Hand and Wrist Surgery - part 4 pptx

V A S C U L A R D I S O R D E R S
162
Host factors also influence the prognosis of extravasation injuries. Advanced age,
immune compromise, nutritional deficits, steroid dependency, and preexisting pe-
ripheral vascular disease are all common host factors that can greatly amplify the
damage caused by any given extravasation event.
Remember that the mainstay of conservative management is elevation, use of a
cool compress, and a loosely wrapped splint to protect and rest the injured part. Al-
though it may seem obvious, make sure that the offending intravenous catheter is
removed so that no more agent can extravasate, and make sure that the affected ex-
tremity is not further compromised by tight circumferential items such as jewelry,
hospital identification bracelets, or tight bandages. Application of heat to the af-
fected area often makes the local swelling much worse and should be avoided. Mark
the affected area of the limb with an ink marker so that improvement or worsening
can be easily noted as time passes. Save whatever intravenous equipment and drug
bags are present initially so that the offending agent and circumstances of extravasa-
tion can be clearly and thoughtfully assessed. Injection of antidote material into the
affected area may be occasionally indicated for specific cases (i.e., hydrofluoric acid
or powerful vasoconstrictor extravasations), but in most cases such injections
should be avoided because they will only increase local tissue pressures, increase the
likelihood of tissue death or vascular compromise, and inconsistently reach the of-
fending agent.
Surgical intervention is an immediate requirement if compartment syndrome or
compromise of a major vessel is present. Surgical drainage and decompression of an
extravasation injury is also helpful if large volumes of agent are involved, or if the
offending agent is a vesicant and the necrosis interval has not yet expired. Once this
interval has passed, surgical intervention may be better delayed until clear demar-
cation of dead tissue has occurred. After thorough debridement of dead tissue, flap
coverage or other complex reconstructive procedures may be warranted based on
the size of the remaining soft tissue defect.

Nonsurgical Management
This patient presented with a severe, acute left forearm compartment syndrome.
All circumferential appliances and intravenous lines were removed from the affected
extremity, including the blood pressure cuff, hospital identification bracelet, and
20-gauge angiocatheter. This situation represented a surgical emergency, and all
other immediate care required operative intervention.
Surgical Management
The patient was taken to the operating room immediately for emergency fas-
ciotomies. A dorsal, longitudinal incision was made from the lateral epicondyle to
the mid-carpus, and the dorsal forearm fascia was completely released. A palmar
incision was then performed, from the antecubital region to the mid-palm in the
hand. The lacertus fibrosus was released, as well as the entire volar forearm fascia.
The deep volar compartment was also explored and the fascia overlying the deep
volar muscle layer was released. Distally, a carpal tunnel release was also performed
(Figs. 26–4 and 26–5).
Upon release of these compartments, ~250 cc of clear fluid was drained from the
wounds. Laboratory analysis of this fluid suggested it was a mixture of plasma and
E X T R A V A S A T I O N I N J U R I E S
163
Figure 26–4. The palmar surface of the left forearm immediately
following fasciotomy.
electrolyte solution. Neither the dorsal nor palmar forearm and wrist incisions
could be closed primarily and no attempt was made to do so.
Postoperative Care
The patient returned to the operating room multiple times over the next 3 weeks
for wound debridements. After the swelling subsided and the wounds were stable,
meshed full-thickness skin grafts were applied for soft tissue coverage.
Analysis of Case
In the case history presented, the patient suffered a major extravasation injury from
electrolyte solution intended to replace lost volume from bleeding. Several factors

made this extravasation injury particularly severe. First, the patient had epinephrine
infused with the electrolyte solution, which as an extravasant acted as a local vaso-
constrictor and greatly worsened local ischemia. Second, because the patient was
obtunded, recognition of the injury was significantly delayed and the patient de-
veloped a compartment syndrome, probably due both to the amount of fluid ex-
travasated as well as to the vasoconstrictive nature of the agent. Third, the presence
of constrictive devices around the extremity also contributed in some fashion to
the severity of injury. Not only did the patient have a hospital identification band
wrapped tightly around her wrist, the frequent blood pressures that were taken with
an automatic cuff situated at the upper left arm may also have restricted venous out-
flow and added to congestion in the extremity. It is also noteworthy that an infusion
pump was used, which can produce dramatic extravasation effects by forcing fluid
into the extremity. All of these factors can add up and produce a more severe injury
than would have otherwise occurred with intravenous fluid extravasation.
This case also illustrates that the presence of peripheral pulses does not exclude a
compartment syndrome or suggest that severe local soft tissue injury is not present.
Furthermore, although it may seem obvious, the infusion should be turned off and
the intravenous catheter removed immediately once a potential extravasation prob-
lem has been identified. Of note in this case presentation is that the patient may have
received a significant additional amount of electrolyte and epinephrine solution for
Figure 26–5. The dorsal surface of the left forearm immediately
following fasciotomy.
V A S C U L A R D I S O R D E R S
164
some period of time after abnormality first presented in the left forearm because no
one bothered to turn off the intravenous line and move it to another location.
Suggested Readings
Benson LS, Sathy MJ, Port RB. Forearm compartment syndrome due to automated
injection of computed tomography contrast material. J Orthop Trauma 1996;10:
433–436.

