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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_926_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •1.5 Wound Healing in Hernia Patients
- •1.6 Main Points
- •References
- •2: An Introduction to Complex Systems Science and Its Application to Hernia Surgery
- •2.1 Introduction
- •1: The Biology of Hernia Formation
- •1.1 Introduction
- •1.2 The Connective Tissue
- •1.2.1 Collagen
- •1.2.2 Matrix Metalloproteinases
- •1.3 Inheritance and Genetics
- •2.2.2 Minimizing Pain and Enhancing Recovery (A Multimodal Effort)
- •2.3 Application of These Tools to a Local Hernia Program
- •2.4 Summary
- •Suggested Reading
- •3: Evaluating Outcomes and Evidence in Hernia Repair
- •3.1 Introduction
- •3.2 Recurrences
- •3.2.1 Importance of Study Methodology
- •3.2.2 Importance of Length of Follow-Up
- •3.2.3 Importance of Outcome Assessment
- •3.2.4 Importance of Follow-Up Percentages
- •3.2.5 Importance of Outcome Reporting
- •3.3 Complications
- •3.3.3 Seroma
- •3.3.4 Surgical Site Infections
- •3.3.5 Surgical Site Occurrences
- •3.4 Patient Reported Outcomes Measurement and Quality of Life
- •3.4.1 Generic Quality of Life Scores
- •3.4.2 Visual Analogues Scale (VAS) for Pain
- •3.4.3 Verbal Rating Scale (VRS)
- •3.4.4 Carolina Comfort Scale™ (CCS™)
- •3.4.5 Inguinal Pain Questionnaire (IPQ) and Ventral Hernia Pain Questionnaire (VHPQ)
- •3.4.6 Hernia-Related Quality-of-Life (HerQles)
- •3.4.7 European Registry for Abdominal Wall Hernias QoL Score (EuraHS-QoL Score)
- •References
- •4: Inguinal Hernia Epidemiology
- •4.1 Introduction
- •4.2 Age and Gender
- •4.3 Inheritance
- •4.4 Occupation
- •4.5 Obesity
- •4.6 Comorbidities
- •4.7 Inguinal Hernia Recurrence
- •References
- •5: Inguinal Anatomy
- •5.1 Overview
- •5.2 Embryology
- •5.3 Gross Anatomy
- •5.3.3 Inguinal (Poupart’s) Ligament
- •5.3.4 Lacunar (Gimbernat’s) Ligament
- •5.3.5 Pectineal (Cooper’s) Ligament
- •5.3.6 Conjoined “Tendon”
- •5.3.7 Hesselbachs Triangle
- •5.3.8 Fossae of the Anterior Abdominal Wall
- •5.3.9 The Femoral Sheath and Femoral Canal
- •5.4 Pathophysiological Variants
- •5.4.1 Hernias
- •5.4.2 Hydrocele
- •5.4.3 Cryptorchidism
- •References
- •6: Diagnostic Considerations in Inguinal Hernia Repair
- •6.1 Introduction
- •6.2 Herniography
- •6.3 Ultrasonography
- •6.4 Computed Tomography
- •6.5 Magnetic Resonance Imaging
- •6.6 Summary
- •References
- •7: Overview of Modern Surgical Techniques in Inguinal Hernia Repair
- •References
- •8: Anesthetic Considerations in Inguinal Hernia Repair
- •8.1 Introduction
- •8.2 Options for Anesthesia in Inguinal Hernia Repair
- •8.2.1 Local Anesthesia
- •8.2.1.1 Patient Selection
- •8.2.1.2 Technique for Local Anesthesia: Open Approach
- •8.2.2 General Anesthesia
- •8.2.2.2 Optimizing Postoperative Recovery from General Anesthesia
- •8.2.3 Regional/Spinal Anesthetic
- •8.3 Epidemiology and Current Trends
- •8.3.1 Anesthesia and Operative Approach
- •8.3.2 Current Guidelines and Recommendations
- •8.3.3 Cost Considerations
- •8.4 Patient Satisfaction and Long-Term Quality of Life
- •8.5 Conclusions
- •References
- •9: The Shouldice Repair 2016
- •9.1 Preamble
- •9.2 History
- •9.2.1 Anatomy
- •9.3.2 The Hernia Sac
- •9.3.3 The Cribriformis Fascia
- •9.3.4 Resection of the Cremaster
- •9.3.5 Relaxing Incision
- •9.3.6 Sutures and Stainless Steel
- •9.3.7 Cost
- •9.4 Surgery: Technical Aspects
- •9.4.1 Sedation
- •9.4.2 Local Anesthesia
- •9.4.3 Dissection
- •9.5 Reconstruction
- •9.6 Statistics and Results
- •9.7 Results
- •9.7.1 Findings
- •9.8 Complications
- •9.2.2 Weight Control
- •9.2.3 Local Anesthesia
- •9.2.4 Early Ambulation
- •9.3 General Principles
- •9.3.1 Division of the Posterior Inguinal Wall
- •9.9 Pain
- •9.9.1 Dysejaculation
- •9.9.1.1 Mesh Removal, Explantations
- •9.9.2 Literature
- •9.10 Conclusion
- •References
- •10: Lichtenstein Tension-Free Hernioplasty
- •10.1 Introduction
- •10.2 Preoperative Management
- •10.3 Materials
- •10.4 Operative Technique
- •10.4.1 Positioning and Preparation
- •10.4.2 Anesthesia and Sedation
- •10.5 Operative Steps
- •10.6 Postoperative Management
- •10.7 Associated Risks and Complications
- •10.9 Discussion
- •10.10 Conclusion
- •References
- •11: The Gilbert Bilayer Connected Device (PHS) and Other Mesh Repairs
- •11.1 Principles of Hernia Repair: The Ideal Technique
- •11.2 Quality of Life Issues: Improving Outcomes and Patient Satisfaction
- •11.3 “Tailored” Surgery: Selection of Technique
- •11.4 Suture Techniques
- •11.5 Mesh Repairs
- •11.5.1 Onlay
- •11.5.2 Mesh Plug Repairs
- •11.5.3 Pre-peritoneal Mesh Repairs
- •11.5.4 Laparoscopic Mesh Repairs
- •11.5.5 Combined Anterior and Posterior Repair: The Prolene Hernia System (PHS)
- •11.6 Technique of Local Anesthesia
- •11.6.1 PHS Insertion Technique
- •11.7 Preparation of the Anterior Space
- •11.9 Preparation and Insertion of the PHS Underlay
- •11.10 Small Indirect Hernias
- •11.11 Large Indirect Hernias
- •11.12 Deployment of the Underlay: Indirect Hernias
- •11.13 Application of the PHS Overlay
- •11.14 Femoral Hernias
- •11.15 Post-op Care: Instructions
- •11.16 Results
- •11.17 Other Mesh Products
- •11.18 Conclusions
- •References
- •12: Laparoscopic TAPP Repair
- •12.1 Introduction
- •12.2 History
- •12.3 Preoperative Considerations
- •12.4 Operative Technique
- •12.5 TAPP Versus TEP
- •12.6 Summary
- •References
- •13: Laparoscopic Totally Extraperitoneal (TEP) Inguinal Hernia Repair
- •13.1 History and Introduction
- •13.2 Totally Extraperitoneal Hernia Repair (TEP)
- •13.2.1 Suggested Equipment
- •13.2.2 Positioning and Draping
- •13.2.3 Incision and Pre-peritoneal Access
- •13.2.4 Pre-peritoneal Space Creation
- •13.2.5 Trocar Insertion
- •13.2.7 Dissection of the Hernia Sac
- •13.2.7.1 Direct Hernias
- •13.2.7.2 Indirect Hernias
- •13.2.8 Mesh Application
- •13.2.8.1 Type and Size of Mesh
- •13.2.8.2 Mesh Preparation
- •13.2.8.3 Mesh Introduction and Application
- •13.2.8.4 Mesh Fixation
- •13.2.8.5 Repair Check
- •Contralateral Side Exploration
- •13.2.9 Special Consideration
- •13.2.9.1 E-TEP
- •13.2.9.2 Obesity
- •13.2.9.3 Recurrent Hernias
- •13.2.9.5 Incarcerated and Strangulated Hernia
- •13.2.10 Postoperative Care
- •13.2.10.1 Hospital Stay and Recovery
- •13.2.10.2 Pain
- •13.2.11 Complications
- •13.2.11.1 Major Intra-operative Complications
- •Urinary Bladder Injury
- •13.2.11.2 Postoperative Complications
- •Urinary Retention
- •Seroma and Hematoma
- •Chronic Pain
- •Genitourinary Complications
- •Mesh Infection
- •Recurrence
- •References
- •14: Emerging Technology: Open Approaches to Preperitoneal Inguinal Hernia Repair
