to considerable suffering from conditions not readily cured by surgery [8]. Fifty-five percent of women with pelvic organ prolapse (POP) have

Table 49.1  Overall means and standard deviations (SD) of various measurements of individual readers Observer UGN #1 UGN #2 RAD #1 RAD #2 CRS #1 CRS #2

LH length (mm) 50.42 (SD: 4.18) 48.62 (SD: 4.87) 48.71 (SD: 4.84) 47.55 (SD: 5.62) 47.95 (SD: 4.20) 47.20 (SD: 4.05)

LH width (mm) 35.03 (SD: 3.50) 34.21 (SD: 3.30) 33.76 (SD: 3.50) 33.54 (SD: 3.32) 34.52 (SD: 3.38) 34.06 (SD: 2.96)

LH area (cm2) 10.48 (SD: 1.51) 10.60 (SD: 1.31) 10.72 (SD: 1.70) 11.76 (SD: 1.35) 10.82 (SD: 1.60) 10.14 (SD: 1.60)

Urethral thickness (mm) 12.82 (SD: 1.6) 13.06 (SD: 1.41) 12.86 (SD: 1.73) 12.61 (SD: 1.32) 12.23 (SD: 1.77) 12.30 (SD: 1.44)

ARA (degrees) 133.1 (SD: 12.3) 144.2 (SD: 7.03) 143.04 (SD: 12.5) 141.1 (SD: 7.99) 143.8 (SD: 9.97) 136.1 (SD: 5.94)

From Santoro et al. [6], with permission ARA anorectal angle, CRS colorectal surgeon, LH levator hiatus, RAD radiologist, UGN urogynecologist Table 49.2  Interobserver, intra- and interdisciplinary repeatability of three-dimensional endovaginal ultrasound parameters Repeatability Overall Intradisciplinary  UGN #1 vs. UGN #2  RAD #1 vs. RAD #2  CRS #1 vs. CRS #2 Interdisciplinary  RADs vs. CRSs  RADs vs. UGNs  UGNs vs. CRSs

LH length LH width LH area Urethral thickness ARA ICC 95% CI ICC 95% CI ICC 95% CI ICC 95% CI ICC 95% CI 0.655 0.509–0.794 0.889 0.822–0.940 0.810 0.707–0.894 0.624 0.472–0.772 0.331  0.179–0.528 0.643 0.359–0.819 0.889 0.773–0.948 0.717 0.473–0.860 0.981 0.958–0.991 0.883 0.761–0.945 0.910 0.815–0.958

0.857 0.713–0.932 0.660 0.385–0.829 0.893 0.781–0.950 0.601 0.298–0.795 0.887 0.770–0.947 0.735 0.501–0.869

0.035 −0.339–0.402 0.569  0.252–0.777 0.216 −0.167–0.544

0.677 0.514–0.815 0.915 0.855–0.956 0.639 0.467–0.790 0.897 0.826–0.946 0.694 0.536–0.826 0.874 0.790–0.934

0.831 0.724–0.909 0.651 0.482–0.798 0.851 0.755–0.921 0.565 0.380–0.739 0.783 0.656–0.882 0.671 0.506–0.811

0.434  0.241–0.639 0.327  0.139–0.549 0.204  0.032–0.431

From Santoro et al. [6], with permission ARA anorectal angle, CI confidence interval, CRS colorectal surgeon, ICC interclass correlation coefficient, LH levator hiatus, RAD radiologist, UGN urogynecologist

49  Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage

visible major LAM damage compared to 15% of women with normal support, making it the strongest known factor to be associated with both vaginal birth and POP [9]. The ability to diagnose injury to the LAM relies on advancements in imaging. Levator ani avulsion as imaged by transperineal ultrasound appears to double the risk of any significant anterior and central compartment prolapse [10].

49.2.1 Prevalence of Pelvic Floor Injury Following Vaginal Delivery During parturition, the levator ani muscle (LAM) stretches beyond its limits in some women [11] in order to allow passage of a term infant [12]. Researchers have calculated maximum stretch ratios of 2.28–3.26 of the levator muscle. However, striated muscle in nonpregnant animals allows a maximum stretch ratio of only 1.5 [13]. Interestingly, as all women sustain overstretching of the pelvic floor, only some  will have levator trauma. Alperin et  al. studied ­pregnancy-­induced adaptations in the pelvic floor muscles of rat models [14]. They demonstrated that the changes in pelvic floor muscles occur by adding sarcomeres to increase muscle fiber length. The largest change in muscle fiber length occurred in the muscle known to have the shortest fibers, namely, the coccygeus muscle of the levator ani. Furthermore, they found a substantial increase in extracellular matrix. This increase in extracellular matrix is thought to provide additional support to the coccygeus muscle [14]. Studies have shown that LAM injury occurs in 13–36% of women who deliver vaginally [15]. There are various definitions of levator ani injury, according to mode of assessment and imaging modality. Furthermore, timing of ultrasound assessment following delivery can impact on the incidence of LAM injury. Most authors have used avulsion of the muscles as the end point of the study. However, (3D) EVUS has found that up to 35% of women may have hematoma formation shortly after their first vaginal delivery [16]. Assessment of the levator muscles is essential for a complete understanding of pelvic floor anatomy abnormalities, as well as of pelvic floor dysfunction. There have been many studies that have investigated predictive modeling of vaginal birth-induced LAM injury. In our study of the predictive role of obstetric variables for obstetric outcomes and birth-related levator ani muscle (LAM) trauma, we evaluated minimal levator hiatus circumference (MLHC) and the ratio of fetal head circumference to MLHC = head-induced stretch ratio (HISR) as an indicator of the discrepancy between passage and passing canal. To derive the true impact of baby’s mass on the levator ani musculature, we devised the levator ani stretch ratio (LASR), which was calculated by multiplying the HISR and the baby’s weight. Mean HISR and LASR values were ­statistically different across all binary outcome categories, with one exception for HISR and levator ani injury. The odds

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ratios for LASR indicated positive and statistically significant associations with all obstetric outcomes examined. The probability of the LASR correctly classifying those with the adverse obstetric outcome, as estimated by the area under the curve, ranged from 0.64 to 0.80 with the strongest discriminatory ability observed for severe LAM trauma. We concluded that fetal head circumference/mother MLHC ratio (HISR) is associated with longer length of second stage of labor, assisted delivery, and increased severity of perineal trauma. Similar associations were observed for LASR, but in addition, LASR had good discriminatory ability to identify severe LAM trauma (Table 49.7.) [17].

49.2.2 Levator Ani Injury and Hematomas There are various definitions of levator ani injury, according to mode of assessment and imaging modality. Most authors have used avulsion of the muscles as the end point of the study. However, more recent publications using 3D EVUS have found that up to 50% of women may have hematoma formation after their first delivery (Fig. 49.13). Assessment

Fig. 49.13  Schematic representation of the 3D endovaginal ultrasound image in the axial plane of the minimal hiatal dimensions. The landmarks are visible: pubic bone (PB), urethra (U), vagina (V), anal canal (A), levator ani muscle (L). The asterisk represents a right levator ani muscle hematoma in the immediate postpartum (© Shobeiri)

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of the levator muscles is essential for a complete understanding of pelvic floor anatomy abnormalities, as well as of pelvic floor dysfunction. It has been accepted that obstetric trauma is the main etiological factor in the development of LAM avulsion. As stated, trauma can occur by stretching of the inner part of the LAM (namely, the pubococcygeus part of the muscle), and by disconnection of its insertion from the inferior pubic ramus and the pelvic side wall [11]. A recent review found a 13–36% incidence of LAM avulsion following the first vaginal delivery [18]. Overall, the highest incidence (39.5%) was found in a prospective study where women were seen in the early postpartum period, using transperineal ultrasound. The authors attributed this higher incidence to the difficulty in differentiating fluid collections from LAM avulsion [19]. In our opinion, they used transperineal ultrasound, which is less discriminatory for the different parts of the LAM. Another more recent study evaluated the LAM shortly after childbirth using EVUS in a prospective study [16]. A total of 114 women underwent EVUS early postpartum. In 27 women (23.7%), the investigators found well-delineated, hypoechoic areas consistent with hematomas (Fig. 49.14). Importantly,

there was 100% agreement between the investigators for the presence of a hematoma. Hematomas away from the LAM attachment zone to the pubic bone resolved. Hematomas that were found at the area of attachment of the pubococcygeus part of the LAM to the pubic bone manifested as pubococcygeus avulsions 3  months postpartum. Hematomas were significantly associated with episiotomy, instrumental delivery, and increased hiatal measurements. Palpation of LAM avulsion, according to a previously described protocol [20], was unreliable early postpartum, as only seven avulsions were diagnosed using the finger as an instrument. In an additional, smaller, group of women, the investigators did not find hematomas but avulsion of the pubococcygeus part of the LAM in the early postpartum period. The overall incidence of LAM avulsion was 12.0% 3  months postpartum. The authors therefore concluded that hematomas in the pubococcygeus part of LAM, where it is supposed to be attached to the pubic bone, always result in avulsion diagnosed 3  months postpartum. On the other hand, one third of avulsions confirmed at 3 months postpartum are not preceded by a hematoma at the site of LAM attachment to the pubic bone but could be seen as an avul-

Fig. 49.14  Schematic representation of the 3D endovaginal ultrasound image in the axial plane of the minimal hiatal dimensions. The landmarks are visible: pubic bone (PB), urethra (U), vagina (V), anal canal (A), levator ani muscle (L). Part 1: the asterisk represents a bilateral hematoma in the muscles. Please note that the attachments to the pubic

bone remain intact within a few hours following vaginal delivery. Part 2: the asterisk represents a bilateral postpartum defect where the levator ani muscle hematomas used to be, in the same patient, 3 months following delivery (From van Delft [16])

49  Three-Dimensional and Dynamic Endovaginal Ultrasonography for Pelvic Organ Prolapse and Levator Ani Damage

sion in the early postpartum period [16]. The authors speculated that a hematoma is formed when muscle is torn away from the tendinous attachment. However, no hematoma is formed when the tendon or pubovisceral enthesis is avulsed from the pubic bone, due to the avascular nature of the trauma [21]. The resolution of hematomas at or away from the attachment zone of LAM to the pubic bone directs to the body’s ability to heal itself [22].

