Phẫu Thuật Tái Tạo Bàn Tay Và Chi Trên

Hand and Upper Extremity Reconstruction
204
TABLE 14.4 Ulnar nerve palsy
Problem
Options for treatment
Clawing deformity
and asynchronous
motion
Lumbrical bar splint
MP volar capsulorrhaphy (Zancolli)
Dorsal bone block
Pulley advancement
Tendon grafts from dorsal carpal ligaments
to lateral bands (Fowler tenodesis)
Weakness of grip,
clawing, and
asynchronous
motion
FDS to intrinsic apparatus (Stiles–Bunnell
transfer)
FDS lasso to annular pulley (Zancolli)
FCR to intrinsic apparatus
ECRB with plantaris graft to lateral bands
(Brand or palmaris longus)
Weakness of
thumb adduction
ECRB to adductor pollicis
FDS ring to adductor pollicis
EIP to fi rst dorsal interosseus
Accessory APL to fi rst dorsal interosseus
les tendon, with careful attention to avoid the sural nerve.
The plantaris tendon is identifi ed, released distally, and
tagged with a 3/0 braided, non-absorbable suture for han-
dling. A closed tendon stripper is run along the tendon and
the plantaris is harvested. The plantaris graft is used for
two portions of the operation: to augment the adductor-
plasty and to use for clawing control. A portion of the graft
is cut at a length adequate to span the APL to the fi rst dorsal
interosseous tendon. This tendon segment is saved in a wet
sponge.
The remaining plantaris tendon is used as a four-tailed
graft. The central 3 cm segment will be used as an anchor
to the ECRB and preserved. The ends of the tendon are split
longitudinally through the midline to create four ‘tails’ that
will be individually sutured to the interossei distally (Fig.
14.10).
The proximal portions of the interossei are excised
through the incision at the metacarpal bases and a radial
incision is made at the junction of the glabrous and non-
glabrous skin along each fi nger. A tail of the plantaris graft
is passed through the interspace, volar to the deep trans-
verse metacarpal ligament, and then attached to the radial
lateral band using 4/0 Ethibond suture in a Pulvertaft weave
at the level of the transverse fi bers. If a Pulvertaft weave is
not possible because of limited graft excursion or tendon
thickness, they may be sutured end to end or side to side
if necessary. The proximal end of the graft is passed sub-
cutaneously into the proximal wound where the ECRB
tendon lies, and the central, unsplit portion is secured to
the ECRB (Fig. 14.10).
A 3 cm incision centered along the ulnar thumb MP
joint is made overlying the adductor aponeurosis. An inci-
sion in line with the distal palmar crease is made overlying
the ring metacarpal. The ring superfi cialis is identifi ed and
transected as the ring fi nger is held fl exed. A subcutaneous
tunnel is made by passing a curved hemostat from the
thumb wound over the palmar fascia and exiting through
the volar ring fi nger wound. The superfi cialis tendon is
drawn through the subcutaneous tunnel and secured to the
tendon of the adductor pollicis using a 3/0 Ethibond suture
weave (Fig. 14.11A).
An incision is made at the base of the radial side of the
wrist at the junction of the glabrous and non-glabrous skin.
The accessory APL is identifi ed and transected at its inser-
tion at the base of the trapezium or scaphoid. This acces-
sory APL slip is withdrawn proximally and the plantaris
graft is interwoven with it. A subcutaneous tunnel is created
from the dorsoradial index fi nger wound to the proximal
wound. The APL–tendon graft complex is then drawn into
the distal wound and interwoven into the tendon of the fi rst
dorsal interosseous tendon (Fig. 14.11B).
After wound closure and dressing, a splint is applied
with the wrist in 30º of dorsifl exion and the MP joints in
40º of fl exion. A separate thumb spica is applied to hold
the thumb at full opposition. The splint is maintained
postoperatively for 4 weeks, after which time a lumbrical
bar splint with a thumb spica extension is used for protec-
tion, and active range of motion is initiated.
hyperextension; tenodesis linking MP and PIP extension;
and tenodesis linking MP fl exion and PIP extension with
wrist fl exion.
The effective function of tendon transfers depends on
the structure to which the transfer is attached. When the
tenodesis extends from a point distal to the wrist to the
proximal phalanx, MP hyperextension occurs. When
the tenodesis extends from a point distal to the wrist and
is attached to the lateral band, linked MP and PIP extension
occurs. When the tenodesis extends from a point proximal
to the wrist and extends to the proximal phalanx, linked
MP fl exion and PIP extension is produced.1
Numerous authors have espoused different methods to
restore intrinsic function.18,19,24–27 Although each patient
should be considered individually, our favored techniques
include transfer of the FDS ring to the adductor pollicis,
accessory abductor pollicis longus to the fi rst dorsal interos-
seous, and transfer of the ECRB to address clawing and
improve pinch strength.
Operative technique
Brand transfer and FDS/APL for power pinch
A transverse incision proximal to the dorsal extensor reti-
naculum extending from the fi rst dorsal compartment to
the third dorsal compartment is made. The ECRB attach-
ment to the third metacarpal and accessory slip of the
abductor pollicis longus (APL) is identifi ed. The accessory
APL is usually the most volar in the cluster of tendons in
the fi rst dorsal compartment. A second, 5 cm transverse
incision is made at the base of the intermetacarpal spaces.
The ECRB attachment is identifi ed and the ECRB is released
and drawn into the proximal wound.
A 5 cm incision is made on the lateral border of the
ankle centered between the lateral malleolus and the Achil-

Tendon Transfers
205
FIGURE 14.10 Brand transfer. A Harvest of ECRB from base of third metacarpal. B After harvest of the plantaris tendon, the ends are split to
form four tails. C The plantaris tendon is attached to the end of the ECRB. D Each limb is passed underneath the transverse metatarsal ligament
on the radial side of each digit and E attached to the lateral band.
Incision to release
ECRB from base
of metacarpal
Incision to harvest
ECRB
Each limb of plantaris
graft is passed through
intermetatarsal
space
Plantaris graft
Plantaris graft sutured
to end of ECRB; passed
through substance of ECRB
Each limb of plantaris
graft sutured to radial
lateral band
Plantaris graft passed palmar to
transverse metacarpal ligament
A
B
D
E
C

Hand and Upper Extremity Reconstruction
206
FIGURE 14.11 Transfers for power pinch. A The FDS ring is transferred over the palmar fascia and inserted into the adductor pollicis.
B Accessory dorsal interosseus and a graft is transferred into the fi rst dorsal interosseus.
F
G
FIGURE 14.10, cont’d F The plantaris tendon has been harvested with a tendon stripper. G The tendon graft is split into four strips to connect
the extensor carpi radialis brevis with the radial lateral band of index through small fi ngers. Prepared extensor indicis pollicis and fl exor
digitorum superfi cial ring transfers are also seen.
FDS ring tunnelled
over palmar fascia
Inserted into
adductor pollicis
Plantaris graft
Accessory APL
Woven into first
dorsal interosseus
muscle
A
B

Tendon Transfers
207
Optimizing outcomes
●
Tensioning of the four-tailed graft is diffi cult and should
be performed with the wrist in neutral. The ring and little
fi ngers should fl ex to approximately 40º, whereas the
index and middle fi ngers should fl ex to approximately
30º.
●
The superfi cialis tendon should be sutured with the thumb
MP joint fl exed and fully adducted. With wrist dorsifl exion,
the thumb should adduct against the palm.
●
The palmaris graft from the accessory APL should be sutured
to the tendon of the fi rst dorsal interosseous tendon with
the index fi nger fully adducted. When the wrist is ulnarly
deviated, the index fi nger should abduct.
Complications
The Andre-Thomas sign describes fl exion of the wrist with
attempted IP extension.28 When the ECRB is transferred
there is a loss of wrist extensor power. Subsequently, if
there is persistent asynchrony of digital fl exion, the wrist
fl exion that is seen with the Andre-Thomas sign may actu-
ally be exacerbated as the patient continues to try to com-
pensate. There is the potential for multiple tendon grafts
to be needed if one plantaris tendon is insuffi cient.
An accessory APL is present in 90% of the population;
however, in the event that the APL is not present, the
surgeon should be prepared to perform an EIP transfer if
needed. Finally, with superfi cialis harvest for opponens-
plasty, PIP fl exion deformity or hyperextension may
occur.
CONCLUSIONS
It is important for a hand surgeon to be familiar with
tendon transfers. Over the past century, the diverse tech-
niques have converged into a set of reliable, reproducible
transfers that can be applied to a majority of the functional
defi cits encountered in practice. Knowledge of the various
transfer options can be useful in complex or unusual cir-
cumstances and combined nerve palsies.
REFERENCES
1. Smith RJ. Tendon transfers of the hand and forearm. Boston:
Little, Brown, 1987.
2. von Recklinghausen H. Gliedermechanik und
Lahmungsprosthesen. Berlin: Springer Verlag, 1920.
3. Brand PW. Clinical mechanics of the hand. St Louis: CV Mosby,
1985; 23.
4. Smith RJ. Indications for tendon transfers to the hand. Hand Clin
1986; 2: 235–237.
5. Pulvertaft RG. Tendon grafts for fl exor tendon injuries in
the fi ngers and thumb. J Bone Joint Surg 1956; 38B: 175–194.
6. Starr CL. Army experiences with tendon transference. J Bone Joint
Surg 1922; 20: 3–21.
7. Zachary RB. Tendon transplantation for radial paralysis. Br J Surg
1946; 33:358–364.
8. Chuinard RG, Boyes JH, Stark HH, et al. Tendon transfers for
radial nerve palsy: Use of superfi cialis tendons for digital
extension. J Hand Surg 1978; 3: 560–570.
9. Bunnell S. Opposition of the thumb. J Bone Joint Surg 1938;
20:269–284.
10. Sebastin MJ, Puhaindran ME, Lim AY, et al. The prevalence
of absence of the palmaris longus – a study in a Chinese
population and a review of the literature. J Hand Surg 2003; 30:
525–527.
11. Troha F, Baibak GJ, Kelleher JC. Frequency of the palmaris longus
tendon in North American Caucasians. Ann Plast Surg 1990; 25:
477–478.
12. Wissinger HA, Singsen EG. Abductor digiti quinti opponensplasty.
J Bone Joint Surg 1977; 59A: 895–898.
13. Burkhalter W, Christensen RC, Brown P. Estensor indicis proprius
opponensplasty. J Bone Joint Surg 1973; 55A: 725–732.
14. Noorda RJP, Havge JJ, deGroot PJM, et al. Index fi nger extension
and strength after extensor indicis proprius transfer. J Hand Surg
1994; 19A: 844–849.
15. Browne EZ, Teavue MA, Snyder CC. Prevention of extensor lag
after indicis proprius tendon transfer. J Hand Surg 1979; 4:
168–172.
16. Riordan DC. Surgery of the paralytic hand. Instructional Course
Lectures 1959; 16: 79–90.
17. Cooney WP, Linscheid RL, An KN. Opposition of the thumb: An
anatomic and biomechanical study of tendon transfers. J Hand
Surg 1984; 9A: 777–786.
18. Cawrse MH, Sammut D. A modifi cation in technique of abductor
digiti minimi (Huber) opponensplasty. J Hand Surg 2003; 28B:
233–237.
19. Froment J. La paralysie de l’adducteur du pouce et le signe de le
prehension. Rev Neurol (Paris) 1914; 28.
20. Jeanne M. La deformation du pouce dans la paralysie cubitale. Bull
Mem Soc Chir 1915; 41: 703.
21. Goldfarb CA, Stern PJ. Low ulnar nerve palsy. J Am Soc Surg
Hand 2003; 3: 14–26.
22. Smith RJ. Extensor carpi radialis brevis tendon transfer for
thumb adduction – A study of power pinch. J Hand Surg 1983; 8:
4–15.
23. Hamlin C, Littler JW. Restoration of power pinch. J Hand Surg
1980; 5: 396–401.
24. Burkhalter WE, Strait JL. Metacarpophalangeal fl exor replacement
for intrinsic paralysis. J Bone Joint Surg 1973; 55A:1667–1676.
25. Brand PW. Tendon grafting. J Bone Joint Surg 1961; 43B:
444–453.
26. Zancolli EA. Structural and dynamic bases of hand surgery.
Philadelphia: JB Lippincott, 1968.
27. Leddy JP, Stark HH, Ashworth CR, et al. Capsulodesis and pulley
advancement for the correction of claw-fi nger deformity. J Bone
Joint Surg 54A: 1465–1471.
28. Andre-Thomas T. Le tonus du poignet dans la paralysie du nerf
cubital. Paris Med 1917; 25: 473.

209
C H A P T E R
15
Techniques for Treating Finger Infections
Loree Kalliainen
INTRODUCTION
Finger infections are common. The incidence is probably
underestimated because many are treated using basic wound
care by patients and by physicians other than hand sur-
geons. This chapter focuses on the evaluation and manage-
ment of serious acute fi nger infections that involve several
tissue layers and spread along planes or invade into joint
spaces. The etiology of fi nger infections is most commonly
related to penetrating injuries (e.g., human or animal bites,
deep space penetration with contaminated items, or retained
foreign objects), but hand and fi nger infections may also be
associated with crush injuries, abrasions, hematogenous
spread, or systemic conditions such as tuberculosis, dia-
betes, and renal transplantation.1–7 The introduction of
contaminated agents into a closed space, combined with
inadequate cleansing, leads to an ideal opportunity for the
development of infection. For patients with inadequate host
defenses, the risk of infection is likely to increase.7–9 Up
to 80% of fi nger infections are caused by Staphylococcus
aureus.10–15 If the patient is immunocompromised, the
infections are more likely to be polymicrobial, and chronic
infections may be due to mycobacteria or other uncommon
organisms.1,4,7,16 The outcome of fi nger infections is poor
when treatment is delayed.1,7,13,17–21
INDICATIONS AND CONTRAINDICATIONS
In the author’s experience, by the time a hand surgery
consultation is requested for a fi nger infection, that infec-
tion can rarely be managed by oral antibiotics alone. A brief
course of intravenous antibiotics may occasionally be suc-
cessful, but operative intervention should not be delayed if
the infection does not respond within 12–24 hours of intra-
venous antibiotic treatment. Drainage of infection should
be performed if there is a deep abscess or rapidly spreading
infection, concern for septic arthritis, or pyogenic fl exor
tenosynovitis. The threshold for surgery may also be lowered
for patients with peripheral neuropathy who have a dimin-
ished pain response to infection, immunosuppression, or
who are unable to participate in a physical examination
because of poor mental status or advanced age.
The most common organism to cause hand infections
is Staphylococcus aureus, and, alarmingly, the incidence
of methicillin-resistant S. aureus (MRSA) has increased to
40–50% of community-acquired Staphylococcus infections.
Vancomycin, gentamicin, and trimethoprim/sulfamethoxa-
zole currently have a high degree of effi cacy in the treat-
ment of MRSA, but individual surgeons should consult
their institution’s annual antimicrobial profi le.10,11 Other
common organisms causing fi nger infections are Strepto-
coccus spp., Pseudomonas aeruginosa, Serratia spp., Gram-
negative rods, Pasteurella multocida, Eikenella corrodens,
and mycobacteria.13–15
Summary: Indications for surgical management
of fi nger infections
Indications
●
Infection that has not responded to antibiotics within 24
hours
●
Infection that is showing signs of progression despite
antibiotics
●
Joint space infections
●
Grossly contaminated wounds with retained foreign objects
●
Spontaneous drainage of purulence through the skin
●
Infection associated with signs of systemic illness
●
Immunocompromised patient
Contraindications
●
Cellulitis without abscess formation
●
Herpetic whitlow

Hand and Upper Extremity Reconstruction
210
Surgical exploration should be undertaken if the infec-
tion does not improve after 24 hours of parenteral anti-
biotics, or if there are signs of progression. Postoperatively,
parenteral antibiotics can be continued for 1–3 days. If
there is no improvement within 2 days, a return to the
operating room should be planned for re-exploration.22
Once all purulence has been drained, necrotic tissue debri-
ded, and the infection is resolving, the antibiotics may be
changed to an oral form. Deeper infections and joint infec-
tions should be treated for 10–14 days. A shorter course
(5–7 days) may be appropriate for more superfi cial infec-
tions.1,7,13,20 Patients who are severely immunocompro-
mised and who have complex fi nger infections may need a
protracted course of parenteral antibiotics, and an infec-
tious disease consultation may be benefi cial.
Purulent or suppurative fl exor tenosynovitis is diag-
nosed by the presence of Kanavel’s signs. First described in
1912, the four signs are fusiform digital swelling, fl exed
posture of the digit, pain with passive extension of the digit,
and pain with palpation over the fl exor sheath (Fig. 15.1).14
If three or four signs are present, there is a strong likelihood
that there is purulence in the fl exor tendon sheath.23
Septic arthritis is characterized by pain, edema, and
reduced motion. The digit may be subconsciously held by
the patient in a fl exed posture to minimize pain. On physi-
cal examination there will be extreme pain with axial
loading of the joint, in addition to the signs above. The
erythrocyte sedimentation rate and C-reactive protein are
generally elevated, but the white blood count is elevated less
than 50% of the time. Acutely, the X-ray will generally be
unremarkable, and obvious bone changes consistent with
joint destruction predict a poorer outcome.13,18,24 This is
a surgical emergency because retained purulent material
within the joint can cause destruction of the articular car-
tilage in less than a day.13,24 Joint infection can also be
caused by hematologic seeding, and a recent history of
invasive procedures such as colonoscopy might be reveal-
ing.24 Infections can be confused with other infl ammatory
processes such as gout, but it is safer to explore an unin-
fected joint than risk the problems associated with joint
destruction in an untreated septic joint.
Paronychia and felons are the most commonly seen
fi nger infections.25 When they are detected early, treatment
is associated with rapid resolution and minimal functional
impairment. If treatment is delayed, the infections may be
associated with tissue loss, osteomyelitis, fl exor tenosyno-
vitis, and septic arthritis. A paronychia is related to loss of
integrity between the nail and the nail fold by the inocula-
tion of bacteria. The presentation ranges from cellulitis and
edema of the paronychium (the nail folds lateral and medial
to the nail plate) to abscess beneath the fi nger nail (Fig.
15.2). If there is no purulence below the nail, and no ‘point-
ing’ of abscess or purulence that is beginning to ‘point’
(whitish discoloration with thinning of the skin), non-
operative care with warm water soaks and oral antibiotics
should be adequate. In the presence of purulence, operative
management is indicated and the lateral 3–4 mm of the nail
plate may need to be elevated and removed.
Felons are closed space infections of the volar pads of
the thumb or fi ngers. They are diagnosed by erythema and
edema limited to the distal phalanx, occasional ‘pointing’
of abscess, increasing pain, and a history of a puncture or
abrasion in a dirty environment. Depending on the size of
the underlying abscess, there may be a palpable area of
fl uid.12,15,18
FIGURE 15.1 The middle fi nger displaying three of Kanavel’s signs:
fusiform swelling, erythema, and fl exed posture.
FIGURE 15.2 Ring fi nger showing a paronychia with a subungual
abscess.