Bowers DG, Lynch JB. Adriamycin extravasation. Plast Reconstr Surg 1978;61:
86–92.
Brown AS, Hoelzer DJ, Piercy SA. Skin necrosis from extravasation of intravenous
fluids in children. Plast Reconstr Surg 1979;64:145–150.
Gault DT. Extravasation injuries. Br J Plast Surg 1993;46:91–96.
Larson DL. What is the appropriate management of tissue extravasation by anti-
tumor agents? Plast Reconstr Surg 1985;75:397–402.
Linder RM, Upton J, Osteen R. Management of extensive doxorubicin hydro-
chloride extravasation injuries. J Hand Surg 1983;8:32–38.
Loth TS, Eversmann WW. Extravasation injuries in the upper extremity. Clin Orthop
1991;272:248–254.
Loth TS, Eversmann WW. Treatment methods for extravasations of chemothera-
peutic agents: a comparative study. J Hand Surg 1986;11A:388–396.
Loth TS, Jones DEC. Extravasations of radiographic contrast material in the upper
extremity. J Hand Surg 1998;13A:407–410.
Luedke DW, Kennedy PS, Rietschel RL. Histopathogenesis of skin and subcuta-
neous injury induced by Adriamycin. Plast Reconstr Surg 1979;63:463–465.
Mabee JR, Bostwick TL, Burke MK. Iatrogenic compartment syndrome from hyper-
tonic saline injection in Bier block. J Emerg Med 1993;12:473–476.
Scuderi N, Onesti MG. Antitumor agents: extravasation, management, and surgical
treatment. Ann Plast Surg 1994;32:39–44.
Seyfer AE. Injection and extravasation injuries. In: Hand Surgery Update. Rose-
mont, IL: American Academy of Orthopaedic Surgeons; 1996:405–411.
Seyfer AE. Upper extremity injuries due to medications. J Hand Surg 1987;12A:
744–750.
Seyfer AE, Solimando DA. Toxic lesions of the hand associated with chemotherapy.
J Hand Surg 1983;8:39–42.
Stanley D, Conolly WB. Iatrogenic injection injuries of the hand and upper limb.
J Hand Surg 1992;17B:442–446.
Section VI

Contractures
Dupuytren’s Contracture
Jack Abboudi and David S. Zelouf
Stiff Joints
Shelly M. Sailer
D U P U Y T R E N ’ S C O N T R A C T U R E
167
PEARLS
• The tabletop test is positive
when the patient cannot
place his or her open hand
flap onto a table surface due
to flexion contractures. This
finding may prompt considera-
tion for surgical treatment.
• Counsel patients with early dis-
ease as to your indications for
operative treatment. This may
help the patient seek reevalu-
ation at an appropriate point
for surgery before severe con-
tractures form.
• MP contracture correction
tends to produce more satisfy-
ing results than PIP correction.
• Cleland’s ligaments, the deep
transverse metacarpal liga-
ment, and the flexor tendon
sheath are not involved in the
disease.

