Review of Plastic Surgery – Donal W. Buck II

Common Wrist/Carpal Fractures
189
18
■ Can progress to arthritis and SNAC (scaphoid nonunion
advanced collapse) wrist deformity.
■ Occurs often with missed scaphoid fractures in young
athletic patients.
■ Treatment: Bone grafting
○ Nonvascularized bone grafting (e.g., iliac crest, distal
radius) can be used for treatment of severe humpback
deformity.
○ Vascularized bone grafting (e.g., retrograde distal
radius bone flap, medial femoral condyle flap) is
indicated for most nonunions.
3. Other carpal fractures (in order of frequency)
• Triquetrum fractures
■ Patients present with pain over the triquetrum.
■ Dorsal lip fractures are the most common.
• Treatment options
■ Long arm thumb spica cast immobilization for 6 to
8 weeks
○ Indicated for nondisplaced, distal pole fractures
○ For proximal pole fractures, immobilization is often
recommended for 6 months.
■ ORIF
○ Indicated in distal pole fractures displaced >1 mm,
unstable transverse or oblique wrist fractures, and/or
most proximal pole fractures.
○ Often performed with compression screw fixation
(see Table 18.1)
• Scaphoid nonunion or malunion (“humpback deformity”)
can occur after scaphoid fracture.
■ Higher risk with more proximal fractures
Stage III
Stage IV
Stage I
Stage II
B
Figure 18.6, cont’d.

Carpal Injuries and Hand Arthritis
190
■ Treatment: Most can be treated with cast immobilization
for 4 to 6 weeks.
• Trapezium fractures
■ Often associated with other fractures (e.g., distal radius,
metacarpals)
■ Often result from an impaction force of the thumb
metacarpal into the trapezium
■ Trapezial ridge fractures can occur from a direct blow
(e.g., from a baseball).
■ Treatment: Nondisplaced ridge fractures may be treated
with cast immobilization; however, displaced fractures of
the trapezium require open reduction and internal
fixation (e.g., compression screw, K wire).
• Hamate fractures
■ Relatively rare, although fractures of the hook of the
hamate are more common in athletes (e.g., baseball
players, golfers, tennis and racquet ball players)
■ The hook protrudes from the base of the hamate into
the hypothenar musculature and is at risk for direct
force.
■ Characterized by chronic pain at the base of the
hypothenar eminence, which is worse with grasping, and
occasionally ulnar nerve paresthesias
■ Hook of hamate fractures require special carpal tunnel
views on X ray for visualization.
■ Treatment: Nondisplaced, acute fractures can be treated
with cast immobilization; however, displaced or chronic
fractures are often treated with excision of the hook of
hamate fragment.
Reprinted from Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C., et al.
(Eds.), 2011. Green’s Operative Hand Surgery, 6th ed. Elsevier,
639–707.
Table 18.1  Algorithm for Acute Scaphoid
Fracture Management
TYPE OF FRACTURE
TREATMENT
Stable Fractures, Nondisplaced
Tubercle fracture
Short arm cast for 6 to 8 weeks
Distal third fracture/incomplete
fracture
Short arm cast for 6 to 8 weeks
Waist fracture
• Long arm thumb spica cast
for 6 weeks, short arm cast
for 6 weeks or until CT
confirmed healing
• Percutaneous or open
internal fixation
Proximal pole fracture,
nondisplaced
Percutaneous or open internal
fixation
Unstable Fractures
• Displacement >1 mm
• Lateral intrascaphoid angle
>35 degrees
• Bone loss or comminution
• Perilunate fracture/dislocation
• Dorsal intercalated segmental
instability alignment
Dorsal percutaneous/open screw
fixation
Figure 18.7.  Recommended preferred positions for arthrodesis of
finger joints. (Reprinted from Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C.,
et al. [Eds.], 2011. Green’s Operative Hand Surgery, 6th ed. Elsevier, 389–406.
Copyright Elizabeth Martin.)
5°
5°
5°
40°
45°
25°
30°
35°
40°
55°
50°
0°– 5°
Osteoarthritis of the Hand and Wrist
1. Osteoarthritis (OA) of the small joints of the hand is
relatively common and can cause significant pain, deformity,
or stiffness.
• The distal interphalangeal (DIP) joints are most commonly
involved, followed by the proximal interphalangeal (PIP)
joints, and metacarpal phalangeal (MCP) joints.
• The treatment of small-joint arthritis centers on optimal
medical management (especially for inflammatory
arthritis), patient selection, and relative active and passive
joint motion.
• The primary surgical procedures for the stiff arthritic finger
are arthroplasty and arthrodesis.
■ Arthroplasty requires adequate soft tissue and
ligamentous support for stability.
○ Silicone and pyrolytic carbon implants available
◆ Silicone lacks stability, especially with side-to-side
force, when compared to pyrolytic carbon
implants, and has a high rate of implant fatigue.
◆ Pyrolytic carbon implants have high revision rates.
■ Arthrodesis: Indicated for painful, unstable, or deformed
digits with loss of motor control or inadequate bony
stock to support a prosthesis or digits with intractable
pain that have failed all other conservative measures (see
Figure 18.7)

Rheumatoid Arthritis (RA) of the Wrist and Hand
191
18
2. Basilar/first carpometacarpal (CMC) joint arthritis
• The thumb accounts for 50% of all hand function.
• Arthritis of the trapeziometacarpal joint is very common
and prevalence increases with age.
• Many patients will remain asymptomatic and symptoms do
not necessarily correlate with findings on plain
radiographs.
■ Patients typically complain of difficulty opening jars or
pain with pinch grip. Stiffness and pain at rest are
typically present in late-stage disease.
• Diagnosis and staging of the disease can be made using
plain radiographs (see Table 18.2).
• Treatment is focused on patients with significant pain,
thumb weakness, and instability, which can lead to
functional deficits. Options include
■ Conservative treatments: Nonsteroidal anti-
inflammatory drugs (NSAIDs), splinting, corticosteroid
injections
○ First-line treatment
■ Arthroscopy
○ Often reserved for early-stage-I disease that has failed
conservative treatment
○ Synovectomy, debridement, and capsulorrhaphy of
the volar beak ligament can all be performed.
■ Arthroplasty
○ Often reserved for stage-II to -IV disease, with loss of
articular cartilage
○ Performed with either trapeziectomy alone or in
combination with ligament reconstruction and flexor
carpi radialis (FCR) tendon interposition (ligament
reconstruction tendon interposition [LRTI] CMC
arthroplasty).
Table 18.2  Eaton Classification
STAGE
RADIOGRAPHIC CHARACTERISTICS
Stage I
Normal or slightly widened trapeziometacarpal joint
Trapeziometacarpal subluxation up to 1 3 of articular
surface
Normal articular contours
Stage II
Decreased trapeziometacarpal joint space
Trapeziometacarpal subluxation up to 1 3 of articular
surface
Osteophytes or loose bodies <2 mm
Stage III
Decreased trapeziometacarpal joint space
Trapeziometacarpal subluxation >1 3 of articular surface
Osteophytes or loose bodies ≥2 mm
Subchondral cysts or sclerosis
Stage IV
Involvement of the scaphotrapezial joint or less
commonly the trapeziotrapezoid or trapeziometacarpal
joint of the index
Data from Eaton, R.G., Littler, J.W., 1973. Ligament reconstruction
for the painful thumb carpometacarpal joint. J. Bone Joint Surg. Am.
55 (8), 1655–1666.
○ Regardless of technique, postoperative spica cast or
splint immobilization of the thumb is critical to
preserve length and prevent subsidence.
■ Arthrodesis
○ Usually preferred over arthroplasty for patients <50
years old with arthritis of the trapeziometacarpal joint
only, who wish to maintain grip and pinch strength
○ Also indicated when other reconstructions have failed
○ Fuse the thumb in 35 degrees of radial and palmar
abduction with 15 degrees of pronation and 10 degrees
of extension.
3. Carpal arthritis
• Often caused by avascular necrosis of the scaphoid or
lunate or secondary to trauma (e.g., chronic SL injury,
distal radius fracture, SNAC or SLAC wrist, etc.)
• Characterized by significant pain, stiffness, and functional
limitations
• Treatment options are directed at eliminating pain and
include
■ Radial styloidectomy
○ Reserved for patients with arthritis confined to the
radial styloid
■ Denervation of the wrist through partial neurectomy of
the anterior interosseus nerve and posterior interosseus
nerve (PIN)
■ Proximal row corpectomy
○ Indicated when the capitate and lunate fossa of the
radius are spared from arthritic changes
○ Removal of the scaphoid, lunate, and triquetrum
(“proximal row”) converts the wrist into a hinge joint
through articulation of the capitate with the radius.
■ 4-corner fusion
○ Indicated in advanced stages of SLAC or SNAC wrist,
with involvement of the lunocapitate joint
○ Involves scaphoidectomy with fusion of the lunate,
capitate, triquetrum, and hamate
■ Total wrist arthrodesis
○ Reserved for cases of advanced arthritis with
involvement of the midcarpal joint and lunate fossa
or as a salvage procedure when other reconstructive
options have failed
○ Involves fusion of the radiocarpal, midcarpal, and
third CMC joints with a dorsal plate or
intramedullary pin
Rheumatoid Arthritis (RA) of the Wrist
and Hand
1. Systemic autoimmune disorder that affects 1% of adults, with
a female predilection and genetic component
2. Characterized by synovial inflammation of the joints of the
hand and wrist, resulting in joint destruction, deformity, and
functional disability
• RA can also be associated with extra-articular disease
including soft-tissue nodules, vasculitis, pericarditis,

Carpal Injuries and Hand Arthritis
192
4. Joint involvement follows a predictable pattern: MCP, PIP,
and wrist joint involvement first, followed by knees, hips,
shoulders, and elbows.
• Unlike in OA, the DIP joints are often spared.
5. Wrist involvement
• Progresses from inflammation to carpal instability, ulnar
translocation of the carpus, caput ulnae (dorsal dislocation
of the ulnar head, carpal supination, and volar subluxation
of the extensor carpi ulnaris [ECU]), extensor tendon
synovitis and rupture, and ankylosis or instability.
6. Finger involvement
• MCP joint: Progresses to volar subluxation and ulnar
deviation
• PIP joint: Progresses to swan-neck deformity or
boutonniere deformity (see Figures 18.8 and 18.9)
7. Management of RA is often multimodal and involves
NSAIDs, corticosteroids, and disease-modifying
antirheumatic drugs (DMARDs) (e.g., methotrexate,
azathiropine, anti-TNF[alpha] agents, etanercept, and
infliximab) as well as surgery for specific indications.
8. The goals of surgery for RA include pain reduction, cessation
of disease progression, and improved function and
appearance.
• In general, stage and perform surgery first on proximal
joints and then proceed distally.
peripheral neuropathy, conjunctivitis, and pulmonary
disease.
3. Diagnosis is largely clinical and based on established criteria
(see Table 18.3).
• The presence of anemia, rheumatoid factor (RF), and
elevated erythrocyte sedimentation rate (ESR) is suggestive
of disease.
• RF is a marker for RA and also correlates with severity of
disease.
Table 18.3  Diagnostic Criteria for Rheumatoid Arthritis
CRITERION
DETAILS
1. Morning stiffness
1 hour
2. Soft-tissue swelling
3 or more joints
3. Soft-tissue swelling
Symmetric
4. Soft-tissue swelling of hand
MCP, PIP, wrist joints
5. Subcutaneous nodules
Rheumatoid nodules
6. Seropositivity
Rheumatoid factor
7. Typical radiographic findings
Periarticular erosions/
osteopenia, hand or wrist
Reprinted from Neligan, P.C., Chang, J. (Eds.), 2013. Plastic Surgery,
vol. 6, 3rd ed. Elsevier.
MCP, Metacarpal phalangeal; PIP, proximal interphalangeal.
Figure 18.8.  A, Swan-neck deformity originating from a mallet finger, with subsequent increased extension force at the PIP joint.
B, Swan-neck deformity originating at the PIP joint, with volar plate attenuation and possible FDS rupture due to PIP synovitis, and
subsequent dorsal subluxation of the lateral bands. FDS, Flexor digitorum superficialis; PIP, proximal interphalangeal. (Reprinted from Neligan,
P.C., Chang, J. [Eds.], 2013. Plastic Surgery, vol. 6, 3rd ed. Elsevier.)
Dorsal subluxation of lateral band
PIP synovitis leading to attenuation of
volar plate and possible FDS rupture
Attenuated or ruptured terminal tendon (mallet finger)
Increased pull at PIP joint
Contracted triangular ligament
$
%

Other Inflammatory Disorders of the Wrist and Hand
193
18
• Preoperatively, cervical spine radiographs in flexion and
extension must be obtained to evaluate for atlantoaxial
instability, which is common in RA patients.
9. Treatment options include
• Synovectomy: Removal of painful inflammatory pannus
and synovitis unresponsive to medical treatment
• Distal ulna resection (“Darrach” procedure): Indicated for
caput ulna syndrome with extensor tendon ruptures or
intractable pain with DRUJ instability
■ Can lead to worsening of ulnar drift of the carpus
because the ulnar stop has been removed
• Wrist arthrodesis: Indicated for severe disease and
instability
• MCP/PIP arthroplasty: Indicated for pain and loss of
function due to MCP deformity
■ Silicone is preferred in RA patients because of soft-tissue
laxity and joint instability.
■ Pyrocarbon implants can be used for MCP arthroplasty
but should be limited to young patients with stable soft
tissues.
• MCP/PIP arthrodesis: Indicated in patients who desire
effective pain relief and will accept the loss in motion or
those with retractable pain despite other procedures
• Treatment of swan-neck deformity depends on the severity
of joint disease, presence of intrinsic tightness, and relative
motion of the PIP joint.
■ Options include splinting (early disease with full PIP
flexion and no intrinsic tightness), intrinsic release,
sublimus sling procedure, PIP arthrodesis, and PIP
arthroplasty.
• Tendon ruptures
■ Caused by attrition of tendon from tendon friction over
a bony prominence, synovitis of the tendon, or vascular
disruption of the tendon.
■ Most common tendons to rupture are the extensor
tendons on the ulnar aspect of the hand secondary to
caput ulnae (e.g., “Vaughn-Jackson syndrome”: rupture
of extensor digiti minimi [EDM] and extensor digitorum
communis [EDC] to the small, ring, and long fingers),
the EPL tendon, and the flexor pollicis longus (FPL)
tendon (from a “Mannerfelt lesion”: Volar osteophyte of
the scaphoid).
○ Compression of the PIN can mimic EPL rupture
(distinguished by absence of tenodesis effect with true
rupture).
■ Treatment follows traditional tendon repair principles,
with addition of osteophyte removal and Darrach
procedure in caput ulna.
• Trigger finger
■ Caused by synovitis and nodule formation of the flexor
tendons
■ Treatment involves corticosteroid injection and flexor
tenosynovectomy with removal of intratendinous
nodules.
■ Never release the A1 pulley in rheumatoid arthritis
patients because this can worsen the patient’s ulnar drift.
Other Inflammatory Disorders of the Wrist
and Hand (see Table 18.4)
1. Scleroderma
• A rare autoimmune connective tissue disease characterized
by systemic sclerosis of multiple tissues including the skin,
blood vessels, heart, lung, gastrointestinal tract, and kidneys
• Can present as limited cutaneous disease or CREST
(calcinosis, Raynaud’s phenomenon, esophageal
dysmotility, sclerodactyly, and telangiectasia) syndrome
• Finger deformities are related to contracture of skin with
development of flexion contractures and ulcerations.
■ Most common lesion is PIP flexion contracture
■ Treat soft-tissue loss conservatively, with topical
antimicrobials and minimal debridement.
■ For severe PIP contracture with intact skin, arthrodesis
may be indicated, and phalanx shortening may be
required to relieve pressure on overlying skin.
■ Occasionally, amputation is required.
Volar subluxation of lateral band
PIP synovitis
Attenuated central slip
Contracted oblique retinacular
ligament
Figure 18.9.  Boutonniere deformity secondary to synovitis at the PIP joint, with attenuation of the central slip, and subsequent volar
subluxation of the lateral bands. (Reprinted from Neligan, P.C., Chang, J. [Eds.], 2013. Plastic Surgery, vol. 6, 3rd ed. Elsevier.)

Carpal Injuries and Hand Arthritis
194
Suggested Readings
Amadio, P.C., Shin, A.Y., 2011. Chapter 12: Arthrodesis and arthroplasty of
small joints of the hand. In: Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C.,
et al. (Eds.), Green’s Operative Hand Surgery, 6th ed. Elsevier, pp. 389–406.
Barron, O.A., Catalano, L.W., 2011. Chapter 13: Thumb basal joint arthritis.
In: Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s
Operative Hand Surgery, 6th ed. Elsevier, pp. 407–426.
Carlsen, B.T., Bakri, K., Al-Mufarrej, F.M., et al., 2013. Chapter 20:
Osteoarthritis of the hand and wrist. In: Neligan, P.C., Chang, J. (Eds.), Plastic
Surgery, vol. 6, 3rd ed. Elsevier, pp. 411–448.
Chang, J., Valero-Cuevas, F., Hentz, V.R., et al., 2013. Chapter 1: Anatomy
and biomechanics of the hand. In: Neligan, P.C., Chang, J. (Eds.), Plastic
Surgery, vol. 6, 3rd ed. Elsevier, pp. 1–46.
Chung, K.C., Haase, S.C., 2013. Chapter 8: Fractures and dislocation of the
wrist and distal radius. In: Neligan, P.C., Chang, J. (Eds.), Plastic Surgery,
vol. 6, 3rd ed. Elsevier, pp. 161–177.
Geissler, W.B., Slade, J.F., 2011. Chapter 18: Fractures of the carpal bones. In:
Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative
Hand Surgery, 6th ed. Elsevier, pp. 639–707.
Nelson, D.L., Gellman, H., Distal Fractures of the Radius Treatment &
Management. Emedicine.com. Found at:
article/1245884-treatment Accessed on October 20, 2014.
Sammer, D.M., Chung, K.C., 2013. Chapter 19: Rheumatologic conditions of
the hand and wrist. In: Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, vol. 6,
3rd ed. Elsevier, pp. 371–410.
Wolfe, S.W., 2011. Chapter 17: Distal radius fractures. In: Wolfe, S.W.,
Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand
Surgery, 6th ed. Elsevier, pp. 561–638.
Yao, J., Ahubhav, J., 2010. Chapter 44: Carpus: perilunate and greater arc
injuries. In: Slutsky, D.J. (Ed.), Principles and Practice of Wrist Surgery,
1st ed. Saunders, pp. 473–484.
2. Gout
• Hyperuricemia that progresses to recurrent bouts of acute
arthritis
• Gout affects 1% of adults, with a male predilection.
• Risk factors: Obesity, alcoholism, hypertension, renal
disease, cyclosporine, and hydrochlorothiazide
• Triggers include stress, fevers, surgery, dehydration,
alcohol, oatmeal, mushrooms, lentils, and spinach.
• Characterized by an exquisitely painful, edematous, and
erythematous joint
■ Diagnosed by arthrocentesis with presence of
monosodium urate crystals
• As the disease progresses, systemic symptoms (fever, chills,
sweats) and chronic polyarticular arthritis with tophi
development are common.
■ Radiographic findings in chronic gout include bony
erosions with sclerotic margins.
• Treatment is largely medical and includes NSAIDs (e.g.,
indomethacin), colchicine, and corticosteroids for acute
attacks and colchicine or the xanthine oxidase inhibitor
allopurinol for prophylaxis.
■ Surgery is reserved to selective arthrodesis for intractable
joint pain or functional deficit and complete excision of
painful, debilitating tophi.
Table 18.4  Characteristics of Other Rheumatologic Conditions of the Hand
CONDITION
SEROLOGY
RADIOGRAPHS
EXAMINATION
Psoriatic arthritis
Negative
Erosions
Resorption
Osteolysis
Periostitis
Ankylosis (PIP)
Juxta-articular bone formation
“Pencil in cup” (DIP)
Psoriasis
Nail abnormalities, dactylitis
PIP flexion contracture
Opera glass hand swan-neck deformity
SLE
ANA
Anti-DNA, antiphospholipid
antibody
Leucopenia
Hemolytic anemia
Thrombocytopenia
Preservation of joints
Secondary OA
Deformity similar to that seen in RA
Malar rash
Discoid rash
Serositis
Other
Scleroderma
ANA
Anticentromere
Antitopoisomerase I
Anti-RNA polymerase
Tuft resorption
Secondary OA
Cutaneous telangiectasia
Raynaud’s
Cutaneous sclerosis
Ischemic ulceration
Joint contracture due to skin contracture
Gout
Hyperuricemia
Negatively birefringent
crystals (synovial analysis)
Sclerotic joint margins
Overhanging edges
Erosion from tophi (late)
Joint destruction (late)
Red, hot, swollen joint
MTP of great toe involvement
Tophi
Reprinted from Neligan, P.C., Chang, J. (Eds.), 2013. Plastic Surgery, vol. 6, 3rd ed. Elsevier.
ANA, Antinuclear antibody; DIP, distal interphalangeal; MTP, metatarsophalangeal; OA, osteoarthritis; PIP, proximal interphalangeal;
RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.