- •14.1 Introduction
- •14.2.1 Indications and Contraindications
- •14.2.2 Preoperative Preparation
- •14.2.3 Anesthesia
- •14.3 The Grid-Iron Repair
- •14.4 Bilayer Mesh Device Repair (Prolene Hernia System™/Ultrapro Hernia System™)
- •14.5 The Kugel Approach
- •14.6 The Transinguinal Polysoft™ Technique
- •14.7 The Transrectus Sheath Preperitoneal Mesh Technique (TREPP)
- •14.8 The Onstep Technique
- •14.8.1 Postoperative Recommendations
- •References
- •15: Emerging Technology: SILS Inguinal Hernia Repair
- •15.1 Introduction
- •15.2 Methodology
- •15.2.1 Using the S-Shaped Retractors
- •15.2.2 Balloon Dissection of the Extraperitoneal Space
- •15.2.3 Telescopic Dissection of the Extraperitoneal Space
- •15.2.4 Preparation of the Triport+ Device
- •15.2.7 Principles of Dissection During a TEP Repair
- •15.2.8 Telescopic Dissection of the Extraperitoneal Space
- •15.2.9 Insertion of the Mesh
- •15.2.11 Closure of the Umbilical Wound
- •15.2.12 Discharge Instructions and Follow-Up
- •15.3 Discussion
- •15.4 Conclusion
- •References
- •16: Emerging Technology: Robotic Inguinal Hernia Repair
- •16.1 Introduction
- •16.2 Rationale
- •16.3 Techniques for Robotic Inguinal Hernia
- •16.4 Literature
- •16.5 Controversies for Robotic Inguinal Hernia Repair
- •16.6 Future Directions for Robotic Inguinal Hernia Repair
- •References
- •17: Outcomes in Inguinal Hernia Repair
- •References
- •18: Prevention and Evaluation of Chronic Groin Pain
- •18.1 Risk Factors
- •18.2 Selection of Patients
- •18.3 Selection of Technique and Approach
- •18.5 Choose the Mesh: Lightweight vs. Heavyweight
- •18.6 Choose the Fixation
- •18.7 Clinical Assessment
- •References
- •19: An Approach to Inguinal Pain
- •References
- •20: Surgical Management of Chronic Groin Pain
- •20.1 Introduction
- •20.2 Nonoperative Approach
- •20.3 Operative Techniques
- •20.3.1 Recurrence
- •20.3.2 Neuropathic Pain
- •20.3.3 Meshoma
- •20.3.4 Orchialgia
- •20.4 Conclusions
- •References
- •21: Groin Pain in Athletes
- •21.1 Introduction
- •21.1.1 Epidemiology
- •21.2.1 Background
- •21.2.2 British Hernia Society: Manchester
- •21.2.4 Doha v Manchester
- •21.4 What Are the Main Investigations That Are Required for Athletes Presenting with Inguinal-Related Groin Pain?
- •21.5.1 Active Rehabilitation
- •21.5.2 Surgical Intervention
- •21.6 Conclusion
- •References
- •22: The Treatment of Incarcerated and Strangulated Inguinal Hernias
- •22.1 Introduction
- •22.2 Incidence
- •22.3 Presentation
- •22.4 Diagnosis
- •22.5 Repair
- •22.5.1 Open Repair
- •22.5.2 Role of Mesh Repair
- •22.5.3 Role of Laparoscopic Repair
- •22.5.4 Hernioscopy
- •22.6 Summary
- •References
- •23: Introduction and Epidemiology of Incisional Hernias and the Argument for Mesh in Incisional Hernia Repair
- •23.1 Historical Brief
- •23.2 Prevalence and Cost
- •23.3 Risk Factors for Incisional Hernia
- •23.4 The Argument for Mesh
- •References
- •24: Abdominal Wall Anatomy
- •24.1 Clinical Anatomy
- •24.1.1 Overview
- •24.1.2 Layers of the Abdominal Wall
- •24.1.2.1 Fascia
- •24.1.2.2 Musculature
- •24.1.3 Neurovascular Anatomy
- •24.1.3.1 Nerves
- •24.1.3.2 Vessels
- •24.1.4 Layers of the Groin
- •24.1.4.1 Fascia
- •24.1.4.2 Contents
- •24.1.4.3 Neurovascular
- •24.1.4.4 Anatomic Regions
- •24.2 Physiology of the Abdominal Wall
- •24.2.1 Overview
- •24.2.2 Normal Function
- •24.2.2.1 Dynamic Function
- •24.2.2.2 Respiratory Function
- •24.2.3 Anatomic Abnormalities
- •24.2.3.1 Diastasis Recti
- •24.2.3.2 Ventral Hernia
- •References
- •25: Hernia Prevention and the Importance of Laparotomy Closure
- •25.1 Introduction
- •25.2 Risk Factors
- •25.2.1 Patient-Related Risk Factors
- •25.2.2 Operative Factors
- •25.3 Methods of Closure
- •25.3.1 Continuous or Interrupted Sutures
- •25.3.2 Suture Length to Wound Length Ratio
- •25.3.3 Layered Closure or Mass Closure
- •25.3.4 Stitch Size
- •25.3.5 Suture Material
- •25.3.6 Prophylactic Mesh Augmentation
- •25.4 Future Directions
- •References
- •26: The Use of Prophylactic Mesh in the Prevention of Incisional and Parastomal Hernia Repair
- •26.1 Introduction
- •26.2 Parastomal Hernia
- •26.2.1 Introduction
- •26.3 Conclusion
- •References
- •27: Preoperative Optimization and Enhanced Recovery Protocols in Ventral Hernia Repair
- •27.1 Introduction
- •27.2 Preoperative Optimization
- •27.2.1 Obesity
- •27.2.2 Smoking
- •27.2.3 Diabetes
- •27.2.4 Nutrition and Metabolic Control
- •27.3 Peri- and Postoperative Optimization
- •27.3.1 Surgical Site Infection
- •27.3.2 Skin Preparation and Decolonization Protocols
- •27.3.3 Perioperative Antibiotics
- •27.3.4 Postoperative Blood Glucose Management
- •27.4 Conclusion
- •References
- •28: Overview of Operative Approaches and Staging Systems for Ventral/Incisional Hernia Repairs
- •28.1 Introduction
- •28.2.2 Ventral Hernia Working Group
- •28.3 Ventral Hernia Staging System
- •28.5 Outcomes
- •28.6 Summary
- •References
- •29: Onlay Ventral Hernia Repair
- •29.1 Introduction
- •29.3 Clinical Data
- •29.4 Contemporary Onlay Ventral Hernia Repair with Fibrin Glue Fixation
- •29.5 Discussion
- •References
- •30: Retrorectus Hernia Repair and Transversus Abdominis Release
- •30.1 Introduction
- •30.2 Indications
- •30.3 Technical Description
- •30.3.1 Retrorectus Hernia Repair
- •30.3.2 The Transversus Abdominis Release Procedure
- •30.4 Outcomes
- •30.5 Pearls
- •30.6 Conclusion
- •References
- •31: Anterior Component Separation Techniques
- •31.1 Introduction
- •31.2.1 Overview
- •31.2.2 Evolution
- •31.2.3 Technique
- •31.2.4 Outcomes
- •31.2.5 Challenges and Pitfalls
- •31.3.1 Overview
- •31.3.2 Evolution
- •31.3.3 Technique
- •31.3.4 Outcomes
- •31.3.5 Challenges and Pitfalls
- •31.4.1 Overview
- •31.4.2 Evolution
- •31.4.3 Technique
- •31.4.4 Outcomes
- •31.4.5 Challenges and Pitfalls
- •31.5 Conclusion
- •References
- •32: Endoscopic Component Separation Techniques
- •32.1 Background/Historical Perspective
- •32.2 Indications for ECS
- •32.3 Contraindications for ECS
- •32.4 Operative Steps
- •32.4.1 Preoperative Preparation
- •32.4.2 Techniques of ECS
- •32.4.3 Operative Technique
- •32.4.3.1 Transfascial Approach
- •32.4.3.3 Endoscopic Subcutaneous CS Approach
- •32.4.4 Pearls and Pitfalls
- •32.4.5 Evaluation of Results
- •32.5 Conclusion
- •References
- •33: Alternate Methods to Components Separation
- •33.1 Introduction
- •33.2 Operative Technique
- •33.2.3 Step Three: Create the Peritoneal Flaps
- •33.2.4 Step Three: Develop the Sublay Plane
- •33.2.5 Step Four: Close the Peritoneal Cavity
- •33.2.6 Step Five: Insert the Mesh
- •33.2.7 Step Six: Complete the Fascial Closure