49.2.3 Levator Ani Avulsion Levator ani avulsion injury was originally defined as “a discontinuity between the inferior pubic rami and the puborectalis muscle” by perineal pelvic floor ultrasound. A complete defect was diagnosed if the reference slide and slices 2.5 mm and 5 mm cranial to it showed a sonographic defect [10]. The authors also described a scoring system where defects were scored according to the number of slices in which a discontinuity of the muscle with the pelvic side wall was documented, with a minimum score of 0 and a maximum score of 16 in a patient with complete bilateral avulsion [23]. Levator avulsion diagnosed by transperineal ultrasound appears to double the risk of significant anterior and central compartment prolapse, with less effect on posterior compartment prolapse [10]. Using MRI, DeLancey et  al. described levator ani defects and scored left and right muscle defects separately. A score of 0 was assigned if no damage was visible, 1 if less than half of the muscle was missing, 2 if more than half, and 3 if the complete muscle bulk was lost. The total score was the sum of both sides, ranging from 0 to 6 and categorized as follows: 0, normal or no defect; 1–3, minor defect; and 4–6, major defect [9]. Miller et al. described a muscle tear if fibers were absent in at least one 4 mm section or two or more adjacent 2 mm sections in both the axial and coronal planes, rated for both sides separately. They also distinguished between subtle (equivocal muscle fiber loss), low-­grade (muscle fiber loss of 50%) [24]. Obstetric levator avulsion is an important risk factor for prolapse. In a study of vaginally parous women with or without levator avulsion, 5–15 years after delivery, using perineal three-dimensional pelvic floor ultrasound, levator avulsion was identified in 15% (66/453) patients. A history of forcepsassisted delivery was strongly associated with levator avulsion (45% vs. 8%; p  50% muscle loss; 3, total absence of the muscle) on each side based on thickness and detachment from the pubic bone (Table 49.3). Each muscle pair score ranged from 0, indicating no defects, to maximum score of 6, indicating total muscle absence. For the entire LAM group, a cumulative LAD score that ranged between 0 and 18 was possible. Scores were categorized as 0–6, mild (Fig. 49.15); 7–12, moderate (Fig. 49.16); and >13, severe deficiency (Fig. 49.17) [30]. All the correlation coefficients at the individual sites as well as

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Table 49.3  Endovaginal ultrasound validated scoring system for levator ani muscle deficiency (LAD) Score (L) Puboanalis (PA + PP) (R) Puboanalis (PA + PP) (L) Puborectalis (R) Puborectalis (L) Pubovisceralis (IC + PC) (R) Pubovisceralis (IC + PC)

0 (no muscle damage)

1 (mild abnormality)

2 (moderate abnormality)

3 (complete muscle loss)

Subtotal 0–3

Total 0–18

IC iliococcygeus, L left, PA puboanalis, PC pubococcygeus, PP puboperinealis, R right

Fig. 49.15  3D ultrasound volume of a normal nulliparous woman with levator ani deficiency score of 0. Anus (A), puboanalis (PA), puborectalis (PR), pubic symphysis (PS), pubococcygeus (PV), urethra (U), vagina (V) (From Rostaminia et al. [30], with permission)

Fig. 49.17  The axial view of pelvic floor muscles with severe levator ani muscle deficiency. Asterisk denotes a missing muscle, and numbers are muscle scores. Anus (A), puboanalis (PA), puborectalis (PR), pubic symphysis (PS), pubovisceralis (PV), vagina (V) (From Rostaminia et al. [30] with permission) Table 49.4  Distribution of stages of prolapse and associated total levator ani deficiency (LAD) scores Stage 0 Stage 1 Stage 2 Stage 3 Stage 4

n (%) 50 (22.7) 57 (25.9) 60 (27.3) 43 (19.6) 10 (4.6)

LAD score (median, range) 6 (0, 18) 8 (0, 18) 10 (0, 18) 14 (6, 18) 13 (9, 18)

p Valuea 8 items

NR

NR

NR

Yes

Yes

NR

1999

12

0–48

Yes 44 to >12 items

Yes

Yes

Yes

Yes

Yes

Yes

2000

11

0–39

No

NR

NR

NR

Yes

Yes

NR

2005

6

NR

Yes 30 to >6 items

Yes

Yes

Yes

Yes

Yes

Yes

2007

16

0–73

Yes 80 to >16 items

Yes

Yes

Yes

Yes

Yes

NR

2007

8

0–31

No

Yes

Yes

NR

NR

Yes

NR

2009

3

0–100 No

Yes

Yes

NR

Yes

Yes

Yes

61  Patient-Reported Outcome Assessment in Constipation and Obstructed Defecation

PROM for constipation. It implies passive overflow fecal incontinence due to rectal fecal impaction. In the original study, this item was separately analyzed and finally kept with the statement of “The item of ‘oozing liquid stool’ was chosen by only 16% of the sample. Because of this result, the alpha coefficient was recomputed with the item deleted. The result was a lower alpha (0.67). Further analysis of individual responses revealed that subjects with the highest scores were the ones who chose the item. Therefore, it was left in the scale” [5]. The CAS was subsequently modified and validated for use in women during pregnancy, being revised to a 5-point rating scale (score range: 0–32) instead of an original 3-point scale [17]. At present, the CAS is rarely used, although its Italian version was validated in 2012 [18]. Constipation Scoring System (CSS) (Table  61.3) is an eight-item self-report scale designed to diagnose constipation and evaluate its symptomatic severity. Each item is rated with 5-point Likert scale from 0 to 4 except for the item of “type of assistance,” which is rated with 3-point scale from 0 to 2, and the total CSS score ranges between 0 and 30 [6]. Table 61.2  Constipation Assessment Scale (CAS) [5] Item Abdominal distention or bloating Change in the amount of gas passed rectally Less frequent bowel movements Oozing liquid stool Rectal fullness or pressure Rectal pain with bowel movement Small volume of stool Urge but inability to pass stool

0 No problem No problem No problem No problem No problem No problem No problem No problem

1 Some problem Some problem Some problem Some problem Some problem Some problem Some problem Some problem

2 Severe problem Severe problem Severe problem Severe problem Severe problem Severe problem Severe problem Severe problem

Score range: 0–16

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Although it is sometimes referred as Cleveland Clinic Constipation Score or Wexner Constipation Score, it should be called CSS to avoid the confusion with Cleveland Clinic Florida Fecal Incontinence Score (CCFIS) that is also called Wexner score [19]. The original 12 items were generated through patient interview and were reduced to the final eight items based on some statistical analysis although its details were not described in the original CSS paper [6]. The CSS was evaluated in 68 patients with colonic inertia and 164 patients with pelvic outlet obstruction as well as in 50 nonconstipated patients. Their diagnosis was confirmed with colonic transit study, anorectal physiology testing, defecography, and anal electromyography. Its discriminant validity was confirmed by differentiating between constipated and nonconstipated patients, and the physiological tests were used to establish convergent validity. However, the internal consistency, test– retest reliability, and responsiveness were not reported in the CSS paper [6]. It is reported that a score of more than 15 is the definition of “constipation” in the CSS study because 97% of the entire group of constipated patients had a score greater than 15. However, this must be interpreted with caution. This study included 68 patients with “colonic inertia,” which was defined as “the presence of at least 80 percent of transit markers scattered diffusely throughout the colon on the fifth day after ingestion,” citing the study by Hinton et al. [20]. In the study by Hinton et al. [20], however, nonconstipated subjects “passed 80% of the markers within five days.” In other words, constipation was defined as “the presence of more than 20 percent of transit markers on the fifth day after ingestion” according to the Hinton’s study. Therefore, the 68 patients in the CSS study had severe slow transit constipation, namely “colonic inertia,” and a CSS score of more than 15 is NOT the definition of “constipation” but could imply “severe constipation.” One of the characteristics unique to CSS is the item of “History: duration of constipation,” which is not included in any other PROM for constipation except for PAC-SYM. Long

Table 61.3  Constipation Scoring System (CSS) [6] Item Frequency of bowel movements Difficulty: painful evacuation effort Completeness: feeling incomplete evacuation Pain: abdominal pain Time: minutes in lavatory per attempt Assistance: type of assistance Failure: unsuccessful attempts for evacuation per 24 h History: duration of constipation (year)

0 1–2 times per 1–2 days Never Never Never Less than 5 Without assistance Never 0

Score range: 0–30 The cutoff score for the diagnosis of “severe constipation” is more than 15

1 2 times per week Rarely Rarely Rarely 5–10 Stimulant laxatives 1–3 1–5

2 Once per week

3 Less than once per week Sometimes Usually Sometimes Usually Sometimes Usually 10–20 20–30 Digital assistance – or enema 3–6 6–9 5–10 10–20

4 Less than once per month Always Always Always More than 30 – More than 9 More than 20

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history of constipation does not necessarily mean severe constipation, because some patients with no symptoms of constipation due to appropriate medical therapy can have a long history of constipation. Another problem of including “the duration of constipation” is that the CSS score does not become zero even if the constipation is completely cured with some appropriate therapy. For the assessment of treatment, therefore, modified CSS (mCSS) can be proposed, in which one item of “the duration of constipation” is deleted from the original CSS with the mCSS score ranging between 0 and 26. In spite of these problems and insufficient evidence of reliability and validity, CSS has been popular and is still widely used at present in clinical studies, particularly among colorectal surgeons, probably because it is easy to administer, and its questions seem appropriate to evaluate symptoms of constipation. Patient Assessment of Constipation Symptom (PAC-­ SYM) questionnaire (Table  61.4) is a self-report measure

T. Mimura

consisting of 12 items in three domains that include “abdominal symptoms” (four items), “rectal symptoms” (three items), and “stool symptoms” (five items) [7]. Each symptom is rated with a 5-point Likert scale from 0 (=absence of symptoms) to 4 (=very severe) with each domain and the total score being calculated as an average score raging between 0 and 4. A formal questionnaire table exactly presenting the 12 items of PAC-SYM is not available in the original paper [7], but it can be obtained in another literature by Neri et al. [21]. The original 44 items were generated through literature review and patient interview, and they were reduced to the final 12 items based on the evaluation of information redundancy, floor and ceiling effects, and internal consistency. Because a high correlation was observed between the frequency items and the severity items, and given the clinical meaningfulness of severity ratings for symptoms, the frequency items were deleted. Moreover, the exploratory factor analysis and multitrait analysis identified original five Table 61.4 Patient Assessment of Constipation–Symptom (PAC-­ domains, including “abdominal symptoms,” “rectal sympSYM) [7] toms,” “stool symptoms,” “systemic symptoms,” and “urgency symptoms.” Because the two domains of “systemic Item 0 1 2 3 4 Abdominal symptom symptoms” and “urgency symptoms” were considered cliniDiscomfort in your Absent Mild Moderate Severe Very cally separate from the constipation symptom domain, they abdomen severe were deleted, resulting in the final three domains with 12 Pain in your abdomen Absent Mild Moderate Severe Very items. severe The PAC-SYM was evaluated in 216 patients with chronic Bloating in your Absent Mild Moderate Severe Very idiopathic constipation. It is one of the most formally and abdomen severe Stomach cramps Absent Mild Moderate Severe Very meticulously developed and validated PROMs, in which all severe of the internal consistency (Cronbach’s alpha = 0.89), test– Rectal symptoms retest reliability (intraclass correlation coefficient  =  0.75), Painful bowel moveAbsent Mild Moderate Severe Very content validity, convergent validity, discriminant validity, ments severe and responsiveness were confirmed. Its convergent validity Rectal burning during or Absent Mild Moderate Severe Very after a bowel movement severe was demonstrated with the comparison between PAC-SYM Absent Mild Moderate Severe Very Rectal bleeding or scores and the investigator and subject global rating of consevere tearing during or after stipation severity on a 7-point scale (absent to very severe). bowel movement Its discriminant validity was confirmed by comparing Stool symptoms responders with nonresponders to treatment (mean total Absent Mild Moderate Severe Very Incomplete bowel severe movement like you did scores, 0.63 for responders vs. 1.44 for nonresponders, not finish P = 0.0001). Absent Mild Moderate Severe Very Bowel movement that The reliability, validity, and responsiveness of PAC-SYM were too hard severe were also confirmed for opioid-induced constipation in 680 Bowel movement that Absent Mild Moderate Severe Very patients with chronic lower back pain [22]. Furthermore, the were too small severe Absent Mild Moderate Severe Very Straining or squeezing minimal important difference of “−0.6” for clinical practice severe to try to pass bowel and “−0.75” for clinical trials was proposed for the threshold movements of reduction in total PAC-SYM score to be used in defining a Feeling like you had to Absent Mild Moderate Severe Very meaningful clinical response [23]. severe pass a bowel movement, Modified PAC-SYM (M:PAC-SYM) was proposed, but you could not For total score, the scores of nonmissing items were summed and claiming that only a minority of patients reported any rectal divided by the total number of nonmissing items (total score range: tearing (38%) [21]. Deletion of such item (rectal bleeding or 0–4) tearing during or after bowel movement) led to a 11-item For subscales, the scores of nonmissing items within the subscale were summed and divided by the total number of nonmissing items for that version, and the remaining two items in the original “rectal” domain in PAC-SYM were merged into “stool” domain in subscale (subscale score range: 0–4)

