Phẫu Thuật Tạo Hình (Tập 6): Bàn Tay Và Chi Trên – Neligan (Ấn bản 4)

479
The stiff hand
Bone
Bone block or exostosis can also cause flexion contracture.
Extension contracture
Limitation of flexion (extension contracture) (Fig. 21.2) can be
caused by one or more structures on the dorsal aspect of the
joint.1,2 However, they too can result from a “jamming” effect
of volar structures that block flexion, such as a bone block or
palmar plate adhesions.
Skin
This usually results from scar contracture.
Long extensors
Tendon shortening or adhesions limit joint flexion. With
extensor tendon adhesions, active extension of the joint is
limited or absent, and active extension falls short of passive
extension.
Intrinsic muscles
Intrinsic contracture may follow ischemia, or muscle fibrosis
may occur for non-ischemic reasons (rheumatoid arthritis,
cerebral palsy). The “intrinsic plus” position of the hand is
one in which the fingers are flexed at the MP joints and
extended at the interphalangeal joints.3 A “saddle deformity”4
results from adhesions between lumbrical and interosseous
muscles. With active intrinsic contraction, painful impinge­
ment on the deep transverse metacarpal ligament occurs with
limitation of flexion (the transverse metacarpal ligament is the
“saddle” and the two muscles are the “legs of the rider”).
Capsular and pericapsular structures
Dorsal capsule
The dorsal capsule may become scarred and contribute to
extension contracture.
Collateral ligaments
Adhesions to the head of the proximal bone may limit flexion.
In contrast to flexion contracture, which is more common in
interphalangeal joints (especially proximal), stiffness in exten­
sion from collateral ligament shortening is more likely at MP
joints. Collateral ligaments at the MP joints are relaxed in
extension and taut in flexion.5 Loss of MP joint flexion can
come about simply from immobilization in the incorrect,
extended position. Collateral ligaments are at their tightest
(the cam arc effect of the metacarpal head) at a range between
70° and 90° flexion.
Volar plate
Flexion is prevented by volar plate adhesions to the palmar
surface of the proximal bony head. Palmar plate adhesions
and collateral ligament tightness may both be causes of MP
joint extension contracture.1 They may be distinguished from
each other. If the collateral ligaments are contracted, finger
abduction–adduction in extension (normally about 45°) is
greatly reduced. When palmar plate is the sole cause,
attempted passive flexion produces an opening of the dorsal
aspect of the joint. The volar lip at the base of the proximal
phalanx jams against the adherent volar plate, and the
Capsular and pericapsular structures
Collateral ligament
The collateral ligament at the PIP joint is taut in all positions
of the joint and collateral ligaments are taut in flexion only at
the MP joints.3 Thus, collateral ligament shortening never
produces a flexion contracture at either joint. However, col­
lateral ligament adherence to the lateral aspect of the proximal
phalanx when the finger is flexed, does play a role in PIP joint
flexion contracture.
Volar plate
When other structures are the primary cause of the flexion
contracture, the volar plate becomes contracted at an early
stage, especially at the interphalangeal joints.
Accessory collateral ligaments, transverse retinacular ligaments,
and intrinsic tendons
Contracture of accessory ligaments, adherence of fibers of the
transverse retinacular ligament to the collateral ligaments,
and adhesions of intrinsic tendons in the lumbrical canals
may cause flexion of MP joints.
Dorsal adhesions
Generally with flexion contracture, tightness of structures on
the flexor aspect of the joint exists. However, joint extension
may sometimes be prevented by incongruity of articular
surfaces or adhesion of dorsal capsule or of an extensor
tendon to the articular surface of the head of the proximal
bone. In such a case, there is not only a flexion contracture but
also limitation of flexion.
Fig. 21.1  Flexion contracture may result from tightness of structures volar to the
joint, including skin, flexor tendon sheath, tendons, volar palmar plate, and
accessory collateral ligaments. In addition, a bone block may impede joint motion,
whereas dorsal tendon adhesions may limit the ability to extend the joint.
Skin
Collateral ligament
Bony block
Palmar plate
Flexor tendon
Extensor tendon

480
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
loose body in the joint. Computed tomography scanning may
help in arriving at the correct diagnosis.
Seesaw effect
This results when a contractural element spans two joints.
Presence of this sign helps in the diagnosis of structures that
potentially contribute to a stiff joint.7 If one joint in a contracted
system is flexed, the other joint can then be extended, and vice
versa. This is seen, for example, when a longitudinal volar
skin scar crosses both proximal and distal interphalangeal
joints. The distal interphalangeal (DIP) joint can be extended
only if the PIP joint is flexed. A similar effect is seen with
adherent extrinsic flexor or extensor tendons (Fig. 21.4). For
example, flexion of MP joints in the presence of a flexor tendon
adhesion over the proximal phalanx has no effect on the
flexion contracture of the PIP joint. If the adhesion lies proxi­
mal to the MP joint, flexion of that joint results in correction
of the contracture apparently present in the PIP joint. Further­
more, with flexor tendon adhesions, passive flexion of the
affected joint exceeds active flexion, provided the extensor
tendon is healthy. Similarly, in the presence of a Volkmann
contracture of the flexors in the forearm, passive extension of
the finger joints is reduced with the wrist extended and not if
the wrist is flexed.
If the extrinsic extensor tendon is adherent to the metacar­
pal, the limitation of extensor tendon excursion distal to that
joint prevents simultaneous flexion of MP and PIP joints. This
is the test for extrinsic tightness (Fig. 21.5A).8,9 The test of
Bunnell for intrinsic tightness results from the seesaw phe­
nomenon in which the band acts across two joints but is
an extensor of one joint and a flexor of the adjacent joint.10 If
the intrinsic musculotendinous system is foreshortened,
unaffected (loose) collateral ligaments allow the flexion force
to rock the dorsal lip away from the metacarpal head, felt as
a subtle dorsal recess between head and base. This sign should
always be sought intraoperatively as a residual impediment
to passive flexion after tight collateral ligaments have been
released.
Painful resistance to passive PIP joint flexion may indicate
volar plate injury (volar plate test).6 Pain results from synovial
involvement, and the most common cause is volar plate avul­
sion with or without a small bone fragment torn from the base
of the middle phalanx. Positive volar plate test at 6–9 months
following injury indicates that volar plate repair of the middle
phalanx may be necessary.
Transverse retinacular ligaments
Transverse retinacular ligaments may be adherent to the
lateral capsular ligament at the PIP joint.
Flexor tendon adherence
Flexor tendon adherence within the sheath may be sufficiently
bulky to block full flexion of the interphalangeal joint.
Bone
This may be a true block or result from intraarticular incon­
gruity. Chondral fractures may not be radiographically appar­
ent and so may present a diagnostic problem (Fig. 21.3).
Persistent waxing and waning joint swelling with limited
flexion may result from a chondral fracture, which is more
likely at the MP joint. Questioning the patient may lead to
recollection of an injury that could have caused the proximal
phalangeal base to impinge on the metacarpal head. Surgical
exploration may reveal the chondral fracture and consequent
Fig. 21.2  (A) Extension contracture may result from tightness
of dorsal structures, including skin, extensor tendons, collateral
ligaments and joint capsule, as well as from a bone block.
Volar structures may also impede the ability to flex the joint.
(B) In addition, adhesions in the lumbrical canal and of the
transverse retinacular ligament fibers may impede both flexion
and joint extension.
A
B
Skin
Capsule
Sheath of flexor tendons
Collateral ligament
Common extensor tendon
Transverse retinacular ligament
Palmar plate
Flexor tendon
Extensor tendon
Lateral tendon

481
The stiff hand
Fig. 21.3  (A) This patient had an
osteochondral fracture involving the
metacarpal head after a finger “jam” and
presented with inability to flex at the
metacarpophalangeal joint and joint
swelling. The fracture involved about
one-third of the articular surface but was
still attached by a single collateral
ligament. (B) Bone fixation restored perfect
joint function.
A
B
Fig. 21.4  By adjusting the joints proximal to the joint that
appears to be the cause of the contracture, the primary
problem may be revealed. (A) If a patient has a proximal
interphalangeal (PIP) flexion contracture, flexion of the
metacarpophalangeal (MP) joint in the presence of flexor
tendon adhesion at the proximal phalanx has no effect on the
PIP flexion contracture. (B) If the flexor tendon adhesion is
proximal to the MP joint, flexion of that joint will result in
correction of the PIP joint contracture.
A
B
extension of the MP joint, either actively or passively, increases
the tone in the system and restrains flexion of the PIP joint.
This is tested by passively extending the MP joint and pas­
sively flexing the PIP joint (Fig. 21.5B). If flexion of the PIP
joint is greater when the MP joint is flexed than when it is
extended, intrinsic tightness is present. In the swan-neck
deformity, not only is there an extension contracture of the
PIP joint, but that joint hyperextends because of volar plate
laxity. There is dorsal displacement of the lateral bands at the
PIP joint. This slackens the distal tension on the extensor
mechanism because of the fixed attachment of the central
tendon at the PIP joint. Thus there is unopposed force of the
flexor digitorum profundus at the distal joint, which then
drops into flexion (Fig. 21.6A).9
A similar volar to dorsal seesaw effect occurs at the DIP
joint secondary to action of the oblique retinacular ligament

482
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
Fig. 21.5  (A) Test for extrinsic tightness. When the metacarpophalangeal (MP) joint is flexed (arrow), passive proximal interphalangeal (PIP) joint flexion is increasingly
difficult. (B) Test for intrinsic tightness. When the MP joint is extended (arrow), passive PIP joint flexion is more difficult. (C) Boutonnière test. The oblique retinacular
ligament is foreshortened so that when the PIP joint is extended (arrow), passive DIP joint flexion is difficult. (D) Central slip tendon excision is performed for extrinsic
extensor tightness and wing tendon excision (oblique fibers and lateral bands) for intrinsic tightness – either of which might cause PIP hyperextension.
A
C
B
D
When extrinsic extensor
mechanism is tight
When intrinsic extensor
mechanism is tight
Direction of clinician pressure
Direction of clinician pressure
Direction of clinician pressure
Resected oblique fibers and
lateral band of extensor hood
Resected central tendon
Fig. 21.6  (A) Swan-neck deformity with hyperextension at the
proximal interphalangeal (PIP) joint. Dorsal displacement of
the lateral bands slackens distal extensor tension, and so the
unopposed flexor digitorum profundus draws the distal
interphalangeal (DIP) joint into flexion. (B) Boutonnière
deformity. The PIP joint drops into flexion because of central
slip attenuation, and the lateral bands move volar. Excess
extensor pull bypasses the PIP joint and hyperextends the DIP
joint. The oblique retinacular ligament foreshortens.
A
B
Lateral band displaced dorsal
Lateral band displaced volar
Insertion of central tendon
Attenuated central tendon insertion
Volar plate
Oblique retinacular ligament

483
The stiff hand
of the joint (Fig. 21.8B). The volar plate is not attached to the
proximal phalanx as this would prevent full extension. The
assembly lines are the two ridges on the volar lateral surfaces
of the phalanx to which are attached the flexor sheath, Cleland
ligaments, Grayson ligaments, oblique retinacular ligaments,
and transverse retinacular ligaments, and the transverse
metacarpal ligament and MP joint volar plate more proxi­
mally. Normally, there is no ligament structure between the
volar plate of the PIP joint and the assembly line or extension
of that joint would not be possible. Two bands (checkreins)6,12,13
form between the lateral proximal volar plate and the assem­
bly lines after injury. These are pathologic structures (Fig.
21.9). They are thicker at the base attached to the volar plate
and have a thinner, longer proximal apex attached to the
assembly line. The communicating artery of the vincula
system passes deep to the checkreins. With interphalangeal
joint contracture, it is the checkreins that mainly prevent
extension. Division of these checkreins and accessory collat­
eral ligaments enables extension at the interphalangeal joint
to be achieved when surgery is required. It is virtually never
necessary to divide collateral ligaments.
and lateral bands, resulting in extension contracture at that
joint. This occurs with the boutonnière deformity. When the
central tendon insertion into the dorsal base of the middle
phalanx ruptures or attenuates, the PIP joint drops into flexion
and the lateral bands move volar to the axis of motion of that
joint.11 They will foreshorten and adhere in that position.
Excess extensor pull that secondarily bypasses the PIP joint is
imposed dorsally at the DIP joint with consequent recurvature
at that joint (Fig. 21.6B). The oblique retinacular ligament is
an extensor of the DIP joint and a flexor of the PIP joint.11 It
also foreshortens and this permits the DIP joint to be flexed
as long as the PIP joint is maintained in flexion. Passively
extending the PIP joint brings the DIP joint into extension,
making passive flexion increasingly more difficult. This
maneuver is the boutonnière test (Fig. 21.5C).
Volar plate and collateral ligament changes
Changes in the volar plate and collateral ligaments occur with
flexion contractures. Flexion and extension contractures can
occur at the PIP joint. In contrast, at the MP joints, extension
contractures occur, but flexion contracture is rare due to volar
plate and collateral ligament anatomy. The volar plate at MP
joints is different anatomically from that of interphalangeal
joints.
The protected position of MP joints is in flexion. The cam
and volar flare shape of the metacarpal head places collateral
ligaments in greatest tension during flexion (Fig. 21.7). The
MP joint volar plate has crisscrossing bands of fibers that
expand with joint extension and are collapsible with flexion.6
Thus, the volar plate at the MP joint is considerably longer in
extension than in flexion (Fig. 21.8A).
In contrast, the interphalangeal joint collateral ligaments
do not change in tightness with joint flexion and extension.
The volar plate is relatively uncollapsible. Rather, the volar
plate slides proximally and distally with flexion and extension
Fig. 21.7  Cam-like action of the collateral ligaments at
the metacarpophalangeal (MP) joint. Collateral ligaments
are in greatest tension during flexion because of the cam
and volar flare shape of the metacarpal head.
Metacarpal head is wider on
volar aspect and stretches
collateral ligament in flexion
The longer radius of the metacarpal in
flexion stretches the collateral ligaments
Clinical tips
Post-traumatic contractures
• Dorsal hand edema
• Negative hand position driven by hydraulic MP joint fluid
accumulation
• Reciprocal tone in tendons
• Wrist flexed, finger MP extended
• Finger MP extended, PIP flexed
• Fixed extension at MP and fixed flexion at PIP with time
• MP collaterals and PIP volar plate tight

484
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
is minimal and the ligaments are taut. After injury, edema
fluid drives the MP joints hydraulically into extension. In this
position, tension is increased in the flexors and decreased in
the extensors. Thus, fingers flex at PIP and DIP joints. There
is no hydraulic drive at PIP or DIP joints because there is only
minimal change in collateral ligament tightness and fluid
capacity of flexed versus extended interphalangeal joints.
Positional changes in interphalangeal joints are thus second­
ary to changes in MP joints. Slight wrist flexion occurs in the
neglected edematous hand because total power of flexors
exceeds the extensors.16 Post-burn claw contractures from
dorsal hand burns similarly drive the MP joints into fixed
extension and the PIP joints into flexion. Thus, the traumatized
hand, susceptible to joint stiffness, must be appropriately
immobilized by placing it in the intrinsic plus position with
MP joints in flexion and interphalangeal joints in extension.
Patient selection
These measures may be more effective early on after the injury
during the edema phase and subsequent collagen phase of
Basic science/disease process
Injury, infection, excessive immobilization, and inappropriate
splinting of the hand all predispose to joint stiffness. The
initial response to any insult of the hand is edema formation.
Unless edema accumulation is prevented, joints assume the
posture in which their ligaments are most relaxed.1,14,15 Liga­
ment contracture and fibrosis then cause joints to become
immobile in this abnormal position (Fig. 21.10), which is:
■ Wrist: flexion
■ Thumb: adduction
■ MP joint: extension
■ PIP joint: flexion.
This is the negative or injured hand position; wrist position
and MP joint posture are the keys to its development. When
the wrist is allowed to flex, increased tone in the extrinsic
extensor tendons causes MP joints to extend. When nearly
fully extended, the MP joint has maximum capsule and col­
lateral ligament laxity as well as intracapsular fluid capacity.
When the MP joint is fully flexed, intracapsular fluid capacity
Fig. 21.8  (A) Crisscrossing bands of fibers make up the
metacarpophalangeal (MP) joint volar plate, and these allow
expansion with joint extension. (B) The volar plate at the proximal
interphalangeal (PIP) joint is relatively uncollapsible. In contrast to
the MP joint, the PIP volar plate slides proximally and distally with
joint flexion and extension.
A
B
Distal slide
Proximal slide
MP flexion
PIP flexion
PIP extension
MP extension

485
The stiff hand
severely after splint removal. Finally, active muscle contrac­
tion may be able to achieve complete joint range of motion,
and the patient may then experience only morning stiffness
that finally progressively resolves.
For PIP joint flexion contractures, the patient may wear a
nighttime progressive static splint (Fig. 21.11). With a Joint Jack
(Joint Jack Company, Glastonbury, CT), the patient tightens
the screw every 2 or 3 min as tolerated, starting 1 h before
bedtime. The screw can then be loosened half a turn at bedtime
for comfort. A Joint-Jack may be difficult to keep in position
on the little finger because its proximal base tends to rock off
the ulnar border of the palm. In that case, a custom palm-
based thermoplastic splint with Velcro straps that can be
tightened over the PIP joint may be appropriate. High com­
pression foam built into the brace supports the distal phalanx.
For PIP joint flexion contractures of more than 60°, these
splints may be inappropriate because they will place undue
extension stress on the DIP joint. These splints must be fitted
with care to avoid hyperextension stress at the DIP joint. The
volar distal pressure should be on the volar plate of the DIP
joint and not at the fingertip. Splints such as Wire-Foam finger
extension splints (DeRoyal LMB Hand Rehab Products, San
Luis Obispo, CA) are less bulky and may be more acceptable
for daytime use by the active patient. Serial finger casting,
with a new cast replaced every 3 days, may be helpful in a
difficult, seemingly unresponsive case or when PIP joint
flexion is >60°.
PIP joint extension contractures rarely occur as pure joint
contractures. They nearly always involve structures other
than joint capsule, such as extensor mechanism adhesions. A
joint strap may be placed around the middle phalanx and the
finger positioned in maximum passive flexion (Fig. 21.12).
With time, the strap is tightened to increase flexion. Snug
Coban wrapping about the palm and finger can accomplish
the same objective.
A variety of flexion splints are available that place a static
flexion force across MP joints when there are extension con­
tractures at those joints. One such chronic progressive flexion
splint is the Knuckle-Jack splint (Joint-Jack Company, East
Hartford, CT).7
Treatment/surgical technique
PIP joint flexion contracture of more than 70° is unlikely to
respond effectively to non-operative therapy alone. Further­
more, once a plateau in improvement has been reached with
non-operative measures and there is still a functionally
impairing residual deformity, surgery is indicated. Radio­
graphic changes within a joint or an obstructing bone block
may also persuade one to undertake surgery. Once swelling
has resolved, and if the joint range of motion reaches an
abrupt stop rather than having a gradual increase in resistance
to passive motion, clinical judgment would make one believe
that maximum benefit has been reached from splinting.
PIP joint flexion contracture
It is important to first evaluate whether there is shortage of
skin. Prolonged joint contracture, even without soft-tissue
scar, may result in longitudinal shortening of soft tissues. One
may decide to make a mid-volar longitudinal incision that is
broken up into multiple Z-plasties as the access incision. For
Fig. 21.9  (A) Checkreins are attached by a broad base to the volar plate, and a
tapering apex is attached to the assembly line. (B) Release of the proximal
interphalangeal (PIP) flexion contracture requires excision of the checkreins, with
care taken not to injure the transverse communicating vessel between the two
digital arteries.
A
B
Cut checkrein
wound healing, when fluid can be displaced and collagen
remodeled. Once a scar and fibrosis have reached maturity, it
is less likely to respond to non-operative measures. These
measures include splinting. Other hand therapy endeavors
such as edema reduction (by extremity elevation and com­
pression gloves), moist heat, and ultrasound may enhance the
beneficial response achieved by splinting.17 Splinting involves
the application of a non-elastic force in the direction of the
desired correction. Initial splinting displaces tissue fluid
during 5–12 min. This is the rapid gain phase of splinting.
Only once this tissue edema has been displaced can the
external forces of the splint result in collagen remodeling.
Rapid deformity recurrence after a period of splinting should
not discourage the patient because this is due to redistribution
of tissue fluid originally displaced by exercise. Only if pro­
longed, will splinting eventually have the desired effect on
collagen.18 As weeks pass, patients notice that less time and
force are necessary to achieve the desired result and that the
finger returns to its contracted position more slowly and less