- •33.3 Postoperative Complications
- •References
- •34: Plastic Surgery Considerations for Abdominal Wall Reconstruction
- •34.1 Introduction
- •34.2 Perforator Preservation
- •34.3 Skin Management
- •34.3.1 Panniculectomy
- •34.4 Dead Space Obliteration
- •34.5 Tissue Expansion
- •34.7 Negative Pressure Wound Therapy
- •34.7.2 Incisional Negative Pressure Wound Therapy
- •34.8 Conclusion
- •References
- •35: Robotic Transabdominal Preperitoneal (rTAPP) Hernia Repair for Ventral Hernias
- •35.1 Introduction
- •35.1.1 Surgical Anatomy
- •35.1.2 Preoperative Considerations
- •35.2 r-TAPP Hernia Repair for Umbilical or Small Mid-Abdominal Incisional Hernia Repair
- •35.2.1 Patient Positioning
- •35.2.2 Port Positioning, Docking, and Instrumentation
- •35.2.4 Primary Closure of Defect
- •35.3 rTAPP Repair of Atypical Hernias
- •35.3.1 Introduction
- •35.4 rTAPP Repair of Suprapubic Hernias
- •35.4.1 Patient Positioning, Trocar Placement, and Docking
- •35.4.2 Operative Steps
- •35.5 rTAPP Repair of Morgagni Hernias
- •35.5.1 Clinical Anatomy
- •35.5.2 Patient Positioning, Trocar Placement, and Docking
- •35.5.3 Operative Steps
- •35.6 Conclusion
- •References
- •36: Robotic IPOM-Plus Repair
- •36.1 Introduction
- •36.3 Surgical Technique
- •36.3.1 Patient Positioning
- •36.3.2 Trocar Placement
- •36.3.3 Docking
- •36.3.4 Adhesiolysis
- •36.4 Closure of the Defect
- •36.4.2 Closure of the Port Defects
- •36.5 The da Vinci Xi
- •36.6 Pearls
- •References
- •37: Laparoscopic Closure of Defect
- •37.1 Introduction
- •37.2 Concept of Defect Closure
- •37.2.1 Abdominal Wall Mechanics
- •37.2.2 Functional and Dynamic Repair
- •37.3 Advantages of Defect Closure
- •37.4 Disadvantages of Defect Closure
- •37.5 Patient Selection
- •37.7 Summary
- •References
- •38: Treatment of Incarcerated and Strangulated Ventral and Incisional Hernias
- •38.1 Introduction
- •38.2 Natural History
- •38.3 Clinical Presentation and Diagnosis
- •38.4 Surgical Management
- •38.4.1 Open Repair
- •38.4.2 Laparoscopic Repair
- •38.4.4 Contaminated Operative Field
- •38.5 Summary
- •References
- •39: Treatment of Atypical Hernias
- •39.1 Introduction
- •39.2 Preoperative Planning
- •39.3 Subxiphoid Hernias
- •39.3.1 Surgical Anatomy
- •39.3.2 Open Repair
- •39.3.3 Laparoscopic Repair
- •39.4 Subcostal Hernias
- •39.5 Suprapubic Hernias
- •39.5.1 Surgical Anatomy
- •39.5.2 Open Repair
- •39.5.3 Laparoscopic Repair
- •39.6 Flank Hernias
- •39.6.1 Surgical Anatomy
- •39.6.2 Open Repair
- •39.6.3 Laparoscopic Repair
- •39.6.4 Extraperitoneal Repair
- •39.7 Additional Considerations for Atypical Hernias
- •39.7.1 Tissue Sealant Fixation of Mesh
- •39.7.2 Bone Anchor Fixation of Mesh
- •39.8 Robotic Hernia Repair
- •References
- •40: Umbilical Hernias
- •40.1 Introduction
- •40.2 Elective Presentation
- •40.2.1 Management Strategies
- •40.3 Special Circumstances
- •40.3.1 Acute
- •40.3.2 Concomitant Repair
- •40.3.3 Cirrhosis
- •40.3.4 Pregnancy
- •40.4 Future Needs
- •40.5 Conclusions
- •References
- •41: Diastasis Recti
- •41.1 Introduction
- •41.2 Anatomy
- •41.3 Etiology
- •41.4 Diagnosis
- •41.5 Treatment
- •41.5.1 Exercise
- •41.5.2 Abdominoplasty
- •41.5.3 Plication of the Linea Alba
- •41.5.4 Fascial Plication and Onlay Mesh
- •41.5.5 Retrorectus Repair with Sublay Mesh
- •41.6 Endoscopic/Laparoscopic
- •41.7 Complications
- •41.8 Summary
- •References
- •42: Evisceration and Dehiscence
- •42.1 Introduction
- •42.2 Incidence and Risk Factors Relating to Dehiscence/Evisceration
- •42.2.1 Patient
- •42.2.2 Operation
- •42.2.3 Surgical Technique
- •42.2.4 Postoperative Period
- •42.4 Outcomes of Patients
- •References
- •43: Treatment of the Open Abdomen
- •43.1 Introduction
- •43.2.2 Damage Control Surgery (DCS)
- •43.3 Temporary Abdominal Closure Techniques
- •43.3.1 Historical Perspective
- •43.3.1.1 Skin Only Closure and Loose Packing
- •43.3.1.2 Esmarch Closure
- •43.3.1.3 Zipper Closure
- •43.3.2 Current Methods of Temporary Abdominal Closure
- •43.3.2.1 Silos, e.g., Bogota Bag
- •43.3.2.3 Negative Pressure Wound Therapy (NPWT)
- •43.3.2.6 Bridging Mesh and Planned Hernia
- •43.4.1 Delayed Primary Fascial Closure
- •43.4.2 Effect of Temporary Abdominal Closure Method on Fascial Closure Rate
- •43.4.3 Component Separation
- •43.5 Complications
- •43.6 Nutritional Considerations
- •43.7 Conclusions
- •References
- •44: Parastomal Hernia
- •44.1 Introduction
- •44.2 Diagnose and Incidence
- •44.3 Symptoms, Patient Information and Risk Factors
- •44.6 Treatment Options and Outcomes
- •44.7 Mesh Types
- •44.8 Prevention of Parastomal Hernia
- •44.9 Summary
- •References
- •45: Progressive Preoperative Pneumoperitoneum (PPP)
- •45.1 Introduction
- •45.3 Loss of Domain, Pathophysiology
- •45.5 Hernia Surgery with Loss of Domain
- •45.6 Preoperative Progressive Pneumoperitoneum
- •45.7 Objectives of the PPP
- •45.8 PPP Physiology
- •45.10 Preparing for PPP
- •45.12 Conclusions
- •45.13 Clinical Case
- •References
- •46: Botulinum Toxin Use in Complex Abdominal Wall Hernias
- •46.1 Introduction
- •46.2.1 Preclinical Studies
- •46.2.2 Clinical Observations
- •46.3 Technique
- •46.5 Proposed Indications
- •46.6 Future Directions
- •46.7 Conclusions
- •References
- •47: Hernia Repair in Undeserved Areas
- •47.1 Epidemiology
- •47.2 Operative Technique
- •47.2.1 The Use of Low-Cost Mesh
- •47.2.2 Logistics and Education
- •References
- •48: Social Media and Education in Hernia Repair
- •48.1 Introduction
- •48.2 Social Media: Background
- •48.3 International Hernia Collaboration
- •48.4 Interactive Learning
- •48.7 Interdisciplinary Collaboration
- •48.8 Conclusion
- •References
- •49: Robotic Ventral Hernia Repair
- •49.1 Introduction
- •49.2 Overview of Current Literature
- •49.3 Patient Selection
- •49.4 Surgical Technique
- •49.5 Double-Dock Approach
- •49.6 Single-Dock Techniques
- •49.6.1 Single-Dock Retromuscular Repair
- •49.6.2 Single-Dock Preperitoneal Repair
- •49.6.3 Single-Dock Epigastric and Suprapubic Repair
- •49.7 Outcomes
- •49.8 Conclusion
- •References
- •50: Management of Mesh Infection
- •50.1 Introduction
- •50.2 Epidemiology and Pathogenesis
- •50.3 Mesh Material and Structure
- •50.4 Management of Mesh Infections
- •50.4.1 Mesh Salvage
- •50.4.2 Mesh Type
- •50.4.3 Mesh Position
- •50.4.4 Percutaneous Drainage
- •50.4.5 Negative Pressure Wound Therapy
- •50.4.6 Mesh Excision
- •50.5 Prevention of Mesh Infection
- •50.6 Conclusion
- •References
- •Index

Contributors
xiii
Brian Jacob, M.D. Icahn School of Medicine at Mount Sinai, New York, NY, USA
Jeffrey E. Janis, M.D., F.A.C.S. Department of Plastic Surgery, The Ohio State University
