The Wrist and Hand

The boutonnière deformity is a functionally compromising
posturing of the digit. The deformity may follow trauma to the central
slip portion of the extensor mechanism. It may occur from a laceration
involving the proximal interphalangeal (PIP) joint or from a closed,
axial force applied to the digit resulting in a rupture of the central
slip. More commonly, the boutonnière deformity is caused by central
slip attenuation due to PIP joint destruction from rheumatoid
arthritis. Much like a small bouquet of flowers protruding through a
buttonhole in the lapel of a suit, the proximal interphalangeal joint
protrudes through the attenuated extensor mechanism of the digit.

The essential features of a boutonnière deformity
include hyperextension of the metacarpal phalangeal (MCP) joint,
flexion contracture of the proximal interphalangeal (PIP) joint,
hyperextension of the distal interphalangeal (DIP) joint, and
incompetence or attenuation of the central portion of the extensor
mechanism (Figure 14-1). The deformity can be
classified as either mild, moderate, or severe. The PIP joint
contracture in the mild or moderate varieties is considered passively
correctable, while the PIP joint contracture in the severe boutonnière
deformity is rigid or fixed and is not passively correctable.

Treatment of boutonnière deformity is more or less
prophylactic in the case of open or closed trauma of the extensor
mechanism. Lacerations of the central slip demand careful scrutiny and
prompt attention to prevent flexion posturing of the PIP joint and
ultimate failure of the extensor mechanism. In the event of a closed
rupture, the central slip is treated by splinting. Alternatively, the
boutonniere deformity seen in rheumatoid arthritis may be treated with
PIP joint synovectomy or reconstruction of the extensor mechanism when
the deformity is mild or moderate. In advanced cases, PIP joint
arthrodesis (fusion) or joint replacement arthroplasty is needed. In
general, soft tissue reconstruction of the boutonnière deformity has
been disappointing. The results from treatment with arthrodesis have
been more predictable.

Carpal tunnel syndrome is the most common clinical
entity seen by the hand surgeon, with some reporting that the condition
affects up to 10% of the general population—an estimated cost to the
U.S. medical system well beyond $1,000,000,000. When considering time
lost from work, the cost to society as a whole is substantial. Risk
factors for the condition include female, diabetes, hypothyroidism,
obesity, pregnancy, rheumatoid arthritis, gout, precious trauma,
acromegaly, smoking, old age, peripheral neuropathy, occupational
vibrational exposure, and renal disease.

It has been established that venous blood flow and
axonal transport within the median nerve is compromised with carpal
tunnel pressures of 30 mm Hg. This is a carpal canal pressure
clinically achievable in the carpal tunnel patient. Pressures in excess
of 30 m Hg have been shown in the patient who frequently flexes and
extends the wrist, pronates and supinates the forearm, or repeatedly
grasps objects. The consequence of chronic compression is damage to the
epineural covering of the median nerve resulting in diminished
conduction velocity.

The diagnosis of carpal tunnel syndrome is based on
information gathered from the history, physical examination, and
electrodiagnostic studies. The classic complaint from the patient
bothered by carpal tunnel syndrome is paresthesias at night.
Paresthesias are typically tingling or numbness in the median nerve
distribution of the hand. However, paresthesias can be characterized by
some patients as “pins and needles,” burning, or simply pain. Secondary
symptoms include paresthesias encountered while holding a book or
newspaper (“reading paresthesias”) or paresthesias encountered while
driving (“driving paresthesias”). Other complaints vary from
“clumsiness” of the hands, such that objects are often dropped and fine
digital tasks are difficult, to

generalized hand weakness. In the elderly complaints of “constant numbness” are often heard.

Provocative testing includes Phalen’s test, Tinel’s test
at the wrist, or the carpal tunnel compression test (Durkan’s test).
The carpal tunnel compression test is generally regarded as the most
sensitive. This test is administered by holding pressure directly over
the median nerve at the wrist. A positive test is acknowledged when the
patient experiences paresthesias in the median nerve distribution
within 30 seconds of the onset of the test. The most predictable
sensory test to evaluate carpal tunnel syndrome is the Semmes-Weinstein
monofilament test, where threshold testing of sensation is performed
using various sizes of nylon filaments. Vibrometry has also been shown
to be a useful sensory test for carpal tunnel syndrome.

Although recommended by most, efficacy of the
electrodiagnostic testing for diagnosing carpal tunnel syndrome is
debated by some. Finsen et al. reported in one
series that 22% of patients who had normal nerve electrodiagnostic
studies had a good outcome following carpal tunnel release surgery,
indicating a substantial false-positive rate for the testing.
Electrodiagnostic tests include the nerve conduction velocity (NCV)
measurements and the electromyogram (EMG). The NCV is considered
positive for carpal tunnel syndrome when the median motor distal
latency is >4.5 ms or the distal sensory latency is >3.5 ms. In
more advanced cases, diminished action potential may also be seen. On
the EMG portion of the study, the presence of positive sharp waves,
increased insertional activity, decreased muscle recruitment, or
polyphasic activity is indicative of substantial nerve dysfunction.

The mainstay of nonoperative management is nocturnal
splinting, particularly for mild or moderate carpal tunnel syndrome.
When consistently used for a period of 4 to 6 weeks, permanent relief
of symptoms can ensue. Other nonoperative measures include nonsteroidal
anti-inflammatory agents (NSAIDs), carpal tunnel injections,
ultrasound, phonophoresis, nerve gliding or stretching, and vitamin B₆.
No data shows any clear advantage of adding these measures with or
instead of splinting. Corticosteroid injections have been shown to have
long-term efficacy in only 22% of patients with symptoms longer than 1
year. Relief of symptoms following injections has been shown to
correlate as a predictor of surgical success. Work modifications to
prevent sustained wrist movements or provocative wrist positioning may
play a greater role than any of the nonoperative measures except
splinting. Some studies have suggested the preventative effect of wrist
and hand exercises in certain occupational environments.