Techniques for Treating Finger Infections
211
Immunocompromised patients are at greater risk for
developing fi nger infections. The threshold for surgical
intervention should be lowered in these patients, and mul-
tiple debridements and prolonged courses of antibiotics
may be needed to clear the infection.7,21,24
Contraindications to surgical exploration are few. Cel-
lulitis without suspicion of underlying purulence should
be treated with a course of antibiotics. It is important to
remember that the dorsal aspect of the hand can become
quite edematous without underlying abscess. Abscesses
may track in a volar to dorsal direction, but this is generally
accompanied by tenderness and discoloration and may be
associated with spontaneous drainage through the thinner
dorsal skin (Fig. 15.3A–C). Herpetic whitlows are often
seen on the fi ngertips. They may be preceded by a tingling
or burning prodrome, may be associated with erythema and
edema in addition to small vesicles, and may be associated
with intense pain. The edema is less pronounced than is
seen with felons (Fig. 15.4). Incisions should not be made
into herpetic lesions because systemic spread may occur.15
PREOPERATIVE HISTORY
AND CONSIDERATIONS
As with any injury, it is important to obtain a thorough
history from the patient. Important information includes
the position of the hand during the injury, whether the
injury was penetrating or blunt, the environment in which
the injury occurred, and whether a relatively clean instru-
ment or a dirty one was involved. The presence of foreign
bodies should always be considered, especially in wounds
that are not healing as rapidly as expected. Pieces of plant
material, glass, metal, fabric, and animal teeth are easily
missed in initial examinations of wounds, especially if the
wound is extensive.
If there is a possibility that a radio-opaque object was
left in the wound, X-rays in three planes should be obtained.
If the wound is not healing, and the mechanism of injury
involves organic matter or glass, an MRI or ultrasound may
be indicated,26,27 but in these cases it may be most reason-
able simply to explore the wound if the problem is well
localized. In patients who have no history of a penetrating
injury, the history should focus on other major medical
problems or potential sources of hematogenous spread.
If surgery is performed, intraoperative cultures of tissue
or purulent matter should be sent for Gram stain, culture,
and sensitivities. Tissue and abscess contents are preferable
to wound swabs for accurate diagnosis.28 The microbiology
laboratory should be contacted if there are concerns for the
presence of unusual organisms such as mycobacteria or
fungi, so that appropriate culture media can be used.
OPERATIVE APPROACHES
Purulent fl exor tenosynovitis
Anatomy
Purulent fl exor tenosynovitis (also called suppurative teno-
synovitis) is caused by inoculation of bacteria into the fl exor
A
B
C
FIGURE 15.3 A The middle fi nger showing a dorsal abscess that
is related to superfi cial trauma. B The hemostat is tracking the
subcutaneous plane from dorsal to volar. C The volar incision was
extended in a Bruner fashion to follow the path of purulence along
the fl exor sheath.

Hand and Upper Extremity Reconstruction
212
tendon sheath.14 Infections of the tendon sheath may also
be chronic and associated with mycobacteria.16 The sheath
is comprised of two layers: an inner visceral layer and an
outer parietal layer. It extends along the fl exor tendons from
the base of the distal phalanx to a level just proximal to the
metacarpophalangeal joint. The fl exor sheath of the small
fi nger is usually associated with the ulnar bursa, which
extends through the palm and carpal tunnel just proximal
to the transverse carpal ligament. The ulnar bursa also
encloses the other fl exor tendons in the mid and proximal
palm, and it may communicate with the radial bursa, which
extends along the fl exor pollicis longus tendon. This asso-
ciation may allow infections to track between fi ngers, and
a careful physical examination should document the
involvement of areas other than the obviously involved
digit.1,14 The fl exor tendon sheath is a closed space contain-
ing protein-rich nutrient synovial fl uid that promotes bacte-
rial growth. If bacteria growth cannot extrude toward the
skin, the abscess tracks along the sheath proximally into
the palm and wrist. As is generally good practice with the
hand examination, moving toward the point of maximal
pain to determine the extent of the infection minimizes
pain and anxiety. For infection that has been present without
treatment for more than a few days, the patient must be
informed of the possibility of rupture of the fl exor tendon.
Elevated pressure in digits with purulent fl exor tenosyno-
vitis may be associated with tissue damage.17 Depending
on the situation, tendon rupture may necessitate delayed
multistage reconstruction or amputation of the digit (Fig.
15.5A,B). The outcome of tendon reconstruction is not
good if infection-associated tendon rupture has occurred.
Minimal volar approach
The author’s preferred approach to a straightforward case
of purulent fl exor tenosynovitis is via a minimal volar
approach under conscious sedation in the operating
room.19,22 Wrist and digital blocks are performed with 7–
10 mL of a 1 : 1 mix of lidocaine and bupivacaine with
epinephrine prior to skin cleansing. The arm is elevated
above the heart, and pressure is held over the radial and
ulnar arteries for 2 minutes. A non-sterile proximal forearm
FIGURE 15.4 Healing herpetic whitlow lesions.
A
B
FIGURE 15.5 A This is a woman with long-standing diabetes and a
fi ngertip ulcer with purulent discharge. The fi nger was notable for
fusiform swelling, erythema, tenderness, and the inability to fl ex.
B Exploration revealed spontaneous rupture of the fl exor tendons.
The fi nger was amputated.

Techniques for Treating Finger Infections
213
or upper arm tourniquet is then infl ated. Loupe magnifi ca-
tion is recommended.
The tendon sheath and tendon are exposed at the level
of the distal interphalangeal (DIP) joint via a transverse
incision, and at the level of the A1 pulley in the distal palm
via a longitudinal incision. The distal incision should be
just through the dermis laterally and medially, and fi ne
scissors are used to spread the soft tissue and expose the
tendon sheath. Care should be taken to avoid transecting
the terminal branches of the digital nerves. If the inciting
wound is over the volar proximal phalanx and the distal
aspect of the fi nger is not grossly involved, the distal inci-
sion may be made at the level of the proximal interphalan-
geal (PIP) joint. When the tendon sheath is opened, any
purulent matter or cloudy fl uid should be cultured for
aerobes, anaerobes, and special organisms (if indicated).
The proximal incision should be made over the A1 pulley
at the level of the metacarpal head as for a trigger fi nger
release. The author prefers longitudinal incisions because
they readily allow the extensile exposure. Senn retractors
are used to expose the tendon sheath and protect the neu-
rovascular bundles. The A1 pulley is incised with a no. 15
blade and divided with small tissue scissors.
A small pediatric feeding tube is passed into the tendon
sheath in a proximal to distal direction at the level of the
A1 pulley. It can be challenging to insert the tube into the
sheath past the level of the PIP.29 The tube can be passed
along the side of the fl exor digitorum profundus. Gently
irrigate the tube with sterile saline. When fl uid fl ows out
of the DIP-level incision, the tube is in an appropriate posi-
tion (Fig. 15.6A,B). Irrigate the sheath until the fl uid is
clear, and attach the tube to a bag of injectable sterile saline
marked clearly as to its use.
If the preoperative examination reveals pain and swell-
ing in the volar wrist, or if milking the sheath from proxi-
mal to distal in the hand expresses cloudy fl uid or gross
purulence, a curvilinear incision should be made in the
distal forearm to examine the fl exor tendons and bursae.
This is especially true for infections along the fl exor pollicis
longus (FPL) tendon sheath. An incision over the palmaris
longus tendon in the forearm is versatile, but if there is only
suspicion of FPL involvement, the incision can be made
over the fl exor carpi radialis (FCR) tendon. Ulnar retraction
of FCR reveals the FPL tendon. Usual caution should be
taken to avoid the palmar sensory branch of the median
nerve, which branches from the median nerve about 6 cm
proximal to the wrist crease and travels along the radial
aspect of the FCR tendon. If more than one fi nger is
involved, a larger midpalm incision should be made in a
Bruner fashion. An additional irrigation tube may be placed
proximally if the infection has tracked that far.
Allow the fl uid to drain via gravity at 20 mL/h. Do not
try to rapidly force fl uid into the sheath with an injection
pump or syringe, because the fl uid can leak into the sub-
cutaneous space and can potentially create increased pres-
sure in the fi nger. Slow continuous irrigation is less painful
to the patient. Secure the drain to the skin of the palm with
a single 3/0 nylon suture, taking care not to compress the
tube. Tape the tube longitudinally to the arm to avoid it
being inadvertently pulled out. Close the palmar wound
loosely with skin sutures. A well-padded plaster or fi ber-
glass dorsal splint is placed with the hand in the position
of safety (wrist slightly extended, metacarpal joints fl exed,
and interphalangeal joints in neutral). The irrigation will
make the dressing wet, and an absorbent pad wrapped
around the arm is helpful in keeping the bed dry. The pad
can be replaced as needed by the nursing staff. If the splint
is dorsal and the hand is resting in an elevated position on
a pillow or foam wedge, it will usually rest in a palm-down
fashion, and the splint will get less wet and be more likely
to stay intact. The dorsal position also allows the surgical
team to look under the wraps at the wound without com-
pletely removing the dressing and potentially dislodging the
irrigation tube. Depending on the severity of the infection
and concomitant medical problems, the author’s preference
is to keep the drain in place for 24–72 hours. Once the drain
is removed, the therapist can educate the patient on active
motion.
A
B
FIGURE 15.6 A A 21-month-old child with a human bite and fl exor
tenosynovitis. B A pediatric feeding tube was inserted in the fl exor
sheath. The bitten tissue over the volar PIP joint was sharply excised.

Hand and Upper Extremity Reconstruction
214
Volar Bruner approach
The entire sheath may be exposed via Bruner incisions (Fig.
15.7) if there are multiple areas of erosion through the skin
along the fl exor sheath; if there has been widespread damage
to the volar skin; if there is concern of retained foreign
material due to an injection injury; or if there is concern
about a necrotizing process. The wound may be left open
and closed in a delayed fashion, or loosely tacked closed at
the time of the surgical drainage. Wet to damp coarse mesh
gauze or feeding tube irrigation may be used.
Postoperative wound care
Numerous methods of postoperative wound care have been
described: catheter irrigation, fi nger soaks in sterile water,
sterile saline, or tap water, wet to damp dressing changes
with coarse mesh gauze, non-stick dressings with Vaseline-
impregnated gauze, or silver-impregnated antimicrobial
dressings. Skin cleansers such as Techni-Care may be
useful acutely, but detergents, iodine, and peroxide may
delay healing.30,31 One should consider the effi cacy, ease,
patient comfort, and cost associated with each of these
treatments. There is no evidence to support any of these
methods.9,28,32
Felon/paronychia
Anatomy
Paronychia is an infection of the tissues around the nail
bed. The paronychium is the tissue folds lateral and medial
to the nail; the eponychium is the fold proximal to the nail;
the hyponychium is the tissue just distal and volar to the
nail. The perionychium is the complex of the nail, nail bed,
and paronychial folds.12 Paronychial infections can spread
beneath the nail, or may spontaneously decompress around
the nail fold.
A felon is an infection isolated to the digital pulp. The
anatomy is unique: the digital skin of the volar pad is
attached to the periosteum by multiple septa encasing fat
and sweat glands.12,25
Surgical drainage
If the infection has not responded to a short course of warm
soaks and oral antibiotics, surgical drainage should be per-
formed. In many cases this can be done in a minor proce-
dure room or offi ce setting using a digital block and fi nger
tourniquet. A thorough history should reveal the mecha-
nism and suggest infective organisms that may be consid-
ered as etiologic agents. Purulent materials should be sent
for culture.
The method for draining a paronychia is chosen accord-
ing to the extent and location of the abscess. If the skin
over the abscess appears to be attenuated, one can make a
longitudinal incision over the point of maximal swelling
running parallel to the paronychial fold. If the edema and
cellulitis are more diffuse, inserting a fi ne tissue scissor
below the surface of the nail into the fold and spreading
will drain the abscess. If there is evidence of subungual
purulence, elevating and removing the lateral or medial 3–
4 mm of nail plate will allow drainage. If the infection
involves the paronychium and eponychium and appears to
be associated with a deeper proximal abscess, an incision
should be made at each juncture of the paronychial and
eponychial folds and extended proximally perpendicular to
the fold. The eponychial fold is elevated, the wound irri-
gated, and a small wick left in place. Two sutures should
be placed to realign the nail fold.
Felons should be drained through a minimal longitudi-
nally directed incision. If the infection is coming to a point,
the incision should be made over the apex. If the area of
involvement is symmetrical over the pulp, the incision can
be made in one of several locations (Fig. 15.8). Avoid making
an incision that traverses more than two sides of the fi n-
gertip (i.e., the fi sh-mouth incision). This incision creates
a proximally based volar fl ap and frees the volar pad from
the bone. It rarely heals well, and can be chronically deform-
ing and uncomfortable.25 It is preferable to keep the incision
off of the distal tip of the fi nger; lateral or medial incisions
work well. A small curved tissue scissors should be placed
just superfi cial to the periosteum and spread to allow drain-
age of all pockets of purulence across the volar pad of the
fi nger. The wound should be copiously irrigated with saline.
Obviously devitalized tissue should be excised. The wound
should not be closed.
A
B
FIGURE 15.7 A Severe purulent fl exor tenosynovitis tracking into the
palm with destruction of the A1 and A2 pulleys. B The wound healed
by secondary intention.

Techniques for Treating Finger Infections
215
Postoperative care
A small Penrose drain or piece of gauze wick may be left in
the wound for 1–2 days to allow it to drain. The fi ngertip
can be soaked in saline or tap water for 10 minutes three
times a day, or irrigated with a small syringe until the acute
infl ammation and drainage have subsided.
Septic arthritis
Anatomy of small joints
The interphalangeal joints are uniaxial (hinge) joints sup-
ported on the palmar side by a thick volar plate and laterally
and medially by the collateral and accessory collateral liga-
ments. The volar plate and collateral ligaments are attached,
adding to the stability of the joint. The dorsal capsule is
fairly thin and the joint is protected largely by the extensor
tendon mechanism. Because of the relative thinness of the
dorsal capsule, intra-articular infections spontaneously
extend dorsally more frequently than in any other direction.
Interphalangeal joints have a high level of congruency and
are inherently stable. They have minimal rotatory motion,
and movement is largely limited to fl exion and extension.
Exposure
A dorsal midline curvilinear incision is appropriate for
access to the joint. When possible, it is preferable to avoid
splitting the tendon because early movement is advisable
after drainage of the joint. Cultures should be taken, copious
irrigation performed, and the wound closed loosely (if at
all). If the joint shows evidence of destruction, it is likely
that an arthrodesis will be indicated for joint stability and
minimization of pain. The arthrodesis should be delayed
until the infection is cleared and the wounds healed.
Postoperative care
A small drain or irrigation catheter may be left in the
wound. The patient should be warned that stiffness, pain,
and arthritis are not uncommon after joint infections13,21,24
FIGURE 15.8 Acceptable incisions for drainage of a felon along the
volar pad and midaxial line of the fi nger.
(Fig. 15.9). Taking the patient back to the operating
room for a second or third look is reasonable if pain, swell-
ing, or redness are not abating within 24–48 hours
postoperatively.
Subcutaneous abscess
Anatomy
Abscesses occasionally undermine the skin widely and
cause overlying necrosis but do not invade into the tendon
sheaths or joints (Fig. 15.10). This is more common over
the dorsal aspect of the fi nger owing to the thinner skin,
but it is possible for felons also to rupture through the volar
pad if suffi ciently neglected. This infection is often seen
in people who have poor general health maintenance
practices.
FIGURE 15.9 X-ray showing septic arthritis caused by a cat bite.
FIGURE 15.10 A dorsal subcutaneous abscess which did not invade
the interphalangeal joint or track volarly. After surgical debridement,
it healed by secondary intention.

Hand and Upper Extremity Reconstruction
216
Exposure
This infection can usually be managed in the minor proce-
dure room under local anesthesia and a digital tourniquet.
All grossly necrotic tissue must be sharply excised and the
wound undermined with a hemostat or other small probe.
Care should be taken to stop debriding when the tissue
begins to ooze, as aggressive debridement may necessitate
more extensive reconstruction.
Postoperative care
Care for this wound is as previously mentioned with soaks
or irrigation, but because of the loss of skin, reconstruction
with skin grafts or local fl aps may be indicated once the
infection has resolved. Antibiotics should be tailored to the
infective organism, and the choice of antibiotic should
refl ect the possibility of poor compliance on the patient’s
part. It may be desirable to see this patient several times
a week to ensure compliance with care and ongoing
healing.
POSTOPERATIVE CARE
Early involvement by a qualifi ed hand therapist is benefi cial
for outcome.1,18,37 They are able to assist the patient perform
protected movements, carry out treatments that hasten the
resolution of infl ammation, encourage psychological as well
as physiological adaptation to the injury, and recognize
patients who are not progressing as expected and for whom
additional treatment may be indicated.
CONCLUSION
Finger infections can be associated with impressive infl am-
mation. As is true in all wounds, rapid progression through
the infl ammatory phase into the building and remodeling
Optimizing outcomes
●
Prompt surgical treatment
●
Appropriate use of antibiotics
●
Assurance that infection is completely drained
●
Meticulous tissue handling technique
●
Judicious debridement of tissue with removal of all foreign
matter
●
Irrigation or soaking
●
Early motion
●
Reduce infl ammation through therapy
COMPLICATIONS AND SIDE EFFECTS OF
FINGER INFECTIONS AND THEIR CARE
All digital infections can be complicated by skin loss, stiff-
ness, chronic edema, prolonged infl ammation, osteomyeli-
tis, and pain. Infections can be inadequately treated if the
infective organism is drug resistant or unusual. Surgical
intervention can be associated with inadvertent injury to
nerves, arteries, and tendons, and failure to adequately
debride necrotic tissue or remove all foreign material. Costs
include hospitalization, surgery, time lost from employ-
ment and diffi culty with activities of daily living. Later
attempts to reconstruct tissues could be associated with
recurrence of infections.33,34 Complications can be more
specifi c to various infections: purulent tenosynovitis can
cause tendon rupture; septic arthritis can progress to oste-
oarthritis or osteomyelitis.
Acute bacterial fi nger infections may be confused with
myriad other medical conditions, including gout, calcium
pyrophosphate deposition disease, herpetic whitlow, spider
bites, metastatic cancer, rheumatoid arthritis, and fl ares of
other arthritides. Infections caused by mycobacteria may be
indolent and persistent, resisting resolution with standard
antibiotics and wound care.35,36
Clinical Pearls
Organisms that may have pathognomonic characteristics:
●
Staphylococcus spp. are pyogenic
●
Streptococcus spp., Sporothrix schenkii, and mycobacteria
are associated with lymphangitis
●
Streptococcus may have a rapid course with systemic signs
of illness
●
Sporothrix schenkii have violaceous ulcers along the
lymphatic channels
●
Pseudomonas has a sweet and musty odor and may have a
greenish color
●
Polymicrobial infections have a foul malodor and dark tan
purulence
●
Clostridia have a sharp and pungent odor with tissue
necrosis
●
Mycobacteria are associated with chronic course, are non-
responsive to antibiotics and require aggressive surgical
treatment
●
Herpetic whitlow is characterized by small vesicles, possibly
preceded by a prodrome and accompanied by
disproportionate pain
Organisms may be more frequently seen in certain clinical
settings
●
Pasteurella multocida is associated with animal bites
●
Eikenella corrodens is associated with human bites
●
Pseudomonas aeruginosa and Serratia spp. are associated
with intravenous drug abuse, diabetes mellitus, and
immunocompromised individuals
●
Sporothrix infections are associated with rose thorn
punctures
●
Mycobacteria are associated with traumatic fresh or salt
water exposures
●
Fungal infections are found in immunocompromised patients