486
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
dorsolateral skin incision may also adequately expose the
extensor hood.
The transverse retinacular ligament fibers are divided and
the lateral band is elevated while the central slip insertion is
preserved.2,6 The dorsal joint capsule is incised and the joint
passively flexed. Extensor tendon adhesions to the dorsum of
the proximal phalanx are released. If the jump phenomenon
occurs after dorsal capsulotomy, the most dorsal fibers of both
collateral ligaments are cut until there is no residual jumping.
In the presence of severe intra-articular fibrosis, both collateral
ligaments may need to be divided and a small dissector used
to free volar plate adhesions (without detaching the volar
plate from its distal insertion).
Partial resection of the appropriate portion of the extensor
mechanism in carefully selected cases is helpful in those
patients who have intrinsic tightness or extrinsic extensor
tendon tightness (see Fig. 21.5). In patients with extrinsic
extensor tightness, the central tendon portion is resected. In
those with intrinsic tightness, only the lateral bands and
oblique fibers of the extensor hood are resected.22 Sagittal
band fibers are left intact because they are the prime method
through which extension is transmitted to the MP joint from
the extensor mechanism
Once the finger has been stiff in extension, the flexor
tendons frequently become adherent in their bed. The opera­
tor should return and check function of these tendons by
making a counterincision in the palm or forearm.2,6 By place­
ment of traction on the flexors, the fingers should fully flex.
Failure for this to occur necessitates performance of a flexor
tenolysis as well. An excellent method of anesthesia adminis­
tration when performing a tenolysis, is to use the tumescent
technique of local anesthesia infiltration using a mixture of
severe accompanying soft-tissue contracture, a transposition
flap from the dorsolateral surface of the homolateral digit
(Joshi flap)19 (Fig. 21.13) or cross-finger flap from an adjacent
finger, or homodigital island flap may be planned.20 If there is
no soft-tissue deficit, any conventional volar zigzag type
surgical approach may be used.21
Shortened checkrein ligaments are the primary abnormal­
ity.12,13 If a flexor tendon injury was the initiating event, a
flexor tenolysis or secondary repair may be required. The
flexor sheath just distal to the A2 pulley and the checkreins
are cut free from their attachments to the proximal edge of the
volar plate (see Fig. 21.9). Gentle passive extension may be
required to break up other adhesions after checkrein resection
to achieve full joint extension.
A “jumping” sensation is occasionally noted as the PIP joint
is fully extended once checkrein release has been done. This
is secondary to a cam effect of the collateral ligament and is
relieved by cutting only the most dorsal fibers of both col­
lateral ligaments.6
Tightness of the oblique retinacular ligaments may also
contribute to the PIP joint flexion contracture, especially in
association with DIP joint hyperextension in the boutonnière
deformity. Transection of the oblique retinacular ligament is
then indicated.
PIP joint extension contracture
A mid-dorsal longitudinal curvilinear surgical incision affords
the luxury of not needing to close the entire incision proxi­
mally or distally, provided an adequate soft-tissue flap covers
the extensor mechanism. In this way, soft-tissue closure will
not limit the flexion achieved as a result of the joint release. A
Fig. 21.10  (A) Posture of the relaxed uninjured hand.
(B) Edema accumulates in the available space on the dorsum
of the injured hand, drawing the wrist into flexion, the
metacarpophalangeal joints into hyperextension, the proximal
interphalangeal joints into flexion, and the thumb into
adduction.
A
B

487
The stiff hand
Postoperative care
Extremity elevation reduces postoperative edema. A postop­
erative splint applied during the first week maintains the
restored joint position. Thereafter, active mobilization is
begun. Daily application of splints as well as a continuous
night splinting is sometimes necessary for several weeks to
months postoperatively to help minimize the risk of contrac­
ture recurrence. Continuous passive motion (CPM) may be a
useful modality to maintain joint motion but it is not a sub­
stitute for maintaining active motion and tendon gliding and
excursion.
Outcomes, prognosis, and complications
Full extension of PIP joint flexion contractures after operative
release occurs in 96% of cases.12,13 There is frequently relapse,
lidocaine with epinephrine added. This enables the so-called
“wide-awake” method of local anesthetic infiltration, avoid­
ing the paralytic effects of prolonged tourniquet ischemia or
of a regional block, and ensuring full cooperation of the
patient. The end-point of the tenolysis or joint release is
achieved only when the patient can actively reproduce normal
function on the operating table.23
MP joint extension contracture
A longitudinal dorsal skin incision is used. Sagittal band hood
fibers are retracted distally and the dorsal capsule is tran­
sected.2,6,24 As the joint is flexed passively, one may note that
the tight collateral ligament cannot pass over the condyles on
the volar aspect of the metacarpal head. In such circumstances,
it is necessary to transect the collateral ligaments proximally
at their attachments to the metacarpal head. It may be neces­
sary, as with extension contractures of the PIP joint, to free
volar plate adhesions by inserting a blunt dissector into the
volar plate pocket dorsal to that structure. If the jump phe­
nomenon is encountered, it is managed in a fashion similar to
that of the PIP joints.
Fig. 21.11  (A) Custom palm-based night proximal interphalangeal (PIP) extension
splint. (B) Joint Jack splint. (C) Wire-Foam PIP extension splint.
A
B
C
Fig. 21.12  A flexion strap can be progressively tightened around the hand and
finger for treatment of a proximal interphalangeal joint extension contracture.
A
B

488
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
and ischemic and develop postoperative necrosis. Necrotic
skin flaps may leave tendons and their sheaths exposed and
in danger of desiccation, necessitating secondary soft-tissue
reconstruction. Skin flap marginal necrosis may also lead to
secondary wound healing and adverse scarring with relapse
of contractures.
Excessive and unwarranted attempts at release of the volar
plates, accessory collateral ligaments, and collateral ligaments,
and use of excessive passive extending force in treatment of
PIP joint flexion contracture may result in the joint subluxing
into hyperextension. This results in a significant postoperative
problem and the finger must then be held in a flexed position
until adequate scarring heals the torn ligaments.
though not complete recurrence, of the deformity despite
adequate release and good postoperative management. After
PIP joint flexion contracture release in patients with Dupuy­
tren contractures, there is reported relapse in those with
severe contractures from a preoperative mean of 78° to a
postoperative mean of 36°.25 With severe PIP flexion contrac­
tures, one can seldom expect to regain normal extension,
although the deformity can be improved.
Neurovascular injury may occur during surgical release.
However, even if there has not been a sharp injury to the
digital neurovascular structures, ischemia to the finger may
result from neurovascular overstretch when the finger has
been previously flexed for a long time. Skin flaps may be thin
Fig. 21.13  (A) Proximal interphalangeal (PIP) flexion contracture caused by
longitudinal soft-tissue pterygium. (B,C) PIP soft-tissue transverse release that
incorporates a Joshi transposition flap in the planning. (D) Soft-tissue release and
flap transposed. (E) Flap inset and donor defect on ulnar side of digit is closed with
hypothenar full-thickness skin graft.
A
B
C
D
E

489
The spastic hand in cerebral palsy
Table 21.1  House functional classification for cerebral palsy
Grade
Designation
Activity level
0
Does not use
Does not use
1
Poor passive
assist
Uses as stabilizing weight only
2
Fair passive assist
Can hold onto object placed in
hand
3
Good passive
assist
Can hold onto object and stabilize
it for use by other hand
4
Poor active assist
Can actively grasp object and
hold it weakly
5
Fair active assist
Can actively grasp object and
stabilize it well
6
Good active assist
Can actively grasp an object and
then manipulate it against other
hand
7
Spontaneous use,
partial
Can perform bimanual activities
easily and occasionally uses
the hand spontaneously
8
Spontaneous use,
complete
Uses hand completely
independently without reference
to the other hand
(Reproduced with permission from House JH, Gwathmey FW, Fidler MO. A
dynamic approach to the thumb-in-palm deformity in cerebral palsy. J Bone
Joint Surg Am. 1981;63:216–225.)
Cartilage necrosis may result at the distal end of the proxi­
mal phalanx when it is brought into full extension from a
flexed position because of excessive pressure now applied on
the fully extended joint surface.26 Risk of overstretched neu­
rovascular ischemia and cartilage necrosis may be heightened
if a Kirschner wire has been used to temporarily fix the PIP
joint in extension to maintain the contracture release.
A hyperextending force of the DIP joint by an improperly
placed Joint Jack splint that applies excessive pressure on the
fingertip may cause iatrogenic functional problems at the DIP
joint. Dysesthesias to the fingertip, stiffness in both flexion
and extension, and reflex sympathetic dystrophy are potential
complications of contracture release.
Secondary procedures
A relapse of a functionally impairing PIP joint flexion contrac­
ture may necessitate disarticulation amputation at the PIP
joint or bone shortening at the PIP joint arthrodesis site with
fusion in a more favorable position. Either of these two options
may be considered in the primary treatment of the patient
who is too frail to undergo any other surgical management or
the patient who lacks the motivation needed for successful
postoperative management. The patient who is a heavy
smoker and has a longstanding severe flexion contracture
(more than 70°) of the PIP joint may also potentially be best
served by PIP joint disarticulation amputation or perhaps
fusion.
The spastic hand in cerebral palsy
Diagnosis/patient presentation
Treatment of cerebral palsy necessitates accurate assessment
of the clinical problem, non-surgical modalities, as well as
surgical treatment. Overall upper extremity function is classi­
fied by the nine-level House activity scale (Table 21.1).27 Surgi­
cal intervention has been shown to improve limb function by
2.6 functional levels.
Patient selection
The age of the patient is important and the child should be at
least 6 or 7 years old to cooperate with the preoperative
assessment and postoperative therapy. The type of palsy is
important and may be spastic, ataxic, or choreoathetotic. The
last is a contraindication to tendon transfers. Surgery for
athetoid patients usually will involve only joint stabilization
through fusions such as at the MP joint of the thumb. The
patients who derive the most benefit from surgery usually
have spastic hemiparesis.28 A hand with poor sensibility is less
likely to be used after reconstructive surgery. Some believe
that an intelligence quotient of >70 is desirable if surgery
is contemplated, but others feel that intellect is less
important.29,30
Non-surgical treatment
Non-surgical modalities include splinting, occupational
therapy, and pharmacologic intervention. Splinting may help
prevent joint contractures. This requires a high level of
compliance from patients and caregivers. It may also be a
necessary component of postoperative management. Many
medications have been used, some of which have significant
adverse drug reactions. The most commonly used are intra­
muscular injection of botulinum toxin A and intrathecal
baclofen. Botulinum toxin injection relaxes muscles that may
then be responsive to splinting and stretching in therapy.
Surgical technique
The typical spastic posture of the upper limb includes shoul­
der internal rotation, elbow flexion, forearm pronation, wrist
flexion and ulnar deviation, thumb-in-palm, and clenched fist
(Fig. 21.14). A thorough preoperative analysis of the pattern
of spasticity is required and an assessment of joint contrac­
tures that may need to be released. Assessment of passive
range of motion must be done slowly to overcome muscle
spasticity. Joint contractures are assessed by evaluating par­
ticular muscles. Thus, positioning the wrist joint in flexion
will allow passive finger extension if there is no joint
contracture.
Spastic muscles need to be either released or weakened by
lengthening to correct muscle imbalance around joints. At the
wrist, there is usually poor volitional control of extensor carpi
radialis longus, extensor carpi radialis brevis (ECRB), and
extensor carpi ulnaris (ECU) and there is spastic overpull of
flexor carpi radialis (FCR) and flexor carpi ulnaris (FCU). One
next assesses which muscles are weak or have poor motor
control. These flaccid muscles need to be augmented by
tendon transfer. Finally, assess which muscles are available for
transfer. Those under good voluntary control are the best for
tendon transfer, though transfer of a spastic muscle may

490
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
50°) demand attention to biceps, brachialis, and possibly
brachioradialis. Antecubital soft-tissue paucity may become
apparent after the release, necessitating Z-plasty or even a flap
(Fig. 21.15). If brachioradialis needs to be released, this can be
done distally and the muscle turned up into the antecubital
fossa for wound coverage and a skin graft placed over it.
Lacertus fibrosus is released and Z-lengthening of the
biceps tendon done. If residual unacceptable contracture
remains, then stepwise release of brachialis (which is weak­
ened by intramuscular incision into the fibrous septae) and
of the brachioradialis (either proximally or distally) is per­
formed.28,31 Less severe flexion contracture can be treated by
fractional biceps tendon lengthening (a series of transverse
step cuts in the tendon). This retains biceps strength better
than Z-lengthening. Postoperative elbow extension splinting
is done for 4 weeks, followed by progressive range of motion
and intermittent extension splinting.
Forearm pronation
This deformity has been classified into four groups28,32:
■ Group I: Active supination beyond neutral
■ Group II: Active supination less than neutral
■ Group III: No active supination; free passive supination,
but with active pronator teres
■ Group IV: No active supination; tight passive
supination.
When treating the forearm pronation deformity in isolation,
recommendations are: no surgery for group I; pronator qua­
dratus release with or without FAR for group II; pronator
teres release for group III, and pronator quadratus release
and FAR for group IV. FAR consists of excision of a 2-cm
transverse strip of fascia from the flexor–pronator mass as
well as division of all fascial septae. This allows muscle fibers
to be stretched, so releasing myostatic contracture without
cutting tendons. Pronator teres re-routing involves taking
down the distal insertion with a distal cuff of periosteum
and then re-routing it through an interosseous membrane
window and reattaching to the dorsoradial side of the radius
with a suture anchor. Alternatively, a Z-tenotomy of pronator
teres distal insertion is done, re-routing the distal segment
around the radial side of the radius and reattaching the
two ends.
However, often the forearm pronation deformity cannot be
taken out of context with the wrist and finger flexion deformi­
ties. A flexor–pronator muscle slide used for the latter prob­
lems will often significantly improve forearm pronation, as
will the Green FCU transfer for active wrist extension.33
Wrist flexion
It is important to note the amount of digital flexor tightness
that is also present. Digital flexor tightness can be quantitated
by measurement of the Volkmann angle (Fig. 21.16). The wrist
is flexed with the digits held extended. Wrist is then passively
extended as much as possible while keeping digits extended.
Full wrist extension can be accomplished in the absence of
flexor tendon tightness. With digital flexor contracture, the
wrist cannot be extended to neutral. As digits are extended,
with wrist extended, one can assess selective digital spas­
ticity. When PIP joint extension is limited, flexor digitorum
superficialis (FDS) spasticity is suspected (flexor digitorum
weaken the overpowered side and utilize it to strengthen the
weaker side of the unbalanced joint. Severe joint contractures
or joint instability may necessitate joint fusion.
Surgical treatment options by type of deformity
Shoulder
Shoulder surgery is rarely indicated. Occasionally, Z-
lengthening of pectoralis major through a deltopectoral inci­
sion is done together with Z-lengthening of the subscapularis
(or simple division by myotomy or recession from the scapula,
which maintains subscapularis integrity) may be necessary.
With a tight adduction contracture, there may be a soft-tissue
deficit requiring flap reconstruction (although this is more
frequently necessary with tight shoulder adduction contrac­
tures that may occur with spastic post-traumatic or stroke
brain injury). Latissimus dorsi and teres major transfer to the
posterolateral humerus at the greater tuberosity is seldom
required, as is an external rotational humeral osteotomy.
Elbow
Mild flexion contractures may be improved simply by the
necessary surgical procedures directed towards forearm pro­
nation and wrist flexion (flexor–pronator muscle slide; or
flexor aponeurotic release (FAR)) as these muscles cross the
elbow. More significant flexion contractures (usually >40° or
Fig. 21.14  Typical spastic hemiplegic posture of the upper extremity shows
shoulder internal rotation, elbow flexion, forearm pronation, wrist flexion and ulnar
deviation, thumb-in-palm, and clenched fist deformities.

491
The spastic hand in cerebral palsy
profundus (FDP) spasticity may also be present). If full PIP
joint extension is possible, but DIP joints do not extend, FDP
spasticity is present.
The Zancolli classification of active finger and wrist exten­
sion is helpful (Table 21.2).34 In the patient with active wrist
extension, spastic wrist flexion, and no significant digital
flexor tightness, a FAR procedure along with fractional
lengthening of the FCU, Z-lengthening of the FCR, and release
of palmaris longus may be required. In contrast, the patient
with flexed fingers, but relatively little spasticity of wrist
flexors, may benefit from fractional lengthening of the
involved finger flexors. If the fingers can be extended only
with the wrist in moderate flexion, then one can perform wrist
flexor releases and additional finger flexor fractional length­
ening. However, a flexor–pronator muscle slide will address
simultaneous wrist and finger flexion and the forearm prona­
tion deformity (Fig. 21.17 and Video 21.1
).
Fig. 21.15  (A) Release of an elbow flexion contracture often results in a soft-tissue
antecubital defect. (B,C) A transposition fasciocutaneous flap will cover the exposed
vital structures in the antecubital fossa and then the donor defect over the proximal
forearm muscles can be replaced with a split-thickness skin graft. (D) Final elbow
extension accomplished.
A
B
C
D
Clinical tips
Flexor–pronator slide
• Allows each muscle to slide distally differentially, with each
finding its “new” place of attachment
• Identify and mobilize median and ulnar nerve first before
commencing release.
• Anterior interosseous nerve and artery are “safely” reflected
volarly.
• May need to divide origin of posterior interosseous artery
for mobilization of the deepest fibers of FDS to middle and
ring fingers
• Splint wrist and fingers for 5–6 weeks to allow muscles to
attach at new sites of origin
• Continue night position splinting.
• Flexion strength may take some months to return.

492
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
Only once the acute flexor spasm has been released is it pos­
sible to accurately assess if there is active wrist extension. This
may be addressed by ECU transfer to ECRB or by brachiora­
dialis transfer. Alternatively, the author has found that FCU
can be transferred (and will have sufficient strength) several
months after a flexor–pronator muscle slide has been per­
formed. This may greatly improve grasp by removing the
habitual grasp pattern of simultaneous wrist flexion. The
fingers and wrist and elbow are splinted for 4 weeks postop­
eratively, with continued wrist splinting for another 6 weeks,
and night positional splinting of the fingers.
Wrist fusion by proximal row carpectomy (PRC) and using
those removed carpal bones for graft is reserved for very
severe wrist flexion contractures (often with a non-functional
hand). Shortening accomplished by PRC may reduce the need
to shorten finger flexors.
Correction of wrist and finger flexion deformities may
unmask intrinsic hand tightness. A simultaneous thenar
release can be done through a curvilinear thenar inci­
sion (avoiding the median motor nerve branch), but the
author prefers to address finger swan-neck deformities at a
later date.
Fig. 21.16  Volkmann test for digital flexor tendon tightness.
When wrist extension is less than neutral (Volkmann’s angle),
surgical intervention is indicated.
A
B
Volkmann’s angle
Table 21.2  Zancolli classification of active finger and wrist
extension
Level
Designation
Description
1
Minimal flexion
spasticity
Can completely extend the fingers
with a neutral position of the wrist
or with <20° of flexion
2
Moderate flexion
spasticity
Fingers can be actively extended but
only with >20° of flexion
2A
Can actively extend, partially or
totally, the wrist with the fingers
flexed
2B
Cannot actively extend the wrist with
the fingers flexed because of
flaccid paralysis of the wrist
extensor muscles
3
Severe flexion
spasticity
Cannot extend the fingers even with
maximal flexion of the wrist
(Reproduced with permission from Zancolli EA, Zancolli ER Jr. Surgical
management of the hemiplegia spastic hand in cerebral palsy. Surg Clin North
Am. 1981;61:395–406.)

