Plastic Surgery: Volume 6: Hand and Upper Limb (Plastic Surgery, 6) [5 ed.] 9780323810432, 9780323873826, 9780323810371, 0323810438

Table of contents :
Any screen. Any time. Anywhere.
Plastic Surgery
Copyright
Contents
Video Contents
Lecture Video Contents
Preface to the Fifth Edition
List of Editors
List of Contributors
Acknowledgments
Dedication
1
1 Anatomy and biomechanics of the hand
Introduction
Skin, subcutaneous tissue, and fascia
Bones and joints
Hand elements
The wrist
Joint motion
The thumb
Muscles and tendons
Extrinsic extensors (Video 1.1 )
Pronators and supinators
Extrinsic flexors (Video 1.3 )
The retinacular system
Intrinsic muscles (see Video 1.2 )
Blood supply
Peripheral nerves
Conclusion
References
2
2 Examination of the upper extremity
Obtaining a patient history
Patient demographics
Current complaint
Medical history
Allergies and medications
Social history
Physical examination specific to the hand
Inspection
Discoloration
Deformity
Muscular atrophy
Trophic changes
Swelling
Skin creases
Palpation
Assessment of musculotendinous function
Posture
Motion
Power
Examination of the muscles of the hand
Examination of the extrinsic muscles
Flexor digitorum profundus muscle
Flexor profundus test (Video 2.1 )
Flexor digitorum superficialis muscle
Flexor sublimis test (Video 2.2 )
Flexor pollicis longus muscle
Milking test of the finger and thumb flexor tendons (Video 2.3 )
Extensor pollicis brevis and abductor pollicis longus muscles
Finkelstein test
Eichoff test (Video 2.5 )
Extensor carpi radialis longus and brevis muscles
Extensor pollicis longus muscle (Video 2.6 )
Extensor digitorum communis muscles (Video 2.7 )
Extrinsic tightness test
Extensor indicis proprius muscle
Extensor digiti minimi muscle
Extensor carpi ulnaris muscle
Examination of the intrinsic muscles
Thenar muscles (Video 2.8 )
Adductor pollicis muscle
Interosseous and lumbrical muscles (Video 2.9 )
Intrinsic tightness test (Bunnell)
Lumbrical-plus test
Hypothenar muscles
Assessment of stability
Scaphoid shift test (Watson) (Video 2.10 )
Finger extension test
Triquetrolunate ballottement test and the lunotriquetral shuck test
Distal radioulnar joint instability test
Ulnocarpal abutment test
The ulnar fovea sign (Video 2.11 )
Pisiform gliding test
Midcarpal instability test
Extensor carpi ulnaris synergy test
Assessment of peripheral nerves
Signs and tests for peripheral nerves
Tinel's sign
Phalen's test
Froment's test
Jeanne's sign
Wartenberg's sign
Other signs associated with ulnar nerve palsy
Tests for evaluating sensory nerve function
Two-point discrimination (2PD) test (Videos 2.12 and 2.13 )
Semmes–Weinstein monofilament test (Video 2.14 )
Moberg's pick-up test
Assessment of the vascular system
Allen's test (Video 2.15 )
Digital Allen's test (Video 2.16 )
Physical examination specific to the forearm
The interosseous membrane of the forearm (IOM)
Distal membranous portion
Middle ligamentous portion
Proximal membranous portion
Measurement of forearm rotation
Measurement of the muscle strength of the forearm
Supination
Pronation
Physical examinations specific to the elbow
Bony landmarks of the elbow
Ligaments of the elbow
Lateral ligament complex
Lateral ulnar collateral ligament
Radial collateral ligament
Annular ligament
Accessory collateral ligament
Medial collateral ligament complex
Instability of the elbow joint
Posterolateral rotatory instability
The pivot shift test
Measurement of malrotation of the distal humerus
Physical examination of thoracic outlet syndrome
Classification
Anatomy
Provocative maneuver
Adson test (Video 2.17 )
The neck tilting
The costoclavicular compression test
Wright test
Roos extended arm stress test (Video 2.18 )
Morley's test
Physical examination of the upper extremity in children
References
3
3 Diagnostic imaging of the hand and wrist
Introduction
Historical perspective
Radiography
Evaluation of the hand
Special views in the hand
Pediatric hand radiographs
Wrist evaluation
Wrist evaluation in distal radius fractures
Ultrasonography
Introduction
Masses
Injuries and degenerative conditions
Compressive neuropathies
Disadvantages
Ultrasound at the bedside
Computed tomography
Fractures and dislocations
Other applications of CT
Magnetic resonance imaging
MRI basics
Clinical applications of MRI
MRI for soft-tissue masses
Ganglion cysts
Giant cell tumors of the tendon sheath (GCTTS)
Lipomas
Hemangiomas
Enchondromas
MRI for wrist and hand trauma
Occult scaphoid and carpal fractures
Ligamentous injuries of the hand and wrist
Thumb ulnar collateral ligament injuries
Scapholunate interosseous ligament injury
MRI for evaluating ulnar-sided wrist pain
TFCC tears
Ulnocarpal abutment
DRUJ instability and tendinopathies
MRI for evaluation of fracture nonunion
MRI for avascular necrosis (AVN) in scaphoid fracture non-union
Kienbock's disease
Osteomyelitis
Vascular imaging techniques for the upper extremity
Radionuclide imaging
Safety in fluoroscopy
Future directions – Artificial Intelligence in radiology and point of care imaging
References
4
4 Anesthesia for upper extremity surgery
Introduction
Anatomy
Perineurial environment
Microneuroanatomy
Sonoanatomy
Pharmacology of local anesthetics
Pharmacokinetics
Toxicity
Vasoconstrictors
LA selection
Regional anesthesia techniques
Digital block
Wrist block
Intravenous regional anesthesia (Bier block)
Interscalene block
Supraclavicular block
Infraclavicular block
Axillary block
Wide-awake local anesthesia no tourniquet (WALANT)
Technique
Complications
Peripheral nerve injury
Local anesthetic toxicity
Vascular injury
Infection
Outcomes
Clinical outcomes and patient satisfaction
Operating room cost and efficiency
Special considerations
Cardiac patients
Pediatric patients
Perioperative pain management
Peripheral catheters
Preemptive analgesia
Chronic postoperative pain
References
5
5 Principles of internal fixation
Introduction
Patient selection
Fracture considerations
Patient-­specific considerations
Preoperative imaging
Treatment/­surgical technique
Preoperative planning
Fracture reduction
Intraoperative imaging
Arthroscopy
Fixation principles
Absolute stability and interfragmentary compression
Relative stability
Methods of fixation
Kirschner wires
Tension band constructs
External fixation
Interfragmentary lag screws
Compression plating
Bridge plating
Locked plating
Postoperative care
Summary
References
6
6 Nail and fingertip reconstruction
Introduction
Anatomy
Surface anatomy
Vascularity
Nerve supply
Physiology
Function
Acute injury
Epidemiology
Subungual hematoma
Treatment
Lacerations
Treatment
Postoperative care
Distal phalanx fractures
Initial evaluation
Treatment
Secondary procedures
Reconstruction
Nail ridge
Split nail
Treatment
Pterygium
Treatment
Nonadherence (onycholysis)
Treatment
Nail absence (anonychia)
Treatment
Cornified nail bed
Treatment
Nail spikes and cysts
Treatment
Hooked nail
Treatment
Eponychial deformities
Treatment
Hyponychial defects
Treatment
Pigmented lesions
Patient presentation
Subungual melanoma
Treatment
Pincer nail
Treatment
Reconstruction of fingertip injuries
Reconstructive principles
Flap selection
Skin grafting
Patient selection
Treatment: Local flaps
Volar V–­Y advancement (Atasoy, Kleinert)
Lateral V–­Y advancement flaps (Kutler)
Visor flap
Homodigital flaps
Reverse homodigital flap
Moberg flap
Heterodigital flaps
The cross-­finger flap
Thenar crease flap
Littler neurovascular island flap
Dorsal metacarpal artery flaps
Additional considerations
Completion amputation
Healing by secondary intention
Antibiotics
Summary
References
7
7 Hand fractures and joint injuries
Introduction
Anatomy
Classification of fractures and dislocations
Fracture stabilization/­fixation and return to function
Pediatric fractures
Open fractures
Bone gaps
Diagnosis
Treatment: fingers
Phalangeal fractures and dislocations
DIP joint fractures and dislocations
Middle phalanx shaft fractures
PIP joint injuries
Middle phalanx base articular fractures
External fixation
Technique of external fixation
Internal fixation
Technique of HHRA (Video 7.2 )
Proximal phalanx head fractures
Technique of open reduction and internal fixation (ORIF) of unicondylar fractures
Proximal phalanx shaft and base fractures
MCP joint fractures and dislocations
Metacarpal fractures
Indications for operative treatment of metacarpal fractures
Metacarpal head fractures
Metacarpal neck fractures
Metacarpal shaft fractures
Multiple metacarpal fractures
Technique of ORIF of multiple metacarpal fractures
CMC dislocations/­fracture dislocations
Treatment: thumb
MCP joint injuries
Stener lesion
Surgical repair of an acute UCL tear
Reconstruction of chronic UCL tear with tendon graft
Thumb metacarpal fractures
Thumb CMC joint injuries
Pediatric fractures
Proximal phalanx neck fractures
Complications
Secondary procedures
Malunion correction
Non-­union correction
Hardware removal, tenolysis, capsulotomy
Future directions
References
8
8 Fractures and dislocations of the wrist and distal radius
Introduction
Historical perspective
Basic science/­disease process
Anatomy
Biomechanics
Mechanisms of injury
Diagnosis/­patient presentation
History
Physical examination
Diagnostic tests
Patient selection
Treatment and surgical techniques
Scaphoid fractures
Scaphoid non-­union
Scapholunate ligament injury
Lunotriquetral ligament injury
Perilunate dislocation
Distal radius fractures
Ulnar styloid fractures
Future directions
References
9
9 Flexor tendon injuries and reconstruction
Introduction
Historical perspective
Basic science
Anatomy
Flexor tendon healing
Biomechanics of tendon repairs and gliding
Diagnosis
Treatment/­surgical techniques
Primary and delayed primary repairs
Indications and contraindications
Anesthesia
Surgical techniques
Zone 1 injuries
Zone 2 injuries (Videos 9.1–­9.6)
Zone 3, 4, and 5 injuries
FPL injuries
Injuries in children
Partial tendon lacerations
Closed rupture of the flexor tendons and pulleys
Postoperative care
Duran–­Houser method
Early active motion
Author's preferred combined passive–­active method (Nantong regimen)
Delayed motion exercises
Outcomes, prognosis, and complications
Secondary procedures
Free tendon grafting
Indications and contraindications
Donor tendons
Operative techniques
Staged tendon reconstruction
Indications
Techniques
The first stage
The second stage
Tenolysis
Indications
Anesthesia
Operative techniques
Postoperative treatment
Future directions
References
10
10 Extensor tendon injuries
Introduction
Historical perspective
Basic science/disease process
Anatomy of the extensor tendons
Extrinsic muscles
Intrinsic muscles
Functional anatomy
Linked chains
Functions of the intrinsic muscles
Extrinsic muscle function
Mechanisms of joint extension
Diagnosis/patient presentation
Elson test
Patient selection
Treatment/surgical technique
Suturing techniques
Zone I
The mallet finger
Open injuries
Chronic injuries
Zone II
Zone III (Video 10.1 )
Closed injuries
Open lacerations
Zone IV
Zone V
Human bite injuries
Sagittal band injuries
Zone VI
Zone VII
Zones VIII/IX
Postoperative care
Short arc motion
Dynamic splinting with passive extension
Relative motion splinting
Outcomes, prognosis, and complications
Outcomes
Complications
Secondary procedures
The mallet finger
The swan-neck deformity
The boutonnière deformity
Preoperative considerations
Tenotomy
Secondary reconstruction of the extensor tendon
Delayed sagittal band reconstruction (Video 10.2 )
The missing tendon: tendon transfers versus tendon grafting (Video 10.3 )
Soft-tissue management and staged reconstruction in combined injuries
Conclusion
Future directions
References
11
11 Replantation
Introduction
Basic science/­disease process
Pathophysiology of ischemia and reperfusion
Historical perspective
Diagnosis/­patient presentation
Transportation
Replant centers
Patient selection
Indications and contraindications
Treatment/­surgical technique
Operative sequence
Bone fixation
Tendon repair
Artery repair
Vein repair
Nerve repair
Skin closure
Special circumstances
Thumb replantation
Multiple digits
Proximal amputations
Distal amputations
Ring avulsion injuries/­degloving injuries/­avulsion amputation
Ectopic transplantation
Pediatric replantation
Postoperative care
Anticoagulation
Postoperative monitoring
Postoperative therapy
Psychosocial aspects of replantation
Future directions
References
12
12 Reconstructive surgery of the mutilated hand
Introduction
Goal of management of mutilated hand injury
Assessment of the mutilated hand
To salvage or not to salvage? Value of scoring and classification systems
Debridement
Envisioning the plan of reconstruction
Vascular reconstruction in the mutilated upper extremity
Stabilization of the skeleton
Soft-­tissue cover
Timing of soft-­tissue cover
The role of negative pressure wound therapy (NPWT) in a mutilated hand
Type of cover
Making the final choice
Pedicled groin flaps
Anatomy
Technique
Lower abdominal flaps
Anatomy
Technique
Pedicled radial forearm flap
Anatomy
Technique
Posterior interosseous reverse forearm flap
Anatomy
Technique
Lateral arm free flap
Anatomy
Technique
Anterolateral thigh free flap
Anatomy
Technique
Gracilis free flap (for cover and for function)
Anatomy
Technique
Major degloving injuries of the upper limb
Basic principles
Degloving injury of the hand
Degloving injury of the thumb
Degloving injury of the fingers
Degloving of the proximal upper limb
Muscle, tendon, and nerve repair
Total primary reconstruction vs. staged reconstruction
Secondary reconstruction
Secondary procedures on bones and joints
Coverage of large defects around the elbow
Free fibula transfer for long segment proximal bone defects
Anatomy
Technique
Secondary reconstruction of musculotendinous units
Restoration of motion at the elbow
Pedicled pectoralis major flap
Pedicled latissimus dorsi flap
Anatomy
Technique
Management of compartment loss
Free functioning muscle transfer (FFMT)
Nerve reconstruction
Secondary reconstruction of digital losses: toe transfers
Thumb reconstruction
Second toe for thumb reconstruction
Complications
References
13
13 Thumb reconstruction: Non-­microsurgical techniques
Introduction
Historical perspective
Basic science/­disease process
Diagnosis/­patient presentation
Patient selection
Treatment/­surgical technique
Distal third
Middle third
Proximal third
Prosthetics
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Future directions
References
14
14 Thumb reconstruction: Microsurgical techniques
Introduction
Historical perspective
Diagnosis/patient presentation
The initial operation
Patient selection
Patient factors
Timing: primary versus secondary reconstruction
Injury factors
Decision-making for the thumb
Decision-making for fingers
Decision-making for the metacarpal hand
Treatment/surgical technique
General principles in vascular dissection
General principles in recipient preparation
General guidelines in donor closure
General principles in flap inset
Specific operations
Trimmed great toe (Video 14.1 )
Second toe: total and partial (Video 14.2 )
Third toe
Modified wraparound flaps: great and second toes
Neurosensory lateral great-toe pulp flaps
First-web neurosensory flap
Combined second- and third-toe transplantation (Video 14.3 )
Vascularized joint transfer for metacarpophalangeal joint reconstruction of the thumb
Postoperative care
Immediate postoperative period
Motor rehabilitation
Sensory rehabilitation
Outcomes, prognosis, and complications
Outcomes and prognosis
Range of motion
Strength assessment
Appearance and sensory outcomes
Donor site outcome evaluation
Complications
Secondary procedures
Debates in thumb reconstruction with toe-to-hand surgery
Future directions
References
15
15 Infections of the hand
Introduction
Historical perspective
Basic science/­disease process
Causative organisms
Diagnosis/­patient presentation
Fingertip
Fingertip infections
Paronychia
Felon
Finger
Pyogenic flexor tenosynovitis
Hand
Deep space infections
Wrist/­forearm
Necrotizing soft-­tissue infection
Joints
Septic arthritis
Bone
Osteomyelitis
Atypical infections
Mycobacterial infections
Fungal infections
Mimics of infection
Gout
Pseudogout
Pyogenic granuloma
Pyoderma gangrenosum
Patient selection
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Future directions
References
16
16 Tumors of the hand
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient history
Physical examination
Laboratory studies
Imaging
Biopsy
Resection
Utility of multidisciplinary team approach
Treatment/surgical treatment by tissue of origin
Skin tumors
Cutaneous horn
Epidermal inclusion and sebaceous cysts
Verruca vulgaris
Nevi
Keratoacanthoma
Dermatofibroma
Seborrheic keratosis
Actinic keratosis
Basal cell carcinoma
Squamous cell carcinoma
Melanoma
Merkel cell carcinoma
Synovial lesions
Ganglion cysts
Giant cell tumor (pigmented villonodular synovitis)
Nerve tumors
Schwannoma/neurilemoma
Neurofibroma
Lipofibromatous hamartoma
Fat tumor: lipoma
Fibrous tissue lesions
Benign lesions
Sarcomas
Vascular lesions
Hemangioma
Vascular malformations
Glomus tumor
Pyogenic granuloma
Muscle lesions
Myositis ossificans
Osteoid osteoma
Leiomyoma
Rhabdomyosarcoma
Cartilage and bone tumors
Enchondroma
Osteochondroma
Solitary unicameral bone cyst
Aneurysmal bone cyst
Giant cell tumor of bone
Osteosarcoma
Chondrosarcoma
Staging and treatment of musculoskeletal sarcomas
Metastases
Postoperative care
Outcomes, prognosis, and complications
Future directions
References
17
17 Dupuytren’s disease
Basic science and disease process
Heredity
Cellular and molecular processes
Genes and epigenetic modifications
Inflammation
Myofibroblasts, fibroblasts and extracellular matrix (ECM)
Surgical anatomy of the palmar fascia in the hand and fingers and involvement in Dupuytren’s disease
Clinical disease process
Clinical assessment
Differential diagnosis
Grading
Indications for treatment
Shared decision-making
Treatments
Early stage DD
Steroids
Radiotherapy
Late stage DD
Non-surgical
Collagenase clostridium histolyticum (CCH)
Surgical
Percutaneous needle fasciotomy (PNF)/needle aponeurotomy (NA)
Open fasciotomy
Fasciectomy
Skin
Fascia
Dermofasciectomy
Joints
Others
External fixation and distraction
Amputation
Rehabilitation
Outcome, prognosis, and complications
Repeated procedures
Complications
Collagenase (CCH)
Percutaneous needle fasciotomy (PNF)/needle aponeurotomy (NA)
Fasciectomy
Dermofasciectomy (DF)
Salvage surgery
Arthrodesis of the PIP joint
Amputation
Future directions
Acknowledgments
References
18
18 Osteoarthritis in the hand and wrist
Introduction/epidemiology
Historical perspective
Basic science/disease process
Pathophysiology
Diagnosis
Management of OA of the fingers
Distal interphalangeal joint (DIP) arthritis
Diagnosis
Indications for surgery
Cheilectomy
Biomechanical effects of DIP fusion
DIP arthrodesis
Indications
Techniques
Interosseous wiring
K-wire fixation
Tension band wiring
Axial compression screw
Complications of DIP fusion
Infection
Non-union
DIP arthroplasty
Mucous cyst
Proximal interphalangeal (PIP) joint arthritis
Management
PIP arthrodesis
Techniques
Crossed K-wire technique
Tension band wire technique
Compression screw
Plating
PIP arthroplasty
Silicone interposition arthroplasty
Technique
Surface replacement arthroplasty with nonconstrained implants
Patient selection
Technique for nonconstrained or semiconstrained PIP arthroplasty
Postoperative therapy for PIP arthroplasty
Outcomes and complications of PIP arthroplasty
Metacarpophalangeal (MCP) joint arthritis
Anatomy and biomechanics
Resection and resurfacing arthroplasty
Implant arthroplasty
Hinged prostheses
Silicone constrained prostheses
Surface replacement prostheses
PyroCarbon arthroplasty
Technique for MCP joint arthroplasty with PyroCarbon implant
MCP arthrodesis
Vascularized joint transfer/costochondral replacement
Management of OA of the thumb
Thumb metacarpophalangeal (MCP) joint arthritis
Trapeziometacarpal arthritis
Etiology and epidemiology
Anatomy and biomechanics
Diagnosis and classification
Nonoperative treatment
Surgical procedures for stage I disease
Thumb TMC arthroscopy
Dorsal wedge extension osteotomy
Volar ligament reconstruction
Technique for Eaton–Littler procedure
Procedures for stage II–IV disease
Trapeziectomy alone
Surgical technique for simple trapeziectomy
Trapeziectomy with ligament reconstruction and/or tendon interposition
Prosthetic arthroplasty
Trapeziometacarpal arthrodesis
Technique for arthrodesis
OA of the wrist
Etiology
Patient evaluation
Surgical treatment
Technique for dorsal approach to the wrist
Radial styloidectomy
Neurectomy
Proximal row carpectomy
Four-corner fusion
Radioscapholunate fusion
Total wrist arthrodesis and total wrist arthroplasty
Future directions
References
19
19 Rheumatologic conditions of the hand and wrist
Introduction
Basic science/disease process
Etiology
Pathogenesis
Medical management
Diagnosis/presentation
Wrist involvement
Finger and thumb involvement
Patient selection
Perioperative considerations
Goals of surgery
Sequence of surgery
Treatment/surgical technique
Operations at the wrist level
Wrist synovectomy/dorsal tenosynovectomy
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Distal ulna resection (Darrach procedure)
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Partial wrist arthrodesis (radioscapholunate arthrodesis)
Postoperative care
Complete wrist arthrodesis
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Total wrist arthroplasty
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Operations for the hand and fingers
MCP synovectomy and soft-tissue reconstruction
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
MCP arthroplasty (silicone)
Postoperative care
PIP arthroplasty
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
MCP and IP arthrodesis
Postoperative care
Outcomes, prognosis, and complications
Correction of swan-neck deformity
Postoperative care
Correction of boutonnière deformity
Postoperative care
Outcomes, prognosis, and complications
Correction of thumb deformities
Postoperative care
Outcomes, prognosis, and complications
Tendon surgery and carpal tunnel syndrome
Carpal tunnel syndrome
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Flexor tendon ruptures
Postoperative care
Outcomes, prognosis, and complications
Trigger fingers
Postoperative care
Outcomes, prognosis, and complications
Extensor tendon ruptures
Postoperative care
Outcomes, prognosis, and complications
Other rheumatologic disorders of the hand and wrist
Seronegative spondyloarthropathies
Systemic lupus erythematosus
Scleroderma
Postoperative care
Crystalline arthropathy (gout)
Crystalline arthropathy (pseudogout)
Differentiating acute gout or pseudogout attack from septic arthritis
DECT scan
JAK inhibitors
Summary
Future directions
References
20
20 Occupational disorders of the hand
Introduction
Patient history and examination
Knowledge of the disease process and its causation
The role of force and repetition
Specific occupational disorders of the hand and wrist
Tendinopathies
Lateral epicondylitis
Trigger finger
De Quervain’s tenosynovitis
Extensor carpi ulnar tendinitis
Flexor carpi radialis tenosynovitis and flexor carpi ulnaris tenosynovitis
Nerve compression
Median neuropathy: carpal tunnel syndrome (CTS)
Vascular disorders
Hypothenar hammer syndrome
Hand–arm vibration syndrome (HAVS)
Bone and joint problems
Osteoarthritis
Distal interphalangeal joint arthritis
Proximal interphalangeal joint arthritis
Metacarpophalangeal joint arthritis
Carpometacarpal joint arthritis
Return to work
Measuring impairment
Summary and future directions
References
21
21 Nerve entrapment syndromes
Pathophysiology of chronic nerve compression
Double-crush syndrome
Clinical examination of upper extremity nerve entrapments
Manual muscle testing algorithm (Video 21.1 )
Scratch collapse test (Video 21.2 )
Electrodiagnostic studies (EDS)
Median nerve entrapments
Carpal tunnel syndrome
Anatomy
Etiology
History
Clinical examination
Other diagnostic tools
Patient selection
Non-operative treatment
Treatment/surgical technique
Wide-awake OCTR
Endoscopic carpal tunnel release (ECTR)
OCTR vs. ECTR
Ultrasound-guided carpal tunnel release (usCTR)
Outcomes and complications
Median nerve entrapments in the elbow and forearm
Background
Lacertus syndrome
Anatomy
History
Clinical examination
Non-operative treatment
Wide-awake surgical release
Superficialis syndrome – AIN syndrome
History
Clinical examination
Non-operative treatment
Surgical release
Ulnar nerve entrapments
Ulnar nerve compression in Guyon's canal
Background
Anatomy
History
Clinical examination
Surgical release
Cubital tunnel syndrome
Anatomy
History
Clinical examination
Non-surgical treatment
Surgical release
In situ decompression – the authors' preferred technique
Simple decompression
Endoscopic decompression
Submuscular–subcutaneous transposition
Medial epicondylectomy
Outcomes and complications
Radial nerve entrapments
Wartenberg's syndrome – entrapment of the SBRN
Anatomy
History and clinical examination
Non-surgical treatment
Surgical release
Radial tunnel syndrome – PIN compression in the proximal forearm
Anatomy
History
Clinical examination
Non-operative treatment
Surgical release
Outcomes following surgery
Lateral intermuscular syndrome – radial compression in the distal upper arm
Anatomy
History and clinical examination
Non-surgical treatment
Surgical release
Triangular interval syndrome – radial compression in the proximal upper arm
Anatomy
History and clinical examination
Non-surgical treatment
Surgical release
Other nerve compressions of the upper extremity
Quadrilateral space syndrome – axillary nerve entrapment
Anatomy and etiology
History
Clinical examination
Other diagnostic tools
Non-surgical treatment
Surgical release
Musculocutaneous nerve compression
Anatomy and etiology
History and clinical examination
Non-surgical treatment
Surgical release
Suprascapular nerve compression
Anatomy and etiology
History and clinical examination
Other diagnostic tools
Non-surgical treatment
Surgical release
Dorsal scapular nerve compression
Anatomy and etiology
History and clinical examination
Non-surgical treatment
Surgical release
Future directions
R­ef­er­en­ces
22
22 Peripheral nerve repair and reconstruction
Introduction
Basic science and natural history
Anatomy
Gross anatomy: the upper extremity
The neuron and supporting cells
The nerve trunk
Blood supply
Physiology
Degeneration and regeneration
The distal nerve segment
Diagnosis and presentation
Formal classification of injury
Neuropraxia
First-degree injury
Axonotmesis
Second-degree injury
Third-degree injury
Neurotmesis
Fourth-degree injury
Fifth-degree injury
Sixth-degree injury
Clinical examination
Functional evaluation
Electromyography/neurography
Wound inspection
Patient selection
Type of nerve injury
Condition of the wound
Treatment and surgical techniques
Immediate compared with delayed nerve repair
General principles
Timing
Surgical approach
Principles of nerve repair
General principles (Videos 22.1 & 22.2 )
Epineurial compared with fascicular repair
End-to-side nerve repair
Wound closure and immobilization
Nerve reconstruction
Autografts
Approach and preparation
Nerve ends
The gap
Length of graft
Harvest of the graft
Coaptation and maintenance
Donor nerves
Sural nerve
Medial and lateral antebrachial cutaneous nerves
The terminal branch of the posterior interosseous nerve
Superficial sensory branch of the radial nerve
Other
Tubular repair and artificial conduits
Biological conduits
Processed nerve allografts (Video 22.3 )
Non-degradable conduits
Biodegradable conduits
Fillers
Other techniques
Nerve transfers
Postoperative care
General aspects
Postoperative movement training
Sensory re-education
Cortical reorganization
Sensory re-education in phase 1
Improving effects of sensory re-education – phase 2
Outcome
Assessment of outcome
General aspects
BMRC
The Rosen score
Factors that affect outcome
General aspects
Age
Digital nerves
Nerve trunks
Level of injury
Type of repair
Type of injury
Postoperative dysfunction
General aspects
Complex regional pain syndrome
Other factors
Future perspectives
Acknowledgments
References
23
23 Brachial plexus injuries: adult and pediatric
Introduction
History of brachial plexus reconstruction
Adult brachial plexus injury
General principles in BPI management
Anatomy
Gross anatomy
Microanatomy
Level of brachial plexus injury
Patterns of brachial plexus injury
Pathophysiology and degree of nerve injury
Timing of brachial plexus exploration
Clinical evaluation
Etiology of adult brachial plexus injury
Patient history
Preoperative evaluation and diagnosis
Motor examination
Sensory examination
Plain X-ray and imaging studies
Electrodiagnostic studies
Vascular injury
Surgical treatment and techniques
Different incision lines for different approaches
Landmarks and key points for supraclavicular dissection
Landmarks and key points for infraclavicular dissection
Surgical techniques
Level I injury
Nerve transfer
Extraplexus nerve transfer
Intraplexus nerve transfer
Closed-target nerve transfer (or distal nerve transfer)
End-to-side neurorrhaphy nerve transfer
Reconstructive strategies
Shoulder
Elbow
Finger
Pedicled muscle transfer
Functioning free muscle transplantation (FFMT)
Level II injury
Level III injury
Level IV injury
Postoperative management and rehabilitation
Palliative reconstruction for sequelae deformities
Outcome evaluation
Conclusion
Future directions
Pediatric brachial plexus injury (obstetric brachial plexus palsy)
Introduction
Infant obstetric brachial plexus palsy
Clinical presentation
Clinical examination
Timing of surgery
Preoperative preparation
Surgical technique
Reconstructive strategies
Pure rupture injury
Rupture injury associated with root avulsion
Postoperative management
Outcome assessment
Results
Sequelae obstetric brachial plexus palsy
Shoulder deformity reconstruction
Elbow deformity reconstruction
Forearm and hand deformity reconstruction
Conclusion
Future directions
R­ef­er­en­ces
24
24 Tetraplegia
Introduction
Basic science/disease process
Classification of the tetraplegic upper extremity
Patient presentation and patient selection
Forming a team
Timing
Patient evaluation/selection
Treatment/surgical technique (Table 24.2)
General guidelines for reconstruction
Tendon transfers
Nerve transfers
Surgical reconstruction
IC group 0 (high cervical spinal cord injuries)
Elbow extension
Biceps-to-triceps tendon transfer
Surgical technique
Postoperative rehabilitation
Deltoid-to-triceps transfer36
Surgical technique (Fig. 24.7)
Postoperative rehabilitation
Nerve transfer for elbow extension
IC groups 1 and 2
Improving wrist extension
Postoperative rehabilitation
Side-to-side sutures
Restoring key pinch
Split FPL-to-EPL interphalangeal stabilization
ELK-tenodesis
Flexor pollicis longus tenodesis (passive key pinch)
Postoperative rehabilitation
Nerve transfers
IC group 2 and some IC group 3
Restoring active key pinch by BR-to-FPL transfer
Surgical planning
Operative procedure
Postoperative rehabilitation
IC groups 3, 4, and 5
Restoring active key pinch, grasp, and release in one operative stage
The single-stage grip and release procedure55 (Video 24.1 )
Surgical order of procedures
Intrinsic stabilization
Zancolli “lasso” procedure
House intrinsic tenodesis
ECU tenodesis
Postoperative rehabilitation
Other considerations
Nerve transfers for hand function
Supinator to posterior interosseus nerve transfer
Patient selection
Surgical technique
Postoperative care
Nerve transfer for pinch and grasp
IC groups 6, 7, 8, and 9
Spasticity
Future directions
Functional neuromuscular stimulation
Outcomes and complications
Conclusions
References
25
25 Tendon transfers
Introduction
General principles of tendon transfers
Bone and soft-­tissue healing
Selection of donor muscle–­tendon
Expendability
Strength
Amplitude
Direction of transfer and integrity
Timing of tendon transfers
Surgical techniques
Radial nerve palsy
Indications
Timing
Operations
Standard FCU transfer (Figs. 25.3–­25.6)
FCR transfer (Fig. 25.8)
Boyes flexor digitorum superficialis transfer (Fig. 25.9)
Outcomes
Low median nerve palsy
Anatomical considerations
Timing
Operations
Burkhalter extensor indicis proprius transfer (Fig. 25.10)
Bunnell ring finger flexor digitorum superficialis transfer (Fig. 25.12)
Camitz palmaris longus transfer (Fig. 25.15)
Other opposition tendon transfers (Table 25.3)
High median nerve palsy
Indications
Operations
Outcomes
Low ulnar nerve palsy
Indications
Timing
Static procedures to correct clawing of the fingers
Tendon transfers to correct clawing
Modified Stiles–­Bunnell transfer (see Fig. 25.27)
Brand EE4T transfer (Fig. 25.28)
Brand EF4T transfer (Fig. 25.29)
Fritschi PF4T transfer
Tendon transfer to correct ulnar deviation of the small finger
Tendon transfers to provide adduction of the thumb
Ring finger flexor digitorum superficialis adductor transfer
Smith extensor carpi radialis brevis adductor transfer (Fig. 25.31)
Tendon transfers to provide index finger abduction
Neviaser accessory abductor pollicis longus and free tendon graft (Fig. 25.32)
High ulnar nerve palsy
Outcomes
Tendon transfers for combined nerve injuries
Tendon transfers for low median–­low ulnar nerve palsy
Tendon transfers for high median–­high ulnar nerve palsy
Tendon transfers for reconstruction after trauma
Tendon transfers to restore thumb extension
Tendon transfers to restore finger extension
Tendon transfers to restore thumb flexion
Tendon transfers to restore finger flexion
Summary
Future directions
References
26
26 Nerve transfers
Introduction
Basic science
Diagnosis and patient presentation
Patient history
Physical examination
Imaging
Electrodiagnostic testing
Patient selection
Examples of nerve transfer procedures for specific injury patterns
Upper plexus injury
Specific patient exam findings
Reconstruction techniques
Use of spinal accessory nerve (cranial nerve XI) to suprascapular nerve transfer (motor)
Use of triceps to axillary nerve transfer (motor component)
Use of the double fascicular nerve transfer (motor)
Other potential donors to restore elbow flexion
Lower plexus injury
Specific patient exam findings
Reconstruction techniques
Complete/­near-­complete plexus injury
Specific patient exam findings
Reconstruction techniques
Use of spinal accessory and intercostal nerves as donors (motor)
Discussion of cross C7 transfer, phrenic nerve transfers (motor)
Median nerve injury
Specific patient exam findings
Reconstruction techniques
Use of radial to median branch nerve transfers (motor)
Use of brachialis branch to AIN branch nerve transfer
Use of adjunct tendon transfers to augment nerve transfers
Ulnar nerve injury
Specific patient exam findings
Reconstruction techniques
Use of median to ulnar branch nerve transfers (motor)
Use of adjunct tendon transfers to augment nerve transfers
Radial nerve injury
Specific patient exam findings
Reconstruction techniques
Use of median to radial branch nerve transfers
Use of adjunct tendon transfers to augment nerve transfers
Sensory nerve injury
Restoration of key sensory functions
Use of ulnar to median branch nerve transfers (sensory)
Use of median to ulnar branch nerve transfers (sensory)
Use of median and ulnar nerve transfers to restore first webspace sensation in C5–­C6 root level brachial plexus injury (se ...
Use of median to radial nerve transfers (sensory)
Use of radial to axillary nerve transfers (sensory)
Postoperative care
Postoperative wound care
Complications
Rehabilitation
Postoperative patient evaluation
Outcomes and prognosis
Secondary procedures
Future directions
References
27
27 Free-functioning muscle transfer
Introduction
Historical perspective
Patient selection
Preoperative planning
Selecting the donor muscle
Selecting the axon source
Surgical technique of the free-functioning gracilis transfer
Preparing the recipient site
Harvesting the gracilis muscle
Muscle transfer to restore finger flexion
Muscle transfer to restore finger extension
Muscle transfer to restore thumb opposition
Muscle transfer to restore elbow flexion
Complications
Future directions
References
28
28 The ischemic hand
Introduction
Historical perspective
Raynaud’s phenomenon
Basic science
Anatomy
Embryology
Arterial system in the forearm, hand, and digits
Superficial palmar arch
Deep palmar arch
Surgical landmarks of superficial and deep palmar arch
Digital arteries
Micro-arterial system
Physiology of blood flow
Hemodynamics
Cellular control mechanisms
Pathophysiology
Emboli
Trauma
Systemic disease
Diagnosis/patient presentation
Evaluation
History and physical examination
Diagnostic investigations
Capillaroscopy
Ultrasound
Duplex ultrasonography
Isolated cold stress testing
Infrared thermography
Laser speckle contrast imaging
Conventional angiography
MR and CT angiography
Patient selection
Acute ischemia
Acute arterial injury
Arterial emboli
Iatrogenic injuries
Cannulation injury
Arterial injection injuries
Acquired arteriovenous fistula
Chronic ischemia
Arterial thrombosis
Aneurysm
Buerger’s disease
Connective tissue disorders
Vasospastic disease
Treatment
Non-surgical treatment
Environmental modification
Medical management
Pharmacological agents
Thrombolytic therapy
Botulinum toxin A therapy
Biofeedback
Surgical treatment
Embolectomy
Sympathectomy
Leriche sympathectomy (arteriectomy)
Periarterial sympathectomy
Classic sympathectomy
Extended or radical digital sympathectomy
Arterial reconstruction
Wrist inflow artery reconstruction (ulnar artery, radial artery, and superficial palmar arch)
Digital artery reconstruction
Other surgical options
Balloon angioplasty with stenotic lesion
Venous arterialization
Fat grafting
Treatment algorithm
Postoperative care
Outcomes, prognosis, and complications
Future directions
References
29
29 The spastic hand
Introduction
Cerebral palsy
Cerebrovascular accident (CVA)
Traumatic brain injury (TBI)
Spinal cord injury
Patient presentation
Clinical examination
Resting posture of the upper limb
Evaluation of spasticity
Muscle contracture
Joint deformity
Motor assessment
Sensory examination
Functional assessment
General preoperative assessment
Other neurological impairments
Imaging and electromyography
The role of botulinum toxin
Technique
Patient selection and timing of surgery
Treatment
Rebalancing the forces
Reducing spasticity
Partial neurectomy
Neurosurgical procedures
Muscle contracture
Tenotomy
Muscle release
Joint contracture
Tendon transfers
Most frequent procedures
At the elbow level
At the forearm level
At the wrist level
At the finger level
Swan-neck deformity
Intrinsic contracture
At the thumb level
Future directions
Conclusions
References
30
30 The stiff hand
Introduction
Etiology, basic science, anatomy, and clinical examination
Treatment
Nonoperative intervention
PIP joint flexion contracture
PIP joint extension contracture
MCP joint extension contracture
Tendon gliding
PIP joint extension lag
Motor retraining
Operative intervention
Anesthesia
MCP joint extension contracture
PIP joint flexion contracture
PIP joint extension contracture
Outcomes
Future directions
References
31
31 The painful hand
Introduction
Assessment
Mechanism of injury
Penetrating injury
Blunt or “closed” injuries
Subjective descriptors
Patient-­reported measures
Clinical examination
Diagnosis/­pathologies
Neuritis
Neurostenalgia
Symptomatic post-­traumatic neuroma
Spinal nerve root avulsion (deafferentation)
Causalgia
Complex regional pain syndrome
Atraumatic neuropathy
Non-­surgical management
Physical therapies
Psychological therapies
Co-­occurring psychiatric and psychological disorders
Features of psychological assessment
Patient-­reported measures
Pain Catastrophizing Scale (PCS)
Pain Self-­Efficacy Questionnaire (PSEQ)
Psychological therapeutic interventions
Cognitive Behavioral Therapy
Acceptance and Commitment Therapy
Pharmacological therapies
Specific medications
Gabapentinoids
Tricylic antidepressants (TCAs)
Nonsteroidal anti-­inflammatory drugs and opioids
Infusions and topical treatments
Abuse and withdrawal
Side-­effects and interactions
Surgical treatment
Operative procedures
Treatment for neurostenalgia: neurolysis
Treatment of symptomatic post-­traumatic neuroma
Graft reconstruction
Neuroma relocation
Targeted muscle re-­innervation
Spinal nerve root re-­implantation after brachial plexus avulsion injury
Dorsal root entry zone procedure
Summary
References
32
32 Congenital hand I: Embryology, classification, and principles
Introduction
Limb development
Classification
Assessment and principles of treatment
Limb development (embryology)
Overview of upper limb morphogenesis
The molecular control of limb outgrowth and patterning
Limb vasculature
Skeletogenesis
Myogenesis
Innervation
The development/differentiation of specific tissues
Anomalies of limb development and their classification
Background
Problems of the Swanson classification
The OMT classification
Assessment of the child and family
The clinic
History
Examination
Investigations
Diagnosis
Principles of surgical management
Indications
Function
Appearance
Timing
References
33
33 Congenital hand II: Malformations – whole limb
Poland syndrome
Introduction
Basic sciences/disease processes
Diagnosis/patient management
Patient selection, treatment, and surgical plan
Emergent complications
Psychosocial concerns
Functional and aesthetic problems
Management of the underdeveloped or absent pectoralis major
Management of hand differences
Postoperative care
Outcome, prognosis, and complications
Secondary and additional procedures
Future directions
Ulnar dimelia and mirror hand
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment and surgical technique
Outcome, prognosis, and complications
Secondary procedures
Radioulnar synostosis
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Osteotomy through synostosis
Osteotomies through the diaphyseal portion of radius and ulna
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Future directions
Madelung deformity
Introduction
Basic science/disease process
Genetic associations
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Physiolysis and ligament release
Radial osteotomy
Ulnar epiphysiodesis
Ulnar osteotomy
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Future directions
References
34
34 Congenital hand III: Malformations – abnormal axis differentiation – hand plate: proximodistal and radioulnar
Proximodistal
Brachydactyly
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Postoperative care
Outcome, prognosis, and complications
Symbrachydactyly
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Non-vascularized toe phalanx transfers
Free vascularized toe-to-hand transfers
Distraction lengthening
Postoperative care
Outcome, prognosis, and complications
Transverse deficiency
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Outcome, prognosis
Cleft hand
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Transverse bones
Border digit syndactyly
First webspace reconstruction
Cleft closure
Thumb reconstruction
Postoperative care
Outcome, prognosis, and complications
Radioulnar
Radial longitudinal deficiency, hypoplastic thumb
Introduction
Basic science/disease process
Diagnosis/patient presentation
Type 1 thumb hypoplasia
Type 2 thumb hypoplasia
Type 3A thumb hypoplasia
Type 3B thumb hypoplasia
Type 4 thumb hypoplasia
Type 5 thumb hypoplasia
Patient selection
Treatment/surgical technique (see Algorithms 34.1 & 34.2)
Type 1 hypoplastic thumbs
Type 2 and 3A hypoplastic thumbs
First webspace deepening
Opposition transfer
ADM (Huber) opposition transfer
FDS opposition transfer with UCL reconstruction
Type 3B, 4, and 5 hypoplastic thumbs
Pollicization
Type 0 and 1 RLD forearms
Joint release and tendon transfer
Type 2 RLD forearms
Radius lengthening
Type 3, 4, and 5 RLD forearms
Soft-tissue release and bilobed flap
Precentralization soft-tissue distraction
Centralization
Ulna osteotomy
Postoperative care
Opposition transfer, collateral ligament reconstruction
Pollicization
Joint release and tendon transfer (type 0 and 1 RLD forearm)
Soft-tissue release and bilobed flap
Precentralization soft-tissue distraction, centralization
Outcome, prognosis, and complications
Secondary procedures
Ulnar longitudinal deficiency
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Polydactyly
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Radial polydactyly
Type I and II
Type III and IV
Type V and VI
Ulnar polydactyly
Type A
Type B
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Triphalangeal thumb
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Abnormally shaped phalanx (delta, trapezoid, rectangle, angular epiphysis)
Delta middle phalanx
Trapezoid or rectangle middle phalanx
Angular epiphysis
Five-fingered hand
Narrow first webspace
Thumb opposition
Associated polydactyly, primarily radial polydactyly
Outcome, prognosis, and complications
Future directions
References
35
35 Congenital hand IV: Malformations – abnormal axis differentiation – hand plate: unspecified axis
Syndactyly
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Creation of a web
Treating the lateral soft tissue defects
Separation of the fingertips
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Clinodactyly
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Kirner deformity
Introduction
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Apert hand
Introduction
History
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical technique
Separation of fingers
Thumb and first web
Additional procedures
Feet
Postoperative care
Outcomes, prognosis, and complications
Complications
Secondary procedures
References
36
36 Congenital hand V: Deformations and dysplasias – variant growth
OMT classification of deformation
Pediatric trigger thumb
Basic science/disease process
Diagnosis/patient presentation
Patient selection (Algorithm 36.1)
Treatment/surgical technique (Fig. 36.1)
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Congenital trigger fingers
Basic science/disease process
Diagnosis/patient presentation (Algorithm 36.2)
Patient selection
Treatment/surgical technique (see Video 36.2 Algorithm 36.3)
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Constriction ring sequence
Basic science/disease process
Diagnosis/patient presentation
Patient selection
In utero diagnosis (Algorithm 36.4)
Postnatal presentation (Algorithm 36.5)
Later presentations (Algorithm 36.6)
Treatment/surgical technique
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
OMT classification of dysplasia
Macrodactyly
Basic science/disease process
Diagnosis/patient presentation (Algorithm 36.7)
Flatt type 1: Macrodactyly with fibrolipomatous hamartoma
Flatt type 2: Macrodactyly with neurofibromatosis
Flatt type 3: Osteohypertrophic macrodactyly
Flatt type 4: Macrodactyly with hemihypertrophy
Treatment/surgical technique
Strategies to slow growth
Treatment of the nerves and blood vessels
Strategies to reduce volume
Amputation
Postoperative care
Outcome, prognosis, and complications
Secondary procedures
Future directions
References
37
37 Congenital hand VI: Dysplasias – tumorous conditions
Introduction
Diagnosis/patient presentation
Treatment/surgical technique
Postoperative care
Vascular anomalies
Vascular tumors
Infantile hemangioma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Congenital hemangioma (CH)
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Vascular tumors
Pyogenic granuloma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Capillary malformation
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Lymphatic malformation
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Outcomes, prognosis, and complications
Venous malformation
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Conservative treatment
Minimally invasive treatment
Surgical treatment
Outcomes, prognosis, and complications
Arteriovenous malformation
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Fibro-adipose vascular anomaly (FAVA)
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Vascular malformations with overgrowth – CLOVES syndrome
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Peripheral nerve tumors
Neurofibroma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Schwannoma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Adipose lesions of nerve
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Malignant peripheral nerve sheath tumor
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Connective tissue dysplasias
Infantile digital fibromatosis
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Juvenile aponeurotic fibroma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Infantile myofibromatosis
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Lipoblastoma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Infantile fibrosarcoma
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Skeletal dysplasias
Osteochondromatoses – multiple hereditary exostosis
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Osteochondromatoses – metachondromatosis
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Enchondromatoses – multiple enchondromatosis (Ollier disease)
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Enchondromatoses – Maffucci syndrome
Basic science/disease process
Diagnosis/patient presentation
Treatment/surgical technique
Future directions
References
38
38 Congenital hand VII: Dysplasias – congenital contractures
Arthogryposis
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical care
Humeral external rotation osteotomy
Elbow extension contracture release
Active elbow flexion transfers
Wrist contracture correction
Finger and thumb contracture correction
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Future directions
Camptodactyly
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical care
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Future directions
Thumb-in-palm deformity
Basic science/disease process
Diagnosis/patient presentation
Patient selection
Treatment/surgical care
Postoperative care
Outcomes, prognosis, and complications
Secondary procedures
Future directions
References
39
39 Growth considerations in the pediatric upper extremity
Introduction
Basic science/disease process
Anatomy and physiology of the epiphyseal growth plate
Vascular anatomy of the growth plate
Growth plate closure and skeletal age assessment during puberty
Diagnosis/patient presentation
Conditions affecting the growth plate
Trauma
Incidence and distribution in the upper extremity
Classification of physeal fractures
Treatment of physeal fractures
Tumor
Bone sarcoma involving the epiphysis
Congenital chondrodysplasia
Patient selection
Treatment/surgical technique
Treatment of physeal arrest
Observation
Completion of a partial physeal arrest and epiphysiodesis
Physeal distraction
Bar resection
Corrective osteotomies, lengthening or shortening
Epiphyseal transfer of the proximal fibular epiphysis
Indications
Vascular supply of the proximal fibular epiphysis
Harvest technique of the proximal fibula based on the tibialis anterior artery (Video 39.1)
Skin incision
Exposure of the anterior tibial pedicle
Dissection of the peroneal nerve at the fibular neck
Section of the interosseous membrane and distal osteotomy
Harvest of the biceps femoris tendon and capsulotomy of the proximal tibiofibular joint
Final dissection of the proximal portion of the vascular pedicle
Postoperative care
Donor site
Recipient site
Outcomes, prognosis, and complications
Secondary procedures
Donor site
Recipient site
Future directions
References
40
40 Treatment of the upper extremity amputee
Introduction
Principles of prosthetic reconstruction
Improve the soft tissues to help wear a prosthesis
Understand that the type of prosthetic is based on patient needs and amputation level
Passive/aesthetic devices
Body-powered devices
Externally powered prosthesis
Hybrid devices
Understand prosthetic attachment systems
Plan for the means of prosthetic control
Treat upper extremity pain and phantoms
Treatment of upper extremity amputees
Principles of acute upper extremity amputation surgery
Surgery for the shoulder disarticulation level amputee
Surgery for the transhumeral amputee
Surgery for the transradial level amputee
Surgery for the wrist disarticulation amputee
Surgery for the partial hand amputee
Surgery for the patient with digit amputations
Future directions
Conclusion
References
41
41 Upper extremity composite allotransplantation
Introduction
Evolution of upper extremity vascularized composite allotransplantation
Immunology of vascularized composite allotransplantation
Experimental background and scientific basis for upper extremity transplantation
Chronology of clinical upper extremity allotransplantation
Historical development and milestones
Clinical experience with upper extremity allotransplantation
Program, patient, procedural, and protocol-related considerations
Program establishment and implementation
Donor and recipient selection
Procedural aspects
Donor limb procurement
Recipient surgery
Protocol-related considerations
Maintenance immunosuppression
Rehabilitation and functional assessment after upper extremity allotransplantation
Assessment for rejection (host-versus-graft reaction)
Immunologic monitoring
World experience and surgical outcomes
Unique aspects of vascularized composite allotransplantation
Emerging insights in vascularized composite allotransplantation
Cortical plasticity and neuro-integration
Chronic rejection
Tolerance approaches and immunomodulatory strategies
Future directions of upper extremity reconstructive transplantation
References
42
42 Aesthetic hand surgery
Introduction
Relevant anatomy
Basic aesthetics of the hand
The aging process
Grading systems
Patient management
Rejuvenation of the epidermis and dermis
Non-surgical management
Topicals
Chemical peels
Microdermabrasion
Laser therapy
Q-switch lasers
Intermittent pulsed light
Photodynamic therapy
Non-ablative non-fractionated lasers
Non-ablative fractionated lasers
Ablative lasers
Radiofrequency
Dorsal vein prominence
Non-surgical management
Sclerotherapy
Endovenous ablation
Surgical management
Phlebectomy
Volume restoration
Non-surgical management
Injectables
Hyaluronic acid
Poly-L-lactic acid
Calcium hydroxyapatite
Injection technique
Surgical management
Autologous fat grafting
Author’s preferred technique
Skin excision
Arthroplasty/arthrodesis
Skin excess
Articular aging
Future directions
Adipose-derived stem cells
Platelet-rich plasma
Allograft adipose matrix
Conclusions
References
43
43 Hand therapy
Patient evaluation
Occupation-based assessments
Impairment-based assessments
Rehabilitation following tendon injury
Extensor tendon injury
Zone I/II
Zone III/IV
Zone V–VII
Thumb
Flexor tendon injury
Timing
Positioning
Motion
Tenolysis
Tendon transfer
Rehabilitation following nerve injury
Nerve decompression
Carpal tunnel release
Cubital tunnel release
Nerve repair
Sensory re-education
Desensitization
Nerve transfer
Motor re-education
Anterior interosseous nerve to ulnar motor nerve
Rehabilitation following fractures
Protective phase
Restorative phase
Strengthening and functional phase
Metacarpal fractures
Proximal/middle phalanx fractures
Distal phalanx fractures
Rehabilitation following replantation
Future directions
References
Confidence is ClinicalKey

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Front Matter

Fifth Edition

Plastic Surgery Hand and Upper Extremity Volume Six

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 Hand and Upper Extremity Volume Six Volume Editor

James Chang MD

Johnson & Johnson Distinguished Professor and Chief Division of Plastic Surgery Stanford University Medical Center Palo Alto, CA, 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 6 ISBN: 978-0-323-81043-2 Volume 6 Ebook ISBN: 978-0-323-87382-6 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

Index

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

926 951



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

xviii

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 This latest volume represents the world’s brightest minds in hand and microvascular surgery. I am indebted to my colleagues and friends from around the globe for their hard work and eloquent writing, and to our talented staff at Elsevier. It is our hope that this text will continue to serve as a guide for the optimal treatment of all our patients with hand problems. I am fortunate to have two families to thank: the students, residents, fellows, and faculty at Stanford University who stimulate and enrich me intellectually; and my own loved ones, my wife, Dr. Harriet Walker Roeder, and daughters, Julia, Kathleen, and Cecilia, who challenge and delight me in every way. James Chang, MD

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

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 Access video and video lecture content for this chapter online at Elsevier eBooks+

SYNOPSIS

ƒ The hand is an incredibly designed structure with complex anatomy and precise biomechanics. The hand must be able to produce adequate force to allow performance of activities of daily living. Furthermore, it must ensure coordination of the fingers for precise prehension and fine motor tasks. ƒ In order to achieve an optimal functional and aesthetic outcome in patients requiring hand surgery, it is thus essential to fully understand the detailed bone, muscle–tendon, aponeurotic, vascular, nerve, and lymphatic components. ƒ Additional challenges arise from the range of possible movements of various articular surfaces, assisted by muscle action and ligamentous support. ƒ In this chapter, we present the various elements that compose the hand as well as explanations of the biomechanical principles. These are updated according to the latest literature. Additionally, clinical examples will be used to illustrate anatomic principles.

Introduction During the Renaissance, Vesalius corrected early misconceptions and brought gross anatomy into proper focus. Since that time, many investigators have embellished the basic structural studies with functional, physiologic, and philosophical observations. The forearm and hand have been prominently included in those observations. Sir Charles Bell (1834),1 in his thought-provoking volume The Hand – Its Mechanism and Vital Endowments as Evincing Design, presented a concept of hand anatomy that places it in proper context with the position of humans in the animal kingdom. Duchenne (1867) carried out detailed analysis of muscular function by isolated electrical stimulation, described in his classic volume Physiologie des Mouvements.2 Frederick Wood-Jones (1920) probed more extensively into comparative anatomy and anthropology

in his excellent work The Principles of Anatomy as Seen in the Hand.3 Allen B. Kanavel (1925) published his monograph Infections of the Hand, which reported detailed analysis of the spaces and synovial sheaths.4 Surgery of the Hand by Sterling Bunnell (1944) became an indispensable reference during World War II.5 Emanuel B. Kaplan (1953) produced the nicely illustrated, detailed volume Functional and Surgical Anatomy of the Hand.6 Detailed studies of the integration of the intrinsic and extrinsic muscles operating the polyarticular digits may be found in the work of Landsmeer,7–10 Kaplan,11 Eyler and Markee,12 Stack,13 Tubiana and Valentin,14 and others. More recently, newer flaps intrinsic to the hand and upper extremity have been developed from more detailed investigation into vascular anatomy.15,16 Lastly, Berger,17 Viegas et al.,18 and others have expanded our knowledge of the ligamentous anatomy of the wrist. As a functional puppet, the hand responds to human desires; its motor performance is initiated by the contralateral cerebral cortex. The conscious demands relayed to the hand and forearm from the central nervous controlling mechanism are sent as movement commands. At subconscious levels, such a movement command is broken down, regrouped, coordinated, and sent on as a signal for fixation, graded contraction, or relaxation of a specific muscular unit. The degree of contraction or relaxation is then modified by relayed evidence that the motion created is that desired by the person. The modifying factors arrive centrally from a multiplicity of sensory sources such as the eye, peripheral sensory end organs, and muscle or joint sensory endings. The surgeon planning reconstructive surgery on the upper extremity must be aware not only of the complex anatomy of the hand and arm, but also of the physiologic interplay of balanced muscular functions under the influence of complex central nervous coordination. The maintenance of physiologic viability by the central and peripheral circulatory and lymphatic systems must also concern the reconstructive surgeon.

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CHAPTER 1  • Anatomy and biomechanics of the hand

This chapter addresses the fundamentals of hand and upper extremity anatomy and highlights clinical pearls, new anatomic descriptions that may aid surgery of the hand, and the fundamentals of biomechanics relevant to the hand surgeon. Illustrations and dissection videos are included for the reader to review important anatomic concepts.

Skin, subcutaneous tissue, and fascia There is great disparity in the character of the skin and soft-tissue envelope covering the dorsum of the hand and that covering the palm. Dorsal skin is thin and pliable, anchored to the deep investing fascia by loose, areolar tissue. These characteristics, coupled with the fact that the major venous and lymphatic drainage in the hand courses dorsally, serve to explain why hand edema is first evident dorsally. The prominent, visible veins in the subcutaneous tissue make it the standard site in which to evaluate venous filling and limb venous pressure  on physical examination. The same characteristics make the dorsum of the hand vulnerable to skin avulsion injuries. Palmar skin, in contrast, is characterized by a thick dermal layer and a heavily cornified epithelial surface. The skin is not as pliable as dorsal skin, and it is held tightly to the thick fibrous palmar fascia by diffusely distributed vertical fibers between the fascia and dermis. Stability of palmar skin is critical to hand function. At the same time, if scar fixation or loss of elasticity occurs in palmar skin, contractures and functional loss result. The skin of the palm is laden with a high concentration of specialized sensory end organs and sweat glands. The surgeon must understand the relationship of the palmar skin creases and the underlying joints in order to plan precise placement of skin incisions for exposure of joints and their related structures (Box 1.1 & Fig. 1.1). Examination of hand skin during normal ranges of motion in various planes is important in planning incisions or geometrically rearranging lacerations that might result in disabling scar contractures. Most loss of elasticity and some longitudinal shortening are compensated for adequately by mobility and elasticity of the uninjured dorsal skin. On the palmar aspect, however, scar shortening and inelasticity of the skin may result in contracture. The nature of palmar skin, its

stabilizing fixation to the palmar fascia, and its position on the concave side of the hand are the bases for such contractures. Littler outlined the specific sites in the palm where a longitudinal scar would impede extension.20 For example, in each digit, the geometry has been worked out by noting each joint axis and the kissing surfaces of the palmar skin in full flexion. These diamond-shaped skin surfaces should not be shortened and rendered inelastic by longitudinal scars if  ­limitation of extension is to be avoided (Fig. 1.2). The palmar fascia consists of resistant fibrous tissue arranged in longitudinal, transverse, oblique, and vertical fibers (Fig.  1.3). The longitudinal fibers concentrate at the proximal origin of the palmar fascia at the wrist, taking origin from the palmaris longus when it is present (in about 80–85% of individuals). The fascia at this level is separable from the underlying flexor retinaculum/carpal ligament, being identified by the longitudinal orientation of its fibers in contrast to the transverse fibers of the retinaculum. The palmar fascia fibers fan out from this origin, concentrating in flat bundles to each of the digits. Generally, the fibers spread at the base of each digit and send minor fibers to the skin and the bulk of fibers distal into the fingers, where they attach to tissues making up the fibrous flexor sheath of the digits. There are attachments of the fascia to the volar plate and intermetacarpal ligaments at each side of the flexor tendon sheath at the level of the metacarpal heads. Transverse fibers are concentrated in the midpalm and the webspaces. The midpalmar transverse fibers, although intimately associated with the longitudinal bundles, lie deep to them and are inseparable from the vertical fibers that concentrate into septa between the longitudinally oriented structures passing to the fingers. This system of palmar transverse fibers makes up what Skoog (in 1967) called the transverse palmar ligament.21 In fact, the transverse fibers form the roof of tunnels at this point that act as pulleys for the flexor tendons proximal to the level of the digital pulleys. Biomechanical evaluation of

BOX 1.1  Clinical pearl: Kaplan’s cardinal line Hand anatomist Emanuel Kaplan described specific surface lines that would aid surgeons in locating key structures in the palm of the hand. The cardinal line has often been misquoted; therefore we refer to Kaplan’s classic hand text, Functional and Surgical Anatomy of the Hand.19 Kaplan’s cardinal line is drawn from the apex of the first webspace to the distal edge of the pisiform bone (see Fig. 1.1). Two longitudinal lines are drawn from the ulnar aspect of the middle finger and the ulnar aspect of the ring finger. These will cross the cardinal line. The intersection of the cardinal line and the longitudinal line from the ulnar side of the middle finger corresponds to the motor branch of the median nerve. The intersection of the cardinal line and the longitudinal line from the ulnar side of the ring finger corresponds to the hook of the hamate. The motor branch of the ulnar nerve is found on the cardinal line, equidistant between the hamate and pisiform. See Kaplan’s original text for additional surface markings.

A

Hook of hamate B

Kaplan’s cardinal line Pisiform

Figure 1.1  Kaplan’s cardinal line, along with lines from the ulnar aspect of the middle finger and the ulnar aspect of the ring finger. Point A corresponds with the motor branch of the median nerve and point B with the motor branch of the ulnar nerve.

Skin, subcutaneous tissue, and fascia

3

b

a

d

c

A

B

Figure 1.2  (A,B) Schematic representation of the joint axes. The longitudinal dimensions in the midpalmar and mid-dorsal aspect of the digits change maximally. The midaxial line through the three joint axes does not change in length with flexion and extension. Palmar incisions placed longitudinally produce contracture if they pass across the palmar diamonds delineated by lines joining the joint axes (after Littler). Transverse incisions avoid the occurrence of flexion scar contractures. The same principle applies at the wrist. (Redrawn after Chase RA. Atlas of Hand Surgery, vol 1. Philadelphia: WB Saunders, 1973.)

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CHAPTER 1  • Anatomy and biomechanics of the hand

Palmaris longus tendon

Palmar branch of ulnar nerve

Branch of superficial radial nerve to skin of lateral thenar area

Pisiform Deep palmar branch of ulnar artery and deep branch of ulnar nerve

Palmar carpal ligament (thickening of deep antebrachial fascia continuous with extensor retinaculum)

Superficial branch of ulnar nerve Ulnar artery Palmaris brevis muscle

Palmar branch of median nerve

Hypothenar muscles

Thenar muscles

Palmar aponeurosis

Recurrent (motor) branch of median nerve to thenar muscles

Palmaris brevis muscle (reflected)

Minute fasciculi attach palmar aponeurosis to dermis

Anterior (palmar) views

Palmar digital nerves from superficial branch of ulnar nerve to 5th and medial half of 4th fingers

Palmar aponeurosis

Transverse fasciculi

Palmar digital arteries and nerves

Superficial transverse metacarpal ligaments

Figure 1.3  Superficial dissection of the palm, showing orientation of the palmar fascia. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Bones and joints

Vertical fibers

5

Bones and joints Hand elements

Figure 1.4  The palmar fascia with its longitudinal, transverse, and vertical fibers. The longitudinal fibers take origin in the palmaris longus (when present). Transverse fibers are concentrated in the distal palm supporting the web skin and in the midpalm as the transverse palmar ligament. Vertical fibers extend superficially as multiple, tiny tethering strands to stabilize the thick palmar skin. The deep vertical components concentrate in septa between the longitudinally oriented structures in the fingers. (Redrawn after McCarthy JG. Plastic Surgery. Philadelphia: WB Saunders, 1990.)

the palmar aponeurosis pulley has demonstrated that isolated sectioning did not change the work of flexor tendons or load efficiency.22 Nevertheless, this pulley has been implicated as contributing to the etiology of trigger finger.23 Longitudinal fibers pass toward the palmar surface of the thumb, but these fibers are generally less numerous and sometimes difficult to identify. The thumb fibers blend into the deep fascia overlying the thenar muscles. The ulnar extreme palmar fascia blends with the hypothenar fascia. The proximal one-third of this border is the attachment site of the palmaris brevis muscle. Laterally, the muscle attaches to the hypothenar skin and hypothenar fascia. The vertical fibers of the palmar fascia, which lie superficially to the tough triangular membrane made up by the longitudinal and transverse fibers, consist of abundant vertical fibers to the palm dermis (Fig. 1.4). Deep to the palmar fascia, the vertical fibers coalesce into septa, or the “perforating fibers of Legueu and Juvara”,24 forming compartments for flexor tendons to each digit and separate compartments for the neurovascular bundles together with the lumbrical muscles. There are eight such compartments which extend proximally to about the midpalm. Proximal to this, there is a common central compartment.25 The marginal septa extend more proximally than the seven intermediate septa closing the central compartment laterally and medially. The major septum between the index flexor tendons and the neurovascular and lumbrical space to the third interspace attaches to the third metacarpal, dividing the thenar or adductor space from the midpalmar space. Knowledge of these vertical compartments aids dissection and identification of structures in operations such as trigger-finger release, sympathectomy, and Dupuytren’s fasciectomy (Fig. 1.5). In the fingers, two important bands of fascia are named Grayson’s ligaments and Cleland’s ligaments. Grayson’s ligaments are volar to the neurovascular bundles and are quite flimsy. The much stouter Cleland’s ligaments are dorsal to the neurovascular bundles. These two fascial sheets help contain and protect the ulnar and radial digital arteries and nerves (Fig. 1.6).

The ability of the hand to resist and create powerful gross action, combined with its capacity to perform intricate fine movements in multiple planes, reflects the masterful construction of its supporting architecture. Reducing the hand to its supporting skeleton and its restraining ligaments reveals the architectural basis for its varied function. A study of the range of joint motions in the hand and forearm with all motor elements removed discloses the full range and limitations that the skeleton imposes on hand function. The hand skeleton is divisible into four elements: The fixed unit of the hand, consisting of the second and third metacarpals and the distal carpal row. The thumb and its metacarpal with a wide range of motion at the carpometacarpal joint. Five intrinsic muscles and four extrinsic muscles are specifically influential on thumb positioning and activity. The index digit with independence of action within the range of motion allowed by its joints and ligaments. Three intrinsic and four extrinsic muscles allow such digital independence. The third, fourth, and fifth digits with the fourth and fifth metacarpals. This unit functions as a stabilizing vise to grasp objects for manipulation by the thumb and index finger, or in concert with the other hand units in powerful grasp (Fig. 1.7). The distal row of carpal bones forms a solid architectural arch with the capitate bone as the keystone. The articulations of the distal carpals with one another, the intercarpal ligaments, and the important transverse carpal ligament (flexor retinaculum) maintain a strong, fixed transverse carpal arch. Projecting distally from the central third of this arch are the fixed central metacarpals, the second and third. Littler called this the “fixed unit of the hand”. It forms a fixed transverse arch of carpal bones and a fixed longitudinal arch created by the anatomic convexity of the metacarpals. As a stable foundation, this unit creates a supporting base for the three other mobile units. This central beam moves as a unit at the wrist under the influence of the prime wrist extensors (the extensor carpi radialis longus and brevis) and the prime wrist flexor, the flexor carpi radialis. These major wrist movers insert on the second and third metacarpals. Thus, the fixed central unit is positioned for activity of the adaptive elements of the hand around it. The distal row of carpal bones constitutes a fixed transverse arch. At the level of the metacarpal heads, the transverse arch of the hand becomes mobile, which is possible because the first metacarpal moves through a wide range of motion at the saddle-like carpometacarpal joint. The loose capsular ligaments and the shallow saddle articulation between the first metacarpal and the trapezium allow circumduction of the mobile first metacarpal. Its range of motion is checked by these capsular ligaments, including the volar beak ligament, and by its attachment to the fixed hand axis through the adductor pollicis, the first dorsal

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CHAPTER 1  • Anatomy and biomechanics of the hand

Pronator quadratus muscle Flexor carpi radialis tendon Common flexor sheath (ulnar bursa)

Tendinous sheath of flexor pollicis longus (radial bursa) Flexor retinaculum (transverse carpal ligament) (reflected ) Flexor digitorum profundus tendons Tendinous sheath of flexor pollicis longus (radial bursa) Fascia of adductor pollicis muscle

Flexor digitorum superficialis tendons

Thenar space

Common flexor sheath (ulnar bursa) (opened)

(deep to flexor tendon and 1st lumbrical muscle)

Lumbrical muscles in fascial sheaths

(Synovial) tendon sheath of finger

Midpalmar space

Lumbrical muscles in fascial sheaths (cut and reflected )

(deep to flexor tendons and lumbrical muscles) Fibrous and synovial (tendon) sheaths of finger (opened)

Annular and cruciform parts (pulleys) of fibrous sheath over synovial sheath of finger

Flexor digitorum superficialis tendon Flexor digitorum profundus tendon

Midpalmar space Palmar aponeurosis

Septa forming canals Profundus and superficialis flexor tendons to 3rd digit Septum between midpalmar and thenar spaces

Thenar space

Common palmar digital artery and nerve

Flexor pollicis longus tendon in tendon sheath (radial bursa)

Lumbrical muscle in its fascial sheath

Extensor pollicis longus tendon

Flexor tendons to 5th digit in common flexor sheath (ulnar bursa)

Adductor pollicis muscle

Hypothenar muscles Dorsal interosseous fascia Dorsal subaponeurotic space Dorsal fascia of hand Dorsal subcutaneous space

Palmar interosseous fascia Palmar interosseous muscles Dorsal interosseous muscles Extensor tendons

Figure 1.5  These deep palmar and midpalmar axial views of the hand reinforce the concept of distinct anatomic compartments separated by fascia. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Bones and joints

7

Figure 1.6  The components of the digital fascia that help to anchor the axial plane skin are Grayson’s ligaments palmar to the neurovascular bundles and Cleland’s ligaments dorsal to the bundles. (Redrawn after McCarthy JG. Plastic Surgery. Philadelphia: WB Saunders, 1990.)

interosseous, and the fascia and skin of the first webspace. The mobile fourth and fifth metacarpal heads move dorsally and palmarly in relation to the central hand axis by limited mobility at the carpometacarpal joints. These metacarpal heads are tethered to the central metacarpals by the intermetacarpal ligaments. The latter unite adjacent metacarpophalangeal volar plates, which are an intimate part of the joint capsules. When the head of the first metacarpal is palmar-abducted by thenar muscles innervated by the median nerve, and the fourth and fifth metacarpals are palmar-abducted by the hypothenar muscles innervated by the ulnar nerve, a volar, concave, transverse metacarpal arch is created, approximating a semicircle. The mobile metacarpal heads are pulled dorsally by extrinsic extensor tendons when the thenar and hypothenar muscles relax. It is obvious that a flaccid paralysis of the intrinsic muscles of the hand in median and ulnar nerve palsy will produce a flattened or even reversed transverse metacarpal arch. The active production of a semicircular transverse arch by the thenar and hypothenar muscles creates the proper circumferential arrangement of the ­metacarpophalangeal joints for convergence of the fingers in flexion. In this position the fingers, flexing at the metacarpophalangeal joints only, converge, forming with the thumb a cone, the apex of which lies over the anatomic center of the hand (Fig.  1.8). A vertical line dropped from the apex of the cone to the center of its base will strike the

Figure 1.7  Exploded view of the functional elements of the hand: (1) the thumb and its metacarpal with a wide range of motion at the carpometacarpal joint; (2) the index digit with independence of action in several planes; (3) the third, fourth, and fifth digits with the fourth and fifth metacarpals; and (4) the fixed unit consisting of the carpals with the fixed transverse carpal arch and the second and third metacarpals forming a fixed longitudinal arch. (Redrawn after McCarthy JG. Plastic Surgery. Philadelphia: WB Saunders, 1990.)

Figure 1.8  When the adaptive arch is semicircular, the fingers converge in a cone over the anatomic center of the hand – the long-finger metacarpophalangeal joint. (From McCarthy JG. Plastic Surgery. Philadelphia: WB Saunders, 1990.)

Cleland’s ligament Grayson’s ligament

Neurovascular bundle

Lateral digital sheet

Natatory ligament Pretendinous band Common digital artery

Spiral band

Transverse fibers of palmar aponeurosis

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CHAPTER 1  • Anatomy and biomechanics of the hand

third metacarpophalangeal joint. This point at the apex of the transverse metacarpal arch is the anatomic center of the hand. With the fingers fully abducted, the tips form radii of equal length from the anatomic center of the hand. The same radius projected proximally falls at the wrist joint. The most important single motor operating the central hand beam at the wrist level is the extensor carpi radialis brevis, which works against gravity, positioning the pronated hand into extension. In the absence of any other motors it pulls the central third metacarpal into extension, making it the apex of the passively created transverse metacarpal arch.

The wrist The wrist joint is the site for major postural change between the arm beam and the working hand end piece (Fig. 1.9). It has a multiarticulated architecture that creates a potentially wide range of motion in flexion, extension, radial deviation, ulnar deviation, and circumduction. The distal radioulnar joint allows pronation and supination of the hand as the radius rotates around the head of the ulna. The proximal row of carpal bones (scaphoid, lunate, triquetrum, pisiform) articulates with the distal radius and ulna, providing the ability to flex and extend the hand and perform radial and ulnar deviation. The distal carpal row (trapezium, trapezoid, capitate, and hamate), along with the second and third metacarpals, forms the “fixed unit” of the hand. The radiocarpal joint includes the carpal bones and the distal radius (Fig. 1.10). The principal articulation of the carpus is with the distal surface of the radius. The articular surface of the radius slopes in several planes. In the radial-to-ulnar plane, the radius exhibits an average slope of 22°. In the dorsal-to-palmar plane, the articular surface of the radius ­ slopes 12° with the dorsal surface more distal than the palmar surface. Fractures of the distal radius frequently result in a loss

of the normal radiocarpal configuration in one or both planes. A loss of the normal dorsal-to-palmar tilt of the articular surface will result in a change in the biomechanical properties of the wrist joint, which may lead to degenerative arthritis. The relationship of the length of the radius to the length of the ulna is fairly constant in individuals and is termed ulnar variance. The distal ulna will complete the curve of the articular surface of the radius. If the end of the ulna falls short of this curvature, the condition is termed ulnar negative variance. If the ulna extends distal to this imaginary extension, the condition is termed ulnar positive variance. Either condition may lead to wrist problems. Ulnar negative variance is associated with a higher incidence of Kienböck’s disease, avascular necrosis of the lunate. Ulnar positive variance greater than 2–3 mm is associated with ulnar impaction (Fig. 1.11). Gilula and others have described several anatomic features that denote normal extracarpal and intracarpal architecture.26 A line that follows the proximal articular contours of the proximal row of carpal bones circumscribes a smooth arc, termed the greater arc (Fig. 1.12). A disruption in the smooth appearance of this arc is one of the signs of carpal abnormality, such as abnormal rotation of one of the bones of the proximal carpal row, as would be seen with disruption of the scapholunate ligament. Similarly, the joint line between the proximal and distal row of carpal bones circumscribes another smooth arc, termed the lesser arc. The presence of abnormalities in either of these arcs may be an indication of carpal pathology, either acute or chronic. The scaphoid and lunate bones of the proximal carpal row form the convex articular counterparts of the concave distal radius for the major wrist articulation. In fact, the articular surface of the radius is divided into scaphoid and lunate fossae (Box 1.2). The triquetrum articulates with the lunate in the proximal row, and with the hamate across the midcarpal joint.

Posterior (dorsal) view

Anterior (palmar) view

Radius

Radius

Ulna Ulnar styloid process

Radial styloid process

Lunate

Scaphoid Tubercle of scaphoid

Triquetrum

Ulna Ulnar styloid process

Tubercle of trapezium

Hamate

Hamate

Trapezoid

Capitate

1

5 2

3

Metacarpal bones

4

Radial styloid process

Pisiform Triquetrum

Hook of hamate

Scaphoid

Lunate

Pisiform

Trapezium

Dorsal tubercle of radius

Trapezium Trapezoid

Capitate

5

1 4

3

2

Metacarpal bones

Figure 1.9  Palmar and dorsal views of the bones of the wrist. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Bones and joints

Olecranon

Right radius and ulna in supination: anterior view

9

Right radius and ulna in pronation: anterior view

Trochlear notch Coronoid process

Head

Radial notch of ulna Ulnar tuberosity

Neck

Oblique cord Ulnar tuberosity

Oblique cord

Radial tuberosity

Radius

Ulna

Radius

Anterior surface

Anterior surface

Ulna

Lateral surface Posterior border

Anterior border Anterior border

Posterior surface Interosseous membrane

Interosseous border Interosseous border

Interosseous membrane

Dorsal tubercle Groove for extensor pollicis longus muscle Groove for extensor digitorum and extensor indicis muscles Styloid process of ulna

Groove for extensor carpi radialis longus and brevis muscles Area for extensor pollicis brevis and abductor pollicis longus muscles

Styloid process Styloid process

Radius

Ulna Ulnar notch of radius

Styloid process

Styloid process

Area for scaphoid bone

Area for lunate bone

Carpal articular suface

Coronal section of radius demonstrates how thickness of cortical bone of shaft diminishes to thin layer over cancellous bone at distal end

Figure 1.10  Relationship of the radius and ulna at the proximal and distal radioulnar joints. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

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CHAPTER 1  • Anatomy and biomechanics of the hand

The pisiform is essentially a floating bone, unimportant for carpal stability. All four of the bones in the distal carpal row present articular surfaces for junction with the metacarpals. The distal carpal row forms a solid architectural arch with the central capitate as the keystone. The nature of the articulations of the distal carpals with one another, and of the carpal ligament (flexor retinaculum), is such that they make up a strong and fixed transverse carpal arch (Box 1.3 & Fig. 1.13).

BOX 1.3  Clinical pearl: Checking for malrotation The tubercle of the scaphoid is found at the distal flexion crease of the wrist joint, lateral to the tendon of the flexor carpi radialis. It is an important skeletal landmark in evaluating digital malrotations. Normally, each finger points to the scaphoid tubercle when individually flexed. A finger that points away from the tubercle may do so because of destructive flattening of the carpal arch. More commonly, it may result from malrotation following a metacarpal or phalangeal fracture (Fig. 1.13).

Figure 1.11  X-ray of ulnar positive variance: this patient has ulnar-sided wrist pain due to ulnar impaction syndrome.

Figure 1.12  Gilula’s lines showing the greater arc and lesser arc of the carpal bones. (Reproduced from Hentz VR, Chase RA. Hand Surgery: A Clinical Atlas. Philadelphia: WB Saunders, 2001.)

Scaphoid

BOX 1.2  Clinical pearl: Blood supply to the scaphoid Investigations by Gelberman and Menon have described two main vessel systems that perfuse the scaphoid via ligamentous attachments.27 The superficial palmar branch of the radial artery contributes a volar blood supply that feeds the distal scaphoid. The dorsal carpal branch of the radial artery contributes a dorsal blood supply that also primarily feeds the distal scaphoid. Therefore, the proximal scaphoid is poorly vascularized and is susceptible to nonunion after proximal pole fracture.

Figure 1.13  Each finger in correct alignment points to the tubercle of the scaphoid when flexed individually. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. 1. Philadelphia: WB Saunders, 1973.)

Bones and joints

The complex motions of the wrist are a product of the collected movements of the carpal bones in various planes and degrees of rotation relative to one another. The motion of any one carpal bone is a consequence of several factors. The first factor is the contour of the bone and the arrangements of its articular surfaces. The second is the degree of freedom afforded by intrinsic ligaments, which are ligaments originating from one carpal bone and inserting on another carpal bone, and by extrinsic ligaments, which are ligaments arising from the radius or ulna and attaching to a carpal bone or bones. This complex set of ligaments and the shape of the intercarpal and radiocarpal articulations control movement because no muscles arise or insert on any of the carpal bones except for the pisiform. This unique adaptation of nature avoids the need for a thickly muscled wrist and hand unit. It permits great flexibility in positioning the hand in space without the need for sets of muscle agonists and antagonists to control the several degrees of freedom of movement. The proximal row of carpal bones is anchored to the radius by a series of stout palmar ligaments arising primarily from the radius and by an additional set of stout ligaments arising from the ulna and the palmar portion of the triangular fibrocartilage complex (TFCC). The TFCC separates the distal end of the ulna from the ulnar-sided carpal bones and serves to suspend the distal ulna to the radius at the distal radioulnar joint. These primary extrinsic palmar ligaments take the form of an inverted “V” with its apex pointed distally. The three most predominant nerves innervating the TFCC are the dorsal cutaneous branch of the ulnar nerve (100%), the medial antebrachial cutaneous nerve (91%), and the volar branch of the ulnar nerve (73%). Other nerves play a minor role in the innervation of the triangular fibrocartilage complex: the anterior interosseous nerve, the posterior interosseous nerve, and the palmar branch of the median nerve.28 Dorsally, the extrinsic radiocarpal ligament complex is thinner and is primarily a condensation of capsular tissues, except for two stout structures, the dorsal intercarpal ligament joining the distal pole of the scaphoid and the triquetrum, and the dorsal radiocarpal ligament. According to work by Viegas, these two dorsal ligaments form a unique lateral “V” configuration that allows variation in length by changing the angle of the “V” while maintaining a stabilizing force on the scaphoid during wrist range of motion.29 The intrinsic ligaments are broad, stout structures that link one carpal bone to another, either within the proximal or distal row, or linking one carpal row to the other. The two most significant intrinsic ligaments are the scapholunate ligament and the lunotriquetral ligament. The scapholunate ligament anchors the scaphoid to the lunate to allow these two carpal bones to move in synchrony. Berger has subdivided this U-shaped structure into three regions: dorsal, proximal, and palmar.30 The dorsal region is thick and controls scapholunate stability. The proximal portion, composed mainly of fibrocartilage, and the palmar region, with thin and obliquely oriented fibers, are less important for stability.31 The lunotriquetral ligament is also composed of dorsal, proximal, and palmar portions. There is less motion between these two c­arpal bones. Disruption of either the scapholunate or lunotriquetral ligaments may lead to wrist

11

instability because the normal restraints on synchronous motion are removed.

Joint motion The bony anatomy of the hand is presented in Fig.  1.14. Normal metacarpophalangeal joint motion in the fingers ranges from 0 to 90°. Lateral activity in the metacarpophalangeal joints is limited by the rein-like collateral ligaments. These ligaments are loose and redundant when the metacarpophalangeal joints are in extension, allowing maximal medial and lateral deviation. As the metacarpophalangeal joint is flexed, the cam effect of the eccentrically placed ligaments and the epicondylar bowing of the collateral ligaments result in tightening and strict limitation of lateral mobility (Fig.  1.15). The fingers that have been fixed in extension during a period of healing have had the stage set for collateral ligament shrinkage and locking of the metacarpophalangeal joints in hyperextension. The proximal interphalangeal joint can be pushed to 110° of flexion, but extension usually cannot be carried beyond 5° of hyperextension because of the ligamentous volar plate, which is an inseparable part of the joint capsule. The medial and lateral collateral ligaments are a part of the capsule. They are radially fixed in a manner that allows no medial or lateral deviation of the joint in any position. The shape of the articular joint surface also strongly contributes to this stability in lateral motion. The distal interphalangeal joints of the fingers can be pushed into about 90° of flexion before they are limited by the dorsal joint capsule and extensor mechanism. The distal interphalangeal joints extend to 30° of hyperextension. There is no lateral mobility in these joints with the collateral ligaments intact. The collateral ligaments of the distal interphalangeal joints are simply thickened medial and lateral portions of the joint capsule.

Biomechanical concept Joint motion Brand and Hollister, in their textbook Clinical Mechanics of the Hand, discuss how joints move.32 An axis of rotation of a joint refers to a line fixed to the proximal bone about which the motion of the distal bone appears to be a pure rotation. For the simple (hinge type) interphalangeal joints of the fingers, the motion occurs only in flexion and extension; the axis of rotation is perpendicular to the sagittal plane and is located in the distal head of the phalanx proximal to the joint. A related concept is that of the degrees of freedom of a joint. The degrees of freedom of a joint are the minimum number of axes of rotation that can be used to describe completely the motion of the bone distal to the joint. The wrist as a whole, for example, has two degrees of freedom (flexion–extension and radial–ulnar deviation), represented by two nearly perpendicular axes of rotation.33 The kinematics of more complex joints such as the thumb carpometacarpal joint34 or the intercarpal joints35 is still the subject of research and thought to have at least two degrees of freedom with nonintersecting, nonperpendicular axes of rotation.

12

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Scaphoid and Tubercle

Carpal bones

Lunate Triquetrum

Trapezoid

Carpal bones

Pisiform

Trapezium and Tubercle

Capitate Hamate and Hook

1

Sesamoid bones

2

3

4

5

Base Shafts Head

Metacarpal bones

Base Shafts Head

Proximal phalanges

Right hand: anterior (palmar) view

Base Shafts Head

Middle phalanges

Base Shafts Tuberosity Head

Distal phalanges

Carpal bones

Lunate Scaphoid Capitate Trapezoid Trapezium Carpal bones

Triquetrum Hamate Base Shafts Head

Metacarpal bones

Middle phalanges

Distal phalanges

5

4

3

2

Base Shafts Head

Proximal phalanges

Right hand: posterior (dorsal) view

1

Base Shafts Head

Base Shafts Tuberosity Head

Figure 1.14  Bony anatomy of the wrist and hand. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Bones and joints

Hyperextension

45° Position of rest

13

BOX 1.4  Clinical pearl: Checkrein ligaments

Maximum mobility

Flexion

Minimum mobility

Figure 1.15  The true collateral ligaments of the metacarpophalangeal joint are loose in extension but tight in flexion of the joint as a result of the cam effect of the metacarpal head in relationship to the proximal phalanx. This accounts for the lack of lateral mobility of the joint when it is flexed. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. 1. Philadelphia: WB Saunders, 1973.)

In each finger, there is no difference between the radii of curvature of the ulnar and radial condyles of the middle phalanx head. Conversely, the radius of curvature of the distal phalanx ulnar groove is significantly greater than that of the radial groove. This asymmetry between the distal phalanx grooves and the middle phalanx results in a translational component during the flexion of the distal interphalangeal joint that may contribute to degenerative changes and development of arthritis.36 The proximal and distal interphalangeal joints are hinge joints: lateral motion is limited in all phases of flexion and extension by radially oriented collateral ligaments, which are tight at any angle. The metacarpophalangeal joints, in contrast, allow motion through several axes. The capsule, including the collateral ligaments and volar plate, is quite lax, allowing medial and lateral deviation, flexion, extension, and thereby circumduction and a small degree of distraction. In the absence of other sources of stabilization, upon cutting of the collateral ligaments the metacarpophalangeal joint becomes a flail, unstable mechanism. Nature, fortunately, has created another source of lateral stability – the interosseous muscles. By virtue of the selective variable pull, the interossei normally influence lateral motion in the metacarpophalangeal joint to the extent allowed by the unyielding collateral ligaments. If the collateral ligaments are sacrificed, the interossei remain the sole source of lateral stability. When there is intrinsic (ulnar) paralysis, if the collateral ligaments are sacrificed, all lateral stability is lost and disastrous ulnar deviation occurs. At the interphalangeal joints lateral stability is again dependent on the collateral ligaments, but at this level there

Checkrein ligaments are, in fact, abnormal structures that are found only after fibrosis of the proximal interphalangeal joint occurs.37 The volar lateral ridges of the proximal phalanx are termed “assembly lines” and represent a coalition of the flexor sheath and Cleland’s and Grayson’s ligaments. Normally, there is no connection between the volar plate and these assembly lines. However, in the proximal interphalangeal joint with a flexion contracture, fibrosis has occurred and stout checkrein “ligaments” have formed from the volar plate that prevent full joint extension.

is no second line of defense. The collateral ligaments of the interphalangeal joints, therefore, cannot be sacrificed without creating a lateral instability that is curable only by fusion of the interphalangeal joints. Palmar or volar plates are found in the metacarpophalangeal and interphalangeal joints where they reinforce the joint capsules, enhance joint stability, and limit hyperextension. The  plates of the metacarpophalangeal and interphalangeal joints are structurally and functionally similar. The volar plates of the metacarpophalangeal joints are the sites of insertion of the intermetacarpal ligaments, which limit separation or fanning of the metacarpal heads. The volar plate is fixed to that portion of the capsule that originates from the proximal phalanx, and therefore the plate moves with the proximal phalanx in flexion and extension. Dorsal to this ligament on each side of the metacarpal heads are sagittal bands that connect the volar plates to the tendon of the extensor digitorum and to the extensor expansion. The volar plates to the proximal and distal interphalangeal joints are also stout structures that may become scarred in cases of fracture-dislocation and may ultimately lead to joint flexion contractures (Box 1.4).

The thumb The thumb occupies the extreme radial position in the transverse arch of the hand. The column of bones making up the thumb architectural base comprises the two phalanges, the metacarpal, and the trapezium. Its formula differs from that of the remaining digits by virtue of its two named phalanges rather than three. From a functional point of view, however, the thumb metacarpal can be compared to a proximal phalanx and the trapezium to a grossly foreshortened metacarpal. This suggests that the thumb is a digit recessed by a short metacarpal (the trapezium) with the proximal phalanx loosely syndactylized to the second metacarpal. There is no clear evidence to support this point of view phylogenetically, but it seems sensible in understanding the gross anatomy of the thumb’s architecture. Like the finger metacarpophalangeal joints, the thumb’s metacarpotrapezial (also known as the carpometacarpal) joint has the greatest degree of freedom of any in the digital rays. The metacarpotrapezial joint is a synovial joint separated and distinct from the general intercarpal joints of the wrist. The trapezium itself articulates with the trapezoid and scaphoid with ligamentous restraints that sharply limit trapezial motion in relationship to the carpus (Fig. 1.16).

14

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Index finger DP Hinge Thumb

MP Hinge

DP

PP

PP

Wide ROM

MC

MC

Trapezium

Limited ROM

Scaphoid

Capitate

Figure 1.16  The osteoarticular column of the thumb as compared with that of a finger. The trapezium in this comparison is the equivalent of a foreshortened metacarpal, and the metacarpotrapezial joint of the fingers. MC, Metacarpal; PP, proximal phalanx; DP, distal phalanx; ROM, range of motion. (Redrawn after Chase RA. Anatomy of the thumb. In: Strickland J (ed.), The Thumb. Edinburgh: Churchill Livingstone, 1989.)

The uniquely wide range of thumb motion as compared with that of the remaining digits is attributable largely to the joint between the base of the first metacarpal and the trapezium. In simplest terms, it is described as a biconcave double saddle joint with a permissively loose capsule. That combination allows movements best described as flexion, extension, adduction, and abduction through infinite combinations that result in circumduction. The thumb rotates as a cone with its apex at a point where the axes of flexion–extension and abduction–adduction cross within the carpometacarpal joint.38–40 The first carpometacarpal joint is best described as a double saddle where one saddle sits atop another, allowing three degrees of motion: (1) flexion–extension; (2) abduction– adduction; and (3) medial rotation–lateral rotation.41 As the thumb rocks along the central ridge of the trapezial saddle in abduction and adduction, the metacarpal saddle’s extensions over the trapezial saddle engage the trapezial saddle’s medial or lateral condylar parts along the central axis. The axis line is curved in such a way that when the metacarpal is adducted, it locks into medial rotation, and when it is abducted, it locks into lateral rotation. This accounts for the sweep of the thumb in adduction to abduction along the transverse arch of the metacarpal heads. This mandatory rotation into medial rotation on adduction helps to position the thumb for pulp-to-pulp opposition of the thumb to the fingers. In neutral position the axis of the trapezium, represented by its central ridge, sits at about 60° from a line through the heads of the central stable

second and third metacarpals. The base of the first metacarpal has a quadrilateral articular surface that is a complementary match to the articular surface of the trapezium. Its concavity is slightly exaggerated on the ulnar volar side by a protrusion or “beak” for insertion of the important anterior oblique carpometacarpal ligament, commonly referred to as the “volar beak” ligament. As in some other joints in the body (e.g., the shoulder), stability and close coaptation of the joint surfaces between the trapezium and the first metacarpal are dependent on the presence of operational muscles and tendons. As noted above, there is a lot of slack in the joint capsule, allowing a wide range of motion, including joint distraction of up to 3 mm.42 An important stabilizing capsular ligament for the first carpometacarpal joint is the anterior oblique carpometacarpal ligament or volar beak ligament referred to above. It extends like the leg of a person seated in the trapezial saddle extending from the “beak” of the first metacarpal to the anterior crest of the trapezium and adjacent intercarpal ligaments. It retains the fragment of bone fractured free from the base of the metacarpal as the metacarpal displaces radially in Bennett’s fracture. In advanced metacarpotrapezial joint arthritis it weakens and attenuates, as also does the intermetacarpal ligament, allowing radial subluxation of the metacarpotrapezial joint.43 The ligament at the radial border of the joint is like a radial collateral ligament and is referred to as the dorsoradial or anteroexternal ligament. Thus, the radial side of the joint support is the right anteroexternal ligament, which inserts close to but beneath the insertion of the abductor pollicis longus on the radial base of the first metacarpal. It forms part of the joint capsule and then attaches to the anterior crest of the trapezium. Dorsally, one sees the posterior oblique ligament crossing the dorsal joint capsule from the radially positioned posteroexternal tubercle of the trapezium to attach to the ulnar base of the first metacarpal. There is a stout intermetacarpal ligament between the base of the first metacarpal and the adjacent base of the second metacarpal, and good evidence that this ligament together with the anterior oblique ligament is a key to prevention of radial subluxation of the metacarpotrapezial joint, as seen in arthroses of the joint.44 Function and range of motion within the limits imposed by these ligaments are influenced by the extrinsic and intrinsic muscles of the thumb and the external forces applied to the thumb. Bettinger and Berger have updated this ligamentous anatomy to include 16 different ligaments that are thought to stabilize the trapezium and trapeziometacarpal joint.45 The first metacarpophalangeal joint differs from other metacarpophalangeal joints in several respects in both anatomic make-up and function. Generally, the first metacarpophalangeal joint range of motion in flexion and extension, as well as abduction and adduction, is less than that in the finger metacarpophalangeal joints. The metacarpal and proximal phalanx are more stout in order to accommodate to greater forces normally borne by the thumb in pinching and grasping. The head of the first metacarpal is different because the radial articular prominence is larger than the ulnar. The articular surface of the proximal phalanx is fashioned reciprocally to match. The collateral ligaments are similar to those of finger metacarpophalangeal joints. The metacarpophalangeal portion is taut in flexion and looser in extension. In

Bones and joints

15

Triceps brachii muscle

Superior ulnar collateral artery (anastomoses distally with posterior ulnar recurrent artery)

Brachioradialis muscle Ulnar nerve Extensor carpi radialis longus muscle Medial epicondyle of humerus Common extensor tendon Olecranon of ulna Extensor carpi radialis brevis muscle

Anconeus muscle

Extensor digitorum muscle

Flexor carpi ulnaris muscle

Extensor digiti minimi muscle

Extensor carpi ulnaris muscle

Abductor pollicis longus muscle

Extensor pollicis brevis muscle

Extensor pollicis longus tendon Extensor carpi radialis brevis tendon Extensor retinaculum (compartments numbered)

Extensor carpi radialis longus tendon

Superficial branch of radial nerve

Dorsal branch of ulnar nerve

Extensor carpi ulnaris tendon

6 5

Extensor digiti minimi tendon

4

1 3 2

Abductor pollicis longus tendon Extensor pollicis brevis tendon Extensor pollicis longus tendon

Extensor digitorum tendons Extensor indicis tendon Anatomical snuffbox

5th metacarpal bone

Figure 1.17  The anatomy of the extensor muscles: superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

extension, the portion of the fanlike collateral ligaments to the palmar plate is taut; thus, adduction and abduction are limited in both extension and flexion.46 Some pronation but no supination is allowed at the metacarpophalangeal joint

when it is in extension. In supination, the joint locks into a stable position for secure grasping. The sturdy fibrocartilaginous volar plate of the metacarpophalangeal joint extends from the palmar base of the proximal

16

SECTION I

Branches of brachial artery

CHAPTER 1  • Anatomy and biomechanics of the hand

Middle collateral branch of deep brachial artery

Superior ulnar collateral Inferior ulnar collateral (posterior branch)

Medial intermuscular septum

Lateral intermuscular septum Brachioradialis muscle

Ulnar nerve Posterior ulnar recurrent artery

Extensor carpi radialis longus muscle

Medial epicondyle of humerus

Lateral epicondyle of humerus

Common extensor tendon (partially cut )

Triceps brachii tendon (cut )

Olecranon of ulna

Extensor carpi radialis brevis muscle

Anconeus muscle

Supinator muscle

Flexor carpi ulnaris muscle

Posterior interosseous nerve

Recurrent interosseous artery

Pronator teres muscle (slip of insertion)

Posterior interosseous artery

Radius

Ulna

Posterior interosseous nerve

Extensor pollicis longus muscle

Abductor pollicis longus muscle

Extensor indicis muscle

Extensor pollicis brevis muscle

Anterior interosseous artery (termination)

Extensor carpi radialis brevis tendon Extensor carpi radialis longus tendon

Extensor carpi ulnaris tendon (cut ) Extensor digiti minimi tendon (cut ) Extensor digitorum tendons (cut )

6 5

Extensor retinaculum (compartments numbered)

5th metacarpal bone

4

3

2

1

Radial artery 1st metacarpal bone 2nd metacarpal bone 1st dorsal interosseous muscle

Figure 1.18  The anatomy of the extensor muscles: superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

phalanx to the neck of the metacarpal. It regularly incorporates two sesamoid bones, one medial and one lateral to the flexor pollicis longus.

The nature of the condyle of the proximal phalanx of the interphalangeal joint to the thumb is such that, upon flexion of the joint, pronation of the distal phalanx occurs.

Bones and joints

Note: Anconeus muscle not shown because it is extensor of elbow

Medial epicondyle

17

Medial epicondyle Olecranon Lateral epicondyle

Extensors of wrist

Common extensor tendon

Extensor carpi radialis longus

Olecranon

Extensor carpi radialis brevis

Lateral epicondyle

Extensor carpi ulnaris

Extensor digitorum and extensor digiti minimi (cut away)

Common extensor tendon Ulna

Interosseous membrane

Extensors of digits (except thumb)

Radius Extensor digitorum Extensor digiti minimi

Ulna

Extensor indicis

Extensors of thumb Abductor pollicis longus Extensor pollicis brevis Extensor pollicis longus

Extensor indicis tendon

Extensor digitorum and extensor digiti minimi tendons (cut)

Right forearm: posterior (dorsal) views A

B

Figure 1.19  (A,B) The anatomy of the extensor muscles: superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

18

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Muscles and tendons Extrinsic extensors (Video 1.1

)

Extensor muscles lie on the dorsum of the forearm and hand and are innervated by the radial nerve (Figs. 1.17–1.19). The brachioradialis is a flexor of the elbow joint but is included with the extensor muscles because it is supplied by the radial nerve. The brachioradialis and the extensor carpi radialis longus originate from the lateral supracondylar ridge of the humerus. The four superficial extensors (extensor carpi radialis brevis, extensor digitorum communis, extensor digiti minimi, and extensor carpi ulnaris) originate from the common extensor tendon which is attached to the supracondylar ridge and the lateral epicondyle. The extensors can be divided by function. The extensor carpi radialis longus and brevis, and the extensor carpi ulnaris Biomechanical concept Muscle structure Muscles are composed of tissue that can actively contract under the influence of the brain and spinal cord to produce hand and finger motion and forces by pulling on bones via tendons.47,48 Muscle tissue is composed of parallel arrangements of muscle fibers that can actively shorten and passively resist stretching, but cannot actively lengthen. The muscles of the hand anchor to bone at either end, typically by a short tendon at their origin (proximal end) and a long tendon at their insertion (distal end). Muscle fibers run along the length of the muscle attaching to tendon at either end. The aponeurosis is the transitional region where the contractile fibers of the muscle interdigitate with the collagen fibers that form the tendon. Tendons are stout parallel bundles of collagen fibers that often cross multiple joints of the hand before inserting into bone. Some tendons of the hand are atypical as they bifurcate or combine before inserting into bone to form the extensor mechanism (or extensor hood) of the fingers. The lumbrical muscle is atypical as it both originates from and inserts on to tendon (the flexor profundus tendon and the extensor mechanism, respectively) and has no direct bony attachment. Striated muscle fibers are themselves parallel assemblies of similarly long cells with multiple nuclei containing sarcomeres, the fundamental contractile unit of muscle tissue. At the biochemical level, sarcomeres are interdigitated filaments of f-actin and myosin proteins. Muscle activation and contraction occur when a neural command causes the release of calcium ions inside the muscle cell to cause the free end of the myosin filaments to “ratchet” past the f-actin filaments to increase the overlap between them by metabolizing adenosine triphosphate, an important source of energy fueling cellular processes. The maximal force a muscle can produce is proportional to the number of parallel muscle fibers that compose it (physiological cross-sectional area), and the angle the fibers make with the line of action of the tendons (pennation angle). Mammalian muscle tissue is considered to produce a maximal stress of around 35 N/cm2, which is a remarkable ratio of force per unit weight that is difficult to match artificially. In addition, the connective tissue that holds together the muscle fibers grants muscle tissue passive viscoelastic properties.

serve to extend the wrist. The extensor digitorum communis, extensor indicis proprius, and the extensor digiti minimi are finger extensors. Three extrinsic extensors assist in thumb motion: abductor pollicis longus, extensor pollicis brevis, and extensor pollicis longus. The extensor retinaculum prevents bowstringing of tendons across the wrist (Fig.  1.20). Six extensor compartments exist (see Video 1.1 and Fig. 1.21): (1) abductor pollicis longus and extensor pollicis brevis; (2) extensor carpi radialis longus and extensor carpi radialis brevis; (3) extensor pollicis longus; (4) extensor digitorum communis and extensor indicis proprius; (5) extensor digiti minimi; and (6) extensor carpi ulnaris. Extension of the phalanges of the fingers and thumb is dependent both on long extensors at the metacarpophalangeal joints and on an interplay between the long extensors and intrinsic muscles at the interphalangeal joints. The extensor digitorum is a series of tendons with a common muscle belly that enters into the central extensor of each of the fingers. There are intertendinous bridges between these separate tendons over the dorsum of the hand. Independent long extensor power is supplied to the index finger through the extensor indicis and to the little finger through the extensor digiti ­minimi. In each case the independent extensor lies on the ulnar side of the long extensor tendon to these two fingers from the extensor digitorum (Fig. 1.22). Each of the three extrinsic muscles to the thumb on its extensor surface inserts on one of the thumb bones. The Biomechanical concept The extensor mechanism of the fingers (Fig. 1.23) The extensor tendons are attached by dorsal expansions or dorsal hoods (see Video 1.2 ). These expansions are divided into three structures. (1) Lateral bands pass on either side of the proximal phalanx and extend all the way to the distal phalanx. The lumbrical and dorsal and palmar interossei muscles contribute to the lateral bands. (2) A single central slip passes down the middle of the finger, ending at the base of the middle phalanx. (3) The retinacular ligament runs obliquely along the middle phalanx, and connects the fibrous digital sheath on the volar side of the phalanges to the extensor expansion. The extensor hood of the fingers is an example of tendons bifurcating and recombining in an intricate network that results in complex muscle actions. For example, extensor muscles can extend the proximal interphalangeal joints, and intrinsic muscles can simultaneously flex the metacarpophalangeal joint and extend the interphalangeal joints.49 The effect of each muscle at each joint, however, may depend on finger posture and the distribution of tendon ­tension. Detailed cadaver studies have shown that, although the change in length of the different components of the extensor hood is relatively small,50,51 their spatial orientation varies considerably from one finger configuration to another, and it has been suggested that the extensor mechanism may act as a floating net to amplify tendon forces52,53 or to coordinate joint motion.54,55 However, the anatomy of the insertion of the extrinsic and intrinsic muscles is quite complex and shows variations in the geometry of muscle bellies and insertion tendons.56,57

Muscles and tendons

Posterior (dorsal) view Extensor carpi ulnaris – Compartment 6 Extensor digiti minimi – Compartment 5 Extensor digitorum Extensor indicis

Compartment 4

Extensor pollicis longus – Compartment 3 Extensor carpi radialis brevis Extensor carpi radialis longus

Compartment 2

Abductor pollicis longus

Plane of cross section shown below

Extensor pollicis brevis

Compartment 1

Extensor retinaculum

Radial artery in anatomical snuffbox Abductor digiti minimi muscle

Dorsal interosseous muscles

Intertendinous connections

Transverse fibers of extensor expansions (hoods)

Cross section of most distal portion of forearm Extensor retinaculum Extensor pollicis longus – Compartment 3 Compartment 4

Compartment 5

Extensor digitorum and extensor indicis

Extensor carpi radialis longus

Extensor digiti minimi

5 Compartment 6

Extensor carpi radialis brevis

Extensor carpi ulnaris

6

3

4

2 1

Compartment 2

Extensor pollicis brevis Abductor pollicis longus

Ulna

Compartment 1

Radius

Figure 1.20  The extensor retinaculum and extensor compartments. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

19

20

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Extensor carpi radialis longus Extensor pollicis longus

Extensor carpi radialis brevis Extensor pollicis brevis Abductor pollicis longus

interosseous artery (Fig.  1.25). The supinator originates from the lateral epicondyle of the humerus and inserts on the proximal third of the radius. It is innervated by the deep branch of the radial nerve and is a primary supinator, assisted by the biceps brachii.

Extrinsic flexors (Video 1.3 Extensor digiti minimi Extensor carpi ulnaris

Extensor digitorum Intertendinous connection

Figure 1.21  The extensor compartments. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

)

Flexion of the phalanges into the palm is a complicated motion representing the sum of actions of the long flexors (profundus and superficialis) and long extensors (extensor digitorum, extensor digiti minimi, and extensor indicis), modified and enhanced by the intrinsic muscles (interossei and lumbricals) (Figs. 1.26–1.31). The long flexors to the fingers are responsible for flexion of the interphalangeal joints and are supplements to active flexion of the metacarpophalangeal joints and the wrist joint.58 Biomechanical concept

Extensor indicis

Extensor digitorum Extensor digiti minimi

Figure 1.22  Anatomic relations of the extensor digitorum, extensor indicis, and extensor digiti minimi muscles. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

abductor pollicis longus inserts on the metacarpal where it primarily radially abducts the metacarpal, but since it bridges the wrist it secondarily radially deviates the wrist. The extensor pollicis brevis inserts on the proximal phalanx, so that it primarily acts as an extensor of the metacarpophalangeal joint but acts at the other joints with the abductor pollicis longus. The extensor pollicis longus inserts on the distal phalanx and is the primary extensor of the interphalangeal joint. It secondarily acts to extend and dorsally abduct the other two thumb joints.

Muscle force production Muscles can produce force in different ways.59 Concentric contractions occur when muscle fibers can shorten to induce tendon stretch, tendon excursion, and/or joint motion. Eccentric contractions occur when tendon forces overpower the passive and active force the muscle can produce and the muscle fibers lengthen during muscle activation. Isometric contractions occur when the muscle is not allowed to shorten (calling this state of the muscle a “contraction”, when in reality it remains the same length, is a historical artifact). The structural and biochemical properties of the sarcomere make the exact magnitude of muscle force for a given level of neural excitation a function of length of the fibers, velocity at which fibers shorten or lengthen, and its previous activation history. The force–length relationship of muscle (sometimes called the Blix curve) indicates that there is an optimal length of the fiber at which maximal force can be produced, and it drops at longer or shorter fiber lengths (Fig. 1.32). Thus, the length at which the muscle is placed in reconstructive surgeries or tendon transfers can greatly influence the force the muscle can produce postoperatively. The force–velocity relationship of muscle indicates that muscle force drops greatly from its isometric level when muscle fibers shorten rapidly during concentric contractions, and rises to a plateau almost double its isometric level when muscle fibers lengthen rapidly during eccentric contractions (Fig. 1.33).

Pronators and supinators The pronator teres originates from the common flexor origin and inserts at the midportion of the radius (Fig. 1.24). It is innervated by the median nerve and is a primary forearm pronator and a weak forearm flexor. The pronator quadratus is a short wide muscle that spans transversely across the distal radius and ulna. It is also innervated by the median nerve and is a forearm pronator. At the upper border of the pronator quadratus muscle, the anterior interosseous artery pierces the interosseous membrane and reaches the back of the forearm, where it anastomoses with the dorsal

The flexors are located on the volar side of the forearm and wrist and are innervated by the median nerve, except the flexor carpi ulnaris, and the flexor digitorum profundus to the ring and small fingers, which are innervated by the ulnar nerve (see Figs. 1.26–1.31). The flexor carpi radialis, flexor carpi ulnaris, and palmaris longus provide wrist flexion. The digital flexors (flexor digitorum superficialis, flexor digitorum profundus, and flexor pollicis longus) pass through the carpal tunnel to provide dual flexion to the fingers and single flexion to the thumb (see Video 1.3 ).

Muscles and tendons

Insertion of central band of extensor tendon to base of middle phalanx Slips of long extensor tendon to lateral bands

Triangular aponeurosis

Interosseous muscles

Long extensor tendon

Extensor expansion (hood)

21

Posterior (dorsal) view

Metacarpal bone

Insertion on extensor tendon to base of distal phalanx

Interosseous tendon slip to lateral band

Lateral bands

Lumbrical muscle

Extensor expansion (hood)

Lateral band

Insertion of extensor tendon to base of middle phalanx

Part of interosseous tendon passes to base of proximal phalanx and joint capsule

Long extensor tendon

Central band

Insertion of extensor tendon to base of distal phalanx

Metacarpal bone

Finger in extension: lateral view Collateral ligaments

Vinculum breve

Vincula longa

Flexor digitorum profundus tendon

Interosseous muscles

Flexor digitorum superficialis tendon

Lumbrical muscle Collateral ligament

Insertion of small deep slip of extensor tendon to proximal phalanx and joint capsule

Extensor tendon

Attachment of interosseous muscle to base of proximal phalanx and joint capsule

Insertion of lumbrical muscle to extensor tendon

Palmar ligament (plate) Flexor digitorum superficialis tendon (cut)

Interosseous muscles Lumbrical muscle

Collateral ligaments

Finger in flexion: lateral view

Flexor digitorum profundus tendon (cut) Palmar ligament (plate)

Note: Black arrows indicate pull of long extensor tendon; red arrows indicate pull of interosseous and lumbrical muscles; dots indicate axis of rotation of joints

Figure 1.23  The extensor mechanism of the fingers. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

22

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Right forearm: anterior view Pronated position

Supinated position

Lateral epicondyle

Medial epicondyle

Medial epicondyle

Lateral epicondyle

Supinator

Pronator teres

Ulna Radius Ulna

Radius

Pronator quadratus

Figure 1.24  The forearm pronators and supinators. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

The flexor digitorum superficialis tendon lies palmar (superficial) to the profundus tendon in the palm.60 It flattens, then splits at the level of the proximal phalanx, and its two tails surround the profundus, decussating behind the

profundus to insert on the middle phalanx. The flexor digitorum profundus perforates the flexor digitorum superficialis to run superficially along the length of the proximal and middle phalanges to insert at the base of the distal phalanx.

Muscles and tendons

Anterior interosseous artery

Pronator quadratus

Figure 1.25  Anatomic relations between the pronator quadratus muscle and the anterior interosseous artery. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

The superficialis and profundus flexors contribute most of the force for digital flexion. The flexor digitorum profundus of the index finger is unique in that it has an independent muscle belly. The flexor pollicis longus inserts at the distal phalanx of the thumb (Box 1.5). In the finger and distal palm, the flexor tendons pass through a fitted fibrous flexor sheath that has thickened areas. The tendons at this level are surrounded by synovial sheaths. The flexor pollicis longus is the interphalangeal flexor of the thumb equivalent to the finger profundi. The flexor digitorum profundus is the only muscle that flexes the distal interphalangeal joint. Testing for profundus function requires observation of active flexion of the distal interphalangeal joint. Selected flexion of one or more of the metacarpophalangeal joints, or either the proximal or distal interphalangeal joint, depends on stabilizing fixation of the remainder by flexor–extensor interplay. Elimination of any single motor element reduces the selective adaptability of a finger. As noted above, a muscle may positively influence any joint between its site of origin and its insertion. The flexor digitorum profundus muscle originates in the forearm, and its tendon therefore bridges the wrist joint, the metacarpophalangeal joint, the proximal interphalangeal joint, and the distal interphalangeal joint before it inserts on the distal phalanx. It may flex any of these joints, depending on the dynamic fixation of the others. Fixation of the distal interphalangeal joint converts the profundus tendon into a functional superficialis tendon by recessing its prime site of action to the proximal interphalangeal joint. By combined fixation of any of the joints, the profundus tendon may primarily flex any selected one. It is intriguing to realize that under certain conditions the flexor profundus may accentuate extension of the proximal interphalangeal joint. The profundus pulling primarily at the distal interphalangeal joint may flex it acutely. In flexing the distal interphalangeal joint, the insertion of the extensor mechanism is advanced distally. This advancement, combined with either a contraction or fixation of the lateral bands, results in extension of the proximal interphalangeal joint. This effect is easily aborted by the intact flexor superficialis, whose prime flexion function is exerted on the proximal interphalangeal joint. Absence of the superficialis, whether

23

occasioned by injury or by tendon graft replacement of the profundus only, results not infrequently in flexion of the distal interphalangeal joint with recurvatum deformity at the proximal interphalangeal joint. This can be corrected by fusion of the distal interphalangeal joint, making the profundus a functional superficialis, or by tenodesis or capsulodesis of the proximal interphalangeal joint in mild flexion. It is wise to keep in mind the innumerable functional circumstances that can be created by selective interplay of multiple motor forces exerted through a series of interdependent joints.63

Biomechanical concept The shape of hand muscles Many muscles of the hand depart from the simple fusiform (fish-like) shape seen in most textbooks. Many are flat, while others have multiple bellies. The interosseous muscles, for example, are bipennate. That is, a central common tendon is pulled on by fibers originating in different bones. The opposite arrangement is also found in muscles like the flexor superficialis of the fingers, which originate in a short belly that leads to a tendon that inserts in a second larger belly that then subdivides into four branches, each with a superficialis tendon to each finger. While it is possible to find muscle fibers that fire only when one finger is being flexed,61,62 the degree to which force production in each belly is independent of the others is still unknown. Moreover, most extrinsic flexor and extensor muscles have tendons that are connected by thin strands of collagen at the level of the metacarpals that prevent independent motions of the fingers (try to extend the ring finger with all other fingers flexed). Other muscles such as the adductor pollicis have a fan-shaped origin where the resultant force at the insertion tendon depends on the distribution of force among muscle fibers. Whether or not muscle fibers fire in synchrony to produce a consistent resultant force, or if the fibers can be subdivided in functional regions to produce different resultant forces, is still unknown.

Biomechanical concept Moment arms The moment arm of a tendon about an axis of rotation of a joint is defined as the shortest distance between the axis of rotation and the tendon as it crosses the joint (Fig. 1.34). This distance can vary with joint angle because of the suspension system of pulleys guiding flexor tendons, and/or the curved but not circular contour of the joint surfaces guiding extensor tendons.63 The greater the moment arm, the greater the excursion of a tendon (and change in length of a muscle) that accompanies a given angle of rotation of the joint. Similarly, the moment of force (rotational action) of a tendon force about an axis of rotation increases with the magnitude of the moment arm of the tendon. These relationships between moment arm and tendon excursion/force assume hinge-type joints without sliding actions, which holds well for most finger joints. Note that a tendon that crosses a joint with multiple degrees of freedom (such as the thumb carpometacarpal joint) will have simultaneous and different actions about each axis of rotation.

24

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Medial antebrachial cutaneous nerve

Biceps brachii muscle

Ulnar nerve

Brachial artery and median nerve

Triceps brachii muscle Lateral antebrachial cutaneous nerve (terminal musculocutaneous nerve) Medial intermuscular septum Brachialis muscle

Ulnar artery

Medial epicondyle of humerus

Biceps brachii tendon

Common flexor tendon

Radial artery

Pronator teres muscle Bicipital aponeurosis Flexor carpi radialis muscle

Brachioradialis muscle

Palmaris longus muscle

Extensor carpi radialis longus muscle

Superficial flexor muscles

Flexor carpi ulnaris muscle

Extensor carpi radialis brevis muscle

Flexor digitorum superficialis muscle Flexor pollicis longus muscle and tendon Palmaris longus tendon Radial artery

Median nerve

Palmar carpal ligament (continuous with extensor retinaculum)

Thenar muscles

Palmar aponeurosis

Dorsal branch of ulnar nerve

Ulnar artery and nerve

Pisiform

Palmar branch of median nerve

Hypothenar muscles

Figure 1.26  The anatomy of the flexor muscles, from superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

The gross anatomic configuration and function of the extrinsic digital flexor tendons have been known since anti­ quity. The great growth in our knowledge and understanding of functional biomechanics, muscle physiology, tendon

nutrition, and blood supply has influenced the management of problems involving these important flexor tendons. The long flexor tendons cross multiple joints. The tendon–muscle unit has an effect on each joint it crosses, which is altered

Muscles and tendons

Ulnar nerve Ulnar artery

Palmaris longus Brachioradialis

Flexor carpi ulnaris

Radial artery

Flexor digitorum superficialis

Flexor carpi radialis

Figure 1.27  The anatomy of flexor muscles in relation to surrounding neurovascular elements. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

by the positioning of the other joints in the linkage system. Thus, the influence of the long flexor tendon on one joint in the system is augmented by the function of its antagonists at each of the other joints it crosses. For example, a digital flexor tendon aids in flexing the wrist, but its flexion capability within the digit at the metacarpophalangeal joints and interphalangeal joints is increased by wrist extension using wrist extensors, which in fact are antagonists to the digital flexors at the wrist. This is the simplified definition of synergistic function – finger flexion augmented by wrist extension, and vice versa. Synergistic and antagonistic groups of muscles in hand function must be considered when functional substitution by tendon transfers is contemplated. Obviously, certain groups of muscles have developed functional synergism, which makes readjustment natural when one group is transferred to take on the function of the other. Examples of such natural synergism are the united functions of the wrist flexors and digital flexors or the wrist extensors and digital flexors. In its course from forearm to fingers, the digital profundus flexor crosses the palmar aspect of the wrist joint, the metacarpophalangeal joint, and the interphalangeal joints. The relationship of the tendon to the joint axes is maintained by retinacular structures, or pulleys. This prevents the bowstring effect, which would allow the tendon to move away from the joint axis, changing the moment arm and therefore the force exerted at that joint by the flexor tendon. The finely balanced relationship between the flexor muscle–tendon unit at each joint in the series may be disrupted by such a change. Such alterations can be compensated for, to some extent, by graded, proportional changes in the controlled power of antagonists, but the physiologic balance may be interfered with.

The retinacular system The large, restraining pulley at the wrist, which serves all the long digital flexors, is the transverse carpal ligament (Fig. 1.35). It bridges the volar surface of the carpals from the pisiform and hook of the hamate medially to the scaphoid tubercle and trapezium laterally. It confines the nine extrinsic flexor tendons and the median nerve within the carpal tunnel, and prevents bowstringing of the flexor tendons at the wrist.

25

Three pulleys housing the flexor pollicis longus within the thumb are usually present. The proximal annular pulley is at the level of the metacarpophalangeal joint arising from the volar plate and base of the proximal phalanx. The distal annular pulley is located over the volar plate of the interphalangeal joint. Between the two is a single oblique pulley that originates proximally on the ulnar side of the middle phalanx, where it also gains fibers from the adductor pollicis before it extends to the middle one-third of the radial palmar surface of the middle phalanx. The oblique pulley must be preserved in order to prevent bowstringing of the flexor pollicis longus tendon. Four or five discrete annular pulleys and three cruciate bands are ordinarily present in the fingers (Fig.  1.36). The most proximal pulley (A1) begins 0.5 cm proximal to the metacarpophalangeal joint. It is anchored to the volar plate and the proximal phalanx. Just distal to it is the second annular band (A2), which is the largest pulley, extending to nearly the proximal one-half of the proximal phalanx. The first cruciform band (C1) lies distal to A2 and well proximal to the proximal interphalangeal joint. The third annular pulley (A3) lies over the proximal interphalangeal joint arising from its volar plate. The second cruciate ligament (C2) is at the base of the middle phalanx. The fourth annular pulley (A4) lies over the middle one-third of the middle phalanx, and just distal to it is the third cruciate (C3). Often it is possible to identify thickening of the sheath over the distal interphalangeal joint, which, when present, is designated the fifth annular pulley (A5). The A2 and A4 pulleys insert directly into bone over the proximal and middle phalanges, respectively. In contrast, A1, A3, and A5 are narrower, more flexible, and insert mostly into the volar plate; additionally, with the cruciate pulleys, they permit compression without impingement and expansion during finger flexion and extension, respectively. The pulleys are strategically placed to maintain the relationship of the flexor tendons to the axis of each finger joint, thus preventing the bowstring effect. The A2 and A4 pulleys are crucial to prevent bowstringing. The gaps between pulleys allow unrestrained flexion and extension of the joints by folding and pleating of the thin sheath between pulleys. The synovial sheaths are closed sacs around the tendons composed of a visceral layer on the tendon surface and a parietal layer on the fibrous sheath surface. The thumb synovial sheath is continuous from the wrist to the distal extreme of the flexor pollicis longus. The digital synovial sheaths for the index, long, and ring fingers usually start at the level of the distal palmar crease and extend to the distal interphalangeal joints. Often the little-finger sheath extends more proximally to communicate with a common sheath around the finger flexors and then across the wrist to the distal forearm, where tendons pass through the carpal tunnel. During embryonic development, synovial sacs form where the flexor tendons are subject to restraint by retinacula. The tendon invaginates into the sac, creating a two-layered, closed synovial membrane around the tendon. The tendon carries its segmental nutrient vessels, and thus with invagination a mesentery-like mesotenon is formed. As time passes, and where the tendon has great excursion in relationship to adjacent bone, the mesentery refines itself to tiny, flexible bands, or vincula. At the sites of insertion, where differential motion

26

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Flexor digitorum superficialis muscle (radial head)

Median antebrachial vein Pronator teres muscle

Anterior branch of medial antebrachial cutaneous nerve

Radial artery and superficial branch of radial nerve

Flexor pollicis longus muscle

Radius

Interosseous membrane

Brachioradialis muscle

Flexor carpi radialis muscle

Cephalic vein and lateral antebrachial cutaneous nerve (from musculocutaneous nerve) Supinator muscle

Ulnar artery and median nerve Palmaris longus muscle Flexor digitorum superficialis muscle (humeroulnar head)

Deep branch of radial nerve

Common interosseous artery

Extensor carpi radialis longus muscle

Ulnar nerve

Extensor carpi radialis brevis muscle

Flexor carpi ulnaris muscle

Extensor digitorum muscle

Basilic vein

Extensor digiti minimi muscle

Flexor digitorum profundus muscle Ulna and antebrachial fascia

Extensor carpi ulnaris muscle

Anconeus muscle

Flexor carpi radialis muscle

Posterior antebrachial cutaneous nerve (from radial nerve)

Brachioradialis muscle Radial artery and superficial branch of radial nerve

Palmaris longus muscle Flexor digitorum superficialis muscle

Flexor pollicis longus muscle

Median nerve

Extensor carpi radialis longus muscle and tendon

Ulnar artery and nerve Flexor carpi ulnaris muscle

Radius

Anterior interosseous artery and nerve (from median nerve)

Extensor carpi radialis brevis muscle and tendon

Flexor digitorum profundus muscle Ulna and antebrachial fascia

Abductor pollicis longus muscle

Interosseous membrane and extensor pollicis longus muscle

Extensor digitorum muscle Extensor digiti minimi muscle

Posterior interosseous artery and nerve (continuation of deep branch of radial nerve)

Extensor carpi ulnaris muscle

Palmaris longus tendon

Flexor carpi radialis tendon

Median nerve

Radial artery

Flexor digitorum superficialis muscle and tendons Flexor carpi ulnaris muscle and tendon

Brachioradialis tendon

Ulnar artery and nerve

Abductor pollicis longus tendon

Dorsal branch of ulnar nerve

Superficial branch of radial nerve

Flexor digitorum profundus muscle and tendons

Extensor pollicis brevis tendon

Antebrachial fascia

Extensor carpi radialis longus tendon

Ulna Extensor carpi ulnaris tendon

Extensor carpi radialis brevis tendon

Pronator quadratus muscle and interosseous membrane

Flexor pollicis longus muscle

Extensor indicis muscle and tendon

Extensor pollicis longus tendon

Extensor digiti minimi tendon Radius

Extensor digitorum tendons (common tendon to digits 4 and 5 at this level)

Figure 1.28 The anatomy of the flexor muscles, from superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)  

Muscles and tendons

Note: Brachioradialis muscle not shown because it is flexor of elbow Medial epicondyle Lateral epicondyle Common flexor tendon

Flexor carpi radialis

Palmaris longus

Flexor carpi ulnaris

Radius Ulna

Pisiform Hook of hamate Palmar aponeurosis (cut)

Right forearm: anterior (palmar) view Figure 1.29  The anatomy of the flexor muscles, from superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

27

28

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Biceps brachii muscle

Ulnar nerve

Median nerve

Brachialis muscle

Brachial artery Lateral antebrachial cutaneous nerve (cut ) (from musculocutaneous nerve)

Medial intermuscular septum Pronator teres muscle (humeral head) (cut and reflected )

Radial nerve Deep branch Superficial branch

Medial epicondyle Flexor carpi radialis and palmaris longus tendons (cut )

Biceps brachii tendon

Anterior ulnar recurrent artery

Radial recurrent artery

Flexor digitorum superficialis muscle (humeroulnar head)

Radial artery

Ulnar artery Supinator muscle

Common interosseous artery Pronator teres muscle (ulnar head) (cut )

Brachioradialis muscle

Anterior interosseous artery Pronator teres muscle (cut )

Flexor carpi ulnaris muscle Flexor digitorum superficialis muscle

Flexor digitorum superficialis muscle (radial head)

Ulnar artery Flexor pollicis longus muscle

Palmar carpal ligament (continuous with extensor retinaculum) with palmaris longus tendon (cut and reflected )

Flexor carpi radialis tendon (cut )

Ulnar nerve and dorsal branch Median nerve Palmar branches of median and ulnar nerves (cut ) Pisiform Deep palmar branch of ulnar artery and deep branch of ulnar nerve Superficial branch of ulnar nerve

Superficial palmar branch of radial artery

Flexor retinaculum (transverse carpal ligament)

Figure 1.30  The anatomy of the flexor muscles, from superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Muscles and tendons

29

Medial epicondyle

Medial epicondyle

Lateral epicondyle

Lateral epicondyle

Common flexor tendon Coronoid process Coronoid process Interosseous membrane Interosseous membrane Radius Radius Flexor digitorum superficialis

Flexor digitorum profundus

Flexor pollicis longus

Radius

Radius

Ulna

Ulna

Flexor digitorum superficialis tendons (cut away)

Right forearm: anterior (palmar) views Figure 1.31  The anatomy of the flexor muscles, from superficial to deep. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

30

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Maximal isometric force (for a given activation level)

between the bone and tendon is least, the mesenteric configuration persists, as it does for flexor tendons in the hand outside the confining tunnels. The vincula brevia form the residual mesotenon at the sites of insertion of the profundus

BOX 1.5  Clinical pearl: Independent and common flexor muscles The flexor profundi to the third, fourth, and fifth fingers work from a common muscle belly. Acting in unison, they fit the architectural concept of this unit as a stable vise for grasping objects. The independent function of the index profundus frees the index finger for use with the thumb to manipulate an object grasped by the vise-like ulnar unit. Independence of action is well developed in the superficialis muscles and the intrinsic muscles.

Fmax

and superficialis tendons on the phalanges (Fig.  1.37). The vincula longa are the flexible, vessel-carrying bands to each tendon in the area where the complete mesotenon has disappeared (Fig. 1.38). Because the cell population of tendons is sparse, metabolic demand is low and cells can survive with minimal nutritional support. The longitudinal blood supply to a tendon comes from its musculotendinous junction and its insertion site into bone. The segmental blood supply derives from the mesotenon where a mesotenon exists and from the vincula within the digital sheaths. It is now clear that synovial fluid within the sheath supplies nutrition to the tendon much as synovial fluid in a joint supports cartilage. This fact has altered thinking about the necessity for adhesion formation to ensure cell survival within a lacerated tendon stripped of blood supply or within tendon grafts. On the basis of the anatomy of the flexor tendons and the associated synovial and fibrous sheaths, the area traversed by the tendons is divided into clinically important zones (Fig. 1.39).

0.5 Fmax

0 0.5 Resting length

Resting length

1.5 Resting length

Muscle fiber length (normalized to resting fiber length)

Figure 1.32  The Blix curve. The maximal force is plotted on the vertical axis, and the muscle fiber length is plotted on the horizontal axis. There is an optimal length of the fiber at which maximal force can be produced, and this drops at longer or shorter fiber lengths.

Percent maximal isometric force

Lengthening

Shortening

180%

100%

  Zone

-0.8

1 is the area traversed by the flexor digitorum profundus distal to the insertion of the flexor digitorum superficialis on the middle phalanx.   Zone 2 extends from the proximal end of zone 1 to the proximal end of the digital fibrous sheath.   Zone 3 is the area traversed by the flexor tendons in the palm and is free of fibrous pulleys. It extends, therefore, from the proximal end of the finger pulley system (Al) to the distal end of the wrist retinaculum, the transverse carpal ligament.

0.8

0.0 Relative shortening velocity (resting lengths/sec)

Figure 1.33  The force–velocity curve. The percentage of maximal isometric force is plotted on the vertical axis, and the relative shortening velocity is plotted on the horizontal axis. Therefore, muscle force drops from its isometric level when muscle fibers shorten rapidly during concentric contractions and rises to a plateau almost double its isometric level when muscle fibers lengthen rapidly during eccentric contractions.

Joint angle x

Pulley

lan Ph a

Phalanx

Pulley

Moment arm

Moment arm

Joint axis

Joint axis

Tendon Moment arm Moment arm

Tendon

Moment arm

Figure 1.34 The moment arm is defined as the shortest distance between the axis of rotation and the tendon as it crosses the joint.  

Muscles and tendons

Thumb pulleys

Annular Oblique Annular

to as the ulnar bursa. Each index, long, and ring finger has a flexor synovial sheath from the point of insertion of the profundus tendon to the level of the distal palmar crease in the palm. The deep space beneath the flexor tendons is divided into two compartments by the heavy vertical septum from the palmar fascia to the third metacarpal. Ulnar to the septum is the midpalmar space, and radial to it lies the thenar space. The thenar space straddles the adductor pollicis muscle like two legs extending between the adductor and deep flexors on the palmar side, and between the adductor and the first dorsal interosseous on the dorsal side. Infection starting in the digital synovial sheaths may extend proximally to the deep palmar spaces.

Intrinsic muscles (see Video 1.2 A

B Finger pulleys

A1

A2

C1

A3 C2 A4 C3 A5

C A1 A2 C1 C2 C3 D

A3 A4 A5

Transverse carpal ligament

Figure 1.35  (A–D) The flexor tendon pulley system for fingers and thumb. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. II. Philadelphia: WB Saunders, 1984.)   Zone

4 is the carpal tunnel. It extends from the distal to the proximal borders of the transverse carpal ligament.   Zone 5 extends from the proximal border of the transverse carpal ligament to the musculotendinous junctions of the flexor tendon (Box 1.6). A knowledge of the classical anatomy of the synovial sheaths and potential anatomic spaces in the hand is essential for proper diagnosis and treatment of serious hand infections. The flexor tendons are shrouded in synovial sheaths, particularly where there is flexion mobility in the longitudinal arch of each ray and at the wrist. The synovial sheath of the flexor pollicis longus generally extends from the flexor insertion to a point proximal to the wrist flexor retinaculum. The same is true of the synovial sheath around the little-finger flexors, but as the little-finger sheath approaches the proximal palm just distal to the carpal tunnel, it expands to encompass the flexors of the ring, long, and index fingers. At this point it is referred

31

)

Intrinsic muscles arise and insert within the hand (Figs. 1.40 & 1.41). They can be divided into four groups. The thenar muscles are a group of four muscles consisting of the abductor pollicis brevis, flexor pollicis brevis, opponens pollicis brevis, and the adductor pollicis brevis. The abductor pollicis brevis, opponens pollicis brevis, and superficial head of flexor pollicis brevis are median-innervated whereas the adductor pollicis brevis and the deep head of the flexor pollicis brevis are ulnar-innervated. The hypothenar muscles are all innervated by the ulnar nerve. These four muscles include the palmaris brevis, abductor digiti minimi, flexor digiti minimi brevis, and opponens digiti minimi. Lumbricals originate from flexor digitorum ­ profundus tendons and insert on the radial aspect of the extensor mechanisms, distal to the metacarpophalangeal joint. They contribute to the flexion of metacarpophalangeal joints and the extension of the interphalangeal joints (Video 1.4 ). The index and middle-finger lumbricals are innervated by the  median nerve, whereas the ring and small-finger lumbricals are innervated by the ulnar nerve. The tiny lumbrical muscles harmonize function between the lateral band interphalangeal extensor mechanism and the flexor digitorum profundus. They have a moving site of origin from the profundus tendon. As the flexor profundus contracts, the lumbrical origin moves proximally. At the same time, the lumbrical insertion moves distally as the extensor is advanced by interphalangeal flexion. The separation of its insertion and origin makes the lumbrical more effective in flexing the metacarpophalangeal joint. Conversely, with a change in balance of power, the lumbrical tends to pull the profundus distally as it shortens the lateral bands. This combination of profundus relaxation and lateral band pull results in extension at the interphalangeal joints. Despite the fact that lumbricals have the smallest cross-sectional area in the upper extremity, they have the greatest number of muscle spindles, which are responsible for gathering proprioceptive input. They play an important role in the sensory feedback of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints of the fingers. Specifically, the lumbrical muscles may be important for forming a precision pinch comprised by the first three digits.64 All interossei are ulnar-innervated. There are three volar muscles and four dorsal muscles. The interossei originate from the metacarpals and form the lateral bands with the lumbricals. The interosseous muscles function as ulnar and

32

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Usual arrangement

Common variation

Tendinous sheath of flexor pollicis longus (radial bursa) Intermediate bursa (communication between common flexor sheath [ulnar bursa] and tendinous sheath of flexor pollicis longus [radial bursa])

Common flexor sheath (ulnar bursa) Thenar space Midpalmar space

Lumbrical muscles (in fascial sheaths) (Synovial) tendon sheaths of fingers

Lumbrical muscles: schema

Flexor digitorum profundus tendons

1st and 2nd lumbrical muscles (unipennate)

3rd and 4th lumbrical muscles (bipennate)

Camper chiasm

Flexor digitorum superficialis tendons (cut)

Note: Flexor digitorum superficialis and profundus tendons encased in synovial sheaths are bound to phalanges by fibrous digital sheaths made up of alternating strong annular (A) and weaker cruciform (C) parts (pulleys). A1

C1

A2

C2

A3

C3

A4

C4

A5

Tendons of flexor digitorum superficialis and profundus muscles

(Synovial) tendon sheath

Palmar ligaments (plates)

Figure 1.36 Orientation of the flexor tendon sheaths, flexor tendons, and pulleys. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)  

Muscles and tendons

33

Flexor digitorum profundus Superficial palmar arch Flexor digitorum superficialis Vinculum breve

Zones

Superficialis insert

I

Proximal A3 Distal Distal A2

Figure 1.37  Flexor digitorum superficialis and profundus; lateral view of the hand. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

Middle

Proximal A1

II

Proximal

III Transverse carpal ligament

IV

V FDP tendon Vincula brevia Vinculum longus profundus

Vinculum longus superficialis

Carpal tunnel

Figure 1.39  Flexor tendon zones are classified for their relevance to flexor tendon injuries. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. II. Philadelphia: WB Saunders, 1984.)

BOX 1.6  Clinical pearl: Examination of extrinsic flexors

FDS tendon

Mesotenon

Figure 1.38  The common configuration of the vincula. FDP, Flexor digitorum profundus; FDS, flexor digitorum superficialis. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. II. Philadelphia: WB Saunders, 1984.)

radial deviators of the fingers as well as flexors of the metacarpophalangeal joints and extensors of the interphalangeal joints. The dorsal interossei act as abductors from the axis of the hand, which falls in the middle of the long finger. The long finger moves both radially and ulnarly under the influence of the second and third dorsal interossei. The abductor digiti minimi is the dorsal interosseous equivalent of the little finger. The palmar interossei adduct the fingers to the hand axis. The pull of all the interossei palmar to the axis of the metacarpophalangeal joints and dorsal to the interphalangeal joint axis acts to flex the metacarpophalangeal joints and extend the interphalangeal joints. The position assumed is called the “intrinsic plus” posture (Figs. 1.42 & 1.43; Box 1.7).

The function of the flexor digitorum profundus can be confined by active flexion of the distal interphalangeal joint. It is the only flexor of this joint. Since a muscle–tendon unit affects every joint between its origin and insertion, the flexor digitorum profundus may also flex the proximal interphalangeal joint. This makes the diagnosis of superficialis nonfunction more difficult. Each superficialis flexor has its own muscle belly, and each acts independently of the others. The profundus flexors are not as independent, since there is a common muscle for the long, ring, and little finger profundus tendons, and a variable degree of interconnection between these and the index finger profundus. The diagnosis of disruption of flexor digitorum superficialis function is confirmed by checkreining the profundus by holding the other fingers in extension while the patient actively attempts to flex the finger whose superficialis is being tested. Flexion of the finger at the proximal interphalangeal joint while the distal interphalangeal joint remains loosely extended confirms the functional integrity of the flexor digitorum superficialis.

With the hand axis or fixed unit in position, the metacarpal arch is adjusted primarily by the thenar and the hypothenar muscle groups. The median nerve generally innervates all the thenar muscles on the radial side of the flexor pollicis longus. These two and one-half muscles (the abductor pollicis brevis, opponens pollicis, and superficial head of the flexor pollicis brevis) are positioning muscles that act to bring the first metacarpal into palmar abduction, thus increasing the concavity of the transverse metacarpal arch. This in turn prepares the thumb for proper pulp-to-pulp opposition with the fingers.

34

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Radial artery and venae comitantes

Ulnar artery with venae comitantes and ulnar nerve

Flexor carpi radialis tendon

Flexor carpi ulnaris tendon

Tendinous sheath of flexor pollicis longus (radial bursa)

Common flexor sheath (ulnar bursa) containing superficialis and profundus flexor tendons Pisiform

Median nerve

Deep palmar branch of ulnar artery and deep branch of ulnar nerve

Palmaris longus tendon and palmar carpal ligament

Superficial branch of ulnar nerve

Transverse carpal ligament (flexor retinaculum)

Palmar digital nerves to 5th finger and medial half of 4th finger

Thenar muscles

Median nerve

Proper palmar digital nerves of thumb

Common flexor sheath (ulnar bursa)

(Synovial) tendinous sheath of flexor pollicis longus (radial bursa)

2nd, 3rd, and 4th lumbrical muscles (in fascial sheaths)

Superficial palmar arterial and venous arches

(Synovial) flexor tendon sheaths of fingers

Probe in 1st lumbrical fascial sheath

Superficial palmar branch of radial artery and recurrent branch of median nerve to thenar muscles

Common palmar digital artery Proper palmar digital arteries Septa from palmar aponeurosis forming canals

Ulnar artery and nerve

Palmar aponeurosis (reflected)

Common palmar digital branches of median nerve (cut)

Anterior (palmar) views

Hypothenar muscles Proper palmar digital nerves of thumb Fascia over adductor pollicis muscle 1st dorsal interosseous muscle Probe in dorsal extension of thenar space deep to adductor pollicis muscle Thenar space (deep to flexor tendons and 1st lumbrical muscle) Septum separating thenar from midpalmar space Common palmar digital artery Proper palmar digital arteries and nerves Annular and cruciform parts of fibrous sheath over (synovial) flexor tendon sheaths

Common flexor sheath (ulnar bursa) 5th finger (synovial) tendinous sheath Probe in midpalmar space Midpalmar space (deep to flexor tendons and lumbrical muscles) Insertion of flexor digitorum superficialis tendon Insertion of flexor digitorum profundus tendon

Figure 1.40  Superficial and deep intrinsic muscles in the hand. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Muscles and tendons

Radial artery and palmar carpal branch

35

Pronator quadratus muscle Ulnar nerve

Radius

Ulnar artery and palmar carpal branch

Superficial palmar branch of radial artery

Flexor carpi ulnaris tendon

Flexor retinaculum (transverse carpal ligament) (reflected )

Palmar carpal arterial arch Pisiform

Opponens pollicis muscle

Median nerve

Branches of median nerve to thenar muscles and to 1st and 2nd lumbrical muscles

Abductor digiti minimi muscle (cut) Deep palmar branch of ulnar artery and deep branch of ulnar nerve

Abductor pollicis brevis muscle (cut )

Flexor digiti minimi brevis muscle (cut)

Flexor pollicis brevis muscle

Opponens digiti minimi muscle Deep palmar (arterial) arch

Adductor pollicis muscle

Palmar metacarpal arteries Common palmar digital arteries

1st dorsal interosseous muscle

Deep transverse metacarpal ligaments

Branches from deep branch of ulnar nerve to 3rd and 4th lumbrical muscles and to all interosseous muscles

Ulna

Anterior (palmar) view Lumbrical muscles (reflected )

Radius

Palmar interosseous muscles (unipennate)

Ulna

Radius

Deep transverse metacarpal ligaments

1

2

3

Radial artery

Abductor pollicis brevis muscle

Abductor digiti minimi muscle

Dorsal interosseous muscles (bipennate)

4

3

2

1

Anterior (palmar) view

Tendinous slips to extensor expansions (hoods)

Posterior (dorsal) view Note: Arrows indicate action of muscles.

