Plastic Surgery: Volume 4: Trunk and Lower Extremity (Plastic Surgery, 4) [5 ed.] 9780323810418, 9780323873802, 9780323810371, 0323810411

Table of contents :
Any screen. Any time. Anywhere.
Front Matter
Fifth Edition
Copyright
Contents
Video Contents
Volume One
Volume Two
Volume Three
Volume Four
Volume Five
Volume Six
Lecture Video Contents
Volume One
Volume Two
Volume Three
Volume Four
Volume Five
Volume Six
Preface to the Fifth Edition
List of Editors
List of Contributors
Acknowledgments
Dedication
1
1 Comprehensive lower extremity anatomy
The gluteal region
Gluteal skeletal structure
Gluteal fascial anatomy
Muscles of the buttocks
Gluteal vasculature
Gluteal innervation
The thigh
Thigh skeletal structure
Thigh fascial composition
Thigh musculature
Thigh vasculature
Profunda femoris
Lateral circumflex femoral arterial system
Clinical correlation – approach to LCFA as recipient vessel for free tissue transfer in the vessel depleted lower extremity
Clinical correlation – anterolateral thigh flap
Medial circumflex femoral arterial system
Profunda femoris perforating branches
Innervation of the thigh
Motor innervation
Cutaneous innervation
The leg
Knee skeletal structure
Leg skeletal structure
Clinical correlation – fibular flap
Leg fascial composition
Lower leg compartments
Clinical correlation – compartment syndrome and leg compartment release technique
Leg musculature
Anterior compartment
Lateral compartment
Posterior compartment – superficial layer
Posterior compartment – deep layer
Clinical correlation – approach to leg vessels as recipients for free tissue transfer
Posterior tibial
Anterior tibial
Peroneal
Leg vasculature
Leg nerve anatomy
Lower leg motor innervation
Lower leg cutaneous innervation
The ankle and foot
Ankle and foot skeletal structure
Ankle
Foot
Ankle and foot fascial composition
Extensor retinacula
Flexor retinaculum
Peroneal retinaculum
Plantar fascia
Fascial compartments of the foot
Foot musculature
Foot and ankle vasculature
Dorsalis pedis artery
Posterior tibial artery – medial and lateral plantar arteries
Peroneal arterial branches
Ankle and foot nerve anatomy
Foot cutaneous innervation
Foot motor innervation
Conclusion
REFERENCES
2
2 Management of lower extremity trauma
Introduction
Basic science
Inflammatory response to injury
Diagnosis and patient presentation
Initial assessment and management
A: Airway and cervical spine protection
B: Breathing
C: Circulation and bleeding control
D: Disability and level of consciousness
E: Exposure and environmental control
Secondary survey
Extremity examination
Vascular evaluation
Compartment syndrome
Grading system
Patient selection
Amputation versus salvage
Degloving soft-tissue injury
Treatment and surgical techniques
Timing of reconstruction and negative-pressure wound therapy (NPWT) in open fracture
Reconstructive surgery
Skin grafting
Local, regional, and propeller flaps
Free flaps and perforator flaps
Skeletal reconstruction
Recipient vessel dissection in trauma
Arterial anastomosis in extremity vessels
Flaps and skin from spare parts: fillet flap and tissue harvest
Flaps in pediatric patients
Complications
Amputation and limb pain
Avascular necrosis (AVN)
Morel–Lavallée lesion
Summary
References
3-1
3.1 Lymphedema: introduction and editors’ perspective
References
3-2
3.2 Imaging modalities for diagnosis and treatment of lymphedema
Introduction
Lymphoscintigraphy
Technique
Diagnosis and staging
Applications in lymphatic surgery
Limitations
Near-infrared fluorescent imaging
Technique
Diagnosis and staging
Applications in lymphatic surgery
Limitations
Ultrasonography
Technique
Diagnosis
Applications in LVA procedures
Applications in free lymphatic tissue transplantation
Limitations
Magnetic resonance imaging
Technique
Diagnosis and lymphedema evaluation
Applications in lymphatic surgery
Limitations
Further imaging modalities
Computed tomography angiography
Bioimpedance spectroscopy
Laser tomography
Photoacoustic imaging
Imaging modality selection algorithm
Diagnosis
Treatment plan
Imaging modalities for LVA procedures
Imaging modalities for free lymphatic tissue transfer
Conclusion
REFERENCES
3-3
3.3 Lymphaticovenular bypass
Introduction
Background
Clinical approach
Diagnostic evaluation
Diagnosis on clinical grounds is inadequate
History and physical examination
Confirmatory studies
Staging
Patient selection
Surgical technique (Video 3.3.1)
Incision placement
Dissection
Anastomosis
Postoperative care
Lymphaticovenular bypass for subclinical lymphedema
Conclusion
References
3-4
3.4 Vascularized lymph node transplant
History of VLNT
Mechanism of VLNT
Indications for VLNT
Types of VLNT
Inguinal/­Groin
Surgical anatomy and technique
Supraclavicular
Surgical anatomy and technique (Video 3.4.1 )
Lateral thoracic
Surgical anatomy and technique
Submental
Surgical anatomy and technique (Fig. 3.4.7)
Intra-­abdominal donor sites
Surgical anatomy and technique
Outcomes
Complications
Summary
References
3-5
3.5 Debulking strategies and procedures: liposuction of leg lymphedema
Introduction
Excess subcutaneous adiposity and chronic lymphedema
Other research regarding adipose tissue deposition
How to assess the efficacy of liposuction
Preoperative planning
Operative technique
Postoperative care
Controlled compression therapy
Volume measurements
How CCT and liposuction works in clinical practice –­ an example
Controlled compression therapy (CCT)
Liposuction and postoperative success
Complications
The lymphedema team
How liposuction helps
Lymph transport system and liposuction
When to use liposuction to treat lymphedema –­ patient selection
When liposuction should never be used
Can the outcome be reproduced?
References
3-6
3.6 Debulking strategies and procedures: excision
Chen-­modified Charles procedure
Anatomy
Patient selection (Algorithms 3.6.1–­3.6.3)
Preparation before surgery (Fig. 3.6.1)
Surgical techniques for modified Charles procedure (Fig. 3.6.1)
Transfer of lymph node flap with Chen-­modified Charles procedure (Video 3.6.1 )
Postoperative care
Outcomes of modified Charles procedure
Radical reduction with preservation of perforators (RPP procedure)18,19
Patient selection
Surgical techniques for RPP procedure
Outcomes of RPP procedure
Excisional therapy for genital lymphedema20–­23
Follow-­up
Surgical limitations
Other options if debulking procedure fails
Summary
References
4
4 Lower extremity sarcoma reconstruction
Introduction
Soft-­tissue and bone sarcomas
Sarcomas in the lower extremity
Basic science/­disease process
Epidemiology soft-­tissue sarcomas
Bone sarcomas
Tumor growth and metastasizing
Historical perspectives
Diagnosis/­patient presentation/­imaging
Patient profile/­general considerations/­treatment planning
Patient profile
General considerations
Treatment planning (Algorithm 4.1)
Surgery
Radiotherapy
Chemotherapy
Treatment/­surgical resection techniques
Biopsy techniques
Fine-­needle or core-­needle aspirations
Excisional biopsy
Incisional biopsy
Re-­operative biopsies and surgical revisions
Surgical technique for definitive resection
Soft tissue sarcomas (STS)
Vascular involvement
Nerve involvement
Osseous involvement
Primary osseous sarcomas
Specimen handling
Wound closure
Lymph node dissection
Indications for amputation
Reconstructive options for lower extremity preservation
Soft tissue
Neuromuscular unit
Skeletal reconstruction
Vascular surgery
Complex approaches
Postoperative care
Immediate postoperative care
Oncologic postoperative care and follow-­up
Secondary procedures
Early secondary procedures –­ soft tissue
Early secondary procedures –­ skeleton
Late secondary procedures
Outcomes, prognosis, and complications
Outcomes and prognosis
Soft tissue sarcomas
Bone sarcomas
Complications –­ management of recurrent disease
References
5
5 Reconstructive surgery: lower extremity coverage
Introduction
History
Principles
The value of autologous tissue
The reconstructive elevator
Skin grafts and substitutes
Approach by location (local flaps)
Thigh
Lower leg
Microvascular free tissue transfer
Treatment approach
Preoperative evaluation
Primary limb amputation
Debridement
Timing of reconstruction
Selection of recipient vessel and microanastomosis
Special considerations
Osteomyelitis
Diabetes
Coverage after tumor ablation
Exposed prosthesis
Soft-­tissue expansion
Postoperative care
Monitoring
Management of flap complications
Secondary operations
Muscle/­musculocutaneous flaps
Tensor fascia lata
Rectus femoris
Biceps femoris
Gracilis
Soleus
Gastrocnemius
Fasciocutaneous/­perforator flap
Propeller flaps
Groin/­SCIP (superficial circumflex iliac perforator)
Medial thigh/­anteromedial perforator and gracilis perforator
Lateral thigh/­profunda femoris perforator flap
Anterolateral thigh perforator
Sural
TAP (thoracodorsal artery perforator)
Compound flaps
Supermicrosurgery
References
6-1
6.1 Diagnosis, treatment, and prevention of lower extremity pain
Introduction
Etiology of lower extremity pain
Overview
Symptomatic neuroma
Symptomatic stump neuroma
Phantom limb pain
Complex regional pain syndrome
Diagnosis and patient selection
Clinical history
Physical exam
Diagnostics
Surgical candidates and preoperative counseling
Treatment options for lower extremity pain
Overview
Neuroma excision
Targeted muscle reinnervation
Regenerative peripheral nerve interface
General principles for amputations
Postoperative management
Prevention of lower extremity pain
Overview
Primary physiologic nerve stabilization at time of amputation
Alternative treatment measures
Physical therapy
Nerve stimulators
Peripheral nerve ablation
Amputation
Conclusion
References
6-2
6.2 Targeted muscle reinnervation in the lower extremity
Introduction
Physiology of targeted muscle reinnervation
Indications for targeted muscle reinnervation in the lower extremity
General concepts and principles
Expendable motor target
Anatomic feasibility of transfer
Axonal capture
Nerve transposition with proximal transfer
Maintain proximal nerve function
Evaluate proximal compression points
Targeted muscle reinnervation in primary amputations
Overview
Perioperative evaluation and multidisciplinary care
Operative technique in below-knee amputations
Operative technique in knee disarticulations
Operative technique in above-knee amputations
Outcomes
Targeted muscle reinnervation in secondary amputations
Overview
Operative technique for superficial peroneal nerve
Operative technique for tibial nerve
Operative technique for saphenous nerve
Operative technique for sural nerve
Operative technique for deep peroneal nerve
Operative technique for sciatic nerve
Operative technique for posterior femoral cutaneous nerve
Outcomes
Targeted muscle reinnervation in very proximal lower extremity amputations
Targeted muscle reinnervation in minor amputations of the foot
Targeted muscle reinnervation for symptomatic neuromas in non-amputees
Overview
Operative technique for superficial peroneal nerve
Operative technique for deep peroneal nerve
Operative technique for saphenous nerve
Operative technique for sural nerve
Operative technique for tibial nerve
Operative technique for femoral cutaneous nerves
Outcomes
Future directions
Conclusions
References
6-3
6.3 Lower extremity pain: regenerative peripheral nerve interfaces
Introduction
Pathophysiology of neuropathic lower extremity pain from symptomatic neuromas
Wallerian degeneration and symptomatic neuroma formation
Central sensitization
Presentation and diagnosis of neuropathic lower extremity pain from symptomatic neuromas
Treatment of lower extremity pain from symptomatic neuromas
Regenerative peripheral nerve interface
In vivo testing of RPNIs
Clinical outcomes using RPNIs
Technique to perform RPNI surgery
Preoperative considerations
Surgical technique and operative pearls
Postoperative care
Future directions
Conclusion
Disclosure statement
References
7
7 Skeletal reconstruction
Introduction
Biology of bone healing and grafting
Historical perspective
Methods of skeletal reconstruction
Bone graft
Healing process
Surgical indication
Masquelet technique
Donor sites
Bone pedicled and free flaps
Fibular flap
Iliac crest flap
Medial femoral condyle flap
Other bone flaps
Vascularized epiphyseal reconstruction
Allograft
Capanna technique
Distraction osteogenesis
Patient evaluation
Reconstruction by anatomic areas
Pelvis
Femur
Double-barrel fibular flap
Fibular flap plus allograft
Tibia
Fibular flap
Fibular flap plus allograft
Foot
Iliac crest flap
Medial femoral condyle flap
Postoperative care
Postoperative monitoring
Postoperative aesthetic considerations
Conclusion
References
8
8 Foot reconstruction
Introduction
Angiosomes of the foot
Clinical relevance of the angiosome model
Patient evaluation and diagnosis
Clinical history
Limb function
Wound assessment
Vascular work-up
Sensorimotor examination
Gait analysis and skeletal stability
Management
Compartment syndrome
Wound infection and directed antibiotic therapy
Biofilm
Acute vs. chronic wounds
Surgical preparation of the wound bed
Wound healing adjuncts
External fixation
Surgical techniques for soft-tissue reconstruction
Options for wound closure
Reconstruction by anatomic location
Anterior ankle and dorsal foot
Extensor digitorum brevis muscle flap
Lateral supramalleolar flap
Free tissue transfer
Plantar forefoot
Local fasciocutaneous flaps
Fillet of toe flap
Free tissue transfer
Forefoot amputations
Plantar midfoot
Local fasciocutaneous flaps
Local muscle flaps
Free tissue transfer
Midfoot amputations
Plantar hindfoot and medial/lateral ankle
Intrinsic muscle flaps
Abductor hallucis brevis muscle flap
Flexor digitorum brevis muscle flap
Abductor digiti minimi muscle flap
Medial plantar artery flap
Posterior heel pad flaps
Lateral calcaneal flap
Sural artery flap
Free tissue transfer
Hindfoot amputations
Achilles/malleolar region
Local fasciocutaneous and pedicled flaps
Free tissue transfer
Below-knee amputation
Below-knee amputation technique
Postoperative care
Outcomes
Summary
References
9-1
9.1 Diabetic foot: introduction
Introduction
Scope and trends
Mortality
Costs
Risk factors for diabetic foot wounds
Neuropathy
Ischemia
Deformity
Patient-centered outcomes
Multidisciplinary team and beyond
IWGDF practical guidelines
Conclusion
REFERENCES
9-2
9.2 Diabetic foot: management of wounds and considerations in biomechanics and amputations
Principles of wound healing
General
Wound bed management
Eradication of infection
Debridement
Topical products and dressings
Skin substitute grafts
Negative pressure wound therapy
Hyperbaric oxygen therapy
Optimization of tissue healing potential
Biomechanical considerations
General
Normal gait
Pathologic gait
Deformity and balance
Accommodative treatment modalities
Total contact casts
Removable walking casts
Miscellaneous offloading strategies
External fixation
Corrective treatment modalities
Soft-tissue correction
Osseous correction
Examples of corrective treatment modalities
Increased ankle plantarflexion (equinus)
Tendo-Achilles lengthening (TAL)
Gastrocnemius recession (GR) and gastrocnemius–soleus recession (GSR)
Increased ankle dorsiflexion (calcaneus)
Increased (flexible) foot varus
Anterior tibial tendon transfer
Posterior tibial tendon transfer
Increased (rigid and/or severe) foot varus/valgus
Partial foot amputations
General
Tissue handling
Toe amputation
Partial ray amputation
Transmetatarsal amputation
Lisfranc amputation
Chopart amputation
Partial calcanectomy amputation
Conclusion
References
9-3
9.3 Diabetic foot: management of vascularity and considerations in soft-tissue reconstruction
Introduction
Reconstructive options
Reconstructive ladder and elevator
Superficial wounds and skin grafts
Local flaps
Free tissue transfer
Flap composition
Functional and aesthetic considerations
Donor site morbidity
Free tissue transfer in the patient with diffuse vascular calcifications
Surgical planning
Vascular considerations
Angiosomes
Preoperative evaluation and optimization for free flap reconstruction
Infection control and wound bed preparation
Vascular
Thrombophilia assessment
Medical optimization
Biomechanical examination
Cases
References
10
10 Trunk anatomy
Surface anatomy and skin considerations (Fig. 10.1)
Skin perfusion and angiosome concept (Fig. 10.2)
Anterior chest
Axilla
Back
Abdomen and flank
Groin
Perineum
Buttock
Bones
References
11
11 Reconstruction of the chest
Introduction
Etiology
Infected sternotomy wounds and mediastinitis
Ventricular assist device infections
Cardiac implantable electronic device infections
Empyema and bronchopleural fistula
Chest wall tumors
Osteoradionecrosis
Traumatic chest wall wounds
Chest wall biomechanics and pathophysiology
Respiration
Sternal continuity
Flail chest
Sternal–rib stability
Evaluation of the defect and functional goals
Medical optimization and preparation of the wound bed
Skeletal reconstruction
Sternal fixation
Management of sternal defects
Rib fixation
Management of rib defects
Soft-tissue reconstruction
Pectoralis major
Rectus abdominis
Latissimus dorsi
Serratus anterior
External oblique
Omentum
Free tissue transfer
Postoperative care
Congenital chest wall deformities
Pectus excavatum
Pectus carinatum
Poland syndrome
Anterior thoracic hypoplasia
Sternal cleft
Conclusion
References
12
12 Reconstruction of the posterior trunk
Introduction
Anatomy
Posterior trunk perforators
Principles of perforasome theory
Principle 1
Principle 2
Principle 3
Principle 4
Flaps for reconstruction of the posterior trunk
Trapezius
Scapular and parascapular
Latissimus dorsi
Paraspinous muscle
Intercostal artery perforator
Lumbar artery perforator
Gluteus maximus
Multi-perforator
Other flaps
Pull-through VRAM
Omental flap
External oblique flap
Special clinical scenarios
Spinal surgery, pseudomeningocele, and cerebrospinal fluid leaks
Congenital malformations
Perioperative care
Preoperative assessment and planning
Operative approach and action
Postoperative care and follow-through
Techniques for soft-tissue reconstruction in the posterior trunk
Adjacent tissue transfer/pedicled perforator flaps
Free tissue transfer
Algorithmic approach to reconstruction of the posterior trunk
Midline wounds
Non-midline wounds
Non-midline cervical wounds
Non-midline upper thoracic wounds
Non-midline middle thoracic wounds
Non-midline lumbar wounds
Conclusion
References
13
13 Abdominal wall reconstruction
Introduction
Abdominal wall anatomy and physiology
Blood supply to the abdominal skin and musculature
Nerve supply and innervation of the muscles
Abdominal wall muscle function
Tissue apposition
Midline laparotomy closure
Tissue interaction with sutures
Optimal midline closure technique
Midline hernia repair
Umbilical and epigastric hernia repair
Midline incisional hernia repair
The need for mesh
Mesh types
Mesh coatings, mesh placement, and fibrovascular ingrowth
Optimal hernia closure with mesh (Algorithm 13.1)
Surgical technique for clean open midline incisional hernia repair
Surgical technique for clean midline incisional hernia repair under tension
Surgical technique for clean-­contaminated, contaminated, and dirty midline hernias
Flank hernias
Abdominal wall soft-­tissue management (Algorithm 13.2)
Conclusion
References
14-1
14.1 Gender confirmation surgery: diagnosis and management
Epidemiology
Change in coverage over time – Affordable Care Act
WPATH
Expanded societal support/paradigm shift
Terminology
WPATH Standards of Care
Mental health practitioners
Adolescent therapy
Hormone therapy
Multidisciplinary treatment
Patient satisfaction following gender confirmation surgery
Barriers to patient care
Preoperative assessment
Goals of therapy
Congruent genitalia
Surgical goals
Vaginoplasty
Chest surgery
Phalloplasty/metoidioplasty
Arrangements for aftercare
Conclusion
REFERENCES
14-2
14.2 Gender confirmation surgery, male to female: vaginoplasty
Preoperative assessment
Penile inversion vaginoplasty
Patient positioning and preparation
Harvest of skin flaps and grafts
Penile disassembly and inversion
Dissection of vaginal cavity
Creation of neoclitoris
Inset of grafts/flaps and closure
Intestinal vaginoplasty
Peritoneal flaps
Complications
Postoperative care
Role of the pelvic floor physical therapist
Benefits of postoperative vaginal dilation
Conclusion
References
14-3
14.3 Gender affirmation surgery, female to male: phalloplasty and correction of male genital defects
Patient selection
Mental health
Hormone replacement therapy
Preoperative evaluation
Phalloplasty
Perineal masculinization – reconstruction of the pars fixa urethra, vaginectomy, and scrotoplasty
Radial forearm phalloplasty
Preoperative considerations
Surgical markings
Surgical technique
Flap harvest
Tubing
Glansplasty
Groin preparation
Forearm donor site closure
Pars fixa and pendulans anastomosis: radial forearm free flap (RFFF)
ALT phalloplasty
Preoperative considerations
Surgical markings
Surgical technique
Flap harvest
Tubing
Glansplasty
Groin preparation and flap transfer
Donor site closure
Urethral anastomosis and closure: ALT
Postoperative care
Secondary procedures
Glansplasty and coronaplasty
Debulking
Urethral tube formation
Phallopexy
Erectile implant placement
Fat grafting
Tattooing
Complications of phalloplasty
Meatal stenosis
Urethral strictures
Urethrocutaneous fistula
Urethral hair or residual suture
Metoidioplasty
Surgical technique
Secondary procedures
Complications of metoidioplasty
Considerations in other genital defects
Genital flaps
Genital replantation
References
14-4
14.4 Breast, chest wall, and facial considerations in gender affirmation
Introduction
WPATH guidelines
Chest masculinization
Preoperative considerations
Technique selection
Periareolar technique
Circumareolar or extended circumareolar techniques
Double incision with free nipple grafts
Inferior pedicle technique
Postoperative considerations and complications
Breast augmentation
Preoperative considerations
Operative principles
Facial feminization surgery
Anatomy
Preoperative planning
Hairline, forehead, and brow
Midface
Rhinoplasty
Lips
Chin and mandible
Laryngeal prominence
Adjunct cosmetic procedures
Conclusions
References
15
15 Reconstruction of acquired vaginal defects
Introduction
Historical perspective
Anatomic considerations
Diagnosis
Patient selection/preoperative considerations
Treatment/surgical technique
Additional surgical considerations
Postoperative care
Immediate perioperative period
Long-term care
Complications, prognosis, and outcomes
Complications
Prognosis and outcomes
References
16
16 Pressure sores
Introduction
Terminology
Epidemiology and cost
Anatomic distribution
Historical perspective
Basic science
Pressure
Shear and friction
Moisture
Malnutrition
Neurological injury
Biofilm and inflammatory milieu
Diagnosis
Staging (Table 16.1, Fig. 16.4)
Patient evaluation
Osteomyelitis
Psychological evaluation
Patient selection
Treatment
Prevention
Risk assessment
Skin care
Incontinence
Spasticity
Pressure relief
Nutrition
Medical management
Pressure relief
Spasticity
Malnutrition
Tobacco and electronic cigarette use
Infection
Wound care (Table 16.3)
Negative-pressure wound therapy
Glucose control
Manipulating the local wound milieu
Surgical management
Setting expectations
Surgical guidelines
Debridement
Procedure selection
Muscle and myocutaneous flaps
Fasciocutaneous and perforator flaps
Free flaps
Tissue expansion
Reconstruction by anatomic site
Sacral pressure ulcer
Selected technique: gluteal myocutaneous rotation flap (Fig. 16.13, Box 16.2)
Ischial pressure ulcer
Selected flap: V–Y hamstring advancement (Fig. 16.14)
Trochanteric pressure ulcer
Selected procedure: V–Y tensor fasciae latae flap tensor fasciae latae rotation flap
Hip joint infection
Heel pressure ulcer
Bone resection
Postoperative care
Outcomes, prognosis, and complications
Complications
Secondary procedures
References
17
17 Perineal reconstruction
Introduction
History of perineal reconstruction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Skin graft reconstruction
Regional skin flaps
Rectus-based reconstruction
Gracilis flap
Anterolateral thigh flap
Singapore flap
Posterior thigh flap
Perforator flaps
Free flap
Minimally invasive flap harvest
Special considerations – sphincter reconstruction
Postoperative care
Outcomes, prognosis, complications
References
18
18 Burn, chemical, and electrical injuries
SYNOPSIS
Epidemiology
Risk factors
Evolution of burn medicine
Pathophysiology of burn injuries
Thermal (high temperature) burns
Flash and flame burns
Scald burns
Hot object “contact burns”
Tar and asphalt burns
Electrical injury
Radiation Injuries
Frostbite
Burn injury in children
Chemical injuries and burns
Acid burns
Hydrochloric and sulfuric acids
Nitric acid
Chromic acid
Hydrofluoric acid
Alkali burns
Sodium hypochlorite
Cement (calcium hydroxide)
Physiological consequences of thermal skin burns
Zones of burn tissue injury
Local injury progression
Systemic injury progression
Acute burn trauma management
Initial evaluation and treatment in the field
Initial hospital management
Initial burn wound diagnosis and management
Epidermal (superficial) burn wounds
Superficial partial-thickness burn wounds
Deep partial-thickness burn wounds
Full-thickness burn wounds
Facial burn considerations
Quantifying the fractional area of the burn wounds
Inhalation injury
Carbon monoxide intoxication
Cyanide intoxication
Airway management
Fluid resuscitation
Resuscitation fluid composition and administration
Vital organ function monitoring
Management of the burn wound
Wound dressings
Topical antimicrobials
Physiological wound dressings
Biological wound dressings or grafts
Operative wound closure
Management of tar burns
Treatment of electrical injuries
Treatment of radiation injury
Treatment of chemical injuries
Effect of burn trauma on metabolism30–32
Nutritional management
Nutrition formulae
Pain control
Complications
Skin graft loss
Invasive wound infection
Adrenal insufficiency
Circumferential limb compression with vascular compromise
Compartment syndromes
Deep venous thrombosis
Systemic inflammatory response syndrome
Sepsis
Rehabilitation
Managing scar hypertrophy and contracture
References
19
19 Extremity burn reconstruction
Introduction
Burns of the upper extremity
Edema
Infection
Operative wound management of acute burns of the extremities
Tangential excision
Fascial excision
Salvage surgery in acute fourth degree burns
Correction of post-burn deformities of the hand
Management of individual deformities
Dorsal hand contractures
Volar hand and digital contractures
First web contracture
Deformities of the thumb
Swan neck deformities
Boutonnière deformity
The burns syndactyly
The burnt little finger
Management of digital losses
Management of heterotopic ossification in burns
Electrical burns to the upper limb
Reconstructive surgery for low voltage electrical injuries
Reconstructive surgery in high voltage electrical burns
Surgery in the acute phase
Provision of soft-tissue cover
Timing of soft-tissue cover
Type of soft-tissue cover
Reconstruction of nerves and tendons
Axillary contracture
Elbow contracture
Skin substitutes
Marjolin ulcer
Therapy considerations
Pressure garments
Silicone
Emollients
Scar massage
Intralesional injections
Lasers
Reconstruction of lower extremity burns
Surgery in the acute phase
Surgery for wound healing and prevention of contractures
Treatment of lower limb contractures
References
20
20 Management of the burned face and neck
Introduction
Anatomy and pathophysiology
Acute facial burn management
General principles
Emergency care
Burn wound dressing
Surgical management of the facial burn wound – early excision
Salient principles in early excision of facial burns
Procedure of facial wound excision
Post-excision options
Allograft and split skin use
Skin grafting – salient points
Other options for post-excision cover
Acellular dermis
Xenograft
Matriderm and Integra
Cultured epithelial autograft
Challenges of specific parts of the face
Periocular burns
Nose and ears
Lips
Scalp
Neck burns
Surgical management of the facial burn wound – delayed surgery
Aftercare and early scar management
Ancillary measures
Psychosocial rehabilitation
Management of facial post-burn deformities
Presentation to the surgeon
The consultation
Planning
Photography during planning
General principles of post-burn facial reconstruction
Timing of surgery
Reconstructive options
Skin grafts
Flaps
Z-plasty
Tissue expansion and flap advancement
Melanin transfer for hypopigmentation
Serial excision
Hair transplantation
Fat grafting beneath scars
Tattooing
Lasers
Management of keloids
Reconstruction of specific areas
Scalp
Forehead
Eyebrows
Ears
Eyelids/periorbital region
Principles for eyelid contracture release
Surgical technique of ectropion release
Upper lid release (Video 20.2)
Lower lid release
Calculation of graft requirement (Video 20.2 )
Postoperative care
Partial or complete loss of the eyelids
Nose
Altered surface texture or discoloration
Elevated nasal tip and alar margins
Scarred and shortened columella
Full-thickness loss of parts of the nose
Cover
Lining
Skeletal support
Nostril stenosis or complete block
Cheeks
Healing by secondary intention
Primary closure and serial excision
Skin grafts
Tissue expansion
Flap cover
Lips and perioral region
Minor hypertrophic scarring of the upper lip
Scarring with/without shortening of the upper lip
Lower lip ectropion with or without mandible deformities
Microstomia
Macrostomia
Perioral scar bands
Pseudomicrogenia
Splints
Neck
Airway problems
Technical pointers for a release of severe neck contracture
Multi-part involvement of face
Acid burns
Future directions
Stem cells
Cell spray devices
3D printing
Face transplantation
Conclusion
References
21
21 Pediatric burns
Introduction
Basic science
Epidemiology
Risk factors
Pathophysiology
Prevention
Initial assessment
Primary survey
Secondary survey
Wound assessment
Initiating fluid resuscitation
Procedures
Triage and disposition
Minor burns
Child abuse and neglect
Wound management
Wound care
Surgical care
Medical management
Analgesia and sedation
Inhalation injury
Nutrition and metabolism
Sepsis
Rehabilitation
Physical and occupation therapy
Scar management
Pruritus
Reconstruction
General principles
Traditional burn reconstruction
Laser
References
Confidence is ClinicalKey

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Fifth Edition

Front Matter

Plastic Surgery Lower Extremity, Trunk and Burns Volume Four

Cover illustration “The Plastic Surgery Huddle” The concept and inspiration for the cover art was derived from a situation that we as plastic surgeons are all familiar with. It is that special time when you know there is a new or interesting case happening down the hall in your hospital. It might be a complex reconstruction, a new flap design or an unusual presentation. There is a buzz and a crowded OR with extra residents, Fellows, students, and colleagues around the table. The “Plastic Surgery huddle” includes additional hands scrubbed-in to assist, wanting to be involved, to learn, and to experience the innovation that is being performed. It is always dynamic, and it is always a learning situation. The color arrangement of the surgical caps/hats around the OR table is intentional. It borrows from the artist’s color wheel, which includes primary colors (red, yellow, and blue) and the secondary colors (orange, purple, and green). All the different colours are meant to represent the dynamic and unique diversity of our discipline as well as the sharing of ideas and collaboration that we all strive to promote in our wonderful specialty of Plastic Surgery. John L. Semple MD, MSc, FRCSC, FACS, LLD Head, Division of Plastic Surgery Women’s College Hospital Professor, Department of Surgery University of Toronto

Content Strategist: Lauren Boyle, Belinda Kuhn Content Development Specialists: Kathryn DeFrancesco, Rebecca Gruliow, Grace Onderlinde, Kevin Travers Project Managers: Anne Collett, Joanna Souch, Julie Taylor Designer: Miles Hitchen Marketing Manager: Mary McCabe-Dunn Video Liaison: Nicholas Henderson

Fifth Edition

Plastic Surgery Lower Extremity, Trunk and Burns Volume Four Volume Editors

David H. Song

Joon Pio Hong

MD, MBA, FACS Physician Executive Director and Chairman Plastic Surgery Georgetown University Washington, DC, United States

MD, PhD, MMM Professor Plastic Surgery Asan Medical Center University of Ulsan Seoul, Korea; Adjunct Professor Plastic and Reconstructive Surgery Georgetown University Washington, DC, United States

Editor-in-Chief

Multimedia Editor

Peter C. Neligan

Daniel Z. Liu

MB, FRCS(I), FRCSC, FACS

MD

Professor Emeritus Surgery, Division of Plastic Surgery University of Washington Seattle, WA, United States

Reconstructive Microsurgeon Oncoplastic and Reconstructive Surgery City of Hope Chicago Zion, IL, United States

For additional online figures, videos, and video lectures visit Elsevier eBooks+

London, New York, Oxford, Philadelphia, St Louis, Sydney 2024

Copyright Elsevier 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899

PLASTIC SURGERY, FIFTH EDITION Copyright © 2024, Elsevier Inc. All rights reserved.

First edition 1990 Second edition 2006 Third edition 2013 Fourth edition 2018 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www. elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Volume 4 ISBN: 978-0-323-81041-8 Volume 4 Ebook ISBN: 978-0-323-87380-2 6 volume set ISBN: 978-0-323-81037-1

Printed in India Last digit is the print number: 9 8 7 6 5 4 3 2 1

Contents Preface to the Fifth Edition xxvii List of Editors xxviii List of Contributors xxix Acknowledgmentsl Dedicationli

17 Skin grafting

206

18 Tissue engineering

220

19 Repair, grafting, and engineering of cartilage

235

20 Repair and grafting of bone

265

21 Repair and grafting of peripheral nerve

295

22 Repair and grafting fat and adipose tissue

309

23 Vascular territories

321

Shawn Loder, Benjamin Levi, and Audra Clark Ramin Shayan and Karl-Anton Harms Wei Liu, Guangdong Zhou, and Yilin Cao

Iris A. Seitz, Chad M. Teven, Bryce Hendren-Santiago, and Russell R. Reid

Volume One: Principles edited by Geoffrey C. Gurtner and Andrea L. Pusic

1 Plastic surgery and innovation in medicine

1

2 History of reconstructive and aesthetic surgery

9

Peter C. Neligan

Riccardo F. Mazzola and Isabella C. Mazzola

3 Applying psychology to routine plastic surgery practice24 Nichola Rumsey and Alex Clarke

4 The role of ethics in plastic surgery and medico-legal issues in plastic surgery

32

5 Business principles for plastic surgeons 6 Value-based healthcare

Hollie A. Power, Kirsty Usher Boyd, Stahs Pripotnev, and Susan E. Mackinnon J. Peter Rubin

Steven F. Morris and G. Ian Taylor

24 Flap physiology, classification, and applications346 Joon Pio Hong and Peter C. Neligan

37

25 Principles and techniques of microvascular surgery

414

60

26 Tissue expansion and implants

442

27 Principles of radiation therapy

452

8 Pre- and intra-operative imaging for plastic surgery83

28 Lymphedema: pathophysiology and basic science

472

9 Patient safety in plastic surgery

29 Benign and malignant nonmelanocytic tumors of the skin and soft tissue

490

Michele A. Manahan and B. Aviva Preminger C. Scott Hultman

Justin M. Broyles, Clifford C. Sheckter, and Anaeze C. Offodile 2nd

7 Digital photography in plastic surgery Daniel Z. Liu

66

Arash Momeni and Lawrence Cai

Jessica Erdmann-Sager and Christopher J. Pannucci

10 Anesthesia and pain management in plastic surgery Paul N. Afrooz and Franklyn P. Cladis

11 Evidence-based medicine and health services research in plastic surgery Sophocles H. Voineskos, Lucas Gallo, Andrea L. Pusic, and Achilleas Thoma

12 Patient-reported outcomes in plastic surgery

Sophocles H. Voineskos, Danny Young-Afat, Madelijn Gregorowitsch, Jonas A. Nelson, Anne F. Klassen, and Andrea L. Pusic

94 101 115 135

146

14 Principles of cancer management

153

15 Wound healing

163

16 Scar prevention, treatment, and revision

186

Stav Brown and Babak J. Mehrara

Kristo Nuutila, David E. Varon, and Indranil Sinha Michelle F. Griffin, Evan Fahy, Michael S. Hu, Elizabeth R. Zielins, Michael T. Longaker, and H. Peter Lorenz

Britta A. Kuehlmann, Eva Brix, and Lukas M. Prantl Stephanie K. Schaub, Joseph Tsai, and Gabrielle M. Kane

Stav Brown, Michelle Coriddi, and Babak J. Mehrara

Rei Ogawa

13 Health services research in plastic surgery Jacqueline N. Byrd and Kevin C. Chung

Fu-Chan Wei, Sherilyn Keng Lin Tay, and Nidal F. Al Deek

30 Melanoma521 Sydney Ch’ng and Alexander H.R. Varey

31 Implants and biomaterials

544

32 Transplantation in plastic surgery

555

33 Technology innovation in plastic surgery: a practical guide for the surgeon innovator

568

34 Robotics in plastic surgery

582

35 Digital technology in plastic surgery

594

Dharshan Sivaraj, Dominic Henn, Timothy W. King, and Kellen Chen Yannick F. Diehm, Valentin Haug, Martin Kauke-Navarro, and Bohdan Pomahac

David Perrault, Leila Jazayeri, and Geoffrey C. Gurtner Karim A. Sarhane and Jesse C. Selber Lynn Jeffers, Hatem Abou-Sayed, and Haley M. Jeffers

36 Aesthetic improvement through noninvasive technologies613 Stelios C. Wilson and Charles H. Thorne

37 Education and teaching in plastic surgery Lydia Helliwell and Johanna N. Riesel

619

vi

Contents

38 Global plastic surgery

625

9.5 Facelift: Platysma-SMAS plication

203

9.6 Facelift: Lateral SMASectomy facelift

212

9.7 Facelift: The extended SMAS technique in facial rejuvenation

219

9.8 High SMAS facelift: combined single flap lifting of the jawline, cheek, and midface

236

9.9 The lift-and-fill facelift

282

9.10 Neck rejuvenation

301

9.11 Male facelift

319

Section I: Aesthetic Anesthesia Techniques 3 Essential elements of patient safety in aesthetic plastic surgery 18

9.12 Secondary facelift irregularities and the secondary facelift

345

4 Pain management in plastic surgery

9.13 Perioral rejuvenation, including chin and genioplasty390

Johanna N. Riesel, Peter Nthumba, George Ho, and Amanda Gosman

39 Gender-affirming surgery

Shane D. Morrison, William M. Kuzon Jr., and Jens U. Berli

Miles G. Berry, James D. Frame III, and Dai M. Davies

634

Index652

Daniel C. Baker and Steven M. Levine

James M. Stuzin

Volume Two: Aesthetic edited by J. Peter Rubin and Alan Matarasso

1 Managing the aesthetic surgery patient Michelle B. Locke and Foad Nahai

2 Principles of practice management and social media for cosmetic surgery Ashley N. Amalfi, Josef G. Hadeed, and Smita R. Ramanadham

1

Stav Brown, Justin L. Bellamy, and Rod J. Rohrich

13

Jeremy T. Joseph, Gabriele C. Miotto, Felmont F. Eaves III, and Galen Perdikis Anna R. Schoenbrunner and Jeffrey E. Janis

5 Anatomic blocks of the face and neck Stelios C. Wilson and Barry Zide

6 Local anesthesia Malcolm D. Paul

Section II: Aesthetic Surgery of the Face 7 Non-surgical skin care and rejuvenation Zoe Diana Draelos

8.1 Editors’ perspective: injectables and non-surgical resurfacing techniques J. Peter Rubin

Timothy Marten and Dino Elyassnia

25

James E. Zins and Jacob Grow Timothy Marten and Dino Elyassnia

Timothy Marten and Dino Elyassnia

Ali Totonchi and Bahman Guyuron

33 42

9.14 Facial feminization

404

10 Editors’ perspective: brow and eye

424

11 Forehead rejuvenation

425

12 Endoscopic brow lift

441

Patrick R. Keller, Matthew Louis, and Devin Coon Alan Matarasso

47 53

Richard Warren

Renato Saltz and Eric W. Anderson

13 Blepharoplasty453 Julius Few Jr., and Marco Ellis

8.2 Injectables and resurfacing techniques: Soft-tissue fillers

54

8.3 Injectables and resurfacing techniques: Botulinum toxin/neurotoxins

73

14 Secondary blepharoplasty

484

15 Asian facial cosmetic surgery

513

16 Facial fat grafting

559

17 Editors’ perspective: nose

567

96

18 Nasal analysis and anatomy

568

8.6 Minimally invasive multimodal facial rejuvenation118

19 Open technique rhinoplasty

581

Kavita Mariwalla

Rawaa Almukhtar and Sabrina G. Fabi

8.4 Injectables and resurfacing techniques: Lasers in aesthetic surgery

Jonathan Cook, David M. Turer, Barry E. DiBernardo, and Jason N. Pozner

8.5 Injectables and resurfacing techniques: Chemical peels Richard H. Bensimon and Peter P. Rullan

84

Seth Z. Aschen and Henry M. Spinelli Jong Woo Choi, Tae Suk Oh, Hong Lim Choi, and Clyde Ishii Francesco M. Egro, Sydney R. Coleman, and J. Peter Rubin Alan Matarasso

Luiz S. Toledo

Rod J. Rohrich and Paul N. Afrooz Rod J. Rohrich and Paul N. Afrooz

20 Closed technique rhinoplasty

607

9.1 Editors’ perspective: surgical facial rejuvenation130

21 Airway issues and the deviated nose

647

9.2 Facial anatomy and aging

22 Secondary rhinoplasty

662

23 Otoplasty and ear reduction

681

24 Hair restoration

690

Alan Matarasso

Bryan Mendelson and Chin-Ho Wong

131

9.3 Principles and surgical approaches of facelift 149 Richard J. Warren

9.4 Facelift: Facial rejuvenation with loop sutures: the MACS lift and its derivatives 180 Patrick Tonnard, Alexis Verpaele, and Rotem Tzur

Mark B. Constantian

Ali Totonchi, Bryan Armijo, and Bahman Guyuron David M. Kahn, Danielle H. Rochlin, and Ronald P. Gruber Charles H. Thorne

Alfonso Barrera and Victor Zhu

Contents

vii

Section III: General Aesthetic Surgery 25.1 Editors’ perspective: liposuction

700

25.2 Liposuction: a comprehensive review of techniques and safety

Volume Three: Craniofacial, Head and Neck Surgery and Pediatric Surgery

701

Part 1: Craniofacial, Head and Neck Surgery: edited by Richard A. Hopper

J. Peter Rubin

Gianfranco Frojo, Jayne Coleman, and Jeffrey Kenkel

1 Management of craniomaxillofacial fractures

25.3 Correction of liposuction deformities with the SAFE liposuction technique

723

26 Editors’ perspective: abdominal contouring

731

Simeon H. Wall Jr. and Paul N. Afrooz Alan Matarasso

27 Abdominoplasty732 Alan Matarasso

28 Lipoabdominoplasty with anatomical definition: a new concept in abdominal aesthetic surgery 775 Osvaldo Ribeiro Saldanha, Andrés F. Cánchica Cano, Taisa Szolomicki, Osvaldo Saldanha Filho, and Cristianna Bonetto Saldanha

2

Srinivas M. Susarla, Russell E. Ettinger, and Paul N. Manson

2 Scalp and forehead reconstruction

39

3 Aesthetic nasal reconstruction

52

Alexander F. Mericli and Jesse C. Selber Frederick J. Menick

4 Auricular construction

Dale J. Podolsky, Leila Kasrai, and David M. Fisher

110

5 Secondary treatment of acquired cranio-orbital deformities138 Allan B. Billig and Oleh M. Antonyshyn

29 Editors’ perspective: truncal contouring

785

6.1 Computerized surgical planning: introduction 155

30 Bra-line back lift

786

6.2 Three-dimensional virtual planning in orthognathic surgery

157

31 Belt lipectomy

792

6.3 Computerized surgical planning in head and neck reconstruction

173

7 Introduction to post-oncologic reconstruction

188

834

8 Overview of head and neck soft-tissue and bony tumors

190

34 Circumferential approaches to truncal contouring: lower bodylift with autologous gluteal flaps for augmentation and preservation of gluteal contour

841

9 Post-oncologic midface reconstruction: the Memorial Sloan-Kettering Cancer Center and MD Anderson Cancer Center approaches

217

35.1 Editors’ perspective: buttock augmentations

854

10 Local flaps for facial coverage

229

35.2 Buttock augmentation with implants

855

11 Lip reconstruction

256

J. Peter Rubin

Joseph Hunstad and Saad A. Alsubaie Amitabh Singh and Al S. Aly

32 Circumferential approaches to truncal contouring in massive weight loss patients: the lower lipo-bodylift Dirk F. Richter and Nina Schwaiger

33 Circumferential approaches to truncal contouring: autologous buttocks augmentation with purse-string gluteoplasty Joseph P. Hunstad and Nicholas A. Flugstad

Robert F. Centeno and Jazmina M. Gonzalez J. Peter Rubin

Jose Abel De la Peña Salcedo, Jocelyn Celeste Ledezma Rodriguez, and David Gonzalez Sosa

819

Constantino G. Mendieta, Thomas L. Roberts III, and Terrence W. Bruner Margaret Luthringer, Nikita O. Shulzhenko, and Joseph F. Capella

37 Medial thigh

Samantha G. Maliha and Jeffrey Gusenoff

878 891

38 Post-bariatric reconstruction

898

39 Energy devices in aesthetic surgery

919

Jonathan W. Toy and J. Peter Rubin David Turer, Jonathan Cook, Jason Pozner, and Barry DiBernardo

40 Aesthetic genital surgery Gary J. Alter

Pradip R. Shetye and Srinivas M. Susarla

Maureen Beederman, Adam S. Jacobson, David L. Hirsch, and Jamie P. Levine Zoe P. Berman and Eduardo D. Rodriguez

35.3 Buttock shaping with fat grafting and liposuction869 36 Upper limb contouring

Richard A. Hopper

926

Index951

Sydney Ch’ng, Edwin Morrison, Pratik Rastogi, and Yu-Ray Chen

Matthew M. Hanasono and Peter G. Cordeiro Nicholas Do and John Brian Boyd Julian J. Pribaz and Mitchell Buller

12 Oral cavity, tongue, and mandibular reconstructions275 Ming-Huei Cheng

13 Hypopharyngeal, esophageal, and neck reconstruction302 Min-Jeong Cho and Peirong Yu

14 Secondary facial reconstruction

336

15 Facial paralysis

359

Afaaf Shakir and Lawrence J. Gottlieb

Simeon C. Daeschler, Ronald M. Zuker, and Gregory H. Borschel

16 Surgical management of facial pain, including migraines390 Anna Schoenbrunner and Jeffrey E. Janis

17 Facial feminization

Luis Capitán, Daniel Simon, and Fermín Capitán-Cañadas

400

viii

Contents

Part 2: Pediatric Surgery: edited by Joseph E. Losee 18 Embryology of the craniofacial complex Jingtao Li and Jill A. Helms

442 451

19.2 Rotation advancement cheiloplasty

456

19.3 Extended Mohler repair

488

Philip Kuo-Ting Chen and Lucia Pannuto

808

25.3 Multisutural syndromic synostosis

827

Sameer Shakir and Jesse A. Taylor

Richard A. Hopper and Benjamin B. Massenburg

Section I: Clefts 19.1 Unilateral cleft lip: introduction

Joseph E. Losee and Michael R. Bykowski

25.2 Nonsyndromic craniosynostosis

25.4 Neurosurgical and developmental issues in craniosynostosis849 Alexandra Junn, John T. Smetona, Michael Alperovich, and John A. Persing

26 Craniofacial microsomia

859

27 Idiopathic progressive hemifacial atrophy

887

28 Robin sequence

902

29 Treacher Collins syndrome

923

21.2 Straight line repair with intravelar veloplasty (IVVP)542

Section III: Pediatrics 30 Congenital melanocytic nevi

935

21.3 Double opposing Z-palatoplasty

549

31 Vascular anomalies

952

21.4 Buccal myomucosal flap palate repair

557

32 Pediatric chest and trunk deformities

974

21.5 The buccal fat pad flap

567

33 Pediatric tumors

988

34 Conjoined twins

1001

Roberto L. Flores

19.4 Anatomic subunit approximation approach to unilateral cleft lip repair

499

20 Repair of bilateral cleft lip

519

21.1 Cleft palate: introduction

538

Raymond W. Tse and David M. Fisher

John B. Mulliken and Daniel M. Balkin Michael R. Bykowski and Joseph E. Losee

Brian Sommerlad

Jordan N. Halsey and Richard E. Kirschner Robert Joseph Mann

James D. Vargo and Steven R. Buchman

21.6 Oral fistula closure

Mirko S. Gilardino, Sabrina Cugno, and Abdulaziz Alabdulkarim

21.7 Alveolar clefts

Katelyn Kondra, Eloise Stanton, Christian Jimenez, Erik M. Wolfswinkel, Stephen Yen, Mark Urata, and Jeffrey Hammoudeh

575 583

21.8 Orthodontics in cleft lip and palate management592 Alvaro A. Figueroa, Alexander L. Figueroa, Gerson R. Chinchilla, and Marta Alvarado

21.9 Velopharyngeal dysfunction

Richard E. Kirschner, Hannah J. Bergman, and Adriane L. Baylis

Craig B. Birgfeld and Scott P. Bartlett Peter J. Taub, Kathryn S. Torok, Daniel H. Glaser, and Lindsay A. Schuster Sofia Aronson, Chad A. Purnell, and Arun K. Gosain Irene Mathijssen

Sara R. Dickie, Neta Adler, and Bruce S. Bauer Arin K. Greene and John B. Mulliken Han Zhuang Beh, Andrew M. Ferry, Rami P. Dibbs, Edward P. Buchanan, and Laura A. Monson Matthew R. Greives, George Washington, Sahil Kapur, and Michael Bentz

Anna R. Carlson, Gregory G. Heuer, and Jesse A. Taylor Index1011

Volume Four: Lower Extremity, Trunk and Burns edited by David H. Song and Joon Pio Hong

618

1 Comprehensive lower extremity anatomy Rajiv P. Parikh and Grant M. Kleiber

2 Management of lower extremity trauma Hyunsuk Peter Suh

1 52

21.10 Secondary deformities of the cleft lip, nose, and palate

636

Section I: Lower Extremity Surgery 3.1 Lymphedema: introduction and editors’ perspective76

21.11 Cleft and craniofacial orthognathic surgery

661

Section II: Craniofacial 22 Pediatric facial fractures

3.2 Imaging modalities for diagnosis and treatment of lymphedema 78

708

3.3 Lymphaticovenular bypass

Han Zhuang Beh, Rami P. Dibbs, Andrew M. Ferry, Robert F. Dempsey, Edward P. Buchanan, and Larry H. Hollier Jr. Stephen B. Baker, Brian L. Chang, and Anusha Singh

John T. Smetona, Jesse A. Goldstein, Michael R. Bykowski, and Joseph E. Losee

102

747

3.5 Debulking strategies and procedures: liposuction of leg lymphedema

111

775

3.6 Debulking strategies and procedures: excision 120

24 Craniofacial clefts

25.1 Craniosynostosis: introduction

Christopher R. Forrest and Johanna N. Riesel

92

3.4 Vascularized lymph node transplant

726

James P. Bradley and Henry K. Kawamoto Jr.

Balazs Mohos and Chieh-Han John Tzou

Wei F. Chen, Lynn M. Orfahli, and Vahe Fahradyan

23 Orbital hypertelorism

Eric Arnaud, Giovanna Paternoster, Roman Khonsari, Samer E. Haber, and Syril James

Joon Pio Hong and David H. Song

Rebecca M. Garza and David W. Chang

Håkan Brorson

Hung-Chi Chen and Yueh-Bih Tang

Contents

4 Lower extremity sarcoma reconstruction Andrés A. Maldonado, Günter K. Germann, and Michael Sauerbier

128

5 Reconstructive surgery: lower extremity coverage154 Joon Pio Hong

6.1 Diagnosis, treatment, and prevention of lower extremity pain 180 Brian L. Chang and Grant M. Kleiber

6.2 Targeted muscle reinnervation in the lower extremity Brian L. Chang and Grant M. Kleiber

6.3 Lower extremity pain: regenerative peripheral nerve interfaces

Nishant Ganesh Kumar, Theodore A. Kung, and Paul S. Cederna

7 Skeletal reconstruction

Marco Innocenti, Stephen Kovach III, Elena Lucattelli, and L. Scott Levin

8 Foot reconstruction

Romina Deldar, Zoe K. Haffner, Adaah A. Sayyed, John S. Steinberg, Karen K. Evans, and Christopher E. Attinger

9.1 Diabetic foot: introduction

Kevin G. Kim, Paige K. Dekker, John D. Miller, Jayson N. Atves, John S. Steinberg, and Karen K. Evans

190 203

Brian L. Chang, Banafsheh Sharif-Askary, and David H. Song

311 327

12 Reconstruction of the posterior trunk

354

13 Abdominal wall reconstruction

388

Reuben A. Falola, Nicholas F. Lombana, Andrew M. Altman, and Michel H. Saint-Cyr Gregory A. Dumanian

14.1 Gender confirmation surgery: diagnosis and management407 Loren Schechter and Rayisa Hontscharuk

14.2 Gender confirmation surgery, male to female: vaginoplasty414 Loren Schechter and Rayisa Hontscharuk

14.3 Gender affirmation surgery, female to male: phalloplasty; and correction of male genital defects421 Alexander Y. Li, Walter C. Lin, and Bauback Safa

14.4 Breast, chest wall, and facial considerations in gender affirmation 439 Kaylee B. Scott, Dana N. Johns, and Cori A. Agarwal

17 Perineal reconstruction

489

Section III: Burn Surgery 18 Burn, chemical, and electrical injuries

501

19 Extremity burn reconstruction

538

20 Management of the burned face and neck

561

21 Pediatric burns

589

Ping Song, Hakim Said, and Otway Louie

Raphael C. Lee and Chad M. Teven

S. Raja Sabapathy, R. Raja Shanmugakrishnan, and Vamseedharan Muthukumar

Sebastian Q. Vrouwe and Lawrence J. Gottlieb

edited by Maurice Y. Nahabedian

265

Paige K. Dekker, Kevin G. Kim, and Karen K. Evans



462

Ibrahim Khansa and Jeffrey E. Janis

Volume Five: Breast

9.3 Diabetic foot: management of vascularity and considerations in soft-tissue reconstruction 296

11 Reconstruction of the chest

16 Pressure sores

228

Jayson N. Atves, John D. Miller, and John S. Steinberg

J. Andres Hernandez, Andrew Nagy Atia, and Scott Thomas Hollenbeck

452

Leila Jazayeri, Andrea L. Pusic, and Peter G. Cordeiro

Index610

9.2 Diabetic foot: management of wounds and considerations in biomechanics and amputations270

Section II: Trunk, Perineum, and Transgender 10 Trunk anatomy

15 Reconstruction of acquired vaginal defects

Vinita Puri and Venkateshwaran Narasiman

210

ix

Section I: Aesthetic Breast Surgery 1 Preoperative assessment and planning of the aesthetic breast patient Kiya Movassaghi and Christopher N. Stewart

1

2 Current status of breast implants

13

3 Primary breast augmentation with implants

28

Patrick Mallucci and Giovanni Bistoni Charles Randquist

4 Autologous fat transfer: fundamental principles and application for breast augmentation 52 Roger Khalil Khouri, Raul A. Cortes, and Daniel Calva-Cerquiera

5 Augmentation mastopexy

69

6 Mastopexy after massive weight loss

83

7 Prevention and management of complications following breast augmentation and mastopexy

92

Justin L. Perez, Daniel J. Gould, Michelle Spring, and W. Grant Stevens Francesco M. Egro and J. Peter Rubin

M. Bradley Calobrace and Chester J. Mays

8 Short scar breast reduction

Elizabeth Hall-Findlay, Elisa Bolletta, and Gustavo Jiménez Muñoz Ledo

102

9 Reduction mammaplasty with inverted-T techniques131 Maurice Y. Nahabedian

10 Breast implant illness: diagnosis and management154 Caroline A. Glicksman and Patricia McGuire

11 Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL): diagnosis and management160 Mark W. Clemens, Eliora A. Tesfaye, and Anand Deva

x

Contents

12 A critical analysis of irrigation solutions in breast surgery Grace Keane, Marissa M. Tenenbaum, and Terence M. Myckatyn

13 Imaging and surveillance in patients with breast implants Bradley Bengtson, Patricia McGuire, Caroline Glicksman, and Pat Pazmiño

174

182

191

15 Management strategies for gynecomastia

200

Michele Ann Manahan

16 Management options for gender affirmation surgery of the breast Ara A. Salibian, Gaines Blasdel, and Rachel Bluebond-Langner

207

Section II: Reconstructive Breast Surgery 17 Preoperative evaluation and planning for breast reconstruction following mastectomy222 Saïd C. Azoury and Liza C. Wu

18 Perfusion assessment techniques following mastectomy and reconstruction Alex Mesbahi, Matthew Cissell, Mark Venturi, and Louisa Yemc

234

19 Introduction to prosthetic breast reconstruction239 Maurice Y. Nahabedian

20 One- and two-stage prepectoral reconstruction with prosthetic devices

Alberto Rancati, Claudio Angrigiani, Maurizio Nava, Dinesh Thekkinkattil, Raghavan Vidya, Marcelo Irigo, Agustin Rancati, Allen Gabriel, and Patrick Maxwell

21 One-stage dual-plane reconstruction with prosthetic devices Brittany L. Vieira and Amy S. Colwell

247

265

293

Kiya Movassaghi and Christopher N. Stewart

25 Management of complications of prosthetic breast reconstruction Nima Khavanin and John Y.S. Kim

Jin Sup Eom and Hyunho Han

32 Autologous breast reconstruction with the superficial inferior epigastric artery (SIEA) flap

413

33 Introduction to autologous reconstruction with alternative free flaps

420

34 Gluteal free flaps for breast reconstruction

424

Pierre Chevray

Maurice Y. Nahabedian

Salih Colakoglu and Gedge D. Rosson

35 Autologous breast reconstruction with medial thigh flaps 433 Venkat V. Ramakrishnan and Nakul Gamanlal Patel

36 Autologous breast reconstruction with the profunda artery perforator (PAP) flap

450

37 Autologous reconstruction with the lumbar artery perforator (LAP) free flap

461

38 Hybrid breast reconstruction: combining flaps and implants

468

39 Innervation of autologous flaps

475

40 Stacked and conjoined flaps

481

41 Management of complications following autologous breast reconstruction

488

Adam T. Hauch, Hugo St. Hilaire, and Robert J. Allen, Sr.

Phillip Blondeel and Dries Opsomer

Aldona J. Spiegel and Janak A. Parikh

Anne C. O’Neill, Vincent J. Choi, and Stefan O.P. Hofer

23 Two-stage prosthetic reconstruction with total muscle coverage Colleen M. McCarthy and Peter G. Cordeiro

371

Adrian McArdle and Joan E. Lipa

Nicholas T. Haddock and Sumeet S. Teotia

280

24 Skin reduction using “smile mastopexy” technique in breast reconstruction

30 Autologous breast reconstruction with the DIEP flap

Arash Momeni, Hani Sbitany, and Suhail K. Kanchwala

22 Two-stage dual-plane reconstruction with prosthetic devices Ara A. Salibian and Nolan S. Karp

355

Dennis C. Hammond

31 Autologous breast reconstruction with the free TRAM flap 396

14 Breast implant explantation: indications and strategies to optimize aesthetic outcomes Connor Crowley, M. Bradley Calobrace, Mark W. Clemens, and Neil Tanna

29 Breast reconstruction with the latissimus dorsi flap

298

42 Enhanced recovery after surgery (ERAS) protocols in breast surgery: techniques and outcomes498 Nicholas F. Lombana, Reuben A. Falola, John C. Cargile, and Michel H. Saint-Cyr

43 Secondary procedures following autologous reconstruction516 Jian Farhadi and Vendela Grufman

44 Introduction to oncoplastic breast surgery

526

45 Partial breast reconstruction using reduction and mastopexy techniques

533

Maurice Y. Nahabedian

304

26 Secondary refinement procedures following prosthetic breast reconstruction

317

27 Introduction to autologous breast reconstruction with abdominal free flaps

46 Oncoplastic breast reconstruction: local flap techniques547

336

47 Surgical and non-surgical management of breast cancer-related lymphedema

Roy de Vita and Veronica Vietti Michelina

Maurice Y. Nahabedian

28 Breast reconstruction with the pedicle TRAM flap Jake C. Laun and Julian J. Pribaz

Albert Losken, Nusaiba F. Baker, and Alexandre Munhoz

Moustapha Hamdi and Claudio Angrigiani

340

Ketan M. Patel, Emma C. Koesters, Rachel Lentz, and Orr Shauly

556

Contents

48 Breast reconstruction and radiotherapy: indications, techniques, and outcomes

Jaume Masià, Cristhian D. Pomata, and Javier Sanz

567

49 Robotic-assisted autologous breast reconstruction581 Karim A. Sarhane and Jesse C. Selber

50 Total breast reconstruction by external vacuum expansion (EVE) and autologous fat transfer (AFT)

590

51 Current options for nipple reconstruction

603

Andrzej Piatkowski and Roger K. Khouri David Chi and Justin M. Sacks

Index610

Introduction:  Plastic surgery contributions to hand surgery James Chang

Section I: Principles of Hand Surgery 1 Anatomy and biomechanics of the hand

James Chang, Anais Legrand, Francisco J. Valero-Cuevas, Vincent R. Hentz, and Robert A. Chase

liii

1

3 Diagnostic imaging of the hand and wrist

70

4 Anesthesia for upper extremity surgery Eugene Park, Jonay Hill, Vanila M. Singh, and Subhro K. Sen

5 Principles of internal fixation

Margaret Fok, Jason R. Kang, Christopher Cox, and Jeffrey Yao

Section II: Trauma Reconstruction 6 Nail and fingertip reconstruction Amanda Brown, Brian A. Mailey, and Michael W. Neumeister

95 109

123

8 Fractures and dislocations of the wrist and distal radius

173

9 Flexor tendon injuries and reconstruction

193

Jin Bo Tang

10 Extensor tendon injuries

Kai Megerle and Karl-Josef Prommersberger

230

11 Replantation250 Dong Chul Lee and Eugene Park

12 Reconstructive surgery of the mutilated hand 272 S. Raja Sabapathy and Hari Venkatraman

13 Thumb reconstruction: Non-­microsurgical techniques305 Jeffrey B. Friedrich, Nicholas B. Vedder, and Elisabeth Haas-Lützenberger

14 Thumb reconstruction: Microsurgical techniques320 Nidal F. Al Deek and Fu-Chan Wei

17 Dupuytren’s disease

384

18 Osteoarthritis in the hand and wrist

411

19 Rheumatologic conditions of the hand and wrist

449

20 Occupational disorders of the hand

491

Section IV: Nerve Disorders 21 Nerve entrapment syndromes

499

22 Peripheral nerve repair and reconstruction

526

23 Brachial plexus injuries: adult and pediatric

552

James K-K. Chan, Paul M.N. Werker, and Jagdeep Nanchahal Paige M. Fox, J. Henk Coert, and Steven L. Moran

Simon Farnebo, Johan Thorfinn, and Lars B. Dahlin Johnny Chuieng-Yi Lu and David Chwei-Chin Chuang

24 Tetraplegia585 Carina Reinholdt and Catherine Curtin

25 Tendon transfers

605

26 Nerve transfers

638

27 Free-functioning muscle transfer

665

Section V: Challenging Disorders 28 The ischemic hand

680

29 The spastic hand

704

30 The stiff hand

716

31 The painful hand

735

Neil F. Jones

Kirsty Usher Boyd, Ida K. Fox, and Susan E. Mackinnon

Hee Chang Ahn, Jung Soo Yoon, and Neil F. Jones

147

Steven C. Haase and Kevin C. Chung

356

Kashyap K. Tadisina, Justin M. Sacks, and Mitchell A. Pet

Simeon C. Daeschler, Kristen M. Davidge, Leila Harhaus, and Gregory H. Borschel

7 Hand fractures and joint injuries

Warren C. Hammert and Randy R. Bindra

16 Tumors of the hand

Elisabet Hagert and Donald Lalonde

49

Alphonsus K.S. Chong, Janice Liao, and David M.K. Tan

337

Andrew O’Brien, Ryan P. Calfee, Jana Dengler, and Amy M. Moore

Celine Yeung and Steven J. McCabe

2 Examination of the upper extremity Ryosuke Kakinoki

Section III: Specific Disorders 15 Infections of the hand

Douglas M. Sammer and Kevin C. Chung

Volume Six: Hand and Upper Extremity

xi

Caroline Leclercq, Nathalie Bini, and Charlotte Jaloux



David T. Netscher, Rita E. Baumgartner, Kimberly Goldie Staines, and Logan W. Carr Hazel Brown, Anna Berridge, Dennis Hazell, Parashar Ramanuj, and Tom J. Quick

Section VI: Congenital Disorders 32 Congenital hand I: Embryology, classification, and principles 746 Michael Tonkin and Kerby C. Oberg

33 Congenital hand II: Malformations – whole limb

770

34 Congenital hand III: Malformations – abnormal axis differentiation – hand plate: proximodistal and radioulnar

790

Aaron Berger, Soumen Das De, Bhaskaranand Kumar, and Pundrique Sharma

Brinkley K. Sandvall and Charles A. Goldfarb

xii

Contents

35 Congenital hand IV: Malformations – abnormal axis differentiation – hand plate: unspecified axis

824

36 Congenital hand V: Deformations and dysplasias – variant growth

842

Christianne A. van Nieuwenhoven

Wee Leon Lam, Xiaofei Tian, Gillian D. Smith, and Shanlin Chen

37 Congenital hand VI: Dysplasias – tumorous conditions868 Amir H. Taghinia and Joseph Upton

38 Congenital hand VII: Dysplasias – congenital contractures898 Ellen Satteson, Paul C. Dell, Xiao Fang Shen, and Harvey Chim

39 Growth considerations in the pediatric upper extremity909 Marco Innocenti and Sara Calabrese

Section VII: New Directions 40 Treatment of the upper extremity amputee Gregory Ara Dumanian, Sumanas W. Jordan, and Jason Hyunsuk Ko

930

41 Upper extremity composite allotransplantation949 Christopher D. Lopez, Joseph Lopez, Jaimie T. Shores, W.P. Andrew Lee, and Gerald Brandacher

42 Aesthetic hand surgery

963

43 Hand therapy

983

David Alan Kulber and Meghan C. McCullough

Wendy Moore, Minnie Mau, and Brittany N. Garcia Index999

Video Contents Volume One Chapter 8: Pre- and intra-operative imaging for plastic surgery 8.1: Injection and monitoring of indocyanine green (ICG) using SPY for real-time lymphatic mapping in patients with lymphedema Arash Momeni and Lawrence Cai

Chapter 15: Wound healing 15.1: Treatment of left ischial pressure ulcer Kristo Nuutila, David E. Varon, and Indranil Sinha

Chapter 17: Skin grafting 17.1: Harvesting a split-thickness skin graft Dennis P. Orgill

Chapter 19: Repair, grafting, and engineering of cartilage 19.1: Surgical procedure of the implantation of in vitro engineered human ear cartilage 19.2: Follow-up analysis of auricular shape and structure, and mechanical property Wei Liu, Guangdong Zhou, and Yilin Cao

Chapter 27: Principles of radiation therapy 27.1: CT simulation and patient setup 27.2: Treatment planning Stephanie K. Schaub, Joseph Tsai, and Gabrielle M. Kane

Chapter 34: Robotics in plastic surgery 34.1: Robotic microsurgery 34.2: Robotic rectus abdominis muscle flap harvest 34.3: Trans-oral robotic surgery 34.4: Robotic latissimus dorsi muscle harvest 34.5: Robotic lymphovenous bypass Jesse C. Selber

Chapter 39: Gender-affirming Surgery 39.1: Pre-operative markings for double incision and free nipple grafting mastectomy. 39.2: Surgical approach to double incision and free nipple grafting mastectomy Edwin Wilkins, Shane D. Morrison, and Martin P. Morris 39.3: Creation of tube-in-tube phalloplasty Jens Urs Berli and Srdjan Kamenko 39.4: Surgical approach to penile inversion vaginoplasty Shane D. Morrison, Martin P. Morris, and William M. Kuzon

Volume Two

Chapter 9.3: Principles and surgical approaches of facelift 9.3.1: Parotid masseteric fascia 9.3.2: Anterior incision 9.3.3: Posterior incision 9.3.4: Facelift skin flap 9.3.5: Buccal fat pad elevation 9.3.6: Facial fat injection Richard J. Warren 9.3.7: Anthropometry, cephalometry, and orthognathic surgery Jonathon S. Jacobs, Jordan M.S. Jacobs, and Daniel I. Taub

Chapter 9.4: Facelift: Facial rejuvenation with loop sutures: the MACS lift and its derivatives 9.4.1: Loop sutures MACS facelift Patrick L. Tonnard

Chapter 9.5: Facelift: Platysma-SMAS plication 9.5.1: Platysma-SMAS plication Dai M. Davies and Miles G. Berry

Chapter 9.9: The lift-and-fill facelift 9.9.1: Adjunctive fat grafting during facelift 9.9.2: Face-lift incision planning Rod J. Rohrich and Erez Dayan

Chapter 9.10: Neck rejuvenation 9.10.1: Intraoperative dissection demonstrating the location of the great auricular nerve during facelift surgery 9.10.2: Intraoperative demonstration of facelift maneuvers in the midface that contribute to neck rejuvenation 9.10.3: Simulated components of neck rejuvenation approached through the submental incision on a fresh cadaver dissection James E. Zins and Jacob Grow 9.10.4: The anterior only approach to the neck James E. Zins, Colin M. Morrison, and C.J. Langevin

Chapter 9.14: Facial feminization 9.14.1: Markings for hairline lowering surgery 9.14.2: Burring of lateral orbital rim 9.14.3: Burring of mandibular body Patrick R. Keller, Matthew Louis, and Devin Coon

Chapter 11: Forehead rejuvenation 11.1: Traditional open brow lift 11.2: Endoscopic brow lift 11.3: Modified lateral brow lift 11.4: Gliding brow lift Richard Warren

Chapter 8.3: Injectables and resurfacing techniques: Botulinum toxin/neurotoxins

Chapter 13: Blepharoplasty

8.3.1: Botulinum toxin injection technique Rawaa Almukhtar and Sabrina G. Fabi

13.1: Perioribital rejuvenation Julius Few Jr. and Marco Ellis

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Video Contents

Chapter 15: Asian facial cosmetic surgery

Chapter 38: Post-bariatric reconstruction

15.1: Nonincisional double eyelidplasty Yeon Jun Kim 15.2: Incisional double eyelidplasty – pretarsal preparation Hong Lim Choi 15.3: Double fold fixation Hong Lim Choi 15.4: Lateral canthal lengthening Yeon Jun Kim 15.5: Medial epicanthoplasty 15.6: Eyelidplasty: Non-incisional method 15.7: Rhinoplasty 15.8: Subclinical ptosis correction (total) 15.9: Secondary rhinoplasty: septal extension graft and costal cartilage strut fixed with K-wire Kyung S. Koh, Jong Woo Choi, and Clyde H. Ishii

38.1: Post-bariatric reconstruction – bodylift procedure J. Peter Rubin and Jonathan W. Toy

Chapter 16: Facial fat grafting 16.1: Structural fat grafting of the face Sydney R. Coleman and Alesia P. Saboeiro

Volume Three Chapter 3: Aesthetic nasal reconstruction 3.1: The three-stage folded forehead flap for cover and lining 3.2: First-stage transfer and intermediate operation Frederick J. Menick

Chapter 4: Auricular construction 4.1: Total auricular construction Akira Yamada

Chapter 5: Secondary treatment of acquired cranio-orbital deformities

Chapter 19: Open technique rhinoplasty

5.1: Temporalis muscle flap 5.2: Orbitozygomatic osteotomy Oleh M. Antonyshyn

19.1: Open technique rhinoplasty Allen L. Van Beek

Chapter 8: Overview of head and neck soft-tissue and bony tumors

Chapter 23: Otoplasty and ear reduction 23.1: Setback otoplasty Leila Kasrai

Chapter 24: Hair restoration 24.1: My preferred hair transplantation technique: A 28 year experience Alfonso Barrera and Victor Zhu

Chapter 27: Abdominoplasty 27.1: Abdominoplasty markings 27.2: Secondary abdominoplasty Alan Matarasso

Chapter 28: Lipoabdominoplasty with anatomical definition: a new concept in abdominal aesthetic surgery 28.1: Lipoabdominoplasty (including secondary lipo) Osvaldo Ribeiro Saldanha, Sérgio Fernando Dantas de Azevedo, Osvaldo Ribeiro Saldanha Filho, Cristianna Bonetto Saldanha, and Luis Humberto Uribe Morelli

Chapter 35.2: Buttock augmentation with implants 35.2.1: Buttock augmentation Terrence W. Bruner, José Abel De la Peña Salcedo, Constantino G. Mendieta, and Thomas L. Roberts

Chapter 36: Upper limb contouring 36.1: Brachioplasty Joseph F. Capella, Margaret Luthringer, and Nikita Shulzhenko 36.2: Upper limb contouring Joseph F. Capella, Matthew J. Travato, and Scott Woehrle

8.1: Surgical approaches to the facial skeleton Yu-Ray Chen, You-Wei Cheong, and Alberto Cordova-Aguilar

Chapter 10: Local flaps for facial coverage 10.1: Facial artery perforator flap 10.2: Local flaps for facial coverage Peter C. Neligan

Chapter 12: Oral cavity, tongue, and mandibular reconstructions 12.1: Profunda artery perforator flap for tongue, inferior maxilla and lower lip defects 12.2: Osteomyocutaneous peroneal artery-based combined flap for reconstruction of type II mandibular defects Ming-Huei Cheng

Chapter 13: Hypopharyngeal, esophageal, and neck reconstruction 13.1: Reconstruction of pharyngoesophageal defects with the anterolateral thigh flap Peirong Yu

Chapter 15: Facial paralysis 15.1: Facial paralysis Eyal Gur 15.2: Facial paralysis 15.3: Cross facial nerve graft 15.4: Gracilis harvest Peter C. Neligan 15.5: Intraoperative gracilis stimulation 15.6: Intraoperative facial nerve stimulation Simeon C. Daeschler, Ronald M. Zuker, and Greogry H. Borschel

Chapter 37: Medial thigh

Chapter 16: Surgical management of facial pain, including migraines

37.1: Thighplasty Samantha G. Maliha and Jeffrey Gusenoff

16.1: Frontal trigger site injection Jeffrey E. Janis and Anna Schoenbrunner

Video Contents

Chapter 17: Facial feminization

Chapter 23: Orbital hypertelorism

17.1: Forehead reconstruction 17.2: Lower jaw and chin contouring Fermin Capitán-Cañadas, Luis Capitán, and Daniel Simon

23.1: Box-shift osteotomy Eric Arnaud

Chapter 19.2: Rotation advancement cheiloplasty 19.2.1: Repair of unilateral cleft lip Philip Kuo-Ting Chen, M. Samuel Noordhoff, Frank Chun-Shin, Chang, and Fuan Chiang Chan 19.2.2: Unilateral cleft lip and palate Philip Kuo-Ting Chen and Lucia Pannuto

Chapter 19.4: Anatomic subunit approximation approach to unilateral cleft lip repair 19.4.1: Medial lip checkpoints David M. Fisher and Raymond W. Tse 19.4.2: Unilateral cleft lip repair – anatomic subunit approximation technique David M. Fisher

Chapter 21.2: Straight line repair with intravelar veloplasty (IVVP) 21.2.1: Straight line repair of the palate with intravelar veloplasty (IVVP) Brian Sommerlad

xv

Chapter 28: Robin sequence 28.1: Tongue lip adhesion technique demonstrated and narrated by the senior author 28.2: Mandibular distraction Arun K. Gosain and Chad A. Purnell

Chapter 29: Treacher Collins syndrome 29.1: Lateral canthotomy 29.2: Ptosis correction 29.3: Dermisfat graft cheek Irene Mathijssen

Chapter 31: Vascular anomalies 31.1: Lip hemangioma Arin K. Greene

Chapter 32: Pediatric chest and trunk deformities 32.1: Cleft sternum 32.2: Thoracic ectopia cordis Han Zhuang Beh, Andrew M. Ferry, Rami P. Dibbs, Edward P. Buchanan, and Laura A. Monson

Chapter 21.3: Double opposing Z-palatoplasty 21.3.1: The Furlow double-opposing Z-palatoplasty Richard E. Kirschner and Jordan N. Halsey

Chapter 21.6: Oral fistula closure 21.6.1: Mobilization of the BFP flap for interposition Mirko S. Gilardino, Sabrina Cugno, and Abdulaziz Alabdulkarim

Volume Four Chapter 3.2: Imaging modalities for diagnosis and treatment of lymphedema

21.7.1: Alveolar bone graft: bone morphogenic protein & demineralized bone matrix Katelyn Kondra, Eloise Stanton, Christian Jimenez, Erik M. Wolfswinkel, Stephen Yen, Mark Urata, and Jeffrey Hammoudeh

3.2.1: ICG lymphangiography for lymphatic mapping before LVA procedure 3.2.2: Microscope-integrated NIRF imaging confirms LVA patency after the anastomosis 3.2.3: UHF-US records the contraction of a functional lymph vessel Balazs Mohos and Chieh-Han John Tzou

Chapter 21.9: Velopharyngeal dysfunction

Chapter 3.3: Lymphaticovenular bypass

21.9.1: Adequate velopharyngeal closer for speech 21.9.2: Velopharyngeal incompetence 21.9.3: Velopharyngeal insufficiency Richard E. Kirschner and Adriane L. Baylis

3.3.1: Supermicrosurgical lymphaticovenicular anastomosis Wei F. Chen, Lynn M. Orfahli, and Vahe Fahradyan

Chapter 21.7: Alveolar clefts

Chapter 21.10: Secondary deformities of the cleft lip, nose, and palate 21.10.1: Abbé flap Larry H. Hollier Jr. and Han Zhuang Beh 21.10.2: Complete takedown 21.10.3: Definitive rhinoplasty Evan M. Feldman, John C. Koshy, Larry H. Hollier Jr., and Samuel Stal 21.10.4: Thick lip and buccal sulcus deformities Evan M. Feldman and John C. Koshy

Chapter 21.11: Cleft and craniofacial orthognathic surgery 21.11.1: Le Fort I BSSO and genioplasty 21.11.2: Genioplasty 21.11.3: Patient recovery from orthognathic surgery Stephen B. Baker

Chapter 3.4: Vascularized lymph node transplant 3.4.1: Supraclavicular lymph node flap harvest Rebecca M. Garza and David W. Chang 3.4.2: Recipient site preparation for vascularized lymph node transfer – axilla David W. Chang

Chapter 3.5: Debulking strategies and procedures: liposuction of leg lymphedema 3.5.1: Liposuction of leg lymphedema: tips and tricks for a successful surgery Håkan Brorson

Chapter 3.6: Debulking strategies and procedures: excision 3.6.1: Charles procedure Peter C. Neligan

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Video Contents

Chapter 4: Lower extremity sarcoma reconstruction 4.1: Case example of a synovial sarcoma in the proximal leg. 4.2: Result 11 years after tumor removal and latissimus dorsi transplantation. Andrés A. Maldonado, Günter K. Germann, and Michael Sauerbier

14.3.6: Radial forearm phalloplasty: venous anastomoses and closure Alexander Y. Li, Walter C. Lin, and Bauback Safa

Chapter 14.4: Breast, chest wall, and facial considerations in gender affirmation

Chapter 5: Reconstructive surgery: lower extremity coverage

14.4.1: Facial feminization: operative technique Kaylee B. Scott, Dana N. Johns, and Cori A. Agarwal

5.1: Anterolateral thigh flap harvest Michel Saint-Cyr

Chapter 17: Perineal reconstruction

Chapter 6.2: Targeted muscle reinnervation in the lower extremity 6.2.1: Targeted muscle reinnervation in the lower extremity Brian L. Chang and Grant M. Kleiber

Chapter 6.3: Lower extremity pain: regenerative peripheral nerve interfaces 6.3.1: Intraoperative demonstration of sciatic nerve neuroma 6.3.2: Demonstration of autologous free skeletal muscle grafts harvested from the lower extremity for RPNIs Nishant Ganesh Kumar, Theodore A. Kung, and Paul S. Cederna

Chapter 7: Skeletal reconstruction 7.1: Harvesting technique of fibular free flap 7.2: Harvesting technique of iliac crest free flap Marco Innocenti, Stephen Kovach III, Elena Lucattelli, and L. Scott Levin 7.3: Medial femoral condyle/medial geniculate artery osseocutaneous free flap dissection Stephen Kovach III and L. Scott Levin

Chapter 9.2: Diabetic foot: management of wounds and considerations in biomechanics and amputations 9.2.1: AT and PT tendon transfers 9.2.2: Cadaver dissection lab: percutaneous tendo-achilles lengthening and vertical contour calcanectomy Jayson N. Atves

Chapter 11: Reconstruction of the chest 11.1: Sternal rigid fixation David H. Song and Michelle C. Roughton

Chapter 12: Reconstruction of the posterior trunk 12.1: Posterior trunk reconstruction with keystone flap Reuben A. Falola, Nicholas F. Lombana, Andrew M. Altman, and Michel H. Saint-Cyr

Chapter 13: Abdominal wall reconstruction 13.1: Ventral hernia repair using narrow well-fixed retrorectus mesh 13.2: “Pumpkin-teeth” flaps for creation of neo-umbilicus Gregory A. Dumanian

Chapter 14.3: Gender affirmation surgery, female to male: phalloplasty; and correction of male genital defects 14.3.1: Right radial forearm phalloplasty: history and markings 14.3.2: Radial forearm phalloplasty: flap donor nerve harvest 14.3.3: Radial forearm phalloplasty: flap shaping 14.3.4: Radial forearm phalloplasty: flap harvest 14.3.5: Radial forearm phalloplasty: vascular anastomoses

17.1: Discovering the role of robotically harvested rectus abdominis muscle flaps in the management of pelvic defects Geraldine T. Klein, Chad M. Bailey, John C. Pederson, Jesse C. Selber, and Louis L. Pisters

Chapter 20: Management of the burned face and neck 20.1: Application of collagen sheet on a partial thickness burn of face 20.2: Resurfacing a post burn scarred face with large full thickness grafts from expanded lower abdominal skin Vinita Puri and Venkateshwaran Narasiman

Chapter 21: Pediatric burns 21.1: Fractional CO2 laser for hypertrophic burn scars Sebastian Q. Vrouwe and Lawrence J. Gottlieb

Volume Five Chapter 3: Primary breast augmentation with implants 3.1: Skin incision and mono-polar needle electrocautery 3.2: Dissection through the deep dermis and subcutaneous fat 3.3: Entrance into the subpectoral space 3.4A: Insertion of the implant – Keller funnel 3.4B: Insertion of the implant – Motiva funnel 3.5: Marking, before performing lucky-8-stitch Charles Randquist

Chapter 5: Augmentation mastopexy 5.1: Preoperative markings for a single-stage augmentation mastopexy 5.2: Augmentation mastopexy W. Grant Stevens

Chapter 8: Short scar breast reduction 8.1: Breast mobility Elizabeth Hall-Findlay, Elisa Bolletta, and Gustavo Jiménez Muñoz Ledo 8.2: SPAIR technique Dennis C. Hammond

Chapter 14: Breast implant explantation: indications and strategies to optimize aesthetic outcomes 14.1: Demonstration of capsulotomy 14.2: Demonstration of a partial capsulectomy 14.3: Demonstration of total capsulectomy showing intact capsule and implant after removal Connor Crowley, M. Bradley Calobrace, Mark W. Clemens, and Neil Tanna

Chapter 15: Management strategies for gynecomastia 15.1: Surgical management of gynecomastia Michele Ann Manahan

Video Contents

15.2: Ultrasound-assisted liposuction Charles M. Malata

Chapter 16: Management options for gender affirmation surgery of the breast 16.1: Preoperative markings and surgical technique for gender affirming double-incision mastectomy Ara A. Salibian, Gaines Blasdel, and Rachel Bluebond-Langner

Chapter 18: Perfusion assessment techniques following mastectomy and reconstruction 18.1: Perfusion imaging as a decision-making tool within the operating room 18.2: ICG fluorescence imaging to determine the extent of perfusion for a perforator flap Alex Mesbahi, Matthew Cissell, Mark Venturi, and Louisa Yemc

Chapter 21: One-stage dual-plane reconstruction with prosthetic devices 21.1: Intraoperative technique: Immediate subpectoral direct-to-implant reconstruction with ADM Brittany L. Vieira and Amy S. Colwell

Chapter 24: Skin reduction using “smile mastopexy” technique in breast reconstruction 24.1: Marking for smile mastopexy 24.2: Operative procedure for smile mastopexy Kiya Movassaghi and Christopher N. Stewart

Chapter 25: Management of complications of prosthetic breast reconstruction

xvii

26.10: Balcony technique for reduction/augmentation mastopexy. Roy de Vita and Veronica Vietti Michelina

Chapter 28: Breast reconstruction with the pedicle TRAM flap 28.1: Unilateral breast reconstruction with a pedicled TRAM flap 28.2: Bilateral breast reconstruction with pedicled TRAM flaps 28.3: Abdominal donor site closure for bilateral TRAM flap Julian Pribaz and Jake Laun 28.4: The bikini inset Jake Laun Paul D. Smith, and Julian Pribaz 28.5: Demonstration of a bipedicled folded TRAM design Julian Pribaz, Jake Laun, Alex Girardot

Chapter 29: Breast reconstruction with the latissimus dorsi flap 29.1: Immediate latis marks 29.2: Delayed latis marks Dennis C. Hammond

Chapter 30: Autologous breast reconstruction with the DIEP flap 30.1: Incision of the anterior rectus fascia 30.2: Incision between the fascial rents 30.3: Intramuscular dissection of the perforator 30.4: Microvascular flap transfer, part 1 30.5: Microvascular flap transfer, part 2 30.6: Drainless progressive tension closure Adrian McArdle and Joan E. Lipa

25.1: Intra-operative video demonstrating poorly incorporated ADM along the inferolateral breast pocket following tissue expander removal 25.2: Patient presents following left sided mastectomy and tissue expander placement with a palpable seroma and fluid wave along the medial breast pocket 25.3: Patient underwent bilateral breast reconstruction following left skin-sparing mastectomy and prophylactic right nipple-sparing mastectomy Nima Khavanin and John Kim

Chapter 31: Autologous breast reconstruction with the free TRAM flap

Chapter 26: Secondary refinement procedures following prosthetic breast reconstruction

34.1: Superior gluteal artery perforator (SGAP) flap 34.2: Inferior gluteal artery perforator (IGAP) flap Peter C. Neligan

26.1: Preoperative 26.2: Postoperative 26.3: Lipoaspiration for lipofilling 26.4: Lipofilling on multiple plane with a fanning technique 26.5: Complete resolution of bilateral animation deformity and capsular contracture in a right breast reconstruction following radiotherapy and left simmetrization 26.6: Complete resolution of bilateral animation deformity and capsular contracture in a right breast reconstruction following radiotherapy and left simmetrization 26.7: Complete resolution of animation deformity after exchange of implant and change of implant placement with prepectoral implant based breast reconstruction. 26.8: Complete resolution of animation deformity after exchange of implant and change of implant placement with prepectoral implant based breast reconstruction. 26.9: Postoperative result in motion after nipple sparing mastectomy with prepectoral implant based breast reconstruction.

Chapter 35: Autologous breast reconstruction with medial thigh flaps

31.1: Elevation of the free TRAM flap Hyunho Han and Jin Sup Eom 31.2: Inset of TRAM flap in delayed breast reconstruction Jin Sup Eom

Chapter 34: Gluteal free flaps for breast reconstruction

35.1: Transverse upper gracilis (TUG) flap 1 Peter C. Neligan 35.2: Transverse upper gracilis (TUG) flap 2 Venkat V. Ramakrishnan

Chapter 36: Autologous breast reconstruction with the profunda artery perforator (PAP) flap 36.1: Profunda artery perforator flap. Adam T. Hauch, Hugo St. Hilaire, and Robert J. Allen Sr.

Chapter 42: Enhanced recovery after surgery (ERAS) protocols in breast surgery: techniques and outcomes 42.1: Traditional transversus abdominis plane block administration by chapter’s senior author

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Video Contents

42.2: Serratus anterior plane and PECS I block administration by chapter’s senior author Nicholas F. Lombana, Reuben A. Falola, John C. Cargile, and Michel H. Saint-Cyr

Chapter 44: Introduction to oncoplastic breast surgery 44.1: Partial breast reconstruction using reduction mammoplasty Maurice Y. Nahabedian

Chapter 47: Surgical and non-surgical management of breast cancer-related lymphedema 47.1: Lymphovenous bypass for BCRL 47.2: Composite SCIP vascularized lymph node transplant Ketan Patel

Volume Six Chapter 1: Anatomy and biomechanics of the hand 1.1: The extensor tendon compartments 1.2: The contribution of the interosseous and lumbrical muscles to the lateral bands 1.3: Extrinsic flexors and surrounding vasculonervous elements, from superficial to deep 1.4: The lumbrical plus deformity 1.5: The sensory and motor branches of the median nerve in the hand James Chang, Vincent R. Hentz, Robert A. Chase, and Anais Legrand

Chapter 2: Examination of the upper extremity 2.1: Flexor profundus test in a normal long finger 2.2: Flexor sublimis test in a normal long finger 2.3: The milking test of the fingers and thumb in a normal hand 2.4: Dynamic tenodesis effect in a normal hand 2.5: Eichhoff test 2.6: Extensor pollicis longus test in a normal person 2.7: Test for the extensor digitorum communis (EDC) muscle in a normal hand 2.8: Test for assessing thenar muscle function 2.9: The “cross fingers” sign 2.10: Scaphoid shift test 2.11: Ulnar fovea sign 2.12: Static two-point discrimination test (s-2PD test) 2.13: Moving 2PD test (m-2PD test) performed on the radial or ulnar aspect of the finger 2.14: Semmes Weinstein monofilament test: The patient should sense the pressure produced by bending the filament 2.15: Allen’s test in a normal person 2.16: Digital Allen’s test 2.17: Adson test 2.18: Roos test Ryosuke Kakinoki

Chapter 3: Diagnostic imaging of the hand and wrist 3.1: Scaphoid lunate dislocation Alphonsus K.S. Chong, David M.K. Tan 3.2: Right wrist positive midcarpal catch up clunk

3.3: Wrist ultrasound Alphonsus K.S. Chong

Chapter 4: Anesthesia for upper extremity surgery 4.1: Supraclavicular block Subhro K. Sen

Chapter 5: Principles of Internal Fixation 5.1: Dynamic compression plating and lag screw technique Christopher Cox 5.2: Headless compression screw 5.3: Locking vs. non-locking plates Jeffrey Yao and Jason R. Kang

Chapter 7: Hand fractures and joint injuries 7.1: PIP volar approach for ORIF Warren C. Hammert and Randy R. Bindra 7.2: Hemi-hamate arthroplasty Warren C. Hammert 7.3: MCP dislocation Warren C. Hammert and Randy R. Bindra 7.4: Metacarpal shaft ORIF narrated 7.5: Bennet reduction Warren C. Hammert

Chapter 9: Flexor tendon injuries and reconstruction 9.1: Zone II flexor tendon repair 9.2: Incision and feed tendon forward 9.3: Distal tendon exposure 9.4: Six-strand M-Tang repair 9.5: Extension-flexion test – wide awake 9.6: How to pass FDP tendon through a palm incision Jin Bo Tang

Chapter 10: Extensor tendon injuries 10.1: Secondary suture of central slip 10.2: Sagittal band reconstruction 10.3: Setting the tension in extensor indicis transfer Kai Megerle

Chapter 11: Replantation 11.1: Replantation Dong Chul Lee 11.2: Hand replantation James Chang

Chapter 12: Reconstructive surgery of the mutilated hand 12.1: Debridement technique James Chang

Chapter 13: Thumb reconstruction: Nonmicrosurgical techniques 13.1: First dorsal metacarpal artery (FDMA) flap 13.2: Osteoplastic thumb reconstruction Jeffrey B. Friedrich

Chapter 14: Thumb reconstruction: Microsurgical techniques 14.1: Trimmed great toe 14.2: Second toe for index finger

Video Contents

14.3: Combined second and third toe for metacarpal hand Nidal F. Al Deek

Chapter 17: Dupuytren’s disease 17.1: Surgical technique of PNF 17.2: Surgical technique of LF James K-K. Chan, Paul M.N. Werker, and Jagdeep Nanchahal

Chapter 18: Osteoarthritis in the hand and wrist 18.1: Ligament reconstruction tendon interposition arthroplasty of the thumb carpometacarpal joint James W. Fletcher

Chapter 19: Rheumatologic conditions of the hand and wrist 19.1: Silicone metacarpophalangeal arthroplasty Kevin C. Chung and Evan Kowalski 19.2: Extensor tendon rupture and end-side tendon transfer James Chang

Chapter 21: Nerve entrapment syndromes 21.1: The manual muscle testing algorithm 21.2: Scratch collapse test – carpal tunnel Elisabet Hagert 21.3: Injection technique for carpal tunnel surgery Donald Lalonde 21.4: Carpal tunnel and cubital tunnel releases in the same patient in one procedure with field sterility: Part 1 – local anesthetic injection for carpal tunnel Donald Lalonde and Michael Bezuhly 21.5: Wide awake carpal tunnel surgery Donald Lalonde 21.6: Endoscopic carpal tunnel release 21.7: Clinical exam and surgical technique – Lacertus syndrome Elisabet Hagert 21.8.1: Triple nerve release 1 21.8.2: Triple nerve release 2 21.8.3: Triple nerve release 3 Donald Lalonde 21.9: Carpal tunnel and cubital tunnel releases in the same patient in one procedure with field sterility: Part 2 – local anesthetic injection for cubital tunnel Donald Lalonde and Michael Bezuhly 21.10: Injection technique for cubital tunnel surgery 21.11: Wide awake cubital tunnel surgery Donald Lalonde 21.12: Clinical exam and surgical technique – Radial tunnel syndrome 21.13: Clinical exam and surgical technique – Lateral intermuscular syndrome 21.14: Clinical exam and surgical technique – Axillary nerve entrapment Elisabet Hagert

Chapter 22: Peripheral nerve repair and reconstruction 22.1: Suture repair of the cut digital nerve 22.2: Suture repair of the median nerve Simon Farnebo, Johan Thorfinn, and Lars B. Dahlin

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Chapter 23: Brachial plexus injuries: adult and pediatric 23.1: Supraclavicular brachial plexus dissection Johnny Chuieng-Yi Lu and David Chwei-Chin Chuang 23.2: Nerve transfer results 1 23.3: Nerve transfer results 2 23.4: Operative demonstration of 1) Contralateral C7 to innervate injured median nerve via free vascularized ulnar nerve graft, 2) 3rd to 5th intercostal nerve transfer to musculocutaneous nerve for a patient with right total root avulsion 23.5: Nerve transfer results 3 23.6: Nerve transfer results 4 David Chwei-Chin Chuang 23.7: Long-term result after total left brachial plexus palsy reconstruction Johnny Chuieng-Yi Lu and David Chwei-Chin Chuang 23.8: Nerve transfer results 5 David Chwei-Chin Chuang

Chapter 24: Tetraplegia 24.1: The single-stage grip and release procedure 24.2: Postoperative results after single-stage grip release procedure in OCu3-5 patients 24.3: Postoperative function after grip release procedure Carina Reinholdt and Catherine Curtin

Chapter 26: Nerve transfers 26.1: Guyon’s canal release and carpal tunnel release – extended Susan E. Mackinnon and Andrew Yee

Chapter 27: Free-functioning muscle transfer 27.1: Gracilis functional muscle harvest Gregory H. Borschel

Chapter 28: The ischemic hand 28.1: Extended sympathectomy of the radial, ulnar and common digital arteries for Raynaud’s phenomenon Neil F. Jones 28.2: Radial artery reconstruction with cephalic vein graft 28.3: Ulnar artery reconstruction with DIEA graft Hee Chang Ahn and Jung Soo Yoon

Chapter 29: The spastic hand 29.1: Hyperselective neuroectomy musculo-cutaneous Caroline Leclercq, Nathalie Bini, and Charlotte Jaloux

Chapter 30: The stiff hand 30.1: Volkmann angle allowing finger extension 30.2: Post-Operative demonstration 30.3: Joint demonstration after three days in a resting splint 30.4: Full function of joints during hockey practice 30.5: Weak grip strength, enough to impact work efficiency 30.6: Improved grip after elevating the original flap David T. Netscher, Rita E. Baumgartner, Kimberly Goldie Staines, and Logan W. Carr

Chapter 31: The painful hand 31.1: Surgical intervention: nerve root avulsion injuries 31.2: Surgical intervention: decompression and neurolysis Hazel Brown, Anna Berridge, Dennis Hazell, Parashar Ramanuj, and Tom J. Quick

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Video Contents

Chapter 32: Congenital hand I: Embryology, classification, and principles

Chapter 39: Growth considerations in the pediatric upper extremity

32.1: Pediatric trigger thumb release James Chang

39.1: Epiphyseal transplant harvesting technique Marco Innocenti and Sara Calabrese

Chapter 33: Congenital hand II: Malformations – whole limb

Chapter 41: Upper extremity composite allotransplantation

33.1: Function of left hand of patient in Figure 33-4 33.2: Congenital radioulnar synostosis of the right forearm and narrowing of the proximal radioulnar joint on the left forearm Aaron Berger, Soumen Das De, Bhaskaranand Kumar, and Pundrique Sharma

41.1: Upper extremity composite tissue allotransplantation W.P. Andrew Lee and Vijay S. Gorantla

Chapter 36: Congenital hand V: Deformations and dysplasia – variant growth 36.1: Surgical release of trigger thumb 36.2: Surgical release of trigger finger Wee Leon Lam, Xiaofei Tian, Gillian D. Smith, and Shanlin Chen 36.3: Thumb hypoplasia Amir H. Taghinia and Joseph Upton III

Chapter 37: Congenital hand VI: Dysplasia – tumorous conditions 37.1: Excision of venous malformation Joseph Upton III and Amir H. Taghinia

Chapter 42: Aesthetic hand surgery 42.1: Injection of radiesse using a bolus technique 42.2: Post-injection massage 42.3: Markings for autologous fat grafting 42.4: A fanning technique is used to maximize surface area contact between the fat and recipient tissues David Alan Kulber and Meghan C. McCullough

Chapter 43: Hand therapy 43.1: Fabrication of the RMA orthosis Wendy Moore, Minnie Mau, and Brittany N. Garcia

Lecture Video Contents Volume One Chapter 1: Plastic surgery and innovation in medicine Plastic surgery and innovation in medicine Peter C. Neligan

Chapter 25: Principles and techniques of microvascular surgery Principles and techniques of microvascular surgery Fu-Chan Wei, Sherilyn Keng Lin Tay, and Nidal F. Al Deek

Chapter 26: Tissue expansion and implants

Chapter 7: Digital photography in plastic surgery

Tissue expansion and implants Britta A. Kuehlmann, Eva Brix, and Lukas M. Prantl

Digital photography in plastic surgery

Chapter 27: Principles of radiation therapy

Daniel Z. Liu Chapter 8: Pre-and intra-operative imaging for plastic surgery Pre- and intra-operative imaging in plastic surgery Arash Momeni and Lawrence Cai

Chapter 16: Scar prevention, treatment, and revision Scar prevention, treatment, and revision Michelle F. Griffin, Evan Fahy, Michael S. Hu, Elizabeth R. Zielins, Michael T. Longaker, and H. Peter Lorenz

Principles of radiation therapy Stephanie K. Schaub, Joseph Tsai, and Gabrielle M. Kane

Chapter 29: Benign and malignant nonmelanocytic tumors of the skin and soft tissue Benign and malignant nonmelanocytic tumors of the skin and soft tissue Rei Ogawa

Chapter 39: Gender-affirming surgery Gender-affirming surgery Shane D. Morrison, William M. Kuzon Jr., and Jens U. Berli

Chapter 17: Skin grafting Skin grafting Shawn Loder, Benjamin Levi, and Audra Clark

Chapter 19: Repair, grafting, and engineering of cartilage Repair, grafting, and engineering of cartilage Wei Liu, Guangdong Zhou, and Yilin Cao

Chapter 20: Repair and grafting of bone Repair and grafting of bone Iris A. Seitz, Chad M. Teven, Bryce Hendren-Santiago, and Russell R. Reid

Chapter 21: Repair and grafting of peripheral nerve Repair and grafting of peripheral nerve Hollie A. Power, Kirsty Usher Boyd, Stahs Pripotnev, and Susan E. Mackinnon

Chapter 22: Repair and grafting fat and adipose tissue Repair and grafting fat and adipose tissue J. Peter Rubin

Chapter 23: Vascular territories Vascular territories Steven F. Morris and G. Ian Taylor

Chapter 24: Flap physiology, classification, and applications Flap physiology, classification, and applications Joon Pio Hong and Peter C. Neligan Flap pathophysiology and pharmacology Cho Y. Pang and Peter C. Neligan

Volume Two Chapter 5: Anatomic blocks of the face and neck Anatomic blocks of the face and neck Stelios C. Wilson and Barry Zide

Chapter 7: Non-surgical skin care and rejuvenation Non-surgical skin care and rejuvenation Zoe Diana Draelos

Chapter 8.2: Injectables and resurfacing techniques: Soft-tissue fillers Injectables and resurfacing techniques: soft-tissue fillers Kavita Mariwalla

Chapter 8.3: Injectables and resurfacing techniques: Botulinum toxin/neurotoxins Injectables and resurfacing techniques: botulinum toxin/neurotoxins Rawaa Almukhtar and Sabrina G. Fabi

Chapter 8.4: Injectables and resurfacing techniques: Lasers in aesthetic surgery Injectables and resurfacing techniques: Lasers in aesthetic surgery Jonathan Cook, David M. Turer, Barry E. DiBernardo, and Jason N. Pozner

Chapter 8.5: Injectables and resurfacing techniques: Chemical peels Injectables and resurfacing techniques: Chemical peels Richard H. Bensimon and Peter P. Rullan

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Lecture Video Contents

Chapter 9.2: Facial anatomy and aging

Chapter 11: Forehead rejuvenation

Facial anatomy and aging Bryan Mendelson and Chin-Ho Wong

Forehead rejuvenation Richard Warren

Chapter 9.3: Principles and surgical approaches of facelift

Chapter 12: Endoscopic brow lift

Principles and surgical approaches of facelift Richard J. Warren

Endoscopic brow lifting Renato Saltz and Eric W. Anderson

Chapter 13: Blepharoplasty

Chapter 9.4: Facelift: Facial rejuvenation with loop sutures: the MACS lift and its derivatives

Blepharoplasty Julius Few Jr. and Marco Ellis

Facelift: Facial rejuvenation with loop sutures: the MACS lift and its derivatives Patrick Tonnard, Alexis Verpaele, and Rotem Tzur

Chapter 14: Secondary blepharoplasty Secondary blepharoplasty Seth Z. Aschen and Henry M. Spinelli

Chapter 9.5: Facelift: Platysma-SMAS plication

Chapter 15: Asian facial cosmetic surgery

Facelift: Platysma-SMAS plication Miles G. Berry, James D. Frame III, and Dai M. Davies

Asian facial cosmetic surgery Jong Woo Choi, Tae Suk Oh, Hong Lim Choi, and Clyde Ishii

Chapter 9.6: Facelift: Lateral SMASectomy facelift

Chapter 16: Facial fat grafting

Facelift: Lateral SMASectomy facelift Daniel C. Baker and Steven M. Levine

Facial fat grafting Francesco M. Egro, Sydney R. Colman, and J. Peter Rubin

Chapter 18: Nasal analysis and anatomy

Chapter 9.7: Facelift: The extended SMAS technique in facial rejuvenation

Nasal analysis and anatomy Rod J. Rohrich and Paul N. Afrooz

Facelift: The extended SMAS technique in facial rejuvenation James M. Stuzin

Chapter 19: Open technique rhinoplasty

Chapter 9.8: High SMAS facelift: Combined single flap lifting of the jawline, cheek and midface High SMAS facelift: combined single flap lifting of the jawline, cheek and midface Timothy Marten and Dino Elyassnia

Chapter 9.9: The lift-and-fill facelift The lift-and-fill facelift Stav Brown, Justin L. Bellamy, and Rod J. Rohrich

Chapter 9.10: Neck rejuvenation Neck rejuvenation James E. Zins and Jacob Grow

Chapter 9.11: Male facelift Male facelift Timothy Marten and Dino Elyassnia

Open technique rhinoplasty Rod J. Rohrich and Paul N. Afrooz

Chapter 20: Closed technique rhinoplasty Closed technique rhinoplasty Mark B. Constantian

Chapter 21: Airway issues and the deviated nose Airway issues and the deviated nose Ali Totonchi, Bryan Armijo, and Bahman Guyuron

Chapter 22: Secondary rhinoplasty Secondary rhinoplasty David M. Kahn, Danielle H. Rochlin, and Ronald P. Gruber

Chapter 23: Otoplasty and ear reduction Otoplasty and ear reduction Charles H. Thorne

Chapter 24: Hair restoration

Chapter 9.12: Secondary facelift irregularities and the secondary facelift

Hair restoration Alfonso Barrera and Victor Zhu

Secondary facelift irregularities and the secondary facelift Timothy Marten and Dino Elyassnia

Chapter 25.2: Liposuction: a comprehensive review of techniques and safety

Chapter 9.13: Perioral rejuvenation, including chin and genioplasty

Liposuction: A comprehensive review of techniques and safety Gianfranco Frojo, Jayne Coleman, and Jeffrey Kenkel

Perioral rejuvenation, including chin and genioplasty Ali Totonchi and Bahman Guyuron

Chapter 25.3: Correction of liposuction deformities with the SAFE liposuction technique

Chapter 9.14: Facial femininization Facial feminization Patrick R. Keller, Matthew Louis, and Devin Coon

Correction of liposuction deformities with the SAFE liposuction technique Simeon H. Wall Jr. and Paul N. Afrooz

Lecture Video Contents

Chapter 27: Abdominoplasty Abdominoplasty Alan Matarasso

Volume Three

Chapter 30: Bra-line back lift

Chapter 1: Management of craniomaxillofacial fractures

Bra-line back lift Joseph Hunstad and Saad A. Alsubaie

Management of craniomaxillofacial fractures Srinivas M. Susarla, Russell E. Ettinger, and Paul N. Manson

Chapter 31: Belt Lipectomy

Chapter 2: Scalp and forehead reconstruction

Belt lipectomy Amitabh Singh and Al S. Aly

Scalp and forehead reconstruction Alexander F. Mericli and Jesse C. Selber

Chapter 32: Circumferential approaches to truncal contouring in massive weight loss patients: the lower lipo-bodylift

Chapter 3: Aesthetic nasal reconstruction

Circumferential approaches to truncal contouring in massive weight loss patients: the lower lipo-bodylift Dirk F. Richter and Nina Schwaiger

Chapter 33: Circumferential approaches to truncal contouring: autologous buttocks augmentation with purse-string gluteoplasty Circumferential approaches to truncal contouring: autologous buttocks augmentation with purse-string gluteoplasty Joseph P. Hunstad and Nicholas A. Flugstad

Chapter 34: Circumferential approaches to truncal contouring: Lower bodylift with autologous gluteal flaps for augmentation and preservation of gluteal contour Circumferential approaches to truncal contouring: Lower bodylift with autologous gluteal flaps for augmentation and preservation of gluteal contour Robert F. Centeno and Jazmina M. Gonzalez

Chapter 35.2: Buttock augmentation with implants Buttock augmentation with implants Jose Abel De la Peña Salcedo, Jocelyn Celeste Ledezma Rodriguez, and David Gonzalez Sosa

Chapter 35.3: Buttock shaping with fat grafting and liposuction

Aesthetic nasal reconstruction Frederick J. Menick

Chapter 4: Auricular construction Auricular construction Dale J. Podolsky, Leila Kasrai, and David M. Fisher

Chapter 8: Overview of head and neck soft-tissue and bony tumors Overview of head and neck soft-tissue and bony tumors Sydney Ch'ng and Edwin Morrison

Chapter 9: Post-oncologic midface reconstruction: the Memorial Sloan-Kettering Cancer Center and MD Anderson Cancer Center Approaches Post-oncologic midface reconstruction: the MSKCC and MDACC approaches Matthew M. Hanasono and Peter G. Cordeiro

Chapter 10: Local flaps for facial coverage Local flaps for facial coverage Nicholas Do and John Brian Boyd

Chapter 11: Lip reconstruction Lip reconstruction Julian J. Pribaz and Mitchell Buller Complex lip reconstruction: local flaps Julian J. Pribaz Total lip reconstruction Julian J. Pribaz

Buttock shaping with fat grafting and liposuction Constantino G. Mendieta, Thomas L. Roberts III, and Terrence W. Bruner

Chapter 12: Oral cavity, tongue, and mandibular reconstructions

Chapter 36: Upper limb contouring

Oral cavity, tongue, and mandibular reconstructions Ming-Huei Cheng

Upper limb contouring Margaret Luthringer, Nikita O. Shulzhenko, and Joseph F. Capella

Chapter 38: Post-bariatric reconstruction Post-bariatric reconstruction Jonathan W. Toy and J. Peter Rubin

Chapter 40: Aesthetic genital surgery Aesthetic genital surgery Gary J. Alter

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Chapter 13: Hypopharyngeal, esophageal, and neck reconstruction Hypopharyngeal, esophageal, and neck reconstruction Min-Jeong Cho and Peirong Yu

Chapter 15: Facial paralysis Facial paralysis Simeon C. Daeschler, Ronald M. Zuker, and Gregory H. Borschel

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Lecture Video Contents

Chapter 19.1: Unilateral cleft lip: introduction

Chapter 12: Reconstruction of the posterior trunk

Unilateral cleft lip Joseph E. Losee and Michael R. Bykowski

Reconstruction of the posterior trunk Reuben A. Falola, Nicholas F. Lombana, Andrew M. Altman, and Michel H. Saint-Cyr

Chapter 20: Repair of bilateral cleft lip Repair of bilateral cleft lip John B. Mulliken and Daniel M. Balkin

Chapter 21.1: Cleft palate: introduction Cleft palate Michael R. Bykowski and Joseph E. Losee

Chapter 21.4: Buccal myomucosal flap palate repair Buccal myomucosal flap palate repair Robert Joseph Mann

Chapter 25.2: Nonsyndromic craniosynostosis Nonsyndromic craniosynostosis Sameer Shakir and Jesse A. Taylor

Chapter 28: Robin sequence Robin sequence Sofia Aronson, Chad A. Purnell, and Arun K. Gosain

Chapter 31: Vascular anomalies Vascular anomalies Arin K. Greene and John B. Mulliken

Volume Four Chapter 2: Management of lower extremity trauma Management of lower extremity trauma Hyunsuk Peter Suh

Chapter 3.3: Lymphaticovenular bypass Lymphaticovenular bypass Wei F. Chen, Lynn M. Orfahli, and Vahe Fahradyan

Chapter 3.4: Vascularized lymph node transplant Vascularized lymph node transplant Rebecca M. Garza and David W. Chang

Chapter 3.6: Debulking strategies and procedures: excision Debulking strategies and procedures: excision Hung-Chi Chen and Yueh-Bih Tang

Chapter 5: Reconstructive surgery: lower extremity coverage Reconstructive surgery: lower extremity coverage Joon Pio Hong

Chapter 11: Reconstruction of the chest Reconstruction of the chest Brian L. Chang, Banafsheh Sharif-Askary, and David H. Song

Chapter 13: Abdominal wall reconstruction Abdominal wall reconstruction Gregory A. Dumanian

Chapter 14.1: Gender confirmation surgery: diagnosis and management Gender confirmation surgery: diagnosis and treatment Loren Schechter and Rayisa Hontscharuk

Chapter 15: Reconstruction of acquired vaginal defects Reconstruction of acquired vaginal defects Leila Jazayeri, Andrea L. Pusic, and Peter G. Cordeiro

Chapter 16: Pressure sores Pressure sores Ibrahim Khansa and Jeffrey E. Janis

Chapter 17: Perineal reconstruction Perineal reconstruction Ping Song, Hakim Said, and Otway Louie

Volume Five Chapter 3: Primary breast augmentation with implants Primary breast augmentation with implants Charles Randquist

Chapter 4: Autologous fat transfer: Fundamental principles and application for breast augmentation Autologous fat transfer: fundamental principles and application for breast augmentation Roger Khalil Khouri, Raul A. Cortes, and Daniel Calva-Cerquiera

Chapter 5: Augmentation mastopexy Augmentation mastopexy Justin L. Perez, Daniel J. Gould, Michelle Spring, and W. Grant Stevens

Chapter 9: Reduction mammaplasty with inverted-T techniques Reduction mammaplasty with inverted-T techniques Maurice Y. Nahabedian

Chapter 20: One- and two-stage prepectoral reconstruction with prosthetic devices One- and two-stage prepectoral reconstruction with prosthetic devices Alberto Rancati, Claudio Angrigiani, Maurizio Nava, Dinesh Thekkinkattil, Raghavan Vidya, Marcelo Irigo, Agustin Rancati, Allen Gabriel, and Patrick Maxwell

Lecture Video Contents

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Chapter 21: One-stage dual-plane reconstruction with prosthetic devices

Chapter 48: Breast reconstruction and radiotherapy: indications, techniques, and outcomes

One-stage dual-plane reconstruction with prosthetic devices Brittany L. Vieira and Amy S. Colwell

Breast reconstruction and radiotherapy: indications, techniques, and outcomes Jaume Masià, Cristhian D. Pomata, and Javier Sanz

Chapter 27: Introduction to autologous breast reconstruction with abdominal free flaps Introduction to autologous breast reconstruction with abdominal free flaps Maurice Y. Nahabedian

Volume Six Chapter 1: Anatomy and biomechanics of the hand

Chapter 29: Breast reconstruction with the latissimus dorsi flap

Anatomy and biomechanics of the hand James Chang, Anais Legrand, Francisco J. Valero-Cuevas, Vincent R. Hentz, and Robert A Chase

Breast reconstruction with the latissimus flap Dennis C. Hammond

Chapter 7: Hand fractures and joint injuries

Chapter 30: Autologous breast reconstruction with the DIEP flap Autologous breast reconstruction with the DIEP flap Adrian McArdle and Joan E. Lipa

Chapter 34: Gluteal free flaps for breast reconstruction Gluteal free flaps for breast reconstruction Salih Colakoglu and Gedge D. Rosson

Chapter 35: Autologous breast reconstruction with medial thigh flaps Autologous breast reconstruction with medial thigh flaps Venkat V. Ramakrishnan and Nakul Gamanlal Patel

Chapter 36: Autologous breast reconstruction with the profunda artery perforator (PAP) flap Autologous breast reconstruction with the profunda artery perforator (PAP) flap Adam T. Hauch, Hugo St. Hilaire, and Robert J. Allen Sr.

Chapter 37: Autologous reconstruction with the lumbar artery perforator (LAP) free flap Autologous reconstruction with the lumbar artery perforator (LAP) free flap Phillip Blondeel and Dries Opsomer

Chapter 40: Stacked and conjoined flaps

Hand fractures and joint injuries Warren C. Hammert and Randy R. Bindra

Chapter 8: Fractures and dislocations of the wrist and distal radius Fractures and dislocations of the wrist and distal radius Steven C. Haase and Kevin C. Chung

Chapter 11: Replantation Replantation Dong Chul Lee and Eugene Park

Chapter 13: Thumb reconstruction: Nonmicrosurgical techniques Thumb reconstruction: Non-microsurgical techniques Jeffrey B. Friedrich, Nicholas B. Vedder, and Elisabeth Haas-Lützenberger

Chapter 14: Thumb reconstruction: Microsurgical techniques Thumb reconstruction: Microsurgical techniques Nidal F. Al Deek and Fu-Chan Wei

Chapter 21: Nerve entrapment syndromes Nerve entrapment syndromes Elisabet Hagert and Donald Lalonde

Chapter 22: Peripheral nerve repair and reconstruction Peripheral nerve repair and reconstruction Simon Farnebo, Johan Thorfinn, and Lars B. Dahlin

Stacked and conjoined flaps Nicholas T. Haddock and Sumeet S. Teotia

Chapter 24: Tetraplegia

Chapter 43: Secondary procedures following autologous reconstruction

Tetraplegia Carina Reinholdt and Catherine Curtin

Secondary procedures following autologous reconstruction Jian Farhadi and Vendela Grufman

Chapter 25: Tendon transfers Tendon transfers Neil F. Jones

Chapter 44: Introduction to oncoplastic breast surgery

Chapter 26: Nerve transfers

Introduction to oncoplastic breast surgery Maurice Y. Nahabedian

Nerve transfers Kirsty Usher Boyd, Ida K. Fox, and Susan E. Mackinnon

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Lecture Video Contents

Chapter 30: The stiff hand The stiff hand David T. Netscher, Rita E. Baumgartner, Kimberly Goldie Staines, and Logan W. Carr

Chapter 31: The painful hand Clinical assessment of the function of the sympathetic nervous system Clinical assessment of the function of the nervous system: Hoffman-Tinel Test Hazel Brown, Anna Berridge, Dennis Hazell, Parashar Ramanuj, and Tom J. Quick

Chapter 39: Growth considerations in the pediatric upper extremity Growth considerations in the Pediatric upper extremity Marco Innocenti and Sara Calabrese

Chapter 40: Treatment of the upper extremity amputee Treatment of the upper extremity amputee Gregory Ara Dumanian, Sumanas W. Jordan, and Jason Hyunsuk Ko

Preface to the Fifth Edition This is the 5th edition of Plastic Surgery but the third and last edition for which I have been lucky enough to be Editor-in Chief. Looking back on the almost 15 years I have been involved in this series, I marvel at how many advances have been made in the specialty in that relatively short time. My predecessors, Drs. McCarthy and Mathes, who edited the 1st and 2nd editions, did so by themselves. When I took over the 3rd edition I realized that the specialty had become so complex that one person could not possibly have the bandwidth to do justice to all the information that an encyclopedic series such as this demands. I therefore introduced separate editors for each volume, bringing their subspecialty expertise to each volume, helping to highlight advances in their areas of subspecialty as well as identifying leaders in the field and up-and-coming authorities to author the various chapters. In this edition we have increased the number of volume editors. This reflects the ever-increasing complexity as well as the most recent advances in each area. In this 5th edition, Andrea Pusic joins Geoff Gurtner in Volume 1; Alan Matarasso teams up with Peter Rubin in Volume 2; Richard Hopper has replaced Ed Rodriguez (who did an outstanding job but, because of increased work demands, had to step down) and edited Volume 3 with Joe Losee; JP Hong joined David Song in Volume 4. Mo Nahabedian in Volume 5 and Jim Chang in Volume 6 updated both of those volumes. Developments continue within the specialty and we have endeavored to capture them in this edition. Dr. Daniel Liu, the multimedia editor has, once again, done an amazing job in compiling and editing the media content. In the 3rd edition we compiled multiple movies to complement the text. In the 4th edition we considerably expanded the list of videos and added lectures to accompany selected chapters. Many of these presentations were done by the chapter authors; the rest were compiled by Dr. Liu and myself from the content of the individual chapters. We have kept many of the movies and lectures from the previous editions and added to them yet again. A significant feature in this edition is the artwork on the cover. I am truly indebted to John Semple, a friend and former colleague of mine in Toronto, for providing this original piece of art. As well as being a talented and widely published plastic surgeon, John is an artist and a musician as well as being Fellow of the Canadian National Geographic Society, well known for his research on climate change in the Himalayas. I asked John if he would consider doing a painting for the cover of this edition and was delighted when he accepted.