493
The spastic hand in cerebral palsy
Fig. 21.17  A flexor–pronator muscle slide is an extensive procedure that involves
identification of all neurovascular structures in the forearm and release of the
muscular origins so that a distal slide can occur. (A) Wrist and digit contractures.
(B) Muscle origin releases. (C) Muscle advancement. (D) Thenar intrinsic release.
(E) Passive correction accomplished.
A
B
C
D
E
Thumb
Deformity as described by House and modified by Tonkin
et al.35 is a useful classification (Table 21.3). If the deformity is
adduction without MP or IP joint deformity, then release of
adductor pollicis is performed in conjunction with first
webspace Z-plasty. Release of the dorsal fascia or even first
dorsal interosseous release may also be required. If there is
tight thumb adduction with MP joint flexion (without signifi­
cant IP joint deformity), then also release the flexor pollicis
brevis though the same incision.36 If both MP and IP joints are
flexed together with thumb adduction, then add flexor pollicis

494
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
previously described releases. One must assess extrinsic thumb
extensor function. If there is a functioning extensor pollicis
longus (EPL) and weak abduction, re-routing EPL is helpful.
EPL is transected proximal to the IP joint, the extensor mecha­
nism is repaired, and the proximal end is re-routed through the
first dorsal compartment and reattached to the radial side of
the extensor mechanism, so changing its vector direction30 or
into the proximal phalanx. If there is MP joint hyperextension,
then the re-routed EPL is inserted into the radial side of the
distal metacarpal.37 If there is no EPL function, brachioradialis
to abductor pollicis longus transfer can be performed.
With MP joint hyperextension instability, then either a
volar tenodesis or capsulodesis of the joint must be done or
MP joint fusion performed.
Finger swan-neck deformity
If there is mild deformity, secondary to intrinsic spasticity,
extrinsic silver ring splints may be used, or intrinsic muscle
slide performed (Fig. 21.18). With a concomitant thumb
adductor spasticity, and if a temporary ulnar nerve block
favorably affects both the thumb-in-palm deformity and
intrinsic finger spasticity, then one may, on occasion, consider
ulnar motor neurectomy in Guyon’s canal. With more severe
PIP joint instability, an FDS distal slip tenodesis secured to the
proximal phalanx works well (Fig. 21.19).38
Table 21.3  Modified House classification of thumb deformity
Type
Deforming forces
Thumb position
1. Intrinsic
Adductor pollicis
Metacarpal adduction
1st dorsal interosseous
MCP joint flexion
Flexor pollicis brevis
IP joint extension
2. Extrinsic
Flexor pollicis longus
MCP joint flexion
IP joint flexion
Metacarpal adduction
less marked
3. Combined
Adductor pollicis
Metacarpal adduction
1st dorsal interosseous
MCP joint flexion
Flexor pollicis brevis
IP joint flexion
Flexor pollicis longus
(True “thumb-in-palm”
deformity)
MCP, Metacarpophalangeal; IP, interphalangeal.
(Reproduced with permission from Tonkin MA, Hagrick NC, Eckersley JR, et al.
Surgery for cerebral palsy part III: classification and operative procedures for
thumb deformity. J Hand Surg Br. 2001;26:465–470.)
Fig. 21.18  (A) Patient with residual swan-neck deformities and intrinsic muscle contractures following more proximal release. (B) Interosseous muscle slide. (C,D) Final
ability to flex and extend the fingers.
A
B
C
D
longus (FPL) lengthening through a separate incision, per­
forming either fractional lengthening or Z-lengthening (for
more severe IP joint flexion).
In a patient who does not have sufficient antagonistic
strength, tendon transfers will be needed to augment these

495
The spastic hand following stroke and traumatic brain injury
have MP joint flexion and PIP joint hyperextension. The
Bunnell test will further confirm intrinsic spasticity. Patients
who present with swan-neck deformity and full MP joint
extension upon active digital extension have this deformity
from overpull of the long digital extensors. Surgical treat­
ment of the former is done through a transverse incision in
the palm and fractional lengthening of lumbricals and volar
and dorsal interossei,40 avoiding the first dorsal interosseous
if possible to reduce the risk of weakened pinch strength.
Extensor digitorum communis overpull, on the other hand, is
treated by central slip tenotomy about 1 cm proximal to the
PIP joint.
PIP joint volar tenodesis may be required as a concomitant
procedure if the volar plate is very lax or has been described
as the sole treatment of swan-neck deformity. This is done by
either using a slip of FDS tendon41 or using lateral bond
translocation.42
The spastic hand following stroke and
traumatic brain injury
Patient selection
The principles of assessment and treatment are very similar
to cerebral palsy. Procedures for flexed fingers are divided
into functional procedures or those that are hygiene proce­
dures.43 The results of surgery are better when deformities are
corrected early, before fixed joint contractures have developed.
Surgery should not be considered as a treatment of last resort.
“Non-functional” surgical procedures may actually help
overall bodily function. For example, in spite of not having
active function in the upper extremity after spastic releases,
dressing may be facilitated or positioning the hand on a
walker may improve ambulation.
Fingernails may dig into the palm and palm skin may be
macerated. Clenched fist is often accompanied by a flexed
wrist. Assess for active finger flexion. If the PIP joints flex
while DIP joints remain extended, there is spasticity in the
FDS rather than FDP.
Surgical technique
If there is skin maceration and no volitional flexion, then
significant lengthening of flexor tendons is required and
superficialis-to-profundus (STP) transfer is performed. At
best, a mass action grasp pattern is achieved with the STP
transfer and, at worst, passive restraint to extension is accom­
plished rather than a “floppy hand” with joint instability if
simple tenotomies were to be performed. Associated proce­
dures may be required such as thenar release and Z-lengthening
of wrist flexors.
If there is volitional control of extrinsic finger flexors,
and if the degree of flexion contracture is less severe, then
fractional lengthening of FDS, FDP, and even FPL is done
by sharply incising the intramuscular tendon fibers. A short
volar splint may be used for postoperative comfort, but
active exercises are begun immediately. A flexor–pronator
muscle slide may sometimes be used for a more global
correction of flexed elbow, forearm pronation, wrist and
finger flexion.
Fig. 21.19  A residual hyperextension swan-neck deformity at the PIP joint may be
treated by (A) a proximal intrinsic release and (B) tenodesis using a distally based
slip of, flexor digitorum superficialis that is re-routed back around the origin of the
flexor tendon sheath or anchored into bone of the proximal phalanx.
A
B
Hints and tips
Spastic swan-neck deformity
• Differentiate between intrinsic “tightness” and “tightness” of
extrinsic extensors.
• The former is treated by intrinsic release (dorsally) or volar
fractional lengthening.
• The latter is treated surgically by central slip (“Fowler”)
tenotomy.
• “Mild” swan-neck may be treated by figure-of-eight splinting.
Swan-neck deformity may result from either intrinsic spastic­
ity or overpull of digital extensors. Each will cause overstretch
of the PIP volar plate, resulting in hyperextension at that joint.
Accurate diagnosis is essential, therefore, for proper surgical
treatment.39
These two variants of swan-neck deformity are distin­
guished by observing the MP joint position during active
digital extension. Patients with intrinsic muscle spasticity

496
SECTION III
CHAPTER 21 • The stiff hand and the spastic hand
surgical treatment. With this approach, one can assess func­
tional outcome in the operating room. The patient can imme­
diately see the outcome while pain-free. This technique also
serves as a bridge to ongoing postoperative hand therapy.
Biochemical and mechanical scar modification are ongoing
directions for research. The introduction of corrective surgery
will bring about all the phases of wound healing once again
with inflammation, edema, collagen deposition, and scar
remodeling. The postoperative problem of new scar forma­
tion following joint releases and tenolyses remain an issue.
In the area of spasticity, gait analysis has been pivotal in
evaluating the lower extremity. We are now gaining insights
from motion analysis laboratories for the upper extremity.
This will not only help in the preoperative analysis of spastic
problems but will also help in assessing postoperative func­
tional outcomes.
Conclusions
Contractures in the upper extremity result not only from joint
pathology but also from disorders of periarticular structures
as well as tendon adhesions and muscle imbalance. The
correct treatment is predicated on making the appropriate
diagnosis. A variety of specific disorders are known to lead to
contractures, but the most common conditions that the hand
surgeon will have to treat are the consequences of trauma.
Meticulous postoperative therapy and splinting are essential
to optimize best functional outcome.
Future directions
With regard to joint contractures and stiff joints, wide-awake
local anesthesia technique has added an extra dimension to
1. Lister G. The Hand: Diagnosis and Indications. 3rd ed. New York, NY:
Churchill Livingstone; 1993:191–198.
2. Curtis RM. Stiff finger joints. In: Grabb WC, Smith JW, eds. Plastic
Surgery. 3rd ed. Boston, MA: Little Brown; 1979:598–603.
3. Smith RJ. Nonischemic contractures of the intrinsic muscles of the
hand. J Bone Joint Surg Am. 1971;53:1313–1331. This is a classic article
that very lucidly describes the pathologic anatomy and treatment of the
disorders of the intrinsic hand muscles.
10. Eaton RG. The extensor mechanism of the fingers. Bull Hosp Joint
Dis. 1969;30:39–47. Another classic article that has stood the test of time
and is recognized for its practical approach to the extensor mechanism and
contributions to finger contractures.
12. Watson HK, Light TR, Johnson TR. Check-rein resection for flexion
contracture of the middle joint. J Hand Surg Am. 1979;4:67–71. This
article describes in detail the role of the volar plate in PIP flexion
contractures and the importance of identifying the pathologically
disordered checkrein ligaments.
19. Joshi BB. Dorsolateral flap from same finger to relieve flexion
contracture. Plast Reconstr Surg. 1972;49:186–189.
28. Lomita C, Ezaki M, Oishi S. Upper extremity surgery in children
with cerebral palsy: review article. J Am Acad Orthop Surg.
2010;18:160–168. This is a very concise article that is packed with
practical information. It is a systematic review that includes spasticity of
the elbow, forearm, wrist, thumb, and fingers in sequence.
30. Manske PR. Redirection of extensor pollicis longus in the treatment
of spastic thumb-in-palm deformity. J Hand Surg Am. 1985;10:
553–560.
32. Gschwind CR. Surgical management of forearm pronation. Hand
Clin. 2003;19:639–655.
35. Tonkin MA, Hagrick NC, Eckersley JR, et al. Surgery for cerebral
palsy part III: classification and operative procedures for thumb
deformity. J Hand Surg [Br]. 2001;26:465–470. Another practical guide
that classifies thumb deformity into “intrinsic” and “extrinsic”
contractures or a combination of the two. This analysis of the deformity
then translates into a useful surgical treatment algorithm.
Access the complete reference list online at

496.e1
References
References
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Surgery. 3rd ed. Boston, MA: Little Brown; 1979:598–603.
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23. Lalonde DH. Wide awake flexor tendon repair. Plast Reconstr Surg.
2009;123:623–625.
24. Buch VI. Clinical and functional assessment of the hand after
metacarpal phalangeal capsulotomy. Plast Reconstr Surg.
1974;53:452–457.
25. Weinzweig N, Culver JE, Fleegler EJ. Severe contractures of the
proximal interphalangeal joint in Dupuytren’s disease combined
fasciectomy with capsuloligamentous release versus fasciectomy
alone. Plast Reconstr Surg. 1996;97:560–566.
26. Field PL, Hueston JT. Articular cartilage loss in long-standing
immobilization of interphalangeal joints. Br J Plast Surg.
1970;23:186–191.
27. House JH, Gwathmey FW, Fidler MO. A dynamic approach to the
thumb-in-palm deformity in cerebral palsy. J Bone Joint Surg Am.
1981;63:216–225.
28. Lomita C, Ezaki M, Oishi S. Upper extremity surgery in children
with cerebral palsy: review article. J Am Acad Orthop Surg.
2010;18:160–168. This is a very concise article that is packed with
practical information. It is a systematic review that includes spasticity of
the elbow, forearm, wrist, thumb, and fingers in sequence.
29. Zancolli VA, Goldner LJ, Swanson AB. Surgery of the spastic hand
in cerebral palsy: report of the Committee on Spastic Hand
Evaluation. J Hand Surg Am. 1983;8:766–772.
30. Manske PR. Redirection of extensor pollicis longus in the treatment
of spastic thumb-in-palm deformity. J Hand Surg Am. 1985;10:
553–560.
31. Tonkin MA. The upper limb in cerebral palsy. In: Gupta A, Kay SPJ,
Scheker LR, eds. The Growing Hand. London: Mosby; 2000:447–459.
32. Gschwind CR. Surgical management of forearm pronation. Hand
Clin. 2003;19:639–655.
33. Green WT, Banks HH. Flexor carpi ulnaris transplant and its use in
cerebral palsy. J Bone Joint Surg Am. 1962;44:1343–1352.
34. Zancolli EA, Zancolli ER Jr. Surgical management of the hemiplegia
spastic hand in cerebral palsy. Surg Clin North Am. 1981;61:395–406.
35. Tonkin MA, Hagrick NC, Eckersley JR, et al. Surgery for cerebral
palsy part III: classification and operative procedures for thumb
deformity. J Hand Surg [Br]. 2001;26:465–470. Another practical guide
that classifies thumb deformity into “intrinsic” and “extrinsic”
contractures or a combination of the two. This analysis of the deformity
then translates into a useful surgical treatment algorithm.
36. Van Heest A, House J. Management of the spastic hand. In: Mathes
SJ, Hentz VR, eds. Plastic Surgery. 2nd ed. Philadelphia, PA:
Saunders/Elsevier; 2006:543–553.
37. Van Heest AE. Surgical technique for thumb-in-palm deformity in
cerebral palsy. J Hand Surg Am. 2011;36:1526–1531.
38. Swanson AB. Surgery of the hand in cerebral palsy and the
swan-neck deformity. J Bone Joint Surg Am. 1960;42:951–964.
39. Carlson MG, Gallagher K, Spirtos M. Surgical treatment of
swan-neck deformity in hemiplegic cerebral palsy. J Hand Surg Am.
2007;32:1418–1422.
40. Matsuo T, Matsuo A, Hajime T, et al. Release of flexors and intrinsic
muscles for finger spasticity in cerebral palsy. Clin Orthop Relat Res.
2001;384:162–168.
41. Swanson AB. Treatment of the swan-neck deformity in the cerebral
palsied hand. Clin Orthop. 1966;48:167–171.
42. Tonkin MA, Hughes J, Smith KL. Lateral band translocation for
swan-neck deformity. J Hand Surg Am. 1992;17:260–267.
43. Hisey MS, Keenan MAE. Orthopedic management of upper
extremity dysfunction following stroke or brain injury. In: Green
DP, Hotchkiss RN, Pederson WC, eds. Green’s Operative Hand
Surgery. 4th ed. Philadelphia, PA: Churchill Livingstone;
1999:287–324.

SECTION III • Acquired Non-traumatic Disorders
22 
Ischemia of the hand
Hee Chang Ahn and Neil F. Jones
SYNOPSIS
■ Upper extremity ischemia is caused by many etiologies and may be
classified into acute and chronic cases.
■ A precise understanding of arterial anatomy is pertinent to preoperative
diagnosis, patient selection, and operative procedure.
■ A history of cold intolerance, Raynaud’s phenomenon, and frequency
of ischemic pain is important. Color changes, ulcerations, and
infections are evaluated.
■ Non-invasive vascular examination includes measurement of fingertip
temperatures, Doppler ultrasound, segmental arterial pressures, and
capillaroscopy.
■ Various pharmacologic agents can be used to counteract the
sympathetic effect on the muscular layers of the arterial wall in a
conservative medical approach.
■ Surgical intervention is directed at interrupting the sympathetic
innervation of the muscle layer, by physical dilatation of the obstructed
lumen, or by microsurgical reconstruction of the occluded lumen.
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Introduction
Hand ischemia occurs when the vascular system is no longer
able to transport blood efficiently because of trauma, constric­
tion, obstruction, or vasospasm. It is the critical vascular event
that results in eventual tissue necrosis and even amputation
without proper management. Compared with the lower
extremity, the symptomatology and presentation is varied in
the upper limb and it is frequently underdiagnosed. Upper
extremity ischemia is caused by many etiologies3 and may be
classified into acute and chronic cases (Box 22.1). Any micro­
vascular injury that diminishes the vascular flow induces the
acute ischemic conditions of the hand. Systemic, congenital,
and genetic problems also cause chronic ischemic conditions.
Raynaud’s phenomenon is a well-known vasospastic condi­
tion that affects 5–10% of the general population.4,5 Primary
Raynaud’s disease occurs in the absence of any underlying
condition whereas secondary Raynaud’s syndrome is associ­
ated with other vasospastic conditions.
Fuchs classified arterial disease according to the three arterial
layers: the intima, media, and adventitia. Several of the most
frequent pathologic processes (atherosclerosis, intimal hyper­
plasia) originate in the intimal layer. Endothelial disruption
produces thrombotic occlusion and embolization.6 The media
consists of smooth muscle cells, fibroblasts, and elastic tissue.
Atherosclerosis also influences the loss of tissue integrity. The
media can become chronically dilated in a diffuse (ectasia) or
localized (aneurysm) pattern. The adventitia is involved in
diffuse pathologic entities (arteritis, Buerger’s disease). Jones
categorized hand ischemia into subgroups of acute and chronic
disease. There are multiple causes of upper extremity ischemia
(see Box 22.1),3 but a classification system based on the under­
lying pathophysiologic mechanism responsible for producing
the ischemia would seem to be most appropriate as a rationale
for suitable treatment. Jones described five main pathophysi­
ological mechanisms of hand ischemia: emboli, thrombosis,
occlusive disease, vasospasm, and low-flow states.7
Regardless of its causes, ischemia of the hand is manifested
by color and temperature changes, pale fingers, cold intoler­
ance, numbness, digital ulcerations, and gangrenous changes.
Despite appropriate treatments, such as smoking cessation,
cold avoidance, biofeedback techniques, and pharmacological
therapy, ischemia commonly progresses to the eventual con­
sequence of amputation.8–13 This chapter provides an insight
to accurate diagnosis and appropriate treatment to avoid
devastating tissue losses.
Raynaud’s phenomenon
Raynaud’s disease is a rare disorder but it is an important
cause of upper limb ischemia. This entity is often confused
with Raynaud syndrome. Raynaud’s phenomenon in patients
  Access video content for this chapter online at expertconsult.com

497.e1
Historical perspective
Historical perspective
Maurice Raynaud described Raynaud’s phenomenon in 1862
and attributed the condition that bears his name to overactiv­
ity of the sympathetic nervous system, but a review of his
cases reveals that most of his patients probably had small-
vessel occlusive disease. He hypothesized that “local asphyxia
of the extremities” was a result of “increased irritability of the
central parts of cord presiding over vascular innervations.”1
Lewis first postulated a peripheral rather than central
mechanism for Raynaud’s disease caused by a “spasm of
digital arteries”. He stated that “the abnormal element in the
reaction to cold is a direct reaction and due to a peculiar
condition of the vessel wall locally: it is not the result of a
reflex through the vasomotor nerves.” However, the patho­
physiology remained poorly understood.2

498
SECTION III
CHAPTER 22 • Ischemia of the hand
3. No evidence of underlying organic disease
4. Symptoms present for at least 2 years.
Merritt,15 and Blunt and Porter16 argued that these criteria are
confusing and perhaps obsolete, considering that Raynaud’s
phenomenon can be present for an average of 11.5 years prior
to diagnosis of an underlying connective tissue disease.17
Furthermore, in one study using sensitive laboratory testing
of patients with Raynaud’s disease, more than one-half of
patients were found to have some evidence of an underlying
systemic disease.18
The relationship between vasospasm in Raynaud’s phe­
nomenon and occlusive disease continues to be controversial.
Some researchers have suggested that occlusive disease may
initiate vasospasm via humoral and/or sympathetic media­
tors. This concept is supported by the fact that excision of the
occluded arterial segment in patients with traumatic ulnar
artery thrombosis (hypothenar hammer syndrome) will
improve the digital vasospasm often seen in this disorder.19
Vasospastic symptoms in patients with connective tissue
disorders may also be related to an underlying abnormality
of the vessel wall. Intimal hyperplasia, thrombosis, fibrosis,
embolism, adventitial thickening, aneurysm formation, and
calcification have all been found in patients with Raynaud’s
phenomenon.20,21 The question remains whether these changes
are responsible for the vasospastic symptoms or merely
potentiate vasospasm initiated at another site. Therefore,
bypass of distal arterial occlusions may not only provide
oxygen delivery via increased blood flow to the hand but also
may remove a potential source of vasospasm.
Basic science
Anatomy
Embryology
The limb buds appear at 4 weeks of embryonic life as lateral
swellings and the forearm vasculature evolves through several
stages between 4 and 8 weeks (see Chapter 25). A median
artery, ulnar artery, and radial artery arise in order from the
brachial artery at the elbow, but the median artery involutes
as the radial and ulnar arteries provide the majority of blood
flow to the hand.
Arterial system in the forearm, hand, and digits
Variations in the vascular pattern of the deep and superficial
palmar arches and the common digital arteries are frequent.
Therefore, a precise understanding of arterial anatomy is
pertinent to preoperative diagnosis, patient selection, and
operative procedure.
Superficial palmar arch
The superficial palmar arch may be classified as either “com­
plete” or “incomplete”. This classification provides the sim­
plest understanding of the anatomy of the arches.22 Gellman
et al. defined an arch to be complete if there was an anasto­
mosis between the vessels constituting it and an incomplete
arch as having an absence of communication or anastomosis
between the vessels constituting the arch.23 Coleman and
Anson also described an incomplete superficial arch as one
with upper extremity ischemia is common and classically
consists of an orderly progression of color changes (white,
blue, and then red) and symptoms in the affected hand sec­
ondary to vasospasm. Pallor is followed by a cyanotic appear­
ance, and culminates with reactive hyperemia and burning
pain or dysesthesias. This classic pattern occurs in about two-
thirds of affected patients. In 1932, Allen and Brown proposed
that Raynaud syndrome/phenomenon be differentiated from
Raynaud’s disease in that no underlying organic cause can be
found in Raynaud’s disease.14 They listed the following crite­
ria as necessary for the diagnosis of Raynaud’s disease:
1. Bilateral symptoms
2. Absence of gangrene
BOX 22.1  Etiology of acute and chronic ischemia of the hand
• Atherosclerosis: proximal (more common) or distal
• Buerger’s disease
• Cervical rib compression
• Connective tissue disease
•
Scleroderma
•
Mixed connective tissue disease
•
Systemic lupus erythematous
•
Rheumatoid arthritis
•
Wegener’s granulomatous
• Emboli
•
Atrial fibrillation
•
Myocardial infarction
•
Poststenotic dilatation of subclavian artery
• Iatrogenic
•
Brachial artery: cardiac catheterization
•
Radial artery: arterial pressure cannulation
•
Hemodialysis access: shunts and fistulas
• Intra-arterial drug injection
• Myeloproliferative and immunologic disorder
•
Polycythemia
•
Leukemia
•
Myeloma
•
Cryoglobulinemia
• Renal vascular disease
• Post-irradiation
• Septicemia
• Trauma
•
Shoulder dislocation
•
Supracondylar fracture of the humerus
•
Posterior dislocation of the elbow
•
Hypothenar hammer syndrome
• Toxins
•
Heavy metals
•
Vinyl chloride
•
Others
• Vibratory tool disease
(Reproduced with permission from Jones NF, Emerson ET. Interposition vein
graft configurations for microsurgical revascularization of the ischemic hand.
Tech Hand Up Extrem Surg. 1999;3:121–130.)