Figure 1.41  Superficial and deep intrinsic muscles in the hand. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

36

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

BOX 1.7  Clinical pearl: Examination of intrinsic muscles Examination of the hand for finger intrinsic function requires little more than an understanding of the anatomy described above and its related function. Function of the interossei may be assessed by asking the patient to adduct and abduct the fingers from the hand axis in the middle of the long finger. The ability to flex the metacarpophalangeal joints with the interphalangeal joints extended (“intrinsic plus” posture) confirms interosseous function. Paralysis is reflected by clawing of the fingers with hyperextension of the metacarpophalangeal joints and flexion of the interphalangeal joints on attempts actively to extend the fingers (“intrinsic minus”). Lumbrical function is best reflected by having the patient fully flex the finger (extrinsic flexor function), then move the finger smoothly into extension at the interphalangeal joints while holding active flexion at the metacarpophalangeal joint. Tightness or contracture of the interossei results in inability actively or passively to flex the interphalangeal joints while the metacarpophalangeal joint is extended. Inability to flex the interphalangeal joints may be a result of fixation of the extrinsic extensor tendons proximal to the metacarpophalangeal joint. Testing to differentiate these two possible etiologies is done by passively extending, then passively flexing, the metacarpophalangeal joint while assessing the degree of passive extension of the interphalangeal joints. If the interphalangeal joints passively extend when the metacarpophalangeal joint is extended, the interosseous muscle and tendon are short. If, by contrast, the interphalangeal joints extend when the metacarpophalangeal joint is passively flexed, the extrinsic extensor is adherent proximal to the metacarpophalangeal joint (Fig. 1.43).

Figure 1.42  All interossei act as prime flexors of the metacarpophalangeal joints since they pass palmar to the joint axis. Extensions into the lateral bands result in extension of the interphalangeal joints. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. 1. Philadelphia: WB Saunders, 1973.)

Adhesion

A

Fibrosed

B

Figure 1.43  (A,B) Testing for tightness or shortening of the interosseous muscles as a cause of passive extension contracture of the interphalangeal joint. The metacarpophalangeal joint is passively extended and the interphalangeal joints passively extend. If the cause of extensor tightness at the interphalangeal joint is a result of long extensor adhesions to the metacarpal, the interphalangeal joints will passively extend on passive flexion of the metacarpophalangeal joint. (Redrawn after Chase RA. Atlas of Hand Surgery, vol. II. Philadelphia: WB Saunders, 1984.)

Blood supply

BOX 1.8  Clinical pearl: Dynamics of hand function The central backbone of the hand is positioned in extension by the very important extensor carpi radialis brevis and longus. Flexion is affected by the flexor carpi radialis. All three muscles insert on the central two metacarpals (the second and third). These key motors are responsible for positioning the hand axis in preparation for operation of the adaptive hand elements around it. There are numerous other modifying motors to adjust the hand axis in the exact position desired, such as the flexor carpi ulnaris and extensor carpi ulnaris, which produce ulnar deviation. The fixed unit of the hand is extended from the radius at the radiocarpal joint. The entire complex is a beam attached to the ulna by the distal radioulnar joint, the interosseous membrane, and the proximal radioulnar articulation. Rotation around the fixed ulna in supination and pronation is largely under the influence of the median-innervated pronator teres and pronator quadratus and the radial-innervated supinator. The biceps and ­brachioradialis augment supination.

The thumb is steadied in position by contraction of the antagonist muscles to the abductors and the thumb adductor. Both the adductors and the abductors support flexion of the metacarpophalangeal joint to prevent recurvatum at this joint on pinching, which may occur with paralysis of either or both  (Froment’s sign). With graded relaxation of the abductors, the adductor will dominate and pull the thumb against the side of the hand. The carpometacarpal joint is a saddle joint with a lax capsule. This allows a wide range of circumduction motion and even a small degree of distraction of the joint on traction. Stability of the thumb root is heavily dependent on the muscles affecting it. The radial-innervated extensor ­pollicis longus and brevis and abductor pollicis longus secure the metacarpal dorsally. Opposing this to achieve stability are two groups of intrinsic muscles that, together with the extensor and dorsal abductor, triangulate the metacarpal. These two intrinsic groups are the median-innervated palmar abductors (the  abductor pollicis brevis, opponens pollicis, and superficial head of the flexor pollicis brevis) and the ulnar-innervated adductors (the adductor pollicis, first dorsal interosseus, and deep head of the flexor pollicis brevis). When there is paralysis of any of the three major motor nerves, thumb stability is compromised. In median nerve palsy, the positioning muscles of the thenar eminence are lost, resulting in inability to oppose the thumb for pulp-to-pulp opposition with other digits. Ulnar nerve palsy results in adduction weakness and imbalance of the structures influencing the metacarpophalangeal joint. Radial nerve palsy destroys extension and dorsal abduction function, with resultant adduction contracture that becomes fixed after an extended period of unopposed adduction. The ulnar nerve innervates the hypothenar muscle group, which serves further to develop the concavity of the transverse metacarpal arch (Box 1.8).

Blood supply The vascular inflow to the upper arm and hand is a continuation of the axillary artery to the brachial artery. The brachial

37

artery is palpable just medial to the biceps tendon at the level of the elbow. The brachial artery branches into the radial and ulnar arteries at the bicipital aponeurosis of the elbow (Fig.  1.44). Supplementary arteries in the forearm include the anterior interosseous artery, the posterior interosseous artery, and the median artery. The radial artery continues distally in the forearm between the brachioradialis and flexor carpi radialis muscles. At the wrist, the radial artery is located near the styloid process of the radius, and then travels dorsally, crossing the ­“anatomic snuffbox” deep to the tendons of the abductor pollicis ­longus, extensor pollicis brevis, and extensor pollicis longus (Fig. 1.45). In the hand, it penetrates between the first and second metacarpal bones, through an arcade in the first ­dorsal interosseous muscle, to enter the palm and form the deep ­palmar arch. A superficial branch of the radial artery arises at the level of the distal radius before the artery enters the “snuffbox” and courses over or through the abductor pollicis brevis to contribute to the superficial palmar arch. This branch contributes blood supply to the skin over the thenar area and underlying intrinsic muscles of the thumb. The ulnar artery is the other major branch of the brachial artery. Soon after the takeoff of the ulnar artery, the common interosseous artery originates and itself branches into the anterior and posterior interosseous arteries. The ulnar artery continues in the forearm under the flexor carpi ulnaris muscle. At the wrist, it lies radial to the pisiform and ulnar to the hook of the hamate and travels into the hand through Guyon’s canal, deep to the palmaris brevis and the hypothenar fascia. Here it divides into a deep palmar branch and a superficial palmar branch. The superficial branch becomes the dominant contributor to the superficial palmar arch. The superficial arch crosses the palm at the level of the fully abducted thumb. The deep branch contributes to the deep palmar arch. In general, the blood supply of the hand is conveniently divided into palmar vessels, which are subdivided into a superficial and a deep layer, and a single dorsal layer (Fig. 1.46).65 For example, the superficial vascular arch and its branches constitute the superficial group, the deep arch and the palmar metacarpal branches make up the deep layer, and the dorsal arch with its dorsal metacarpal branches forms the dorsal distribution (Box 1.9). The superficial palmar arch gives rise to three common digital arteries and multiple branches to intrinsic muscles and skin. The deep vascular arch lies at the proximal ends of the metacarpals deep to all the flexor tendons. It arises chiefly from the radial artery and becomes an arch by anastomosis with the deep branch of the ulnar artery. The deep arch is the major source of blood supply to the thumb and to the radial side of the index finger. This blood supply comes from the first of the four palmar metacarpal arteries. The first metacarpal artery is the prime source of blood supply to the radial and ulnar proper digital arteries of the thumb and the radial proper digital artery of the index finger. These digital arteries generally receive collateral branches from the superficial palmar arch as well. After giving its branch to the index finger, the first metacarpal artery becomes the primary source of blood supply to the thumb and is frequently called the princeps pollicis (Box 1.10).

38

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Anterior view Deltoid muscle Coracobrachialis muscle Short head (cut )

Biceps brachii muscle

Intercostobrachial nerve

Long head (cut ) Medial brachial cutaneous nerve

Musculocutaneous nerve Brachialis muscle

Radial nerve

Biceps brachii muscle (cut ) and tendon

Ulnar nerve

Lateral antebrachial cutaneous nerve (from musculocutaneous nerve) Radial nerve

Medial antebrachial cutaneous nerve

Deep branch

Median nerve

Superficial branch

Brachial artery

Supinator muscle

Bicipital aponeurosis

Brachioradialis muscle

Humeral head (cut)

Radial artery

Ulnar head

Pronator teres muscle (partially cut ) Median nerve Flexor pollicis longus muscle Flexor carpi radialis tendon (cut ) Flexor retinaculum (transverse carpal ligament) Superficial branch of radial nerve Recurrent (motor) branch of median nerve to thenar muscles

Pronator teres muscle

Flexor carpi radialis muscle (cut) Humeroulnar head Radial head

Flexor digitorum superficialis muscle (cut)

Flexor digitorum profundus muscle Flexor carpi ulnaris muscle Ulnar artery and nerve Dorsal branch of ulnar nerve Flexor digitorum superficialis tendons (cut) Deep palmar branch of ulnar artery and deep branch of ulnar nerve Superficial branch of ulnar nerve Superficial palmar arch (cut)

Common palmar digital branches of median nerve Proper palmar digitial branches of median nerve

Common palmar digital branch of ulnar nerve Communicating branch of median nerve with ulnar nerve Proper palmar digital branches of ulnar nerve

Figure 1.44  Upper arm vascular anatomy and surrounding structures. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Peripheral nerves

Extensor pollicis brevis Superficial branch of radial nerve Abductor pollicis longus

Extensor pollicis longus

Figure 1.45  The anatomic snuffbox. The superficial branch of the radial nerve can be palpated by stroking along the extensor pollicis longus. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

The dorsal arteries originate proximally from the posterior interosseous artery and a dorsal perforating branch of the anterior interosseous artery. These arteries are joined by branches from the radial and ulnar arteries to form a dorsal carpal arch. Dorsal metacarpal arteries arise from this arch and extend distally to the margins of the fingers.66–70 These dorsal arteries are joined by a varying number of vessels perforating from the deep palmar metacarpal arteries. In fact, the dominant supply to the dorsal metacarpal arteries may come from these perforators. Dorsal arteries to the thumb come from branches of the radial artery before it plunges through the first dorsal interosseous arcade. Thus, the dorsal arterial blood supply of the thumb is similar to that of the fingers (Box 1.11). Veins generally follow the arterial pattern in the deep system as venae comitantes. An abundant superficial system of venous drainage also exists (Fig.  1.47). Ultimately, these superficial veins contribute to the cephalic and basilic veins of the upper extremities. Lymphatic drainage terminates in the axillary, supraclavicular, and subclavicular nodes.

Peripheral nerves The peripheral nerves to the upper extremity have anatomic relationships of great importance to the surgeon. For example, one needs to know the anatomic availability for nerve block and sites where nerves are subject to compression or injury. Sites of particular susceptibility to injury coincide quite accurately with the sites chosen for anesthesia. With the ability to perform fascicular and group fascicular repair of nerves in addition to epineurial repair, it is important for surgeons to understand the generic internal structure of peripheral nerves. The epineurium is the tubular fibrous support structure surrounding the entire nerve; it also courses between the fascicles. Subdivisions consisting of multiple fascicles within the nerve are covered by epineurium. Each fascicle is covered by perineurium. Within each fascicle are separate axons, some myelinated and some unmyelinated. Motor, sensory, and sympathetic fibers are present within each

39

peripheral nerve. Blood vessels are found on the epineurial surface and in the internal supporting structure of the nerve. The internal topography is plexus-like, as described in detail in the classic monograph by Sunderland.70 The radial nerve arises from the posterior cord of the brachial plexus (C6–8). As the nerve passes the distal humerus, muscular branches innervate the brachioradialis and extensor carpi radialis longus muscles (Fig. 1.48). The radial nerve divides into terminal deep and superficial branches at the proximal forearm (Fig.  1.49). The deep posterior interosseous nerve supplies the supinator as well as muscles in all the extensor compartments: extensor carpi radialis brevis, extensor digitorum communis, extensor digiti minimi, extensor carpi ulnaris, extensor indicis proprius, extensor pollicis longus, extensor pollicis brevis, and abductor pollicus longus muscles. Finally, the deep posterior interosseous nerve terminates to supply carpal joint sensation. The dorsal or superficial branch of the radial nerve courses through the forearm in relationship to the brachioradialis muscle on the radial side of the arm. The superficial branch of the radial nerve crosses the “anatomic snuffbox” between the extensor pollicis brevis and the extensor pollicis longus in the loose subcutaneous tissue. Here it exchanges fibers with terminal branches of the lateral antebrachial cutaneous nerve. The area the superficial branch of the radial nerve supplies is the skin of the dorsum of the hand over the radial two-thirds, the dorsum of the thumb, and the index, long, and half of the ring finger proximal to the distal ­interphalangeal joint. The median nerve arises from the lateral and medial cords of brachial plexus (C5–T1) (Fig. 1.50). In the forearm, muscular branches supply the pronator teres, flexor carpi radialis, palmaris longus, and flexor digitorum superificialis muscles. The anterior interosseous branch of the median nerve innervates the flexor pollicis longus, flexor digitorum profundus (index and middle finger), and pronator quadratus muscles, and provides wrist sensation. Proximal to the wrist and running between the flexor carpi radialis and palmaris longus tendons, the palmar cutaneous branch provides lateral palmar sensation (Fig. 1.51). As the median nerve passes through the carpal tunnel, the recurrent motor branch innervates the thenar muscles (abductor pollicis brevis, opponens pollicis, and flexor pollicis brevis (superficial head). Sensory branches supply digital nerves to the thumb, index, and middle fingers, as well as the radial aspect of the ring finger (Video 1.5 ). Lastly, the ulnar nerve enters the upper extremity as a branch of the medial cord of the brachial plexus (C8–T1) (Fig.  1.52). Muscular branches innervate the flexor carpi ulnaris and flexor digitorum profundus muscles to the ring and small fingers. The palmar cutaneous branch of the ulnar nerve provides sensation to the hypothenar eminence and medial portion of the palm. The dorsal branch of the ulnar nerve courses around the ulnar aspect of the forearm in its distal one-fourth after branching from the main trunk at a variable site in the distal one-third of the forearm. It passes from its position deep to the flexor carpi ulnaris out through the dorsal fascia to become subcutaneous (Fig. 1.53). This sensory nerve branches to innervate the ulnar portion of the dorsum of the hand, the dorsum of the little finger, and at least part of the dorsum of the ring finger. In contrast, the main

40

CHAPTER 1  • Anatomy and biomechanics of the hand

SECTION I

Radial artery

Ulnar artery and nerve Palmar carpal ligament (continuous with extensor retinaculum)

Median nerve and palmar branch Superficial palmar branch of radial artery

Flexor retinaculum (transverse carpal ligament)

Abductor pollicis brevis muscle (cut )

Deep palmar branch of ulnar artery and deep branch of ulnar nerve

Opponens pollicis muscle

Superficial branch of ulnar nerve

Flexor pollicis brevis muscle

Common flexor sheath (ulnar bursa)

Recurrent (motor) branch of median nerve to thenar muscles

Superficial palmar (arterial) arch

Proper digital nerves and arteries to thumb

Common palmar digital nerves and arteries Communicating branch of median nerve with ulnar nerve

Adductor pollicis muscle

Proper palmar digital nerves and arteries

Branches of median nerve to 1st and 2nd lumbrical muscles Flexor tendons, synovial and fibrous sheaths

Branches of proper palmar digital nerves and arteries to dorsum of middle and distal phalanges

Ulnar artery and nerve Radial artery

Palmar carpal branches of radial and ulnar arteries

Median nerve

Pisiform

Superficial palmar branch of radial artery Deep palmar (arterial) arch and deep branch of ulnar nerve Princeps pollicis artery

Deep palmar branch of ulnar artery and deep branch of ulnar nerve Branches to hypothenar muscles Superficial branch of ulnar nerve

Proper digital arteries and nerves of thumb

Hook of hamate Distal limit of superficial palmar arch Radialis indicis artery Palmar metacarpal arteries Common palmar digital arteries Proper palmar digital arteries Proper palmar digital nerves from median nerve

Deep palmar branch of ulnar nerve to 3rd and 4th lumbrical, all interosseous, adductor pollicis, and deep head of flexor pollicis brevis muscles Communicating branch of median nerve with ulnar nerve Proper palmar digital nerves from ulnar nerve

Figure 1.46  Hand vascular anatomy and surrounding structures. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Conclusion

41

BOX 1.9  Clinical pearl: The Allen’s test

BOX 1.11  Clinical pearl: Dorsal metacarpal artery flaps

This test may be used to assess the competence of the major arterial contributors to blood supply in the hand and the functional efficiency of the vascular arches in the hand. Palpate the radial and ulnar pulses at the wrist and prepare to compress these arteries. Have the patient make a very tight fist. Compress the arteries and ask the patient to extend the digits. The hand will be blanched white. Release pressure on one of the arteries and observe the return of a red flush on the hand. Normally, the flush is immediate and progresses across the whole hand without delay. This confirms the patency of the artery and the competence of circulatory collaterals through the vascular arches. The test may be performed to confirm the competence of each of the two major arteries before surgery or to check their competence after repair, thrombectomy, manipulation, or injury. The Allen’s test principle may be used in clinically assessing the competence of the two proper digital arteries in the fingers. It may be done by observing return of color after compression of both arteries and release of one to the digit. Compress one artery, then the other, and then both to note the individual proper artery contribution to cutaneous blood supply. The technique may be useful when one is planning an island pedicle flap from a donor finger whose digital artery may have been damaged by an injury proximal to the finger.

The dorsal arterial circulation of the hand is the source of multiple intrinsic hand flaps. The radial artery and the dorsal carpal arch give off the first and second metacarpal arteries which run in the intermetacarpal spaces between the thumb and index finger, and the index finger and middle finger, respectively. The third metacarpal artery is much smaller and is less reliable for flap transfer. Although multiple uses and variations have been described, the simplest method to catalogue these flaps is by artery and by direction of flow. Therefore, both the first and second dorsal metacarpal arteries may be used in an anterograde or retrograde fashion. The first dorsal metacarpal artery (FDMA) has been found to originate from the dorsal radial artery, just distal to the extensor pollicis longus tendon. In a series of 30 hand dissections, 90% of hands had superficial or fascial FDMAs, 40% of hands had a deep intramuscular branch, and 30% had both vessels present.67 The external diameter averaged 1.0–1.5 mm at the largest part. This vessel can be used to harvest a pedicled island flap of skin from the dorsum of the index proximal phalanx innervated by a branch of the radial sensory nerve.68 In the anterograde fashion, this flap may reach about the dorsum of the radial two-thirds of the hand, and even to a portion of the volar hand. The reach of the FDMA flap can be extended distally if designed in a retrograde fashion.69 The second dorsal metacarpal artery (SDMA) was found in 29 of 30 (97%) hands dissected. The origin of this vessel varied, including from the dorsal carpal arch, radial artery, FDMA, and the posterior interosseus artery. Once the SDMA reached the index finger extensor tendons, the vessel passed deep to the tendons and within the fascia of the second dorsal interosseous muscle. The SDMA branched and became superficial at the level of the ­metacarpophalangeal joints. The pedicle, being more central than the FDMA, can nearly reach the entire dorsum of the hand and can also be extended in a retrograde fashion, to reach the level of the proximal interphalangeal joints of the index and middle fingers.70

BOX 1.10  Clinical pearl: The relative size of digital vessels Although two digital arteries (radial and ulnar) usually perfuse each finger, there are differences in the diameter of the radial versus ulnar digital arteries.66 In the thumb, the ulnar digital artery is usually much larger. The index finger is similarly ulnar-dominant whereas the small finger is radial-dominant. The arteries to the middle and ring fingers do not have appreciable size differences between radial and ulnar sides. This anatomic variation may be important in finding adequate vessels for microanastomosis during replantation or revascularization.

sensory branch forms the ulnar digital nerve to the small finger and the common digital nerve which divides into the small-finger radial digital nerve and the ring-finger ulnar digital nerve. The deep motor branch of the ulnar nerve passes through the pisohamate and opponens tunnel in company with the deep branch of the ulnar artery. It courses with the deep vascular arch across the depths of the palm, giving off motor branches to the four hypothenar muscles (abductor digiti minimi, opponens digiti minimi, flexor digiti minimi brevis, and palmaris brevis), all the interossei, the two ulnar lumbricals, and the thumb intrinsics ulnar to the flexor pollicis longus – the adductor pollicis brevis and the flexor pollicis brevis (deep head). Essentially, the flexor pollicis longus divides the hand into a median and ulnar-innervated portion from the motor standpoint. The ulnar nerve is far less important from the standpoint of hand sensation but is very important for its motor innervation of all the hypothenar muscles and interossei. In addition, it innervates the thumb adductor,

the deep head of the flexor pollicis brevis, and the two ulnar lumbricals. Classically, all the intrinsic muscles on the radial side of the flexor pollicis longus are median nerve-innervated (the abductor pollicis brevis, opponens, and superficial head of the flexor pollicis brevis). All other intrinsic muscles in the hand receive their innervation from the ulnar nerve. The two tiny radial lumbricals (median nerve innervated) are the only exceptions to this axiom (Boxes 1.12 & 1.13).

Conclusion In the human hand, the complicated motor balance at each joint resulting from contraction, fixation, or relaxation of opposing muscle groups is worthless in the absence of the precisely fitted elements in the skeletal architecture. The skeletal framework with its restraining ligaments is beautifully designed but

42

SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Anterior (palmar) view

Posterior (dorsal) view

Cephalic vein

Basilic vein

Posterior antebrachial cutaneous nerve (from radial nerve) Lateral antebrachial cutaneous nerve (from musculocutaneous nerve)

Anterior branch and Posterior branch of medial antebrachial cutaneous nerve

Accessory cephalic vein

Median basilic vein

Median cephalic vein

Bicipital aponeurosis

Cephalic vein

Basilic vein

Note: In 70% of cases, a median cubital vein (tributary to basilic vein) replaces median cephalic and median basilic veins

Palmar branch of median nerve Intercapitular veins

Accessory cephalic vein Posterior branch of lateral antebrachial cutaneous nerve (from musculocutaneous nerve)

Perforating veins

Median antebrachial vein

Superficial branch of radial nerve

Posterior branch of medial antebrachial cutaneous nerve

Posterior antebrachial cutaneous nerve (from radial nerve)

Cephalic vein Basilic vein Extensor retinaculum Palmar branch of ulnar nerve Dorsal branch of ulnar nerve Palmar carpal ligament (continuous with extensor retinaculum) Palmar aponeurosis

Dorsal branch of ulnar nerve Dorsal metacarpal veins

Superficial branch of radial nerve Dorsal venous network

Intercapitular veins

Superficial transverse metacarpal ligament

Proper palmar digital nerves and palmar digital veins

Dorsal digital nerves and veins

Figure 1.47  The superficial and deep venous drainage system of the hand and arm. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Conclusion

Dorsal scapular nerve (C5)

Posterior view

Supraspinatus muscle Suprascapular nerve (C5, 6) Levator scapulae muscle (supplied also by branches from C3 and C4)

Deltoid muscle Teres minor muscle Axillary nerve (C5, 6) Superior lateral brachial cutaneous nerve

Rhomboid minor muscle

Radial nerve (C5, 6, 7 , 8, T1) Inconstant contribution

Rhomboid major muscle

Inferior lateral brachial cutaneous nerve

Posterior antebrachial cutaneous nerve Infraspinatus muscle Teres major muscle

Lateral intermuscular septum

Lower subscapular nerve (C5, 6) Posterior brachial cutaneous nerve (branch of radial nerve in axilla) Long head Triceps brachii muscle

Brachialis muscle (lateral part; remainder of muscle supplied by musculocutaneous nerve)

Lateral head Medial head Brachioradialis muscle Triceps brachii tendon Medial epicondyle

Extensor carpi radialis longus muscle

Olecranon Anconeus muscle

Extensor carpi radialis brevis muscle

Extensor digitorum muscle Extensor carpi ulnaris muscle

Figure 1.48  The proximal radial nerve wraps posteriorly around the humerus and then proceeds in a dorsal–radial direction distally. (Reprinted with permission from www. netterimages.com © Elsevier Inc. All Rights Reserved.)

43

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SECTION I

CHAPTER 1  • Anatomy and biomechanics of the hand

Inconstant contribution

Radial nerve (C5, 6, 7, 8, T1) Superficial (terminal) branch

Posterior view

Deep (terminal) branch Lateral epicondyle Anconeus muscle Brachioradialis muscle Extensor carpi radialis longus muscle Supinator muscle Extensor carpi radialis brevis muscle

Extensor-supinator group of muscles

Extensor carpi ulnaris muscle Extensor digitorum muscle and extensor digiti minimi muscle Extensor indicis muscle Extensor pollicis longus muscle Abductor pollicis longus muscle Extensor pollicis brevis muscle Posterior interosseous nerve (continuation of deep branch of radial nerve distal to supinator muscle) Superficial branch of radial nerve

From axillary nerve

Superior lateral brachial cutaneous nerve

Inferior lateral brachial cutaneous nerve Posterior brachial cutaneous nerve From radial nerve Posterior antebrachial cutaneous nerve Superficial branch of radial nerve and dorsal digital branches

Dorsal digital nerves Cutaneous innervation from radial and axillary nerves

Figure 1.49  The radial nerve in the forearm innervates the extensor muscles and then lends sensibility to the radial dorsal aspect of the hand. (Reprinted with permission from www.netterimages.com © Elsevier Inc. All Rights Reserved.)

Conclusion

Anterior view

45

Note: Only muscles innervated by median nerve shown

Musculocutaneous nerve

Median nerve (C5, 6, 7, 8, T1) Medial Posterior Lateral

Inconstant contribution

Pronator teres muscle (humeral head)

Cords of brachial plexus

Medial brachial cutaneous nerve

Articular branch

Medial antebrachial cutaneous nerve

Flexor carpi radialis muscle

Axillary nerve Palmaris longus muscle

Radial nerve

Pronator teres muscle (ulnar head)

Ulnar nerve

Flexor digitorum superficialis muscle (turned up) Flexor digitorum profundus muscle (lateral part supplied by median [anterior interosseous] nerve; medial part supplied by ulnar nerve) Anterior interosseous nerve Flexor pollicis longus muscle Pronator quadratus muscle

Cutaneous innervation

Palmar branch of median nerve

Thenar muscles

Abductor pollicis brevis Opponens pollicis Superficial head of flexor pollicis brevis (deep head supplied by ulnar nerve)

1st and 2nd lumbrical muscles

Palmar view Communicating branch of median nerve with ulnar nerve Common palmar digital nerves

Dorsal branches to dorsum of middle and distal phalanges

Proper palmar digital nerves

Posterior (dorsal) view Figure 1.50 The median nerve classically lends sensibility to the palmar aspect and the distal dorsum of the thumb, index, long, and radial half of the ring fingers. Intrinsic muscles radial to the flexor pollicis longus and the two radial lumbricals receive motor innervation from the median nerve. (Reprinted with permission from www.netterimages. com © Elsevier Inc. All Rights Reserved.)  

46

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CHAPTER 1  • Anatomy and biomechanics of the hand

Median nerve Flexor digitorum superficialis

Palmar cutaneous Flexor retinaculum (cut) branch

Figure 1.51  The palmar cutaneous branch of the median nerve travels superficial to the flexor retinaculum of the hand while the remaining portion of the median nerve travels deep. (Upper limb cadaver dissection, Stanford University Division of Clinical Anatomy. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

BOX 1.12  Clinical pearl: Median and ulnar nerve lacerations The ulnar and median nerves are frequently injured just proximal to the wrist. The nerves are quite superficial and it is a region where injuries to all structures are frequent. Median palsy alone results in anesthesia over the important exploring and manipulating digits (the thumb, index, and long fingers, and part of the ring finger) on the palmar surface. The median positioning muscles of the thumb become paralyzed, resulting in an inability to position the thumb for pulp-to-pulp opposition with other digits. In addition, the two radial lumbricals are paralyzed, but this may be barely perceptible functionally. There is a constant midvolar blood vessel on the median nerve that helps in its identity and in achieving very accurate axial rotation to perfect end-to-end opposition. The ulnar nerve divides into a deep motor branch and a superficial sensory branch just beyond the pisiform. Occasionally, stab wounds of the hand result in transection of the motor branch with no sensory loss. A guide to proper fascicular orientation in the ulnar nerve is the fact that one can identify that portion destined to be the deep or superficial branches well above the wrist.

BOX 1.13  Clinical pearl: Crowded areas with unyielding boundaries Flexion and extension motions in the hand occur at two levels, the wrist and the finger joints. Flexion at these joints would surely create volar bowstringing at the long flexor tendons unless it were prevented by fixed retinacular conduits at these points. At the wrist the flexor retinaculum is the fixed roof of the carpal tunnel. The fibrous flexor sheath in the digits forms a fitted pulley system with condensed thickening in the areas of greatest fulcrum responsibility. At the wrist and in the digital fibrosynovial sheaths, anatomic structures create full occupancy. Any addition, whether it be more structures, postinjury or inflammatory swelling of the contents, or inflammatory tightening of the sheath, sets the stage for an inflammatory reaction and adhesion formation. At the wrist, the median nerve passes beneath the flexor retinaculum and the transverse carpal ligament as the most superficial structure in this crowded space. It is subject to compression injury when swelling occurs within the carpal tunnel. Just proximal to the wrist, the ulnar nerve passes from beneath the flexor carpi ulnaris along the radial side of the easily palpable pisiform. At this point the nerve enters a fibromusculofascial space that is tubular in configuration, crossing the entire length of the carpus. This is Guyon’s tunnel, which is quite separate from the carpal tunnel, through which the median nerve and longitudinal structures to the digits pass. Guyon’s tunnel starts at a hiatus formed by the distal edge of the volar carpal ligament superficially and the proximal edge of the transverse carpal ligament deeply. The pisiform forms the ulnar side of the tunnel, and fibers from the volar carpal ligament that plunge down to join the underlying transverse carpal ligament form the radial wall. There is no fibrous roof on the proximal part of the tunnel until the pisohamate arcade fibers are encountered distally. The roof of the tunnel, therefore, consists of a thick layer of fascia continuous with the hypothenar fascia and generally a part of the palmaris brevis muscle. Through this rather soft hiatus, the superficial branch of the ulnar artery and the arterial branches to the palmaris brevis and overlying skin pass, together with the superficial branches of the ulnar nerve. Within Guyon’s tunnel the ulnar nerve lies ulnar to the artery, and the division of the ulnar nerve into its deep motor branch and two superficial branches is evident. After the superficial branches of the artery and nerve emerge through the roof of the tunnel, the deep artery and deep branch of the ulnar nerve enter the pisohamate tunnel beneath the pisohamate arcade. Although the tunnel of Guyon is devoid of a thick, fibrous roof, it is nonetheless covered by palmaris brevis fascia, creating an unyielding space, and its contents are therefore subject to compression from a variety of causes. Repeated trauma, as when one uses the heel of the hand to pound objects, may result in swelling of the tissues and resultant hypertrophy and fibrosis or hemorrhage in the tunnel, which may squeeze the nerve or artery, or both. Ganglia, tumors, or displaced bone may cause compression in the ulnar tunnel, just as occurs with the median nerve in the carpal tunnel.

Conclusion

47

Ulnar Nerve Anterior view

Note: Only muscles innervated by ulnar nerve shown Ulnar nerve (C7, 8, T1) (no branches above elbow) Inconstant contribution

Medial epicondyle

Articular branch (behind condyle)

Cutaneous innervation

Flexor digitorum profundus muscle (medial part only; lateral part supplied by anterior interosseous branch of median nerve)

Palmar view

Flexor carpi ulnaris muscle (drawn aside)

Dorsal branch of ulnar nerve

Posterior (dorsal) view

Flexor pollicis brevis muscle (deep head only; superficial head and other thenar muscles supplied by median nerve)

Adductor pollicis muscle

Palmar branch

Superficial branch Deep branch Palmaris brevis Abductor digiti minimi Flexor digiti minimi brevis

Hypothenar muscles

Opponens digiti minimi Common palmar digital nerve Communicating branch of median nerve with ulnar nerve Palmar and dorsal interosseous muscles 3rd and 4th lumbrical muscles (turned down) Proper palmar digital nerves (dorsal digital nerves are from dorsal branch) Dorsal branches to dorsum of middle and distal phalanges

Figure 1.52 The ulnar nerve classically gives sensory innervation to the little finger and the ulnar half of the ring finger. All hypothenar muscles, all interossei, the two ulnar lumbricals, the adductor pollicis, and the ulnar half of the flexor pollicis brevis are usually innervated by the ulnar nerve. (Reprinted with permission from www.netterimages. com © Elsevier Inc. All Rights Reserved.)  

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CHAPTER 1  • Anatomy and biomechanics of the hand

Extensor retinaculum

Flexor carpi ulnaris

Dorsal branch of ulnar nerve

Figure 1.53  The dorsal branch of the ulnar nerve. (Upper limb cadaver dissection, Stanford University Division of Plastic Surgery. © 2015 James Chang, Anais Legrand. All Rights Reserved.)

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is useless without proper dynamic motor tension. The anatomic presence of both architecture and functioning muscles is only serviceable when there is integrity of the central nervous control mechanisms. As a unified interrelated melding of these elements emerges, hand function becomes the marvelous adaptable fact that it is in humans. Its function is modified and further refined by sensory integrity. Sensation is protective and influential on central motor function. Moreover, special sensation as it resides in the hand makes the hand a special sense organ with which human beings explore their environment. From a practical standpoint, surgeons need repeatedly to remind themselves of the anatomic basis for diagnosis and management of surgical problems in the hand.

References

References 1. Bell C. The Hand – Its Mechanism and Vital Endowments as Evincing Design. London: William Pickering; 1834. This treatise by Sir Charles Bell is a literary classic that should be read by any student of hand surgery and anatomy. 2. Duchenne G.B. Physiologie des mouvements. Trans. Kaplan, EB. Philadelphia: J. B. Lippincott; 1959 (Paris: Baillière, 1867). 3. Wood-Jones F. The Principles of Anatomy as Seen in the Hand. Philadelphia: Blakiston, Son; 1920. 4. Kanavel AB. Infections of the Hand. Philadelphia: Lea and Febiger; 1925. 5. Bunnell S. Surgery of the Hand. Philadelphia: J. B. Lippincott; 1944. This is the first edition of the first modern textbook in hand surgery, written by Sterling Bunnell, widely regarded as the father of American hand surgery. 6. Kaplan EB. Functional and Surgical Anatomy of the Hand. Philadelphia: J. B. Lippincott; 1953. 7. Landsmeer JM. Anatomy of the dorsal aponeurosis of the human finger and its functional significance. Anat Rec. 1949;104:31–44. 8. Landsmeer JM. Anatomical and functional investigations on the articulation of the human fingers. Acta Anat. 1955;25:1–69. 9. Landsmeer JM. A report on the coordination of the interphalangeal joints of the human finger and its disturbances. Acta Morphol Neerl Scand. 1958;2:59–84. 10. Landsmeer JM. The coordination of finger joint motions. J Bone Joint Surg. 1963;45A:1654–1662. 11. Kaplan EB. The participation of the metacarpophalangeal joint of the thumb in the act of opposition. Bull Hosp Joint Dis. 1966;27:39–45. 12. Eyler DL, Markee JE. The anatomy of the intrinsic musculature of the fingers. J Bone Joint Surg. 1954;36A:1–9. 13. Stack HG. A study of muscle function in the fingers. Ann R Coll Surg Engl. 1963;33:307–322. 14. Tubiana R, Valentin P. L’extension des doigts. Rev Chir Orthop. 1963;49:543. 15. Zancolli EA, Angrigiani C. Posterior interosseous island forearm flap. J Hand Surg. 1988;13B:130–135. 16. Earley MJ, Milner RH. Dorsal metacarpal flaps. Br J Plast Surg. 1987;40:333–341. 17. Berger RA. The gross and histologic anatomy of the scapholunate interosseous ligament. J Hand Surg. 1996;21:170–178. In this journal article, Dr. Berger clearly describes the unique anatomy of the scapholunate interosseous ligament. He discusses clinical implications of the anatomy for injury patterns and repair/reconstruction. 18. Viegas SF, Yamaguchi S, Boyd NL, et al. The dorsal ligaments of the wrist: anatomy, mechanical properties, and function. J Hand Surg. 1999;24:456–468. 19. Kaplan EB. Functional and Surgical Anatomy of the Hand. Philadelphia: J. B. Lippincott; 1953. 20. Littler JW. Hand, wrist, and forearm incisions. In: Littler JW, Cramer LM, Smith JW, eds. Symposium on Reconstructive Hand Surgery. St. Louis: C.V. Mosby; 1974. 21. Skoog T. The transverse elements of the palmar aponeurosis in Dupuytren’s contracture. Scand J Plast Reconstr Surg. 1967;1:51–63. 22. Phillips C, Mass D. Mechanical analysis of the palmar aponeurosis pulley in human cadavers. J Hand Surg Am. 1996;21:240–244. 23. Sherman PJ, Lane LB. The palmar aponeurosis pulley as a cause of trigger finger. A report of two cases. J Bone Joint Surg Am. 1996;78: 1753–1754. 24. Legueu F, Juvara E. Des aponèvroses de la paume de la main. Bull Mem Soc Anat Paris. 1892;67:383. In this original manuscript, Legueu and Juvara perform anatomic dissections to outline the palmar aponeurosis of the hand. The vertical fibers that bear the authors' names are described. These vertical fibers separate the neurovascular and flexor tendon compartments within the palm. 25. Bojsen-Moller F, Schmidt L. The palmar aponeurosis and the central spaces of the hand. J Anat. 1974;117:55–68. 26. Gilula LA. Carpal injuries: analytic approach and case exercises. Am J Radiol. 1979;133:503–517.

48.e1.e

27. Gelberman RH, Menon J. The vascularity of the scaphoid bone. J Hand Surg. 1980;5:508–513. The authors perform dye injection studies to determine the vascular anatomy to the scaphoid. The relative decreased blood flow to the proximal pole has implications for poor healing of scaphoid fractures in this region. 28. LaPorte DM, Shar Hashemi S, Lee Dellon A. Sensory innervation of the triangular fibrocartilage complex: a cadaveric study. J Hand Surg Am. 2014;39:1122–1124. 29. Viegas SF. The dorsal ligaments of the wrist. Hand Clin. 2001;17:65–75. 30. Berger RA. The gross and histologic anatomy of the scapholun ate interosseous ligament. J Hand Surg. 1996;21:170–178. 31. Berger RA, Imeada T, Berglund L, et al. Constraint and material properties of the subregions of the scapholunate and interosseous ligament. J Hand Surg. 1999;24:953–962. 32. Brand P, Hollister A. Clinical Mechanics of the Hand. St. Louis: Mosby-Year Book; 1999. 33. Youm Y, McMurtry RY, Flatt AE, et al. Kinematics of the wrist – I. An experimental study of radial-ulnar deviation and flexionextension. J Bone Joint Surg. 1978;60A:423–431. 34. Hollister A, Giurintano DJ, Buford WL, et al. The axes of rotation of the thumb interphalangeal and metacarpophalangeal joints. Clin Orthop Relat Res. 1995;320:188–193. 35. Wolfe SW, Neu C, Crisco JJ. In vivo scaphoid, lunate, and capitate kinematics in flexion and in extension. J Hand Surg Am. 2000;25: 860–869. 36. Graham KS, Goitz RK, Kaufmann RA. Curvatures of the DIP joints of the hand. Hand (NY). 2014;9:522–528. 37. Watson HK, Light TR, Johnson TR. Checkrein resection for flexion contracture of the middle joint. J Hand Surg. 1979;4:67–71. 38. Eaton RG, Littler JW. A study of the basal joint of the thumb. J Bone Joint Surg. 1969;51A:661–668. 39. Dahhan P, Fischer L, Alliey Y. The trapeziometacarpal articulation. Anat Clin. 1980;2:43–56. 40. Cooney WP, An KN, Daube JR, et al. Electromyographic analysis of the thumb: a study of isometric forces in pinch and grasp. J Hand Surg. 1985;10A:202–210. 41. Kuczynski K. The thumb and the saddle. Hand. 1975;7:120–122. 42. Kuczynski K. Carpometacarpal joint of the human thumb. J Anat. 1974;118:119–126. 43. Tubiana R. The Hand. Vol. II. Philadelphia: W. B. Saunders; 1985. 44. Pagalidis T, Kuczynski K, Lamb DW. Ligamentous stability of the base of the thumb. Hand. 1981;13:29–36. 45. Bettinger PC, Berger RA. Functional ligamentous anatomy of the trapezium and trapeziometacarpal joint (gross and arthroscopic). Hand Clin. 2001;17:151–168. 46. Aubriot JH. The metacarpophalangeal joint of the thumb. In: Tubiana R, ed. The Hand. Philadelphia: W. B. Saunders; 1981:184. 47. Lieber RL. Skeletal Muscle Structure and Function: Implications for Rehabilitation and Sports Medicine. Baltimore: Williams and Wilkins; 1992. 48. Enoka RM. Neuromechanics of Human Movement. Champaign, IL: Human Kinetics; 2001. 49. Garcia-Elias M, An KN, Berglund L, et al. Extensor mechanism of the fingers: I. A quantitative geometric study. J Hand Surg Am. 1991;16:1130–1140. 50. Hurlbut PT, Adams BD. Analysis of finger extensor mechanism strains. J Hand Surg Am. 1995;20:832–840. 51. Garcia-Elias M, An KN, Berglund L, et al. Extensor mechanism of the fingers: II. Tensile properties of components. J Hand Surg Am. 1991;16:1130–1140. 52. Valero-Cuevas FJ, Zajac FE, Burgar CG. Large index-fingertip forces are produced by subject-independent patterns of muscle excitation. J Biomech. 1998;31:693–703. 53. Sancho-Bru JL, Perez-Gonzalez A, Vergara-Monedero M, et al. 3-D dynamic model of human finger for studying free movements. J Biomech. 2001;34:1491–1500. 54. Leijnse JN, Bonte JE, Landsmeer JM, et al. Biomechanics of the finger with anatomical restrictions – the significance for the exercising hand of the musician. J Biomech. 1992;25:1253–1264.

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55. Leijnse JN, Snijders CJ, Bonte JE, et al. The hand of the musician: kinematics of the bidigital finger system with anatomical restrictions. J Biomech. 1993;26:1169–1179. 56. Ikebuchi Y, Murakami T, Ohtsuka A. The interosseous and lumbrical muscles in the human hand, with special reference to the insertions of the interosseous muscles. Acta Med Okayama. 1988;42:327–334. 57. Zancolli E, Cozzi EP. Atlas of Surgical Anatomy of the Hand. New York: Churchill Livingstone; 1992. 58. Chase RA. Surgical anatomy of the hand. Surg Clin North Am. 1964;44:1349. 59. Zajac FE. How musculotendon architecture and joint geometry affect the capacity of muscles to move and exert force on objects: a review with application to arm and forearm tendon transfer design. J Hand Surg Am. 1992;17:799–804. 60. Agee J, McCarroll HR, Hollister AM. The anatomy of the flexor digitorum superficialis relevant to tendon transfers. J Hand Surg Br. 1991;16B:68–69. 61. Burgar CG, Valero-Cuevas FJ, Hentz VR. Fine-wire electromyographic recording during force generation. Application to index finger kinesiologic studies. Am J Phys Med Rehabil. 1997;76:494–501.

62. Stack HG. A study of muscle function in the fingers. Ann R Coll Surg Engl. 1963;33:307–322. 63. Tubiana R, ed. The Hand. Philadelphia: Saunders; 1981. 64. Wang K, McGlinn EP, Chung KC. A biomechanical and evolutionary perspective on the function of the lumbrical muscle. J Hand Surg Am. 2014;39:149–155. 65. McFadden JA, Gordon L. Arterial repair at the digital and palmar level. In: Blair WF, ed. Techniques in Hand Surgery. Baltimore: Williams and Wilkins; 1996:398–406. 66. Earley MJ, Milner RH. Dorsal metacarpal flaps. Br J Plast Surg. 1987; 40:333–341. 67. Small JO, Brennan MD. The first dorsal metacarpal artery neurovascular island flap. J Hand Surg. 1987;13B:136–145. 68. Maruyama Y. The reverse dorsal metacarpal flap. Br J Plast Surg. 1990;43:24–27. 69. Hao J, Liu X, Ge B, et al. The second dorsal metacarpal flap with vascular pedicle composed of the second dorsal metacarpal artery and the dorsal carpal branch of radial artery. Plast Reconstr Surg. 1993;92:501–506. 70. Sunderland S. Nerves and Nerve Injuries. 2nd ed. New York: Churchill Livingstone; 1978.

SECTION I  •  Principles of Hand Surgery

2 Examination of the upper extremity Ryosuke Kakinoki

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SYNOPSIS

ƒ Physical examination of the upper extremity starts with a detailed and accurate patient history. ƒ Physical examination of the upper extremity consists of inspection, palpation, measurement of length, girth, and ranges of motion, assessment of stability, and detailed assessment of the associated nerve and vascular systems. ƒ Thorough understanding of the anatomy, physiology, and biomechanics of the upper extremity is essential to perform a physical examination correctly and to make a correct diagnosis of pathologic conditions of the upper extremity. ƒ Examiners must master correct physical examination techniques based on the anatomy, physiology, and biomechanics. ƒ The entire upper extremity should be examined, even if the patient’s complaint focuses only on the hand. ƒ It is essential to master correct techniques of physical examination to identify the pathologic conditions of patients. ƒ Examiners should have their own routine protocol of examination of the upper extremity so as not to leave a part unexamined. ƒ Comparison of the affected upper extremity with the contralateral ­unaffected one helps examiners identify pathologic conditions. ƒ Imaging modalities such as X-rays, CT or MRI should be used to ­confirm the diagnosis drawn from the physical examinations.

Obtaining a patient history The patient history can be the most important tool in developing an accurate diagnosis. The history should not only detail the patient’s current complaint, but should also document other elements of the patient’s history which may be of great significance for interpreting the patient’s current problem and choosing between treatment options. A patient history should include information on the patient’s demographics, current complaint, medical history, allergies, medications, and socioeconomic status. The time course of the patient history ­interview should also be documented.

Patient demographics The patient’s name, age, occupation, hand dominance, and hobbies should be documented. Information about previous injuries or diseases should be obtained regardless of whether they seem to be related to the patient’s current complaint.

Current complaint All information on the patient’s current problem, including symptoms of pain, numbness, tingling (paresthesia), weakness, dislocation, coldness, clumsiness, or poor coordination and clicking or snapping should be documented. Each symptom should be characterized according to its location, intensity, duration, frequency, radiation and associated symptoms. The patient history should include information on activities or treatments that aggravate or ameliorate the symptoms. It is also important to record the time and place at which the initial injury occurred and the mechanism. In trauma cases, the following data are especially important: 1. The time of the injury and the interval between the injury and the patient’s presentation should be determined. The interval between an injury and revascularization of amputated fingers has a great effect on the outcome of replantation surgery. 2. The environment in which the injury occurred is important. Whether an injury occurred in a dirty or a clean environment may determine whether infection is likely to be present. 3. The mechanism of injury is also important. For example, information on the posture of the fingers and hand at the time of a tendon laceration is helpful for locating a transected tendon stump. 4. Any previous treatment associated with the injury is documented. In non-trauma cases, the following data are especially significant: 1. The time at which symptoms such as pain, abnormal sensation, swelling or stiffness began and the subsequent progression of the symptoms is critical.

50

2. 3. 4. 5.

SECTION I

CHAPTER 2  • Examination of the upper extremity

The effects of the symptoms on the patient’s daily life, hobby or job are unique to that patient. One must also ascertain whether or not the symptoms are limited to one part of the body. Activities or postures that aggravate or ameliorate the symptoms are also discussed. The association between time and the intensity of symptoms must be carefully documented (e.g., whether pain increases just after waking up in the morning or during the night).

Medical history The patient’s health status may influence diagnosis and treatment. Before starting treatment, it is essential to determine whether the patient has diabetes, or cardiac, pulmonary, and/ or renal disease and whether the patient has a history of rheumatologic disease. Documentation of the family’s medical history may be helpful for making an accurate diagnosis and for choosing an appropriate treatment if the disease is hereditary. Patients and their families should be questioned about previous problems associated with bleeding and anesthesia. It is also important to determine the course of any prior surgery.

Allergies and medications The patient history should include data on any medications that the patient is taking. Previous allergic reactions to foods or medications should be noted. People who are allergic to shellfish are often allergic to contrast media that contain iodine.

Social history The social history includes the patient’s use of tobacco and alcohol. The amount of tobacco and alcohol used should be documented. Substance abuse and infection with hepatitis virus or human immunodeficiency virus (HIV) should also be noted. The patient’s hobbies or sports should be documented because these activities often determine the most appropriate treatment.

Physical examination specific to the hand Accurate diagnosis of hand problems depends on a systematic, careful physical examination. Physical examination should be performed routinely following a specific protocol. Even if the patient complains of a problem limited to the hand, the physical examination should start at the neck and shoulder region because the hand is suspended by the bones of the forearm, which connect proximally to the elbow joint, which in turn is stabilized by the humerus and the shoulder joint. In addition, numbness of the hand may be associated with cervical problems. These elements (inspection, palpation, measurement of range of motion, musculotendinous assessment, stability assessment, nerve assessment, and vascular assessment) should be included in the examination procedure for patients with problems of the upper extremities. An understanding of the interrelationships among these elements is helpful for drawing accurate diagnostic conclusions. Repeated physical

examinations reveal how symptoms change over time, which is important for assessing the effectiveness of the treatment.

Inspection When inspecting the upper extremities, it is essential to compare the affected extremity with the contralateral extremity because the latter can be used as a normal reference if the injury is unilateral.

Discoloration An abnormal skin color or a change in the color of the skin of the upper extremity is indicative of a wide variety of problems. Infections often cause swelling and patches of redness with proximal streaking. Vascular problems caused by arterial inflow insufficiency often present as pale-colored and the distal part of the upper limb appears to have shrunk, whereas those caused by venous outflow insufficiency present as a purple or dark red discoloration and a swollen limb. The color of a hematoma can be used to estimate the interval since the trauma occurred. A fresh hematoma has purple or blue patches, which then become green and finally yellow.

Deformity Fractures, tumors, arthritis, and some infectious conditions can cause deformities of the upper extremity. Fractures of the phalanges of the fingers frequently result in angular rotation or malrotation of the fingers. When the fingers are held up, the point at which the long axes of the fingers converge corresponds with the position of the scaphoid tubercle. However, the long axis of a malrotated finger deviates from the position of the scaphoid.

Muscular atrophy It is important to determine whether atrophied muscles are innervated by specific peripheral nerves. If the atrophic muscles are innervated by a specific nerve, the atrophy may have been caused by a peripheral nerve disorder. Muscular atrophy may occur under systemic neural or muscular pathological conditions; in most of these cases, the atrophy is symmetrical in the bilateral extremities. Generally, neurogenic diseases involve muscles in the distal part of the extremity and muscular diseases involve the proximal part of the extremity. The girths of the arm (a portion measured should be noted, like the arm girth 20 cm distal to the acromion) and forearm (a portion with the maximum diameter of the forearm) of both upper extremities should be measured routinely because this often reveals a loss of muscle mass, which may not be obvious to the eye.

Trophic changes Trophic changes are associated with an abnormality of the sympathetic nervous system. Increased hair growth or abnormal perspiration of the hands is often observed in chronic regional pain syndrome.

Swelling Swelling can be identified by comparison with the uninvolved extremity. Localized swelling indicates recent

Physical examination specific to the hand

51

trauma or inflammation. Diffuse swelling is often caused by infection. General swelling may originate from a lymphatic or venous obstruction. Swelling of the dorsum of the hand is also common.

The active range of motion of a joint is that which occurs when the patient contracts his or her muscles. The active range of motion is affected by tendon excursion, the posture of the hand and fingers, nerve function, and muscular strength.

Skin creases

Power

Disappearance of skin creases is indicative of loss of motion of the joint under the creases and can be helpful in determining the validity of a complaint of an inability to move the fingers or upper extremities. Clear finger creases over joints that a patient claims he or she is unable to flex or extend indicate that the patient moves the joint. In such cases, the patient may be malingering or may have a psychiatric condition in which he or she cannot recognize motion of the joint.

Muscle power is classed according to the Medical Research Council scale, which ranges from zero to five (0–5) (Table 2.1).1 Grip strength is a good indicator of the global muscle strength of the upper extremity. Grip strength is measured using a dynamometer with the shoulder and elbow joints stabilized. The patient grips the dynamometer with the elbow straightened beside the trunk in the standing position or flexed 90° in the sitting position. Measurement of pinch grip strengths includes the average of three grip strength trials on the affected and unaffected hands using a Jamar pinch gauge in two different postures. These include a lateral pinch grip measured between the thumb pulp and the radial aspect of the second digit, and a thumb–forefinger pinch grip measured between the tips of the thumb and forefinger (Fig. 2.1). For both grips, the shoulder is adducted and neutrally rotated, and the forearm and wrist are in a closely neutral and comfortable position.

Palpation Palpation is a powerful maneuver for identifying masses, abnormal skin temperature, areas of tenderness, crepitance, clicking or snapping, and effusion. Masses in the deep layer can be detected by palpation before they emerge as masses under the skin. When performing palpation, special attention should be paid to differences in hardness or mobility relative to that of the surrounding tissue. For example, subtle palpation can identify a palmar bowstring of a flexor tendon in a patient who complains of lack of finger flexion after an injury of the flexor pulleys.

Assessment of musculotendinous function The integrity of the tendon and the strength of the muscle should be considered when conducting a musculotendinous assessment.

Posture When musculotendinous units are examined, it should be kept in mind that the muscle strength and ranges of motion of the hand and digits change depending on the posture of the wrist, forearm or digits. For example, the range of motion of the distal interphalangeal (DIP) joint of a finger is less when the proximal interphalangeal (PIP) joint is passively extended than when the PIP joint is flexed.

Motion Both passive and active ranges of motion should be documented. The range of motion of both the contralateral healthy limb and the affected limb should be measured and compared. The range of motion may be affected by the posture of the adjacent joints. For example, active and passive distal interphalangeal (DIP) joint flexion is limited when the proximal interphalangeal (PIP) joint of the same finger is extended. When the wrist joint is flexed, the active range of finger flexion decreases. The range of motion of a joint should be measured in a posture that permits maximum motion. The passive range of motion is measured by holding proximal and distal to the joint in question and then moving the joint from one limit of motion to the other in the absence of any muscular contraction by the patient. A limited range of passive motion is associated with joint stiffness and/or soft-tissue contracture.

Examination of the muscles of the hand There are many muscles and tendons in the hand. Muscles, the origin and insertion of which are both distal to the wrist joint, are called intrinsic muscles. Muscles extending across the wrist joint are called extrinsic muscles. Other muscles often compensate for a nonfunctioning muscle, in which case the nonfunctioning muscle appears to function. To evaluate muscle function, each muscle should be evaluated in a posture or situation in which the cooperative muscles do not function. For example, the extensor pollicis longus (EPL) can compensate for impaired thumb adduction. Even when the thumb adductors do not function because of ulnar nerve palsy, patients may be able to adduct the thumb using a functional EPL. The presence of abnormal muscles or an abnormal linkage of tendons should sometimes be considered. The flexion function of the PIP joint of a finger is generally accepted to be independent of that of the other fingers because the flexor digitorum superficialis (FDS) tendon of each finger has its own muscle belly. The motion of the FDS tendon of the small finger is often linked to that of the ring and/or the long finger and the PIP joint flexion of the small finger often coordinates with

Table 2.1  Medical Research Council scale

Grade

Physical examination findings

0

No contraction

1

Flicker or trace contraction

2

Active movement with gravity eliminated

3

Active movement against gravity

4

Active movement against gravity and resistance

5

Normal power

(Reproduced with permission from: Seddon HJ. Peripheral Nerve Injuries. Medical Research Council Special Report Series, 282. London: HMSO; 1954.)

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SECTION I

CHAPTER 2  • Examination of the upper extremity

Flexor sublimis test (Video 2.2

)

Purpose: This test is used to assess the continuity, excursion, and muscle power of each of the flexor digitorum superficialis tendons. Maneuver: The patient’s hand is placed palm up on a table. The examiner presses down on the distal phalanges of all fingers except that of the finger to be tested to keep the MCP, PIP, and DIP joints of the other fingers in full extension. The patient is then asked to flex the finger to be tested. Each finger is tested individually. The FDS moves when the other fingers are kept fully extended.

Flexor pollicis longus muscle The flexor pollicis longus (FPL) inserts on the palmar surface of the distal phalanx of the thumb and can be tested by asking the patient to flex the interphalangeal (IP) joint of the thumb.

A

Milking test of the finger and thumb flexor tendons (Video 2.3

)

Purpose: To evaluate the continuity and excursion of the extrinsic flexors of the thumb and fingers. This test and the dynamic tenodesis test (Video 2.4 ) are useful for distinguishing nerve palsy from tendon rupture. Maneuver: The patient is asked to place the dorsum of the forearm and the hand on a table and to relax. The examiner pushes down on the musculotendinous junctions of the flexor tendons around the palmar aspect of the mid-forearm. If the tendons have normal excursion and no adhesions, the fingers and thumb flex as the forearm is pushed down.

Extensor pollicis brevis and abductor pollicis longus muscles B

Figure 2.1  Lateral pinch (A) and thumb–forefinger tip pinch (B) grips.

that of the ring and/or long fingers.2 The extensor digitorum manus brevis is sometimes present in the middle finger and causes dorsal wrist pain.3

Examination of the extrinsic muscles Flexor digitorum profundus muscle The flexor digitorum profundus (FDP) tendons insert on the palmar surface of the distal phalanx of the fingers. Because the FDP muscles share a common origin, holding the DIP joint of a finger in full extension may prevent motion of all FDPs.

Flexor profundus test (Video 2.1

)

Purpose: This test is used to assess the continuity, excursion, and muscle power of each of the FDP tendons. Maneuver: The patient’s hand is placed palm up on a table. The examiner presses down on the proximal and middle phalanges of the target finger to keep the metacarpophalangeal (MCP) and PIP joints in extension and asks the patient to flex the DIP joint. The test should be performed on each finger.

Flexor digitorum superficialis muscle The flexor digitorum superficialis (FDS) tendons insert on the proximal half of the palmar surface of the middle phalanx of the fingers. Because each FDS tendon has its own muscle belly, its function is independent of the FDS of the adjacent fingers.

The extensor pollicis brevis (EPB) inserts at the dorsal base of the proximal phalanx of the thumb. It is sometimes connected to the EPL. The abductor pollicis longus (APL) has several tendon slips and inserts at the dorsolateral base of the thumb metacarpal and trapezium. Both tendons pass through the first dorsal compartment at the wrist (the APL tendon lies radial to the EPB in the compartment). Because the EPB is a phylogenetically new muscle, it often shows extremely poor development or even complete absence. The number of the APL tendon slips is usually greater when the EPB is absent than that when the EPB is present. When the patient abducts the thumb maximally, the EPB and APL tendons as well as the EPL tendon merge under the skin over the radiodorsal side of the wrist and create the snuffbox. The EPB and APL tendons are palpable as taut tendons in the radiopalmar border of the snuffbox. The tendinitis of the EPB and APL at the radial wrist level is known as de Quervain’s tenosynovitis. There are two provocative tests for diagnosing de Quervain’s tenosynovitis.

Finkelstein test Purpose: To detect de Quervain’s tenosynovitis. Maneuver: The patient places the hand on a table with the thumb up. The examiner pushes down on the proximal phalanx of the thumb. A patient with de Quervain’s tendinitis will experience pain or discomfort in the first extensor compartment of the wrist.

Eichoff test (Video 2.5

)

Purpose: To detect de Quervain’s tenosynovitis. Maneuver: The patient is asked to hold the thumb with the four flexed fingers of the affected hand. The hand is deviated

Physical examination specific to the hand

ulnarly by the examiner. A patient with de Quervain’s tenosynovitis will experience pain or discomfort in the first extensor compartment of the wrist.

Extensor carpi radialis longus and brevis muscles The extensor carpi radialis longus (ECRL) and brevis (ECRB) tendons insert at the dorsal bases of the second and third metacarpal bones, respectively. The function of these muscles is to extend the wrist joint. Because the functional axis of the ECRL deviates radially, the ECRL extends the wrist dorso­ radially. When the ECRB does not function, extension of the wrist deviates radially because of the intact ECRL tendon. The extensor digitorum communis (EDC) tendon also may function as a wrist extensor. To remove the EDC contribution to wrist extension, the patient is asked to make a fist and then extend the wrist. Making a fist eliminates EDC function.

Extensor pollicis longus muscle (Video 2.6

)

The extensor pollicis longus (EPL) passes through the third dorsal compartment, turns radially at the Lister’s tubercle and inserts at the dorsal base of the distal phalanx of the thumb. The EPL extends the IP joint of the thumb. The hand is placed palm down on a table with the thumb adducted. The patient is asked to lift only the thumb off the surface of the table, keeping the thumb adducted. The taut EPL tendon is palpable in the radiodorsal aspect of the wrist. Clinical tip The EPL tendon is often connected to the extensor pollicis brevis (EPB) tendon. Although the EPL tendon is not functioning, the thumb IP joint can be extended by means of the force of the EPB tendon. When examining EPL function, one must eliminate EPB function by stabilizing the thumb MCP joint.

Extensor digitorum communis muscles (Video 2.7

)

The extensor digitorum communis (EDC) tendons pass through the fourth extensor compartment and insert at the dorsal base of the middle phalanges of the fingers. They mainly extend the MCP joint, while the intrinsic extensors extend the PIP and DIP joints. EDC function is examined by asking the  patient to lift the MCP joints of four fingers (the index to the small finger) keeping the PIP and DIP joints flexed.

53

small finger EDC tendon at the MCP joint level. Because the EDM tendon is usually divided into two tails distally, both tails of the tendon must be transected when the tendon is transferred. This tendon is evaluated by asking the patient to straighten the small finger when the other fingers are flexed into a fist.

Extensor carpi ulnaris muscle The extensor carpi ulnaris (ECU) tendon passes through the sixth extensor compartment and inserts on the dorsal base of the fifth metacarpal bone. The function of this tendon is ulnar deviation of a wrist that is held extended. The wrist cannot be extended dorsally only by the ECU. This tendon is evaluated by asking the patient to make a fist and to lift and deviate the wrist ulnarly. The tendon is palpable radial to the ulnar styloid process.

Examination of the intrinsic muscles Thenar muscles (Video 2.8

)

The thenar muscles cover the thumb metacarpal and consist of three muscles: the abductor pollicis brevis, the flexor pollicis brevis, and the opponens pollicis. The muscles move the thumb into opposition, enabling the thumb to touch the fingertips when the nails are parallel. These muscles are evaluated by asking the patient to place the dorsum of the hand flat on a table and to raise the thumb until it is perpendicular to the palm. The patient is then asked to resist a downward force by the examiner on the thumb.

Adductor pollicis muscle The adductor pollicis (ADP) muscle arises from the third metacarpal and inserts to the ulnar base of the proximal phalanx of the thumb. Some fibers of the ADP extend dorsally to form an extensor apparatus for the thumb. Together with the first dorsal interosseous muscle, the ADP approximates the thumb to the second metacarpal.

Interosseous and lumbrical muscles (Video 2.9

)

The extensor indicis proprius (EIP) tendon passes through the fourth extensor compartment at the wrist deep to the EDC tendon and merges with the ulnar side of the index finger EDC tendon over the MCP joint. The function of the EIP is to extend the MCP joint of the index finger, which is isolated from the extension of the MCP joints of the other fingers. The EIP is functional if the patient can straighten the index finger completely when the other fingers are flexed in a fist.

The interosseous and lumbrical muscles flex the MCP joints and extend the PIP and DIP joints of the fingers. In addition, four dorsal interosseous muscles abduct the thumb and the radial three fingers and three palmar interosseous muscles adduct the fingers. The second and third dorsal interosseous muscles are evaluated by asking the patient to place the hand flat on a table and then to stretch the long finger upward (i.e., to hyperextend it) and to deviate it radially and ulnarly. Patients with ulnar nerve palsy cannot do this because of loss of power in the interosseous muscles (the Pitres–Testut sign). The first palmar interosseous and the second dorsal interosseous muscles are tested by crossing the index and middle fingers (“crossed fingers” sign). The patient is asked to cross a flexed long finger over the index finger or to cross a flexed index finger over the long finger when the palm and the ring and little fingers are placed flat on a table. (Finger abduction refers to movement away from the long finger; finger adduction refers to movement toward the long finger.)

Extensor digiti minimi muscle

Intrinsic tightness test (Bunnell)

The extensor digiti minimi (EDM) tendon passes the fifth extensor compartment and merges with the ulnar side of the

Purpose: This test assesses the contracture of the interosseous muscles.

Extrinsic tightness test The PIP joint is more easily flexed when the MCP joint is kept extended than when it is flexed, signifying that tightness of the extrinsic muscles is present.4

Extensor indicis proprius muscle

54

SECTION I

CHAPTER 2  • Examination of the upper extremity

A

A

B

Figure 2.3  Lumbrical muscle tightness test. Because the lumbrical muscle connects the flexor digitorum profundus tendon and the radial lateral band of the extensor tendon, the PIP and DIP joint are apt to be extended when the patient intends to flex the finger (paradoxical movement). (A) Normal. (B) Abnormal, with lumbrical tightness causing extension of the finger.

B

Figure 2.2  Intrinsic tightness test. If there is a tightness of the interosseous muscles, the PIP joint can be more easily flexed when the MCP joint is held flexed than when the MCP joint is extended. (A) The MCP joint is extended. (B) The MCP joint is flexed.

Maneuver: The PIP joint is more easily flexed when the MCP joint is flexed than when it is extended (0° extended position) if tightness of the interosseous muscles is present (Fig. 2.2).5 The test can be performed using radial and ulnar deviation of the finger to distinguish between tightness of the radial and ulnar lateral bands.

Lumbrical-plus test The lumbrical muscle connects the flexor digitorum profundus tendon and the radial lateral band of each extensor tendon. The PIP and DIP joints are apt to be extended when a patient with lumbrical muscle tightness intends to flex a finger.6 The finger flexion is thus blocked (paradoxical movement of the finger) (Fig. 2.3). This movement is often seen in the situation of FDP tendon repair using a tendon graft, which is longer than the appropriate length.

Figure 2.4  The collateral ligament of the MCP joint. The proper portion of the collateral ligament is relaxed when the joint is extended (top) and is tight when the MCP joint is flexed (bottom). The smaller accessory portion has the opposite effect.

Hypothenar muscles The hypothenar muscles (the abductor digiti minimi, the flexor digiti minimi, the opponens digiti minimi, and the palmaris brevis muscle) abduct the small finger, moving it away from the other fingers.

Assessment of stability The tightness of the ligaments around a joint, morphology of the surface of a joint, and musculotendinous balance around a joint are useful indices of joint stability.

The stability of ligaments is tested by holding the portions distal and proximal to the joint and gently moving the joint passively to stress the ligaments that stabilize the joint. When assessing joint stability, the biomechanical and physiological properties of the ligaments should be taken into consideration and the stress forces applied should be appropriate for the ligament in question. For example, the bilateral collateral ligaments of the finger MCP joints tighten when the joint is in the flexed position (Fig. 2.4), whereas those of the PIP joints tighten when the joints are

Physical examination specific to the hand

55

Clinical tip Assessment of the lateral instability of the MCP and PIP joints of fingers The straight portions of the bilateral collateral ligaments of the finger MCP joints tighten when the joint is in the flexed position, whereas those of the PIP joints tighten when the joints are in an extended position. The lateral instability of the MCP joints is assessed with the joint in full flexion, and the PIP joints should be checked with joint in the neutral position.

Scaphoid shift test (Watson) (Video 2.10

A

)

Purpose: This test was originally developed to detect loosening or disruption of the scapholunate interosseous ligament. This test can also be used to detect a scaphoid fracture or scapholunate advanced collapse (SLAC) arthritis. Maneuver: When the wrist deviates radially, the scaphoid rotates palmarly, and the palmar prominence of the tubercle of the scaphoid thus becomes evident. However, when the wrist deviates ulnarly, the scaphoid rotates dorsally and the bony prominence is less evident. The examiner holds the dorsum of the patient’s hand with his or her fingers and places his or her thumb onto the radial palmar wrist to palpate the bony prominence of the scaphoid tubercle. When the examiner holds the patient’s hand and deviates the wrist radially and ulnarly, he or she will feel the motion of the bony prominence under his or her thumb. When the examiner feels the palmar movement of the bony prominence of the scaphoid tubercle when moving the patient’s wrist from the ulnar to the radial deviation, he or she pushes dorsally up on the tubercle against the force of the palmar movement. If scapholunate ligament insufficiency is present, the examiner will feel a clunk on the thumb over the distal tubercle.7

Finger extension test

B

Figure 2.5  Rupture of the radial collateral ligament of the index finger PIP joint. Measure the opening angle of the affected joint under the radial and ulnar stress forces on X-ray films and compare the angle with that of the corresponding normal joint of the opposite hand. (A) Affected finger. (B) Normal opposite finger.

in an extended position. The lateral instability of the MCP joints is assessed at the fully flexed position, and the PIP joints should be checked at the neutral position. It is useful to measure the opening angle of the affected joint under stress using X-rays and to compare the opening angle of the affected joint with that of the corresponding healthy joint of the opposite hand (Fig. 2.5). Assessment of the stability of wrist joints is complex and difficult. The stability of the wrist joint is determined by the stability of the radiocarpal, ulnocarpal, distal radioulnar, and midcarpal joints. Special tests for assessing the stability of specific ligaments or imaging tools such as X-rays, CT or MRI may be helpful in making a diagnosis.

Purpose: To detect the pre-dynamic rotary subluxation of the scaphoid (dorsal wrist syndrome).8 Maneuver: When being asked to extend the DIP and PIP joints of all fingers fully, keeping the wrist and the MCP joints of all fingers in a full-flexed position, patients with overloaded scapholunate ligaments (pre-dynamic rotary subluxation of the scaphoid) experience pain around the scapholunate joint in the dorsal wrist.

Triquetrolunate ballottement test and the lunotriquetral shuck test Purpose: To evaluate the stability of the lunotriquetral ligament. Maneuver: The examiner places his or her thumb dorsally over the triquetrum and the index finger palmarly over the pisiform bone to keep the triquetrum–pisiform unit between the thumb and index finger. The examiner then places his or her opposite thumb on the dorsum of the lunate and pushes it palmarly down. If there is triquetrolunate ligament incompetence, the examiner will feel palmar movement of the lunate and the patient will complain of pain in the wrist (Fig. 2.6).9 The lunotriquetral shuck test is similar to the triquetrolunate ballottement test. The patient is asked to place the elbow on a table with the forearm in neutral rotation. The examiner’s thumb is placed over the dorsal side of the lunate just beyond the radiolunate joint. The examiner’s opposite thumb pushes

56

SECTION I

CHAPTER 2  • Examination of the upper extremity

A

Maneuver: The deep layers of the dorsal and palmar ligaments of the distal radioulnar joint (DRUJ) comprise the triangular ligament of the triangular fibrocartilage complex (TFCC) and play a primary role to stabilize the DRUJ. The deep dorsal ligament becomes taut when the forearm is supinated and the deep palmar ligament is taut when the forearm is pronated. The deep layers of the palmar and dorsal ligaments thus restrict dorsal and palmar shift of the ulnar head, respectively. The examiner sits opposite the patient at a table. The patient’s elbow is flexed 90° and placed on the table. The patient’s forearm is fully pronated and the examiner places his or her thumb on the palmar aspect of the ulnar head and pushes dorsally upward. This maneuver should be repeated on the healthy wrist. If abnormal dorsal movement of the distal ulna is felt with the thumb, insufficiency of the deep layer of the palmar distal radioulnar ligament (palmar portion of the triangular ligament of the TFCC) is present. Next, the patient’s forearm is fully supinated and the examiner places his or her thumb on the dorsum of the distal ulna and pushes palmarly down. If abnormal palmar movement of the distal ulna compared with that of the opposite wrist is felt with the thumb, insufficiency of the deep layer of the dorsal distal radioulnar ligament (­dorsal portion of the triangular ligament of the TFCC) is present (Fig. 2.8).11 Clinical tip Dorsal instability of the ulna is assessed with the forearm fully pronated and palmar instability of the ulna is assessed with the forearm fully supinated.

B

Figure 2.6  (A,B) Triquetrolunate ballottement test.

Ulnocarpal abutment test Purpose: To evaluate TFCC injuries and ulnar impaction syndrome. Maneuver: The examiner places a thumb on the patient’s distal ulna and holds the patient’s hand with the remaining four fingers. The patient’s forearm is stabilized by the examiner’s opposite hand. The patient’s wrist is fully deviated ulnarly and the forearm is pronated and supinated. A patient with a TFCC injury or ulnar impaction syndrome may complain of ulnar wrist pain and a click or pop may be felt when the examiner’s thumb is placed on the ulnocarpal joint (Fig. 2.9).12

The ulnar fovea sign (Video 2.11

Figure 2.7  Lunotriquetral shuck test.

the palmar side of the pisiform dorsally to load the pisotriquetral joint. In lunotriquetral ligament incompetence, the triquetrum–pisiform unit is moved dorsally and the patient will complain of pain in the lunotriquetral joint (Fig. 2.7).10

Distal radioulnar joint instability test Purpose: To evaluate the integrity of the deep layer of the ­dorsal or palmar distal radioulnar ligaments.

)

Purpose: To evaluate TFCC avulsion at the ulnar fovea and/or ulnotriquetral ligament tear. Maneuver: The patient’s upper limb should be relaxed and the examiner should hold the patient’s hand to keep the forearm in neutral rotation and wrist in neutral flexion-extension and slightly radially deviated position. The ulnar fovea sign is positive if the patient complains of exquisite pain and tenderness when the examiner presses the soft-tissue space surrounded by the ulnar styloid process, flexor carpi ulnaris tendon, volar surface of the ulnar head, and the pisiform with the thumb tip. This tenderness must be replicable when this procedure is repeated (Fig. 2.10).13,14

Pisiform gliding test Purpose: To evaluate arthritis in the pisotriquetral joint. Maneuver: The examiner palpates the pisiform and pushes it down against the triquetrum and applies shear force between

Physical examination specific to the hand

Loosened deep dorsal radioulnar ligament

57

Loosened deep palmar radioulnar ligament

Ulna Ulna Radius Radius Taut deep palmar radioulnar ligament A

Push

Taut deep dorsal radioulnar ligament B

Push

Figure 2.8  Distal radioulnar joint (DRUJ) instability test. (A) Examination for the palmar instability of the DRUJ. The examiner pushes the ulna head from the palmar side when the forearm is pronated to examine the deep palmar distal RU ligament. The deep palmar ligament is taut in the forearm pronated. (B) Examination for the dorsal instability of the DRUJ. The examiner pushes the ulna head from the dorsal side when the forearm is supinated to examine the deep dorsal distal RU ligament. The deep dorsal ligament is taut in the forearm supinated.

the two bones. If there is arthritis in the pisotriquetral joint, the patient will feel pain in the joint during this maneuver (Fig. 2.11).

Midcarpal instability test Purpose: To evaluate midcarpal stability. Maneuver: The examiner places a thumb on the dorsal midcarpal joint and holds the patient’s affected hand with the remaining four fingers. The patient’s forearm is stabilized by the examiner’s opposite hand. A patient with midcarpal instability will complain of pain in the midcarpal joint when the wrist is deviated ulnarly or radially. Patients with dorsal intercalary segmental instability (DISI) often complain of pain in the ulnodorsal portion of the midcarpal joint, and a click or pop may be felt when the wrist is deviated ulnarly.

Extensor carpi ulnaris synergy test Extensor carpi ulnaris (ECU) tendinitis is a cause of ulnarsided wrist pain. The ECU synergy test is a provocative test, indicating ECU tendinitis, which is often hard to distinguish from TFCC injuries.

Purpose: To detect ECU tendinitis. Maneuver: The patient’s forearm is held fully supinated. The examiner asks the patient to abduct all fingers and applies a counterforce to the index and small fingers sufficient to prevent abduction of the index and small fingers. A patient with ECU tendinitis will experience pain in the sixth extensor compartment (Fig. 2.12).15

Assessment of peripheral nerves Evaluation of peripheral nerves should include both motor and sensory function. To evaluate the motor function of the hand, it is necessary to understand not only the anatomy and biomechanics of the muscles of the upper extremity but also the peripheral innervation of the muscles. An understanding of the order in which branches of the nerves innervate muscles is important for assessing nerve recovery after a nerve injury or a compression neuropathy. Sensibility testing also relies on knowledge of peripheral nerve anatomy. It is essential to understand which parts of the  hand are innervated by which peripheral nerves. Peripheral nerve palsy should be diagnosed using motor and

SECTION I

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CHAPTER 2  • Examination of the upper extremity

Supination

Ulnar deviation and axial loading

Pronation

Ulnar deviation and axial loading

Figure 2.9  Ulnocarpal abutment test. The wrist is subjected to ulnar deviation and axial forces with the forearm fully supinated or pronated.

Triquetum UTL

UCLC Lunate

Tear Push

Fovea DPL Ulna

A

Radius

B

Figure 2.10 The ulnar fovea sign. The tenderness over the ulnar fovea (positive ulnar fovea sign) strongly supports the foveal disruption of the TFCC. DPL, Deep palmar ligament; UCLC, ulnocarpal ligamentous complex; UT, ulnotriquetral ligament.  

Physical examination specific to the hand

59

sensory evaluation. When the outcome of a motor assessment does not coincide with that of a sensory assessment, abnormal innervation of muscles or an unusual connection between peripheral nerves should be considered. The Martin–Gruber connection is an abnormal innervation of the median nerve to the motor branch of the ulnar nerve. Patients with cubital tunnel syndrome and this nerve connection may have a sensory palsy of the ulnar nerve without motor palsy. Comprehensive sensibility evaluation includes static and dynamic two-point discrimination (2PD) testing, Semmes– Weinstein monofilament testing, vibrotactile threshold testing, and cold–heat testing. The 2PD test evaluates the tactile sensation of the skin and assesses density of the perception receptors in the skin. Stimuli generated by the static 2PD test are mainly sensed by Merkel cells (slow-adapting mechanoreceptors), while the main receptors of stimuli generated by the moving 2PD test are Meissner corpuscles (quick-adapting receptors). In the static 2PD test, a caliper is applied longitudinally to the digit and the smallest distance between the tips of the caliper that the patient can distinguish is measured. The moving 2PD test is the smallest perceived distance between the tips of a caliper that is moved longitudinally along the ulnar or radial aspect of the finger.16 The normal distance is 3 mm for the moving 2PD test and 6 mm for the static 2PD test of the fingertips. The Semmes–Weinstein test evaluates the pressure perception of the skin of the fingers and assesses the threshold of the perception receptors in the skin. This test is conducted by touching the fingers with filaments of various diameters.16 The vibrotactile test also assesses the threshold of the perception receptors and is performed using two types of tuning forks with 30 cycles per second (cps) and 250 cps. The vibrating forks are touched on the area examined and whether patients can recognize the vibration is examined. Main receptors of stimuli generated by the tuning forks with 250 cps are Pacinian corpuscles, while those by the forks with 30 cps are Meissner corpuscles. In the cold–heat test, the perception of heat is evaluated by touching the skin with a test tube containing water at 40–45°C and the perception of cold is tested using a test tube containing water at 10°C. Stimuli of the cold–heat test are mainly sensed by free nerve endings of the skin (Table 2.2).

Figure 2.11  Pisiform gliding test.

Clinical tip

Figure 2.12  Extensor carpi ulnaris synergy test. The patient is asked to abduct the fingers with the forearm fully supinated. The examiner applies counterforce to the index and little fingers.

Ulnar nerve palsy occurring distal to the FDP muscle branches demonstrates more severe claw deformity than that occurring proximal to the branches. This is because the FDP tendons continue to flex the ring and little fingers, which accentuates the hyperextension of the MCP joints and flexion of the PIP and DIP joints.

Table 2.2  Specific sensory testing and main receptors

Test

Perception

Main receptor

Type of adaptation

Evaluation of innervation

Static 2PD

Tactile

Merkel cell

Slowly

Density

Moving 2PD

Tactile

Meissner corpuscle

Quickly

Density

Tune fork (250 cps)

Vibration

Pacinian corpuscle

Quickly

Threshold

Tune fork (30 cps)

Vibration

Meissner corpuscle

Quickly

Threshold

S–W test

Pressure

Merkel cell

Slowly

Threshold

cps, Cycles per second. (Reproduced with permission from Bell-Krotosoki J, Tomancik E. The repeatability of testing with Semmes–Weinstein monofilaments. J Hand Surg. 1987;12 A:155–161.)

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CHAPTER 2  • Examination of the upper extremity

Signs and tests for peripheral nerves Tinel's sign Purpose: To detect nerve regeneration. Maneuver: When the examiner taps on a peripheral nerve distal to a nerve injury such as a compression neuropathy or a laceration, the patient will experience tingling that radiates distally along the course of the nerve. This phenomenon is called a Tinel's sign. The most distal point of the pain indicates the site at which axon sprouting has occurred. Peripheral nerve recovery after a nerve injury can be assessed by observing the advancement of Tinel's sign along the nerve (approximately 1 mm/day of advancement).

Phalen's test Purpose: This test is used as a provocative test specific to carpal tunnel syndrome. Maneuver: With the elbow in neutral position, the patient’s wrist is held in maximum palmar flexion for up to 2 min. This increases pressure on the carpal tunnel and provokes paresthesia in the area innervated by the median nerve in patients with carpal tunnel syndrome (Fig. 2.13). Maximum extension of the wrist also increases pressure on the carpal tunnel. This is called the reverse Phalen’s test.

lateral instability of the joint secondary to weakness of the thumb adductors.

Wartenberg's sign Purpose: To assess the motor function of the ulnar nerve. Maneuver: The patient is asked to keep the fingers adducted with the MCP, PIP, and DIP joints fully extended. If the patient has motor dysfunction of the ulnar nerve, the small finger deviates away from the ring finger because the third palmar interosseous muscle does not function and the extensor digiti minimi muscle abducts the small finger (Fig. 2.15).

Other signs associated with ulnar nerve palsy Duchenne's sign: If the FDP muscles are functioning and the intrinsic muscles are paralyzed (low-level ulnar nerve palsy), the ring and little fingers show hyperextension of the MCP joint and flexion of the PIP and DIP joints (claw finger deformity). André–Thomas sign: A conscious effort to extend the fingers by tenodesing the extensor tendons with palmar flexion of the wrist only increases the claw deformity. Bouvier maneuver: When hyperextension of the MCP joint of the ring and little fingers is corrected, the flexion of the PIP and DIP joints of the fingers is reduced.

Froment's test Purpose: To assess motor function of the ulnar nerve. Maneuver: The patient is asked to hold a piece of paper between the ulnar tip of the thumb and the radial tip of the index fingers. The examiner slowly pulls the paper away from the patient while encouraging the patient to hold on to it. Patients with normal strength of the first dorsal interosseous and adductor pollicis muscles keep the IP joint of the thumb extended. If the patient has weakness of thumb adduction caused by ulnar nerve palsy, the patient attempts to hold the paper by flexing the thumb IP joint using the flexor pollicis longus and (hyper)extends the thumb MCP joint to stabilize it (Jeanne's sign). Such patients also flex the PIP joint and hyperextend the DIP joint of the index finger to compensate for weakness of MCP joint flexion of the index finger (Fig. 2.14).

Jeanne's sign

Figure 2.14  Froment’s sign. A patient with left ulnar nerve palsy attempts to hold the paper by flexing the thumb IP joint using the flexor pollicis longus and hyperextending the thumb MCP joint to stabilize it. He also demonstrates flexion of the PIP joint and hyperextension of the DIP joint of the index finger to compensate for weakness of MCP joint flexion of the finger (Jeanne’s sign).

Purpose: To assess motor function of the ulnar nerve. Maneuver: When patients with ulnar nerve dysfunction attempt a lateral or key pinch of the thumb, they hyperextend the thumb MCP joint, which locks it to compensate for the

Figure 2.15 Wartenberg’s sign. A patient with left ulnar nerve palsy demonstrates inability to perform adduction of the left little finger when he attempts to adduct all fingers.  

Figure 2.13  Phalen’s test.

Physical examination specific to the hand

The Pitres–Testut sign: This maneuver reveals the function of the second and third interosseous muscles. The patient is asked to place the hand flat on a table and then to stretch the long finger upward (i.e., to hyperextend it) and to deviate it radially and ulnarly. The “crossed fingers” sign (see Video 2.9 ): The function of the first palmar interosseous and the second dorsal interosseous muscles is evaluated by this sign. The patient is asked to cross a flexed long finger over the index finger or to cross a flexed index finger over the long finger when the palm and the ring and little fingers are placed flat on a table.

Tests for evaluating sensory nerve function Two-point discrimination (2PD) test (Videos 2.12 and 2.13

)

Purpose: To evaluate the tactile sensation of the skin and assess density of the perception receptors of the skin. Maneuver: In the static 2PD test, a caliper is applied longitudinally to the digit and the smallest distance between the tips of the caliper that the patient is able to distinguish is measured. In the dynamic 2PD test, the distance between the tips of a caliper that is moved longitudinally along the ulnar or radial aspect of the finger is measured.15 The normal distance is 3 mm for the moving 2PD test and 6 mm for the static 2PD test. Although it is known that the main receptors for the static 2PD test are Merkel cells (slow-adapting mechanoreceptors) and those for the moving 2PD test are Meissner corpuscles (quick-adapting mechanoreceptors), the results of the 2PD test reflect the functions of multiple sensory receptors in the skin. This test is best for evaluation of nerve lacerations.

Semmes–Weinstein monofilament test (Video 2.14

61

Table 2.3  Semmes–Weinstein test

Evaluator size

Pressure force (g)

Color

Interpretation

1.65–2.83

0.008–0.07

Green

Normal

3.32–3.61

0.16–0.4

Blue

Normal

3.84–4.31

0.6–2

Purple

Diminished light touch sensation

4.56–4.93

4–8

Red

Diminished protective sensation

5.07–6.45

10–180

Red

Loss of protective sensation

6.65

300

Red

Deep pressure sensation only

(Reproduced with permission from: Bell-Krotosoki J, Tomancik E. The repeatability of testing with Semmes–Weinstein monofilaments. J Hand Surg. 1987; 12 A:155–161.)

)

Purpose: To evaluate the pressure perception threshold of the skin. Stimuli generated by this test are mainly sensed by Merkel cells (slow-adapting mechanoreceptors). Maneuver: Filaments of various diameters are used. The patient places a finger on a table with the palm up and closes his or her eyes. The tip of a filament is held vertically against the skin of the finger and sufficient force is applied to bend the filament before allowing it to return to the vertical position. The filament should remain in contact with the skin surface after the force is released. If the patient senses the pressure applied by the filament, other filaments of decreasing diameter are used until the patient no longer senses the pressure. The size of the smallest-diameter filament that can be sensed by the patient is recorded (Table 2.3).17 Clinical tip Touching the tip of the filament on the skin should be so gentle that patients cannot recognize the touch of the filament tip on the skin. Patients have to recognize the bending pressure produced by the filaments. Some patients misunderstand that the test is whether they recognize the initial touch sensation of the filaments or not.

Moberg's pick-up test Purpose: To generally evaluate the motor and sensory function of the hand. This test is applied to patients with median nerve injuries or injuries of both the ulnar and median nerves.

Figure 2.16  Moberg pick-up test. A patient with eyes open or closed picks up small items on a cloth mat and puts them into the box. The time required to finish the task is recorded.

Maneuver: Small items such as a button, a key, and a paperclip are placed on a cloth mat. The patient is asked to pick up each item and put it into a small box as quickly as possible with their eyes open and again with their eyes closed. The times required to finish these tasks are measured (Fig. 2.16).18

Assessment of the vascular system There are two types of vascular problems: arterial and venous insufficiency. Vascular problems are assessed according to the color, capillary refill, pressure (turgor), and temperature of the affected part. Arterial interruption causes a pale white or grayish discoloration of the affected area. Venous blockage results in blood congestion, which causes a purple–blue discoloration. Capillary refill is indicative of the circulation status of the digits. When the fingertip or nail bed is depressed, the area under pressure turns white. When the pressure is released, the area should turn pink within 2 seconds. A delay in refill is indicative of an arterial inflow problem. Prompt refilling may indicate venous congestion. A decrease in skin pressure or temperature may also indicate vascular problems.

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CHAPTER 2  • Examination of the upper extremity

The Allen’s test (see Videos 2.15 and 2.16 ) is helpful for determining if there is an intact circulatory connection between the radial and ulnar arteries in the hand. If there is an intact circulatory path between the two arteries, the hand may be nourished by either of the arteries.18 This test is essential for assessing the vascularity of the hand before harvesting radial or ulnar forearm flaps. If both arteries are not patent, pedicled forearm flap elevation may compromise the vascularity of the hand. To assess the circulatory connection between the radial and ulnar palmar digital arteries, the same maneuver is performed at the base of the fingers and thumb (digital Allen’s test [see Video 2.16 ]). If there is no circulatory connection between the palmar digital arteries, pedicled island flap harvest should be avoided.

The IOM is divided into three portions. Each portion contains several fibers that connect the radius and the ulna (Fig. 2.17).22

Distal membranous portion Dorsal oblique band (DOB): This band functions as a stabilizer of the DRUJ, in particular by restricting a palmar shift of the ulna in the supination position.23

Middle ligamentous portion a.

Allen's test (Video 2.15 ) Purpose: To assess the blood supply of the radial and ulnar arteries to the hand. Maneuver: The patient places the dorsum of the hand on a table. The examiner compresses the patient’s radial and ulnar arteries at the wrist to occlude both arteries. The patient is then asked to make and release a tight fist repeatedly to exsanguinate the hand, after which the fingers are held in a relaxed position. The examiner releases the pressure on the radial artery while keeping pressure on the ulnar artery. The time taken for blood to return to the hand and fingers is noted. A normal interval for this process is 2–5 seconds. The procedure is repeated for the ulnar artery.19

Digital Allen's test (Video 2.16

The interosseous membrane of the forearm (IOM)

)

Purpose: To assess the blood supply of the radial and ulnar palmar digital arteries to the finger. Maneuver: The patient is asked to place the dorsum of the finger to be tested flat on a table. The examiner compresses the ulnar and radial side of the patient’s fingertip with his or her two fingers and moves them proximally to exsanguinate the finger to be tested. The examiner then releases the pressure on the radial palmar digital artery while maintaining pressure on the ulnar digital artery. The time taken for blood to return to the finger is noted. A normal interval for this process is ≤3 seconds. The procedure is repeated for the palmar ulnar digital artery of the finger. A delay in the return of blood to the finger indicates that the blood flow of the radial or ulnar palmar digital arteries is impaired.

b. c.

Central band (CB): This is the strongest fiber of the IOM and extends from the proximal radius to the distal ulna. When the radial head removed, the CB carries 71% of the overall mechanical stiffness of the forearm.21 Distal ligament of accessory band (DLAB). Proximal ligament of accessory band (PLAB).

Proximal membranous portion a. b.

Distal oblique accessory cord (DOAC). Proximal oblique cord (POC): a stabilizer of the proximal radioulnar joint.

Among these fibers, the DOB and CB are isometric components and their lengths do not change during forearm rotation.24 By contrast, the POC is shorter when the forearm is in

DOB

Distal membranous portion

(DL)AB

Middle ligamentous complex

CB (PL)AB

Physical examination specific to the forearm The main functions of the forearm are to transmit force between the elbow and hand and to enable pronation and supination. According to a cadaveric study, 80% of an axial load applied to the wrist is transmitted to the radius and 20% is transmitted to the ulna. The axial force is distributed to the radiocapitellar and ulnohumeral joints in a 60 : 40 ratio, respectively. Some 20% of an axial force applied to the radius is therefore transferred to the ulna through the interosseous membrane (IOM).20 After resection of the radial head, 90% of an axial load applied to the forearm is transferred through the IOM.21

Dorsal oblique accessory cord Proximal membranous portion

Proximal oblique cord

Ulna

Radius

Figure 2.17  Interosseous membrane of the forearm. CB, Central band; (DL)AB, distal ligament of accessory band; DOB, dorsal oblique band; (PL)AB, proximal ligament of accessory band.

Physical examinations specific to the elbow

a neutral or supination position than when it is in a pronation position. The length of the DOAC shortens as the forearm is rotated from pronation to supination.

Measurement of forearm rotation The patient should be seated on a chair with the elbow joints tucked in lateral to the abdomen. The patient is asked to grasp a pen in each hand and to rotate the forearm. The angle between the pen and a line perpendicular to the floor should be measured.

Measurement of the muscle strength of the forearm Supination The main supinators of the forearm are the supinator muscle and the biceps brachii muscle. The extensor carpi radialis longus (ECRL) and brachioradialis (BR) muscles act as the forearm supinators when the forearm is pronated.

Pronation The main pronators are the pronator teres and pronator quadratus (PQ) muscles. The flexor carpi radialis and palmaris longus muscles also act as forearm pronators. The BR muscle is a forearm pronator when the forearm is in the supinated position. A recent study revealed that the PQ is responsible for 20% of forearm pronation, except when in the fully pronated position.25 The muscle power of the PQ should be measured when the elbow joint is fully flexed to eliminate the effects of the other pronators. Pronation or supination strength is evaluated with the elbow joint at 90° of flexion. Pronation strength is measured by grasping the wrist with the forearm in a neutral or supination position. To test supination strength, the forearm should be in a neutral or pronation position.

Physical examinations specific to the elbow Bony landmarks of the elbow The medial epicondyle, lateral epicondyle, and the tip of the olecranon are located along a straight line (Hüter’s line) when the elbow is extended and form an equilateral triangle (Hüter’s triangle) when the elbow is flexed (Fig. 2.18). This feature is helpful for identifying a deformity of the distal humerus and elbow joint caused by fracture, malunion, dislocation or growth disturbances. On the lateral aspect, the capitellum of the humerus and the radial head are easily palpable. The extensor muscles originate from the lateral epicondyle. The radial nerve is palpable in the interface between the BR muscle and the brachialis muscle. On the anterior aspect, the cubital fossa is bordered by the BR muscle laterally and the pronator teres muscle medially. The musculocutaneous nerve is located deep to the brachioradialis muscle and medial to the biceps brachii tendon. The pulsation of the brachial artery is palpable, as it lies medial to

63

the biceps brachii tendon and deep to the lacertus fibrosus. The median nerve is located just medial to the brachial artery under the lacertus fibrosus, which can cause median nerve palsy (pronator teres syndrome). In the medial aspect, the ulnar nerve groove is palpable between the medial epicondyle and the ulna. The ulnar nerve is sometimes palpated as a strand in the posterior aspect of the groove. In some patients with ulnar nerve palsy, a dislocated ulnar nerve is palpable over the epicondyle when the elbow is flexed. On the posterior aspect, the olecranon and olecranon fossa of the humerus are easily palpated. The triceps brachii tendon is attached to the olecranon.

Ligaments of the elbow Lateral ligament complex The lateral ligament complex consists of the following four ligaments (Fig. 2.19).

Lateral ulnar collateral ligament The lateral ulnar collateral ligament originates from the lateral epicondyle, blends with the fibers of the annular ligament and terminates at the tubercle of the crest of the supinator. It functions as a primary stabilizer of the joint when a varus stress is applied.

Radial collateral ligament This structure originates from the lateral epicondyle and terminates in the annular ligament. The ligament is located near the axis of the elbow joint and is uniformly taut during elbow motion.

Annular ligament This ligament originates from the anterior margin of the sigmoid notch and inserts on the posterior notch of the sigmoid of the ulna to connect the radial head to the ulna.

Accessory collateral ligament The ligament blends with the inferior margin of the annular ligament to support the annular ligament during varus stress.

Medial collateral ligament complex The medial collateral ligament complex consists of three portions: the anterior bundle, the posterior bundle, and the transverse ligament. The transverse ligament is not considered functional. The posterior bundle is clinically insignificant with regard to the stability of the elbow joint. Contracture of the posterior bundle generates extension contracture of the elbow joint. The anterior bundle functions as the prime stabilizer of the elbow joint against valgus stress (Fig. 2.20).

Instability of the elbow joint The elbow joint is stabilized by the medial collateral ligament (MCL) complex, the lateral collateral ligament (LCL) complex, the joint capsule, and the osteochondral articulation. The MCL, joint capsule, and osteochondral articulation contribute equally to restrain valgus displacement of the elbow joint when the joint is extended. The MCL contributes more than the osteochondral articulation to restrain valgus

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CHAPTER 2  • Examination of the upper extremity

SECTION I

M

O

L

O

L

M

Figure 2.18  Bony landmarks of the elbow. The medial (M) epicondyle, (L) lateral epicondyle, and the tip of the (O) olecranon locate on a straight line when the elbow is extended and form an equilateral triangle when the elbow is flexed.

Radial collateral ligament

Anterior bundle

Annular ligament

Lateral ulnar collateral ligament

Accessory collateral ligament

Figure 2.19  Lateral complex of the elbow.

Transverse ligament

Figure 2.20  Medial complex of the elbow.

Posterior bundle

Physical examinations specific to the elbow

A

65

B

Figure 2.21  Assessment of the lateral instability of the elbow. (A) Varus instability of the elbow is examined with the humerus in full internal rotation. (B) Valgus instability is assessed with the humerus in full external rotation.

displacement when the joint is flexed. The osteochondral articulation contributes more than the LCL to restrain varus displacement, especially in the flexed position. When examining instability of the elbow joint, the elbow should be placed in a position in which other factors that affect its stability (articulation and tension of the joint capsule) are minimized. To assess collateral ligament integrity, the elbow should be flexed by about 15°. This position relaxes the anterior capsule and unlocks the olecranon from the fossa. Varus instability of the elbow is therefore assessed with the humerus in full internal rotation and varus stress is applied to the slightly flexed joint. By contrast, valgus instability of the elbow is evaluated with the humerus in full external rotation while valgus stress is applied to the joint in slight flexion (Fig. 2.21).26

Clinical tip Collateral ligament integrity of the elbow should be assessed with the elbow in about 15° flexion, which relaxes the anterior capsule and unlocks the olecranon from the fossa. Varus instability of the elbow is assessed with the humerus in full internal rotation and varus stress is applied to the slightly flexed joint. Valgus instability of the elbow is evaluated with the humerus in full external rotation while valgus stress is applied to the joint in slight flexion.

Posterolateral rotatory instability Insufficiency (loosening, rupture or laceration) of the lateral ulnar collateral ligament causes posterolateral instability of the elbow joint. Posterolateral rotatory instability (PLRI) is evaluated using the pivot shift test maneuver.26

The pivot shift test The patient is placed in a supine position with the shoulder and elbow flexed at 90°. The examiner stands cephalad to the patient. The examiner grasps the patient’s forearm in a fully supinated position and extends the elbow slowly, applying valgus and axial compressions to the joint. If the patient has lateral collateral ligament insufficiency, these maneuvers cause rotatory subluxation in the ulnohumeral joint. The examiner continues to extend the elbow slowly. As the elbow joint approaches extension, the radial head is suddenly dislocated anteriorly. The prominence of the radial head disappears and a skin dimple appears. The dislocated radial head is repositioned by flexion of the elbow (Fig. 2.22).27

Measurement of malrotation of the distal humerus Patients in whom fractures of the distal humerus have not been treated correctly often demonstrate malrotation of the distal humerus, which restricts the functional arc of the shoulder joint. Malrotation of the distal humerus is easily assessed. The patient is asked to stand and flex the trunk more than 90° forward. The patient is then asked to extend both shoulder joints maximally with the elbow joints in 90° of flexion.

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SECTION I

Subluxation

CHAPTER 2  • Examination of the upper extremity

Axial compression

Valgus

Supination

A

B

Figure 2.22  Pivotal shift test of the elbow. (A,B) Subluxation.

The angles formed between the floor and the forearms are measured. The malrotation angle of the affected distal humerus can be measured by comparing it with that of the contralateral normal side (Fig. 2.23).

Physical examination of thoracic outlet syndrome Thoracic outlet syndrome (TOS) is a broad term that refers to compression of the neurovascular structures in the area just above the first rib and behind the clavicle resulting in upper extremity symptoms. It represents a constellation of symptoms.

Classification TOS is usually classified into two groups: neurogenic and vascular. The neurogenic group is caused by compression or

Figure 2.23  Assessment of malrotation of the humerus. The patient is asked to stand and flex the trunk more than 90° forward with the bilateral shoulder joints extended maximally and the elbow joints in 90° of flexion. The angles formed between the floor and the forearms are measured.

irritation of the brachial plexus trunks and comprises 90% of the TOS. The neurogenic type can be divided into three types, depending on involvement of cervical nerve roots: the upper type (C5, C6, C7 spinal nerve involvement), lower type (C8, T1 spinal nerve involvement), and the combined type. The lower and combined types comprise 85–90% of all patients with TOS. Some 40–50% of TOS is associated with distal compression neuropathies, such as carpal tunnel, pronator teres, cubital tunnel, and radial tunnel syndromes.25 The vascular group is subtyped into the venous type and arterial type. The venous type comprises 70–80% of the vascular group of TOS. The symptoms include pain, swelling, distended vein, and discoloration of the affected upper limb. Compression of the subclavian vein does not occur in the interscalene space because it passes anterior to the anterior scalene muscle, but usually occurs at the area between the anterior scalene insertion to the first rib and at the costocoracoid ligament and subclavius tendon insertion of the first rib. This type sometimes develops into thrombosis formation in the subclavian vein (Paget–Schroetter syndrome). The arterial type comprises only 20–30% of the vascular group and occurs with direct pressure of the cervical rib, or an abnormal middle scalene muscle to the first rib, or anomalous bandlike structure under the subclavian artery.28 Trauma to the neck, shoulder girdle, and upper extremity, particularly the lower trunk and C8–T1 spinal nerves, is thought to play an important role in developing the symptoms of thoracic outlet syndrome. The trauma can be a single blow or a repetitive, strenuous type.28

Anatomy The brachial plexus trunks and subclavian vessels are subject to compression or irritation in three spaces at the thoracic outlet region. The most important of these spaces is the interscalene space (triangle), which is also the most proximal. This space is bordered by the anterior scalene muscle anteriorly, the middle scalene muscle posteriorly, and the medial surface

Physical examination of thoracic outlet syndrome

67

Anterior scalene

Middle scalene

Phrenic nerve Long thoracic nerve 1st rib

Interscalene space

Costoclavicular space

Subpectoral minor space

Figure 2.24  The three spaces that potentially entrap the neurovascular bundle in patients with the thoracic outlet syndrome.

of the first rib inferiorly. This area may be small at rest and may become even smaller in the posture with elevation or hyperabduction of the upper limb, which moves the scapula posteroinferiorly, resulting in the access of the clavicle to the first rib. The anomalous structures, such as fibrous bands, cervical ribs, and anomalous muscles, may constrict this space further. The second space is the costoclavicular space, which is bordered anteriorly by the middle third of the clavicle, posteromedially by the first rib, and posterolaterally by the upper border of the scapula. The last space is the subpectoralis minor space beneath the coracoid process just deep to the pectoralis minor tendon (Fig. 2.24).

radial artery pulsation disappears or is diminished, the test is positive. This test is considered sensitive to compression in the interscalenus space (Fig. 2.25).29

Provocative maneuver

The patient is asked to inhale deeply and hold the breath. The examiner depresses the patient’s shoulder of the involved limb. Patients with TOS complain of symptoms such as heaviness, pain, numbness or tingling in the limb, and the pulsation of the radial artery is often diminished. This maneuver calls attention to compression in the costoclavicular space (Fig. 2.26).

Adson test (Video 2.17 ) The patient is asked to inhale deeply with the chin up and tilt the neck toward the involved arm holding the breath. If the

The neck tilting The patient is asked to inhale deeply and tilt the neck to the opposite direction of the involved arm holding the breath. In patients with TOS, this action produces arm heaviness, numbness, and tingling in the fingers or/and arm, with some pain.

The costoclavicular compression test

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CHAPTER 2  • Examination of the upper extremity

Figure 2.25  Adson test is sensitive to entrapment of the neurovascular bundle in the interscalene space (arrows) by Adson test.

Figure 2.27  The neurovascular bundle can be potentially entrapped in the costoclavicular space (red arrow) and the subpectoralis minor space (black arrow) by Wright test.

Wright test The examiner holds the patient’s arm in 90° abduction with the elbow 90° flexed, and rotates the arm externally. If the pulsation is diminished and the symptoms are provoked by this maneuver, the test is positive. Entrapment of the ­ neurovascular bundle at the subpectoralis minor space or the costoclavicular space can make the test positive (Fig. 2.27).30

Roos extended arm stress test (Video 2.18

)

The patient is asked to hold both arms with the shoulders in 90°-abduction and 90°-external rotation position and open and close the hands repetitively. If the patient develops any fatigue, pain, numbness or tingling in the hand or arm within 3 min, the test is positive.31

Morley's test Figure 2.26  The costoclavicular compression test is considered to detect the entrapment in the costoclavicular space (arrow).

The patient complains of pain, numbness, tingling or uncomfortable feelings when the examiner pushes the patient’s brachial plexus in the supraclavicular fossa.

Physical examination of the upper extremity in children

These provocative tests should be performed on the bilateral upper limbs and the outcomes of the involved limb should be compared with those of the opposite one, because the tests can be positive in a normal person.

Physical examination of the upper extremity in children Communication with very young children is often difficult or  impossible and young children are not able to articulate their symptoms. A fatty subcutaneous tissue layer often prevents doctors from identifying a deformity or swelling. It is often difficult to locate the source of pain because children tend to complain that the pain is everywhere. Questioning of the parents and family of the patient is sometimes helpful

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for making a diagnosis. Physical examination should include observing the child’s activities when he or she is held by a parent or is playing. Valuable information in terms of the usage and dexterity of the upper extremity can be obtained by observing children playing with age-appropriate toys or props. The affected limb should be examined from the tip of fingers to the hemithorax, which should be compared with the contralateral limb to confirm the anomaly. The ­physical examination should include not only a musculoskeletal examination but also a nervous system examination. Primitive reflexes, including the Moro reflex, the systemic tonic neck response, the mouth lip reflex, and palmar grasp stimulation are used to assess neuromuscular function in newborns. As these patients age, gross movement patterns and integration of the affected hand into functional activities can be assessed.

References

References 1. Seddon HJ. Peripheral Nerve Injuries. Medical Research Council Special Report Series. London: HMSO; 1954:282. 2. Tan JS, Oh L, Louis DS. Variations of the flexor digssitorum superficialis as determined by an expanded clinical examination. J Hand Surg Am. 2009;34A:900–906. 3. Ranade AV, Rai R, Prabhu LV, et al. Incidence of extensor digitorum brevis manus muscle. Hand (N Y). 2008;3:320–323. Small vestigial extensor tendons are sometimes found in the long and ring fingers beside the extensor digitorum communis tendons, which are called the extensor digitorum brevis manus. This muscle is often found as a soft tissue mass and sometimes causes pain in the dorsum of the hand. 4. Eaton RG. The extensor mechanism of the fingers. Bull Hosp Joint Dis. 1969;30:39–47. 5. Harris Jr C, Riordan DC. Intrinsic contracture in the hand and its surgical treatment. J Bone Joint Surg. 1954;36A:10–20. 6. Parkes A. The “lumbrical plus” finger. J Bone Joint Surg. 1971;53B: 236–239. 7. Watson HK, Ryu J, Akelman E. Limited triscaphoid intercarpal arthrodesis for rotatory subluxation of the scaphoid. J Bone Joint Surg. 1968;68:245–349. Watson described his original maneuver of the so-called “scaphoid test” in this article. This maneuver has been modified by several authors and is now recognized as the “scaphoid shift test”, which is a useful physiological examination to identify the instability of the scapholunate ligament complex. 8. Yasuda M, Masada K, Takeuchi E. Dorsal wrist syndrome repair. Hand Surg. 2004;9:45–48. 9. Reagan DS, Linscheid RL, Dobyns JH. Lunotriquetral sprains. J Hand Surg Am. 1984;9A:502–514. 10. Kleinman WB. The lunotriquetral shuck test. Am Soc Surg Hand Corr News. 1985:51. 11. Kleinman WB. Stability of the distal radioulnar joint: biomechanics, pathophysiology, physical diagnosis and restoration of function: what we have learned in 25 years. J Hand Surg Am. 2007;32A: 1086–1106. The author describes detailed anatomy and biomechanics of the ulnar side of the wrist, including the TFCC. The deep layer of the distal radioulnar ligament plays an important role to stabilize the distal radioulnar joint. The dorsal deep layer of the ligament becomes tight in the supinated forearm and the palmar deep layer increases the strain in the pronated forearm. 12. Tay SC, Tomita K, Berger RA. The “ulnar fovea sign” for defining ulnar wrist pain: an analysis of sensitivity and specificity. J Hand Surg Am. 2007;32A:438–444. 13. Tatebe M, Nishizuka T, Hirata H, Nakamura R. Ulnar shortening osteotomy for ulnar-sided wrist pain. J Wrist Surg. 2014;3:77–84. 14. Tay SC, Tomita K, Berger RA. The "ulnar fovea sign" for defining ulnar wrist pain: an analysis of sensitivity and specificity. J Hand Surg Am. 2007;32(4):438–444. 15. Ruland RT, Hogan CJ. The ECU synergy test: an aid to diagnose ECU tendonitis. J Hand Surg Am. 2008;33A:1777–1782.

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16. Dellon AL. The moving two-point discrimination test: clinical evaluation of the quickly-adapting fiber/receptor system. J Hand Surg Am. 1978;3:474–481. 17. Bell-Krotosoki J, Tomancik E. The repeatability of testing with Semmes–Weinstein monofilaments. J Hand Surg Am. 1987;12A:155–161. 18. Moberg E. Objective methods for determining the function value of sensibility in the hand. J Bone Joint Surg. 1958;40B:476. 19. Allen EV. Thromboangitis obliterans: methods of diagnosis of chronic occlusive arterial lesions distal to the wrist with illustrative cases. Am J Med Sci. 1929;178:237–244. 20. Halls AA, Travill A. Transmission of pressures across the elbow joint. Anat Rec. 1960;150:243–248. 21. Hotchkiss RN, An KN, Sowa DT, et al. An anatomic and mechanical study of the interosseous membrane of the forearm: pathomechanics of proximal migration of the radius. J Hand Surg Am. 1989;14A:256–261. When the radial head was resected, 90% of the axial load applied to the wrist joint was transmitted to the ulna through the interosseous membrane. The central band of the interosseous membrane provided 71% of the overall mechanical stiffness of the forearm. 22. Noda K, Goto A, Murase T, et al. Interosseous membrane of the forearm: an anatomical study of ligament attachment locations. J Hand Surg Am. 2009;34A:415–422. 23. Stuart PR, Berger RA, Linscheid RL, et al. The dorsopalmar stability of the distal radioulnar joint. J Hand Surg Am. 2000;25A:689–699. 24. Moritomo H, Noda K, Goto A, et al. Interosseous membrane of the forearm: length change of ligaments during forearm rotation. J Hand Surg Am. 2009;34A:685–691. 25. McConkey MO, Schwab TD, Travlos A, et al. Quantification of pronator quadratus contribution to isometric pronation torque of the forearm. J Hand Surg Am. 2009;34A:1612–1617. 26. Morrey BF. The Elbow and Its Disorders. 3rd ed. Philadelphia: WB: Saunders; 2000. 27. O’Driscoll SW, Bell DF, Morrey BF. Posterolateral rotatory instability of the elbow. J Bone Joint Surg. 1991;73A:440–446. The authors addressed grades of dislocation of the joint caused by lateral ligament insufficiency (from instability of the joint to complete dislocation) and described a maneuver of the pivot shift test that was provocative of the elbow dislocation due to the lateral ligament instability. 28. Atasoy E. A hand surgeon’s experience with thoracic outlet compression syndrome. J Hand Surg Am. 2010;35A:1528–1538. 29. Adson AW. Surgical treatment for symptoms produced by cervical ribs and the scalenus anticus muscle. Surg Gynecol Obstet. 1947;85:687–700. 30. Wright CJS. The neurovascular syndrome produced by hyperabduction of the arms. Am Heart J. 1945;29:1–19. 31. Roos DB. New concepts of thoracic outlet syndrome that explain etiology, symptoms, diagnosis, and treatment. Vasc Surg. 1979;13:313–321.

SECTION I  •  Principles of Hand Surgery

3 Diagnostic imaging of the hand and wrist Alphonsus K.S. Chong, Janice Liao, and David M.K. Tan

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SYNOPSIS

ƒ Radiographs form the cornerstone of diagnostic imaging of the hand and wrist, and are usually the first imaging modalities performed following clinical evaluation. ƒ The keys to obtaining the most information from radiographs are ordering the correct radiographs for the situation, and ensuring the radiograph is appropriately taken. ƒ A systematic and careful examination of the radiograph is necessary to glean the often subtle findings in the hand and wrist. ƒ Clinical evaluation with plain radiographs often provides sufficient information for clinical decision-making. ƒ Computed tomography (CT) scans, ultrasound, magnetic resonance imaging (MRI), and other advanced imaging modalities can supplement information from plain radiographs in selected situations. On occasion, they may be the primary imaging study performed. ƒ These advanced imaging modalities allow today’s clinician to visualize disorders that would previously have required open surgery or biopsy.

Introduction   A proper

and directed history-taking followed by a careful examination of both hands and wrists forms the foundation of making a clinical differential diagnosis in hand conditions.   Appropriate investigations are then ordered to help confirm the clinical diagnosis.   Diagnostic imaging modalities are often the first-line investigations ordered, as many clinical conditions in the hand and wrist can be seen visually.   Technological advances in many advanced imaging modalities like ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI), have led to them being applied for use in the hand and wrist. This increases clinician choices for diagnostic imaging of a suspected clinical condition.   The radiograph, despite its simplicity and age, still forms the foundation of imaging of hand and wrist conditions.

In many clinical situations, an appropriately chosen and well-taken set of radiographs may be all the diagnostic imaging required.   The key to obtaining the most information from a radiograph is to understand which radiographs are appropriate for each clinical situation, and how to obtain good-quality radiographs for evaluation.   Advanced imaging modalities may then be ordered to provide additional information for decision-making.   This chapter will equip the reader with practical information about the different imaging modalities available for the hand and wrist.   It will start from the foundation of radiographs, covering the appropriate views, how they are taken, and how best to evaluate them. Following which, the advanced imaging techniques will be described in turn, emphasizing their applications in the hand and wrist.

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Radiography Radiography is the cornerstone in diagnostic imaging of the hand and wrist. It should be the first imaging modality for the diagnosis of most hand and wrist disorders.3 The plain radiograph is inexpensive in relation to other imaging modalities, technically easy to perform, and widely available. The correct radiograph taken in an appropriate manner provides much imaging information to the attending clinician. In many hand and wrist conditions, radiography may also be the only imaging modality required for definitive diagnosis and assessment.

Evaluation of the hand The three basic radiographs to evaluate the hand are: posteroanterior (PA), oblique, and true lateral views. The radiographs

Historical perspective

Historical perspective The origins of diagnostic radiology are of particular significance to hand surgery. The first radiograph of human anatomy after the discovery of X-rays by Wilhelm Conrad Roentgen was that of his wife’s hand in 1895. The medical community was quick to see the potential applications of this technology, and radiographs were rapidly adopted for clinical use. As a result, Roentgen is considered the father of diagnostic radiology, and his discovery led him to win the first Nobel Prize in Physics in 1901. Plain X-ray radiographs are still the first-line imaging modality for the diagnosis of most hand and wrist disorders. Plain film radiography has progressed from a tedious process using an acetate-based film to one that applies digital technology. In newer facilities, widespread adoption of digital technology has led to radiographs that are not printed on film, but viewed on the computer screen. Beyond technology, the development of special views through positioning of the patient or machine, and stress application, has enabled improvements in imaging of specific disorders. The development of water-soluble contrast dyes allowed the use of X-rays to perform arthrography.

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CT, MRI, and ultrasound are advanced imaging technologies that have become widely adopted for musculoskeletal imaging, including the hand and wrist. Improvements in hardware technology, software, and imaging protocols have resulted in improved imaging of bone, joints, and soft tissue. These technologies have enabled detailed visualization and assessment of the musculoskeletal system and its disorders in a noninvasive manner. Prior to these technologies, many of these disorders would have required open surgery or biopsy for diagnosis. Improvements in imaging modalities and technology are only part of the equation for the advances made in musculoskeletal imaging. Equally important has been the parallel development of musculoskeletal radiology as a distinct subspecialty.1,2 The dedication of musculoskeletal radiologists has been instrumental in developing their field, and subspecialty training of future musculoskeletal radiologists. These radiologists can better appreciate the often subtle findings on imaging, leading to improved diagnosis. This has translated to earlier and more effective clinical care and improved outcomes. Musculoskeletal radiology continues to progress at a rapid pace as both a clinical specialty and in technological advances. Building on its strong foundations, musculoskeletal imaging will continue to be a crucial pillar in the diagnosis and assessment of hand and wrist disorders.

Radiography

should be performed in a standardized fashion to allow proper evaluation (Figs. 3.1 & 3.2). Specialized views are required to assess specific areas not well seen in the above views. The PA hand view provides a useful overview of the skeletal structure of the hand. Fractures, osseous tumors, and even soft-tissue masses (Fig. 3.3) can be seen on this view. The oblique view of the hand is useful to assess the metacarpals, as a true lateral view of the hand will lead to an overlapping of the second to fifth metacarpals. In the common boxer’s or fifth metacarpal neck fracture, this view allows an assessment of the amount of angulation of the fracture. Incident beam of X-ray perpendicular to the X-ray cassette Beam direction and central position: A Wrist PA – centered over capitate B Hand PA – centered over 3rd metacarpal midshaft Shoulder abducted 90º Elbow flexed 90º

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In hand radiographs, begin by assessing the overall alignment of the metacarpals and phalanges. The individual bones should then be evaluated in terms of cortical shape and integrity, as well as bony quality. Fractures are usually easy to detect, although a careful review is necessary in the case of undisplaced or minimally displaced fractures. Osseous tumors are identified by an area of different lucency in the bone. There may be changes in the outline of the bone. Enchondromas are common benign bony tumors in the hand. They can result in pathological fractures, so an assessment of the bone for such pathology should be done, particularly if the trauma resulting in the injury is trivial (Fig. 3.4). Osteomyelitis typically occurs in the hand following open injuries (Fig. 3.5). The joints should then be assessed, starting from the carpometacarpal joints (CMCJs) and working distally. The CMCJs may be dislocated following injury. These injuries are uncommon but are difficult to diagnose. In a normal hand X-ray the second to fifth CMCJs should be clearly visible on the PA view (Fig. 3.6).4 The loss of these features in the second to fifth CMCJs is usually due to a fracture dislocation of one or more of the CMCJs. However, an improperly performed hand radiograph can also give this impression. Fisher et al. described a systematic approach to evaluating the PA view of the hand for dislocations of the fourth and fifth CMCJs.4 In subluxation of the fifth CMCJ, the base of the fifth metacarpal is usually offset ulnarly compared to the hamate (Fig. 3.7). Several views have been suggested to confirm this diagnosis. The true lateral of the hand provides a useful way to assess the CMCJ for any signs of dislocation and oblique views may also be helpful5,6; if the diagnosis is

Figure 3.1  The posteroanterior (PA) radiograph of the hand and wrist is taken in the position shown. For the hand radiograph, the beam is centered over the midshaft of the third metacarpal. For the wrist radiograph, it is centered over the capitate.

Incident beam of X-ray perpendicular to the X-ray cassette and centered over the third metacarpophalangeal joint

Thumb and index fingertip brought close; hand lies in 45º of pronation

Forearm resting on table and pronated, radius, and third metacarpal collinear

Figure 3.2  The oblique hand radiograph is taken with the hand positioned as shown. This position provides a good non-overlapping view of the metacarpals. The view is not adequate for assessment of the digits; separate lateral views of the digits should be performed if necessary.

Figure 3.3  This female patient presented with a soft-tissue mass over the ulnar side of the middle finger. The radiograph shows the outline of the soft-tissue mass with scalloping of the ulnar border of the middle phalanx. Histology of the mass showed this to be a pigmented villonodular synovitis.

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Figure 3.4  This nurse presented with pain at the base of her right ring finger after transferring a patient from his bed to a chair. The radiograph shows a partial articular fracture of the base of the proximal phalanx of the right ring finger. The area of lucency just at the fracture site and minor trauma were suspicious for a pathological fracture.

Figure 3.6  In a normal hand radiograph, the second to fifth carpometacarpal joints should be well visualized, as shown. The articular surfaces should be profiled without overlap, parallel to each other, and have distinct cortical rims.

still uncertain, a CT scan of the hand including the CMCJs will confirm the diagnosis.7 The more distal joints are then evaluated, from the metacarpophalangeal joints to the proximal interphalangeal joints and distal interphalangeal joints. A normal joint should be completely congruent with a visible joint space. Osteoarthritis commonly affects the interphalangeal joints and thumb CMCJs. It is often demonstrable on radiographs by narrowing of the joint space, subchondral sclerosis, osteophytes, and deformity (Fig. 3.8).

Special views in the hand (Box 3.1)

Figure 3.5  This elderly man presented with increasing pain and redness in the finger. The radiograph shows a destructive lesion of the distal phalanx and head of the middle phalanx. This is consistent with osteomyelitis. A differential diagnosis would be that of a malignant bone tumor. These are much rarer, and usually due to metastatic disease in terminally ill patients.

A true lateral radiograph of the finger is needed to complete an assessment of the digit. Hand radiographs alone are insufficient for assessment. This is because the oblique view of the hand does not provide an adequate lateral profile of the digit and interphalangeal joint spaces to supplement the PA view. With only a PA view, subtle fractures, fracture displacement, or joint subluxation of the fingers may not be apparent. Metacarpal head fractures may also be difficult to assess and the Brewerton view8 will give additional information to the standard hand radiographs. To assess the thumb, specialized views are also necessary as the thumb lies in an oblique plane relative to the other digits in the usual hand radiograph. A true PA and lateral view of the thumb is obtained to allow proper radiographic assessment of the thumb. One common condition in the thumb for which radiographs are performed is that

Radiography

73

Figure 3.7  This radiograph shows a dislocation of the fifth carpometacarpal joint. Note the ulnar offset of the fifth metacarpal with loss of the normal articular space.

BOX 3.1  Special hand and thumb views Brewerton view Purpose: To obtain tangential views of the metacarpal heads – for evaluation of metacarpal head fractures and erosive changes in rheumatoid arthritis Positioning: With the palm facing up, the MCPJs are flexed 65° with the posterior aspect of the fingers in contact with the cassette, and beam angled at 15° from the ulnar side of the hand

Betts/Gedda view Purpose: To obtain a true lateral view of the TMCJ, and see the trapezium in profile Positioning: Palm of the hand must be placed flat on the cassette with the hand and forearm pronated, with the beam is then directed 5–10° distal to proximal

Robert's view Purpose: To obtain a true AP view of the TMCJ Positioning: The hand and forearm is hyperpronated such that the dorsum of the thumb lies on the cassette, with the beam angled 15° from the vertical

Figure 3.8  Osteoarthritis of the distal interphalangeal joints of middle and ring fingers. There is loss of joint space, and osteophytes are clearly seen on this lateral view.

of basal joint or trapeziometacarpal joint (TMCJ) arthritis (Fig. 3.9). This condition is graded radiologically using the Eaton classification.9 The irregular saddle shape of the trapezium makes visualization of the bone difficult, and the

Betts view will allow all four articulations of the trapezium to be visible without overlap (Fig. 3.10). The ulnar collateral ligament of the thumb metacarpophalangeal joint is commonly injured in forceful thumb abduction. Less commonly the radial collateral ligament may also be injured. Lateral stress application during the posteroanterior thumb radiograph can be helpful to assess if the ligament injuries are complete or partial. Ultrasonography and MRI are alternatives to assess this injury.10,11

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Figure 3.9  The trapeziometacarpal joint shows narrowing of the joint space with osteophytes and joint subluxation.

Pediatric hand radiographs Evaluation of the pediatric hand, especially after injury, is often more difficult than in adults. All carpal bones and epiphyses in the hand lack ossification in the newborn. The ossification centers then appear in a well-recognized sequence,12 as detailed in Table 3.1. The staggered ossification of the various carpal bones (Fig. 3.11) and the presence of the growth plate may confuse the examiner as to whether a fracture is present or not. A misdiagnosis rate of 8% for pediatric hand fractures was found in one study.13 There are several reasons for this. Clinical evaluation in children is more difficult, the more so the younger the child. It may not be possible to localize the site of the problem clearly, e.g., the site of injury following trauma. Proper standardized views may also be difficult to obtain. Other reasons for misdiagnosis include missing additional fractures and using an X-ray that was obscured by dressings.13 When the clinical suspicion remains high and the films obtained are inadequate, the radiograph should be repeated, either the same day or at another time when the patient is more cooperative. Similar views taken of the opposite uninjured limb are also helpful for evaluation. Growth plate-related injuries are common in children. These injuries can be classified according to the system described by Salter and Harris (Fig. 3.12).14 The Salter–Harris type II fracture injury is the most common type of growth plate injury seen in the hand.

Wrist evaluation A properly performed set of orthogonal wrist radiographs forms the basis of an effective evaluation of the wrist.15,16 This is especially important when indices are being measured. The wrist has numerous asymmetrically arranged bones, so a

methodical assessment of the bones, joints, and overall alignment of the wrist is necessary. Obtaining proper views for wrist radiographs (see Fig. 3.1; Fig. 3.13; see Fig. 3.18) requires careful positioning which may be difficult to achieve in patients with pain or limitations in motion of the affected upper limb (Box 3.2). The wrist radiograph is first evaluated by checking the overall alignment of the bones of the wrist, starting with the distal radius and ulna, progressing to the carpal bones and metacarpal bases. Gilula described three smooth arcs made by the articular surfaces of the proximal and distal carpal row bones in a normal wrist PA radiograph (Fig. 3.14).17 A loss of the normal contour usually indicates a disruption in the normal arrangement of these carpal bones. A common cause of this is a perilunate dislocation (Fig. 3.15). Lunotriquetral (LT) dissociation is another cause of the loss of the normal Gilula’s lines. Care must be taken when interpreting these findings in an asymptomatic patient as radial or ulnar deviation of the wrist can introduce a break in the arcs.3,18 The overall relationship between the different bones can also be assessed using two common parameters: the carpal height ratio and ulnar variance. These provide a quantitative assessment of the structural integrity of the carpal rows, and the relationship of the distal radius and ulna articular surfaces, respectively. The carpal height ratio (Fig. 3.16)19,20 gives a measure of the distance between the distal articular surface of the radius to the proximal articular surface of the third metacarpal base. A loss of this distance is seen in collapse of a carpal bone, for example Kienbock’s disease (avascular necrosis [AVN] of the lunate) or in malrotation of the carpal bones, for example in rheumatoid arthritis or scapholunate (SL) dissociation. A ratio is used instead of actual dimensions to correct for variability in carpal bone sizes.

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Table 3.1  Appearance of ossification centers and fusion of epiphyses in children

Females

Males

Appearance of capitate and hamate

3 months

3 months

Appearance of distal radius ossification center

10 months

1 year 3 months

Appearance of phalanges and metacarpal ossification center

10 months to 2 years

14 months to 3 years

Fusion of phalangeal and metacarpal epiphyses

13–15 years

14–16 years

Fusion of distal radius and ulna epiphyses

15–17 years

17–19 years

A

Commonest order of ossification: 1 Capitate 2 Hamate 3 Triquetrum 4 Lunate 5 Scaphoid 6 Trapezium 7 Trapezoid 8 Pisiform

B

Figure 3.10  (A) Hand radiograph showing a trapezium fracture. (B) The Bett’s view demonstrates the trapezial fracture and the step in the articular surface clearly.

The ulnar variance provides a measure of the height difference between distal radius and ulnar articular surfaces. There are several ways to measure the ulnar variance.21,22 We prefer the technique of the perpendiculars (Fig. 3.17). It is easy to perform and has been shown to have higher intra- and interobserver reliability.23,24

1

2 8

3

7

6

5 4

Figure 3.11  Commonest order of ossification: capitate, hamate, triquetrum, lunate, scaphoid, trapezium, trapezoid, and pisiform. Note the position of the growth plates on the proximal ends of the phalanges and first metacarpal. In the remaining ulnar four metacarpals, the growth plate is on the distal end of the bone.

A proper PA and lateral radiograph of the wrist (Fig. 3.18; see Fig. 3.13) is the first necessary imaging for the evaluation of a suspected distal radioulnar joint (DRUJ) instability. Radiographic findings associated with this injury include widening of the DRUJ, a fracture of the ulnar styloid base, or a displaced fracture from the ulnar fovea. On the lateral view, there is loss of the normal radioulnar overlap. A comparison radiograph of the contralateral normal wrist is helpful if the findings

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CHAPTER 3  • Diagnostic imaging of the hand and wrist

are unclear. The application of volar or dorsal-directed stress is also helpful in cases of suspected DRUJ instability (Fig. 3.19). Scaphoid fractures are the commonest carpal fracture. The shape of the scaphoid bone does not lend itself well to evaluation by just two orthogonal views, so a “scaphoid series” of X-rays is usually done (Fig. 3.20 and Box 3.3). Fractures of the hook of the hamate are uncommon but disabling. A carpal tunnel view is helpful to diagnose this injury (Fig. 3.21), although a CT scan can also provide the definitive diagnosis. Injuries to the wrist ligaments, for example the SL ligament, can lead to carpal instability. In severe cases, this can be seen

A

B

on the usual wrist views as loss of the normal relationships between the carpal bones. In SL instability, this is typically seen as a dorsal intercalated segmental instability deformity (Fig. 3.22) with an increase in the SL angle, and dorsal tilt in the radiolunate angles (Fig. 3.23). However, in milder forms of BOX 3.2  Assessing quality of wrist radiographs There are criteria for acceptable wrist views. The posteranterior (PA) view is assessed using the position of the ulnar styloid and extensor carpi ulnaris tendon groove.15 The lateral view is assessed using the radioulnar overlap and scaphopisocapitate relationships.16

C

Most common

3 2 1 D

E

Crush injury of growth plate

Figure 3.12  (A–E) The Salter–Harris classification of epiphyseal plate injuries. (Redrawn after Salter RB, Harris R. Injuries involving the epiphyseal plate. J Bone Joint Surg Am. 1963;45:587–621.)

A

B

Figure 3.14  In a normal posteroanterior wrist radiograph, three smooth curved non-overlapping lines can be drawn on the proximal and distal cortical surfaces of the proximal carpal bones (lines 1 and 2) and proximal surface of the distal carpal row (line 3). A disruption or step-off indicates a loss of the normal carpal bone relationships.

Figure 3.13  Normal wrist radiograph. (A) In the posteroanterior view, note the lateral position of the ulnar styloid and position of the extensor carpi ulnaris groove. It lies radial to the straight line that passes tangential to the radial edge of the ulnar styloid at the fovea. This indicates a good posteroanterior view. (B) On the lateral view, there is good radioulnar overlap.

Radiography

77

3 Level of ulna distal cortical rim

2 Perpendicular to axis through volar ulnar sclerotic rim line of distal radius

Ulnar variance

1 Longitudinal axis of radius

Figure 3.17  Ulnar variance is measured on a true neutral posteroanterior view of the wrist. First (1) a line along the longitudinal axis of the radius is drawn. Next (2) a line perpendicular to this line through the volar ulnar sclerotic rim of the distal radius is drawn. Finally (3) a line parallel to this second line at the level of the distal cortical rim of the ulna is drawn. The distance between these two parallel lines is the ulnar variance.

Beam direction

Figure 3.15  This radiograph shows a perilunate fracture dislocation with disruption of the normal smooth carpal arcs. There are associated radioulnar shaft fractures.

Elbow flexed 90º L1

X-ray cassette Wrist neutral – no palmar or dorsiflexion

Radius, wrist and 3rd metacarpal collinear

Figure 3.18  A true lateral view of wrist is taken in the position shown.

L2

rL1

CR

Figure 3.16  (1) Carpal height ratio = carpal height (L2)/third metacarpal length (L1). Normal is 0.54 ± 0.03. (2) Revised carpal height ratio = carpal height (L2)/ heights of capitate (rL1). (3) Capitate–radius index (CR). This is the shortest line between two eccentric arches of the carpal rows. The line is moved until the shortest distance is measured. Mean CR index 0.999 ± 0.034. Values less than 0.92 are abnormal.

instability, ­application of loads and/or positioning of the wrist are necessary to bring out these dynamic changes in carpal relationships. The clenched-fist PA series of the wrist is one technique used to diagnose dynamic carpal instability (Fig. 3.24). Ulnar abutment syndrome is a common cause of ulnarsided wrist pain. The use of a clenched-fist pronated view of the wrist enhances the ulnar variance and may demonstrate the abutment (Fig. 3.25).24

Wrist evaluation in distal radius fractures Distal radius fractures are the commonest fractures encountered in the emergency room.25 Loss of the normal distal radius indices (Figs. 3.26 & 3.27) due to fracture displacement can affect final outcome. Unstable and displaced fractures are commonly treated with plates and screws. Screws placed subchondrally offer the greatest rigidity in fixation. However, conventional wrist views do not allow accurate assessment of screw position, especially when a distal fracture line compels the surgeon to place the screws in close proximity to the radiocarpal joint. This is because standard views do not compensate for the normal anatomic tilt of the radius. Radiographs angled 22° lateral and 11° posteroanterior (Fig. 3.28) enable tangential X-ray exposure to the articular surface and facilitate this assessment after fixation. With increasing using of volar plates for treatment of distal radius fractures, extensor tendon rupture from screw protrusion dorsally is a concern. Detection of dorsal screw protrusion from a lateral X-ray has a sensitivity of only 56%,26 and on average, protrusion of the radial-most screw can only be detected at a minimum

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Ultrasound uses the acoustic properties of generated sound waves to form images.32 An ultrasound transducer generates the sound waves in pulses. When the transducer is applied over the surface of the part to be examined, the sound waves pass through tissues. At the junction of two tissues, an acoustic interface occurs. When the sound waves meet an acoustic interface, some of the sound wave energy is reflected, while the rest continues to be transmitted deeper. The greater the differences in material properties of the adjacent tissues, the more energy is reflected. The reflected sound wave is received in the transducer. This is then converted to an electrical signal for processing. The greater the sound reflected, the larger the amplitude of the reflected wave, and consequently, the brighter the image. The primary mode used in hand surgery is the B-mode where two dimensional images are created by simultaneous scanning the area of interest with a linear array of transducers. This provides a cross-sectional image with the horizonal and vertical directions corresponding to the real distances in tissue and the grayscale corresponding to the echo strength.

Masses

Figure 3.19  Stress view: true lateral of the wrist. Notice the loss of radioulnar overlap due to the dorsal subluxation of the distal radioulnar joint. The pisiform lies between the volar aspect of the scaphoid and capitate, so the view is accurate.

of 6.5 mm of protrusion.27 Special X-ray views can be done to improve detection of screw protrusion (Box 3.4 and Fig. 3.29). The availability of fluoroscopy in many clinics and operating rooms allows the dynamic assessment of many hand and wrist conditions. Smaller, lower cost, and lower radiation28 mini C-arms have also lowered the barrier to acquiring such facilities. The clinician can operate the C-arm to obtain the best view and view changes in the relationships of the bones “live” with motion, loading, or application of stress. Fluoroscopy is helpful for assessing carpal instability, including SL injuries29 (Video 3.1 ) and midcarpal instability (Video 3.2 ), guiding percutaneous insertion of implants, and assessing the position of implants.30

Ultrasonography Introduction Ultrasound is widely used in hand surgery. The ultra-high frequency probes and smaller probe sizes allow higher-quality images of the hand and wrist (Video 3.3 ).31 Ultrasound’s safety, portability, and relatively low cost have supported wider adoption.32 Beyond its accessibility and lack of radiation exposure, one additional advantage of ultrasound over other forms of advanced imaging, like CT scanning or MRI, is that it allows dynamic and real-time assessment. The addition of Doppler imaging enhances the information provided by the ultrasound study.31

In assessment of masses, ultrasound is most useful for differentiating ganglia from other solid masses in the wrist. To detect the presence and nature of blood vessels within a mass such as a vascular malformation, the Doppler mode is used. The Doppler effect occurs when there is relative motion between the sound’s source (blood flow) and the receiver. When blood flow moves toward a receiver, a higher-pitch sound is produced. When blood flows away from the receiver, a lower-pitch sound is produced. Color Doppler produces a color-coded map to superimpose onto a B-mode image. As ganglions are the most common wrist and hand mass, the use of ultrasound is more informative than plain radiographs and sufficient imaging assessment, unless atypical features (heterogeneity, solid lesions) are found. In the latter case, MRI should be performed.33

Injuries and degenerative conditions Ultrasound is helpful for various tendon, pulley, and ligament injuries and for degenerative conditions such as trigger finger and DeQuervain’s tenosynovitis.34 For example, trigger finger is usually easily diagnosed by clinical examination. However, in certain situations, e.g., grade 1 trigger or triggering in atypical patients (e.g., young patients or where a mass effect is suspected), ultrasound can both diagnose the trigger and reveal any underlying cause.35 In trigger finger, ultrasound has also been used to guide steroid injection and percutaneous release.36,37 Carpal ligament injuries and triangular fibrocartilage (TFCC) tears can be assessed using ultrasonography.38 For TFCC tears, ultrasonography has been shown to have good correlation with MRI.39 The Stener lesion is an important surgical indication in the acute ulnar collateral ligament injury of the thumb metacarpophalangeal joint. Ultrasound has been shown to be excellent at differentiating Stener lesions from non-displaced UCL tears.40 One major advantage of musculoskeletal ultrasound is the ability to do real-time and dynamic assessments. An area in the hand and wrist where this is particularly useful is in the assessment of tendons. For example, flexor tendon bowstringing due

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79

Figure 3.20  Scaphoid series to assess for a scaphoid fracture. Notice the fracture is best seen in the scaphoid view on the lower left corner of the series.

BOX 3.3  Scaphoid series The scaphoid view of the wrist addresses the normal foreshortening of the scaphoid seen on the conventional posteroanterior (PA) wrist radiograph. The view is taken with the wrist ulnarly deviated and the X-ray tube angled 20–30°. Several other views are helpful for assessment of the scaphoid: a pronated oblique view (to view the distal third and tubercle of the scaphoid better), a supinated view (to assess the dorsoradial ridge of scaphoid and pisiotriquetral articulation), and a lateral view to help assess a humpback deformity.

to pulley rupture can be dynamically demonstrated on ultrasound by the patient. Tendinopathies, partial and complete tendon tears, or lacerations can also be demonstrated (Fig. 3.30).

Compressive neuropathies Ultrasonography of the carpal tunnel may be helpful to assess compressive neuropathies. The median nerve is enlarged in

carpal tunnel syndrome, with changes in the echogenicity of the nerve. The most consistent finding across the studies is the increase of the cross-sectional area of the median nerve at the level of the pisiform bone.41 Although nerve conduction studies have been shown to have greater diagnostic sensitivity than ultrasound, the high positive predictive value of ultrasound makes it suitable as a screening test.42 Ultrasound is also useful for clinical assessment if other causes of carpal tunnel syndrome are suspected (e.g., mass lesions in the carpal tunnel or tenosynovitis).

Disadvantages Ultrasound has its disadvantages (Table 3.2). It only allows a small field of view, so is best used for a focused examination of a small area. Differentiation of different soft-tissue tumors of the hand and wrist, apart from ganglia, is also inadequate.43 However, with ganglion being the most common cause of tumors in the hand, ultrasound would be an ideal first-line investigation.

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L

C

S

R

P HH

A

B

C

D

Tz A

Normal 30–80º

E Scapholunate angle

B

Figure 3.21  (A) Carpal tunnel view of the wrist demonstrating several structures: trapezium (Tz), pisiform (P), and hook of hamate (HH). A fracture across the hook of the hamate is indicated by the black arrow. The trapezial ridge (indicated by white arrow) is an unusual site for fractures that is best seen on this projection. (B) Same patient with carpal tunnel view of the same wrist following open reduction and screw fixation. Notice that the fracture line is no longer visible.