In both the 3rd and 4th editions, we started the process of organizing the content with face-to-face meetings with the volume editors as well as the Elsevier team. Because of COVID, this was not possible for this edition so it was all planned via video conferencing. We held regular online meetings between Elsevier and the volume editors during the whole production process. This proved not only to be convenient, but extremely efficient. We went through the 4th edition volume by volume, chapter by chapter, decided what needed to stay, what needed to be added, what needed to be revised, and what needed to be changed. We also decided who should write the various chapters, keeping many existing authors, replacing others, and adding some new ones; we did this in order to really reflect the changes occurring within the specialty. Apart from the updated content, there is a lot that is new in each volume of this edition. We have new chapters on patient-reported outcome measures (PROMs), on education and teaching in Plastic Surgery, on gender-affirmation surgery, lymphedema, local anesthetic blocks in aesthetic surgery, facial feminization, diabetic foot management, to name but some. We have also added multiple algorithms for various conditions, all in an effort to make the text easier to use and more approachable. In my travels around the world since the 3rd edition was published, I’ve been struck by the impact this publication has had on the specialty and, more particularly, on training. Everywhere I go, I’m told how the text is an important part of didactic teaching and a font of knowledge. It was gratifying to see the 3rd edition translated into Portuguese, Spanish, and Chinese. The 4th edition has been equally successful. When I first took over as Editor-in-Chief of this series, Elsevier wanted a new edition to be produced every 5 years. At first I thought that was too ambitious, but as this 5th edition is published I am struck, once again, by the extent of what has changed and how the specialty has continually developed, as evidenced by the number of completely new chapters (34), not to mention all the updated ones. I hope this 5th edition continues to contribute to the specialty, remains a resource for practicing surgeons, and continues to prepare our trainees for their future careers in Plastic Surgery. Peter C. Neligan Phoenix, AZ March, 2023

List of Editors Editor-in-Chief Peter C. Neligan, MB, FRCS(I), FRCSC, FACS Professor Emeritus Surgery, Division of Plastic Surgery University of Washington Seattle, WA, United States

Volume 3: Pediatric Surgery Joseph E. Losee, MD Ross H. Musgrave Professor of Pediatric Plastic Surgery Department of Plastic Surgery University of Pittsburgh Medical Center Chief, Division of Pediatric Plastic Surgery UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA, United States

Volume 1: Principles Geoffrey C. Gurtner, MD, FACS Professor and Chair, Department of Surgery Professor of Biomedical Engineering College of Medicine University of Arizona Tucson, AZ, United States

Volume 4: Lower Extremity, Trunk and Burns David H. Song, MD, MBA, FACS Physician Executive Director and Chairman Plastic Surgery Georgetown University Washington, DC, United States

Andrea L. Pusic, MD Chief, Division of Plastic and Reconstructive Surgery Brigham and Women’s Hospital Boston, MA, United States

Joon Pio Hong, MD, PhD, MMM Professor, Plastic Surgery Asan Medical Center University of Ulsan Seoul, Republic of Korea Adjunct Professor Plastic and Reconstructive Surgery Georgetown University Washington, DC, United States

Volume 2: Aesthetic J. Peter Rubin, MD, FACS Professor and Chair, Department of Plastic Surgery Professor of Bioengineering University of Pittsburgh Pittsburgh, PA, United States

Volume 5: Breast Maurice Y. Nahabedian, MD, FACS Former Professor of Plastic Surgery Johns Hopkins University, Georgetown University, and the Virginia Commonwealth University Private practice – National Center for Plastic Surgery McLean, VA, United States

Alan Matarasso, MD, FACS Clinical Professor of Surgery Systems Chief of Cosmetic Surgery Hofstra School of Medicine-Northwell Health System New York, NY, United States

Volume 6: Hand and Upper Extremity James Chang, MD Johnson & Johnson Distinguished Professor and Chief Division of Plastic Surgery Stanford University Medical Center Palo Alto, CA, United States

Volume 3: Craniofacial, Head and Neck Surgery Richard A. Hopper, MD, MS Chief, Division of Craniofacial and Plastic Surgery Surgical Director, Craniofacial Center Seattle Children’s Hospital Marlys C. Larson Professor Department of Surgery University of Washington Seattle, WA, United States

Multimedia editor

Daniel Z. Liu, MD Reconstructive Microsurgeon Oncoplastic and Reconstructive Surgery City of Hope Chicago Zion, IL, United States

List of Contributors The editors would like to acknowledge and offer grateful thanks for the input of all previous editions’ contributors, without whom this new edition would not have been possible. VOLUME ONE Hatem Abou-Sayed, MD, MBA, FACS Private Practice Plastic Surgeon Tim Sayed MD, P.C. La Jolla and Newport Beach, CA; Co-Founder and Chief Medical Officer YesDoctor Irvine, CA; Co-Founder and Chief Medical Officer Elevai Labs Newport Beach, CA, United States Paul N. Afrooz, MD Resident Plastic and Reconstructive Surgery University of Pittsburgh Medical Center Pittsburgh, PA, United States Nidal F. Al Deek, MD, MSc Associate Professor of Surgery Division of Plastic and Reconstructive Microsurgery Cleveland Medical Center, University Hospitals Case Western Reserve School of Medicine Cleveland, OH, United States; Chang Gung Memorial Hospital, and Chang Gung School of Medicine Taipei, Taiwan Jens U. Berli, MD Associate Professor Division Chief Plastic Surgery Department of Surgery Oregon Health and Science University Portland, OR, United States Kirsty Usher Boyd, MD, FRCSC Associate Professor Division of Plastic Surgery The Ottawa Hospital University of Ottawa Ottawa, ON, Canada Eva Brix, MD Consultant Plastic Surgeon Department of Plastic, Hand, and Reconstructive Surgery University Hospital Regensburg Regensburg, Germany Stav Brown, MD Research Fellow Plastic and Reconstructive Surgery Memorial Sloan Kettering Cancer Center New York, NY, United States Justin M. Broyles, MD Assistant Professor of Surgery Plastic and Reconstructive Surgery Harvard Medical School, Brigham and Women’s Hospital Boston, MA, United States

Jacqueline N. Byrd, MD, MPH, MS Research Fellow Surgery, Center for Health Outcomes and Policy University of Michigan Ann Arbor, MI; Resident Surgery University of Texas Southwestern Dallas, TX, United States Lawrence Cai, MD Division of Plastic and Reconstructive Surgery Stanford University Medical Center Palo Alto, CA, United States Yilin Cao, MD, PhD Professor Shanghai 9th People’s Hospital Shanghai Jiao Tong University School of Medicine Shanghai, China Kellen Chen, PhD Assistant Research Professor Department of Surgery Department of Biomedical Engineering College of Medicine University of Arizona – Tucson Tucson, AZ, United States Sydney Ch’ng, MBBS, PhD, FRACS Associate Professor Faculty of Medicine and Health The University of Sydney Sydney, NSW, Australia Kevin C. Chung, MD, MS Professor of Surgery Section of Plastic Surgery University of Michigan; Chief of Hand Surgery University of Michigan; Assistant Dean for Faculty Affairs University of Michigan Ann Arbor, MI, United States Franklyn P. Cladis, MD, FAAP Associate Professor of Anesthesiology Department of Anesthesiology The Children’s Hospital of Pittsburgh of UPMC; Program Director, Pediatric Anesthesiology Fellowship The Children’s Hospital of Pittsburgh of UPMC Pittsburgh, PA, United States Audra Clark, MD Assistant Professor General Surgery University of Texas Southwestern Dallas, TX, United States

Alex Clarke, DSc honoris causa, DClinPsych, MSc, BSc (Hons), AFBPS Visiting Professor, Chartered Clinical and Health Psychologist Centre for Appearance Research UWE Bristol Bristol, United Kingdom Michelle Coriddi, MD Attending Plastic Surgery Memorial Sloan Kettering Cancer Center New York, NY, United States Yannick F. Diehm, MD, MSc Resident Doctor Department of Hand, Plastic and Reconstructive Surgery BG Trauma Center Ludwigshafen Ludwigshafen, Germany Jessica Erdmann-Sager, MD, FACS Assistant Professor Harvard Medical School Division of Plastic Surgery Brigham and Women’s Hospital Newton, MA, United States Evan Fahy, MD Clinical Research Fellow Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States Lucas Gallo, MD, MSc, PhD(c) Resident Physician Clinician Investigator Program; Division of Plastic Surgery, Department of Surgery McMaster University Hamilton, ON, Canada Amanda Gosman, MD Professor and Chief of Plastic Surgery Director of Craniofacial and Pediatric Plastic Surgery UC San Diego School of Medicine San Diego, CA, United States Madelijn Gregorowitsch, MD, PhD, MHSc General Practitioner in Training and Clinical Epidemiologist The Julius Center, University Medical Center Utrecht Utrecht, The Netherlands Michelle F. Griffin, MBChB, PhD Clinical Research Fellow Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States

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List of Contributors

Geoffrey C. Gurtner, MD Professor and Chair Department of Surgery Professor of Biomedical Engineering College of Medicine University of Arizona Tucson, AZ, United States Karl-Anton Harms, MBBS O’Brien Institute Department St Vincent’s Institute for Medical Research Melbourne, VIC, Australia Valentin Haug, MD Resident Doctor Department of Hand, Plastic and Reconstructive Surgery BG Trauma Center Ludwigshafen Ludwigshafen, Germany Lydia Helliwell, MD Plastic, Hand and Reconstructive Surgeon Brigham and Women’s Hospital Harvard Medical School Boston, MA, United States Bryce Hendren-Santiago, BS Medical Student Pritzker School of Medicine University of Chicago Chicago, IL, United States Dominic Henn, MD Department of Plastic Surgery University of Texas Southwestern Medical Center Dallas, TX, United States George Ho, MD Division of Plastic, Reconstructive and Aesthetic Surgery Department of Surgery University of Toronto Toronto, ON, Canada Joon Pio Hong, MD, PhD, MMM Professor Plastic Surgery Asan Medical Center, University of Ulsan Seoul, Republic of Korea; Adjunct Professor Plastic and Reconstructive Surgery Georgetown University Washington, DC, United States Michael S. Hu, MD Clinical Research Fellow Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States C. Scott Hultman, MD, MBA Professor and Vice Chair Department of Plastic Surgery Johns Hopkins University School of Medicine; Director Burn Center Johns Hopkins Bayview; Fellowship Director Burn Surgical Critical Care Johns Hopkins Bayview Baltimore, MD, United States

Leila Jazayeri, MD Microsurgery Fellow Plastic and Reconstructive Surgery Memorial Sloan Kettering New York, NY, United States

Daniel Z. Liu, MD Reconstructive Microsurgeon Oncoplastic and Reconstructive Surgery City of Hope Chicago Zion, IL, United States

Haley M. Jeffers Student Harvard University Boston, MA, United States

Wei Liu, MD, PhD Professor Plastic and Reconstructive Surgery Shanghai 9th People’s Hospital Shanghai Jiao Tong University School of Medicine Shanghai, China

Lynn Jeffers, MD, MBA, FACS Chief Medical Officer CommonSpirit/Dignity Health St. John’s Regional Medical Center and St. John’s Hospital Camarillo, CA Plastic Surgery Private Practice Oxnard and Camarillo, CA, United States Gabrielle M. Kane, MB, BCh, EdD, FRCPC Professor Emeritus Radiation Oncology University of Washington Seattle, WA, United States Martin Kauke-Navarro, MD Resident Physician Department of Surgery, Division of Plastic Surgery Yale School of Medicine New Haven, CT, United States Timothy W. King, MD, PhD, MSBE, FAAP, FACS Stuteville Division Chief of Plastic and Reconstructive Surgery Professor, Department of Surgery Loyola Stritch School of Medicine Maywood, IL; Plastic Surgery Site Director Department of Surgery Hines VA Hospital Hines, IL, United States Anne F. Klassen, BA(Hons), DPhil Professor Department of Pediatrics McMaster University Hamilton, ON, Canada Britta A. Kuehlmann, Dr. med. Postdoctoral Research Fellow Plastic Surgery Stanford University Palo Alto, CA, United States; Plastic Aesthetic Surgeon, Scientist and Founder, CEO and MD of CINEOLUX Düsseldorf, North Rhine-Westphalia, Germany WiIliam M. Kuzon Jr., MD, PhD Reed O. Dingman Professor of Surgery Department of Surgery University of Michigan Ann Arbor, MI, United States Benjamin Levi, MD Dr. Lee Hudson-Robert R. Penn Chair in Surgery Associate Professor in the Department of Surgery University of Texas Southwestern Medical Center, Dallas, TX, United States

Shawn Loder, MD Resident Department of Plastic Surgery University of Pittsburgh Pittsburgh, PA, United States Michael T. Longaker, MD, MBA, FACS Deane P. and Louise Mitchell Professor of Plastic Surgery Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States H. Peter Lorenz, MD Pediatric Plastic Surgery Service Chief and Professor Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States Susan E. Mackinnon, MD, FRCSC, FACS Minot Packer Fryer Professor of Surgery Director of the Center for Nerve Injury and Paralysis Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, MO, United States Michele A. Manahan, MD, MBA, FACS Professor of Clinical Plastic and Reconstructive Surgery Department of Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States Isabella C. Mazzola, MD Attending Plastic Surgeon Klinki für Plastiche und Ästhetische Chirurgie Klinikum Landkreis Erding Erding, Germany Riccardo F. Mazzola, MD Plastic Surgeon Department of Specialistic Surgical Sciences Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico Milan, Italy Babak J. Mehrara, MD Chief Plastic and Reconstructive Surgery Memorial Sloan Kettering Cancer Center; Member Plastic and Reconstructive Surgery Memorial Sloan Kettering Cancer Center New York, NY; Professor Plastic and Reconstructive Surgery Weill Cornell Hospital New York, NY, United States

List of Contributors

Arash Momeni, MD Director, Clinical Outcomes Research Division of Plastic and Reconstructive Surgery Stanford University Medical Center Palo Alto, CA, United States

David Perrault, MD Division of Plastic and Reconstructive Surgery Stanford University Stanford, CA, United States

Steven F. Morris, MD, MSc, FRCS(C) Professor Department of Surgery Dalhousie University Halifax, NS, Canada

Bohdan Pomahac, MD Professor of Surgery Chief, Division of Plastic and Reconstructive Surgery Frank F. Kanthak Professor of Surgery Department of Surgery Yale School of Medicine New Haven, CT, United States

Shane D. Morrison, MD, MS Assistant Professor Division of Plastic Surgery, Department of Surgery Seattle Children’s Hospital; Division of Plastic Surgery, Department of Surgery University of Washington Medical Center Seattle, WA, United States

Hollie A. Power, MD, FRCSC Assistant Professor Division of Plastic Surgery, Department of Surgery University of Alberta Edmonton, AB, Canada

Peter C. Neligan, MB, FRCS(I), FRCSC, FACS Professor Emeritus Surgery, Division of Plastic Surgery University of Washington Seattle, WA, United States

Lukas M. Prantl, MD, PhD University Center for Plastic, Reconstructive, and Hand Surgery University Hospital Regensburg Regensburg, Germany

Jonas A. Nelson, MD, MPH Assistant Professor Department of Surgery Memorial Sloan Kettering New York, NY, United States

B. Aviva Preminger, MD, MPH, FACS Preminger Plastic Surgery New York, NY, United States

Peter Nthumba, MD, MSc AIC Kijabe Hospital Department of Plastic Surgery Vanderbilt University Medical Center Nashville, TN, United States Kristo Nuutila, MSc, PhD Principal Research Scientist US Army Institute of Surgical Research San Antonio, TX; Associate Professor of Surgery Uniformed Services University of the Health Sciences Bethesda, MD, United States Anaeze C. Offodile 2nd, MD, MPH Assistant Professor Department of Plastic and Reconstructive Surgery University of Texas MD Anderson Cancer Center; Assistant Professor Department of Health Services Research University of Texas MD Anderson Cancer Center Houston, TX, United States Rei Ogawa, MD, PhD, FACS Professor Department of Plastic, Reconstructive and Aesthetic Surgery Nippon Medical School Tokyo, Japan Christopher J. Pannucci, MD, MS Plastic and Microvascular Surgeon Private Practice Plastic Surgery Northwest Spokane, WA, United States

Karim A. Sarhane, MD, MSc General, Laparoscopic, and Peripheral Nerve Surgeon Burjeel Royal Hospital, Al Ain Abu Dhabi United ArabEmirates Stephanie K. Schaub, MD Assistant Professor Department of Radiation Oncology University of Washington School of Medicine Seattle, WA, United States Iris A. Seitz, MD, PhD Edward-Elmhurst Healthcare Naperville, IL, United States Jesse C. Selber, MD, MPH, FACS Professor, Vice Chair, Director of Clinical Research Department of Plastic Surgery MD Anderson Cancer Center Houston, TX, United States Ramin Shayan, MBBS, PhD, FRACS(Plast) Associate Professor O’Brien Institute Department St. Vincent’s Institute for Medical Research Melbourne, VA, Australia

Stahs Pripotnev, MD, FRCSC Assistant Professor Division of Plastic Surgery Roth | McFarlane Hand and Upper Limb Centre Western University London, ON, Canada

Clifford C. Sheckter, MD Assistant Professor Plastic and Reconstructive Surgery Stanford University Stanford, CA; Associate Director Regional Burn Center Santa Clara Valley Medical Center San Jose, CA, United States

Andrea L. Pusic, MD Professor Chief, Division of Plastic and Reconstructive Surgery Brigham and Women’s Hospital Boston, MA, United States

Indranil Sinha, MD Plastic and Reconstructive Surgery Brigham and Women’s Hospital; Associate Professor Harvard Medical School Boston, MA, United States

Russell R. Reid, MD, PhD Professor Surgery/Section of Plastic and Reconstructive Surgery University of Chicago Medicine Chicago, IL, United States

Dharshan Sivaraj, BS Research Fellow Division of Plastic Surgery, Department of Surgery Stanford University University of Arizona – Tucson Tucson, AZ, United States

Johanna N. Riesel, MD Pediatric Craniofacial and Plastic Surgery The Hospital for Sick Children Toronto, ON, Canada J. Peter Rubin, MD Professor and Chair Department of Plastic Surgery University of Pittsburgh; Professor Bioengineering University of Pittsburgh Pittsburgh, PA, United States Nichola Rumsey, BSC, MSc, PhD Professor Emerita Centre for Appearance Research UWE Bristol Bristol, United Kingdom

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Sherilyn Keng Lin Tay, MRCS, MSc, FRCS(Plast) Consultant Plastic Surgeon Plastic Surgery Glasgow Royal Infirmary Glasgow, United Kingdom G. Ian Taylor, AO, FRACS Professor Department of Anatomy and Physiology University of Melbourne; Department of Plastic Surgery Royal Melbourne Hospital Melbourne, VIC, Australia Chad M. Teven, MD, MBA, FACS, HEC-C Assistant Professor of Surgery (Clinical) Northwestern University Feinberg School of Medicine Chicago, IL, United States

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List of Contributors

Achilleas Thoma, MD, MSc, FRCS(C), FACS Clinical Professor, Department of Surgery Associate Member, Department of Health Research Methods, Evidence and Impact (HEI) McMaster University Hamilton, ON, Canada Charles H. Thorne, MD Chairman Department of Plastic Surgery Lenox Hill Hospital New York, NY, United States Joseph Tsai, MD, PhD Department of Radiation Oncology University of Washington School of Medicine Seattle, WA, United States Alexander H.R. Varey, MBChB, MRCS, FRACS, FRCS(Plast), PhD Clinical Associate Professor Faculty of Health and Medicine University of Sydney; Faculty Member Melanoma Institute Australia Sydney; Staff Specialist Plastic and Reconstructive Surgery Westmead Hospital Sydney, NSW, Australia David E. Varon, BS University of Michigan Medical School Ann Arbor, MI, United States Sophocles H. Voineskos, MD, MSc Assistant Professor Division of Plastic Surgery, Department of Surgery University of Toronto Toronto, ON, Canada Fu-Chan Wei, MD, FACS Professor Plastic and Reconstructive Surgery Chang Gung Memorial Hospital Kweishan, Taoyuan, Taiwan Stelios C. Wilson, MD Private Practice Charles H. Thorne MD Plastic Surgery New York, NY, United States Danny Young-Afat, MD, PhD, MHSc Plastic Surgeon and Clinical Epidemiologist Department of Plastic and Reconstructive Surgery Amsterdam University Medical Center Amsterdam, The Netherlands Guangdong Zhou, MD, PhD Professor Plastic and Reconstructive Surgery, Shanghai Key Laboratory of Tissue Engineering Research Shanghai 9th People’s Hospital Shanghai Jiao Tong University School of Medicine Shanghai, China Elizabeth R. Zielins, MD Clinical Research Fellow Stanford University School of Medicine Division of Plastic and Reconstructive Surgery Stanford, CA, United States

VOLUME TWO Paul N. Afrooz, MD Private Practice Miami, FL, United States Rawaa Almukhtar, MD, MPH Scripps Medical Group Dermatology San Diego, CA, United States Saad A. Alsubaie, MD, FACS, FRCSC Asthetic Plastic Surgeon North Texas Plastic Surgery Dallas, TX, United States Gary J. Alter, MD Assistant Clinical Professor Division of Plastic Surgery University of California Los Angeles, CA, United States Al S. Aly, MD Professor of Plastic Surgery Department of Plastic Surgery University of Texas Southwestern Medical Center Dallas, TX, United States Ashley N. Amalfi, MD Board Certified Plastic Surgeon Quatela Center for Plastic Surgery Rochester, NY; Clinical Assistant Professor of Surgery Division of Plastic Surgery University of Rochester School of Medicine Rochester, NY, United States Eric W. Anderson, MD Resident Plastic Surgery University of Utah Salt Lake City, UT, United States Bryan Armijo, MD Plastic Surgery Dallas Plastic Surgery Institute Dallas, TX, United States Seth Z. Aschen, MD Weill Cornell Medical College Division of Plastic and Reconstructive Surgery Weill Cornell Medicine New York, NY, United States Daniel C. Baker, MD Professor of Surgery Institute of Reconstructive Plastic Surgery New York University Medical Center Department of Plastic Surgery New York, NY, United States Alfonso Barrera, MD, FACS Clinical Assistant Professor Plastic Surgery Baylor College of Medicine Houston, TX, United States Justin Bellamy, MD Board Certified Plastic Surgeon West Palm Beach, FL, United States Richard Hector Bensimon, MD Medical Director Plastic Surgery Bensimon Center Portland, OR, United States

Miles G. Berry, MS, FRCS (Plast) Aestheticus Plastic and Aesthetic Surgery London Welbeck Hospital London, UK Stav Brown, MD Research Fellow Plastic and Reconstructive Surgery Memorial Sloan Kettering Cancer Center New York, NY, United States Terrence W. Bruner, MD, MBA AnMed Health Cosmetic and Plastic Surgery Anderson, SC, United States Andrés F. Cánchica Cano, MD Plastic and Reconstructive Surgeon Private Practice Medellín, Colombia Joseph Francis Capella, MD Chief, Post-bariatric Body Contouring Division of Plastic Surgery Hackensack University Medical Center Hackensack, NJ, United States Robert F. Centeno, MD, MBA Medical Director St. Croix Plastic Surgery & MediSpa; Chief Medical Quality Officer Governor Juan F. Luis Hospital & Medical Center Christiansted, US Virgin Islands Sydney R. Coleman, MD Assistant Clinical Professor Plastic Surgery University of Pittsburgh Medical Center Pittsburgh, PA, United States Mark B. Constantian, MD Adjunct Clinical Professor Surgery (Plastic Surgery) University of Wisconsin School of Medicine Madison, WI; Visiting Professor Department of Plastic Surgery University of Virginia Health System Charlottesville, VA, United States Jonathan Cook, MD Plastic Surgeon Private Practice Sanctuary Plastic Surgery Boca Raton, FL, United States Hong Lim Choi JW Plastic Surgery Clinic Seoul, Republic of Korea Jong Woo Choi, MD, PhD, MMM Professor Department of Plastic and Reconstructive Surgery University of Ulsan College of Medicine Asan Medical Center Seoul, Republic of Korea Jayne Coleman Professor Department of Anesthesiology and Pain Medicine University of Texas Southwestern Medical Center Dallas, TX, United States

List of Contributors

Devin Coon, MD, MSE Associate Professor of Plastic Surgery and Biomedical Engineering Department of Plastic and Reconstructive Surgery Johns Hopkins University Baltimore, MD, United States Dai M. Davies, FRCS Consultant and Institute Director Institute of Cosmetic and Reconstructive Surgery London, UK Jose Abel De la Pena Salcedo, MD, FACS Plastic Surgeon Director Instituto de Cirugia Plastica SC Huixquilucan, State of Mexico, Mexico Daniel A. Del Vecchio, MD, MBA Instructor in Surgery Massachusetts General Hospital Boston, MA, United States Zoe Diana Draelos, MD Consulting Professor Department of Dermatology Duke University School of Medicine Durham, NC, United States Barry DiBernardo, MD, FACS Clinical Associate Professor, Plastic Surgery Rutgers, New Jersey Medical School Newark, NJ; Director, New Jersey Plastic Surgery Montclair, NJ, United States Felmont F. Eaves, III, MD, FACS Adjunct Professor of Surgery (Plastic), Emory University ME Plastic Surgery Founder, Executive Chair, and Chief Medical/ Technical Officer, Brijjit Medical, Inc. Atlanta, GA, United States Francseco M. Egro, MD, MSc, MRCS Associate Professor Department of Plastic Surgery University of Pittsburgh Medical Center Pittsburgh, PA, United States Dino Elyassnia, MD, FACS Plastic Surgeon Private Practice Marten Clinic of Plastic Surgery San Francisco, CA, United States Marco Ellis, MD Assistant Professor Plastic Surgery Northwestern Medicine, Feinberg School of Medicine Chicago, IL, United States Sabrina G. Fabi, MD Volunteer Assistant Clinical Professor Department of Dermatology University of California San Diego, San Diego, CA; Associate Dermatology Cosmetic Laser Dermatology San Diego, CA, United States

Julius Few Jr., MD Director Plastic Surgery The Few Institute for Aesthetic Plastic Surgery Chicago, IL Clinical Professor Plastic Surgery University of Chicago Pritzker School of Medicine Chicago, IL Health Science Clinician Northwestern University Plastic Surgery Chicago, IL, United States Nicholas A. Flugstad, MD Plastic Surgeon Denton Plastic Surgery Denton, TX, United States James D. Frame III, MBBS, FRCS, FRCSEd, FRCS(Plast) Professor of Aesthetic Plastic Surgery Anglia Ruskin University Chelmsford, Essex, UK Gianfranco Frojo, MD Plastic Surgeon Private Practice Virginia Beach, VA, United States Jazmina M. Gonzalez, MD Plastic and Cosmetic Surgery Younger Image Plastic Surgery Center Vienna, VA, United States David Gonzalez Sosa, MD Plastic and Reconstructive Surgery Hospital Quirónsalud Torrevieja Alicante, Spain Jacob Grow, MD Plastic Surgery Associate Plastic Surgery Southern Indiana Aesthetic & Plastic Surgery Columbus, IN, United States Ronald P. Gruber, MD Adjunct Clinical Professor Division of Plastic and Reconstructive Surgery Stanford University Stanford, CA; Clinical Professor Division of Plastic and Reconstructive Surgery University of California San Francisco San Francisco, CA, United States Jeffrey Gusenoff, MD Professor of Plastic Surgery Department of Plastic Surgery University of Pittsburgh Pittsburgh, PA, United States Bahman Guyuron, MD Emeritus Professor Plastic Surgery Case Western Reserve University Cleveland, OH, United States Josef G. Hadeed, MD, FACS Plastic Surgeon Hadeed Plastic Surgery Beverly Hills, CA, United States

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Joseph Hunstad, MD Plastic Surgeon Plastic Surgery Hunstad-Kortesis-Bharti Center for Cosmetic Plastic Surgery and Medical Spa Huntersville, NC, United States Clyde Ishii, MD John A. Burns School of Medicine Department of Surgery University of Hawaii Honolulu, HI; Assistant Clinical Professor of Surgery University of Hawaii Honolulu, HI; Chief, Plastic Surgery Department of Surgery Shriners Hospital Honolulu, HI, United States Jeffrey E. Janis, MD Professor of Plastic Surgery, Neurosurgery, Neurology, and Surgery Department of Plastic and Reconstructive Surgery Chief of Plastic Surgery, University Hospital Department of Plastic and Reconstructive Surgery Ohio State University Wexner Medical Center Columbus, OH; Past President, American Society of Plastic Surgeons, American Council of Academic Plastic Surgeons, American Hernia Society, and Migraine Surgery Society United States Jeremy T. Joseph, MD Plastic and Reconstructive Surgery Resident Department of Surgery Eastern Virginia Medical School Norfolk, VA, United States David M. Kahn, MD Associate Professor of Plastic Surgery Division of Plastic Surgery Stanford University, Palo Alto, CA, United States Patrick R. Keller, MD Resident Physician Department of Plastic and Reconstructive Surgery Johns Hopkins University Baltimore, MD, United States Jeff Kenkel, MD Professor and Chair Department of Plastic Surgery University of Texas Southwestern Medical Center Dallas, TX, United States Jocelyn Celeste Ledezma Rodriguez, MD Private Practice Guadalajara, Jalisco, Mexico Steven Levine, MD Assistant Professor of Surgery Department of Surgery Hofstra Medical School – Northwell Health System, New York, NY, United States

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List of Contributors

Michelle Locke, MBChB, MD, FRACS (Plastics) Plastic and Reconstructive Surgeon Department of Plastic Surgery Middlemore Hospital Auckland; Associate Professor Department of Surgery University of Auckland Auckland, New Zealand Matthew Louis, MD Resident Physician Department of Plastic and Reconstructive Surgery Johns Hopkins University Baltimore, MD, United States Margaret Luthringer, MD Resident Division of Plastic and Reconstructive Surgery Rutgers New Jersey Medical School Newark, NJ, United States Samantha G. Maliha, MD,MS Resident Physician Plastic Surgery University of Pittsburgh Pittsburgh, PA, United States Kavita Mariwalla Director Dermatology Mariwalla Dermatology West Islip, NY, United States Timothy Marten, MD, FACS Private Practice Founder and Director Marten Clinic of Plastic Surgery San Francisco, CA, United States Alan Matarasso, MD, FACS Clinical Professor of Surgery Systems Chief of Cosmetic Surgery Hofstra School of Medicine-Northwell Health System New York, NY, United States Bryan Christopher Mendelson, AM, FRCSE, FRACS, FACS, Diplomate American Board of Plastic Surgery Plastic Surgeon Aesthetic Plastic Surgery The Centre for Facial Plastic Surgery Melbourne, VIC, Australia Constantino G. Mendieta, MD Board Certified Plastic and Reconstructive Surgeon Miami, FL, United States Gabriele C. Miotto, MD Private Practice Adjunct Associate Professor, Division of Plastic Surgery Emory School of Medicine Atlanta, GA, United States Foad Nahai, MD Professor of Surgery Emory University Atlanta, GA, United States

Tae Suk Oh, MD, PhD Professor Department of Plastic and Reconstructive Surgery University of Ulsan College of Medicine Asan Medical Center Seoul, Republic of Korea Sabina Paiva, MD Serviço de Cirurgia Plástica Dr. Osvaldo Saldanha Santos, São Paulo, Brazil Malcolm Paul, MD Clinical Professor of Surgery Department of Plastic Surgery University of California, Irvine, CA, United States Galen Perdikis, MD Chair, Professor Department of Plastic Surgery Vanderbilt University Medical Center Nashville, TN, United States Jason Pozner, MD Adjunct Clinical Faculty Plastic Surgery Cleveland Clinic Florida, Weston, FL; Sanctuary Plastic Surgery Boca Raton, FL, United States Smita R. Ramanadham, MD, FACS Board-certified Plastic Surgeon SR Plastic Surgery P.C Montclair and East Brunswick, NJ, United States Dirk F. Richter, MD Institut ID Aesthetic Surgery and Regenerative Medicine Cologne, Germany Danielle H. Rochlin, MD Plastic Surgery Resident Division of Plastic and Reconstructive Surgery Stanford University Palo Alto, CA, United States Thomas L. Roberts, III Plastic Surgery Center of the Carolinas Spartanburg, SC, United States Rod J. Rohrich, MD Clinical Professor of Plastic Surgery Baylor College of Medicine Past Chair/Distinguished Professor of Plastic Surgery University of Texas Southwestern Medical Center Founding Partner Dallas Plastic Surgery Institute Dallas, TX, United States Peter J. Rubin, MD Professor and Chair Plastic Surgery University of Pittsburgh Pittsburgh, PA; Professor Bioengineering University of Pittsburgh Pittsburgh, PA, United States

Peter P. Rullan, MD Medical Director, Dermatology Institute Chula Vista, CA; Volunteer Clinical Faculty Department of Dermatology University of California San Diego, CA, United States Cristianna Bonetto Saldanha, MD Plastic and Reconstructive Surgeon Santos, São Paulo, Brazil Osvaldo Ribeiro Saldanha, MD, PhD Plastic Surgery Service Osvaldo Saldanha Santos, São Paulo, Brazil; Director of Plastic Surgery Services Department Metropolitan University of Santos – UNIMES São Paulo, Brazil Osvaldo Saldanha Filho, MD Plastic and Reconstructive Surgeon Santos, São Paulo, Brazil Renato Saltz, MD, FACS Adjunct Professor University of Utah Saltz Plastic Surgery and Spa Vitoria Salt Lake City and Park City, UT, United States Anna Schoenbrunner, MD, MAS Department of Plastic and Reconstructive Surgery Ohio State University Columbus, OH, United States Nina Schwaiger, Dr. Plastic and Aesthetic Surgery Clinic Dr. Reba Hanover, Germany Nikita O. Shulzhenko, MD Resident Division of Plastic and Reconstructive Surgery Rutgers New Jersey Medical School Newark, NJ, United States Amitabh Singh, MBBS, MS, DNB, MCh Plastic Surgery Fortis Memorial Research Institute Gurgaon, India Henry M. Spinelli, MD Clinical Professor Surgery and Neurological Surgery Plastic Surgery and Neurological Surgery New York Presbyterian Weill Cornell Medicine New York, NY, United States James M. Stuzin, MD Clinical Professor (Voluntary) Plastic Surgery University of Miami School of Medicine Miami, FL, United States Taisa Szolomicki, MD Plastic and Reconstructive Surgeon Balneário Camboriú, Santa Catarina, Brazil Charles H. Thorne, MD Chairman Department of Plastic Surgery Lenox Hill Hospital New York, NY, United States

List of Contributors

Luiz Toledo, Prof., Dr. Private Practice Plastic Surgery MMC Polyclinic Dubai, United Arab Emirates; Private Practice Plastic Surgery Hospital Saint Louis Lisbon, Portugal Patrick Tonnard, MD, PhD Plastic Surgeon Coupure Centre for Plastic Surgery Ghent, Belgium Ali Totonchi Professor Case Western Reserve University Plastic Surgery MetroHealth Medical Center Cleveland, OH, United States Jonthan W. Toy, MD, FRCSC Associate Clinical Professor Plastic Surgery University of Alberta Edmonton, AB, Canada Rotem Tzur, MD Private Practice Tel Aviv, Israel David Turer, MD, MS Assistant Professor Plastic Surgery University of Pittsburgh Pittsburgh, PA, United States Alexis Verpaele, MD, PhD Plastic Surgeon Coupure Centre for Plastic Surgery Ghent, Belgium Simeon Wall Jr., MD, FACS Director The Wall Center for Plastic Surgery Shreveport, LA; Assistant Clinical Professor Department of Plastic Surgery UT Southwestern Medical Center Dallas, TX; Assistant Clinical Professor Department of Surgery LSU Health Sciences Center at Shreveport Shreveport, LA, United States Richard J. Warren, MD, FRCSC Clinical Professor Division of Plastic Surgery University of British Columbia Vancouver, BC, Canada Stelios C. Wilson, MD Plastic Surgeon Charles H. Thorne MD Plastic Surgery New York, NY, United States Chin-Ho Wong, MBBS, MRCSE, MMed (Surg), FAMS (Plast Surg) Plastic Surgeon Plastic Surgery W Aesthetic Plastic Surgery Singapore

Victor Zhu, MD, MHS Department of Plastic Surgery Kaiser Permanente San Francisco San Francisco, CA, United States Barry M. Zide, MD, DMD Professor Plastic Surgery NYU Langone Health New York, NY, United States James E. Zins, MD Chair, Department of Plastic Surgery Cleveland Clinic Cleveland, OH, United States

VOLUME THREE Neta Adler, MD Plastic Surgeon Ann & Robert H. Lurie Children’s Hospital of Chicago Chicago, IL, United States Abdulaziz Alabdulkarim, MD, FRCSC Craniofacial Surgery Fellow Division of Plastic, Reconstructive and Aesthetic Surgery McGill University Health Center Montreal, QC, Canada; Department of Plastic Surgery Prince Sattam Bin Abdulaziz University Kharj, Riyadh, Saudi Arabia Michael Alperovich, MD, MSc Division of Plastic Surgery Yale School of Medicine New Haven, CT, United States Marta Alvarado, DDS, MS Orthodontist Department of Orthodontics Facultad de Odontología Universidad de San Carlos de Guatemala Guatemala City, Guatemala Oleh M. Antonyshyn, MD Professor Plastic Surgery University of Toronto Toronto, ON, Canada Eric Arnaud, MD Unité fonctionnelle de chirurgie craniofaciale, Service de Neurochirurgie Pédiatrique, Hôpital Necker – Enfants Malades, Assistance Publique – Hôpitaux de Paris, Centre de Référence Maladies Rares CRANIOST, Filière Maladies Rares TeteCou, ERN Cranio Paris, France; Clinique Marcel Sembat, Ramsay Générale de Santé Boulogne-Billancourt, France Sofia Aronson, MD Resident Physician Division of Plastic Surgery Northwestern University Feinberg School of Medicine Chicago, IL, United States

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Stephen B. Baker, MD, DDS Professor and Program Director Plastic Surgery Medstar Georgetown University Hospital Washington, DC; Medical Director Craniofacial Program Inova Children’s Hospital Falls Church, VA; Attending Physician Plastic Surgery Children’s National Medical Center Washington, DC, United States Daniel M. Balkin, MD, PhD Instructor in Surgery Harvard Medical School Department of Plastic and Oral Surgery Boston Children’s Hospital Boston, MA, United States Scott P. Bartlett, MD Professor of Surgery Department of Surgery University of Pennsylvania Philadelphia, PA; Mary Downs Endowed Chair in Craniofacial Treatment and Research Division of Plastic Surgery Children’s Hospital of Philadelphia Philadelphia, PA, United States Bruce S. Bauer, MD Chief Division of Plastic Surgery NorthShore University HealthSystem Highland Park, IL; Clinical Professor of Surgery Department of Surgery University of Chicago Pritzker School of Medicine Chicago, IL, United States Adriane L. Baylis, PhD, CCC-SLP Speech Scientist Department of Plastic and Reconstructive Surgery Nationwide Children’s Hospital Columbus, OH; Director, VPD Program and Co-Director, 22q Center Department of Plastic and Reconstructive Surgery Nationwide Children’s Hospital Columbus, OH; Associate Professor-Clinical Department of Plastic Surgery Ohio State University College of Medicine Columbus, OH, United States Maureen Beederman, MD Assistant Professor Department of Surgery, Section of Plastic and Reconstructive Surgery University of Chicago Chicago, IL, United States Han Zhuang Beh, MD Cleft, Craniofacial and Pediatric Plastic Surgeon Plastic Surgery Cook Children’s Hospital Fort Worth, TX, United States

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List of Contributors

Michael Bentz, MD, FAAP, FACS Chairman, Division of Plastic Surgery Department of Surgery University of Wisconsin Madison, WI; Vice Chair of Clinical Affairs Department of Surgery University of Wisconsin Madison, WI, United States Hannah J. Bergman, MD Plastic and Reconstructive Surgery The Center for Plastic Surgery at CoxHealth Springfield, MO; Clinical Instructor of Surgery University of Missouri School of Medicine Columbia, MO, United States Zoe P. Berman, MD Postdoctoral Research Fellow Hansjörg Wyss Department of Plastic Surgery NYU Langone Health New York, NY; Resident Physician Department of General Surgery Maimonides Medical Center Brooklyn, NY, United States Allan B. Billig, MD Department of Plastic, Reconstructive, and Hand Surgery Hadassah University Medical Center Jerusalem, Israel Craig B. Birgfeld, MD Associate Professor Department of Surgery Division of Plastic and Reconstructive Surgery University of Washington Craniofacial Fellowship Director Seattle Children’s Hospital Seattle, WA, United States Gregory H. Borschel, MD, FACS, FAAP James Joseph Harbaugh, Jr. Professor of Plastic Surgery Department of Plastic Surgery Riley Hospital for Children Indianapolis, IN, United States John Brian Boyd, MB, ChB, MD, FRCS, FECSC, FACS Chief of Plastic Surgery Department of Surgery Harbor-UCLA Torrance, CA; Professor of Surgery Department of Surgery University of California, Los Angeles Los Angeles, CA, United States James P. Bradley, MD Professor and Vice Chairman Plastic and Reconstructive Surgery Northwell Health New York, NY, United States Edward P. Buchanan, MD, FACS Professor, Director of Cleft Care, Program Director Craniofacial Fellowship Department of Surgery Baylor College of Medicine Houston, TX, United States

Steven R. Buchman, MD M. Haskell Newman Professor in Plastic Surgery Department of Surgery University of Michigan Medical School Ann Arbor, MI; Professor of Neurosurgery (Joint Appointment) Department of Neurosurgery University of Michigan Medical School Ann Arbor, MI; Director, Craniofacial Anomalies Program Department of Surgery University of Michigan Medical Center Ann Arbor, MI; Chief, Pediatric Plastic Surgery CS Mott Children’s Hospital Ann Arbor, MI, United States Mitchell Buller, MEng, MD Resident Physician Plastic Surgery University of South Florida Tampa, FL, United States Michael R. Bykowski, MD Assistant Professor, Department of Plastic Surgery Surgical Director, Vascular Anomalies Center Surgical Director, Craniofacial Scleroderma Center Division of Pediatric Plastic Surgery UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA, United States Luis Capitán, MD, PhD Director and Head Surgeon Surgical Department The Facialteam Group Marbella, Málaga, Spain Fermín Capitán-Cañadas, PhD R&D Director Department of Research and Development The Facialteam Group Marbella, Málaga, Spain Anna R. Carlson, MD Fellow in Craniofacial Surgery Plastic Surgery Children’s Hospital of Philadelphia Philadelphia, PA, United States Sydney Ch’ng, MBBS, PhD, FRACS Associate Professor Faculty of Medicine and Health University of Sydney Sydney, NSW, Australia Brian L. Chang, MD Resident Department of Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States Philip Kuo-Ting Chen, MD Director Craniofacial Center Taipei Medical University Hospital Taipei; Professor of Surgery Taipei Medical University Taipei, Taiwan

Yu-Ray Chen, MD Professor of Surgery Gung University Chang Gung Memorial Hospital Taipei, Taiwan Ming-Huei Cheng, MD, MBA Professor A+ Surgery Clinic Taoyuan, Taiwan Gerson R. Chinchilla, DDS, MS Director Department of Orthodontics Facultad de Odontología Universidad de San Carlos de Guatemala Guatemala City, Guatemala Min-Jeong Cho, MD Assistant Professor Department of Plastic and Reconstructive Surgery The Ohio State University Columbus, OH, United States Peter G. Cordeiro, MD The William G Cahan Chair in Surgery Plastic and Reconstructive Surgery Service Memorial Sloan Kettering Cancer Center Professor of Surgery Weil Medical College of Cornell University New York, NY, United States Sabrina Cugno, MD, MSc, FRCSC, FACS, FAAP Division of Plastic, Reconstructive and Aesthetic Surgery Montreal Children’s Hospital McGill University Health Center Montreal, QC, Canada Simeon C. Daeschler, MD, Dr. med Postdoctoral Fellow Neuroscience and Mental Health Program SickKids Research Institute The Hospital for Sick Children (SickKids) Toronto, ON, Canada Robert F. Dempsey, MD, FACS, FAAP Assistant Professor Division of Plastic Surgery Department of Surgery Texas Children’s Hospital Baylor College of Medicine Houston, TX, United States Rami P. Dibbs, MD Plastic Surgery University of Texas Medical Branch Galveston, TX, United States Sara R. Dickie, MD Clinician Educator Surgery University of Chicago Hospital, Pritzker School of Medicine Chicago, IL; Attending Surgeon Section of Plastic and Reconstructive Surgery NorthShore University HealthSystem Northbrook, IL, United States Nicholas Do, MD Assistant Professor Plastic Surgery Harbor-UCLA Medical Center Torrance, CA, United States

List of Contributors

Russell E. Ettinger, MD Assistant Professor Craniofacial & Plastic Surgery Seattle Children’s Hospital Seattle, WA; Assistant Professor Plastic Surgery University of Washington Seattle, WA, United States Andrew M. Ferry, MD Clinical Research Fellow Division of Plastic Surgery, Michael E. DeBakey Department of Surgery Baylor College of Medicine Houston, TX; Clinical Research Fellow Division of Plastic Surgery, Department of Surgery Texas Children’s Hospital Houston, TX, United States

Mirko S. Gilardino, MD, MSc, FRCSC, FACS Chief Division of Plastic, Reconstructive and Aesthetic Surgery McGill University Health Center Montreal, QC; Director, H.B. Williams Craniofacial and Cleft Surgery Unit Montreal Children’s Hospital Montreal, QC, United States Daniel H. Glaser, MD, MPH Clinical Fellow Division of Pediatric Rheumatology UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA; Assistant Professor of Clinical Pediatrics (Rheumatology) Department of Pediatrics Yale University School of Medicine New Haven, CT, United States

Alexander L. Figueroa, DMD Adjunct Attending Orthodontist Rush Craniofacial Center Division of Plastic Surgery, Department of Surgery Rush University Medical Center Chicago, IL, United States

Jesse A. Goldstein, MD Associate Professor, Department of Plastic Surgery Craniofacial Surgery Fellowship Director Division of Pediatric Plastic Surgery UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA, United States

Alvaro A. Figueroa, DDS, MS Adjunct Associate Professor Rush Craniofacial Center Division of Plastic Surgery, Department of Surgery Rush University Medical Center Chicago, IL, United States

Arun K. Gosain, MD Children’s Service Board Professor and Chief Stanley Manne Children’s Research Institute Ann & Robert H. Lurie Children’s Hospital of Chicago Chicago, IL, United States

David M. Fisher, MB, BCh, FRCSC, FACS, MFA Medical Director, Cleft Lip and Palate Program Plastic Surgery The Hospital for Sick Children (SickKids) Toronto, ON; Professor Department of Surgery University of Toronto Toronto, ON, Canada Roberto L. Flores, MD Joseph G. McCarthy Associate Professor of Reconstructive Plastic Surgery Hansjörg Wyss Department of Plastic Surgery NYU Langone Health New York, NY, United States Christopher R. Forrest, MD, MSc, FRCSC, FACS Chief, Division of Plastic and Reconstructive Surgery The Hospital for Sick Children (SickKIds) Professor and Chair, Division of Plastic, Reconstructive and Aesthetic Surgery Department of Surgery, Temerty Faculty of Medicine University of Toronto Toronto, ON, Canada

Lawrence J. Gottlieb, MD Professor of Surgery Section of Plastic and Reconstructive Surgery, Department of Surgery University of Chicago Chicago, IL, United States Arin K. Greene, MD, MMSc Vascular Anomalies and Pediatric Plastic Surgery Endowed Chair Department of Plastic and Oral Surgery Boston Children’s Hospital Boston, MA; Professor of Surgery Harvard Medical School Boston, MA, United States Matthew R. Greives, MD, MS Thomas D. Cronin Chair of Plastic Surgery Division of Plastic Surgery, Department of Surgery McGovern Medical School at the University of Texas Health Sciences Center at Houston Houston, TX, United States Samer E. Haber, MD Unité fonctionnelle de chirurgie craniofaciale, Service de Neurochirurgie Pédiatrique, Hôpital Necker – Enfants Malades, Assistance Publique – Hôpitaux de Paris; Centre de Référence Maladies Rares CRANIOST, Filière Maladies Rares TeteCou, ERN Cranio Paris, France

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Jordan N. Halsey, MD Assistant Professor Plastic Surgery Johns Hopkins All Children’s Hospital Saint Petersburg, FL, United States Jeffrey Hammoudeh, DDS, MD, FACS Associate Chief Plastic and Maxillofacial Surgery University of Southern California Children’s Hospital Los Angeles Los Angeles, CA, United States Matthew M. Hanasono, MD Professor, Deputy Chair, and Fellowship Program Director Department of Plastic Surgery University of Texas MD Anderson Cancer Center Houston, TX, United States Jill A. Helms, DDS, PhD Professor Department of Surgery Stanford University Stanford, CA, United States Gregory G. Heuer, MD, PhD Associate Professor of Neurosurgery Perelman School of Medicine at the University of Pennsylvania Children’s Hospital of Philadelphia Philadelphia, PA, United States David L. Hirsch, MD, DDS, FACS Professor of OMFS/dental Medicine Zucker School of Medicine at Hofstra-Northwell SVP, Dental Medicine Service Line, Northwell Health System Chair of Dental Medicine/OMFS at Long Island Jewish, North Shore, Lenox Hill Hospital New York, NY, United States Larry H. Hollier Jr., MD Surgeon in Chief Texas Children’s Hospital Professor Department of Surgery Baylor College of Medicine Houston, TX, United States Richard A. Hopper, MD, MS Chief Division of Craniofacial and Plastic Surgery Seattle Children’s Hospital Seattle, WA; Surgical Director Craniofacial Center Seattle Children’s Hospital Seattle, WA; Marlys C. Larson Professor Department of Surgery University of Washington Seattle, WA, United States Adam S. Jacobson, MD, FACS Chief, Division of Head and Neck Surgery Co-Director, Head and Neck Center Director, Fellowship in Head and Neck Oncologic and Reconstructive Surgery Department of Otolaryngology – Head and Neck Surgery New York University – Langone Health New York, NY, United States

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List of Contributors

Syril James, MD Unité fonctionnelle de chirurgie craniofaciale, Service de Neurochirurgie Pédiatrique, Hôpital Necker – Enfants Malades, Assistance Publique – Hôpitaux de Paris; Centre de Référence Maladies Rares CRANIOST, Filière Maladies Rares TeteCou, ERN Cranio Paris, France; Clinique Marcel Sembat, Ramsay Générale de Santé Boulogne-Billancourt, France Jeffrey E. Janis, MD Department of Plastic and Reconstructive Surgery Ohio State University Wexner Medical Center Columbus, OH; Past President, American Society of Plastic Surgeons, American Council of Academic Plastic Surgeons, American Hernia Society, and Migraine Surgery Society, United States Christian Jimenez, BS Medical Student Plastic and Reconstructive Surgery Keck School of Medicine of USC Los Angeles, CA, United States

Jamie P. Levine, MD Associate Professor Plastic Surgery NYU Langone Medical Center New York, NY; Chief of Microsurgery New York, NY, United States Jingtao Li, DDS, PhD Associate Professor Oral & Maxillofacial Surgery West China Hospital of Stomatology Sichuan University Chengdu, Sichuan, China Joseph E. Losee, MD Vice Dean for Faculty Affairs, University of Pittsburgh School of Medicine Dr. Ross H. Musgrave Endowed Chair in Pediatric Plastic Surgery Professor and Executive Vice Chair, Department of Plastic Surgery Division Chief, Pediatric Plastic Surgery, UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA, United States

Alexandra Junn, MD Department of Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States

Robert Joseph Mann, MD, FACS Senior Surgeon & Surgical Committee Member, Global Smile Foundation Executive Director of the Michigan / Ohio Chapter of Healing the Children Grand Rapids, MI, United States

Sahil Kapur, MD Resident Physician Division of Plastic Surgery University of Wisconsin Madison, WI, United States

Paul N. Manson, MD Distinguished Service Professor Plastic Surgery Johns Hopkins University Baltimore, MD, United States

Leila Kasrai, MD, MPH, FRCSC Division of Plastic Surgery St Joseph’s Health Centre Toronto, ON, Canada

Benjamin B. Massenburg, MD Resident in Plastic and Reconstructive Surgery Department of Surgery Division of Plastic and Reconstructive Surgery University of Washington Seattle, WA, United States

Henry K. Kawamoto Jr., MD, DDS Clinical Professor, Emeritus Surgery, Division of Plastic Surgery University of California, Los Angeles Los Angeles, CA, United States Roman Khonsari, MD, PhD Unité fonctionnelle de chirurgie craniofaciale Service de chirurgie maxillofaciale et chirurgie plastique, Hôpital Necker – Enfants Malades, Assistance Publique – Hôpitaux de Paris; Centre de Référence Maladies Rares CRANIOST, Filière Maladies Rares TeteCou, ERN Cranio; Faculté de Médecine, Université Paris Cité Paris, France Richard E. Kirschner, MD Chair Department of Plastic and Reconstructive Surgery Nationwide Children’s Hospital Columbus, OH; Professor Pediatrics and Plastic Surgery Ohio State University College of Medicine Columbus, OH, United States Katelyn Kondra, MD Department of Plastic and Maxillofacial Surgery Children’s Hospital Los Angeles Los Angeles, CA, United States

Irene Mathijssen, MD, PhD, MBA-H Professor and Head of Department Plastic and Reconstructive Surgery and Hand Surgery Erasmus Medical Center Rotterdam, The Netherlands Frederick J. Menick, MD Medical Director, Cleft Lip and Palate Program Plastic Surgery The Hospital for Sick Children (SickKids) Toronto, ON; Professor Department of Surgery University of Toronto Toronto, ON, Canada Alexander F. Mericli, MD, FACS Associate Professor Plastic Surgery University of Texas MD Anderson Cancer Center Houston, TX, United States Laura A. Monson, MD Assistant Professor Department of Surgery Division of Plastic Surgery Houston, TX, United States

Edwin Morrison, LLB, BComm (Hons Eco), MBBS, FRACS Plastic and Reconstructive Surgery St Vincent’s Hospital Melbourne, VIC; Plastic and Reconstructive Surgery Peter Mac Hospital Melbourne, VIC, Australia John B. Mulliken, MD Professor of Surgery Harvard Medical School Department of Plastic and Oral Surgery Boston Children’s Hospital Boston, MA, United States Lucia Pannuto, MD Fellow Craniofacial surgery Taipei Medical University Hospital Taipei, Taiwan Giovanna Paternoster, MD Unité fonctionnelle de chirurgie craniofaciale, Service de Neurochirurgie Pédiatrique, Hôpital Necker – Enfants Malades, Assistance Publique – Hôpitaux de Paris; Centre de Référence Maladies Rares CRANIOST, Filière Maladies Rares TeteCou, ERN Cranio Paris, France John A. Persing, MD Emeritus Professor of Surgery Division of Plastic Surgery Yale School of Medicine New Haven, CT, United States Dale J. Podolsky, BSc, BESc, MD, PhD, FRCSC Surgeon Craniofacial Surgery The Hospital for Sick Children (SickKids) Toronto, ON, Canada Julian J. Pribaz, MD Professor of Surgery Department of Plastic Surgery University of South Florida Tampa, FL, United States Chad A. Purnell, MD Assistant Professor Division of Plastic, Reconstructive, and Cosmetic Surgery University of Illinois-Chicago Chicago, IL; Craniofacial Surgeon Department of Plastic Surgery Shriners Hospitals for Children – Chicago Chicago, IL, United States Pratik Rastogi, MBBS (Hons), GDAAD, MS, FRACS (PRS) Consultant Plastic and Reconstructive Surgeon St George Hospital Sydney, Australia Johanna N. Riesel, MD Assistant Professor, Division of Plastic and Reconstructive Surgery The Hospital for Sick Children (SickKIds) Division of Plastic, Reconstructive and Aesthetic Surgery Department of Surgery, Temerty Faculty of Medicine University of Toronto Toronto, ON, Canada

List of Contributors

Eduardo D. Rodriguez, MD, DDS Professor and Chair Hansjörg Wyss Department of Plastic Surgery NYU Langone Health New York, NY, United States

Eloise Stanton, BA Medical Student Plastic and Reconstructive Surgery Keck School of Medicine of USC Los Angeles, CA, United States

Anna Schoenbrunner, MD, MAS Department of Plastic and Reconstructive Surgery The Ohio State University Columbus, OH, United States

Srinivas M. Susarla, DMD, MD, FACS, FAAP Associate Professor Oral and Maxillofacial Surgery University of Washington School of Dentistry Seattle, WA; Associate Professor Surgery (Plastic) University of Washington School of Medicine Seattle, WA, United States

Lindsay A. Schuster, DMS, MS Director, Cleft-Craniofacial Orthodontics Pediatric Plastic Surgery UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA; Associate Professor of Plastic Surgery Department of Plastic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA, United States Jesse C. Selber, MD, MPH, FACS Associate Professor Plastic Surgery University of Texas MD Anderson Cancer Center Houston, TX, United States Afaaf Shakir, MD Resident Section of Plastic and Reconstructive Surgery Department of Surgery University of Chicago Chicago, IL, United States Sameer Shakir, MD Assistant Professor Division of Pediatric Plastic Surgery, Children’s Wisconsin Department of Plastic Surgery, Medical College of Wisconsin Milwaukee, WI, United States Pradip R. Shetye, DDS, BDS, MDS Associate Professor (Orthodontics), Director of Craniofacial Orthodontics, and Director of Craniofacial Orthodontic Fellowship Hansjörg Wyss Department of Plastic Surgery NYU Langone Health New York, NY, United States Daniel Simon, DMD Director and Head Surgeon Surgical Department The Facialteam Group Marbella, Málaga, Spain Anusha Singh, MD, MSc Resident Physician Department of Plastic Surgery MedStar Georgetown University Hospital Washington, DC, United States John T. Smetona, MD Craniofacial and Pediatric Plastic Surgery Director of Orthognathic Surgery Advocate Health Oak Lawn, IL, United States Brian Sommerlad, MBBS, DSc(Med) UCL(Hon), FRCS, FRCSE(Hon), FRCPCH, FRCSLT(Hon) Honorary Consultant Plastic Surgeon Department of Plastic Surgery Great Ormond Street Hospital for Children London, United Kingdom

Peter J. Taub, MD, MS Professor and System Chief Division of Plastic and Reconstructive Surgery Icahn School of Medicine at Mount Sinai New York, NY; Director, Cleft and Craniofacial Center Division of Plastic and Reconstructive Surgery Icahn School of Medicine at Mount Sinai New York, NY, United States Jesse A. Taylor, MD Chief, Division of Plastic, Reconstructive, and Oral Surgery Department of Surgery Children’s Hospital of Philadelphia Philadelphia, PA, United States Kathryn S. Torok, MD Co-Director, Pediatric Craniofacial Scleroderma Center UPMC Children’s Hospital of Pittsburgh Pittsburgh, PA; Associate Professor of Pediatrics Pediatric Rheumatology University of Pittsburgh School of Medicine Pittsburgh, PA, United States Raymond W. Tse, MD, FRCSC Associate Professor Craniofacial and Plastic Surgery Seattle Children’s Hospital Seattle, WA, United States Mark Urata, MD, DDS Chief Division of Plastic and Reconstructive Surgery Keck School of Medicine of USC Los Angeles, CA; Chair Division of Oral and Maxillofacial Surgery Ostrow School of Dentistry of USC Los Angeles, CA; Associate Dean of Surgery and Hospital Affairs Ostrow School of Dentistry of USC Los Angeles, CA; Division Head Division of Plastic and Maxillofacial Surgery Children’s Hospital Los Angeles Los Angeles, CA, United States James D. Vargo, MD Craniofacial and Pediatric Plastic Surgeon Plastic Surgery Children’s Hospital and Medical Center Omaha, NE; Assistant Professor of Plastic Surgery Department of Surgery University of Nebraska Medical Center Omaha, NE, United States

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George Washington, MD Resident Plastic and Reconstructive Surgery University of Texas Health Science Center at Houston Houston, TX, United States Erik Wolkswinkel, MD Assistant Professor Division of Plastic and Reconstructive Surgery Oregon Health & Science University Portland, OR, United States Stephen Yen, DMD, PhD Division of Dentistry and Orthodontics Children’s Hospital Los Angeles Los Angeles, CA, United States Peirong Yu, MD Professor Plastic Surgery University of Texas MD Anderson Cancer Center Houston, TX, United States Ronald M. Zuker, MD, FRCSC, FACS, FRCSEd(Hon) Professor of Surgery Department of Surgery University of Toronto Toronto, ON; Staff Plastic and Reconstructive Surgeon Department of Surgery The Hospital for Sick Children (SickKids) Toronto, ON, Canada

VOLUME FOUR Cori A. Agarwal, MD Associate Professor Plastic Surgery University of Utah Salt Lake City, UT, United States Andrew M. Altman, MD Associate Professor Department of Surgery Baylor Scott & White/Texas A&M Temple, TX, United States Andrew Nagy Atia, MD Department of Surgery Division of Plastic, Maxillofacial, and Oral Surgery Duke University Hospital Durham, NC, United States Christopher E. Attinger, MD Chief, Division of Wound Healing Department of Plastic Surgery Georgetown University Hospital Washington, DC, United States Jayson N. Atves, DPM, AACFAS Assistant Professor Plastic Surgery Georgetown University Washington, DC; Program Director MedStar Georgetown University Hospital Foot and Ankle Research Fellowship Washington, DC, United States

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List of Contributors

Håkan Brorson, MD, PhD Professor, Senior Consultant Plastic Surgeon Department of Clinical Sciences Lund University Plastic and Reconstructive Surgery Skåne University Malmö, Sweden; Professor Faculty of Medicine Esculera de Graduados, Asociación Médica Buenos Aires, Argentina; Professor Lund University Cancer Centre Lund, Sweden Paul S. Cederna, MD Chief of Plastic Surgery Robert Oneal Professor of Plastic Surgery Professor of Biomedical Engineering Section of Plastic Surgery, Department of Surgery University of Michigan Ann Arbor, MI, United States Brian L. Chang, MD Resident Department of Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States David W. Chang, MD Professor Department of Surgery University of Chicago Chicago, IL, United States Hung-Chi Chen, MD, PhD, FACS Professor Department of Plastic Surgery China Medical University Hospital Taichung, Taiwan Wei F. Chen, MD, FACS Professor of Plastic Surgery Head, Regional Microsurgery and Supermicrosurgery Co-director, Center for Lymphedema Research and Reconstruction Department of Plastic Surgery Cleveland Clinic Cleveland, OH, Unites States Peter G. Cordeiro, MD, FACS Professor of Surgery Weil Medical College of Cornell University New York, NY; William G. Cahan Chair in Surgery Plastic and Reconstructive Surgery Service Memorial Sloan Kettering Cancer Center Westfield, NJ, United States Paige K. Dekker, MD Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States Romina Deldar, MD PGY-4, General Surgery MedStar Georgetown University Hospital Washington, DC, United States

Gregory A. Dumanian, MD Stuteville Professor of Surgery Division of Plastic Surgery Northwestern Feinberg School of Medicine Chicago, IL, United States Karen K. Evans, MD Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States Vahe Fahradyan, MD Assistant Professor Division of Plastic and Reconstructive Surgery Mayo Clinic Rochester, MN, United States Reuben A. Falola, MD, MPH Postdoctoral Research Fellow Plastic & Reconstructive Surgery Baylor Scott & White Temple, TX, United States Rebecca M. Garza, MD Rebecca Garza Plastic Surgery Schererville, IN, United States Günter K. Germann, MD, PhD Professor of Plastic Surgery Department of Plastic, Reconstructive, Hand and Aesthetic Surgery ETHIANUM Clinic Heidelberg Heidelberg, Germany Lawrence J. Gottlieb, MD, FACS Professor of Surgery Section of Plastic & Reconstructive Surgery University of Chicago Chicago, IL, United States Zoe K. Haffner, BS Medical Student Georgetown University School of Medicine Washington, DC, United States J. Andres Hernandez, MD, MBA Resident Physician Division of Plastic, Maxillofacial and Oral Surgery Duke University Hospital Medical Center Durham, NC, United States Scott Thomas Hollenbeck, MD, FACS Plastic and Reconstructive Surgery Duke University Durham, NC, United States Joon Pio Hong, MD, PhD, MMM Professor Plastic Surgery Asan Medical Center University of Ulsan Seoul, Republic of Korea; Adjunct Professor Plastic and Reconstructive Surgery Georgetown University Washington, DC, United States Rayisa Hontscharuk, MD, MSc, FRCSC Plastic, Reconstructive and Aesthetic Surgeon Private Practice Toronto Plastic Surgery Toronto, ON, Canada

Marco Innocenti, MD Chairman and Professor of Plastic Surgery University of Bologna Director of Orthoplastic Surgery Department Rizzoli Institute Bologna, Italy Jeffrey E. Janis, MD Professor of Plastic Surgery, Neurosurgery, Neurology, and Surgery Department of Plastic and Reconstructive Surgery Ohio State University Wexner Medical Center Columbus, OH; Chief of Plastic Surgery, University Hospital Department of Plastic and Reconstructive Surgery Ohio State University Wexner Medical Center Columbus, OH, United States Leila Jazayeri, MD Microsurgery Fellow Plastic and Reconstructive Surgery Memorial Sloan Kettering Cancer Center New York, NY, United States Dana N. Johns, MD Assistant Professor Plastic Surgery University of Utah Salt Lake City, UT, United States Ibrahim Khansa, MD, FAAP, FACS Assistant Professor of Plastic and Reconstructive Surgery Department of Plastic and Reconstructive Surgery Nationwide Children’s Hospital Columbus, OH, United States Kevin G. Kim, MD Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States Grant M. Kleiber, MD Attending Surgeon, Assistant Professor Plastic and Reconstructive Surgery MedStar Georgetown University Hospital MedStar Washington Hospital Center Washington, DC, United States Stephen Kovach III, MD Herndon B. Lehr Endowed Associate Professor Division of Plastic Surgery, Department of Orthopaedic Surgery University of Pennsylvania Philadelphia, PA; Assistant Professor Department of Orthopaedic Surgery University of Pennsylvania Philadelphia, PA, United States Nishant Ganesh Kumar, MD House-Officer Section of Plastic Surgery, Department of Surgery University of Michigan Ann Arbor, MI, United States Theodore A. Kung, MD Associate Professor Section of Plastic Surgery Department of Surgery University of Michigan Ann Arbor, MI, United States

List of Contributors

Raphael C. Lee, MS (BmE), MD, ScD, FACS, FIAMBE Paul and Allene Russell Distinguished Service Professor Emeritus Departments of Surgery, Medicine, Molecular Engineering and Molecular Biosciences University of Chicago Chicago Electrical Trauma Rehabilitation Institute Chicago, IL, United States L. Scott Levin, MD, FACS Chair Orthopaedic Surgery Perelman School of Medicine at the University of Pennsylvania Philadelphia, PA, United States Alexander Y. Li, MD, MS Surgeon Plastic and Reconstructive Surgery Stanford Hospital and Clinics Palo Alto, CA, United States Walter C. Lin, MD, FACS Attending Surgeon Reconstructive Microsurgery The Buncke Clinic San Francisco, CA, United States Nicholas F. Lombana, MD, BS Associate Professor Department of Surgery Baylor Scott & White/Texas A&M Temple, TX, United States Otway Louie, MD Associate Professor Surgery University of Washington Medical Center Seattle, WA, United States Elena Lucattelli, MD Breast Unit A. Franchini Hospital Santarcangelo di Romagna, Italy Andrés A. Maldonado, MD, PhD Plastic Surgery University of Getafe Madrid, Spain; Department of Plastic, Hand and Reconstructive Surgery BG Unfallklinik Frankfurt Frankfurt, Germany John D. Miller, DPM Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States Balazs Mohos, MD Microsurgery Fellow Plastic and Reconstructive Surgery, Department of Surgery Hospital of Divine Savior (Göttlicher Heiland Krankenhaus) Vienna, Austria; Heart and Vascular Center, Semmelweis University Budapest, Hungary; Plastic and Reconstructive Surgery, Department of Surgery County Hospital Veszprem Veszprem, Hungary

Vamseedharan Muthukumar, DNB, M Ch, DrNB, MRCS Junior Consultant, Department of Plastic Surgery Ganga Hospital Coimbatore, Tamil Nadu, India Venkateshwaran Narasiman, MS, MCh. Plastic Surgery Consultant Plastic Surgeon Director- Wound Clinic Jupiter Hospital, Thane, Maharashtra, India; Hon. Visiting Consultant Seth G S Medical College and KEM Hospital Mumbai, India Lynn M. Orfahli, MD Resident Division of Plastic and Reconstructive Surgery University of Colorado Aurora, CO, United States Rajiv P. Parikh, MD, MPHS Attending Surgeon, Assistant Professor Plastic and Reconstructive Surgery MedStar Georgetown University Hospital MedStar Washington Hospital Center Washington, DC, United States Vinita Puri, MS (General Surgery), MCh (Plastic Surgery) Professor and Head Department of Plastic Surgery Seth G S Medical College and KEM Hospital Mumbai, Maharashtra, India Andrea L. Pusic, MD Chief Plastic and Reconstructive Surgery Brigham and Women’s Hospital Boston, MA, United States S. Raja Sabapathy, MS, MCh, DNB, FRCSE, FAMS, Hon FRCSG, Hon FRCS (Eng), Hon FACS, DSc (Hon) Chairman Department of Plastic Surgery, Hand Surgery, Reconstructive Microsurgery, and Burns Ganga Hospital Coimbatore, Tamil Nadu, India Hakim Said, MD, FACS Clinical Associate Professor Division of Plastic Surgery University of Washington Seattle, WA, United States Bauback Safa, MD, MBA, FACS Attending Surgeon Reconstructive Microsurgery The Buncke Clinic San Francisco, CA; Adjunct Clinical Faculty Division of Plastic and Reconstructive Surgery Stanford University Palo Alto, CA, United States Michel H. Saint-Cyr, MD, FRCSC Professor Plastic Surgery Banner MD Anderson Cancer Center Phoenix, AZ, United States

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Michael Sauerbier, MD, PhD PROFESSOR SAUERBIER Private Practice for Hand and Plastic Surgery Bad Homburg v.d. Höhe, Germany Adaah A. Sayyed, BS Medical Student Georgetown University School of Medicine Washington, DC, United States Loren Schechter, MD Professor of Surgery Division of Plastic Surgery Rush University Medical Center Chicago, IL, United States Kaylee B. Scott, MD Resident Physician Division of Plastic Surgery University of Utah Salt Lake City, UT, United States R. Raja Shanmugakrishnan, MS, DNB, MRCS Consultant, Department of Plastic and Burns Surgery Ganga Hospital Coimbatore, Tamil Nadu, India Banafsheh Sharif-Askary, MD Resident Department of Plastic and Reconstructive Surgery MedStar Georgetown University Hospital Washington, DC, United States David H. Song, MD, MBA Physician Executive Director and Chairman Plastic Surgery Georgetown University Washington, DC, United States Ping Song, MD Virginia Hospital Center Department of Plastic and Reconstructive Surgery Arlington, VA, United States John S. Steinberg, DPM Professor Plastic Surgery Georgetown University School of Medicine Washington, DC, United States Hyunsuk Peter Suh, MD, PhD Associate Professor Plastic Surgery Asan Medical Center Seoul, Republic of Korea Yueh-Bih Tang, MD, PhD Professor in Plastic Surgery National Taiwan University Hospital Taipei; Attending Plastic Surgeon Far Eastern Memorial Hospital New Taipei City, Taiwan Chad M. Teven, MD, MBA, FACS, HEC-C Assistant Professor of Surgery (Clinical) Division of Plastic Surgery Northwestern University Feinberg School of Medicine Chicago, IL, United States

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List of Contributors

Chieh-Han John Tzou, MD, PhD, MBA Director of Plastic and Reconstructive Surgery Hospital of Divine Savior (Göttlicher Heiland Krankenhaus) Vienna; Associate Professor of Plastic and Reconstructive Surgery Faculty of Medicine Sigmund Freud University Vienna; Director Lymphedema and Facial Palsy Center TZOU MEDICAL Vienna, Austria Sebastian Q. Vrouwe, MD, FRCSC Assistant Professor of Surgery Section of Plastic & Reconstructive Surgery University of Chicago Chicago, IL, United States

VOLUME FIVE Allen Gabriel, MD, FACS Plastic Surgeon Vancouver, WA; Clinical Professor Plastic Surgery Loma Linda University Medical Center Loma Linda, CA, United States Robert J. Allen Sr., MD Director Microsurgical Breast Reconstruction Department Ochsner Baptist Hospital New Orleans, LA; Clinical Professor of Plastic Surgery Department of Plastic and Reconstructive Surgery Louisiana State University New Orleans, LA, United States Claudio Angrigiani, MD Director Oncoplastic Surgery Hospital de Clínicas José de San Martín University of Buenos Aires Buenos Aires, Argentina Eric Michel Auclair, MD Plastic Surgeon Clinique Nescens Paris, France Saïd C. Azoury, MD Assistant Professor of Surgery (Plastic Surgery) Division of Plastic Surgery University of Pennsylvania Philadelphia, PA; Assistant Professor of Orthopaedic Surgery Orthopedic Surgery University of Pennsylvania Philadelphia, PA, United States Nusaiba F. Baker, PhD MD PhD Student Medicine Emory University Atlanta, GA, United States

Bradley P. Bengtson, MD, FACS Founder and CEO Bengtson Center for Aesthetics and Plastic Surgery Grand Rapids, MI; Associate Professor Department of Surgery Michigan State University Grand Rapids, MI, United States Giovanni Bistoni, MD Department of Surgery “Pietro Valdoni” Plastic Surgery Unit Policilinico Umberto I, University of Rome “Sapienza” Rome, Italy Gaines Blasdel, BS Research Associate Department of Urology NYU Langone Health New York City, NY; University of Michigan Medical School Ann Arbor, MI, United States Phillip Blondeel, MD, PhD, FCCP Professor Plastic and Reconstructive Surgery Ghent University Ghent, Belgium Rachel Bluebond-Langner, MD Associate Professor of Plastic Surgery Hansjörg Wyss Department of Plastic Surgery NYU Grossman School of Medicine New York, NY, United States Elisa Bolletta, MD, MRBS (Master’s Degree in Surgical Oncology, Reconstructive and Aesthetic Breast Surgery) Department of Plastic and Reconstructive Surgery Policlinico Sant’Orsola-Malpighi IRCCS Bologna, Italy M. Bradley Calobrace, MD Gratis Clinical Faculty Department of Plastic Surgery University of Louisville; CaloAesthetics Plastic Surgery Center Louisville, KY, United States Daniel Calva-Cerquiera, MD Miami Breast Center Miami, FL, United States John C. Cargile, MD Department of Anesthesiology Baylor Scott & White Memorial Hospital Temple, TX, United States Pierre Chevray, MD, PhD Plastic Surgeon Institute for Reconstructive Surgery Houston Methodist Hospital Houston, TX; Associate Professor Surgery Weill Cornell Medical College New York, NY; Adjunct Associate Professor Surgery Baylor College of Medicine Houston, TX, United States

David Chi, MD, PhD Resident Physician Division of Plastic and Reconstructive Surgery Washington University in St. Louis St. Louis, MO, United States Vincent J. Choi, BSc (Med), MBBS, MS, FRACS (Plast) Plastic Surgery University Health Network, University of Toronto Toronto, ON, Canada Matthew Cissell, DHSc, PA-C Surgical Physician Assistant National Center for Plastic Surgery McLean, VA, United States Salih Colakoglu, MD Assistant Professor Department of Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States Amy S. Colwell, MD Professor Division of Plastic Surgery Massachusetts General Hospital, Harvard Medical School Boston, MA, United States Raul A. Cortes, MD Miami Breast Center Miami, FL, United States Mark W. Clemens II, MD, MBA, FACS Professor Plastic Surgery MD Anderson Cancer Center; Associate Vice President Perioperative Services MD Anderson Cancer Center Houston, TX, United States Peter G. Cordeiro, MD Attending Surgeon Department of Surgery Memorial Sloan Kettering Cancer Center; Professor of Surgery Weil Medical College of Cornell University New York, NY, United States Connor Crowley, MD Resident Doctor Department of Surgery Northwell New Hyde Park, NY, United States Anand Deva, MBBS(Hons), MS, FRACS Professor Plastic and Reconstructive Surgery Integrated Specialist Healthcare Miranda, NSW, Australia Roy de Vita Chief Plastic and Reconstructive Surgery Department Regina Elena National Cancer Institute Rome, Italy Francesco M. Egro, MD, MSc, MRCS Associate Professor, Department of Plastic Surgery Associate Professor, Department of Surgery University of Pittsburgh Pittsburgh, PA, United States

List of Contributors

Jin Sup Eom, MD, PhD Professor Plastic Surgery Asan Medical Center University of Ulsan, College of Medicine Seoul, Republic of Korea Reuben A. Falola, MD, MPH Postdoctoral Research Fellow Division of Plastic and Reconstructive Surgery Baylor Scott & White Medical Center Temple, TX, United States Jian Farhadi, MD, PD Professor Plastic Surgery Group Zurich; Professor University of Basel Basel, Switzerland Caroline A. Glicksman, MD, MSJ Assistant Clinical Professor Department of Surgery Hackensack Meridian School of Medicine Nutley, NJ, United States Daniel J. Gould, MD, PhD Surgeon, Private Practice Gould Plastic Surgery Beverly Hills, CA, United States Vendela Grufman, MD Consultant Plastic Surgery Plastic Surgery Group Zurich, Switzerland Nicholas T. Haddock VC Business Affairs, Associate Professor Department of Plastic Surgery University of Texas Southwestern Dallas, TX, United States Elizabeth J. Hall-Findlay, MD, FRCSC Private Practice Banff Plastic Surgery Banff, AB, Canada Moustapha Hamdi, MD, PhD Professor Plastic and Reconstructive Surgery Brussels University Hospital Brussels, Belgium Dennis C. Hammond, MD Assistant Program Director Grand Rapids Plastic Surgery Residency Spectrum Health Grand Rapids, MI, United States Hyunho Han, MD, PhD Associate Professor Asan Medical Center University of Ulsan, College of Medicine Seoul, Republic of Korea Adam T. Hauch, MD, MBA Assistant Professor of Clinical Surgery Department of Surgery Louisiana State University New Orleans, LA, United States Stefan O.P. Hofer, MD, PhD, FRCSC Professor of Plastic Surgery University Health Network, University of Toronto Toronto, ON, Canada

Marcelo Irigo, MD Chief Plastic Surgery Hospital Italiano La Plata La Plata, Argentina Suhail K. Kanchwala, MD Associate Professor of Surgery Division of Plastic Surgery University of Pennsylvania Philadelphia, PA, United States Nolan S. Karp, MD Professor of Plastic Surgery Hansjörg Wyss Department of Plastic Surgery NYU Grossman School of Medicine, New York, NY, United States Grace Keane, MD Resident Physician Plastic and Reconstructive Surgery Washington University School of Medicine Saint Louis, MO, United States Nima Khavanin, MD Resident Physician Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States Roger Khalil Khouri, MD, FACS Medical Director Miami Breast Center Miami, FL; Professor Department of Surgery Florida International University School of Medicine Miami, FL, United States John Y.S. Kim, MD, MA Professor Department of Surgery Northwestern University Chicago, IL, United States Emma C. Koesters, MD Assistant Professor Plastic and Reconstructive Surgery University of Southern California Los Angeles, CA, United States Jake C. Laun, MD Assistant Professor Department of Plastic Surgery University of South Florida Tampa, FL, United States Patricia McGuire, MD, FACS Clinical Instructor of Surgery Washington University St Louis, MO, United States Gustavo Jiménez Muñoz Ledo, MD Private Practice Phi Aesthetics León Guanajuato, México Anne C. O’Neill, MBBCh, MMedSci, FRCS(Plast), MSc, PhD Associate Professor of Plastic Surgery University Health Network, University of Toronto Toronto, ON, Canada

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Andrzej Piatkowski, MD, PhD Associate Professor Department of Plastic and Reconstructive Surgery Maastricht University Medical Centre, MUMC+ Maastricht, The Netherlands Rachel Lentz, MD Assistant Professor Plastic and Reconstructive Surgery University of Washington Seattle, WA, United States Joan E. Lipa, MD, MSc, FRCSC, FACS Associate Professor Department of Surgery, Division of Plastic, Reconstructive & Aesthetic Surgery University of Toronto; Active Staff Sunnybrook Health Sciences Centre Toronto, ON, Canada Nicholas F. Lombana, MD Plastic Surgery Resident Division of Plastic and Reconstructive Surgery Baylor Scott & White Medical Center Temple, TX, United States Albert Losken, MD, FACS Emory University Division of Plastic and Reconstructive Surgery Emory University Hospital Atlanta, GA, United States Patrick Mallucci, MD Director of Plastic Surgery Mallucci London London, United Kingdom Michele Ann Manahan, MD, MBA, FACS Professor of Clinical Plastic and Reconstructive Surgery Vice Chair of Faculty and Staff Development and Well-Being Department of Plastic and Reconstructive Surgery Johns Hopkins Hospital Baltimore, MD, United States Past President, MedChi, The Maryland State Medical Society Jaume Masià, MD, PhD Chief and Professor Plastic Surgery Sant Pau University Hospital (Universitat Autonoma de Barcelona) Barcelona, Spain Chester J. Mays, MD Plastic Surgeon CaloAaesthetics Plastic Surgery Center CaloAesthetics Plastic Surgery Louisville, KY, United States Patrick Maxwell, MD Plastic Surgeon Assistant Professor of Surgery Vanderbilt University Nashville, TN, United States

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List of Contributors

Adrian McArdle, MBBCh, MD, FRCSI, FEBOPRAS Assistant Professor Department of Surgery, Division of Plastic, Reconstructive and Aesthetic Surgery University of Toronto; Division of Plastic and Reconstructive Surgery Trillium Health Partners Toronto, ON, Canada Colleen M. McCarthy, MD, MHS Attending Surgeon Department of Surgery Memorial Sloan Kettering Cancer Center New York, NY, United States Alexandre Munhoz, MD, PhD Plastic Surgery Hospital Sírio-Libanês São Paulo; Professor Plastic Surgery Instituto do Câncer do Estado de São Paulo São Paulo, SP, Brazil Alex Mesbahi, MD, FACS Founding Partner National Center for Plastic Surgery McLean, VA, United States Arash Momeni, MD, FACS Director, Clinical Outcomes Research Division of Plastic & Reconstructive Surgery Stanford University Medical Center Palo Alto, CA, United States Kiya Movassaghi, MD, DMD, FACS Assistant Clinical Professor; Director, Aesthetic Surgery Fellowship at Movassaghi Plastic Surgery Division of Plastic Surgery Oregon Health & Science and University Portland, OR, United States Terence M. Myckatyn, MD, FACS, FRCSC Professor, Plastic and Reconstructive Surgery Washington University School of Medicine Saint Louis, MO, United States Maurizio Nava, MD Breast & Plastic Surgeon Assistant Professor of Surgery University of Milan Milan, Italy Maurice Y. Nahabedian, MD, FACS Former Professor of Plastic Surgery Johns Hopkins University, Georgetown University and the Virginia Commonwealth University Private practice- National Center for Plastic Surgery Mclean, VA, United States Dries Opsomer, MD Plastic Surgery OLV Aalst Aalst, Belgium Janak A. Parikh, MD, MSHS Resident Plastic Surgery Houston Methodist Houston, TX, United States

Ketan M. Patel, MD Assistant Professor Plastic and Reconstructive Surgery University of Southern California Los Angeles, CA, United States Nakul Gamanlal Patel, BSc(Hons), MBBS(Lond), FRCS(Plast) Consultant Plastic Surgeon Department for Plastic Surgery and Burns University Hospitals of Leicester Leicester, United Kingdom Pat Pazmiño Associate Professor Division of Plastic Surgery University of Miami Miller School of Medicine Miami, FL, United States Justin L. Perez, MD Plastic Surgeon Medical Director, Marina Plastic Surgery MarinaRox Aesthetic Fellowship Marina del Rey, CA, United States Cristhian D. Pomata, MD, MSc Associate Plastic Surgery Clinica Planas Barcelona, Spain Julian J. Pribaz, MD Professor of Surgery Department of Plastic Surgery University of South Florida Tampa, FL, United States

Justin M. Sacks, MD, MBA, FACS Chief Division of Plastic and Reconstructive Surgery Sidney M. Jr. and Robert H. Shoenberg Professor of Surgery Washington University in St. Louis School of Medicine St. Louis, MO, United States Michel H. Saint-Cyr, MD, MBA, FRCSC Professor Department of Plastic and Reconstructive Surgery Banner M.D. Anderson Cancer Center Phoenix, AZ, United States Javier Sanz, MD, PhD Associate Professor Pompeu Fabra University Barcelona Radiation Oncologist Radiation Oncology Department Hospital del Mar Barcelona, Spain Hugo St. Hilaire, MD, DDS, FACS Clinical Professor of Surgery Division Chief Plastic and Reconstructive Surgery Louisiana State University Baton Rouge, LA, United States Ara A. Salibian, MD Assistant Professor Plastic & Reconstructive Surgery University of California, Davis School of Medicine Sacramento, California, United States

Venkat V. Ramakrishnan, MS, FRCS, FRACS (Plastic Surgery) Consultant Plastic Surgeon St. Andrews Centre for Plastic Surgery Broomfield Hospital UK Chelmsford, Essex, United Kingdom

Karim A. Sarhane, MD, MSc General, Laparoscopic and Peripheral Nerve Surgeon Burjeel Royal Hospital, Al Ain Abu Dhabi, UAE

Agustin Rancati, MD Department of Surgery Hospital Británico Buenos Aires Buenos Aires, Argentina

Hani Sbitany, MD Professor of Surgery Division of Plastic Surgery Mount Sinai Medical Center New York, NY, United States

Alberto Rancati, MD, PhD Breast & Plastic Surgery Assistant Professor Surgery Florida International University – FIU Miami, FL, United States Charles Randquist, MD Plastic Surgeon Victoriakliniken Saltsjöbaden, Sweden Gedge D. Rosson, MD Associate Professor Department of Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States J. Peter Rubin, MD, MBA, FACS Chair, Department of Plastic Surgery at UPMC and the University of Pittsburgh UPMC Endowed Professor of Plastic Surgery Professor of Bioengineering University of Pittsburgh Pittsburgh, PA, United States

Jesse C. Selber, MD, MPH, FACS Professor, Vice Chair, Director of Clinical Research Department of Plastic Surgery MD Anderson Cancer Center Houston, TX, United States Orr Shauly Resident Physician Plastic and Reconstructive Surgery Emory University School of Medicine Atlanta, GA, United States Aldona J. Spiegel, MD Houston Methodist Institute for Reconstructive Surgery Houston Methodist Hospital Houston, TX, United States Michelle Spring, MD, FACS Mountain West Plastic Surgery  Kalispell, MT, United States Sandpoint, ID, United States

List of Contributors

Grant Stevens, MD Professor Emeritus of Surgery Founder, Marina Plastic Surgery Associates Keck School of Medicine of USC Los Angeles, CA, United States Christopher N. Stewart, MD Plastic Surgeon Private Practice New Beautiful You Casper, WY, United States Neil Tanna, MD, MBA Professor Plastic Surgery Zucker School of Medicine at Hofstra/Northwell Hempstead, NY; Associate Program Director Plastic Surgery Northwell Health; Vice President, Women’s Surgical Services Northwell Health Great Neck, NY, United States Marissa Tenenbaum, MD Associate Professor of Surgery Director of Aesthetic Surgery Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, MO, United States Sumeet S. Teotia, MD, FACS Professor, Department of Plastic Surgery Director, Breast Reconstruction Program Simmons Cancer Center University of Texas Southwestern Medical Center Dallas, TX, United States Eliora A. Tesfaye, MD Plastic Surgery M.D. Anderson Cancer Center Houston, TX; Virginia Commonwealth University Richmond, VA, United States Dinesh Thekkinkattil, MD Oncoplastic Breast Surgeon Lincoln County Hospital Lincoln, UK Mark L. Venturi, MD, FACS Founding Partner National Center for Plastic Surgery McLean, VA, United States Raghavan Vidya, MD Oncoplastic Breast Surgeon Royal Wolverhampton Hospital Birmingham University Birmingham, UK Brittany L. Vieira, MD Resident Physician Division of Plastic and Reconstructive Surgery Massachusetts General Hospital Boston, MA, United States Veronica Vietti Michelina, MD Plastic and Reconstructive Surgery Department Regina Elena National Cancer Institute Rome, Italy

Liza C. Wu, MD Associate Professor PRIVÉ Plastic Surgery Boca Raton, Florida, United States Louisa Yemc, PA-C Surgical Physician Assistant National Center for Plastic Surgery McLean, VA, United States VOLUME SIX Hee Chang Ahn, MD, PhD Professor Plastic and Reconstructive Surgery CHA University Bundang Medical Center Seongnam, Gyeonggi-do, Republic of Korea Nidal F. Al Deek, MD, MSc Consultant Plastic and Reconstructive Surgery Chang Gung Memorial Hospital Taipei, Taiwan Rita E. Baumgartner, MD Attending Physician Panorama Summit Orthopedics Frisco, CO, United States Aaron Berger, MD, PhD Chief/Medical Director of Programs in Pediatric Hand, Brachial Plexus and Peripheral Nerve Division of Plastic Surgery Nicklaus Children’s Hospital Miami, FL; Clinical Assistant Professor Division of Plastic Surgery Florida International University School of Medicine Miami, FL; Voluntary Assistant Professor Department of Orthopedic Surgery University of Miami Miller School of Medicine Miami, FL, United States Anna Berridge, MBBS, BSc, FRCS (Tr & Orth) Consultant Orthopaedic Hand and Wrist Surgeon Ipswich Hospital East Suffolk and North Essex Foundation Trust Ipswich, United Kingdom Randy R. Bindra, MChOrth, FRCS Professor Orthopaedic Surgery Griffith University and Gold Coast University Hospital Gold Coast, QLD, Australia Nathalie Bini, MD Pediatric Orthopedics Regina Margherita Hospital Turin, Italy Gregory H. Borschel, MD, FACS, FAAP, FAAPS James Harbaugh Professor of Surgery Indiana University School of Medicine Chief of Plastic Surgery, Riley Hospital for Children Indianapolis, Indiana, United States

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Kirsty Usher Boyd, MD, FRCSC Associate Professor Division of Plastic Surgery The Ottowa Hospital University of Ottawa Ottawa, ON, Canada Gerald Brandacher, MD Scientific Director Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States Amanda Brown, MD Division of Plastic and Reconstructive Surgery St. Louis University School of Medicine St. Louis, MO, United States Hazel Brown, MSc Advanced Physiotherapy, BSc Hons Physiotherapy, Post Grad Dip Orthopaedic Medicine Clinical Specialist Physiotherapist Peripheral Nerve Injury Unit Royal National Orthopaedic Hospital Stanmore, United Kingdom Sara Calabrese, MD Plastic Reconstructive and Aesthetic Surgery Resident Plastic, Reconstructive and Aesthetic Surgery Department Careggi University Hospital Florence, Italy Ryan P. Calfee, MD, MSc Professor Orthopedic Surgery Washington University School of Medicine in St. Louis St. Louis, MO, United States Logan W. Carr, MD Attending Physician Division of Plastic Surgery Westchester Medical Center Valhalla, NY; Associate Professor of Surgery New York Medical College Valhalla, NY, United States James K-K. Chan, MA(Cantab), DPhil(Oxon), FRCS(Plast) Consultant Hand, Plastic and Reconstructive Surgeon Department of Plastic Surgery Stoke Mandeville Hospital Aylesbury; Clinical Lecturer Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences University of Oxford Oxford, United Kingdom James Chang, MD Johnson & Johnson Distinguished Professor and Chief Division of Plastic Surgery Stanford University Medical Center Palo Alto, CA, United States

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List of Contributors

Robert A. Chase, MD Emile Holman Professor of Surgery (Emeritus) Department of Surgery Stanford University Stanford, CA, United States

Lars B. Dahlin, MD, PhD Professor Hand Surgery Department of Translational Medicine Malmö, Sweden

Paige M. Fox, MD, PhD Department of Surgery, Division of Plastic and Reconstructive Surgery Stanford University School of Medicine Stanford, CA, United States

Shanlin Chen, MD, PhD Professor and Consultant Orthopaedic Surgeon Chief, Department of Hand Surgery Beijing Ji Shui Tan Hospital National Center for Orthopedics Beijing, China

Soumen Das De, MBBS, FRCS, MPH Consultant Department of Hand and Reconstructive Microsurgery National University Health System Singapore

Jeffrey B. Friedrich, MD, FACS Professor of Surgery and Orthopedics Department of Surgery University of Washington Seattle, WA, United States

Harvey Chim, MD Professor Plastic and Reconstructive Surgery University of Florida College of Medicine Gainesville, FL, United States

Kristen M. Davidge, MD, MSc, FRCSC Plastic and Reconstructive Surgeon Department of Surgery Hospital for Sick Children Toronto; Assistant Professor Department of Surgery University of Toronto; Associate Scientist Child Health and Evaluative Sciences Sick Kids Research Institute Toronto, ON, Canada

Alphonsus K.S. Chong, MBBS Associate Professor Department of Orthopaedic Surgery National University of Singapore; Group Chief and Senior Consultant Department of Hand and Reconstructive Microsurgery National University Health Systems Singapore David Chwei-Chin Chuang, MD Professor Department of Plastic and Reconstructive Surgery Chang Gung Memorial Hospital, Linkou Branch Gueishan District, Taoyuan City, Taiwan Kevin C. Chung, MD, MS Professor of Surgery Section of Plastic Surgery University of Michigan; Chief of Hand Surgery University of Michigan Ann Arbor, MI, United States J. Henk Coert, MD, PhD Professor Plastic Surgery UMC Utrecht Utrecht, The Netherlands Christopher Cox, MD Orthopedic Hand Surgery Kaiser Permanente Walnut Creek, CA, United States Catherine Curtin, MD Professor Department of Surgery Palo Alto VA Palo Alto, CA; Professor Department of Surgery Stanford University Palo Alto, CA, United States Simeon C. Daeschler, MD, Dr. med Postdoctoral Fellow Neuroscience and Mental Health Program SickKids Research Institute, Hospital for Sick Children (SickKids) Toronto, ON, Canada

Paul C. Dell, MD Professor Department of Orthopaedic Surgery and Sports Medicine University of Florida College of Medicine Gainesville, FL, United States Jana Dengler, MD, MASc Assistant Professor Department of Surgery University of Toronto; Staff Physician Department of Surgery Sunnybrook Health Sciences Program Toronto, ON, Canada Gregory Ara Dumanian, MD Stuteville Professor of Surgery Division of Plastic Surgery Northwestern Feinberg School of Medicine Chicago, IL, United States Simon Farnebo, MD, PhD Professor Department of Biomedical and Clinical Sciences and Department of Plastic Surgery, Hand Surgery, and Burns Faculty of Medicine and Health Sciences Linköping University Linköping, Sweden Margaret Fok, MBChB, FRCSE(Ortho), FHKAM (Orthopaedic Surgery) Associate Consultant Department of Orthopaedics and Traumatology Queen Mary Hospital Hong Kong; Honorary Clinical Assistant Professor Department of Orthopaedics and Traumatology The University of Hong Kong Hong Kong Ida K. Fox, MD Professor of Plastic Surgery Department of Surgery Washington University School of Medicine in St. Louis St. Louis, MO, United States

Brittany N. Garcia, MD Hand and Upper Extremity Surgery University of Utah Department of Orthopedic Surgery Salt Lake City, UT, United States Charles A. Goldfarb, MD Executive Vice Chair Orthopedic Surgery Washington University School of Medicine in St. Louis; Professor Orthopedic Surgery Washington University School of Medicine in St. Louis St Louis, MO, United States Kimberly Goldie Staines, OTR, CHT Visiting Researcher Michael E. DeBakey Veterans Affairs Medical Center Houston, TX; Adjunct Faculty Department of Immunology, Allergy, and Rheumatology Baylor College of Medicine Houston, TX, United States Elisabeth Haas-Lützenberger, MD Division of Hand, Plastic and Aesthetic Surgery University Hospital LMU Munich Munich, Germany Steven C. Haase, MD, FACS Professor Surgery University of Michigan Health Ann Arbor, MI, United States Leila Harhaus, MD, Prof. dr. med. Chief, Department for Handsurgery, Peripheral Nerve Surgery and Rehabilitation Vice Chair, Department for Hand, Plastic and Reconstructive Surgery, Microsurgery, Burn Center BG Trauma Hospital Ludwigshafen; Chair, Section Upper Extremity, Orthopedic University Hospital Heidelberg University of Heidelberg Heidelberg, Germany Elisabet Hagert, MD, PhD Associate Professor Department of Clinical Science and Education Karolinska Institute Stockholm, Sweden; Head of Hand Surgery Department of Surgery Aspetar Orthopedic- and Sports Medicine Hospital Doha, Qatar

List of Contributors

Warren C. Hammert, MD Professor of Orthopedic and Plastic Surgery Orthopedic Surgery Duke University Durham, NC, United States Dennis Hazell, RN, MChiro, Independent Prescriber Clinical Nurse Specialist Peripheral Nerve Injury Unit Royal National Orthopaedic Hospital Stanmore, United Kingdom Vincent Henta, MD Professor of Surgery, Emeritus Plastic Surgery Stanford University Stanford, CA, United States

Jason Hyunsuk Ko, MD, MBA, FACS Associate Professor Division of Plastic and Reconstructive Surgery Northwestern University Feinberg School of Medicine Chicago; Associate Professor Department of Orthopedic Surgery Northwestern University Feinberg School of Medicine Chicago, IL, United States

Vincent R. Hentz, MD Professor of Surgery, Emeritus Department of Plastic Surgery Stanford University Stanford, CA, United States

David A. Kulber, MD Professor of Surgery Cedars Sinai Medical Center and USC Keck School of Medicine; Director of Hand and Upper Extremity Surgery Program Director Marilyn and Jeffrey Katzenberg Hand Fellowship Department of Orthopedic Surgery, Cedars Sinai Medical Center; Director of the Plastic Surgery Center of Excellence Cedars Sinai Medical Center Los Angeles, CA, United States

Charlotte Jaloux, MD Assistant Professor Hand and Limb Reconstructive Surgery Timone University Hospital - APHM Marseille, France

Bhaskaranand Kumar, MBBS, MS (Ortho) Formerly Professor and Head Department of Orthopaedic Surgery Kasturba Medical College Manipal, India

Neil F. Jones, MD, FRCS, FACS Distinguished Professor of Plastic and Reconstructive Surgery Distinguished Professor of Orthopedic Surgery Ronald Reagan UCLA Medical Center and David Geffen School of Medicine University of California, Los Angeles; Consultant in Hand Surgery and Microsurgery Division of Plastic and Reconstructive Surgery Shriners Hospital for Children Los Angeles, CA, United States

Donald Lalonde, HonsBSc, MSc, MD, FRCSC, DSc Professor Plastic Surgery Dalhousie University Saint John, NB, Canada

Jonay Hill, MD Private practice Park City, Utah, United States

Sumanas W. Jordan, MD, PhD Division of Plastic and Reconstructive Surgery Northwestern University Chicago, IL, United States Ryosuke Kakinoki, MD, PhD Professor of Hand Surgery and Microvascular Reconstructive Surgery Orthopedic Surgery Kindai University Osaka-sayama Osaka, Japan Jason R. Kang, MD Kaiser Permanente Physician Orthopedics Department Garfield Specialty Care Center San Diego, CA, United States Marco Innocenti, MD Chairman and Professor of Plastic Surgery University of Bologna; Director of Orthoplastic Surgery Department Rizzoli Institute Bologna, Italy

Wee Leon Lam, MBChB, FRCS(Plast) Consultant Plastic and Hand Surgeon Department of Plastic and Reconstructive Surgery Royal Hospital for Children and Young People Edinburgh; Honorary Clinical Senior Lecturer University of Edinburgh Edinburgh, United Kingdom Caroline Leclerq, MD Consultant Hand Surgeon Institut de la Main Clinique Bizet Paris; Consultant Hand Surgeon Neuro-orthopaedic Rehabilitation CRN Coubert Coubert; Consultant Hand Surgeon Neuro-paediatric Rehabilitation Hôpital National Saint Maurice Saint Maurice, France Dong Chul Lee, MD Attending Physician Plastic and Reconstructive Surgery Gwangmyeong Sungae Hospital Gwangmyeong, Gyeonggi-do, Republic of Korea

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W.P. Andrew Lee, MD Provost and Dean Office of Provost University of Texas Southwestern Medical Center Dallas, TX, United States Anais Legrand, MD Postdoctoral Research Fellow Plastic & Reconstructive Surgery Stanford University Medical Center Palo Alto, CA, United States Janice Liao, MBBS, MRCS, FAMS Consultant Department of Hand and Reconstructive Microsurgery National University Health Systems Singapore Christopher D. Lopez, MD Resident Physician Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States Joseph Lopez, MD, MBA Chief of Pediatric Head and Neck Surgery Head and Neck Surgery AdventHealth for Children Orlando, FL, United States Johnny Chuieng-Yi Lu, MD, MSCI Associate Professor Department of Plastic and Reconstructive Surgery Chang Gung Memorial Hospital, Linkou Branch Gueishan District, Taoyuan City, Taiwan Susan E. Mackinnon, MD, FRCSC, FACS Minot Packer Fryer Professor of Surgery Director of the Center for Nerve Injury and Paralysis Professor of Plastic and Reconstructive Surgery Division of Plastic and Reconstructive Surgery Washington University School of Medicine St. Louis, MO, United States Brian A. Mailey, MD Associate Professor of Surgery Division Chief Plastic and Reconstructive Surgery Chief Pediatric Plastic Surgery Cardinal Glennon Children’s Hospital Pandrangi Family Endowed Professor of Plastic Surgery St. Louis University School of Medicine St. Louis, MO, United States Minnie Mau, OT, CHT/L Occupational Therapist, Certified Hand Therapist Hand Therapy Stanford Health Care Redwood City, CA, United States Steven J. McCabe, MD, MSc, FRCS(C) Director of Hand Program Department of Surgery University of Toronto Toronto, ON, Canada Meghan C. McCullough, MD, MS Plastic and Reconstructive Surgery Cedars Sinai Hospital Los Angeles, CA, United States

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List of Contributors

Kai Megerle, MD, PhD Professor and Chief Center for Hand Surgery, Microsurgery and Plastic Surgery Schoen Clinic Munich Munich, Germany Amy M. Moore, MD Professor and Chair Plastic and Reconstructive Surgery The Ohio State University Columbus, OH, United States Wendy Moore, OTR/L, CHT Assistant Manager Rehab Services Hand Therapy Stanford Health Care Redwood City, CA, United States Steven L. Moran, MD Professor of Plastic Surgery and Orthopedic Surgery Mayo College of Medicine and Science Mayo Clinic, Rochester, MN, United States Jagdeep Nanchahal, BSc, PhD, FRCS(Plast) Professor Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences University of Oxford Oxford, United Kingdom David T. Netscher, MD Professor Division of Plastic Surgery, Department of Orthopedic Surgery Baylor College of Medicine Houston, TX, United States Michael W. Neumeister, MD Professor and Chairman Surgery SIU School of Medicine; The Elvin G. Zook Endowed Chair in Plastic Surgery SIU School of Medicine, Springfield, IL, United States Christianne A. van Nieuwenhoven, MD, PhD Plastic Surgeon/Hand Surgeon Plastic and Reconstructive Surgery and Hand Surgery Erasmus Medical Center Rotterdam Rotterdam, The Netherlands Kerby C. Oberg, MD, PhD Professor and Vice Chair Pathology and Human Anatomy Loma Linda University Loma Linda, CA, United States Andrew O’Brien, MD, MPH Clinical Instructor, Housestaff Plastic and Reconstructive Surgery The Ohio State University Medical Center Columbus, OH, United States

Eugene Park, MD Pediatric Hand and Plastic Surgeon Plastic Surgery Shriners Children’s Philadelphia; Clinical Assistant Professor Orthopedic Surgery Sidney Kimmel Medical Center of Thomas Jefferson University Philadelphia, PA, United States Mitchell A. Pet, MD Assistant Professor Surgery Washington University School of Medicine in St. Louis St. Louis, MO, United States Karl-Josef Prommersberger, Prof. dr. Professor Krankenhaus St. Josef Clinic for Elective Hand Surgery Schweinfurt, Germany Tom J. Quick, MB, MA(hons)Cantab, FRCS(Tr & Orth) Associate Professor Institute of Orthopaedics and Musculoskeletal Science University College London London; Consultant Surgeon Peripheral Nerve Injury Unit Royal National Orthopaedic Hospital London, United Kingdom Parashar Ramanuj, MBBS, BSc(Hons) London Spinal Cord Injury Centre Royal National Orthopaedic Hospital Stanmore; Clinical Director Mental Health and Community Programmes Imperial College Health Partners London; Senior Research Fellow RAND Europe Cambridge, United Kingdom Carina Reinholdt, MD, PhD Senior Consultant in Hand Surgery Center for Advanced Reconstruction of Extremities Sahlgrenska University Hospital Mölndal; Assistant Professor Department of Hand Surgery Institute for Clinical Sciences Sahlgrenska Academy Göteborg, Sweden Justin M. Sacks, MD, MBA, FACS Shoenberg Professor of Plastic Surgery Chief, Division of Plastic and Reconstructive Surgery Director – Microsurgery Fellowship Division of Plastic and Reconstructive Surgery Department of Surgery Washington University in St. Louis School of Medicine St. Louis, MO, United States

Douglas M. Sammer, MD Professor Plastic Surgery and Orthopedic Surgery University of Texas Southwestern Medical Center at Dallas Dallas, TX, United States Brinkley K. Sandvall, MD Assistant Professor Department of Plastic Surgery Texas Children’s Hospital Baylor College of Medicine Houston, TX, United States Ellen Satteson, MD Assistant Professor, Research Director Plastic and Reconstructive Surgery University of Florida Gainesville, FL, United States Subhro K. Sen, MD Clinical Associate Professor Plastic Surgery Stanford University Medical School Palo Alto, CA, United States Pundrique Sharma, BSc(Hons) PhD, MBBS, FRSC(Plast) Consultant Plastic Surgeon Alder Hey Children’s Hospital Liverpool, United Kingdom Xiao Fang Shen, MD Vice-Director Pediatric Orthopedic (Hand Surgery) Children’s Hospital Affiliated to Soochow University Suzhou, Jiangsu, China Jamie T. Shores, MD Clinical Director of Hand and Upper Extremity Transplantation Plastic and Reconstructive Surgery Johns Hopkins University School of Medicine Baltimore, MD, United States S. Raja Sabapathy, MS, MCh, DNB, FRCSE, FAMS, Hon FRCSG, Hon FRCS, Hon FACS, DSc (Hon) Chairman Department of Plastic Surgery, Hand and Reconstructive Microsurgery and Burns Ganga Hospital Coimbatore, Tamil Nadu, India Vanila M. Singh, MD, MACM Clinical Associate Professor Anesthesiology, Perioperative, and Pain Medicine Stanford University Stanford, CA, United States Gillian D. Smith, MBBCh Consultant Hand and Plastic Surgeon Plastic Surgery Great Ormond Street Hospital London, United Kingdom Kashyap K. Tadisina, MD Assistant Professor Division of Plastic and Reconstructive Surgery Department of Surgery University of Miami Miller School of Medicine Miami, FL, United States

List of Contributors

Amir H. Taghinia, MD, MPH Attending Surgeon Department of Plastic Surgery Boston Children’s Hospital; Associate Professor of Surgery Harvard Medical School Boston, MA, United States David M.K. Tan, MBBS, MMED (Surgery) Senior Consultant Department of Hand and Reconstructive Microsurgery National University Health Systems Singapore Jin Bo Tang, MD Professor and Chair Department of Hand Surgery Affiliated Hospital of Nantong University; Chair The Hand Surgery Research Center Affiliated Hospital of Nantong University Nantong, Jiangsu, China Johan Thorfinn, MD, PhD Associate Professor Department of Biomedical and Clinical Sciences and Department of Plastic Surgery, Hand Surgery, and Burns Faculty of Medicine and Health Sciences Linköping University Linköping, Sweden Xiaofei Tian, MSc Professor Department of Burns and Plastic Children’s Hospital of Chongqing Medical University Chongqing, China

Michael Tonkin, MBBS, MD, FRACS, FRCSE(Orth) Professor Emeritus University of Sydney Medical School University of Sydney Sydney, NSW, Australia Joseph Upton, MD Attending Surgeon Shriners Children’s Hospital; Professor of Surgery Harvard Medical School Boston, MA, United States Francisco J. Valero-Cuevas, PhD Professor of Biomedical Engineering Professor of Biokinesiology and Physical Therapy The University of Southern California Los Angeles, CA, United States Hari Venkatramani, MS, MCh, DNB, EDHS Senior Consultant Plastic Surgery, Hand and Reconstructive Microsurgery Ganga Hospital Coimabatore, Tamil Nadu, India Nicolas B. Vedder, MD Professor of Surgery and Orthopedics Chief of Plastic Surgery Department of Surgery University of Washington Seattle, WA, United States

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Celine Yeung, MSc, MD, FRCSC Plastic, Reconstructive and Aesthetic Surgery Department of Surgery University of Toronto Toronto, ON, Canada Fu-Chan Wei, MD, FACS Professor Plastic and Reconstructive Surgery Chang Gung Memorial Hospital Kweishan, Taoyuan, Taiwan Paul M.N. Werker, MD, PhD, FEBOPRAS, FEBHS Professor and Chair Plastic Surgery University Medical Centre Groningen Groningen, The Netherlands Jeffrey Yao, MD Professor Orthopedic Surgery Stanford University Medical Center Menlo Park, CA, United States Jung Soo Yoon, MD, PhD Assistant Professor Plastic and Reconstructive Surgery Dongguk University Ilsan Hospital Goyang, Gyeonggi-do, Republic of Korea

Acknowledgments My wife, Gabrielle Kane, continues to encourage me in my work but gives constructive criticism bolstered by her medical expertise as well as by her knowledge and training in education. I can never repay her. The editorial team at Elsevier have made this series possible. Belinda Kuhn, once again, leads the group and is the Content Strategist. Through the years I’ve been involved with this project Belinda has been a constant support, an amazing resource, and a good friend. Unlike the previous editions which were managed through the London office, this edition has been directed through the Philadelphia office led by Katie De Francesco. The Elsevier production team, as always, has been vital in moving this project along. The volume editors, Geoff Gurtner and Andrea Pusic in Volume 1, Peter Rubin and Alan Matarasso in Volume 2, Richard Hopper and Joe Losee in Volume 3, David Song and JP Hong in Volume 4, Mo Nahabedian in Volume 5, and Jim Chang in Volume 6, have shaped and refined this 5th edition, making vital changes to keep the series relevant and up to date. Dan Liu has, once again, taken masterful charge of the

media content. This series is a team effort and wouldn’t exist without these wonderful people. This is the last edition I will edit. It has been an honor, an enormous privilege, and a work of love to do so. Peter C. Neligan, MB, FRCS(I), FRCSC, FACS I would like to thank all the authors for their commitment to producing this volume, my colleagues and residents at MedStar Health and Georgetown University School of Medicine, who work tirelessly to advance Plastic Surgery; my parents, who first inspired me to seek knowledge; and most importantly my wife, Janie, and my daughters, Olivia, Ava, and Ella, without whom this and all work loses meaning and significance for me. David H. Song, MD, MBA, FACS

Dedication Dedicated to all teachers, peers, and trainees in Plastic Surgery

1 Comprehensive lower extremity anatomy Rajiv P. Parikh and Grant M. Kleiber

SYNOPSIS

ƒ Success in lower extremity reconstruction is dependent on a comprehensive understanding of structural and functional anatomy. An anatomic- and defect-specific approach to lower extremity reconstruction enables the surgeon to provide tailored solutions for both the preservation and restoration of a functional limb. ƒ A comprehensive appreciation for normal lower extremity anatomy and anatomical variants is critical to functional limb salvage when treating lower extremity pathology. ƒ The reconstructive surgeon may be also be called upon to harvest tissue for transfer from the many potential donor sites in the lower extremity. ƒ This chapter aims to provide a comprehensive review of the three-dimensional anatomy of the lower extremity to facilitate operative and clinical decision-making. ƒ A detailed description is given of each region of the lower extremity with respect to skeletal support, musculofascial anatomy, vascularity, lymphatic drainage, peripheral nerves, and skin and soft-tissue elements. ƒ A broad overview of available soft-tissue donor sites from each region, donor sites for bone grafts, anatomic basis of common lower extremity flaps, surgical approaches to lower extremity recipient vessels, and common points of nerve injury and entrapment are included to provide a clinically relevant discussion for anatomy of the lower extremity as a framework for common challenges in reconstructive surgery.

The gluteal region Gluteal skeletal structure The pelvis consists of the two paired hip bones and the midline sacrum, articulating together at the two sacroiliac joints. The hip bones are formed by the fusion of the ilium, pubis, and ischium. These three bony regions of the pelvis coalesce to form the acetabulum. The large thick bony prominences of

the pelvis serve as attachments for the muscles of the hip and thigh (Fig. 1.1). These prominences also become clinically relevant in contributing to the formation of pressure ulcers, most commonly over the ischial tuberosity, sacrum, and greater trochanter. Dense ligaments stabilize and distribute the numerous opposing forces acting on the pelvis. The sacrospinous ligament runs from the sacrum to the ischial spine, bounding the greater sciatic foramen. The sacrotuberous ligament attaches the sacrum to the ischial tuberosity and encloses the lesser sciatic foramen. Running from the anterior superior iliac spine (ASIS) to the pubic tubercle is the inguinal ligament. The action of the multiple flexors, extensors, and internal and external rotators on the hip joint serves to stabilize and position the torso during the complex process of ambulation.

Clinical correlation – iliac crest bone graft The iliac crest serves as a versatile source of autogenous bone graft to reconstruct a variety of defects. Bone grafts can be cortical, cancellous, or corticocancellous in composition. Cortical bone is structurally stable with osteoconductive properties and ideally suited for structural defects requiring immediate mechanical stability. Cancellous bone is osteoinductive, osteogenic, and osteoconductive, undergoes rapid remodeling and vascularization, and is ideally suited for non-unions and bony fusion. Cancellous bone can be obtained between the inner and outer table of the ilium. The anterior and posterior iliac crest are common donor sites for cancellous and corticocancellous bone grafts, with 13 cm3 and 30 cm3 average graft volumes available from the anterior and posterior crest, respectively (Fig. 1.2).1 Anteriorly, bone graft is most commonly harvested from the iliac tubercle, 3–4 cm posterior and parallel to the ASIS to maximize available bone and minimize risk to the lateral femoral cutaneous nerve. The iliac crest lies deep to a musculofascial layer from the external oblique and the iliacus muscle. The ilioinguinal nerve runs along the medial surface of the iliacus muscle and is at risk during harvest from the anterior crest. The anterior iliac crest provides

CHAPTER 1  • Comprehensive lower extremity anatomy

2

Anterior View Origin of psoas major m. from sides of vertebral bodies, intervertebral discs, and transverse processes (T12–L4)

Iliacus m. Sartorius m. Rectus femoris m. Obturator internus and superior and inferior gemellus mm. Piriformis m. Gluteus minimus m. Vastus lateralis m. Intertrochanteric line Vastus medialis m. Vastus intermedius m.

Origins Insertions

Piriformis m. Pectineus m. Adductor longus m. Adductor brevis m. Gracilis m. Obturator externus m. Adductor magnus m. Quadratus femoris m. Iliopsoas m. Gluteus maximus m.

Posterior View Gluteus medius m. Gluteus minimus m. Tensor fasciae latae m. Sartorius m.

Superior gemellus m. Inferior gemellus m. Quadratus femoris m.

Rectus femoris m. Obturator externus m. Gluteus medius m. Quadratus femoris m. Iliopsoas m.

Obturator internus m. Articularis genus m.

Gluteus maximus m.

Adductor magnus m. Biceps femoris (long head) and semitendinosus mm.

Adductor magnus m.

Semimembranosus m.

Iliotibial tract

Pectineus m. Vastus medialis m.

Biceps femoris m.

Adductor longus m. Rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis via patellar ligament A

Sartorius m. Pes Gracilis m. anserinus Semitendinosus m. Adductor magnus m. Gastrocnemius m. (medial head)

Vastus lateralis m. Adductor magnus m. Adductor brevis m. Vastus intermedius m. Biceps femoris m. (short head) Adductor magnus m. Vastus lateralis m.

Plantaris m. Gastrocnemius m. (lateral head) Popliteus m.

Semimembranosus m. Popliteus m. Note: Width of zone of attachments to posterior aspect of femur (linea aspera) is greatly exaggerated

B

Figure 1.1  Bony attachments of buttock and thigh muscles. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

twice the volume of packed cancellous bone compared to the distal radius or olecranon. Alternatively, tricortical bone grafts can be harvested from the inner and outer table of the anterior ilium and corticocancellous bone grafts can be harvested to include either the inner or outer table. Posteriorly, the bone is thickest and best harvested in the area superior to a line connecting the posterior superior iliac spine (PSIS)

and the apex of the sacroiliac joint. Harvesting from an area approximately 4 cm distal to the PSIS prevents violation of the sacroiliac joint.2 Unicortical and corticocancellous bone grafts can be obtained from the outer table of the posterior ilium and additional cancellous bone harvested from the inner table of the ilium. The iliac crest can also provide vascularized bone for a variety of composite soft-tissue and bone

The gluteal region

3

Table 1.1  Mathes–Nahai classification system for muscle vascular supply Iliac tubercle

PSIS

Muscle vascular supply type

Description

I

Single vascular pedicle

II

Dominant vascular pedicle and one or more minor pedicles

III

Two dominant pedicles

IV

Segmental vascular pedicles

V

Single dominant vascular pedicle and secondary segmental pedicles

ASIS

Figure 1.2  Harvest sites for iliac crest bone graft. (Redrawn from Ebraheim NA, Elgafy H, Xu R. Bone-graft harvesting from iliac and fibular donor sites: techniques and complications. J Am Acad Orthop Surg. 2001;9(3):210–218.)

defects. Corticocancellous, vascularized bone can be obtained from the outer cortex of the ilium on the lateral half of the iliac crest, supplied by the ascending branch of the lateral femoral circumflex system.3 The inner cortex of the ilium, supplied through nutrient branches off the deep circumflex iliac artery, is another common source of vascularized iliac bone.

Gluteal fascial anatomy The fascial system of the gluteal region and the lower extremity contains various permutations of a nearly continuous superficial fascial and a deep fascial layer. The superficial system is located in the subcutaneous fat. The deep fascial layer is thicker and frequently can be seen as a dual-layered fibrous band. It usually lies directly over the underlying limb musculature and its proper fascia. The superficial fascia of the gluteal region is contiguous with that over the lower back and continues inferiorly into the proximal thigh. The deep fascia covering the gluteal muscles varies in thickness. Over the maximus it is thin, but over the anterior two-thirds of the medius it thickens and forms the gluteal aponeurosis. This is attached to the lateral border of the iliac crest superiorly, and splits anteriorly to enclose the tensor fasciae latae and posteriorly to enclose the gluteus maximus.

Muscles of the buttocks The gluteus maximus is the largest muscle in the body and lies most superficially in the gluteal region, originating from the posterior gluteal line of the ilium and the dorsal portion of the sacrum (Fig. 1.3). The superficial fibers coalesce into a thick tendinous expansion which contributes to the iliotibial band of the fascia lata, while the deep fibers insert on the gluteal tuberosity of the femur. The gluteus maximus acts as a

hip extensor when the hip is in a flexed position. In a standing position, the gluteus maximus dorsally rotates the pelvis and torso, maintaining stability. The vascular supply is primarily derived from the inferior gluteal vessels, which supply the inferior two-thirds of the muscle. The superior gluteal vessels supply the superior portion and the first perforator branch of the profunda femoris contributes to the vascular supply of the muscle laterally. For ease of description, the Mathes–Nahai classification system is used when discussing muscle vascularity (Table 1.1).4 The gluteus maximus has a type III vascular supply, with two dominant pedicles from the superior and inferior gluteal arteries. Innervation to the gluteus maximus is provided by the inferior gluteal nerve. Underneath the gluteus maximus lie three bursae: the trochanteric, gluteofemoral, and ischiofemoral bursae, which allow frictionless movement over its underlying structures. The gluteus medius, situated immediately deep to the gluteus maximus, arises from the outer surface of the iliac wing and inserts on the greater trochanter of the femur. It is innervated by the superior gluteal nerve and functions to abduct the hip and medially rotate the femur. Blood supply to this muscle is from the deep branch of the superior gluteal artery and from the trochanteric connection. The gluteus minimus lies deep to the gluteus medius and arises from the outer surface of the ilium. Its fibers join the aponeurosis of the gluteus medius to insert on the greater trochanter, and the two muscles function together to abduct the hip. The gluteus minimus is innervated by the superior gluteal nerve and receives blood supply from the superior gluteal artery and trochanteric connection. Several small muscles arise from the medial pelvis and insert on the greater trochanter of the femur, functioning collectively to rotate the hip externally. These muscles include piriformis, superior and inferior gemellus, quadratus femoris, obturator internus, and obturator externus.

Gluteal vasculature The superior gluteal artery (SGA) is the last branch of the posterior trunk of the internal iliac artery. It exits the pelvis through the greater sciatic foramen superior to the piriformis, dividing into two branches (Fig. 1.4). The deep branch runs deep to the gluteus medius, dividing into superior and inferior branches. The superior branch travels laterally to the anterior superior

CHAPTER 1  • Comprehensive lower extremity anatomy

4

Superficial dissection

Deeper dissection Iliac crest Gluteal aponeurosis over Gluteus medius muscle Gluteus minimus muscle Gluteus maximus muscle Piriformis muscle Sciatic nerve Sacrospinous ligament Superior gemellus muscle Obturator internus muscle Inferior gemellus muscle Sacrotuberous ligament Quadratus femoris muscle Ischial tuberosity Semitendinosus muscle Greater trochanter Biceps femoris muscle (long head) Adductor minimus part of Adductor magnus muscle Semimembranosus muscle Iliotibial tract Gracilis muscle Biceps femoris muscle Short head Long head Semimembranosus muscle Semitendinosus muscle Popliteal vessels and tibial nerve Common fibular (peroneal) nerve Plantaris muscle Gastrocnemius muscle Medial head Lateral head Sartorius muscle Popliteus muscle Tendinous arch of Soleus muscle Plantaris tendon (cut)

A

B

Figure 1.3  Muscles of hip and thigh: posterior views. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The gluteal region

Deep dissection Superior clunial nerves Gluteus maximus muscle (cut) Medial clunial nerves Inferior gluteal artery and nerve Pudendal nerve Nerve to obturator internus (and superior gemellus)

Iliac crest Gluteal aponeurosis and gluteus medius muscle (cut) Superior gluteal artery and nerve Gluteus minimus muscle Tensor fasciae latae muscle Piriformis muscle Gluteus medius muscle (cut) Superior gemellus muscle

Posterior femoral cutaneous nerve

Greater trochanter of femur

Sacrotuberous ligament Ischial tuberosity Inferior clunial nerves (cut) Adductor magnus muscle Gracilis muscle Sciatic nerve Muscular branches of sciatic nerve

Obturator internus muscle Inferior gemellus muscle Gluteus maximus muscle (cut) Quadratus femoris muscle Medial circumflex femoral artery Vastus lateralis muscle and iliotibial tract

Semitendinosus muscle (retracted)

Adductor minimus part of adductor magnus muscle

Semimembranosus muscle

1st perforating artery (from profunda femoris artery)

Sciatic nerve Articular branch Adductor hiatus Popliteal vein and artery Superior medial genicular artery Medial epicondyle of femur Tibial nerve Gastrocnemius muscle (medial head) Medial sural cutaneous nerve Small saphenous vein

Adductor magnus muscle 2nd and 3rd perforating arteries (from profunda femoris artery) 4th perforating artery (from profunda femoris artery) Long head (retracted) Short head

Biceps femoris muscle

Superior lateral genicular artery Common fibular (peroneal) nerve Plantaris muscle Gastrocnemius muscle (lateral head) Lateral sural cutaneous nerve

Figure 1.4  Arteries and nerves of thigh: deep dissection (posterior view). (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

5

6

CHAPTER 1  • Comprehensive lower extremity anatomy

iliac spine and connects with the ascending branch of the lateral circumflex femoral and the deep circumflex iliac. The inferior branch supplies the gluteus medius and minimus, and later joins with the lateral circumflex femoral. The superficial branch of the superior gluteal artery pierces the gluteus maximus, connecting intramuscularly with branches of the inferior gluteal artery, and sending musculocutaneous perforators to the overlying skin. The inferior gluteal artery (IGA) branches from the anterior trunk of the internal iliac and exits the pelvis through the greater sciatic foramen below the piriformis. It runs deep to the gluteus maximus, supplying it and its overlying skin with musculocutaneous perforators. The descending branch of the inferior gluteal artery continues down the posterior thigh, between the semitendinosus and biceps femoris, running with the posterior cutaneous nerve and connecting with the perforating branches to supply the skin.5

Clinical correlation – SGAP and IGAP flaps and SGA as a recipient vessel Perforating branches from the SGA and IGA can be used to perfuse free and pedicled flaps to reconstruct a variety of soft-tissue defects. There is considerable variability in size, location, and branching pattern of perforators in the gluteal region. Generally, the superior gluteal region is perfused by perforators from the SGA and the inferior gluteal region is perfused by perforators from the IGA. SGA perforators can be reliably found medial and adjacent to a line drawn from the PSIS to the greater trochanter and range in number from 5 to 11 perforators. The mean size of SGA perforators is 0.6 mm; however, there is always a perforator greater than 0.8 mm in diameter and, on average, at least 4 perforators per side greater than 0.8 mm.6 Perforator lengths for pedicle use vary from 4 cm to 10 cm and are dependent on the extent of dissection to the source vessel. The thickness and size of subcutaneous tissue that can be reliably perfused by SGA perforators follows the perforasome theory.7 Flaps harvested on the superficial fascial plane can be “ultra-thin”, with thickness ranging from 5 mm to 11 mm and an average flap size of 125 cm2.8 IGA perforators range in number from 4 to 12 perforators each side, with a mean diameter of 0.4 to 0.6 mm, and perforator lengths vary from 4 cm to 14 cm.6,9 Perforators from the IGA can perfuse an average of 175 cm2 of subcutaneous tissue, with thickness ranging from 1 cm to 6 cm depending on indication and patient body habitus.9 The SGA is also a valuable recipient vessel in the setting of complex posterior trunk, lumbosacral spine, and/or pelvic defects requiring free tissue transfer for reconstruction. There is a dearth of suitable recipient vessels for lower back and/or pelvic reconstruction. The superior gluteal artery and accompanying vein are reliable recipient vessels and have a predictable size, location, and length.

Approach to SGA as recipient vessel A follow-the-perforator approach is an efficient way to identify the underlying main SGA. By identifying the perforators on the skin with Doppler probe based on the aforementioned anatomical relationships, the surgeon can then dissect the perforator to the source SGA where the caliber is more suitable for microvascular anastomoses. Dissection through the fascia and proceeding deep in the plane between the piriformis and gluteus is necessary. There is often a moderate amount of intramuscular dissection required and it is critical to ligate

branches off the SGA to facilitate exposure. At this level, the caliber is often 2–4 mm. We recommend dissection to obtain a length of at least 4–5 cm on the recipient SGA as this allows the vessel to be brought more superficial to avoid anastomosis in a deep hole. Selecting a donor flap with a longer pedicle and deep self-retaining retractors also decrease the technical difficulty of anastomosis to the SGA.

Gluteal innervation The posterior cutaneous nerve of the thigh exits the pelvis with the inferior gluteal vessels (Fig. 1.4). Several branches will curl around the inferior border of the gluteus maximus and run superiorly to innervate the overlying skin of the buttocks, while the posterior cutaneous nerve continues to descend down the posterior thigh deep to the fascia lata, sending segmental cutaneous branches to the skin of the posterior thigh. The gluteal muscles are innervated by the superior and inferior gluteal nerves. The superior gluteal nerve runs with the superior gluteal artery and divides into superior and inferior branches, which course respectively with the superior and inferior branches of the deep superior gluteal artery, supplying the gluteus medius and minimus. The inferior branch runs laterally to also innervate the tensor fascia latae. The inferior gluteal nerve runs with the inferior gluteal artery, exiting the pelvis below the piriformis and entering the gluteus maximus.

The thigh The thigh region is generally defined as the cylindrical proximal portion of the lower extremity that extends from the infragluteal crease and the inguinal ligament distally to the tibiofemoral joint. The thigh aids in trunk support and positioning of the knee in space, serving a critical role in ambulation. The muscles of the thigh are some of the largest in the body and often have redundant or overlapping function. Similarly, the corresponding fasciocutaneous coverage in the thigh is relatively redundant. Thorough knowledge of thigh anatomy is key for taking advantage of these redundancies and utilizing the thigh as a generous source of donor tissue for local, regional, and distant reconstructive surgical options.

Thigh skeletal structure The femur is the longest bone in the body and the predominant bone in the thigh region. The femoral head articulates with the pelvic acetabulum to form the only true ball-and-socket joint in the body, allowing for stability under load as well as smooth multiplanar movement. Two bony prominences emanate from the femoral neck at about 90° from each other – the greater and lesser trochanters. These femoral prominences primarily serve as insertion sites for hip actors (Fig. 1.1). The action of multiple flexors, extensors, and internal and external rotators on the hip joint serves to stabilize and position the torso during the complex process of ambulation. The vascular supply of the femoral bone arises from multiple sources. The femoral head and neck are encircled by an arterial anastomosis between the medial and lateral circumflex arteries with lesser contribution by the superior and inferior gluteal vessels. The femoral shaft has multiple nutrient

The thigh

foramina supplied by branches from the second perforating artery from the profunda femoris. These foramina usually run along the linea aspera on the posterior surface of the femur in the middle one-third of the femoral shaft. Periosteal vascularity along the femur receives vascular input from either the perforating branches of the profunda or directly from the profunda femoris. The distal metaphyseal region of the femur also has multiple vascular foramina that are derived from the genicular arterial system.