Techniques for Treating Finger Infections
217
phases is ideal.38 Minimization of infl ammation is ensured
by early recognition of the problem, surgical drainage of
abscess, surgical removal of foreign material, appropriate
use of effective antibiotics, and collaboration with occupa-
tional therapists. Under the guidance of an occupational
therapist, the patient can be provided with a home program
for movement and edema control. If these points are
attended to, and if the patient does not have comorbid
conditions that compete with healing, the infection should
rapidly abate and a reasonable outcome should be
expected.
REFERENCES
1. Boles SD, Schmidt CC. Pyogenic fl exor tenosynovitis. Hand Clin
1998; 14: 567–578.
2. Brook I. Management of human and animal bite wounds: an
overview. Adv Skin Wound Care 2005; 18: 197–203.
3. Chang MC, Huang YL, Liu Y, Lo WH. Infectious complications
associated with toothpick injuries of the hand. J Hand Surg [Am]
2003; 28: 327–331.
4. Marculescu CE, Berbari EF, Cockerill FR III, Somon DR. Unusual
aerobic and anaerobic bacteria associated with prosthetic joint
infections. Clin Orthop Relat Res 2006; 451: 55–63.
5. Rowe JG, Amadio PC, Edson RS. Sporotrichosis. Orthopedics
1989; 12: 981–985.
6. Karanas YL, Yim KK. Mycobacterium tuberculosis infection of the
hand: a case report and review of the literature. Ann Plast Surg
1998; 40: 65–67.
7. Francel TJ, Marshall KA, Savage RC. Hand infections in the
diabetic and the diabetic renal transplant recipient. Ann Plast Surg
1990; 24: 304–309.
8. Klein MB, Chang J. Management of hand and upper-extremity
infections in heart transplant recipients. Plast Reconstruct Surg
2000; 106: 598–601.
9. Wysocki AB. Evaluating and managing open skin wounds:
colonization versus infection. AACN Clinical Issues: Adv Pract
Acute Crit Care 2002; 13: 382–397.
10. LeBlanc DM, Reece EM, Horton JB, Janis JE. Increasing incidence
of methicillin-resistant Staphylococcus aureus in hand infections:
a 3-year county hospital experience. Plast Reconstruct Surg 2007;
119: 935–940.
11. Kiran RV, McCampbell B, Angeles AP, et al. Increased prevalence
of community-acquired methicillin-resistant Staphylococcus aureus
in hand infections at an urban medical center. Plast Reconstruct
Surg 2006; 118: 161–166.
12. Zook EG. Understanding the perionychium. J Hand Ther 2000;
13: 269–275.
13. Murray PM. Septic arthritis of the hand and wrist. Hand Clin
1998; 14: 579–587.
14. Small LN, Ross JJ. Suppurative tenosynovitis and septic bursitis.
Infect Dis Clin North Am 2005; 19: 991–1005.
15. Gaar E. Occupational hand infections. Clin Occup Environ Med
2006; 5: 369–380.
16. Neviaser RJ. Tenosynovitis. Hand Clin 1989; 5: 525–531.
17. Schnall SB, Vu-Rose T, Holtom PD, et al. Tissue pressures in
pyogenic fl exor tenosynovitis of the fi nger. Compartment
syndrome and its management. J Bone Joint Surg 1996; 78:
793–795.
18. Glass KD. Factors related to the resolution of treated hand
infections. J Hand Surg [Am] 1982; 7: 388–394.
19. Harris PA, Nanchahal J. Closed continuous irrigation in the
treatment of hand infections. J Hand Surg [Br] 1999; 24:
328–333.
20. Gosain AK, Markison RE. Catheter irrigation for treatment of
pyogenic closed space infections of the hand. Br J Plast Surg 1991;
44: 270–273.
21. Boustred AM, Singer M, Hudson DA, Bolitho GE. Septic arthritis
of the metacarpophalangeal and interphalangeal joints of the hand.
Ann Plast Surg 1999; 42: 623–628.
22. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation
is as effective as open drainage for treatment of pyogenic fl exor
tenosynovitis. Ann Plast Surg 2002; 49: 350–354.
23. Schecter WP, Markison RE, Jeffrey RB, et al. Use of sonography in
the early detection of suppurative fl exor tenosynovitis. J Hand Surg
[Am] 1989; 14: 307–310.
24. Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev
2002; 15: 527–544.
25. Canales FL, Newmeyer WL 3rd, Kilgore ES Jr. The treatment of
felons and paronychias. Hand Clin 1989; 5: 515–523.
26. Russell RC, Williamson DA, Sullivan JW, et al. Detection of
foreign bodies in the hand. J Hand Surg [Am] 1991; 16: 2–11.
27. Peterson JJ, Bancroft LW, Kransdorf MJ. Wooden foreign bodies:
imaging appearance. Am J Roentgenol 2002; 178: 557–562.
28. Campton-Johnston S, Wilson J. Infected wound management:
advanced technologies, moisture-retentive dressings, and die-hard
methods. Crit Care Nurs Q 2001; 24: 64–77.
29. Rosenbaum DH Jr, Degnan GG. Facilitating diffi cult catheter
passage. Orthop Rev 1993; 22: 396–398.
30. Wilson JR, Mills JG, Prather, ID, Dimitrijevich SD. A toxicity of
skin and wound cleansers used on in vitro fi broblasts and
keratinocytes. Adv Skin Wound Care 2005; 18: 373–378.
31. Grubbs BC, Statz CL, Johnson EM, et al. Salvage therapy of open,
infected surgical wounds: a retrospective review using Techni-Care.
Surg Infect 2000; 1: 109–114.
32. Leaper DJ. Silver dressings: their role in wound management. Int
Wound J 2006; 3: 282–294.
33. Ammon P, Stockley I. Allograft bone in two-stage revision of
the hip for infection. Is it safe? J Bone Joint Surg 2004; 86:
962–965.
34. Hart JP, Eginton MT, Brown KR, et al. Operative strategies in
aortic graft infections: is complete graft excision always necessary?
Ann Vasc Surg 2005; 19: 154–160.
35. Regnard PJ, Barry P, Isselin J. Mycobacterial tenosynovitis of the
fl exor tendons of the hand. A report of fi ve cases. J Hand Surg [Br]
1996; 21: 351–354.
36. Hess CL, Wolock BS, Murphy MS. Mycobacterium marinum
infections of the upper extremity. Plast Reconstruct Surg 2005;
115: 55e–59e.
37. Mancini LH, Fort LK. Rehabilitation of the infected hand. Hand
Clin 1989; 5: 635–641.
38. Menke NB, Ward KR, Witten TM, et al. Impaired wound healing.
Clin Dermatol 2007; 25: 19–25.

219
C H A P T E R
16
Dupuytren’s Contracture
Warren C. Hammert
INTRODUCTION
Our understanding of Dupuytren’s disease and the contrac-
ture process has evolved over the years. We have progressed
from the early description of contracture release1 to our
current understanding and many treatment modalities.
Multiple treatment techniques have been described, ranging
from simple division of the contracted fascia to attempted
complete excision of the diseased tissue.
The evolution of our understanding of Dupuytren’s
disease and its early treatment dates back to the late 18th
and early 19th centuries.2 The condition was ultimately
named after Baron von Dupuytren, who described his tech-
nique for release of the contracture in the 1830s.
In order to understand the process, one must have a
clear understanding of the nomenclature and the biology
behind the process.3 A nodule is the early palpable mass in
the palm. In addition to the clinical description, it can also
be used to describe a histologic pattern. The term band is
used to describe normal fascia and the term cord describes
the diseased fascia. The term diathesis is used to describe
a more aggressive, severe form that begins earlier in life
and often involves multiple sites (plantar aspect of the
feet: Ledderhose’s disease; the penis: Peyronie’s disease;
and the dorsal aspect of the PIP joints: Garrod’s knuckle
pads) in addition to involvement of the palmar aspect of
the hands.
HISTOLOGY
The nodules do not occur randomly, but at points along
the axis of the digital rays. They progress to a cord and the
resultant contracture.4 The myofi broblast is the cell that
has been implicated in the contracture process.5,6 This has
been demonstrated in studies showing that Dupuytren’s
fi broblasts consistently generate greater contractile forces
than the controls, with those derived from the nodule
having the greatest contraction.7–9 These cells contain
myosin and actin, which induce the contraction. The myo-
fi broblasts connect to each other via tight junctions and
fi bronectin. They are located in an extracellular matrix and
contain glycosaminoglycan as well as collagen types I and
III.10,11 Multiple other tissue factors for this disease, includ-
ing basic fi broblast growth factor,12,13 transforming growth
factors β1 and 2,14–16 epidermal growth factor,16 platelet-
derived growth factor,17 nerve growth factor,18 and matrix
metalloproteinases,19 have been implicated, but the exact
mechanism that stimulates the myofi broblasts to begin the
contractile process has not been elucidated.20
Three histologic phases have been described in the
disease process: proliferative, involutional, and residual.
The proliferative phase is characterized by an increased
amount of immature fi broblasts and myofi broblasts,
minimal extracellular matrix, and increased numbers of
pericytes to create increased, disorganized cellularity. The
involutional phase is characterized by a reduction in the
number of fi broblasts and myofi broblasts, and increasing
organization. The ratio of type III to type I collagen is
increased, and the myofi broblasts align along the axis of the
collagen bundles. In the residual phase the myofi broblasts
essentially disappear, leaving densely packed bundles of
collagen fi brils.
GENETICS/CAUSE
Although the true etiology is unknown, most studies indi-
cate a higher incidence in populations of northern Europe
and persons of northern European ancestry.21 There appears
to be an autosomal dominant pattern of inheritance with
variable penetration. The prevalence increases with increas-
ing age and the disease is more common in males.22
In addition, environmental infl uences may play a role, as
it is more commonly seen in Indian patients living in
England.23
In spite of attempts to determine the true cause of
Dupuytren’s disease, its true etiology has eluded us. It has
been linked to many different processes, but these processes
do not affl ict most patients. It is often seen in diabetics,24
but this form is somewhat different and more commonly
affects the radial aspect of the hand. Alcohol has been
reported to be associated, but the cause and effect

Hand and Upper Extremity Reconstruction
220
relationship is not clear.25–27 The increased association with
epilepsy is related to medications used to treat epilepsy,
rather than to the disease itself.27,28 There is no evidence
that treating any of these conditions will affect the Dupuy-
tren’s process; the treatment should be directed towards the
hand and not the systemic process.
ANATOMY AND PATHOLOGY
A clear knowledge of the anatomy of the normal palmar
fascia is essential to understanding the disease process and
its management. As the palmar fascia extends distally from
the palm into the digits, it is divided into three anatomic
layers. In the palm, the palmaris longus continues distally
as the palmar fascia. These longitudinal fi bers of the palmar
fascia run superfi cial (volar) to the transverse fi bers. At the
distal end of the transverse fi bers, the longitudinal fi bers
split into three layers (Fig. 16.1A–C). The fi rst layer inserts
into the skin between the distal palmar crease and the pal-
modigital crease, and is known as the pretendinous band.
These fi bers insert at a more proximal location along the
ulnar aspect of the hand and move distally as they progress
A
Pretendinous bands
(longitudinal)
Transverse
fibers
Natatory ligament
(distal commissural
ligament)
Natatory ligament
(proximal
commissural
ligament)
Layer 1 -
Pretendinous band
Layer 2 -
Spiral bands (deep to
neurovascular bundles)
Transverse fibers
Neurovascular
bundles
Layer 3 -
Deepest layer (passing
around MP joints)
Pretendinous band
B
C
Grayson’s ligament
(superficial to
neurovascular bundle)
Natatory ligament
Neurovascular bundle
Pretendinous band
Transverse fibers of
palmar fascia
Spiral band
Lateral digital sheet
Cleland’s ligament
(deep to the
neurovascular bundle)
FIGURE 16.1 A Diagram of anatomy of palmar fascia and
pretendinous bands. B Diagram of palmar fascia as it separates into
three layers at level of MP joint. C Diagram of layers of digital fascia.

Dupuytren’s Contracture
221
towards the radial side. The second layer dives deep to the
neurovascular bundle and becomes continuous with the
lateral digital sheet. This layer is known as the spiral band,
and is responsible for displacement of the neurovascular
bundle. The third layer continues deeper, passing around
the fl exor tendons along the side of the metacarpophalan-
geal (MP) joint.29,30
As the pretendinous bands become involved and con-
tracture develops, they are termed pretendinous cords and
cause contracture of the MP joints. As the deeper layers of
fascia contract, they contribute to contracture of the proxi-
mal interphalangeal (PIP) joint. The central cord is a lon-
gitudinal continuation of the pretendinous cord and inserts
along the base of the middle phalanx. The lateral cord is
an extension from the natatory ligament to the lateral
digital sheet. In the small fi nger, it attaches to the abductor
digiti minimi and contributes to PIP joint contracture. The
spiral cord develops from the second layer of fascia, as an
extension of the pretendinous band. After wrapping around
the neurovascular bundle, it joins the lateral digital sheet
and causes contracture of the PIP joint through the attach-
ment of Grayson’s ligaments to the fl exor sheath and skin
(Fig. 16.2A,B). Occasionally, distal extension will contrib-
ute to contraction of the DIP joint.30,31
Some individuals will have isolated digital involvement.
In this scenario, the cord originates from the periosteum
at the base of the proximal phalanx in conjunction with
adjacent ligaments and intrinsic tendons. It can proceed
in an oblique direction to displace and then cross the neu-
rovascular bundles before inserting on the bone and/or
fl exor tendon sheath of the middle phalanx.32 In some
cases it will continue distally, deep to the neurovascular
bundle, and attach to the distal phalanx, causing DIP joint
contractures, and is known as the retrovascular cord
(Fig. 16.3A, B).30
The thumb is much less commonly involved than the
ulnar aspect of the hand and has a different pattern of
contracture, as the natatory ligament and the proximal
commissural ligament are responsible. These are parallel
structures that run transversely across the fi rst web space,
from the radial aspect of the thumb to the radial aspect of
the index fi nger in the region of the MP joint and the meta-
carpal, rather than extending into the thumb (Fig. 16.1A).
Thus, contracture results in an adduction contracture of
the thumb, rather than fl exion of the IP joint.30,33
INDICATIONS AND CONTRAINDICATIONS
Indications
Progression of disease
● Functional disability
● Hygiene issues (inability to keep hand clean and skin
healthy).
Goal of surgery
● Release the contracture (or at least improve it)
● Dupuytren’s disease cannot be cured and the tissue can
not be totally removed.
Contraindications
● Stable disease without functional impairment
● Medical conditions preventing safe surgical procedure
● Unable to participate in postoperative rehabilitation
program.
The mere presence of Dupuytren’s disease is not an
indication for surgical intervention. The most important
considerations are the degree of functional loss and the rate
of progression. There are many patients who notice a
A
Lateral digital sheet
Spiral band
Grayson’s ligament
Neurovascular
bundle
Pretendinous band
Lateral digital sheet
Spiral cord
Grayson’s ligament
Neurovascular
bundle displaced
toward midline by
contracted spiral cord
B
FIGURE 16.2 A Diagram of fascial layers involved in spiral band.
B Diagram of spiral band as it contracts and becomes spiral cord.

Hand and Upper Extremity Reconstruction
222
nodule in the palm, which may develop into a small cord,
but which does not cause any functional disability. These
patients can be followed using Houston’s tabletop test (Fig.
16.4). If the patient places his or her hand fl at on the table
and there is no separation between the palm or digit and
the table, it is reasonable to teach the patient what to look
for and see them again if contracture begins to develop. If
the hand does not lie fl at on the table, it can be placed with
the ulnar side against the table and the digits actively
extended. The hand is then traced on a piece of paper and
the patient is taught how to check for progression of the
contracture by periodically checking to see whether the
hand lies within this outline. This will help objectively
determine the rate of progression. In addition, measure-
ments of contracture and range of motion are measured at
the affected joints.
As a general rule, MP joint contractures can be corrected
even when severe and long-standing. The PIP joint is much
less forgiving and it is more diffi cult to maintain long-term
correction. Taking into consideration the loss of function
and progression of the contracture, the author will consider
(but not always perform) surgery when there is an MP joint
contracture of 30º or more and any degree of PIP joint
contracture.
The patient must have a clear understanding and real-
istic expectations. In general, they must be able to comply
with the prescribed postoperative therapy program to have
a good outcome. There are, however, some patients whose
ability to comply with the therapy program is limited but
who may still be candidates for surgery. These are patients
with severe contractures whose hygiene and wounds are
problematic. This situation may occur in a patient who has
had a stroke, resulting in limited ability to comply with
therapy, but whose contracture is severe, resulting in mac-
eration of the tissue in the palm and inability to keep the
hand clean. These patients are often candidates for more
limited procedures, such as fasciotomy.
A
Central cord
Retrovascular cord
Cleland’s ligaments
(deep to
retrovascular cord)
B
FIGURE 16.3 A Diagram of fascia and components of retrovascular
cord. B Clinical photo of contracture involving PIP and DIP joints with
retrovascular cord.
FIGURE 16.4 Houston’s table top test – the patient places the hand
fl at on the table. Inability to place the hand fl at on the table is
secondary to contracture of the MP joint, PIP joint, or both and may
be an indication for surgery.

Dupuytren’s Contracture
223
PREOPERATIVE HISTORY AND
CONSIDERATIONS
Currently, the treatment of Dupuytren’s disease is still
surgical. Oral non-steroidal anti-infl ammatory medications
have been suggested, but have not been found to be effec-
tive. Triamcinolone injections have been shown to slow the
growth process, but not eliminate it. 34 Collagenase injec-
tions have shown promise and are in the third stage of
clinical trials, but are currently not available for routine
use.35 In those patients who for medical reasons are not
good candidates for surgery, or who may not be able to
complete the required therapy, fasciotomy can be performed
as an offi ce-based procedure and has been shown to be
effective in the management of MP joint contractures.36
The procedure can be performed under local anesthesia.
This cord can be sharply transected with an 11 blade or an
18-gauge needle, allowing the involved digit to be straight-
ened. As this is a blind procedure, there is the possibility
of injury to tendons or neurovascular structures, and
recurrence is more likely.
The patient must understand that there are risks
involved with the procedure and that the goal is to release
the contracture, not to remove or cure the disease. Injury
to the digital nerves or vessels is rare, but can occur even
with an experienced surgeon. Contractures, especially at
the PIP joint, may not be completely released, and recur-
rence and extension of disease are common.37 Radiographs
should be obtained to look for underlying osteoarthritis, as
this makes postoperative stiffness more likely. This should
be discussed with the patient before surgery.
The procedure is generally completed on an outpatient
basis under regional or general anesthesia. Prior to the
surgery, a decision must be made about management of the
skin, the contracted fascia, and the joints. Decisions regard-
ing the skin include orientation of the incision and the
method of closure, and whether a dermofasciectomy would
be benefi cial, as some feel the skin may be the source of
recurrence.38 The skin can be incised in a zigzag fashion
initially, or a straight longitudinal incision can be used,
with conversion of the straight line to a zigzag orientation
by z-plasties (Fig. 16.5). Options for closure include closing
the entire incision or leaving a transverse portion open to
heal secondarily.39,40 A dermofasciectomy can be used which
involves simultaneous excision of the skin and contracted
fascia and replacing the skin with full-thickness grafts.
Multiple variations of these skin incisions and methods
of closure have been proposed, and all can be used
successfully.
The decision regarding management of the fascia con-
siders the amount to be excised: complete excision of all
involved fascia (fasciectomy) versus removal of a portion
(fasciotomy). Variations of complete removal have been
proposed and include radical fasciectomy, which involves
extensive removal of palmar fascia in the hope of reducing
the chance of recurrence, and a more limited fasciectomy,
which involves the removal of diseased fascia causing the
contracture in the involved digit.
Management of the MP joint is typically straightforward
as removal of the fascia almost always allows complete
extension of the joint. Management of the PIP joints is
more diffi cult. Depending on the duration and severity of
the contracture, removal of the involved fascia may not
completely release the joint. It is generally accepted that if
the joint is within 30º of full extension following fasciec-
tomy, further efforts to release the contracture are not
benefi cial in the long term. If the residual contracture is
greater than 30º, it is probably benefi cial to address the PIP
joint by releasing the check-rein ligaments of the volar
plate, followed by the accessory collateral ligaments and
the proper collateral ligaments, checking for PIP joint exten-
sion following each step and stopping when the contracture
is less than 30º. If these maneuvers are not successful,
further efforts are not going to be benefi cial in the long
term.
Although it is not routinely performed, patients
with severe PIP joint contractures may be candidates
for PIP joint arthrodesis. This will allow shortening of the
digit, which will reduce the tension on the neurovascular
bundle when the digit is straightened, and allow the joint
to maintain a functional position following osseous
healing.
C
A
B
FIGURE 16.5 Diagram of commonly used skin incisions for exposure
of contracted fascia. A Multiple V-Y incisions. B Straight-line incision
closed with multiple z-plasties. C Zigzag (Bruner) incisions.