Wexner Medical Center, Columbus, OH, USA
Johannes Jeekel, M.D., Ph.D. Neuroscience, Erasmus University Medical Center, Rotterdam,
Zuid Holland, The Netherlands
Kristian K. Jensen, M.D. Digestive Disease Center, Bispebjerg Hospital, Copenhagen,
Denmark
Lars N. Jorgensen, M.D., Dr.M.Sc. Bispebjerg Hospital, Digestive Disease Center,
Copenhagen, Denmark
Ibrahim Khansa, M.D. Department of Plastic Surgery, The Ohio State University Wexner
Medical Center, Columbus, OH, USA
Andreas Koch, M.D., F.A.C.S. Day Surgery and Hernia Center, Cottbus, Germany
Leonard Frederik Kroese, M.D. Department of Surgery, Erasmus University Medical
Center, Rotterdam, Zuid Holland, The Netherlands
David M. Krpata, M.D. Department of General Surgery, Cleveland Clinic, Cleveland, OH,
USA
Johan Frederik Lange, M.D., Ph.D. Department of Surgery, Erasmus University Medical
Center, Rotterdam, Zuid Holland, The Netherlands
Havenziekenhuis Rotterdam, Rotterdam, Zuid Holland, The Netherlands
Mike K. Liang, M.D. Department of Surgery, University of Texas Health Science Center at
Houston, Houston, TX, USA
Adriana Hernández López, M.D., F.A.C.S. Department of General Surgery, The American
British Cowdray Hospital IAP, Mexico City, Distrito Federal, Mexico
Ian T. MacQueen, M.D. Department of Surgery, David Geffen School of Medicine at the
University of California, Los Angeles, Los Angeles, CA, USA
Mohammed Al Mahroos, M.D., F.R.C.S. Department of Surgery, McGill University
Health Centre, Montreal, QC, Canada
Arnab Majumder, M.D. Department of Surgery, University Hospitals Cleveland Medical
Center, Cleveland, OH, USA
Robert G. Martindale, M.D., Ph.D. Department of Surgery Oregon Health and Science
University, Portland, OR, USA
Kendall R. McEachron, M.D. Department of Surgery, University of Minnesota, Minneapolis,
MN, USA
Justin M. Milligan, M.D. Department of General Surgery, New Hanover Regional Medical
Center, Wilmington, NC, USA
Agneta Montgomery, Ph.D. Department of Surgery, Skåne University Hospital, Malmö,
Skåne University Hospital, Malmö, Sweden
Alexandra M. Moore, M.D. Department of Surgery, David Geffen School of Medicine at
UCLA, Los Angeles, CA, USA
Andrea Morlacchi, M.D. University of Insubria, Istituto Clinico Sant’Ambrogio, Center of
Research and High Specialization for the Pathologies of Abdominal Wall and Surgical
Treatment and Repair of Abdominal Hernia, Milan, Italy

xiv
Filip Muysoms, M.D., Ph.D. Dienst Algemene Heelkunde, Maria Middeleares Hospital,
Ghent, Belgium
Maurice Y. Nahabedian, M.D., F.A.C.S. Department of Plastic Surgery, Georgetown
University Hospital, Washington, DC, USA
Pär Norden Department of Surgical and Perioperative Sciences, Umeå University, Umeå,
Sweden
Yuri William Novitsky, M.D., F.A.C.S. Department of Surgery, University Hospitals
Cleveland Medical Center, Cleveland, OH, USA
Sean B. Orenstein, M.D. Department of Surgery, Oregon Health & Science University,
Portland, OR, USA
Eric M. Pauli, M.D. Department of Surgery, Penn State Hershey Medical Center, Hershey,
PA, USA
William F. Powers IV, M.D. Department of Surgery, New Hanover Regional Medical
Center, Wilmington, NC, USA
Charles D. Procter Jr., M.D., F.A.C.S., F.A.S.M.B.S. Department of Surgery, Piedmont
Atlanta Hospital, Atlanta, GA, USA
Archana Ramaswamy, M.D. Department of Surgery, University of Minnesota, Minneapolis
VA Medical Center, Minneapolis, MN, USA
Contributors
Bruce Ramshaw, M.D., F.A.C.S. Department of Surgery, University of Tennessee Medical
Center, Knoxville, TN, USA
Michael J. Rosen, M.D. Department of General Surgery, Cleveland Clinic, Cleveland, OH,
USA
John Scott Roth, M.D., F.A.C.S. Division of General Surgery, Department of Surgery,
University of Kentucky College of Medicine, Lexington, KY, USA
Estefanía J. Villalobos Rubalcava, M.D. Department of General Surgery, The American
British Cowdray Hospital IAP, Mexico City, Distrito Federal, Mexico
David L. Sanders, BSc, MBCHB, FRCS, MD, PG Department of Upper GI Surgery, North
Devon District Hospital, Raleigh Park, Barnstaple, UK
Yasmine Shafik, M.B.B.S. King Abdulaziz Medical City, Ministry of the National Guard
Health Affairs, Jeddah, Saudi Arabia
Charles P. Shahan, M.D., M.S. Department of Surgery, University of Tennessee Health
Science Center, Memphis, TN, USA
Aali J. Sheen, MD, FRCS (Eng), FRCS (Gen Surg) Department of General Surgery, Central
Manchester University, Hospital NHS Foundation Trust, Oxford Road, Manchester, UK
Department of Healthcare Sciences, Manchester Metropolitan University, Oxford Road,
Manchester, UK
Maarten Simons, M.D., Ph.D. Department of Surgery, OLVG Hospital Amsterdam,
Amsterdam, The Netherlands
Kyle Stigall, B.S. University of Kentucky College of Medicine, Lexington, KY, USA
Nathaniel F. Stoikes, M.D. Department of Minimally Invasive Surgery, University of
Tennessee Health Science Center, Memphis, TN, USA

Contributors
xv
Paul Tenzel, M.D. Department of Surgery, New Hanover Regional Medical Center,
Wilmington, NC, USA
Shirin Towfigh, M.D., F.A.C.S. Department of Surgery, Beverly Hills Hernia Center, Cedars
Sinai Medical Center, Beverly Hills, CA, USA
Hanh Minh Tran, MA, MD, PhD, MBA, FRCS (Eng) The Sydney Hernia Specialists
Clinic, Sydney, NSW, Australia
Mai Dieu Tran, D.M.D. The Sydney Hernia Specialists Clinic, Sydney, NSW, Australia
Bruce R. Tulloh, M.S., F.R.A.C.S., F.R.C.S.Ed. Department of Upper GI Surgery, Royal
Infirmary of Edinburgh, Edinburgh, Scotland, UK
Gabriëlle H. van Ramshorst, M.D., Ph.D. VU University Medical Center, Amsterdam, The
Netherlands
Melina Vassiliou, M.D. F.R.C.S.C., M.Ed. Department of Surgery, McGill University
Health Centre, Montreal, QC, Canada
Guy Voeller, M.D. Department of Surgery, University of Tennessee Health Science Center,
Memphis, TN, USA
Kevin B. Walker, M.D. Department of Anesthesiology, Greenville Health System, Greenville,
SC, USA
Jeremy A. Warren Greenville Health System, University of South Carolina School of
Medicine—Greenville, Greenville, SC, USA
David Webb Jr., M.D. Department of Surgery, University of Tennessee Health Science
Center, Memphis, TN, USA
Adam Weir, M.B.B.S., Ph.D., Doctor. Aspetar Orthopaedic and Sports Medicine Hospital,
Doha, Qatar
Alexandra Weir, M.D. Department of Surgery, Maricopa Integrated Health System, Phoenix,
AZ, USA
Zachary F. Williams, M.D. Department Surgery, New Hanover Regional Medical Center,
Wilmington, NC, USA
Jerrold Young, M.D. Hernia Institute of Florida, Miami, FL, USA
DeWitt Daughtery Department of Surgery, University of Miami Miller School of Medicine,
Miami, FL, USA
Benjamin Zendejas, M.D., M.Sc. Department of Surgery, Mayo Clinic, Rochester, MN, USA