Clinical correlation – medial femoral condyle flap The arterial anatomy of the distal femur, specifically the medial femoral condyle and supracondylar region, has clinical significance as it is the anatomical basis for the medial femoral condyle (MFC) vascularized corticoperiosteal flap (Fig. 1.5). This flap can be harvested as a corticoperiosteal free or pedicled flap with or without cancellous bone and provides an excellent option for transfer of vascularized bone in the treatment

Descending genicular artery

Adductor magnus tendon

Superomedial genicular artery

Medial collateral ligament

Figure 1.5  The medial femoral periosteal bone flap.

7

of recalcitrant fracture nonunions.10 The vascular supply to the MFC is derived from the descending genicular artery (DGA) and/or the superior medial genicular artery. The DGA, the longer and larger of the two vessels, is a medial branch off the superficial femoral artery and originates just proximal to the adductor hiatus, approximately 14 cm proximal to the knee joint. The DGA is the dominant vessel to the medial femoral condyle 90% of the time, has a mean pedicle length of 8 cm, and has a proximal diameter of at least 1.5 mm, suitable for microsurgical anastomosis.11,12 The superior medial genicular artery, a branch off the popliteal artery, has a smaller vessel diameter of 0.8 mm and pedicle length of 5 cm, and therefore is less utilized when harvesting a flap.11 The osteoarticular branch of the DGA provides periosteal perfusion, and there are numerous intraosseous perforators to the MFC. Paired venae comitantes provide venous drainage for the MFC flap, often converging to form the short descending genicular vein.

Thigh fascial composition The thigh has a superficial and deep fascial system. The superficial fascia lies within the subcutaneous fat of the thigh encircling the entire structure. Superficial vessels and nerves pass along and pierce this fascia as they travel to the skin. The thickness of the fascia varies throughout the thigh but thickens proximally in the inguinal region. At the inguinal ligament the superficial fascia fuses with the deep thigh fascia. The deep fascia is a tough, well-vascularized fibrous tissue that lies beneath the superficial fascia and the subcutaneous fat. This fibrous structure encircles and constrains the thigh musculature in a near-complete sheath. There is varying terminology used to describe the deep fascia of the thigh and this is often a source of confusion. The deep fascia of the thigh is also called investing fascia or the fascia lata. For simplicity and consistency, it will be referred to as the deep fascia in this text. The deep fascia of the thigh attaches posteriorly to the sacrum and coccyx, anteriorly to the inguinal ligament, and laterally to the iliac crest. At the inguinal ligament, where the superficial fascia joins the deep fascia, there is an opening in both fascial layers called the fossa ovalis. The great saphenous vein, superficial branches of the femoral artery, and lymphatics pass through this opening between the deep and the superficial layers of the thigh (Fig. 1.6). This opening is covered by a membranous layer of the superficial fascia called the cribriform fascia. A thickening of the fibrous tissues is present on the lateral aspect of the deep fascia and is termed the iliotibial band or tract (Fig. 1.7). The iliotibial band is proximally attached to the tensor fascia latae muscle and together this myofascial unit aids in maintaining knee extension. Septa pass from the deep fascial sheath to the bones underneath, confining the functional muscle groups within osteofascial compartments. In addition to separating musculature, fascial planes also provide pathways for vessel perforators to travel from deeper vasculature to the overlying skin. There are three functional compartments of the thigh: anterior, posterior, and medial. The anterior compartment contains the knee extensor muscles; the posterior compartment comprises knee flexors; and the medial compartment retains the hip adductors (Fig. 1.8). The medial and lateral intermuscular septa travel from the fascia lata to attach to the femur on the linea aspera along its posterior aspect. These septa then divide the anterior compartment from the posterior compartments and partition

CHAPTER 1  • Comprehensive lower extremity anatomy

8

Anterior view Inguinal lig. (Poupart) Superficial circumflex iliac v. Saphenous opening (fossa ovalis) Lateral cutaneous n. of thigh

Anterior femoral cutaneous nn. of thigh (from femoral n.)

Branches of lateral sural cutaneous n. (from common fibular [peroneal] n.)

Posterior view

Femoral v. Medial cluneal nn. (from dorsal rami of S1, 2, 3) Superficial external pudendal v.

Branches of posterior cutaneous n. of thigh

Infrapatellar branch of saphenous n. Great saphenous v. Saphenous n. (terminal branch of femoral n.) Small saphenous v.

Cutaneous branch of obturator n. Lateral sural cutaneous n. (from common fibular [peroneal] n.)

Great saphenous v. Medial sural cutaneous n. (from tibial n.) Sural n.

Small saphenous v. and lateral dorsal cutaneous n. (from sural n.)

A

Branches of lateral cutaneous n. of thigh

Cutaneous branches of obturator n.

Branches of saphenous n.

Dorsal digital nn. and vv.

Inferior cluneal nn. (from posterior cutaneous n. of thigh)

Great saphenous v.

Superficial fibular (peroneal) n.

Dorsal metatarsal vv.

Superior cluneal nn. (from dorsal rami of L1, 2, 3)

Superficial epigastric v.

Lateral calcaneal branches of sural n. Medial calcaneal branches of tibial n.

Dorsal venous arch Dorsal digital n. and v. of medial side of great toe Dorsal digital branch of deep fibular (peroneal) n.

B

Plantar cutaneous branches of lateral plantar n. Plantar cutaneous branches of medial plantar n.

Figure 1.6  Surface anatomy: superficial veins and nerves. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

the thigh musculature according to knee function. Only the anterior and posterior compartments have definite fascial boundaries. The medial (adductor) compartment is not a true anatomical compartment as it has no defined intermuscular septa separating it. The muscles of the adductor compartment – gracilis, pectineus, adductor longus, adductor brevis, and adductor magnus – form a functional compartment in the proximal aspect of the thigh.

Thigh musculature The three compartments of the thigh are a well-organized way to approach the thigh musculature (Table 1.2). There are 17 muscles that course through the region of the thigh. The anterior thigh compartment contains the sartorius, articularis genu, and quadriceps femoris comprising the rectus femoris, vastus lateralis, intermedius, and medialis. These muscles are the primary knee extensors. All of the anterior compartment muscles share a single articular function, with the exception of the sartorius and the rectus femoris, which cross both the hip joint and the knee joint. The sartorius muscle is the most superficial muscle of the thigh. It obliquely crosses the anterior

thigh from superolateral to medial inferior. The proximal end of the sartorius makes up one of the three limbs of the femoral triangle: the medial border of the sartorius makes up the lateral side, the medial border of the adductor longus makes up the medial side, and the inguinal ligament makes up the superior limb (Fig. 1.9). The femoral triangle denotes the region where the femoral artery, nerve, and vein are transiently uncovered superficially by muscle in the proximal thigh. Here, all three structures radiate multiple branches in multiple directions to supply the vasculature and innervation to the groin region, lower abdomen, and proximal thigh. As the femoral artery, vein, and nerve descend distally in the thigh, they dive under the adductor longus and then proceed to the adductor canal. At the distal end of the sartorius, the muscle inserts on the proximal, medial surface of the tibia. The sartorius inserts in this region above the gracilis, which then inserts above the semitendinosus (Fig. 1.10). This three-muscle insertion point forms the pes anserinus. The superficial location of the sartorius muscle and its proximity to the femoral triangle make it an ideal flap for muscle transposition coverage over proximal thigh wounds with vessel or prosthetic graft exposure. The vascular anatomy of the sartorius muscle is traditionally

The thigh

External oblique muscle

Iliac crest

Gluteal aponeurosis over gluteus medius muscle

Anterior superior iliac spine

Sartorius muscle Gluteus maximus muscle Tensor fasciae latae muscle

Rectus femoris muscle

Vastus lateralis muscle

Iliotibial tract

Long head Biceps femoris muscle Short head

Lateral condyle of tibia and Gerdy’s tubercle

Semimembranosus muscle Lateral patellar retinaculum Fibular collateral ligament Patella Plantaris muscle Extensor digitorum longus muscle Gastrocnemius muscle (lateral head)

Head of fibula

Fibularis (peroneus) longus muscle

Patellar ligament

Tibialis anterior muscle

Figure 1.7  Muscles of hip and thigh: lateral view. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

9

CHAPTER 1  • Comprehensive lower extremity anatomy

10

Thigh: Serial Cross-Sections Sartorius muscle Deep artery and vein of thigh Pectineus muscle lliopsoas muscle

Fascia lata Branches of femoral nerve Femoral artery and vein Adductor longus muscle Great saphenous vein

Rectus femoris muscle

Obturator nerve (anterior branch)

Vastus medialis muscle

Adductor brevis muscle

Lateral cutaneous nerve of thigh

Obturator nerve (posterior branch)

Vastus intermedius muscle Femur

Gracilis muscle

Vastus lateralis muscle

Adductor magnus muscle

Tensor fasciae latae muscle

Sciatic nerve

lliotibial tract

Posterior cutaneous nerve of thigh

Gluteus maximus muscle

Semimembranosus muscle Semitendinosus muscle Biceps femoris muscle (long head)

Vastus medialis muscle Rectus femoris muscle

Medial intermuscular septum of thigh

Vastus intermedius muscle Vastus lateralis muscle Iliotibial tract Lateral intermuscular septum of thigh Biceps femoris muscle

Short head Long head

Semitendinosus muscle Semimembranosus muscle

Sartorius muscle Nerve to vastus medialis muscle Saphenous nerve

in adductor canal

Femoral artery and vein Great saphenous vein Adductor longus muscle Gracilis muscle Adductor brevis muscle Deep artery and vein of thigh Adductor magnus muscle

Rectus femoris tendon Vastus intermedius muscle lliotibial tract Vastus lateralis muscle Articularis genus muscle Lateral intermuscular septum of thigh Femur Biceps femoris muscle Common fibular (peroneal) nerve Tibial nerve

Posterior intermuscular septum of thigh Sciatic nerve Vastus medialis muscle Sartorius muscle Saphenous nerve and descending genicular artery Great saphenous vein Gracilis muscle Adductor magnus tendon Popliteal vein and artery Semimembranosus muscle Semitendinosus muscle

Figure 1.8  Thigh: serial cross-sections. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

Anterior compartment

Hip-related

Anterior superior iliac spine (ASIS)

ASIS and ilium

Shaft of femur – upper intertrochanteric line, base of greater trochanter, lateral linea aspera, lateral supracondylar ridge, and lateral intermuscular septum Shaft of femur – lower intertrochanteric line, spiral line, medial linea aspera, and medial intermuscular septum

Sartorius

Rectus femoris

Vastus lateralis

Vastus medialis

4

5

6

Thoracic and lumbar spine (T12– L5)

Psoas major

2

3

Pelvis – iliac fossa

Iliacus

Origin

1

Muscle

Table 1.2  Thigh musculature

Quadriceps tendon–patella tendon–tibial tuberosity

Quadriceps tendon–patella tendon–tibial tuberosity (lateral aspect)

Quadriceps tendon–patella tendon–tibial tuberosity

Medial, proximal tibia (pes anserinus)

Lesser trochanter of femur – middle region

Lesser trochanter of femur – inferior edge

Insertion

Knee extension, patellar stabilization

Knee extension

Hip flexion and knee extension

One dominant and minor pedicles (type II)

One dominant and minor pedicles (type II)

Segmental (type IV)

–

–

Flap blood supply type

Branch of superficial One dominant and femoral artery minor pedicles (dominant); distal (type II) branches of the superficial femoral artery (minor), branches of descending genicular artery (minor)

Descending branch of LCFA (dominant); transverse branch of LCFA (minor), posterior branches of profunda femoris (minor), branch of superior genicular artery (minor)

Descending branch of LCFA (dominant); ascending branch of LCFA (minor), muscular branch of superficial femoral artery (minor)

Multiple branches for the superficial femoral artery

–

Hip flexion and internal rotation Flexes, abducts, and external rotates thigh at hip; flexes, internally rotates leg at knee

–

Blood supply

Hip flexion and internal rotation

Function

(Continued)

Femoral nerve (posterior division)

Femoral nerve (posterior division)

Femoral nerve (posterior division)

Femoral nerve (anterior division)

Lumbar spinal nerves

Femoral nerve – intraabdominal

Innervation

The thigh 11

Posterior compartment Long head: ischial tuberosity – posterior surface Short head: linea aspera – middle third and lateral supracondylar ridge of femur

Ischial tuberosity – medial surface

Ischial tuberosity – lateral surface

Semitendinosus

Semimembranosus

10

11

Femur – anterior, distal surface of shaft

Articularis genu

8

Biceps femoris

Shaft of femur – inferior one-third

Vastus intermedialis

7

9

Origin

Muscle

Table 1.2  Thigh musculature —cont’d

Medial condyle

Medial, proximal tibia (pes anserinus) – below gracilis insertion

Lateral condyle of tibia & head of fibula

Apex of suprapatellar bursa

Quadriceps tendon–patella tendon–tibial tuberosity

Insertion

Extends hip, flexes, and medially rotates the knee

Extends hip, flexes, and medially rotates the knee

Long head: extends knee Both heads: flexes and laterally rotates knee

Retracts bursa as knee extends

Knee extension

Function

First perforating branch of profunda femoris (dominant); muscular branch of inferior gluteal artery (minor), descending branch of MCFA, inferior medial genicular artery

First perforating branch of profunda femoris (dominant); inferior gluteal artery branch (minor), second or third perforating branch of profunda (minor), superficial femoral artery branch (minor)

Long head: first perforating branch of profunda femoris (dominant); inferior gluteal artery branch (minor), second perforating branch of profunda (minor); short head: second or third perforating branch of profunda (dominant); superior lateral genicular artery (minor)

Direct branch of profunda femoris

Lateral direct branch from the profunda femoris (dominant); medial direct branch from the profunda femoris (minor)

Blood supply

One dominant and minor pedicles (type II)

One dominant and minor pedicles (type II)

One dominant and minor pedicles (type II)

–

One dominant and minor pedicles (type II)

Flap blood supply type

Tibial nerve

Tibial nerve

Long head: tibial nerve Short head: common peroneal nerve

Femoral nerve (posterior division)

Femoral nerve (posterior division)

Innervation

12 CHAPTER 1  • Comprehensive lower extremity anatomy

Pubic bone – ischiopubic ramus

Pubic bone

Gracilis

Pectineus

14

15

16

Iliac crest

Pubic bone – superior and inferior ramus

Adductor brevis

13

Tensor fascia latae

Pubic bone – pubic tubercle

Adductor longus

12

17

Pubic bone – ischiopubic ramus

Adductor magnus

Origin

LCFA, lateral circumflex femoral artery; MCFA, medial circumflex femoral artery.

Extracompartmental

Adductor compartment

Muscle

Table 1.2  Thigh musculature

Iliotibial tract– lateral tibia condyle (anterior surface)

Proximal femur – below the lesser trochanter

Medial, proximal tibia (pes anserinus), below the sartorius

Femur – superior aspect of linea aspera

Femur – inferior aspect of linea aspera

Femoral shaft, inferior – lower gluteal line and linea aspera

Insertion

Maintains knee extension (assists gluteus maximus) and hip abduction

Hip adduction, knee flexion, and internal rotation

Hip adduction, knee flexion, and internal rotation

Hip adduction

Hip adduction, internal hip rotation

Hip adduction, internal hip rotation

Function

Ascending branch of the LCFA

Branches from the MCFA, common femoral, and obturator arteries

Ascending branch of MCFA (dominant); 1–2 branches from the superficial femoral artery

Variable – branch of profunda femoris versus branch from MCFA; obturator artery

Branch from profunda femoris (artery to the adductors); branches from MCFA, distal branch from the superficial femoral artery

Branches from the obturator, profunda femoris, and superficial femoral arteries

Blood supply

One dominant artery (type I)

–

One dominant and minor pedicles (type II)

–

–

–

Flap blood supply type

Superior gluteal nerve

Femoral nerve (anterior division)

Obturator nerve (anterior division)

Obturator nerve (anterior division)

Obturator nerve (anterior division)

Obturator nerve (posterior division)

Innervation

The thigh 13

CHAPTER 1  • Comprehensive lower extremity anatomy

14

Anterior superior iliac spine Lateral femoral cutaneous nerve Inguinal ligament Iliopsoas muscle

Superficial dissections Lateral femoral cutaneous nerve (cut)

Tensor fasciae latae muscle (retracted)

Sartorius muscle (cut)

Gluteus minimus and medius muscles

Superficial circumflex iliac vessels Superficial epigastric vessels

Iliopsoas muscle Femoral nerve, artery, and vein

Superficial and Deep external pudendal vessels

Pectineus muscle

Lateral circumflex femoral artery

Profunda femoris (deep femoral) artery

Rectus femoris muscle

Adductor longus muscle

Vastus lateralis muscle

Adductor canal (opened by removal of sartorius muscle)

Vastus medialis muscle Femoral sheath

Saphenous nerve

Femoral nerve, artery, and vein

Nerve to vastus medialis muscle

Pectineus muscle Profunda femoris (deep femoral) artery Gracilis muscle Adductor longus muscle Sartorius muscle

Vastus medialis muscle Fascia lata (cut) Rectus femoris muscle Vastus lateralis muscle Tensor fasciae latae muscle A

Adductor magnus muscle

Saphenous nerve and saphenous branch of descending genicular artery Articular branch of descending genicular artery (emerges from vastus medialis muscle) Patellar anastomosis Infrapatellar branch of Saphenous nerve

Anteromedial intermuscular septum covers entrance of femoral vessels to popliteal fossa (adductor hiatus) Sartorius muscle (cut) Superior medial genicular artery (from popliteal artery) Inferior medial genicular artery (from popliteal artery)

B

Figure 1.9  Arteries and nerves of thigh: anterior views. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

described as a type IV, segmental pattern. Six to eight muscular branches enter the sartorius along the length of the muscle from different source vessels. The proximal third is supplied by branches from the superficial circumflex iliac and the lateral circumflex femoral arteries. The middle third receives multiple branches from the superficial femoral artery. The

distal third of the muscle is supplied by muscular branches of the descending genicular and superomedial genicular arteries (Fig. 1.11).13 A recent anatomic study has challenged this purely segmental classification, demonstrating two dominant vascular pedicles.14 This renewed anatomical understanding of the sartorius muscle suggests that it may be based on a

The thigh

Vastus medialis Sartorius Gracilis Semimembranosus

15

Superficial circumflex iliac artery Common femoral artery Lateral circumflex iliac artery

Semitendinosus Profunda femoris artery

Patellar ligament Gastrocnemius

Superficial femoral artery

Tibial tuberosity

Descending genicular artery

Superior medial genicular artery Popliteal artery

Figure 1.10  Pes anserinus.

single pedicle, and therefore have a larger arc of rotation for wound coverage. The quadriceps muscles act as a unit through the patella and the patellar tendon to extend the lower leg at the knee. Knee extension is critical in ambulation and upright posture maintenance. The redundancy in function of these four muscles ensures this ability and removal of one of the quadriceps muscles can usually be tolerated with appropriate centralization techniques of the remaining musculature and physical therapy. This recovery potential is a primary factor in the ability to use the type II rectus femoris muscle for regional and distant reconstructions. The dominant pedicle from the descending branch of the lateral circumflex artery allows for wide transposition of the rectus femoris muscle or musculocutaneous flap with minimal impact on knee function.15 The posterior compartment musculature comprises the knee flexion muscles, colloquially known as the hamstrings (Table 1.2). The biceps has two heads, each with a slightly different origin and action. All three of these muscles span the posterior knee, with the tendons of the semitendinosus and

Figure 1.11  Segmental blood supply to the sartorius muscle. (Redrawn from Buckland A, et al. Neurovascular anatomy of sartorius muscle flaps: implications for local transposition and facial reanimation. Plast Reconstr Surg. 2009;123:44–54.)

semimembranosus traveling medially and forming one border of the popliteal fossa and the biceps femoris tendon traveling laterally and forming the other border (Fig. 1.12). The adductor compartment contains the adductor magnus, brevis, and longus, as well as the gracilis and pectineus muscles

CHAPTER 1  • Comprehensive lower extremity anatomy

16

Iliac crest

Gluteus maximus muscle

Anterior superior iliac spine Iliacus muscle

Semitendinosus muscle

Psoas major muscle

Biceps femoris muscle (long head)

Inguinal ligament

Adductor magnus muscle

Pubic tubercle Semimembranosus muscle

Iliopsoas muscle Tensor fasciae latae muscle

Iliotibial tract

Pectineus muscle

Gracilis muscle

Adductor longus muscle

Biceps femoris muscle (short head) Semimembranosus muscle

Gracilis muscle

Semitendinosus muscle

Sartorius muscle

Popliteal vessels and tibial nerve Common fibular (peroneal) nerve

Rectus femoris muscle

Plantaris muscle

Vastus lateralis muscle

Gastrocnemius muscle

Vastus medialis muscle Rectus femoris tendon Lateral patellar retinaculum Patella Medial patellar retinaculum Patellar ligament

B

Sartorius tendon Gracilis tendon

Superficial dissection: posterior view

Pes anserinus

Semitendinosus tendon Tibial tuberosity

A

Superficial dissection: anterior view

Figure 1.12  Muscles of the thigh. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

(Fig. 1.13). All five muscles cross the hip joint but only the gracilis crosses the knee. The gracilis is also the most superficial muscle of the adductor compartment. It begins from its origin on the pubic bone as a flat, broad muscle that tapers down into a narrow tendon that inserts into the pes anserinus. The gracilis is often harvested for wound coverage and can be transferred as a pedicled flap for local coverage or a free flap for distant reconstruction. It can also be harvested with its nerve supply

for functional upper extremity reconstruction or facial reanimation. The gracilis has a type II vascular supply, perfused from a dominant medial circumflex femoral artery pedicle, with three to six muscular branches entering the muscle on the deep surface adjacent to a branch of the obturator nerve and each branch proceeding distally in an independent, longitudinal manner, allowing for muscle subdivision when necessary.16,17 As opposed to the gracilis, the remainder of the adductor muscles

The thigh

17

Muscles of Hip and Thigh Anterior view: deep dissection Pectineus m. (cut and reflected) Anterior superior iliac spine Superior ramus of pubis Anterior inferior iliac spine Capsule of hip joint Greater trochanter of femur Iliopsoas m. (cut) Pectineus m. (cut and reflected) Adductor brevis m. (cut and reflected) Vastus intermedius m. Adductor longus m. (cut and reflected) Femoral a. and v. passing through tendinous hiatus of adductor magnus m. Vastus medialis m. (cut) Rectus femoris tendon (cut)

Adductor longus m. (cut and reflected) Adductor brevis m. (cut) Pubic tubercle Gracilis m. (cut) Obturator externus m. Quadratus femoris m. Adductor magnus m. (Adductor minimus m.) Openings for perforating branches of deep femoral a. Medial epicondyle of femur

Vastus lateralis m. (cut)

Gracilis m. (cut)

Lateral epicondyle of femur Patella Fibular collateral ligament

Tibial collateral ligament

Lateral patellar retinaculum Head of fibula Patellar ligament

Medial patellar retinaculum Sartorius tendon (cut) Semitendinosus tendon Tuberosity of tibia

Figure 1.13  Muscles of the thigh, deep dissection: anterior view. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

do not lend themselves easily for flap transposition due to their position and muscular structure. The tensor fascia latae is not classically designated in the previously described compartments but included in the discussion of the thigh because of its intimate relation to thigh musculature and utility in reconstructive surgery. The tensor fascia latae lies on the proximal lateral aspect of the thigh originating from the iliac crest. As it descends distally, it is enveloped by the two layers of the iliotibial band (Figs. 1.7 and 1.9). The tensor fascia latae muscle usually ends in the proximal third of the thigh but can extend down to the lateral femoral condyle. Its blood supply is from the ascending or transverse branch of the lateral circumflex femoral arterial system. This allows the muscle and fascia to be included with other flaps based off the same system if such a composite reconstruction is required.

Thigh vasculature The primary blood supply to the lower extremity is the femoral artery (Fig. 1.14). It courses with the femoral vein through the femoral sheath, a short canal composed of the continuation of the transversalis fascia anteriorly and the iliac fascia posteriorly. These fascial layers fuse with the vascular adventitia approximately 4 cm inferior to the inguinal ligament. The femoral artery crosses beneath the sartorius muscle and enters Hunter’s canal, a fibromuscular canal bounded laterally by the vastus medialis, inferiorly by the adductor longus and magnus, and anteromedially by the sartorius. The femoral artery exits Hunter’s canal through the adductor hiatus, entering the popliteal fossa, at which point it is referred to as the popliteal artery.

CHAPTER 1  • Comprehensive lower extremity anatomy

18

Rectus femoris ALT Ascending branch of lateral circumflex femoral artery Medial circumflex femoral artery Transverse branch of lateral circumflex femoral artery Second perforating artery

Femoral artery Deep artery of thigh First perforating artery

TFL for tongue Lateral Femoral Circumflex

Third perforating artery Descending genicular artery Descending branch of lateral circumflex femoral artery Superior lateral genicular artery

Articular branch of descending genicular artery Saphenous branch of descending genicular artery Superior medial genicular artery

Inferior lateral genicular artery Circumflex peroneal branch of posterior tibial artery

Inferior medial genicular artery Popliteal artery

Anterior tibial artery Peroneal artery

Anterior lateral malleolar artery

Lateral tarsal artery

Posterior tibial artery

Anterior medial malleolar artery Dorsal pedis artery Medial tarsal artery Arcuate artery

Lateral Iliac Crest

Figure 1.15  Lateral circumflex femoral artery system. ALT, anterolateral thigh; TFL, tensor fasciae latae. (Courtesy of Lawrence Gottlieb.)

ligament, then the femoral artery branches into the profunda femoris and the SFA. The profunda femoris usually branches from the posterolateral aspect of the femoral artery then passes deep to the adductor longus muscle, between the insertions of the lateral and medial intermuscular septa, and runs posterior to the linea aspera of the femur (Figs. 1.8 and 1.15).

Profunda femoris In the thigh, the profunda femoris is the predominant blood supply source. There are some important contributions to thigh musculature by the SFA (the adductors, sartorius, and the vastus medialis), but the main vascular distribution for the three thigh compartments arises from the profunda femoris. The majority of the pedicles to thigh musculature arise in the proximal two-thirds of the thigh from the six major branches of the profunda femoris: the lateral and medial circumflex arteries and four perforating arteries (Fig. 1.16).

Lateral circumflex femoral arterial system Figure 1.14  Femoral and profunda arteries.

In the proximal thigh, the femoral artery bifurcates 4 cm inferior to the inguinal ligament into the profunda femoris (also called the deep femoral artery) and the superficial femoral artery (SFA). Although there is some debate over the terminology of the femoral artery’s origin and distal progression, it is usually described as follows: the external iliac artery becomes the femoral artery after it crosses the inguinal

The lateral circumflex femoral arterial system is particularly relevant to the reconstructive surgeon due to the popularity of flap options that can be harvested on it. Classically, the lateral circumflex femoral artery (LCFA) is described as the second major branch off the profunda femoris, splitting into the ascending, transverse, and descending branches (Fig. 1.17). The ascending branch travels along the intertrochanteric line, supplying the greater trochanter, the tensor fascia latae, anterior iliac crest, and the skin overlying the hip before connecting with the superior gluteal and deep circumflex iliac vessels. The transverse branch passes through the vastus lateralis and

The thigh

19

Superficial epigastric artery Tensor fasciae latae Lateral circumflex femoral artery Ascending branch of lateral circumflex femoral artery

Transverse branch of lateral circumflex femoral artery Deep artery of thigh Femoral artery

Superficial circumflex iliac artery Lateral circumflex femoral artery Ascending branch of lateral circumflex femoral artery Transverse branch of lateral circumflex femoral artery Medial circumflex femoral artery

Superficial external pudendal artery Deep external pudendal artery Deep artery of thigh

Femoral artery

Descending branch of lateral circumflex femoral artery

Descending genicular artery

Vastus intermedius

Vastus lateralis

Descending branch of lateral circumflex femoral artery

Rectus femoris

Figure 1.17  Profunda femoris perforating branches.

Figure 1.16  Lateral circumflex femoral artery (LCFA).

curls posteriorly around the femur, joining with the medial circumflex artery. The descending branch usually travels in the intermuscular septum between the vastus intermedius and the overlying rectus femoris. From these branches, cutaneous perforators either travel through the musculature (musculocutaneous perforators) or between the musculature along the intervening fibrous septa (septocutaneous perforators). There is great variability in the LCFA system and the classical description of the location of the vessels and their courses does not always hold. In 20% of cases, the take-off of the

lateral circumflex femoral artery is from a different source vessel than the profunda femoris. It can arise from the common femoral artery itself, present as a split artery traveling from the femoral artery and the profunda femoris separately, from a common origin for the profunda femoris and the medial circumflex femoral artery (MCFA), from the MCFA, or even from the external iliac artery.18 In spite of this multiplicity of anatomic variations, the LCFA system provides a robust interconnected blood supply to skin, muscle, fascia, and bone. This can be exploited for a plethora of flap compositions in a variety of orientations. The numerous independent branches of the LCFA system allow for construction of chimeric flaps with multiple tissue types, including anterolateral thigh skin, fascia lata, vastus lateralis, rectus femoris, tensor fascia latae, and lateral iliac crest (Fig. 1.15).

20

CHAPTER 1  • Comprehensive lower extremity anatomy

Clinical correlation – approach to LCFA as recipient vessel for free tissue transfer in the vessel depleted lower extremity The distal aspect or descending branch of the LCFA can often be utilized as a salvage recipient vessel option in lower extremity reconstruction. In major oncological resections of the proximal lower leg/knee or traumatic injuries with a large zone of injury, there may not be sufficient recipient vessels in the lower leg for free tissue transfer. In these circumstances, a primary vein graft or arteriovenous loop can be performed from the distal LCFA to perfuse the transferred flap. In our experience, the challenging aspect of this approach is not only selecting the vessel where there is sufficient caliber for arterial anastomosis, but also where the accompanying vein is not diminutive to avoid a large size mismatch. This is typically more proximal than one would initially anticipate, and thus a vein graft is almost always required. A 10–12 cm incision can be made overlying the intermuscular septum in the mid-thigh. Identification of the septum and the approach to the LCFA is similar to harvest of a vastus lateralis or anterolateral thigh free flap. Elevation and medialization of the rectus femoris is critical. We recommend identifying the LCFA proximally first and then dissecting distally as the descending branch or distal continuation can become intermuscular and less predictable more distally in the thigh. A deep Adson–Beckman retractor and/or dull fish hooks/lone star retractors facilitate exposure for anastomoses and obviate the need for retraction assistance. If necessary to avoid muscular compression on the vein graft following anastomoses in the thigh, a trough can be created on the superficial aspect of the vastus lateralis muscle.

Clinical correlation – anterolateral thigh flap The anterolateral thigh flap (ALT), based on the LCFA system, is one of the most popular soft-tissue flaps for microvascular tissue transfer in reconstructive surgery. There is considerable variability in the arterial anatomy of the ALT flap. Most commonly, perforators from the descending branch of the LCFA supply the ALT flap. However, in up to 44% of cases, there is an oblique branch, arising most commonly from the descending branch of the LCFA or, less frequently, from the transverse branch of the LCFA, which provides the dominant perforator supply to the ALT flap.18,19 When an oblique branch is present, in over 90% of cases it will supply an additional codominant pedicle to the rectus femoris muscle.20 The implication of this is that an ALT flap can be reliably harvested on either pedicle without compromising perfusion to the rectus femoris. The superior-most cutaneous perforator is reliably located approximately 17 cm inferior to the ASIS along a line from the ASIS to the lateral patella.21 The majority of cutaneous perforators will be found within a 3-cm radius around the midpoint of this line.22,23 Septocutaneous perforators to the ALT flap, which allow for more efficient dissection than musculocutaneous perforators, can be expected to be present in nearly 20% of cases, and are more common in the proximal thigh. A major benefit of the ALT flap is the potential for a long vascular pedicle. With a proximal harvest, the pedicle ranges from 4 to 8 cm; however, when harvested distally, the pedicle can reach 20 cm in length.18

Medial circumflex femoral arterial system The MCFA emerges from the medial and posterior aspect of the profunda, winds around the medial side of the femur, passes between the pectineus and psoas major, and then between the obturator externus and the adductor brevis to supply the adductor compartment (Fig. 1.17). As the artery passes between the quadratus femoris and the adductor magnus, it splits into descending and transverse branches. The transverse branch passes posteriorly to the femur and joins the transverse branch of the LCFA and the inferior gluteal artery, known as the cruciate connection. The descending branch of the MCFA branches into several muscular branches to supply the gracilis muscle. The MCFA system mirrors the LCFA system as a nexus of branches that supply multiple different muscles and cutaneous regions. Branches of the MCFA are typically smaller than those of the LCFA. However, patients with small or absent LCFA perforators tend to have larger branches from the MCFA, suggesting a reciprocal dominance of blood supply.24

Profunda femoris perforating branches There are typically four perforating branches of the profunda femoris that arise distal to the circumflex arteries. Their name is derived from the course of the vessels traveling posteriorly near the linea aspera of the femur. These vessels perforate the tendon of the adductor magnus under small tendinous arches to supply the posterior thigh. The first perforating branch emerges from the profunda femoris above the adductor brevis, the second from in front of the adductor, and the third immediately below it. The distal aspect of the profunda becomes the fourth perforator (Fig. 1.17). The first perforating branch supplies the adductor brevis, adductor magnus, biceps femoris, and gluteus maximus. The second perforating branch is larger than the first and divides into an ascending and descending branch. These branches supply the posterior compartment muscles and the endosteal blood supply to the femoral bone. The third and fourth perforating branches also supply the posterior femoral muscles and join with branches of the MCFA and the popliteal artery.

Innervation of the thigh Motor innervation The nerve supply of the compartments in the thigh follows a “one compartment, one nerve” pattern. The femoral nerve supplies the anterior compartment, the obturator nerve supplies the medial compartment, and the sciatic nerve supplies the musculature of the posterior compartment. Innervation to the thigh is derived originally from the lumbosacral plexus. The femoral nerve, arising from the L2–L4 nerve roots, passes beneath the inguinal ligament and splits into anterior and posterior divisions around the lateral femoral circumflex artery (Fig. 1.18). The anterior division supplies motor innervation to the sartorius and gives off the intermediate and medial cutaneous nerves of the thigh. The posterior division of the femoral nerve provides motor innervation to the quadriceps, sensory fibers to the knee joint, and also gives rise to the saphenous nerve. The obturator nerve, also arising from the L2–L4 spinal roots, enters the thigh through the obturator foramen and splits

The thigh

Lateral femoral cutaneous nerve (L2, 3) Femoral nerve (L2, 3, 4)

T12 L1 L2 L3 L4

Lumbar plexus

Obturator nerve Lumbosacral trunk Iliacus muscle Psoas major muscle (lower part) Articular branch Sartorius muscle (cut and reflected) Lateral femoral cutaneous nerve

Pectineus muscle

Rectus femoris muscle (cut and reflected) Quadriceps femoris muscle

Anterior cutaneous branches of femoral nerve

Vastus intermedius muscle

Sartorius muscle (cut and reflected)

Vastus medialis muscle

Saphenous nerve

Vastus lateralis muscle Articularis genus muscle

Infrapatellar branch of saphenous nerve

Medial crural cutaneous nerves (branches of saphenous nerve)

Note: Only muscles innervated by femoral nerve shown

Cutaneous innervation

A

B

Figure 1.18  Femoral nerve and lateral cutaneous femoral nerves. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

21

22

CHAPTER 1  • Comprehensive lower extremity anatomy

into anterior and posterior branches. The anterior branch of the obturator nerve provides motor innervation to the adductor longus brevis and gracilis, sensory innervation to the hip joint, and communicates with the saphenous nerve to innervate the medial leg. The posterior branch of the obturator nerve innervates the adductor magnus, and supplies sensory innervation to a portion of the knee joint capsule. The sciatic nerve is the largest nerve in the body, arising from the L4–S3 nerve roots and entering the thigh through the sciatic foramen inferior to the piriformis (Fig. 1.19). It divides into its two major components, the tibial and the common peroneal nerve, at a variable point within the thigh. The tibial nerve supplies all hamstring muscles with the exception of the short head of the biceps femoris, which is innervated by the common peroneal nerve.

Cutaneous innervation The cutaneous innervation of the thigh is shared by two pure cutaneous nerves directly branching from the lumbosacral plexus (lateral and posterior femoral cutaneous nerves) and cutaneous branches from two mixed nerves (femoral and obturator) (Figs. 1.18–1.20). The lateral femoral cutaneous nerve arises from the dorsal branches of the second and third lumbar rami. It travels from intra-abdominal and behind the descending colon to exit to the thigh underneath or through the inguinal ligament. The nerve may become entrapped or compressed at this point in a condition known as meralgia paresthetica. The lateral femoral cutaneous nerve divides into an anterior and posterior branch. The anterior branch pierces the fascia lata and becomes superficial ~10 cm below the anterior superior iliac spine. The posterior branch pierces the fascia lata more superiorly than the anterior branch. The posterior branch supplies the cutaneous region around the greater trochanter and midthigh. The anterior branch supplies the anterolateral skin of the thigh down to the knee. The posterior femoral cutaneous nerve arises from the first and second sacral rami. It leaves the pelvis via the greater sciatic foramen and descends distally under the gluteus maximus with the inferior gluteal vessels. It travels down the thigh superficial to the long head of the biceps femoris but still under the fascia lata. It pierces the deep fascia behind the knee and its terminal branches continue down to the midcalf. The posterior femoral cutaneous nerve supplies the majority of the posterior thigh skin via branches that pierce the fascia lata to travel superficially. The skin over the popliteal fossa is also supplied by the posterior femoral cutaneous nerve. The femoral nerve course has been described previously. Its anterior division supplies the medial superior and inferior thigh skin by way of the intermediate cutaneous and medial cutaneous nerve of the thigh. The obturator nerve arises from the second to fourth lumbar rami. It exits the pelvis, initially descending within the psoas major then finally through the obturator foramen, anterosuperior to the obturator vessels. It branches into an anterior and posterior division. The branches off the anterior division give cutaneous innervation to the inferomedial thigh (Fig. 1.20).

The leg As the lower extremity extends distally, the anatomic structures narrow significantly, and the tissues become more compact.

The amount of redundant soft tissue present in the thigh is not available in the leg, and there is less redundancy of similar functioning muscles. These issues make the leg more of a target for tissue reconstruction, rather than a source of donor tissue.

Knee skeletal structure The knee is the largest synovial joint in the body. It comprises the two largest long bones of the body (femur and tibia) and the largest sesamoid bone (patella). The tendons of the vastus lateralis, vastus medialis, vastus intermedialis, and rectus femoris all come to a confluence at the superior surface of the patella and then insert on the smooth proximal region of the tibial tuberosity as the patellar tendon (Fig. 1.21). The tibial tuberosity is a small, raised triangular area where the anterior condylar surfaces merge. The primary functional role of the patella is to assist in knee extension, amplifying the extensor force by 30%.25 The knee comprises two joints, the patellofemoral and the tibiofemoral joint. The patellofemoral joint assists in producing leg flexion and extension at the tibiofemoral joint. The tibiofemoral joint is a bicompartmental synovial joint whose stability and range of motion are governed by a complex interplay between the bony anatomy and its soft-tissue constraints. The femoral condyles, their articular surfaces on the tibia, and the intercondylar regions are all uniquely and asymmetrically shaped. This gives the knee lateral translocation and rotational movement beyond any hinge joint. The medial collateral ligament, lateral collateral ligament, posterior cruciate, anterior cruciate, popliteofibular, transverse, coronary, and tibiofibular ligaments all work in cooperation with the muscular attachments to provide knee joint stability. The medial and lateral menisci are semilunar cartilaginous structures connected to the surrounding peripheral ligaments that deepen the articulation surface between the tibia and the femoral condyles.

Leg skeletal structure The shafts of both the tibia and the fibula form triangular cross-sectional shapes. The apex of the tibia is oriented anteriorly with a smooth curvilinear medial surface and a shelf-like lateral surface that brackets the lateral compartment musculature. The triangular apex of the fibula is oriented lateral and 90° to that of the tibia. The interosseous membrane crosses the leg in the anterior one-third area and is attached between the interosseous crests of the tibia and the fibula (Fig. 1.22). The vascular supply to the tibia and fibula is provided from multiple sources. The tibia receives major endosteal vascularity through the proximal nutrient foramen that lies near the soleal line, a bony ridge on the posterior-superior aspect of the tibia that serves as the origin of the soleus, flexor digitorum longus, and tibialis posterior muscles (Fig. 1.22).26 The endosteal blood supply to the tibia enters this area after branching off the posterior tibial artery as it exits the popliteal fossa. This branch may also stem from the popliteal bifurcation of the anterior tibial artery and the tibioperoneal trunk. The periosteal supply to the tibial shaft arises from multiple segmental branches directly from the anterior tibial artery and from perforating branches from the surrounding musculature. The distal tibia is supplied by branches from the connection around the ankle between the peroneal and posterior tibial vessels. The fibular shaft receives its endosteal blood supply from a branch of the peroneal artery that enters the bone through

The leg

23

Posterior femoral cutaneous nerve (S1, 2, 3) Greater sciatic foramen Inferior clunial nerves Sciatic nerve (L4, 5, S1, 2, 3)

Perineal branches

Common fibular (peroneal) division of sciatic nerve

Tibial division of sciatic nerve Long head (cut) of biceps femoris muscle

Short head of biceps femoris muscle

Adductor magnus muscle (also partially supplied by obturator nerve)

Cutaneous innervation

Long head (cut) of biceps femoris muscle

Semitendinosus muscle Semimembranosus muscle Tibial nerve

Common fibular (peroneal) nerve

Articular branch

Posterior femoral cutaneous nerve

Articular branch Plantaris muscle Medial sural cutaneous nerve

Lateral sural cutaneous nerve

Sural communicating branch

Gastrocnemius muscle Sural nerve Soleus muscle

Medial sural cutaneous nerve From sciatic nerve

Tibial nerve Medial calcaneal branches Medial and lateral plantar nerves A

Common fibular (peroneal) nerve via lateral sural cutaneous nerve

Superficial fibular (peroneal) nerve Sural nerve

Lateral calcaneal branches

Tibial nerve via medial calcaneal branches

Lateral dorsal cutaneous nerve B

Figure 1.19  Sciatic nerve (L4, L5; S1, S2, S3) and posterior femoral cutaneous nerve (S1, S2, S3). (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

CHAPTER 1  • Comprehensive lower extremity anatomy

24

L1

Iliohypogastric nerve

L2

Lumbar plexus

L3

Ilioinguinal nerve

L4

Genitofemoral nerve

Lumbosacral trunk

Lateral femoral cutaneous nerve

Femoral nerve Obturator externus muscle Obturator nerve (L2, 3, 4)

Posterior branch

Articular branch Adductor brevis muscle Anterior branch

Adductor longus muscle (cut) Adductor magnus muscle (ischiocondylar, or “hamstrings”, part supplied by sciatic [tibial] nerve)

Posterior branch

Cutaneous branch

Gracilis muscle

Articular branch to knee joint

Adductor hiatus

Note: Only muscles innervated by obturator nerve shown

Cutaneous innervation

A

Figure 1.20  Obturator nerve. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

B

The leg

25

Knee Joint Lateral view

Medial view

IIiotibial tract

Sartorius m.

Vastus lateralis m.

Biceps femoris m., long head, short head

Gracilis m. Semitendinosus m. Semimembranosus m.

Vastus medialis m.

Bursa under iliotibial tract Fibular collateral ligament and bursa Plantaris m. Biceps femoris tendon and bursa Common peroneal n. Head of fibula Gastrocnemius m.

Adductor magnus tendon Tibial collateral ligament, parallel fibers, oblique fibers Bursa under semimembranosus tendon

Rectus femoris tendon Patella Lateral patellar retinaculum Medial patellar retinaculum

Anserine bursa under semitendinosus, gracilis, and sartorius tendons

Joint capsule

Soleus m.

Gastrocnemius m.

Patellar ligament

Peroneus longus m. Tibialis anterior m.

Popliteus m.

Tuberosity of tibia B

A

Anterior view

Femur Articularis genus m.

Vastus lateralis m. Iliotibial tract Lateral patellar retinaculum Lateral condyle of femur Fibular collateral ligament and bursa Biceps femoris tendon and bursa Bursa under iliotibial tract Insertion of iliotibial tract to oblique line of tibia Common peroneal n. Head of fibula Peroneus longus m. C

Extensor digitorum longus m. Tibialis anterior m.

Vastus medialis m. Rectus femoris tendon Patella Medial condyle of femur Medial patellar retinaculum Tibial collateral ligament Semitendinosus, gracilis, and sartorius tendons Anserine bursa Medial condyle of tibia Patellar ligament Tuberosity of tibia Gastrocnemius m.

Figure 1.21  Knee joint (lateral, medial, and anterior views). (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

a nutrient foramen in the middle one-third of the shaft. The nutritive branch enters the fibula on the posteromedial surface, posterior to the interosseous membrane.27 The fibula also receives a periosteal blood supply from multiple branches from the peroneal artery. The fibular head receives a separate blood supply. The anterior tibial artery gives off recurrent branches and both the inferior lateral genicular arteries may supply the fibular head and neck. The distal metaphyseal region of the fibula is supplied by the ankle connection between the peroneal and posterior tibial vessels similar to the distal tibia.

Clinical correlation – fibular flap The fibular flap is a workhorse flap in microvascular reconstruction of bony defects. The proximal 6 cm of the fibula

should be maintained to protect the peroneal nerve and the attachments of the peroneus muscles, and the distal 6 cm should be preserved to maintain ankle stability. To reliably harvest this as an osteocutaneous flap, incorporation of peroneal artery perforators is essential. Peroneal artery perforators to the skin can be identified using common anatomic landmarks: the proximal fibular head is the proximal landmark and the lateral malleolus is the distal landmark, creating the fibular axis. The highest concentration of septocutaneous perforators is found at the 60% mark from the fibular head to the lateral malleolus.28 Therefore, to reliably capture these perforators, the cutaneous paddle should be designed over the third quarter of the fibula, or centered between 20 and 25 cm from the fibular head in adult patients.29 The flap can also be harvested as a bone only flap (Fig. 1.23).

CHAPTER 1  • Comprehensive lower extremity anatomy

26

Anterior view

Posterior view Gastrocnemius muscle (medial head)

Plantaris muscle Gastrocnemius muscle (lateral head)

Iliotibial tract Biceps femoris muscle

Popliteus muscle Semimembranosus muscle

Fibularis (peroneus) longus muscle

Sartorius muscle Gracilis muscle Semitendinosus muscle

Extensor digitorum longus muscle

Quadriceps femoris muscle via patellar ligament

Pes anserinus Popliteus muscle Soleus muscle

Tibialis posterior muscle

Tibialis anterior muscle Flexor digitorum longus muscle

Extensor hallucis longus muscle

Fibularis (peroneus) brevis muscle

Fibularis (peroneus) tertius muscle

Origins Insertions Note: Attachments of intrinsic muscles of foot not shown

Tibialis posterior muscle

Flexor hallucis longus muscle

Fibularis (peroneus) brevis muscle Plantaris muscle Soleus and gastrocnemius muscles via calcaneal (Achilles) tendon

Fibularis (peroneus) brevis muscle Tibialis anterior muscle

Fibularis (peroneus) tertius muscle Extensor digitorum longus muscle

A

Flexor hallucis Extensor longus muscle hallucis longus muscle B

Figure 1.22  Bony attachments of muscles of leg. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

Fibularis (peroneus) longus muscle Flexor digitorum longus muscle

The leg

27

Leg fascial composition

Lower leg compartments

The fascial structure of the leg is in continuation with the fascial system of the thigh. The superficial fascia of the leg lies within the subcutaneous tissue. It is often present in two or more layers of areolar tissue, but the layers can also be densely adherent and appear as one. In the leg, the greater and lesser saphenous veins and the sural and saphenous nerve travel along the superficial fascia (Fig. 1.24). The deep fascia of the leg (also called the investing fascia or fascia cruris) constrains the leg musculature. The deep fascia is actually a continuation of the deep fascia of the thigh and receives fascial expansions from the tendons of the knee extensors and flexors. The deep fascia varies in thickness in different regions and is closely attached to the tissue structures beneath it. The interosseous membrane of the leg is a band of dense fibrous fibers oriented obliquely that extends between the interosseous crests of the tibia and the fibula (Fig. 1.24). It separates the anterior and posterior compartments of the leg. The muscles which lie directly on the membrane (tibialis anterior, extensor hallucis longus, tibialis posterior, flexor hallucis longus) use the membrane as a muscular origin. At the superior aspect of the interosseous membrane is an oval aperture that allows for passage of the anterior tibial vessels traveling from the popliteal bifurcation in the popliteal fossa to the anterior leg. At the inferior edge of the interosseous membrane there is another opening that allows for the passage of perforating branches from the distal peroneal artery.

Intermuscular septa radiate from the tibia and fibula to the investing deep fascia and divide the leg musculature into compartments (Fig. 1.24). These compartments organize the musculature into groups of similar function. These intermuscular septa divide the leg into anterior, lateral, and posterior compartments. The boundaries of the anterior muscle compartment are the tibial surface medially, the interosseous membrane as the floor, the deep fascia as the roof, and the intermuscular septum, which divides the anterior compartment from the lateral compartment, as the lateral wall. The lateral compartment boundaries are as follows: the floor is the anterior surface of the fibula, the roof is the investing fascia of the leg, and the other wall is the intermuscular septum dividing the lateral from the posterior compartment. The posterior compartment is the largest of the three major compartments and lies posterior to the interosseous membrane. The transverse intermuscular septum creates a division line from the lateral deep fascia wall to the medial deep fascia wall separating the posterior compartment into the deep and superficial layers. The superficial layer is the only compartment that does not have a bony component. The medial surface of the tibia is bare, with no muscular peripheral coverage and therefore there is no medial compartment.

Figure 1.23 Fibular free flap.  

Clinical correlation – compartment syndrome and leg compartment release technique The functional advantage of osteofascial compartment organization can turn problematic when the compartment volume is pathologically expanded against its fascial constraints. Trauma, infection, and intravenous extravasation of liquids can increase compartmental volume through edema, inflammation, and/or direct volume addition.30 As the volume of a compartment increases, so does the intracompartmental pressure due to the rigid nature of the fascial boundaries. As intracompartmental pressure rises above capillary and arterial filling pressure, perfusion and vascular inflow decreases, leading to tissue ischemia. Because the investing fascia of the leg is thickest on the anterior surface, the anterior compartment is the least expansile of the four major compartments of the leg. The posterior aspect of the investing fascia of the leg is more pliable; therefore, the superficial posterior compartment is much more expansile and slightly less at risk for compartment syndrome. A two-incision lateral and medial approach provides safe and efficient access to release all four compartments in the supine position. The lateral incision can be made 2 cm anterior to the fibula and extending from just distal to the fibular head to a few centimeters above the lateral malleolus. This is carried down through the anterior compartment fascia and then the lateral compartment fascia. Care should be taken to avoid iatrogenic injury to the superficial peroneal nerve. The medial incision can be made 2 cm posterior to the medial border of the tibia and carried down through the superficial posterior compartment. Care is taken to avoid iatrogenic injury to the saphenous nerve and greater saphenous vein during the medial approach. The gastrocnemius and soleus should then be retracted to gain exposure to the deep posterior compartment fascia, which is incised and released of the tibia.

CHAPTER 1  • Comprehensive lower extremity anatomy

28

Deep fascia of leg (crural fascia)

Interosseous membrane

Anterior compartment Extensor muscles Tibialis anterior Extensor digitorum longus Extensor hallucis longus Fibularis (peroneus) tertius Anterior tibial artery and veins Deep fibular (peroneal) nerve

Tibia Deep posterior compartment Deep flexor muscles Flexor digitorum longus Tibialis posterior Flexor hallucis longus Popliteus Posterior tibial artery and veins Tibial nerve Fibular (peroneal) artery and veins

Anterior intermuscular septum Lateral compartment Fibularis (peroneus) longus muscle Fibularis (peroneus) brevis muscle Superficial fibular (peroneal) nerve

Transverse intermuscular septum Superficial posterior compartment Superficial flexor muscles Soleus Gastrocnemius Plantaris (tendon)

Posterior intermuscular septum Fibula A

Deep fascia of leg (crural fascia)

Cross-section just above middle of leg Tibialis anterior muscle Extensor hallucis longus muscle Extensor digitorum longus muscle

Anterior tibial artery and veins and deep fibular (peroneal) nerve Tibia Interosseous membrane

Superficial fibular (peroneal) nerve

Great saphenous vein and saphenous nerve

Anterior intermuscular septum

Tibialis posterior muscle

Deep fascia of leg (crural fascia) Fibularis (peroneus) longus muscle

Flexor digitorum longus muscle Fibular (peroneal) artery and veins

Fibularis (peroneus) brevis muscle

Posterior tibial artery and veins and tibial nerve

Posterior intermuscular septum Fibula

Flexor hallucis longus muscle

Lateral sural cutaneous nerve

Deep fascia of leg (crural fascia)

Transverse intermuscular septum

Plantaris tendon

Soleus muscle Gastrocnemius muscle (lateral head) B

Sural communicating branch of lateral sural cutaneous nerve

Gastrocnemius muscle (medial head) Medial sural cutaneous nerve Small saphenous vein

Figure 1.24  Leg: cross-sections and fascial compartments. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

Leg musculature Anterior compartment The composition of the compartments of the leg follows a congruent order, with the muscular components of each

compartment sharing similar functions. The anterior compartment comprises four muscles (tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius), one major artery (anterior tibial), and one major mixed nerve (deep peroneal) (Figs. 1.25 and 1.26). These muscles are responsible for dorsiflexion of the ankle, foot, and toes. The

Vastus lateralis muscle

Dorsal digital branches of deep fibular (peroneal) nerve

Extensor hallucis brevis tendon

Extensor hallucis longus tendon

Tendon

Short head

Head of fibula

Inferior lateral genicular artery

Common fibular (peroneal) nerve

Fibular collateral ligament

Biceps femoris muscle

Long head

B

Fibularis (peroneus) longus tendon passing to sole of foot

Inferior fibular (peroneal) retinaculum

Superior fibular (peroneal) retinaculum

(Subtendinous) bursa of tendocalcaneus

Calcaneal (Achilles) tendon

Lateral malleolus

Fibula

Fibularis (peroneus) brevis muscle and tendon

Fibularis (peroneus) longus muscle and tendon

Soleus muscle

Gastrocnemius muscle

Medial branch of deep fibular (peroneal) nerve

Tibialis anterior tendon

Medial malleolus

Extensor hallucis longus muscle

Soleus muscle

Gastrocnemius muscle

Tibia

Tibial tuberosity

Insertion of sartorius muscle

Patellar ligament

Joint capsule

Infrapatellar branch (cut) of Saphenous nerve (cut)

Inferior medial genicular artery

Medial patellar retinaculum

Tibial collateral ligament

Superior medial genicular artery

Patella

Vastus medialis muscle

Figure 1.25  Muscles of leg (superficial dissection): anterior view. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

A

Dorsal digital nerves

Extensor digitorum brevis tendons

Fibularis (peroneus) tertius tendon

Extensor digitorum longus tendons

Inferior extensor retinaculum

Lateral malleolus

Superior extensor retinaculum

Fibula

Extensor digitorum longus muscle

Fibularis (peroneus) brevis muscle

Superficial fibular (peroneal) nerve (cut)

Tibialis anterior muscle

Fibularis (peroneus) longus muscle

Head of fibula

Common fibular (peroneal) nerve

Inferior lateral genicular artery

Biceps femoris tendon

Lateral patellar retinaculum

Superior lateral genicular artery

Iliotibial tract

Rectus femoris tendon (becoming quadriceps femoris tendon)

Muscles of Leg (Superficial Dissection): Anterior View

5th metatarsal bone

Fibularis (peroneus) tertius tendon

Fibularis (peroneus) brevis tendon

Extensor digitorum longus tendons

Extensor hallucis longus tendon

Extensor digitorum brevis muscle

Inferior extensor retinaculum

Superior extensor retinaculum

Extensor hallucis longus muscle and tendon

Extensor digitorum longus tendon

Superficial fibular (peroneal) nerve (cut)

Extensor digitorum longus muscle

Tibialis anterior muscle

Tibial tuberosity

Patellar ligament

Lateral condyle of tibia

Lateral patellar retinaculum

Patella

Superior lateral genicular artery

Quadriceps femoris tendon

Iliotibial tract

Vastus lateralis muscle

The leg 29

30

CHAPTER 1  • Comprehensive lower extremity anatomy

Superior medial genicular artery

Superior lateral genicular artery

Quadriceps femoris tendon

Fibular collateral ligament

Tibial collateral ligament

Lateral patellar retinaculum

Medial patellar retinaculum

Iliotibial tract (cut) Biceps femoris tendon (cut) Inferior lateral genicular artery Common fibular (peroneal) nerve Head of fibula Fibularis (peroneus) longus muscle (cut) Anterior tibial artery Extensor digitorum longus muscle (cut) Superficial fibular (peroneal) nerve Deep fibular (peroneal) nerve Fibularis (peroneus) longus muscle

Infrapatellar branch of saphenous nerve (cut) Inferior medial genicular artery Saphenous nerve (cut) Patellar ligament Insertion of sartorius tendon Anterior tibial recurrent artery and recurrent branch of deep peroneal nerve Interosseous membrane Tibialis anterior muscle (cut) Gastrocnemius muscle

Extensor digitorum longus muscle Fibularis (peroneus) brevis muscle and tendon

Soleus muscle Tibia Superficial fibular (peroneal) nerve (cut) Extensor hallucis longus muscle and tendon (cut)

Fibularis (peroneus) longus tendon Perforating branch of fibular (peroneal) artery Anterior lateral malleolar artery Lateral malleolus and arterial network Lateral tarsal artery and lateral branch of deep fibular (peroneal) nerve Extensor digitorum brevis and extensor hallucis brevis muscles (cut) Fibularis (peroneus) brevis tendon Posterior perforating branches from deep plantar arch

Interosseous membrane Anterior medial malleolar artery Medial malleolus and arterial network Dorsalis pedis artery Tibialis anterior tendon Medial tarsal artery Medial branch of deep fibular (peroneal) nerve Arcuate arter y Deep plantar artery

Extensor digitorum longus tendons (cut)

Dorsal metatarsal arteries

Extensor digitorum brevis tendons (cut)

Extensor hallucis longus tendon (cut)

Dorsal digital arteries Branches of proper plantar digital arteries and nerves

Extensor hallucis brevis tendon (cut) Dorsal digital branches of deep fibular (peroneal) nerve

Figure 1.26  Muscles of leg (deep dissection): anterior view. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

tibialis anterior is the most superficial muscle in the compartment, overlying the anterior tibial vessels and the deep peroneal nerve in the proximal leg. Its tendon passes through the medial compartments of the superior and inferior extensor retinacula to insert on the medial cuneiform and first metatarsal

base. Its specific mechanism of action is foot dorsiflexion and inversion. The tibialis receives its blood supply from the anterior tibial artery, usually in branches organized in two columns. These columns give off 8–12 branches which segmentally supply the muscle. The extensor digitorum longus

The leg

lies lateral to the tibialis anterior in the anterior compartment, travels distally in the lateral aspect of the ankle and transitions to tendon around the same point as the tibialis anterior. It divides into four slips that proceed to the second through fifth toes. The extensor digitorum longus extends the toes, dorsiflexes synergistically with the tibialis anterior and extensor hallucis, as well as everts the foot. It has a segmental blood supply from the anterior tibial artery similar to that of the tibialis anterior. The extensor hallucis longus shares the origin of the extensor digitorum longus but inserts on the base of the distal phalanx of the first toe. Its mechanism of action is dorsiflexion of the first toe and foot. Like all muscles in the anterior compartment, its blood supply is segmental from the anterior tibial artery. This segmental vascularity limits the mobility and arc of rotation of anterior-compartment muscle flaps. The peroneus tertius is a muscle unique to the human species. Along with the popliteus, it is the shortest muscle in the leg. Its mechanism of action is to work in collaboration with the other muscles of the anterior compartment to dorsiflex and evert the foot. All the muscles of the anterior compartment are innervated by the deep peroneal nerve.

Lateral compartment The lateral compartment is comprised of only two muscles – the peroneus longus and brevis, which originate from, and are anatomically related to, the fibula (Figs. 1.24 and 1.25). The peroneus longus is the more superficial of the two and has a more superior origin on the fibula than the brevis (Table 1.3). Both muscles transition to tendons at the ankle, course in a groove behind the lateral malleolus, and ultimately travel on the plantar surface of the foot to their insertions. The peroneus brevis inserts on the plantar surface of the base of the fifth metatarsal. The peroneus longus crosses the foot traveling beneath the midsole musculature to insert on the plantar surface of the base of the first metatarsal. Both muscles work together to evert and plantarflex the foot. The blood supply for both muscles is the same, type II, with the major pedicle branching from the peroneal artery in the proximal one-third and a distal minor branch coming off the anterior tibial artery in the distal two-thirds of the muscles. There is no major vessel within the lateral compartment, so both pedicles must traverse the intermuscular septa to reach their target muscles. Both muscles are innervated by the superficial branch of the peroneal nerve.

Posterior compartment – superficial layer The posterior compartment is the largest compartment of the leg and is divided into deep and superficial layers by the deep transverse fascia. The superficial group contains four muscles – medial and lateral gastrocnemius, soleus, and plantaris (Fig. 1.24). The gastrocnemius and plantaris muscles originate on the femur and insert on the calcaneus (Table 1.3). Therefore, these muscles cause activity on both the knee (flexion) and ankle joints (plantar flexion). The medial head of the gastrocnemius is larger and longer than the lateral head. The proximal aspect of the gastrocnemius defines the inferior border of the popliteal fossa (the superior border is marked by the terminus of the biceps femoris, semitendinosus, and semimembranosus). The lateral head overlies the biceps femoris and the medial head overlies the semimembranosus. The muscle mass

31

of the gastrocnemius extends to midcalf and transitions to its tendinous component more proximally than the soleus muscle. Of note, in 10%–30% of individuals, a sesamoid bone can be present in the proximal tendon of the lateral head of the gastrocnemius. Located behind the femoral condyle, this sesamoid body is called the fabella and can be either fibrocartilaginous or bony. Radiographically, the fabella can mistakenly be identified as a foreign body or an osteophyte.31 Each head of the gastrocnemius is supplied by a sural branch off the popliteal artery. The medial sural artery always arises more proximally from the popliteal artery than the lateral, usually at the level of the tibiofemoral joint line. Each sural artery enters the deep surface of the gastrocnemius at about the midpoint of the popliteal fossa, paired with a motor branch from the tibial nerve. These muscles follow a single major pedicle vascular supply pattern (type I), but also have some small connecting vessels between the muscle heads. The plantaris muscle is a small, expendable muscle that lies between the gastrocnemius muscles and the soleus. It is absent in approximately 10% of the population and its tendon, often used as a source for tendon grafting, is located medial and anterior to the Achilles tendon.32 The soleus is a broad, flat muscle that works synergistically with the other muscles of the compartment to plantarflex the foot. In the proximal calf, the gastrocnemius overlies the soleus. However, the muscle belly of the soleus continues much more distally than the gastrocnemius until its musculotendinous transition into the Achilles. The tendons of the gastrocnemius, soleus, and plantaris coalesce to create the broad, thick Achilles tendon which inserts into the posterior calcaneus. The soleus has a type II blood supply with three major dominant pedicles feeding it from the popliteal, peroneal, and posterior tibial arteries. Proximally, near the soleal origin, the popliteal artery sends two branches to the soleus; just below the tibioperoneal bifurcation, the peroneal artery contributes two branches; and the posterior tibial artery delivers two major pedicle branches in the proximal one-third of soleus. Additionally, there are minor pedicles that flow as segmental branches from the posterior tibial artery in the distal one-third of the leg. Because of the multiple different vascular supplies, basing an entire soleus muscle flap off one or two closely related pedicles usually results in some ischemia of the muscle area most distant from the arterial inflow. Of note, the muscles of the superficial posterior compartment create a “muscle pump” effect which helps facilitate venous return. There is an intramuscular venous plexus within the soleus that is important for adequate lower extremity venous return, especially when upright position is maintained. Consequently, most distal deep venous thromboses are seen in either the soleus or gastrocnemius.

Posterior compartment – deep layer The deep posterior compartment is comprised of four muscles – popliteus, flexor digitorum longus, flexor hallucis longus, and tibialis posterior (Table 1.3). These muscles function to flex the toes and plantarflex the ankle. All muscles in this compartment are innervated by the tibial nerve (Fig. 1.27). The popliteus is a flat muscle that travels obliquely across the popliteal fossa from its origin on the posterior aspect of the lateral femoral condyle to the posterior aspect of the proximal tibial shaft. The popliteus is characterized as the muscle that “unlocks” the knee joint from full extension. It rotates the tibia

Superficial posterior compartment

Lateral compartment

Anterior compartment

Medial gastrocnemius

Peroneus brevis

6

7

Peroneus longus

Peroneus tertius

4

5

Extensor hallucis longus

3

Medial femoral condyle

Shaft of fibula

Shaft of fibula

Shaft of fibula and interosseous membrane

Shaft of fibula and interosseous membrane

Extensor digitorum Shaft of fibula longus and interosseous membrane

2

Shaft of tibia and interosseous membrane

Origin

Tibialis anterior

Muscle

1

Table 1.3  Leg musculature

Calcaneum via Achilles tendon

Base of fifth metatarsal bone

Base of first metatarsal and medial cuneiform

Base of fifth metatarsal bone

Base of distal phalanx of big toe

Extensor expansion of lateral four toes

Medial cuneiform and base of first metatarsal

Insertion

Plantarflexes foot; flexes leg

Plantarflexes foot; everts foot at subtalar and transverse tarsal joints; supports lateral longitudinal arch

Plantarflexes foot; everts foot at subtalar and transverse tarsal joints; supports lateral longitudinal and transverse arches of foot

Dorsiflexes (extends) foot; everts foot at subtalar and transverse tarsal joints

First-toe dorsiflexion

Foot and II–V toe dorsiflexion and foot eversion

Foot dorsiflexion and inversion

Function

Blood supply

Anterior tibial

Medial gastrocnemius

Peroneus brevis

Peroneus longus

Peroneus tertius

Posterior tibial

Peroneal

Peroneal

Anterior tibial

Extensor Anterior tibial hallucis longus

Extensor digitorum longus

Tibialis anterior Anterior tibial

Muscle

One vascular pedicle (I)

Dominant pedicle and minor pedicle(s) (II)

Dominant pedicle and minor pedicle(s) (II)

Segmental (IV)

Segmental (IV)

Segmental (IV)

Segmental (IV)

Flap blood supply type

Tibial nerve

Superficial peroneal nerve

Superficial peroneal nerve

Deep peroneal nerve

Deep peroneal nerve

Deep peroneal nerve

Deep peroneal nerve

Innervation

32 CHAPTER 1  • Comprehensive lower extremity anatomy

Soleus

10

Flexor digitorum longus

Flexor hallucis longus

Tibialis posterior

12

13

14

Popliteus

Plantaris

9

Deep posterior 11 compartment

Lateral gastrocnemius

Muscle

8

Table 1.3  Leg musculature

Shafts of tibia and fibula and interosseous membrane

Shaft of fibula

Shaft of tibia

Lateral condyle of femur

Shafts of tibia and fibula

Lateral supracondylar ridge of femur

Lateral femoral condyle

Origin

Foot plantarflexion

Plantarflexes foot; flexes leg

Plantarflexes foot; flexes leg

Function

Tuberosity of navicular bone and the medial cuneiform

Base of distal phalanx of big toe

Distal phalanges of lateral four toes

Plantarflexes foot; inverts foot at subtalar and transverse tarsal joints; supports medial longitudinal arch of foot

Flexes distal phalanx of big toe; plantarflexes foot; supports medial longitudinal arch

Flexes distal phalanges of lateral four toes; plantarflexes foot; supports medial and lateral longitudinal arches of foot

Shaft of medial Flexes leg; unlocks tibia full extension of knee by laterally rotating femur on tibia

Calcaneum via Achilles tendon

Calcaneum

Calcaneum via Achilles tendon

Insertion

Tibialis posterior

Flexor hallucis longus

Flexor digitorum longus

Popliteus

Soleus

Plantaris

Lateral gastrocnemius

Muscle

Posterior tibial and peroneal

Peroneal branches

Posterior tibial branches

Medial and lateral genicular arteries

Posterior tibial

Posterior tibial

Posterior tibial

Blood supply

Segmental (IV)

Segmental (IV)

Segmental (IV)

Segmental (IV)

Dominant pedicles and minor pedicle (II)

Segmental (IV)

One vascular pedicle (I)

Flap blood supply type

Tibial nerve

Tibial nerve

Tibial nerve

Tibial nerve

Tibial nerve

Tibial nerve

Tibial nerve

Innervation

The leg 33

CHAPTER 1  • Comprehensive lower extremity anatomy

34

Common fibular (peroneal) nerve

Tibial nerve (L4, 5; S1, 2, 3)

Articular branch Lateral sural cutaneous nerve (cut)

Medial sural cutaneous nerve (cut)

Medial calcaneal branches (S1, 2)

Articular branches

Medial plantar nerve (L4, 5)

From tibial nerve

Plantaris muscle

Lateral plantar nerve (S1, 2)

Gastrocnemius muscle (cut)

Saphenous nerve (L3, 4)

Nerve to popliteus muscle Popliteus muscle

B

Sural nerve (S1, 2) via lateral calcaneal and lateral dorsal cutaneous branches

Cutaneous innervation of sole

Interosseous nerve of leg Soleus muscle (cut and partly retracted) Flexor digitorum longus muscle Tibialis posterior muscle Flexor hallucis longus muscle Sural nerve (cut) Lateral calcaneal branch Medial calcaneal branch Flexor retinaculum (cut)

A

Lateral dorsal cutaneous nerve

Flexor retinaculum (cut) Tibial nerve Medial calcaneal branch Medial plantar nerve Flexor digitorum brevis muscle and nerve Abductor hallucis muscle and nerve Flexor hallucis brevis muscle and nerve 1st lumbrical muscle and nerve Common plantar digital nerves Proper plantar digital nerves

Lateral calcaneal branch of sural nerve Lateral plantar nerve Nerve to abductor digiti minimi muscle Quadratus plantae muscle and nerve Abductor digiti minimi muscle Deep branch to interosseous muscles, 2nd, 3rd, and 4th lumbrical muscles and Adductor hallucis muscle Superficial branch to 4th interosseous muscle and Flexor digiti minimi brevis muscle Common and Proper plantar digital nerves

C

Note: Articular branches not shown Figure 1.27  Tibial nerve. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The leg

medially on the femur to allow the beginning of knee flexion. The flexor digitorum longus descends down the leg, and its tendon courses posterior to the medial malleolus and across the sole of the foot to insert to the plantar surfaces of the base of the distal phalanges. The flexor hallucis longus travels from the fibular origin down to the ankle with most of the muscle belly uniquely still present at the calcaneal level. It crosses the sole of the foot under the flexor digitorum longus to insert into the base of the plantar surface of the first-toe distal phalanx. Slips of tendons connect the flexor digitorum longus and the flexor hallucis longus. This allows coordinated flexion between the great toe and the other toes to maintain balance. The blood supply for the flexor digitorum longus comes from multiple segmental branches of the posterior tibial artery. The flexor hallucis longus, originating from the fibula, is supplied by the peroneal artery via multiple segmental branches. The tibialis posterior is the deepest muscle of the posterior compartment. As the tibialis posterior progresses to the musculotendinous junction, it courses behind the medial malleolus with the flexor digitorum longus and crosses the plantar surface of the foot beneath the flexor retinaculum, inserting onto the navicular and the medial cuneiform. It receives a segmental blood supply from multiple branches of the posterior tibial artery (Fig. 1.28).

Leg vasculature The lower leg is entirely supplied by branches from the popliteal artery (Fig. 1.29). The popliteal artery is an extension of the femoral artery after it exits the adductor canal and crosses the popliteal fossa. Prior to entering the fossa, it gives off multiple genicular branches which form a rich vascular plexus that wraps anteriorly around the knee. The superior genicular arteries connect with descending branches from the lateral circumflex femoral artery and superficial femoral artery (Fig. 1.17). As the popliteal artery exits the popliteal fossa at the distal edge of the popliteus, it produces its first terminal branch, the anterior tibial artery. The anterior tibial artery passes between the heads of the tibialis posterior and penetrates through the oval aperture in the superior aspect of the interosseous membrane. It then enters the anterior compartment, and descends along the anterior surface of interosseous membrane until it reaches the ankle. At the ankle, the anterior tibial artery is positioned midway between the lateral and medial malleoli on the anterior surface of the ankle and enters the foot as the dorsalis pedis artery. After the anterior tibial artery branches from the popliteal artery, there is usually a short segment of vessel known as the tibioperoneal trunk, that divides into the peroneal and posterior tibial vessels (Fig. 1.30). Both arteries remain in the deep layer of the posterior compartment with the peroneal artery traveling deeper and laterally, closely related to the fibula. The posterior tibial artery descends down the leg, initially slightly more superficial than the peroneal artery, and then courses deeper to just under the deep transverse fascia. As it progresses distally, it becomes more superficially located until it is only covered by skin and subcutaneous fat as it traverses the ankle posterior to the medial malleolus. The tibial nerve runs with the posterior tibial artery in the calf. Approximately five fasciocutaneous perforators emerge between the flexor digitorum longus and the soleus to pass through the deep fascia

35

to the skin (Fig. 1.31). As the posterior tibial artery rounds the medial malleolus, it divides into its terminal branches – the medial and lateral plantar arteries.

Clinical correlation – approach to leg vessels as recipients for free tissue transfer Lower extremity reconstruction often requires free tissue transfer. Understanding the approach to dissect and expose the three main potential recipient vessels, posterior tibial, anterior tibial, and peroneal, is critical for efficient microsurgery.

Posterior tibial The distal posterior tibial artery is frequently utilized as a recipient vessel for microsurgical reconstruction of the lower extremity. At the ankle level, the artery runs anterior to the tibial nerve and flexor hallucis longus tendon and posterior to the tibialis posterior and flexor digitorum longus tendons. It is quite superficial and efficient access is consistently attainable. A Doppler probe can identify the vessel above the level of the ankle. A longitudinal incision is designed with the proximal aspect shifted to get out of the zone of injury. The incision is carried down through skin and retinaculum until the artery and accompanying vein(s) are visualized. If access is required more proximal in the lower leg, the vessel is deeper in the posterior compartment, overlying the tibialis posterior muscle, and requires retraction/dissection of the gastrocnemius and soleus muscles. At the mid-lower leg level, we recommend a medial longitudinal incision, like that used for a pedicled soleus flap harvest. Identification of a perforator to the soleus muscle will allow the surgeon to dissect this perforator deep to the source posterior tibial vessels. All muscle branches can be ligated to facilitate muscular retraction and self-retainer placement for microvascular anastomoses.

Anterior tibial The anterior tibial vessel is reliably found in the distal lower extremity above the ankle between the TA and EHL tendons. A Doppler probe is used to design a longitudinal incision to access the vessels. Palpation of the tibial spine provides a good landmark as the TA tendon is lateral to this. Dissection is carried down through the retinaculum and the vessels are just deep to this level. The deep peroneal nerve accompanies the AT vessels and care should be taken to avoid iatrogenic injury to this nerve (Fig. 1.32). Proximally, the AT vessels are deeper, and more dissection and retraction of the TA muscle is required for appropriate exposure. Microvascular anastomoses to the AT vessel is progressively more challenging as one goes more proximal due to the depth of the vessels in this region and multiple muscular branches coming off that require ligation.

Peroneal On occasion, access to the peroneal artery in the lower extremity is required for microvascular anastomoses. The distal continuation of the peroneal artery or the perforating branch may have a suitable caliber for anastomosis and can be accessed via a lateral approach with the patient supine. A Doppler probe can be utilized to identify the vessel distally near the lateral malleolus. However, most commonly, access to the peroneal artery requires resection of a portion of the fibula bone. A small segment of the fibula can be resected to visualize the peroneal artery and accompanying vein(s)

36

CHAPTER 1  • Comprehensive lower extremity anatomy

Superior medial genicular artery Gastrocnemius muscle (medial head) (cut) Sural (muscular) branches Popliteal artery and tibial nerve Tibial collateral ligament Semimembranosus tendon (cut) Inferior medial genicular artery

Superior lateral genicular artery Plantaris muscle (cut) Gastrocnemius muscle (lateral head) (cut) Fibular collateral ligament Biceps femoris tendon (cut) Inferior lateral genicular artery Head of fibula Common fibular (peroneal) nerve

Popliteus muscle Posterior tibial recurrent artery Tendinous arch of soleus muscle Posterior tibial artery Flexor digitorum longus muscle

Soleus muscle (cut and reflected) Anterior tibial artery

Fibular (peroneal) artery

Tibial nerve Flexor hallucis longus muscle (retracted) Tibialis posterior muscle

Fibular (peroneal) artery

Calcaneal (Achilles) tendon (cut)

Flexor digitorum longus tendon

Interosseous membrane Perforating branch Communicating branch

of fibular (peroneal) artery

Tibialis posterior tendon

Fibularis (peroneus) longus tendon

Medial malleolus and posterior medial malleolar branch of posterior tibial artery

Fibularis (peroneus) brevis tendon

Flexor retinaculum Medial calcaneal branches of posterior tibial artery and tibial nerve Tibialis posterior tendon Medial plantar artery and nerve Lateral plantar artery and nerve Flexor hallucis longus tendon 1st metatarsal bone

Lateral malleolus and posterior lateral malleolar branch of fibular (peroneal) artery Superior fibular (peroneal) retinaculum Lateral calcaneal branch of fibular (peroneal) artery Lateral calcaneal branch of sural nerve Inferior fibular (peroneal) retinaculum Fibularis (peroneus) brevis tendon Fibularis (peroneus) longus tendon Flexor digitorum longus tendon 5th metatarsal bone

Figure 1.28  Muscles, arteries, and nerves of leg: deep dissection (posterior view). (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The leg

37

Femoral artery Adductor magnus tendon Tibial nerve Gastrocnemius medial head Popliteal artery

Gastrocnemius lateral head

Popliteus Soleus

Peroneal artery Peroneus longus

Flexor digitorum longus

Flexor hallucis longus

Posterior tibial artery Tibialis posterior

Flexor hallucis longus

Peroneus brevis Peroneal artery Communicating branch Perforating branch

Calcaneal tendon

Figure 1.29  The popliteal artery.

Figure 1.30  Posterior tibial and peroneal artery and tibial nerve.

CHAPTER 1  • Comprehensive lower extremity anatomy

38

Femoral artery Vastus medialis

Descending genicular artery

Saphenous artery

Adductor magnus tendon

Gastrocnemius perforators Popliteal artery Gastrocnemius

Perforators from anterior tibial artery Gastrocnemius

Soleus

Perforators from peroneal artery

Tibialis posterior

Tibialis anterior

Peroneal artery

Posterior tibial artery Extensor digitorum longus Fasciocutaneous perforators Peroneus longus

Peroneus brevis

Calcaneal branch of peroneal artery

Flexor digitorum longus

Anterior perforating branch of peroneal artery

Calcaneal tendon

Bifurcation of lateral and medial plantar artery

A Anterior tibial/dorsal pedis perforators

B

Figure 1.31  Leg vasculature.

Calcaneal branch of posterior tibial artery

The leg

39

of the leg, it gives off its motor innervation to the muscles of the lateral compartment. The superficial peroneal nerve continues to the lateral compartment, piercing the fascia between the distal and middle thirds. Here it bifurcates into medial and lateral branches, which provide innervation to the skin of the lower leg and foot. The deep peroneal nerve begins its course splitting from the common peroneal nerve between the fibula and the proximal part of the peroneus longus. It crosses medially from the lateral leg compartment to the deep aspect of the anterior compartment. There, it travels down the leg in front of the interosseous membrane, behind the extensor digitorum longus. It descends to the ankle alongside the anterior tibial artery and sends terminal branches into the foot joints and first web space.

Lower leg motor innervation The motor innervation of the leg muscles follows a “one compartment, one nerve” principle. The muscles of the anterior compartment are innervated by the deep peroneal nerve; the muscles of the lateral compartment are innervated by the superficial peroneal nerve; and the muscles of the posterior compartment (both superficial and deep layers) are innervated by the tibial nerve.

Lower leg cutaneous innervation

Figure 1.32  Anterior tibial artery incision and deep peroneal nerve (retracted).

deep. This should be performed at least 6 cm proximal to the lateral malleolus. The approach is similar to the harvesting of a bone only fibular flap, except the proximal bone cut only needs to be 3–4 cm above the distal bone cut to provide a sufficient window.

Leg nerve anatomy Leg innervation is derived from the tibial and peroneal branches of the sciatic nerve. The sciatic nerve bifurcates into the tibial and common peroneal nerves in the popliteal fossa. The tibial nerve continues down the deep posterior compartment running alongside the posterior tibial artery (Fig. 1.28). It innervates all the musculature of both the deep and superficial posterior compartments. The tibial nerve accompanies the posterior tibial artery to the ankle and they course together behind the medial malleolus under the flexor retinaculum. As the tibial nerve leaves the ankle and enters the plantar surface of the foot it bifurcates into the medial and lateral plantar nerves. In the popliteal fossa, the common peroneal nerve branches off laterally from the sciatic nerve and then passes from the posterior to the lateral aspect of the leg. It curves laterally around the fibular neck, passing beneath the posterior crural intermuscular septum which acts as an anatomic compression point. The peroneal nerve continues deep to the peroneus longus, the extensor digitorum longus, and the tibialis anterior. The nerve divides into superficial and deep peroneal nerves beneath the peroneus longus (Fig. 1.33). The superficial peroneal nerve travels distally down the leg between the peroneus and the extensor digitorum longus. In the proximal two-thirds

Cutaneous innervation of the leg is shared by branches of the major mixed nerves of the lower extremity (femoral and sciatic nerves) and the posterior cutaneous nerve of the thigh (Figs. 1.18 and 1.19). The nerves that innervate the skin surfaces of the knee and leg are: saphenous, posterior femoral cutaneous, common peroneal, superficial peroneal, and sural nerves. The saphenous nerve branches from the femoral nerve in the middle one-third of the thigh. It travels within the adductor canal, passing medially and underneath the sartorius, then heading superficially between the sartorius and gracilis. Here, the saphenous nerves pierces the fascia and enters the subcutaneous space. As it descends inferiorly, it gives off an infrapatellar branch that innervates the medial knee and medial crural branches that supply the entire medial leg. The posterior femoral cutaneous nerve, described in detail earlier in the chapter, sends off multiple branches to the posterior thigh and continues distally to innervate the posterior knee where it also forms communicating branches with the sural nerve. The course of the common peroneal nerve in the proximal leg has previously been discussed. As it curves lateral to the fibula neck the common peroneal nerve gives off cutaneous branches that innervate the lateral knee skin. Beneath the peroneus longus muscle, the common peroneal nerve divides into superficial and deep peroneal nerves (Fig. 1.33). The superficial peroneal nerve is responsible for the cutaneous nerve supply for the middle one-third area of the anterolateral leg (Fig. 1.33). The superficial peroneal nerve cutaneous innervation continues distally to the anterior ankle. Both the superficial and the deep peroneal branches exit the ankle into the foot to give dorsal cutaneous innervation. In the dorsal foot, the deep peroneal nerve courses below the superior extensor retinaculum, whereas the superficial peroneal nerve passes above the retinaculum in the subcutaneous space. The majority of the dorsal foot is innervated by the

CHAPTER 1  • Comprehensive lower extremity anatomy

40

Common fibular (peroneal) nerve (phantom)

Lateral sural cutaneous nerve (phantom)

Articular branches Biceps femoris tendon Recurrent articular nerve Common fibular (peroneal) nerve (L4, 5; S1, 2)

Head of fibula

Fibularis (peroneus) longus muscle (cut)

Extensor digitorum longus muscle (cut)

Deep fibular (peroneal) nerve

Tibialis anterior muscle

Cutaneous innervation

Superficial fibular (peroneal) nerve

Branches of lateral sural cutaneous nerve

Fibularis (peroneus) longus muscle

Extensor digitorum longus muscle

Extensor hallucis longus muscle

Fibularis (peroneus) brevis muscle Lateral sural cutaneous nerve Medial dorsal cutaneous nerve

Intermediate dorsal cutaneous nerve

Inferior extensor retinaculum (partially cut)

Lateral dorsal cutaneous nerve (branch of sural nerve)

Dorsal digital nerves A

Superficial fibular (peroneal) nerve Lateral branch of deep fibular (peroneal) nerve to Extensor hallucis brevis and Extensor digitorum brevis muscles Medial branch of deep fibular (peroneal) nerve

Deep fibular (peroneal) nerve

Sural nerve via lateral dorsal cutaneous branch B

Figure 1.33  Common fibular (peroneal) nerve. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The ankle and foot

peroneal nerve; only the first webspace is innervated by the deep peroneal nerve. The cutaneous innervation of the lateral side of the dorsum of the foot is also provided by the sural nerve via the lateral dorsal cutaneous branch. The sural nerve system is an intercommunicating complex of nerve branches that travel between the common peroneal and the tibial nerves. There is a medial sural branch from the tibial nerve that supplies the medial posterior portion of the leg and a lateral sural nerve from the common peroneal nerve that supplies the lateral posterior portion of the leg. The true sural nerve is composed of several different possible intercommunicating cutaneous branches of the leg. The branches coalesce in the proximal leg and form the sural nerve. The sural nerve pierces the deep fascia of the leg at the inferior edge of the gastrocnemius head median raphe. It travels down the leg in the subcutaneous space with the lesser saphenous vein. It innervates the distal one-third of the posterolateral leg. The sural nerve is of specific clinical importance as it is commonly harvested for use as a nerve graft. The distal sural nerve is located approximately 1 cm posterior to the lateral malleolus and has an intimate relationship with the short saphenous vein.33 This superficial location, the relatively small number of branches present, and the tolerable anesthetic defect in the lateral lower leg and foot left after harvest, make the use of the sural nerve graft very appealing for nerve reconstruction.

The ankle and foot The ankle and foot region has significant functional responsibility for ambulation and upright positioning. It is an area of frequent concern in reconstructive surgery, as there is only thin soft-tissue coverage over highly complex and compact osteoligamentous structures. Adequate ambulation and balance rely on a proper interplay between proprioception and sensation, musculotendinous performance, and bony alignment. Proficient reconstruction of the ankle and foot requires a focus on maintaining these essential anatomic interactions.

Ankle and foot skeletal structure There are 28 major bones in the human foot. The bony arrangement produces an intricate system, reinforced by the surrounding ligament system that supports the entire weight of the body. The ankle is the region of transition from the leg to the foot and orientation of bones and muscles from vertical to horizontal.

Ankle The ankle comprises two joints: (1) the ankle joint – the articulation between the distal surfaces of the fibula (lateral malleolus) and tibia (medial malleolus) to the superior aspect of the talus; and (2) the subtalar joint – the articulation of the inferior aspect of the talus to the superior aspect of the calcaneus and four bones (lateral malleolus, medial malleolus, talus, and calcaneus). Strong ligaments support this structure throughout its multiplanar movement. The anterior and posterior inferior tibiofibular ligaments, the interosseous ligament, and the interosseous membrane act synergistically to stabilize the joint. The ankle joint is a hinged synovial joint with plantarflexion and dorsiflexion movements, but the addition

41

of the subtalar joint allows the ankle to have comprehensive range of motion, including rotational and inversion–eversion movements.

Foot The tarsal bones are arranged in a proximal and distal row, analogous to the carpal bones in the wrist. The talus and calcaneus make up the proximal row in the foot, while the medial, intermediate, and lateral cuneiforms and the cuboid comprise the distal row. The navicular bone is interspersed between the talus and the cuneiform. The bones of the toes are very similar to the hand with the second through fifth toes consisting of metatarsal, proximal, middle, and distal phalanges. The first toe – similar to the thumb – does not contain a middle phalanx (Fig. 1.34).

Ankle and foot fascial composition The retinacula of the ankle are important structural elements for maintaining normal function of the foot. They restrain the tendons crossing the ankle, preventing bowstringing and subluxation. Additionally they keep the tendons closely adapted to the bony structure of the ankle for maximum stability. Three retinacula separate the musculotendinous units crossing the ankle into groups: the extensor retinacula on the dorsum of the foot, the flexor retinaculum on the medial ankle, and the peroneal retinaculum on the lateral ankle.

Extensor retinacula Two retinacular bands restrain the dorsal tendons of the foot and ankle – the superior and inferior extensor retinacula. This retinacular system contains the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius (Table 1.4). The superior extensor retinaculum attaches to the distal tibia and fibula just superior to the malleoli. The inferior extensor retinaculum is a Y-shaped band inserting laterally on the superior calcaneus, and medially on the medial malleolus and the plantar aponeurosis (Fig. 1.35).

Table 1.4  Retinacular contents at the ankle Extensor retinaculum Anterior tibial vessels Deep peroneal nerve Tibialis anterior Extensor hallucis longus Extensor digitorum longus Peroneus tertius Flexor retinaculum Tibialis posterior Flexor digitorum longus Posterior tibial vessels Tibial nerve Flexor hallucis longus Peroneal retinaculum Peroneus longus tendon Peroneus brevis tendon

CHAPTER 1  • Comprehensive lower extremity anatomy

42

Bones of Foot Plantar view Dorsal view

Lateral tubercle Medial tubercle

Calcaneus Body Fibular (peroneal) trochlea

Posterior process

Groove for tendon of flexor hallucis longus Trochlea Neck Head

Tarsal sinus Transverse tarsal joint Cuboid

Medial tubercle

Talus

Posterior process Head Transverse tarsal joint

Navicular Tuberosity

Tuberosity of 5th metatarsal bone

Lateral Intermediate Medial

Cuneiform bones

Lateral Intermediate Medial

Cuneiform bones

Base

5

4

3

2

1

Cuboid Tuberosity Groove for fibularis (peroneus) l longus tendon

Navicular Tuberosity

Tarsometatarsal joint

Metatarsal bones

Tuberosity of 5th metatarsal bone Base

Tarsometatarsal joint Calcaneus

Shaft (body)

Metatarsal bones

Phalanges Proximal

Head

Middle

Talus

2

1

3

4

5

Shaft (body)

A

Proximal

Head Phalanges

Base

Head Talus

Head

Middle

B

Tuberosity

Shaft (body)

Base Shaft (body) Head Base Head Base Tuberosity

Medial Lateral

Sesamoid bones

Base

Distal

Tuberosity Medial process Lateral process Sustentaculum tali Groove for tendon of flexor hallucis longus Fibular (peroneal) trochlea

Lateral tubercle

Distal

Transverse tarsal joint Navicular

Neck

Intermediate Lateral

Trochlea

Cuneiform bones

Lateral process Tarsometatarsal joint

Posterior process

Metatarsal bones Tarsal sinus

Calcaneus

Medial view

4

Fibular (peroneal) trochlea Tuberosity Groove for fibularis (peroneus) longus tendon

Phalanges

2 3

Body

Transverse tarsal joint

5

Navicular Tuberosity Cuboid Tuberosity Groove for fibularis (peroneus) longus tendon

Tuberosity of 5th metatarsal bone

Cuneiform bones

Intermediate Medial

Tarsometatarsal joint

Lateral view

Neck

Talus Head Trochlea Posterior process

Metatarsal bones

C Phalanges

2 1

Tuberosity of 1st metatarsal bone

D

Sesamoid bone

Tuberosity Groove for tendon of flexor hallucis longus

Calcaneus

Sustentaculum tali

Figure 1.34  Bones of the foot. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

Flexor retinaculum The flexor retinaculum (also called the laciniate ligament) is a medial ankle-located fascial band that restricts bowstringing of the plantar-flexing tendons traveling from the leg to the foot behind the medial malleolus (Fig. 1.36). The retinaculum is attached to the medial malleolus and fans out to the calcaneus and plantar aponeurosis. The flexor retinaculum retains the tendons of the flexor digitorum longus, flexor hallucis longus, and the tibialis posterior, the posterior tibial vessels, and

the tibial nerve (Table 1.4). The tendons are usually located anteriorly and the neurovascular structures posteriorly. An osteoligamentous passageway is created by the flexor retinaculum superficially and deeply by the talus and calcaneus. This structure is also called the tarsal tunnel and is analogous in many ways to the carpal tunnel of the hand. Both tunnels contain flexor tendons and a mixed motor and sensory nerve that gives supply to intrinsic muscles and the glabrous skin of the distal extremity. There is very little elasticity in the ligament roofs of both tunnels and none in the bony floor. As

The ankle and foot

Superficial fibular (peroneal) nerve (cut) Fibularis (peroneus) brevis muscle Fibularis (peroneus) longus tendon Extensor digitorum longus muscle and tendon Superior extensor retinaculum Fibula Perforating branch of fibular (peroneal) artery

Tibialis anterior tendon Anterior tibial artery and deep fibular (peroneal) nerve Tibia Extensor hallucis longus tendon Tendinous sheath of extensor digitorum longus Medial malleolus Tendinous sheath of tibialis anterior

Lateral malleolus and anterior lateral malleolar artery

Tendinous sheath of extensor hallucis longus

Inferior extensor retinaculum

Anterior medial malleolar artery

Lateral tarsal artery and lateral branch of deep peroneal nerve (to muscles of dorsum of foot)

43

Dorsalis pedis artery and medial branch of deep fibular (peroneal) nerve Medial tarsal artery

Fibularis (peroneus) brevis tendon Tuberosity of 5th metatarsal bone Fibularis (peroneus) tertius tendon Extensor digitorum brevis and extensor hallucis brevis muscles Extensor digitorum longus tendons Lateral dorsal cutaneous nerve (continuation of sural nerve) (cut) Dorsal metatarsal arteries Dorsal digital arteries

Arcuate artery Deep plantar artery passing between heads of 1st dorsal interosseous muscle to join deep plantar arch Extensor hallucis longus tendon Extensor expansions

Dorsal digital branches of deep fibular (peroneal) nerve

Dorsal digital branches of superficial fibular (peroneal) nerve

Dorsal branches of proper plantar digital arteries and nerves

Figure 1.35  Muscles of dorsum of foot: superficial dissection. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

44

CHAPTER 1  • Comprehensive lower extremity anatomy

Flexor digitorum longus

Soleus

Superior extensor retinaculum Posterior tibial artery

Tibialis anterior tendon and sheath Medial malleolus

Tibial nerve

Inferior extensor retinaculum Synovial sheath of extensor hallucis longus

Extensor hoods

Abductor hallucis Medial plantar artery Lateral plantar artery

Flexor retinaculum Calcaneal tendon

Figure 1.36  Fascial components of foot.

the tarsal tunnel courses distally, it becomes septated into a medial and lateral tarsal tunnel, which contain the medial and lateral plantar neurovascular structures.

skin ligaments (Fig. 1.37). It is joined at a right angle, just distal to the metatarsal heads, by the transverse metatarsal ligament. The plantar fascia is not uniform in its consistency; it is strongest and thickest centrally and thins laterally and distally.

Peroneal retinaculum

Fascial compartments of the foot

On the lateral aspect of the ankle, the tendons of the peroneus longus and brevis are held in position by a dual-positioned fascial band – the peroneal retinaculum. The superior peroneal retinaculum extends from the posterior surface of the lateral malleolus to the calcaneus. The inferior peroneal retinaculum retains the tendons by attaching from the inferolateral surface of the calcaneus and inserting on the superior surface of the calcaneus The peroneal retinaculum retains only two structures: the peroneus longus tendon and the peroneus brevis tendon (Table 1.4). As the peroneal artery passes distally from the leg to the foot, it exits from the deep region of the ankle to pass superficial to the peroneal retinaculum and provides vascular supply to the calcaneal and lateral malleolar regions of the ankle.

The foot can be divided into several distinct fascial compartments (Table 1.5). These divide the foot musculature into distinct functional units. The plantar compartments include the medial, central, lateral, and interosseous compartments. The central compartment is further subdivided into an adductor, deep, and superficial compartments (Fig. 1.38). The interosseous compartment is actually four separate spaces divided by the metatarsals. There are several distinct fascial layers in the dorsum of the foot, but this can effectively be thought of as a single functional compartment. Similar to the leg, conditions that cause increased intracompartmental pressure can lead quickly to compartment syndrome of the foot. Release of the surrounding fascial attachments is essential to avoid tissue ischemia and necrosis. Crush injuries, calcaneal fractures, and tarsometatarsal joint dislocations are the most common causes for foot compartment syndrome.

Plantar fascia The plantar fascia (also called the plantar aponeurosis) is a thick fibrous band which constrains the intrinsic structures of the foot deeper to it and serves as the fixed base for the densely adherent glabrous skin superficial to it. It is analogous to the palmar fascia of the hand in providing a stable base for overlying skin to resist shear forces and to facilitate ambulation. In the multilayered sole of the foot, the plantar fascia is the first defined structure beneath the subcutaneous fat. Proximally, the plantar fascia is attached to the calcaneus, and distally, it divides into five slips which are joined by transverse fibers and then insert to the dermis beyond the metatarsal heads via retinacula cutis

Foot musculature The foot and ankle are acted upon by both extrinsic and intrinsic musculature. The extrinsic muscles all originate from proximal to the foot and have been described in the leg section. The intrinsic muscles of the foot originate and insert within the foot and act primarily on the toes. Their secondary function is to maintain posture balance through stabilization of the osteocartilaginous architecture of the foot. The plantar muscles of the foot can be thought of as organized by layers from the sole of the foot progressing deep to

The ankle and foot

Superficial transverse metatarsal ligaments

Proper plantar digital arteries and nerves

Superficial branch of medial plantar artery

Transverse fasciculi

Digital slips of plantar aponeurosis

Lateral plantar fascia

Medial plantar fascia

Cutaneous branches of lateral plantar artery and nerve Cutaneous branches of medial plantar artery and nerve

Lateral band of plantar aponeurosis (calcaneometatarsal ligament)

Plantar aponeurosis

Medial calcaneal branches of tibial nerve and posterior tibial artery Tuberosity of calcaneus with overlying fat pad (partially cut away)

Figure 1.37  Sole of foot: superficial dissection. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

45

CHAPTER 1  • Comprehensive lower extremity anatomy

46

Table 1.5  Fascial compartments of the foot Plantar Medial compartment

Contains abductor hallucis and flexor hallucis brevis

Central compartment

Contains flexor digitorum brevis, lumbricals, flexor accessorius, and adductor hallucis

Lateral compartment

Contains abductor digiti minimi and flexor digit minimi brevis

Interosseous compartment

Contains the seven interossei

Dorsal compartment

Although several fascial layers in dorsum, effectively there is one dorsal compartment

the bony structures (Table 1.6). The first layer consists of muscles found just beneath the plantar aponeurosis – the flexor digitorum brevis, the abductor hallucis, and the abductor digiti minimi (Fig. 1.39). These muscles extend from calcaneus to toes and create a functional group that assists in maintaining foot concavity. All three have been described as local pedicled muscle flaps, and all have type I vascular supply. The flexor digitorum brevis is supplied by branches of the posterior tibial artery via the medial and lateral plantar arteries on its proximal deep surface. The abductor hallucis is supplied by a dominant pedicle on its deep surface and by a branch of the medial plantar artery in the proximal foot. The abductor digiti minimi muscle receives its dominant pedicle from a lateral branch of the proximal lateral plantar artery.

Four interosseus compartments (dorsal 4 plantar interosseus muscles)

The first layer for the plantar foot is separated from the second layer by the tendons of the extrinsic muscles of the flexor digitorum longus and the flexor hallucis longus. Also, the medial and lateral plantar artery and nerve course in this intermediary plane (Fig. 1.40). The second layer consists of the quadratus plantae muscle and the lumbrical muscles of the foot. The foot lumbricals follow the same course as those of the hand, and flex the metatarsophalangeal joints and extend the interphalangeal joints. The third layer consists of the flexor hallucis brevis, the adductor hallucis, and flexor digiti minimi brevis (Fig. 1.40). These form a small, deep intrinsic musculature that contributes in the maintenance of the longitudinal plantar arch and participates in the stabilization of intrinsic foot osteoligamentous intercalation and balance. The fourth layer is the interosseous compartment, which contains both the plantar and the dorsal interossei. The three plantar interosseous muscles adduct the toes. The four dorsal interosseous muscles abduct the toes. The adduction– abduction activity of the interossei is based through the axis of the second toe, making this toe the least mobile at the metatarsophalangeal joints. Tendons of the tibialis posterior and the peroneus longus are considered part of the fourth layer. The dorsum of the foot contains two muscles – the extensor digitorum brevis and extensor hallucis brevis (Fig. 1.35). These muscles perform accessory toe extension function to the extrinsic toe extensors. The extensor digitorum brevis extends the second through fifth toes while the extensor hallucis brevis extends the great toe. The extensor digitorum brevis receives its blood supply from the lateral tarsal artery, a branch off the dorsalis pedis. The extensor digitorum brevis is a useful muscle flap for small skin defects of the proximal foot and ankle. It can also be used as joint interposition

Medial compartment

Flexor hallucis brevis muscle

Flexor digiti minimi brevis

Abductor hallucis muscle Abductor digiti minimi muscle Lateral compartment Superficial central compartment (flexor digitorum brevis)

A

Adductor compartment (adductor hallucis)

Deep central compartment (quadratus plantae) Dorsal fasciotomy incisions

B

Medial fasciotomy incisions

Figure 1.38  Muscles of the foot and ankle. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The ankle and foot

47

Table 1.6  Muscles of the foot

Plantar musculature First layer

Abductor hallucis Flexor digitorum brevis Abductor digiti minimi

All three extend from calcaneus to toes and create a functional group that assists in maintaining foot concavity

Second layer

Flexor digitorum accessorius Lumbrical muscles

Injury to the motor supply branch for the tibial nerve to the lumbricals can cause clawing of the toes

Third layer

Flexor hallucis brevis Adductor hallucis Flexor digiti minimi brevis

Highly interrelated musculature that contributes in the maintenance of the longitudinal plantar arch

Fourth layer (interosseous compartment)

Dorsal interossei Plantar interossei

The adduction–abduction activity of the interossei is based through the axis of the second toe (dissimilar from the third finger in the hand). Therefore the second toe is the least mobile of the metatarsophalangeal joints. Tendons of the tibialis posterior and the peroneus longus are considered part of the fourth layer

Dorsal musculature

Extensor digitorum brevis

Additional extensor of toes, if it or the extensor digitorum longus is cut, the toes still extend and do not impede ambulation. Useful muscle flap for small skin defects and as joint interposition to prevent fusion (e.g., calcaneonavicular bar). Major vascular pedicle from dorsalis pedis perforator and minor pedicle from peroneal artery perforator

Extensor hallucis brevis

Closely associated with the extensor digitorum brevis and sometimes considered variant slip of the extensor digitorum brevis

to prevent fusion in nearby tarsal joints (e.g., calcaneonavicular bar).

Foot and ankle vasculature The foot and ankle receive blood supply from three proximal sources: the dorsalis pedis artery, the terminal branches of the posterior tibial artery, and the terminal branches of the peroneal artery.

Dorsalis pedis artery The dorsalis pedis is a direct extension from the anterior tibial artery and is the major vascular supply for the dorsum of the foot. It passes from underneath the extensor retinaculum and travels underneath the extensor digitorum brevis, passing between the tendons of the extensor hallucis longus medially and the extensor digitorum longus laterally. As it crosses over the tarsus and continues over the space between the first and second metatarsal, it gives off a major terminal branch that dives deep between the first intermetatarsal space and joins the lateral plantar artery to complete the plantar arterial arch (Fig. 1.41). This branching is significant because it provides communication between the dorsal foot circulation, primarily supplied by the dorsalis pedis, with the plantar circulation, supplied by the posterior tibial artery (via the lateral and medial plantar arteries). Another major terminal branch from the dorsalis pedis is the first dorsal metatarsal artery that courses distally and supplies the dorsal skin of the first and second toes. In the mid-forefoot, the dorsalis pedis (and variably the first dorsal metatarsal artery) gives off septocutaneous

branches that supply the dorsal skin of the medial two-thirds of the foot. This area of skin can be harvested with the dorsalis pedis artery as a fasciocutaneous dorsalis pedis flap.

Posterior tibial artery – medial and lateral plantar arteries The posterior tibial artery runs beneath the flexor retinaculum and splits into the medial and lateral plantar artery as it enters the sole of the foot in between the first and second layers (Fig. 1.40). The bifurcation occurs under the abductor hallucis muscle, and both the lateral and medial plantar arteries arborize to give branches to the toes. The medial plantar artery has a smaller caliber than the lateral plantar artery, runs along the medial side of the foot, and contributes to the plantar digital arteries of the first through third toes. The lateral plantar artery is analogous to the ulnar artery in the hand and similarly is the dominant blood supply for the plantar arterial arch (Fig. 1.41). At the first intermetatarsal space, a perforating branch from the dorsalis pedis traverses the foot to the plantar surface and connects with the plantar arterial arch via the lateral plantar artery. Together, the dorsalis pedis branch and the lateral plantar arch feed the toes through metatarsal branches. These branches join with branches from the medial plantar artery to complete the connecting blood supply to the toes.

Peroneal arterial branches In the distal leg, the peroneal artery primarily contributes to the ankle blood supply (Fig. 1.42). The terminal branches of the

CHAPTER 1  • Comprehensive lower extremity anatomy

48

Proper plantar digital branches of medial plantar nerve

Proper plantar digital branches of lateral plantar nerve Proper plantar digital arteries

Common plantar digital arteries from plantar metatarsal arteries Lumbrical muscles Fibrous sheaths of flexor tendons

Flexor digitorum brevis tendons overlying Flexor digitorum longus tendons

Superficial branch of medial plantar artery Lateral head and Medial head of flexor hallucis brevis muscle Flexor hallucis longus tendon

Plantar metatarsal branch of lateral plantar artery Abductor hallucis muscle and tendon Flexor digiti minimi brevis muscle Flexor digitorum brevis muscle

Abductor digiti minimi muscle (deep to lateral plantar fascia) Plantar aponeurosis (cut) Medial process and Lateral process of Tuberosity of calcaneus

Medial calcaneal branches of tibial nerve and posterior tibial artery

Figure 1.39  Muscles of sole of foot: first layer. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

The ankle and foot

Muscles of the Sole of the Foot: Second Layer

Muscles of the Sole of the Foot: Third Layer

Proper plantar digital branches of medial plantar nerve

Proper plantar digital branches of medial plantar nerve

Proper plantar digital branches of lateral plantar nerve

Flexor digitorum longus tendons

Proper plantar digital branches of lateral plantar nerve

Proper plantar digital branch of superficial branch of medial plantar artery

Flexor digitorum brevis tendons Fibrous sheaths (opened) Sesamoid bones

Anterior perforating arteries to dorsal metatarsal arteries

Common plantar digital nerves and arteries

Tendons of lumbrical muscles (cut) Sesamoid bones

Lumbrical muscles Lateral head and Medial head of flexor hallucis brevis muscle

Flexor digiti minimi brevis muscle

Flexor hallucis longus tendon Abductor hallucis tendon and muscle (cut)

Superficial branch and Deep branch of lateral plantar nerve

Flexor digitorum longus tendons Flexor digitorum brevis tendons (cut) Flexor digiti minimi brevis muscle Plantar metatarsal arteries Plantar interosseous muscles Superficial branch of lateral plantar nerve

Flexor digitorum longus tendon Superficial and deep branches of medial plantar artery

Lateral plantar nerve and artery

Medial plantar artery and nerve

Deep plantar arterial arch and deep branches of lateral plantar nerve Tuberosity of 5th metatarsal bone

Quadratus plantae muscle

Peroneus brevis tendon

Tibialis posterior tendon

Abductor digiti minimi muscle (cut) Nerve to abductor digiti minimi muscle (from lateral plantar nerve)

Flexor hallucis longus tendon

Peroneus longus tendon and fibrous sheath

Posterior tibial artery and tibial nerve (dividing)

Quadratus plantae muscle (cut and slightly retracted ) Lateral plantar artery and nerve

Flexor retinaculum

Flexor digitorum brevis muscle and plantar aponeurosis (cut)

A

Lateral calcaneal nerve and artery (from sural nerve and fibular [peroneal] artery)

49

Abductor digiti minimi muscle (cut)

Abductor hallucis muscle (cut)

Lateral calcaneal artery and nerve

Medial calcaneal artery and nerve Tuberosity of calcaneus

Transverse head and Oblique head of adductor hallucis muscle Medial head and Lateral head of flexor hallucis brevis muscle Superficial branches of medial plantar artery and nerve Flexor hallucis longus tendon (cut) Abductor hallucis muscle (cut) Deep branches of medial plantar artery and nerve Flexor digitorum longus tendon (cut) Tibialis posterior tendon Medial plantar artery and nerve Flexor hallucis longus tendon Flexor retinaculum Abductor hallucis muscle (cut) Flexor digitorum brevis muscle and plantar aponeurosis (cut) Medial calcaneal artery and nerve

Tuberosity of calcaneus

B

Figure 1.40  Muscles of sole of foot: second layer. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

peroneal artery join with the lateral malleolar and calcaneal branches of the posterior tibial artery system at the posterior ankle and heel. The peroneal artery usually terminates at the level of the calcaneus. Depending on the size and perfusion from the posterior tibial and anterior tibial arterial systems, the peroneal artery system may have an expanded contribution to the foot and ankle vascular supply. A dominant peroneal artery is seen in 7%–12% of the population. In up to 5%, the peroneal artery may be the only blood supply to the foot, known as peronea arteria magna.34,35 These variants stress the importance of preoperative evaluation of the leg vasculature prior to fibula harvest.

Ankle and foot nerve anatomy Foot cutaneous innervation The cutaneous innervation of the foot is shared by the superficial peroneal, the deep peroneal, saphenous, sural and tibial terminal branches (medial calcaneal, medial plantar, and lateral plantar) nerves (Fig. 1.41). As discussed above, the dorsum of the foot is innervated mostly by the superficial peroneal nerve. The first webspace is supplied by the deep peroneal nerve, and the lateral foot by the sural nerve. The saphenous nerve innervates the proximal anteromedial foot and ankle. The cutaneous sensation of the sole of the foot is

primarily innervated by the tibial nerve and its branches  – medial calcaneal, medial plantar, and lateral plantar (Fig. 1.27).

Foot motor innervation The motor supply to the intrinsic muscle of the foot comes from the same nerves as the cutaneous innervation and is organized similarly. The dorsal muscles of the extensor hallucis brevis and the extensor digitorum brevis are innervated by the deep peroneal nerve. All the intrinsic muscles of the plantar surface are innervated by the tibial nerve via the medial and lateral plantar nerves. The medial and lateral plantar nerves follow the course of the corresponding medial and lateral plantar arteries. The medial plantar nerve follows an innervation pattern similar to the median nerve. The muscles to the great toe (abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and first lumbrical) and the medial plantar cutaneous region, including the first through third toes, are supplied by the medial plantar nerve. The lateral plantar nerve mirrors the ulnar nerve as it innervates the deep muscles (interossei, second through fourth lumbricals, adductor hallucis, flexor digitorum brevis and flexor digitorum accessorius, and abductor digiti minimi) and the lateral side of the plantar skin, including the fourth and fifth toes.

CHAPTER 1  • Comprehensive lower extremity anatomy

50

Dorsal view Medial dorsal cutaneous nerve Supplies skin on medial sides and dorsum of foot and adjacent sides of 2nd and 3rd toes

Intermediate dorsal cutaneous nerve Supplies skin on lateral side of dorsum of foot, ankle, and adjacent sides of 3rd, 4th and 5th toes

Deep peroneal Superficial nerve Supplies peroneal the muscles: tibialis nerve anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius of the ankle joint

Anterior tibial artery

Sural nerve Supplies dorsal and calcaneal areas of the skin of the foot

Lateral tarsal Lateral dorsal arteries cutaneous nerve (branch of the sural nerve) Tibial nerve Posterior tibial artery

A

Dorsal digital arteries

Dorsal metatarsal arteries

Arcuate artery

Medial tarsal arteries

Dorsalis pedis artery

Anterior and Anterior posterior medial lateral malleolar malleolar arteries arteries

Saphenous nerve Supplies the skin on the medial side of the foot, and often the alluvial metatarsophalangeal joint Saphenous nerve

Plantar view Medial plantar nerve Sensitivity of skin of sole of foot, both sides of 1st, 2nd, 3rd and medial toes, and medial aspect of the 4th toe, as well as joints of tarsus and metatarsus of the related toes

Superficial and deep peroneal nerve

Anterior and posterior medial malleolar arteries

Anterior tibial artery

Sural nerve Tibial nerve Posterior tibial artery

Proper plantar digital arteries

B

Common plantar digital arteries

Plantar metatarsal arteries

Plantar arch

Lateral dorsal cutaneous nerve

Lateral plantar nerve Sensitivity of skin of 5th toe and lateral aspect of the 4th one. Supplies deep muscles of foot

Figure 1.41  Anatomy of the foot: nerves. (Netter illustration from www.netterimages.com. Copyright Elsevier Inc. All rights reserved.)

Conclusion

51

Conclusion The reconstructive surgeon may be called upon to treat specific tissue defects of the lower extremity, or to harvest tissue for transfer from the many potential donor sites in the lower extremity. Therefore, an intricate understanding of the structural and functional anatomy of the lower extremity is essential. This chapter provides the reader with a comprehensive review of the three-dimensional anatomy of the lower extremity. With a thorough anatomical foundation, the reconstructive options discussed in the following chapters will be better appreciated. It is our goal that this chapter serve as a valuable resource for readers of all experience levels to facilitate operative planning and clinical decision-making in reconstructive surgery.

Figure 1.42  The peroneal artery.

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51.e1

CHAPTER 1  • Comprehensive lower extremity anatomy

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2 Management of lower extremity trauma Hyunsuk Peter Suh

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SYNOPSIS

ƒ Lower extremity trauma is commonly associated with other organ injuries. ƒ A primary survey is essential to quickly recognize life-threatening conditions and perform critical interventions as early as possible. ƒ The initial assessment of extremity trauma involves evaluating vessel, bone, nerve, and soft-tissue injury, and checking for compartment syndrome. ƒ A multidisciplinary approach with an orthoplastic concept is applied from diagnosis to rehabilitation. ƒ The decision for limb amputation is not determined by a scoring system. ƒ The concept of wound healing and a skilled microsurgery technique are required for complex lower extremity reconstruction. ƒ Substantial effort and time should be devoted to successful limb salvage.

Introduction Injury is the leading cause of death and disability in all age groups, causing approximately 5 million deaths worldwide annually, accounting for 9% of all deaths.1,2 In the United States, unintentional injuries or accidents are the third leading cause of death in all age groups, accounting for 6% of all deaths in 2018. Indeed, unintentional injuries are the leading cause of death in the population aged 1–44 years. The relative burden of mortality from injury is far more significant at younger ages, accounting for 31.8% of all deaths for the 1–9 year age group, 38.3% in the 10–24 year age group, and 34.0% in the 25–44 year age group.3 In developing countries, injuryrelated mortality rates are even higher than those in developed countries.1 Trauma to the lower extremities is a common injury pattern observed in emergency medical and surgical practice.

The management of lower extremity injuries involves a multidisciplinary approach. Initial assessment begins with the primary investigation of life-threatening injuries based on the Advanced Trauma Life Support (ATLS) protocol, which is a standardized acute care system that aims to reduce trauma mortality during the golden hour.4,5 Following the initial evaluation of the medical condition and spinal cord injury, a thorough investigation of the extremity injury is initiated by the trauma team, which includes general surgery, vascular surgery, orthopedic surgery, and plastic surgery specialists. This integrated access to the patients, also known as Levin’s concept of orthopedic approach, should be applied from the emergency room to prevent amputation, restore limb function, and improve the quality of life outcome in patients with lower extremity injury.6 With a multidisciplinary team approach, surgical debridement of the necrotic tissue and external fixation of the fractured bone is followed by immediate flap coverage or delayed flap surgery after wound care. In cases of bone loss, bone graft or vascularized bone graft can be performed as a delayed procedure or by immediate bone flap coverage simultaneously with soft-tissue coverage (Algorithm 2.1).

Basic science Inflammatory response to injury Without medical treatment, most patients with major trauma die due to blood loss. This first began to change in the 16th century when the French surgeon Ambroise Paré was the first to ligate arteries during amputation. Treatment improved over the following centuries, especially after the outbreak of World War II. Most patients who would have died in earlier times are now being saved thanks to advances in bleeding control.7,8 However, more than 6% of survivors of massive hemorrhage develop septic complications, with 20% of patients developing

Diagnosis and patient presentation

Algorithm 2.1 During hospital stay

In emergency room

• Initial assessment of the patient • Multidisciplinary trauma team involvement • Stabilize the patient

• Initial assessment of lower extremity • Evaluation of limb injury • Vessel injury, soft tissue, and bone injury • Limb revascularization if necessary • Fasciotomy if needed

• Initial management of lower extremity • Early serial surgical debridement • NPWT • Fixation of unstable limb

• Definitive management of lower extremity • Soft-tissue coverage +/- internal fixation early • Bone flap or delayed bone graft for bone defect

• Rehabilitation and functional improvement • Rehabilitation • Debulking and functional surgery

Simple workflow for the management of lower extremity trauma.

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syndrome (CARS), which can be described as postinflammatory immunosuppressive status.22 This feedback loop is characterized by increased levels of anti-inflammatory cytokines and cytokine antagonists.15 The anti-inflammatory response limits progressive tissue damage and maintains homeostasis to prevent further organ damage. In the balancing process of proinflammatory and anti-inflammatory reactions, the response can either be stabilized at baseline or progress to persistent inflammation, immunosuppression, and catabolism syndrome (PICS), with an increased risk of MOF and sepsis during the critical care period (Fig.  2.1B).23 Plastic surgeons should evaluate the general condition and immune response of the patient and accordingly decide when to reconstruct the defect of the limb or other parts of the body, not only for successful reconstructive surgery limb salvage but also to save the patient.

Diagnosis and patient presentation Initial assessment and management Lower extremity trauma is often accompanied by polytrauma,24–26 and more than one-third of patients with multiple trauma have a significant lower extremity injury.24 The initial treatment of patients with multiple trauma should involve rapid assessment and management. For immediate evaluation, emergency trauma care should be well organized according to the concepts of triage, resuscitation, diagnosis, and therapeutic intervention.26,27 The Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach is used to rapidly recognize life-threatening conditions and perform critical interventions first. This approach can save valuable time in the early stage of treatment in poly-trauma cases immediately upon arrival to the emergency room.

A: Airway and cervical spine protection multi-organ failure (MOF). The activation of the immune system following trauma is vital for the protection and healing of the wound. Following severe trauma, the human body responds similarly to systemic inflammatory response syndrome (SIRS) and sepsis,12–14 and bacterial pathogens and injury cause similar immunologic responses at the genomic and transcriptomic levels.15 This similarity previously led to the assumption that post-traumatic SIRS was a response to bacterial inoculation. However, it is now considered to be a sterile process. This response is a combination of proinflammatory and anti-inflammatory responses, which start within 30 min of a major injury to favor blood loss and tissue damage rather than infection.7 SIRS results from the release of damage-associated molecular patterns or alarmins after tissue injury.16–18 Recognition of these patterns leads to the activation of immune cells, such as neutrophils and monocytes, and the rapid generation of C3, C5a, and interleukins, which activate the inflammatory process and can cause early MOF (Fig.  2.1A).17,19–21 The post-traumatic immune system has a balancing compensatory anti-inflammatory response to dampen the inflammatory reaction, termed compensatory anti-inflammatory response 9–11

In the initial evaluation of a trauma patient, the airway should be assessed first. If the patient can respond in a normal voice, the airway is patent. Signs of a partially obstructed airway include noisy breathing and increased breathing effort.28,29 A  reduced level of consciousness is a common sign of airway obstruction. Maxilla and mandible fractures can cause airway obstruction, and untreated airway obstruction rapidly leads to cardiac arrest. A head-tilt and chin-lift maneuver can secure the airway with spinal immobilization.26 Foreign materials in the airway should be removed, and suction of the airways should be performed frequently to remove blood or vomit. If the patient has reduced consciousness, a cervical spine injury is presumed, and cervical spine protection should be used throughout the evaluation process.29 A neck collar can be applied to stabilize the cervical spine.

B: Breathing The thorax and neck should be inspected, auscultated, and palpated to determine if the patient is breathing. Additionally, signs of accessory muscle work, chest symmetry, and nasal

CHAPTER 2  • Management of lower extremity trauma

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Proinflammation

Early multiorgan failure and early death

Proinflammation

RS

ST

SIRS Rapid recovery CARS

CARS

Days to weeks

Days to weeks Anti-inflammation

Anti-inflammation B

A Proinflammation

Persistent inflammation SIRS

PICS CARS Immunosuppression Anti-inflammation C

Week to months

Figure 2.1  (A–C) Inflammatory response to injury.

flaring should be looked for, and the chest should be percussed for dullness and resonance. If there is hypotension, cyanosis, neck vein distension, and tracheal deviation, tension pneumothorax should be suspected, and proper management must be performed promptly.25,26,29,30

C: Circulation and bleeding control Capillary refill and pulsation can be assessed in any setting. Electrocardiography monitoring and blood pressure measurements should also be performed. In trauma patients, hemorrhage is the leading cause of preventable death. Cardiac arrest caused by hemorrhagic shock is difficult to reverse. Hemorrhagic shock can also lead to a progressive loss of consciousness in patients with hypotension. External bleeding from the wound can be controlled by direct compression and hemostatic dressing or with a tourniquet for a limited time.25,26 Crystalloid is the fluid of choice for initial resuscitation in trauma patients with bleeding.26

D: Disability and level of consciousness The level of consciousness, blood glucose level, pupil size, and motor/sensory status should be checked. The Glasgow Coma Scale (GCS) can be used to objectively describe brain injury in trauma patients.31,32 If the GCS is ≤8 in trauma cases, severe brain damage can be presumed, and endotracheal intubation is recommended to secure a definite airway.26,29 Reduced consciousness induced by hypoglycemia can easily be corrected with oral or intravenous glucose.

E: Exposure and environmental control The patient must be undressed, and the entire body should be examined for hidden injuries, rashes, bites, or other lesions. After the examination, a warm blanket or warming device should be provided to prevent hypothermia.26 Extremities should be splinted if fractures are suspected to reduce pain and blood loss.

Diagnosis and patient presentation

Secondary survey When the patient has been stabilized after the primary evaluation, a secondary survey should be conducted; this is a rapid but more thorough head-to-toe examination. The delayed diagnosis and management of occult injuries can lead to worsened morbidity and mortality. A secondary survey is a thorough inspection of lacerations, bruising, and deformity to identify hidden fractures, injuries, or bleeding by the palpation of each part of the body. To check the back of the patient, the log-roll method should be used in cases of spinal injury.26,33 In-depth history-taking is crucial for understanding the mechanism of trauma and anticipating the possible injuries that are yet to be found during the secondary survey. Essential radiographs, including those of the cervical spine, chest, and pelvis, should be taken. The serial extended Focused Assessment Sonography in Trauma (FAST) is used to identify bleeding from internal organs, pericardial tamponade, pneumothorax, and hemothorax.34 In severely injured patients, the whole-body computed tomography (WBCT) scan protocol, including the brain, spine, chest, abdomen, pelvis, and extremities, can be used to rapidly assess the whole body for injuries and reduce the number of CT scans.26,35 Laboratory studies, including hematologic and chemistry profiles, arterial blood gas, blood type and screen, glucose, cardiac marker, coagulation battery, lactate, pregnancy test, and toxicology screen can be performed. Severe rhabdomyolysis, which can induce acute kidney injury, can occur in up to 6.2% of cases of blunt trauma, and it is recommended to check the urine myoglobin level.36 However, several studies have shown that the laboratory tests have few positive findings.37–39 Prophylactic antibiotics can reduce ventilator-associated pneumonia and empyema in penetrating head trauma and penetrating chest trauma cases. For hollow viscus injury in patients with abdominal trauma, a prophylactic antibiotic is recommended for 24 h. In an open fracture, prophylactic antibiotics covering Gram-positive organisms are administered as soon as possible, and Gram-negative covering agents are added if there is a type III fracture.40 Tetanus immunoglobulin (TIG) with tetanus toxoid (Tt) should be administered to patients without complete immunization or those who have not received a booster within 10 years, regardless of the severity of the wound.41

Extremity examination After identifying the injuries during the initial and secondary surveys, an in-depth evaluation of the extremities should be performed for vascular, nerve, bone, tendon, and soft-tissue injuries. As early diagnosis and treatment of vascular injury are crucial for limb salvage, vascular evaluation should be prompt and accurate.