Hand and Upper Extremity Reconstruction
224
In rare situations, amputation should be considered.
This would most likely involve a patient who has a problem
with hygiene who is unable to cooperate with the required
therapy.
OPERATIVE APPROACH
bundles can be identifi ed along each side of the pretendi-
nous cord as they emerge from the distal aspect of the
transverse fascia. After identifi cation of the neurovascular
bundle, the diseased pretendinous cord is transected dis-
tally (Fig. 16.6C), which should allow full extension of the
MP joint.
Management of the fascia causing contracture of the PIP
joint requires a thorough understanding of the anatomy, as
the neurovascular bundle is often displaced both centrally
and superfi cially. With the neurovascular bundles visual-
ized, the skin incision is carried distally to the level of the
PIP joint. This can be designed as a zigzag Bruner-type
incision or a straight-line incision, which is subsequently
broken with z-plasties. These fl aps are elevated at the level
of the fascia, with all the subcutaneous tissue on the skin
fl ap. Following fl ap elevation, the neurovascular bundles are
protected and kept under direct visualization while the
diseased fascia is excised. This will require excision of the
spiral cord, which wraps around the neurovascular bundle,
attaching to the lateral digital sheath, and Grayson’s liga-
ment. Occasionally, a central cord will be present and
extends from the region of the pretendinous cord to the
region of the PIP joint. When both of these cords are present,
the neurovascular bundle will be sandwiched between them.
Occasionally, spiral bands will be present on both sides of
the digit, pulling both neurovascular bundles together in
the midline. Once the contracted fascia is exposed to its
distal extent, and the neurovascular bundle has been identi-
fi ed and protected, the fascia is divided. Effort is made not
to disrupt the fl exor sheath (Figs 16.7 and 8).
The PIP joint itself is now evaluated. Sometimes, it can
be fully extended with gentle pressure. Occasionally, a
cracking sound will be heard, which is the result of rupture
of the vincula. There is considerable debate about the man-
agement of the PIP joint following excision of the con-
tracted fascia. If the joint cannot be extended, a goniometer
is used to measure the remaining contracture. If this is less
than 30º I do not attempt further release, as the subsequent
edema slows the recovery process and long-term mainte-
nance of the fi nal extension is usually not accomplished
(Fig. 16.9). If the contracture is more than 30º I feel it is
worth attempting further joint release. The fl exor sheath is
opened and the check-rein ligaments (proximal extensions
of the volar plate at the PIP joint) are released along the
radial and ulnar aspects. The joint is gently extended and
again measured. If the contracture is still greater than 30º,
the accessory collateral ligaments are released from their
attachment to the volar plate, the joint is gently extended,
and the remaining contracture is again measured. If still
greater than 30º the proper collateral ligaments are released,
which will allow full extension of the PIP joint.41 In patients
with severe PIP joint contractures, long-term maintenance
is unlikely even with PIP joint capsulotomy.42
The tourniquet is defl ated and pressure is held during
the reperfusion phase until the hyperemia has resolved.
The perfusion of the digits and skin fl aps is evaluated and
hemostasis obtained with bipolar electrocautery. Digital
perfusion may be delayed secondary to vasospasm from
manipulation of the digital arteries, but should return if the
Pearls and technical points
Understand the normal and diseased (contracted)
palmar fascia
●
Pretendinous cord
●
Spiral cord
●
Central cord
●
Retrovascular cord
MP joint contracture
●
Exposure of cord
●
Preservation of transverse fi bers of palmar fascia
●
Excise cord from proximal to distal with direct visualization
of the neurovascular bundle
PIP joint contracture
●
Exposure of cord to distal extent
●
Identify neurovascular bundles proximally
●
Excise cord with direct visualization of neurovascular bundles
●
Fixed joint contracture following fasciectomy
●
Less than 30º – accept
●
Greater than 30º – joint release
●
Volar plate – check-rein ligaments
●
Accessory collateral ligaments
●
Proper collateral ligaments
The procedure is performed under either regional or
general anesthesia. The author prefers regional, as this will
typically allow the patient to return home with the block
still in effect, making him/her more comfortable. A pneu-
matic tourniquet is placed on the upper arm. Prior to infl a-
tion, the skin incisions are outlined with a marking pen. A
variety of incisions can be used effectively, but the author
generally prefers a zigzag type of incision, modifi ed, if nec-
essary, by creating a transverse limb in the distal palmar
crease and the palmodigital crease (Fig. 16.6A). An
Eschmarch wrap is used to exsanguinate the upper extrem-
ity and the tourniquet is infl ated to 100 mmHg above the
preoperative systolic pressure. I begin the operation by
incising and elevating the palmar fl aps to expose the entire
area of the diseased, contracted fascia, from the proximal
palm to the palmodigital crease (Fig. 16.6B). The skin fl aps
should be elevated at the level of the palmar fascia, keeping
all the subcutaneous fat on the fl ap, exposing the longitu-
dinal contracted palmar cords (pretendinous cords) and the
non-contracted transverse bands. The digital neurovascular
bundles will lie deep to the transverse fascia and are pro-
tected at this level. The transverse fascia is not diseased
and does not need to be completely removed. The longitu-
dinal pretendinous cord is divided proximally and elevated
to the distal aspect of the transverse fascia, which will
coincide with the distal palmar crease. The neurovascular

Dupuytren’s Contracture
225
arteries have not been damaged. On rare occasions the
digital vessels are intact, but there is inadequate perfusion
secondary to stretching of the digital vessels. In this case,
the digit is fl exed to alleviate the tension on the vessel and
circulation will be restored. If circulation is not restored,
the digital artery must be reconstructed,43 and this may
require vein grafts.
The skin fl aps are again evaluated. If there are large
areas of buttonholing or areas of devascularization, these
should be resected and replaced by skin grafts. If there is a
shortage of skin due to the prolonged fl exed position, the
skin can be advanced distally, leaving the palm open in the
region of the distal palmar crease: the open palm technique,
often incorrectly referred to as the McCash technique. (The
open palm technique involves leaving a transverse portion
of the palmar incision open and allowing it to heal second-
arily.) The McCash operation, as originally described,
involved extensive undermining of the skin, tunneling from
the palmar incisions to the digital incisions, and advance-
ment of the skin distally to close the fi nger wounds, while
A
B
C
FIGURE 16.6 Clinical case involving MP joint contracture of the ring
fi nger. A Zigzag skin incision outlined along the palmar cord.
B Exposure of palmar cord. C Appearance of wound following
removal of cord.

Hand and Upper Extremity Reconstruction
226
leaving the palm open. The skin incisions are closed and
covered with a non-adherent dressing. I prefer a bulky soft
dressing without a plaster splint, as the patients seem more
comfortable, but a plaster splint is also acceptable.
Alternative technique: dermofasciectomy
In cases of recurrent disease, or where the skin is adherent
to the underlying contracted fascia, which is presumably
infi ltrated by myofi broblasts, the skin and involved fascia
can be removed as a composite resection. This will allow
correction of the skin shortage and produce ‘fi rebreaks.’
(When the skin is excised and replaced with a skin graft,
as in dermofasciectomy, large skin grafts can be used to
replace skin shortage and the skin graft replaces the native
skin (which is potentially infi ltrated with myofi broblasts),
creating an area of normal skin (skin graft) between two
areas of potentially diseased skin (native skin infi ltrated
with myofi broblasts), which is referred to as a ‘fi rebreak’.)
Although this does not eliminate the possibility of recur-
rence, there are reports of lower rates of recurrence.44–46 The
procedure still involves identifi cation and protection of the
neurovascular bundles and excision of the diseased fascia,
followed by joint release if necessary. The tourniquet is
defl ated and hemostasis obtained. The size of the defects
is measured with the digits in full extension and full-thick-
ness grafts are harvested, typically from the upper inner
arm. The grafts are sutured in place and a bolster dressing
is applied, followed by a plaster splint with the MP joints
in slight fl exion (30º) and the IP joints extended. I prefer
to leave the dressing/splint in place for 7–10 days and delay
therapy until the graft has taken.
Recurrence
Unfortunately, recurrence of disease is common. In patients
who have had previous surgery for Dupuytren’s disease, the
surgeon should attempt to discern between true recurrence
(Dupuytren’s disease in the same area) or extension of
disease (nodules and cords that develop in other unoperated
areas).47 This sounds straightforward, but is often diffi cult
to determine. The important point is whether there has
been a previous dissection, as the anatomy will not be
predictable, making the operation more diffi cult and time-
consuming. In addition, recurrence and altered sensation
are common when operating on patients with recurrent
Dupuytren’s disease.48
There is no way to predict which patients will develop
recurrence, and no evidence linking recurrence to inade-
quate excision at the initial operation. Management of the
skin and PIP joint is the critical factor in recurrent disease.
With signifi cant skin involvement, dermofasciectomy is
often preferred. When operating in a previously dissected
region of the palm or digit it can be very diffi cult to clearly
identify the neurovascular bundles, and it is often advanta-
geous to identify them proximally in unoperated tissue and
follow them distally. Management of the PIP joint can be
diffi cult, and if the contracture is severe, arthrodesis can be
effectively used to prevent recurrent, problematic PIP joint
A
B
C
FIGURE 16.7 Clinical case involving isolated PIP joint contracture.
A Prior to excision. B and C Following excision through transverse
incisions.

Dupuytren’s Contracture
227
A
B
C
FIGURE 16.8 Clinical case involving PIP and DIP joint contractures.
A Appearance prior to incision. B Exposure of cord (note retrovascular
cord associated with ulnar neurovascular bundle). C Appearance of
incision immediately following closure (note the initial pale
appearance of digit and skin fl aps, which resolved with warm
irrigation).
contracture. The remainder of the procedure is the same as
for primary disease.
OPTIMIZING OUTCOMES
As with many operations, a complete understanding of the
normal and pathologic anatomy is essential. Patients must
have realistic expectations and understand that the proce-
dure is designed to relieve, or at least improve, the contrac-
ture, but not to remove all the Dupuytren’s tissue. They
must be able to comply with the postoperative therapy
program and understand that prolonged night-time splint-
ing is often necessary to maintain optimal surgical results.
If these conditions are met, the chances are that the patient
will have a good result.
PITFALLS TO AVOID
● Nerve injury: neurovascular bundles will be displaced
toward the midline in the fi nger

Hand and Upper Extremity Reconstruction
228
D
E
FIGURE 16.8, cont’d D Appearance following healing. E Flexion
following therapy.
● Arterial injury: critical ischemia may develop, requiring
microsurgical reconstruction
● Devascularization of skin fl aps: resect and replace with
full-thickness skin grafts
● Hematoma: meticulous hemostasis prior to wound
closure
COMPLICATIONS
Unfortunately, the complication rate following surgery for
Dupuytren’s contracture can be high and has been reported
to be as high as 17%.49 Complications can result from
intraoperative damage to structures or from early postop-
erative events. Late postoperative events, such as recurrence
of contracture or extension of disease, should be considered
adverse outcomes not complications.
Intraoperative complications include injury to tendons
and neurovascular structures, and devascularization of skin
fl aps. Tendon injury should not occur, as one should be
able to delineate clearly between tendon and contracted
fascia. Injury to neurovascular structures typically occurs
in the digit and is due to displacement of the neurovascular
bundle by the spiral cord. When displaced, the digital vessel
or nerve may appear as contracted fascia and be inadver-
tently transected. This can occur when the surgeon mistak-
enly identifi es a strand of fascia as a digital nerve and
transects the true nerve, or when a dorsal branch of the
digital nerve is mistakenly identifi ed as the proper digital
nerve and protected while the true nerve is transected. If
the transected nerve is identifi ed, this should be repaired
primarily or with a graft. If a digital vessel is found to be
transected repair should be attempted, as recurrence of the
contracture may require a repeat operation and injury to
the other vessel would compromise digital survival.
Often, diseased fascia is adherent to the skin and eleva-
tion of skin fl aps results in a buttonhole. This may com-
promise the circulation and result in delayed wound healing.
Occasionally there may be inadequate perfusion to the digit

Dupuytren’s Contracture
229
A
B
C
D
FIGURE 16.9 Clinical case involving middle and ring MP joints and signifi cant ring fi nger PIP joint contracture. A and B preoperative photos.
C Intraoperative photo prior to removal of cord. D Residual PIP joint contracture. This was less than 30º, so a decision was made not to proceed
with joint release.
secondary to vasospasm from stretching of the digital
vessels, as the vessels become shortened with prolonged
fl exion. If this does not resolve, the digit should be fl exed
to a point that allows for reperfusion.
Early postoperative events are typically related to wound
healing, for example hematoma formation, skin fl ap necro-
sis, or infection. Great care should be taken to prevent
hematoma formation, and the judicious use of Penrose
drains will often prevent fl uid from accumulating under
skin fl aps. When a hematoma is noted, the patient should
be taken back to the operating room for evacuation and
evaluation of the wound. The hematoma creates a dead
space and stimulates mediators of infl ammation, resulting
in fi brosis and increased scarring. In addition, the

Hand and Upper Extremity Reconstruction
230
hematoma is a nidus for infection. Skin necrosis typically
occurs from the initial procedure (buttonholing, or the cre-
ation of fl aps that are too thin) or from adequate fl aps that
become ischemic secondary to pressure from a fl uid collec-
tion. If there is a large amount of skin necrosis, this should
be debrided and consideration given to skin grafting the
defect.
Late postoperative events involving signifi cant pain,
swelling, stiffness, or vasomotor changes should be treated
aggressively to reduce the chance of developing a chronic
regional pain syndrome.
POSTOPERATIVE CARE
A good postoperative program is essential to success.50
There is no consensus as to whether the use of a postopera-
tive plaster splint is necessary. In addition, the optimal
position for postoperative splinting has been debated, with
no clear consensus. Some advocate the position of function
with the MP joint fl exed and the IP joints extended, whereas
others advocate extending both the MP and the PIP
joints.
In cases without skin grafts (which are the majority) the
author places the patient in a bulky soft dressing and has
them see the therapist on the second or third postoperative
day. They receive instructions in wound care, edema
control, and active range of motion exercises. They also are
fi tted with a custom Orthoplast resting splint with both the
MP and PIP joints in extension. This is removed for hygiene
purposes and exercises. Cases managed with an open palm
technique typically heal remarkably well, often with a scar
that is diffi cult to discern. The patient is instructed on local
wound care, coverage with a non-adherent dressing, and the
importance of digital motion during the healing process.
The healing time is variable, depending on the patient and
the size of the wound, but is often complete in several
weeks.
In cases with a skin graft, I prefer to place a bolster over
the graft and use a postoperative splint with the MP joints
slightly fl exed (approximately 30º) and the PIP joints in full
extension. The splint is left undisturbed for 7–10 days and
then removed for evaluation of the graft. If the graft is
adherent, it is covered with a non-adherent dressing, an
Orthoplast splint is made, and gentle active range of motion
exercises are begun to restore fl exion. If the graft has not
taken, the cause must be determined (hematoma or fl uid
collection under the graft, inadequate immobilization,
infection, etc.) and a decision must be made as to whether
it is best to return to the operating room for repeat grafting
or allow the wound to heal secondarily.
The most important aspect of the postoperative course
is to regain full fl exion. This must be achieved even if it
means allowing some residual fl exion contracture to occur,
as the patient will function much better with full fl exion
and limited extension than with full extension and limited
fl exion. In cases with residual PIP contracture and full
fl exion, dynamic splinting may help improve the contrac-
ture and, at the least, prevent it from becoming worse.
Static night-time splinting is benefi cial, as PIP joint con-
tractures are apt to recur. There is no optimal duration of
splinting and this is patient dependent, but the author typi-
cally recommends a minimum of several months.
CONCLUSION
Most of the current research on Dupuytren’s disease has
been in the basic science arena, with efforts to improve our
understanding of the disease process. The basic surgical
tenets have not changed much over the years. Current
advances in non-surgical treatment, such as the use of col-
lagenase, will probably make current treatments obsolete,
making an offi ce-based injection for rupture of the cord the
standard of care. In addition, further research into the
basic science of the pathogenesis may some day allow us
to determine susceptible individuals and thus stop the
process before it begins. Until then, we must continue to
treat this problem with the time-honored method of surgi-
cal fasciectomy.
The variability of the disease due to the duration and
severity of contracture has precluded researchers from ana-
lyzing outcomes as has been done for other upper extremity
disorders, such as carpal tunnel syndrome and distal radius
fractures. In spite of a paucity of objective data, the subjec-
tive improvement in function makes this a worthwhile
procedure.
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Hand Clin 1999; 15: 167–174.