499
Basic science
When the superficial arch is well developed, the deep
palmar arch is correspondingly less developed and vice versa.
A reciprocal inverse relationship was also found between the
common palmar digital arteries and the palmar metacarpal
arteries.22,30,33,34
Digital arteries
The ulnar digital arteries of the thumb and index finger are
larger than the radial digital arteries. The radial digital artery
is larger in the ring and small fingers. The difference between
the radial and ulnar digital arteries is statistically significant
only in the border digits. The anatomy of the thumb digital
arteries is unique. The blood supply of the thumb comes
mainly from the princeps pollicis artery, the terminal branch
of the superficial palmar arch, and the first dorsal metacarpal
artery. There are numerous sources of blood supply from the
radial and ulnar arteries, including the palmar ulnar, palmar
radial, dorsal ulnar and dorsal radial arteries. The first palmar
metacarpal artery is absent in about 2% of patients.22,31 This
accounts for the tolerance to ischemia by the thumb due to
numerous collateral blood vessels.
According to the Hagan–Poiseuille’s law, the blood viscos­
ity, diameter, length and the pressure gradient influence flow
through the digital arteries, and larger digital arteries can
carry more blood. Strauch and de Moura described the
numerous interconnections between the digital arteries
beyond the metacarpophalangeal joints. These connections
play an important role in hand ischemia if segmental arterial
obstruction develops.34
Micro-arterial system
Microvascular vessels are defined as having a diameter of
<100 µm. Their role is to deliver oxygen and nutrients at a
cellular level. They consist of nutritional capillary and ther­
moregulatory vessels.33 In the digits, 80–90% of the total flow
passes through thermoregulatory beds and 10–20% are
involved in capillary nutrition.35 In pathologic states, cellular
hypoperfusion leads to ischemic symptoms and imbalance in
the distribution of thermoregulatory and nutritional flow,
resulting in cell death or damage.
Physiology of blood flow
Hemodynamics
Koman et al.24 described macrovascular structures that are
defined as vessels >100 µm. Their function is to deliver nutri­
ents to the microvascular beds, provide adequate capacity for
arteriovenous thermoregulatory flow, and drain nutritional
and thermoregulatory beds.
Cellular control mechanisms
Blood flow does not only follow principles of fluid dynamics.
There is compensation between arterial dilatation, collateral
vessels, and resistance in the peripheral circulation. In a normal
extremity, blood flow in the hand depends on sympathetic
tone, metabolic demands, environmental events, local factors,
and circulating humoral mediators. Alpha-adrenergic control
is the dominant control arm of vasoconstriction; however,
vasodilatation is initiated by endothelium-derived relax­
ing factor. Active vasoconstriction and vasodilatation may
“in which the contributing arteries do not anastomose, or
when the ulnar artery fails to reach the thumb and index
finger.”22 Koman et al.24 also reported a complete arch in 78.5%
of extremities. Gellman et al. reported a complete arch in 38
of 45 specimens studied (84.4%). In contrast to these studies,
Fazan25 reported that only 43% of right hands and 52% of left
hands had complete arches.
Multiple variations of the superficial palmar arch have
been classified into subgroups. According to Gellman’s study,
complete arches have been divided into five subgroups:
■ Type A: The radioulnar arch is formed by anastomosis
between the superficial volar branch of the radial artery
and the continuation of the ulnar artery.
■ Type B: The superficial arch is formed by a continuation
of the ulnar artery and even provides common digital
vessels to the thumb and index webspace.
■ Type C: The median and ulnar arteries combine to form
the superficial arch without a contribution from the radial
artery.
■ Type D: This is characterized by all three vessels (radial,
median, ulnar) contributing to the arches.
■ Type E: A branch from the deep palmar arch
communicates with an ulnar artery-initiated superficial
arch.
The main branches from the superficial palmar arch are the
three common digital arteries to the index–middle, middle–
ring, and ring–small finger webspaces22,26 and the proper
digital artery to the ulnar border of the small finger.23,27,28
When the princeps pollicis artery and a vessel to the radial
side of the index finger (index radial digital artery) originate
from the superficial palmar arch, this should be named as the
first common digital artery.27,29
Deep palmar arch
The deep palmar arch is less variable than the superficial arch.
The radial artery forms the deep arch when it passes from
dorsal to palmar by piercing the two heads of the first dorsal
interosseous muscle. The arch then curves along the bases of
the metacarpal bones. The deep arch may anastomose with
one or both volar branches of the ulnar artery.23,30 At least one
of the deep volar branches was present in all individuals in a
recent study. The deep palmar arterial arch travels across the
palm, deep to the flexor tendons, at the level of the carpometa­
carpal joints to connect with a deep arterial branch from the
ulnar artery.22,31 The deep palmar arch gives rise to as many
as five palmar metacarpal arteries that pass distally to the
level of the metacarpal heads, where they branch dorsally to
join the dorsal metacarpal arteries and also connect to the
common digital artery through a small palmar arterial branch.
Nystrom et al. described three palmar and three dorsal arches
that connect the four forearm arteries (ulnar, median, radial,
and interosseous arteries). Dorsal metacarpal arteries that
originate from the dorsal carpal arches pass to their respective
webspaces distally, where they join perforating vessels from
the palmar circulation.32
The most consistent of the dorsal vessels supplying the
dorsal carpal rete, which consists of numerous small, thin
vessels (0.3–0.5 mm), is the radial dorsal carpal branch. It
branches off the radial artery 10–15 mm distally to the radial
styloid.23

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SECTION III
CHAPTER 22 • Ischemia of the hand
Because of its anatomic configuration within Guyon’s
canal, the ulnar artery is particularly vulnerable to mechani­
cal injury. The hook of the hamate bone presses against the
superficial palmar branch of the ulnar artery in Guyon’s canal,
leading to the development of progressive periadventitial
scarring, damage to the media, disruption of the internal
elastic lamina, intimal damage, and subintimal hematoma
of the ulnar artery. These events are postulated to be the
pathophysiological mechanism whereby repetitive trauma
causes thrombosis in competitive athletes (volleyball, karate,
handball, and baseball).40–42
“Vibration white finger” or vibration-induced Raynaud’s
phenomenon is also related to repetitive trauma in workers
who frequently use drills, jackhammers, and chainsaws.
High-frequency vibration is assumed to affect the response
of the sympathetic vasoconstrictor nerves and receptors, not
only to mechanical- but also to thermal-induced pain.43,44
Radial artery catheterization frequently results in radial
artery thrombosis, although it is frequently asymptomatic
because of communication between the radial and ulnar
arterial systems. However, if the patient has an incom­
plete superficial palmar arch, distal ischemia may occur.23
Cardiac catheterization via the brachial artery may result
in thrombosis and distal emboli, with an incidence of
approximately 0.6%.45
Arteriovenous shunt operations in renal failure patients
may also result in hand ischemia. The arteriovenous shunt
may redirect a critical volume of blood flow away from the
hand, resulting in a “steal” phenomenon producing severe
motor and sensory deficits.46,47
Systemic disease
Systemic disease may produce distal hand ischemia and/or
Raynaud’s symptoms, including connective tissue disease,
vasculitis, malignancy, septicemia, arteriosclerosis, Buerger’s
disease, polycythemia, cryoglobulinemia, and chemical
toxicity.15
Diagnosis/patient presentation
Evaluation
Evaluation of vascular competency should define the patient’s
vascular anatomy and function under stressed and unstressed
conditions. Therefore, a combination of studies is needed.
Most importantly, a complete history and physical examina­
tion is essential in establishing a diagnosis. Investigations
including non-invasive or invasive vascular studies may be
required for exact evaluation of the patient’s status. The
patient’s symptoms and studies are carefully reviewed to
identify those patients who require surgical intervention.
History and physical examination
A history of cold intolerance, Raynaud’s phenomenon (Fig.
22.1), and frequency of ischemic pain is important, as is
smoking history; occupation involving repetitive injury or
vibration trauma, and systemic disease including diabetes,
cardiac disease, arrhythmias, drug use, blood dyscrasias, and
peripheral neurological abnormalities. Unilateral Raynaud’s
be initiated by a central control process mediated through
peripheral neural structures or circulatory factors or by local
autoregulation, which is metabolic or myogenic. Metabolic
autoregulation occurs in response to local metabolic needs
and is mediated by decreased oxygen and build up of adenos­
ine and potassium.36 Myogenic autoregulation is mediated
via transmural pressure and stretch-operated calcium chan­
nels.37 The microcirculation is also affected by endothelial
factors within blood vessels. The endothelium plays a major
role in control of vasomotor tone and blood fluidity, lipid
metabolism, and finally angiogenesis. The endothelium has
been recognized as an active tissue responsible for elaborating
both vasodilatory and vasoconstrictor substances. Endothelial
cells respond to differences in intravascular pressure due to
variations in the size of the lumen by releasing endothelium-
derived relaxing factor.38 Endothelium-derived relaxing factor
produces active vasodilatation, and endothelin is a potent
vasoconstrictor. Both compounds are released from the endo­
thelial cells to regulate vascular flow. Endothelial cells can
also release thromboxane A2, prostacyclin, and molecules of
thrombomodulin and heparan sulfate.
Pathophysiology
As described previously, Fuchs classified arterial disease
according to the three arterial layers: intima, media, and adven­
titia. Several pathologic processes (atherosclerosis, intimal
hyperplasia) originate from this intimal layer. Endothelial
disruption produces thrombotic occlusion and embolization.4
The media consists of smooth muscle cells, fibroblasts, and
elastic tissue. Atherosclerosis leads to loss of tissue integrity,
and the media becomes chronic dilated in a diffuse (ectasia)
or localized (aneurysm) pattern. The adventitia is involved
in diffuse pathologic conditions (arteritis, Buerger’s disease).
A classification system based on the underlying patho­
physiological mechanism responsible for producing the
ischemia would seem to be most appropriate as a rationale
for determining treatment. The pathological processes that
produce ischemia in any end organ (and the hand can be con­
sidered such an end organ) are emboli, “sludging” of blood
in low-flow states, thrombosis, external compression, intimal
proliferation progressing to occlusion (arteriosclerosis), and
vasospasm.5
Emboli
Large emboli from the heart due to atrial fibrillation or myo­
cardial infarction lodging at the bifurcation of the brachial
artery are best managed by embolectomy by a vascular
surgeon. However, smaller emboli or “micro-emboli” dis­
lodged from an ulcerated atherosclerotic plaque in a large
artery may lodge in the distal radial and ulnar arteries and
digital arteries, and result in digital ulcerations or gangrene.
Trauma
Traumatic causes of ischemia can be occupational, iatrogenic,
or secondary to an injury. Hypothenar hammer syndrome
(HHS) first described by Van Rosen in 1934 is an uncommon
cause of secondary Raynaud’s phenomenon, and occurs
mainly in patients who use the hypothenar part of their hand
as a hammer.39

501
Diagnosis/patient presentation
Diagnostic investigations
Non-invasive vascular examination includes measurement of
fingertip temperatures, Doppler ultrasound, segmental arte­
rial pressures, and capillaroscopy.
Capillaroscopy
The capillaries of the nail fold can be examined directly by
specialized dynamic videophotometric capillaroscopy, which
provides measurements of capillary diameter, red blood cell
velocity, and total flow. It can be difficult to perform in 10–12%
of individuals due to anomalous vessel orientation, varying
length of capillary loops, hyperkeratotic skin, or dense pig­
mentation. Dynamic capillary videomicroscopy allows direct
assessment of nutritional perfusion and arteriovenous shunt­
ing, and provides objective evidence of the effects of systemic
disease on the microcirculation and objective confirmation of
any improvement with medical intervention.25
Ultrasound
The pencil Doppler probe can also be used to assess the
patency of the distal radial and ulnar arteries at the wrist and
the dorsal branch of the radial artery as it passes through the
webspace, the superficial palmar arch, the common digital
arteries, and each proper digital artery on the radial and ulnar
aspects of each digit. Jones found the pencil Doppler probe to
be the simplest, most informative technique providing precise
determination of the patency of the arterial structures. Doppler
evidence of occlusion of either the distal radial or ulnar arter­
ies is one of the primary criteria for proceeding to invasive
arteriography.1,5
Segmental arterial pressures of the brachial artery at the
elbow and the distal radial and ulnar arteries at the wrist may
be measured with a pencil Doppler probe. A radial-brachial
index (RBI) and a digital-brachial index (DBI) can be calcu­
lated with a value of ≤0.7 indicating that arterial outflow to
the hand is decreased.54
Duplex ultrasonography
A duplex ultrasonogram is non-invasive, repeatable, and can
be used for follow-up investigation. Its most important
advantage is presenting real-time blood flow information
(Fig. 22.2).55,56
Isolated cold stress testing
Cold stress testing was developed to provide an evaluation of
the digital response to physiologic stress. Digital temperatures
or digital plethysmography (pulse volume recordings) are
measured before, during, and after application of a cold
stress-immersion in cold water or a cold chamber at 4°C.57 If
the fall in digital temperature or drop in pulse volume record­
ing can be partially ameliorated by a prior injection of local
anesthetic, this implies that vasospasm is a likely mechanism
for the ischemia.
Infrared thermography
Infrared thermography (IRT) provides a measure of the
decreased skin temperature of patients with hand ischemia
due to decreased superficial skin blood flow.44 The advantage
Fig. 22.1  Triphasic color changes. (A) Fingers turn white. (B) Fingers turn purple.
A
B
symptoms are especially suspicious and are usually indicative
of occlusive disease on the affected side.
McCabe et al. and Troum et al. developed a questionnaire
that can be used to assess the severity of cold sensitivity and
quantify the magnitude, duration, and frequency of vasospas­
tic symptoms and their effect on function.48,49
A thorough examination of the upper extremity for previ­
ous trauma, old scars or operative incisions, skin color, tem­
perature, presence of digital ulcers, and motor and sensory
evaluation of the three peripheral nerves should be routine.
Observation of blood flow in the fingernails may help to
diagnose ischemia due to connective tissue disease.25,50
Palpation may detect an abnormal mass or thrill. The
brachial, radial, and ulnar arterial pulses are also palpated.
The Allen test allows rapid evaluation of the patency of radial
and ulnar arterial inflow into the hand. A digital Allen test can
occasionally be performed either by forcing blood out of the
finger or by sequential compression of the digital arteries.51,52
Color changes, ulcerations, and infections are evaluated.
Non-healing ulcerations and/or impending gangrene associ­
ated with unilateral Raynaud’s symptoms are presumptive
evidence of thrombosis or embolism.25,53

502
SECTION III
CHAPTER 22 • Ischemia of the hand
of IRT is that it is non-invasive, easy to use and inexpensive
(Fig. 22.3). However, it is influenced by the ambient tem­
perature, and skin temperature itself does not reveal the
condition of a blood vessel and cannot visualize the site of
stenosis.
Angiography
Potential disadvantages of conventional angiography include
bleeding, allergic response to the contrast media, and X-ray
exposure. A major problem with invasive angiography is the
vessel spasm induced by the contrast media (Fig. 22.4).23,56,58
This can be circumvented by performing angiography under
a brachial plexus block or by preventing vasoconstriction by
intra-arterial injection of 4 mg phentolamine.59
Angiography defines the site and extent of thrombosis or
occlusion of the distal radial and ulnar arteries and even the
common digital and proper digital arteries.23,58,60 Jones5 has
suggested some criteria for angiographic investigation of
upper extremity ischemia as follows: (1) unilateral Raynaud’s
phenomenon; (2) progressive digital ulceration or gangrene
despite good medical management; (3) recurrent digital
ulceration; (4) Doppler evidence of occlusion of a major inflow
artery; and (5) acute onset of ischemic symptoms.
Magnetic resonance and computed
tomography angiography
More recently, high-resolution contrast-enhanced magnetic
resonance (MR) angiography and computed tomography
(CT) angiography continue to be refined to compete with
conventional angiography.61 Even though enhanced MR
angiography and CT angiography are non-invasive, the
resolution still does not allow the same visualization of the
digital arteries compared with conventional angiography.
Currently, if the surgeon requires accurate visualization of
the digital arteries, conventional angiography is still preferred
(Fig. 22.5).
Fig. 22.3  Infrared thermography. (A) Normal temperature in the palm.
(B) Ischemic fingers.
A
B
Fig. 22.4  Brachial angiography showing localized occlusion of the ulnar artery.
Fig. 22.2  Duplex ultrasonogram.