Vascular evaluation If there are the so-called “hard signs” of vascular injury (such as apparent arterial bleeding, expanding hematoma, absence of distal pulsation, audible bruit, palpable thrill, or signs of distal ischemia [the five “P’s”: pain, pallor, paralysis, paresthesia, and poikilothermia]), immediate vascular surgery consultation and intervention is recommended to reduce the

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ischemic time in case of associated vascular injuries.42–45 Even in patients with palpable pulsation of the distal vessels, there can be occult or progressive vascular damage that requires operative intervention.46 The incidence of arterial injuries in patients with “soft signs” of vascular injury (such as cool limb, nonexpanding hematoma, changing in color, nonpulsatile bleeding, a history of arterial bleeding at the scene, or injury near the major artery) ranges from 3% to 25%.44,45,47–49 Point-of-care color duplex ultrasonography can be used to detect significant injuries as a screening study and to assist in the decision-making process, but CT angiography or conventional angiography is necessary to confirm the presence of hidden injuries.43,50–52 Duplex ultrasonography is combination of real-time imaging with Doppler velocimetry, which can demonstrate anatomical injury and flow status. Duplex ultrasonography has high specificity and accuracy exceeding 95%; however, it is less sensitive compared to other modalities and, when lesions are detected, angiography is also usually performed before any surgery.53 In addition, ultrasonography may not be appropriate in open trauma and may be limited in assessing arterial flow when there is a presence of collateral vessels.54 Previously, conventional arteriography was the modality of choice to evaluate for arterial injury. However, conventional angiography is a relatively time-consuming and invasive procedure and requires specialized personnel for all hours. Well-recognized complications include arteriovenous fistulae or pseudo-aneurysms, and vessel injury, which are reported to be as high as 9%.55 Recently, multidetector computed tomographic angiography (MDCTA) became the initial diagnostic radiographic modality in patients suspected to have peripheral vascular injuries associated with extremity trauma. MDCTA is easily accessible, fast, noninvasive and has high spatial and temporal resolution compared with conventional angiography. It is known to have diagnostic sensitivity higher than 95% and specificity higher than 98%.56,57 Compared to MDCTA, magnetic resonance (MR) angiography is more time consuming, provides inferior visualization of surrounding bony structures and atherosclerosis, and is more sensitive to motion artifacts.58 Images of vessel evaluation is useful in further reconstructive surgery. In severe lower limb trauma, recipient vessels in the zone of trauma may be transected, crushed, or thrombosed. Failure to identify the extent of injury to the recipient vessels can have disastrous consequences to any reconstruction with local flaps or free tissue transfer.59

Compartment syndrome Compartment syndrome, a time-sensitive surgical emergency, is a devastating complication of trauma. It is common with lower leg injuries and occurs in 1%–10% of traumas involving lower leg fracture or soft-tissue injury.60 Compartment syndrome occurs when there is increased pressure within a compartment, which compromises the circulation to the nerves, muscles, and soft tissues within that limited space. It can result from tissue edema or hematoma within the compartment that exceeds the limits of the passive stretching of the surrounding fascia. The diagnosis of compartment syndrome starts from the physical examination and the observation of six cardinal clinical manifestations (6 P’s: pain, poikilothermia, paresthesia, paralysis, pulselessness, and pallor). The earliest indicator is severe pain, which does not improve with position change

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CHAPTER 2  • Management of lower extremity trauma

and is aggravated by the passive stretching of the muscle within the compartment. However, in trauma patients, even without compartment syndrome, pain is common and severe if the patient has a fracture or crushing injury of the limb, making it difficult for the surgeon to make the decision to perform invasive fasciotomy surgery. It is well known that compartment pressure >30 mmHg or 90 mmHg

1

Transient hypotension

2

Persistent hypotension

3

Age 50 years

3

Note: Score doubled for ischemia >6 h.

different, and an MESS >8 predicts in-hospital amputation in only 43.2% of the patients.74,77 Moreover, there is a consensus that the loss of plantar sensation, that is, tibial nerve injury, is a crucial factor in salvaging a limb and is thought to be an indication for amputation.73 However, in recent studies, patients with salvaged insensate limbs had no adverse outcomes compared to those who had sensation. In addition, more than half of the patients with an insensate foot regained sensation within 2 years.80 Unfortunately, no randomized controlled trial (RCT) has been conducted on limb salvage and amputation issues with a high level of evidence. In addition, there is a low possibility that RCTs will be performed because of ethical issues in the decision-making process. Most studies that analyze the amputation rate, risk factors, and outcomes are retrospective studies. In a retrospective study, there is an unequal group of patients, and the decision-making is affected by the operator’s own philosophy or algorithm, which may represent a selection bias that blurs the causal relationship between the risk factors and the salvage rate. For this reason, many studies have shown a wide range of amputation rates in the same fracture grade or a group of the same risk factors. It cannot be overemphasized that successful management of the injuries and salvaging the limb are mainly dependent on the effort and technique of the surgeons involved in the trauma team, and not on a low score in the selected scoring system. The primary goal in trauma reconstruction is to restore and maintain function, with stable skeletal support and stable surrounding soft tissue without chronic pain/ infection, and a good aesthetic outcome without compromising the function.

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Degloving soft-tissue injury A degloving injury is the avulsion of soft tissue and detachment of the skin and subcutaneous tissue from the underlying fascia. Prompt suturing of the detached tissue to the original position without tension is usually performed in the early period of care.81 This represents an excellent option if the perfusion to the distal part of the avulsion flap is intact. However, if the perfusion is insufficient, the successful attachment of a thick avulsion flap to the wound base is difficult. In contrast, without proper debridement of the necrotic tissue, infection, fasciitis, or sepsis can develop in the patient. Therefore, it is crucial to perform appropriate debridement and determine the margin of the part of the flap that lacks perfusion. Evaluation of tissue vascularization is primarily based on bleeding from the margin of the skin, the skin color, or on a pinprick over the skin flap to delineate the region with proper perfusion. However, this process can be demanding, and the results may vary depending on the surgeon’s experience. In the initial debridement, near-infrared indocyanine green (ICG) fluorescence angiography can be helpful in assessing the devascularized area through visualization.82 If there is an area of skin that is intact but has no perfusion, split-thickness or full-thickness skin grafts can be harvested from the avulsed skin when it is still viable and can be grafted83 after debridement of the wound, immediately or in a delayed fashion. As there is no absolute method for estimating the line of demarcation, surgeons should check the viability of the avulsed skin within a short time interval and perform additional debridement if needed.

Treatment and surgical techniques Timing of reconstruction and negativepressure wound therapy (NPWT) in open fracture In 1986, Godina published his landmark article on microsurgical reconstruction of complex extremity trauma and provided evidence for reconstruction within the first 72 h of injury.84 A large series of more than 500 patients showed a lower incidence of flap failure and postoperative infection in the early reconstruction group than in patients in whom reconstruction was performed after 72 h. Although Godina’s original work established a guideline for early free flap reconstruction in extremity trauma reconstruction, there are limitations for the application of this strategy. First, his analysis did not control for surgeon bias, which is the learning curve in the early stages of clinical practice. The flap failure rate was 26% in the first 100 cases, which were mostly delayed flaps, compared to only 4% in his last 100 cases, which were mostly performed within 3 days of injury. Second, Godina included upper extremity trauma cases in the series, which affected the outcome of the data analysis. Third, there is no detailed information on why patients underwent delayed reconstruction. The timing of the surgery can be determined by surgeon preference but can also be affected by various factors, such as transfer from other hospitals, the patient’s general condition or other life-threatening injuries, and the capacity of the hospital and faculties. If the patient has multiple traumas with additive intensive care, they will have a

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CHAPTER 2  • Management of lower extremity trauma

higher chance of morbidity, and there will be less chance of early surgery, which will increase the complication rate for the delayed reconstruction group. As early surgery is not an option for these patients, the patient group should be analyzed separately to reduce selection bias. Despite the confounding factors, the concept of early coverage of extremity trauma wounds has become the gold standard, due to the reduced scarring and fibrosis in the zone of injury. After Godina’s landmark paper, several recent studies showed that flap coverage could be performed in a subacute period, which lasts from 1 week to several months after trauma, as a delayed reconstruction with a similar flap success rate.85,86 In addition, a meta-analysis in 2018, which analyzed 43 retrospective case report articles, demonstrated that early freeflap reconstruction performed within the first 72 h showed a decreased rate of flap failure and infection. Importantly, 135 early reconstruction cases, 862 delayed reconstruction cases, and 93 late reconstruction cases were included in the study. The reconstruction timing in this study shows that many surgeons still perform delayed reconstruction because of many practical issues in clinical practice. Recently, some reports advocated for delayed reconstruction with similar reconstruction results. A retrospective study by Lee et al. in 2019 analyzed 358 cases of lower extremity injury, and demonstrated that the flap reconstruction performed within 10 days of injury had similar flap total failures and major complication rates as the reconstructions performed within the first 3 days of injury.87,88 In addition, retrospective studies showed no significant difference in flap success and complication rate between the timing groups divided as 15 days, 21 days, and 30 days.89–91 Although the debate regarding the reconstruction timing is ongoing, immediate reconstruction is, if the general condition of the patient permits, the timing of choice for lower extremity injury. However, delayed reconstruction can also be successful if the surgery has to be delayed because of clinical issues (Figs. 2.2 & 2.3). Again, the main issue with this debate is the absence of high-level evidence. The limitation of this retrospective review is the selection bias in the patient groups. The patients in the retrospective study had no standardized treatment protocol or reconstruction algorithm, and the patient groups were not randomized before the study. In some cases, patients with different degrees of injury and soft-tissue conditions can be categorized as the same category and compared in the same study group. One factor that extends the golden time period for reconstruction of lower extremity injury is the introduction of NPWT as an advanced wound management modality, which has now become universal. When immediate wound coverage cannot be performed during the acute phase because of medical instability, undemarcated wounds with blunt soft-tissue injury, or unavailability of hospital faculty, NPWT can be applied as a bridge therapy during the interval between debridement and definitive flap coverage. Use of NPWT during wound care leads to a low postoperative infection rate and a flap success rate as high as that of the flap reconstructions performed in the acute phase.92 Compared to the same subacute group, the patients who underwent NPWT had lower overall complication, infectious complication, and flap-related complication rates.93 Regardless of the usefulness of NPWT, it is essential to realize that NPWT is a temporary dressing modality in most cases, and can reduce the depth of

the wound and decrease the need for flap coverage in limited circumstances.94 However, it cannot replace the need for serial surgical debridement, fasciotomy, or definitive flap surgery in most soft-tissue injuries in lower extremity trauma. In addition, the advancements in bone fixation, antibiotic cement, and beads might play a role in expanding the period for successful reconstruction.95 The salvage of a functioning lower limb is a result of the timely intervention by surgeons and other medical personnel in a multidisciplinary team. For a reconstructive microsurgeon, it is crucial to understand the fundamental management steps in various individual situations and demonstrate good skills at each point of the process over time.

Reconstructive surgery All options should be considered for lower extremity reconstruction to achieve rapid wound healing, better esthetic results, and the best functional outcome, with minimal donor site morbidity. It is important to check that the wound bed is well prepared for the coverage, and to perform serial debridement if there is a sign of infection or severe contamination. If the wound and surrounding tissue are mostly in the inflammatory phase of the wound healing process, coverage surgery should be postponed, and antibiotics and proper debridement should be performed first. The following sections provide a brief overview of the surgical options for wound coverage in lower extremity trauma.

Skin grafting Although the free flap has evolved into a thin perforator flap with minimal morbidity, skin grafting is still a useful mainstay of treatment for lower extremity full-thickness skin defects. Skin grafting can be performed in a short operation time and has a high success rate.96 Moreover, it can be used to cover extensive soft-tissue defects, degloving injuries, or friction injuries of the foot dorsum,97 or even a defect with a small segment of avascular area by the bridging phenomenon.98,99 However, a full-thickness skin graft has limited donor sites, which is insufficient for extensive lower extremity trauma wounds, and split-thickness skin grafts usually have poor elasticity and limited range of motion of the joint due to contracture or hypertrophic scar. Case reports have suggested that these limitations can be improved by using alternative dermal substitutes, including allogenic dermis or artificial dermis with collagen matrix, to show better functional and esthetic outcomes.100,101 Wound bed preparation is critical to achieve successful “take” of the skin graft as a skin graft cannot survive on a nonviable wound bed. There should be pinpoint bleeding from the entire wound bed, but not from the visible vessels on the surface (Fig. 2.4).

Local, regional, and propeller flaps An advancement flap or propeller flap has the advantage of replacing like with like and has no need for the microsurgical procedures102 (Figs. 2.5 & 2.6). However, this is only possible when there is healthy tissue near the defect without soft-tissue injury, which is not the case in many lower limb traumas. It also has a higher complication rate, including partial necrosis, than free flap surgery,103,104 and often fails to cover the most critical

Treatment and surgical techniques

59

B

F

A

D

C

E

Figure 2.2  (A) Open tibiofibular fracture of the left leg after a traffic accident in a 74-year-old patient. A plastic surgeon and orthopedic surgeon examined the patient at the emergency room. As the wound is clearly demarcated and clean, emergency flap coverage was planned with a multidisciplinary team via the orthoplastic approach. (B) The patient was transferred from the emergency room to the operation room for fixation and flap coverage within 12 h of trauma. The external fixator was placed posteriorly on the medial side to allow easy access to the anterior tibial artery. Complete debridement of the wound was possible. (C) The flap was elevated based on the medial branch of the superficial circumflex iliac artery from the ipsilateral side. (D) The size of the flap was 14 × 8 cm. (E) The flap was sutured without tension. (F) One year postoperatively, the patient could ambulate without pain.

point of soft-tissue defect leading to the need for an additional free flap to cover it (Fig. 2.7). Additionally, in the lower leg, if the width of the propeller flap is >3 cm, there is a high chance of creating a skin graft that is aesthetically unpleasant. Adjacent muscle flaps are useful for the knee and the midthird of the lower leg. The medial or lateral gastrocnemius muscle flap can be used to cover the knee and the upper one-third of the lower leg.105 For the mid-third defect, the soleus muscle flap can be used.106,107 The main limitation of

the regional muscle flap is that it frequently requires an additional skin graft and it is only possible to cover small defects (50% of the circumference or with a segment of loss 6 cm are considered a reasonable indication for a vascularized bone flap, which allows for early definitive bony reconstruction. A free fibular flap based on the peroneal artery has a straight shape, sufficient length, mechanical strength, and the possibility of folding the graft into a double-barrel reconstruction suitable for tibia and femur reconstruction. The vascularized iliac bone flap can also be used; however, it has disadvantages regarding the shape, short length (10% larger than the non-­swollen leg), liposuction can be performed if the patient wants a normalization of the leg volume.

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References

References 1. Brorson H, Svensson H. Complete reduction of lymphoedema of the arm by liposuction after breast cancer. Scand J Plast Reconstr Surg Hand Surg. 1997;31(2):137–­143. 2. Brorson H, Svensson H. Liposuction combined with controlled compression therapy reduces arm lymphedema more effectively than controlled compression therapy alone. Plast Reconstr Surg. 1998;102(4):1058–­1067. discussion 1068. 3. Wojnikow S, Malm J, Brorson H. Use of a tourniquet with and without adrenaline reduces blood loss during liposuction for lymphoedema of the arm. Scand J Plast Reconstr Surg Hand Surg. 2007;41(5):243–­249. 4. Brorson H. Liposuction normalizes lymphedema induced adipose tissue hypertrophy in elephantiasis of the leg –­ a prospective study with a ten-­year follow-­up. Plast Reconstr Surg. 2015;136(4 Suppl): 133–­134. 5. Brorson H. Complete reduction of arm lymphedema following breast cancer –­ a prospective twenty-­one years’ study. Plast Reconstr Surg. 2015;136(4 Suppl):134–­135. 6. Hoffner M, Ohlin K, Svensson B, et al. Liposuction gives complete reduction of arm lymphedema following breast cancer treatment –­ a 5-­year prospective study in 105 patients without recurrence. Plast Reconstr Surg Glob Open. 2018;6(8):e1912. 7. Boccardo F, Casabona F, De Cian F, et al. Lymphatic microsurgical preventing healing approach (LYMPHA) for primary surgical prevention of breast cancer-­related lymphedema: over 4 years follow-­up. Microsurgery. 2014;34(6):421–­424. 8. Feldman S, Bansil H, Ascherman J, et al. Single institution experience with Lymphatic Microsurgical Preventive Healing Approach (LYMPHA) for the primary prevention of lymphedema. Ann Surg Oncol. 2015;22(10):3296–­3301. 9. Gebruers N, Verbelen H, De Vrieze T, Coeck D, Tjalma W. Incidence and time path of lymphedema in sentinel node negative breast cancer patients: a systematic review. Arch Phys Med Rehabil. 2015; 96(6):1131–­1139. 10. Cook JA, Hassanein AH. ASO Author reflections: immediate lymphatic reconstruction: a proactive approach to breast cancer-­ related lymphedema. Ann Surg Oncol. 2021;28(3):1388–­1389. 11. Sleigh BC, Manna B. Lymphedema. Treasure Island, FL: StatPearls Publishing; 2021. Available at: https://­www.ncbi.nlm.nih.gov/­ books/­NBK537239/­. 12. Olszewski WL. Lymph stasis. In: Boca Raton, Ann Arbor, eds. Pathophysiology, Diagnosis and Treatment. 1st ed. Boston, London: CRC Press; 1991:648. 13. Mihara M, Hara H, Hayashi Y, et al. Pathological steps of cancer-­ related lymphedema: histological changes in the collecting lymphatic vessels after lymphadenectomy. PLoS One. 2012;7(7): e41126. 14. Bagheri S, Ohlin K, Olsson G, Brorson H. Tissue tonometry before and after liposuction of arm lymphedema following breast cancer. Lymphat Res Biol. 2005;3(2):66–­80. 15. Brorson H, Ohlin K, Olsson G, Långström G, Wiklund I, Svensson H. Quality of life following liposuction and conservative treatment of arm lymphedema. Lymphology. 2006;39(1):8–­25. 16. Hoffner M, Bagheri S, Hansson E, Manjer J, Troeng T, Brorson H. SF-­36 shows increased quality of life following complete reduction of postmastectomy lymphedema with liposuction. Lymphat Res Biol. 2017;15(1):87–­98. 17. Brorson H, Ohlin K, Olsson G, Nilsson M. Adipose tissue dominates chronic arm lymphedema following breast cancer: an analysis using volume rendered CT images. Lymphat Res Biol. 2006;4(4):199–­210. 18. Brorson H, Ohlin K, Olsson G, Karlsson MK. Breast cancer-­related chronic arm lymphedema is associated with excess adipose and muscle tissue. Lymphat Res Biol. 2009;7(1):3–­10. 19. Hoffner M, Peterson P, Mansson S, Brorson H. Lymphedema leads to fat deposition in muscle and decreased muscle/­water volume after liposuction: a magnetic resonance imaging study. Lymphat Res Biol. 2018;16(2):174–­181.

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20. Trinh L, Peterson P, Brorson H, Mansson S. Assessment of subfascial muscle/­water and fat accumulation in lymphedema patients using magnetic resonance imaging. Lymphat Res Biol. 2019;17(3):340–­346. 21. Trinh L, Peterson P, Leander P, Brorson H, Mansson S. In vivo comparison of MRI-­based and MRS-­based quantification of adipose tissue fatty acid composition against gas chromatography. Magn Reson Med. 2020;84(5):2484–­2494. 22. Vague J, Fenasse R. Comparative anatomy of adipose tissue. Section 5. In: Renold AE, Cahill GF, eds. American Handbook of Physiology. Washington, DC: American Physiology Society; 1965:25–­36. 23. Ryan TJ. Lymphatics and adipose tissue. Clin Dermatol. 1995;13(5): 493–­498. 24. Mattacks CA, Sadler D, Pond CM. The control of lipolysis in perinodal and other adipocytes by lymph node and adipose tissue-­derived dendritic cells in rats. Adipocytes. 2005;1(1):43–­56. 25. Pond CM. Adipose tissue and the immune system. Prostaglandins Leukot Essent Fatty Acids. 2005;73(1):17–­30. 26. Borley NR, Mortensen NJ, Jewell DP, Warren BF. The relationship between inflammatory and serosal connective tissue changes in ileal Crohn’s disease: evidence for a possible causative link. J Pathol. 2000;190(2):196–­202. 27. Sadler D, Mattacks CA, Pond CM. Changes in adipocytes and dendritic cells in lymph node containing adipose depots during and after many weeks of mild inflammation. J Anat. 2005;207(6): 769–­781. 28. Harvey NL, Srinivasan RS, Dillard ME, et al. Lymphatic vascular defects promoted by Prox1 haploinsufficiency cause adult-­onset obesity. Nat Genet. 2005;37(10):1072–­1081. 29. Schneider M, Conway EM, Carmeliet P. Lymph makes you fat. Nat Genet. 2005;37(10):1023–­1024. 30. Jones B, Fishman EK, Hamilton SR, et al. Submucosal accumulation of fat in inflammatory bowel disease: CT/­pathologic correlation. J Comput Assist Tomogr. 1986;10(5):759–­763. 31. Lantz M, Vondrichova T, Parikh H, et al. Overexpression of immediate early genes in active Graves’ ophthalmopathy. J Clin Endocrinol Metab. 2005;90(8):4784–­4791. 32. Karlsson T, Karlsson M, Ohlin K, Olsson G, Brorson H. Liposuction of breast cancer-­related arm lymphedema reduces fat and muscle hypertrophy. Lymphat Res Biol. 2022;20(1):53–­63. 33. Zampell JC, Aschen S, Weitman ES, et al. Regulation of adipogenesis by lymphatic fluid stasis: part I. Adipogenesis, fibrosis, and inflammation. Plast Reconstr Surg. 2012;129(4): 825–­834. 34. Aschen S, Zampell JC, Elhadad S, Weitman E, De Brot M, Mehrara BJ. Regulation of adipogenesis by lymphatic fluid stasis: part II. Expression of adipose differentiation genes. Plast Reconstr Surg. 2012; 129(4):838–­847. 35. Levi B, Glotzbach JP, Sorkin M, et al. Molecular analysis and differentiation capacity of adipose-­derived stem cells from lymphedema tissue. Plast Reconstr Surg. 2013;132(3):580–­589. 36. Dayan JH, Wiser I, Verma R, et al. Regional patterns of fluid and fat accumulation in patients with lower extremity lymphedema using magnetic resonance angiography. Plast Reconstr Surg. 2020;145(2): 555–­563. 37. Zhang J, Hoffner M, Brorson H. Adipocytes are larger in lymphedematous extremities than in controls. J Plast Surg Hand Surg. 2022;56(3):172–­179. 38. Tambour M, Holt M, Speyer A, Christensen R, Gram B. Manual lymphatic drainage adds no further volume reduction to complete decongestive therapy on breast cancer-­related lymphoedema: a multicentre, randomised, single-­blind trial. Br J Cancer. 2018;119(10): 1215–­1222. 39. Campisi C, Bellini C, Campisi C, Accogli S, Bonioli E, Boccardo F. Microsurgery for lymphedema: clinical research and long-­term results. Microsurgery. 2010;30(4):256–­260. 40. Campisi CC, Ryan M, Boccardo F, Campisi C. A single-­site technique of multiple lymphatic-­venous anastomoses for the

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42. 43.

44. 45. 46. 47. 48. 49.

50.

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CHAPTER 3.5  • Debulking strategies and procedures: liposuction of leg lymphedema

treatment of peripheral lymphedema: long-­term clinical outcome. J Reconstr Microsurg. 2016;32(1):42–­49. Baumeister RG, Siuda S, Bohmert H, Moser E. A microsurgical method for reconstruction of interrupted lymphatic pathways: autologous lymph-­vessel transplantation for treatment of lymphedemas. Scand J Plast Reconstr Surg. 1986;20(1):141–­146. Baumeister RG, Mayo W, Notohamiprodjo M, Wallmichrath J, Springer S, Frick A. Microsurgical lymphatic vessel transplantation. J Reconstr Microsurg. 2016;32(1):34–­41. Vignes S, Brorson H. Comment on “Clinical and psychosocial outcomes of vascularized lymph node transfer for the treatment of upper extremity lymphedema after breast cancer therapy”. Ann Surg Oncol. 2017;24(Suppl 3):559–­560. Cheng MH, Loh CYY, Lin CY. Outcomes of vascularized lymph node transfer and lymphovenous anastomosis for treatment of primary lymphedema. Plast Reconstr Surg Glob Open. 2018;6(12):e2056. Brorson H, Svensson H, Norrgren K, Thorsson O. Liposuction reduces arm lymphedema without significantly altering the already impaired lymph transport. Lymphology. 1998;31(4):156–­172. Greene AK, Voss SD, Maclellan RA. Liposuction for swelling in patients with lymphedema. N Engl J Med. 2017;377(18):1788–­1789. van de Pas CB, Boonen RS, Stevens S, Willemsen S, Valkema R, Neumann M. Does tumescent liposuction damage the lymph vessels in lipoedema patients? Phlebology. 2020;35(4):231–­236. Brorson H, Ohlin K, Olsson G, Svensson B, Svensson H. Controlled compression and liposuction treatment for lower extremity lymphedema. Lymphology. 2008;41(2):52–­63. Klernas P, Johnsson A, Boyages J, Brorson H, Munnoch A, Johansson K. Quality of life improvements in patients with lymphedema after surgical or nonsurgical interventions with 1-­year follow-­up. Lymphat Res Biol. 2020;18(4):340–­350. Lee D, Piller N, Hoffner M, Manjer J, Brorson H. Liposuction of postmastectomy arm lymphedema decreases the incidence of erysipelas. Lymphology. 2016;49(2):85–­92.

51. Brorson H. Liposuction in arm lymphedema treatment. Scand J Surg. 2003;92(4):287–­295. 52. Damstra RJ, Voesten HG, Klinkert P, Brorson H. Circumferential suction-­assisted lipectomy for lymphoedema after surgery for breast cancer. Br J Surg. 2009;96(8):859–­864. 53. Schaverien MV, Munro KJ, Baker PA, Munnoch DA. Liposuction for chronic lymphoedema of the upper limb: 5 years of experience. J Plast Reconstr Aesthet Surg. 2012;65(7):935–­942. 54. Boyages J, Kastanias K, Koelmeyer LA, et al. Liposuction for advanced lymphedema: a multidisciplinary approach for complete reduction of arm and leg swelling. Ann Surg Oncol. 2015;22(Suppl 3): S1263–­1270. 55. Greene AK, Maclellan RA. Operative treatment of lymphedema using suction-­assisted lipectomy. Ann Plast Surg. 2016;77(3): 337–­340. 56. Lamprou DA, Voesten HG, Damstra RJ, Wikkeling OR. Circumferential suction-­assisted lipectomy in the treatment of primary and secondary end-­stage lymphoedema of the leg. Br J Surg. 2017;104(1):84–­89. 57. McGee P, Munnoch DA. Treatment of gynaecological cancer related lower limb lymphoedema with liposuction. Gynecol Oncol. 2018; 151(3):460–­465. 58. Stewart CJ, Munnoch DA. Liposuction as an effective treatment for lower extremity lymphoedema: a single surgeon’s experience over nine years. J Plast Reconstr Aesthet Surg. 2018;71(2):239–­245. 59. Granoff MD, Johnson AR, Shillue K, et al. A single institution multi-­disciplinary approach to power-­assisted liposuction for the management of lymphedema. Ann Surg. 2020 Published online ahead of print. 60. Granoff MD, Pardo J, Singhal D. Power-­assisted liposuction: an important tool in the surgical management of lymphedema patients. Lymphat Res Biol. 2021;19(1):20–­22.

SECTION I  •  Lower Extremity Surgery

3.6 Debulking strategies and procedures: excision Hung-­Chi Chen and Yueh-­Bih Tang

Access video and video lecture content for this chapter online at Elsevier eBooks+

­

Anatomy An important anatomic detail is that the Chen-­ modified Charles procedure consists of preserving the lesser saphenous vein along with its superficial branch. The excisional procedure can be combined with lymphatic microsurgery. A circumferential incision is marked with two wedge incisions on

Patient selection (Algorithms 3.6.1–3.6.3) ­

In advanced lymphedema, chronic inflammation and repeated episodes of infection lead to gradual fibrosis of subcutaneous tissue and skin, causing destruction of lymphatic channels, and it is not suitable for microsurgical lymphovenous anastomosis.1,2 The most important goal of treatment for lymphedema is control or eradication of infection. In particular, prevention of toe infection has proven to be an important step in controlling cellulitis of the lower limb. Historically, the Charles procedure3 was first described in 1940. The Charles procedure was a common treatment to decrease lymphatic load and to control infection. Patients with primary or secondary advanced lower limb lymphedema with induration, fibrosis, brawny leather-­like skin, “squared-­off” toes, hyperkeratosis, and multiple fistulas can be treated with the Charles procedure. Potential complications of the Charles procedure are wound breakdown, hyperkeratosis, ulceration, and aggravation of foot lymphedema. To prevent these problems, many authors have described a modified Charles procedure. Van der Walt et al.4 presented a modified Charles procedure, applying negative-­dressing after the initial debulking surgery, and then they delayed the skin grafting by 5–­7 days. The excisional procedure may be simultaneously performed with toe amputations.5 The excisional procedure can be combined with lymph node flap transfer,6–11 as in the Chen-­modified Charles procedure, in which 10 steps are different from the original Charles procedure.

the proximal thigh, one on the medial aspect and the other on the lateral. Distally at the foot and toes, markings are placed at the mid-­lateral and medial aspect of the foot, above the heel, and on the dorsum of the toes and web spaces, preserving the web spaces between the toes. The treatment of toes depends on different severity of toe involvement.

The International Society of Lymphology divides the severity of lymphedema into three stages.11 Karri et al.12 reported a modified staging system, dividing the severity of the pathology into four stages. According to their system, advanced lymphedema is characterized by irreversible skin fibrosis (IIIb); and non-­ pitting edema, with leather-­ like skin, skin crypts, and ulcer, without or with involvement of the toes (stage IVa and IVb, respectively). In advanced lymphedema, the most important goal of treatment is control or eradication of infection. Toes are the major source of infection, especially in older patients. Toe crowding, nail infections, skin changes such as verrucous hyperkeratosis, and poor hygiene can all contribute to infection of toes, which may ascend to the foot or even proximal leg. If the toes are affected but left untreated, the patient will invariably have recurrent infections with a compromised result.

Preparation before surgery (Fig. 3.6.1)  

Chen-­modified Charles procedure

On hospital admission, the circumference of the affected limb is measured by a plastic surgery specialist nurse. Measurements are taken at four levels: midfoot, ankle (between medial and lateral malleoli), mid-­calf (15 cm below knee joint), and mid-­ thigh (15 cm above knee joint). Routine preoperative investigations are performed and anesthetic consultation is provided. Antibiotics13 are given according to bacterial culture one hour before induction and continued postoperatively for three days.

Chen-­modified Charles procedure

Algorithm 3.6.1 Conservative treatment

No improvement

LVA

Improvement

No improvement

LNF + Suction lipectomy

Conservative treatment

121

transition from the distal grafted thigh to the skin flaps of proximal thigh. Suction drains are left in situ. A full-­thickness skin graft (FTSG) is taken from the wedge-­excised tissues and is used for grafting at the dorsum of the foot. (FTSG on the dorsum of the foot results in a more resistant skin graft with less hypertrophic scarring and can prevent later friction with the compression garment.) The tourniquet is re-­inflated, and the split-­thickness skin graft is applied circumferentially with 0.5–­1 cm edge overlap to prevent gap formation between the sheets of skin grafts, which may arise because of swelling. This is aimed at minimizing the formation of hypertrophic scar. Finally, nonadherent dressings, bulky gauze, compression wrap, and a posterior splint are applied. The tourniquet is then deflated. Elevation of the limb and thus avoidance of shearing force ensures STSG take on the posterior surface of the leg and thigh.

Transfer of lymph node flap with Chen-­ modified Charles procedure (Video 3.6.1

)

No improvement

RPP

Lymphedema of the upper limb.

Surgical techniques for modified Charles procedure (Fig. 3.6.1)  

The patient is positioned supine, and a pneumatic tourniquet is placed on the proximal thigh and inflated to 375 mmHg following exsanguination. Split-­ thickness skin graft (STSG) is harvested from the entire circumference of the affected limb in a proximal to distal (axial) direction with the thickness of 12/­1000 of an inch. It is imperative that the lengths of the harvested STSG are as long as possible. The STSG can thus be “wrapped” around the limb in a circular fashion. Consequently, the risk of hypertrophic scar formation is minimized. The harvested STSG sheets are fenestrated. The leg is denuded down to the deep fascia. To access the posterior surface of the limb, a 3-­mm K-­pin is drilled through the distal tibia and the limb is suspended from a stand. This pin can also help to elevate the leg after surgery and is usually removed five days postoperatively at bedside. The fibrosclerotic lymphedematous tissue is then separated from the deep fascia using blunt and sharp dissection. The thickened deep fascia is also trimmed to its normal size. Toes are amputated if there are recurrent infections, verrucous hyperkeratosis, or osteomyelitis. Otherwise, nails and nail beds are removed, and the defect is closed using C–­V or rotation advancement flaps, to preserve toe length. The tip of the distal phalanx of the toe can be shortened by 0.5 cm if there is any tension during wound closure. The procedure of excision and control of the major bleeders should be completed within two hours of tourniquet ischemia time. Therefore, a team of surgeons is necessary. While waiting for hemostasis, the proximal thigh can be debulked. Two wedge excisions are made starting at the medial and lateral mid-­axial lines. The resultant soft tissue on anterior and posterior thigh flaps is thinned tangentially to 2 cm and sutured together to the deep fascia to allow a smoother

Harvesting of the right side supraclavicular lymph node flap has been described in our previously published article.14 The anatomical landmarks of the flap were the sternocleidomastoid muscle anteriorly, the trapezius muscle posteriorly, the clavicle inferiorly, and the external jugular vein, which was also included with the flap and was used for the second venous anastomosis. The main lymph nodes are deep to the omohyoid muscle, and careful dissection should be performed so as not to separate the lymph nodes from the underlying transverse cervical artery (TCA). The concomitant vein was also identified and included with the flap. The skin paddle could be harvested with safety, unless careless dissection separates the skin paddle from the underlying soft tissue. Using a Doppler, the direct perforator from the TCA to the skin paddle can be identified. One arterial and two venous anastomoses are performed at the recipient site. STSG or local flaps are used to cover the lymph node flap. The Chen-­modified Charles procedure can be performed in a single stage or in two stages (Fig. 3.6.2). In the two-­ stage setting, the lymph node transfer can be performed before or after the modified Charles procedure. The major advantage of the two-­stage technique is that it ensures the flap survival because it does not require compression for the STSG after the modified Charles procedure. The disadvantage is that it requires two surgical procedures. In our experience, the favored lymph node flaps used in the Chen-­modified Charles procedure are the supraclavicular lymph node flap and right gastroepiploic lymph node flap, which is harvested with the laparoscopic method to minimize the morbidity of the donor site.

Postoperative care The patient is encouraged to keep the leg elevated for five days postoperatively. Leg elevation is encouraged for the next two weeks, and a compression stocking is worn after four weeks. Physiotherapy and long-­term limb compression are commenced subsequently.

Outcomes of modified Charles procedure Extensive reduction of the lymphedematous limb for advanced lymphedema can be achieved with this procedure (Fig. 3.6.3). Potential complications of this procedure are wound

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CHAPTER 3.6  • Debulking strategies and procedures: excision

Algorithm 3.6.2 Suspected lymphedema

Clinical examination

Differential diagnosis

No lymphedema

Lymphedema

History

Assessment

Diagnosis

• • • • •

Circumference measurement Skin tonicity Lymphoscintigraphy MR lymphography Photographic evaluation

Clinical stage (ISL)

Stage 0

Stage I

Stage II

Observation

CDT

CDT

Stage III

Fibrosis(+) CDT

LVA

LNF

Fibrosis (+++) Elephantiasis Recurrent infection

LNF Gastroepiploic LNF Supraclavicular LNF

RPP

LNF+modified Charles procedure

Liposuction

Assessment and treatment algorithm for lower limb lymphedema.

Algorithm 3.6.3 StageI–IIb

Stage IIb

Stage III

No improvement

Excision + skin graft

CDT

No improvement

LVA

Algorithm for genital lymphedema.

breakdown, loss of skin graft, hyperkeratosis, ulceration, and aggravation of foot lymphedema. It is possible to improve the postoperative results and eliminate the risk of recurrence by combining this procedure with a lymph node flap transfer. The main mechanism of the lymph node flap transfer is the lymphaticovenous connection. After the implantation of the lymph nodes, spontaneous regeneration of lymphatic channels between the lymph nodes and the surrounding lymphedematous tissue will occur and then the lymph is drained to the venous system through the lymphaticovenous connections inside the lymph node flap.15,16 On the basis of this mechanism, we supercharged the lymph node flap with two venous anastomoses to maximize the lymph drainage into the venous system. In our practice, none of the patients experienced aggravation of the lymphedema in the foot as the transferred lymph node flap had a protective role. In addition, in our cases we had a low incidence of postoperative infection. The transferred lymph node flap contains macrophages and lymphocytes, which have the ability to capture and destroy pathogens from sites of

Chen-­modified Charles procedure

123

A

B

C

D

E

F

Figure 3.6.1 (A) Good exsanguination is very important to minimize blood loss. The patient may lose a significant amount of blood if the bleeding is not well controlled. (B) The area of excision for the indurated skin and subcutaneous tissue is very large. However, we should still be patient to do it carefully. This is a very laborious procedure, and multiple plastic surgeons are required for the procedure of excision and hemostasis. (C) This picture shows the very large area of excision in the modified Charles procedure. (D) Advanced lymphedema was due to repetitive occurrences of infection. The skin was very thick and fibrotic, like leather. The subcutaneous tissue was also as hard as rock, which could not be removed with suction lipectomy. Also, LVA would not work for this patient. (E) Intraoperative picture after the modified Charles procedure. The strips of split skin graft were arranged in a circular manner. (F) Full-­thickness skin graft was put over the dorsum of the foot to prevent future ulcer due to frequent friction with the compression garment.  

infection. This immunological mechanism of the lymph nodes can explain the reduction of the infection rate of the affected limb after lymph node flap transfer.17 The 10 steps in the modified Charles procedure include: 1. Design: the extent of the excisional procedure must be from foot to at least mid-­thigh. The key to success in treating advanced cases resides in radical reduction of the lymphatic load. For the proximal half of the thigh,

2. 3.

suction lipectomy and wedge resection should be done. In other words, minimal subcutaneous tissue is left in order to prevent later occurrence of repetitive infection. The depth of excision is down to the fascia, which is evenly shaved to less than 1 mm in thickness. Keep bleeding to a minimum. Apply tourniquet carefully before harvesting split-­thickness skin graft. The sheets of skin graft are wrapped with wet gauze.

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A

CHAPTER 3.6  • Debulking strategies and procedures: excision

B

C

D

4. Use split-­thickness skin graft for the leg and thigh, but full-­thickness skin graft for the dorsum of the foot. For coverage at the dorsum of the foot, full-­thickness skin graft is better than split-­thickness skin graft because there will be less chance of ulcer after surgery. 5. The sheets of split skin graft should be arranged in a circular fashion, instead of a longitudinal fashion, because a longitudinal scar will cause more problems than a circular scar, especially at the areas around the ankle or knee joints. 6. Between the sheets of split skin graft there should be 0.5–­ 1 cm of overlapping, because on the second or third day after surgery there will be more tissue swelling, which may cause gaps between sheets of skin graft if there is no overlapping during surgery. 7. A 3-­mm K-­pin is drilled through the tibia to provide suspension of the leg during and after surgery, so that the skin graft at the posterior side of the leg is not exposed to shifting and does not get lost. Complete take of the skin graft is essential to prevent scar and subsequent recurrence of infection. 8. Complete the excision procedure within 2 hours. Then release the sterile tourniquet and get good hemostasis, followed by wet dressing over the skin defects of the foot, leg, and thigh. 9. Apply skin grafts over the skin defects. Take full-­ thickness skin graft from the wedge resection at bilateral aspects of the proximal thigh, and apply it over the dorsum of the foot. The rest of the skin defects at the leg and thigh are covered with split skin graft, which has been harvested from the leg and thigh at the beginning of surgery, as mentioned before. 10. Dressing change is performed from 24 to 72 hours after surgery, depending on the condition before surgery. If there is an ulcer with infection before surgery, dressing change can be done at 24 hours postoperatively. Additional options include: a. The use of VAC. The skin graft can be fenestrated. VAC devices can be used to prevent complications leading to loss of skin graft. b . Hyperbaric oxygen may be helpful when the tissue bed is indurated with suboptimal blood supply or in the situation of peripheral arterial occlusive disease. c . Re-­grafting for dorsum of foot. If there are skin crypts or verrucous hyperkeratosis at the dorsum of the foot and distal leg later, they should be excised to form a smooth surface, and a new skin graft should be placed. Results of the Chen-­modified Charles procedure for advanced lymphedema are: (1) delayed healing: 4%; (2) verrucous hyperkeratosis or skin crypts requiring redrafting for dorsum of foot: 14%; (3) cellulitis 2 years after surgery: 11%; (4) chronic ulcer: 3%; (5) infection of toes requiring further surgery: 21%.

E

Figure 3.6.2 (A) A case of right lower limb lymphedema with severe fibrosis. The patient received a modified Charles procedure and then lymph node flap transfer. She had no more episodes of infection after surgery. This is the front view of the patient before surgery. (B) Posterior view of the lower limbs. (C) Front view at 3 years of follow-­up. (D) Posterior view at 3 years of follow-­up. (E) Supraclavicular lymph node flap was transferred to the ankle in the second stage. The donor site of the lymph node flap was inconspicuous.  

Radical reduction with preservation of perforators (RPP procedure)18,19 The blood supply for the skin of the upper limb is originated from one source in the arm and two sources in the forearm. The bi-­pedicle design of the medial and lateral skin flaps

Radical reduction with preservation of perforators (RPP procedure)

125

A

D

B

C

E

Figure 3.6.3 (A) This 56-­year-­old woman had very severe lymphedema of the right lower limb since 19 years of age. The right lower limb was huge and she always stayed on the bed. Every time she tried to move out of bed, there would be 5 liters of blood being drained into the right lower limb, and when she lay on the bed again the 5 liters of blood would come back to join the cardiovascular system. The big shifting of intravascular fluid had caused cardiopulmonary dysfunction with cardiomegaly. Therefore, she was told she would have only three years of survival because of heart failure. We performed the modified Charles procedure and used abdominal skin for coverage. We also transferred lymph node flap to the right foot for improvement of lymphatic circulation of the sole of the foot in the second stage. This was the picture before surgery. (B) The lateral view of the huge lower limb. (C) A team of 6 surgeons participated in the surgery in order to achieve efficient resection and hemostasis. Two anesthesiologists were in charge of the anesthesiology. One chest physician and two cardiologists also came to monitor the cardiopulmonary functions during surgery. (D) A total of 47 kg of indurated skin and subcutaneous tissue was removed in the surgery. It was equivalent to one-third of her body weight. That was why many physicians had to come and help. (E) Since then she did not develop cellulitis of the right lower limb. After wound healing and two months of physiotherapy she went home and found a new boyfriend while working in a restaurant.  

ensures blood supply for the skin from above and below the elbow. The vascular supply of the arm is from septocutaneous or musculocutaneous perforators, or from direct perforators arising from the brachial artery. The forearm is supplied by septocutaneous or musculocutaneous perforators or direct perforators from the radial, ulnar, and posterior interosseous arteries. The radial artery has 9 to 17 fasciocutaneous branches, next to the radial recurrent artery which arises near the origin of the radial artery. The ulnar artery, next to the anterior and

posterior ulnar recurrent arteries and the common interosseous artery, gives off 3 to 5 fasciocutaneous branches between the flexor carpi ulnaris and the flexor digitorum superficialis muscles.

Patient selection The indications for RPP procedure are as follows: (1) stage IIIb patients who failed medical treatment; (2) for patients with advanced lymphedema who are destined to undergo modified

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CHAPTER 3.6  • Debulking strategies and procedures: excision

Charles procedure but have a higher risk with potential complications; (3) as an adjunct to other treatment modalities (e.g., lymph node flaps).

Surgical techniques for RPP procedure In the lower limb, perforators from posterior tibial and peroneal arteries are mapped with a hand-­ held Doppler above the levels of the medial and lateral malleoli, respectively. In the middle of the leg, one large perforator is identified on the medial and lateral side, supplying the medial and lateral skin flaps, respectively. The normal diameter of these perforators ranges from 1 to 3 mm for both artery and vein. A 2-­cm “cuff” of fascia and fat is preserved around the two main perforators in the medial and lateral skin flaps. If several large perforators are found, the one located close to the center and far from the preserved medial and lateral tissue over the malleoli is marked. The ellipse represents the area of skin that will be excised with preservation of skin perforators. The skin flap is retracted by two skin hooks, and the subcutaneous tissue is grasped using Allis clamps. The subcutaneous fat is tangentially excised until the skin flap is approximately 5 mm in thickness, preserving the subdermal venous plexus and minimal subdermal fat. The size of these ellipses depends on the expected amount of debulking. One should initially make conservative markings and, if necessary, more skin can be resected after preservation of skin perforators. Care is taken to preserve the superficial peroneal nerve and sural nerve. Loupes magnification is used for this part of the procedure. The subcutaneous tissue and skin around the medial and lateral malleoli are left untouched. The tourniquet is deflated for hemostasis. The skin ellipses along with underlying subcutaneous fat are then excised. The resultant wound edges are approximated to see if further skin excision is possible. Otherwise, suction drains are introduced, and the wounds are closed. In the upper limb, the presence of radial and ulnar arteries is confirmed by using a hand-­held Doppler. The ellipse of skin marks the area of skin that needs to be excised for the debulking of the forearm. The size of these skin ellipses depends on the expected amount of resection. Like the leg, the elliptical markings serve two purposes. They allow for a skin excision without dog-­ears and provide wider access. Care is taken to preserve the medial and lateral cutaneous nerves of the forearm, especially the cutaneous branch of the ulnar nerve around the elbow. The vascular branches are identified during elevation of the medial and lateral skin flaps. The areas on the medial and lateral aspect of the forearm, around the wrist, are left untouched. Using two skin hooks, the skin flap is elevated. The incisions are made down to the deep fascia. All the tissue layers above the fascia are elevated, and the procedure is carried out in the same manner as already described. The large veins are preserved as far as possible. Then, using Allis clamps, the subcutaneous fat is grasped and pulled backward and downward. A minimal thickness of 5 mm of skin flap is raised, preserving the subdermal venous plexus and minimal subdermal fat. The tourniquet is deflated for hemostasis. The skin is approximated and assessed to see if any further skin excision is needed. The wound is then closed over suction drains.

Outcomes of RPP procedure The average percentage of circumferential reduction for all patients above the knee was 51%, below the knee 66%, at the ankle 44%, and at the level of the foot 41%. The overall

circumferential reduction for the lower limb lymphedema was 52%. Complications consisted of cellulitis in 18% of the patients, seroma in 6.7% of the patients, and hematoma 6.7% of the patients. There was no incidence of wound breakdown or skin flap necrosis. In 13.3% of the patients, there were complaints of numbness in the extremity, which had not resolved within a year. Most patients complained of a transient numbness of the leg that resolved within six months. For the upper limb, the average circumferential reduction above and below the elbow, at the wrist, and the hand were 15.1%, 20.7%, 0.5%, and 3.6%, respectively. Statistical analysis showed significant circumference reduction above and below the elbow but not at the wrist and hand. There were no cases of wound breakdown, skin necrosis, or cellulitis in the postoperative period. Some 36.3% of the patients complained of mild numbness confined to the vicinity of the surgical incisions. All lymphedema reductions were completed in one stage.

Excisional therapy for genital lymphedema20–23 ­

Filariasis is the most frequent cause of genital lymphedema (GL), but other clinical conditions such as cancer therapies, hidradenitis suppurativa, or heart, liver, and kidney dysfunctions are more common causes in developed countries. Less frequently, GL occurs after injection of exogenous substances, like paraffin or silicone. The involvement of external genitalia accounts for 0.6% of lymphedema cases worldwide. Conservative CDT therapy is considered the mainstay treatment for the common limb lymphedema, but its application for GL is limited, due to the shape and location of genitalia. In cases of severe fibrosis, direct excision becomes necessary. Recurrent infections and limitations in daily activities, hygiene procedures, and social and sexual life make GL extremely uncomfortable with severe impairment of quality of life. On admission to our unit, patients with GL were staged according to the International Society of Lymphology (ISL) system. The treatment algorithm applied in our unit is presented as Algorithm  3.6.3. Stage I and mild presentations of  stage II were approached with conservative therapy first, consisting of compression and elevation of positions. In cases of failure with conservative management for 3 months, physiologic surgery with lymphovenous anastomosis (LVA) was proposed for stages I and II. For chronic and progressive stage III GL, excisional procedures were the solution in order to reduce fibrotic tissue accumulation and functional impairments. Among the debulking surgeries for GL, the Charles procedure is considered the earliest and most radical one, and it has been described for the scrotum or for both scrotum and penis. Debulking procedure was carried out with circumcision, by removing all the affected skin and subcutaneous tissues deep to the fascia, carefully preserving testes and spermatic cords. Scrotal septum was preserved to achieve favorable appearance, and the tunica vaginalis was identified and inverted. Moreover, when feasible, still patent subcutaneous lymphatic vessels were visualized with injections of ICG, and were preserved. Before closure, testicles and spermatic cords were sutured together with absorbable stitches, in order to prevent formation of bifid scrotum. Local skin flaps allowed coverage of scrotum structures, taking care to perform a midline suture to the retained scrotal septum in order to reconstruct

Summary

the scrotal raphe. When complete coverage with flaps was not possible, meshed split-­thickness skin grafts (STSG) could resemble scrotal rugae and positional gravity progressively expanded the graft, giving it a natural pendulous appearance. When penis was involved, the dartos was preserved during excision, in order to enhance subsequent extensibility and mobility. When the skin is affected, excision was carried out until the coronal sulcus or to the glans to reduce the risk of recurrence. For the penis, coverage with unmeshed STSG was recommended for sexually active patients. The graft was secured at the penis base and the neo-­raphe. Postoperative CDT was prescribed for at least 6 months, in order to prevent recurrences. Physiologic procedures added to GL treatment, such as LVA, were described by Mukenge et  al.,24 where the anastomosis was carried out between the lymphatic vessels of the spermatic funiculus and branches of the spermatic veins. Outcomes were assessed in terms of edema reduction and ISL stage regression, skin quality, and reported outcomes of functions. In a recent study of 19 GL patients in our unit, 18 patients (94.7%) experienced complete resolution of GL, and there was no relapse with follow-­up for at least 8 months. Patients who were treated with surgical excision reported difficulties in urinating prior to treatment, having to compress the swollen penis thirty minutes before urine could pass. After surgery, the urine passage was smooth with no necessity for compression. More patients with longer follow-­up will be necessary to reach consistent results and give more support to the treatment protocol described above.

Follow-­up In terms of long-­term follow-­up for patients with advanced lymphedema after modified Charles procedure, the patients are followed up regularly every 3 months. When the patients have recurrent infection, there are three possibilities: a. Infection from the toes or web spaces. Usually it is an infection with a combination of bacteria and fungus. Under such circumstances the patients are advised to receive amputation of second and fourth toes to allow for good hygiene care. This would not affect normal walking of the patients. Unusually we see patients with severe infection of all toes; we advise them to receive amputation of all toes to get rid of infection sources. b. There is appearance of verrucous hyperkeratosis or skin crypts at the distal leg and dorsum of foot. This is due to inadequate removal of subcutaneous tissue, which causes recurrent infection. The solution would be excision of the verrucous hyperkeratosis and skin crypts, leaving only a minimal amount of tissue above the fascia to allow for re-­grafting with split skin graft, which is harvested from the proximal thigh. c. Some plastic surgeons only perform the modified Charles procedure for the leg but not up to the

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127

thigh. This is not enough for patients with advanced lymphedema; we should further reduce the lymphatic loading to the minimum. At the junction of the skin graft and the preserved skin flap in the thigh, we should perform wedge resection so that there is no sharp step between these two zones. In our experience, all patients could be treated successfully and minimize the chance of infection down to less than once per year. In our hands, the modified Charles procedure is a good procedure with the revision surgeries as described above in a., b., and c.

Surgical limitations Because the skin graft does not have sebaceous glands or sweat glands, the patients should put enough lubricant over the skin graft every day to prevent chronic inflammation of the skin graft. Other good hygiene care should be instructed by special nurses in the outpatient clinic. The other limitation for the modified Charles procedure is for patients with severe comorbidities such as uremia, heart disease, or metastatic cancers.

Other options if debulking procedure fails Debulking procedures have cascades, with the modified Charles procedure as the last choice. If the patients do not have contraindications as described above, we could achieve good results by using the modified Charles procedure with subsequent revision surgeries as described above. If all debulking procedures have failed, the last option is amputation. We had two patients who had below-­knee amputation due to osteomyelitis of the leg because they lost follow-­up and the infection involved the bone.

Summary For lymphedema most methods of treatment are palliative. Surgical techniques for lymphedema are reserved for patients who fail medical treatment. Many plastic surgeons consider the original Charles procedure as old and outdated because of its complications and unsatisfactory aesthetic results. We believe that in selected cases of advanced lymphedema, the Chen-­modified Charles procedure can be performed (even with toe amputations) for prevention of potential infection. Lymph node transfer can be combined with the extensive excisional procedure, and is a reliable method for treating advanced lower limb lymphedema. When used in properly selected patients, RPP is an excisional technique based on angiosome principles and application of perforator skills to the surgical reduction of lymphedema. With this procedure, long-­lasting and cosmetically appealing results are achieved in a single-­stage procedure.

References

References 1. Warren AG, Brorson H, Borud LJ, et al. Lymphoedema. A comprehensive review. Ann Plast Surg. 2007;59:464–­472. 2. Gloviczki P. Principles of surgical treatment of chronic lymphoedema. Int Angiol. 1999;18:42–­46. 3. Dumanian GA, Futrell JW. The Charles procedure: misquoted and misunderstood since 1950. Plast Reconstr Surg. 1996;98(7):1258–­1263. 4. Chen HC, Garb BB, Salgado CJ, et al. Elective amputation of the toes in severe lymphoedema of the lower leg: rationale and indications. Ann Plast Surg. 2009;63(2):193–­197. 5. Van der Walt JC, Perks TJ, Zeeman BJ, et al. Modified Charles procedure using negative pressure dressings for primary lymphedema: a functional assessment. Ann Plast Surg. 2009;62: 669–­675. 6. Sapountzis S, Ciudad P, Lim SY, et al. Modified Charles procedure and lymph node flap transfer for advanced lower extremity lymphedema. Microsurgery. 2014;34(6):434–­447. 7. Gharb BB, Rampazzo A, Spanio di Spilimbergo S, et al. Vascularized lymph node transfer based on the hilar perforators improves the outcome in upper limb lymphedema. Ann Plast Surg. 2011;67: 589–­593. 8. Lin CH, Ali R, Chen SC, et al. Vascularized groin lymph node transfer using the wrist as a recipient site for management of postmastectomy upper extremity lymphedema. Plast Reconstr Surg. 2009;123:1265–­1275. 9. Fanzio PM, Singha D, Becker C. Combined radical excision and free microsurgical lymph node transfer for treatment of lower extremity lymphedema. Eur J Plast Surg. 2012;35:565–­568. 10. Sapountzis S, Singhal D, Rashid A, et al. Lymph node flap based on the right transverse cervical artery as a donor site for lymph node transfer. Ann Plast Surg. 2014;73(4):398–­401. 11. International Society of Lymphology. The diagnosis and treatment of peripheral lymphedema: Consensus Document of the International Society of Lymphology. Lymphology. 2013;46(1):1–­11. 12. Karri V, Yang MC, Lee IJ, et al. Optimizing outcome of Charles procedure for chronic lower extremity lymphoedema. Ann Plast Surg. 2011;66(4):393–­402.

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13. Badger C, Preston N, Seers K, et al. Antibiotics/­anti B inflammatories for reducing acute episodes in lymphoedema of the limb (Review). Cochrane Collab. 2008;2:1–­15. 14. Yeo MS, Lim SY, Kiranantawat K, Ciudad P, Chen HC. A comparison of vascularized cervical lymph node transfer with and without modified Charles’ procedure for the treatment of lower limb lymphedema. Plast Reconstr Surg. 2014;134(1):171e–­172e. 15. Koshima I, Kawada S, Moriguchi T, et al. Ultrastructural observations of lymphatic vessels in lymphoedema in human extremities. Plast Reconstr Surg. 1996;97(2):397–­405. 16. Szuba A, Shin WS, Strauss HW, et al. The third circulation: radionuclide lymphoscintigraphy in the evaluation of lymphedema. J Nucl Med. 2003;44:43. 17. Agko M, Ciudad P, Chen HC. Staged surgical treatment of extremity lymphedema with dual gastroepiploic vascularized lymph node transfers followed by suction-­assisted lipectomy-­a prospective study. J Surg Oncol. 2018;117(6):1148–­1156. 18. Salgado CJ, Mardini S, Spanio S, et al. Radical reduction of lymphedema with preservation of perforators. Ann Plast Surg. 2007;59:173–­179. 19. Salgado CJ, Suma P, Gharb BB, et al. Radical reduction of upper extremity lymphedema with preservation of perforators. Ann Plast Surg. 2009;63(3):302–­306. 20. Dandapat MC, Mohapatro SK, Patro SK. Elephantiasis of the penis and scrotum. A review of 350 cases. Am J Surg. 1985;149:686–­690. 21. Aulia I, Yessica EC. Surgical management of male genital lymphedema: a systematic review. Arch Plast Surg. 2020;47(1):3–­8. 22. Lim KH, Speare R, Thomas G, Graves P. Surgical treatment of genital manifestations of lymphatic filariasis: a systematic review. World J Surg. 2015;39(12):2885–­2899. 23. Torio-­Padron N, Stark GB, Foldi E, et al. Treatment of male genital lymphedema: an integrated concept. J Plast Reconstr Aesthet Surg. 2015;6:262–­268. 24. Mukenge SM, Catena M, Negrini D, et al. Assessment and follow-­up of patency after lymphovenous microsurgery for treatment of secondary lymphedema in external male genital organs. Eur Urol. 2011;60:1114–­1119.

SECTION I  •  Lower Extremity Surgery

4 Lower extremity sarcoma reconstruction Andrés A. Maldonado, Günter K. Germann, and Michael Sauerbier

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SYNOPSIS

ƒ Any lesion in the lower extremity with a clinical history of pain, continuous growth, size over 5 cm, or deep subfascial localization is suspicious of a sarcomatous malignancy and should be surgically biopsied according to established surgical rules. ƒ Still the single statistically proven modality of curing sarcomas and prolonging postsurgical lifespan is surgical excision with wide margins resulting in a postoperative R0-­status. To date, no other neoadjuvant or postoperative treatment modality can replace this approach. If wide margins cannot be achieved, adjuvant therapy is indicated for extremity preservation. ƒ Plastic surgical lower extremity sarcoma reconstruction is  –­ especially in bone sarcoma reconstruction  –­ the classical field of an interdisciplinary, multimodal approach, most commonly working together with tumor and orthopedic surgeons, oncologic radiotherapists, oncologists and radiologists. ƒ Modern oncoplastic reconstructive surgery can provide adequate reconstructive options for almost any defect size and composition, and so radical tumor excision can be combined with over 95% extremity preservation today. ƒ The plastic reconstructions in sarcoma-­related limb-­sparing surgery (LSS) are often demanding and complex and consist of the full spectrum of plastic surgical options. They should be performed in specialized centers and specifically adapted to the patient and case profile.

Introduction Soft-­tissue and bone sarcomas

 

Soft-­tissue tumors are a highly heterogeneous group of about 100 different tumor entities, which are still classified histogenetically according to the main adult tissue component they resemble most. The malignant subgroup among them is called sarcomas, which not only have the potential to grow locally invasive or even demonstrate destructive growth but also have a variable risk of recurrence and metastatic potential. As the term “sarcoma” (derived from the Greek word σαρξ “sarx” = “meat”) itself does not necessarily imply fast, expansive growth or metastasis, a

further subclassification system into more aggressive sarcomas (high-­grade, poorly differentiated) or less aggressive (low-­grade, well differentiated) types does exist. Some lesions like the atypical fibroxanthoma are called “pseudosarcomas”, as they demonstrate a benign clinical course but are histologically malignant. However, usually well-­differentiated tumors show low-­grade characteristics and vice versa. Primary bone sarcomas are even less frequent than soft-­ tissue sarcomas, and most malignant osseous lesions are metastatic, especially in advanced age. Despite having a low incidence, bone sarcomas have a high significance for both patient and surgeon due to their impact on extremity function and overall mobility. Limb-­preserving surgery after wide tumor resections frequently poses a real challenge for the reconstructive surgeon. Sarcomas can occur in every part of the body, as they derive from mesodermic tissue such as muscle, nerve, bone cartilage, blood vessels, or fat. The therapeutic mainstay for soft-­tissue sarcomas is based on surgical excision. However, previous radical concepts in STS surgery have been gradually replaced by more moderate approaches with function and limb-­ sparing resections combined with radiotherapy, chemotherapy, and/­or isolated limb perfusion.1 The complexity of the surgical resection and the subsequent plastic surgical reconstruction differs considerably depending on the localization. Like any oncologic discipline, sarcoma treatment is a typical field of modern interdisciplinary and multimodal therapy. Lower extremity sarcoma reconstruction is  –­ especially in bone sarcoma reconstruction  –­ also a fascinating field for an effective interaction between the surgical disciplines of radiologists, orthopedic, oncologic, pediatric, and podiatric surgeons and plastic reconstructive (micro-­)surgeons. Modern plastic reconstructive surgery can provide adequate reconstructive options for almost any defect size and composition, so considerations about defect size should not play a role during tumor excision. Today, over 95% of the extremities can be preserved after radical tumor excision, and to close large defects and to largely preserve function of the extremity by transplantation of muscles, tendons, and bones

Basic science/­disease process

as well as transplantations of nerves and blood vessels.2 The plastic reconstructive procedures are often demanding and complex and frequently encompass the full spectrum of plastic surgical options. These procedures may be best performed in specialized centers where regimens individually adapted to patient and case profiles may be optimized.3

Sarcomas in the lower extremity Sarcomas in the lower extremity are more common than in the upper limb (74% vs. 26%) and represent the most common location of sarcomas in the body overall (45%).4 Currently, they are safely treatable by extremity preservation in most cases, if properly performed according to the rules described in this chapter and in the pertinent current literature. In this context, several studies have now demonstrated that limb-­sparing surgery (LSS) is oncologically not inferior to amputation in the treatment of lower extremity sarcoma.5 While amputation was still the keystone of previous surgical therapy several decades ago, it usually represents only an important last line therapeutic modality today. The common misconceptions that amputations have a better outcome both in tumor safety and quality of life have both definitely been proven wrong.6–8 Sarcomas are rare, and a “soft-­tissue swelling” is often misinterpreted by both patient and physician because of this fact. This can considerably delay proper diagnosis. Still, tumor manifestations in the extremities are often detected a bit earlier than in the trunk, as the extremities are constantly under personal “visual” control in daily life. This might be even truer for tumors on the upper extremity than on the lower. Due to the highly functional anatomy of our extremities with vessels, nerves, tendons, bones, and muscles in the close vicinity, even smaller tumors can represent a challenge to both the resecting tumor surgeon as well as the reconstructive plastic surgeon. Preservation of the lower extremity in sarcoma reconstruction differs from alike manifestations in the upper extremity9 in several key points that have to be considered carefully:   Stability and weight-­bearing capability are usually regarded higher than functional mobility or range of motion in the lower extremity.   Postoperative appearance is usually less important. In most urban cultures the reconstructed legs with their scars and possible voluminous flaps can easily be hidden in clothing and have a less important role in social interaction than the upper extremity (i.e., handshaking).   Weight-­bearing demands are higher and atherosclerotic vessel damage and orthostatic venous pressure are more profound in the lower extremity. Both may play a major role in free tissue transfer.   Nerve regeneration is less successful in the lower extremity at any age.   Wound healing is slower, and the risk for an infectious complication is higher. ­

13,460 and 5350 cases, respectively (www.seer.cancer.gov). There is no overall significant gender predisposition. The median age at diagnosis is 60 years old, with two incidence peaks, at 50 and 80 years old; 25% of diagnostic sarcomas are more than 75 years.10 With about 45% of all sarcomas occurring in the lower extremity, 15% in the upper extremity, 10% in the head and neck region, 15% in the retroperitoneal space, and the remaining 15% in the abdomen and the chest wall,11 the musculoskeletal system of the extremities and the abdominal and thoracic walls are the most common predilection sites. Extremity sarcomas are most common in the thigh (50%–­60%). While most cases of soft-­ tissue sarcomas are sporadic, there are some genetic and non-­genetic risk factors summarized in Table 4.1. Up to 60% of all soft-­tissue sarcomas contain a somatic mutation of p53.12 A detailed description of the various risk factors is beyond the scope of this chapter, but there are several strong associations to be mentioned: a history of radiation exposure accounts for up to 5.5% of all sarcomas. The risk is dose dependent, and the latency period between radiation and clinical tumor manifestation is around 5 years. Over 80% of radiation-­associated sarcomas are high-­grade types.13 Neurofibromatosis type NF-­1 is strongly associated with the cumulative lifetime risk of up to 13% for the occurrence of malignant peripheral nerve sheath tumors (MPNST).

Table 4.1  Predisposing factors for soft-­tissue sarcomas Genetic

Soft-­tissue sarcomas are a rare disease entity with an incidence range from 1.8 to 5:100,000 in adults and 10%–­15% in children. The estimated new cases and deaths in the USA in 2021 are

Neurofibromatosis NF-­1 (von Recklinghausen disease) Retinoblastoma Gardner syndrome Werner syndrome Bloom syndrome Fumarate hydratase leiomyosarcoma syndrome Diamond–­Blackfan anemia

Mechanical

Li–­Fraumeni syndrome Postparturition

Chemical

Chronic irritation Polyvinylchloride (PVC) Hemochromatosis Dioxin (TCDD) “Agent Orange”

Radiation

Arsenic Traumatic–­accidental

Lymphedema

Post-­therapeutic Parasitic (filariasis)

Basic science/­disease process Epidemiology soft-­tissue sarcomas

129

Iatrogenic Stewart–­Treves syndrome Infectious (viral)

Congenital Kaposi sarcoma (HHV-­8)

HHV-­8, human herpes virus 8; TCDD, 2,3,7,8-­tetrachlorodibenzodioxin.

130

SECTION I

CHAPTER 4  • Lower extremity sarcoma reconstruction

The sarcoma subtype is determined by light and electron microscopy, immunohistochemistry, and cytogenetic analysis. If it results in a tumor that cannot be designated accordingly, a descriptive evaluation is given for an “unclassified sarcoma”. Obtaining reference pathologies for soft-­and bone-­tissue sarcomas should be standard, as the rate of diagnostic agreement among specialists is below 75%.5,14 The most common histopathologic subtype distribution in extremities in the largest series in the literature is shown in Fig. 4.1.

population. Chondrosarcomas are slow growing and relatively resistant to adjuvant therapy. Ewing sarcoma is classically located in the femur diaphysis in teenagers, and only 20% occur in middle-­aged adults. If found extradiaphyseal, it is very common in the pelvis. It is the most common primary bone malignancy of the fibula. The Ewing sarcoma is very sensitive for radiation therapy.

Bone sarcomas

Sarcomas in the extremity may spread locally by continuous expanding growth irrespective of anatomic borders. In many cases it mistakenly seems that the tumor has developed a bordering capsule to surrounding “healthy tissue”. However, this capsule is part of the tumor, and soft-­tissue satellite-­like or intraosseous skip-­lesion tumor manifestations are beyond this capsule. This fact represents the main justification for a modern wide resection concept in sarcoma surgery. Hematogenic spread is most common in soft-­tissue and bone sarcomas. For lower extremity tumors, the primary site for metastasis is the lung. Lymphatic metastases are present in less than 5% of all soft-­tissue sarcomas (rhabdomyosarcoma, angiosarcoma, and epithelioid-­like sarcoma).17,18

About 2600 new primary bone sarcomas occur each year in the USA (www.seer.cancer.gov). The overall median age at diagnosis is 39 years. Many predisposing factors for bone sarcomas are similar to those for soft-­tissue sarcomas (like retinoblastoma, Li–­Fraumeni syndrome, radiation, and others) (Table 4.1). Paget disease, bone infarction, and fibrous dysplasia may also represent risk factors for bone sarcomas. The most common type is the osteogenic sarcoma, which has a predilection for the metaphyses around the knee in about 50% of cases. It is the third most common cancer in the young (www.nhs.uk) with a second peak around age 60. The male to female ratio is almost 2:1 in large studies, and for this specific tumor the median age at diagnosis is 17 years. Only 6.4% present initially with pathologic fractures, whereas the majority are detected in the workup of a painful mass or swollen extremity.15,16 It commonly arises in the medulla, but as a juxtacortical osteogenic sarcoma it arises from the external surface  –­ most commonly the posterior aspect of the femur. The spindle cell mesenchymal sarcoma group contains chondrosarcomas, intraosseous malignant fibrous histiocytomas (MFHs), and fibrosarcomas. The tumors of this group only have an incidence of about two-­thirds of the incidence of osteogenic sarcomas and primarily occur in an older

9%

38%

12%

14%

Leiomyosarcoma Fibrosarcoma Synovial sarcoma Liposarcoma MFH

27%

Figure 4.1 Distribution of histopathologic types in extremity soft-­tissue sarcomas. MFH, malignant fibrous histiocytoma. (From: Weitz J, Antonescu CR, Brennan MF. Localized extremity soft tissue sarcoma: improved knowledge with unchanged survival over time. J Clin Oncol. 2003;21:2719–­2725.)  

Tumor growth and metastasizing

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Diagnosis/­patient presentation/­imaging A detailed history and physical examination is the first initial and very important step to professional tumor surgery. In sarcomatous lesions, the patient often relates the tumor causally to an –­ often minor –­ traumatic event, bringing the lesion into clinical attention to the patient. Acute trauma, however, is not a proven predisposing factor for sarcoma development. Because of this, there is often a considerable time lag between this initial recognition and the first presentation of the lesion to a medical professional. Furthermore, the rationale of the lesion is often erratically misinterpreted and then causes a variety of inadequate treatments by both lays and physicians, further delaying proper diagnosis. The average duration of any symptoms before seeing a physician is 6 months in all soft-­tissue sarcomas, but possibly shorter in extremity manifestation.7 So in adults, lesions that (1) have not disappeared after 4 weeks, (2) are located subfascially or in the popliteal or groin flexion creases, (3) continue to grow or are symptomatic (i.e., pain and paresthesias), or (4) are already larger than 5 cm on detection should generally be biopsied as they are highly suspicious for malignancy. It is not unusual that sarcomas are found by physicians in the context of a workup for a completely different medical problem (i.e., chronic venous insufficiency in the leg). Coincidental findings like articular pain and joint effusions are common especially with osseous sarcomas, whereas clinically manifest neurovascular symptoms are relatively rare at initial presentation. Two-­thirds of sarcoma patients present with a painless mass during their first clinical examination, and only one-­third have current pain or have had a history of pain in the affected region.

Historical perspectives

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Phemister in his article “Conservative Bone Surgery in the Treatment of Bone Tumors”.19 After WWII more surgeons began to explore limb-­salvaging The term sarcoma was first used by Abernethy in 1804 and resection instead of amputation. It became clear that obtaining was based on the gross characteristic of the tumors. Codman adequate surgical margins is a key issue for cases with resectfounded the first Bone and Soft Tissue Sarcoma Registry in able tumors according to their pathologic characteristics. Their 1909, containing information on the diagnosis and treatment work established the principles of today’s limb-­salvaging surof bone. In 1829 Jean Cruveilhier published a two-­volume gery despite the limited reconstructive modalities at that time. work on pathologic anatomy, containing a substantial amount The surgical treatment of malignant bone tumors was revof information about sarcomas as they are understood today. olutionized in the early 1970s by the development of chemoSince then, the classical treatment of a sarcoma in the therapy, improved diagnostic radiology by more accurate lower extremity was amputation, accounting for relatively CT and MRI scanners, advances in reconstructive surgery, low recurrence rates, but with a severe impact on the integ- improvements in orthopedic oncologic surgery, and, evenrity of the patient. In 1879 Samuel W. Gross published his tually, the establishment of multidisciplinary tumor centers. experiences with 165 sarcoma cases of the long bones, in These advances are mainly responsible for the reduction in which he advocated early amputation despite the prevailing local recurrences after limb-­salvaging procedures by allowing operative mortality rate of 30%. Based on his study, limb-­ a better patient selection and a more accurate preoperative salvaging resection inevitably led to local recurrence, metasta- planning. sis, and death. Following this study, an even more aggressive During these developments, many sophisticated plastic approach to bone tumors was popularized, but survival rates surgical techniques were developed in a fascinating hisdid not improve significantly. This stimulated the first adju- tory that is covered in a different volume of this textbook. vant radiation treatment of bone tumors. Most of the techniques were focused on soft-­tissue reconHowever, the mortality rate of radiated patients equaled struction, but later composite tissue transplants and grafts the mortality rate of patients who underwent amputation. The were improved as well. Many new techniques were derived first neoadjuvant protocol was developed in 1940 by Cade and from trauma surgery, the treatment of congenital disorders, Ferguson, who combined preoperative radiation followed by or tumor surgery elsewhere in the body and did not specifiamputation 6 months later in metastasis-­free patients. The cally relate to the development of sarcoma surgery, but were aim of the protocol was to avoid unnecessary amputation. quickly adapted to limb-­preserving tumor reconstruction. The transition between amputation surgery and limb-­ Sophisticated pedicled reconstructive methods like cross-­ sparing surgery was less of a plastic surgical issue than an leg flaps, tubed pedicled flaps, or fibula pro tibia transfers oncologic–­orthopedic development: reconstructive proce- were standard procedures in early LSS until reconstructive dures after sarcoma resection were very uncommon until the microvascular surgery was integrated into the plastic surginumber of limb-­preserving resections increased. cal armamentarium. Episodic anecdotes reporting on limb salvage appear Modern reconstructive approaches integrate the latas early as 1895, when Mikulicz described two resection est advances in orthopedic surgery, such as modular and arthrodeses of the knee for distal femoral lesions in Europe. custom-­ made tumor prostheses for long bone and joint Sauerbruch in Germany described his “Umkippplastik” in replacement, with the full spectrum of the plastic surgi1922 as the precursor of today’s rotationplasty. A first sys- cal reconstructive ladder20 or elevator21 including chimeric tematic approach to limb salvage was suggested in 1940 by multi-­tissue-­type free flaps in limb-­sparing lower extremity sarcoma reconstruction.

Historical perspectives

Patient profile/­general considerations/­treatment planning

The thorough physical examination is not only focused on the affected extremity but includes the complete body. The pertaining lymph node stations should be examined as well, even though lymphatic spread is uncommon in the majority of all sarcoma types. The general health status should be assessed and optimized by all relevant medical specialties. This is especially important in multimorbid patients with concomitant acute and chronic comorbidities in the context of the planned operative procedures. Terminal illnesses and comorbidities have to be taken into consideration for the extent of both resection and reconstructive surgery. Clinical assessment and staging of the patient must be completed by adequate imaging diagnostics for evaluating local and generalized tumor manifestations. Any imaging of the tumor region must be performed before any surgical biopsy as the latter may confound the picture to a considerable extent. Gadolinium contrast-­enhanced magnetic resonance imaging (MRI) is currently the diagnostic mainstay to define exact tumor location, its relation to neighboring neurovascular structures and muscular compartments, to determine its homogeneity, integrity, and vascularization, and its presumed main tissue component. MRI is specifically useful for detecting skip lesions. It allows 3D planning of the resection and helps to assess the necessary reconstruction procedures preoperatively. Modern spiral computerized tomography (CT) scans are indispensable for clarifying the detailed anatomy of osseous sarcomas, determining the extent to which skeletal structures are affected by neighboring soft-­tissue tumors, and aiding in operative planning of these sarcomatous entities. Thoracic and abdominal CT scans are the diagnostics of choice for staging of high-­grade sarcomas of the extremities and detect intrapulmonary and abdominal metastases. In recurrent disease, positron emission tomography (PET) CT can augment the information about suspicious lesions in selected cases, though not accepted as a standard instrument for the preoperative workup (see Chapter 7).22–24 CT angiography with 3D reconstructions is a valuable tool in determining the overall vascular status of the affected leg, the underlying generalized vessel disease, and the vascularity of the tumor, and showing vascular displacements, collateral perfusion systems, vessel invasion, and tumor-­ related occlusion. They also provide valuable information about the feasibility of microvascular anastomoses and the presence of suitable recipient vessels, especially in elderly patients. Plain X-­ray films demonstrate specific periosteal or cortical signs, osteolysis, and paraosseous calcifications in diaphyseal and metaphyseal bony lesions. Even today, a plain radiograph remains the diagnostic method of choice for primary bone sarcomas (Fig.  4.2). A plain chest radiograph is still considered the standard for clinical staging in low-­grade extremity lesions. Ultrasound with or without contrast media is a cheap, fast, and painless adjunctive diagnostic measure that may be especially helpful in highly vascularized tumors. Ultrasound was often the diagnostic device of coincidental tumor findings but is also used for getting an initial overall picture of the lesion. A 99m-­Tc-­pyrophosphate bone scan is essential to bone tumor staging and screening for multicentric disease or metastases. ­

131

Onion ring sign Spiculae Codman’s triangle (singular periosteal lamella) Solid periosteal reaction

Extended osteolysis

Piecemeal lesions

Tumor permeation

Figure 4.2 Typical radiologic features of malignant and benign primary osseous tumors.  

A special laboratory workup for soft-­tissue sarcomas does not exist, whereas elevated alkaline phosphatase and lactate dehydrogenase over 400 U/­L are independent predictors of an unfavorable outcome in bone sarcomas.25

Patient profile/­general considerations/­ treatment planning Patient profile The goals of surgery in sarcoma reconstruction in the lower extremity depend on the individual case profile, which is composed of personal factors and the available reconstructive options. The most important personal factors that need to be taken into consideration are age, size, and weight; concomitant chronic diseases relevant to general health and operability; medications; social status; functional and aesthetic conceptions; previous operations; and tissue quality of the affected extremity. The pertinent reconstructive options that need to be discussed with the patient are the relevant operative methods according to the applicable steps of the reconstructive ladder, counterweighing their advantages and disadvantages for the actual tumor stage, location, oncologic safety, and potential adjuvant procedures (i.e., irradiation).

General considerations Above all, the prime goal should be an R0-­resection with tumor-­ free and adequately wide margins, which provides

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Algorithm 4.1 Histologic diagnosis of suspicious tumor (core needle or incisional biopsy)

Staging • Chest CT • Contrast-enhanced MRI of local tumor

STS – Primary disease (if metastasic disease – special consideration in extremity board)

Intermediate or high-grade STS

Low-grade STS

Surgery

Surgery pre- or postoperative RT

If no R0, evaluation for: • Re-resection (incl. amputation) • CHT • Observation

Downstaging

If no R0, evaluation for: • Re-resection • RT • Observation

R0 possible with acceptable functional outcomes

Unresectable or R0 only possible with adverse functional outcomes

Preoperative ILP preoperative RT preoperative CHT

Evaluation for: • Amputation • Palliative surgery • RT boost • CHT • Observation

Algorithm for the treatment of non-­intra-abdominal soft-­tissue sarcoma. (From: Harati K, Lehnhardt M. The changing paradigm of resection margins in sarcoma resection. Innov Surg Sci. 2017;2(4):165–­170.)

the best chance of complete surgical cure of the disease. This might create a considerable surgical defect and can imply major surgical reconstructive procedures for the patient. The extent of adequate wide tissue resection is almost never realized by the patient presenting with a palpable mass and has to be explained to him or her in detail. If surgical cure is not possible, resection of as much tumor mass as possible (tumor debulking) is paramount (R1/­R2) and usually followed by adjuvant radio-­and (less frequently) chemotherapy according to the recommendations of a multidisciplinary tumor board. At this point, the reconstructive goal should aim for a functional lower extremity capable of full weight-­bearing that appears as aesthetically pleasing as possible in the given case and circumstances. The surgical therapy should create a status for the patient to be integrated in social life, allowing him or her to wear normal clothing and

having a closed skin envelope. In selected cases, creating a stable open chronic wound is the only remaining palliative option; however, it should be free of copious discharge and secretions and avoid any olfactory nuisances. For example, a stable open wound producing minimal drainage that can be treated by daily dressing changes at home may offer a higher quality of life than performing another resection and reconstructive effort that may force the patient to stay in the clinic during his or her last days.

Treatment planning (Algorithm 4.1)  

Each case should be discussed in the multidisciplinary tumor board with all relevant medical disciplines involved in the setup of a treatment plan (tumor surgeon, medical oncologist, orthopedic surgeon, plastic surgeon, internal medicine,

Patient profile/­general considerations/­treatment planning

psychologist, radiologist, oncologic radiotherapy specialist, prosthetic technician, etc.). For optimal planning and strategy development, all diagnostic procedures, the radiologic imaging, and the definitive histology should already be present (see below). Even during the worst pandemic period of SARS-­ CoV-­2, some sarcoma centers were able to implement pathways and structures to keep this important multidisciplinary approach.26 A thorough and complete discussion of the tumor board treatment recommendations are explained to and discussed with the patient including all operative options (including amputation) and neoadjuvant or adjuvant chemo-­or radiotherapy. It is important for many patients to have an outline of the timeframe for the various surgical or multimodal therapeutic options. Finally, tumor staging is done according to the current staging systems for soft-­ tissue sarcomas. The American Joint Committee on Cancer (AJCC) eighth edition system is designed for extremity sarcomas, including most but not all histologic subtypes. The major changes in the eighth edition of the AJCC staging for bone and soft-­tissue sarcomas are the following four points: (i) Tumors are described separately according to the primary sites. For bone sarcoma, three tumor locations are described: (a) appendicular skeleton, trunk, skull and facial bones; (b) spine; and (c) pelvis. Meanwhile, four tumor locations are described for soft-­tissue sarcoma: (1) trunk and extremity; (2) retroperitoneum; (3) head and neck; and (4) visceral sites. (ii) Histologic grading system in bone sarcoma is changed to three-­grade classifications. (iii) For soft-­tissue sarcoma, any TN1M0 tumor in the trunk and extremity is classified as stage IV, whereas for the retroperitoneal tumor, any TN1M0 remains as stage IIIB. (iv) For soft-­tissue sarcomas in the trunk, extremity, and retroperitoneum, tumor size was classified into four categories: (a) ≤5 cm; (b) >5 cm and ≤10 cm; (c) >10 cm and ≤15 cm and (d) >15 cm. In addition, the notation about the depth of the tumor (superficial or deep from the superficial fascia) has been eliminated.27 Dermatofibrosarcoma protuberans (DFSP) and angiosarcoma, among others, are exempt from staging with the AJCC. For primary bone sarcomas like the osteogenic sarcoma, the Musculoskeletal Tumor Society (MSTS) (Table 4.2) staging

Table 4.2  Musculoskeletal Tumor Society staging system

Stage

Characteristic

IA

Low-­grade, intracompartmental

IB

Low-­grade, extracompartmental

IIA

High-­grade, intracompartmental

IIB

High-­grade, extracompartmental

IIIA

Low-­or high-­grade, intracompartmental with metastases

IIIB

Low-­or high-­grade, extracompartmental with metastases

(Reproduced from Papagelopoulos PJ, Mavrogenis AF, Mastorakos DP, et al. Current concepts for management of soft tissue sarcomas of the extremities. J Surg Orthop Adv. 2008;17:204–­215.)

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system is used. This classification was established in 1980 by Enneking.28 For bone sarcomas, orthopedic surgeons frequently refer to the MSTS system for bone tumors, and it is still the primary staging system taught in many training programs despite major evidence-­based updates to the AJCC system, including demarcations based on the tumor size, anatomic site of a primary tumor, and location of metastases.29

Surgery If complete tumor resection is possible (R0) with acceptable functional outcome, no other treatment modality provides better cure for sarcomas than adequate surgery. Oncologic safety is paramount, but preservation of the leg or foot should be achieved to preserve patient integrity, which is usually possible. Isolated limb perfusion, chemotherapy, or radiotherapy should be preoperatively considered if complete tumor resection is not possible (R1) or if R0 is only possible with adverse functional outcomes.1 This could avoid the need for prosthesis adaptation and use and prosthesis-­related problems. Several considerations in sarcoma-­ related defect reconstruction need to be mentioned that differ from sarcoma-­ related surgery at the upper extremity. The capability for stable weight-­bearing is more important than joint mobility in the lower extremity, whereas preservation or restoration of sensitivity is less important on the leg and foot than on the arm or hand. While sensitivity should be preserved as much as possible, in selective cases, asensitive “stilt-­legs” are considered superior to amputations, especially in elderly patients that would have problems adapting to prosthesis handling. Not being able to preserve the main nerves and thereby sensitivity is not an indication for amputation by itself!

Radiotherapy Radiotherapy is the primary adjunctive treatment method in sarcoma management today. Neoadjuvant radiation in large sarcomas uses external beam irradiation that helps in tumor shrinkage and thickening of the tumor capsule, which facilitates adequate resection and the achievement of negative margins during wide resection and reduces potential surgical tumor seeding. The disadvantages of preoperative irradiation are a higher rate of wound healing complications compared to postoperative radiotherapy and the creation of necrotic tumor material for the pathologist.6 However, preoperative radiotherapy did not increase the risk of acute wound or microvascular complications when combined with free flap reconstruction, and was associated with fewer late recipient-­site complications than adjuvant irradiation.30 The European Society for Medical Oncology (ESMO) recommendation favors adjuvant radiotherapy when tumor size is above 5 cm or deeply located or high grade and when R1 resection occurs.31 In the context of neoadjuvant radiotherapy, NBTXR3 is a new class of radioenhancer and shows efficiency in localized sarcoma in a phase 1–­2 study.32 NBTXR3 follows by radiotherapy improved responses rate, with correct tolerance in comparison with radiotherapy alone. Intraoperative radiation comprises a single dose electron radiation and has indications for use in the lower extremity for locations around the groin and foot. It is especially effective when the tumor dose is increased relative to the normal

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tissue dose. However, its availability is limited even in modern tumor centers. Postoperative irradiation is done with brachytherapy and electron beam therapy both used in solitary and combination regimens. Brachytherapy is especially useful after resection of local recurrences in a previously irradiated field.

Chemotherapy

the disadvantage of not representing the tumor tissue components correctly, especially in larger tumors, which makes it very difficult for the histopathologist to find the exact diagnosis, perform the necessary number of different studies, and determine the correct grading. However, if combined with CT scan or ultrasound-­guided needle placement, core biopsies may achieve a correct diagnosis in up to 90% of cases under optimal circumstances. Fine-­ needle aspirations only reach 56%–­72%.36–38 While single core biopsies may harvest too little tissue for an extensive pathologic workup with several stainings and immunohistochemical diagnostics, they provide the advantage of gathering tissue from different parts of the tumor to create a comprehensive picture.38 Both methods are atraumatic and only very rarely cause dangerous tumor-­cell dissipating hematomas. In several institutions, core biopsies are reserved for surgically unresectable tumors (i.e., retroperitoneal lesions) to determine tissue type and guide an eventual neoadjuvant therapy,7 while others use it as a prime diagnostic tissue sampling method.38 In summary, fine needle biopsies do not have a place in sarcoma diagnosis in the lower extremities, and both core biopsy and open surgical biopsy are very operator dependent: if poorly performed, the risk of getting an inadequate diagnostic sample or tumor seeding is high, respectively.38–40 Bone-­forming lesions are very difficult to adequately sample percutaneously, and open biopsies are preferable.41 ­

To date, any adjuvant or neoadjuvant chemotherapy for sarcomas should only be conducted in clinical studies (EORTC, COSS, EURO-­ Ewing, etc.). The role of perioperative chemotherapy remains controversial in both neoadjuvant and adjuvant settings. Adjuvant chemotherapy can be proposed as an option to the high-­risk individual patient for a shared decision-­making with the patient. Analysis by subgroups in meta-­analysis revealed benefit preferentially to the soft-­tissue mass located in extremities and chest wall. If the decision is made to use chemotherapy as upfront treatment, it may well be used preoperatively. A local benefit may be gained, facilitating surgery, in addition to the systemic one. Neoadjuvant chemotherapy with anthracyclines plus ifosfamide for at least three cycles can be viewed as an option in the high-­risk individual patient.31,33 The various protocols are beyond the scope of this chapter and are changing rapidly. The reader is therefore advised to consult the pertinent most recent literature on that matter. Isolated limb perfusion (ILP) can be proposed in selected locally advanced marginally resectable soft-­ tissue sarcoma of extremity. A meta-­analysis for isolated limb perfusion of extremity soft-­tissue sarcoma demonstrated overall response rate of 73.3% and complete response rate of 25.8%.34 The procedure mainly involves a 60 min perfusion with melphalan and TNF-­α under mild hyperthermia, achieving a limb preservation rate of 72%–­96%, with an overall response rates from 72% to 82.5% and an acceptable toxicity according to the Wieberdink scale. The local failure rate is 27% after a median follow up of 14–­31 months compared to 40% of distant recurrences after a follow-­up of 12–­22 months. Currently there is no consensus regarding the benefit of ILP per histotype, and the value of addition of radiotherapy or systemic treatment.35

Treatment/­surgical resection techniques Histologic confirmation, grading, and subtyping of the presumed malignant sarcomatous tumor on the lower extremity must be achieved before the overall treatment strategy is planned in the tumor board and definitive, usually more extensive, surgery is initiated. However, not all known biopsy techniques are useful for a correct and safe diagnosis of a sarcoma.

Biopsy techniques Fine-­needle or core-­needle aspirations These techniques gain only a very small amount of tissue even in the hands of an experienced clinician. While tissue aspiration with a 23-­gauge needle usually harvests only a very small number of cells, the volume of tissue gained from a core-­needle biopsy is a bit higher. Still, both methods have

­

Excisional biopsy Excisional biopsies aim for the removal in toto of all tumor tissue with primary closure of the surrounding tissue and are therefore reserved for lesions less than 3–­5 cm in diameter and with epifascial location. As the definitive diagnosis is not known beforehand, no tissue margin of defined thickness is left with this procedure. Any surgical biopsy on the lower extremity should be performed with a pressurized tourniquet (no exsanguination!) if tumor location permits. The bloodless field not only aids in exact and atraumatic safe dissection but also inhibits possible tumor cell contamination during surgery. Before incising the skin, it is absolutely necessary that the surgeon already imagines any secondary, definitive tumor resections and has possible muscle and tendon transfers and local flap options in mind. The biopsy incision should interfere as little as possible with these factors. Usually, a longitudinal incision as short as possible for an adequate exposure directly over the tumor is made, providing the shortest reasonable access route to the neoplasm. The tumor should be excised in a no-­touch/­no-­see technique including any pseudocapsule (if present) without opening it. Any “shelling-­out” of the tumor should not be performed as in sarcomas this capsule is part of the tumor and its remaining walls do contain tumor cells. After the excision, it may be useful to mark the resection bed with titanium or vitallium microclips to make later excision easier, if malignancy was affirmed. Localization sutures are fixed to the tumor, and both instruments and gloves are changed. Meticulous hemostasis and the placement of a closed suction drainage within the wound to prevent possible tumor seeding through a hematoma are paramount before a multilayered skin closure is done. The skin should be closed with single interrupted stitches or intracutaneous sutures. Mattress

Treatment/­surgical resection techniques

sutures or separate drainage perforations leave stitch marks too far away from the incision and, as they all have to be excised in case of malignancy, this would enlarge the amount of tissue to be resected. A sterile circular compressive dressing is placed, and the affected extremity is immobilized  –­ especially in procedures close to joints. Temporary splinting for a few days assists well here.7

Incisional biopsy The surgical resection of a representative part of the sarcoma is the gold standard in diagnosis of extremity tumors for any lesions that are larger than 3–­5 cm and of subfascial location (Case study  4.1). This technique should only be performed by an experienced surgeon, as the gathering of respective tissue specimens and the handling of the tissue is crucial to the success of the procedure. The advantages of getting adequate tissue for a full range of diagnostics greatly outweigh the disadvantages by opening the tumor and introducing the potential for tumor cell seeding in the path of the access route. Again, the procedure should be performed with a tourniquet, as detailed dissection is possible and intraoperative

Case study 4.1 (Fig. 4.4)  

A 35-­year-­old male presented with a growing tumor and painless swelling in his right quadriceps muscle. The patient referred this to a blunt trauma while playing soccer 6 months ago. Ultrasound and contrast-­enhanced MRI demonstrated a large intramuscular tumor suspicious for a liposarcoma (Fig. 4.4A & B). Histology was verified with incision biopsy. Staging with abdominal and thoracic CT scan showed no distant metastases. The treatment protocol was discussed in the local tumor board and wide excision of the tumor was performed (Fig. 4.4C). As four-­fifths of the quadriceps muscle had to be resected (Fig. 4.4D), a free functional musculocutaneous latissimus dorsi flap was harvested (Fig. 4.4E) and connected to local vessels. Nerve coaptation was done to a branch of the femoral nerve close to the groin that could be spared from the resection. The muscle transplant was fixed at the anterior superior iliac spine, and the remaining vastus medialis head and its tendon were woven into the quadriceps tendon and fixed securely with 1-­0 non-­resorbable sutures. To assist leg function until the latissimus muscle was reinnervated, we simultaneously also transferred a functional biceps femoris flap through a separate posterior incision (Fig. 4.4F) around the distal lateral femur and sutured it into the new latissimus–­quadriceps–­tendon extensor apparatus with an adequate pretension. The muscle bulk of the latissimus easily obliterated the space of the resected quadriceps muscle, while the skin island served for tension-­ free closure of the integument. For protection of the tendomuscular reconstructions, an external fixator across the knee was applied for 6 weeks. Healing was uneventful, and the pathology showed clear and adequate margins (R0 situation). The fixator was removed in an outpatient procedure and physiotherapy begun. At 3 months after the resection and simultaneous reconstruction procedure, the patient showed an almost completely normal gait (Fig. 4.4G & H).

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contamination of surrounding tissue areas during resection of the histologic specimen with potentially tumor-­cell-­containing blood is minimized. The guidelines for the skin incision are practically the same as for the excisional biopsies with regard to keeping any further operative options in mind. An incision parallel to the axis of the extremity is made. It should be as short as possible for an adequate exposure directly over the tumor providing the shortest reasonable access route to the neoplasm. The incision must not unnecessarily interfere with later procedures needed to cover the defect. A properly conducted incision biopsy should harvest a relevantly large, at least 2 × 1 × 1 cm, tissue block from all areas of the tumor including the capsule. It is a common misconception to want to gain tissue only from the central portion, as this area often contains considerable amounts of necrotic tissue that are not adequate for pathology and makes definitive histologic classification impossible. The tissue block removed should be manipulated as little as possible and should not come into contact with the wound edges of the surgical access route. Any instrument used to hold or manipulate the biopsy specimen must not be used for wound closure or retraction, etc. After removal of the tumor block, localization sutures are tied and both instruments and gloves are changed. Meticulous hemostasis and the placement of closed suction drainage within the wound to prevent possible tumor seeding through a hematoma are paramount before a multilayered skin closure is done. The skin should be closed with single interrupted stitches or intracutaneous sutures. Mattress sutures or separate drainage perforations leave stitch marks too far away from the incision and, as they all have to be excised in case of malignancy, this would enlarge the amount of tissue to be resected. A sterile circular compressive dressing is placed, and the affected extremity is ­immobilized –­ especially in procedures close to joints. Temporary splinting or an external fixator for a few days serves the purpose here. When mounting an external fixator to the affected lower extremity at the time of biopsy, care must be taken not to interfere with the later resection margins for definitive tumor resection. Preoperative findings of intraosseous skip lesions in bone sarcomas must be taken into consideration in this context. A fixator pin must never be set into an area for later resection, or the pin tract has to be included in the resection specimen. Both incisional and excisional biopsies are not intended to adequately remove the tumor according to oncologic rules. Therefore, temporary vacuum-­ assisted closure techniques should be avoided and are rarely required anyway. Their angiogenetic potential and the risk of dissipation of tumor-­ cell-­containing wound secretions into the rest of the wound may negatively affect local oncologic safety. Larger studies are missing, however.

Re-­operative biopsies and surgical revisions Tumor centers frequently have to perform a surgical revision to confirm the diagnosis of sarcoma or to accomplish the correct surgical–­oncological treatment. After previous attempts of inadequate biopsy or even after surgery that was intended to be definitive and curative, a re-­operation is considered mandatory if at least one of the following situations is present:

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Hahn 1884

Wittek 1906

Codvilla 1909

Brandes 1913

Moszkowicz 1917

Stracker 1926

Davis 1944

Muller 1963

Blauth 1963

Dederich 1965

Ferrand 1966

Zanoli 1966

Ferrand 1966

Blauth 1971

Allgöwer 1963

Eckeu Kyambi 1975

Figure 4.3 Historical overview of various fibula-­pro-­tibia techniques for lower leg reconstruction.  

  Only

inadequate tissue material for definitive histology was gained at the first operation.   Previous resections have not been performed according to current oncologic guidelines (see Case study 4.2). Some indicators for a re-­operation are incisions placed horizontally to the axis of the extremity and opening up several muscle compartments, intact nerve function after “resection of a malignant peripheral nerve sheath tumor”, or normal leg motor function after “radical excision of extensor or flexor muscles”.   A clinically unsuspicious and presumably benign tumor was resected with the techniques of benign tumor surgery, but the postoperative histopathologic workup showed an unexpected malignancy.   A tumor was resected during a non-­oncologic surgery and detected in the postoperative workup (“unplanned excision”).   The tumor surface was visible intraoperatively.   Previous operating room (OR) reports describe an “easy shelling-­out from a capsule”, but clinical and/­or histologic and/­or radiographic workup confirms a highly suspicious lesion or malignancy. A sarcoma resection out of its pseudocapsule results in local recurrences in up to 90% of patients.11   The patient presents with early local tumor recurrence, despite a “radical resection” being stated in the previous OR report.

Case study 4.2 (Fig. 4.5)  

This 48-­year-­old male patient was referred to us with a horizontal (non-­oncologic) incision of the right anterior lower leg (Fig. 4.5A & B) after a non-­oncologic resection of an MFH leaving positive margins (R1) elsewhere. Re-­operation with a wide excision (9 × 8 cm) (Fig. 4.5C & D) was performed in our center, and the defect closed with a pedicled medial gastrocnemius muscle flap (Fig. 4.5E) and split-­thickness skin graft from the ipsilateral thigh. Histology now showed adequately wide and clear margins of this R0 resection. Further healing was uneventful. Fig. 4.5G–I demonstrate follow-­up results at 3 months after flap transposition and defect closure. ­

  Previous

OR reports state a “compartment resection” in the axilla or around the elbow, popliteal fossa, or groin (which is anatomically not possible).   OR and pathologic reports differ considerably in amount and integrity of the resected tumor.   Any remaining tumor is present in any postoperative imaging (MRI). In all these situations, at least an R1 situation must be anticipated. The secondary resection should follow the exact principles of the surgical technique for definitive resection described

Treatment/­surgical resection techniques

137

A D

G

B E

C

F

H

Figure 4.4 (A,B) Contrast-­enhanced magnetic resonance imaging demonstrating a large intramuscular tumor suspicious for a liposarcoma. (C) Tumor specimen after wide excision, including the incision biopsy scar. (D) The quadriceps muscle had to be resected subtotally. (E) This free functional musculocutaneous latissimus dorsi flap was harvested and revascularized to local vessels. Nerve coaptation was done to a branch of the femoral nerve close to the groin that could be spared from the resection. (F) To assist leg function this pedicled biceps femoris flap was rerouted around the distal lateral femur and woven into the new latissimus–­quadriceps–­tendon extensor apparatus. (G,H) Clinical result 3 months after resection.  

below. The previous tumor bed should not be opened or visualized at all. If macroscopically visible remaining tumor is encountered during surgery (R2 situation), the secondary revisional surgery may at least reduce the situation into an R1 situation (Table 4.3). Following these revisional surgeries, radiotherapy is usually indicated for a reduction in the probability of local tumor recurrence.

Surgical technique for definitive resection Soft tissue sarcomas (STS) As soon as the definitive histology is found and the tumor type, grading, and staging of the disease has been completed in the multidisciplinary workup, definitive surgery is initiated. If the tumor is deemed to be resectable and no neoadjuvant therapy or isolated extremity perfusion was planned, the therapy of choice today is a wide excision with adequate margins. Before any definitive surgery is performed, the reconstructive

Table 4.3  World Health Organization classification of tumor resection margins R0

Resection with microscopically tumor-­free specimen margins

R1

Resection with microscopically tumor-­positive specimen margins

R2

Resection with macroscopically remaining tumor

strategy should be planned as meticulously as possible. It is necessary to fully inform the patient about the expected extent and length of the procedure and of possible donor sites of flaps, nerves, vessels, or skin grafts, etc. Furthermore, the anesthesiologic risk and invasiveness of monitoring should be explained to the patient and planned accordingly with the anesthesiologist. Also, placement of vascular access routes and regional pain catheters are important in that aspect. A well planned patient positioning on the OR table can allow a simultaneous team approach by oncologic and plastic surgeons and save a considerable amount of operative time.

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A

B

C

D

E

F

G

H

I

­ ­ ­ Figure 4.5 (A,B) Clinical situation on admission after non-axial (i.e., non-oncologic) incision biopsy and secondary non-oncologic resection of a malignant fibrous histiocytoma (MFH) with positive margins (R1) elsewhere. (C) Intraoperative picture after wide R0 excision (9 × 8 cm). (D) Excised specimen including the scar of the former biopsy and primary resection. (E) A pedicled medial gastrocnemius muscle flap was used for closure. (F) Serial incision of the muscle tendon and fascia was performed to expand the reach of the flap and to allow supple wound closure. (G–I) Clinical result 3 months after resection and flap closure.  

 

 

­

Treatment/­surgical resection techniques

Definitive sarcoma resection with a curative approach should be performed in a bloodless field with a pneumatic tourniquet or even temporary occlusion of the iliac or femoral artery by vascular surgery techniques. This reduces not only the risk for potential hemorrhage-­induced contamination of the field with tumor cells but blood loss in general and is mandatory for a detailed dissection. The resection must include all previous skin incisions, all previous stitch marks, and drain sites with a margin of 4 cm of healthy skin around them. This margin is also true for any ulcerated tumor locations. If the previous incision was performed properly, it creates an elliptical defect along the longitudinal axis of the leg. The advantages of this orientation are the preservation of the remaining subdermal lymph vessels and the ease in wound closure. After adequate epifascial mobilization, the muscle fascia is opened and the sarcoma is resected with a no-­touch/­no-­see technique leaving a cuff of macroscopically unaffected tissue of 2–­5 cm around it. Still there are no conclusive studies about the exact margins in sarcoma surgery, but many centers have recommend a margin of 2 cm from the deep surface of the tumor and 4–­5 cm laterally.6,7,36,42 More recent studies could not establish a strong association between radical resections and improved local control or survival. Previous radical concepts in STS surgery have been gradually replaced by more moderate approaches with function-­and limb-­sparing resections combined with radiotherapy. Here, the margin status appears to be of prognostic significance. However, several large retrospective analyses have presented inconsistent results, questioning the independent prognostic impact of surgical margins.1 Any palpable pseudocapsule of the tumor belongs to the tumor itself and should be resected but not opened or seen at all, otherwise the procedure is regarded as an R1-­resection. The tumor should not be retracted or manipulated with sharp or pointed-­tipped instruments and should be resected in continuity with the skin island containing the previous incision.

Vascular involvement Relevant deep vascular structures that are not directly infiltrated or encased in the tumor can usually be treated by longitudinal opening of the vascular adventitia opposite the tumor and subsequent microsurgical stripping of the adventitia under loupe magnification and en bloc with the tumor. Accompanying veins are usually ligated and included in this specimen if venous drainage of the extremity is still guaranteed in a different compartment. Preoperative MRI helps in this decision, otherwise the affected vessels have to be resected en bloc and replaced by a venous patch (less common), a vein graft, or, less commonly, an artificial vessel graft material (i.e., Gore-­Tex). Any arterial side branches that do not lead into the tumor should be evaluated as possible recipient vessels for microvascular tissue reconstruction and be preserved. Preservation of septal branches or muscular vessels that are outside the tumor resection area may lifeguard local or regional muscle and skin flaps that can not only aid in postoperative dead-­space elimination and wound closure but also in simple primary wound healing. Extraneous vessel ligation should therefore be avoided. If the superficial venous systems (great and lesser saphenous veins) are not included in the resected sarcoma specimen,

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they should be preserved together with their subcutaneous branches if possible. This prevents venous congestion if the deep venous systems close to the tumor must be resected as mentioned above, adding to the radicality and safety. While there should always be an adequate arterial perfusion of the lower extremity after tumor removal, only the main arteries are reconstructed immediately. Interpositional vein grafts for large vein reconstruction in tumor patients have a higher risk of thrombotic failure than in traumatic cases and should be reserved for selected cases only.

Nerve involvement The same dissection strategy applies to the main nerves in the lower extremity (Video 4.1 ). Any affected epineural tissue or connective tissue around the nerve inside the safety margin around the tumor should be stripped or removed with careful microsurgical techniques. If only a few fascicles of an important main nerve trunk are adherent to the tumor, it is considered acceptable to resect these and leave the unaffected nerve bundles intact for some basic motor function and sensitivity. If a major nerve is encased completely, it must be resected and should be reconstructed primarily or secondarily (see Chapter 6).

Osseous involvement For soft-­tissue tumors in the lower extremity that are not primary osseous sarcomas and growing close to bone, the appropriate treatment has to be guided by clinical judgment and preoperative MRI and CT scan. Real bony arrosion is relatively rare, and periosteal stripping, decortication, and partial bone resection are reasonable methods to comply with safe margins according to the principles of wide resection. However, these procedures weaken the bone mechanically in an area where later adjuvant radiotherapy further weakens the bone in the beam to an extent that may actually cause spontaneous fractures. Together with a systemically prevalent osteoporosis, this poses a considerable risk for spontaneous fractures.7,43 Any resection of weight-­bearing bones and joint segments should be balanced carefully against the complexity to reconstruct them. Frequently, the preservation of important skeletal structures permits quality of life to a degree that is comparable to an acceptable oncologic risk. Nevertheless, the full range of the plastic reconstructive operative armamentarium including bone flaps should be evaluated in providing the best outcome for the patient (see Chapter 6).

Primary osseous sarcomas Primary osseous sarcomas may be diagnosed relatively accurately by plain radiographic imaging alone. The biopsy techniques are the same as in soft-­tissue sarcomas, with the addition of opening up the bone cortex with a round burr hole under X-­ ray-­assisted localization; gaining the biopsy; obtaining wound swabs for bacteria, fungi, and tuberculosis (differential diagnosis); and closing the hole with alloplastic hemostatic material.41 Wide surgical resection is also the treatment of choice for primary osseous sarcomas with comparable later reconstructive demands. Sometimes, the biopsy procedure may cause structural instability and external casts, splints, or external

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fixators are necessary. The method of choice for postresection leg stabilization should at best be determined before biopsy. If external fixators are planned for a definitive skeletal stabilization, the montage may already be applied during biopsy if the diagnosis is verified by a pathognomonic bone X-­ray.

Specimen handling If the resection is completed, the tumor and the tumor bed are photographed and the specimen is removed. It is extremely important to clearly mark the decisive anatomic landmarks and the topographic orientation of the tumor in its previous bed to allow unequivocal and exact determination of margins by the pathologist. Optimally, the examining histopathologist is present at this stage of the procedure. The surgeon has to ensure that any identifying orientation markings on the tumor are not shifted or torn off during transport.

Wound closure Before wound closure, meticulous hemostasis and the placement of sufficient closed suction drains are necessary. Skin closure should be done in a multilayered fashion exerting detailed care for exact approximation of the wound edges in order to avoid any wound-­healing disturbances that might hinder fast implementation of radiation therapy. Primary wound closure is dependent on the size of the tumor and the location in the leg. In the thigh, primary wound closure after wide resection is frequently possible, whereas around the knee and distally from it in the lower leg this is usually not feasible. The tumor resection bed should be narrowed by appropriate muscular and fascial sutures to prevent seroma and hematoma collection in it. Naturally, this usually applies for tumor locations at the thigh or proximal lower leg only. Any wound closure must aim for a stable skin closure with only minor tension for fast primary wound healing and must avoid stretching of thinned-­ out, unsupported adipofascial skin flaps over empty wound cavities or bony protuberances. Wound closure must not be a trade-­off against the appropriate radicality in tumor resection, especially in the context of available modern plastic surgical reconstructive options. If closed suction drainage is used, the drains should exit the skin close to the surgical incision edge (in case re-­resection or RT is indicated).44 It is often quite useful to immobilize the operated leg with a splint for postoperative handling, analgesia, and aiding in hemostasis. A sterile circular compressive dressing is placed as well. However, in the case of a flap reconstruction, many surgeons defer from using this option because of the fear of compression forces onto the flap or the microvascular pedicle. An interim placement of external fixators is very useful in this context. They easily permit the bedside elevation of the operated extremity, especially in cases with free flaps that may not be dressed with circular bandages in the first postoperative days. External fixators may help in later daily wound care and aid in safe and fast flap healing, but may also be mounted in the proximal and distal metaphyses when a diaphyseal resection must be performed, or for interim stabilization until a surgical arthroplasty is healed or an orthopedic joint replacement is performed. Depending on the patient and case profile, an immediate reconstruction may not be possible due to a variety of reasons.

Cardiovascular instability, ventilation problems, a large blood loss, or unexpected surgical findings may render a continuation of the operation too dangerous, especially in patients with several comorbidities or advanced biologic age. In these cases, temporary vacuum-­ assisted wound closure may be used until final reconstruction. There is no evidence in the literature that these angiogenesis-­promoting subatmospheric pressure devices have negative effects on oncologic safety after a wide resection that was intended to remove all neoplastic tissue including an appropriate safety margin.45,46 This is in contrast to the situation after incisional or excisional biopsies where they are not recommended for use (see above).

Lymph node dissection Less than 5% of all sarcomas spread in a lymphatic way. Therefore there is no indication for a standardized simultaneous dissection of the relevant lymph node areas (i.e., popliteal fossa/­groin) if the region is not clearly involved clinically or radiographically. A lymph node dissection should always be performed, however, in sarcomatous tumor entities that are known for their lymphatic spread like the rhabdomyosarcoma, angiosarcoma, and epitheloid-­like sarcoma subtypes. If regional lymph node metastases are present, a radical lymphadenectomy significantly improves median survival.17,18

Indications for amputation In selected cases, amputation of the leg must be considered the best option for the patient despite very detailed imaging techniques, modern oncologic resection strategies, advanced sophisticated plastic reconstructions, and advances in radiologic and chemotherapeutic therapeutic regimens. Primary amputations for treatment of lower extremity sarcomas are necessary in less than 5% of all patients and in less than 15% in recurrences while demonstrating a comparable long-­term survival.6–8 Amputations are chosen as an adequate primary therapy, if significant medical comorbidities prevent the safe completion of a major tumor resection with immediate defect reconstruction. Usually, these cases are very rare, and almost always the reconstruction can be deferred to a secondary operation. Modern advances in anesthesiology and intensive care medicine usually allow long procedures to be performed safely. The only exceptions where an immediate reconstruction must be performed are immediate revascularization procedures in cases with extensive main arterial involvement. Extensive lower limb reconstruction procedures also have to be balanced cautiously against amputation in para-­or tetraplegic patients or patients with severe cerebral impairment who are bedridden for lifetime. If the tumor demonstrates transmetatarsal growth, penetrates the interosseus membrane in the lower leg, already shows locoregional dissemination (for example with rhabdomyosarcomas), or the patient presents with a very large and extensively ulcerated tumor with circular leg involvement, an amputation may be inevitable. Primary multicomponent sarcomas in the proximal thigh may be treated best with an amputation as well as extensive tumor recurrences after exhaustion of all adjuvant or surgical modalities. Uncontrollable chronic diseases that are not acceptable for major (microvascular) procedures or render the preservation ­

Reconstructive options for lower extremity preservation

of the sarcoma-­infested extremity useless can make an amputation inevitable. Examples are open ulcers because of chronic venous insufficiency or atherosclerotic occlusive disease in the same leg, an ipsilateral unrelated tumor, or a history of previous trauma with subsequent subclinical osteitis. The latter could reactivate in the context of major surgery or adjuvant therapy. Furthermore, the predictable inability to reconstruct a stable extremity and/­or wounds that are not suitable for safe conservative wound care and patient handling are an indication for amputation, if the full reconstructive spectrum has been evaluated for leg salvage and a suitable solution was not found. This might include the unavailability of relevant donor sites for (microvascular) extremity reconstruction. Lastly, patient preference in favor of amputation is very rare after thorough information about modern reconstructive possibilities but has to be respected in selected cases.

Reconstructive options for lower extremity preservation Plastic surgical involvement in sarcoma treatment already begins during tumor resection. Several examples that demand plastic surgical and microsurgical knowledge during skin incision, tissue dissection, and neurovascular preparation have already been mentioned above. In general, the plastic surgical reconstruction follows the reconstructive ladder with the lowest rung being the least invasive method (secondary healing) and the highest rung representing customized chimeric multicomponent free flaps. Like in many other reconstructive problems, the best option for the individual patient must be chosen regardless of whether it requires more complicated surgery (“reconstructive elevator”).20,21,47 The following subsections demonstrate the vast diversity of plastic surgical methods, also found elsewhere in this book in detail. For sarcoma reconstruction, the surgeon has to keep in mind that pre-­or postoperative radiation or previous chemotherapy can spoil his or her success rate, especially in complicated microvascular reconstructions. The use of large recipient vessels outside the radiation field, supple soft-­tissue closure, and as little foreign material as possible are proven ways for successful surgery.

Soft tissue Soft-­tissue coverage for sarcoma reconstruction must always be seen in the context of preoperative and adjuvant radiotherapy. The goals are obliteration of dead space, closure of large skin defects with tension-­free wound closure, preservation of thin but viable skin edges by supporting them with voluminous muscle flaps, and to cushion exposed bony prominences around the tibia, joints, or amputation stumps.48 Local and regional fasciocutaneous flaps are slightly superior to skin-­grafted muscle transposition flaps (i.e., medial or lateral gastrocnemius head or peroneus brevis) in terms of fast wound healing and radiation resistance. They might be of limited availability after large tumor resection. Local perforator flaps are very useful for primary reconstructions. However, if the area was irradiated, the perforators in the field are less reliable and extremely difficult to dissect due to fibrosis or

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became very small and fragile.49 Furthermore, the skin quality and elasticity is inferior for donor site closure in secondary reconstructions with local flaps. Useful pedicled regional flaps to cover defects in the thigh may be harvested from the deep inferior epigastric artery system of the lower abdomen (i.e., transverse rectus abdominis myocutaneous, vertical rectus abdominis myocutaneous, deep inferior epigastric perforator, and rectus abdominis muscle) or from the buttock area (superior gluteal artery perforator and inferior gluteal artery perforator). The latter may have a suitable rotation radius if isolated on their respective perforators (Case study 4.3). Microvascular free flaps from all over the body may be used for lower extremity reconstruction and are chosen according to the defect geometry and depth, location, and functional requirements. For secondary reconstructions, recipient vessels are rare or fragile, if the area was irradiated, and a preoperative angiogram is warranted. Sensate flaps (i.e., lateral arm flap) should be considered for weight-­bearing areas at the foot or on amputation stumps.

Neuromuscular unit Resected main nerves can be microsurgically reconstructed with multiple cable grafts from the sural nerve or other donor sites according to the cross-­section of the recipient nerve (see Case study 4.4). Meticulous technique and the use of an operative microscope are paramount. In selected sarcoma resections that include bone and nerves, the bone may be restabilized with shortening of the extremity (see Case study  4.5). This

Case study 4.3 (Fig. 4.6)  

This 56-­year-­old male patient demonstrated a large intramuscular tumor highly suspicious of a soft-­tissue sarcoma in the proximal left thigh close to the groin. His clinical complaints were swelling and pain over 6 months. MRI demonstrated close proximity to the superficial femoral vessels; however, the femoral nerve could not be identified in the MRI (Fig. 4.6A & B). The incisional biopsy showed a highly malignant synovial-­ cell sarcoma (G3). After preoperative planning in the tumor board, a wide resection including most of the extensor muscles (Fig. 4.6C) was performed according to oncologic guidelines, yielding a 23 × 18 × 20 cm large tissue specimen including the tumor (Fig. 4.6D–F). The femoral nerve was encased by tumor tissue and required resection according to oncologic principles. From the contralateral abdomen, a pedicled vertical musculocutaneous rectus abdominis muscle (VRAM) flap (30 × 18 cm) was harvested and transferred into the defect (Fig. 4.6G & H). Additionally, the biceps femoris as well as the semitendinosus muscles was transferred to the remnants of the patellar tendon to reconstruct knee extension. The postoperative course was uneventful with the exception of a small wound dehiscence applicable for conservative local wound care at the mid-­abdomen flap harvest site. The patient underwent radiation therapy as well as chemotherapy due to metastases in the lung. Two years postsurgery the patient was able to extend his leg and had no recurrence of the tumor or the metastases in the lung (Fig. 4.6I). ­

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Case study 4.4 (Fig. 4.7)

Case study 4.5 (Fig. 4.8)

A 6 × 7 × 5 cm large painless mass was detected in the right calf of this 31-­year-­old male patient. Contrast-­enhanced MRI showed a lesion highly suspicious for a soft-­tissue sarcoma. This diagnosis was confirmed by a longitudinal incision biopsy according to oncologic guidelines, and the definitive tumor resection was planned (Fig. 4.7A). The tumor resection was performed according to international standards for wide excision to leave a cuff of tissue surrounding the tumor of at least 2 cm to the depth and at least 4 cm to the sides (Fig. 4.7B & C). Due to encasement of the posterior tibial vessels and the tibial nerve by the tumor, they had to be resected as well (Fig. 4.7D). The tibial nerve was immediately reconstructed microsurgically by a free sural nerve harvested from the contralateral side (Fig. 4.7E & F). The sural nerve was doubled as a cable graft to allow cross-­sectional matching to the tibial nerve and was set at 180° to improve neurotization. The resection defect was controlled for a perfect hemostasis, and drains were placed. As the tumor provided a “tissue-­ expansion-­like” stretching of the calf, the wound could easily be closed primarily without having relevant dead spaces or skin “tenting” over unsupported wound cavities (Fig. 4.7G). Further follow-­up showed uneventful healing and recurrence of sensation at the plantar side of the foot after 2 years.

A 70-­year-­old female complained of a painless mass in the lower extremity (Fig. 4.8A). The preoperative MRI imaging showed a tumor in the posterior and lateral compartment that also affects the fibula (Fig. 4.8B). Due to the overall age and the amount of resection, which included the peroneal vessels, a preoperative angiogram was done demonstrating a well-­vascularized tumor as well as appropriate vessels for a free tissue transplantation and limb perfusion (posterior tibial vessels, Fig. 4.8C). After an incisional biopsy, which demonstrated a liposarcoma G2, the planned resection was outlined (Fig. 4.8D) and a 13 × 11 cm specimen resected en bloc including a fibula segment (Fig. 4.8E & F). The defect was closed with a free fasciocutaneous parascapular flap, and radiation therapy was initiated. After 2 years, the patient was doing well without any metastases or local tumor recurrence (Fig. 4.8G).

 

scales down the soft-­tissue defect, facilitates wound closure, and can make primary nerve coaptation possible. Depending on the muscular units that have to be resected, muscle or tendon transfers may be performed primarily (see Case study  4.6). Biceps tendon (with or without semitendinosus tendon) or posterior tibial transfers are the most common transfers in the lower extremity to reconstruct knee extension and foot elevation, respectively (see Case study 4.1). Tenodeses may preserve muscular power in partially resected compartments (i.e., adductors) and allow muscular stabilization of joints. Of course, free functional muscle transfers (i.e., mm. gracilis and gastrocnemius)50 are very useful in young patients with high neuroregenerative potential as well.

Skeletal reconstruction Reconstruction of the skeleton after resection of soft-­tissue sarcomas involving bone secondarily and primary osseous sarcomas are the main interdisciplinary field of orthopedic and plastic surgeons, also named “orthoplastic surgery”.51 Expandable and non-­expandable tumor prostheses, Van Ness or Borggreve rotationplasty,52 resection arthroplasties, distraction osteogenesis, segment transport, or total joint replacements commonly belong to the orthopedic techniques (see Case study  4.7). However, a combination of the above with pedicled or free vascularized bone may benefit the patient and augment the therapeutic armamentarium. Therefore this “orthoplastic approach” does not only refer to post-­traumatic reconstructions but is a fruitful strategy for oncologic plastic surgery as well. In selected cases, a variety of traditional techniques like fibula-­ pro-­ tibia transfer require microsurgical dissection of the pedicle (Fig.  4.3) or an orthopedic osteosynthesis in the

 

Case study 4.6 (Fig. 4.9)  

A newborn male patient presented with a 3 × 3 cm tumor on the dorsum of the right foot. Preoperative MRI imaging and incisional biopsy were carried out (Fig. 4.9A & B). The histology revealed a congenital rhabdomyosarcoma. After chemotherapy, wide resection (5 × 7 cm) was performed. All extensor tendons were resected (Fig. 4.9C & D). The reconstruction was performed with a free latissimus dorsi flap. In addition, the extensor tendons were reconstructed by transplanting the superficial toe extensors from the opposite side (Fig. 4.9E). Note the free function of the foot without tumor recurrence 11 years after resection (Video 4.2 ).

Case study 4.7 (Fig. 4.10)  

Fig. 4.10A shows the foot of a 51-­year-­old-­female with a mass 5 × 5 cm at the dorsum of the right foot. Diagnostic MRI demonstrated a tumor that encased the extensor tendons of the first ray (Fig. 4.10B). The incisional biopsy (Fig. 4.10C) confirmed an MFH G2. A wide excision including the extensor tendons of the first ray, the dorsal half of the first and second metatarsal bones, as well as the capsule of the metatarsophalangeal joint 1 was performed (Fig. 4.10D). Due to the resulting instability of this joint of the first ray an immediate arthrodesis was carried out and the defect covered with a free ALT perforator flap. One year after the operation and radiation therapy the patient was tumor free and able to walk and exercise (Fig. 4.10E).

metaphyseal area may benefit from additional vascularized bone from a composite flap to augment the construction. Very useful flaps here are the latissimus bone flap and the (para-­) scapular bone flap with a lateral and or medial scapular bone segment of up to 11 × 3 cm that provides coverage or filling of extensive soft-­tissue defects or prosthetic material. For smaller defects around the foot, composite flaps like the osteofasciocutaneous lateral arm flap, which also can be harvested with a piece of humeral bone, are useful.53 Large defects of the long bones are more difficult to reconstruct with autologous tissue in the lower extremity than in the upper.54 This is due to the geometrical and size mismatch of the

Reconstructive options for lower extremity preservation

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B

A

C

D

F

E

Figure 4.6 (A,B) Large intramuscular tumor highly suspicious of a soft-tissue sarcoma in the proximal left thigh close to the groin with close proximity to the superficial femoral vessels; however, the femoral nerve could not be identified in the MRI. (C) After the incisional biopsy, wide resection including most of the extensor muscles was planned. (D,E) Resection specimen 23 × 18 × 20 cm including the tumor. (F) The femoral nerve was encased by tumor tissue and had to be resected according to oncologic principles. (G) A contralateral pedicled vertical musculocutaneous rectus abdominis muscle flap (30 × 18 cm) was harvested. (H) Flap closure of the defect. (I) Clinical picture 2 years after surgery.  