233
C H A P T E R
17
Nerve Reconstructive Techniques
in the Hand
Thomas H. Tung
INTRODUCTION
Nerve injuries in the upper extremity can cause permanent
impairment and have devastating consequences. Direct
primary repair should be performed if possible. Large nerve
gaps, proximal injuries and avulsion-type injuries prohibit
direct repair and mandate secondary nerve reconstruction
after the patient has recovered from the acute injury. Time
constraints due to muscle atrophy after denervation and
degeneration of the neuromuscular junction adversely infl u-
ence the outcome. Until the last century, the results of
nerve repair in the extremity, and especially of the brachial
plexus, were viewed with pessimism. In the latter half of
the 20th century, advances in peripheral nerve surgery,
including improvements in nerve repair and grafting tech-
niques, knowledge of the internal topography, injury pattern
and regenerative ability of the peripheral nerve, have con-
tributed to the improvement of outcomes.
Advances in nerve repair and improved understanding
of the internal topography of the nerve have contributed to
the development of nerve transfers. Nerve to nerve transfers
offer a superior alternative for functional restoration in
isolated or multiple nerve injuries when early reinnervation
of the target organ is necessary, such as in proximal injuries
or delayed treatment. Expendable sensory or motor axons
close to the organ allow for earlier regeneration and pre-
clude the need for nerve grafts. This chapter describes the
assessment of and criteria for nerve transfers, as well as the
management and surgical techniques for well-established
nerve transfer procedures.
NERVE REPAIR
Indications
● Transection of motor nerve; tension-free repair is pos-
sible to restore motor function.
● Transection of sensory nerve; tension-free repair is pos-
sible to restore critical sensation or to prevent neuroma
formation.
Contraindications
● Nerve injury in which primary repair will place excessive
tension on the repair, or where postural positioning is
required to minimize tension (for example bending the
elbow to repair the lacerated ulnar nerve).
Preoperative and operative considerations
After transection of a peripheral nerve, the nerve segment
distal to the injury will undergo wallerian degeneration and
the proximal nerve will undergo traumatic degeneration for
a variable distance. Crush and avulsion injuries will produce
a greater longitudinal zone of injury and degeneration than
a sharp transection. Regeneration will then occur from the
proximal nerve by the formation of regenerating units as
each single axon ‘sprouts’ multiple axons that represent the
minimum functional unit for regeneration (Fig. 17.1). The
goal of a good nerve repair is to contain and permit the
growth of these regenerating units into the remaining endo-
neurial tubes of the degenerated distal nerve, with minimal
loss of sprouting axons at the repair site. Regenerating
axons that are lost in the extraepineurial environment will
contribute to a painful neuroma and may compromise
target organ reinnervation. Optimal target organ reinnerva-
tion requires that motor, sensory, and autonomic axonal
pathways be restored such that distal organs are reinner-
vated by axons of the appropriate modality.
Operative technique
Nerve repairs may be performed using either an epineurial
or a fascicular suturing technique (Fig. 17.2). The superior-
ity of one method over the other has never been conclu-
sively demonstrated, either clinically or experimentally, and
therefore there is no general consensus as to which is better.
Intuitively, there would seem to be greater potential for the
proper alignment of axonal pathways of the appropriate
modality with the fascicular repair, but for several reasons
this is not realized clinically. Because the proper identifi ca-

Hand and Upper Extremity Reconstruction
234
tion of fascicular function is diffi cult practically, it is
possible that the direct suturing of groups of fascicles unin-
tentionally results in improper alignment and modality
mismatching, which then guarantees loss of functional
recovery. There may also be more intraneural scarring
because of the greater manipulation and suturing required
for a fascicular repair. Although the epineurial repair tech-
nique is not as precise with regard to fascicular alignment,
it may better allow neurotropic factors to infl uence the
direction of regeneration of individual fascicles and result
in comparable or better overall fascicular alignment, result-
ing ultimately in an equivalent functional outcome.
It is probably best to use aspects of both fascicular and
epineurial repair techniques, depending on the nature and
location of the injury and the fascicular arrangement of the
injured nerve. With an acute, clean transection and with
the aid of appropriate magnifi cation, anatomic vascular
markings on the epineurium can be relatively easily aligned,
and an epineurial repair should suffi ce. If there is a proxi-
mal injury, the nerve is more likely to have a mono- or
oligofascicular pattern at that level where an epineurial
repair is again appropriate. Further distally, however, there
will be a polyfascicular arrangement with a grouped fascicu-
lar pattern. Because of variations in the size of the groups
and the diameter of the individual fascicles, it is often pos-
sible to match the proximal and distal ends with enough
certainty to proceed with a grouped fascicular repair. Alter-
natively, a fascicular group can be repaired if its function is
clear, and the remainder of the nerve can be repaired with
epineurial sutures. A minimum number of fi ne microsu-
tures should be used, avoiding neural tissue itself. The
nerve repair must be tension free and adjacent joints should
be moved to note any tension at the repair site. Any fl exion
or extension of the extremity or digit to facilitate a direct
repair should be avoided.
Postoperative care
Primary repairs should be immobilized for approximately
1–2 weeks, depending on the laxity at the repair site(s) and
their ability to accommodate the full range of joint motion.
Motion should then be encouraged to minimize scarring
and adhesions around the nerve.
NERVE GRAFTING
Indications
● For the reconstruction of any critical motor or sensory
nerve in which primary repair without excessive tension
is not possible.
Growth cones with filopodia
Schwann cells
Basal lamina
FIGURE 17.1 After transection of a single axon, multiple axons will ‘sprout’ from the proximal nerve stump forming a regenerating unit,
whereas wallerian degeneration will occur distal to the injury.
A
B
FIGURE 17.2 A Standard epineurial suture technique. B Group
fascicular suture technique.

Nerve Reconstructive Techniques in the Hand
235
● Reconstruction of proximal injury to prevent neuroma
formation but in which motor restoration may not be
realistic.
● Nerve transfer for which a direct repair between the
donor and recipient nerve is not possible
Contraindications
● Primary nerve repair should be performed whenever pos-
sible to maximize axonal input to target organs.
Preoperative and operative considerations
The use of nerve grafts is necessary when a tension-free
primary repair is not possible. The critical length of a nerve
gap for which a nerve graft is required will vary depending
on the injured nerve and its anatomical location. For
example, a nerve in the forearm can be mobilized both
proximally and distally for a considerably greater distance
than a digital nerve to overcome a small nerve gap. In par-
ticular, anterior transposition of the ulnar nerve can provide
enough mobility to overcome a gap of several centimeters
to permit an acceptable primary repair. Millesi has made
the distinction between a nerve defect and a nerve gap. A
nerve defect is the actual amount of nerve tissue that is
lost, whereas a nerve gap is the distance between the proxi-
mal and distal ends of an injured nerve irrespective of
whether nerve tissue is missing or not. If there is no actual
loss of nerve tissue (nerve defect), the nerve gap results from
scarring and contracture of the proximal and distal nerve
stumps. If nerve tissue is lost, the nerve gap results from
the combination of the nerve defect and contracture. A
nerve gap will always be equal to or greater than the nerve
defect, depending on the amount of contracture or displace-
ment of the proximal and distal nerve segments. The pres-
ence of a nerve defect will complicate attempts to properly
align injured fascicles, and it may be impossible to do so
with large nerve defects because the topographical anatomy
will vary considerably between the proximal and distal
stumps. The association of long nerve grafts with a less
optimal outcome may also be due to a more severe and
higher level of injury, both of which may lead to more
extensive neuronal cell death.
Operative technique
Many of the principles of primary nerve repair are applica-
ble to nerve grafting as well. The proximal and distal nerve
ends must be prepared with the excision of all neuroma and
scar tissue, and both the proximal and distal suture sites of
the graft must be tension-free throughout the full range of
motion of the injured region. It also remains essential that
every attempt be made to align fascicles of the appropriate
modality at the proximal and distal ends of the graft. Fre-
quently it is not possible to distinguish between motor and
sensory fascicles because at the proximal stump of a high
injury the fascicles may be mixed. At the distal end, however,
fascicular function can usually be identifi ed and the distal
end of the nerve graft can be sutured selectively to the
desired fascicle(s), usually motor. The non-critical sensory
fascicles are excluded to optimize the restoration of critical
motor function.
The most commonly used donor nerves for grafting are
the sural and the medial antebrachial cutaneous (MABC)
nerves. The sural nerve is preferable in most cases because
of minimal donor morbidity and the long length of nerve
graft available. A single longitudinal incision on the poste-
rior lower leg and calf will allow identifi cation of all sural
communicating branches and suffi cient access for harvest-
ing additional nerve graft material. Smaller step incisions
may also be used, with or without the aid of a specialized
sural nerve harvester or tendon stripper, but care must be
taken and additional incisions may be needed to avoid
damage to the donor nerve when managing the communi-
cating branches. Up to 30–40 cm of graft length can usually
be obtained. The MABC is also commonly used, especially
in brachial plexus reconstructions, because it is often non-
functional and therefore has no donor morbidity. The donor
scar lies in the brachial sulcus of the medial arm, which is
often required for the exposure and reconstruction of the
injured nerves. Use of only the anterior branch will further
minimize donor site morbidity if the nerve is functional.
Up to 20 cm of nerve graft material of substantial size can
typically be harvested. Other potential nerve grafts, depend-
ing on the size and length required, include the lateral
antebrachial cutaneous (LABC) nerve and the radial sensory
nerve for proximal radial nerve injuries because the sensory
nerve will usually be dissected and excluded from the distal
repair to optimize the recovery of motor function.
Nerve laceration injuries can often be repaired primarily
if managed acutely. Most delayed or secondary reconstruc-
tions will require nerve graft reconstruction because of
nerve contracture as well as the need to trim scar tissue
from the nerve stumps, which may inhibit regeneration. If
there is a signifi cant component of crush or avulsion injury,
then nerve repair should be delayed for about 3 weeks, at
which time the zone of injury will be more clearly discern-
ible at the time of surgery to allow for adequate resection
of all injured areas. If reoperation is deemed too risky or
undesirable because of a need for vascular reconstruction,
anticipation of intense scarring at the operative fi eld, or
poor patient condition, a generous resection of the injured
nerve should be performed at the initial surgery and imme-
diate nerve grafting performed to avoid secondary nerve
grafting in an unfavorable condition.
We advocate nerve graft repair of any nerve injury in
which primary repair is not possible. Most injuries after 1
or 2 weeks will develop so much scarring and contracture
of the nerve ends that primary repair will result in excessive
tension at the repair site or may not even be possible.
Delayed reconstructions will require resection of neuroma
and scar tissue from both the proximal and distal nerve
stumps, which will result in even larger nerve gaps. Lacera-
tions of the median and ulnar nerves at the wrist or forearm
should be reconstructed in a cabled fashion because of their
larger size, and usually the sural nerve or the MABC is used
as the graft. The median and ulnar nerves will usually
require up to three to fi ve cables, depending on the size of

Hand and Upper Extremity Reconstruction
236
the grafts, for the optimal size match (Fig. 17.3). An attempt
should always be made to align the fascicular groups as
anatomically as possible to provide appropriate motor or
sensory innervation of distal targets (Fig. 17.4).
High nerve injuries at the elbow or further proximally
should be reconstructed early to permit reinnervation of
critical motor targets. If reconstruction is being performed
secondarily, we advocate graft reconstruction to manage
pain due to neuroma formation, but we will perform nerve
transfers to reinnervate critical muscles if the timing and
distance will not permit successful muscle recovery prior to
degeneration and fi brosis of motor endplates. If there is no
pain or neuroma formation at the injury site, we do not
reconstruct the nerve gap but rely on nerve transfers for
motor and sensory reconstruction.
Nerve gaps of the common or proper digital nerves will
usually require a smaller graft such as the lateral ante-
brachial cutaneous nerve (LABC) from the proximal or mid
forearm. The length of nerve graft used to reconstruct a gap
should provide for tension-free nerve coaptation to permit
early full range of motion and minimize the need for post-
operative immobilization. Splinting may be desirable ini-
tially to minimize swelling and for the patient’s comfort,
but otherwise is often not necessary.
Postoperative care
Nerve graft reconstructions should be immobilized for
approximately 1 week, because there should be no tension
at the repair site and the graft should be made long enough
to easily accommodate the full range of joint motion.
Motion should then be encouraged to minimize scarring
and adhesions around the nerve.
NERVE CONDUITS
Indications
● Reconstruction of a sensory nerve gap of no more than
3 cm.
Contraindications
● Reconstruction of a motor nerve gap remains controver-
sial and the use of a nerve graft is considered by most
to be more appropriate.
Preoperative and operative considerations
Because of the donor site morbidity associated with nerve
graft harvest, the use of readily available nerve conduits
continues to be investigated experimentally and is being
used clinically by some with success. A number of different
biodegradable conduits of varying materials and sizes are
currently available for clinical use, including nerve wraps
that allow the surgeon to tailor the conduit diameter to
meet his or her particular needs. Non-degradable nerve
tubes are not preferred because of the potential for foreign
body reaction and additional scarring. It has been shown
experimentally that inserting a small segment of nerve
tissue in the middle of the conduit, or pieces of morcellized
nerve within the conduit, will improve regeneration and
may even allow regeneration across a somewhat longer
nerve gap. The current recommendations for their use
include the reconstruction of nerve gaps of no more than
3 cm in small-diameter sensory nerves. A conduit should
be used for a gap of no more than 5 mm if reconstructing
a larger-diameter nerve.
FIGURE 17.3 Standard cable nerve graft technique for reconstruction
of large-caliber nerves, with care taken to align fascicular groups as
anatomically as possible.
A
B
FIGURE 17.4 A Median nerve injury in the distal forearm resulting in
a 5.5 cm nerve gap following neuroma excision. B Reconstruction
with sural nerve graft using fi ve cables.

Nerve Reconstructive Techniques in the Hand
237
Operative technique
The technique involves inserting the nerve stump into the
conduit for approximately 2–3 mm and securing it with
nylon microsutures, which can be performed in a horizontal
mattress fashion to help guide the nerve stump into the
tube (Figs 17.5, 17.6).
Postoperative care
Nerve conduit reconstructions should be immobilized for
approximately 1 week because there should be no tension
at the fi xation sites throughout the full range of joint
motion. Motion should then be encouraged to minimize
scarring and adhesions around the repair.
NERVE TRANSFERS OF THE UPPER EXTREMITY
Nerve transfers have conventionally been reserved for severe
root avulsion injuries of the brachial plexus in which recon-
struction with nerve grafts is not possible.1 Even when a
root stump is available, the use of nerve grafts for such
proximal injuries is frequently associated with a poor
outcome because of the long distance over which nerve
regeneration must occur to reach target muscles. To improve
outcomes in this group of patients, the technique of nerve
transfer was applied as a natural extension of the use of
tendon transfers and the principles of motor re-education
and rehabilitation. As our experience with nerve transfers
has increased and we have observed better functional
results, we have used this technique with increasing fre-
quency in a broader range of patients, including those
with more distal and isolated nerve trauma and those for
whom tendon transfers is conventionally recommended.
The advantages typically include less operative time, less
morbidity and shorter recovery times, and faster target
muscle reinnervation with less atrophy and motor endplate
fi brosis.
Principles of nerve transfer
Many of the considerations for tendon transfer also apply
to nerve transfer. The selected donor nerve(s) must be
redundant and/or expendable. It is preferable that the donor
nerve branch innervates a muscle that acts synergistically
with the target muscle to simplify and facilitate postopera-
tive rehabilitation and motor re-education. If no other
options are available, a nerve branch to a muscle that is not
synergistic or even antagonistic may be transferred, but
postoperative therapy will be more diffi cult and less intui-
tive and may lead to a less optimal result. Nerve transfers
have several advantages over tendon transfers, including
minimal dissection around the target muscle. Such dis-
section may lead to scarring and limited excursion and
strength.2,3 Nerve transfers are also capable of restoring
sensory as well as motor function, and can reinnervate
several muscles in a group with a single donor nerve.
With proximal nerve injuries, a distal nerve transfer
converts a high proximal lesion to a low distal injury in
terms of recovery and reinnervation time. We often perform
distal nerve transfers simultaneously with proximal nerve
graft reconstruction to avoid the formation of a painful
proximal neuroma. The choice of donor nerve is also based
on the proximity to the motor endplate of the target muscle
for a direct transfer using a primary repair, but a nerve graft
is occasionally necessary. Internal neurolysis can often be
used to obtain more length on the donor and recipient nerve
branch from the main nerve to allow a primary repair
whenever possible.4,5
Indications and timing
Because of the excellent results that can be obtained from
nerve transfer, we advocate its use in almost any case in
which regeneration distance and time to reinnervation
can be signifi cantly reduced to improve outcome. It is also
used to avoid surgery under unfavorable tissue conditions,
FIGURE 17.5 Suture technique for nerve gap reconstruction using
nerve conduit. Proximal and distal nerve ends are invaginated into
the tube for 2–3 mm.
FIGURE 17.6 Nerve conduits used to reconstruct the radial sensory
and lateral antebrachial cutaneous nerve (LABC) gaps following injury
and neuroma formation.

Hand and Upper Extremity Reconstruction
238
especially when other critical structures have already been
reconstructed, for example vascular injuries. Currently, our
recommendations include the following:
● Brachial plexus injuries in which only very proximal or
no nerve is available for grafting.
● High proximal injuries that require a long distance for
regeneration.
● Avoidance of scarred areas in critical locations with
potential for injury to critical structures.
● Major limb trauma with segmental loss of nerve
tissue.
● As an alternative to nerve grafting when time from
injury to reconstruction is prolonged.
● Partial nerve injuries with a defi ned functional loss.
● Spinal cord root avulsion injuries.
● Nerve injuries in which the level of injury is uncertain,
such as with idiopathic neuritides or radiation trauma
and nerve injuries with multiple levels of injury.
Recovery of motor function depends on a critical number
of motor axons reaching the target muscle to reinnervate
muscle fi bers within a critical period. In adults, reinnerva-
tion of denervated muscles is generally not possible after
12–18 months because of degeneration of the motor end-
plates. Axonal regeneration occurs at a rate of 1 inch/month,
or 1–1.5 mm/day.6 The use of distal nerve transfers can
signifi cantly prolong the ‘window’ of opportunity for surgi-
cal intervention after injury. A distal nerve transfer within
centimeters of the neuromuscular junction of the target
muscle will still have the potential for successful reinnerva-
tion even if performed late (8–10 months) after the
injury.
NERVE TRANSFERS FOR MEDIAN NERVE PALSY
Indications
● Isolated functional defi cits of forearm pronation, thumb
opposition, or fi nger fl exion within 8 months of the
inciting event.
Contraindications
● Functional defi cit of a duration of 1 year or more.
Preoperative considerations
We have used motor nerve transfers reliably to restore pro-
nation, thenar muscle function, and fl exor pollicis longus
(FPL) function. If loss of pronation exists as an isolated
defi cit, a redundant or expendable branch from the ulnar
or median nerve itself may be used to reinnervate the pro-
nator teres (see Operative Approach for Pronation, below).24
The branches (usually two) to the pronator are found proxi-
mally at the level of the antecubital fossa. Nerve stimula-
tion is used to identify the multiple branches of the median
nerve. There are usually two or more branches to the FDS,
and one or two can be transferred directly to the branches
of the pronator teres by direct repair. The pollicis longus
(PL), if present, or fl exor carpi radialis (FCR) branches may
also be used. If the median nerve is not available to provide
donor motor axons, then a redundant branch to the fl exor
carpi ulnaris (FCU) from the ulnar nerve can be used.
In the case of combined ulnar and median nerve palsy
with intact shoulder and elbow function, such as in C8–T1
avulsions, we prefer to transfer the extensor carpi radialis
brevis (ECRB) and supinator branches of the radial nerve to
the pronator teres branch and anterior interosseous nerve
(AIN). If these branches are not available, and the FCU
muscle is functional, a redundant FCU branch of the ulnar
nerve can be used. This will require a separate incision over
the course of the ulnar nerve for its anterior transposition
to facilitate a direct tension-free transfer. We have also
transferred the brachioradialis branch of the radial nerve to
the proximal AIN, with either a medial antebrachial cuta-
neous (MABC) or medial brachial cutaneous (MBC) nerve
graft to restore fi nger fl exion.
Thumb opposition can be effectively corrected with
standard tendon transfers; however, the terminal AIN at
the wrist may be used to reinnervate the motor branch of
the median nerve with a short nerve graft. In the case of
an isolated palsy of the FPL, another expendable motor
branch of the median nerve, such as that to the PL, FDS
or FCR, may be used as donor axons for transfer to the FPL
branch.
Operative approach for pronation
A longitudinal volar incision is used to expose the median
nerve, and the branches to the pronator teres are identifi ed
as the most proximal. A nerve stimulator is used to verify
loss of function to the pronator teres, and these branches
are divided as far proximally as possible. An FDS or PL
branch is the preferred donor nerve for transfer, and these
are dissected as far distally to the muscle as possible. A
direct repair is performed using standard microneuro surgical
technique (Fig. 17.7). The forearm is pronated and supi-
nated prior to the repair to ensure a tension-free repair. The
wound is closed in layers, usually with insertion of a pain
pump and a drain. A posterior splint with the elbow fl exed
to 90º is used, leaving the fi ngers, wrist and shoulder free.
On postoperative day 2 the splint, drains and pain pump
are removed, and the patient is placed in a protective sling
for an additional 2 weeks.
Operative approach: radial-to-median
nerve transfer
A longitudinal incision is made in the proximal volar
forearm just below the antecubital fossa in the lateral third
of the forearm. We perform a step-cut lengthening of the
pronator teres tendon to decompress and facilitate exposure
of the median nerve. Its branches are identifi ed and dis-
sected, and loss of function is verifi ed. The critical target
motor branches are those to the pronator teres and the AIN.
Lateral dissection is then carried out beneath the wrist
extensors to expose the radial nerve. The ECRB branch is
readily identifi ed and verifi ed using a standard nerve stimu-
lator, but exposure of the supinator branch for transfer will