Martin D. Zielinski, M.D. Department of Surgery, Mayo Clinic, Rochester, MN, USA
Adrian Murillo Zolezzi, M.D. Department of General Surgery, The American British
Cowdray Hospital IAP, Mexico City, Distrito Federal, Mexico
Terri Zomerlei, M.D. Department of Plastic Surgery, The Ohio State University Wexner
Medical Center, Columbus, OH, USA

The Biology of Hernia Formation
Nadia A. Henriksen, Kristian K. Jensen,
and Lars N. Jorgensen
1.1 Introduction
Hernia formation is a multifactorial process involving
endogenous factors including age, gender, anatomic variations, and inheritance and exogenous factors such as smoking, comorbidity, and surgical factors (Fig. 1.1) [1]. However,
these factors alone do not explain why some develop abdominal wall hernias. Already in 1924, the anatomist Sir Arthur
Keith proposed that surgeons should try to perceive tendons
and fascia as living structures in order to understand the hernia disease properly [2]. Research on synthesis and breakdown of connective tissue in relation to pathophysiological
mechanisms of hernia formation is important to comprehend
herniogenesis and to select a proper treatment strategy for
the individual patient.
1.2 The Connective Tissue
1
1.2.1 Collagen
Collagen is synthesized by fibroblasts in a complex process
involving extensive modifications before the mature collagen fibril is formed (Fig. 1.2) [4]. The amino acid hydroxyproline is almost unique for collagen and is used for
quantitation of collagen in certain tissues. The collagen protein consists of a triple helix, and the enzyme lysyl oxidase
(LOX) mediates the formation of both intra- and intermolecular cross-links between the collagen fibrils contributing
to the special strength and stability of the collagen protein.
There are 28 genetically different types of human collagen [5]. The skin and fascia consist mainly of type I collagen
with smaller amounts of type III and V collagen. The same
collagen fiber can comprise both type I and III collagens.
The more type III collagen relative to type I collagen, the
thinner and weaker the fiber. Type V collagen is essential
during collagen maturation, as it is involved in the initiation
of fibril formation.
The connective tissue comprises the extracellular matrix
(ECM) and the cells within. The ECM contains proteoglycans and proteins, such as collagen and elastin, which
together form a dense network important for tissue stability.
In healthy tissue, regeneration of ECM involves a controlled
balance between degradation of old and damaged proteins
and synthesis of new ones [3]. In hernia patients, this balance
may be disturbed leading to altered tissue turnover and
impaired tissue quality.
N.A. Henriksen, M.D., Ph.D. (*)
Department of Surgery, Zealand University Hospital,
Lykkebaekvej 1, Koege 4600, Denmark
e-mail: nadiahenriksen@gmail.com
K.K. Jensen, M.D. • L.N. Jorgensen, M.D., Dr.M.Sc.
Digestive Disease Center, Bispebjerg Hospital,
Bispebjerg Bakke 23, Copenhagen NV 2400, Denmark
e-mail: mail@kristiankiim.dk; larsnjorgensen@hotmail.com
© Springer International Publishing Switzerland 2017
W.W. Hope et al. (eds.), Textbook of Hernia, DOI 10.1007/978-3-319-43045-4_1
1.2.2 Matrix Metalloproteinases
Matrix metalloproteinases (MMPs) constitute a family of 23
zinc-dependent proteases important for collagen remodeling.
The MMPs are divided into groups based on their structure
and function. The most important with regard to hernias and
collagen are the collagenases (MMP-1, MMP-8, and MMP-
13) and the gelatinases (MMP-2 and MMP-9). The collagenases unwind the triple-helical collagens into gelatin, and
then the gelatinases cleave the denatured collagen [6].
1.3 Inheritance and Genetics
Some patients seem to be especially susceptible to hernia
development [7]. Patients operated on for abdominal aortic
aneurysms have a higher risk of developing an incisional
hernia postoperatively as opposed to patients operated on for
1

2
N.A. Henriksen et al.
Fig. 1.1 Endogenous and
exogenous factors involved in
hernia formation (Reproduced
with permission from: Jansen
PL et al. The biology of
hernia formation. Surgery
2004)
endogenous
triggers
age
gender
adipositas
predisposition
exogenous
triggers
smoking
malnutrition
steroids
macrophages
fibroblasts
lymphocytes
proteases
cytokines
collagen
metabolism
restitution
hernia
relapse
Fig. 1.2 Collagen synthesis and maturation in healthy tissue and in patients with hernias (Reproduced with permission from: Henriksen NA et al.
Connective tissue alteration in abdominal wall hernia. Br J Surg 2011)
aortoiliac occlusive disease [8]. Patients with rare connective
tissue disorders such as Marfan’s syndrome and Ehlers–
Danlos syndrome have an earlier onset and a higher risk of
hernia development [9–11]. Further, patients with direct
inguinal, bilateral inguinal, or recurrent inguinal hernia are
at higher risk of ventral hernia formation [12–14], suggesting a systemic predisposition to hernia formation.
Emerging evidence suggests that inguinal hernias represent an inherited disease; however the inheritance pattern
remains to be clarified [15]. There is increased risk of
developing an inguinal hernia, if a first-degree relative has a
history of inguinal hernia repair. Most of the literature on
groin hernia inheritance includes hernias in children and
does not distinguish between indirect and direct hernias.

1 The Biology of Hernia Formation
3
Furthermore, the strongest inherited predisposition for hernia disease is found in females with inguinal hernias [16,
17]. As groin hernias in children and females most often are
of the indirect type [18, 19], the demonstrated inheritance
patterns may be associated with indirect inguinal hernias.
Thus, it is possible that it is the anatomic defect of a patent
processus vaginalis that is inherited and not a defect in collagen turnover.
It has not yet been possible to identify gene defects
involved in hernia formation for clinical use. A polymorphism in the regulatory region of the COL1A1 gene and a
missense point mutation in the elastin gene have been demonstrated in a smaller population of patients with both indirect and direct inguinal hernias [20, 21]. A recent
genome-wide association study including more than 5000
patients with a history of indirect or direct inguinal hernia
repair identified four genetic susceptibility loci for inguinal
hernia including WT1, EFEMP1, EBF2, and ADAMTS6 [22].
WT1 and EFEMP1 may be important in connective tissue
turnover through their effect on ECM enzymes including
MMPs. The ADAMTS proteins are related to MMPs in
structure and function and play a role in ECM homeostasis.