PITFALLS
• Procedures performed by
“limited exposure” still require
adequate visualization of the
neurovascular structures that
may be displaced from their
normal location.
• Neurovascular structures may
be displaced superficially and
toward the midline of the digit
by the spiral cord and should
not be assumed to be in their
anatomic position. Generally,
tracing the neurovascular
structures is easier in a proxi-
mal to distal direction starting
just distal to the transverse
carpal ligament.
• Neurovascular structures are
displaced more toward the
midline and more superficial
with increasing PIP contracture.
27
Dupuytren’s Contracture
Jack Abboudi and David S. Zelouf
History and Clinical Presentation
A 51 year-old right hand dominant construction supervisor presented with a 2- to
3-year history of a progressive right ring finger contracture. He denies a history of
trauma. He is of Scottish descent, and his father has undergone bilateral Dupuytren’s
contracture releases. The patient denies a history of diabetes or other medical ill-

nesses, and he is taking no medications.
Physical Examination
A prominent cord is noted in the palm in line with the ring finger extending to the
level of the proximal interphalangeal (PIP) flexion crease. There was a prominent
nodule present over the palmar aspect of the proximal phalanx, with a 60-degree
metacarpophalangeal (MP) contracture and a 10-degree PIP contracture (Fig. 27–1).
The left hand exhibited early palmar disease with no contracture. No knuckle pads
were noted, and there was no involvement of the plantar surfaces of the feet.
Radiographic Findings
Plain x-rays of the right hand were unremarkable.
Differential Diagnosis
Dupuytren’s contracture
Joint flexion contracture
Scar contracture
Flexor tendon bowstring
Tendon adhesions
Tumor (i.e., fibrosarcoma)
Figure 27–1. Preoperative
clinical photo.
C O N T R A C T U R E S
168
Diagnosis
Dupuy tren’s Cont rac ture
Dupuytren’s disease has been attributed to genetic lines of Viking heritage and
northern European lineage with an autosomal-dominant pattern of inheritance.
The condition presents most frequently in males and after the age of 40. Clinical
features include painless palmar pitting, cords, and nodules frequently in line with
the small and ring finger. Many structures, described as “ligaments” and “bands” in
their normal state, are referred to as “cords” in the diseased state (Fig. 27–2). The
spiral cord is a continuum of the diseased spiral band, lateral digital sheet, and

Grayson’s ligament. The spiral cord is pulled to the midline with contracture, caus-
ing the neurovascular bundle to wrap around the straightening and tightening cord.
The natatory cord can be palpated in the web space, and its contracture deviates the
digit from the midline at the MP joint. See the suggested readings, later, for more
comprehensive descriptions of the pathoanatomy. Disease progression generally
leads to characteristic flexion deformities of the MP and the PIP joint. Associated
findings include dorsal knuckle pads (Garrod’s nodules), thickening of plantar tis-
sue in the foot (Lederhose’s disease), and penile fascia (Peyronie’s disease).
Indications for surgical correction of Dupuytren’s contracture depend greatly on
the impact of the deformity on the patient’s ability to perform activities of daily liv-
ing and the ability and willingness of the patient to participate in the postoperative
rehabilitation. Hard-and-fast, objective surgical indications are difficult to define.
The “tabletop test” provides the earliest sign of significant flexion contracture, al-
though this test alone is not always an indication for surgery. The test is positive
when the patient cannot fully flatten his or her hand against a table surface. Gener-
ally, flexion deformities of the MP joints are better tolerated by the patient and are
relatively easier to correct, as MP flexion is a relatively “safe” position that maintains
A B
Figure 27–2. Anatomy of normal (A) and contractured (B) digits.
D U P U Y T R E N ’ S C O N T R A C T U R E
169
collateral ligament length. On the other hand, PIP deformities interfere more with
hand function and are more difficult to correct, as PIP flexion is a relatively “unsafe”
position that allows for volar plate contracture. Therefore, PIP flexion deformities
are stronger indications for surgery at earlier stages than are MP deformities.
At the microscopic level, Dupuytren tissue demonstrates an abundance of normal
fibroblastic and myofibroblastic cells. The local abundance of these cells explains
some of the other molecular findings attributed to Dupuytren tissue such as in-
creased amount of type III collagen. The fibroblastic and myofibroblastic prolifera-
tion has been localized around occluded microvessels, and seems to be a cellular