Tendon Injuries
and Reconstruction
Chapter
19 
Flexor Tendon Anatomy (see
Figures 19.1-19.4)
1. There are 12 flexor tendons in the hand and forearm.
Common flexor group arises near the medial epicondyle.
Most are median n. innervated, except the flexors to the 4th
and 5th digits and interossei.
• Finger flexors
■ Flexor digitorum superficialis (FDS)
○ Separate muscle belly origin, allowing independent
finger motion
○ Tendons superficial to the flexor digitorum
profundus (FDP) tendons up to their bifurcation into
slips at the metacarpophalangeal (MCP) joint, where
they travel around the FDP tendon, dive deep, rejoin
to form Camper’s chiasm, and insert onto the middle
phalanx
○ Flexes the proximal interphalangeal (PIP) joint
■ FDP
○ Common muscle belly origin
♦ Because of this common origin, shortening of FDP
tendon or overtightening of repair can lead to
decreased grip strength and decreased flexion of
the uninjured digits (“quadrigia” effect).
○ Inserts into the volar aspect of the distal phalanx
○ Flexes the distal interphalangeal (DIP) joint
○ Lumbrical muscles originate from FDP tendon in the
palm.
♦ Proximal migration of the FDP after injury leads
to lumbrical contracture and paradoxical extension
of the PIP joint when attempting to flex the MCP
joint (“lumbrical plus” deformity). Can address
through division of the lumbrical
■ Flexor pollicis longus (FPL)
○ Arises from the midaspect of the radial shaft and
interosseous membrane
○ The only tendon inside the flexor sheath of the
thumb; inserts onto the distal phalanx
○ Flexes the thumb interphalangeal (IP) joint
• Wrist flexors
■ Flexor carpi radialis (FCR)
○ Inserts onto the base of the 2nd and 3rd metacarpals
■ Flexor carpi ulnaris (FCU)
○ Inserts onto the base of the 5th metacarpal, hook of
hamate, and pisiform
○ Overlies ulnar artery and nerve
♦ Laceration to FCU is concerning for injury to the
ulnar a. and n.
■ Palmaris longus (PL)
○ Absent in ~15% to 20%
○ Ends in the fan-shaped palmar fascia
○ Lies volar to median nerve traveling within carpal
canal
○ Lacerations to PL are concerning for median nerve
laceration.
• Intrinsic flexors
■ Interossei muscles act as prime flexors of the MCP joints
and extensors of the IP joints through their pull on the
lateral bands (see Figure 19.5).
2. Flexor tendon healing
• Nutrition of flexor tendons occurs through the synovial
sheath, insertion, and vincula, which provide blood vessels
directly to the tendon proper (see Figure 19.6).
3. Flexor tendon zones: Divisions of the flexor tendon anatomy
within the hand that have important implications in
fundamentals of repair (see Figure 19.7)
4. Carpal canal anatomy: Contains 9 tendons (4 FDS, 4 FDP,
and 1 FPL) and the median nerve. Anatomic relationships
within the canal are consistent; knowledge of these
relationships is important when repairing injuries in this zone
(zone 4).
• FDS tendons to the ring and middle finger lie most volar,
followed by the FDS tendons to the index and small fingers
deep to this.
• FDP tendons lie on the dorsal floor of the carpal canal.
• FPL tendon lies radial, deep, and adjacent to the scaphoid
and trapezium
General Flexor Tendon Repair Principles
1. Indications and contraindications to flexor tendon repair (see
Box 19.1)
2. Primary tendon repair with atraumatic techniques is critical
to minimize the risk for postrepair adhesions.

Tendon Injuries and Reconstruction
196
Figure 19.1.  The anatomy of the flexor muscles: Superficial to deep. (Reprinted with permission from © Elsevier Inc. All Rights
Reserved.)
Note: Brachioradialis muscle not shown
because it is flexor of elbow
Lateral epicondyle
Medial 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

General Flexor Tendon Repair Principles
197
19
Figure 19.2.  The anatomy of the flexor muscles: Superficial to deep. (Reprinted with permission from © Elsevier Inc. All Rights
Reserved.)
Ulnar nerve
Median nerve
Brachial artery
Medial intermuscular septum
Pronator teres muscle (humeral head)
(cut and reflected )
Flexor carpi radialis and palmaris
longus tendons (cut )
Flexor digitorum superficialis
muscle (humeroulnar head)
Medial epicondyle
Biceps brachii muscle
Brachialis muscle
Lateral antebrachial cutaneous nerve (cut )
(from musculocutaneous nerve)
Radial nerve
Deep branch
Superficial branch
Biceps brachii tendon
Radial recurrent artery
Radial artery
Supinator muscle
Brachioradialis muscle
Pronator teres muscle (cut )
Flexor digitorum superficialis
muscle (radial head)
Anterior ulnar recurrent artery
Ulnar artery
Common interosseous artery
Pronator teres muscle (ulnar head) (cut )
Anterior interosseous artery
Flexor carpi ulnaris muscle
Flexor digitorum superficialis muscle
Ulnar artery
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
Flexor retinaculum
(transverse carpal ligament)
Superficial branch of ulnar nerve
Superficial palmar branch
of radial artery
Flexor carpi radialis
tendon (cut )
Palmar carpal ligament
(continuous with extensor
retinaculum) with palmaris
longus tendon (cut and reflected )
Flexor pollicis longus muscle

Tendon Injuries and Reconstruction
198
Figure 19.3.  The anatomy of the flexor muscles: Superficial to deep. (Reprinted with permission from © Elsevier Inc. All Rights
Reserved.)
Medial epicondyle
Lateral epicondyle
Common flexor tendon
Coronoid process
Interosseous membrane
Radius
Medial epicondyle
Lateral epicondyle
Coronoid process
Interosseous
membrane
Radius
Flexor digitorum superficialis
Flexor digitorum profundus
Flexor pollicis longus
Ulna
Radius
Radius
Flexor digitorum superficialis
tendons (cut away)
Ulna
Right forearm:
anterior (palmar) views

General Flexor Tendon Repair Principles
199
19
• Epitendinous sutures can add strength to the repair site
and smooth the approximation of tendon ends to help
resist gapping during tendon movement.
5. Partial tendon lacerations
• Lacerations <50% to 60% of the tendon do not require
repair.
• Trim frayed edges to prevent a trigger site within the
annular pulley system.
6. Annular pulley disruptions
• In the fingers, the A2 and A4 pulleys are the largest and
most important to hand function.
■ Complete laceration of the A2 pulley leads to decreased
motion at the PIP joint, with an increased moment arm
and power.
3. Strength of the tendon repair is affected by
• Number of core suture strands across the repair site
■ Strength proportionate to the number of strands
• Tension of the repair
■ Relevant to gap formation and stiffness
• Suture characteristics
■ Tendon–suture locking technique, diameter of suture
locks, suture caliber and material
• Holding capacity of the tendon
• Early mobilization and range of motion may also increase
the strength of repair.
4. Recommended repair technique: A 3-0 or 4-0 core coated
nylon or woven/braided polyester suture (4 to 6 strands) on a
tapered needle (with approximately 1 cm of tendon purchase),
with a locking tendon–suture junction and a 6-0 nylon
epitendinous suture
Figure 19.4.  The flexor tendon pulley system for fingers and thumb. (Redrawn after Chase, R.A., 1984. Atlas of Hand Surgery, vol. 2. WB Saunders,
Philadelphia.)
Annular
Oblique
A2
C1
A3 C2 A4 C3 A5
Annular
Thumb pulleys
Finger pulleys
A1
A2
C1
A3
C2
A4
C3
A5
Transverse carpal
ligament
A
C
D
B
A1

Tendon Injuries and Reconstruction
200
Figure 19.5.  All interossei act as prime flexors of the
metacarpophalangeal joints because they pass palmar to the joint
axis. Extensions into the lateral bands result in extension of the IP
joints. (From Chase, R.A., 1973. Atlas of Hand Surgery, vol. 1. WB Saunders,
Philadelphia.)
Figure 19.6.  Insertions and relative positions of the flexor
digitorum superficialis (FDS) and flexor digitorum profundus (FDP)
tendons and vincula. Each of the FDS and FDP tendons has two
vincula, one short and one long. The relationships of the FDS and
FDP tendons are complex in the middle part of the proximal
phalanx under the A2 pulley (zone 2C). (Reprinted from Neligan P.C.,
Buck D.W. [Eds.], 2014. Core Procedures in Plastic Surgery, Elsevier, 358-374.)
FDP tendon
Vinculum longus
FDS tendon
Vincula brevia
Vinculum brevia
Vinculum longus
Figure 19.7.  Division of the flexor tendons into 5 zones according
to anatomical structures of the flexor tendons, presence of the
synovial sheath, and the transverse carpal ligament. (Reprinted from
Neligan, P.C., Buck, D.W. [Eds.], 2014. Core Procedures in Plastic Surgery.
Elsevier, 358–374.)
1
1
2
2
3
3
4
5
Reprinted from Neligan, P.C., Buck, D.W. (Eds.), 2014. Core
Procedures in Plastic Surgery. Elsevier, 358–374.
BOX 19.1  PRIMARY FLEXOR TENDON REPAIRS
Indications
• Clean-cut tendon injuries
• Tendon cut with limited peritendinous damage; no
defects in soft-tissue coverage
• Regional loss of soft-tissue coverage or fractures of
phalangeal shafts (borderline indications)
• Within several days or at most 3 or 4 weeks after
tendon laceration
Contraindications
• Severe wound contamination
• Bony injuries involving joint components or extensive
soft-tissue loss
• Destruction of a series of annular pulleys and lengthy
tendon defects
• Experienced surgeons unavailable
• Incision of the A2 pulley up to 12 or 2/3rds its length, or
release of the entire A4 pulley, can be tolerated without
significant functional deficits.
■ May be required for assistance with repair
• In the thumb, A1 and oblique pulleys are most important
to function.
7. Common complications of tendon repairs
• Adhesions
■ Can develop from traumatic technique during repair,
excessive scarring, and prolonged immobilization

Flexor Tendon Injuries
201
19
■ Adhesions of the flexor tendons will prevent extension,
but allow continued flexion of the involved finger.
■ Treatment: Tenolysis
• Rupture
■ Most commonly occurs within 1 to 2 weeks and at suture
knots
■ Can often be primarily repaired if occurs within the first
few weeks (up to 1 month) after the initial surgery
■ Secondary tendon grafts, or staged reconstruction with
Hunter rods, may be required in the presence of delayed
rupture, multiple surgical failures, and retraction or
excessive scarring.
○ One-stage tendon grafting is contraindicated in joints
with absent passive range of motion.
8. Early postoperative motion of repaired tendons is critical for
prevention of adhesions and strengthening the repair.
• Motion typically begins 2 to 5 days after repair.
• Indications for prolonged immobilization include tendon
repairs in children (often immobilized at 3 to 3.5 weeks),
noncompliant patients, and tendon injury associated with
underlying fractures.
• Early postoperative motion protocols
■ Early passive motion
○ Allows active extension with passive flexion
(“Kleinert” method)
■ Early active motion
○ Under supervision, allows active extension and active
flexion.
■ Combined passive-active motion
Flexor Tendon Injuries
1. Zone-1 injury
• Affects the FDP tendon only
• Characterized by inability to flex the DIP
• Tendon may be held out to length by vinculum
• Distal injuries often require pull-out suture over buttons or
bone-anchor screws because distal tendon stump is too
short (<~1 cm) for direct end-to-end suture repair.
• Proximal zone injuries are usually amenable to direct
suture repair.
• Take care to preserve the A4 pulley.
• Avulsion and fracture/avulsion injuries of the FDP tendon
(“jersey finger” injuries) require special consideration (see
Chapter 16: Hand Fractures and Dislocations)
2. Zone-2 injury
• Often involves both FDP and FDS tendons
• May disrupt the vincula, with retraction of the proximal
tendon ends into the palm
■ Flexion of the MCP and PIP joints may bring the tendon
end into sight; otherwise, a counter incision in the palm
is necessary.
• Adequate exposure requires Bruner incisions and windows
or releases within the synovial sheath and/or pulley system.
■ Attempts to preserve the A2 pulley (at least 13 to 12) are
important, functionally.
■ If the A2 pulley is lacerated completely, it can be
reconstructed with a free tendon graft or fascia graft
(e.g., extensor retinaculum or tensor fascia lata).
• Many surgeons advocate repairing both FDP and FDS
tendons.
3. Zones–3 to 5 injury
• Repair techniques almost identical to those for zone 2
• Injuries in zones 3 to 5 have better prognosis because of a
richer vascular supply and less constricting tissue overlying
the tendons (i.e., pulleys).
■ Zone-5 repairs have the best outcomes because of the
greater area allowed for tendon gliding.
■ Zone-4 injuries are often associated with concomitant
injuries to the median n.
• Spaghetti wrist
■ Wrist laceration/injury with transection of a majority of
tendons, vessels, and nerves (at least 10 out of 15 of these
structures, excluding the palmaris)
■ May require lengthy repair, with intermittent deflation
and reinflation of the tourniquet during surgery to allow
episodic hand perfusion
○ Often allow 20 to 30 minutes of perfusion between
2-hour intervals of tourniquet ischemia.
4. FPL injury
• Repair techniques and principles similar to those for repair
of the FDP tendon in the fingers
• Proximal tendon end frequently retracts into the thenar
musculature.
• Closed injuries can occur with fracture and/or rupture
from attrition (e.g., scaphoid malunion).
5. Stenosing tenosynovitis (“trigger” finger/thumb)
• Characterized by entrapment of the flexor tendon at the A1
pulley, resulting in pain and catching, popping, or
“locking” of the involved digit during flexion and
extension
■ Occasionally, the digit can become locked in the flexed
position and require passive extension of the digit with
the uninvolved hand.
■ May be associated with a painful, palpable nodule along
the flexor tendon
• Caused by hypertrophy of the A1 pulley or occasionally
intratendinous swelling
• Treatment: Initial treatment is conservative with splinting
and corticosteroid injection. Surgical release of the A1
pulley (open or percutaneous) can be performed in severe
cases (active locking) and for triggering that has failed
conservative treatment.

Tendon Injuries and Reconstruction
202
Figure 19.8.  The anatomy of the extensor muscles: Superficial to deep. (Reprinted with permission from © Elsevier Inc. All
Rights Reserved.)
Superior ulnar collateral artery
(anastomoses distally with
posterior ulnar recurrent artery)
Ulnar nerve
Medial epicondyle of humerus
Olecranon of ulna
Anconeus muscle
Flexor carpi ulnaris muscle
Extensor carpi ulnaris muscle
Triceps brachii muscle
Brachioradialis muscle
Extensor carpi radialis longus muscle
Common extensor tendon
Extensor carpi radialis brevis muscle
Extensor digitorum muscle
Extensor digiti minimi muscle
Abductor pollicis longus muscle
Extensor pollicis brevis muscle
Extensor pollicis longus tendon
Extensor carpi radialis brevis tendon
Extensor carpi radialis longus tendon
Superficial branch of radial nerve
Abductor pollicis longus tendon
Extensor pollicis brevis tendon
Extensor pollicis longus tendon
Anatomical snuffbox
1
2
3
4
5
6
Extensor carpi ulnaris tendon
Extensor digiti minimi tendon
Extensor digitorum tendons
Extensor indicis tendon
5th metacarpal bone
Dorsal branch of ulnar nerve
Extensor retinaculum
(compartments numbered)
Extensor Tendon Anatomy
(see Figures 19.8-10)

Flexor Tendon Anatomy
203
19
Figure 19.9.  The anatomy of the extensor muscles: Superficial to deep. (Reprinted with permission from © Elsevier Inc. All
Rights Reserved.)
Middle collateral branch of
deep brachial artery
Lateral intermuscular septum
Brachioradialis muscle
Extensor carpi radialis longus muscle
Lateral epicondyle of humerus
Common extensor tendon (partially cut )
Extensor carpi radialis brevis muscle
Supinator muscle
Posterior interosseous nerve
Pronator teres muscle (slip of insertion)
Radius
Posterior interosseous nerve
Abductor pollicis longus muscle
Extensor pollicis brevis muscle
Extensor carpi radialis brevis tendon
Extensor carpi radialis longus tendon
1
2
3
4
5
6
Radial artery
1st metacarpal bone
2nd metacarpal bone
1st dorsal
interosseous muscle
5th metacarpal bone
Extensor retinaculum
(compartments numbered)
Extensor digitorum tendons (cut )
Extensor digiti minimi tendon (cut )
Extensor carpi ulnaris tendon (cut )
Anterior interosseous artery
(termination)
Extensor indicis muscle
Extensor pollicis longus muscle
Ulna
Posterior interosseous
artery
Recurrent interosseous
artery
Flexor carpi ulnaris
muscle
Anconeus muscle
Olecranon of ulna
Triceps brachii tendon
(cut )
Medial epicondyle of
humerus
Posterior ulnar recurrent
artery
Ulnar nerve
Medial intermuscular
septum
Inferior ulnar collateral
(posterior branch)
Superior ulnar collateral
Branches of
brachial artery

Tendon Injuries and Reconstruction
204
Figure 19.10.  The extensor mechanism of the fingers. Black arrows indicate pull of long extensor tendon; red arrows indicate pull of
interosseous and lumbrical muscles; dots indicate axis of rotation of joints. (Reprinted with permission from © Elsevier Inc. All
Rights Reserved.)
Insertion of central band of extensor
tendon to base of middle phalanx
Triangular aponeurosis
Slips of long
extensor tendon
to lateral bands
Extensor
expansion
(hood)
Long extensor
tendon
Interosseous muscles
Metacarpal bone
Posterior
(dorsal)
view
Insertion on extensor tendon
to base of distal phalanx
Lateral bands
Interosseous
tendon slip
to lateral band
Lumbrical muscle
Part of interosseous tendon
passes to base of proximal
phalanx and joint capsule
Extensor expansion (hood)
Long extensor tendon
Metacarpal bone
Interosseous muscles
Lumbrical muscle
Flexor digitorum
profundus tendon
Lateral band
Central band
Insertion of extensor tendon
to base of middle phalanx
Insertion of extensor
tendon to base
of distal phalanx
Finger in
extension:
Lateral view
Collateral
ligaments
Vinculum
breve
Vincula
longa
Flexor digitorum
superficialis tendon
Collateral ligament
Extensor tendon
Insertion of small deep slip of extensor
tendon to proximal phalanx and joint capsule
Attachment of interosseous muscle to
base of proximal phalanx and joint capsule
Insertion of lumbrical
muscle to extensor tendon
Finger in flexion:
Lateral view
Palmar ligament (plate)
Flexor digitorum
superficialis tendon (cut)
Collateral ligaments
Flexor digitorum
profundus tendon (cut)
Palmar ligament (plate)
Interosseous muscles
Lumbrical muscle