Surgical treatment of carpal tunnel syndrome is
considered when two of the following criteria are meet following at
least a 3-month course of nonoperative care: persisting symptoms,
positive physical examination, and positive electrodiagnostic testing.
Absolute indications for surgery are constant paresthesias, thenar
atrophy, and markedly delayed median motor nerve conduction velocity or
abnormal EMG testing. The surgical procedure consists of increasing the
volume of the carpal canal by transecting the transverse carpal
ligament. An MRI study has shown that division of the transverse carpal
ligament expands the volume of the carpal canal by as much as 25%. In
some instances, such as in rheumatoid arthritis, the addition of a
flexor tenosynovectomy is needed. The surgical procedure is most
commonly performed through a small longitudinal incision at the base of
the palm, in line with the ring finger. Care must be taken to avoid
injury to the thenar motor branch of the median nerve, which has
variable anatomy. Misplaced or transverse incisions about the wrist may
jeopardize the palmar cutaneous branch of the median nerve. Other
reported complications with open carpal tunnel decompression include
ulnar nerve and artery injury.

An alternative technique to the open carpal tunnel
decompression is the endoscopic carpal tunnel release. Various authors
have reported success rates equal to the open carpal tunnel release
with less scar tenderness and quicker return to work. Concerns still,
however, remain regarding the safety and efficacy of the endoscopic
technique. Van Heest et al., Lee et al., and Schwartz et al., have
reported incomplete release of the transverse carpal ligament using the
endoscopic technique in cadaver models. Devastating complications such
as median nerve transection and flexor tendon transection have been
reported causing some to carefully scrutinize the routine use of the
endoscopic technique.

Irrespective of the method of surgical decompression
chosen, it has been well established that success from carpal tunnel
surgery can approach 98% when only subjective complaints are
considered. It has been generally held that these results diminish with
age. It has been shown that workers applying for worker’s compensation
can be anticipated to have worse overall results and a slower recovery
compared to a similar group of patients not submitting worker’s
compensation claims.

In 1766, Hunter introduced the term algodystrophy in describing pain of uncertain origin. In 1864 Mitchell introduced the term causalgia to describe nerve pain following an amputation. More recently Evans forwarded the term reflex sympathetic dystrophy
(RSD) to identify a condition that included pain, swelling,
hyperhydrosis, skin color changes, skin temperature changes, stiffness,
and underlying osteoporosis, with all symptoms potentially reversible
with stellate ganglion blockade. Other terms often used in place of RSD
include Sudeck’s atrophy, shoulder-hand syndrome, or “allodynia.”
These complex and often confusing terms for pain of uncertain origin
has lead to the classification system of complex regional pain syndrome
(CRPS) typed I and II. Simply stated, CRPS type I is a condition
whereby pain had developed following an inciting painful circumstance.
In this condition the pain, however, seems to develop out of proportion
to the clinical situation. Associated findings include edema, skin
blood flow changes, and abnormal sudomotor activity such as
hyperhydrosis. CRPS type II has a similar clinical presentation but is
associated with a known nerve injury. The predominant symptoms and
findings of the initial stage are constant pain, hyperhydrosis, and a
hypersensitivity to touch. The second stage of the condition is
characterized more by stiffness and pain, while in stage III patients
experience diminished pain but overall disuse of the extremity. The
pathophysiology of CRPS is still unknown.

To date the most reliable tool for the diagnosis of CRPS
is the physical examination. Other less reliable tests include the
three-phase bone scan, thermography, the quantitative sudomotor axon
reflex test (QSART), and plain radiography. Increased uptake is
anticipated in the later phases of the bone scan while osteopenia is a
later finding in the CRPS patient. CRPS I has been reported to occur
following as many as 25% of all distal radius fractures. A risk factor
is displacement requiring reduction. It is generally regarded that
those patients experiencing CRPS of an extremity are at greater risk of
recurrent symptoms following a surgical procedure.

The initial treatment of CRPS requires prompt
recognition and diagnosis. Most patients diagnosed within the first 6
to 8 weeks respond favorably to treatment. Initially, hand therapy
plays an important role in the treatment of CRPS. Such techniques as
massage, edema control, gentle passive motion (to prevent contracture),
contrast baths, and use of the transelectrical stimulator unit (TENS)
have proven effective. The key concept to remember when embarking on
hand therapy is the patient must be exercised within the limits of
pain, otherwise a flare-up of the condition may result. Initial drug
therapies have included the use of β-blocker medication (propranolol),
calcium channel blockers medication (nifedipine), guanethidine,
neurontin (anticonvulsant medication), nasal calcitonin, and 6-day
medrol dose packs—all with some limited success. The role of NSAIDs,
although theoretically attractive, has shown limited benefit.

In patients with CRPS I or II, pain may be
sympathetically mediated or sympathetically independent. In those with
sympathetically mediated pain, stellate ganglion blocks may be
diagnostic as well as curative for the condition. Multiple such
injections may be necessary to realize a benefit and are indicated when
other above-mentioned measures are not effective. Surgical stellate
ganglion ablation is yet another treatment alternative.

Congentital anomalies of the upper limb account for over
10% of all birth defects. The limb bud forms adjacent to the fifth
through seventh cervical somites and can be visualized at day 25
following fertilization. During the ensuing 25 days the limb develops
rapidly with individual digits and web spaces well defined. It is
during this period of embryogenesis that anomalies occur due to either
malformation, deformation, disruption, or dysplasia. Syndactyly
(incompletely separated digits) and polydactyly (extra digits) are
generally considered the most common forms of congenital hand
anomalies. Certain anomalies may be associated with midline congenital
defects such as those affecting the heart, lungs, or kidneys, while
other congenital hand anomalies may appear as isolated events.
Appropriate pediatric and medical genetic workup is recommended in all
patients with upper extremity congenital anomalies. Surgery is often
necessary in these children with a goal of completing all hand
reconstruction by the time hand preference is established, which is
approximately 2 years of age.