61  Patient-Reported Outcome Assessment in Constipation and Obstructed Defecation

745

Table 61.5  Knowles–Eccersley–Scott Symptom (KESS) questionnaire [8] Item 1.   Duration of constipation

0 0–18 months

2.  Laxative use

None

3.  Frequency of bowel movements (using current therapy) 4.  Unsuccessful evacuatory attempts 5.   Feeling incomplete evacuation 6.   Abdominal pain 7.  Bloating

1–2 times/1–2 days 2 or less times per week Never/rarely Occasionally

Less than once per week Usually

Never Never Never

Occasionally Occasionally Visible to others

8.  Enema/digitation

None

9.  Time taken (minutes in 20 (or all life)

Regular, long duration

–

Always Always Severe with vomiting Manual evacuation always –

Rarely Rarely Perceived by patient only Enema/suppositories occasionally 5–10

Enema/suppositories regular 10–30

Regular, long duration, ineffective Less than once per 2 weeks Always = manual evacuation Usually Usually Severe causing satiety or nausea Manual evacuation occasionally > 30

Rarely

Occasionally

Usually

Always

Occasionally hard

Always hard

Always hard, usually pellet-like

–

– –

Score range: 0–39 Rarely ≤25% of time, occasionally =25–50%, usually ≥50% of the time The cutoff score for the diagnosis of constipation is 10

M:PAC-SYM because they were moderately correlated with “stool” domain. Consequently, the M:PAC-SYM consists of only two domains including “abdominal” (four items) and “stool” (seven items). The authors concluded that “the rectal domain may not represent a relevant cluster of symptoms for patients with chronic constipation” and that M-PAC-SYM “might better represent symptom severity of most patients seeking care in gastroenterology referral centers” [21]. Another and more major problem of PAC-SYM is the lack of item regarding bowel movement frequency and its reason. In the process of the item reduction, overlap between the PAC-SYM and Patient Assessment of Constipation Quality of Life (PAC-QOL) questionnaire [13] was examined. The instruments were finalized on the basis of consideration of the joint results, and two items from the original PAC-SYM including “decreased appetite” and “less frequent bowel movements than desired” were identified as more appropriate to measure the quality of life and were included in the final version of the PAC-QOL. Therefore, it is recommended to utilize “full PAC,” which means the usage of both PAC-SYM and PAC-QOL at the same time, for the evaluation of constipation [7, 24]. It is also recommended that “when used without the PAC-QOL, a frequency item should be asked in addition to the PAC-SYM,” which effectively means that the PAC-SYM alone is not enough to evaluate the symptomatic severity of constipation. PAC-SYM has been popular and is widely used at present in clinical studies, particularly among gastroenterologists. It is probably because it possesses good reliability, validity,

and responsiveness with the minimal important difference established. PAC-SYM is also appropriate to use with PAC-­ QOL as the “full PAC,” while it is not suitable to use on its own to evaluate the symptomatic severity due to its development process. Knowles–Eccersley–Scott Symptom (KESS) questionnaire (Table  61.5) is an 11-item interviewer-led questionnaire to assist in diagnosing constipation and in discriminating among pathophysiologic subgroups of slow transit constipation and rectal evacuatory disorders [8]. Each symptom is rated with a 4- or 5-point Likert scale either from 0 to 3 or from 0 to 4, and the total KESS score ranges between 0 and 39. The 11 items were developed by incorporating items from CSS [6] and Rome II criteria. The formal item generation and reduction were not performed, and the content validity was not examined. KESS was evaluated in 71 patients with intractable constipation and 20 healthy controls. Although its convergent validity against CSS and discriminant validity with healthy controls were confirmed, its reliability and responsiveness were not formally examined. The KESS was able to predict which patients had pure slow transit constipation or rectal evacuatory disorder for 55% (95% CI: 43–67%). The cutoff score for constipation was >10 with both a sensitivity and specificity of 100%. KESS was further validated in 105 patients with constipation, and the overall prediction of the correct pathophysiologic subgroup was reported to be 47% [25]. In clinical studies, the KESS has been less frequently utilized than

746

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Table 61.6  Chinese Constipation Questionnaire (CCQ) [9] Item 1. Severity of false alarm: feeling like you have to pass a stool, but you cannot 2. Frequency of 5 was determined to discriminate between constipated patients and controls with both a sensitivity and specificity of 91%. The CCQ has rarely been utilized since its development although it is one of the most formally and rigorously validated PROMs. There are possible two reasons for this. First, the CCQ was validated only in Chinese and requires another validation study of its English version to be reliably used in English. Second, a formal questionnaire table exactly presenting the six items of CCQ was not provided in the original paper. Constipation Severity Instrument (CSI) (Table 61.7) is a 16-item self-report measure designed to assess constipation severity and identify subtypes of constipation, including obstructed defecation and slow transit constipation [10]. The CSI consists of three subscales that include “obstructed def-

ecation” (six items), “colonic inertia” (six items) and “pain” (four items). Each symptom is rated with a 5-point Likert scale either from 0 to 4 or from 1 to 5, and the total CSI score ranges between 0 and 73. The original 80 items were generated through literature review and patient interview, which were reduced to the final 16 items by exploratory and confirmatory analysis. The CSI was evaluated in 191 constipated patients and 103 healthy volunteers. Its reliability of internal consistency (Cronbach’s alpha = 0.9) and test–retest reliability (intraclass correlation coefficient = 0.91) was demonstrated. Content validity, convergent validity against PAC-SYM, and discriminant validity were confirmed, while responsiveness was not examined. The CSI has rarely been utilized since its development although it was formally developed and meticulously validated. It is probably because the CSI has too many items and its rating is rather complicated although its authors claimed, “The CSI is a short, easy to use, reliable, and valid instrument to assess constipation severity and identify subtypes of constipation.” Obstructed Defecation Syndrome (ODS) score (Table  61.8) is an eight-item interviewer-led questionnaire specifically designed to assess obstructed defecation syndrome (ODS), in which the stool in the rectum cannot be evacuated sufficiently or comfortably due to various pathophysiologies, including pelvic floor incoordination, rectocele, and rectal intussusception [11]. Each symptom is rated with a 5-point Likert scale from 0 to 4 except for the item of “stool consistency,” which is rated with a 4-point scale from 0 to 3, and the total ODS score ranges between 0 and 31. The eight items were developed by incorporating items from CSS [6] and KESS [8] with taking into account the definition of constipation by Rome II criteria. The formal item generation and reduction were not performed, and the content validity was not examined. The ODS score was evaluated in 76 patients with ODS and 30 healthy controls. Its test–retest reliability was confirmed by the Bland–Altman plot, and relatively weak internal consistency (Cronbach’s alpha = 0.51) was demonstrated. Discriminant validity with healthy controls was confirmed, while convergent validity and responsiveness were not examined. The ODS score is suitable and frequently used in evaluating the ODS symptomatic severity and the effect of treatments for ODS. There is another scale, called Longo’s ODS score, that is designed to evaluate ODS. It is specifically used to evaluate the efficacy of a surgical procedure, called Stapled Transanal Rectal Resection (STARR), for the treatment of rectocele and/or rectal intussusception [26]. This score, however, has never been formally validated to examine its reliability and validity. Bowel Function Index (BFI) (Table 61.9) is a three-item clinician-administered and patient-reported questionnaire,

61  Patient-Reported Outcome Assessment in Constipation and Obstructed Defecation

747

Table 61.7  Constipation Severity Instrument (CSI) [10] Item Obstructed Defecation Subscale CSI 1. Incomplete bowel movements (a) How often do you experience incomplete bowel movements?

0

1

Usually Occasionally Sometimes experience this experience experience this this

(b)  How severe is this symptom for you?

Never experience this (Skip to #2) –

(c)  How much does this bother you?

–

CSI 2. Straining/difficulty in having a bowel movement (a)  How often do you experience this? Never experience this (Skip to #5) (b)  How severe is this for you? –

(c)  How much does this bother you?

–

2

3

4

5

Always experience this

–

Not at all severe (Most of my BM comes out)

Mild

Somewhat Severe severe (I bear down hard)

Not at all bothersome

A little bothersome

Somewhat Very bothersome bothersome

Usually Occasionally Sometimes experience this experience experience this this

Always experience this

Not at all severe (I push a little)

Mild

Somewhat Severe severe (I bear down hard )

Not at all bothersome

A little bothersome

Somewhat Very bothersome bothersome

Extremely severe (I push on my belly, grunt and bear down very hard) Extremely bothersome –

Extremely severe (I push on my belly, grunt and bear down very hard ) Extremely bothersome

Colonic Inertia Subscale CSI 3. Think about when you are having difficulty with your bowel habits: During a typical month, how many times do you usually have a bowel movement? (please check only one) A few times Once per Once every 2 Once a month N/A—I never Daily per week week weeks have difficulty with my bowel habits CSI 4. Infrequent bowel movement (less than 1 bowel movement every 3 days) – Always Usually Occasionally Sometimes (a) How often do you experience infrequent Never experience this experience experience experience bowel movement? experience this this this this (Skip to #5 ) Extremely Mild Somewhat Severe (b)  How severe is this symptom for you? – Not at all severe severe severe (I can go up to (I go 1–2 (I go almost 4 weeks times per everyday) without going) week) (c)  How much does this symptom bother you? – Not at all A little Somewhat Very Extremely bothersome bothersome bothersome bothersome bothersome CSI 5. Lack of urge to have a bowel movement (BM) (a)  When you lack the urge to have a BM, how severe is this for you? Extremely Mild Somewhat Severe Not at all Never severe severe severe experience (I don’t have (I only (I have a this any sensation in have a pretty good the pelvic area) vague sense when I sense that I have to go) might have to go) (b)  When you lack the urge to have a BM, how much does this bother you? Not at all A little Somewhat Very Extremely Never bothersome bothersome bothersome bothersome bothersome experience this (continued)

748

T. Mimura

Table 61.7 (continued) Item 0 1 2 3 4 Pain Subscale: Rectal/anal pain due to your bowel problems CSI 6. During the last month, on average how severe was the pain in your rectum/anus? Mild Somewhat Severe Extremely I haven’t severe severe experienced this CSI 7. Rate the level of your rectal/anal pain at the present moment No pain Mild Somewhat Severe Extremely severe severe CSI 8. How much suffering do you experience because of rectal/anal pain? Severe Extremely None Mild Somewhat suffering severe suffering severe suffering CSI 9. During the last month, due to your bowel habits, how often have you had bleeding during/after a bowel movement? Never Rarely Occasionally Usually Always

5

―

― ―

―

Score range: 0–73

Table 61.8  Obstructed Defecation Syndrome (ODS) score [11] Item Mean time spent at the toilet N attempts to defecate per day Anal/vaginal digitation

0 1 2 3 4 30 min 20 min 1

2

Never

>1/month, Once a 1/month, Once a 1/month, Once a 1/month, Once a 1cm (compared Valsalva maneuver with at rest, line 1). (a) At rest. (b) Valsalva maneuver. AC

795

b a

anal canal, ARJ anorectal junction, B bladder, R rectum, SP symphysis pubis, U urethra

796

a

S. M. Murad-Regadas et al.

b

Fig. 64.19  Dynamic 3D transvaginal and transrectal ultrasonography technique (TTUS). Using intrarectal gel. Transvaginal approach. (a) At rest. The angle is measured at the intersection of the longitudinal axis of

a

Fig. 64.20  Dynamic 3D transvaginal and transrectal ultrasonography technique (TTUS). Using intrarectal gel – transvaginal approach. (a) At rest. The angle is measured at the intersection of the longitudinal axis of the anal canal, and a line is drawn along the posterior border of the

the anal canal, and a line is drawn along the posterior border of the rectal wall (lines). (b) Increased angle during straining (lines). EAS external anal sphincter, IAS internal anal sphincter, PR puborectalis muscle

b

rectal wall (lines). (b) Decreased angle (anismus) during straining (lines). EAS external anal sphincter, IAS internal anal sphincter, PR puborectalis muscle

64  Echodefecography: Technique and Clinical Application

a

Fig. 64.21  Dynamic 3D transvaginal and transrectal ultrasonography technique. Using intrarectal gel—Transrectal approach—the vagina maintains a straight horizontal position during defecatory effort. (a) Patient without rectocele—the vagina maintains a straight horizontal position during defecatory effort. (b) Patient with grade III rectocele.