Flexor Tendon Anatomy
205
19
• Extensor compartment 2: Extensor carpi radialis longus
(ECRL) and extensor carpi radialis brevis (ECRB)
■ Insert on the 2nd and 3rd metacarpal base, respectively
■ ECRB is the prime wrist extensor (because of insertion).
• Extensor compartment 3: EPL
■ Crosses wrist above extensor compartment 2 and then
reorients around Lister’s tubercle to the thumb
■ Vulnerable to rupture (e.g., distal radius fractures)
■ Laceration or rupture of the EPL prevents extension of
the thumb IP and ability to “lift” the thumb off of a
tabletop.
• Extensor compartment 4: Extensor digitorum communis
(EDC) and extensor indicis proprius (EIP)
■ EIP rests ulnar and deep to the EDC tendon to the index
finger.
■ Posterior interosseus n. lies deep to extensor
compartment 4.
• Extensor compartment 5: EDM
■ Typically has 2 tendon slips
■ Rests ulnar and deep to the EDC tendon to the small
finger
• Extensor compartment 6: Extensor carpi ulnaris (ECU)
■ ECU functions as a wrist extensor, part of the triangular
fibrocartilage complex (TFCC), and major stabilizer of
the distal radioulnar joint (DRUJ).
9. The intrinsic extensors
• The palmar interossei arise from the medial side of the
2nd, 4th, and 5th metacarpal, cross volar to the MCP joint,
and join the extensor apparatus at the level of the proximal
phalanx.
■ Function to adduct the fingers, flex the MCP joint, and
extend the IP joints
• The dorsal interossei arise from the adjacent sides of the 5
metacarpal bones and join the extensor apparatus.
■ Function to abduct the fingers, flex the MCP joint, and
extend the IP joints
• The lumbrical muscles arise from the radial side of the
FDP tendons at the level of the metacarpal and join the
extensor apparatus on the radial side.
■ Function primarily as IP extenders
10. Extensor tendon zones: Divisions of the extensor tendon
anatomy within the hand that have important implications in
fundamentals of repair (see Figure 19.11)
1. The extensor muscles are located on the dorsum of the hand
and forearm and are all innervated by the radial n.
2. The common extensor tendon arises from the lateral
epicondyle of the humerus.
3. The extensor retinaculum prevents bowstringing of the
extensor tendons across the wrist.
4. Unlike the flexor tendons, the extensor tendons do not lie
within synovial sheaths.
5. Extension of the phalanges is dependent on the extrinsic
extensors at the MCP joints, and the extrinsic and intrinsic
muscles at the IP joints.
• The sagittal bands help to centralize the extensor tendons
over the MCP joint to maximize function and prevent
hyperextension.
• At the level of the proximal phalanx, the extensor tendons
split into the central band and two lateral bands that merge
with the intrinsic muscles to form the extensor apparatus.
• The central slip inserts at the base of the middle phalanx,
whereas the terminal tendon inserts at the base of the distal
phalanx.
• The extensor pollicis longus (EPL) inserts on the base of
the thumb distal phalanx, whereas the extensor pollicis
brevis (EPV) inserts on the base of the proximal phalanx.
6. The extensor digitorum tendons arise from a common muscle
belly, and only the index (extensor indices pollicis) and small
fingers (extensor digiti minimi [EDM]) have independent
extensors.
7. The extensor digitorum tendons are interconnected by
intertendinous bridges (juncturae) that can provide some
backup finger extension (albeit weak) in the setting of
proximal extensor tendon injury.
• Testing each finger individually against resistance can
overcome this backup and uncover an extensor tendon
injury.
8. There are 6 dorsal extensor compartments at the wrist;
knowledge of their location and contents is important.
• Extensor compartment 1: Abductor pollicis longus (APL)
and EPB
■ APL tendon can have multiple slips.
■ May have septations between APL and EPB
■ Dorsal sensory branch of the radial n. lies superficial to
extensor compartment 1

Tendon Injuries and Reconstruction
206
• After nonviable tissue has been debrided, fractures must be
stabilized and soft-tissue coverage provided before tendon
reconstruction.
■ Many surgeons aim for soft-tissue coverage within 72
hours.
• Complete primary tendon repair if it is possible; if not,
tendon reconstruction is required and can be performed at
the time of soft-tissue coverage by primary grafting or
transfers.
• With advent of microsurgery, many surgeons perform
single-stage bone fixation, tendon reconstruction, and
soft-tissue coverage.
■ The anterolateral thigh flap has become a workhorse flap
for this indication.
7. Common extensor tendon repair complications
• Adhesions
■ Treatment includes hand therapy and splinting, followed
by tenolysis.
■ Occasionally capsulotomies, collateral ligament release,
and/or flexor tendon tenolysis are also necessary for
range-of-motion improvements.
• Rupture
■ Sagittal band ruptures result in subluxation of the
extensor tendon at the MCP joint.
• Swan-neck deformity
■ Characterized by DIP flexion and PIP hyperextension
■ Often caused by an untreated “mallet finger” or volar
plate laxity
■ Treatment options: Fowler tenotomy (central slip
release), tendon reconstruction, tenodesis of the FDS
(when volar plate laxity is the cause)
• Boutonniere deformity
■ Characterized by DIP hyperextension and PIP flexion
■ Caused by disruption of the central slip or volar
subluxation of the lateral bands
■ Treatment options: Acute treatment of central slip
injuries includes splinting in extension; treatment of
boutonniere is challenging and includes extensor tendon
tenotomy, tendon relocation or grafting, and central slip
reconstruction.
8. As with flexor tendons, postoperative therapy is critical to
successful treatment of these injuries.
• Mallet injuries (zone 1) and closed ruptures of the central
slip (zone 3) require strict immobilization.
• Immobilization is also considered for injuries proximal to
the extensor retinaculum (zones 8 and 9).
• Early controlled dynamic motion is often recommended
for injuries in zones 3 to 5.
Extensor Tendon Injuries
1. Zone-I injury
• Characterized by flexion at the DIP joint without active
extension (mallet finger)
• Causes include laceration and/or avulsion.
General Extensor Tendon Repair Principles
1. Suture techniques are dependent on the location of the injury
because the tendons become thin and flat distally.
2. Injuries proximal to zone 6 can be repaired in similar fashion
as that for flexor tendons because of their size (core suture
plus epitendinous suture).
3. Minimal changes in tendon length can cause significant
alterations in range of motion because the excursion
amplitude of extensor tendons is limited.
4. Closed ruptures of the extensor tendon at the level of the DIP
and PIP joints are often treated conservatively.
5. Lacerations in zone 5 (over the MCP joints) are frequently
caused by “fight bites” and are prone to infection.
• Treatment: Surgical debridement, antibiotics, splinting,
and primary or delayed tendon repair
6. Because of the superficial nature of the extensor tendons,
complex injuries to the dorsal hand can involve skin, tendon,
and bone.
• Adequate debridement of nonviable tissue is the critical
first step.
Figure 19.11.  The zones of extensor tendon injuries. (Reprinted from
Neligan, P.C., Buck, D.W. [Eds.], 2014. Core Procedures in Plastic Surgery.
Elsevier, 309–341.)
1
2
3
4
5
6
7
8
9
10
11
12
13
14

Extensor Tendon Injuries
207
19
the proximal tendon end will be found proximal with
the hand in the open position.
■ Concomitant sagittal band injuries can be treated
conservatively with buddy taping or splinting in cases
with stable tendon injuries, partial lacerations, or closed/
spontaneous ruptures; in cases with unstable tendon
injuries or old sagittal band injuries, suture repair is
recommended.
6. Zone-6 injury
• In this zone, the tendon is often of similar caliber to a
flexor tendon and thus can be repaired in similar fashion:
With a core suture and an epitendinous suture.
• Early active motion protocols will reduce tendon
adhesions.
7. Zone-7 injury
• Injuries in this zone typically involve open lacerations with
multiple tendon involvement or closed rupture associated
with underlying fractures or arthritis (e.g., EPL rupture
associated with distal radius fractures or rheumatoid
arthritis).
• Open lacerations at this level often require opening of the
extensor retinaculum for exposure and repair.
• Concomitant nerve injury is also common; repair if
present.
• Treatment: Surgical repair with core and epitendinous
sutures
■ Closed ruptures of the EPL tendon often cannot be
repaired primarily because of the possibility for
unacceptable tendon shortening in these cases; therefore,
primary tendon transfer (EIP to EPL) is preferred.
8. Zones–7 and 9 injury
• Often associated with injuries to the musculotendinous
junctions and muscle bellies
• Treatment: Surgical repair of tendons and/or fascial layers
with brief postoperative immobilization (3 to 4 weeks) is
recommended.
■ Concomitant nerve injuries must be repaired as well.
9. de Quervain’s disease
• Characterized by entrapment of the APL and EPB tendons
at the 1st extensor compartment, resulting in radial-sided
wrist pain and swelling, which is worse with thumb motion
• Caused by tension on the tendons in the 1st extensor
compartment, which produces friction with subsequent
swelling and/or narrowing of the compartment
• Diagnosed by localized pain and swelling over the 1st
dorsal compartment, ~1 cm proximal to the radial styloid,
and severe pain when the wrist is forced into ulnar
deviation with the thumb adducted into the palm (positive
“Finkelstein’s” test)
■ Differential diagnosis: 1st carpometacarpal arthritis,
intersection syndrome
• Treatment: Initial treatment is conservative with rest,
splinting, and corticosteroid injection. Surgical release of
the 1st dorsal compartment for recurrent disease
■ Must ensure release of all tendon slips and septae within
the compartment to optimize success of surgical release.
• Treatment: Closed injures are treated with splinting of the
DIP in extension for 8 weeks continuously, followed by
nighttime splinting for 2 to 6 weeks.
■ Treat open injuries open.
○ In most cases, skin-only laceration repair with
splinting will allow healing strong enough for
extension function.
■ In avulsion injuries with bone fragments > one third of
the articular surface, K-wire fixation can be used.
■ Alternative options include extension block pinning.
2. Zone-II injury
• Characterized by inability to extend the DIP joint
• Caused primarily by lacerations or crush injuries
• Treatment: Explore acute lacerations to rule out tendon
involvement.
■ Partial lacerations (<50% tendon substance) do not
require repair.
■ Complete lacerations (or partial lacerations >50%)
require suture repair.
■ Avoid significant shortening of the tendon to prevent
flexion of the DIP.
3. Zone-3 injury
• Characterized by flexed PIP without active PIP extension
• Caused by disruption of the central slip through both
closed and open injuries
• Can lead to boutonniere deformity if not properly treated
■ As the lateral bands migrate volarly, they will lead to
flexion contracture of the PIP joint with hyperextension
of the DIP.
• Treatment options: Extension splinting of the PIP, K-wire
fixation with the joint in extension, tendon reinsertion
with bone anchors
■ In open injuries, exploration is warranted.
■ Clean injuries can be repaired primarily with sutures.
■ Do not have staged reconstruction for contaminated
injuries or those with significant tendon loss.
4. Zone-4 injury
• The extensor becomes broader over the proximal phalanx,
resulting in many partial lacerations.
• Tendon injuries in zone 4 are often associated with
proximal phalanx fractures.
• The tendon is in close proximity to the proximal phalanx
in this zone; therefore, adhesions are relatively common
and may require secondary tenolysis.
• Treatment: Surgical repair and early active motion
5. Zone-5 injury
• At this level, the extensor mechanism includes the tendon
and the sagittal bands.
■ The tendon is relatively broad, so complete lacerations
are uncommon.
• Commonly caused by human bite injuries (“fight bite”)
• Treatment: Surgical exploration and washout, especially if
“fight bite” is suspected
■ If the injury occurred with a clinched fist, the tendon
injury commonly occurs proximal to the skin tear, and

Tendon Injuries and Reconstruction
208
2. Technical considerations
• Depending on the location and size of the distal and
proximal tendon stumps, the graft can be secured through
varying techniques.
■ Distally, can be sewn directly to residual stump, buried
under an osteoperiosteal flap, or secured over a button.
■ Proximally, either at the palm or in the forearm, the
graft is secured to the native stump through a Pulvertaft
weave (see Figure 19.12)
10. Intersection syndrome
• Characterized by pain and swelling overlying the 2nd
extensor compartment (ECRL and ECRB) in the location
where the APL and EPB cross over (or “intersect”) this
compartment.
• Caused by friction and swelling of the 2nd extensor
compartment associated with activities requiring repetitive
wrist motion (e.g., rowing, weightlifting)
• Diagnosed by localized pain, swelling, and crepitus 4 cm
proximal to the wrist joint
• Treatment: Initial treatment is conservative with splinting
and corticosteroid injection into the 2nd extensor
compartment. Surgical release of the 2nd extensor
compartment is indicated for recurrent or persistent
disease.
Tendon Grafting (see Box 19.2)
Reprinted from Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, vol. 6,
3rd ed. Elsevier, 178–209.
BOX 19.2  TENDON GRAFTING AND STAGED
RECONSTRUCTION
Indications
• Tendon injuries not treated within about 1 month after
injuries
• Rupture of the tendon repairs at primary or delayed
primary stages
• Tendon injuries not indicated for primary repair
• Badly scarred digits are indicative for staged tendon
reconstruction
Essential Requirements
• Supple passive motion of the hand
• Soft-tissue conditions: Good
• Sufficient time passed after initial tendon injury: 3
months
Contraindications
• Joint motion very limited (but may be suitable for staged
reconstruction)
• Presence of soft-tissue wounds or defects and fractures
not well healed
Figure 19.12.  Skin incision and the method of free tendon grafting
to reconstruct the function of digital flexion. As many annular
pulleys as possible are preserved. The junction is placed at either
palm or distal forearm. The graft is weaved with the digital flexor
through holes in the tendons created by a knife. (Reprinted from
Neligan, P.C., Chang, J. [Eds.], 2013. Plastic Surgery, vol. 6, 3rd ed. Elsevier,
178–209.)
1. Most common tendon donor sites
• PL
■ From ipsilateral limb
■ Useful for palm-to-fingertip grafts
■ Absent in 15% of hands
■ Take care to protect median n. during harvest
• Plantaris
■ Can obtain graft up to 25 cm; useful for long distal
forearm-to-fingertip grafts
■ Absent in 7% to 20% of limbs
■ Care must be taken to protect tibial n. during harvest
• Toe extensors
■ Extensor digitorum longus tendons to the 2nd to 4th toes
• Other potential options
■ EIP, FDS to the 5th finger, ECRL or ECRB, Allograft
tendon
• Postoperatively, immobilization is recommended for at
least 3 weeks followed by graded motion protocols.
3. Staged tendon reconstruction
• Indications: Severely scarred digits
• Stage 1: Excision of tendon and scar, preservation or
reconstruction of pulleys, and insertion of a Hunter rod
(Silicone tendon implant)
■ The Hunter rod will stimulate formation of a
pseudosheath
• Stage 2: The Hunter rod is replaced with a tendon graft
■ Typically occurs 3 months after the first stage.

High Median Nerve Palsy
209
19
Radial Nerve Palsy
1. Functional deficits
• Wrist extension
• Finger extension at the MCP joints
• Thumb extension and radial abduction
2. Tendon transfers for radial n. palsy
Tendon Transfers
1. Indications
• Paralyzed muscle secondary to peripheral nerve, brachial
plexus, or spinal cord injury
• Direct muscle or tendon injury (open and closed rupture/
injuries)
• Restore balance to hands affected by neurological disease
2. Basic principles of tendon transfer (see Box 19.3)
Table 19.1  Tendon Transfers for Radial Nerve Palsy
STANDARD FCU
TRANSFER
FCR TRANSFER
BOYES
SUPERFICIALIS
TRANSFER
PT to ECRB
PT to ECRB
PT to ECRB
FCU to EDC
FCR to EDC
FDS of ring finger to
EDC middle, ring,
and small fingers
PL to EPL
PL to EPL
FDS middle finger to
EIP and EPL
FCR to APL and EPB
Reprinted from Neligan, P.C., Buck, D.W. (Eds.), 2014. Core
Procedures in Plastic Surgery. Elsevier, 393–413.
APL, Abductor pollicis longus; ECRB, extensor carpi radialis brevis;
EDC, extensor digitorum communis; EIP, extensor indicis proprius;
EPB, extensor pollicis brevis; EPL, extensor pollicis longus; FCR, flexor
carpi radialis; FCU, flexor carpi ulnaris; FDS, flexor digitorum
superficialis; PL, palmaris longus; PT, pronator teres.
Reprinted from Neligan, P.C., Buck, D.W. (Eds.), 2014. Core
Procedures in Plastic Surgery. Elsevier, 393–413.
BOX 19.3  BASIC PRINCIPLES OF TENDON TRANSFERS
Soft-tissue equilibrium
Full passive range of motion of involved joints
Adequate amplitude of donor muscle
Adequate excursion of donor muscle
Direct line of pull
Single function for each transferred tendon
Synergy of transfer
3. Technical considerations
• The timing of transfers can be classified as early,
conventional, or late
■ Early: Performed simultaneously with peripheral n.
repair, or before the expected time of reinnervation of
the muscle to act as an internal splint and serve as a
temporary substitute for the paralyzed muscle until
reinnervation occurs
■ Conventional: Performed after failed reinnervation
(typically 3 months after the expected time of
reinnervation)
■ Late: Performed for chronic deficits, beyond 3 months
from time of expected reinnervation.
• List in order of priority (and approach in this way) the
specific functions of the hand that need to be restored.
• Success depends on preventing scarring or adhesions along
the path of the transferred tendon and a patient who will
be compliant with postoperative restrictions and therapy.
• Transfers should only act across one joint and perform a
single function.
• Use Pulvertaft weave tendon junctures when possible.
• The power of the transferred muscle tendon is typically
downgraded one level after the transfer procedure;
therefore, place the transferred tendon at slightly greater
resting tension than that in the donor site.
• The potential excursion of the donor muscle–tendon unit
must be sufficient to restore the lost function.
■ Finger flexor excursion amplitude: 7 cm
■ Finger extensor excursion amplitude: 5 cm
■ Wrist flexor/extensor excursion amplitude: 3.3 cm.
■ The tenodesis effect may increase the effective amplitude
of a tendon transfer by 2.5 cm.
Low Median Nerve Palsy
1. Distal to innervation of the extrinsic forearm flexors (thus,
extrinsic flexors are intact)
2. Functional deficits
• Loss of thumb opposition
• Numbness over the thumb, index, and long fingers and
radial half of the ring finger
3. Tendon transfer for low median n. palsy (opponensplasty)
• EIP-to–abductor pollicis brevis (APB) transfer
• Bunnell transfer: Ring-finger FDS to APB
■ Contraindicated if concomitant injury to FDS, combined
low median/high ulnar n. palsy (ring-finger FDS is only
remaining ring-finger flexor), or low median/low ulnar
n. palsy (ring-finger FDS needed to correct clawing)
• Huber transfer: ADM to APB
• Camitz transfer: PL to APB
High Median Nerve Palsy
1. Injury proximal to innervation of the extrinsic forearm
flexors
2. Functional deficits
• Thumb flexion at IP joint
• Thumb opposition
• Index and long-finger flexion at PIP and DIP
3. Tendon transfers for high median n. palsy
• Thumb flexion: BR to FPL
• Opposition: See above.