Gout is most commonly a result of an underexcretion of
uric acid that leads to the deposition of monosodium urate crystals and
intermittent acute articular swelling, which is termed acute gouty
arthritis. Occasionally the syndrome can also occur due to the
overproduction of uric acid. Gout is approximately 10 times more common
in men than women and has a predilection for middle-aged

males.
The attacks often occur suddenly and are characterized by severe pain,
warmth, and erythema. The consumption of alcohol, trauma, or acute
medical illnesses can cause an attack. Attacks often also occur
following a surgical procedure. Monosodium urate crystals have a lower
solubility quotient at colder temperatures; therefore some have
speculated that this is the cause for the gout commonly affecting the
distal aspects of the extremities. Gout can affect the wrist, MCP, PIP,
and DIP joints. In fact, its sudden onset can lure the unsuspecting
medical student toward acute septic arthritis. The diagnosis of acute
gouty arthritis is made by joint aspiration of negative birefringent,
monosodium urate crystals. The treatment of gout generally does not
require surgery. Colchicine, NSAIDS, or corticosteroid medication is
used in the treatment of acute gout. Chronic tophaceous gout is treated
with allopurinol. Occasionally, gouty tophi require surgical
debridement, particularly from the carpal tunnel following the
development of secondary carpal tunnel syndrome.

Calcium pyrophosphate dihydrate deposition (CPPD), or
pseudogout, occurs due to the deposition of birefringent CPPD crystals
into the joint, activating an inflammatory cascade. In these patients,
sudden swelling, pain, and warmth occur. The wrist and the MCP joints
are the most commonly affected joints of the upper extremity. And like
gout, it can be misdiagnosed as infection. The condition more
frequently occurs in the older age groups, particularly females. In
these patients, chondrocalcinosis is frequently seen on plain
radiographs, particularly in the triangular fibrocartilage of the wrist
(Figure 14-7). Trauma and acute medical
illnesses can trigger attacks. Similar to gout, treatment is primarily
nonsurgical. For the wrist, joint aspiration with injection of 10 mg of
Kenalog is generally successful in minimizing an acute attack. For
other joints in the hand, NSAIDS may be useful.

Degenerative arthritis or osteoarthritis of the hand and
wrist is one of the more common afflictions seen in society. Causes
include posttraumatic, post-repetitive stress, or idiopathic, and may
be symmetrical or bilateral. This condition distinguishes itself from
the systemic and symmetrical inflammatory arthropathies. Patients often
complain of localized pain following certain provocative activities.
There may be swelling and pain with passive range of motion, which are
hallmarks of arthritis in general. A history of fracture may be related
but this is not always the case. Scapholunate advanced collapse (SLAC)
wrist is a type of degenerative arthritis of the wrist that primarily
affects the radio-scaphoid articulation and spares the radiolunate
articulation (Figure 14-8). Advanced cases have
midcarpal joint involvement with resulting loss of carpal height and
migration of the capitate proximally between the scaphoid and lunate
articulation. This is easily identifiable on plain wrist radiographs.
Patients may relate a history of wrist ligamentous injury, such as a
scapholunate ligament disruption, or radiographs may reveal an old
scaphoid nonunion. Most of these patients display weak grip and
diminished range of motion. In a study of over 200 wrists with primary
osteoarthritis of the wrist, the SLAC wrist pattern was identified as
the most common pattern. Initial nonoperative measures include activity
restriction, splinting, NSAIDs, and injections. Although many patients
may remain without symptoms for years, some patients require operative
intervention for relief of pain. Temporizing operative treatment
includes wrist debridement and de-innervation procedures where the
radiocarpal articular branches of the anterior and posterior
interosseous are cut in an effort to relieve pain. Salvage procedures
for SLAC wrist include removal of the scaphoid with midcarpal fusion
(scaphoidectomy with four-corner fusion); removal of the scaphoid,
lunate, and triquetrum thus shortening the carpus and allowing the head
of the capitate to articulate in the lunate fossa (proximal

row carpectomy); and complete wrist fusion. The choice of operative treatment is individualized.

Scapho-trapezial-trapezoidal arthritis (STT arthritis)
is a form of thumb base arthritis. In these patients articulation
involving the scaphoid, the trapezium, and the trapezoid degenerates.
These patients may localize their discomfort at the base of the thumb
joint or in the wrist in general. This form of degenerative arthritis
is less common than SLAC wrist but is also recognized as either
posttraumatic or idiopathic. Patients will experience difficulties with
pinch tasks in particular. Initial treatment is also nonoperative
similar to the treatment for SLAC wrist. Operative treatment has
classically been the STT fusion. Problems with this operation have
included persistant pain and nonunion of the fusion mass. This outcome
has prompted some authors to recommend the same treatment that will be
discussed for degenerative arthritis of the thumb: removal of the
trapezium and tendon reconstruction of the ligaments of the base of the
thumb.

Thumb carpometacarpal joint osteoarthritis is one of the
most common forms of arthritis in the body. Females in the sixth and
seventh decade of life are approximately eight times more likely to
develop the condition than males. Patients complain of pain at the base
of the thumb with most activities of daily living, such as turning keys
or pinching objects between the thumb and index finger. The thumb axis
itself may be misshapen with the first web space narrowed and the thumb
MCP joint hyperextended to aid in grasping objects. Radiographs show
narrowing of the carpometacarpal joint of the thumb (Figure 14-9). Initial nonoperative treatment includes thumb-spica splinting,

NSAIDs, and injections. If patients fail to respond to these
nonoperative measures, surgery may prove helpful. Surgery entails
removal of the arthritic CMC joint by complete trapezium removal and
harvest of the flexor carpi radialis (FCR) tendon. The FCR tendon is
used to recontruct the primary ligamentous stabilizer of the basilar
thumb joint—the anterior oblique retinacular ligament. One long-term
study showed high patient satisfaction at 10 years average follow-up.
Although initial success was reported, long-term failures with the
Silastic trapezial implant has been well recognized, due primarily to
wear debris from the implant and subsequent fracture. The use of the
Silastic trapezial implant is no longer recommended.