503
Patient selection
neurologic deficits are very important, but the presence of
a distal pulse is not reliable in the evaluation of vascular
integrity (Box 22.2). Immediate diagnosis is crucial in patients
with acute ischemia of the hand, and this has been accom­
plished most expeditiously with Doppler examination and
angiography.
Arterial emboli
The heart is the most common origin for arterial emboli. Acute
onset of pallor, pain, coolness, paresthesias, and pulselessness
should lead to strong suspicion for embolism. Ischemia will
produce muscle paralysis after an embolus proximal to the
forearm muscles, but paralysis is not present in distal emboli.
Segmental arterial pressures are helpful, and arteriography of
the entire upper extremity will determine if there is a more
proximal arterial source of emboli and also will help differen­
tiate embolism from acute arterial thrombosis.66
Iatrogenic injuries
■ Cannulation of the radial artery
■ Catheterization through the brachial artery
■ Harvest of radial artery for coronary artery bypass
■ Harvest of the radial forearm flap
■ Drug injection injury
■ Acquired arteriovenous fistula – for dialysis in renal
failure.
Cannulation injury
Radial artery cannulation injuries have increased because of
the increased frequency of arterial blood pressure monitoring.
Repeated injury to the radial artery can cause acute thrombo­
sis with distal embolization, pseudoaneurysm, and arterio­
venous fistula. Because of concomitant endothelial injury in
cannulation injuries of the radial artery, immediate resection
of the involved segment and reconstruction with an arterial
or vein graft is more effective than thrombectomy with small
Fogarty catheters.
Patient selection
Acute ischemia
Acute arterial injury
Acute ischemia of the hand may occur following laceration of
the brachial, radial, and ulnar arteries. Closed vascular injuries
are often caused by high-energy trauma with accompanying
fractures.62 High-energy trauma may cause hemorrhage,
thrombosis, incomplete vessel injury with development of
an aneurysm, compartment syndrome, or progressive throm­
bosis and distal embolization.63 Specific injuries of the upper
extremity that may result in ischemia of the hand include
shoulder dislocation, posterior dislocation of the elbow, and
supracondylar fracture of the humerus. Diagnosis is usually
not difficult in patients with significant hemorrhage and distal
ischemia. Undetected injury to non-critical vessels may result
in a false aneurysm or formation of an arteriovenous fistula.64
Thal described the indications for operative exploration.65
Physical findings of a pulsatile hematoma, a thrill, an
audible bruit, decreased peripheral pulses, or associated
Fig. 22.5  Computed tomography angiography.
Hints and tips
Diagnostic approach
1. A history of Raynaud’s phenomena is usually very
diagnostic. Patients can bring digital photos of the color
changes in their hands.
2. Thermal scan is a very easy tool for checking the
temperature of various parts of the hand.
3. Even though arteriography is invasive, it is the most
valuable investigation for detecting arterial abnormalities of
the hand – obstruction, stenosis, ectasia, coiling, aneurysm,
velocity of flow.
4. Occupational history is important for “vibration white finger”.
BOX 22.2  Signs of arterial injury
Hard signs
• Distal circulatory deficit
•
Ischemia
•
Absent or diminished pulses
• Bruit
• Expanding or pulsatile hematoma
• Arterial bleeding
Soft signs
• Small or moderate-sized hematoma
• Adjacent nerve injury
• Shock unexplained by other injuries
• Penetrating wound overlying course of major artery
(Reproduced with permission from Thal ER, Synder WH, Perry MO. Vascular
injuries of the extremities. In: Rutherford RB (ed.). Vascular surgery, 4th edn.
Philadelphia, PA: WB Saunders; 1995:713–735.)

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CHAPTER 22 • Ischemia of the hand
uncommon. Rarely nerve compression may cause pain or
sensory abnormalities. An aneurysm is readily identified by
a Doppler duplex ultrasonogram. Arteriography defines the
extent of involvement and allows for evaluation of collateral
flow for preoperative planning.73
Arteritis
Buerger’s disease
Buerger’s disease or thromboangiitis obliterans is an inflam­
matory disease of the small and medium-sized vessels of the
upper and lower extremities.74 Diagnosis is dependent on five
criteria: (1) smoking history; (2) onset before 50 years of age;
(3) arterial lesions below the knee; (4) upper limb involvement
or migratory phlebitis; and (5) absence of atherosclerotic risk
factors other than smoking. Surgical treatment by interposi­
tion or bypass vein grafting has been ineffective because the
process occurs in the very distal vessels.
Connective tissue disorders
■ Systemic sclerosis (scleroderma)
■ Mixed connective tissue disease
■ Systemic lupus erythematosus
■ Wegner’s granulomatosis.
Ischemic symptoms in connective tissue disorders should be
investigated with non-invasive modalities first, such as seg­
mental arterial pressure measurements, pulse volume record­
ings, and cold stress testing. Angiography is necessary if
surgery is contemplated.
Vasospastic disease
1. Primary Raynaud’s disease
2. Secondary Raynaud’s syndrome.
As described previously, the medical literature relevant to
vasospastic disease or Raynaud’s syndrome is confusing
and at times misleading. Koman24 described the criteria of
Raynaud’s disease and Raynaud’s phenomenon (Box 22.3,
Table 22.1).
Vasospastic conditions are either defined as primary with
absence of an identifiable etiology or secondary associated
Arterial injection injuries
Self-inflicted or inadvertent drug injection arterial injuries
result in severe acute ischemia due to chemical endarteritis,
arterial blockage by acid crystals, activation of the clotting
cascade, and secondary vasospasm, which causes severe
vasoconstriction and widespread thrombosis. Diagnostic
modalities are the same as in other vascular injuries.67
Acquired arteriovenous fistula
Arteriovenous fistulas may occur following trauma or infec­
tion but are usually created surgically to provide vascular
access for patients undergoing hemodialysis.68 End-to-end
radial artery to cephalic vein anastomosis may result in both
ischemic and neurological complications related to a “steal”
phenomenon.69
Side-to-side
anastomosis
(radiocephalic
arteriovenous fistula) also may reduce digital blood flow to
the thumb because of proximal shunting.70 Dialysis access-
associated “steal” syndrome occurs in 2–4% of surgically
created arteriovenous fistulas.71 Diagnosis is usually obvious.
For traumatic or post-injection fistulas, duplex sonogram
imaging, technetium scanning, or MR angiography are
diagnostic. Arteriography is usually not necessary unless
embolization is selected as a treatment option.
Chronic ischemia
Arterial thrombosis
The ulnar artery is the most common site for thrombosis in
the upper extremity. The anatomy of Guyon’s canal leaves the
ulnar artery vulnerable at the hook of the hamate.54
Repetitive trauma may damage the intima and cause
hypothenar hammer syndrome. Ischemic pain or paresthesias
in the ulnar two digits, color changes, and tenderness are the
usual signs at presentation. Allen’s test will show poor inflow
through the ulnar artery. Digital plethysmography (pulse
volume recordings) quantifies the degree of compromised
perfusion. Duplex sonogram or MR angiography will reveal
occlusion of the ulnar artery. Arteriography may show the
diagnostic “corkscrew” sign of hypothenar hammer syndrome
due to alternating segmental stenoses.72
Radial artery thrombosis occurs much less frequently
compared to ulnar artery thrombosis. Ischemic pain and cold
intolerance are confined to the thumb and index finger. Diag­
nostic modalities are similar to those described for ulnar
artery thrombosis.
Vibration-induced “white finger syndrome” represents
thrombosis of the digital arteries, and occurs most frequently
in the index finger. A digital Allen test is helpful, but an
ultrasonogram and angiography is diagnostic.44
Aneurysm
Upper extremity aneurysms may be divided into two types.
True aneurysms contain three layers of the arterial wall
whereas a false aneurysm or pseudoaneurysm lacks endothe­
lial cells. A true aneurysm occurs most frequently in areas of
repetitive trauma or is related to atherosclerosis. A pseudoa­
neurysm is usually the result of a penetrating injury.
A painless, palpable mass is highly suspicious of an
aneurysm but signs and symptoms of ischemia are very
BOX 22.3  Criteria defining Raynaud’s disease
• Characteristic triphasic digital color changes
• Bilateral hand movement
• Absence of occlusive disease
• Absence of gangrene or trophic changes (fingertip trophic
findings permissible)
• Absence of identifiable systemic disease (e.g., collagen vascular
disorder)
• Symptoms at least 2 year’s duration
• Female predominance
(Data from Dabich L, Bookstein JJ, Zweifler A, et al. Digital arteries in patients
with scleroderma. Arteriographic and plethysmographic study. Arch Intern Med.
1972;130:708–714.)

505
Treatment
interrupting the sympathetic innervation of the muscle layer
or by physical dilatation of the obstructed lumen or by micro­
surgical reconstruction of the occluded lumen.
Non-surgical treatment
Environmental modification
Cessation of smoking, avoidance of cold exposure, and limita­
tion of activities that precipitate symptoms are fundamental.
Cigarette smoking increases vasoconstrictor tone and alters
blood coagulability; both are detrimental to a patient with
ischemic disease. Nicotine patches may be used because they
do not impair nutritional blood flow.25 It is important that
patients are aware of the relationship between cold and emo­
tional stress and the reflex vasospasm in their hands.57 Most
patients intuitively avoid these circumstances but should also
be instructed in protective techniques.
Medical management
Pharmacological agents
Drug therapy is aimed at mitigating the sympathetic
hyperactivity in vasospastic and occluded arteries. Topical
nitroglycerine is a simple first-line treatment in an attempt to
relieve the pain associated with digital ulcerations. Currently,
calcium channel blockers are the optimal choice for vaso­
spastic symptoms,75 by preventing calcium influx in vascular
smooth muscle cells, which, in turn, ameliorates sympatheti­
cally driven vasoconstriction. Nifedipine, 10–30 mg orally
three times a day, or in a long-acting form (30–60 mg/day)
sustained-release capsules once or twice a day is most com­
monly used.11
Both tricyclic antidepressants and selective serotonin reup­
take inhibitors have also proved efficacious in the treatment
of chronic pain due to ischemia. However, some drugs that
directly affect sympathetic tone (α-adrenergic antagonists) are
often difficult for patients to tolerate due to their side effects.76,77
Local anesthetic blockade and intra-arterial vasodilators such
as reserpine and guanethidine have been used systemically
and by local injection, but long-term benefit has not been
achieved.78
For treatment of obstructive Raynaud’s syndrome, vasodi­
lator drugs that alter prostaglandin metabolism (prostaglan­
din E1, prostacyclin and its analogues), and rheologic agents
(aspirin, pentoxifylline, piracetam) have been advocated.15
Some success has been reported with intra-arterial adminis­
tration of prostaglandin E1, a potent vasodilator and inhibitor
of platelet aggregation.74
Recently, Van Beek et al. described a novel use for Botox
(botulinum toxin A) in the management of vasospastic disor­
ders.75 Injection of botulinum toxin A into the hand appears
to have a beneficial effect on intractable digital ulcerations and
rest pain in patients with severe vasospastic disorders.79
Thrombolytic therapy
Thrombolytic agents may be helpful for an embolic occlu­
sion of a small vessel, especially if the agent is administered
shortly after the acute embolic event. They can also be used
preoperatively as an adjunct to vessel repair by lysing clot
that is obscuring an underlying vascular abnormality (e.g.,
with an underlying cause. Based on this terminology, Rayn­
aud’s disease is primary and all other conditions are second­
ary.25 The vessels in primary Raynaud’s disease are not
diseased, hence the prognosis is benign. Because the structure
of the artery is normal, arterial reconstruction is not necessary,
but occasionally patients who are refractory to medical treat­
ment may be candidates for cervical sympathectomy or digital
sympathectomy.
In comparison to primary Raynaud’s disease, secondary
Raynaud’s syndrome has a more severe prognosis, which is
primarily related to the severity of the underlying disease.15
Surgical treatment of the ischemia in secondary Raynaud’s
syndrome includes digital sympathectomy and arterial
reconstruction.
Treatment
A detailed history, physical examination, and differential
diagnosis are the first steps in the management of ischemia
of the hand. An arteriogram is essential to evaluate the arterial
system of the entire upper extremity from the aortic arch
to the digital arteries. The aims of treatment are to restore
blood flow to an ischemic limb, prevent thromboembolic
complications, and preserve hand function by avoiding sec­
ondary muscle ischemia and necrosis through compartment
syndrome.
Treatments are selected according to the cause of ischemia,25
with options ranging from environmental modification to
surgical intervention. Various pharmacologic agents can be
used to counteract the effect of humoral factors on the mus­
cular layers of the arterial wall in a conservative medical
approach, whereas surgical intervention is directed at
Table 22.1  Raynaud’s disease versus Raynaud syndrome
Characteristics
Disease
Syndrome
History
Triphasic color change
Yes
Yes
Age >40
No
Yes
Progression rapid
No
Yes
Underlying disease
No
Yes
Female predominance
Frequent
Occasional
Physical examination
Trophic findings (ulcer,
gangrene)
Infrequent
Frequent
Abnormal Allen test
No
Common
Asymmetric findings
Infrequent
Frequent
Laboratory testing
Blood chemistry
Normal
Frequently abnormal
Microangiography
Normal
Frequently abnormal
Angiography
Normal
Frequently abnormal
(Reproduced with permission from Koman LA, Ruch DS, Smith BP, et al.
Vascular disorders. In: Green DP, Hotchkiss RN, Pederson WC (eds). Green’s
Operative Hand Surgery. New York, NY: Churchill Livingstone; 1999:2254–2302.)

506
SECTION III
CHAPTER 22 • Ischemia of the hand
flow across the fistula by narrowing the fistula with bands.
Even with precise intraoperative monitoring, this technique
failed because of a high rate of fistula thrombosis.92 Berman
et al.93,94 reported successful distal revascularization–interval
ligation in more than 90% of patients.
Sympathectomy
When medical management has failed to control rest pain,
or there is impending infarction of digits, or non-healing
of ischemic ulcerations, digital artery sympathectomy is
indicated.
Most of the sympathetic nerves in the upper extremity
emerge from the spinal cord with the ventral roots of the
second and third thoracic nerves95 and are widely dispersed
in the brachial plexus to the forearm and hand.90,96 Cervi­
cal sympathectomy has a long history in the treatment of
secondary vasospasm, but has currently lost favor because
it has a high relapse rate and is essentially of no benefit in
connective tissue disease.15,95 Pick96 first noted in his dissec­
tions of the sympathetic nervous system that some of the
sympathetic nerves bypass the sympathetic trunk and pass
first with proximal somatic nerves and then in the periarterial
adventitia to the digits. Failure of cervical sympathectomy for
upper extremity vasospastic disease may be due to branches
that bypass the cervicothoracic sympathetic trunk and are
not interrupted during the operative procedure of cervical
sympathectomy.90,91
Sympathetic nerve branches pass from the peripheral
nerves to adjacent arteries at intervals along the extremity and
travel in the perivascular tissue including the large and easily
identifiable nerve of Henle. This nerve accompanies the ulnar
artery along its course from forearm to the hand, supplying
several large segments to the ulnar artery.97 Pick96 identified
individual sympathetic nerve branches to the arterial struc­
tures from the wrist to the digits, providing a basis for the
current approach to surgical sympathectomy of the hand and
digits.98 This anatomic concept has provided the basis for two
types of peripheral sympathectomy.
Leriche sympathectomy (arteriectomy)
Leriche advocated excision and ligation of the thrombosed or
diseased arterial segment to improve collateral circulation
and interrupt the vasomotor disturbance. If there is adequate
collateral flow, excision of a thrombosed arterial segment
without reconstruction interrupts sympathetic control over
the distal vessels and reduces vasospasm. Several surgeons
determine intraoperatively whether adequate collateral flow
exists (e.g., after excision of a segment of ulnar artery) by
measuring digital arterial pressures.54,88,99 Zook et al.100 have
applied the Leriche sympathectomy concept to the digits by
excising segments of occluded digital arteries when digital
artery bypass was not possible.
Periarterial sympathectomy
Flatt90 first introduced the concept of a sympathectomy at the
digital level to apply its effect more distally in the extremity.
Surgical stripping of the adventitia from arteries to interrupt
the sympathetic innervation to the smooth muscle in the
vessel media has been tried in situations of acute vasospasm
following trauma or during microsurgery. However, this
aneurysm), permitting the surgeon to plan reconstruction of
the vessel abnormality.80 Successful salvage of hand ischemia
events has also been described with a combination of PGE1 and
local fibrinolytic therapy with tissue plasminogen activator
(rt-PA).81 Although some authors82 have doubted the benefit of
fibrinolytic agents for treatment of a preformed thrombus in a
small (0.82–1.5 mm) vessel, low-dose streptokinase has been
shown to be clinically effective for a thrombus in the hand
if the drug is administered locally as a continuous infusion
within 36 h after the onset of symptoms.83 Anticoagulation
using intravenous heparin to prevent the propagation of
thromboemboli and permit early lysis of thrombotic arterial
occlusions should be instituted intraoperatively.84–86 The role
of low-molecular weight heparin in contrast to intravenous
heparin has not been addressed thus far. McClinton made the
following suggestions to increase the likelihood of success:
initiate the infusion as soon as possible, be alert to the effect of
systemic anticoagulation, and proceed with surgical explora­
tion if no lysis occurs after the initial 2-h high-dose treatment.
Steroids and iloprost (a prostacyclin analogue with potent
vasodilating and anti-aggregant properties) have anecdotal
results.84,86 The role of phosphodiesterase inhibitors such as
sildenafil has yet to be determined.
Biofeedback
Biofeedback training to develop central nervous system control
over peripheral autonomic functions involves instruction in
techniques that allow the conscious regulation of autonomic
body processes. This entails consciously increasing digital
blood flow or temperature.87
Biofeedback improves symptoms most effectively in
patients with Raynaud’s disease, vasospasm from non-neural
or non-vascular etiology, and Raynaud’s phenomenon with
adequate collateral circulation. However, it tends not to be
helpful in secondary vasospastic disease.
Thermal biofeedback is effective in primary vasospastic
disease increasing digital flow, raising digital temperatures, and
reducing cold-induced symptoms 2–3 years after treatment.15,25,88
Surgical treatment
Surgical intervention should be considered in patients who
are refractory to medical treatment. Surgical options include
reconstruction or bypass of occluded vessels by microvascular
reconstruction with or without vein grafts and/or modifica­
tion of sympathetic tone.49,89–91 Sympathetic tone may be
reduced by (1) proximal cervicothoracic sympathectomy, (2)
Leriche sympathectomy (resection and ligation of a throm­
bosed or occluded arterial segment), (3) peripheral periarterial
sympathectomy, and (4) new techniques in balloon angio­
plasty with periarterial sympathectomy.
Embolectomy
Emboli can be removed through a brachial arteriotomy and
passage of catheters both proximally and distally. Number 2
or 3 Fr Fogarty catheters can usually be threaded all the way
into the hand. If distal pulses do not return following restora­
tion of flow, completion angiography is mandatory.
In high-flow arteriovenous malformations when emboli
diminished the blood flow, initial attempts to preserve the
fistula and relieve the vascular steal were aimed at reducing