A smaller genome profiling study analyzing fascia and skin
biopsies of patients with recurrent incisional hernias found
an altered expression of the GREM1 gene [23]. GREM1 is a
regulator of tissue differentiation and related to fibrosis,
which could explain its association to incisional hernia recurrence. Furthermore, altered gene expressions were found for
COL1A2, COL3A2, and LOX in patients with recurrent
incisional hernias.
1.4 Role of Collagen Turnover in Hernia
Formation
Studies on the morphology of the fascial tissue surrounding
inguinal hernias found lower total collagen content in
patients with inguinal hernias compared with individuals
without inguinal hernia [24–29]. Furthermore, the fascial
collagen architecture appears altered as described histologically by an uneven distribution of collagen fibers, thinner
collagen fibers, inflammation, and degeneration of muscle
fibers [24, 30–32].
The collagen quality seems to be more important than the
collagen quantity. In fascia from hernia patients, there is less
type I collagen relative to type III collagen resulting in a
decreased type I to III collagen ratio and thinner collagen
fibers with less tensile strength [33, 34]. These alterations are
also present at the mRNA level suggesting that the problem
appears during collagen synthesis [35]. A decreased type I to
III collagen ratio is also present in skin biopsies from hernia
patients, suggesting that the connective tissue alterations are
systemic [36].
The reason for the altered collagen quality and the
decreased type I to III ratio remains to be clarified. It has
been suggested that altered activity levels of the enzymes
involved in the collagen synthesis and maturation process
may play a role. Decreased activity of lysyl oxidase results in
decreased cross-linking of collagen fibrils [37], which is
essential for collagen strength and stability (Fig. 1.2). In
addition, recent studies found systemically decreased turnover of type V collagen both in patients with inguinal hernia
and in patients with incisional hernia. Type V collagen is
necessary for initiation of collagen fibril formation, and
decreased levels of type V collagen may thereby impair the
collagen synthesis [38, 39].
Alternatively, the reduced collagen quality may be associated with altered ECM homeostasis. MMP-2 is increased
both locally and systemically in men with inguinal hernia,
suggesting a higher MMP-2 activity causing increased collagen breakdown [40–42]. No convincing results exist presently with regard to other MMPs or MMP involvement in the
development of incisional hernias.
Overall, the collagen alterations found in patients with
inguinal hernias are more pronounced in patients with direct
hernias as opposed to patients with indirect hernias, suggesting that an imbalance in collagen turnover is especially
important in the formation of direct hernias.
1.5 Wound Healing in Hernia Patients
The wound healing process is complex and involves important steps in ECM turnover, which are important in the
understanding of secondary hernia formation, that are incisional or recurrent hernias.
First step of the wound healing process includes vasoconstriction and clot formation secondary to activation of both
platelets and the coagulation cascade. The following inflammatory phase initiates the immune response in order to eliminate bacteria from the wound. A wound colonized with
bacteria at a high tissue concentration will not heal properly
as illustrated by the fact that surgical site infection is a wellknown risk factor for incisional hernia formation [43].
During the inflammatory response, several growth factors
are involved, which among others activate fibroblasts leading
to the proliferative phase of wound healing beginning on day
3. This involves fibroblast and myofibroblast proliferation,
followed by migration, leading to wound contraction. The
fibroblasts produce type I and III procollagens and deposit
ECM. In unwounded dermis, there is 80 % type I collagen
and 20 % type III collagen, whereas there is 40 % type III
collagen in wounded dermis, resulting in thinner collagen
fibers with less strength. Lastly, the remodeling phase takes
place and may last up to 2 years. During this phase, the
immature type III collagen is replaced by the mature and

4
N.A. Henriksen et al.
stronger type I collagen [44]. Any imbalance in this process
may lead to hernia formation. Interestingly, the type I to III
collagen ratio is even more decreased in patients with secondary hernias as compared with patients with primary hernias, suggesting that hernia recurrence is also associated
with collagen imbalance [36].
The final strength of the wound depends on the respective
anatomic region, and the duration and quality of the wound
healing process. However, surgically traumatized fascial or
aponeurotic tissues never regain their original strength, indicating that a midline aponeurotic scar is relatively weak
despite uncomplicated healing conditions. It has been demonstrated that minor mechanical stress impacts positively on
wound healing in various tissues. Sutured wounds of aponeurosis benefit from mechanical stress in terms of organization and alignment of collagen fibrils as well as enhanced
maturation of collagen cross-linking [45].
Apart from infection, other exogenous factors may be
involved in the development of secondary hernias. Smoking
is a well-known risk factor for both incisional and recurrent
inguinal hernias [46, 47]. In smokers, the function of the
fibroblasts is compromized and the collagen synthesis is
decreased leading to delayed wound healing, possible wound
dehiscence, and ultimately hernia formation [48, 49].
Future research on the biology of hernia formation may
focus on developing serological markers enabling identification of patients at high risk of developing secondary hernias,
thus opening up for preventive measures such as prophylactic mesh placement after elective non-hernia surgery.
1.6 Main Points
• Hernia formation is multifactorial
• Inguinal hernias represent inherited disease, but both the
inheritance pattern and involved gene defects remain to
be clarified
• Type I to III collagen ratio is decreased in patients with
hernias resulting in thinner and weaker collagen fibers
• The connective tissue alterations found in patients with
hernias are pronounced in patients with direct and recur-
rent inguinal hernias as opposed to patients with indirect
inguinal hernias
References
1. Jansen PL, Mertens PP, Klinge U, Schumpelick V. The biology of
hernia formation. Surgery. 2004;136(1):1–4. doi:10.1016/j.
surg.2004.01.004.
2. Read RC. Arthur Keith, the anatomist who envisioned herniosis.
Hernia. 2007;11(6):469–71. doi:10.1007/s10029-007-0273-9.
3. Stamenkovic I. Extracellular matrix remodelling: the role of matrix
metalloproteinases. J Pathol. 2003;200(4):448–64. doi:10.1002/
path.1400.
4. Henriksen NA, Yadete DH, Sorensen LT, Agren MS, Jorgensen
LN. Connective tissue alteration in abdominal wall hernia. Br
J Surg. 2011;98(2):210–9. doi:10.1002/bjs.7339.
5. Kadler KE, Baldock C, Bella J, Boot-Handford RP. Collagens at a
glance. J Cell Sci. 2007;120(Pt 12):1955–8. doi:10.1242/jcs.03453.
6. Murphy G, Nagase H. Progress in matrix metalloproteinase
research. Mol Aspects Med. 2008;29(5):290–308. doi:10.1016/j.
mam.2008.05.002.
7. Zoller B, Ji J, Sundquist J, Sundquist K. Shared and nonshared
familial susceptibility to surgically treated inguinal hernia, femoral hernia, incisional hernia, epigastric hernia, and umbilical
hernia. J Am Coll Surg. 2013;217(2):289–99.e1. doi:10.1016/j.
jamcollsurg.2013.04.020.
8. Henriksen NA, Helgstrand F, Vogt KC, Jorgensen LN, Bisgaard
T. Risk factors for incisional hernia repair after aortic reconstructive surgery in a nationwide study. J Vasc Surg. 2013;57(6):1524–
30e1–3. doi:10.1016/j.jvs.2012.11.119.
9. Thomas GP, Purkayastha S, Athanasiou T, Darzi A. General surgical manifestations of Marfan’s syndrome. Br J Hosp Med.
2008;69(5):270–4.
10. Liem MS, van der Graaf Y, Beemer FA, van Vroonhoven
TJ. Increased risk for inguinal hernia in patients with Ehlers-Danlos
syndrome. Surgery. 1997;122(1):114–5.
11. Girotto JA, Malaisrie SC, Bulkely G, Manson PN. Recurrent ventral herniation in Ehlers-Danlos syndrome. Plast Reconstr Surg.
2000;106(7):1520–6.
12. Ruhl CE, Everhart JE. Risk factors for inguinal hernia among
adults in the US population. Am J Epidemiol. 2007;165(10):1154–
61. doi:10.1093/aje/kwm011.
13. Henriksen NA, Sorensen LT, Bay-Nielsen M, Jorgensen LN. Direct
and recurrent inguinal hernias are associated with ventral hernia
repair: a database study. World J Surg. 2013;37(2):306–11.
doi:10.1007/s00268-012-1842-3.