Fig. 64.22  Dynamic 3D transvaginal and transrectal ultrasonography technique. Using intrarectal gel—Transrectal approach.(a) Patient with intussusception—rectal wall infolding into the rectum

797

b

Rectocele grade (sagittal plane) is measured by one line placed in the initial straining position (1), and the other line drawn at the point of maximal straining (2). The distance between the two lines (vaginal wall positions) determines the grade of the rectocele (3)

798

a

S. M. Murad-Regadas et al.

b

Fig. 64.23  Patient with grade II or III sigmoidocele/enterocele—bulges downward to the pelvis. (a) Patient without rectocele. (b) Patient with grade II rectocele

References 1. Regadas FSP, Murad-Regadas SM, Lima DMR, et  al. Anal canal anatomy showed by three-dimensional anorectal ultrasonography. Surg Endosc. 2007;21:2207–11. 2. Murad-Regadas SM, Regadas FSP, Rodrigues LV, et  al. A novel three-dimensional dynamic anorectal ultrasonography technique (echodefecography) to assess obstructed defecation, a comparison with defecography. Surg Endosc. 2008;22:974–9. 3. Santoro GA, Wieczorek AP, Dietz HP, et al. State of the art: an integrated approach to pelvic floor ultrasonography. Ultrasound Obstet Gynecol. 2011;37:381–96. 4. Barthet M, Portier F, Heyries L.  Dynamic anal endosonography may challenge defecography for assessing dynamic anorectal disorders: results of a prospective pilot study. Endoscopy. 2000;32: 300–5. 5. Beer-Gabel M, Teshler M, Schechtman E, Zbar AP. Dynamic transperineal ultrasound vs. defecography in patients with evacuatory difficulty: a pilot study. Int J Colorectal Dis. 2004;19:60–7. 6. Dietz HP, Steensma AB. Posterior compartment prolapse on two-­ dimensional and three-dimensional pelvic floor ultrasound: the distinction between true rectocele, perineal hypermobility and enterocele. Ultrasound Obstet Gynecol. 2005;26:73–7. 7. Perniola G, Shek C, Chong CC, et al. Defecation proctography and translabial ultrasound in the investigation of defecatory disorders. Ultrasound Obstet Gynecol. 2008;31:567–71. 8. Steensma AB, Oom DMJ, Burger CW, Schouten WR. Assessment of posterior compartment prolapse: a comparison of evacuation proctography and 3D transperineal ultrasound. Colorectal Dis. 2010;12:533–9. 9. Regadas FSP, Haas EM, Jorge JM, et  al. Prospective Multicenter Trial comparing Echodefecography with defecography in the

assessment of anorectal dysfunctions in patients with obstructed defecation. Dis Colon Rectum. 2011;54:686–92. 10. Murad-Regadas SM, Soares GS, Regadas FSP, et al. A novel three-­ dimensional dynamic anorectal ultrasonography technique for the assessment of perineal descent, compared with defaecography. Colorectal Dis. 2012;14:740–7. 11. Santoro GA, Wieczorek AP, Stankiewicz A, et al. High-resolution three-dimensional endovaginal ultrasonography in the assessment of pelvic floor anatomy: a preliminary study. Int Urogynecol J Pelvic Floor Dysfunct. 2009;20:1213–22. 12. Murad-Regadas SM, Bezerra LR, Silveira CR, et  al. Anatomical and functional characteristics of the pelvic floor in nulliparous women submitted to three-dimensional endovaginal ultrasonography: case control study and evaluation of interobserver agreement. Rev Bras Ginecol Obstet. 2013;35:123–9. 13. DeLancey JL.  Anatomy. In: Cardozo L, Staskin D, editors. Textbook of female urology and urogynecology. London: Isis Medical Media; 2010. p. 112–24. 14. Lammers K, Futterer JJ, Prokop M, Vierhout ME, Kluivers KB. Diagnosing pubovisceral avulsions: a systematic review of the clinical relevance of a prevalent anatomical defect. Int Urogynecol J. 2012;23:1653–64. 15. Snooks SJ, Setchell M, Swash M, Henry MM. Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet. 1984;2:546–50. 16. DeLancey JO, Kearney R, Chou Q, Speights S, Binno S. The appearance of levator ani muscle abnormalities in magnetic resonance images after vaginal delivery. Obstet Gynecol. 2003;101:46–53. 17. Dietz HP, Lanzarone V.  Levator trauma after vaginal delivery. Obstet Gynecol. 2005;106:707–12. 18. Dietz HP, Steensma AB.  The prevalence of major abnormali ties of the levator ani in urogynaecological patients. BJOG. 2006;113:225–30.

64  Echodefecography: Technique and Clinical Application 19. Abdool Z, Shek KL, Dietz HP.  The effect of levator avulsion on hiatal dimension and function. Am J Obstet Gynecol. 2009;201:89. e81–5. 20. Lammers K, Futterer JJ, Inthout J, et  al. Correlating signs and symptoms with pubovisceral muscle avulsions on magnetic resonance imaging. Am J Obstet Gynecol. 2013;208:148.e141–7. 21. Murad-Regadas SM, Fernandes GO, Regadas FS, et al. Assessment of pubovisceral muscle defects and levator hiatal dimensions in women with faecal incontinence after vaginal delivery: is there a correlation with severity of symptoms? Colorectal Dis. 2014;16:1010–8. 22. Murad-Regadas SM, Fernandes GO, Regadas FS, et al. Usefulness of anorectal and endovaginal 3D ultrasound in the evaluation of

799 sphincter and pubovisceral muscle defects using a new scoring system in women with fecal incontinence after vaginal delivery. Int J Colorectal Dis. 2017;32:499–507. 23. Murad-Regadas SM, Pinheiro Regadas FS, Rodrigues LV, et  al. Correlation between echodefecography and 3-dimensional vaginal ultrasonography in the detection of perineal descent in women with constipation symptoms. Dis Colon Rectum. 2016;59(12):1191–9. 24. Murad-Regadas SM, Regadas Filho FS, Regadas FS, et al. Use of dynamic 3-dimensional transvaginal and transrectal ultrasonography to assess posterior pelvic floor dysfunction related to obstructed defecation. Dis Colon Rectum. 2014;57(2):228–36.

Evacuation Proctography

65

Magdalena Maria Woźniak, Aleksandra Stankiewicz, Alexander Clark, and Andrzej P. Wieczorek

Learning Objectives

• To gain an overview on how evacuation proctography should be performed and interpreted • To become familiar with normal findings and the ways of interpretation • To understand the most frequent pathological findings which can be diagnosed with evacuation proctography

pacemakers, or of greater relevance to pelvic floor investigation, sacral nerve stimulators (SNS).

65.2 Patient Preparation

Before the procedure itself, it is very important to obtain a complete clinical history with particular attention to abdominal and pelvic surgery, clinical conditions (such as diabetes, hypothyroidism, and systemic disorders), and drug consumption. Other clinical history should be recorded as fol65.1 Introduction lows: the period of dyschezia, the frequency of defecation per week, the time required for usual defecation, the sense of Constipation is the most common digestive complaint, tenesmus or incomplete evacuation, the specific pose during effecting up to 20% of the population, with considerable defecation, and the use of any specific maneuver (digitation), healthcare, social, and economic implications [1]. Evacuation laxative or enema [3]. proctography also referred to as defecography has been Proctography is recognized by patients as an embarrassestablished as a particularly useful fluoroscopic examination ing and stressful examination, and thus, the patient should be for diagnosis in patients with constipation, where constipa- informed in advance about the procedure and its particular tion is due to obstructed defecation, because it enables a steps. To perform a correct examination cooperation with the functional, real-time assessment of the defecation mechanics patient is essential. The entire procedure should be explained in an almost physiologic setting. When combined with phys- to the patient first so that the patient follows actual instrucical examination, evacuation proctography allows accurate tions of the examination correctly in a relaxed and comfortand expanded assessment of the underlying pathology and able condition [3]. helps to guide future intervention [2]. Despite recent Preparation of the bowel with laxatives or enemas is not advances in magnetic resonance (MR) defecography, this mandatory. In some institutes, however, the patient can technique still represents a widely available and cost-­ undertake a rectal cleansing enema at home a few hours effective diagnostic tool [3]. Furthermore, some patients will before the examination because a limited bowel preparation be unsuitable for MRI having implanted devices such as will be more comfortable for the patient and will also provide a more standardized examination [3]. In some centers for the same purposes, the administration of two glycerin suppositories to empty the rectum is recognized as useful, M. M. Woźniak (*) · A. P. Wieczorek although also not obligatory [4]. Department of Pediatric Radiology, Medical University of Lublin, Children’s University Hospital, Lublin, Poland e-mail: [email protected]; [email protected] A. Stankiewicz · A. Clark Imaging Department, University Hospitals of North Midlands NHS Trust, Keele University, Stoke-on-Trent, UK e-mail: [email protected]; [email protected] © Springer Nature Switzerland AG 2021 G. A. Santoro et al. (eds.), Pelvic Floor Disorders, https://doi.org/10.1007/978-3-030-40862-6_65

801

802

M. M. Woźniak et al.

65.3 Examination Technique Rather than actually reproducing the physiological process of normal defecation, defecography is a study of voluntary evacuation; hence, the term “evacuation proctography” is often preferred [5] and will be further used in this chapter. The concept of radiological investigation of rectal evacuation in constipated patients is not new [6], although the proctographic technique widely practiced today is based on the initial description of Mahieu in the early 1980s [7, 8].

65.3.1 Small Bowel, Rectal and Vaginal Opacification, and Defecation In our institution (University Hospital of North Midlands), evacuation proctography is performed as follows: The patient drinks 400–600 ml of oral barium suspension to opacify the small bowel and about 1 h later is taken to the fluoroscopy room by the advanced practitioner in radiography who will perform the test. Here, the patient is reminded of what the procedure entails, and they have the opportunity to ask any questions regarding the examination. Subsequently, the patient lies on a bed in the left lateral decubitus position, and 10 ml of barium is administered into the vagina. Then 150  ml of barium sulfate for oral suspension (E Z HD), which is mixed immediately before use with warm water to a “toothpaste” consistency, is injected into the rectum gently using an enema catheter. The enema catheter is removed, and the patient walks 3 m to the commode chair. The examination takes place with the patient seated, following the below instructions: (a) “Relax,” then “squeeze and lift,” and then “relax.” This is captured with video fluoroscopy and is an indication of pelvic floor level and puborectalis contraction. (b) The next is to “push” out the rectal paste, also under fluoroscopic screening. “Push” is repeated until all the paste is evacuated or if a diagnosis of rectal prolapse is made. If patients are unable to empty, they are asked to try to evacuate on a normal toilet in privacy before a final fluoroscopic assessment. (c) Some practitioners will obtain a post-evacuation spot radiograph after full evacuation. In our practice, spot exposures are only acquired where there is a history of rectopexy. In such cases, one spot film is acquired at rest and another at maximum strain. These radiographs should show the position of clips or staples and any excess movement of these when pushing to empty the rectum.