Nerve Reconstructive Techniques in the Hand
239
require further distal dissection and splitting of the supina-
tor muscle. These branches are then divided as distally as
possible, and the target median nerve branches are divided
as proximally as possible to allow direct coaptation of the
appropriate nerve branches (Figs 17.8, 17.9). The forearm
is pronated and supinated to ensure a tension-free repair.
The wound is closed in layers, usually with insertion of a
pain pump and a drain. A posterior splint with the elbow
fl exed to 90º is used, leaving the fi ngers, wrist and shoulder
free. On postoperative day 2 the splint, drains and pain
pump are removed, and the patient is placed in a protective
sling for an additional 2 weeks.
NERVE TRANSFERS FOR RADIAL
NERVE PALSY
Indications
● Isolated functional defi cits of wrist extension and fi nger,
thumb extension within 8 months of the inciting
event.
Contraindications
● Functional defi cit of 1 year or more duration.
Preoperative considerations
Motor branches of the median nerve are available and in
close proximity to the radial nerve for use as donor nerves
for transfer (Fig. 17.10). Expendable motor branches with
minimal or no donor morbidity include the palmaris longus
branch, a portion or all of the FCR branches, and a redun-
dant fl exor digitalis superioris (FDS) branch. All are readily
identifi ed and dissected in the proximal forearm. The use
of a donor nerve branch from a muscle that is synergistic
to the target muscle will facilitate postoperative therapy and
motor re-education. However, a nerve from a non-synergis-
tic muscle or even an antagonistic muscle (less ideal) to the
target muscle can be used. Motor re-education will be more
diffi cult for the patient, however, and the use of additional
Pronator teres
branches
Median nerve
FCR and
Palmaris
longus
branches
FDS branch
FIGURE 17.7 Nerve transfer reconstruction for pronation. Redundant
motor branch to fl exor digitorum superfi cialis (FDS) is transferred
directly to the pronator branch of the median nerve. Portions of the
fl exor carpi radialis (FCR) or palmaris longus branches could also be
used.
ECRB
branch
Sensory
branch
PIN
Supinator
branch
Median nerve
Pronator
teres
branch
AIN
Median nerve
FIGURE 17.8 Radial-to-median nerve transfer. The radial and median
nerves are exposed through the same incision in the volar proximal
forearm. Proximal motor branches of the radial nerve including the
extensor carpi radialis brevis (ECRB) and supinator motor branches,
and the median nerve including the pronator teres and anterior
interosseous nerve (AIN) branches are mobilized. A direct transfer is
performed from the ECRB to pronator branches, and the supinator
branch to the AIN.

Hand and Upper Extremity Reconstruction
240
assistance such as audio and/or visual biofeedback may help
to correctly recruit the target muscles and to minimize
co-contraction of the antagonistic muscles. Nevertheless,
an excellent functional result is still possible for a compli-
ant patient with a good understanding of the motor re-
education strategies and appropriate hand therapy. Whereas
median and radial nerve functions are non-synergistic,
certain movements are complementary based on the teno-
desis effect. Wrist extension increases the passive tension
of the fl exor tendons and thereby passively causes fi nger
fl exion and augments fl exion strength, whereas wrist fl exion
has the opposite effect. Because of this, the use of a donor
nerve branch that innervates fi nger fl exion (FDS) rather
than wrist fl exion (FCR/PL) is complementary for wrist
extension (ECRB). Similarly, a donor nerve branch that
innervates wrist fl exion (FCR) is better suited for fi nger
extension (posterior interosseous nerve (PIN)).
Wrist extension also requires greater force than fi nger
extension. The excellent functional results we have seen
with this nerve transfer are also due in part to the relatively
greater number of motor axons transferred to the ECRB
than to the PIN branches. There is a slight size match dis-
crepancy between the two nerve branches, the PIN being
larger than the ECRB branch. By contrast, the two donor
branches from the median nerve are similar in size. Thus
the wrist extensor reinnervates a relatively greater percent-
age of motor axons.
Operative approach: median-to-radial
nerve transfer
An incision is made in the proximal volar forearm just
below the antecubital crease. The median nerve and its
branches are identifi ed deep beneath the fl exor/pronator
muscles with intraoperative nerve stimulation, including
those to the FDS, FCR, and palmaris longus (PL), the ante-
rior interosseous (AIN) and the main median nerve (Fig.
17.11). Through the same incision, the radial sensory nerve
is identifi ed laterally beneath the mobile wad muscles and
followed proximally to identify the target motor branches,
the PIN and the branch to the ECRB. In preparation for
A
B
FIGURE 17.9 A Wide exposure of volar proximal forearm with vessel
loops around radial and median nerve branches. B Direct end-to-end
transfer of ECRB to pronator branch, and supinator branch to AIN.
ECRB
branch
Sensory
branch
PIN
Median nerve
Redundant
FDS branch
FCR/PL
branch
Radial nerve
FIGURE 17.10 Median-to-radial nerve transfer. Similar exposure of
radial and median nerve branches in proximal forearm through single
longitudinal incision. Motor branch to FDS, FCR or palmaris longus of
median nerve transferred directly to ECRB and PIN branches of radial
nerve.

Nerve Reconstructive Techniques in the Hand
241
nerve transfer, the radial nerve branches to the ECRB and
the PIN are divided as proximally as possible to maximize
length for the transfer. The branch to the FDS and the
FCR/PL branch of the median nerve are then divided as
distally as possible to allow a direct tension-free end-to-end
coaptation to the ECRB branch and the PIN, respectively,
using standard microneurosurgical technique (Fig. 17.12).
Transection of the supinator branch of the radial nerve will
facilitate transposition and provide longer reach of the PIN
towards the median nerve for a direct nerve transfer.
SENSORY NERVE TRANSFERS
Restoring sensation to the hand is essential for optimal
functional reconstruction, and sensory nerve transfers may
be performed primarily or secondarily at the level of the
distal forearm or hand in conjunction with motor nerve
transfers. Transfer at a distal level converts a high-level
injury to a low-level one and permits a more rapid recovery
of sensation to facilitate postoperative therapy and motor
re-education. The ulnar nerve can be used to restore more
critical median nerve sensation in high median nerve inju-
ries, and the nerve transfer can be performed at the level of
the hand as a direct nerve transfer. The common and proper
digital nerves are dissected in the palm to the level of the
web space, and the nerve branch to the fourth web space
proximally is transferred directly to the branch to the fi rst
web space distally in an end-to-end fashion (Fig. 17.13).
Non-critical sensation of the long and ring fi ngers can be
improved by transfer in an end-to-side fashion to the func-
tional digital branches of the ulnar nerve to restore protec-
tive sensation, with no donor morbidity to the ulnar nerve
(Fig. 17.14). The branch to the third web space can also be
used to restore more critical border digit sensation in a
FIGURE 17.11 Proximal exposure of median nerve just below elbow
with vessel loops around AIN, FDS and FCR/PL motor branches.
FIGURE 17.12 Radial and median nerve branches divided and
transposed for transfer of FDS to ECRB branch and palmaris longus or
part of FCR to PIN.
Ulnar digital
nerve of
thumb
4th web
sensory
nerve
Radial digital
nerve of index
FIGURE 17.13 Sensory transfer of ulnar common digital nerve to the
fourth web space to the fi rst web space in median nerve injury to
restore critical digital sensation.

Hand and Upper Extremity Reconstruction
242
similar manner in the palm, or a sensory fascicular transfer
technique at the level of the wrist and distal forearm can
be performed. Because the internal topography of the
median and ulnar nerves at that level is well established,
the fascicular components of each nerve are readily identi-
fi ed and dissected. In particular, the fascicle to the third
web space is readily dissected from the median nerve to the
level of the mid-forearm. However, the sensory components
of the ulnar nerve to the fourth web space and to the ulnar
border of the small fi nger are not readily separable at this
level. Therefore, we prefer dissection in the hand when
using only the fourth web space branch as donor nerve, and
fascicular transfer at the distal forearm when using the
whole sensory component of the ulnar nerve to the hand
as the recipient or donor nerve. When performing internal
neurolysis of the median nerve, usually four fascicular
groups are easily dissected, with the group innervating the
third web space located the most medially. In the ulnar
nerve at the wrist, the motor fascicle is located medially
and the sensory fascicles make up the lateral half. As with
all nerve transfers, the donor fascicle or nerve branch is
divided as distally as possible, and the recipient fascicle or
nerve branch is divided as proximally as possible to maxi-
mize length for transposition and minimize tension at the
coaptation sites. The fascicular transfer technique at the
wrist has the advantage of avoiding incisions on the palm,
avoiding potential injury to the palmar vascular arches, and
can be combined with other procedures typically performed
at the wrist or distal forearm.
Optimizing outcomes: motor and
sensory re-education
The long-term focus of rehabilitation is on motor and/or
sensory re-education. As with tendon transfers, the patient
must learn and be able to coordinate synchronized move-
ment. Following nerve transfer, the cortical command
required to initiate target muscle contraction is different
from that previously experienced. The patient ‘relearns’
motor control of the reinnervated target muscle by activat-
ing the nerve to the donor muscle, which now stimulates
the reinnervated muscle (see Fig. 17.8).5 This concept is
similar to the re-education needed after tendon transfers.
In addition, the ability to restore sensation can only improve
recovery, but does not guarantee optimal function. Sensory
re-education begins when the patient begins to perceive
input stimulus from the reinnervated territory. Cortical
remapping occurs from continued sensory input from the
newly innervated areas.
CONCLUSIONS
Over the last century, signifi cant advances in peripheral
nerve surgery have been made. The introduction of micro-
surgery has transformed nerve surgery into a sophisticated
specialty with techniques that produce consistent results.
The combined experience from brachial plexus surgery,
tendon transfers, and motor and sensory re-education has
allowed the development of nerve transfer techniques as a
reliable surgical option for the reconstruction of nerve inju-
ries. In the last decade, reconstruction of upper plexus
injuries in our institution has progressed from the use of
long nerve grafts to distal elegant nerve transfers. The need
to expose and explore the brachial plexus is reserved for
tumor cases and other special circumstances. Our use of
nerve transfers far removed from the zone of injury allows
us to restore function and sensibility in shorter operative
time, through smaller incisions, with less morbidity, and
to achieve comparable or better functional results than in
the past.
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Ulnar digital
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small finger
2nd and 3rd
web sensory
nerves
FIGURE 17.14 For non-critical digit sensation following median
nerve injury, end-to-side transfer of common digital nerves to the
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essentially no donor morbidity.

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245
C H A P T E R
18
Brachial Plexus Reconstructive Techniques
Lynda Yang and Kevin C. Chung
INTRODUCTION
Brachial plexus injuries lead to paresis or paralysis of the
upper extremity. Motor vehicle accidents cause approxi-
mately 70% of adult brachial plexus injuries (BPI),1 and
such injuries lead to signifi cant socioeconomic diffi culties
for these newly disabled patients who are usually 15–25-
year-old males.2–4 As the number of accidents from high-
speed motor vehicle collisions and dangerous sporting
events increases, the prevalence of BPI is also increasing
worldwide.3,5–9 The care of patients with BPI continues to
evolve: outcomes will be enhanced by improvements in
surgical techniques, by advances in nerve regeneration
research, and by the development of novel pharmacological
agents. This chapter presents the key concepts underlying
the current surgical management of BPI.
Appropriate surgical management of patients with bra-
chial plexus injuries depends on an understanding of the
physiology of nerve injury/regeneration and brachial plexus
anatomy. In 1943, Seddon10 proposed a system for classify-
ing nerve injury that is still useful today; this system con-
sists of neurapraxia, axonotmesis, and neurotmesis (Fig.
18.1). Neurapraxia refers to the segmental interruption of
the myelin sheaths, leaving the axons and surrounding
connective tissues intact; this type of injury recovers spon-
taneously within a few weeks. Axonotmesis refers to the
interruption of both the myelin sheath and the axons, but
with sparing of the surrounding connective tissues (intact
Schwann cell basal lamina): this injury may recover spon-
taneously within months to years if axonal regeneration is
able to progress across the injury zone. Neurotmesis refers
to the interruption of all of the elements, including the
axons, the myelin sheaths, and the surrounding connective
tissues; spontaneous recovery does not occur.
To select the appropriate timing for diagnostic electro-
physiologic studies, one must recognize the concept of
Wallerian degeneration. When the structure of the axon is
disrupted, the neuron itself is damaged; the distal portion
of the axon, which is disconnected from the cell body,
undergoes granular disintegration of the cytoskeleton and
axoplasm over several days to weeks. Early after injury,
until the distal axons are totally degenerated, motor con-
ductivity and/or sensory nerve potentials still can be
observed. Therefore, electrodiagnostic studies used to
predict the severity of the lesion and to guide treatment
recommendations should not be performed within several
weeks of the injury.
Regeneration of the interrupted axon towards its correct
muscular target depends on guidance by the basal Schwann
cell lamina (axonotmesis) or grafted basal lamina (neurot-
mesis). The axons of the proximal stump will sprout, and
a growth cone leads each sprout. The distal stump degener-
ates, and axonal and myelin debris will be cleared away by
macrophages (Wallerian degeneration) to prepare the distal
stump for reception of the outgrowing axonal sprouts. The
‘growing point’ of the regenerating axons can produce par-
esthesias when tapped (Tinel’s sign). When the outgrowing
stump of axonal growth cones is halted by scar tissue at the
point of injury, a neuroma forms.
Functional recovery relies on regenerating axons that
can grow to reach their target muscle before the denervated
muscle degenerates. Unfortunately, the rate of axonal
regeneration is quite slow, at approximately 1 mm/day.
Therefore, axonotmetic injury to the supraclavicular bra-
chial plexus requires months to years before the recovering
axon reaches the distal musculature. After long periods of
denervation, the distal musculature will have degenerated
and the joints may develop contractures. Research into
expediting nerve regeneration is under way, but adjunctive
pharmacologic agents to enhance nerve regeneration are not
yet ready for clinical use.
Another key to understanding the operative manage-
ment of BPI is a thorough understanding of the normal
anatomy of the brachial plexus. The brachial plexus is
comprised of the nerve structures by which the central

Hand and Upper Extremity Reconstruction
246
nerve system communicates with the upper extremity. It
has fi ve roots (C5–T1), three trunks (upper, middle, and
lower), six divisions (two divisions, anterior and posterior,
per trunk), three cords (lateral, posterior and medial), and
fi ve terminal nerve branches (musculocutaneous, radial,
axillary, median, and ulnar; Fig. 18.2). Grossly, the brachial
plexus emerges in the posterior triangle of the neck
(bordered by the sternocleidomastoid, trapezius, clavicle
and occiput; Fig. 18.3) Note that the spinal accessory nerve
emerges posterior to the sternocleidomastoid, two-thirds of
the way up from the sternum to the mastoid, and travels
relatively superfi cially towards the trapezius. More specifi -
cally, the trunks of the brachial plexus emerge within
the interscalene triangle bordered by the anterior scalene,
middle scalene, and the clavicle (Fig. 18.4). The subclavian
artery also travels through the interscalene triangle, whereas
the subclavian vein travels anterior to the anterior scalene.
The nerve roots contributing to the trunks exit from their
neural foramina and run along the bony groove between the
anterior and posterior tubercles of the vertebrae. These
bony ‘chutes’ are well formed for the nerves comprising the
upper trunk (C5, C6), and more abbreviated for the nerves
comprising the lower trunk. In addition, there is less con-
nective tissue binding the lower nerve roots to the bony
chutes than in the upper nerve roots. Consequently, the
lower nerve roots (C8, T1) are prone to preganglionic (avul-
sion) injury, whereas the nerves comprising the upper trunk
tend to sustain postganglionic injury.
The anterior scalene attaches to the anterior tubercle of
the transverse process of the vertebrae and the clavicle, and
the middle scalene attaches to the posterior tubercle of the
transverse process; the anterior tubercle of C6 is particu-
larly bulbous (Chassignac’s tubercle) and can be used as an
intraoperative marker. The brachial plexus is intimately
associated with prominent vasculature. In the supraclavicu-
lar region, the subclavian vessels are in close proximity to
the lower roots/lower trunk. In the infraclavicular region
the cords surround the axillary artery, and in the arm the
median nerve travels with the brachial artery.
Basement membrane
Myelin sheath
Axon
Neurapraxia
Axonotmesis
Neurotmesis
FIGURE 18.1 Seddon’s classifi cation of nerve injury: neurapraxia,
axonotmesis, neurotmesis.
Branches
Cords Divisions Trunks
Roots
C4
C6
T1
FIGURE 18.2 Brachial plexus: fi ve roots (C5–T1), three trunks (upper,
middle, lower), six divisions (anterior and posterior divisions per
trunk), three cords (lateral, posterior, medial), and fi ve branches
(musculocutaneous, radial, axillary, median, ulnar.)
Sternocleidomastoid muscle
Trunks of brachial plexus
Accessory nerve
Phrenic nerve
Middle scalene muscle
Anterior scalene muscle
FIGURE 18.3 Brachial plexus emerging from the posterior triangle of
the neck.