507
Treatment
technique may be ineffective because of the vasoconstrictive
effect on the smooth muscle by humoral factors, including
catecholamines encountered in ischemic conditions.
By directly removing the sympathetic nerve input from the
arteries, it is possible to block alternative sympathetic path­
ways or receptor upregulation. Flatt divided connections car­
rying sympathetic nerve fibers between the digital nerve and
digital artery by stripping a 3–4 mm long segment of adventi­
tia from the common digital artery; eight patients had variable
relief of their symptoms. Wilgis10,91 extended this surgical dis­
section to include a 2 cm segment of the common and proper
digital arteries and used preoperative anesthetic blockade to
predict which patients would benefit from the procedure. Both
Flatt and Wilgis noted symptomatic relief in patients with
primary vasospastic disease but did not achieve consistently
good results in patients with connective tissue diseases.
Jones101 introduced a more radical digital sympathectomy,
with an extended digital sympathectomy for patients with
connective tissue disease both to interrupt the sympathetic
fibers and to remove fibrous tissue that encircles and com­
presses the arteries. Both the radial and ulnar arteries at the
wrist are exposed and stripped over a 3 cm distance. The
incision for the ulnar artery is extended into the palm in an
inverted J-shaped fashion so that the entire ulnar artery and
superficial palmar arch can be stripped of adventitia and
sympathetic nerve fibers. The common and proper digital
arteries are stripped from their origin to the base of the fingers,
but not as far as the proximal interphalangeal joint, under the
operating microscope. If the thumb and index finger are
involved, the dorsal branch of the radial artery102 is stripped
from the anatomic snuffbox to the origin of the deep palmar
arch. The high incidence of ulnar artery occlusion has been
previously mentioned in connective tissue disorders. In such
patients, if there is sufficient distal arterial run-off, microsurgi­
cal bypass grafting from the proximal ulnar artery to the
superficial palmar arch or common digital arteries can be
performed.15,101,103 Koman et al.104 demonstrated that sympa­
thectomy can increase the percentage of nutritional blood
flow with resultant healing of ulcers and gangrene.
The authors suggest that two different sympathectomy
procedures should be considered depending on the severity
of the disease: In a limited digital sympathectomy, adventitia
is stripped from the radial and ulnar digital arteries and
common digital arteries (Video 22.1
). In an extended,
radical digital sympathectomy, adventitia is stripped from the
radial and ulnar arteries, the common digital arteries and the
proper digital arteries (Figs. 22.6 & 22.7).105 Long-term follow
up of peripheral sympathectomy was reported recently.106
Because of the myogenic nature of the spasm, treatment
may not just be directed towards the autonomic nervous
system. The principle of mechanical dilatation is based on the
observation of Bard,107 who noticed that a vessel in a state of
tonic contraction may respond by reflex dilatation when
mechanical dilatation is applied. Vessel constriction should
not be treated by physical dilatation until the nature of the
lesion has been determined, intimal damage with or without
thrombosis has been excluded, and if pharmacologic treat­
ment has been ineffective. A closed technique may be tried
initially in which heparinized saline solution is injected under
pressure between occluding vascular clamps. An arteriotomy
may be required and the vessel dilated with a small Fogarty
catheter.
Arterial reconstruction
For small partial arterial injuries, closure in a transverse direc­
tion prevents narrowing of the lumen. Even with significant
(up to 60%) arterial narrowing after transverse closure, flow
is not affected.108 A vein patch can be used to close a more
extensive partial injury.65,88 Sharp arterial transections can
often be repaired end-to-end if the vessel ends are mobilized
sufficiently. More extensive untidy arterial injuries commonly
require a reversed vein graft interposed between the proximal
and distal arterial ends. The cephalic, basilic, distal greater
saphenous, and distal lesser saphenous veins are used most
frequently. Some 10–30% more length of vein than is esti­
mated, is harvested and then the vein graft is reversed or the
valves incised. For axillary and brachial arterial injuries, the
greater saphenous vein is preferred.64,65 A local forearm vein
can be used for distal brachial, radial, and ulnar artery repairs
when the extremity has not sustained significant additional
soft-tissue trauma. If forearm trauma precludes use of a local
vein graft, leg or dorsal foot veins are used.64
Arterial reconstruction for symptomatic thrombosis or
occlusion can be managed by ligation alone, excision with
end-to-end repair, or excision and interposition grafting.
Surgical indications include (1) absence of an alternative arte­
rial inflow, (2) two or more levels of occlusion that compromise
potential collateral flow, (3) thrombosis extending beyond the
origins of the common digital vessels, and (4) incomplete
deep and superficial arches. The major indication for arterial
reconstruction is inadequate perfusion with a DBI of <0.7; if
an appropriate risk–benefit ratio exists, arterial reconstruction
should be performed.25
Surgical techniques include:
1. In situ and non-reversed vein grafts
2. Interposition reversed vein grafts
3. Interposition arterial grafts (Video 22.2
)
4. Arterialization of venous flow
5. Free omental transfer.
The goal of arterial reconstruction is to increase digital
blood flow and restore nutritional flow. Successful arterial
Clinical tips
Periarterial sympathectomy
1. A palmar incision along a skin crease will result in a less
prominent scar and less contracture postoperatively.
2. Two step incisions along the horizontal palmar crease are
sufficient to expose the common digital arteries.
3. The entire superficial palmar arch can be exposed through
a longitudinal palmar crease incision.
4. The vena comitantes may also be removed with the
periarterial adventitia, but it may result in postoperative
edema of the hand.
5. Periarterial sympathectomy is routinely performed on both
the radial and ulnar arteries at the wrist level and the
second, third, and fourth common digital arteries in primary
Raynaud’s disease. However, sympathectomy of the proper
digital arteries may also be necessary for “vibration white
finger” disease and systemic sclerosis.

508
SECTION III
CHAPTER 22 • Ischemia of the hand
Fig. 22.6  Limited digital sympathectomy: (A) Preoperative. (B) Operative view.
(C) Schematic drawing. (D) Postoperative view.
B
C
D
A

509
Treatment
Fig. 22.7  Radical digital sympathectomy: (A) Radical sympathectomy of
common and proper digital arteries in the palm and digits. (B) Schematic
drawing of radical digital sympathectomy.
B
A
reconstruction in patients with underlying collagen vascular
disease increases total digital blood flow and nutritional flow,
diminishes symptoms, and promotes healing of ulcers.109
Regardless of the etiology, the level and extent of occlu­
sion, the adequacy of collateral flow, and any component of
sympathetic overactivity obviously influence the results of
reconstruction for arterial thrombosis and occlusion.
Jones advocated that if by stringent clinical and angio­
graphic criteria, segmental thrombosis or occlusions are
identified in the distal radial and/or ulnar arteries and the
superficial palmar arch, and if adequate distal “run-off” can
be demonstrated in the common digital arteries, microsurgi­
cal revascularization should be considered in patients with
symptomatic hand ischemia unresponsive to medical man­
agement.5 Jones described four basic vein graft configurations
that have evolved for revascularization of the hand, and this
classification may be helpful in planning surgery.1
For short segmental occlusions or thrombosis of the ulnar
artery in Guyon’s canal, end-to-end anastomosis of a vein
graft or arterial graft from the ulnar artery in the distal forearm
to the distal ulnar artery just proximal to the superficial
palmar arch is classified as a type I configuration.
Occlusion of the distal radial artery is much rarer in com­
parison to ulnar artery occlusion. End-to-end anastomosis
of a vein graft or arterial graft from the distal radial artery
in the forearm to the deep palmar arch or princeps pollicis
artery in the thumb–index webspace is classified as a type II
configuration.
If the superficial palmar arch is involved but the common
digital arteries are spared, reconstruction of the superficial
palmar arch may become necessary with end-to-end anas­
tomosis of the vein or arterial graft to the ulnar artery in the
distal forearm and end-to-side anastomoses of the common
digital arteries to the interposition vein graft. This type III
configuration is commonly required in systemic disease
manifest by secondary Raynaud’s disease. In this situation, a
deep inferior epigastric arterial graft may be more useful than
a vein graft. The deep inferior epigastric artery has numerous

510
SECTION III
CHAPTER 22 • Ischemia of the hand
Early excision of true or false aneurysms of the radial or
ulnar arteries is strongly advocated to prevent distal emboli­
zation. An intraoperative Digital/Brachial Artery Index less
than 0.7 after aneurysm excision indicates the need for arterial
reconstruction.54 Postoperative care and surgical outcomes are
similar to those after reconstruction of ulnar artery thrombosis
(Fig. 22.9).
Mycotic aneurysms are secondary to hematogenous or
local bacterial infection that weakens the vessel wall and
virtually all are now due to intravenous drug abuse.73 Infec­
tion producing a soft-tissue swelling overlying an artery
should be evaluated for the possibility of a false aneurysm to
avoid an ill-advised incision and drainage procedure. If clini­
cal examination is not conclusive, duplex scanning should be
diagnostic. Excision and ligation of the artery are preferred if
the feeding vessel is not critical to limb survival, otherwise
excision and vein bypass around the infected area will restore
arterial inflow.
Balloon angioplasty for stenotic lesions
Ahn applied the technique of balloon angioplasty to treating
patients with secondary Raynaud’s syndrome who had an
arterial stenosis of their radial and ulnar arteries diagnosed
by arteriography.114 After adventitial stripping of the affected
radial and ulnar arteries, palmar arch, and common digital
arteries, vessel dilatation was performed using a percutane­
ous transluminal coronary angioplasty balloon catheter. The
balloon was inserted through a branch of the ulnar artery and
advanced from the main artery through Guyon’s canal, into
the palmar arch and common digital arteries. Sequential dila­
tation of any stenotic segment was performed by inflation of
the balloon to 6 atmospheres for 40 seconds.
Balloon catheter dilatation is a useful adjunct procedure
and may potentiate the effects of digital sympathectomy. The
technique can also be used for incomplete arterial occlusions
up to 15 cm in length and may eliminate the need for inter­
position vein grafts (Fig. 22.10).
branches that can be used to reconstruct a new palmar arch
with end-to-end anastomoses to the common digital arteries.
End-to-end anastomoses are easier to perform compared with
end-to-side anastomoses if an interposition vein graft is used
which may also cause turbulent flow.
There are other technical advantages to using an autolo­
gous deep inferior epigastric artery graft. The size match
between the inflow ulnar artery and the proximal epigastric
artery is excellent.110 The deep inferior epigastric artery tapers
as it gives off branches and the size of these distal branches
is a close match for anastomoses to the common digital arter­
ies (Fig. 22.8).
In a type IV configuration, two interposition vein grafts or
two deep inferior epigastric artery grafts are used to revascu­
larize the superficial palmar arch or common digital arteries
from the distal ulnar artery and the deep palmar arch or
princeps pollicis artery from the distal radial artery.111
In the Wake Forest classification of occlusive/vasospastic/
vaso-occlusive disease (Table 22.2), Koman et al. recom­
mended that arterial reconstruction is indicated in patients
with refractory symptoms and inadequate collateral circula­
tion (groups IIB and IIIB), and should be individualized in
groups IIA and IIIA.24
Aneurysms
Treatment options include: (1) resection and ligation112; (2)
excision of the damaged wall and “patch” grafting; (3) resec­
tion with end-to-end repair; and (4) resection with an inter­
position graft, depending on collateral flow and vasomotor
tone.113
Table 22.2  Wake Forest classification of occlusive/vasospastic/
vaso-occlusive disease
Group
Etiology
Comments
I
Raynaud’s disease
Idiopathic
II
Raynaud’s syndrome
Collagen vascular disease
  A
Adequate circulation
  B
Inadequate circulation
III
Secondary vasospasm/
occlusive disease
Vascular injury
  A
Adequate circulation
Occlusion/embolus
  B
Inadequate circulation
IV
Secondary vasospasm
Non-vascular injury
Nerve/bone/soft tissue
damage
(Reproduced with permission from Koman LA, Ruch DS, Smith BP, et al.
Vascular disorders. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s
operative hand surgery. New York: Churchill Livingstone; 1999:2254–2302.)
Clinical tips
Interposition vessel grafts
1. Volar wrist veins are very useful for interposition grafts for
the proper digital arteries.
2. The deep inferior epigastric artery (DIEA) is a good source
for superficial palmar arch and ulnar artery obstruction. The
vessel diameters of the DIEA are a good match for the
proximal ulnar artery and distal palmar arch. Branches of
the DIEA are also a good match for the common digital
arteries.
3. The cephalic vein is a useful donor vein for radial artery
obstruction. It can be harvested through the same incision.
The radial artery graft is placed superficial to the abductor
pollicis longus (APL), extensor pollicis brevis (EPB), and
extensor pollicis longus (EPL) tendons to prevent the
compression of the graft by these tendons.
4. Distal anastomoses into the digital arteries are very
challenging in the ischemic hand because of the obliterated
artery. The intima of the artery is markedly thickened in
secondary Raynaud’s syndrome.
5. Graft anastomoses should be performed into healthy
recipient vessels with good inflow and a normal appearing
intima.
6. The hand and wrist should be immobilized in a short arm
splint for at least 1 week.

511
Balloon angioplasty for stenotic lesions
D
A
B
C
Fig. 22.8  Arterial graft using deep inferior epigastric artery (DIEA). (A) Occluded
ulnar artery. (B) DIEA graft. (C) DIEA graft anastomosed between the ulnar artery
and palmar arch. (D) Schematic drawing of the ulnar artery to the superficial palmar
arch reconstruction.

512
SECTION III
CHAPTER 22 • Ischemia of the hand
over 20 cases, and showed significant improvement in pain
and ulceration after the procedure.116,117
The recipient vein is prepared by removing the valves at
the level of the metacarpal necks. The cephalic vein is well
suited for this procedure because it has great interconnections
with the dorsal venous system of the hand, which potentially
allows for a single proximal anastomosis. Arterial branches
are then ligated and the proximal end-to-side anastomosis is
performed. Postoperative thrombosis and swelling of the limb
may result.
A new blood supply can be supplied indirectly to the hand,
by a second technique. A free omental flap is harvested and
placed beneath the dorsal skin of the forearm and hand, and
the superior gastro-epiploic artery and vein anastomosed to
the brachial artery and cephalic vein at the elbow.116,117
Treatment algorithm
All patients with chronic ischemia of the hand should obvi­
ously be treated pharmacologically with topical nitroglyc­
erin, calcium channel blockers, vasodilators, and possibly
botulinum toxin.75 Patients with ischemic pain often follow
an intractable course and surgical intervention is frequently
Other surgical options
Surgeons have investigated alternative options to salvage
severely ischemic limbs when standard arterial bypass proce­
dures are not possible. Two salvage procedures for impending
digital loss are reversal of blood flow through the upper
extremity veins and vascularized omental transfer to the
dorsum of the hand.
King et al.115 reported arterialization of the venous system
of the upper limb based on in situ vein bypass. In situ vein
bypass is a standard vascular surgery technique that involves
complete exposure of the chosen vein and ligation of all its
branches. A small valvulotome is used to divide each half of
the bicuspid valves in the vein all the way to the metacarpal
heads distally. The vein is then anastomosed to a proximal
artery (usually end-to-end to the brachial artery), shunting
arterial blood through the vein into the hand. Patients are
heparinized after this procedure. Pederson has used the
concept of reverse venous flow to improve vascularity in
severe hand ischemia. He anastomosed the distal portion of
either the radial or ulnar artery to suitable hand veins, thereby
creating a reverse-flow situation in an attempt to improve
capillary perfusion. He reported his personal experience in
Fig. 22.9  Ulnar artery aneurysm treated by resection and interpositional vein graft.
(A) Aneurysm. (B) Resection. (C) Interpositional vein graft.
A
B
C

513
Postoperative care
In a patient with Raynaud’s phenomenon unresponsive to
pharmacological treatment, if angiography reveals no evi­
dence of occlusion of the main inflow radial and ulnar arteries
and satisfactory visualization of the three common digital
arteries, digital sympathectomy should be considered.101,106
If angiography reveals stenosis or occlusion of the radial or
ulnar arteries over a distance of <3 cm, balloon angioplasty
may be considered so that expansion of the vessel lumen may
increase digital blood flow. Balloon angioplasty can also be
combined with radical sympathectomy.
If angiography demonstrates segmental occlusions of the
main inflow radial and/or ulnar arteries but there is satisfac­
tory “run-off” in the common digital arteries, microsurgical
revascularization of the superficial palmar arch from the ulnar
artery and much less frequently microsurgical revasculariza­
tion of the deep palmar arch from the radial artery can be
considered.
Despite more complicated harvesting, a deep inferior epi­
gastric artery graft may allow end-to-end anastomoses of the
branches of the arterial graft to the common digital arteries,
whereas an interposition vein graft requires end-to-side
anastomoses. However, the more extensive the involvement
of the ulnar or radial arteries, the more likely that an interposi­
tion vein graft rather than an interposition arterial graft is
required.114
If the symptoms of chronic ischemia are localized to a
single finger and angiography reveals a discrete segment of
occlusion of a proper digital artery, resection of the segment
of proper digital artery and reconstruction with an interposi­
tion vein graft or arterial graft may occasionally be considered
(Fig. 22.11).118 Balloon angioplasty of a stenotic common
digital artery or proper digital artery is very difficult and may
result in vessel rupture.114
inevitable. Established gangrene, osteomyelitis, and septic
arthritis usually require a digital amputation. Amputations
are effective in relieving patients’ pain, for which they are
very grateful.
Arteriography, MR angiography or duplex ultrasound will
allow delineation of the exact site and extent of any stenosis
or complete occlusion, and assist in surgical planning. Indica­
tions for arteriography with the intent of surgical revascular­
ization include the following:
■ unilateral Raynaud’s phenomenon;
■ progressive digital ulceration or gangrene despite good
medical management;
■ recurrent digital ulceration; and
■ Doppler evidence of occlusion of a major artery.5
Specific indications for surgical intervention in patients with
chronic ischemia of the hand have been suggested.5,101 Options
for surgical intervention include digital sympathectomy,
balloon angioplasty, and microsurgical revascularization
using interposition vein grafts or arterial grafts. In some
patients these procedures can be combined.
Fig. 22.10  Balloon angioplasty. (A) Ballooning of stenotic ulnar artery.
(B) Ballooning of the palmar arch.
A
B
Clinical tips
Management strategy
1. Medication with calcium channel blockers is acceptable in
both primary Raynaud’s disease and secondary Raynaud’s
syndrome. However, patients with secondary Raynaud’s
syndrome usually need periarterial sympathectomy or
vascular reconstruction.
2. Balloon angioplasty is useful in selected cases of stenosis
and short occluded segments.
3. Arterial reconstruction with interposition grafts in Raynaud’s
syndrome may be performed earlier than before the
appearance of gangrene of the fingers.
4. Amputation of gangrenous fingertips should be
conservative to preserve the length and shape of fingers in
women. Small ulcers may heal spontaneously after
improvement in vascular inflow.
5. Ischemic pain usually improves after appropriate surgery to
increase blood flow.
Postoperative care
After microsurgical revascularization procedures, a single
bolus of heparan (1000–2400 IU, intravenous push) is
administered immediately before the microsurgical clamps

514
SECTION III
CHAPTER 22 • Ischemia of the hand
Fig. 22.11  Proper digital artery reconstruction with reverse vein graft.
(A) Preoperative. (B) Angiogram showing occlusion of the proper digital arteries to
the middle finger. (C) Occlusion of the ulnar digital artery. (D) Resection and
interposition vein graft. (E) Postoperative.
A
B
C
D
E

515
Future directions
renal vascular disease. Hartzell et al. reported that long-term
follow-up of 27 patients revealed that while digital sympa­
thectomy healed digital ulcers and decreased the number of
ulcers in vasospastic disease in autoimmune patients, the
efficacy was much lower in patients with vasospasm second­
ary to atherosclerosis. This might explain why the prognosis
is worse in patients with underlying diabetes. Patients with
chronic ischemia of their hands due to scleroderma show
improvement after digital sympathectomy and microsurgical
revascularization, but because of progression of the underly­
ing disease, there is a significant recurrence of digital ulcers
2 years after surgery.21 Therefore, these procedures should
be considered palliative rather than curative. Since digital
sympathectomy and microsurgical revascularization cannot
usually be repeated, recurrence of digital ulcerations may
ultimately require amputations. Jones101 has suggested that
the hand be considered an “end organ” just like the heart,
brain, and kidneys and therefore hand ischemia may reflect
similar pathology in these other organs.
Secondary procedures
Secondary procedures after digital sympathectomy or micro­
surgical revascularization are rare because of the postopera­
tive scarring from the original operation. Revision surgeries
at the same location are usually not advised. Digital amputa­
tion or even ray amputation would be a last option should the
ischemia progress.
Future directions
Occlusive/thrombotic disease of the inflow ulnar and radial
arteries to the hand will still be managed by excision of the
occluded or thrombosed segment and interposition vein or
arterial grafting. Technically proficient hand surgeons may
be inclined to utilize the same excision and grafting of an
occluded segment of the proper digital arteries in affected
fingers. However, the newer technique of balloon angioplasty
may eliminate the necessity for interposition vein or arterial
grafting within the fingers themselves.
Even though there are anecdotal reports of the successful
use of botulinum toxin and fat grafting for vasospastic condi­
tions causing ischemia of the hand, more rigorous randomized
trials will be necessary in the future. Finally, newer pharma­
cologic agents may be developed to treat Raynaud’s phenom­
enon, but digital sympathectomy may still be indicated for
those patients with increasing frequency and increasing sever­
ity of their Raynaud’s symptoms. The results of digital sym­
pathectomy in patients with connective tissue disorders will
only be palliative and dependent on the progression of the
underlying disease.
are removed and either heparin is maintained for 7 days, or
dextran 40 is administered intravenously at 25 cc/h for 5 days.
If there is extensive intimal damage or vascular compromise,
full heparinization and conversion to Coumadin is advisable.
A bulky hand and forearm dressing with a dorsal plaster
of Paris splint is applied with the hand in a functional posi­
tion. A drain is left in place for 12–36 h. Circulation to the
fingertips is assessed every hour for 6 h and then every 4 h
for 24 h. Critical arterial reconstructions are monitored in the
same way as replantations. Changes in color and capillary
refill; temperature monitoring (loss of >2°C in 1 h); pencil
Doppler monitoring or pulse oximetry can be used. If seda­
tion is required, chlorpromazine (25 mg orally three times
daily) is prescribed. The patient obviously discontinues
smoking and avoids caffeine consumption. The patient is
discharged home on aspirin 81 mg daily and continued for up
to 3 months.
Sutures are removed at 10–14 days postoperatively. The
hand is protected for 2–6 weeks in a lightweight splint and
the patient is instructed to avoid any trauma to the surgical
site. Some residual cold sensitivity, soreness, pillar-type palm
pain, and ulnar nerve irritability are expected. Return to work
is based on job type after 6–12 weeks, no athletic or work
restrictions are necessary if the patient is asymptomatic.
Outcomes, prognosis, and
complications
Complications after surgical intervention for ischemia of the
hand include impaired healing of the incision, dehiscence,
infection, stiffness of the fingers, and specifically after micro­
surgical revascularization, thrombosis of the anastomoses.
After digital sympathectomy, patients usually report
improvement in their symptoms of pain and cold tolerance,
reduction in the frequency and severity of Raynaud’s epi­
sodes, and healing of digital ulcers.101
Microsurgical revascularization increases distal arterial
perfusion, reduces symptoms of ischemic pain, promotes
healing of ulcers, and prevents progression to gangrene in
hands without adequate collateral circulation.101 Koman et al.
have demonstrated that this is due to an increase in the ratio
of nutritional to total flow without increasing total microvas­
cular perfusion within digits.104 Patency rates of 80–90% can
be expected of interposition vein grafts for hypothenar
hammer syndrome, but thrombosis of the grafts can occur and
symptoms return in longer follow-up. Of 106 interposition
vein graft reconstructions of the ulnar artery, 87 (82%)
remained patent.40,99,119–122
The prognosis for patients with chronic ischemia of their
hands depends on the etiology, the severity, the response to
treatment, and progression of the underlying condition.101,123
Prognosis seems to be worse in patients with diabetes and