14. Alnassar S, Bawahab M, Abdoh A, Guzman R, Al Tuwaijiri T,
Louridas G. Incisional hernia postrepair of abdominal aortic occlusive and aneurysmal disease: five-year incidence. Vascular.
2012;20(5):273–7. doi:10.1258/vasc.2011.oa0332.
15. Burcharth J, Pommergaard HC, Rosenberg J. The inheritance of
groin hernia: a systematic review. Hernia. 2013;17(2):183–9.
doi:10.1007/s10029-013-1060-4.
16. Jones ME, Swerdlow AJ, Griffith M, Goldacre MJ. Risk of congenital inguinal hernia in siblings: a record linkage study. Paediatr
Perinat Epidemiol. 1998;12(3):288–96.
17. Sawaguchi S, Matsunaga E, Honna T. A genetic study on indirect
inguinal hernia. Jinrui Idengaku Zasshi. 1975;20(3):187–95.
18. Rowe MI, Copelson LW, Clatworthy HW. The patent processus
vaginalis and the inguinal hernia. J Pediatr Surg. 1969;4(1):102–7.
19. Koch A, Edwards A, Haapaniemi S, Nordin P, Kald A. Prospective
evaluation of 6895 groin hernia repairs in women. Br J Surg.
2005;92(12):1553–8. http://dx.doi.org/10.1002/bjs.5156.
20. Sezer S, Simsek N, Celik HT, Erden G, Ozturk G, Duzgun AP, et al.
Association of collagen type I alpha 1 gene polymorphism with inguinal
hernia. Hernia. 2014;18(4):507–12. doi:10.1007/s10029-013-1147-y.
21. Rodrigues C, Yoo J, Rodrigues Jr A. Elastin (ELN) gene point mutation in patients with inguinal hernia. Genet Mol Biol. 2006;29(1):
45–6. http://dx.doi.org/10.1590/S1415-47572006000100009.
22. Jorgenson E, Makki N, Shen L, Chen DC, Tian C, Eckalbar WL,
et al. A genome-wide association study identifies four novel susceptibility loci underlying inguinal hernia. Nat Commun. 2015;6:10130.
doi:10.1038/ncomms10130.
23. Calaluce R, Davis JW, Bachman SL, Gubin MM, Brown JA, Magee
JD, et al. Incisional hernia recurrence through genomic profiling: a pilot
study. Hernia. 2013;17(2):193–202. doi:10.1007/s10029-012-0923-4.
24. Wagh PV, Leverich AP, Sun CN, White HJ, Read RC. Direct inguinal herniation in men: a disease of collagen. J Surg Res.
1974;17(6):425–33.

1 The Biology of Hernia Formation
5
25. Rodrigues Jr AJ, Rodrigues CJ, da Cunha AC, Jin Y. Quantitative
analysis of collagen and elastic fibers in the transversalis fascia in
direct and indirect inguinal hernia. Rev Hosp Clin Fac Med Sao
Paulo. 2002;57(6):265–70.
26. Ozdogan M, Yildiz F, Gurer A, Orhun S, Kulacoglu H, Aydin
R. Changes in collagen and elastic fiber contents of the skin, rectus
sheath, transversalis fascia and peritoneum in primary inguinal hernia patients. Bratisl Lek Listy. 2006;107(6–7):235–8.
27. Casanova AB, Trindade EN, Trindade MR. Collagen in the transversalis fascia of patients with indirect inguinal hernia: a casecontrol study. Am J Surg. 2009;198(1):1–5. doi:10.1016/j.
amjsurg.2008.07.021.
28. Pans A, Albert A, Lapiere CM, Nusgens B. Biochemical study of
collagen in adult groin hernias. J Surg Res. 2001;95(2):107–13.
doi:10.1006/jsre.2000.6024.
29. Meyer AL, Berger E, Monteiro Jr O, Alonso PA, Stavale JN,
Goncalves MP. Quantitative and qualitative analysis of collagen
types in the fascia transversalis of inguinal hernia patients. Arq
Gastroenterol. 2007;44(3):230–4.
30. Szczesny W, Glowacka K, Marszalek A, Gumanski R, Szmytkowski
J, Dabrowiecki S. The ultrastructure of the fascia lata in hernia
patients and healthy controls. J Surg Res. 2012;172(1):e33–7.
doi:10.1016/j.jss.2011.09.004.
31. Amato G, Agrusa A, Romano G, Salamone G, Gulotta G, Silvestri
F, et al. Muscle degeneration in inguinal hernia specimens. Hernia.
2012;16(3):327–31. doi:10.1007/s10029-011-0890-1.
32. Friedman DW, Boyd CD, Norton P, Greco RS, Boyarsky AH,
Mackenzie JW, et al. Increases in type III collagen gene expression
and protein synthesis in patients with inguinal hernias. Ann Surg.
1993;218(6):754–60.
33. Rosch R, Junge K, Knops M, Lynen P, Klinge U, Schumpelick
V. Analysis of collagen-interacting proteins in patients with incisional hernias. Langenbecks Arch Surg. 2003;387(11–12):427–32.
doi:10.1007/s00423-002-0345-3.
34. Klinge U, Si Z, Zheng H, Schumpelick V, Bhardwaj R, Klosterhalfen
B. Collagen I/III and matrix metalloproteinases (MMP) 1 and 13 in
the fascia of patients with incisional hernias. J Invest Surg.
2001;14(1):47–54. http://dx.doi.org/10.1080/089419301750072202.
35. Si Z, Bhardwaj R, Rosch R, Mertens PR, Klosterhalfen B, Klinge
U. Impaired balance of type I and type III procollagen mRNA in
cultured fibroblasts of patients with incisional hernia. Surgery.
2002;131(3):324–31.
36. Peeters E, De Hertogh G, Junge K, Klinge U, Miserez M. Skin as
marker for collagen type I/III ratio in abdominal wall fascia. Hernia.
2013. doi:10.1007/s10029-013-1128-1.
37. Pascual G, Rodriguez M, Mecham RP, Sommer P, Bujan J, Bellon
JM. Lysyl oxidase like-1 dysregulation and its contribution to direct
inguinal hernia. Eur J Clin Invest. 2009;39(4):328–37.
doi:10.1111/j.1365-2362.2009.02099.x.
38. Henriksen NA, Mortensen JH, Sorensen LT, Bay-Jensen AC, Agren
MS, Jorgensen LN, et al. The collagen turnover profile is altered in
patients with inguinal and incisional hernia. Surgery.
2015;157(2):312–21. doi:10.1016/j.surg.2014.09.006.
39. Henriksen NA, Mortensen JH, Lorentzen L, Agren MS, Bay-Jensen
AC, Jorgensen LN, et al. Abdominal wall hernias-A local manifestation of systemically impaired quality of the extracellular matrix.
Surgery. 2016. doi:10.1016/j.surg.2016.02.011.
40. Jain V, Srivastava R, Jha S, Misra S, Rawat NS, Amla DV. Study of
matrix metalloproteinase-2 in inguinal hernia. J Clin Med Res.
2009;1(5):285–9. doi:10.4021/jocmr2009.12.1281.
41. Smigielski J, Kolomecki K, Ziemniak P, Drozda R, Amsolik M,
Kuzdak K. Degradation of collagen by metalloproteinase 2 in
patients with abdominal hernias. Eur Surg Res. 2009;42(2):118–21.
doi:10.1159/000187643.
42. Pascual G, Rodriguez M, Gomez-Gil V, Trejo C, Bujan J, Bellon
JM. Active matrix metalloproteinase-2 upregulation in the abdominal skin of patients with direct inguinal hernia. Eur J Clin Invest.
2010;40(12):1113–21. doi:10.1111/j.1365-2362.2010.02364.x.
43. Jensen KK, Krarup PM, Scheike T, Jorgensen LN, Mynster
T. Incisional hernias after open versus laparoscopic surgery for
colonic cancer: a nationwide cohort study. Surg Endosc. 2016.
doi:10.1007/s00464-016-4779-z.
44. Velnar T, Bailey T, Smrkolj V. The wound healing process: an overview of the cellular and molecular mechanisms. J Int Med Res.