Brachial Plexus Reconstructive Techniques
247
INDICATIONS AND CONTRAINDICATIONS
FOR SURGERY
Understanding the indications and contraindications for
surgical management of BPI depends on understanding the
type of injury. Brachial plexus injuries can be classifi ed in
several ways. Anatomically, they can be considered to be
supraclavicular (roots, trunks), retroclavicular (divisions),
and infraclavicular (cords, terminal branches). Most
injuries occur to the roots and trunks in the supraclavicular
region. Supraclavicular injuries can also be classifi ed as pre-
or postganglionic, with profound surgical implications. A
preganglionic injury results in permanent paralysis of the
muscles innervated by the avulsed roots, complete sensory
loss of the corresponding dermatomes, and most impor-
tantly, the lack of spontaneous recovery. A postganglionic
injury potentially retains the function of the cell body
within the ventral horn of the spinal cord, and under the
appropriate conditions these neurons may regenerate axons.
Brachial plexus injury can be open or closed. Open injuries
include sharp lacerations and missile wounds, whereas
closed injuries include traction or compressive injuries.
Current guidelines recommend early repair of clean sharp
nerve lacerations, and the delayed (by weeks) repair of
ragged or dirty nerve lacerations. Missile wounds with vas-
cular injury should be explored acutely. Early intervention
is generally not recommended in closed injuries because of
the potential for neurapraxia. Spontaneous regeneration,
when it occurs, yields superior functional outcomes com-
pared to surgical repair or reconstruction. Consideration of
the clinical implications of these issues led Kline11 to
propose an algorithm for the surgical management of
peripheral nerve and brachial plexus injuries (Fig. 18.5).
PREOPERATIVE HISTORY
AND CONSIDERATIONS
When considering surgical treatment, the surgeon ought
to weigh the potential benefi ts versus the impending risks
of the operation. Estimation of the risk–benefi t ratio of the
treatment requires careful history taking and a detailed
physical examination. Well-intentioned but inappropriate
procedures can result in worsening symptoms or creating
new defi cits. The following is not meant to describe a com-
prehensive neurological examination of the upper extremity
peripheral nerve system (refer to Aids to the Examination
of the Peripheral Nerve System12), but will provide a few
pearls ‘for guidance’.
The history should include the patient’s description of
the timing and quality of the motor and sensory defi cits,
pain, paresthesias, other symptoms, and also the mecha-
nism of injury. For example, a road rash over the shoulder
may point towards an injury resulting from traction of the
brachial plexus when the arm is distracted in the opposite
direction of the head, which implies injury to the upper
brachial plexus (Erb’s palsy). In contrast, a road rash on the
underside of the arm, axilla, and/or side of torso points
towards an injury that results from traction of the arm in
the fully abducted position, implying injury to the lower
brachial plexus (Klumpke’s palsy). Likewise, a similar acute
presentation from falling 3 feet (more consistent with
neurapraxia) versus ejection from a high-speed motor
vehicle has very different implications for treatment.
The physical examination can be categorized as follows.
A vascular assessment for the presence of peripheral pulses
must be performed. Inspection of the affected limb can
reveal changes in skin turgor and coloration, which may
point towards denervated dermatomes. A comprehensive
assessment of the musculature, coupled with a thorough
understanding of brachial plexus anatomy, can lead to an
accurate determination of the identity and the severity of
injured nerves and their anatomic level of involvement.
Although the spinal accessory nerve is not considered to be
part of the brachial plexus, examination of trapezius func-
tion will determine whether the spinal accessory nerve can
be a potential donor in future neurotization procedures.
Diaphragmatic function should be assessed by plain radio-
graph or ultrasound, because denervation of the diaphragm
can imply a preganglionic lesion. The sensory examination
can confi rm the suspicion of the relevant lesion, and the
quality of the extremity pain can aid in the localization of
the lesion. For example, constant aching can indicate deaf-
ferentation pain, which accompanies an avulsion injury,
whereas sharp, stabbing pains are more consistent with
postganglionic lesions. The presence of Horner’s syndrome
(an interruption of sympathetic fi bers marked by constricted
pupil, drooping eyelid, and lack of sweating on the face) is
consistent with a preganglionic lesion. Serial palpation and
percussion along the suspected path of the injured nerve
can detect a distally traveling Tinel’s sign of neural regen-
Middle scalene
Subclavian artery
Brachial plexus
Anterior scalene
Well-formed “chute”
First rib
FIGURE 18.4 Brachial plexus emerging from the interscalene
triangle.

Hand and Upper Extremity Reconstruction
248
eration. Finally, examination of the range of motion of the
joints of the upper extremity can detect joint contractures
and signify the need for more aggressive physical therapy.
Electrodiagnostic studies (EDS) can aid in defi ning the
site of injury and the potential for reinnervation of affected
musculature. Baseline EDS are best performed 3 or more
weeks after injury. Serial EDS can document clinically sig-
nifi cant regeneration. Lack of innervation of paraspinal
muscles implies a proximal injury within the brachial
plexus. Sensory nerve action potentials (SNAPs) and
somatosensory evoked potentials (SSEPs) are also useful in
determining the site of injury.
Radiographic studies should include cervical spine and
chest radiographs, which may reveal associated fractures of
the cervical vertebrae, clavicle, scapula or ribs, and demon-
strate an elevated hemidiaphragm (phrenic nerve injury).
Post-myelography computerized tomography (CT) and MRI
can be used to detect pseudomeningoceles, which may be
associated with preganglionic injuries and require extra-
plexal nerve transfer procedures. The resolution provided
by current standard imaging techniques is as yet unable to
demonstrate direct evidence for the interruption of nerve
structures.
When operative treatment is contemplated, the sur-
geon should gauge the patient’s expectations. Similarly, the
patient should understand the reconstructive priorities
when spontaneous recovery of function is unlikely. Patience
is needed from both patient and practitioner. Most sur-
geons consider restoration of elbow fl exion to be of the
highest priority. Shoulder abduction and stability, hand
sensibility, wrist extension and fi nger fl exion, wrist fl exion
and fi nger extension, and intrinsic function of the hand
follow in order of priority.13,14
OPERATIVE APPROACH
The successful brachial plexus operation depends on not
only a thorough understanding of the nerve connections
within the plexus, but also on the vital structures surround-
ing the brachial plexus.
Supraclavicular exposure
The supraclavicular brachial plexus is exposed in the pos-
terior triangle of the neck (Fig. 18.6, black arrow). The
patient is supine, with a roll under the scapulae and the
head turned towards the opposite direction with the neck
in gentle extension (Fig. 18.6). If there is a need to acquire
a sural nerve graft, a roll is also placed under the buttock
to internally rotate and fl ex the ipsilateral leg. The lower
part of the face, neck, shoulder, entire chest and leg are
prepared for surgery.
A curvilinear incision extending from the sternocleido-
mastoid to the trapezius is made approximately 1.5 cm
above the clavicle. The platysma is incised perpendicular to
its fi bers, and a generous subplatysmal dissection is per-
Evaluation
yrujni d
e
s
olC
yrujni n
e
p
O
Brachial plexus injury
Primary or
early repair
(within 3 d)
Sharp
Nerve divided
sharply
Blunt
Nerve contused
Epineureum ragged
"Tack" to adjacent
tissue planes
Secondary repair
at 3 wks
Exploration,
Repair/Reconstruction
With intraoperative
monitoring, >3 months
No regeneration
(No recovery)
Regeneration
(Recovery)
Clinical assessment,
EMGs, Radiographs,
CT-myelogram, MRI
Laceration/
transection
Lesion in continuity from
stretch/contusion.
Compression, ischemic,
electric, injection, or
latrogenic injury
FIGURE 18.5 Algorithm for the surgical
management of peripheral nerve and
brachial plexus injuries.

Brachial Plexus Reconstructive Techniques
249
formed. The external jugular vein is often encountered and
must be retracted or ligated when necessary. The position
of the spinal accessory nerve is relatively superfi cial as it
courses from the posterior aspect of the sternocleidomas-
toid muscle (two-thirds of the distance from the sternum
to the mastoid) towards its insertion in the trapezius (Fig.
18.7). Identifi cation of the spinal accessory nerve along its
course is crucial to preserve trapezius function and to use
its branches for a donor for nerve transfer. An intraopera-
tive nerve stimulator can be used to identify and confi rm
this nerve.
The lateral margin of the sternocleidomastoid muscle is
identifi ed, with its sternal and clavicular heads. The lateral
aspect of the clavicular head is released to facilitate expo-
sure. The supraclavicular nerves (sensory nerve branches of
the ansa cervicalis, C2–C4) are identifi ed along their super-
fi cial craniocaudal course and likewise preserved for ana-
tomical landmarks and as potential donors for nerve graft
material. The supraclavicular nerves are followed proxi-
mally until the C4 spinal nerve root is identifi ed; a branch
from this nerve can be followed to the phrenic nerve, which
derives from C3, C4, and C5. The phrenic nerve is dis-
sected along its length on the anterior aspect of the anterior
scalene muscle. One should carefully mobilize the phrenic
nerve to preserve the function of the diaphragm. Periodic
stimulation of the nerve with an intraoperative nerve
stimulator will confi rm the intraoperative integrity of the
nerve.
The lateral edge of the anterior scalene muscle is identi-
fi ed. The scalene fat pad is released from this border in a
cranial to caudal direction, then in a medial to lateral direc-
tion to refl ect the fat pad laterally. When releasing the fat
pad deep in this region during the exposure of the left
supraclavicular brachial plexus, one should preserve or
ligate the thoracic duct to avoid chyle leakage. The omohy-
oid muscle is identifi ed along its course toward the supra-
scapular notch, and can be tagged and divided. Note that
preserving this muscle to identify the suprascapular notch
can facilitate the identifi cation of the suprascapular nerve
(see below), especially in patients whose anatomy is dis-
torted by trauma.
The phrenic nerve courses lateral to medial toward the
diaphragm, whereas the contents of the plexus and the
surrounding nerves course from medial to lateral. As the
phrenic nerve approaches the lateral edge of the anterior
scalene, the C5 spinal nerve root emerges (Fig. 18.8). Fol-
lowing the C5 root distally leads to the upper trunk, and
following the upper trunk proximally will lead to the C6
spinal nerve root. The C6 spinal nerve root is located caudal
and dorsal to the C5 spinal nerve root. The anterior tuber-
cle of C6 is very prominent (Chassignac’s tubercle).
The C7, C8, and T1 spinal nerve roots are sequentially
more caudal and dorsal. The transverse cervical artery and
vein cross the C7 spinal nerve root and can be ligated.
FIGURE 18.6 Incisions. Black arrow indicates incision for
supraclavicular approach to brachial plexus. Red arrow indicates
standard deltopectoral approach to the infraclavicular brachial plexus.
FIGURE 18.7 Spinal accessory nerve in its superfi cial course from the
sternocleidomastoid to the trapezius.
FIGURE 18.8 C5 root emerging at the junction of the phrenic nerve
with the lateral edge of the anterior scalene.
C5
Phrenic nerve
Anterior scalene
Upper trunk

Hand and Upper Extremity Reconstruction
250
Following the C7 spinal nerve distally will reveal the middle
trunk. The C8 and T1 spinal nerves combine quickly to
form the lower trunk, which is adjacent to the subclavian
vessels. The roots of the lower trunk surround the fi rst rib;
therefore, care should be taken to avoid injury to the pleura.
Should more proximal exposure of the nerve roots be neces-
sary, the lateral edge of the anterior scalene muscle and the
bony ‘chutes’ conducting the spinal nerve roots can be
resected. Occasionally, clear fl uid may be observed during
the proximal exposure of the spinal nerve roots, indicating
the presence of a pseudomeningocele and probably an
avulsed root.
The next step is to identify the suprascapular nerve and
the divisions of the upper trunk. The upper trunk can be
seen to ‘split’ into three separate structures: from lateral to
medial the suprascapular nerve, the posterior division, and
the anterior division (Fig. 18.9). The divisions of the bra-
chial plexus can often be exposed by downward retraction
of the clavicle. Should a more extensive exposure of
the divisions be necessary, a clavicle osteotomy may be
performed.
A commonly encountered situation in the traumatic
injury of the supraclavicular brachial plexus is an upper
trunk neuroma. Following the exposure described, intra-
operative nerve action potentials (NAPs) are measured. A
non-conducting upper trunk neuroma is generally resected.
A common strategy to repair this lesion comprises the fol-
lowing: (1) spinal accessory to suprascapular nerve transfer;
(2) graft repair from the C5 spinal nerve to the posterior
division of the upper trunk; and (3) graft repair from the
C6 spinal nerve to the anterior division of the upper
trunk.
Infraclavicular exposure
The infraclavicular brachial plexus is exposed through the
deltopectoral groove. The patient is placed in the supine
position and a linear incision made from the clavicle toward
the axilla, in line with the deltopectoral groove (see Fig.
18.6). The cephalic vein is visualized within the groove and
can be retracted laterally or ligated. If needed, a portion of
the pectoralis muscle can be detached from the inferior
surface of the clavicle and from the humerus. The cuff of
tendon from the humerus is tagged to facilitate later
repair.
The coracoid process of the scapula as well as the ten-
dinous attachment of the pectoralis minor will be promi-
nent. Blunt dissection will separate the pectoralis minor
from the surrounding tissues. Once the pectoralis minor
tendon has been isolated, it may be divided. It is convenient
to place sutures into the tendon on either side of the divided
tendon for retraction and reapproximation.
Division of the pectoralis minor will reveal the infra-
clavicular brachial plexus lying immediately underneath.
When the arm is at or lower than the plane of the shoulder,
the most superfi cial structures are the lateral cord with its
lateral branch leading to the musculocutaneous nerve and
its medial branch leading to the median nerve. The medial
cord may be identifi ed medial and slightly posterior to the
axillary artery, and the lateral branch of the medial cord
will lead to the median nerve (the medial branch continues
down the arm as the ulnar nerve). Exposure of the posterior
cord and its axillary and radial nerve branches is best
accomplished in the region lateral to the axillary artery.
OPTIMIZING OUTCOMES
Patient selection, an understanding of their expectations,
and a thorough knowledge of the anatomical caveats result-
ing in the thoughtful surgical planning of the repair/
reconstruction can facilitate an optimal outcome.
Diagnosis of root avulsion
Diagnosing nerve root avulsion is crucial to optimize the
outcome of the reconstructive strategy used in brachial
plexus surgery. Currently, no single diagnostic study can
provide either direct evidence of root avulsion or enough
predictive value to diagnose this condition.15–18 The diagno-
sis of an avulsion injury should not be missed because an
avulsed root eliminates the option of a direct primary repair
of the relevant neural elements and necessitates the use of
other reconstructive options.
Available investigative modalities include computerized
tomography–myelography (CT–myelography), MRI, pre-
and intraoperative EDS, and a thorough neurologic exami-
nation. CT–myelography can document the presence of
pseudomeningoceles, implying the presence of root avul-
sion. Rarely, the rootlets may be directly visualized;
however, this study has an approximately 10% rate of false
positives and false negatives.15,18 MRI of the cervical spine
can also document pseudomeningoceles and occasionally
may be of suffi ciently high resolution to demonstrate the
FIGURE 18.9 The suprascapular nerve and the divisions of the upper
trunk.
CN XI
Posterior division
Anterior division
Suprascapular n.

Brachial Plexus Reconstructive Techniques
251
disconnected neural elements.17 Preoperative EDS include
electromyography (EMG) and NAPs. Testing one muscle
cannot defi nitively exclude root avulsion because each
muscle is innervated by more than one nerve root. EMG
can also demonstrate denervation of posterior myotomes,
but the reliability of this fi nding in predicting avulsion
injury varies. A more reliable electrodiagnostic modality to
evaluate for avulsion injury is the absence of motor action
potentials coupled with the presence of a sensory NAP from
the analogous insensate dermatome. An avulsion injury
will interrupt the continuity of the cells of the dorsal gan-
glion (sensory) to the spinal cord, but not the distal exten-
sion of the sensory axon to the periphery; therefore,
somatosensory evoked potentials (SSEPs) will be absent in
the presence of sensory nerve action potentials (SNAPs).
Similar logic is applied to the intraoperative assessment of
the SSEPs from direct stimulation of the nerve root. The
absence of SSEPs in the presence of rapid NAPs provides
strong evidence for an avulsion injury.19,20
Further confi rmation of root avulsion results from a
thorough neurological examination and knowledge of bra-
chial plexus anatomy. The phrenic nerve, dorsal scapular
nerve, and long thoracic nerve arise proximally from the
roots soon after they exit the neural foramen. Consequently,
a raised hemidiaphragm (phrenic nerve), paralyzed levator
scapulae (dorsal scapular), and/or paralyzed serratus ante-
rior (long thoracic nerve) imply a very proximal (potential
avulsion) injury to the relevant nerve roots. The presence
of ptosis, miosis, and anhydrosis of the ipsilateral face is
consistent with Horner’s syndrome. Horner’s syndrome
implies injury to the upper thoracic sympathetic ganglion,
which is again located adjacent to the nerve root as it exits
the neural foramen. Lastly, the patient’s report of deaffer-
entation pain (continuous burning or compressive pain)
will support the diagnosis of brachial plexus avulsion.
Extensile exposure
Brachial plexus exploration should not be considered a
minimally invasive procedure in current practice. Incom-
plete dissection of the appropriate plexal elements can
result in a suboptimal outcome. The dissection of unin-
jured as well as injured nerves helps orient the surgeon
when the anatomy may be distorted by the injury, and can
also expose sensory nerves to be used for grafts. Identifi ca-
tion of healthy proximal and distal recipient targets for
grafts or nerve transfers is crucial to maximizing the poten-
tial for functional regeneration.21
Surgical options
The knowledge of and ability to combine relevant surgical
nerve repair/reconstructive options is key to achieving
an optimal functional outcome. The increase in surgical
options during brachial plexus operations has paralleled the
advances in microsurgical techniques and the increas-
ing availability of reliable intraoperative electrodiagnostic
studies. Standard options to be considered for surgical repair
or reconstructive strategy include neurolysis, direct nerve
repair, nerve repair with graft, and nerve transfers
(neurotization).
Neurolysis is the removal of scar tissue from around the
nerve (external neurolysis) or between fascicles (internal
neurolysis) if the nerve is injured asymmetrically. Dis-
section is begun with proximal and distal uninjured nerve
ends towards the involved injured segment. Intraoperative
EDS can determine whether the injured segment can
conduct electric signals. The presence of nerve action
potentials across an involved segment implies that neuroly-
sis alone is adequate for neural recovery.22
Direct (end-to-end) repair is possible only if a short
nerve gap exists after resection of the non-functioning
neural segment. Direct repair is preferred over indirect
(graft) repair because of the better functional results.22
Tension across the repair must be avoided to reduce the
risk of failure of regeneration. Tension can be reduced by
proximal and distal mobilization of the nerve, internal neu-
rolysis for transposition of the involved fascicles (not rec-
ommended usually because of the scarring from the internal
nerve dissection), and optimal positioning of the surround-
ing soft tissues/bony elements to shorten the nerve gap
distance. The authors prefer the mobilization technique, for
example by performing anterior transposition of the ulnar
nerve to gain 3–4 cm of extra nerve advancement. Direct
repair is performed by coapting the ends with either sutures
(6/0 to 8/0 Ethilon or Prolene) or by approximating the ends
with fi brin glue.
A graft (indirect repair) is needed when the gap that
exists after resection of the non-functioning neural segment
is too large for direct approximation without tension. The
length of the graft should be the length of the gap plus 10%.
Autograft is usually used, derived from the sural nerve,
antebrachial cutaneous nerve, or superfi cial radial nerve (if
not functioning), because these small-caliber grafts achieve
better results (faster revascularization) than larger-caliber
ones.23 Coaptation of the ends of the graft to the proximal
and distal stumps is similar to that used for the direct
repair.
The introduction of increasingly creative nerve transfers
(neurotization) has transformed the surgical arena for bra-
chial plexus injuries, especially in the context of avulsion
injury.24,25 Neurotization has changed the outlook for the
‘unrepairable’ avulsion injury to a ‘reconstructable’ one by
coapting a proximal functional nerve donor with a distal
denervated nerve to reinnervate the latter with healthy
donor axons. Reported nerve transfer techniques include
neurotization of the spinal accessory to the suprascapular
nerve26–29 or radial fascicular to axillary nerve30,31 to achieve
shoulder abduction, intercostal32–34 medial pectoral35,36
phrenic37,38 ulnar fascicular nerve transfer to the musculo-
cutaneous nerve,39,40 the double fascicular transfer (ulnar
fascicular to musculocutaneous and median fascicular to
brachialis)41–43 for elbow fl exion (Fig. 18.10), and contralat-
eral C7 spinal nerve for intraplexal repair.43,44 Recovery of
the translated function appears to rely on cortical plastic-
ity.46 Fascicle(s) from the functioning ulnar nerve can be
transferred to the nerve branches of the biceps and/or bra-
chialis to regain elbow fl exion.