A

Dorsal tilt of >15º DISI

Normal is ±15º

F Capitolunate angle

G Radiolunate angle

Figure 3.23  Carpal indices. Axes are drawn based on the true lateral wrist radiograph. (A) The scaphoid (S) is represented by a tangential line that connects the two palmar convexities of the bone. (B) The lunate (L) axis is perpendicular to a line that joins the two distal horns of the bone. (C) The capitate (C) axis is determined by the center of the two proximal and distal articular surfaces. (D) The axis of the radius (R) is obtained by tracing perpendicular lines to its distal third and connecting the center of these lines. (E) Normal scapholunate angles. (F) Normal capitolunate angles. (G) Normal radiolunate angles. DISI, dorsal intercalated segmental instability.

B

Figure 3.22 DISI is the acronym for dorsal intercalated segmental instability. The term “intercalated segment” refers to the proximal carpal row bones. (A) This row has no direct musculotendinous insertions, hence it is “intercalated”. “Dorsal” refers to the dorsiflexion of the lunate seen in the radiograph. A scapholunate dissociation is the commonest cause of a DISI deformity, and will show an increased scapholunate angle as above. (B) On the posteroanterior view, the scaphoid will appear flexed and foreshortened with a positive cortical ring sign as seen.  

Ultrasonography

A

81

B

Figure 3.24  These radiographs show a patient with dynamic scapholunate instability. The scapholunate interval is normal on an unloaded wrist (A), but widens on clenching the fist (B).

A

B

Figure 3.25 This patient presented with signs and symptoms of ulnar carpal abutment. The positive ulnar variance (A) is increased with the pronated clenched-fist view (B).  

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Incident beam of X-ray perpendicular to the X-ray cassette and centered over the wrist joint

B

A

C

PA wrist

PA wrist

Lateral wrist

A: Radial height. Normal = 11–12mm, Range = 8–18mm B: Radial inclination. Normal = 22–23º, Range = 13–30º C: Volar tilt. Normal = 11–12º, Range = 0–28º

Figure 3.26  Normal distal radius indices. PA, Posteroanterior.

Firm soft radiolucent support inclining elbow at 22º to horizontal

X-ray cassette

Figure 3.28  Position of the limb and direction of X-ray beam for an anatomical tilt lateral view of the distal radius. This view is very helpful for assessing screw position when applying plates and screws close to the articular surface in distal radius fractures.

Figure 3.27  Distal radius fracture with loss of the normal radial height, inclination, and volar tilt.

The problem of anisotropy can lead to reduced echogenicity when tendons are being imaged. Anisotropy is a phenomenon where the echogenicity of the tendon changes when the incidence of the sound beam changes. This can lead to the operator mistaking anisotropy for pathology like tendon degeneration. A careful complete assessment of suspected tendon lesions will detect this phenomenon.44 Although ultrasound is operator-dependent, this deficiency can be mitigated by having well-defined scanning protocols to

reduce intra- and inter-rater variation45 and incorporation of intelligent systems to aid diagnosis.46

Ultrasound at the bedside Clinician-operated ultrasound assessment is gaining traction.32 Point-of-care ultrasound is more accessible than ever, with the availability of highly portable, high-resolution, and affordable ultrasound machines. Current portable ultrasound

Ultrasonography

BOX 3.4  Additional views for assessment of dorsal screw penetration from distal radius Supinated This view aligns the X-ray beam to the radial side of the dorsal cortex, allowing easier detection of prominent screws in the first and second dorsal compartment.

Pronated This view aligns the X-ray beam to the dorsal-ulnar corner of the distal radius and allow easier detection of prominent screws in the fourth extensor compartment.

Dorsal horizon view

devices come in a range of sizes, budgets, and features that will fit different practices, and are effective in trained persons.47 At the most compact end, the device consists of just a probe that can integrate with a smartphone or tablet, making it truly a stethoscope replacement. A key limiting factor in wider adoption of ultrasound at consults is clinician competency in ultrasound use. A short training exposure has been shown to be sufficient to teach specific competencies,48 but for a wider skill repertoire, comprehensive training and supervised practice is necessary. The availability of simulators and online training courses lowers the bar for individuals interested in acquiring these skills.

This view is done with the wrist hyperflexed and the X-ray beam aimed along the longitudinal axis of the radius.

A

B

C

83

Figure 3.29  (A) Standard PA and lateral wrist X-rays showing a distal radius fracture post-fixation. (B) Supination and pronation views showing dorsal screw penetration. (C) Dorsal horizon view showing dorsal screw penetration.

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Table 3.2  Advantages and disadvantages of ultrasound

Advantages

Disadvantages

• No ionizing radiation • Allows real-time and dynamic assessment by operator • Not affected by metallic implants • Able to guide procedures • Relatively cheap to acquire and operate

• Very limited field of view • Limited penetration • Highly operatordependent • Limited usefulness for assessment of softtissue masses

Table 3.3  Advantages and disadvantages of computed tomography (CT)

A

Advantages

Disadvantages

• Quick scanning with modern machines • Capacity to image in any anatomic plane (multiplanar imaging) and threedimensional reconstruction • Excellent for assessing complex or poorly visualized fractures in the hand and wrist • CT angiography can be performed at the same sitting to assess the vascular tree

• Inferior to magnetic resonance imaging for imaging of soft tissue • Requires expose to ionizing radiation • Prone to artifacts from patient movement and implants

Fractures and dislocations

B

Figure 3.30  This patient presented with difficulty in finger flexion after an injury. Ultrasonography showed a partial tear of flexor tendon at the level of the head of middle phalanx, more obvious on flexion against resistance (dark area, arrowed on longitudinal section (B) and between calipers on transverse section (A)). (Courtesy of Dr. Ian Tsou, Singapore.)

Computed tomography CT is a key advanced imaging modality for the assessment of hand and wrist disorders, particularly those affecting the bones and joints. Advances in CT scanning technology have resulted in shorter scanning times, and allow manipulation and reformatting of the CT data for image reconstruction in multiple planes and the development of three-dimensional images. The advantages and disadvantages of CT are shown in Table 3.3.

CT is useful in evaluation of the hand and wrist for bony and joint injuries that are not well visualized or assessed using radiographs. Examples of these include scaphoid fractures, CMC joint injuries (see discussion in radiography section, above), and other articular fractures (Fig. 3.31). Scaphoid fractures are often difficult to detect on plain radiology after an acute injury. A repeat radiograph several weeks later or other radiological investigations like CT scan, MRI, and bone scans are often employed to detect an occult scaphoid fracture.49 In one study, multidetector CT was shown to be as effective as MRI in the detection of such occult fractures.50 In the management of scaphoid fractures, CT scan is useful in evaluating fracture union,51 as plain radiography has been shown to have poor interobserver agreement for assessing scaphoid union.52 CT scans along the long axis of the scaphoid53 improve the ability to evaluate the scaphoid for fractures, and assess for any displacement or humpback deformity.54 CT scan is also useful for the evaluation of other carpal fractures.55 Wrist radiographs provide a first evaluation of the distal radius fractures. In an acute fracture, patient positioning is hindered by pain, and suboptimal radiographs are common. Radiography can over- and underestimate the articular stepoff in 30% of intra-articular fractures.56 CT scans of the wrist can improve assessment, which has an impact on clinical decision-making (Fig. 3.32). CT scanning and three-dimensional reconstruction are also helpful in complex fractures of the distal radius and ulna to help in surgical planning. In distal radius malunion, CT is recommended to assess the deformity57 and as a basis for computer-assisted surgical techniques.58,59

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85

A

Figure 3.32  Coronal computed tomography (CT) image of distal radius fracture. Extension into the radiocarpal joint is seen here but not on the plain radiograph. CT is helpful for the assessment of intra-articular distal radius fractures with respect to articular involvement and incongruity, fragment number, and fragment orientation.

B

Figure 3.31  This displaced fracture of the radial condyle of the proximal phalanx (small finger) is well visualized on the computed tomography (A) and (B), but obscured on plain radiograph. There is a concomitant fracture of phalanx base, seen in (B).

CT is also helpful in suspected DRUJ instability. A proper lateral view of the wrist is the key initial imaging. There are several pitfalls associated with this. Proper positioning of the wrist for a proper lateral wrist radiograph or stress views may not be possible because of pain or other factors. The instability may be subtle, manifesting only in certain wrist positions or under load. Bilateral axial cut CT scans of the wrists in the neutral, pronated, and supinated position provide critical information to allow better evaluation of these injuries (Fig. 3.33). For CT evaluation of DRUJ instability, different radiographic parameters have been described.60–63 Our institution uses the subluxation ratio method described by Park and Kim.64

Other applications of CT CT is also helpful for the evaluation of bony tumors in the hand. CT can help characterize the bony tumor and assess for bony destruction. In these situations, MRI is often complementary. Fine-cut CTs are the modality of choice for osteoid osteoma.65 There are limitations to the use of CT. Soft-tissue resolution is limited, so it is less useful than MRI for imaging soft-tissue disorders. Artifacts from various sources, including patient movement and metal implants, hinder evaluation. Software

Figure 3.33  Axial computed tomography cut of distal radioulnar joint in neutral position shows dorsal subluxation of the left joint (right image). This can be quantified by the use of indices.

techniques can be used to limit these artifacts, but often at the cost of resolution at the site of interest.66 The usefulness of CT is often enhanced when coupled with volume-rendering techniques. These allow clearer imaging of subtle fractures and complex injuries. They are also helpful in the evaluation of suspected infections or neoplastic disease. After operative fixation of fractures, volume rendering can improve the quality of imaging by eliminating streak artifacts.67 Using intravenous contrast, CT angiography can be performed (see section on vascular imaging techniques for the upper extremity, below).

Magnetic resonance imaging MRI of the hand and wrist has come to the forefront in the last decade. It is the preferred modality for imaging soft tissue, particularly those associated with trauma and neoplastic conditions. Larger and more powerful magnets, improved

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Table 3.4  Advantages and disadvantages of magnetic resonance imaging (MRI)

Advantages

Disadvantages

• Capacity to image in any anatomic plane (multiplanar imaging) • High soft-tissue contrast with indication of tissue composition • No ionizing radiation • Acquisition of three-dimensional volume data using gradient echo sequences • Non-invasive imaging of blood vessels and other structures without the use of contrast (e.g., MR arthrography)

• The high cost of equipment • Image artifacts from motion and ferromagnetic objects • Inferior to computed tomography for imaging of cortical bone • Contraindicated in patients with cardiac pacemakers, aneurysm clips, metallic foreign body, claustrophobia

gradient strength and speed, dedicated coils providing favorable signal-to-noise ratios, and the capability of supporting small fields of view enable visualization of pathology in exquisite anatomic detail. The advantages and disadvantages of MRI are shown in Table 3.4.

MRI basics MRI employs magnetic fields and radiowaves rather than ionizing radiation. The magnetic field is generated by an electromagnetic coil with field strengths ranging from 1.5 to 3.0 Tesla (T) (15,000–30,000 gauss). Gradient (secondary) magnets finetune and focus the MRI on specific areas of interest. MRI coils send and receive radiofrequency pulses that are used to create images. In general, the smaller the coil and the more centrally located an anatomic structure is within the coil, the sharper the image and the higher the signal-to-noise ratio. MR differentiates tissues such as fat, muscle, bone, blood, and water on the basis of their innate magnetic characteristics and the varying tissue concentration of hydrogen ions (protons). Each proton spins like a top, around an axis. In the absence of a magnetic field, their axes are randomly oriented and produce no net magnetic effect. In the MRI scanner, the magnetic field generated causes the axes of rotation of the protons to align themselves with the longitudinal axes of the magnet. Gradient magnets change the alignment of the rotating protons whilst radiofrequency pulses from the coils excite the protons to a higher energy level. Cessation of radiofrequency stimulation induces a tiny current within the surrounding coil which can be detected and amplified to give a signal. The time taken for a proton to become magnetized is known as the T1 relaxation time and the time taken for the proton to be demagnetized is known as the T2 relaxation time. The amount of energy released by a tissue is directly proportional to its concentration of protons. It is also the varying concentration of protons between different tissues that allows them to be magnetized and demagnetized differentially. This is the basis of differentiating the soft tissues. The relevant signals of different tissues on T1- and T2weighted images are shown in Table 3.5. Water can be categorized into free water and bound water. Free water is found mostly in extracellular fluid whilst bound water is mostly in intracellular fluid. Free water has long

Table 3.5  Signal intensities of tissues on T1- and T2-weighted magnetic resonance images

Tissue

Signal T1weighted image

Signal T2weighted image

Fluid (free water)

Low

High

Fluid (proteinaceous)

Intermediate

High

Fat

High

High

Muscle

Intermediate

Intermediate

Cartilage

Intermediate

High

Cortical bone

Low

Low

Bone marrow (yellow)

High

Intermediate

Bone marrow (red)

Low

Intermediate

T1 and T2 relaxation times. Hence it typically shows low signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Water that is not free is usually bound to proteins which inhibit motion. This preferentially shortens the T1 relaxation time more than the T2 relaxation time, hence the T1 signal is usually of intermediate to high intensity. Examples of proteinaceous fluid include abscesses, synovial fluid, and purulent collections.

Clinical applications of MRI MRI for soft-tissue masses MRI is the preferred modality for imaging soft-tissue masses in the hand and wrist. The majority of soft-tissue masses in the hand and wrist are benign.68 MRI characteristics of the common tumors are well described in literature and references.69–71 MRI, with its multiplanar imaging capability, tissue characterization of lesions, and ability to define relationship of lesions to surrounding tissue and vessels (including tumor invasion), allows one in many circumstances to arrive at a ­specific diagnosis.

Ganglion cysts Ganglia show low to intermediate signals on T1-weighted images and high signals on T2-weighted images. They may be uniloculated or multiloculated and contain proteinaceous synovial fluid. This accounts for its isointense or slightly hypointense signal on T1-weighted images compared to muscle (Fig. 3.34). Demonstration of a stalk can usually reveal its site of origin. Hemorrhage into a ganglion cyst can result in high signal intensity on T1-weighted images. A ganglion shows no enhancement on administration of intravenous gadolinium; however, its capsule and septa will usually show enhancement. Ganglion cysts occurring in “classic” locations such as the dorsum of the wrist can usually be diagnosed clinically and do not require MRI. However, MRI is especially useful to locate occult ganglion cysts too small to palpate.

Giant cell tumors of the tendon sheath (GCTTS) Synonymous with focal pigmented villonodular synovitis, these benign tumors of synovial origin typically occur in the digits

Magnetic resonance imaging

A

87

B

Figure 3.34  This patient presented with a firm mass in the left thenar eminence that was difficult to characterize clinically. Radiographs were normal. (A) Magnetic resonance imaging shows a mass with typical high signal intensity during the T2-weighted sequence. (B) A sagittal fat suppression short tau inversion recovery sequence shows the stalk of the ganglion connecting to the sheath of the flexor carpi radialis (indicative arrow) with the scaphoid (S) in close relation.

A

B

Figure 3.35  This man presented with a firm painless enlarging mass over the dorsum of the left hand. Magnetic resonance imaging shows a low signal intensity mass over the third carpometacarpal junction, seen on (A) sagittal T1-weighted sequence and (B) axial T2-weighted sequence.

over the volar aspect, and arise from the tendon sheath, joint capsule, fascia, or ligaments. They contain multinucleated giant cells and have intra- and extracellular hemosiderin deposition. On MRI, GCTTS appear as solid masses, hypointense on both T1and T2-weighted images. The low signal is due to the paramagnetic effect of hemosiderin deposition. On T1-and T2-weighted images, these masses appear isointense with skeletal muscle.

Uniform enhancement is seen following administration of intravenous gadolinium contrast (Fig. 3.35).

Lipomas Lipomas are less common in the hand and wrist than in other parts of the body. In the hand, they usually occur over the

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palmar aspect, either in the thenar or hypothenar eminence or in the mid-palmar space. They show the same homogeneous high signal intensity as fat on T1-weighted images and superficial lipomata can appear inconspicuous. They show low signals on short tau inversion recovery (STIR) and T2-weighted sequences. The presence of distinct nodules or solid components may suggest a liposarcoma.

Hemangiomas Hemangiomas are benign tumors classified into capillary, cavernous, and venous types. T1-weighted signal intensity varies from low, to high, depending on the amount of fat contained. On T2-weighted sequences, they tend to be lobulated with well-­defined borders and very high signal intensity from pooled blood. A lace-like pattern of enhancement may be seen on T1-weighted images due to fibrofatty elements. Signal voids may be present on all MR sequences as a consequence of phleboliths within the hemangiomas. The heterogeneous nature of hemangiomas thus makes preoperative diagnosis by MRI less certain.68

Enchondromas Enchondromas are the most common benign tumors of bone that are found in the hand. Problems associated with enchondromas are pathological fractures and the rare occurrence of malignant transformation. Radiography demonstrates a lytic expansile lesion with a clear zone of transition and speckled calcifications. Cortical thinning is present and may be associated with a pathological fracture. On MRI, they appear as high-signal-intensity lobulated tumors on fat suppression (FS) STIR and T2-weighted sequences. They show low to intermediate signal intensity on T1-weighted sequences.

MRI for wrist and hand trauma This application of MRI has become more widespread in the last two decades, in particular for ligamentous injuries. A further advantage of MRI is its superior imaging of bone marrow and vascularity of bone with a wide range of applications, including diagnosing AVN, marrow edema, and inflammation, as well as infection.

Occult scaphoid and carpal fractures MRI is the most sensitive and specific imaging modality for occult scaphoid fractures, although its cost may be greater or equitable compared to the classic diagnostic algorithm.72,73 An area of a linear band of low signal intensity on T1-weighted sequences, coupled with an area of high signal intensity on FS T2-weighted sequences or STIR sequences, has the highest combined sensitivity and specificity. Cortical fracture lines are best seen on a STIR or gradient echo (GRE) sequence. Use of MRI for diagnosis of radiographically occult fractures is not limited to the scaphoid, but includes other carpal bone fractures which are difficult to image on radiography.18 The added value of using MRI for detection of occult carpal bone fractures is that it also demonstrates ligament injuries which can clinically mimic carpal fractures (Fig. 3.36). Bone bruising, a term synonymous with bone contusion, exhibits exactly the same MRI findings as occult fractures do with the exception of a cortical break. This diagnosis

Figure 3.36  This patient presented with persistent dorsoradial-sided wrist pain after a fall. He had initially been seen by a general practitioner and diagnosed as having a sprain. Magnetic resonance imaging coronal fast spin echo proton density sequences with fat suppression showed two areas (white arrows) of high signal intensity in the scaphoid proximal pole and waist (associated with fracture). The signal enhancement in the proximal pole is due to an injury of the scapholunate ligament, noting a normal ligamentous structure of the lunotriquetral ligament (black arrow).

is made in the setting of a positive history of p ­ receding trauma and positive MRI findings, as described above.

Ligamentous injuries of the hand and wrist Suspected ligamentous injures of the hand and wrist are probably the most common indication for ordering an MRI. SL and LT ligament tears as well as tears of interphalangeal or metacarpophalangeal joint ligaments are frequent clinical problems. Another large group of wrist conditions – ulnar-sided wrist pain, including but not limited to tears of the TFCC, ulnocarpal abutment, DRUJ, and tendinitis – is considered separately in the next section. An intact ligament is shown as a homogeneous black signal or band on a proton density-weighted GRE sequence or a T1-weighted spin echo sequence on coronal slices. An abnormal ligament shows increased signal intensity on T2-weighted sequences or STIR sequences, segmental defect, increased length, thickening, thinning, and nonvisualization.74 MR arthrography can be performed with saline or dilute gadolinium injected into the joint, enhancing the detection of ligaments and TFCC perforations.

Thumb ulnar collateral ligament injuries A poorly treated complete tear of the ulnar collateral ligament of the thumb metacarpophalangeal joint can lead to painful and chronic instability. MRI is valuable in assessing for complete ligamentous disruption, a diagnosis that may be difficult to make in early or acute presentations (Fig. 3.37). Such imaging helps exclude a Stener lesion, where the adductor aponeurosis becomes interposed between the two ends of the ruptured ligament, preventing ligament healing.

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89

commonest cause of carpal instability. Early recognition of SL instability allows treatment and prevention of late arthritis. Features which support a tear of the SL ligament include widening of the SL interval, fluid signal traversing the SL or LT ligaments on the fat-suppressed fast spin echo (FSE) T1weighted sequence, or STIR sequence (Fig. 3.38). Proton density sequences as well as T2-weighted sequences with FS can also reveal morphological abnormalities and absence of the SL ligament. The same criteria also apply for evaluating the less common LT ligament injuries.

MRI for evaluating ulnar-sided wrist pain Ulnar-sided wrist pain is a common and challenging problem. Causes of ulnar-sided wrist pain include injuries to the TFCC, LT ligament injuries, and ulnocarpal abutment syndrome. Other diagnoses include fractures and non-union of fractures, especially of the ulnar styloid, DRUJ problems, and tendinopathies.

TFCC tears A

Scapholunate interosseous ligament injury

TFCC injuries are classified into two groups: those occurring acutely and degenerative lesions. In the latter group, lesions occur in the central portion of the TFCC and the incidence increases with advancing age. Acute traumatic tears of the TFCC usually occur following a forced axial load of the wrist in an extended and ulnar-deviated position. Acute tears of the TFCC resulting in detachment from the fovea or detachment from its radial border can result in DRUJ instability. The gold standard for evaluation of TFCC injuries is arthroscopy. MRI has been increasingly used for imaging the TFCC. The sequence which best demonstrates the TFCC is the FS FSE T1-weighted and GRE T2 sequence.75 GRE sequences which mimic FS FSE T1-weighted sequences such as the proton density-weighted GRE sequence depicts TFCC disruptions even more distinctly (Fig. 3.39). With the advent of 3.0-T MRI machines, the sensitivity and specificity of MRI for detection of TFCC lesions exceed that of 1.5-T machines.76,77

Ulnocarpal abutment

B

Figure 3.37 This 15-year-old girl presented with pain at the ulnar aspect of the metacarpophalangeal joint of her right thumb after an abduction injury from a fall. Plain posteroanterior and lateral radiographs showed no abnormalities. Clinical assessment for joint instability was difficult because of her anxiety and pain and a magnetic resonance imaging scan was performed. The coronal fast spin echo proton density sequence, a variant form of gradient echo sequences, reveals a distal avulsion/rupture (A) of the ulnar collateral ligament (black arrow). The radial collateral ligament on the other hand is intact and smoothly inserts or joins the base of the proximal phalanx of the thumb. (B) The short tau inversion recovery sequence shows bright signal intensity (black arrow) at the site of rupture seen on the proton density sequence, correlating with an acute tear or rupture of the ligament.

This is the most common intrinsic wrist ligament injury. Presentations vary from occult SL joint ganglions, dynamic SL instability, to static SL dissociation. SL dissociation is the

This is a degenerative condition related to excessive load-bearing across the ulnar side of the wrist. An ulna positive variance may be present. Radiography may be normal or may show subchondral cyst formation in the lunate and/or triquetrum. Stress films can demonstrate dynamic increase in ulnar length relative to the radius (pronated grip film of the wrist). MRI shows foci of low signal intensities in the lunate and triquetrum and occasionally in the ulnar head, reflecting chondromalacia. On FS STIR or FS T2-weighted sequences, these same areas show bright signal intensities from bone marrow edema or secondary to the presence of cyst formation (Fig. 3.40).

DRUJ instability and tendinopathies CT is the preferred imaging modality for DRUJ instability and subluxation. MRI, however, allows visualization of the ligaments and the insertion of the TFCC into the fovea, which contributes to stability of the DRUJ. Furthermore, high signal intensities on FS STIR sequence will suggest reactive marrow edema from persistent DRUJ instability and synovitis. The relationship of the ulnar head to the distal end of the radius and DRUJ subluxation is best assessed on an axial FSE

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A

B

Figure 3.38  This patient presented with right-sided wrist pain. He had tenderness over the scapholunate junction over the dorsum of the wrist. Radiography showed a normal scapholunate angle on lateral wrist projections and no widening of the scapholunate interval on posteroanterior projections of the wrist. Magnetic resonance imaging coronal fast spin echo proton density sequences with fat suppression (A) showed widening of the scapholunate (SL) interval (star) with absence of the membranous portion of the ligament. The membranous portion of the lunotriquetral (LT) ligament is intact (white arrow). The next sequence (B) shows a more dorsal section of the proximal carpal row with an intact LT ligament (black arrow) and disrupted SL ligament with abnormal fluid signal traversing it and a thickened and fibrillar morphology (white arrow).

A

B

Figure 3.39  This 27-year-old male presented with right ulnar-sided wrist pain of 1 year’s duration. There was a preceding history of a fall during rollerblading. Magnetic resonance imaging proton density-weighted sequences show that the portion of the triangular fibrocartilage (small arrow) that inserts into the fovea (big arrow) has been avulsed off its insertion (A). In a different patient, the triangular fibrocartilage with its insertion into the fovea preserved (white arrow) is shown (B). This patient had instead a scapholunate ligament injury.

T1-weighted sequence. A halo of high signal enhancement can be seen in tendinopathies on axial slices during an FS STIR sequence or an FS T2-weighted sequence. In addition, there may be thickening of the tendon and abnormal signal within the tendon itself on coronal slices.

MRI for evaluation of fracture nonunion Scaphoid fractures are prone to non-union. Radiography to assess for fracture healing lacks a high degree of sensitivity and specificity. The MRI criterion to assess union is the

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MRI for avascular necrosis (AVN) in scaphoid fracture non-union The proximal pole of the scaphoid is prone to AVN following a fracture due to its retrograde vascular axis pattern.79 Radiographs can show changes associated with AVN, including sclerosis of the proximal fragment, osseous absorption, and cysts. MRI can detect AVN at an earlier stage. Knowing the vascularity of the proximal fragment guides clinical decision-making, including whether to use vascularized or non-vascularized grafts. Low signal intensity of the proximal fragment on T1-weighted sequences indicates replacement of the normal marrow with fibrous tissue. High signal intensity of the proximal pole on gadolinium contrast-enhanced study suggests that vascularity is preserved. This finding has not been consistently proven in all studies, and the relative enhancement should be significantly greater than the surrounding carpal bones.78

Kienbock's disease A

presence on T1-weighted sequences of normal signal intensity

Idiopathic AVN of the lunate is relatively uncommon when compared with post-traumatic AVN of the scaphoid. A negative ulnar variance has been shown to be associated with an increased risk of Kienbock’s disease. MRI is of value in detecting early disease, prognosticating, and for monitoring revascularization of the lunate following treatment.80 AVN of the lunate is suggested by low signal intensity on T1-weighted sequence as marrow is replaced by fibrous tissue. Areas of high signal intensity may be seen on FS T2-weighted sequence or FSE FS STIR sequences, suggesting marrow edema or neovascularization (Fig. 3.41). Low signal intensity on such sequences likely indicates established ischemic necrosis without any further bone reactive changes.

Osteomyelitis

B

Figure 3.40  This patient presented with persistent right ulnar-sided wrist pain of 6 months’ duration and he complained of inability, in particular in hammering objects. He had tenderness over the ulnar fovea and a positive ulnocarpal grind. Plain film radiography (A) showed no fractures of the ulnar styloid. There was, however, a subchondral cyst seen in the proximal ulnar corner of the lunate (black arrow) and there was positive ulnar variance (white arrow). On magnetic resonance imaging, the fat suppression short tau inversion recovery sequence showed high signal intensity in the same corresponding area of the lunate (B). Note that the triangular fibrocartilage and the ulnar head (white arrows) show no signal enhancement which would typify more advanced involvement.

crossing the previous fracture line.78 Non-union is shown by the presence of high signal intensity at the fracture line on FS STIR or FS T2-weighted sequences or the GRE equivalents.

Osteomyelitis of the hand and wrist bones is relatively uncommon. It is usually a consequence of previous surgical intervention for fractures or other procedures. Traditionally, either scintigraphy or MRI has been used when plain film radiography has been negative in suspected osteomyelitis. MRI has the advantage of discriminating marrow abnormalities from joint and soft-tissue changes. Areas of marrow involvement will show low signal on T1-weighted sequence and high signal intensity on T2-weighted sequence.

Vascular imaging techniques for the upper extremity Digital subtraction angiography (DSA) is the gold standard for vascular imaging of the extremities.81,82 Improvements in CT angiography and magnetic resonance angiography (MRA) make them increasingly viable alternatives in vascular imaging of the upper extremity. Arterial imaging of the upper limb is usually performed in two different clinical settings: the detection of extremity vascular injury following trauma to the limb, and assessment of vascular disorders involving the upper limb. The indications for angiography following trauma are: decreased or absent pulse or blood pressure, cold limb, bruit

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A

B

Figure 3.41  A karate enthusiast presented with right wrist central dorsal pain of gradual onset that was associated with morning stiffness as well as weakness of grip over the passage of time. Radiography was normal aside from the suggestion of an area of faint linear sclerosis in the lunate. Magnetic resonance imaging fast spin echo T1-weighted sequence showed loss of normal marrow signal affecting the radial corner of the lunate (black arrow) (A). Fast spin echo fat suppression short tau inversion recovery sequences showed diffuse marrow enhancement (long white arrow), sparing only the proximal ulnar tip of the lunate (short white arrow) (B).

or murmur, uncontrolled bleeding or increasing hematoma, neurologic deficit, and proximity of the injury to vascular structures.83 When the clinical condition warrants immediate surgery, conventional angiography is contraindicated. Knife injuries (80%) and blunt trauma (67%) are more likely

to be associated with vascular abnormalities, followed by gunshot wounds (44%).83 DSA has a role in the assessment of the vascular tree in peripheral arteriosclerotic disease, connective tissue diseases, thoracic outlet syndrome, and Raynaud’s phenomenon. It is also useful for assessing arteriovenous fistulas and vascular tumors and malformation of the upper limb. CT angiography (CTA) is less invasive than DSA and can additionally assess vessel wall and extraluminal pathology. The data obtained allow reconstruction in three-dimensional and multiple planes. The advancements in CT technology, new protocols, and availability of CTs in proximity of many emergency departments have made CTA an increasingly attractive option for the assessment of the extremity vascular tree following trauma.84,85 In extremity trauma, CTA can identify arterial injuries, including pseudoaneurysm, active arterial hemorrhage, arteriovenous fistulas, occlusion, intimal injury, or vasospasm.86 Venous injury may also be assessed. CTA has also been shown to be useful in the evaluation of suspected extremity vascular trauma in pediatric patients.87 In pediatric patients, CTA allows imaging of the vascular tree where DSA is often not possible. The indications for CTA are similar to that of DSA. There are limitations with use of CTA for evaluation following trauma. For example, differentiation of a tapered contour deformity of CTA, which may variously represent dissection, intimal injury, vasospasm, or adjacent hematoma, is difficult.84 Imaging of the distal vascular tree is also difficult. DSA also offers an advantage where there is a possibility of endo­ vascular treatment, for example in an arteriovenous fistula. The sensitivity and specificity of CT arteriography have been shown to be 95.1% and 98.7% in cases of suspected vascular injury following blunt or penetrating injury.88 MRA offers advantages over conventional DSA for extremity vascular imaging. MRA is less invasive, does not require iodinated contrast, and can simultaneously demonstrate extraluminal disease.89 The angiographic effect in MRA is created by various techniques with or without contrast enhancement with gadolinium chelate agent. The use of contrast-enhanced MRA with a dedicated surface coil enables quick and highquality examination of the hand vascular tree.90 MRA of the wrist and hand has a potential number of indications for its use and has been employed successfully in imaging of vascular malformations, vascular trauma, and vascular occlusion. MRA is performed making use of a coronal volume three-dimensional spoiled GRE time-of-flight sequence and dynamic administration of intravenous gadolinium contrast with image acquisition using a wrist coil. The inherent contrast from protons in flowing blood relative to the saturated protons in the stationary soft tissue produces the image which is formulated based on an MR algorithm which deletes the signal from the soft tissue. MRA has the potential to depict pathologic change in vessels of up to 1 mm in diameter and can reliably show the superficial and deep palmar arches of the hand (Fig. 3.42). Some of the disadvantages of MRA include the inferior resolution of vasculature at 1 mm diameter or less, susceptibility to motion artifacts, as well as flow artifacts at sites of severe stenosis or thrombosis where a high signal intensity91 may be mistaken for flowing blood. MRA is useful in patients with renal impairment where intravascular ionic contrast could cause further nephrotoxic damage, as well as in pediatric patients.

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imaging is its lack of specificity. This is because the tracers used reflect function. The imaging detail required to differentiate physiological and pathological processes is often lacking in these scans. Therefore, it is most useful as a screening tool. The most common radionuclide musculoskeletal imaging is bone scintigraphy with technetium-99m-labelled diphosphonates. The three-phase bone scan is highly sensitive for osteomyelitis. However, similar findings can be mimicked by conditions such as tumors, fractures, and joint neuropathy. The use of indium-111-labeled autologous leukocytes can improve its specificity.91 Bone scintigraphy is also useful for diagnosis of complex regional pain syndrome (reflex sympathetic dystrophy),93 occult fractures of the scaphoid,94 and metastatic disease.95 Newer modalities, such as the combination of scinti­graphy with morphologic information, e.g., single-photon emission CT/CT can improve diagnostic yields in the extremity.96

Safety in fluoroscopy A

B

Figure 3.42  This 23-year-old female had a previous excision of arteriovenous malformation more than 5 years ago and now presents with skin changes suggestive of recurrence. Magnetic resonance angiography delineates the palmar arch well and in addition shows blushes of bright signal intensity over the thumb pulp, the first web area, and over the index finger (A). This correlated well with the pigmented changes (arrowed) seen on the clinical photo (B).

Radionuclide imaging Radionuclide imaging is a highly sensitive imaging modality92 with applications in hand and wrist conditions. It can be positive even when conventional imaging techniques are unable to visualize the condition. The main limitation of radionuclide

Fluoroscopy is a powerful imaging tool allowing operative and dynamic assessment of the bones and joints of the hand. As the surgeon is often the operator of the machine, this causes exposure to both direct and scattered radiation. Such radiation exposure is an occupational risk, with potential serious effects. There was a report suggesting an increased cancer risk in orthopedic surgeons working in an institution with poor compliance to use of radiation protective measures when working with standard C-arm devices.97 Another study found a 1.9-fold increased prevalence of cancer and 2.9-fold increased prevalence of breast cancer in female orthopedic surgeons when compared with the women of similar age and race.98 Radiation exposure is directly related to the distance from the X-ray source. This relationship is described by the inverse square law. In practical terms, a doubling of the distance from the source reduces the exposure 4 times. Conversely, a halving of the distance results in a four-fold increase in radiation exposure. Some basic knowledge and precautions will minimize radiation to the worker during its operation (Box 3.5). The choice of fluoroscopy affects the potential radiation exposure. Compared to conventional fluoroscopy, mini C-arm fluoroscopy has been shown to emit about half the radiation exposure.99 However, if the surgeon places his or her hand in the path of the X-ray beam during intraoperative use of the mini C-arm, there is a decreased source-to-skin distance resulting in higher radiation exposure to the hand than when using the standard C-arm.2,100 While the mini C-arm fluoroscopy has been widely adopted in hand surgery, we need to exercise caution during its use to ensure safety of both the surgeon and the patient.

Future directions – Artificial Intelligence in radiology and point of care imaging The application of Artificial Intelligence (AI) is the next big leap in medical radiology following digitalization. Virtual fluoroscopy and software to optimize image acquisition speed and positioning of an intraoperative C-arm would mitigate the radiation risks associated with fluoroscopy.101 AI image interpretation is the domain of keenest interest to clinicians,

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BOX 3.5  Methods to reduce radiation exposure Increasing the distance between the personnel and the source of radiation is key, as it has been shown that the rate of radiation exposure drops significantly beyond the path of the radiation beam and is minimal beyond 15 cm from the point of focus on the image intensifier.99 1. Increasing distance from radiation source • Placement of the limb directly on the image intensifier (when using mini C-arms) • Uninvolved personnel to position themselves away from the radiation source 2. Shielding • Lead gowns • Lead-lined operating rooms • Protective goggles • Radiation attenuation gloves for operators placing their hands near radiation source • Shielding for anaesthetists and patients 3. Minimizing radiation use • Increasing accuracy of fluoroscopy by using laser beams • Collimation • Avoiding long exposure time

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and remarkable strides have been made in this area. There is already good evidence showing that intelligent systems perform as well as clinicians in diagnosis of fractures and other musculoskeletal conditions.102,103 It is a matter of when rather than whether these systems will enter clinical use, initially to support physician reporting, but possibly supplanting it in some use cases. AI’s influence on radiology will extend to other use cases that affect clinical care. These domains include decision systems to help physicians order the right radiological examinations and radiologists use the right protocol. AI will also feature greatly in emerging areas as such radiomics and quantitative image analysis.104 Point-of-care imaging, often acquired and interpreted by the clinician, is being increasingly used. This marks a swing towards decentralization of some radiology services. In musculoskeletal imaging, ultrasound is most ready for this shift, but the other imaging modalities, including the portable MRI and nuclear imaging may follow.105 Ultrasound has already been shown to be cost effective in different clinical settings (Acebes, Van Schaik).106,107 Increasing portability, sophistication and affordability of the equipment will accelerate this trend of point-of-care imaging. To capture the most value from these trends, training, of both of the clinician and support staff, and a re-design of clinical operations will be necessary.

References

References 1. Sofka CM, Pavlov H. The history of clinical musculoskeletal radiology. Radiol Clin North Am. 2009;47(3):349–356. 2. Vosbikian MM, Ilyas AM, Watson DD, Leinberry CF. Radiation exposure to hand surgeons’ hands: a practical comparison of large and mini C-arm fluoroscopy. J Hand Surg Am. 2014;39(9): 1805–1809. 3. Peh WC. Modern imaging of the musculoskeletal system: is there still a role for radiography? Singapore Med J. 2002;43(8):385–386. 4. Fisher MR, Rogers LF, Hendrix RW. Systematic approach to identifying fourth and fifth carpometacarpal joint dislocations. AJR Am J Roentgenol. 1983;140(2):319–324. 5. Parkinson RW, Paton RW. Carpometacarpal dislocation: an aid to diagnosis. Injury. 1992;23(3):187–188. 6. Gurland M. Carpometacarpal joint injuries of the fingers. Hand Clin. 1992;8(4):733–744. 7. Chong AK, Chew WY. An isolated ring finger metacarpal shaft fracture?--beware an associated little finger carpometacarpal joint dislocation. J Hand Surg Br. 2004;29(6):629–631. 8. Lane CS. Detecting occult fractures of the metacarpal head: the Brewerton view. J Hand Surg Am. 1977;2(2):131–133. 9. Eaton RG, Littler JW. Ligament reconstruction for the painful thumb carpometacarpal joint. J Bone Joint Surg Am. 1973;55(8):1655–1666. 10. Ebrahim FS, De Maeseneer M, Jager T, Marcelis S, Jamadar DA, Jacobson JA. US diagnosis of UCL tears of the thumb and Stener lesions: technique, pattern-based approach, and differential diagnosis. Radiographics. 2006;26(4):1007–1020. 11. Hergan K, Mittler C, Oser W. Ulnar collateral ligament: differentiation of displaced and nondisplaced tears with US and MR imaging. Radiology. 1995;194(1):65–71. 12. Gilsanz VRO. Indicators of Skeletal Maturity in Children and Adolescents. New York: Springer-Verlag; 2005. 13. Chew EM, Chong AK. Hand fractures in children: epidemiology and misdiagnosis in a tertiary referral hospital. J Hand Surg Am. 2012;37(8):1684–1688. 14. Salter RB. Injuries of the epiphyseal plate. Instr Course Lect. 1992;41:351–359. 15. Levis CM, Yang Z, Gilula LA. Validation of the extensor carpi ulnaris groove as a predictor for the recognition of standard posteroanterior radiographs of the wrist. J Hand Surg Am. 2002;27(2):252–257. 16. Yang Z, Mann FA, Gilula LA, Haerr C, Larsen CF. Scaphopisocapitate alignment: criterion to establish a neutral lateral view of the wrist. Radiology. 1997;205(3):865–869. 17. Gilula LA. Carpal injuries: analytic approach and case exercises. AJR Am J Roentgenol. 1979;133(3):503–517. 18. Peh WC, Gilula LA. Normal disruption of carpal arcs. J Hand Surg Am. 1996;21(4):561–566. 19. Bouman HW, Messer E, Sennwald G. Measurement of ulnar translation and carpal height. J Hand Surg Br. 1994;19(3):325–329. 20. McMurtry RY, Youm Y, Flatt AE, Gillespie TE. Kinematics of the wrist. II. Clinical applications. J Bone Joint Surg Am. 1978;60(7):955–961. 21. Kristensen SS, Thomassen E, Christensen F. Ulnar variance determination. J Hand Surg Br. 1986;11(2):255–257. 22. Palmer AK. Triangular fibrocartilage disorders: injury patterns and treatment. Arthroscopy. 1990;6(2):125–132. 23. Steyers CM, Blair WF. Measuring ulnar variance: a comparison of techniques. J Hand Surg Am. 1989;14(4):607–612. 24. Shin AY, Deitch MA, Sachar K, Boyer MI. Ulnar-sided wrist pain: diagnosis and treatment. Instr Course Lect. 2005;54:115–128. 25. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26(5):908–915. 26. Thomas AD, Greenberg JA. Use of fluoroscopy in determining screw overshoot in the dorsal distal radius: a cadaveric study. J Hand Surg Am. 2009;34(2):258–261.

94.e1

27. Maschke SD, Evans PJ, Schub D, Drake R, Lawton JN. Radiographic evaluation of dorsal screw penetration after volar fixed-angle plating of the distal radius: a cadaveric study. Hand (N Y). 2007;2(3):144–150. 28. Badman BL, Rill L, Butkovich B, Arreola M, Griend RA. Radiation exposure with use of the mini-C-arm for routine orthopaedic imaging procedures. J Bone Joint Surg Am. 2005;87(1):13–17. 29. Kwon BC, Baek GH. Fluoroscopic diagnosis of scapholunate interosseous ligament injuries in distal radius fractures. Clin Orthop Relat Res. 2008;466(4):969–976. 30. Bain GI, Hunt J, Mehta JA. Operative fluoroscopy in hand and upper limb surgery. One hundred cases. J Hand Surg Br. 1997;22(5):656–658. 31. Wong DC, Wansaicheong GK, Tsou IY. Ultrasonography of the hand and wrist. Singapore Med J. 2009;50(2):219–225. quiz 226. 32. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: part 1. Fundamentals. PM R. 2009;1(1):64–75. 33. Teh J. Ultrasound of soft tissue masses of the hand. J Ultrason. 2012;12(51):381–401. 34. Diop AN, Ba-Diop S, Sane JC, et al. [Role of US in the management of de Quervain’s tenosynovitis: review of 22 cases]. J Radiol. 2008;89(9 Pt 1):1081–1084. 35. Guerini H, Pessis E, Theumann N, et al. Sonographic appearance of trigger fingers. J Ultrasound Med. 2008;27(10):1407–1413. 36. Bodor M, Flossman T. Ultrasound-guided first annular pulley injection for trigger finger. J Ultrasound Med. 2009;28(6):737–743. 37. Kuo LC, Su FC, Tung WL, Lai KY, Jou IM. Kinematical and functional improvements of trigger digits after sonographically assisted percutaneous release of the A1 pulley. J Orthop Res. 2009;27(7):891–896. 38. Renoux J, Zeitoun-Eiss D, Brasseur J-L. Ultrasonographic study of wrist ligaments: review and new perspectives. Semin Musculoskelet Radiol. 2009;13(01):055–065. 39. Keogh CF, Wong AD, Wells NJ, Barbarie JE, Cooperberg PL. High-resolution sonography of the triangular fibrocartilage: initial experience and correlation with MRI and arthroscopic findings. Am J Roentgenol. 2004;182(2):333–336. 40. Melville D, Jacobson JA, Haase S, Brandon C, Brigido MK, Fessell D. Ultrasound of displaced ulnar collateral ligament tears of the thumb: the Stener lesion revisited. Skeletal Radiol. 2013;42(5):667–673. 41. Beekman R, Visser LH. Sonography in the diagnosis of carpal tunnel syndrome: A critical review of the literature. Muscle & Nerve. 2003;27(1):26–33. 42. Pastare D, Therimadasamy AK, Lee E, Wilder-Smith EP. Sonography versus nerve conduction studies in patients referred with a clinical diagnosis of carpal tunnel syndrome. J Clin Ultrasound. 2009;37(7):389–393. 43. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: part 2. Clinical applications. PM R. 2009;1(2):162–177. 44. Connolly DJA, Berman L, McNally EG. The use of beam angulation to overcome anisotropy when viewing human tendon with high frequency linear array ultrasound. Br J Radiol. 2001;74(878):183–185. 45. Gellhorn AC, Carlson MJ. Inter-rater, intra-rater, and inter-machine reliability of quantitative ultrasound measurements of the patellar tendon. Ultrasound Med Biol. 2013;39(5):791–796. 46. Choi YJ, Baek JH, Park HS, et al. A computer-aided diagnosis system using artificial intelligence for the diagnosis and characterization of thyroid nodules on ultrasound: initial clinical assessment. Thyroid. 2017;27(4):546–552. 47. European Society of Radiology. ESR statement on portable ultrasound devices. Insights Imaging. 2019;10(1):89. 48. Zumsteg JW, Ina JG, Merrell GA. Evaluation of the acquisition of ultrasound proficiency in hand surgery fellows. J Ultrasound Med. 2019;38(8):2111–2117. 49. Brookes-Fazakerley S, Kumar A, Oakley J. Survey of the initial management and imaging protocols for occult scaphoid fractures in UK hospitals. Skeletal Radiology. 2009;38(11):1045–1048. 50. Memarsadeghi M, Breitenseher MJ, Schaefer-Prokop C, et al. Occult scaphoid fractures: comparison of multidetector CT and MR imaging – initial experience. Radiology. 2006;240(1):169–176.

94.e2

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51. Dias JJ. Definition of union after acute fracture and surgery for fracture nonunion of the scaphoid. J Hand Surg. 2001;26(4):321–325. 52. Dias J, Taylor M, Thompson J, Brenkel I, Gregg P. Radiographic signs of union of scaphoid fractures. An analysis of inter-observer agreement and reproducibility. J Bone Joint Surg Br. 1988;70-B(2):299–301. 53. Sanders WE. Evaluation of the humpback scaphoid by computed tomography in the longitudinal axial plane of the scaphoid. J Hand Surg Am. 1988;13(2):182–187. 54. Lozano-Calderon S, Blazar P, Zurakowski D, Lee S-G, Ring D. Diagnosis of scaphoid fracture displacement with radiography and computed tomography. J Bone Joint Surg Am. 2006;88(12):2695–2703. 55. Kaewlai R, Avery LL, Asrani AV, Abujudeh HH, Sacknoff R, Novelline RA. Multidetector CT of carpal injuries: anatomy, fractures, and fracture-dislocations. Radiographics. 2008;28(6):1771–1784. 56. Cole RJ, Bindra RR, Evanoff BA, Gilula LA, Yamaguchi K, Gelberman RH. Radiographic evaluation of osseous displacement following intra-articular fractures of the distal radius: reliability of plain radiography versus computed tomography. J Hand Surg Am. 1997;22(5):792–800. 57. Slagel BE, Luenam S, Pichora DR. Management of post-traumatic malunion of fractures of the distal radius. Hand Clin. 2010;26(1):71–84. 58. Athwal GS, Ellis RE, Small CF, Pichora DR. Computer-assisted distal radius osteotomy. J Hand Surg Am. 2003;28(6):951–958. 59. Murase T, Oka K, Moritomo H, Goto A, Yoshikawa H, Sugamoto K. Three-dimensional corrective osteotomy of malunited fractures of the upper extremity with use of a computer simulation system. J Bone Joint Surg Am. 2008;90(11):2375–2389. 60. Mino DE, Palmer AK, Levinsohn EM. The role of radiography and computerized tomography in the diagnosis of subluxation and dislocation of the distal radioulnar joint. J Hand Surg Am. 1983;8(1):23–31. 61. Mino DE, Palmer AK, Levinsohn EM. Radiography and computerized tomography in the diagnosis of incongruity of the distal radio-ulnar joint. A prospective study. J Bone Joint Surg Am. 1985;67(2):247–252. 62. Wechsler RJ, Wehbe MA, Rifkin MD, Edeiken J, Branch HM. Computed tomography diagnosis of distal radioulnar subluxation. Skeletal Radiol. 1987;16(1):1–5. 63. Lo IK, MacDermid JC, Bennett JD, Bogoch E, King GJ. The radioulnar ratio: a new method of quantifying distal radioulnar joint subluxation. J Hand Surg Am. 2001;26(2):236–243. 64. Park MJ, Kim JP. Reliability and normal values of various computed tomography methods for quantifying distal radioulnar joint translation. J Bone Joint Surg Am. 2008;90(1):145–153. 65. Assoun J, Richardi G, Railhac JJ, et al. Osteoid osteoma: MR imaging versus CT. Radiology. 1994;191(1):217–223. 66. Barrett JF, Keat N. Artifacts in CT: recognition and avoidance. Radiographics. 2004;24(6):1679–1691. 67. Pretorius ES, Fishman EK. Volume-rendered three-dimensional spiral CT: musculoskeletal applications. Radiographics. 1999;19(5):1143–1160. 68. Capelastegui A, Astigarraga E, Fernandez-Canton G, Saralegui I, Larena JA, Merino A. Masses and pseudomasses of the hand and wrist: MR findings in 134 cases. Skeletal Radiol. 1999;28(9):498–507. 69. Peh WC, Truong NP, Totty WG, Gilula LA. Pictorial review: magnetic resonance imaging of benign soft tissue masses of the hand and wrist. Clin Radiol. 1995;50(8):519–525. 70. Teh J, Whiteley G. MRI of soft tissue masses of the hand and wrist. Br J Radiol. 2007;80(949):47–63. 71. Ergun T, Lakadamyali H, Derincek A, Tarhan NC, Ozturk A. Magnetic resonance imaging in the visualization of benign tumors and tumor-like lesions of hand and wrist. Curr Probl Diagn Radiol. 2010;39(1):1–16. 72. Amrami KK. Magnetic resonance arthrography of the wrist: case presentation and discussion. J Hand Surg Am. 2006;31(4):669–672. 73. Jenkins PJ, Slade K, Huntley JS, Robinson CM. A comparative analysis of the accuracy, diagnostic uncertainty and cost of imaging modalities in suspected scaphoid fractures. Injury. 2008;39(7):768–774.

74. Steinbach LS, Smith DK. MRI of the wrist. Clin Imaging. 2000;24(5):298–322. 75. Nakamura T, Yabe Y, Horiuchi Y. Fat suppression magnetic resonance imaging of the triangular fibrocartilage complex. Comparison with spin echo, gradient echo pulse sequences and histology. J Hand Surg Br. 1999;24(1):22–26. 76. Anderson ML, Skinner JA, Felmlee JP, Berger RA, Amrami KK. Diagnostic comparison of 1.5 Tesla and 3.0 Tesla preoperative MRI of the wrist in patients with ulnar-sided wrist pain. J Hand Surg Am. 2008;33(7):1153–1159. 77. Magee T. Comparison of 3-T MRI and arthroscopy of intrinsic wrist ligament and TFCC tears. AJR Am J Roentgenol. 2009;192(1):80–85. 78. Karantanas A, Dailiana Z, Malizos K. The role of MR imaging in scaphoid disorders. Eur Radiol. 2007;17(11):2860–2871. 79. Gelberman RH, Gross MS. The vascularity of the wrist. Identification of arterial patterns at risk. Clin Orthop Relat Res. 1986;202:40–49. 80. Sowa DT, Holder LE, Patt PG, Weiland AJ. Application of magnetic resonance imaging to ischemic necrosis of the lunate. J Hand Surg Am. 1989;14(6):1008–1016. 81. McDonald Jr. EJ, Goodman PC, Winestock DP. The clinical indications for arteriography in trauma to the extremity. A review of 114 cases. Radiology. 1975;116(1):45–47. 82. Rieger M, Mallouhi A, Tauscher T, Lutz M, Jaschke WR. Traumatic arterial injuries of the extremities: initial evaluation with MDCT angiography. AJR Am J Roentgenol. 2006;186(3):656–664. 83. McCorkell S, Harley J, Morishima M, Cummings D. Indications for angiography in extremity trauma. Am J Roentgenol. 1985;145(6):1245–1247. 84. Shah N, Anderson SW, Vu M, Pieroni S, Rhea JT, Soto JA. Extremity CT angiography: application to trauma using 64-MDCT. Emerg Radiol. 2009;16(6):425–432. 85. Fishman EK, Horton KM, Johnson PT. Multidetector CT and three-dimensional CT angiography for suspected vascular trauma of the extremities. Radiographics. 2008;28(3):653–665. 86. Miller-Thomas MM, West OC, Cohen AM. Diagnosing traumatic arterial injury in the extremities with CT angiography: pearls and pitfalls. Radiographics. 2005;25(Suppl 1):S133–S142. 87. Hsu CS, Hellinger JC, Rubin GD, Chang J. CT angiography in pediatric extremity trauma: preoperative evaluation prior to reconstructive surgery. Hand (N Y). 2008;3(2):139–145. 88. Soto JA, Mãnera F, Morales C, et al. Focal arterial injuries of the proximal extremities: helical CT arteriography as the initial method of diagnosis. Radiology. 2001;218(1):188–194. 89. Stepansky F, Hecht EM, Rivera R, et al. Dynamic MR angiography of upper extremity vascular disease: pictorial review. Radiographics. 2008;28(1). e28-e28. 90. Connell DA, Koulouris G, Thorn DA, Potter HG. Contrastenhanced MR angiography of the hand. Radiographics. 2002;22(3):583–599. 91. Palestro CJ, Love C, Schneider R. The evolution of nuclear medicine and the musculoskeletal system. Radiol Clin North Am. 2009;47(3):505–532. 92. Love C, Din AS, Tomas MB, Kalapparambath TP, Palestro CJ. Radionuclide bone imaging: an illustrative review. Radiographics. 2003;23(2):341–358. 93. Wuppenhorst N, Maier C, Frettloh J, Pennekamp W, Nicolas V. Sensitivity and specificity of 3-phase bone scintigraphy in the diagnosis of complex regional pain syndrome of the upper extremity. Clin J Pain. 2010;26(3):182–189. 94. Beeres FJ, Rhemrev SJ, den Hollander P, et al. Early magnetic resonance imaging compared with bone scintigraphy in suspected scaphoid fractures. J Bone Joint Surg Br. 2008;90(9):1205–1209. 95. Hage WD, Aboulafia AJ, Aboulafia DM. Incidence, location, and diagnostic evaluation of metastatic bone disease. Orthop Clin North Am. 2000;31(4):515–528. vii. 96. Linke R, Kuwert T, Uder M, Forst R, Wuest W. Skeletal SPECT/CT of the peripheral extremities. AJR Am J Roentgenol. 2010;194(4):W329–335. 97. Mastrangelo G, Fedeli U, Fadda E, Giovanazzi A, Scoizzato L, Saia B. Increased cancer risk among surgeons in an orthopaedic hospital. Occup Med (Lond). 2005;55(6):498–500.

References

98. Chou LB, Cox CA, Tung JJ, Harris AH, Brooks-Terrell D, Sieh W. Prevalence of cancer in female orthopaedic surgeons in the United States. J Bone Joint Surg Am. 2010;92(1):240–244. 99. Athwal GS, Bueno Jr RA, Wolfe SW. Radiation exposure in hand surgery: mini versus standard C-arm. J Hand Surg Am. 2005;30(6):1310–1316. 100. Singer G, Herron B, Herron D. Exposure from the large C-arm versus the mini C-arm using hand/wrist and elbow phantoms. J Hand Surg Am. 2011;36(4):628–631. 101. De Silva T, Punnoose J, Uneri A, et al. Virtual fluoroscopy for intraoperative C-arm positioning and radiation dose reduction. J Med Imaging (Bellingham). 2018;5(1):015005. 102. Olczak J, Fahlberg N, Maki A, et al. Artificial intelligence for analyzing orthopedic trauma radiographs. Acta Orthop. 2017;88(6):581–586. 103. Jones RM, Sharma A, Hotchkiss R, et al. Assessment of a deeplearning system for fracture detection in musculoskeletal radiographs. NPJ Digit Med. 2020;3:144.

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104. Gyftopoulos S, Lin D, Knoll F, Doshi AM, Rodrigues TC, Recht MP. Artificial Intelligence in musculoskeletal imaging: current status and future directions. AJR Am J Roentgenol. 2019;213(3):506–513. 105. Iksung K. A portable, low-cost, 3D-printed main magnetic field system for magnetic imaging. Annu Int Conf IEEE Eng Med Biol Soc. 2017;2017:3533–3536. 106. Acebes C, Harvie JP, Wilson A, Duthie J, Bowen F, Steven M. Clinical usefulness and patient satisfaction with a musculoskeletal ultrasound clinic: results of a 6-month pilot service in a Rheumatology Unit. Rheumatol Int. 2016;36(12):1677–1681. 107. Van Schaik GWW, Van Schaik KD, Murphy MC. Point-of-care ultrasonography (POCUS) in a community emergency department: an analysis of decision making and cost savings associated with POCUS. J Ultrasound Med. 2019;38(8):2133–2140.

SECTION I  •  Principles of Hand Surgery

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

Access video content for this chapter online at Elsevier eBooks+

SYNOPSIS

ƒ Optimal perioperative anesthetic outcomes are achieved by a thorough understanding of anatomy, pharmacology, techniques, and potential complications. ƒ Local anesthetics (LA) make regional anesthesia possible by preventing the propagation of nerve conduction and by inhibiting or relieving pain. ƒ Ultrasound guidance in the use of regional anesthesia has decreased the need for high volumes of anesthetic. ƒ Use of wide-awake local anesthesia with no tourniquet (WALANT) techniques can help fast track upper extremity procedures in the operating room and clinic settings.

Introduction The goal of anesthesia for hand and upper extremity procedures is to provide a comfortable and safe experience for the patient during surgery. Many options are available for anesthesia, with respective benefits and risks. The decision regarding which anesthetic technique is chosen depends on various factors, including the extent, site, and expected duration of surgery; need for sedation; general medical health of the patient, and personal preference. General anesthesia techniques can be applied for hand and upper extremity procedures the same as for procedures elsewhere. In addition, regional anesthesia techniques can be applied for procedures involving the upper extremity when used in the proper setting and patient population. Adjunctive measures are used to augment local anesthetics to provide longer duration of action, lower risk of adverse systemic effects, and less bleeding at the surgical site. Optimal perioperative anesthetic outcomes are achieved by a thorough understanding of anatomy, pharmacology, techniques, potential complications, and general pain management.

Anatomy The brachial plexus arises from the ventral rami of nerves C5–8 and T1, with variable contributions from C4 and T2 (Fig. 4.1). These rami unite and diverge forming the roots, trunks, divisions, cords, and terminal nerves of the brachial plexus. C5 and C6 roots form the superior trunk, C7 becomes the middle trunk, and C8 and T1 form the inferior trunk between the anterior and middle scalene muscles. The three trunks then divide into anterior and posterior divisions, coursing over the first rib and lateral to the subclavian artery. The divisions then reunite to form cords. The anterior divisions of the superior and middle trunk form the lateral cord, while the anterior division of the inferior trunk forms the medial cord. The posterior divisions of all three trunks form the posterior cord. The cords are named according to their anatomic relationship with the axillary artery. The cords then divide once again to become the terminal branches of the brachial plexus. The lateral cord gives rise to the musculocutaneous nerve and contributes to the median nerve. The medial cord also contributes to the median nerve and gives rise to the ulnar nerve and the medial brachial and antebrachial cutaneous nerves. The posterior cord becomes the axillary and radial nerves.1 Additional nerves outside the brachial plexus can be important for complete anesthesia of the upper extremity. The supraclavicular nerve (C3–4) provides sensory innervation to the “cape” of the shoulder, and the intercostobrachial nerve (T2) innervates the skin of the medial upper arm and axilla. Knowledge of brachial plexus anatomy and the dermatomes supplied (Figs. 4.2 & 4.3) enables selective regional anesthesia.

Perineurial environment The axillary sheath is the connective tissue surrounding the neurovascular structures of the brachial plexus. It originates as a continuation of the prevertebral fascia and joins the fascia

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CHAPTER 4  • Anesthesia for upper extremity surgery

SECTION I

C5 C6 C7 C8 T1

ROOTS 3 TRUNKS DIVISIONS

from C4

3 Ventral 3 Dorsal

C5

3 CORDS

Suprascapular nerve R IO ER E P SU DDL MI IOR ER F IN

TERMINAL BRANCHES

RAL

LATE

C6 C7 C8 T1

PO

Radial nerve Median nerve

Radial nerve Median nerve

Long thoracic nerve

R STERIO

Axillary nerve

!st rib

Ulnar nerve

L

MEDIA

Ulnar nerve Subscapular nerve Thoracodorsal nerve Median cutaneous nerve of forearm Median cutaneous nerve of arm Musculocutaneous nerve

Figure 4.1  Brachial plexus anatomy.

Radial nerve

Median antebrachial cutaneous nerve Ulnar nerve

(posterior antebrachial cutaneous nerve)

(posterior (inferior Axillary nerve brachial lateral cutaneous cutaneous nerve) nerve)

Musculocutaneous nerve (lateral antebrachial cutaneous nerve) Radial nerve (superficial branch)

Radial nerve (inferior lateral brachial cutaneous nerve) Axillary nerve

Median nerve

Median nerve Radial nerve

Musculocutaneous nerve (lateral antebrachial cutaneous nerve) Intercostobrachial cutaneous nerve Supraclavicular nerve (cervical plexus)

(palmar branch) Ulnar nerve (palmar digital branch)

Intercostobrachial Median antebrachial cutaneous nerve and medial brachial cutaneous nerve Supraclavicular nerve (cervical plexus)

Figure 4.2  Upper extremity nerve innervation (arm pronated).

Figure 4.3  Upper extremity nerve innervation (arm supinated).

of the biceps and brachialis muscles distally. This connective tissue extends inward, forming septa between components of the plexus and creating fascial compartments for each nerve.2 Controversy exists regarding the ability of the septa to limit the spread of local anesthetics within the sheath. Some investigators report that these fascial compartments limit the

circumferential spread of local anesthetics and that injected solutions spread longitudinally up and down the nerve and remain compartmentalized. This concept provides a rational explanation for the occurrence of a rapid and profound block of one nerve, yet partial or absent block in other nerves during brachial plexus blockade.3 Other investigators propose that

Pharmacology of local anesthetics

these septa are incomplete and form small bubble-­like pockets when solution is injected. They found that single injections of dye solutions into the axillary sheath resulted in immediate staining of median, radial, and ulnar nerves, despite the presence of septa. These data demonstrate that there are connections between compartments within the sheath, and may explain why single injection techniques have success rates comparable with multiple injection techniques during blockade of the brachial plexus.4

Microneuroanatomy Peripheral nerves are composed of fascicles of individual nerve fibers surrounded by endoneurium. Groups of fascicles are contained within the epineurium. As the nerve travels away from the spinal cord, fascicle numbers increase, while fascicle size decreases.5 The nerve roots contain large fascicles, demonstrating a monofascicular or oligofascicular pattern, while a multifascicular pattern is found more distally.6,7 While the amount of neural tissue remains constant, the amount of non-­neural connective tissue increases from proximal to distal. The ratio of neural to non-­neural tissue changes from 1 : 1 in the proximal plexus to 1 : 2 in the more distal plexus.2,7 The presence of non-­ neural tissue may explain why injections within the epineurium rarely result in neural injury.6

Sonoanatomy The shape and echogenicity of a nerve determine its ultrasound appearance. Structures that strongly reflect ultrasound waves generate large signal intensities and appear white or hyperechoic. In contrast, hypoechoic structures weakly reflect ultrasound waves and appear darker.8 Peripheral nerves show a mixture of hypoechoic and hyperechoic structures constituting a typical “honeycomb” structure.9 Hypoechoic structures seen with ultrasound correspond to neural tissue, while hyperechoic areas correlate with connective tissue.10 Ultrasound imaging of the proximal brachial plexus usually shows hypoechoic structures reflecting an oligofascicular pattern. Distal brachial plexus structures display a more hyperechoic, honeycomb appearance, reflecting a multifascicular pattern.7

Pharmacology of local anesthetics Local anesthetics (LA) make regional anesthesia possible by preventing the propagation of nerve conduction and inhibiting or relieving pain.11 LA are primarily weak bases that attach to sites of the sodium channel in nerves and prevent the movement of the sodium ion through the nerve pores, which temporarily halts nerve conduction.12 Local anesthetics are classified as amides or esters, based on the chemical structure. Most local anesthetics used in regional anesthesia are amides (e.g., “-­caines”). The structure of a typical local anesthetic consists of a lipophilic head, a hydrophilic tail, and a chain linking the head and tail which is either an amide or ester and determines the classification of the type of LA. Alteration of the structure of the LA affects the various actions of the LA itself and is important when making the choice of which LA to use. For example, increasing the alkyl substitution on the aromatic ring increases its lipid solubility,

97

thereby increasing its potency. Allergic reactions to local anesthetics are more common with esters and rare with amides.

Pharmacokinetics Local anesthetics differ from other drugs because they are directly delivered at their site of action. Efficacy depends on the amount of LA that reaches the nerve and proximity to the nerve. Diffusion of local anesthetic is dependent on the amount of connective tissue and adipose tissue that is present in the area of the block.

Toxicity Local anesthetic toxicity has been a concern since its first use in nerve blockade. Regardless of which local anesthetic is injected, traditional methods have required large volumes for successful regional anesthesia such as with brachial plexus blockade or Bier blocks. Frequent aspiration and incremental dosing are imperative, as is communication with the patient to detect early signs of potential intravenous injection before progression to signs and symptoms of toxicity. Factors such as drug dose, rate of absorption, biotransformation, and elimination of the drug from the circulation are determinants of the plasma concentration of local anesthetics. Fortunately, one of the benefits of ultrasound guidance in the use of regional anesthesia has been the decreased need for large volumes.13 High plasma levels may be a consequence of direct intravascular injection, plasma absorption, and/­or certain underlying medical conditions of the patient (i.e., hypoproteinemia in renal or hepatic disease). Elevated intravascular levels of LA may result in minor CNS symptoms such as dizziness, ringing in the ears, and may proceed to more intense symptoms of loss of consciousness, and seizures. At even higher levels, cardiac arrhythmias ensue, including complete cardiovascular collapse. Use of LA in regional anesthesia demands an appreciation of these toxicities. Understanding agent-­ specific toxic levels is vital – as much as the preparation for these unintended events. Adjuncts such as epinephrine affect absorption and elimination. The use of epinephrine as a marker of intravascular injection is warranted in almost all situations. Exceptions include those cases where the vasoconstriction resulting from epinephrine may in fact compromise the blood flow to the area. Physicians must be prepared with monitors, emergency drugs, and airway supplies to facilitate treatment of LA-­ related toxicity. Toxicity related to LA can include but is not limited to oxygen desaturation, hypotension, bradycardia, and seizures. The extent of toxicity is determined by the specific drug’s intrinsic properties as well as the plasma level of the LA. The safety of LA is an essential aspect of regional anesthesia and is dependent on the skill of the physician, placement of the needle, the drug utilized, and patient health. All of these factors must be considered when determining the appropriate procedure and LA dose.14 Bupivacaine has been in use for many years and has the highest cardiotoxicity potential due to its intrinsic properties. Although the cardiac system is generally resistant to the effects of LA, bupivacaine is the notable exception. An overdose is more likely to result in cardiovascular collapse compared with other LA. This cardiac collapse is difficult

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SECTION I

CHAPTER 4  • Anesthesia for upper extremity surgery

to treat traditionally with ACLS/­ CPR alone. Recent case studies have demonstrated that intravenous (IV) infusion of Intralipid, an emulsified fat, may be successful in ameliorating cardiotoxicity associated with local anesthetics by acting as a “sink”.

Table 4.1  Commonly used agents in upper extremity regional anesthesia Lidocaine

Prototype amide

Vasoconstrictors With the addition of vasoconstrictors such as epinephrine or phenylephrine to the LA anesthetic solution, the systemic absorption rate of an LA can be decreased.14 The dose of bupivacaine increases from 3.5 to 4.0 mg/­kg. This action of epinephrine is more significant with lidocaine as the upper limit increases from 3.0 to 7.0 mg/­kg. Vasoconstrictors allow the physician to identify an intravascular injection sooner rather than later, due to the development of tachycardia with an intravascular injection.15 The block can be halted immediately, possibly preventing a more serious intravascular complication. Vasoconstrictors result in decreased plasma uptake and increased duration of local anesthetic effect.16

Most widely used local anesthetic Can be used in almost any peripheral block 1.5% or 2% with or without epinephrine is most commonly used for surgical anesthesia

Mepivacaine

Intermediate duration Similar to lidocaine Less vasodilatation Ineffective as topical agent 1.5% mepivacaine is the most commonly used agent in regional anesthesia

Bupivacaine

One of the most commonly used local anesthetics in regional and infiltration anesthesia Long-­acting

LA selection

High quality sensory anesthesia relative to motor blockade

The choice of a LA depends on toxicity (as discussed previously), duration of effect, and time to onset (Table 4.1). Duration is important when considering surgical times when the block is the primary anesthetic. In such instances, the longer-­acting agents such as ropivacaine or bupivacaine have the distinct advantage as they often can outlast the surgery and offer the greater benefits of postoperative pain management. Time to onset is also an important factor. Most of the time, regional anesthesia is done prior to the surgery and a fast time to onset is highly desirable. Each LA has its own time to onset or latency. Various factors can shorten this latency, including the addition of bicarbonate, higher dose, and needle location. The recent use of ultrasound allows for a more precise needle placement, which in turn allows for quicker onset. The choice of local anesthetic affects the quality of the block, time to onset, and duration of action (Table  4.2).15 Quicker onset generally leads to quicker clearance. Lidocaine and mepivacaine, agents with intermediate duration, have a short latency period which is further shortened by the addition of bicarbonate as mentioned above. In comparison, bupivacaine and ropivacaine, two long-­acting agents used commonly in regional anesthesia, have a longer latency period, and are not able to mix with bicarbonate due to precipitation concerns. Some may consider mixing two agents together to achieve the quicker onset effect and the longer duration of anesthesia/­ analgesia. These mixtures can be about 50 : 50; however, it can vary depending on the experience and training of the anesthesiologist. The toxicity of mixtures is additive and the mixture does not lower the overall toxicity.17 Another consideration is the differential blockade, as nerves are blocked unequally and at different rates. Nerve blockade proceeds in the following order: sympathetic nerves, pin-­prick sensation, touch, temperature, and finally, motor.18 This is an important attribute of bupivacaine, as one can provide improved analgesia without much motor blockade in the postoperative period if an infusion is run at analgesic doses. Optimally, an LA with sensory selectivity is desired.

Most commonly used for epidural and spinal Refractory cardiac arrest with 0.75% concentration. Interaction with cardiac Na+ channels “fast in, slow out” Disruption of atrioventricular nodal conduction Depression of myocardial contractility Indirect effects mediated by CNS Limitations on total dose of bupivacaine given Ropivacaine

Developed due to cardiotoxicity related to bupivacaine Long-­acting Slightly less potent than bupivacaine Higher concentrations fastens its onset and density of block Reduced CNS/­CV toxicity compared to bupivacaine

Regional anesthesia techniques Regional anesthesia has been shown to be an excellent anesthetic modality for upper extremity surgery. This relates to long-­lasting pain relief, reduced opioid-­related side effects during the first 24 hours after surgery, and expedited hospital discharge.2,19 Despite this, many patients still receive other types of anesthesia for a variety of reasons. Alternatives to regional anesthesia include general anesthesia, monitored anesthetic care (MAC), or simple local anesthetic infiltration without blockade of the brachial plexus or selected nerves. The factors involved in determining suitability of an anesthetic include patient preference, surgeon preference, relative and absolute contraindications to regional anesthesia, as well as type of surgery. General anesthesia has been utilized for many years with a safety record that has improved significantly

Regional anesthesia techniques

99

Table 4.2  Comparative pharmacology and current use of local anesthetics

pKa

Non-­ ionized (%) at pH 7.4

Potencya

Max. dose (mg) for infiltrationb

Duration after infiltration (min)

Topical

Infiltration

Intravenous regional

Peripheral block

Epidural

Spinalc

Procaine

8.9

3

1

500

45–60

No

Yes

No

Yes

No

Yes

Chloroprocaine Tetracaine

8.7

5

2

600

30–60

No

Yes

No

Yes

Yes

Yes (?)

8.5

7

8

−

−

Yes

No

No

No

No

Yes

Lidocaine

7.9

24

2

300

60–120

Yes

Yes

Yes

Yes

Yes

Yes (?)

Mepivacaine

7.6

39

2

300

90–180

No

Yes

No

Yes

Yes

Yes (?)

Prilocaine

7.9

24

2

400

60–120

No

Yes

Yes

Yes

Yes

Yes (?)

Bupivacaine, levobupivacaine

8.1

17

8

150

240–480

No

Yes

No

Yes

Yes

Yes

Ropivacaine

8.1

17

6

200

240–480

No

Yes

No

Yes

Yes

Yes

Classification and compounds Esters

Amides

Relative potencies vary based on experimental model or route of administration. b Dosage should take into account the site of injection, use of a vasoconstrictor, and patient-­related factors. c Use of lidocaine, mepivacaine, prilocaine, and chloroprocaine for spinal anesthesia is controversial and evolving (see text). a

over the past decades.20 Due to respiratory depression, general anesthesia requires airway management not routine in regional anesthesia, local anesthesia or in monitored anesthetic care. Additionally, patients who undergo general anesthesia may experience hemodynamic variations that may be significant in those with cardiac disease. All patients who will undergo any type of anesthesia need to have standard ASA monitors, which include pulse oximetry, blood pressure monitoring, and electrocardiogram monitoring as well as intravascular access established in the non-­operative limb. The use of ultrasound-­guided blocks has gained significant momentum in the last decade. The benefits of ultrasound include shortened time to onset, enhanced visualization of the nerve target and surrounding structures such as arteries, veins, muscle, and other soft tissues, needle visualization, visualization of the local anesthetic and its spread, and anomalies of anatomy.21 Combining the traditional technique of peripheral nerve stimulation with ultrasound has not demonstrated notable benefits, although that has been a common practice, particularly for difficult cases. Surprisingly, there have been no studies that demonstrate improved safety with ultrasound over the technique of peripheral nerve stimulation.22,23

Digital block Digital nerve blockade is easy to perform and provides useful anesthesia for a variety of surgical procedures or injuries isolated to a digit. Many techniques for performing digital nerve blocks have been described. These techniques rely on anesthesia of the volar common digital nerves derived from the median and ulnar nerves as well as the dorsal digital branches of the radial nerve. The authors’ preferred technique for digital blockade involves volar and dorsal injections. The hand is placed palm up and the skin is cleansed. Using a small needle, 5 mL of local anesthetic such as 1% lidocaine or 0.25% bupivacaine is

injected into the subdermal space directly overlying the A1 pulley of the involved finger. A wheal is slowly raised. The hand is then turned palm down and an additional 2–3 mL of local anesthetic is injected into the subcutaneous tissue over the dorsum of the finger, just distal to the metacarpophalangeal joint. The use of epinephrine in digital blocks was, in the past, a controversial subject. Despite the admonition against epinephrine use in numerous medical textbooks, no case of digital gangrene has been reported in the literature resulting solely from the use of epinephrine with a local anesthetic. A number of studies have demonstrated epinephrine can be safely used as an adjunct for digital block anesthesia. A randomized, prospective, blinded study with over 3000 consecutive cases showed no cases of infarction, necrosis or tissue loss.24 Epinephrine can be added to local anesthetics to lengthen the duration of action, lessen bleeding, reduce the need for a tourniquet, and reduce the risk of adverse systemic effects.25 Clinical tip Injection technique Use a small needle, such as 27-­or 30-­gauge, and a slow injection technique to deliver the local anesthetic. Smaller needle size with gentle insertion have been shown to result in less painful injections.26

Wrist block When the entire hand requires anesthesia, a wrist block is appropriate. A wrist block is the technique of blocking the median, ulnar, and radial nerves at the level of the wrist. Similar to the digital block, it is easy to perform, has minimal complications, and is highly effective.

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CHAPTER 4  • Anesthesia for upper extremity surgery

The patient should be supine with the arm abducted and wrist in slight dorsiflexion. The median nerve is located between the tendons of the palmaris longus (PL) and the flexor carpi radialis (FCR). The palmaris longus tendon is usually the more prominent of the two; the median nerve passes just radial to it. The ulnar nerve passes between the ulnar artery and tendon of the flexor carpi ulnaris (FCU). The tendon of the flexor carpi ulnaris is superficial to the ulnar nerve. The superficial branch of the radial nerve runs along the medial aspect of the brachioradialis muscle. It then passes between the tendon of the brachioradialis and radius to pierce the fascia on the dorsal aspect. Just above the radial styloid process, it gives digital branches for the dorsal skin of the thumb, index finger, and lateral half of the middle finger. The median nerve is blocked by inserting a 25-­gauge needle between the tendons of the palmaris longus and flexor carpi radialis at a 30° angle. The needle is inserted until it pierces the deep fascia. Piercing of the deep fascia may be appreciated with a fascial “click”. Local anesthetic, 3–5 mL, is injected. There should be no resistance to the injection as the local anesthetic travels up and down the carpal tunnel. The ulnar nerve is anesthetized by transversely inserting the needle under the tendon of the FCU muscle close to its distal attachment proximal to the ulnar styloid. The needle is advanced 5–10 mm past the FCU tendon. The syringe is aspirated to confirm that it is not intravascular in the ulnar artery. Local anesthetic solution, 3–5 mL, is then injected. A subcutaneous injection of 2–3 mL of local anesthesia just above the tendon of take back the FCU is also advisable in blocking the cutaneous branches of the ulnar nerve. The radial nerve is essentially anesthetized with a field block. This blockade requires a more extensive infiltration because of the less predictable anatomic location and division into multiple, smaller, cutaneous branches. Local anesthetic, 5 mL, is injected subcutaneously just above the radial styloid, aiming medially. The infiltration is then extended laterally, using an additional 5 mL of local anesthetic.

Intravenous regional anesthesia (Bier block) A Bier block is indicated for brief surgery of the hand or forearm (up to 1 hour). This technique relies on diffusion of local anesthetic from the venous system to nearby nerves. The operative extremity is exsanguinated using an Esmarch bandage. A double tourniquet is inflated sequentially from distal to proximal. The distal tourniquet is then deflated to allow local anesthetic to penetrate that area. Local anesthetic solution is then injected through a small IV catheter placed in the hand of the arm to be anesthetized. A total of 50 mL of 0.5% lidocaine is commonly used. Of note, the patient should have a separate IV on the nonoperative limb to be available for sedation and/­or emergency access. Anesthesia onset is within minutes. Patients may complain of tourniquet pain after 30 min, at which time the distal cuff is inflated and the proximal cuff is released. At the conclusion of surgery, the tourniquet is deflated, and there is a rapid resolution of anesthesia. To prevent local anesthetic toxicity, the tourniquet should not be deflated before 30 min have elapsed after drug infusion. Advantages of a Bier block include its safety profile, simplicity, and reliability. However, its use is limited to short procedures due to tourniquet discomfort, and it offers no postoperative analgesia.

Interscalene block Indications for an interscalene block include surgery of the shoulder, distal clavicle, acromioclavicular joint, and proximal humerus. The block is performed at the level of C5–C7 nerve roots, providing anesthesia to the shoulder and upper arm. Proximal spread of local anesthetic to C3–4 will also anesthetize the cape of the shoulder. Ulnar nerve distribution is usually spared with this technique. The nerve roots lie in a groove between the anterior and middle scalene muscles, posterolateral to the sternocleidomastoid muscle and phrenic nerve. To perform the block, the patient is placed in a semi-­ recumbent position. When using the nerve stimulation technique, the interscalene groove is palpated at the level of C6 and the needle is advanced in a slight posterocaudad direction. A twitch of the bicep, tricep, or distal muscle is sought. When using ultrasound, the C5–7 roots form a characteristic “stoplight” appearance as they lie sequentially between the scalene muscles. The nerves are identified, and local anesthetic is deposited circumferentially around the nerves (Fig. 4.4). Complications and side effects specific to this block are ipsilateral phrenic nerve palsy, Horner’s syndrome, hoarseness from blockade of the recurrent laryngeal nerve, and vascular puncture or injection; the carotid artery, internal and external jugular veins, and vertebral artery are in close proximity to the nerves of interest.

Supraclavicular block The supraclavicular approach to the brachial plexus provides more reliable and effective regional anesthesia to the upper extremity than other approaches.27 Indications for the supraclavicular approach include surgery of the upper extremity including the arm, elbow, and hand. Though the supraclavicular block can also be used for shoulder surgery, it may require some supplementation of the supraclavicular nerve (C3–C4).2 With ultrasound assistance, it is easy to appreciate the continuum that exists within the brachial plexus. Moving the ultrasound probe up or down, the brachial plexus will change a block from an interscalene block to a supraclavicular block. With the gain in popularity with ultrasound, there has been a resurgence in the supraclavicular block as the concerns of pneumothorax have diminished. In a recent study of 510 patients who underwent ultrasound-­guided supraclavicular blocks, none were found to have a pneumothorax.28 The supraclavicular block is performed with the probe placed in the supraclavicular fossa (Video 4.1 ). The sonoanatomy includes the subclavian artery, which is the primary landmark in this block. The brachial plexus (trunks and/­or divisions of the plexus) lies superior (posterior) and lateral to the artery in a majority of patients and appears as a “bunch of grapes” or several round structures with a dark interior (hypoechoic) and a bright outline (hyperechoic outer circle). Once an adequate view is identified, the area is prepped and draped in a sterile fashion. The needle is then aligned with the probe in what is referred to as an “in-­plane” technique. The needle appears on screen to move in a lateral to medial fashion. Once the needle is seen, placement should be carefully done with frequent aspiration. It may take 2–3 needle placements to ensure adequate coverage of the brachial plexus (Fig. 4.5). The most common side effects include hemidiaphragmatic paresis secondary to phrenic nerve block, ipsilateral

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Anterior scalene Middle scalene

Phrenic nerve

Thyroid cartilage Middle scalene

Sternocleidomastoid (cut)

Cricoid cartilage External jugular vein Anterior scalene

A

Clavicle

Clavicle B

Subclavian artery 1st rib Subclavian vein

Cricoid cartilage

C

Horner’s syndrome, and ipsilateral nasal congestion. Other risks include infection, bleeding, nerve injury, and pneumothorax. Nerve stimulation technique of the supraclavicular block is less frequently performed due to the concerns and risk of pneumothorax. There are other suitable alternatives if the ultrasound view is difficult to obtain.

Figure 4.4  (A,B) Interscalene block, functional anatomy, and (C) technique.

Infraclavicular block Indications for an infraclavicular block are the same as for the supraclavicular approach. The main difference is that the infraclavicular approach generally preserves pulmonary function by avoiding a block of the diaphragm, which is possible with the supraclavicular approach. The infraclavicular

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Sternocleidomastoid (cut)

C3

Axillary block

Vertebral artery

C4

Middle scalene

C5 Phrenic nerve C6 Accessory phrenic nerve

Clavicle

1st rib

achieved, the needle’s direction should be redirected by 5° at a time. Some anesthesiologists may seek both the medial and lateral cord if the posterior cord is difficult to find in order to improve success rates. The risks of the infraclavicular block include infection, bleeding, nerve injury, and pneumothorax.

Sternocleidomastoid (cut) Anterior scalene

Figure 4.5  Functional anatomy of supraclavicular block.

approach is a block of the brachial plexus at the level of the lateral, medial and posterior cords. These cords are named for their relationship to the axillary artery, although this relationship can have many variations.29 In the United States, the most common approach for the infraclavicular block is using the coracoid process as a landmark, both with ultrasound guidance, as well as with peripheral nerve stimulation. Ultrasound-­ guided infraclavicular blocks are performed with the probe placed just medial to the coracoid process and below the clavicle. Important sonoanatomy includes the axillary artery with the three cords surrounding the artery in a U-­shaped fashion. The approach includes an in-­plane technique with the needle aligned with the probe in a 45° angle aiming in a cephalad to caudad direction. The needle is placed just posterior to the axillary artery, which, when the LA is injected, provides coverage to all three cords in a U-­shaped spread (Fig. 4.6). Use of the nerve stimulator with the infraclavicular approach is quite common and may be considered to be less difficult by some than ultrasound-­guided infraclavicular block. In order to perform the infraclavicular block, the coracoid process is identified and marked. Once this is achieved, the physician will measure 2 cm medial and 2 cm inferior – this marks the nerve stimulator needle entry point. The nerve stimulator is turned to 1.0 mA. The needle is advanced in a direction that is perpendicular to the floor. It is important to note, as with other blocks, that there should be frequent aspiration throughout the block in order to minimize the risk of intravascular injection. As the needle is advanced, stimulation of the posterior cord is sought (extension of the elbow, wrist or fingers) and maintained at 0.5 mA. If the correct stimulation of muscle groups is not

An axillary block is indicated for surgery of the hand and forearm. It is performed at the level of the terminal branches of the brachial plexus. The radial, median, and ulnar nerves are positioned around the axillary artery, and the musculocutaneous nerve resides in the coracobrachialis muscle, lateral to the neurovascular bundle. The distribution of anesthesia includes the entire arm, except for the medial strip of skin in the upper arm, which is supplied by the intercostobrachial nerve from T2 (Fig. 4.7). For this block, the arm is abducted and the elbow flexed. When using the nerve stimulation technique, the axillary artery is palpated high in the axilla and the needle is directed lateral, medial, and posterior to the artery to stimulate the median, ulnar, and radial nerves, respectively. Obtaining two or more separate twitches, and therefore injecting local anesthetic near two or more nerves, improves block success.30 The musculocutaneous nerve is then blocked by directing the needle laterally into the coracobrachialis muscle, obtaining a twitch of the bicep muscle, and depositing additional local anesthetic. When using ultrasound, the probe is placed transversely on the upper arm near the axilla, perpendicular to the axillary artery. The artery and nerves of interest are visualized. The needle is advanced in a lateral to medial direction, and local anesthetic is deposited around each nerve. The axillary approach to the brachial plexus has potential benefits for certain patient populations, such as patients with pulmonary disease, because the phrenic nerve will not be affected. This block may also be superior in patients with coagulopathies, since the area is superficial and easily compressible if vascular puncture occurs. One disadvantage of this block is that the needle must be repositioned multiple times to adequately block all of the nerves, potentially increasing the risk of vascular puncture or causing more patient discomfort. Additionally, the arm must be abducted in order to have adequate access to the upper arm and axilla, which may be difficult in some patients such as those with injuries.

Wide-awake local anesthesia no tourniquet (WALANT) The use of lidocaine with epinephrine in hand surgery has grown rapidly in the past two decades with the introduction of the wide-awake local anesthesia no tourniquet (WALANT) technique. The primary advantage of WALANT is that it obviates the need for tourniquet use and eliminates the risks associated with sedation. Other benefits include decreased resource utilization and waste,31 decreased cost to patients and surgeons alike,32 and the ability to have patients cooperate during ­complex reconstruction procedures.

Complications

103

C4 C5 C6

Anterior scalene (cut) C7

Subclavian vein Axillary artery

T1

Pectoralis minor (cut) Sternocleidomastoid (cut) Clavicle (cut) First rib Musculocutaneous nerve Median nerve Ulnar nerve Radial nerve Axillary nerve

Figure 4.6  Functional anatomy of infraclavicular block.

The use of epinephrine in the digits has historically been frowned upon due to its vasoconstrictive effects, but a substantial body of evidence has disproven the myth that epinephrine use in the fingers causes ischemic necrosis.33–36 If a finger remains persistently pale after epinephrine use, phentolamine can be used as an effective reversal agent. WALANT can be used to perform a broad range of hand surgery procedures from carpal tunnel releases to wrist arthroscopy. WALANT is particularly useful during flexor tendon reconstruction. Patient cooperation during this procedure allows the surgeon to dial in the optimal tension for repair.

Complications associated with regional anesthesia present a rare but significant risk to patients undergoing surgery of the upper extremity. Serious complications include neurologic injury, seizures, and cardiac arrest. Other risks associated with regional anesthesia are hematoma, infection, and block-­ specific complications such as pneumothorax. A large French prospective study reported an incidence of severe complications related to peripheral nerve blocks to be 48 h), and ICU admission.47,48 A careful evaluation of the risk-­to-­benefit ratio should be made prior to placing nerve blocks in infected or immunocompromised patients.2,46

Outcomes Upper extremity surgery can be performed successfully under both general anesthesia (GA) and regional anesthesia (RA). The potential benefits of RA techniques in outpatient surgery include improved clinical outcomes, patient satisfaction, efficiency, and reduced cost.49 However, GA is still widely used for outpatient surgery, and many of the newer anesthetic agents are short-­acting with fewer side effects and better recovery profiles as compared with older agents. Additionally, many anesthesiologists are more familiar and comfortable with providing GA compared with RA.50,51

Clinical outcomes and patient satisfaction Several studies comparing regional anesthesia to general anesthesia for upper extremity surgery have demonstrated more favorable clinical outcomes with regional anesthesia, in terms of improved pain control, less nausea and vomiting, and fewer opioid-­related side effects. Other benefits include patients feeling more alert, tolerating oral intake sooner, and ambulating sooner.49,50 While improved clinical outcomes have been shown for RA in the immediate postoperative period, long-­term benefits are still undefined. In a study comparing RA to GA in patients undergoing outpatient hand and wrist surgery, patients having RA had better initial analgesia and faster recovery but both groups had a similar degree of pain and need for oral analgesics 48 h postoperatively.49 In another study comparing RA to GA in ambulatory hand surgery, patients in the RA group had significantly less postoperative pain before hospital discharge, but on postoperative days 1, 7, and 14, there were no differences in pain, opioid consumption, adverse effects, pain–disability index, or satisfaction.50 Improved functional capacity has been demonstrated in patients having lower extremity surgery with continuous RA techniques. A study of patients undergoing outpatient shoulder and foot surgery under RA with continuous outpatient perineural infusions of local anesthetics demonstrated optimized functional recovery, analgesia, and patient satisfaction for 3 days postoperatively.52 Further studies are necessary to determine if RA for upper extremity surgery has a benefit after the immediate postoperative period in terms of pain control, adverse effects, and functional capacity. Patient satisfaction, although difficult to define, is usually high, with both regional and general anesthesia. Improved patient satisfaction with RA techniques may be a result of improved analgesia and fewer side effects.53 Studies showing lower patient satisfaction with RA techniques often cite tourniquet pain and discomfort during the nerve block placement as causes of dissatisfaction.54

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Clinical tip Benefits of a regional anesthesia service and outpatient clinic A 24-­hour regional anesthesia service can expand care to patients who present during off-­hours with traumatic injuries. Blocks are placed in the emergency department for patients with fractures, traumatic amputations, and other injuries hours prior to their scheduled surgery. This offers the benefit of decreased opioid use during admission and decreased side effects such as delirium. A regional anesthesia outpatient clinic permits walk-­ins from home or from their surgeon’s office to be evaluated for postoperative neuropathies, catheter management, or other related concerns. The benefits of a regional anesthesia clinic include reduced emergency department admissions, early diagnosis and management of neuropathies, and improved patient satisfaction.

Patients having RA for upper extremity surgery who experience superior pain control and fewer side effects may potentially have a shorter PACU stay. A meta-­analysis of RA versus GA for ambulatory anesthesia showed that patients receiving RA had an increased ability to bypass the PACU and/­or a decreased PACU time.53 To date, studies demonstrating an overall cost reduction for intraoperative and postoperative care during upper extremity surgery have compared GA to intravenous regional anesthesia (Bier block). The IVRA group had significant cost-­savings attributed to lower anesthetic drug and equipment costs, shorter OR times, shorter PACU times, and shorter nursing times.55,56 In contrast, a retrospective comparison of costs for RA and GA techniques demonstrated a cost disadvantage for brachial plexus regional anesthesia, although recovery room costs were not included in this analysis.57 More research is needed to determine if RA techniques for upper extremity surgery show a significant cost reduction when compared with other anesthetic techniques.

Operating room cost and efficiency

Special considerations

Several investigators have sought to determine if regional anesthesia is superior to general anesthesia in terms of operating room (OR) efficiency and costs. Some potential areas to improve efficiency and reduce costs are OR utilization time and recovery room time. Some studies suggest that in order to save OR time through the use of regional anesthesia techniques, nerve blocks must be performed outside the operating room. In this case, the cost of valuable OR time is spared and efficiency is maximized because patients are ready for surgery as soon as they enter the operating room.50 Others have reported similar OR times for RA versus GA techniques even when the blocks were performed in the operating room. This was attributed to the combination of fast-­acting local anesthetics, the ability for surgeons to prepare the patients while the nerve blocks took full effect, and faster emergence time compared to GA.49

Cardiac patients

Clinical tip Benefits of an out-­of-­OR regional team Having a separate, out-­of-­OR regional anesthesia team offers several benefits. Efficiency is improved when blocks are placed in the preoperative holding area rather than the operating room. An out-­of-­OR team has the freedom and availability to place rescue blocks in the recovery room and bolus, reposition, or replace catheters placed preoperatively. Additionally, blocks can be placed in the emergency department, hospital ward, or intensive care unit for patients with acute pain such as dressing changes and other non-­operative pain. The addition of a block nurse to the regional anesthesia service improves efficiency. The block nurse assists the team by placing IVs, applying monitors to the patients, preparing drugs and supplies, and directing the pre-­procedure “time-­out”. Other responsibilities include assisting with documentation and patient follow-­ups.

Patients with cardiac disease, including those with cardiac dysfunction and low ejection fractions, conduction abnormalities or ongoing ischemia, should be given consideration for regional anesthesia for upper extremity cases when indicated. Regional anesthesia allows patients the usual advantages of perioperative analgesia and possibly avoidance of general anesthesia.20 General anesthesia, while very safe, can cause hemodynamic variations during the induction of anesthesia, intubation, emergence from anesthesia and possibly during surgical stimulation or bleeding. In this patient population, variations in blood pressure and heart rate can have significant consequences. The prospect of regional anesthesia and analgesia allows the patient to avoid hemodynamic fluctuations, thus minimizing risk. Patients with cardiac disease may be anticoagulated for a variety of reasons. In these patients, the risks and benefits of the block must take into consideration the possibility of an increased likelihood of bleeding during a nerve block with a resultant hematoma and nerve compression.

Pediatric patients The pediatric population warrants special considerations when considering the type of anesthetic for surgery. These include anatomic and physiologic differences when compared with adult counterparts. Regional anesthesia offers the advantage of intraoperative and postoperative analgesia for the pediatric population. While still receiving a general anesthesia in most cases, the pediatric patient may benefit from a regional anesthetic as a result of decreased requirements for inhalational agents, leading to improved respiratory status.58 Improved respiratory status decreases the chance of laryngospasm on emergence. There are additional benefits of comfort for the patient’s family, observing a more comfortable and pain-­free child in the recovery room. Overall, there is less stress for all involved.59

Perioperative pain management

The types of blocks performed on pediatric patients are generally performed with the patient under GA. It is not until the child is older and demonstrating a level of maturity that the block can be performed on the awake patient. When a block is performed on an asleep patient, there is an elevated risk of nerve injury as the patient cannot relay the sensation of paresthesias and pain from the rare event of neural trauma. Overall, regional anesthetic techniques are considered safe with an extremely low incidence of complications.60 Ultrasound guidance is strongly recommended when considering regional anesthesia as part of the anesthetic in infants and children. The increased assistance provided in locating sonographic landmarks and nerve targets are of great benefit.61–63

Perioperative pain management For upper extremity surgery, the use of regional anesthesia with local anesthetics is primarily motivated by the desire to avoid general anesthesia. It has resulted in lower postoperative opiate usage and therefore alleviation of opiate-­related side effects.64 This approach has become, in many ways, the standard of care in upper extremity cases.

Peripheral catheters Peripheral nerve blockade is safe and provides postoperative analgesia through the use of long-­acting local anesthetics and/­ or continuous infusions through peripheral nerve catheters.65 Outpatient catheters have become very common. Catheters provide longer-­acting pain relief over single-­shot techniques and benefit patients who undergo more painful surgical procedures, patients with chronic pain, and patients who are unable to tolerate opioids for various reasons. Peripheral nerve catheters are usually placed preoperatively by the anesthesiologist when the initial nerve block is performed. Alternatively, a catheter may be placed in the postoperative period if the patient experiences severe pain. Continuous catheters do not delay discharge in outpatient surgery as they can be managed at home by the patient.

Clinical tip Use and protocols for ambulatory catheters and pain pumps For upper extremity procedures, the infraclavicular approach is preferred over the supraclavicular approach because there is less catheter migration at this location, possibly due to the anchoring of the catheter by the pectoralis muscles or the decreased amount of skin movement with activity. Patients are sent home with a catheter and an elastomeric pain pump with an on-­demand button function. The pumps are set at a basal rate at 6 mL/­hour (on average) with a bolus option of 5 mL every 30 minutes. The pumps are filled to 550 mL and usually last roughly 3 days, depending on the number of boluses activated by the patient. Patients remove the catheters themselves at home. The patients are instructed on the use and care of the catheter and pump prior to discharge and are sent home with an instruction pamphlet and a 24-­hour number to call for any questions or concerns.

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Preemptive analgesia Preemptive analgesia is a pain management technique initiated prior to incision, which continues during the surgical procedure to reduce ongoing changes that occur in the body as a result of surgical incision and stimulation.66 The rationale is that by preemptively blocking the nociceptive transmission onslaught that occurs with surgical incision, there will be less pain in the postoperative period and thus less need for consumption of opiates with fewer side effects. The duration of treatment includes the entire time that the noxious stimulation of surgery and its inflammatory injuries occur (intraoperative and early postoperative period).66 Opiate-­ related side effects of sedation, nausea, respiratory depression, ileus, and urinary retention can impact patient safety and satisfaction, discharge or patient admission, particularly in the outpatient setting, thereby affecting cost issues. Multimodal analgesic regimens have been developed featuring the peripheral nerve block in order to improve perioperative outcomes for minimally invasive procedures. There has been much controversy surrounding the relevance and effectiveness of preemptive analgesia. Although the benefits have been established to some degree in animal studies, it has had questionable effect in human studies to date.67 Many physicians practice with the belief that there is some preemptive analgesic effect. Some suggest that there is greater complexity in pain pathways than our understanding, and that studies are too simplistic. However, there is little doubt that excellent pain management in the pre-­and postsurgical area contributes to an overall improved pain experience. A meta-­analysis demonstrated that analgesia in the preoperative period lowered opiate consumption when the preemptive treatment was epidural analgesia, local infiltration, and systemic non-­steroidal anti-­inflammatory drugs (NSAIDs).68 The findings were equivocal with opioids and NMDA receptors alone. Certain studies go further to demonstrate that the preemptive analgesia associated with ketamine or a cox-­2 analgesic gives additional benefit pre-­incision. One such study looked at patients about to undergo upper limb surgery under axillary brachial plexus blockade.69 The study examined the addition of a long-­ acting NSAID, ampiroxicam, versus placebo given 3 h prior to surgery. A  significant improvement occurred in patients who received the NSAID when compared to those in the placebo group. The treated patients consumed significantly less opiates and therefore were less likely to develop narcotic side effects such as sedation, nausea, constipation, or urinary retention. Nociceptive afferent transmission is known to be sensitive to inflammation and NSAIDs are postulated to have this effect via their anti-­inflammatory action. Another study retrospectively reviewed a multimodal, preemptive pathway for patients undergoing major knee or hip surgery featuring peripheral nerve blocks, and found that patients were better able to participate in postoperative rehabilitation, were eligible for hospital discharge sooner, initiated earlier ambulation, experienced lower perioperative pain scores, and experienced reduced postoperative nausea and vomiting when compared with more traditional PCA ­measures.70 These findings advocate for the preemptive ­ multimodal analgesic regimen.

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Chronic postoperative pain The development of postoperative pain after surgery is due to complex pathways  – endocrine, metabolic, and inflammatory  – that trigger a prolonged state of excitation of the spinal cord.71 Various chemicals released during and soon after surgical incision may induce conversion of high threshold nociceptors into low threshold receptors, via a process called peripheral sensitization. This complex process eventually leads to release of cellular mediators in the recuperative period resulting in central sensitization and chronic pain.72 Chronic pain is, among other factors, linked to patients with severe postoperative pain.15,73 While the development of chronic pain following surgery has lacked a spotlight in the medical literature, it is a reality that needs to be considered particularly in patients who may be at higher risk of developing chronic pain.74 Inadequately treated postoperative pain is a major source of patients’ dissatisfaction with their overall surgical experience.75 Severe pain in the postoperative period correlates to a greater likelihood of developing chronic pain.76 There are a number of risk factors77 for developing severe postoperative pain (Box 4.1).

Access the reference list online at   Elsevier eBooks+

BOX 4.1  Risk factors for severe postoperative pain • • • • • • • • •

Preoperative pain Prior use of opiates Female gender Non-­laparoscopic surgery Knee and shoulder surgery Psychosocial vulnerability Repeat surgery Intensity of early postoperative pain Surgical approach with risk of nerve damage

It is imperative that postoperative pain be treated effectively, possibly with a multimodal approach that considers preemptive analgesia and its potential benefits. It is crucial to identify those patients who have a greater likelihood of developing severe postoperative pain, not only to minimize the likelihood of developing chronic pain, but also to improve the patient’s experience in the perioperative period.

References

References 1. Brown DL. Atlas of Regional Anesthesia. 3rd ed. Philadelphia: Saunders; 2006. 2. Neal JM, Gerancher JC, Hebl JR, et al. Upper extremity regional anesthesia: essentials of our current understanding, 2008. Reg Anesth Pain Med. 2009;34:134–170. 3. Thompson GE, Rorie DK. Functional anatomy of the brachial plexus sheaths. Anesthesiology. 1983;59:117–122. 4. Partridge BL, Katz J, Benirschke K. Functional anatomy of the brachial plexus sheath: implications for anesthesia. Anesthesiology. 1987;66:743–747. 5. Kawai H, Kawabata H. Brachial Plexus Palsy. Singapore: World Scientific; 2000. 6. Moayeri N, Bigeleisen PE, Groen GJ. Quantitative architecture of the brachial plexus and surrounding compartments, and their possible significance for plexus blocks. Anesthesiology. 2008;108:299–304. 7. van Geffen GJ, Moayeri N, Bruhn J, et al. Correlation between ultrasound imaging, cross-­sectional anatomy, and histology of the brachial plexus: a review. Reg Anesth Pain Med. 2009;34:490–497. 8. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-­guided regional anesthesia. Part I: understanding the basic principles of ultrasound physics and machine operations. Reg Anesth Pain Med. 2007;32:412–418. 9. Schafhalter-­Zoppoth I, Gray AT. The musculocutaneous nerve: ultrasound appearance for peripheral nerve block. Reg Anesth Pain Med. 2005;30:385–390. 10. Thoirs K, Scutter S, Wilkinson M. The ulnar nerve at the elbow: an anatomic, sonographic, and histology comparison. J Diagn Med Sonogr. 2003;19:16–23. 11. Hadzic A, Vloka JD. New York School of Regional Anesthesia. Peripheral Nerve Blocks. New York: McGraw-­Hill Health Professions Division; 2004. 12. Covino BG, Scott DB. Handbook of Epidural Anaesthesia and Analgesia. Orlando: Grune & Stratton; 1985:175. 13. Ponrouch M, Bouic N, Bringuier S, et al. Estimation and pharmacodynamic consequences of the minimum effective anesthetic volumes for median and ulnar nerve blocks: a randomized, double-­blind, controlled comparison between ultrasound and nerve stimulation guidance. Anesth Analg. 2010;111:1059–1064. 14. Gerancher J, Weller R. Plastic surgery. In: Hentz VR, Mathes SJ, eds. Plastic Surgery. Philadelphia: Saunders Elsevier; 2006 15. Bridenbaugh PO, Cousins MJ. Neural Blockade in Clinical Anesthesia and Management of Pain. 3rd ed. Philadelphia: Lippincott-­Raven; 1998:xxii, 1177. 16. Bernards CM, Kopacz DJ. Effect of epinephrine on lidocaine clearance in vivo: a microdialysis study in humans. Anesthesiology. 1999;91:962–968. 17. Spiegel DA, Dexter F, Warner DS, et al. Central nervous system toxicity of local anesthetic mixtures in the rat. Anesth Analg. 1992;75:922–928. 18. Raj PP. Textbook of Regional Anesthesia. New York: Churchill Livingstone; 2002. xix, 1083. 19. Klein SM, Evans H, Nielsen KC, et al. Peripheral nerve block techniques for ambulatory surgery. Anesth Analg. 2005;101:1663–1676. 20. Pierce Jr. EC. The 34th Rovenstine Lecture. 40 years behind the mask: safety revisited. Anesthesiology. 1996;84:965–975. 21. Neal JG, Cox MJ, Drake DB, et al. The ASRA evidence-­based medicine assessment of ultrasound-­guided regional anesthesia and pain medicine: Executive summary. Reg Anesth Pain Med. 2010;35:S1–S9. 22. Koff MD, Cohen JA, McIntyre JJ, et al. Severe brachial plexopathy after an ultrasound-­guided single-­injection nerve block for total shoulder arthroplasty in a patient with multiple sclerosis. Anesthesiology. 2008;108:325–328. 23. Zetlaoui PJ, Labbe JP, Benhamou D. Ultrasound guidance for axillary plexus block does not prevent intravascular injection. Anesthesiology. 2008;108:761.

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24. Lalonde D, Bell M, Benoit P, et al. Multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase A. J Hand Surg Am. 2005;30:1061–1067. 25. Wilhelmi BJ, Blackwell SJ, Miller JH, et al. Do not use epinephrine in digital blocks: myth or truth? Plast Reconstr Surg. 2001;107:393–397. 26. Gill HS, Prausnitz MR. Does needle size matter? J Diabetes Sci Technol. 2007;1:725–729. 27. Winnie AP, Collins VJ. The subclavian perivascular technique of brachial plexus anesthesia. Anesthesiology. 1964;25:353–363. 28. Perlas A, Lobo G, Lo N, Brull R, et al. Ultrasound-­guided supraclavicular block: outcome of 510 consecutive cases. Reg Anesth Pain Med. 2009;34:171–176. 29. Sauter AR, Smith HJ, Stubhaug A, et al. Use of magnetic resonance imaging to define the anatomical location closest to all three cords of the infraclavicular brachial plexus. Anesth Analg. 2006;103:1574–1576. 30. Sorenson EJ. Neurological injuries associated with regional anesthesia. Reg Anesth Pain Med. 2008;33:442–448. 31. Leblanc MR, Lalonde J, Lalonde DH. A detailed cost and efficiency analysis of performing carpal tunnel surgery in the main operating room versus the ambulatory setting in Canada. Hand. 2007;2(4): 173–178. 32. Chatterjee A, McCarthy JE, Montagne SA, Leong K, Kerrigan CL. A cost, profit, and efficiency analysis of performing carpal tunnel surgery in the operating room versus the clinic setting in the United States. Ann Plast Surg. 2011;66(3):245–248. 33. Lalonde D, Bell M, Benoit P, Sparkes G, Denkler K, Chang P. A multicenter prospective study of 3,110 consecutive cases of elective epinephrine use in the fingers and hand: the Dalhousie Project clinical phase. J Hand Surg. 2005;30(5):1061–1067. 34. Chowdhry S, Seidenstricker L, Cooney DS, Hazani R, Wilhelmi BJ. Do not use epinephrine in digital blocks: myth or truth? Part II. A retrospective review of 1111 cases. Plast Reconstr Surg. 2010;126(6): 2031–2034. 35. Fitzcharles-­Bowe C, Denkler K, Lalonde D. Finger injection with high-­dose (1:1,000) epinephrine: Does it cause finger necrosis and should it be treated. Hand. 2007;2(1):5–11. 36. Muck AE, Bebarta VS, Borys DJ, Morgan DL. Six years of epinephrine digital injections: absence of significant local or systemic effects. Ann Emerg Med. 2010;56(3):270–274. 37. McKee DE, Lalonde DH, Thoma A, Glennie DL, Hayward JE. Optimal time delay between epinephrine injection and incision to minimize bleeding. Plast Reconstr Surg. 2013;131(4):811–814. 38. Auroy Y, Benhamou D, Bargues L, et al. Major complications of regional anesthesia in France: The SOS Regional Anesthesia Hotline Service. Anesthesiology. 2002;97:1274–1280. 39. Neal JM, Bernards CM, Hadzic A, et al. Practice advisory on neurologic complications in regional anesthesia and pain medicine ASRA. Reg Anesth Pain Med. 2008;33:404–415. 40. Neal JM, Barrington MJ, Brull R, et al. The Second ASRA Practice Advisory on Neurologic Complications Associated with Regional Anesthesia and Pain Medicine, Executive Summary 2015. Reg Anesth Pain Med. 2015;40:401–430. 41. Neal JM, Bernards CM, Butterworth 4th JF, et al. Practice advisory on local anesthetic systemic toxicity ASRA. Reg Anesth Pain Med. 2010;35:152–161. 42. Ben-­David B, Stahl S. Axillary block complicated by hematoma and radial nerve injury. Reg Anesth Pain Med. 1999;24:264–266. 43. Zipkin M, Backus WW, Scott B, et al. False aneurysm of the axillary artery following brachial plexus block. J Clin Anesth. 1991;3:143–145. 44. Horlocker TT, Wedel DJ, Rowlingson JC, et al. Regional anesthesia in the patient receiving antithrombotic or thrombolytic therapy: American Society of Regional Anesthesia and Pain Medicine Evidence-­Based Guidelines, 3rd edn. Reg Anesth Pain Med. 2010;35:64–101. 45. Capdevila X, Pirat P, Bringuier S, et al. Continuous peripheral nerve blocks in hospital wards after orthopedic surgery: a

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multicenter prospective analysis of the quality of postoperative analgesia and complications in 1,416 patients. Anesthesiology. 2005;103:1035–1045. 46. Hebl JR, Neal JM. Infectious complications: a new practice advisory. Reg Anesth Pain Med. 2006;31:289–290. 47. Horlocker TT, Wedel DJ. Regional anesthesia in the immunocompromised patient. Reg Anesth Pain Med. 2006;31:334–345. 48. Wedel DJ, Horlocker TT. Regional anesthesia in the febrile or infected patient. Reg Anesth Pain Med. 2006;31:324–333. 49. Hadzic A, Arliss J, Kerimoglu B, et al. Comparison of infraclavicular nerve block versus general anesthesia for hand and wrist day-­case surgeries A. Anesthesiology. 2004;101:127–132. 50. McCartney CJ, Brull R, Chan VW, et al. Early but no long-­term benefit of regional compared with general anesthesia for ambulatory hand surgery. Anesthesiology. 2004;101:461–467. 51. Epple J, Kubitz J, Schmidt H, et al. Comparative analysis of costs of total intravenous anaesthesia with propofol and remifentanil vs. balanced anaesthesia with isoflurane and fentanyl. Eur J Anaesthesiol. 2001;18:20–28. 52. Capdevila X, Dadure C, Bringuier S, et al. Effect of patient-­ controlled perineural analgesia on rehabilitation and pain after ambulatory orthopedic surgery: a multicenter randomized trial. Anesthesiology. 2006;105:566–573. 53. Liu SS, Strodtbeck WM, Richman JM, et al. Comparison of regional versus general anesthesia for ambulatory anesthesia: a meta-­ analysis of randomized controlled trials A. Anesth Analg. 2005;101:1634–1642. 54. De Andrés J, Valía JC, Gil A, et al. Predictors of patient satisfaction with regional anesthesia. Reg Anesth. 1995;20:498–505. 55. Chan VW, Peng PW, Kaszas Z, et al. Comparative study of general anesthesia A, intravenous regional anesthesia, and axillary block for outpatient hand surgery: clinical outcome and cost analysis. Anesth Analg. 2001;93:1181–1184. 56. Chilvers CR, Kinahan A, Vaghadia H, et al. Pharmacoeconomics of intravenous regional anaesthesia vs general anaesthesia for outpatient hand surgery. Can J Anaesth. 1997;44:1152–1156. 57. Schuster M, Gottschalk A, Berger J, et al. Retrospective comparison of costs for regional and general anesthesia techniques A. Anesth Analg. 2005;100:786–794. 58. Shandling B, Steward DJ. Regional analgesia for postoperative pain in pediatric outpatient surgery. J Pediatr Surg. 1980;15: 477–480. 59. Leak WD, Winchell SW. Regional anesthesia in pediatric patients: review of clinical experience. Reg Anesth Pain Med. 1982;7:64–65. 60. Giaufre E, Dalens B, Gombert A. Epidemiology and morbidity of regional anesthesia in children: a one-­year prospective survey of the French-­Language Society of Pediatric Anesthesiologists. Anesth Analg. 1996;83:904–912.

61. Lönnqvist PA. Is ultrasound guidance mandatory when performing paediatric regional anaesthesia? Curr Opin Anesthesiol. 2010;23:337–341. 62. Marhofer P, Chan VW. Ultrasound-­guided regional anesthesia: current concepts and future trends. Anesth Analg. 2007;104:1265–1269. 63. Marhofer P, Frickey N. Ultrasonographic guidance in pediatric regional anesthesia Part 1: Theoretical background. Paediatr Anaesth. 2006;16:1008–1018. 64. Richman JM, Liu SS, Courpas G, et al. Does continuous peripheral nerve block provide superior pain control to opioids? A meta-­ analysis. Anesth Analg. 2006;102:248–257. 65. Jin F, Chung F. Multimodal analgesia for postoperative pain control. J Clin Anesth. 2001;13:524–539. 66. Kissin I. Preemptive analgesia at the crossroad. Anesth Analg. 2005;100:754–756. 67. Moiniche S, Kehlet H, Dahl JB. A qualitative and quantitative systematic review of preemptive analgesia for postoperative pain relief: the role of timing of analgesia. Anesthesiology. 2002;96:725–741. 68. Ong CK, Lirk P, Seymour RA, et al. The efficacy of preemptive analgesia for acute postoperative pain management: a meta-­ analysis. Anesth Analg. 2005;100:757–773. 69. Hebl JR, Dilger JA, Byer DE, et al. A pre-­emptive multimodal pathway featuring peripheral nerve block improves perioperative outcomes after major orthopedic surgery. Reg Anesth Pain Med. 2008;33:510–517. 70. Sai S, Fujii K, Hiranuma K, et al. Preoperative ampiroxicam reduces postoperative pain after hand surgery. J Hand Surg Br. 2001;26:377–379. 71. Joshi GP, Ogunnaike BO. Consequences of inadequate postoperative pain relief and chronic persistent postoperative pain. Anesthesiol Clin North Am. 2005;23:21–36. 72. Warfield CA, Bajwa ZH. Principles and Practice of Pain Medicine. 2nd ed. New York: McGraw-­Hill; 2004. xxiii, 938. 73. Gerbershagen HJ, Dagtekin O, Rothe T, et al. Risk factors for acute and chronic postoperative pain in patients with benign and malignant renal disease after nephrectomy. Eur J Pain. 2009;13:853–860. 74. Asokumar B. Regional anesthesia and analgesia: prevention of chronic pain. Anesth Analg. 2008;12:199–202. 75. Tong D, Chung F, Wong D. Predictive factors in global and anesthesia satisfaction in ambulatory surgical patients. Anesthesiology. 1997;87:856–864. 76. Yarnitsky D, Crispel Y, Eisenberg E, et al. Prediction of chronic post-­operative pain: pre-­operative DNIC testing identifies patients at risk. Pain. 2008;138:22–28. 77. Perkins FM, Kehlet H. Chronic pain as an outcome of surgery: a review of predictive factors. Anesthesiology. 2000;93:1123–1133.

SECTION I  •  Principles of Hand Surgery

5 Principles of internal fixation Margaret Fok, Jason R. Kang, Christopher Cox, and Jeffrey Yao

Access video content for this chapter online at Elsevier eBooks+

SYNOPSIS

ƒ Careful preoperative planning facilitates safe and expeditious surgery. ƒ Ligamentotaxis relies on the intact soft-­tissue envelope. By applying linear traction, it indirectly reduces fragments via the intact periosteum, ligaments, and soft tissues. ƒ The most appropriate method of fracture fixation depends on a careful assessment of the fracture characteristics and patient-­related factors. ƒ Postoperative care should aim for early mobilization if fixation permits in order to avoid the development of hand and wrist stiffness.

Introduction Fracture care was significantly advanced in the twentieth century with the introduction of new techniques and instrumentation for internal and external fixation.1,2 Today’s hand surgeon must be well versed in the spectrum of available techniques of fracture fixation to provide optimal care for the myriad of bony injuries that occur within the purview of a hand surgery practice. Fixation of fractures in the hand is notoriously difficult given the relatively small size of the osseous structures and complexity of the surrounding anatomy.3 The aim of this chapter is not to review every possible technique of fracture fixation in the hand, but rather, to present basic concepts and general techniques useful in routine fracture care. In general, we base our fracture management on the Arbeitsgemeinschaft für Osteosynthesefragen (AO) principles (Box 5.1).4

BOX 5.1  AO principles 1. Anatomical fracture reduction 2. Appropriate stability of the fixation construct 3. Preservation of blood supply and soft-­tissue attachments to fracture fragments 4. Early and safe mobilization

Patient selection Fracture considerations Fracture assessment must begin with a careful, complete history and physical examination. Was the mechanism of injury a high-­or low-­energy trauma? How much time has elapsed since the fracture and the current presentation? Does the patient require early return to functional activities, or does he/­she have low daily demands? Does the patient have multiple injuries, or is this an isolated injury? Are there open wounds or significant soft-­ tissue damage? Is there angular or rotational displacement? It is noted that the vast majority of fractures that are non-­displaced or minimally displaced with adequate soft-­tissue integrity are intrinsically stable and amenable to treatment with nonoperative methods.1,5,6

Patient-­specific considerations Apart from fracture fixation, commitment from the patient to follow the rehabilitation protocol is essential to achieve favorable outcomes.7 Failure to comply with immobilization, follow-­up care, therapy recommendations, or weight-­bearing restrictions may compromise results. These include patients with mental incapacity and/­or patients with neuromuscular disorders such as epilepsy and Parkinsonism. Certain host factors may increase susceptibility to fracture and/­or surgical wound healing. Systemic risk factors for poor healing potential include: diabetes mellitus,8 immunocompromised state, advanced age,9 and smoking. Local risk factors include: skin quality, integrity of soft tissue, and underlying bone quality (e.g., the presence of osteoporosis/­osteopenia or a lytic bone cyst). The type of hardware utilized, and its corresponding tension created across the wound may also play a role. Failure to recognize and address these factors may result in poor outcomes. Patients with an elevated risk for wound problems should be counseled accordingly and managed with

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alternative strategies where appropriate. Non-­modifiable risk factors should be recognized and taken into consideration during decision-­making. Modifiable risk factors should be addressed and optimized before, during, and after fracture treatment.

Preoperative imaging

fragments to other fragments is critical in achieving a satisfactory reduction in the face of comminution. Due to the small size of the oseesous structures, forceps or wires used for temporary fixation should be carefully thought out so as to not interfere with the planned definitive fixation.

Reduction hints and tips

Proper radiographic assessment requires a minimum of two orthogonal views with the X-­ ray beam centered near the fracture to minimize distortion. Factors to carefully evaluate include: 1. Location of fracture (articular, metaphyseal, diaphyseal) 2. Pattern (transverse, oblique, spiral) 3. Presence of comminution 4. Displacement 5. Angulation (sagittal, coronal, and axial/­rotational planes) 6. Potential deforming forces acting across the fracture site

Reduction forceps

Occasionally, advanced imaging with computed tomography (CT) scans10,11 or magnetic resonance imaging (MRI) may be indicated to further characterize complex fracture patterns or to evaluate for occult injuries to the bones or soft tissue.12 After careful consideration of the fracture pattern in the context of the injured patient, a decision must be made regarding nonoperative versus operative treatment.

Reduction hints and tips

Reduction forceps may be useful to achieve and maintain fracture reduction in fixation of larger fragments. One tine of the forceps is introduced firmly onto a fragment and the other tine is used to tease another fragment into the appropriately reduced position. Careful pronation and supination movements while applying the forceps may allow for the restoration of length, angulation and rotation in difficult fractures. One has to be mindful of not to crush or shatter the fragments with excessive compression of the clamps.

Kirschner wires (K-­wires) In fracture reduction, K-­wires may be used to temporarily secure fractures that are already reduced. They may be used to reduce the fractures indirectly like preventing volar joint subluxation in bony mallet and preventing dorsal joint subluxation in PIP joint fracture dislocation15 (Fig. 5.1). In addition, they may be bent and inserted as an intramedullary pin, reducing the fracture and fixing it as a 3-­point fixation, or a few K-­wires can be inserted together into the intramedullary canal (Fig. 5.2) and are used as a canal filler in metacarpal fractures.16 They may be applied in a unicortical fashion and utilized as “joysticks” or “handles” to manipulate pieces into the appropriate position. After attaining the desired position, they are often advanced across the fracture site to transition them from a reduction aid into a tool of temporary or definitive fixation.  

Treatment/­surgical technique

 

Preoperative planning Similar to the “reconstructive ladder” concept for management of soft-­tissue defects, the surgeon should, in general, use the simplest method that will reliably produce excellent clinical results. Planning should include every detail of the proposed operation. This includes patient positioning, operating room setup, type of imaging (fluoroscopy) and instruments desired, implants needed, surgical approach, fracture fixation constructs, and consideration of backup plans. The time spent on planning will save operative time, decrease staff frustration, and ensure the availability of appropriate tools in order to enable the surgery to run in a safe, smooth, and efficient manner.

Fracture reduction Fracture reduction may be obtained by closed or open means. For closed reductions, pulling linear traction across the fracture site is usually required. This utilizes the phenomenon of ligamentotaxis,13,14 whereby intact periosteum, soft-­tissue attachments, and ligaments help to realign bony fragments as they are stretched. For open reductions, the fracture site is exposed and reduction is obtained through a combination of external manipulation and instruments placed within the fracture site. The reduction can be provisionally held with reduction forceps or Kirschner wires. The concept of reducing the number of fragments by temporary or final fixation of

Reduction hints and tips Kapandji (intrafocal) pinning17–21 This is a special type of application of a K-­wire utilized in distal radius fractures. The wire is introduced through the fracture site (intrafocally). The pin is then tilted in the desired direction of the reduction, then advanced through the far cortex. This has particular applicability to the restoration of volar tilt and radial inclination in distal radial fracture. This may be employed as either temporary or definitive fixation.

Reduction hints and tips Temporary/­supplemental external fixation For selected, extremely difficult fractures, an external fixator may be utilized to hold traction, neutralize shortening, and apply ligamentotaxis to assist with fracture reduction.

Treatment/­surgical technique

A

111

B

Figure 5.1  K-­wire is used as extension block to reduce fracture dislocation of the proximal phalangeal joint of the left little finger. (A) Preoperative radiograph; (B) postoperative radiograph. (Courtesy of and copyright Dr Esther Chow.)

A

B

Figure 5.2  This 75-­year-­old man had multiple injuries after being run over by a truck. He sustained fractures of all metacarpals (A). Relative stability through usage of multiple K-­wires (B) was elected to minimize further soft-­tissue disruption.

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Intraoperative imaging Fluoroscopy provides a valuable adjunct to many fracture fixation surgeries. A complete review of the physics and principles of fluoroscopy is beyond the scope of this chapter, but a few points are worth mentioning. For upper extremity surgery, either an image intensifier or a “mini” fluoroscopic unit may be employed. For the vast majority of hand surgery cases a “mini” fluoroscopy unit provides adequate visualization with greater mobility and less radiation.22–25 Many different operating room setups may be employed, but patient positioning should be confirmed preoperatively to allow for adequate fluoroscopic visualization during surgery. We typically position the mini fluoroscopic unit parallel to the bed, oriented from the foot toward the axilla, so that the patient’s arm can be adducted off of the hand table to provide unobstructed views. The region being examined should always be centered on the detector of the fluoroscopic unit to minimize the distortion from the “parallax” effect. Multiple views are often necessary to determine fracture reduction or hardware position in all planes. In some instances, especially for carpal, metacarpal and proximal phalangeal fractures, the fracture configuration and reduction are difficult to appreciate in true lateral view due to the overlap of bone. Multiple oblique views are needed to evaluate the fracture pattern and subsequent fixation. It may also be helpful to orient the beam directly down a placed K-­wire or screw to precisely visualize its placement. Specific knowledge of certain anatomic regions may also be helpful. For instance, when imaging the distal radius, inclining the wrist approximately 20–30° from a true lateral can provide better visualization of the cortex of the lunate facet to evaluate for screw penetration into the radiocarpal joint.26–28, Live, dynamic fluoroscopy may be useful to examine the stability across a fracture site with controlled motion and the integrity of adjacent collateral ligaments and to evaluate for intra-­ articular screw penetration.

Arthroscopy The use of arthroscopy to assess articular reduction in fracture fixation is growing in popularity in recent decades. This includes its use in the management of distal radius fractures and base of metacarpal fractures 29–32 (Fig.  5.3). It has the

A

theoretical advantage of achieving better articular congruity than fluoroscopic-­assisted technique which may in turn prevent secondary osteoarthritis.31,33,34 A complete review of the technical tips in performing arthroscopic-­assisted fracture reduction is beyond the scope of this chapter. Yet, one must include this as part of the preoperative planning and ensure the operative staff is familiar with all of the required instruments used. The operating room setup and patient positioning must be considered when both fluoroscopy and arthroscopy are required.

Fixation principles The hand and wrist are prone to develop stiffness.7 Apart from restoring alignment and attaining bone union, one of the purposes of surgery is to provide the initial inherent stability to allow for early mobilization.1 Surgery must be appreciated as an additional trauma to the soft tissue. Internal fixation should attain fracture stability and allow at least some immediate postoperative controlled/supervised mobilization. Immobilization should be kept minimal in order to prevent excessive stiffness.1

Absolute stability and interfragmentary compression Absolute stability is employed when fracture fragments are reduced anatomically and secured with rigid fixation. Interfragmentary compression is a critical component of fixation when the surgeon attempts to achieve absolute stability.35,36 This compression, when combined with anatomic reduction, leads to microscopic interdigitation of fracture ends, thus minimizing the distance required for cells to travel from one side of the fracture to the other. The fracture heals by primary bone healing and histologically with “cutting cones” that facilitate direct healing of one fragment to another (Fig. 5.4). Minimal to no fracture callus is observed. This may be achieved via a variety of methods discussed below, including lag screws, compression plates, and tension bands. Interfragmentary compression should be used in the fixation of intra-­articular fractures when possible, to rigidly fix the articular surface and allow for early mobilization. It should be avoided in highly comminuted fractures, as overzealous compression may lead to excessive collapse and shortening.

B

­ ­ Figure 5.3 Arthroscopic views of an intra-articular distal radius fracture showing pre-reduction (A) and post-reduction status (B). (Copyright by Dr Margaret Fok.)  

­

Treatment/­surgical technique

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A

B

Figure 5.4  Compressed osteotomy site. Note the migration of osteocytes across the fracture line, an example of contact healing. (Hematoxylin and eosin: magnification ×100.)

C

Relative stability Relative stability is important when treating comminuted fractures where anatomical reduction is not possible or in cases where closed reduction is elected. With relative stability, the primary focus is on restoring the anatomic relationship of the neighboring articular surfaces in length, alignment, and rotation. Some micromotion occurs at the fracture site, and, in fact, is conducive to this type of healing (secondary bone healing). Stability, however, must be adequate to maintain alignment and prevent excessive motion at the fracture sites. In contrast to primary bone healing via absolute stability, secondary bone healing occurs via progression through cartilaginous intermediaries and fracture callus is typically observed. Relative stability is typically achieved with external fixation, bridge plating, or intramedullary fixation. This concept, in general, is not commonly applied to articular fractures.

Methods of fixation Kirschner wires Kirschner wires (K-­wires) are inexpensive and simple, yet versatile tools to assist with fracture fixation. They may be inserted in either a percutaneous or open fashion and appropriate insertion causes minimal tissue trauma. They may be implemented either as provisional or definitive fixation.37,38 When used for definitive fixation, relative stability is generally obtained and healing occurs with callus formation. Insertion of K-­wires may be either directly across a fracture site or in an intramedullary fashion, commonly used in metacarpal fracture16 (see Fig. 5.2). The main limitation of K-­wires is that they do not allow for interfragmentary compression and may loosen over time, leading to implant migration. Sizes of Kirschner wires are usually reported either in terms of inches or millimeters. For instance, a 0.062-­inch K-­wire is the same caliber as a 1.6-­mm K-­wire. Sizes typically utilized in hand surgery range from 0.035 inches (0.9 mm) to 0.079 inches (2.0 mm), although larger wires may be used for specific circumstances. Most wires are available in either smooth or threaded varieties. Smooth wires allow for easy removal in a clinic setting, but are also more prone to unintended migration.

D

E

Figure 5.5  Tension band technique. (A) Transverse midshaft proximal phalangeal fracture with volar angulation and displacement. (B) Reduction without fixation allows compression of the volar cortex during digital flexion but unacceptable dorsal cortical instability, causing an unacceptable gap. (C) A figure-­of-­eight tension band wire is applied dorsal to the central axis of the proximal phalanx. (D) The loops on either side of the tension band are tightened simultaneously to achieve symmetric tension on both sides of the fracture. After the tension band wire is applied, the compressive forces created during digital flexion are evenly distributed across the entire fracture site. The tension band wire absorbs an amount of tension equal to the compression at the fracture site. (E) Dorsal view of the tightened tension band wire. Holes may be drilled in the bone, and the ends of the wire loops may be inserted into these holes to minimize soft-­tissue irritation. (Modified from Freeland AE. Hand Fractures: Repair, Reconstruction and Rehabilitation. Philadelphia: Churchill Livingstone; 2000:42.)

Threaded wires have a tendency to follow prior tracts within bone; advancing them with the drill on reverse somewhat negates this tendency.

Tension band constructs When bone is subjected to eccentric axial forces, one side of the bone is subjected to compression forces and the opposite side to tensile forces. A tension band,39–42 either in the form of a wire construct or a plate, aims to convert this eccentric tensile force into compression to assist with fracture compression and healing (Fig. 5.5). This concept is most applicable to simple, transverse fractures in the diaphyseal region and requires an intact cortex (no comminution) on the compression side. To accomplish this conversion of eccentric forces into compression, the tension band must be placed on the tension surface. Fortunately, in the hand, this is on the dorsal

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side of the metacarpals and the phalanges, allowing easier surgical access. As the patient actively flexes the fingers, the force of flexion on the annular pulleys is transmitted directly to the attached bone, and the vectors of force are through the volar cortex toward one another. Because the tension band fixes the dorsal cortex stably, the effect is to force the volar cortices against each other and, by this process, produce further compression of the fragments, thus attaining absolute stability. The exact configuration of the wires may vary with the individual fracture, but most commonly consists of a “figure-­ of-­eight” construct with dorsally crossed wires (Fig.  5.6). Typically, this is employed by passing the wire either through a drill hole or under a tendinous origin/­insertion on each side of the fracture. The wire can then be twisted to reduce and compress the fracture. Depending on the specific situation, one may use a twist on either side of the bone,

A

B

Figure 5.6  (A) A displaced transverse fracture of the mid-­diaphysis of the middle phalanx resulting from a glancing blow to the dorsum of the long finger. (B) Application of a tension band wire resulting in good interdigitation of the fracture so that it was held securely against rotational forces. (From Freeland AE, Jabaley ME, Hughes JL. Stable Fixation of the Hand and Wrist. New York: Springer-­Verlag; 1985:89.)

combine K-­wires with the intraosseous wires, or many other techniques. In the hand, 28-­gauge wire is adequate for a tension band in small phalanges; 26-­gauge wire serves in larger phalanges and metacarpals. Rotation may be controlled and stability augmented by accurately interdigitating the jagged edges of fracture fragments together (Table 5.1). A specific form of intraosseous wiring,43 the 90-­90 technique (Fig.  5.7), is useful, especially for arthrodesis, replantation, and transverse fractures. Although not a tension band strictly speaking, it is a rigid enough construct that it will permit immediate motion.

External fixation External fixation provides a useful, versatile option for fracture stabilization. This typically consists of pins placed on either side of the fracture with the pins connected to each other through an external apparatus. This may be employed as either temporary or definitive fixation.44 Reduction may be achieved through ligamentotaxis.13,44,45 While this may be used with any fracture, it serves a particular purpose when there is severe fracture comminution (Fig. 5.8) and/­or an element of soft-­tissue loss requiring reconstruction, thus minimizing the risk of infection when compared with internal implants. External fixators can typically be inserted through small incisions away from the fracture site and zone of injury, thus avoiding violation of the fracture hematoma. Knowledge of local anatomy together with proper techniques of pin insertion should be used to avoid damage to neurovascular structures/­collateral ligaments. For instance, when placing an external fixator for a distal radius fracture, great care should be used to avoid damage to the radial sensory nerve. Most authors advocate using an open approach and identifying the radial sensory nerve in this instance, although others have advocated percutaneous placement of the pins in a more dorsal position.46 Two main categories of external fixators exist: non-­bridging and bridging. Non-­bridging fixators47 only span the fracture site, while bridging fixators also span a joint. Bridging fixators are more often used with metaphyseal fractures and fractures associated with severe soft-­tissue injuries. Bridging fixators may also be combined with limited K-­wire or internal fixation for comminuted articular fractures.21,48,49 When bridging joints, care must be taken to avoid unwanted overdistraction.50 Some specialized bridging fixators are hinged to allow mobilization of the spanned joint.51,52 (Fig. 5.9) Relative stability is achieved

Table 5.1  Techniques for internal fixation

Interosseous wire (gauge)

Kirschner wire (diameter inches)

Interosseous (lag) screw (mm)

Plate (mm)

Distal phalanx

28

0.028/­0.035

1.3/­1.5

N/­A

Middle phalanx

28

0.035

1.3/­1.5

1.3/­1.5

Proximal phalanx

26/­28

0.045

1.5/­2.0

1.5/­2.0

Metacarpal

26

0.045/­0.062

1.5/­2.0

2.0

Carpal

24/­26

0.045/­0.062

1.5/­2.0/­2.4

2.0/­2.4

Distal radius

2.4/­2.7

Treatment/­surgical technique

A

B

115

C

Figure 5.7  This 37-­year-­old male had a saw injury to the palm of the hand. In addition to multiple tendon injuries, he sustained a severe injury to the cartilage of the thumb metacarpophalangeal joint (A). A primary fusion was elected with usage of 90-­90 interosseous wires and a supplemental K-­wire (B,C).

A

Figure 5.8  (A,B) A spanning external fixator has been applied to this highly comminuted fifth metacarpal shaft fracture.

B

with any method of external fixation and healing occurs with abundant callus via secondary bone healing.

Interfragmentary lag screws Lag screws (Fig.  5.10 & 5.11) provide compression between two fragments to achieve absolute stability. These may be used alone, in combination with another method of fixation, or through a plate. Lag screws are most useful in simple oblique or spiral fractures,53 but also may be used to piece together comminuted fractures. The utility of lag screws is very limited in the fixation of transverse fractures as proper orientation perpendicular to the fracture is difficult. If the trajectory of the

lag screw is not perpendicular to the plane of the fracture, a shear force is introduced.

Key concept Lagging by technique vs. lagging by design Insertion of a lag screw can be accomplished in two ways. Lagging by technique relies on screw placement technique to achieve interfragmentary compression, whereas lagging by design applies the design features of the screw to achieve compression.

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CHAPTER 5  • Principles of internal fixation

A

B

C

D

Figure 5.9  Dynamic external fixator. (A) A 35-­year-­old man sustained a closed base of middle phalangeal fracture of the middle finger and ring finger. (B) Radiograph illustrating the application of dynamic splints to both middle and ring finger. The fracture was reduced by ligamentotaxis (C). (D) Clinical photo illustrating the movement of the proximal interphalangeal joint of the middle and ring fingers with the splint in situ. (Courtesy of and copyright Dr Esther Chow.)

When placing a lag screw by technique, a proper site of insertion is selected first (see Fig.  5.10 and Video 5.1 ). Ideally, lag screws should be positioned perpendicular to the plane of the fracture. Long spiral fractures may be fixed with lag screws in different planes, but perpendicular to the fracture at each position. Screws placed too close to fracture edges may lead to fracture propagation. Second, the near cortex is overdrilled with a drill size equivalent to or slightly larger than the outer thread diameter of the planned screw. This allows the screw to “glide” through the near cortex as the screw is tightened. Next, the far cortex is drilled with a smaller drill size equivalent to the core diameter of the planned screw. Tapping may be done at this stage. However, most modern screws are self-­tapping. Next, the near cortex is countersunk. This increases the contact area of the screw head on the near cortex, thus distributing the forces more evenly and avoiding the high contact pressure that may lead to fracture propagation from the drill site into the fracture site. Countersinking also decreases

the prominence of the screw head, decreasing irritation of the overlying soft tissues. Finally, the screw length is measured with a depth gauge and the appropriate length screw is inserted. Visible compression across the fracture site is frequently observed. Care should be taken to avoid overcompression. In practice, caution must be used when utilizing lag screws in finger fractures especially in the metaphyseal region, as the cortex is thin, the bone is soft and the soft tissue overlying the far side of the fracture is easily irritated if the screw is too long. Lagging by design may be achieved by utilizing specially designed implants. Two types of screws commonly employed are partially threaded screws (Fig.  5.12) and headless compression screws. Partially threaded screws have threads at the tip of the screw but no threads below the screw head that allows the screw to glide through the near cortex. They may be placed after drilling bicortically with the core-­diameter drill and then placing the screw, which saves time intraoperatively. The utility of partially threaded screws may be limited by the relatively large size of the implant in many regions of

Treatment/­surgical technique

117

A

B

2.4

C

1.8

D

E 2.4

F

G

H

I

the hand and wrist. Another type of compression screw is the headless compression screw (Fig. 5.13 and Video 5.2 ). This screw has threads of varying pitches. The threads with greater pitch within one fragment lead to more travel per turn within that fragment compared to the finer pitch threads in the other fragment (Fig.  5.14). Thus, compression is achieved as the screw is advanced. A classic example is its use in scaphoid fractures (see Fig. 5.13 and Video 5.2 ).

Compression plating Compression plating is a method of obtaining absolute ­stability and interfragmentary compression through a specific method of plate application. This particular plating method is typically employed for oblique or transverse fractures.

Figure 5.10  Lag screw technique. A long oblique metacarpal fracture (A) is reduced and secured with a pointed reduction forceps. (B) A glide hole is drilled perpendicular to the fracture in the near cortex with a 2.4 mm drill bit. A drill guide is used to protect adjacent soft tissue and to prevent skating of the drill bit on the bone. (C) The opposite end of this double-­ended drill guide inserts into the 2.4 mm gliding hole. It has an internal diameter of 1.8 mm. A concentric 1.8 mm core hole is drilled in the opposite cortex (D). A countersink fashions an area in the proximal half of the dorsal cortex to correspond to and seat the screw head (E). A depth gauge determines the appropriate screw length (F). A 2.4 mm tap threads the core hole of the opposite cortex (G). A tap sleeve is used to protect the adjacent soft tissues. (This step may be omitted for self-­tapping screws.) A 2.4 mm screw is inserted. As the screw glides through the proximal hole, its head engages the proximal cortex (H). A second screw is applied in a manner similar to the first but in a plane perpendicular to the long metacarpal axis, thus satisfying the need for a neutralization screw (I). (Redrawn after Freeland AE. Hand Fractures: Repair, Reconstruction and Rehabilitation. Philadelphia: Churchill Livingstone; 2000:42.)

For transverse fractures (Fig. 5.15), the fracture is provisionally reduced and the plate is affixed to one side of the fracture in a neutralization fashion (holes drilled centrally within the screw holes of the plate). Next, a hole is drilled eccentrically (the portion of screw hole farthest away from the fracture) on the opposite side of the fracture. As the screw head engages the plate, it slides down the incline of the screw hole in the plate, thus causing the screw/­plate interface to translate toward the fracture site, leading to interfragmentary compression. In oblique fractures (Fig. 5.16), the plate should be affixed first to the side of the fracture that allows for an acute angle (or axilla) to be created between the undersurface of the plate and the fragment. This allows for the second fragment to be compressed into the axilla, thus entrapping the fragment and assisting with reduction and compression. If the opposite

118

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CHAPTER 5  • Principles of internal fixation

Head

Shaft

Length

Pitch

Core diameter

Figure 5.12  Anatomy of a partially threaded screw.

A

B

Figure 5.11  This 34-­year-­old woman sustained an oblique fracture of the ring finger proximal phalanx (A). Absolute stability was achieved through usage of multiple lag screws (B). Note that the screws are placed in different planes, but perpendicular to the fracture at each site.

sequence was done and an obtuse angle was created, further compression would lead to shortening and displacement of the fracture. An angled lag screw through the plate placed perpendicular to the fracture may be added to provide further interfragmentary compression.