Ulnar impaction syndrome occurs when a mismatch in
lengths occurs between the ulna and the radius such that the ulna is
longer than the radius. The result is that the ulna impales the lunate
or possibly the triquetrum during ulnar deviation of the wrist.
Coincident with ulnar impaction, the triangular fibrocartilage complex
(TFCC) is generally torn or frayed due to the impaction process. The
patients complain of ulnar-sided wrist pain with strong grip, which
results in ulnar deviation of the wrist. Causes of ulnar impaction
syndrome may be posttraumatic or developmental. Initial treatment is
nonoperative and includes long arm splinting and NSAIDs. Failure of
nonoperative treatment may indicate the patient for operative
intervention. The principle of surgical treatment is ulnar shortening.
This joint-leveling procedure requires an osteotomy of the ulna at the
metaphyseal or diaphyseal junction, necessitating internal fixation
with plates and screws. Another less desirable option is distal ulnar
resection, also referred to as Darrach procedure. The Darrach procedure
is more appropriately performed in the elderly, debilitated individual,
as it is not as well tolerated in the young active patient.

The extensor pollicis brevis (EPB) tendon and two
abductor pollicis longus (APL) tendons are generally contained within
the most radial condensation of the extensor retinaculum system, the
first dorsal compartment. DeQuervain’s syndrome generally occurs
following certain repetitive wrist movements that cause friction within
the first dorsal compartment. Anatomic variations such as more than two
APL tendons or multiple septations within the first dorsal compartment
may predispose to development of the syndrome. In cadaver studies,
first dorsal compartment septations have been found in approximately
one-third of individuals. In one study, Jackson et al.,
reported 67% incidence in patients undergoing surgical treatment for
DeQuervain’s syndrome. Space occupying lesions such as ganglion cysts
also contribute to narrowing of the first dorsal compartment.

Repetitive friction then leads to swelling and narrowing
of the compartment resulting in radial-sided wrist pain. Patients will
complain of soreness and tenderness at the base of the thumb
exacerbated by ulnar deviation of the wrist, strong grasp, or thumb
pinch. Inspection will find swelling of the radial side of the wrist in
most cases. Physical examination will find tenderness and often warmth
directly over the first dorsal compartment. In certain advanced cases,
audible squeaking occurs with active thumb movements. The classic test
confirming the diagnosis of DeQuervain’s syndrome is Finklestein’s
test. This test is performed with the thumb slightly flexed and
abducted into the palm and the wrist ulnarly deviated. A positive test
is one where pain is reproduced compared to the contralateral,
unaffected side. Often the test is performed incorrectly with the
patient clasping the thumb into the palm and the wrist ulnarly
deviated. This maneuver, if done vigorously, causes pain in most
anyone. If the reader doubts this, he is encouraged to try the maneuver
on himself.

Initial treatment for DeQuervain’s syndrome is
nonoperative. The patient is fitted with a volar forearm-based,
thumb-spica splint for nighttime use. A small, lower profile,
hand-based splint may be used for daily activities if suited to the
patient’s lifestyle. NSAIDS may also be of value and should be
considered if not contraindicated due to GI intolerance. Additionally,
a corticosteriod injection into the first dorsal compartment may
provide sustained relief. In one study, Weiss et al.
reported that injection was just as effective in DeQuervain’s syndrome
as splinting alone or splinting combined with injection. In another
study of 63 patients, 71% of patients had sustained relief of their
symptoms with one first dorsal compartment injection. Skin
depigmentation and fat atrophy are known complications of
corticosteroid injections of the wrist.

If a 6 to 8 month period of nonoperative treatment
fails, then operative intervention can be considered. Surgical
treatment is release of the first dorsal compartment under local
anesthesia. This is performed through a longitudinal incision directly
overlaying the first dorsal compartment. Branches

of
the superficial radial nerve are particularly vulnerable with this
procedure. Care must be exercised in protecting these branches as
injury to them can cause substantial disability. Other reported
complications of this procedure include volar subluxation of the first
dorsal compartment contents and hypertrophic scar formation. It is for
these reasons most prefer a prolonged trial of nonoperative therapy.

Dupuytren’s contracture is a thickening and subsequent contraction of the palmar aponeurotic fascia (Figure 14-10).
Due to factors that are poorly understood, fibroblasts transform to
myofibroblasts with contractile elements (smooth muscle actin) and
attach to the cells of the palmar aponeurosis. Trauma has also been
mentioned as a possible cause. As the disease progresses, the affected
tissues shorten as a unit, ultimately resulting in digital
contractures. Along with the digital contracture, skin dimpling may
occur. Dupuytren’s diathesis generally implies a more advanced form of
the disease, including “knuckle pads” (thickening over the extensor
surfaces of the PIP joints), plantar fibromas (lederhosen disease), and
fasciitis of the penis (Peyronie’s disease). The disease has a genetic
predisposition, as males of Northern European descent are more commonly
affected. Incidence among affected families has been reported to
approach 70%. Although the genetic predisposition in Dupuytren’s
disease has been well established, the condition is seen more commonly
in patients with seizures, patients who use alcohol and tobacco, and
patients with diabetes. Also, the combination of carpal tunnel
syndrome, trigger finger, and Dupuytren’s contracture has been
appreciated in the diabetic population. The most commonly affected
digit is the ring finger, but any finger can be affected. The prodrome
of Dupuytren’s contracture is inflammation with tenderness in the palm.
Later, contracture ensues on an unpredictable course. The bands of
palmar fascia are termed cords when
affected by Dupuytren’s disease. The most common pattern of cord
development is the pretendinous cord in the palm, which progresses to
cause a MCP joint contracture. The pretendinous cord develops directly
over the flexor tendon system in the palm. Secondarily, a PIP joint
contracture may develop due to the formation of a spiral cord that is
the condensation of several diseased fascial bands in the finger. The
most notable is Grayson’s ligament that is a digital aponeurotic
element attaching to skin volar to the digital nerve and artery. The
spiral cord is so named because it often entraps the digital nerve and
the digital artery along the radial or ulnar borders of the finger.
Following the acute inflammatory prodrome stage of the disease, pain is
usually not encountered as the contracture progresses. At some point,
patients seek medical attention due to the inability to straighten
their hands, making tasks such as shaking hands or donning gloves
difficult. In extreme cases, the contracture can become so severe that
palmar maceration develops, posing a hygiene problem.