Hand and Upper Extremity Reconstruction
252
The more widespread use of neurotization to optimize
the outcomes from brachial plexus surgery has led to much
debate regarding the best choice of nerve transfer technique,
and recent literature favors the use of directed discrete
transfers to achieve a specifi c function.25,28 However, one
must remember that intraplexal repair (direct or graft),
when available, should be performed, with augmentation
by extraplexal nerve transfers because of the relatively
few extraplexal transfer possibilities available in a severely
injured brachial plexus.47
For delayed presentations (longer than 1 year) after bra-
chial plexus injury, nerve reconstruction is not possible
because of denervation to the muscles. In these situations,
free muscle transfers are the only option to regain elbow
fl exion and rudimentary fi nger fl exion. In the fi rst opera-
tion, a gracilis muscle is used to replace the biceps function.
The proximal muscle is anchored to the clavicle and the
distal tendon is woven to the biceps tendon. The obturator
nerve from the gracilis muscle is coapted to the distal end
of the spinal accessory nerve, which is usually functional.
The vessels are repaired to the thoracoacromial vessels.
This is a highly complex operation that may give a rather
gratifying outcome of about 70–90º of elbow motion.
Patients usually detect voluntary muscle contraction at 4–6
months after the operation. In a second-stage operation
once the patient has attained suffi cient elbow fl exion,
another gracilis muscle is used to power fi nger fl exion. The
proximal muscle is attached to the second or third rib and
the distal tendons are woven to the fl exor tendons in the
proximal forearm. The third, fourth and fi fth intercostal
nerves are used to provide motor nerve input, and the tho-
racodorsal vessels from the axilla are used for blood fl ow.
The outcome of this second-stage procedure is less satisfy-
ing. Patients can attain rather modest fi nger fl exion and the
hand is used mainly as a hook. The fi ngers extend by teno-
desis effect, which is produced when the wrist fl exes by
gravity. In patients with limited hand function, the wrist
should not be fused. The loss of tenodesis function from
an injudicious wrist fusion procedure will markedly hamper
an already limited hand function.
COMPLICATIONS AND SIDE EFFECTS
Complications
can
occur
during
brachial
plexus
operations, but can be minimized by a thorough under-
standing of not only the nerve anatomy but also the sur-
rounding soft tissue and musculoskeletal anatomy. Russell
and Kline’s48 review includes the following categories of
injury: neural, vascular, orthopedic, pneumothorax, and
wound problems.
A common neural injury that occurs during the supra-
clavicular brachial plexus exploration is to the phrenic
nerve. This is particularly vulnerable in its location super-
fi cial to the anterior scalene and deep to the sternocleido-
mastoid. Identifi cation of the nerve and careful mobilization
early in the dissection will allow it to be protected during
the remainder of the operation. One must avoid inadvertent
retraction of the anterior scalene muscle as the neural
foramen is approached. Another nerve that is vulnerable
because of its superfi cial anatomy is the spinal accessory
nerve. When using a transverse incision, the surgeon should
identify the spinal accessory nerve as it travels within the
superfi cial adipose tissue anterior to the trapezius muscle.
The nerve should be mobilized and traced proximally
towards its emergence from the posterior aspect of the
sternocleidomastoid, two-thirds of the way from the
sternum to the mastoid process. Use of a nerve stimulator
is helpful. During an infraclavicular brachial plexus explo-
ration, the superfi cial position of the musculocutaneous
nerve should be recognized to avoid accidental retraction of
the nerve with the surrounding muscle. Placing the arm in
the same plane as or lower than the shoulder, the lateral
cord/musculocutaneous nerve becomes the most superfi cial
structure under the pectoralis minor.
Vascular injury occurs most commonly in the depths of
the scalene triangle, usually during exposure of the lower
nerve roots. The anterior scalene, as it attaches to the fi rst
rib, separates the subclavian vein from the artery. Injury
can occur to the parent vessels or to their smaller branches
in this region. Small branch injuries are amenable to bipolar
coagulation or suture repair; however, signifi cant arterial
injury will require an emergent vascular or thoracic consul-
tation. To avoid arterial injury, frequent digital palpation,
dissection parallel to the artery, and the addition of an
infraclavicular exposure can be useful. Because the brachial
plexus is intimate with the subclavian vessels, a nerve
injury can be accompanied by a vascular injury. A careful
examination of the affected limb, which includes evaluating
distal pulses, is crucial, and when necessary, an angiogram
may be performed prior to surgery.
Postoperative orthopedic issues occur most commonly
when the clavicle is divided during brachial plexus explora-
tion. Although visualization of the brachial plexus is easier
FIGURE 18.10 Nerve anatomy. Black arrows indicate the lateral
cutaneous nerve of the forearm (branch of musculocutaneous nerve).
White arrow indicates the branch of the musculocutaneous nerve
going to the biceps. Green arrow indicates the branch of the
musculocutaneous nerve going to the brachialis. Dotted black
indicates ulnar nerve. Dotted white indicates median nerve.

Brachial Plexus Reconstructive Techniques
253
with a clavicular osteotomy, postoperative non-union and/
or callus formation can be troublesome. Placing a surgical
sponge around the exposed clavicle for retraction should
reveal all the necessary anatomy.
Pneumothorax can occur with violation of the pleura
when dissecting the lower supraclavicular plexus or in
harvesting of intercostal nerves. When a pleural injury is
noted by bubbling of air during a Valsalva maneuver, it is
treated by suture repair of the pleura with or without placing
a chest tube. Routine postoperative chest X-rays will iden-
tify the presence or absence of a pneumothorax.
Wound problems can arise from the accumulation of
blood, lymph, or spinal fl uid in the wound or pleural cavity
after brachial plexus exploration. The thoracic duct tra-
verses the region of dissection over the left side, and if vio-
lated, the thoracic duct or its branches must be coagulated.
Unnoticed violation of this lymph channel can lead to a
lymphocele or chylothorax, which may require re-explora-
tion, chest tube placement, or thoracic duct ligation.
POSTOPERATIVE CARE
Documenting recovery after brachial plexus surgery relies
on clinical and electrophysiological examinations. Patients
should be informed that recovery is a long process, which
may last 3–5 years. Preserving range of motion of the joints
in the affected extremity is paramount. Physical therapy is
recommended for range of motion as well as for maintain-
ing strength in the unaffected muscles.
Although recovery from brachial plexus operations has
improved with increasingly creative surgical options, a mul-
tidisciplinary approach will be required for optimal restora-
tion of function in the injured limb. The treatment of
pain by subspecialized anesthesiologists using gabapentin,
certain tricyclic antidepressants, or by neurosurgeons
employing dorsal root entry zone (DREZ) procedures, can
aid in recovery. In addition, reconstructive procedures using
free gracilis muscle transfer to regain elbow fl exion and
some fi nger motion may be considered for those who are
motivated and request these complex options.
CONCLUSION
Adult brachial plexus injuries can be devastating, and the
long-term implications of such injuries are often not under-
stood by patients or their families. Communication between
the patient and the surgeon to manage expectations and to
help adapt to unrecoverable functional defi cits will optimize
outcomes. These injuries are challenging for the managing
healthcare practitioner: the treating practitioner must rely
upon an understanding of the anatomy, clinical acumen,
appropriate use of ancillary radiographic and electrodiag-
nostic studies to determine the proper course, and timing
for offering surgical options. With improved microsurgical
techniques, the potential development of pharmacological
agents, and the increasingly creative reconstructive options
offered by multidisciplinary teams, the outlook for patients
suffering severe brachial plexus injures will continue to
improve.
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Reinnervation of avulsed brachial plexus using the spinal accessory
nerve. Surg Neurol 1990; 33: 7–11.
30. Kawai H, Akita S. Shoulder muscle reconstruction in the upper
type of the brachial plexus injury by partial radial nerve transfer to
the axillary nerve. Tech Hand Upper Extrem Surg 2004; 8: 51–55.
31. Witoonchart K, Leechavengvongs S, Uerpairojkit C, et al. Nerve
transfer to deltoid muscle using the nerve to the long head of the
triceps, part I. an anatomic feasibility study. J Hand Surg [Am]
2003; 28: 628–632.
32. Friedman AH, Nunley JA 2nd, Goldner RD, et al. Nerve
transposition for the restoration of elbow fl exion following brachial
plexus avulsion injuries. J Neurosurg 1990; 72: 59–64.
33. Malessy MJ, Thomeer RT. Evaluation of intercostal to
musculocutaneous nerve transfer in reconstructive brachial plexus
surgery. J Neurosurg 1998; 88: 266–271.
34. Waikakul S, Wongtragul S, Vanadurongwan V. Restoration of
elbow fl exion in brachial plexus avulsion injury. Comparing spinal
accessory nerve transfer with intercostal nerve transfer. J Hand
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35. Blaauw G, Slooff AC. Transfer of pectoral nerves to the
musculocutaneous nerve in obstetric upper brachial plexus palsy.
Neurosurgery 2003; 53: 338–341; discussion 341–332.
36. Samardzic M, Grujicic D, Rasulic L, Bacetic D. Transfer of the
medial pectoral nerve. myth or reality? Neurosurgery 2002; 50:
1277–1282.
37. Luedemann W, Hamm M, Blomer U, et al. Brachial plexus
neurotization with donor phrenic nerves and its effect on
pulmonary function. J Neurosurg 2002; 96: 523–526.
38. Songcharoen P. Brachial plexus injury in Thailand: a report of 520
cases. Microsurgery 1995; 16: 35–39.
39. Oberlin C, Ameur NE, Teboul F, et al. Restoration of elbow
fl exion in brachial plexus injury by transfer of ulnar nerve fascicles
to the nerve to the biceps muscle. Tech Hand Upper Extrem Surg
2002; 6: 86–90.
40. Teboul F, Kakkar R, Ameur N, et al. Transfer of fascicles from
the ulnar nerve to the nerve to the biceps in the treatment of
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1485–1490.
41. Liverneaux PA, Diaz LC, Beaulieu JY, et al. Preliminary results
of double nerve transfer to restore elbow fl exion in upper type
brachial plexus palsies. Plast Reconstruct Surg 2006; 117:
915–919.
42. Mackinnon SE. Preliminary results of double nerve transfer
to restore elbow fl exion in upper type brachial plexus
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1274.
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reinnervation of the biceps and brachialis muscles with a double
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978–985.
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255
C H A P T E R
19
Techniques for Nerve
Compression Syndromes
David J. Slutsky
INTRODUCTION
A neuropathy may be defi ned as any disorder that results
in abnormal nerve function. Neuropathies are frequently
associated with a number of systemic disorders, such as
diabetes, hypothyroidism, alcoholism, vitamin B12 defi -
ciency, and lead intoxication. The neuropathy may be focal
or restricted to a specifi c anatomical location. Many of
these focal neuropathies arise as a result of nerve compres-
sion, although traction injuries can play a signifi cant role.
Nerve anatomy and physiology
The connective tissue of nerves includes the outer epineu-
rial layer, which contains loosely woven collagen fi bers and
elastin. The epineurium protects the nerve from compres-
sion and stretching and therefore tends to be thicker in
places that experience repetitive shear force, such as the
cubital tunnel at the elbow. The perineurium separates
groups of fascicles and constitutes a diffusion barrier, which
protects the axons from infection and chemical insult. The
perineurium is relatively unyielding, and this property can
lead to a mini-compartment syndrome when the endoneu-
rial pressure increases. The individual axons are surrounded
by the endoneurium, which provides support and a frame-
work for regeneration of nerve fi bers after injury.
Nerve compression
In early nerve compression the symptoms are caused by
vascular impairment, and the initial changes occur at the
blood–nerve barrier. Fluid shifts that occur with limb posi-
tion result in endoneurial edema.1 There is no lymphatic
drainage of the endoneurial space, and so endoneurial
edema clears slowly. The edema cuts off the blood supply
by compressing the arterioles that course through the peri-
neurium obliquely.3 This impairs the Na+/K+ exchange
pump that is ATP dependent. This ultimately results in
a reversible metabolic conduction block, leading to
paresthesia.4
The dramatic relief of symptoms that sometimes occurs
after surgical decompression also suggests an ischemic eti-
ology to compression neuropathies. The mechanical source
of compression may obstruct venous return, resulting in
segmental anoxia, capillary vasodilatation and edema. The
edema compounds the compressive effects and leads to
abnormal axonal and cellular exchange. Surgical release of
compressed nerves at this early stage generally yields good
results. Prolonged compression, however, results in intra-
neural fi brosis, after which nerve recovery is less likely to
occur.
Nerves are viscoelastic and can change their length in
order to accommodate the myriad combination of joint
positions. Nerves have a longitudinal blood supply that is
reinforced periodically by segmental perforators. They are
surrounded by a vascularized gliding layer to facilitate the
nerve gliding that accompanies joint movement. Chronic
compression leads to infl ammation and secondary fi brosis
to disrupt this gliding layer, ultimately leading to nerve
tethering. Any compressive neuropathy therefore frequently
has a component of traction neuropathy as well. Traction
alone can cause conduction block. Nerves can only elongate
by 8% until there is a disruption of the blood supply.5 Trac-
tion therefore leads to nerve ischemia with secondary
impairment of the Na+/K+ pump to cause a conduction
block. This is clinically manifested as numbness or pares-
thesia. Many of the provocative tests for nerve compression
induce relative nerve ischemia in the already susceptible
nerves through manual pressure, awkward joint positioning
and/or traction to elicit numbness or paresthesia in the
distribution of that specifi c nerve. A knowledge of the
normal nerve course and topographic anatomy is thus
essential.

Hand and Upper Extremity Reconstruction
256
ELECTRODIAGNOSTIC STUDIES
Ancillary testing cannot replace a detailed history and thor-
ough examination of the upper limb, but it can provide a
means for staging the degree of neuropathy and ruling out
more generalized disorders that may masquerade as a focal
neuropathy.
Nerve fi bers show varying susceptibility to compres-
sion.6 The large fi bers are more vulnerable to compression
and ischemia. The neurophysiology of electrical recording
is such that the recording electrode will detect activity in
the largest myelinated fi bers fi rst, because these fi bers
conduct at the fastest rates and have a lower depolarization
threshold than the small unmyelinated nerves. Latency and
conduction velocity depend on the time that elapses from
stimulation of the nerve to the fi rst recording. If only a
fraction of the large thick myelinated fi bers remain and
transmit impulses, the recorded latency and conduction
velocity remain normal because the recording electrode
mostly detects the fastest fi bers.7 The electrical conduction
in smaller, less myelinated or non-myelinated nerves is
much slower, and hence not usually detected in a routine
nerve conduction study (NCS). Large myelinated and small
unmyelinated fi bers can be affected differently.
Connective tissue changes follow after focal nerve fi ber
changes. The large myelinated nerves undergo segmental
demyelination, whereas the small unmyelinated nerves
undergo degeneration and regeneration. Normal fascicles
are adjacent to abnormal fascicles. The nerve conduction
study only tests the faster-conducting fi bers. This explains
the seeming paradox of the patient who has established
carpal tunnel syndrome but yet normal electrodiagnostic
studies. It is the worst fascicles that produce symptoms,
but it is the best fascicles that account for the normal nerve
conduction studies.8
With early compression the symptoms are intermittent,
and the edema is reversible. When there are constant symp-
toms, there is usually myelin damage and/or chronic endo-
neurial edema. This demyelination is responsible for the
slowing of nerve conduction. If the compression continues,
some of the axons will die. If there are fewer nerve fi bers,
the size of the electrical charge will be smaller, leading to
smaller amplitudes. When there is sensory or motor loss,
there is usually degeneration of nerve fi bers. Despite the
restoration of neural blood fl ow following nerve decompres-
sion, remyelination of the axon is often incomplete, which
accounts for persistently abnormal nerve conduction even
though the patient may be without symptoms.9
Quantitative sensory testing (QST)
Quantitative sensory testing is reportedly more sensitive
than the NCS because only 25% of the large myelinated
nerve fi bers need to be conducting normally in order to yield
a normal nerve conduction test. Nerve density is defi ned as
the number of nerve fi bers per mm2. The nerve threshold
is the minimum amount of force necessary to cause the
touch receptors to fi re. With nerve degeneration it is more
diffi cult to distinguish two points from one point. Static
and moving two-point discrimination typically tests the
density of innervation. Threshold tests would include
vibrometry and Semmes–Weinstein monofi lament testing
(SWT). Vibrometry is relatively insensitive to early changes
and is not commonly used. Semmes–Weinstein testing
involves placing nylon fi laments of varying thickness on the
skin until the patient can detect the touch of specifi c fi la-
ment thickness. The test is repeated with varying diameter
fi laments until the threshold is determined. Abnormal
SWT is consistent with nerve demyelination.
MEDIAN NEUROPATHIES
DISTAL MEDIAN NEUROPATHY
Carpal tunnel syndrome
Anatomy
The carpal tunnel is open-ended proximally and distally, but
behaves like a closed compartment physiologically and
maintains its own distinct tissue fl uid pressure levels. It is
a fi bro-osseous canal that is bound by the concave arch of
the carpal bones dorsally and the fl exor retinaculum pal-
marly. The hook of the hamate, triquetrum, and pisiform
form the ulnar border; the radial border consists of the
scaphoid, trapezium, and the fascial septum overlying the
FCR. The fl exor retinaculum consists of three zones: a
proximal zone that is continuous with the deep forearm
fascia, a central zone that is composed of the transverse
carpal ligament (TCL), and a third zone that consists of the
aponeurosis between the thenar and hypothenar muscles.13
The median nerve at the wrist has approximately 30 fasci-
cles. The motor recurrent branch often consists of two fas-
cicles that are situated in a volar position, with the various
sensory groups in the radial, ulnar and dorsal positions of
the main trunk. The motor branch can be separated from
the main trunk without harm for up to 100 mm proximal
to the thenar muscles.14 The sensory fi bers travel within the
common digital nerves to the thumb, index and middle
fi ngers, as well as the communicating branch to the third
web space.
Pathophysiology
There are two potential sites of compression anatomically.
The fi rst is at the proximal edge of the TCL, where com-
pression may be produced by acute wrist fl exion. This
accounts for the positive Phalen’s test (wrist fl exion test) in
CTS. The second is adjacent to the hook of the hamate
where an hourglass deformity of the median nerve may be
seen. Patients with compression in this area will have a
positive median nerve compression (Durkan’s) test but a
negative Phalen’s test.15 Compression within the carpal
tunnel may also result from any lesion that takes up space
within the canal, such as fl exor tenosynovitis, hematoma,
palmar carpal dislocation, distal radius fractures, tumors
and ganglia. Although many cases have been attributed to
a non-specifi c synovitis, synovial biopsies typically fail to