A

B

Bridge plating

Figure 5.13   A 20-­year-­old woman fell onto her wrist and sustained a left scaphoid fracture (A). A headless compression screw is used for fixation (B). This device allows for interfragmentary compression while avoiding screw-­head prominence when treating intra-­articular fractures.

Bridge plating (Fig. 5.17) is a useful method of relative stability for stabilization of comminuted metaphyseal and diaphyseal fractures where anatomic reduction is either not possible or would require extensive dissection.54 Ideally, the fracture site should not be opened with this technique to avoid unnecessary surgical trauma to the surrounding soft tissues and allow for the preservation of vascularity to the comminuted fragments. Bridge plates are used in a similar manner to that of an external fixator and can be applied across a joint (Fig. 5.18). The principal goal is to restore length, alignment, and rotation

Figure 5.14  Headless compression screw. Headless compression screws have threads with variable pitch so that the screw advances at a different rate in the proximal and distal bone fragments as the screw is inserted. This achieves compression at the fracture site without the prominence of a screw head at an articular surface.

Treatment/­surgical technique

Dorsal view

119

Lateral view

A

B

C

Plate

Plate D Bone

Figure 5.15  Compression plate. This illustration demonstrates the application of a mini compression plate to a reduced transverse fracture of the mid-­metacarpal shaft. The straight miniplate has a graduated bend of about 5° centered at the middle of the plate. (A) Two neutral (centered) screws secure the plate to the left (distal) of the fracture. (B) A drill hole is placed eccentrically away from the fracture site in the first plate hole to the right of the fracture. (C) A screw is inserted in the eccentric drill hole. (D) As the screw is tightened and the screw head engages the plate, translation of the plate and bone in opposite directions causes compression at the fracture site. (E) After compression is obtained, a neutral drill hole is centered in the remaining plate holes. If further compression is desired a second offset hole may be used instead. (F) A neutral screw is inserted, completing the fixation. (Redrawn from Freeland AE. Hand Fractures: Repair, Reconstruction and Rehabilitation. Philadelphia: Churchill Livingstone; 2000:53.)

Bone

E

F

2 NS

A

1 NS

3 OS

4 NS

B

2 NS

1 NS

5 CS

3 OS

4 NS

C

Figure 5.16 Compression plate – compression screw (CS) within the plate. (A) Lateral view of a short oblique mid-diaphyseal metacarpal fracture in the coronal plane. (B) The fracture is reduced and a tension band plate is applied, compressing the fracture. It is essential to place the offset mini compression screw (OS) eccentrically away from the triangle of bone that is compressed into the “axilla” of the miniplate. (C) A large screw is placed across the fracture site, adding compression and stability. (Redrawn from Freeland AE. Hand Fractures: Repair, Reconstruction and Rehabilitation. Philadelphia: Churchill Livingstone; 2000:55.)  

 

­

120

SECTION I

CHAPTER 5  • Principles of internal fixation

A

B

C

D

Figure 5.17 Bridging plate. (A,B) Radiographs showing a comminuted fracture of proximal phalanx of left index finger. (C,D) Bridging plate was placed at the dorsal aspect of proximal phanlanx. (Copyright Dr Margaret Fok.)  

Treatment/­surgical technique

121

A B

C

D

of the proximal and distal fragments. Healing is indirect via callus formation. Alternatively, if inadequate bone is thought to be present to allow healing, this technique may be supplemented with a staged bone grafting procedure to stimulate healing (Fig. 5.19). The bridge plate concept is a powerful one, but the drawback is that an additional surgery is necessary for the removal of the implants.

Locked plating Locking plates allow for the creation of angular stable constructs to share load across a healing fracture (see

Figure 5.18  Spanning plate. (A,B) Radiographs showing fracture dislocation of right fifth carpal metacarpal joint (CMCJ) in a 25-­year-­old man. (C,D) Fracture and joint were reduced and fixed with a locking plate across the CMCJ. It was later removed when the fracture healed. (Copyright Dr Margaret Fok.)

Video 5.3 ). Special threads on the screw heads themselves allow for interdigitation with threads located within the screw hole of the plate.2 The resultant angular stable construct is no longer reliant on screw thread purchase within bone and may present an advantage in osteoporotic bone or in low-­density metaphyseal bone. Failure of this construct is not at the screw/­plate interface, but rather would represent catastrophic failure of the entire construct from the bone. Furthermore, because purchase within the far cortex is not mandatory, screws may be used in a unicortical fashion, thus avoiding soft-­tissue irritation in the tissues overlying the far side of the fracture.

122

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CHAPTER 5  • Principles of internal fixation

Figure 5.19  Bridge plate. A complicated fracture in the first metacarpal with comminution and bone loss has been excised and filled with an autogenous graft. This plate provides a modicum of compression and screws through it further stabilize the graft. (Reproduced with permission from Freeland AE, Jabaley ME, Hughes JL. Stable Fixation of the Hand and Wrist. New York: Springer-­Verlag; 1986:248.)

Locked plates may be applied in a variety of methods, depending on the particular fracture pattern (see Fig. 5.17 & 5.18). Compression, if desired, may be achieved through lag screws (either outside or through the plate) or usage of non-­ locked eccentrically placed compression screws (depending on plate selected).

Postoperative care The hand and wrist are prone to stiffness. Where possible, fixation should be stable enough to allow for early postoperative mobilization without allowing unintended motion across the

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fracture site.1,7 In certain circumstances such as the protection of any tendon repairs or the presence of associated injuries, the addition of external splints may be applied postoperatively to allow for controlled movement.7 Immobilization following fracture fixation may be done for several reasons including: need to protect the soft tissues during initial wound healing, desire to mitigate the possibility of secondary loss of reduction, protection of any neurovascular repairs, and inability of the patients to follow the rehabilitation protocol (e.g., children). Joint immobilization following fracture fixation may result in increased stiffness due to either tendon adhesions or capsular contraction. In the setting of articular fractures, unwanted alterations in cartilage physiology occur with immobilization. Several studies have showed a protective effect of early motion on cartilage following articular injury.55,56 Furthermore, some degree of micromotion across the fracture site may be beneficial for fracture healing, as illustrated in the examples of bridge plating and external fixation. This micromotion facilitates callous formation through the secondary bone healing pathway.

Summary Hand surgeons must be familiar with various aspects of proper fracture care and fixation. Decisions regarding optimal treatment rely heavily on careful consideration of patient-­ related factors and a detailed analysis of fracture morphology. Once operative management is chosen, a myriad of options are available. Comprehensive preoperative planning should be done to shorten operative times and ensure that adequate instrumentation is available. The type of stability desired, planned operative sequence, and desired implants should all be included in the preoperative plan. A thorough understanding of the key concepts underlying proper operative fracture care should lead to excellent surgical outcomes.

References

References 1. Harness NG, Meals RA. The history of fracture fixation of the hand and wrist. Clin Orthop Relat Res. 2006;445:19–29. 2. Mudgal CS, Jupiter JB. Plate and screw design in fractures of the hand and wrist. Clin Orthop Relat Res. 2006;445:68–80. 3. Henry MH. Fractures of the proximal phalanx and metacarpals in the hand: preferred methods of stabilization. J Am Acad Orthop Surg. 2008;16:586–595. 4. Helfet DL, Haas NP, Schatzker J, et al. AO philosophy and principles of fracture management-­its evolution and evaluation. J Bone Joint Surg Am. 2003;85-­A:1156–1160. 5. Logters TT, Lee HH, et al. Proximal phalanx fracture management. Hand. 2017;13:376–383. 6. Fok MWM, Ip WY, et al. Ten year results using a dynamic treatment for proximal phalangeal fractures of the hands. Orthopedics. 2013;36: 348–352. 7. Hardy MA. Priciples of metacarpal and phalangeal fracture management: a review of rehabilitation concepts. J Orthop Sports Phys Ther. 2004;34:781–799. 8. 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. J Bone Joint Surg Am. 2010;92:287–295. 9. Cowie J, Anakwe R, McQueen M. Factors associated with one year outcome after distal radius fracture treatment. J Orthop Surg. 2015;23(1):24–28. 10. Katz MA, Beredjiklian PK, Bozentka DJ, Steinberg DR. Computed tomography scanning of intraarticular distal radius fractures: does it influence treatment. J Hand Surg Am. 2001;26(3):415–421. 11. Welling RD, Jacobson JA, et al. MDCT and radiography of wrist fractures: radiographic sensitivity and fracture patterns. AJR Am J Roentgenol. 2008;190:10–16. 12. Jorgsholm P, Thomsen N, et al. MRI shows a high incidence of carpal fractures in children with posttraumatic radial sided wrist tenderness. Acta Orthop. 2016;87:533–537. 13. Agee JM. Distal radius fractures. multiplanar ligamentotaxis. Hand Clin. 1993;9:577–585. 14. Dee W, Klein W, Rieger H. Reduction techniques in distal radius fractures. Injury. 2000;31:48–55. 15. Newington DP, Davis TRC, Barton NJ. The treatment of dorsal fracture dislocation of the proximal interphalangeal joint by closed reduction and Kirchner wire fixation: a 16 year follow up. J Hand Surg Eng. 2001;26:537–540. 16. Corkum JP, Davison PG, Lalonde DH. Systematic review of the best evidence in intramedullary metacarpal fractures. Hand. 2013;8: 253–260. 17. Dowdy PA, Patterson SD, King GJ, et al. Intrafocal (Kapandji) pinning of unstable distal radius fractures: a preliminary report. J Trauma. 1996;40:194–198. 18. Kapandji A. [Internal fixation by double intrafocal plate. Functional treatment of non articular fractures of the lower end of the radius (author’s transl)] [in French]. Ann Chir. 1976;30:903–908. 19. Kapandji A. [Intra-­focal pinning of fractures of the distal end of the radius 10 years later] [in French]. Ann Chir Main. 1987;6: 57–63. 20. Silverman AT, Paksima N. Biplanar Kapandji intrafocal pinning of distal radial fractures. Am J Orthop (Belle Mead NJ). 2004;33: 40–41. 21. Trumble TE, Wagner W, Hanel DP, et al. Intrafocal (Kapandji) pinning of distal radius fractures with and without external fixation. J Hand Surg Am. 1998;23:381–394. 22. Athwal GS, Bueno Jr RA, Wolfe SW. Radiation exposure in hand surgery: mini versus standard C-­arm. J Hand Surg Am. 2005;30: 1310–1316. 23. Giordano BD, Baumhauer JF, Morgan TL, Rechtine 2nd GR. Patient and surgeon radiation exposure: comparison of standard and mini-­C-­arm fluoroscopy. J Bone Joint Surg Am. 2009;91: 297–304.

122.e1

24. Giordano BD, Ryder S, Baumhauer JF, DiGiovanni BF. Exposure to direct and scatter radiation with use of mini-­c-­arm fluoroscopy. J Bone Joint Surg Am. 2007;89:948–952. 25. Sinha S, Evans SJ, Arundell MK, Burke FD. Radiation protection issues with the use of mini C-­arm image intensifiers in surgery in the upper limb. Optimisation of practice and the impact of new regulations. J Bone Joint Surg Br. 2004;86:333–336. 26. Soong M, Got C, Katarincic J, Akelman E. Fluoroscopic evaluation of intra-­articular screw placement during locked volar plating of the distal radius: a cadaveric study. J Hand Surg Am. 2008;33:1720–1723. 27. Marsland D, Hobbs CM, Sauve PS. Volar locking plate fixation of distal radius fracture: use of an intra-­operative “carpal shoot through” view to identify dorsal compartment and distal radioulnar joint screw penetration. Hand. 2014;9:516–521. 28. Vaiss L, Ichihara S, et al. The utility of the fluoroscopic skyline view during volar locking plate fixation of distal radius fractures. J Wrist Surg. 2014;3:245–249. 29. Culp RW, Johnson JW. Arthroscopically assisted percutaneous fixation of Bennett fractures. J Hand Surg Am. 2010;35:137–140. 30. del Pinal F. Technical tips for (dry) arthroscopic reduction and internal fixation of distal radius. J Hand Surg Am. 2011;36: 1694–1705. 31. Doi K, Hatori Y, et al. Intra-­articular fractures of the distal aspect of the radius: arthroscopically assisted reduction compared with open reduction and internal fixation. J Bone Joint Surg Am. 1999;81: 1093–1110. 32. Yamazaki H, Uchiyama S, et al. Arthroscopic assistance does not improve the functional or radiographic outcome of unstable intra-­articular distal radial fractures treated with a volar locking plate: a randomized controlled trial. Bone Joint J. 2015;97:957–962. 33. Pomares G, Strugarek-­Lecoanet C, Dap F. Dautel. Bennett fracture: arthroscopically assisted percutaneous screw fixation versus open surgery: functional and radiological outcomes. Orthop Traumatol Surg Res. 2016;102:357–361. 34. Burnier M, Le Chatelier Riquier M, Herzberg G. Treatment of intra-­articular fracture of distal radius fractures with fluoroscopic only or combined with arthroscopic control: a prospective tomodensitometric comparative study of 40 patients. Orthop Traumatol Surg Res. 2017;104:89–93. 35. Bagby GW, Janes JM. The effect of compression on the rate of fracture healing using a special plate. Am J Surg. 1958;95:761–771. 36. Perren SM, Huggler A, Russenberger M, et al. The reaction of cortical bone to compression. Acta Orthop Scand Suppl. 1969;125: 19–29. 37. Belsky MR, Eaton RG, Lane LB. Closed reduction and internal fixation of proximal phalangeal fractures. J Hand Surg Am. 1984;9:725–729. 38. Gregory S, Lalonde DH, Fung Leung LT. Minimally invasive finger fracture management: wide-­awake closed reduction, K wire fixation, and early protected movement. Hand Clin. 2013;30:7–15. 39. Allende BT, Engelem JC. Tension-­band arthrodesis in the finger joints. J Hand Surg Am. 1980;5:269–271. 40. Jupiter JB, Sheppard JE. Tension wire fixation of avulsion fractures in the hand. Clin Orthop Relat Res. 1987:113–120. 41. Safoury Y. Treatment of phalangeal fractures by tension band wiring. J Hand Surg Br. 2001;26:50–52. 42. Pehlivan O, Kiral A, Solakoglu C, et al. Tension band wiring of unstable transverse fractures of the proximal and middle phalanges of the hand. J Hand Surg [Br]. 2004;29:130–134. 43. Lister G. Intraosseous wiring of the digital skeleton. J Hand Surg Am. 1978;3:427–435. 44. Agee JM. External fixation. Technical advances based upon multiplanar ligamentotaxis. Orthop Clin North Am. 1993;24:265–274. 45. Agee JM. Application of multiplanar ligamentotaxis to external fixation of distal radius fractures. Iowa Orthop J. 1994;14:31–37. 46. Emami A, Mjoberg B. A safer pin position for external fixation of distal radial fractures. Injury. 2000;31:749–750. 47. Eichenbaum MD, Shin EK. Nonbridging external fixation of distal radius fractures. Hand Clin. 2010;26:381–390, vi–vii.

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48. Weil WM, Trumble TE. Treatment of distal radius fractures with intrafocal (kapandji) pinning and supplemental skeletal stabilization. Hand Clin. 2005;21:317–328. 49. Egol K, Walsh M, et al. Briding external fixation and supplementary Kirchner wire fixation versus volar locking plating for unstable fractures of the distal radius – a randomized prospective trial. Bone Joint J. 2008;90:1214–1221. 50. Loebig TG, Badia A, Anderson DD, Baratz ME. Correlation of wrist ligamentotaxis with carpal distraction: implications for external fixation. J Hand Surg Am. 1997;22:1052–1056. 51. Hove LM, Krukhaug Y, Revheim K, et al. Dynamic compared with static external fixation of unstable fractures of the distal part of the radius: a prospective, randomized multicenter study. J Bone Joint Surg Am. 2010;92:1687–1696. 52. Ng CY, Oliver CW. Fracture of the proximal interphalangeal joint of the fingers. J Bone Joint Surg Br. 2009;91:705–712.

53. Horton TC, Hatton M, Davis TR. A prospective randomized controlled study of fixation of long oblique and spiral shaft fractures of the proximal phalanx: closed reduction and percutaneous Kirschner wiring versus open reduction and lag screw fixation. J Hand Surg Br. 2003;28:5–9. 54. Hanel DP, Lu TS, Weil WM. Bridge plating of distal radius fractures: the Harborview method. Clin Orthop Relat Res. 2006;445:91–99. 55. Salter RB, Simmonds DF, Malcolm BW, et al. The biological effect of continuous passive motion on the healing of full-­ thickness defects in articular cartilage. An experimental investigation in the rabbit. J Bone Joint Surg Am. 1980;62: 1232–1251. 56. Salter RB. The physiologic basis of continuous passive motion for articular cartilage healing and regeneration. Hand Clin. 1994;10:211–219.

SECTION II  •  Trauma Reconstruction

6 Nail and fingertip reconstruction Amanda Brown, Brian A. Mailey, and Michael W. Neumeister

SYNOPSIS

ƒ Fingertip and nail bed injuries are the most common injuries of the hand. ƒ Large subungual hematomas should be drained to relieve pressure and pain; small and asymptomatic hematomas ( 50% of the nail bed

Leave in place, unless pain syptoms are present

> 48 hours old

< 48 hours old

No fracture, no pain

Fracture, severe pain

Leave in place

Attempt trephination

No fracture or laceration, intact nail

Children < 5 years old

Children > 5 years old

Leave in place

Trephination alone

Fracture or lacerated nail bed present

Remove nail, repair nail bed if lacerated, K-wire fixation for unstable, displaced fractures and protect nail bed

Treatment algorithm for subungual hematoma.

The mechanism of injury generally constitutes a deforming force, which compresses the nail bed between the nail and the distal phalanx. A subungual hematoma results from injury to the nail bed, causing bleeding beneath the nail (Algorithm 6.1). Most commonly, injury to the nail bed is a simple laceration (Fig. 6.4A ), especially18 when the object causing the injury is small or sharp. A stellate laceration (Fig. 6.4B) occurs after compression with larger objects causing a bursting injury. Severe crush of the nail bed (Fig. 6.4C) is commonly caused by a wider, greater force of compression. Avulsion injuries (Fig. 6.4D) are the least common.18 Fingertip avulsions are most commonly result from being crushed in a house door.19 Most avulsions are partial avulsions of the fingertip; however, complete amputations are not unusual. Complete or partial avulsions heal exceptionally well in children, especially before adolescence, in comparison to adults.20 In fact, the literature suggests that children younger than 2 years are likely to show full distal tip recovery following amputation when managed without repair.19

Subungual hematoma Subungual hematoma formation causes separation of the nail from the nail bed. The pressure of bleeding in this closed space

frequently results in throbbing pain as pressure to the nail bed rises. Hematoma drainage is thus indicated for pain relief.

Treatment The current recommended method for drainage of an acute (less than 48 hours) subungual hematoma is trephination.21 Drainage is performed with a heated (red-­hot), sterile paper clip, battery-­ operated cautery, 18-­gauge needle,22 or 2-­mm punch biopsy,23,24 or in children, an insulin-­syringe needle may be used.25 The heated object burns a hole through the nail and is cooled by the underlying hematoma. The hole is made large enough to ensure prolonged drainage of the hematoma. A small hematoma will be incorporated into the nail and travel distally with nail growth. The decision to perform trephination is made by the size of hematoma and symptoms; not all hematomas require drainage. The extent of underlying nail bed injury is difficult to assess with a subungual hematoma. Some advocate the use of ultrasound to detect nail bed injuries.26 If there is minimal disruption of the nail bed, normal nail growth is expected. However, if a significant disruption of the nail bed is present, there is higher risk of nail deformity if the nail bed is not repaired. Therefore, whether a subungual hematoma should be drained with the nail left intact or the nail removed, and

Acute injury

A

B

127

C

Figure 6.5  An 11-­year-­old male crushed his left index finger in a fence and suffered (A) an avulsion injury of the nail plate with a stellate laceration of the nail bed in the sterile matrix with an intact germinal matrix. (B) The nail was taken off with a Freer elevator, the nail bed and hyponychium were repaired, and the nail plate replaced. (C) 4 months after injury and repair (left index finger) compared to the uninjured right index fingernail.

the nail bed repaired is debatable. In the past, removal of the nail for inspection of the nail bed with repair, as needed, was advocated for hematomas undermining more than 25% of the nail. Simon and Wolgin27 examined the nail beds of 47 patients presenting to the emergency department with a subungual hematoma and found that a hematoma >50% had a 60% incidence of laceration requiring repair. Repair of the nail bed was advocated with a hematoma >50% or an associated distal phalanx fracture. Many studies have shown that trephination has an equivalent cosmetic outcome and comparable rate of complications in the vast majority of cases.28–­30 At the University of Pittsburgh, a 2-­year prospective, observational study was designed to examine the outcome of 48 patients with subungual hematomas treated with drainage alone. No complications of nail deformity were found with this treatment, regardless of the size of hematoma or presence of fracture.31 Roser and Gellman32 compared three treatment groups in a prospective study of 52 children with subungual hematomas. A total of 26 fingers were treated with nail removal and repair of the nail bed. Drainage only was performed in 11 fingers, and 16 of 27 fingers were observed. No notable difference in outcome was found between the groups, regardless of hematoma size. It was concluded that nail removal and nail bed exploration are not justified in children with subungual hematoma with an intact nail and nail margin. A systematic review in 2012 evaluated four articles comparing nail bed repair with simple decompression and concluded the outcome of nail cosmesis did not differ by the mode of treatment.33 Leaving the nail in place is recommended for most subungual hematomas with an intact nail. Exceptions may include children or patients with concern for an optimally aesthetic nail. If the nail is broken or the edge disrupted, removal of the nail and exploration of the nail bed are advised (Fig. 6.5). The acutely painful subungual hematoma should be decompressed, whether done by trephination or nail removal.

Hints and tips Nail bed repair The nail bed handles like wet tissue paper; each suture should be thrown with two bites. Be conservative with the placement of sutures. The goal is simple –­reapproximation. Tension on the nail bed suture line will lead to excessive scarring.

Lacerations Avulsion of the nail, or nonadherence of the nail to the nail bed, is an indication for nail removal. Any loose nail should be trimmed and only enough of the nail that allows adequate exposure and repair of the nail bed laceration should be removed. Complete removal of the nail is not always necessary. With middle to distal nail bed injuries, it may be possible to leave the proximal nail undisturbed within the nail fold.

Treatment Exploration of the nail bed is performed with digital block, anesthesia, and tourniquet (e.g., a half-­inch Penrose drain or cut-­out from a sterile glove). The nail plate is gently removed from the nail bed with a small periosteal elevator or iris scissors. Careful removal of the nail is important to avoid further injury to the nail bed. Once removed, the nail is scraped to remove residual soft tissue, then soaked in povidone-­iodine (Betadine) solution. The nail bed is examined with loupe magnification. It is better to leave ragged edges and allow the replaced nail to mold the edges than to debride and cause tension on closure. Careful undermining of the edges may assist in reducing tension on closure. A double-­armed 7-­0 chromic suture on an ophthalmic needle is recommended. The suture

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is cut in half to provide a second stitch because the small ­needle is commonly bent during the repair. Reapproximation of the more complex stellate laceration and crush injury is more difficult. In these types of injuries, it may appear to be missing fragments. However, they are often present, attached to the undersurface of the nail. Small fragments should be gently removed with a periosteal elevator and used as a nail bed graft. A split-­or full-­thickness nail bed graft up to 1 cm in diameter will usually survive, even when it is placed directly on the distal phalanx cortex.7 Blood supply to the graft is established by inosculation and vascular ingrowth from the periphery. The scenario with nail bed fragments attached to the nail commonly occurs in avulsion type of injuries. To avoid further insult to the nail bed, leaving the large nail bed fragment on the nail is recommended. The edges of the nail are trimmed a few millimeters to expose the nail bed for suturing into the defect. Avulsion of the bed often occurs at the level of the germinal matrix and proximal nail fold, leaving a distally based nail bed flap of germinal or sterile matrix (Fig. 6.6A). The nail bed remains attached to the nail, avulsing the germinal matrix off the bone and out of the nail fold (Fig. 6.6B). The nail and germinal matrix must be separated, and the germinal matrix replaced and sutured back into the nail fold (Fig. 6.6C). The nail fold is exposed with unilateral or bilateral incisions perpendicular to the lateral corners of the eponychium. The incisions should be made at a 90° angle to the eponychium to prevent a notch deformity (Fig. 6.6D). If the laceration occurs at the junction of the ventral and dorsal roof of the nail fold, suture approximation may not be possible. In this case, a horizontal mattress stitch is placed through the proximal end of the avulsed nail bed and brought out through the nail wall. This will secure the nail bed within the nail fold. The eponychial incisions are then reapproximated with 5–­0 or 6–­0 nylon after nail bed repair. Loss of small areas of nail bed may be replaced with split-­ thickness nail bed grafts from adjacent uninjured nail bed, harvested carefully with a No. 15 scalpel blade (Fig. 6.7A,B). A split-­thickness nail bed graft may be harvested from an adjacent noninjured finger (risky) or an amputated finger. A split toenail bed graft may also be used acutely and avoids the possible deformity of an adjacent nail (Fig. 6.7C–­H).34 With exception of the great toe, the nail bed from the other toes is not large enough to supply enough graft for an entire finger nail bed. On completion of the nail bed repair, the nail is removed from the povidone-­iodine solution and a hole made in the nail away from the site of injury. The hole allows drainage of the subungual space after reinsertion of the nail into the nail fold. The nail is placed within the nail fold to mold the edges of the repair, to act as a splint for tuft or phalangeal fractures, to prevent formation of synechiae between the nail fold and the injured nail bed, and to protect the tender fingertip. The nail is held in place with a 5-­0 nylon suture placed distally through the nail and hyponychial region. On rare occasions with severe injury to the fingertip, a mattress suture may be placed proximally through the nail fold. If the nail is not available or is in small fragments, a piece of silicone sheeting (reinforced 0.020-­ inch-­ thickness silastic) may be shaped to fit beneath the nail fold and secured proximally through the nail fold (Fig. 6.8 ). Unlike the nail, the

silastic sheet is soft and easily slips from beneath the nail fold if it is secured only distally. Non-­adherent gauze may also be placed within the nail fold if no nail or silicone sheet is available. Hints and tips Nail plate replacement Trim the nail plate of sharp contours. Place the nail plate under the eponychial fold for a distance of 2–­3 mm. An absorbable suture can be used to hold the nail plate in place as an alternative to nylon. This will avoid painful suture removal.

Postoperative care The fingertip is dressed in nonadherent gauze, 2-­inch roll gauze, and a four-­prong splint to protect the repair. At 3–­7 days after repair, the holding suture is removed, especially if it is in the proximal nail fold position. The authors have observed stitch track formation in the nail fold if the stitch is left in place longer than 7–­10 days. If not disturbed, the nail will frequently adhere to the nail bed for 1–­3 months as the new nail forms beneath. Fingertip tenderness is usually less with the nail replaced.

Distal phalanx fractures Initial evaluation Distal phalanx fractures are found in approximately 50% of nail bed injuries and result in a higher incidence of secondary nail deformities.18 Therefore, multiple-­view radiographs of the distal phalanx are recommended. A Seymour fracture presents in children with the appearance of an elongated nail. The fracture occurs through the physis with interposed soft tissue, usually consisting of nail bed matrix but can include other tissues, like eponychial fold.

Treatment Treatment of non-­displaced distal fractures consists of nail bed repair and replacement of the nail. The nail acts as an excellent splint for the fracture. Small, displaced tuft fractures and most stable distal fractures can be reduced with reapproximation of the nail bed and replacement of the nail. Larger displaced fractures or unstable fractures require longitudinal or cross K-­wire fixation. Care must be taken to put the pin in the medullary cavity of the bone (see Fig. 6.9 ). K-­wires traversing the nail bed can cause a painful ridging deformity. Tuft fractures are the most common fracture seen in a patient with a subungual hematoma and an intact nail fold.20 Tuft fractures typically require finger splinting for at least 14  days; however, they may not require a splint at all. Zook et al.18 reported that distal phalanx or tuft fractures were associated with the occurrence of nail surface irregularities. Since then, it has been traditionally believed that bone continuity provides a smooth scaffold for the nail bed, which is considered necessary for natural-­appearing nail bed production. Range of motion exercises should begin without delay.

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A

D

Figure 6.6  (A) When the proximal nail is flipped out of the nail fold and is lying on top of it, one must remove the nail and explore the nail bed. (B) There is almost always a nail bed laceration with stripping of the germinal matrix up with the nail or a Salter fracture of the distal phalanx. (C) The laceration must be replaced and repaired. (D) Radial incisions are made in the eponychium to access the nail fold. It is almost impossible to replace the nail in the nail fold without its total removal and then sliding it back. (© Southern Illinois University School of Medicine.)

A

B

C

D

E

F

G

H

Figure 6.7 (A) A crushing injury to the tip of the finger with laceration of the surrounding skin. (B) After the skin is sutured, an area of cortex is seen. (C) A split-thickness sterile ­ ­ matrix graft is removed from an adjoining area on the finger or toe. Back-and-forth sawing with a scalpel blade will remove a small fragment of nail bed, which is slightly curved after the nail has been removed. The white line of the sharp edge of the blade should always be able to be seen so that the graft is not taken too thick with a resultant deformity. (D) The fragment of nail bed taken. (E) If a larger piece of nail bed graft is needed, it may be taken from proximal to distal; the tip of the knife blade is used to dissect up the split-thickness layer of nail bed. (F) The large toe after removal of the split-thickness nail bed graft. (G) A split-thickness nail bed graft is sutured into place over the periosteum without any manipulation of the cortex. (H) One year later, good regrowth of the nail and adherence are shown. (© Southern Illinois University School of Medicine.)  

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Secondary procedures

Treatment

Reconstruction

Scar must be minimized to allow normal nail production. Scar within the sterile matrix can occasionally be treated with excision and primary closure. The excised defect is frequently too wide to be approximated without tension and requires repair with a split-­thickness sterile nail bed graft from the same digit or a toe. In germinal matrix injuries, Johnson37 recommended releasing incisions in the lateral paronychial folds with bilateral central advancement of the germinal matrix, but our experience with this technique has been disappointing in traumatic deformities. Replacement of germinal matrix with sterile matrix will not be successful because sterile matrix grafts do not produce a nail. Split-­thickness germinal matrix grafts also do not produce hard nail growth. The germinal matrix defect requires repair with a full-­thickness germinal matrix nail bed graft.34,38 The second-­toe germinal matrix is a good option with its similar shape and size; the large toe is a second choice (Fig. 6.12). The patient is warned that use of the toenail germinal matrix will eliminate hard nail growth on the toe. This second-­toe nail defect is frequently more acceptable to patients than a defect of the great toenail. In the case of an existing bone spur, the nail bed is lifted free, and the spur is removed with rongeurs to produce a flat surface, and the nail bed is replaced.

The painful nonadherent, split, or hooked nail, may hinder work productivity in the laborer. For others, nail deformities, such as nail ridges, grooves, or absence of the nail may create self-­consciousness or an unsightly appearance. Goals for reconstruction should be based on concerns and wishes of the individual patient. Surgical measures often improve function and appearance but often do not produce a normal nail. The best chance for restoring a normal nail is at time of the initial repair. Most nail deformities are secondary to scarring of the nail bed with subsequent disruption of nail growth. Like other scars, it is recommended to wait at least 8–­12 months after injury before consideration of reconstruction. With scar remodeling, small nail deformities may resolve significantly or completely. Common secondary nail deformities seen after nail bed injury include nail ridging, splitting, nonadherence, absence, cornified nail bed, hook and spikes, or cysts.

Nail ridge Nail ridges are secondary to an irregularly healed distal phalanx fracture or scar within the nail bed. Nail ridges may also occur secondary to a K-­wire placed between the sterile matrix and the periosteum on reduction of a phalanx fracture (Fig. 6.9  ). The longitudinal ridges of the sterile matrix determine the direction of longitudinal growth35; as a result, it is important to match the direction of the defect during harvesting and grafting of a nail bed to avoid the growth of ridged-­appearing nails.36 Longitudinal irregularities result in longitudinal ridges or grooves. Transverse irregularities beneath the nail bed result in corresponding transverse grooves or ridges or distal nonadherence. Correction of this deformity requires excision of the scar or irregular bone edge to form a flat, smooth nail bed surface.7,17 A defect that cannot be reapproximated primarily requires use of a nail bed graft. Transverse nail ridges may develop secondary to hypoxia from ischemic injury or tourniquet hemostasis. The ridges resolve with correction of the inciting factor and subsequent new nail growth.

Split nail A split nail is often secondary to longitudinal scarring of the germinal or sterile matrix. Unlike the germinal and sterile matrices, the scar does not produce nail cells, resulting in splitting of the nail. Scar within the germinal matrix can split the nail from its most proximal aspect. Scar within the sterile matrix disrupts the progressive addition of nail cells to the volar nail, leading to detachment of the nail plate (Fig. 6.10 ). Other causes of split nails include bone spurs beneath the nail bed, eponychial pterygium resulting from failure of the dorsal roof matrix to detach from the nail, and scar formation between the dorsal roof and ventral floor of the nail fold. Although longitudinal splits are most common, a horizontal split has been reported; it caused a diagonal scar in the matrix and formation of a portion of the nail on each side (Fig. 6.11  ). The nail was produced within both folds, forming a horizontally split nail.

Pterygium Splitting of the nail may also be caused by a pterygium. A pterygium of the eponychium results from adherence of the eponychium or dorsal roof of the nail fold to the nail plate or nail bed during healing. A web between the eponychium and nail bed will result in splitting of the nail as it grows distally from the nail fold (Fig. 6.13 ).

Treatment Simple pterygia are amenable to warm water soaks until the eponychium can be bluntly separated from the nail. Sharp dissection of the eponychium from the dorsal nail is performed if blunt dissection is unsuccessful. Separation between the dorsal roof and nail is then maintained with nonadherent gauze or a silastic sheet. This allows epithelialization of the undersurface of the nail fold. If adherence persists between the dorsal roof and the ventral floor (matrix) of the nail fold, it must be divided surgically. Once the nail fold has been redesigned, maintenance of the separation must be achieved with nail, silicone sheet, or gauze until healing occurs. If a large raw surface is present after freeing, a split-­thickness sterile matrix graft can be placed on the raw surface of the dorsal roof. If the scar has completely replaced the normal germinal matrix, a full-­thickness germinal matrix graft is necessary.

Nonadherence (onycholysis) Nonadherence of the nail is the most common post-­traumatic nail deformity. This occurs secondary to nail bed scarring and is often found immediately distal to transverse or diagonally oriented nail bed scars or bone irregularities. The scar interrupts the progressive addition of nail cells from the sterile matrix to the volar nail plate, causing detachment of the nail. The nail is unable to reattach to the nail bed distally.39

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B

C

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D

Figure 6.12  (A) Avulsion of a portion of the germinal matrix with a split nail. (B) The sterile matrix has been reapproximated after resection of the scar, and a toe germinal matrix graft is shown before insertion in the germinal matrix. (C) Insertion of the germinal matrix graft as a free graft into the sterile matrix. (D) At 6 months, the graft of germinal matrix is shown to be growing nail. (© Southern Illinois University School of Medicine.)

Distal nonadherence may lead to problems with subungual hygiene, an unstable nail when picking up small objects, pain from repeated avulsions when catching the nail on objects or may simply be an aesthetic concern.

be unpredictable and at times unsuccessful secondary to non-­ take or shrinkage of the graft. Patients should be informed of the risk of toenail deformity and a possible suboptimal outcome. The most reliable and normal-­appearing nail is constructed with a free vascularized dorsal tip of the toe.44–­47 This proTreatment cedure can be technically difficult, requiring microsurgical Nonadherence secondary to a nail bed scar is corrected with expertise, and produces scarring of the foot from harvest of scar excision and primary closure or closure with a split-­ the vascular pedicle. thickness sterile matrix graft from the adjacent nail bed or Skin grafts, as opposed to nail bed grafts, have been used toenail bed.39–­41 with some success to mimic the nail. This method has been Malalignment of distal phalanx fractures may cause non- advocated for treatment of traumatic nail absence and conadherence. Prevention begins with accurate alignment of the genital nail absence in which multiple digits are involved fracture at initial repair. Secondary deformities caused by bone (Fig. 6.14). The scar is excised from the fingertip in the shape exostosis, bone angulation, or non-­union will require revision. of a larger than normal nail (10% larger) and replaced with The exostosis should be removed to form a flat surface for the a similarly shaped split-­or full-­ thickness skin graft. Full-­ sterile matrix and subsequent nail adherence. Bone angula- thickness grafts can be placed proximally and distally to tion may require osteotomy of the distal phalanx to re-­form simulate a white lunula and hyponychia, respectively. An a flat surface. artificial nail can then be fixed to the healed skin with glue, but patients may have difficulties maintaining the nail in place with glue alone. To aid in nail adherence, Buncke and Nail absence (anonychia) Gonzalez48 reconstructed the proximal fold using a prosthesis Any process, including trauma, infection, and burn, which wrapped in split-­thickness skin graft and buried it under the destroys the nail matrix will lead to an absent nail. Frequently, dorsal finger skin. Artificial nails were then secured beneath small nail remnants will remain that can cause other second- the new fold. Unfortunately, the fold was only temporary and ary deformities. Nail absence is also rarely seen as a congeni- slowly disappeared with time. Baruchin et  al.49 described an tal deformity known as anonychia. osseointegrated anchorage device to secure the artificial nail.

Treatment

Cornified nail bed

Free partial and composite nonvascularized nail grafts have been described by McCash42 and Lille et al.43 for reconstruction of absent nails. Both germinal and sterile matrices are needed for total reconstruction of a nail bed. Zook recommended a full-­thickness second-­toe germinal and sterile matrix graft to approximate the width of the fingernail.9 To match the length of the fingernail, a split-­thickness sterile matrix graft from another toe is placed distal to the free composite graft. The large toenail is used for thumbnail reconstruction. Results can

With ablation of the germinal matrix, nail production ceases. However, an intact sterile matrix will continue to produce varying amounts of keratinous material, resulting in a cornified nail bed.

Treatment Treatment for a cornified nail bed includes excision of the sterile matrix and replacement with a split-­thickness skin graft.

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the tip of the finger. Healing of a distal amputation site by secondary intention may also pull the nail bed volarly over the tip. Because the growing nail follows the direction of the nail bed, the nail grows in a hooked fashion, curving around the fingertip.

Treatment

Figure 6.14   A nail-­shaped split-­thickness skin graft is placed on the dorsum of the finger to mimic a nail. (© Southern Illinois University School of Medicine.)

Overproduction of keratinous material from the sterile matrix can also occur beneath a nail from chronic repetitive partial avulsion, allowing build-­up beneath the distal nail, leading to nonadherence. Treatment includes removal of the nail to a point just proximal to this area of overproduction. The keratinous material is scraped from the nail bed with a scalpel blade. The nail is then able to adhere to the nail bed during distal growth. The process may need to be repeated if overproduction on the exposed nail bed occurs more quickly than nail growth (Fig. 6.15 ). Sterile matrix grafts may be necessary if scraping is unsuccessful (Fig. 6.16 ).

This deformity can be avoided during repair of the acute injury by following two rules. The nail bed should never be pulled over the tip of the distal phalanx. If bone support beneath the nail bed is missing, it must be replaced, or the nail bed shortened to match the length of the remaining distal phalanx. Correction of the hooked nail secondary to the distal nail being pulled over the tip comprises release of contracted soft tissue, return of the nail bed to its normal position, and replacement of fingertip soft tissue. A full-­thickness skin graft, V–­Y advancement flap, cross-­finger flap, or proximal thenar crease flap can be used to augment the tip and reposition the nail bed on the dorsum of the distal phalanx.50 When bony support is missing, the options are either to shorten the nail bed or add bony support to maintain length. Non-­vascularized bone grafts have been placed distally with successful initial support of the nail bed. However, they often resorb with time, and the correction is lost.7 Osteotomy and distraction of the distal phalanx with placement of a bone graft between the distracted segments has been proposed to decrease the incidence of graft resorption but may be technically difficult. Bubak et  al.51 described a repair of a hooked nail deformity using a composite second-­toe graft for tip support. A fishmouth incision is made in the hyponychium and carried proximally on the lateral aspects of the digit until the nail bed is released. An elliptical, transverse wedge of skin and pulp is excised from the second toe and placed beneath the released nail bed. Good results were reported with a 2-­year follow-­up. Free vascularized second-­toe tip (bone, soft tissue, and nail bed) transfer has been presented as a more permanent yet more complex option.45

Eponychial deformities

On elimination of the nail bed or amputation of the distal phalanx, care must be taken to excise the germinal matrix completely. Any residual matrix allows continued production of nail cells. These cells produced within a closed space form nail cysts and the cells that can grow distally form nail spikes.

Eponychial deformities occur as sequelae after trauma, burns, tumor, infection or any process causing direct destruction of the nail fold tissue. As the tissues heal, scar contractures create the final deformity. Loss of eponychium causes more of an aesthetic defect than a functional one. Notching or loss of the eponychium exposes more of the proximal nail and results in loss of nail shine. Despite this change in appearance, there is no effect on nail growth.

Treatment

Treatment

Treatment consists of complete surgical removal of the cyst or spike along with the residual matrix. These deformities are seen more commonly after revision amputations performed in the emergency department.

The three-­dimensional structure of the nail fold makes reconstruction difficult. Multiple local rotation flaps have been described. Reconstruction of a nail fold with both inner and outer surfaces has been described with use of rotation flaps lined with split-­thickness skin grafts.17 Hayes52 used distally based ulnar finger flaps for creation of the nail fold without reconstruction of the inner surface. Kasai and Ogawa53 modified Hayes’ technique of distally based ulnar finger flaps by using the local tissue to reconstruct the inner surface. The scarred eponychial tissue is incised proximally and turned

Nail spikes and cysts

Hooked nail The hooked nail is a nail that hooks volarly during distal growth. This deformity is commonly seen after tight closure of tip amputations. On closure, the nail bed is pulled around

Acute injury

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C

Figure 6.17  (A) Loss of eponychium secondary to trauma with resultant irregularity and roughness of the nail. (B) One year after a full-­thickness composite graft of second-­ toe dorsal roof transfer to the finger. Note the improvement in the contour and shine of the dorsum of the nail. (C) The eponychial graft was taken from the second toe and here shows essentially no deformity. (© Southern Illinois University School of Medicine.)

over distally to form the nail roof. An ulnar, dorsal flap is then raised on a distal base and placed on top of the new roof to form the new eponychium, with split-­thickness skin grafting of the donor site. Achauer and Welk54 described a one-­ stage reconstruction of the burn-­ scarred eponychium with dorsal transposition of bilateral proximally based lateral digit flaps. A composite eponychial graft of skin and dorsal roof from the first or second toe to the eponychial defect is recommended. This eponychial graft has been found to improve appearance and restore the shine to the nail (Fig. 6.17). The eponychial flap is a technique used for fingertip injur­ ies when the eponychium is intact. This flap lengthens the appearance of the visible nail. It was first presented in 1998 by Bakhach55 and is indicated for fingertip injuries with a resultant small stump of intact nail and nail bed. The procedure consists of incising the dorsal eponychium with two radial incisions, elevating the dorsal eponychium as a flap and suturing it down in a more proximal location. This can be done at the time of acute injury or as a later reconstructive procedure.56

Hyponychial defects The keratinous plug of the hyponychium may hypertrophy secondary to acute or chronic trauma to the distal nail and hyponychium. When this occurs, it may protrude beyond the nail and cause pain when it is bent or pressed with use of the finger. It may also produce an unsightly protrusion from under the nail (Fig. 6.18 ). Loss of the hyponychium results in lack of support of the nail and a hook nail deformity. To prevent hygiene and cosmetic issues, patients must keep their nails trimmed. Alternatively, further shortening of the digit or nail bed ablation would be required.

Treatment Treatment for the hypertrophic hyponychium requires determination of the inciting activity, which is often something

that causes acute or chronic irritation. Initial management consists of avoidance of process producing the pathology. If irritation cannot be avoided or if symptoms persist despite avoidance, excision of the hypertrophic hyponychium and coverage with a split-­ thickness sterile matrix graft have resulted in a high incidence of symptom relief. The split-­ thickness sterile matrix graft is carried out in the same manner as with replacement for avulsion of a portion of the sterile matrix or scar excision.

Pigmented lesions The differential diagnosis for pigmentation of the nail bed is complex; it includes subungual hematoma, foreign body, onychomycosis nigricans, junctional nevi, pyogenic granuloma, paronychia, vascular lesion, melanonychia striata, melanoma in situ, and malignant melanoma.57 Although most pigmented lesions of the nail are benign, they should be evaluated carefully to rule out malignancy.

Patient presentation The history of the pigmentation is generally the most valuable aspect to making the diagnosis. Trauma may cause bands of pigment, especially in darkly pigmented individuals. Development of pigment in adults, even without a known history of trauma, is often secondary to a subungual hematoma, but the differential diagnosis of malignant melanoma must be considered (Algorithm 6.2). These suspicious areas can be monitored by scratching the nail at the proximal and distal edges of the pigment with a scalpel blade or 18-­gauge needle (Fig. 6.19). Distal migration of pigmentation over 3–­ 4  weeks, together with the scratch marks suggests a hematoma. However, if the scratch marks move distally, away from the pigment, this suggests foreign body, nevus, or melanoma. The evaluation of nail clippings can also provide some diagnostic value.58 To do this, a sample at least 4 mm in length is required and can be used to diagnose a number of conditions, including melanonychia, subungual hematoma, onychomycosis and others.58

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Algorithm 6.2 Subungual pigmentation

History of trauma Yes

No

Traumatic pigmentation most likely

3-4 weeks later

*Scratch nail at proximal and distal edges of pigment with scalpel or syringe and recheck in 3-4 weeks

Scratch test *

Distal migration of pigment and scratch marks

Distal migration of scratch marks alone

Most likely subungual hematoma

Foreign body, nevus, or melanoma

3-4 weeks later

Nail clipping evaluation or biopsy

Differential diagnosis of malignant melanoma.

Melanonychia striata is defined as any linear tan-­brown-­ black pigment of the nail bed that is carried into the nail as growth occurs. This pigmentation is caused by focal increase in the number or function of melanocytes. Melanonychia striata is common in individuals with darkly pigmented skin but uncommon in those with fair skin (Fig. 6.20). Subungual nevi produce pigmentation within the nail bed and the ventral nail. These pigmented nevus cells are derived from neural crest cells and are frequently present at birth or shortly thereafter. The nail is frequently pigmented with elevation and ridging (Fig. 6.21). Fleegler and Zeinowicz59 recommended nail bed biopsy of dark streaks present at or shortly after birth because of the danger of malignant degeneration at puberty. Melanocytic hyperplasia without atypia can be observed. However, complete excision with reconstruction of the nail bed is advised if atypical cells are found.

Subungual melanoma

Figure 6.19  Scratching of the nail proximal and distal to the pigment to determine whether the pigment is in the nail or in the nail bed. (© Southern Illinois University School of Medicine.)

Nail melanoma is an infrequent cause of brown-­black nail color compared to other melanocytic and nonmelanocytic pigmentations. More common causes of nail discoloration are subungual hematoma, exogenous pigmentations and melanonychia, which are all benign. In a review of 100 patients seen at a dermatology clinic for nail discoloration, 25 required additional evaluation, but only one had a melanocytic pigmentation that required a

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frictional melanonychia. Next, the appearance of the nail itself can provide diagnostic information, including trauma, psoriasis, and nail tumors (onychopapilloma, onychomatricoma, Bowen’s disease). Nail clippings can also be used to assist in the diagnosis. Finally, if the diagnosis has not been determined then removal of the nail plate and a histopathologic evaluation of tissue is required.60 Subungual melanoma represents only 1–­2% of all cutaneous melanoma and usually affects the thumb or big toe.61 An important clinical clue to subungual melanoma is characterized by extension of brown or black pigment from the mail bed, matrix and nail plate to the adjacent cuticle and proximal or lateral nail folds; this is known as Hutchinson’s nail sign. There are two stages to melanoma growth. The first stage is superficial, radial growth under the nail plate, followed by a vertical growth. At this stage, the lesion begins to develop a more dramatic change in appearance.

Treatment

Figure 6.20  The melanocytic streaks in an African American patient after trauma to the perionychium (arrowhead). (© Southern Illinois University School of Medicine.)

Figure 6.21   A newly occurring pigmented streak that originates in the germinal matrix or proximal to the observable pigment. (© Southern Illinois University School of Medicine.)

surgical evaluation.60 Most lesions can be diagnosed by history alone. The first determination is to decide if the pigment is due to melanin within the nail. This step can help exclude exogenous pigmentations, fungal melanonychia, and subungual hematoma. Examining the other digits can reveal racial melanonychia, effects of systemic drugs or pregnancy, endocrine disorders and

The historic standard treatment recommendation for subungual melanoma has been en bloc partial or complete digit amputation. This strategy was considered the safest means of obtaining clear margins, preventing recurrence and metastasis. This rationale, however, was not based on clear scientific evidence, but rather the principles of wide excision for what was thought to be an aggressive malignancy. Current evidence suggests this disease is not more aggressive than their more common cutaneous counterpart of similar depth.62,63 The original evidence to support these recommendations came from Dasgupta et al. in 1965.64 They presented 34 patients with subungual melanoma treated with amputation at different levels. Three patients who underwent a less aggressive form of amputation recurred and subsequently died from their disease. Based on these findings, it was determined that local amputation was not an adequate resection. However, it should be noted that they did not present the depth of these lesions and half of the patients in the study were being treated for recurrent melanoma or already had regional lymph node metastases at time of treatment. Therefore, the conclusions derived from Hutchinson’s and Dasgupta’s findings regarding aggressive amputation are not appropriately supported by their evidence. Today, interphalangeal joint amputations are the most commonly performed treatments for this disease. However, digit sparing procedures in appropriately selected cases have also been successfully performed. The precedent for digit sparing came from a study in 1992 by Park et  al.65 In this paper, the authors described treating subungual melanoma in situ without amputation. This was followed by a number of series in the literature presenting similar experiences with variable results, but not infrequent recurrence. Today, it seems wide excision can be an option for patients with melanoma in situ. However, they should be followed closely for signs of disease recurrence. A complete discussion and further in-­depth review of available literature is available in a paper presented by Cochran et al. in the August 2014 issue of Plastic and Reconstructive Surgery.66

Pincer nail Pincer nail deformity is described as lateral hooking or excessive transverse curvature of the nail plate, unilaterally or bilaterally (Fig. 6.22). The progressive tubing of the nail eventually

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CHAPTER 6  • Nail and fingertip reconstruction

or international centers.69 For soft-­tissue fingertip injuries, local flaps were preferred over secondary intention or skin grafts more commonly in surgeons with a plastic surgery background or with more than 30 years of experience.69 Younger surgeons were also more likely to perform skeletal shortening than those with more than 5 years’ experience.69 The Allen classification70 is commonly used to describe the level of fingertip injury, as thought of in a transverse amputation. Type 1 injuries involve the pulp only. A type 2 injury also involves the nail bed. Concomitant distal phalangeal fractures with associated pulp and nail represents a type 3 injury and the type 4 injury occurs more proximal with involvement at the level of the lunula. Figure 6.22  Unilateral pincer nail deformity. (© Southern Illinois University School of Medicine.)

pinches off the nail bed and hyponychium, resulting in an unaesthetic, painful nail. Pincer nail is most commonly seen in middle-­aged to elderly women. The cause of the pincer nail is not known.

Treatment Previous treatments have included resection of a wedge of the phalanx to flatten the nail edges and release of the nail bed with a medial longitudinal nail bed incision and split-­thickness skin graft coverage of the resultant triangular defect.67 They have been largely unsuccessful. Brown et  al.68 have advocated the use of dermal graft strips between the lateral nail bed and the distal phalanx periosteum for elevation of the lateral borders of the nail bed. The nail is removed, and incisions are made at the tip of the digit to allow freeing and elevation of the paronychial folds from the periosteum (Fig. 6.23 ). The dermal grafts are placed within this space to maintain the elevation and to flatten the nail bed. Our preferred technique is a modification of this, using human acellular dermal matrix in place of autologous dermal strips. We have achieved equally good correction of pincer nail without the addition of an additional donor defect. In more severe cases, the pain from a pincer nail deformity may be severe enough to warrant surgical ablation of the nail bed, especially if other forms of reconstruction are unsuccessful.

Reconstruction of fingertip injuries Reconstructing defects on the fingers requires thorough knowledge of a variety of coverage options. Treatment possibilities range from simple, including an occlusive dressing to allow healing by secondary intention, to extremely complex, including free pulp transfer. As the surgeon considers each possibility to obtain definitive closure, one must also integrate the priorities of function, contour, stability, and the anticipation for further reconstructive surgery. The reconstructive decision is based on characteristics of the defect, including size, shape, location, and availability of donor sites. Age, occupation, and individual attributes of the patient ultimately play the largest role in appropriate selection of the reconstructive plan. The final decision is made by the patient; however, the surgeon may affect this choice. A survey sent out to American Association for Hand Surgery members revealed that US and private practice physicians were less likely to perform replantations than academic

Reconstructive principles The principles of wound management in the traumatized digit or hand are the same basic guidelines that apply to the rest of the body and include irrigation, debridement, and restoration of vascularity. Stabilization of fractures and repair of specialized tissues such as nerve and tendon become the second priority, followed by the definitive soft-­tissue coverage. The skin of the hand and the fingers varies from palmar to dorsal sides. The palmar aspect is covered with glabrous skin notable for its limited sheer, high friction coefficient and papillary ridges, which create the characteristic fingerprint. Numerous fibrous septae compartmentalize subcutaneous tissue of the palm with fibers from the underlying dermis to the musculoskeletal structures below. The mid-­axial line of each digit is formed by connecting the lateral volar finger crease at the distal interphalangeal joint (DIP), proximal interphalangeal joint (PIP), and metacarpal phalangeal (MCP) joint. It is at this line that the transition from the glabrous to nonglabrous skin of the hand occurs. The mida­xial line corresponds to the midline of the phalanx. Whereas the true midlateral line of the finger corresponds to the location of the neurovascular bundle. The dorsal skin is relatively soft, pliable, and thin. It is devoid of the fibrous septae observed in the volar skin.14 The importance of understanding the difference of glabrous and nonglabrous skin comes to light when one observes one of the dictums of reconstructive surgeons to replace “like with like”. Local flaps that include glabrous skin should be considered first for glabrous defects. The relative limi­ted and inelastic quality of glabrous skin on the body prevents reconstruction of large glabrous defects with similar tissue. In such cases, alternative strategies must be employed, including using spare parts in a multi-­digit injury, use of multiple grafts for a single defect, leaving wounds with non-­ vital structures exposed to heal by secondary intention or coverage with nonglabrous skin. Dorsal skin more closely resembles skin on the anterior trunk and defects of the dorsal hand and fingers can readily be closed with other similar quality skin.

Flap selection A multitude of available flaps can produce good outcomes for both the recipient and donor site. Each flap has inherent advantages and drawbacks. Ultimately, flap selection is dependent upon variables such as size, shape, location of the defect, and the characteristics of the tissue lost. The hand surgeon must select the most ideal flap to restore as many as possible of the native skin characteristics present prior to the defect, and to provide the quickest means of wound closure. Efficient wound closure becomes a higher priority to prevent finger stiffness and maximize hand function.

Reconstruction of fingertip injuries

Fingertip injuries should be thoroughly irrigated and debrided of foreign material and nonviable tissue before closure is attempted. If the entire defect cannot be closed primarily, the wound can be partially closed, and the remainder allowed to heal by secondary intention. Suture selection varies by surgeon preference. If possible, the wound should be closed with a chromic or other resorbable suture. Nylon sutures in the fingertip are not usually necessary; they are uncomfortable to remove in the early follow-­up periods. The wound is covered with a non-­stick dressing like Xeroform or other minimal adherence dressing. Daily dressing changes permits rapid wound healing. Early motion is encouraged to prevent stiffness at the DIP or PIP joints. Larger wounds can heal by secondary intention if bone, tendon, or neurovascular structures are not exposed. Wounds up to 2–­3 cm may be allowed to heal by re-­epithelialization, but both surgeon and patient must be aware that closure may take 4–­6 weeks (Fig. 6.24 ). Previously, authors advocated that defects >1 cm should be closed with local flaps.71 However, secondary intention offers many advantages over flap closure, including improved contour, sensation, and lack of donor site morbidity.72

Skin grafting

137

over tendons can provide an interface that accepts a skin graft and prevents scar adhesion formation that prevents motion (Fig. 6.25). Distal fingertip amputations often comprise skin, subcutaneous fat, and a portion of the nail bed. The amputated part may be replaced as a composite graft after defatting, called a cap graft.74 The overall success rate of composite grafts is poor in the adult population and better in children 10 mm

Reduction and pinning

Volar base of distal phalanx subluxed in volar direction compared to middle phalanx

Reduction and pinning

Mallet fracture (closed)

Mallet fractures. Most mallet fractures can be managed with splinting. Operative treatment generally involves reduction and pinning as the nail matrix, extensor, and flexor tendons, and bone quality generally preclude plate fixation. If the joint is congruent, extension splinting with the PIP joint free is preferred. In the event there is a large, displaced fragment (generally >10 mm) or volar subluxation of the distal phalanx, reduction and pinning can be helpful. Treatment always involves a discussion with the patient or the risks and potential complications with any approach.  

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of malrotation, which is best evaluated with the fingers in flexion. Any malrotation is an indication for reduction and stabilization. Oblique fractures tend to be unstable, even following closed reduction, and often result in shortening, which is poorly tolerated by the extensor mechanism. Spiral fractures shorten and rotate. Therefore, these fractures are usually best treated with stabilization. Stiffness is common following these injuries, making postoperative rehabilitation important to optimize the outcome. Plate and screw fixation can provide good stability and allow early motion, but hardware tends to irritate extensor tendons, often resulting in adhesions, necessitating removal and tenolysis to improve tendon gliding. Lag screws are better tolerated than plates, but still require soft-­tissue dissection, which can result in adhesions and limit postoperative motion. K-­wire fixation can often be accomplished with minimal soft-­tissue stripping, providing functional stable fixation, and can easily be removed following healing. The fixation is not rigid, so the rehabilitation program cannot be as aggressive, generally focusing on active motion without resistance. These fractures take longer to heal due to the higher ratio of cortical to cancellous bone (in comparison to the proximal phalanx and metacarpal) but are usually stable enough for K-­wire removal between 4 and 6 weeks. Radiographic healing may take up to 4 months. A removable orthosis for protection and protected motion with buddy strapping is instituted to maximize motion.

fractures (involving the insertion of the central slip of the extensor mechanism), the volar base, resulting dorsal subluxation of the middle phalanx, avulsion of the collateral ligaments, or pilon type of fracture involving the dorsal and volar margins, with a depressed central articular fragment (Fig. 7.4). Fractures involving the proximal phalanx head can involve one or both condyles and can occur with or without proximal extension. Pure dislocations result from hyperextension and an axial load. They are often dorsal dislocations and are managed similar to the DIP joint, with an initial trial of closed reduction (with the wrist and fingers flexed and distal pressure on the base of the middle phalanx). When successful, a dorsal blocking splint and early active flexion can produce good results. When reduction cannot be completed by closed means, open reduction is indicated, either through a volar or midlateral approach.14 Volar dislocations are less common but can lead to late deformities if not recognized and treated.15 The central slip is often injured and can result in late boutonnière deformities. Following reduction, splinting the PIP joint in extension and active flexion of the DIP joint will allow gliding of the lateral bands. Active flexion can be started around 3 weeks,

PIP joint injuries Injuries around the PIP joint are challenging to treat and good outcomes can be difficult to obtain. Stiffness is common and causes difficulty with gripping and grasping activities, as well as fine dexterity. The small size of the articular fracture fragments can make it difficult to maintain reduction. The goal in treating injuries of the PIP joint is to create a congruent joint and begin a rehabilitation program aimed at restoring motion. The PIP joint functions as a hinge joint with approximately 100° of motion in the sagittal plane (flexion/­extension) and minimal motion in the coronal or axial planes. The base of the middle phalanx is a biconcave surface with a central ridge. The volar lateral aspects of the bone are the sites of insertion of the proper collateral ligaments. The volar plate is a fibrocartilaginous structure, which provides additional stability to the joint. It has thicker fibers that insert laterally and thinner fibers that insert centrally to the base of the middle phalanx and proximal extensions (checkrein ligaments), which attach to the periosteum on the proximal phalanx. The volar base of the middle phalanx and its curvature play an important role in stability, preventing dorsal subluxation of the middle phalanx. The head of the proximal phalanx contains two condyles, separated by a groove or sulcus. There is a slight difference on the size of each condyle, allowing the fingers to converge in flexion. The index and middle fingers have a slightly larger radial condyle while the small finger has a slightly larger ulnar condyle. Injuries involving the PIP joint can involve fracture of the base of the middle phalanx, the head of the proximal phalanx, a pure dislocation, or any combination of these. Fractures involving the base of the middle phalanx include dorsal base

A

B

C

Figure 7.4  Classification of PIP joint fracture dislocations. (A) Volar base fracture resulting in dorsal subluxation of the middle phalanx. (B) Dorsal base fracture resulting in volar subluxation of the middle phalanx. (C) Pilon type fracture with dorsal and volar base fractures and comminuted, depressed central articular surface.

Treatment: fingers

as further immobilization of the PIP joint may result in permanent stiffness. Irreducible dislocations are due to an interposed central slip or collateral ligament and require open reduction through a dorsal approach, allowing direct inspection of the central slip.

153

Unstable Tenuous

Middle phalanx base articular fractures

Stable

Dorsal fracture dislocations of the PIP joint result from an axial load in a dorsal direction or longitudinal direction when the finger is slightly flexed (Algorithm 7.2). These are much more common than volar fracture dislocations, which result from an axial load in a volar direction or hyperextension and axial load. The dorsal fracture dislocations are classified according to the amount of the articular surface involved. Fractures involving 50% are unstable and result in dorsal subluxation of the middle phalanx (Fig. 7.5).16 Lateral radiographs should be carefully evaluated for the “V sign”, indicative of dorsal subluxation (Fig. 7.6). The two condyles of the proximal phalanx should be superimposed, and the base of the middle phalanx should be collinear with the head of the proximal phalanx. There should be a smooth curvature of the joint surface, with a consistent space between the proximal and middle phalanx. If there is convergence of the joint space creating a dorsal “V”, the patient may be able to flex the digit at the PIP joint, but this occurs through a hinge process rather than rotation, and the joint surface will degenerate.

Figure 7.5  Stability of PIP fracture dislocations. Fractures involving 50% are unstable and have resultant dorsal subluxation.

Figure 7.6  The lateral “V” sign indicating dorsal subluxation of the middle phalanx and associated hinging with flexion.

Algorithm 7.2

No Dorsal subluxation/ Lateral V sign Yes Middle phalanx base dorsal fracture dislocation

Splinting and early motion

Reducible with less than 30º flexion

Arthritic or stiff joint at baseline No arthritis and good motion prior to injury

Extension block splinting or pinning

External fixation and early motion

ORIF if fragments amenable to screw, cerclage wire, or plate and screw Comminuted fragment not amenable to repair –Hemi-hamate replacement

PIP dorsal fracture dislocations. The decision for treatment is based on the alignment of the joint and the presence of “dorsal V sign”. If not present, early motion is instituted. If present and correctable with flexion of 30° or less, dorsal extension block splinting or pinning can be performed. If persistent subluxation, consider surgical treatment. If the ­ joint is stiff at baseline, arthritic, or the patient is not highly motivated, external fixation with K-wires is our preferred treatment. If there is good motion at baseline and no pre-­ existing arthrosis, we prefer ORIF. If the fragments are amenable to fixation, we perform ORIF with screws, plate and screws, or cerclage wire. If the fragments are comminuted and not amenable to ORIF, we replace the base of the middle phalanx with a hemi-hamate graft. ­

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Treatment is directed at recreating a congruent joint surface and restoring motion. Stable fractures and those which are classified as tenuous but maintain stable reduction and a congruent joint with no more than 30° of flexion can be managed nonoperatively with a dorsal extension block splint. Active flexion is initiated and extension is allowed short of the point of subluxation. These patients should be followed closely to ensure that subluxation of the joint does not develop. Unstable fractures, or those in which a congruent joint cannot be established with 10% of the articular surface, or those with articular incongruity are best treated with open reduction and stabilization.57,58 Isolated ligamentous injuries can be more challenging to diagnose. Avulsion from the proximal phalanx is five times more common than midsubstance tears or avulsion from the metacarpal.59

Stener lesion In 1962, Stener described the injury where the complete ulnar collateral ligament tear retracted proximally, and the adductor aponeurosis was interposed between the ligament and the site of avulsion along the base of the proximal phalanx (Fig. 7.15). Without contact between the ligament and bone, healing cannot occur and chronic instability will result.60 A complete rupture and retraction of the ligament is necessary for the Stener lesion to occur and therefore it is important to differentiate between partial or complete tears without retraction and those where the ligament has retracted proximal to the adductor aponeurosis. Unfortunately, there is not an absolute clinical criterion for making this diagnosis. The MCP joint is observed for swelling and tenderness along the ulnar side. A palpable mass at the level of the metacarpal neck may be consistent with the retracted ulnar collateral ligament (UCL). The joint should be tested in both flexion and extension, checking for a definite endpoint and comparing to the opposite thumb. Multiple reports exist in the literature, all using different clinical criteria for diagnosis of a complete tear.61–­64 Stress radiographs may assist in making the diagnosis. In addition, MRI and ultrasound can be used in cases of uncertainty following clinical exam and plain radiographs. When a Stener lesion is present, operative treatment is required. Open ligament repair is the most common procedure performed, but arthroscopic repositioning of the ligament has been described, placing the ligament deep to the adductor aponeurosis and allowing it to heal to the bone.65,66 Delayed presentation may make it difficult to repair the ligament primarily and reconstruction may be indicated. With late presentation, radiographs should be evaluated for presence of arthritis and when present, arthrodesis should be considered. Reconstruction techniques produce dynamic (tendon transfers and adductor advancement) and static reconstructions (creation of a static restraint to radial-­directed stress with a graft). Dynamic reconstructions typically involve transfer of a tendon to stabilize the MCP joint. Procedures include transfer of the extensor indicis proprius (EIP) to the extensor mechanism, transfer of the extensor pollicis brevis (EPB) to the ulnar side of the proximal phalanx,67,68 and advancement of the adductor.69 The adductor is transferred from its insertion on the sesamoid to the proximal phalanx. Static reconstructions involve replacement of the ligament with a graft, such as palmaris longus tendon, through holes created in the metacarpal and proximal phalanx.57

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CHAPTER 7  • Hand fractures and joint injuries

SECTION II

Adductor aponeurosis

Adductor aponeurosis

Ulnar collateral ligament

A

B

C

D

Figure 7.15  Stener lesion of the MCP joint of the thumb. (A) Normal relationship of the adductor aponeurosis. With a radial directed stress (B), the ligament is avulsed from the bone and retracts proximal to the adductor aponeurosis (C). When the joint is reduced, the adductor is interposed between the ligament and bone (D), preventing healing.

Primary repair can be completed as long as there is adequate ligament to repair. When the procedure is greater than 6 weeks following the injury, the surgeon should be prepared to proceed with reconstruction in the event the ligament is not amenable to primary repair. Repair or reattachment too distal or volar will result in loss of flexion and placement too dorsal may result in persistent instability. With an acute injury, it is often possible to determine the site of avulsion and reattach it to the site of avulsion. The ligament runs from dorsal to volar in a proximal to distal direction. The origin of the proper collateral ligament is 7 mm proximal to the joint and 3 mm from the dorsal cortex. The insertion of the base of the proximal phalanx is located 3 mm distal to the joint and 3 mm from the volar cortex (Fig. 7.16).63 Reattachment can be completed using suture anchors or a pull-­out suture exiting the opposite side tied over a button or directly over the bone. Radial collateral ligament injuries are much less common than their ulnar counterparts. On the radial side of the thumb, the abductor aponeurosis is broad, covering a larger percentage of the joint and there is no interposition of the aponeurosis between the ligament and the bone (Stener lesion). Tear of the RCL typically results from forced adduction on a flexed joint. The dorsal capsule tears along the radial aspect and the proximal phalanx pronates around the intact UCL, creating a prominence of the radial aspect of the metacarpal head. The location of the tear is more variable than the UCL counterpart, with equal frequency between proximal and distal avulsions56 and mid-­substance tears.57

Surgical repair of an acute UCL tear The skin incision is outlined in a straight or lazy “S” configuration from the ulnar base of the proximal phalanx to the dorsal aspect of the metacarpal head/­neck region (Fig. 7.17). After the skin incision is completed, spreading to the level of the adductor aponeurosis is carefully performed. Care should

7 mm

3 mm 8 mm 8 mm

3 mm

Proper collateral ligament Accessory collateral ligament

3 mm

Figure 7.16  Location of thumb MCP joint UCL on metacarpal and proximal phalanx. The ligament runs from dorsal to volar in a proximal to distal direction. The origin of the proper collateral ligament is 7 mm proximal to the joint and 3 mm from the dorsal cortex. The insertion of the base of the proximal phalanx is located 3 mm distal to the joint and 3 mm from the volar cortex.

be taken to identify the cutaneous branch of the radial nerve, as injury to this structure can cause a painful neuroma, compromising the final outcome. When a Stener lesion is present, the ligament will be identified proximal to the adductor aponeurosis. The adductor aponeurosis is incised, splitting the fibers until the base of the proximal phalanx can be identified. The ligament is debrided of hematoma and fibrous tissue in preparation for repair. The joint can be opened and irrigated to remove hematoma and the site of attachment is identified. When a larger fragment of bone is present, this can be reduced and secured with a screw or K-­wires. When the fragment is small, it can be excised, and the ligament repaired to the site of avulsion with a suture anchor. The adductor aponeurosis is

Treatment: thumb

167

A A

B

B

Figure 7.17  Surgical repair of thumb MCP joint UCL. (A) Preoperative clinical photograph illustrating laxity at the MCP joint. (B) Intraoperative photograph illustrating suture anchor in the base of the proximal phalanx with suture through the UCL.

repaired, and the skin is closed. If there is a concern about the stability of the repair, a K-­wire can be placed across the joint, but this is generally not necessary. A plaster thumb spica splint is applied, leaving the IP joint free and converted to a short arm cast at 1 week. Motion of the IP joint is encouraged to prevent adhesions of the extensor tendons. At 4 weeks, the cast is removed, and a therapy program is instituted to regain motion. A thermoplastic orthosis is used between exercises with avoidance of radial directed stress. Pinch strengthening is begun at 10 weeks and unrestricted activities are allowed at 12 weeks. Final motion is typically 80% of the non-­injured side with grip and pinch strength approximately 90% of the contralateral side.

Reconstruction of chronic UCL tear with tendon graft This creates a static restraint to radial directed stress and although not the same as the ligament prior to the injury, can provide a stable thumb MCP joint. The approach to the

Figure 7.18  Technique of thumb MCP joint UCL reconstruction with palmaris longus tendon graft. (A) Intraoperative exposure of the joint following resection of scar and remnants of UCL. (B) Tendon graft secured to the proximal phalanx in preparation for securing to metacarpal.

joint is the same as for acute repairs. After exposing the joint, the remaining collateral ligament is excised. The site of origin and insertion of the graft is identified (Fig.  7.18). A  tendon graft is harvested using palmaris longus when present or a strip of flexor carpi radialis (FCR) in the event the palmaris longus is not present. The graft can be attached either through drill holes or with tenodesis screws (alternatively, the collateral ligament can be left attached to the metacarpal and the graft secured to the native ligament). The tendon is attached to the metacarpal head just dorsal to the dorsal volar axis, approximately 8 mm from the joint surface. The proximal phalanx insertion site is 3 mm from the volar cortex and 3 mm distal to the joint. The tendon can be attached to the bone with suture anchors, biotenodesis screws or transosseous sutures. The joint is pinned in slight flexion and ulnar deviation. The adductor aponeurosis and skin incisions are closed and a thumb spica splint is applied. Postoperative rehabilitation is similar to acute repairs except the joint is immobilized for 6 weeks and pinching is avoided for 3 months. Unrestricted activities are allowed at 4–­5 months. Motion tends to be less following reconstructions than acute repairs, but 70% of the flexion/­extension and 80% grip and pinch strength can often be obtained. The goal of the reconstruction is to produce a stable painless

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thumb and the slight loss of motion is compensated for at the CMC joint.

Thumb metacarpal fractures Fractures of the thumb metacarpal are more tolerant of displacement and rotation due to the motion in three planes (flexion/­extension, abduction/­adduction, pronation/­ supination). Fractures can occur through the shaft or the base at the metaphyseal–­diaphyseal junction. Angulation 30 mmHg or within 30 mm of diastolic pressure should be treated with urgent fasciotomies, thereby releasing the interosseous, thenar, hypothenar, adductor pollicis muscles, and transverse carpal ligament.

Secondary procedures Secondary procedures can be performed to correct a problem, such as malunion or non-­union, or in an attempt to improve motion for stiff digits. All wounds should be healed, and soft tissues supple before secondary procedures are performed.

A

B

Malunion correction Malunion typically occurs as angular or rotational deformities. Correction of an angular malunion involves an opening or closing wedge osteotomy with internal fixation.85 Closing wedge osteotomies are easier to perform and are stable, while opening wedge osteotomies often require bone graft. These are best treated at the site of the malunion. Rotational malunions are treated with derotational osteotomies. These can be performed as transverse86,87 or step-­ cut osteotomies88–­90 and rigid fixation is used to provide stability and early motion (Fig. 7.21). Intra-­articular malunions can be corrected with an intra-­articular91 (Fig. 7.22) or extra-­articular92 osteotomy.

Non-­union correction Non-­unions are rare in the hand but can be managed by following principles of non-­union reconstruction in long bones.93 Any underlying infection should be treated, and a good soft-­tissue envelope should be present prior to reconstruction. Hypertrophic non-­unions demonstrate bone formation around the fracture without bridging bone at the non-­union site. These will typically heal if stability and compression are provided at the non-­union site. Atrophic non-­unions require bone grafting in addition to internal fixation. Metabolic conditions, such as vitamin D deficiency, should be evaluated with blood tests and corrected if necessary, as low vitamin D levels will prevent ossification.

C

Figure 7.21 (A–C) Diagram demonstrating step-cut osteotomy for correction of malunion. This can be used in the metacarpal or phalanx. The distal transverse cut is in the direction of malrotation, so the dorsal surface closes as the malrotation is corrected.  

­

­

Secondary procedures

171

B

A

D

C

E

F

G

Figure 7.22 Technique for correction of intra-articular malunion of the proximal phalanx head with condylar advancement osteotomy. (A) A longitudinal osteotomy is created into the site of the intra-articular malunion, the condyle is advanced and rotated into proper alignment and secured with screws, leaving the proximal shaft defect to heal secondarily. Clinical example: (B) preoperative radiograph; (C) intraoperative photograph of articular malunion prior to osteotomy; (D) intraoperative photograph following condylar advance osteotomy and fixation. Postoperative posteroanterior (E) and lateral (F) radiographs and clinical example in flexion (G).  

­

­

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Hardware removal, tenolysis, capsulotomy Patients with residual stiffness may benefit from secondary procedures to improve motion. When internal fixation with plates and screws has been used for initial treatment of the fracture, adhesions between the plate and the extensor tendons

Clinical tips Tenolysis • Tenolysis can be performed as a wide-­awake procedure, using local anesthesia with epinephrine, avoiding the use of a tourniquet. • Tenolysis knives are specifically designed to free adhesions between tendon and bone, flexor sheath and the tendons themselves. • Active motion after releasing adhesions will often allow rupture of additional adhesions, illustrating when adequate release has been completed. • Begin therapy, focusing on active motion, immediately following the release. This can be demonstrated in the operating room when done wide-­awake.

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often occur. Removal of the hardware and extensor tenolysis will often improve flexion. Indications include a motivated patient who will be compliant with the postoperative therapy program, complete osseous healing, and supple soft tissues with passive motion that is greater than active motion. When joints become stiff, the results are much less predictable and outcomes not as good. Results following release of MCP extension contractures are better than PIP flexion or extension contracture release.

Future directions There have been few substantial advances in management of hand fractures over the last decade. K-­wires are still commonly used and provide functionally stable fixation. Ideally, something to minimize adhesions, whether something used locally or systemically, or increase the rate of bony healing could improve motion and ultimate outcome. The understanding and use of intramedullary fixation for metacarpal fractures and more recently phalanx fractures have the advantage of early motion and more rigid fixation, potentially allowing better outcomes. Comparative studies including randomized trials comparing fixation methods may help surgeons determine optimal treatments.

References

References 1. Karl JW, Olson PR, Rosenwasser MP. The epidemiology of upper extremity fractures in the United States, 2009. J Orthop Trauma. 2015;29(8):e242–­e244. 2. Kozin SH, Thoder JJ, Lieberman G. Operative treatment of metacarpal and phalangeal shaft fractures. J Am Acad Orthop Surg. 2000;8(2):111–­121. 3. Leversedge FJ. Anatomy and pathomechanics of the thumb. Hand Clin. 2008;24(3):219–­229, v. 4. Seitz Jr. WH, Shimko P, Patterson RW. Long-­term results of callus distraction-­lengthening in the hand and upper extremity for traumatic and congenital skeletal deficiencies. J Bone Joint Surg Am. 2010;92(Suppl 2):47–­58. 5. Marino JT, Ziran BH. Use of solid and cancellous autologous bone graft for fractures and nonunions. Orthop Clin North Am. 2010;41(1): 15–­26. table of contents. 6. Schneider LH. Fractures of the distal phalanx. Hand Clin. 1988;4(3): 537–­547. 7. Wehbe MA, Schneider LH. Mallet fractures. J Bone Joint Surg Am. 1984;66(5):658–­669. 8. Kalainov DM, Hoepfner PE, Hartigan BJ, Carroll Ct, Genuario J. Nonsurgical treatment of closed mallet finger fractures. J Hand Surg Am. 2005;30(3):580–­586. 9. Hamas RS, Horrell ED, Pierret GP. Treatment of mallet finger due to intra-­articular fracture of the distal phalanx. J Hand Surg Am. 1978;3(4):361–­363. 10. Leinberry C. Mallet finger injuries. J Hand Surg Am. 2009;34(9): 1715–­1717. 11. Rocchi L, Genitiempo M, Fanfani F. Percutaneous fixation of mallet fractures by the "umbrella handle" technique. J Hand Surg Br. 2006; 31(4):407–­412. 12. Schneider LH. A simple fixation method for unstable bony mallet finger. J Hand Surg Am. 2005;30(3):626–­627; author reply 627. 13. Palmer AK, Linscheid RL. Irreducible dorsal dislocation of the distal interphalangeal joint of the finger. J Hand Surg Am. 1977;2(5): 406–­408. 14. Green SM, Posner MA. Irreducible dorsal dislocations of the proximal interphalangeal joint. J Hand Surg Am. 1985;10(1):85–­87. 15. Peimer CA, Sullivan DJ, Wild DR. Palmar dislocation of the proximal interphalangeal joint. J Hand Surg Am. 1984;9A(1):39–­48. 16. Kiefhaber TR, Stern PJ. Fracture dislocations of the proximal interphalangeal joint. J Hand Surg Am. 1998;23(3):368–­380. 17. Hamilton SC, Stern PJ, Fassler PR, Kiefhaber TR. Mini-­screw fixation for the treatment of proximal interphalangeal joint dorsal fracture-­dislocations. J Hand Surg Am. 2006;31(8):1349–­1354. 18. Blazar PE, Robbe R, Lawton JN. Treatment of dorsal fracture/­ dislocations of the proximal interphalangeal joint by volar plate arthroplasty. Tech Hand Up Extrem Surg. 2001;5(3):148–­152. 19. Eaton RG, Malerich MM. Volar plate arthroplasty of the proximal interphalangeal joint: a review of ten years’ experience. J Hand Surg Am. 1980;5(3):260–­268. 20. Williams RM, Hastings 2nd H, Kiefhaber TR. PIP fracture/­ dislocation treatment technique: use of a hemi-­hamate resurfacing arthroplasty. Tech Hand Up Extrem Surg. 2002;6(4):185–­192. 21. Williams RM, Kiefhaber TR, Sommerkamp TG, Stern PJ. Treatment of unstable dorsal proximal interphalangeal fracture/­dislocations using a hemi-­hamate autograft. J Hand Surg Am. 2003;28(5):856–­865. 22. Badia A, Riano F, Ravikoff J, Khouri R, Gonzalez-­Hernandez E, Orbay JL. Dynamic intradigital external fixation for proximal interphalangeal joint fracture dislocations. J Hand Surg Am. 2005; 30(1):154–­160. 23. Ellis SJ, Cheng R, Prokopis P, et al. Treatment of proximal interphalangeal dorsal fracture-­dislocation injuries with dynamic external fixation: a pins and rubber band system. J Hand Surg Am. 2007;32(8):1242–­1250. 24. Ruland RT, Hogan CJ, Cannon DL, Slade JF. Use of dynamic distraction external fixation for unstable fracture-­dislocations of the proximal interphalangeal joint. J Hand Surg Am. 2008;33(1):19–­25.

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25. Agee JM. Unstable fracture dislocations of the proximal interphalangeal joint. Treatment with the force couple splint. Clin Orthop Relat Res. 1987(214):101–­112. 26. Weiss AP. Cerclage fixation for fracture dislocation of the proximal interphalangeal joint. Clin Orthop Relat Res. 1996(327):21–­28. 27. Dionysian E, Eaton RG. The long-­term outcome of volar plate arthroplasty of the proximal interphalangeal joint. J Hand Surg Am. 2000;25(3):429–­437. 28. Calfee RP, Kiefhaber TR, Sommerkamp TG, Stern PJ. Hemi-­hamate arthroplasty provides functional reconstruction of acute and chronic proximal interphalangeal fracture-­dislocations. J Hand Surg Am. 2009;34(7):1232–­1241. 29. McAuliffe JA. Hemi-­hamate autograft for the treatment of unstable dorsal fracture dislocation of the proximal interphalangeal joint. J Hand Surg Am. 2009;34(10):1890–­1894. 30. Meyer ZI, Goldfarb CA, Calfee RP, Wall LB. The central slip fracture: results of operative treatment of volar fracture subluxations/­dislocations of the proximal interphalangeal joint. J Hand Surg Am. 2017;42(7):572 e571-­572 e576. 31. Doering TA, Greenberg AS, Tuckman DV. Dorsal plating for intra-­ articular middle phalangeal base fractures with volar instability. Hand (N Y). 2019;14(5):620–­625. 32. Weiss AP, Hastings 2nd H. Distal unicondylar fractures of the proximal phalanx. J Hand Surg Am. 1993;18(4):594–­599. 33. Belsky MR, Eaton RG, Lane LB. Closed reduction and internal fixation of proximal phalangeal fractures. J Hand Surg Am. 1984; 9(5):725–­729. 34. Page SM, Stern PJ. Complications and range of motion following plate fixation of metacarpal and phalangeal fractures. J Hand Surg Am. 1998;23(5):827–­832. 35. del Pinal F, Moraleda E, Ruas JS, de Piero GH, Cerezal L. Minimally invasive fixation of fractures of the phalanges and metacarpals with intramedullary cannulated headless compression screws. J Hand Surg Am. 2015;40(4):692–­700. 36. Patel MR, Bassini L. Irreducible palmar metacarpophalangeal joint dislocation due to junctura tendinum interposition: a case report and review of the literature. J Hand Surg Am. 2000;25(1):166–­172. 37. Betz RR, Browne EZ, Perry GB, Resnick EJ. The complex volar metacarpophalangeal-­joint dislocation. A case report and review of the literature. J Bone Joint Surg Am. 1982;64(9):1374–­1375. 38. Chin SH, Vedder NB, MOC-­PSSM CME. article: metacarpal fractures. Plast Reconstr Surg. 2008;121(1 Suppl):1–­13. 39. Kuokkanen HO, Mulari-­Keranen SK, Niskanen RO, Haapala JK, Korkala OL. Treatment of subcapital fractures of the fifth metacarpal bone: a prospective randomised comparison between functional treatment and reposition and splinting. Scand J Plast Reconstr Surg Hand Surg. 1999;33(3):315–­317. 40. Hunter JM, Cowen NJ. Fifth metacarpal fractures in a compensation clinic population. A report on one hundred and thirty-­three cases. J Bone Joint Surg Am. 1970;52(6):1159–­1165. 41. Jahss S. Fractures of the metacarpals: a new method of reduction and immobilzation. J Bone Joint Surg Am. 1938;20:726–­731. 42. Hofmeister EP, Kim J, Shin AY. Comparison of 2 methods of immobilization of fifth metacarpal neck fractures: a prospective randomized study. J Hand Surg Am. 2008;33(8):1362–­1368. 43. Martinez-­Catalan N, Pajares S, Llanos L, Mahillo I, Calvo E. A prospective randomized trial comparing the functional results of buddy taping versus closed reduction and cast immobilization in patients with fifth metacarpal neck fractures. J Hand Surg Am. 2020;45(12):1134–­1140. 44. Brown PW. The management of phalangeal and metacarpal fractures. Surg Clin North Am. 1973;53(6):1393–­1437. 45. Foucher G. "Bouquet" osteosynthesis in metacarpal neck fractures: a series of 66 patients. J Hand Surg Am. 1995;20(3 Pt 2):S86–­S90. 46. Hastings 2nd H. Unstable metacarpal and phalangeal fracture treatment with screws and plates. Clin Orthop Relat Res. 1987(214):37–­52. 47. Boulton CL, Salzler M, Mudgal CS. Intramedullary cannulated headless screw fixation of a comminuted subcapital metacarpal fracture: case report. J Hand Surg Am. 2010;35(8):1260–­1263.

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SECTION II

CHAPTER 7  • Hand fractures and joint injuries

48. ten Berg PW, Mudgal CS, Leibman MI, Belsky MR, Ruchelsman DE. Quantitative 3-­dimensional CT analyses of intramedullary headless screw fixation for metacarpal neck fractures. J Hand Surg Am. 2013;38(2):322–­330.e322. 49. Seitz Jr WH, Gomez W, Putnam MD, Rosenwasser MP. Management of severe hand trauma with a mini external fixateur. Orthopedics. 1987;10(4):601–­610. 50. Drenth DJ, Klasen HJ. External fixation for phalangeal and metacarpal fractures. J Bone Joint Surg Br. 1998;80(2):227–­230. 51. Ashmead Dt, Rothkopf DM, Walton RL, Jupiter JB. Treatment of hand injuries by external fixation. J Hand Surg Am. 1992;17(5): 954–­964. 52. Hoang D, Vu CL, Jackson M, Huang JI. An anatomical study of metacarpal morphology utilizing CT scans: evaluating parameters for antegrade intramedullary compression screw fixation of metacarpal fractures. J Hand Surg Am. 2021;46(2):149 e1-­149.e8. 53. Dunleavy ML, Candela X, Darowish M. Morphological analysis of metacarpal shafts with respect to retrograde intramedullary headless screw fixation. Hand (N Y). 2020:1558944720937362 [online ahead of print]. 54. Garcia-­Elias M, Bishop AT, Dobyns JH, Cooney WP, Linscheid RL. Transcarpal carpometacarpal dislocations, excluding the thumb. J Hand Surg Am. 1990;15(4):531–­540. 55. Gurland M. Carpometacarpal joint injuries of the fingers. Hand Clin. 1992;8(4):733–­744. 56. Camp RA, Weatherwax RJ, Miller EB. Chronic posttraumatic radial instability of the thumb metacarpophalangeal joint. J Hand Surg Am. 1980;5(3):221–­225. 57. Smith RJ. Post-­traumatic instability of the metacarpophalangeal joint of the thumb. J Bone Joint Surg Am. 1977;59(1):14–­21. 58. Husband JB, McPherson SA. Bony skier’s thumb injuries. Clin Orthop Relat Res. 1996(327):79–­84. 59. Bowers WH, Hurst LC. Gamekeeper’s thumb. Evaluation by arthrography and stress roentgenography. J Bone Joint Surg Am. 1977;59(4):519–­524. 60. Stener B. Skeletal injuries associated with rupture of the ulnar collateral ligament of the metacarpophalangeal joint of the thumb. A clinical and anatomical study. Acta Chir Scand. 1963;125:583–­586. 61. Smith RJ, Peimer CA. Injuries to the metacarpal bones and joints. Adv Surg. 1977;11:341–­374. 62. Palmer AK, Louis DS. Assessing ulnar instability of the metacarpophalangeal joint of the thumb. J Hand Surg Am. 1978;3(6): 542–­546. 63. Heyman P, Gelberman RH, Duncan K, Hipp JA. Injuries of the ulnar collateral ligament of the thumb metacarpophalangeal joint. Biomechanical and prospective clinical studies on the usefulness of valgus stress testing. Clin Orthop Relat Res. 1993(292):165–­171. 64. Heyman P. Injuries to the ulnar collateral ligament of the thumb metacarpophalangeal joint. J Am Acad Orthop Surg. 1997;5(4): 224–­229. 65. Ryu J, Fagan R. Arthroscopic treatment of acute complete thumb metacarpophalangeal ulnar collateral ligament tears. J Hand Surg Am. 1995;20(6):1037–­1042. 66. Slade 3rd JF, Gutow AP. Arthroscopy of the metacarpophalangeal joint. Hand Clin. 1999;15(3):501–­527. 67. Sakellarides HT, DeWeese JW. Instability of the metacarpophalangeal joint of the thumb. Reconstruction of the collateral ligaments using the extensor pollicis brevis tendon. J Bone Joint Surg Am. 1976;58(1):106–­112. 68. Ahmad I, DePalma AF. Treatment of game-­keeper’s thumb by a new operation. Clin Orthop Relat Res. 1974;103:167–­169. 69. Neviaser RJ, Wilson JN, Lievano A. Rupture of the ulnar collateral ligament of the thumb (gamekeeper’s thumb). Correction by dynamic repair. J Bone Joint Surg Am. 1971;53(7):1357–­1364. 70. Imaeda T, An KN, Cooney 3rd WP, Linscheid R. Anatomy of trapeziometacarpal ligaments. J Hand Surg Am. 1993;18(2):226–­231.

71. Cooney 3rd WP, Chao EY. Biomechanical analysis of static forces in the thumb during hand function. J Bone Joint Surg Am. 1977;59(1): 27–­36. 72. Cooney 3rd WP, Lucca MJ, Chao EY, Linscheid RL. The kinesiology of the thumb trapeziometacarpal joint. J Bone Joint Surg Am. 1981; 63(9):1371–­1381. 73. Jakobsen CW, Elberg JJ. Isolated carpometacarpal dislocation of the thumb. Case report. Scand J Plast Reconstr Surg Hand Surg. 1988;22(2):185–­186. 74. Watt N, Hooper G. Dislocation of the trapezio-­metacarpal joint. J Hand Surg Br. 1987;12(2):242–­245. 75. Eaton RG, Littler JW. Ligament reconstruction for the painful thumb carpometacarpal joint. J Bone Joint Surg Am. 1973;55(8): 1655–­1666. 76. Simonian PT, Trumble TE. Traumatic dislocation of the thumb carpometacarpal joint: early ligamentous reconstruction versus closed reduction and pinning. J Hand Surg Am. 1996;21(5): 802–­806. 77. Pellegrini Jr. VD. Fractures at the base of the thumb. Hand Clin. 1988;4(1):87–­102. 78. Langhoff O, Andersen K, Kjaer-­Petersen K. Rolando’s fracture. J Hand Surg Br. 1991;16(4):454–­459. 79. Buchler U, McCollam SM, Oppikofer C. Comminuted fractures of the basilar joint of the thumb: combined treatment by external fixation, limited internal fixation, and bone grafting. J Hand Surg Am. 1991;16(3):556–­560. 80. Schuind F, Noorbergen M, Andrianne Y, Burny F. Comminuted fractures of the base of the first metacarpal treated by distraction-­ external fixation. J Orthop Trauma. 1988;2(4):314–­321. 81. Al-­Qattan MM. Phalangeal neck fractures in children: classification and outcome in 66 cases. J Hand Surg Br. 2001;26(2):112–­121. 82. Al-­Qattan MM. Juxta-­epiphyseal fractures of the base of the proximal phalanx of the fingers in children and adolescents. J Hand Surg Br. 2002;27(1):24–­30. 83. Al-­Qattan MM, Hashem FK, Rasool MN, Elshayeb A, Hassanain J. A unique fracture pattern of the proximal phalanx in children: fractures through the phalangeal neck with an attached dorsal bony flange. Injury. 2004;35(11):1185–­1191. 84. Botte MJ, Davis JL, Rose BA, et al. Complications of smooth pin fixation of fractures and dislocations in the hand and wrist. Clin Orthop Relat Res. 1992(276):194–­201. 85. Freeland AE, Lindley SG. Malunions of the finger metacarpals and phalanges. Hand Clin. 2006;22(3):341–­355. 86. Buchler U, Gupta A, Ruf S. Corrective osteotomy for post-­traumatic malunion of the phalanges in the hand. J Hand Surg Br. 1996;21(1): 33–­42. 87. Trumble T, Gilbert M. In situ osteotomy for extra-­articular malunion of the proximal phalanx. J Hand Surg Am. 1998;23(5): 821–­826. 88. Jawa A, Zucchini M, Lauri G, Jupiter J. Modified step-­cut osteotomy for metacarpal and phalangeal rotational deformity. J Hand Surg Am. 2009;34(2):335–­340. 89. Lucas GL. Rotational step-­cut osteotomy for treatment of metacarpal and phalangeal malunion. J Hand Surg Am. 1992;17(3):583. 90. Manktelow RT, Mahoney JL. Step osteotomy: a precise rotation osteotomy to correct scissoring deformities of the fingers. Plast Reconstr Surg. 1981;68(4):571–­576. 91. Teoh LC, Yong FC, Chong KC. Condylar advancement osteotomy for correcting condylar malunion of the finger. J Hand Surg Br. 2002;27(1):31–­35. 92. Harness NG, Chen A, Jupiter JB. Extra-­articular osteotomy for malunited unicondylar fractures of the proximal phalanx. J Hand Surg Am. 2005;30(3):566–­572. 93. Jupiter JB, Koniuch MP, Smith RJ. The management of delayed union and nonunion of the metacarpals and phalanges. J Hand Surg Am. 1985;10(4):457–­466.

SECTION II  •  Trauma Reconstruction

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

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SYNOPSIS

ƒ Wrist injuries are common, and proper management relies on an understanding of normal anatomy, alignment, and kinematics. ƒ Scaphoid fractures can be subtle, and due to the precarious blood ­supply to this bone, may go on to non-­union if not properly managed. ƒ Indications for scapholunate ligament repair and/­or reconstruction depend on the patient’s symptoms and on the chronicity of the injury. ƒ For distal radius fractures requiring stabilization, external fixation and dorsal plating have largely been supplanted by volar fixed-­angle locking plates, which provide the necessary stability for fracture healing, even in osteoporotic individuals. ƒ Ulnar styloid fractures only require fixation in the setting of distal ­radioulnar joint instability.

Introduction The wrist is a complex articulation that connects the hand to the forearm. Entire textbooks have been devoted to detailed

discussions of the anatomy, physiology, and pathology of this important joint. This chapter will review some of the more common injury patterns seen in the wrist, including fractures of the carpal bones, ligamentous injuries of the wrist, and fractures of the distal radius and ulna. The epidemiology of wrist fractures has been investigated in detail. Each year, nearly 1.5 million hand and wrist fractures are estimated to occur in the United States, accounting for 1.5% of all emergency department visits.1 Of these, approximately 208,000 are carpal fractures. The scaphoid is the carpal bone most commonly fractured; it accounts for 60–80% of all carpal fractures.2,3 Incidence estimates range from 2.9/­10,000 person-­years in the United Kingdom4 to 12.1/­10,000 person-­years in the US military population.5 The highest incidence is found in the 20–24-­year-­old age group, and there is a clear male predominance.4,5 Distal radius fractures are the most common upper extremity fracture; the annual incidence is estimated at ­ 643,000 fractures per year in the United States.1 When the incidence is examined by age, there are two distinct peaks identified (Fig.  8.1), representing the 5–14-­year-­old group

Fracture incidence (per 10,000 person-years)

60 50 40 30 20 10 0

0–4

5–14

15–24

25–34

35–44

45–54

Age (years)

55–64

65–74

75–84

85+

Figure 8.1  Age-­related variation in radius/­ulna fracture incidence. (Data from Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26:908–915.)

Historical perspective

Historical perspective The carpus was not well described until the 1500 s, when Andreas Vesalius first identified the eight carpal bones. Before then, drawings of the hand connected the metacarpals directly to the distal radius, with no mention of wrist anatomy. Carpal bones are generally named for their shapes. For example, the scaphoid resembles a boat, whereas the lunate resembles the crescent moon. The names of the carpal bones were not solidified until 1955 when Nomina Anatomica established the official nomenclature for the carpal bones that we use today (Fig. 8.2).7 Historically, the carpal bones have been grouped together in various ways, based on function and kinematics. The earliest classification separates the wrist joint into two rows, consisting of the distal carpal row (trapezium, trapezoid, capitate, hamate) and the proximal carpal row (scaphoid, lunate, triquetrum). The carpus can also be divided into columns: a radial column (scaphoid, trapezoid, trapezium), a central column (lunate, capitate), and an ulnar column (triquetrum, hamate). The pisiform bone is not involved in wrist motion, so it is not typically included in these groupings. Trapezoid

Trapezium Scaphoid

Capitate

Hook of hamate

Lunate Triquetrum

Hamate

Pisiform

Figure 8.2  Posteroanterior radiograph of the wrist, with carpal bones identified.

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Abraham Colles (1773–1843) is credited with the first clinical description of fractures of the distal radius. His 1814 manuscript provides an eloquent description of closed reduction and splinting, in an era before the development of radiographs, anesthesia, and plaster-­ of-­ Paris. On the results of treatment, he proclaimed, “The cases treated on this plan have all recovered without the smallest defect or deformity of the limb, in the ordinary time for the cure of fractures.”8 More than 200 years later, closed reduction and immobilization is still the predominant method of treatment for distal radius fractures, though internal fixation has been steadily gaining in popularity.9 It is now commonly believed that restoration of anatomic alignment of the distal radius leads to better outcomes, although the age and activity level of the patient certainly contribute to this equation. To achieve these ends, technology has advanced to allow for precise fracture fixation with a variety of techniques. Over the past several decades, pins-­ and-­ plaster and external fixation systems have largely given way to internal fixation methods, heavily encouraged by AO (Arbeitsgemeinschaft für Osteosynthesefragen). AO is a Swiss organization started in the late 1950s for promoting more consistent fracture care, chiefly using rigid internal fixation. Despite the development of hundreds of fixators, plates, rods, and other devices, there is little high-­level evidence to support the use of one technique over another. In some ways, Colles’ conservative approach was probably correct – many patients, especially the low-­demand elderly population, achieve excellent outcomes even in the presence of significant malunion or malalignment.10 Many textbooks discourage the use of eponyms, believing them to be of historical interest only. However, the various eponyms for distal radius fractures often convey precise information regarding the fracture pattern and the type of injury sustained. The major eponyms for distal radius fractures are: Colles fracture (extra-­articular fracture with dorsal displacement of distal fragment) (Fig.  8.3A); Smith fracture (also called reverse Colles fracture; extra-­articular with volar displacement of distal fragment) (Fig.  8.3B); Barton fracture (intra-­articular shear fracture of the radiocarpal joint, may be dorsal or volar) (Fig.  8.3C,D); and Chauffeur fracture (intra-­ articular fracture involving the radial styloid) (Fig. 8.3E). For some cases, these eponyms may help in selecting a treatment modality.

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A

D

SECTION II

CHAPTER 8  • Fractures and dislocations of the wrist and distal radius

C

B

E

Figure 8.3  Examples of common distal radius fracture eponyms: (A) Colles fracture, (B) Smith fracture, (C) dorsal Barton fracture, (D) volar Barton fracture, and (E) Chauffeur fracture.

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CHAPTER 8  • Fractures and dislocations of the wrist and distal radius

(55.7/­ 10,000 person-­ years) and the 75–84-­ year-­ old group (35.2/­10,000 person-­years). Although a common injury, these fractures should never be treated casually. There is significant potential for patient disability if these injuries are not managed with great care and expertise. Khan and Giddins’ review of hand and wrist surgery negligence claims in the UK from 1995–2001 revealed that wrist fracture was the most common condition in which negligence was alleged, comprising 48% of claims.6

Access the Historical Perspective section, including Figs. 8.2 & 8.3, online at Elsevier eBooks+

Basic science/­disease process Anatomy Normal anatomy of the wrist is covered in detail in Chapter 1 of this volume. However, there are a few points that merit emphasis in this chapter with regard to these injuries. The vascularity of the scaphoid bone bears particular consideration. The scaphoid bone has a single dominant vascular pedicle that enters from the distal pole of the bone. Therefore, the proximal pole relies wholly on the intramedullary blood supply for survival. It is for this reason that proximal pole fractures typically take longer to heal and have increased incidence of non-­union. Furthermore, in cases of non-­union, the proximal pole is susceptible to avascular necrosis, which further complicates these injuries.11 Detection of ligamentous injuries of the wrist is made easier by attention to the Gilula arcs (Fig. 8.4). Dr. Gilula, a radiologist, described three arcs that can be noted on the posteroanterior radiograph of the wrist, formed by the proximal and distal articular surfaces of the proximal row, and the proximal articular surface of the distal row. Increased joint space or deviation of carpal bones from these lines is indicative of wrist instability.12

The bones of the wrist are linked by a complex system of intrinsic and extrinsic ligaments (Fig.  8.5). The strength of these wrist ligaments helps determine the injury patterns observed. For example, the very strong short radiolunate ligament tends to resist lunate dislocation, retaining the lunate in its fossa on the distal radius in all but the most severe traumas. Instead, the surrounding carpal bones typically dislocate away from the lunate. This perilunate pattern of injury has been described in stages by Mayfield (Fig. 8.6): (I) rupture of the scapholunate interosseous ligament; (II) capsular disruption through the space of Poirier, an area of inherent weakness of the volar capsule between the lunate and capitate; and (III) rupture of the lunotriquetral interosseous ligament. If the dislocated carpus rebounds, then the capitate will settle into the lunate fossa, and the lunate rotates volarly (IV), hinged on the short radiolunate ligament (Fig. 8.7).13,14 Injury patterns are also influenced by the details of bony anatomy and structure. For example, both the diaphysis and the articular surface of the distal radius have thicker cortical bone than is found at the metaphysis. The thinner cortical bone at the metaphysis is what makes it vulnerable to fracture, especially in the osteoporotic population. Furthermore, within the metaphysis, there is a distinct difference between the dorsal and volar cortices. The dorsal cortex is much thinner, resulting in extensive comminution in most cases of distal radius fracture from falls on outstretched hands, where the force is directed in a volar-­to-­ dorsal direction. The extensor pollicis longus (EPL) is the tendon most likely to rupture after a distal radius fracture. Of note, rupture is more common with non-­displaced fractures, and has been reported in cases of wrist injury without fracture. The etiology of this appears to be related to interruption of the tendon’s nutritional supply, leading to attritional rupture. This most commonly occurs at the Lister tubercle, where there is a natural watershed area of this tendon’s intrinsic blood supply. If the extrinsic (diffusion-­mediated) nutritional supply is also interrupted by fracture callus, fracture displacement, or swelling from edema or hematoma, rupture of the EPL can occur.15

Biomechanics

Figure 8.4  The Gilula arcs are used to detect alterations in carpal alignment and stability. The lines are defined by (1) the proximal and (2) the distal articular surface of the proximal row, as well as (3) the proximal articular surface of the distal row.

The biomechanics of the hand and wrist were reviewed in Chapter 1, but there are a few points to revisit here. Disruption of the normal linkages between the bones of the wrist – whether due to ligamentous rupture or fracture – can lead to carpal instability. The concept of carpal instability has evolved rapidly over the past 50 years as we have learned more about the ways in which the wrist bones move (kinematics) and transfer a load (kinetics). Specifically, a wrist is unstable if it is unable to transfer functional loads without sudden changes in stress on the articular cartilage, and if it is unable to maintain motion throughout its range without sudden alterations of intercarpal alignment.16 Carpal instability has been thoughtfully classified into four major patterns (Table 8.1). Carpal instability dissociative (CID) occurs when there is a disruption within or between the bones of the same carpal row. Carpal instability non-­dissociative (CIND) refers to a disruption between the distal radius and the proximal carpal row, or between the proximal and distal carpal rows. When a combination of elements of both CID and CIND exist, it is referred to as carpal instability complex (CIC). Finally, when the instability is an adaptive response to a

Basic science/­disease process

4

5

H Dorsal intercarpal ligament

3

2 Td

C

2

1

1 Tm

Tm

Td

3

4 5

C

Radioscaphocapitate ligament

L S

Dorsal radiocarpal ligament U

Long radiolunate ligament

R

Pisohamate ligament

H

S P

P L

Ulnotriquetral ligament

Tr

Ulnocapitate ligament Ulnolunate ligament

Short radiolunate ligament

A

175

Palmar radioulnar ligament

B

Capitotrapezoid ligament

2

1 Tm Trapeziotrapezoid ligament Scaphotrapezium trapezoid ligament Scaphocapitate ligament Scapholunate ligament

3

Td

4

C

5

H P

S L

Tr

Capitohamate ligament Triquetrohamate ligament Triquetrocapitate ligament Lunotriquetral ligament

C

Figure 8.5 (A) Dorsal extrinsic wrist ligaments. (B) Volar extrinsic wrist ligaments. (C) Intrinsic wrist ligaments. C, Capitate; H, hamate; L, lunate; P, pisiform; R, radius; S, scaphoid; Td, trapezoid; Tm, trapezium; U, ulna.  

 

 

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SECTION II

Table 8.1  Patterns of carpal instability

Pattern

II III

I

Example(s)

Carpal instability Disruption within or dissociative (CID) between bones of the same carpal row

Scapholunate dissociation; scaphoid non-­union

Carpal instability non-­dissociative (CIND)

Disruption at the radiocarpal or midcarpal joints, with intact proximal and distal rows

Midcarpal instability

Carpal instability complex (CIC)

Derangement both within and between carpal rows (CID plus CIND)

Perilunate dislocation with ulnar translation

Carpal instability adaptive (CIA)

Instability due to injury proximal or distal to wrist

Distal radius malunion

Data from International Wrist Investigators’ Workshop Terminology Committee. Wrist: terminology and definitions. J Bone Joint Surg Am. 2002;84-­A(Suppl 1):1–73.

IV

Figure 8.6  Mayfield stages of perilunate instability: (I) scapholunate ligament rupture; (II) volar capsule tear at the spae of Poirer; (III) lunotriquetral ligament rupture; (IV) lunate dislocation.

A

Definition

B

problem proximal or distal to the wrist itself, it is called carpal instability adaptive (CIA).17 Carpal kinematics has perhaps the biggest clinical impact on scaphoid fractures and scapholunate ligament injuries. The proximal carpal row is “pre-­tensioned”, with the scaphoid subject to a flexion moment, and the triquetrum tending to follow an extension moment. Any breakage of the connections within this row, whether intracarpal (e.g., scaphoid fracture) or intercarpal

Figure 8.7  Lateral radiograph examples of (A) perilunate dislocation and (B) lunate dislocation injury patterns.

Diagnosis/­patient presentation

(e.g., scapholunate ligament rupture), will result in carpal instability because the disconnected carpal bones rotate in opposite directions. This natural tendency for the components in this row to fall away from each other is in part responsible for the high rate of complications after these types of injury. Two particular instability patterns that result from CID within the proximal row are dorsal intercalated segment instability (DISI) and volar intercalated segment instability (VISI) (Fig. 8.8). DISI deformity is commonly associated with scapholunate ligament disruption or displaced scaphoid fractures, whereas VISI deformity is associated with lunotriquetral ligament disruption. Because of the scaphoid’s natural tendency to flex when loaded, delayed treatment of comminuted fractures of the scaphoid waist tend to result in the so-­ called “humpback deformity” (Fig.  8.9). This term describes the shape of the scaphoid as seen on lateral tomograms, reflecting malunion of the bone with an abnormally acute angle between the proximal and distal poles of the scaphoid.18

DISI

Normal

177

VISI

A

Mechanisms of injury In elderly osteoporotic patients, wrist injuries are commonly seen after falls from a standing height (fragility fractures). Very often, this is an extra-­articular fracture with apex volar angulation, the so-­ called “Colles fracture” (see Fig.  8.3). Patients sustaining one fragility fracture are at risk for future fragility fractures. This population should have appropriate screening, diagnosis, and treatment of underlying osteopenia or osteoporosis.19 The younger population typically experiences fractures caused by higher energy injuries, such as motor vehicle collisions or sports-­related trauma, resulting in more complex fracture patterns. With increasing force of injury, the chance of associated carpal fracture, intercarpal ligament injury, and/­or triangular fibrocartilage complex injury increases.

B

Diagnosis/­patient presentation History A detailed history begins with careful documentation of the circumstances or mechanism of the injury. Patients involved in high-­energy falls or collisions should be evaluated for associated injuries by an emergency medicine physician or trauma specialist. The patient’s handedness, occupation, important hobbies or recreational activities, medical and surgical history, and social history should be recorded. It is important to ask about numbness and/­or tingling in the hand, because these patients are prone to acute carpal tunnel syndrome which may need to be addressed at the time of operation.

Physical examination The examination of the patient’s upper extremity should be thorough and systematic. Although the focus of this chapter is on the wrist, both the elbow and the hand should be included in the scope of examination, to avoid missing associated injuries. Examination begins with inspection. The signs of acute trauma should be noted: wounds, ecchymosis, bleeding,

C

Figure 8.8  (A) Lunate position in DISI and VISI deformities of the wrist. X-­rays of (B) DISI and (C) VISI deformities.

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patient. Upon releasing pressure, a clunk may be detected, indicating the self-­reduction of the scaphoid back over the dorsal rim of the radius. A painful Watson test in the absence of an obvious clunk may be a sign of scapholunate ligament damage without complete disruption of the ligament. The lunotriquetral interosseous ligament can be assessed by the Kleinman shear test (Fig.  8.11). The examiner grasps the patient’s wrist in one hand, specifically applying stabilizing pressure over the lunate, which is palpable dorsally just beneath the fourth extensor compartment tendons. With the other hand, the examiner applies dorsally directed pressure over the pisiform, which applies a shear force directed across the lunotriquetral articulation.21 Laxity can be assessed by further grasping the pisiform and triquetrum “unit” and moving it both palmarly and dorsally in a “shucking”-­type maneuver. This latter is referred to as the lunotriquetral ballottement test.22 Pain and/­or instability may indicate injury or ­disruption of the lunotriquetral ligament.

Diagnostic tests Figure 8.9  Fracture at the waist of the scaphoid, resulting in a humpback deformity.

swelling, etc. Subacute or chronic changes may be more subtle, and comparison to the patient’s contralateral uninjured extremity can be helpful in detecting slight differences in swelling, alignment, and skin characteristics. Palpation of the extremity can help localize the site of injury. The examining surgeon should be familiar with the topography of the wrist and be able to identify injury to specific structures by careful, systematic palpation. For instance, focal tenderness just distal to the Lister tubercle could indicate injury to the scapholunate interosseous ligament, whereas pain with palpation of the floor of the anatomic snuffbox may signify a scaphoid waist fracture. Before assessing the range of motion or performing any provocative testing, it is important to review the radiographs of the extremity to rule out any unstable fractures that might be displaced or otherwise worsened by vigorous physical examination. While assessing the patient’s active and passive range of motion, palpation over the joints being moved can yield other useful information about crepitus, clicks, or clunks in the wrist. A complete examination should also include assessment of grip strength, pinch strength, and sensibility. It is particularly important to detect median neuropathy in wrist injury patients, because acute carpal tunnel syndrome may require treatment. Provocative testing of specific intrinsic ligaments of the wrist can be valuable in reaching a diagnosis but should be conducted with caution when unstable fractures are present to avoid unwanted fracture displacement. The Watson scaphoid shift test stresses the scapholunate ligament to detect injury or instability (Fig. 8.10). The examiner applies pressure (typically with the thumb) over the distal scaphoid tubercle, while moving the patient’s wrist from ulnar to radial deviation.20 In ulnar deviation, the scaphoid is extended, whereas in radial deviation it is flexed. Thus, in the intact wrist, the scaphoid’s ligamentous attachments resist subluxation during this maneuver. However, in cases of scapholunate dissociation, the scaphoid may be forced dorsally out of the scaphoid fossa into a painful position for the

At a minimum, assessment of wrist injuries should include four radiographs: posteroanterior (PA), oblique, lateral, and PA ulnar deviation. The ulnar deviation view is particularly important in detecting scaphoid injuries. The lateral view can evaluate the relationship between scaphoid and lunate; the normal scapholunate angle is between 30° and 60° (Fig. 8.12). Another helpful view for detecting dynamic instability of the scapholunate ligament is the clenched fist view. When making a tight fist, load is placed across the wrist, and the capitate is driven toward the scapholunate articulation, which will make scapholunate ligament laxity or rupture more evident. To increase the accuracy of the diagnosis, both anteroposterior (AP) and PA stress views should be considered.23

Figure 8.10  Watson scaphoid shift test.

Patient selection

Pisiform

Triquetrum Lunate

179

(normal = 21–25°), and volar tilt (range 2–20°, average = 11°) help define the extent of fracture displacement (Fig. 8.13).24 Cross-­ sectional imaging modalities, such as computed tomography (CT) and magnetic resonance imaging (MRI), are also used routinely to investigate wrist injuries. CT is an X-­ray-­ based modality, and as such it is best for assessing complex fracture-­dislocation patterns. In particular, CT can help assess joint congruity and/­or depressed articular fragments. CT is also better than MRI at determining osseous healing across a fracture site. On the other hand, MRI is the preferred modality for assessing non-­osseous structures and has the added benefit of providing some information about vascularity of parts of the carpus. MRI technology continues to evolve, and modern machines can detect very small ligamentous injuries. When the modalities of MRI and arthrography are combined, even small perforations in the interosseous ligaments can be detected. Clinical tip

Figure 8.11  Kleinman shear test.

CT scans are better at showing fracture details and bony bridging/­healing. MRIs are better at showing soft-­tissue injury, occult (non-­displaced) fractures, and bony edema.

The use of bone scans has decreased substantially over the years because of the effectiveness of MRIs. Nevertheless, bone scans are still helpful in identifying “hot areas” of the wrist in difficult cases when the etiology of the patient’s wrist pain is uncertain. However, the nonspecific nature of the bone scan limits its usefulness in the evaluation of most injuries. Diagnostic wrist arthroscopy, while more invasive than the tests mentioned above, must still be considered the “gold standard” for detecting intra-­articular wrist injuries. In a recent systematic review comparing MRI results with findings at arthroscopy, the negative predictive value of MRI for scapho­ lunate injury ranged from 72% to 94%.25 In other words, MRI can never completely rule out ligamentous injury in the wrist. One pitfall associated with the increasingly widespread use of MRI is the inevitable detection of “false-­positive” findings in the wrist. It is not uncommon to find multiple minor abnormalities on high-­resolution wrist MRI, many of which have nothing to do with the patient’s complaints. Therefore, it is important for the treating physician to use MRI wisely, in cases where there is reasonable suspicion of injury or occult pathology, rather than use it indiscriminately. If the results of the MRI are going to have no impact on the treatment plan for the patient, one should reconsider if it is worth spending resources on this expensive examination.

Patient selection Figure 8.12  The normal angle between the mid-­axis of the scaphoid to the lunate ranges from 30° to 60° (average 47°).

With regard to distal radius fractures, there are a few key metrics that help guide management, and plain radiographs are generally sufficient to determine these measurements. Changes in radial height (normal = 10–13 mm), radial inclination

Indications for fixation of scaphoid fractures are fairly well-­ established. Because displaced scaphoid fractures cannot be reduced in a closed fashion, open reduction and internal fixation (ORIF) is required to restore anatomic alignment. This is important to facilitate healing in the scaphoid, due to its tenuous blood supply, and to restore normal scaphoid shape and alignment, which is important for carpal kinematics.26 Other relative indications are listed in Box 8.1. Operative fixation of non-­displaced scaphoid fractures has been debated. Advocates cite many advantages, including

180

A

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CHAPTER 8  • Fractures and dislocations of the wrist and distal radius

B

C

Figure 8.13  (A) Radial height measured as the distance between two lines, the first line perpendicular to the longitudinal axis of the radius and intersecting the distal surface of the ulnar head, and the second line that passes through the distal tip of the radial styloid. (B) Radial inclination represented by the angle between the line perpendicular to the longitudinal axis of the radius and a second line connecting the ulnar aspect of the distal radius and the tip of the radial styloid. (C) Volar tilt is the angle between the line perpendicular to the longitudinal axis of the radius and a line along the distal articular surface of the radius.

BOX 8.1  Relative indications for scaphoid fracture fixation Displaced fractures Proximal pole fractures (regardless of displacement) Fractures associated with perilunate injuries Open fractures Fractures in multiply injured patients Fractures not healing after a trial of immobilization (3–4 months)

earlier return to active military duty and increased quality-­ adjusted life-­years.27,28 Despite some evidence of improved functional outcomes and less time off work, surgical treatment does present some risk of complications and should not be considered lightly, since the majority of these fractures will heal with immobilization alone.29,30 Acute scapholunate ligament injuries require operative repair to maintain carpal alignment and avoid collapse which can lead to predictable patterns of wrist arthritis.31 However, unlike bone fixation, which reliably leads to union in most cases, techniques for repair of interosseous ligaments are not as predictable. Furthermore, the healing capacity of intercarpal ligaments seems to deteriorate over time, so patients presenting more than 6 weeks after injury may not have any suitable ligament remnants to attempt an operative repair. The evidence favoring acute repair of lunotriquetral tears is less convincing. Many authors believe a trial of nonoperative

treatment with immobilization is indicated prior to considering operative repair.22,32 The American Academy of Orthopedic Surgeons has published guidelines regarding treatment of distal radius fractures.33 Non-­displaced distal radius fractures typically heal with immobilization alone and do not require surgical intervention. Displaced distal radius fractures should undergo a reduction maneuver before deciding if surgery is needed. Stable fractures that remain reduced will not require an operation but should be followed weekly for 2–3 weeks to be sure the fracture does not collapse or re-­displace. Although the available evidence does not lend itself to many definitive recommendations, there is moderate evidence to support operative fixation of fractures with post-­reduction radial shortening >3 mm, dorsal tilt >10°, and/­or intra-­articular displacement or step-­off >2 mm.33 Despite the existence of these guidelines, patient selection does not depend on X-­ray findings alone. A patient’s overall health, comorbidities, pre-­ injury activity level, job requirements, and expectations all play a role in the decision for surgery. This concept is exemplified in the ongoing investigation of the optimal treatment of distal radius fractures in the elderly.34,35 With the development of volar fixed-­angle plates with locking screws, fixation of distal radius fractures quickly became easier and more predictable, especially for fragility fractures in older adults.36,37 This has led to an increase in the operative management of these fractures in the elderly, increasing from 3% in 1996 to 16% in 2005.9 Without surgery, these fractures predictably result in malunion, with the majority having

Treatment and surgical techniques

less-­than-­excellent radiographic results.38 However, patient-­ reported outcome studies have shown that older adults tolerate greater degrees of malalignment without difficulty.39 Therefore, an independent, active retiree might do better with surgical fixation, whereas a low-­demand, infirm patient of the same age might do better with nonoperative treatment.

Treatment and surgical techniques Scaphoid fractures The scaphoid appears to be in the shape of a cashew nut and can be divided into three anatomic segments: distal pole (tubercle), waist, and proximal pole. Due to the distally located blood supply, fractures of the distal pole or tubercle heal reliably with 6–8 weeks of immobilization, and rarely need surgical fixation unless significantly displaced. However, as the location of the fracture line moves more proximally, the incidence of non-­union increases, and any measurable displacement increases this risk. Even non-­displaced proximal pole fractures will take considerable time to heal if treated

A

D

B

181

nonoperatively; cast treatment can last as long as 6–9 months before healing is confirmed. Internal fixation of scaphoid fractures is most commonly accomplished with a headless compression screw. Placement of the screw can be challenging, as complete visualization of the scaphoid is difficult, and the screw should be placed down the long axis of the bone for best bony purchase with least risk of extrusion. We advocate a dorsal approach for proximal pole fractures; waist fractures can be repaired through a volar or dorsal approach. Although minimally invasive (percutaneous) techniques have been developed for scaphoid fractures, these are not for the novice hand surgeon.40 The dorsal approach for ORIF of a scaphoid fracture (Fig. 8.14A) begins with a longitudinal incision just distal and ulnar to the Lister tubercle, extending over the dorsal wrist (Fig. 8.14B). The third compartment is identified through this incision, and EPL is partially released, without completely opening the compartment. With EPL protected, the wrist capsule is opened longitudinally to expose the scaphoid, identify the fracture, and examine the nearby scapholunate ligament. The fracture is then reduced; this can be aided by bone reduction forceps, or another similar instrument.41 The wrist is then

C

E

Figure 8.14  (A) Scaphoid fracture to be treated with ORIF using a screw. (B) The incision is made ulnar to the Lister tubercle. (C) Two K-­wires are passed into the scaphoid, one of which is the guidewire for the cannulated screw. (D) Finally, a compression screw is inserted into the bone. (E) Final fracture reduction showing the screw placement.

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flexed to fully expose the proximal pole, and the guidewire for the cannulated headless compression screw is placed down the long axis of the bone. Ideally, a second wire should be added to prevent displacement of the fracture during drilling and screw placement (Fig.  8.14C). This stabilizing wire should be placed across the fracture into the trapezium for maximum stability, but it must not interfere with screw placement. Multiplanar mini C-­arm fluoroscopy is used to confirm that the guidewire is through the central axis of the scaphoid and that the fracture is reduced. Most screw sets utilize a measuring tool at this point to select a screw length, based on the length of guidewire that is protruding from the bone. Clinical tip When basing the scaphoid screw measurement on the guidewire, one must take into account the position of the wire relative to the distal cortex. If the wire abuts the distal cortex, at least 2 mm should be subtracted from the given measurement to ensure the screw does not penetrate into the scaphotrapezial joint. Generally, screw measurements are around 22–24 mm for men and 18–20 mm for women.

A cannulated drill or reamer is then used to gently drill the hole by hand, frequently checking progress using fluoroscopy. Consider advancing the guidewire into the trapezium to stabilize it further before drilling. It is important to maintain a straight trajectory with the drill and avoid bending the guidewire, to avoid damaging or breaking the wire. The cannulated screw is then placed on the guidewire and advanced across the fracture line (Fig. 8.14D). The K-­wires are then removed, final position of the screw is verified with fluoroscopy, and the incision closed (Fig. 8.14E).

Scaphoid non-­union Scaphoid non-­union is not an uncommon occurrence, both because scaphoid fractures can be missed upon initial examination, and because the scaphoid’s precarious blood supply puts it at risk. Many of those who suffer from a scaphoid non-­union are active young adults who are involved in athletic activities, and their fracture was either misdiagnosed as a sprain, or not diagnosed at all. The natural history of scaphoid non-­union is not precisely known. It is clear that there is an increased risk of post-­traumatic arthritis  – the scaphoid non-­union advanced collapse (SNAC) wrist – due to the disruption of the proximal row biomechanics. What is not known is the incidence of symptoms, since many asymptomatic patients never present for treatment of their non-­union.42 Asymptomatic patients do not need surgical intervention but should probably be followed periodically to monitor for the development of symptoms and/­or radiographic signs of arthritis. Patients with symptomatic scaphoid non-­ union may be candidates for operative treatment.43 Advanced imaging is indicated to determine the exact deformity present in the scaphoid and may also provide clues as to the vascularity of the proximal fragment. Correction of a “humpback” deformity (see Fig.  8.9) is easiest from the volar approach, as it requires the fracture site to be opened and a structural bone graft from either the iliac crest or from the distal radius

inserted to restore the height of the scaphoid (Fig. 8.15). This approach can also be used to treat established malunion of the scaphoid with similar deformity. If there is concern for avascular necrosis, vascularized bone grafting should be considered to increase the blood flow to the scaphoid. Typically, this situation arises in proximal pole fractures, and dorsal approach is preferred. Pedicled grafts from the dorsal distal radius, such as those based on the 1,2-­intercompartmental supraretinacular artery, reach the scaphoid easily.44 Although more technically demanding, a free vascularized bone graft from the medial femoral condyle is another option (Fig. 8.16).45 A modification of the medial femoral condyle flap, termed the medial femoral trochlea flap, has been developed to address the non-­salvageable proximal pole. This flap is an osteocartilaginous construct that can be used to replace the entire proximal pole of the scaphoid, as long as one takes the time to precisely “carpenter” the graft to the correct shape.46,47 Although logic dictates that there must be some disadvantage to the loss of the scapholunate ligament, it does not appear that these patients develop automatic instability. In fact, authors have shown that scapholunate stability can be effectively restored by “overstuffing” the scaphoid dimensions using a larger-­than-­anatomic graft to reconstruct this troublesome carpal bone.48

Scapholunate ligament injury Scapholunate ligament injury is the most common form of carpal instability. It is critical to establish the chronicity of the injury before developing a treatment plan. Acute scapholunate injuries present with localized pain and swelling, but rarely have dramatic findings on radiographs. The diastasis between scaphoid and lunate and the DISI deformity that characterize this injury often develop over time as secondary supporting structures attenuate and degenerate (Fig.  8.17). If radiographs are normal, identification of these injuries demands a high degree of clinical suspicion and may require confirmation with MRI arthrography or arthroscopy. Acute partial tears will not have any gross instability and should heal with 4–6 weeks of immobilization alone. Acute complete tears should be treated with open repair of the ligament using suture anchors or other suitable method. The repair should be protected with scapholunate and scaphocapitate (midcarpal) pinning for 8 weeks to allow the ligament to heal. Many surgeons reinforce such acute repairs with additional capsulodesis, especially in subacute repairs.49 Repairs delayed greater than several weeks may be difficult, as the ligament remnants tend to deteriorate over time.31 For patients with chronic tears, the treatment becomes more complex (see Algorithm 8.1). Patients with a reducible scapholunate diastasis without arthritic changes may benefit from reconstruction. Arthroscopy is often utilized to determine the status of the cartilaginous surfaces and the reducibility of the carpals, but sometimes a final decision can only be made after open exploration of the joint. It is important to discuss all potential options with the patient prior to surgery. Reconstruction of chronic scapholunate dissociation can take many forms. For an easily reducible diastasis with some

Treatment and surgical techniques

183

B

A

D

C

E

F

­ of a 22-year-old ­ ­ patient with scaphoid non-union. ­ Figure 8.15 (A) X-rays (B) Volar approach, showing the defect in the scaphoid after non-union debridement. (C) Outline of the volar distal radius vascularized bone graft, pedicled on a portion of the pronator quadratus muscle. (D) Bone graft mobilized, prior to inset. (E) Bone graft inset into the scaphoid defect. (F) Fixation was performed with Kirschner wires.  

­

 

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CHAPTER 8  • Fractures and dislocations of the wrist and distal radius

A

B

C

Figure 8.16  (A) The medial femoral condyle flap is taken from the leg and (B,C) grafted into the wrist.

Clinical tip A good indicator of the “reducibility” of chronic scapholunate dissociation is the ease with which the diastasis can be corrected using K-­wire “joysticks” in the bones to manipulate them. If the scapholunate articulation can be reduced without permanently deforming 0.062-­inch K-­wire joysticks, then reconstruction can be considered.

If the ligament is not repairable, there have been many strategies developed to restore the scapholunate linkage, usually relying on tendon grafts to perform some variety of tenodesis between the unstable bones. Our preferred technique uses a slip of the flexor carpi radialis (FCR) tendon passed through a drill hole in the scaphoid, woven through the dorsal radiocarpal ligament, and secured to the lunate, which has been referred to as a three-­ligament tenodesis (Fig. 8.19).50 If uncorrected, scapholunate dissociation can lead to wrist arthritis. Depending on the stage of arthritis at presentation, various salvage procedures may be indicated. These are addressed more fully in Chapter 18 of this volume.

Lunotriquetral ligament injury Figure 8.17  A widened interval between scaphoid and lunate as a result of a scapholunate ligament tear.

ligament remnants present, repair with capsulodesis can be performed, much like in a more acute injury. Our preference is to perform a dorsal capsulodesis by inserting a mini-­bone anchor into the distal pole of the scaphoid (Fig. 8.18) to anchor this part of the scaphoid to the dorsal wrist capsule, thereby preventing volar flexion of the scaphoid and subsequent impingement on the radial styloid.

Lunotriquetral ligament injuries are more subtle than scapho­ lunate ligament tears. A true lunotriquetral diastasis is rarely seen on radiographs, although a mild VISI deformity or minor disruption in the first Gilula arc may help identify the injury (Fig.  8.20). Because of this subtlety, these injuries are rarely diagnosed acutely. If no collapse (VISI deformity) is present, both acute and chronic injuries can be treated initially with immobilization and other conservative measures. Operative intervention is reserved for those wrists that progress to symptomatic VISI deformity, or otherwise fail nonoperative management. Surgical treatment options include ligament repair,

Treatment and surgical techniques

185

Algorithm 8.1 NO

NO

What is the status of the ligament? Incomplete Tear

Complete Tear

Consider pinning +/- capsulodesis

Is the ligament repairable?

YES

Ligament repair +/capsulodesis

Is scaphoid alignment normal (radioscaphoid angle >45°)?

YES

Bone-ligamentbone reconstruction

Are the cartilage surfaces of the radiocarpal and midcarpal joints normal?

Is the abnormal carpal alignment reducible?

YES Ligament reconstruction with tendon graft (e.g., three-ligament tenodesis)

NO

Partial wrist fusion to maintain alignment (e.g., STT or SC fusion)

YES

NO Salvage procedure (e.g., PRC or scaphoidectomy and four-corner fusion)

Scapholunate ligament injury.

carpi ulnaris tendon passed through drill holes in these bones has been used with some success to recreate the lunotriquetral linkage and is superior to repair in chronic cases.32,51 Ulnar shortening osteotomy can be useful in unloading a painful ulnocarpal joint, as in cases of ulnocarpal abutment leading to lunotriquetral injury, and may help to re-­tension secondary stabilizers in these cases.52

Perilunate dislocation

Figure 8.18  A mini-­bone anchor used to anchor the distal pole of the scaphoid to prevent its flexion, which can cause arthritis change at the radial styloid.

ligament reconstruction, arthrodesis, and ulnar-­shortening osteotomy. Lunotriquetral ligament repair is technically challenging, typically requiring both dorsal and volar approaches. The ligament tends to be short and is not amenable to repair in chronic injuries. Reconstruction with a slip of the extensor

Perilunate injuries are usually diagnosed immediately, as these patients present with a major wrist injury and often have acute median neuropathy (Fig.  8.21A). Reduction should be performed immediately to alleviate this pressure on the nerve and restore carpal alignment. This maneuver typically requires sedation, analgesia, and distraction. With careful manipulation of the wrist into extension, while applying traction, the capitate can be re-­located onto the lunate in most cases. If the lunate is completely dislocated into the carpal tunnel, gentle volar pressure should be used to relocate it back into its place between capitate and radius. Patients presenting in a delayed fashion will be more difficult to reduce. If reduction is not possible, consideration should be given to a more urgent operative intervention, especially in patients with ongoing nerve impingement. For definitive repair, we believe both dorsal and volar approaches are required.13 Volarly, an extended carpal tunnel incision is performed, crossing the wrist crease (Fig.  8.21B). After reducing the lunate, the volar capsule tear is closed using permanent sutures. This repair often incorporates closure of the space of Poirier as well as repair of the volar lunotriquetral ligament, if sutures are placed deep enough. Proponents of a dorsal-­only approach to this injury argue that these ligaments are nicely opposed after reduction, and sutures are unnecessary.14 However, given the need for carpal tunnel decompression in most of these patients, we perform the capsular repair through this incision as well.

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B

A

C

Figure 8.19  (A) PA X-­ray showing mild scapholunate diastasis and cortical ring sign. (B) Intraoperative view of chronic scapholunate dissociation. L, Lunate; S, scaphoid. (C) Three-­ ligament tenodesis. DRC, dorsal radiocarpal ligament; FCR, flexor carpi radialis tendon. (D) Postoperative X-­ray showing properly extended scaphoid, bone anchors, and protective K-­wires.

D

A dorsal wrist exposure (Fig.  8.21C) is then used to confirm accurate carpal alignment, pin the reduced carpus, and repair the dorsal scapholunate ligament, typically with suture anchors. A capsulodesis can be added to reinforce the repair. The pins are cut below the surface of the skin, to remain in place for 8 weeks (Fig.  8.21D). We prefer burying the pins to reduce the risk of postoperative pin track infection. Interestingly, although the lunate is often stripped of all its attachments in this type of injury, avascular necrosis of the lunate is rare in these patients.

Clinical tip In perilunate dislocations, it is important to make sure the carpus is “rebuilt” with the lunate in neutral position (no DISI or VISI). We begin by placing a temporary pin across the radiolunate joint, with the lunate in neutral position, verified with lateral fluoroscopy. The scaphoid and triquetrum are then reduced to the lunate and pinned in the appropriate reduced position. After repairing the dorsal ligaments, the radiolunate pin is removed.

Treatment and surgical techniques

Figure 8.20  Disruption of the first Gilula arc as a result of a lunotriquetral ligament injury.

Distal radius fractures Most distal radius fractures present as closed injuries; those that fail conservative treatment can be electively fixed on an outpatient basis, preferably within one week. If fixed within this time frame, we find that most fragments are easily reducible, and the deposition of healing callus that can obscure an accurate reduction is minimized. However, there are a few situations where more urgent intervention might be needed. Open fractures of the distal radius are a surgical emergency, especially if there is gross contamination of the fracture site. Any fracture-­related wound more than a tiny puncture should probably be washed out formally in the operating room to reduce the risk of osteomyelitis. Patients with median nerve symptoms that do not improve after reduction of the fracture should be considered for an acute carpal tunnel release. It is our experience that these patients typically have a prolonged recovery due to their nerve contusion/­ crush injury, so relieving any ongoing compression of the nerve can be important to their ultimate recovery. If median nerve symptoms do improve with fracture reduction, the carpal tunnel should still be released at the time of fracture fixation. Operative treatments for distal radius fractures include percutaneous K-­wire fixation, external fixation, internal fixation, or combinations of these techniques. Internal fixation can

187

be further subdivided into dorsal plating, volar plating, and fragment-­specific plating configurations. The introduction of volar fixed-­angle plates with locking screws has revolutionized the treatment of these fractures.36 Historically, the dorsal approach was thought to be safer, as it avoided the important neurovascular structures found at the volar wrist. Furthermore, dorsal buttress plates seemed more logical, since these fractures tend to displace dorsally. However, dorsal plating was soon found to be associated with many complications, especially extensor tendon ruptures, due to the difficulty of protecting these soft tissues from the hardware in this location. The modern volar approach is intended to overcome the problems of dorsal plating. The advantage of the volar plating technique is the ability to place the plate under the pronator quadratus muscle, which can shield the plate from injuring the overlying tendons and nerves. In addition, the introduction of locking screws made rigid fixation from the volar side possible irrespective of the amount of comminution of the dorsal metaphysis (Fig. 8.22). Traditional non-­locking screws must adequately engage both cortices in order to secure the plate to bone using friction. While locking screws do engage the bone to some extent, they also have threads on the screw head to engage the plate itself. This prevents the screw from “toggling” due to pressure across the fixed fracture. Furthermore, each screw can be firmly positioned in space to lend three-­dimensional support beneath the articular surface of the radius. This construct is rigid enough to allow for early gentle motion of the wrist in routine cases. Volar plating does have several nuances that one must pay attention to during exposure to prevent unnecessary complications.53 First, the volar incision must be made radial to the FCR tendon to protect the palmar cutaneous branch of the median nerve, which is usually found immediately ulnar to the FCR at the wrist (see Clinical Tip). Next, instead of incising the pronator quadratus down the middle, the muscle should be elevated as an ulnarly based flap by dividing its insertion on the radius. This makes coverage of the plate easier at the conclusion of the case. For the distal locking screws, the lengths should be measured very carefully. We advocate using screws 2 mm shorter than the depth gauge measurement to prevent screw-­tip related injuries to the extensor tendons. Biomechanical studies suggest these screws only need reach 75% of the distance across the metaphysis to provide adequate fracture stabilization.54 Finally, once the plate has been completely installed, fluoroscopy should be performed in multiple planes to ensure correct implant and screw position. Specifically, an offset lateral view should be used to examine the radiocarpal joint. By angling the wrist about 30° (equal to the radial inclination of the joint), one can get a view down the articular surface to make sure no distal screws penetrate the joint (Fig. 8.23). Adhering to these guidelines will allow for effective plating, with minimal complications. Clinical tip The palmar cutaneous branch of the median nerve usually lies ulnar to the FCR tendon, but several anatomic variations have been described. For example, the nerve may lie within the FCR tendon sheath, or cross over its volar surface at the distal forearm. Caution should be exercised during the surgical exposure of the distal radius to avoid injury to this important sensory nerve.

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B

A

C

D

Bridge plating of distal radius fractures can be accomplished by placement of a long dorsal plate which spans the wrist, extending from the radius diaphysis proximal to the fracture distally to the second or third metacarpal (Fig. 8.24). This plate acts as an “internal external fixator”, which can be used to offload and distract the fracture site. This can improve reduction via ligamentotaxis and protect against early loading of the joint, which might overwhelm tenuous fixation constructs. A recent systematic review found that this technique was most commonly used for comminuted, intra-­ articular

Figure 8.21  (A) Lateral X-­ray showing perilunate dislocation. (B) Extended carpal tunnel release, showing lunate in the carpal tunnel. L, lunate. (C) Dorsal wrist exposure, after lunate has been reduced. Note the complete disruption of the scapholunate ligament. C, Capitate; DR, distal radius; H, hamate; L, lunate; S, scaphoid; Tq: triquetrum. (D) Postoperative X-­ray showing bone anchors and protective K-­wires across scapholunate, scaphocapitate, and lunotriquetral articulations.

distal radius fractures and resulted in overall functional wrist range of motion, moderate patient-­reported disability, and a 13% complication rate at average 24 month follow-­up.55

Ulnar styloid fractures The distal radioulnar ligaments connect the distal radius to the ulna, inserting via the triangular fibrocartilage complex (TFCC) to both the fovea and the styloid of the ulna. Because of this mechanical connection, the ulnar styloid often sustains

Future directions

A

189

Figure 8.22  (A) A complex distal radius fracture that has been (B) reduced using a volar locking plate. Note the displacement of the ulnar styloid fracture, which does not need to be fixated because the distal radioulnar joint is stable with manual testing.

B

some degree of an avulsion fracture when distal radius fractures displace (see Fig.  8.22). Even in cases where the ulnar styloid is not fractured, avulsion injuries of the TFCC can lead to instability of the distal radioulnar joint (DRUJ). For this reason, the stability of this joint should be tested in every case of distal radius fracture. When instability is detected, it should be addressed by performing fixation of the styloid fracture, or by repair of the TFCC attachment in cases without styloid fracture. In some ways, the ulnar styloid fracture is analogous to the volar lip avulsion fracture seen in PIP joint hyperextension injury: it serves as a marker of injury severity but does not need to be treated unless instability is present. Despite evidence of ulnar styloid non-­union in many cases, patients without DRUJ instability do very well without ulnar styloid fixation.56 Biomechanical studies have shown that DRUJ stability in these cases can be maintained by the distal oblique bundle of the interosseous membrane.57 This makes it all the more important to obtain anatomic distal radius reductions, so that the appropriate tension on the interosseous membrane is maintained.58 In cases where the DRUJ is unstable, the ulnar styloid can be fixed with tension-­band constructs or small “hook plates”, which have recently been developed (Fig. 8.25). Hardware in this location is not particularly dangerous to the nearby tendons, but is often symptomatic to the patient, since it is on the subcutaneous border of the wrist and forearm, without much soft-­tissue padding to cover the hardware.

Future directions Figure 8.23  Fluoroscopic 30° offset lateral view, showing that each of the distal screws is outside the radiocarpal joint.

Although vascularized bone grafting (in both pedicled and free-­flap iterations) has become a very popular method of

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A

B

C

D

­ of a 75-year-old ­ ­ woman with a very distal, comminuted, displaced distal radius fracture. (C) Fixation required a volar plate to buttress the Figure 8.24 (A,B) X-rays fragments, and a bridge plate to further offload and stabilize, due to the very distal nature of the fracture. (D,E) X-rays after removal of the temporary bridge plate, showing the healed fracture. (F,G) Wrist motion at final follow-up.  