Tendon Injuries and Reconstruction
210
Combined Nerve Palsy
1. Low median/Low ulnar
• Most common combined nerve injury (extrinsic flexors
intact)
• Typically a result of open laceration/“spaghetti wrist”
• Characterized by sensory loss over the palmar aspect of the
hand, claw hand, and Wartenberg’s sign
• Goals of reconstruction
■ Restore thumb adduction for key pinch: ECRB with
tendon graft to adductor tubercle of the thumb
metacarpal
○ Ring-finger FDS is also an option
■ Restore opposition: EIP transfer to the APB tendon
■ Correction of finger clawing: ECRL or PL transfer
extended by 4 tendon grafts to the radial lateral bands or
A2 pulleys (e.g., Brand EP4T transfer)
■ Sensory restoration: If nerve repair or nerve graft has
failed, can consider superficial radial n. transfer to the
distal median n.
2. High median/high ulnar
• Characterized by findings in low/low injury (above), with
no active flexion of the fingers or thumb
• Transfers often performed in stages
• Goals of reconstruction
■ Restore finger and thumb flexion
○ Thumb: Brachioradialis (BR) transfer to FPL
○ Fingers: ECRL transfer with grafts to the four FDP
tendons
■ Restore key pinch: ECRB with graft to adductor
tubercle/adductor pollicis insertion
■ Restore opposition: EIP transfer to the APB tendon
■ Correct clawing: If above transfers have been performed,
there are no expendable wrist extensors for correction of
clawing. If above transfers have not been performed,
transfer of the ECRB to the intrinsics has been described.
■ Restoration of wrist flexion: ECU to FCU
Tendon Transfers for Muscle Spasticity
1. Classically involves patients with spasticity syndromes (e.g.,
cerebral palsy)
2. Goals of treatment: Improve digital contractures, assist with
hand hygiene by getting digits out of fixed flexed position
within the palm
3. Common deformities
• Thumb-in-palm deformity: One of the most important
factors affecting good hand function in these patients (see
Table 19.2)
• Finger flexion: Side-to-side tenodesis of index and
long-finger FDP to the ulnar innervated FDP (ring and
small)
■ ECRL tendon transfer to FDP, or index and long, can
also be performed, especially if power flexion is required.
Ulnar Nerve Palsy
1. Low ulnar n. palsy: Injury distal to innervation of the ring
and small-finger FDP and FCU
2. High ulnar n. palsy: Injury proximal to innervation of the
ring and small-finger FDP and FCU
3. Functional deficits
• Clawing
■ Hyperextension of the MCP joint, flexion at the PIP and
DIP joints (“Duchenne” sign) secondary to flexor/
extensor imbalance
■ Involves only the ring and small fingers in low ulnar n.
palsy but will affect all four fingers in combined median
and ulnar n. palsy
• Loss of key pinch
■ Secondary to paralysis of the adductor pollicis, 12 of the
flexor pollicis brevis (FPB), and the 1st dorsal
interosseous m.
■ Compensatory activation of FPL, producing IP flexion
(“Froment’s” sign) and MCP hyperextension (“Jeanne’s”
sign) with forceful pinch
• Ulnar deviation of the small finger (“Wartenberg’s” sign)
■ Secondary to paralysis of the 3rd palmar interosseous m.
and unopposed action of the EDM
• Weak flexion of the ring- and small-finger DIP
• Weak wrist flexion (high ulnar n. palsy)
4. Tendon transfers for ulnar n. palsy
• Correction of clawing: ECRB extended with tendon grafts
to the radial lateral bands (“Brand” transfer: ECRB,
extensor route, 4-tailed graft, or extensor-to-extensor
4-tailed [EE4T] transfer)
■ Can also use ECRL (“Brand EF4T” transfer: ECRL,
flexor route, 4-tailed graft), PL, FCR, Zancolli lasso
procedure (FDS tendon is split into two slips that are
wrapped around the A1 pulleys and secured to each
other), or Stiles-Bunnell transfer (FDS split into two
slips and secured to radial lateral bands).
• Restore key pinch (thumb adduction): ECRB extended
with tendon graft to adductor pollicis
■ Use of the ring-finger FDS, BR, ECRL, and EIP has also
been described.
• Correct ulnar deviation of small finger: Ulnar half of EDM
passed volar and sutured to the insertion of the radial
collateral ligament of the MCP or looped under the A2
pulley and secured to itself
• Restore flexion of ring- and small-finger DIP: Side-to-side
tenodesis of the ring- and small-finger FDP tendons to the
middle-finger FDP tendon (median n. innervated).

Free Functioning Muscle Transfers
211
19
3. The transplanted muscle must be able to generate sufficient
force to power the desired function.
4. The transplanted muscle must be placed at the same resting
tension as that in the donor site.
5. Requirements for free functional muscle transfer
(see Box 19.4)
• Fist-in-palm deformity: Classically treated with FDS to
FDP transfer (superficialis-to-profundus [STP] transfer).
■ FDS and FDP tendons identified in the distal forearm
○ The FDP tendons are sutured together distally, and
the FDS tendons are sutured together proximally if
there is little digital function.
■ The FDS tendons are transected distally, and the FDP
tendons are transected proximally.
■ The FDS tendons are then sutured side to side to the
FDP tendons.
Common Tendon Transfers for
Reconstruction after Trauma
1. Closed EPL rupture after distal radius fracture
• Classically occurs at Lister’s tubercle
• Etiology: Ischemia of tendon secondary to tenosynovial
edema and attrition over the radial cortex
• Treatment: EIP-to-EPL transfer
2. Restoration of finger extension after trauma
• Etiology: Complex dorsal hand trauma with soft-tissue
damage and tendon loss
• Treatment: Similar transfers used in radial n. palsy (FCU,
FCR, or FDS of long and ring fingers to EDC)
3. Laceration or rupture of FPL
• Treatment: Ring-finger FDS to FPL
4. Volar crush or avulsion injuries involving the extrinsic flexor
muscles
• Treatment: ECRL with grafts to all 4 FDP tendons or free
functioning muscle transfer (e.g., gracilis)
Free Functioning Muscle Transfers
1. Indicated when no simpler alternative is available
2. Complex procedure that requires strict patient compliance
and meticulous microsurgical technique
Adapted from Anastakis D., Manktelow R., 2005. Free functioning
muscle transfers. In: Green’s operative hand surgery, 5th ed. Elsevier,
Philadelphia.
BOX 19.4  REQUIREMENTS FOR FREE FUNCTIONAL
MUSCLE TRANSFER
• Available, undamaged motor nerve, artery, and vein at
the site of muscle transplantation
• Adequate skin coverage for the distal half of the muscle
• Supple joints and gliding tendons
• Good hand sensibility and intrinsic function
• Adequate antagonist muscle function
• Good patient motivation
• No simpler solution for patient’s problem
Table 19.2  Classifications of Thumb-in-Palm Deformity
TYPE
DESCRIPTION
INVOLVED
ELEMENTS
1
Simple metacarpal
adduction contracture
Spastic adductor
and 1st dorsal
interosseous
2
Metacarpal adduction
contracture with MP
flexion deformity
Spastic adductor,
1st dorsal
interosseous, FPB
3
Metacarpal adduction
contracture with MP
hyperextension/instability
Spastic adductor,
1st dorsal
interosseous, EPB
4
Metacarpal adduction
contracture, MP and IP
flexion deformities
Spastic adductor,
1st dorsal
interosseous, FPL
Reprinted from Wolfe, S.W., Hotchkiss, R.N., Pederson, W.C., et al.
(Eds.), 2011. Green’s Operative Hand Surgery, 6th ed. Elsevier,
1139–1172.
EPB, Extensor pollicis brevis; FPB, flexor pollicis brevis; FPL, flexor
pollicis longus; IP, interphalangeal; MP, metacarpophalangeal.
Suggested Readings
Carlson, M.G., 2011. Chapter 35: Cerebral palsy. In: Wolfe, S.W., Hotchkiss,
R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand Surgery, 6th ed.
Elsevier, pp. 1139–1172.
Davis, T.R.C., 2011. Chapter 34: Median and ulnar nerve palsy. In: Wolfe,
S.W., Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand
Surgery, 6th ed. Elsevier, pp. 1093–1138.
Harvey, I., Borschel, G.H., 2013. Chapter 35: Free-functioning muscle transfer
in the upper extremity. In: Neligan, P.C., Chang, J. (Eds.), Plastic Surgery,
vol. 6, 6th ed. Elsevier, pp. 777–788.
Ingari, J.V., Green, D.P., 2011. Chapter 33: Radial nerve palsy. In: Wolfe,
S.W., Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand
Surgery, 6th ed. Elsevier, pp. 1075–1092.
Jones, N.F., 2013. Chapter 34: Tendon transfers in the upper extremity. In:
Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, vol. 6, 3rd ed. Elsevier,
pp. 745–776.
Magerle, K., Germann, G., 2013. Chapter 10: Extensor tendon injuries. In:
Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, vol. 6, 3rd ed. Elsevier,
pp. 210–227.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
19: Essential anatomy of the upper extremity. Elsevier, pp. 309–341.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
20: Examination of the upper extremity. Elsevier, pp. 342–357.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
21: Flexor tendon injuries and reconstruction. Elsevier, pp. 358–374.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
22: Nerve transfers. Elsevier, pp. 375–392.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
23: Tendon transfers in the upper extremity. Elsevier, pp. 393–413.
Neligan, P.C., Buck, D.W., 2013. Core Procedures in Plastic Surgery. Chapter
24: Extensor tendon injuries. Elsevier, pp. 414–426.
Seiler, J.G., 2011. Chapter 7: Flexor tendon injury. In: Wolfe, S.W., Hotchkiss,
R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand Surgery, 6th ed.
Elsevier, pp. 189–206.
Strauch, R.J., 2011. Chapter 6: Extensor tendon injury. In: Wolfe, S.W.,
Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand
Surgery, 6th ed. Elsevier, pp. 159–188.
Tang, J.B., 2013. Chapter 9: Flexor tendon injury and reconstruction. In:
Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, vol. 6, 3rd ed. Elsevier,
pp. 178–209.
Taras, J.S., Kaufman, R.A., 2011. Flexor tendon reconstruction. In: Wolfe,
S.W., Hotchkiss, R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand
Surgery, 6th ed. Elsevier, pp. 207–238.
Wolfe, S.W., 2011. Chapter 62: Tendinopathy. In: Wolfe, S.W., Hotchkiss,
R.N., Pederson, W.C., et al. (Eds.), Green’s Operative Hand Surgery, 6th ed.
Elsevier, pp. 2067–2088.

SECTION 5: Integument
Wound Healing and
Tissue Expansion
Chapter
20 
1. Wound healing phases
• Hemostasis: Platelet plug, fibrin clot, vasoconstriction. α
granules in the platelets release cytokines such as platelet-
derived growth factor (PDGF), transforming growth factor
(TGF), and basic fibroplast growth factor (bFGF).
• Inflammatory: Activated to cleanse and prepare wound for
healing
■ Polymorphonuclear (PMN) leukocytes: Initial 24 to
48 hours. Act as defensive units, phagocytosing bacteria
and foreign debris from the wound to prevent infection
○ Phagocytosed by macrophages and destroyed
■ Macrophage: Dominant cell between 48 and 72 hours
(key regulatory cell). Functions to phagocytose bacteria
and dead tissue. Secretes collagenases and cytokines
responsible for proliferation of fibroblasts, resulting in
collagen production, and endothelial cells, resulting in
angiogenesis
• Proliferative/fibroplastic: 3 to 5 days after injury, fibroblasts
migrate into the wound and become predominant cell
type. They begin to lay down new collagen. At first, type 3
is greater than type 1 but is eventually replaced by type 1 to
the normal ratio (4:1, T1:T3).
■ It is during this time that the greatest rate of collagen
synthesis occurs in the wound.
■ Contraction begins and continues into remodeling
phase.
• Remodeling begins day 21. Cross-linking and organization
of collagen fibers (procollagen is cleaved into collagen)
■ Net amount of collagen is constant because there is an
equal amount of degradation and synthesis.
■ Wound becomes stronger because of cross-linking.
○ Maximum tensile strength is achieved after ~12
weeks.
♦ 80% by 60 days
2. Wound healing process
• Epithelial cell migration: Initiated by loss of contact
inhibition and occurs from the periphery of the wound
and adnexal structures
■ Cell division occurs in 48 to 72 hours, resulting in a thin
epithelial cell bridge across the wound.
■ Epidermal growth factors play a key role.
■ Can be delayed by retinoids (Accutane/isotretinoin)
■ Can be stimulated by tretinoin (Retin-A)
○ Promotes epithelialization by stimulating mitotic
activity and decreasing the turnover of follicular
epithelial cells
○ Often used as a pretreatment in patients undergoing
chemical peeling and laser skin resurfacing to
accelerate wound healing
• Myofibroblasts: Involved in wound contraction and play
no role in epithelialization
• Collagen deposition is seen in the remodeling phase of
wound healing.
• Fibronectin produced by fibroblasts serves as an adhesion
molecule, anchoring cells to collagen or proteoglycan
substrates.
• Release of cytokines from platelets plays an important role
in the initiation of the hemostatic initial phase.
3. Growth factors involved in wound healing process (see
Table 20.1)
4. Important nutrients for wound healing
• Vitamin C: Collagen cross-linking via the hydroxylation of
proline and lysine to hydroxyproline and hydroxylysine,
respectively
■ Lack of cross-linking results in impaired collagen
synthesis and a decrease in collagen tensile strength.
Collagen-containing tissues, such as skin, dentition,
bone, and blood vessels, are therefore affected, leading to
the development of scurvy.
○ Hallmark signs of scurvy: Hemorrhaging in any organ
(ie, petechiae, swollen gums), loss of dentition, and a
lack of osteoid formation
○ Seen in patients who are severely malnourished, have
a history of alcoholism, or have restrictive diets for
medical, social, or economic reasons
• Folate and vitamin B6 (pyridoxine) are integral in DNA
synthesis and cellular proliferation.
• Vitamin A is an essential factor in epithelialization and
fibroblast proliferation.
■ Impairment of wound healing caused by use of
corticosteroids can be reversed by the oral
administration of vitamin A (retinoic acid), 15,000 IU
daily, for 7 days.
• Vitamin E is a strong antioxidant and immune modulator.

Wound Healing and Tissue Expansion
213
20
Table 20.1  Partial List of Growth Factors Present in the Wound Site
GROWTH FACTOR
ABBREVIATION
GROWTH FACTOR
CELLULAR SOURCE
TARGET CELLS
BIOLOGIC ACTIVITY
CTGF
Connective tissue growth factor
Fibroblasts, endothelial cells
Fibroblasts
Downstream of TGF-β1
EGF
Epidermal growth factor
Platelets, macrophages,
keratinocytes
Keratinocytes, fibroblasts,
endothelial cells
Proliferation, chemotaxis
FGF-1, FGF-2,
FGF-4
Fibroblast growth factor-1, -2,
and -4
Macrophage, fibroblasts,
endothelial cells
Keratinocytes, fibroblasts,
endothelial cells,
chondrocytes
Angiogenesis,
proliferation, chemotaxis
FGF-7 (KGF-1),
FGF-10 (KGF-2)
Fibroblast growth factor-7
(keratinocyte growth factor-1),
fibroblast growth factor-10
(keratinocyte growth factor-2)
Fibroblasts
Keratinocytes
Proliferation, chemotaxis
IGF-1/Sm-C
Insulin-like growth factor-1/
somatostatin-C
Fibroblasts, macrophages,
serum
Fibroblasts, endothelial
cells
Proliferation, collagen
synthesis
IL-1α and IL-1β
Interleukin-1α and -1β
Macrophages, neutrophils
Macrophages, fibroblasts,
keratinocytes
Proliferation, collagenase
synthesis, chemotaxis
PDGF
Platelet-derived growth factor
Macrophage, platelets,
fibroblasts, endothelial cells,
vascular smooth-muscle cells
Neutrophils,
macrophages, fibroblasts,
endothelial cells, vascular
smooth-muscle cells
Chemotaxis, proliferation,
matrix production
TGF-α
Transforming growth factor-α
Macrophages, platelets,
keratinocytes
Keratinocytes, fibroblasts,
endothelial cells
Proliferation
TGF-β1 and -β2
Transforming growth factor-β1
and β2
Macrophages, platelets,
fibroblasts, keratinocytes
Inflammatory cells,
keratinocytes, fibroblasts
Chemotaxis, proliferation,
matrix production (fibrosis)
TGF-β3
Transforming growth factor-β3
Macrophages
Fibroblasts
Antiscarring
TNF-α
Tumor necrosis factor-α
Neutrophils
Macrophages,
keratinocytes, fibroblasts
Activation of growth factor
expression
VEGF
Vascular endothelial cell
growth factor
Macrophages, keratinocytes,
fibroblasts
Endothelial cells
Angiogenesis
Modified from Lorenz, H.P., Longaker, M.T., 2000. Wounds: biology, pathology, and management. In: Norton, J., Barie, P., Bollinger, R., et al.
(Eds.), Surgery: Basic Science and Clinical Evidence, 2nd ed. Springer, New York, 191–208.
• Zinc is one of the most important micronutrients because
it acts as a cofactor for numerous metalloenzymes and
proteins.
■ Essential for proper protein (like collagen) and nucleic
acid synthesis
• Silicone/silicone sheeting
■ Exact mechanism of action unknown
■ Most widely accepted hypothesis is that there is an
increase in hydration resulting from occlusion
○ Studies have either ruled out or not supported
alteration of cytokine levels, direct chemical effects,
increased oxygen tension, or pressure.
■ Some postulate that their effect is associated with the
generation of an increased static electronegative field by
the silicone.
■ To be effective, it must be worn for at least 12 hours/day
for 3 months or longer.
5. Systemic factors affecting wound healing (see Table 20.2)
• Diabetes mellitus adversely affects healing by altering
circulation, attenuating inflammation, reducing tissue
oxygenation, and adversely affecting glucose metabolism,
resulting in stress hyperglycemia.
• Malnutrition, including caloric, protein, vitamin, and
mineral insufficiency, impairs the immune system, prevents
tissue repair, and may lead to progression or recurrence of
a wound.
• Aging is associated with reduced production of collagen
and angiogenesis and a diminished response to
environmental stresses.
• By reducing inflammation, steroids impair angiogenesis,
fibrogenesis, and wound contraction; reduce wound
strength; and delay healing.
• Other factors such as infection, smoking, poor tissue
oxygenation, radiation, chemotherapy, and the presence of
foreign bodies or cancer within a wound are also associated
with poor healing.
• Anemia, even to severe levels, when circulation is
maintained has not been found to impair wound healing.
6. Collagens
• Type 1: Mature skin, tendon, bone
• Type 2: Hyaline cartilage, eye
• Type 3: Papillary dermis, arteries, intestinal walls, uterus,
hypertrophic/keloid scars
• Type 4: Basement membrane

Wound Healing and Tissue Expansion
214
Table 20.2  Factors that May Impair Normal Healing and Lead to Chronic Nonhealing Wounds
ETIOPATHOLOGY
EXAMPLES
Vascular
Arterial
Arteriosclerosis, arterial aneurysm, fat embolism with arterial obstruction,
hypertension (Martorell ulcer)
Lymphatic
Lymphatic edema, lymphangiodysplasia
Venous
Chronic venous insufficiency, necrotizing thrombophlebitis
Mixed arteriovenous
Combined arteriosclerosis with venous insufficiency, arteriovenous malformations/
dysplasia; steal phenomenon (e.g., arteriovenous shunts, vascular compression/
obstruction; due to tumors, enlarged lymphatic nodes, etc.)
Vasculitis
Wegener’s granulomatosis, Churg-Strauss vasculitis, Henoch-Schönlein purpura,
Sneddon syndrome, systemic lupus erythematosus, rheumatoid arthritis, Felty
syndrome, Takayasu arteriitis, polyarteritis nodosa, Kawasaki syndrome, pyoderma
gangrenosum, necrobiosis lipoidica diabeticorum, thromboangiitis obliterans
(Buerger’s disease), allergic reactions
Vasculopathic syndromes
Raynaud’s syndrome, systemic scleroderma, CREST, Klippel-Trenaunay syndrome,
proteus syndrome, CLOVES syndrome, Kasabach-Merritt syndrome
Physical, chemical,
and biological causes
Pressure
Immobility, intra- and postoperative bedding, tight shoes and casts, compression
therapy
Trauma
Lacerations, any type of soft-tissue and bone injury, vascular rupture
Thermal
Burns/frostbite, electrical injury (electrical current/high voltage/lightning)
Radiation
Radiation therapy
Chemical-toxic
Extravasation, chemical burns (acids/bases), sclerotherapy
Infections
Erysipelas, necrotizing fasciitis, septic cutaneous embolism, osteomyelitis,
complications after cutaneous infection
Herpes simplex, cytomegalovirus, human immunodeficiency virus, syphilis, leprosy,
tuberculosis
Tropical ulcers, parasitic and vermicular infections
Neuropathic
Posttraumatic
Spinal lesions with palsy, peripheral nerve injury
Congenital
Spina bifida, syringomyelia, multiple sclerosis, neurological syndromes
Systemic neuropathic diseases
Diabetes mellitus, ethylene oxide toxic neuropathy, degenerative central and
peripheral neuropathies
Poliomyelitis, leprosy, tabes dorsalis
Hemopathological
Systemic diseases
Polycythemia vera, sickle-cell anemia, other anemias, thalassemia,
thrombocythemia vera, thrombocytopenic purpura, increased blood viscosity
(paraneoplastic, paraproteinemia, hyperglobulinemia, leukemia), complication after
blood transfusion
Disturbed hemostasiology
Factor V Leiden syndrome, antiphospholipid syndrome, disturbed fibrinolysis,
factor-XIII deficiency syndrome, antithrombin-III deficiency, proteins C and S
deficiency, Marcumar necrosis, disseminated intravascular coagulation, necrosis
due to vitamin K antagonist therapy
Neoplastic diseases
Cutaneous tumors
Basal and squamous cell carcinoma, melanoma, Bowen syndrome, Marjolin ulcer
(scar carcinoma), tumors with cutaneous metastasis or penetration (e.g., Paget
syndrome)
Therapeutic modalities
Steroids, vaccination ulcer (BCG), cytostatic drugs, NSAIDs, extravasation of
various drugs
Systemic diseases
Hepatic and/or renal insufficiency, immunosuppression, sarcoidosis,
homocysteinemia, hemochromatosis
Other causes
Alcoholism, obesity, gout, smoking, advanced age, malnutrition (e.g., vitamin,
protein, and micronutrient deficiency; scurvy); psychiatric diseases with self-
harming, neglect, intravenous drug abuse; foreign bodies/projectiles with fistulas
Reprinted from Neligan, P.C, Chang, J. (Eds.), 2013. Plastic Surgery, 3rd ed. Elsevier.
BCG, Bacillus Calmette-Guérin; CLOVES, congenital lipomatous overgrowth, vascular malformations, epidermal nevi, and spinal/skeletal;
CREST, calcinosis, Raynaud’s syndrome, esophageal dysmotility, sclerodactyly, and telangiectasia; NSAIDs, nonsteroidal anti-inflammatory drugs.
• Type 5: Found within the basement membrane in lesser
amounts than type-4 collagen
7. Negative pressure wound therapy (NPWT) effects
on wound
• The most likely mechanism by which NPWT expedites
healing is deformation of the wound.
■ Causes both macrodeformation and microdeformation
of a wound
○ Macrodeformation maintains approximation of the
tissues, preventing loss of domain and facilitating
earlier closure by delayed primary or secondary
intention.
○ Microdeformation at the interface of the sponge and
wound bed changes cell shape, which then affects
gene transcription via the cytoskeleton
(mechanotransduction).