response to local tissue ischemia. This may explain the association of Dupuytren’s
contracture with conditions that predispose to tissue ischemia, such as alcohol use,
smoking, and age.
The myofibroblasts share cellular characteristics between fibroblasts and smooth
muscle cells and are concentrated within the palmar nodules. The contractile ele-
ments of this cell type produce a progressive pull through the Dupuytren cords
that leads to the characteristic flexion deformity. Residual myofibroblasts within
the dermis and epidermis after surgical excision of diseased tissue have been impli-
cated in the recurrence of the contracture. This notion is supported by the lower
recurrence rate seen with palmar skin excision and full-thickness skin grafting after
fasciectomy.
Surgical Management
The patient was treated with a subtotal palmar and digital fasciectomy. He was
brought to the operating room where, under axillary anesthesia, Brunner incisions
were utilized to expose the pretendinous cord (Fig. 27–3). An early spiral cord was
encountered at the level of the PIP joint. After both neurovascular bundles were
identified and protected, the involved palmar fascia was excised and sent to the
pathology laboratory for gross and histologic analysis. At the conclusion of the pro-
cedure, complete correction was obtained at both the MP and PIP joints. The
tourniquet was deflated prior to closure, and brisk capillary refill was noted imme-
diately. The wounds were closed with interrupted 5–0 nylon sutures, and a short
arm plaster splint was placed, immobilizing the MP joints in 30 degrees of flexion,
with the PIP joints comfortably extended.
Figure 27–3. Intraopera-
tive photo demonstrating
pretendinous cord.
C O N T R A C T U R E S
170
Postoperative Management
A follow-up examination was done on the third postoperative day, at which time

the patient’s dressing was removed. Inspection revealed minimal swelling, with well-
vascularized flaps. A light dressing was applied and occupational therapy was insti-
tuted with a certified hand therapist, consisting of active, active assisted, and passive
range-of-motion exercises. A resting night splint was fashioned with the ring finger
in full extension, to be worn for 3 months. A follow-up visit at 3 months revealed an
excellent early result, with full correction, and full flexion (Fig. 27–4).
Alternative Methods of Management
There are no proven nonoperative modalities that can reverse or even halt the devel-
opment of cords, nodules, and contractures. A significant number of patients develop
progression of their flexion contractures and involvement of other digits, although the
risk and the rate of progression are variable and difficult to predict. There are reports
of rare cases of disease regression. Therefore, the unpredictable natural history of this
disease may present a sense of “efficacy” to some patients who try nonoperative
modalities, and they should at least be counseled accordingly. The future may hold
promise for the treatment of Dupuytren’s contracture with collagenase injections into
the diseased cords, and such protocols are currently under investigational study.
Historically, radical palmar fasciectomy was performed as an attempt to rid the
patient of all diseased tissue. However, recurrences were still noted, and this proce-
dure has fallen out of favor due to associated wound complications and patient
morbidity.
Segmental fasciectomy has been described as a method of correcting the flexion
contracture with segmental excision of diseased tissue through multiple incisions.
Full-thickness skin grafting at these multiple incisions can theoretically prevent recur-
rence at those sites and provide “fire breaks” against full-length cord recurrence. Skin
grafting techniques can also be done in conjunction with standard partial fasciectomy.
Fasciotomy can be performed through a limited exposure to release the cords and
provide correction of the contracture. This procedure does not attempt removal of
diseased tissue; however, it does provide a method for contracture correction in the
debilitated patient.
A B

Figure 27–4. Three-month clinical follow-up demonstrating full extension (A) and flexion (B).
D U P U Y T R E N ’ S C O N T R A C T U R E
171
Severe or recalcitrant deformities can ultimately be treated with amputation or
ray resection. In such cases, all involved palmar skin should be excised and free skin
grafting or dorsal skin should be used for flap closure if needed. Corrective os-
teotomies that change the arc of motion to a more functional zone and joint fusions
have been utilized in problem cases as well.
Correction of the contracture changes the lay of the palmar skin and may present
areas not amenable to direct closure of the original incision lines. Different incisions
and techniques related to wound closure have been described, and the surgeon
should be familiar with each one and understand how to utilize them as the need
arises.
Generally, a standard Brunner zigzag incision is used for less severe contractures,
and can be closed in V-Y fashion for added coverage. The transverse limb of the
V-Y closure can be left open to relieve skin tension. In more severe contractures, a
straight incision in line with the ray of the digit can be divided into multiple
Z-plasty angles to provide exposure and to increase palmar skin length at closure.
Ultimately, the finger can be flexed to gain direct closure, and small parts of the in-
cision over the finger can be left to granulate, provided there is no direct exposure of
bone, tendon, or neurovascular structures.
There is extensive literature about an “open palm” technique that leaves the pal-
mar part of the incision open to gain length. After surgery, the wound is cared for
with daily dressing changes and closes via wound contracture over 3 to 5 weeks.
Some have used the “open palm” technique routinely, and report a lower complica-
tion rate and better motion with this technique.
Complications
Although most of the complications related to Dupuytren’s contractures are related
to the surgical treatment of the disease, prolonged nonsurgical treatment of this
condition can allow for severe contracture formation that makes salvage of the digit