516
SECTION III
CHAPTER 22 • Ischemia of the hand
3. Jones NF, Emerson ET. Interposition vein graft configurations for
microsurgical revascularization of the ischemic hand. Tech Hand
Up Extrem Surg. 1999;3:121–130. Despite the various causes of upper
extremity ischemia, the presenting symptoms are usually predictable.
These symptoms constitute acute ischemia, digital ulcers, and gangrene,
Raynaud’s phenomena, or claudication with exercise. For segmental
arterial occlusive diseases in selected patients, microsurgical
revascularization with bypass vein grafts may be effective. This study
reviews such cases that are bypassable with vein grafts, and proposes a
classification system for distal upper extremity bypass vein grafts.
7. Jones NF. Acute and chronic ischemia of the hand:
pathophysiology, treatment, and prognosis. J Hand Surg Am.
1991;16:1074–1083. Fifty patients with acute and chronic ischemia of the
hand were investigated using various methods over 4 years. For many
causes of the ischemia, medical management with emergent intra-arterial
streptokinase, heparin, or dextran was used, along with nifedipine and
pentoxifylline in chronic cases. Surgical treatment such as stellate
ganglion blocks, microsurgical revascularization, and digital
sympathectomy was used. Eighteen patients underwent amputation due
to end-stage gangrene, and long-term follow-up revealed 20% incidence
of recurrent digital ulcerations.
12. Wilgis EF. Evaluation and treatment of chronic digital ischemia.
Ann Surg. 1981;193:693–698. Forty-two patients were evaluated and
treated for chronic digital ischemia. Manifestations of pain, severe cold
intolerance and occasional tip ulceration were seen despite conservative
treatment of vasodilators, tobacco abstinence, and beta-blockers. Direct
microvascular reconstruction, thermal biofeedback, and digital
sympathectomy were performed with improvement in 70% of patients.
21. Jones NF, Imbriglia JE, Steen VD, et al. Surgery for scleroderma of
the hand. J Hand Surg Am. 1987;12:391–400. Out of 813 consecutive
patients with scleroderma, 31 underwent one or more surgical
procedures. Raynaud’s phenomenon and digital tip ulcerations were
controlled with vasodilators and meticulous local wound care. Frank
gangrene was usually managed conservatively until autoamputation, but
23 digital amputations had to be performed. Digital sympathectomy and
micro-revascularization were performed in selected patients. Arthrodesis
was performed in patients with severe digital contractures.
25. Fazan VP, Borges CT, Da Silva JH, et al. Superficial palmar arch:
an arterial diameter study. J Anat. 2004;204:307–311. Symptomatic
vascular disorders of the upper extremity interfere with health-related
quality of life, diminish function, and have a negative impact on patients
and society. Although less prevalent than ischemic lesions of the lower
extremity, heart, or brain, upper extremity vascular morbidity is a
significant social burden. Aberrant microvascular flow secondary to acute
or chronic trauma, congenital deformity, systemic processes, or genetic
influences affect over 10% of the general population and 20–30% of
premenopausal women. Pain, cold intolerance, numbness, ulceration, or
gangrene can result from these vascular insufficiencies or incompetencies.
Abnormal perfusion may occur secondary to congenital or acquired
events that affect vascular structures, vascular function, or both.
Vascular insufficiency occurs due to blood flow compromise with
decreased cellular perfusion and resultant cell damage, cellular injury,
and pain. Various approaches to diagnosis and management of vascular
disorders based on physiologic factors are covered.
60. Kim YH, Ng SW, Seo HS, et al. Classification of Raynaud’s disease
based on angiographic features. J Plast Reconstr Aesthet Surg.
2011;64:1503–1511. We analyzed the angiographic features of the arterial
supply of the hand at three levels: (1) radial or ulnar, (2) palmar arch
and common digital, and (3) digital vessels. Subsequent surgical
interventions were tailored according to disease types, and these included
combinations of: digital sympathectomy, balloon angioplasty, and
end-to-end interposition venous or arterial grafting. We classified
Raynaud’s disease into six types: type I and II involve the radial or ulnar
arteries. Type I (27.3%) showed complete occlusion, while type II
(26.2%) involved partial occlusion. Type IIIa (27.1%) showed tortuous,
narrowed or stenosed common digital and digital vessels. Type IIIb
(1.4%) is a subset which involved the digital vessel of the index finger
related to exposure to prolonged vibration. Type IV and V showed global
involvement from the main to digital vessels. Type IV (13.7%) showed
diffused tortuosity, narrowing, and stenosis. Type V (4.3%) is the most
severe, with paucity of vessels and very scant flow. Nearly half (47%) of
the patients had associated systemic disease. This new classification
provides objective and valuable information for decision-making
regarding choice of surgical procedures for the treatment of patients with
Raynaud’s disease that had failed conservative therapy.
79. Neumeister MW. Botulinum toxin type A in the treatment of
Raynaud’s phenomenon. J Hand Surg Am. 2010;35:2085–2092.
Raynaud’s patients were injected with 50 to 100 units of
onabotulinumtoxin A to improve perfusion of the digits. An institutional
review board-approved retrospective review was undertaken to analyze
outcomes. Laser Doppler scans were performed before and after injection
to quantitatively measure perfusion. A total of 14 men and 19 women
with Raynaud’s phenomenon were injected with onabotulinumtoxin.
Botulinum toxin appears to improve perfusion of the hand after direct
injection around the neurovascular bundles. Further investigations are
warranted to identify the exact mode of action in relieving vasospasm
and alleviating pain.
90. Flatt AE. Digital artery sympathectomy. J Hand Surg Am.
1980;5:550–556.
91. Wilgis EF. Digital sympathectomy for vascular insufficiency. Hand
Clin. 1985;1:361–367.
101. Jones NF. Ischemia of the hand in systemic disease. The potential
role of microsurgical revascularization and digital sympathectomy.
Clin Plast Surg. 1989;16:547–556.
103. Jones NF, Raynor SC, Medsger TA. Microsurgical revascularisation
of the hand in scleroderma. Br J Plast Surg. 1987;40:264–269.
104. Koman LA, Smith BP, Pollock FE Jr, et al. The microcirculatory
effects of peripheral sympathectomy. J Hand Surg Am.
1995;20:709–717.
106. Murata K, Omokawa S, Kobata Y, et al. Long-term follow-up of
peripheral sympathectomy for chronic digital ischemia. J Hand
Surg Eur Vol. 2012;37:788–793. This study investigates long-term
clinical results (>10 years) of periarterial sympathectomy in chronic
ischemic digits compared with intermediate-term results (3 years).
Periarterial sympathectomy via the palm and volar wrist was carried out
on 11 hands of seven patients with digital ischemia but no gangrene or
severe ulceration. The periarterial sympathectomy via the palm and wrist
could prevent long-term aggravation of symptoms of chronic digital
ischemia when combined with adequate postoperative drug therapy.
109. Savvidou C, Tsai TM. Long-term results of arterial sympathectomy
and artery reconstruction with vein bypass technique as a salvage
procedure for severe digital ischemia. Ann Plast Surg. 2013;70:168–
171. The aim of this study is to present a combined treatment of arterial
sympathectomy and artery reconstruction with vein bypass technique in
patients with severe digital ischemia. In all, 22 patients representing 53
digits received treatment during a 15-year period. Skin color and trophic
changes including ulcers, necrosis, and amputation; pain level according
to the visual analog scale; and functional assessment based on the
disabilities of the arm, shoulder, and hand questionnaire were recorded.
Based on the results of this study, vascular reconstruction combined with
sympathectomy may be indicated on an individualized basis for patients
with digital ischemia. This procedure can lead to healing of skin trophic
changes, diminution of pain, avoidance of amputation, and long-term
improvement in life quality.
111. Masden DL, Seruya M, Higgins JP. A systematic review of the
outcomes of distal upper extremity bypass surgery with arterial
and venous conduits. J Hand Surg Am. 2012;37:2362–2367. The aim
of the authors was to conduct a systematic review of literature evaluating
efficacy of venous and arterial grafts for distal upper extremity bypass
surgery. Manual review produced 42 studies based on inclusion criteria
of reported distal upper extremity bypass surgery, complete information
on graft type used, examined patency of reconstruction, and described
method for determining patency. In 145 patients, 152 grafts were
performed for upper extremity revascularization, including 120 grafts for
revascularization of distal ulnar artery circulation, 31 for distal radial
artery circulation, and one for both distal ulnar and radial artery
occlusions. Overall patency rate was 87% at an average follow-up of
34 months. This review showed a high patency rate and clinical efficacy
of distal upper extremity bypass surgery with a mean follow-up of almost
3 years. There may be a benefit of using arterial versus venous conduits,
although further examination is needed given the small number of
arterial reconstructions reported.
123. Hartzell TL, Makhni EC, Sampson C. Long-term results of
periarterial sympathectomy. J Hand Surg Am. 2009;34:1454–1460.
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516.e1
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extremity ischemia, the presenting symptoms are usually predictable.
These symptoms constitute acute ischemia, digital ulcers, and gangrene,
Raynaud’s phenomena, or claudication with exercise. For segmental
arterial occlusive diseases in selected patients, microsurgical
revascularization with bypass vein grafts may be effective. This study
reviews such cases that are bypassable with vein grafts, and proposes a
classification system for distal upper extremity bypass vein grafts.
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hand were investigated using various methods over 4 years. For many
causes of the ischemia, medical management with emergent intra-arterial
streptokinase, heparin, or dextran was used, along with nifedipine and
pentoxifylline in chronic cases. Surgical treatment such as stellate
ganglion blocks, microsurgical revascularization, and digital
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intolerance and occasional tip ulceration were seen despite conservative
treatment of vasodilators, tobacco abstinence, and beta-blockers. Direct
microvascular reconstruction, thermal biofeedback, and digital
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25. Fazan VP, Borges CT, Da Silva JH, et al. Superficial palmar arch:
an arterial diameter study. J Anat. 2004;204:307–311. Symptomatic
vascular disorders of the upper extremity interfere with health-related
quality of life, diminish function, and have a negative impact on patients
and society. Although less prevalent than ischemic lesions of the lower
extremity, heart, or brain, upper extremity vascular morbidity is a
significant social burden. Aberrant microvascular flow secondary
to acute or chronic trauma, congenital deformity, systemic processes,
or genetic influences affect over 10% of the general population and
20–30% of premenopausal women. Pain, cold intolerance, numbness,
ulceration, or gangrene can result from these vascular insufficiencies
or incompetencies. Abnormal perfusion may occur secondary to
congenital or acquired events that affect vascular structures, vascular
function, or both. Vascular insufficiency occurs due to blood flow
compromise with decreased cellular perfusion and resultant cell
damage, cellular injury, and pain. Various approaches to diagnosis and
management of vascular disorders based on physiologic factors are
covered.
26. Ger R, Abrahams P, Olson TR. Essentials of Clinical Anatomy. 2nd
ed. New York, NY: Parthenon; 1996.
27. Clemete CD. Anatomy. A Regional Atlas of the Human Body. 4th ed.
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28. Agur AMR. Grant’s Atlas of Anatomy. 9th ed. Baltimore, MD:
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29. Al-Turk M, Metcalf WK. A study of the superficial palmar arteries
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30. Karlsson S, Niechajev IA. Arterial anatomy of the upper extremity.
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31. Ikeda A, Ugawa A, Kazihara Y, et al. Arterial patterns in the hand
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J Hand Surg Am. 1988;13:501–509.
32. Nystrom NA, Fedele G, Zoldos J. Intrinsic vascular anatomy of the
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33. Edwards EA. Organization of the small arteries of the hand and
digits. Am J Surg. 1960;99:837–846.
34. Strauch B, de Moura W. Arterial system of the fingers. J Hand Surg
Am. 1990;15(1):148–154.
35. Clemete CD. Functional Anatomy of the Circulation to the Lower
Extremities. The Circulation to the Skin. Chicago, IL: Year Book
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36. Rich NM, Baugh JH, Hughes CW. Acute arterial injuries in
Vietnam: 1,000 cases. J Trauma. 1970;10:359–369.
37. Faber JE, Meininger GA. Selective interaction of alpha-
adrenoceptors with myogenic regulation of microvascular smooth
muscle. Am J Physiol. 1990;259:H1126–H1133.
38. Cooke JP. Endothelium-derived factors and peripheral vascular
disease. Cardiovasc Clin. 1992;22:3–17.
39. Marie I, Herve F, Primard E, et al. Long-term follow-up of
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40. Koman LA, Urbaniak JR. Ulnar artery insufficiency: a guide to
treatment. J Hand Surg Am. 1981;6:16–24.

516.e2
SECTION III
CHAPTER 22 • Ischemia of the hand
41. Pineda CJ, Weisman MH, Bookstein JJ, et al. Hypothenar hammer
syndrome. Form of reversible Raynaud’s phenomenon. Am J Med.
1985;79:561–570.
42. Sharma R, Ladd W, Chaisson G, et al. Images in cardiovascular
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43. Ekenvall L, Lindblad LE, Carlsson A, et al. Afferent and efferent
nerve injury in vibration white fingers. J Auton Nerv Syst.
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44. Ziegler S, Zoch C, Gschwandtner M, et al. Thermoregulation and
rheological properties of blood in primary Raynaud’s phenomenon
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Environ Health. 2005;78:218–222.
45. Babu SC, Piccorelli GO, Shah PM, et al. Incidence and results of
arterial complications among 16,350 patients undergoing cardiac
catheterization. J Vasc Surg. 1989;10:113–116.
46. Schanzer H, Schwartz M, Harrington E, et al. Treatment of
ischemia due to “steal” by arteriovenous fistula with distal artery
ligation and revascularization. J Vasc Surg. 1988;7:770–773.
47. Odland MD, Kelly PH, Ney AL, et al. Management of
dialysis-associated steal syndrome complicating upper
extremity arteriovenous fistulas: use of intraoperative digital
photoplethysmography. Surgery. 1991;110:664–669;
discussion 9–70.
48. McCabe SJ, Mizgala C, Glickman L. The measurement of cold
sensitivity of the hand. J Hand Surg Am. 1991;16:1037–1040.
49. Troum SJ, Smith TL, Koman LA, et al. Management of vasospastic
disorders of the hand. Clin Plast Surg. 1997;24:121–132.
50. Sumner DS. Evaluation of acute and chronic ischemia of the upper
extremity. In: Rutherford RB, ed. Vascular Surgery. 4th ed.
Philadelphia, PA: WB Saunders; 1995:918–935.
51. Allen EV. Thromboangiitis obliterans: methods of diagnosis of
chronic occlusive arterial lesions distal to the wrist with
illustrative cases. Am J Med Sci. 1929;178:237–244.
52. Ruch DS, Aldridge M, Holden M, et al. Arterial reconstruction for
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53. Bouhoutsos J, Morris T, Martin P. Unilateral Raynaud’s
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54. Zimmerman NB. Occlusive vascular disorders of the upper
extremity. Hand Clin. 1993;9:139–150.
55. Schmidt WA, Wernicke D, Kiefer E, et al. Colour duplex
sonography of finger arteries in vasculitis and in systemic
sclerosis. Ann Rheum Dis. 2006;65:265–267.
56. Balas P, Katsogiannis A, Katsiotis P, et al. Comparative study of
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57. Koman LA, Nunley JA, Goldner JL, et al. Isolated cold stress
testing in the assessment of symptoms in the upper extremity:
preliminary communication. J Hand Surg Am. 1984;9:305–313.
58. Arneklo-Nobin B, Albrechtsson U, Eklof B, et al. Indications for
angiography and its optimal performance in patients with
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59. Vaughan RS, Lawrie BW, Sykes PJ. Use of intravenous regional
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60. Kim YH, Ng SW, Seo HS, et al. Classification of Raynaud’s disease
based on angiographic features. J Plast Reconstr Aesthet Surg.
2011;64:1503–1511. We analyzed the angiographic features of the
arterial supply of the hand at three levels: (1) radial or ulnar, (2) palmar
arch and common digital, and (3) digital vessels. Subsequent surgical
interventions were tailored according to disease types, and these
included combinations of: digital sympathectomy, balloon angioplasty,
and end-to-end interposition venous or arterial grafting. We classified
Raynaud’s disease into six types: type I and II involve the radial
or ulnar arteries. Type I (27.3%) showed complete occlusion, while
type II (26.2%) involved partial occlusion. Type IIIa (27.1%) showed
tortuous, narrowed or stenosed common digital and digital vessels.
Type IIIb (1.4%) is a subset which involved the digital vessel of the
index finger related to exposure to prolonged vibration. Type IV and
V showed global involvement from the main to digital vessels. Type IV
(13.7%) showed diffused tortuosity, narrowing, and stenosis. Type V
(4.3%) is the most severe, with paucity of vessels and very scant flow.
Nearly half (47%) of the patients had associated systemic disease. This
new classification provides objective and valuable information for
decision-making regarding choice of surgical procedures for the
treatment of patients with Raynaud’s disease that had failed conservative
therapy.
61. Winterer JT, Ghanem N, Roth M, et al. Diagnosis of the
hypothenar hammer syndrome by high-resolution contrast-
enhanced MR angiography. Eur Radiol. 2002;12:2457–2462.
62. Fitridge RA, Raptis S, Miller JH, et al. Upper extremity arterial
injuries: experience at the Royal Adelaide Hospital, 1969 to 1991.
J Vasc Surg. 1994;20:941–946.
63. Raskin KB. Acute vascular injuries of the upper extremity. Hand
Clin. 1993;9:115–130.
64. Hess AV. Treatment of vascular injuries from penetrating and
nonpenetrating trauma. Hand Clin. 1999;15:249–259, viii.
65. Thal ER, Snyder WH, Perry MO. Vascular injuries of the
extremities. In: Rutherford RB, ed. Vascular Surgery. 4th ed.
Philadelphia, PA: WB Saunders; 1995:713–735.
66. Maiman MH, Bookstein JJ, Bernstein EF. Digital ischemia:
angiographic differentiation of embolism from primary arterial
disease. AJR Am J Roentgenol. 1981;137:1183–1187.
67. Silverman SH, Turner WW Jr. Intraarterial drug abuse: new
treatment options. J Vasc Surg. 1991;14:111–116.
68. Rich NM, Hobson RW 2nd, Collins GJ Jr. Traumatic arteriovenous
fistulas and false aneurysms: a review of 558 lesions. Surgery.
1975;78:817–828.
69. Redfern AB, Zimmerman NB. Neurologic and ischemic
complications of upper extremity vascular access for dialysis.
J Hand Surg Am. 1995;20:199–204.
70. Bussell JA, Abbott JA, Lim RC. A radial steal syndrome with
arteriovenous fistula for hemodialysis. Studies in seven patients.
Ann Intern Med. 1971;75:387–394.
71. Shemesh D, Mabjeesh NJ, Abramowitz HB. Management of
dialysis access-associated steal syndrome: use of intraoperative
duplex ultrasound scanning for optimal flow reduction. J Vasc
Surg. 1999;30:193–195.
72. Hammond DC, Matloub HS, Yousif NJ, et al. The corkscrew sign
in hypothenar hammer syndrome. J Hand Surg [Br].
1993;18:767–769.
73. McClinton MA. Tumors and aneurysms of the upper extremity.
Hand Clin. 1993;9:151–169.
74. Shionoya S. Buerger’s disease (thromboangiitis obliterans). In:
Rutherford RB, ed. Vascular Surgery. 4th ed. Philadelphia, PA: WB
Saunders; 1995:235–245.
75. Van Beek AL, Lim PK, Gear AJ, et al. Management of vasospastic
disorders with botulinum toxin A. Plast Reconstr Surg.
2007;119:217–226.
76. Cardelli MB, Kleinsmith DM. Raynaud’s phenomenon and
disease. Med Clin North Am. 1989;73:1127–1141.
77. Czop C, Smith TL, Rauck R, et al. The pharmacologic approach to
the painful hand. Hand Clin. 1996;12:633–642.
78. Arquilla B, Gupta R, Gernshiemer J, et al. Acute arterial spasm in
an extremity caused by inadvertent intra-arterial injection
successfully treated in the emergency department. J Emerg Med.
2000;19:139–143.
79. Neumeister MW. Botulinum toxin type A in the treatment of
Raynaud’s phenomenon. J Hand Surg Am. 2010;35:2085–2092.
Raynaud’s patients were injected with 50 to 100 units of
onabotulinumtoxin A to improve perfusion of the digits. An institutional
review board-approved retrospective review was undertaken to analyze
outcomes. Laser Doppler scans were performed before and after injection
to quantitatively measure perfusion. A total of 14 men and 19 women
with Raynaud’s phenomenon were injected with onabotulinumtoxin.
Botulinum toxin appears to improve perfusion of the hand after direct
injection around the neurovascular bundles. Further investigations are