­

­

Future directions

191

F

E

G

Figure 8.24  Cont’d

treating scaphoid proximal pole non-­union with avascular necrosis (AVN), it is not clear exactly when this procedure should be used. Results of these interventions are reported with a wide range of success in the literature. One reason for the variability in results is rooted in the difficulty of standardizing the diagnosis of AVN; another derives from the challenges in recording the exact location of the non-­union in the proximal pole. Establishing guidelines or algorithms for these cases will require additional data from future studies.59 Scapholunate ligament repair and reconstruction continues to be a problem that many hand surgeons feel is largely unsolved. While many procedures have been advocated for acute repair and for chronic reconstruction, most of these options require complex surgeries, prolonged immobilization, and yield inconsistent results. A promising new area of research is developing around the use of various products

(e.g., suture tape) designed to augment the surgical repair of ligamentous structures.60 The Wrist and Radius Injury Surgical Trial (WRIST) concluded enrollment in December 2016 after screening 2190 patients. This 24-­center international randomized controlled trial sought to elucidate differences between outcomes of distal radius fracture treatment in patients over the age of 60. There were three treatment groups: percutaneous fixation with K-­wires, external fixation, and internal fixation with a volar locking plate. A separate group of patients who received nonoperative treatment were also followed for the duration of the study. One of the largest trials of its kind in the hand surgery literature, WRIST has yielded a wealth of new know­ ledge on multiple aspects of distal radius fracture treatment and continues to generate new publications as the wealth of data is reviewed.35

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B

Bonus images for this chapter can be found online at Elsevier eBooks+ Figure 8.2 Posteroanterior radiograph of the wrist, with carpal bones identified. Figure 8.3 Examples of common distal radius fracture eponyms: (A) Colles fracture, (B) Smith fracture, (C) dorsal Barton fracture, (D) volar Barton fracture, and (E) Chauffeur fracture.

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Figure 8.25  Options for ulnar styloid fixation include (A) K-­wires, with or without a tension band, and (B) ulnar hook plate, which works well for larger styloid or ulnar head fractures.

References

References 1. Chung KC, Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am. 2001;26: 908–915. 2. Hove LM. Fractures of the hand. Distribution and relative incidence. Scand J Plast Reconstr Surg Hand Surg. 1993;27:317–319. 3. Dunn AW. Fractures and dislocations of the carpus. Surg Clin North Am. 1972;52:1513–1538. 4. Duckworth AD, Jenkins PJ, Aitken SA, et al. Scaphoid fracture epidemiology. J Trauma Acute Care Surg. 2012;72:E41–E45. 5. Wolf JM, Dawson L, Mountcastle SB, Owens BD. The incidence of scaphoid fracture in a military population. Injury. 2009;40: 1316–1319. 6. Khan IH, Giddins G. Analysis of NHSLA claims in hand and wrist surgery. J Hand Surg Eur. 2010;35:61–64. 7. Johnson RP. The evolution of carpal nomenclature: a short review. J Hand Surg Am. 1990;15:834–838. 8. Colles A. On the fracture of the carpal extremity of the radius. Edinb Med Surg J. 1814;10:182–186. 9. Chung KC, Shauver MJ, Birkmeyer JD. Trends in the United States in the treatment of distal radial fractures in the elderly. J Bone Joint Surg Am. 2009;91:1868–1873. 10. Gehrmann SV, Windolf J, Kaufmann RA. Distal radius fracture management in elderly patients: a literature review. J Hand Surg Am. 2008;33:421–429. 11. Panagis JS, Gelberman RH, Taleisnik J, Baumgaertner M. The arterial anatomy of the human carpus. Part II: the intraosseous vascularity. J Hand Surg Am. 1983;8:375–382. 12. Nagle DJ. Evaluation of chronic wrist pain. J Am Acad Orthop Surg. 2000;8:45–55. 13. Kozin SH. Perilunate injuries: diagnosis and treatment. J Am Acad Orthop Surg. 1998;6:114–120. 14. Budoff JE. Treatment of acute lunate and perilunate dislocations. J Hand Surg Am. 2008;33:1424–1432. 15. Kozin SH, Wood MB. Early soft-­tissue complications after fractures of the distal part of the radius. J Bone Joint Surg Am. 1993;75: 144–153. 16. No authors listed. Definition of carpal instability. The Anatomy and Biomechanics Committee of the International Federation of Societies for Surgery of the Hand. J Hand Surg Am. 1999;24:866–867. 17. International Wrist Investigators’ Workshop Terminology Committee Wrist: terminology and definitions. J Bone Joint Surg Am. 2002;84-­A (Suppl 1):1–73. 18. Amadio PC, Berquist TH, Smith DK, Ilstrup DM, Cooney 3rd WP, Linscheid RL. Scaphoid malunion. J Hand Surg Am. 1989;14: 679–687. 19. Shoji MM, Ingall EM, Rozental TD. Upper extremity fragility fractures. J Hand Surg Am. 2021;46(2):126–132. 20. Watson HK, Ashmead DT, Makhlouf MV. Examination of the scaphoid. J Hand Surg Am. 1988;13:657–660. 21. Kleinman WB. Physical examination of the wrist: useful provocative maneuvers. J Hand Surg Am. 2015;40:1486–1500. 22. Reagan DS, Linscheid RL, Dobyns JH. Lunotriquetral sprains. J Hand Surg Am. 1984;9:502–514. 23. Schreibman KL, Freeland A, Gilula LA, Yin Y. Imaging of the hand and wrist. Orthop Clin North Am. 1997;28:537–582. 24. Goldfarb CA, Yin Y, Gilula LA, et al. Wrist fractures: what the clinician wants to know. Radiology. 2001;219:11–28. 25. Andersson JK, Andernord D, Karlsson J, Fridén J. Efficacy of magnetic resonance imaging and clinical tests in diagnostics of wrist ligament injuries: a systematic review. Arthroscopy. 2015;31: 2014–2020.e2. 26. Haisman JM, Rohde RS, Weiland AJ. Acute fractures of the scaphoid. J Bone Joint Surg Am. 2006;88:2750–2758. 27. Davis EN, Chung KC, Kotsis SV, et al. A cost/­utility analysis of open reduction and internal fixation versus cast immobilization for acute nondisplaced mid-­waist scaphoid fractures. Plast Reconstr Surg. 2006;117:1223–1235. discussion 1236–1238.

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28. Bond CD, Shin AY, McBride MT, Dao KD. Percutaneous screw fixation or cast immobilization for nondisplaced scaphoid fractures. J Bone Joint Surg Am. 2001;83-­A:483–488. 29. Buijze GA, Doornberg JN, Ham JS, et al. Surgical compared with conservative treatment for acute nondisplaced or minimally displaced scaphoid fractures: a systematic review and meta-­ analysis of randomized controlled trials. J Bone Joint Surg Am. 2010;92:1534–1544. 30. Dias JJ, Wildin CJ, Bhowal B, Thompson JR. Should acute scaphoid fractures be fixed? A randomized controlled trial. J Bone Joint Surg Am. 2005;87:2160–2168. 31. Kuo CE, Wolfe SW. Scapholunate instability: current concepts in diagnosis and management. J Hand Surg Am. 2008;33:998–1013. 32. Shin AY, Battaglia MJ, Bishop AT. Lunotriquetral instability: diagnosis and treatment. J Am Acad Orthop Surg. 2000;8:170–179. 33. Lichtman DM, Bindra RR, Boyer MI, et al. Treatment of distal radius fractures. J Am Acad Orthop Surg. 2010;18:180–189. 34. Wrist and Radius Injury Surgical Trial (WRIST) Study Group Reflections 1 year into the 21-­Center National Institutes of Health-­funded WRIST study: a primer on conducting a multicenter clinical trial. J Hand Surg Am. 2013;38:1194–1201. 35. Chung KC, Kim HM, Malay S, Shauver MJ. WRIST Group. Predicting outcomes after distal radius fracture: a 24-­center international clinical trial of older adults. J Hand Surg Am. 2019;44(9):762–771. 36. Chung KC, Petruska EA. Treatment of unstable distal radial fractures with the volar locking plating system. J Bone Joint Surg Am. 2006;88:2687–2694. 37. Orbay JL, Fernandez DL. Volar fixed-­angle plate fixation for unstable distal radius fractures in the elderly patient. J Hand Surg Am. 2004;29:96–102. 38. Young BT, Rayan GM. Outcome following nonoperative treatment of displaced distal radius fractures in low-­demand patients older than 60 years. J Hand Surg Am. 2000;25:19–28. 39. Grewal R, MacDermid JC. The risk of adverse outcomes in extra-­ articular distal radius fractures is increased with malalignment in patients of all ages but mitigated in older patients. J Hand Surg Am. 2007;32:962–970. 40. Merrell G, Slade J. Technique for percutaneous fixation of displaced and nondisplaced acute scaphoid fractures and select nonunions. J Hand Surg Am. 2008;33(6):966–973. 41. Chung KC. A simplified approach for unstable scaphoid fracture fixation using the Acutrak screw. Plast Reconstr Surg. 2002;110: 1697–1703. 42. Kozin SH. Incidence, mechanism, and natural history of scaphoid fractures. Hand Clin. 2001;17:515–524. 43. Kawamura K, Chung KC. Treatment of scaphoid fractures and nonunions. J Hand Surg Am. 2008;33:988–997. 44. Sheetz KK, Bishop AT, Berger RA. The arterial blood supply of the distal radius and ulna and its potential use in vascularized pedicled bone grafts. J Hand Surg Am. 1995;20:902–914. 45. Jones Jr DB, Moran SL, Bishop AT, Shin AY. Free-­vascularized medial femoral condyle bone transfer in the treatment of scaphoid nonunions. Plast Reconstr Surg. 2010;125:1176–1184. 46. Higgins JP, Burger HK. Proximal scaphoid arthroplasty using the medial femoral trochlea flap. J Wrist Surg. 2013;2:228–233. 47. Bürger HK, Windhofer C, Gaggl AJ, Higgins JP. Vascularized medial femoral trochlea osteocartilaginous flap reconstruction of proximal pole scaphoid nonunions. J Hand Surg Am. 2013;38(4): 690–700. 48. Capito AE, Higgins JP. Scaphoid overstuffing: the effects of the dimensions of scaphoid reconstruction on scapholunate alignment. J Hand Surg Am. 2013;38:2419–2425. 49. Szabo RM. Scapholunate ligament repair with capsulodesis reinforcement. J Hand Surg Am. 2008;33:1645–1654. 50. Garcia-­Elias M, Lluch AL, Stanley JK. Three-­ligament tenodesis for the treatment of scapholunate dissociation: indications and surgical technique. J Hand Surg Am. 2006;31:125–134. 51. Wagner ER, Elhassan BT, Rizzo M. Diagnosis and treatment of chronic lunotriquetral ligament injuries. Hand Clin. 2015;31:477–486.

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52. Mirza A, Mirza JB, Shin AY, et al. Isolated lunotriquetral ligament tears treated with ulnar shortening osteotomy. J Hand Surg Am. 2013;38:1492–1497. 53. Chung KC, Petruska EA. Treatment of unstable distal radial fractures with the volar locking plating system. Surgical technique. J Bone Joint Surg Am. 2007;89(Suppl 2 Pt. 2):256–266. 54. Wall LB, Brodt MD, Silva MJ, Boyer MI, Calfee RP. The effects of screw length on stability of simulated osteoporotic distal radius fractures fixed with volar locking plates. J Hand Surg Am. 2012;37(3):446–453. 55. Fares AB, Childs BR, Polmear MM, Clark DM, Nesti LJ, Dunn JC. Dorsal bridge plate for distal radius fractures: a systematic review. J Hand Surg Am. 2021;46(7):627.e1-­627.e8. 56. Sammer DM, Shah HM, Shauver MJ, Chung KC. The effect of ulnar styloid fractures on patient-­rated outcomes after volar locking

57. 58. 59. 60.

plating of distal radius fractures. J Hand Surg Am. 2009;34: 1595–1602. Moritomo H. The distal interosseous membrane: current concepts in wrist anatomy and biomechanics. J Hand Surg Am. 2012;37: 1501–1507. Ross M, Di Mascio L, Peters S, et al. Defining residual radial translation of distal radius fractures: a potential cause of distal radioulnar joint instability. J Wrist Surg. 2014;3:22–29. Higgins JP, Giladi AM. Scaphoid nonunion vascularized bone grafting in 2021: is avascular necrosis the sole determinant? J Hand Surg Am. 2021;46(9):801–806.e2. Thompson RG, Dustin JA, Roper DK, Kane SM, Lourie GM. Suture tape augmentation for scapholunate ligament repair: a biomechanical study. J Hand Surg Am. 2021;46(1):36–42.

SECTION II  •  Trauma Reconstruction

9 Flexor tendon injuries and reconstruction Jin Bo Tang

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SYNOPSIS

ƒ Tendons transmit forces generated by muscles to move joints or to create action power. Flexor tendon injuries are common, but recovery of satisfactory function, particularly after injuries within the digital sheath, is sometimes difficult. Lacerated flexor tendons should be treated by primary surgical repair whenever possible. ƒ The current trend of end-­to-­end surgical tendon repairs is to use multistrand core sutures (four-­strand repairs such as cruciate, double Tsuge, Strickland, modified Savage, or six-­strand repairs such as modified Savage, Tang, or triple Kessler). ƒ In tendon repairs in the digital sheath area, a number of surgeons advocate that the A2 pulley can be released up to two-­thirds of its length, and the A4 pulley can be entirely released when necessary and tendon repair is in the proximity of the pulley, given the integrity of the other pulleys. The release may reduce the resistance to tendon motion and the chance of repair ruptures. ƒ Postoperatively, early tendon mobilization should always be employed, except in children or in some rare instances; motion protocols vary greatly among different treatment centers. ƒ Repair rupture, adhesion formation, and joint stiffness are major complications of primary surgery. ƒ Combined use of multistrand core repairs, release of constricting pulley parts, and well-­designed postoperative combined passive and active motion protocols –­that do not overload, but sufficiently move the ­tendon –­can help minimize adhesions, avoid repair ruptures, and restore optimal function. Full extension and flexion of the operated digit should be tested right after repair, ideally in a wide-­awake setting, to ascertain no gapping of the repair and smooth tendon gliding. ƒ Secondary surgeries include tenolysis, free tendon grafting, and staged tendon reconstruction. Tenolysis is indicated when restricting adhesions hamper tendon gliding and soft tissues and joint conditions of the hand are favorable. Free tendon grafting is a salvage operation for failed primary repairs, delayed treatment (>1 month) of an acute cut, or lengthy tendon defects. Staged reconstruction is indicated in case of extensive scar formation or multiple failed surgeries. Preservation or reconstruction of major annular pulleys is vital to restoring function of the digits during these secondary surgeries.

ƒ Closed rupture of flexor tendons usually requires surgical repair. ƒ Success of flexor tendon surgery is very expertise-­dependent. A thorough mastery of anatomy and meticulous surgical technique are requirements for satisfactory restoration of function.

Introduction Tendons are composed of dense connective tissues that transmit forces generated by muscles to move the joints or to create action power. Functionally, the hand is dependent upon the integrity and ample gliding of the tendons. Among all the tendons in the body, those in the hand are most frequently injured, due to their length and the varied nature of the activities of the hand. The pursuit of ideal repair techniques has drawn the attention of surgeons ever since hand surgery became a subspecialty. For over a century, flexor tendon repairs have presented challenges to hand surgeons. Difficulties in restoration of function of digital flexor tendons relate chiefly to the intricate anatomy of flexor tendon systems: the coexistence of superficialis and profundus tendons within a tight fibro-­osseous tunnel. Peritendinous adhesions jeopardize tendon gliding. Tendons within the synovial sheath (intrasynovial tendons) were once considered to lack self-­reparative capacity; therefore, ingrowth of adhesions from peritendinous tissues was believed to be a prerequisite in the tendon healing process.1–­4 As the concepts regarding tendon healing biology evolved, tendon cells have been proven capable of proliferating and of producing collagen to heal tendons.5–­10 However, the tendon is innately low in cell density and growth factor activity, limiting its early healing strength. In the early and middle twentieth century, secondary tendon grafting dominated the repair of digital flexor tendons. During this period, tendon implants were developed for staged tendon reconstruction. However, as the practice of primary repair prevailed in recent decades, the number of cases indicated for secondary tendon grafting or staged

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reconstruction decreased drastically. Primary repair of injured digital flexor tendons was pioneered by Verdan11 and Kleinert et  al.12 in the 1960s and is the essential approach underlying current practice. Current primary repair and early tendon motion are based on the recognition of intrinsic healing capacity of the tendon in the 1970s and 1980s by Lundborg, Manske et al., and Gelberman et al.5–­10 Nevertheless, despite the widespread use of primary repairs, surgical outcomes remained unpredictable, and sometimes even disappointing. In the last two to three decades, major efforts were thus devoted to tackling this problem, with the goal of achieving consistently optimal outcomes and minimizing repair ruptures and adhesions. In this regard, a number of multistrand core surgical repairs –­ such as Savage, Strickland, cruciate, Lim–­ Tsai, or Tang techniques13–­19  –­have been developed to replace weaker, conventional two-­ strand repairs. Subdivisions of zones 1 and 2 of digital flexor tendon systems were proposed by Moiemen and Elliot20 and Tang,21 which offer precise nomenclature in recording the locations of tendon cuts, discussing treatments, and comparing outcomes. Surgical procedures to release critical parts of the pulleys have been advocated by Tang22 and Kwai Ben and Elliot23 to decompress the tendon and “free” tendon motion. In the past few years, we have witnessed reports in which repair ruptures have been minimized, with recovery of excellent or good function in the majority of cases.19,24,25 These recent reports represent some remarkable steps towards satisfactory flexor tendon repairs and highlight the promise of predictable tendon repairs (Box 9.1).

BOX 9.1  General tips for surgeons of flexor tendon repairs 1. Repairing flexor tendons is based on a thorough mastery of anatomy and biomechanics. The surgeon should know the anatomy in detail, including the lengths of major pulleys, characteristic changes in the diameter of the sheath, and tendon gliding amplitude. 2. Primary repairs should be performed by experienced surgeons whenever possible. 3. Mastery of atraumatic techniques is essential for the operator. The outcomes of the repairs are very expertise-­dependent; repair of tendons by an inexperienced surgeon is a frequent cause of tendon adhesions and poor function, and thus should be avoided. 4. Conventional two-­strand repairs are weak; stronger surgical repairs are preferable. 5. Complete closure of the tendon sheath is not necessary. Venting of a part of sheath (7–10 mm

Gapping

Tension

Loose repair

B

Solution : Repair with a certain light tension

Figure 9.28  Two bad repairs decrease the strength: (A) a repair with short core suture purchase and (B) a loose repair. Sufficient core suture purchase and a certain pre-­tension favor resisting gapping and decrease the chance of repair failure during tendon motion after surgery.

BOX 9.4  Recommended surgical tendon repair requirements

C

Figure 9.27  Three simple, common methods of peripheral suture. (A) Simple running peripheral suture. (B) Running locking peripheral suture. (C) Several sparely located peripheral stitches: from upper to lower, circle sutures, cross sutures, and combined circle and cross sutures.

tendons appear edematous, and in cases with delayed primary repairs. In performing the delayed repair, the author finds it almost impossible to repair the FDS tendon in zone 2 C, because some degree of collapse or narrowing of the A2 pulley is inevitable, and the tendons are often edematous. In zone 2B, where the FDS tendon is bifurcated into two slips, the author uses two Tsuge repairs separately in each tendon slip; when the laceration is close to the insertion, the tendon slips are anchored to the phalanx. Treatment of the FDS tendon in zone 2D is straightforward, similar to the FDP tendon except that the FDS is flatter and four or fewer strands are used.

• More than two strands as the core repair –­four or six strands recommended. • Certain tension across the repair site –­10% shortening of tendon segment after repair. • Core suture purchase: 7–­10 cm. • Locking tendon–­suture junctions in core suture. • Diameter of the locks: 2 mm or over. • Suture calibers: 3-­0 or 4-­0 for core suture. • A variety of nylon sutures, or other sutures. • A simple running or locking peripheral suture. • Minimal separate stitches of peripheral suture if core repair is extremely strong. • Avoid extensive exposure of sutures over the tendon surface.

In deciding surgical options relating to both the FDS and the pulleys, the author generally seeks to appropriately decrease the gliding contents (by not repairing or excising the FDS tendon) or enlarge the sheath (when both tendons are repaired primarily or only the FDP tendon is repaired at the delayed stage). The underlying idea is that the fibro-­osseous digital flexor sheath tunnel is comparable to a tight fascia compartment of extremities; the edematous and healing tendons are compromised easily. Release of compression of the tendon to avoid overloading it during motion can be more vital to the success of treatment than providing it with sufficient surgical strength.

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A

Figure 9.29  The constricting A4 pulley sometimes presents an obstacle for the passage of the flexor digitorum profundus tendon.

B Midline incision

Figure 9.30  The A4 pulley and a part of its adjacent sheath were vented to allow tendon passage in this patient. Other parts of the sheath were not violated. In this case, the flexor digitorum profundus tendon was repaired with a six-­strand original Tang repair with three groups of looped sutures. Lateral incision

Surgical options currently advised to deal with the tendons and pulleys in the most complex areas of finger flexor tendons are summarized in Table 9.1. Once surgeons have completed surgical repair of the tendon, and vented the pulleys in case of need, an intraoperative test –­ “digital extension–­flexion test” –­should be performed before closure of surgical incisions.149 Detailed in Box 9.6, this test consists of three parts: full extension of the operated digit, flexion of the digit from full extension to flexion, and finally maximal digital flexion (Fig. 9.38). If the repair fails this test, the repair should be either redone or enhanced, or the annular pulley proximal to the repair vented further, depending on the circumstance. If the repair is a wide-­awake surgery, the patient should move the digit actively on the operating table, which offers the most objective measure of quality of the repair (Fig. 9.39). If a repair fails the test intraoperatively, this poor repair is bound to gapping or disruption in later early active motion; therefore it should be revised before leaving the operating table.

Shortening

C

Figure 9.31  A case of delayed primary repair. (A) An intact A4 pulley was seen. (B) The A4 pulley was cut open entirely to allow tendon repair. The flexor digitorum profundus tendon was repaired with a six-­strand asymmetric Kessler repair (see Fig. 9.26C). (C) Methods of venting a pulley: midline cut, lateral cut, or shortening.  

Treatment/­surgical techniques

211

BOX 9.5  When and how to vent the A4 pulley for tendon repair 1. The A4 pulley is located at the middle part of the middle phalanx, about 5 mm long. 2. The A4 pulley is rigid, constrictive, and narrow. 3. When this pulley prevents smooth passage of the retracted FDP tendon underneath, or when the pulley is found to prevent smooth gliding of the repaired FDP tendon during digital extension–­flexion test (see Box 9.6 for method detail), this pulley can be entirely vented after the surgeon confirms that all other annular pulleys are intact. 4. The A3 pulley should usually be preserved. In the rare case when the A3 pulley has to be vented, any synovial sheath proximal to the A3 should be entirely preserved. 5. The entire length of the sheath–­pulley venting should be less than 1.5–­2 cm over the middle phalanx area. 6. The method of venting is (1) direct cut along the palmar midline of the pulley, or (2) direct cut along the lateral side of the pulley, or (3) resection of this pulley if it has been embedded inside adhesions and fibrosis.  

Figure 9.34  The proximal tendon stump was passed underneath the preserved portion of the A2 pulley. The tendon was repaired with the six-­strand M-­Tang technique.

Figure 9.35  Follow-­up 6 months after surgery. Full flexion of the finger, with no loss of digital flexion and no tendon bowstringing. Figure 9.32  A case of ruptured primary repair referred to the author. Direct repair of the ruptured flexor digitorum profundus tendon was performed 3 weeks after the first tendon repair. The flexor tendons and the A2 pulley were found embedded within scars.

Figure 9.33  The A2 pulley was partially excised and the intact part of the A2 pulley was released from the scar. The ragged tendon ends were trimmed to fresh tendon surfaces.

Figure 9.36  Full extension of the fingers, without extension deficits of the finger joints.

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CHAPTER 9  • Flexor tendon injuries and reconstruction

SECTION II

A5

A

B

C3

A4

C 2 A3

C1

A2

A1

Tendon laceration

A5

C3

A4

D

C1

A2

A1

Sheath–pulley release

Tendon laceration

C

C2 A3

Sheath–pulley release

Tendon laceration

Sheath–pulley release

Tendon laceration

Sheath–pulley release

Figure 9.37  Drawings depicting the length and areas of release of the pulley–­sheath complex to decompress the repaired tendons, without bowstringing or loss of tendon function. (A) Release of the entire A4 pulley when the flexor digitorum profundus tendon has been cut around the A4 pulley and the tendon cannot pass easily beneath this pulley during surgery. (B) Release of a part of the sheath distal to the A2 pulley and the distal half of the A2 pulley, when the tendons are cut a little distal to the A2 pulley. (C) Release of a short part of the sheath distal to the A2 pulley and the distal two-­thirds of the A2 pulley when repairing tendons cut at the edge of, or in the distal part of, the A2 pulley. (D) Release of the proximal two-­thirds of the A2 pulley when repairing a cut in the middle, or proximal part of, the A2 pulley.

Zone 3, 4, and 5 injuries The repair techniques for injured flexor tendons proximal to zone 2 are almost identical to those used in zone 2. These zones have a better prognosis because of richer vascularity around the tendon and lack of constricting pulleys over the tendons. Adhesions in these areas are less likely to impede tendon motion. Zone 4 tendon injuries are frequently accompanied by lacerations to the median nerve. The transverse carpal ligament may be partly or entirely opened to facilitate repairs and left partly open after tendon repairs. Zone 5 tendon injuries usually present as multiple tendon lacerations with neurovascular injuries. A wrist with transection of a majority of tendons, vessels, and nerves (at least 10 out of 15 of these structures, excluding palmaris longus) is called a “spaghetti” wrist.180–­184 A “spaghetti” wrist was reported to have an adverse effect on the recovery of the independent FDS action but not on the recovery of digital range of motion.184 In zone 5, repair of the FDS tendon is preferred, and early postoperative tendon motion is advised,184–­186 which favors independent movement of the superficialis. However, the FDS tendon to the little finger may be absent or too slender to repair.

FPL injuries Repair of the injured FPL tendon in the thumb usually follows the same principles and methods of repairs of the FDP

tendon in fingers. Multistrand repairs are advised, and one or two pulleys can be vented to free tendon motion. Reports have shown that conventional two-­strand repairs have a risk of rupture as high as 17%.25,172 Later, Giesen et al.25 reported no ruptures and good function after use of a six-­strand Tang method without peripheral sutures in repairing 50 FPL tendons. The oblique pulley is often vented to access the tendon when the cut is in zone 2. A strong six-­strand repair is suggested, with sparse peripheral suture (Fig. 9.40). In repairing the FPL tendon, the proximal cut end of the tendon frequently retracts into the thenar muscles. This end can be retrieved with the techniques described for retracted FDS and FDP tendons. If the proximal stump of the FPL tendon has retracted proximal to the thenar muscles, a separate incision just distal to the carpal tunnel or in the forearm is required to locate the stump. In the forearm, the FPL stump usually lies deep to the FCR tendon and the radial artery.

Injuries in children Flexor tendon repairs in children have a better prognosis than those in adults.187–­191 As children may be less compliant with instructions to limit movement, the repaired digits are usually immobilized for 3–­3.5 weeks after surgery. Either a two-­strand or a four-­strand repair can be used. In practice, many surgeons use a two-­strand repair and achieve good return of function. The outcomes appear unaffected by whether

Treatment/­surgical techniques

213

Table 9.1  Summary of mechanical basis and surgical options advised to deal with the flexor digitorum superficialis (FDS) tendon and pulleys in zone 2 of the finger

Investigations

Area of FDS insertion (2 A)

Distal to A2 pulley (2B)

Beneath A2 pulley (2 C)

Proximal to A2 pulley (2D)

FDS tendon

Insertion

2 slips, dorsal to FDP, with vincula

Bifurcation

One single band, flattened palmar to FDP

Pulleys

A4, C2, narrow

A3, C1

A2, narrow

A1, PA

FDS tendon

No gliding

Not constricting FDP

Constricting FDP, as a moving and second “pulley”

Little constriction

Pulleys

A4 release is feasible112

May incise one pulley107

Partial release is feasible22,111,112

Repair174,179

Resection or do not repair21,23,150 Resect one slip101

Anatomic

Biomechanical

Clinical options FDS tendon

Pulleys

A4 venting19,23,172

Repair both tendons when possible

Partial release19,23,150,172 Pulley shortening or plasty100,175

FDP, Flexor digitorum profundus; PA, palmar aponeurosis.

BOX 9.6  When and how to perform an extension–­flexion test • This test should be performed after any kind of primary repair of flexor tendons in the digital and palm area, to make sure the repair is strong and that tendon gliding is smooth before closure of surgical incisions. • There are three parts to this test. Part 1: Full passive extension of the digit that has undergone surgery by the operator, to confirm that the tendon repair site has no gapping. • Part 2: From the fully extended position, the operated digit is passively flexed to moderate degrees, to confirm that the tendon and the repair site can glide smoothly. • Part 3: Further pushing the digit to full or almost full flexion, to confirm that the tendon repair site does not impinge against rigid annular pulleys. • If tendon gapping is found with digital extension, the repair should be reinforced, or if annular pulleys block tendon gliding with digital flexion, the pulleys should be vented, according to guidelines for treatment of pulleys. • The results of the above tests are included in the operative notes and the therapists are informed.

a two-­or four-­strand repair is used or whether the tendon is moved or immobilized early after surgery.189,190 Navali and Rouhani189 reported that both a two-­strand and  four-­strand repair achieved good functional return, with no difference in range of active digital motion between the two methods. Elhassan et al.190 reported that early postoperative motion and immobilization did not affect outcomes in children aged 2–­14 years with injuries in zones 1 and 2.

Partial tendon lacerations Laceration through less than 60% of the diameter of the tendon does not necessitate a repair by core sutures. An

increased risk of triggering, entrapment, or ruptures is associated with partial laceration over 60%.192–­196 For lacerations less than 60%, the tendon wound can be trimmed to lessen the chance of entrapment by pulley edges and friction against the sheath. Alternatively, the cut portion of the tendon can be repaired with epitendinous stitches to smooth the tendon surface and to strengthen the tendon. Laceration of 60–­80% requires at least an epitendinous repair197–­200 and is better repaired using a two-­strand core suture through the cut portion. Laceration of 80–­90% is treated identically to a complete laceration.

Closed rupture of the flexor tendons and pulleys Traumatic FDP tendon avulsion from the tendon–­ bone junction accounts for a major portion of closed rupture cases.201–­204 The injury mechanism is hyperextension of the DIP joint, which subjects the FDP tendon to excessive load. The tendon disrupts at its insertion to the distal phalanx. Athletic injuries can lead to this type of injury. In football, wrestling, or rugby, when one player grabs another’s jersey, a finger gets caught and pulled, resulting in disruption of flexor tendons. This injury (“jersey finger”) is seen most commonly in the ring finger. Closed tendon ruptures at the wrist can be associated with fractures in carpal bones.204 Flexor pulleys are prone to sprains and ruptures during climbing. Rupture of the pulleys occurs in up to 20% of climbers.205 The A2 pulley of the ring finger is the most often injured. Closed pulley ruptures are treated conservatively or by surgical reconstruction. Leddy and Packer201 classified close tendon ruptures into the following types: Type I: The FDP tendon is avulsed from the phalanx and retracts into the palm. The vincula of the FDP tendon are disrupted. There is no active flexion of the DIP

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CHAPTER 9  • Flexor tendon injuries and reconstruction

Confirm no gapping

retracts beyond the middle phalanx and even into the palm. In treating type IV injuries, the bony fragment is attached into the distal phalanx first; then the avulsed tendon is advanced. Postoperatively, the DIP joint is immobilized for 4–­5 weeks, or a gentle motion regime is prescribed. Early recognition of closed tendon ruptures is of paramount importance. In the cases of late diagnosis, primary repair is difficult or even impossible. Chronic cases require free tendon grafting.

A Confirm smooth gliding on digital flexion

Postoperative care With the exception of a few instances  –­such as tendon repairs in children, adults who are unable to follow through the protocol, or associated with complex fractures  –­motion of repaired tendons should be initiated from the early postsurgical period. Combined passive–­ active flexion protocols are the mainstream protocols, replacing passive flexion-­only protocols.150,161,206–­212 The passive flexion-­only protocols such as Duran–­Houser method is reserved only for those who cannot do active flexion exercises.

B Confirm pulley does not impinge on tendon gliding

C

Figure 9.38  Extension–­flexion test of the repaired tendon before closure of surgical incision. (A) Full extension of the digit. (B) Motion from full extension to flexion. (C) Completing the maximal flexion. In wide-­awake surgical settings, the digital motion is active, providing the best measure of quality of surgical repair.

joint. A tender mass is present in the palm. The tendon should be reinserted within 7–­10 days before the sheath collapses, which may prevent advancing the tendon distally. Muscle contracture may also prevent tendon advancement. Type II: The FDP tendon retracts to the level of the PIP joint. This is the most common type. The sheath is not compromised, and muscle contracture does not develop easily. Repair may be attempted 1 month after injury. Type III: A large bone fragment is attached to the FDP tendon. This bone fragment frequently prevents the tendon from retraction proximal to the A4 pulley. Bony fixation using a K-­wire or a screw usually suffices. Type IV: The FDP tendon avulses from the bony fragment. This type was added by Smith.202 The avulsed tendon

Duran–­Houser method This was a controlled passive finger flexion protocol introduced by Duran and Houser in the 1970s.209 A dorsal splint was applied with the wrist in 20° flexion, the MCP joint in 50° flexion, and the IP joints were allowed full extension (Fig. 9.41). Within the first 4.5 weeks, the patients performed 10 passive DIP joint extensions with PIP and MCP joint flexions, and 10 passive PIP joint extensions with MCP and DIP joint flexions hourly within the splint (see Fig. 9.41).

Early active motion In the late 1980s and early 1990s, protocols containing early active tendon motion components emerged. One requirement is that the tendon repairs be strong enough to tolerate the tension during the motion. In 1989, Belfast surgeons devised an active motion protocol,211 which was later known as “Belfast method”. Postoperatively, a splint is applied from the elbow to the fingertips with the wrist in mid-­flexion, the MCP joint at slightly less than 90° flexion, and the IP joints straight. The exercises commence 48 hours after surgery, consisting of two passive movements followed by two active movements and are performed at 2-hour intervals. During the first week, the PIP joint is actively flexed through about 30° and the DIP joint through 5–10°. In subsequent weeks, the range of active motion is gradually increased. The splint is removed by the sixth week and blocking exercises of the IP joints are initiated when necessary. Variants of the Belfast method have been reported. In one of the variants, the “Billericay regimen”, the wrist and the MCP joint are kept in a splint at 30° flexion, respectively, and the splint is removed by the fifth week. The patient is instructed to perform 10 repetitions of exercise hourly.212

Postoperative care

Author's preferred combined passive–­active method (Nantong regimen)

215

session of motion. After surgery, the hand is protected in a dorsal splint, with the wrist at 20–­30° flexion, MCP joint at slight flexion, and the IP joints in extension for the initial 2.5 or 3 weeks (3 weeks or slightly longer when the trauma is severe or digital edema is remarkable) (see Fig. 9.41).19 Either a plaster splint or thermoplastic splint can be used. The wrist can be placed at a

The key components of this regimen are true active flexion of the repaired digits and sufficient runs of the repaired tendon in each

A

B

C

D

E

F

­ Figure 9.39 Primary tendon repair of the tendon in the A2 pulley area (zone 2 C) under a wide-awake setting. (A) The first injection of 5 mL of the 1% lidocaine with 1 : 100 000 to the palm 30 minutes before surgery. (B) The second injection was given 15 minutes later, to the proximal part of the digit, followed immediately by injection to the middle and distal parts of the digit (C,D). (E) A close-up M-Tang repair. Note that the ­ view of making the first anchor of the looped suture to the tendon in the six-strand ­ ­ site of needle entry is 1 cm away from the cut end and the size of the lock is large. (F) The U-shaped repair with the first looped suture was completed. Two strands of centrally placed looped sutures was added later to complete the six-strand core repair. (D) After completion of the six-strand repair and simple peripheral suture, the patient actively extended (G) and actively flexed (H) the digit to check quality of the repair. (I) Pictures taken 5 months later showing full recovery.  

 

 

 

­

­

­

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CHAPTER 9  • Flexor tendon injuries and reconstruction

G

H

I

Figure 9.39  Cont’d

neutral position instead. The patients do not exercise the digits in the initial postoperative days; exercise starts at 3–­5 days after surgery. The patient is instructed to perform at least 4–­6 sessions of combined passive–­active motion daily across the morning, noon, evening, and before sleep, with each session lasting for 15-­20 minutes. More sessions can be implemented as needed, while hourly exercises are not required. At the beginning of each exercise session, the finger is passively flexed 10–­30 times to lessen the overall resistance of finger joints and soft tissues during subsequent active flexion. The passive motion is followed by actively flexing the finger with gentle force at least 30–­40 times up to the range the patients feel comfortable with (usually from full extension to one-­third or one-­half of entire flexion range, and may even increase to two-­thirds if achieved with ease). In each exercise session of 15–­ 20 minutes, the patient usually actively flexes the finger for about 60–­80 times. The active flexion can be slow and gentle, and should not performed against resistance. Active flexion over full range is not encouraged, unless it can be achieved very easily. In this 2.5-­to 3-­week period, full active extension is particularly encouraged, and prevention of extension deficits rather than achieving full range active flexion is emphasized. After above initial 2.5 weeks (or 3 weeks, or slightly later), a new splint is made, and the wrist is splinted at 30° extension (Fig.  9.42). Exercise of finger flexion, both passively and actively, is emphasized in this period. Active motion up to the midrange is required, and is increased gradually

over two-­thirds (or full range). Digital flexion from the mid-­ range to full range, in particular over the final one-­third of the flexion range, usually encounters greater digital stiffness. In this period, we ensure passive flexion over a full range to decrease joint stiffness and gradually increase the range of active flexion approaching full flexion range, but discourage active forceful flexion of the finger over the final range where the tendon is subjected to the greatest load and is more vulnerable to rupture (see Figs.  9.8, 9.42, & 9.43). Differential FDS and FDP motion exercise is encouraged throughout the first 5 weeks. From the sixth week, full active finger flexion  is encouraged (which can be started earlier when the flexion is judged to have less resistance). From 6 or 8 weeks, the splint is removed or used only at night or when going out. Strong surgical repairs together with necessary venting of the pulleys have bestowed greater freedom in wrist positions after surgery. The wrist can be protected in any positions except for remarkable flexion or extension. The author now uses a dorsal plaster splint to protect the wrist in neutral or slight extension throughout the exercise period. Often a  shorter splint is used (to about 10 cm above the wrist) to protect zone 1 and 2 repairs (Figs. 9.43 & 9.44). In performing the combined passive-active digital motion exercises as detailed earlier, the author regularly asks the patient to remove the splint to do out-­ of-­ splint motion. Therefore, changing splinting position at 2.5 or 3 weeks after surgery is no longer necessary. The is a simplified Nantong regimen

Postoperative care

A

217

B

C

­ ­ Figure 9.40 (A) Oblique pulley was released in the thumb. (B) The cut FPL tendon was repaired with the six-strand M-Tang technique, with slightly tensioned (bulky) repair site when the proximal stump is fixed by a needle. (C) The repair site is flatter after the needle was removed.  

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CHAPTER 9  • Flexor tendon injuries and reconstruction

SECTION II

A

Duran and Houser passive motion regimen

B

Nantong regimen

Figure 9.41  (A) Duran and Houser passive tendon motion regimen. (B) Nantong regimen. Passive flexion of the fingers over 10–­30 times, followed by active flexion to one-­ or two-­thirds of the entire arc of finger flexion for at least 30-40 times in a session. The patient performs 4–6 such exercise sessions daily.

Postoperative care

219

The First 2.5 Weeks

Emphasis on full digital extension

Partial active digital flexion and full passive digital flexion The Second 2.5 Weeks

Emphasis on full active digital flexion

Figure 9.42  The author’s combined passive–­active motion protocol. This protocol is divided into two 2.5-­(or 3-­) week periods, or into two 3-­week periods when trauma to the digit is severe or edema of the hand is remarkable. In the first 2.5 weeks, with wrist in slight flexion, finger extension is emphasized. Only partial active digital flexion is allowed, but full range of passive motion is implemented. In the second 2.5 weeks, with wrist in extension, full active finger flexion is encouraged. This protocol incorporates the concept of synergistic wrist and finger motion. When the wrist is flexed, finger extension is less tensed; when the wrist is extended, finger flexion is less tensed.

with out-of-splint exercise. The patient is instructed to do 4–6 sessions (each session of 15–20 minutes) of the out-ofsplint exercise at home daily. The out-­of-­splint motion is safe and more efficient. Out-­of-­splint motion is even easier and more beneficial for a patient with a repair in the little finger. The splint is put back after each exercise session. It must be noted that the early active motion protocols used in 1990s (Belfast regimen or Billericay regimen) and the recent protocols (such as Nantong regimen) are remarkably different. The Belfast regimen and Billericay regimen have only 2–­10 repetitions of active flexion in each session, which is remarkably fewer in number and duration of active digital flexion in each session than the recent regimen. The early regimen is insufficient in term of the cycles and duration of active digital flexion, which may be the reasons why they did not improve outcomes. Sufficient number of cycles and duration of each exercise session are keys to early active motion. The author often checks with or explains to his patients these therapy details.

Delayed motion exercises Delaying motion exercises, i.e., immobilization over the first 2 weeks, can be a right choice for some patients. A patient with distal zone 1 direct end-­to-­end repair, the terminal part

of the FDP tendon has little need of gliding and adhesions have almost no impact on digital motion. The author immobilizes the wrist in 20–­30° of flexion and the MCP joint in slight flexion for 2 weeks with a short dorsal splint. From the third week, the digit is passively moved within the splint. From the fifth week, the patient performs active digital flexion with the splint removed; the splint is not discarded until week 7. A severely traumatized hand after repair of multiple structures also benefits from such delayed exercises. The above-­ described protocols represent several distinct categories of exercise. While the key points of the passive–­active motion regimen are respected currently (Box 9.7), upon applying to individual patients, surgeons or therapists should incorporate refinements. In patients with severe edema of the hand or trauma to multiple digits, motion exercise can be delayed for a few days, and more sessions of passive digital motion should be integrated. Table  9.2 is the straightforward scale that the author uses to record the severity of digital edema for setting timing and intensity of exercise. Other factors such as joint stiffness, soft-­tissue conditions, and extensor tethering should also be considered in adjusting the regime.213 From communications with many hand surgeons and therapists, the author has found that hand centers around the globe actually use some kinds of variants of these protocols after zone 1 and 2 repairs.149,214 Motion regimes for zone 4

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CHAPTER 9  • Flexor tendon injuries and reconstruction

A

B

A

B

Figure 9.43  The out-of-splint partial-range active flexion. (A) Early active motion to full extension. (B) Active flexion to the half or two-thirds of the flexion arc in the first 3 weeks.

and 5 repairs are generally not as complex as those described above. It is a common practice to commence exercise 4 or 5 days after surgery because adhesions only start to develop from 10 days to 2 weeks after surgery. Experimental evidence supporting later commencement of tendon motion a few days after surgery were offered by Zhao et  al.118 of the Amadio group, and the author’s colleagues Xie et al.119 and Cao et al.122 Digital edema increases resistance to motion, which peaks at 3–­5 days.120–­122 Both Zhao et al.118 and Cao et al.122 suggest that motion be commenced later (5 days after surgery).

Outcomes, prognosis, and complications Review of outcomes reported over decades showed excellent or good active range of finger motion in more than three-­ quarters of primary tendon repairs.14,17,19–­21,25,179,211,212,214–­232 In the earlier part of this period, the rupture rates ranged from 4 to 10% in the finger flexors and from 3 to 17% in the FPL tendon of the thumb.14,17,179,215–­228 Adhesions remained the most common complication, preventing satisfactory return of active joint motion. Finger joint stiffness was reported fairly frequently as well. Most of these reports came from the finest

C

Figure 9.44  The postoperative protection and motion. (A) Neutral wrist position with a short forearm splint. (B) Out-­of-­splint motion exercise. (C) In later weeks, specific motion exercise of the distal interphalangeal joint is often necessary to correct mild to moderate stiffness, which develops 3–­4 weeks after surgery.

hand centers in the world, and each team was supervised by at least one surgeon with expertise in treating tendon injuries. The outcomes in a general hospital setting may actually reflect a lower level of success. Flexor tendon repairs might have been unsuccessful in a larger proportion of patients, with

Outcomes, prognosis, and complications

BOX 9.7  When to begin and how to perform early active motion • Early active motion of the surgically repaired digit is a component of an early passive–­active motion regime, which should be performed together with passive motion in each exercise session with the protection of a dorsal splint (or out-­of-­splint exercise in very compliant patients). • Early active motion should be initiated on day 3, 4, or 5 after surgery, not necessarily starting on day 1. Delaying the early motion for a few days decreases pain and avoids peak digital edema. • Early active motion can be delayed to around the end of week 1 if remarkable digital edema is drastic and wound conditions do not allow earlier motion. However, passive hand motion should be implemented earlier to decrease the risk of joint stiffness and edema. • At least 4–­6 sessions of exercise are necessary daily, distributed across the day and evening. Each session lasts 15–20 minutes and includes no fewer than 40 runs of active digital flexion. More exercise sessions should be added if possible. • In each session, passive motion always precedes active digital flexion. The finger should be flexed passively and extended 20–­ 30 times (or more) before starting active finger flexion. • In performing active finger flexion, the patient should be instructed to perform partial range active flexion in the first 2.5 or 3 weeks, i.e., active flexion over the first one-­half or two-­third parts of the entire flexion arc, avoiding the final part of active flexion or making a fist. • Full range of active flexion is allowed 3–­4 weeks after surgery.

Table 9.2  Severity of digital edema

Grade

Description

0 (none)

Swelling is absent

1 (slight)

Swelling is minimal or mild

2 (moderate)

Swelling is prominent, with increase in digital diameter

3 (severe)

Swelling with openings in skin incisions

a greater incidence of repair ruptures, adhesion formations, or digital joint contracture. Nevertheless, the past 30 years have seen impressive improvements in outcomes of flexor tendon repairs. In the late 1980s and early 1990s, Small et  al.211 and Cullen et  al.179 used a two-­strand repair and postoperative active motion and had repair ruptures in 6–­9% of the repairs, with overall good or excellent results in 78% of the digits. Elliot et al.212 reported a series of 233 patients with complete division of the digital flexor tendons, treated with a two-­strand core repair with a controlled active motion regimen. Thirteen (5.8%) fingers and five (16.6%) thumbs suffered tendon ruptures during the mobilization. In the same period, multistrand core repairs were reported by Savage and Risitano,14 and Tang et  al.17,215 together with active or passive–­active motion therapies. Trumble et al.229 used a four-­strand Strickland core suture and a running epitendinous suture to repair zone 2 flexor tendon lacerations in 119 digits (103 patients) in a multicenter prospective randomized trial. They documented significantly greater range of digital motion, smaller digital flexion contractures, and greater patient satisfaction in the active motion group than in the passive motion group. Two digits had tendon ruptures in each group. The study supports the combination of multistrand tendon repair and early active motion. Later reports of Pan et al.,207 Tang et al.,231 and Giesen et al.232

221

give support to early active digital flexion exercise. Rupture rates do not increase in tendons with strong surgical repair and early active flexion.206,207,230–­232 Of note, reports of multistrand core sutures in the recent decade documented minimal or zero repair ruptures.207,230–­232 A stronger surgical repair combined with release of the pulleys offered great safety to the postoperative active motion exercise. After combined use of multistrand repairs and pulley releases, the majority of the cases had good to excellent active range of digital motion with zero tendon ruptures.19,24,25 The author’s own clinical outcomes also indicate that good-­to-­excellent return of function can be achieved fairly consistently by means of multistrand tendon repairs, venting of pulleys, and well-­designed combined passive and active motion protocols (Boxes  9.8  &  9.9). For many years, the author has not had rupture of the tendons after multistrand repairs in the patients performing out-­of-­splint early active motion. BOX 9.8  Methods to optimize outcomes 1. Master tendon anatomy in detail and use atraumatic techniques throughout surgery. 2. To expose the tendons, open a window in the synovial sheath, or open the A2 partially or the entire A4 pulley if the repair site overlaps or is located just distal to these structures. 3. May release the distal two-­third parts of the A2 pulley, where it is the most narrow and most constrictive to the tendons, when the FDP tendon is cut just distal or under the pulley. 4. Adopt a stronger and more secure core suture method. 5. Add peripheral sutures to smooth the repair and to prevent gap formation. 6. Properly combine passive and active finger motion into postoperative motion protocols. Fully extend and flex the finger passively, followed by active finger flexion over a certain range. Active motion over the final one-­half or one-­third is discouraged in the initial weeks to avoid tendon overload (rupture). Postoperatively, apply motion therapy for at least 5–­6 weeks. 7. Passive finger motion before active motion substantially decreases the overall resistance to digital motion, lessening the chance of repair ruptures during active motion. 8. Surgical tendon repairs are performed by experienced surgeons, and the unit should have established postsurgical rehabilitation guidelines.

BOX 9.9  What are the most important factors during surgery? 1. Two essential goals must be achieved: maintaining sufficient purchase length (> 0.7–­1.0 cm) of the core suture –­most vital for the suture’s anchor in the tendon, and maintaining tension in the sutures placed in the tendon –­critical to prevent gapping between stumps. 2. The suture’s holding –­a grasp or a lock –­in the tendon should be at least 2 mm or greater. Small grasps or locks are pulled out easily. 3. Increasing the diameter of suture from 4-­0 to 3-­0 can increase the core suture strength; but with sutures of either caliber, at least four strands are needed for any zone 1–­3 repairs. 4. Even a robust repair may fail if the tendon impinges against a pulley or is tightly constricted by narrow pulleys. Therefore, properly venting pulleys when necessary is just as important as employment of a robust repair.

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The Strickland criteria (Table 9.3) are the most commonly used methods in assessment of outcomes.15 The Moiemen and Elliot criteria (Table 9.3),20 which specifically evaluate the active range of flexion of the DIP joint, are favored by surgeons who record outcomes of zone 1 repair. The Buck-­Gramcko method is used often by German-­speaking hand societies.153 Among the less popular methods currently used are White, Tubiana, and tip-­to-­palm distance methods. The author currently uses a criterion that implements a more stringent measure of range of active finger motion into the grading system (see Table 9.3).19 Outcomes of flexor tendon repairs are affected by patient age, extent and zones of injuries, timing of the repairs, postoperative exercise, and the expertise of the surgeon. Results of tendon repairs in children are generally better than those in adults. Tendon repairs associated with extended soft-­tissue damage or accompanied by phalangeal fractures are likely to have worse outcomes.

Secondary procedures Secondary tendon repairs are achieved by free tendon grafting or staged reconstruction. These procedures are reserved for tendons that could not be repaired primarily or for lengthy tendon defects (Box  9.10). These techniques, developed by the early masters of hand surgery,38–­42,233–­243 remain largely unchanged today despite refinements in tendon junction methods, use of novel suture materials, and

Table 9.3  Criteria of assessment of functional outcomes of flexor tendon repairs

% return of motiona

Function grade

Strickland criteria (1980) 85–­100 (>150°)

Excellent

70–­84 (125–­149°)

Good

50–­69 (90–­124°)

Fair

0–­49 (62°)

Excellent

70–­84 (51–­61°)

Good

50–­69 (37–­50°)

Fair

0–­49 (30,000, and Cr >2 mg/­dL were all risk factors for death.51

Secondary procedures Clinical tips Secondary procedures • Once the infection is eradicated, secondary procedures can optimize function. • Scar contractures can be treated with Z-­plasty releases to improve joint excursion. • Flexor tenolysis may improve function after pyogenic flexor tenosynovitis but there must be: • Tissue equilibrium • Plateaued progression with hand therapy • Significantly greater passive than active range of motion of the digit • Patient compliance with hand therapy and a home exercise program. • Arthrodesis is a reasonable solution to the painful stiff joint with arthrosis after infection. • Amputation is always a consideration as a secondary procedure or immediate salvage depending on the extent of infection. • When amputating digits for infection, amputate through joints with preservation of the articular surface on the proximal bone to keep that portion of the skeleton sealed.

After eradication or control of infection, secondary procedures may be required to optimize function. Even straightforward soft-­tissue infections may leave scars that contract or limit joint excursion. For these superficial scars, we have had good success with standard Z-­ plasty scar rearrangement to restore tension-­free motion. Tenolyses of the flexor or extensor tendons may be needed following either subcutaneous abscesses, deep space infections, or flexor tenosynovitis.

Future directions

When considering tenolysis, it is important that the soft tissues have reached an equilibrium at which point recurrent transient swelling has ceased and the tissues have softened from a hardened or “woody” state common after trauma. Second, patience is warranted in allowing the patient to truly plateau with therapy before adding another surgical insult to the digit. The patient should have significantly more passive than active range of motion to expect improvement from tenolysis. One must also consider each patient’s ability to participate in appropriate therapy as the success of tenolyses is strongly dependent on the postoperative course. Arthrodeses are a more common secondary procedure after intra-­articular infections. Arthrodesis is a reasonable solution to the painful stiff joint with arthrosis after infection. The authors recommend performing arthrodeses through prior incisions if possible and taking care to raise full-­thickness flaps for exposure. For the interphalangeal joints, these flaps can raise the extensor apparatus with the skin as a single layer. In the hand and wrist, the authors have not routinely considered arthroplasty after infection. Despite being feasible after debridement and a prolonged course of antibiotics, arthroplasty is not expected to increase motion in what are usually stiff affected joints. Lastly, amputation is always a consideration as a secondary procedure or immediate salvage depending on the infection. Persistent osteomyelitis or recalcitrant soft-­tissue infections (e.g., fungal) are certainly well treated with amputation.

Access the reference list online at   Elsevier eBooks+

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Likewise, amputation for the post-­infected digit that is either persistently hypersensitive or bypassed secondary to pain and stiffness is often the best option for the hand. When amputating digits for infection, the authors prefer to amputate through joints with preservation of the articular surface on the proximal bone to keep that portion of the skeleton sealed. For ray resections after infection, the authors recommend avoiding osteotomy and transposition of an adjacent metacarpal as that necessitates internal fixation and requires healing at the transposition site.

Future directions The identification and treatment of hand infections have remained relatively unchanged since first described by Allen Kanavel in 1905. A clear understanding of hand anatomy and pathophysiology is important for early identification and effective medical and surgical management. Over the past few decades, the incidence and prevalence of MRSA infections have continued to plague appropriate antibiotic care, and further resistance to once effective alternatives is also on the rise.98 Additionally, atypical infections, such as mycobacterial, fungal, and viral infections, cause delays in diagnosis and treatment. As such, apt recognition of hand infections, and the development of effective antibiotic coverage is imperative for adequate treatment of infections.

References

References 1. Kono M, Stern PJ. The history of hand infections. Hand Clin. 1998; 14(4):511–­518. vii. 2. Gahhos FN, Ariyan S. Hippocrates, the true father of hand surgery. Surg Gynecol Obstet. 1985;160(2):178–­184. 3. Kanavel A. An anatomical and clinical study of acute phlegmons of the hand. Surg Gynecol Obstet. 1905;1:221–­259. 4. Kanavel A. Infections of the Hand. 2nd ed. Philadelphia: Lea & Febiger; 1914. 5. Flynn JE. Modern considerations of major hand infections. N Engl J Med. 1955;252(15):605–­612. 6. Pallin DJ, Egan DJ, Pelletier AJ, et al. Increased US emergency department visits for skin and soft tissue infections, and changes in antibiotic choices, during the emergence of community-­associated methicillin-­resistant Staphylococcus aureus. Ann Emerg Med. 2008;51 (3):291–­298. 7. Tosti R, Ilyas AM. Empiric antibiotics for acute infections of the hand. J Hand Surg Am. 2010;35(1):125–­128. 8. Fowler JR, Ilyas AM. Epidemiology of adult acute hand infections at an urban medical center. J Hand Surg Am. 2013;38(6):1189–­1193. 9. Houshian S, Seyedipour S, Wedderkopp N. Epidemiology of bacterial hand infections. Int J Infect Dis. 2006;10(4):315–­319. 10. Türker T, Capdarest-­Arest N, Bertoch ST, et al. Hand infections: a retrospective analysis. PeerJ. 2014;2:e513. 11. Robson MC, Heggers JP. Delayed wound closure based on bacterial counts. J Surg Oncol. 1970;2(4):379–­383. 12. Barbieri RA, Freeland AE. Osteomyelitis of the hand. Hand Clin. 1998;14(4):589–­603. ix. 13. Gunther SF, Gunther SB. Diabetic hand infections. Hand Clin. 1998; 14(4):647–­656. 14. Stern PJ, Staneck JL, McDonough JJ, Neale HW, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5 Pt 1):553–­559. 15. Pang H-­N, Teoh L-­C, Yam AKT, Lee JY-­L, Puhaindran ME, Tan AB-­H. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742–­1748. 16. McDonald LS, Bavaro MF, Hofmeister EP, Kroonen LT. Hand infections. J Hand Surg Am. 2011;36(8):1403–­1412. 17. Osterman M, Draeger R, Stern P. Acute hand infections. J Hand Surg Am. 2014;39(8):1628–­1635. quiz 1635. 18. Bach HG, Steffin B, Chhadia AM, Kovachevich R, Gonzalez MH. Community-­associated methicillin-­resistant Staphylococcus aureus hand infections in an urban setting. J Hand Surg Am. 2007;32(3): 380–­383. 19. Harrison B, Ben-­Amotz O, Sammer DM. Methicillin-­resistant Staphylococcus aureus infection in the hand. Plast Reconstr Surg. 2015;135(3):826–­830. 20. Abrams RA, Botte MJ. Hand infections: treatment recommendations for specific types. J Am Acad Orthop Surg. 1996;4(4):219–­230. 21. Covey DC, Albright JA. Clinical significance of the erythrocyte sedimentation rate in orthopaedic surgery. J Bone Joint Surg Am. 1987;69(1):148–­151. 22. Patel DB, Emmanuel NB, Stevanovic MV, et al. Hand infections: anatomy, types and spread of infection, imaging findings, and treatment options. Radiographics. 2014;34(7):1968–­1986. 23. Palestro CJ, Love C, Tronco GG, Tomas MB, Rini JN. Combined labeled leukocyte and technetium 99m sulfur colloid bone marrow imaging for diagnosing musculoskeletal infection. Radiographics. 2006;26(3):859–­870. 24. Rockwell PG. Acute and chronic paronychia. Am Fam Physician. 2001;63(6):1113–­1116. 25. Brook I. Paronychia: a mixed infection. Microbiology and management. J Hand Surg Br. 1993;18(3):358–­359. 26. Bednar MS, Lane LB. Eponychial marsupialization and nail removal for surgical treatment of chronic paronychia. J Hand Surg Am. 1991;16(2):314–­317. 27. Shafritz AB, Coppage JM. Acute and chronic paronychia of the hand. J Am Acad Orthop Surg. 2014;22(3):165–­174.

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28. McGinley KJ, Larson EL, Leyden JJ. Composition and density of microflora in the subungual space of the hand. J Clin Microbiol. 1988;26(5):950–­953. 29. Hurst LC, Gluck R, Sampson SP, Dowd A. Herpetic whitlow with bacterial abscess. J Hand Surg Am. 1991;16(2):311–­314. 30. Imahara SD, Friedrich JB. Community-­acquired methicillin-­resistant Staphylococcus aureus in surgically treated hand infections. J Hand Surg. 2010;35(1):97–­103. 31. Watson PA, Jebson PJ. The natural history of the neglected felon. Iowa Orthop J. 1996;16:164–­166. 32. Doyle JR. Anatomy of the flexor tendon sheath and pulley system: a current review. J Hand Surg Am. 1989;14(2 Pt 2):349–­351. 33. Schnall SB, Vu-­Rose T, Holtom PD, Doyle B, Stevanovic M. Tissue pressures in pyogenic flexor tenosynovitis of the finger. Compartment syndrome and its management. J Bone Joint Surg Br. 1996;78(5): 793–­795. 34. Yi A, Kennedy C, Chia B, Kennedy SA. Radiographic soft tissue thickness differentiating pyogenic flexor tenosynovitis from other finger infections. J Hand Surg Am. 2019;44(5):394–­399. 35. Schecter WP, Markison RE, Jeffrey RB, Barton RM, Laing F. Use of sonography in the early detection of suppurative flexor tenosynovitis. J Hand Surg Am. 1989;14(2 Pt 1):307–­310. 36. Yates MC, Chiasson KF, Pacheco ZS, Gullett JP, Denney BD, Pigott DC. Point-­of-­care ultrasound diagnosis of flexor tenosynovitis caused by an unusual pathogen. Oxf Med Case Reports. 2020;2020(12). omaa115. 37. Prunières G, Igeta Y, Hidalgo Díaz JJ, et al. Ultrasound for the diagnosis of pyogenic flexor tenosynovitis. Hand Surg Rehabil. 2018;S2468–­1229(18):30061–­30066. 38. Jardin E, Delord M, Aubry S, Loisel F, Obert L. Usefulness of ultrasound for the diagnosis of pyogenic flexor tenosynovitis: a prospective single-­center study of 57 cases. Hand Surg Rehabil. 2018;37(2):95–­98. 39. Frenkel Rutenberg T, Velkes S, Sidon E, et al. Conservative treatment for pyogenic flexor tenosynovitis: a single institution experience. J Plast Surg Hand Surg. 2020;54(1):14–­18. 40. DiPasquale AM, Krauss EM, Simpson A, Mckee DE, Lalonde DH. Cases of early infectious flexor tenosynovitis treated non-­surgically with antibiotics, immobilization, and elevation. Plast Surg (Oakv). 2017;25(4):272–­274. 41. Draeger RW, Bynum DK. Flexor tendon sheath infections of the hand. J Am Acad Orthop Surg. 2012;20(6):373–­382. 42. Gutowski KA, Ochoa O, Adams WP. Closed-­catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350–­354. 43. Neviaser RJ. Closed tendon sheath irrigation for pyogenic flexor tenosynovitis. J Hand Surg Am. 1978;3(5):462–­466. 44. Giladi AM, Malay S, Chung KC. A systematic review of the management of acute pyogenic flexor tenosynovitis. J Hand Surg Eur Vol. 2015;40(7):720–­728. 45. Burkhalter WE. Deep space infections. Hand Clin. 1989;5(4):553–­559. 46. Jebson PJ. Deep subfascial space infections. Hand Clin. 1998;14(4):557–­566. viii. 47. Angoules AG, Kontakis G, Drakoulakis E, Vrentzos G, Granick MS, Giannoudis PV. Necrotising fasciitis of upper and lower limb: a systematic review. Injury. 2007;38(Suppl 5):S19–­26. 48. Wong C-­H, Chang H-­C, Pasupathy S, Khin L-­W, Tan J-­L, Low C-­O. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85(8): 1454–­1460. 49. Giuliano A, Lewis F, Hadley K, Blaisdell FW. Bacteriology of necrotizing fasciitis. Am J Surg. 1977;134(1):52–­57. 50. Morgan MS. Diagnosis and management of necrotising fasciitis: a multiparametric approach. J Hosp Infect. 2010;75(4):249–­257. 51. Anaya DA, McMahon K, Nathens AB, Sullivan SR, Foy H, Bulger E. Predictors of mortality and limb loss in necrotizing soft tissue infections. Arch Surg. 2005;140(2):151–­157. discussion 158. 52. Childers BJ, Potyondy LD, Nachreiner R, et al. Necrotizing fasciitis: a fourteen-­year retrospective study of 163 consecutive patients. Am Surg. 2002;68(2):109–­116.

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SECTION III

CHAPTER 15  • Infections of the hand

53. Wong C-­H, Khin L-­W, Heng K-­S, Tan K-­C, Low C-­O. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32(7):1535–­1541. 54. Corona PS, Erimeiku F, Reverté-­Vinaixa MM, Soldado F, Amat C, Carrera L. Necrotising fasciitis of the extremities: implementation of new management technologies. Injury. 2016;47(Suppl 3): S66–­S71. 55. Fernando SM, Tran A, Cheng W, et al. Necrotizing soft tissue infection: diagnostic accuracy of physical examination, imaging, and LRINEC score: a systematic review and meta-­analysis. Ann Surg. 2019;269(1):58–­65. 56. Abdullah M, McWilliams B, Khan SU. Reliability of the Laboratory Risk Indicator in Necrotising Fasciitis (LRINEC) score. Surgeon. 2019;17(5):309–­318. 57. Hodgins N, Damkat-­Thomas L, Shamsian N, Yew P, Lewis H, Khan K. Analysis of the increasing prevalence of necrotising fasciitis referrals to a regional plastic surgery unit: a retrospective case series. J Plast Reconstr Aesthet Surg. 2015;68(3):304–­311. 58. Chauhan A, Wigton MD, Palmer BA. Necrotizing fasciitis. J Hand Surg Am. 2014;39(8):1598–­1601. quiz 1602. 59. Babiker A, Li X, Lai YL, et al. Effectiveness of adjunctive clindamycin in β-­lactam antibiotic-­treated patients with invasive β-­haemolytic streptococcal infections in US hospitals: a retrospective multicentre cohort study. Lancet Infect Dis. 2021;21(5):697–­710. 60. Andreoni F, Zürcher C, Tarnutzer A, et al. Clindamycin affects group A streptococcus virulence factors and improves clinical outcome. J Infect Dis. 2017;215(2):269–­277. 61. Shewring DJ, Trickett RW, Subramanian KN, Hnyda R. The management of clenched fist “fight bite” injuries of the hand. J Hand Surg Eur Vol. 2015;40(8):819–­824. 62. Chang C-­P, Hsiao C-­T, Lin C-­N, Fann W-­C. Risk factors for mortality in the late amputation of necrotizing fasciitis: a retrospective study. World J Emerg Surg. 2018:13. 63. Khamnuan P, Chongruksut W, Jearwattanakanok K, Patumanond J, Tantraworasin A. Necrotizing fasciitis: epidemiology and clinical predictors for amputation. Int J Gen Med. 2015;8:195–­202. 64. Ravindran V, Logan I, Bourke BE. Medical vs surgical treatment for the native joint in septic arthritis: a 6-­year, single UK academic centre experience. Rheumatology (Oxford). 2009;48(10):1320–­1322. 65. Piper D, Smith G, Archer JE, Woffenden H, Bose D. Management of native joint septic arthritis, serial aspiration vs. arthroscopic washout during the COVID-­19 pandemic. Cureus. 2020;12(11): e11391. 66. Sammer DM, Shin AY. Comparison of arthroscopic and open treatment of septic arthritis of the wrist. J Bone Joint Surg Am. 2009;91(6):1387–­1393. 67. Sinha M, Jain S, Woods DA. Septic arthritis of the small joints of the hand. J Hand Surg Br. 2006;31(6):665–­672. 68. Wittels NP, Donley JM, Burkhalter WE. A functional treatment method for interphalangeal pyogenic arthritis. J Hand Surg Am. 1984;9(6):894–­898. 69. Boustred AM, Singer M, Hudson DA, Bolitho GE. Septic arthritis of the metacarpophalangeal and interphalangeal joints of the hand. Ann Plast Surg. 1999;42(6):623–­628. discussion 628-­629. 70. Giuffre JL, Jacobson NA, Rizzo M, Shin AY. Pyarthrosis of the small joints of the hand resulting in arthrodesis or amputation. J Hand Surg Am. 2011;36(8):1273–­1281. 71. Waldvogel FA, Papageorgiou PS. Osteomyelitis: the past decade. N Engl J Med. 1980;303(7):360–­370. 72. Gold RH, Hawkins RA, Katz RD. Bacterial osteomyelitis: findings on plain radiography, CT, MR, and scintigraphy. AJR Am J Roentgenol. 1991;157(2):365–­370. 73. Klifto CS, Gandi SD, Sapienza A. Bone graft options in upper-­ extremity surgery. J Hand Surg Am. 2018;43(8):755–­761. 74. Tabib W, Haddad H. Management of second metacarpal chronic osteomyelitis by induced membrane technique. Case Reports Plast Surg Hand Surg. 2018;5(1):49–­53.

75. Hara A, Yokoyama M, Ichihara S, Kudo T, Maruyama Y. Masquelet technique for the treatment of acute osteomyelitis of the PIP joint caused by clenched-­fist human bite injury: a case report. Int J Surg Case Rep. 2018;51:282–­287. 76. Pruzansky ME, Lee Y, Pruzansky J. Masquelet technique for phalangeal reconstruction and osteomyelitis. Tech Hand Up Extrem Surg. 2020;25(1):52–­55. 77. Rossello C, Antonini A, Zoccolan A, Burastero G, Rossello MI. Reconstructive surgery for thumb osteomyelitis: a new way of remodelling the vascularized medial femoral condyle flap. A case report. Handchir Mikrochir Plast Chir. 2019;51(6):440–­443. 78. Scaglioni MF, Chang EI, Gur E, et al. The role of the fibula head flap for joint reconstruction after osteoarticular resections. J Plast Reconstr Aesthet Surg. 2014;67(5):617–­623. 79. Elhassan BT, Wynn SW, Gonzalez MH. Atypical infections of the hand. J Am Soc Surg Hand. 2004;4(1):42–­49. 80. Hurst LC, Amadio PC, Badalamente MA, Ellstein JL, Dattwyler RJ. Mycobacterium marinum infections of the hand. J Hand Surg. 1987; 12(3):428–­435. 81. Flondell M, Ornstein K, Björkman A. Invasive Mycobacterium marinum infection of the hand. J Plast Surg Hand Surg. 2013;47(6):532–­534. 82. Reis FJJ, Cunha AJLA, Gosling AP, Fontana AP, Gomes MK. Quality of life and its domains in leprosy patients after neurolysis: a study using WHOQOL-­BREF. Lepr Rev. 2013;84(2):119–­123. 83. Al-­Qattan MM, Al-­Namla A, Al-­Thunayan A, Al-­Omawi M. Tuberculosis of the hand. J Hand Surg Am. 2011;36(8):1413–­1421. quiz 1422. 84. Chan E, Bagg M. Atypical hand infections. Orthop Clin North Am. 2017;48(2):229–­240. 85. Ely JW, Rosenfeld S, Seabury Stone M. Diagnosis and management of tinea infections. Am Fam Physician. 2014;90(10):702–­710. 86. Coleman NW, Fleckman P, Huang JI. Fungal Nail Infections. J Hand Surg. 2014;39(5):985–­988. 87. Jones NF, Conklin WT, Albo VC. Primary invasive aspergillosis of the hand. J Hand Surg. 1986;11(3):425–­428. 88. Olorunnipa O, Zhang AY, Curtin CM. Invasive aspergillosis of the hand caused by Aspergillus ustus: a case report. Hand (N Y). 2010; 5(1):102–­105. 89. Epstein MD, Segalman KA, Mulholland JH, Orbegoso CM. Successful treatment of primary cutaneous Aspergillus flavus infection of the hand with oral itraconazole. J Hand Surg Am. 1996;21(6):1106–­1108. 90. Banerjee S, Dooley TP, Gilroy S, Parkinson JR. Blastomycotic osteomyelitis: an unusual cause of hand swelling. J Hand Surg. 2017;42(11). 932.e1-­932.e6. 91. Vitale MA, Roden AC, Rizzo M. Tenosynovitis of the wrist and thumb and carpal tunnel syndrome caused by Histoplasma capsulatum: case report and review of the literature. Hand (N Y). 2015;10(1):54–­59. 92. Liang KV, Ryu JH, Matteson EL. Histoplasmosis with tenosynovitis of the hand and hypercalcemia mimicking sarcoidosis. J Clin Rheumatol. 2004;10(3):138–­142. 93. Al-­Qattan MM, Al Mazrou AM. Mucormycosis of the upper limb. J Hand Surg. 1996;21(2):261–­262. 94. Moran SL, Strickland J, Shin AY. Upper-­extremity mucormycosis infections in immunocompetent patients. J Hand Surg Am. 2006; 31(7):1201–­1205. 95. Lineberry KD, Boettcher AK, Blount AL, Burgess SD. Cutaneous mucormycosis of the upper extremity in an immunocompetent host: case report. J Hand Surg Am. 2012;37(4):787–­791. 96. Witthaut J, Steffens K, Koob E. Reliable treatment of pyogenic granuloma of the hand. J Hand Surg Br. 1994;19(6):791–­793. 97. Elliott DC, Kufera JA, Myers RA. Necrotizing soft tissue infections. Risk factors for mortality and strategies for management. Ann Surg. 1996;224(5):672–­683. 98. Kistler JM, Thoder JJ, Ilyas AM. MRSA incidence and antibiotic trends in urban hand infections: a 10-­year longitudinal study. Hand (N Y). 2019;14(4):449–­454.

SECTION III  •  Specific Disorders

16 Tumors of the hand Kashyap K. Tadisina, Justin M. Sacks, and Mitchell A. Pet

SYNOPSIS

ƒ Benign and malignant tumors of the hand arise from distinct tissue types. ƒ The majority of these tumors are benign. ƒ Accurate assessment, diagnosis, and treatment will optimize clinical outcomes. ƒ Reconstructive procedures of the hand and upper extremity should be performed only after the diagnosis is confirmed and appropriate surgical margins are achieved.

  Surgical

incisions must be planned carefully with definitive surgery in mind, utilizing a longitudinal incision in line with or parallel to a potential limb salvage procedure.   Reconstructive procedures, in the setting of a neoplasm of the hand, are performed only after the final pathological diagnosis and clear resection margins are established.   An understanding of both oncologic and reconstructive principles is required in order to achieve an optimal clinical outcome. Clinical tips

Introduction   Most

tumors of the hand are benign, recognized early, and treated by excision.   Ninety-five percent of hand tumors that do not involve the skin are benign.   Malignant tumors of the hand can be divided into two categories: primary and metastatic. Primary tumors can arise from the skin (e.g., melanoma, basal, and squamous cell carcinoma), soft tissues (e.g., sarcoma), or bone (e.g., osteosarcoma). Metastatic disease originates most commonly from cancers of the breast, kidney, thyroid, lung, and colon.   Appropriate evaluation, diagnosis, and treatment for tumors of the hand are required for optimal patient care. A careful history and physical examination will rapidly focus the investigation of a suspicious mass found in the hand.   Magnetic resonance imaging (MRI) has become the “gold standard” to evaluate soft-tissue masses for malignancy. Computed tomography (CT) is preferred for osseous lesions.   Incisional or excisional biopsy is required for definitive diagnosis in many cases.

Most hand tumors: • arise from any cell type • are benign • are treated with a favorable prognosis. When in doubt: • perform excisional biopsy • plan incisions carefully • keep definitive surgery in mind.

Basic science/disease process Tumors of the hand can arise from the skin, adipose tissue, synovium, tendons, cartilage, bones, muscles, fibrous tissue, nerves, and blood vessels. The majority of hand tumors are benign, most are recognized early, and the prognosis is typically good.1,2 Malignant tumors can rarely occur in the hand and can be divided into two categories: primary and metastatic. Additionally, premalignant lesions such as actinic keratoses and atypical nevi can occur on the hand. In this chapter, benign and malignant tumors are classified and discussed by their tissues of origin. Understanding the origin of hand lesions will assist in accurate diagnosis and appropriate therapeutic interventions.3

Diagnosis/patient presentation

The management of hand tumors requires the hand surgeon to function as both oncologic surgeon and reconstructive surgeon. A complete understanding of both oncologic and reconstructive principles is therefore required to achieve an optimal outcome. The role of the oncologic surgeon is to eradicate the tumor completely, which can compromise both aesthetics and function. In contrast, the role of the reconstructive surgeon is to optimize hand function. Balancing these sometimes competing goals can be challenging.4 In management of particularly complex or atypical cases, the authors advocate multidisciplinary team care which should necessarily include surgical and/or musculoskeletal oncologic colleages. An effective strategy to evaluate, diagnose, and treat tumors of the hand and associated upper extremity is required for optimal patient care. A systematic approach with a high index of suspicion for complex disease is warranted. A proposed algorithm is presented here: 1. Have a diagnostic tree when evaluating any mass. 2. Recognize aggressive features. 3. Image thoughtfully, typically with radiographs, CT, and/or MRI.5 4. Perform a biopsy which avoids tumor spillage and facilitates limb preservation. 5. Involve multidisciplinary team members when necessary. 6. Perform oncologically sound extirpative surgery. 7. Reconstruct form and function.

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commonly from breast, kidney, thyroid, lung, and colon cancers. The patient should also be questioned about rheumatologic conditions, such as gout, psoriasis, and rheumatoid arthritis. The age of the patient should be considered when evaluating a mass in the hand. Certain masses are specific to certain age groups. For instance, bone cysts are typically seen in adolescents and young adults, whereas metastatic tumors in the hand are rare under the age of 50 years.7 Conversly, if a “typical” mass is present at an “atypical” age, clinical suspicion should be high for a more serious disease process. Questions about previous biopsies or excisions will complete a thorough historical evaluation of the patient with a hand tumor. Pathology specimen slides and reports for previous biopsies or excisions will need to be obtained and reviewed. Prior operative reports will help clarify the diagnosis and optimize future surgical interventions in instances in which the current pathology is unknown. Clinical clues History • • • • •

Rheumatoid arthritis – rheumatoid nodule Gout – tophus Severe and unrelenting pain - suggestive of malignancy Cold sensitivity: subungual lesion – glomus tumor Pain relieved by nonsteroidal anti-inflammatory drugs (NSAIDs) – osteoid osteoma • Trauma – epidermal inclusion cyst or atypical infection

Diagnosis/patient presentation Patient history

Physical examination

Patients often present with a preliminary diagnosis of “ganglion cyst” or “bone spur” from referring physicians. It is imperative to disregard assumed diagnoses and perform a complete evaluation. While most hand masses are benign, one cannot overstate the importance of recognizing malignancies and other unusual cases early in the course of treatment and evaluation. Patients frequently present in a delayed fashion, particularly with malignancies, as they may have been asymptomatic, misdiagnosed, or experienced some element of denial/neglect. A thorough history and physical examination remain the foundation of proper initial diagnosis. Questions concerning the history of the tumor are solicited. These include duration, changes in size or color, associated pain, and occurrence of ulceration. Pain can signify a malignancy or a mass that has encroached upon neurologic structures. The sensitivity of the mass to cold or heat needs to be clarified, as the former typifies a glomus tumor.6 Inquiring about risk factors for tumors of the hand will inform the differential diagnosis. The patient should be questioned about a history of cutaneous malignancies, extensive sun exposure or sunburns as a child, chemical and ionizing radiation exposure, and trauma or infections. Screening for non-cutaneous malignancies must also be performed, as metastatic disease can present in the upper extremity, most

The physical examination of the hand involves a complete examination of the skin, tendons, muscles, ligaments, bones, and neurovascular structures. An evaluation of the regional lymph nodes for adenopathy is important for assessing the malignant potential of a hand mass.8,9 Color and texture changes are noted, and an examination for ulceration, erythema, and edema is performed. Transillumination of the mass can be helpful in distinguishing between solid and cystic etiologies. The lesion is palpated, and the mass size is appreciated along with its shape. The mobility of the mass is assessed to determine whether it is fixed to underlying anatomic structures, and mobility may differ depending on the direction of displacement. Having the patient flex and extend the fingers and wrist will further delineate whether the lesion is associated with tendons or deeper structures within the joints. A complete vascular examination with palpation of pulses is required. If pulses are not palpable, an Allen’s test using a Doppler can be used to define the vascular status of the hand and upper extremity. Neurologic testing of fine and gross motor and sensory function is also performed. When benign lesions are to be followed clinically, photographic documentation is an essential tool to judge the rate of growth over time. Measuements and photographs are also recommended for patients with multiple and subtle lesions.

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SECTION III

CHAPTER 16  • Tumors of the hand

Laboratory studies Laboratory studies are helpful in determining the etiology of some hand tumors. Workup should be targeted based upon a differential diagnosis developed after examination. Labs can often help differentiate infectious from non-infectious etiologies. As a basic principle, even in the case of normal labs, presumed neoplasms without a clear diagnosis shoud be cultured, and those presumed infectious should undergo pathologic examination. Elevated white blood cell (WBC) count and inflammatory markers can support an infectious etiology, but it should be noted that not all infectious processes of the hand will generate a substantial leukocytosis. Normal inflammatory labs do not rule out processes such as osteomyelitis. Serum calcium, phosphorus, and alkaline phosphatase levels are often increased in patients with metastatic tumors, and alkaline phosphatase is also increased in patients with osteosarcoma. An erythrocyte sedimentation rate assesses for inflammation; the rate is often increased in Ewing’s sarcoma, lymphoma, and myeloma. In male patients older than 50 years with blastic hand lesions on radiography, a serum prostate-specific antigen (PSA) test should be performed to investigate the possibility of metastatic prostate cancer. Clinical tips Laboratory tests • • • • •

Increased ESR: Ewing’s sarcoma, lymphoma, myeloma Increased Ca++: metastatic tumors Increased alkaline phosphatase: osteosarcoma Males, age >50, and blastic bone lesions: check PSA Increased WBC: Indicates infection, but infectious etiologies are not ruled out in the absence of elevated WBC

Imaging Multiple radiologic modalities are available for imaging benign and malignant hand lesions and masses. Radiographs are not essential for most skin lesions. However, radiographs are required for very large skin lesions when there is clinical suspicons of possible bony erosion/invasion. The architecture of the mass as it relates to the cortex of the associated bone can be determined rapidly by X-ray. Sharp cortical margins usually indicate a benign process, while a “moth-eaten” or destroyed cortex often indicates a malignant process. Erosions and periosteal elevation on X-rays can signify a potential malignancy or an infectious process. Soft-tissue calcifications may signify a malignancy (Fig. 16.1). Ultrasonography can be helpful in assessing soft-tissue masses. This technique is noninvasive and inexpensive. Ultrasonography can determine if a tumor is solid or cystic and differentiate between a discrete mass and diffuse edema. In many instances, ultrasonography can be used to guide needle biopsy. This is particularly useful in the pedatric population to limit radiation exposure and the need for sedation, which is often needed to facilitate cross-sectional imaging in this population.

Figure 16.1  In this proximal phalanx lesion of the thumb a destroyed cortex potentially indicates a malignant process.

Scintigraphy or bone scanning is beneficial in screening for skeletal masses. This technique is sensitive in isolating abnormalities, but the findings are not very specific for malignancy. For example, there is intense uptake with osteoid osteoma, a benign bone tumor. Bone scans are very helpful when searching for sources of metastasis in the workup of hand and upper extremity primary malignancies. With the emergence of routine cross-sectional imaging techniques, this modality is becoming less commonly used for diagnosis. CT is extremely useful for the assessment of bones and cortical destruction. CT scans have markedly greater bony resolution than standard radiographs. If bone involvement by the mass is equivocal on X-ray, CT is the next appropriate radiographic modality. CT also distinguishes calcification patterns from ossification and is superior in assessing periosteal versus endosteal reactions. MRI is superior to CT for the evaluation of soft-tissue masses. It has become the gold standard to evaluate soft-tissue masses for malignancy.10 The MRI study should include T1-weighted, fat-suppressed T2-weighted, and short tau inversion recovery (STIR) images. The contrast agent gadolinium can further enhance the visualization of soft-tissue tumors. An MRI study obtained with various views can clearly delineate the extent of soft-tissue involvement prior to operative intervention. A drawback of MRI is that it cannot reliably distinguish between benign and malignant processes. In addition, for MRI of hand masses, a dedicated hand coil is required.

Biopsy Based upon the clinical, imaging, and lab workup, the surgeon will work with the patient to choose a course of

Diagnosis/patient presentation

watchful waiting versus need for biopsy. The goal of biopsy is to obtain an accurate sample of tissue, facilitate treatment of the tumor if needed, without compromising definitive treatment. While no evidence-based guidelines exist for exactly which masses require biopsy, a general rule of thumb is to biopsy any mass that is symptomatic or growing.11,12 Various methods of obtaining biopsies exist, including punch biopsy, core needle (interventional radiology assisted), open incisional, or open excisional. Each biopsy option has its advantages and disadvantages. Proper technique impacts the quality of results. When navigating through methods of biopsy, there are important principles to keep in mind. Masses should be characterized as well-defined or ill-defined based on clinical history, exam, and imaging results.12 Simple masses localized to the skin only can be sampled with a punch biopsy. Masses that are smaller (3 cm), proximal to the metacarpophalangeal joint, progressive in size, painful, illdefined, in an atypical location, or with overlying skin changes are amenable to core needle biopsy or open incisional biopsy.12 Particularly difficult masses or those with high suspicion for malignancy may benefit from multidisciplinary consultation with a musculoskeletal radiologist and interventional radiol­ ogist to assist in biopsy.13,14 Punch biopsy is performed with a hollow circular-shaped sharp instrument that allows en bloc resection to the desired depth of tissue based on pressure. The mass can then be harvested directly from the biopsy device and sent for pathologic examination. In a closed or core needle biopsy, a needle or trephine is used to obtain samples. Core needle biopsy is typically indicated for masses in difficult locations (intra-osseous lesions, deeper tissues). This technique is favored due to its high accuracy, low likelihood of misdiagnosis, low cost, and minimally invasive nature.15 These biopsies must be coordinated with a musculokeletal/interventional radiologist to optimize results (Figs. 16.2 & 16.3).

While useful in metastatic workup, tissue samples from closed biopsy are sometimes inadequate for initial diagnosis in cases where the tumor is heterogeneous, or the pathology is unclear.16 Open biopsies should be performed by hand surgeons who are familiar with the principles of musculoskeletal oncology and target anatomy. Longitudinal incisions should be in line with or parallel to incisions that would be used in a later limb salvage procedure if the tumor proves to be malignant. If a tourniquet is used, the upper extremity must not be exsanguinated because doing so may cause spread of malignant cells into the lymphatics. Meticulous hemostasis should be maintained, and adjacent anatomic compartments should not be violated. An important tenet is to biopsy all infections and culture all masses.3,17 Chronic infections can masquerade as malignancies, and masses can result from subclinical infections. Open excisional biopsies are performed by making an incision directly over the mass of interest, dissecting the mass from surrounding soft tissues and removing it. It is important to note that adjacent tissue is not removed and cells from the mass may remain within the excision site. If the mass proves to be benign, this excisional biopsy is the definitive procedure. If a malignancy is identified in this way, resection with margins is usually indicated. Open incisional biopsies are done as a precursor to formal resection of masses, with the goal of identifying origin of masses prior to further definitive surgical planning without contaminating tissue planes. Through a longitudinal incision and abiding by the above-mentioned principles, a piece of the mass of interest is removed for pathologic examination. This technique may also be employed after an indeterminate or inconclusive closed needle biopsy. Once a biopsy has been obtained, the type of specimen sent must be carefully selected, as the accuracy of pathologic assessment is dependent on the type of specimen obtained. A frozen-section analysis can be performed to assess the adequacy of the tissue sample. However, the accuracy of frozen-section diagnosis is only 80%, whereas permanent-section diagnosis is 96% accurate.

Figure 16.3 Anteroposterior view of fluoroscopic-assisted fourth metacarpal biopsy for suspected osteomyelitis.  

Figure 16.2 CT-guided bone biopsy of giant cell tumor of the distal radius.  

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CHAPTER 16  • Tumors of the hand

Clinical tips Types of biopsy • Punch • Core needle (assisted by interventional radiologist): difficult location, deeper • Incisional biopsy: larger (>3 cm), proximal to metacarpophalangeal joint • Excisional biopsy: small (1–2 mm thick, a 1–2-cm margin is used; for lesions >2 mm thick, a 2-cm margin is used. The risk of metastasis is 5–12% for thin (65 years) with significant sun exposure history. Malignant transformation is associated with Merkel cell polyomavirus in a large majority of cases. Current guidelines are based on relatively low levels of evidence with an evolving body of literature. Current standards of treatment include a clinical nodal exam and local excision with 1–2-cm margins and SLNB at time of resection for clinically node-negative disease. SLNB-negative disease can be treated with post-resection radiation therapy for locoregional control, although survival benefit of this has not been well established. SLNBpositive disease is treated with completion lymph node dissection and adjuvant radiation, chemotherapy, and/or immunotherapy. Given the complexity and aggressive nature of this disease, a multidisciplinary team approach is advocated by most expert43, 44

Figure 16.24  Volar wrist ganglion cyst. The cyst is a mucinous-filled structure associated with joint capsules, tendons, and tendon sheaths. The etiology of these cystic structures is presumed to be secondary to synovial herniation and trauma.

Synovial lesions Ganglion cysts Ganglion cysts are the most common soft-tissue tumors of the hand and upper extremity (Figs. 16.24 & 16.25). Ganglion cysts are mucin-filled structures associated with joint capsules, tendons, or tendon sheaths. The etiology of these cystic structures is presumed to be secondary to synovial herniation and trauma.45 In the hand, ganglion cysts typically occur in the dorsal carpal region (60–70%) and originate from the scapholunate interosseous ligament. The volar carpal region is the next most commonly involved region, with 20% of ganglion cysts originating from the scapho-trapezio-trapezoid ligament. Ganglion cysts are also found on the volar retinaculum (10– 20%). Ganglion cysts found on the dorsal proximal interphalangeal joint associated with osteoarthritis are termed mucous cysts (Fig. 16.26 & 16.27). These are treated by excision of the cyst along with associated osteophytes. If atypical presentations occur or if clinical examination does not clarify a potential ganglion cyst, then ultrasonography or MRI can be helpful in determining a diagnosis.

A

B

Figure 16.25  (A,B) Dorsal wrist ganglion cyst.

Treatment/surgical treatment by tissue of origin

A key point in the treatment of ganglion cysts is to clarify their benign nature for the patient. Patients often seek reassurance when confronted with this lesion. The natural course of volar retinaculum ganglion lesions is spontaneous resolution

369

in almost two-thirds of patients. Aspiration of these masses results in complete resolution in the same proportion of patients. Aspiration of volar and dorsal ganglions in other locations with fenestration techniques has improved results. However, recurrence is still observed.45 The definitive management is surgical excision. For larger ganglions in the volar and dorsal regions of the hand, removal of the ganglion with its stalk and a portion of the cuff of the joint capsule is required. The capsule is not repaired so as not to limit motion. Arthroscopic removal of ganglion cysts in the dorsal region of the wrist is currently being performed. Success rates have been favorable, although long-term follow-up data are currently lacking.

Giant cell tumor (pigmented villonodular synovitis)

Figure 16.26  Mucous cyst of the dorsal middle finger. Ganglions found on the dorsal proximal interphalangeal joint associated with osteoarthritis are termed mucous cysts. Excision of the cyst along with excision of osteophytes must be performed to treat this clinical entity completely.

Figure 16.27  Mucous cyst of the dorsal middle finger treated with excisional biopsy and reconstruction with a bilobed flap.

Giant cell tumors are the second most common soft-tissue masses in the hand (Figs. 16.28 & 16.29). A giant cell tumor is a benign tumor containing multinucleated giant cells and xanthoma cells. Giant cell tumors are found in synovial fluidproducing sites such as joints, capsular ligaments, and tendon sheaths.46,47 They are slow-growing and can have a mass effect on adjacent structures, at times indenting cortical bone. They are firm, nodular, and non-tender. Most commonly, they are found over the volar aspect of the hand. The treatment for this tumor is careful, complete excision. When dissecting these tumors out of the hand, the surgeon must be aware of nerve displacement. The main problem with these masses is the potential for recurrence; the recurrence rate has been reported to be 5–50%. A malignant form of this tumor has been described, but is extremely rare.

Figure 16.28  Preoperative photograph of giant cell tumor of the tendon sheath (pigmented villonodular synovitis). A benign tumor containing multinucleated giant cells and xanthoma cells found in synovial fluid-producing sites such as joints, capsular ligaments, and tendon sheaths.

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CHAPTER 16  • Tumors of the hand

A

B

Figure 16.29  Intraoperative photograph (A) and post resection specimen (B) of giant cell tumor of the tendon sheath.

Nerve tumors

Lipofibromatous hamartoma

Schwannoma/neurilemoma

Lipofibromatous hamartoma represents a fibrofatty infiltration of the nerves (Fig. 16.33). This tumor is most commonly found in the median nerve. In a child who presents with carpal tunnel syndrome, lipofibromatous hamartoma should be considered part of the differential diagnosis.49 Exploration of the mass reveals fusiform swelling of the nerve without invasion into perineural tissue. Interfascicular resection is not possible, and in fact, is contraindicated for the treatment of this lesion. Instead, simple decompression is recommended. Gradual deterioration of nerve function can occur; only then should resection and nerve grafting be considered.

Schwannomas, the most common benign nerve tumors of the hand, arise from Schwann cells (Figs. 16.30 & 16.31). The presentation of schwannoma is one of a slow-growing, well-circumscribed, eccentric, and essentially painless mass.48 However, there may be a neurologic deficit or pain if the lesion is in the distribution of motor or sensory nerves. Schwannomas are mobile transversely, not longitudinally. They are typically found on the volar surface of the hand and forearm in the fourth to sixth decades of life. The treatment for schwannoma is to “shell it out” from surrounding intact nerve fascicles, under magnification. The risk of a postoperative neurologic deficit is 4%. There are very rare reports of malignant transformation.

Neurofibroma Neurofibromas are benign, slow-growing tumors arising within nerve fascicles (Fig. 16.32). The lesions appear histologically as diffuse growths of Schwann cells, fibrous tissue, and axons. When groups of these lesions are encountered, von Recklinghausen’s disease or neurofibromatosis should be considered as a diagnosis. The treatment for neurofibromas is excision; however, this is likely to require segmental nerve resection with or without nerve grafting based on the anatomy of the tumor in that normal nerve fascicles are incorporated into the tumor. Malignant transformation of neurofibroma is possible, and rapid enlargement may indicate malignant transformation.2 In patients with neurofibromatosis, malignant degeneration into malignant peripheral nerve sheath tumors can occur.

Fat tumor: lipoma A lipoma is a benign tumor composed of adipose tissue (Figs. 16.34 & 16.35). Lipomas can be located subcutaneously or intramuscularly. If present in the carpal tunnel or Guyon’s canal, lipomas can lead to nerve compression. Lipomas typically have a longstanding history with very slow growth. Physical examination and history will invariably lead to the diagnosis. If imaging is warranted, X-rays will reveal lucent soft-tissue shadows, and MRI will show a signal intensity consistent with adipose tissue. The treatment of lipoma is simple excisional biopsy consisting of a marginal resection. The well-defined margins of the tumor make excision technically straightforward. The primary indication for excision is size increase and mass effect (nerve compression). The malignant form of this mass, liposarcoma, has rarely been reported in the hand.

Treatment/surgical treatment by tissue of origin

A

371

B

Figure 16.30  Large Schwannoma found incidentally during vascular access placement. Also called neurilemmoma. This soft-tissue mass arises from Schwann cells and is typically found on the volar surface of the hand and forearm.

A

B

Figure 16.31  Post excision specimen of large Schwannoma (A) and intact nerves after resection (B).

Fibrous tissue lesions Benign lesions The majority of the lesions of fibrous tissue found in the hand are benign. These include simple scars, hypertrophic

scars, and keloid tissue. Hypertrophic scars are confined within the original wound margins, whereas keloids grow beyond these margins. Both exhibit increased cellularity and vascularity. Other benign fibrous tumors found in the hand include juvenile aponeurotic fibroma, desmoid tumors, fibrous histiocytoma, and Dupuytren’s nodules.

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CHAPTER 16  • Tumors of the hand

Figure 16.32  Neurofibroma, a benign slow-growing tumor arising within nerve fascicles. When encountered in groups, von Recklinghausen’s disease or neurofibromatosis should be considered as a diagnosis.

Synovial sarcoma is among the more common sarcomas in the hand and wrist. This malignant soft-tissue tumor occurs near tendons and joints and may invade bone. Its most common presentation in the upper extremity is that of a firm, indolent, painless mass on the dorsum of the hand.8 It typically presents in young adults to middle-aged patients. Synovial sarcoma is a very aggressive tumor. Treatment is wide or radical surgical excision. Nodal status must be evaluated because of the high rates (50%) of metastasis from this mass. Adjuvant radiotherapy or chemotherapy is recommended. Epithelioid sarcoma is the most common malignant softtissue tumor of the upper extremity (Fig. 16.37). It most commonly appears on the hand and forearm in adolescents and young adults as a firm, slow-growing mass.8 Epithelioid sarcoma can affect the digits and palm with proximal spread along tendon sheaths. Favorable prognosis has been associated with more distal location of sarcoma (i.e., fingertip).51 It can be misdiagnosed as a wart or an ulcer. Treatment of epithelioid sarcoma is wide or radical excision. Nodal status needs to be evaluated as metastasis is typically to regional lymph nodes. While amputation used to be commonplace for treatment of upper extremity sarcomas, recently there has been shift toward limb preservation, as long-term data has not shown a clear advantage to radical resection.52 This has been facilitated by tremendous advances in the multidisciplinary management of sarcoma. These include neoadjuvant chemotherapy and radiotherapy which can be used to reduce tumor size thus enabling neurovascular-sparing resections that preserve limb function. Complex free flap reconstructions are now routinely being performed to preserve limbs that, due to locally advanced disease, would have been previously amputated.

Vascular lesions Hemangioma

Figure 16.33  Lipofibromatous hamartoma. This mass is a fibrofatty infiltration of the nerves, most commonly found in the median nerve. In a child who presents with carpal tunnel syndrome, this should be considered part of the differential diagnosis.

Sarcomas Malignant fibrous histiocytoma is the most common soft-tissue sarcoma in adults (Fig. 16.36).49,50 It develops in the sixth to eighth decades of life. This tumor presents as a painless enlarging mass that is most common in the forearm. Treatment is wide excision or amputation. Neoadjuvant therapy can be administered to reduce tumor bulk and avoid amputation of the limb. A metastatic workup is required, with the most common site of metastasis being the lungs.

Hemangiomas are benign capillary malformations. They can present as superficial, cutaneous lesions; as deep, cavernous lesions; or as a mixture of the two forms (Fig. 16.38). Hemangiomas typically are not present at birth but appear in the first month of life. They are characterized by a rapid growth phase during the first year. The rate of involution is 50% by 5 years of age and 70% by 7 years of age.53 Treatment is typically observation, as most will involute. However, propranolol, laser therapy, systemic steroids, intralesional steroids, and interferon have all been shown to have beneficial effects. When hemangiomas become symptomatic in adults, they require a marginal resection. Even after resection, these lesions can recur. Infantile hemangiomas can be associated with Kasabach– Merritt syndrome (Fig. 16.39). This aggressive hemangioendothelioma leads to a consumptive coagulopathy secondary to platelet trapping. High-dose steroids and vincristine have been used to treat this syndrome.54 Maffucci syndrome is a condition characterized by multiple hemangiomas and enchondromas.55 The digits in patients with this condition are short and angulated. There is a risk of malignant transformation of the enchondromas and hemangiomas into chondrosarcomas and angiosarcomas.

Treatment/surgical treatment by tissue of origin

A

373

B

Figure 16.34  Intraoperative photograph of a large lipoma of the palm. This lesion is a benign tumor composed of adipose tissue. Commonly they are located subcutaneously or intramuscularly in the upper extremity.

(Fig.  16.40). These are considered “low-flow” tumors. Treatment is generally limited to lesions that are painful, or symptomatic from a functional or aesthetic standpoint, and may include observation, anticoagulation, laser therapy, sclerosing agents, or excision.56 Large and/or complex vascular malformations should be managed in the context of a multidisciplinary team which may include dermatology, plastic surgery, diagnostic/interventional radiology, genetics, and hematology/ocology. “High-flow” vascular malformations have arterial or arteriovenous components. These masses have a high potential for rapid expansion. Treatment of these tumors involves preoperative embolization followed by excision.

Glomus tumor

Figure 16.35  Post-resection intraoperative photograph of a large lipoma of the palm.

Vascular malformations Vascular malformations are typically present at birth, in contrast to hemangiomas, and represent malformed vascular channels. Malformations are described as capillary, venous, lymphatic, or mixed venous–lymphatic malformations

A glomus tumor is a benign tumor of the neuromyoarterial apparatus, which is responsible for controlling circulation to the skin. Glomus tumors frequently present subungually (Fig. 16.41). The classic triad of symptoms is cold hypersensitivity, intermittent severe pain, and point tenderness. 6,57 Diagnostic workup for a suspected glomus tumor should include radiography and MRI. Radiographs reveal a “scalloped” osteolytic defect. MRI will commonly reveal a high-signal-intensity lesion. Excisional biopsy is usually curative.

Pyogenic granuloma Pyogenic granuloma is a progressively growing vascular lesion (Fig. 16.42). Pyogenic granulomas of the hands are commonly found

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SECTION III

A

CHAPTER 16  • Tumors of the hand

C

B

D

E

Figure 16.36  Malignant fibrous histiocytoma. This sarcoma presents as a painless enlarging mass commonly found on the upper extremity. Treatment for this tumor is wide excision with mandatory metastatic evaluation. (A) Dorsal hand lesion. (B) Specimen revealing composite resection involving extensor tendons. (C) Wide local excision with proximal and distal extensor tendons tagged for reconstruction. (D) Dorsalis pedis flap elevation, including dorsal foot extensors. (E) Postoperative flap.

on the fingers. The lesion begins as a solitary “red” nodule and progresses to a chronically inflamed vascular lesion. The exact etiology is unknown.56 Current beliefs are that the lesion begins with trauma followed by a subsequent subclinical infection and poor re-epithelialization. Treatment modalities range from excision with 1-mm margins, to curettage, to topical silver nitrate.

Muscle lesions Myositis ossificans In myositis ossificans, benign ossification occurs in muscles and other soft tissues (Fig. 16.43). The etiology can be traumatic. In the upper extremity, the deltoid and brachialis muscles are involved most frequently. Over time, the volume of heterotopic bone will diminish.

Osteoid osteoma Osteoid osteoma represents a benign bone-forming lesion typically affecting the distal radius, carpus, and phalanges (Fig. 16.44). These bone tumors rarely form in the hand (50%)

Pain management

Big issue

Little problem

Orthopedic Surgery and Traumatology, they concluded that surgical repair of brachial plexus lesions could not guarantee effective and predictable results.2 The advances of microsurgical repair brought forth the concept of nerve grafting to bridge two ruptured stumps of a completely disrupted nerve with minimal tension. The traditional perspective was attempting primary repair of nerve gaps through mobilization of the nerve ends and keeping joints flexed, sometimes even beyond the “critical resection length”, to avoid rupturing. Such tension would risk rupturing at the nerve coaptation site. It was then that autologous nerve grafting between two nerve stumps was introduced, and Hanno Millesi would improve the functional outcomes by applying microsurgical techniques.3–5 His contributions included (1) differentiating normal and pathological tissue under microscope, (2) minimizing inadvertent manipulation to healthy fascicles; and (3) using multiple cable grafting instead of one large diameter nerve graft to improve perfusion. This contribution would greatly influence the principles of peripheral nerve reconstruction and serve as the principle for connecting ruptured roots to target nerves. Applications of nerve grafting in brachial plexus become limited when the proximal root is avulsed, and therefore nerve transfer using healthy, expendable donors became the next popular trend. Nerve transfer is defined as division of a healthy donor nerve and transfer to a denervated recipient nerve. In 1903, Harris and Low was the first to propose suturing the distal stump of the damaged spinal nerve to healthy contiguous nerve.6 In 1913, Tuttle used the anterior terminal branch of the 4th cervical nerve to repair half of the distal stump of the upper trunk in a patient with avulsed 5th and 6th cervical nerves.7 In 1948, Lurje suggested phrenic nerve, long thoracic nerve, medial pectoral nerve, lateral pectoral nerve, anterior rami of radial nerve, and subscapularis nerve as donor nerves for transfer to the upper trunk in an effort to restore shoulder and elbow function.8 Narakas termed nerve transfer as a type of neuroneural neurotization and recognized that distal nerve transfer would only benefit if the site of reconstruction was closer to the target muscle.9 By the 1990s, the Oberlin transfer of 10% of the ulnar nerve to the motor nerve of the biceps marked a new era for nerve transfer.10 Leechavengvongs found that >95% of patients achieved elbow flexion of M3 or more, with no subjective deficit in grip strength.11 Mackinnon modified the technique to include flexor carpi radialis, flexor digitorum superificialis, palmaris longus of the median nerve for transfer to the brachialis branch of the musculocutanaeous nerve (MCN), while specifically delineated the flexor carpi ulnaris (FCU) branch of the ulnar nerve to transfer to the biceps branch.12,13 Transfer of the branch to the long head of the triceps,14 or the medial head of

the triceps to the target axillary nerve for deltoid reinnervation15 or transfer of the terminal anterior interosseous nerve to the deep motor branch of the ulnar nerve for reinnervating hand intrinsics16 would become common reconstructive methods that grew popular due to operating outside of the zone of injury. In total root avulsion (TRA) where the paucity of donor nerves on the injured side limits the options for nerve transfer, surgeons have turned to expandable nerves from the healthy side via nerve grafts to the injured side or employing functioning free muscle transplantation (FFMT) as a two-stage procedure to restore elbow and finger flexion. Gu used the contralateral C7 root to innervate the nerves of the injured side via a pedicled vascularized ulnar graft application to innervate the median or musculocutaneous nerve.17 Chuang used a one-stage free vascularized ulnar nerve graft to bridge the gap between the contralateral C7 and the median nerve of the affected side as a one-stage procedure, or followed with free functioning gracilis muscle transplantation as a two-stage procedure to augment finger flexion.18 Wang modified the CC7 transfer technique by passing the donor through the neck via the prespinal route and then directly coapting the C7 root to the lower trunk to increase chance of finger flexion, but with occasional need of humeral shortening osteotomy.19 Other donor nerves include the use of the contralateral medial pectoral nerve as a donor nerve to innervate the injured MCN with sural nerve graft as the bridge.20 Meanwhile, with the advances in microsurgical techniques, application of FFMT in brachial plexus reconstruction became popular.21–23 Gracilis myocutaneous flap is the most frequently used donor muscle, in which the overlying skin flap is used for monitoring.24 Donor nerves include the spinal accessory nerve, intercostal nerves, phrenic nerve, and anterior interosseous nerve neurotized by the vascularized ulnar nerve graft.25,26 Doi described a two-stage method where upon the first gracilis flap is used to restore elbow flexion and wrist extension, and the second gracilis flap is used to restore finger flexion.27 Such methods have gained popularity, giving the brachial plexus surgeon more options to reconstruct patients.

Adult brachial plexus injury General principles in BPI management Adult brachial plexus injury (BPI) is characterized by many complex problems, including (1) anatomy; (2) level of BPI; (3) diverse injury patterns; (4) unpredictable nerve degeneration

Adult brachial plexus injury

Clinical tips • The evolution of brachial plexus reconstruction has undergone dramatic changes in attitude and approach throughout the past several decades. • BPI has many complex issues such as anatomy, pathophysiology (level of injury, timing of operation), and surgical options. • Categorizing the level of BPI by "number", level I–IV is critical. • Timing of nerve exploration is dependent upon the degree of nerve injury. Debate between early (within one month) and delayed early (within 3–5 months after injury) nerve exploration exists. The latter is becoming more popular. • Clinical evaluation is the most essential step for preoperative and postoperative decision-making. • Imaging studies can help the diagnosis, especially for level I (root) injury. • Correct prediction of the level of injury can help avoid unnecessarily long incision and dissection.

and regeneration; (5) difficult physical examination and diagnosis; (6) challenging nerve surgery; (7) long rehabilitation and follow-up; (8) different palliative surgeries for sequelae deformity; (9) no consensus of outcome evaluation; and (10) difficult pain management. Many reconstructive microsurgeons show great interest, but are greatly frustrated by this field.

Anatomy Gross anatomy The brachial plexus is a large plexus which has the most complex structures in the peripheral nerve system. It locates superficially between two highly mobile structures, neck and arm, causing its susceptibility to injury, especially traction injury. The brachial plexus is formed by the anterior primary rami of the lower cervical (C5–8) and the first thoracic (T1) spinal nerves, which give motor innervation to muscles of the shoulder, including all anterior and posterior chest muscles related to glenohumeral joint movement, muscles of the entire upper limb, and sensory innervation of the entire upper limb except the skin on some parts of the medial aspect of the upper arm (T2 zone). Not infrequently, the C4 and T2 spinal nerves also contribute nerve fibers to it. Whenever the C4 contribution is large and the T1 contribution is small, the brachial plexus is called a “prefixed brachial plexus”. When the C5 contribution is small and T2 contribution is large, it is termed a “postfixed brachial plexus”. Clinically, the prefixed type is more common than the postfixed. But postfixed plexus in adult BPI has been rarely seen, probably because the injuries are either so extensive that further dissection of C8–T1 is hazardous and unnecessary, or the injuries are diagnosed not to involve C8–T1 so that further identification is also unnecessary. Each spinal nerve is formed by the joining of the ventral root (motor fibers) and the dorsal root (sensory fibers). Each root is formed by a number of rootlets which exit from each spinal cord. These separate rootlets can be defined on magnetic resonance imaging (MRI) with three or four bands in the upper cervical roots

555

(C5–7) and two bands of rootlets in the lower roots (C8–T1). The dorsal roots carry sensory information to the central nervous system (retrograde afferent), while the ventral roots convey motor fibers to the muscles (antegrade efferent). The cell bodies (neurons) of the motor fibers are located in the anterior horn of the spinal cord, while the cell bodies of the sensory fibers reside in the dorsal root ganglion located within the intervertebral foramen, immediately outside the dura mater of the spinal cord. The ventral and dorsal roots carry with them an extension of the arachnoid and dura which forms the root sleeve, where the root sleeve attaches to the ventral root and ganglion to form the sheath of the spinal nerve so that the cerebrospinal fluid space does not extend beyond the intervertebral foramen. The anatomy detailed here describes the location of level I (Fig. 23.1). The dorsal and ventral roots unite a few millimeters distal from the ganglion to form a spinal nerve, a mixed nerve, which goes through the interscalene space between the scalene anterior and middle muscles. Nerves arising from the anterior primary ramus include branch to scalene muscles (C5–8), branch to longus colli muscle (C5–8), the long thoracic nerve (C5–7), a portion of phrenic nerve (C5), and a portion of the dorsal scapular nerve (C5). The anatomy detailed here describes the location of level II (see Fig. 23.1). Just out of the scalene muscles the five postganglionic spinal nerves make a first union to form the three trunks: upper (formed by C5 and C6), middle (C7 itself), and lower trunk (formed by C8 and T1 spinal nerves). Two branches are given off from the upper trunk: the nerve to the subclavius muscle and the suprascapular nerve. Each trunk divides into anterior and posterior divisions just proximal to or directly under the clavicle, retroclavicular. Lateral pectoral nerve is formed from anterior divisions of the upper and middle trunk to innervate the clavicular part of pectoralis major muscle; medial pectoral nerve is formed from the anterior division of the lower trunk to innervate the sternal part of the pectoralis major muscle.

Level IV

Level III Level II

Level I

Level I Lesions inside the bone Level II Lesions inside the muscle Level III Lesions pre-and retroclavicular Level IV Lesions infraclavicular

Figure 23.1  Anatomy and numbered level of brachial plexus injury (see the text).

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SECTION IV

CHAPTER 23  • Brachial plexus injuries: adult and pediatric

The anatomy detailed here describes the location of level III (see Fig. 23.1). Infraclavicularly the nerves exchange fibers and form the second union, just distal to the clavicle, and are termed “cords”. The lateral cord is formed by the fusion of the two anterior divisions of the upper and middle trunks, containing fibers derived from C5 through C7. The posterior cord joining all three posterior divisions, containing fibers derived from C5 through C8. The medial cord is simply continuation of the anterior division of the lower trunk, containing fibers from C8 and T1. The subclavian artery becomes the axillary artery at the lateral border of the first rib. Names for the cord relationship are based on the axillary artery. Lateral and medial cords pass anterior, and the posterior cord passes posterior to the axillary artery. The cords run anterior to the subscapularis muscle, just distally behind the pectoralis minor muscle. Each cord has two or more terminal branches to the periphery. The medial and lateral cords, giving one or two terminal branches, join in a Y-shape to form the median nerve. Other main terminal branches of the cords contain the musculocutaneous nerve from the lateral cord, the ulnar nerve from the medial cord, the axillary and radial nerve from the posterior cord. The anatomy detailed here describes the location of level IV (see Fig. 23.1). Numerous anatomical variations of the brachial plexus do exist28–30 and should be always kept in mind. For example, the musculocutaneous nerve may sometimes arise from the median nerve and not from the lateral cord. In some rare cases of C5–6 root avulsion, the musculocutaneous nerve is still found to be functional because part of the musculocutaneous nerve derives from the median with its origins from C7.

and infraclavicular34,39; four levels as preganglionic root, postganglionic root, trunk and division, cord and terminal branches,31,37 etc. These numerous classifications have made the understanding of the anatomy of the brachial plexus complex and confusing. The most confusing aspect is the so-called postganglionic root (Fig. 23.2). In fact, after the dorsal root ganglion, both ventral and dorsal roots continue for only a few millimeters (3), serratus anterior (M>3)

Impossible

Yes

No need to DD

(C) When supraspinatus (M3), LD (M>3) (C-2) when C-PM (M3), LD (M>3)

High possible level III

(C-3) when C-PM (M4000 g) in cephalic presentation, underweight babies ( 4000 g) in cephalic presentation, underweight babies (4000 g), shoulder dystocia, cephalopelvic disproportion, forceps or vacuum suction delivery, or poor technique of delivery. I-OBPP may also occur during difficult breech presentation or in fetal distress (such as septicemia) during Cesarean section. Associated injuries with birth palsy can be seen, including fracture (ipsilateral or contralateral clavicle, humerus, femur or ribs), respiratory insufficiency (asphyxia) due to diaphragm palsy, ecchymosis (neck, chest, face or upper back), and wry neck (torticollis). Although the cause of I-OBPP is still a subject of debate (some believe it can be of intrauterine origin), the author believes that it is caused by obstetric trauma and not due to intrauterine compression neuropathy. All of the author’s intraoperative findings in I-OBPP have been similar to adult brachial plexus traction injury (avulsion, rupture with neuroma and mixed with muscles), not like the picture of compression neuropathy, which presents with pseudoneuroma and is rarely mixed with muscle fibers.

Clinical presentation Determining the relationship between I-OBPP and S-OBPP and predicting the progressive changes in I-OBPP with age

Pediatric brachial plexus injury (obstetric brachial plexus palsy)

575

A

A

B

Figure 23.16  (A,B) A 4-year-old girl shows isolated type 5 (Klumpke) palsy of her right upper limb. B

Figure 23.15  (A) A 2-month-old infant shows improving shoulder abduction of his right upper limb; (B) a 3-month-old infant shows improving elbow flexion of her right upper limb. Both were type 1 OBPP with no need for primary nerve surgery.

is a great challenge.76 Different surgeons have different opinions about clinical presentation of the I-OBPP. In general, there are five types of clinical presentation in I-OBPP: type 1 (or Erb) palsy, which involves deficits of C5 and C6, resulting in a posture of shoulder abduction or internal rotation, elbow extension, and forearm pronation (Fig. 23.15); type 2 (or extended Erb) palsy, which extends further deficits to C7 or C8, resulting in a posture of type 1 with wrist flexion (waiter tip deformity); type 3 and 4 palsies involve the entire plexus (global palsy), resulting in a flail arm without or with a Horner syndrome, respectively; type 5 (or Klumpke) palsy, which involves isolated lower plexus, resulting in only paralyzed hand (Fig. 23.16). In non-operated cases, type 1 or 2 is much more common than type 3 or 4. But in operated cases it is reversed, global palsy more than Erb’s. Type 5 palsy is rarely seen, only in about 1%. In about 1% of I-OBPP cases, the injury

is bilateral but predominantly on one side, and it is frequently seen in breech delivery or Cesarean section with fetal distress.

Clinical examination Newborns are difficult to examine thoroughly. A precise muscle or sensory examination of an infant is impossible. The evaluation chart used for adult BPI (see Fig. 23.5) is not practical. Evaluation should include parents’ observation at home, especially during bathing or dressing, and examiner’s observation in clinic. The infant is placed in the lateral decubitus position with normal side down. The examiner then tickles the baby (tickling test, Fig. 23.17A), or covers the infant face with a towel (towel test, Fig. 23.17B) and uses this to evaluate dynamic movements of the infant’s shoulder, elbow, and hand. An M2 (movement with weight eliminated) muscle strength score in a newborn infant is sufficient to predict a good result when the infant grows. In I-OBPP there is no need to see M4 or M5 muscle strength as in adult BPI. Horner’s syndrome with signs of ptosis or miosis may disappear with time, indicating that the T1 has a stretch but not an avulsion injury,

576

SECTION IV

CHAPTER 23  • Brachial plexus injuries: adult and pediatric

A

B

Figure 23.17  (A) Tickling test and (B) towel test to examine the I-OBPP.

or that T1 has a good connection with T2 (postfixed brachial plexus). An ipsilateral clavicle fracture is usually a good prognostic sign due to traction force divergence. However, a contralateral clavicle fracture is usually a bad prognostic sign as this indicates a high energy traction force. Ideally the infant should be followed up after birth and then at 1-month interval until the decision to operate or not is made. Neurophysiologic studies are not performed routinely. EMG in I-OBPP is usually positive and too optimistic, and may not be accurate enough to predict useful function. Even intraoperative EMG can be misleading. Improving techniques of MRI are now useful to evaluate level I and II lesions as in adult BPI, and are becoming our routine investigation for preoperative imaging (Fig. 23.18). CT-myelogram can also be useful.

Timing of surgery Gilbert89 recommends surgical intervention for infants without evidence of elbow flexion by 3 months. Terzis and Papakonstantinou90 emphasize that the presence of total palsy with Horner’s syndrome warrants earlier surgical intervention at 2 months of age. Clarke and Curtis85 advocate that failure to perform a “cookie test” (i.e., to place a cookie in the mouth by 9 months of age) is an indication for exploration. Our results84 indicate that shoulder and elbow recovery were not different when surgery was performed at 2 months

or at 11 months of age. Even patients who received primary nerve surgery beyond one year of age also showed significant improvement in shoulder and elbow function, but no improvement at all in hand function. In addition, our previous results showed similar improvement of shoulder function in late palliative reconstructions for late OBPP patients compared to those who underwent primary early nerve surgery for I-OBPP.78 However, recovery of hand function with secondary reconstructive methods was far inferior to those who had early nerve surgery for hand function.49 The ideal opportunity for improving hand function is by performing nerve surgery early. Our results demonstrate that Gilbert’s “rule of 3 months” overestimates the poor results of shoulder and elbow function. However, Clarke and Curtis’s “ rule of 9 months” underestimates the poor results of forearm and hand function. The presence of poor shoulder and elbow function in I-OBPP is not an urgent indication for surgery. However, hand palsy is an urgent condition, indicating early surgical intervention. Therefore, our recommended timing of surgery falls between that of Gilbert and Clarke. A global palsy with absence of biceps function and little or no hand function is an indication for early exploration within 3 months. However, in the presence of wrist extension and finger flexion, an additional 3 months of observation is recommended. If by 6 months of age there continues to be no improvement in elbow flexion, then exploration is indicated. If poor shoulder or elbow function persists by one year of age, surgery is indicated too. However, poor hand function at this late age is not an indication for exploration as it is too late. The observation of M2 wrist extension or interphalangeal extension on clinical examination may imply that C7 may be injured (more often with avulsion), but C8 and T1 are intact, warranting an additional 3-month period of observation until the child reaches 6 months.

Preoperative preparation Treating an OBPP patient is treating the whole family. A thorough explanation of the risks and benefits of surgery to the patient’s family is very important, including preoperative diagnosis, surgical risks, postoperative care and rehabilitation, long-term follow-up, possible outcomes, and possible subsequent operations. After intubation, central venous pressure and arterial lines with long catheters should be secured in the femoral vessels. Those two vessel lines are crucial during the operation and for the first 3 days of postoperative care. Sometimes inguinal exploration of the femoral vessels is required to facilitate catheterization.

Surgical technique Incision lines, dissection, and brachial plexus exploration are all similar to adult BPI, except: 1. The platysma in infants is very thin and scarce, resulting in an incision directly superficial to the surface of the sternocleidomastoid muscle. 2. The phrenic nerve should be isolated and well protected. Care should be taken during the operation to avoid excessive traction as this may prolong the extubation time due to transient palsy of the diaphragm. 3. All spinal nerves, C5–T1, should be identified and examined.

Pediatric brachial plexus injury (obstetric brachial plexus palsy)

A

B

C

D

577

Figure 23.18   A 3-month-old I-OBPP. (A) T2 MRI, coronal view to locate the level of cervical spine. (B) MRI 3D, coronal view, T2 normal on right side; MRI 3D: FIESTA and CPR techniques: (C) ventral roots and (D) dorsal root show left C7–C8–T1 root avulsion.

4.

5.

The scalenus anterior muscle is usually segmentally excised, permitting exposure of the level II spinal nerves and release of compression of the subclavian artery. Lesion-in-continuity of the upper and middle trunks is commonly seen, requiring microneurolysis to evaluate the severity of scarring and judge the degree of nerve injury. If the scar is dense and the axis of the nerve, proximal and distal segments, is badly torted, resection of the neuroma and nerve grafts is required.

6.

7.

When the lesions are more distal, involving the divisions (level III injury), the incision is then extended to the deltopectoral groove, exposing Chuang’s triangle (see Fig. 23.8). The supra- and infraclavicular fossa are connected by opening the space under the subclavius muscle. The clavicle can be elevated easily without clavicle osteotomy. Nerve grafts are commonly harvested from both the sural and saphenous nerves. If necessary, medial cutaneous nerve of the arm, superficial radial nerve, and lateral antebrachi cutaneous nerve from the injured limb are other sources.

578

SECTION IV

CHAPTER 23  • Brachial plexus injuries: adult and pediatric

Reconstructive strategies

Table 23.10  Reconstructive strategies for isolated rupture injury

Two groups of spinal nerve injury are classified based on intraoperative findings: (A) pure rupture injury (40%, 47/118); and (B) rupture injury associated with root avulsion (60%, 71/118) (Table 23.8). C5 and C6 tend to be ruptured; but C8-T1 tend to be avulsed (Table 23.9). If C8 is avulsed, T1 tends to be avulsed too but partially. Once C8 T1 avulsion occurs, a ruptured C7 tends to have more proximal avulsion injury too. In global palsy, incidence of three-trunk rupture is about 5% (6/118). Preoperative MRI can be very helpful as a diagnostic tool to see level I or II injury.

Pure rupture injury Except 6 patients who had rupture of all three trunks, the majority of patients (41 patients, 41/47, 87%) had rupture injury involving the upper and/or middle trunk. The reconstructive procedures consisted of microneurolysis and nerve grafts. Reconstructive strategies in these pure rupture injury groups varied based on intraoperative findings and judgment. The majority of patients received C5 nerve grafting to the suprascapular nerve and posterior division of the upper trunk for shoulder, and C6 nerve grafting to the anterior division of the upper trunk for elbow function instead of proximal upper trunk nerve grafting to the distal upper trunk (Table 23.10). Four to six cable nerve grafts (2–3 cm in length) are usually required for coaptation. A ruptured C7 has a high incidence of accompanying avulsion. The proximal stump of C7 was

Table 23.8  Intraoperative findings of obstetric brachial plexus palsy (1992–2004, Chang Gung Memorial Hospital) Ruptured injury alone

47 (40%)

Rupture of UT

17

Rupture of UT and MT

24

Rupture of UT, MT, and LT

6

Rupture and avulsion injury

72 (60%)

One-root avulsion

18

Two-root avulsion

28

Three-root avulsion

17

Four-root avulsion

9

Total patients

119

LT, lower trunk; MT, middle trunk; UT, upper trunk.

Table 23.9  Incidence of type of injury on different spinal nerves (1992–2004, Chang Gung Memorial Hospital)

Rupture

Avulsion

C5

117

12

C6

95

42

C7

49

79

C8

9

71

T1

8

39

Trunk rupture

Nerve reconstructive strategy

Upper trunk

C5-ng-SS and PD C6-ng-AD

Upper and middle

C5-ng-SS and PD C6-ng-AD C7-ng-C7

Upper and middle and lower

C5-ng-SS and PD C6-ng-AD C7-ng-C7 LT-ng-LT

AD, Anterior division of the upper trunk; LT, lower trunk; ng, nerve graft; PD, posterior division; SS, suprascapular nerve; UT, upper trunk.

therefore routinely repaired to the distal stump of C7 via nerve grafts. There were few patients who received longer nerve grafting (4-6 cm in length) from supraclavicular spinal nerves to the infraclavicular selected target nerves (posterior and lateral cord). Table 23.10 shows our reconstructive strategies for pure rupture injury.

Rupture injury associated with root avulsion A total of 72 patients (60%) were included in this series. Once avulsion occurs it tends to involve at least 2 roots (75%). This type of reconstruction depends on the number of root avulsions, and the remaining proximal neural resources. In global palsy, restoration of hand function becomes the first priority, followed by elbow flexion and then shoulder function (Table 23.11). In I-OBPP, C5 is usually ruptured, not avulsed (see Table 23.9). The proximal C5 stump can be a source for selective neurotization to the C8 or lower trunk (intraplexus neurotization). The frequency of nerve transfers increases if associated root avulsion increases, including intercostal nerve transfer for elbow or finger flexion, XI nerve transfer for the shoulder, or intraplexus transfer from C5 or C6 to the C8 or median nerve for hand function in three- or four-root avulsion. Intercostal nerve transfer, either to the musculocutaneous nerve for elbow, or to the median nerve for hand function is an effective procedure in infant patients (much better than in adults). Few patients need contralateral C7 transfer,69 branch of ulnar nerve transfer (Oberlin method10) or combined branch of median nerve (Mackinnon method12) transfer. Table 23.11 shows our reconstructive strategies for rupture injury associated with root avulsion. In this series of patients, 10 cases of I-OBPP were operated on late, at 1 year of age or older (range, 1 year to 2 years 6 months). Most of these patients showed poor spontaneous recovery of shoulder and/or elbow function prior to surgery. Primary nerve surgery for these late operative cases showed encouraging results in shoulder and elbow function recovery, but few gained recovery of hand function.

Postoperative management A rigid premade neck splint is placed on every patient immediately postoperatively (Fig. 23.19). Total operative time is on average 8 hours, with a range of 6–10 hours. Postoperatively

Pediatric brachial plexus injury (obstetric brachial plexus palsy)

579

Table 23.11  Nerve reconstructive strategy for rupture injury associated with root avulsion

Nerve reconstructive strategy Root avulsion

For shoulder

For elbow

One

C5

XI-SS

C6-ng-(major) AD and (minor) PD

C7

C5-ng-SS and PD

C6-ng-AD

C5, C6 (minor)-C7

C8

C5-ng-SS and PD

T3–5 ICNMCn

C6-ng-C8 (C7-ng-C7)

T1

C5-ng-SS and PD

C6-ng-AD

C7-ng-C7; C8-ng-C8

C5 and C6

XI-SS

T3–5ICNMCN

C8-ng-C8

C6 and C7

XI-SS

C5-ng-C6

C6-ng-C8

C7 and C8

XI-SS

T3–5ICNMCN

C6-ng-C8 (or median)

C8 and T1(8)

XI-SS

T3–5ICNMCN

(C7-ng-C7)

C5–7

XI-SS

T3–5ICNMCN

C6–8

XI-SS

T3–5ICNMCN

C5-ngmedian

C7, C8, and T1

C6-ng-SS and PD

T3–5ICNMCN

C5-ngmedian

C6–T1

C5-ng-SS and PD

T3–4 ICNMCN

T5–7ICNmedian

C5-ng-SS and PD

T3–5ICNMCN

CC7T-ng-C8

Two

Three

Four

For hand

A

AD, anterior division of the upper trunk; MCN, musculocutaneous nerve; ng, nerve graft; PD, posterior division; SS, suprascapular nerve; XI, spinal accessory nerve.

B

the patient is transferred to the intensive care unit after extubation. The patient is cared for in the head-up position to avoid dyspnea due to any temporary palsy of the diaphragm. The patient is kept in the intensive care unit for 3–5 days, and then transferred to the general ward for an additional 2 days. Total hospitalization is approximately 1 week. The neck splint is kept in place for 4 weeks. Follow-up at regular intervals (the first month postoperatively and then every 4 months afterwards) is performed for a minimum of 4 years. Home electrical muscle stimulation (twice daily for 15–20 minutes each) is started 4 weeks after surgery and performed for approximately 1 year or until muscle function reaches M2 level. There are two important exercises for prevention of shoulder adduction contracture: pull-up bar exercise (stretching exercise), and swimming (dynamic exercise), where both upper limbs are exercised simultaneously.

the lesions (i.e., aberrant reinnervation), complexity of the repair (i.e., different surgical strategies), complexity of limb involvement (shoulder, elbow, forearm, and hand), and finally the young age of the patients, which makes cooperation difficult. The reported methods of functional assessment include the MRC muscle grading system, Gilbert and Tassin Muscle Grading System, Clark and Curtis active movement scale, Narakas’ Grading System, and others.71–74 For result assessment the author prefers to follow all patients for a minimum of four years and outcomes are then categorized as “Good”, “Fair” or “Poor” based on the degree of shoulder abduction, external rotation, elbow flexion and extension, and finger flexion (Table 23.12).

Outcome assessment

Results

There is a lack of consensus with regards to the optimal method of assessing results. This is partly due to the complexity of

The overall results in C5 nerve grafting, especially to the suprascapular nerve and posterior division of the upper

Figure 23.19  (A,B) Postoperative neck splint.

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SECTION IV

CHAPTER 23  • Brachial plexus injuries: adult and pediatric

Table 23.12  Postoperative functional assessment of obstetric brachial plexus palsy

Good

Fair

Poor

Shoulder abduction

>120°

90–120°

90°

60–90°

2 mm shorter than ulna

Normal, radioulnar synostosis, or congenital dislocation of the radial head

2

Hypoplastic or absent

Absence, hypoplasia, or coalition

Hypoplasia

Hypoplasia

3

Hypoplastic or absent

Absence, hypoplasia, or coalition

Physis absent

Variable hypoplasia

4

Hypoplastic or absent

Absence, hypoplasia, or coalition

Absent

Absent

5

Hypoplastic or absent

Absence, hypoplasia, or coalition

Absent

AbsentIncludes humerus deficiencies

From Bayne LG, Klug MS. Long-term review of the surgical treatment of radial deficiencies. J Hand Surg Am. 1987;12:169–179; James MA, McCarroll HR Jr, Manske PR. The spectrum of radial longitudinal deficiency: a modified classification. J Hand Surg Am. 1999;24:1145–1155; Goldarb CA, Manske PR, Busa R, Mills J, Carter P, Ezaki M. Upper extremity phocomelia re-examined: a longitudinal dysplasia. J Bone Joint Surg Am. 2005;87(12):2639–2648.

hypoplasia may occur in isolation. The index (and middle) finger(s) may also be abnormal (e.g., more stiff, more differences in myotendinous units, etc.) when the forearm is more severely affected, a finding which has direct treatment implications.

Type 1 thumb hypoplasia Type 1 thumbs are mildly affected and may go undiagnosed. The thumbs are more petite – shorter and narrower in girth, the first webspace mildly shallow, but with well-formed intrinsic and extrinsic muscles.

Type 2 thumb hypoplasia Type 2 thumbs have intrinsic muscle differences. The thumbs are petite, there is thenar atrophy, and possible MCP joint instability from a lax collateral ligament (ulnar collateral ligament [UCL] ± radial collateral ligament [RCL]). Flexion and extension creases are relatively normal as the extrinsic myotendinous units are not affected. When not detected early, type 2 thumbs may go unnoticed and manifest when children are older and there is increased difficulty with more complex tasks.

Type 3A thumb hypoplasia Type 3A thumbs have added extrinsic myotendinous differences, but the TMC joint remains stable. Tendons may be aberrant or absent. The metacarpal is often narrow. Intrinsic and extrinsic myotendinous differences exist (Fig. 34.15). Type 3A thumbs may be quite anatomically abnormal and challenging to reconstruct, especially with pollex abductus.21,112

Type 3B thumb hypoplasia The hallmark of type 3B thumbs is that the TMC joint is unstable. The proximal aspect of the thumb metacarpal is deficient, though the distal portion of the metacarpal exists. Intrinsic and extrinsic myotendinous units are abnormal. Often some diminutive thenar muscles are present (Fig. 34.16).

Type 4 thumb hypoplasia Type 4 thumbs, also referred to as “pouce flottant”, have a stalk which contains only a neurovascular bundle and no bone. The metacarpal is entirely absent. Phalanges are present within the distal portion of the digit.

Type 5 thumb hypoplasia Type 5 thumbs are entirely absent. A modification to the Blauth classification was recently suggested in order to be more inclusive and provide a framework for describing the small proportion of severely affected RLD hands that do not fit into the 1–5 system.113 Adding type 6 thumb hypoplasia was proposed in order to describe an absent thumb and index finger with or without additional missing digits.113 Due to the high incidence of associated medical and musculoskeletal anomalies among patients with RLD, comprehensive assessment and thorough physical examination is essential.89,93 Two large studies found approximately onethird had a concomitant syndrome.89,93 Goldfarb et al. found most patients had additional medical or musculoskeletal anomalies and that those with isolated thumb hypoplasia and forearm type 0 RLD were less likely to have comorbidities than patients with more severe forearm involvement.93 A basic workup including a complete blood count, renal ultrasound, electrocardiogram, echocardiogram, spine exam, and spine radiographs is indicated in all patients with RLD. We often recommend testing for Fanconi anemia given the grave consequences of missing the diagnosis.114 Additional testing is based on evaluation by a geneticist. Initial hand and upper extremity radiographs can be obtained closer to 6–12 months of age to allow additional structures to ossify and existing structures to grow and be better visualized.

Patient selection Thumb reconstruction is based on the severity of thumb hypoplasia. The breakpoint in decision-making for many surgeons

SECTION VI

802

CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

D

C

B

A

E

F

G

Figure 34.12  Types of radial longitudinal deficiency: (A) type N, (B) type 0, (C) type 1, (D) type 2, (E) type 3, (F) type 4, (G) type 5. (Courtesy of Charles A. Goldfarb, MD.)

Radioulnar

Type I

Type II

Extrinsic and intrinsic present

Extrinsic present intrinsic absent

Type IIIA

Type IIIB

Type IV

Type V

Figure 34.13  Classification of thumb hypoplasia. (With permission from Herring JA, Tachdjian MO. Texas Scottish Rite Hospital for Children. Tachdjian's Pediatric Orthopaedics, 4th ed. Philadelphia, PA: Saunders/Elsevier; 2008.)

is type 3 A and milder thumbs are reconstructed, and type 3B and more severe thumbs are treated with index finger pollicization.115 Those in Asian cultures are more likely to reconstruct type 3B and even type 4 thumbs compared to Western surgeons.

803

Radiographs and clinical examination can be helpful determining type 3 A versus 3B. With time, children will ignore an unstable type 3B thumb and bypass it, preferring the index and middle (or ring and small) fingers for side-to-side pinch (Fig. 34.17). This often makes the discussion with parents about reconstruction versus ablation and pollicization somewhat easier as parents can see the child does not use the diminutive thumb. Radiographs help delineate the anatomy of the metacarpal base, but delayed ossification can make radiographs less reliable early on. Nonetheless, the decision to remove a type 3B thumb can still be difficult for families as the thumb is substantial in size. In some children, the index finger will “autopollicize”. This refers to the index finger pronating, the index/middle finger webspace widening, and intermetacarpal ligament loosening – changes which are secondary to a tendency to preferentially attempt to use the index finger somewhat like a thumb (Fig. 34.18). This is an encouraging finding and is an indicator of the quality of the index finger and the potential to use it in its new position post-pollicization. When examining a child, if the predominant pattern of use is ulnar prehension (primary use of the ring and small fingers), then we advise significant caution when considering a pollicization. The tendency to prefer using the ring and small fingers is based on quality of the digits and motion. Ulnar prehension is present in children with more severe forearm deformity, radial wrist deviation, and more abnormal index finger anatomy. In our experience, these patients are usually not ideal candidates for pollicization, and we consider it carefully. Occasionally, the index finger is still pollicized with the idea that it serves as a post, but we recommend carefully watching patterns of use and assessing the quality of the index finger. Outcomes in these children are often humbling, as they may ignore the neo-thumb and maintain ulnar prehension since it is more dexterous and facile (Fig. 34.19). Reconstruction of type 2 and 3 A hypoplastic thumbs considers three features: narrow first webspace, lack of opposition, and instability of the MCP joint. One or more of these features may be present, and each should be individually addressed. Opposition tendon transfers are commonly performed using abductor digiti minimi (ADM) or flexor digitorum superficialis (FDS) to the middle or ring finger.116,117 One advantage to using FDS is the excess tendon length which can be simultaneously used for MCP joint collateral ligament reconstruction.116 Extensor indicis proprius (EIP) opposition transfer is not typically performed, as tendons on the radial side of the forearm may be underdeveloped and less optimal donors in RLD. Resection of tethering tendinous interconnections in pollex abductus deformity removes deforming forces and permits active motion at the MCP and IP joints. However, in some cases, the extrinsic flexor tendon may be absent and the interconnection more likely represents a malpositioned flexor pollicis longus (FPL).21 The ideal time for reconstruction of a hypoplastic thumb is debatable – many surgeons recommend surgery at approximately 2 years of age while others recommend waiting until closer to school age. Part of the timing dilemma is related to FDS tendon transfer and the drilling of a bone tunnel across the metacarpal; waiting until the metacarpal is large enough to accommodate this often corresponds to a delayed timeframe. Likewise, participation and compliance with postoperative

804

SECTION VI

A

CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

B

C

Figure 34.14  Patient with bilateral RLD previously treated with bilateral index finger pollicizations. (A) Right forearm type 4. (B) Photograph highlights limb length discrepancy – the more severely affected forearm is substantially shorter. (C) Left forearm type 0. (Courtesy of The Royal Children’s Hospital. Melbourne, Australia.)

A

B

Figure 34.15  (A) A type 3A hypoplastic thumb. (B) MCP joint UCL instability. (Courtesy of Brinkley K. Sandvall, MD.)

rehabilitation after opposition transfer is more likely with an older child. Pollicization at 18–24 months of age is reasonable. At this point, developmentally, children are starting to perform more complex tasks, and the hand has had time to nearly double in size since birth making the procedure more straightforward. Older age is not a contraindication to pollicization in a patient who is otherwise a good candidate. While there is merit to cortical plasticity, studies have not been able to show a definite advantage when pollicization is performed younger.118

Additionally, there are reports of older children successfully integrating and using their pollicized digits.118 Clearly, if the index is the most radial digit (type 5 thumb hypoplasia) and is used for pinch with the middle finger, then it is likely to also be used in its new neo-thumb position as it is cortically represented as the radial post. When treating the forearm in RLD, overarching goals are to address family expectations, improve deformity/appearance, and improve function. Surgical principles are to correct radial deviation/the position of the hand, balance the wrist on the forearm, maintain wrist and finger motion, and allow growth

Radioulnar

Figure 34.16   A type 3B hypoplastic thumb. (Courtesy of Brinkley K. Sandvall, MD.)

805

Figure 34.18  Index finger “autopollicizing”. (Courtesy of Brinkley K. Sandvall, MD.)

Figure 34.19  Maintained ulnar prehension after bilateral pollicization. (Courtesy of The Royal Children’s Hospital, Melbourne, Australia.) A

B

Figure 34.17  (A) Patient bypassing her type 3B hypoplastic thumb and using index/middle finger for pinch. (B) Patient with right type 3B and left type 4 hypoplastic thumbs using bilateral index/middle fingers for grasp. (Courtesy of Brinkley K. Sandvall, MD.)

of the forearm. While there is agreement on general goals and principles, there is substantial variability in practice patterns among experienced pediatric hand surgeons – internationally – but also among centers in North America.115 Stretching a radially deviated wrist should start as early as possible and can be initiated in the newborn nursery. When the child is large enough, splinting begins – often around 3 months of age. The splint is worn at night-time and intermittently during the daytime for at least the first year. Surgery to improve hand and wrist position is often performed around 12–24 months of age, prior to surgery on the thumb or index finger. Our primary considerations when making decisions about treatment of the forearm in RLD include severity of RLD, wrist motion, unilateral versus bilateral, pattern of prehension, and the potential for pollicization.