difficult if not impossible. Surgical complications of Dupuytren’s contracture fa-
sciectomy are numerous, and many can be avoided or minimized with meticulous
surgical technique.
Vascular compromise of the digit is an immediate concern at the time of surgery.
Meticulous technique and fine dissection of the neurovascular bundles prevent
iatrogenic injury to those structures. Once the fasciectomy is complete, the tourni-
quet should be deflated. Vascular refill of the operated digits may lag behind the
other digits, but should be normal within a few minutes. If, after observation, the
finger is still blanched, flexion of the digit relieves tension from the neurovascular
bundles that may have shortened with longstanding Dupuytren’s contracture. In
such a situation, the digits need not be splinted in extension, as MP and PIP exten-
sion can be addressed with gradual postoperative therapy. Vasospasm may compro-
mise vascular flow and can be alleviated by bathing the vessels with warm saline
solution or with plain lidocaine.
Hematoma formation can be minimized with meticulous hemostasis once the
tourniquet is deflated after fasciectomy. Penrose drains can be placed as wick-type
drains at multiple points along the closure. Some have advocated use of suction
drainage that can be removed in the recovery room prior to discharge or at an early
postoperative visit. The “open palm” technique provides a large surface for drainage,
and hematoma formation is minimized with this technique.
C O N T R A C T U R E S
172
Skin sloughing is a concern due to the multiple thin flaps developed during the
exposure. When designing the initial incision, the surgeon should survey the topog-
raphy of the palmar skin for any particularly adherent areas. The dissection of these
areas generally renders the skin particularly thin, and should not be planned at the
base of the flaps where they may compromise the vascular supply of the whole flap.
Rather, the incision should be planned through these troublesome spots.
Loss of flexion can occur after Dupuytren’s contracture release, and can signifi-
cantly restrict maximal grip strength, especially when involving the ring and small

fingers. Preoperatively, virtually all patients with Dupuytren’s contractures have full
flexion of the involved digits, barring any other underlying pathology. Postopera-
tively, the surgeon and patient are both quite focused on restoration of extension
and should also be vigilant regarding maintenance of flexion.
Recurrence of disease and extension of the disease to other digits are common after
primary surgical treatment of Dupuytren’s contractures, and patients should be
counseled about this preoperatively. These patients tend to present at a younger age
with multiple digit and bilateral hand involvement. Surgical treatment of this sub-
group is plagued with technical difficulties, higher recurrence rates, and prolonged
postoperative recovery.
Reflex sympathetic dystrophy has been reported in less than 10% of patients and re-
quires prompt diagnosis and treatment.
Suggested Readings
Badalamente MS, Hurst LC. The biochemistry of Dupuytren’s disease. Hand Clin
1999;15:35–42.
Benson LS, Williams CS, Kahle M. Dupuytren’s contracture. J Am Acad Orthop
Surg 1998;6:24–35.
Boyer MI, Gelberman RH. Complications of the operative treatment of Dupuytren’s
disease. Hand Clin 1999;15:161–166.
Burge P. Genetics of Dupuytren’s disease. Hand Clin 1999;15:63–71.
Crowley B, Tonkin MA. The proximal interphalangeal joint in Dupuytren’s disease.
Hand Clin 1999;15:137–147.
Elliot D. The early history of Dupuytren’s disease. Hand Clin 1999;15:1–19.
Hurst LC. Dupuytren’s fasciectomy: zig-zag plasty technique. In: Blair WF, ed.
Techniques in Hand Surgery. Baltimore: Williams & Wilkins; 1996:519–532.
Hurst LC, Badalamente MA. Nonoperative treatment of Dupuytren’s disease.
Hand Clin 1999;15:97–107.
Jabaley ME. Surgical treatment of Dupuytren’s disease. Hand Clin 1999;15:109–126.
Lubahn JD. Dupuytren’s fasciectomy: open palm technique. In: Blair WF, ed. Tech-
niques in Hand Surgery. Baltimore: Williams & Wilkins; 1996:508–518.