In 1831, Dupuytren outlined the first treatment for the
disease that came to bear his name, although the nature of this disease
had been described years earlier by Felix Plater, Henry Cline, and Sir
Ashley Cooper. For many years a variety of nonoperative treatments have
been tried, all without success but, as Dupuytren first described,
surgery is the preferred treatment for this condition. Although simple
transection of the pretendinous cords is a viable option in the elderly
or the debilitated patient, the

surgery
for symptomatic Dupuytren’s contracture has evolved into a formal
fasciectomy of the involved palmar tissue. The indications for surgery
are debilitating contracture of the MCP joints or any contracture of
the PIP joint. Contractures of the MCP joints are easily corrected
under most circumstances. In contrast, contractures of the PIP joints
are often incompletely corrected and are fraught with recurrence.

Dupuytren’s fasciectomy can be performed through the
standard zigzag Bruner incisions, unless the deformity is severe. With
severe contracture, the fundamental problem becomes one of skin
coverage after the fascia is removed and the contracture corrected. In
severe cases of Dupuytren’s contracture, a longitudinal incision with
multiple opposing Z-plasties can be utilized to expand the coverage
potential of the existing skin. Alternatively, McCash described a
technique whereby fasciectomy skin incisions can be made in the
transverse skin creases of the palm and the digits, without closure.
The wounds then heal by secondary intention so motion is not inhibited
following complex wound coverage procedures. Another alternative is
performing the standard Bruner incision and leaving portions of that
wound open following fasciectomy, either in the palm or in the digit.
Yet another option is dermofasciectomy where diseased fascial elements
are excised along with overlying skin and the resulting defect skin
grafted. Whatever the surgical technique employed, the dissection of
the palmar fascial can be tedious, particularly in advanced or
recurrent cases. Extreme care must be exercised in dissecting the
diseased fascial cords from the digital nerves and arteries because
nerve injury or even nerve division can result.

One of the greatest challenges for the patient and the
hand surgeon is maintaining the improvements in MCP and PIP motion
following fasciectomy. Maintaining motion improvements requires close
postoperative supervision by a hand therapist. Within the first 3 to 5
days the dressing is changed, and the patient is placed in an extension
splint. Care is taken to not cause ischemia of the palmar skin flaps.
It is important to also start active flexion exercises of the MCP and
PIP joints. The patient’s progress must be closely monitored and the
exercise protocol modified as necessary to achieve the optimal balance
between achieving digital extension and maintaining composite finger
flexion.

Most patients are satisfied with the surgical outcome of
palmar fasciectomy, although complete corrections of PIP joint
contractures are rarely achieved. Recurrence of Dupuytren’s contracture
following fasciectomy has been well recognized with the incidence
approaching 50% in some series. Complications of fasciectomy surgery
for Dupuytren’s contracture include digital nerve neuropraxia and
digital sensory compromise, digital nerve division, digital ischemia,
wound healing problems, and complex regional pain syndrome type 1 or
type 2. Surgery for recurrent disease can be challenging even for the
most experienced surgeons, with complications such as amputation having
been reported.

Keinbock’s disease is osteonecrosis of the lunate. By a
mechanism that still is not entirely understood, the blood flow to the
lunate bone of the wrist is compromised to such an extent that
osteonecrosis ensues and collapse and fragmentation of the bone occurs
over time. The end result can be degenerative arthritis of the
radiocarpal joint and pain. Various predisposing factors exist.
Approximately 75% of wrists with Keinbock’s disease have a shorter ulna
compared to the radius, as measured at the wrist (ulnar negative
variance). Also, the slope of the distal radius articular surface has
been shown to be more horizontal in patients with Keinbock’s disease.
Approximately one-fourth of lunate are thought to have a single vessel
blood supply. Some believe that osteonecrosis of the lunate occurs
subsequent to a single fracture although others have suggested
repetitive microfracture of the bone. In reality, cause of Keinbock’s
is most likely multifactorial.

Keinbock’s is more common in males that females.
Approximately 50% of patients relate a history of trauma. Most complain
of dorsal wrist pain and stiffness. Physical examination may reveal
diminished range of motion, grip weakness, and tenderness over the
radiocarpal joint. Some patients present with symptoms of carpal tunnel
syndrome. Keinbock’s can be staged radiographically into one of six
categories. Stage 0: normal plain radiographs of the wrist with
abnormal MRI scan of the lunate. Stage 1: fracture of the lunate
without collapse of the bone. Stage 2: sclerosis of the lunate without
collapse of the bone. Stage 3a: lunate collapse without loss of height
of the wrist (Figure 14-13). Stage 3b: Collapse of the wrist. Stage 4: degenerative changes of the wrist joint secondary to Keinbock’sdisease.

The natural history of Keinbock’s disease is not
entirely known. In patients with stage 0 and stage 1 disease,
immobilization and nonoperative support may suffice. Patients with
stage 2 and stage 3a disease

who
continue with symptoms are generally indicated for surgery. The
surgical procedures for patients with stage 2 and stage 3a Keinbock’s
disease can be divided into two broad categories: joint-leveling
procedures and revascularization procedures. The most commonly
performed among these procedures is the radial shortening osteotomy.
This procedure is indicated in patients who have a short ulna and the
goal of surgery is to shorten the radius to “level” it with the ulna.
The exact reason why this procedure is effective is still unknown. The
most commonly performed revascularization procedures for Keinbock’s
disease is a pedicled vascularized bone graft harvested from the
dorsal, distal radius. For patients with symptomatic stage 4 disease
and some patients with stage 3b disease, reconstructive salvage surgery
of the wrist is indicated. This salvage surgery may include a partial
(maintains some element of wrist range of motion), or a complete wrist
fusion or a proximal row carpectomy (removal of the lunate bone along
with the scaphoid and triquetral bone). Proximal row carpectomy allows
the capitate to articulate in the lunate fossa. A prerequisite for this
operation is maintenance of a good distal radius articular surface.