516.e3
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SECTION III • Acquired Non-traumatic Disorders
23 
Neuropathic pain in the upper extremity
Catherine Curtin
SYNOPSIS
■ Pain is a common issue for those who care for people with disorders
of the upper limb, ranging from mild musculoskeletal pain to complex
regional pain syndrome.
■ Neuropathic pain is often the cause of persistent surgical pain.
■ Neuropathic pain is defined by the International Association for the
Study of Pain (IASP) as pain caused by a lesion or disease of the
somatosensory nervous system.
Introduction
Pain is a common issue for those who care for people with
disorders of the upper limb, ranging from mild musculoskel­
etal pain to complex regional pain syndrome.1 There is the
“healthy pain” that protects the injured limb while the tissue
heals. Then there is the persistent pain after surgery or trauma
that continues long after the tissue has healed. This persistent
pain becomes a pathologic process and is most commonly
neuropathic in origin. Post-traumatic and post-surgical neu­
ropathic pain will be the focus of this chapter.2
Neuropathic pain is defined by the International Asso­
ciation for the Study of Pain (IASP) as “pain caused by a
lesion or disease of the somatosensory nervous system.”3
Neuropathic pain is seen in many clinical settings such as
nerve compression and nerve injury. Perhaps the most
frustrating presentation of neuropathic pain is the pain
that occurs after a technically perfect surgery. Every
surgeon wants better outcomes. Early recognition and treat­
ment of neuropathic pain will improve outcomes in these
challenging cases.
Pain and surgery have always been intertwined. From
before the advent of anesthesia, surgeons strove to increase
their speed to reduce their patients’ suffering. Dr. Mitchell
described neuropathic pain in a book explaining his expe­
rience with nerve injuries treated during the Civil War.4
Throughout the treatise, he noted intense pain associated
with these nerve injuries and uses the term causalgia to
explain this “burning pain”. Surgeons have continued to try
and improve the treatment of nerve pain. We have changed
techniques, medications, and added other treatments. The
knowledge of neuropathic pain and its mechanisms has
greatly expanded since Dr. Mitchell’s time, but to this day,
neuropathic pain remains a challenging problem. This chapter
will provide the reader with information on the diagnosis
and treatments available for the common complaint of
neuropathic pain.
Terminology
Before progressing too far into this topic, it is first important
to understand some basic definitions of terminology used
within the pain field. Below are the IASP definitions for
common pain vocabulary.
1. Allodynia: pain due to a stimulus that does not
normally provoke pain. Example: “It hurts when the
wind blows on my arm.”
2. Dysesthesia: an unpleasant abnormal sensation.
Example: “My arm feels like it is rubbed raw by sand
paper when my shirt touches it.”
3. Hyperalgesia: increased pain from a stimulus that
normally provokes pain. Example: “Even a small bump
feels like a sledge hammer hit me.”
Another term to be clarified is complex regional pain syn­
drome (CRPS). CRPS represents a severe subset of patients
who have neuropathic pain as well as other symptoms
impacting the skin and tissues of the injured area. This term
CRPS is often used inappropriately, resulting in confusion and
fear associated with the diagnosis of CRPS. This confusion is
likely due to two factors. First is that the terminology for
CRPS has changed with increased understanding of the
pathophysiology. Mitchell first named it “causalgia”, where
he described patients with nerve injuries, burning pain, glossy
skin, and changes in hair and nails. In 1946, this process was

518
SECTION III
CHAPTER 23 • Neuropathic pain in the upper extremity
Epidemiology
There are several anatomic reasons that the limbs are at par­
ticular risk for the development of neuropathic pain. Chronic
pain after extremity injury occurs in up to 79% of patients
having surgery for traumatic injury to the feet and hands.11–12
First, the upper limb is richly innervated, putting more nerves
at risk of injury after trauma. Second, the nerves of the upper
limb travel long distances crossing multiple joints with wide
arcs of motion, so the nerves need to glide. Thus, trauma and
scarring can tether a nerve resulting in repeated traction of
the nerve. Finally, there are several tight areas along the course
of the nerves, so an injured swollen nerve is at risk for second­
ary entrapments. All these anatomic characteristics of the
renamed reflex sympathetic dystrophy.5 But as all cases did
not seem to be sympathetically mediated, so a group of pain
researchers again changed the taxonomy to complex regional
pain syndrome in 1995.6 CRPS has been subdivided this into
two groups – type 1 (no known nerve injury) and type 2
(known nerve injury). There remains controversy whether
this subdivision of CRPS is useful, as some believe all CRPS
is mediated by some type of nerve injury, whether it can be
identified or not.7
The second issue with CRPS is that there is no test to
confirm the diagnosis; CRPS is a diagnosis based on history
and physical exam. All patients with CRPS must have pain
disproportionate to the trauma. The patients must also have
a constellation of other sudomotor symptoms to receive a
diagnosis of CRPS. What symptoms make a diagnosis of
CRPS has been debated in the pain field, further adding to the
confusion.8 Table 23.19 presents the list of physical exam find­
ings required for a diagnosis for CRPS based upon a consensus
meeting of pain researchers in Budapest. Fig. 23.1A,B shows
two hands with typical physical exam findings seen in the
setting of CRPS. One thing about CPRS is clear: this complica­
tion has a great negative impact on the patient’s quality of
life.10
Table 23.1  Diagnostic criteria for complex regional pain
syndrome (CRPS)
Must report at least one
symptom in three of the
following categories:
Must display at least one
sign* at time of evaluation
in at least two of the
following categories:
1. Sensory: Reports of
hyperalgesia and/or
allodynia
1. Sensory: Evidence of
hyperalgesia (to pinprick)
and/or allodynia (to light
touch and/or deep somatic
pressure and/or joint
movement)
2. Vasomotor: Reports of
temperature asymmetry and/
or skin color changes and/or
skin asymmetry
2. Vasomotor: Evidence of
temperature asymmetry and/
or skin color changes and/or
asymmetry
3. Sudomotor/edema: Reports
of edema and/or sweating
changes and/or sweating
asymmetry
3. Sudomotor/edema:
Evidence of edema and/or
sweating changes and/or
sweating asymmetry
4. Motor/trophic: Reports of
decreased range of motion
and/or motor dysfunction
(weakness, tremor, dystonia)
and/or trophic changes (hair,
nail, skin)
4. Motor/trophic: Evidence of
decreased range of motion
and/or motor dysfunction
(weakness, tremor, dystonia)
and/or trophic changes (hair,
nail, skin)
*A sign is counted only if it is observed at time of diagnosis.
(Reproduced with permission from Harden RN, Oaklander AL, Burton AW, et al.
Complex regional pain syndrome: practical diagnostic and treatment guidelines.
Pain Med. 2013;14:180–229.)
Fig. 23.1  (A) Hand in patient with complex regional pain syndrome (CRPS): note
the shiny skin and edema. (B) Hand in CRPS: note the subtle color changes.
A
B

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Diagnosis
Psychological factors
There are many studies looking to associate pre-existing
psychological conditions with the development of neuropathic
pain. These studies often have significant limitations and
results have been mixed. The overall theory is that patients
with increased psychological distress have higher concentra­
tions of circulating catecholamines, which makes them more
sensitized to pain. Two psychological factors commonly dis­
cussed in relation to development of pain after trauma/
surgery are depression and pain catastrophizing.
Depression
Depression has long been thought to be associated with pain,
and studies have shown correlations between depression and
pain after surgery.27,28 However, for much of the literature, it
is difficult to assess the directionality of this relationship –
does the depression cause the pain or is the pain causing the
depression? The literature is mixed on this question, but a
pooling of the available data found enough evidence to
support depression as a risk factor for chronic post-surgical
pain. 29 There are short forms to assess for depression in the
clinic. One example is the Patient Health Questionnaire
(PHQ-9), which has only nine questions.30
Pain catastrophizing (PC)
There is increasing evidence that PC may be one of the most
important psychological factors associated with prolonged
pain after surgery. PC is a cognitive style in which patients
have a “set of exaggerated and ruminating negative cogni­
tions and emotions during actual or perceived painful stimu­
lation.”31 These patients feel helpless and say things like “this
is the worst pain in the world.” The Pain Catastrophizing
Scale has 13 questions and was developed to capture the PC
traits.32 PC has been found to be associated with poorer out­
comes after distal radius fracture.33 PC has been shown in
meta-analysis to be one of the strongest predictors of pro­
longed pain after knee arthroplasty.34 PC can be addressed
with cognitive–behavioral therapy and there is increased
interest in this psychological trait as a potential target for
“pre-habilitation” before surgery.
Immobilization
Immobilization is often required to protect healing tissue.
However, immobilization is not a benign intervention, and
there is increasing evidence that immobilization can contrib­
ute to neuropathic pain.35 It makes intuitive sense that immo­
bilization, which prevents nerve gliding in an inflamed tissue
bed, is not ideal. A study putting healthy volunteers in a cast
for a month found that the subjects developed some of the
changes associated with CRPS.36 Another study also found
that those immobilized after surgery had increased inflamma­
tory factors as well as trophic factors similar to CRPS.37
Diagnosis
Localizing the pain generator can be challenging to providers,
as the patient’s perception of neuropathic pain often is not
dermatomal. It is difficult to target interventions when the
upper limb mean that injury can result in irritated painful
nerves.13
Surgical trauma can be the inciting factor for chronic pain.
The literature has noted that persistent pain occurs in 20–50%
of surgical patients.14 Carpal tunnel has a 20% rate of persis­
tent pain. The most common complication after trigger finger
release and distal radius fractures is pain.15–16 The mechanism
of post-surgical chronic pain is thought to be persistent firing
of nerves injured at the time of surgery.2 Every surgical inci­
sion cuts cutaneous nerves and for a subset of patients this
injury results in chronic pain. The mystery is: Why do many
patients develop peri-incisional numbness after surgery but a
subset of patients develops neuropathic pain? Later in the
chapter we will discuss risk factors associated with persistent
post-surgical pain.
Although neuropathic pain is not uncommon after surgery,
the incidence of post-surgical CRPS is fortunately rare. Post-
surgical CRPS is a devastating complication, preventing
return of function and often causing prolonged disability. A
few upper limb surgeries are particularly at risk for CRPS.
CRPS after distal radius fracture care is well described, occur­
ring in 1–30% of patients17–19 CRPS has also been described
after palmar fasciectomy with rates reported as high as 17%.20
Occasionally the patient with the seemingly smallest of
traumas will develop CRPS.
Early recognition and treatment of the patient with CRPS
is critical, as anecdotal evidence suggests that early interven­
tion improves outcomes.
Risk factors
Much effort has been devoted assessing the risk factors associ­
ated with developing neuropathic pain, with the goal of
identifying those at risk prior to surgery. Pain is clearly a
complex multifactorial process but some patient characteris­
tics have repeatedly been associated with post-surgical pain
development. In 2017, there is no definitive risk assessment
for postoperative pain. Listed below are some of the factors
that have data suggesting an association with pain after
surgery.
Gender
The available evidence clearly shows that women and
men have different pain experiences. Women are more at
risk for developing chronic pain and CRPS.21 An overall
epidemiologic study found CRPS incidence 4 : 1 women
to men.22 Jellead looked prospectively at distal radius
fractures treated with a cast and found 32% developed
CRPS and that women had a 5.77 greater odds of being
in the CRPS group.17 Sennwald found that 40% of women
who had Dupuytren’s release developed CRPS.20 Overall,
the data suggests women are at higher risk for pathologic
pain processes and that surgeons should be aware of this
heightened risk.23–24
High preoperative pain
Multiple studies have found that the patients with high
preoperative pain values are more at risk of severe acute
postoperative pain, which puts them at risk for chronic
pain.21,25–26

520
SECTION III
CHAPTER 23 • Neuropathic pain in the upper extremity
Fig. 23.2  Woman with complex regional pain syndrome (CRPS): note the posture
with which she holds her arm.
Fig. 23.3  Patient with a scar neuroma: note the tethered area was site of maximal
tenderness.
Clinical diagnostics
Specific tests in the physical examination
Motor examination  If the patient can tolerate it, a focused
motor examination can provide useful information. Nerve
entrapment can result in subtle changes in strength. The
maneuvers proposed by Hagert are useful for assessing nerve
entrapments.41 This examination technique assesses bilateral
muscle strength simultaneously. By testing bilateral muscle
groups at the same time, the examiner can see subtle
differences between the two sides, suggesting areas of nerve
pathology.
Cold perception  Patients with nerve injuries or entrapments
will often have changes in perception of temperature and
these changes can localize injured nerves. In clinic, a quick
inexpensive way to assess cold perception is to place a piece
of ice in the finger of an exam glove and test the patient’s cold
perception on various nerve distributions.
Tinel’s sign  The Tinel’s sign has long been used to assess
nerve pathology. It is easy and quick and can help localize
areas of nerve compression. However, this test has low
sensitivity/specificity and wide variability between providers.42,43
Thus Tinel’s sign provides information but should be used as
one small piece of a full physical exam.
patient reports, “the whole arm hurts.” Strategies to diagnose
neuropathic pain and to localize pain generator(s) are pre­
sented below.
Patient history
There are several clues in the patient history to suggest a
neuropathic component to the pain. The first is the pain
quality. Neuropathic pain is often described as burning or
shooting. However, neuropathic pain can also be described as
dull or sore.38–40 Thus, pain quality can help diagnose but
should not rule out neuropathic pain. Pain severity can also
provide a clue. Severe pain without a clear cause can point to
activation of the somatosensory nervous system. If the pain is
out of proportion to the injury, a neuropathic component is
suspected. Pain duration beyond the time that tissue has
healed points to a pathologic pain process, often of neuro­
pathic origin.2
Physical examination
Physical examination can help differentiate neuropathic
from musculoskeletal pain. The examination can also help
localize area(s) of nerve irritation that are contributing to the
pain. First, the examination should begin with inspection. If
the patient is uncomfortable, apprehensive, and distressed
before the examination begins, this can suggest that the
pain has become a pathologic process (Fig. 23.2). Next, the
provider should assess for the physical signs associated
with CRPS such as edema, shiny skin, and temperature
changes (see Table 23.1). These same physical exam find­
ings can be found in patients with neuropathic pain who
do not meet the criteria for a diagnosis of CPRS. The pres­
ence of these trophic signs does suggest a neuropathic pain
component.
After the patient has been inspected, the provider should
begin with gentle palpation. Allodynia or pain to light tough
suggests a neuropathic pain process. If light touch of the skin
is painful or unpleasant, then the pain is not generated from
a deeper musculoskeletal problem.
After surgery, patients can have persistent pain from a
“scar neuroma”. These patients will have tenderness to light
touch or manipulation localized over the scar. Often the scar
will be tethered or depressed at the area of maximal tender­
ness (Fig. 23.3).
The provider should then perform a standard full
upper extremity examination looking for other potential
causes of the pain. There are several specific tests that
will help with identifying areas of symptomatic nerve
entrapments.

521
Diagnosis
Fig. 23.4  Magnetic resonance imaging of the ulnar nerve.
Clinical tips
Scratch collapse test  This is a newer test that is a useful
addition to the physical exam.44,45 For this technique, the
patient is seated with upper arms at their sides and elbows at
90° of flexion. The patient is asked to resist as the examiner
pushes medially on forearm (loading shoulder external
rotation). The examiner then lightly scratches the skin directly
over the area of the suspected nerve entrapment. Then the
examiner immediately repeats the loading of the shoulder
external rotation. If the patient’s external rotation is weaker, i.e.,
“collapses”, this is a positive test. This test is particularly
useful for less common proximal nerve entrapments such as
radial tunnel, pronator syndrome, and thoracic outlet. The
scratch collapse test is one more tool to help localize an area
of nerve pathology.
Diagnostic testing
Neuro-diagnostic testing  Neuro-diagnostic studies are key
diagnostic tests for assessing peripheral nerve pathology.
These studies can assess for neuropathy, localize nerve
compression, and exclude more proximal spinal pathology.
After trauma, patients have swelling, which can result in painful
nerve entrapments, such as carpal tunnel syndrome. Treating
the nerve entrapment is a key part to treating the pain.
However, it is important to understand the limitations of these
studies. There are patients with symptomatic nerve
entrapments with normal neuro-diagnostic tests.46 This is
particularly true for proximal nerve entrapments such as radial
tunnel or thoracic outlet. Remember, a negative nerve study
does not rule out entrapment. These tests, like many of the
others, provide one more piece of information for consideration.
Ultrasound  Ultrasound is being increasingly utilized in
evaluating nerve pathology.47,48 Ultrasound is attractive as it is
not painful, dynamic, and does not expose the patient to
radiation. Ultrasound can identify swelling and changes in
nerve architecture. As the nerves become smaller, the utility of
ultrasound decreases. At this time, the role of ultrasound in
the diagnosis of nerve injury/entrapments in the upper limb is
still evolving.
Magnetic resonance imaging (MRI)  MRI technology
continues to improve, resulting in more detailed imaging of the
nerves. However, like ultrasound, as the nerves become
smaller, the utility of the exam decreases. MRI neurogram is a
technique specifically designed to image nerves and it can
also provide information about the surrounding tissue
(presence of ganglions, etc.).49 MRI neurogram assesses
T2-weighted images looking for increased signal that identify
the area of nerve injury or entrapment.50,51 MRI neurogram is
currently useful for looking at larger nerve lesions such as
thoracic outlet and cubital tunnel (Fig. 23.4).
Hybrid imaging techniques such as positron emission
tomography (PET)/MRI are new innovations that expand the
information provided. In this technology, the patient undergoes
a PET scan and MRI of the affected area. Then the anatomic
images of the MRI and the biological marker images of the
PET are overlapped, providing more detail on the pathologic
process52 (Fig. 23.5).
Diagnostic blocks  Diagnostic blocks with local anesthetic
are the most important tool for identifying the area of pain
generation. If a patient has significant pain relief after a block,
then the pain generator is somewhere distal to the blocked
nerve. Diagnostic blocks are also useful as blocking one nerve
can unmask a second site of pain. These anesthetic blocks
can be done by the surgeon or in collaboration with a pain
medicine specialist. There are several steps, described below,
that are needed to ensure the diagnostic block generates the
most useful information.
Fig. 23.5  Positron emission tomography (PET) magnetic resonance imaging (MRI)
showing the merging of the bright PET signal on the anatomy of the MRI. (Courtesy
of Sandip Biswal.)