 

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G

H

I

Figure 4.6, cont’d

largest human bone flaps, that is free fibula and vascularized iliac crest (deep circumflex iliac artery flap). However, vascularized bone is a vital, dynamic, growing, infection-­resistant, and relatively radiation-­resistant tissue. The various methods for single and double fibula reconstruction of extensive long bone defects in the lower extremity are discussed elsewhere in this book and apply to sarcoma reconstruction alike (see Chapter 7). In the context of adjuvant radiotherapy, avascular autologous or allogeneic bone grafts, with their high complication rate of fracture, infection, slow integration, and creeping substitution, should be used very carefully and only in selected cases. When using these grafts, there should be special emphasis on ample vascularization of the surrounding soft-­tissue bed and obliteration of any dead spaces around the bone. This optimizes creeping substitution of the avascular allograft and reduces the probability of graft exposure after radiation. Combination techniques using an avascular structural allograft with a vascularized free fibula inside, as described by Capanna, offer promising results especially for extensive skeletal defects in young tumor patients (see Case study 4.8).55,56 This hot dog–­like construct combines optimal vascularization of the vascularized autologous fibula with the structural stability of the geometrically matched allograft “shell”. The osteosynthetic stabilization of this construct over the length of a long bone and in metaphyseal areas may be a compromise as the vascular pedicle and vascularization of the inner fibula must be preserved. Burring a trough into the allograft for guiding the peroneal pedicle through the allograft cortex to the recipient vessels has proven quite useful.56,57

Case study 4.8 (Fig. 4.11)  

The patient was a 12-­year-­old girl with an osteosarcoma of the right distal femur (Fig. 4.11A). She received four cycles of neoadjuvant chemotherapy consisting of doxorubicin and intra-­ arterial cisplatin. A total segment of 15 cm was then resected from the femur, with the distal transepiphyseal cut 3 cm proximal to the lateral joint line of the knee. A 2 cm fibula bone flap was harvested (Fig. 4.11B). The bone defect was repaired with an intercalary allograft and a vascularized fibula bone flap placed into the medullary canal of the allograft (Fig. 4.11C). The vascular pedicle of the fibula flap was brought out through a side hole burred into the allograft. The allograft was fixed to the native bone with a 12-­hole lateral locking plate (Fig. 4.11D). Proximally, 4 cm of vascularized fibula bone flap was inserted into the host femur, and distally 2 cm of fibula flap was inserted into the host femur (Fig. 4.11E). Microvascular anastomoses were performed end-­to-­end to branches of the femoral artery and vein. Postoperatively, the patient received two additional cycles of chemotherapy. At 2 months, radiographs showed signs of healing with no complications, and touch weight-­bearing was started. At 5 months, radiographs showed a small amount of callus formation and remodeling at the proximal and distal allograft–­host junctions (Fig. 4.11F). The patient was allowed partial weight-­bearing on the leg with a limit of 10–­20 pounds. Another 6 months later, the patient progressed to full weight-­bearing, with the restrictions of no running and no sports activity until full radiographic union (Fig. 4.11G). Case courtesy of David W. Chang, MD, MD Anderson Cancer Center, Houston, TX, USA.39

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D

A E

F B

C

G

­ Figure 4.7 (A) A 6 × 7 × 5 cm large painless mass in the right calf suspicious for a soft-tissue sarcoma. A longitudinal incision biopsy according to oncologic guidelines and the definitive tumor resection was planned. (B,C) The tumor resection was performed according to international standards for wide excision to leave a cuff of tissue surrounding the tumor of at least 2 cm to the depth and at least 4 cm to the sides. (D) Posterior tibial vessels and tibial nerve were encased and had to be resected as well. (E,F) The tibial nerve was immediately reconstructed microsurgically by a free sural nerve harvested from the contralateral side. The sural nerve was doubled as a cable graft to allow crosssectional matching to the tibial nerve and was set at 180° to improve neurotization. (G) Postoperative view after primary closure without having relevant dead spaces or skin “tenting” over unsupported wound cavities.  

 

 

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D A

E B

F

C

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Figure 4.8 (A) Clinical picture of a painless mass in the right lower extremity. (B) Preoperative MRI showing a tumor in the posterior and lateral compartment also affecting the fibula. (C) Preoperative angiogram demonstrating a well-vascularized tumor including the peroneal vessels. (D) After an incisional biopsy, which demonstrated a liposarcoma G2, the planned resection was outlined. (E) En bloc resection, 13 × 11 cm large specimen including a fibula segment. (F) The tumor was not seen during surgery and was covered well with muscle according to adequate tumor margins. (G) Clinical picture 2 years after free parascapular flap closure.  

 

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Reconstructive options for lower extremity preservation

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C

A D

B

E

Figure 4.9 (A) Preoperative MRI a tumor on the dorsum of the right foot a few days postpartum. (B) Macroscopic image of the tumor after incisional biopsy 3 weeks postpartum. The histology revealed a congenital rhabdomyosarcoma. (C) Intraoperative finding after wide excision, down to the bony structures and resection of all extensor tendons after neoadjuvant chemotherapy. (D) Resection defect 5 × 7 cm after opening the tourniquet. Temporary alloplastic soft-­tissue coverage was carried out up to histological status confirmation. (E) The defect was covered with a free latissimus dorsi flap. The extensor tendons were reconstructed by transplanting the superficial toe extensors from the opposite side.  

Vascular surgery Main arteries that need to be resected together with the tumor should be reconstructed immediately by interpositional vein grafts in the lower leg. Proximal to the knee, autologous vein grafts may be too small and alloplastic material may be considered as an alternative for vessel replacement or extra-­anatomic bypasses. It is paramount to ensure a good soft-­tissue coverage for these materials to

prevent exposure, which is easier to achieve in the thigh than in the lower leg. In selected cases, a temporary arteriovenous loop connected to large-­bore vessels proximal to the recipient area offers large-­diameter vascular access for microvascular anastomosis distant to any previously scarred or irradiated area. For the proximal thigh and groin area, even the contralateral femoral vessels can be used as recipients for a cross-­over

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Figure 4.10 (A) A 51-­year-­old-­female with a 5 × 5 cm large mass at the dorsum of the right foot. (B) Preoperative MRI showing encasement of the extensor tendons of the first ray. (C) Clinical picture after incisional biopsy. (D) Clinical picture after wide excision including the extensor tendons of the first ray, the dorsal half of the first and second metatarsal bone, as well as the capsule of the metatarsophalangeal joint 1. (E) One year after the operation and radiation.  

graft.58 If available, autologous vein grafts should be used for vessel reconstruction. In selected cases with tumor-­related resection of main arteries, a simultaneous defect coverage and vessel reconstruction can be provided by flow-­through flaps (i.e., anterolateral thigh (ALT), radial forearm, and free fibula). Due to the high rate of venous graft occlusion for vein reconstruction in oncologic patients, the procedure should be done only in selected cases.59 One of the reasons for this might be the use of longer vein grafts in oncologic surgery than in trauma patients, which are more prone to thrombosis. Compared to trauma cases, venous outflow compromise by invasive tumor growth occurs more slowly, and the dynamic nature of the lower leg venous system almost always allows the development of sufficient venous collaterals, if the affected deep veins are resected.

Complex approaches For complex defects, free microvascular composite flaps from the subscapular, external iliac, or lateral circumflex femoral vessel systems provide large, multilobed transplants with a variety of different tissues for simultaneous soft-­tissue and skeletal reconstruction.60 Chimeric flaps further expand this enormous variability (i.e., free fibula with ALT). In selected cases, where amputation or segment amputation is inevitable, the distal limb segments are viable and healthy. According to the spare-­part principle of plastic surgery, the tissue may be transferred as a composite fillet flap,61,62 either pedicled or free microvascular, onto the amputation site providing length and suitable tissue quality for coverage. Preservation or coaptation of the contained nerves may achieve a sensate flap of excellent quality and skin texture.

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Figure 4.11 (A) The right distal femur of a 12-­year-­old girl showing an osteosarcoma. (B) A 21 cm fibula bone flap was harvested. (C) The 15 cm long intercalary allograft and a vascularized fibula bone flap placed into the medullary canal of the allograft. (D) Fixation of the allograft with a 12-­hole lateral locking plate. (E) Postoperative radiograph. Proximally, 4 cm of vascularized fibula bone flap was inserted into the host femur diaphysis, and distally 2 cm of fibula flap was inserted into the host femur metaphysis. (F) Radiograph 5 months later, showing a small amount of callus formation and remodeling at the proximal and distal allograft–­host junctions. (G) Radiograph after 11 months before progression to full weight-­bearing. ( Figure 4.11D: Courtesy of Dr. David W. Chang, Department for Plastic Surgery, MD Anderson Cancer Center, Houston, TX.)  

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Postoperative care Immediate postoperative care A firm concept of postoperative care is very important following biopsies, definitive sarcoma resection, and after any reconstructive surgical procedures for a variety of reasons. The postoperative protocol after incisional or excisional biopsies is focused on the prevention of hematoma and seroma formation and thereby possible tumor spread. While meticulous hemostasis and drainage placement is paramount (see techniques section), postoperative fluid collections in the resection bed and in tissue planes can be prevented effectively by bed rest, elevation of the affected lower extremity, and immobilization by external fixators or splints. Circular elastic bandaging and compressive dressings are also helpful. Most reconstructive procedures in sarcoma surgery with larger lesions need defect closure with flaps of some kind. Lower extremities that were reconstructed with local, regional, or free flaps need to be positioned in a slightly elevated position for 5–­7 days to accommodate the circulation rearrangements in the flap tissue and to prevent early venous congestion in the transplanted tissue. Frequent flap perfusion monitoring is paramount in the first days and ensures immediate intervention should a pedicle thrombosis or hematoma occur. Patients with neoadjuvant chemotherapy or preoperative intra-­arterial perfusion are at high risk for vascular complications in this context. Following this period of elevation, orthostatic “flap training” can be initiated with lowering the reconstructed extremity for 5 min t.i.d. associated with external compression by elastic bandaging. After this, the flap is clinically evaluated, and the procedure can be extended in increments of 5–­15 min daily over the next week until 1 h is accumulated. This allows reasonable intervals for early gait training and mobilization by stage-­adapted physiotherapy. Compressive bandaging should be replaced by custom-­fit compressive garments worn for at least 6 months for all soft-­ tissue flap reconstructions of the lower extremity except pure osseous flap reconstructions. Usually, garment wearing is initiated when the sutures are removed and the wound is healed. Postoperative weight-­bearing depends on the bony resection and reconstruction procedures that were performed, the hardware used for osteosynthesis, and the bone quality. The mobilization schedule should be determined exclusively by the operating surgeon. Serial roentgenograms or CT scans help in determination of the bone healing and regained functional stability of the extremity.

Oncologic postoperative care and follow-­up Patients after sarcoma resection with adequate margins and R0 situation need postoperative adjuvant radiation therapy under most circumstances, especially in tumors that are classified as high-­grade (G2/­G3). Only superficial, low-­grade lesions with tumor-­free wide margins may be treated with wide resection only. The radiation oncologists start with the therapy according to the appropriate treatment protocols established by the tumor board decision as soon as the wound is healed. If any unexpected oncologically relevant factors

occurred during resection or reconstruction (inappropriate or positive margins, vessel invasions, histology, etc.), the new findings should be presented in the tumor board as the treatment plan needs to be revised accordingly. This is also true for any late follow-­up findings, which imply a change in the normal course of healing by emerging local recurrences or distant metastases. The modalities or patient follow-­up after completion of resection and possible adjuvant treatment are not clearly defined in the literature. The following investigations are well accepted in the current literature:   Thoracic CT scan. Distant metastases in lower extremity sarcomas almost exclusively occur through hematogenous spread into the lung with only a few exceptions (see above). It should be repeated every 3 months.   Contrast-­enhanced MRI of the primary tumor site every 3 months. This should always be evaluated by or together with the surgeons. MRI is also the diagnostic method of choice for evaluating lymphatic spread if applicable. However, MRI criteria of tumor stability or progression may not correlate with the tumor status correctly.   Serial radiographs of the primary tumor location at least every 6 months if the skeleton was affected by the primary tumor or included in resection or reconstruction. The osteointegration of prosthetic material, bony healing, bone grafts, or transplants are controlled more frequently in the postoperative period anyway. A CT scan should be performed if the information by the plain radiograph is insufficient or suspicious findings occur.   New imaging techniques evaluating the metabolic activity of tumor material like PET (or PET-­CT) or magnetic resonance spectroscopy (MRS) are promising. While this is a fast developing field and the numbers of tracers are increasing, these methods are increasingly accurate in controlling preoperative response to adjuvant therapy and postoperative follow-­up. No commonly accepted follow-­ up schedule exists for sarcomas so far, and patients should be integrated into suitable studies.

Secondary procedures Early secondary procedures  –­ soft tissue After the initial tumor resection and extremity reconstruction is performed successfully and the wounds are healed, in the majority of cases plastic surgical therapy must continue during or after a possible radiotherapy to optimize the overall result. Despite adequate healing during the primary reconstructive phase, wound healing disturbances, fistulas, and incision breakdowns may occur during the scheduled radiation cycles. If the initial soft-­tissue closure was supple enough, early wound excision and secondary closure may suffice in minor cases. However, larger skin breakdowns may lead to exposure of functional structures like tendons, vessels, nerves, and bones, which need to be covered urgently to prevent radiation-­induced osteitis, vessel thrombosis, or tissue necrosis. Local flap solutions are only possible, however, if the appropriate vessels are still intact, as mentioned before.

Secondary procedures

With the radiation cycles completed, many patients experience fibrosis, scar formation, contractures, and tendon adhesions. Early function-­ improving procedures include tenolyses, contracture and scar releases, serial excisions, or tendon transfers that were not possible or justified primarily. It is often very difficult to evaluate during tumor resection, if any remaining musculature or nerves fascicles will suffice for an adequate basic motor function. A typical example for a secondary procedure like this is the posterior tibial tendon transfer for a clinical drop-­foot caused by a muscular or neural insufficiency of the peroneal compartment. Neuroma formation or nerve entrapments in irradiated and fibrotic tissue should be approached with desensitization and conservative therapy first, but frequently may require early operative neurolyses. Contour-­improving procedures of bulky transferred tissue should be performed not earlier than 6 months to be less independent from the vascular pedicle. They follow standard plastic surgical debulking techniques like direct sequential flap excision, tangential subcutaneous thinning, tangential thinning, and secondary resurfacing with split-­or full-­thickness skin grafts in muscle flaps or aspiration lipectomy. The same time frame applies to secondary procedures for forming amputation stumps. However, additive procedures on amputated legs like cushioning and stump lengthening by local and free flaps or sensitization by transfer of neurotized transplants can be planned earlier than 6 months after the amputation.

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arthroplasties, the functional outcome often cannot be adequately assessed until complete mobilization of the patient has taken place. If joint salvage surgery was not successful primarily, resulting in an unstable or painful joint with a severely impaired range of motion, secondary arthroplasties, joint replacement surgery, or arthrodeses may be necessary. If the limb-­preserving surgery consisted of a shortening of the limb, secondary distraction osteogenesis for extremity length adaptation can now be performed with all the soft tissue healed and the radiation therapy completed. However, docking failures are more frequent in irradiated patients. Corticocancellous augmentation is then needed to achieve stability.

Late secondary procedures

The number of patients that are long-­term survivors after successful sarcoma therapy in the lower extremity is constantly increasing. A considerable number of them need late secondary reconstructions or surgical corrections of their reconstructed leg. The plastic surgical therapy at this stage aims to correct the sequelae of the previous interdisciplinary plastic surgical, radiologic, and orthopedic therapy. Though not life-­or limb-­saving anymore, these procedures are nevertheless important to help the patients complete their personal and social coping after the disease and to improve quality of life. Scar releases and flap debulkings because of functional and aesthetic reasons that began in the early secondary stage Early secondary procedures  –­ skeleton frequently need revisions for several years. Irradiation may As mentioned above, skeletal reconstruction and stabilization leave a hard, constrictive, and fibrotic soft-­tissue integument should be performed as completely as possible during the pri- behind, which may be painful in rest and in motion or while mary reconstructive stage. Usually, orthopedic prosthetic joint wearing clothing and shoes. If postirradiation ulcers and or long bone replacements do not need any secondary surgery unstable scars further deteriorate the situation, the plastic if the initial montage demonstrated uneventful osteointegra- surgeon must be aware of late local recurrences and secondtion. Prosthetic replacement is mostly used in primary osseous ary malignancies in the affected area. Excision of the lesions sarcomas with large skeletal defects after resection. However, or the constricted scarred skin and transfer of unimpaired infection, mechanical failure, and loosening are among the healthy tissue by local, regional, or free tissue transfer can most common prosthetic complications in the context of radio-­ improve the patient’s quality of life considerably. Of course, and chemotherapy. Major revision surgery is therefore needed, any excised tissue from these areas must be evaluated which is described in the pertinent orthopedic literature. histopathologically. If plastic surgical reconstruction of the lower limb skeleton Peripheral neuropathies are less common after irradiawas performed by free autologous bone grafts, vascularized tion but more common after chemotherapy and may cause bone transplants, avascular allogeneic bone grafts, or combi- disabling chronic pain to the patient. Frequently, the nerve nations of the above, osseous healing is often slow in sarcoma is relatively healthy, but entrapped and fixed by surroundpatients, especially if the radiation field encompasses the zone ing dense, fibrotic, and irradiated tissue. Adequate therapy of skeletal reconstruction. Therefore augmentation of previ- consists of careful neurolysis, rerouting, and wrapping of the ously inserted bone transplants or revision of pseudarthroses nerve in well-­vascularized tissue by microsurgical methods. with corticocancellous bone packing is quite often necessary –­ Late secondary procedures after implantation of major especially in non-­vascularized grafts. At this stage, the osteo- hardware like modular prostheses or total joint replacements synthesis may also be changed to a more stable and definitive may include hardware exchange due to wear, mechanical failmethod if the primary one has failed. ure, or loosening. The microvascular medial femoral condyle corticoperiosLong-­term sarcoma survivors with a previous lower limb teal flap may be a useful tool to provide vascularity and osteo- amputation may experience stump problems like retracted soft genic potential for recalcitrant pseudarthroses in a previously tissue with insufficient soft-­tissue coverage of the bone, skin irradiated field.63,64 folds that impair proper wear of the prosthesis, painful neuroSarcoma-­ related partial joint resections in the weight-­ mas, and trophic skin changes. Many patients are very experibearing lower extremity may be critical. Painless function enced with their prosthesis and ask for specific plastic surgical with an acceptable range of motion must be the reconstruc- stump corrections. In selected cases, this might include microtive goal. Especially after partial joint resections or resection vascular free flap transfers, preferably with sensate flaps.

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CHAPTER 4  • Lower extremity sarcoma reconstruction

Outcomes, prognosis, and complications Outcomes and prognosis Several specialized evaluation scores do exist (Musculoskeletal Tumor Society (MSTS),65 Toronto Extremity Salvage Score (TESS),66 European Organization for Research and Treatment of Cancer (EORTC QLQ-­C30)) that rate various sets of subjective and objective parameters for functionality, quality of life, emotional, and social factors.67

Soft tissue sarcomas The current age-­adjusted death rate for soft-­tissue sarcomas is 1.3 per 100,000/­year, based on data between 2001 and 2005.4 A recent series, from the Memorial Sloan Kettering Cancer Center (MSKCC), of 1706 patients with primary and secondary STS of the extremities with a mean follow-­up of 55 months demonstrated a 5-­year disease-­specific survival rate of 85% in patients treated between 1997 and 2001. This number did not differ significantly from the survival rate in the previously treated patients from this group. The same was true for the subset of high-­risk patients in this group with a 5-­year disease-­ specific survival rate of 61% in those treated between 1997 and 2001. This indicates that the prognosis for patients with extremity soft-­tissue sarcomas has not changed over the last 20 years. Throughout this period, tumor depth, size, grade, margins, presentation status, location (proximal vs. distal), and certain histopathologic subtypes as well as patient age remained significant prognostic factors (Table 4.4).4 Steinau et al. report about 85 soft-­tissue sarcomas in the lower extremity among 744 sarcoma patients between 1980 and 1996. Mean age at presentation was 42.9 years (range 6–­80 years), with 38 patients being previously operated elsewhere. Eighteen patients had 2–­9 recurrences. Still, in 81 patients

(95.3%) an R0 resection with curative intention could be performed, whereas 4 patients underwent a palliative resection due to multilocular distant metastases. In 41/­ 81 patients extensive tissue defects resulted after the resection and 17 local and 24 free flaps were needed for closure. Thirteen patients received a simultaneous tendon transfer with defect closure to improve their gait. In 18 patients with local skeletal infiltration, special plastic surgical bone reconstructions, conventional partial foot amputations, or atypical hindfoot amputations were done. All of these patients received individualized orthopedic shoe and inlay adaptions and finally achieved (with and without these shoes) a better gait and ability to do sports, in comparison with patients who received lower leg prostheses. In 2 patients, a transtibial amputation was inevitable. In this group of 85 patients, a mean survival of 132 months and a 5-­year survival rate of 62% was found.7 The Finnish experience, with 73 patients with lower limb soft-­ tissue sarcomas who received limb-­ salvage surgery, reports a 5-­year local recurrence-­free survival rate of 82%, a metastasis-­free survival of 59%, a disease-­free survival of 56%, and a disease-­specific overall survival of 70% over a follow-­up time of 65.9 months. Three-­quarters of the patients were able to walk normally or had only minor walking impairment. They emphasize that microsurgery is an essential part of modern tumor surgery.60 Long-­term survivors have a higher probability of experiencing both sequelae of their primary plastic surgical treatment (i.e., contractures, bulky flaps, and unstable scars) and secondary malignomas (i.e., postradiation angiosarcomas). A large study from an interdisciplinary sarcoma center in Germany had a mean follow-­up of 36 months for 167 patients with extremity liposarcomas. Over this time, only 5 (3%) of the patients had to undergo amputation throughout this period. A clear margin R0 resection could be achieved in 158 patients. The authors report an overall 5-­year survival rate of 79%, though the study collective was biased in favor of extensive and previously operated cases due to the reference center status of the clinic. Patients with primary tumors had a 5-­year

Table 4.4  Prognostic factors in soft-­tissue sarcoma therapy

Factor

Distant recurrence-­free survival

Local recurrence-­free survival

Relapse-­free survival

Disease-­specific survival

Age >50 years

–­

–­

–­

–­

Recurrent sarcoma

–­

–­

–­

–­

Size >5 cm

–­

–­

–­

–­

Deep location

–­

High-­grade

–­

–­ –­

Proximal position

–­ –­

Histology Fibrosarcoma

–­

Leiomyosarcoma

–­

Positive microscopic margin

–­

–­

–­

–­

–­

–­

Time period of treatment Minus symbols indicate an independent adverse prognostic factor, and blank fields indicate a non-­independent prognostic factor. (Adapted from Weitz J, Antonescu CR, Brennan MF. Localized extremity soft tissue sarcoma: improved knowledge with unchanged survival over time. J Clin Oncol. 2003;21: 2719–­2725.)

Outcomes, prognosis, and complications

survival rate of 90%, and an overall number of 37 local recurrences were found. The myxoid liposarcoma was responsible for most recurrences. Patients with recurrent tumors had a 5-­year survival rate of 69%.42

Bone sarcomas The European Osteosarcoma Intergroup reports a 57% 5-­year survival rate in a patient group of 202 patients with a 49%–­ 85% limb salvage rate. An important finding of this study was that patients having undergone limb salvage surgery with later local recurrence had a slightly better survival rate than primarily amputated patients (37% vs. 31% at 5 years).15,16 Marulanda et al. stated that for osteosarcoma patients there is no difference in survival between amputations and properly performed limb-­salvaging procedures. Carty et al. reported their results after LSS of 20 intra-­ articular knee osteosarcoma patients and their reconstruction with endoprostheses. Evaluation was done by MSTS and TESS scores, and moderate to high function was achieved.67 A Norwegian study, involving 118 patients with osteosarcomas or Ewing sarcoma in the extremities, evaluated the long-­term functional outcome at a minimum of 5 years after treatment. The function was evaluated with the MSTS and TESS scores while quality of life was assessed using the Short Form-­36 (SF-­36). The mean age at follow-­up was 31 years (15–­ 57 years), and the mean follow-­up was 13 years (6–­22 years). A total of 67 patients (57%) initially had limb-­sparing surgery, but 4 had a secondary amputation. The median MSTS score was 70% (17%–­100%), and the median TESS was 89% (43%–­ 100%). The amputees had a significantly lower MSTS score than those with limb-­sparing surgery (p  4 ribs > > 5 cm diameter

Soft-tissue defect

Bone graft mesh

Latissimus dorsi Serratus anterior Rectus abdominis External oblique Omentum

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CHAPTER 11  • Reconstruction of the chest

Algorithm 11.2 Medical optimization

Systemic medical conditions • Stabilized from acute trauma and/or infection • Determined optimal timing of chemotherapy and/or radiation therapy • Smoking cessation > 4 weeks pre-operatively • BMI < 30 • Discussion of stopping steroids and other immunosuppressants

Glycemic control • Hemoglobin A1c < 6%–7% • Perioperative glucose < 200 mg/dL

Nutrition • Pre-albumin > 15 mg/dL • Albumin > 3.5 g/dL • Transferrin > 200 mg/dL

Wound bed optimization

Infection Trauma • Grossly rid of nonviable soft tissue and bone • Critical structures repaired

• Grossy rid of nonviable soft tissue and bone • Quantitative tissue culture < 105 organisms/gram • Infected prosthetics removed/exchanged if possible

Cancer • Grossly rid of nonviable soft tissue and bone • Negative pathologic margins

Algorithms for medical optimization prior to chest wall reconstruction.

evaluated for cancer recurrence and for osteomyelitis. Sternal and rib non-union should be managed with debridement of the non-union site to healthy, pinpoint bleeding, creating sites amenable for new osteosynthesis. Infected chest wall wounds should be debrided until the wound bed looks grossly healthy and non-infected. Tissue cultures should be taken at time of initial washout and following subsequent debridements to tailor antibiotics. The infectious disease team should be consulted to guide antibiotic choice and duration of treatment. There is debate on the importance of staging closure versus single-stage debridement and closure. On one hand, attempting immediate closure of an infected wound is counterintuitive, and allowing a second look to debride and having the culture data help guide the clinical decision on aggressiveness of the next debridement goes in favor for staged closure. On the other hand, several reports have been published that there may not be a significant difference in rates of re-operation and mortality between single-stage and multi-stage closures or between closure over positive or negative wound cultures.64–66 Best practice is to look at each case individually and not adopt a rigid over-arching algorithm. If there is gross purulence or necrotic tissue at time of initial debridement, fluid surrounding bone or

prosthetics, cultures positive for more virulent or drug-resistant organisms, or in patients with comorbidities that pre-dispose to infection or poor healing (smokers, diabetics, ESRD, immunocompromised, malnourished, etc.), it is reasonable to stage closure and temporize the patient with dressings or negative pressure wound therapy (NPWT). An otherwise healthy patient with a wound that is not grossly infected or necrotic may be considered for a single stage debridement and closure. The soft-tissue components of the wound should be sharply debrided until the entire wound surface demonstrates pinpoint bleeding. If the sternum or ribs appear infected, a sample should be sent to evaluate for osteomyelitis, as that will impact duration of postoperative antibiotics. In patients with sternotomies, the medial edges of the sternum should be debrided until pinpoint medullary bleeding is observed. The infected bone must be debrided, but it is important to do so judiciously to allow for the possibility of later sternal fixation. A radical bony debridement is often not necessary, as sternal salvage can be safely achieved using a combination of sound clinical assessment of the viability and vascularity of the bone with or without a bacteriologic assessment of the infected bone.62 If using quantitative bacteriologic assessments, a bacteria load greater than 105 organisms per gram of

Skeletal reconstruction

tissue should be considered not ready for closure.15 Any obviously infected or colonized wires, plates, and screws should be removed. If the infection involves any mediastinal structures, debridement should be performed alongside the cardiothoracic surgery team. If other cardiopulmonary prosthetics, such as VADs, grafts, etc., appear to be infected, a discussion should be made with the patient and cardiothoracic surgery team about the role for exchange. The literature is inconclusive regarding the benefit of device salvage versus exchange, and the decision should be made in a case-by-case fashion. Following the debridement, the wound should be thoroughly irrigated, making sure to use warm, physiologic-temperature solution so as to not cause arrhythmias. The team should consider switching gloves and setups following irrigation. In patients undergoing staged debridements, one should strongly consider treating the wound with NPWT over conventional dressing changes. The wound vac is easier to manage on the floor or ICU, does not require nursing or physician-driven bedside dressing changes, and prevents additional contamination of the wound by other nosocomial organisms. Studies have demonstrated that NPWT, when compared to traditional dressing changes, is associated with decreased time to definitive closure, decreased risk of recurrent infections, and decreased hospital stay.67,68 One review did raise some concerns with NPWT as a bridging treatment, citing risks of ventricular rupture, cardiac arrhythmias, and retained sponges as potential complications.69 To minimize the risk of the potential wound VAC-associated complications, one should first apply the less-adherent V.A.C. WHITEFOAM sponge onto any of the mediastinal structures. Furthermore, NPWT with instillation has been demonstrated, though not specifically with infected chest wall wounds, to be superior to traditional NPWT.70,71 Saline is the conventional fluid for instillation, but antimicrobial solutions such as acetic acid,

A

B

Figure 11.5 (A,B) Cerclage parasternal wires to assist with sternal plating.  

335

sodium hypochlorite, hypochlorous acid, etc. may also be used to decrease bioburden of the infected wounds.

Skeletal reconstruction Sternal fixation Unless the sternum is entirely resected or debrided away, the sternal edges should be fixated together for optimal cardiopulmonary biomechanics and function. The two most common methods of sternal fixation are cerclage wiring (CW) and rigid plate fixation (RPF). The vast majority of sternotomies are closed with CW. This method of fixation is performed using 6- to 8-gauge stainless steel wires. Peri-sternal or parasternal wires are placed in the intercostal spaces at the lateral border of the sternum (Fig. 11.5). Trans-sternal wires are passed through the anterior and posterior tables of the sternum, approximately 1 cm in from the lateral edge. Parasternal and trans-sternal wires are most commonly placed in simple, interrupted fashion, but can be placed in figure-of-eight fashion spanning one or more rib spaces. The advantage of figure-of-eight sutures is that they increase the surface area of wire that is in contact with the sternum and increasing the length of bone which the wire would have to cut through to tear as the shearing forces are oblique as opposed to perpendicular. Double-stranded wires can be used to theoretically provide greater fixation while providing more resistance to transverse sternal fractures. The Robicsek weave technique involves running a single wire parasternally along one hemisternum from manubrium to xiphoid, alternating anterior and posterior to the costal cartilages, and then running it back up to be tied at the manubrium.72 After

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CHAPTER 11  • Reconstruction of the chest

placement of all wires, heavy clamps should be placed on each, so that the wires can be pulled vertically up to reduce the sternal edges. This can be facilitated using bone-reducing clamps. Once the sternal edges are brought together, the wires should be tightened by twisting the two ends of the wires to the endpoint where the sternal edges are together without gapping but prior to the wires cutting into the sternum. The strength of CW fixation is dependent on the breaking strength (gauge) of wires used, number of wires, location of wires, and the tightness and applied stress when tightening the wires. A general rule-of-thumb to follow is use one wire for every 10 kg of patient weight. A minimum of seven wires should be used as using six or fewer wires is associated with increased risk of deep sternal infections.73 The wires should be placed along the vertical length of the sternum, particularly the manubrium and caudal body and xyphoid area. With regard to technique of placement, simple vs. figure-of-eight, and single vs. double wires, there is no clear-cut best wiring technique, and a case-by-case decision should be made.74 CW has the benefits of low expense, expedient closure, provides circumferential compression, and are easy to remove in re-operations. The major disadvantage is that cerclage wiring does not provide rigid fixation – allowing some motion and separation at the fracture site under normal physiologic loads – and therefore is associated with non-union and infection rates of about 5% among all sternotomies and up to 15% in high-risk patients.17,47,75 Sternal bands and polymer cable ties made of poly-ethyl-ether-ketone (PEEK) are alternatives to CW. They are similar in the sense that they do not provide rigid fixation and instead try to force the medial edges together. Both have the advantage over CW of being wider and stronger, theoretically providing a more stable fixation and decreased risk of cutting through the sternum.74 The primary alternative to CW is RPF with titanium plates and screws (Fig. 11.6, Video 11.1 ). Rigid, loading bearing fixation is the preferred means of bony fixation in other parts of the body because of its superiority in achieving osteosynthesis. RPF was initially performed using mandibular

A

B

reconstruction plates with bicortical screws that required pre-drilling. These initial hardware systems, in addition to being more expensive than CW, were challenging to customize and contour to individual sternums, ran the risk of damaging underlying mediastinal structures when drilling, and delayed opening the sternum in cases of emergent re-operation. Modern sternal plating systems include SternaLock, Talon, LactoSorb, and Flexigrip. As an example, the SternaLock system uses low-profile, 1.6 mm titanium plates and 2.4 mm screws that are threaded to grip the cancellous medullary bone, engage the posterior cortex, and lock into the plate at a 90° angle. The screws are self-drilling, and the length of the needed screw can be measured using the depth gauge while the sternum is still in discontinuity, which allows for proper screw capture of the posterior table without fear of drilling into the mediastinum. The thickness of the sternum can also be measured preoperatively on CT. The set comes with multiple plate designs, all of which are two-sided and bendable to allow for patient-specific contouring. The most common construct is use of a single 4-hole L plate for the manubrium and two 8-hole X plates for the superior body and inferior body. These plates are designed to be cut in the middle with standard wire cutters that would be used to cut the wires used in CW in cases of emergent re-entry into the chest. The screw holes can be salvaged by using 2.7 mm emergency screws. The newer SternaLock 360 set also includes a cerclage band that locks into the plate and adds circumferential osteotomy compression on top of the rigid fixation provided by the plate. Prior to plating the sternum, the sternum needs to be reduced using bone-reducing forceps and/or selectively placed wires. The sternal thickness at the manubrium and along the length of the body should be measured first to allow for proper screw length selection. After reducing the sternum, the pectoralis major should be dissected off the anterior portion of the sternum. The plating system can then be applied. The stability of the sternum should be manually tested. Cerclage wires may be left in if they provide additional stability.

Figure 11.6  Sternal non-union (A) treated with removal of cerclage wires and placement of sternal plates (B).

Skeletal reconstruction

A human cadaver study demonstrated that the amount of intrathoracic pressure required to create a 2 mm sternal separation was 355 mmHg in cadavers treated with rigid plate fixation compared to 183 mmHg in cadavers treated with cerclage wiring.76 Additional studies have demonstrated a biomechanical advantage of rigid fixation over cerclage wiring.77 Because the sternal plates take the weight-bearing load off of the sternum, more osteoporotic or damaged but potentially salvageable bone, that otherwise would not hold cerclage wires, can still be plated. Multiple studies have demonstrated excellent sternal union rates with primary sternal plating. Raman et al. looked at cardiac patients with three or more risk factors for mediastinitis and demonstrated that the 320 patients treated prophylactically with RPF had lower rates of mediastinitis (0% vs. 13%) and perioperative deaths (3.8% vs. 8.6%) compared to 215 patients treated with CW.18 Sinno et al. found that patients treated with RPF, compared to patients left in sternal discontinuity, had significantly less sternal pain (11% vs. 67%), sternal instability (11% vs. 25%), time in the ICU (1.5 vs. 7.5 days), and time intubated (0.8 vs. 2.2 days).78 Allen et al. conducted a randomized controlled trial featuring 116 patients treated with RPF and 120 patients treated with CW. They found the RPF cohort had significantly better sternal pain, improved quality of life, and decreased overall healthcare costs.44 The RPF cohort also had significantly greater sternal healing and union rates at 3 and 6 months as determined by blinded, radiologist-driven CT analysis.79 80% of patients treated with RPF achieved radiographic union compared to 67% of patients treated with CW.79 The rate of cumulative 6-month complications including superficial wound infection, deep wound infection, and painful non-union was 0% in the rigid fixation group, compared to 5% in the CW group.79 The cumulative 6-month healthcare costs were similar between the two groups: 32,439 vs. 34,085 USD.79 Raman et al. randomized 140 “high-risk” patients, defined as those with two or more risk factors for sternal wound complications, to RPF or CW. 70% of patients treated with RPF achieved radiographic union at 6 months, compared to 24% of patients with CW.80 The RPF group also had lower patient-reported pain.80 Use of sternal plating systems is still met with some resistance because of the increased time and cost relative to wiring, the relative rarity of sternal non-union in comparison to nonunion of other fractures, and the fact that it takes more time to remove the plating systems in case of emergent re-operation.81 Although the upfront cost of the plating system is greater than that for wiring, when taking into account the costs associated with postoperative complications, rigid sternal fixation was found to have a significantly lower overall cost of care by nearly 10,000 USD.17 A meta-analysis of 427 patients in randomized controlled trials and 1025 patients in cohort studies demonstrated no overall difference in infection rates between RPF and CW.82 However, secondary analyses looking at patients with multiple risk factors for complications demonstrated the RPF was associated with a 77% risk reduction in sternal complications compared to CW.82 Any patients referred to plastic surgery for sternal reconstruction should be viewed as high risk for wound complications regardless of etiology. While the decision of how to best prophylactically fixate the sternum is up to the cardiothoracic surgeon, there is strong evidence in favor of RPF over CW in both clinical and patient-reported outcomes.

337

Management of sternal defects Large chest wall tumors that involve the sternum and severe chest wall trauma and infections that require total or sub-total resection of the sternum can result in bony defects that are too large to allow for primary union. If the defect includes the articulating costal cartilages or the clavicles, it is impor­ tant to reconstruct those components in addition to the sternal defect. Strengthening or re-creating the sternoclavicular joint is important to maintain chest wall integrity with upper extremity movements. Options include autologous grafts and flaps, cadaveric grafts, biologic scaffolds, and prosthetics. Though no large comparative studies have evaluated outcomes between the options, each has its purported benefits, and selection is ultimately up to surgeon comfort and specific patient characteristics. Bony autografts are a valid option in patients with sternal defects from tumor resection, while patients with sternal defects as a result of deep sternal infections often have comorbidities or are too acutely ill to consider an additional donor site. Iliac crest is among the most commonly reported donors.83–85 A non-vascularized segment of the inner table of one or both of the iliac crests can be harvested and then secured to the edges of the sternal defect using wires or plates. The natural curvature of the inner table allows it to provide a concave sternum, providing more space and better contour to the chest wall. Piotrowski et al. described their technique of harvesting 7 × 5 cm inner table iliac crest grafts from both sides, suturing the two grafts together, and using the graft to reconstruct total sternal defects.86 Cancellous iliac crest bone graft with sternal plating can be used to treat sternal non-union.87 Autologous rib can be harvested, and various osteotomies can be made to customize the length, width, and thickness of the bone graft to fill the defect.88 Rib has the benefit of easy access at the same surgical site but the risk of destabilizing the thoracic cage, so one must carefully plan the number and size of rib graft taken. Vascularized bone flaps are an option for healthier patients who may benefit from a more robust and larger bony reconstruction. Options include vascularized iliac crest, fibula, and scapula.89 The internal thoracic vessels, which should be easily accessible, can be used for vascular inflow and outflow. Other options, which are farther away and require either greater pedicle dissection or interpositional vein graft, include the subscapular, lateral thoracic, and thoracoacromial systems. Cadaveric sternal or fibular allograft can be considered in patients who may not tolerate or want a donor site procedure but want the benefits of a biologic construct.90–93 Transverse plates are used to fixate the allograft to the remaining right and left hemi-sternums or to the ribs. A minimum of two transverse plates should be used. The osteotomy sites can be reinforced with cancellous bone autograft or allograft. Kalab et al. used this technique in 10 patients with large sternal defects from deep sternal wound infections and, despite medical complications in some patients, reported good chest stability in all 10 patients.90 Biologic meshes made of porcine acellular dermal matrix (ADM) have also been used to reconstruct sternal defects (Fig.  11.7).94 While theoretically infection-resistant and promoting tissue ingrowth, these meshes do not have the same rigidity and structural support as prosthetic meshes. There is also hesitation to use these meshes because of potential herniation of mediastinal contents into the bony defect once

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Figure 11.7  (A–C) Use of biologic mesh to reconstruct sternal and anterior rib defect and coverage with vertical rectus abdominis flap (VRAM) flap.

the mesh incorporates. The ADM can be anchored to the surrounding ribs and sternum using fiberwire suture screws and additionally to deep fascia using sutures. Multiple alloplastic materials have been used to reconstruct bony defects. The ideal prosthetic is malleable enough to be contoured to fit the defect while rigid enough to prevent paradoxical chest wall motion. It should be physically and chemically inert and allow for ingrowth of native tissue to reduce the risk of infection. The prosthetic should be radiolucent to minimize interference with postoperative imaging and radiation therapy, given that the most common indication for the use of these prosthetics is in tumor resection. Polypropylene (Marlex) mesh, expanded polytetrafluoroethylene (ePTFE, Gore-Tex) mesh, polyester fiber (Mersilene) mesh, titanium mesh, and methyl methacrylate are some of the most common prosthetics used to reconstruct sternal defects.95–107 Polypropylene mesh is highly malleable and allows tissue ingrowth but is not very rigid. Gore-Tex is a double-sided mesh with a smooth, inert side that can be placed against the mediastinal structures and an indented, microporous side to better facilitate overlying vascularized tissue adhesion and ingrowth. Titanium mesh is more rigid and osteoconductive than polypropylene but not as malleable. Methyl methacrylate is the most rigid but difficult to mold to fit the defect and carries the risk of thermal injury. Sandwich techniques have been described which position methylmethacrylate or stainless steel between polypropylene mesh, such that the methylmethacrylate or steel rigidly fills the bony void, while the mesh can be positioned anterior and posterior

to the bony margins and secured using sutures.101–104 Acellular dermal matrix can also be used as part of the sandwich and is best positioned on the mediastinal side. When placing the mesh, 1–2 cm of mesh should overlap the healthy bony defect edges. These prosthetics can be secured to the edges of the bony defect using cortical screws, transosseous steel wires, or sutures. If the sternoclavicular joint is unstable, the mesh can be wrapped around the clavicle prior to securing to the ribs or sternum, recreating the effects of the stabilizing ligaments.108 Most studies have reported reasonable clinical outcomes with high rates of chest wall stability and low rates of infection, but the literature is lacking in robust outcome metrics and comparative studies.95–107 Customized 3D-printed titanium implants can be constructed using CT imaging and CAD software to fill a planned defect following surgical resection of a chest wall tumor.109–112 These implants can be designed to replace the sternum and the medial edges of the ribs and then the overlapping titanium implant can be fixated to the healthy ribs or residual sternum with screws. More recently, customized carbon fiber or hybrid titanium and porous polyethylene implants have been used with the purported benefits of better facilitating tissue ingrowth and less interference with postoperative imaging and radiotherapy.113,114 These implants can be designed with holes for screws, wires, or sutures to fasten the implant to native ribs and sternum. Several tissue-engineered constructs have been developed to repair or regenerate bony defects. Those that have been attempted for sternal wounds include poly-L-lactic acid,

Skeletal reconstruction

calcium hydroxyapatite, tricalcium phosphate, and various scaffolds combining those materials with autologous osteogenic cells.115 The lack of current outcome data has prevented the widespread use of any of these biologic constructs. There are little data in the literature regarding comparative efficacy or relative complications between the many options for bony defect reconstruction. One should consider overall and acute health of the patient to determine if subjecting the patient to another donor site for autologous reconstruction is viable. Infected wounds always perform better with autologous or biologic materials over synthetic prosthetics. Treatment of sternal non-union involves creating fresh osteotomy sites with pinpoint medullary bleeding on either hemisternum along the length of the original non-union. The sternal edges should be reduced and plated together. Placement of autologous and cadaveric cancellous bone graft can promote sternal union.

Rib fixation Principles of rib fixation will be briefly discussed as management of acute rib fractures is typically performed by trauma or cardiothoracic surgeons, and thoracotomies are performed with partial rib resection as opposed to opening osteotomies. The clinical significance of rib fractures increases with the number of ribs involved, as increasing number of ribs fractured is associated with increased risk of pneumonia, respiratory compromise, and mortality.116 This risk increases when multiple adjacent ribs are fractured in two or more places, creating a flail chest. Prompt, appropriate identification and management of these fractures is critical as operative fixation is associated with decreased time on the ventilator, need for tracheostomy, risk of pneumonia, and mortality in the correct patient population.116 Indications for operative management include three or more displaced rib fractures, flail segment including sternal flail or fractures, or in patients who require a thoracotomy or VATS for another indication. Otherwise, the vast majority of rib fractures can be managed nonoperatively with pain control and incentive spirometry. The major complications of nonoperative management are non-union and intercostal nerve entrapment leading to chronic pain and disability.117 The skin incision should be designed to allow access to all the fractured ribs. Elevate subcutaneous flaps to expose the chest wall musculature. The muscle fibers should be split and retracted parallel to the direction of the fibers. The fracture site should be exposed while minimizing stripping of the intercostal attachments and periosteum to preserve blood supply to the fracture. The thickness of the rib should be measured to prevent drilling into the pleura. The rib edges should be brought into reduction and held with clamps. The fracture site can also be accessed minimally invasively using a videoassisted approach. Multiple plating systems exist including RibFix Blu MatrixRib, RibLoc U Plus, etc. Most plating systems use low-profile, approximately 1.6 mm thick titanium plates, with some sets having pre-set 8-, 12-, 16-, and 24-hole plates and others having a universal 8-hole plate as well as custom plates for each rib. Some plates have a U-shaped design on the ends which will capture the anterior and posterior edges of the ribs, allowing for easier fracture reduction. Some sets have 2.4-mm self-drilling locking screws designed to capture cancellous

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bone, while others require pre-drilling, which comes at the risk of injuring the pleura.

Management of rib defects Rib defects large enough to hinder respiratory biomechanics should be reconstructed. As a general rule of thumb, patients with a resection of four or more ribs or defects with a diameter of 5 cm or greater should undergo skeletal reconstruction because of the risk of flail chest and/or lung herniation. This rule is more of a guideline, as the most important question to assess is whether or not the thoracic cage is stable. Defects that are located more posteroaxially or superiorly do not affect respiratory function as much because of the support provided by the scapula and shoulder girdle. Defects up to 10 cm in diameter in the apical posterior chest wall have been described to not significantly alter pulmonary function.118 Patients who have undergone or will undergo radiation can also tolerate greater larger defects as radiation-induced fibrosis of the soft tissues provides more chest wall rigidity. Salo and Tukiainen presented 135 patients undergoing chest wall reconstruction following oncologic resection over a 19-year period, and they had lower thresholds for bony reconstruction.119 For anterior or anterolateral defects of one to two ribs, they performed a mesh-only reconstruction, and for anterior or anterolateral defects of three or more ribs, they performed a methyl methacrylate mesh sandwich reconstruction.119 Inferior and posterolateral rib defects generally did not undergo reconstruction.119 Traditionally, rib defects were reconstructed with autologous tissue. Bone grafts from other ribs, iliac crest, and fibula can be used to span the defect and stabilized with sutures, steel wires, or plates and screws. Fascial grafts are another option, with donor sites including the tensor fascia lata and dura. The downside is while the fascia is initially rigid, it tends to become more flaccid overtime, leading to chest wall instability. Cadaveric bone grafts and skin substitutes have also been reported, but autologous bone and synthetic meshes are more favorable (Fig. 11.8). Human alloderm has been use to reconstruct large defects. There is a risk of thoracic bulges or hernias given the bioprosthetic’s tendency to remodel, but paradoxical chest wall motion has not been reported even when used to reconstruct large defects. Xenograft meshes such as Surgigis (small intestine submucosa), Permacol (porcine dermis), Strattice (porcine dermis), CollaMend (porcine dermis), or bovine products such as Tutopatch (pericardium) and SurgiMend (dermis) have all be trialed. These bioprosthetics better promote native tissue ingrowth, making them more resistant to infection and useful in contaminated fields. Giordano et al. found that patients reconstructed with synthetic mesh had a 33% rate of surgical site complications compared to a 16% rate for patients treated with ADM.120 Alloplastic reconstruction is now the most common method of rib reconstruction. Aside from cost, these implants have no donor site morbidity, are available off the shelf, and do not add additional operative time. As with alloplasts used for sternal reconstruction, the ideal prosthetic is inexpensive, easy to use, rigid enough to provide stability while flexible enough to be molded to the defect, inert, promotes vascularized tissue ingrowth, and radiolucent. Meshes include those made of polypropylene knitted meshes (Marlex, Prolene), polyester (Mersilene, Dacron), polyglycolic acid, expanded polytetrafluoroethylene (e-PTFE, Gore-Tex), polydioxanone (PDS),

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polyglactin (Vicryl), PTFE and carbon (Proplast), and stainless steel. The meshes should be contoured to provide 1–2 cm of overlap in all directions and secured with sutures, screws, or wires while under tension. Securing these flexible meshes under tension is important to prevent warping during respiration. Bicortical holes in the ribs can be made using a drill or penetrating clamps to allow for suture passage. The mesh can be positioned on the anterior (onlay) or posterior (underlay) aspect of the defect. The anesthesia team should be asked to expand the lungs with PEEP to a normal tidal volume to best determine the size of the defect that needs to be reconstructed. More rigid constructs can be created with sandwich techniques whereby polymethylmethacrylate (PMMA), silicone, rubber, carbon fiber, etc. is positioned between two pieces of mesh. The rigid component should be designed to fit exactly into the defect or slightly smaller so as to not create a restrictive effect on pulmonary function, while the mesh should be

Figure 11.8  Use of synthetic mesh to reconstruct diaphragmatic defect (A), biologic mesh to reconstruct rib defect (B), and covered with free ALT flap (C,D).

designed with a 1–2 cm overlap. The rigid component can be molded in situ or on the back table. If using PMMA in situ, be sure to irrigate continuously to avoid thermal injury. Lardinois et al. reported that 92% of patients with anterolateral chest wall defects treated with a Mersilene–PMMA–Mersilene sandwich had concordant chest wall motion according to cine-MRI, while 8% demonstrated rigidity and 0% with paradoxical movement or implant dislocation.121 Weyant et al. found that patients undergoing mesh-only and rigid mesh composites had similar respiratory outcomes and rates of complications; defect size was the more significant predictor of complications.122 While the meshes are permeable, the rigid PMMA, silicone, etc. constructs are not. A permeable prosthetic better prevents seromas but comes at the downside of difficulty controlling the pleural space and pleural fluid. The rigidity of the PMMA can also cause increased pain and higher rates of infection.

Soft-tissue reconstruction

Stainless steel or titanium bars and plates can be used to span the rib defects, providing skeletal continuity between the resected edges. Coonar et al. described their technique using STRATOS titanium rib bridges, which is a construct of a rigid, size-adjustable connecting bar that attaches to the remaining cut ends of the rib via clips that crimp to the posterior surface of the ribs.123 These bar-rib constructs can be further bolstered by securing a mesh to the posterior surface of the surrounding ribs.124,125 Rare and more novel reconstructive options include custom-designed 3D-printed ribs or tissue-engineered ribs from autogenous mesenchymal stem cells obtained from bone marrow seeded into processed rib cadaveric allografts.126,127 Wang et al. reconstructed 10 rib tumor defects with 3D printed PEEK implants and reported no complications with only a 14% decrease in postoperative pulmonary function.128 There is little data comparing all the possible reconstructive options. Our approach is to fasten ADM under tension to the posterior surface of the thoracic cage, providing a nice biologic covering over the pleura, followed by a semi-rigid titanium mesh. Management of rib non-union involves creating fresh osteotomy sites to have adjacent, healthy, bleeding bone edges. The rib edges should be brought into reduction and fixated using plates and screws. Autologous or cadaveric cancellous bone graft can be placed if the defect is small enough.129–131 Another option is to resect the non-union site, leaving a large enough gap to reduce the pathologic rib movement and risk of nerve entrapment.131

Soft-tissue reconstruction Superficial wounds without exposed bone, prosthetics, or other critical structures may be treated nonoperatively with wound care or with operative debridement and closure. One study comparing nonoperative and operative treatment of superficial chest wall wounds demonstrated no difference in wound complications or infections but significantly decreased time to complete healing and hospital visits with the operative group.132 The decision whether to treat operatively or nonoperatively should be discussed with the patient and dependent on factors such as size of the wound, patient’s comorbidities, patient’s ability to perform wound care, and patient’s preference for quicker wound healing versus the added risks of anesthesia. Deeper wounds, those with exposed bone, prosthetics, or other critical structures, significant dead space, or in patients with risk factors for wound complications should be treated aggressively with robust soft-tissue coverage. The soft-tissue flaps must be well-vascularized, cover the critical structures, obliterate deadspace, and minimize donor site morbidity. Use of regional chest wall muscles for reconstruction is well-­ tolerated without significant morbidity. Reconstruction using the accessory muscles of respiration – pectoralis, scalenes, sternocleidomastoid, rectus abdominis, obliques – has no well-documented negative effect on inspiration.133

Pectoralis major Pectoralis major is a broad, fan-shaped muscle overlying the superior portion of the anterior chest wall (Fig. 11.9). The

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clavicular head originates from the anterior surface of the medial half of the clavicle. The sternocostal head originates from the anterior surface of the sternum, the superior six costal cartilages, and the aponeurosis of the external oblique. The muscle fibers converge to a flat tendon that inserts into the superomedial humerus in the bicipital groove to flex, internally rotate, and adduct the humerus. This muscle also serves as the foundation for the female breast. It has a dual blood supply from the axillary artery and the internal mammary artery. The muscle receives a dominant pedicle from the pectoral branch of the thoracoacromial artery. After the thoracoacromial artery pierces the clavipectoral fascia, it divides into its four branches, and the pectoral branch enters the deep surface of the pectoralis major, encased in the fascia separating it from the pectoralis minor, at the junction of the lateral and middle third of the clavicle. The pectoral branch further divides to form intramuscular arterial arcades with the lateral thoracic artery and the intercostal branches of the internal mammary artery. The lateral thoracic artery branches off the axillary artery just posterior to the pectoralis minor and pierces the clavipectoral fascia lateral to the pectoralis minor and then runs in the same plane as the pectoral branch. In some people, the lateral thoracic artery is the dominant blood supply to the pectoralis major.134 Segmental pedicles from the IMA traverse the intercostal spaces to supply the sternocostal head of the pectoralis major. These vessels then anastomose with branches of the pectoral branch and lateral thoracic within the muscle. The pectoralis major can be advanced and/or rotated based on the pectoral branch of the thoracoacromial artery (Fig. 11.10). The medial sternocostal attachments of the pectoralis should be released while staying on top of the ribs. The vertically oriented segmental pedicles from the IMA should be clipped in the intercostal spaces. After all the medial muscle fiber origins are released, one enters an avascular plane between the pectoralis major and the underlying ribs, intercostal muscles, and pectoralis minor laterally. The pectoralis advancement flap is most commonly used to cover sternal wounds in combination with a contralateral pectoralis advancement flap, pectoralis turnover flap, or any other flap. If sternal continuity is able to be achieved, bilateral pectoralis advancement flaps can be raised to provide a tensionless muscle layer closure over the sternum. To maximize medial advancement, the deep dissection plane can be developed underneath the pectoralis major laterally all the way to the lateral chest wall subcutaneous fat. Skin flaps can be raised, if needed, off the muscle fascia to achieve a tensionless skin closure. With just dissection off the rib cage, the pectoralis advancement flap is typically insufficient to cover wounds of the inferior one-third of the sternum – where the muscle fibers peter out as it runs confluent with the external oblique fascia – or to obliterate deadspace in the mediastinum in patients left in sternal discontinuity. To cover inferior sternal wounds, release of the inferior attachments of the sternum can be continued inferiorly to include the anterior rectus sheath to allow for mobilization of the abdominal wall to cover any exposed inferior sternum or VAD prosthetics. Inferior coverage and/or filling of the mediastinum can be achieved by releasing the pectoralis’s attachments to the clavicle and the external oblique aponeurosis and then making a separate incision in the deltopectoral groove to release the insertion on the humerus. This may also reduce the risk of

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Figure 11.9  Pectoralis major muscle flap vascular anatomy.

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Figure 11.10  (A,B) Bilateral pectoralis major muscle flap advancement for sternal coverage.

Rectus abdominis

mechanical dehiscence if the patient attempts to contract the pectoralis major postoperatively. The pedicle can be dissected all the way to the origin of the thoracoacromial artery to create an islandized muscle flap. The muscle can then be fully rotated to cover defects of any portion of the sternum, fill in deadspace between the sternal edges, or be used to wrap around vascular grafts or other prosthetics.135 The pectoralis can be turned over based on the segmental pedicles from the IMA. The pectoralis turnover flap requires an intact ipsilateral IMA, which oftentimes is harvested in cardiac bypass procedures or may be damaged by the infection, trauma, or tumor. An incision in the deltopectoral groove is made to release the insertion off the humerus, which enables use of the entire muscle for coverage. Alternatively, a counter incision in the lateral anterior chest can be made to divide the muscle vertically, leaving some muscle still attached to the humerus. The dissection occurs in the same plane, between subcutaneous tissue and muscle fascia anteriorly and between the pectoralis major and the pectoralis minor, ribs, and intercostal muscles posteriorly. Dissection should stop a couple of centimeters from the lateral edge of the sternum to protect the segmental pedicles. When turned over, the pectoralis major can be rotated to cover the full length of the sternum or placed between the sternal edges, if the sternum is left in discontinuity. The muscle can be split into superior and inferior halves in the direction of the muscle fibers. This allows each half to be rotated, independently. When combined with a contralateral

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pectoralis advancement flap, the entire length of the sternum can be covered. The pectoralis major is a very versatile muscle, and one can take advantage of its dual and robust vascular anatomy to design flaps, using one or both muscles, to cover nearly any sternal defect. The pectoralis advancement flap is generally well tolerated with minimal donor site morbidity if the insertion is maintained. The pectoralis turnover flap comes with the aesthetic loss of the anterior axillary fold. From the head and neck cancer literature, the pectoralis turnover or significant rotation of the pectoralis advancement can lead to decreased shoulder function.136

Rectus abdominis The rectus abdominis is a long, flat, paired muscle of the anterior abdominal wall (Fig. 11.11). It originates from the pubis and inserts onto the costal cartilages of the 5th to 7th ribs and the xiphoid to power trunk flexion. The paired muscles are joined in the midline by the linea alba. Additional tendinous intersections subdivide each muscle transversely. The muscle has two dominant pedicles, the superior and deep inferior epigastric arteries, and receives additional blood flow from the intercostal arteries.137 The IMA divides into the musculophrenic artery, which courses inferolaterally and branches to

Superior epigastric artery

Inferior epigastric artery B A

Figure 11.11  Rectus abdominis muscle flap vascular anatomy.

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form choke anastomoses with the intercostal arteries, and the superior epigastric artery. The superior epigastric artery exits the mediastinum between the xiphoid and the diaphragm and descends on the posterior aspect of the costal margins of the inferior ribs before entering the posterior aspect of the rectus sheath. There is some variability, but the superior epigastric artery typically has two parallel branches, which may branch before or after the artery enters the muscle, and the pedicle may enter intramuscularly early or run for some distance along the deep surface before entering the muscle. The branches of the superior epigastric artery anastomose with the ascending intramuscular branches of the deep inferior epigastric artery. The costomarginal artery is an intramuscular arterial arcade connecting the deep superior epigastric artery with the 8th intercostal artery just below the costal margin, which allows the muscle to survive solely on the supply from the intercostal arteries. The deep inferior epigastric artery branches from the external iliac artery and ascends obliquely towards the rectus abdominis. The artery enters the deep surface of the muscle at or just inferior to the arcuate line. Once within the muscle, the artery has one to three intramuscular branches that anastomose with the descending branches of the superior epigastric artery. Multiple musculocutaneous perforators branch vertically up to supply the overlying skin. When used in chest wall reconstruction, the rectus abdominis is best based superiorly, as inferiorly based flaps cannot be advanced or rotated enough to cover sternal or thoracic defects. The flap can be raised muscle-only or with a skin paddle measuring about 25 × 6 cm. The skin is incised, and dissection continues to the anterior rectus sheath, preserving any skin perforators if using a skin paddle. The anterior rectus sheath is incised, balancing taking enough fascia to preserve the skin perforators while leaving enough to minimize hernia risk. An avascular plane between the deep surface of the muscle and the posterior sheath or transversalis fascia should be entered to facilitate the dissection. Dissection should begin inferiorly, eventually identifying the deep inferior epigastric

A

B

artery to be ligated. Dissection can then continue superiorly and requires division of the tendinous inscriptions to the anterior surface of the rectus abdominis. As one approaches the costal margin, the connecting arteries from the intercostals will be encountered. This blood supply should be maintained if possible but can be sacrificed if it is a tethering point. The superior epigastric artery is the dominant supply to this flap, but a superiorly based rectus abdominis flap can still be raised if the ipsilateral internal mammary artery has been harvested or resected. The blood supply from the intercostal arteries is sufficient to perfuse the flap via the intramuscular anastomoses between the 8th intercostal artery and the epigastrics.138 This flap can be augmented by maintaining length on the deep inferior epigastric artery to supercharge the flap via a microanastomosis to the contralateral internal mammary artery or the axillary system (Fig. 11.12).139 To maximize the arc of advancement and rotation, the muscle can be released from its insertions on the costal cartilages and xiphoid, and the single superior epigastric pedicle can be skeletonized. The major drawback to this flap is risk of a bulge or hernia, so the fascia should be repaired primarily, and mesh reinforcement should be considered. The superiorly based rectus abdominis can be rotated to cover the full length of the sternum, and harvesting with a skin paddle allows for a complete skin closure when there is a deficit of native chest skin. The muscle can be placed deep within the mediastinum, which is useful in cases of infected aortic grafts or VAD outflow tracts and still allows for closure of the sternum. Alternatively, if the sternum is left in discontinuity, the rectus abdominis can be placed in between the sternal edges to both obliterate the mediastinal deadspace and help prevent pain from the sternal edges. The rectus abdominis has a large arc of rotation and is very useful for most lateral thoracic wounds. It can function alone as coverage for non-­ critical rib defects or be used to cover rib defects reconstructed with prosthetic meshes or autograft or allograft constructs. The muscle can also be used to protect bronchial stumps or as

Figure 11.12  (A,B) VRAM flap based on intercostal artery and supercharged to the contralateral IMA for sternal coverage.

Rectus abdominis

Latissimus dorsi

salvage flaps for empyema or bronchopleural fistula. In those cases, the muscle can be tunneled subcutaneously toward the defect, a neighboring rib can be resected to facilitate inset without kinking the pedicle, and the flap can sit nicely in the intrathoracic space.140 If the muscle is not enough, a skin paddle that is de-epithelialized can provide additional bulk.

The latissimus dorsi is a large, flat muscle that covers the mid and lower back (Fig. 11.13). It has multiple origins: the spinous processes of the T7–L5 vertebrae, the thoracolumbar fascia, the iliac crest, the inferior ribs, and the scapula. The

Thoracodorsal artery

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Figure 11.13 Latissimus dorsi muscle flap vascular anatomy.  

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muscle converges to a flat, broad tendon and inserts onto the intertubercular groove of the humerus to power adduction, extension, and internal rotation of the humerus. This muscle is intimately associated with multiple other trunk muscles. The trapezius lies superficial to the posteromedial fibers and the superior aspect of the tendinous origin off the thoracolumbar spine. The external oblique fibers abut the anterior and inferior edge of the latissimus as it originates off of the most inferior ribs. The serratus anterior lies on the deep surface of the latissimus, and the muscles interdigitate at the level of the 10th to 12th ribs. The inferior border of the teres major is often adherent to the superior border of the latissimus. The latissimus has a dual blood supply from the thoracodorsal artery and the posterior intercostal arteries. The thoracodorsal artery arises from the subscapular artery and enters the deep surface of the latissimus about 4 cm distal to the scapular border, 2–3 cm lateral to the medial border of the muscle, and 5 cm from the posterior axillary fold. Within the muscle, the artery divides into transverse and vertical branches.141 The vertical branch runs parallel along the lateral border of the muscle, while the transverse branch runs parallel to the superior border of the muscle. Both branches have multiple branches that frequently form large choke anastomoses with each other and to the blood supply from the posterior intercostals. This branching pattern allows for raising just a portion of the latissimus muscle or for raising a split muscle flap. The other blood supply is from segmental pedicles from the posterior intercostal and lumbar arteries. These segmental pedicles are arranged into medial and lateral rows, 5–10 cm from the posterior midline. Flaps based on this segmental blood supply are useful for posterior trunk reconstruction but cannot be used for chest wall defects. Raising the latissimus dorsi flap for chest wall reconstruction is performed in similar fashion as when it is used in breast reconstruction. The patient should be placed in lateral decubitus or prone position. The muscle can be harvested with a straight or lazy S incision from the posterior axillary fold coursing inferomedially towards the posterior iliac crest. The flap can also be raised with a skin paddle about 18 × 8 cm in dimension. The anterior border needs to be freed from the serratus anterior, preserving the serratus branch of the thoracodorsal artery in case, as this artery can supply the muscle should the pedicle be damaged. The superior border needs to be separated from the teres major, trapezius, and scapula. Once freed from the surrounding musculature, the origins from the posterior spine and thoracolumbar fascia can be divided to allow quick dissection in the avascular plane on the deep surface towards the neurovascular hilum. To maximize rotation and advancement of the muscle, the pedicle can be skeletonized, and the muscle can be released off its humeral insertion. The branch to the serratus and circumflex scapular artery can be ligated to allow for pedicle dissection to the origin of the subscapular artery. The muscle is then placed in the axilla to allow for proper inset after patient is repositioned. Removing a 1 cm segment out of the thoracodorsal nerve will create a denervated flap. The latissimus dorsi can easily reach and cover defects of the anterolateral chest wall and sternum (Fig. 11.14). With skeletonization of the pedicle and division of the insertion, it can be used to fill central mediastinal defects. This flap is particularly useful to cover lateral thoracic defects with non-­ critical rib resections by itself, prosthetic meshes for rib defects,

or in the setting of osteoradionecrosis.142 The latissimus dorsi is a robust and reliable flap to prophylactically protect bronchial stumps or to obliterate deadspace with empyema or bronchopleural fistulas.143 A remote window into the thorax can be made by removing one to two ribs, tunneling the muscle intrathoracically toward the defect without kinking the pedicle, and then suturing the muscle to the parietal pleura and/or ribs. This was the most common flap used by Salo and Tukiainen to cover oncologic chest wall defects.119 Harvest of this muscle causes shoulder weakness and girdle instability, which while not affecting activities of daily living in most patients, can produce notable deficits in patients who rely on walkers, wheelchairs, or crutches for mobility.144–146 There is a high risk of seromas, which can be reduced with quilting sutures and drains. Finally, there is the aesthetic deformity as a result of loss of the posterior axillary fold.147,148

Serratus anterior The serratus anterior is a small, thin, multi-pennate muscle of the lateral chest wall (Fig. 11.15). There are multiple originating slips that attach to the 1st to 8th or 9th ribs, and these fibers converge to form three vertically oriented parts that insert onto the superior angle, medial border, and inferior angle of the scapula. The serratus anterior protracts and stabilizes the scapula and assists in upward rotation. It has a dual blood supply via the thoracodorsal artery and the lateral thoracic artery.149 The thoracodorsal artery gives off a branch to the serratus anterior 3–6 cm before supplying the latissimus dorsi. This branch enters the posterolateral border of the serratus anterior. The lateral thoracic artery enters the anterior and superior aspect of the muscle. The serratus anterior is an excellent flap to cover lateral thoracic defects as it can often be harvested without an additional incision. If used to cover a more anterior defect, a longitudinal incision can be made along the midaxillary line. The latissimus dorsi which lies posteromedial and superficial to the serratus anterior should be dissected off. In this plane, one should find the thoracodorsal artery entering the latissimus dorsi, and if traced proximally, one should find the branch to the serratus anterior. Electrocautery should then be used to release the originating fibers from the ribs. Once released, an avascular plane should be entered to allow for easy dissection and mobilization of the deep surface of the muscle. The muscular insertions onto the scapula should then be released. Additional pedicle length can be attained by ligating the thoracodorsal artery distal to the takeoff of the serratus branch, and similar to the latissimus dorsi, can be dissected proximally to the origin of the subscapular artery. However, doing so means the ipsilateral latissimus dorsi can no longer be used should the serratus anterior fail. The serratus anterior and latissimus dorsi can be raised together on the thoracodorsal artery in cases of very large defects. Maintaining the superior insertion of the serratus onto the scapula helps retain function and prevent scapular winging.150 While the serratus can be used to cover most lateral thoracic wounds, the latissimus is often preferred because of its larger size and ease of harvest. The best use of the serratus anterior is to fill intrathoracic defects (Fig. 11.16). Because the muscle is smaller than the latissimus, it is easily tunneled through a small thoracotomy window and can fill intrathoracic deadspace, especially in the setting of partial lung resection or

Rectus abdominis

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Figure 11.14  (A–D) Latissimus dorsi myocutaneous flap used to reconstruct a defect following resection of a chronic anterolateral chest wall wound.

to secondarily treat empyema or bronchopulmonary fistula, without being too bulky as to impede lung expansion.151,152

External oblique The external oblique is a thin but broad muscle of the anterior abdominal wall (Fig. 11.17). It originates via multiple fibers from the 5th to 12th ribs and then expands to a broad aponeurosis which inserts onto the xiphoid, iliac crest, pubic crest, and anterior superior iliac spine and then runs confluent with the linea alba and inguinal ligament. The blood supply enters posteriorly from the lateral cutaneous branches of eight lower posterior intercostal arteries, which also provides perforating branches to the skin. The external oblique can be raised as a muscle-only or as a myocutaneous flap with the skin of almost the entire hemiabdomen. The linea semilunaris is identified, which allows one to develop the plane between the tendinous portions of the external and internal oblique, and then between the two muscle bellies. Dissection can continue in this avascular plane out

laterally, which allows for upward mobilization of the flap. Fascia should be preserved if possible, but if harvested, the abdominal wall should be reinforced with mesh. This flap is excellent for covering more inferior lateral thoracic wounds, those that may be out of reach for the latissimus dorsi. Patients with more skin laxity oftentimes have a greater arc of rotation. Harvest of the muscle itself has minimal effect on the abdominal wall, as the other muscles compensate. It is important to understand the risks of abdominal bulges and hernias depending on the amount of fascia resected and method of repair.

Omentum The omentum is composed of visceral fat and blood vessels which arises from the greater curve of the stomach and is also attached to the transverse colon (Fig. 11.18). It has two dominant pedicles, the right and left gastroepiploic arteries. Although its reach makes it best suited for defects of the lower anterior chest, the pedicle length can easily be elongated

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Subclavian artery

Thoracodorsal artery

A

A

B

A

B

CB

Figure 11.15  Serratus anterior muscle flap vascular anatomy.

with division of the internal arcades. Additionally, the omentum can be used to obliterate large intrathoracic dead spaces and can easily be covered with a skin graft. The malleable nature of the flap also allows for its use to wrap grafts thereby providing a stable, well-vascularized bolster to these vital structures. Omental flaps also are thought to harbor additional immunologic characteristics, which together with its considerable vascularity, may explain better control of sternotomy infections as compared to pedicled muscle flaps.153–155 A drawback of the omental flap is the manner in which C it is harvested. Open harvest requires a laparotomy incision which comes with an increased risk of peritoneal infection, intra-abdominal adhesions, and small bowel obstruction. Laparoscopic-assisted omental harvest has demonstrated promising results in terms of feasibility and safety, avoiding obvious morbidity of the laparotomy incision and offering the advantage of less pain, more rapid recovery, and lower risk of abdominal wall herniation.156,157 While larger scale studies are needed, there appear to be low rates of major intra-abdominal complication. Laparoscopic harvest techniques may be best suited for complex patients with multiple comorbidities.158,159 Using this technique, the omentum is detached from the colon from the hepatic to the splenic angle. A superior port is

C

Figure 11.16  (A–C) Serratus anterior used to cover intrathoracic defect.

often used to open the lesser sac, allowing better visualization of the gastric wall. The greater omentum is then mobilized from the greater curvature of the stomach. While it can be based on either gastroepiploic artery, the right gastroepiploic is often isolated and ligated in order to mobilize the flap off the longer left gastroepiploic artery.160,161 Finally, the flap is affixed to the chest wall to provide further stability and prevent migration.

Rectus abdominis

A

B

349

C

Figure 11.17  External oblique muscle flap vascular anatomy.

Omentum

Original incision

Incision

Omentum A

B

C

Left gastroepiploic vessels divided

Figure 11.18  Omentum flap vascular anatomy.

While laparoscopic harvest may be useful for complex patients, it may not be appropriate in a subset of cardiothoracic patients who may not tolerate pneumoperitoneum because of the increased risk of pulmonary compromise and hemodynamic instability.162–167 Due to reduced visualization there is also increased risk of splenic injury, and more difficulty in identifying the vascular pedicle.167 To pass the omentum from the abdomen into the thoracic cavity, it can be passed subcutaneously over the costal margin or through the diaphragm. For trans-diaphragmatic

interpolation, the flap is mobilized through a cruciate incision in the right diaphragm as the liver helps to buttress the incision and prevent diaphragmatic hernia (Fig. 11.19 & 11.20). Furthermore, right-sided transposition obviates the need to navigate the flap around the heart. Care must be taken when interpolating the omentum as it is often of very little substance and can easily be avulsed during passage through the diaphragm. Strategies to protect the omentum during transposition include placing the omentum into a bowel bag. The empty bag can be passed from the mediastinum into the

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Left lobe of liver Incision in diaphragm

Omentum passing through diaphragm into thoracic cavity

Stomach

Figure 11.19  Trans-diaphragmatic tunneling of omentum.

abdomen via the diaphragm incision, past the left lobe of the liver. The omentum is then gently packed into the bowel bag with tension transferred to the bowel bag rather than the omentum during interpolation. Hernia development is another well-recognized complication of the omentum-based chest reconstruction. Hernias can occur either through a diaphragmatic defect or through a ventral defect after subcutaneous tunneling, with rates ranging from 3% to 12%.168–171 While it may be tempting to make the diaphragmatic defect as small as possible to avoid hernia formation, this technique may increase the risk of pedicle compression and subsequent ischemia of the transposed flap. Caution is also advised for patients with prior laparotomy incisions as the omentum may have significant intra-abdominal adhesions or have been previously resected.

Free tissue transfer Although there are plentiful regional flap options to reconstruct chest wall defects, occasionally, distant vascularized tissue is the best reconstructive option. Chimeric or composite grafts such as those off of the circumflex scapular system, thoracodorsal system, circumflex iliac system, and others are viable options. Such flaps can reconstruct both the bony and soft-tissue defect. Recipient vessels include the internal mammary and axillary systems.

Postoperative care Proper postoperative incision care is paramount. The incision should be kept clean, dry, and dressed until fully healed. Use of NPWT along the incision can help decrease tension across the incision, promote peri-incisional vascularity, and allow for fluid extravasation. The incision should be monitored closely postoperatively for any signs of infection or dehiscence and promptly treated. Drains should be used to allow drainage

of postoperative fluid, especially in cases of large flap dissections or when prosthetic meshes or rigid constructs are used, as they are naturally seroma-genic. Drain output and quality should be monitored daily. External, compressive vests reduce mechanical stress and act as shock absorbers when patients experience physiologic stresses of breathing, coughing, upper extremity movement, etc. Multiple studies have demonstrated that the use of supportive vests is associated with decreased risk of wound complications, shorter hospital stay, and decreased rates of re-hospitalization and re-operation.172,173 Supportive surgical bras can help decrease tension on midline incisions in patients with breast ptosis or macromastia. All patients with infectious chest wounds should be treated with antibiotics postoperatively at the discretion of the infectious disease team based on operative cultures. It is impor­ tant to communicate with the infectious disease team about the gross appearance of the wound, depth of the infection, and take cultures to allow for optimal antibiotic selection and duration. Patients with recurrent infections or those with prosthetics that need to remain in place should be considered for long-term antibiotic suppression. Patients with clean chest wall wounds do not need antibiotics outside of the perioperative setting. Inpatient physical and occupational therapy should treat the patient and instruct how to adhere to appropriate activity restrictions. “Sternal precautions” is a commonly used term but inconsistently defined. These activity restrictions generally include no lifting more than 5–10 pounds, no reaching behind the back, no pushing or pulling through the arms, try to keep arms adducted, try to hug a pillow when coughing or sneezing, etc. for 6–8 weeks. Some studies have found the initial activity restrictions too aggressive and advocate for more lenient restrictions. Several reviews have demonstrated no significant difference in wound healing complications in patients on strict activity restrictions compared to patients who are told to allow pain to limit their physical activities.174–176

Congenital chest wall deformities

351

B

A

C

Figure 11.20  (A–C) Reconstruction of lateral chest wall wound with biologic mesh and omentum flap.

Congenital chest wall deformities Management of congenital chest wall deformities is challenging as it requires good communication with the patient and family about realistic expectations and goals of reconstruction. One must decide on timing of surgery, balancing desire for prompt reconstruction with skeletal immaturity. The axial skeleton continues to grow until adulthood, which will impact the decision on what form of skeleton reconstruction to use.

Pectus excavatum Pectus excavatum is the most common congenital chest wall anomaly with an incidence of 1/300–1/400. This condition affects males in a 3:1 ratio and is characterized by a concave deformity of the sternum and parasternal ribs.177

Asymptomatic, minor cases can be treated conservatively with close observation and physical therapy to strengthen the chest wall musculature. The aesthetic deformity can be treated in adulthood using implants or fat grafting.178 The two most common techniques to correct the deformity in childhood, if causing cardiopulmonary compromise, are the Ravitch and Nuss procedures, both of which have evolved in the decades since they were initially described.179 The Ravitch procedure uses a single 8–12 cm transverse incision to remove the deformed costal cartilages to allow for expansion of the rib cage with axial skeletal growth, correction of the concave deformity, and bolstering of the sternum in its corrected position using a synthetic, absorbable mesh to the surrounding ribs. The Nuss procedure uses two 2–4 cm transverse incisions on either side of the chest, limits the osteotomy and rib resection, and uses a metal bar – that has to be removed in a later separate surgery – to correct the sternal deformity.

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Pectus carinatum Pectus carinatum is characterized by a convex deformity of the chest such that the sternum is protruded with depressions along the parasternal ribs, creating a pigeon-like appearance. This condition can cause pain and decreased pulmonary function because of a restricted vital capacity. Unless the patient has significant cardiopulmonary compromise, it is best to treat these patients nonoperatively.180 External bracing can mold the still pliable chest wall to correct for the deformity. In patients who require surgery during childhood or adolescence, the Ravitch and Nuss procedures to reset the costosternal junctions and properly position and bolster the sternum can be used.

Poland syndrome Poland syndrome is a congenital syndrome characterized by underdeveloped chest wall and ipsilateral brachysyndactyly. The chest wall deformity varies but can include absence of the pectoralis major (commonly the sternocostal portion), absence or hypoplasia of the pectoralis minor, absence of the ribs (most commonly 2nd–5th parasternally) and other rib anomalies, absence of the intercostal muscles, deformities of the sternum including pectus carinatum, pectus excavatum, and sternal cleft, and varying deformities or absence of the breast and nipple–areolar complex. Occasionally, other regional muscles such as the latissimus dorsi, serratus, or trapezius may be involved. The incidence is around 1/30,000, is more common in males, and is thought to be due to a vascular injury of the subclavian artery, and the resultant hypoperfusion to the chest wall and upper extremity lead to underdevelopment.181 Several classification systems have been proposed stratified on severity of the chest wall, upper extremity, and breast deformities.182,183 In rare presentations, children with Poland syndrome may have cardiopulmonary compromise related to their chest wall deformity. Those patients should undergo early surgery

with reconstruction of the defect using an absorbable prosthetic. The Ravitch or Nuss procedure can be performed to reconstruct and stabilize the sternum and ribs. Surgery at such an early age is avoided if possible as more trauma to the growing thoracic skeleton may lead to growth restriction.181 The vast majority of patients should undergo surgery after skeletal and breast maturity are reached, which allows for simultaneous chest wall and breast reconstruction. The defects and/or abnormalities of the ribs and sternum can be reconstructed using mesh, titanium bars and plates, custom 3D-printed implants, or autologous tissue. Sometimes regional flaps need to be performed for adequate soft-tissue coverage. Preoperative imaging via CT or MRI helps surgical planning. Reconstruction of the breast and nipple–areolar complex depends on severity but options include implants with or without tissue expansion, fat grafting, or regional or free tissue transfer (Fig. 11.21).

Anterior thoracic hypoplasia Anterior thoracic hypoplasia is often confused with Poland syndrome as patients similarly present with a sunken unilateral chest wall, hypoplasia of the ipsilateral breast, and a superiorly displaced nipple–areolar complex. The major difference is that patients with anterior thoracic hypoplasia have a normal pectoralis major muscle and normal sternal position. These patients rarely have cardiopulmonary issues, and the aesthetic breast deformity can be treated with augmentation mammaplasty.184

Sternal cleft Sternal clefts are rare congenital chest wall deformities and classified as either complete, involving the full vertical length of the sternum, or partial, involving just the superior or inferior portion of the sternum.185 Clinical presentation varies from asymptomatic, to frequent pulmonary infections, to

A

Figure 11.21  (A,B) Right-sided Poland syndrome treated with fat grafting from the left chest.

B

Conclusion

ectopia cordis, in which the heart herniates out from the thoracic cavity. Surgical correction should occur in early infancy to protect the heart. Preoperative workup should include an echocardiogram, CT, and/or MRI. In patients with a present, but split, sternum, primary fixation should be performed. Partial defects can be converted to complete defects to facilitate this. If the articulating ribs or clavicles prevent primary sternal union, chondrotomies or osteotomies at the junction of the medial one-third of the clavicle can be performed to bring the sternal edges together. The donor defects can be reinforced with a biologic or synthetic absorbable mesh. The periosteum on the sternal edges can be elevated and sewed retrosternally to provide another layer of repair over the heart.186 Bony autograft or allograft can also be used to fill the sternal defect.

Access the reference list online at   Elsevier eBooks+

353

Conclusion Chest wall defects are varied and can be incredibly challenging to treat given the many systemic patient factors playing into optimal wound healing. Fortunately, there are plentiful robust options for both bony and soft-tissue reconstruction, as well as significant research and biomedical advances that will continue to advance this field. This chapter reviews the etiology of chest wall wounds, what to think about from a biomechanical and pathophysiologic standpoint, how to evaluate the wound and determine the reconstructive goals, and an algorithm for optimal wound bed preparation, multidisciplinary care, both bony and soft-tissue reconstruction, and perioperative considerations.

References

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surgery outcomes in patients with deep sternal wound infection after cardiac surgery. J Plast Surg Hand Surg. 2020;54(3):182–186. 67. Cowan KN, Teague L, Sue SC, Mahoney JL. Vacuum-assisted wound closure of deep sternal infections in high-risk patients after cardiac surgery. Ann Thorac Surg. 2005;80(6):2205–2212. 68. Fuchs U, Zittermann A, Stuettgen B, Groening A, Minami K, Koerfer R. Clinical outcome of patients with deep sternal wound infection managed by vacuum-assisted closure compared to conventional therapy with open packing: a retrospective analysis. Ann Thorac Surg. 2005;79(2):526–531. 69. White BM, Meyer DL, Harlin SL. Is negative-pressure wound therapy a "bridge to reconstruction" for poststernotomy mediastinitis? A systematic review. Adv Skin Wound Care. 2019; 32(11):502–506. 70. Kim PJ, Attinger CE, Constantine T, et al. Negative pressure wound therapy with instillation: international consensus guidelines update. Int Wound J. 2020;17(1):174–186. 71. Giri P, Krishnaraj B, Chandra Sistla S, et al. Does negative pressure wound therapy with saline instillation improve wound healing compared to conventional negative pressure wound therapy? A randomized controlled trial in patients with extremity ulcers. Ann Med Surg (Lond). 2020;61:73–80. 72. Robicsek F, Daugherty HK, Cook JW. The prevention and treatment of sternum separation following open-heart surgery. J Thorac Cardiovasc Surg. 1977;73(2):267–268. 73. Friberg O, Dahlin LG, Söderquist B, Källman J, Svedjeholm R. Influence of more than six sternal fixation wires on the incidence of deep sternal wound infection. Thorac Cardiovasc Surg. 2006; 54(7):468–473. 74. Cataneo DC, Dos Reis TA, Felisberto G, Rodrigues OR, Cataneo AJM. New sternal closure methods versus the standard closure method: systematic review and meta-analysis. Interact Cardiovasc Thorac Surg. 2019;28(3):432–440. 75. Park JS, Kuo JH, Young JN, Wong MS. Rigid sternal fixation versus modified wire technique for poststernotomy closures: a retrospective cost analysis. Ann Plast Surg. 2017;78(5):537–542. 76. Fawzy H, Alhodaib N, Mazer CD, et al. Sternal plating for primary and secondary sternal closure; can it improve sternal stability? J Cardiothorac Surg. 2009;4:19. 77. Ozaki W, Buchman SR, Iannettoni MD, Frankenburg EP. Biomechanical study of sternal closure using rigid fixation techniques in human cadavers. Ann Thorac Surg. 1998;65(6): 1660–1665. 78. Sinno H, Dionisopoulos T. Open reduction internal fixation poststernotomy mediastinitis. Plast Surg Int. 2013;2013:57. 1685 79. Allen KB, Thourani VH, Naka Y, et al. Rigid plate fixation versus wire cerclage: patient-reported and economic outcomes from a randomized trial. Ann Thorac Surg. 2018;105(5):1344–1350. 80. Raman J, Lehmann S, Zehr K, et al. Sternal closure with rigid plate fixation versus wire closure: a randomized controlled multicenter trial. Ann Thorac Surg. 2012;94(6):1854–1861. 81. Nazerali RS, Hinchcliff K, Wong MS. Rigid fixation for the prevention and treatment of sternal complications. Ann Plast Surg. 2014;72(Suppl 1):S27–S30. 82. Tam DY, Nedadur R, Yu M, Yanagawa B, Fremes SE, Friedrich JO. Rigid plate fixation versus wire cerclage for sternotomy after cardiac surgery: a meta-analysis. Ann Thorac Surg. 2018;106(1): 298–304. 83. Drinnon KD, Sherali S, Cox CT, MacKay BJ. Sternal tumor resection and reconstruction using iliac crest autograft. Plast Reconstr Surg Glob Open. 2020;8(8):e3002. 84. Cara JA, Laclériga AF, Cañadell J. Iliac allograft used for sternal reconstruction after resection of a chondrosarcoma. Int Orthop. 1993;17(5):297–299. 85. Ren P, Zhang J, Zhang X. Resection of primary sternal osteosarcoma and reconstruction with homologous iliac bone: case report. J Formos Med Assoc. 2010;109(4):309–314. 86. Piotrowski JA, Fischer M, Klaes W, Splittgerber F. Autologous bone transplant after sternal resection. J Cardiovasc Surg (Torino). 1996;37(6 Suppl 1):179–181.

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87. Bertin KC, Rice RS, Doty DB, Jones KW. Repair of transverse sternal nonunions using metal plates and autogenous bone graft. Ann Thorac Surg. 2002;73(5):1661–1662. 88. Li W, Zhang G, Ye C, Yin D, Shen G, Chai Y. Autogenous rib graft for reconstruction of sternal defects. J Thorac Dis. 2014;6(12):1851–1852. 89. Heller L, Huang WC, Chen HC, Lu CT, Lin SL. Vascularized iliac bone flap used for sternum reconstruction after resection of chondrosarcoma. Plast Reconstr Surg. 2002;110(4):1088–1091. 90. Kaláb M, Karkoška J, Kamínek M, et al. Reconstruction of massive post-sternotomy defects with allogeneic bone graft: four-year results and experience using the method. Interact Cardiovasc Thorac Surg. 2016;22(3):305–313. 91. Kaláb M, Karkoška J, Kamínek M, Šantavý P. Successful three-year outcome in a patient with allogenous sternal bone graft in the treatment of massive post-sternotomy defects. Int J Surg Case Rep. 2015;7C:6–9. 92. Nahabedian MY, Riley LH, Greene PS, Yang SC, Vander Kolk CA. Sternal stabilization using allograft fibula following cardiac transplantation. Plast Reconstr Surg. 2001;108(5):1284–1288. 93. Ersoy C, Özyüksel A, Malkoç M, et al. Fibula allograft sandwich technique for the reconstruction of sternal nonunion after cardiac surgery. Ann Thorac Surg. 2014;98(2):e51–e53. 94. Ely S, Gologorsky RC, Hornik BM, Velotta JB. Sternal reconstruction with non-rigid biologic mesh overlay. Ann Thorac Surg. 2020;109(5):e357–e359. 95. Koto K, Sakabe T, Horie N, et al. Chondrosarcoma from the sternum: reconstruction with titanium mesh and a transverse rectus abdominis myocutaneous flap after subtotal sternal excision. Med Sci Monit. 2012;18(10):CS77–CS81. 96. Yang H, Tantai J, Zhao H. Clinical experience with titanium mesh in reconstruction of massive chest wall defects following oncological resection. J Thorac Dis. 2015;7(7):1227–1234. 97. Zhang Y, Li JZ, Hao YJ, et al. Sternal tumor resection and reconstruction with titanium mesh: a preliminary study. Orthop Surg. 2015;7(2):155–160. 98. Akiba T, Marushima H, Nogi H, et al. Chest wall reconstruction using Gore-Tex® dual mesh. Ann Thorac Cardiovasc Surg. 2012;18(2):166–169. 99. Huang H, Kitano K, Nagayama K, et al. Results of bony chest wall reconstruction with expanded polytetrafluoroethylene soft tissue patch. Ann Thorac Cardiovasc Surg. 2015;21(2):119–124. 100. Hameed A, Akhtar S, Naqvi A, Pervaiz Z. Reconstruction of complex chest wall defects by using polypropylene mesh and a pedicled latissimus dorsi flap: a 6-year experience. J Plast Reconstr Aesthet Surg. 2008;61(6):628–635. 101. Motono N, Shimada K, Kamata T, Uramoto H. Sternal resection and reconstruction for metastasis due to breast cancer: the Marlex sandwich technique and implantation of a pedicled latissimus dorsi musculocutaneous flap. J Cardiothorac Surg. 2019;14(1):79. 102. Gayer G, Yellin A, Apter S, Rozenman Y. Reconstruction of the sternum and chest wall with methyl methacrylate: CT and MRI appearance. Eur Radiol. 1998;8(2):239–243. 103. Haraguchi S, Hioki M, Hisayoshi T, Yamashita K, Koizumi K, Shimizu K. Resection of sternal metastasis from endometrial carcinoma followed by reconstruction with sandwiched marlex and stainless steel mesh: report of a case. Surg Today. 2006;36(2): 184–186. 104. Haraguchi S, Yamashita Y, Yamashita K, Hioki M, Matsumoto K, Shimizu K. Sternal resection for metastasis from thyroid carcinoma and reconstruction with the sandwiched Marlex and stainless steel mesh. Jpn J Thorac Cardiovasc Surg. 2004;52(4):209–212. 105. Kilic D, Gungor A, Kavukcu S, et al. Comparison of mersilene mesh-methyl metacrylate sandwich and polytetrafluoroethylene grafts for chest wall reconstruction. J Invest Surg. 2006;19(6): 353–360. 106. Weyant MJ, Bains MS, Venkatraman E, et al. Results of chest wall resection and reconstruction with and without rigid prosthesis. Ann Thorac Surg. 2006;81(1):279–285. 107. Shah NR, Ayyala HS, Tran BNN, Therattil PJ, Keith JD. Outcomes in chest wall reconstruction using methyl methacrylate prostheses:

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a review of the literature and case series utilizing a novel approach with biologic mesh. J Reconstr Microsurg. 2019; 35(8):575–586. 108. Collaud S, Pfofe D, Decurtins M, Gelpke H. Mesh-bone cement sandwich for sternal and sternoclavicular joint reconstruction. Eur J Cardiothorac Surg. 2013;43(3):643–645. 109. Dzian A, Živcˇák J, Penciak R, Hudák R. Implantation of a 3D-printed titanium sternum in a patient with a sternal tumor. World J Surg Oncol. 2018;16(1):7. 110. Demondion P, Mercier O, Kolb F, Fadel E. Sternal replacement with a custom-made titanium plate after resection of a solitary breast cancer metastasis. Interact Cardiovasc Thorac Surg. 2014;18(1):145–147. 111. Turna A, Kavakli K, Sapmaz E, et al. Reconstruction with a patient-specific titanium implant after a wide anterior chest wall resection. Interact Cardiovasc Thorac Surg. 2014;18(2):234–236. 112. Aranda JL, Jiménez MF, Rodríguez M, Varela G. Tridimensional titanium-printed custom-made prosthesis for sternocostal reconstruction. Eur J Cardiothorac Surg. 2015;48(4):e92–e94. 113. Wang B, Guo Y, Tang J, Yu F. Three-dimensional custom-made carbon-fiber prosthesis for sternal reconstruction after sarcoma resection. Thorac Cancer. 2019;10(6):1500–1502. 114. Oswald N, Senanayake E, Naidu B, Khalil H, Bishay E. Chest wall mechanics in vivo with a new custom-made three-dimensionalprinted sternal prosthesis. Ann Thorac Surg. 2018;105(4): 1272–1276. 115. Cataneo DC, Dos Reis TA, Felisberto G, Rodrigues OR, Cataneo AJM. New sternal closure methods versus the standard closure method: systematic review and meta-analysis. Interact Cardiovasc Thorac Surg. 2019;28(3):432–440. 116. Martin TJ, Eltorai AS, Dunn R, et al. Clinical management of rib fractures and methods for prevention of pulmonary complications: a review. Injury. 2019;50(6):1159–1165. 117. Fabricant L, Ham B, Mullins R, Mayberry J. Prospective clinical trial of surgical intervention for painful rib fracture nonunion. Am Surg. 2014;80(6):580–586. 118. Seder CW, Rocco G. Chest wall reconstruction after extended resection. J Thorac Dis. 2016;8(Suppl 11):S863–S871. 119. Salo JTK, Tukiainen EJ. Oncologic resection and reconstruction of the chest wall: a 19-year experience in a single center. Plast Reconstr Surg. 2018;142(2):536–547. 120. Giordano S, Garvey PB, Clemens MW, et al. Synthetic mesh versus acellular dermal matrix for oncologic chest wall reconstruction: a comparative analysis. Ann Surg Oncol. 2020; 27(8):3009–3017. 121. Lardinois D, Müller M, Furrer M, et al. Functional assessment of chest wall integrity after methylmethacrylate reconstruction. Ann Thorac Surg. 2000;69(3):919–923. 122. Weyant MJ, Bains MS, Venkatraman E, et al. Results of chest wall resection and reconstruction with and without rigid prosthesis. Ann Thorac Surg. 2006;81(1):279–285. 123. Coonar AS, Qureshi N, Smith I, Wells FC, Reisberg E, Wihlm JM. A novel titanium rib bridge system for chest wall reconstruction. Ann Thorac Surg. 2009;87(5):e46–e48. 124. Berthet JP, Wihlm JM, Canaud L, et al. The combination of polytetrafluoroethylene mesh and titanium rib implants: an innovative process for reconstructing large full thickness chest wall defects. Eur J Cardiothorac Surg. 2012;42(3):444–453. 125. Berthet JP, Solovei L, Tiffet O, et al. Chest-wall reconstruction in case of infection of the operative site: is there any interest in titanium rib osteosynthesis? Eur J Cardiothorac Surg. 2013;44(5): 866–874. 126. Xie HQ, Huang FG, Zhao YF, et al. Tissue-engineered ribs for chest wall reconstruction: a case with 12-year follow-up. Regen Med. 2014;9(4):431–436. 127. Simal I, García-Casillas MA, Cerdá JA, et al. Three-dimensional custom-made titanium ribs for reconstruction of a large chest wall defect. European J Pediatr Surg Rep. 2016;4(1):26–30. 128. Wang L, Huang L, Li X, et al. Three-dimensional printing PEEK implant: a novel choice for the reconstruction of chest wall defect. Ann Thorac Surg. 2019;107(3):921–928.

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SECTION II

CHAPTER 11  • Reconstruction of the chest

129. Hernandez MC, Reisenauer JS, Aho JM, et al. Bone autograft coupled with locking plates repairs symptomatic rib fracture nonunions. Am Surg. 2018;84(6):844–850. 130. de Jong MB, Houwert RM, van Heerde S, de Steenwinkel M, Hietbrink F, Leenen LPH. Surgical treatment of rib fracture nonunion: a single center experience. Injury. 2018;49(3):599–603. 131. Fabricant L, Ham B, Mullins R, Mayberry J. Prospective clinical trial of surgical intervention for painful rib fracture nonunion. Am Surg. 2014;80(6):580–586. 132. Zeitani J, Bertoldo F, Bassano C, et al. Superficial wound dehiscence after median sternotomy: surgical treatment versus secondary wound healing. Ann Thorac Surg. 2004;77(2):672–675. 133. Netscher DT, Baumholtz MA. Chest reconstruction: I. Anterior and anterolateral chest wall and wounds affecting respiratory function. Plast Reconstr Surg. 2009;124(5):240e–252e. 134. Freeman JL, Walker EP, Wilson JS, Shaw HJ. The vascular anatomy of the pectoralis major myocutaneous flap. Br J Plast Surg. 1981; 34(1):3–10. 135. Brutus JP, Nikolis A, Perreault I, Harris PG, Cordoba C. The unilateral pectoralis major island flap, an efficient and straightforward procedure for reconstruction of full length sternal defects after postoperative mediastinal wound infection. Br J Plast Surg. 2004;57(8):803–805. 136. Refos JW, Witte BI, de Goede CJ, de Bree R. Shoulder morbidity after pectoralis major flap reconstruction. Head Neck. 2016;38(8): 1221–1228. 137. Moon HK, Taylor GI. The vascular anatomy of rectus abdominis musculocutaneous flaps based on the deep superior epigastric system. Plast Reconstr Surg. 1988;82(5):815–832. 138. Jacobs B, Ghersi MM. Intercostal artery-based rectus abdominis transposition flap for sternal wound reconstruction: fifteen-year experience and literature review. Ann Plast Surg. 2008;60(4): 410–415. 139. Yamamoto Y, Nohira K, Shintomi Y, Sugihara T, Ohura T. “Turbo charging” the vertical rectus abdominis myocutaneous (turboVRAM) flap for reconstruction of extensive chest wall defects. Br J Plast Surg. 1994;47(2):103–107. 140. Hallock GG. Intrathoracic application of the transverse rectus abdominis musculocutaneous flap. Ann Plast Surg. 1992;29(4): 357–361. 141. Tobin GR, Schusterman M, Peterson GH, Nichols G, Bland KI. The intramuscular neurovascular anatomy of the latissimus dorsi muscle: the basis for splitting the flap. Plast Reconstr Surg. 1981;67(5):637–641. 142. Makboul M, Salama Ayyad MA. Is myocutaneous flap alone sufficient for reconstruction of chest wall osteoradionecrosis? Interact Cardiovasc Thorac Surg. 2012;15(3):447–451. 143. Eggers C. The treatment of bronchial fistulae. Ann Surg. 1920; 72(3):345–351. 144. Russell RC, Pribaz J, Zook EG, Leighton WD, Eriksson E, Smith CJ. Functional evaluation of latissimus dorsi donor site. Plast Reconstr Surg. 1986;78(3):336–344. 145. Fraulin FO, Louie G, Zorrilla L, Tilley W. Functional evaluation of the shoulder following latissimus dorsi muscle transfer. Ann Plast Surg. 1995;35(4):349–355. 146. Laitung JK, Peck F. Shoulder function following the loss of the latissimus dorsi muscle. Br J Plast Surg. 1985;38(3):375–379. 147. Delay E, Gounot N, Bouillot A, Zlatoff P, Comparin JP. [Breast reconstruction with the autologous latissimus dorsi flap. Preliminary report of 60 consecutive reconstructions]. Ann Chir Plast Esthet. 1997;42(2):118–130. 148. 19Titley OG, Spyrou GE, Fatah MF. Preventing seroma in the latissimus dorsi flap donor site. Br J Plast Surg. 1997;50(2):106–108. 149. Arnold PG, Pairolero PC, Waldorf JC. The serratus anterior muscle: intrathoracic and extrathoracic utilization. Plast Reconstr Surg. 1984;73(2):240–248. 150. Arnold PG, Pairolero PC. Intrathoracic muscle flaps: An account of their use in the management of 100 consecutive patients. Ann Surg. 1990;211:656–660. discussion 660–662.

151. Chen JT, Bonneau LA, Weigel TL, et al. A twelve-year consecutive case experience in thoracic reconstruction. Plast Reconstr Surg Glob Open. 2016;4(3):e638. 152. Asaad M, Van Handel A, Akhavan AA, et al. Muscle flap transposition for the management of intrathoracic fistulas. Plast Reconstr Surg. 2020;145(4):829e–838e. 153. Milano CA, Georgiade G, Muhlbaier LH, Smith PK, Wolfe WG. Comparison of omental and pectoralis flaps for poststernotomy mediastinitis. Ann Thorac Surg. 1999;67(2):377–380; discussion 380–381. 154. Lopez-Monjardin H, de-la-Pena-Salcedo A, Mendoza-Munoz M, Lopez-Yanez-de-la-Pena A, Palacio-Lopez E, Lopez-Garcia A. Omentum flap versus pectoralis major flap in the treatment of mediastinitis. Plast Reconstr Surg. 1998;101(6):1481–1485. 155. Meza-Perez S, Randall TD. Immunological functions of the omentum. Trends Immunol. 2017;38(7):526–536. 156. Mathisen DJ, Grillo HC, Vlahakes GJ, Daggett WM. The omentum in the management of complicated cardiothoracic problems. J Thorac Cardiovasc Surg. 1988;95(4):677–684. 157. Weinzweig N, Yetman R. Transposition of the greater omentum for recalcitrant median sternotomy wound infections. Ann Plast Surg. 1995;34(5):471–477. 158. Acarturk TO, Swartz WM, Luketich J, Quinlin RF, Edington H. Laparoscopically harvested omental flap for chest wall and intrathoracic reconstruction. Ann Plast Surg. 2004;53(3):210–216. 159. Pechetov AA, Esakov YS, Makov MA, Okonskaya DE, Basylyuk AV, Khlan TN. [Laparoscopic-assisted harvesting of omental flap in chest wall reconstruction for deep sternal wound infection]. Khirurgiia (Mosk). 2017(8):18–23. 160. Ferron G, Garrido I, Martel P, et al. Combined laparoscopically harvested omental flap with meshed skin grafts and vacuumassisted closure for reconstruction of complex chest wall defects. Ann Plast Surg. 2007;58(2):150–155. 161. Powers JC, Fitzgerald JF, McAlvanah MJ. The anatomic basis for the surgical detachment of the greater omentum from the transverse colon. Surg Gynecol Obstet. 1976;143(1):105–106. 162. Hultman CS, Carlson GW, Losken A, et al. Utility of the omentum in the reconstruction of complex extraperitoneal wounds and defects: donor-site complications in 135 patients from 1975 to 2000. Ann Surg. 2002;235(6):782–795. 163. Avital S, Rosin D, Brasesco O, et al. Laparoscopic mobilization of an omental flap for reconstruction of an infected sternotomy wound. Ann Plast Surg. 2002;49(3):307–311. 164. Saltz R. Endoscopic harvest of the omental and jejunal free flaps. Clin Plast Surg. 1995;22(4):747–754. 165. Corral CJ, Prystowsky JB, Weidrich TA, Harris GD. Laparoscopicassisted bipedicle omental flap mobilization for reconstruction of a chest wall defect. J Laparoendosc Surg. 1994;4(5):343–346. 166. Domene CE, Volpe P, Onari P, et al. Omental flap obtained by laparoscopic surgery for reconstruction of the chest wall. Surg Laparosc Endosc. 1998;8(3):215–218. 167. Kamei Y, Torii S, Hasegawa T, Nishizeki O. Endoscopic omental harvest. Plast Reconstr Surg. 1998;102(7):2450–2453. 168. Boiskin I, Karna A, Demos TC, Blakeman B. Herniation of the transverse colon: an unusual complication of pedicled omentoplasty. Can Assoc Radiol J. 1995;46(3):223–225. 169. Massard G, Wilk A, Dumond P, Rodier-Bruant C, Wihlm JM, Morand G. [Diaphragmatic hernia complicating omentoplasty after thoracic wall excision. Reflections apropos of 2 cases]. Ann Chir Plast Esthet. 1992;37(3):329–332. 170. van Garderen JA, Wiggers T, van Geel AN. Complications of the pedicled omentoplasty. Neth J Surg. 1991;43(5):171–174. 171. Hultman CS, Culbertson JH, Jones GE, et al. Thoracic reconstruction with the omentum: indications, complications, and results. Ann Plast Surg. 2001;46(3):242–249. 172. Caimmi PP, Sabbatini M, Kapetanakis EI, et al. A randomized trial to assess the contribution of a novel thorax support vest (corset) in preventing mechanical complications of median sternotomy. Cardiol Ther. 2017;6(1):41–51.

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procedures for pectus excavatum: considering the patients’s perspective. Ann R Coll Surg Engl. 2016;98(8):581–585. 180. Buziashvili D, Gopman JM, Weissler H, Bodenstein L, Kaufman AJ, Taub PJ. An evidence-based approach to management of pectus excavatum and carinatum. Ann Plast Surg. 2019;82(3): 352–358. 181. Moir CR, Johnson CH. Poland’s syndrome. Semin Pediatr Surg. 2008;17(3):161–166. 182. Romanini MV, Calevo MG, Puliti A, et al. Poland syndrome: a proposed classification system and perspectives on diagnosis and treatment. Semin Pediatr Surg. 2018;27(3):189–199. 183. Romanini MV, Torre M, Santi P, et al. Proposal of the TBN classification of thoracic anomalies and treatment algorithm for Poland syndrome. Plast Reconstr Surg. 2016;138(1):50–58. 184. Spear SL, Pelletiere CV, Lee ES, Grotting JC. Anterior thoracic hypoplasia: a separate entity from Poland syndrome. Plast Reconstr Surg. 2004;113(1):69–77. discussion 78–79. 185. Blanco FC, Elliott ST, Sandler AD. Management of congenital chest wall deformities. Semin Plast Surg. 2011;25(1):107–116. 186. de Campos JR, Das-Neves-Pereira JC, Velhote MC, Jatene FB. Twenty seven-year experience with sternal cleft repair. Eur J Cardiothorac Surg. 2009;35(3):539–541.

SECTION II  •  Trunk, Perineum, and Transgender

12 Reconstruction of the posterior trunk Reuben A. Falola, Nicholas F. Lombana, Andrew M. Altman, and Michel H. Saint-Cyr

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Introduction Wounds of the posterior trunk can arise as a result of trauma, tumor ablation, chronic pressure, or congenital defects. Management of these wounds can be quite challenging for the reconstructive surgeon given the relative lack of soft-tissue laxity, dearth of microsurgical recipient vessels, and dependent anatomical location. Of note, there are the many vital structures that traverse this anatomical region, including structures involved in neurological signaling, respiratory function, visceral protection, and postural support, and exposure or violation of these structures increases the risk of postoperative morbidity and mortality.1–9 Compounding these challenges may be other elements of the patient history, including the presence of irradiation, spinal hardware, fulminant infection, or cerebrospinal fluid leak. As a result of the above challenges, healing by secondary intention or skin grafting are frequently suboptimal, especially for intermediate and deep posterior trunk wounds.1,9–14 Muscle and myocutaneous flaps based on the latissimus dorsi and trapezius muscles are robust, well-vascularized flaps that are considered the traditional first-line options for reconstruction in the posterior trunk. Early studies demonstrated superior outcomes of muscle flaps compared to random pattern fasciocutaneous flaps or primary closure, especially in the presence of infection.9,15,16 This may be due to improved delivery of antibiotics and immune cells, superior tissue oxygenation and wound coverage, and inhibition of bacterial growth when compared to muscle-sparing flaps.15,17–19 Newer studies, however, have challenged these beliefs, producing data to support the use of perforator flaps, even for large wounds.6,20–26 Perforator flaps can offer reliable wound healing, cosmesis, and an improved comorbidity profile when compared to muscle-based flaps.22–24,26,27 However, the steep technical learning curve and decreased tissue bulk compared to

muscle-containing flaps may limit the use of perforator flaps in the posterior trunk. Flaps based on multiple perforators may address concerns related to limited tissue bulk and can efficiently recruit large areas of soft tissue in a relatively simple operation. Once mastered, perforator flaps offer a robust, secondary reconstructive option for soft-tissue defects in the posterior trunk, especially when muscle preservation is desired.6,20,21,23–26,28,29 An algorithmic approach to posterior trunk reconstruction starts with categorization of the wound depth as superficial, intermediate, or deep. Superficial wounds can typically be managed with local wound care. Intermediate and deep wounds often require recruitment of soft tissues for filling of empty space and resurfacing. These wounds are further classified by their midline or non-midline position and by their location within the four posterior trunk regions (posterior cervical, upper thoracic, middle thoracic, and lumbar). Flap selection is then narrowed to locoregional options based on these coordinates. Free tissue transfer is typically considered an option of last resort. Wound characteristics such as size, depth, and the presence of hardware are then considered when deciding which soft and bony tissue component to include within the flap. Midline wounds differ from non-midline wounds in that there is a higher risk of complication by spinal involvement and/or spinal leak. As a result, midline wounds typically require two full layers of vascularized muscle or fascia for definitive closure. For non-midline wounds, or midline wounds without spinal exposure, soft-tissue needs within the wound will dictate the variable inclusion of vascularized muscle, fascia, subcutaneous tissues, and skin.21,30 Regardless of flap selection, the following principles serve to optimize soft-tissue reconstruction in the posterior trunk: debridement of all devitalized tissues, recruitment of well-vascularized tissue outside of the zone of injury, obliteration of empty space, coverage of vital structures/ hardware with adequate tissue bulk, and a tension free

Anatomy

closure.21,30 Appropriate flap selection minimizes patient morbidity while maximizing functionality. A sound reconstructive plan should include a multidisciplinary approach with neurosurgery and/or orthopedic surgery when indicated. This chapter synthesizes the current literature on reconstruction of the posterior trunk and provides an algorithmic approach, which can serve as a starting point when addressing the myriad challenges present within this anatomical region.

Anatomy The back comprises 18% of total body surface area with anatomical boundaries beginning at the superior margin of the posterior trunk, demarcated by a line connecting the spinous process of the “vertebra prominens”, or C7, to the acromial angle of both shoulders. The inferior margin lies just above the bilateral iliac crests, and lateral margins extend to the mid-axillary line on either side of the trunk. The muscles of the back are organized into three groups. The extrinsic or superficial muscle group aids in limb movement and contains the trapezius, latissimus dorsi, levator scapulae, and rhomboids (Fig. 12.1). The intermediate muscle group aids in respiratory effort and is composed of the serratus posterior inferior and serratus posterior superior (see Fig. 12.1). The deep or intrinsic group is further subdivided into two main subgroups: the erector spinae and the transversospinalis (Fig. 12.2). The erector spinae include the iliocostalis, longissimus, and spinalis muscles, commonly referred to as the “paraspinous” muscle, and are the main spinal extensors, in addition to aiding in lateral bending and in rotation of the spine (see Fig. 12.2). The transversospinalis subgroup includes the semispinalis, multifidus, and spinal rotators, which aid in posterior and lateral bending of the spine and rotation (see Fig. 12.2). The gluteal muscles lay caudal to the inferior boundary of the back, and as a result of their proximity to this region, are frequently involved in locoregional posterior trunk reconstruction, especially for wounds in the lumbar region (Fig. 12.3). The muscles and soft tissues of the back are well vascularized and are fed both by axial vessels and dorsal branches of the intercostal and lumbar arteries. The skin and intrinsic muscles of the back are innervated primarily by the dorsal rami of the spinal nerves while extrinsic muscles are innervated by the ventral rami. Sensory innervation takes on a dermatomal pattern. The back can also be divided into four descriptive subregions from cephalad to caudad, for the purposes of grouping locoregional reconstructive options. This includes the posterior cervical, upper thoracic, middle thoracic, and lumbar subregions (Fig. 12.4).9

Posterior trunk perforators Perforating vessels in the posterior trunk branch off of the axial blood supply and are categorized by the course taken towards their termination point. There are three types of perforators31,32 (Fig. 12.5): 1. Musculocutaneous (indirect muscle) perforators course through the muscle, perforate the outer layer of deep fascia, then supply the overlying skin

2. 3.

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Septocutaneous (indirect septal) perforators course through the septum, perforate the outer layer of deep fascia, then supply overlying skin Direct cutaneous perforators, which perforate the deep fascia only and then supply the overlying skin

Perforasomes are distinct regions of tissue within a vascular territory that is supplied by perforating blood vessels (Fig. 12.6). A central dense vascular network progressively decreases in concentration towards the periphery of the perforasome. Multiple perforasomes are linked, directly or indirectly, by vessels that branch out radially from the periphery.33–36 A line drawn transversely across the lower margin of the 12th rib divides the posterior trunk into the upper back (thoracic) and lower back (lumbar) regions, which correlate with the two major perforator densities within the region (Figs. 12.7–12.9).26 In a cadaveric study of posterior trunk perforators, conducted by Aho et al., 393 perforators were dissected to help elucidate their distribution within the two groupings in this region.26 The first perforator grouping is the thoracic cluster, which, based on cadaveric studies, has a mean of 17.8 perforators, located within 10–20 cm of the C7 reference point (see Figs. 12.7–12.9; Table 12.1). The center of the thoracic cluster has a perforator density of 0.3/cm2, reflecting a three-times higher average likelihood of containing a perforator than surrounding tissues (see Figs. 12.7 & 12.8, Table 12.1).26 The second perforator grouping is the lumbar cluster, which has a mean of 21.5 perforators located within 10–20 cm of the coccygeal reference point (see Figs. 12.7 & 12.8; Table 12.2).26 The center of the lumbar cluster has a perforator density of 0.3/cm2, reflecting a two-times higher average likelihood of containing a perforator than surrounding tissues (see Fig. 12.7 & 12.8, Table 12.2).26 Some of the lumbar perforators cross the midline and join contralateral perforators via direct and indirect flow.26 It is important to appreciate the “watershed” areas of low perforator density between the thoracic and lumbar perforasomes during flap design (see Figs. 12.7).

Principles of perforasome theory There are four main principles that define perforasome theory.

Principle 1 Each perforasome is connected to adjacent perforasomes via two main mechanisms: direct flow via linking vessels or indirect flow via the subdermal plexus (Fig. 12.10). Hypoperfusion, therefore, captures adjacent perforasomes.30

Principle 2 The vascular density of a given perforator is determined by the most proximal distance of the flap edge and flap width relative to the perforator location. This relationship subsequently defines the angle of perfusion. A decreasing number of linking vessels correlates with a decreasing angle of perfusion. The orientation of linking vessels corresponds to the orientation of maximal flap vascularity. Thus, the orientation of flap design should be parallel to the linking vessels to allow for optimal vascularity.30

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SECTION II

Superior nuchal line

Splenius capitis muscle

External occipital protuberance

Accessory nerve (XI) Levator scapulae muscle

Posterior triangle of neck Sternocleidomastoid muscle

Rhomboid minor muscle

Trapezius muscle

Rhomboid major muscle Supraspinatus muscle

Spine of scapula

Infraspinatus muscle

Infraspinous fascia

Spine and acromion of scapula

Teres minor muscle Deltoid muscle

T1

Teres minor muscle Spinous processes of thoracic vertebrae

T6

Teres major muscle

Latissimus dorsi muscle (cut) Lower digitations of serratus anterior muscle

Teres major muscle Latissimus dorsi muscle

T12 Digitations of external oblique muscle

External oblique muscle Lumbar triangle (Petit) with internal oblique muscle in its floor

Serratus posterior inferior muscle Thoracolumbar fascia over deep muscles of back (erector spinae)

Iliac crest Medial Lateral

Posterior cutaneous branches (from medial and lateral branches of dorsal rami of thoracic spinal nerves)

Figure 12.1  Extrinsic muscles of the back. The extrinsic muscles of the back include the two workhorse flaps in the region: the latissimus dorsi and trapezius muscle flaps. Variations of these flaps allow for a variety of closure options in the posterior trunk region. (From Kaminsky DA. The Netter Collection of Medical Illustrations – Respiratory System, 2nd ed. Elsevier, 2011. Copyright, Netter Images. Variant Image ID: 58515.)

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Rectus capitis posterior minor m.

Superior nuchal line of skull

Obliquus capitis superior m.

Posterior tubercle of atlas (C1)

Rectus capitis posterior major m.

Longissimus capitis m.

Obliquus capitis inferior m.

Semispinalis capitis m.

Longissimus capitis m. Splenius capitis and splenius cervicis mm.

Semispinalis capitis m. (cut) Spinalis cervicis m.

Serratus posterior superior m.

Spinous process of C7 vertebra Iliocostalis m. Erector spinae muscle

Longissimus cervicis m. Iliocostalis cervicis m.

Longissimus m.

Iliocostalis thoracis m. Hook

Spinalis m.

Spinalis thoracis m. Longissimus thoracis m. Serratus posterior inferior m.

Iliocostalis lumborum m. Spinous process of T12 vertebra

Tendon of origin of transversus abdominis m.

Transversus abdominis m. and tendon of origin

Internal oblique m. External oblique m. (cut)

Thoracolumbar fascia (cut edge)

Iliac crest

Figure 12.2  Intrinsic muscles of the back. The intrinsic muscles of the back include the paraspinous (erector spinae) muscle group, which are often utilized for the deep layer of a multilayered closure of midline back wounds. (From Cleland J. Orthopaedic Clinical Examination, 4th ed. Elsevier, 2021. Copyright, Netter Images. Variant Image ID: 32799.)

Principle 3 Preferential filling of perforasomes occurs within perforators of the same source artery followed by perforators of an adjacent source. When designing the optimal flap, it is important to center flaps over known perforators and to incorporate as many dominant linking vessels and multiple perforators from the same source artery. Further, larger flaps should incorporate tissues that originate away from the zone of injury, a practice which allows for more robust vascular support, but may not always prevent hypoperfusion in the distal tip.30

Principle 4 Mass vascularity of a perforator is found adjacent to articulations and directed away from the same articulation. Midpoint perforators, also known as linking vessels, are found between two adjacent perforators and exhibit a bidirectional flow pattern.30

Flaps for reconstruction of the posterior trunk Trapezius The trapezius, a Mathes and Nahai type II muscle, receives its blood supply from the ascending and descending branches of transverse cervical artery (TCA), with minor contributions from branches of the occipital artery and intercostal perforators (Fig. 12.11; see Fig. 12.1). The spinal accessory nerve provides motor innervation (cranial nerve XI) and branches of C3 and C4 provide motor and sensory innervation. The external anatomical boundaries of the trapezius form a triangle, the base of which is marked by the midline of the back, extending from the external occipital protuberance to T12. This muscle then tapers laterally toward the base of the scapula, covering

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Superficial dissection

Iliac crest Gluteal aponeurosis over gluteal medius m. Gluteus maximus m.

Semitendinosus m. Biceps femoris m. (long head)

Adductor magnus m.

Iliotibial tract

Semimembranosus m. Gracilis m.

Biceps femoris m. Short head Long head

Deep dissection Iliac crest Gluteus maximus m. (cut)

Gluteal aponeurosis and gluteus medius m. (cut) Superior gluteal a. and n. Gluteus minimus m.

Inferior gluteal a. and n. Pudendal n. Nerve to obturator internus (and superior gemellus) Posterior cutaneous n. of thigh Sacrotuberous lig. Ischial tuberosity Sciatic n.

Tensor fasciae latae m. Piriformis m. Gluteus medius m. (cut) Superior gemellus m. Greater trochanter of femur Obturator internus m. Inferior gemellus m. Quadratus femoris m. Medial circumflex femoral a.

Muscular branches of sciatic n. Semitendinosus m. (retracted)

Adductor magnus m.

Semimembranosus m.

Figure 12.3  Muscles of the gluteal region. Due to its proximity to the lumbar region of the posterior trunk, gluteal flaps are often utilized for reconstruction of inferiorly located back wounds. (From Hansen JT. Netter’s Clinical Anatomy, 5th ed. Elsevier, 2021. Copyright, Netter Images. Variant Image ID: 9409.)

an area of 34 × 18 cm. The trapezius muscle originates along the superior nuchal line, the external occipital protuberance (nuchal ligament), the thoracic vertebrae, and the supraspinous ligaments. Insertion points include the scapular spine, acromion, and the lateral third of the clavicle. Elevation of the trapezius proceeds inferiorly to superiorly, and flap reach is increased by removing attachments to the scapular spine. The flap is typically utilized as an advancement, rotation, or turnover flap with muscle and myocutaneous variations (see Fig. 12.11).3,10,21,37–41 Care should be taken when harvesting

the trapezial flap, as aggressive muscle harvest and/or nerve injury can result in winging of the scapula. The dorsal scapular artery perforator (DSAP) and the superficial cervical artery perforator (SCAP) form the basis of the trapezial perforator flap, a muscle-sparing variation first described by Sadigh and colleagues in 2014 (Fig. 12.12; see Fig. 12.9).42 There is also some contribution from the posterior intercostal arteries (see Fig. 12.9). The dorsal scapular artery (DSA) and the superficial cervical artery (SCA) are the deep and superficial branches of the TCA, respectively.

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Posterior cervical

Upper thoracic

Middle thoracic

Lumbar

Figure 12.4  Regions of the posterior trunk. The four reconstructive regions of the posterior trunk are shown below. The regions each contain a preferred flap option, which can serve as a starting point to help to guide reconstructive efforts. (Redrawn from Hallock GG. Reconstruction of posterior trunk defects. Semin Plast Surg. 2011;25(1):78. Thieme Medical Publishers.) Type A

Figure 12.6  Distribution of thoracic and lumbar perforators. The posterior trunk contains perforator “hot spots”, regions in which the likelihood of finding a perforator is high. The cluster of perforators decreases in density toward the periphery. (Redrawn from Mohan AT, Rammos CK, Akhavan AA, et al. Evolving concepts of keystone perforator island flaps (KPIF). Plast Reconstr Surg. 2016;137(6):1909–1920.)

Type B

Type C

Figure 12.5  Classification of perforator flaps. Perforators can be classified into direct cutaneous (type A), septocutaneous (type B), and musculocutaneous (type C) branches.

Figure 12.7  Thoracic and lumbar perforator densities. The posterior trunk contains perforator “hot spots”, regions in which the likelihood of finding a perforator is high. The cluster of perforators decreases in density towards the periphery. (Copyright Mayo Foundation for Medical Education and Research, all rights reserved.)

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As a result, flap harvest spares the subscapular system (see Fig. 12.13), which can be unavailable after tumor ablation or multiple prior attempts at reconstruction.43 The trapezial perforator flap not only preserves muscle function but has the added benefit of a limited donor site that can be well hidden

under clothes. It provides a thin, flexible flap with skin paddles up to 25 × 15 cm that are ideal for coverage of superficial defects in the posterior cervical and upper thoracic regions, or even as a free flap.44 The DSA courses beneath the levator scapulae and rhomboid minor muscles, then branches between the rhomboid minor and major, perforating the fascia as the superficial dorsal scapular artery (SDSA). The SDSA then runs along the medial border of the scapula, deep to the trapezius, and sends out 1–2 perforators to the muscle and skin, located ~1–2 cm medial to the lower trapezial border. Alternatively, the DSA can originate directly from the third part of the subclavian artery.43 Due to its large arc of rotation, the trapezial perforator flap can reach ipsilateral and contralateral occipital, cervical, and upper thoracic wounds as a pedicled flap.43 Skin grafts can be utilized to aid closure if larger skin paddles are harvested.

A

B

Figure 12.8  Heat map of posterior trunk perforator density. The “heat map” image below represents the density of perforators contained in the (A) thoracic and (B) lumbar regions of the posterior trunk. (From Aho JM, Laungani AT, Herbig KS, Wong C, Kirchoff RW, Saint-Cyr M. Lumbar and thoracic perforators: vascular anatomy and clinical implications. Plast Reconstr Surg. 2014;134(4):635e–645e.)

Figure 12.9  Distance of thoracic and lumbar perforators from midline (left vs. right). A cadaveric study was conducted to determine the average perforator distance from the midline in the thoracic and lumbar posterior trunk clusters. The individual means of thoracic perforator distance to the left (top left) and right (top right) of the midline are shown below. The grand mean distance from midline of both left and right thoracic perforators is 14.11 cm (9.34 SD). The individual means of lumbar perforator distance from left (bottom left) and right (bottom right) of the midline are also shown. The grand mean distance from midline of both left and right lumbar perforators is 9.59 cm (5.14 SD).

Table 12.1  Distance of thoracic perforators from midline (left vs. right)

Location of thoracic perforators Left

Right Mean (SD) distance (cm)

Cadaver

No. of perforators

From C7 reference point

1

16

2

15

3

Mean (SD) distance (cm)

From midline

No. of perforators

From C7 reference point

From midline

4.99 (3.10)

8.96 (6.57)

17

5.84 (3.92)

9.92 (8.74)

3.87 (3.53)

20.27 (6.41)

19

6.12 (3.62)

15.89 (8.24)

13

7.95 (7.06)

9.28 (6.96)

16

5.59 (4.54)

5.49 (3.19)

4

22

8.14 (5.05)

19.60 (9.82)

15

9.63 (4.85)

17.27 (10.15)

5

15

7.15 (8.25)

15.96 (8.30)

16

7.17 (5.94)

16.16 (10.37)

Total

81

6.51 (5.74)

15.29 (9.14)

83

6.80 (4.71)

12.96 (9.44)

Mean (SD) overall distances are 6.66 (5.23) cm from C7 and 14.11 (9.34) cm from the midline (n = 164).