Fig. 65.1  Evacuation proctography. Normal anatomy. A (arrow) anal canal, R rectum, SB opacified small bowel, V (dotted arrow) vagina

Without interruption, the evacuation process takes less than 30 s in physiologic conditions [3, 9]. Normal anatomy is demonstrated in Fig. 65.1. Most authors consider proctography to be more physiological when performed with the patient in the seated position, although in immobile or incontinent patients, the procedure may successfully be performed with the patient in the left lateral decubitus position [10]. Indeed, comparative studies suggest that although static findings differ, dynamic patterns are essentially similar [11]. In some institutions, cystocolpoproctography is performed. The bladder is first filled through a catheter, and static and dynamic images are obtained during rest and maximum strain. Then the bladder is emptied, and the vagina is opacified followed by the rectum, as described above [12]. Clearly, more invasive than basic proctography, dynamic cystocolpoproctography has the advantage of providing a more detailed assessment of pelvic floor dysfunction [13, 14]. However, dynamic magnetic resonance imaging (MRI)

65  Evacuation Proctography

has found an increasing role in imaging multicompartment pelvic organ prolapse [15].

65.4 Image Analysis 65.4.1 Parameters 65.4.1.1 Anorectal Angle (ARA) The anorectal angle (ARA) is measured between the longitudinal axis of the anal canal and the posterior rectal line, parallel to the longitudinal axis of the rectum. It can be difficult to measure because the posterior wall of the rectum is often not clearly delineated and the angle becomes highly subjective [16]. At rest, the physiologic range is 65–100° without noticeable differences between men and women [9, 17]. ARA is an indirect indicator of the puborectalis muscle activity. During muscle contraction, ARA becomes more acute while during relaxing phase it becomes obtuse. 65.4.1.2 Anorectal Junction (ARJ) The second important parameter for evaluation is the shift of the anorectal junction (ARJ) during straining. ARJ is the uppermost point of the anal canal. The line drawn between the ischial tuberosities is called the bi-ischiatic line and can be used as a fixed bony landmark. Another fixed reference point is represented by the tip of the coccyx. The craniocaudal migration of ARJ indirectly represents the elevation and descent of pelvic floor. The reproducibility and reliability of these two parameters as usually measured have been confirmed, but their clinical significance is still controversial [9]; hence, some experienced practitioners do not routinely measure them. 65.4.1.3 Pubococcygeal Line (PCL) Pubococcygeal line (PCL) is the line between the inferior margin of pubic symphysis and the sacrococcygeal junction.

65.4.2 Normal Findings 65.4.2.1 Rest At rest, the anal canal is closed, and the rectum assumes its normal upright configuration [7]. The impression of the puborectal sling is visible on the posterior wall of the lower rectum, and the ARA is about 90° [3]. The position of the pelvic floor is often inferred by reference to the pubococcygeal line (PCL), although the side of the commode or inferior margins of the ischial tuberosities are useful approximations. Perineal descent is measured from this line to the ARJ and may be up to 1.8 cm at rest [18], although usually less in younger patients [19] and often

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greater in the elderly [20]. Some pelvic floor descent during evacuation is considered normal, and a descent of up to 3 cm from the rest position to anal canal opening is acceptable [18, 21]. The anorectal angle (ARA) has received considerable attention, although absolute measurements are of questionable clinical use. Qualitative assessments of changes in the ARA in individual patients are more useful than absolute angle measurements. The puborectalis length (PRL) can be estimated by measuring the distance between the ARA and symphysis pubis. However, as for the ARA, qualitative assessment of the PRL in individuals is of greater use than reliance on absolute measurements.

65.4.2.2 Squeeze/Strain (Push) During voluntary contraction of the pelvic floor (squeeze), the ARA decreases to about 75°, and the ARJ migrates cranially. The puborectal impression becomes more evident because of the contraction of levator ani [3]. While the patient is asked to push or strain to empty, the ARA increases with partial to complete loss of puborectal impression and the pelvic floor descends. The degree of caudal migration of ARJ is considered normal when less than 3 cm relative to the resting position. 65.4.2.3 Evacuation The emptying phase of the proctogram gives important information about rectal structure and function. During evacuation, wide opening of the anal canal and funneling of the anorectum are seen with near complete loss of puborectal sling impression [2, 3]. In the normal patient, the anal canal should open fully within a couple of seconds, and evacuation should then proceed promptly and to completion. It is important to remember that in essence, only contrast below the first rectal fold is expected to be evacuated during the examination; retained contrast above the first fold is a normal finding [21]. The ARA increases with the relaxation of the anal sphincter and puborectalis muscle. Typically, the ARA should increase by around 20–30°, and the PRL should increase by around 3–4 cm [18], although absolute measurements are of limited value for individual patients [7]. At the end of evacuation, the rectum is empty and its walls collapse. Eventually, the rectum is restored to its original resting condition. The rate and degree of contrast emptying is highly relevant in the diagnosis of functional disorders of defecation. This was described first by Mahieu et al. who divided the normal proctogram into five elements: increase in the ARA, obliteration of the puborectalis impression, wide opening of the anal canal, evacuation of rectal contents, and lack of significant pelvic floor descent [21]. Although later refined, this initial description remains a very useful baseline of normality.

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65.4.2.4 Recovery After evacuation is complete, the anal canal should close, the ARA recover, and the pelvic floor return to its normal baseline position. Post-toilet imaging may be required, particularly in those suspected of retained barium within rectoceles [7] and to visualize rectal prolapse previously obscured by retained rectal barium.

65.4.3 Pathological Findings 65.4.3.1 Abnormal Pelvic Floor Descent Pelvic floor descent is defined as the distance moved by the ARJ at rest to the point of anal canal opening and is considered abnormal if it exceeds 3 cm. It is important to note the resting position of the pelvic floor. In those with fixed pelvic floor descent at rest, the ARJ commonly lies 4 cm below the pubococcygeal line although moves little during evacuation [22]. Excessive pelvic floor descent, or descending perineum syndrome, is suggestive of pelvic floor weakness, although the exact etiology and significance remain controversial. It has been mainly attributed to pelvic/pudendal neuropathy [23, 24], although other etiological factors have been identified such as greater parity [25, 26], elderly age [19], dystocias and obstinate constipation, or even more recently genetic factors [27]. There is also a well-described association with anterior rectal mucosal prolapse [28] and with prolonged straining [18], which is suggested as the underlying common etiology for both conditions. In addition incontinence is frequently associated with perineal descent syndrome [3]. Although perineal descent can be assessed clinically, evacuation proctography is more reliable, not least because patients are seated and strain maximally to the point of anal canal opening [7]. The main radiographic feature is the caudal migration of the anorectal junction more than 3 cm during straining. The anorectal angle is more than 130o at rest and increases to more than 155° during straining [29, 30]. On balance, excessive pelvic floor descent is a common proctographic finding, although its exact significance and cause is not yet fully explained (Fig. 65.2). 65.4.3.2 Anismus (Dyssynergic Defecation) There exist a large group of constipated patients who complain of inability to evacuate but in whom no significant underlying structural abnormality is found [31], but in whom there is an inability for pelvic floor muscles to relax in concert to allow defecation and in some there may be inappropriate contraction of the pelvic floor during defecation. The phenomenon has been variously labeled anismus, spastic pelvic floor syndrome, dyskinetic puborectalis muscle syndrome, and paradoxical puborectalis syndrome [32], reflecting the as-yet obscure etiology. However, the frequent success of biofeedback therapy is good evidence that the

Fig. 65.2  Abnormal pelvic floor descent and bulging of the anterior rectal wall (rectocele, arrow)

condition is both real and, in part, behavioral in origin. It is thus an important diagnosis to make in constipated patients with symptoms of rectal obstruction [7, 33]. Although the diagnosis of animus may be suggested by anorectal physiology, proctography has an important diagnostic role. Various proctographic abnormalities have been described including lack of pelvic floor descent and paradoxical contraction of the puborectalis muscle when attempting to defecate. In practice, elevation of the pelvic floor and reduction in the ARA are rare, but no movement (descent or ARA widening) of the opacified pelvic structures on attempted defecation is a more commonly seen pattern with anismus. Also described are a narrow anal canal and acute anorectal angulation [34]. However, these observations may be found in normal controls and are in themselves unreliable distinguishing features [35, 36]. A further finding is a prominent puborectal impression in the posterior lower rectum throughout the examination, due to failure of puborectalis to relax appropriately. Indeed, another less specific feature is an aberrantly deep impression of the puborectalis sling on the posterior lower rectal wall at rest [2, 3], thought to be caused by the presence of a hypertrophic puborectalis muscle, but this finding is also seen in some normal individuals [36]. A more reliable assessment is based on the rate and completeness of evacuation. Patients with anismus classically demonstrate delay in anal canal opening and prolonged incomplete evacuation [35, 36]. Evacuation time longer than 30 s is highly predictive of dyskinetic puborectalis muscle syndrome, having a positive predictive value of 90% [37]. Evacuation may eventually proceed to completion in some patients, but only after repeated straining. Care must always be taken, however, when diagnosing anismus simply on the presence of prolonged evacuation. Inadequate straining and patient

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embarrassment may both simulate the condition and should be recognized by the radiologist.

65.4.3.3 Intussusception and Rectal Prolapse Rectal intussusception is a concentric invagination or infolding of the entire rectal wall into the rectal lumen during straining or defecation. It may be classified as intrarectal, intraanal, or total (external) rectal prolapse, where the rectum passes through the anal canal. The etiology of rectal intussuscepting is not clear; however, it is more common in multiparous women [25, 26], suggesting it may be a sign of more global pelvic floor damage. Although originally postulated as a cause of obstructed defecation [38], intussusceptions seems more likely a secondary phenomenon, occurring as it does at the end of evacuation rather than preceding it [7]. There is, however, a very strong association with solitary rectal ulcer syndrome (SRUS), a condition related to chronic straining. Patients with SRUS present with rectal bleeding, mucus discharge, and symptoms of obstructed defecation. The proctographic diagnosis is not clear-cut, and there is often difficulty in distinguishing from normal mucosal descent [7]. It usually begins at 6–8 cm above the anal canal as an invagination of one of the valves of Houston [39]. Some degree of rectal intussusception is seen in normal volunteers [17], although symptomatic patients tend to have more advanced findings [40]. The categorization of intussusceptions into intrarectal and intraanal is undoubtedly very useful, as it seems likely that all intussusceptions commences in the rectum and descends toward the anal canal. Furthermore, there is no clear definition of purely intrarectal intussusception [21]. However, the presence of transverse or oblique infolding of abnor-

a

b

mally wide rectal wall of more than 3 mm thickness, which is presented as a funnel or ring-­like configuration during straining, represents intussusception [3]. Rectal collapse may mean normal folds mimic intussusception in the lateral view [40], and thus repeat examination in the AP projection may be required [7]. Minor degrees of infolding of less than 3  mm thickness represent mucosal prolapse and are probably not significant. Once the intussusception enters the anal canal, diagnosis is more clear-cut. The canal is seen to splay on both the lateral and AP views, as it is filled by the descending intussusceptum. Perhaps a more robust method has been recently described whereby the ratio of the intussuscipiens diameter and intussusceptum diameter are calculated [41]. A ratio of more than 2.5 is highly suggestive of true intussusception. An advantage of this technique is the relative nonambiguity of the intussuscipiens and intussusceptum borders and the nondependence on technical factors. In complete rectal prolapse, dilatation of the anal canal is evident during evacuation, and an infolding of the rectal wall invaginates into the lumen. Descent can be so dramatic as to pass through the anus and prolapsed externally [3]. The Oxford grading system is widely used to describe rectal prolapse on clinical and imaging assessment. It divides prolapse into internal rectal prolapse and external. Internal rectal prolapse is further subdivided into rectal intussusception (grade I—descent to the proximal limit of the rectocele; grade II—descent into the rectocele) and rectoanal intussusception (grade III—descent to the top of the anal canal; grade IV—descent into anal canal); while external rectal prolapse corresponds to grade V, when rectal prolapse protrudes from the anus [42] (Figs. 65.3 and 65.4).