806

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

In patients with type 0, 1, and 2 RLD forearms, nonoperative care may be appropriate. However, surgery to balance the tendons or to lengthen the radius are considered based on exact deficiency and family preferences. Release of tight structures on the radial aspect of the wrist and tendon transfers can improve alignment, increasing ulnar deviation and wrist extension.119 The goal with lengthening the radius is to provide additional support for the carpus. In patients with type 3, 4, and 5 RLD forearms, consensus on management is lacking.115 Patient and family desires play a key role in decision-making. Treatment options include observation, soft-tissue release and realignment, centralization with or without distraction, extra-articular skeletal realignment, and free skeletal transfer. There is no question that some children with RLD forearm differences function well without surgery. This fact has led some surgeons to recommend nonoperative care for most patients. However, other patients and families become frustrated and seek direct intervention to improve alignment with hopes for functional and aesthetic improvement. There are data to suggest that centralization improves finger motion and strength.120 Reasons to centralize include the potential to open up space on the radial hand for a pollicized digit, the ability to achieve a longer and more stable hand–forearm unit, and the possibility of improved aesthetics. Reasons to avoid centralization include stiffness, growth impairment from ulna physeal injury, satisfactory function without intervention, and the likelihood of recurrence. Patients with a stiff elbow rely on wrist radial deviation to bring their hand closer to their face – and a straighter, stiffer, more centralized wrist risks downgrading function. Similarly, in children with persistent ulnar patterns of prehension, straightening the wrist takes their ring and small fingers away from midline (away from their working space, contralateral hand, and face), and may hinder function. In these patients, we avoid formal centralization. Centralization alone is rarely our preferred choice. We find it challenging and have significant concern about causing injury to the physis. We only perform centralization alone if the wrist can be passively positioned to neutral. If it is not possible to passively correct the deformity, then our preference is to perform distraction prior to centralization. Distraction prior to centralization (precentralization soft-tissue distraction) facilitates centralization by stretching tight radial and volar structures.121,122 Gradual stretching of the soft tissue allows more complete and tension-free alignment of the carpus on the ulna. Tension at the time of centralization could theoretically cause pressure-induced injury to the distal ulnar physis, and distraction minimizes this risk. Notching has been used to facilitate reduction and increase stability of the construct; however, this technique is rarely utilized today given the risk to the ulna physis. Distraction minimizes the need to resect part of the carpus or ulna (notch the carpus or notch the ulna) in order to achieve appropriate alignment.123 An alternative treatment to centralization (with or without distraction) in type 3, 4, and 5 forearms is soft-tissue release and a local flap/bilobed flap. With mild forearm RLD, the skin and soft-tissue tightness is not severe enough to need adjacent tissue transfer, and thus this technique is primarily for type 3, 4, and 5 forearms. The primary goals of this surgery are to release tight deforming structures, improve wrist mobility, and improve resting posture of the wrist while minimizing

the risk of physeal injury and stiffness. Different flap designs have been devised to redistribute the lax soft tissue on the ulnar side of the wrist.124,125. A volar bilobed flap is our treatment of choice in many children with type 3, 4, and 5 forearms, especially when the elbow is stiff or if an ulnar pattern of prehension exists. If the ulna is bowed more than 30°, we perform a closing wedge osteotomy to realign it. This is often performed in conjunction with the above listed procedures. Despite significant shortening, ulna lengthening is rarely indicated. Occasionally, due to a functional need in adolescence, we will perform this surgery. However, the complication rate is high and the process arduous for both patient and family. Vilkki described a vascularized free second toe metatarsophalangeal joint transfer for type 4 RLD forearms after distraction.126,127 The goal is to provide additional support for the radial side of the wrist with preservation of growth.

Treatment/surgical technique (see Algorithms 34.1 & 34.2) Type 1 hypoplastic thumbs These usually do not require surgery. Rarely, first webspace deepening is indicated.

Type 2 and 3A hypoplastic thumbs First webspace deepening Various local flap designs have been described to deepen the first webspace – and each has advantages and disadvantages, with various theoretical changes in first webspace contour. We have found many different flap designs suffice. One should be wary of small flaps with narrow tips. A 4-flap Z-plasty is our preferred method and is raised in standard fashion. It is important to evaluate the underlying muscle and fascia and consider incising the adductor pollicis and/or first dorsal interosseous (FDI) muscle fascia if tight. If severely constricted, releasing the FDI origin from the thumb metacarpal can achieve additional gains, but we often find releasing the fascia alone achieves sufficient release. Skin incisions may double as access for the approach during MCP joint stabilization (Fig. 34.20).

Opposition transfer ADM (Huber) opposition transfer

An incision is made along the ulnar border of the small finger from the base of the proximal phalanx along the hypothenar eminence to the wrist flexion crease. The ADM muscle is separated from the other hypothenar muscles and raised distal to proximal (releasing its two-tailed insertion first). At the proximal aspect, beware of the neurovascular bundle entering the deep and radial aspect of the muscle. A wide subcutaneous tunnel is made from the pisiform to the radial aspect of the thumb MCP joint along the thenar eminence. The muscle is passed through the tunnel and secured with the wrist in extension and the thumb in abduction and opposition.

FDS opposition transfer with UCL reconstruction Incisions are designed at the ring finger A1 pulley, the carpal tunnel (or distal forearm, depending on preference in pulley), and at the radial and ulnar aspects of thumb MCP joint. The

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the index finger may be more distal volarly near the index PIP flexion crease or more proximal near the index MCP flexion crease – and each has implications on how the skin is redraped and the first webspace is closed. Once skin incisions are chosen, the remaining steps proceed similarly.128,129 The index metacarpal is transected through the physis, and it is important to ablate the physis. The amount to shorten the index finger can be estimated by the distance from the tip of the index finger to the PIP joint of the middle finger. When transposing the index finger, it is important to flex the metacarpal head (and thus hyperextend the index MCP joint) – and secure it with suture in this position – so that it rests in a position which will not allow further hyperextension later.

Clinical tip

A

B

Figure 34.20  (A,B) First webspace 4-flap Z-plasty, adductor pollicis and first dorsal interosseous fascia released. (Courtesy of Brinkley K. Sandvall, MD.)

FDS tendon is isolated at the A1 pulley of the ring finger and also at the distal aspect of the carpal tunnel (or in the distal forearm) and retrieved through the proximal incision. A pulley is formed using the transverse carpal ligament (or a hemislip of flexor carpi ulnaris just proximal to the pisiform). The FDS is passed through the pulley. A wide subcutaneous tunnel is made from the radial aspect of the thumb MCP joint across the thenar eminence to the pulley, and the FDS tendon passed through the tunnel. A K-wire is placed across the IP and MCP joints for stability. A drill hole is made through the thumb metacarpal head radial to ulnar. Branches of the radial sensory nerve are protected. Often a size 2.0–2.5 drill bit is sufficient to pass a hemi-slip of FDS through the metacarpal head. A loop of a large monofilament suture can be used to pass the tendon radial to ulnar. We use the entire width of the tendon for the opposition transfer, but often pass only a hemislip of it through the bone tunnel for ligament reconstruction in order to avoid making the bone tunnel too large. Tension of the tendon transfer is set with the wrist in extension and the thumb in abduction and opposition. The tendon is secured to the bone and surrounding soft tissue on the radial side of the thumb, near where the abductor pollicis brevis insertion would be. Tension is assessed with tenodesis. UCL ligament reconstruction is completed by securing the distal stump of FDS to the base of the proximal phalanx. This is completed with suture to the bone, over the native ligament(s). If the RCL is also insufficient, the extra tendon on the radial side can be similarly used to add support.

Type 3B, 4, and 5 hypoplastic thumbs Pollicization Various skin incisions have been described and have advantages and disadvantages.128,129 The circumferential incision on

Flexing the index metacarpal head (hyperextending the native index MCP joint) and securing the neo-TMC joint in a hyperextended position is important to avoid secondary deformity. A native TMC joint does not hyperextend, but a native MCP joint does. To account for these differences, securing the native MCP in a hyperextended position at the time of pollicization removes the potential for it to hyperextend later. Some prefer K-wires to secure the thumb. Our preference is to use sutures alone. Securing the metacarpal head on both the volar and dorsal side provides sufficient stability.

Type 0 and 1 RLD forearms Joint release and tendon transfer Our technique is the same as described by Mo and Manske.119 Detach the tight radial wrist extensor(s) from their distal origin. Release the tight radial wrist capsule dorsal and volar. Detach extensor carpi ulnaris (ECU) just proximal to its insertion and transfer it to the dorsal wrist capsule to augment wrist extension. Transfer the radial wrist extensor to the native insertion site of the ECU tendon, converting it to an ulnar deviator. A K-wire can be inserted across the radiocarpal joint (Fig. 34.21).

Type 2 RLD forearms Radius lengthening We prefer a unilateral fixator and cross pin the proximal radius and ulna. We also pin the carpus to the radius (cartilaginous component) to avoid lengthening dorsal or volar to the carpus. The fixator is applied, osteotomy performed, and distractor activated (Fig. 34.22).

Type 3, 4, and 5 RLD forearms Soft-tissue release and bilobed flap A bilobed flap can be designed either dorsal or volar.125 We prefer the volar design due to improved visualization of structures and minimized scarring on the presenting surface of the arm (Fig. 34.23). Skin flaps are designed at right-angles

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

Algorithm 34.1 The wrist in RLD “St. Louis Protocol” 0,1

Joint release and tendon transfer (@18 months)

Lengthen radius with unilateral or ringed fixator (@18 months)

Substantial development of radius 2

Treat like forearm 3,4,5

Diminutive radius

Bilobe flap (@18-36 months) (+ consider ulna osteotomy if >30° of ulna angulation)

Ulnar prehension ALL TYPES FOREARM RLD @ birth start stretch regularly to correct radial deviation and flexion

Resting angulation 30° of ulna angulation) (@18-24 months)

Hypoplastic thumb reconstruction vs. pollicization (6 months later)

Resting angulation >45° and not passively correctable

Pre-centralization distraction with ring fixator (@24-30months)

If severe recurrent wrist deformity, see Algorithm 34.2

3,4,5

Radial prehension

Decisions for intervention vary based on the health of the child and family preferences. The algorithm here assumes several family conversations and a desire to intervene. Bold text shows the most common pathway. After wrist intervention, all children splint at night until skeletal maturity.

Algorithm 34.2 The wrist in RLD “St. Louis Protocol” Continue stretching

Ulna epiphysis present / ossified?

NO YES

Release and epiphyseal ulnocarpal arthrodesis At or near skeletal maturity?

Recurrent wrist deformity (severe)

Begin stretching

NO YES

Complete wrist fusion

Decisions for intervention vary based on the health of the child and family preferences. The algorithm here assumes several family conversations and a desire to intervene. This algorithm applies to post-centralization patients with severe recurrent deformity and to patients with untreated/persistent late-presenting wrist deformity. The ulna epiphysis often ossified around 12 years of age.

to each other. The pinch test on the ulnar side determines the width of each flap, as the ulnar side must close primarily. The flaps are equal lengths and widths and are raised subfascial. Care is taken to not delaminate the skin from the subcutaneous tissue and fascia during elevation and transposition. The ulnar nerve and artery are protected. The radial artery may be absent. The median nerve is often the most radial

structure. Tight fascial bands on the radial aspect of the wrist are released. The radial wrist flexor is often diminutive and tight and is usually released rather than transferred. Finger flexors are preserved. It is possible to dissect to the dorsal radial side of the wrist through the volar bilobed flap incisions. We avoid dissection around the distal ulnar physis. The hand and wrist are stabilized with a K-wire from the second

Radioulnar

A

B

809

C

Figure 34.21  Type 1 RLD forearm tendon transfers. (A) Preoperative radiograph. (B) Intraoperative tendon transfer. (C) Postoperative radiograph. ECRB, Extensor carpi radialis brevis; ECU, extensor carpi ulnaris. (Courtesy of Charles A. Goldfarb, MD.)

more appropriate given its ability to correct three-dimensional deformity and its stability. Lengthening of the soft tissues is quite gradual and should not be at the pace required for bone lengthening; rather, 1–2 turns/day (each turn 0.25 mm) is appropriate. Rapid correction can traumatize the physis of the distal ulna. Once correction is achieved, we allow the fixator to remain in place for another 2–4 weeks to allow soft-tissue edema to resolve (see Fig. 34.24).

Centralization Through an L-shaped dorsal incision, the dorsal and radial neurovascular structures are dissected off the tight radial fibrous structures. The extensor retinaculum is divided and the finger extensors retracted. The dorsal, radial, and volar wrist capsule, as well as tight fibrous tissue, is incised. Once the soft-tissue release is performed, the carpus is placed on the end of the ulna without tension. Alignment is maintained with one or two K-wires which remain in place for 6 months. The extensor retinaculum is repaired, and ECU is advanced and repaired.

Ulna osteotomy Figure 34.22  Radiograph showing radius lengthening with a unilateral fixator. (Courtesy of Charles A. Goldfarb, MD.)

or third metacarpal across the carpus. If the wire is passed into the ulna, care is taken to only pass the wire once to minimize injury to the physis. The K-wire maintains maximal correction during healing. A closing wedge osteotomy of the ulna is simultaneously performed if bowing is greater than 30° (see description below).

Precentralization soft-tissue distraction The technique proceeds as previously described.122 A ring fixator or a unilateral fixator may be used. We find the ring fixator

While most frequently performed either at the time of soft-tissue release and bilobed flap or at the time of centralization, it can be performed separately. The degree of ulna bowing is assessed. At the mid-diaphyseal apex, a small incision is made and dissection carried down to the ulna. A closing wedge osteotomy is performed and stabilized with a K-wire.

Clinical Tip While various treatment options exist for the wrist in RLD, the key to each is to preserve growth of the ulna and to avoid traumatizing the distal ulna physis. Balance can be challenging, and recurrence of deformity is common.

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

A

C

B

Figure 34.23  Volar bilobed flap. (A) Flap design. (B) Flap elevation and rotation. (C) Flap inset. (Courtesy of Michael Galvez, MD.)

Postoperative care Opposition transfer, collateral ligament reconstruction The patient is placed in a short arm thumb spica splint for 5 weeks, after which the K-wire is removed and the patient transitions to a removable thumb spica maintaining wide palmar abduction and initiates hand therapy. Begin active range of motion, focusing on thumb abduction and opposition and MCP joint flexion and extension. Remove the splint for hygiene and light exercises. Start passive exercises at 8 weeks, light functional strengthening, and transition the splint to night-time only for one more month.

Pollicization

Figure 34.24  Precentralization soft-tissue distraction with a ring fixator. (Courtesy of Charles A. Goldfarb, MD.)

The patient is placed in a long arm soft cast or similar bulky bandage for 3 weeks. After this, transition to a night-time forearm-based thumb spica splint, with the thumb in opposition, allowing free motion during the day and play activities (active flexion/opposition activities). Taping can be used to position the thumb in a position of function during the daytime. At 8 weeks, begin gentle passive range of motion and progressive strengthening. Continue night-time splinting until 3 months postoperatively. It may take up to one year to regain active movement of the pollicized digit.

Radioulnar

Joint release and tendon transfer (type 0 and 1 RLD forearm) The postoperative cast and K-wire are removed after 6–8 weeks. Splinting and exercises are initiated and continue for several weeks.

Soft-tissue release and bilobed flap The K-wire is removed after 4 weeks, and the patient is transitioned into a forearm-based splint and begins range of motion and stretching. Avoid passive flexion and radial deviation. Light active use of the hand begins. Splinting transitions to night-time only at 12 weeks and continues, ideally, until skeletal maturity.

Precentralization soft-tissue distraction, centralization Vigilant pin care is performed. Outpatient therapy is three times a week while the fixator is in place for finger and elbow motion. At the time of distractor removal and centralization, a long arm plaster splint is placed. Active and passive digit range of motion is initiated. At 2 weeks, the splint is converted to a cast for a total of 6 weeks of immobilization. At 6 weeks after surgery, the patient transitions to a removable splint which is slowly weaned but continues for 6 months. At 6 weeks, light active use of the hand begins. K-wires are removed 6 months postoperatively and active wrist range of motion begins. Night-time splinting continues until skeletal maturity.

A

Outcome, prognosis, and complications Reconstructing a type 2 or 3A hypoplastic thumb does not provide a “normal” thumb. MCP motion is decreased after ligament reconstruction, and many hypoplastic thumbs already have decreased IP motion due to extrinsic tendon differences. However, increased stability and opposition strength improves function.116 After FDS opposition transfer ± collateral ligament reconstruction, Vuillermin et al. found grip and pinch strengths were just under half of “normal” and that type 2 thumbs had significantly greater grip and pinch strengths compared to type 3A thumbs.116 Manske et al. found pollicized digits were used in 84% of activities, with increased use for handling large objects (92%) and less use for small objects (77%).118 Results were not influenced by patient age at the time of operation.118 Tonkin et al. studied function as it related to RLD and compared patients with normal or near normal forearms to those with forearm and wrist anomalies.130 They found that despite RLD and compromised strength, all of the pollicized digits were used for some tasks – but not all tasks.130 Expected total active motion is approximately 50% of a normal thumb, grip strength 21%, pinch strength 25%.118,131,132 In general, children with pollicized digits improve dexterity and strength with growth (Fig. 34.25).132–134 Patient-reported appearance outcomes after pollicization are lacking. Many studies have assessed caregiver/parent,

B

C

Figure 34.25 (A–C) Pollicized digit being used well. (Courtesy of The Royal Children’s Hospital, Melbourne, Australia.)  

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

therapist, and/or surgeon perspectives, yet few studies have included patient perspectives on hand appearance.130–132,134–136 Hovius et al. assessed the impact of RLD on appearance post-pollicization.131 They compared patients with mild RLD to those with severe RLD and found no statistically significant difference in patient or parent-reported thumb appearance.131 In a study assessing surgeon, therapist, and caregiver perspectives, narrow girth, angulation, and excess length negatively impacted appearance scores (Fig. 34.26).135 There is some credence to the notion that “if it works like a thumb, it looks like a thumb”, and Zlotolow et al. have tried to delineate which objective criteria correlate with subjective impressions.136 In an analysis of complications, suboptimal outcomes, and functional deficiencies after pollicization, poor opposition and limited extension were the two most common functional limitations.137 Suboptimal outcomes related to first webspace contracture.137 Acute complications after pollicization mainly relate to perfusion.137 One should assess if insufficiency is arterial or venous and take standard measures to treat vasospasm. It is critical to ensure there is no kinking of or tension on the vascular pedicles. Anticipating swelling that will ensue is important, so a loose but secure dressing should be applied. In patients with type 0 RLD forearms, release and tendon transfers can augment ulnar deviation and wrist extension, and results show improved resting posture as well as active and passive wrist motion.119 It is generally though that centralization improves appearance, but whether it improves function remains unsettled. A large study by Kotwal et al. comparing radiographic and functional outcomes after nonoperative treatment and operative treatment (centralization or radialization) in type 3 and 4 RLD forearms, concluded that surgery improved appearance, function, and ease of performance of activities compared to nonoperative management.120 Ekblom et al. studied adults with RLD and concluded that grip strength, key pinch, forearm length, elbow motion, and digit motion seemed to be more important for activity and participation than radial angulation of the wrist.138

Recurrent radial deviation after centralization is common and is due to residual muscle/tendon imbalance and lack of a stable wrist platform. Despite recurrence, centralization with and without distraction results in improved alignment of the wrist.139–142 Damore et al. found that patients with the greatest preoperative deformity also had the greatest amount of recurrence.139 While distraction facilitates centralization, it has not been found to prevent recurrent deformity.140 Some have found less recurrent radial deviation with notched centralization.109 While notching increases the stability of the hand/wrist/forearm construct, it commonly results in decreased wrist motion and may result in a shorter forearm. Sestero et al. studied deleterious effects of centralization on growth of the ulna in RLD.109 They found that centralization significantly decreased growth potential of the ulna, their centralized patients only achieving 48% of the length of the unaffected ulna (versus 68% of length in the nonoperative group). Additionally, notching resulted in shorter forearms than those that were non-notched.109 In a study by Vuillermin et al. assessing results of soft-tissue release and bilobed flap in patients with forearm RLD at an average of 9 years post operation, resting wrist radial deviation improved by an average of 24°, active wrist flexion–extension arc was 73°, and age at time of surgery did not correlate with maintained correction over time.125 Patient-reported happiness with appearance and satisfaction were excellent.125 Additionally, they found no effect on ulna growth as occurs with centralization procedures.143 Their results for resting wrist radial deviation after soft-tissue release and bilobed flap compare similarly with results after centralization reported by Damore et al.139 Some have abandoned centralization in favor of soft-tissue release and bilobed flap.115,144

Secondary procedures In the pollicized digit, the first volar interosseous is not a strong adductor, and unfortunately, there is not another good substitute for the absent adductor pollicis. On the contrary, poor opposition after pollicization can be augmented with an opposition transfer, and this is often done closer to school age. Limited extension may require exploration with extensor tendon imbrication or possibly epiphyseal arthrodesis of the PIP joint of the pollicized digit (MCP joint of the new “thumb”).137 A digit that is not positioned well is less likely to be useful, and occasionally, an osteotomy to reposition the base into more palmar abduction is performed. Instability at the neo-TMC is also possible and requires secondary surgery for stabilization. Growth through the metacarpal physis causes excess length and an unfavorable appearance and is treated with physeal ablation and shortening. In post-centralization patients with severe recurrent deformity and in patients with untreated/persistent late-presenting wrist deformity, complete wrist fusion at skeletal maturity or epiphyseal arthrodesis (physeal-sparing) when the distal ulna physis is still open can be performed (see Algorithm 34.2).145

Ulnar longitudinal deficiency Figure 34.26  Photograph comparing left index pollicization to contralateral unaffected thumb showing differences in girth and nail width. (Courtesy of The Royal Children’s Hospital, Melbourne, Australia.)

Introduction Ulnar longitudinal deficiency (ULD) is about 4 to 10 times less common than RLD.146,147 It is usually unilateral and

Radioulnar

sporadic.1,148,149 Unlike RLD, ulnar deficiency is not associated with systemic conditions and disruptions in organogenesis.149 However, it can be associated with musculoskeletal differences (e.g., proximal femoral focal deficiency, fibular deficiency, club feet, absent patella, and congenital scoliosis).148,149 As aptly noted by Broudy and Smith in 1979, ulnar deficiency is not simply the postaxial counterpart of radial deficiency.149

Basic science/disease process An insult to the ZPA is responsible for ULD.94 The ZPA is located on the ulnar (posterior) side of the developing hand plate and disturbances are thought to result from a disrupted gradient of Shh, with ulnar side development dependent on Shh.97–100 Severity of ULD is related to both the timing and the severity of the insult.150

Diagnosis/patient presentation Hand differences in ULD are strikingly variable. However, a few characteristics are most common – ectrodactyly (missing digits), syndactyly, and thumb differences.151 The vast majority of patients with ULD and hand differences have ectrodactyly (approximately 90%).148,149,151,152 The syndactyly may be simple or complex and often the bony anatomy is striking.148,149,151 The thumb may be hypoplastic.148,149,151–153 Metacarpal synostosis is also common and may not be evident except on radiographs.148,149,152,154–156 While RLD hand differences are isolated to the radial side of the hand, the hand differences in ULD are highly variable, and thumb anomalies are commonly seen. Carpal bone anomalies are also common (Fig. 34.27).148,149,152,157 A classification system describing hand differences in ULD was developed by Cole and Manske and has similarities to the one Manske described for central deficiency (Table 34.4).151 It focuses on development the thumb and first webspace, as that is the most common surgical indication in patients with

813

ULD.151 Hands may have additional differences (e.g., ectrodactyly or syndactyly of other digits, etc.), but this particular system focuses on the radial side of the hand. Many classification systems describe forearm and elbow characteristics in ULD.148,158–161 ULD usually affects the entire limb, although occasionally only the hand plate is affected.152 The Bayne and Klug classification is one of the commonly used classification systems – and two additions have been made to the original description – type 0 for hand plate only ULD and type 5 for more severe deficiency and a single arm/ forearm bone (Table 34.5, Fig. 34.28).108,152,161 The forearm in ULD is usually short. As elbow flexion and extension is normally a reflection of the ulnohumeral joint, elbow motion may be limited. However, even without normal joint development, elbow motion is often remarkably good. In patients without a proximal ulna (or with a very rudimentary proximal ulna), elbow motion occurs through the radiohumeral joint. Classically, patients may have an appearance suggesting that the arm is “on backward” due to a combination of internal rotation a bowed forearm

Table 34.4  Classification of hand differences in ulnar longitudinal deficiency

Type

Characteristics

A

Normal first webspace and thumb

B

Mild first webspace and thumb deficiency. Normal intrinsic and extrinsic myotendinous structures

C

Moderate to severe first webspace and thumb deficiency. Potential lack of opposition, malposition of the thumb, first webspace syndactyly, abnormal extrinsic and intrinsic musculotendinous function, and/or thumb in the plane of the fingers

D

Absent thumb

From Cole RJ, Manske PR. Classification of ulnar deficiency according to the thumb and first web. J Hand Surg. 1997;22 A:479–488.

Table 34.5  Classification of the forearm in ulnar longitudinal deficiency

Figure 34.27  Bilateral hand radiographs demonstrating common hand differences in ULD – ectrodactyly, thumb hypoplasia, metacarpal synostosis, carpal coalition. (Courtesy of Brinkley K. Sandvall, MD.)

Type

Characteristics

0

Normal-length ulna with hand anomalies

I

Hypoplasia of ulna (presence of distal and proximal epiphysis)

II

Partial aplasia of ulna (absence of distal or middle one-third)

III

Total aplasia (complete absence of ulna)

IV

Radiohumeral synostosis

V

Severe radiohumeral synostosis with humeral bifurcation or large medial condyle

From Goldfarb CA, Manske PR, Busa R, Mills J, Carter P, Ezaki M. Upperextremity phocomelia reexamined: a longitudinal dysplasia. J Bone Joint Surg Am. 2005;87:2639–2648; Havenhill TG, Manske PR, Patel A, Goldfarb CA. Type 0 ulnar longitudinal deficiency. J Hand Surg. 2005;30 A:1288–1293; Bayne LG. Ulnar club hand (ulnar deficiencies). In: Green DP, ed. Operative Hand Surgery. Vol 1, 3rd ed. New York: Churchill Livinstone; 1993.

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

B

A

D

E

C

E

Figure 34.28  Types of ulnar deficiency: (A) type 0, (B) type I, (C) type II, (D) type III, (E) type IV, (F) type V. (Courtesy of Charles A. Goldfarb, MD.)

(Fig. 34.29). Unlike RLD, there has been no established correlation between the severity of forearm and the severity of hand involvement in ULD.151 Assessment of and referral to an appropriate specialist is warranted for additional evaluation of the lower extremities and spine.

Patient selection Indications for surgery on the hand in patients with ULD relate most commonly to either syndactyly reconstruction or thumb and first webspace reconstruction. Thumb and first webspace reconstruction in ULD follows principles outlined in the prior section on thumb hypoplasia. On rare occasions,

metacarpal synostosis may be excised to improve digit alignment, most commonly for the 4th–5th metacarpal.162 Indications for surgery on the forearm in patients with ULD are primarily bowing that interferes with function or aesthetics – and rarely instability or ulnar deviation at the wrist. Severe bowing may be treated with an osteotomy. Forearm lengthening is rarely indicated. Some children with radiohumeral synostosis may benefit from an external rotation ± flexion osteotomy. The goal is to improve function by facilitating midline function. We perform this closer to school age or even older once functional assessments can be more reliably performed. We do not attempt to restore motion across the synostosis as no technique is reliable for motion restoration. Treatment of wrist ulnar deviation in ULD is much

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815

Basic science/disease process Radial polydactyly is most frequently sporadic and unilateral and is not associated with systemic medical conditions.164 Incidence varies depending on the population studied, but it affects approximately 1 in 1000 live births and is most common in populations of European descent.164–169 Ulnar polydactyly is frequently autosomal dominant with variable penetrance. It is commonly bilateral and may also affect the feet. Type B ulnar polydactyly, a small extra digit attached by a skin bridge, is more common and in the US presents ten times more frequently in African Americans than in individuals of European ancestry.168,170 In contrast, type A polydactyly, a more completely formed extra digit, is less common and is present relatively equally among White and Black populations.168,170,171 Type A polydactyly in White individuals may be syndromic.1,172

Diagnosis/patient presentation

Figure 34.29  Patient with left ULD and appearance of the arm “on backward”. (Courtesy of Charles A. Goldfarb, MD.)

less commonly indicated than treatment of radial deviation in RLD. When an ulnar anlage is tethering and increasing deformity/ulnar deviation (Bayne II forearm), release of the distal portion can be performed.

Clinical tips • Given the unilateral nature of most cases of ULD, function is typically well maintained. Nonetheless, maximizing hand function via the thumb and first webspace can be helpful. • Despite a bowed and abnormal appearance of the forearm, rarely is a corrective osteotomy helpful. When indicated, a closing wedge osteotomy in the older child may be performed.

Polydactyly Introduction Polydactyly encompasses extra digits on the radial (preaxial), central, or ulnar (postaxial) hand. Radial and ulnar polydactyly are far more common, and this section will focus on these diagnoses. Radial polydactyly is often referred to as a thumb duplication or split thumb. Split thumb is the more accurate, patient-focused definition as both digits are small. In contrast, the term “duplicated” thumb suggests two normal-sized thumbs, an imprecise notion which can be disappointing and problematic for families, especially after surgical reconstruction (Fig. 34.30).163 Ulnar polydactyly is far more common and, typically, more straightforward to treat.

In radial polydactyly, each thumb is hypoplastic. However, one is usually more well formed and dominant – both anatomically and functionally. Most commonly, it is the radial thumb that is less well formed. The nail, skeletal alignment, ligaments, intrinsic muscles, and extrinsic myotendinous units are each affected. The thumb is examined for alignment, length, girth, nail plate width, flexion and extension creases, first webspace, joint stability, and muscle bulk. Thumb flexion and extension, adduction, palmar abduction, opposition, and active and passive motion at the TMC, MCP, and IP joints are assessed. It can be helpful to compare the affected thumb to the contralateral unaffected thumb. The more proximal the level of duplication, the more likely the first webspace is narrowed. Shallow flexion and/or extension creases suggest underdevelopment of joints and myotendinous units. Decreased passive motion at joints suggests abnormal articular surface development. A pollex abductus deformity is a hypoplastic thumb with interconnections along the radial side of the thumb between the flexor and extensor tendons.110 It is classically described in hypoplastic thumbs but may be present in radial polydactyly as well. The abnormal line of pull of the tendons leads to malalignment of the osteoarticular construct if not addressed. The most commonly used classification system for radial polydactyly is the Wassel–Flatt classification, which is a radiographic classification based on the degree of and level of skeletal duplication – bifid versus duplicated, distal to proximal.69,173 It gained wide acceptance as a simple, clear, and easy-to-use system (Fig. 34.31). However, the Wassel–Flatt classification system has been criticized as it is not inclusive of all presentations of radial polydactyly, and thus not representative of the entire spectrum of complexity.174–177 Inclusion of triphalangeal thumb as type VII in the Wassel–Flatt radial polydactyly classification has been controversial – and Adrian Flatt recommended it be separated and excluded from the classification system, considering it a distinct thumb difference.69 Whether included in the classification or not, patients with a triphalangeal component must be considered uniquely different from typical radial polydactyly patients.

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A

B

Figure 34.30  (A,B) Right split thumb size compared to contralateral unaffected thumb. (Courtesy of Brinkley K. Sandvall, MD.)

I

II

III

IV

V

VI

VII

Figure 34.31  Wassel–Flatt classification of radial polydactyly. (From Wassel HD. The results of surgery for polydactyly of the thumb. A review. Clin Orthop Relat Res. 1969;64:175-193.)

Clinical tip Interestingly, many advocate renaming the Wassel classification the “Flatt classification”. Harry Wassel was a hand surgery fellow under Adrian Flatt at the University of Iowa in 1969 when he published the classification system; however, Dr. Flatt was not acknowledged as a mentor or coauthor. Dr. Flatt started the first academic hand surgery unit in the United States at the University of Iowa, was a president of the American Society for Surgery of the Hand and founded the Journal of Hand Surgery. The term “Flatt Classification” is now favored by many in the pediatric hand surgery literature in order to give appropriate recognition to Dr. Flatt.176,178

Ulnar polydactyly is most commonly classified as a type A or B, as described by Temtamy and McKusick.179 Type A is an extra small finger which has an osseous connection to the

hand; it is typically a well-formed extra digit.179 Type B is the more common presentation and in which the supernumerary digit stalk is only skin, subcutaneous tissue, and neurovascular bundle – there is no bony connection.179 The stalk may be very narrow or a bit more robust. Type A ulnar polydactyly has diverse morphology. Pritsch et al. described a classification system for type A ulnar polydactyly which includes five subtypes based on whether the duplicated digit’s skeletal origin is articular or bony (Table 34.6).180

Patient selection Radial and ulnar polydactyly are treated surgically. In addition to the clear aesthetic concerns, there are also functional concerns as the extra digit can limit motion and can interfere with function of the other digits. Radial polydactyly and type A ulnar polydactyly are typically surgically

Radioulnar

817

Table 34.6  Classification of type A ulnar polydactyly

Type

Description

1. Metacarpal type

Fully developed 6th ray

2. Metacarpophalangeal type (most common)

On the radial aspect of 5th digit, the distal portion of the metacarpal is intercalated

3. Phalangeal type

On the ulnar aspect of the 5th digit, either as a separate hypoplastic 6th metacarpal or fused to the 5th metacarpal

4. Intercalated type

Arises from the metacarpophalangeal joint of the 5th digit

5. Fully developed type

Arises from bifid 5th proximal phalanx

From Pritsch T, Ezaki M, Mills J, Oishi SN. Type A ulnar polydactyly of the hand: a classification system and clinical series. J Hand Surg. 2013;38 A:453–458.

A

treated around 12–18 months of age. Type B ulnar polydactyly can be treated in the newborn nursery, in the clinic, or in the operating room at a time and age that is convenient. The neuroma from ligating the digit occasionally becomes symptomatic and can be managed later in life. Alternatively, when the stalk is wider, formal excision in the operating room is performed at 6–12 months of age (delayed in order to minimize anesthetic risk). It is important to set expectations before surgery and ensure the family understands the different size(s) of the polydactylous digit(s). If the contralateral thumb is unaffected, baseline differences in width, girth, and nail plate size can be demonstrated, explaining that those difference will persist postoperatively.

Treatment/surgical technique Certain principles are paramount: 1. Identify the digit to maintain/reconstruct and the digit to excise. 2. Create a skin incision to accomplish reconstruction goals and avoid scar contracture. 3. Use all available tissue to normalize anatomy, realign the osteoarticular column and articular surfaces, reconstruct ligaments, and rebalance myotendinous units.

Radial polydactyly Type I and II The diminutive thumb is removed, and the dominant thumb is realigned. Skin is incised on either the dorsal or radial side, skin flaps are elevated, and the extensor mechanism is inspected. The extensor tendon to the diminutive digit is either excised or transferred to the dominant thumb. The flexor tendon to the diminutive digit is transected and not commonly transferred. The neurovascular bundle is preserved. The collateral ligament is raised as a periosteal sleeve and later attached to the dominant thumb.181 The diminutive phalanx is removed. The IP joint is assessed and if a separate facet is present, it is removed with either a scalpel or

B

Figure 34.32  (A,B) Photograph of a right thumb after the Bilhaut–Cloquet procedure compared to the contralateral unaffected left thumb which highlights nail deformity and difference in width. (Courtesy of Brinkley K. Sandvall, MD.)

an osteotome and rongeur. Articular alignment is assessed, and a closing wedge osteotomy is performed, if necessary, to align the joint surfaces. The bone is stabilized with a K-wire. The skin is carefully repaired. Some of the soft-tissue bulk can be used to augment the pulp. When the two thumbs are similar in size, some advocate for the Bilhaut–Cloquet procedure which resects the central portion of each distal phalanx and combines the two lateral portions.182 However, difficulties often arise with physeal growth, nail bed/plate deformity, and joint stiffness (Fig. 34.32), and most surgeons have therefore abandoned this technique.183–185 Alternatively, a modified version combines a portion of the osseous and soft-tissue structures from each while preserving the entire epiphysis of one of the digits in an effort to mitigate some of these risks.186 In our opinion, both of these procedures have a very limited role.

Type III and IV These digits may be divergent, convergent, or aligned (Fig. 34.33). The smaller digit is removed. The tips may be separate or the skin syndactylized to various degrees. If the lateral nailfold needs to be reconstructed, it should be transferred from the digit being removed by excising the central tissue and transferring the radial paronychium. If the thumbs are similar size, then the radial one is usually removed in an effort to preserve the MCP joint UCL. Surgical technique proceeds in a similar manner to that described above. The MCP joint articular surface is assessed. It is important to remove a duplicated facet and realign malaligned articular surfaces with an extra-articular osteotomy. The periosteal sleeve with the collateral ligament is preserved during these steps. The thumb is stabilized with a K-wire for 5 weeks. Extrinsic tendons are realigned and thenar muscles are transferred and reinserted. The first webspace should be inspected and deepened with an adjacent tissue transfer if indicated.

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attention to surgical detail. Precise reconstruction of the osteoarticular column and realignment of the intrinsic and extrinsic myotendinous units will decrease many of these concerns. We recommend correcting all structures during the initial operation in order to prevent secondary deformity and decrease the need for revision. In a review of long-term outcomes more than 10 years after radial polydactyly reconstruction, the revision rate was 19%, and most patients underwent revision for painful joint instability.187 Another study reported significantly decreased satisfaction if there was persistent joint angulation.163 In a comparative study evaluating the Bilhaut procedure versus resection and reconstruction for treatment of radial polydactyly types II and IV, aesthetic results were more likely perceived as pleasing after conventional reconstruction.185

Secondary procedures

Figure 34.33  Wassel–Flatt type IV, divergent–convergent. (Courtesy of Charles A. Goldfarb, MD.)

Type V and VI Reconstruction is similar to that mentioned above. The first webspace is more likely to be affected and require deepening. Carefully inspect the overall alignment and have a low threshold to perform an osteotomy to improve it.

Ulnar polydactyly Type A Principles and techniques are similar to those described in radial polydactyly. If hypothenar muscles insert onto the duplicated digit, they are transferred to the remaining small finger.

Instability may be treated with either ligament reconstruction or delayed fusion. Painful instability is an indication for either arthrodesis or chondrodesis and is based on bony development. Correction of secondary deformity requires identifying the cause as treatment may require osteotomies, ligament reconstruction, and/or extrinsic tendon realignment. Treatment of a zigzag deformity may require osteotomies at two different levels in order to realign the skeleton and tendons (Fig. 34.34).

Triphalangeal thumb Introduction The two most common triphalangeal thumb (TPT) phenotypes are isolated TPT and TPT with radial polydactyly.188 TPT can be sporadic or autosomal dominant with variable expressivity.189 When inherited, it is often bilateral.168 TPT with radial polydactyly is highly associated with a positive family history.188 Several syndromes may be associated with TPT (e.g., Holt–Oram, Fanconi anemia, VACTERL).188

Type B

Basic science/disease process

An elliptical incision is made around the base of the stalk and is extended proximally along the hypothenar eminence. The neurovascular bundle is dissected proximal. A traction neurectomy is performed, taking care to not injure the ulnar digital neve to the remaining small finger. The skin is trimmed and closed.

One of the genes responsible for TPT has been isolated to 7q36 and is autosomal dominant.189,190 Additional genetic assessment is likely to identify additional genetic anomalies.

Postoperative care Ligament reconstructions and osteotomies are protected for 5 weeks with a Kirschner wire and a thumb spica cast. After wire removal, the patient is transitioned to a removable thumb spica splint which is weaned over the next several weeks.

Outcome, prognosis, and complications A smaller pulp, narrower nail, and decreased motion at the IP joint are unavoidable and most notable in type I and II split thumbs. However, nail deformity, malalignment, instability, and growth disturbance can be minimized with proper

Diagnosis/patient presentation TPT thumb can vary considerably in appearance, though the most common type is an opposable thumb with a small, extra middle phalanx. The extra phalanx can have variable size and shape (triangle, trapezoid, rectangle), which impacts overall thumb length and angulation. A triangle-shaped bone causes notable angular deformity (Fig. 34.35); this same effect can be seen with a triangular-shaped (or angular) epiphysis. If the extra phalanx is sizable, then the thumb will appear long. Mobility and stability of each joint is assessed. The digit may have the appearance of a finger and be in the plane of the palm rather than in a position of palmar abduction, a finding referred to as a five-fingered hand (Fig. 34.36). The thumb may be quite hypoplastic with a shallow first webspace and underdeveloped thenar muscles leading to insufficient opposition.

Radioulnar

A

B

819

C

Figure 34.34  Wassel–Flatt type VI thumb with secondary zigzag deformity after incomplete correction at the initial surgery. (A) Preoperative radiograph. (B) Preoperative photograph. (C) Immediate postoperative photograph after two osteotomies and UCL reconstruction. (Courtesy of Brinkley K. Sandvall, MD.)

are organized by shape of the extra phalanx, others by treatment options, and still others by the relationship of the triphalangeal digit to a duplicated (or triplicated) digit.69,173,194–198 The Rotterdam classification was developed to provide a more comprehensive framework to capture the full spectrum and complex presentations of radial polydactyly and triphalangeal thumb, and it uses the Wassel–Flatt classification as its foundation (Fig. 34.38).69,173,174

Patient selection While the length of the thumb is always assessed, there are five main considerations in the treatment of triphalangeal thumb: 1. Abnormally shaped phalanx (delta, trapezoid, rectangle, angular epiphysis) 2. Five-fingered hand 3. Narrow first webspace 4. Thumb opposition 5. Associated anomalies, primarily radial polydactyly

Figure 34.35  Left triphalangeal thumb with a triangle-shaped extra phalanx and fingertip deviation. (Courtesy of Brinkley K. Sandvall, MD.)

When syndromic, the thumb is usually more severely hypoplastic and non-opposable.188 Additional findings such as syndactyly, polydactyly (radial or ulnar), and lower extremity differences including great toe duplication may coexist (Fig. 34.37).191–193 Several classification systems have been described, and each has focused on different aspects of triphalangeal thumb. Some

While TPT may cause functional difficulties, appearance of the thumb is a consideration as well.199 Functional issues usually relate to angular deformity, a narrow first webspace, lack of opposition from hypoplastic or absent intrinsic muscles, and/or a thumb that is not positioned well/is in the plane of the palm. A thumb that is excessively long or deviated is generally thought to have a less ideal appearance. There is no consensus recommendation on timing for surgery, and controversy exists over the ideal age. Consideration is given to growth potential, potential for articular surface remodeling, cooperation with postoperative care, and overall size of the thumb. We believe the potential for joint remodeling is better when the patient is less than 4 years of age and so typically perform surgery early (18–24 months). It is important to have a stable, well-positioned thumb when developing patterns of prehension around 2 years of age. If the child is not using the thumb like a thumb, consideration is

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Figure 34.36  Bilateral five-fingered hands. (Courtesy of Charles A. Goldfarb, MD.)

B

A

C

D

Figure 34.37 (A–D) Patient with bilateral TPT and radial polydactyly and bilateral great toe duplication. (Courtesy of The Royal Children’s Hospital, Melbourne, Australia.)  

Radioulnar

I

II

T Triplication

III

Tph Triphalangism

IV

V

VI

Triplication on different levels associated with triphalangism

H Hypoplastic/floating

VII

D Deviation

821

VIII

S Symphalangism

Figure 34.38  The Rotterdam classification of radial polydactyly and triphalangeal thumb. (From Zuidam JM, Selles RW, Ananta M, Runia J, Hovius SE. A classification system of radial polydactyly: inclusion of triphalangeal thumb and triplication. J Hand Surg Am. 2008;33(3):373–377.)

given to operating earlier in order to facilitate functional use. Osteotomies and/or arthrodeses to improve alignment do not rely on articular remodeling and so are often performed when the child is a bit older.

Treatment/surgical technique Abnormally shaped phalanx (delta, trapezoid, rectangle, angular epiphysis) Delta middle phalanx Remove the triangle-shaped extra phalanx and rebalance the collateral ligaments by tightening the one on the convex side. A Z-plasty on the concave side facilitates skin and soft tissue rebalancing. Shorten the extensor mechanism. In children less than 6 years, there is a good expectation for articular remodeling, and this is our preferred technique. However, when the patient is older than 6 years, we consider an ostectomy and arthrodesis as described below.

Trapezoid or rectangle middle phalanx For trapezoid or rectangle middle phalanx (Fig. 34.39) closing wedge osteotomies may include resection and arthrodesis of the distal joint (or the joint with less motion). This is performed through a dorsal approach using fluoroscopic imaging and usually K-wires for fixation. As additional ossification is needed, this intervention is typically performed at an older age.

Angular epiphysis An abnormally shaped epiphysis requires patience before treatment as the epiphysis must be sufficiently large to allow safe intervention and maintain growth. Treatment may be delayed until skeletal maturity depending on size and ossification.

Five-fingered hand Pollicization is our preferred technique for treatment of a five-fingered hand (Fig. 34.40). Attention must be given

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

A

B

Figure 34.39  (A) Radiograph and (B) photograph showing a left trapezoid-shaped extra middle phalanx. (Courtesy of Brinkley K. Sandvall, MD.)

to recreating a broad first webspace. The technique is similar to that described in the section on thumb hypoplasia. Alternatively, a “rotation shortening osteotomy with abduction at the metacarpal level” (ROAMC), which leaves the native TMC joint intact, has been described.200,201

Narrow first webspace For mild to moderate narrowing of the first webspace, local flaps can be used. In severe cases, reverse radial forearm flaps or free fasciocutaneous flaps may be used.202

Thumb opposition Standard opposition tendon transfers are performed. Steps are described in the section on thumb hypoplasia. If the triphalangeal thumb is severely hypoplastic, consideration is given to ablation and pollicization rather than reconstruction.

Associated polydactyly, primarily radial polydactyly When TPT and radial polydactyly coexist, we reconstruct the “best” thumb. Radiographs and clinical examination help with this determination. The extra digit is removed through standard techniques described in the section on polydactyly. If the triphalangeal thumb is preserved (as it typically is), treatment of the extra phalanx proceeds as described above (see Fig. 34.40). Clinical tips • Care of the child with a triphalangeal thumb is complex, and families often have experience given strong inheritance patterns. While early intervention is preferred for both functional and remodeling potential reasons, patience may be required based on the size of the extra phalanx and physeal proximity. In addition, careful assessment for potential associated anomalies in addition to the extra bone is required, and additional reconstruction may be necessary.

• An incision on either the dorsum of the thumb or on the concave side of the extra phalanx can be utilized. While both are effective, we now prefer an incision on the concave side for ease of exposure and phalanx excision. • Stability of the reconstructed thumb is not typically an issue, with pinning for 5 weeks; however, regaining mobility, especially in older children, can be difficult.

Outcome, prognosis, and complications TPTs (both operated and nonoperated) have diminished strength.203 Zuidam et al. found TPT grip strength 70% and opposition strength 63% compared to age-adjusted normal values.203 In a group of adults with nonoperated TPTs, though patient-reported thumb function was good, appearance scores were low, implying dislike of the thumb.199 TPT metacarpals may have abnormal physeal plate positions (most commonly distal) and unpredictable growth, potentially resulting in longer thumbs than anticipated.204

Future directions The OMT classification for congenital upper extremity anomalies continues to be optimized through updates and improves our ability to categorize individuals based on phenotypes, our understanding of genetics, and limb development differences. Many of our classification challenges are due to limitations in our understanding. With additional research, correct categorization of these anomalies will become elucidated. As the OMT classification becomes more widely utilized, it will facilitate population-based comparisons and clarify the true epidemiology of congenital upper limb anomalies. We should strive to utilize validated patient-reported outcome measures in order to better assess long-term functional outcomes and satisfaction with appearance.

Radioulnar

A

C

823

B

D

Figure 34.40  Patient with triphalangeal thumb and radial polydactyly treated with removal of the polydactylous digit and pollicization. (A) Preoperative photograph. (B) Preoperative radiograph. (C,D) Postoperative photographs. (Courtesy of The Royal Children’s Hospital, Melbourne, Australia.)

Prosthetics are often hot, heavy, expensive, and cumbersome, especially if the child has an unaffected contralateral extremity. The results from James et al imply that current prostheses are not normalizing function – and that there is

Access the reference list online at   Elsevier eBooks+

room for improvement.68 As technology improves, prosthetics are likely to grow in popularity, and 3D printing offers exciting possibilities.

References

References 1. Online Mendelian Inheritance in Man, OMIM®. McKusick– Nathans Institute of Genetic Medicine, Johns Hopkins University (Baltimore, MD). https://omim.org/. 2. Bell J. The Treasury of Human Inheritance: On Hereditary Digital Anomalies. London: Cambridge University Press; 1951. 3. Ghani HA. Modified dorsal rotation advancement flap for release of the thumb web space. J Hand Surg Br. 2006;31(2):226–229. 4. Buck-Gramcko D. Syndactyly between the thumb and index finger. In: Buck-Gramcko D, ed. Congenital Malformation of the Hand and Forearm. New York: Churchill Livingstone; 1998:141–147. 5. Coombs CJ, Thomas DJ. The Manta Ray flap: a technique for first web space release. Tech Hand Up Extrem Surg. 2010;14(1):41–45. 6. Oberg KC, Feenstra JM, Manske PR, Tonkin MA. Developmental biology and classification of congenital anomalies of the hand and upper extremity. J Hand Surg Am. 2010;35(12):2066–2076. 7. Ekblom AG, Kaurell T, Arner M. Epidemiology of congenital upper limb anomalies in Stockholm, Sweden, 1997 to 2007: application of the Oberg, Manske, Tonkin classification. J Hand Surg Am. 2014;39(2):237–248. 8. Fernandez-Teran M, Ros MA. The apical ectodermal ridge: morphological aspects and signaling pathways. Int J Dev Biol. 2008;52(7):857–871. 9. Bavinck JN, Weaver DD. Subclavian artery supply disruption sequence: hypothesis of a vascular etiology for Poland, Klippel– Feil, and Möbius anomalies. Am J Med Genet. 1986;23(4):903–918. 10. Miura T, Nakamura R, Horii E. The position of symbrachydactyly in the classification of congenital hand anomalies. J Hand Surg Br. 1994;19(3):350–354. 11. Blauth W, Gekeler J. Morphology and classification of symbrachydactyly. Handchirurgie. 1971;3(4):123–128. 12. Manske PR. Symbrachydactyly instead of atypical cleft hand. Plast Reconstr Surg. 1993;91(1):196. 13. Kallemeier PM, Manske PR, Davis B, Goldfarb CA. An assessment of the relationship between congenital transverse deficiency of the forearm and symbrachydactyly. J Hand Surg Am. 2007;32(9):1408–1412. 14. Yamauchi Y, Tanabu S. Symbrachydactyly. In: Buck-Gramcko D, ed. Congenital Malformations of the Hand and Forearm. London: Churchill Livingstone; 1998:149–158. 15. Ogino T, Minami A, Kato H. Clinical features and roentgenograms of symbrachydactyly. J Hand Surg Br. 1989;14(3):303–306. 16. Catena N, Divizia MT, Calevo MG, et al. Hand and upper limb anomalies in Poland syndrome: a new proposal of classification. J Pediatr Orthop. 2012;32(7):727–731. 17. Koehler DM, Goldfarb CA, Snyder-Warwick A, Roberts S, Wall LB. Characterization of hand anomalies associated with Möbius syndrome. J Hand Surg Am. 2019;44(7):548–555. 18. De Smet L, Fabry G. Characteristics of patients with symbrachydactyly. J Pediatr Orthop B. 1998;7(2):158–161. 19. Devriendt K, De Smet L, De Boeck K, Fryns JP. DiGeorge syndrome and unilateral symbrachydactyly. Genet Couns. 1997;8(4):345–347. 20. Blauth W, Schneider-Sickert F. Numerical variations. Congenital Deformities of the Hand: An Atlas on Their Surgical Treatment. Berlin: Springer-Verlag; 1981:120–121. 21. Manske PR, McCarroll HR Jr, James M. Type III-A hypoplastic thumb. J Hand Surg Am. 1995;20(2):246–253. 22. Langer JS, Manske PR, Steffen JA, et al. Thumb in the plane of the hand: characterization and results of surgical treatment. J Hand Surg Am. 2009;34(10):1795–1801. 23. Wolff H. Diskussion zu Lexer; Gelenktransplantation. Verhandlungen der Deutschen Gesellschaft fur Chirurgie. Berlin: Congress 39; 1910. 24. Patterson RW, Seitz Jr. WH. Nonvascularized toe phalangeal transfer and distraction lengthening for symbrachydactyly. J Hand Surg Am. 2010;35(4):652–658. 25. Goldberg NH, Watson HK. Composite toe (phalanx and epiphysis) transfers in the reconstruction of the aphalangic hand. J Hand Surg Br. 1982;7(5):454–459.

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26. Netscher DT, Lewis EV. Technique of nonvascularized toe phalangeal transfer and distraction lengthening in the treatment of multiple digit symbrachydactyly. Tech Hand Up Extrem Surg. 2008;12(2):114–120. 27. Cavallo AV, Smith PJ, Morley S, Morsi AW. Non-vascularized free toe phalanx transfers in congenital hand deformities – the Great Ormond Street experience. J Hand Surg Br. 2003;28(6):520–527. 28. Buck-Gramcko D. The role of nonvascularized toe phalanx transplantation. Hand Clin. 1990;6(4):643–659. 29. Gohla T, Metz Ch, Lanz U. Non-vascularized free toe phalanx transplantation in the treatment of symbrachydactyly and constriction ring syndrome. J Hand Surg Br. 2005;30(5):446–451. 30. Radocha RF, Netscher D, Kleinert HE. Toe phalangeal grafts in congenital hand anomalies. J Hand Surg Am. 1993;18(5):833–841. 31. James MA, Durkin RC. Nonvascularized toe proximal phalanx transfers in the treatment of aphalangia. Hand Clin. 1998;14(1):1–15. 32. Buck-Gramcko D, Pereira JA. Proximal toe phalanx transplantation for bony stabilization and lengthening of partially aplastic digits. Ann Chir Main Memb Super. 1990;9(2):107–118. 33. Goodell PB, Bauer AS, Sierra FJ, James MA. Symbrachydactyly. Hand. 2016;11(3):262–270. 34. Lister G. Microsurgical transfer of the second toe for congenital deficiency of the thumb. Plast Reconstr Surg. 1988;82(4):658–665. 35. Jones NF, Kaplan J. Indications for microsurgical reconstruction of congenital hand anomalies by toe-to-hand transfers. Hand. 2013;8(4):367–374. 36. Richardson PW, Johnstone BR, Coombs CJ. Toe-to-hand transfer in symbrachydactyly. Hand Surg. 2004;9(1):11–18. 37. Foucher G, Medina J, Navarro R, Nagel D. Toe transfer in congenital hand malformations. J Reconstr Microsurg. 2001;17(1):1–8. 38. Schenker M, Wiberg M, Kay SP, Johansson RS. Precision grip function after free toe transfer in children with hypoplastic digits. J Plast Reconstr Aesthet Surg. 2007;60(1):13–23. 39. Jones NF, Hansen SL, Bates SJ. Toe-to-hand transfers for congenital anomalies of the hand. Hand Clin. 2007;23(1):129–136. 40. Kay SP, Wiberg M. Toe to hand transfer in children. Part 1: technical aspects. J Hand Surg Br. 1996;21(6):723–724. 41. Miyawaki T, Masuzawa G, Hirakawa M, Kurihara K. Bonelengthening for symbrachydactyly of the hand with the technique of callus distraction. J Bone Joint Surg Am. 2002;84(6):986–991. 42. Netscher DT, Lewis EV. Technique of nonvascularized toe phalangeal transfer and distraction lengthening in the treatment of multiple digit symbrachydactyly. Tech Hand Upper Ext Surg. 2008;12(2):114–120. 43. Kessler I, Baruch A, Hecht O. Experience with distraction lengthening of digital rays in congenital anomalies. J Hand Surg Am. 1977;2(5):394–401. 44. Netscher DT. Applications of distraction osteogenesis. Clin Plast Surg. 1998;25(4):561–566. 45. Heitmann C, Levin LS. Distraction lengthening of thumb metacarpal. J Hand Surg Br. 2004;29(1):71–75. 46. Tonkin M, Deva A, Filan S. Long term follow-up of composite non-vascularized toe phalanx transfers for aphalangia. J Hand Surg Br. 2005;30(5):452–458. 47. Carroll RE, Green DP. Reconstruction of the hypoplastic digits using toe phalanges. J Bone Joint Surg Am. 1975;57:727–730. 48. Rank BK. Long-term results in epiphyseal transplants in congenital deformities of the hand. Plast Reconstr Surg. 1978;61(3):321–329. 49. Jones NF. Nonvascularized toe phalangeal bone grafts for congenital anomalies of the hand. J Am Soc Surg Hand. 2004;4:27–34. 50. Netscher DT, Richards WT. Rational treatment for multiple digit congenital absence: case report and distraction lengthening for symbrachydactyly. Ann Plast Surg. 2006;56(2):211–215. 51. Bourke G, Kay SPJ. Free phalangeal transfer: donor-site outcome. Br J Plast Surg. 2002;55(4):307–311.

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CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

52. Garagnani L, Gibson M, Smith PJ, Smith GD. Long-term donor site morbidity after free nonvascularized toe phalangeal transfer. J Hand Surg Br. 2012;37(4):764–774. 53. Gilbert A. Toe transfers for congenital hand defects. J Hand Surg Am. 1982;7(2):118–124. 54. Kay SP, Wiberg M, Bellew M, et al. Toe to hand transfer in children. Part 2: Functional and psychological aspects. J Hand Surg Br. 1996;21(6):735–745. 55. Van Holder C, Giele H, Gilbert A. Double second toe transfer in congenital hand anomalies. J Hand Surg Br. 1999;24(4):471–475. 56. Foucher G, Medina J, Navarro R, et al. Toe transfer in congenital hand malformation. J Reconstr Microsurg. 2001;17(1):1–7. 57. Bellew M, Haworth J, Kay SP. Toe to hand transfer in children: ten year follow up of psychological aspects. J Plast Reconstr Aesthet Surg. 2011;64(6):766–775. 58. Kaplan JD, Jones NF. Outcome measures of microsurgical toe transfers for reconstruction of congenital and traumatic hand anomalies. J Pediatr Orthop. 2014;34(3):362–368. 59. Foucher G, Pajardi G, Lamas C, Medina J, Navarro R. Progressive bone lengthening of the hand in congenital malformations: 41 cases. Rev Chir Orthop Reparatrice Appar Mot. 2001;87(5):451–458. 60. Heo CY, Kwon S, Back GH, Chung MS. Complications of distraction lengthening in the hand. J Hand Surg Eur. 2008;33(5):609–615. 61. Wynne-Davies R, Lamb DW. Congenital upper limb anomalies: an etiologic grouping of clinical, genetic, and epidemiologic data from 387 patients with “absence” defects, constriction bands, polydactyly, and syndactylies. J Hand Surg Am. 1985;10(6 Pt 2):958–964. 62. Saunders JW. The proximo-distal sequence of origin of the parts of the chick wing and the role of the ectoderm. J Exp Zool. 1948;108(3):363–403. 63. Summerbell D. A Quantitative analysis of the effect of excision of the AER from the chick limb-bud. J Embrylol Exp Morph. 1974;32(3):651–660. 64. Knight JB, Pritsch T, Ezaki M, Oishi S. Unilateral congenital terminal finger absences: a condition that differs from symbrachydactyly. J Hand Surg Am. 2012;37(1):124–129. 65. Scotland TR, Galway HR. A long-term review of children with congenital and acquired upper limb deficiency. J Bone Joint Surg Br. 1983;65(3):346–349. 66. Postema K, van der Donk V, van Limbeek J, Rijken RA, Poelma MJ. Prosthesis rejection in children with a unilateral congenital arm defect. Clin Rehabil. 1999;13(3):243–249. 67. Davids JR, Wagner LV, Meyer LC, Blackhurst DW. Prosthetic management of children with unilateral congenital below-elbow deficiency. J Bone Joint Surg Am. 2006;88(6):1294–1300. 68. James MA, Bagley AM, Brasington K, Lutz C, McConnell S, Molitor F. Impact of prostheses on function and quality of life for children with unilateral congenital below-the-elbow deficiency. J Bone Joint Surg Am. 2006;88(11):2356–2365. 69. Flatt AE. The Care of Congenital Hand Anomalies. St.Louis: Mosby; 1977:328–341. 70. Kosher RA, Savage MP, Chan SC. In vitro studies on the morphogenesis and differentiation of the mesoderm adjacent to the apical ectodermal ridge of the embryonic chick limb-bud. J Embryol Exp Morphol. 1979;50:75–97. 71. Naruse T, Takahara M, Takagi M, Oberg KC, Ogino T. Busulfaninduced central polydactyly, syndactyly and cleft hand or foot: a common mechanism of disruption leads to divergent phenotypes. Dev Growth Differ. 2007;49(6):533–541. 72. Ogino T. Teratogenic relationship between polydactyly, syndactyly, and cleft hand. J Hand Surg Br. 1990;15(2):201–209. 73. Zlotogora J. On the inheritance of the split hand/split foot malformation. Am J Med Gen. 1994;53(1):29–32. 74. Duijf PH, van Bokhoven H, Brunner HG. Pathogenesis of split-hand/split-foot malformation. Hum Mol Genet. 2003;12(Spec No 1):R51–R60. 75. Manske PR, Halikis MN. Surgical classification of central deficiency according to the thumb web. J Hand Surg Am. 1995;20(4):687–697.

76. Watari S, Tsugue T. A classification of cleft hands based on clinical findings. Plast Reconstr Surg. 1979;64(3):381–389. 77. Nutt JN, Flatt AE. Congenital central hand defect. J Hand Surg. 1981;6(1):48–60. 78. Tada K, Yonenobu K, Swanson AB. Congenital central ray deficiency in the hand – a survey of 59 cases and subclassification. J Hand Surg Am. 1981;6(5):434–441. 79. Sandzen SC. Classification and functional management of congenital central defect of the hand. Hand Clin. 1985;1(3):483–498. 80. Saito H, Seki T, Suzuki Y, et al. Operative treatments for various types of the cleft hand. Seikeigeka. 1978;29:1551–1553. 81. Ogino T. Cleft hand. Hand Clin. 1990;6(4):661–671. 82. Miura T, Komada T. Simple method for reconstruction of the cleft hand with an adducted thumb. Plast Reconstr Surg. 1979;64(1):65–67. 83. Hentz VR, Littler JW. Congenital anomalies of the upper extremity. In: Converse JM, ed. Reconstructive Plastic Surgery. 2nd ed. Philadelphia: WB: Saunders and Company; 1977:3306–3349. 84. Rider MA, Grindel SI, Tonkin MA, Wood VE. An experience of the Snow–Littler procedure. J Hand Surg Br. 2000;25(4):376–381. 85. Buck-Gramcko D. Cleft hands: classification and treatment. Hand Clin. 1985;1(3):467–473. 86. Ueba Y. Plastic surgery for the cleft hand. J Hand Surg Am. 1981;6(6):557–560. 87. Upton J. Simplicity and treatment of the typical cleft hand. Handchir Mikrochir Plast Chir. 2004;36(2-3):152–160. 88. Upton J, Taghinia A. Correction of the typical cleft hand. J Hand Surg Am. 2010;35(3):480–485. 89. Forman M, Canizares MF, Bohn D, et al. Association of radial longitudinal deficiency and thumb hypoplasia: an update using the CoULD registry CoULD Study Group. J Bone Joint Surg Am. 2020;102(20):1815–1822. 90. Lamb DW. Radial club hand: a continuing study of sixty-eight patients with one hundred and seventeen club hands. J Bone Joint Surg Am. 1977;59(1):1–13. 91. Bayne LG, Klug MS. Long-term review of the surgical treatment of radial deficiencies. J Hand Surg Am. 1987;12(2):169–179. 92. James MA, McCarroll R, Manske PR. Characteristics of patients with hypoplastic thumbs. J Hand Surg Am. 1996;21(1):104–113. 93. Goldfarb CA, Wall L, Manske PR. Radial longitudinal deficiency: the incidence of associated medical and musculoskeletal conditions. J Hand Surg. 2006;31(7):1176–1182. 94. Saunders JW, Gasseling MT. Ectodermal–mesodermal interactions in the origin of limb symmetry. In: Fleischmajer R, Billingham RE, eds. Epithelial–Mesenchymal Interactions. Baltimore, MD: Williams & Wilkins; 1968:78–79. 95. Tickle C. The number of polarizing region cells required to specify additional digits in the developing chick wing. Nature. 1981;289(5795):295–298. 96. Saunders JW. The experimental analysis of chick limb bud development. In: Hinchliff JR, Balls M, eds. Vertebrate Limb and Somit Morphogenesis. Cambridge: Cambridge University Press; 1977:1–24. 97. Johnson RL, Riddle RD, Tabin CJ. Mechanisms of limb patterning. Curr Opin Genet Dev. 1994;4(4):535–542. 98. Johnson RL, Riddle RD, Laufer E, Tabin C. Sonic hedgehog: a key mediator of anterior-posterior patterning of the limb and dorso-ventral patterning of axial embryonic structures. Biochem Soc Trans. 1994;22(3):569–574. 99. Riddle RD, Johnson RL, Laufer E, Tabin C. Sonic hedgehog mediates the polarizing activity of the ZPA. Cell. 1993;75(7):1401–1416. 100. Tickle C, Summerbell D, Wolpert L. Positional signaling and specification of digits in chick limb morphogenesis. Nature. 1975;254(5497):199–202. 101. Goldarb CA, Wustrack R, Pratt JA, Mender A, Manske Thumb function and appearance in thrombocytopenia absent radius syndrome. J Hand Surg Am. 2007;32(2):157–161.

References

102. Oishi SN, Carter P, Bidwell T, Mills J, Ezaki M. Thrombocytopenia absent radius syndrome: presence of brachiocarpalis muscle and its importance. J Hand Surg Am. 2009;34(9):1696–1699. 103. Wall LB, Piper SL, Habenicht R, Oishi SN, Ezaki M, Goldfarb CA. Defining features of the upper extremity in Holt–Oram syndrome. J Hand Surg Am. 2015;40(9):1764–1768. 104. Gluckman E. Bone marrow transplantation in Fanconi’s anemia. Stem Cells. 1993;11(Suppl 2):180–183. 105. Verlinsky Y, Rechitsky S, Schoolcraft W, Strom C, Kuliev A. Preimplantation diagnosis for Fanconi anemia combined with HLA matching. JAMA. 2001;285(24):3130–3133. 106. Josefson D. Couple select healthy embryo to provide stem cells for sister. BMJ. 2000;321(7266):917. 107. James MA, McCarroll Jr HR, Manske PR. The spectrum of radial longitudinal deficiency: a modified classification. J Hand Surg Am. 1999;24(6):1145–1155. 108. Goldfarb CA, Manske PR, Busa R, Mills J, Carter P, Ezaki M. Upper-extremity phocomelia reexamined: a longitudinal dysplasia. J Bone Joint Surg Am. 2005;87(12):2639–2648. 109. Sestero AM, Van Heest A, Agel J. Ulnar growth patterns in radial longitudinal deficiency. J Hand Surg Am. 2006;31(6):960–967. 110. Tupper J. Pollex abductus due to congenital malposition of the flexor pollicis longus. J Bone Joint Surg Am. 1969;51(7):1285–1290. 111. James MA, Green HD, McCarroll R, Manske PR. The association of radial deficiency with thumb hypoplasia. J Bone Joint Surg Am. 2004;86(10):2196–2205. 112. Graham TJ, Louis DS. A comprehensive approach to surgical management of the type IIIA hypoplastic thumb. J Hand Surg Am. 1998;23(1):3–13. 113. Chang PS, Goldfarb CA, Bae DS, et al. Defining features of hand anomalies in severe thumb hypoplasia: a classification modification. J Hand Surg Am. 46(5):422. 2021;e1–422:e5. 114. Auerbach AD. Diagnosis of Fanconi anemia by diepoxybutane analysis. Curr Protoc Hum Genet. 2015;85:8.7.1–8.7.17. 115. Wall LB, Kim DJ, Cogsil T, Goldfarb CA. Treatment of radial longitudinal deficiency: an international survey. J Hand Surg Am. 2021;46(3):241.e1–241.e11. 116. Vuillermin C, Butler L, Lake A, Ezaki M, Oishi S. Flexor digitorum superficialis opposition transfer for augmenting function in types II and IIIA thumb hypoplasia. J Hand Surg Am. 2016;41(2):244–249. 117. Wall LB, Patel A, Roberts S, Goldfarb CA. Long-term outcomes of Huber opposition transfer for augmenting hypoplastic thumb function. J Hand Surg Am. 2017;42(8):657.e1–657.e7. 118. Manske PR, Rotman MB, Dailey LA. Long-term functional results after pollicization for the congenitally deficient thumb. J Hand Surg Am. 1992;17(6):1064–1072. 119. Mo JH, Manske PR. Surgical treatment of type 0 radial longitudinal deficiency. J Hand Surg Am. 2004;29(6):1002–1009. 120. Kotwal PP, Varshney MK, Soral A. Comparison of surgical treatment and nonoperative management for radial longitudinal deficiency. J Hand Surg Eur Vol. 2012;37(2):161–169. 121. Kessler I. Centralisation of the radial club hand by gradual distraction. J Hand Surg Br. 1989;14(1):37–42. 122. Goldfarb CA, Murtha YM, Gordon JE, Manske PR. Soft-tissue distraction with a ring external fixator before centralization for radial longitudinal deficiency. J Hand Surg Am. 2006;31(6):952–959. 123. Nanchahal J, Tonkin MA. Pre-operative distraction lengthening for radial longitudinal deficiency. J Hand Surg Br. 1996;21(1):103–107. 124. VanHeest A, Grierson Y. Dorsal rotation flap for centralization in radial longitudinal deficiency. J Hand Surg Am. 2007;32(6):871–875. 125. Vuillermin C, Wall L, Mills J, et al. Soft tissue release and bilobed flap for severe radial longitudinal deficiency. J Hand Surg Am. 2015;40(5):894–899. 126. Vilkki SK. Distraction and microvascular epiphysis transfer for radial club hand. J Hand Surg Br. 1998;23(4):445–452. 127. Vilkki SK. Vascularized metatarsophalangeal joint transfer for radial hypoplasia. Semin Plast Surg. 2008;22(3):195–212. 128. Manske PR. Index pollicization for thumb deficiency. Tech Hand Up Extrem Surg. 2010;14(1):22–32.

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129. Taghinia AH, Upton J. Index finger pollicization. J Hand Surg Am. 2011;36(2):333–339. 130. Tonkin MA, Boyce DE, Fleming PP, Filan SL, Vigna N. The results of pollicization for congenital thumb hypoplasia. J Hand Surg Eur Vol. 2015;40(6):620–624. 131. de Kraker M, Selles RW, van Vooren J, Stam HJ, Hovius SE. Outcome after pollicization: comparison of patients with mild and severe longitudinal radial deficiency. Plast Reconstr Surg. 2013;131(4):544–551. 132. Netscher DT, Aliu O, Sandvall BK, et al. Functional outcomes of children with index pollicizations for thumb deficiency. J Hand Surg Am. 2013;38(2):250–257. 133. Kollitz KM, Tomhave W, Van Heest AE, Moran SL. Change in hand function and dexterity with age after index pollicization for congenital thumb hypoplasia. Plast Reconstr Surg. 2018;141(3):691–700. 134. Aliu O, Netscher DT, Staines KG, Thornby J, Armenta A. A 5-year interval evaluation of function after pollicization for congenital thumb aplasia using multiple outcome measures. Plast Reconstr Surg. 2008;122(1):198–205. 135. Goldfarb CA, Deardorff V, Chia B, Meander A, Manske PR. Objective features and aesthetic outcome of pollicized digits compared with normal thumbs. J Hand Surg Am. 2007;32(7):1031–1036. 136. Zlotolow DA, Tosti R, Ashworth S, Kozin SH, Abzug JM. Developing a pollicization outcomes measure. J Hand Surg Am. 2014;39(9):1784–1791. 137. Goldfarb CA, Monroe E, Steffen J, Manske PR. Incidence and treatment of complications, suboptimal outcomes, and functional deficiencies after pollicization. J Hand Surg Am. 2009;34(7):1291–1297. 138. Ekblom AG, Laurell T, Arner M. Epidemiology of congenital upper limb anomalies in Stockholm, Sweden, 1997 to 2007: application of the Oberg, Manske, and Tonkin classification. J Hand Surg Am. 2014;39(2):237–248. 139. Damore E, Kozin SH, Thoder JJ, Porter S. The recurrence of deformity after surgical centralization for radial clubhand. J Hand Surg Am. 2000;25(4):745–751. 140. Manske MC, Wall LB, Steffen JA, Goldfarb CA. The effect of soft tissue distraction on deformity recurrence after centralization for radial longitudinal deficiency. J Hand Surg Am. 2014;39(5):895–901. 141. Dana C, Auregan JC, Salon A, et al. Recurrence of radial bowing after soft tissue distraction and subsequent radialization for radial longitudinal deficiency. J Hand Surg Am. 2012;37(10):2082–2087. 142. Goldfarb CA, Klepps SJ, Dailey LA, Manske PR. Functional outcome after centralization for radius dysplasia. J Hand Surg Am. 2002;27(1):118–124. 143. Vuillermin C, Butler L, Ezaki M, Oishi S. Ulna growth patterns after soft tissue release with bilobed flap in radial longitudinal deficiency. J Pediatr Orthop. 2018;38(4):244–248. 144. Wall LB, Ezaki M, Oishi SN. Management of congenital radial longitudinal deficiency: controversies and current concepts. Plast Reconstr Surg. 2013;132(1):122–128. 145. Pike JM, Manske PR, Steffen JA, Goldfarb CA. Ulnocarpal epiphyseal arthrodesis for recurrent deformity after centralization for radial longitudinal deficiency. J Hand Surg Am. 2010;35(11):1755–1761. 146. Froster UG, Baird PA. Upper limb deficiencies and associated malformations: a population-based study. Am J Med Genet. 1992;44(6):767–781. 147. Koskimies E, Lindfors N, Gissler M, Peltonen J, Nietosvaara Y. Congenital upper limb deficiencies and associated malformations in Finland: a population-based study. J Hand Surg Am. 2011;36(6):1058–1065. 148. Swanson AB, Tada K, Yonenobu K. Ulnar ray deficiency: its various manifestations. J Hand Surg Am. 1984;9(5):658–664. 149. Broudy AS, Smith RJ. Deformities of the hand and wrist with ulnar deficiency. J Hand Surg Am. 1979;4(4):304–315. 150. Ogino T, Kato H. Clinical and experimental studies on ulnar ray deficiency. Handchir Mikrochir Plast Chir. 1988;20(6):330–337.

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SECTION VI

CHAPTER 34  • Congenital hand III: Malformations – hand plate: proximodistal and radioulnar

151. Cole RJ, Manske PR. Classification of ulnar deficiency according to the thumb and first web. J Hand Surg Am. 1997;22(3):479–488. 152. Havenhill TG, Manske PR, Patel A, Goldfarb CA. Type 0 ulnar longitudinal deficiency. J Hand Surg Am. 2005;30(6):1288–1293. 153. Johnson J, Omer GE Jr. Congenital ulnar deficiency: natural history and therapeutic implications. Hand Clin. 1985;1(3): 499–510. 154. Ogino T, Kato H. Clinical features and treatment of congenital fusion of the small and ring finger metacarpals. J Hand Surg Am. 1993;18(6):995–1003. 155. Blair WF, Shurr DG, Buckwalter JA. Functional status in ulnar deficiency. J Pediatr Orthop. 1983;3(1):37–40. 156. Carroll RE, Bowers WH. Congenital deficiency of the ulna. J Hand Surg Am. 1977;2(3):169–174. 157. Horii E, Miura T, Nakamura R. Ulnar ray deficiency. A report of a family. J Hand Surg Br. 1994;19(2):244–247. 158. Miller JK, Wenner SM, Kruger LM. Ulnar deficiency. J Hand Surg Am. 1986;11(6):822–829. 159. Kummel W. Die Missbildungen der Extremitaeten durch Defekt, Verwachsung und Ueberzahl. Cassel, Germany: T.G. Fisher; 1895. 160. Ogden JA, Watson HK, Bohne W. Ulnar dysmelia. J Bone Joint Surg Am. 1976;58(4):467–475. 161. Bayne LG. Ulnar club hand (ulnar deficiencies). In: Green DP, ed. Operative Hand Surgery. Vol 1. New York, NY: Churchill Livingstone; 1993:251–548. 162. Gottschalk HP, Bednar MS, Moor M, Light TR. Metacarpal synostosis: treatment with a longitudinal osteotomy and bone graft substitute interposition. J Hand Surg Am. 2012;37(10):2074–2081. 163. Goldfarb CA, Patterson JM, Maender A, Manske PR. Thumb size and appearance following reconstruction of radial polydactyly. J Hand Surg Am. 2008;33(8):1348–1353. 164. Ezaki M. Radial polydactyly. Hand Clin. 1990;6(4):577–588. 165. Baek GH. Duplication. In: Abzug JM, Kozin SH, Zlotolow DA, eds. The Pediatric Upper Extremity. New York, NY: Springer-Verlag; 2015:325–368. 166. Goldfarb CA, Wall LB, Bohn DC, Moen BA, Van Heest AE. Epidemiology of congenital upper limb anomalies in a midwest United States population: an assessment using the Oberg, Manske, and Tonkin classification. J Hand Surg Am. 2015;40(1):127–132. 167. Sesgin MZ, Stark RB. The incidence of congenital defects. Plast Reconstr Surg Transplant Bull. 1961;27:261–267. 168. Temtamy SA, McKusick VA. The genetics of hand malformations. Birth Defects Orig Artic Ser. 1978;14:i-xviii,1–619. 169. Giele H, Giele C, Bower C, Allison M. The incidence and epidemiology of congenital upper limb anomalies: a total population study. J Hand Surg Am. 2001;26(4):628–634. 170. Watson BT, Hennrikus WL. Postaxial type-B polydactyly. Prevalence and treatment. J Bone Joint Surg Am. 1997;79(1):65–68. 171. Woolf CM, Myrianthopoulos NC. Polydactyly in American Negroes and Whites. J Hum Genet. 1973;25(4):397–404. 172. Biesecker LG. Polydactyly: how many disorders and how many genes? 2010 update. Dev Dyn. 2011;240(5):931–942. 173. Wassel HD. The results of surgery for polydactyly of the thumb. A review. Clin Orthop Relat Res. 1969;64:175–193. 174. Zuidam JM, Selles RW, Ananta M, Runia J, Hovius SE. A classification system of radial polydactyly: inclusion of triphalangeal thumb and triplication. J Hand Surg Am. 2008;33(3):373–377. 175. Chung MS, Baek GH, Gong HS, Lee HJ, Kim J, Rhee SH. Radial polydactyly: proposal for a new classification system based on the 159 duplicated thumbs. J Pediatr Orthop. 2013;33(2):190–196. 176. Manske MC, Kennedy CD, Huang JI. Classifications in brief: the Wassel classification for radial polydactyly. Clin Orthop Relat Res. 2017;475(6):1740–1746. 177. Hu CH, Thompson ER, Agel J, et al. A comparative analysis of 150 thumb polydactyly cases from the CoULD registry using the Wassel–Flatt, Rotterdam, and Chung classifications. J Hand Surg Am. 2021;46(1):17–26.

178. Waters PM, Bae DS. Pediatric Hand and Upper Limb Surgery: A Practical Guide. Philadelphia, PA: Lippincott Williams &Wilkins; 2012. 179. Temtamy S, McKusick VA. Synopsis of hand malformations with particular emphasis on genetic factors. Birth Defects Orig Art Ser. 1969;3:125–184. 180. Pritsch T, Ezaki M, Mills J, Oishi SN. Type A ulnar polydactyly of the hand: a classification system and clinical series. J Hand Surg Am. 2013;38(3):453–458. 181. Manske PR. Treatment of duplicated thumb using a ligamentous/ periosteal flap. J Hand Surg Am. 1989;14(4):728–733. 182. Bilhaut M. Guerison d’un pouce bifide par un nouveau procède operatoire. Congr Fr Chir. 1890;4:576–580. 183. Tada K, Yonenobu K, Tsuyuguchi Y, Kawai H, Egawa T. Duplication of the thumb. A retrospective review of two hundred and thirty-seven cases. J Bone Joint Surg Am. 1983;65(5):584–598. 184. Townsend DJ, Lipp EB Jr, Chun K, Reinker K, Tuch B. Thumb duplication, 66 years’ experience—a review of surgical complications. J Hand Surg Am. 1994;19(6):973–976. 185. Dijkman RR, Selles RW, Hülsemann W, et al. A matched comparative study of the Bilhaut procedure versus resection and reconstruction for treatment of radial polydactyly types II and IV. J Hand Surg Am. 2016;41(5):73–83. 186. Baek GH, Gong HS, Chung Ms, Oh JH, Lee YH, Lee SK. Modified Bilhaut–Cloquet procedure for Wassel type-II and III polydactyly of the thumb. J Bone Joint Surg Am. 2007;89(3):534–541. 187. Stutz C, Mills J, Wheeler L, Ezaki M, Oishi S. Long-term outcomes following radial polydactyly reconstruction. J Hand Surg Am. 2014;39(8):1549–1552. 188. Potuijt JWP, Galjaard RH, van der Spek PJ, et al. A multidisciplinary review of triphalangeal thumb. J Hand Surg Eur Vol. 2019;44(1):59–68. 189. Zguricas J, Snijders PJ, Hovius SE, et al. Phenotypic analysis of triphalangeal thumbs and associated hand malformations. J Med Genet. 1994;31(6):462–467. 190. Heutink P, Zguricas J, van Osterhout L, et al. The gene for triphalangeal thumb maps to the subtelomeric region of chromosome 7q. Nat Genet. 1994;6(3):287–292. 191. Haas SL. Three phalangeal thumbs. Am J Roentgenol. 1939;42:677–782. 192. Phillips RS. Congenital split foot (lobster claw) and triphalangeal thumb. J Bone Joint Surg. 1971;53(2):247–257. 193. Miura T, Nakamura R, Horii E, et al. Three cases of syndactyly, polydactyly, and hypoplastic triphalangeal thumb (Haas’s malformation). J Hand Surg Am. 1990;15(3):445–449. 194. Wood VE. Treatment of the triphalangeal thumb. Clin Orthop Relat Res. 1976;120:188–200. 195. Wood VE. Polydactyly and the triphalangeal thumb. J Hand Surg Am. 1978;3(5):436–444. 196. Miura T. Triphalangeal thumb. Plast Reconstr Surg. 1976;58(5): 587–594. 197. Buck-Gramcko D, Behrens P. Classification of polydactyly of the hand and foot. Handchir Mikrochir Plast Chir. 1989;21(4):195–204. 198. Blauth W, Olason AT. Classification of polydactyly of the hands and feet. Arch Orthop Trauma Surg. 1988;107(6):334–344. 199. Zuidam JM, de Kraker M, Selles RW, Hovius SER. Evaluation of function and appearance of adults with untreated triphalangeal thumbs. J Hand Surg Am. 2010;35(7):1146–1152. 200. Hovius SE, Zuidam JM, de Wit T. Treatment of the triphalangeal thumb. Tech Hand Up Extrem Surg. 2004;8(4):247–256. 201. Hovius SER, Potuijt JWP, van Nieuwenhoven CA. Triphalangeal thumb: clinical features and treatment. J Hand Surg Eur Vol. 2019;44(1):69–79. 202. Upton J, Havlik RJ, Coombs CJ. Use of forearm flaps for the severely contracted first web space in children with congenital malformations. J Hand Surg Am. 1996;21(3):470–477. 203. Zuidam JM, Selles RW, Hovius SER. Thumb strength in all types of triphalangeal thumb. J Hand Surg Eur Vol. 2012;37(8):751–754. 204. Zuidam JM, Dees EEC, Lequin MH, Hovius SER. The effect of the epiphyseal growth plate on the length of the first metacarpal in triphalangeal thumb. J Hand Surg Am. 2006;31(7):1183–1188.

 

SECTION VI • Congenital Disorders

35

Congenital hand IV: Malformations – abnormal axis differentiation – hand plate: unspecified axis Christianne A. van Nieuwenhoven

SYNOPSIS

ƒ Syndactyly is one of the most common congenital differences in the upper extremity. It can be classified as incomplete (soft tissue only, not extending to the tip), complete (soft tissue only, extending to the tip), complex (with distal bony union) or complicated (with more than only distal bone fusion). The timing of surgery depends on the fingers involved and the type of syn­ dactyly. In simple digit 3–4 syndactyly there is no hurry, while in a hidden synpolydactyly, release is performed at an earlier stage. When bony fusion accompanies syndactyly (complex/complicated), these fusions should be separated early to prevent asymmetric growth if the fused fingers have different lengths. Creating a web, reconstructing a nailfold, and adding skin to the inner borders of the digits in complete syndactyly are three key elements in the separation of the involved digits. ƒ Clinodactyly is derived from “klineia” (to bend, incline or slope) and “dactylos” (finger, toe). The term is used for a deviated finger in a radio­ ulnar direction. The deviation is caused by an abnormally shaped bone. The middle phalanx of the little finger and the proximal phalanx of the thumb are the most frequently involved. Treatment can be a closed wedge osteotomy, reversed wedge osteotomy or an opening wedge osteotomy with or without bone graft, or a physiolysis in a bracketed epiphysis. ƒ The Kirner deformity is a rare congenital difference of the hand, char­ acterized by a volarly directed curvature of the distal phalanx of usually the little finger. Diagnosis is mostly made after an age of 5 years, and patients might be referred with “missed finger fracture”. Physical ex­ amination and radiographs will underscore the diagnosis with the volar curvature present as well as aberrant physis and diaphysis. Treatment is directed to an aesthetic rather than a functional improvement. ƒ Apert syndrome (acrocephalosyndactyly) is characterized by craniosyn­ ostosis with complex acrosyndactyly of both hands and feet. Common features of the hands in Apert syndrome are: brachyclinodactyly of the thumb, complex syndactyly of index/long/ring finger, symbrachyphalangism, and simple syndactyly of the fourth web. Three different types of hand mal­ formations can be recognized: the flat, “spade” hand (type I), the constricted cupped, “mitten” hand (type II), and the coalesced “rosebud” hand (type III). ƒ The surgical goal in correction of Apert syndrome is correction of clino­ dactyly of the thumb, release of thumb and index or deepening of the first web, and separation of the fingers. If present, fourth–fifth finger metacar­ pal synostoses can be separated. The sequence of these corrections is dependent on the hand type and the experience of the surgeon.

Syndactyly Introduction Syndactyly is one of the most common congenital hand malfor­ mations, with an incidence of approximately 1 in 2000 to 3000 live births. Familial syndactyly is reported in 15–40% of syndac­ tylies.1 It is more common in populations of European descent than in people from African descent. The inheritance pattern is believed to be autosomal dominant, with a variable penetrance and expression, but sporadic syndactyly occurs as well. About 50% of patients have bilateral involvement. Males are more affected than females, varying from 46% to 84% more. The web that is involved varies, as listed here: third web 50%; fourth web 30%; second web 15%, and first web 5%.2 It can appear isolated or in association with other deformities in the upper or lower extremity, or as part of a syndrome (such as Poland syndrome or Apert syndrome). Syndactyly can be associated with polydactyly and/or clefting (as in synpolydactyly, Greig syndrome, oculo­ dentodigital syndrome, and cleft hand), and can be present in the radial fingers in ulnar longitudinal deficiency. In syndromes, the first web and second webs are more likely to be involved. Syndactyly can be classified by clinical description or on an anatomical basis, or with a genetic and molecular approach.1 The most commonly used classification is divided as: incom­ plete (soft tissue only, not extending to the tip), complete (soft tissue only, extending to the tip), complex (with distal bone union) or complicated (with more than only distal bone fusion) (Fig. 35.1). When only skin is involved, as in complete and incomplete syndactyly, the unfortunate term “simple” is used, although treatment of the cutaneous form is not nec­ essarily simple. Complications during the primary operation might result in frequent revisions during growth.

Basic science/disease process In the developing limb bud, fingers become apparent at day 41–43 and are fully separated at day 53.3–5 Apoptosis is

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Figure 35.1  (A) Incomplete, (B) complete, (C) complex, and (D) complicated syndactyly.

needed for separation of the fingers. This process is mediated by BMP-4 (bone morphogenic protein) in a distal to proximal direction, thus explaining the clinical phenotypes.6,7 Current understanding relates these anomalies to differentiation dis­ turbances in the developing hand plate.8

Diagnosis/patient presentation Syndactyly can be present in a large variety of forms, as it is only a descriptive term. The fingers can be normal or anom­ alous; the number of affected fingers can differ, as well as the nature of involvement (Fig. 35.2). In the patient with cutaneous syndactyly, only the soft tis­ sues between the fingers are attached. These skin bridges can vary from supple/wide to tight, influencing the flap possi­ bilities during surgery, and warranting the possible necessity for skin grafting. In the incomplete form, the distal boundary usually ends just before the proximal interphalangeal joint (PIPJ). In complete syndactyly, the nails can range from sep­ arated with full pulps of the affected fingers (see Fig. 35.2) to

conjoined nails with ridges and insufficient pulp for either side (Fig. 35.3). If the involved fingers have normally devel­ oped phalanges, the joints and tendons are mostly normal. If not, like in symbrachydactyly, the tendons and joints might be affected as well. Neurovascular bundles might bifurcate more distally, forcing the surgeon to choose. When fingers are of unequal length, the longest finger will tend to bend and rotate more during growth especially if the distal ends are fused. Complex syndactyly with distal bone fusion involving only two fingers can be recognized by a tapered distal end with inward rotation of the fingers and abnormally ridged or con­ fluent nails (Fig. 35.4). When more fingers are distally fused, they can be flat to very cupped with anomalous nails, abnor­ mal bones with different lengths, and abnormally located, and with insufficiently developed or undeveloped joints. Complicated syndactyly is characterized by an abnormal bone structure inside the syndactyly with fusions, rudimen­ tary bones, missing bones, abnormal joints, and sometimes crossed bones.3

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CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

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Figure 35.2  Incomplete syndactyly on the right hand and complete on the left in the same patient. (A) Pulp and nails are developed in a normal fashion. (B) Lateral nail folds on the syndactylized side are involved.

Figure 35.3  Complex syndactyly. The nails and distal phalanx are rotated and less wide. Pulp and lateral nail folds on the syndactylized side are involved. After release, a rotational defect can be expected.

Patient selection In most patients, except for the very mild incomplete syn­ dactylies, surgical treatment is indicated, and with regard to syndactyly, the question rather is when and how. Timing of treatment is controversial in pediatric hand surgery. The pri­ mary goal of the operation is improvement of hand function, and with that in mind, the operative treatment could be post­ poned until no adverse effects on hand function and motor development are to be expected.

Early indications for surgery are syndactylies between fingers of unequal length; and/or distal bone fusions; and in complex or complicated acrosyndactyly, especially if the thumb is involved. These early indications are to prevent asymmetric growth and/or to create a possibility to grasp when the first web is involved.9 The release can be performed from 6 months onward, especially when multiple webs and two hands are involved. In the simple third web syndactyly, an operation can be safely delayed until an age of 18 months. Some advantages of postponing surgery until 18 months of age are a safer anesthesia,10 decrease of subcutaneous fat allowing easier mobilization of the skin flaps, and a larger hand with less risk of web creep (the hand doubles in size in the first 3 years of life). Contraindications for surgery might be a syndactyly with fully fused phalanges, or with support of only one metacarpal bone (“super digit”). If surgical separa­ tion is possible, it might result in deviation of the fingers and insufficient motion. In complicated syndactylies, the anatom­ ical support for the individual fingers is often not enough to have them function sufficiently following separation. Careful assessment of the maturity of each individual finger is necessary before release of syndactyly is undertaken. The choice to separate can be extremely difficult, especially in symbrachy­ dactyly and synpolydactyly. The biggest challenge is to convince parents or children, who often request to separate these fingers.

Treatment/surgical technique The goal of syndactyly treatment is to create as normal a webspace as possible at the right level in which the sep­ arated fingers are allowed normal movement. Treatment of syndactyly should not only address the key points of adequate release but also in the least number of operations while minimizing complications.10 Release of syndactyly requires separation of conjoined skin and subcutaneous tissue preserving integrity of the neurovas­ cular bundles. Furthermore, coalesced Cleland and Grayson

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Figure 35.4  Complicated syndactyly. (A) Dorsal view. (B) Radiograph

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Figure 35.5  Polysyndactyly. (A) Preoperative radiograph. (B) Postoperative radiograph with removal of the polydactyly combined with the desyndactylization.

ligaments and existing sites of osseous union are divided. On the dorsal side, subcutaneous fat can be removed, but care has to be taken to prevent damage to the neurovascular bundles when defatting volar flaps. The lateral digital flaps should be designed in a zigzag fashion to avoid longitudinal scar contracture. For safety reasons, two adjacent complete syndactylous fin­ gers are not separated at the same time as vascular anatomy can be different, and skin flaps may be limited. In short multiple syndactylous fingers, for instance, dominant digital vessels may only exist on the lateral sides of the conjoined fingers. Sometimes it is necessary to sacrifice one of the vessels in a distal bifurca­ tion. The nerves in these cases can mostly be dissected more

proximally. In young children, bone or cartilaginous fusions can be separated by knife or osteotome.9 Care should be taken to remove a possible hidden polydactyly. Especially in cases where the 4th web is involved, a polydactylous distal phalanx and/or remnant of the middle phalanx may be present (Fig. 35.5).

Creation of a web The web in syndactyly can basically be created by a dorsal flap, a palmar flap or a combination of both. These techniques had already been practiced in the second half of the nineteenth cen­ tury and are still used today. To these techniques have been

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CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

added flaps with slightly different design or flaps more proximal from the dorsum of the hand.11–16 The author’s preference is for a large dorsal flap because the wings will cover partly the lateral side of the proximal phalanx, and the tip is interdigitated on the palmar side, thus preventing linear scars in the web itself as well as on the palmar side. In an effort to prevent skin grafts, dorsal metacarpal flaps have been used to create the web, followed by primary closure of the fingers.15–18 However, these techniques leave a conspicuous scar on the dorsal side of the hand. To prevent web creep in the future, a dorsal flap is used that will cover the newly made web without scars that might inter­ fere during growth. In addition, the appearance of the hand is important. Visible skin grafts on the dorsal hand, that will darken in time, are experienced as aesthetically less pleasing by patients. Therefore, a flap is chosen that will allow for primary closure on the dorsal hand and fingers with the skin grafts at the midlateral sides of the fingers, if grafts are needed at all (Figs. 35.6 & 35.7). For the first web, different kinds of Z-flaps (four-flap, dou­ ble, double-opposing, five-flap) or transposition flaps from the dorsum of the hand and index or thumb are used depending on the width and depth of the created defect following release. Also, pedicled flaps and free flaps have been proposed for the larger defects.19 In the first web, the release of the tight fascia on the first dorsal interosseous muscle in combination with the

Treating the lateral soft tissue defects In syndactyly, the shortage of skin is very often underesti­ mated. In the regular simple syndactyly, skin shortage is at least 36% of the circumference of the finger which is sepa­ rated. Cronin has popularized the zigzag skin separation distal to the flap for web reconstruction.21 The created tri­ angular flaps provide coverage at the proximal interphalan­ geal joint. The triangular flaps can either be fully or partially interdigitated depending on the extent of the skin shortage. In this way, the areas for skin grafting can be diminished and placed on less demanding parts of the fingers. Full-thickness skin grafts (FTSG) are mostly used to cover the defects (see Fig. 35.6). The donor site for skin grafts is traditionally the groin. However, this skin will be more pigmented in time and may grow hair after puberty. Therefore, our preferred donor sites are the elbow or wrist crease, as these scars will

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Figure 35.6 (A–C) Creation of webspace for repair of syndactyly.  

fascia on the adductor muscle is essential to create a deeper web. Sometimes even the insertion of the adductor muscle is shifted more proximally to open the web. Upton has published an excellent overview of all the different flaps for web recon­ struction.3 For incomplete syndactyly, many variations of rotat­ ing Z-flaps have been described for web reconstruction.20

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Figure 35.7  Two years after desyndactylization of an incomplete syndactyly of the third web. (A) Complete view. (B) Detail.

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Figure 35.8  Healing of the pulp by secondary intention. (A) Preoperative. (B) Postoperative.

diminish over time. A longitudinal scar on the volar side of the lower arm, or at the level of the hypothenar area, will give aesthetically unpleasing scars. If a large area needs to be grafted, as in multiple involved webs, or Apert’s hands, the skin in the abdominal skin crease can be harvested exten­ sively over and over, with a scar that will be covered by underwear or swimwear.

Separation of the fingertips If the nails are separately developed in complete syndactyly, the pulp can be separated and the skin advanced to the rim. If the nails are partly fused with a deep furrow and indentation on the pulp side, then simple separation and primary closure is often still possible. If the nails are conjoined, with minimal

ridges, nail wall reconstruction with flaps might be necessary. Buck-Gramcko has introduced the pedicled pulp flaps for nail wall reconstruction from the adjacent finger pulp.22 The disad­ vantage of these flaps is the flattened aspect of the fingertips and involved lateral borders. Alternatives include the use of a thenar flap, but this has the disadvantage that the finger has to be supple to reach the thenar easily and it is a two-stage procedure.23 The defects on the lateral fingertips may alterna­ tively be covered by a FTSG, with an insufficient synonychial reconstruction as a result. With rounded fingertips as a goal and inspired by the sec­ ondary healing in fingertip injuries, the author now leaves the syndactylized sides of the fingers open for secondary healing, with esthetically pleasing results and no synonychial compli­ cations (Fig. 35.8).

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CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

Surgical pearl Syndactyly release: a personal approach When performing a syndactyly release, my personal approach is not limited to a fixed sequence with regard to dissection of the flaps and neurovascular bundle. But there are some key features I would like to share. If you are a beginner, take your time; your patient needs it. The desyndactylization part is the shorter part of the operation, but after identifying the bifurcation of the digital artery, the closing of the flaps takes time. Take your time and “find the Zen” of closing the flaps and placing the full-thickness skin grafts. – Choose a flap dorsally (see Fig. 35.6) that will not give scars in the web. – Draw the middle of the finger dorsally, this will help with positioning the wings of the flap. – Identify the middle of the metacarpal heads. – The distal part of the flap is at two-thirds to three-quarters of the length of the proximal phalanx. – Use big zigzag flaps, the small ones might become full-thickness skin grafts. – Draw lines from the tip of the zigzag to the opposite side, perpendicular to the axis of the finger. This will help in locating the tip of the zigzag on the volar side of the opposite finger. – Mark the volar little V flap more proximal than the location of the actual web. – Start the incision dorsally and elevate the flaps. – The bifurcation of the dorsal vein is a giveaway for the level of the digital artery bifurcation. – Dissect from distal to proximal on the dorsal side, leaving the volar skin intact. – Dissect the arterial bifurcation from the dorsal side; it is easier! – When there is a big discrepancy in finger length, adjust your drawings on the volar side if needed. – Defat only the dorsal skin if necessary. Particularly in synpolydactyly, extra fat is present. – Start closing by approximating the middle of the dorsal flap to the tip of the volar V flap. In that way, the arterial bifurcation is protected. – Finally, take your time with skin grafting. All the time spent will contribute to the ultimate result.

Postoperative care Paraffin gauze is applied on the wounds and grafts, followed by moist dressings creating a wedge between the involved fin­ gers, then synthetic cotton, and an elastic bandage. It is very important to prevent the wedge from dislocating. This might give skin bridging in the web with a synechia as a result. The elbow, forearm, and hand are subsequently covered with a longitudinal adhesive bandage to prevent removing the dressing (Fig. 35.9). It is important to position the elbow at 90° flexion. The general concept among most authors is to perform wound inspection in the first 2 weeks after operation.11,22. However, for the past 5 years, we have introduced a 6-week period of initial dressing and immobilization with less com­ plications and workload for the doctor, and more importantly, for the parents. Only one direct postoperative outpatient clinic contact is needed before starting hand therapy (if necessary). Further immobilization is dependent on surgery for associ­ ated malformations.

Figure 35.9  Author’s preferred bandage used after pediatric hand cases

In complex syndactyly, with a tight synostosis between both distal phalanges, a rotation and deviation of the fin­ gers can be present. In most cases, this will resolve after the child has trained the intrinsics that have not been used before the desyndactylization. A minor distal rotation will still be present, but the deviation will resolve. It is import­ ant to explain this to the parents with regard to managing expectations.

Outcomes, prognosis, and complications The desyndactylization has a low complication rate in gen­ eral, with only 0.3% directly related complications in a cohort of 2047 patients.24 Early complications include graft loss, flap necrosis, infection, or even complete adhesion of the fingers. The latter is mostly due to postoperative infection or insuffi­ cient application of a postoperative bandage. Web creep is the migration of the web more distally during growth and has been reported to be from 0% to 12% depending on the used techniques, the long-term followup, and the variety of included patients. Reoperations have been performed for web creep in up to 8% of patients.18,25–28 Factors influencing web creep include complex syndac­ tyly, inadequate flap design, the use of split-thickness skin grafts (STSGs), secondary healing after graft loss, and infection.29 With regard to skin grafts, while FTSGs have a better skin quality than STSGs, they can also create problems such as graft loss, skin contracture, web creep, hair growth, hyper­ pigmentation, and hypertrophic scarring.16,22,30–34 Skin contrac­ tures from using STSGs are reported to occur in 40%, while this was only 22% when using FTSGs.32 Flexion contractures are reported in a series with long-term follow-up to be 13% and rotation and lateral deviation in 12%. Hair growth when using FTSGs from the groin is reported as being 71%.28 Leaving small areas open between numerous triangular flaps seems to result in less scarring and there is no difference in web creep versus the classical approach. Very rarely, patients will develop a hypertrophic or keloid scar after a syndactyly reconstruction (Fig. 35.10). An incidence of 0.7% (8 patients) has been reported with primary digital enlargement as a risk factor (7 out of 8 patients). Treatment with pressure, corticosteroids, and re-excision was unsuccessful in 8 patients. Two patients treated with methotrexate adjunct to

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Figure 35.10  (A) Keloid after syndactyly release of the third web in a patient with an overgrowth syndrome. (B) Removal of keloid after institution of oral methotrexate. (C) Keloid formation under methotrexate, not caused by a surgical scar but after a superficial abrasion of the first web by a splint and of the fingers by a pressure glove, ironically to prevent keloid formation.

surgery had a near normal healing.35,36 More recently, intra­ lesional bleomycin has been used with promising results.37 Fortunately, this functionally and aesthetically limiting com­ plication is very rare. As a result, specific literature on treating keloids after syndactyly release is very sparse. In a group treated with dorsal metacarpal flaps or extended dorsal interdigital flaps and primary closure, results were bet­ ter, avoiding all the problems with skin grafts.15,16,18 However, in a systematic review comparing skin graft techniques with dorsal metacarpal flaps, no superior outcomes could be attributed to the different techniques. In our opinion, the scar on the dorsal side of the hand is aesthetically displeasing (see Fig. 35.11B). In complex and complicated syndactylies following sep­ aration, rotated and deviated fingers can occur as well as

insufficient functioning of the individual separated fingers. Joint instabilities are also possible and may be underesti­ mated. This is especially true for the polysyndactylies. The joint contracture therefore is a consequence of the initial defor­ mity and difficult to treat. Patients should be followed until the end of growth to detect later problems, such as web creep, scar contractures (Fig. 35.11), and bony deviations due to different types of delta phalanges. Revision of residual syndactyly is often under­ taken, especially at the first web in more complex cases.

Secondary procedures Scar contracture release and re-deepening of webs with or without flaps may be necessary in cases of symbrachydactyly

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SECTION VI

CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

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Figure 35.11  (A) Scar contracture after desyndactylization using a dorsal and volar V-flap. (B) 3 months after web deepening and Z-plasties.

or synpolydactyly, which are not able to extend their involved fingers actively, probably due to an aberrant anatomy of the intrinsic muscles (see Fig. 35.11). In complicated syndactylies, for instance polysyndactyly, ligament reconstructions, osteot­ omies, chondrodesis and arthrodeses may be necessary. These operations are tailored to anatomical differences, active and passive function, and most importantly, the patient’s wishes.

Clinodactyly Introduction Clinodactyly is derived from “klineia” (to bend, incline or slope) and “dactylos” (finger, toe). It is defined as a radio­ ulnar deviation of fingers and lateromedial deviation of toes. The angle of deviation defining clinodactyly varies among authors from >8° to >15°.38,39 Clinodactyly is a symptom and not a disease. It may be isolated, usually involving the little finger, or it may be associated with other congenital malfor­ mations, such as in complex syndactyly of multiple webs, in Down syndrome, Rubinstein–Taybi syndrome, Apert syn­ drome or oculodental digital dysplasia. Burke described 25 syndromes associated with clinodactyly.38 Clinodactyly might inhibit function when the thumb or index finger is involved (Fig. 35.12), or is of cosmetic concern even if only a minor deviation is present in the little finger. The incidence varies from 1% to 19.5%, depending on the degree of angulation used to determine clinodactyly and the population studied.39 Brachymesophalangism is the most frequently encountered form of clinodactyly and probably the most common hand dif­ ference. The articular surfaces of the proximal and distal inter­ phalangeal joints are not perpendicular to the longitudinal

Figure 35.12  Clinodactyly of the index finger combined with a hypoplastic index finger and thumb.

axis due to the abnormally shaped bone. The middle to distal phalanx ratio is 1 : 1, compared with 1.3 : 1 in normal fingers. Secondly, an aberrant growth plate surrounding one side of the abnormally shaped bone in a C-shape results in deviation at the involved joint(s). Names for this type of phalangeal appearance are delta phalanx, triangular bone and longitudi­ nally bracketed epiphysis.39–42 Reports suggest that anomalies

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with a delta phalanx should be clearly distinguished from the classic clinodactyly.43 As it is not clear, the author would reserve clinodactyly for a congenital difference with or without a C-shaped epiphysis. Angulations after injury to the growth plate in an otherwise normal finger or a deviation in a joint following syndactyly release are secondary conditions.

Basic science/disease process Clinodactyly is considered to be a congenital deformity at the phalangeal level. The mode of inheritance of clinodactyly is as an autosomal dominant trait with incomplete penetrance.44 The middle phalanx is ossified later in embryonic develop­ ment than the other phalanges, and latest in the little finger. Brachyphalangism therefore appears most in the little finger, followed by the thumb and ring finger.45 In proximal phalan­ ges, however, aberrant growth plates also occur, resulting in clinodactyly and brachyphalangism, and often in selective fin­ gers. The exact etiology is still unknown.

Diagnosis/patient presentation The most common form of clinodactyly is seen in the middle phalanx of the little finger presenting with an inward deviation of more than 10°. It is mostly isolated and bilateral. A positive family history in these patients is frequent. The little fingers mostly do not scissor over or under the ring finger, making this deformity more an aesthetic than a functional problem. Scissoring can also be prevented by abducting the little finger at the metacarpophalangeal joint. The deviation is clinically not only visible at the PIPJ but also at the DIPJ. Observation in these patients is appropriate, and when deviation increases over time, surgical correction can be considered. In the minority of cases, the little finger has a deviation that inter­ feres with function, since correction in flexion or with abduc­ tion is insufficient. Deviations in these cases are more notable at 30–40° degrees or more, with surgery then being indicated. Some patients will present with pain at the proximal inter­ phalangeal joint, and the inability to control the range of motion in the finger joints, with unstable finger joints. They typically present in the teenage years, when appearance is important to them as well. The author’s personal opinion is that there is an imbalance of the intrinsic tendons across the proximal interphalangeal joint (longer ulnar side, shorter radial side) with insufficient control, possibly subluxating tendons and lack of stability. The middle phalanx acts as an intercalated segment. When correcting these cases, attention should be given to the soft tissues. An X-ray of the finger in two directions will not always elu­ cidate the exact bony anomaly, especially not in very young children where the majority of the phalanx is still cartilage. The contour of the radial side of the phalanx in clinodactyly of the little finger is rounded in those cases, with only a mal­ formed metaphysis and diaphysis visible (Fig. 35.13). The bracketed epiphysis will only show later in development.

Patient selection Clinodactyly in the little finger without functional impair­ ment can be observed and treated if the deviation worsens in time. In those patients where function is impaired, one can decide to correct the deviation. As mentioned, time and

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Figure 35.13  (A) A 2-year-old patient with a clinodactyly of the middle phalanx of the little finger. (B) One year after modified Vickers’ release, note the improved alignment of the phalanges achieved in 1 year without osteotomy.

procedure are much debated. In a more severe deviation with a longitudinally bracketed epiphysis, the author’s approach is resection of the lateral (epi)physis without interposition of fat. In severe deviations, this correction might need to be repeated. This should be communicated with the parents care­ fully. Osteotomy with or without bone graft is used in older patients with no physis or epyphysis left. In syndromic clino­ dactyly, correction of clinodactyly depends very much on the associated abnormalities.

Treatment/surgical technique Despite the high prevalence, the management of clinodactyly is still a topic of debate and controversy. Timing and type of surgical treatment is still debated, with numerous options described:   Opening wedge osteotomy with or without bone graft   Opening wedge   Closing wedge osteotomy   Reversed wedge osteotomy   Dome osteotomy   Physiolysis with or without fat interposition. These osteotomies have all been recommended, and all have a different degree of surgical difficulty. Although a clos­ ing wedge osteotomy is technically relatively simple and advised for moderate and severe deviations (>30°),46 the affected finger will further shorten.45 An open wedge osteot­ omy lengthens the digit, but it is more demanding and may allow the formation of a bony bridge crossing to both phy­ ses, limiting further growth.47 The advantage of the reverse wedge is that no other donor site is necessary. However, with the same disadvantage of a new bony bridge, mimicking the

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CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

bracketed epiphysis. In the open wedge technique and in the reverse wedge technique, the graft is transfixed with either a percutaneous Kirschner (K)-wire or with a suture to hold the bone graft in position. In more severe deviations, bony correction alone will not be enough. Release of soft tissue (fibrous tissue and the skin) on the contracted side will be necessary. The thenar musculature at its insertion on the distal phalanx of the radially deviated thumb should also be released in thumb clinodactyly; other­ wise, recurrence is inevitable. Tightening of soft-tissue struc­ tures, especially collateral ligaments on the convex side, can also be useful. Vickers described the physiolysis procedure, excising the continuous region of the midzone of the eiphysial bracket of the middle phalanx via a lateral incision. The bone is further removed in this region with a burr or curette. The remaining cavity is filled with a fat graft. This allows the phalanx to grow longitudinally with correction of the deviation of the finger during growth. This operation has worked well in younger children (under the age of 6 years), with a mean angular cor­ rection of 18°. In more severe clinodactyly cases with a trap­ ezoidal phalanx (>40°), a mean correction of more than 20° was observed.48,49 In a retrospective comparison of the Vickers’ physiolysis with osteotomy for the primary treatment of clin­ odactyly, the physiolysis group had minimal complications and need for revision, and being more effective in cases with deviations less than 55°.50 Under loupe magnification, via a mid-lateral incision on the radial side, the radial physis and epiphysis is removed after retraction of the neurovascular bundle and elevation of the periosteum. Care must be taken to maintain the proximal and distal physis and to remove the complete midsection of the physis-ephysis. The latter can be performed by dissect­ ing until reaching cancellous bone. Fat can be harvested and interpositioned, however, the author has not used fat grafts, with the same results (see Fig. 35.13). In severe clinodactyly, the physiolysis technique can be combined with a dome oste­ otomy and a Z-plasty to increase the longitudinal correction.

Postoperative care In the physiolysis technique, the operated finger can be casted for approximately 2 weeks. In the osteotomy techniques, 4–6 weeks immobilization is often carried out. After the immo­ bilization period, patients are allowed to mobilize the digit normally.

Outcomes, prognosis, and complications Reversed wedge osteotomies normally heal well. Slight angu­ lations in the dorsal-palmar plane following surgery mostly disappear during growth. In open wedge osteotomies, skin and ligament release can be insufficient, leading to skin tight­ ness and recurrence of angulation. Furthermore, they may lead to more revisions compared to the physiolysis.50 In phys­ iolysis, results in children over 5 years are lessthan in younger children. The angular correction in patients with a deviation more than 40–55° preoperatively is significantly more than compared with fingers deviating less than 40°.49,50 Complications of the bone can be malunion or malrotation. Non-union in children is very rare. Even if the X-ray demon­ strates a non-consolidated osteotomy, the fibrous tissue

bridging the two parts can prevent movement and will have no clinical implications. Furthermore, extensor tendon adhe­ sions can result in a mallet like deformity. In some cases, stiff­ ness of joints can occur. Pain is rarely an issue.

Secondary procedures Secondary procedures mainly address recurrence of the devi­ ation either by insufficient release or excision of the physis or by inadequate soft-tissue release. A new osteotomy and soft-tissue release can be performed.

Kirner deformity Introduction Kirner first described the deformity as a different appearance of the distal phalanx of the little finger51 and it is character­ ized by a volarly directed curvature. The incidence is 0.1–0.3% in clinical populations, with a female predominance 2 : 1.52–54 Kirner deformity is progressive during growth. It is painless, but patients may have a swelling of the distal interphalangeal joint of the involved finger. The nail follows the direction of the curvature of the phalanx in the proximal to distal direction. In addition, the nail might have a curvature on the paronychium as well, giving the nail a watch-glass appearance. Bilateral, symmetrical involvement is common, and involvement of fin­ gers other than the little finger is rare.52 When asymmetrical, the right hand is involved more often.55

Basic science/disease process The etiology of the Kirner deformity is unknown, however, several theories have been proposed to explain the abnormal appearance of the distal phalanx on physical and radiologic examination. Aseptic necrosis, osteochondritis, osteomalacic change and axial distortion, lysis between diaphysis and eph­ ysis are only a few of the proposed etiologies. Abnormal ten­ don insertions distal to the physis with deforming forces were believed to be the cause of the deformity,56,57 as were insertions of the flexor digitorum profundus into the physis itself.58 In recent MRI evaluations in Kirner deformity, the flexor digito­ rum profundus insertion was normal,59,60 there were no signs of infection,60 and an L-shaped physis was noted as a possible cause.59 During the treatment of these MRI-assessed Kirner deformity cases, a cartilaginous layer was found dorsal to the flexor digitorum profundus and volar to the diaphyseal part of the distal phalanx, and histologically proven to be hyaline cartilage in one patient.59 These radiological, surgical and his­ tological findings support the hypothesis that an L-shaped physis, as a volar bracketed epiphysis, influences the growth of the distal phalanx in Kirner deformity.

Diagnosis/patient presentation Typically, patients present after an age of 5 years with a pro­ gressive curvature during growth of the distal phalanx of the little finger. No history of trauma or infection is given at pre­ sentation, although some parents mention minor entrapments of the little finger at a younger age. Patients might be referred

Kirner deformity

A

B

C

835

D

Figure 35.14  (A) Kirner deformity of the little finger. Note the curved distal phalanx at the tip. (B) Clinical aspect of the finger with the distinct curvature. (C) After double osteotomy at the metaphysis and distal tip proximal to the corona. (D) Postoperative improvement of the aspect of the distal phalanx and nail.

of this deformity is important to differentiate it from physeal fractures, infections, and mallet fingers.

Patient selection Kirner deformity of the little finger typically goes without functional impairment and can be observed and treated if the curvature worsens in time, and if the patient finds it aestheti­ cally displeasing. No normal appearance of the nail and distal phalanx will be achieved. This should be communicated with the parents carefully. Figure 35.15  X-ray of a young child with a Kirner deformity.

Treatment/surgical technique

as a fingertip injury after a mild trauma, with the deformity being noticed only at that point in time. At inspection the volar curvature of the little finger is noted without signs of previous trauma or infection. Physical exam­ ination might reveal an extension lag of the distal interphalan­ geal joint, and together with the aspect of the distal phalanx might look like a mallet finger (Fig. 35.14). Radiographs will reveal the abnormal curvature of the dis­ tal phalanx with a widened, L-shaped physis and a narrow diaphysis (Fig. 35.15). Distal interphalangeal joint subluxation might be noticed, as is a hyperextension in this joint despite the mallet-like appearance on physical examination. The site of curvature in Kirner deformity can be described and depends on age: at the ephiphyseal line in young children, the diaphysis in teenagers, and at the distal tip in patients older than 15 years.52,55 Generally, the deformity results in little functional deficit, and treatment can be directed to restoration of the appearance. Several treatment options have been introduced. Awareness

The treatment goal is to decrease the curvature of the distal phalanx appearance. Treatment starts with removal of the nail plate followed by a midlateral/midaxial incision on the ulnar side of the little finger. Exposure on the volar surface of the distal phalanx is obtained by retracting the flexor dig­ itorum profundus tendon. Just volar to the distal phalanx and proximal to the tendon insertion, a fibrous tissue can be found and removed. This is the volar part of the bracketed L-shaped epiphysis as described before. In children younger than 10 years, one could argue to treat those patients with only this Vickers’ release as treatment for the Kirner defor­ mity, without osteotomies that might cause nailbed injury and thus introducing a new aesthetic aberrant feature to the nail (Fig. 35.16). When the curvature is severe or a patient is not likely to outgrow the curvature, one or two osteotomies can be performed with a 2 mm osteotome. Care should be taken to only involve 75% of the volar phalanx in the osteot­ omy, ensuring the integrity of the dorsal cortex and nailbed. The position of the osteotomies is dependent on the type of curvature. After the osteotomies are performed, the dorsal

836

SECTION VI

CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

Apert hand Introduction

A

B

Figure 35.16  Drawing of the Vickers’ technique for Kirner deformity. (A) Correction of the distal phalanx with Vickers’ technique by removing the fibrous tissue (in red) on the volar proximal side of the bone, and dorsal to the flexor digitorum profundus. The dotted red lines depict the osteotomies as performed in direct bony correction. (B) After direct bony correction with osteotomies.

cortex is straightened gently, leaving the dorsal cortex, peri­ osteum, and nail bed intact. An axial 6-mm K-wire is used for bony fixation. In small children, an above-elbow plaster is given for 6 weeks, since finger-based splints will be lost or swallowed. In older patients, a finger-based splint can be considered.

Postoperative care Immobilization is necessary after osteotomy and K-wire fix­ ation. Because the surface of the bone that needs to heal is sparse, K-wire fixation will be needed for 6 weeks. After 6 weeks, the K-wire is removed. During the 6 weeks of K-wire fixation, the hand is immobilized to prevent micro-move­ ments of the K-wire and prevent possible infection. For K-wires immobilizing the finger joints, children are very for­ giving with regard to stiffness, unlike adults.

Outcomes, prognosis, and complications The success is much related to the expected outcome of the patient. In these cases, where aesthetics is the main problem, careful explanation of the achievable goals is the mainstay of a successful treatment. Other complications include pin track infection, nailbed injury, and insufficient relief of the curvature of the distal phalanx.

Secondary procedures When corrected insufficiently, or in severe curvatures, a sec­ ond osteotomy might be necessary.

Apert syndrome is also called acrocephalosyndactyly type I syndrome and is characterized by craniosynostosis combined with acrosyndactyly together with other important distin­ guishing features. Except for the craniosynostosis, the mid­ face is underdeveloped and retruded, a highly arched palate or cleft palate may occur, with dental and ocular abnormal­ ities, hearing loss and/or inner ear anomalies, and airway obstruction. Most patients will have neurological anomalies. In contrast to very early reports, the neurodevelopmental out­ comes may be more promising since surgical management of the skull has improved and is accessible at an earlier stage for patients.61 Additional distinguishing features are cardiovas­ cular abnormalities, gastrointestinal issues, anomalies of the genitourinary tract, and skin differences. The hand difference consists of complex syndactyly and symphalangism (congenital ankylosis of the proximal phalan­ geal joints) of the fingers of both hands and radial clinodac­ tyly of the thumbs in a symmetrical way. Common features of the hands in Apert syndrome are: brachyclinodactyly of the thumb, complex syndactyly of index/long/ring finger, sym­ brachyphalangism, and simple syndactyly of the fourth web. Three different types of hand malformations can be recog­ nized: the flat, “spade” hand (type I), the constricted cupped, “mitten” hand (type II), and the coalesced “rosebud” hand (type III). The little finger is usually the best finger with a sim­ ple syndactyly at the fourth web. Both feet are also affected in a similar fashion. The craniofacial features in Apert syndrome consist of a variety of skull deformities originating from premature clo­ sure of the coronal and often lamboid sutures of the skull, and a midface hypoplasia. These deformities can lead to a high incidence of intracranial pressure and obstructive sleep apnea. Craniofacial operations include early cranial vault expansion and if indicated, midface advancement is performed later in life. Other differences are oily skin, hyperhydrosis, decreased eyesight and hearing, and increased strabismus. In the lower extremity, the hips become increasingly stiff over time. The knees demonstrate mild to moderate genu valgum. The feet have simple and complete syndac­ tyly. If present, medial polydactyly is mostly at the base of the first metatarsal. Furthermore, a polydactyly of the sec­ ond toe might be present. The foot deformity causes shoe fitting problems and an abnormal gait, and possible pain due to callouses over the prominent second and third meta­ tarsal heads. The acrosyndactyly of the feet is encountered less, in contrast to the hands. However, the problems caused by the foot deformity in Apert disease may be restricting to patients. In recent years, treatments have been introduced to improve the aspect of the foot by desyndactylization in the less severe cases, and osteotomies to address the pronounced metatarsals at the ball of the foot and the malformation of the calcaneal bone. In managing all of the different features in Apert syndrome, it is important that the comprehensive care is provided by spe­ cialized teams with a holistic and lifelong approach, including psychosocial support, with improvement of the quality of life for children and adults with Apert syndrome as a goal.

Apert hand

History Apert, a French physician in Paris, reported nine collected cases in 1906, but probably Wheaton was the first to describe it fully in 1894.62

Table 35.1  Apert syndrome: common features of hands in Apert syndrome

Thumb

Digit 2, 3, 4

Digit 5

Type I

Brachyclinodactyly Incomplete 1st web syndactyly

Symphalangism Complex syndactyly

Simple (incomplete) syndactyly of 4th web or separate digit MC 4–5 synostosis possible

Type II

Brachyclinodactyly Simple (incomplete) syndactyly

Symphalangism Complex syndactyly

Complete syndactyly Duplication P3 possible MC 4–5 synostosis possible

Type III

Brachydactyly Complex syndactyly Paronychial infections Skin maceration

Symphalangism Complex syndactyly Paronychial infections Skin maceration

Complete syndactyly Duplication P3 possible MC 4–5 synostosis possible

Basic science/disease process The birth prevalence of Apert syndrome ranges from 1 : 40,000 to 1 : 160,000 live births, the lowest incidence being in Hispanics and the highest in Asians. Males and females are equally affected.63,64 In the author’s series, the male to female ratio was 1.5 : 1. A relation between advanced pater­ nal age and increased incidence of Apert syndrome has been reported.65 Apert syndrome is caused by a mutation in the gene encod­ ing fibroblast growth factor receptor-2 (FGFR 2). The gene map locus is 10q26. Two mutations are well recognized and are related to substitutions at two amino acid positions: patho­ genicp.Pro253Argvariant and pathogenicp.Ser252Trpvariant in FGFR2. More severe involvement of the hand and foot is mostly related to the Pro253Argvariant. In our series, nearly all type III Apert hands were attributed to this mutation, how­ ever studies also suggest no clear correlation.66 Most cases are sporadic, but autosomal dominant inheritance has been reported.67,68

Diagnosis/patient presentation Apert syndrome individuals have a normal intellect or mild intellectual disability, however some will have moderate to severe intellectual disability.69–71 Children raised within the family have better outcomes than institutionalized children.69 Since management of Apert syndrome improved over the past years, the neurodevelopmental outcome might be more prom­ ising and dependent on the timing of the first craniectomy and the presence or absence of structural brain malformations.61 With regard to skeletal development, there is characteris­ tically a progressive fusion of several bones, including bones of the skull, hands and feet with involvement of the carpus and tarsus, and cervical vertebrae.72 The hands and feet draw attention since they are most visible, however, all joints are involved, with decreased ambulation and limitations in daily life as a result. When focusing on the upper extremity, shoulder motion is restricted and will decrease with age. At birth, patients mostly present with a marked deltoid muscular atrophy. They have an anterior subluxation of the humeral head with a glenohu­ meral dysplasia.73 This will lead to a decreased anteflexion and abduction of the shoulder, limiting performance of over­ head tasks.74 The elbow differences can differ more extensively between patients. The function can be slightly decreased but mostly does not worsen over time.73 Upton classified the Apert syndrome hand into type I, II, and III for ease of clinical decision-making (Table 35.1). In the type I hand there is a radially deviated short thumb, and there­ fore, a shallow first web. The index, long, and ring fingers display complete or complex syndactyly. The little finger is attached by a simple complete or incomplete syndactyly and can mostly move at the distal interphalangeal joint. The meta­ carpophalangeal joints have a restricted but adequate range of motion.

837

MC, Metacarpal; P, distal phalanx.

In the type II hand, the thumb is radially deviated and has an incomplete or complete simple syndactyly with the index. The index, long, and ring fingers are distally fused at phalan­ geal level. Due to this osseous fusion, a curve in the palm with divergent metacarpals is created. The little finger is attached to the ring with a mostly complete but simple syndactyly. In the type III hand (“rosebud” hand) the thumb, index, long, and ring are distally fused either cartilaginous or bony attachments. The thumb can be very difficult to identify sep­ arately from the index. The little finger is united to the ring by simple complete syndactyly. The nails can be confluent or have ridges indicating the distal finger underneath. Proximal synostosis at the base of the fourth–fifth metacarpal can be present, as well as carpal fusions.75 In our series of 66 patients, the ratio of type III : type II : type I hand was 4:3:3, although Upton reported that type III is the most uncommon. In addition to the description of the different types, in the type III hand, fingernails growing through surrounding skin frequently cause tedious paronychial infections. The flexion creases are shallow or absent at the fingers, except for the distal interphalangeal joint of the little finger. Dimples on the dorsum indicate the metacarpophalangeal joints. Distal to the metacarpophalangeal joints, neurovascular structures can vary considerably in branching, or are absent. Distal in the hand, tendons can have a different shape and course, and will be flatter than normal. In most cases, the pulley system is either hypoplastic or absent. Regarding the thumb, adduction, palmar abduction, and flexion are mostly present. The first dorsal interosseous is hypertrophic and fan-shaped, extend­ ing to the delta phalanx of the thumb in the more severe types. The abductor pollicis brevis muscle (APB) is anomalous as it inserts into the radial aspect of the distal phalanx of the thumb

838

SECTION VI

CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

causing radial deviation.76 Lumbricals, if present, act as meta­ carpophalangeal joint flexors. The hypothenar muscles are present and normal. The proximal phalanx of the thumb is abnormal and trian­ gular-shaped. The interphalangeal joint and the carpometa­ carpal joint have little motion, while the metacarpophalangeal joints are mobile. With skeletal maturity, the interphalangeal joint fuses after first being segmented. The distal phalanx and nail matrix are broad.77,78 Symphalangism at the proximal interphalangeal joints of the index, long, and ring finger is a persistent finding. In border digits (the index and the little finger), the epiphyseal growth plate can be aberrant at the metacarpophalangeal joint, causing lateral deviation following separation. The severity of the deformity of the feet does not correlate to the hands. Blauth described three types of syndactyly in Apert feet, with type III being the most common.79 However, polydactyly has not been included, and in situations where syndactyly and polydactyly of the feet need to be described, the Rotterdam foot classification introduced by Burger can be used.80 The feet are involved with polydactyly of the hallux or second toe and syndactyly of mostly the second to fourth web, but all webs may be involved. Synostosis of the tarsals and

metatarsals will evolve in time. The first metatarsal is short with a shift in weight-bearing from the first metatarsal to the second. The second to fourth metatarsals are longer than the first metatarsal and are forced to grow in a plantar fashion, causing a bulge on the plantar metatarsal phalangeal level with callus formation. These progressive foot deformities will lead to pain and limitations of daily activities and the neces­ sity to wear adjusted footwear.81

Patient selection Many articles have been published on treatment timing in Apert syndrome.75,77,82–84 Most advocate to diminish the num­ ber of operations by releasing as many fingers as possible in one session. The way this is accomplished varies among authors (Table 35.2).

Treatment/surgical technique Separation of the thumb and fingers, correction of deviated thumbs, and mobilization of the little finger in as few oper­ ations as possible is the surgical goal. The author’s preferred method is illustrated in Table 35.3 and Figs. 35.17 and 35.18.

Table 35.2  Reported treatments in Apert syndrome

Upton75

Fearon82

Guero84

Chang83

Bilateral 1–6 months of age

Both hands and feet 9–12 months of age

Bilateral 9–10 months of age

Bilateral 6–15 months of age

1st webspace with dorsal skin flap Resection index 4th web release Incision of nailfold/macerations

Deepening of 1st web and 3rd web one hand Release of 2nd and 4th web on other hand Similar releases on feet

1st web release with Buck– Gramcko flap Release APB Release of 4th web for a three-fingered hand Release of 3rd web for a four-fingered hand

Release of border digits

Within 6 months of 1st stage Unilateral Before 3 years of age

3 months after 1st stage

Unilateral; 6 months between unilateral stages

Unilateral Before age 2; 3 months between unilateral stages

Long-ring release Re-deepening 1st-web

Release of the remaining webs on both feet and hands

In four-fingered hand: release of 4th web In three-fingered hand: release of 2nd web, removal of 4th ray

Release of middle digit mass Excision of bone, leaving three digits Opening wedge osteotomy thumb clinodactyly

Two-stage syndactyly release of all fingers and toes

Three/four fingers and thumb

Three/four fingers and thumb

First stage

Second stage

Goal

Additional 4–6 years

9–12 years

Metacarpal synostosis correction Thumb clinodactyly correction Re-deepening 1st web

Dorsal osteotomies at PIP for anatomic position Correction radial clinodactyly Addressing foot disorders if present

APB, Abductor pollicis brevis; PIP, proximal interphalangeal joint.

Apert hand

839

Table 35.3  Apert syndrome – author’s preferred treatment

Stage

Age

Procedures

Types

First

6 months

Both hands Thumb separation with tailor made dorsal flap with straight line incision distally 1st web deepening with double-opposing Z-plasty Index amputation if necessary 2nd and 4th web separation with volar and dorsal flap with straight line incision distally Longitudinal osteotomy of the acrosyndactyly of the middle and ring finger Possibly 2nd, 3rd, 4th distal digit separation with volar and dorsal flap Skin release radial side thumb with Z-plasty and release of APB Dome osteotomy of clinodactyly of thumb

All types Type II and III Type I Only severe type III All types All types Only type I Type I, II, III Type I, II, III

Second

9 months

Both hands 3rd web separation with volar and dorsal flap with straight line incision distally Re-deepening of the 1st web Synostosis MC 4–5

In all types In all types If necessary, in all types If present

APB, Abductor pollicis brevis; MC, metacarpal.

A

B

C

Figure 35.17  Type II Apert hand after stage I: syndactyly release of the second and fourth web and correction of the thumb. (A) Large dorsal V-flap with straight incision to distal. (B) Large volar V-flap with straight incision to distal. (C) The straight incision on the volar side is connected to the incision on the dorsal side without Buck–Gramcko flaps.

Separation of fingers In general, dorsal flaps are used to create webs. For the remain­ ing distal syndactyly, fingers can be separated by zigzag inci­ sions, or straight incisions in the fingers with symphalangism. Nail walls can be reconstructed with flaps from the adjacent finger pulp. In type I hands, all webs can be addressed in one operation, further decreasing the number of operations. In type II and III hands, during the desyndactylization of the sec­ ond and fourth web, it is possible to do an osteotomy of the bony fusion of the remaining web(s). This will lead to a wider and flattened nail complex, facilitating the following desyn­ dactylization and giving better results (Fig. 35.19). The residual defects are covered with skin grafts. Chang only used local flaps and skin grafts, while Zuker et al. and Kay use groin flaps for the central digits and the first web, respectively.19,83 Often, further corrections are necessary to deepen webs.

Habenicht uses small external fixators to transversely dis­ tract the complicated and complex syndactyly of the central fingers, with separation of the distal bone fusions. The created skin is used for coverage of the defects instead of skin grafts.85 Other methods such as Silastic sheets and tissue expanders to separate fingers have been abandoned.86

Thumb and first web A well-separated thumb is crucial in these hands. In a shallow first web (in the type I hand), a four- or five-flap Z-plasty can be utilized. In a complete or nearly complete syndactyly (in the type II hand), a large dorsal flap is used to create a first web.22 Tight fascia around the adductor muscle is released to open up the first web. Preferably, a hand with four fingers and a thumb is created. In the type III hand, however, it can be necessary to sacrifice the index finger to create a useful first web with a dorsal flap.87

840

SECTION VI

CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

B

A

Figure 35.18  (A) After separation and positioning of the volar and dorsal V-flap. (B) Skin graft at either side. The lateral sides of the distal part of the distal phalanx are not covered by a skin graft, but will heal by secondary intention, thus improving the aspect of the pulp.

A

B

Figure 35.19  (A) Type II Apert hand with angulated nails and distal phalanges in the acrosynostosis of the third and fourth finger. (B) Two months after a longitudinal osteotomy of the acrosynostosis performed in stage I. The nails are wider and the angulation flattens.

Clinodactyly of the thumb is often corrected in the sec­ ond stage because of more skeletal growth by then. The tight skin on the radial side at interphalangeal joint level can be released with a Z-plasty. The APB is released from the distal phalanx when treating the clinodactyly. The triangular bone is treated as in clinodactyly with an opening wedge osteotomy or a dome osteotomy. There is a tendency to treat the thumb

clinodactyly and APB release at the first operation, interfering the pull of the APB on the deviation of the thumb as soon as possible. Dao et al. considered the abnormal radiodistal insertion of the APB responsible for the deviation of the thumb and released the APB muscle and tendon distally without per­ forming a corrective osteotomy.76 In the type III hand, the

Apert hand

841

thumb is short and has less bone volume distally, therefore, an opening wedge osteotomy is performed, secured by a lon­ gitudinal K wire. Due to the increased bony healing in Apert disease, this will suffice.

can be used. Despite the skin abnormality in Apert syndrome, no additional problems are seen using this bandage regimen. In the postoperative treatment of feet, a walking cast is pro­ vided directly after the operation for 3–4 weeks.

Additional procedures

Outcomes, prognosis, and complications

Synostosis, if present, at the proximal fourth–fifth metacar­ pal should be separated early to improve function of the fifth ray in this rather stiff hand. Aberrant growth plates at the index and little finger can cause clinodactyly after separation. Osteotomies may be needed secondarily to correct this devi­ ation. Even without aberrant growth plates, the border dig­ its tend to deviate. Lengthening procedures of especially the thumb and the fingers are performed to improve appearance and also function in type III hands with short thumbs.

Hand function is improved the most if the thumb is separated together with separation of the little finger, as it is the best finger. In this way, the thumb can adduct powerfully with the ulnar proximal part of the thumb. Also, a sort of tripod pinch with the more mobile little finger is ensured. Movement of the fingers, except the little finger, is only at the metacarpo­ phalangeal joint. Lengthening of the thumb and separation of the remaining fused fingers does not improve function con­ siderably; however, it is sometimes requested to improve the appearance.

Feet The treatment of the feet is still much debated, and it is only for the last few years that it has received the attention it deserves with regard to surgical treatment. Where previous treatment was focused on orthopedic shoes, today, attention is given to the syndactyly, the plantar protrusion of the metatar­ sal heads of the second to fourth toe, the short first metatarsal, and the hindfoot differences. Based on personal experience, only a desyndactylization of the first web is performed if the hallux is prohibiting the “normal” growth of the second toe. Furthermore, an osteotomy of the metatarsals protruding into the plantar foot is an easy operation to perform, with less effort for the patient but with a huge benefit with regards to improvement in ambulation. With all the new experience on treatment of the foot, only limited data is available.88 But with increasing data, more information can be shared on how to help Apert patients have less foot pain, in conventional or normal-looking shoes, for longer ambulatory distances.

The hyperhidrosis and oily skin make the skin grafts prone to maceration, skin slough, and even infection. Barot and Caplan reported a 22% partial skin graft loss.89 Guero operates on these children in winter, to diminish sweaty bandages and casts.77 Secondary procedures for web contractures are there­ fore common. The revision rate for secondary web contracture varies among authors from 3% to 18%.77,82,83,89 Revising web contractures depends very much on the surgeon’s idea of con­ tracture and the functional gain in Apert hands after release. Patients rarely complain of web contractures. Other described interventions are amputation of a finger due to limited open­ ing of the first webspace or because of ankylosis.

Secondary procedures Secondary operations include: deepening with advancement of the primary flap or skin grafting the newly created defect   Wedge osteotomies of the border digits as necessary to correct the deviation following separation due to partial closure of the epiphyseal plate   Extra thumb lengthening is sometimes required in very short thumbs in type III hands.   Web

Postoperative care Postoperatively, the hand is carefully dressed and is covered by a small plaster splint. Over this plaster, a completely cover­ ing adhesive bandage is applied preventing elbow extension. At the outpatient clinic 6 weeks later, the hand is inspected and if wound healing is achieved after 6 weeks, the hand(s)

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References

References 1. Temtamy SA, McKusick VA. The genetics of hand malformations. Birth Defects Orig Artic Ser. 1978;14(3):i–xviii, 1–619. 2. Dobyns JH, Doyle JR, Von Gillern TL, Cowen NJ. Congenital anomalies of the upper extremity. Hand Clin. 1989;5(3):321–342; discussion 39–40. 3. Upton J. Failure of differentiation and overgrowth. In: Neligan PC, ed. Plastic Surgery. 2nd ed. Philadelphia, PA: Saunders Elsevier; 2006:265–322. 4. Sadler TW. Langman's Medical Embryology. 8th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2000. 5. Streeter GL. Developmental horizons in human embryos; a review of the histogenesis of cartilage and bone. Contrib Embryol. 1949;33(213-221):149–168. 6. Bakrania P, Ugur Iseri SA, Wyatt AW, et al. Sonic hedgehog mutations are an uncommon cause of developmental eye anomalies. Am J Med Genet A. 2010;152A(5):1310–1313. 7. Malik S. Syndactyly: phenotypes, genetics and current classification. Eur J Hum Genet. 2012;20(8):817–824. 8. Ogino T. Teratogenic relationship between polydactyly, syndactyly and cleft hand. J Hand Surg Br. 1990;15(2):201–209. 9. Buck-Gramcko D. Progress in the treatment of congenital malformations of the hand. World J Surg. 1990;14(6):715–724. 10. Dao KD, Shin AY, Billings A, Oberg KC, Wood VE. Surgical treatment of congenital syndactyly of the hand. J Am Acad Orthop Surg. 2004;12(1):39–48. 11. Smith PJ, Harrison SH. The “seagull” flap for syndactyly. Br J Plast Surg. 1982;35(3):390–393. 12. Bauer TB, Tondra JM, Trusler HM. Technical modification in repair of syndactylism. Plast Reconstr Surg (1946). 1956;17(5):385–392. 13. Niranjan NS, Azad SM, Fleming AN, Liew SH. Long-term results of primary syndactyly correction by the trilobed flap technique. Br J Plast Surg. 2005;58(1):14–21. 14. Colville J. Syndactyly correction. Br J Plast Surg. 1989;42(1):12–16. 15. Hsu VM, Smartt Jr JM, Chang B. The modified V–Y dorsal metacarpal flap for repair of syndactyly without skin graft. Plast Reconstr Surg. 2010;125(1):225–232. 16. Sherif MM. V–Y dorsal metacarpal flap: a new technique for the correction of syndactyly without skin graft. Plast Reconstr Surg. 1998;101(7):1861–1866. 17. Ekerot L. Correction of syndactyly: advantages with a non-grafting technique and the use of absorbable skin sutures. Scand J Plast Reconstr Surg Hand Surg. 1999;33(4):427–431. 18. Ekerot L. Syndactyly correction without skin-grafting. J Hand Surg Br. 1996;21(3):330–337. 19. Kay S, Coady M. The role of microsurgery and free tissue transfer in the reconstruction of the paediatric upper extremity. Ann Acad Med Singap. 1995;24(4 Suppl):113–123. 20. Foucher G, Medina J, Navarro R, Pajardi G. [Value of a new first web space reconstruction in congenital hand deformities. A study of 54 patients]. Chir Main. 2000;19(3):152–160. 21. Cronin TD. Syndactylism: results of zig-zag incision to prevent postoperative contracture. Plast Reconstr Surg (1946). 1956;18(6): 460–468. 22. Buck-Gramcko D. Congenital malformations. J Hand Surg Br. 1990;15(2):150–152. 23. van der Biezen JJ, Bloem JJ. The double opposing palmar flaps in complex syndactyly. J Hand Surg Am. 1992;17(6):1059–1064. 24. Canizares MF, Feldman L, Miller PE, Waters PM, Bae DS. Complications and Cost of syndactyly reconstruction in the United States: analysis of the Pediatric Health Information System. Hand (N Y). 2017;12(4):327–334. 25. Jose RM, Timoney N, Vidyadharan R, Lester R. Syndactyly correction: an aesthetic reconstruction. J Hand Surg Eur Vol. 2010;35(6):446–450. 26. Frick L, Fraisse B, Wavreille G, Fron D, Martinot V. [Results of surgical treatment in simple syndactyly using a commissural dorsal flap. About 54 procedures]. Chir Main. 2008;27(2-3):76–82.