Wound Healing and Tissue Expansion
215
20
♦ These microdeformational forces stimulate cellular
proliferation and angiogenesis in the wound.
• NPWT prevents desiccation of the wound.
■ The semiocclusive polyurethane drape maintains a
favorable, moist wound environment.
• NPWT decreases matrix metalloproteinase activity in the
wound.
■ Elevated matrix metalloproteinases inhibit wound
healing and neovascularization.
• NPWT decreases exudate of the wound by removing excess
fluid through suction.
■ Removes toxic inflammatory mediators and proteinases
■ Improves the diffusion of oxygen and nutrients to the
wound
• Contraindication: Gross bacterial infection
8. Skin substitutes
• Integra: Bilayer dermal replacement product that is
composed of a biodegradable bovine collagen
glycosaminoglycan (GAG; collagen-GAG) matrix
underlayer with a silicone outer layer
■ FDA on-label indication is for burn reconstruction.
■ Has been used in reconstruction of wounds with
exposed bone without periosteum, exposed cartilage
without perichondrium, and exposed tendon without
paratenon
■ The collagen-GAG matrix serves as scaffolding for the
ingrowth of cells and neovascularization.
○ After 2 to 4 weeks, the silicone outer later is removed
and a thin split-thickness skin graft completes the
reconstruction by providing epithelial cells over the
neovascularized dermal replacement.
■ Advantages: Availability of large quantities, simple and
reliable to use, pliability and cosmetic appearance of the
resulting cover, less wound contraction
• Biobrane: Temporary; constructed of an inner layer
composed of nylon and collagen, covered by an outer
silicone film
■ Useful as temporary coverage of burn wounds, where it
helps prevent evaporative loss (due to the silicone outer
layer) and subsequent wound desiccation
■ Reported to decrease wound pain and provide a barrier
to bacterial infection
■ Removed either before permanent grafting or after
epithelialization of the wound has occurred.
• Dermagraft: Dermal substitute composed of neonatal
foreskin fibroblasts cultured on a polyglactin mesh;
generally used in the treatment of diabetic foot ulcers,
where it often is combined with meshed skin grafts
• TransCyte: Similar to Biobrane but has an added biologic
layer derived from neonatal fibroblasts that are seeded onto
the nylon matrix to produce type-1 collagen, fibronectin,
and glycosaminoglycans
■ Removed either before skin grafting or after
epithelialization of the wound
■ Has been shown to decrease pain and time to
epithelialization
• Apligraf: Permanent, constructed of type-1 bovine
collagen and cultured neonatal human fibroblasts and
keratinocytes
■ Generally used in the treatment of venous ulcers and
diabetic foot ulcers
■ Long-term durability makes it an inappropriate choice
in situations with a full-thickness defect with exposed
vital structures.
• Cultured epidermal autografts: Patient’s own keratinocytes
expanded in tissue culture (2 to 3 weeks)
■ No donor site limitations
○ Useful with significant burns and limited donor site
availability
■ No dermal matrix tissue used; thus, the graft lacks the
elastic quality of normal skin or even split-thickness skin
grafts
○ Results in stiff wounds with limited motion in the
face and around joints
■ The lack of a dermis results in very slow basement
membrane formation, producing frequent blistering and
shearing
■ Use is somewhat limited by high cost and delay in
availability because the tissue is cultured.
■ Low resistance to infection (102 bacteria will result in
infection)
• Acellular dermal matrices: Cadaveric (or porcine) dermis
that is processed to be acellular and nonimmunogenic and
then freeze-dried for preservation.
■ Provides a substrate for tissue ingrowth; however, it does
not bring in any blood supply
■ Use described in the literature for abdominal wall
reconstruction, lower eyelid reconstruction, breast
reconstruction, lining of breast implant capsules, and
cleft palate repair
9. Dressings
• Silver ions kill a broad spectrum of bacteria. No resistant
organisms have been identified, and it is nontoxic to
human cells.
• Alginates absorb up to 20 times their weight and are used
to exudate wounds.
• Films and transparent dressings are waterproof and would
be impermeable to bacterial contamination.
• Hydrogels are generally waterproof and would prevent
bacterial contamination.
10. Extravasation injuries
• Cytotoxic and hyperosmolar agents may result in local
tissue necrosis.
■ Doxorubicin (Adriamycin) associated with severe
soft-tissue necrosis and warrants close follow-up for
early surgical debridement, if needed.
○ Dilution with saline or hyaluronidase may be
helpful.
• High-volume injuries may cause compartment syndrome
and limb ischemia.
■ Higher-risk groups include children, the elderly, and
intensive care/chronically ill patients.

Wound Healing and Tissue Expansion
216
• Interventions standard to all extravasation injuries, include
splinting, elevation, local dressings, and close serial
examination
11. Enzymatic debriding agents
• Main drawbacks: Not sufficient for significant levels of
necrotic tissue burden
• These ointments can cause burning and they may be
diluted with a hydrogel to reduce pain.
■ Papain is a potent digestant of nonviable protein
material but does not affect healthy tissues.
○ Urea increases the digestive potency of papain.
○ Dressings containing silver ions inactivate papain.
■ Collagenases are another class of commonly used
enzymatic debridement agents.
○ Work slowly
12. Effects of radiation on skin
• Permanent and may present either acutely or in delayed
fashion, even years after the original radiation insult
• The mechanism of injury: Through free radical production,
which directly damages the DNA
■ Acute changes: Erythema and edema of the skin,
vasodilation with endothelial edema, and lymphatic
obliteration
■ Chronic changes: Capillary thrombosis and subsequent
inadequate tissue oxygenation/development of
nonhealing ulcers
13. Abnormal scarring (2:1 ratio, T1:T3 collagen)
• Keloid scars: Scarring with hypertrophy beyond original
borders
■ May develop months after injury, seldom regresses, and
is not associated with contractures
■ More frequent in darker-skinned individuals
■ Extremely high recurrence rate (up to 80% for excision
alone)
■ Radiation therapy effective method to prevent keloid
scarring
○ External beam irradiation decreased recurrence rates
of 12% to 27%, but this may be associated with
pigmentary changes
■ Other methods (intralesional injection of corticosteroids,
interferon, retinoic acid, and 5-fluorouracil) have
recurrence rate of 50%.
○ Intralesional corticosteroid relieves symptoms of
itching and burning.
■ Pressure therapy has been found to be helpful in
decreasing keloid recurrence but requires ongoing
treatment for 3 to 10 months, which may not be
acceptable.
○ Mode of action (MOA): Local tissue hypoxia, reduced
fibroblast proliferation, and reduced collagen
synthesis
○ Required pressure: 24 and 30 mm Hg
■ Commonly found on deltoid, upper back, chest, and
earlobes
■ Histopathology: Extensive, random collagen fibers in
bundles. Fibroblasts have increased proliferation rates
and decreased apoptosis (when compared with those
from hypertrophic scars), decreased density of blood
vessels, relatively acellular absent myofibroblasts,
elevated TGF-β.
• Hypertrophic scars: Boundaries of original scar maintained
■ Develop soon after the injury (within 6 to 8 weeks).
■ Can worsen up to 6 months but subside with time
■ Can produce contractures and have a predilection to
occur over the flexor surface of joints
■ Histopathology: Increased density of blood vessels,
increased myofibroblasts
• Both hypertrophic and keloid scars are raised,
erythematous, and often pruritic.
14. Wound dehiscence
• Early wound dehiscence (immediate postoperative period)
may be caused by patient movement.
• Late wound dehiscence is often due to underlying seroma,
although infection and skin necrosis can occur.
15. Hyperbaric oxygen
• Proven utility in conditions such as osteomyelitis,
necrotizing infections, ischemia reperfusion injury, and
diabetic lower extremity (LE) wounds
• No proven utility in the treatment of extravasation injury,
pressure sores, or pyoderma gangrenosum
16. Chronic wounds: Interruption in the natural sequence of
wound healing involving a highly regulated cascade of events
among many cell types, soluble factors, and matrix
components; prolonged inflammatory phase
• The chronic wound microenvironment: Imbalance between
matrix-degrading enzymes and their inhibitors
■ Metalloproteinase levels are elevated, resulting in
extracellular matrix degradation.
■ Proinflammatory cytokines are elevated, which leads to
an increase in protease activity and a decrease in
protease inhibitor and growth factor levels.
○ Results in decreased matrix deposition, which
prevents epithelization and healing
■ Tissue oxygen tension is abnormally low in the central
aspect of chronic wounds.
17. Tissue expansion (TE)
• Results in increased cell division through stretch-induced
signal transduction pathways involving growth factors, the
cytoskeleton, and protein kinases
■ Net result is an increase in protein synthesis,
keratinocyte growth, and new skin production to restore
resting tension
• Cells in adjacent, nonexpanded areas are not affected,
expanded cells do not undergo apoptosis followed by
cellular replacement, and expansion of the intracellular
cytoskeleton alone does not result in increased tissue
generation.
• Several experimental animal studies have shown increased
flap survival following TE, similar to that seen with the
delay effect. It has been shown to occur with both
random-patterned and island flaps.

Wound Healing and Tissue Expansion
217
20
• TE increases the amount of locally available tissue,
preserves sensation, and maintains hair follicles and
adnexal structures.
• When performing expansion, place the largest tolerated
expander(s) in the subgaleal plane.
■ Rectangular and crescent-shaped prostheses provide
more expansion than circular devices.
• To account for tissue recoil, continue expansion until the
expanded flap is ~20% larger than the expected defect.
• Disadvantages: Prolonged time to complete the expansion
process (up to 3 months is not uncommon), need for at
least two operations, and a high rate of complication (6%
to 48%)
■ Common problems include infection, prosthesis
exposure or extrusion, hematoma, flap necrosis, skull
erosion, alopecia, and wide scars. (see Figure 20.1 and
Table 20.3)
• Large bundles of compacted collagen fibrils have been
demonstrated within the expanded dermis, and the total
collagen content of the flap is increased, although the
dermis is thinner.
• TE also results in an increase in the total surface area of the
flap; however, tensile strength and elasticity are decreased.
• Histopathologic examination demonstrates thinning of the
dermis, but the stratum spinosum of the epidermis
becomes thickened.
• Creep: Mechanical stretching changes the orientation of
elastic fibers and collagen.
• Stress relaxation: During a period of time when skin is
stretched to a certain length, the amount of force necessary
to maintain that length is decreased.
18. Scalp reconstruction with TE
• In patients with nearly 50% scalp loss, TE will provide the
optimal functional and aesthetic outcome.
Figure 20.1.  The temporal patterns of repair phase, cellular influx, and vascular response during wound repair. The time points are
approximate, and overlap occurs during these repair events. (Reprinted from Lorenz, H.P., Longaker, M.T., 2000. Wounds: Biology, Pathology, and
Management. Springer-Verlag, New York.)
Major
event
Clot formation
Hemostasis
Growth factor
elaboration
Collagen deposition
Collagen cross linking
Repair
phase
Inflammatory
Proliferation
Remodeling
Fibroblasts
Lymphocytes
Macrophages
Neutrophils
Cellular
influx
Vascular
response
Vasoconstriction
Injury
3 days
7 days
Time
3 weeks
1-2 years
Vasodilation
Table 20.3  Diagnostic Criteria for Distinction between Hypertrophic Scars and Keloids
HYPERTROPHIC SCAR
KELOID
Clinical symptoms
Remain within the boundaries of the wound
Grow beyond the wound borders
Rarely more than 1 cm in thickness or width
Size variations; growth may be widespread, vertical, or both
Form scar contractures
No contractures
Less pruritic and painful
Pruritic and painful
Occur after injury only: Disruption of skin continuity, burns
Spontaneous appearance without skin injury possible
Generally arise within 4 weeks, grow intensely for several
months, then regress often within 1 year
Appear within several months after initial scar, then
gradually proliferate indefinitely
Occur on points with excessive tensile forces: Across joint
surfaces, sternum, neck, palm, and soles after injury
Occur often on the chest, shoulders, trunk, back of the
neck, and earlobes; rarely on the palms or soles
Regress spontaneously
Do not regress spontaneously
Histological features
Fine and thin collagen fibers oriented parallel to the
epidermis
Large and thick collagen fibers; closely packed collagen
fibrils; increased ratio of type-2 to type-3 collagen
Nodules with increased fibroblast density
Increased fibroblast density in enlarging borders, acellular
in keloid center
Presence of α-smooth-muscle actin-expressing
myofibroblasts is typical
Lack of α-smooth-muscle actin-expressing myofibroblasts
Reprinted from Neligan, P.C., Chang, J. (Eds.), 2013. Plastic Surgery, 3rd ed. Elsevier.

Wound Healing and Tissue Expansion
218
Hsu, A., Mustoe, T.A., 2010. Chapter 1: The principles of wound healing. In:
Weinzweig, J. (Ed.), Plastic Surgery Secrets Plus. Mosby, pp. 3–7.
Leedy, J.E., Janis, J.E., Rohrich, R.J., 2005. Reconstruction of acquired scalp
defects: an algorithmic approach. Plast. Reconstr. Surg. 116 (4), 54e–72e.
Marks, M.W., Argenta, L.C., 2013. Chapter 27: Principles and applications of
tissue expansion. In: Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, 3rd ed.
Elsevier, pp. 622–653.
Mirastschijski, U., Jokuszies, A., Vogt, P.M., 2013. Chapter 15: Skin wound
healing. In: Neligan, P.C., Chang, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier,
pp. 26–296.
Sen, C.K., Roy, S., 2013. Chapter 14: Wound healing. In: Neligan, P.C.,
Chang, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier, pp. 240–266.
Suggested Readings
Buchanan, E.P., Lorenz, H.P., 2009. Chapter 3: Wound healing, including
fetal skin healing. In: Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.),
Plastic Surgery: Indications and Practice, 1st ed. Elsevier.
Buck, D.W., Galiano, R.D., 2013. Chapter 3: Wound care. In: Thorne, C.H.,
Chung, K.C., Gosain, A.K., et al. (Eds.), Grabb and Smith Plastic Surgery.
7th ed. Wolters Kluwer, pp. 58–75.
Desai, K.K., Hahn, E., Pulikkotill, B., et al., 2012. Negative pressure wound
therapy. Clin. Plast. Surg. 39 (3), 311–324.
Gantwerker, E.A., Hom, D.B., 2012. Skin: histology and physiology of wound
healing. Clin. Plast. Surg. 39 (1), 85–97.
Gurtner, G.C., Wong, V.W., 2013. Chapter 2: Wound healing: abnormal and
normal. In: Thorne, C.H., Chung, K.C., Gosain, A.K., et al. (Eds.), Grabb and
Smith Plastic Surgery. 7th ed. Wolters Kluwer, pp. 42–57.

Soft-Tissue and
Hand Infections
Chapter
21 
Bites
1. Human bites
• Generally polymicrobial: Staphylococcus aureus,
Streptococcus, Corynebacterium, Eikenella corrodens, and
anaerobics
• Eikenella species unique to human bites
■ Treat with penicillin including ampicillin and
amoxicillin
■ Eikenella species are resistant to clindamycin.
• Note that fight bites require operative exploration and
washout because bacteria can be inoculated into joint
spaces and spread proximally by extensor tendon motion.
2. Dog bites
• Immediately irrigate wounds with saline and wash with
soap and/or Betadine
• Leave puncture wounds open to heal by secondary intent.
• Lacerations can be repaired after copious irrigation if
wound appears clean.
• Penicillin antibiotics most commonly used
• Must be concerned about rabies
■ If a known animal, it should be quarantined for at least
10 days.
■ If an unknown animal, rabies prophylaxis is indicated.
○ Rabies prophylaxis
◆ If prior vaccination: Wash wound thoroughly and
provide booster vaccine.
◆ If no prior vaccination: Wash wound thoroughly,
administer rabies vaccine and rabies
immunoglobulin.
3. Cat bites
• Cat bites tend to result in puncture wounds that can seal
quickly; therefore, incision and drainage is recommended.
• High rate of infection from cat bites
• Many infections are polymicrobial; however, Pasteurella
multocida is unique to cat bites.
■ Pasteurella is resistant to cephalexin and cefazolin.
■ Treat with amoxicillin-clavulanate or fluoroquinolone
and clindamycin for penicillin-allergic patients.
■ Preferred treatment for pediatric patients is
trimethoprim-sulfamethoxazole (Bactrim) and
clindamycin.
4. Snake bites
• The majority of snakebites are from pit vipers.
• Treat with immediate immobilization to prevent spread of
venom, tetanus prophylaxis, broad-spectrum antibiotics,
and observation for venom inoculation (worsening edema,
pain, ecchymosis, altered mental status, coagulopathy,
compartment syndrome).
• Antivenin is indicated for progressive injury or symptoms.
■ If nonurgent, skin test first for hypersensitivity reaction
is preferred.
• Avoid debridement and/or tourniquet application
5. Spider bites
• Brown recluse spider
■ Venom inoculation causes a dermonecrotic reaction:
Blistering, ischemia, ulceration at the bite site.
■ Treat with Dapsone.
○ Watch for hematologic side effects.
• Black widow spider
■ Venom is a neurotoxin that causes severe muscle pain
and cramping. Late findings include abdominal pain,
tremors, emesis, excessive salivation, and shock.
■ Treat with calcium gluconate and benzodiazepines (e.g.,
diazepam).
■ Spider antivenin can be used in immunocompromised
patients.
6. Scorpion stings
• Stings are typically self-limiting in adults.
• Symptoms include severe localized pain and hyperesthesia
and can progress to blurry vision, strabismus, dyspnea,
dysphagia, incontinence, fevers, and muscle contraction.
• Treat initially with cold compresses and observation.
• In children, symptoms can be more severe.
■ Treat with admission, monitoring, and potentially
intubation for airway protection.
• Avoid debridement and tourniquet application.
7. Special considerations
• Tetanus prophylaxis
■ If prior vaccination
○ Tetanus-prone wound (contaminated, etc.):
Administer tetanus booster if last dose occurred more
than 5 years before new injury.