c

Fig. 65.3  At rest (a), and pushing/straining (b, c). Moderate rectocele (R) and internal rectal prolapse Oxford grade 2 (arrows) are demonstrated. Note clear demarcation of vagina (dotted arrow)

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a

b

Fig. 65.4  A 60-year-old lady with recurrent symptoms of obstructed defecation syndrome. (a) Initially, a small rectocele is seen. Note sacral nerve stimulator (SNS). (b) In the same patient, during straining, circumferential rectal prolapse (Oxford grade 4) is also demonstrated (arrow)

a

b

c

Fig. 65.5 (a) During “squeeze and lift”—puborectalis contraction. (b) At rest, the pelvic floor level is unremarkable. (c) On straining—pelvic floor descent and anorectal angle widening are noted. There is a small

rectocele and a circumferential rectal mucosal prolapse (arrows) descending into the rectocele, but no intussusception into the anal canal (Oxford grade 2)

65.4.3.4 Rectocele Rectocele is an anterior bulge of the rectal wall wider than 2 cm in the anteroposterior diameter [4]. The depth of a rectocele is measured from the anterior border of the anal canal to the anterior border of the rectocele. A distance of 4 cm as large [7] (Figs. 65.5 and 65.6). This condition is more commonly found in females because of the laxity of the rectovaginal septum. Outpouchings smaller than 2  cm are frequently found in asymptomatic females [17]. The condition is more common in multiparous women (particularly those who have

undergone instrumental delivery), and a defect in the rectovaginal septum has been suggested as the causal mechanism [43]. There is also a clear association with symptoms of obstructed defecation [44] although in itself, the mere presence of a rectocele has limited clinical meaning [45]. On evacuation proctography, an anterior outpouching of the anterior rectal wall bulges and displaces the opacified vaginal lumen during straining and evacuation. A rectocele does not necessarily impede evacuation, but retention of stool within a rectocele may lead to a sense of incomplete evaluation and the need for digitation to complete evacuation [3].

65  Evacuation Proctography

Fig. 65.6  Large rectocele measuring 50 mm is shown. There is predominantly posterior, rectal mucosal prolapse, which intussuscepts the anal canal—Oxford grade 3 (arrow). R rectocele

Of more relevance, however, is barium trapping at the end of evacuation defined as retention of >10% of the area [46] and is related to the size of the rectocele [47]. A pressure drop within “trapping” rectoceles has been demonstrated [46], which explains the relief obtained by patient digitation, when pressure is applied on the perineum and posterior vagina to complete rectal emptying [48]. Indeed, the effect of digitation may be imaged during proctography after careful discussion with the patient. Proctography has an important role in triaging patients for surgical treatment. The patients with an underlying functional disorder of defecation tend to respond poorly to surgery and benefit from biofeedback. Patients with proctographic evidence of significant looking structural abnormalities are more likely to benefit from surgery. Interestingly, however, even patients who obtain symptomatic relief from surgical repair of a rectocele may still have proctographic evidence of a rectocele on postoperative imaging [49], suggesting that factors other than the anatomical abnormality give rise to symptoms. Rarely, the rectum may be herniated in a posterolateral direction through a defect in the levator ani, commonly related to childbirth [7].

65.4.3.5 Enterocele and Sigmoidocele An enterocele is diagnosed when small bowel loops enter the potential space between the rectum and vagina (rectogenital space) (Fig. 65.7). When a loop of sigmoid enters and widens the rectovaginal septum, it is a sigmoidocele (Fig. 65.8). They result from the herniation of the peritoneal sac into the

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Fig. 65.7  A 6.5-cm rectocele (R) is formed by a loop of the rectum (including rectosigmoid) folded anterior to the anus under a large enterocele (E). Circumferential (posterior predominant) rectal mucosal prolapse (arrow) is demonstrated, with intra anal intussusception to the anal verge (Oxford grade 4)

Fig. 65.8  Large sigmoidocele (S). A small- to moderate-sized anterior rectocele (R) measuring 23 mm is demonstrated. There is also a rectal prolapse, including prolapse of the rectocele roof, which intussuscepts into the anus almost to the anal verge (Oxford grade 4)

rectovaginal space. The diagnosis of an enterocele on proctography is more reliable if oral contrast has been administered before the examination. On proctography, descent of

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barium-filled ileal loops is evident during evacuation in the space between the rectum and vagina that is widened. Widening of this space, or the presence of air in this space, is also an indirect sign of enterocele when opacification of ileal loops is not achieved [2, 3]. The rectogenital space widens as evacuation occurs (and after it) when pressure from the ­adjacent full rectum is reduced, and as such, enteroceles are usually diagnosed at the end of the procedure [7]. Formation can be prevented by filling of the rectogenital space with any other structure such as a cystocele or large rectocele, and for this reason, the bladder should be emptied prior to rectal evacuation when performing extended proctography [7]. Enteroceles may also only become apparent after repeated straining, and some authors recommend post-toilet strain images to increase diagnosis [14]. Kelvin et al. found over 40% of enteroceles were diagnosed only on the post-toilet images [50]. Prior hysterectomy is a major precipitating cause of enteroceles, but there is also an association with multiparity, age, obesity, and connective tissue disorders. Patients typically complain of pelvic pressure or dragging, but it is increasingly clear that, contrary to popular belief, enteroceles are not a cause of obstructed defecation [51]. Herniation of the sigmoid into the rectogenital space (sigmoidocele) is significantly less common than an enterocele, although symptoms may be more severe. Diagnosis is based on the barium-filled sigmoid or fecal contents within the sigmoid seen anterior to the rectum. Unlike enteroceles, there is some evidence that large sigmoidoceles can themselves cause obstructed defecation. The advent of newer MRI techniques hold considerable promise in the diagnoses of enteroceles and other forms of pelvic herniation and are discussed elsewhere [52]. The study by van Gruting et al. compared four different imaging techniques used in the assessment of posterior compartment disorders in patients with obstructed defecation syndrome. It showed that evacuation proctography is not the best available method for all conditions but showed the highest diagnostic accuracy for rectal intussusception. Therefore, evacuation proctography should remain the examination of choice in cases of clinically suspected rectal intussusception [53]. Furthermore, not all patients can undergo MRI having pacemakers or SNS.

65.5 Conclusions Evacuation proctography is a long-established reliable and reproducible technique, as well as a cost-effective and easily assessable procedure for evaluation of defecation disorders. However, the diagnosis of defecation abnormalities may not always be straightforward because the pathological imaging findings overlap with appearances seen in normal and asymptomatic individuals. This method has the highest

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accuracy in diagnosing rectal intussusception [53]. Moreover, controversies exist as to the interpretation and clinical utility of the technique due to absent or imperfect reference standards for comparison. The main limitation of this technique is patient’s exposure to ionizing radiation in comparison to MR defecography, but MR defecography is limited due to its high costs and still low availability. However, when performed in specialized centers by welltrained and experienced personnel, this technique still plays a very important role in management of patients with defecation dysfunctions.

Take-Home Message

Evacuation proctography remains the main radiological examination in the assessment of posterior compartment disorders in patients with constipation and obstructed defecation, especially when rectal intussusception is suspected.

References 1. Higgins PD, Johanson JF.  Epidemiology of constipation in North America: a systematic review. Am J Gastroenterol. 2004;99(4):750–9. 2. Kim NY, Kim DH, Pickhardt PJ, Carchman EH, Wald A, Robbins JB.  Defecography: an overview of technique, interpretation, and impact on patient care. Gastroenterol Clin North Am. 2018;47(3):553–68. 3. Kim AY. How to interpret a functional or motility test - defecography. J Neurogastroenterol Motil. 2011;17(4):416–20. 4. Mezwa DG, Feczko PJ, Bosanko C.  Radiologic evaluation of constipation and anorectal disorders. Radiol Clin North Am. 1993;31(6):1375–93. 5. Bruch HP, Fischer F, Schiedeck TH, Schwandner O. [Obstructed defecation]. Chirurg. 2004;75(9):861–70. 6. D’Hoore A, Penninckx F.  Obstructed defecation. Colorectal Dis. 2003;5(4):280–7. 7. Taylor SA. Defecographic study of rectal evacuation in constipated patients. In: Santoro GA, Di Falco G. Benign anorectal diseases: diagnosis with endoanal and endorectal ultrasound and new treatment options. Springer Milan; 2006. p. 231–41. 8. Zonca G, De Thomatis A, Marchesini R, Sala S, Bozzini B, Cozzi G, et al. The absorbed dose to the gonads in adult patients undergoing defecographic study by digital or traditional radiographic imaging. Radiol Med. 1997;94(5):520–3. 9. Choi JS, Wexner SD, Nam YS, Mavrantonis C, Salum MR, Yamaguchi T, et al. Intraobserver and interobserver measurements of the anorectal angle and perineal descent in defecography. Dis Colon Rectum. 2000;43(8):1121–6. 10. Poon FW, Lauder JC, Finlay IG. Technical report: evacuating proctography--a simplified technique. Clin Radiol. 1991;44(2):113–6. 11. Jorge JM, Ger GC, Gonzalez L, Wexner SD. Patient position during cinedefecography. Influence on perineal descent and other measurements. Dis Colon Rectum. 1994;37(9):927–31. 12. Kelvin FM, Maglinte DD. Dynamic cystoproctography of female pelvic floor defects and their interrelationships. AJR Am J Roentgenol. 1997;169(3):769–74.