Few injuries are as devastating functionally to the hand
and wrist as median, ulnar, or radial nerve palsies. The vast majority
of radial nerve palsy is posttraumatic, but can also occur as a
complication of elective surgery of the upper extremity, a residual of
birth palsy, or the consequence of cervical spine disc disease. Tendon
transfers provide an option to restore lost motor function. The ideal
tendon transfer is one in which the tendon’s muscle has normal
strength, has a straight line of pull, and provides adequate excursion.
Additionally, the tendon should originally have a function synergistic
or “opposite” to the tendon function for which it is substituted.
Naturally, the tendon to be transferred must be expendable.

Loss of median nerve function at or above the elbow
results in a high median nerve palsy. The consequences of a high median
nerve palsy is loss of palmar sensation along the volar aspect of the
thumb, index, long, and radial border of the ring finger. Motor
strength deficits include loss of thumb opposition (loss of abductor
pollicis brevis), loss of thumb interphalangeal (IP) joint flexion
(loss of flexor pollicis longus muscle function), and loss of index
distal interphalangeal joint flexion (flexor digitorum profundus
function). Restoration of thumb IP joint flexion can be restored using
a transferred brachioradialis muscle (radial nerve innervated) to the
FPL tendon. Restoration of FDP function of the index finger can be
accomplished using the extensor carpi radialis longus (radial nerve
innervated) tendon rerouted to the index FDP tendon in the mid forearm.
Lastly, thumb opposition can be restored with transfer of the abductor
digiti minimi muscle (ulnar nerve innervated).

Radial nerve palsy is particularly compromising to the
function of the hand because extension posturing of the wrist (the
prehensile position) is lost. This positioning of the hand increases
grip power as well as the all-important hand function of grasp and
release. The radial nerve is particularly vulnerable as it spirals
around the humerus midshaft, against which it is closely applied. The
radial nerve palsy is most often caused by injuries following a spiral
fracture of the humerus. The sharp bony ends of the fracture can impale
the radial nerve along its course. Loss of radial nerve function at
this level results in loss of wrist and finger extension. This is known
as “wrist drop.” Tendon transfers for radial nerve palsy include flexor
carpi radialis (FCR) transfer to extensor digitorum communus (EDC)
tendons, pronator teres to extensor carpi radialis brevis tendon, and
palmaris longus to the rerouted extensor pollicis longus (EPL) tendon.
These transfers are then subsequently fired by flexion of the wrist
causing tension on the transferred tendons (tenodesis) of the wrist.

Without question, the most devastating injury to the
hand is the ulnar nerve palsy. The ulnar nerve supplies sensation to
the volar aspect of the small finger as well as the small finger side
of the ring finger. Motor function deficits following ulnar nerve palsy
include loss of hand muscle function (intrinsic muscle function), which
includes digital side-to-side movements as well as “thumb pinch”
function. This results in substantial impairment in hand strength and
digital mobility. Ulnar nerve injuries higher (more proximal) in the
arm result in the loss of DIP joint flexion. Profound hand wasting
accompanies ulnar nerve dysfunction.

Various signs of ulnar nerve palsy have been described.
The classic “clawhand” of ulnar nerve palsy is known as Duchenne’s
sign. Wartenberg’s sign is the inability to pull in (adduct) the small
finger against the ring finger. Froment’s sign is the hyperflexion of
the thumb IP joint to substitute for the lack of thumb-pinch power
against the index finger. Weakness of DIP joint flexion due to loss of
FDP

function
of the ring and small finger is known as Pollock’s sign. The flattening
of the natural metacarpal arch of the hand seen in association with
hand muscle wasting is known as Masse’s sign.

Tendon transfers for ulnar nerve palsy are limited in
their ability to restore hand strength. The ECRB tendon can be
transferred to the thumb proximal phalanx to provide thumb pinch
(adduction) while the extensor pollicis brevis (EPB) tendon is
transferred to the index interosseous muscle. Additionally, the thumb
MCP joint may be fused to prevent thumb hyperextension and instability.
The combination of these surgeries has been reported to restore
approximately 50% of the lost pinch strength.

Rheumatoid arthritis affects approximately 1% of the
population with females affected twice as often as males. It is a
systemic condition that causes a symmetrical polyarthritis. In the hand
and the wrist joint, the distal radioulnar joint and the
metacarpophalangeal joints are commonly affected. Patients usually
present between ages 40 and 60 with joint pain and stiffness and
occasionally fever. In the hand, synovial swelling is first seen
followed by ligamentous failure, joint subluxation, and ultimately
joint erosions and destruction. Initial treatment of rheumatoid
arthritis in the hand includes medical therapy and resting night
splints. Early on, medical therapy may consist of NSAIDs and rest
splints but potential remittive therapy is usually necessary.
Aggressive medical management often includes low dose oral
corticosteroids and immunosuppressive agents such as methotrexate,
Imuran (azathioprine), or Arava (leflunomide). Newer biological agents
include Enbrel (etanercept), Humira (adalimumab), and Remicade
(infliximab), which act by inhibiting tumor necrosis factor. These
biologic response modifiers may be combined with more traditional
agents such as methotrexate. Whether or not these treatments will make
surgery less necessary has been suggested but not yet established.

If synovitis persists following at least 3 months of
medical management, then surgical synovectomy is indicated to prevent
extensor tendon rupture. Similarly, synovitis of the wrist joint or the
metacarpophalangeal joints may not respond to medical management and
surgical synovectomy may be indicated. The indications for MCP and
wrist joint synovectomy are less clear but in the absence of joint
destruction, most agree that joint surgery can be delayed. MCP joint
synovectomy should be considered in those patients with recalcitrant
synovitis who have no radiographic evidence of joint destruction.