Soft-Tissue and Hand Infections
220
○ Non-tetanus-prone wound (clean): Administer
tetanus booster if last dose occurred more than 10
years from new injury.
■ If no prior vaccination
○ Tetanus immunoglobulin
Necrotizing Soft-Tissue Infections
1. Necrotizing fasciitis: A progressive soft-tissue infection
affecting skin, subcutaneous tissue, and fascia and sparing
muscle
• Extremely high mortality and rapid progression
• Can result from minor trauma or hematogenous spread
■ Most patients have predisposing morbidity, placing them
at risk.
○ Immunocompromised
○ Diabetes
○ Renal failure
○ Substance abuse
■ Head and neck infections can result from pharyngeal
abscesses, tonsillar abscesses, and dental abscesses.
• Requires emergent debridement of all devitalized tissue
2. Classification
• Type 1 (75% of cases): Polymicrobial, mixed aerobic and
anaerobic infections (non-group-A Streptococcus)
■ Treat with ampicillin-sulbactam, clindamycin,
ciprofloxacin, or gentamicin.
• Type 2: Monomicrobial, group-A Streptococcus
(Streptococcus pyogenes)
■ Treat with clindamycin and penicillin.
3. Progression of infection
• Initial cellulitis stage: Tenderness, erythema, edema, warm
skin, fever
■ May have increased white blood cells (WBCs),
thrombocytopenia, hyperkalemia
• Cellulitis progresses to ischemia with severe pain, crepitus,
and bullae formation.
• Final stage characterized by frank necrosis, anesthesia, and
“dishwater” drainage.
4. Principles of management
• Fluid resuscitation
• Intravenous antibiotics
• Emergent surgical debridement
■ Include fasciotomies in setting of compartment
syndrome.
■ Many require multiple trips to the operating room for
serial debridement.
• Hyperbaric oxygen is indicated as an adjunct to surgical
debridement for patients with persistent or extensive
necrosis.
• Negative pressure wound therapy (NPWT) is often used as
a bridge to reconstruction after debridement.
5. Fournier’s gangrene
• A necrotizing soft-tissue infection of the perineum
• Risk factors: Diabetes, alcoholism, smoking, leukemia,
immunocompromised
• Rapid progression and high mortality
• Treat as above and include antibiotic coverage for
anaerobic clostridium species.
Other Common Soft-Tissue Infections
1. Methicillin-resistant Staphylococcus aureus (MRSA)
• Increasingly common flora, especially in the nares
• More virulent and resistant to penicillins and
cephalosporins
• Suspect in patient with persistent infection in setting of
penicillin antibiotic treatment.
■ Treat with vancomycin, linezolid, trimethoprim-
sulfamethoxazole (Bactrim), or clindamycin.
• Nasal mupirocin (Bactroban) can be used to decolonize
patients who are noted to be carriers by nasal culture.
2. Orbital cellulitis
• Signs
■ Edema of the upper and lower eyelids
■ Erythema and cellulitis in the periorbital region
■ Proptosis
■ Pain with globe movement
• Diagnosis: Computed tomography (CT) scan
• Treatment: Broad-spectrum intravenous antibiotics and
operative drainage
3. Purpura fulminans
• Signs: Acute onset of hemorrhagic bullae formation,
desquamation, bilateral symmetric gangrene, and shock
• Rapid progression, with high mortality
■ Most common pathogens are Neisseria meningitides and
MRSA
• Typically involves pediatric patients
• Treatment: Supportive care, broad-spectrum intravenous
antibiotics, and activated protein C
■ Delay surgery until demarcation occurs, except in the
setting of acute wound infection or compartment
syndrome.
4. Hidradenitis suppurativa
• A defect of the follicular epithelium causing follicle
occlusion, rupture, and formation of abscesses and sinus
tracts, which leads to chronic apocrine gland inflammation
and secondary bacterial infections
• Commonly affects hair-bearing regions with apocrine
glands and skin folds (e.g., axilla, groin, perineum).
• Most common pathogens are Staphylococcus aureus and
Streptococcus viridans.
• Treatment: Antibiotics and incision and drainage of acute
abscesses followed by wide excision of all involved skin and
sinus tracts with healing by secondary intent or grafting
5. Toxic shock syndrome
• Signs: Fever, hypotension, diffuse macular rash, and
desquamation of the palms and soles 2 weeks after onset of
symptoms
• Can occur after surgery, trauma, or retained foreign bodies
(e.g., nasal packing, tampons, etc.)

Hand Infections
221
21
• Most common pathogens are Staphylococcus aureus and
Streptococcus viridians.
■ Treat with penicillin or 1st-generation cephalosporin.
• Other potential organisms
■ Neisseria species
○ Often develops without history of trauma
(hematogenous spread).
○ Gram positive diplococci on gram stain of joint fluid
○ No incision and drainage necessary because Neisseria
does not destroy joint cartilage
○ Treatment: Aspiration of joint fluid, intravenous
3rd-generation cephalosporin (e.g., ceftriaxone)
■ Serratia species
○ Often affects patients with history of diabetes,
immunosuppression, or intravenous drug abuse
■ Tuberculosis infections can masquerade as tenosynovitis
or arthritis.
○ Diagnosis is made by the presence of rice bodies on
imaging studies.
4. Paronychia
• Infection of the nail fold
• Often present without any specific history of trauma or
exposure
• Most common pathogens are Staphylococcus aureus and
group-A Streptococcus pyogenes.
■ Streptococcal toxic shock syndrome characterized by
severe disproportionate pain, with potential progression
to coagulopathy and organ failure
• Treatment: Supportive care and antibiotics
6. Wound infections
• Can develop after surgery, trauma, injury
• Risk factors can include host (diabetes, malnutrition,
obesity, ischemia, steroid use, immunosuppression),
wound (presence of nonviable tissue, foreign bodies,
contamination), and procedural (length of operation)
characteristics.
■ Of the wound factors, contamination portends the
highest risk.
• Treatment: Drainage and/or debridement, antibiotics,
supportive care
Hand Infections
1. Hand abscess
• Often complex due to deep communication with anatomic
hand spaces
■ Horseshoe abscess: Communication of flexor sheath
infection with Parona space in the distal forearm
○ Parona space: Potential space in the distal forearm
that joins the radial and ulnar bursa, superficial to the
pronator quadratus, and contiguous with the
midpalmar and thenar space
○ Treat with aggressive debridement of the digit and
Parona space (can access through an extended carpal
tunnel incision).
■ Collar button abscess: Tracks from dorsal to volar within
the web space via the palmar fascia
○ Hallmark sign: Finger abduction away from the
affected web space
○ Treat with dorsal and volar incision and drainage and
intravenous antibiotics (see Figure 21.1).
2. Flexor tenosynovitis
• Kanavel’s signs: Fusiform swelling, partially flexed finger
posturing, pain over the flexor sheath, pain with passive
extension
• Most common pathogens are Staphylococcus aureus or
Eikenella corrodens through human bite injuries.
• Treatment: Intravenous antibiotics, irrigation of the flexor
tendon sheath
■ Can access flexor sheath through incisions at the A1 and
A5 pulley or distal flexor crease (see Figure 21.2)
3. Septic arthritis
• Infection of the joint space
• Signs: Joint edema, pain with motion and joint impaction,
erythema, limited motion
• Diagnosis: Aspiration of the joint
■ Elevated synovial fluid WBC count (>50,000 to 100,000)
with predominance of neutrophils is the most sensitive
marker of septic arthritis.
Figure 21.1.  Deep spaces of the hand. (Reprinted from Neligan, P.C.,
Chang, J. [Eds.], 2013. Plastic Surgery, 3rd ed. Elsevier, 333–345.)
Septum of 3rd
metacarpal
Thenar space
Thenar muscles
Hypothenar
muscles
Midpalmar
space

Soft-Tissue and Hand Infections
222
• Treatment
■ Acute paronychia: Removal of a segment of the nail
plate and antibiotics
○ May require incision within the nail fold for drainage
○ Most common pathogens are Staphylococcus aureus
and Streptococcus.
■ Chronic paronychia: Removal of a segment of the nail
plate and antifungal medication
○ May require marsupialization of the paronychia with
healing by secondary intent if antifungal medication
fails
○ Most common pathogen is candida.
5. Felon (see Figure 21.3)
• Infection of the volar pad of a finger after a traumatic
puncture injury
■ Complex infections because of the multiple fibrous
septae within the finger pads
• Signs: Severe pain, swelling
• Treatment: Incision and drainage (with care to divide the
fibrous septae) and antibiotics
Figure 21.2.  Hand incisions. (Reprinted from Neligan, P.C., Chang, J. [Eds.], 2013. Plastic Surgery, 3rd ed. Elsevier, 333–345.)
Thenar +/– carpal
tunnel extension
Closed irrigation
A1 pulley
Hypothenar
incision
Dorsal thenar incision
Collar button incision
No incision (web space)
Brunner incision
Midpalmar space incision
Figure 21.3.  A, Anatomy of a felon; B,C, options for felon
incisions. (Reprinted from Neligan, P.C., Chang, J. [Eds.], 2013. Plastic
Surgery, 3rd ed. Elsevier, 333–345.)
Midlateral incision
Volar midline incision
Felon
$
%
&

Hand Infections
223
21
6. Herpetic whitlow
• A lesion on the finger or thumb secondary to the herpes
simplex virus
• Signs: Pain, multiple vesicles on an erythematous base
• Risk factors: Immunocompromised patients
• Diagnosis: Tzanck smear shows giant cells.
• Treatment: Acyclovir (oral or topical) only; surgical incision
or debridement may result in superinfection or encephalitis.
7. Sweet syndrome
• Also known as acute febrile neutrophilic dermatosis.
• Signs: Fever and painful erythematous skin lesions that
primarily appear on the arms, neck, face, and back
• Diagnosis: Biopsy reveals neutrophilic infiltration of the
dermis and epidermis.
• Treatment: Corticosteroid administration
8. Atypical mycobacterial infections
• Resulting from exposure to ocean water, aquatic life, or
marine environments
• Most common pathogen is Mycobacterium marinum.
• Signs: Tenosynovitis signs without pain
9. Vibrio vulnificus infections
• Infections resulting from exposure to water, raw aquatic
life, or puncture wounds from fish and/or stingrays
• Signs: Pain, cellulitis, severe edema, and hemorrhagic
bullae formation
• Can progress to bacteremia and systemic symptoms
• High mortality rate
• Treatment: Intravenous fluoroquinalone (or a
3rd-generation cephalosporin with a tetracycline) and
supportive care (see Table 21.1)
Suggested Readings
Brinster, N.K., Liu, V., Hafeez, D., et al. (Eds.), 2011. Dermatopathology.
Saunders.
Dodds, S.D., 2010. Chapter 11: Hand infections and injection injuries. In:
Trumble, T.E., Rayan, G.M., Budoff, J.E., et al. (Eds.), Principles of Hand
Surgery and Therapy, 2nd ed. Elsevier, pp. 193–200.
Masden, D.L., Forthman, C.L., 2014. Hand infections. In: Cameron, J.L.,
Cameron, A.M. (Eds.), Current Surgical Therapy, 11th ed. Saunders,
pp. 724–732.
O’Neal, P.B., Itani, K.M., 2014. Necrotizing skin and soft tissue infections.
In: Cameron, J.L., Cameron, A.M. (Eds.), Current Surgical Therapy, 11th ed.
Saunders, pp. 745–750.
Bidic, S.M., Schaub, T., 2013. Chapter 16: Infections of the hand. In: Neligan,
P.C., Chang, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier, pp. 333–345.
Shenoy, E.S., Hooper, D.C., 2013. Chapter 38: Skin and soft tissue infections.
In: Parsons, P.E., Wiener-Kronish, J.P. (Eds.), Critical Care Secrets, 5th ed.
Mosby, pp. 262–270.
Slavin, E.M., 2013. Chapter 184: Skin and soft-tissue infections. In: Adams,
J.G. (Ed.), Emergency Medicine Clinical Essentials, 2nd ed. Saunders,
pp. 1550–1554.
Durand, M.L., 2015. Chapter 118: Periocular infections. In: Bennett, J.E.,
Dolin, R., Blaser, M.J. (Eds.), Principles and Practice of Infectious Diseases,
8th ed. Saunders, pp. 1432–1438.
Evans, D.C., Steinberg, S.M., 2011. Chapter 135: Infections of skin, muscle,
and soft tissue. In: Vincent, J.L., Abraham, E., Moore, F.A., et al. (Eds.),
Textbook of Critical Care, 6th ed. Saunders, pp. 1028–1035.
Norris, R.L., Auerbach, P.S., Nelson, E.E., et al., 2012. Chapter 22: Bites and
stings. In: Townsend, C.M., Beauchamp, R.D., Evers, B.M., et al. (Eds.),
Sabiston Textbook of Surgery, 19th ed. Saunders, pp. 548–562.
Fagan, S., Chai, J., Spies, M., et al., 2012. Chapter 43: Exfoliative diseases of
the integument and soft tissue necrotizing infections. In: Herndon, D.N. (Ed.),
Total Burn Care, 4th ed. Elsevier, pp. 471–481.
Table 21.1  General Recommendations for Hand Infections
INFECTION
LIKELY ORGANISM(S)
INITIAL ANTIBIOTIC THERAPY*
SURGICAL THERAPY
Cellulitis
Staphylococcus or
Streptococcus
Cephalexin. Use clindamycin or
trimethoprim-sulfamethoxazole (Bactrim) for
suspected MRSA
Only indicated for associated abscess
Abscess
Staphylococcus
Vancomycin. Add piperacillin-tazobactam
(Zosyn) for diabetic/immunocompromised
patients
Immediate drainage (no closure), soaks, and
motion 1 day after surgery
Flexor
tenosynovitis
Staphylococcus, anaerobes,
polymicrobial
Ampicillin-sulbactam (Unasyn). Replace
Unasyn with Zosyn for diabetic/
immunocompromised patients and add
vancomycin if suspect possible MRSA
Consider 12- to 24-hour observation for early
signs; otherwise, drainage of flexor sheath (no
closure), soaks, and motion 1 day after surgery
Septic
arthritis
Staphylococcus
Vancomycin. Add ceftriaxone if suspect
Neisseria gonorrhoeae
Immediate drainage (no closure), soaks, and
motion 1 day after surgery
Animal bite
Pasteurella multocida is
classic, but Staph, Strep, and
anaerobes are common
Unasyn or oral (PO) equivalent. If penicillin
allergic, consider fluoroquinolone and
clindamycin
Clean thoroughly in ER and observe closely for
signs of deep infection. Cat teeth inoculate the
deep tissues, so consider incising the puncture
site to facilitate drainage. Dog teeth tear local
tissues; wound will usually drain spontaneously
Human bite
Eikenella corrodens is classic,
but Staph, Strep, and
anaerobes are common
Unasyn or PO equivalent. If penicillin
allergic, consider fluoroquinolone and
clindamycin
Clean thoroughly in ER and observe closely for
signs of a deep infection (e.g., abscess, FTS,
etc.). “Fight bites” require immediate drainage,
even in the absence of overt infection
Necrotizing
fasciitis
Streptococcus or
polymicrobial
Vancomycin and clindamycin and
piperacillin-tazobactam (Zosyn)
Emergent radical debridement(s), hemodynamic
monitoring, possible amputation
Gas gangrene
Clostridium perfringens, Strep
pyogenes, Staph aureus,
Vibrio vulnificus, polymicrobial
Vancomycin and clindamycin and
piperacillin-tazobactam (Zosyn). Consider
high-dose penicillin.
Emergent radical debridement(s), hemodynamic
monitoring, possible amputation
Reprinted from Cameron, J.L., Cameron, A.M. (Eds.), 2014. Current Surgical Therapy, 11th ed. Saunders, 724–732.
FTS, Flexor tenosynovitis.
*Antibiotic coverage should be adjusted once cultures are back to decrease the creation of antibiotic-resistant organisms and to minimize drug
side effects to the patient.

Burns and Burn Reconstruction
Chapter
22 
Initial Evaluation
1. Burn severity or “degree”: Described based on depth of injury
• First degree (“superficial” partial thickness): Superficial,
erythema, sometimes painful, epidermal integrity intact
• Second degree (“deep” partial thickness): Blisters,
erythema, edema, very painful, epidermis violated, injury is
into dermis
• Third degree (full thickness): Charred or translucent,
“white” color, mild pain, pin prick absent
2. Burn volume: Described by total body surface area (TBSA)
involved
• “Rule of nines” (see Figure 22.1)
• Lund and Browder method (see Figure 22.2)
3. Burn center referrals
• Outcomes of burns better at high-volume centers
• Criteria for referral to an accredited burn center (American
Burn Association) (see Box 22.1)
Burn Physiology
1. The three zones of a burn
• Zone of coagulation: Central area of nonviable tissue
Figure 22.1.  Estimation of burn size using the “rule of nines.” BSA, Body surface area.
Part
Arm
Head and neck
Leg
Anterior trunk
Posterior trunk

Child
Adult

9%
9%

18%
10%

14%
18%

18%
18%

18%
18%
9%
1%
Front
18%
Back
18%
18%
18%
9%
9%
% of total BSA
Front
18%
Back
18%
18%
9%
9%
14%
14%
• Zone of stasis: Threatened area with initial perfusion that
can progress to ischemia
■ Progression can be prevented with adequate
resuscitation
• Zone of hyperemia: Outer area of viable tissue (see
Figure 22.3)
2. Burns >30% TBSA are associated with a systemic
inflammatory response and general down-regulation of the
immune system, including
• Diminished activation of complement and decrease in
levels of circulating immunoglobulins (levels may take 2
to 4 weeks to recover as patient condition improves)
• Up-regulation of proinflammatory cytokines TNF-α,
interleukin-1 (IL-1), IL-8, and integrins that promote
neutrophil chemotaxis, extravasation, and tissue necrosis
• Reduced B-lymphocyte function, T-helper-cell function,
and cytotoxic T-lymphocyte function
■ Contributes to delayed allograft rejection, suppression of
graft versus host disease, and skin hypersensitivity
• Increased T-suppressor function

Burn Physiology
225
22
Figure 22.2.  Estimation of burn size using the Lund and Browder method. (Reprinted from Herndon, D.N. [Ed.], 2012. Total Burn Care. Elsevier, 93–102.)
Age
0–1
1–4
5–9
10–14
15
A – ½ of head
9½%
8½%
6½%
5½%
4½%
B – ½ of one thigh
9½%
8½%
6½%
5½%
4½%
C – ½ of one leg
9½%
8½%
6½%
5½%
4½%
Adult
3½%
3½%
3½%
3½%
3½%
3½%
A
A
B
B
C
C
B
B
C
C
1½%
1½%
1½%
1½%
1½%
1½%
1½%
1½%
2½%
2½%
4¾%
4¾%
4¾%
4¾%
1¾%
1¾%
1%
1%
1%
13%
13%
2%
2%
2%
2%
1¾%
1¾%
Figure 22.3.  Jackson’s three zones of injury on an ankle burn.
a, Zone of coagulation; b, zone of stasis; c, zone of hyperemia.
(Reprinted from Herndon, D.N. [Ed.], 2012. Total Burn Care, 4th ed. Elsevier,
125–130.)
a
b
c
BOX 22.1  BURN CENTER REFERRAL CRITERIA
1. Partial-thickness burns >10% TBSA
2. Burns that involve the face, hands, feet, genitalia,
perineum, or major joints
3. Full-thickness burns in any age group
4. Burns caused by electric current including lightning
5. Chemical burns
6. Inhalation injury
7. Burn injury in patients with preexisting medical
disorders that could complicate management, prolong
recovery, or affect mortality
8. Any patient with burns and concomitant trauma (such
as fractures) in whom the burn injury poses the
greatest risk of morbidity or mortality. In such cases,
if the trauma poses the greater immediate risk, the
patient may be stabilized in a trauma center before
transfer to a burn center
9. Burned children in a hospital without qualified
personnel or equipment for the care of children
10. Burn injury in a patient who will require special social,
emotional, or rehabilitative intervention
Adapted from American Burn Association, 2011. Advanced Burn
Life Support Course Provider Manual. American Burn Association,
Chicago, IL, 25–26.
TBSA, Total body surface area.