65  Evacuation Proctography 13. Maglinte DD, Kelvin FM, Hale DS, Benson JT.  Dynamic cystoproctography: a unifying diagnostic approach to pelvic floor and anorectal dysfunction. AJR Am J Roentgenol. 1997;169(3):759–67. 14. Kelvin FM, Maglinte DD.  Dynamic evaluation of female pelvic organ prolapse by extended proctography. Radiol Clin North Am. 2003;41(2):395–407. 15. Roos JE, Weishaupt D, Wildermuth S, Willmann JK, Marincek B, Hilfiker PR.  Experience of 4 years with open MR defecography: pictorial review of anorectal anatomy and disease. Radiographics. 2002;22(4):817–32. 16. Penninckx F, Debruyne C, Lestar B, Kerremans R. Observer variation in the radiological measurement of the anorectal angle. Int J Colorectal Dis. 1990;5(2):94–7. 17. Shorvon PJ, McHugh S, Diamant NE, Somers S, Stevenson GW. Defecography in normal volunteers: results and implications. Gut. 1989;30(12):1737–49. 18. Jorge JM, Habr-Gama A, Wexner SD.  Clinical applications and techniques of cinedefecography. Am J Surg. 2001;182(1):93–101. 19. Pinho M, Yoshioka K, Ortiz J, Oya M, Keighley MR. The effect of age on pelvic floor dynamics. Int J Colorectal Dis. 1990;5(4):207–8. 20. Oettle GJ, Roe AM, Bartolo DC, Mortensen NJ. What is the best way of measuring perineal descent? A comparison of radiographic and clinical methods. Br J Surg. 1985;72(12):999–1001. 21. Bartram C.  Dynamic evaluation of the anorectum. Radiol Clin North Am. 2003;41(2):425–41. 22. Mahieu P, Pringot J, Bodart P.  Defecography: I.  Description of a new procedure and results in normal patients. Gastrointest Radiol. 1984;9(3):247–51. 23. Parks AG, Porter NH, Hardcastle J. The syndrome of the descending perineum. Proc R Soc Med. 1966;59(6):477–82. 24. Jorge JM, Wexner SD, Ehrenpreis ED, Nogueras JJ, Jagelman DG.  Does perineal descent correlate with pudendal neuropathy? Dis Colon Rectum. 1993;36(5):475–83. 25. Karasick S, Spettell CM. Defecography: does parity play a role in the development of rectal prolapse? Eur Radiol. 1999;9(3):450–3. 26. Karasick S, Spettell CM. The role of parity and hysterectomy on the development of pelvic floor abnormalities revealed by defecography. AJR Am J Roentgenol. 1997;169(6):1555–8. 27. Vijayvargiya P, Camilleri M, Cima RR.  COL1A1 mutations presenting as descending perineum syndrome in a young patient with hypermobility syndrome. Mayo Clin Proc. 2018;93(3):386–91. 28. Tsiaoussis J, Chrysos E, Glynos M, Vassilakis JS, Xynos E. Pathophysiology and treatment of anterior rectal mucosal prolapse syndrome. Br J Surg. 1998;85(12):1699–702. 29. Ekberg O, Nylander G, Fork FT.  Defecography. Radiology. 1985;155(1):45–8. 30. Kuijpers HC, Schreve RH, ten Cate Hoedemakers H. Diagnosis of functional disorders of defecation causing the solitary rectal ulcer syndrome. Dis Colon Rectum. 1986;29(2):126–9. 31. Turnbull GK, Bartram CI, Lennard-Jones JE. Radiologic studies of rectal evacuation in adults with idiopathic constipation. Dis Colon Rectum. 1988;31(3):190–7. 32. Halligan S, Bartram CI. The radiological investigation of constipation. Clin Radiol. 1995;50(7):429–35. 33. Bleijenberg G, Kuijpers HC. Treatment of the spastic pelvic floor syndrome with biofeedback. Dis Colon Rectum. 1987;30(2):108–11. 34. Kuijpers HC, Bleijenberg G. The spastic pelvic floor syndrome. A cause of constipation. Dis Colon Rectum. 1985;28(9):669–72. 35. Halligan S, Bartram C.  Proctographic diagnosis of anismus. Dis Colon Rectum. 1998;41(8):1070–1.

809 36. Halligan S, Bartram CI, Park HJ, Kamm MA. Proctographic features of anismus. Radiology. 1995;197(3):679–82. 37. Halligan S, Malouf A, Bartram CI, Marshall M, Hollings N, Kamm MA.  Predictive value of impaired evacuation at proctography in diagnosing anismus. AJR Am J Roentgenol. 2001;177(3):633–6. 38. Wallden L. Roentgen examination of the deep rectogenital pouch. Acta Radiol. 1953;39(2):105–16. 39. Karasick S, Karasick D, Karasick SR. Functional disorders of the anus and rectum: findings on defecography. AJR Am J Roentgenol. 1993;160(4):777–82. 40. Dvorkin LS, Gladman MA, Epstein J, Scott SM, Williams NS, Lunniss PJ.  Rectal intussusception in symptomatic patients is different from that in asymptomatic volunteers. Br J Surg. 2005;92(7):866–72. 41. Pomerri F, Zuliani M, Mazza C, Villarejo F, Scopece A.  Defecographic measurements of rectal intussusception and prolapse in patients and in asymptomatic subjects. AJR Am J Roentgenol. 2001;176(3):641–5. 42. National Institute for Health and Care Excellence (NICE) Interventional Procedures Programme. Interventional procedures overview of laparoscopic ventral mesh rectopexy for internal rectal prolapse. Guidelines; 2018. 43. Gill EJ, Hurt WG.  Pathophysiology of pelvic organ prolapse. Obstet Gynecol Clin North Am. 1998;25(4):757–69. 44. van Dam JH, Ginai AZ, Gosselink MJ, Huisman WM, Bonjer HJ, Hop WC, et al. Role of defecography in predicting clinical outcome of rectocele repair. Dis Colon Rectum. 1997;40(2):201–7. 45. Halligan S, Thomas J, Bartram C.  Intrarectal pressures and balloon expulsion related to evacuation proctography. Gut. 1995;37(1):100–4. 46. Halligan S, Bartram CI.  Is barium trapping in rectoceles significant? Dis Colon Rectum. 1995;38(7):764–8. 47. Kelvin FM, Maglinte DD, Hornback JA, Benson JT.  Pelvic prolapse: assessment with evacuation proctography (defecography). Radiology. 1992;184(2):547–51. 48. Siproudhis L, Dautreme S, Ropert A, Bretagne JF, Heresbach D, Raoul JL, et  al. Dyschezia and rectocele--a marriage of convenience? Physiologic evaluation of the rectocele in a group of 52 women complaining of difficulty in evacuation. Dis Colon Rectum. 1993;36(11):1030–6. 49. Van Laarhoven CJ, Kamm MA, Bartram CI, Halligan S, Hawley PR, Phillips RK. Relationship between anatomic and symptomatic long-term results after rectocele repair for impaired defecation. Dis Colon Rectum. 1999;42(2):204–10; discussion 10–1. 50. Kelvin FM, Hale DS, Maglinte DD, Patten BJ, Benson JT. Female pelvic organ prolapse: diagnostic contribution of dynamic cystoproctography and comparison with physical examination. AJR Am J Roentgenol. 1999;173(1):31–7. 51. Halligan S, Bartram C, Hall C, Wingate J.  Enterocele revealed by simultaneous evacuation proctography and peritoneography: does “defecation block” exist? AJR Am J Roentgenol. 1996;167(2):461–6. 52. Healy JC, Halligan S, Reznek RH, Watson S, Bartram CI, Phillips R, et  al. Dynamic MR imaging compared with evacuation proctography when evaluating anorectal configuration and pelvic floor movement. AJR Am J Roentgenol. 1997;169(3):775–9. 53. van Gruting IMA, Stankiewicz A, Kluivers K, De Bin R, Blake H, Sultan AH, Thakar R. Accuracy of four imaging techniques for diagnosis of posterior pelvic floor disorders. Obstet Gynecol. 2017;130(5):1017–24.

The Abdominal Approach to Rectal Prolapse

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Sthela M. Murad-Regadas, Rodrigo A. Pinto, and Steven D. Wexner

Learning Objectives

• Describe and discuss multiple surgical techniques that have been developed to treat rectal prolapse, each with advantages and disadvantages; • Analyze many treatment options developing over the years and develop an individualized plan for management of each patient according to the severity and frequency of symptoms, full anorectal examination, associated dysfunctions, and conditions of the patient; • Demonstrate and discuss the result in the literature concerning multiple surgical techniques that have been developed to treat rectal prolapse.

66.1 Introduction Full-thickness rectal prolapse is defined as the protrusion of all layers of the rectal wall through the anal sphincters [1]. If the prolapsed rectal wall does not protrude through the anus, it is called intussusception or internal rectal prolapse [2, 3]. Mucosal prolapse is the protrusion of only the rectal mucosa.

S. M. Murad-Regadas (*) Colorectal Surgery at University Hospital, School of Medicine, Federal University of Ceara, Fortaleza, Ceara, Brazil Anorectal Physiology and Pelvic Floor Unit, Sao Carlos Hospital, Fortaleza, Ceara, Brazil e-mail: [email protected] R. A. Pinto Department of Gastroenterology, Service of Colorectal Surgery, Hospital das Clínicas, University of São Paulo School of Medicine, São Paulo, Brazil e-mail: [email protected] S. D. Wexner Digestive Disease Center, Department of Colorectal Surgery, Cleveland Clinic Florida, Weston, FL, USA e-mail: [email protected]

Complete rectal prolapse has been reported since the Egyptian and Greek ancient civilizations [4]. The first written report dates from 1500 BC, by Ebers Papyrus [5]. Over the years, multiple treatments came and went. Mickulicz [6] popularized the perineal amputation in 1888, and Lockhart-­ Mummery [7], in 1910, performed a perineal procedure for the treatment of rectal prolapse. In 1912, Moschowitz [8] started the abdominal repair. The estimated incidence of rectal prolapse is 4 per 1000 population, being more common in elderly females after the fifth decade. The female to male ratio ranges from 6:1 to 10:1. Among children, males and females are equally affected, usually by the age of 3 years [9, 10].

66.2 Etiology The anatomical basis for rectal prolapse is a deficient pelvic floor through which the rectum herniates [3, 11–13]. The exact way that the prolapse takes place is not completely understood, thus it is based on theories. Rectal prolapse as an intussusception of the rectal wall was first described by Hunter [14] and confirmed by Broden and Snellman [11] with cineradiography. Complete rectal prolapse is thought to be a process that starts within 6–8 cm of the anal verge, continuing through the anal canal, and everting onto the perineum [11, 15, 16]. The lower rest and squeeze pressures found in the anal manometries of these patients compared to normal control subjects support this theory [17]. However, defecographic studies have found that in patients with intussusception, the risk of developing rectal prolapse was small, which contradicts this theory [18, 19]. Parks et al. postulated the theory that repeated stretching of the pelvic floor muscles can injure the pudendal nerves and can be a part of the cause of rectal prolapse [20]. This suggested mechanism is supported by some surgeons who have detected a frequent association between neurogenic fecal incontinence and rectal prolapse [12, 13]. However, the improvement of fecal incontinence after surgery, and the

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electromyographic findings of normal innervation in patients with rectal prolapse challenge this proposal. Lax lateral ligaments combined with an atonic condition of the muscles of the pelvic floor and the anal canal could be the main cause of rectal prolapse [11, 12]. In addition, the lack of normal fixation of the rectum, with a mobile mesorectum and a laxity of the lateral ligaments, may predispose to and/or be associated with rectal prolapse [12, 21, 22]. Regardless of which theory is chosen, the following anatomic findings are commonly associated with rectal prolapse: abnormally deep cul-de-sac, loss of posterior fixation of the rectum, laxity of the anal sphincters, and redundant sigmoid colon. All of the procedures described to date attempt to correct some or all these abnormalities.