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Table 12.2  Distance of lumbar perforators from midline (left vs. right)

Location of lumbar perforators Left

Right

Cadaver

No. of perforators

Mean (SD) distance (cm)

Mean (SD) distance (cm)

From midline

No. of perforators

From coccyx

From coccyx

From midline

1

22

2

10

13.29 (4.89)

6.98 (4.89)

21

13.63 (3.83)

6.40 (2.93)

18.35 (4.36)

8.07 (2.79)

22

13.61 (6.75)

9.27 (2.95)

3 4

17

15.62 (8.32)

7.69 (4.96)

13

16.91 (10.27)

8.69 (4.66)

25

16.53 (9.58)

14.69 (5.71)

38

19.43 (7.07)

11.65 (4.49)

5

21

18.68 (8.35)

11.33 (3.85)

27

17.49 (7.95)

7.70 (5.66)

Total

95

16.28 (7.82)

10.21 (5.61)

121

16.66 (7.48)

9.11 (4.70)

Mean (SD) overall distances are 16.49 (7.62) cm from the coccyx and 9.59 (5.14) cm from the midline (n = 216).

Anterolateral thigh perforator complex

Anteromedial thigh perforator complex

Descending branch to the subdermal plexus Linking vessel

Linking vessel Fascia Suprafascial plexus Adipose layer Subdermal plexus Skin

Figure 12.10  Perforasome theory. Each perforasome communicates with adjacent perforasomes via two main mechanisms: direct flow through linking vessels, which travel in the suprafascial plexus, and indirect flow through non-linking vessels that travel in the subdermal plexus. Communication between linking and non-linking vessels may also be seen.

In a cadaveric study performed by Nyemb et al., trapezial perforator location was assessed.45 In a majority of cases (78%), an average of 16 (range 9–27) perforating arteries can be found within 5–6 cm on either side of the midline, with an average diameter of 0.6 mm (range 0.1–2.6 mm).45 The line of perforators lies within fixed external landmarks, such as the scapular spine laterally, the scapular tip caudally, and the cranial margin of the trapezius, which can be used when designing trapezial perforator flaps.45

Scapular and parascapular The scapular and parascapular flaps are part of the subscapular system (Fig. 12.13). The scapular flap is an axial flap with blood supply provided by the transverse branch of the circumflex scapular artery (CSA). The CSA arises from the subscapular artery and occasionally directly from the axillary artery, before penetrating the triangular space formed by the teres muscles and the long head of the triceps. The flap is oriented parallel to the spine of the scapula (Figs. 12.13 & 12.14). The midline of the flap can be visualized as a horizontal line extending from 2 cm above the posterior axillary crease to the vertebral column. The distal extent of the scapular flap extends midway between the midline of the back and the medial border of the

scapula. The scapular flap is raised from medial to lateral and can include both fasciocutaneous and bony components, with dimensions typically up to 10 × 25 cm. A larger, 50 × 10 cm bi-scapular flap has been described by anastomosing the flap to the contralateral circumflex scapular artery.46 The vascular pedicle is typically 7–10 cm, which may be lengthened up to 14 cm by including the subscapular vessel.47 The arterial and venous caliber of the source vessels ranges from 2 to 4 mm. Donor sites less than 10 cm may be closed primarily, while larger donor sites may require skin grafting for coverage. Other regional flaps may be harvested simultaneously with the scapular flap, including the parascapular, latissimus dorsi, and serratus flaps. A thin, circumflex scapular artery perforator flap can also be raised based off perforating vessels arising within 1.5 cm of the CSA bifurcation, either from the main or descending branch.48–50 The CSA bifurcation is commonly found within the omotricipital space, a triangular region bordered by the teres minor and major muscles superiorly and the long head of triceps laterally.48–50 The parascapular flap is similar in characteristics to the scapular flap and provides another option for fasciocutaneous flap reconstruction from the subscapular system (see Figs. 12.13 & 12.14). It is supplied by the descending branches of the CSA, with multiple radial arteries off the descending

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anastomosing the distal end of the thoracodorsal artery and subscapular vein, forming a reverse flow flap orientation.50

Latissimus dorsi

A

Spinal accessory nerve (XI) Superficial branch of the transverse cervical artery Dorsal scapular nerve B

Deep branch of the transverse cervical artery

Figure 12.11  Trapezius flap. The dissection plane and blood supply to the trapezius muscle flap. (A) Demonstrates the anatomic dissection of a trapezius muscle flap. The deep and superficial branches of the transverse cervical artery are noted with red and the spinal accessory nerve is noted with yellow. (B) Illustrates the above photograph with identification of important structures. (From Wei FC, Mardini S. Flaps and Reconstructive Surgery, 2nd ed. Elsevier, 2017, Fig. 39.3.)

branch providing blood flow for an inframammary extended circumflex scapular flap. The parascapular flap is oriented vertically, parallel to the lateral scapular border (see Figs. 12.13 & 2.14). The midline of the parascapular flap can be visualized as a vertical line extending from the triangular space towards the posterior iliac spine. Additional length can be obtained by following the contour of the inframammary crease. Based off radial branches of the descending branch of the circumflex scapular artery, the inframammary extended circumflex scapular flap can reach dimensions upwards of 10 × 30 cm and has the benefit of improved donor site scar aesthetics.21,50 Because their vascular pedicles arise from the same source artery, the parascapular flap can be raised simultaneously with the scapular flap and/or other flaps emanating from the subscapular system, with the convenience of a single anastomosis at the subscapular vessels (see Fig. 12.13).51–53 The resultant chimeric flaps can incorporate the latissimus dorsi and/or serratus anterior muscles, which can allow for coverage of larger defects.50–53 The arc of rotations for flaps in the subscapular system allows them to reach the shoulder, axilla, and lateral thoracic wall. The pedicle can be lengthened by

The latissimus dorsi (LD), a Mathes and Nahai type V muscle, is another flap originating from the subscapular system (Fig. 12.15; see Figs. 12.1 & 12.13). It receives blood primarily from the thoracodorsal artery via the subscapular artery, and secondarily from segmental perforating branches of intercostal and lumbar arteries. Innervation is from the thoracodorsal nerve, and it is the largest flap that can be harvested off a single vascular pedicle. External anatomical boundaries are formed by the midline of the back, the posterior superior iliac crest, and the inferior angle of the scapula. The LD originates from the outer region of the superior iliac crest and the thoracolumbar fascia and spinous processes (T7–L5) posteriorly; it then extends superolaterally as broad, fan-like muscle, with dimension up to 20 × 40 cm. The LD gradually tapers and inserts into the intertubercular groove of the humerus, forming the posterior axillary fold (see Fig. 12.13). The LD flap is typically raised inferiorly to superiorly and can include muscular and fasciocutaneous components. A vascular pedicle ranging from 5–15 cm can be harvested, depending on the degree of thoracodorsal artery dissection down to its origin at the subscapular artery.14,21,54 As a pedicled flap, the LD can reach as far caudally as the lumbosacral region.14,21,55 Within the substance of the LD muscle, the artery divides into a transverse branch and a descending branch. A split LD flap variation, based on one of these branches, or a muscle sparing LD, can be raised to minimize muscle morbidity. Skin paddles up to 22 × 15 cm can be included for coverage. Because the LD can survive on its secondary segmental blood supply, a medially based, “reverse flow” musculocutaneous LD flap is an alternative for reconstruction in the middle thoracic and lumbar regions (see Figs. 12.1 & 12.15).14,21,54,55 In this version, the thoracodorsal pedicle is sacrificed, and the flap is fed by the T9–T11 posterior intercostal artery perforators. The pedicle may also be lengthened via placement of a vein graft.56 The LD is also the most common flap used in free tissue transfers within the posterior trunk, most commonly for reconstruction of lumbosacral defects.57 This is due to the large thoracodorsal artery diameter, with arterial and venous calibers ranging from 2 to 5 mm. Free tissue transfer with the LD is commonly successful even after the muscle has been irradiated.14,21 If greater length is required to bridge the distance between the flap and a non-local recipient vessel, vein grafts or arteriovenous loops can be utilized (see Free tissue transfer below). The LD can also be raised as a chimeric flap for coverage of larger defects by including other flaps within the subscapular system, including serratus, scapular, and/or parascapular flaps.51–53 The thoracodorsal artery perforator (TDAP) flap can be raised as a fasciocutaneous or cutaneous flap, sparing the LD muscle (Fig. 12.16). The TDAP flap offers consistent, long perforators, with single perforators reportedly able to support flaps up to 18 × 55 cm in size.25,58–61 Like the LD flap, the long pedicle of the TDAP flap makes it favorable for use in free tissue transfer.58 The thoracodorsal vessels course along the deep surface of the LD muscle, divide into the transverse branch and the lateral or vertical branch, typically situated at 45° angles from one another. A cadaveric dissection conducted by Heitmann et al. identified a total of 64 musculocutaneous perforators larger than 0.5 mm in 20 specimens.62 Of the 64 perforators, 36 were from

Flaps for reconstruction of the posterior trunk Dorsal scapular artery Posterior intercostal arteries

363

Dorsal scapular artery Posterior intercostal arteries

Trapezius

Trapezius

A

B

Figure 12.12  Trapezius flap variations. The trapezius flap is a versatile flap that can be based either on its primary or secondary blood supply, allowing for great flexibility in flap design. (A) Demonstrates a turnover trapezius muscle flap based off the posterior intercostal arteries. (B) Demonstrates a fasciocutaneous pedicled perforator flap based off the dorsal scapular artery. (From Wei FC, Mardini S. Flaps and Reconstructive Surgery, 2nd ed. Elsevier, 2017, Fig. 17.9.) Parascapular skin flap

Subscapular artery

Axillary artery

Axillary artery Thoracodorsal nerve

Circumflex scapular artery

Pectoralis minor

Subscapular artery Humerus Long head of triceps

Thoracodorsal artery Long thoracic nerve Circumflex scapular artery Teres major Thoracodorsal artery and nerve

Serratus anterior (flipped out) Latissimus dorsi (flipped back)

Figure 12.13 Subscapular system. The subscapular system is the origin of the axial blood supply for many flaps within the upper thoracic and middle thoracic posterior trunk region. This anatomical relationship can be exploited in the creation of large chimeric flaps that can be raised on a single pedicle.  

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Circumflex scapular artery (cutaneous branch)

Transverse branch

Circumflex scapular artery

Scapular skin paddle

Vertical branch

Parascapular skin paddle

Thoracodorsal artery Subscapular artery

Figure 12.14  Scapular and parascapular flaps. The scapular and parascapular flaps are based off the circumflex scapular artery. The scapular flap is oriented parallel to the scapular spine, while the parascapular flap is oriented perpendicular to it.

Thoracodorsal artery

Axillary artery

Figure 12.16  Thoracodorsal artery perforator (TDAP) flap variations. The TDAP flap is based off perforators from either the transverse or vertical branch of the thoracodorsal artery. (Redrawn from Wolff KD, Hölzle F. Scapular flap. In: Raising of Microvascular Flaps. Springer, Cham; 2018.) Posterior intercostal arteries

Latissimus dorsi

A

Latissimus dorsi

B

Figure 12.15  Latissimus dorsi flap variations. The latissimus dorsi flap is a versatile flap that can be based either on its primary or secondary (segmental) blood supply, allowing for great flexibility in flap design. (A) Is a traditional latissimus dorsi flap based off the thoracodorsal artery, this can be used as a locoregional flap or a free flap. (B) Demonstrates a turnover latissimus dorsi muscle flap based off the posterior intercostal arteries. (From Wei FC, Mardini S. Flaps and Reconstructive Surgery, 2nd ed. Elsevier, 2017, Fig. 17.10.)

the descending branch and 28 from the transverse branch.62 A direct cutaneous branch was also noted in 11 dissections.62 These branches follow an intramuscular course before continuing as skin perforators. The first perforator typically arises 6–8 cm

below the posterior axillary fold and 2 cm medial to the posterior axillary line. Each of roughly three subsequent perforators arise at 1.5–4 cm intervals inferiorly. The perforators range from 0.3 to 0.6 mm in diameter. After locating the perforator, dissection

Flaps for reconstruction of the posterior trunk

proceeds until the desired pedicle length is obtained. Care must be taken to preserve the thoracodorsal nerve.25 Three flap variations can be raised from the thoracodorsal artery perforators including the musculocutaneous perforator, the thoracodorsal artery perforator (TDAP) flap based on the septocutaneous perforator, and the lateral thoracic artery perforator (LTAP) flap based on the direct cutaneous perforator from the lateral thoracic artery (see Fig. 12.16).61–64 The TDAP, however, predominates due to a long vascular pedicle (18 cm) and large diameter vessels. This provides a greater ease of anastomosis to recipient vessels outside the zone of injury, with an option of end-side placement, thus preserving flow in receptor vessels.65 Modifications can be made to the TDAP flap to increase flap length and bulk, including pre-expansion.66 More than one perforator from the same thoracodorsal vessel branch can be incorporated, and the surrounding subcutaneous fat can be harvested by angling the subcutaneous dissection obliquely from the skin paddle.66,67 The TDAP flap orientation is configured along the axis of the linking vessels, allowing for inter-perforator flow. Further benefits to utilization of the TDAP flap for reconstruction of the posterior trunk include the availability of chimeric variations with other flaps in the subscapular system (see Figs. 12.13 & 12.16).51–53 Common chimeric flap combinations include the TDAP and LD and the TDAP and serratus anterior muscle.68,69 Scapular bone may also be added when osseous reconstruction is required. The TDAP is an ideal perforator flap in the posterior trunk due to its ease of harvest, soft-tissue bulk, and minimal morbidity.63,68,69

365

Necrotic tissue Fascia Incised fascia

Latissimus dorsi/ trapezius

Cutaneous perforator

Longissimus Iliocostalis

Lateral perforator

Spinalis

Medial perforator

A

Exposed instrumentation

Raise flaps

Paraspinous muscle The paraspinous (PS), or erector spinae, are a group of intrinsic muscles that includes the longissimus, iliocostalis, and spinalis (Figs. 12.17 & 12.18; see Fig. 12.2). They are located within the paravertebral gutters on either side of the spinal column. The PS muscles extend from the lumbosacral to thoracic region, originating from the sacrum, iliac crest, lamina, and transverse processes of the vertebrae and inserting into the posteromedial aspect of the ribs, with insertions into the occiput at the most superior extent (see Fig. 12.2).70 The blood supply to the PS muscles is provided by the intercostal arteries, segmental branches from the aorta, which give deep and lateral perforators to the muscle.70 Thus, the PS is classified as a Mathes and Nahai type IV muscle. Exposure and harvest of the PS flap for closure of upper thoracic defects requires dissection of the overlying trapezius, rhomboid major, and serratus posterior superior muscles (see Figs. 12.1 & 12.2).70 Alternatively, dissection of the thoracolumbar fascia, latissimus dorsi, and serratus posterior inferior muscles is necessary for exposure and harvest of the paraspinous muscle in the middle thoracic region (see Figs. 12.1 & 12.2). The PS flap is commonly utilized as a bipedicled or turnover flap, although osseo-muscular flaps, as initially described by Mustardé, can also be harvested by fracturing of the transverse processes of the vertebrae.21,71 Flap design should incorporate well-perfused tissues with perforators based outside the zone of injury. Bipedicled PS flap elevation incorporates the lateral column perforators and proceeds in a medial to lateral direction (see Fig. 12.18). Attachments to the medial spinal process and the transverse process are removed (see Figs. 12.17 & 12.18). The flap remains in continuity at the superior and inferior muscle segments, ensuring adequate segmental perfusion while

B

Extend flaps

C Figure 12.17  Paraspinous muscle flap. The midline spinal wound below is complicated by exposed hardware and potential for cerebrospinal fluid leak. A paraspinous muscle flap can be used for deep closure of the defect. Paraspinal perforators originate from the dorsal intercostal artery (DICA). The perforators split into the medial and lateral branch. The medial branch may be sacrificed to increase advancement of the flap. The blood supply for the paraspinous (erector spinae) flap enters from the deep aspect of the muscle. (A,B) The fascia is incised laterally, and the attachments to the spine and transverse processes are released medially and on the deep muscle surface to increase flap advancement toward the midline. (C) The flap is approximated in the midline in a “vest-over-pants”, overlapping fashion. For added security, a second superficial closure with vascularized trapezius or latissimus muscle can be performed.

allowing the medial portion of the flap to advance toward the midline defect (see Fig. 12.18). Flap advancement can be increased by cauterization of medial perforators.29,70 Because the bipedicled design can limit flap excursion, a superiorly based, unipedicled flap based on intramuscular longitudinal

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B

E

H

C

D

F

G

I

J

Figure 12.18  Paraspinous and latissimus dorsi muscle flaps. Case example of a 65-year-old female patient with a history of lumbar scoliosis with a midline posterior trunk defect and spinal hardware after lumbar arthrodesis. The patient underwent reconstruction with paraspinous and latissimus dorsi muscle flaps. (A–C) Dissection and mobilization of the paraspinous muscle complex was performed with cautery dissection in the superficial plane, from the midline laterally for approximately 7 cm starting on the left. This dissection was performed for the length of the defect and then repeated on the right side. (D–F) Good paraspinous approximation was obtained along the full length of the defect. (G,H) The latissimus dorsi muscles, superficial to the paraspinous muscles along the length of the defect, were dissected and mobilized to provide an additional layer of muscle flap coverage. (I,J) The paraspinous muscle then latissimus dorsi muscle flaps were co-apted in the midline by placement of interrupted 0 Vicryl figure-ofeight sutures.

Flaps for reconstruction of the posterior trunk

K

367

L

Figure 12.18, cont’d  (K) Two superficial 15 F Blake drains were placed and brought out the patient’s left side (deep drain placed by neurosurgery on right side). The wound was closed in a multilayered fashion and reinforced with horizontal mattress sutures. (L) An incisional wound vacuum-assisted closure (VAC) device was then applied.

vessels is another alternative, which can be raised bilaterally up to T10.21,29 Removal of attachments from the posterosuperior iliac crest, quadratus lumborum, and thoracolumbar fascia can also increase flap advancement. When the fascial incision is placed on the lateral aspect of the erector spinae fascia, a turnover flap can be performed. The flap is raised from lateral to medial, and the medial perforator row is preserved. The lateral flap edges are then transposed toward the midline, while ensuring good opposition under minimal tension. A history of bilateral laminectomies increases the likelihood of damaged medial intercostal perforators and segmental pedicles from the posterior intercostals. In such cases, a turnover PS flap may be unreliable.70

Intercostal artery perforator If multiple primary and secondary options for posterior trunk reconstruction have been utilized or are otherwise unavailable, an intercostal artery perforator (ICAP) flap can be utilized for wound coverage. The intercostal artery has four regions including the vertebral, intermuscular, rectus segments, and costal groove segments, which has the largest perforators. Perforators from the intercostal artery can supply a flap up to 18 × 12.5 cm. Excision of the cephalad rib can increase the arc of rotation of the flap; however, this increases morbidity. The flap can also be sensate with addition of the nerve.21 The extensive network of intercostal artery perforators (ICAP) from the lower nine intercostal spaces forms the largest angiosome in the posterior trunk (Fig. 12.19).72 The vertebral segment of the posterior intercostal artery produces dorsal, collateral, and nutrient branches, accompanied by a single nerve and vein.6 There are many options for flaps based on the intercostal perforators, which follow the curve of the thoracic cavity and includes, from posterior to anterior, the dorsal intercostal artery perforator (DICAP), dorsolateral intercostal artery perforator (DLICAP), lateral

intercostal artery perforator (LICAP), and anterior intercostal artery perforator (AICAP) (see Fig. 12.19). Each of these flap options can be raised as island flap, V–Y advancement flap, and propeller flap.73 The DICAP flap can be found within 5 cm lateral to the midline of the back, from T3 to T11, posteriorly. The DLICAP flap is found up to 2 cm off the mid-scapular line at the 8th–11th intercostal spaces. The LICAP flap is located at the intersection of the midaxillary line and the inferior border of the corresponding rib, at the 3rd–11th intercostal spaces. The AICAP flap is found 1–3 cm from the lateral sternal border at the 1st–9th intercostal spaces. ICAP flaps can be raised off a single perforator with a skin paddle width ranging from 8 to 15 cm,74–76 although skin graft closure of the donor site may be necessary for widths greater than 8 cm.74 Multiple perforators can be included in the flap design for larger defects. The risk of venous congestion, a common complication encountered with ICAP flaps, can be minimized by limiting the amount of flap skeletonization and leaving an island of soft tissue around the perforator artery.74 Due to an extensive network of nine bilateral perforator arteries, the ICAP flap variations have a high capacity for mobilization, allowing great flexibility for use in defects all over the posterior trunk.72,74 The DICAP flap, the posterior-most ICAP option, has been shown to be a reliable flap for reconstruction of superficial defects in the posterior trunk (see Fig. 12.19). In a study of 20 patients with tumor extirpation defects in the posterior trunk, only one DICAP flap developed complications.77 The single complication was minor marginal flap necrosis, which subsequently healed uneventfully and without intervention. The majority of DICAP flaps were raised on a single perforator (60%) and mobilized either in V–Y (11) or propeller fashion (9).77 Flaps ranging from 4 × 6 to 6 × 14 cm in dimension were used to cover defects up to 6 × 8 cm.77 On average, the operative time was 70 minutes.77 Variations of the ICAP flap continue to be a safe, reliable option for resurfacing defects in the posterior trunk.

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DICAP

LICAP

AICAP

Figure 12.19  Intercostal artery perforator (ICAP) flap variations. ICAP flap options from posterior to anterior, include the dorsal intercostal artery perforator (DICAP), dorsolateral intercostal artery perforator (DLICAP), lateral intercostal artery perforator (LICAP), and anterior intercostal artery perforator (AICAP). (Adapted from Hamdi M, Van Landuyt K, de Frene B, et al. The versatility of the inter-costal artery perforator (ICAP) flaps. J Plast Reconstr Aesthet Surg. 2006;59(6):644–652.)

Lumbar perforating arteries

Lumbar muscles and arterial perforators A

Lumbar flap design for second and fourth perforators B

Figure 12.20  Lumbar artery perforators (A) and flap design (B). The lumbar muscles and their relationship to the lumbar perforators are shown. (From Zenn M, Jones G. Reconstructive Surgery: Anatomy, Technique, and Clinical Application. CRC Press; 2012.)

Lumbar artery perforator A pedicled lumbar artery perforator (LAP) flap can be used for reconstruction of lumbosacral defects (Figs. 12.20–12.25; see Fig. 12.1). Four pairs of lumbar arteries originate from the posterior surface of the abdominal aorta (L1–L4), extending posteriorly around the bodies of the vertebrae and continuing as perforators to the lumbar tissues (see Fig. 12.20).

A 5th perforating vessel (L5) originates from the iliolumbar arteries, fed by the iliac system (see Fig. 12.20). Lumbar perforators arising from L1–L3 run between the erector spinae and the quadratus lumborum muscles, and the last two pairs (L4–L5) run anterior to the quadratus lumborum muscles and lateral to the erector spinae musculature. The perforators pierce the transversus abdominis aponeurosis and course either directly through or just lateral to the erector

Flaps for reconstruction of the posterior trunk

A

369

B

Figure 12.21  CT image of lumbar artery perforator. A preoperative computed tomographic angiogram (CTA) or magnetic resonance angiogram (MRA) can help to choose and localize the best perforator, which is then confirmed preoperatively with the Doppler. Below, are axial CTA images of a right (A) and left (B) lumbar artery perforator.

A

B

C

Figure 12.22 Lumbar artery pedicled perforator. A case example of an 81-year-old male who underwent preoperative radiotherapy and operative resection of a back sarcoma is shown below. The defect was reconstructed with a lumbar artery pedicled perforator flap, designed as a propeller flap around the chosen perforator to allow for rotation of no more than 180°. (A,B) Skin laxity in this case would have allowed designing the flap in several directions. The horizontal axis was chosen to follow the direction of the lumbar angiosomes. (C) The flap was elevated, rotated, and inset. An immediate postoperative image is shown. Harvest the flap in areas of minimal tension so that the donor site can be closed primarily.  

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B

Figure 12.23  Superior gluteal artery perforator flap. (A) A case example of a sacral pressure ulcer on a paraplegic patient is shown. The ulcer was covered with a propeller flap design, based on a superior gluteal artery perforator. The distance between the perforator and the distal portion of the flap is slightly longer than the distance between the perforator and the furthest part of the wound to avoid closure under tension. (B) Flap inset into defect.

Figure 12.24  Lumbar artery perforator. Below is a case example of a 77-year-old, multi-comorbid female patient with a history of sarcoma on her back, initially treated with radiotherapy, and reconstruction with a rhomboid flap. The sarcoma eventually recurred requiring surgical management for tumor resection and soft-tissue reconstruction. A large, 33 × 15 cm lumbar artery perforator propeller flap was raised with minimal skeletonization, and rotated 90° and advanced prior to inset. Partial flap loss can be appreciated in the distal tip of flap. This patient exhibited a large degree of soft-tissue laxity in the lumbar region, and thus the wound was able to be closed primarily.

spinae, and finally through the thoracolumbar fascia. They then immediately bifurcate or trifurcate into smaller vessels, supplying soft tissues in the lumbar region. The first pair of LAPs can be visualized on surface anatomy, extending inferolaterally along the inferior margin of the 12th rib. The second and third LAPs cluster in the midline, close to the L2 and L3 vertebrae. The L4 LAPs pierce

the thoracolumbar fascia roughly 7–10 cm from the midline, on a horizontal plane drawn between the two posterior superior iliac crests.78,79 A LAP flap harvested too far laterally may be subject to fat necrosis and sequelae related to poor perfusion. Flaps as large as 15 × 26 cm can be supported by perforators in this region. The pedicle of the LAP flap tends to be short, ~2–3 cm, and arterial/venous grafting may be required to extend its reach. Innervation is provided by the superior cluneal nerves (L1–L3). The arterial diameter is ~1 mm, and the vein is commonly larger than the artery. An early study by Kato et al. found that, in general, the L2 and L4 perforators are the largest in diameter and length, and thus ideal for flap design.80 Another study, however, by Bissell et al., found that L1 and L4 LAPs are the best choice due to statistically higher perforator numbers (p40 years of age or is at risk for DVT. Oral estradiol is an option if the patient is 1 cm), we will utilize a composite technique and harvest a 2.2 cm section of areola and a separate portion of the papilla. The grafts are placed on a moistened gauze on the back table for later use. The previously drawn mastectomy ellipses are then incised and carried down to the breast capsule. Skin flaps are raised in the plane separating the breast capsule and overlying the skin and subcutaneous tissue. As with the previous techniques, it is essential that the subcutaneous tissue is preserved, and that the dissection plane follows the breast capsule precisely to avoid overthinning of the skin flap and a hollowed-out appearance. Firm counter-traction of the breast tissue facilitates the dissection. These flaps are elevated to the extent of the pre-marked breast footprint, with care to remove all breast tissue in the axillary tail to prevent unwanted fullness. It is important that the inferior skin flaps are thinned adequately, and that the dissection is carried out past the marked IMF. As with the other techniques, the breast mound is elevated from the pectoralis fascia; this is thought to decrease postoperative pain, bleeding, and seroma formation. After the mastectomy is completed, the skin flaps are temporarily stapled closed, and the patient is then sat up to assess scar position, shape, and symmetry. Adjustments are made with the

patient sitting up through a combination of tailor-tacking and staples until optimal scar position is obtained. The patient is returned to a supine position, skin is trimmed, and hemostasis is ensured. A 15 F round drain is placed in the mastectomy cavity and secured in place. The wound is then closed in layers. At this point we proceed with free nipple grafting. After the mastectomy is completed and closed, the position for the NAC is determined. The patient is sat upright on the operating table and the lateral border of the pectoralis muscle is palpated and marked. Paper templates are used to determine the NAC position. The templates are placed approximately 1.5–2.5 cm above and medial to the pectoralis borders, with final position based on body habitus and surgeon aesthetic judgment21 (Fig. 14.4.6). The most common error is leaving the NACs too high and too medial, and it is important to avoid this and position the NAC near the inferior insertion and lateral border of the pectoralis for optimal aesthetics.21,22,29 Once the appropriate position has been determined, the patient is returned to a supine position. Because of the tendency for the grafted NACs to elongate in a vertical direction over time along the lines of tension, we have found that modification of the recipient site to a horizontal oval shape has been an effective method to create a final round shape. We begin by drawing the 2.2 cm circle at the optimally determined location of the NAC as described above. In order to orient the oval, a line is drawn through the circle perpendicular to the incision in the direction of greatest tension (Fig. 14.4.7). The circle is then converted to a horizontally oriented oval

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CHAPTER 14.4  • Breast, chest wall, and facial considerations in gender affirmation

2.5c

m

1.5c

m

A

B

C

Figure 14.4.7  Modified free nipple graft recipient site. Once placement has been determined, the recipient site is converted to an oval shape due to the tendency of nipple grafts to elongate vertically over time. (A) The solid black line is the lower incision. Dashed line is the direction of greatest tension. Final dimensions of the graft recipient site are 2.5 cm width × 1.5 cm height. (B,C) Oval is de-epithelialized and graft inset.

A

B

C

Figure 14.4.8  Preoperative and postoperative photos of chest masculinization using the double incision technique with free nipple grafts. (A) The lateral view demonstrates significant skin laxity with an acute IMF angle. (B) Anteroposterior view shows NACs below the position of the pectoralis border. (C) Postoperative result demonstrates scars camouflaged along the inferior border of the pectoralis muscle.

with the vertical height along this line. Through experience, we have found that oval dimensions of 1.5 cm in height × 2.5 cm in width yield a nearly round NAC in most cases, but these dimensions may need to be adjusted as deemed necessary based on skin tension. This oval is then de-epithelialized for graft placement. The oval recipient site compensates for nipple graft distortion due to the direction of skin tension, with the end result being an NAC that will be more circular over time (see Fig. 14.4.7C). After securing the graft, pressure bolsters are placed and left in place for one  week. As for other mastectomy techniques, gauze and a compression vest are placed. The compression vest, drains, and, if applicable, the nipple graft pressure bolster are left in place for one  week. At the first postoperative visit, the bolsters are removed, and grafts and incisions inspected. Drains are removed once they are draining less than 30 mL per day. Patients continue to wear their compression vest for a total of 2–4 weeks. The scars for the double incision technique are well camouflaged if placed along the inferior border of the pectoralis muscle (Fig. 14.4.8).

Inferior pedicle technique It is also possible to keep the NACs connected on a dermoglandular inferior pedicle, which has the possibility of retained NAC sensation and a more natural appearance of the NAC by avoiding a skin graft. The disadvantage is the bulge that is invariably left by the pedicle, which detracts from the chest contours. Advocates have stated that in heavier patients, the residual

bulk is not prominent and that for some patients it is an acceptable trade-off.24,29 Wilson et al. found this technique to be used 15.7% of the time, but in our practice it is almost never used, preferring the free nipple graft technique for optimal contours.28

Postoperative considerations and complications There is high satisfaction reported with all chest masculinization, regardless of technique.6–8,28,30 Hematoma is the most common acute complication after chest masculinization, ranging from 3% to 5% in the double incision techniques and 10% to 15% in the periareolar and circumareolar techniques, the difference presumably due to the limited exposure in the latter.22–25,28,31 Other complications include seroma formation and infection, which are relatively infrequent and typically managed conservatively.25 NAC partial or complete loss can occur but is rare, provided the dermal pedicle is maintained and the NACs are bolstered appropriately, depending on technique. Revisions for redundant skin and dog-ears are common, ranging from 8% to 40% in the literature, and are significantly higher in the periareolar and circumareolar techniques.23,25 Most revisions are minor and can be performed under local anesthetic. Overall, chest masculinization has high patient reported satisfaction rates and is effective at reducing gender dysphoria and improving quality of life in transmasculine individuals.6–8,28,30

Breast augmentation

Breast augmentation Breast augmentation is desired in nearly half of transwomen, and the number of transfeminine augmentations performed is steadily increasing.4,32 This procedure has been found to significantly improve quality of life and psychosocial well-­ being, and high satisfaction rates have been reported following surgery.33,34

Preoperative considerations The previously mentioned WPATH Standards of Care should be followed when evaluating a patient for breast augmentation.2 Though hormone therapy is not universally required, estrogen use for 1–2 years prior to surgery can improve cosmetic outcome. Estrogen is the key hormone responsible for female secondary sex characteristics, and is often administered in combination with androgen blockers, such as spironolactone, which also possesses anti-androgen and breast-enhancing effects. Studies suggest that breast growth begins to occur at 3 to 6 months following initiation of estrogen therapy, with maximum growth occurring at 2 years post-initiation.35,36 Optimal breast growth is not typically reached, with most patients only achieving Tanner stage II or III breasts even after a year of hormonal therapy, necessitating breast augmentation to achieve a more feminine chest.37 A thorough medical history should be collected, which includes personal or family history of venous thromboembolism or breast cancer. Estrogen may contribute to an increased risk of venous thromboembolism and should be stopped 2 weeks prior to surgery and resumed 2–4 weeks following surgery, though this is controversial.38 Patients should be counseled on smoking and nicotine product cessation at least 4 weeks prior to surgery and 4 weeks following surgery to prevent wound healing complications.19 Patients should also be screened for prior silicone breast injections, which may be more common in the transgender population and contribute to an increased risk of infection postoperatively.39 Physical examination should note the quality of the skin envelope and any asymmetries in the breast or chest wall. Patients should be made aware of these asymmetries and should be informed that they may persist following the operation. Measurements, such as base width, sternal notch-to-nipple distance, and nipple-to-IMF distance, should be collected, which will aid in implant selection, further described below. Patient expectations and desires should be discussed, as well as any limitations of the procedure to meet these expectations. The patient should be made aware of the risks and benefits of breast augmentation more broadly, including capsular contracture, rupture, infection, hematoma, asymmetry, migration, and breast implant-associated anaplastic large cell lymphoma.37,40,41 Patients should be informed of FDA recommendations for MRI screening of silicone implants for rupture, 3 years after the initial placement and every 2 years after that.42

Operative principles Cosmetic breast augmentation is commonly performed by many plastic surgeons. There are some important anatomical differences between a chest wall that is phenotypically male

445

and phenotypically female, however, and care should be taken to adjust the breast augmentation procedure accordingly to obtain a satisfactory cosmetic result. When compared to the cis-female chest, the cis-male chest has a larger pectoralis muscle, a wider sternal border, more inferiorly and laterally set nipples, smaller nipple diameter, a larger horizontal chest width, a more superior IMF, and a larger breast base width. Additionally, with the use of hormonal therapy, transwomen may develop more “bud”-like breast development centered beneath the NAC rather than more widely distributed, similar in character to gynecomastia.37 Implant selection is a shared decision between the patient and surgeon. Decision-making tools exist for implant selection and operative planning, which tend to emphasize degree of soft-tissue coverage, breast base width, and IMF location as important considerations.37,43–47 These principles are generally applicable to breast implant selection in the patient seeking transfeminine breast augmentation; however, some anatomic distinctions create nuances. The larger breast base width and chest horizontal width generally favor the selection of higher volume implants; however, a tighter skin envelope may impose some limitations with regard to implant profile. Preoperative markings include the midline of the chest, position of the IMF, location of the planned new IMF, and medial and lateral limits of the dissection pocket. The patient is positioned supine with arms out and secured to armboards to allow the surgeon to sit the patient upright intra-operatively to assess implant position and symmetry. Antibiotics are administered prior to incision to minimize the risk of postoperative infection. An inframammary incision is advocated by some authors due to ease of adjustment of the IMF, although a periareolar incision is also commonly used with good results (Fig. 14.4.9). Adjustment of the IMF is necessary in either scenario to improve lower pole expansion. Multiple authors suggest using the radius of the implant (base width × 0.5) to calculate the appropriate distance from the nipple to the IMF.37,44,48 Subtracting the preoperative nipple-to-IMF distance from this number dictates the appropriate amount of IMF lowering that must be performed. This formula allows half of the implant to sit in the lower pole pocket, which prevents superior implant displacement and downward-pointing nipples. The location of the new IMF should be reinforced by tacking Scarpa’s fascia to the chest wall at the conclusion of the case. Implants can be placed in the submuscular, subfascial, or subcutaneous plane. Many surgeons who perform transfeminine breast augmentation choose to place implants in the subcutaneous position, with dissection performed in the plane above the prepectoral fascia.37,49 The rationale for using this plane is to minimize the risk of severe animation deformity and implant displacement, due to an enlarged pectoralis muscle and more challenging submuscular pocket dissection on a male chest.37 Submuscular or dual plane placement may be warranted in thin patients with otherwise inadequate soft-tissue coverage, however. Subfascial implant placement, beneath the prepectoral fascia, has also been described with promising results.49 The implant pocket is typically centered beneath the NAC and designed for a precise fit of the selected implant. There must be a balance, however, as centering implants under the more widely spaced NACs can result in lateralized implants and a lack of central cleavage. Adjustment can be performed with more medial

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A

B

C

D

Figure 14.4.9  (A–D) Pre- and postoperative results of transfeminine breast augmentation using a periareolar technique. A 520 cc silicone implant was selected based on a preoperative base diameter of 13.5 cm.

dissection, with release of some of the pectoralis major sternal insertions. Care must be taken to avoid excessive release, however, which can result in medial implant migration and symmastia. If there is intra-operative uncertainty regarding implant sizing or satisfaction with pocket dissection, saline sizers can be inserted into the pocket and the patient can be sat up. Once the pocket has been adequately dissected and the implant size has been chosen, copious irrigation of the pocket is performed using a triple-antibiotic or povidone-iodine solution. Implants are then placed using a no-touch technique, and a multi-layer closure is performed. At the conclusion of the case, the patient is placed in a postsurgical bra or compression garment. Patients are typically advised to continue to wear this garment, or a sports bra without underwire, for the first several weeks to provide support and help reduce swelling. They are also advised to avoid strenuous activity or heavy lifting for a period of 4 to 6 weeks following surgery. If implants are noted to be superiorly migrating, a breast band may be provided to provide downward compression. Fat grafting can be performed as an adjunctive procedure to enhance medial fullness of the augmented breast. This procedure consists of liposuction followed by sterile fat preparation and injection. The amount of permanent take of the injected volume of fat is unpredictable; however, the procedure can be performed serially for optimal results. Common donor sites of fat include the abdomen, flanks, and thighs. Revisionary and adjunctive procedures may not be covered by insurance, however, which is important to discuss with patients preoperatively.

Tissue expanders are not commonly used in transfeminine breast augmentation due to cost and desire for a single-stage approach, though they may be warranted in patients with particularly poor soft-tissue quality who desire larger implants. Breast augmentation in both cis and transwomen has a high satisfaction rate and a favorable complication profile. Patients report improved satisfaction with breasts, psychosocial well-being, and sexual well-being following augmentation.33,34,50,51 Complication rates of 0.5%–2.0% have been described, with hematoma being the most cited complication.32,52 This is similar to the complication profile observed in the cisgender cohort.

Facial feminization surgery Facial feminization surgery was pioneered by Dr. Douglas Ousterhout in the late 1980s, who initially focused on recontouring the upper facial bony skeleton.53 Over the last 40 years, these techniques have expanded to address discrepancies between the masculine and feminine bony skeleton and soft tissue of the upper, middle, and lower face. The most common of these procedures include orbit contouring, brow lift, hairline advancement, fat grafting to temples, cheeks, and lips, rhinoplasty, upper lip lift, mandibuloplasty, and chondrolaryngoplasty.54 Non-surgical alternatives or adjuncts to these procedures have also been reported, including fillers for lip and malar augmentation as well as neurotoxins for lateral brow elevation and treatment of rhytids.55 Facial feminization surgery is attained or desired in 45% of transwomen.4 It is a rewarding but challenging endeavor for both the patient and

Facial feminization surgery

surgeon and requires complete investment on behalf of the surgeon in taking care of the entire patient with the help of a well-organized multidisciplinary team.56

Anatomy Facial feminization requires an understanding of the anatomic differences between the male and female face that convey masculinity and femininity. While there are innumerable quantifiable variances, several critical differences are worth highlighting. Differences in the upper-third of the face are most notable with regard to frontal bone, orbits, hairline, and brow position. The male forehead is flatter with prominent supraorbital bossing secondary to large frontal sinuses and greater thickness of the supraorbital ridge.53,54,57 The male hairline tends to be M-shaped with varying degrees of recession, as opposed to O-shaped in the female, and sits 7–8 cm above the center point of the eyebrows compared to 5.5–5.8 cm in the female face.54,58 In the female skeleton, relative to the upper face, the orbits are higher, more rounded, and appear larger, leading to a softer appearance.54 The female eyebrow is more curved than the male, arching over instead of at the supraorbital ridge with its peak at the lateral limbus, and it sits above the bony orbit rim, whereas the male eyebrow sits at or below the orbit rim. The female midface has wider zygomatic bones with more prominent, but delicate malar eminences resulting in a rounder or more heart-shaped contour compared to the squarer male contour. This female contour can be perceived as an inverted triangle drawn by connecting a line between the two malar eminences to the chin point.59 The nose is overall smaller in females with a more concave dorsum. The glabellar angle is additionally more obtuse, as is the nasolabial angle (greater tip rotation: 100–105°) with a narrower alar base and increased tip projection.60 The malar fat pads are fuller in the female face, providing a softness and fullness to the anterior cheek that is not present in the male face.54 With regard to the lower face, overall lip height is greater in males than females.61 Females have greater upper incisor show in repose and a smaller proportion of upper lip cutaneous height to vermilion height.62 The lower face is dominated by the shape and size of the mandible. Males have a wider bigonial angle secondary to greater bony volume as well as bulk of the masseter, conveying a squarer appearance to the male face.63 The female chin is narrow, shorter, and less projected than the male chin, and can be described as a softer, rounder, and less prominent feature.63 Finally, the thyroid cartilage is more prominent in males secondary to a more acute angle at the laryngeal prominence.

Preoperative planning Though WPATH does not provide preoperative guidelines for facial feminization surgery, criteria similar to those proposed for breast/chest surgery should be followed.2 While facial feminization can be a life-saving procedure, protecting the patient from assault, bullying, and alleviating gender dysphoria, some insurance companies still consider it to be cosmetic and thus do not cover it. In addition to standard preoperative counseling, discussing coverage issues with patients is paramount. Preoperative imaging is critical for surgical planning. Plan films or CT scans can be used to evaluate the size of the frontal

447

sinus, thickness of the frontal bone, dimensions of the chin, fullness of the angle of the mandible, and course of the inferior alveolar nerve. Information gained from imaging allows the surgeon to select the most appropriate techniques.

Hairline, forehead, and brow Hairline shape and position is extremely important to address during feminization of the face. Both lowering and reshaping of the hairline can be performed via a trichophytic (beveled cut) incision 4–5 mm behind the hairline to allow regrowth of hair through the maturing scar. The incision is then transitioned at the temporal recession region into the hair to a more traditional bicoronal type incision. The scalp is then raised in a subgaleal plane back to the occiput to allow for anterior movement of the scalp flap to the desired position of the new hairline. Serial galeotomies may need to be performed if adequate advancement is not achieved after elevation of the flap.58 Additional reshaping of the leading edge of the central hairline may also be needed to create the appropriate feminine shape. The galea of the scalp flap should be sutured down to the forehead periosteum to prevent retraction of the hairline. More recently, follicular unit method for hair transplantation has been used in conjunction at the time of hairline advancement to completely fill in the temporal hollows. The follicular units are harvested from a crescent of temporal scalp that is removed during the hairline advancement procedure.58 Feminization of the forehead was first thoroughly studied by Dr. Douglas Ousterhout. He originally classified foreheads into three types, which has subsequently been modified into four types by Dr. Jordan Deschamps-Braly58 (Fig. 14.4.10). Several methods of forehead recontouring have been described since the original report by Dr. Ousterhout,53 and choosing the correct technique can be done based off of the Deschamps-Braly classification system (Fig. 14.4.11). The most common forehead type is type III. Feminization of a type III forehead utilizes removing the anterior table of the frontal sinus in the area of the glabellar ridge, followed by contouring of the removed bone segment and setback of this segment with microplates, in addition to burr contouring of the supraorbital bar and lateral orbit rims to decrease thickened areas and soften the orbital shape54,57,64 (Fig. 14.4.12). Access incisions include trichophytic or bicoronal incisions depending on hairline repositioning and need for a direct brow lift. Once bony work is complete, a direct brow lift can be performed by either removing a strip of forehead skin if a trichophytic incision is used, or a strip of scalp if a bicoronal incision is used (Fig. 14.4.13). Reported patient satisfaction is high, though complications can be serious, and include mucocele formation, malunion of anterior table segments, and alopecia.57,64

Midface The goals of midface contouring include providing a rounder appearance of the facial contour while highlighting the malar prominences but minimizing the overall mass of this region of the face. Feminizing the malar region can often be done with fat grafting to increase malar volume.65 Cheek augmentation can also be accomplished with alloplastic implants including both silicone and porous polyethylene implants inserted through an upper gingivobuccal sulcus incision if significant deficiency in the region is noted.

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SECTION II

Type I

Absent or very hypoplastic frontal sinus Type III

CHAPTER 14.4  • Breast, chest wall, and facial considerations in gender affirmation

Type II

Present sinus and glabellar ridge in good AP position with recessed forehead Type IV

Rhinoplasty Feminizing rhinoplasty utilizes traditional open and closed rhinoplasty techniques to address the nasal dorsum, width of the bony vault, nasal length, tip projection and rotation, and alar width.60,69,70 The nasal dorsum is typically addressed by performing a bony or component dorsal hump reduction, as needed, to increase the concavity of the dorsum in profile as well as create a more obtuse nasofrontal angle. Nasal bone osteotomies and infracturing can narrow a widened bony nasal vault. Tip rotation is achieved with tip rotation sutures, cephalic trim, and columellar strut grafts. Further tip work including caudal septal reduction can decrease the length of the nose, and suturing of the alar domes can also be utilized to refine tip shape and narrow the domes. Often alar base reduction is needed to harmonize the ala to the new smaller, feminine nose (Fig. 14.4.14). During these procedures, it is important that aesthetic assessment and operative principles are still followed to appropriately individualize treatment, achieve an aesthetic as well as feminine result, and minimize the numerous complications that can lead to a poor outcome.71

Lips Lip lift procedures convey more feminine, as well as aesthetically pleasing, proportions to the upper lip.72 The goals of this operation include reducing the height of the cutaneous upper lip, increasing the height of the red vermilion, enhancing pout, achieving aesthetically pleasing dental show, and hiding the visible scar at the nasal base.73 The superior incision or final scar line is marked at the junction of the nasal base and upper lip and the planned amount of skin resection is measured with calipers at reference points based on the desired amount of upper lip height and incisal show (typically 5–10 mm simulated with a pinch technique). Meticulous atraumatic technique during excision and closure is critical to minimize aberrant scarring, which is the most common complication with this procedure.

Chin and mandible

Prominence of glabellar ridge with present sinus

Entire forehead and glabellar ridge are under-projected

Figure 14.4.10  Deschamps-Braly forehead classifications. Forehead type is determined by presence or absence of the frontal sinus, in addition to glabellar ridge, and forehead anterior–posterior position. Surgical technique is determined based on forehead type.

While performed less frequently, procedures to the zygoma can also be used to feminize the midface. The sandwich zygomatic osteotomy is an effective technique for increasing zygomatic width that involves a transoral osteotomy of the zygoma and lateral translation of the osteotomized segment with placement of an alloplastic or autogenous bone graft.66 Segmentalized osteotomies of the entire zygomaticomaxillary complex have also been described to increase the projection of the entire zygoma in relation to the upper third and remainder of the midface.67,68

Mandibular recontouring focuses on softening the mandibular angle to decrease bigonial distance and lend a more ovoid shape to the face, as well as narrowing the width and height of the chin.74 Both genioplasty and mandibular angle reduction can be performed concomitantly through intraoral gingivobuccal sulcus incisions to minimize external scars. Mandibular angle reduction can be performed using high speed burrs to reduce the prominences of the angle, body, and external oblique ridge while taking care to avoid damage to the dental roots or inferior alveolar nerve.75 Osteotomies can additionally be utilized for bony reduction in patients with more prominent angles, with subsequent fine contouring with burrs.76,77 The excess bulk of the masseter is a masculinizing feature which typically is reduced secondary to atrophy after stripping of the pterygomasseteric sling, though adjunct botulinum toxin injections can be utilized.59 Feminizing genioplasty is aimed at reducing the prominence of the chin in the horizontal and vertical dimensions. While subtle changes can be made with burring or contouring, reduction genioplasty typically lends better results in our observations. A labial sulcus incision is utilized for

Facial feminization surgery

449

Deschamps-Braly forehead type

Type I

Type II

Type III

Type IV

Burr contouring of glabellar ridge and orbits

Burr down glabellar ridge slightly and fill in recessed area above glabellar ridge with bone substitute, along with burr contouring of orbits

Cranial setback of anterior table of glabellar ridge overlying the frontal sinus and burr contouring of the orbits

Fill in glabellar ridge and recessed area above glabellar ridge with bone substitute, along with burr contouring of orbits

Figure 14.4.11  Surgical algorithm for forehead feminization. Forehead type is determined using the Deschamps-Braly forehead classifications (see Fig. 14.4.10), and surgical technique is dictated by forehead type.

A

B

Figure 14.4.12  (A,B) Intra-operative feminization of a type III forehead. Cranioplasty setback of the anterior table with burr contouring of the orbit rims was performed.

access while leaving a cuff of mentalis for later resuspension. T-shaped osteotomies with both horizontal and midline vertical components and removal of a predetermined segment of bone allow the surgeon to reduce the height, width, and prominence of the chin.58,74 These segments are subsequently fixated with miniplates to each other and the native mandible, ensuring a smooth contour/transition between the bony segments. As with traditional aesthetic genioplasty, the mental nerves must be carefully protected and inferior tooth roots avoided. Mentalis resuspension is critical, as is the performance of a watertight mucosal closure to minimize the chance of salivary leak and hardware infection.

Laryngeal prominence The laryngeal prominence, formed by the junction of the anterior borders of the thyroid cartilage laminae, is a

definitive masculine secondary sexual characteristic.78 As such, many transwomen desire removal of this prominence. Chondrolaryngoplasty, or tracheal shave, reduces the masculinizing laryngeal prominence and is a powerful feminizing tool.79,80 Variations in technique of this procedure exist. The incision can be placed submental, at the cervicomental junction or directly over the laryngeal prominence. Dissection is carried down, and the strap muscles are separated in the midline to expose the thyroid cartilage. Once adequate exposure of the thyroid cartilage is obtained, needle localization of the vocal cords can be performed to verify the level of insertion. A flexible fiberoptic laryngoscope is placed down the laryngeal mask airway to visualize the vocal cords. A 22-gauge needle is placed through the trachea below the proposed area of resection and the insertion of the cords is localized and marked externally. Resection must stay 2 mm above this point

SECTION II

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CHAPTER 14.4  • Breast, chest wall, and facial considerations in gender affirmation

B

A

Figure 14.4.13  (A) Pre- and (B) postoperative photos of type III forehead feminization and adjunct procedures. Cranioplasty setback of the anterior table with burr contouring of the orbit rims, direct brow lift, corrugator resection, upper lip lift, and fat grafting.

A

B

C

D

Figure 14.4.14  (A–D) Pre- and postoperative photos of facial feminization. Procedures performed included cranioplasty setback of the anterior table with burr contouring of the orbit rims, direct brow lift, corrugator resection, upper lip lift, rhinoplasty with alar base reduction, reduction genioplasty, and fat grafting.

to prevent damage to the vocal cord insertion.81 A subperichondrial plane is then entered and excess thyroid cartilage is removed via excision with a scalpel and careful burring to reduce its projection and create smooth, natural contour to the neck (Fig. 14.4.15). Complications include bleeding in the neck, odynophagia, hoarseness, damage to the vocal cords, and destabilization of the epiglottis. Important precautions include meticulous hemostasis during the procedure and postoperative monitoring for hematoma. Needle localization of vocal cord insertion can decrease the risk of vocal cord damage.54,78

and lower blepharoplasty, face and neck lift, and skin treatments to achieve desired results from the feminizing procedures.54 Facial feminization procedures are continuing to evolve in the landscape of technical refinements, cultural and institutional acceptance, and more critical assessment of outcomes. There is an increase in research dedicated to further improving these procedures and incorporating facial feminization into the overall care of the transgender patient. Importantly, studies have demonstrated improvements in quality of life and high patient satisfaction after facial feminization.82,83

Adjunct cosmetic procedures

Conclusions

In addition to facial feminization surgeries, some patients may require cosmetic facial rejuvenation procedures such as upper

Gender-affirming surgeries are critical and medically necessary elements in the treatment of gender dysphoria. The

Conclusions

A

B

C

D

E

F

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Figure 14.4.15  (A–F) Laryngeal prominence reduction using chondrolaryngoplasty. Resected thyroid cartilage specimen measuring approximately 2.5 cm × 3.5 cm yielded a feminizing result.

discussed treatments represent the most widely used and safest techniques, endorsed by board-certified plastic surgeons. The goal for gender-affirming surgeries is to improve the congruence between an individual’s gender identity and their sex assigned at birth. There is a growing body of literature that demonstrates improved quality of life, reduction in the

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symptoms of gender dysphoria, and high patient satisfaction following these gender-affirming surgeries. Standardized and validated assessments of patient-reported outcomes are still lacking, and future efforts should be aimed at better understanding long-term effects on patient quality of life with validated measures.54

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CHAPTER 14.4  • Breast, chest wall, and facial considerations in gender affirmation

44. Tebbetts JB, Adams WP. Five critical decisions in breast augmentation using five measurements in 5 minutes: the high five decision support process. Plast Reconstr Surg. 2006;118(7 Suppl): 35S–45S. 45. Maxwell GP, Gabriel A. Bioengineered breast: concept, technique, and preliminary results. Plast Reconstr Surg. 2016;137(2):415–421. 46. Salibian AA, Frey JD, Karp NS. Strategies and considerations in selecting between subpectoral and prepectoral breast reconstruction. Gland Surg. 2019;8(1):11–18. 47. Wan D, Rohrich RJ. Modern primary breast augmentation: best recommendations for best results. Plast Reconstr Surg. 2018;142(6): 933e–946e. 48. Bengston B. The inframammary fold: Histologic and anatomic description, classification and definitions, and options for repair and reinforcement. In: Spear S, ed. Surgery of the Breast: Principles and Art. 3rd ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2011. 49. Mehra G, Kaufman-Goldberg T, Meshulam-Derazon S, Boskey ER, Ganor O. Use of the subfascial plane for gender-affirming breast augmentation: a case series. Plast Reconstr Surg Glob Open. 2021;9(1):e3362. 50. Alderman A, Pusic A, Murphy DK. Prospective analysis of primary breast augmentation on body image using the BREAST-Q: results from a nationwide study. Plast Reconstr Surg. 2016;137(6):954e–960e. 51. McCarthy CM, Cano SJ, Klassen AF, et al. The magnitude of effect of cosmetic breast augmentation on patient satisfaction and health-related quality of life. Plast Reconstr Surg. 2012;130(1): 218–223. 52. Fakin RM, Zimmermann S, Kaye K, Lunger L, Weinforth G, Giovanoli P. Long-term outcomes in breast augmentation in trans-women: a 20-year experience. Aesthet Surg J. 2019;39(4): 381–390. 53. Ousterhout DK. Feminization of the forehead: contour changing to improve female aesthetics. Plast Reconstr Surg. 1987;79(5):701–713. 54. Morrison SD, Vyas KS, Motakef S, et al. Facial feminization: systematic review of the literature. Plast Reconstr Surg. 2016;137(6): 1759–1770. 55. Ascha M, Swanson MA, Massie JP, et al. Nonsurgical management of facial masculinization and feminization. Aesthet Surg J. 2019;39(5):NP123–NP137. 56. Spiegel JH. Challenges in care of the transgender patient seeking facial feminization surgery. Facial Plast Surg Clin North Am. 2008;16(2):233–238. viii. 57. Spiegel JH. Facial determinants of female gender and feminizing forehead cranioplasty. Laryngoscope. 2011;121(2):250–261. 58. Deschamps-Braly JC. Facial gender confirmation surgery: facial feminization surgery and facial masculinization surgery. Clin Plast Surg. 2018;45(3):323–331. 59. Altman K. Facial feminization surgery: current state of the art. Int J Oral Maxillofac Surg. 2012;41(8):885–894. 60. Bellinga RJ, Capitán L, Simon D, Tenório T. Technical and clinical considerations for facial feminization surgery with rhinoplasty and related procedures. JAMA Facial Plast Surg. 2017;19(3):175–181. 61. Anic-Milosevic S, Mestrovic S, Prlic’ A, Slaj M. Proportions in the upper lip-lower lip-chin area of the lower face as determined by photogrammetric method. J Craniomaxillofac Surg. 2010;38(2):90–95. 62. Farkas LG, Katic MJ, Hreczko TA, Deutsch C, Munro IR. Anthropometric proportions in the upper lip-lower lip-chin area of the lower face in young white adults. Am J Orthod. 1984;86(1): 52–60.

63. Becking AG, Tuinzing DB, Hage JJ, Gooren LJ. Transgender feminization of the facial skeleton. Clin Plast Surg. 2007;34(3): 557–564. 64. Capitán L, Simon D, Kaye K, Tenorio T. Facial feminization surgery: the forehead. Surgical techniques and analysis of results. Plast Reconstr Surg. 2014;134(4):609–619. 65. Piombino P, Marenzi G, Dell’Aversana Orabona G, Califano L, Sammartino G. Autologous fat grafting in facial volumetric restoration. J Craniofac Surg. 2015;26(3):756–759. 66. Mommaerts MY, Abeloos JV, De Clercq CA, Neyt LF. The ’sandwich’ zygomatic osteotomy: technique, indications and clinical results. J Craniomaxillofac Surg. 1995;23(1):12–19. 67. Lundgren TK, Farnebo F. Midface osteotomies for feminization of the facial skeleton. Plast Reconstr Surg Glob Open. 2017;5(1):e1210. 68. Natghian H, Farnebo F, Lundgren KC. Management of the midface in the transgender patient. J Craniofac Surg. 2019;30(5):1383–1386. 69. Hage JJ, Vossen M, Becking AG. Rhinoplasty as part of genderconfirming surgery in male transsexuals: basic considerations and clinical experience. Ann Plast Surg. 1997;39(3):266–271. 70. Noureai SA, Randhawa P, Andrews PJ, Saleh HA. The role of nasal feminization rhinoplasty in male-to-female gender reassignment. Arch Facial Plast Surg. 2007;9(5):318–320. 71. Rohrich RJ, Ahmad J. A practical approach to rhinoplasty. Plast Reconstr Surg. 2016;137(4):725e–746e. 72. Lee DE, Hur SW, Lee JH, Kim YH, Seul JH. Central lip lift as aesthetic and physiognomic plastic surgery: the effect on lower facial profile. Aesthet Surg J. 2015;35(6):698–707. 73. Salibian AA, Bluebond-Langner R. Lip lift. Facial Plast Surg Clin North Am. 2019;27(2):261–266. 74. Morrison SD, Satterwhite T. Lower jaw recontouring in facial gender-affirming surgery. Facial Plast Surg Clin North Am. 2019;27(2):233–242. 75. Shams MG, Motamedi MH. Case report: feminizing the male face. Eplasty. 2009;9:e2. 76. Becking AG, Tuinzing DB, Hage JJ, Gooren LJ. Facial corrections in male to female transsexuals: a preliminary report on 16 patients. J Oral Maxillofac Surg. 1996;54(4):413–418; discussion 419. 77. Li J, Hsu Y, Khadka A, Hu J, Wang Q, Wang D. Surgical designs and techniques for mandibular contouring based on categorisation of square face with low gonial angle in orientals. J Plast Reconstr Aesthet Surg. 2012;65(1):e1–8. 78. Therattil PJ, Hazim NY, Cohen WA, Keith JD. Esthetic reduction of the thyroid cartilage: a systematic review of chondrolaryngoplasty. JPRAS Open. 2019;22:27–32. 79. Deschamps-Braly JC, et al. First female-to-male facial confirmation surgery with description of a new procedure for masculinization of the thyroid cartilage (Adam’s apple). Plast Reconstr Surg. 2017;139(4): 883e–887e. 80. Wolfort FG, Dejerine ES, Ramos DJ, Parry RG. Chondrolaryngoplasty for appearance. Plast Reconstr Surg. 1990;86(3):464–469; discussion 470. 81. Spiegel JH, Rodriguez G. Chondrolaryngoplasty under general anesthesia using a flexible fiberoptic laryngoscope and laryngeal mask airway. Arch Otolaryngol Head Neck Surg. 2008;134(7):704–708. 82. Ainsworth TA, Spiegel JH. Quality of life of individuals with and without facial feminization surgery or gender reassignment surgery. Qual Life Res. 2010;19(7):1019–1024. 83. Raffaini M, Magri AS, Agostini T. Full facial feminization surgery: patient satisfaction assessment based on 180 procedures involving 33 consecutive patients. Plast Reconstr Surg. 2016;137(2):438–448.

 

 

SECTION II • Trunk, Perineum, and Transgender

15 Reconstruction of acquired vaginal defects Leila Jazayeri, Andrea L. Pusic, and Peter G. Cordeiro

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Introduction Acquired vaginal defects most commonly result from the resec­ tion of pelvic malignant neoplasms. Advanced colorectal carcino­ mas frequently involve the posterior vaginal wall. Carcinoma of the bladder may extend into the anterior vaginal wall. Primary tumors of the vaginal wall may result in any number of vaginal defects. Local extension or recurrence of uterine or cervical malig­ nant neoplasms can necessitate pelvic exenteration and total vagi­ nal resection. Trauma or burns to the vaginal area may also result in vaginal distortion; however, the relatively protected position of the vagina makes these deformities much less common. Irrespective of their etiology, vaginal defects may range from a small mucosal defect to total circumferential loss. In addition, tumor ablation may necessitate the resection of nearby pelvic contents and/or vulvar and perineal tissue. The subsequent pelvic dead space or resulting perineal defects are critical considerations in the final reconstruction.

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Anatomic considerations The close anatomic relationship between the bladder, vagina, and rectum needs to be well appreciated by the reconstructive surgeon. Ligamentous support of these organs is interrelated, and surgical dissection of any one structure may lead to pro­ lapse and herniation of the remaining components. In addition, pelvic exenteration may disrupt or devascularize the pelvic floor musculature. The pelvic sidewalls define a fixed anatomic space that, once cleared of the pelvic organs, will either delin­ eate a dead space or invite small-bowel prolapse and adhesions. The vagina is essentially a distensible cylindrical pouch (Fig. 15.1). Normal length is 6–7.5 cm along its anterior wall and

9 cm along the posterior wall.8 It is constricted at the introitus, dilated in the middle, and narrowed near its uterine extremity. In its normal anatomic position, the vagina tilts posteriorly as it extends up into the pelvis, forming a 90° angle with the uterus. Careful orientation of the neovagina is important to successful reconstruction and ultimate sexual function. The introitus is a frequent site of contracture after reconstruction, and any distor­ tion of its normal position relative to other structures such as the urethral orifice, perineal body, and anus should be addressed. If no resection of the external vulva and perineum is required, great care must be taken to avoid their distortion because this may also have an impact on sexual function and body image.

Diagnosis The classification of acquired vaginal defects is based on their anatomic location (Fig. 15.2). This classification will help to guide reconstructive efforts. There are two basic types of vaginal defects: partial (type I) and circumferential (type II). These basic types can be further subclassified. Type IA defects are partial, and involve the anterior or lateral wall. These defects may result from the resection of urinary tract malignant neoplasms or pri­ mary malignant neoplasms of the vaginal wall. Type IB defects are partial, and involve the posterior wall. These defects, which tend to be the most common type of vaginal defect requiring reconstruction, result primarily from extension of colorectal car­ cinomas. Type IIA defects are circumferential defects involving the upper two-thirds of the vagina. These defects are typically the result of uterine and cervical diseases. Type IIB defects are circumferential, total vaginal defects that are commonly the result of pelvic exenteration. These defects result in considerable soft-tissue loss, dead space, as well as distortion of the introitus. In addition to the vaginal defect one must consider the extent of the pelvic dead space in ablative surgeries such as abdomi­ nal perineal resection (APR) and pelvic exenterations. In an APR the entire rectum, anal canal, and anus are removed and a permanent colostomy is created. When pelvic exenteration is performed all the organs from the pelvic cavity are removed.

Historical perspective

Historical perspective Whereas small partial vaginal defects are common and usu­ ally repaired primarily, larger defects caused by ablative surgeries such as abdominal perineal resections (APRs) and pelvic exenterations usually require flap reconstruction. APRs are performed for very low rectal tumors. In this pro­ cedure, the entire rectum, anal canal, and anus are removed, and a permanent colostomy is created. Perineal wound com­ plications such as delayed healing and infection are common in these patients, especially those who have undergone irradi­ ation. Major wound complications have been reported in 20%– 51% of patients following APR when defects have been closed primarily.1 When APR was first described in 1908, the perineal wound was left open and allowed to heal by secondary inten­ tion.2 This approach led to serious morbidity associated with delayed wound healing, and was subsequently replaced by primary closure with suction drains and then delayed recon­ struction. This approach was also problematic, especially for irradiated wounds as the wounds broke down commonly and

452.e1

delayed reconstruction was difficult. Today, immediate local or regional flaps are the most common approach to managing these large APR defects. Pelvic exenteration (PEX) may be required when rectal can­ cers have invaded adjacent structures such as the uterus or bladder. In these cases, a partial or total vaginectomy is often necessary. When pelvic exenteration was first performed in the 1940s, the operative mortality was greater than 20%.3 Today, perioperative mortality is 2%–4%.4,5 The historical approach to these defects is similar to that of the APR defect: wounds left open to heal by secondary intention, or primary closure over drains with delayed reconstruction if the wound broke down. Today, many APR and PEX defects are immediately reconstructed using flaps. Despite the change in approach to these defects, close to 50% of patients experience postoper­ ative complications within 30 days of the procedure.6 Even with immediate flap reconstruction to improve vascularity and to decrease dead space, wound complications occur in 20%–30% of these patients.1,6,7 Other significant complications include infection, intestinal adhesions, fistulas, and pelvic herniation.

Patient selection/preoperative considerations

453

The urinary bladder, urethra, rectum and anus are removed in addition to the vagina, cervix, uterus, fallopian tubes, ovaries, and in some women, the vulva, and in men, the prostate. In this procedure both a colostomy and urinary diversion are created.

Patient selection/preoperative considerations A

P

Figure 15.1  Vaginal vault. A, anterior; P, posterior.

Type I: partial defect Type IA

A

P

Type IB

A

Anterior wall

P

A

Lateral wall

P

Posterior wall

A

B Type II: circumferential defect Type IIA

A

Type IIB

A

P

P

Successful management of patients undergoing vaginal recon­ struction is dependent upon a multidisciplinary approach. The oncologic and reconstructive surgeons need to commu­ nicate well in terms of the surgical approach, expected defect, possible stoma positioning, and the reconstructive options that are available to that specific patient.1 The anesthesia team needs to be well advised of the nature of the procedure and the hemodynamic stress that can be expected intra-­operatively. Also, early involvement of a psychiatrist and a sex therapist may be warranted. The radiation oncologist is an important participant in the overall treatment plan. Many patients have had previous radiotherapy or will undergo neoadjuvant chemoradiation, and many other patients may be receiving intra-operative radiotherapy or placement of a brachytherapy cannula. The radiotherapy plan has important implications for the choice of flap as both the recipient and donor sites can be affected by radiation injury. In addition, the medical oncologist should be involved with the decision-making as many patients may receive neoadjuvant or adjuvant chemotherapy. Surgical pro­ cedures should be timed to minimize the effects of chemother­ apy on wound healing, as well as to avoid unnecessary delays in starting chemotherapy protocols. Most important to the success of the reconstruction is the full and informed involvement of the patient and her family. It is important to be specific about the goals of vaginal recon­ struction with patients, which include effective wound healing and restoration of body image and sexual function (Box 15.1). For those women motivated to preserve sexual function, a com­ prehensive program of sexual rehabilitation may be warranted.9 Ratliff et al. investigated sexual adjustment after vaginal recon­ struction with gracilis myocutaneous flaps and found that, although 70% of patients were judged to have a physically ade­ quate vagina, fewer than 50% resumed sexual activity.10 Absence of pleasure (37%), problems with vaginal dryness (32%), excess secretions (27%), self-consciousness about ostomies (40%), and self-consciousness about nudity in front of their partner (30%) were the most considerable concerns. Preoperative and postop­ erative counseling, in addition to postoperative rehabilitation strategies (vaginal dilators, lubricants, topical estrogens), have

BOX 15.1  The major goals of vaginal reconstruction Total

Upper two-thirds C

D

Figure 15.2 Classification system of acquired vaginal defects. (A,B) Type I: partial defect. (A) Type IA: partial defect of the anterior or lateral wall. (B) Type IIB: partial defect of the posterior wall. (C,D) Type II: circumferential defect. (C) Type IIA: circumferential defect of the upper two-thirds. (D) Type IIB: circumferential, total defect. A, anterior; P, posterior.  

• To promote effective wound healing, facilitating postoperative radiation therapy and chemotherapy • To decrease pelvic dead space, thus decreasing fluid loss, metabolic demands, and infection • To restore the pelvic floor, preventing herniation and small-bowel fistula • To re-establish body image • To re-establish sexual function

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CHAPTER 15  • Reconstruction of acquired vaginal defects

been suggested as the best way to influence these outcomes positively and give patients the best hope of functional and psychological recovery.9,11 The psychologist and sex therapist should be an integral part of the ablative–reconstructive team. In addition, at most tertiary care institutions, specialized nurs­ ing teams can help the patient and her family prepare for the psychological distress that they may experience.

Treatment/surgical technique There are five basic goals in vaginal reconstruction (Box 15.1). Selection of the optimal reconstructive method to achieve these goals is based on the type of defect, the surgical approach, the need for radiation, and the characteristics of the patient. Small defects that can be closed without tension can be closed pri­ marily. In the case of the irradiated wound, however, one must proceed cautiously with primary closure. Rarely is primary closure alone an adequate alternative in oncology patients. Proceeding along the reconstructive ladder, regional flaps continue to be the most frequently used and effective pro­ cedures. Many flaps have been described, none of which is ideal for all defect types (Table 15.1). To simplify surgical Table 15.1  Previously described flap options for vaginal reconstruction

Defect type

Flap option

IA

Singapore flaps (aka pudendal fasciocutaneous flap)

IB

Pedicled rectus myocutaneous flap Pedicled rectus musculoperitoneal flap Muscle-sparing rectus myocutaneous flap

IIA/B

Vertical rectus abdominis myocutaneous Gracilis Singapore flaps Pedicled jejunum Sigmoid colon

decision-making, a reconstructive algorithm has been devel­ oped on the basis of defect type (Algorithm 15.1).12 Type IA defects, which involve only the anterior or lateral vaginal walls, usually require little tissue bulk and small to moderate surface coverage. The modified Singapore (vulvo­ perineal or pudendal thigh) fasciocutaneous flap is ideal in this setting.13–15 It provides a highly vascularized, reliable, and pliable flap that conforms well to the surface of the vaginal cylinder. This flap is based on the posterior labial arteries and innervated by perineal branches of the posterior cutaneous nerve of the thigh. The flaps are raised in the thigh crease, lateral to the hair-bearing labia majora, and may be designed to measure 9 × 4 cm to 15 × 6 cm.13–15 The posterior skin margin is marked at the level of the posterior fourchette (Fig. 15.3A). The skin, subcutaneous tissue, deep fascia of the thigh, and epimysium of the adductor muscles are raised (Fig. 15.3B). Posteriorly, the base of the flap is undermined at the subcu­ taneous level to facilitate rotation and insetting. Depending on the defect, unilateral or bilateral flaps may be developed (Fig. 15.3C). The flaps may be inset by tunneling under the labia majora or by division of the labia at the level of the four­ chette. The donor site is closed primarily (Fig. 15.3D & 15.4). Type IB defects, which encompass the posterior vaginal wall, frequently require greater soft-tissue bulk to fill the dead space made by resection of the rectum. Here, the preferred choice is the pedicled rectus myocutaneous flap. This highly reliable flap provides both a large surface area and large volume. The skin can be used to replace the entire posterior vaginal wall. The healthy muscle and subcutaneous tissue bring well-vascu­ larized tissue to the pelvis, obliterate dead space, and separate the contents of the abdominal cavity from the zone of injury. When used for vaginal reconstruction, the flap is based on the deep inferior epigastric vessels that arise from the external iliac arteries and enter the rectus muscle along its posterolateral surface 6–7 cm above its insertion on the pubis (Fig. 15.5). In planning the flap, one must ensure that these vessels are not divided as part of the cancer resection. One must also ensure that the muscle itself is not violated during placement of the stoma. Stoma planning requires communication between the reconstructive surgeon and the colorectal surgeon. Usually the stoma is placed on the patient’s left side, thus sparing the right rectus for reconstruction. If there is only one available rectus

Algorithm 15.1 Vaginal Defect Type I Partial

Type II Circumferential

Type IA Anterior or lateral wall

Type IB Posterior wall

Type IIA Upper two-thirds

Type IIB Total

Singapore

Rectus

Rolled rectus or colon

Bilateral gracilis

Algorithm for reconstruction of the vagina based on defect type.

Treatment/surgical technique

A

B

C

D

455

Figure 15.3  (A–D) Modified Singapore fasciocutaneous flap. See text for details.

A

C

B

Figure 15.4  (A) Marking of the modified Singapore fasciocutaneous flap. (B) Flap elevation. (C) Flap inset.

for both stoma placement and the reconstructive donor site, the colorectal surgeon may be able to place the stoma through an empty rectus sheath, or through the external oblique. In cases of an open abdominal resection, communication with the colorectal surgeon is also required for incision planning. If the right rectus is to be used for reconstruction, ask the colorectal surgeon not to plan the abdominal incision around the left side of the umbilicus, as this will lead to vascular compromise of the umbilicus when harvesting the rectus flap.

Either a vertical or transverse skin island design may be used for the rectus myocutaneous flap, depending on the size of the defect and the characteristics of the patient’s abdomi­ nal wall. For posterior wall reconstruction, the vertical rectus abdominis myocutaneous (VRAM) design is usually prefera­ ble because it maximizes blood supply by centering the skin island over the medial and lateral rows of perforators, and does not interfere with the contralateral muscle and stoma placement.

SECTION II

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CHAPTER 15  • Reconstruction of acquired vaginal defects

Both the vertical and transverse rectus abdominis myocuta­ neous flaps can be designed up to 10 × 20 cm in size with easy donor site closure. When the flap is inset into a posterior-wall defect, care must be taken to avoid constriction or tension on the vascular pedicle as this is the principal cause of flap fail­ ure. Leaving the distal muscle insertion intact to decrease ten­ sion on the pedicle is helpful in this regard (Fig. 15.6). The rectus abdominis musculoperitoneal flap is a modi­ fication rectus flap for type I vaginal defects where a patch of posterior rectus sheath and peritoneum above the arcuate line is harvested with the rectus to the exact dimensions of the resected vaginal mucosa. The pedicled flap is then transposed into the vaginal canal and the peritoneal patch is sutured to the edges of the vaginal mucosa. This technique avoids the need for harvesting skin and anterior rectus sheath. The peri­ toneum has been shown to re-epithelialize to squamous epi­ thelium, making it indistinguishable from vaginal mucosa.16 Harvest of a rectus abdominis muscle flap can also be done both laparoscopically and robotically.17–19 These modifications are evolving with promising outcomes to complement lap­ aroscopic and robotic colorectal, urologic, and gynecologic resections.20,21 When harvesting a rectus abdominis muscle flap, laparoscopically or robotically, the anterior rectus sheath remains intact. Dissection begins with incising the peritoneum and posterior rectus sheath at the arcuate line. The muscle is exposed and dissected off the anterior rectus sheath. After mobilization of the entire muscle, the inferior pedicle of the flap is identified and isolated, and the superior rectus muscle is divided. The flap is then mobilized with a portion of the poste­ rior rectus sheath, above the arcuate line, to facilitate reconstruc­ tion of the posterior vaginal defect. Once harvested, the flap can be positioned and sutured in place with an assistant working

Figure 15.5  Pedicled rectus myocutaneous flap.

A

B

C

Figure 15.6 (A–C) Rotation and insetting of a pedicled vertical rectus abdominis myocutaneous flap for a posterior wall defect.  

Treatment/surgical technique

through the peritoneal wound. The musculoperitoneal flap can be contoured to the vaginal defect and allowed to mucosalize over time. Type IIA defects are circumferential defects involving the upper two-thirds of the vagina and, like type IB defects, they are well reconstructed with the pedicled rectus myocutaneous flap due to its skin and soft-tissue bulk. The rectus is preferable to bilateral gracilis flaps because the intervening vulvar and pelvic floor musculature prohibits transfer of the gracilis to the defect. When using the rectus myocutaneous flap for these defects, the cutaneous portion of the flap is tubed. A trans­ verse skin island is easier to manipulate and leaves a slightly longer pedicle than the VRAM. A flap width of 12–15 cm will provide a neovagina with a 4-cm diameter.22,23 Once tubed, the flap is then sutured to the remaining vaginal cuff from above (Fig. 15.7). The sigmoid colon or jejunum may also be used to recon­ struct type IIA defects for patients in whom the rectus flap cannot be utilized. For the sigmoid colon flap, a segment of colon is isolated and pedicled on a branch of the inferior mesenteric artery.24 For the jejunum flap, a 15-cm segment of jejunum is isolated and pedicled on the fourth branch of the superior mesenteric artery, approximately 30 cm distal to the ligament of Treitz.25 For both of these flaps the bowel is

stapled closed superiorly, and sutured inferiorly to the vag­ inal cuff. Excessive secretions and unpleasant odor persist as common complaints of patients, limiting the usefulness of these techniques.26 Type IIB defects are circumferential defects involving the entire vagina and frequently the introitus. These are usually total pelvic exenteration defects. Given the need for a large skin island, bilateral gracilis flaps are a good reconstructive choice for these defects. The subcutaneous tissue and muscle of the two conjoined flaps will provide a large volume of soft tissue that can obliterate the dead space within the pelvis. The vascu­ lar supply of the gracilis flap is the medial femoral circumflex artery, which enters the gracilis muscle 7–10 cm below the pubic tubercle (Fig. 15.8A). An elliptical skin island approximately 6 × 20 cm can be designed centered over the proximal two-thirds of the muscle, with the anterior border of the incision lying on a line between the pubic tubercle and the semitendinosus ten­ don. Once elevated, the flaps are tunneled subcutaneously into the vaginal defect (Fig. 15.8B,C). The flaps are then sutured in the midline, and a neovaginal pouch is formed (Fig. 15.8D,E). The neovaginal pouch is then inserted into the defect, and the proximal flap edges are sutured to the introitus (Fig. 15.8F & 15.9). The flap can maintain some sensation for pressure through branches of the obturator nerve.27

A

Figure 15.7 (A,B) Tubing and insetting a pedicled rectus flap for a circumferential defect.  

457

B

SECTION II

458

CHAPTER 15  • Reconstruction of acquired vaginal defects

A

B

C

D

E

F

Figure 15.8  (A–F) Anatomy, design, elevation, and insetting of bilateral gracilis flaps for a type IIB defect. See text for details.

Additional surgical considerations While many patients can be reconstructed by using an algo­ rithm based on defect type, a few may require a modified approach. In addition to the type of vaginal defect, con­ sideration should be given to patient-specific risk factors,

the surgical approach, the surrounding surgical defect, and the need for radiation and/or chemotherapy. Obesity, for example, has been shown to be a significant risk fac­ tor for poor wound healing after rectus flap reconstruc­ tion.28,29 Obese patients with type IIB defects therefore may be better reconstructed with thin, bilateral Singapore flaps.

Treatment/surgical technique

A

459

B

Figure 15.9  (A,B) Postoperative results of a vaginal reconstruction using bilateral gracilis flaps.

Alternatively, the rectus may be used without its cutaneous portion and a skin graft applied directly to the muscle over a vaginal stent. In elderly patients or patients with signifi­ cant comorbidities who are unlikely to resume intercourse after reconstruction, a full vaginal reconstruction may be omitted. Using a rectus muscle flap to obliterate dead space within the pelvis may still be of wound-healing benefit to these patients. In addition to patient-specific risk factors, consider­ ation must be given to both the surgical approach and the surrounding surgical defect. For patients with colorectal, gynecologic, and urologic cancers, laparoscopic and robotic surgical techniques are emerging as the preferred surgical approach. Laparoscopic colorectal resection now accounts for well over 40% of all resections, and robotic techniques are quickly increasing in popularity.20,21,30 Minimally invasive surgery (MIS) for colon and rectal cancer is now universally accepted as providing equivalent outcomes to open sur­ gery with added benefits of earlier return of bowel function, shortened length of stay, and better cosmesis.21,31 To main­ tain the benefits of either laparoscopic or robotic surgery, a reconstructive surgeon without the expertise to harvest an abdominal flap laparoscopically or robotically, may opt for a gracilis or fasciocutaneous perineal flap. In the setting of MIS, these flaps may be preferred to minimize donor site morbidity associated with an open abdominal flap, including hernias, later return of bowel function, and scarring. These considerations, however, must be weighed against the result­ ing surgical defect. When the ablative surgeon resects nearby pelvic contents, the resulting non-collapsible dead space may

need to be addressed regardless of the surgical approach. Such is the case in low rectal tumors requiring APR or more advanced rectal cancers requiring pelvic exenteration, both of which result in a poorly vascular dead space often requiring chemoradiotherapy. In these cases local flaps can be used to obliterate the non-collapsible dead space with vascularized tissue. Butler compared immediate VRAM flap reconstruc­ tion of irradiated APR wounds that could have been closed primarily versus primary closure.32 The flap group had sig­ nificantly lower incidence of perineal abscess (9% versus 37%, p = 0.002), major perineal wound dehiscence (9 versus 30%, p  =  0.014) and drainage procedures required for perineal/ pelvic fluid collection (3% versus 25%, p  =  0.003) than the control group. Although both groups could have been closed primarily, bringing in healthy vascularized tissue reduced major perineal wound complications by filling the dead space, separating the bowel from the underlying perineum, and closing the perineal skin defect with non-irradiated flap skin. In a review of APR reconstruction with a VRAM com­ pared to gluteal fasciocutaneous and gracilis myocutaneous flaps, the overall rate of any perineal wound or flap compli­ cations among VRAM patients was significantly lower than gluteal and gracilis flaps.30 This should be taken into account when weighing the risks and benefits of flap choice even in the setting of exenterative MIS. Finally, in patients with previous vaginal reconstruction and recurrent disease, the choice of regional flap may be extremely limited, perhaps warranting free flap reconstruc­ tion.33,34 Several pedicled perforator flaps are good alternative options in these cases. Examples include the muscle-sparing

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CHAPTER 15  • Reconstruction of acquired vaginal defects

vertical rectus,35 the deep inferior epigastric perforator (DIEP) flap,36,37 superior and inferior gluteal artery perforator (SGAP, IGAP) flaps,38 anterior lateral thigh (ALT) flaps,39 as well as free-style perforator flaps.40

Postoperative care Immediate perioperative period At the end of the reconstructive case, it is imperative to leave a pelvic drain in place in order to drain the fluid that will inevitably collect in any remaining dead space. While these drains typically drain a large amount, the goal should be to keep it in place until the patient is mobile and the drainage begins to decrease, rather than reaching below a certain set point. Postoperatively, careful attention must also be paid to the patient’s hemodynamic and nutritional support. All patients should receive deep vein thrombosis prophylaxis. They should be placed on a fluidized mattress and given instructions not to sit for a minimum of four weeks. Positioning is difficult due to these restrictions, and patients should be encouraged to lie on either side, stand, or walk. Prophylactic perioperative antibi­ otics are often used.

Long-term care The placement of a vaginal stent intra-operatively is not rou­ tine for all flap reconstructions. However, once the flap is healed, gradual dilatation with a lubricator may be important in order to increase the size of the orifice. If the patient wishes to use the neovagina for intercourse, she must be told that dil­ atation must be continued on an ongoing and regular basis for life. Dilatation can begin at approximately 2 months post-­ reconstruction, as long as everything is well healed. Custom dilators are usually constructed for each patient. Estrogen creams applied to reconstructed type I defects can also be helpful to maintain lubrication.

Complications, prognosis, and outcomes Complications The principal early complications after vaginal reconstruc­ tion include infection and pelvic abscess, delayed wound healing, and flap loss. While the risk of infection and pelvic abscess is decreased when flap reconstruction is performed after vaginal resection, it still remains significant rang­ ing in the literature between 3% and 16%.30 Perioperative antibiotics, adequate drainage, and patient positioning, as mentioned in the previous section, are all important preven­ tive measures. Once a pelvic infection is established, per­ cutaneous or operative drainage is generally necessary to prevent worsening sepsis. The incidence of perineal wound complications varies in the literature as well. However,

once stratified by flap type, VRAM flaps may be superior to perineal and gracilis flaps with rates of reported perineal wound complications of 15.8%, 16.4%, and 26.8% among VRAM patients41–43 compared to 42.5%, 44.2%, and 44.4% among perineal and gluteal flaps44–46 and 37.0%, 68.0%, and 40% among gracilis flap patients.47–49 Radiotherapy, obesity, and smoking are all risk factors for poor wound healing that should be considered preoperatively. The most com­ mon location for wound separation is the posterior per­ ineal closure site, which usually responds to conservative management. Flap loss, both partial and complete, is a major postoper­ ative problem that will delay adjuvant therapy and increase morbidity of the patient. The incidence of flap loss depends on the type of flap used, surgical technique, and patient characteristics. When used for vaginal reconstruction, the VRAM flap is highly reliable with less than 5% incidence of total or partial flap loss; gracilis myocutaneous flaps are less reliable with 10% to greater than 20% incidence of total or partial flap loss.30,50,51 The success rate of both of these flaps depends on careful attention to design and surgical technique. Partial flap loss may be managed by debride­ ment and local wound care. In the setting of irradiated tissue, full debridement and reconstruction with an alter­ native flap may be required. In general, the overall compli­ cation rate for the VRAM is lower than either the gracilis or Singapore flaps in vaginal reconstruction (36%, 53%, and 44%, respectively).30 In addition to complications at the site of the vaginal reconstruction, one must also consider potential donor site complications. For all potential donor sites, hypertrophic scarring, infection, and wound-healing problems must be considered. Harvesting the rectus myocutaneous flap for vaginal reconstruction carries the risk of abdominal bulge or hernia (which may be as high as 66.7%).52 However, com­ paring abdominal complications in similar patients without flap reconstruction shows similar abdominal complication rates, thus questioning whether harvesting the rectus mus­ cle adds significant morbidity to these patients.52 Thigh abscess or hematoma, infection, sensory anomalies, or hypertrophic scarring are the most common complications in patients who have had their gracilis muscles harvested, occurring in up to 40% of patients.51 When compared to abdominal or perineal flaps, the prevalence of donor site hematoma is statistically significantly higher with graci­ lis flaps, occurring in 16% of patients undergoing perineal reconstruction.1

Prognosis and outcomes After pelvic exenteration, 5-year survival among patients with gynecologic cancer is 60%.53 Among APR patients, 5-year survival is 60%–80%.54 For the patients who do well with their disease and ultimately achieve wound healing, sexual function and body image are fundamental quality-oflife issues. Vaginal reconstruction has been associated with improved body image and sexual function.9,55 In a pooled analysis of patients undergoing vaginal reconstruction by local flaps, 122 of 246 (50%) resumed sexual activity post­ operatively.50 Anatomic reconstruction of the vagina does not equate with restoration of sexual function for a variety

Complications, prognosis, and outcomes

of reasons. In a review of 44 patients who had undergone bilateral gracilis flap reconstruction, Ratliff et al. found that 33% of patients complained of vaginal dryness, whereas 28% complained of excess vaginal secretions. Twenty per­ cent thought their neovagina was too small, whereas 5% found it to be too large. Eighteen percent had flap prolapse,

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461

and a further 18% had pain with intercourse.10 The most impor­ tant determinant of postoperative sexual activity, however, is prior sexual activity, and this is not affected by the type of reconstruction.50 Extensive preoperative coun­ seling is essential to ensure realistic patient expectations regarding postoperative sexual function.

References

References 1. Copeland-Halperin LR, Stewart T, Chen Y, Funderburk CD, Freed GL. Perineal reconstruction following abdominoperineal resection: comprehensive review of the literature. J Plast Reconstr Aesthet Surg. 2020;73(11):1924–1932. 2. Miles. A method of performing abdominoperineal resection for adenocarcinoma of the low rectum. Lancet. 1908:1812–1813. 3. Brunschwig A. Complete excision of pelvic viscera for advanced carcinoma; a one-stage abdominoperineal operation with end colostomy and bilateral ureteral implantation into the colon above the colostomy. Cancer. 1948;1(2):177–183. 4. Matsuo K, Matsuzaki S, Mandelbaum RS, et al. Hospital surgical volume and perioperative mortality of pelvic exenteration for gynecologic malignancies. J Surg Oncol. 2020;121(2):402–409. 5. Vigneswaran HT, Schwarzman LS, Madueke IC, et al. Morbidity and mortality of total pelvic exenteration for malignancy in the US. Ann Surg Oncol. 2021;28(5):2790–2800. 6. Crystal DT, Zwierstra MJ, Blankensteijn LL, et al. Immediate reconstruction after colorectal cancer resection: a cohort analysis through the National Surgical Quality Improvement Program and Outcomes Review. Ann Plast Surg. 2020;84(2):196–200. 7. Block LM, Hartmann EC, King J, Chakmakchy S, King T, Bentz ML. Outcomes analysis of gynecologic oncologic reconstruction. Plast Reconstr Surg Glob Open. 2019;7(1):e2015. 8. Luo J, Betschart C, Ashton-Miller JA, DeLancey JO. Quantitative analyses of variability in normal vaginal shape and dimension on MR images. Int Urogynecol J. 2016;27(7):1087–1095. 9. Huffman LB, Hartenbach EM, Carter J, Rash JK, Kushner DM. Maintaining sexual health throughout gynecologic cancer survivorship: a comprehensive review and clinical guide. Gynecol Oncol. 2016;140(2):359–368. 10. Ratliff CR, Gershenson DM, Morris M, et al. Sexual adjustment of patients undergoing gracilis myocutaneous flap vaginal reconstruction in conjunction with pelvic exenteration. Cancer. 1996;78(10):2229–2235. 11. Del Pup L, Villa P, Amar ID, Bottoni C, Scambia G. Approach to sexual dysfunction in women with cancer. Int J Gynecol Cancer. 2019;29(3):630–634. 12. Cordeiro PG, Pusic AL, Disa JJ. A classification system and reconstructive algorithm for acquired vaginal defects. Plast Reconstr Surg. 2002;110(4):1058–1065. 13. Tham NL, Pan WR, Rozen WM, et al. The pudendal thigh flap for vaginal reconstruction: optimising flap survival. J Plast Reconstr Aesthet Surg. 2010;63(5):826–831. 14. Woods JE, Alter G, Meland B, Podratz K. Experience with vaginal reconstruction utilizing the modified Singapore flap. Plast Reconstr Surg. 1992;90(2):270–274. 15. Ohmaru Y, Sakata K, Hashiguchi SI, Tanaka H, Rikimaru H, Kiyokawa K. A new modified pudendal thigh flap of vaginoplasty including reconstruction of vaginal vestibule. Case Rep Plast Surg Hand Surg. 2017;4(1):21–26. 16. Gupta V, Lennox GK, Covens A. The rectus abdominus myoperitoneal flap for vaginal reconstruction. Gynecol Oncol Rep. 2020;32:100567. 17. Pang JH, Patel SA, King SA, Curcillo PG 2nd, Weiss ES, Buchanan DR. Reduced-port approach to laparoscopic flap harvest (RALFH): an anterior sheath sparing rectus abdominis flap. J Plast Reconstr Aesthet Surg. 2017;70(5):710–712. 18. Pedersen J, Song DH, Selber JC. Robotic, intraperitoneal harvest of the rectus abdominis muscle. Plast Reconstr Surg. 2014;134(5): 1057–1063. 19. Winters BR, Mann GN, Louie O, Wright JL. Robotic total pelvic exenteration with laparoscopic rectus flap: initial experience. Case Rep Surg. 2015;2015:835425. 20. Agochukwu N, Bonaroti A, Beck S, Liau J. Laparoscopic harvest of the rectus abdominis for perineal reconstruction. Plast Reconstr Surg Glob Open. 2017;5(11):e1581. 21. Hammond JB, Howarth AL, Haverland RA, Rebecca AM, Yi J, Bryant LA, et al. Robotic harvest of a rectus abdominis muscle flap

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35. 36. 37.

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40. 41. 42.

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after abdominoperineal resection. Dis Colon Rectum. 2020;63(9): 1334–1337. Tobin GR, Pursell SH, Day Jr. TG. Refinements in vaginal reconstruction using rectus abdominis flaps. Clin Plast Surg. 1990;17(4):705–712. Holman FA, Martijnse IS, Traa MJ, et al. Dynamic article: vaginal and perineal reconstruction using rectus abdominis myocutaneous flap in surgery for locally advanced rectum carcinoma and locally recurrent rectum carcinoma. Dis Colon Rectum. 2013;56(2):175–185. Sahakitrungruang C, Atittharnsakul P. Sigmoid flap: a novel technique for perineal and neovaginal reconstruction after abdominoperineal resection with near total vaginectomy for locally advanced rectal cancer. J Am Coll Surg. 2010;210(2):e5–e8. Chen HC, Chana JS, Feng GM. A new method for vaginal reconstruction using a pedicled jejunal flap. Ann Plast Surg. 2003;51(4):429–431. Erman Akar M, Özkan Ö, Özkan Ö, Colak T, Gecici O. Sexual function and long-term results following vaginal reconstruction with free vascular jejunal flap. J Sex Med. 2013;10(11):2849–2854. Martello JY, Vasconez HC. Vulvar and vaginal reconstruction after surgical treatment for gynecologic cancer. Clin Plast Surg. 1995;22(1):129–140. Berger JL, Westin SN, Fellman B, et al. Modified vertical rectus abdominis myocutaneous flap vaginal reconstruction: an analysis of surgical outcomes. Gynecol Oncol. 2012;125(1):252–255. Westbom CM, Talbot SG. An algorithmic approach to perineal reconstruction. Plast Reconstr Surg Glob Open. 2019;7(12):e2572. Johnstone MS. Vertical rectus abdominis myocutaneous versus alternative flaps for perineal repair after abdominoperineal excision of the rectum in the era of laparoscopic surgery. Ann Plast Surg. 2017;79(1):101–106. Pai A, Marecik S, Park J, Prasad L. Robotic colorectal surgery for neoplasia. Surg Clin North Am. 2017;97(3):561–572. Butler CE, Gundeslioglu AO, Rodriguez-Bigas MA. Outcomes of immediate vertical rectus abdominis myocutaneous flap reconstruction for irradiated abdominoperineal resection defects. J Am Coll Surg. 2008;206(4):694–703. John HE, Jessop ZM, Di Candia M, Simcock J, Durrani AJ, Malata CM. An algorithmic approach to perineal reconstruction after cancer resection--experience from two international centers. Ann Plast Surg. 2013;71(1):96–102. Stechl NM, Baumeister S, Grimm K, Kraus TW, Bockhorn H, Exner KE. [Microsurgical reconstruction of the pelvic floor after pelvic exenteration. Reduced morbidity and improved quality of life by an interdisciplinary concept]. Der Chirurg Zeitschrift fur alle Gebiete der operativen Medizen. 2011;82(7):625–630. Weiwei L, Zhifei L, Ang Z, Lin Z, Dan L, Qun Q. Vaginal reconstruction with the muscle-sparing vertical rectus abdominis myocutaneous flap. J Plast Reconstr Aesthet Surg. 2009;62(3):335–340. Ang Z, Qun Q, Peirong Y, et al. Refined DIEP flap technique for vaginal reconstruction. Urology. 2009;74(1):197–201. Wang X, Qiao Q, Burd A, et al. A new technique of vaginal reconstruction with the deep inferior epigastric perforator flap: a preliminary report. Plast Reconstr Surg. 2007;119(6):1785–1790. discussion 1791. Wagstaff MJ, Rozen WM, Whitaker IS, Enajat M, Audolfsson T, Acosta R. Perineal and posterior vaginal wall reconstruction with superior and inferior gluteal artery perforator flaps. Microsurgery. 2009;29(8):626–629. Zelken JA, AlDeek NF, Hsu CC, Chang NJ, Lin CH, Lin CH. Algorithmic approach to lower abdominal, perineal, and groin reconstruction using anterolateral thigh flaps. Microsurgery. 2016;36(2):104–114. Hashimoto I, Abe Y, Nakanishi H. The internal pudendal artery perforator flap: free-style pedicle perforator flaps for vulva, vagina, and buttock reconstruction. Plast Reconstr Surg. 2014;133(4):924–933. Buchel EW, Finical S, Johnson C. Pelvic reconstruction using vertical rectus abdominis musculocutaneous flaps. Ann Plast Surg. 2004;52(1):22–26. Chessin DB, Hartley J, Cohen AM, Mazumdar M, Cordeiro P, Disa J, et al. Rectus flap reconstruction decreases perineal wound

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44. 45. 46. 47. 48.

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CHAPTER 15  • Reconstruction of acquired vaginal defects

complications after pelvic chemoradiation and surgery: a cohort study. Ann Surg Oncol. 2005;12(2):104–110. Lefevre JH, Parc Y, Kernéis S, et al. Abdomino-perineal resection for anal cancer: impact of a vertical rectus abdominis myocutaneus flap on survival, recurrence, morbidity, and wound healing. Ann Surg. 2009;250(5):707–711. Arnold PB, Lahr CJ, Mitchell ME, et al. Predictable closure of the abdominoperineal resection defect: a novel two-team approach. J Am Coll Surg. 2012;214(4):726–732. discussion 732–733. Hainsworth A, Al Akash M, Roblin P, Mohanna P, Ross D, George ML. Perineal reconstruction after abdominoperineal excision using inferior gluteal artery perforator flaps. Br J Surg. 2012;99(4):584–588. Winterton RI, Lambe GF, Ekwobi C, et al. Gluteal fold flaps for perineal reconstruction. J Plast Reconstr Aesthet Surg. 2013;66(3):397–405. Persichetti P, Cogliandro A, Marangi GF, et al. Pelvic and perineal reconstruction following abdominoperineal resection: the role of gracilis flap. Ann Plast Surg. 2007;59(2):168–172. Shibata D, Hyland W, Busse P, et al. Immediate reconstruction of the perineal wound with gracilis muscle flaps following abdominoperineal resection and intraoperative radiation therapy for recurrent carcinoma of the rectum. Ann Surg Oncol. 1999;6(1):33–37. Vermaas M, Ferenschild FT, Hofer SO, Verhoef C, Eggermont AM, de Wilt JH. Primary and secondary reconstruction after surgery of

50.

51. 52.

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the irradiated pelvis using a gracilis muscle flap transposition. Eur J Surg Oncol. 2005;31(9):1000–1005. McArdle A, Bischof DA, Davidge K, Swallow CJ, Winter DC. Vaginal reconstruction following radical surgery for colorectal malignancies: a systematic review of the literature. Ann Surg Oncol. 2012;19(12):3933–3942. Nelson RA, Butler CE. Surgical outcomes of VRAM versus thigh flaps for immediate reconstruction of pelvic and perineal cancer resection defects. Plast Reconstr Surg. 2009;123(1):175–183. Devulapalli C, Jia Wei AT, DiBiagio JR, et al. Primary versus flap closure of perineal defects following oncologic resection: a systematic review and meta-analysis. Plast Reconstr Surg. 2016;137(5):1602–1613. Westin SN, Rallapalli V, Fellman B, et al. Overall survival after pelvic exenteration for gynecologic malignancy. Gynecol Oncol. 2014;134(3):546–551. Hawkins AT, Albutt K, Wise PE, Alavi K, Sudan R, Kaiser AM, et al. Abdominoperineal resection for rectal cancer in the twentyfirst century: indications, techniques, and outcomes. J Gastrointest Surg. 2018;22(8):1477–1487. Mirhashemi R, Averette HE, Lambrou N, et al. Vaginal reconstruction at the time of pelvic exenteration: a surgical and psychosexual analysis of techniques. Gynecol Oncol. 2002;87(1):39–45.

SECTION II  •  Trunk, Perineum, and Transgender

16 Pressure sores Ibrahim Khansa and Jeffrey E. Janis

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SYNOPSIS

ƒ Pressure sores are a common problem associated with great morbidity and cost. ƒ The etiology of pressure sores is multifactorial, and includes pressure, friction, shear, moisture, malnutrition, and infection. ƒ Successful treatment of pressure sores requires a multidisciplinary evaluation in order to accurately stage wounds, identify/eradicate wound/ bone infection, minimize risk factors for recurrence, and optimize wound healing potential. ƒ Prevention and treatment of pressure sores should focus on correcting risk factors and optimizing the condition of the patient, including social support. Operative reconstruction should be delayed until the patient is optimized. ƒ As with any wound, pressure sores involving infected soft tissue and/ or bone must be thoroughly debrided prior to definitive closure. The lack of overt signs of infection should not give the surgeon a false sense of comfort, as biofilm is usually still present. ƒ Locoregional fasciocutaneous and musculocutaneous flaps remain workhorse flaps, allowing for adequate padding, dead space obliteration, and readvancement/rerotation as needed. ƒ Prevention remains the most effective treatment of pressure sores.

Introduction Terminology The term pressure ulcer applies specifically to any injury to the skin and underlying tissue that is due to pressure. The terminology is quite imprecise: while an ulcer usually refers to an open wound, not all pressure ulcers are open (for example, stage I pressure ulcers and deep tissue injuries are usually closed at the time of diagnosis). Synonyms of pressure ulcer are also imprecise, namely decubitus ulcer, which implies that the ulcer occurred from lying down – the Latin word decumbere means “to lie down”. In reality, many types of pressure ulcers

are not due to lying down. For example, ischial pressure ulcers are due to sitting on poorly padded surfaces for prolonged periods of time. Some pressure ulcers on the leg are due to a poorly padded cast, while others on the ear are due to prolonged wear of nasal cannulas in hospitalized patients. The terms pressure ulcer and pressure sore are likely the best terms to use when describing these lesions (Video Lecture 16.1 ).

Epidemiology and cost Pressure ulcers are fairly common among the elderly, critically ill, and spinal cord injury population. Every year, approximately 2.5 million patients develop pressure ulcers in the United States.1 In 1999, 14.8% of patients in acute care facilities had a pressure ulcer,2 7.1% of which were facility-acquired. In 2009, those prevalence rates were 12.3% and 5%, respectively.3 Overall prevalence rates were highest in long-term acute care facilities (22%), while facility-acquired rates were highest in adult intensive care units (ICUs). Overall, pressure ulcer prevalence does not appear to be decreasing over the past few decades, despite significant advances in treatment and prevention. Particular populations have been identified as particularly high risk. There is a strong association between hip fractures and pressure ulcers, with incidences ranging from 8.8% to 55%.4–6 In patients with spinal cord injury (SCI), the incidence of pressure ulcers has been reported to be as high as 60%.7,8 Pressure ulcers also constitute a significant economic burden on the healthcare system. However, calculating the exact financial costs associated with pressure ulcers is complex, since many patients are admitted with pressure ulcer-related problems, such as septicemia, and carry pressure sore as a secondary diagnosis. The National Pressure Ulcer Advisory Panel (NPUAP) has estimated the cost to treat and heal hospital-acquired pressure sores to be up to $100,000 per patient.9 When taking the additional costs, both surgical and non-surgical, of managing pressure sores at nursing homes and home care facilities into consideration, the annual financial

Basic science

Anatomic distribution Classically, in the early acute phase after SCI, the sacral area tends to be the most common site of pressure sores as patients are treated for their initial injuries in the supine position. In the later phases after SCI, ischial pressure ulcers become more common as patients begin to sit up. Overall, the most common location for pressure ulcers is the sacrum (28% to 36%), followed by the heel (23% to 30%) and the ischium (17% to 20%).1,14–16

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Basic science Multiple studies describe risks associated with the development of pressure sores.1,27,28 Fisher et al. found that increased age, male sex, friction, shear, moisture, malnutrition, immobility, and altered sensorium all independently place patients at risk of developing pressure sores.27 More recently, Baumgarten et al. found that increased age, male sex, moisture caused by incontinence, poor nutrition, and immobility limiting turning in bed all correlated with the diagnosis of pressure sores.28 Recognition of these factors has led to the understanding of pressure sores as multifactorial entities.

Pressure As their name implies, the main culprit in pressure ulcer formation is pressure, specifically sustained external pressure exceeding the closing pressure of nutrient capillaries.29,30 In 1930, Landis performed a classic series of experiments and found that the average capillary closing pressure is approximately 32 mmHg.31 Fronek and Zweifach later reported similar findings, noting perfusion pressures between 20 and 30 mmHg (Fig. 16.1).32 Lindan et al. measured pressure points33: when supine, the highest pressure is applied to the sacrum, buttocks, heel, and occiput, all of which are subjected to pressures of roughly 50–60 mmHg. When sitting, pressures up to 100 mmHg are applied over the ischial tuberosities (Fig. 16.2).

120 100 80 mmHg

burden in the United States was estimated by the Agency for Healthcare Research and Quality at approximately $11 billion in 2006.10 Ten years later, Padula et al. estimated the cost to have increased to $26.8 billion annually.11 In 2002, the Center for Medicare & Medicaid Services (CMS) identified eight hospital-acquired complications as never events. These never events include hospital-acquired stage III and IV pressure ulcers. In 2008, CMS implemented the Hospital-Acquired Conditions (HACs) initiative, a policy that denies reimbursement for these preventable conditions.12 Waters et  al. analyzed data from 1381 US hospitals between July 2006 and December 2010, comparing the rate of stage III/ IV pressure sores before and after the implementation of the HACs initiative.13 Unfortunately, the initiatives did not seem to lead to a decrease in the incidence of pressure ulcers over that four year period.

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Figure 16.1  Pressure in various components of the tissue microcirculation (diameter in μm). (Data from Fronek K, Zweifach BW. Microvascular pressure distribution in skeletal muscle and the effects of vasodilation. Am J Physiol. 1975;228:791; reprinted with permission from Woolsey RM, McGarry JD. The cause, prevention, and treatment of pressure sores. Neurol Clin. 1991;9:797).

However, simply applying pressure in excess of these levels does not necessarily result in tissue ischemia. Much of the pressure applied to tissues is sustained by the connective tissues surrounding the blood vessels. Furthermore, autoregulatory mechanisms tend to vasodilate blood vessels in response to pressure, a process known as pressure-induced vasodilation, which will be discussed in more detail in the Neurological Injury section below.31,34 Efforts have been made to quantify the degree and time of pressure necessary to cause tissue damage. Dinsdale found that pressure roughly double capillary closing pressure, applied for 2 hours, resulted in irreversible ischemic damage to tissue.35 Pressures below this threshold were unlikely to cause tissue necrosis. Kosiak et  al. noted similar findings in dog tissues, but noted that if the pressure was released every 5 minutes, no injury occurred.36 Groth noted, in rabbits, that higher pressures caused damage in shorter amounts of time.37 Husain had similar results in a rat model, also noting that pressure applied over a large area was less injurious than when applied over a smaller one.29 Furthermore, various tissues have different susceptibility to pressure. Nola and Daniel both noted that muscle was more susceptible to pressure injury than skin, requiring less pressure for a shorter duration, likely owing to its increased metabolic demands.38,39

Shear and friction Friction is the force resisting relative motion between the patient’s skin and other surfaces, such as bedding, transfer devices (sheets, rollers, slide boards), various appliances and orthotics, and mobility devices such as wheelchair cushions. Excess friction causes direct injury to the skin, consisting of abrasions, blisters, and even tears in patients with fragile skin (Fig. 16.3).40,41 While relatively minor in isolation, such injuries may potentiate further damage. As the integrity of the skin is compromised, transepidermal water loss increases and allows moisture to accumulate. Moisture, in turn, increases the coefficient of friction and promotes adherence to sheets and other contact surfaces, leading to a positive feedback loop.42 Shear, on the other hand, represents the deep tissue injury that occurs as a result of friction. When friction causes the skin and subcutaneous tissue to move in relation to the deeper

Historical perspective

Historical perspective Pressure sores are an ancient problem, observed at autopsy of Egyptian mummies.17 As early as the 16th century, Ambrose Paré recognized the importance of pressure and nutrition in the treatment of these lesions.18 By 1873 Sir James Paget correctly surmised that pressure led to compression of the cutaneous vasculature, leading to necrosis.19 Though he incorrectly attributed them to central nervous system lesions, in 1878 Charcot provided a detailed description of what he termed decubitus ominosus,20 noting not only the clinical manifestations of the disease but the poor prognosis they portended. Though well over a century old, Charcot’s description could be applied to any number of modern patients with pressure sores of various stages: The skin there has a rosy hue, sometimes it is dark red, and even violet, but the dolor disappears momentarily on pressure with the finger. […] On the morrow, or after-morrow, vesiculae or bullae make their appearance toward the central part of the erythematous patch; […] The subcutaneous connective tissue, and sometimes

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even the subjacent muscles are themselves already invaded by sanguine infiltration. […] The eschars, if they but attain a certain extent, constitute, as you are aware, dangerous foci of infection; and, in fact, putrid intoxication, denoted by a more or less intense remittent fever. In 1938, John Staige Davis was the first to suggest reconstructing the fragile scar of a healed pressure ulcer with a flap.21 However, it was not until 1945 that Lamon described the first closure of open pressure sores.22 Thereafter, surgical treatment of pressure sores gained immediate attention, and by the end of the decade most of the surgical techniques used in the treatment of pressure sores today had been reported, including excision of bony prominences,23 use of flaps,24,25 tension-free closure, and back-grafting of donor sites.26 In the following decades, wound care became ever more complex, and numerous technical refinements were developed, but the basic concepts of patient optimization, complete debridement, and tension-free soft-tissue coverage have remained constant.

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CHAPTER 16  • Pressure sores

SECTION II

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Figure 16.3  Pressure, shear, and friction are related but distinct forces which contribute to pressure sore development.

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of shear: patients in the semi-Fowler’s position or sliding down in a wheelchair both experience significant shear over the lower back and buttocks.46 This can explain why wheelchair-bound patients may still develop a sacral pressure sore if they are not sitting upright in their chair, despite the fact that theoretically the ischial tuberosities should be bearing the majority of their weight.

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Figure 16.2  Distribution of pressure in a healthy adult male while (A) supine, (B) prone, (C) sitting with feet hanging freely, and (D) sitting with feet supported. Values expressed in mmHg. (Adapted with permission from Lindan O, Greenway RM, Piazza JM. Pressure distribution on the surface of the human body I. Evaluation in lying and sitting positions using a “bed of springs and nails”. Arch Phys Med Rehabil. 1965;46:378).

tissues, blood vessels are stretched, angulated, and potentially injured.43,44 Shear forces potentiate the effects of pressure,40,41 acting in synergy to cause tissue injury. Dinsdale noted that addition of shear forces greatly decreased the amount of pressure needed to cause ulceration in a pig model, concluding that “a shear force is more disastrous than a vertical force”.35 Goossens et al. noted similar results in human subjects, finding that the addition of a small shear component drastically reduced the level of pressure needed to cause critical ischemia over the sacrum.45 Transferring patients, sliding or dragging them in bed, “boosting” them up in bed, or allowing them to elevate themselves in bed by pushing with elbows and heels all cause significant shear.41 Certain positions also cause elevated levels

Moisture Moisture also potentiates the effects of pressure. Moisture increases the coefficient of friction between the skin and other surfaces, making friction and shear injuries more likely.42 Moisture also directly causes skin maceration and breakdown.47 Though excess moisture can have many causes, urinary and fecal incontinence are common in patients with pressure sores, with rates from 20% to 77% for urinary incontinence48,49 and 17% to 50% for fecal incontinence.50 In addition to causing excess moisture, urine also negates the acidic pH of skin through the introduction of nitrogen derivatives. Fecal contamination introduces a large bacterial load. Lowthian noted a fivefold increase in pressure sores in patients who were incontinent, though he did not distinguish between urinary and fecal incontinence.47 While some studies have found a relationship between urinary incontinence and pressure sores,51 others have failed to find a correlation while noting a significant correlation between fecal incontinence and pressure sores.52–54 While excess moisture is clearly deleterious, the opposite is also true. Excessively dry skin is prone to cracking, has decreased tensile strength and lipid content, and impaired

Patient evaluation

barrier function, and this appears to be an independent risk factor for pressure ulceration.55,56 Thus the importance of controlling the microclimate around the patient’s skin within specific parameters.

Malnutrition Malnutrition, manifested by low serum albumin, prealbumin, or transferrin levels, is a common comorbidity in patients in pressure ulcers.57 The prevalence of malnutrition ranges from 1%–4% in elderly patients living at home, to 20% in hospitalized patients and 37% in institutionalized patients.58 Protein malnutrition impairs wound healing and increases the risk of wound infection.59,60 In addition, protein malnutrition, as measured by low serum albumin, is an independent predictor of postoperative mortality.61–64 The importance of nutrition for pressure ulcer healing will be discussed in more detail later in this chapter.

Neurological injury Pressure sores are the most common complication65,66 and the second most common cause of hospital admission67 in patients with a spinal cord injury (SCI). While this is mostly due to the loss of protective sensation, there is also a large role for the loss of pressure-induced vasodilation. In healthy individuals, moderate pressure over tissue is known to induce vasodilation in that tissue, leading to increased blood flow.68 This pressure-induced vasodilation is mediated by a local reflex loop, whereby local sensory nerves detect pressure and induce the release of calcitonin gene-related peptide, which mediates vasodilation.68 In patients with impaired peripheral nerve function, such as diabetics, paraplegics, and the elderly, pressure-induced vasodilation is lost, making tissues much more susceptible to ischemia as a result of local pressure.69,70 Another neurologic issue that may potentiate the formation of pressure ulcers is spasticity, which affects up to 78% of SCI patients one year after injury.71 Spasticity is characterized by hyperreflexia, clonus, and increased muscle tone. While it is not included in most pressure sore risk scales, it directly increases mechanical stress, alters weight distribution, and complicates patient positioning, skin inspection, and hygiene.72

Biofilm and inflammatory milieu Chronic wounds seldom exhibit overt signs of infection (erythema, purulence). Instead, bacteria in chronic wounds are often encased in a extracellular polymeric substance (EPS), forming what is known as biofilm.73 Biofilm infections are problematic in pressure ulcers for several reasons. Biofilm infections are difficult to diagnose using traditional culture techniques.74 Instead, biofilm requires advanced diagnostic techniques such as polymerase-chain reaction and scanning electron microscopy.75,76 In addition, bacteria encased in biofilm are much more recalcitrant to topical and systemic antibiotic therapy than bacteria in the planktonic state.77 This is because the EPS acts as a barrier to antibiotic diffusion, and bacteria in biofilm exist in a low metabolic state.76 Biofilms are also known to promote an inflammatory milieu that inhibits wound healing. This milieu is rich in proteases and ceramidase, both of which cause wound and

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skin degradation.78 Biofilm promotes the influx of numerous but ineffective host neutrophils. Those neutrophils in turn produce reactive oxygen species that further exacerbate the inflammatory milieu.75 Pressure ulcers have an imbalance of matrix metalloproteinases (MMPs). MMPs are zinc-dependent proteases, which are capable of degrading various extracellular matrix proteins, and which play a role in cell proliferation, differentiation, apoptosis, angiogenesis, and host immunity.79 Under homeostatic conditions, a balance must be maintained between MMPs and their counterparts, namely tissue inhibitors of metalloproteinases (TIMPs) in order to maintain orderly formation/degradation of extracellular matrices. In chronic wounds from 56 patients with stage III/IV pressure sores, Ladwig et al. found that as chronic wounds heal, the ratio of MMP-9:TIMP-1 decreases, thus suggesting that higher levels of MMP-9 and TIMP-1 are necessary for appropriate healing of chronic wounds and may serve as markers of healing/ non-healing.80 Pressure ulcers are also known to have decreased levels of cytokines that promote wound healing, such as platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), epidermal growth factor (EGF), and transforming growth factor-beta (TGF-β).81

Diagnosis Staging (Table 16.1, Fig. 16.4) The most commonly used staging classification for pressure ulcers is the one originally developed by Shea,82 and modified by the National Pressure Sore Advisory Panel Consensus Development Conference in 2007.29 Though used in basic form for many years, two additional definitions, suspected deep-tissue injury and unstageable, have been added relatively recently to the NPUAP system. “Stage” is somewhat of a misnomer, as it implies a progression that does not reflect reality. Stage IV ulcers do not necessarily start as stage I ulcers, a fact emphasized by the addition of the suspected deep-tissue injury classification. Likewise, healing pressure sores do not progress in reverse order but instead granulate and close by secondary intention in the absence of surgical treatment. Though panel members were aware of these issues, the term “stage” was retained due to its historical use and widespread adoption.

Patient evaluation When evaluating a new patient with a pressure sore, several factors must be considered. Both the wound and the patient should be meticulously examined. A wound history, noting the onset, duration, prior treatments and procedures, and wound care regimen, should be documented. Wounds should be measured in three dimensions, with notes made regarding any tunneling or undermining. The tissue at the margins of the wound should be examined for any signs of occult deep-tissue injury, infection, and scarring. The base of the wound should be characterized, noting the presence of eschar, slough, or

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Table 16.1  Staging of pressure ulcers

Stage

Description

I

Intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared with adjacent tissue. Stage I may be difficult to detect in individuals with dark skin tones. May indicate “at risk” persons (a heralding sign of risk).

II

Partial-thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising.† This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation.

III

Full-thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, and muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage III pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and stage III ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable.

IV

Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often includes undermining and tunneling. The depth of a stage IV pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue, and these ulcers can be shallow. Stage IV ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable.

Unstageable

Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth and therefore stage cannot be determined. Stable (dry, adherent, intact, without erythema, or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should not be removed.

(Reproduced with permission from: Tchanque-Fossuo C, Kuzon WM. An evidence-based approach to pressure sores. Plast Reconstr Surg. 2011;127:932).

other necrotic tissue. If necrotic material obscures the base of the wound, it should be debrided until a full assessment can be performed. Granulation should be noted in terms of both character and percentage of the wound bed covered. Exposed tissues, such as bone, tendon, or joint, should be noted. If easily accessible, the bone should be characterized as hard, soft, or obviously necrotic. The amount and character of the wound exudate should be documented as well. A measuring tape and camera can improve documentation and make tracking progression easier.83 Attention should also be paid to the risk factors specific to pressure sores. An attempt should be made to identify the etiology of the patient’s pressure sore, though it is often multifactorial. Sources of friction, shear, and pressure should be evaluated, and recommendations for proper pressure relief surfaces and skin care regimens made as appropriate. If incontinence is present an effort should be made to control this, possibly involving the assistance of other specialties. Likewise, spasticity should be evaluated and, if needed, controlled medically or surgically. Nutrition should be evaluated with serum albumin and prealbumin. If needed, nutrition should be supplemented, and progress of therapy monitored with weekly serum studies. Any underlying medical problems, such as hypertension, diabetes, or history of cardiac disease, should be investigated and optimized. A reasonable initial set of studies would include a complete blood count, basic metabolic panel, creatinine, and blood urea nitrogen. Albumin and prealbumin should be obtained at the initial consult and regularly thereafter to evaluate for malnutrition and follow the progression of therapy. C-reactive protein and erythrocyte sedimentation

rate (ESR) can be obtained to evaluate for osteomyelitis, though they will almost certainly be positive when deep ulcers are present. The evaluation of the pressure sore patient for osteomyelitis is discussed in the next section. Unlike core-needle and open surgical biopsy, swab cultures of the open pressure sore are of little value and should not be used to direct antibiotic therapy.84

Osteomyelitis Osteomyelitis has been known for years to cause wound infection and breakdown after reconstruction85,86 (Fig. 16.5, Algorithm 16.1). Therefore, the diagnosis of osteomyelitis must be established before surgical reconstruction is undertaken. The gold-standard for the diagnosis of osteomyelitis remains open bone biopsy. This technique also allows for identification of the pathogenic organisms, thereby facilitating tailored antibiotic therapy. However, attempts have been made to identify less invasive diagnostic modalities. Some individual modalities have been attempted in isolation, but have not been found to be accurate. The clinical assessment of bone (firm versus soft and crumbly) is a poor predictor of osteomyelitis.87 Lewis et  al. found that a combination of white blood cell count, ESR, and two-view X-ray was an easy, accurate, and noninvasive method to diagnose osteomyelitis,88 with a sensitivity of 89% and a specificity of 88%. Only one positive test was needed to make the diagnosis. In contrast, they found that isolated radiographic imaging (CT or X-ray) has limited sensitivity (10%–30%), but high specificity (90%–100%).

Patient evaluation

A

B

C

D

E

F

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Figure 16.4  The National Pressure Ulcer Advisory Panel staging system. (A,E) Stage I: Intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. (B,F) Stage II: Partial-thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. This should not be used to describe skin tears, tape burns, perineal dermatitis, maceration, or excoriation. (C,G) Stage III: Full-thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. (D,H) Stage IV: Full-thickness tissue loss with exposed bone, tendon, or muscle. Exposed bone is sufficient but not necessary to define a stage IV pressure sore. Slough or eschar may be present on some parts of the wound bed. Often includes undermining or tunneling. May extend into muscle and/or supporting structures (e.g., fascia, tendon, or joint capsule), making osteomyelitis possible. Bone/tendon is visible or directly palpable. (I) Suspected deep-tissue injury: Purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. The wound may evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment. (J) Unstageable: Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown) and/or eschar (tan, brown, or black) in the wound bed. Until the base of the wound is exposed, the true depth, and therefore stage, cannot be determined.

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G

H

I

J

Figure 16.4, cont’d

Rubayi found that nuclear bone scans tend to have limited utility in chronic pressure ulcers, as they are nonspecific, and therefore have a high rate of false positivity for osteomyelitis.89 MRI has been found to have an overall accuracy of 97%, sensitivity of 98%, and specificity of 89%.90 Not only is MRI accurate, but it also helps define the extent of infection, which can guide surgical resection. Han et al. analyzed the results of two-stage surgical management, consisting of wound debridement and Jamshidi core needle bone biopsy at the first operation, followed by delayed wound closure86 (Fig. 16.6). If the biopsy results were positive, closure was delayed for 6 weeks while the osteomyelitis was treated with antibiotics; otherwise the wound was closed once biopsy results were available. The authors also noted that bone cultures alone were not as useful as bone cultures and histopathology of the bone biopsy together, and found that the biopsy had positive and negative predictive values of 93% and 100%, respectively. These results are in keeping with several other studies that support the utility of bone biopsy in the diagnosis of osteomyelitis.91–94 Marriott and Rubayi have used the results of bone biopsy to determine the duration of antibiotic therapy, in some cases truncating treatment if pathology reveals only chronic osteomyelitis.95 Ultimately, the combination of MRI with bone biopsy allows high diagnostic accuracy, while identifying the extent of disease and the pathologic organism.

Psychological evaluation Psychological problems are common in the pressure sore population, with a diagnosis of major depression in SCI patients ranging from 22% to 47.4%.96–98 Risk factors for depression include female gender, younger age, multiple previous operations for pressure sores. Foster et al. suggest that psychological factors may play a role in pressure ulcer recurrences.99

Patient selection All patients with pressure sores should be optimized with regard to the risk factors already enumerated. It is worth remembering that pressure sores are rarely life-threatening, and there is no need to rush to treatment or surgery if the patient has not been optimized. Many superficial wounds will heal with conservative therapies if correctable risk factors are identified and addressed. On the other hand, a patient who is malnourished, bedbound on an inappropriate mattress, with undiagnosed osteomyelitis, is doomed to failure regardless of the surgical technique used. A judgment must be made whether a wound is likely to heal by secondary intention or whether a flap is required to resurface the wound and/or fill dead space after debridement. In general, stage I and II pressure sores can be treated nonoperatively, while stage III and IV ulcers require flaps.

Treatment

A

469

B

C

D

Figure 16.5  (A–D) Bone scan, computed tomography, and magnetic resonance imaging of severe sacral osteomyelitis. (Reprinted with permission from Han H, Lewis VL, Weidrich VA, et al. The value of Jamshidi core needle bone biopsy in predicting postoperative osteomyelitis in grade IV pressure ulcer. Plast Reconstr Surg. 2002;111:118).