Burns and Burn Reconstruction
226
leucopenia, cross-reactive with sulfa allergies, cannot
penetrate eschar or cartilage
• Mafenide acetate (Sulfamylon)
■ Advantages: Broad-spectrum antimicrobial coverage,
penetrates eschar and cartilage, useful in setting of burn
wound infection and suppurative chondritis
■ Disadvantages: Painful when applied, can cause
metabolic acidosis, secondary to inhibition of carbonic
anhydrase
5. Surgical management/burn reconstruction
• Operative excision and grafting are recommended for burn
wounds that are not likely to reepithelialize and heal within
3 weeks.
■ The practice of early burn wound excision and grafting
has reduced mortality from burn wound sepsis.
• Debride partial-thickness wounds with tangential excision
until pinpoint bleeding is obtained, then perform skin
graft.
• Skin substitutes may be used in patients who may not have
enough donor site availability for burn wound coverage.
■ Cultured epidermal autografts: Ex vivo expansion of
donor keratinocytes
○ Advantages: Can obtain ~10,000-fold expansion;
available in spray form
○ Disadvantages: Lack dermal component, rendering
these grafts fragile and highly susceptible to sheer
forces; grown with murine fibroblasts and fetal calf
serum, which can contribute to rejection, infection
• Escharotomy
■ Indications: Full-thickness circumferential skin burns
that can cause ischemia to a distal extremity or part
from development of compartment syndrome
■ Symptoms
○ Dry, pale/whitish skin, nonblanching, insensate
○ “5 Ps”: pain, pallor, poikilothermia, paresthesia,
pulselessness
■ Perform at bedside as soon as the patient stabilized
■ Make incisions in the following orientation and with a
depth into the subcutaneous fat:
○ Arm/forearm: Longitudinal medial and lateral
○ Hand: Thenar/hypothenar, dorsal incisions 3×
between metacarpals, digital midlateral lines
○ Chest wall: Midline, + /− transverse
○ Thigh/leg: Longitudinal medial and lateral
○ Foot: Dorsal, medial, lateral
• Reconstruction of burn wounds can be performed through
skin grafts, pedicled flaps, and/or free flaps.
■ Delay free flaps for at least 6 weeks after debridement in
burn patients secondary to a hypercoagulable state; leads
to an increased risk of microvascular thrombosis.
Burn Complications
1. Postburn contracture
• Reduced motion secondary to scar contracture
■ Especially common around joints
Burn Management
1. Fluid resuscitation
• High-volume resuscitation is warranted in burns >20%
TBSA
• Parkland formula
■ (4 mL/kg) × (weight in kg) × (% TBSA) = total fluid to
be infused over 24-hour period.
■ Give half of this in the first 8 hours from the time
that the burn injury occurred (not from time of
presentation).
■ Give remaining half during the next 16 hours.
• Titrate fluid resuscitation to urine output.
■ Adults: 12 cc/kg/hr
■ Pediatrics: 1 cc/kg/hr
■ Urine output can be falsely elevated with elevated urine
glucose (glycosuria), thereby overestimating a patient’s
fluid status.
○ When following urine output in these patients, obtain
a urinalysis to check for the presence of glucose.
2. Supportive care
• Systemic prophylactic antibiotics and steroids have not
been shown to improve outcomes.
■ Antibiotics are indicated in the presence of cellulitis,
purulent drainage, and active infection.
○ Most common organisms are methicillin-resistant
Staphylococcus aureus, Pseudomonas, and Klebsiella.
○ Initial coverage using broad-spectrum antibiotics
(e.g., vancomycin and piperacillin-tazobactam)
followed by culture-directed therapy
• Children are at high risk for hypoglycemia in the first 24
hours following a burn due to limited hepatic glycogen
stores.
• Most common cause of death is bronchopneumonia.
3. Burn nutrition
• Large burns are associated with hypermetabolism.
• Elevated daily protein requirement for burn patients
■ Adults: 1 to 2 g/kg/day
■ Pediatrics: 2 to 3 g/kg/day
• Excessive carbohydrate/glucose administration can result in
excessive water and carbon monoxide generation, leading
to increasing edema and difficulty in weaning ventilator
support.
• Enteral feeding is preferred to parenteral nutrition.
4. Topical antimicrobial agents
• Silver nitrate
■ Advantages: Can provide antimicrobial coverage and
some hemostasis
■ Disadvantages: Must be frequently reapplied, stains
tissue black, can cause electrolyte disturbances and
methemoglobinemia
• Silver sulfadiazine (Silvadene)
■ Advantages: Broad-spectrum antimicrobial
coverage
■ Disadvantages: Forms a yellowish-gray pseudoeschar
that must be removed before reapplication, can cause

Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis
227
22
2. Initial management
• Rapid rewarming will decrease further tissue damage by
reversing vasoconstriction and preventing ice crystal
formation.
■ Preferred method is hot water bath at 40° C (104° F to
107° F) for 15 to 30 minutes.
■ Do not use a radiant heat source.
• Anti-inflammatory medications: NSAIDs or COX-2
inhibitors are beneficial for vasodilatory effects and
antiplatelet aggregation.
• Debride clear blisters that contain inflammatory mediators.
■ Do not debride hemorrhagic blisters because this can
promote dessication and necrosis.
• Allow time for tissue demarcation.
■ Early debridement and amputation only if there is
evidence of infection
■ Bone scans can assist with predicting the level of
amputation.
• In severe frostbite with absent pulses: Emergent
angiography and tissue plasminogen activator (tPA)
infusion.
■ Decreases rate of amputation if given within 24 hours
of injury
Stevens-Johnson Syndrome/Toxic
Epidermal Necrolysis
1. May begin 1 to 3 weeks after starting a specific medication
(e.g., phenobarbital, Dilantin, sulfa, allopurinol, various
antibiotics, NSAIDs).
2. Characterized by
• Epidermal sloughing in conjunction with mucosal
inflammation and ulceration
• Several days of nonspecific symptoms rapidly progressing
to exfoliating rash
3. Slough >10% TBSA is best treated in a burn center.
4. Treatment is supportive.
• Fluid resuscitation
• Burn wound care including early debridement and coverage
■ Often requires use of synthetic skin substitutes
○ For example, allograft, xenograft, Biobrane
Suggested Readings
Borghese, L., Masellis, A., Masellis, M., 2013. Chapter 19: Extremity burn
reconstruction. In: Neligan, P.C. (Ed.), Plastic Surgery, 3rd ed. Elsevier,
pp. 435–455.
Burns, J.L., Phillips, L.G., 2006. Chapter: Burns. In: McCarthy, J.G., Galiano,
R.D., Boutros, S.G. (Eds.), Current Therapy in Plastic Surgery. Saunders,
pp. 71–76.
French, L.E., Prins, C., 2012. Chapter 20: Erythema multiforme, Stevens-
Johnson syndrome and toxic epidermal necrolysis. In: Bolognnia, J.L., Jorizzo,
J.L., Schaffer, J.V. (Eds.), Dermatology, 3rd ed. Elsevier, pp. 319–333.
Herndon, D.N. (Ed.), 2012. Total Burn Care, 4th ed. Elsevier.
Klein, M.B., 2013. Chapter 22: Reconstructive burn surgery. In: Neligan, P.C.
(Ed.), Plastic Surgery, 3rd ed. Elsevier, pp. 500–510.
Spence, R.J., 2013. Chapter 21: Management of facial burns. In: Neligan, P.C.
(Ed.), Plastic Surgery, 3rd ed. Elsevier, pp. 468–499.
Steinstraesser, L., Al-Benna, S., 2013. Chapter 18: Acute management of burn/
electrical injuries. In: Neligan, P.C. (Ed.), Plastic Surgery, 3rd ed. Elsevier,
pp. 393–434.
• Can occur through extrinsic and intrinsic means
■ Extrinsic contractures: Tissue loss in distant sites leads to
distortion and limitations through tension.
■ Intrinsic contractures: Distortion and
limitations secondary to tissue loss within the
affected area
• Can prevent functional deficits from contractures through
splinting
■ Appropriate positions for postburn splinting
○ Neck: Slight extension
○ Shoulder: Fully abducted to 90 degrees
○ Elbow: Fully extended at 180 degrees
○ Wrist: Neutral or slightly extended
○ Hand: Intrinsic plus (“safe”) position
• Most common locations for postburn contracture release
(in order of frequency)
■ Neck
■ Axilla
■ Elbow
■ Trunk
■ Knee
■ Hand
2. Scar alopecia
• Occurs commonly from scalp burns
• Tissue expansion is the preferred method of treatment for
large areas.
■ Can reconstruct up to 50% of the scalp through tissue
expansion
3. Ectropion
• Most common complication following burns to the
eyelid
• If ectropion is related to skin deficiency only, preferred
treatment is contracture incision and placement of
full-thickness skin graft.
Electrical Injury
1. Occurs often to electricians and linemen or can occur
through lightning injury
2. Electrical injury is the primary cause of compartment
syndrome in the burn patient.
• Greatest risk for compartment syndrome with exposure to
>1000 V (reported incidence of ~30%)
3. Deep periosseus tissues are at highest risk for injury because
of the high heat capacity of bone.
4. If compartment syndrome is a concern, perform fasciotomy
in standard fashion.
• Missed compartment syndrome from electrical injury can
lead to a high rate of amputation.
Frostbite
1. Frostbite injury occurs through severe vasoconstriction and
intravascular ice crystal formation, leading to ischemia and
tissue necrosis.

Benign Skin Conditions
and Skin Disorders
Chapter
23 
Common Benign Skin Lesions
1. Keratocanthoma (see Figure 23.1)
• Benign tumor that behaves like a squamous cell carcinoma
(SCC) and is difficult to differentiate histologically
• Characterized by rapid growth with a central crater/keratin
plug
• Can spontaneously regress
• Treatment recommendation: Excision
• Risk factors: Chronic sun exposure, increasing age, male
gender, fair skin
• Characterized by a rough, erythematous papule with a
white to yellowish scale or plaque
• Treatment: Cryosurgery, photodynamic therapy, medical
treatment (e.g., topical or intralesional 5-fluorouracil
[5FU], topical imiquimod)
Figure 23.1.  Keratoacanthoma on the nose. (Reprinted from Neligan,
P.C. [Ed.], 2013. Plastic Surgery, vol. 1, 3rd ed. Elsevier, 707–742.)
A
Figure 23.2.  Actinic keratoses (AKs). A, Multiple AKs on the face
of an elderly woman with fair complexion, blue eyes, and moderate-
to-severe photodamage; the AKs vary in size from a few millimeters
to >1 cm. On the left forehead, the red nodule with slight scale-
crust represents a well-differentiated SCC.
2. Actinic keratosis (AK; also known as solar keratosis, senile
keratosis; see Figure 23.2)
• Extremely common skin lesions reportedly affecting up to
12% of the population
• Benign, premalignant lesion that can progress to SCC
■ Estimated rate of conversion to SCC is 13% to 20% over
10 years for lesions that are untreated.
• More than 80% occur on sun-exposed/sun-damaged areas
such as the head, neck, and upper extremities (e.g., dorsal
hand/forearm).

Common Benign Skin Lesions
229
23
B, Pink-colored, atrophic AK with minimal
scale on the forehead. C, Numerous hypertrophic AKs on the
bald scalp with hypopigmentation at sites of previous treatment.
D, Multiple large, hypertrophic AKs on the shin of an elderly
woman; note the thick scale. (Reprinted from Bolognia, J.L., Jorizzo, J.L.,
Schaffer, J.V. [Eds.], 2012. Dermatology, 3rd ed. Elsevier, 1773–1793.
B, Courtesy Iris Zalaudek, M.D.; D, Courtesy Jean L. Bolognia, M.D.)
B
C
D
Figure 23.2, cont’d. 
3. Seborrheic keratosis (SK; also known as a senile wart) (see
Figure 23.3)
• Benign skin growth originating from the basal and
squamous cells of the epidermis
• Characterized by well-circumscribed, waxy lesions that are
occasionally pigmented and have a “stuck-on” appearance
• Must be differentiated from AK, basal cell carcinoma
(BCC), and melanoma
• Sudden appearance of multiple SKs can be a marker of
internal malignancy.
• Treatment: Laser therapy, cryotherapy, electrosurgery, and
excision
Figure 23.3.  Example of a large seborrheic keratosis. Notice the
waxy, stuck-on appearance. (Reprinted from Neligan, P.C. [Ed.], 2013.
Plastic Surgery, vol. 1, 3rd ed. Elsevier, 707–742. Courtesy Lorenzo Cerroni,
M.D.)
4. Nevus sebaceous (“nevus sebaceous of Jadassohn”) (see
Figure 23.4)
• A benign hamartoma confined to the head and neck regions
• Can have malignant degeneration into BCC
• Characterized by a waxy, smooth or papillated, hairless,
salmon-colored patch or thickening on the scalp that
typically presents at birth
• Treatment: Excision
Figure 23.4.  Nevus sebaceous. A typical lesion on the scalp
of a prepubertal male. (Reprinted from Habif, T.P. [Ed.], 2010. Clinical
Dermatology: A Color Guide to Diagnosis and Therapy, 5th ed. Elsevier,
776–800.)

Benign Skin Conditions and Skin Disorders
230
5. Juvenile melanoma (“Spitz nevus”; see Figure 23.5)
• Benign pigmented skin lesion typically found in children or
young adults
• Difficult to distinguish from melanoma clinically and
histologically
• Characterized by a red, pink, or brown papule or nodule
with rapid growth
• Treatment: Complete excision with negative margins; if
any concern for melanoma, obtain appropriate margins
based on depth.
Figure 23.5.  Spitz nevus. Red, dome-shaped papule on the ear of
a child. (Reprinted from Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. [Eds.], 2012.
Dermatology, 3rd ed. Elsevier, 1851–1883. Courtesy Ronald P. Rapini, M.D.)
Figure 23.6.  Nevus of Ota (oculodermal melanocytosis). Unilateral,
bluish-gray discoloration of the face, which is either mottled or
confluent. There is also involvement of the sclera. (Reprinted from
Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. [Eds.], 2012. Dermatology, 3rd ed.
Elsevier, 1851–1883.)
6. Nevus of Ota (see Figure 23.6)
• Benign blue nevus that is present within the dermatome of
the first and second branches of the trigeminal nerve
• Most commonly affects Asian females
• Bimodal distribution: Early infancy and early adolescence
• Caused by dermal proliferation of melanocytes
• Treatment: Laser (e.g., Q-switched ruby, alexandrite);
dermabrasion, peels, or cryotherapy have also been used.
9. Blue nevus
• Also caused by dermal melanocytosis
• Characterized by a well-circumscribed, firm, blue-
pigmented nodule/papule
• Three subtypes: Common, cellular (can invade the
subcutaneous tissue), and combined (combined with a
pigmented nevus or a Spitz nevus)
• Treatment: Biopsy for suspicious lesions; simple excision
(see Figure 23.8)
10. Rosacea (“acne rosacea”; see Figure 23.9)
• Common, benign facial condition with both vascular
(flushing/blushing) and inflammatory (papules/pustules)
aspects
• Characterized by erythema, telangiectasia, flushing/
blushing, and papules and pustules on the face, especially
the forehead, cheeks, nose, and periorbita
7. Nevus of Ito
• Often considered a subtype of nevus of Ota
• Occurs in the acromiodeltoid region.
• Treatment: Similar to nevus of Ota
8. Mongolian spot (also known as congenital dermal
melanocytosis; see Figure 23.7)
• A common benign proliferative disorder that affects the
majority of Native American, Asian, and Hispanic infants
• Caused by entrapment of melanocytes within the dermis
during development
• Characterized by multiple bluish-gray spots or a large
patch covering the lumbosacral region
• Lesions typically disappear by 10 years of age.
• Treatment: Observation because most disappear without
treatment; lasers for severe cases.
Figure 23.7.  Dermal melanocytosis (Mongolian spots) in a child
with type-1 neurofibromatosis. Surrounding each café-au-lait macule
is an absence of the characteristic blue discoloration. (Reprinted
from Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. [Eds.], 2012. Dermatology, 3rd ed.
Elsevier, 1851–1883.)

Common Benign Skin Lesions
231
23
Figure 23.8.  Common blue nevus. A, A well-circumscribed, blue, dome-shaped papule. B, Histologically, heavily pigmented, spindle-shaped
melanocytes as well as melanophages are within the dermis; the melanocytes are denser than in dermal melanocytosis or nevus of Ota.
(Reprinted from Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. [Eds.], 2012. Dermatology, 3rd ed. Elsevier, 1851–1883.)
A
B
• Exacerbated by hot foods and drinks, alcohol, heat,
sunlight, and topical skin creams
• Treatment: Avoidance of exacerbating factors, sunscreen,
topical treatment of papules/pustules (e.g., Isotretinoin),
long-term oral antibiotics
• Chronic rosacea can lead to granuloma formation, deep
inflammation, and scarring with subsequent irreversible
hypertrophy (“granulomatous rosacea” or “rhinophyma”
when it involves the nose).
■ Treatment of rhinophyma generally consists of
tangential excision of involved skin, electrosurgery, and/
or carbon dioxide laser resurfacing.
Figure 23.9.  Rosacea and rhinophyma. Chronic rosacea of the
nose has caused irreversible hypertrophy (rhinophyma). (Reprinted
from Habif, T.P. [Ed.], 2010. Clinical Dermatology: A Color Guide to Diagnosis
and Therapy, 5th ed. Elsevier, 217–263.)
11. Chondrodermatitis nodularis helicis (see Figure 23.10)
• Uncommon lesion that frequently occurs on the lateral
surface of the helix and occasionally the antihelix in men
over the age of 40
• Characterized by a small, painful, dull red to white nodule
with a central scale and underlying erosion or ulceration
on the ear
• Treatment: Simple excision of the nodule with removal of
involved underlying cartilage to reduce recurrence
Figure 23.10.  Chondrodermatitis nodularis. Shown is an early
lesion with a central crust on the most common site, the apex of
the helix. (Reprinted from Habif, T.P. [Ed.], 2010. Clinical Dermatology: A Color
Guide to Diagnosis and Therapy, 5th ed. Elsevier, 776–800.)