The distal radioulnar joint (DJUJ) may be the first
joint affected in patients with rheumatoid arthritis. DRUJ subluxation
is often observed and as the distal ulna becomes eroded, rupture of the
overlying extensor digiti quinti minimi (EDQM) tendon can occur. The
result is the Vaughan-Jackson sign, which is a prominent distal ulna
with the inability to extend the small finger. In these patients,
extensor tenosynovectomy is indicated with EDQM reconstruction. A
side-to-side tendon repair to the adjacent EDC to ring finger can
accomplish EDQM reconstruction. In these patients it is also incumbent
to stabilize the distal radioulnar joint. This is most commonly done
with a distal radioulnar joint fusion with the creation of a more
proximal pseudoarthrosis (Suave-Kapandji procedure). As disease
progresses, the remainder of the wrist joint becomes involved, further
destruction of the wrist may occur, and wrist arthrodesis may be
necessary. Wrist arthrodesis is a reliable procedure well suited for
providing pain relief. Alternatively, a total wrist replacement can be
considered in low demand individuals with bilateral disease. Total
wrist arthroplasty is contraindicated in patients with previous
infection. The failure rate with total wrist replacement approaches 25%
at intermediate-term follow-up in one recent series. The most common
mode of failure is distal component loosening.

Progression of the rheumatoid hand deformity includes
MCP joint destruction with subluxation of the joint and drift of the
digits toward the small finger side of the hand (ulnar drift).
Tightness of the surrounding soft tissue structures ultimately prevents
correction of this deformity (intrinsic muscle tightness). Wrist
involvement may also occur with sliding of the carpal bones toward the
ulna (ulnar translation of the carpus) as ligamentous destruction
occurs (Figure 14-14). These patients also
commonly have pain and have noticed a recent decline in overall hand
performance. These patients are reasonable candidates for MCP joint
arthroplasties. The Swanson flexible silicone implant that has been in
service for well over 35 years functions as a spacer following
resection of the destroyed MCP joint. It has been well recognized that
these implants typically fracture but remain in service for

years, continuing to function as a spacer. Hansraj et al.
has reported a 90% 10-year survival rate with this spacer. The
biomechanical shortfall of the Swanson Silastic implant is the amount
of bone and soft tissue resection needed for implantation of the
device. Current alternatives to the Silastic implants are surface
replacement arthroplasties that attempt to recreate the normal
articular surface anatomy while requiring less soft tissue resection
for implantation of the device. Further follow-up data on these newer
generation devices are needed.

Stenosing tenosynovitis condition is a mechanical
problem of a mismatch in size of the flexor tendons within their flexor
tendon sheath. The result is a bunching or catching of the tendons as
they pass through the orifice of the A1 pulley. This mismatch in size
results in the mechanical problem of triggering that is the clinical
hallmark of the condition. A fibrocartilagenous dysplasia develops at
the A1 pulley, leading to a similar lesion on the corresponding surface
of the flexor tendon. This results in degenerative tendinopathy over
time. The process can occur at any digit but more commonly affects the
ring finger. Patients usually present with a complaint of a painful
catching of the finger with gripping. In more advanced cases, the
finger may be locked in flexion and very painful to reduce. The
patients may complain of the occurrence more in the morning hours than
later in the day. Prior to experiencing the triggering or catching
symptoms, patients may just have a tender and sore flexor tendon sheath
that is aggravated by activities. On physical examination, actual
triggering may not be elicited but tenderness directly over the A1
pulley usually is. The condition is more frequently seen in patients
with rheumatoid arthritis, gout, diabetes, and degenerative arthritis.
Patients usually present in the fifth to seventh decade of life.

Initial treatment is nonoperative. Simple splinting with
the use of NSAIDs has been shown to be effective in some patients.
Injection of corticosteroid into the flexor tendon sheath has been
shown to be effective in 70% of patients. Another study has shown the
percentage to increase to 84% when a regimen of two injections is used.
Alternatively, reports of splint therapy alone have yielded improvement
in 66% of patients. The trigger finger injection is performed using a
25-gauge needle and 1 cc of lidocaine and 10 mg of Kenalog solution or
an equivalent of another water insoluble steroid preparation. Water
insoluble steroid preparations are longer acting. The lidocaine steroid
preparation is injected into the flexor tendon sheath at the level of
the A2 pulley, and the examiner palpates the filling of the sheath.
Flexor tendon sheath release or trigger finger release is indicated
when nonoperative management fails. This is done at the opening of the
flexor tendon sheath, or at the level of the A1 pulley. Results
approaching 100% in appropriately indicated patients were recently
reported by Turowski et al. An alternative to
open trigger finger release is percutaneous flexor tendon sheath
release. This technique employs a 20-gauge needle placed percutaneously
at the level of the A1 pulley. The needle is manipulated such that the
A1 pulley is cut by the bevel of the needle. Complications of this
technique include scoring of the tendon.

Similar to the boutonnière deformity of the digit, the
swan-neck deformity may cause substantial functional limitation. It can
arise following trauma but more typically is seen in the context of the
rheumatoid hand. The essential features of the digital swan-neck
deformity include hyperextension of the PIP joint and flexion of the
DIP joint subsequent to incompetence of the PIP joint volar plate (Figure 14-15).
The swan-neck deformity is often accompanied by the presence of
intrinsic tightness. In this condition the interosseous muscles of the
hand become contracted, which causes tightness of the lateral band
portion of the extensor mechanism. With the metacarpal phalangeal (MCP)
joint extended, the lateral band portion of the extensor mechanism is
placed on stretch, causing tightness of the terminal tendon. This
imbalance then causes restriction in the passive or active flexion of
the PIP joint. A simple test for intrinsic tightness involves
hyperextending the PIP joint and then examining the passive range of
motion (ROM) of the PIP joint. Patients with intrinsic tightness of a
digit experience diminished passive range of motion at the PIP joint
when the test is performed.

Digits with a swan-neck deformity may be classified into
four stages. Stage 1 is a finger with a swan-neck deformity and no
limitation of PIP joint ROM. Stage 2 is a swan-neck digit with
limitation of ROM with certain positions of the MCP joint. Stage 3 is a
digit with limitations of PIP ROM in any MCP position. Stage 4 is fixed
and rigid swan-neck deformity. The stage 4 swan-neck deformity in the
rheumatoid is characterized by advance PIP joint destruction.