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27. D’Arcangelo M, Gilbert A, Pirrello R. Correction of syndactyly using a dorsal omega flap and two lateral and volar flaps. A long-term review. J Hand Surg Br. 1996;21(3):320–324. 28. Lumenta DB, Kitzinger HB, Beck H, Frey M. Long-term outcomes of web creep, scar quality, and function after simple syndactyly surgical treatment. J Hand Surg Am. 2010;35(8):1323–1329. 29. Hutchinson DT, Frenzen SW. Digital syndactyly release. Tech Hand Up Extrem Surg. 2010;14(1):33–37. 30. Eaton CJ, Lister GD. Syndactyly. Hand Clin. 1990;6(4):555–575. 31. Toledo LC, Ger E. Evaluation of the operative treatment of syndactyly. J Hand Surg Am. 1979;4(6):556–564. 32. Brown PM. Syndactyly – a review and long term results. Hand. 1977;9(1):16–27. 33. Deunk J, Nicolai JP, Hamburg SM. Long-term results of syndactyly correction: full-thickness versus split-thickness skin grafts. J Hand Surg Br. 2003;28(2):125–130. 34. Percival NJ, Sykes PJ. Syndactyly: a review of the factors which influence surgical treatment. J Hand Surg Br. 1989;14(2):196–200. 35. Muzaffar AR, Rafols F, Masson J, Ezaki M, Carter PR. Keloid formation after syndactyly reconstruction: associated conditions, prevalence, and preliminary report of a treatment method. J Hand Surg Am. 2004;29(2):201–208. 36. Tolerton SK, Tonkin MA. Keloid formation after syndactyly release in patients with associated macrodactyly: management with methotrexate therapy. J Hand Surg Eur Vol. 2011;36(6): 490–497. 37. Khan HA, Sahibzada MN, Paracha MM. Comparison of the efficacy of intralesional bleomycin versus intralesional triamcinolone acetonide in the treatment of keloids. Dermatol Ther. 2019;32(5): e13036. 38. Burke F, Flatt A. Clinodactyly. A review of a series of cases. Hand. 1979;11(3):269–280. 39. Wood VE, Flatt AE. Congenital triangular bones in the hand. J Hand Surg Am. 1977;2(3):179–193. 40. Jaeger M, Refior HJ. The congenital triangular deformity of the tubular bones of hand and foot. Clin Orthop Relat Res. 1971;81: 139–150. 41. Theander G, Carstam N. [Longitudinally bracketed diaphysis]. Ann Radiol (Paris). 1974;17(4):355–360. 42. Choo AD, Mubarak SJ. Longitudinal epiphyseal bracket. J Child Orthop. 2013;7(6):449–454. 43. Jones GB. Delta Phalanx. J Bone Joint Surg Br. 1964;46:226–228. 44. Hersh AH, Demarinis F, Stecher RM. On the inheritance and development of clinodactyly. Am J Hum Genet. 1953;5(3):257–268. 45. Al-Qattan MM. Congenital sporadic clinodactyly of the index finger. Ann Plast Surg. 2007;59(6):682–687. 46. Ali M, Jackson T, Rayan GM. Closing wedge osteotomy of abnormal middle phalanx for clinodactyly. J Hand Surg Am. 2009;34(5):914–918. 47. Light TR, Ogden JA. The longitudinal epiphyseal bracket: implications for surgical correction. J Pediatr Orthop. 1981;1(3): 299–305. 48. Vickers D. Clinodactyly of the little finger: a simple operative technique for reversal of the growth abnormality. J Hand Surg Br. 1987;12(3):335–342. 49. Caouette-Laberge L, Laberge C, Egerszegi EP, Stanciu C. Physiolysis for correction of clinodactyly in children. J Hand Surg Am. 2002;27(4):659–665. 50. Gillis JA, Nicoson MC, Floccari L, Khouri JS, Moran SL. Comparison of Vickers’ physiolysis with osteotomy for primary correction of clinodactyly. Hand (N Y). 2020;15(4):472–479. 51. Wurfel A, Hofmann-von Kap-herr S, Schumacher R. [Kirner deformity]. Klin Padiatr. 1995;207(6):356–358. 52. Sugiura Y. Polytopic dystelephalangy of the fingers. Pediatr Radiol. 1989;19(6–7):493–495. 53. David TJ, Burwood RL. The nature and inheritance of Kirner’s deformity. J Med Genet. 1972;9(4):430–433. 54. Freiberg A, Forrest C. Kirner’s deformity: a review of the literature and case presentation. J Hand Surg Am. 1986;11(1):28–32.

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SECTION VI

CHAPTER 35  • Congenital hand IV: Malformations – hand plate: unspecified axis

55. Satake H, Ogino T, Eto J, Maruyama M, Watanabe T, Takagi M. Radiographic features of Kirner’s deformity. Congenit Anom (Kyoto). 2013;53(2):78–82. 56. Carstam N, Eiken O. Kirner’s deformity of the little finger. Case reports and proposed treatment. J Bone Joint Surg Am. 1970;52(8): 1663–1665. 57. Benatar N. Kirner’s deformity treated by distal detachment of the flexor digitorum profundus tendon. Handchir Mikrochir Plast Chir. 2004;36(2-3):166–169. 58. Dubrana F, Dartoy C, Stindel E, Fenoll B, Le Nen D, Lefevre C. [Kirner’s deformity. 4 case reports and review of the literature]. Ann Chir Main Memb Super. 1995;14(1):33–37. 59. Fairbank SM, Rozen WM, Coombs CJ. The pathogenesis of Kirner’s deformity: a clinical, radiological and histological study. J Hand Surg Eur Vol. 2015;40(6):633–637. 60. Lee J, Ahn JK, Choi SH, Koh EM, Cha HS. MRI findings in Kirner deformity: normal insertion of the flexor digitorum profundus tendon without soft-tissue enhancement. Pediatr Radiol. 2010;40(9): 1572–1575. 61. Wenger TL, Hing AV, Evans KN. Apert syndrome. In: Adam MP, Mirzaa GM, Pagon RA, et al., eds. GeneReviews(®). Seattle, WA; 1993. 62. Mantilla-Capacho JM, Arnaud L, Diaz-Rodriguez M, Barros-Nunez P. Apert syndrome with preaxial polydactyly showing the typical mutation Ser252Trp in the FGFR2 gene. Genet Couns. 2005;16(4): 403–406. 63. Tolarova MM, Harris JA, Ordway DE, Vargervik K. Birth prevalence, mutation rate, sex ratio, parents’ age, and ethnicity in Apert syndrome. Am J Med Genet. 1997;72(4):394–398. 64. Cohen Jr MM, Kreiborg S, Lammer EJ, et al. Birth prevalence study of the Apert syndrome. Am J Med Genet. 1992;42(5):655–659. 65. Glaser RL, Broman KW, Schulman RL, Eskenazi B, Wyrobek AJ, Jabs EW. The paternal-age effect in Apert syndrome is due, in part, to the increased frequency of mutations in sperm. Am J Hum Genet. 2003;73(4):939–947. 66. Park WJ, Theda C, Maestri NE, et al. Analysis of phenotypic features and FGFR2 mutations in Apert syndrome. Am J Hum Genet. 1995;57(2):321–328. 67. Journeau P, Lajeunie E, Renier D, Salon A, Guero S, Pouliquen JC. Syndactyly in Apert syndrome. Utility of a prognostic classification. Ann Chir Main Memb Super. 1999;18(1):13–19. 68. Slaney SF, Oldridge M, Hurst JA, et al. Differential effects of FGFR2 mutations on syndactyly and cleft palate in Apert syndrome. Am J Hum Genet. 1996;58(5):923–932. 69. Renier D, Arnaud E, Cinalli G, et al. [Mental prognosis of Apert syndrome]. Arch Pediatr. 1996;3(8):752–760. 70. David DJ, Anderson P, Flapper W, Syme-Grant J, Santoreneos S, Moore M. Apert syndrome: outcomes from the Australian Craniofacial Unit’s Birth to Maturity Management Protocol. J Craniofac Surg. 2016;27(5):1125–1134. 71. Fernandes MB, Maximino LP, Perosa GB, Abramides DV, Passos-Bueno MR, Yacubian-Fernandes A. Apert and Crouzon

72.

73. 74. 75. 76. 77. 78. 79. 80.

81.

82. 83. 84. 85. 86. 87. 88. 89.

syndromes – cognitive development, brain abnormalities, and molecular aspects. Am J Med Genet A. 2016;170(6):1532–1537. Schauerte EW, St-Aubin PM. Progressive synosteosis in Apert’s syndrome (acrocephalosyndactyly), with a description of roentgenographic changes in the feet. Am J Roentgenol Radium Ther Nucl Med. 1966;97(1):67–73. Kasser J, Upton J. The shoulder, elbow, and forearm in Apert syndrome. Clin Plast Surg. 1991;18(2):381–389. McHugh T, Wyers M, King E. MRI characterization of the glenohumeral joint in Apert syndrome. Pediatr Radiol. 2007;37(6): 596–599. Upton J. Apert syndrome. Classification and pathologic anatomy of limb anomalies. Clin Plast Surg. 1991;18(2):321–355. Dao KD, Shin AY, Kelley S, Wood VE. Thumb radial angulation correction without phalangeal osteotomy in Apert’s syndrome. J Hand Surg Am. 2002;27(1):125–132. Guero S, Vassia L, Renier D, Glorion C. Surgical management of the hand in Apert syndrome. Handchir Mikrochir Plast Chir. 2004;36(2-3): 179–185. Fereshetian S, Upton J. The anatomy and management of the thumb in Apert syndrome. Clin Plast Surg. 1991;18(2):365–380. Blauth W, von Torne O. [“Apert’s foot” (in acrocephalo-syndactyly) (author’s transl)]. Z Orthop Ihre Grenzgeb. 1978;116(1):1–6. Burger EB, Hovius SE, Burger BJ, van Nieuwenhoven CA. The Rotterdam Foot Classification: a classification system for medial polydactyly of the foot. J Bone Joint Surg Am. 2016;98(15): 1298–1306. Calis M, Oznur A, Ekin O, Vargel I. Correction of brachymetatarsia and medial angulation of the great toe of Apert foot by distraction osteogenesis: a review of 7 years of experience. J Pediatr Orthop. 2016;36(6):582–588. Fearon JA. Treatment of the hands and feet in Apert syndrome: an evolution in management. Plast Reconstr Surg. 2003;112(1):1–12; discussion 3-9. Chang J, Danton TK, Ladd AL, Hentz VR. Reconstruction of the hand in Apert syndrome: a simplified approach. Plast Reconstr Surg. 2002;109(2):465–470; discussion 71. Guero SJ. Algorithm for treatment of apert hand. Tech Hand Up Extrem Surg. 2005;9(3):126–133. Lohmeyer JA, Hulsemann W, Mann M, Habenicht R. Transverse soft tissue distraction preceding separation of complex syndactylies. J Hand Surg Eur Vol. 2016;41(3):308–314. Ashmead D, Smith PJ. Tissue expansion for Apert’s syndactyly. J Hand Surg Br. 1995;20(3):327–330. Van Heest AE, House JH, Reckling WC. Two-stage reconstruction of Apert acrosyndactyly. J Hand Surg Am. 1997;22(2):315–322. Casula I, Guero S. Helal metatarsal osteotomy in Apert foot. J Pediatr Orthop. 2021;41(1):56–60. Barot LR, Caplan HS. Early surgical intervention in Apert’s syndactyly. Plast Reconstr Surg. 1986;77(2):282–287.

 

SECTION VI • Congenital Disorders

36

Congenital hand V: Deformations and dysplasias – variant growth Wee Leon Lam, Xiaofei Tian, Gillian D. Smith, and Shanlin Chen

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SYNOPSIS

ƒ In the Oberg, Manske, Tonkin (OMT) classification, “Deformation” refers to disruption of a limb that has already been formed. This category previously included constriction band sequence and congenital trigger digits, although the latter has been removed in the latest OMT update. ƒ Trigger thumbs are common. Surgical correction remains the mainstay of treatment although conservative management is increasingly practiced worldwide. ƒ Trigger fingers are much less common. Surgical correction requires an appreciation of the anatomical anomalies that may be present, and an algorithmic strategy to treat these anomalies. ƒ “Constriction ring sequence” refers to a wide-ranging list of conditions characterized by encircling rings to digits or limbs. A management algorithm includes early surgical release to maintain limb viability, or delayed reconstruction to optimize hand function and appearance. ƒ “Dysplasia” refers to a group of conditions in the OMT classification which exhibit variant growth either of a hyperplastic or hypoplastic nature. Overgrowth conditions such as macrodactyly, neurofibromatosis or vascular anomalies may present as enlarged limbs or digits. ƒ Macrodactyly is a rare and potentially disfiguring condition, usually caused by PIK3CA gene mutation in the m-TOR pathway. Strategies to optimize hand function and appearance include slowing down growth, soft tissue debulking, shortening or amputation.

OMT classification of deformation In 2013, the Swanson classification for congenital hand dif­ ferences was replaced by a new system, the Oberg, Manske, Tonkin (OMT) system, proposed at the recommendation of the International Federation of Societies for Surgery of the Hand (IFSSH) Scientific Committee for Congenital Conditions.1 This followed growing dissatisfaction with inability of the former to classify certain conditions, such as symbrachydactyly and

cleft hand, together with the rapid progression of knowledge in developmental biology and molecular genetics. The OMT system provides a logical classification system in combin­ ing etiology and morphology. The system consists of four main groups: malformations, deformations, dysplasias, and syndromes. The OMT has undergone several changes since its original description. The “Deformation” group was initially reserved for conditions resulting from a disruption of any portion of a limb that has already been formed, consisting of constriction ring sequence (related to amniotic banding), arthrogryposis, and trigger digits. Any condition resulting from deformations or dis­ ruptions as a result of other causes, e.g., viral infection, vascular insults, or mechanical damage, was meant to be listed under the subcategory of “Not otherwise specified” or “Others”. In subsequent modifications and updates, arthrogryposis was removed from the deformation category to “Malform­ ation – dorsal/ventral axis” as well as “Syndromes” and then subsequently to “Dysplasia”. In the 2020 OMT update, “trigger digit” (both trigger thumbs and trigger fingers) was finally removed, due to lack of evidence that the condition is truly congenital in nature.2 At present, the deformation group consists of “Constriction ring sequence” and “Not otherwise specified” (Table 36.1). For the purpose of this chapter, how­ ever, the conditions of constriction ring sequence and trigger digits will be discussed.

Pediatric trigger thumb Congenital trigger thumb was classified under Deformation (IIB) in the original OMT classification1 but was removed in the 2020 update.2 Considerable debate remains as to whether trigger thumb in children is a congenital condition and there­ fore the term “pediatric trigger thumb” will be used for the remainder of the chapter. Pediatric trigger thumb remains one of the commonest conditions faced by any practicing pediatric hand surgeon.

Pediatric trigger thumb

Table 36.1  The Oberg, Manske, Tonkin (OMT) classification: Deformation. Changes to grouping of conditions from 2010 to 2020

2010

2013, 2015, 2017

2020

2. Deformations A. Constriction ring sequence B. Arthrogryposis C. Trigger digits D. Not otherwise specified

2. Deformations A. Constriction ring sequence B. Trigger digits C. Not otherwise specified

II. Deformations A. Constriction ring sequence B. Not otherwise specified

Basic science/disease process Pediatric trigger thumb is a stenosing tenovaginitis affecting the flexor pollicis longus (FPL) tendon as it passes underneath the A1 pulley at the volar aspect of the metacarpophalangeal (MCP) joint. The exact pathophysiology remains unknown; whether there is a pre-existing anatomical disorder that pre­ disposes triggering, i.e., rendering it a congenital difference, is undetermined. In addition, it is also unknown why there is a much higher incidence of pediatric trigger thumb in compari­ son to its finger or adult counterparts. It is a relatively straightforward task when explaining to a parent that their child has a congenital hand difference if there was an obvious hand difference at birth. However, pediatric trigger thumb is rarely encountered at birth; Kikuchi and Ogino3 reported an incidence of 3.3 per 1000 live births and Ger et al.4 mentioned an even rarer incidence of around 1 in 2000 live births. Moon et al.5 examined 7700 infants at birth and found no incidence of the condition. Rodgers and Waters6 published similar findings with 1046 infants and found no incidence of trigger thumbs, either. The proponents of a congenital theory argued that bilateral pediatric trigger thumbs have been found in identical twins.7 In addition, pediatric trigger thumb typically presents with a higher-than-average incidence of bilateral occurrence in non-identical twins. The question remains: why are there so many children with trigger thumbs, mostly presenting around the same age group, around 1–2 years of age, but not at birth? One possibility is a developmental error in the vicinity of the A1 pulley at the child’s thumb MCP joint that simply predisposes to an inflammatory condition and entrapment of the FPL tendon. Another possibility is trauma, causing a narrowing of the fibro-osseous space at the level of the MCP joint. The definition of trauma remains vague; in one of the author’s (W.L.) experience involving a review of 70 consecu­ tive trigger thumbs, 33% made their first presentation to the emergency department with “a history of trauma”, but none were subsequently found to have any injuries. Children are naturally more hypermobile and there may be a tendency for the MCP joint to hyperextend and narrow the fibro-osseous space; however, hyperextension should be a transient move­ ment causing very little permanent effects on tendon gliding. Perhaps a combination of trauma, hyperextension in a natu­ rally occurring tight space, can predispose some children to triggering of the thumb.

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Diagnosis/patient presentation As mentioned, pediatric trigger thumb rarely presents at birth or earlier than 1 year of age, although this may reflect a failure to recognize the condition rather than its true absence. The newborn child tends to hold the thumb within the palm for months, and even to the most observant parent a deformity is only picked up when the child starts to reach out and grab objects, often around the age of 6 months. The parent notices that the child is unable to extend the thumb with the inter­ phalangeal (IP) joint in a fixed flexion deformity, or that the child is unable to flex the thumb (an extension deformity), or that flexion and extension is accompanied by pain, or an observable “clicking” movement. Older children (above the age of 3 years) may use the contralateral hand to free the thumb. A severity score8,9 has been suggested where grade 0 implies that the IP joint can be actively extended to at least 0 degrees without triggering; grade 1where the IP joint can be extended actively but with triggering; grade 2 where pas­ sive, but not active extension, is possible, with triggering; and grade 3 where the IP joint is fixed in a flexed or occasionally an extended position. This classification is useful for communica­ tion but does not take into account symptoms of pain, which may be determinant in whether treatment is performed. On examination, the surgeon may feel a lump in the volar aspect of the thumb MCP joint, called a “Notta’s nodule”, pathognomonic of swelling in the FPL tendon. It is important to differentiate this from a sesamoid bone, which may also feel like a prominence, but a Notta’s nodule should be more pal­ pable and moves with flexion of the FPL tendon, unlike a sesa­ moid bone which remains in the same position. The examiner can also try and gently extend the IP joint passively and feel the nodule give way as the FPL tucks underneath the A1 pul­ ley, provided this is not too painful for the child. Often, the thumb is stuck in flexion and cannot be extended, and exam­ ination can only be confirmed with palpation of a nodule and a flexed thumb. Finally, it is important to differentiate a trigger thumb from a congenital clasped thumb; the former presents with flexion deformities at the IP joint and the latter, at the MCP joint, frequently accompanied by deficiencies in the first webspace.

Patient selection (Algorithm 36.1) The obvious treatment for a child presenting with pediatric trigger thumb deformity is to “straighten the thumb” or to improve the range of movement of the IP joint. Management of a trigger thumb, however, remains controversial, for the following reasons. Firstly, is active treatment needed? Does the thumb suffer from long-term issues if it is not fully straightened? Reports of deformities in the IP joint, includ­ ing contracture, radial deviation, and rotational deformity with compensatory MCP joint hyperextension and even nail deformities in untreated trigger thumbs have been reported,10 but these are not widely observed. Finally, the impact of the appearance of a permanently flexed thumb remains unknown, both on the parents and children. Secondly, there are continued reports that the pediatric trigger thumb resolves spontaneously. Ger et al.4 observed that none of their patients demonstrated any resolution after almost 4 years of waiting; in contrast, Chalise et al.11 found a

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

Algorithm 36.1 Suspected trigger thumb

Wait and review when child is older than 2

Discharge

Below 2 years old?

Yes

No

Grade 0 Able to actively extend and flex (with palpable lump)

Grade 1 Active extension possible, with triggering

No

Painful?

Grade 2 Passive extension possible, with triggering

Grade 3 IP joint fixed in passive or active extension

Consider surgery Yes

Observe 6 months with splinting and stretching as tolerated

Yes

Improvement?

No

Decision-making in the treatment of pediatric trigger thumb.

high rate of resolution, although this was only in stages 1 and 2, i.e., when the thumb is not fixed, and recommended a con­ servative approach with stretching, and surgery reserved for grade 3 trigger thumbs. Thirdly, is surgery the best method of treatment? Since Jahss12 prioritized surgery as the only treatment for trigger thumbs, there has been a recent move towards conserva­ tive management. A resolution rate of about 30% has been reported13 if the child presents before 1 year old, but this dra­ matically decreases as the child gets older. Watanabe et al.8 recommended a conservative approach in grades 1 and 2 but surgery in grade 3 and reported a final satisfactory rate of 96% with abnormal motion in about 59% of thumbs. Finally, Baek et al.14 reported a spontaneous resolution rate of >75% after a follow-up of at least 5 years; in the remaining 25%, there

was at least some improvement. They admitted that fine motor movement may be adversely affected by an incomplete resolution and recommended waiting until 5 years of age to decide surgery, but not beyond that. Tan et al.15 found a high success rate with conservative treatment, especially in very young children, but attributed it to the use of splints. Finally, Lee et al.16 recommended splinting with good results but cau­ tioned that not all thumbs would regain normal movement. A cursory glance at the literature would perhaps reveal an East–West divide, with conservative management favored in Asian countries but surgical release in Western ones. The higher rate of success with conservative management in the East may be attributable to the increased hypermobility in children or other cultural factors, including compliance. Overall, the indications for surgery would therefore appear

Pediatric trigger thumb

to be a child presenting after the age of 2 and before 5, with a fixed flexion (or extension) deformity, or an intermittently triggering thumb that is painful. A desire for a full correction of the IP joint, for whatever reasons, including appearance, may be another indication (see Algorithm 36.1)

naturally hyperextended MCP joint and this often-overlooked posture should be made known to the parent. Once released, however, the IP joint thumb extension should eventually approach that of the normal side over time. Surgery is typically carried out as a general anesthetic day case, under tourniquet control and loupe magnification. A transverse incision is preferred rather than a Bruner one, sit­ uated at the base of the thumb. There are usually three natu­ rally occurring thumb creases and the incision is placed in the center one. It is helpful to mark the midline axis of the thumb for reference, as rotation of the thumb can easily occur during assistance and inadvertently displace the digital nerves into the center of the operative field (Video 36.1 ). The initial incision is kept superficial, sufficient to visualize the initial appearance of fat and the rest of the dissection performed with tenotomy scissors. Once the proximal edge of the A1 pulley is visualized, a longitudinal window is made in the pulley with a scalpel, until the FPL tendon fibers are visual­ ized, and the rest of the pulley release is completed distally with scissors. The use of a blunt retractor should allow direct visualization of the divided pulley, which would appear as a “V”, with the apex situated distally. The tips of the scis­ sors are then inserted and under direct observation, the last fibers of the A1 pulley are divided, and the cut edges should appear parallel to each other. The direction of release should be kept in the midline to avoid damaging the digital neuro­ vascular bundles, although some surgeons prefer to keep it slightly radial, to avoid cutting the origin of the oblique pul­ ley. However, a slightly radial release must be balanced with

Clinical tips Trigger thumb • To ensure optimal visualization of the A1 pulley and protection of the neurovascular bundles, avoid rotation of the thumb during surgery or assistance. • Draw a line in the longitudinal axis of the thumb as a reference to keep orientation during surgery. • Ensure adequate distal and proximal release of the A1 pulley and check excursion of the flexor pollicis longus (FPL) tendon after release. • Do not excise Notta’s nodule on the FPL tendon. • Be aware that the thumb may not achieve a symmetrical position to the normal contralateral thumb, especially if it has been flexed for a long time.

Treatment/surgical technique (Fig. 36.1) Preoperatively, in unilateral cases, it is important to warn par­ ents that the thumb may not straighten to the same degree as the contralateral normal one. Children often present with a

A

B

C

D

Figure 36.1 Steps in surgical release of pediatric trigger thumb. (A) Transverse crease incision. (B) Release of A1 pulley, initially with scalpel and then with scissors. (C) Check for full tendon excursion after pulley release. (D) Postoperative appearance at 3 months showing a completely straight left thumb with full range of motion.  

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

the risk of damaging the radial digital nerve, which usually lies in a more midline position during surgery. Once released, the IP joint should straighten naturally but as mentioned, the degree of extension may not immediately be identical to the contralateral thumb. However, the IP joint should move freely without any evidence of triggering at this stage and a passive tenodesis test should produce full IP joint extension. A skin hook retractor is then used on the lower skin edge to allow visualization of the proximal part of the wound and to release any existing tight bands. The FPL tendon is then retracted out of the wound to check for full excursion and to break up any adhesions. Notta’s nod­ ule is observed and, if present, no attempts should be made to excise it, as this would cause more inflammation. Wound clo­ sure is achieved with interrupted 6-0 Vicryl Rapide sutures. The hand is dressed with the thumb extended, and the tip exposed in an older child and a full boxing glove in a younger child.

Postoperative care The wound is checked at 2 weeks and dressings removed to usually reveal a straight thumb that can move freely. Before removal of dressings, the parents are warned again that the posture of the thumb may not be identical to the other. Physiotherapy is very rarely required as the child makes full use of the thumb immediately. The child is then seen at 3 months postoperatively, and very often, the posture of the operated thumb is observed to be symmetrical to the other.

Outcome, prognosis, and complications The outcome of surgery is usually excellent, in all aspects including parental satisfaction for scar, pain, and ease of care. The overall incidence of complication is around 1–2%, mainly in the area of wound infections.17 Occasionally, there is resid­ ual triggering, or the thumb remains in a flexed position, and the common reasons are inadequate release or tendon adhe­ sions, and a period of splinting should be allowed to see if the condition improves. There is perhaps a higher incidence of true recurrence in children with more hypermobility but evidence for this is lacking.

Secondary procedures If there is true recurrence or if the thumb remains stuck in flexion, a trigger release can be performed in the same man­ ner. However, imaging investigations are recommended to ensure there are no other pathologies that may account for the triggering.

Congenital trigger fingers The incidence of pediatric trigger finger is about ten times less common than its thumb counterpart, and much rarer as compared to its adult counterpart.18 There remains a paucity of evidence about its etiology and the best way to treat this condition. As mentioned, trigger digits have recently been removed in the most recent update of the OMT classification2 over controversies as to whether this is an acquired or congen­ ital condition.

Basic science/disease process Like trigger thumb, there is little evidence of pediatric trig­ ger finger being present at birth.5 They have been reported in children as early as 3 weeks, with the majority presented before 8 months of age.19 Despite its unknown etiology, how­ ever, most authors reported recurrent anatomical anomalies accounting for the triggering, which may support the case for a congenital cause. Schaverien and colleagues20 classified the anatomical anomalies into three groups: (1) tendon anomaly (tendon nodules, wide flexor tendons); (2) abnormal relation­ ship between the flexor digitorum superficialis (FDS) and pro­ fundus (FDP), such as a proximal or narrow decussation of FDS or aberrant connections between the flexor tendons; and (3) narrowing of the pulley system which can affect A1, A2 or A3 pulleys. A plausible causative explanation can therefore be a child born with these predisposition anatomical anomalies, presenting with a trigger finger following a subsequent “acute on chronic” event.20 Rarer conditions that can also increase the contents of the sheath and cause triggering include inflamma­ tory synovitis from juvenile rheumatoid arthritis, post-trau­ matic calcific tendonitis, benign osteochondromas21 or mucopolysacchariodosis type 1 (Hurler’s syndrome). If there is any evidence of systemic involvement, referral to a rheuma­ tologist is warranted. Radiographs are unlikely to be helpful, but ultrasound examination may reveal the underlying etiol­ ogy and location of entrapment.

Diagnosis/patient presentation (Algorithm 36.2) Although patients with pediatric trigger finger can present early,19 the age of presentation is usually slightly older, as com­ pared to pediatric trigger thumb.22 One or more digits may be affected, although the middle is the commonest.19 Other important differential diagnoses to exclude include campto­ dactyly or aberrant muscles of the forearm, including isolated congenital deficiency of the extensor mechanism or contracture of the long flexors. Camptodactyly-arthropathy-coxa varapericarditis syndrome (CACP) is a rare autosomal recessive condition which can present with multiple fixed flexion con­ tractures, in which surgery should be avoided. On physical examination, the child may present with a persistently flexed digit when attempting to open the hand, while others demon­ strate a decreased active range of motion, or normal range with frank triggering, which may be painful or painless. An older child would often use the other hand to open the digit. A Notta’s nodule, similar to that found in trigger thumbs, can often be palpable in the region of the A1 pulley. An abnor­ mally proximal FDS decussation can similarly be felt as a prominence traveling under the A1 pulley, as the finger flexes and extends.

Patient selection There are fewer specific data on the non-surgical man­ agement of pediatric trigger finger as compared to trigger thumb, in part due to the grouping of both conditions in ear­ lier publications. Bae et al.22 observed patients for a minimum of 6 months to determine if spontaneous resolution might occur, except in those who presented with locked digits. The

Congenital trigger fingers

systematic review by Womack et al.18 reported a total of 64 digits that received initial nonoperative treatment, with res­ olution in 37 triggering digits (57.8%). A period of observa­ tion for 6 months to a year is probably reasonable, unless the child reports pain or functional limitations, or if the other hand is constantly required to help release the digit. Unlike adults, a corticosteroid injection cannot be routinely admin­ istered in younger children because of the reduced tolerance to pain and injection.

847

• Release A1 pulley first and check for excursion of the flexor digitorum superficialis (FDS) and profundus (FDP) tendons. If triggering persists, check for distal pathology. • If necessary, excise one slip of the FDS tendon to ensure free gliding of both FDS and FDP postoperatively. • If recurrence occurs, consider undiagnosed systemic cause or imaging modalities to exclude other anatomical reasons for triggering.

Treatment/surgical technique (see Video 36.2 ; Algorithm 36.3)

Clinical tips Trigger finger

Unlike adult trigger finger, the surgical release of pediatric finger should be performed in anticipation of certain anatom­ ical variations, with defined strategies to address these. The surgery is usually performed under general anesthesia and tourniquet control. A Bruner type incision, allowing an exten­ sile approach to the A1 to A4 pulleys is planned, although the

• Trigger finger is an uncommon condition in children. Exclude any systematic associations and if in doubt, refer to a pediatric rheumatologist. • Use a Bruner incision with extensile options to expose A1–A4 pulleys.

Algorithm 36.2 Exclude differential diagnoses, e.g., camptodactyly and if necessary, investigate for underlying systemic conditions

Suspected trigger finger

Splinting and therapy Review at 6-12 months

Able to actively extend and flex painlessly (with palpable lump)

Discharge

Observation for another 12 months

Yes

Improvement?

Decision-making in the management of pediatric trigger finger.

Active extension possible, with triggering

Passive extension only possible, with triggering

No

Consider surgery

Finger fixed in flexion, or no passive or active movement possible

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

Algorithm 36.3

Trigger finger release

Skin closure Early active mobilization

Full passive extension with no further triggering

Resect one slip of FDS

Bruner incision to expose A1 pulley Release A1 pulley

Yes

Passive extension possible but with continued triggering OR Passive extension not possible

Tight FDS decussation proximal to A1 pulley?

No

Extend Bruner incision Expose A3 pulley and free adhesions between FDS/FDP

No

Improvement?

Yes

Surgical algorithm for pediatric trigger finger.

initial incision should only be to identify and release the A1 pulley. The cause of triggering can be identified at this stage if it is due to a Notta’s nodule or proximal decussation of the FDS tendon, but in any case, release of the A1 pulley should resolve the problem in the majority of cases. The finger may remain slightly flexed at rest, as compared to a normal cascade, especially if the triggering has been for a long period of time, however, it should improve in passive extension without much resistance. The FDS and FDP tendons are then retracted with a tendon hook to check for distal sites of triggering. If triggering is still present, the incision is extended to expose the A2 to A4 pulleys. The A3 pulley is opened and the FDS tendon slips are inspected, and any adhesions freed. Finally, an ulnar slip of the FDS should be resected if there is continued resistance to gliding or triggering. This stepwise approach is recommended by most authors,1,4,5 although others have a lower threshold for routine resection of one slip of the FDS.22 Once an adequate

release is achieved, skin closure is completed with absorbable sutures and a bulky soft dressing is applied.

Postoperative care Although no routine postoperative splinting is required for most cases, early active mobilization is encouraged. However, a finger splint can be worn intermittently in patients for a few weeks followed by gentle stretching, if the finger was not completely straight after release, due perhaps to central slip attenuation or adhesions.

Outcome, prognosis, and complications Reports of outcomes for trigger finger have been limited by the rarity of this condition and small number of patients. Most are case series with variations in reporting what a “successful”

Constriction ring sequence

outcome is: resolution of the triggering, return to function or achieving a full range of movement. There is no evidence-based algorithmic pathway that incorporates nonoperative manage­ ment although the algorithm in Algorithm 36.3 offers a reason­ able pathway. The results of primary surgery appear favorable, with success rates above 90%.19,22

Secondary procedures Recurrence can be due to inadequate first surgeries, misdiag­ nosis of a camptodactyly or a missed diagnosis of an underly­ ing inflammatory condition, and for this reason, re-exploration should consider concomitant synovial biopsy as well as blood tests for juvenile rheumatoid arthritis.20 Finally, anomalous mus­ cles should be suspected; Bae et al.22 reported an abnormal mus­ cle belly during revision surgery, arising from the FDS tendon proximal to the A1 pulley and responsible for the triggering. The patient’s symptoms resolved after resection of the muscle.

Constriction ring sequence Constriction ring sequence (CRS) is a common sporadic condi­ tion of encircling constriction rings to the limbs. Often affect­ ing multiple limbs at multiple levels, the condition ranges from simple bands without any distal deficit to potentially serious sequelae including associated lymphedema, vascular com­ promise and potential risk of amputations at multiple ­levels. Distal structures in the fingers and toes may be hypoplastic but structures proximal to the rings are normal. In the current OMT classification, CRS is the only named condition under Deformation after the removal of trigger digits.2 This implies that the constriction and deformation happens after the limb is already formed. However, a view of cases shows that the limb or digit beyond the ring can be normal, distorted or can be rel­ atively underdeveloped, suggesting that the insult to the area can occur in variable points in the limb development or may not represent deformation but instead a failure of formation. CRS is one of the most common congenital hand conditions, with an incidence estimated as 1 in 1200 live births. A Swedish study suggested a much lower incidence of 3 per 100,000 live births23 and a study in Western Australia24 had a prevalence of 6 per 100,000 live births. Bilateral involvement is frequent and there is no gender preference.

Basic science/disease process There are two main theories as to the etiology of this condition: 1. Intrinsic theory 2. Extrinsic theory The intrinsic theory was proposed by Streeter in 1930 and suggests a defect in the germ cells. This would account for the coexistence of clefts in the palate and face and for some of the deficiencies distal to constriction rings. Misoprostol, a pros­ taglandin analogue, administered to terminate a pregnancy, can produce similar defects. Webster25 attributes the develop­ ment of CRS secondary to impaired blood flow causing vas­ cular disruption or compromise. Recent genetic studies have begun to identify intrinsic, genetic factors that may predis­ pose infants to the development of disruptions such as those seen in amniotic band syndrome.

849

The extrinsic theory suggests an intrauterine disruption that may be traumatic, vascular or iatrogenic which causes detach­ ment of strands of amnion which wrap around the digits causing rings, syndactyly and amputation when these constrict the digits tightly. This disruption may be related to premature membrane rupture, intrauterine death of a twin pregnancy or iatrogenic injury from chorionic villus sampling or any form of fetoscopy. The extrinsic theory fails to explain why there is an intact amni­ otic sac in some infants, why there are a high number of mal­ formations affecting internal organs in some patients, and why it oftentimes affects only part of the circumference of the digits.

Diagnosis/patient presentation The patient may present in fetal life with an ultrasound scan suggesting amputations distally of the fingers or a tight con­ striction around one or more limbs. It is common to have mul­ tiple limbs involved and frequently, in the lower limb, this is associated with talipes equinovarus. Facial and palatal clefts are less common associations. It is more frequent with prema­ ture and low birthweight babies, which may account for its slightly higher incidence in twin pregnancies. Postnatally, there may be residual remnants of amnion wrapped around the digits immediately after birth (Fig. 36.2). The constriction rings may occur anywhere along the limbs, but frequently affect the digits and may be at multiple lev­ els, both in the limbs and the digits. The rings are usually cir­ cumferential and vary in apparent depth (Figs. 36.3 & 36.4). Occasionally, there are missing digits, and the remnants of these are found with the placenta at delivery or growing at erroneous sites such as scalp or knee. Over the long bones, these may be sufficiently deep to compress both nerves and vessels, leading to both short-term pain and color changes and long-term issues with growth, function and sensation (see Fig. 36.3). In the digits, constriction rings often follow a sloping pattern that would fit with an external entanglement. CRS may cause digits to fuse together, commonly with an acrosyndactyly pattern. Where this happens, the linkages may be minor and loose, when the length and quality of each digit is clear, or complex and tight, when it is unclear which distal end belongs to which digit and even which digit is amputated and which hypoplastic (see Figs. 36.5 & 36.6). These hypoplastic digits lack normal structures distally, including neurovascular bundles beyond the bands, and may present with bony syndactyly, requiring a staged approach to separation. Any of the amputated digits may be thin and pointed with poor skin cover over the bony stump or be floppy and bulky distally. Lymphedematous tissues distal to the bands may add additional bulk and contribute to the poor appearance of the hand or foot. This is particularly true in the digits. The main differential diagnosis is Adams-Oliver syndrome, which is extremely rare. This is a genetic condition, usually of autosomal dominant inheritance, presenting with distal digi­ tal hypoplasia and amputations of the digits, similar to those seen with constriction rings and associated with cutis aplasia of the scalp. Patterson26 classified CRS into four groups, although poten­ tially all may present on the same hand: 1. Simple constriction rings – usually seen over the proximal and/or middle phalanges of the fingers and toes, although they can occur more proximally in the limb.

SECTION VI

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

A

B

C

Figure 36.2  (A) Deep constriction band with amniotic tissues present in the forearm of a newborn, with distal lymphedema. (B,C) Following removal of the tissues, the lymphedema resolved with no distal limb compromise.

Figure 36.4  Mild constriction ring in the left wrist of a 2-year-old child presenting with a combined median and ulnar nerve palsy.

Figure 36.3  Severe untreated constriction ring in the upper arm of a 20-year-old female with radial nerve palsy. Release of the band is unlikely to lead to any nerve recovery.

2. 3.

Constriction ring with secondary lymphedema distal to the ring so that there is distal swelling which may be progressive. Acrosyndactyly – where there is distal fusion which may be soft tissue or bony but proximally there is separation

of the digits in the form of fistulas. These are often described as sinuses, but these epithelial-lined tracts extend from the dorsum to the volar aspect of the hand. They are frequently associated with distal amputations. The digits distally may be hypoplastic. There are three types of acrosyndactyly: (a) distal fusion with webs at normal height (b) distal fusion with incompletely formed webs proximally

Constriction ring sequence

4.

(c) fusion distally with only narrow openings proximally. Amputations – these can be multiple to whole limbs or to multiple or single digits.

Patient selection The following algorithms describe the treatment pathways for different presentations of CRS.

In utero diagnosis (Algorithm 36.4) In utero treatment for CRS is reserved for those with impending limb amputation and does involve risks for both the mother and the fetus which need to be weighed before proceeding. It will not prevent pre-existing developmen­ tal deficiencies but can potentially prevent worsening of deformities. In a review by Gueneuc et al.27 about fetoscopic release of bands, 75% achieved a functional limb with a 15% risk of complications and 7.7% risk of fetal death – this was considered by the authors to be an acceptable compli­ cation rate.

Figure 36.5  Acrosyndactyly in the left hand of newborn. Note the impending threat to vascularity of the distal part of the thumb, leading to autoamputation.

851

Postnatal presentation (Algorithm 36.5) When there is vascular compromise or rapidly increasing lymphedema at birth, a simple longitudinal incision in the band under local anesthetic over a safe area may be per­ formed to salvage a digit or a limb. Any obvious amniotic tissues may be removed (see Fig. 36.2). Later, formal excision may be required. When there is evidence of major nerve com­ pression, e.g., nerve palsy, early excision may give the best chance of recovery. If there is no sign of recovery after decom­ pression, nerve grafting can be considered, but results are dis­ appointing (see Fig. 36.4 and Fig. 36.7), The result of surgical nerve decompression is poor; previous authors28 reported nerve palsies associated with CRS but no recovery following band releases and decompression of the nerves. It is widely assumed that the anatomy proximal to the site of constriction (or amputation) is always developmentally normal, but we have found a global nerve hypoplasia proximal to the bands, even in the case of very mild constrictions.29 Nerve develop­ ment, as one of the later processes to occur in limb embryo­ genesis, is particularly susceptible to earlier insults affecting both the vasculature and musculature.

Later presentations (Algorithm 36.6) When there is a complex picture of acrosyndactyly, the ini­ tial aim is to separate the digits to see what residual length is present and to allow normal growth – depending on the com­ plexity. This may need to be in more than one stage. Release of any residual proximal syndactyly should be deferred; the aim in short digits should be to release as proximally as the bifurcation, with the use of full-thickness skin graft if needed (see Fig. 36.6, and Figs. 36.8 & 36.9). Toe-to-hand transfer is particularly suitable when the thumb has been shortened by amputation or when multiple digits are affected on one hand. The normality of structures immediately proximal to the band makes surgery straightfor­ ward and a reliably good outcome should be expected if the toes are unaffected. When there are simple bands causing only aesthetic issues, operating early may mean later revisions, and parents should be counseled about the increased incidence of further surgeries.

Figure 36.6 A 6-week-old baby with constriction ring sequence of the right hand. There is acrosyndactyly of the index, ring, and little fingers with volar displacement of the middle finger.  

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

Algorithm 36.4 Antenatal diagnosis

No

Yes

Limb threatening ?

Yes

No

Consider fetal surgery

Antenatal counseling

Decision-making in the management of constriction ring sequence (antenatal diagnosis).

A

B

Figure 36.7  (A,B) Persistent combined median and ulnar nerve palsy, following release of the ring.

Clinical tips Constriction ring sequence • Remove any visible amniotic remnants at birth and release loose areas of acrosyndactyly under local anesthesia. • Early vascular compromise on a digit can be improved using a longitudinal incision under local anesthesia with a beveled needle on the dorsum.

• Do not excise circumferentially in one stage distally on a hypoplastic digit – treat the dorsum first. • Do not use a subcuticular suture for circumferential excisions as this creates a purse-string effect. • Skin obtained from the depths of the fistulas in acrosyndactyly is fragile and does not make good material for a webspace. Use a new flap where possible. • Use skin from excision of the bands to provide full-thickness skin graft for web releases.

Constriction ring sequence

853

Algorithm 36.5 Vascular compromise

No

Yes

Immediate longitudinal release of band under LA or remove any obvious amniotic tissues

Remnants of amniotic tissue / narrow connections

Increasing lymphedema

Incise longitudinally under LA within 6/52

Tight limb band

Multiple bands close together

Single band

Excise circumferentlially under GA within 6/52

If can't excise together, excise most proximal first

Neurological compromise to limb

Yes

No

Nerve conduction studies after 3/12

PIan other surgery required

No improvement, consider nerve grafting

Decision-making in the management of constriction ring sequence (early postnatal diagnosis). GA, General anesthesia.

Treatment/surgical technique For emergency decompression with vascular compromise or progressive lymphedema, all loose amniotic tissues should be removed, and in many cases. a short longitudinal incision across the band is sufficient with a plan for later

elective excision. Minor bands are treated for aesthetics only and treatment may best be deferred until the child is much older. Traditional techniques for excision of deep bands required multiple Z-plasties in the skin, combined sometimes with opposing Z-plasties in the underlying fat, raising separate fat

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

Algorithm 36.6 Deep digital bands with static lymphedema

Acrosyndactyly

Yes

Yes

No

Release by 6/12

No

Release by 1yr

Release timed in relation to other needs

Fingers/ thumb absent but toes present

No

Yes

Digital bands

Syndactyly

Offer toe-to-hand transfer

Deepening of webs proximal to normal level with FTSG

Good digit distally

Poor digit distally

Excise circumferentially prior to school entry

Excise in 2 stages, dorsally first

Short straight digits Offer distraction osteogenesis as teenager

Poor skin cover as grows

Bony shortening

Local flaps

Cosmetic prostheses

Decision-making in the management of constriction ring sequence (later or non-urgent management). FTSG, Full-thickness skin graft.

Constriction ring sequence

855

Figure 36.8  Three months postoperatively, following separation of digits at 6 months and resurfacing of digits with full-thickness skin grafts. There remains a deep band in the index finger.

Figure 36.9  Following further surgeries to release the constriction band on the index finger and to deepen the first web.

flaps to fill out the hourglass contour and treating only half the circumference of the limb or digit at a time. These techniques are largely obsolete. It is clear that in most cases, direct excision of the band including the skin up to the shoulders of the band followed by direct closure can be performed circumferentially in a single procedure. The band needs to be fully excised, and this is always more extensive than it appears and is frequently adherent to the deep mus­ cle fascia and in close proximity to major nerves and vessels which must be preserved. Sometimes subcutaneous longitudi­ nal fasciotomies are also performed to avoid muscle herniae. Direct suture is usually possible except in cases where there is a large discrepancy in circumference between the proximal and distal sides of the band and here “Y to V” plasties are ideal; the “V” from the proximal side of the incision insets into the distal incision.

In those cases, when distally there is major hypoplasia, it may be wise to stage the excision over part of the circum­ ference at a time.30 With rings at the digital level with distal hypoplasia, there may not be any viable vessels distally and here release should not be circumferential. The dorsal release gives the greater benefit, and the volar release may not be required unless there is tethering or contracture, as they may not be as obvious. Release of acrosyndactyly should be performed early to allow optimum growth of digits (see Figs. 36.6, 36.8, & 36.9). Release may be challenging, and the use of lacrimal probes may help in distinguishing the separate digits. The complex cases may need staging to maintain maximum amounts of tissue. It may become clearer once the thumb and the little finger are separated from the others. Then, planning to leave sufficient skin bridge to act as a random pattern flap and allow venous

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CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

drainage, the other digits should be separated, taking care to look for neurovascular structures whilst doing so. If the planned incision is found to be potentially compromising of digit viabil­ ity if the operation proceeds, then stopping at that point and returning once this is healed is better than losing a digit. Skin graft is usually required, as tight closure will compromise those digits of tenuous viability but may be taken from other rings. There is often some lymphedematous tissue dorsally which may be debulked, giving additional skin for grafting. An alter­ native in severe cases is the use of a small bony distractor such as the Cubefix fixator to help distract existing tissues. Later incomplete syndactyly release ought to be to a more proximal level than normal to make the apparent length of the digits greater. Toe-to-hand transfer will give benefit for ampu­ tated digits but is usually not performed before 18 months of age and only if the digits are present and the family agree to this. Where bands are involving the toes, this may be less reliable.

Postoperative care Postoperatively, dressings can be a soft padded dressing applied to the hand and secured with tape to the forearm and immobilized in a Tubigrip sling. This is left in place for 2–3 weeks and with a plan made at the initial surgery whether a dressing change under sedation or general anes­ thetic is likely to be required. Usually, the dressing change is performed in an outpatient setting and unless the first web has been released, postoperative splintage is not required. In a situation where surgery needs to be staged, 3 months between procedures is adequate unless the patient forms hypertrophic scars, when prolonging the interval between releases would be advisable.

Outcome, prognosis, and complications As mentioned, the prognosis where there is proximal neurop­ athy is guarded as the nerve palsy may not recover. The limb is also unlikely to grow normally or become normally sensate so there is a risk of neuropathic injury later in life. Functionally, for most patients the degree of functional difficulty varies according to the number of fingers and the length of those digits left and the presence of functioning thumbs. What is present usually functions well but where amputations are present, the reduced length reduces the span available, and loss of IP joints reduces the grip strength. Toe-to-hand transfer allows the use of the normal proximal structures present and may be of huge functional benefit in these patients, where multiple amputations limit grip strength and fine manipulative skill. Residual lymphedema in a limb has the usual increased risk of infection and needs aggressive acute antibiotic man­ agement. It is rare, however, that infections are sufficiently problematic to require prophylactic antibiotics. Aesthetic appearance in the limbs themselves may be good. The traditional multiple Z-plasties used to excise the bands removed the contour defect but the extent of scarring was a source of complaint later in childhood, and modern straightline techniques should leave better scarring. However, within the hand it is frequently suboptimal, even after multiple procedures and many secondary surgeries are necessary to optimize this. The pattern of digit amputation is usually

particularly unattractive and the digits themselves look thin in places and bulging in others.

Secondary procedures Commonly, these patients have multiple procedures as some may need to be staged and others repeated as the child grows. The major secondary procedures they may require are: 1. Toe-to-hand transfer, if toes are available and the family agrees to this surgery. 2. Distraction osteogenesis – this is usually at metacarpal level to improve grasp, span, and digital length. It is used where toes are not available for transfer or the family decline this surgery 3. Shortening of bone or local flaps to fingertips – as the child reaches teenage years, the fingertip tissue can become tight in its soft tissue envelope creating local ischemia and pain. Surgery can advance local tissue, if available, but otherwise requires shortening of the bone.

OMT classification of dysplasia In the OMT system, the dysplasias group was initially designed to include conditions associated with cellular atypia and tumor formation. The 2010 version was separated into two main categories: “Hypertrophy” for limb anomalies that were disproportionately large, e.g., macrodactyly, and “Tumorous conditions”. In subsequent updates and revisions, the cat­ egory rapidly expanded to include several sub-categories according to tissue type, especially in the tumorous category, including vascular, neurological, connective tissues and skele­ tal. Hypertrophy conditions were divided into “whole limb”, focusing on hemihypertrophy, and “partial limb”, focusing on macrodactyly (Table 36.2). In the 2020 version, the term “hypertrophy” was changed to “variant growth” as it was noted that in dysplasia, aberrant tissues could be hypoplastic as well as hyperplastic. In addi­ tion, the term “partial limb” was more accurately changed to “isolated”. The focus of this portion of the chapter is on mac­ rodactyly of the upper limb/hand.

Macrodactyly Macrodactyly of the hand is a rare congenital malformation, characterized by a disproportionate increase in the size of one or multiple digits (Fig. 36.10). In severe cases, the entire hand or ipsilateral upper limb can be involved, termed macrochiria and macromelia respectively (Fig. 36.11). Macrodactyly is an “overgrowth” disorder and is classified in the updated OMT classification, under Dysplasia – variant growth/isolated (see Table 36.2).2 Digital overgrowth can also be a manifestation of other sys­ temic overgrowth disorders such as type I neurofibromatosis, vascular hemangiomas or Proteus syndrome, each of which is under separate OMT categories (Dysplasia – tumorous/neu­ rological; Dysplasia – tumorous/vascular; and Syndromes, respectively). The focus of this chapter is on primary macro­ dactyly although some of the management principles can be

Macrodactyly

Table 36.2  The Oberg, Manske, Tonkin classification: Dysplasia. Changes to grouping of conditions from 2010 to 2020

2010

2013, 2015, 2017

2020

3. Dysplasias

3. Dysplasias

III. Dysplasias

A. Hypertrophy 1. Macrodactyly 2. Upper limb 3. Upper limb and macrodactyly

A. 1. 2.

Hypertrophy Whole limb i. Hemihypertrophy ii. Aberrant flexor/extensor/intrinsic muscle Partial limb i. Macrodactyly ii. Aberrant intrinsic muscles of hand

A. 1. 2.

Variant growth Diffuse (Whole limb) i. Hemihypertrophy ii. Aberrant flexor/extensor/intrinsic muscle Isolated i. Macrodactyly ii. Aberrant intrinsic muscles of hand

B. 1. 2. 3. 4.

Tumorous conditions Vascular i. Hemangioma ii. Malformation Neurological i. Neurofibromatosis Connective tissue i. Juvenile aponeurotic fibroma ii. Infantile digital fibroma Skeletal i. Osteochondromatosis ii. Enchondromatosis iii. Fibrous dysplasia iv. Epiphyseal abnormalities

B. 1. 2. 3. 4.

Tumorous conditions Vascular i. Hemangioma ii. Malformation iii. Others Neurological i. Neurofibromatosis ii. Others Connective tissue i. Juvenile aponeurotic fibroma ii. Infantile digital fibroma iii. Others Skeletal i. Osteochondromatosis ii. Enchondromatosis iii. Fibrous dysplasia iv. Epiphyseal abnormalities v. Pseudoarthrosis vi. Other

C. 1. 2.

Congenital contracture Arthrogryposis multiplex congenita i. Amyoplasia ii. Distal arthrogryposis iii. Other Isolated i. Camptodactyly ii. Thumb in palm deformity iii. Other

B. Tumorous conditions

A

Figure 36.10 (A) Static and (B) progressive macrodactyly.  

B

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SECTION VI

CHAPTER 36  • Congenital hand V: Deformations and dysplasias – variant growth

Figure 36.12  Macrodactyly of the right index and middle finger. Hypertrophy of nerve and adipose tissues can be seen to occur from the level of the 2nd common digital nerve bifurcation, a phenomenon known as “nerve-oriented macrodactyly”. Figure 36.11  Macrodactyly with macromelia.

applied to other conditions of overgrowth. There is no con­ clusive data on the prevalence of macrodactyly. According to Flatt, macrodactyly accounted for 0.9% of all upper limb deformities. Other studies reported a low prevalence of mac­ rodactyly of approximately 1 per 18,000.31

Basic science/disease process There is increasing evidence that the dysplastic growth in macrodactyly is caused by a post-zygotic somatic mutation in the PIK3CA gene, creating a mosaicism.32 PIK3CA is a compo­ nent of the mechanistic target of rapamycin (MTOR) pathway which plays a central role in regulating human metabolism processes such as growth, proliferation and apoptosis. Where there is no evidence of mosaicism, the etiology of macrodac­ tyly remains unknown. The nerves in macrodactylous digits are usually dispropor­ tionately enlarged, although it is not known whether or how this relates to the surrounding secondary tissue hypertrophy. When dysplastic changes occur in the territory of an abnor­ mal nerve, it is termed a “nerve territory-oriented macrodac­ tyly” (Fig. 36.12). The most common microscopic findings in nerve hypertrophy are thickening of the epineurium, second­ ary to infiltration by abnormal adipose tissues and fibrosis (Fig. 36.13). Other common findings in macrodactyly can be found in the overlying skin, e.g., pachyderma (thickening of the overlying dermis), reduction in the number of sweat glands, excess subcutaneous fat and in the underlying skele­ ton, e.g., enlarged phalangeal medullary canal and thickening of trabeculae and periosteum.

Diagnosis/patient presentation (Algorithm 36.7) A diagnosis of macrodactyly can be made if there is primary dis­ proportionate enlargement or growth of digits, either alone or when accompanied by a more diffuse upper limb hypertrophy, after excluding secondary causes like tumors, vascular malfor­ mations and other systemic abnormalities. The child must be

Figure 36.13  Microscopic view of resected nerve from a patient with macrodactyly. There is proliferation of fat and fibrous tissue extraneurally and within the epineurium of the nerve.

screened for any such systemic disorders or secondary causes, which can potentially be life-threatening if left untreated. Macrodactyly can be divided into two types according to the history of growth of the affected digit: static and progressive macrodactyly.33 Static macrodactyly refers to an enlarged digit that is present at birth, but where the subsequent growth rate is proportional to that of the other fingers. Progressive macrodac­ tyly refers to a digit that grows at a rate that is disproportion­ ately faster than the other digits. This division may have clinical significance; a static macrodactyly can often be observed for longer periods of time before surgical intervention and debulk­ ing procedures are more promising in producing a final satis­ factory result, whereas progressive macrodactyly may warrant more aggressive treatment, including digital amputation, to preserve hand function, and the results are less likely to pro­ duce satisfactory digit function and appearance. There is no predominant pattern in isolated macrodactyly but when multiple digits are involved, the index and middle

Macrodactyly

Algorithm 36.7

Macrodactyly

Static

Progressive

Test for PIK3CA for research reasons

Test for PIK3CA for therapeutic options

Possible to make functionally and aesthetically acceptable digit

4 or more digits involved

30 degrees - Functional impairment - Failed splinting/stretching

FDS tendon

Anomalous muscle insertion

Mild/moderate skin deficiency

Z-plasty

Severe skin deficiency

Modified Malek flap

Tight tendon

Tenotomy

Tight tendon + weak extension

Tenotomy + transfer to LB

Lumbrical

Release

FDI

Release

Supple

Pinning

Fixed

Checkrein/ACL release + pinning

PIP joint

Surgical algorithm for severe camptodactyly. ACL, Accessory collateral ligament; FDI, first dorsal interosseous; FDS, flexor digitorum superficialis; LB, lateral band.

Thumb-in-palm deformity

described, most begin with a Z-plasty to address the volar skin deficiency. Systematic evaluation of potential anatomic contributions to the contracture is then performed. If the FDS tendon is tight, a tenotomy can be performed with or without transfer to the lateral bands to augment extension. Anomalous insertions of the lumbrical and/or interosseous muscles are released if present. If the PIP joint is contributing to the contracture, the checkrein and accessory collateral ligaments should be released. Temporary pinning of the joint with a Kirschner wire can be used to hold it in extension for 2–3 weeks postoperatively. In cases where the PIP joint is rigid, a modified Malek flap has been described to provide an extensive skin release with exposure of all necessary structures for systematic contracture release and FDS transfer. This proximally based homodigital island flap is dissected distal to proximal, leaving fat overlying the flexor tendons at the level of the middle phalanx for subsequent full-thickness skin grafting to address the skin shortage following release. Dissection proceeds deeper, just over the flexor sheath and radial neurovascular bundle, once the PIP is reached, leaving the flap pedicled on the ulnar neurovascular bundle.38

Postoperative care A course of postoperative splinting followed by hand therapy to optimize range of motion is typically used, regardless of surgical technique. A Kirschner wire may be used to hold the PIP in extension for 2–3 weeks postoperatively as well.

Outcomes, prognosis, and complications In patients younger than 3 years of age, a stretching protocol has been shown to significantly improve camptodactyly flexion contractures in patients with mild (60°) contractures. Degree of pretreatment contracture, however, did significantly correlate with the contracture improvement ratio, with milder contractures demonstrating greater improvement.36 Progressive splinting has also been associated with significant contracture improvement, particularly in type I infantile camptodactyly. A study including 24 fingers with splinting initiated by 2.5 years of age, an average flexion contracture of 23° improved to 4° with an average follow-up of 36 months.32 Reported postoperative outcomes are favorable for those patients in whom nonoperative measures are inadequate, particularly in patients with a supple PIP joint preoperatively.39 A systematic review including 187 patients in 14 studies undergoing surgical correction of camptodactyly reported an average flexion contracture improvement ranging from 30° to 77°.34 Foucher et al. report an improvement of surgical failure from 45.5% to 11% after implementing an algorithm of systematic release of involved anatomic structures similar to that described earlier in this chapter.38 Reported surgical complications include contracture recurrence, pain, stiffness, ankylosis, osteoarthritis, loss of flexion, and traction neurovascular injuries with a reoperation rate as high as 11%.34 Because the complication rate for surgical management is typically higher than that of nonoperative management, surgery is reserved for more severe, recalcitrant or resistant contractures. One must embark on surgery with caution; postoperative extension contractures may be more function-limiting than the original problem itself.

905

Secondary procedures Patients with persistent or recurrent contracture following surgery may rarely benefit from a revision capsulotomy or contracture release. A corrective osteotomy can also address persistent joint deformity. For patients with severe contracture and limited range of motion despite surgical release, a PIP arthrodesis may be used to place the digit in a more functional position.

Future directions Studies evaluating appropriate duration of trialing nonoperative interventions prior to proceeding with surgery would be beneficial. Furthermore, the implementation of a unified classification system for the various etiologies and presentations of camptodactyly would better allow comparisons between studies.

Thumb-in-palm deformity Congenital thumb-in-palm or clasped thumb deformity encompasses a spectrum of flexion contractures of the thumb, which can occur in isolation or in association with distal arthrogryposis, cerebral palsy, or MASA (mental retardation, aphasia, shuffling gait, thumb adduction) syndrome.

Basic science/disease process Although a variety of anatomic abnormalities have been noted in patients with clasped thumb, an underlying imbalance in flexion/extension or abduction/adduction forces contributes to its development. When occurring in isolation, clasped thumb has been classified into three categories:40,41 Type I: Absent or hypoplastic extensor mechanism with supple joints Type II: Absent or hypoplastic extensor mechanism with joint and first webspace contractures and collateral ligament and thenar muscle abnormalities Type III: Associated with arthrogryposis or another syndrome When occurring in patients with AMC or DA, the thumbin-palm deformity involves an extension contracture at the carpometacarpal metacarpal (CMC) joint and flexion and adduction contracture at the metacarpophalangeal (MCP) joint. In contrast, the opposite is seen in patients with amyoplasia. Abnormalities are less common in the extensor mechanism than in cases of isolated clasped thumb.

Diagnosis/patient presentation After birth, infants hold the thumb in the palm clasped beneath the other digits, for the first 3–4 months of life, so a clasped thumb deformity, while congenital and therefore present at birth, may not initially be apparent. This can make its presentation more difficulty to distinguish from a trigger thumb, which is acquired and not present at birth.

Patient selection Surgical intervention for clasped thumb deformity should be considered in patients with a persistent functional impairment

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SECTION VI

CHAPTER 38  • Congenital hand VII: Dysplasias – congenital contractures

after a trial of splinting, particularly those with inadequate motion to perform a thumb-to-palm pinch. In patients with thumb-in-palm deformity related to arthrogryposis, particularly amyoplasia, patients must have active motion, particularly of the flexor pollicis longus (FPL), to benefit from surgery.

Treatment/surgical care Regardless of the etiology, splinting beginning at the time of diagnosis is the first-line treatment for thumb-in-palm deformity, as this is most efficacious in the first 2 years of life. When surgical correction is warranted, the chosen technique depends on the deformity and underlying etiology. In patients with a type I clasped thumb, release of the skin and subcutaneous tissue contributing to the first webspace contracture may be adequate. Function of a weak or absent extensor tendon may be augmented with a tendon transfer. The extensor indicis proprius (EIP) is classically used, but transfers of the FDS and abductor digiti minimi (ADM) have also been described.41 The transferred tendon is secured to the diminutive native extensor, when present, or the base of the proximal phalanx. When a first webspace contracture is present, such as in type II deformities, a tissue rearrangement or local flap is used to treat the skin deficiency. Skin grafting, four-flap Z-plasty, dorsal rotation-advancement flap, and index flap (Figs. 38.7 & 38.8) have been described.41–45 In addition to

A

B

C

D

E

F

Clinical tips Keys to first webspace release for thumb-in-palm deformity Transposition flap designed on dorsoradial index finger Incision along first webspace to release skin contracture Release of intermetacarpal fascia, adductor pollicis, first dorsal interosseous and/or CMC joint Pinning of thumb in abduction and extension Transposition of index finger flap with full-thickness skin graft to donor site

release of the skin contracture, release of the intermetacarpal fascia, adductor pollicis, first dorsal interosseous, and/or CMC joint may be needed.43 Arthrogryposis patients with a thumb-in-palm deformity require a different surgical approach depending on the position of the CMC and MCP joints (Algorithm 38.2). Typically, joints that are supple with a passively correctable contracture can be addressed with tendon transfer whereas fixed joint contractures require a chondrodesis. With the CMC extension and MCP flexion seen in AMC, an EIP tendon transfer is used to augment extension with an MCP chondrodesis if there is a fixed deformity. The flexed CMC and extended MCP

Figure 38.7  (A,B) Patient with isolated clasped thumb. (C,D) Markings for palmar incision to facilitate release of tight adductor pollicis and first dorsal interosseous with index flap for widening first webspace. (E,F) Following release and index flap transfer with pinning to hold thumb in abduction.

Thumb-in-palm deformity

A

B

C

D

E

F

907

Figure 38.8  (A) Patient with distal arthrogryposis with adduction contracture of the thumb with tight first webspace and camptodactyly of the digits. (B,C) Markings for index flap to correct thumb abduction and camptodactyly releases of the digits. (D) After transfer of index flap to thumb and full-thickness skin grafting of digits with Kirschner wire placement. (E,F) Postoperative correction of contractures.

in patients with amyloplasia, however, can be more difficult to address with a goal of achieving either a thumb-to-palm or thumb-to-digit pinch function, depending on the active motion of the other digits. Regardless of CMC and MCP position, these patients typically require a first webspace release as described previously.

Algorithm 38.2

Thump-in-palm deformity

Postoperative care

CMS extended MCP flexed

CMS flexed

MCP supple

MCP flexed

EIP to EPL

EIP to EPL MCP Chondrodesis

MCP flexed Reorientation osteotomy EIP to EPL +/-MCP chondrodesis

MCP extended Reorientation osteotomy

Arthrogryposis thumb-in-palm surgical algorithm. CMC, Carpometacarpal; EIP, extensor indicis proprius; EPL, extensor pollicis longus; MCP, metacarpophalangeal.

Following contracture release, a 4-week course of immobilization with a thumb spica splint or cast is completed. Sometimes a Kirschner wire is used to help maintain thumb extension and abduction during early healing. This is followed by a regimen of hand therapy to work on gradual thumb flexion in conjunction with splint weaning.

Outcomes, prognosis, and complications Early splinting has shown good efficacy, particularly with type I deformities. In two studies, including 27 type I patients, nonoperative management was successful in all patients with none requiring surgical intervention.46,47 Among patients with type II and III deformities undergoing

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SECTION VI

CHAPTER 38  • Congenital hand VII: Dysplasias – congenital contractures

first webspace release with extensor augmentation, FPL lengthening, and/or MCP capsulotomy, 12 of 16 patients were reported to have a good or excellent outcome based on degree of MCP extension and CMC radial abduction. In another series of 28 hands, 24 thumbs had excellent abduction and MCP stabilization, and all patients were satisfied with their results.47 Although reported complication rates are low, patients undergoing surgery for thumb-in-palm deformity are at risk of undercorrection or recurrence of their contracture, stiffness, and neurovascular injury. When an osteotomy or chondro­ desis is performed, there is a risk of non-union or malunion; flap necrosis can occur with first webspace release.46

Secondary procedures Patients undergoing reorientation osteotomy before the age of 7 may require repeat osteotomy due to bony remodeling.

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Similarly, webspace contracture may recur as a child ages and require additional release.

Future directions Patients with type III clasped thumb, particularly those with poor baseline function such as with amyoplasia, tend to be among those with fair or poor outcomes. Advanced techniques to improve functional outcomes in these groups would be beneficial.

Acknowledgment We would like to thank Dr. Alphonsus Chong for contributing images for cases shown in Figs. 38.6 and 38.7.

References

References 1. Cachecho S, Elfassy C, Hamdy R, Rosenbaum P, Dahan-Oliel N. Arthrogryposis multiplex congenita definition: update using an international consensus-based approach. Am J Med Genet Part C Semin Med Genet. 2019;181(3):280–287. 2. Fahy MJ, Hall JG. A retrospective study of pregnancy complications among 828 cases of arthrogryposis. Genet Couns. 1990;1(1):3–11. 3. Hall JG, Reed SD, Greene G. The distal arthrogryposes: Delineation of new entities: review and nosologic discussion. Am J Med Genet. 1982;11(2):185–239. 4. Griffet J, Dieterich K, Bourg V, Bourgeois E. Amyoplasia and distal arthrogryposis. Orthop Traumatol Surg Res. 2021;107(1S):102781. 5. Bamshad M, Van Heest AE, Pleasure D. Arthrogryposis: a review and update. J Bone Joint Surg Am. 2009;91(Suppl 4):40–46. 6. Goldfarb CA, Ezaki M, Wall LB, Lam WL, Oberg KC. The Oberg– Manske–Tonkin (OMT) classification of congenital upper extremities: update for 2020. J Hand Surg Am. 2020;45(6):542–547. 7. Hall JG, Reed SD, Driscoll EP. Part I. Amyoplasia: a common sporadic condition with congenital contractures. Am J Med Genet. 1983;15(4):571–590. 8. Bernstein RM. Arthrogryposis and amyoplasia. J Am Acad Orthop Surg. 2002;10(6):417–424. 9. Lester R. Problems with the upper limb in arthrogryposis. J Child Orthop. 2015;9(6):473–476. 10. Zlotolow DA. Arthrogryposis. In: Green’s Operative Hand Surgery. 7th ed. Philadelphia, PA: Elsevier; 2017:1365–1390. 11. Wall LB, Calhoun V, Roberts S, Goldfarb CA. Distal humerus external rotation osteotomy for hand position in arthrogryposis. J Hand Surg Am. 2017;42(6):473.e1–473.e7. 12. Ramirez RN, Richards CJ, Kozin SH, Zlotolow DA. Combined elbow release and humeral rotational osteotomy in arthrogryposis. J Hand Surg Am. 2017;42(11):926.e1–926.e9. 13. Oishi S, Agranovich O, Zlotolow D, et al. Treatment and outcomes of arthrogryposis in the upper extremity. Am J Med Genet Part C Semin Med Genet. 2019;181(3):363–371. 14. Cao J, Stutz C, Beckwith T, Browning A, Mills J, Oishi SN. Elbow release and tricepsplasty in arthrogrypotic patients: a long-term follow-up study. J Hand Surg Am. 2020;45(6):549.e1–549.e7. 15. Richards C, Ramirez R, Kozin S, Zlotolow D. The effects of age on the outcomes of elbow release in arthrogryposis. J Hand Surg Am. 2019;44(10):898.e1–898.e6. 16. Gogola GR, Ezaki M, Oishi SN, Gharbaoui I, Bennett JB. Long head of the triceps muscle transfer for active elbow flexion in arthrogryposis. Tech Hand Up Extrem Surg. 2010;14(2):121–124. 17. Chomiak J, Dungl P, Včelák J. Reconstruction of elbow flexion in arthrogryposis multiplex congenita type I: Results of transfer of pectoralis major muscle with follow-up at skeletal maturity. J Pediatr Orthop. 2014;34(8):799–807. 18. Sochol KM, Edwards G, Stevanovic M. Restoration of elbow flexion with a free functional gracilis muscle transfer in an arthrogrypotic patient using a motor nerve to pectoralis major. Hand. 2020;15(5): 739–743. 19. Takagi T, Seki A, Kobayashi Y, Mochida J, Takayama S. Isolated muscle transfer to restore elbow flexion in children with arthrogryposis. J Hand Surg Asian-Pacific Vol. 2016;21(1):44–48. 20. Zargarbashi R, Nabian MH, Werthel JD, Valenti P. Is bipolar latissimus dorsi transfer a reliable option to restore elbow flexion in children with arthrogryposis? A review of 13 tendon transfers. J Shoulder Elb Surg. 2017;26(11):2004–2009. 21. Hagemann C, Stücker R, Breyer S, Kunkel POS. Nerve transfer from the median to musculocutaneous nerve to induce active elbow flexion in selected cases of arthrogryposis multiplex congenita. Microsurgery. 2019;39(8):710–714. 22. Smith DW, Drennan JC. Arthrogryposis wrist deformities: results of infantile serial casting. J Pediatr Orthop. 2002;22(1):44–47. 23. Foy CA, Mills J, Wheeler L, Ezaki M, Oishi SN. Long-term outcome following carpal wedge osteotomy in the arthrogrypotic patient. J Bone Joint Surg Am. 2013;95(20):1–6.

908.e1

24. Oishi SN, Foy CA, Wheeler L, Ezaki M. Carpal wedge osteotomy in the arthrogrypotic patient. JBJS Essent Surg Tech. 2014;4(4):e20. 25. Van Heest AE, Rodriguez R. Dorsal carpal wedge osteotomy in the arthrogrypotic wrist. J Hand Surg Am. 2013;38(2):265–270. 26. Oliveira RK, de, Marques F, da S, Praetzel RP, Bayer LR, Delgado PJ, Ribak S. Biplanar carpal wedge osteotomy in the treatment of the arthrogrypotic patients. Rev Bras Ortop (English Ed). 2018;53(6): 687–695. 27. Wenner SM, Saperia BS. Proximal row carpectomy in arthrogrypotic wrist deformity. J Hand Surg Am. 1987;12(4):523–525. 28. Littman A. Camptodactyly. A kindred study. JAMA. 1968;206(7): 1565–1567. 29. Wall LB, Ezaki M, Goldfarb CA. Camptodactyly treatment for the lesser digits. J Hand Surg Am. 2018;43(9):874.e1–874.e4. 30. Smith PJ, Grobbelaar AO. Camptodactyly: a unifying theory and approach to surgical treatment. J Hand Surg Am. 1998;23(1): 14–19. 31. Deng H, Deng S, Xu H, et al. Exome sequencing of a pedigree reveals S339L mutation in the TLN2 gene as a cause of fifth finger camptodactyly. PLoS One. 2016;11(5):1–9. 32. Benson LS, Waters PM, Kamil NI, Simmons BP, Upton W. Camptodactyly: classification and results of nonoperative treatment. J Pediatr Orthop. 1994;14(6):814–819. 33. Bates SJ, Hansen SL, Jones NF. Reconstruction of congenital differences of the hand. Plast Reconstr Surg. 2009;124(Suppl. 1): 128–143. 34. Wang AMQ, Kim M, Ho ES, Davidge KM. Surgery and conservative management of camptodactyly in pediatric patients: a systematic review. Hand. 2020;15(6):761–770. 35. Hong SW, Kim J, Kwon OS, Lee MH, Gong HS, Baek GH. Radiographic remodeling of the proximal phalangeal head using a stretching exercise in patients with camptodactyly. J Hand Surg Am. 2020;45(5):e1–e10. 36. Rhee SH, Oh WS, Lee HJ, Roh YH, Lee JO, Baek GH. Effect of passive stretching on simple camptodactyly in children younger than three years of age. J Hand Surg Am. 2010;35(11): 1768–1773. 37. Hori M, Nakamura R, Inoue G, et al. Nonoperative treatment of camptodactyly. J Hand Surg Am. 1987;12(6):1061–1065. 38. Foucher G, Loréa P, Khouri RK, Medina J, Pivato G. Camptodactyly as a spectrum of congenital deficiencies: a treatment algorithm based on clinical examination. Plast Reconstr Surg. 2006;117(6): 1897–1905. 39. Foucher G. “Bouquet” osteosynthesis in metacarpal neck fractures: a series of 66 patients. J Hand Surg Am. 1995;20(3 Part 2):86–90. 40. McCarrol H. Congenital flexion deformities of the thumb. Hand Clin. 1985;1(3):567–575. 41. Mih AD. Congenital clasped thumb. Hand Clin. 1998;14(1):77–84. 42. Mahmoud M, Abdel-Ghani H, Elfar JC. New flap for widening of the web space and correction of palmar contracture in complex clasped thumb. J Hand Surg Am. 2013;38(11):2251–2256. 43. Abdel-Ghani H, Mahmoud M, Shaheen A, Abdel-Wahed M. Treatment of congenital clasped thumb in arthrogryposis. J Hand Surg Eur Vol. 2017;42(8):794–798. 44. Abdel Ghani H. Modified dorsal rotation advancement flap for release of the thumb web space. J Hand Surg Am. 2006;31(2): 226–229. 45. Ezaki M, Oishi SN. Index rotation flap for palmar thumb release in arthrogryposis. Tech Hand Up Extrem Surg. 2010;14(1):38–40. 46. Tsuyuguchi Y, Masada K, Kawabata H, Kawai H, Ono K. Congenital clasped thumb: a review of forty-three cases. J Hand Surg Am. 1985;10(5):613–618. 47. Ghani HA, El-Naggar A, Hegazy M, Hanna A, Tarraf Y, Temtamy S. Characteristics of patients with congenital clasped thumb: a prospective study of 40 patients with the results of treatment. J Child Orthop. 2007;1(5):313–322.

 

SECTION VI • Congenital Disorders

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

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SYNOPSIS

ƒ Skeletal growth is possible because of the presence of an active physis. ƒ The physis is a temporary anatomical structure physiologically regulated by several factors. It can be hindered by congenital conditions (chondrodysplasias), direct damage, or interruption of its blood supply. ƒ Regardless of its etiology, when the physis and or the epiphysis are damaged in a skeletally immature individual, three main issues must be addressed: restoration of longitudinal growth, restoration of joint congruency and function, and replacement of the osseous defect. ƒ Therapeutic options include completion of epiphyseal arrest, resection of the physeal bar, and epiphyseal distraction. ƒ Where there is involvement of the whole epiphysis, autologous epiphyseal transfer may achieve the dual goals of restoring joint function and growth potential. The longer the period of time between the epiphyseal insult and the expected end of growth, the stronger the indication for surgical treatment.

Introduction   The

growth plate is a temporary anatomical entity, which allows axial growth in long bones. Once skeletal maturity is approached, the function of the growth plate gradually decreases and eventually stops.   Trauma, infection, irradiation, thermal injury, tumors, and congenital disorders may affect the growth plate and interfere with the growth process.   Any damage to the growth plate in a skeletally immature individual leads to growth disturbance with deformity and/or length discrepancy.   Goals of the surgical treatment should be restoration of the physiological growth, prevention of angular deformities, and correction of established deviation of bones and joints (Video Lecture 39.1 ).

Basic science/disease process Anatomy and physiology of the epiphyseal growth plate The physis (also known as growth plate, epiphyseal plate, epiphyseal growth plate, epiphyseal cartilage) is a highly specialized and organized cartilaginous structure derived from the mesoderm. It develops in the bone bud, secondary to the primary ossification centers (metaphysis) and is responsible for longitudinal and circumferential bone growth.1 The physis must be distinguished from the epiphysis, or secondary ossification center (Fig. 39.1). The physis consists of proliferating chondrocytes surrounded by synthesized extracellular matrix. The extracellular matrix is composed of water, collagen fibrils (mainly types II, IX, X, and XI) and proteoglycans (aggrecan, decorin, annexin II, V, and VI) arranged to form a sort of sponge with very small pores.2 This arrangement confers peculiar mechanical properties that permit the physis to be “hard” when an axial load is applied rapidly (a jumping child) or “soft” when deformed slowly (when chondrocytes secrete new extracellular matrix).3 The physis is traditionally divided into horizontal zones of chondrocytes at different stages of maturation (see Fig. 39.1). The resting zone (reserve zone or germinal matrix), immediately adjacent to the epiphysis, contains small, uniform, irregularly scattered chondrocytes, also referred to as stem cells, with low rates of proliferation but rich in storage materials (lipids and cytoplasmic vacuoles) for later growth.4,5 The resting zone is responsible for protein synthesis and for maintaining a germinal structure. Injury to this layer results in cessation of growth. When chondrocytes enter into the proliferative zone they undergo rapid duplication, increase the synthesis of collagen, in particular types II and XI,4 and become flat and well

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SECTION VI

CHAPTER 39  • Growth considerations in the pediatric upper extremity

Vascular anatomy of the growth plate Secondary ossification center/epiphysis Epiphyseal artery

Germinative zone Proliferative zone Hypertrophic zone

Ring of LaCroix Zone of Ranvier Metaphyseal artery

Physis

Zone of enchondral ossification

Periosteal sleeve Primary ossification center

Figure 39.1  Cross-sectional anatomy of the physis.

organized into longitudinal columns. Mitotic activity is present only at the base of these columns. This layer is responsible for longitudinal growth of the bone via active cell division. These first two zones have an abundant extracellular matrix that confers a great deal of mechanical strength, in particular in response to shear forces. Further morphological changes – maturation, degeneration, and provisional calcification – take place in the transformation (or hypertrophic) zone, divided into upper and lower hypertrophic zones. The presence of provisional calcification4–6 confers shear resistance to the lower hypertrophic zone. In contrast, the upper hypertrophic zone containing scant extracellular matrix is the weakest portion of the physis and it is here that most injury or alteration to the physis occurs.7–9 In continuity with the metaphysis is the zone of endochondral calcification where the mineralization process of the matrix becomes more intensive. The periphysis is a fibrochondroosseous structure that surrounds the physis of tubular bones and plays an important role in skeletal development10 (see Fig. 39.1): (1) it allows gradual circumferential growth of the physis; (2) it continues to maintain its transverse diameter11; and (3) it is critical to the overall stability of the growth plate and to support for the physis bone–cartilage junction.11–13 The part of the periphysis adjacent to the epiphysis is a wedge-shaped group of germinal cells known as the zone of Ranvier, while the part adjacent to the metaphysis is known as the ring of LaCroix. Histologically, the Ranvier and LaCroix zones are a single structure (see Fig. 39.1). Chondrocyte proliferation and differentiation in the physis, and therefore longitudinal skeletal growth, are regulated at both a systemic and local level.14 A number of endocrine, paracrine, and autocrine factors and their respective receptors are involved in this process. Amongst these, the parathyroid hormone-related protein (PTHrP) and the Indian hedgehog (Ihh) play a prominent role in skeletal maturation.1,15–18 There is also mechanical control of growth, which is important in pediatric orthopedic surgery because it is the basis of the widely used epiphysiodesis and epiphyseal distraction procedures.3

The epiphyseal and physeal cartilage vascular anatomy in newborn and early postnatal life is integral to long-bone development and differs from later postnatal periods. In late fetal and early postnatal life, epiphyseal cartilage canals (or transphyseal vessels) are seen passing through the physeal cartilage and communicating with the metaphyseal marrow. Such vessels play an active role in forming the secondary ossification centers18–20 but their primary earlier function is to provide nutrition by diffusion to epiphyseal chondrocytes. The transphyseal vessels are constantly obliterated several months after birth. Once the obliteration has occurred, the physeal cartilage becomes an avascular structure supplied by the epiphyseal vessels by diffusion, and by the metaphyseal vessels invading the lowermost regions of the hypertrophic zone.21,22 The main vascular supply to the germinal zone is from the epiphyseal vessels. Two types of epiphyseal vascularization are described.23 Type A epiphyses are almost entirely covered by articular cartilage, and the epiphyseal vessels enter the epiphysis after traversing the perichondrium. With this anatomical configuration, the blood supply to the epiphysis, and consequently to the germinal zone, is susceptible to damage if the epiphysis is separated from metaphysis. Type B epiphyses are only partially covered by articular cartilage. Their blood supply enters from the epiphyseal side and is protected from vascular injury during separation. The proximal femur and proximal radius are the only two examples of type A epiphyses.

Growth plate closure and skeletal age assessment during puberty It is generally assumed that long bone physes close at 14 years of skeletal age in females and at 16 years in males while the axial skeleton completes its development later.24–26 In 50% of normal children and adolescents, skeletal age does not differ from chronological age.27 Prediction of limb length discrepancy and final standing height, as well as decisions regarding when to perform an epiphysiodesis, are first subjected to determination of skeletal age. A complication unique to physeal injuries is growth disturbance. Once damage to the physis has occurred, the predicted amount of growth remaining from that specific physis must be determined to plan the treatment. This can be accomplished by determining the skeletal age of the patient and then using information on physeal growth rates and patterns assembled by Green and Anderson.28–32 Treatment decisions are often made during puberty. Puberty is the period of time in the growing individual characterized by a significant increase in growth rate.33,34 In girls, puberty starts at 11 years and ends at 13 years of skeletal age; in boys, it starts and ends 2 years later (13 years and 15 years of skeletal age).27 Peak height growth and Tanner stage 235 signal the beginning of puberty. The 2 years of pubertal growth spurt are known as the acceleration phase followed by a deceleration phase that continues until skeletal maturity. The radiographic markers currently used to assess skeletal age are all based on the appearance of ossification centers in specific skeletal segments at specific times. Several age

Basic science/disease process

assessment methods are based on the use of anteroposterior radiographs of the left hand and wrist.36–39 Other methods use left elbow radiographs.27,40 The axial skeleton can also be used to determine the skeletal age: Risser sign41 is based on the appearance of the left iliac apophysis of the pelvis. However, other radiographs can be used to assess skeletal age.27 Different assessment methods become helpful at different ages. The Greulich and Pyle atlas36 is probably the most common and widely used method to assess skeletal age. This technique, however, has some limitations, especially during puberty because it does not make it possible to assess skeletal age at 6-month intervals during the 2 years of peak growth

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rate.27 On the other hand, during the pubertal acceleration phase, the elbow, at the level of the distal epiphysis ossification centers and the olecranon apophysis, undergoes peculiar and identifiable morphological changes every 6 months27,40 (Figs. 39.2 & 39.3). Elbow ossification centers always appear in a determined sequence (the mnemonic is CRITOE: capitellum, radial head, internal (medial) epicondyle, trochlea, olecranon, external (lateral) epicondyle). The ages of appearance, as a general guide, are 1–3–5–7–9–11 years. During the acceleration phase, the skeletal age is best assessed with X-rays of the left hand and left elbow.42–45 In the deceleration phase, the growth rate decreases significantly.

Humerus Ulna

A

Olecranon

B

D

C

E

Figure 39.2  Olecranon maturation according to Dimeglio et al., with significant changes occurring every 6 months. (A) Two ossification centers (girls 11 years; boys 13 years); (B) half-moon shape (girls 11.5 years; boys 13.5 years); (C) rectangular shape (girls 12 years; boys 14 years); (D) beginning of fusion (girls 12.5 years; boys 14.5 years); and (E) complete fusion (girls 13 years; boys 15 years). 35

ELBOW CLOSURE Fusion distal phalanx of the thumb Girls: Age 13 Boys: Age 15

Risser still 0 prior to elbow closure Triradiate cartilage closure Girls: Age 12 Boys: Age 14

'Acceleration' phase

Risser I: Distal phalanx fusion Girls: Age 13.5 (Menarche) Boys: Age 15.5 Risser II: Proximal phalanx fusion Risser III: Greater trochanter fusion Intermediate phalanx fusion Risser IV: Ulnar epiphysis fusion 'Deceleration' phase

Beginning of puberty

Risser V:

Girls: Age 11 Boys: Age 13

Radial epiphysis fusion END OF GROWTH

Figure 39.3 Pubertal diagram. Acceleration phase, between skeletal age of 11 and 13 years in girls and 13 and 15 years in boys; Risser sign is 0. End of the acceleration phase, complete elbow and distal phalanx of the thumb closure; Risser sign is still 0.  

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

The remaining growth in both boys and girls is around 6 cm, of which 4.5 cm belong to the trunk and skull. During this phase, the most useful tools for skeletal age assessment are again the left hand and the Risser stage. Regardless of the assessment method used, skeletal age alone is not enough, and it should be related to other clinical and radiological findings such as standing and sitting height, Tanner stage, and annual growth rate.

Diagnosis/patient presentation Conditions affecting the growth plate A complication unique to physeal injuries is growth disturbance. Trauma is the most common cause of physeal injury and growth disturbance, but physeal growth arrest may as well occur after infection, tumor, irradiation, thermal injury, laser beam exposure, and sequelae of Blount’s disease (growth disorder with bowing of the tibia).46–49

Trauma Incidence and distribution in the upper extremity Physeal injuries represent 15–30% of all fractures in children50–54 and frequently involve the upper extremities.53,55 The incidence varies with age, with a peak in adolescence.53,55,56 The upper hypertrophic zone, just above the area of provisional calcification, is the weakest layer of the physis and where most injuries to the physis occur.7–9 This observation implies that, after most injuries, the germinal layer of the physis remains intact and attached to the epiphysis. Consequent normal growth should resume unless insult to the blood supply of the germinal layer or development of a “bony bridge” across the injured physis occurs.57

Classification of physeal fractures Several classification systems for physeal injuries have been described.58–64 The Salter and Harris classification (Fig. 39.4)65 is by far the most widely used system. This classification helps to distinguish different types of fractures and provides prognostic information as well. In Salter–Harris type I (see Fig. 39.4), the injury is a separation of the epiphysis from the metaphysis. It occurs entirely through the physis and therefore the surrounding bone is not involved. It is rare and tends to be

Type I

Type II

seen in infants or pathologic fractures, such those secondary to rickets or scurvy. Because the germinal layer remains with the epiphysis, growth is not hindered unless blood supply is interrupted (traumatic separation of the proximal femoral epiphysis). Often, X-rays of a child with a type I Salter–Harris fracture will appear normal. Healing of type I fractures tends to be rapid, and complications are rare. In Salter–Harris type II injury (see Fig. 39.4), the fracture extends along the hypertrophic zone of the physis but then it continues and exits through the metaphysis. This is the most common type of growth plate fracture, and tends to occur in older children. The epiphyseal fragment contains the entire germinal layer as well as a metaphyseal fragment, known as Thurston Holland’s sign. The periosteum on the side of the metaphyseal fragment is usually intact and provides stability after reduction. Growth disturbance is uncommon because the germinal layer remains intact. In Salter–Harris type III injury (see Fig. 39.4), the fracture starts through the hypertrophic zone and exits through the epiphysis. These injuries also tend to affect older children. By definition, type III fractures cross the germinal layer and are usually intra-articular. Consequently, they raise concerns about growth and, when displaced, they require anatomic, and often open, reduction. In Salter–Harris type IV injury (see Fig. 39.4), the fracture starts from the metaphysis and then extends through the physis and into the epiphysis. By definition, these fractures disturb the germinal layer and are usually intra-articular. Consequently, these injuries may impair normal growth and affect articular congruency. In type IV injuries, an anatomic reduction is mandatory in order to prevent osseous bridging across the physis and to restore the articular surface. A Salter–Harris type V injury (see Fig. 39.4) occurs when the physis is crushed from a pure compression force. It is so rare that some authors question whether such an injury exists.66 For those authors who have reported on this injury,65,67 it carries the most concerning prognosis as the growth disturbance is almost a rule. It often requires later surgical treatment to restore limb length and alignment. Despite being widely used, the Salter–Harris classification excludes a few physeal injuries: the Rang’s type VI epiphyseal injury,62,63 which represents an injury to the perichondral ring, and two additional injuries described in the Peterson classification system (Fig. 39.5),56 which is very similar to the Salter– Harris scheme. The Peterson type I fracture is a transverse

Type III

Type IV

Type V

Figure 39.4 Salter–Harris classification of physeal fractures. (Redrawn after Salter RB, Harris R. Injuries involving the epiphyseal plate. J Bone Joint Surg Am. 1963;45:587–621.)  

Diagnosis/patient presentation

Type I

Type II

Type III

Type IV

Type V

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Type VI

Figure 39.5  Peterson classification of physeal fractures. Type VI injuries are open and associated with loss of the physis. (Redrawn after Peterson HA. Physeal fractures: part 3. Classification. J Pediatr Orthop. 1994;14:439.)

fracture of the metaphysis that extends longitudinally into the physis. Clinically, this type of fracture is commonly seen in the distal radius. The Peterson VI fracture is an open injury associated with loss of the physis.

Treatment of physeal fractures Growth plate injuries that are less severe and occur closer to the time of closure of the growth plate, carry the best prognosis. More severe injuries occurring in younger patients require observation and possibly treatment to prevent problems. The principles of treatment of physeal fractures are the same as those involved in the treatment of all fractures, with a few important considerations. The goal in the treatment of physeal injuries is to obtain and maintain an acceptable reduction while avoiding any further damage to the germinal layer of the physis during reduction. Thus the most important goal, and the most subjective one, is to establish the limits of acceptable reduction. The age of the patient, the location and displacement of the fracture, and the time elapsed since the injury must all be taken into consideration when assessing a non-anatomic reduction. Although animal studies have not shown that delay in reduction produces a growth disturbance,68 the recommendation is to accept any displacement in type I and II injuries after 7–10 days9,69 and rather plan an osteotomy later. As a general rule, the remodeling potential is inversely proportionate to the age of the patient and is also related to the location and type of injury. Consequently, a greater deformity can be accepted in younger children. Because type III and IV injuries are by definition intra-articular, the focus must be on achieving an anatomic reduction regardless of the age of the patient and the time that has elapsed since the injury. Once the physeal fracture has been reduced, the reduction can be maintained with cast, pins, internal fixation, or combinations of these three.

Tumor Bone sarcoma involving the epiphysis Most of the common primary malignant bone tumors occur in patients aged under 30 years.70 Typically, osteosarcoma and Ewing sarcoma are found in adolescents and young adults, but they may also be diagnosed during infancy. The current approach to systemic therapy70 includes preoperative (neoadjuvant) chemotherapy and postoperative (adjuvant)

chemotherapy for both osteosarcoma and Ewing sarcoma. Radiotherapy is indicated only in Ewing sarcoma and it may be the only local treatment in cases of tumor in unfavorable locations, such as spine and pelvis, and in all cases where radical surgery is unlikely to be successful. Postoperative radiotherapy is indicated in all cases of intralesional resections with the aim of reducing the risk of local recurrence. With advances in bone reconstruction, the role of surgery has become predominant in the treatment of primary bone tumors, and the percentage of limb salvage versus amputation has significantly increased. In the upper limb, bone sarcomas are more frequently located in the distal radius and proximal humerus. Although the tumor is usually initially located at the metaphyseal level, the growth plate and the physis are always to be considered as a possible target of sarcoma invasion. From a functional standpoint, it is critical to know whether the surgical resection may spare the epiphysis or not. In the past, the growth plate was thought to be a biologic barrier to bone tumor invasion71–73; unfortunately this theory has not proven to be valid74–76 (Fig. 39.6). The current view is that invasion of the physis must always be suspected when the tumor is located in the proximity of the growth plate and all patients should be investigated with magnetic resonance imaging (MRI). In the event of epiphyseal involvement, the oncological resection must include the epiphysis and the only possible reconstructive option for such a defect in the pediatric age group is autologous epiphyseal transplant.

Congenital chondrodysplasia Chondrocyte proliferation and differentiation in the physis, and therefore skeletal growth, are regulated by various endocrine, paracrine, and autocrine factors. Any disturbance of the epiphyseal growth plate physiology and development results in various skeletal abnormalities known as dysplasia or chondrodysplasia. These cases may also require reconstruction to maintain growth.

Patient selection When the physis is damaged and deformity results or is foreseen, several treatment options are available. The best treatment for a growth plate injury depends on the individual situation. Although physeal injuries are common, problems arising are rare, occurring in only 1–10% of all physeal

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

fractures.9,53,56 Comminuted fractures, high-energy injuries, and physeal injuries that cross the germinal layer are more prone to result in physeal arrest with subsequent growth disturbance. Physeal injuries are most common in adolescents close to skeletal maturity. In these individuals, the remaining growth is limited.9,53,56 Consequently, even when it occurs, physeal arrest will produce minimal or no length discrepancy or angular deviation, and will seldom require treatment. Growth disturbance resulting from a physeal fracture is usually evident 2–6 months after the injury, but it may take up to a year to manifest.9 This information is important both to warn the parents about possible complications and to anticipate close long-term follow-up. In fact, the management of a post-traumatic growth disturbance is easier when directed exclusively towards treating the arrest rather than tackling both the arrest and the acquired deformity. Growth disturbance is usually a consequence of the development of a bony bridge, or bar, across the physis.57 However, when the injury only reduces rather than stops the growth rate of a portion of the physis, it may still produce asymmetric

growth and angular deformity with no development of a bony bridge.77 If the bony bar involves a large portion of the physis, it may stop the physeal growth completely. However, in most cases, the bony bar is confined to a rather small portion of the physis, and the growth stops only at that point. The remaining healthy physis continues to grow, creating a tethering effect which may produce either a shortening or a progressive significant angular deformity, or both. The extent and location of the bar, the skeletal age of the patient, and the amount of growth remaining from the physis must all be determined to plan the treatment of a physeal bar appropriately. Plain radiography, tomography, computed tomography (CT), or MRI46,78–81 may all be used to assess the anatomy of a physeal bar. MRI is by far the preferred method currently used to investigate physeal anatomy.82–85 In particular, fat-suppressed, 3D, gradient-recalled echo sequences can provide an accurate 3D reconstruction of the physis and estimate the percentage of physeal arrest.85 The classification of partial physeal arrests is based on their location within the physis (Fig. 39.7): peripheral (type A) or central (type B or C). In type B, the bar develops in the center of the physis and is surrounded by a perimeter of healthy physis. This may create a tethering effect that “tents” the epiphysis, leading to joint deformity. In type C (central) the bar traverses the entire physis (front to back or side to side) while the physis on both sides of the bar is normal.

Treatment/surgical technique Treatment of physeal arrest Different treatment options are available for the management of physeal arrests. These options include observation, completion of a partial physeal arrest, epiphysiodesis, physeal bar resection, or physeal distraction. The appropriate treatment strategy involves intimate knowledge of the patients, risk/ benefits of the various approaches, a specific estimate of the physeal injury extent and of the remaining time to skeletal maturity. These findings can be then applied to the treatment algorithm presented in Algorithm. 39.1.

Observation

Figure 39.6  Osteosarcoma involving the proximal epiphysis and the adjoining diaphysis in a 6-year-old child.

Type A

Observation may be the best option when the physeal bar involves the entire physis with complete growth arrest if existing limb length inequality and/or angular deformity are acceptable, or if the individual is close to skeletal maturity with little longitudinal growth remaining.

Type B

Type C

Figure 39.7 Classification of physeal bars. Type A, peripheral; type B, central, surrounded by normal physis; type C, central, traversing the physis.  

Treatment/surgical technique

915

Algorithm 39.1 90%

No consequences No treatment

10%

Decision-making process

PHYSEAL INJURY

Extent of physeal arrest Established deformities : Physeal bar Bone length discrepancy Angular deviation

Partial

Complete

Remaining time to skeletal maturity

Short

Long

Observation

Acceptable

Completion of arrest / Epiphysiodesis

Foreseen unacceptable

Physeal bar Resection if present

Already unacceptable

Corrective osteotomies Bone lengthening

Epiphyseal reconstruction

Algorithm for treatment of physeal injuries. Although physeal injuries are common, problems arising are rare, occurring in only 1–10% of all the lesions. Optimal treatment strategy can be determined by evaluating (1) the extent of the physeal injury grouped as partial (50%), (2) the remaining time to skeletal maturity grouped as short (1 yr), (3) the established skeletal/articular deformities grouped as acceptable, foreseen unacceptable, and already unacceptable.

Completion of a partial physeal arrest and epiphysiodesis Completion of a partial physeal arrest may be indicated if there is an acceptable existing angular deformity that may become clinically unacceptable if left untreated. To avoid significant limb shortening of the upper extremity, the surgeon must evaluate the predicted remaining growth and foresee a lengthening procedure if necessary. In the upper extremity limb, length discrepancy is a relative issue but the asynchronous rate of longitudinal growth between two bones in an anatomic region where the two bones are paired in close longitudinal relationship, as in the forearm, or asynchronous growth in an anatomic region where the harmonic activity of several physes contributes to the final size and shape of the bone, such as the distal humerus, might lead to a great risk of anatomic distortion. If the likelihood of length inequality is high, epiphysiodesis of a non-injured physis should be performed at the time of completion of the physeal arrest. Epiphysiodesis is an established method of limb length equalization or angular deformity correction in children and adolescents with projected limb length discrepancies

at maturity as great as 5 or 6 cm. It consists of temporarily stopping or permanently destroying the activity of the whole or just a part (hemiepiphysiodesis) of the growth plate. First introduced by Phemister in 1933,86 epiphysiodesis has evolved into various reversible or irreversible, open or percutaneous techniques, with and without instrumentation. The ideal tool should be minimally invasive, have minimal morbidity, and be reliably reversible. Pitfalls include errors in the prediction of growth and planning of the surgery. In particular, with non-reversible techniques, timing must be precise. Overcompensation for limb length discrepancy or creation of an opposite angular deformity can be very distressing for the patient, family, and surgeon. Although many different techniques have proven their efficacy, percutaneous epiphysiodesis using transphyseal screws combines the minimal invasiveness of a percutaneous technique with reversibility.87

Physeal distraction Physeal distraction is an alternative treatment for partial physeal arrest. Physeal distraction uses the growth plate as a zone of least resistance. It involves the damaged physis and

CHAPTER 39  • Growth considerations in the pediatric upper extremity

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therefore acts at the site of the deformity. It requires a force to be applied longitudinally across the physis, permitting both lengthening and angular correction on multiple planes, with external control of the correction until consolidation. Prior resection of the bony bar is not necessary. A distinction must be made between distractional epiphysiolysis and chondrodiastasis,88,89 chondrodiastasis,90 and hemichondrodiastasis.91 The chondrodiastasis technique employs large forces or rapid rate of distraction (> 1 mm/day) or both.92 This provokes a distraction and opening of the physis that provides a rapid in situ correction from the bony bar without prior bar resection, but almost invariably it produces a premature physeal fusion.93,94 This notion limits the indications to patients nearing skeletal maturity and preventive lengthening according to predicted limb length discrepancy.94,95 In the literature, physeal distraction techniques are mostly reported for the treatment of lower limb deformities and little is known about their application in the upper limb.

Bar resection If a portion of the physis has prematurely closed, but the reminder of the physis is healthy and there is substantial growth remaining, resection of the physeal bar and insertion of interposition materials are indicated. This technique in fact preserves longitudinal bone growth ability.96,97 The procedure was first introduced by Langenskiöld and has been documented in both human and animal models.47,79,96,98–101 The surgical technique of bar resection consists in removing the bone bridge along with the neighboring portions of metaphysis and epiphysis and filling the cavity with an inert material that will prevent recurrence of physeal bar formation (Fig. 39.8). Type A peripheral bars can be removed under direct vision, taking care to resect a wide cuff of periosteum. Type B and C central bars need to be approached through a window in the metaphysis or through an osteotomy (see Fig. 39.8A–C). Their resection may be facilitated by the use of fluoroscopy, fiberoptic lighting, and dental mirrors, as well as magnifying loupes (see Fig. 39.8C). Physeal bar resection is recommended when all the following conditions are present: the remaining physis must be undamaged and must be large enough to permit growth to continue; and there should be a significant amount of growth

A

remaining in that physis before physiologic physeal closure. Bars involving more than 50% of the physeal surface are unlikely to respond to surgical treatment.48,62,79,96–98,100 Despite the acceptance that younger patients, with higher growth potential, will benefit from physeal bar resection, there is still no agreement in quantifying the amount of this growth potential.79,98,101 According to Bright,102 indications for a bone bridge resection are as follows: there must be more than 50% of remaining healthy physis; the expected physeal growth must last for 2 years or more; there must be good soft-tissue coverage of the lesion; and, in the case of growth arrest due to infection, the infection must have been absent for more than 1 year. Once the bar is completely resected, various interpositional materials can be used to fill the void and prevent transphyseal bone bridge formation.62,79,98 Of the interposition materials described, fat is the most commonly used.96,103 It has the advantage of being autologous and immediately available. Failure to prevent re-formation of the physeal bridge104,105 may be due to the fact that fat may not provide adequate hemostasis of the cavity and may migrate.97,106 Silicone (Silastic) has been experimentally used in both human and animal studies with good results,102,107 but Silastic has been withdrawn from the market.99 Methylmethacrylate, commercially known as Cranioplastic (Codman/Integra LifeSciences, Mansfield, MA), is a material used to fill partial defects of the skull, is radiolucent, and is thermally non-conductive. The advantage as an interposition material97 is that its solid structure may help to support an epiphysis if a large metaphyseal defect has been created.106 It may, however, damage the healthy physis because of heat produced by the exothermic reaction during the solidifying phase.108 It may also be problematic to remove if further reconstructive procedures are required. Rarely, it can migrate from the physis into the diaphysis, and cause a pathological fracture.109 Expanded polytetrafluoroethylene (ePTFE) membrane (Gore-Tex dura substitute; W. L. Gore & Associates, Flagstaff, AZ) is generally used as an artificial dura substitute. The advantages of ePTFE membrane are that it is inert, non-reactive, unaffected by long-term exposure within the body,110 easy to handle, and provides good hemostasis. The disadvantage is that, being a soft material, it does not provide sufficient mechanical support and it is therefore only recommended when the resected area is at most 30% of the cross-section of the physis.111

B

Figure 39.8 (A) Central bar. (B) Bar resection through metaphyseal approach. (C) Assessing the resection.  

C

Treatment/surgical technique

Bone wax is readily available and commonly used in medical applications to control bleeding. It has been successfully used as interposition material with the advantages of being inexpensive and permitting good hemostasis. It is not associated with excessive complications.112 The disadvantage is that it does not offer a good mechanical support to the physis after bar resection. Regardless of which interposition material is selected, the purpose is to fill the cavity created in the physis with the material so that bar formation is prevented. After bar resection, radiographic markers should be placed on each side of the physis to assess growth resumption. Results after bar resection are variable. Even with appropriate patient selection and standardized operative technique, failure may result. Graft dislocation out of the cavity is one of the causes of failure.113 It is therefore recommended that the interposition material be anchored so that it will not dislodge, allowing bleeding into the cavity.97 It is important that, even when growth resumes, premature closure of the physis is to be expected.56,79,98,106,113 Physeal bar resection with interposition of certain materials plays a role in the treatment of partial physeal arrest; however, its results are relatively modest.

Corrective osteotomies, lengthening or shortening Epiphysiodesis and resection of the bone bridge with the insertion of interposition materials96,97 are the two main methods to treat partial physeal arrest that also prevent further progression of angular deformity. In addition, for mild deformities of less than 20°, we can expect spontaneous remodeling after bar resection,96,97,114 although this has not been universally reported.77 When an angular deformity is already evident, corrective osteotomy is indicated because remodeling sufficient to correct the deformity cannot be expected. Corrective osteotomy should be considered for any angular deformity that is judged to be “clinically unacceptable”.79,97,98,106 It is well known that the physeal growth rate responds to the force applied on the physis itself: growth is stimulated by both mild tension and mild compression.115 However, according to the Hueter–Volkmann principle,116 when compression on the growth plate exceeds a certain level, growth is indeed suppressed.115 If the compression is applied only on one side of the physis, worsening of the deformity may ensue. Improved alignment may therefore facilitate more normal growth. Bone lengthening involves the principle of distraction-induced osteogenesis and the use of an external fixator. Because of the non-weight-bearing status of the upper extremity, limb length discrepancy of the upper limbs is better tolerated and of less functional and cosmetic significance than their counterparts in the lower extremity. For these reasons, along with the incumbent risks associated with the surgery, indications for bone-lengthening procedures in the upper extremities are confined to selected cases.104,117–128 Reported complications of upper limb lengthening include pin tract infections, complications related to callus stability and formation (callus deformities after fixator removal, re-fractures, and malunions), diminished range of motion, elbow flexion contractures, pin-related nerve injuries,

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temporary radial nerve paresis as a complication of humeral lengthening, and sympathetic dystrophy.129–133 Considerable morbidity results from nerve injury secondary to the transfixing wires.132,133 In addition, in distraction lengthening of the upper limb, the bone formation takes longer compared to the lower limb because of the lack of weight-bearing. Therefore, the external fixator must be kept on for several months. The length of treatment further decreases patient compliance and can be a major issue in young children and adolescents.

Epiphyseal transfer of the proximal fibular epiphysis The first reports of free non-vascularized epiphyseal transplant date back to the end of the nineteenth century.134–136 All attempts in the pre-microsurgical era had discouraging results in terms of graft survival and growth. Early revascularization of the growth plate was identified as the crucial condition in determining success.137 In the past 30 years, advancements in microvascular surgery led to experimental research with several studies proving the feasibility of vascularized epiphyseal transfer in animal models.138–146 In the 1980s, this procedure was successfully introduced into clinical practice.147–149 These first encouraging results convinced the scientific community to refine further the technique and expand its indications. During the past 15 years, an increasing number of papers have successfully reported on limited series of reconstruction of either the proximal humerus or the distal radius and ulna with this technique.150–160

Indications The main indications for epiphyseal reconstruction are loss of an epiphysis following trauma, tumor resection, or infection in children. Vascularized epiphyseal transfer is a procedure that can simultaneously achieve the double goal of reconstructing a lost joint and maintaining growth potential. Because of its biological and morphological characteristics, the proximal fibula is by far the best donor site for reconstruction of large bone defects of the upper extremity. In fact, unlike other bone segments suggested for vascularized epiphyseal reconstruction,161,162 the proximal end of the fibula contains a true epiphysis with a growth plate that, if properly revascularized, maintains its growth potential at the recipient site. In addition, the fibula is a tubular bone with a long expendable diaphysis that is perfectly suited for upper limb reconstruction, allowing safe and stable bone fixation. The two most common locations of bone sarcomas of the upper extremity in the pediatric age group are the distal metaepiphysis of the radius and the proximal humerus, with a slightly higher incidence for the latter. Due to morphological and dimensional similarities, the proximal fibula is ideal for distal radius reconstruction.157 In addition, under the influence of a new biomechanical environment, the plasticity of the immature bone allows remarkable remodeling of the epiphysis after its transfer into the new anatomic location. Since the forearm is a two-bone segment and severe wrist deformity may result from asymmetrical growth of radius and ulna, the younger the patient, the greater is the indication for epiphyseal transfer in this location.

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

Case study Resection of the entire radius for sarcoma Sometimes the extension of the sarcoma is so wide that resection of the entire radius is required (Fig. 39.9). In such case, the reconstruction with proximal fibular epiphysis is particularly demanding. It is actually impossible to restore the entire length of the radius and, in addition, the absence of interosseous membrane would lead to unacceptable instability and proximal migration of the graft. In the two cases of our series, we performed a bone fixation of the fibula to the midshaft of the ulna in a neutral pronation/ supination (Fig. 39.10A). This is a type of radioulnar synostosis, which provides a stable neoradius with the only drawback of eliminating pronation and supination. The only conceptual concern that may be related to this choice is the risk to have a divergent growth of the two bones, because the ulna is straight and the new radius has an angle of about 45° with the longitudinal axis of the forearm. However, in our case, longitudinal remodeling occurred and over the years the distal portion of the new radius migrated medially toward the ulna (see Fig. 39.10B), thus improving the stability of the joint and its function (Fig. 39.11).

A

Figure 39.9  Sarcoma involving extensively the radius. Resection of the entire bone is required.

Despite the anatomic mismatch between the fibular head and the glenoid fossa and the difference in transverse diameter of the shafts between the humerus and the fibula,151 autologous proximal fibular transplant remains the best option for autogenous reconstruction of the proximal humerus (Fig. 39.12). Over time, the fibular diaphysis undergoes hypertrophy, which minimizes the size discrepancy. Moreover, remodeling of the fibular head, although less impressive than in distal radius reconstruction, is expected, leading to more than acceptable shoulder joint stability and function (Fig. 39.13). Since the proximal growth plate is responsible for 80% of humeral bone growth,152 in case of massive bone losses of the distal humeral epiphysis, there is no need to transfer a vascularized proximal fibular epiphysis, as required in distal radius or proximal humerus reconstruction. A satisfactory osteo-articular reconstruction can be obtained by the use of a single-step technique to reconstruct humeral epiphysis and diaphysis following Ewing’s sarcoma resection using a

B

Figure 39.10  (A) Bone fixation of the fibula to the midshaft of the remaining ulna. Radioulnar synostosis in neutral pronation/supination position is created, providing a stable neoradius but eliminating pronation and supination. (B) Longitudinal remodeling of the physis occurred over the years.

vascularized prefabricated bony flap of iliac crest and fibula grafts153 (Fig. 39.14). Proximal fibula epiphyseal transfer has proven to be an excellent option in limb salvage surgery in pediatric oncologic cases. Congenital differences of the upper limb, such as radial

Treatment/surgical technique

919

Figure 39.11  Long-term clinical outcome: functional flexion–extension of the wrist and wrist stability are restored after surgery.

Figure 39.13  Reconstruction of the proximal humerus at 5-year follow-up. The transferred proximal fibula underwent significant remodeling and hypertrophy as well as enough longitudinal growth to prevent limb length discrepancy.

Figure 39.12  In proximal humerus reconstruction, the smaller fibula is usually inserted inside the humeral medullar canal with a periosteal flap overlapping the bony junction. This type of assemblage improves stability and ability to heal. Vascular anastomoses are usually performed end-to-end to the deep humeral vessels.

Figure 39.14  MRI (T1 weighted, coronal) showing an Ewing’s sarcoma of the right humerus after preoperative chemotherapy without proximal epiphyseal involvement in a 5-year-old male patient.

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dysplasia, may also benefit from this surgical procedure. These cases, though, raise a few concerns and considerations: the new radius may be expected to grow more than the native ulna, which usually is hypoplastic, thus developing wrist instability and ulnar deviation. Limited literature is available on epiphyseal transfer for radial dysplasia, with encouraging results reported by Yang et al.,163 only on Bayne and Klug type III radial longitudinal deficiency. There is no report on long-term outcomes that could help to validate the technique.149,156,164 Autologous distal humerus osteoarticular reconstructions have been described in the literature, but published case numbers are small with heterogeneous diagnosis. The nonmicrosurgical options are limited to allograft, prosthesis, or composite of both (APC – Allograft Prosthesis Composites). Custom-made hemiarthroplasty of the distal humerus is another option, with concerns regarding elbow stability. Moreover, in case of subtotal humerus resection, prosthetic anchorage into the small residual proximal humerus would not be possible, and prosthetic reconstruction would require a total humerus custom-made lengthening hemiarthroplasty.154 Autologous reconstruction represents an alternative to endoprosthesis, which is burdened by a high risk of complications and surgical revisions. Vascularized epiphyseal transplant based on the anterior tibial vascular system is a long and demanding procedure with high rate of complications, although transient, at the donor site. For these reasons, the cost–effectiveness ratio should be carefully evaluated. From personal experience of 30 cases, we have concluded that distal radius reconstruction is indicated up to 13 years of age because the radius and ulna require symmetrical growth until skeletal maturity. On the other hand, the humerus tolerates well a length discrepancy from both functional and cosmetic standpoints, setting the age limit for such a procedure at around 10 years of age.165

acceptable blood supply to the growth plate based solely on the peroneal artery. Although this is probably anatomically possible if enough soft tissue is left around the fibular neck, further experiences151,159 have had disappointing results on the growth rate of grafts supplied by the peroneal artery alone. The use of a bipedicled graft has been suggested,147,149,151 with the purpose of providing two separate blood supplies to the epiphysis and the diaphysis. This option, however, is technically demanding, time-consuming, and requires two anastomoses at the recipient site. In addition, the physis is very susceptible to ischemia, and normal growth can be expected only if ischemia time is less than 3 hours.171 For these reasons, a single-pedicled graft is definitely a better choice. The anterior tibial system has proven to be adequate in supplying both the epiphysis and the shaft, and it is therefore the preferred pedicle for such a graft (Fig. 39.15). A potential disadvantage to the use of the anterior tibial vascular system is that the pedicle is very short (the distance between the division of the popliteal artery and the origin of the recurrent branch at the fibular neck). To overcome this issue, it has been suggested to use a reverse-flow pedicle.151,157,164 In this way,

Vascular supply of the proximal fibular epiphysis In the past 30 years, the vascular anatomy of the proximal fibular epiphysis has been extensively investigated in order to define the best pedicle supplying both the epiphysis and the diaphysis of such a graft. There is general agreement that the proximal epiphysis of the fibula is supplied by two vascular sources: (1) the lateral inferior genicular artery; and (2) the recurrent branches of the anterior tibial artery. The role of the two systems is differently emphasized according to different authors,166–170 but the majority of reports confirm that the anterior tibial artery provides the major contribution to the blood supply of the proximal fibular growth plate. Summarizing the data available in the literature, the lateral inferior geniculate artery mostly supplies the capsule of the proximal tibiofibular joint, the anterior and posterior recurrent branches of the anterior tibial artery supply the epiphysis, and the peroneal artery supplies the fibular shaft. It has also been experimentally demonstrated168,169 that the anterior tibial artery is able to vascularize the proximal two-thirds of the fibular diaphysis through tiny musculoperiosteal perforators that distribute to the periosteum of the shaft. Almost all possible vascular pedicle combinations have been described in use in clinical practice. Pho et al. reported on 3 cases148 where the peroneal artery was used as the pedicle, postulating that the presence of intercommunicating branches between the metaphyseal and epiphyseal systems allowed for

Epiphyseal recurrent branch Anterior tibial artery

Periosteal branches to fibula

Figure 39.15  The anterior tibial artery supplies the growth plate and proximal epiphysis by means of a recurrent epiphyseal branch and the proximal two-thirds of the diaphysis by means of musculoperiosteal perforator branches.

Treatment/surgical technique

921

long vessels are provided, allowing comfortable anastomosis at the recipient site.

Harvest technique of the proximal fibula based on the tibialis anterior artery (Video 39.1 ) The flap includes the proximal fibular epiphysis and a variable amount of the adjoining diaphysis. The epiphyseal articular surface is oriented upward and medially to form the proximal tibiofibular joint. The biceps femoris tendon and the lateral collateral ligament are inserted in the lateral and proximal aspect of the epiphysis, which is also where the origins of the peroneus longus and extensor digitorum longus muscles are located. The common peroneal nerve crosses the fibular neck, moving toward the anterior compartment of the leg. The superficial branch is located in the space between the extensor digitorum longus and peroneus longus muscles, while the deep branch reaches the interosseous membrane and joins the anterior tibial vessels, giving several motor branches to the surrounding muscles. Proceeding proximally, the dissection of the vascular pedicle with preservation of the motor branches becomes increasingly demanding because of the increasing number of motor branches surrounding the vessels. The harvest technique (Video 39.1 ) has been refined over the years and has been finally described in detail172,173 with the purpose of standardizing it and making it reproducible. The aim of the procedure is to harvest the proximal fibula, preserving the blood supply to both the epiphysis and diaphysis with the least possible local morbidity. The following step-bystep description is the optimal surgical sequence according to the experience of the senior author (M.I.).

Skin incision The surgical approach is developed in the plane between tibialis anterior and extensor digitorum longus muscles because this allows for direct visualization of the neurovascular bundle. The skin incision is therefore located in the anterolateral aspect of the leg and is extended proximally up to the neck of the fibula where it proceeds posteriorly and proximally over the biceps femoris tendon (Fig. 39.16A,B).

Peroneal nerve

Incision

A

B

Figure 39.16  (A,B) An anterolateral approach is used for the harvest of the proximal fibula based on the anterior tibial vascular system. The skin incision is on the projection of the intermuscular space between the tibialis anterior and extensor digitorum longus muscles. The incision is prolonged proximally and posteriorly over the tendon of biceps femoris muscle.

Exposure of the anterior tibial pedicle The anterior tibial artery and veins lie on the interosseous membrane. The peroneal nerve surrounds the vessel according to a very intricate tridimensional pattern and delivers several motor branches to the muscles of the anterior compartment of the leg (Fig. 39.17). These motor branches are more numerous in the proximal part of the leg, and it is therefore recommended to start the dissection distally and proceed proximally, maintaining the same plane to the fibular neck. Great care should be taken not only in dissecting the nerve from the vessels but also in preserving the small perforator branches of the anterior tibial artery that pierce the extensor digitorum longus and peroneus longus muscles, interposed between the vascular pedicle and the fibular shaft, supplying the periosteum of the proximal two-thirds of the diaphysis.

Dissection of the peroneal nerve at the fibular neck The point where the peroneal nerve approaches the fibular neck is an important anatomic landmark. The nerve is in close contact with the bone and is covered by the proximal portion of extensor digitorum longus and peroneus longus muscles,

Figure 39.17  During the diaphyseal dissection of the pedicle, great care must be paid to isolating the peroneal nerve and its motor branches to the muscles of the anterior compartment.

which must be sharply divided in order to expose and protect the nerve and its motor branches (Fig. 39.18). Medially, at the same level, the recurrent epiphyseal branch of the anterior tibial artery rises from the main artery and pierces the muscular

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

cuff and feeds the epiphysis. Its direct dissection is unnecessary and potentially dangerous; it is therefore recommended to preserve the proximal insertion of the muscles attached to the proximal epiphysis in order to protect the fragile epiphyseal vascular network. Biceps femoris tendon

Peroneal nerve Fibular epiphysis

Anterior tibial artery

Section of the interosseous membrane and distal osteotomy The interosseous membrane must be sharply detached from the tibia, and all the soft tissue interposed between it and the vascular bundle must be carefully protected (Fig. 39.19). The perforator vessels to the shaft of the fibula branch off laterally and pierce the of extensor digitorum longus and peroneus longus muscle bellies. In order to maintain the vascular connection between the artery and bone, a longitudinal strip of muscle approximately 1 cm wide should be preserved around the harvested fibula (Fig. 39.20). The fibula is cut distally at

Tibialis anterior

Peroneus longus Extensor digitorum longus

Figure 39.19  Sharp detachment of the interosseous membrane from the tibia. Note the location of the vascular pedicle and its relationship to the peroneal nerve. Anterior tibial artery and vein

A

Tibialis anterior Peroneus longus Tibia Extensor digitorum longus Fibula

B

Figure 39.18  (A,B) The peroneal nerve is an important landmark in proximal dissection. The nerve is exposed in its intramuscular portion by means of sharp section of the extensor digitorum longus and peroneus longus muscles. The muscular cuff proximal to the section must be left intact because it protects the recurrent branch to the growth plate of the anterior tibial artery.

Figure 39.20  The perforator branches to the diaphysis are too small and fragile to allow a direct intramuscular dissection. It is therefore suggested that a strip of muscle containing the perforators be left intact between the vascular pedicle and the bone.

Treatment/surgical technique

the desired length, and an extra portion of periosteum is left in order to improve healing capacity at the recipient site. The anterior tibial artery and veins are ligated as distally as possible to obtain a long reverse-flow pedicle.

Harvest of the biceps femoris tendon and capsulotomy of the proximal tibiofibular joint The insertions of the biceps femoris tendon and the lateral collateral ligaments are almost at the same point at the apex of the fibula. The tendon should be divided in two strips (Fig. 39.21): the posterior portion is harvested with the fibula to provide additional soft tissue useful for stabilization of the recipient joint; the anterior half is used to reinforce the lateral collateral ligament after its reinsertion on the lateral aspect of tibial metaphysis by means of staples or transosseous sutures. Gentle external rotation of the fibula allows for the division of the medial and posterior capsule of the proximal tibiofibular joint after coagulation of the lateral inferior genicular artery.

Final dissection of the proximal portion of the vascular pedicle The anterior tibial artery should be dissected up to the division of the popliteal artery (Fig. 39.22). The recurrent branch rises from the anterior tibial artery approximately 2 cm distal to its origin, and is often difficult to identify. For this reason, it is advisable to preserve all the small vessels, which pierce the muscular cuff toward the fibular epiphysis. After release of the tourniquet, the muscular cuff surrounding the epiphysis, the diaphyseal periosteum, and the medullary canal are carefully inspected. After a few seconds, bleeding should be observed at the three levels, confirming the successful harvest of the proximal fibula, based on the anterior tibial artery pedicle (Fig. 39.23). Due to low tolerance to ischemia, it is suggested to wait 20–30 min before clipping and dividing the proximal pedicle. Details regarding technical pearls are given in Box 39.1; about the selection of flap vena comitantes in Box 39.2; osteosynthesis in Box 39.3; and selection of recipient vessels in Box 39.4.

BOX 39.1  Surgical tips for harvest of proximal fibula flap • Start dissection distally: this approach simplifies the dissection of the peroneal nerve from the vascular pedicle. • Save a strip of muscle between the vascular pedicle and the fibular diaphysis to avoid injury to the tiny musculoperiosteal branches. • Identify the peroneal nerve at the neck of the fibula and carefully dissect the muscular belly of peroneus longus and extensor digitorum longus. • The muscular cuff surrounding the epiphysis must remain attached to the epiphysis because it contains the recurrent branch. • In cases of intersection of the motor nerve to the tibialis anterior muscle and the recurrent branch, a section of the nerve as close as possible to the muscle and subsequent microsurgical neurorraphy are needed. • After the harvest of the fibula, a meticulous reconstruction of the lateral collateral ligament is needed. The ligament should be reinforced with the residual strip of biceps femoris tendon and finally reinserted on the lateral aspect of the tibia.

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BOX 39.2  Selection of flap venae comitantes The proximal epiphyseal fibular transfer based on the anterior tibial artery is a reverse-flow flap; however, an adequate venous return is guaranteed by the presence of several small shunts that interconnect the two venae comitantes, allowing the reverse venous flow to bypass the valves. Due to this intricate pattern of valves and shunts, usually, only one of the two venae comitantes has adequate return flow: it is instrumental, for a good outcome, to identify which one it is. After 20–30 min with the tourniquet down, the two venae comitantes are ligated and divided proximally leaving intact the flow through the artery. Within a couple of minutes, the venous flow is inverted and bleeding is evident from one of the two venae comitantes. The bleeding vein is tagged to be anastomosed at the recipient site (Fig. 39.24). During the dissection of the vascular bundle care must be taken not to interrupt these delicate venous shunts.

BOX 39.3 Osteosynthesis Humerus reconstruction The humerus is a single bone segment with a high mechanical stress, particularly in case of rotation against resistance. For this reason, a stable bone fixation must be provided; long plates are therefore preferred over less invasive options such as K-wires and screws. However, the implant cannot be too stiff for risk of fracture at the level of the most proximal screw, which is the weakest point of the implant (Fig. 39.25A). In order to provide a more elastic and less invasive bone fixation, we advocate the use of locking compression plates (LCP). The fibula is usually placed for a couple of centimeters in the medullary canal of the distal stump of the humerus and a periosteal flap is wrapped around the bony junction. Then a long LCP plate is placed. Three bicortical screws are used in the humeral portion while few unicortical screws are used in the fibular portion (see Fig. 39.25B). This type of assemblage provides a very stable bone fixation at the junction between fibula and humerus and a minimally invasive and elastic fixation in the fibular segment.

Radius reconstruction Similarities in size and shape between the radius and the fibula facilitates osteosynthesis in the forearm. Also in this case, LCP plates are the preferred method of bone fixation. As an alternative, lag screws and step-cut osteotomy may be used. The wrist joint is temporarily stabilized with a K-wire which is usually removed 1 month after surgery, in addition the strip of biceps femoris tendon is woven in the residual capsule in order to provide additional stability to the joint. By contrast, the distal radioulnar joint is intentionally left lax without any type of stabilization in order to maintain full range of pronation and supination.

BOX 39.4  Selection of recipient vessels The harvest of the fibula based on a reverse-flow anterior tibial artery pedicle allows for a long distal pedicle, which may be easily anastomosed to the recipient vessels. In humeral reconstruction, the deep brachial artery, satellite of the radial nerve, is usually preferred for end-to-end anastomosis with the fibular vessels. If the venae comitantes are too small, the cephalic vein or one of the venae comitantes of the brachial artery may be chosen for venous anastomosis. In case of radius reconstruction, there are more choices. When the radial artery is resected together with radius, the proximal stump can be easily anastomosed with the fibular pedicle end to end: Alternatively, the anterior interosseous artery may be used end-to-end because its sacrifice has a negligible impact on hand blood supply.

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

Biceps femoris tendon

Head of fibula Peroneus longus

Extensor digitorum longus

Figure 39.22  After release of tourniquet and 20–30 min of reperfusion of the flap, the tibialis anterior artery is ligated and severed just distal to its emergence from the popliteal artery.

1

Tibialis anterior

Biceps femoris tendon (cut) Head of fibula Peroneus longus Extensor digitorum longus

A

Fibula (cut)

Superficial peroneal nerve Tibialis anterior

2

Deep peroneal nerve

B

Figure 39.21  (A,B) The biceps femoris tendon is longitudinally divided in two strips. One is harvested with the bone flap and may be used to improve the stability of the joint after the transfer. The second one is fixed to the lateral aspect of the tibia to reinforce the lateral collateral ligament.

Figure 39.23  At the end of the dissection, before severing the vascular pedicle, the tourniquet is released to reset the ischemia time. Bleeding should be observed from both the epiphysis and the medullar canal after a few minutes. 1, posterior articular capsule is severed; 2, bleeding from the bone is observed.

Outcomes, prognosis, and complications Normal flow

Case study

925

Inverted flow Proximal

Distal humerus osteoarticular reconstruction The surgical plan is aimed to achieve distal humerus osteoarticular reconstruction by means of a prefabricated vascularized iliac crest and fibula graft (Fig. 39.26). In the case presented here, a double-curved-S-incision was used, starting proximally at the coracoid process, into a delto-pectoral approach, and extending to the lateral aspect of the arm and elbow. Insertions of the deltoid, pectoralis major, latissimus dorsi and teres major muscles were cut from the humerus. A careful blunt dissection was performed to separate and protect the neurovascular bundle (median nerve, and the brachial artery and vein). The radial nerve in the arm and the ulnar nerve in the epitroclear fossa were identified and protected. The biceps muscle was preserved while portions of the brachialis, brachioradialis and triceps muscles were resected due to the tumor. An elbow arthrotomy sparing the medial and lateral ligaments was performed and the proximal humerus was cut with an oscillating saw 1.5 cm below the proximal growth plate. Frozen section of the residual medullary canal ensured a negative margin. Simultaneously, we harvested the contralateral vascularized bony flaps. A 4×3 cm iliac crest graft was shaped to recreate the humeral epiphysis and fixed to a 13 cm long fibula flap with two 2.4 mm screws, then the two pedicles were anastomosed in an end-to-end fashion. The construct was inserted in the recipient site and, under fluoroscopic control, fixed with the proximal part of the humerus with a 2.7 mm T-plate and screws (Box 39.5). Due to the small size of the residual proximal humerus, the osteosynthesis was performed across the growth plate with the insertion of two epiphyseal screws. Medial and lateral collateral ligaments of the elbow were fixed on the iliac bone with suture anchors and the deep brachial artery with its venae comitantes were used as donor vessels for end-to-end anastomoses. The radial nerve was transposed anteriorly to avoid nerve compression (Fig. 39.27). The elbow joint was stabilized with a temporary transolecranon Kirschner wire, local muscle/tendons were reinserted, with the pectoralis major sutured onto the deltoid and the brachioradialis muscle onto the triceps. Under fluoroscopic control, tibiofibular metaphyseal synostosis at the donor-site ankle was performed with a 2.7 mm screw. Surgical sites were closed primarily and one suction drain was placed in each of them (Box 39.6).

Postoperative care Donor site In order to protect the reconstructed lateral collateral ligament, a cast at 30° flexion of knee and neutral ankle position is applied. In children below the age of 8 years, the cast is maintained for 4 weeks; in older and compliant children, the cast may be substituted after 2 weeks with a brace of appropriate size, for a total of 4 weeks of immobilization. The rehabilitation program is started

Venous valve

Venous shunt

Bleeding comitans

A

Distal

B

Figure 39.24  (A) Pattern of valves and shunts of venae comitantes. (B) When the flow is inverted, bleeding is usually evident from one of the two venae comitantes.

at 1 month postoperatively with the aim of recovering full motion of the knee without compromising stability (Box 39.7).

Recipient site A long spica cast or a shoulder brace is applied for 4 weeks after distal radius and proximal humerus reconstruction. The rehabilitation program follows the immobilization period and must take into account different variables such as type and stability of bone fixation, amount of muscles excised during the resection, and age and compliance of the patient. As for distal humerus reconstruction, the arm is kept immobilized in a Desault bandage for 4 weeks. One month after surgery, the trans-olecranon Kirschner wire is removed, and the shoulder and arm brace are kept for another 4 weeks, encouraging daily progressive and careful elbow passive mobilization. Active mobilization training of the shoulder and elbow is started at 8 weeks (Figs. 39.28 & 39.29).

Outcomes, prognosis, and complications Analysis of the results takes into account the survival of the grafts, as well as their consolidation, longitudinal growth, and remodeling. In a personal series of 27 cases of upper limb skeletal reconstruction after bone sarcoma resection with

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

A

Figure 39.26  Schematic picture of the construct inserted into the arm and, under fluoroscopic control, fixed to the proximal part of the humerus with a 2.7-mm T-plate and screws.

B

Figure 39.25  (A) Humerus implant: the weakest portion of the implant is at the passage between the hardware and the bone, with higher risk of fracture at these levels especially in case of rigid implants. (B) More elastic and less invasive bone fixation.

BOX 39.5  Equipment preferences for distal humerus osteoarticular reconstruction by means of a prefabricated iliac crest and fibula free flap • Cortical 2.4-mm screws for fixation of the fibula flap to the iliac crest flap • 2.7-mm plate with cortical screws to fix the flaps to the proximal humerus • Kirschner wires for temporary fixation and to be used as a guide, under fluoroscopy, for proximal osteotomy • High speed burr to shape the allograft to the adequate size

BOX 39.6  Tips, tricks, and pitfalls • The proximal juxta-articular osteotomy can be performed using Kirschner wires to guide the oscillating saw under fluoroscopy. • In growing children, valgus deformity of the donor site ankle can be expected as a complication of vascularized fibula harvest. In this case, preventive tibiofibular screw fixation was implanted. This is advisable in children if the residual fibula is less than 6 cm in length. • During bony flaps harvesting, the use of piezoelectric surgery provides safe and precise cutting of the bone. • As soon as the proximal osteotomy is healed and solid union is radiographically evident, the proximal epiphyseal screws should be removed and replaced with metaphyseal screws with distal orientation in order to free the growth plate and to avoid epiphysiodesis.

Outcomes, prognosis, and complications

927

Figure 39.27  After the construct was inserted and fixed in the desired position, the radial nerve was transposed anteriorly to avoid nerve compression.

BOX 39.7  Postoperative rehabilitation: donor site • After 4 weeks of immobilization, the cast or the splint are removed and passive range of motion of knee and ankle is initiated. • The use of crutches is virtually impossible because of the surgery involving the upper limb and is therefore avoided. • During the therapy sessions, the child is also helped to get acquainted with the upright position standing only on the nonoperated leg. • The splint is repositioned only at night for 4 more weeks. • A transient palsy of the peroneal nerve occurs in almost all cases. Great care is taken to avoid equinus deformity of the foot with Achilles tendon retraction. A Codivilla spring is used routinely in all cases of peroneal palsy and maintained until complete recovery. Passive mobilization of the ankle is taught to parents and performed 3–5 times per day. • Full weight-bearing is usually possible at 2 months after surgery. • The rehabilitation program is eventually tailored to each patient considering their clinical condition and the necessity of adjuvant chemotherapy.

epiphyseal transplant, all of the transferred bones except one survived and healed with the recipient bone in a period of time ranging from 1 to 2 months. This variability depended on the age of the child and the length of the reconstructed segment. In some cases, the viability of the transplant was confirmed by bone scan. Significant axial growth, calculated by the progressive increase in the distance between the tip of the metal plate used for bone fixation and the apex of the epiphysis of the transferred fibula, has been observed in approximately 70% of cases monitored. Its extent was variable depending on factors that are only partially known, amongst which the patient’s age was predominant. The annual growth trend varied between 0.7 and 1.35 cm (Fig. 39.30), and in all cases, there was prevention of future length discrepancy with the opposite limb. As far as the radius is concerned, symmetrical growth was observed in the neoradius in all cases, not only with respect to the opposite limb, but also to the adjacent ulna, which confirms the integration of the fibula into

Figure 39.28  Postoperative X-ray, latero-lateral projection, at 3 months after primary surgery. The iliac crest flap adequately matches the proximal part of the elbow joint.

Figure 39.29  Postoperative X-ray, posteroanterior projection, at 3 months after primary surgery showed assembling with osteoperiosteal fibula and iliac crest free flaps, to restore the humeral diaphysis and the distal humerus, respectively.

its new anatomical site. The average flexion of the wrist was 75°, while the average extension was 63°. The overall range of movement was equal to on average 70% of the opposite hand, which allowed for excellent functional recovery. The prono-supination range was also restored.

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As for ostearticular distal humerus reconstruction, there were no deep infections at either donor or recipient sites. After 8 months follow-up, bony union was documented radiographically with no signs of local recurrence. No signs of metastasis were detected from the chest computed tomography (CT) scan as well. At latest follow-up at 10 months, the imaging tests confirmed union at the proximal osteotomy and vascularized fibula diaphyseal hypertrophy. At clinical examination, the patient achieved full range of motion of the shoulder. The elbow was stable, with flexion from 45° to 110° and complete pro-supination.

Secondary procedures Secondary procedures may be necessary at both the donor and the recipient site.

Donor site Figure 39.30  Postoperative radiograph and 4-year follow-up of one case of distal radius reconstruction. In this case, the average growth per year was 0.9 cm.

In cases of humeral reconstruction, the functional outcomes were not as positive. The morphological and dimensional discrepancy between the fibular head and the glenoid fossa may lead to proximal migration of the fibular epiphysis and, in some cases, subacromial displacement. Moreover, the extent of soft tissue involved in the neoplasia and consequently removed further hinders functional recovery. In all monitored cases, however, shoulder abduction between 70° and 100° was observed. Premature ossification of the growth plate and consequent end of growth were observed in five cases of humeral reconstruction. Two of these transplants were based on peroneal vessels, which, in our opinion, are not as reliable in ensuring correct epiphyseal perfusion. In the other three cases, the epiphyseal artery was probably damaged during stabilization in the glenohumeral joint. Five fractures of the neohumerus and two of the neoradius were observed. All the fractures but one healed conservatively in due time. Replacement of an inadequate fixation was performed in one case. In four cases of proximal humerus reconstruction, incorrect alignment between the fibula head and glenoid fossa was observed. In these cases, the epiphysis migrated subacromially. The reasons for this complication are the anatomical mismatching between fibular head and glenoid fossa and the extensive oncological excision of muscles and ligaments with consequent joint stability. All the four cases, however, recovered an acceptable range of motion. With transosseous suture of the lateral collateral ligament at the donor site, no residual instability of the knee was ever observed. Neuropraxia of the peroneal nerve occurred in approximately two-thirds of cases. This was probably caused by stretching of small motor branches during the dissection. This deficit resolved spontaneously within 1 year in all but two cases. One of the patients had a permanent residual paralysis of the tibialis anterior and one of the extensor digitorum longus muscles.

In case of permanent palsy of the peroneal nerve, a tendon transfer is indicated to restore the function of the tibialis anterior muscle. In our series, we observed no cases of knee joint instability.

Recipient site A feared complication is the total loss of the graft due to failure to restore its blood supply. We did not observe this complication, but its treatment would require the use of a massive frozen allograft as salvage procedure. In the majority of cases, the fate of an osteoarticular allograft in the medium/long term is a massive resorption of the articular cartilage, which should be treated with a prosthetic replacement of the allogenic humeral head. In our experience, we have observed premature growth arrest, probably due to vascular damage to the physis, in five cases of proximal humerus reconstruction. Despite the limb length discrepancy, all patients have an acceptable function, and no further surgery was required. A relatively frequent complication is graft fracture in proximal humerus reconstruction. In our series, this event was usually successfully treated conservatively with immobilization in a cast. Nonetheless, revision of the hardware and cancellous bone grafting may be considered in cases of displaced fractures.

Future directions Although epiphyseal transfer proved to be a reliable and effective reconstructive option in case of skeletal disorders involving an immature epiphysis, this procedure is not widely used yet. The technique is well standardized, and several papers are now available in the literature reporting, in the vast majority of cases, either the reconstruction of the proximal humerus or the distal radius. In the future, new recipient sites might be added to the classic ones, taking advantage of the high remodeling potential of the immature fibular head. We have recently used this technique for mandible reconstruction on a child affected by osteoblastoma of the mandibular condyle, with

Future directions

encouraging results. In selected cases, other joints might benefit from reconstruction with vascularized proximal epiphyseal transfer. Congenital differences at the wrist level, such as radial and ulnar dysplasia, are now successfully treated with this procedure. A few cases of radial dysplasia have been, indeed,

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reported recently with good results.163 These cases, though, need a longer follow-up to evaluate the growth rate. These initial results are very encouraging, and epiphyseal transfer of the proximal fibula may be a valid alternative to the procedure described by Vilkki,174 which is, at present, the only alternative to the conventional techniques.