Benign Skin Conditions and Skin Disorders
232
Common Benign Skin and Soft-Tissue Masses
1. Lipoma
• Most common benign soft-tissue tumor
• Many subtypes and often classified based on their location
(e.g., intramuscular)
• Patients can have multiple lipomas affecting the
extremities, head, neck, and trunk (“lipomatosis”).
• Has the potential for malignant degeneration to
liposarcoma
■ Rapid growth is a potential sign of liposarcoma.
• Characterized by a soft, spongy, mobile, well-
circumscribed, soft-tissue mass
• Computed tomography (CT) or magnetic resonance
imaging (MRI) may be helpful in diagnosis and surgical
planning.
• Treatment: Complete surgical excision with the capsule to
reduce recurrence
2. Epidermoid cyst (also known as epidermal cyst)
• Characterized by a smooth, dome-shaped, mobile,
subcutaneous, cystic mass, often with a central punctum
• Frequently rupture spontaneously or with external
pressure
• May become inflamed and/or infected
• Treatment: Simple excision, with care to remove the entire
cyst to minimize the risk for recurrence
3. Dermoid cyst
• Congenital subcutaneous cyst that develops along
embryonic fusion lines
• Most commonly occurs on the head and neck (e.g., lateral
brow, glabella, scalp).
• Characterized by a firm, solitary, soft-tissue mass
• Midline dermoid cysts may have intracranial extension;
investigate with CT or MRI before excision.
■ CT findings can include splaying of the nasal bones as
well as defects in the foramen cecum and crista galli.
• Treatment: Simple excision of the entire cyst; if intracranial
involvement is detected, neurosurgical consultation and
craniotomy is required.
4. Acrochordon (“skin tag”)
• Common benign fibroma found in an estimated 25% of
adults
• Most frequently found in the axilla, neck, and inguinal
region of obese patients
• Characterized by small, pedunculated, brownish-red, or
normal skin color superficial skin lesions with a broad-to-
narrow stalk
• Treatment: Scissor excision, simple excision, cryotherapy,
electrodessication
5. Pilomatricoma (also known as a pilomatrixoma or calcifying
epithelioma of Malherbe; see Figure 23.11)
• Benign, firm, cystic nodule that typically occurs in the head
and neck of children
• Calcification can be detected on radiographic studies (e.g.,
ultrasound, X ray, CT, and MRI).
• Treatment: Complete excision to prevent recurrence
6. Trichilemmal cyst
• Arises from the outer root sheath of the hair follicle
• Up to 70% of patients have multiple cysts.
• Characterized by a subcutaneous cyst within the hair-
bearing portion of the scalp
• Treatment: Complete excision
7. Dermatofibroma (also known as fibrous histiocytoma; see
Figure 23.12)
• Caused by the proliferation of fibroblasts, histiocytes, and
vascular endothelial cells within the dermis
• They may not be true tumors but, instead, a reaction to
trauma, viral infection, or insect bites.
• Typically asymptomatic but may present with pruritis and/
or pain
• Characterized by a small, firm, pink-brown nodule on the
extremities, particularly the lower extremity, that retracts
beneath the skin surface with attempts to compress or
elevate it with the thumb and index finger (“retraction
sign” or “Fitzpatrick sign”)
• Treatment: May be observed; however, simple excision is
often performed for symptoms, diagnostic uncertainty, or
cosmetic purposes
Figure 23.11.  Pilomatricoma on the upper eyelid. (Reprinted from
Neligan, P.C. [Ed.], 2013. Plastic Surgery, vol. 1, 3rd ed. Elsevier, 707–742.)
Figure 23.12.  Dermatofibroma. (Reprinted from Neligan, P.C. [Ed.], 2013.
Plastic Surgery, vol. 1, 3rd ed. Elsevier, 707–742.)

Other Skin Disorders
233
23
10. Desmoid tumor
• Characterized by large, well-circumscribed, deep masses
that arise from the muscular aponeurosis
• Most commonly occur on the abdominal wall
• Rarely metastasize, although they can be locally aggressive
with a high recurrence rate
• Diagnosis is often made by clinical exam and CT
or MRI.
• Treatment: Wide local excision with margin clearance,
radiation, and hormonal therapy (e.g., Tamoxifen)
Other Skin Disorders
1. Genetic skin disorders (also known as “genodermatoses”) (see
Table 23.1)
2. Xeroderma pigmentosum (XP)
• Rare, autosomal, recessive skin disorder
• Caused by defective DNA repair mechanisms within the
nucleotide excision repair (NER) pathway associated with
ultraviolet (UV)- light-induced damage
• Characterized by severe photosensitivity to UV radiation
including severe burns and blistering
• Significant risk of skin cancer, often developing within the
first decade of life
8. Neurofibroma
• Benign tumor of the peripheral nerve sheath that arises
from Schwann cells
• Typically found in patients with neurofibromatosis (types 1
and 2)
• Characterized by multiple small, pink or skin colored,
raised nodules
• Can undergo malignant degeneration
• Treatment: Excision, CO2 laser treatment, adjuvant
chemotherapy, and radiation in malignant cases
9. Schwannoma (also known as “neurilemmoma”)
• Benign tumor of the peripheral nerve sheath that arises
from Schwann cells
• Most commonly occurs in the deep soft tissues, along the
main nerve trunks of the extremities, especially the flexor
surface of the arms, wrists, and knees
• Characterized by a solitary, pale pink, or yellowish deep
nodule that may be firm or soft and occasionally painful
■ Often, the mass is mobile in the transverse plane and not
the longitudinal plane
• MRI is useful in diagnosis; displays a well-encapsulated
“egg-shaped” tumor within the nerve sheath that does not
disrupt the nerve fascicles.
• Treatment: Surgical excision
Table 23.1  Key Features of Genodermatoses
SYNDROME
INHERITANCE
GENETIC
MUTATION
NONCUTANEOUS FEATURES
CUTANEOUS FEATURES
Gardner syndrome
(familial adenomatous
polyposis)
AD
APC
GI polyps and adenocarcinoma,
osteomas, supernumerary or
unerupted teeth
Epidermoid cysts, lipomas, Gardner
fibroma, desmoid tumor
Gorlin syndrome
(nevoid BCC
syndrome)
AD
PTCH
Odontogenic keratocysts,
medulloblastoma, calcification of the
falx, bifid ribs, ovarian fibromas,
macrocephaly, frontal bossing, pectus
deformity
Palmar pits, BCCs
Multiple endocrine
neoplasia, type 1
(Wermer syndrome)
AD
MEN1
Endocrine tumors including
parathyroid, pituitary, adrenocortical,
gastrinoma
Multiple angiofibromas, collagenomas,
lipomas
Muir-Torre syndrome
AD
MSH2 and MLH1
Colorectal, breast, genitourinary
cancers
Keratoacanthomas, sebaceous
adenoma, sebaceous epithelioma,
sebaceous carcinoma
Neurofibromatosis
(von Recklinghausen
disease)
AD
Neurofibromin
Lisch nodules of the iris, optic nerve
glioma, sphenoid dysplasia
Café-au-lait macules, axillary freckling,
numerous neurofibromas (often
including plexiform neurofibroma)
Porphyria cutanea
tarda
AD
Uroporphyrinogen
decarboxylase
Liver function abnormalities
Blisters, erosions, milia on the dorsal
hands and photoexposed sites,
hypertrichosis, hyperpigmentation,
sclerodermoid plaques
Tuberous sclerosis
AD
Tuberin (TSC2)
and hamartin
(TSC1)
Retinal nodular hamartoma, cortical
tuber, subependymal nodule,
subependymal giant cell astrocytoma,
epilepsy, mental retardation, cardiac
rhabdomyoma, lymphangiomyomatosis,
renal angiomyolipoma
Adenoma sebaceum (angiofibromas),
periungual fibromas, shagreen patch,
hypopigmented ash leaf macules
Reprinted from Elston, D.M., Ferringer, T., Ko, C.J., et al. (Eds.), 2014. Dermatopathology, 2nd ed. Elsevier, 208–212.
AD, Autosomal dominant; APC, adenomatous polyposis coli; AR, autosomal recessive; BCC, basal cell carcinoma; GI, gastrointestinal;
MEN1, multiple endocrine neoplasia 1; MLH1, mutL homolog 1; MSH2, human mutS homolog 2; PTCH, patched.

Benign Skin Conditions and Skin Disorders
234
• Diagnosis: Largely clinical, although DNA testing is
available; suspect XP in children <2 years old who present
with freckling on sun-exposed skin and severe sunburn
after minimal sun exposure.
• Treatment: UV protection (e.g., sunscreen, skin cover with
clothing/hats, sunglasses, UV protection over windows),
regular skin exams, early excision of skin cancers
3. Calcifying skin disorders (also known as “calcinosis cutis”)
• Characterized by deposition of insoluble calcium salts
within the skin and subcutaneous tissues
• Generally divided into four broad categories
■ Dystrophic: Occurs in the setting of localized tissue
damage with normal metabolic calcium regulation
■ Metastatic: Occurs in the setting of dysfunction in
calcium regulation (e.g., renal failure)
■ Iatrogenic: Calcification related to medial therapy or
testing
■ Idiopathic: Calcification of unknown etiology
• CREST syndrome (calcification, Raynaud’s phenomenon,
esophageal dysmotility, sclerodactyly, telangiectasia)
■ A form of dystrophic calcinosis cutis related to the
autoimmune disease scleroderma
■ Patients typically present with small calcium deposits
over bony prominences and tendons and/or on the
elbows, knees, buttocks, shoulders, and hands.
■ These calcium deposits are painful and can extrude a
white chalky material and ulcerate.
■ Treatment: Low-calcium and -phosphate diet, aluminum
hydroxide, and bisphosphonates; surgical excision of
deposits is reserved for localized painful masses that
limit function.
• Calciphylaxis
■ A form of metastatic calcinosis cutis related to renal
failure that occurs secondary to progressive vascular
calcification with ischemic necrosis of the skin and soft
tissues
■ Patients typically present with multiple, extremely
painful skin lesions that can be violaceous, ulcerated, or
necrotic.
■ High mortality and poor prognosis, with death often
secondary to gangrene and sepsis
■ Risk factors: Female gender, obesity, poor nutritional
status, diabetes
■ Treatment: Low-calcium and -phosphate diet, low-
calcium dialysis, phosphate binders, parathyroidectomy,
and aggressive local wound care; surgical excision/
debridement is generally not recommended.
Suggested Readings
Bolognia, J.L., Schaffer, J.V., Duncan, K.O., et al. (Eds.), 2014. Chapter 95:
Common soft tissue tumors/proliferations. In: Dermatology Essentials. Elsevier,
pp. 934–941.
Fairley, J.A., 2012. Chapter 50: Calcifying and ossifying disorders of the skin.
In: Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. (Eds.), Dermatology, 3rd ed.
Elsevier, pp. 729–736.
Ferringer, T., 2014. Chapter 12: Genodermatoses. In: Elston, D.M., Ferringer,
T., Ko, C.J., et al. (Eds.), Dermatopathology, 2nd ed. Elsevier, pp. 208–212.
Habif, T.P., 2010. Chapter 20: Benign skin tumors. In: Habif, T.P. (Ed.),
Clinical Dermatology: A Color Guide to Diagnosis and Therapy, 5th ed.
Mosby Elsevier, pp. 776–800.
Habif, T.P. (Ed.), 2010. Chapter 7: Acne, rosacea, and related disorders. In:
Clinical Dermatology: A Color Guide to Diagnosis and Therapy. 5th ed.
Elsevier, pp. 217–263.
Habif, T.P., Campbell, J.L., Chapman, M.S., et al. (Eds.), 2011. Chapter 16:
Benign skin tumors. In: Skin Disease. 3rd ed. Elsevier, pp. 424–463.
James, W.D., Berger, T.H., Elston, D.M. (Eds.), 2011. Chapter 28: Dermal
and subcutaneous tumors. In: Andrews’ Disease of the Skin: Clinical
Dermatology. 11th ed. Elsevier, pp. 574–619.
McMasters, K.M., Uris, M.M., 2012. Chapter 32: Melanoma and cutaneous
malignancies. In: Townsend, C.M., Beauchamp, R.D., Evers, B.M., et al.
(Eds.), Sabiston Textbook of Surgery, 19th ed. Elsevier, pp. 742–767.
Ogawa, R., 2013. Chapter 30: Benign and malignant nonmelanocytic tumors
of the skin and soft tissue. In: Neligan, P.C. (Ed.), Plastic Surgery, vol. 1, 3rd
ed. Elsevier, pp. 707–742.
Rabinovitz, H.S., Barnhill, R.L., 2012. Chapter 112: Benign melanocytic
neoplasms. In: Bolognia, J.L., Jorizzo, J.L., Schaffer, J.V. (Eds.), Dermatology,
3rd ed. Elsevier, pp. 1851–1883.
Soyer, H.P., Rigel, D.S., Wurm, E.M.T., 2012. Chapter 108: Actinic keratosis,
basal cell carcinoma and squamous cell carcinoma. In: Bolognia, J.L.,
Jorizzo, J.L., Schaffer, J.V. (Eds.), Dermatology, 3rd ed. Elsevier,
pp. 1773–1793.
Tamura, D., Kraemer, K.H., DiGiovanna, J.J., 2014. Chapter 249: Xeroderma
pigmentosum. In: Lebwohl, M.G., Heymann, W.R., Berth-Jones, J., et al.
(Eds.), Treatment of Skin Disease: Comprehensive Therapeutic Strategies,
4th ed. Elsevier, pp. 808–811.

Malignant Skin Conditions
Chapter
24 
Melanoma
1. Incidence of melanoma is increasing faster than any other
cancer in the United States.
2. Melanoma is most commonly located in the skin but can
occur in the oral mucosa, nasopharynx, esophagus, vagina,
and rectum.
3. Risk factors for melanoma
• Fair skin (e.g., Fitzpatrick I/II), blue eyes, blond/red hair
• Chronic exposure to ultraviolet (UV) radiation (e.g., UVA,
UVB, tanning salons)
• History of sunburns, freckles
• Family history of melanoma (e.g., familial, atypical,
multiple mole-melanoma syndromes; B-K mole syndrome)
• Immunosuppression
• Presence of multiple, giant congenital, or dysplastic nevi
• Xeroderma pigmentosa, BRCA2 mutations
4. The most important factor related to outcome is the depth of
the primary lesion.
• Regional lymph node metastasis is also associated with
poorer prognosis.
5. Diagnosis of melanoma is based on histologic examination;
however, clinical suspicion of lesions that follow the
“ABCDE” guidelines of the American Cancer Society (ACS)
should guide biopsy decisions (see Figure 24.1).
• Asymmetry of the lesion
• Border irregularity
• Color changes or variation
• Diameter >6 mm
• Evolution of the lesion (e.g., change in size, shape,
symptoms, surface characteristics, and/or color)
%
$
Figure 24.1.  Melanoma with characteristic changes. A, Asymmetry of lesion shape. B, Border irregularity.
Continued

Malignant Skin Conditions
236
• “Ugly duckling sign”: Unique appearance of the nevus
relative to the patient’s other nevi
6. Melanoma staging relies on the tumor (T), node (N), and
metastases (M) system established by the ACS.
Table 24.1  Melanoma TNM Classification
TUMOR (T) CLASSIFICATION
TUMOR THICKNESS (BRESLOW DEPTH)
MITOTIC RATE/ULCERATION STATUS
Tis
In situ
None
T1
≤1.0 mm or less
a: Mitosis <1/mm2, no ulceration
b: Mitosis ≥1/mm2, or ulceration
T2
1.01 to 2.0 mm
a: No ulceration
b: Ulceration
T3
2.01 to 4.0 mm
a: No ulceration
b: Ulceration
T4
>4.0 mm
a: No ulceration
b: Ulceration
NODAL (N) CLASSIFICATION
NUMBER OF METASTATIC NODES
NODAL METASTATIC MASS
N1
1
a: Micrometastasis
b: Macrometastasis
N2
2 to 3
a: Micrometastasis
b: Macrometastasis
c: In-transit metastases/satellite lesions
without metastatic nodes
N3
≥4
Matted nodes, in-transit metastases/satellite
lesions with metastatic nodes
METASTASES (M) CLASSIFICATION
SITE OF METASTASES
SERUM LDH LEVEL
M0
None
Normal
M1a
Skin, subcutaneous, distant lymph nodes
Normal
M1b
Lung
Normal
M1c
All other visceral sites, distant metastasis
Normal, elevated
Adapted from How Is Melanoma Skin Cancer Staged? © 2015 American Cancer Society, Inc. All rights reserved.
LDH, Lactase dehydrogenase.
C, Color variegation. D, Diameter >6 mm. (Reprinted from Neligan, P.C. [Ed.], 2013. Plastic Surgery, vol. 1, 3rd ed. Elsevier,
743–785.)
&
'
Figure 24.1, cont’d.

Melanoma
237
24
7. Histologic subtypes/growth patterns
• Superficial spreading
■ Most common pattern (50% to 80%)
■ Radial growth followed by vertical growth phase
• Lentigo maligna melanoma
■ Typically located on sun-exposed areas and grows in a
horizontal pattern
■ Develops within a preexisting lentigo maligna
(“Hutchinson freckle”—flat, brown macule with variable
shades of pigmentation located on sun-exposed areas in
older adults; considered to be melanoma in situ)
• Nodular
■ Second most common pattern (20% to 30%)
■ Early vertical growth phase
• Acral lentiginous
■ Develops on the palms, soles, and subungual region
■ More common in dark-skinned individuals
■ Has the lowest 5-year survival of all melanoma (10% to
20%) and highest recurrence
• Amelanotic and desmoplastic
■ Rare histiologic forms
■ Desmoplastic melanomas are locally aggressive but rarely
metastasize.
8. Biopsy recommendations
• In small cutaneous lesions, excisional biopsy with 1- to
2-mm margins is recommended to establish the Breslow
depth of the lesion
• In larger lesions, or lesions with functional or cosmetic
concerns prohibiting complete excision, an incisional
biopsy (e.g., punch biopsy) can be performed.
• Shave biopsy is generally not recommended unless it is
performed for a suspicious lesion on the nail bed that is
concerning for a subungual melanoma.
Table 24.2  Melanoma Staging
STAGE
T
N
M
0
Tis
N0
M0
IA
T1a
N0
M0
IB
T1b or T2a
N0
M0
IIA
T2b or T3a
N0
M0
IIB
T3b or T4a
N0
M0
IIC
T4b
N0
M0
IIIA
T1a-T4a
N1a or N2a
M0
IIIB
T1b-T4b
N1a or N2a
M0
T1a-T4a
N1b or N2b
M0
T1a-T4a
N2c
M0
IIIC
T1b-T4b
N1b or N2b
M0
T1b-T4b
N2c
M0
Any T
N3
M0
IV
Any T
Any N
M1 (a, b, or c)
Adapted from How Is Melanoma Skin Cancer Staged?
© 2015 American Cancer Society, Inc. All rights reserved.

9. Sentinel lymph node biopsy indications
• Breslow depth >0.76 mm without clinically palpable nodes
• Melanoma of any depth with the presence of ulceration or
high mitotic rate (e.g., >1 mitosis per high-powered field)
• Elective or complete lymph node dissection is generally
performed for patients with palpable lymphadenopathy on
clinical exam or positive sentinel nodes, respectively.
10. Additional workup (see Box 24.1)
Reprinted from Ariyan, S., Berger, A., 2013. Chapter 31: Melanoma.
In: Neligan, P.C. (Ed.), Plastic Surgery, vol. 1, 3rd ed. Elsevier,
743–785.
BOX 24.1  STAGING EVALUATION: TESTS
RECOMMENDED FOR DETERMINATION
OF PRESENCE AND EXTENT
OF TUMOR SPREAD
Primary tumor (no clinical evidence of other
involvement)
Physical examination
Chest radiography
Liver function tests
Lymphoscintigraphy to detect sites of sentinel nodes
(if primary tumor ≥1-mm thick)
Local and regional disease (in-transit lesions or nodal
involvement)
Physical examination
Liver function tests
Computed tomography (CT) scans
Chest and abdomen (to examine lungs and liver)
Pelvis if tumor involves lower extremities
Neck if tumor involves the head and neck
Lymphoscintigraphy to detect sites of sentinel nodes
Additional scans as indicated by clinical signs or
symptoms
Distant organ metastases
Physical examination
Liver function tests and serum lactate dehydrogenase
level
CT scans, as indicated above
Magnetic resonance imaging scans if required to detect
extent of soft-tissue invasion
Positron emission tomography scans to detect extent of
tumor involvement of vital organs (lung, liver, brain)
11. Wide local excision: The mainstay of initial treatment to
decrease the rate of local recurrence (reported to occur in
3% to 20%)
• General recommendations for wide local excision margins
■ Melanoma in situ: 0.5-mm margins
■ Melanoma <1 mm: 1 cm
■ Melanoma 1 to 2 mm: 1 to 2 cm
■ Melanoma 2 to 4 mm: 2 cm
■ Melanoma >4 mm: 2 to 3 cm
• If primary closure of the defect cannot be achieved, delay
reconstruction until permanent pathology preparations
confirming negative margins are finalized.
12. Additional treatment recommendations
• Lentigo maligna: Treat as melanoma in situ
• Subungual melanoma