Patients with suspected deep-tissue injury and unstageable ulcers should be debrided until they can be clearly staged.100 While surgical debridement is the gold standard, other methods can be used as appropriate. While operative treatment is often delayed while the patient is optimized and risk factors corrected, it is a rare patient who never qualifies for any attempt at reconstruction. Obviously critically ill patients who cannot tolerate surgery should be stabilized before any sort of reconstruction is entertained. More uncommon is the patient with multiple severe comorbidities whose risk factors cannot be easily corrected, due to either medical or social factors. In such cases, chronic wound care may be preferable to attempted reconstruction that is doomed to failure and recurrence.

Treatment Prevention Obviously, prevention of pressure sores is preferable to treatment. As healthcare moves toward nonpayment for nosocomial pressure sores, there is an ever-greater incentive to avoid these lesions. However, despite extensive study and recommendations, overall pressure sore rates have changed little in recent years.3,101,102 Some pressure sores may not be preventable,103–105 and using pressure sores as an indicator of quality is a contentious issue, particularly in light of possible negligence litigation.106 However, although no strategy has been found that reduces

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Algorithm 16.1 Grade IV pressure ulcer

Aggressive wound care and nutritional optimization

Effective Jamshidi needle bone biopsy and bone culture

JNBB + Bone cx +

JNBB + Bone cx –

JNBB – Bone cx +

JNBB – Bone cx –

IV antibiotics 6 weeks

IV antibiotics 6 weeks

Elective flap reconstruction

Elective flap reconstruction

Delayed flap reconstruction Partial ostectomy bony prominence

Delayed flap reconstruction Partial ostectomy bony prominence

Continue with IV antibiotics for 2 weeks

Perioperative antibiotics for 48 hours

Effective Jamshidi needle bone biopsy and bone culture

Effective Jamshidi needle bone biopsy and bone culture

Protocol for managing patients with grade IV pressure ulcers. JNBB, Jamshidi core needle bone biopsy; IV, intravenous. (Reprinted with permission from Han H, Lewis VL, Weidrich VA, et al. The value of Jamshidi core needle bone biopsy in predicting postoperative osteomyelitis in grade IV pressure ulcer. Plast Reconstr Surg. 2002;111:118).

pressure sore rates to zero, there are several measures, many of which now constitute standard care, that may contribute to the reduction of pressure sore incidence.56 For the surgeon who is often consulted only after a pressure sore has developed, knowledge of prevention strategies is still critical not only to advise the consultation, but also to optimize the patient before surgery, prevent additional pressure sores from developing, and, perhaps most critically, to prevent postoperative recurrence.

Risk assessment Risk assessment is an essential step in pressure ulcer prevention. Several risk assessment scales have been developed (Braden, Gosnell, Knoll, Norton, Waterlow, and Douglas),107 with each scale having specific merits and limitations. The Norton scale is designed for use in geriatric patients, and includes general physical condition, mental status, activity, mobility, and incontinence.108 Scores range from 5 to 20, with lower scores associated with greater risk. The Braden scale is the most widely used pressure sore risk assessment tool (Table 16.2).109 It incorporates six subscales which assess sensory perception, skin moisture, activity,

mobility, friction and shear, and nutrition. Scores range from 6 to 23, with higher scores indicating a higher risk of pressure ulcers. A score of 16 is generally considered to be the threshold for pressure sore development.109 The Braden scale has a sensitivity of 74%, and a specificity of 68% for predicting pressure ulcers.110 However, the scale is unreliable in patients older than 80 years,111 and it does not include important risk factors such as spasticity. In general, assessment scales are superior to clinical judgment when predicting future pressure ulceration.107 However, there is no evidence that use of risk assessment decreases pressure sore incidence.112–114 Whether this is because interventions are not instituted or are ineffective is unclear.113 Given the recent efforts to improve healthcare quality, Bergman et  al. analyzed one institution’s National Surgical Quality Improvement Program (NSQIP) database to determine adherence to multiple process-based quality indicators, including pressure ulcer risk assessment. While this study only looked at 143 consecutive elective abdominal surgery admissions, authors note an adherence rate of only 35% in the risk assessment for pressure ulcers, supporting the notion that interventions designed to stratify risk remain poorly utilized.115

Treatment

A

B a

b

c

d

C D

Figure 16.6  (A) The Jamshidi bone biopsy needle, cannula, and screw-on cap (a), tapered point (b), pointed stylet to advance cannula through soft tissues (c), and probe to expel specimen from cannula (d). (B) With the stylet locked in place, the cannula is advanced through the soft tissue until bone is reached. The inset is a close-up view showing stylet against bone cortex. (C) The stylet is removed, and the bone cortex is penetrated with the cannula. The cannula is withdrawn, and the procedure repeated with redirection of the instrument to obtain multiple core samples. (D) The probe is then inserted retrograde into the tip of the cannula to expel the specimen through the base (inset). (Reprinted with permission Powers BE, LaRue SM, Withrow SJ, et al. Jamshidi needle biopsy for diagnosis of bone lesions in small animals. J Am Vet Med Assoc. 1988;193:206–207).

Skin care Ideal skin care encompasses cleaning, hydrating, protecting, and replenishing the skin as needed (Box 16.1). Proper skin care can be time- and labor-intensive and is at times neglected by physicians and nurses alike.116 Common recommendations for skin cleansing involve the use of warm soap and water followed by drying by rubbing or patting.117 Washing involves the use of soap and surfactants, which, while effective at removing debris, have the potential to be irritants.118 The alkaline nature of soap also negates the protective natural acidity of the skin, which in turn alters the balance of resident flora on the skin.119 Drying the skin by patting may cause less trauma,120,121 though if it leaves excess moisture on the skin, can lead to maceration and increased vulnerability to friction injuries.122 Many alternative cleansers have been marketed that address the shortcomings of soap and water, but little data exist to recommend any particular product at this time.123

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Maintaining proper skin hydration is most often achieved through the use of emollients, which occlude the skin surface with a hydrophobic layer, and humectants, which attract and absorb water from their surroundings. Numerous formulations exist, many with additional surfactants and emulsifying agents, which vary somewhat in their effectiveness, greasiness, and potential for skin irritation. While the theoretic advantages of treating dry skin are well established,52,54,122 as with cleansers, few data exist to recommend any one hydrating product over another.124,125 Barrier products protect the skin, particularly in the setting of incontinence or in the presence of stomas, fistulas, or wounds. Many preparations consist of a lipid/water emulsion that forms a protective film over the skin. Newer barrier products incorporate a polymer that forms a thin semipermeable membrane over the skin.126 Many incorporate an antiseptic agent such as cetrimide or benzalkonium as well. Again, despite their widespread use and the proliferation of products, data on their effectiveness are scant.127 While data on individual agents are not very robust, there is evidence that a clear skin care protocol can benefit patients. Multiple authors have found that instituting such protocols results in reduction in pressure sore incidence rates.128 Cole and Nesbitt found a reduction from 17.8% to 2% over a 3-year period,129 whereas Lyder et  al. noted an 87% reduction in a nursing home setting.130 Based on the available data, the American Wound Ostomy and Continence Nurses Society has updated their guidelines for skin care.131

Incontinence As noted previously, the relationship between urinary incontinence and pressure sore incidence is not clear, with limited evidence to suggest a causal relationship. Currently, the use of diapers or sanitary pads in conjunction with meticulous skin care is a reasonable option when compared to the risks associated with extended use of a urinary catheter.132 Fecal incontinence, on the other hand, has been shown to be a risk factor for pressure sores. At times fecal incontinence is due to factors that are not easily correctable: cognitive impairment, history of colorectal surgery, radiation proctopathy, inflammatory bowel disease, and various neurological or myogenic disorders of sphincter function are not easily correctable. The bladder and bowel dysfunction of SCI patients requires specific regimens and is generally managed by a specialist.133 However, many measures can be instituted to decrease the impact of fecal incontinence. Possibly the most common predisposing condition to fecal incontinence is fecal impaction, which is common in older adults and may lead to overflow incontinence.134 Conservative measures include diet modification and a wide variety of antimotility agents, including clonidine, cholestyramine, loperamide, codeine, diphenoxylate, and atropine.135,136 Diarrhea may be due to infection, which should be ruled out and treated prior to using antidiarrheal agents. If medical management is unsuccessful, surgery may be considered, ranging from attempts at sphincterplasty to elective diverting colostomy when other options fail.137,138 Though patients and families are often reluctant to proceed with colostomy, there is evidence that overall quality of life is improved in patients with severe fecal incontinence.139

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Table 16.2  The Braden scale for predicting pressure sore risk Sensory perception Ability to respond meaningfully to pressure-related discomfort

1. Completely limited Unresponsive (does not moan, flinch, or grasp) to painful stimuli, due to diminished level of consciousness or sedation or Limited ability to feel pain over most of body

2. Very limited Responds only to painful stimuli. Cannot communicate discomfort except by moaning or restlessness or Has a sensory impairment which limits the ability to feel pain or discomfort over half of body

3. Slightly limited Responds to verbal commands, but cannot always communicate discomfort or the need to be turned or Has some sensory impairment which limits ability to feel pain or discomfort in one or two extremities

4. No impairment Responds to verbal commands. Has no sensory deficit which would limit ability to feel or voice discomfort

Moisture Degree to which skin is exposed to moisture

1. Constantly moist Skin is kept moist almost constantly by perspiration and urine. Dampness is detected every time patient is moved or turned

2. Very moist Skin is often, but not always, moist. Linen must be changed at least once a shift

3. Occasionally moist Skin is occasionally moist, requiring an extra linen change approximately once a day

4. Rarely moist Skin is usually dry; linen only requires changing at routine intervals

Activity Degree of physical activity

1. Bedfast Confined to bed

2. Chairfast Ability to walk severely limited or nonexistent. Cannot bear own weight and/or must be assisted into chair or wheelchair

3. Walks occasionally Walks occasionally during day, but for very short distances with or without assistance. Spends majority of shift in bed or chair

4. Walks frequently Walks outside room at least twice a day and inside room at least once every 2 hours during waking hours

Mobility Ability to change and control body position

1. Completely immobile Does not make even slight changes in body or extremity position without assistance

2. Very limited Makes occasional slight changes in body or extremity position but unable to make frequent or significant changes independently

3. Slightly limited Makes frequent though slight changes in body or extremity position independently

4. No limitation Makes major and frequent changes in position without assistance

Nutrition Usual food intake pattern

1. Very poor Never eats a complete meal. Rarely eats more than half of any food offered. Eats two servings or less of protein (meat or dairy products) per day. Takes fluids poorly. Does not take liquid dietary supplement or Is NPO and/or maintained on clear liquids or IVs for more than 5 days

2. Probably inadequate Rarely eats a complete meal and generally eats only about half of any food offered. Protein intake includes only three servings of meat or dairy products per day. Occasionally will take a dietary supplement or Receives less than optimum amount of liquid diet or tube feeding

3. Adequate Eats over half of most meals. Eats a total of four servings of protein (meat, dairy products) per day. Occasionally will refuse a meal, but will usually take a supplement when offered or Is on a tube-feeding or TPN regimen which probably meets most of nutritional needs

4. Excellent Eats most of every meal. Never refuses a meal. Usually eats a total of four or more servings of meat and dairy products. Occasionally eats between meals. Does not require supplementation

Friction and shear

1. Problem Requires moderate to maximum assistance in moving. Complete lifting without sliding against sheets is impossible. Frequently slides down in bed or chair, requiring frequent repositioning with maximum assistance. Spasticity, contractures, or agitation leads to almost constant friction

2. Potential problem Moves feebly or requires minimum assistance. During a move skin probably slides to some extent against sheets, chair, restraints, or other devices. Maintains relatively good position in chair or bed most of the time but occasionally slides down

3. No apparent problem Moves in bed or chair independently and has sufficient muscle strength to lift up completely during move. Maintains good position in bed or chair

Total score IV, intravenous; NPO, nil per os; TPN, total parenteral nutrition. (Reproduced from www.bradenscale.com.)

Treatment

BOX 16.1  General skin care principles Assess the patient’s skin daily Cleanse skin when indicated using a pH-balanced cleanser Avoid soap and hot water Avoid friction and scrubbing Minimize exposure to moisture (e.g., incontinence, wound leakage) Use skin barrier product to protect vulnerable skin Use emollients to maintain skin hydration

Spasticity Control of spasticity may not only reduce the risk of pressure sores, but may also improve patient reports of pain and ability to perform activities of daily living (ADL).140 However, it is worth noting that in some cases spasticity may increase stability in positioning, facilitate some transfers and ADLs, and prevent osteopenia.141,142 Taken as a whole, the impact of spasticity on quality of life is not straightforward and should be considered before instituting treatment. Physical therapy is the first step in treating spasticity, and an important component of care in SCI patients in general.143 Pharmacologic treatment is the next step. Diazepam, baclofen, clonidine, tizanidine, gabapentin, and dantrolene are commonly used agents.144–147 Each has the potential for side effects, including sedation, nausea, diarrhea, muscle weakness, and cognitive effects, and treatment must be tailored to the individual patient.147,148 Patients who cannot tolerate or do not respond to oral therapy may benefit from intrathecal administration of baclofen.146,149 As the drug directly accesses the central nervous system, systemic side effects are minimized at the cost of the risks of surgery and possible mechanical complications with the pump. Injection with chemodenervating agents, including phenol, ethanol, and botulinum toxin, can be effective.150,151 Reported complications include systemic side effects, vascular complications, skin irritation, and tissue necrosis. Though the effects are temporary, long-term use of chemodenervating agents will result in denervation atrophy. Surgical management of spasticity is an option when medical therapy is insufficient. Baclofen pump implantation is the most common surgical procedure for spasticity in individuals with SCI and has a long history of success.147,152 In select, refractory cases, orthopedic and neurosurgical techniques may be of benefit, though such procedures are not usually aimed primarily at pressure sore prevention. Local tenotomy or tendon transfer has had mixed results in the treatment of spasticity.153 Rhizotomy has been complicated by both inadequate treatment of spasticity154 and severe atrophy,155 depending on the technique employed. Myelotomy and T-myelotomy involving direct sectioning of the spinal cord have been reported to be effective in several case series in patients who did not have hope of regaining motor function,156,157 though the benefits did decrease over time.158

through the use of various surfaces and products, as well as protocols mandating patient repositioning. Though numerous support surfaces exist, most can be divided into two general categories. Constant low-pressure (CLP) devices distribute pressure over a large area to avoid concentrated pressure over bony prominences. These CLP devices include supports with static air, water, gel, bead, silicone, foam, and sheepskin (Fig.  16.7A). On the other hand, alternating-pressure (AP) devices vary the pressure under the patient, avoiding prolonged pressure over a single anatomic point (Fig. 16.7B).159 Two particular types of CLP device deserve special mention, as they are commonly used in the prevention and treatment of pressures sores. Low air loss (LAL) beds float the patient on air-filled cells through which warm air circulates (Fig. 16.8). The circulating air both equalizes pressure exerted on the patient and keeps the skin dry. Properly utilized, LAL surfaces exert less than 25 mmHg on any part of the body.160,161 Air-fluidized (AF) beds circulate warm air through fine ceramic beads, creating a unique support surface, while having a drying effect similar to LAL beds (Fig. 16.9).162,163 With proper use these beds exert less than 20 mmHg on the patient, but are expensive, heavy, and cumbersome.164 There is a daunting body of literature comparing various specific products to one another and with standard hospital beds. Despite these limitations, some general conclusions can be drawn from the literature.165 Considerable evidence exists that the use of a pressure-relieving overlay is superior to a

A

B

Figure 16.7  (A) Constant low-pressure surfaces seek to distribute pressure statically, while (B) alternating-pressure surfaces vary applied pressure over time.

Pressure relief Pressure relief is the mainstay of pressure ulcer prevention. Extensive efforts have been made in modulating the pressure

473

Figure 16.8  Low air loss mattress concept.

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Air flow

Figure 16.9  Fluidized bed.

standard bed in preventing pressure sores. Multiple studies have found decreased incidence and severity of pressure sores in high-risk patients with the use of constant low-pressure devices such as overlays166,167 or sheepskin168–170 when compared to a standard hospital foam mattress. Pooled analysis reveals a relative risk of 0.32.165 Specifically, in the operating room, gel operating table overlays have been shown to reduce the incidence of pressure ulcers.171 Data also support the use of AP devices when compared to standard mattresses. Both Andersen et al.167 and Sanada172 noted a significant reduction in pressure sore incidence with the use of active devices, with a pooled relative risk of 0.31.165 Though several studies have compared CLP and AP devices,173–176 no clear advantage has been identified, despite attempts at pooled analysis.165 LAL, like other CLP surfaces, has been shown to be effective at preventing pressure sores,177,178 with a relative risk estimated at 0.08.165 Comparisons with other CLP devices in regard to prevention are limited, and no clear advantage for either has been demonstrated.179,180 Likewise, though AF beds are perhaps the most effective pressure-relieving devices in widespread use, virtually no data on their role in prevention are available, perhaps because these expensive devices are reserved for treatment. Regardless of the type of mattress used, they lose their ability to disperse interface pressure as the head is elevated to 45° or higher.181 As such, patients should avoid prolonged periods of sitting while on these mattresses. Given the wide array of, yet variable, data on the use of protective surfaces in high-risk patients, the American College of Physicians has formalized recommendations.102 These clinical practice guidelines were developed after critical evaluation of the quality of evidence and strength of recommendations of the available literature. While there is moderate-level evidence demonstrating improved outcomes with the use of static mattresses or overlays (CLPs not including LAL beds), there is only low-level evidence supporting the use of LAL mattress or AP devices.174,176,178,182–184 Moreover, in addition to the increased costs associated with the use of LAL and AP devices, the literature on LAL and AP devices demonstrates no difference or mixed results when compared to static mattresses/overlays. Therefore, the American College of Physicians now recommends that all patients identified as being at increased risk for developing a pressure sore be placed on an advanced static mattress, but recommends against the routine use of AP devices in these patients.102 In addition to support surfaces, patient repositioning is often used in an attempt to prevent pressure sores, though the data are limited. Defloor et al. found a significant reduction in pressure sore incidence when turning every 4 hours combined with a specialized foam mattress was compared to every 2 hours on a regular mattress.185 Given the study design it is

Figure 16.10  Hammocking effect of wheelchair sling seat producing pelvic obliquity. Paraplegics lack innervation of the lower trunk muscles and sit on their coccyx, with exaggerated posterior pelvic tilt. (Reprinted with permission from Letts RM. Principles of Seating the Disabled. Boca Raton, FL: CRC Press; 1991).

difficult to determine the relative contributions of the pressure relief surface and the turning regimen. The ideal interval and posture for repositioning are not clear given the current data.56,186 It bears mention that repositioning is not without its costs, both in terms of nursing time and effort, patient discomfort, and possible dislodgement of catheters and lines, and there is no evidence that more frequent repositioning reduces rates of pressure sores. Cushions for wheelchairs filled with gel, foam, air, or water are available to relieve pressure. A typical wheelchair sling seat exerts a “hammocking” effect that can produce abnormal scoliotic posture and pelvic obliquity (Fig. 16.10). This in turn causes asymmetric pressure on both trochanter and ischium that requires specialized cushions for prevention.187 Hip adduction and internal rotation of thighs, with consequent reduction in stability, are also seen in most paraplegics, who lack trunk or pelvic muscle innervation and tend to sit on their coccyx. Rigid-base cushions provide lumbar support and decrease ischial pressure by allowing wider weight distribution on the posterior thighs.187 A direct correlation between buttock–cushion interface has been noted (Fig. 16.11).188 Houle189 and Souther et al.190 studied the effects of various wheelchair seats and found decreased pressures over the ischium, although none was below the capillary pressure benchmark. The authors recommend additional measures for pressure relief to prevent ulceration. Ragan et al. studied seat interface pressures on wheelchair cushions of various thicknesses.191 They found the highest subcutaneous stress concentrated within 2 cm of the ischial tuberosity. The subcutaneous

Treatment

475

Nonetheless, as mentioned previously current recommendations support the use of low-cost static mattress overlays over high-cost LAL and AP devices.102,164,201

Spasticity Hard surface

Compliant surface

Bottoming out

Figure 16.11  Compressive force exerted on tissue by bone in an individual lying or sitting on (left) a hard surface; (center) an effective pressure-reducing device; and (right) an ineffective pressure-reducing device that “bottoms out”. (Reprinted with permission from Woolsey RM, McGarry JD. The cause, prevention, and treatment of pressure sores. Neurol Clin. 1991;9:797).

pressures decreased with thicker cushions, with the maximum effectiveness obtained with an 8-cm cushion. Increasing the thickness beyond 8 cm did not give further benefit in reducing subcutaneous stress. As with pressure relief mattresses, no data exist to recommend a particular type of cushion over another at this time.165,173,192,193 The development of pressure consciousness by the patient is an essential part of pressure sore prevention.194 Pressure release maneuvers are reinforced to patients and should be performed at least every 15 minutes while the patient is seated.195

Spasticity should be addressed not only to improve patient positioning, weight distribution, and hygiene but also to prevent tension on the healing wound, particularly if surgical intervention is planned.202,203 Spasticity treatment may be complicated by a reluctance to perform surgery or implant devices in a patient with an open wound, though this has been reported with favorable results.203 If pump implantation is not an option, then temporary chemodenervation should be considered, with delayed pump placement once the wound is healed.72

Malnutrition

With adequate care and patient optimization, some limited wounds may heal spontaneously without surgical intervention. The measures implemented in pressure sore prevention become doubly important once the transition is made to treating an established ulcer.

Nutritional optimization must be undertaken to achieve adequate healing.60,204 Nutrition is considered adequate when serum albumin is 3.5 g/dL or greater, and prealbumin is 15 mg/dL or greater, with an upward trend. In malnourished patients undergoing elective surgery, preoperative nutritional supplementation has been shown to decrease infectious205 and noninfectious complications.206 Specifically for pressure ulcers, Keys et  al. found that albumin levels below 3.5 g/dL were associated with ulcer recurrence within 1 year207; thus malnutrition should be corrected preoperatively, and nutritional markers, including albumin and prealbumin, should be followed and trended. Van Anholt et al.208 and Lee et al.209 both found accelerated healing with the use of oral nutritional supplement in randomized controlled trials. Taken together, the American College of Physicians now recommends protein or amino acid supplementation in patients with pressure sores.210 In regard to micronutrient supplementation, there is still little evidence to support routine supplementation of micronutrients such as vitamin C or zinc in the absence of a specific deficiency state.196,211 Though small, a randomized controlled trial of 88 patients failed to demonstrate an increase in the rate of healing of pressure sores.211 Similarly, a double-blind study of 14 patients treated with oral zinc failed to demonstrate any clinical benefit in the treatment of pressure sores.212 One exception is patients on chronic corticosteroids, who have impaired collagen synthesis, and therefore wound healing.60 In those patients, treatment with oral vitamin A 10,000 to 25,000 IU daily for one week preoperatively and 4 days postoperatively mitigates the harmful effects of corticosteroids on wound healing.213

Pressure relief

Tobacco and electronic cigarette use

Pressure relief continues to be critical in the treatment of pressure sores. While more advanced LAL and AF surfaces would in theory be preferred in the treatment of established pressure sores, the literature is mixed on this point. Ferrell et al. found similar results when comparing LAL beds to foam mattresses.199 Ochs et  al. in turn found AF beds to be superior to both standard overlays and LAL beds.200 On the other hand Branom and Rappl found LAL mattresses inferior to an advanced foam surface,179 while Economides et  al. failed to find any superiority of an AF bed over a foam overlay.162

Tobacco and electronic cigarettes contain chemicals, such as nicotine, that act as vasoconstrictors and cause local tissue ischemia.214 Other chemicals or byproducts include carbon monoxide, which displace oxygen from hemoglobin, and hydrogen cyanide, which poisons cellular respiration.215 As a result, tobacco use is known to impede wound healing, and increase the rate of wound healing complications and infections after surgery.216–218 While decades of research have demonstrated the deleterious effects of traditional cigarettes, in the laboratory as well

Nutrition As discussed later in this chapter, nutritional optimization before surgical reconstruction of pressure ulcers is of utmost importance. However, the evidence that pressure sores can be prevented by nutritional supplementation is limited.196 Bourdel-Marchasson and Rondeau found a modest reduction in pressure sore rates when patients were given oral dietary supplementation.197 A more recent meta-analysis by Stratton et  al. found a modest reduction in pressure sore rates in patients treated with enteral tube feeds, estimating that 19.25 patients would need to be given enteral nutritional support to prevent one pressure sore.198

Medical management

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as clinically, uncertainty arose with the recent emergence of electronic cigarettes as to their potential effect on wound healing. However, recent research has demonstrated that electronic cigarettes have virtually the same deleterious effects on wound healing as traditional cigarettes.219,220 For patients being considered for surgery, abstinence from all tobacco products for at least 4 weeks before and after surgery has been shown to reverse those deleterious effects, decreasing wound complication rates to levels similar to nonsmokers.60,221,222

Infection Osteomyelitis is a common complication of deep pressure sores and, as previously mentioned, often mandates operative therapy. Many authors rightly emphasize the importance of adequate debridement in the treatment of osteomyelitis.223 However, biopsy-directed antibiotic therapy is still an impor­ tant adjunct to surgery.86 While traditional therapy calls for 6 weeks of intravenous antibiotic therapy, there is some evidence that shorter courses many be effective.95

Wound care (Table 16.3) Debridement, regardless of the method used, is an essential step in the care of pressure sores.100 Only once the wound is thoroughly debrided can the full extent of the wound be examined and staged. Necrotic material impedes wound healing and acts as a nidus for infection. Traditional wet-to-dry dressings may debride effectively but may remove healthy tissue and granulation in addition to

necrotic tissue.224 They may also aerosolize bacteria from the wound.225 Knowing that wounds heal best in a moist environment, allowing the wound to desiccate in a wet-to-dry dressing is also counterproductive.226 Certain exogenous enzymes can be applied to wounds to digest necrotic tissue and eschar. These enzymes include collagenase, papain/urea, and fibrinolysin/DNAse.227 However, the efficacy of those agents is quite low,228,229 and their use should be reserved for cases where surgical debridement is contraindicated. Biologic debridement is enjoying something of a resurgence, using maggots that consume necrotic material while sparing living tissue. Currently no evidence suggests superiority of one agent over another.230 Ultimately, though many complementary methods of debridement are available, they are no substitute for proper sharp debridement.83 Studies have not consistently found one type of dressing to be superior to others.202,231 Therefore, dressing selection must be guided by the characteristics of the wound. Lionelli and Lawrence review the multitude of dressings available.230 In the context of pressure sores, occlusive films and hydrocolloids are frequently used on more shallow ulcerations, while alginates find use in deeper, heavily exudative wounds (Algorithm 16.2). It is worth noting that, even within a classification, individual products may differ widely in their capacity for absorption, occlusion, permeability, and cohesion.230 As with dressings, numerous topical agents are used in the hopes of improving wound healing. Antiseptic solutions are commonly used in hopes of reducing the bacterial burden of a wound. Dakin’s solution (sodium hypochlorite) is bactericidal, and is an excellent short-term dressing option for dirty wounds.1 Acetic acid is an effective topical antiseptic against

Table 16.3  Overview of wound dressings, in increasing order of absorbency

Type

Characteristics

Advantages

Disadvantages

Form

Frequency

Gauze

Woven cotton or synthetic fibers

Inexpensive; widely available; simplicity

Painful removal; limited absorbency; nonselective debridement; evaporative moisture loss

Sheets, ribbon

Once or twice daily

Low-adherent dressing

Open weave, coated gauze or synthetic material

Transparent; can observe wound; inexpensive; widely available; less painful removal

Low absorbency

Tulles or textiles Every 1–7 days

Films Hydrogel

Semipermeable

Transparent Donate moisture to wound; cooling effect, pain relief

Low absorbency May predispose to maceration,139 yeast140

Sheets Sheet or amorphous gel

Every 1–7 days Every 1–7 days

Hydrocolloid

Polycarboxymethylcellulose, gelatin, pectin, elastomer bound to film

Low–moderate absorbency

May macerate periwound skin or adhere to wound137,138; brown, malodorous exudate141

Sheets, pastes, or hydrofibers

Every 7 days

Foam

Polyurethane or silicone foam

Moderate absorbency; May adhere to wound or cushioning; thermal need secondary dressing insulation

Sheets or pouches

Every 1–7 days

Alginate

Derived from brown seaweed

Highly absorbent; inherently hemostatic

Sheet or fibers

Daily

Foreign-body reaction

(Reproduced with permission from: Jones CM, Rothermel AT, Mackay DR. Evidence-based medicine: wound management. Plast Reconstr Surg. 2017;140:201e).

Treatment

Algorithm 16.2 Wound color

Black (eschar)

Yellow (slough)

Red (granulation)

Hydrogel and transparent film

Exudate quantity

Hydrocoloid

Small

Moderate

Large

Hydrocoloid

Hydrogel and absorbent foam

Alginate and absorbent foam

Suggested guidelines for the use of wound products in the full-thickness, noninfected, chronic wound. (Reprinted with permission from Ladin DA. Understanding dressings. Clin Plast Surg. 1998;25:433).

Pseudomonas species.232 However, while these solutions and others have broad-spectrum antibacterial activity,233–236 they have all been shown to kill fibroblasts and impede wound healing.237–239 Therefore, their use should be limited to a few days. Procellera (Vomaris, Inc., Tempe, Ariz.) is a wound dressing that generates a small electrical field, which has been shown to inhibit biofilm formation in vitro240 and has demonstrated some potential benefit in chronic wounds.241 Silver ion is cytotoxic against most pathogens, with very little known resistance. As a result, dressings containing silver have become very popular. Silver, especially when combined with negative pressure wound therapy, has been found to decrease infection rates and accelerate healing in open infected wounds.242 However, in open wounds without overt signs of infection, including pressure ulcers, silver-containing dressings actually delay healing.241,243,244 Silver ion is toxic to fibroblasts in high concentrations, which limits its utility to the treatment of infected wounds, and for a short amount of time.245,246

Negative-pressure wound therapy Negative-pressure wound therapy (NPWT) entails applying topical negative pressure to a wound. The most common commercially available system, the vacuum-assisted closure (VAC) system, consists of an open-cell polyurethane or polyvinyl alcohol foam sponge with a pore size ranging from 400 to 600 μm in diameter. This sponge is cut to the appropriate dimensions to fill the entire wound. Suction is then

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applied to the sponge after it is covered with an adhesive drape to create an airtight seal. This suction can be adjusted in intensity and frequency. The most common settings are 125 mmHg negative pressure and either continuous or intermittent frequency. NPWT is known to accelerate wound healing. It removes inflammatory exudate, improves blood flow to the wound, and stimulates cellular proliferation.247 Evidence for the use of NPWT in pressure ulcers is somewhat limited, however. Deva et al. noted positive results in treated grade III ulcers but did not utilize any controls.248 Ford et  al. reported improved healing with VAC dressings when compared to standard wound care, but results did not reach significance.249 Joseph noted a greater decrease in wound depth with NPWT dressing when compared to saline dressings, but had limited follow-up and endpoints did not include wound closure.250 On the other hand, Wanner et al. failed to find any advantage to NPWT therapy in treating pressure sores,251 a finding echoed in a larger review by Reddy et  al.201 It is perhaps surprising that more evidence does not support the use of NPWT in this clinical scenario, but it is unclear whether this is due to inadequate data, or a reflection of the altered physiology associated with pressure sores, which at times may render them resilient to closure by secondary intention. Recent modifications of NPWT have sought to further improve its efficacy. Those modifications include NPWT with instillation and dwell time, and incisional NPWT. NPWT with instillation and dwell time (NPWTi-d) is a modification of traditional NPWT where a topical antiseptic solution is instilled into the wound, allowed to dwell (usually for 10 minutes), and then suctioned using the typical negative pressure of 125 mmHg. The cycle is repeated every 2 to 3 hours.252 NPWTi-d has been demonstrated to reduce biofilm burden in chronic wounds significantly more than traditional NPWT.253 Clinically, NPWTi-d has been shown to accelerate healing and shorten length of stay in large complex wounds, compared to traditional NPWT.254,255 Specifically for pressure ulcers, NPWTi-d has been shown to decrease the number of operative debridements necessary, as well as the hospital length of stay. NPWTi-d uses a variety of topical solutions, including normal saline, Dakin’s solution, polyhexanide, and others.256 There is little evidence that antiseptic solutions confer any advantage over normal saline.257 Incisional NPWT refers to the application of NPWT over a closed surgical incision. Incisional NPWT has been shown to decrease wound complications, including dehiscence and infection, in many different types of high-risk surgical incisions.258–267 Similarly, in a study of 37 patients receiving incisional NPWT after pressure ulcer reconstruction, Papp et al found that those patients had a 74% reduction in complications, a 27% reduction in hospital length of stay, and a 78% reduction in the number of open wounds at 3 months, when compared to historical controls who did not receive incisional NPWT.268

Glucose control Poorly controlled serum glucose is another risk factor for infection and wound complications. This is mediated through several mechanisms: compromised microvascular circulation causing decreased wound perfusion,269 decreased fibroblast activity,270 and impaired immune response.271 In patients

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undergoing surgery, even one instance of perioperative hyperglycemia above 200 mg/dL increases the risk of dehiscence significantly.272 Specifically, in patients undergoing pressure ulcer reconstruction, those with poor glycemic control (hemoglobin A1c greater than 6%) are 16 times more likely to develop a major dehiscence after surgery.207

Manipulating the local wound milieu Several studies propose the use of biologic and recombinant agents as possible modalities for the non-surgical treatment of pressure sores. Robson et al. performed a double-blind randomized controlled trial in which 50 patients with stage III/ IV pressure sores were treated with recombinant bFGF; notably, samples from patients treated with recombinant bFGF demonstrated significantly increased fibroblast and capillary formation than other groups.273 Similarly, Rees et al. found that application of recombinant human platelet-derived growth factor-BB to pressure sore wounds resulted in increased healing as compared to placebo. Despite the high cost of recombinant proteins, Robson et  al. suggest that treatment with recombinant cytokines may actually result in a cost reduction as compared to surgical treatment.59 While it remains unlikely that this will become a mainstay therapy, recombinant agents may become an option for patients unable to undergo surgery or as a temporizing treatment until medically optimized for surgical treatment.

Surgical management Setting expectations In the treatment of pressure ulcers, building a trusting patient– physician relationship is essential. Patients must play an active role in their own health and preoperative optimization. On the other hand, the surgeon must set realistic expectations. Pressure ulcer recurrence rates remain high, and the surgeon should aim to underpromise and overdeliver.274

Debridement Thorough, sharp surgical debridement is the cornerstone of the treatment of pressure ulcers.100 Debridement disturbs the bacterial biofilm, and reverts the bacteria in the chronic ulcer to a temporary planktonic state,277,278 during which they are susceptible to topical and systemic antimicrobial therapy. Without thorough debridement and appropriate antibacterial therapy, biofilm is re-established within 72 hours.277 At the time of flap closure, complete excision of the bursa, and debridement of any osteomyelitic bone, are essential. The bursa should be stained with methylene blue to ensure complete excision. Chronic pressure sores will generally have a relatively well-defined bursa in continuity with the base of the ulcer. The bursa and any surrounding scarred tissue, calcifications, or heterotopic ossification should be excised completely, leaving only healthy, pliable tissues (Fig. 16.12). The bursa commonly extends much farther than the surface wound would indicate. Taking a small skin margin around the wound and following the contours of the bursa as it undermines adjacent tissues ensures it is entirely excised. After the initial excision the wound base should be palpated to identify any residual areas of woody, scarred tissues, which require excision. Once the soft tissue has been debrided, the underlying bone must be evaluated and, if necessary, debrided. There should be a very low threshold to debride back to healthy, hard, bleeding bone using an osteotome or rongeurs. A bone biopsy can also be taken at this time if desired. Debridement should never be compromised to facilitate wound closure, as incomplete debridement is a common cause of flap failure. The affected tissue must be debrided radically and flap coverage designed as appropriate to fill the resulting defect, even if this may require larger, or even multiple, flaps for complete obliteration of dead space and wound closure. Another modality for debridement is tangential hydrodebridement (Versajet; Smith & Nephew, Cambridge, England), which uses the Venturi effect to remove a thin layer of tissue

Surgical guidelines In general, pressure ulcers represent a tissue deficiency, and tissue transfer is required. Primary closure tends to have very high recurrence rates due to high tension.95 Similarly, skin grafts are not usually durable enough, and do not provide the bulk needed to prevent recurrence.1 The principles of the surgical treatment of pressure ulcers were first laid by Conway and Griffith over half a century ago,275 and include complete bursectomy, radical ostectomy, filling of dead space and resurfacing with soft-tissue flaps, design of flaps to be larger than necessary, placement of the suture line away from the area of pressure, possible grafting of the donor site, and avoiding violation of territories of flaps that may be necessary in the future. During surgery, special precautions must be taken, including meticulous padding of any area prone to pressure, gentle handling of any contracted joints, normothermia, and avoidance of the depolarizing neuromuscular blocking agent succinylcholine, which can cause hyperkalemia in spinal cord injury patients, due to upregulation of acetylcholine receptors in denervated muscles.276

Figure 16.12  Depiction of excision of bursa and chronic scar tissue.

Treatment

from the wound, and is used until the endpoint of healthy bleeding tissue is reached.279 No large studies have compared the efficacy of hydrodebridement to radical surgical debridement in the management of pressure ulcers.

Procedure selection Once the wound has been adequately debrided, a reconstruction method must be selected. Options for surgical coverage of pressure sores include random skin flaps, muscle flaps with skin graft, myocutaneous, fascial, or fasciocutaneous flaps, free flaps, and tissue expansion.280

Muscle and myocutaneous flaps Traditionally, muscle flaps have been preferred to fasciocutaneous and perforator flaps for the treatment of pressure ulcers due to the belief that they lead to a lower recurrence rate. Recent evidence, however, demonstrates that recurrence rates are similar between muscle flaps, fasciocutaneous flaps, and perforator flaps.281,282 As previously noted, muscle is more susceptible to ischemic necrosis than either skin or subcutaneous tissue,36 at times manifesting in necrotic muscle under intact overlying skin.283 On the other hand, interposing muscle between skin and bone resulted in a decreased rate of skin ulceration in a rat model,38 presumably because the increased mass of muscle can help diffuse the effects of pressure on the skin. Compared with skin grafts and fasciocutaneous flaps, muscle flaps have the advantages of greater bulk for filling the wound cavity and obliterating dead space,274 the ability to cover larger wounds, and a better local vascular supply.284,285 Bruck et  al. found that myocutaneous flaps were more resistant to Staphylococcus aureus and Escherichia coli infection than random skin flaps in pigs.286 Despite their theoretic advantages, whether the improved vascularity of muscle flaps results in clinically significant effects on infection and wound healing when compared to other options has not been determined.287

Fasciocutaneous and perforator flaps In the late 1980s, Kroll, Rosenfield, and Koshima reported favorable pressure ulcer reconstruction outcomes using fasciocutaneous flaps,288,289 thereby challenging the dogma that muscle was necessary. Fasciocutaneous flaps allow muscle preservation, which is especially crucial in ambulatory patients.290 With time, perforator flaps were developed, allowing more versatility with reconstruction.

Free flaps Though not a common option, several authors have described free tissue transfer in the reconstruction of pressure sores, with and without preservation of sensation. Nahai et  al.291,292 and Hill et al.,293,294 among others, have described transferring the tensor fasciae latae muscle–skin unit as a free flap for lower trunk reconstruction. Sensation can reportedly be restored by coapting the lateral femoral cutaneous nerve. Multiple other authors have reported successful pressure ulcer reconstruction using free tissue transfer.295–297

Tissue expansion Tissue expansion is an appealing reconstructive option in elective situations like pressure ulcer reconstruction.298 It can

479

be used to advance sensate skin into the area of the pressure ulcer.299 Several authors have reported the successful use of tissue expansion for pressure ulcer reconstruction.296,300–303 The technique can also be used to pre-expand a musculocutaneous or fasciocutaneous flap before transfer, thereby increasing their reach and potential coverage, and improving their vascularity.300 It should be noted that several studies examining this technique reported high rates of infection and extrusion.296 Therefore, this tissue expansion should only be used judiciously in the reconstruction of pressure ulcers.

Reconstruction by anatomic site Sacral pressure ulcer Surgical options for coverage of a sacral pressure ulcer include the gluteus maximus myocutaneous rotation flap,304 the V–Y myocutaneous advancement flap,305 the superior gluteal artery perforator flap,287 and others274,286,287,301,306–327 (Table 16.4). Parry and Mathes reported favorable results after sacral coverage of pressure sores with bilateral gluteus maximus musculocutaneous advancement flaps in ambulatory patients.320 Foster et al. had high success rates with V–Y gluteus maximus flaps and gluteal island flaps.328 In ambulatory patients, the superior half of the muscle can be used, sparing the inferior half. Borman and Maral describe a modification of the gluteal rotation flap, incorporating a V–Y closure, allowing closure of defects up to 12 cm with a unilateral flap.306 Additional modifications include the expansive gluteus maximus flap described by Ramirez and colleagues,304 which is advanced in a V–Y fashion either unilaterally or bilaterally to cover sacral ulcers. Multiple authors have reported their success with gluteal artery perforator flaps, and variations abound.329–331 Wong et  al. modified the classic gluteal rotation flap to spare the perforators down to the level of the piriformis.332 Xu et  al. designed a multi-island perforator propeller flap for use in large sacral defects.333 Cheong et al. described an innervated variant of the superior gluteal artery perforator flap for sacral coverage.334 Thoracolumbar flaps can also be used to reconstruct sacral pressure ulcers. These are usually based on contralateral lumbar perforators, and often require back-grafting.311,320 These flaps can be designed as perforator flaps,286,287 with the second lumbar perforator being the most commonly used perforator.314

Selected technique: gluteal myocutaneous rotation flap (Fig. 16.13, Box 16.2) One of many options based on the gluteus maximus muscle, the myocutaneous gluteal rotation flap is technically straightforward, keeps scars off pressure-bearing surfaces, and is easily revised or re-rotated.335 The muscle is useful for obliterating the dead space, which is often significant after the preparatory bursectomy and ostectomy. The vascular supply is based on the superior gluteal artery. This vessel can easily be identified in the plane beneath the gluteus maximus immediately superior to the piriformis muscle.

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Table 16.4  Reconstructive options in sacral pressure sores Primary closure White and Hamm, Ann Surg. 1946;124:1136

Gluteal fasciocutaneous rotation–advancement flap with V–Y closure Borman and Maral, Plast Reconstr Surg. 2002;109:23

Reverse dermal graft Wesser and Kahn, Plast Reconstr Surg. 1967;40:252

Bilateral gluteus advancement flap Parry and Mathes, Ann Plast Surg. 1982;8:443

Interiorly based random skin flap Conway and Griffith, Am J Surg. 1956;91:946

Gluteus plication closure Buchanan and Agris, Plast Reconstr Surg. 1983;72:49

Transverse lumbosacral arterial and random flap Hill, Brown, and Jurkiewicz, Plast Reconstr Surg. 1978;62:177

Sensory island flaps Snyder and Edgerton, Plast Reconstr Surg. 1965;36:518 Dibbell, Plast Reconstr Surg. 1974;54:220 Daniel, Terzis, and Cunningham, Plast Reconstr Surg. 1976;58:317 Little, Fontana, and McColluch, Plast Reconstr Surg. 1981;68:175

Thoracolumbar–sacral arterial/random flap Vyas, Binns, and Wilson, Plast Reconstr Surg. 1980;65:159

Gluteal thigh arterialized flap Hurwitz, Swartz, and Mathes, Plast Reconstr Surg. 1981;68:521

Superior gluteus myoplasty Ger, Surgery. 1971;69:106 Ger and Levine, Plast Reconstr Surg. 1976;58:419

Expansive gluteus maximus flap Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg. 1984;74:757

Turnover gluteus myopathy Stallings, Delgado, and Converse, Plast Reconstr Surg 54: 52, 1974

Parasacral perforator-based musculocutaneous flap Kroll and Rosenfield, Plast Reconstr Surg 81: 561, 1988 Koshima et al., Plast Reconstr Surg 91: 678, 1993

Gluteus maximus musculocutaneous flap Minami, Mills, and Pardoe, Plast Reconstr Surg. 1977;60:242

Parasacral perforator-based fasciocutaneous flap Kato et al., Br J Plast Surg. 1999;52:541

Gluteus maximus musculocutaneous island flap Maruyama et al., Br J Plast Surg. 1980;33:150 Stevenson et al., Plast Reconstr Surg. 1987;79:761 Dimberger, Plast Reconstr Surg. 1988;81:567

Parasacral perforator-based fasciocutaneous flap Kato et al., Br J Plast Surg. 1999;52:541

Gluteus maximus fasciocutaneous flap Yamamoto et al., Ann Plast Surg. 1993;30:116 (Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in Plastic Surgery; 2003:25).

Skin incision is marked to follow the contour of the iliac crest and descends inferiorly, staying posterior to the greater trochanter and the footprint of the tensor fasciae latae flaps. Dissection is carried down through the thick subcutaneous tissues and superficial fascia of the hip to the level of the muscle fascia. The fascia and muscle are then divided laterally. It can be helpful to bevel the incision so the muscle and fascia are divided more peripherally than the skin. This both accounts for some degree of muscle retraction and provides extra soft tissue to obliterate dead space and additional fascia for added security and ease of wound closure. The flap should then be undermined in the plane beneath the gluteus maximus. The pedicle can usually be identified at this time with relative ease as it passes superior to the piriformis. It may be easier to proceed from lateral to medial, as scarring and inflammation near the ulcer can impede dissection, and the separation between the hip muscles becomes more distinct as they approach their insertion on the trochanter. If additional length is needed or tension is excessive, the flap can be partially delaminated at either the fascial or subcutaneous level, so long as the major musculocutaneous perforators are identified and protected. The flap is then closed in multiple layers over drains using long-lasting absorbable sutures in the muscle and superficial fascial system, and either staples or nonabsorbable sutures in the skin.

Drains remain in place until output is less than 20–30 cc/ day, though some may opt to use drains for an extended period.

Ischial pressure ulcer Surgical options for coverage of an ischial pressure ulcer include the gluteus maximus myocutaneous rotation flap, the hamstring (posterior thigh) V–Y myocutaneous advancement flap,336 the posterior thigh fasciocutaneous rotation flap,337 the gracilis muscle or myocutaneous flap,338 the inferior gluteal artery perforator flap,339 and others325,340–351 (Table 16.5). Thigh-based flaps for the reconstruction of ischial pressure ulcers include the posterior V–Y advancement flap, which can include the biceps femoris muscle alone in ambulatory patients, or all the hamstring muscles in SCI patients. Another flap is the posteromedial thigh fasciocutaneous flap, which is based on the perforators from either the gracilis or the adductor magnus muscles.352 In addition, the posterior thigh flap can be based on the descending branch of the inferior gluteal artery.286,338,345,353 In addition to the gluteal rotation flap, the superior and inferior gluteal arteries provide multiple options for reconstruction for ischial ulcers. The inferior gluteal artery perforator flap is well suited to ischial reconstruction.288,334,354 It spares muscle, and allows primary closure of the donor site.347 The inferior gluteal artery is located along a line from the posterior

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Figure 16.13  (A–F) Right gluteal musculocutaneous flap.

BOX 16.2  Myocutaneous gluteal rotation flap As always, complete debridement is the key to any flap surgery. This flap can survive entirely on its major vascular pedicle. The muscle can be disinserted and the skin and fascia divided circumferentially without compromising the vascularity of the flap. Creating an island design without tension is preferable to leaving a skin bridge, which results in tension.

superior iliac spine to the ischium, caudal to the piriformis muscle.334 The perforators of the IGA are identified preoperatively using handheld Doppler. The flap is elevated in the suprafascial plane and the perforators are identified. One or

two perforators are chosen and dissected to allow tension-free rotation of the flap into the defect. The sensate tensor fasciae latae flap can be used to cover ischial and trochanteric pressure ulcers,289,292,355 providing protective sensation. Several authors have reported high success rates with this flap.356,357

Selected flap: V–Y hamstring advancement (Fig. 16.14) Flaps from the posterior thigh are common options for ischial reconstruction. They have the advantage of leaving the lateral hip and buttock for use in trochanteric and sacral reconstruction. The V–Y hamstring advancement is a robust flap that is relatively easy to raise and can be readvanced if necessary.337 The vascular supply to the hamstring flap is based on perforators of the profunda femoris, with minor contributions

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Table 16.5  Reconstructive options in ischial pressure sores Primary closure Arregui et al., Plast Reconstr Surg. 1965;36:583

Biceps femoris musculocutaneous flap Tobias et al., Ann Plast Surg. 1981;6:396 Kauer and Sonsino, Scand J Plast Reconstr Surg. 1986;20:129

Random posterior thigh flap ± biceps femoris myoplasty Campbell and Converse, Plast Reconstr Surg. 1954;14:442 Conway and Griffith, Am J Surg. 1956;91:946 Baker, Barton, and Converse, Br J Plast Surg. 1978;31:26

Gluteal thigh flap Hurwitz, Swartz, and Mathes, Plast Reconstr Surg. 1986;20:129

Inferior gluteus maximus musculoplasty Ger and Levine, Plast Reconstr Surg. 1976;58:419

Sliding gluteus maximus flap Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg. 1984;74:757

Inferior gluteus musculocutaneous flap Minami, Mills, and Pardoe, Plast Reconstr Surg. 1977;60:242

Tensor fasciae latae + vastus lateralis Krupp, Kuhn, and Zaech, Paraplegia. 1983;21:119

Interior gluteus musculocutaneous island flap Rajacic et al., Br J Plast Surg. 1994;47:431

Lateral thigh fasciocutaneous flap Maruyama, Ohnishi, and Takeudhi, Br J Plast Surg. 1984;37:103 Hallock, Ann Plast Surg. 1994;32:367

Gracilis musculocutaneous flap Wingate and Friedland, Plast Reconstr Surg. 1978;62:245 Lesavoy et al., Plast Reconstr Surg. 1990;85:390

Anterolateral thigh fasciocutaneous island flap Yu et al., Plast Reconstr Surg. 2002;109:610

Gracilis musculocutaneous flap (with sartorius as a double muscle unit) Apfelberg and Finseth, Br J Plast Surg. 1981;34:41

Rectus abdominis musculocutaneous flap Bunkis and Fudem, Ann Plast Surg. 1989;23:447 Mixter, Wood, and Dibbell, Plast Reconstr Surg. 1990;85:437

Hamstring musculocutaneous flap Hurteau et al., Plast Reconstr Surg. 1981;68:539

Inferior gluteal artery perforator flap Higgins et al., Br J Plast Surg. 2002;55:83

(Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in Plastic Surgery; 2003:27).

from the inferior gluteal, medial circumflex, and superior geniculate arteries. These vessels are generally not specifically identified when elevating the flap, as they are well protected on the deep surface of the muscle. Superiorly the flap is bounded by the gluteal crease or the inferior border of the ulcer. Laterally the flap extends to the posterior border of the tensor fasciae latae, while medially the dissection extends to the adductor magnus. Inferiorly the flap can be extended to the popliteal fossa, though a lesser flap can be designed as needed. The flap is incised and dissection carried down the level of the fascia. The muscles are divided distally at the musculotendinous junction and proximally by elevating the muscles from the ischium, though this step is often partially accomplished during bony debridement of the ischium. Minimal blunt dissection may be performed at the lateral and medial margins to mobilize the flap, but it is generally not necessary to perform a complete dissection on the undersurface of the muscle or to identify the major pedicle of the flap. As with the gluteal rotation flap, it is inset in layers over drains and the donor site is closed in linear fashion.

Trochanteric pressure ulcer Trochanteric ulcers are generally closed with tensor fasciae latae (TFL)289,292,351–353,358–361 or vastus lateralis flaps (Table 16.6).362–365 The TFL can be transferred as a muscle only, myocutaneous, or free flap.289,292,351 A number of perforator flaps have found use in trochanteric reconstruction as well. The anterolateral thigh flap provides an option with considerable flexibility, allowing the option of taking chimeric flaps if necessary.366,367 Flaps based on the gluteal,368 ascending

circumflex,369 or adductor370 perforators all share the advantages of minimal donor morbidity and sparing of muscle for further reconstruction. The adductor perforator flap also has the advantage of being medially based and often outside the field of previous operations.

Selected procedure: V–Y tensor fasciae latae flap; tensor fasciae latae rotation flap The many variations on the tensor fasciae latae flap are common options for dealing with trochanteric ulcers (Fig. 16.15). A fasciocutaneous or musculocutaneous rotation flap is technically straightforward, can reach a variety of defects, and may be readvanced if necessary.371 The blood supply to the tensor fasciae latae is from branches of the lateral circumflex femoral artery, which enter the deep surface of the muscle anteriorly. The proximal, muscular portion of the tensor fasciae latae is relatively small. The distal portion of the muscle consists almost entirely of fascia but still provides perforators to the overlying skin. If necessary, the flap can be extended just proximal to the knee and rotated to cover ischial or even sacral defects, though such extended flaps are not entirely reliable unless delayed. Though the blood supply to this flap is robust and relatively reliable, minor variations are common. If necessary, the flap may be based on alternate branches of the circumflex vessels. If the perforators to the muscle are not usable, dissection of the descending branch of the lateral circumflex allows relatively simple conversion to a pedicled anterolateral thigh flap. The ulcer will generally define the posterior margin of the flap. A line from the anterior superior iliac spine to the knee

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Figure 16.14  (A–E) Right posterior hamstring musculocutaneous V–Y advancement flap.

marks the anterior border of the flap. Flaps up to 15–20 cm proximal to the femoral condyle are very reliable without delay. The inferior point of the flap can be taken just short of the condyle if preferred. Though it may be excessive for single-stage ulcer coverage, a lengthier flap is easier to readvance if necessary. The pedicle is generally roughly 10 cm inferior to the anterior superior iliac spine and 10–15 cm lateral to the pubic tubercle. After incising the skin down to fascia, dissection is easiest distally, where the tensor fasciae latae is essentially entirely fascia. Dissecting under the fascia, it is generally easy to identify the pedicle as the tensor fasciae latae transitions to muscle proximally. The fascia and muscle can then be completely divided and the flap rotated to fill the defect. As with the other flaps discussed in this section, the flap is

then inset in layers over drains and the donor site closed in linear fashion.

Hip joint infection In certain deep pressure ulcers, osteomyelitis occurs in the hip joint and the proximal femur. The surgical procedure in that situation is the Girdlestone procedure.372 This procedure consists of resection of the femoral head and neck. The dead space is then filled with a vastus lateralis muscle flap (Fig. 16.16).373–375

Heel pressure ulcer The posterior heel is the second most common location for a pressure ulcer.1,14–16 Reconstruction of the posterior heel can be challenging due to scarcity of local tissues. Options for

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Table 16.6  Reconstructive options in trochanteric pressure ulcers Anteriorly based random thigh flap Vasconez, Schneider, and Jurkewicz, Curr Probl Surg. 1977;14:1

Tensor fasciae latae musculocutaneous flap, island Kauer and Sonsino, Scand J Plast Reconstr Surg. 1986;20:129

Random bipedicle flap Conway and Griffith, Am J Surg. 1956;91:946

Vastus lateralis myoplasty Minami, Hentz, and Vistnes, Plast Reconstr Surg. 1977;60:364 Dowden and McCraw, Ann Plast Surg. 1980;4:396

Tensor fasciae latae musculocutaneous flap Nahai et al., Ann Plast Surg. 1978;1:372 Hill, Nahai, and Vasconez, Plast Reconstr Surg. 1978;61:517 Withers et al., Ann Plast Surg. 1980;4:31

Vastus lateralis musculocutaneous flap Bovet et al., Plast Reconstr Surg. 1982;69:830 Hauben et al., Ann Plast Surg. 1983;10:359 Drimmer and Krasna, Plast Reconstr Surg. 1987;79:560

Tensor fasciae latae musculocutaneous flap, bipedicle Schulman, Plast Reconstr Surg. 1980;66:740

Gluteus medius tensor fasciae latae musculocutaneous flap Little and Lyons, Plast Reconstr Surg. 1983;71:366

Tensor fasciae latae musculocutaneous flap, V–Y advancement Lewis, Cunningham, and Hugo, Ann Plast Surg. 1981;6: 34 Siddiqui, Wiedrich, and Lewis, Ann Plast Surg. 1993;31:313

Distally based gluteus maximus flap Becker, Plast Reconstr Surg. 1979;63:653

Tensor fasciae latae musculocutaneous flap, innervated Dibbell, McCraw, and Edstrom, Plast Reconstr Surg. 1979;64:796 Nahai, Hill, and Hester, Plast Reconstr Surg. 1981;7:286 Nahai, Clin Plast Surg. 1980;7:51 Cochran, Edstrom, and Dibbell, Ann Plast Surg. 1981;7:286

Gluteal thigh flap Hurwitz, Swartz, and Mathes, Plast Reconstr Surg. 1981;68:521

Expansive gluteus maximus flap Ramirez, Hurwitz, and Futrell, Plast Reconstr Surg. 1984;74:757 Ramirez, Ann Plast Surg. 1987;18:295 (Reproduced from Janis JE, Kenkel JM. Pressure sores. In: Barton FE Jr., ed. Selected Readings in Plastic Surgery, vol. 9, no. 39. Dallas, TX: Selected Readings in Plastic Surgery; 2003:29).

B

Lateral circumflex femoral artery Vastus lateralis C

A D

Figure 16.15  (A–D) Left tensor fasciae latae flap with backgrafting.

Postoperative care

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Figure 16.16  (A–D) Girdlestone arthroplasty.

reconstruction include the reverse sural artery flap,376 medial plantar artery flap,377 and free tissue transfer. The reverse sural artery flap can be raised as a fasciocutaneous or fascial flap. It is located over the calf, from the popliteal fossa superiorly to the mid-calf inferiorly. Its perfusion depends on perforators of the peroneal artery, as well as the vasa nervorum of the sural nerve.378 Despite its versatility, the flap suffers from a high rate of venous congestion. Reliability of the flap can be improved with a surgical delay.14,379,380 The medial plantar artery flap is a fasciocutaneous flap that includes the non-weight-bearing skin of the instep. It is based on the medial plantar artery, a branch of the posterior tibial artery. It is a reliable flap that can provide durable soft-tissue coverage over the heel.381,382

Bone resection Excision of bony prominences under pressure ulcers was first introduced as an adjunct to treatment by Kostrubala and Greeley.23 Conway and Griffith later expanded the excision to a more radical excision, and noted that total ischiectomy led to significantly lower pressure ulcer recurrence rates than partial ischiectomy (3% vs. 38%).274 Total ischiectomy, however, introduces other complications, including an increased risk of contralateral pressure ulcers,383 prompting some authors to attempt contralateral prophylactic ischiectomy. Nevertheless, total bilateral ischiectomy should only be performed in patients with deep, extensive bilateral pressure

ulcers, because this procedure transfers the patient’s weight to the perineum, resulting in a high rate of perineal ulcers and urethrocutaneous fistulas.24,384,385 Patients with osteomyelitis should be treated with partial ostectomy,223,386 with the endpoint being healthy bleeding bone.83 Preoperative MRI is essential to delineate the extent of osteomyelitis and guide bony debridement.387 In patients with osteomyelitis who undergo partial ostectomy, the application of resorbable antibiotic-impregnated beads between the bone and the flap has been shown to decrease pressure ulcer recurrence rates.388 These beads provide relatively high concentrations of antibiotics locally, without the risk of systemic toxicity.

Postoperative care After surgery for reconstruction of pressure ulcers, the same preventive measures that are used to address pressure, shear, friction, moisture, incontinence, spasticity, and nutrition still apply.274,389–393 Traditionally pressure sore patients were kept in bed for 6–8 weeks based on experimental data indicating that wounds reached maximum tensile strength after this period.396 More recent studies have advocated a more rapid progression to sitting. In a prospective, randomized trial Isik et al.397 found equivalent complication rates when comparing 2 and 3 weeks of immobilization, though overall length of stay was similar, and long-term follow-up was deemed inadequate to draw any firm conclusions. Likewise, Foster et al. began a sitting regimen at 10–14 days and had postoperative

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hospital stays averaging 20 days, with short-term success rates of 89%.325 Regardless of how long patients are kept in bed, appropriate prophylaxis for venous thromboembolism must be provided during the period of bedrest. In addition, patients should begin active and passive range-of-motion exercises of the uninvolved extremity early in the postoperative course,195 while the affected extremity can be ranged just prior to initiation of a sitting protocol. A typical regimen involves having the patient sit for 15-minute intervals once or twice a day, then gradually increasing the length and frequency of sitting periods until discharge.389 The surgical site should be carefully monitored for signs of recurrence.195 Prior to discharge, patients should have their support surfaces re-evaluated (Fig. 16.17). This assessment is particularly important in patients who have had bony resections or multiple procedures that may result in altered weight-bearing or pelvic and truncal instability.396 An appropriate seat cushion should be selected, ideally with the assistance of seat mapping. Maximum recommended pressures are 35 mmHg for patients unable to relieve pressure themselves by lifting or leaning and 60 mmHg for those who can.397 After bursectomy and flap reconstruction, there is a large potential space that can lead to seroma, both in the pressure ulcer site, as well as the flap donor site. Closed-suction drains are vital in these operations.398 Those drains should be squeezed size-to-side, emptied whenever 25% full, and kept until their output is 20 cc a day for two consecutive days.399 There may also be a role for applying chlorhexidine-impregnated disks at the drain exit sites to reduce the risk of ascending infection along the drain tubing.59,400

Patient education should also be emphasized postoperatively. Though studies have demonstrated a positive effect of education on patient knowledge,401,402 research relating education to recurrence rates is lacking at this time. However, given the evidence that recurrence rates are associated with poor patient compliance, social factors, and communication barriers,208,403 attempts at addressing these issues through education seem reasonable.

Outcomes, prognosis, and complications The existing literature reports a wide variation in pressure ulcer recurrence rates, ranging from as low as 3%–6%335,385,404 to as high as 33%–100%.336,387,405 Risk factors for recurrence include poorly controlled diabetes mellitus, serum albumin below 3.5 g/dL, age less than 45 years, reoperation, and ischial location.207 Patients with a prior history of complication or recurrence after pressure ulcer reconstruction have a threefold higher risk of reconstructive failure when reconstruction is attempted at the same anatomic site again.207 Patients younger than 45 years are five times more likely to suffer a major dehiscence.207 Evans et al. found that paraplegics had a significantly higher rate of pressure ulcer recurrence than nonparaplegics.406 Disa et al. identified two patients groups at particularly high risk of pressure ulcer recurrence after reconstruction: young patients with post-traumatic paraplegia, and elderly patients with cerebral compromise.387 Tavakoli et al. emphasized the role of

Figure 16.17 Seat mapping. (Reproduced from the University of Washington PM&R website: http://sci.washington.edu/info/forums/reports/pressure_map.asp).  

Secondary procedures

social, psychological, and behavioral factors in pressure ulcer recurrence.397

Complications Potential complications after reconstruction of pressure ulcers include dehiscence, seroma, infection, and hematoma.95 If the pressure ulcer recurs, patient optimization should be reassessed prior to reoperation.99,325 In a longstanding chronic wound, the possibility of malignant degeneration (Marjolin’s ulcer) should be entertained.407 These malignancies may arise in a chronic pressure ulcer after 20 years on average.408 If the wound starts to change, or develops new drainage, biopsy should be considered to rule out malignant transformation.409

Secondary procedures It is critical that, before embarking on revision or repeat flap surgery, the patient be fully re-evaluated. Assuming proper surgical technique, the same risk factors that led to the patient’s original ulcer are likely to be at least partially responsible for recurrence, and neglecting them will reliably result in poor outcomes. Every pressure sore surgery should allow for the possibility of future secondary procedures. Despite favorable initial healing rates, long-term recurrence is common, even in the most favorable series. Assuming basic principles have been adhered to, multiple options should still exist, even in cases of multiple recurrences.

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Figure 16.18 (A–E) Readvanced right gluteal flap for recurrent sacral pressure sore.  

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Figure 16.19  (A–E) Hemicorporectomy with right subtotal thigh flap.

The simplest option may involve readvancing a previously performed flap (Fig. 16.18). Flaps can often be readvanced multiple times, but, as always, excessive tension must be avoided. If tension is an issue, a change of plane, such as advancing a fasciocutaneous flap over a previous musculocutaneous flap, can provide additional length without violating another anatomic region or flap design. If a particular flap has already been readvanced or the tissue is of poor quality due to recurrent ulceration or scarring, a new,

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preferably virgin, anatomic area should be used to address the wound. For example, while flaps from the thigh area are commonly used to address ischial ulcers, a superiorly based gluteal flap can afford coverage if the posterior thigh is no longer a viable option. Amputation and hemicorporectomy are options of last resort in patients with very extensive ulcers, patients who are very ill from their ulcers, and patients with recalcitrant extensive pelvic osteomyelitis410–415 (Fig. 16.19).

References

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26. Conway H, Kraissl CJ. The plastic surgical closure of decubitus ulcers in patients with paraplegia. Surg Gynecol Obstet. 1947;85:321–332. 27. Fisher AR, Wells G, Harrison MB. Factors associated with pressure ulcers in adults in acute care hospitals. Holist Nurs Pract. 2004;18:242–253. 28. Baumgarten M, Margolis DJ, Localio AR, et al. Pressure ulcers among elderly patients early in the hospital stay. J Gerontol A Biol Sci Med Sci. 2006;61:749–754. 29. National Pressure Sore Advisory Panel. Consensus Development Conference Staging System, February 2007. Available at: http://www.npuap.org/pr2.htm. 30. Husain T. An experimental study of some pressure effects on tissues, with reference to the bed-sore problem. J Pathol Bacteriol. 1953;66:347–358. 31. Landis EM. Micro-injection studies of capillary blood pressure in human skin. Heart. 1930;15:209–228. 32. Fronek K, Zweifach BW. Microvascular pressure distribution in skeletal muscle and the effect of vasodilation. Am J Physiol. 1975;228:791–796. 33. Lindan O, Greenway RM, Piazza JM. Pressure distribution on the surface of the human body. I. Evaluation in lying and sitting positions using a “bed of springs and nails”. Arch Phys Med Rehabil. 1965;46:378–385. 34. Holloway GA, Daly CH, Kennedy D, Chimoskey J. Effects of external pressure loading on human skin blood flow measured by 133Xe clearance. J Appl Physiol. 1976;40:597–600. 35. Dinsdale SM. Decubitus ulcers: Role of pressure and friction in causation. Arch Phys Med Rehabil. 1974;55:147–152. 36. Kosiak M, Kubicek WG, Olson M, et al. Evaluation of pressure as a factor in the production of ischial ulcers. Arch Phys Med Rehabil. 1958;39:623–629. 37. Groth KE. Klinische Beobachtungen und experimentelle Studien über die Entstehung des Dekubitus. Acta Chir Scand. 1942;87 (suppl 76):1–209. 38. Nola GT, Vistnes LM. Differential response of skin and muscle in the experimental production of pressure sores. Plast Reconstr Surg. 1980;66:728–733. 39. Daniel RK, Priest DL, Wheatley DC. Etiologic factors in pressure sores: an experimental model. Arch Phys Med Rehabil. 1981;62:492–498. 40. Gerhardt LC, Mattle N, Schrade GU, et al. Study of skin-fabric interactions of relevance to decubitus: friction and contactpressure measurements. Skin Res Technol. 2008;14:77–88. 41. Hanson D, Langemo DK, Anderson J, et al. Friction and shear considerations in pressure ulcer development. Adv Skin Wound Care. 2010;23:21–24. 42. Gerhardt LC, Strassle V, Lenz A, et al. Influence of epidermal hydration on the friction of human skin against textiles. J R Soc Interface. 2008;5:1317–1328. 43. Reichel SM. Shearing force as a factor in decubitus ulcers in paraplegics. J Am Med Assoc. 1958;166:762–763. 44. Reuler JB, Cooney TG. The pressure sore: pathophysiology and principles of management. Ann Intern Med. 1981;94:661–666. 45. Goossens RH, Zegers R, Hoek van Dijke GA, Snijders CJ. Influence of shear on skin oxygen tension. Clin Physiol. 1994;14:111–118. 46. Schubert V, Heraud J. The effects of pressure and shear on skin microcirculation in elderly stroke patients lying in supine or semi-recumbent positions. Age Ageing. 1994;23:405–410. 47. Lowthian P. The distinction between superficial pressure ulcers and moisture lesions. Skinmed. 2007;6:111–112. 48. Resnick NM, Beckett LA, Branch LG, et al. Short-term variability of self report of incontinence in older persons. J Am Geriatr Soc. 1994;42:202–207. 49. Saxer S, Halfens RJ, de Bie RA, Dassen T. Prevalence and incidence of urinary incontinence of Swiss nursing home residents at admission and after six, 12 and 24 months. J Clin Nurs. 2008;17:2490–2496. 50. Chassagne P, Landrin I, Neveu C, et al. Fecal incontinence in the institutionalized elderly: incidence, risk factors, and prognosis. Am J Med. 1999;106:185–190.

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CHAPTER 16  • Pressure sores

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222. Sørensen LT, Karlsmark T, Gottrup F. Abstinence from smoking reduces incisional wound infection: a randomized controlled trial. Ann Surg. 2003;238:1–5. 223. Eckardt JJ, Wirganowicz PZ, Mar T. An aggressive surgical approach to the management of chronic osteomyelitis. Clin Orthop Relat Res. 1994;298:229–239. 224. Jones VJ. The use of gauze: will it ever change? Int Wound J. 2006;3:79–86. 225. Lawrence JC. Dressings and wound infection. Am J Surg. 1994;167:21S–24S. 226. Field FK, Kerstein MD. Overview of wound healing in a moist environment. Am J Surg. 1994;167:2S–6S. 227. Jones CM, Rothermel AT, Mackay DR. Evidence-based medicine: wound management. Plast Reconstr Surg. 2017;140:201e. 228. Health Quality Ontario. Management of chronic pressure ulcers: an evidence-based analysis. Ont Health Technol Assess Ser. 2009;9:1–203. 229. Falabella AF, Carson P, Eaglstein WH, Falanga V. The safety and efficacy of a proteolytic ointment in the treatment of chronic ulcers of the lower extremity. J Am Acad Dermatol. 1998;39:737–740. 230. Lionelli GT, Lawrence WT. Wound dressings. Surg Clin North Am. 2003;83:617–638. 231. Bradley M, Cullum N, Torgerson D, et al. Systematic reviews of wound care management: (2). Dressings and topical agents used in the healing of chronic wounds. Health Technol Assess. 1999;3:1–35. 232. Phillips I, Lobo AZ, Fernandes R, Gundara NS. Acetic acid in the treatment of superficial wounds infected by Pseudomonas aeruginosa. Lancet. 1968;1:11–14. 233. Bellinger CG, Conway H. Effects of silver nitrate and sulfamylon on epithelial regeneration. Plast Reconstr Surg. 1970;45:582–585. 234. Lineaweaver W, Howard R, Soucy D, et al. Topical antimicrobial toxicity. Arch Surg. 1985;120:267–270. 235. Lineaweaver W, McMorris S, Soucy D, Howard R. Cellular and bacterial toxicities of topical antimicrobials. Plast Reconstr Surg. 1985;75:394–396. 236. Kramer SA. Effect of povidone-iodine on wound healing: a review. J Vasc Nurs. 1999;17:17–23. 237. Viljanto J. Disinfection of surgical wounds without inhibition of normal wound healing. Arch Surg. 1980;115:253–256. 238. Kjolseth D, Frank JM, Barker JH, et al. Comparison of the effects of commonly used wound agents on epithelialization and neovascularization. J Am Coll Surg. 1994;179:305–312. 239. Saeg F, Schoenbrunner AR, Janis JE. Evidence-based wound irrigation: separating fact from fiction. Plast Reconstr Surg. 2021;148(4):601e–614e. 240. Banerjee J, Das Ghatak P, Roy S, et al. Silver-zinc redox-coupled electroceutical wound dressing disrupts bacterial biofilm. PLoS One. 2015;10:e0119531. 241. Whitcomb E, Monroe N, Hope-Higman J, Campbell P. Demonstration of a microcurrent generating wound care device for wound healing within a rehabilitation center patient population. J Am Coll Clin Wound Spec. 2013;4:32–39. 242. Khansa I, Schoenbrunner AR, Kraft CT, Janis JE. Silver in wound care-friend or foe? A comprehensive review. Plast Reconstr Surg Glob Open. 2019;7:e2390. 243. Norman G, Dumville JC, Goto S, et al. Antibiotics and antiseptics for pressure ulcers. Cochrane Database Syst Rev. 2016 244. Dumville JC, Keogh SJ, Liu Z, et al. Alginate dressings for treating pressure ulcers. Cochrane Database Syst Rev. 2015 245. Geronemus RG, Mertz PM, Eaglstein WH. Wound healing. The effects of topical antimicrobial agents. Arch Dermatol. 1979;115:1311–1314. 246. Tredget EE, Shankowsky HA, Groeneveld A, Burrell R. A matched-pair, randomized study evaluating the efficacy and safety of Acticoat silver-coated dressing for the treatment of burn wounds. J Burn Care Rehabil. 1998;19:531–537. 247. Singh D, Chopra K, Brown E, et al. Practical things you should know about wound healing and vacuum-assisted closure management. Plast Reconstr Surg. 2020;145:839e. 248. Deva AK, Buckland GH, Fisher E, et al. Topical negative pressure in wound management. Med J Aust. 2000;173:128–131.

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SECTION II

CHAPTER 16  • Pressure sores

249. Ford CN, Reinhard ER, Yeh D, et al. Interim analysis of a prospective, randomized trial of vacuum-assisted closure versus the healthpoint system in the management of pressure ulcers. Ann Plast Surg. 2002;49:55–61. discussion 61. 250. Joseph E, Hamori CA, Bergman S, et al. A prospective randomized trial of vacuum-assisted closure versus standard therapy of chronic nonhealing wounds. Wounds. 2000;12:60–67. 251. Wanner MB, Schwarzl F, Strub B, et al. Vacuum-assisted wound closure for cheaper and more comfortable healing of pressure sores: a prospective study. Scand J Plast Reconstr Surg Hand Surg. 2003;37:28–33. 252. Kim PJ, Attinger CE, Constantine T, et al. Negative pressure wound therapy with instillation: international consensus guidelines update. Int Wound J. 2020;17:174–186. 253. Yang C, Goss SG, Alcantara S, et al. Effect of negative pressure wound therapy with instillation on bioburden in chronically infected wounds. Wounds. 2017;29:240–246. 254. Gabriel A, Kahn K, Karmy-Jones R. Use of negative pressure wound therapy with automated, volumetric instillation for the treatment of extremity and trunk wounds: clinical outcomes and potential cost-effectiveness. Eplasty. 2014;14:e41. 255. Omar M, Gathen M, Liodakis E, et al. A comparative study of negative pressure wound therapy with and without instillation of saline on wound healing. J Wound Care. 2016;25:475–478. 256. Faust E, Opoku-Agyeman JL, Behnam AB. Use of negativepressure wound therapy with instillation and dwell time: an overview. Plast Reconstr Surg. 2021;147:16S. 257. Kim PJ, Attinger CE, Oliver N, et al. Comparison of outcomes for normal saline and an antiseptic solution for negative- pressure wound therapy with instillation. Plast Reconstr Surg. 2015;136:657e–664e. 258. Grauhan O, Navasardyan A, Hetzer R, et al. Prevention of poststernotomy wound infections in obese patients by negative pressure wound therapy. J Thorac Cardiovasc Surg. 2013;145:1387–1392. 259. Grauhan O, Navasardyan A, Tutkun B, et al. Effect of surgical incision management on wound infections in a poststernotomy patient population. Int Wound J. 2014;11(Suppl 1):6–9. 260. Reddy VS. Use of closed incision management with negative pressure therapy for complex cardiac patients. Cureus. 2016;8:e506. 261. Gabriel A, Sigalove SR, Maxwell GP. Initial experience using closed incision negative pressure therapy after immediate postmastectomy breast reconstruction. Plast Reconstr Surg Glob Open. 2016;4:e819. 262. Pachowsky M, Gusinde J, Klein A, et al. Negative pressure wound therapy to prevent seromas and treat surgical incisions after total hip arthroplasty. Int Orthop. 2012;36:719–722. 263. Redfern RE, Cameron-Ruetz C, Beer KJ, et al. Closed incision negative pressure therapy effects on postoperative infection and surgical site complication after total hip and knee arthroplasty. J Arthroplasty. 2017;32:3333–3339. 264. Gunatilake RP, Swamy GK, Brancazio LR, et al. Closed incision negative-pressure therapy in obese patients undergoing cesarean delivery: a randomized controlled trial. AJP Rep. 2017;7: e151–e157. 265. Pleger SP, Nink N, Koshty A, et al. Reduction of groin wound complications in vascular surgery patients using closed incision negative pressure therapy (ciNPT): a prospective, randomised, single-institution study. Int Wound J. 2018;15:75–83. 266. Swift SH, Zimmerman MB, Hardy-Fairbanks AJ. Effect of single-use negative pressure wound therapy on postcesarean infections and wound complications for high-risk patients. J Reprod Med. 2015;60:211–218. 267. Lee K, Murphy PB, Ingves MV, et al. Randomized clinical trial of negative pressure wound therapy for high-risk groin wounds in lower extremity revascularization. J Vasc Surg. 2017;66:1814–1819. 268. Papp AA. Incisional negative pressure therapy reduces complications and costs in pressure ulcer reconstruction. Int Wound J. 2019;16:394–400. 269. Greenhalgh DG. Wound healing and diabetes mellitus. Clin Plast Surg. 2003;30:37–45.

270. Lerman OZ, Galiano RD, Gurtner GC, et al. Cellular dysfunction in the diabetic fibroblast: impairment in migration, vascular endothelial growth factor production, and response to hypoxia. Am J Pathol. 2003;162:303–312. 271. Wukich DK, Lowery NJ, McMillen RL, Frykberg RG. Postoperative infection rates in foot and ankle surgery: a comparison of patients with and without diabetes mellitus. JBone Joint Surg Am. 2010;92:287–295. 272. Endara M, Masden D, Attinger C, et al. The role of chronic and perioperative glucose management in high-risk surgical closures: a case for tighter glycemic control. Plast Reconstr Surg. 2013;132:996–1004. 273. Robson MC, Hill DP, Smith PD, et al. Sequential cytokine therapy for pressure ulcers: clinical and mechanistic response. Ann Surg. 2000;231:600–611. 274. Harrison B, Khansa I, Janis JE. Evidence-based strategies to reduce postoperative complications in plastic surgery. Plast Reconstr Surg. 2016;7 138:51S. 275. Conway H, Griffith BH. Plastic surgery for closure of decubitus ulcers in patients with paraplegia; based on experience with 1,000 cases. Am J Surg. 1956;91:946–975. 276. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006;104:158–169. 277. Attinger C, Wolcott R. Clinically addressing biofilm in chronic wounds. Adv Wound Care. 2012;1:127–132. 278. Wolcott RD, Rumbaugh KP, James G, et al. Biofilm maturity studies indicate sharp debridement opens a time-dependent therapeutic window. J Wound Care. 2010;19:320–328. 279. Liu J, Ko JH, Secretov E, et al. Comparing the hydrosurgery system to conventional debridement techniques for the treatment of delayed healing wounds: a prospective, randomised clinical trial to investigate clinical efficacy and cost-effectiveness. Int Wound J. 2015;12:456–461. 280. Janis JE, Kwon RK, Attinger CE. The new reconstructive ladder: modifications to the traditional model. Plast Reconstr Surg. 2011;127:205S–212S. 281. Sameem M, Au M, Mahoney J, et al. A systematic review of complication and recurrence rates of musculocutaneous, fasciocutaneous, and perforator-based flaps for treatment of pressure sores. Plast Reconstr Surg. 2012;130:67e. 282. Yamamoto Y, Tsutsumida A, Murazumi M, Sugihara T. Long-term outcome of pressure sores treated with flap coverage. Plast Reconstr Surg. 1997;100:1212–1217. 283. Ohura T, Ohura N Jr, Oka H. Incidence and clinical symptoms of hourglass and sandwich-shaped tissue necrosis in stage iv pressure ulcer. Wounds. 2007;19:310–319. 284. Mathes SJ, Alpert BS, Chang N. Use of the muscle flap in chronic osteomyelitis: experimental and clinical correlation. Plast Reconstr Surg. 1982;69:815–829. 285. Mathes SJ, Feng LJ, Hunt TK. Coverage of the infected wound. Ann Surg. 1983;198:420–429. 286. Bruck JC, Buttemeyer R, Grabosch A, Gruhl L. More arguments in favor of myocutaneous flaps for the treatment of pelvic pressure sores. Ann Plast Surg. 1991;26:85–88. 287. Yazar S, Lin CH, Lin YT, et al. Outcome comparison between free muscle and free fasciocutaneous flaps for reconstruction of distal third and ankle traumatic open tibial fractures. Plast Reconstr Surg. 2006;117:2468–2475, discussion 2476–2477. 288. Kroll SS, Rosenfield L. Perforator-based flaps for low posterior midline defects. Plast Reconstr Surg. 1988;81:561–566. 289. Koshima I, Moriguchi T, Soeda S, et al. The gluteal perforatorbased flap for repair of sacral pressure sores. Plast Reconstr Surg. 1993;91:678–683. 290. Higgins JP, Orlando GS, Blondeel PN. Ischial pressure sore reconstruction using an inferior gluteal artery perforator (IGAP) flap. Br J Plast Surg. 2002;55:83–85. 291. Nahai F. The tensor fascia lata flap. Clin Plast Surg. 1980;7:51–56. 292. Nahai F, Hill L, Hester TR. Experiences with the tensor fascia lata flap. Plast Reconstr Surg. 1979;63:788–799.

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320. Parry SW, Mathes SJ. Bilateral gluteus maximus myocutaneous advancement flaps: sacral coverage for ambulatory patients. Ann Plast Surg. 1982;8:443–445. 321. Snyder GB, Edgerton MT Jr. The principle of the island neurovascular flap in the management of ulcerated anesthetic weightbearing areas of the lower extremity. Plast Reconstr Surg. 1965;36:518–528. 322. Stallings JO, Delgado JP, Converse JM. Turnover island flap of gluteus maximus muscle for the repair of sacral decubitus ulcer. Plast Reconstr Surg. 1974;54:52–54. 323. Vyas SC, Binns JH, Wilson AN. Thoracolumbar-sacral flaps in the treatment of sacral pressure sores. Plast Reconstr Surg. 1980;65: 159–163. 324. Wesser DR, Kahn S. The reversed dermis graft in the repair of decubitus ulcers. Plast Reconstr Surg. 1967;40:252–254. 325. Weum S, de Weerd L. The butterfly design as an alternative to the “double-A bilateral flaps for the treatment of large sacral defects. Plast Reconstr Surg. 2008;121:1513–1514. author reply 1514–1515. 326. White JC, Hamm WG. Primary closure of bedsores by plastic surgery. Ann Surg. 1946;124:1136–1147. 327. Yamamoto Y, Ohura T, Shintomi Y, et al. Superiority of the fasciocutaneous flap in reconstruction of sacral pressure sores. Ann Plast Surg. 1993;30:116–121. 328. Foster RD, Anthony JP, Mathes SJ, et al. Flap selection as a determinant of success in pressure sore coverage. Arch Surg. 1997;132:868–873. 329. Seyhan T, Ertas NM, Bahar T, Borman H. Simplified and versatile use of gluteal perforator flaps for pressure sores. Ann Plast Surg. 2008;60:673–678. 330. Basterzi Y, Canbaz H, Aksoy A, et al. Reconstruction of extensive pilonidal sinus defects with the use of S-GAP flaps. Ann Plast Surg. 2008;61:197–200. 331. Cheon YW, Lee MC, Kim YS, et al. Gluteal artery perforator flap: a viable alternative for sacral radiation ulcer and osteoradionecrosis. J Plast Reconstr Aesthet Surg. 2010;63:642–647. 332. Wong CH, Tan BK, Song C. The perforator-sparing buttock rotation flap for coverage of pressure sores. Plast Reconstr Surg. 2007;119:1259–1266. 333. Xu Y, Hai H, Liang Z, et al. Pedicled fasciocutaneous flap of multi-island design for large sacral defects. Clin Orthop Relat Res. 2009;467:2135–2141. 334. Cheong EC, Wong MT, Ong WC, et al. Sensory innervated superior gluteal artery perforator flap for reconstruction of sacral wound defect. Plast Reconstr Surg. 2005;115:958–959. 335. Zomerlei T, Janis JE. Gluteal flaps for sacral ulcers. In: Chung K, ed. Operative Techniques in Plastic Surgery. 1st ed. Wolters Kluwer Health; 2019:1698–1704. 336. Luscher NJ, de Roche R, Krupp S, et al. The sensory tensor fasciae latae flap: a 9-year follow-up. Ann Plast Surg. 1991;26:306–310, discussion 311. 337. James JH, Moir IH. The biceps femoris musculocutaneous flap in the repair of pressure sores around the hip. Plast Reconstr Surg. 1980;66:736–739. 338. Wingate GB, Friedland JA. Repair of ischial pressure ulcers with gracilis myocutaneous island flaps. Plast Reconstr Surg. 1978;62:245–248. 339. Kim YS, Lew DH, Tark KC, et al. Inferior gluteal artery perforator flap: a viable alternative for ischial pressure sores. J Plast Reconstr Aesthet Surg. 2009;62:1347–1354. 340. Ger R, Levine SA. The management of decubitus ulcers by muscle transposition. An 8-year review. Plast Reconstr Surg. 1976;58:419–428. 341. Minami RT, Mills R, Pardoe R. Gluteus maximus myocutaneous flaps for repair of pressure sores. Plast Reconstr Surg. 1977;60:242–249. 342. Campbell RM, Converse JM. The saddle-flap for surgical repair of ischial decubitus ulcers. Plast Reconstr Surg. 1946;1954(14):442–443. 343. Rajacic N, Gang RK, Dashti H, Behbehani A. Treatment of ischial pressure sores with an inferior gluteus maximus

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CHAPTER 16  • Pressure sores

musculocutaneous island flap: an analysis of 31 flaps. Br J Plast Surg. 1994;47:431–434. 344. Baker DC, Barton FE Jr, Converse JM. A combined biceps and semitendinosus muscle flap in the repair of ischial sores. Br J Plast Surg. 1978;31:26–28. 345. Hurteau JE, Bostwick J, Nahai F, et al. V-Y advancement of hamstring musculocutaneous flap for coverage of ischial pressure sores. Plast Reconstr Surg. 1981;68:539–542. 346. Tobin GR, Sanders BP, Man D, Weiner LJ. The biceps femoris myocutaneous advancement flap: a useful modification for ischial pressure ulcer reconstruction. Ann Plast Surg. 1981;6:396–401. 347. Kauer C, Sonsino G. The need for skin and muscle saving techniques in the repair of decubitus ulcers. A consecutive series of 72 patients and 100 ulcers over 5 years (1979/1984). A case report. Scand J Plast Reconstr Surg. 1986;20:129–131. 348. Kroll SS, Hamilton S. Multiple and repetitive uses of the extended hamstring V-Y myocutaneous flap. Plast Reconstr Surg. 1989;84: 296–302. 349. Paletta C, Bartell T, Shehadi S. Applications of the posterior thigh flap. Ann Plast Surg. 1993;30:41–47. 350. Yu P, Sanger JR, Matloub HS, et al. Anterolateral thigh fasciocutaneous island flaps in perineoscrotal reconstruction. Plast Reconstr Surg. 2002;109:610–616, discussion 617–618. 351. Windhofer C, Brenner E, Moriggl B, Papp C. Relationship between the descending branch of the inferior gluteal artery and the posterior femoral cutaneous nerve applicable to flap surgery. Surg Radiol Anat. 2002;24:253–257. 352. Homma K, Murakami G, Fujioka H, et al. Treatment of ischial pressure ulcers with a posteromedial thigh fasciocutaneous flap. Plast Reconstr Surg. 2001;108:1990–1996, discussion 1997. 353. Hallock GG. The random upper posterior thigh fasciocutaneous flap. Ann Plast Surg. 1994;32:367–371. 354. Scheufler O, Farhadi J, Kovach SJ, et al. Anatomical basis and clinical application of the infragluteal perforator flap. Plast Reconstr Surg. 2006;118:1389–1400. 355. Nahai F, Silverton JS, Hill HL, Vasconez LO. The tensor fascia lata musculocutaneous flap. Ann Plast Surg. 1978;1:372–379. 356. Dibbell DG, McCraw JB, Edstrom LE. Providing useful and protective sensibility to the sitting area in patients with meningomyelocele. Plast Reconstr Surg. 1979;64:796–799. 357. Hulsen J, Janis JE. Posterior thigh and hamstring flaps for ischial ulcers. In: Chung K, ed. Operative Techniques in Plastic Surgery. 1st ed. Wolters Kluwer Health; 2019:1705–1714. 358. Cochran JH Jr, Edstrom LE, Dibbell DG. Usefulness of the innervated tensor fascia lata flap in paraplegic patients. Ann Plast Surg. 1981;7:286–288. 359. Lewis VL Jr, Cunningham BL, Hugo NE. The tensor fascia lata V-Y retroposition flap. Ann Plast Surg. 1981;6:34–37. 360. Schulman NH. Primary closure of trochanteric decubitus ulcers: the bipedicle tensor fascia lata musculocutaneous flap. Plast Reconstr Surg. 1980;66:740–744. 361. Withers EH, Franklin JD, Madden JJ Jr, Lynch JB. Further experience with the tensor fascia lata musculocutaneous flap. Ann Plast Surg. 1980;4:31–36. 362. Bovet JL, Nassif TM, Guimberteau JC, Baudet J. The vastus lateralis musculocutaneous flap in the repair of trochanteric pressure sores: technique and indications. Plast Reconstr Surg. 1982;69:830–834. 363. Dowden RV, McCraw JB. The vastus lateralis muscle flap: technique and applications. Ann Plast Surg. 1980;4:396–404. 364. Hauben DJ, Smith AR, Sonneveld GJ, Van der Meulen JC. The use of the vastus lateralis musculocutaneous flap for the repair of trochanteric pressure sores. Ann Plast Surg. 1983;10:359–363. 365. Minami RT, Hentz VR, Vistnes LM. Use of vastus lateralis muscle flap for repair of trochanteric pressure sores. Plast Reconstr Surg. 1977;60:364–368. 366. Chang SH. Anterolateral thigh island pedicled flap in trochanteric pressure sore reconstruction. J Plast Reconstr Aesthet Surg. 2007;60:1074–1075.

367. Mehrotra S. Giant trochanteric pressure sore: use of a pedicled chimeric perforator flap for cover. Indian J Plast Surg. 2009;42:126–129. 368. Coskunfirat OK, Ozgentas HE. Gluteal perforator flaps for coverage of pressure sores at various locations. Plast Reconstr Surg. 2004;113:2012–2017, discussion 2018–2019. 369. Ishida LH, Munhoz AM, Montag E, et al. Tensor fasciae latae perforator flap: minimizing donor-site morbidity in the treatment of trochanteric pressure sores. Plast Reconstr Surg. 2005;116:1346–1352. 370. Hallock GG. The propeller flap version of the adductor muscle perforator flap for coverage of ischial or trochanteric pressure sores. Ann Plast Surg. 2006;56:540–542. 371. Zomerlei T, Janis JE. Tensor fascia lata flap for trochanteric ulcers. In: Chung K, ed. Operative Techniques in Plastic Surgery. 1st ed. Wolters Kluwer Health; 2019:1715–1720. 372. Rubayi S, Pompan D, Garland D. Proximal femoral resection and myocutaneous flap for treatment of pressure ulcers in spinal injury patients. Ann Plast Surg. 1991;27:132–138. 373. Benito-Ruiz J, Baena-Montilla P, Mena-Yago A, Miguel I, Montanana-Vizcaino J. A complicated trochanteric pressure sore: what is the best surgical management? Case report. Paraplegia. 1993;31:119–124. 374. Evans GR, Lewis VL Jr, Manson PN, et al. Hip joint communication with pressure sore: the refractory wound and the role of Girdlestone arthroplasty. Plast Reconstr Surg. 1993;91:288–294. 375. Klein NE, Luster S, Green S, et al. Closure of defects from pressure sores requiring proximal femoral resection. Ann Plast Surg. 1988;21:246–250. 376. Akhtar S, Hameed A. Versatility of the sural fasciocutaneous flap in the coverage of lower third leg and hind foot defects. J Plast Reconstr Aesthet Surg. 2006;59:839–845. 377. Gupta A. The versatile medial plantar artery and its flaps. Ann Plast Surg. 2007;58:348. 378. Aoki S, Tanuma K, Iwakiri I, et al. Clinical and vascular anatomical study of distally based sural flap. Ann Plast Surg. 2008;61:73–78. 379. Baumeister SP, Spierer R, Erdmann D, et al. A realistic complication analysis of 70 sural artery flaps in a multimorbid patient group. Plast Reconstr Surg. 2003;112:129–140. discussion 141–142. 380. Erdmann D, Gottlieb N, Humphrey JS, et al. Sural flap delay procedure: a preliminary report. Ann Plast Surg. 2005;54:562–565. 381. Schwarz RJ, Negrini JF. Medial plantar artery island flap for heel reconstruction. Ann Plast Surg. 2006;57:658. 382. Yang D, Yang JF, Morris SF, et al. Medial plantar artery perforator flap for soft-tissue reconstruction of the heel. Ann Plast Surg. 2011;67:294. 383. Arregui J, Cannon B, Murray JE, O’Leary JJ Jr. Long-term evaluation of ischiectomy in the treatment of pressure ulcers. Plast Reconstr Surg. 1965;36:583–590. 384. Hackler RH, Zampieri TA. Urethral complications following ischiectomy in spinal cord injury patients: a urethral pressure study. J Urol. 1987;137:253–255. 385. Karaca AR, Binns JH, Blumenthal FS. Complications of total ischiectomy for the treatment of ischial pressure sores. Plast Reconstr Surg. 1978;62:96–99. 386. Anthony JP, Mathes SJ. Update on chronic osteomyelitis. Clin Plast Surg. 1991;18:515–523. 387. Schiffman J, Golinko MS, Yan A, et al. Operative debridement of pressure ulcers. World J Surg. 2009;33:1396–1402. 388. Khansa I, Barker JC, Gordillo GM, et al. Use of antibiotic impregnated resorbable beads reduces pressure ulcer recurrence: a retrospective analysis. Wound Repair Regen. 2018;26:221–227. 389. Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure sores. Curr Probl Surg. 1977;14:1–62. 390. Stal S, Serure A, Donovan W, Spira M. The perioperative management of the patient with pressure sores. Ann Plast Surg. 1983;11:347–356.

References

391. Hentz VR. Management of pressure sores in a specialty center. A reappraisal. Plast Reconstr Surg. 1979;64:683–691. 392. Constantian MB, ed. Pressure Ulcers: Principles and Techniques of Management. Boston: Little, Brown; 1980. 393. Disa JJ, Carlton JM, Goldberg NH. Efficacy of operative cure in pressure sore patients. Plast Reconstr Surg. 1992;89:272–278. 394. Levenson SM, Geever EF, Crowley LV, et al. The healing of rat skin wounds. Ann Surg. 1965;161:293–308. 395. Isik FF, Engrav LH, Rand RP, et al. Reducing the period of immobilization following pressure sore surgery: a prospective, randomized trial. Plast Reconstr Surg. 1997;100:350–354. 396. Wagner D, Fox M, Ellis E. Developing a successful interdisciplinary seating program. Ostomy Wound Manage. 1994;40:32–34. 36–38, 40–41. 397. Dover H, Pickard W, Swain I, Grundy D. The effectiveness of a pressure clinic in preventing pressure sores. Paraplegia. 1992;30:267–272. 398. Janis JE, Khansa L, Khansa I. Strategies for postoperative seroma prevention: a systematic review. Plast Reconstr Surg. 2016;138:240. 399. Khansa I, Khansa L, Meyerson J, Janis JE. Optimal use of surgical drains: evidence-based strategies. Plast Reconstr Surg. 2018;141:1542. 400. Degnim AC, Scow JS, Hoskin TL, et al. Randomized controlled trial to reduce bacterial colonization of surgical drains after breast and axillary operations. Ann Surg. 2013;258:240–247. 401. Garber SL, Rintala DH, Holmes SA, et al. A structured educational model to improve pressure ulcer prevention knowledge in veterans with spinal cord dysfunction. J Rehabil Res Dev. 2002;39:575–588. 402. Brace JA, Schubart JR. A prospective evaluation of a pressure ulcer prevention and management E-learning program for adults with spinal cord injury. Ostomy Wound Manage. 2010;56:40–50.

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403. Tavakoli K, Rutkowski S, Cope C, et al. Recurrence rates of ischial sores in para- and tetraplegics treated with hamstring flaps: an 8-year study. Br J Plast Surg. 1999;52:476–479. 404. Stevenson TR, Pollock RA, Rohrich RJ, VanderKolk CA. The gluteus maximus musculocutaneous island flap: refinements in design and application. Plast Reconstr Surg. 1987;79:761–768. 405. Relander M, Palmer B. Recurrence of surgically treated pressure sores. Scand J Plast Reconstr Surg Hand Surg. 1988;22:89–92. 406. Evans GR, Dufresne CR, Manson PN. Surgical correction of pressure ulcers in an urban center: is it efficacious? Adv Wound Care. 1994;7:40–46. 407. Kerr-Valentic MA, Samimi K, Rohlen BH, et al. Marjolin’s ulcer: modern analysis of an ancient problem. Plast Reconstr Surg. 2009;123:184–191. 408. Tutela RR Jr, Granick M, Benevenia J. Marjolin’s ulcer arising in a pressure ulcer. Adv Skin Wound Care. 2004;17:462–467. 409. Esther RJ, Lamps L, Schwartz HS. Marjolin ulcers: secondary carcinomas in chronic wounds. J South Orthop Assoc. 1999;8:181–187. 410. Rubayi S, Ambe MK, Garland DE, Capen D. Heterotopic ossification as a complication of the staged total thigh muscles flap in spinal cord injury patients. Ann Plast Surg. 1992;29:41–46. 411. Georgiade N, Pickrell K, Maguire C. Total thigh flaps for extensive decubitus ulcers. Plast Reconstr Surg. 1956;17:220–225. 412. Niazi ZB, Salzberg CA. Operative repair of pressure ulcers. Clin Geriatr Med. 1997;13:587–597. 413. Barnett CC Jr, Ahmad J, Janis JE, et al. Hemicorporectomy: back to front. Am J Surg. 2008;196:1000–1002. 414. Janis JE, Ahmad J, Lemmon JA, et al. A 25-year experience with hemicorporectomy for terminal pelvic osteomyelitis. Plast Reconstr Surg. 2009;124:1165–1176. 415. Peterson R, Sardi A. Hemicorporectomy for chronic pressure ulcer carcinoma: 7 years of follow-up. Am Surg. 2004;70:507–511.

SECTION II  •  Trunk, Perineum, and Transgender

17 Perineal reconstruction Ping Song, Hakim Said, and Otway Louie

Access video and video lecture content for this chapter online at Elsevier eBooks+

SYNOPSIS

ƒ Surgical site is typically hostile after resection and/or radiation for an underlying condition. ƒ Healthy tissue transfer is usually necessary to mitigate wound-healing challenges. ƒ A proactive surgical approach can help lessen impact of complications.

Introduction Perineal reconstruction poses the challenge of healing a problematic area with multiple site-specific obstacles. Although a number of benign conditions exist which can require resurfacing perineal skin, more frequently reconstruction is needed after treatment of underlying cancer. Modern treatment of malignancies in this region has evolved to more frequently use neoadjuvant radiation therapy, which can yield a high rate of complications at the time of surgical intervention. Local effects of radiation therapy and close proximity (combined in many cases with ostomies) to bowel, reproductive organs and bladder, can all complicate reconstructive flap inset, contaminate the surgical site, and threaten surgical outcomes. Successful reconstruction takes into account these impediments and minimizes the consequences of complications in this hazardous region.

History of perineal reconstruction The evolution of perineal reconstruction over the last century parallels the development of the reconstructive ladder. Since Miles described abdominoperineal resection in 1910 for carcinoma of the rectum, numerous methods of reconstructing the perineum have been described. In his original paper, the perineal wound was simply packed with gauze, with

closure by secondary intention or delayed primary closure.1 Brunschwig’s introduction of pelvic exenteration provided the potential for oncologic cure, but left an even larger pelvic defect with significant associated morbidity.2 This lead to significant morbidity associated with an open perineal wound, and Altmeier subsequently introduced the concept of primary closure of the perineal wound with continuous suction drainage.3 Although there was some degree of success with both primary and secondary closure of the perineum, certain perineal wounds seemed predisposed to breakdown, particularly those that were irradiated and contaminated. Management of the draining perineal wound proved difficult; split-thickness skin grafts were attempted with limited success.4 The advent of axial pattern flaps ushered in the next rung on the reconstructive ladder for perineal reconstruction. Although first applied for coverage of exposed bone in the lower extremity, muscle flaps were soon utilized throughout the body, including the perineum.5 The gluteus maximus flap was described as a potential cure for a chronic perineal sinus.6 The rectus abdominus flap subsequently emerged to be a workhorse in perineal reconstruction.7,8 Transverse, vertical, and oblique skin paddles have been designed and used effectively. The gracilis muscle has also been described extensively for use in the perineum.9,10 More recently, fasciocutaneous flaps have been reported for perineal reconstruction. Wee introduced the concept of neuropudendal thigh flaps for vaginal reconstruction, creating sensate lining for the vaginal wall.11 The anterolateral thigh flap has emerged as a versatile flap that can be applied to perineal reconstruction as well as complex pelvic wounds.12,13 Additionally, the study of angiosomes and perforasomes has identified local and regional flaps of the perineum, which play a role in resurfacing of cutaneous infectious processes and malignancies.14 Finally, advances in microsurgery have allowed free flaps to be performed routinely with reliable results. Although the utility of free flaps in perineal reconstruction has been somewhat limited by the ample locoregional flaps available, there

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have been reports of free flaps for coverage of large defects in the perineal area, particularly in conjunction with sacral defects.15 Moreover, microsurgical techniques developed over the last decade have allowed perforator flaps to be applied to this region of the body as well, based on essentially every regional vascular system.16,17 In summary, significant advances have been made over the past century for perineal reconstruction. The remainder of this chapter will describe in detail some of the flaps routinely used today for perineal coverage, and touch on promising advances in technique that are on the horizon.

Basic science/disease process The processes requiring reconstruction of the perineum can broadly be broken into superficial and deep processes (Table 17.1). Benign conditions primarily include hidradenitis suppurativa, infectious destructive processes such as fasciitis or Fournier’s gangrene, and trauma, but can range to other rarer dermatologic conditions such as pyoderma gangrenosum and vasculitic ulcers. Malignant superficial lesions usually include vulvar cancers and cutaneous lesions in the area, such as extramammary Paget’s disease (Fig. 17.1). These entities have in common the depth of involvement, which typically leaves only an external cutaneous deficit on the perineum (see Fig. 10.18). Radiation treatment for these given wounds is unusual so the surrounding skin is typically healthy. Once the primary process is addressed and resolving, the defect can begin secondary healing. Negative pressure therapy and skin grafts can often play a useful role in shortening the time to healing. Some authors advocate locoregional flaps to hasten treatment for superficial defects, although this has yet to gain universal utility.18 Challenges to healing in this area include a high bacterial bioburden in many of the causative etiologies, an inherently moist surgical site, and pressure, tension, and shearing forces, which threaten to disrupt the site as the patient begins to mobilize. Outcomes are more favorable in this group. Deep defects are primarily the result of malignancy, including colorectal cancer, urologic and gynecologic cancers, most of which originate from and involve pelvic structures.

Abdominoperineal resection or exenteration has been demonstrated to provide the best cure in these cases. Typically, this extensive resection is accompanied by perioperative radiation therapy. Treatment of these more complex defects must be individualized for the missing and exposed structures. The bony pelvis effectively splints open the pelvic outlet, so contraction cannot occur, and seromas are common. Further impediments to healing such as fistulas and radiation changes in the area generally mean these defects are frequently contaminated, prone to infection, and will not heal without the addition of a non-radiated tissue transfer. After extensive resection, large areas of dead space and loss of support allow the abdominal viscera to fall into the irradiated pelvic basin. This can lead to pelvic hernias, adhesions, obstruction, and fistulas, all of which can be disastrous to treat secondarily. Nearby organs such as the bladder or vagina may also be resected in part or whole as part of the treatment course. Finally, the surgical incision is inherently moist, and mobilizing the patient can cause pressure or shearing stresses, further compounding the difficulty of healing a radiated closure at that location. Surgical outcomes reflect the many challenges posed in this group.

Figure 17.1  Extramammary Paget’s disease.

Table 17.1  Perineal reconstruction

Process

Etiology

Complicating factors

Reconstructive options

Superficial (simple, mostly benign)

Hidradenitis suppurativa Necrotizing fasciitis Fournier’s gangrene Trauma Autoimmune ulcers Vulvar cancer

Bacterial bioburden Moisture Mobility

Secondary healing Negative pressure therapy Skin graft Fasciocutaneous perforator flaps

Deep (complex, malignant)

Colorectal cancer Vulvar cancer Vaginal cancer Uterine cancer Bladder cancer

Radiation Ostomies Contamination Dead space Pelvic hernia Moisture Mobility

Rectus abdominis flap Gracilis flap Anterolateral thigh flap Singapore flap Fasciocutaneous perforator flaps Free flap

Patient selection

Diagnosis/patient presentation Patients with superficial disease may present at various stages in their treatment. As a rule, reconstruction should not be initiated until the primary process is identified and resolved with repeated surgical debridement or excisions; underlying medical conditions or autoimmune disorders should be treated. Typically, areas of external pudendal skin are involved and will require resurfacing in some fashion (see Fig. 17.1). Patients with deep disease are typically treated in conjunction with a multidisciplinary oncologic team for an underlying malignancy. Often the extent of the defect is not obvious until after the surgical resection is performed, and must be anticipated in advance. Preoperative consultation is important to manage patient expectations, outline the possible extent of surgery, and prepare for postoperative adversity. Such cases may involve more extensive external pudendal defects (Figs. 17.2 & 17.3) or deeper structures (Fig. 17.4). In the event that vaginal resection is necessary, preferences regarding vaginal versus simple perineal reconstruction should be discussed, along with a thorough dialogue about sexual function. Further details and management of vaginal reconstruction are discussed in depth in Chapter 15.

491

for skin grafting. If the wound fails to begin the healing process despite wound healing optimization, a more complex approach and tissue transfer might be warranted. Especially for superficial malignancies such as vulvar cancer, reconstruction at the time of resection is feasible, and standard in many centers. Application of microsurgical principles for perforator flap dissection has been proposed in that setting. In the case of deeper malignancies, such as colorectal, gynecologic, or urologic cancer, radiation therapy is part of the preoperative routine in most centers. This factor alone is the

Patient selection Patients with superficial defects are more straightforward in management; as their underlying process resolves, the defect begins to heal secondarily, even in response to a conventional wet to moist dressing regimen. Typically, a modest, shallow perineal defect is left. A number of publications support the use of a negative pressure therapy plan to accelerate the healing process. Within a matter of weeks, a healthy wound bed can be established, confirming the suitability of these patients

Figure 17.3  External perineal skin and soft-tissue loss.

Figure 17.2 Post-radiation lymphangiosarcoma after treatment of vulvar cancer.

Figure 17.4 Complex perineal defect involving external skin, soft tissue, vagina, and pelvic floor.  

 

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most significant indication for flap reconstruction at the time of resection. Large prospective series suggest that abdominal-based flaps demonstrate the most favorable outcomes and complication profile in this setting, even compared to thighbased flap reconstruction.19 This must be balanced with the abdominal morbidity of the harvest. Some surgeons prefer to avoid using abdominal flaps if ostomies are necessary on both sides, although these can be inset through the external oblique musculature with no additional morbidity. A vertical skin pedicle provides the most discreet scar, but an oblique paddle can provide more tissue by extending off the muscle, effectively also extending its reach. Pre-existing abdominal wall defects might direct some surgeons to alternative flap options. Nevertheless, Butler has shown no increased incidence of abdominal wall problems after abdominal flap harvest.19,20 Additionally, when faced with large abdominoperineal resection (APR) or pelvic exenteration defects, systematic reviews and meta-analyses have demonstrated the efficacy of muscle flap closure as compared to primary closure in decreasing total and major perineal wound complications.21,22 Rarely, perineal resection can be performed without laparotomy, and this might predispose toward use of a non-abdominal flap option. The complication profile of the gracilis flap is also reasonable, and represents a dramatic improvement over primary closure under these circumstances. Early studies comparing gracilis reconstruction to primary closure demonstrate a dramatic reduction in infectious complications from 46% to 12% with flap reconstruction.23 Limitations are the small muscle bulk and questionable skin island, but recent modifications may address the latter based on capturing additional perforators. The anterolateral thigh flap represents an alternative option with documented excellent reliability for many applications. There is growing literature to support its use as a reliable regional option for perineal reconstruction.24–26 This is especially true if the abdomen cannot serve as a donor site. With the addition of the vastus lateralis muscle, it can also play a role for addressing the dead space left behind after large pelvic defects.27 However, more studies comparing efficacy between rectus abdominis flaps and anterolateral thigh flap with vastus lateralis may corroborate this in time. Some surgeons favor a posterior thigh flap, harvested in similar fashion to the anterolateral thigh flap, but the axial nature of the perfusion off the inferior gluteal artery has been called into question. Recent series document a wound healing complication rate of over 50% using this method,28 which does not compare favorably to abdominal flaps. For defects with less dead space or requiring less bulk, skin flap reconstruction (e.g., Singapore or perforator flaps) can be used, although outcomes data are more mixed and overall less favorable compared to abdominal flaps. Complications are reported to range from 7% to 62%.29–31 Recent outcome studies are not available directly comparing this method to other options in head-to-head fashion, but there is a growing role for local skin flaps in coverage of superficial wounds resultant from cutaneous infections or malignancies. Massive defects in pelvic support may in fact require multiple flaps. Occasionally pelvic floor support is needed in the form of mesh reinforcement. In a hostile, radiated, often contaminated surgical site, prosthetic mesh is contraindicated. Newer bioprosthetic options provide a reinforcement alternative that is more robust in the face of complications.32

Finally, if the two abdominal flaps and eight thigh-based flaps are unavailable or insufficient for the defect, there are several reports of distant flaps used in conjunction with microsurgical transfer. Composite thigh tissues can be transferred en bloc, and large surface area flaps such as the latissimus dorsi have been reported in extreme cases. Laparoscopic or robotic techniques represent a new frontier in both extirpative and reconstructive surgeries. Performing the entirety of an abdominoperineal resection is now possible through incisions that total 2 cm in length. As techniques are developed for resection without an open laparotomy, the necessity for harvesting non-radiated tissue to fill the radiated pelvic basin remains. More challenging is avoiding a midline laparotomy incision for flap harvest, when extirpation avoids its use. Typically this entails harvest of the rectus muscle through the posterior sheath using either a laparoscopic or robotic approach. Laparoscopic tools are widely accessible, but robotic equipment is less widely available, and surgeons trained in using that for reconstruction are rarer still. Yet, plastic surgeons are no strangers to innovation, and it is certain that adoption of robotic techniques will be met by future plastic surgeons within the growing field of minimally invasive reconstruction.

Treatment/surgical technique Skin graft reconstruction Benign, uncomplicated wounds of the perineum that granulate in response to dressing changes or negative pressure therapy can usually be treated in staged fashion with split-thickness skin grafts.

Regional skin flaps Processes such as Fournier’s gangrene may leave more extensive but still subcutaneous defects that can be reconstructed with local flaps. Exposed subcutaneous structures such as testes can be buried under nearby intact thigh skin if available, during the initial debridement phase. Otherwise vacuum-assisted closure therapy can also act as temporary dressing.33 Definitive coverage of the testes can also be achieved with remnant scrotal skin, or local areas of intact skin on the thighs or perineum can also be advanced using a V–Y pattern, rotational, or keystone design to provide resurfacing (Figs. 17.5 & 17.6). Furthermore, skin grafting may serve a role,34,35 but regional skin flaps such as the pudendal thigh flap or anterior lateral thigh flap may provide more reliable, and sensate, scrotal resurfacing.36 In addition, some authors have described tissue expansion in conjunction with regional flaps to augment the amount of subcutaneous coverage available for example in the case of missing scrotal coverage.37 Perforator-based flaps have been described for superficial defects using medial circumflex femoral vessels,18,38 profunda femoris perforating branches,39 and almost any vascular axis in the region.14,16 See Perforator flaps section, below.

Rectus-based reconstruction Rectus-based flaps have emerged as workhorses for more complex perineal reconstruction. These flaps provide well-vascularized tissue with adequate bulk to fill dead space.

Treatment/surgical technique

Figure 17.5  Complex perineal defect with perforators marked.

493

rectus; however, its arc of rotation is limited by the muscle itself, and the bulk of the muscle itself can make insetting difficult, particularly in a narrow male pelvis. The transverse paddle has been well described for perineal reconstruction as well, and provides excellent cosmesis for the donor site.42 Dumanian and others have had success with an oblique design for the rectus flap, noting the long, excellent arc of rotation and thin, reliable skin paddle obtained.43–45 In addition, cadaver injection studies have shown flow in a lateral and superior oblique direction from the periumbilical perforators. After marking the periumbilical perforators with a Doppler, a skin paddle is designed with an axis towards the ipsilateral tip of the scapula, ending at the anterior axillary line. Flaps up to 12 × 30 cm can be obtained with this design. Once the skin paddle has been marked in one of these orientations, the skin incisions are made and dissection carried down to the external oblique and rectus fascia. The skin paddle is dissected circumferentially, approaching the deep inferior epigastric perforators coming through the rectus muscle. The fascia immediately adjacent to these perforators is opened, and the anterior sheath elevated off the rectus muscle. The muscle is then dissected free of the rectus sheath, working down toward the deep inferior epigastric vessels. These are identified lateral to the rectus beneath the arcuate line. The

Figure 17.6  Closure with local skin flaps.

In addition, lining for external or vaginal wall coverage can be obtained if harvested as a musculocutaneous flap. They are known for having a wide arc of rotation with a reliable pedicle. They have been shown to decrease the risk of perineal complications in irradiated APR defects.40 When compared to thigh-based flaps, rectus-based flaps had lower major complications without increased abdominal morbidity.19 The rectus flap can be muscular or myocutaneous, depending on whether external skin or vaginal lining is needed for reconstruction. The right rectus is typically used, saving the left rectus for a colostomy if needed. After the resection is complete, the deep inferior epigastric vessels are examined to confirm they are patent, undamaged by the resection, and preferably pulsatile before proceeding with flap design. The skin paddle is based on the peri-umbilical perforators of the deep inferior epigastric vessels,41 and can be oriented in vertical, transverse, or oblique directions (Figs. 17.7 & 17.8; see Figs.  15.5 & 15.6). The vertical design theoretically includes more perforators as the skin paddle overlies the length of the

Figure 17.7  Design of transverse rectus abdominis myocutaneous (TRAM) flap for perineal and pelvic reconstruction.

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Figure 17.8  Design of oblique rectus abdominis myocutaneous (ORAM) flap for perineal and pelvic reconstruction. Note skin paddle designed around peri-umbilical perforators, extending toward ipsilateral scapular tip.

Figure 17.10  Cutaneous oblique rectus skin paddle tubed for vaginal lining.

Gracilis flap

Figure 17.9  Cutaneous paddle inset for external perineal skin reconstruction.

superior rectus is divided, and the muscle transposed out of the rectus sheath. The vascular pedicle can be mobilized, but does not need to be skeletonized. The insertion of the rectus on the pubis typically does not need to be divided completely, and is left intact at least in part to help prevent traction injury to the pedicle. The flap is then delivered down through the pelvis and out to the perineum (see Fig. 15.6). The requisite skin for external lining or vaginal reconstruction is marked, and the remainder of the skin paddle de-epithelialized and inset under the radiated skin edges (Fig. 17.9). The skin paddle may be tubed if needed for total vaginal reconstruction (Fig. 17.10). The flap is then inset with a layered closure. The fascial donor site is closed primarily if possible, or the remaining anterior and posterior sheaths are sown together and used to span the fascial defect. Bioprosthetic mesh may be used to repair extensive anterior sheath defects. The abdominal skin is closed primarily over closed suction drainage.

The gracilis flap was first introduced in its myocutaneous form by McCraw and used as a healthy tissue to augment genital reconstruction.46 As described, it was based on the medial circumflex femoral vessels to the gracilis muscle, and to the overlying skin. Subsequent studies have shown that the perforators originating from the deep femoral system only pass reliably through the gracilis muscle proximally. To consistently capture the perfusion to distal portions of a longitudinal skin paddle, the fasciocutaneous vascular network around the gracilis muscle must be widely harvested intact from proximal to distal as described by Whetzel.47 A line is drawn from the adductor insertion on the pubis to the semitendinosus muscle at the medial condyle of the knee. Centered on this axis at the anterior edge of the gracilis muscle, the skin flap is designed as a 6–10 cm wide ellipse, which can reach up to 30 cm in length (see Fig. 15.8). This position is slightly more anterior than the traditional design, which failed to harvest peri-gracilis fascia and was associated with a less reliable skin paddle. The skin pattern is incised distally to identify the thin, round gracilis muscle near the knee, and a bowstring technique is used to confirm its course. If necessary, the skin design is adjusted to overlie the anterior edge of the muscle. The paddle is then incised anteriorly, and beveling dissection outward ensures that the gracilis is harvested encased within its surrounding fat, vessels, and fascia, essentially denuding the sartorius and adductor musculature (Fig. 17.11; see Fig 15.8B). The perforating branches off the superficial femoral vessels are divided very close to their take-off, preserving the longitudinal arcade of fasciocutaneous vessels in communication with the primary pedicle off the deep femoral system proximally. The greater saphenous vein is divided proximally and distally and preserved within the substance of the flap as an additional venous conduit. The flap is isolated back to its pedicle off the medial circumflex femoral vessels, usually at 7–10 cm distal from the pubis (see Fig. 15.8 F). Upgoing adductor branches are divided to yield extra length. If needed, the muscular origin is exposed and divided off the pubis to allow rotation of the flap 180° into

Treatment/surgical technique

Vastus medialis

495

Rectus femoris Femur

Adductor longus Superficial femoral artery

Vastus intermedius Vastus lateralis

Sartorius

Figure 17.12  Gracilis myocutaneous flap elevated before inset. Pedicle is visible 7–10 cm from pubis.

Biceps femoris

Gracilis Great saphenous vein

Sciatic nerve Semimembranosus Adductor magnus Semitendinosus

Figure 17.11  Cross-sectional view of gracilis myocutaneous flap harvest. The fasciocutaneous vascular network around the gracilis muscle must be widely harvested to preserve perfusion to the distal tip of the skin. Adductor magnus, vastus medialis, sartorius, and semitendinosus muscles are denuded by the harvest, as described by Whetzel.47

the perineum. To reduce the chance of flap ptosis, the flap is suspended from high within the perineal defect, or into the pelvis if possible. Layered closure over drains completes the inset (Figs. 17.12 & 17.13). Specific utility of the gracilis flap is in providing muscle bulk to obliterate dead space in perineal reconstruction, especially with avoiding abdominal donor site complications.48,49 Additional augmentation to the skin island, by capturing the transverse branch of the medial circumflex system allows a bilobed skin design which serves to increase reliable soft-tissue bulk to be used in perineal reconstruction.50

Anterolateral thigh flap The anterolateral thigh flap was first described by Song in 1984.51 Since that time it has become a valuable tool in the armamentarium of the reconstructive surgeon, with extensive uses in head and neck, trunk, and lower extremity reconstruction.52 Luo first described its use in perineal reconstruction after failed gracilis flaps in 2000.53 Increasing experience with it in perineal reconstruction has confirmed its utility in complex pelvic defects.12,13 It provides a regional flap that can provide large, reliable skin paddles and muscle in the form of the vastus lateralis as well.27

Figure 17.13  Bilateral gracilis myocutaneous flaps for large area external perineal defect.

With the patient in a supine position, a line connecting the anterior superior iliac spine with the superolateral patella is marked (Fig. 17.14). A circle with a 3 cm radius is marked at the center of this longitudinal axis, delineating the most common location of perforators of the descending branch of the lateral femoral circumflex vessels. Locations of perforators are confirmed by Doppler, and the skin paddle is designed as an ellipse centered on these perforators. The anterior incision is made first, dissecting down to the fascia overlying the rectus femoris muscle (Fig. 17.15). Dissection proceeds laterally, either in a subfascial or suprafascial plane, looking for septocutaneous perforators, which are then followed superomedially back to the descending branch of the lateral femoral circumflex vessels. Intramuscular perforators can be harvested with a small cuff of vastus lateralis muscle to minimize risk of injury to the perforators. The posterolateral incision is subsequently made and the harvest completed. The flap can be delivered through either a perineal route or inguinal route, as elegantly described by Yu.54 If a perineal

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Anterior superior iliac spine

Lower outer quadrant of circle with 3 cm radius centered on midpoint of line between lateral patella and anterior superior iliac spine

Figure 17.16  Anterolateral thigh flap delivered under the inguinal ligament into the pelvis, then out through the pelvic defect to fill the pelvic dead space and reconstruct the perineal skin defect. The flap can be tunneled subcutaneously across the thigh if no pelvic defect is present.

Patella

Figure 17.14  Design of anterolateral thigh flap, centered midway along an axis between the anterior superior iliac spine (ASIS) and the superolateral corner of the patella. Lateral femoral cutaneous nerve branch

Tensor fasciae latae Lateral branch of descending branch of lateral femoral circumflex artery Vastus lateralis

Rectus femoris (under fascia)

Figure 17.15  Elevation of anterolateral thigh flap, including skin, soft tissue, fascia, and occasionally a small cuff of muscle. Perforators are pursued toward the septum between the vastus lateralis and rectus femoris, and then followed superomedially up to the descending branch of the lateral circumflex femoral vessels.

skin defect exists, the flap is delivered under the rectus femoris and through a subcutaneous tunnel in the medial thigh to reach the perineum (Fig. 17.16). If the perineal defect can be closed primarily, the inguinal ligament can be divided, and the vastus lateralis muscle delivered intraperitoneally through the abdominal wall to fill any dead space in the pelvis. The flaps are then inset with layered closure and ample drainage. Furthermore, this flap combined with vastus lateralis muscle can provide bulk and coverage for posterior defects involving the sacrum following giant chordoma resections and extended APR defects.55

Singapore flap First reported by Wee, Singapore flaps are fasciocutaneous flaps harvested from the groin ideally using non-hair-bearing skin just lateral to the labia majora.11 These flaps are based on the posterior labial arteries, tracing back from the perineal arteries, which in turn originate from the internal pudendal vessels. A horn-shaped flap up to 15 × 6 cm is designed lateral to the labia majora, and harvested to include deep fascia and adductor epimysium to preserve dermal blood supply. The original description divided the dermis at the base of the design, and tunneled the flap into the defect. In order to maximize perfusion under the most adverse circumstances, Woods subsequently described a modification to avoid dividing the skin at the base of the flap.56 This design added an incision made at the posterior base of the labia majora in order to avoid dividing the dermal circulation to the flap entirely. The released labia are allowed to shift anteriorly, and the flaps are transposed 70° through the release incision into the defect (Fig. 17.17; see Fig. 15.3). Although this method is well established, in some patients it may transpose hair-bearing skin, which can be a liability, especially in vagino-perineal reconstruction. Some populations are less hirsute, and this issue is

Treatment/surgical technique

Design of fasciocutaneous flaps Post exenteration defect

Labia

Defect partially closed

A

B

Divided labia Suturing of paired flaps Neurovascular bundle

Dissected flaps C

D

Continuous everting suture

Neovaginal pouch Closure of donor defect with continuous suture Vaginal pouch inserted into defect

E

F

Figure 17.17  Elevation of pudendal thigh flaps for more extensive, or vaginal defects. (A) Perineal defect. (B) Design of fasciocutaneous flaps along vascular territory of perineal arteries. (C,D) Primary closure of donor sites and suturing of flaps together. (E,F) Inset of flaps into pelvic and perineal defect.

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less important. For use in European populations, however, some groups advocate depilatory treatments prior to this surgery. Newer methods using fasciocutaneous flaps based on other perforators (see Perforator flaps, below) eliminate this issue, and are becoming a preferred solution.

Posterior thigh flap Although this flap has been described based on axial flow from the inferior gluteal artery,57 this pattern of perfusion has been called into question. A significant number of flaps in this distribution are actually based on perforators from the profunda femoris vessels,39 which are frequently divided using the flap design as traditionally described.58,59 This may relate to the high wound healing complication rate (53%) recently reported in a series of these flaps.28 There are settings where this flap can be useful, especially when an abdominal approach is contraindicated and the previous flaps are not available. In such cases, using a profunda femoris perforator flap design is recommended (see Perforator flaps, below). Not all surgeons are comfortable with this style of dissection, and the literature shows far fewer reports of its use in this manner. These various issues prevent it from being a firstline choice in comparison with the better-established and supported flaps above.