2009;37(5):1528–42.
45. Oryan A. Role of collagen in soft connective tissue wound healing.
Transplant Proc. 1995;27(5):2759–61.
46. Sorensen L, Friis E, Jorgensen T, Vennits B, Andersen B, Rasmussen
G, et al. Smoking is a risk factor for recurrence of groin hernia.
World J Surg. 2002;26(4):397–400.
47. Sorensen L, Hemmingsen U, Kirkeby L, Kallehave F, Jorgensen L.
Smoking is a risk factor for incisional hernia. Arch Surg.
2005;140(2):119–23. http://dx.doi.org/10.1001/archsurg.140.2.119.
48. Jorgensen LN, Kallehave F, Karlsmark T, Gottrup F. Reduced collagen
accumulation after major surgery. Br J Surg. 1996;83(11): 1591–4.
49. Sorensen LT. Wound healing and infection in surgery: the pathophysiological impact of smoking, smoking cessation, and nicotine
replacement therapy: a systematic review. Ann Surg. 2012;255(6):
1069–79. doi:10.1097/SLA.0b013e31824f632d.

An Introduction to Complex Systems Science and Its Application to Hernia Surgery
Bruce Ramshaw
2.1 Introduction
The scientific paradigm shift from reductionist to complex
systems science began over a century ago. Around the beginning of the twentieth century, physicists started to understand
the incompleteness of Newtonian physics applied to the real
biologic world. During the past century, many other disciplines have begun to make this shift. From the studies of
systems biology to behavioral economics, the principles of a
reductionist, rational, and static scientific understanding of
our world have been found to be inadequate to explain and
improve our dynamic and ever-changing world. Even the
human genome project, with the unmet potential to discover
the blueprint for the cause of and cure for all of our diseases,
found that our genome was constantly adapting and changing and the idea that we could make a major impact on our
health through only genetic engineering was naïve and misguided. Understanding healthcare as a complex biologic system and applying tools that apply to this reality will result in
a global healthcare system that is based on measuring and
improving the value of care we provide.
A more complete understanding of our world through
the application of complex systems science will allow us
to identify the factors that contribute to both positive and
negative outcomes from definable patient processes and
patient subpopulations. These factors are constantly changing and are interconnected with other factors that contribute
to outcomes. If they are tested in isolation, as attempted in
a prospective, randomized, controlled trial, the potential
measurement of the impact of any one factor will be likely
B. Ramshaw, M.D., F.A.C.S. (*)
Department of Surgery, University of Tennessee Medical Center,
1934 Alcoa Highway, Building D, Suite 285, Knoxville,
TN 37920, USA
e-mail: hernia@utmck.edu
2
inaccurate. It would also only apply to the selected group of
people in which that factor was tested and only in the environment in which that experiment was completed. The tools
we have used to attempt to discover static truths in healthcare will need to be replaced by tools from complex systems
science (also known as information or data science) which
should be applied to all patients (no inclusion or exclusion
criteria) in many different local environments.
Where the reductionist scientific method, which attempts
to prove or disprove a hypothesis, assumes the test environment is static, the complex systems tools for discovery are
intended to be applied to a constantly changing world. Basic
principles in complex systems science include the assumption that many factors that are constantly changing and interacting can have a variety of impacts on the subject (a person/
patient) who is considering a variety of treatment options
and will have a variety of potential outcomes based on the
interaction of the factors related to the patient, the treatment
process in that local environment at one particular moment
in time. A change in any one or more of these factors can lead
to a similar or potentially different outcome from the same
treatment option. Rather than attempting to prove or disprove a hypothesis, tools for discovery in complex systems
science are simply designed to improve whatever is measured within a definable process.
These tools for improvement have been applied and
matured most famously in manufacturing, the automobile
industry, for example. A variety of terms have been applied
to improvement tools such as Lean and Six Sigma, but the
basic concept is the same—the desire to achieve continuous
improvement. One significant point needs to be made about
the application of these tools in manufacturing compared
with healthcare. In manufacturing, these tools are typically
applied to one manufacturing process that is producing one
specified product, a 2016 Ford Mustang, for example. In a
manufacturing process, the steps and factors involved can be
controlled and improved by eliminating variation. Statistical
tools include process control charts to identify inappropriate
or unexpected variation. In a biologic process, such as
© Springer International Publishing Switzerland 2017
W.W. Hope et al. (eds.), Textbook of Hernia, DOI 10.1007/978-3-319-43045-4_2
7

8
healthcare, it is impossible to control the variation. Instead,
the process can be managed through iterative measurement
and improvement of value-based outcomes and through the
identification of patterns and subpopulations. The optimal
variety of options for various subpopulations can be determined with nonlinear complex systems tools such as factor
analysis and predictive analytics. Currently, many reductionist tools for improvement (like a single “best practice,” for
example) are being applied to healthcare as if healthcare was
composed of static, mechanical processes instead of the
realty that we are dealing with complex biologic processes
in healthcare.
Another way improvement tools have been generally misapplied in healthcare is their application to subproccesses
without attention to the impact on the value of whole patient
processes. It should be well accepted that the most important
processes to improve are the entire cycles of patient care for
the many definable patient processes. The concept of a whole
patient process includes the time from the moment of first
symptom to the return to a full quality of life (for acute, curable disease) and in some cases for the entire life of the
patient (for chronic, not currently curable disease). The ultimate outcome measure for the entire cycle of care is value, a
combination of costs, quality measures, and outcome measures from the perspective of the patient, such as patient and
family satisfaction with the care process. Until now, essentially all process improvement attempts in healthcare, like
decreasing central line infection or improving safety in the
operating room, have been attempts at improving a subprocess, not the entire cycle of care for a definable patient care
process. In a complex process, when a subprocess is
improved without attention to the whole process, the result is
suboptimization—improvement of a subprocess will not
lead to improvement of the whole process and will predictably have unintended consequences.
The application of complex systems science to hernia disease is demonstrated in applying the principles of valuebased clinical quality improvement (CQI) principles to the
whole cycle of care for a definable patient care process. This
ideally requires a multidisciplinary team to determine the
appropriate factors (patient and treatment variables) that are
most likely to impact the outcomes that would measure
value for a specific care process. By identifying what data
points and outcome measures should be collected, the team
is providing the programming for what goes in to the computing—a computer program providing data analysis and
data visualization. That same team then attempts to interpret
the significance of the analysis and data visualizations to
generate ideas to improve outcomes that measure value.
This example of a team providing the programming of data,
a computer program providing a variety of data analytics
and visualizations from the data entered, and that same
human team then interpreting the output and using that to
B. Ramshaw
Fig. 2.1 Illustration of the human–computer symbiosis for artificial
intelligence applied to healthcare. The human team identifies the context (patient care process) and programs what data and outcomes to
analyze, the computer can perform a variety of analyses and produce
visualizations, and the human team then interprets the analyses and
visualizations to generate ideas for process improvement
generate ideas for improving the patient care process is an
example of the human–computer collaboration that can be
termed artificial intelligence (Fig. 2.1). Computers have
become immensely powerful at beating human beings in
competitions if rules and answers are known and do not
change. IBM’s successful demonstration of their computer
capabilities at beating the world’s best chess player (IBM’s
Deep Blue vs. Garry Kasparov) and Jeopardy’s greatest
champions (IBM’s Watson vs. Ken Jennings and Brad
Rutter) demonstrate that computing capabilities have overtaken even the greatest human minds in these areas. But this
was never meant to be the greatest potential application of
artificial intelligence. The true potential for artificial intelligence is in the discovery of new ideas, innovations, and
applications that have yet to be applied to improve the value
of a particular process. In the case of hernia disease, we have
generated many examples of attempts to improve the value
of care for patients who have a ventral hernia. We will demonstrate the method and impact of having a dedicated team
(including input from patients and family members) who
determine what factors and outcome measures to use for the
computer analytics and how to interpret the output of the
data analyses and data visualizations to generate value-based
ideas in an attempt to improve outcomes. This is one application of artificial intelligence, a symbiosis between human
teams and computing capabilities, to healthcare. This complex systems science approach to healthcare will become
more and more important as the pace of change in our world
continues to accelerate.
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