Treatment for the swan-neck deformity includes splinting
for the stage 1 deformity, and extensor mechanism reconstruction or
release of tight intrinsic muscles for the stage 2 and 3 deformities.
Arthrodesis or arthroplasty is required for the stage 4 condition. In
general, results for soft tissue reconstruction of the rheumatoid
swan-neck deformity has been disappointing while treatment with
arthrodesis has been more predictable.

Fortunately, malignancy of the hand and wrist is rare.
The most common primary malignant bone tumor of the hand and wrist is
the chondrosarcoma. The chondrosarcoma often develops in relationship
to a preexisting enchondroma, particularly enchondromas associated with
Ollier’s disease. Osteosarcoma is seen less frequently in the hand by
comparison to the lower extremities and is typically seen in an older
population than the classic young adult presentation. Radiation
exposure has been suggested as a possible cause for osteosarcoma
development in the hand. Metastatic tumors to the hand may present as
the original presentation of a previously undiagnosed cancer. The most
common metastatic tumor to the hand is lung and the most common site is
the distal phalanx. Other reported primary sites include the esophagus,
colon, breast, ovary, prostate, bladder, uterus, and thyroid. In one
study, there was only a 6-month average life expectancy of patients
with tumors metastatic to the hand. The most common soft tissue
sarcomas of the hand and upper extremity is the epithelioid sarcoma,
the malignant fibrous histiocytoma (MFH), and the synovial cell
sarcoma. The epithelioid sarcoma is often misdiagnosed at original
presentation leading to delays in treatment. Synovial cell sarcoma
presents associated with the synovial joints of the wrist. They are
slow growing and may go undiagnosed for years. MFH is becoming
increasingly more recognized in the hand, particularly in older adults.
It is often painless, also leading to original misdiagnosis and
treatment delays. Treatment for bone and soft tissue sarcomas are wide
tumor resection and limb salvage reconstruction. Adjuvant chemotherapy
and external beam radiation may prolong survival, depending on the
histologic diagnosis and grade of the tumor.

Vascular insufficiency of the hand and wrist may arise
as result of penetrating trauma, repetitive trauma, primary vasospastic
disease (Raynaud’s disease), or vasospastic disease secondary to
another disorder (Raynaud’s phenomena). Whatever the cause, patients
complain of color changes of the digits anywhere from pale white to
bluish purple. They often experience pain and particularly cold
intolerance. In some advanced conditions, fingertip soft tissue
necrosis may result. Important information to be gained from the
patient is any history of smoking, penetrating or blunt trauma,
repetitive trauma, or excessive occupational vibration exposure. Also,
the examiner should query the patient for a history of malignancy,
blood dyscrasias, or any other hypercoagulable condition. Physical
examination should include an Allen’s test, which assesses the patency
of both the radial and ulnar arteries. In this test, the examiner
occludes both arteries at the wrist and then has the patient
repetitively make a fist in an effort to remove blood from the palm.
Sequentially, the examiner releases pressure from one of the arteries
while continuing to occlude the other. The return of capillary refill
to the palm of the hand is then assessed. The test is then repeated for
the

other
artery. The test can also be performed using a Doppler probe.
Symptomatic, chronic vascular insufficiency of the hand warrants a
workup that includes an upper extremity arteriogram and includes images
of the aortic arch and subclavian arteries. The arteriogram is obtained
to rule out the presence of vascular occlusion anywhere in the vascular
system of the upper extremity. Additionally, an echocardiogram is
obtained to rule out mural thombi in the ventricles of the heart. Other
testing includes the use of noninvasive vascular studies such as
color-duplex imaging, cold immersion testing, and magnetic resonance
angiography.

A primary vasospastic disorder of the digits in which
symmetric discoloration of the digits occur, primarily in females under
the age of 40 is known as Raynaud’s disease. These patients seldom
experience any trophic changes of the digits and have no clinical
evidence of occlusive arterial disease or connective tissue disorder.
The diagnosis is established following 2 years of symptoms.
Alternatively, secondary vasospastic conditions resulting from such
conditions as connective tissue disorders (including scleroderma,
rheumatoid arthritis, systemic lupus erythematosus, vasculitis, and
CREST syndrome), occlusive arterial disease, hematologic disorders, and
occupational trauma is referred to as Raynaud’s phenomena. Patients
developing Raynaud’s phenomena, are typically over age 40, have some
underlying disease, and often experience progressive trophic changes of
the digits. Raynaud’s phenomena is seen in approximately 80% of
patients with scleroderma, 25% of patients with systemic lupus
erythematosus, and 10% of patients with rheumatoid arthritis. Initial
nonoperative treatment of Raynaud’s phenomena includes oral calcium
channel blockers and axillary sympathetic blocks. Anticoagulation
therapy may also have some merit. Patients with continued symptoms but
a favorable response to axillary sympathetic blocks may be good
candidates for peripheral arterial sympathectomy.

Buerger’s disease (thromboangiitis obliterans) is an
inflammatory vascular occlusive disorder related to the use of
nicotine. The condition is more common in men. In these patients,
narrowing of the digital arteries generally occurs resulting in
ischemic finger pain and Raynaud’s phenomena. Smoking cessation arrests
the progression of the disease in most instances.

Hypothenar hammer syndrome is the result of chronic
repetitive trauma to the ulnar side of the wrist, resulting in
thrombosis of the ulnar artery and Raynaud’s phenomena. These patients
often have engaged in activities such as drywall hanging, carpentry, or
other construction activities. In some instances, patients will give a
dramatic history of how they have used the ulnar border of the wrist as
a “hammer” to secure or stabilize objects. These patients often
complain of coldness in the digits, color changes, or frank pain while
engaged in certain occupational maneuvers. Arteriogram shows an ulnar
artery devoid of flow and in many instances markedly diminished or
absent blood flow to the ring and small digits (Figure 14-17).
Treatment in symptomatic individuals requires resection of the
thrombosed ulnar artery segment and superficial palmar arch
reconstruction using a reverse flow vein graft, normally harvested from
a dorsal foot vein. Following ulnar artery reconstruction, symptoms of
ring and small finger ischemia can be expected to improve.