Profunda artery (deep femoral artery)

Perforator flaps There are several regional skin flaps based on the perforasome theory60 that are available in the perineal region. These flaps possess the advantages of well-vascularized soft tissue of similar thickness and quality, and the ability to withstand the shearing and moisture impact that is common in this region. Furthermore, as the use of perforator-based techniques becomes more widespread, a number of fasciocutaneous perforator or free-style flaps have been described with good success in perineal reconstruction. Originally described for vulvar cancer, which results in external cutaneous defects without radiation treatment, a number of authors have reported their usefulness even in settings of deeper resection and radiated tissues. Mostly based on perforators from the internal pudendal artery, these include the Singapore flap, pudendal thigh flap, lotus leaf flap, and gluteal fold flap.16,17,61,62 The latter of these are more recent designs, which are less prone to hair-bearing, thus eliminating the most significant liability of the Singapore flap. Also described are local perforators based on the external pudendal artery, superficial inferior epigastric artery and thigh vessels, either the profunda femoris or medial circumflex femoral arteries (Fig. 17.18). Many of these flaps can be designed remotely enough to yield non-radiated tissue for transposition into the defect.

Gracilis muscle

Medial circumflex femoral artery EPAP flap External pudendal artery

A B

PAP flap

Adductor magnus muscle

C MCFAP flap

Internal pudendal artery

IPAP flap

Figure 17.18  Perforating vessels in the vicinity of the perineum. Several flaps shown based on internal or external pudendal vessels, and the profunda femoris and medial circumflex femoral vessels. EPAP, external pudendal artery perforator; IPAP, internal pudendal artery perforator; MCFAP, medial circumflex femoral artery perforator; PAP, profunda artery perforator.

Outcomes, prognosis, complications

There is growing popularity in the profunda artery perforator flap from the inner thigh. Its popularity can be seen in the field of autologous breast reconstruction, as an alternative free flap option.63–65 More so, the favorable anatomic location makes it a viable option as a regional pedicled flap for perineal reconstruction.66,67 More robust studies in the future may further validate this flap for perineal reconstruction. For both deep and superficial resection defects, multiple perforator flaps, bilaterally, can be employed to provide tissue with minimal morbidity. Hong has provided a straightforward anatomic approach to soft-tissue perineal reconstruction using local perforator flaps.14 As surgeons become more comfortable with perforator flaps, the prevailing algorithms for perineal reconstruction may evolve; the first-line choice of muscle flaps for large pelvic defects may be augmented by perforator flaps for defects involving mainly superficial skin and soft tissues.

Free flap Given the number of reliable local flap options, microsurgical tissue transfer is rarely indicated. In extenuating circumstances, however, large composite flaps of skin and muscle from the thigh can be elevated and re-anastomosed using gluteal recipient vessels.15 Alternatively, the latissimus dorsi muscle can be harvested on the thoracodorsal vascular system and anastomosed to the gluteal vessels.

Minimally invasive flap harvest The rectus flap has emerged to be a workhorse in perineal reconstruction in these settings, as it brings in well-vascularized tissue to an often-irradiated bed with a large amount of dead space. However, the traditional rectus flap harvest involves a midline laparotomy. Minimally invasive abdominoperineal resections and pelvic exenterations are increasingly being used to limit morbidity. In these settings, some groups have explored the possibility of harvesting the rectus flap in a similarly minimally invasive manner. Early experiences focused on endoscopic-assisted harvests. In 1996, Bass described using a balloon dissector to create a plane between the posterior sheath and rectus muscle, followed by CO2 insufflation and rectus harvest.68 Subsequently Friedlander et al. utilized a tripod device to improve visualization during minimally invasive rectus harvest in cadavers.69 Both of these techniques utilized incisions through the anterior sheath. The first clinical case of laparoscopic harvest was performed by Greensmith in 2000.70 In their transperitoneal approach, the rectus is harvested by taking down the posterior sheath. Therefore, no incisions were made in the anterior sheath, decreasing the risk of hernia formation. More recently, Winters et al. reported on the results of robotic total pelvic exenteration in conjunction with a laparoscopic harvested rectus flap.71 Yet another advancement is the use of the robot in rectus flap harvest. Selber reported their experience with the Intuitive Surgical robot, with harvest times of 45 minutes and incisions limited to three ports, totaling 2 inches in length (Video 17.1 ).72 Further collaboration with colorectal and plastic surgeons has shown continued dedication in describing the utility and safety of robot-assisted rectus abdominis muscle harvest for pelvic reconstruction in a recent case series.73,74

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Special considerations – sphincter reconstruction For treatment of rectal cancers in patients seeking to avoid colostomy, some centers have advocated resection with sphincter reconstruction as a strategy. Historically, anal sphincter reconstruction with gluteus maximus muscle was described. But this has been supplanted by functional transfer using one or two gracilis muscles wrapped around a perineal colostomy; this has shown some success, although the morbidity of this approach is high.75 Early authors in the 1950s encountered issues generating resting sphincter tone when using a voluntary muscle to perform an autonomic smooth muscle function. This was addressed using an implantable electrical stimulator (electrically stimulated dynamic graciloplasty), but a high complication rate ultimately led the manufacturer to withdraw the device from the US market in 1999.76 Evolution of this approach has continued in Europe where the device is still available, but one meta-analysis has shown more favorable results using an artificial bowel sphincter (Acticon Neosphincter, American Medical Systems, Minnetonka, MN).77 All methods of sphincter preservation or reconstruction carry a significant (30% to 100%) risk of complications, and a consensus is still not available on the best of these alternatives. The sparse literature regarding graciloplasty may be in part due to the advancements in the colorectal field, as the need for sphincter reconstruction may lessen as indications for sphincter preservation and indications for APR change.78 Or else despite the ability to perform sphincter reconstruction, the traditional abdominal colostomy has been advocated as still having the lowest complication rate for this group of patients.79

Postoperative care The management of these patients follows the basic tenets of surgical postoperative care. A key principle is to avoid excessive pressure on the flap, as this can lead to venous congestion and flap loss. The authors have the patients on bed-rest for several days, followed by progressive ambulation. However, the patients are instructed not to sit upright for several weeks. Drains are typically placed in both the donor site and the perineum. Deep venous thromboprophylaxis in the form of sequential compression devices and subcutaneous heparin is used. Nutrition must be optimized. The patient is seen regularly by all involved teams postoperatively.

Outcomes, prognosis, complications It is important to emphasize that reconstruction of the perineum cannot eliminate complications. In fact, multiple series highlight complications even in the best of circumstances; what has improved with advances in the state of surgical treatment has been the complication profile. In earliest descriptions, extensive abdominoperineal resections and exenterations were accompanied by significant mortality, small bowel obstruction, small bowel fistulae, pelvic abscesses, perineal hernias, and profound interstitial fluid losses through what frequently became a chronic draining

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perineal wound. In contrast, when flaps are used, the small bowels are separated from the radiated pelvic basin, which dramatically reduces or eliminates all these major sequelae in every major series.19,20,40,80 Complications remain at a ­significant incidence of 5%–33% overall, but these manifest a shift toward minor complications. Still present are delayed wound healing at the inset incisions, seromas, or superficial

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dehiscence or infection, but none of these normally requires re-operation. Understanding the vulnerabilities of the ­surgical site and the clinical outcomes data makes it possible to deploy a reliable reconstructive plan that addresses each defect in a patient-specific manner according to the needs of the wound, as well as to limit complications and make perineal reconstruction a relatively safe, optimized process.

References

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67. 68. 69. 70. 71. 72. 73. 74.

75. 76. 77. 78. 79. 80.

“supra-fascial” lotus petal flaps. J Plast Reconstr Aesthet Surg. 2015;68(1):e7–12. Haddock NT, Greaney P, Otterburn D, Levine S, Allen RJ. Predicting perforator location on preoperative imaging for the profunda artery perforator flap. Microsurgery. 2012;32: 507–511. Allen JR Jr, Lee ZH, Mayo JL, Levine J, Ahn C. Allen RJ Sr. The profunda artery perforator flap experience for breast reconstruction. Plast Reconstr Surg. 2016;138:968–975. Largo RD, Chu CK, Chang EI, et al. Perforator mapping of the profunda artery perforator flap: anatomy and clinical experience. Plast Reconstr Surg. 2020;146:1135–1145. Chen YC, Scaglioni MF, Kuo YR. Profunda artery perforator based V-Y rotation advancement flap for total vulvectomy defect reconstruction--a case report and literature review. Microsurgery. 2015;35:668–671. Kosutic D, Bullen T, Fulford P. Profunda artery perforator flap for perineal reconstruction: a new indication. Microsurgery. 2016;36(7):615–616. Bass LS, Karp NS, Benacquista T, Kasabian AK. Endoscopic harvest of the rectus abdominis free flap: balloon dissection in the fascial plane. Ann Plast Surg. 1995;34:274–279. discussion 279–280. Friedlander LD, Sundin J. Minimally invasive harvesting of rectus abdominis myofascial flap in the cadaver and porcine models. Plast Reconstr Surg. 1996;97(1):207–211. Greensmith A, Januszkiewicz J, Poole G. Rectus abdominis muscle free flap harvest by laparoscopic sheath-sparing technique. Plast Reconstr Surg. 2000;105:1438–1441. Winters BR, Mann GN, Louie O, Wright JL. Robotic total pelvic exenteration with laparoscopic rectus flap: initial experience. Case Rep Surg. 2015;2015:835425. Pedersen J, Song DH, Selber JC. Robotic, intraperitoneal harvest of the rectus abdominis muscle. Plast Reconstr Surg. 2014;134:1057–1063. Hammond JB, Howarth AL, Haverland RA, et al. Robotic harvest of a rectus abdominis muscle flap after abdominoperineal resection. Dis Colon Rectum. 2020;63(9):1334–1337. Haverland R, Rebecca AM, Hammond J, Yi J. A case series of robot-assisted rectus abdominis flap harvest for pelvic reconstruction: a single institution experience. J Minim Invasive Gynecol. 2021;28(2):245–248. Rulllier E, Zerbib F, Laurent C, Caudry M, Saric J. Morbidity and functional outcome after double dynamic graciloplasty for anorectal reconstruction. Br J Surg. 2000;87:909–913. Cera SM, Wexner SD. Muscle transposition: does it still have a role? Clin Colon Rectal Surg. 2005;18:46–54. Ruthmann O, Fischer A, Hopt UT, Schrag HJ. Schließmuskelprosthese vs. Ersatzmuskelplastik bei hochgradiger Stuhlinkontinenz? Chirurg. 2006;77:926–938. Denost Q, Rullier E. Intersphincteric resection pushing the envelope for sphincter preservation. Clin Colon Rectal Surg. 2017;30: 368–376. Fischer A, Tarantino I, Warschkow R, Lange J, Zerz A, Hetzer FH. Is sphincter preservation reasonable in all patients with rectal cancer? Int J Colorectal Dis. 2010;25:425–432. Lefevre JH, Parc Y, Kerneis S, et al. Abdomino-perineal resection for anal cancer impact of a vertical rectus abdominis myocutaneus flap on survival, recurrence, morbidity, and wound healing. Ann Surg. 2009;250:707–711.

SECTION III   •  Burn Surgery

18 Burn, chemical, and electrical injuries Raphael C. Lee and Chad M. Teven

SYNOPSIS

Risk factors













ƒ Review diagnostic criteria for the different types of burn injuries. ƒ Review the pathogenesis of the different types of burn injuries. ƒ Review first aid management of burn patients. ƒ Relate extent of burn injury and magnitude of the physiologic stress response. ƒ Review acute management of burn patients, including fluid, nutritional, and wound care. ƒ Review burn wound management. ƒ Learn indications for wound debridement, wound dressing and splinting, and skin grafting. ƒ Discuss advances in rehabilitation of burn trauma survivors. ƒ Aims of burn care: • Rescue: Stop the burn trauma process and provide basic life support. • Resuscitate: Restore vital organ function. • Refer: Triage and possibly transfer to a burn center for multidisciplinary intensive care. • Resurface: Close open wounds as soon as possible. • Reconstruct: Replace damaged anatomic structures. • Rehabilitate: Recover, as far as is possible, physical, emotional, and psychological well-being.

countries where prevention programs are almost non-existent. The international median burn injury death rate is 0.9–1.2 per 100,000 inhabitants per country. In addition, the cost to society in terms of lost wages, acute medical care, and rehabilitation is significant. In 2009, the WFSC noted that the economic direct cost of fire-related losses ranged from 0.06%–0.26% of countries’ gross domestic product (GDP) with the indirect cost ranging from 0.002%–0.95% of GDP. In economically developed nations, 1%–2% of the population receives a burn injury annually, and 10% of those require professional medical attention. Roughly, 10% of those requiring medical attention have major burns that require burn center management.

Epidemiology The capability to produce fire (ca. 900,000 BCE) provided humans with transformative new capabilities that advanced human civilization, but there have been consequences. According to the most recent statistics compiled by the World Health Organization and the World Fire Statistics Center (WFSC), fire causes roughly 6.6 million major burn injuries and 400,000 burn-related deaths every year.1 Major burn trauma is a disease of the poor and disabled. The majority of cases occur in poor neighborhoods and in low-income

Clinically debilitating and life-threatening burn injuries are far more common in economically under-developed communities and nations. Lack of education and awareness regarding the consequences of burn injuries and basic strategies to prevent burn injury are major risk determining factors. In addition to poverty, substance abuse or/and mental illness are significant burn risk factors. For adults, these details include alcoholism, opiate use, senility, psychiatric disorders, and neurological disease such as epilepsy.2 Of course, some types of employment are associated with higher risk of burn injury. Children under 5 years old are also particularly susceptible to burns and account for 75% of all pediatric burns. Scald burns account for about two-thirds of childhood burn injuries.

Evolution of burn medicine Beginning at least 3000 BCE, human suffering from burn trauma resulted in efforts to identify therapies to ameliorate burn morbidity and mortality. In the earliest medical handbook identified (ca. 3rd millennium BCE), an anonymous Sumerian physician documented several burn remedies

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based on plant extracts. Fifteen hundred years later (~1534 BCE), the Egyptian Ebers Papyrus described a topical compound for treatment for burns consisting of extracts of frog, mud, cow dung, ram’s horn, lemon strips, and a variety of other ingredients.3 Around 600 BCE, Sushruta first described classic symptoms associated with severe burn injury including thirst and fever. He was also the first to recommend surgical debridement for burns resulting in loose skin and flesh. The Old Testament of the Bible (Leviticus 13:24–28) lists burn injury of the skin among other dermatologic illnesses. Around 500 BCE, Chinese physicians were using a mixture of tea leaves to treat burns. But the oldest preserved written Chinese scientific description of burn wound treatment dates back to Hong Ge (281–341 CE). His book Zhou Hou Fang (Prescriptions for Emergency) suggested the topical application of two different prescriptions: old (imperative) calcarea optionally blended with plant oil, or the use of pig fat cooked with willow bark.4 The application of these mixtures resulted in reduced numbers of wound infections and has to be regarded as the oldest preserved Chinese description of an anti-infectious astringent to be used in thermal injuries. Hippocrates (460–377 BCE) also wrote extensively on burns. He recognized that significant fluid loss occurred at the burned surface as fluid egressed from blood vessels to form blisters. He also described several aspects of burn management, including hydrating the patient, topical occlusive dressing with tree bark extract containing salicins, and surgery for the most severe cases. Perhaps most importantly, Hippocrates advocated that wound care be performed in aseptic conditions and as quickly and painlessly as possible. Centuries later, the 16th-century German physician Fabricius Hildanus was the first to classify burns into three categories that could be used to guide treatment.5 Around this time, the French surgeon Paré also described areas of the body prone to burn contracture and advocated for early excision of the burn wound. Richter (1788) later wrote on the relationship between burn wound size and prognosis.6 Debates would continue for centuries about how to best classify and treat burn wounds as well as about which factors – in addition to burn wound size – must be considered when predicting outcome. Major advances were made in burn care in the 19th century. The first dedicated burn center opened in 1848 when James Syme, a burn surgeon at the Royal Infirmary in Edinburgh, designated one building for all burn patients. Additionally, physicians described excision of burnt tissue and skin grafting, which led to an important publication in JAMA (1905) advocating for early skin grafting.7 Physicians also began to appreciate the importance of intravenous fluids in acute burn management after Tappeiner (1881) demonstrated that burn physiology results in a hemodynamic picture similar to that of acute pancreatitis.8 Clearly, the largest strides in burn care advances have been made in the last century. Sentinel events such as the World Wars and the discovery of antibiotics facilitated major change in medical and surgical care of burns. During World War I, the British plastic surgeon Sir Harold Gilles performed the first successful autograft. His work also facilitated improved techniques for tangential excision of burned skin, donor site harvest, meshing of skin grafts, and the use of cadaveric grafts. In the 1930s, the Yale surgeon Frank Underhill reported that hypovolemic burn shock occurred in major burn patients and was essentially due to trans-capillary leakage that was

eventually found to be caused by the release of damage associated inflammatory mediators into the systemic circulation.9 Through this process, burn shock may result in decreased intravascular volume, inadequate tissue perfusion, and early post-burn mortality. Stanley Levinson, a surgery resident in Boston at the time, similarly observed that large surface area burn patients often lose fluids at a rate incompatible with life. Drs. Oliver Cope and Francis D. Moore proposed to administer fluid resuscitation, including proteins, at a rate that was linked to the percentage of body surface area burned.2,10 Therefore, he advocated for adequate fluid resuscitation as a cornerstone of acute burn care. Charles Baxter at the Parkland Hospital in Dallas promoted the use of lactated Ringer’s solution over colloid to avoid pulmonary edema. This is called the Parkland Burn Resuscitation Formula.11 Another important shift in burn care was borne from Levinson’s comprehensive description of the pathology and effects of smoke-inhalation injury. This research has led to advances in treating patients with smoke-inhalation injury as well as the initiation of public health safety measures to decrease the risk of smoke inhalation including the development of smoke detectors. The recent improvements in burn care are largely the result of the comprehensive treatment of burn patients in dedicated burn units and a team approach to burn care. Multidisciplinary teams consisting of plastic or general surgeons, intensivists, psychiatrists or psychologists, nurses, dietitians, therapists, pharmacists, social workers, and spiritual leaders are now the standard at burn centers. In addition, a better understanding of acute burn resuscitation, wound care management, and early excision and skin grafting in severe burns has reduced the mortality rate associated with burns.

Pathophysiology of burn injuries Stedman’s Medical Dictionary lists more than 22 types of burn injury including thermal, chemical, electrical, friction, cement, and other “burns”.12 The pathogenesis of each burn type is quite distinct, which causes some confusion because they are all labelled burn injuries. What they do have in common is that the process begins with damaging molecular structure of tissue. Although the treatment of these different injuries would have aspects in common, there are differences that address the specific pathogenesis.

Thermal (high temperature) burns A thermal burn results when tissue temperature exceeds the level in which molecular kinetic energy exceeds the bond energies that stabilize biomolecular structure.13,14 This results from conduction, convection, and/or radiative heating and are usually not spontaneously reversible, although immediate cooling can modify some critical aspects. Thermal burn injury may also result from internal heat generation in diseases such as malignant hyperthermia. The extent of tissue heat damage depends on the tissue type, the immediate tissue temperature history, and the amount of preconditioning. Cells have the capabilities to increase their tolerance to heat stress through an adaptive preconditioning process. This process involves upregulating synthesis of stress proteins that repair or remove heat-damaged molecules, seal membrane disruptions, and suppress oxidation stress. Only when the

Pathophysiology of burn injuries

503

Depth of burn injury 1000 3º

Time (seconds)

100 2º 10 1 Pain threshold

0.1 0.0 44

48

52

56 60 Temperature (°C)

64

68

72

extent of thermal damage exceeds cellular repair capabilities does loss of cell and subsequent tissue viability result, which manifests as a burn injury.14 Basically induced thermal tolerance increases cellular injury repair rates, thus allowing tissues to subsequently survive more than normal heat exposure. Characteristic molecular alterations that occur at supraphysiological temperatures include disruption of cell membranes, aggregation of unfolded proteins, onset of a cellular oxidative stress response to unfolded proteins in cellular organelles and in the cytoplasm, and extracellular damage to collagen, non-collagenous proteins, and activation of degradative proteases, vascular disruption with hemorrhage, blood coagulation, and dehydration. Of course, the skin temperature history (i.e., magnitude and duration) in nearly all cases of skin burn injury is anatomically non-uniform, which results in a non-uniform distribution of thermal burn injury and is clinically classified according to skin burn depth (Fig. 18.1).

Flash and flame burns Although the tissue damage mechanisms associated with “flash” and “flame” burns are similar, they are used in different ways. Both flame and flash phenomena pertain to hot, ionized combustion aerosols emanating from a fire or explosion. Flash and flame burn injuries are the most common cause of adult burn admissions. Flame burns result from exposure to heat produced by an ongoing fire. The exposure likely involves longer contact time because it involves a human response time. This results in deeper burn injuries such as partial- and full-thickness skin burns. In contrast, flash burns result from brief exposure to a propagating thermal energy pulse emanating from ignition of flammable gases, high-energy electrical arc (Fig. 18.2), or ionizing radiation. Although the temperatures of arc or flash may reach 10–20 thousands of degrees, they are composed of gases with very low heat capacity which means the efficiency of heat energy transfer is fortunately low. Because of this and the brief exposure, flash burns usually do not penetrate clothing. Typically, flash burns are manifested only on exposed areas of skin and are superficial.

Scald burns Scald burns result from skin contact with hot liquid or steam. In modern societies, scald burns are second in incidence to

Figure 18.1  The importance of both temperature and time in determining the depth and extent of injury is illustrated by this curve. The threshold for feeling pain precedes injury, and sensation is lost once all cutaneous pain receptors are burned. The data is adapted from various models.

Figure 18.2  Photograph of a gasoline flame burn to the neck and face illustrating the non-uniform heat exposure corresponding to depth of injury from deep partial to epidermal.

flame burns. Most often, the burns result from a cooking accident and often involve a mixture of water and grease. Tragically, children are the most common victims. Scald burn depth is often more difficult to clinically judge because scalds are lower temperature thermal injuries than flame injury (Fig. 18.3). This is particularly true for patients with darker skin. Thus, scald-injured skin’s structural changes are less noticeable compared to flame burns unless there are petechial hemorrhages visible indicating rupture of mid-dermal and subdermal microvasculature. In the absence of petechial hemorrhage, the depth of scald burn skin injuries is often not visually apparent for 48–72 hours when the manifestation of autolytic degradation is obvious. Duration of hot liquid contact is a major deterministic factor in the depth of burn in scald injuries. Thus, hot water immersion scalds are typically deeper than a hot water spill scald with liquid at the same temperature.15 Skin surface contact with 60°C (140°F) water creates a deep dermal burn in 3 seconds but will cause the same injury in 1 second at 69°C (156° F). Also, the burn tends to be a bit deeper in skin folds and clefts. Scald burn damage kinetics depend on the barometric pressure, being slower in higher altitudes than at sea level. Unless superheated at pressures higher than 1 atmosphere or in a

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CHAPTER 18  • Burn, chemical, and electrical injuries

A

B

Figure 18.3  Typical appearance of superficial skin burns from (A) low energy electrical arc flash and (B) sunburn.

microwave, the maximum skin temperature reached in hot water can be 100°C at sea-level. Also, because wet skin cools by evaporation, the duration of tissue contact with scalding temperatures depends on factors that limit evaporation rate such as clothing, oil, or other water vapor barriers. If the water contains oils or lipids, as in soups, evaporative cooling is slowed, resulting in longer burn duration and a deeper skin injury.

Hot object “contact burns” Contact burns involve mechanical contact with a hot, thermally conducting object (e.g., cooking pan or radiator). Domestic contact burns are caused by direct mechanical contact with lit cigarettes, space heaters, stoves, ovens, irons, exhaust pipes, etc. Resultant burn depth depends on the capability to transfer heat energy to the skin. Thus, skin contact with a hot metal rod can be expected to produce a deeper burn than a hot plastic rod at the same temperature. Contact burns are often associated with workplace-related hands, patients prone to seizures, and use of intoxicating substances. They are also seen in elderly people after a loss of consciousness; such a presentation requires a workup of the cause of syncope. In the industrial setting, contact burns commonly result from contact with hot metals, thermoplastic composites, glass, or coals. Because the heat energy transfer is large, contact burns often involve full-thickness skin and subcutaneous tissue.

Tar and asphalt burns Hot tar and asphalt burns occur in workers engaged in surfacing pavement and roads, roofing, and other industrial applications. Tar is an oil composite that solidifies when cooled to body surface temperatures. When hot tar makes contact with skin, it adheres and solidifies in the wound making it difficult to remove without causing further injury. The tar usually retains sufficient heat to produce prolonged damaging temperatures resulting in deep skin burns.16 Tar itself is also chemically toxic to tissues. Often, the tar is cool by the time the patient arrives at the medical facility. Injuries typically occur on the exposed skin

of the face and extremities, and the burn is of variable depth ranging from deep partial to full thickness.

Electrical injury Electrical injuries represent 3%–5% of burn trauma admissions. However, injuries are often among the most devastating and therefore challenging to manage. Electrical injuries are more difficult to clinically assess because tissues can be injured by either or both thermal and non-thermal injury processes.17,18 Furthermore, various modes of electrical injuries can result from electrical current exposure at any frequency in the electromagnetic spectrum (Table 18.1). The abbreviation “DC” (i.e., direct current) indicates the current frequency to be zero, the current flows constantly in one direction, and “AC” (i.e., alternating current) indicates that the current is changing direction of flow (i.e., alternating polarity) with time. The injury mode(s) depend on the voltage, power capacity, and frequency of the power source. The vast major of electrical shock patients seeking medical attention have had contact with commercial electrical power sources which operate between 50 and 60 Hz (i.e., 1 Hz = 1 wave cycle per second). However, electrical power in the form of radiowaves, microwaves, infrared, visible, and ionizing irradiations are also capable of inflicting injury, and they each have unique pathophysiology and clinical manifestations. At frequencies greater than approximately 50,000 Hz (i.e., low frequency radio waves), electrical power can radiate across air gaps from the power source into the body. However, the body does not absorb ambient radio waves very efficiently, so very high power is needed to cause injury. However, a thermal burn injury can result when direct mechanical contact is made with an energy low radiofrequency power source. Electrocautery devices used for surgical procedures operate in the low radiofrequency range. At much higher frequencies, mechanical contract with the conductor is not required for tissue injury. Common domestic microwave ovens operate in the gigahertz frequency range (109 Hz), and infrared food warmers operate in the terahertz (1018 Hz) range. Although they induce electrical current flow in tissues, these devices cause injury by heating rather than cellular disruption by electrical forces

Pathophysiology of burn injuries

Table 18.1  Electrical shock by frequency

Frequency range “Low frequency” (DC – 10 kilohertz)

505

Table 18.2  Thresholds for electrical current effects

General applications

Tissue injury pathway

Physiological consequence of50– 60 Hz current (path: hands to feet)

Threshold current (milliamps)

Commercial electric power; battery power

Joule heating; cell membrane electroporation of nerve and skeletal muscle cells

Tingling sensation/perception

1–4

“No let go”(i.e., hand and forearm skeletal muscle tetany)

16–20

Respiratory muscle paralysis

20–50

Cardiac arrhythmia (possibly VF)

50–120

“Radiofrequency” (10 kilohertz to 10 megahertz)

Radiocommunication; diathermy; electrocautery

Joule heating; dielectric heating of proteins

“Microwave” (10 megahertz to 10 gigahertz)

Microwave heating

Dielectric heating of free water

Terahertz

Industrial and Dielectric heating biomedical imaging of bound water and applications proteins

“Light and ionizing” (1015 hertz and higher)

Photo-optical and ionizing irradiation (ultraviolet, X-ray, gamma, etc.)

Heating and direct protein damage; oxidative damage

(i.e., electroporation). Accidental brief microwave and infrared radiation burns are usually superficial. To summarize the effects of electrical shock over a range of electrical field frequencies, Table 18.1 presents a classification of electrical injury according to frequency regime. Electrical shocks from commercial electrical power are the second most common cause of workplace injury. The clinical manifestations depend on the amount of electrical current, the duration of contact, and the anatomic path of the current through the body. When relating the amount of current to the contact voltage, the length of the current path between electrical contact points, the resistance of skin coverings such as gloves, shoes, and clothing are essential to consider. With moist skin, the VLF electrical resistance of a current path from one hand to the other is about 1000 ohms and from hand to both feet is about 750 ohms. The highly resistive epidermal layer is instantly penetrated by voltages greater than 60–100 volts. For triage purposes, electrical shock injuries are often categorized as “low-voltage” or “high-voltage” depending on whether the contact voltage is below or above 1000 volts, respectively. The scientific basis for this stratification is not clearly defined, but it does correlate with the probability that arc-mediated electrical contact will precede direct body mechanical contact with the energized conductor. For low-voltage shocks, direct mechanical contact with the power source is usually required to initiate current flow, whereas for high-voltage shocks, the current begins to flow through an electrical arc before mechanical contact is made. Some have proposed a mid-voltage (i.e., 400–1000 volts) shock category which makes medical sense in terms of predicting therapy and prognosis.17 In addition, other important injury-determining factor parameters are duration of electrical contact and the anatomic path of the current through the body. For example, although static electrical shocks typically involve more than 1000 volts, they

do not cause injury because the current is small and it only passes on the outer surface of the body. If mechanical contact with the power source occurs, it can be difficult to impossible to voluntarily disconnect from the contact because the skeletal muscle stimulation is dominated by the electrical shock current rather than the central nervous system. Thus, shock times are typically longer in low-voltage shocks. Electrical shock by commercial electrical power can produce a range of neuromuscular effects (Table 18.2). Of course, the most life-threatening is the immediate risk for cardiopulmonary arrest when the current passes through the heart, especially during the myocardial repolarization phase. In the case of contact with an energized high-voltage conductor, electrical arcing will mediate electrical current flow to the victim before mechanical contact. This introduces a third mechanism of injury: mechanical trauma from the thermoacoustic blast. This is a particularly important mechanism of injury and mortality in short circuits involving very high capacity electrical power in a closed space. The gases released from the arc will further short circuit paths that generate thunderous pressures and temperatures. High-voltage contact arcs can reach very high temperatures leading to corneal burns and clothing ignition. A common misconception is to identify skin contact wounds as “entrance” and “exit” wounds. The skin contact wounds resulting from passage of commercial AC current are all “entrance” and “exit” wounds because the current travels in and out of each body contact (Fig. 18.4).18 If the skin is wet, especially from salt water, the skin’s electrical resistance drops allowing subcutaneous tissue damage to occur without skin burns. For electrical shock injury, the skin surface area damage is not reflective of the injury extent. The damage is more volumetric and scattered along the current path, often requiring diagnostic imaging to locate and quantify (Fig. 18.5). Peripheral nerve and skeletal muscle tissues are most vulnerable to the damaging effects of the electrical field during electrical shock. Just 14–16 milliamperes of current passing through the forearm induces tetanic contractions of muscles controlling handgrip, which may prevent a person from voluntarily releasing the electrical conductor (see Table 18.2). Joint dislocations and fractures may result from the muscle spasm as well. A current of 50 milliamperes or more passed through the chest can result in cardiopulmonary arrest within 1 second.19 Non-thermal electric injury to nerves and muscles can occur in milliseconds while taking seconds for burns to occur. Thus brief shocks commonly result in neuromuscular function disturbances in the absence of thermal burns.

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Figure 18.4  Appearance of a full-thickness electrical contact burns resulting from contact with AC electrical power. All contacts are entrance points, and all are exit points because the current is alternating direction of flow during the shock.

Figure 18.5  MR imaging of an electrical injury to the scalp to visualize the extent of tissue damage and secondary edema formation.

Disruption of skeletal muscle membranes leads to release of myoglobin and hemoglobin that enter the circulation and muscle edema, which results in muscle compartment syndromes. Release of myoglobin into the urine is a characteristic feature of severe electrical shock injury. Renal failure may result from intrarenal aggregation of myoglobin. Direct electrical shocks to the head may cause increased intracranial pressure as well. Case reports of electrical injury also have been reported secondary to cardioversion.19 Lightning is another common form of electrical shock. Approximately 200 deaths occur per year in the United States due to lightning injury. Most of the lightning current passes along the skin surface and around the body to ground through the lightning arc. There are often superficial epidermal burn marks that have a characteristic fern-leaf pattern, but the burn does not extend into the dermis for various reasons. Cardiac and central neurological arrest often occurs due to the magnetic pulse-induced electrical currents. Transient central and peripheral neurological arrest is called keraunoparalysis that causes delay in recovery of brain function as well as autonomic nervous system malfunction.20 CNS viability signs are not useful to guide CPR efforts. Thus, CPR should be continued longer than for other causes of cardiac arrest. Peripheral autonomic neurological malfunction can persist for longer time periods in lightning injury survivors.

Radiation Injuries Radiation injury results from tissue absorption of either ionizing or non-ionizing radiating electromagnetic waves or both at doses above tissue tolerance. Sub-atomic particle beam irradiation is classified as ionizing irradiation because it can ionize molecules that absorb the particle. Radiation effects on tissue are dependent on both fraction of the radiation energy absorbed and the relative biological effectiveness of the absorbed radiation on the tissue. Both of these factors depend on the tissue type, water content, oxygenation, and other variables. Regarding non-ionizing radiation, such as infrared or microwave radiation, the radiating energy is absorbed by tissue molecules resulting in tissue heating. Light is absorbed at the sub-molecular level, resulting in heating and shifts in electron orbitals, but does not have enough energy to ionize the molecule. Intense laser light may cause thermal burns or explosive water boiling to disrupt tissues. Non-ionizing radiation from a hot fire or an electrical arc is a frequent cause of industrial thermal burns. Ionizing radiation transmits higher energy and shorter wavelength than non-ionizing radiation. Ionizing radiation disrupts atomic structure and causes chemical reactions in the tissue. In tissue, water is the primary absorber. Ionizing

Pathophysiology of burn injuries

irradiation causes water and molecular oxygen to react and produce hydroxyl radicals with an unpaired electron in the valence shell. Unpaired radicalized electrons on the outer shell are very reactive with other biomolecules causing damage to DNA, proteins, lipids, etc. Most commonly, the cell and extracellular matrix damage is caused by generation of hydroxyl (OH*) free radicals in oxygenated water.21 The higher the tissue water and oxygen content, the greater the radiation-induced cell injury. The intensity of ambient ionizing irradiation energy to which a person can be exposed is measured in Roentgens (R); the amount absorbed into the tissue is measured in Gray (Gy). For a typical person, absorbing X-ray or gamma-ray doses greater than 5 Gray (Joules/kilogram) to a body part like the hand or scalp causes molecular alterations in proteins and nucleic acids that results in radiation fibrosis or burns. With preconditioning that upregulates DNA repair and intracellular protein removal mechanisms, higher doses of radiation could be better tolerated by tissue. Total body absorption of more than 2–3 Gy is associated with a high mortality rate.22 The most common cause of radiation burn is heavy sun exposure. Sunlight produces a wide spectrum of radiating energy from infrared to cosmic energies. In typical sunburn, it is the heavy dose of the infrared heating and ionizing ultraviolet (UV) that does the most damage. Cosmic irradiation also contributes. UV radiation produces aqueous phase oxidative free radicals in the epidermis and dermis. When free radical scavenging mechanisms are exceeded, biomolecular damage occurs. It is rare that the burn depth is greater than epidermal or superficial dermal. Also, nucleic acids are able to directly adsorb some wavelengths of UV radiation known as the UVB wavelength spectrum. UVB radiation causes direct damage to DNA in the form of cross-links and double-stranded breaks. If this damage is not reparable by the cell the result is an increased risk of cell death or malignant transformation. Clinical manifestations are painful partial-thickness burns and blistering. Sunscreen lotions absorb the UV and increase the

amount of sun exposure required to cause a burn. However, until recently they did not totally shield the entire UV range. There is some evidence that use of narrow-band (i.e., UVB) sunblock is associated with other long-term consequences related to prolonged exposure to DNA reactive irradiation outside of the blocked UVB band. Radiation injuries also occur from therapeutic, accidental, space travel, or military use of ionizing irradiation. The molecular target of the radiation depends on the type of radiation.23 Severe immune compromise due to neutropenia and bleeding secondary to thrombocytopenia are seen over a period of 3–5 weeks. At higher levels of exposure (30–100 Gy), the membranes of cells, even non-proliferating nerves and muscle, are damaged leading to loss of tissue viability within 6–24 hours. Radiation injury during space travel is a major unsolved problem. Outside of planetary magnetic fields, the electrons emitted from the sun at relativistic speeds would certainly cause burns and must be shielded. Also, subatomic particles, especially fragments of heavy metal nuclei (High Z), traveling through space are almost impossible to shield.23 Of course, such High Z radiation would damage tissue. Basic differences between modes of cellular burn injury can be appreciated in Fig. 18.6.

Frostbite Tissue tolerance to hypothermic temperatures is tissue type specific. Neurological and neuromuscular tissues stop functioning at temperatures less than 21°C for more than 20–30 minutes because electrical and chemical signaling stops working. Skin tolerates hypothermia for longer time frames (i.e., 19–24 hours). At temperatures below freezing the mechanism of injury changes. Freezing with ice formation in any tissue causes damage by disrupting cell membranes and denaturing cellular proteins. Frostbite is a clinical diagnosis applied to tissues injured by freezing. Freezing temperatures result in disruptive

Tissue cell before injury + - + + +-

+ + + +-

S1

P1

S1

S2

P2

P1 + - + + + --

+ - + ++-

S P1 2

P1

P2

P2

S1 P1

S1

S1

+ - ++ +- -

S2 P1

+ - + + +-

B

C

+ - ++ +-

+

- + ++ -

S1

+ +++ -- -

- + +++ -

A

After radiation injury

+ ++ + -- --

After electrical injury

++ ++ - --

After thermal injury

507

Figure 18.6  Schematic illustration of the different molecular manifestations of thermal, electrical, and radiation burn trauma.

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CHAPTER 18  • Burn, chemical, and electrical injuries

intracellular ice formation and denaturation of proteins.24 Ice formation in tissues concentrates electrolytes around proteins that leads to protein unfolding and aggregation. Tissue freezing also dehydrates cells in addition to promoting ice crystal propagation through cell membranes. The thaw cycle also causes injury by osmotic rupture of tissue cells that survived the freezing process. Loss of circulation in the frozen tissue, as well as the reperfusion consequences on rewarming, also contribute substantially to the molecular denaturation of frostbite injury. Demographically, the majority of frostbite cases arise in the homeless or disabled populations in climates with cold winters. Ethanol consumption accelerates cool-down by increasing vasodilatation and rapid heat loss.25 Most commonly, distal extremities, ears, and other ambient air-exposed areas of the face are involved.26

Burn injury in children Burn injuries in children typically involve home cooking accidents. Another 10% of pediatric burns are due to non-accidental injury, and these burn victims will occasionally have other non-burn-related trauma.27 Diagnosing pediatric burns also involves an investigative component to understand the risk factors that precipitated the burn. A social history is extremely important. Abuse is more common in poor households with single or young parents. Detecting these injuries is important, as many children who are repeatedly abused eventually suffer a fatal injury. Usually children less than 3 years old are affected. As with other non-accidental injuries, the history and the pattern of injury may arouse suspicion (Fig. 18.7). Burn center care with experienced pediatric burn resuscitation and pain management is more important than for young adults.

Chemical injuries and burns Chemical injury occurrences are roughly equally distributed between industrial and domestic situations. They most commonly result from inadvertent contact with toxic polishers, paints, cleaners or solvents. Cement burns make up approximately one-quarter of all chemical burns.28 Current classification of chemical burns began with the efforts of Carl Jelenko III, who proposed stratification of chemical injuries into six broad categories based upon mechanism of action: reducing agents, oxidizing agents, corrosive agents, protoplasmic poisons, desiccants/vesicants, and acids/bases.29 The toxic chemicals involved are often strong acids or alkalis, especially in domestic disputes. Extent of tissue resulting from toxic chemicals are almost always dependent the concentration of the chemical, the duration of contact, mechanism of action of the chemical, and phase of the chemical agent (liquid, solid, or gas). The various mode of tissue damage range from redox reactions, corrosion, denaturation of proteins, disruption of cell membrane lipid bilayers, chelation of important ions, vesicants, and desiccants. Some chemicals actually cause thermal burns through exothermic reactions. Chemicals diffuse into tissues causing damage until they are inactivated by reaction with tissue and/or removed by therapeutic intervention or by blood perfusion of the tissue. Different taxic chemicals behave the differently when in contact with tissue. Tissue injury caused by strong acid spills are characteristically less deep than those caused by strong bases. Acids denature proteins and dehydrate tissues, which makes the tissue less permeable to the acid (i.e., tanning). Tissue injury resulting from contact with strong bases results in hydrolysis, peroxidation and liquefication of tissue lipids. This facilitates tissue penetration to cause deeper penetration and damage to tissues.29 Some toxic chemical injuries to the skin may appear superficial because of minimal discoloration, but are actually deep dermal or full thickness. An example of this type of chemical injury is caused by skin contact with wet cement ( i.e., calcium oxide [CaO]).

Acid burns Hydrochloric and sulfuric acids

Figure 18.7  The anatomic pattern of injury often provides clues to the cause of injury. The burn tideline is associated with sitting in a bath of hot water. The nonburned area in the center of the ring results from contact with the ceramic in the tub, which is a poor conductor of heat.

The most common acid burn injuries in humans result from contact with hydrochloric and sulfuric acids. These acids protonate glycoproteins and lipids, hydrolyze peptide bonds, and denature proteins. The result is denatured and dehydrated skin that resembles a thin, dry scab. Hydrochloric acid is often used in plumbing drain cleaners and in chemistry laboratories. Sulfuric acid has many industrial uses including lead–acid batteries, fertilizer, and wastewater processing. It is highly reactive against protein and lipids in water. It h ­ ydrolytically cleaves peptide bonds and deaminates amino side chains. Both of these acids irreversibly damage the protein or phospholipids leading to molecular denaturation, exposure of hydrophobic groups, coagulation, and dehydration. The skin is white and dry when the damage is superficial and partial thickness, forming a hard, dry eschar under which ulcers may form.

Physiological consequences of thermal skin burns

509

Nitric acid

Sodium hypochlorite

Nitric acid is widely used in industry, especially in organic synthesis, metallurgy, photoengraving, polyurethane manufacturing, etc. Human exposure and contact are common. Nitric acid is very corrosive resulting in protein denaturation and dehydration. It hydrolytically cleaves peptide bonds and deaminates amino side chains. Highly concentrated nitric acid contact rapidly results in a depressed tan-colored scab on the skin. It is usually partial thickness and painful.

Sodium hypochlorite, household bleach, is a common cause of chemical burns. The active metabolite is hypochlorous (OCl−), and toxicity arises from its oxidizing reactions on tissue. The severity of the injury is mostly dependent upon the concentration of the solution as opposed to the duration of exposure. Chemical skin burns from working with household bleach or hair treatment products can infect injury to the epidermis without significant immediate symptoms. Then hours later, painful blisters manifest. Very dilute hypochlorous acid (i.e., Dakin’s solution) is useful for cleaning contaminated wounds.

Chromic acid Chromic acid is commonly used in cleaning metal surfaces. This pungent, viscous, yellow liquid is made up of the active chemical metabolite chromic trioxide (CrO3) in a solution of strong sulfuric acid. Contact leads to a range of irreversible damage to tissue proteins, protein coagulation, blister formation, and ulceration. It reaches peak serum levels by 5 h post-injury. Once in circulation, CrO3 binds to hemoglobin and undergoes tissue uptake by the kidneys, liver, bones, lungs, and spleen within the first 24 h. Nephrotoxic damage leading to renal failure may result. Primary treatment consists of large volume water lavage for 15–20 minutes with a dilute solution of sodium hyposulfite. Then, rinse with buffered phosphate solution made up of 70 g of monobasic potassium phosphate and 180 g of dibasic sodium phosphate in 850 mL of water. Systemic manifestations are treated with 4 mg/kg of 2,3-dimercapto-1-propanol (dithioglycerol) given intramuscularly every 4 h for the first 48 h followed by 2 mg/kg daily for 1 week.

Hydrofluoric acid Hydrofluoric acid is used to etch glass. Exposure is particularly challenging to manage because fluorine is very electronegative. It strongly chelates calcium and thus penetrates tissue deeply, causing injury to nerves and muscles. Small splashes of high-concentration hydrogen fluoride products on the skin may not cause much inflammation or pain but may be fatal. Depending on the concentration and exposure duration of hydrofluoric acid, manifestations can be severe pain at the point of contact or a rash, which evolve into deep, slow-healing burns. Severe pain can occur even if no burns can be seen. Hydrofluoric acid can be toxic to the kidneys and lead to renal failure. Hand contact from hydrogen fluoride may result in persistent pain, bone loss, and injury to nail bed. Eye exposure to hydrogen fluoride may cause prolonged or permanent visual defects, blindness, or total destruction of the eye.

Alkali burns An alkali is a water soluble base compound that when mixed with water produces heat and hydroxide ions. This reaction with water produces a pH that is higher than neutral. Alkalis such as lime, sodium hydroxide, and potassium hydroxide are common in household-cleaning soaps and detergents. Hydroxyl ions oxidize lipids (i.e., saponification) to generate water-soluble lipids. In addition, alkalis act to alter protein structure and disrupt cellular membrane structure. Strong alkalis are highly cytotoxic.30

Cement (calcium hydroxide) Cement burns are a common injury that is classically seen in patients kneeling in concrete. There are many constituents of cement; however, calcium oxide accounts for 65% of the content in the most mixtures. It acts as both a desiccant and an alkali. Injury is caused when calcium oxide reacts with water to become calcium hydroxide. The hydroxide is a strong base and causes tissue injury.

Physiological consequences of thermal skin burns Most burns primarily involve the skin. While other tissues also suffer burns, this discussion will focus on skin burns. The skin is the largest organ of the body and serves multiple functions essential to our survival including (1) transport barrier against evaporative fluid and heat losses; (2) thermal regulation; (3) immune barrier against microbes and foreign chemicals; and (4) sensory receptors that provide information about environment. Burn injuries invariably disrupt these functions. If large enough, the consequences are life-threatening. Burn survival associated with burn injuries is strongly dependent on the age of the patient, the percentage of the entire body surface burned, pre-existing disease, and the presence or absence of smoke inhalation injury. Also, there are major socioeconomic factors. In economically under-developed countries and regions without access to an acute care medical center, death results from acute dehydration and hypothermia. In such locations, initial burn management must control dehydration and hypothermia using fabricated dressings until the patient can be transported to a local or regional medical facility. Without the support of a well-equipped medical facility, individuals that suffer major burn injuries are unlikely to survive more than a few days. In the United States, less than 25% of burn-related deaths occur after the patient arrives in the burn center.

Zones of burn tissue injury Skin burns resulting from contact with a hot object or flames experience a non-uniform temperature history and a nonuniform burn depth (Fig. 18.8). The observable pattern of thermal burn has been traditionally divided into three zones: (1) zone of coagulation; (2) zone of stasis; and (3) zone of hyperemia. These three skin burn injury zones were initially described by Jackson, Topley, and Cason in 1947.31 Each zone has distinctive

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SECTION III

CHAPTER 18  • Burn, chemical, and electrical injuries

Full thickness Partial thickness

Superficial burn

A

Superficial dermal burn

Zone of coagulation (necrosis) Zone of injury (edema and stasis) Zone of hyperemia

Deep dermal burn

Zone of coagulation (necrosis) Zone of injury (edema and stasis) Zone of hyperemia

B

Figure 18.8  (A) Flame burn on abdomen showing zones of injury. Dry full-thickness thermal burn coagulation is in the upper aspect of the wound. Away from the coagulation zone, the injury severity becomes progressively less. (B) Schematic showing zones of injury in deep and superficial dermal burns.

Physiological consequences of thermal skin burns

histological characteristics due to differences in extent of thermal damage to the cells and extracellular matrix. The zone of coagulation (ZoC) represents the most severely heat-damaged tissue with extensive denaturation and coagulation of tissue proteins, tissue dehydration due to exposure of hydrophobic proteins, and disruption of cell organelles of all tissue components include the vasculature. Collagen is the most abundant protein in skin, and it has a melting (i.e., denaturation) temperature of more than 77°C for more than a few seconds. Collagen denaturation is generally thought to be irreversible and requires surgical excision. Sometimes enzymatic debridement is adequate for ZoC contact burns small enough that excision and grafting are not necessary. Moving away from the ZoC area, the next zone of injury is the zone of stasis (ZoS). The ZoS is characterized by cellular swelling, partial extracellular matrix denaturation, and decreased vascular perfusion due to vasospasm. ZoS tissue typically manifests with a wet, pink haze appearance due to light diffracting through edematous and denatured extracellular matrix proteins. Initial resuscitation timing and strategy can influence the survival of tissue in the ZoS. Additional insults, such as ischemia, infection, or edema, can push tissue in this zone toward necrosis. With proper resuscitation and wound care, however, fibroblasts and macrophages in the ZoS recover and the denatured matrix molecular changes may be replaced by wound healing. However, adverse clinical events such as hypotension due to metabolic stress responses, sepsis, cardiopulmonary complications, and wound infection put the survival of ZoS tissue at risk. The next adjacent zone is the zone of hyperemia. In this outermost zone, vascular perfusion is increased by small vessel vasodilation in response to inflammatory cytokines released from the zone of stasis. Histopathology in this zone reveals swollen cells and capillaries, suggestive of cell membrane disruption. The tissue here will invariably recover unless the burn victim suffers prolonged hypotension and/or sepsis. Estimating the depth of a skin burn on the basis of clinical exam is difficult. The depth of a skin burn is not always obvious initially, and experienced experts often disagree. This is particularly true for scald or other low temperature burns in patients with dark skin. Many methods have been proposed to predict the depth of the injury immediately or soon after injury (ultrasound examination, intravenous fluorescent probes), but none has been as reliable as serial examination of the wound. The final depth of the injury typically becomes obvious 48–72 h after injury. Rarely, the thermal injury penetrates into the subcutaneous or deep tissue.

Local injury progression One important goal of resuscitation is to minimize the burn injury extension by conversion of ZoS and ZoH areas to areas of tissue necrosis. Edema and the unfolded protein response (UPR) are thought to be major contributors to burn wound conversion. Burn wound edema formation often follows a biphasic pattern in time. An immediate and rapid increase in the water content of burn tissue is seen in the first hour after injury. A second and more gradual increase in fluid flux of both the burned skin and non-burned soft tissue occurs during the first 12–24 h following burn trauma. The rate of progression of tissue edema is dependent upon the adequacy of resuscitation

511

that is determined by both rate and composition of the fluid administered. Burning temperatures denature intracellular proteins as well as prevent folding of newly synthesized proteins in the endoplasmic reticulum. This leads to local metabolic stress-related UPR that alters cellular energy metabolism to form the oxidative stress, release of inflammatory process mediators, especially in the zone of hyperemia, that extend the volume of injury.32 Release of damage-associated molecular patterns including mitochondria, xanthine oxidase, and other intracellular substances into the circulation generates destructive reactive oxygen species in the tissue as well as the local circulation. This causes thrombosis that potentiates ischemic tissue necrosis. Both complement activation and intravascular stimulation of neutrophils add to small vessel injury. Increased histamine activity, enhanced by the catalytic properties of xanthine oxidase, further increases vascular permeability. As a general rule, the volume of tissue necrosis after an uncomplicated burn injury progresses over 48 hours.

Systemic injury progression Injured cells within perfused burn tissue release into the circulation a “storm” of inflammatory cytokines, including serotonin, bradykinin, prostaglandins, and leukotrienes as well as catecholamines that causes a multi-organ system stress response. These inflammatory cytokines mediate generalized stress responses including altered capillary permeability and generalized third-space loss of intravascular fluid into the extravascular fluid spaces. Inflammatory cytokines also trigger generalized proteolysis, lipolysis, gluconeogenesis, and a hypermetabolic state.33 The severity of the hypermetabolic state scales with amount of tissue damaged. Adding to this effect are consequences of delayed or inadequate fluid resuscitation, particularly in underdeveloped parts of the world, with resultant hemo-concentration that hampers tissue perfusion. Because release of burn tissue products into the circulation have a direct myocardial depression effect as well as altered small vessel dynamics, large burns may result in hypotensive shock once the burn reaches 20%–30% of the total body surface area (TBSA). Splanchnic vasoconstriction, gut ischemia, reperfusion injury, and bacterial translocation are often consequences. The net effect is increased tissue demand for nutrition to support the increased metabolic demand under conditions of reduced nutrient transport that exacerbates burn wound injury pathogenesis. A second stress process begins to occur in major burn patients soon after the first. It is mediated by upregulation of inflammatory cell activity. Defense mechanisms of monocytes, macrophages, and neutrophils are activated in release of cellular breakdown products when they reach the circulation. These are referred to as damage-associated molecular patterns (DAMPs), seen on blood analysis. Among these are tumor necrosis factor (TNF) and other cell damage ligands that cause ubiquitous activation of the master inflammatory gene promoter NF-κB and AP-1, which upregulate biosynthesis and release of multiple inflammatory mediators (i.e., IL-1, IL-6, etc.) leading to systemic inflammatory response syndrome. Concurrent release of soluble burn wound breakdown products actually compromise cell-mediated immune

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CHAPTER 18  • Burn, chemical, and electrical injuries

functions including neutrophil killing of invading pathogens; T cell proliferation and IL-2 production are also suppressed.34 Furthermore, bacterial translocation from the gut into the vascular space results in intense immunological responses. Together, these events lead to the development of a compromised immune defense system and subsequent susceptibility to infection. This response is almost unique to burns and is referred to as the hypermetabolic response; it is associated with generalized catabolic state, multi-organ failure, infections, and early post-burn mortality. As in the treatment of hypovolemic shock, the primary initial therapeutic goal is to quickly restore intravascular fluid volume and to preserve tissue perfusion to minimize tissue ischemia. Burn shock is not easily or fully repaired by isotonic electrolyte fluid resuscitation. Large volumes of resuscitation solution may be required to maintain vascular volume during the first several hours after an extensive burn. Burn shock evolves through a dynamic pathophysiologic process even if hypovolemia is corrected. Increases in pulmonary and systemic vascular resistance (SVR) occur despite adequate preload and volume support. Such cardiovascular dysfunctions can further exacerbate tissue ischemia resulting in a vicious cycle of accelerating organ dysfunction. The critical concept in burn shock is that massive fluid shifts can occur even though total body water remains unchanged.

Hints and tips • Thermal burn results in three distinct burn zones: coagulation, stasis, and hyperemia. • One goal of burn resuscitation is to prevent burn wound conversion to more severe zones. • Major burns (>15%–20% TBSA) require burn center admission (Box 18.1). • Different burn mechanisms lead to different anatomic injury patterns.

BOX 18.1  Burn injuries that should be referred to a burn unit • Partial-thickness burns >15% TBSA and patients requiring burn shock resuscitation • Burns that involve the face, hands, feet, genitalia, perineum, or major joints • Deep partial-thickness burns and full-thickness burns in any age group • Circumferential burns in any age group • Electrical injuries, including lightning injury • Chemical burns • Burns with a suspicion of inhalation injury • Burns of any size with concomitant trauma or diseases that might complicate treatment, prolong recovery, or affect mortality • Diseases associated with burns such as toxic epidermal necrolysis, etc., if the involved skin area is 10% for children and elderly and 15% for adults or any doubt of treatment • Burned children in hospitals without qualified personnel or equipment for the care of children (Modified from: American Burn Association.)

Acute burn trauma management Initial evaluation and treatment in the field Without medical intervention, individuals that suffer a major burn will rapidly succumb to hypothermia and dehydration. The primary effort by first responders should focus on the ABCs of trauma management (i.e., Airway, Breathing, and Circulation). Re-establishing pulmonary ventilation, cardiac output, and control of hemorrhage are immediate life-saving priorities. A quick survey is performed to determine if there are coexisting injuries that may require more urgent treatment than the burn. Once immediate life-saving efforts are completed, it is also important to quickly survey for other forms of associated trauma, then triage to an emergency medical facility. In all cases (especially chemical or electrical injuries), care must be taken to avoid personal injury to the victim and first aid responders by ensuring that the area is safe and that appropriate protective clothing is worn. Basic trauma victim life support protocols should be used to assess and stabilize the patient. Clothing should be removed. If the burn occurred in a closed space, inhalation injury should be ruled out by inspecting the oropharyngeal airway for soot and carbon particulate. Supplemental oxygen by face mask should be given if clinical signs of hypoxia exist or if the patient was retrieved from a closed space fire. The mask should be operated at a flow rate to produce close to 100% O2 until respiratory status can be firmly assessed. In under-developed parts of the world with no healthcare facilities, the priorities are to stop the burn, and fabricate and use occlusive dressings while evacuation is arranged. Another unique aspect of burn care in low-resourced areas is meeting the need for ongoing resuscitation in patients with major burn injuries. Resource-austere environments (RAEs) often do not have adequate sterile intravenous fluids. Under those circumstances oral rehydration solutions, such as the WHO solution, are invaluable. This is stored in rural villages as a dry compound that consists of balanced salts and glucose in a prepared package to which water can be added. Current information suggests that oral rehydration solutions can provide adequate fluid for burns up to 40% TBSA in size. Although results of a large porcine study have shown improved renal function with such solutions, optimization in humans is still needed. Regarding the need for antimicrobial dressings, 0.9% sodium hypochlorite (Dakin’s solution) or iodine-based solutions are often available even in RAEs.35,36 In industrialized communities with modern emergency healthcare facilities, treatment of a burned patient starts with the removal of the patient to a safe location where first aid and Burn Life Support measures can be rendered while the patient is transported to a trauma center. A major burn patient should then be triaged to a trauma center, stabilized, and then transported to the nearest burn unit for definitive management (Box 18.2). Significant benefit can result from cooling the burn wounds and reducing tissue burn conversion.37 While transporting the patient to a medical center, cool the burns by wrapping in a hydrogel blanket or room-temperature water-soaked gauze. Cooling for 20 minutes should achieve near maximum benefit. However, systemic hypothermia and hypotension in patients

Acute burn trauma management

BOX 18.2  Field management of a major burn Perform an ABCDE primary survey: A – Airway with cervical spine control B – Breathing C – Circulation D – Neurological status and pain control E – Environment (heat loss) control F – Initiate fluid resuscitation

with larger burn areas must be avoided. Although immediate burn wound cooling is preferable, application of cooling after a delay of more than half an hour is still beneficial to the burn wound.38

Initial hospital management First steps are to continue resuscitation efforts as indicated. It is also important to survey for other forms of associated trauma and evidence of inhalation injury (see below). The secondary survey should be completed and documented, including relevant history (i.e., time, location, and circumstances of the injury), where the patient was found, and their condition. Past medical and social history, current medication usage, drug allergies, and tetanus status should be determined. It is also important to consider the possibility of non-accidental burns or scalding. A thorough assessment of a person with a burn should then take into account:   The type of burn (e.g., flame, scald, electrical, or chemical)   The depth and TBSA of the burn, and therefore the severity   Signs of inhalation injury (singed nasal hair, black carbon in the sputum, or carbon in the oropharynx)   Any coexisting medical conditions (e.g., cardiac, respiratory, or hepatic disease; diabetes; pregnancy; or immunocompromised state)   Any predisposing factors that may require further investigation or treatment (e.g., a burn resulting from a fit or faint)   The possibility of non-accidental injury   The person’s social circumstances (e.g., ability to self-care or need for admission). If there is evidence of airway injury, it should be secured because upper airway obstruction can develop quickly. Smoke inhalation is a major amplifier of burn mortality. Patients sustaining an inhalation injury may require aggressive airway management to prevent acute obstruction. Most injuries result from the inhalation of smoke containing proinflammatory combustion products. On occasion, steam or super-heated air may directly inflict thermal injury to the upper respiratory tract. Patients who are breathing spontaneously and are at risk for inhalation injury should be placed on humidified air. The FIO2 should be adjusted to maintain adequate hemoglobin saturation.

513

Of course, patients trapped in burning buildings or those caught in an explosion are at higher risk for inhalation injury. These patients may present with complicating factors such as facial burns, singeing of the eyebrows and nasal hair, pharyngeal burns, carbonaceous sputum, or impaired mentation. A progressive change in voice quality or hoarseness, stridorous respirations, or wheezing may be noted. In these patients the upper airway should be evaluated by laryngoscopy, and the tracheobronchial tree should be evaluated by flexible bronchoscopy. Patients who have suffered flame burns in a closed space are also at risk for carbon monoxide poisoning. Endotracheal intubation is indicated by respiratory stridor, hypoxemia with a mask FIO2 of 40%, need for mechanical ventilation, inadequate CNS function for airway protection, edematous orofacial burns, or oropharyngeal edema. If the medical providers have the skill and working equipment to perform an awake fiberoptic intubation, that is the safest method. Diagnosis of significant inhalation injury risk is best made by arterial blood gas measurements and bronchoscopy. Evidence of pulmonary parenchymal edema does not manifest early enough to be used for timely intervention for postburn inhalation injury. Furthermore, the pulse oximeter does not accurately measure oxyhemoglobin in patients with carbon monoxide poisoning because only oxyhemoglobin and deoxyhemoglobin are detected. CO-oximetry measurements are necessary to confirm the diagnosis of carbon monoxide poisoning. Patients with a patent upper airway (absence of stridor), burn size 60 mmHg, PCO2 50%

Death

BOX 18.5  Indications for intubation • • • •

Erythema or swelling of oropharynx on direct visualization Change in voice, with hoarseness or harsh cough Stridor, tachypnea, or dyspnea Carbonaceous particles staining a patient’s face

reflect metabolic acidosis and raised carboxyhemoglobin levels (CO-HgB) but may not show hypoxia. For the same reason pulse oximetry is also inaccurate as it cannot differentiate between oxyhemoglobin and carboxyhemoglobin, and may therefore give misleading results. Treatment is with 100% oxygen with a non-rebreather facemask, which displaces carbon

monoxide from hemoglobin much faster than 21% room air oxygen. Patients with CO-HgB levels greater than 25% have had clinically significant exposure to combustion products and should be ventilated (Table 18.4). The half-life of carboxyhemoglobin is ≈1 hour at an FIO2 near 100%. Treatment of CO-HgB levels greater than 10% is to provide an FIO2 =100% and monitor CO-HgB levels every 1–2  hours. When the CO-HgB drops below 10%, the FIO2 =100% can be adjusted to meet other requirements. Hyperbaric oxygen therapy can reduce the blood half-life of carbon monoxide to 23 minutes. If readily available, hyperbaric oxygen is recommended for patients with carboxyhemoglobin

Acute burn trauma management

levels greater than 25%, myocardial ischemia, cardiac dysrhythmias, or central neurological abnormalities. Hyperbaric oxygen is also recommended by some for pregnant women and young children with carboxyhemoglobin levels of ≥15% to prevent delayed neurological sequelae.

Cyanide intoxication Nitriles, which contain hydrogen cyanide (HCN), are commonly used in industrial solvents, polyurethanes, and vinyl plastic. They all release HCN during burning. HCN is rapidly absorbed in lungs or skin and contributes to the morbidity from smoke inhalation in industrial fires. Cyanide competitively inhibits oxygen binding to hemoglobin and inhibits the cytochromes of oxidative phosphorylation, resulting in metabolic energy depletion. Dicobalt edetate ((Kelocyanor) is a known treatment for massive cyanide poisoning in cases of ingestion or industrial explosion.46 In cases of inhaled cyanide products, the plasma concentration of free cyanide is often low. Use of dicobalt edetate it is also nephrotoxic and should be used only under life-saving conditions. A better approach is to use hydroxocobalamin, which is a vitamin B12 (cyanocobalamin) precursor. In high doses, it binds cyanide and has very low risk of toxic side effects. Other less desirable options are amyl nitrite inhalant or sodium nitrite administered intravenously. They convert hemoglobin to methemoglobin, which has a lower cyanide-binding affinity.

Airway management Pulmonary ventilation support and airway management in this situation are often challenging, and the need for prolonged endotracheal intubation is very common in patients affected by different degrees of respiratory distress syndrome. Despite the use of high-volume low-pressure cuffs, considerable controversy exists among burn surgeons as to whether to

convert endotracheal tubes to tracheostomy in burns patients, particularly when ventilator support is prolonged beyond two weeks or when other airway complications occur, as many studies have recorded high mortality and high tracheostomy complications. Tracheostomies may provide a good portal of entry for microorganisms into the respiratory tract, with a high incidence of respiratory infection and sepsis. In addition, feeding aspirations, obstructive abnormalities, increased incidence of pneumonia, and tracheo-innominate fistulas have been reported as high-morbidity complications of tracheostomies. Long-term sequelae are no less important. Stenosis of the airway, dysphagia, alterations of speech, tracheo-esophageal fistulas, and tracheomalacia can compromise the favorable outcome of this selected group of patients. Every effort should be made to maintain airway pressures at the lowest range, in order to prevent tracheomalacia. Advantages of tracheostomy include minimizing dead space, ease of suctioning, presence of a more secure airway, and ease of movement.

Fluid resuscitation Initiation of intravenous fluid administration should begin immediately in major burn resuscitation. The fluid rate should be adjusted to maintain adequate urine output. Initiation of burn resuscitation IV fluid protocols should be reserved for burns involving greater than 20% TBSA (Table 18.5) or for those patients with associated trauma or electrical injuries. In pediatric patients, fluid resuscitation should be initiated in all infants with burns ≥10% TBSA and in older children with burns ≥15% TBSA. Lactated Ringer’s solution with or without colloid is the most commonly used fluid for burn resuscitation.47 Patients undergoing post-burn fluid resuscitation should have a Foley catheter inserted in order to monitor urine output. Urine output should be used as a measure of renal

Table 18.5  Fluid resuscitation formulae

Formula

Electrolyte

Colloid

Glucose

Brooke

Lactated Ringer’s at 1.5 mL/kg/% TBSA burn

0.5 mL/kg/% TBSA burn

2 L 5% dextrose

Evans

0.9% NaCl at 1 mL/kg/% TBSA burn

1 mL/kg/% TBSA burn

2 L 5% dextrose

Slater

Lactated Ringer’s 2 L/24 h

Fresh frozen plasma at 75 mL/kg/24 h

2 L 5% dextrose

Lactated Ringer’s at 4 mL/kg/% TBSA burn

20%–60% estimated plasma volume

Titrated to urinary output of 30 mL/h

Colloid formulae

Crystalloid formulae Parkland

519

Hypertonic saline formulae Hypertonic saline solution (Monafo)

Maintain urine output at 30 mL/h Fluid contains sodium 250 mmol/L

Modified hypertonic (Warden)

Lactated Ringer’s + 50 mmol/L NaHCO3 for 8 h to maintain UO at 30–50 mL/h Lactated Ringer’s to maintain UO at 30–50 mL/h beginning 8 h post-burn

Dextran formula (Demling)

Dextran 40 in saline at 2 mL/kg/h for 8 h Lactated Ringer’s titrated to maintain urine output at 30 mL/h

Fresh frozen plasma at 0.5 mL/kg/h for 18 h beginning 8 h post-burn

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CHAPTER 18  • Burn, chemical, and electrical injuries

perfusion and to assess fluid balance. In adults, a urine output of 0.5 mL/kg per hour should be maintained during the acute resuscitation period. Intravenous fluid resuscitation of burned children is targeted to a urine output of 1.0 mL/kg/h. The color and consistency of the initial urine in patients with deep thermal burns, blunt trauma, or electrical injury should be monitored. The urine may be dark red, indicating hemoglobinuria or myoglobinuria. These heme-proteins can precipitate in the renal collecting ducts resulting in renal failure. If so, then osmotic or tubular diuretics should also be used to flush the renal collecting ducts to avoid renal failure. In elderly patients, patients with cardiorespiratory disease, and patients who have delayed presentation, consider inserting a central venous pressure line. This can play an important part in the subsequent restoration of volume in a patient with a severe burn. The risks of infection related to a central line are small in the early stages. With current methods of line management these risks are outweighed by the importance of the line for monitoring and access.

A major risk of fluid resuscitation in major burn patients is excessive accumulation of fluid in extracellular interstitial “third space” spaces, which in turn limits nutrient and gas transport between capillaries and cells within tissues. It has been recently demonstrated that opioid pain medications promote third space fluid losses.48 Avoiding continuous infusion of opioids during burn shock in favor of administration of opioids on an as-needed basis reduces third space resuscitation fluid accumulation. This opioid-linked fluid resuscitation problem is called “fluid creep”. Another routine part of fluid resuscitation should be antioxidant therapy, especially vitamin C. The oxidative stress of burn injury leads to peroxidation of capillary membrane lipids and then to loss of capillary transport barrier function. Vitamin C administration at 50–60 mg/kg/h has been shown to reduce fluid resuscitation requirements to maintain urine output and decreased tissue edema.49

Resuscitation fluid composition and administration

Heart rate and urine output are the primary parameters for monitoring fluid therapy in patients with large burns although there is a lack of evidence supporting them. Titrating intravenous fluid administration rate according to body weight is commonly practiced. A minimum of 0.5 mL/kg/h urine output in adults and children is recommended, but 1 mL/kg/h urine output is preferred. Lesser hourly urinary outputs in the first 48 h post-burn almost always represent inadequate resuscitation. Hemodynamic monitoring and treatment of deviation from normovolemia are the fundamental tasks in intensive care. A pulse rate ~110 beats/min or less for adults usually indicates adequate volume, with rates >120 beats/ min usually indicative of hypovolemia. Narrowed pulse pressure provides an earlier indication of shock than systolic blood pressure alone. Noninvasive blood pressure measurements by cuff are inaccurate due to the interference of tissue edema and read lower than the actual blood pressure. An arterial catheter placed in the radial artery is the first choice, followed by the femoral artery. The decision to perform invasive hemodynamic monitoring requires careful consideration. The lack of benefit associated with goal-directed supranormal therapy has resulted in waning enthusiasm for the use of pulmonary artery catheters.

The amount of replacement fluid is predicted from the extent of burn and size of the patient, and fluid replacement should proceed at the same rate as the loss. Fluid administered in excess of the capillary leak is excreted by the kidney or results in increased hydrostatic pressure and extra interstitial edema. Lactated Ringer’s solution most closely resembles the electrolyte content of normal body fluids. Burn fluid resuscitation protocols have evolved considerably over the past half-century. Today, the Parkland formula (and its variations) is the most widely used burn resuscitation guideline. The Advanced Burn Life Support curriculum supports the use of this formula for initial resuscitation in burn injury. It is 4 mL/kg/% TBSA, describing the amount of lactated Ringer’s solution required in the first 24 h after burn injury. Starting from the time of burn injury, half of the fluid is given in the first 8 h, and the remaining half is given over the next 16 h. As an example, by the Parkland formula, a 70 kg patient with a 40% TBSA burn receives (70 × 40 × 4) = 11,200 mL of lactated Ringer’s solution during the first 24 h after the burn (approx. 470 mL/h). In actual practice, these fluid resuscitation guidelines are just useful as starting points in major burn resuscitation. Within the first 30 to 90 minutes, the resuscitation fluid administration rates are adjusted to maintain physiological cardiovascular parameters with the urine output as a useful guide.47 For adults this means that fluid rate is reduced about 10%– 20% per hour if the urine output target is above 0.5 mL/kg (ideal body weight)/h, and in children (under 30 kg of weight) fluid rate is decreased if the urine output target is above 1 mL/ kg/h.47 Some burn centers administer albumin or other colloids during the initial resuscitation period. However, the Parkland formula remains the most common protocol used given the lack of proven survival benefit and increased cost associated with albumin, and a meta-analysis comparing albumin to crystalloid that showed a more than doubled mortality rate with albumin. Administration of albumin, and other colloids, is usually avoided in the first 24 h post-burn, but may have a role in severe burns (>50% TBSA) after the first 24 h.

Vital organ function monitoring

Management of the burn wound The priority in thermal burn wound management is to create a physiologic environment for healing and reduce evaporative losses. In a hospital setting, wounds should be washed with a physiological and sterile solution, then debrided of contaminants and loose nonviable tissue. For treatment of major burns or in cases of smaller deep burns, topical antibiotics are useful to control microbial invasion. This is followed by coverage with sterile dressings that serve as an evaporative barrier and as an immobilizer. Extremity splints also help immobilize and are helpful to reduce edema and pain. There is a wide range of wound products that subserve these purposes. Preferences vary from institution to institution. Some practical first aid tips can make a significant difference to the burn outcome. Small superficial burns are reduced in severity by immediate rapid cooling with running cold

Acute burn trauma management

water for 5 to 10 minutes. Subsequent careful cleaning, immobilization, and barrier protection are the next steps. Topical antibiotics are unnecessary unless there is contamination with foreign material or large surface area involvement. In wilderness situations well away from medical facilities, the management priority for large surface area burn wound care is the control of evaporative and heat losses until evacuation. Cleaned and boiled large plant leaves can serve as occlusive dressing and block the rapidly fatal evaporative fluid loss from a large burn. The inner cambium layer of plants or trees can also be used to provide salicylates to control pain and reduce bacterial and fungal growth. Ideally, the goal of wound management is to create a healing environment that attempts to mimic the in utero environment of a fetal wound. Typically, the wound is covered between dressings with a moist, antimicrobial covering to minimize microbial growth, fluid loss, and painful stimuli and to maximize skin regeneration. Superficial partial-thickness burns heal in a short time and with little pain or contracture with warm, moist, and bacteria-free dressings. Because major burn patients are immunocompromised, it is worthwhile to place these patients in protective isolation to limit contact with hospital-based pathogens, such as multidrug-resistant organisms. This isolation also requires room ventilation which is separate as well. Despite these precautions, many have one or several bouts of infection through the course of their treatment. The skin and gut of the patient are common sources of microbial pathogens, and no known therapy can eliminate these sources of infection. Contamination and then overgrowth of burn wounds by pathogens causing a systemic picture of sepsis typically occur 2–3 weeks after injury. Early enteric feeding and early wound coverage with skin greatly reduce the incidence of burn wound infections. Physiologic wound care helps minimize the chance of infection and maximize healing. The daily dressing changes in burn patients permit inspection of the wound to assess the need for further interventions but, more importantly, offer the chance to remove nonviable tissue. In burn centers, the providers dedicate a large part of the time to gently removing nonviable tissue and proteinaceous debris that have gathered since the last dressing. This leaves a healthy bed for the migration of keratinocytes. For small deep partial- or full-thickness burns that could heal without causing functional limitations, the time for healing can be more than several weeks with a risk of infection especially in resource-poor circumstances. The clinical outcome is far better to treat these wounds by surgical debridement and coverage with skin grafts or an engineered scaffold. For a deep burn over a small area or one with a patchy distribution, the time for healing by secondary intention may be no longer than the healing of a skin graft. For these wounds, surgical debridement and grafting may not be appropriate. After all, it takes a skin graft 7–10 days to stabilize on a wound and about the same amount of time for the donor site to heal.

521

occlusive coverage. This way, some micro-debridement occurs with each dressing change. In RAEs, a topical antiseptic may be applied over this followed by cotton wool or gauze to absorb the exudate. Newer dressings have been introduced that are claimed to be less adherent and allow less water to be lost by evaporation from the wound while also protecting it from external pathogens. Some dressings are meant to provide temporary coverage while others are meant to be permanent. These may further be classified into two groups:   Biologic dressings: These are modified tissues or biomimetic materials which are invaded by wound cells, especially immune cells, when placed on an open viable wound. They have the advantage of assisting the local wound immune defense control surface colonization.   Physiologic dressings: These consist of synthetic biopolymers such as polyethylene glycol, or polyvinyl derivatives which prevent adherence to the wound, and plastic films, which reduce evaporation and contamination.

Topical antimicrobials In the hospital setting, silver ion is the most commonly used topical antibacterial. Historically, silver nitrate, as a 0.5% solution, was widely used to deliver silver ions. It is a bacteriostatic liquid which can be poured into the gauze wound dressings to saturate them. It has a broad antibacterial spectrum but does not diffuse through eschar effectively. Therefore, it is not too effective in reducing colonization beneath the eschar in deeper burns. Also, silver nitrate is not very popular with burn care professionals because it discolors the bedding, floors, and uniforms. A more practical approach is to use nanocrystalline silver-coated dressings like ACTICOAT (Fig. 18.13). When soaked in water, it releases mono- and diatomic silver ions, which can penetrate burn tissue and provide broad-spectrum bactericidal antibacterial coverage. It has to be moistened with pure water rather than salt solutions to release and transport the silver ions into the wound surface to impede bacterial proliferation.

Wound dressings Standard burn dressing consists of sterile evaporative barriers such as petrolatum- or wax-impregnated gauze, which effectively restores the transport barrier function of the epidermis and helps to prevent adherence to the wound. It is often helpful to first apply an absorbing dressing on the wound before

Figure 18.13  Application of a topical antimicrobial silver dressing (ACTICOAT) is helpful to control bacterial proliferation in partial- to full-thickness burn injuries, large surface area burns, heavily contaminated, or immunocompromised patients.

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Silver, like many other transition metals, interferes with bacterial energy metabolism. Other antimicrobial transition metals clinically used are iodine, gold, titanium, platinum, sulfur, and zinc, to name a few. Silver ions are particularly well tolerated by tissue and rapidly cleared in the urine. Another silver compound, silver sulfadiazine, is a very commonly used antimicrobial ointment because it combines the antimicrobial effects of silver and sulfur. It has intermediate eschar penetration and a large antibacterial spectrum. The antibacterial activity lasts 8–10 h, and the dressings are changed once or twice a day. Silver sulfadiazine also contains sulfur. The sulfur also inhibits the cytochromes involved in ATP generation. Thus sulfur is bacteriostatic to many microorganisms including bacteria and fungi. Silver sulfadiazine is a very effective topical antibiotic but causes an exudative reaction in the wound, which discolors the wound and makes it more difficult to clinically assess burn depth. This exudative process is associated with a transient leucopenia in some patients. A switch to a different topical agent for a few days allows the white blood cell count to recover. Restarting silver sulfadiazine rarely causes recurrent leucopenia. Silver sulfadiazine is best indicated for mid to deep partial-thickness burns that clearly require excision and grafting. Mafenide acetate is an inhibitor of bacterial folate metabolism and is bactericidal. It has a molecular weight 50% smaller than silver sulfadiazine and thus is several times more effective in eschar penetration. Use of mafenide acetate on full-thickness burns prevents deeper infections. It is often used on external ear burns because it penetrates and protects the auricular cartilage from infection. Systemic absorption of mafenide acetate, when it is applied to large burns, produces a metabolic acidosis by inhibition of carbonic anhydrase. The effect is usually noted after 3–5 days. Use of the compound on open wounds also causes pain. The pain subsides after several minutes, but patients usually do not like it. Another topical dressing uses Dakin’s solution (0.25% sodium hypochlorite), which is an oxidizing solution that bleaches proteins and lipids. It is good for suppressing bacterial and fungal proliferation but is not effective against bacterial biofilms. Practically, it is useful as a three-timesper-day gauze dressing to reduce devitalized tissue. Dakin’s solution-soaked gauze is often alternated with topical silver sulfadiazine to treat a wound heavily colonized with bacteria. Agents such as povidone-iodine solution and nitrofurazone are still used in RAEs and do not require expensive storage conditions. They are still widely used in many parts of the world where access to agents that require expensive storage is limited. Fortunately, wound infections have decreased during the last two decades largely due to a better understanding of basic wound care principles and prophylactic use of more effective topical antibacterial compounds. Early tangential debridement and coverage of the wound with skin or biological dressings have markedly decreased the opportunity for burn wound infection. Despite meticulous wound care, and even under the most sterile conditions, the patient’s own microbial flora quickly colonizes and then invades the non-perfused burned tissue. Only by removing the devitalized burn tissue and providing biomimetic tissue coverage is native immunity restored and risk of wound infection reduced.

Physiological wound dressings A physiological dressing is designed to replace some of the basic vitally important barrier functions of the skin as well as provide a wound environment that allows cellular immunity to control wound surface bacterial and fungal growth.10,50 Historically, treated xenografts were used. The composite dressing consisting of extracellular matrix proteins anchored to a deformable plastic has been popular with burn surgeons for decades (i.e., Biobrane [Smith & Nephew, London, UK]). There are several similar products. They can help establish physiologic wound control in large percentage surface area burns while the process of autograft coverage takes place. Biobrane is also used to provide a physiologic environment for the healing of superficial burns and donor sites. If applied correctly, Biobrane usually adheres to the wound bed. Left undisturbed, the dressing limits fluid loss and prevents stimulation of the wound. Epidermal regeneration is undisturbed beneath. The dressing falls off once the epithelial layer completely heals underneath, much like a scab falls off an open wound once it is healed. These materials work best on superficial partial-thickness burn wounds and skin graft donor sites that heal in 7–10 days. Placed on wounds that have nonviable tissue or are heavily colonized with bacteria, the materials adhere poorly and as foreign material serve as a nidus for infection much like the burn eschar. These biomaterials have no antimicrobial activity and therefore should not be placed on a contaminated wound. Most of the newly developed synthetic biologic dressings are used mainly in developed countries because most of these products are extremely expensive.

Biological wound dressings or grafts Restoring immune defense boundaries to beyond the healing wound requires restoration of vascular perfusion superficial to the wound. This requires placement of a biologic dressing on the wound that is capable on inducing vascular ingrowth (Table 18.6). The most widely used biologic dressing remains fresh or frozen human cadaveric split-thickness skin. Properly handled, cadaveric skin remains viable and vascularizes (“takes”) when it is placed on a healing wound bed. The allograft’s dermal capillaries imbibe interstitial fluid, proliferate, and form channels with the wound bed 2–5 days after grafting. The process is called inosculation. Once taken, the wound beneath the allograft becomes sterile and less inflamed. Of course, allografts contain foreign proteins that will trigger an immunologic rejection. The immunosuppression manifested in massively burned patients may delay the rejection process some, but eventually the grafts develop an abundant inflammatory cell infiltrate, and the epidermis dies and sloughs from the patient. Loss of the epidermis requires replacement with another set of cadaveric grafts, or, it is hoped, the patient is ready for coverage with permanent autologous tissue. Disease transmission from the donor to the burn patient is possible but occurs rarely. After the epidermis is lost, much of the allograft dermis is remodeled by host cells and becomes permanent. Porcine skin and freeze-dried human cadaveric skin were once routinely used to cover burn patients. But they do not

Acute burn trauma management

523

Table 18.6  Temporary skin substitutes

Product

Source

Layers

Category

Uses

Advantages

Disadvantages

Human allograft

Human cadaver

Epidermis and dermis

Cryostored split-thickness skin

Temporary dressing of partial-thickness and excised burns before autografting or when there is a lack of autograft

A bilayer skin providing epidermal and dermal properties Revascularizes maintaining viability for weeks Dermis incorporates Antimicrobial activity

Epidermis will reject Risk of disease transfer Expensive Need to cryopreserve

Gammagraft

Human cadaver

Epidermis and dermis

Split-thickness skin

Temporary dressing of partial-thickness and excised burns before autografting or when there is a lack of autograft

A bilayer skin providing epidermal and dermal properties Revascularizes maintaining viability for weeks Dermis incorporates

Epidermis will reject Risk of disease transfer Expensive Store at room temperature

Human amnion

Placenta

Amniotic membrane

Epidermis Dermis

Temporary dressing of partial-thickness and excised burns before autografting or when there is a lack of autograft

Acts like biologic barrier of skin Decreases pain Easy to apply, remove Transparent

Difficult to obtain, prepare, and store Must change every 2 days Disintegrates easily Risk of disease transfer Expensive

Pig skin xenograft

Pig dermis

Dermis

Dermis

Temporary dressing of partial-thickness and excised burns before autografting or when there is a lack of autograft

Good adherence Decreases pain More readily available compared to allograft Bioactive (collagen) inner surface with fresh product Less expensive than allograft

Does not revascularize and will slough Short-term use Need to keep the fresh product frozen

Oasis

Xenograft

Extracellular wound matrix from small intestine submucosa

Bioactive dermal-like matrix

Temporary coverage of superficial partialthickness burns, although it has been used for coverage of autograft and for donor

Excellent adherence Decreased pain Provides bioactive dermal-like properties Long shelf-life, store at room temperature Relatively inexpensive

Mainly a dermal analogue Incorporates and may need to be reapplied

Transcyte

Allogenic dermis

Bilayer product Outer: silicone Inner: nylon seeded with neonatal fibroblasts

Bioactive dermal matrix components on synthetic dermis and epidermis

Temporary coverage of superficial partialthickness burns, although it has been used for coverage of autograft and for donor

Bilayer analogue Need to store frozen Excellent adherence to until use a superficial partialRelatively expensive thickness burn Decreases pain Provides bioactive dermal components Maintains flexibility Good outer barrier function

Suprathel

Synthetic copolymer of polylactide, and εcaprolactone

Monolayer

Synthetic epidermis and dermis

Temporary coverage of superficial partialthickness burns, although it has been used for coverage of autograft and for donor

Long shelf-life, store at Relatively expensive room temperature Not absorbent, requires fairly frequent replacement to obviate pooling of exudate and related problems

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take as well as properly preserved frozen cadaveric skin. Thus they tend to detach from the wound bed during dressing changes. However, they do help reduce evaporative fluid and heat loss while they are attached to the burn wounds. Over the past 30 years, both cellular and acellular tissue-engineered biomaterials have served an increasing role in burn wound coverage (Table 18.7). Acellular matrices of collagen and proteoglycans were manufactured and marketed as the first “artificial skin” and are now sold under the name Integra. A thin porous polymer sheet, to serve as a barrier to the air, covers the surface. Engraftment of the material takes approximately 2 weeks, and any disturbance, such as excessive movement, fluid accumulation under the material, or infection, causes loss of the material. Once the matrix is incorporated, the polymer sheeting is replaced with a thin skin graft. Replacement of lost dermis with Integra or similar matrix for closure of deep partial- or full-thickness burns during the initial wound treatment stages will often decrease the need for later scar release surgery by improving the elasticity of the grafted skin. Despite the technical problems with these materials, the advantage of reducing functional and cosmetic deformities from scar contractures makes their use worthwhile in many clinical situations. AlloDerm is chemically treated human cadaver dermis produced from skin allograft in which most non-cross-linked proteins and lipids are removed. It is commercially available as a dermal replacement. As with Integra, however, the engraftment process for the matrix is variable, and the matrix does not support the attachment of cultured epidermal autograft (CEA) well. The rapidity of the engraftment process is likely to depend on growth factors in the matrix material as much as the wound bed on which it is placed. The ability to grow in cell culture and expand isogenic human keratinocytes in tissue culture has made survival possible for burn injuries above 90% TBSA that would not have survived previously. No longer was an adjacent skin source a major limitation for restoration of a keratinizing isogenic epithelial barrier. In a landmark case in 1984, twin children with burns over almost their entire bodies were treated at the

Shriners Burns Institute in Boston with cultured keratinocytes taken from a small biopsy specimen of undamaged axillary skin. During the course of their treatment, the keratinocytes were successfully expanded in tissue culture and used to resurface some of their wounds. Survival of the patients was directly attributed to the use of the technique. Now several biotechnology companies offer the service for a fee. Skin biopsy specimens sent to the company are expanded in culture and returned to the patient, usually in 2–3 weeks. The sheets of CEA are placed directly onto a cleanly debrided wound bed. The grafts survive well, and wounds close much faster than without treatment. Despite its theoretic advantages, CEA has not succeeded in solving wound coverage needs of large percentage surface area burned patients. Covered by CEA, areas around joints and over muscles, such as the face, have little motion and poor function. CEA placed directly on muscle or subcutaneous tissue only gradually forms a basement membrane, in some cases during 6 months. Often a mechanically fragile and unstable epithelial barrier results, which requires replacement over time.

Operative wound closure The main goals of surgical treatment of burn wounds are removal of damaged or devitalized tissue and replacement with viable tissue.51 Early removal of the necrotic tissue decreases wound infections and mortality. Necrotic tissue serves as a growth medium for pathogens, and delays wound healing. Early closure reduces the time of systemic inflammation. The decision to excise and graft a superficial partial thickness burn wound remains one that is based on clinical experience and judgment. If the burn care team believes that the wound will require more than 3–4 weeks of dressing changes before it closes, the functional outcome of excision and grafting is likely superior to allowing the wound to heal by secondary intention. Perhaps the more improved physiological dressings are rebalancing the scale.

Table 18.7  Engineered skin substitutes or scaffolds

Product

Tissue of origin

Layers

Category

Uses

Advantages

Disadvantages

Apligraf

Allogenic composite

Collagen matrix Composite: seeded with human epidermis and neonatal keratinocytes dermis and fibroblasts

Excised deep partial-thickness burn

Readily available

Expensive Vascularizes slowly No epithelial barrier No antimicrobial activity

Epicel

Autogenous keratinocytes

Cultured autologous keratinocytes

Epidermis only

Deep partial- and Readily available full-thickness burns Live cells >30% TBSA

Expensive Vascularizes slowly No epithelial barrier No antimicrobial activity

Alloderm

Allogenic dermis

Acellular dermis (processed allograft)

Dermis only

Deep partial- and Readily available full-thickness burns Live cells

Expensive Vascularizes slowly No epithelial barrier No antimicrobial activity

Integra

Synthetic

Silicone outer layer on bovine collagen GAG and shark chondroitin sulfate dermal matrix

Biosynthetic dermis

Full-thickness burns; definitive “closure” requires skin graft

Expensive Vascularizes slowly No epithelial barrier No antimicrobial activity

Readily available Live cells

Acute burn trauma management

On the other hand, treatment of a deep partial- or full-thickness burn requires excision and skin grafting. Necrotic burn tissue is usually debrided in sequential layers, called tangential excision, until all tissue appears viable. This is associated with significant blood loss and transfusion requirement. In obvious full-thickness burns, the burn can be excised to deep fascia in one stage using cautery to reduce blood loss. For large surface area major burn patients or those with significant comorbid disease, treatment is directed toward preservation of life or limb, and large areas of deep burn must be excised before the necrotic tissue triggers multi-organ stress. In such cases, areas that are more deeply burned may be treated with physiological dressings until healing occurs late or until adequate skin donor sites become available. The main limitation to removal of the burned tissue in large burns is the need to limit blood loss during the debridement.

A

C

B

Blood platelet function often becomes less effective with repeated blood transfusions. Of course, large burn excisions should be conducted only when typed and crossmatched blood is available in the operating room and administered during the excision to prevent hypotension. Clotting factors in the form of fresh frozen plasma and cryopreserved platelets often need to be co-administered as well. Tangential debridement involves removing burn tissue to a depth within the dermis that involves the dermal and subcutaneous capillary network (Fig. 18.14). Methods to limit blood loss such as excision under proximal tourniquet control can reduce blood loss during excision of distal extremity burns but make it difficult to accurately excise the burnt tissue. Topical application of vasoconstrictive agents in lactated Ringer’s (LR) is widely used to limit bleeding. In addition, some surgeons tumesce a LR solution or LR containing

B

C

525

Figure 18.14  (A) Burn wound is marked prior to debridement. (B) Hand scald burn post-debridement. (C) Using a Weck guarded knife for debridement of a hand scald burn.

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1:1,000,000 (w/v) epinephrine beneath the burn wound before excision and donor sites to reduce bleeding. Although some units practice large (>20% TBSA) debridement in one procedure, many burn centers consider it wise to limit each stage of wound debridement by a blood transfusion limit of 20%–40% total blood volume.52 This helps to keep blood replacement, fluid administration, and anesthetic requirements within the range of physiological stress tolerance. Although full-thickness excision to the level of muscle fascia with electrocautery minimizes blood loss, it requires skin grafts on fascia resulting in poor functional and cosmetic results. Autologous split-thickness skin grafts from unburnt areas are the “gold standard” for definitive coverage of burn wounds if enough donor sites are available (Fig. 18.15).51 When available, the extremities, minus the hands and feet, are the best areas for harvesting of skin grafts (Fig. 18.16). The trunk is used next, but obtaining the grafts is technically more challenging because of contour irregularities. Hair-bearing scalp skin is a great but often underused donor site. The scalp skin is thick and re-epithelializes rapidly owing to the density of hair follicles. The scrotum can also be used. Regrowth of the hair is rarely a problem; thus, the donor site is well camouflaged after healing.

Repeated harvesting of skin graft donor sites multiple times is possible, but the donor site must be allowed time to regenerate between harvest procedures. Donor sites should ideally be harvested from areas that optimize color match. Non-meshed (“sheet”) grafts are preferred to improve the cosmetic and functional result. Meshing the skin grafts allows coverage of larger areas. Commercially available skin graft meshers allow expansion ratio of the skin graft either 1.5:1 or 3:1. Meshing improves graft “take” and faster burn coverage; the mesh ­pattern is permanent and unsightly. Sheet grafts are often used on hands and faces, and over any future site for intravenous central lines and tracheostomies to obtain rapid cover. Frozen allografts (Table 18.6) and skin equivalents (Table  18.7) have allowed rapid excisions of extremely large burns and still achieve physiologic closure, with potentially lower mortality in these injuries. Cultured epithelial autografts can also be used to provide temporary burn wound closure while the donor sites heal. The cultured cells can be applied as sheets (available after 3 weeks) or in suspension (available within 1 week). A few burns units use these cells for superficial skin loss or in combination with mesh graft to improve the cosmetic result.

B

A

Figure 18.15  (A) Healed split-thickness graft. (B) Donor site.

A

B

Figure 18.16 (A) Powered dermatome commonly used to harvest skin grafts. (B) Thin split-thickness autograft harvested.  

Acute burn trauma management

For major burn patients that are physiologically unstable, one option is to debride the wounds as much as possible and skin graft the wounds when the patient is more stable. Between the time of excision and the skin grafting procedure, the wounds are covered with a biologic dressing (Fig. 18.17). This allows the wound bed and the patient to recover before harvesting the donor sites. Autograft skin coverage begins as soon as possible to avoid wound colonization with pathogenic microbes that limit graft take. Donor sites harvested more than once heal less rapidly, but the alternatives are limited in these patients with large burns. Unfortunately, this approach is not feasible in less resourced countries. A strategic plan directed toward achieving the best functional outcome should be used in planning skin graft coverage of large surface area burn patients. High priority for early coverage include joints and intravenous access sites, thereafter grafting large torso areas where skin grafts have a high probability for take to decrease the surface area of the injury and reduce physiologic stress. Burns to the hands, neck, and face warrant special consideration, however. To prevent excessive functional impairment to these areas after the burn wounds are healed, these areas should be grafted earlier rather than later. In full-thickness burns to the hands, neck, and face,

A

C

B

527

delay in grafting will result in scar contractures and functional limitations that are difficult to overcome. Thus deep burns to these areas should be grafted early or closed with flaps so that range of motion and hypertrophic scar management can be started early (Box 18.6).

BOX 18.6  Techniques for burn scar reconstruction Without deficiency of tissue • Excision and direct closure • Local tissue rearrangement  

With deficiency of tissue • • • • • • •

Split- and full-thickness skin autografts Local/regional flaps Distant flaps Tissue expansion Free flaps Dermis substitutes, then grafts or flaps Serial excision and direct closure

B

C

Figure 18.17  (A) Integra acellular dermal matrix in place over a full-thickness wound. (B) Well-vascularized Integra graft. (C) Coverage of Integra.

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CHAPTER 18  • Burn, chemical, and electrical injuries

Management of tar burns In order to expedite the cooling and solidification process one should immediately apply cold or ambient temperature water or lotion. One of the biggest challenges in care for tar burn wounds is removing the tar without inflicting further injury to the adjacent tissue. It is rarely possible to nonoperatively remove the tar rapidly, and there is no pressing medical need to do so. In general, it is best to treat the injury as a deep burn with appropriate fluid resuscitation or preparation for skin grafting as needed. Removal of the tar is not essential, but it improves patient comfort. This approach carries the risk of potential conversion of a partial-thickness injury to a full-thickness injury. Mechanical debridement of tar burns is often painful, relatively ineffective, and results in the removal of underlying viable skin and hair follicles, thus extending the depth and area of the dermal injury. In addition, a degree of auto-debridement will occur. If the skin has a light coat of tar and the patient does not complain about the underlying skin or surrounding tissue, leaving the asymptomatic tar in place may be acceptable. Numerous biocompatible compounds have been used to chemically detach the tar from the burn wound with variable results, and selection of the appropriate agent for the removal of adherent tar is still challenging. The detergent surfactant copolymers like polyoxyethylene–sorbitan or poloxamer 188, which are basically emulsifying agents commonly used as a wax base, when applied will separate the tar from the skin. Since they are water soluble, they easily wash off.53 Alternatively silver sulfadiazine, Neosporin (with polyoxyethylene sorbitan as a base), or polysorbate may be left under the bandage on the tar-contaminated burn. The tar comes away with dressing changes.54 With some of these agents, it is recommended to leave it on for 12–48 h at a time until the tar has dissolved. Organic solvents, such as alcohol, acetone, or other organic solvents are not recommended for removing tar from tissue. When these emulsifiers above are not available, common household agents, such as mayonnaise (15–30 min), butter (20–30 min), olive oil, sunflower seed oil (20–30 min), and baby oil (1–1.5 h) placed on sterile gauze and onto the tar, should help to remove tar without further tissue damage over the aforementioned time periods.

Treatment of electrical injuries The majority of people that seek medical attention for electrical shock have experienced brief contacts with an electrically energized conductor, typically 480 volts or less. Usually, they are industrial workers. They will have small puncture wounds at the skin contact points without burn injury to deep tissues. The presenting symptom is pain in the sensory distribution of the shock, a small contact burn, and perhaps soreness from falling. Very few have cardiac abnormalities unless pre-existing cardiac disease exists. Electrical function of the heart should be assessed by an electrocardiogram. It is common practice to continuously monitor cardiac rhythm for the first 24 h after shock if the current passed through the chest or if the patient reports cardiac rhythm disturbance after the shock. If the ECG does not reveal any abnormality, then it is probably unnecessary to place the patient in a cardiac monitored ICU bed for 24 hours.17 If there are no cardiac abnormalities in the emergency ward, it is very

unusual for it to manifest subsequently. Fatal electrocutions usually occur at the time of shock. Because of significant risk of late onset neurological sequelae, these patients should have at least one follow-up with the primary care physician, neurologist, or trauma specialist. Determining risk of cardiac injury by electrical shock requires knowing the voltage drop induced directly across the heart. Low-voltage devices such as modern cardiac defibrillators with contact points on the chest generate enough voltage drop across the heart to transiently electroporate the myocardium, which is done to restore rhythm in a dysrhythmic heart and can damage chest wall muscles.55 If the electrical contact points on the body were hand-to-hand or hand-to-feet, a much higher voltage would be needed. Patients presenting with cardiac arrhythmias or full cardiac arrest should undergo cardiac resuscitation procedures according to American Heart Association guidelines. Once resuscitated, these patients should be admitted and evaluated for myocardial injury while being monitored in an inpatient monitored bed or ICU setting for several days. Patients who have suffered major electrical injuries from high energy electrical power sources are among the most complex trauma patients to manage. They should be admitted to a specialty burn center if possible. Vital organ function should be stabilized as soon as possible. Thorough evaluation to determine the full extent of injury throughout the current path is the next priority while being constantly monitored and receiving fluid resuscitation. Diagnostic imaging is often essential to determine the extent and location of tissue edema. Proton weighted MRI without contrast is best. However, in the setting of a severely injured patient, soft-tissue CT imaging is faster and more practical. The surface area of a burn usually does not factor into fluid resuscitation for electrical injury patients unless they have extensive skin burns as well. If clinical exam reveals a physiologically stressed patient, this suggests significant injury, and a Foley catheter should be placed. If the urine is clear, then fluid administration should be enough to maintain urine output at 1–2 mL/kg/h. After 3–4 hours, a judgment can be made about the severity of injury and whether the intravenous fluids can be reduced to maintain a baseline urine output of 0.5 mL/kg/h. If on the contrary the urine is dark colored due to myoglobin or the blood levels of CK are elevated more than four- to fivefold greater than normal, then intravenous fluid administered should be increased to keep the urine output at 2 mL per kg body weight. If the urine contains visible amounts of myoglobin, alkalinizing agents (e.g., bicarbonate) should be administered to keep the urine pH >8 to reduce the risk of protein aggregation in the renal collecting ducts. Renal failure in severely injured patients must be aggressively avoided because of its associated high mortality. Unfortunately, blood dialysis systems cannot be used to remove myoglobin. If oliguria develops despite maximal fluids, loop diuretics, and urine alkalization, then an osmotic diuretic like mannitol/bicarbonate maybe effective.56 However, it is very important to titrate the urine pH to above 9 to prevent mannitol-induced renal toxicity. If these maneuvers fail, then dialysis will be indicated. Once the urine is clear, the fluid administration can return to the level required to maintain a normal urine output. Electrical contact skin burns are almost always full thickness to the subcutaneous tissues and should be managed the

Acute burn trauma management

same as thermal injuries. Deep tissue injury, usually skeletal muscle, requires early diagnosis of deep muscle injury locations, muscle compartment decompression by fasciotomies as needed, and debridement of nonviable tissue. Muscle debridement should be performed under histological guidance as recommend by Quinby et al.57 Early diagnosis of compartment syndrome is essential for muscle salvage. Manual testing of the compartment pressure is proven to lack adequate sensitivity even by experienced physicians. Various ways can be used to measure the pressure. Elevated pressures over 30 mmHg require fasciotomies of the fascia and epimysial layers in the muscle. Escharotomies and other releases needed to optimize tissue perfusion should be done as soon as feasible. Most electrical shocks involve the hand. When hand edema is present, carpal tunnel Guyon’s canal releases are needed. Doppler and pulse oximeter verification of perfusion in distal tissue is needed. A second-look operation at 48–72 hours is needed for a final muscle debridement.57 Deep wound cover with allograft or composite, with the aim of preserving vital structures, is indicated between debridements. Serial and multiple debridements of wounds, including superficial and deep muscles, must be performed, but nerves, tendons, joints, and bones, even if partially damaged, can be preserved. Further assessment with time to guide reconstruction is appropriate. Once all of the electroporated muscle is removed, wound closure should be accomplished with vascularized tissue. It is safest to connect flap vessels to recipient vessels well outside the zone of maximum injury. Large blood vessels that are damaged should be bypassed by vascular grafting or removal. Injured nerves should be decompressed by tunnel releases and kept physiologically moist for later assessment. Allografts or biologic dressings can be used for interim coverage until the second look procedure and debridement are completed. If needed to fill dead space, vascularized coverage is beneficial but may be technically difficult to achieve in an unstable patient. The vascular damage and resulting thrombotic phenomenon abates during the second week and tissues become less inflamed. This is the time when tissues around the wound withstand manipulation for a local, regional, axial, or free flap. The mortality rate of patients who suffer high-energy electrical burns is high with the main cause of death being multi-organ failure. Once wounds are closed, recovery of nerve and muscle function becomes the next challenge. Nerve releases, nerve grafts, and transfers are often necessary. Amputation and replacement with a prosthesis is often the most cost-effective and rapid approach to regaining productivity. Months after wounds are closed, patients often develop neuromuscular coordination problems, pain syndromes, and neuropsychological disorders that require a team approach to manage.

Treatment of radiation injury Treatment of sunburn injury is complex. There are both ionizing and non-ionizing thermal injury processes involved. Deep sunburns can cause epidermolysis and blistering, which can be very painful. Of course, the first line of therapy is to avoid further sun exposure to the burn area and replace the disrupted barrier functions of the epidermis. Topical analgesic creams are water based and may have temporary effect. It is best to use a wax- or ointment-based barrier

529

to reduce heat and water transport across the wound. Restoring barrier function helps tremendously with pain management. Dressings like Xeroform, Aquacel Ag, or hydrogel sheeting are excellent antimicrobial and evaporative barriers to maintain a physiologic environment for healing and substantially reduce pain. Topical nonsteroidal anti-inflammatory medications reduce the inflammation and inflammation-driven pain.21,22 Oxidative damage is the central mode of injury in ionizing radiation-induced injury. Therefore the administration of antioxidants, e.g., superoxide dismutase (Cu/Zn/Mn-containing SOD), nitroxides (tempol), and aminothiols (amifostine), represents a standard approach and a first-line treatment in clinical therapies for ROI-mediated injury. They scavenge free radicals, protecting cellular components against oxidative damage. N-acetylcysteine (NAC) is another thiol-containing antioxidant that replenishes cellular levels of reduced glutathione, an endogenous antioxidant, as well as scavenging aqueous phase free radicals. These mechanisms allow NAC to serve as a radioprotectant against the oxidative effects of gamma rays and other forms of ionizing radiation. At high radiation doses, it is very difficult to completely block the effects of reactive oxygen intermediates (ROI) production throughout the intracellular water. Consequently, in parallel with the search for efficient antioxidants, sustained research efforts are currently focused on identifying critical targets of the ROIs at the cellular level and on developing effective treatments for restoring these damaged cellular components. Topical occlusive dressings with antimicrobial activity are the first line of therapy for ionizing radiation skin burns. Polyethylene glycol-based waxes help scavenge free radicals and reduce pain and may slow injury progression. Topical antibiotic creams and lotions should be avoided in the acute phase as hydration enhance reactive oxygen species generation. Rather, use anhydrous ointments or gel barriers to maintain an optimal environment for healing. Healing maybe slow, and the full extent of the tissue necrosis is often not clear for weeks to months. Once the acute phase of wound progression and inflammation has subsided, consideration should be given to wound coverage strategy. Skin or flaps from non-irradiated areas are needed to bring in proliferation-competent cells to heal the wound and vascularize grafts. Grafting of adipose-derived stem cells beneath non-healing radiation wounds is finding increased enthusiasm as a technique to restore healing capacity and remodel the stiff and painful fibrotic skin surrounding a radiation wound.

Treatment of chemical injuries The treatment of chemical injuries is stratified into the acute and non-acute stages. The goal of acute care is to reduce the exposure to the drug. The goal of the non-acute stage is to debride and reconstruct the wound. Fundamentally, the extent of injury caused by any toxic chemical in contact with tissue is linked to the concentration and volume of the toxic chemical. Therefore, with few exceptions the treatment is to dilute the chemical and remove it by rinsing the exposed area and using absorbing towels. The most notable exception to that is the treatment of hydrofluoric acid contacts. In addition, one should never try to pH neutralize an acid spill by applying a basic solution and vice-versa. Acid– base reactions are exothermic enough to cause thermal burns.

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Wet clothing, gloves, and other cement-saturated items in contact with the skin should be removed quickly to minimize duration of contact. The next step is dilution with copious water for 15–30 min. Ideally, this would occur immediately after exposure prior to transport to the emergency department.28,29 Once this is done, the contact area should be covered in sterile (or clean) absorbing dressings, and the patient should be transferred to a hospital or acute care clinic for further evaluation and treatment. Anhydrous chemical toxins or metal compounds should be removed by quick surface cleaning with a dry cloth or absorbing powder. Hydrofluoric acid is a water-based material. The HF binds avidly to calcium, i.e., calcium gluconate or other calcium salt. Calcium gluconate (2.5%) gel can be applied to the contact site. This gel is often available where HF is extensively used. It should be quickly massaged with a gloved hand into affected areas until pain has subsided. If pain persists after 30 minutes, consider intravenous administration of 1 amp of 10% calcium gluconate (30 mL) IV over 10 minutes. It can be repeated every 6 hours with lactated Ringer’s administered in between calcium checks until the pain is resolved. The consequences of a delay in receiving medical attention can be fatal as hydrofluoric acid may penetrate into vital tissues through the circulation. Powdered chemicals such as dry concrete, cement, and anhydrous metals should be brushed off of the skin prior to the utilization of irrigation. Water triggers an exothermic reaction which will cause a burn. Similarly, acid or base exposures should never be neutralized with a base or acid. Definitive management through excision and skin grafting may be necessary. We also propose a new classification with an emphasis on treatment modality. Cement burns treatment consists of removing all of the cement and clothing soaked in cement, followed by irrigation with water, and dressing with topical antimicrobial compounds.58 Another common form of chemical injury is exposure to highly concentrated bleach solutions, especially bleaching agents for skin and hair color. In addition to copious irrigation to dilute the bleach, oral and topical vitamin C (ascorbic acid) acts to neutralize the oxidizing effect of the bleach. Immediate cooling with an ice pack in a thin towel can reduce the rate of tissue damage and allow for natural antioxidants to regenerate. A topical NSAID like aloe vera cream, Avosil, or similar can be used to reduce inflammation and pain. Mild acids like citric acids are not appropriate as they enhance the release of chlorine.29 In the second stage of chemical burn care, the objective is to debride nonviable tissues and reconstruct the wounded area as needed. The depth of the injury depends on the chemical agent. Acid burns are usually less deep that alkali burns. Whether skin grafts or flaps will be need will depend on the depth of the injury and will be decided by the surgeon.

Effect of burn trauma on metabolism30–32 Extensive burns elicit a pronounced metabolic response to trauma causing physiologic derangements leading to the hypermetabolic state (Table 18.8). Over weeks post-burn, the hypermetabolic response involves severe catabolism, nitrogen depletion, and loss of lean body mass. This condition is associated with a progressive decline of host defenses that impairs the immunologic response and can lead to sepsis.

Table 18.8  Percentage increase in metabolic rate vs. burn size

% Burn (TBSA)

Metabolic rate (% increase)

20

 30

30

 50

40

 75

50

100

60

100

The burn wound consumes large quantities of energy due to the increased cost of thermal homeostasis, maintaining host defense barriers as well as protein biosynthesis. Burn patients often increase the basal metabolic rate 50%– 100% of the normal resting rate. The main features include increased glucose production, insulin resistance, lipolysis, and muscle protein catabolism. Without adequate nutritional support, patients suffer delayed wound healing, decreased immune function, and generalized weight loss. Many formulas predict the nutritional needs of patients on the basis of lean body mass and percentage TBSA burned (Table 18.9). Increased intake of both nutritional calories and protein are needed to restore the deficit. Using the gut for providing nutrition has several benefits including reduction of translocation of gut microbes into the circulation. Also, the dermis is the organ that converts vitamin D precursor into metabolically active vitamin D3 (VD3).59 VD3 is a primary regulator of innate cellular immune defenses posed by all cells, while it modulates the secondary immune responses of cellular immunity mediated by while blood cells, lymphocytes, eosinophils, basophils, and other cells that constitute the immune organ system. Loss of skin by burn injury and loss of sunlight exposure by prolonged inpatient hospitalization leads to a proinflammatory state. It is therefore critical to maintain VD3 levels within a healthy range of at least 30–70 ng/mL.

Nutritional management Patients fed early have significantly enhanced wound healing and shorter hospital stays.60 Meeting the extensive calorie requirement by oral route alone is practically not possible in the major burn patients.61 Enteral nutrition through nasogastric or nasoduodenal transpyloric tubes are the preferred supplementary route of providing calorie deficit to the acutely injured burn patient. Patients with 20% TBSA burns will be unable to meet their nutritional needs with oral intake alone, and the transpyloric tube should be inserted at admission, as it is better tolerated than if inserted after the return of peristalsis. In the rare case that precludes use of the gastrointestinal tract, parenteral nutrition should be used only until the gastrointestinal tract is functioning. Early enteral nutrition can relieve gastrointestinal damage and maintain the integrity of intestinal mucosa after severe burn.62 Gastrointestinal mucosal lesions take place during ischemia and the reperfusion period after severe burns. Early enteral nutrition can relieve the ischemia and reperfusion injury by means of increasing the ability of eliminating

Acute burn trauma management

531

Table 18.9  Formulae for estimating calorie and protein needs

Formula

Age (years)

% TBSA burn

Calories (kcal) per day

Protein

16–59

Any

(25 × body weight in kg) + (40 × % TBSA burn)

Not calculated

>60

Any

(20 × body weight in kg) + (65 × % TBSA burn)

Adults Curreri Galveston I

>18

Ireton-Jones

>18

Modified >18 Harris-Benedict

(2100 kcal/m2 × TBSA) + (1000 kcal/m2 × % TBSA burn)

Not calculated

Any but must be ventilatordependent

1784 − (11 × age in years) + (5 × weight in kg) + 244 (sex: male = 1; female = 0) + 239 (trauma: yes = 1; no = 0) + 804

Not calculated

50% surface injuries are calculated as a 50% injury]

(3 g × body weight in kg) + (1 g × % burn)

Galveston Infant

0–1

Any

(2100 kcal/m2 × TBSA) + (1000 kcal/m2 × % TBSA burn)

Not calculated

Galveston II

1–11

Any

(1800 kcal/m2 × TBSA) + (1300 kcal/m2 × % TBSA burn)

Not calculated

Galveston Adolescent

12–18

Any

(1500 kcal/m2 × TBSA) + (1300 kcal/m2 × % TBSA burn)

1 g nitrogen = 6.25 g protein; BMR, basal metabolic rate.

oxygen free radicals. The increase of intestinal permeability is one of the early features of intestinal mucosal barrier damage. Early enteral nutrition is an effective method to keep a normal intestinal barrier through burn metabolic stress response. Parenteral nutrition requires additional vascular access with its concomitant risks. It also lacks the beneficial effects of gut mucosal stimulation and protective effects against bacterial translocation and stress hemorrhage. The rigorous schedule of dressing changes for burn wound care, operations, and rehabilitation sessions often interferes with meals. Diminished appetite from high-dose analgesics also contributes to poor feeding. Adequate nutritional support is so critical to recovery from burn injury that most clinicians will place feeding tubes in patients with inadequate oral calorie intake despite the risk of aspiration pneumonia.63,64 Much like fluid resuscitation, the exact nutritional requirements are debatable.63,64 The clinical response of the patient remains the best indication of nutritional repletion during recovery from the injury. The rapidity of epidermal regeneration of superficial burns and donor sites and improving serum nutritional parameters are the best indicators of adequate nutrition. Measurement of the basal metabolic rate also guides nutritional replacement therapy. Measuring weight loss and gain during treatment is not

useful because of the large fluid shifts. Even with adequate nutritional support, most patients lose muscle mass and weight. Optimizing nutrition to cover nutrient utilization is the fundamental goal. Over- or underfeeding increases the risks of complications.

Nutrition formulae The main features include increased glucose production, insulin resistance, lipolysis, and muscle protein catabolism. Without adequate nutritional support, patients have delayed wound healing, decreased immune function, and generalized weight loss. Many formulas predict the nutritional needs of these patients on the basis of lean body mass and percentage TBSA burned. Increased intake of both total calories and protein (1.5–3 g of protein/kg/day) is needed to restore the deficit. Much like fluid resuscitation, the exact nutritional requirements are debatable. The clinical response of the patient remains the best indication of nutritional repletion during recovery from the injury. Close glucose control of 80–110 mg/dL can be achieved using an intensive insulin therapy protocol, leading to decreased infectious complications and mortality rates. Burn

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centers continue to use a variety of formulae to estimate nutrient needs (see Table 18.9). The number of energy estimation formulas has increased in recent years with many developed for specific patient populations. Burn-specific equations have been developed both for pediatric and adult populations.65 A study compared 46 published energy calculations with indirect calorimetry in burn patients and found none precisely estimated calorie needs and most demonstrated some inaccuracy for any given patient. Several studies propose the use of anabolic steroids or growth hormone to reduce muscle catabolism and weight loss during the injury and to enhance weight gain during recovery. It appears that anti-catabolic and anabolic agents can markedly diminish the net catabolism of burn injury during the acute and recovery phases. These agents, in combination with optimum protein intake, appear to be of significant benefit in the metabolic management of the severe burn. Adequate nutritional support from the beginning of acute care is critical to burn patient survival. Therapeutic strategies should aim to prevent body weight losses of more than 10% of the patient’s baseline status because more profound weight loss is associated with significantly worse outcomes. Known consequences of catabolic disorders with loss of lean body mass above 10% include impaired immune function and delayed wound healing. Lean body mass reduction beyond 40% leads to imminent mortality. Therefore complications of ongoing catabolism remain a major cause of morbidity and mortality in severely burned patients.

during dressing changes: limit opiate use to prevent excess interstitial edema that impairs wound nutrition; ensure the safety and comfort of sedated patients both during and post-procedure by frequently assessing pain level and vital signs; and control acute pain during the most painful stages of dressing changes (dressing removal and wound cleansing). Close monitoring of respiratory status is required when consciousness is diminished. More emphasis on pain control not only helps the patient’s psychological wellbeing but may significantly affect physical outcome as well. Painful stimuli influence the release of a number of circulatory factors that affect tissue perfusion, immune system function, and wound healing. Effective management of pain requires a working knowledge of pain neurophysiology and pharmacology. These skills are important for burn care providers. Patients without a substance abuse problem before the injury typically do not develop opiate addiction even after receiving high doses for prolonged periods, but physical dependence often occurs after sustained treatment with opiates. Gradually reducing the doses of opiates as pain diminishes avoids opiate withdrawal. Increasing evidence suggests that methadone is an excellent choice for background pain control in burn patients and has a very low tolerance development rate.

Pain control

Skin graft loss

The adverse sequelae of inadequate pain control in the burn population have been long recognized, yet control of pain remains inadequate globally. The dynamic evolution of the pain both centrally and peripherally, and the many factors that influence pain perception, illustrate the need for a therapeutic plan that is similarly dynamic and flexible enough to cope with the facets of background, breakthrough, procedural, and postoperative pain. Regular, ongoing, and documented pain assessment is key in directing this process. Severe pain with burns is a major physiologic stress that can have a negative impact on the patient’s recovery. Often, bedside procedures require adequate doses of anxiolytics and opiates managed by a skilled intensivist. Particularly painful and anxiety-provoking is the first dressing change after skin grafting. In addition to pain, especially at the donor site, patients often experience great anxiety as they confront their new graft for the first time. Various approaches have been studied to provide sedation, comfort, and pain control. Conventional pharmacotherapy utilizes opioids for analgesia and benzodiazepines for sedation. The risk of apnea may cause the provider to err on the side of administering too little drug. To combat this, some centers offer patient-controlled analgesia (PCA) using propofol. PCS allows the patient to self-titrate to the comfort level desired, which may have the added benefit of allowing the patient to feel in control of the situation. In general, it is helpful to have an anesthesiologist or pain specialist involved in the day-to-day management of burn patients. Providers caring for burn patients should keep in mind several key points in order to optimize pain control

Loss of skin graft is the most common operative complication and is caused by inadequate immobilization, inadequate wound debridement, or formation of blood clot beneath the graft. Infection is usually the direct consequence of failed graft take (Fig. 18.18). Thus, careful placement of dressings to immobilize the graft relative to the wound bed is essential. Some burn surgeons spray freshly applied skin grafts with fibrin sealant to help immobilize the graft and accelerate vascular ingrowth. Unless carefully splinted, avoid circumferential compression dressings on a grafted extremity. Any movement in a grafted and circumferentially wrapped extremity will generate shear stress between underlying muscles and the overlying graft. Early graft inspection on day 2–3 after grafting should be encouraged with removal of any underlying hematoma. After day 3, capillary ingrowth has occurred and would be interrupted by graft movement. If examination shows that the skin grafts are grossly infected, then microbiologic cultures can be performed and appropriate antimicrobial therapy instituted.

Complications

Invasive wound infection In burn patients, systemic antibiotic prophylaxis administered in the first 4–14 days significantly reduces all-cause mortality by nearly a half; limited perioperative prophylaxis reduces wound infections but not mortality.66 Topical antibiotic prophylaxis applied to burn wounds, commonly recommended, has no large beneficial effects. The methodologic quality of the evidence is weak, however, so a large, robust randomized controlled trial is now needed.

Complications

533

needed as well. Patients with premorbid peripheral vascular disease are especially prone. The appropriate level of amputation should be performed as soon as feasible to expedite prosthesis fitting and patient rehabilitation.

Compartment syndromes

Figure 18.18  Appearance of an infected burn wound resulting in systemic sepsis and loss of skin autografts and allografts.

Wound infection should be suspected if the wound becomes increasingly uncomfortable, tachycardic, painful, or malodorous; if cellulitis is observed; or if the patient becomes febrile. Several biopsies from suspicious areas in the burn wound should be sent for microbiology. Since all wounds will be colonized after a few hours, it is best to measure the density of bacteria in the wound. This is called quantitative bacterial culture. Some experience, clean instruments, and training is necessary to accurately perform the test. When the density of bacteria in the wound exceeds 100,000 colony-forming units per gram of tissue (equivalent to 105/gram), then host defense mechanisms are no longer effective. This condition permits invasive wound infection. Treatment of invasive wound infections requires both antibiotics and excision of all infected tissue. Empiric broad-spectrum antibiotic treatment should be started after discussion with the microbiology team. The antibiotic treatment regime can be adjusted to be more specific according to the rapid-slide Gram stain results obtained in a few hours from the biopsy. In 24–48 hours, more specific identification of the bacteria and its antibiotic sensitivities can be used to decide on the antibiotic regime. The recommended choice of antibiotic is guided by the most likely cause of infection, and local patterns of antibiotic resistance should also be considered.

Adrenal insufficiency Some degree of adrenal insufficiency occurs in up to 36% of patients with major burns. Correcting for it is not as simple as administering corticotropin. Probably due to the variation in the stress responses across different patients, there is no statistically resolved association between response to corticotropin stimulation and survival. The clinical relevance of this finding has not been established.

Circumferential limb compression with vascular compromise Partial extremity amputation may be necessary for treatment of loss of tissue viability following major burn injury or frostbite. This most commonly occurs in the distal extremities resulting in loss of digits. However, more proximal amputations may be

Compartment syndrome occurs when the tissue pressure within an enclosed space is elevated above venous pressure. If the pressure exceeds venous pressures, the result is decreased blood flow within the fascial compartment resulting in decreased delivery of metabolic nutrients, decreased oxygen delivery, and decreased removal of metabolic wastes. If the resulting metabolic stress reaches a critical level, cell lysis and increasing pressure results. The final result without treatment within the warm ischemia tolerance time for tissues is tissue necrosis. The occurrence of abdominal compartment syndrome has a similar pathophysiology. Because of the vital organs involved, it can be life-threatening. It results from edema in a major burn patient with capillary leak and undergoing aggressive fluid resuscitation. It is diagnosed by rising airway pressures, decreasing urine output and intra-abdominal pressures greater than 20 mmHg, and evidence for an abdominal organ dysfunction.67 It is associated with renal impairment, gut ischemia, elevated airway ventilation pressures, increased bladder pressures, and cardiac and pulmonary malperfusion. Clinical manifestations include tense abdomen, decreased pulmonary compliance, hypercapnia, and oliguria. Urine output monitoring is not sensitive or specific enough to diagnose abdominal compartment syndrome. Serial close patient monitoring and aggressive treatment should be instituted to avoid this potentially fatal complication. Treatment includes maintaining appropriate intravascular volume, maintaining normal intravascular oncotic pressure, arterial oxygenation, appropriate body positioning, pain management, sedation, nasogastric decompression if appropriate, chemical paralysis if required, and torso escharotomy are all interventions to increase abdominal wall compliance and decrease intra-abdominal pressures. Bladder pressure monitoring should be initiated as part of the burn fluid resuscitation protocol in every patient with 30% TBSA burn. Patients who receive >250 mL/kg of crystalloid in the first 24 hours of resuscitation are at highest risk for developing abdominal compartment syndrome. Percutaneous abdominal decompression is a minimally invasive procedure that should be performed before resorting to laparotomy. If less invasive maneuvers fail, decompressive laparotomy should be performed in patients with abdominal compartment syndrome that is refractory to other therapies.

Deep venous thrombosis Deep venous thrombosis incidence ranges from 1% to 23% in burn patients, and deep venous thrombosis chemoprophylaxis with heparin is recommended. Risk factors include older age, TBSA of greater than 20%, prior history of venous thromboembolism, blood transfusions, use of mechanical ventilation, and African-American race.68 Often coagulopathies develop after multiple transfusions.68 Alteration in clotting parameters can trigger intravascular thrombosis in low flow veins. Deep venous thrombosis is associated with a significant

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increase in burn patient mortality. Although widely practiced, the effectiveness of DVT chemoprophylaxis with heparins is controversial.69

Systemic inflammatory response syndrome There are standardized definitions for sepsis and infection-related diagnoses in burn patients. Patients with large burns have a baseline temperature reset to 38.5°C, and tachycardia and tachypnea may persist for months. Continuous exposure to inflammatory mediators leads to significant changes in the white blood cell count, making leukocytosis a poor indicator of sepsis. Use other clues as signs of infection or sepsis, such as increased fluid requirements, decreasing platelet counts >3 days after burn injury, altered mental status, worsening pulmonary status, and impaired renal function. The term “systemic inflammatory response syndrome” should not be applied to burn patients because patients with large burns are in a state of chronic systemic inflammatory stimulation.

Sepsis Patients with large TBSA burns are immunosuppressed and at increased risk for infections, especially of the wounds, venous access sites, and lungs.70 However, for small TBSA burns, there is no immune-compromise. Small burn wounds (