References

References 1. Burdan F, Szumilo J, Korobowicz A, et al. Morphology and physiology of the epiphyseal growth plate. Folia Histochem Cytobiol. 2009;47:5–16. 2. Allen DM, Mao JJ. Heterogeneous nanostructural and nanoelastic properties of pericellular and interterritorial matrices of chondrocytes by atomic force microscopy. J Struct Biol. 2004;145:196–204. 3. Rauch F. Bone growth in length and width: the yin and yang of bone stability. J Musculoskelet Neuronal Interact. 2005;5:194–201. 4. Ballock RT, O’Keefe RJ. The biology of the growth plate. J Bone Joint Surg Am. 2003;85:715–726. 5. Melrose J, Smith SM, Smith MM, et al. The use of Histochoice for histological examination of articular and growth plate cartilages, intervertebral disc and meniscus. Biotech Histochem. 2008;83:47–53. 6. Sawae Y, Sahara T, Sasaki T. Osteoclast differentiation at growth plate cartilage–trabecular bone junction in newborn rat femur. J Electron Microsc (Tokyo). 2003;52:493–502. 7. Haas S. The localization of the growing point in the epiphyseal cartilage plate of bone. Am J Orthop Surg. 1917;15:563. 8. Harris W. The endocrine basis for slipping of the upper femoral epiphysis. J Bone Joint Surg Br. 1950;32:5. 9. Salter R. Epiphyseal plate injuries. In: Letts R, ed. Management of Pediatric Fractures. New York, NY: Churchill Livingstone; 1994:11. 10. Seeman E. Periosteal bone formation – a neglected determinant of bone strength. N Engl J Med. 2003;349:320–323. 11. Iannotti J, Goldstein S, Khun J, et al. Growth plate and bone development. In: Simon SR, ed. Orthopaedic Basic Sciences. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1994:191. 12. Juster M, Moscofian A, Balmalin-Oligo N. Formation of the skeleton: VIII. Growth of the long bone: periostealization of the metaphyseal bone. Bull Assoc Anat (Nancy). 1975;59:437. 13. Oestreich AE, Ahmad BS. The periphysis and its effect on the metaphysis: I. Definition and normal radiographic pattern. Skeletal Radiol. 1992;21:5. 14. van der Eerden BC, Karperien M, Wit JM. Systemic and local regulation of the growth plate. Endocr Rev. 2003;24:782–801. 15. Kronenberg HM. Developmental regulation of the growth plate. Nature. 2003;423:332–336. 16. Kronenberg HM. PTHrP and skeletal development. Ann N Y Acad Sci. 2006;1068:1–13. 17. Kozhemyakina E, Lassar AB, Zelzer E. A pathway to bone: signaling molecules and transcription factors involved in chondrocyte development and maturation. Development. 2015;142:817–831. 18. Zhu M, Zhang J, Dong Z, et al. The p27 pathway modulates the regulation of skeletal growth and osteoblastic bone formation by parathyroid hormone-related peptide. J Bone Miner Res. 2015;30:1969–1979. 19. Wilsman NJ, van Sickle DC. The relationship of cartilage canals to the initial osteogenesis of secondary centers of ossification. Anat Rec. 1970;168:381–392. 20. Burkus JK, Ganey TM, Ogden JA. Development of the cartilage canals and the secondary center of ossification in the distal chondroepiphysis of the prenatal human femur. Yale J Biol Med. 1993;66:193–202. 21. Trueta J, Morgan JD. The vascular contributions to osteogenesis. J Bone Joint Surg Br. 1960;42B:97–109. 22. Shapiro F. Epiphyseal and physeal cartilage vascularization: a light microscopic and tritiated thymidine autoradiographic study of cartilage canals in newborn and young postnatal rabbit bone. Anat Rec. 1998;252:140–148. 23. Dale GG, Harris WR. Prognosis of epiphyseal separation: an experimental study. J Bone Joint Surg Br. 1958;40B:116–122. 24. Bayley N. Individual patterns of development. Child Dev. 1956;27:45. 25. Prader A. Normal growth and disorders of growth in children and adolescents. Klin Wochenschr. 1981;59:977.

929.e1

26. Westh RN, Menelaus MB. A simple calculation for the timing of epiphyseal arrest: a further report. J Bone Joint Surg Br. 1981;63:117. 27. Canavese F, Charles YP, Dimeglio A. Skeletal age assessment from elbow radiographs. Review of the literature. Chir Organ Mov. 2008;92:1–6. 28. Anderson M, Green W. Lengths of the femur and tibia: norms derived from orthoroentgenograms of children from five years of age until epiphyseal closure. Am J Dis Child. 1948;75:279. 29. Anderson M, Green WT, Messner MB. Growth and predictions of growth in the lower extremities. J Bone Joint Surg Am. 1963;45A:1–14. 30. Anderson M, Messner MB, Green WT. Distribution of lengths of the normal femur and tibia in children from one to eighteen years of age. J Bone Joint Surg Am. 1964;46:1197–1202. 31. Green WT, Anderson M. Experience with epiphyseal arresting correcting discrepancies in length of the lower extremities in infantile paralysis: a method of predicting the effect. J Bone Joint Surg Am. 1947;29:659. 32. Green WeT, Anderson M. Skeletal age and the control of bone growth. Instr Course Lect. 1960;17:199. 33. Dimeglio A. La Croissance en orthopédie. Montpellier: Suramps Medical;; 1987. 34. Exner GU. Normalwerte in der Kinderorthopadie. Wachstum und Entwicklung. Stuttgart: Thieme; 1990. 35. Tanner JM, Whitehouse RH. Clinical longitudinal standards for height, weight, height velocity and weight velocity and stages of puberty. Arch Dis Child. 1976;51:170–179. 36. Greulich WW, Pyle SI. Radiographic Atlas of Skeletal Development of Hand and Wrist. 2nd ed. Stanford, CA: Stanford University Press; 1959. 37. Sempé M, Pavia C. Atlas de la maturation squelettique. Paris: SIMEP; 1979. 38. DeRoo T, Schroder HJ. Atlas van de Skeletale Leeftijd. Dordrecht: Intercontinental Graphics;; 1977. 39. Tanner JM, Whitehouse RH, Marshall WA, et al. Assessment of Skeletal Maturity and Prediction of Adult Height (TW Method). London: Academic Press; 1975. 40. Sauvegrain J, Nahm H, Bronstein N. Etude de la maturation osseuse du coude. Ann Radiol. 1962;5:542–550. 41. Risser JC. The iliac apophysis: an invaluable sign in the management of scoliosis. Clin Orthop. 1958;11:111–119. 42. Dimeglio A. Growth in pediatric orthopaedics. In: Morris T, Weinstein SL, eds. Lovell & Winter's Pediatric Orthopaedics. 6th ed. Philadelphia, PA: Lippincott: Williams and Wilkins; 2005:35–61. 43. Diméglio A, Charles YP, Daures JP, et al. Accuracy of the Sauvegrain method in determining skeletal age during puberty. J Bone Joint Surg Am. 2005;87:1689–1696. 44. Charles YP, Canavese F, Diméglio A. Skeletal age determination from the elbow during pubertal growth. Orthopade. 2005;34: 1052–1060. 45. Charles YP, Daures JP, de Rosa V, et al. Progression risk of idiopathic juvenile scoliosis during pubertal growth. Spine. 2006;31:1933–1942. 46. Birch JG, Herring JA, Wenger DR. Surgical anatomy of selected physis. J Pediatr Orthop. 1984;4:224. 47. Langenskiöld A. Growth disturbances after osteomyelitis of femoral condyles in infants. Acta Orthop Scand. 1984;55:1. 48. Langenskiöld A, Osterman K. Surgical treatment of partial closure of the epiphyseal plate. Reconstr Surg Traumatol. 1979;17:48. 49. Peterson HA, Wood MB. Physeal arrest due to laser beam damage in a growing child. J Pediatr Orthop. 2001;21:335. 50. Bisgard J, Martenson L. Fractures in children. Surg Gynecol Obstet. 1937;65:464. 51. Compere E. Growth arrest in long bones as a result of fractures that include epiphysis. JAMA. 1935;105:2140. 52. Mann DC, Rajmaira S. Distribution of physeal and non-physeal fractures in 2650 long bone fractures in children aged 0–16 years. J Pediatr Orthop. 1990;10:713. 53. Mizuta T, Benson WM, Foster BK, et al. Statistical analysis of incidence of physeal injuries. J Pediatr Orthop. 1987;7:518.

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

54. Worlock P, Stower M. Fracture patterns in Nottingham children. J Pediatr Orthop. 1986;6:656–660. 55. Peterson HA, Madhok R, Benson JT, et al. Physeal fractures: Part 1. Epidemiology in Olmested County, Minnesota, 1979–1988. J Pediatr Orthop. 1994;14:423. 56. Peterson HA. Physeal fractures: Part 3. Classification. J Pediatr Orthop. 1994;14:439. 57. Chung R, Foster BK, Xian CJ. The potential role of VEGF-induced vascularization in the bony repair of injured growth plate cartilage. J Endocrinol. 2014;221:63–75. 58. Aitken A. The end results of the fractured distal radial epiphysis. J Bone Joint Surg Am. 1935;17:302. 59. Aitken A. The end results of the fractured distal tibial epiphysis. J Bone Joint Surg Am. 1936;18:605. 60. Aitken A. End results of fractures of the proximal humeral epiphysis. J Bone Joint Surg Am. 1936;18:1036. 61. Foucher M. De la divulsione des epiphyses. Cong Med Fr (Paris). 1863;1:63. 62. Odgen JA. Skeletal Injury in the Child. Philadelphia, PA: Lea & Febiger; 1981. 63. Odgen JA. Injury to the growth mechanism of the immature skeleton. Skeletal Radiol. 1981;6:237. 64. Poland J. Traumatic Separation of the Epiphyses. London: Smith, Elder; 1898. 65. Salter R, Harris W. Injuries involving the epiphyseal plate. J Bone Joint Surg Am. 1963;45:587. 66. Peterson HA, Burkhart SS. Compression injury of the epiphyseal growth plate: fact or fiction? J Pediatr Orthop. 1981;1:377. 67. Skak SV. A case of partial physeal closure following compression injury. Arch Orthop Trauma Surg. 1989;108:185. 68. Egol KA, Karunakar M, Phieffer L, et al. Early versus late reduction of a physeal fracture in an animal model. J Pediatr Orthop. 2002;22:208. 69. Rang M. Injuries of the epiphysis, growth plate and perichondral ring. In: Rang M, ed. Children's Fractures. Philadelphia, PA: JB Lippincott; 1983:23. 70. Gloeckler Ries LA, Reichman ME, Riedel Lewis D, et al. Cancer survival and incidence from the Surveillance, Epidemiology, and End Results (SEER) program. Oncologist. 2003;8:541–552. 71. Mahboubi S. Radiologic approach to primary bone lesions. In: Pediatric Bone Imaging: A Practical Approach. Boston, MA: Little Brown; 1989:175. 72. Kuettner KE, Pauli BU, Soble L. Morphological studies on the resistance of cartilage to invasion by osteosarcoma cells in vitro and in vivo. Cancer Res. 1978;38:277–287. 73. Brem H, Folkman J. Inhibition of tumor angiogenesis by cartilage. J Exp Med. 1975;141:427–439. 74. Enneking WF, Kagan A. Transepiphyseal extension of osteosarcoma: incidence, mechanism and implications. Cancer. 1978;41:1526–1537. 75. Panuel M, Gentet JC, Scheiner C, et al. Physeal and epiphyseal extent of primary malignant bone tumors. Correlation of preoperative MRI and the pathologic examination. Pediatr Radiol. 1993;23:421–424. 76. Norton KI, Hermann G, Abdelwahab IF, et al. Epiphyseal involvement in osteosarcoma. Radiology. 1991;180:813–816. 77. Herring JA, ed. Tachdjian's Pediatric Orthopaedics. 4th ed. Philadelphia, PA: Saunders Elsevier; 2007. 78. Carlson WO, Wenger DR. A mapping method to prepare for surgical excision of a partial physeal arrest. J Pediatr Orthop. 1984;4:232. 79. Kasser JR. Physeal bar resection after growth arrest about the knee. Clin Orthop Relat Res. 1990;255:68. 80. Loder R, Swinford AE, Kuhns LR, et al. The use of the helical computed tomographic scan to assess bony physeal bridges. J Pediatr Orthop. 1997;17:356. 81. Oestreich AE. Imaging on the skeleton and soft tissue in children. Curr Opin Radiol. 1992;4:55.

82. Cheon JC, Kim IO, Choi IH, et al. Magnetic resonance imaging of the remaining physis in partial physeal resection with graft interposition in a rabbit model. A comparison with physeal resection alone. Invest Radiol. 2005;40:235. 83. Craig JG, Cramer KE, Cody DD, et al. Premature partial closure and other deformities of the growth plate: MR imaging and three dimensional modeling. Radiology. 1999;210:835. 84. Eklund K, Jamarillo D. Patterns of premature physeal arrest: MR imaging of 111 children. AJR Am J Roentgenol. 2002;178:967. 85. Sailhan F, Chotel F, Guibal AL, et al. Three-dimensional MRI imaging in the assessment of physeal growth arrest. Eur Radiol. 2004;14:1600. 86. Phemister DB. Operative arrestment of longitudinal growth of bone in the treatment of deformities. J Bone Joint Surg Am. 1933;15:1–15. 87. Khoury JG, Tavares JO, McConnell S, et al. Results of screw epiphysiodesis for the treatment of limb length discrepancy and angular deformity. J Pediatr Orthop. 2007;27:6. 88. Zazjyalov PV, Plaksin IT. Elongation of crural bones in children using a method of distraction epiphysiolysis. Vestn Khir Im I I Grek. 1967;103:67–70. 89. Zazjyalov PV, Plaksin IT. Distraction epiphyseolysis for lengthening of the lower limbs in children. Khirurgiia (Mosk). 1968;7:121–123. 90. De Bastiani G, Aldegheri R, Renzi Brivio L. Indicazioni particolari dei Fissatori esterni. G Ital Fissatore Esterno. 1979;501:31. 91. Aldegheri R, Trivella G, Lavini F. Epiphyseal distraction. Hemichondrodiatasis. Clin Orthop Relat Res. 1989;241:128–136. 92. De Bastiani G, Aldegheri R, Renzi Brivio L, et al. Chondrodiatasiscontrolled symmetrical distraction of the epiphyseal plate. Limb lengthening in children. J Bone Joint Surg Br. 1986;68:550–556. 93. Kershaw CJ, Kenwright J. Epiphyseal distraction for bony bridges: a biomechanical and morphologic study. J Pediatr Orthop. 1993;13:46–50. 94. Canadell J, de Pablos J. Correction of angular deformities by physeal distraction. Clin Orthop Relat Res. 1992;283:98–105. 95. Langlois V, Laville JM. Physeal distraction for limb length discrepancy and angular deformity. Rev Chir Orthop Reparatrice Appar Mot. 2005;91:199–207. 96. Langenskiöld A. Surgical treatment of partial closure of the growth plate. J Pediatr Orthop. 1981;1:3–11. 97. Peterson H. Partial growth plate arrest and its treatment. J Pediatr Orthop. 1984;4:246–258. 98. Birch JG. Surgical technique of physeal bar resection. Instr Course Lect. 1992;41:445. 99. Bright RW. Operative correction of partial epiphyseal plate closure by osseous-bridge resection and silicone-rubber implant: an experimental study in dogs. J Bone Joint Surg Am. 1974;56:655. 100. Langenskiöld A. An operation for partial closure of an epiphyseal plate in children, and its experimental basis. J Bone Joint Surg Br. 1975;57:325. 101. Langenskiöld A. Partial closure of the epiphyseal plate: principles of treatment. 1978. Clin Orthop Relat Res. 1993;297:4. 102. Bright RW. Partial growth arrest: identification, classification, and the results of treatment. Orthop Trans. 1982;6:65–66. 103. Broughton NS, Dickens DRV, Cole WG, et al. Epiphyseolysis for partial growth plate arrest. J Bone Joint Surg Br. 1989;71B:13–16. 104. Lamoureux J, Verstreken L. Progressive upper limb lengthening in children: a report of two cases. J Pediatr Orthop. 1986;6:481–485. 105. Williamson RV, Staheli LT. Partial physeal growth arrest: treatment by bridge resection and fat interposition. J Pediatr Orthop. 1990;10:769–776. 106. Ogden JA. Current concepts review: the evaluation and treatment of partial physeal arrest. J Bone Joint Surg Am. 1987;69A:1297–1302. 107. Macksoud WS, Bright R. Bar resection and Silastic interposition in distal radial physeal arrest. Orthop Trans. 1989;13:1–2. 108. Cabanela ME, Coventry MB, Maccarty CS, et al. The fate of patients with methyl methacrylate cranioplasty. J Bone Joint Surg Am. 1972;54A:278–281.

References

109. Shea KG, Rab GT, Dufurrena M. Pathological fracture after migration of cement used to treat distal femur physeal arrest. J Pediatr Orthop B. 2009;18:185–187. 110. Setzen G, Williams EF. Tissue response to suture materials implanted subcutaneously in a rabbit model. Plast Reconstr Surg. 1997;100:1788–1795. 111. Inoue T, Naito M, Fujii T, et al. Partial physeal growth arrest treated by bridge resection and artificial dura substitute interposition. J Pediatr Orthop B. 2006;15:65–69. 112. Yoshida T, Kim WC, Tsuchida Y, et al. Experience of bone bridge resection and bone wax packing for partial growth arrest of distal tibia. J Orthop Trauma. 2008;22:142–147. 113. Hasler CC, Foster BK. Secondary tethers after physeal bar resection: a common source of failure? Clin Orthop Relat Res. 2002;405:242–249. 114. Oesterman K. Operative elimination of partial premature epiphyseal closure. An experimental study. Acta Orthop Scand. 1972;147(Suppl):1–79. 115. Frost HM. Biomechanical control of knee alignment: some insights from a new paradigm. Clin Orthop. 1997;335:335–342. 116. Mehlman CT, Araghi A, Roy DR. Hyphenated history: the Hueter–Volkmann law. Am J Orthop. 1997;26:798–800. 117. Bagatur AE, Doúan A, Zorer G. Correction of deformities and length discrepancies of the forearm in children by distraction osteogenesis. Acta Orthop Traumatol Turc. 2002;36:111–116. 118. Hosny GA. Unilateral humeral lengthening in children and adolescents. J Pediatr Orthop B. 2005;14:439–443. 119. Janovec M. Short humerus: results of 11 prolongations in 10 children and adolescents. Arch Orthop Trauma Surg. 1991;111:13–15. 120. Lee FY, Schoeb JS, Yu J, et al. Operative lengthening of the humerus. J Pediatr Orthop. 2005;25:613–616. 121. Mader K, Gausepohl T, Pennig D. Shortening and deformity of radius and ulna in children: correction of axis and length by callus distraction. J Pediatr Orthop B. 2003;12:183–191. 122. Burge P. Lengthening in the upper limb [Editorial]. J Hand Surg Br. 1993;18B:141–143. 123. Dahl MT. The gradual correction of forearm deformities in multiple hereditary exostoses. Hand Clin. 1993;9:707–718. 124. Irani RN, Petrucelli TC. Ulnar lengthening for negative ulnar variance in hereditary multiple osteochondromata. J Pediatr Orthop. 1993;1:143–147. 125. Price CT, Mills WL. Radial lengthening for septic growth arrest. J Pediatr Orthop. 1983;3:88–91. 126. Pritchett JW. Lengthening the ulna in patients with hereditary multiple exostoses. J Bone Joint Surg Br. 1986;68B:561–565. 127. Masada K, Tsuyuguchi Y, Kawai H, et al. Operations for forearm deformity caused by multiple osteochondromas. J Bone Joint Surg Br. 1989;71B:24–29. 128. Linscheid RL. Ulnar lengthening and shortening. Hand Clin. 1987;3:69–78. 129. Abe M, Shirai H, Okamoto M, et al. Lengthening of the forearm by callus distraction. J Hand Surg Br. 1996;21B:151–163. 130. Kiss S, Pap K, Vízkelety T, et al. The humerus is the best place for bone lengthening. Int Orthop. 2008;32:385–388. 131. Paley D. Problems, obstacles, and complications of limb lengthening by the Ilizarov technique. Clin Orthop. 1990;250:81–104. 132. Tetsworth K, Krome J, Paley D. Lengthening and deformity correction of the upper extremity by the Ilizarov technique. Orthop Clin North Am. 1991;22:689–713. 133. Villa A, Paley D, Catagni MA, et al. Lengthening of the forearm by Ilizarov technique. Clin Orthop Relat Res. 1990;250:125–137. 134. Helferich U. Versuche uber die Transplantation des Intermediarknorpels Wachsender. Rohrenknochen Dtsch Z Chirurgie. 1899;51:564. 135. Haas S. The experimental transplantation of the epiphysis with observations on the longitudinal growth of bone. JAMA. 1915;65:1965–1971.

929.e3

136. Biscard JD. Transplanted epiphyseal cartilage. Arch Surg. 1939;39:1028–1030. 137. Harris W, Martin R, Tile M. Transplantation of epiphyseal plates. J Bone Joint Surg Am. 1965;47A:897–914. 138. Donski PK, Carwell GR, Sharzer LA. Growth in revascularized bone grafts in young puppies. Plast Reconstr Surg. 1979;64:239–243. 139. Donski PK, O’Brien BM. Free microvascular epiphiseal transplantation: an experimental study in dogs. Br J Plast Surg. 1980;33:169–178. 140. Bowen CVA. Experimental free vascularized epiphyseal transplants. Orthopedics. 1986;9:893–898. 141. Bowen CVA, O’Brien BM. Experimental study of the microsurgical transfer of growth plates. Can J Surg. 1984;27:446. 142. Bowen CVA, Ethridge CP, O’Brien BM, et al. Experimental microvascular growth plate transfers. Part 1 – Investigation of vascularity. J Bone Joint Surg Br. 1988;70B:305–310. 143. Bowen CVA, O’Brien BM, Gumley GJ. Experimental microvascular growth plate transfers. Part 2 – Investigation of feasibility. J Bone Joint Surg Br. 1988;70B:311–314. 144. Nettelblad H, Randolph MA, Weiland AJ. Physiologic isolation of the canine proximal fibular epiphysis on a vascular pedicle. Microsurgery. 1984;5:98–101. 145. Nettelblad H, Randolph MA, Weiland AJ. Free microvascular epiphyseal plate transplantation. An experimental study in dogs. J Bone Joint Surg Am. 1984;66:1421–1430. 146. Manfrini M, Randolph MA, Andrisano A, et al. Orthotopic knee grafts in rats: a model for growth plate transplantation. Microsurgery. 1988;9:242–245. 147. Tsai TM, Ludwig L, Tonkin M. Vascularized fibular epiphyseal transfer: a clinical study. Clin Orthop. 1986;210:228–234. 148. Pho RW, Patterson MH, Kour AK, et al. Free vascularised epiphyseal transplantation in upper extremity reconstruction. J Hand Surg Am. 1988;13:440–447. 149. Zhong-Wei C, Guang-Jian Z. Epiphyseal transplantation. In: Pho RW, ed. Microsurgical Technique in Orthopaedics. London: Butterworths; 1988:121–128. 150. Wood MB, Gilbert A. Microvascular Bone Reconstruction. London: Martin Dunitz; 1997:85–89. 151. Innocenti M, Ceruso M, Manfrini M, et al. Free vascularised growth plate transfer after bone tumor resection in children. J Reconstr Microsurg. 1998;14:137–143. 152. Pritchett JW. Growth plate activity in the upper extremity. Clin Orthop Relat Res. 1991;268:235–242. 153. Innocenti M, Lucattelli E, Brogi M, Totti F, Campanacci D. Custom-made elbow joint reconstruction with free osteoperiosteal fibula and iliac crest flaps after tumor resection: a case report. J Vis Surg. 2019;5:28–34. 154. Houdek MT, Wagner ER, Wyles CC, Nanos 3rd GP, Moran SL. New options for vascularized bone reconstruction in the upper extremity. Semin Plast Surg. 2015;29(1):20–29. 155. Ad-El DD, Paizer A, Pidhortz C. Bipedicled vascularized fibula flap for proximal humerus defect in a child. Plast Reconstr Surg. 2001;107:155–157. 156. Amr SM, el-Mofty AO, Amin SN. Further experiences with transplantation of the head of the fibula. Handchir Mikrochir Plast Chir. 2001;33:153–161. 157. Innocenti M, Delcroix L, Manfrini M, et al. Vascularized proximal fibular epiphyseal transfer for distal radial reconstruction. J Bone Joint Surg Am. 2004;86A:1504–1511. 158. Bae DS, Waters PM, Sampson CE. Use of free vascularized fibular graft for congenital ulnar pseudoarthrosis; surgical decision making in the growing child. J Pediatr Orthop. 2005;25:755–762. 159. Innocenti M, Delcroix L, Romano GF, et al. Vascularized epiphyseal transplant. Orthop Clin North Am. 2007;38:95–101. 160. Papadopulos NA, Weigand C, Kovacs L, et al. The free vascularized fibula transfer: long term results of wrist reconstruction in young patients. J Reconstr Microsurg. 2009;25:3–13.

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CHAPTER 39  • Growth considerations in the pediatric upper extremity

161. Teot L, Giovannini UM, Colonna MR. Use of free scapular crest flap in pediatric epiphyseal reconstructive procedures. Clin Orthop Relat Res. 1999;365:211–220. 162. Mayr JM, Pierer GR, Linhart WE. Reconstruction of part of the distal tibial growth plate with an autologous graft from the iliac crest. J Bone Joint Surg Br. 2000;82:558–560. 163. Yang J, Qin B, Li P, et al. Vascularized proximal fibular epiphyseal transfer for Bayne and Klug type III radial longitudinal deficiency in children. Plast Reconstr Surg. 2015;135:157e–166e. 164. Sawaizumi M, Maruyama Y, Okaiima K, et al. Free vascularised epiphyseal transfer designed on the reverse anterior tibial artery. Br J Plast Surg. 1991;44:57–59. 165. Innocenti M, Baldrighi C, Menichini G. Long-term results of epiphyseal transplant in distal radius reconstruction in children. Handchir Mikrochir Plast Chir. 2015;47:83–89. 166. Restrepo J, Katz D, Gilbert A. Arterial vascularization of the proximal epiphysis and the diaphysis of the fibula. Int J Microsurg. 1980;2:48–51. 167. Bonnel F, Lesire M, Gomis R, et al. Arterial vascularization of the fibula microsurgical transplant techniques. Anat Clin. 1981;3: 13–23.

168. Taylor GI, Wilson KR, Rees MD, et al. The anterior tibial vessels and their role in epiphyseal and diaphyseal transfer of the fibula: experimental study and clinical applications. Br J Plast Surg. 1988;41:451–469. 169. Menezes-Leite MC, Dautel G, Duteille F, et al. Transplantation of the proximal fibula based on the anterior tibial artery: anatomical study and clinical application. Surg Radiol Anat. 2000;22:235–238. 170. Mozaffarian K, Lascombes P, Dautel G. Vascular basis of free transfer of proximal epiphysis and diaphysis of fibula: an anatomical study. Arch Orthop Trauma Surg. 2009;129:183–187. 171. Stark RH, Matloub HS, Sanger JR, et al. Warm ischemic damage to epiphyseal growth plate: a rabbit model. J Hand Surg Am. 1987;12:54–61. 172. Innocenti M, Delcroix L, Romano GF. Epiphyseal transplant: harvesting technique of the proximal fibula based on the anterior tibial artery. Microsurgery. 2005;25:284–292. 173. Innocenti M, Delcroix L, Manfrini M, et al. Vascularized proximal fibular epiphyseal transfer for distal radial reconstruction. J Bone Joint Surg Am. 2005;87(Suppl 1):237–246. 174. Vilkki SK. Vascularized joint transfer for radial club hand. Tech Hand Up Extrem Surg. 1998;2:126–137.

SECTION VII  •  New Directions

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

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Introduction Upper extremity amputees are different from lower extremity amputees in many aspects. The patients tend to be younger, and their amputations are primarily due to trauma and tumors rather than dysvascular conditions. The patients live longer with their residual limbs, and prosthetic concerns for the two groups of patients dramatically differ. Upper extremity prostheses require more control, more movement, and more precision than those for the lower extremity. Fortunately, upper extremity prostheses have less load-bearing requirements since they do not need to support the weight of the body. The purpose of this chapter is to familiarize the reader with necessary concepts to care for the upper extremity amputee (Algorithm 40.1). Handling of soft tissues, bones, and nerves are reviewed for each of the levels of amputation. Prosthetics and prosthetic control will be a necessary accompaniment of this chapter. Recent advancements in the field, including targeted muscle reinnervation (TMR), regenerative peripheral nerve interfaces (RPNI), and direct skeletal attachment (osseointegration, or OI) will be introduced.

Principles of prosthetic reconstruction Improve the soft tissues to help wear a prosthesis A key principle of prosthetic reconstruction is for the residual limb to be pain-free with stable soft tissues to allow the prosthesis to fit comfortably without causing sores, wounds, or pain generated by the weight of the device. The surgical treatment of patients with unreconstructable upper extremity conditions must consider issues unique to the amputee. The amputation must have durable soft tissues to allow for prosthetic fitting. The soft tissues cannot be overly thick or mobile,

because this impedes transmission of the forces created by the residual muscles on bone. Similarly, the soft tissues cannot be overly thin, or else the slightest trauma or pressure causes breakdown, which can limit prosthesis wear. Standard plastic surgery principles involve common sense and judgment to add soft tissues where there are deficits and to remove soft tissue where there are excesses. For fat, this can involve free fat grafts to the deficient atrophied limb and liposuction or direct excision to circumferentially remove adipose tissue to improve socket fitting, as well as improve function.1 Functionless and excessive soft tissue can be excised to allow the prosthetic jacket to assume a smoother contour. Tissue expansion can be employed to improve soft tissues over bony prominences critical to hold the prosthesis in place (Fig. 40.1). Soft-tissue procedures are valuable to improve joint mobility, as well as to deepen soft-tissue indentations to functionally lengthen a residual limb, much like a 4-flap Z-plasty of the first webspace in the hand (Fig. 40.2). Excessive soft tissues can render the donning of socket liners difficult and can be removed with direct excision and/or with liposuction. Pedicled or free flaps can be used to augment tissue where there are deficits in order to avoid a more proximal amputation. The major downside of soft-tissue surgery is that amputees cannot wear their prosthetics for weeks to months, depending on the time course for swelling to resolve. However, as many of these amputees are young with many years of life expectancy to live with their residual limbs, the efforts to improve the quality of the soft tissues are often worthwhile.

Understand that the type of prosthetic is based on patient needs and amputation level There are four main categories of prostheses, defined by the method used to control the device. There is a rough correlation between prosthetic type and the level of amputation. Selection of a prosthesis also depends on the functional requirements of the patient and the level of financial support available to

Principles of prosthetic reconstruction

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Algorithm 40.1

Upper Extremity Amputation

Shoulder-level

Transhumeral

Transradial

Wrist disarticulation

Hand-level

Consider converting to transradial

Very proximal

Adequate soft tissue? Yes

Yes

Pain

Prosthesis control

TMR RPNI

TMR

OI AMI RPNI

Pain

TMR RPNI

No

Yes

Prosthesis control

TMR

TMR RPNI

OI AMI RPNI

Yes

Yes

Prosthesis control

Pain

TMR

OI AMI RPNI

Pain

TMR RPNI

Tissue expansion Pedicled flap Free flap

Pain

Prosthesis control

Prosthesis control TMR Starfish procedure

TMR

Digit only

Partial hand

RPNI TMR

TMR RPNI

OI AMI RPNI

OI

Algorithm for the management of upper extremity amputation. For abbreviations, see text.

A

B

C

Figure 40.1  (A,B) Patient with a traumatic shoulder disarticulation amputation with painful, unstable scar and skin grafting in the shoulder and axilla that prevent prosthesis wear. (C) After tissue expansion and advancement flap of the soft tissues over the acromion and scapular spine to facilitate prosthesis suspension.

the patient for the device. Prostheses are compared based on issues of weight, durability, speed and accuracy of motion, degrees of freedom of movement, battery life for externally powered devices, and aesthetics.

Passive/aesthetic devices Passive prostheses are the lightest-weight devices because they contain no motors and few mechanical systems. Used predominantly for finger and distal hand amputations,

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Figure 40.2  (A) Patient with a shoulder disarticulation amputation has difficulty with prosthesis suspension. (B) After a pedicled parascapular flap has been used to deepen the soft tissue indentation in the right axilla to functionally “lengthen” his residual shoulder, promoting improved prosthesis suspension.

passive prostheses do not permit any motion, and they are relatively soft and fragile. The primary goal of a passive device is aesthetic so that the upper extremity injury does not garner attention. Some patients use these passive devices to help with holding down objects for manipulation by their non-injured hand. Passive devices can also fill out and support clothing. An aesthetic prosthesis assists patients with addressing issues of body image and self-esteem, with possible functional gains due to a newfound social openness and ability to expose the limb2 (Fig. 40.3). Most of these prostheses are custom-made and require a high level of expertise and artistry on the part of the prosthetist. More recently, 3D printing has made these devices more accessible and less costly. Because intact skin is used to secure the prosthetics in place, some amount of sensory feedback of the residual limb will be lost, which is one drawback to these devices. Osseointegration or direct skeletal attachment of passive prostheses may solve some of these attachment issues and is described below. A well-attached passive prosthesis has the potential to improve function by simply increasing the functional length of amputated digits.

Body-powered devices As the name implies, a body-powered prosthesis is moved by the remaining muscles in the individual’s body. Typically, a harness with a strap that lies over the lower third of the scapula connects to a cable that operates the terminal device, which is sometimes a hook. The Ballif arm of 1812 was one of the first to provide body-powered active control of the terminal prosthetic "hand", as well as to utilize softer materials for the socket. Rather than locking prosthetic fingers into place for a static grip, the Ballif arm utilized cables attached to the shoulder and arm to allow opening and closing of the prosthetic hand. The Civil War created a large number of amputees in the United States, leading to companies such as the A. A. Marks Company (1853) of New York and the J. E. Hanger Company (1861), which is still in existence today. The benefits of body-powered prostheses are that they are relatively lightweight and durable; can be made to be waterproof; and can provide feedback to the user based on the tension in the control cable. Similar to aesthetic devices, 3D printing has lowered the cost of these devices and allowed

Figure 40.3  Multiple digit prostheses for cosmesis.

them to be more "custom" for improved fitting. Body-powered prostheses work best in transradial amputees with good elbow and shoulder function who will use their residual limb for forceful activity. The disadvantages are that they require harnessing, and the user must have the strength and range of motion to pull the cable sufficiently to make the device work in all positions.

Externally powered prosthesis An externally powered prosthesis is powered by batteries contained within the system. The device can be controlled with various inputs, including electromyographic (EMG) signals, force-sensing resistors, pull switches, and push switches.

Principles of prosthetic reconstruction

The most prevalent type of externally powered device is a myoelectric prosthesis control scheme which uses EMG signals from two antagonist muscle contractions to operate two directions of movement. With a simple two-site direct control system, for example, wrist extensor EMG signals control opening of the hand/fingers, while wrist flexor EMG signals control closing. The benefits of myoelectric prostheses are that they require less harnessing than body-powered systems; they can often be operated in more planes of movement; and because there are no cables and straps on the outside of the device, they are aesthetically more appealing than body-powered prosthetics. While some patients prefer an outer covering of their device to appear like skin, others welcome a futuristic appearance with digits made of metal, along with visible joints and articulations. The disadvantages of myoelectric devices are that the batteries and motors make them heavier than body-powered systems; they can be water-resistant but not waterproof; they need to be charged daily; they require more maintenance than body-powered devices; and they are relatively more expensive.3 In addition, myoelectric prostheses require that the electrode sensors that record signals from the muscles to control the device maintain contact with the skin. Thus, they require an intimate fit that may be uncomfortable or not tolerated by fragile skin or by scar tissue. Excessive sweating tends to decrease contact reliability. Additionally, in order for surface sensors to accurately record EMG signals, there must be a very tight socket fit (Fig. 40.4). When planning for a myoelectric prosthesis, the removal of fat surgically can be advantageous to improve signal detection. The removal of subcutaneous fat decreases the resistance between the underlying muscle and skin, thereby increasing the amplitude of the signal and decreasing cross-talk.4 Skin grafts used as part of the closure of the residual limb can be advantageous, as the EMG signal is more easily detected due to the lack of subcutaneous fat. Implantable EMG sensors that transmit a signal to the myoelectric device will avoid these problems of transcutaneous signal detection and are the focus of much research. However, thin wires that exit the skin to provide direct signaling capabilities can break, dislodge, and/or become infected. EMG information can be brought out through the abutment of an osseointegrated prosthesis, but these systems (like the transcutaneous thin wires) are all experimental and are not

Figure 40.4  In order for surface sensors to accurately record EMG signals, there must be a very tight socket fit. (A) A transhumeral socket with embedded electrodes. (B) The socket of this transhumeral myoelectric prosthesis has matching electrodes with pattern recognition capabilities.

A

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available for commercial use. Direct recording and stimulation of the cerebral cortex has been performed in monkeys in order to drive peripheral movement. This brain–machine interface, if successful, could have wide applicability not only for amputees, but also for patients with spinal cord injuries.5

Hybrid devices Hybrid devices combine body-powered components and myoelectric/externally powered components into one device. They are primarily used for transhumeral and shoulder disarticulation prostheses and most commonly include a body-powered elbow and a myoelectric terminal device (hook or hand). This configuration allows both components to be operated simultaneously and provides the increased force of the powered hand for gripping with the lightweight body-powered elbow. Hybrid systems require less battery charge than a fully myoelectric device for transhumeral and shoulder disarticulation patients and are correspondingly less heavy without the additional battery packs and motors required for a fully myoelectric device.

Understand prosthetic attachment systems Liners are the interface between the skin of the residual limb and the prosthetic. Liners need to be easy to apply, comfortable, washable, and replaceable. Typically made from thermoplastic elastomers, silicone, or polyurethane, liners are often "rolled" onto the residual limb from distal to proximal. The thermoplastic elastomers are the softest and most flexible and are used for new amputees. Silicone liners are less flexible but more durable, and polyurethane liners are the most durable and ideal for active individuals. Sensing electrodes can be embedded into these liners in order to improve signal detection for myoelectric prostheses (Fig. 40.5). Sockets are the firm portion of the prosthetic that either wraps around the limb or mirrors the impression of the chest for shoulder-level amputees. Well-fitting sockets distribute forces to avoid pressure sores and achieve comfortable prosthetic device wear. Sensing electrodes for myoelectric devices can be integrated within the inner aspect of the socket. Sockets maintain their connection to the amputee either indirectly through a locking attachment to the liner, via a suction apparatus to the liner, or even with active vacuum pumps.

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Shoulder-level amputees keep the socket in place with straps that encircle the chest. Often, the residual limb has an irregular shape, bony prominences, or irregular soft-tissue coverage that makes these connections difficult to maintain.6 The prosthetic socket must optimize stability while controlling for movement such as slippage, translation, and rotation of the soft tissues and the socket itself.7 Maintenance of a consistent fit over time proves difficult as the contour and volume of the residual limb can change with weight and fluid fluctuations. Transient changes in volume of the limb throughout the day can cause variability in socket fit and comfort even without long-term overall changes in body weight. Poor fitting of a prosthetic can lead to pressure sores, irritation, and pain at pressure points.8 Bursa formation at the end of the bone is a form of an internal pressure sore. These aforementioned limitations cause at least 35% of upper limb amputees to abandon use of their prosthetics.8 Both sockets and liners could be made irrelevant and unnecessary by the development of osseointegration (OI), or direct skeletal attachment.9 The concept that bone and porous titanium establish a durable and secure bond was introduced in the 1960s by Per-Ingvar Brånemark for intraoral indications.10 This work was continued by his son Rickard Brånemark and coworkers, who evaluated the possibility of OI for extremity amputations.11,12 The first OI treatment in an amputee was performed in 1990 on a 25-year-old woman who had undergone bilateral transfemoral amputation at the age of 15 due to a tram accident. A titanium fixture was installed in her right residual femur. The concept of OI is now generally defined as a direct anchorage of an implant into the skeleton by induction of bone healing to the implant surface. The systems typically involve a fixture that is implanted into the intramedullary cavity of the amputated bone (humerus or femur) and an abutment that percutaneously extends from the fixture out through the skin. The prosthesis locks into the end of the abutment, and the abutment is designed to be revisable if there is damage during use, but without the need to change the fixture. The fixture achieves an intimate bone-implant contact due to its porosity, and this provides bacteriologic stability for long-term usage. An additional advantage of the intimate connection between implant and bone is the ability to sense vibrations and pressure, defined as “osseoperception”. Neurophysiologic evidence shows that a proper peripheral feedback pathway can be restored with development of OI implants.13,14 Osseointegration technology is now being broadly applied and implemented around the world as a method for treatment

Figure 40.5  (A,B) Low-profile sensing electrodes can be embedded into the liners in order to improve signal detection for myoelectric prostheses.

of transfemoral and transhumeral amputations – long cylindrical bones that permit the introduction of a central metallic implant. The surgical implantation is generally performed in two stages with stage 1 being exposure of the distal end of the bone, removal of the intramedullary cortex, drilling and subsequent insertion of the implant, and skin closure. Approximately 3–6 months later, stage 2 is completed by opening and thinning the skin envelope, and then a small aperture is created for insertion of the abutment that remains exposed outside the body.

Plan for the means of prosthetic control A prosthesis is only as good as the control signals that it receives from the user. The goal of any prosthesis is to be moved and positioned in space smoothly, quickly, intuitively, and with minimal exertion and mental fatigue to accomplish this task.15 Multifunctional prostheses offer the potential for greater functionality but come at the cost of increased complexity with regard to control strategies. The more proximal the amputation, the more signaling that is required. A trans­ radial amputation only needs to open and close prosthetic "fingers", whereas a patient with a transhumeral amputation requires a control paradigm for both prosthetic elbow and prosthetic hand. Prostheses with both a terminal hand device and a prosthetic elbow require differentiation between signals intended for hand control and those intended for elbow function. This differentiation becomes even more critical when these functions are attempted simultaneously. The cable systems used by body-powered devices provide a reliable method for control but lack fluidity and do not offer simultaneous control of multiple functions. Body-powered prostheses, as previously described, utilize shoulder motions to operate the prosthesis. This is problematic because muscles that are designed for strong movements – such as the latissimus dorsi and the serratus anterior – are required to move accurately and sensitively to control cables and switches. Body-powered devices use non-intuitive shoulder muscles to control a prosthetic elbow or hand. Myoelectric control, derived from surface EMG recording of residual limb muscles, provides prosthetic control without the need for accessory shoulder movement. From the standpoint of aesthetics and comfort, the lack of cables and pulleys is advantageous but is often offset by the bulk of the socket and the increased weight of the motorized device. Another ongoing problem for myoelectric systems is consistent detection of the EMG signal. The surface electrodes can loosen or become dislodged with

Principles of prosthetic reconstruction

active movement of the prosthetic or from sweat on the skin surface. Myoelectric control represented a promising technological advance, but the prosthetic function it provided remained relatively slow and disjointed, thus limiting its applicability. For amputations at or above the elbow, myoelectric control was not intuitive, because the prosthetic terminal device was controlled by muscles that move the elbow. Also, as with body-powered devices, only one joint could be operated at a time. Multifunctional devices required an additional switch or signal to enable the device to change between functions. The potential offered by myoelectric control was realized in 1995, when Kuiken, Childress, and Rymer demonstrated a new myoelectric control strategy called “hyper-reinnervation”,16 which is now generally referred to as “targeted muscle reinnervation (TMR)”. Targeted muscle reinnervation utilizes nerve transfers between the transected brachial plexus nerves and the residual limb muscles to reclaim the neural control information that is lost as a result of transhumeral or higher upper extremity amputation.17 As a result, prosthetic function can be directly coupled with EMG signals corresponding to the nerves responsible for the identical function in the previously intact limb. Going back to the transhumeral amputee, the information still contained in the median, distal radial, and ulnar nerves is amplified with nerve transfers to muscles, while still maintaining intact signals of the musculocutaneous and proximal radial nerves that would control the prosthetic elbow movement. Clinically, this technique yields intuitive and relatively seamless device control. In addition, the increased number of EMG control sites provided by TMR enables simultaneous control of multiple functions. Kuiken and Dumanian reported the first TMR procedure in shoulder disarticulation patients in 2004,18 and in transhumeral amputees in 2008.19 Targeted muscle reinnervation uses a large muscle segment to amplify and spread out the EMG signal to permit transcutaneous signal detection in an “all-natural” manner without transcutaneous wires or other implanted electric devices. Typically, the surgeon will choose a superficial broad muscle as the target and remove overlying fat to facilitate later signal detection. Targeted muscle reinnervation nerve transfers are highly successful in neurotization of the newly denervated muscle, with one study reporting universal success in the nerve transfers providing a useable EMG signal for prosthetic function.20 While the functional capabilities of prosthetic devices once outpaced the amount of information available to control them, the pendulum has now swung the other way. When TMR was first introduced, the number of nerve transfers performed as part of the TMR procedure largely dictated the number of prosthetic functions capable of being controlled. This control strategy, labeled “direct-control”, meant that a single reinnervated muscle segment could be used to control only one function via a single EMG electrode (i.e., reinnervation of the short head of the biceps by the median nerve for hand closure). With a simple two-site direct control system, for example, wrist extensor EMG signals control opening of the hand, while wrist flexor EMG signals control closing of the hand. As innovation has continued, “direct control” now has been supplanted by “pattern recognition”, whereby advanced algorithms are used to correlate the pattern of muscular contractions recorded from many more electrodes. Pattern recognition provides greater flexibility for rehabilitation and has served to markedly improve the functional capacity of the amputee.

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Direct recording of electric signals from nerve, or electroneurography (ENG), is a promising direction of investigation. Rather than sampling a nearby muscle for information, with or without TMR, the nerve itself can be interrogated with electrodes. A central problem for direct ENG control of prostheses is that the signal-to-noise ratio is unfavorable. There is crosstalk between fascicles that makes the control signals less pure. These ENG electrode arrays and cuffs have different designs, and each of them attempts to minimize trauma to the nerve while maximizing the information obtained.21 Examples of these systems include the FINE electrodes (flat interface nerve electrode) that flattens the nerve to achieve closer spatial distancing between internal fascicles and the cuff, the longitudinal intrafascicular electrodes (LIFE) system that introduces a longitudinal needle within the nerve for signal detection, the transverse intrafascicular multichannel electrode (TIME) system that uses transversely oriented needles within nerves, and the Utah slanted electrode array (USEA) system. Not only do these systems help to drive a myoelectric device, but they also serve to restore sensory feedback to the user. Sensory feedback is an underappreciated but important aspect of prosthetic rehabilitation of the amputee.22 Cederna and colleagues developed a biologic amplification system using free muscle grafts wrapped around the ends of nerve that dramatically increased the signal-tonoise ratio of the ENG, permitting greater facility in signal detection.23 Termed a "regenerative peripheral nerve interface", or RPNI, these free muscle grafts amplify the ENG after successful revascularization and reinnervation to the point that muscle contractions can be detected via ultrasound. A significant limitation for all of the aforementioned paradigms that attempt to collect information directly from the nerve (LIFE, TIME, USEA) or from an amplified nerve (RPNI) is the electric systems necessary to bring the signal out from the nerve to the prosthetic device. While direct wires connecting the nerve to the prosthetic are possible, the finer the wire, the more susceptible it would be to infection and breakage. Most recently, a new method to bring out an ENG or EMG signal was devised using the osseointegration abutment to physically bring electric signals from inside the limb out to the prosthetic. Ortiz-Catalan and colleagues have designed an osseointegrated implant with bidirectional communication between the hand and electrodes implanted in the nerves and muscles of the upper arm, known as the e-OPRA (Osseointegrated Prosthesis for the Rehabilitation of Amputees) system. The e-OPRA system requires implantable electrodes to be sutured onto the epimysium of the two heads of the biceps muscles and the long and lateral heads of the triceps in order to obtain muscle control. These electrodes, like conventional surface electrodes, detect signals from the patient’s voluntary contraction in remaining muscles to control motors in the prosthetic hand.24 The e-OPRA device can be combined with TMR and/or RPNI to gain signals of the median, ulnar, and distal radial nerve for intuitive movement of the fingers and wrist, and spiral cuff electrodes can be placed around the ulnar and median nerves to provide sensory feedback to the amputee. These control systems are all exciting developments with high chances of becoming a part of everyday clinical medicine in the future. However, for now, there is no system currently approved by the US Food and Drug Administration (FDA) for directly obtaining EMG or ENG signals for prosthetic control.

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Treat upper extremity pain and phantoms Almost 75% of major limb amputees suffer from residual limb pain (RLP, pain localized to the remaining residual limb) or phantom limb pain (PLP, painful sensations referred to the amputated limb).25 Major limb amputees have reported lower quality of life measures than non-amputees, as patients grapple with alterations in body image, impairment of physical activity, and disruption of valued activities.26 Amputeerelated chronic pain, in either form, is thought to be a major contributor to amputee functionality and overall quality of life due to the impact of pain on patient motivation and prosthesis tolerance. In cross-sectional analysis of the general amputee population, females are more likely to suffer from RLP and PLP than their male counterparts. Additionally, the level of amputation in both upper and lower extremity amputees affects phantom limb pain outcomes, with more proximal amputees carrying a higher risk of PLP than more distal levels. Moreover, proximal upper limb amputees (aboveelbow and shoulder disarticulation levels) carry even higher odds of PLP compared to the more proximal lower limb amputees (above the knee and hemipelvectomy levels).25 Upwards of 80% of upper limb amputees wear a prosthesis for some portion of the day, and it is important to consider the impact of chronic pain conditions on this specific population.27 Furthermore, many patients report that their prosthesis worsens both RLP and PLP, causing them to wear it for significantly fewer hours per day. Post-amputation pain can profoundly affect prosthetic fit and function, thereby decreasing overall quality of life. Targeted muscle reinnervation was initially performed for control of myoelectric prostheses, and there was an initial hesitation before performing the first TMR procedure that the size mismatches between the major mixed nerve found just distal to the brachial plexus cords and the much smaller motor nerves would create neuromas-in-continuity and pain. Rather than causing pain, the early TMR patients (all upper extremity) stated that both their pain and phantom sensations decreased after the procedure. This surprising reduction in pain led to experimental animal work, where TMR demonstrated healing of the terminal nerve ending despite the size mismatch between the major mixed nerve and the smaller motor nerve. Healing of the terminal nerve ending was determined with endpoints of axon number and axon size.28 Clinically, Souza et al. reviewed the first 28 patients having TMR performed at Northwestern University in Chicago, IL and the San Antonio Military Medical Center in San Antonio, TX. Of these initial TMR patients, 58% had pain preoperatively, but only one had pain postoperatively, and this was from a lateral antebrachial cutaneous neuroma that had not been treated.29 This initial retrospective study led to a prospective randomized clinical trial where upper and lower extremity amputees were randomized and blinded to treatment with either TMR or standard neuroma excision and muscle burying. Using the 0–10 point Numeric Rating Scale (NRS) for pain assessments, TMR led to a significant decrease in both phantom pain (−3.2) and neuroma pain (−2.9) with 18 months of follow-up. In comparison, neuroma burying resulted in no significant change in phantom pain (+0.2) and neuroma pain (−0.9) outcomes.30 Patient recruitment numbers were low in this RCT, because patients often did not wish to be randomized – they wanted TMR. Due to significant nerve pain after

nerve burying, 9 of 15 patients in the control group were eventually converted to TMR after at least 1 year of follow-up. In a prospective study of 19 upper extremity amputees who underwent TMR in a non-blinded fashion for the treatment of established pain, both pain and patient-reported outcomes for function improved significantly after TMR.31 The slogan “give the nerve somewhere to go and something to do” was coined to encapsulate the idea that nerve “healing” was achieved with TMR, by the provision of terminal nerve receptors within the muscle. The nerve size mismatches of a large nerve being coapted to a small nerve were simply less important than may have been expected by decades of peripheral nerve surgery teaching. A secret of TMR is that the cut motor nerve never becomes a symptomatic neuroma – explaining the tens of thousands of free muscle flaps successfully transferred by plastic surgeons with little regard for the motor nerve that had supplied the muscle flap. “Healing” the nerve with a nerve transfer is more important than trying to “hide” the nerve in an area not susceptible to trauma and manipulation. Cheesborough and colleagues were the first to perform TMR at the time of an acute traumatic shoulder disarticulation, both to save a second surgery for improved prosthetic control, as well as to potentially prevent the development of pain and phantom sensations.32 Confirming and enlarging on this single case report, Valerio and colleagues demonstrated this improved effect of pain and phantom improvement was possible to achieve prophylactically if TMR were performed at the time of major limb amputation in a series of 51 patients for both upper and lower limbs.33 The comparison group was taken from a matched set of 438 amputees that had not undergone TMR. In this study, TMR was associated with a 3.03 higher odds ratio of decreased phantom limb pain, and 3.92 times higher odds for neuroma pain. O’Brien et al. published outcomes for acute TMR for upper extremity patients, using both the 10-point NRS scale, as well as the Patient-Reported Outcomes Measurement Information Scale (PROMIS), demonstrating that 62% of acute TMR patients described no phantom sensations, in comparison to 24% of controls.34 Half of all patients had no neuroma pain, in comparison to 36% of controls. Similar improvements were demonstrated using PROMIS. Regenerative peripheral nerve interfaces (RPNI), like TMR, were initially conceived for the control of upper extremity prosthetic devices. Similar to TMR, RPNIs were found to help both neuroma pain and phantom limb pain. Conceptually, the mechanism of pain relief for the two surgical techniques – treating the end of the newly freshened nerve – are similar. While TMR channels regenerating axons into a denervated muscle through the established technique of a nerve transfer, RPNIs use a muscle graft (also denervated) that is wrapped around the terminal nerve (Fig. 40.6) and that sprouts nerve receptors during the revascularization process. The nerve reinnervates and helps to revascularize the free muscle graft. The axons reach a terminal nerve receptor in the muscle graft, and healing of the nerve occurs to limit sprouting and disorganized nerve regeneration. While there has not been a randomized clinical trial to evaluate the efficacy of RPNI for pain control, RPNIs were found to decrease local nerve pain and phantom pain both for established amputees and as a prophylaxis against the development of these conditions.35 For established neuromas, 71% of patients reported a reduction in neuroma pain within the residual limb, and there was a 53%

Treatment of upper extremity amputees

Figure 40.6  Regenerative peripheral nerve interface (RPNI). (A) Two sensory nerves after neuroma excision with two free muscle grafts. (B) The free muscle grafts are wrapped around the ends of the terminal nerves to create the RPNI constructs.

A

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B

A

B

C

D

E

F

Figure 40.7  (A,B) Short transradial amputation with radius and ulna bones protruding through healed skin grafts, and a large painful ulnar neuroma is visible along the medial elbow. The patient was unable to wear a prosthesis due to pain and lack of durable soft tissue. (C,D) A free anterolateral thigh (ALT) flap with a segment of vastus lateralis muscle with motor nerve was used for complete soft tissue resurfacing and TMR target for the median nerve. (E,F) All skin grafts were excised and replaced with a durable, well-vascularized ALT flap to promote prosthesis wear. Transhumeral TMR nerve transfers were also performed with median nerve to the vastus lateralis of the flap.

reduction in phantom limb pain. In a retrospective cohort study, patients with the creation of RPNIs at the site of amputated nerves at the time of the index amputation surgery had no symptomatic neuromas compared to 13% in the traction neurectomy group. In addition, 51% of the RPNI patients had phantom limb pain compared to 91% of the control group.36 Hundreds of patients with established neuromas have been treated successfully with RPNIs, and outcome studies of RPNIs for the treatment of these neuromas are soon to be published.

Treatment of upper extremity amputees Principles of acute upper extremity amputation surgery No matter the level, principles exist for performance of upper extremity amputations and for revision surgery in chronic amputees. These principles include the following:

(a) Cover the bone with adequate soft tissue. Granulation coverage and skin grafts over terminal bone may achieve a healed wound in the short-term, but longterm inadequate soft tissue often leads to bone exposure. These bone exposures typically will require a shortening revision amputation at some point in order to wear a prosthetic, but length can also be preserved with a free flap or a pedicled flap to achieve bone coverage (Fig. 40.7). For the upper extremity, pedicled flaps include a latissimus to cover the shoulder and/ or humerus (Fig. 40.8), an oblique rectus abdominus myocutaneous (ORAM) perforator flap – also referred to as a paraumbilical perforator (PUP) flap – to cover the forearm (Fig. 40.9),37 and a pedicled groin flap to cover the distal forearm and hand. (b) Assess the expected joint mobility on the residual limb. In some situations, a higher-level amputation, achieved by removing a non-functioning joint, may be preferable to length, especially considering the abilities of modern prosthetics. For instance, a patient with a dysfunctional, stiff, and possibly painful elbow may be best served with

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CHAPTER 40  • Treatment of the upper extremity amputee

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E

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Figure 40.8  (A–D) Shoulder disarticulation amputee with painful skin graft in the axilla that prevents prosthesis use. (E) A pedicled latissimus dorsi myocutaneous flap was designed to resurface the axilla and also use the thoracodorsal nerve as a target for the ulnar nerve for shoulder-level TMR. (F) The latissimus dorsi myocutaneous flap has been elevated. (G) The painful axillary skin graft has been excised, and the latissimus flap skin paddle was used to resurface the axilla to provide durable, well-vascularized soft tissue to promote prosthesis use. TMR nerve transfers had also been performed. (H–K) The latissimus skin paddle and TMR nerve transfers allowed the patient to later wear a prosthesis without pain.

a transhumeral amputation, as opposed to salvage of a suboptimal transradial amputation. (c) Assess the status of the other limb. If the other limb is uninjured, then the amputated limb will serve as a helper, rather than be required to perform complex tasks. All unilateral amputees achieve better function with their uninjured limb in comparison to their amputated limb that is prosthetically rehabilitated. ( d) Length is not the sine qua non for success. Maintenance of limb length when the residual limb is stiff, painful, and with poor soft tissue coverage does not maximize prosthetic potential. Targeted muscle reinnervation

and/or RPNI treatment of the residual limb at a higher level may achieve better functional outcomes with less pain than a stiff, but longer, residual limb. (e) Is the bone length long enough to achieve function from the next proximal joint? For traditional sockets, prosthetists need approximately two-thirds of the humerus length for the patient to functionally use the shoulder joint, and 5 cm of radius/ulna to have a functioning elbow. Osseointegration will likely change these limitations of short residual limbs. ( f) Consider which muscles remain under cortical control and how best to maintain them. For instance, for a short transradial

Treatment of upper extremity amputees

939

A B

Figure 40.9  (A) A transradial amputee with exposed, protruding bone. The pedicled paraumbilical perforator (PUP) flap is designed on the abdomen similar to an oblique rectus abdominis myocutaneous (ORAM) flap. (B) The PUP flap has been raised and inset as a tubed flap. (C) A short transradial amputee with skin graft and protruding bone with planned PUP flap reconstruction to salvage the elbow joint. (D) After division and inset of the PUP flap to provide durable soft-tissue coverage over the exposed bone and to maintain the elbow joint.

C

amputation, maintenance of the native hand closing/ wrist flexion muscles of the forearm and hand opening/ wrist extension muscles of the extensor wad should be tested for movement before any shortening surgeries are performed. ( g) Assess if there is a more proximal brachial plexus injury. Review of the initial amputation in traumatic cases for history and workup is an important aspect of prosthetic rehabilitation. Targeted muscle reinnervation requires an intact nerve from the cortical brain to the end of the residual limb to achieve reliable motor signals.

Surgery for the shoulder disarticulation level amputee Both acute and chronic shoulder disarticulation patients can be treated with TMR. The indication for surgery is two-fold – to help decrease pain and phantoms, as well as to potentially improve prosthetic rehabilitation with an advanced myoelectric or hybrid device. The surgery has changed little since it was first performed by Dumanian in 2002.18,38 Especially for traumatic injuries, it is important to review medical records and examine the patient to rule out a brachial plexopathy. Contractions of the residual pectoralis major and latissimus muscles are a good sign that no plexus injury is present. Scapula injury, a history of a broken clavicle, and injury photographs demonstrating avulsed nerves are a sign that TMR

D

may be performed distal to the nerve injury and therefore not effective at helping pain. Preoperative X-rays should be performed to determine if the humeral head is still present. When the humerus is absent, the pectoralis major has lost its insertion, leading to a medial translocation of soft tissues and pectoral nerves. The surgical technique for TMR at the shoulder level has been outlined by Gart et al.17 A transverse incision is made 2 fingerbreadths caudal to the clavicle in order to locate the junction of the clavicular and sternal heads of the pectoralis major. The fat and fascia of the pectoralis are raised as a medially based adipofascial flap for later interposition between muscle bellies for improved signal acquisition (Fig. 40.10). This maneuver also exposes the slanted fascial condensation that marks the borders of the sternal and clavicular heads of the pectoralis major. Dissection of this space can be performed bluntly, and the surgeon is in the correct interspace if no nerves or blood vessels require division. The motor nerves to the pectoralis are predominantly in the fat at the same level as the thoracoacromial blood vessels. Typically, there is a medial motor nerve, a motor nerve adjacent to the thoracoacromial vessels, and a lateral nerve that travels through the pectoralis minor to innervate the low lateral section of the pectoralis. The motor nerve to the clavicular head is found immediately adjacent to its vascular pedicle, typically lateral to the midpoint of the bone. While the textbooks concentrate on naming the pectoralis nerves according to from what cords they

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SECTION VII

A

CHAPTER 40  • Treatment of the upper extremity amputee

B

emerge, we tend to name the pectoralis motor nerves from where they exist anatomically. Next, the branches of the brachial plexus are dissected and identified deep to these motor nerves and lateral to the pectoralis minor muscle. In very high injuries, scarring can exist along the cords of the brachial plexus even medial to the pectoralis minor. The nerves at this level are firm and identified by palpation, while still avoiding the pulsatile subclavian artery. The nerves are followed distally, in order to obtain length, and divided. The end-neuromas are typically significantly scarred into position, and they do not require excision so long as the nerve upstream is divided. If the cords are found laterally and more length is needed, they can be delivered medial to the pectoralis minor to achieve more tension-free coaptations. After mobilization of the musculocutaneous, median, ulnar, and medial cutaneous nerves of the arm, the radial nerve is found deep within this space. With a hand-held nerve stimulator, the thoracodorsal nerve is found emanating off of the posterior cord to confirm its identity.

Clinical tips For shoulder-level amputees, it is important to review X-rays to determine whether the humeral head is present. If the humeral head is absent, the pectoralis major and brachial plexus nerve endings will be more medially displaced. Identify the fascial condensation between the clavicular and sternal heads of the pectoralis major to start your dissection. To gain more length on the nerve endings, the brachial plexus cords can be delivered medial to the pectoralis minor.

While the actual nerve transfers depend more on length considerations of the major mixed nerve reaching the pectoralis motor nerve in a tension-free manner, the most common TMR nerve transfer sequence includes the radial nerve coapted to the newly divided thoracodorsal nerve, the musculocutaneous nerve coapted to the motor branch of the clavicular head, and the median and ulnar nerves to the individual motor nerves of the sternal head (Table 40.1 & Fig. 40.11). Without a residual limb, it is only anatomy that can be used to determine nerve identity, and there is much variability.39 We typically avoid nerve transfer to the motor branch of the pectoralis minor as the muscle signal is deep, which limits signal detection, though it is an option for neuroma control. After the

Figure 40.10  (A) The fat and fascia of the pectoralis major are raised as medially based adipofascial flaps for (B) interposition between the sternal and clavicular heads for improved signal acquisition.

nerve transfers are performed using loupe magnification and 7-0 polypropylene suture on a vascular tapered needle, the previously elevated adipofascial flap is then placed between the sternal and clavicular heads of the pectoralis for improved EMG signal separation. While some surgeons use nerve wraps and fibrin glue, the senior author has not employed these adjuncts to date. The patient may resume wearing his/ her original prosthesis when there is adequate wound healing. Therapy can begin several weeks after the nerve transfer procedure,40 and prosthetic fitting for new control sites can occur in 3–6 months, depending on reinnervation. The latissimus muscle, being farthest away from the coaptation site, will take the longest to come under cortical control. As mentioned previously, TMR is not typically performed for patients with severe brachial plexopathies resulting in flail limbs. Targeted muscle reinnervation performed at the level of proximal nerves would not be expected to help with injuries causing pain at the trunk or cord level. Amputation will not relieve neuropathic plexopathy pain but can relieve traction pain at the shoulder. In addition, amputation clearly eliminates the inconveniences associated with having a paralyzed arm. We recommend a transhumeral amputation at 25–30% of humeral length in these instances. This removes the weight of the limb, relieving nerve traction pain, and preserves a nice shoulder and upper arm contour for clothing. Fusion of the shoulder to enhance prosthetic fitting is not recommended. Prosthetic fittings with flail residual limbs have extremely poor outcomes, and a humerus fused in abduction and flexion interferes with some activities, especially positioning in bed.

Surgery for the transhumeral amputee The indications for transhumeral TMR are for treatment or prophylaxis of local nerve pain and phantom limb pain as well as for improved prosthetic control. In these patients, while there is an intuitive elbow flex and extend signal in the biceps and triceps, respectively, the patient has lost the hand open and close signals found in the median, ulnar, and distal radial nerves. The key is to perform nerve transfers to regain the information in these three aforementioned nerves while at the same time not losing the native innervation of the biceps and triceps. Table 40.2 outlines the various TMR nerve transfer options for transhumeral amputees. It is best to mark the midpoints of the biceps and triceps in the preoperative holding area with the patient flexing and extending his/her imaginary elbow, since it is easy to lose orientation in the operating room due to lack of humeral

Treatment of upper extremity amputees

941

Table 40.1  Example pattern of targeted muscle reinnervation nerve transfers in a shoulder disarticulation amputee

New innervation via nerve transfers

Native innervation to preserve

Donor nerve

Recipient nerve

Muscle innervated

Prosthetic signal generated

Musculocutaneous nerve

Pectoral nerve

Clavicular head of pectoralis

Elbow flexion

Median nerve

Pectoral nerve

Upper sternal head of pectoralis

Hand closeWrist flexion

Ulnar nerve

Pectoral nerve

Lower sternal head of pectoralis

Intrinsic handWrist flexion

Radial nerve

Thoracodorsal nerve

Latissimus

Elbow extensionHand open

Residual triceps fibers if humeral head present

Elbow extension

Radial nerve

A

B

C

Figure 40.11  (A) Patient with small humeral remnant undergoing shoulder-level TMR with the incision marked two fingerbreadths caudal to the clavicle. (B) Within the interspace between the clavicular and sternal heads of the pectoralis major, the radial, median, and ulnar nerves are dissected free with hemostats holding them laterally. (C) The musculocutaneous nerve is visible just inferior to the Army–Navy retractor. TMR nerve transfers have been performed to distinct motor nerves to the sternal and clavicular heads of the pectoralis major, along with the thoracodorsal nerve.

Table 40.2  Example pattern of targeted muscle reinnervation nerve transfers in a transhumeral amputee

New innervation via nerve transfers

Native innervation to preserve

Muscle(s) innervated

Prosthetic signal generated

Musculocutaneous nerve motor branch

Short head of biceps

Hand close Wrist flexion

Ulnar nerve*

Musculocutaneous nerve motor branch*

Brachialis*

Intrinsic hand* Wrist flexion*

Radial nerve

Radial nerve motor branch

Lateral head of triceps

Hand open

Musculocutaneous nerve

Long head of biceps

Elbow flexion

Radial nerve

Long and medial heads of triceps

Elbow extension

Donor nerve

Recipient nerve

Median nerve

Performed if sufficient arm length exists that innervated brachialis is present.

*

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CHAPTER 40  • Treatment of the upper extremity amputee

condyles. While the surgery is most facile to perform with a position change to prone for the radial nerve, it has been described from just the supine position.17,41 A longitudinal incision is made on the anterior arm with the aim of separating the long and lateral heads of the biceps brachii ­muscle. While raising an adipofascial flap for improved signal detection and signal separation has been described in the past, modern myoelectric prostheses with pattern recognition render this less important. Dissecting between the two heads of the biceps will reveal the musculocutaneous nerve, which gives off one primary motor branch to each head of the biceps on average 19.6 cm from the anterolateral tip of the acromion (range, 15–25 cm).42 More distally, the musculocutaneous nerve provides 2–3 motor branches to the brachialis for longer transhumeral amputations when the brachialis is still present. One of these motor nerves is found as a continuation of the musculocutaneous nerve, and one branch is found on the medial aspect of the brachialis as in Fig. 40.12. The motor branch to the short (medial) and long (lateral) heads of the biceps brachii are identified, and a vessel loop is placed for later identification, as are the motor branches to the brachialis. It should be noted that the motor branch to the brachialis splits into two separate branches before entering the muscle, so both brachialis motor branches can be used as targets for TMR for the prevention and treatment for pain. Once the motor targets have been identified, a subcutaneous skin flap is elevated to dissect along the medial border of the biceps for identification of the median nerve and the smaller medial antebrachial cutaneous (MABC) nerve. The first (superficial) nerve identified is invariably the MABC,

A

Clinical tips For transhumeral amputees, it is important to preserve volitional elbow flexion and elbow extension for prosthesis control. Transhumeral TMR can be performed through a single anterior incision. When performing separate anterior and posterior incisions, the patient can be positioned supine, lateral decubitus, or flipped from prone to supine, depending on surgeon preference. In long transhumeral amputees, both motor branches to the brachialis muscle can be used as targets for prosthesis and/or neuroma control.

and not the median nerve. The median nerve is identified adjacent to the brachial vessels, anterior to the medial intermuscular septum. The MABC can then be found superficial and slightly posterior to the median nerve and adjacent to the basilic vein. The MABC is smaller than the median and ulnar nerves, but it can still be confused with the ulnar nerve. The median nerve is dissected from surrounding tissues, divided distally, and then mobilized to lie adjacent to the motor nerve of the medial biceps. An end-to-end nerve coaptation is performed without tension with 7-0 polypropylene sutures. It is important to leave the inherent innervation to the long (lateral) head of the biceps for myoelectric prosthesis elbow flexion signal. The ulnar nerve is identified posterior to the MABC and deep to the muscular fascia. The ulnar nerve is coapted to the motor nerve of the brachialis. If the brachialis motor branch is

B

C

D

Figure 40.12  (A) Anterior exposure of transhumeral TMR with the median, ulnar, and medial antebrachial cutaneous (MABC) nerves dissected free. (B) TMR nerve transfers of the median nerve to the medial head of the biceps, ulnar nerve to the brachialis, and MABC to a secondary motor point within the medial head of the triceps have been performed. (C,D) The radial nerve is transferred to the motor branch to the lateral head of the triceps. Note the raised adipofascial flap retracted to the left.

Treatment of upper extremity amputees

not present, the ulnar nerve and the MABC are placed within the newly denervated medial head of the biceps, or else an RPNI is created. This is also done for the lateral antebrachial cutaneous (LABC) nerve. Secondary motor points identified within the long head of the triceps can also be used as potential TMR targets. If an adipofascial flap has been raised, it is then inset between the two heads of the biceps and the incisions are closed. After completing the anterior nerve transfers, the posterior arm is accessed, with or without a position change. A longitudinal incision is made between the long and lateral heads of the triceps brachii muscle. Typically, the heads of the triceps are a bit more difficult to separate than the heads of the biceps, but the interval is easiest to identify proximally (immediately adjacent to the deltoid), so we recommend starting cephalad and dissecting caudally. The nerves are typically identified initially by palpation, and their identity confirmed with a handheld nerve stimulator. Typically, the radial nerve increases in diameter after injury – more so than the median and ulnar nerves. Adjacent to the radial nerve is a 2–3 mm in diameter motor nerve to the lateral head of the triceps. There are on average 2.5 branches to the lateral triceps, located 21.6 cm from the posterolateral tip of the acromion (range, 11–29 cm).42 The distal radial nerve will not stimulate, as there are no forearm muscles present, while the motor nerve to the lateral head produces a strong contraction. The motor nerve to the long head comes off of the radial nerve fairly proximally and is generally not seen.43 The distal radial nerve is transected and transferred in an end-to-end fashion to the motor branch of the lateral head of the triceps. Similar to the anterior arm, the TMR nerve coaptations are performed in a tension-free manner under loupe magnification. It is important to leave the inherent innervation to the long head of the triceps for myoelectric prosthesis elbow extension signal. If an adipofascial flap has been raised, it is then placed between the long and lateral heads of the triceps brachii for improved signal separation for prosthetic elbow extension and terminal device extension.

Surgery for the transradial level amputee The indication for surgery in the transradial amputee is to treat pain and phantoms, to provide improved signaling of myoelectric prostheses, improve soft tissues for wearing of liners and sockets, and on occasion, provide room for the battery of a myoelectric prosthesis. The issue of prosthetic control is fluid and dependent on the available technology of the myoelectric device. The majority of transradial amputees have residual flexor and extensor musculature near the elbow for providing intuitive hand opening and closing signals, but TMR can provide additional signals for specific grasp patterns. Pattern recognition systems that can decode the complex sea of EMG signals for transradial amputations are especially important for transradial patients.44,45 Forearm procedures permit the use of an operating room tourniquet to achieve a bloodless field. Motor nerves should be identified first and enveloped with a vessel loop. Block anesthestics at the supraclavicular and infraclavicular levels should not impede motor nerve stimulation with the use of modern nerve stimulators that remain functional with up to an hour of tourniquet time. In the forearm, the majority of the motor branches to the musculature are in the proximal forearm. For this reason,

943

primary amputations at the wrist or distal forearm level will require a separate incision in the proximal volar forearm. The authors prefer a single volar incision to treat the median, ulnar, radial, and LABC nerves. The volar incision is made over the proximal volar forearm and curves towards the medial epicondyle (Fig. 40.13). For short transradial amputees, especially when performing concurrent TMR, the TMR nerve transfers can be performed through the amputation wound (Fig. 40.14). There are multiple targets available for the median nerve, including the flexor digitorum superficialis (FDS), flexor digitorum profundus (FDP), flexor pollicis longus (FPL), flexor carpi radialis (FCR), and palmaris longus. A principle of TMR for improved prosthetic control is that the target muscle should be superficial, broad, and with redundant function. After opening the forearm fascia, the median nerve is found on the ulnar side of the radial artery, with branches to the FDS and the anterior interosseous nerve (AIN) to the FPL and FDP index. Dissection ulnar to the radial vessels will help identify the median nerve, including the branches to the FDS and the AIN. The median nerve is divided and mobilized to reach one of these motor nerves for a tension-free nerve coaptation. When TMR is performed for prosthetic control, the palmaris longus or the FCR are the targets of choice. One strong wrist/finger flexor and one strong wrist/ finger extensor should be maintained to control standard myoelectric prostheses. The ulnar nerve is coapted to a motor nerve of the FCU, and these motor nerves are relatively proximal and often seen during a standard ulnar nerve decompression surgery. The radial sensory nerve can be accessed through the same volar incision, and it can be found radial to the radial vessels, deep to the brachioradialis. The radial sensory nerve can be transferred to any of the aforementioned motor points in the volar forearm. Alternatively, the radial sensory fascicle can also be dissected through a separate, more proximal dorsal incision and transferred to a motor branch to the brachioradialis. In the volar forearm, the LABC is identified superficially running adjacent to the cephalic vein, and this can also be transferred to a motor branch in the forearm. For patients where the medial antebrachial cutaneous (MABC) is a known source of pain, this nerve can be identified in the subcutaneous plane along the ulnar aspect of the proximal forearm. Table 40.3 outlines the various TMR nerve transfer options for transradial amputees. The length of the residual transradial limb is important. Very long limbs have a pronator quadratus muscle present, and the AIN at this level can be the recipient of the dorsal sensory branch of the radial nerve and/or the LABC. However, very long limbs are on occasion shortened 7–8 cm to provide the room for a battery pack for a myoelectric device. When this is performed, the pronator quadratus can be mobilized on its neurovascular pedicle and be brought towards the donor nerve(s). Alternatives include mobilizing and transposing the radial nerve to the mid-forearm to coapt to an FDS motor nerve, coapting the radial sensory nerve to the motor nerve of the brachioradialis via a separate incision just proximal to the elbow flexion crease, or an RPNI (Fig. 40.15). As the radial nerve is entirely sensory, the superficial nature of the target muscle is not as important. Pierrie et al. have described an innovative TMR technique in transradial amputees for improved myoelectric prosthesis control.46 When TMR is performed for pain and phantoms in trans­ radial amputees, we tend to perform whatever transfer is

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CHAPTER 40  • Treatment of the upper extremity amputee

A

B

C

D

A

Figure 40.13  (A) In a long transradial amputee, all TMR nerve transfers can be performed through a single volar incision in the proximal forearm with an ulnar curve to gain access to the ulnar nerve and motor branch of the flexor carpi ulnaris (FCU). (B) Median nerve branches of the anterior interosseous nerve (AIN) and the motor branch to the flexor digitorum superficialis (FDS) have been dissected and marked with vessel loops. (C) The ulnar nerve has been dissected, along with a motor branch to the FCU, marked with a vessel loop. (D) TMR nerve transfers are then performed. In this view, the radial sensory nerve will be transferred to the motor branch to FDS, and the median nerve will be transferred to the AIN. The ulnar nerve to FCU motor branch transfer is not pictured.

B

C

Figure 40.14  In a short transradial amputee, the TMR nerve transfers can be performed through the wound in the acute setting. (A) TMR nerve transfers of the median nerve to AIN and radial sensory nerve to FDS are pictured. (B) The Army–Navy retractor exposes the ulnar to FCU nerve transfer. (C) Primary skin closure has been performed after TMR nerve transfers through the wound.

Table 40.3  Example pattern of targeted muscle reinnervation nerve transfers in a transradial amputee

New innervation via nerve transfers

Native innervation to preserve

Prosthetic signal generated

Donor nerve

Recipient nerve

Muscle(s) innervated

Median nerve

Anterior interosseus nerve

FPL, FDP to index and long Thumb opposition fingers

Ulnar nerve (±dorsal branch)

Ulnar nerve motor branch

FCU

Finger abduction

Superficial branch of the radial nerve

Radial nerve motor branch Median nerve motor branch

Brachioradialis FDS

N/A (sensory only)

LABC

Median nerve motor branch

FCR

N/A (sensory only)

MABC

Ulnar nerve motor branch

FCU

N/A (sensory only)

Radial nerve

ECRL, ECRB

Wrist extension

Posterior interosseus nerve

ECU, EDC, EIP, EDM, EPL, APL

Wrist extension, hand open

Median nerve

FCR, FDS

Wrist flexion, finger flexion

APL, Abductor pollicis longus; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; ECU, extensor carpi ulnaris; EDC, extensor digitorum communis; EDM, extensor digiti minimi; EIP, extensor indicis proprius; EPL, extensor pollicis longus; FCR, flexor carpi radialis; FCU, flexor carpi ulnaris; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; FPL, flexor pollicis longus.

Treatment of upper extremity amputees

A

B

945

C

Figure 40.15  (A) A large radial sensory neuroma has been dissected in the distal forearm. (B) The radial sensory nerve has been mobilized proximally and free muscle graft has been harvested. (C) After neuroma excision, the cut end of the radial sensory nerve is wrapped with the muscle graft to create the RPNI construct.

Clinical tips Since most transradial amputees have intact, functioning flexor and extensor muscles, they are able to achieve simple hand “open” and “close” signals for myoelectric prostheses. Transradial TMR is usually performed for neuroma control, as opposed to prosthetic control. When performing transradial TMR for neuroma control, a single volar incision can be made in the proximal forearm to perform all nerve transfers. For short transradial TMR, especially in the acute setting, TMR nerve transfers can be performed through the wound.

easiest that requires the least dissection and movement of the donor nerve. For pain control, no set algorithm for nerve transfers is followed, although typically we advocate transferring all sensory and motor nerves, including the MABC and LABC branches. What matters is resecting nerves back to healthy fascicles, and the creation of a tension-free coaptation to a nearby motor nerve (or denervated muscle graft/RPNI) that will permit the channeling of axons into newly denervated motor end-plates and other terminal nerve receptors.

Surgery for the wrist disarticulation amputee If the patient is unlikely to wear a prosthesis, a wrist disarticulation with good soft coverage will give the patient a longer residual limb that will serve as a helper for the opposite arm. When a hand prosthetic is used, the maintenance of the radial and ulnar styloids aids in pronation and supination stability for the prosthesis. However, room is limited for prosthetic components and the devices tend to look bulky. A long transradial amputation generally facilitates better prosthetic fitting than a wrist disarticulation by allowing room for prosthetic components and providing better cosmetic appearance. In terms of techniques, TMR for the wrist disarticulation amputee would be the same as for the transradial amputee, using the AIN to the pronator quadratus as an addition potential target, as described previously.

Surgery for the partial hand amputee Injuries that divide the digital nerves and strip the soft tissues off of the carpal bones may be better served by a wrist disarticulation or a transradial amputation, than by efforts to

Figure 40.16  A young worker had skin grafts applied to a proximal hand stripped of almost all soft tissues in an attempt to “save length.” He later underwent a transradial amputation for treatment of his painful immobile scarred hand.

salvage a scarred and immobile hand for the sake of “preserving length” (Fig. 40.16). Some patients may have some usable wrist flexion and extension and can use the partial hand amputation to "hook" heavy objects (Fig. 40.17). Like other conditions described in this chapter, much depends on the status of the opposite hand. However, if these patients have pain from division of the median, radial, and ulnar nerves from their injury, a more formal amputation with TMR may permit a prosthetic hand and prosthetic fingers to be fitted for improved function.

Surgery for the patient with digit amputations An estimated 45,000 people in the United States annually sustain finger amputations that lead to major impairments in hand function.47 Thumb amputations alone result in a devastating disability with the loss of pinch and grasp decreasing 40% of hand function alone.48 Given the crucial role fingers play in dexterity and performing daily tasks of life, finger and thumb amputations lead to the inability to perform more precise pinch and grip patterns, decreased grip strength, and a measurable loss of a person’s quality of life and independence.49,50 Reconstruction of the amputated digit begins with an evaluation for replantation. Thumbs are typically favored for

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A

CHAPTER 40  • Treatment of the upper extremity amputee

B

C

replantation over other single digits due to the issues of grip and pinch. When replantation is not possible or not thought as a reasonable option, revision amputation is the procedure of choice. Traction neurectomies are performed to potentially keep the nerve ending away from the terminal closure. It is recommended to preserve digit length in these situations so as to increase options of passive prosthetic devices powered by remaining joints such as the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints.3 Another procedure is the "Starfish" procedure, described by Gaston and colleagues, whereby the interossei of the middle and ring fingers are moved to a more superficial location in order to signal a handbased prosthetic that recreates finger flexion and extension for patients with multiple digit losses.51 Several reports have described reconstructive techniques for improving hand mechanics, aesthetics, and functionality after partial amputation of the hand and or fingers.52,53 Due to the advances in microsurgery, many centers now offer autologous reconstruction of the hand and replantation with toe transfers.54,55 Congenital thumb absence is often treated with pollicization, but this procedure is performed less commonly with traumatic thumb loss.56 When these options are not possible, and when patients still desire to improve their finger functionality and aesthetics, prosthetic reconstruction should be considered. Treatment of painful digital nerves from amputations greatly depends on the level of injury. As stated previously, about 6% of patients with digital amputations complain of painful end-neuromas.57 For patients who have developed neuromas of the digital nerves distal to the MCP joint, RPNI is

Figure 40.17  (A) Avulsion amputation specimen in a young male worker that cannot be replanted. (B) Radiograph showing preserved radiocarpal joint. (C) Mobile wrist joint acts as a helper hand. His extensor tendons were reinserted into the carpal bones with bone anchors to provide active wrist extension.

Clinical tips TMR for neuroma control can be performed for digit and partial hand amputations by using motor points within the lumbrical muscles as targets. If the patient and surgeon want to treat digital neuromas in the digit (and not dissect into the palm), RPNI is an alternative that requires obtaining a muscle graft from the forearm or thigh. The Starfish procedure combines TMR and intrinsic muscle mobilization to provide improved intuitive myoelectric prosthesis control for partial hand amputees.

an option in the fingers, using the volar forearm or thigh as a donor site for the muscle graft. Due to a lack of motor nerves in the fingers, TMR for digit amputations requires a nerve coaptation to a lumbrical, dorsal interosseous, volar interosseous, thenar, or hypothenar motor point (Fig. 40.18). The authors believe that TMR has more of a role for more proximal amputations, such as MCP disarticulation and transmetacarpal amputations, whereby the digital nerves can be transferred into motor points in the lumbrical or interossei muscles from either a volar or dorsal approach.58–60 The motor nerves to the interossei run on their deep surface, and so they are most easily found at the time of a proximal removal of the metacarpal. The motor points to the thenar muscles and lumbricals are located volarly. By extending the incision into the palm, the fascia over the lumbrical muscles can be incised, and the nerve stimulator can be used to identify a small motor point within

Future directions

A

B

947

C

Figure 40.18  A manual laborer who had suffered crush injuries to his left hand requiring amputations of the long and small fingers with significant neuroma pain in the transected digital nerves that went to his long finger. TMR nerve transfers of the digital nerves to motor branches in the hypothenar muscles were planned. (A) Two separate motor branches were identified within the hypothenar muscles as TMR targets. (B) The digital neuromas that used to go to the amputated long finger were dissected and (C) mobilized toward the hypothenar region for TMR.

Figure 40.19  A young patient with a recurrent sarcoma in his palm, requiring ray resections of his index and long fingers with the plan for acute TMR. (A,B) Motor branches within the lumbricals were identified and marked with vessel loops during the sarcoma resection. (C) After resection of the recurrent sarcoma with concurrent ray resections. TMR nerve transfers of the digital nerves were then performed to the motor branches of the lumbricals, followed by (D) primary closure of the skin.

A

B

C

D

the muscle that can be used as a target (Fig. 40.19). For dorsal sensory branches of the radial and ulnar nerves, the fascia over the dorsal interossei can be incised and motor points identified for transfer with an intramuscular dissection. Alternatively, the AIN to the pronator quadratus can be used for volar and/ or dorsal sensory branches of the ulnar nerve (Fig. 40.20).

Future directions “Necessity is the mother of invention” is a well-known proverb, and proximal upper extremity amputees needed a better way to control myoelectric prostheses. Targeted muscle reinnervation was initially developed to provide improved real-time, intuitive control to a newer generation of myoelectric prostheses for proximal upper extremity amputees. Since Dumanian and Kuiken first described the use of TMR for shoulder-level and transhumeral amputees in 200418 and 2008,19 respectively, the field of neuroprosthetics has exploded.

Cederna and colleagues later developed RPNI as a new myoelectric prosthetic control strategy to provide even higher fidelity (and decreased signal-to-noise ratios) than what TMR provided.61 The positive effects of TMR and RPNI on neuroma pain and phantom limb pain were a fortuitous byproduct of strategies initially intended to improve prosthesis control in upper extremity amputees that have since been validated with laboratory studies, retrospective analyses, and prospective randomized controlled trials.25,29–31,33,35,36 As the benefits of concurrent TMR at the time of amputation on preventing the development of residual limb pain and phantom limb pain have become increasingly accepted,33,34 we are in the midst of a paradigm shift in terms of how amputations are being performed around the world. While significant progress has been made in terms of improving prosthetic control strategies and decreasing residual limb pain and phantom limb pain – in addition to significant advances in upper limb prosthetic devices – prosthesis suspension, especially for proximal amputees, still relies on

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B

D

C

E

Figure 40.20  (A) The specimen of a multiply recurrent squamous cell carcinoma requiring partial hand amputation. (B) The ulnar aspect of the hand has exposed bone, so soft tissue reconstruction with a reversed ulnar forearm flap has been designed. (C) Acute TMR of the volar and dorsal sensory branches of the ulnar nerve has been planned to the anterior interossesous nerve (AIN), which is exposed by the Army-Navy retractor, as it enters the pronator quadratus. The vessel loop has been used to mark the motor fascicle of the ulnar nerve, which was spared. (D) TMR nerve transfers of the volar and dorsal sensory fascicles of the ulnar nerve were performed into the AIN. (E) Soft-tissue reconstruction of the ulnar hand with reverse ulnar forearm flap.

an external socket and harness, which is limited by the length of the residual limb. This is a significant challenge for shoulder-level and transhumeral amputees. Osseointegration is considered one of the “Holy Grails” for improved prosthesis control, since it provides improved range of motion, strength, as well as awareness of the prosthetic limb via osseoperception.7,62–64 In the US, osseointegration is currently FDA-approved for use in transfemoral amputees, and OI for transhumeral amputees will likely be approved sometime in the near future. Another “Holy Grail” for prostheses is the capability of providing sensory feedback to the amputee, which is something that modalities like TMR [including targeted sensory reinnervation (TSR)] and RPNI can help provide. As mentioned previously, Ortiz-Catalan and colleagues have developed the e-OPRA system, which involves an osseointegrated implant with bidirectional communication between the prosthesis and electrodes implanted in the nerves and muscles of the upper arm.24 The e-OPRA device, currently experimental, can be combined with TMR and/or RPNI to gain signals of the median, ulnar, and distal radial nerve for intuitive movement of the fingers and wrist, and spiral cuff electrodes can be placed around the ulnar and median nerves to provide sensory feedback to the amputee. Another surgical technique, known as the agonist–antagonist myo­ neural interface (AMI) procedure, has demonstrated the ability to provide proprioceptive feedback in lower extremity amputees by employing two muscle-tendon units (one agonist and one antagonist) that allow proprioceptive mechanoreceptors

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within both muscles to close the loop within a bidirectional efferent–afferent neural control system.65–67 The AMI procedure can also be performed in upper extremity amputees. By using normal muscle relationships and tension, AMI can provide proprioceptive feedback to the amputee, which TMR and RPNI cannot provide. Advances in neuroprosthetics and control strategies – along with techniques like OI and AMI – highlight the substantial innovations that have been developed over the past 20 years since TMR was first described, and someday soon standard treatment for a transhumeral amputee may involve the e-OPRA implant with a combination of TMR, RPNI, and AMI techniques. We are witnessing a paradigm shift with regard to amputee care and prosthetics, and future technologies will allow what was once deemed science fiction to become a reality.

Conclusion Amputations are no longer the “end of the road” after traumatic limb loss or after the treatment of tumors.68 Prosthetic rehabilitation of the amputated limb requires surgical planning at the time of amputation, revision surgeries of the amputated limb to maximize function and limit pain, and a dedicated prosthetic team. Surgical treatments, such as soft tissue procedures to add or remove soft tissue, TMR, RPNI, and OI, are all designed so that the amputation marks a new beginning, as opposed to the end of the road, for limb function.

References

References 1. Kuiken TA, Fey NP, Reissman T, Finucane SB, Dumanian GA. Innovative use of thighplasty to improve prosthesis fit and function in a transfemoral amputee. Plast Reconstr Surg Glob Open. 2018;6(1):e1632. 2. Goyal A, Goel H. Prosthetic rehabilitation of a patient with finger amputation using silicone material. Prosthet Orthot Int. 2015;39(4): 333–337. 3. Geary M, Gaston RG, Loeffler B. Surgical and technological advances in the management of upper limb amputees. Bone Joint J. 2021;103-B(3):430–439. 4. Kuiken TA, Lowery MM, Stoykov NS. The effect of subcutaneous fat on myoelectric signal amplitude and cross-talk. Prosthet Orthot Int. 2003;27(1):48–54. 5. London BM, Jordan LR, Jackson CR, Miller LE. Electrical stimulation of the proprioceptive cortex (area 3a) used to instruct a behaving monkey. IEEE Trans Neural Syst Rehabil Eng. 2008;16(1): 32–36. 6. Flaubert JL, Spicer CM, Jette AM, eds. National Academies of Sciences, Engineering, and Medicine. The Promise of Assistive Technology to Enhance Activity and Work Participation. Washington, DC: The National Academies Press; 2017. 7. Souza JM, Mioton LM, Harrington CJ, Potter BK, Forsberg JA. Osseointegration of extremity prostheses: a primer for the plastic surgeon. Plast Reconstr Surg. 2020;146(6):1394–1403. 8. Biddiss EA, Chau TT. Upper limb prosthesis use and abandonment: a survey of the last 25 years. Prosthet Orthot Int. 2007;31(3):236–257. 9. Aman M, Festin C, Sporer ME, et al. Bionic reconstruction: restoration of extremity function with osseointegrated and mind-controlled prostheses. Wien Klin Wochenschr. 2019;131(23–24): 599–607. 10. Brånemark PI, Hansson BO, Adell R, et al. Osseointegrated implants in the treatment of the edentulous jaw. Experience from a 10-year period. Scand J Plast Reconstr Surg Suppl. 1977;16:1–132. 11. Brånemark R, Ohrnell LO, Nilsson P, Thomsen P. Biomechanical characterization of osseointegration during healing: an experimental in vivo study in the rat. Biomaterials. 1997;18(14): 969–978. 12. Brånemark R, Ohrnell LO, Skalak R, Carlsson L, Brånemark PI. Biomechanical characterization of osseointegration: an experimental in vivo investigation in the beagle dog. J Orthop Res. 1998;16(1): 61–69. 13. Thesleff A, Brånemark R, Hakansson B, Ortiz-Catalan M. Biomechanical characterisation of bone-anchored implant systems for amputation limb prostheses: a systematic review. Ann Biomed Eng. 2018;46(3):377–391. 14. Ortiz-Catalan M, Hakansson B, Brånemark R. An osseointegrated human-machine gateway for long-term sensory feedback and motor control of artificial limbs. Sci Transl Med. 2014;6(257):257re6. 15. Ajiboye AB, Weir RF. A heuristic fuzzy logic approach to EMG pattern recognition for multifunctional prosthesis control. IEEE Trans Neural Syst Rehabil Eng. 2005;13(3):280–291. 16. Kuiken TA, Childress DS, Rymer WZ. The hyper-reinnervation of rat skeletal muscle. Brain Res. 1995;676(1):113–123. 17. Gart MS, Souza JM, Dumanian GA. Targeted muscle reinnervation in the upper extremity amputee: a technical roadmap. J Hand Surg Am. 2015;40(9):1877–1888. 18. Kuiken TA, Dumanian GA, Lipschutz RD, Miller LA, Stubblefield KA. The use of targeted muscle reinnervation for improved myoelectric prosthesis control in a bilateral shoulder disarticulation amputee. Prosthet Orthot Int. 2004;28(3):245–253. 19. O’Shaughnessy KD, Dumanian GA, Lipschutz RD, Miller LA, Stubblefield K, Kuiken TA. Targeted reinnervation to improve prosthesis control in transhumeral amputees. A report of three cases. J Bone Joint Surg Am. 2008;90(2):393–400. 20. Salminger S, Sturma A, Roche AD, Mayer JA, Gstoettner C, Aszmann OC. Outcomes, challenges, and pitfalls after targeted muscle reinnervation in high-level amputees: is it worth the effort? Plast Reconstr Surg. 2019;144(6):1037e–1043e.

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21. Rijnbeek EH, Eleveld N, Olthuis W. Update on peripheral nerve electrodes for closed-loop neuroprosthetics. Front Neurosci. 2018;12:350. 22. Nghiem BT, Sando IC, Gillespie RB, et al. Providing a sense of touch to prosthetic hands. Plast Reconstr Surg. 2015;135(6): 1652–1663. 23. Vu PP, Chestek CA, Nason SR, Kung TA, Kemp SWP, Cederna PS. The future of upper extremity rehabilitation robotics: research and practice. Muscle Nerve. 2020;61(6):708–718. 24. Ortiz-Catalan M, Mastinu E, Sassu P, Aszmann O, Brånemark R. Self-contained neuromusculoskeletal arm prostheses. N Engl J Med. 2020;382(18):1732–1738. 25. Mioton LM, Dumanian GA, Fracol ME, et al. Benchmarking residual limb pain and phantom limb pain in amputees through a patient-reported outcomes. Surv. Plast Reconstr Surg Glob Open. 2020;8(7):e2977. 26. Hsu E, Cohen SP. Postamputation pain: epidemiology, mechanisms, and treatment. J Pain Res. 2013;6:121–136. 27. Ostlie K, Lesjo IM, Franklin RJ, Garfelt B, Skjeldal OH, Magnus P. Prosthesis use in adult acquired major upper-limb amputees: patterns of wear, prosthetic skills and the actual use of prostheses in activities of daily life. Disabil Rehabil Assist Technol. 2012;7(6):479–493. 28. Kim PS, Ko JH, O’Shaughnessy KK, Kuiken TA, Pohlmeyer EA, Dumanian GA. The effects of targeted muscle reinnervation on neuromas in a rabbit rectus abdominis flap model. J Hand Surg Am. 2012;37(8):1609–1616. 29. Souza JM, Cheesborough JE, Ko JH, Cho MS, Kuiken TA, Dumanian GA. Targeted muscle reinnervation: a novel approach to postamputation neuroma pain. Clin Orthop Relat Res. 2014;472(10): 2984–2990. 30. Dumanian GA, Potter BK, Mioton LM, et al. Targeted muscle reinnervation treats neuroma and phantom pain in major limb amputees: a randomized clinical trial. Ann Surg. 2019;270(2):238–246. 31. Mioton LM, Dumanian GA, Shah N, et al. Targeted muscle reinnervation improves residual limb pain, phantom limb pain, and limb function: a prospective study of 33 major limb amputees. Clin Orthop Relat Res. 2020;478(9):2161–2167. 32. Cheesborough JE, Souza JM, Dumanian GA, Bueno Jr. RA. Targeted muscle reinnervation in the initial management of traumatic upper extremity amputation injury. Hand (N Y). 2014;9(2):253–257. 33. Valerio IL, Dumanian GA, Jordan SW, et al. Preemptive treatment of phantom and residual limb pain with targeted muscle reinnervation at the time of major limb amputation. J Am Coll Surg. 2019;228(3):217–226. 34. O’Brien AL, Jordan SW, West JM, Mioton LM, Dumanian GA, Valerio IL. Targeted muscle reinnervation at the time of upperextremity amputation for the treatment of pain severity and symptoms. J Hand Surg Am. 2021;46(1):72 e1–72 e10. 35. Santosa KB, Oliver JD, Cederna PS, Kung TA. Regenerative peripheral nerve interfaces for prevention and management of neuromas. Clin Plast Surg. 2020;47(2):311–321. 36. Kubiak CA, Kemp SWP, Cederna PS, Kung TA. Prophylactic regenerative peripheral nerve interfaces to prevent postamputation pain. Plast Reconstr Surg. 2019;144(3):421e–430e. 37. O’Shaughnessy KD, Rawlani V, Hijjawi JB, Dumanian GA. Oblique pedicled paraumbilical perforator-based flap for reconstruction of complex proximal and mid-forearm defects: a report of two cases. J Hand Surg Am. 2010;35(7):1105–1110. 38. Hijjawi JB, Kuiken TA, Lipschutz RD, Miller LA, Stubblefield KA, Dumanian GA. Improved myoelectric prosthesis control accomplished using multiple nerve transfers. Plast Reconstr Surg. 2006;118(7):1573–1578. 39. Mioton LM, Dumanian GA, De la Garza M, Ko JH. Histologic analysis of sensory and motor axons in branches of the human brachial plexus. Plast Reconstr Surg. 2019;144(6):1359–1368. 40. Stubblefield KA, Miller LA, Lipschutz RD, Kuiken TA. Occupational therapy protocol for amputees with targeted muscle reinnervation. J Rehabil Res Dev. 2009;46(4):481–488. 41. Daly MC, He JJ, Ponton RP, Ko JH, Valerio IL, Eberlin KR. A single incision anterior approach for transhumeral amputation targeted muscle reinnervation. Plast Reconstr Surg Glob Open. 2020;8(4):e2750.

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42. Renninger CH, Rocchi VJ, Kroonen LT. Targeted muscle reinnervation of the brachium: an anatomic study of musculocutaneous and radial nerve motor points relative to proximal landmarks. J Hand Surg Am. 2015;40(11):2223–2238. 43. Dumanian GA, Ko JH, O’Shaughnessy KD, Kim PS, Wilson CJ, Kuiken TA. Targeted reinnervation for transhumeral amputees: current surgical technique and update on results. Plast Reconstr Surg. 2009;124(3):863–869. 44. Morgan EN, Kyle Potter B, Souza JM, Tintle SM, Nanos 3rd GP. Targeted muscle reinnervation for transradial amputation: description of operative technique. Tech Hand Up Extrem Surg. 2016;20(4):166–171. 45. Li G, Kuiken TA. EMG pattern recognition control of multifunctional prostheses by transradial amputees. Annu Int Conf IEEE Eng Med Biol Soc. 2009;2009:6914–6917. 46. Pierrie SN, Gaston RG, Loeffler BJ. Targeted muscle reinnervation for prosthesis optimization and neuroma management in the setting of transradial amputation. J Hand Surg Am. 2019;44(6):525e1–525e8. 47. Peterson SL, Peterson EL, Wheatley MJ. Management of fingertip amputations. J Hand Surg Am. 2014;39(10):2093–2101. 48. Li Y, Kulbacka-Ortiz K, Caine-Winterberger K, Brånemark R. Thumb amputations treated with osseointegrated percutaneous prostheses with up to 25 years of follow-up. J Am Acad Orthop Surg Glob Res Rev. 2019;3(1):e097. 49. Goodacre CJ, Bernal G, Rungcharassaeng K, Kan JY. Clinical complications with implants and implant prostheses. J Prosthet Dent. 2003;90(2):121–132. 50. Manurangsee P, Isariyawut C, Chatuthong V, Mekraksawanit S. Osseointegrated finger prosthesis: an alternative method for finger reconstruction. J Hand Surg Am. 2000;25(1):86–92. 51. Gaston RG, Bracey JW, Tait MA, Loeffler BJ. A novel muscle transfer for independent digital control of a myoelectric prosthesis: the Starfish procedure. J Hand Surg Am. 2019;44(2):163 e1–163 e5. 52. Shubinets V, McAndrew C, Mauch J, et al. Partial hand transplant: lessons learned from cadaveric dissection studies. J Hand Surg Am. 2018;43(7):634–640. 53. Wilhelmi BJ, Lee WP, Pagenstert GI, May Jr. JW. Replantation in the mutilated hand. Hand Clin. 2003;19(1):89–120. 54. Buncke GM, Buncke HJ, Lee CK. Great toe-to-thumb microvascular transplantation after traumatic amputation. Hand Clin. 2007;23(1): 105–115. 55. Bueno Jr RA, Battiston B, Ciclamini D, Titolo P, Panero B, Tos P. Replantation: current concepts and outcomes. Clin Plast Surg. 2014;41(3):385–395.

56. Pet MA, Ko JH, Vedder NB. Reconstruction of the traumatized thumb. Plast Reconstr Surg. 2014;134(6):1235–1245. 57. Vlot MA, Wilkens SC, Chen NC, Eberlin KR. Symptomatic neuroma following initial amputation for traumatic digital amputation. J Hand Surg Am. 2018;43(1):86e1–86e8. 58. Daugherty THF, Bueno Jr RA, Neumeister MW. Novel use of targeted muscle reinnervation in the hand for treatment of recurrent symptomatic neuromas following digit amputations. Plast Reconstr Surg Glob Open. 2019;7(8):e2376. 59. Daugherty THF, Mailey BA, Bueno Jr RA, Neumeister MW. Targeted muscle reinnervation in the hand: an anatomical feasibility study for neuroma treatment and prevention. J Hand Surg Am. 2020;45(9):802–812. 60. Elmaraghi S, Albano NJ, Israel JS, Michelotti BF. Targeted muscle reinnervation in the hand: treatment and prevention of pain after ray amputation. J Hand Surg Am. 2020;45(9):884e1–884e6. 61. Vu PP, Vaskov AK, Irwin ZT, et al. A regenerative peripheral nerve interface allows real-time control of an artificial hand in upper limb amputees. Sci Transl Med. 2020;12(533). 62. Potter BK. From bench to bedside: a perfect fit? Osseointegration can improve function for patients with amputations. Clin Orthop Relat Res. 2016;474(1):35–37. 63. Zaid MB, O’Donnell RJ, Potter BK, Forsberg JA. Orthopaedic osseointegration: state of the art. J Am Acad Orthop Surg. 2019;27(22):e977–e985. 64. Overmann AL, Aparicio C, Richards JT, et al. Orthopaedic osseointegration: implantology and future directions. J Orthop Res. 2020;38(7):1445–1454. 65. Clites TR, Carty MJ, Ullauri JB, et al. Proprioception from a neurally controlled lower-extremity prosthesis. Sci Transl Med. 2018;10(443). 66. Srinivasan SS, Herr HM, Clites TR, et al. Agonist–antagonist myoneural interfaces in above-knee amputation preserve distal joint function and perception. Ann Surg. 2021;273(3): e115–e118. 67. Srinivasan SS, Gutierrez-Arango S, Teng AC, et al. Neural interfacing architecture enables enhanced motor control and residual limb functionality postamputation. Proc Natl Acad Sci U S A. 2021;118(9). e2019555118. 68. Herr HM, Clites TR, Srinivasan S, et al. Reinventing extremity amputation in the era of functional limb restoration. Ann Surg. 2021;273(2):269–279.

 

SECTION VII • New Directions

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

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SYNOPSIS

ƒ Upper extremity allografts consist of multiple tissues of variable immunogenicity such as skin, lymph nodes, bone marrow, nerves, vessels, muscles, and bone. ƒ Transplantation can restore the appearance, anatomy, and function of non-salvageable upper extremity loss by replacing “like-with-like” tissue while avoiding donor site morbidity and/or multiple reconstructions. ƒ Vascularized composite allotransplantation (VCA) is not a life-saving procedure but it can significantly enhance a patient’s quality of life. Unlike solid organ transplantation, recipients are otherwise healthy without significant co-morbidities. The risk-benefit consideration for patients must include the potential side effects of long-term immunosuppression – treatment that is necessary for graft survival. ƒ The conventional immunosuppression protocols used in upper extremity VCA are similar to those used in solid organ transplantation and have prevented early graft loss, but not acute rejection. ƒ Acute rejection in vascularized composite allografts can be monitored grossly, thus allowing for rapid intervention as needed. Acute rejection events, when properly managed, do not appear to impact long-term allograft function or survival. ƒ During the past two decades, more than 100 upper extremity transplants have been performed around the world in more than 70 patients with encouraging intermediate to long-term functional and graft survival outcomes. ƒ In order to broaden the application of this life-changing reconstructive modality, future research should focus on investigating novel immunomodulatory approaches that aim to enable long-term allograft survival while minimizing the need for life-long immunosuppression.

Introduction Millions of people each year suffer from major upper extremity trauma, resection of upper extremity tumors, or are born with major congenital defects that require many complex

reconstructive procedures to repair large upper extremity defects. Conventional management of these tissue deficiencies includes prosthetic rehabilitation or autologous reconstruction, but these modalities are often limited by highly variable outcomes.1 There are many factors that adversely affect outcomes from traditional approaches, including a prolonged timeline and cost of rehabilitation, multiple surgeries, limited autologous tissue for reconstruction, and secondary morbidity from extensive autologous donor-site surgery. For complex injuries not amenable to conventional reconstruction, vascularized composite allotransplantation (VCA) can achieve near perfect primary restoration of tissue defects with improved functional and aesthetic outcomes. VCA is a newly developed focus area in transplantation medicine and combines the timetested techniques of reconstructive microsurgery with the immunologic principles of transplantation. The goal of VCA is to improve quality of life for patients with significant composite tissue defects by leveraging the plastic surgery principle of replacing “like with like” to optimize both functional outcomes and aesthetic outcomes. In the US alone, approximately 1,285,000 upper extremity amputations are performed per year.2 In 2005, there were approximately 1.6 million individuals living in the US with upper or lower extremity limb loss.3 Of these 1.6 million patients, nearly 540,000 individuals have had upper extremity amputations. Even if only 1% of these patients were deemed candidates for upper extremity allotransplantation, this would mean that more than 5000 patients could potentially benefit from this life-changing treatment. Thus far, only some 70 patients have undergone upper extremity allotransplantation in the past two decades. However, despite the fact that surgical, immunological, and functional results are highly encouraging, the need for long-term and high-dose immunosuppression to enable graft survival and to treat/reverse acute skin rejection episodes remains a rate-limiting obstacle towards widespread application.4,5 The risks of immunosuppression are significant and include, but are not limited to: infection, cancer, and metabolic derangements. All these risks

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greatly affect the recipient’s quality of life, alter risk profile, and jeopardize the potential benefits of upper extremity transplantation. Furthermore, unlike in solid organs, clinical success is dictated not only by graft acceptance and survival but also by nerve regeneration, which determines ultimate functional outcomes. Novel strategies such as cellular and biologic therapies that integrate the concepts of immune regulation with those of nerve regeneration have shown promising results in small and large animal models. Clinical translation of these insights to upper extremity reconstructive transplantation could further minimize the need of immunosuppression and optimize functional outcomes, enabling greater feasibility and wider application of these procedures as an option for upper extremity amputees.

Evolution of upper extremity vascularized composite allotransplantation Access the Historical Perspective section, including Fig. 41.1, online at: Elsevier eBooks+

Immunology of vascularized composite allotransplantation Research findings in a plethora of translational models have vastly improved our understanding of the immunologic aspects of VCA. We now know that allografts are composed of different tissues, each with its own unique antigenicity as a result of differing antigen expression and presentation mechanisms.69 Each tissue type in a vascularized composite allograft expresses different amounts of major histocompatibility complex (MHC) and tissue-specific antigens – important factors that elicit a recipient’s cellular-mediated immune response.70 Antigen recognition and targeting by the recipient’s immune system also differs among the allograft tissue elements due to differential vascular and lymphatic supply. Cumulatively, these mechanisms explain the pattern of rejection that can be observed in whole limb transplanted allografts. For example, transplanted muscle evokes a primarily cell-mediated immune response, whereas skin is known to induce both cellular and humoral responses.71 Skin and bone marrow are also known to reject earlier and more aggressively than muscle, bone, cartilage, or tendon. Appreciating the relative antigenicity of vascularized composite tissue components informs the development of strategies aimed to attenuate the antigenicity of these components. Furthermore, understanding the relative antigenicity of specific allograft components enables the tailoring of immunosuppression, thus facilitating opportunities to limit immunosuppressants as much as possible.72 Over the past few decades, our understanding of relative antigenicity and humeral/cellular immunity has allowed the testing of several tailored immunosuppressive regimens in small animal (rat) and large animal (porcine, canine, and nonhuman primate) VCA models.

Experimental background and scientific basis for upper extremity transplantation Early rodent limb transplantation recipients immunosuppressed with various combinations of 6-mercaptopurine or derivative azathioprine and prednisone all died from drug-induced side effects prior to onset of macroscopic signs of rejection.73 Even after the introduction of cyclosporine A, the use of high doses of cyclosporine A demonstrated no improvement in limb or animal survival.74–78 In fact, cyclosporine A monotherapy was found to be uniformly unsuccessful in prolonging vascularized composite allograft survival in both small animal and nonhuman primate models.79 Further studies in nonhuman primate models demonstrated that acute rejection could only be prevented with cyclosporine A when trough levels were 3–4 times the level achieved in human solid organ transplantation – levels known to be associated with significant peri-transplant infections and malignancies.80–83 In 1996, Benhaim and colleagues demonstrated that a combination of cyclosporine A with an antimetabolite (such as mycophenolate mofetil) could successfully prolong rat hindlimb allograft survival.84 Benhaim and his team pioneered the concept that predictable, long-term, functional limb allograft survival was feasible. Using a similar regimen, others demonstrated in swine models that long-term survival of fully mismatched composite allografts was feasible.85,86 Since swine and humans share immunological similarities including the structure of MHC and the expression of MHC class II antigens (on endothelial cells, epithelial cells, and dendritic cells),87 these findings provided adequate proof of concept in both small88,89 and large animal models85,86 that human upper extremity allotransplantation was feasible.90 Solid organ transplantation innovation has provided critical information about the immunologic consequences of organ transplantation and the efficacy and toxicity of immunosuppressive drugs. The field of transplantation evolved from transplanted kidneys91 and hearts92,93 to livers,94 lungs,95 pancreas,96 small bowel,97 multiple abdominal viscera,98 bone marrow,99 and, most recently, vascularized composite allografts.100,101 As expected, the initial results of allograft and patient survival after organ transplantation in the 1960s were poor. Editorials in major clinical journals, including the New England Journal of Medicine,102–105 questioned the feasibility and ethical basis of organ transplantation. There was great concern for the adverse effects of chronic immunosuppression, especially the risk of opportunistic infections and malignancies. During the next four decades, due to improvements in immunosuppression and in the management of post-transplant complications, this pessimism abated. Similarly, attempts at upper extremity transplantation,106,107 after three decades of quiescence since the first attempt in Ecuador,46,47 has also been met with vigorous skepticism. Interestingly, most of the criticism has come from hand surgeons.108–114 Most argue that the risks of immunosuppressive therapy are justifiable in potentially life-saving organ transplantation, but not in upper extremity allotransplantation. Furthermore, many hand surgeons argue that the immunological, ethical,115,116 and psychological117 issues associated with hand transplantation still need to be addressed.118 The justification for proceeding with clinical trials of upper extremity transplantation using modern immunosuppression has been based on scientific progress on: (1) the availability

Evolution of upper extremity vascularized composite allotransplantation

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Historical development and milestones The earliest accounts of organ transplantation date to the Chinese physician Pien Chi’ao, who in 500 BCE performed a dual-heart transplant on warriors Gong Hu and Qi Ying.6 In addition, in the Sushruta Samhita, a surgical report written by the Indian surgeon Sushruta who lived around the fifth to sixth century BCE. He describes in detail the techniques of rhinoplasty and pedicled autografts from the forehead, neck, and cheek to restore mutilating injuries of the nose and ear.7–9 About 900 years later, the patron saints Cosmos and Damian are credited with performing the first limb allotransplantation.10–14 Legend has it that around the year 348, they successfully transplanted the right leg of a dead Moor onto the Roman deacon Justinian, after amputating his cancerous/gangrenous leg (Fig. 41.1). The first description of skin allografting was done by the sixteenth-century Italian surgeon Gaspare Tagliacozzi from Bologna, who in his book De curtorum chirurigia per insitionem (“On the surgery of mutilation by grafting”) described a novel method of nasal and aural allo-reconstruction, where he used skin from the inner aspect of the arm from a slave to reconstruct the nose of a wealthy patient who injured it during a sword fight.15–17 In this book, Tagliacozzi goes on to describe one of the first descriptions of tissue rejection, when he discusses the practical difficulty of binding two different individuals (referring to tissue rejection) to one another for a sufficient length of time. It took another 300 years before these “practical difficulties” in transplantation began to be elucidated. During this time, advancements in antisepsis, anesthesia, hemostasis, organ preservation and, most importantly, microvascular surgery led to the rapid progress of reconstructive microsurgery. Alexis Carrel in 1902 described the surgical technique of vascular anastomosis, thus laying the foundation for conventional vascular and microsurgery.18 Carrel successfully obtained the revascularization of experimental organ allografts,19,20 but failed to achieve permanent graft acceptance. Carrel attributed this “organ failure” to vascular complications because he had no knowledge of the process of rejection. In 1932 and 1937, the first attempts at skin grafting were performed between identical twins.21,22 Again, no mention was made of rejection. In 1944, Hall published the first detailed theoretical account of cadaveric donor upper extremity transplantation (at the mid-humeral level).23 In his protocol, Hall described that an experienced surgical team within a well-equipped hospital was needed to perform the procedure. Additionally, his protocol included important and innovative descriptions of organ preservation, osteosynthesis, and vascular anastomoses. Lastly, potential complications related to thrombosis and infections were discussed, but, again, no reference was made to the occurrence of rejection. Strikingly, Hall was not aware that Sir Peter Brian Medawar, a young zoologist in Britain, and Thomas Gibson, a plastic surgeon, had made the historic discovery of the immunologic phenomenon of skin allograft rejection that very same year (1944).24 The challenge of skin transplantation led to the exploration of new frontiers in organ transplantation. In 1954, a plastic surgeon, Joseph E. Murray, with his team members, John P. Merrill and J. Hartwell Harrison in Boston, performed the first successful human kidney transplantation between identical twins.25,26 This was followed in 1957, by the first clinical attempt at allotransplantation of

Figure 41.1  St. Cosmas and St. Damian perform the first human extremity allotransplantation. Per mythology, Christian Roman deacon Justinian had a malignant growth on his leg and fell asleep while praying for a cure in the Church of Cosmas and Damian in Rome. In his dreams, the saints amputated the diseased limb and transplanted the leg of a Moor, brought to the church for burial. The patient awoke and gratefully observed a now healthy leg, though black in color. (Reproduced with permission from Württembergisches Landesmuseum, Stuttgart.)

an en bloc composite digital flexor tendon mechanism by a plastic surgeon, Erle E. Peacock, Jr.27,28 Indeed, it was Peacock who coined the term “composite tissue allograft” to differentiate these transplants that were composed of multiple tissues unlike solid organs.29 Our understanding of the immunologic behavior of allografts lagged behind technical developments in surgery. It was only the knowledge gained from landmark discoveries in the past century30–38 that facilitated the manipulation or suppression of the immune response, allowing successful prolongation of graft survival. After Medawar’s demonstration that rejection was an immunologic event, the next logical question was: Why not prevent this phenomenon by suppressing the immune system? In the 1950s, corticosteroids and irradiation were used for immunosuppression.39,40 In the 1960s, the antimetabolites 6-mercaptopurine and its derivative azathioprine were introduced, along with agents such as antilymphocyte globulin. These drugs were used either alone41,42 or in combination with corticosteroids.43–45 Graft survival improved but surgical outcomes were dismal because these drugs acted indiscriminately and were associated with severe organ-specific and systemic adverse effects. In 1964, the first hand transplantation was performed using pharmacologic immunosuppression.46–48 Dr Gilbert in Guayaquil, Ecuador, transplanted the right forearm of a

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CHAPTER 41  • Upper extremity composite allotransplantation

28-year-old sailor who had lost his limb at the wrist level owing to a hand-grenade explosion the previous day. The donor was a laborer who had died of hematemesis (with gastric bleeding) a few hours earlier. The recipient was given heparin, dextran, and a broad-spectrum antibiotic after the surgery and was maintained on a combination regimen of prednisone and 6-mercaptopurine (6-mercaptopurine was replaced 24 hours later by azathioprine). These drugs are considered primitive according to present day standards, and unfortunately, signs of acute allograft rejection occurred after two and half weeks. The patient was then moved to Peter Bent Brigham Hospital in Boston, where at 3 weeks, aggressive rejection set in, and the forearm had to be re-amputated at 4 cm above the wrist level. Unfortunately, the advanced state of necrosis prevented any histopathologic evaluation of the graft. This bold and pioneering attempt at hand transplantation laid the foundation to the successful attempts yet to come. In 1976, another major breakthrough in transplantation came with the discovery of the immunosuppressive properties of the calcineurin inhibitor cyclosporine A.49,50 In 1978,

cyclosporine was first used clinically in organ51 as well as bone marrow transplantation with remarkable results. The FDA approved cyclosporine A in 1983. Cyclosporine A, along with agents like anti-CD3 antibody (OKT3, introduced in 1981),52 effectively reduced the reliance on high-dose steroids for the prevention of rejection. The calcineurin inhibitor tacrolimus (FK 506) was discovered in 1987,53 clinical trials were conducted in 1989,54 and FDA approval came in 1994. Tacrolimus led to dramatic improvements in solid organ transplantation,55–58 allowing highly immunogenic grafts such as the small bowel to be transplanted.59–61 The success of the calcineurin inhibitors cyclosporine A and tacrolimus made them the cornerstone drugs of the modern era of transplantation.62 The 1990s saw the introduction of novel drugs such as the antimetabolite mycophenolate mofetil63 (MMF, approved by FDA in 1995) and rapamycin64 (sirolimus, discovered in 1976 but approved by FDA only in 1999). Combining these drugs with a calcineurin inhibitor65–68 was found to significantly reduce rejection and improve solid organ graft survival with a reduction in adverse effects.

Clinical experience with upper extremity allotransplantation

of novel immunosuppressive drugs that have improved the efficacy and lower risk profile of immunosuppresion; (2) the availability of highly efficacious treatments for opportunistic fungal or viral infections (such as Pneumocystis carinii and Cytomegalovirus); (3) the development of novel therapeutics for post-transplant malignancies (such as rituximab for post-transplant lymphoproliferative disorder, PTLD); (4) research on immunosuppressive drug regimens based on years of experience with solid organ transplantation; and (5) the success of human transplantation of all individual component tissues of the hand, including skin, muscle, tendons, vessels, nerve, bone, and joint.119

Chronology of clinical upper extremity allotransplantation In September 1991, the first conference on VCA was held in Washington, DC to “determine the clinical feasibility of transplanting limbs in patients with limb loss” and the “direction in which clinically oriented limb transplantation research should head”.120 In November 1997, the 1st International Symposium on VCA was convened in Louisville, Kentucky to discuss the “scientific, clinical and ethical barriers standing in the way of performing the first human hand transplant”. International experts at the meeting predicted that limb transplantation was not far from “becoming a clinical reality”.121 Within the next 22 months, 34 years after the first hand transplantation was performed,46,47 surgeons in Lyon, France, performed the world’s second unilateral hand transplant in September 1998.106,107,122,123 In January 1999, the first unilateral hand transplant in the US was performed in Louisville, Kentucky.124,125 Following these attempts, numerous centers in Europe, Asia, and the US have performed over 70 upper extremity transplantations. Most of these transplantations were wrist to mid-forearm amputations, except for two partial hand grafts in China, one partial hand graft in the US, and two cases of above elbow transplantation.126,127

Clinical experience with upper extremity allotransplantation Program, patient, procedural, and protocol-related considerations Program establishment and implementation Creating a hand transplant program is a task filled with many challenges.128,129 Solid organ transplantation and hand replantation are time-tested procedures and are now the standard of care. Hand transplantation is the amalgamation of the scientific principles of reconstructive surgery and the concepts of organ transplantation. Therefore, the success of any hand transplant program lies in its ability to foster collaboration between a multidisciplinary team comprised of a core group of hand (plastic or orthopedic) and transplant surgeons, psychiatrists, physical therapists, social workers, and transplantation nursing staff to name a few. Although the transplant clinical process is well established, it is also bound by tight

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regulations; this may come as a surprise to reconstructive plastic/hand surgeons who wish to start a hand program. Therefore, the experience of the solid organ transplantation members is essential when negotiating through the regulatory process. Such a joint effort can overcome the challenges that are inherent in a complex therapeutic option that integrates multiple specialties during the planning, procedural, and post-transplant phases.

Donor and recipient selection Successful VCA relies on many factors; our own experience with upper extremity allotransplantation has taught us that proper evaluation, selection, and management of donors and potential recipients are likely the most important determinants of success. Recipient screening and selection is a multistage process, which takes a multidisciplinary look into the patient’s past medical history and pre-transplant life.130 Data on psychological and social factors must be collected and evaluated in order to determine patient eligibility. While these psychological and social aspects of screening are critical, they are also the most difficult to assess. The worldwide experience with upper extremity allotransplantation has shown that only patients who are physically and mentally healthy, with adequate psychological and social support, and highly motivated to undergo long-term (+6 months) intensive rehabilitation and therapy, are “good” candidates for upper extremity transplantation. Decades of experience with solid organ transplantation has provided the field of transplantation medicine with wellestablished criteria for donor and recipient selection. Given that the field of upper extremity allotransplantation is still young, parameters for inclusion and exclusion of donors and recipients have yet to be fully established.131,132 Boxes 41.1 and 41.2 highlight the general selection criteria that have been used in upper extremity allotransplantation. Patients below the age of 18 are generally excluded due to issues of informed consent of an experimental procedure, though this frontier

BOX 41.1  Donor considerations in upper extremity allotransplantation Demographic and phenotypic characteristics Skin color, tone, and texture match Limb size and dimension (bone length and diameter match) Age, sex, race, and ethnicity match if possible Donors must be deceased (brain death declared) Donor limb dissection and procurement must not interfere with organ recovery. Limb usually prepped first, perfused under isolated tourniquet, dissected after cross clamp and retrieved in sequence with heart and lung recovery. This minimizes overall ischemia time History of malignancy (recent or remote) may be an exclusion Paralysis of ischemia or traumatic origin, inherited peripheral neuropathy, infectious, post-infectious or inflammatory neuropathy, toxic neuropathy (i.e., heavy metal poisoning, drug toxicity, industrial agent exposure) or mixed connective tissue disease, severe deforming rheumatoid or osteoarthritis in the limb may be exclusions

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BOX 41.2  Recipient considerations in upper extremity allotransplantation Subjects can be of any race, color, ethnicity, in good health Age range for eligibility is variable but usually over 18 years and under 65 years Subjects with congenital defects (e.g., transverse arrest) are currently excluded It impact of the lack of pre-existing cortical recognition is unknown Blindness is an exclusion in some programs Eyesight is necessary to follow the rigorous rehabilitation process. Additionally, visual feedback is critical for functional recovery Rigorous psychosocial assessment is mandatory Used to determine the motivation for transplantation, emotional and cognitive preparedness for the procedure, body image adaptation, level of realistic expectations regarding post-transplant outcomes, anticipated comfort with the transplant, personality organization/risk of regression, history of medication compliance/substance abuse, potential for compliance, and social support system/family structure Use or attempted use of prostheses prior to transplant is a suggested requirement

has been challenged and is discussed later in this chapter. Furthermore, from experience in solid organ transplantation, it is known that pediatric patients are more likely to develop immunosuppressive-related complications like PTLD, than adults.133 Patients over the age of 65 are also generally excluded because of increased immunosuppression-related complications, limited years of potential gain from the transplant, and decreased nerve regeneration potential. Medical screening of recipients includes a complete medical history and physical examination; routine laboratory studies; blood typing and cross-matching; human leucocyte antigen (HLA) typing; testing for panel-reactive antibodies; and serology for Epstein–Barr virus, cytomegalovirus, HIV, and viral hepatitis. Other tests include radiography (to plan for osteosynthesis), angiography (to exclude abnormal vascular patterns), electro­ myography, nerve conduction velocity, and functional magnetic resonance imaging (fMRI).

Procedural aspects Donor limb procurement Once an immunologically appropriate donor has been identified by the Organ Procurement Organization (OPO), further “matching” is necessary to ensure adequate skin color, gender, age, and length circumference.134 The level of procurement depends on the specific deficit on the recipient. Each recipient should receive a “custom” operation tailored to the respective anatomical deficits (see Algorithm 41.1). For distal forearm

Algorithm 41.1 Distal Forearm

Osteosynthesis: standard distal radius/ulna Muscle needed: recipient extrinsics Nerve level: median, ulnar, radial Vessel level: radial, ulnar

Mid Forearm

Osteosynthesis: mid to distal distal radius/ulna Muscle needed: Recipient flexors/extensors if possible Nerve level: median, ulnar, radial Vessel level: radial, ulnar

Proximal Forearm

Osteosynthesis: proximal radius/ulna Muscle level: Donor flexor/pronator/extensor origins anchored to native medial/lateral epicondyle Nerve level: median, ulnar, radial Vessel level: brachial

Trans Humeral

Osteosynthesis: mid humerus Muscle needed: Brachialis, biceps/triceps from both donor & recipient pectoralis repair Nerve level: median, ulnar, radial Vessel level: brachial, superficial veins

Recipient Defect

The procedure is matched specifically to the level of the recipient defect.

Clinical experience with upper extremity allotransplantation

and mid-forearm transplants, an elbow disarticulation provides enough soft tissue, vessel length, nerve length, and extra skin/bone for transplantation. For proximal trans-humeral transplants, a proximal humeral procurement at the most proximal level possible that can still maintain tourniquet control is usually adequate.135 Proximal arm procurements may often require intrathoracic cannulation and control of the subclavian vessels by the thoracic procurement team. The limb is perfused by cold Histidine–Tryptophan–Ketoglutarate (HTK, Custodiol) or University of Wisconsin (UW) solution based on the individual center preference. Depending on the stability of the donor, level of procurement, and operating room space, upper extremity procurement may occur concurrently, before, or after standard organ procurement. We recommend procurement of the upper extremity before visceral organ procurement to minimize ischemia time as much as possible. Upon completion of hand retrieval (Fig. 41.2), the donor stump is closed, and the body can be fitted with a cosmetic prosthesis, allowing the family the option of an open-casket funeral. Following retrieval, the limb (wrapped in moist sterile gauze and placed in a polyurethane bag) is transported in a sterile container (provided by the OPO) with iced water at 4°C–6°C. Donor spleen and lymph nodes are collected and cell suspensions cryopreserved for future immune assays.

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general anesthesia and induction therapy (most commonly with basiliximab, Simulect; anti-thymocyte globulin, ATG, or alemtuzumab, Campath 1H). Hand transplantation does not differ greatly from replantation. Instrumentation and technique are similar. A two-team approach is used. The donor team prepares the donor limb once received on the back table, tailoring the graft to the needs of the recipient and tagging the structures (Fig. 41.3). The two lead hand transplant surgeons and assistant hand transplant surgeons (dissecting the donor limb) are assisted by one scrub nurse per extremity, two circulators per room, and at least one anesthesiologist. Based on the preoperative assessment of the recipient, tissue requirements from the donor will be known. The team dissecting the recipient must know exactly what measurements are necessary for the donor team to proceed. The recipient team will need to clearly identify the amount of nerve, artery and veins required for transplantation. The sequence of tissue repair is to minimize ischemia time and could depend on surgical preference (Fig. 41.4). Commonly, it includes bony fixation → artery repair → vein repair (revascularization) → tendon repair → nerve repair → skin closure. Our experience has elucidated key principles that are important for the recipient operation. In general, nerve approximation should be performed as distally as possible.

Recipient surgery The recipient procedure is carefully planned prior to procurement and involves close communication between donor and recipient teams. After confirming donor match, the recipient undergoes placement of regional blocks, preparation for

Figure 41.4  Reperfusion after extensor tendon reconstruction but prior to flexor tendon reconstruction. Figure 41.2  Donor graft after isolated perfusion and disarticulation.

Clinical tips Distal forearm allotransplantation

Figure 41.3  Tagging of structures in the donor graft following back-table dissection improves technical success and reduces ischemia time.

Allotransplantation at the distal forearm frequently relies on the recipient’s native extrinsic musculature, which in turn requires the careful approximation of median and ulnar motor fascicles for recovery of intrinsic function. Recipient incisions should create volar and dorsal skin flaps, while donor incisions should create radial and ulnar skin flaps for interdigitation. Tendon approximation can be performed using the Pulvertaft weave technique, facilitating immediate postoperative active/passive range-of-motion. The osteosynthesis can be performed with standard distal radius and ulna fixation techniques. The authors typically perform osteosynthesis first, taking great care to create a stable distal radioulnar joint (DRUJ), followed by arterial and venous anastomoses, followed by reconstruction of the extensors, then flexors, then nerves.

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Clinical tips Mid-forearm allotransplantation Allotransplantation at the mid-forearm necessitates careful assessment of recipient flexor and extensor tendons/muscle (Fig. 41.5). If the flexors and extensors are considered of adequate length with minimal damage, then muscle/epimysial/fascial/tendon repairs are performed. However, postoperative care is especially warranted as these repairs do not lend themselves to vigorous immediate postoperative therapy. The same sequence described above for the distal forearm allotransplantation procedure is used for the mid-forearm procedure. If the recipient extensors and flexors are deemed inadequate, the mid-forearm procedure follows the steps as performed in the proximal forearm allotransplantation procedure (see below), while maintaining the distal level of skeletal osteosynthesis.

Clinical tips Proximal forearm allotransplantation

A

Allotransplantation at the proximal forearm requires the transplantation of donor flexor/extensor muscle groups in order to obtain meaningful digital excursion and strength in the hand. Volar and dorsal skin flaps are created on the recipient limb to protect the antecubital fossa and olecranon while donor limb skin flaps are elevated radially and ulnarly. The new flexor/pronator origins are fixed with bone anchors and sutures on top of the native flexor/pronator muscle mass at the medial epicondyle (Fig. 41.6 A–D). Similarly, the extensor origin is fixated with bone anchors into the lateral epicondyle. Additionally, the annular ligament and radiocapitellar joint capsule of the donor are sutured to the extensor origin of the recipient. The radial nerve can usually be dissected to individual muscles groups such as superficial radial, ECRB branch, posterior interosseus branch, and ECRL branch. We use an end-to-side brachial-to-brachial artery anastomosis to preserve maximum blood flow to the proximal ulna, radius, and native flexor/extensor motor groups. Veins are anastomosed in end-to-end fashion.

Over-dissection of donor arteries should be avoided to prevent postoperative bleeding and to minimize the risk of a persistent inflammatory reaction. The limb should always be kept on sterile ice with an interface between the ice and tissue to prevent thermal injury. Lastly, the authors typically use an implantable venous Doppler on the anastomosed veins and use pulse-oximetry probes on the transplanted hand for oxygenation monitoring.

Protocol-related considerations Maintenance immunosuppression B

Figure 41.5  (A,B) Mid-forearm allotransplantation.

Immunosuppression protocols currently in use for upper extremity allotransplantation have been adapted from solid organ transplantation regimens. The overall amount of immunosuppression required to ensure graft survival is comparable with that used in renal transplantation. Such conventional

Clinical experience with upper extremity allotransplantation

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Clinical tips Transhumerus allotransplantation Allotransplantation at the transhumeral region can be categorized as distal, middle, and proximal. Distal humerus allotransplantation is performed with primary repair of the donor brachialis fascia and biceps/triceps tendon to the recipient brachialis fascia and biceps/ triceps tendons (Fig. 41.6E–H). End-to-end brachial artery/vein (in addition to several superficial vein anastomoses) anastomoses are performed. Fixation is achieved by utilizing single-plate osteosynthesis with the authors preferring a tapered 4.5/3.5 mm stainless steel locking compression plate. Skin flaps are elevated while maintaining skin integrity at the AC fossa and olecranon. In mid-humerus transplantation, one must decide whether the remnant flexor/extensor muscle groups will be adequate for active elbow motion. If one decides to maintain the native biceps and triceps to power the elbow, then muscle-to-muscle approximation is performed with as much tendon/fascia substance as possible. The use of fascial/tendon graft or allograft may be beneficial for strengthening the repair. The brachialis, due to its extensive origin on the humerus, can be transferred with the donor limb and be expected to function if the musculocutaneous nerve is adequately coapted. The same osteosynthesis, nerve repair, and vascular reconstructions are performed as described for the proximal humerus procedure. If one decides to transplant the donor flexor and extensor masses, then the steps for the proximal humerus allotransplantation are followed. For proximal humerus allotransplantation, one may be required to transplant the entire flexor/extensor muscle compartments of the antebrachium (Fig. 41.7). Both the biceps short head and the biceps long head tendons are dissected off their origins on the donor limb. Both of these muscles can be sutured or woven into the recipient short head and long head/conjoint tendons, respectively. This level of transplantation also requires the division of the recipient pectoralis tendon with tagging for future repair. Osteosynthesis is performed utilizing a 4.5 mm locking compression plate which is placed anterolaterally. Once osteosynthesis is complete, the most posterior compartment structures are reconstructed with the recipient and donor triceps muscle/tendons sutured to one another with some tension with the elbow in extension. Next, the radial, ulnar, and median nerves are coapted. Attention is then directed to the arterial and venous anastomoses. The brachial artery on the recipient is anastomosed to axillary artery of the donor limb and the brachial and cephalic veins are anastomosed proximally as well. Lastly, after reperfusion is complete, the biceps long and short head proximal tendons are woven and/or sutured with the elbow in flexion and under some tension, followed by musculocutaneous nerve coaptation. Once this is complete, the pectoralis tendon may be repaired or reinserted with bone anchors if necessary.

A

E

B

F

C

G

immunosuppression has resulted in >95% patient and graft survival at 1 year after upper extremity transplantation.126 The majority of hand transplant patients received either polyclonal (antithymocyte globulins, ATGs) or monoclonal (alemtuzumab, basiliximab) antibody preparations as induction therapy followed by high-dose triple-drug combination for maintenance therapy including tacrolimus, mycophenolate mofetil (MMF), and steroids, though the dose and trough

D

H

Figure 41.6  Proximal forearm and trans-humeral transplantation. (A) Left forearm proximal transplantationpreop; (B) possible donor forearm incisions indicated; (C) post-fixation X-rays; (D) inset of skin flaps; (E) right upper arm transplantation-preop; (F) donor arm procured and demonstrating skin flap incisions; (G) post-fixation X-rays; (H) inset of skin flaps.

levels of each drug differs by center. Such regimens have proven sufficient to prevent early immunologic graft loss but have yet to prevent acute rejection episodes. Some programs follow steroid avoidance regimens, while others rely on monotherapy immunosuppression. Successful reversal of acute rejection episodes (Fig. 41.8) has been achieved using topical clobetasol or tacrolimus ointment with or without short-term bolus steroid doses.136,137

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Rehabilitation and functional assessment after upper extremity allotransplantation Rehabilitation and functional assessment are integral components of successful upper extremity allotransplantation.138 A fully trained hand therapist should be involved in the entire process from initial screening of prospective patients through final discharge. The goal is functional integration of the transplanted hand into the patient’s daily activities. Successful rehabilitation of upper extremity transplant patients follows

A

B

Figure 41.7  (A,B) Use of the high non-pneumatic tourniquet for proximal transhumeral procurement.

A

B

guidelines similar to replant protocols. There are several significant differences, however, such as the screening process for an ideal candidate and the monitoring for signs of rejection. The preoperative evaluation process involves patient acceptance of the amputation, attempted prosthetic use, and the establishment of realistic goals for surgery and outcomes. This includes a full history and physical exam to document the range of motion (ROM) of the available joints; manual muscle testing (MMT) of available muscles; response of the residual forearm musculature to electrical muscle stimulation; documentation of pain and sensitivity complaints; scar quality; level of amputation; sensation; edema; skin and soft-tissue integrity; and circumference of the forearms at varying levels, as well as length of the forearms. Different tests, questionnaires, or instruments can be used to evaluate preoperative functional level and the status of residual muscles that will power the transplanted hand. As appropriate, electrical muscle stimulation, as well as isometric exercise, can help in preoperative strengthening of these muscles. The goals of postoperative therapy, bracing, and splinting are similar to the goals in replantation surgery. Knowledge of the exact level of nerve repair, type of osteosyntheses, and details of tendon repairs are essential in planning of splinting and therapy. Uniquely, the hand therapist can help monitor for signs of rejection as the patient spends considerable time in rehabilitation after surgery. At our institution, a rigorous rehabilitation regimen has been implemented in all patients with 3–6 hours of supervised therapy, 5 days a week during the first 3–6 months postoperatively, depending on the nature and upper extremity level of the transplant. Therapy must consist of passive and active ROM exercises with appropriate static and dynamic splinting to allow for gentle active flexion/extension, and limit adhesions and promote healing. Hand-based splints such as dynamic extension outrigger splints (Fig. 41.9) and anti-claw splints should be used in all patients. The outrigger allows for an intrinsic-plus position, protects flexors and extensors, and enables constant tension

C

Figure 41.8 (A–C) Clinical manifestations of acute skin rejection. These can range from discrete or diffuse maculopapular rash with or without edema and palmar involvement.  

Clinical experience with upper extremity allotransplantation

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throughout the range of controlled motion. Compression gloves are useful in patients with lymphedema. Qualitative and quantitative tests for hand and upper extremity function such as the Carroll score,139 the DASH140 score, and the Hand Transplantation Score System141 may be utilized along with standard tests that evaluate motor and sensory recovery (Tinel’s, Semmes–Weinstein monofilaments, 2PD, dynamometry, peg board tests, etc.). After discharge at 3–6 months postoperatively, communication and coordination with a certified local therapist is critical to ensure follow-up continuity of an intensive regimen and a home therapy exercise routine that is paramount to achieving functionality.

Assessment for rejection (host-versus-graft reaction)

Figure 41.9  Dynamic extension (crane) outrigger splint.

Acute rejection (AR) is a T-cell- and/or antibody-mediated attack of the transplant by the recipient’s immune system resulting in damage and ultimately loss of the graft. We now know that skin is a critical target of rejection and monitoring of the skin by inspection is therefore considered most important for monitoring. Protocol graft-skin biopsies must be routinely performed until the first year plus whenever clinically indicated (visible signs of rejection such as a maculopapular rash). Biopsy samples may be analyzed by means of histology and immunohistochemistry (staining for CD3, CD4, CD8, CD20, and CD68) for quantification and characterization of cellular infiltrates. Scoring for severity of acute rejection is accomplished using established standard grading criteria such as the Banff classification (Fig. 41.10, Table 41.1).142,143 Important clinical characteristics of AR include edema, erythema, escharification, and necrosis. Atypical rejection in the

Normal skin

Grade I

Grade II

Grade III

Grade IVa

Grade IVb

Figure 41.10 The Banff histopathology grading system for acute rejection in skin. Grade IVa and IVb are variants in severity of rejection (Banff Grade IV).  

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Table 41.1  Banff grading scale

Grade

Histopathology of skin

Grade 0

None. Rare inflammatory infiltrates

Grade I

Mild. Mild perivascular lymphocytic and eosinophilic infiltration. No involvement of the overlying epidermis

Grade II

Moderate. Moderate-to-severe perivascular inflammation with or without mild epidermal and/ or adnexal involvement (limited to spongiosis and exocytosis)

Grade III

Dense inflammation and epidermal involvement with epithelial apoptosis, dyskeratosis, and/or keratinolysis

Grade IV

Necrotizing acute rejection. Necrosis of single keratinocytes and focal dermal-epidermal separation

Reproduced with permission from Cendales LC, Kanitakis J, Schneeberger S, et al. The Banff 2007 working classification of skin-containing composite tissue allograft pathology. Am J Transplant. 2008;8(7):1396–1400.

form of scaling, leuconychia or nail dystrophy can also occur (Fig. 41.11).137 Biopsies must also be examined for evidence of chronic rejection (CR), including intimal hyperplasia and subintimal foamy histiocytes in the vessels of the skin or muscle and tissue fibrosis (see Fig. 41.12).

A

Immunologic monitoring Recipient and donor cells must be typed before transplantation for human leukocyte antigens (HLA).144,145 Additionally, DNA samples from recipient/donor must be stored for future typing for MICA (MHC Class I Chain A related) genes in those patients in whom anti-MICA antibody is detected. All sera should be screened by antihuman globulin-enhanced complement-dependent cytotoxicity assays (AHG-CDC), by ELISA (to identify IgG anti-HLA Class I- and Class II-specific antibodies independently) and by Luminex (allows for the identification of anti-MICA antibodies, as well as ascertainment of their donor specificity). The MICA and MICB antigens are expressed on surface of endothelial cells and epithelial cells and elicit a strong antibody response in recipients of solid organ transplants. Cell-mediated immunity may be measured by the ImmuKnow (Cylex) assay that detects adenosine triphosphate (ATP) synthesis in CD4 cells. Immune responses are reported in ng/mL of ATP and categorized as strong (>525), moderate (226–524), or low (