66.3 A  ssessment of Patients with Rectal Prolapse and Associated Symptoms The assessment of patients with rectal prolapse is based on a complete history including the investigation of all pelvic floor compartment involvement, like the severity and frequency of fecal incontinence and constipation/obstructed defecation symptoms as well as urge of urinary incontinence and pelvic organ prolapse symptoms applying score systems and quality of life to quantify the dysfunctions before and after treatment. Other pelvic floor disorders may be present in 8–27% of patients with rectal prolapse [23]. Altman et al. [23] observed an incidence of 48% of genital prolapse and 31% of urinary incontinence in patients with rectal prolapse (Fig.  66.1). Gonzalez-Argente et al. [24] observed a higher incidence of urinary incontinence (58%) and genital prolapse (24%) in patients operated for rectal prolapse. Previous pelvic surgery, obstetric trauma, elevated intra-abdominal pressure, increas-

Fig. 66.1  Rectal and uterine prolapse

S. M. Murad-Regadas et al.

ing age, and chronic constipation are some factors allied with rectal and genital prolapse [23]. Up to 75% patients with rectal prolapse experience fecal incontinence, and 25–50% have significant constipation [23, 24, 26, 27]. Metcalf and Metcalf et al. [28] supposed that an increased external sphincter activity seen by electromyography could be a cause of outlet obstruction and constipation. Reducible protrusion that may be associated with mucous discharge is a common sign of initial prolapse. Prolapse may theoretically be due to bowel movements, straining, and increased intraabdominal pressure. After the diagnosis of prolapse has been made, patients may experience loss of control of stool because of stretching of the sphincter muscles and the pudendal nerves. In addition, bleeding may develop if the rectum remains exposed and therefore becomes traumatized. Full anorectal examination should include inspection of the perineum including the perineal body and urogenital hiatus; urogynecologists will also include the pelvic organ prolapse quantification (POP-Q) [29]. The prolapse may be easily visible on anorectal examination. Otherwise, the patient is asked to sit down on a commode, leaning forward, with the examiner standing behind to confirm the diagnosis. Digital examination may reveal hypotonia or a patulous anus and it is necessary to exclude rectal/pelvic tumor. A reducible protrusion that may be associated with mucous discharge is a common sign of initial prolapse. Prolapse may theoretically be due to bowel movements, straining, and increased intraabdominal pressure. After the diagnosis of prolapse has been made, patients may experience loss of control of stool because of stretching of the sphincter muscles and the pudendal nerves. In addition, bleeding may develop if the rectum remains exposed and therefore becomes traumatized. A search for risk factors should also be considered as well as previous pelvic surgeries. Evaluation of the colon with colonoscopy and barium enema is recommended to exclude coexisting conditions, such as polyps, cancer, and diverticular disease, which may influence the choice of procedure. The colonic transit study is important, especially in patients with associated constipation. Madoff [26] suggested that slow colonic transit time is the primary factor associated with constipation in patients with rectal prolapse. It has also been postulated that an increased sigmoid transit is a significant factor associated with fecal incontinence in patients with rectal prolapse [27]. Symptoms of obstructive defecation in those patients in whom the prolapse cannot be reproduced during the physical examination usually require the use of dynamic evaluation including defecography, dynamic ultrasound with different modalities (transperineal, transrectal, and ecodefecography), and magnetic resonance image (MRI). The findings can reveal associated functional abnormalities such as entero-­

66  The Abdominal Approach to Rectal Prolapse

sigmoidocele, paradoxial contraction of puborectal muscles (anismus), cystocele and vaginal vault prolapse; such tests are useful. The advantage of dynamic images makes it possible to visualize the anatomical structures of the anal canal and pelvic floor. The anorectal and transvaginal ultrasound are important methods in patients with a previous history of vaginal delivery and anorectal and/or low colorectal surgery to identify the anal sphincter or/and levator ani muscle defects. Previous studies have demonstrated levator ani damage in 15–55% after vaginal delivery with MRI and transvaginal ultrasound as well as pelvic organ prolapse and ballooning hiatal dimensions. [30–32] The evaluation with anorectal manometry and electromyography is useful to evaluate the pelvic floor muscles, particularly in patients with preoperative fecal incontinence; also, patients with urinary incontinence may benefit from urodynamic examination to complete the evaluation and allow for concomitant surgical intervention. Although it is not life-threatening, rectal prolapse is an extremely distressing condition that affects patients’ quality of life; therefore, surgical treatment should be considered even in high-risk patients.

66.4 S  election of Patients for Abdominal Procedures Surgical management of full-thickness rectal prolapse aims to eradicate the external prolapse, limit the risk of recurrence, and limit any impairment to bowel function and continence. Additionally, morbidity and mortality rates should be minimal. The lack of any one treatment as a panacea is why multiple surgical approaches are in common use. Perineal procedures are advocated for elderly patients with significant comorbidity, as they are associated with limited surgical stress and relatively low postoperative morbidity. Nevertheless, recurrence rates up to 58% and persistent bowel dysfunction are commonly reported [33–35]. Conversely, the abdominal approaches are associated with lower recurrence rates, which vary from 0 to 20% among different surgeons [36–41]. The reason for this superior durability is not clearly known, but is attributed to the ability to perform a complete rectal mobilization and fixation under direct vision, with no sacrifice to the rectal reservoir. It also offers a more accurate determination of whether to excise or fix any additional redundant bowel that may prolapse [42]. Abdominal procedures are also related to symptomatic improvement and better functional results than perineal operations [34, 37, 43, 44]. The surgical options can be summarized as suture or mesh rectopexy, with or without sigmoid resection. The abdominal approach can be performed with either an open or a laparoscopic approach. Some authors have reported higher morbid-

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ity rates of 15% with open techniques [34, 37, 42]. Furthermore, the laparoscopic approach, first introduced by Berman [45] in 1992, tried to integrate the surgical stress reduction associated with the perineal approach with the lower recurrence rates achieved with abdominal repair. The decision as to whether to perform sigmoid resection is based on bowel function and sphincter muscle status. If the patient has normal bowel function, or constipation associated with normal anal tone, a resection is preferred. Whenever diarrhea or sphincter damage is suspected, maintenance of the sigmoid colon seems to be correlated with better functional results. Choosing the optimal repair for rectal prolapse involves consideration of the patient’s health and the preexisting bowel function as well as any history or physical findings consistent with either constipation or fecal incontinence. Lastly, the individual surgeon’s experience is always an important factor in the decision-making process as to which procedure is most appropriate for the individual patient. This chapter addresses the abdominal approaches for rectal prolapse.

66.5 Abdominal Procedures Multiple abdominal operations for the treatment of rectal prolapse have been described since the beginning of the past century. The procedures that have persisted, and are mostly commonly reported in the literature, are discussed below.

66.5.1 Ripstein Procedure (Anterior Sling Rectopexy) First described by Ripstein [46] in 1952, the procedure consists of insertion of a synthetic mesh or fascia lata to the anterior wall of the mobilized rectum, fixing the mesh to the sacral promontory, and promoting an encirclement of the rectum. The technique restores the posterior curve of the rectum and provides a stiff anterior support (Fig.  66.2). The major problem with this procedure is the development of obstruction due to the anterior mesh, which can cause rectal stenosis and erosion of the mesh into the rectal wall, followed by fistula formation. Kuijpers [12] observed a 7% incidence of stenosis in his experience. Aiming to reduce this complication, Ripstein [46] modified his procedure by including a posterior fixation of the mesh to the sacrum and an intraoperative calibration with a proctoscope to prevent the narrowing. Despite this modification, the complication rate remained high, significantly limiting the use of the technique. Roberts et  al. [47] reviewed their experience with the Ripstein procedure in 135 patients and reported a 52% com-

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Fig. 66.2  Mesh placement in the Ripstein procedure. Supplied courtesy of Dr Amanda M. Dantas

plication rate and an overall recurrence rate of 10%. Furthermore, a review by Madiba et al. [48] also showed a high complication rate, with mortality ranging from 0 to 2.8%, and recurrence rates ranging from 0 to 13%.

66.5.2 Posterior Mesh Rectopexy First described by Wells [49] in 1959, this technique was popular in the UK.  The procedure consists of placement of a prosthetic Ivalon® (polyvinyl alcohol) sponge between the rectum and the promontory in either side of the rectum, after mobilization of the posterior rectal wall (Fig. 66.3). The anterior part of the rectum must stay free to prevent stenosis. The parietal peritoneum is closed to isolate the mesh from the peritoneal cavity. The well-built fibrous reaction promoted by the presence of a foreign body restores the anorectal angle. Novell et al. [50], in a prospective randomized trial comparing the Ivalon sponge to sutured rectopexy, showed similar recurrence rates and higher wound infection in the mesh group. They failed to demonstrate any advantage of the Ivalon rectopexy over the simpler sutured rectopexy. Other nonabsorbable and even absorbable meshes have been introduced, and have undergone evaluation with similar results, including mortality ranging from 0 to 1% and recurrence rates ranging from 0 to 6%, using absorbable [51–53] or nonabsorbable [25, 26, 50–54] meshes. The main concern about the presence of a foreign material is the development of infection and sepsis. Sepsis after mesh placement has varied from 2 to 16% [11, 12, 52, 55– 61]. The performance of a resection associated with de novo

Fig. 66.3  Posterior mesh fixation of the sacral promontory in the Wells procedure. Supplied courtesy of Dr Amanda M. Dantas

mesh insertion may be associated with an increased risk of infection because of the presence of an anastomosis and a new foreign body; thus, the placement of a mesh for rectopexy seems to be reasonable without resection, due to lower mortality and infection rates [52, 53, 62]. The placement of a drain in the presacral space is also recommended while inserting a mesh to prevent infected collections or hematomas [45, 47, 53]. Whenever sepsis occurs, it is worthwhile to remove the mesh [50, 52, 57, 59–61].

66.5.3 Suture Rectopexy First described by Cutait [63] in 1959, the operation involves a mobilization and upward fixation of the rectum to the sacral promontory with two to three unabsorbable sutures on either side of the rectum (Fig. 66.4). The healing process by fibrosis keeps the rectum fixed in the elevated position, preventing recurrence [1]. Despite the sound theory, the recurrence rates range from 0 to 27% [50, 63–67]; however, most reports have included recurrence rates ranging from 0 to 3%. The effect of rectopexy on constipation may include exacerbation of constipation and sometimes the development of a new onset of constipation [67, 68]. Currently, the lower complication rates and similar long-term outcomes associated with the suture rectopexy compared to mesh placement have led surgeons to prefer sutures to foreign material.

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66  The Abdominal Approach to Rectal Prolapse Fig. 66.4  Stitches placed onto the sacral promontory in suture rectopexy. Supplied courtesy of Dr Amanda M. Dantas

Table 66.1  Results of rectopexy with and without sigmoid resection Author Solla et al. [35] Stevenson et al. [72] Aitola et al. [54] Heah et al. [73] Lechaux et al. [69] Ashari et al. [74] Carpelan Holmström et al. [75] Kariv et al. [76] Dulucq et al. [68]

Year 1989 1998 1999 2000 2005 2005 2006 2006 2007

Resection Yes Yes No No Yes Yes Yes No No

Number 102 34 112 25 48 117 85 111 77

Complication (%) 4 13 15 12 5 9 0 – 0

Mortality (%) 0 3 1 0 0 50% improvement 78% 61% 62% 75% 65% 68% 78%

Table 77.2  Fate of individual symptoms (n = 78) Condition Stress incontinence (n = 69) Urge incontinence (n = 44) Frequency only (n = 12) Nocturia (n = 32) Pelvic pain (n = 17)

>50% improvement 57 (82%) 33 (68%) 10 (83%) 29 (90%) 13 (76%)

support the bladder base stretch receptors, thereby preventing urine loss by premature activation of the micturition reflex (urge incontinence). Both the initial data (Table 77.1) [20] and the later data (Table 77.2) [19] indicate that all these functions can be improved with this method, not just the USI which the Kegel method addresses.

77.6.1 How the Skilling Squatting-Based PFR Method Evolved By 1995 it was evident from the surgical data that a substantial percentage of chronic pelvic pain and bladder and bowel dysfunctions in the female could be cured by surgical repair of the pelvic suspensory ligaments. It was hypothesized that a squatting-based regime would strengthen the three directional muscle forces and the ligaments against which they contract; this would improve urethral closure (incontinence) evacuation (bladder emptying) and support of the bladder base stretch receptors (urge incontinence) and enable the now strengthened USLs to better support the Frankenhauser and sacral nerve plexuses, thereby alleviating ICPP.  The standard regime comprised four visits in 3 months. HRT was administered to all patients, electrotherapy 20  min per day for 4 weeks with a 50 Hz probe placed into the posterior fornix of the vagina, squeezing 3 × 12 per day, reverse pushdowns 3  ×  12 per day, and squatting or equivalent up to 20 min per day as part of daily routine (such as household tasks). Of 147 patients (mean age 52.5  years), 53% completed the program. Median QOL improvement reported was 66%, mean cough stress test urine loss reduced from 2.2 (range 0–20.3) to 0.2 (range 0–1.4), p