Lubahn JD. Open-palm technique and soft-tissue coverage in Dupuytren’s disease.
Hand Clin 1999;15:127–136.
Mullins PA. Postsurgical rehabilitation of Dupuytren’s disease. Hand Clin 1999;15:
167–174.
D U P U Y T R E N ’ S C O N T R A C T U R E
173
Rayan GM. Clinical presentation and types of Dupuytren’s disease. Hand Clin
1999;15:87–96.
Rayan GM. Palmar fascial complex anatomy and pathology in Dupuytren’s disease.
Hand Clin 1999;15:73–86.
Ross DC. Epidemiology of Dupuytren’s disease. Hand Clin 1999;15:53–62.
Tomasek JJ, Vaughan MB, Haaksma CJ. Cellular structure and biology of Dupuytren’s
disease. Hand Clin 1999;15:21–34.
Tubiana R. Dupuytren’s disease of the radial side of the hand. Hand Clin 1999;
15:149–159.
Yi IS, Johnson G, Moneim MS. Etiology of Dupuytren’s disease. Hand Clin 1999;
15:43–51.
C O N T R A C T U R E S
174
PEARLS
• Static-progressive and serial
static splinting are very useful
for resolving contractures with
a “hard” end feel.
• Dynamic splinting is most use-
ful i n resolving contractures
with a “soft” end feel.
PITFALLS
• Dynamic splinting forces are
difficult to control, leading to

poor splint compliance.
• Dynamic splinting can cause
inflammation of tissues when
tension is placed too high.
• Static splints do not allow for
active motion while splinted,
possibly contributing to tendon
adhesions.
Figure 28–1. Anteroposterior (AP)
view of the initial injury demonstrates
complete amputations of the index
and small fingers and near amputa-
tions of the long and ring fingers.
28
Stiff Joints
Shelly M. Sailer
His tory and Clinical Presentati on
A 44-year-old right hand dominant cabinet maker presented to the emergency
room after accidentally cutting the fingers of his right hand with a table saw.
Phy sical Examination
The patient completely amputated his index finger through the middle phalanx just
distal to the proximal interphalangeal (PIP) joint and his small finger through the prox-
imal phalanx. The long and ring fingers were lacerated from the volar aspect through
the flexor tendons and distal aspect of the proximal phalanges, but were held on by dor-
sal skin bridges. They were both avascular and insensate. The amputated portions of
the index and small fingers were retrieved, but they were severely mangled and not
amenable to replantation. He was taken to the operating room for immediate surgical
management.
Dia gnostic Studies
Initial radiographs revealed traumatic amputation of the index finger through the

middle phalanx, ring finger at the proximal phalanx, and small finger at the proxi-
S T I F F J O I N T S
175
Figure 28–2. Oblique view of the
initial injury.
mal phalanx, and a unicortical defect of the long finger at the proximal phalanx
(Figs. 28–1 and 28–2).
Postoperative C-arm images demonstrate two Kirschner wires (K-wires) anatomi-
cally reducing the ring finger proximal phalanx fracture and extending through the
PIP joint (Fig. 28–3).
Radiographs taken 8 weeks postoperatively demonstrate union of the ring finger
fracture and complete closure of the unicortical defect of the middle finger.
Figure 28–3. Postoperative
C-arm image demonstrates
fixation of the ring finger
fracture.
C O N T R A C T U R E S
176
Figure 28–4. A metacarpopha-
langeal (MP) blocking splint used
to facilitate active motion at the
interphalangeal joints.
Surgical Management
The ring finger proximal phalanx level amputation was stabilized with two 0.045-
inch crossed K-wires placed across the fracture site. Distally the pins extended
through the PIP joint to provide better fixation of the short remaining distal frag-
ment of the proximal phalanx. Despite near amputation, the long finger proximal
phalanx fracture was found to be stable and did not require fixation. On both the
ring and long fingers, the flexor digitorum profundus (FDP) tendons were repaired
and the flexor digitorum superficialis (FDS) tendons were tenodesed to the FDP

tendons. The radial and ulnar digital arteries and nerves were repaired. The extensor
mechanism was intact in both long and ring fingers. Revision amputations of the
index and small fingers were performed.
A second surgery was ultimately required to regain full active range of motion.
Five months after the initial injury this patient underwent a flexor tenolysis to the
middle and ring fingers after passive range of motion was restored and the scars were
soft and mature.
Postoperative Management
Two weeks after initial surgery, the patient was referred to hand therapy to begin
active motion of the thumb and wrist and only metacarpophalangeal (MP) motion
of the fingers. The MP joints were stiff initially, flexing only 50 degrees, but pro-
gressed to 80 to 100 degrees within 4 weeks. Desensitization activities and com-
pressive wraps were initiated for the index and small finger amputations. The volar
wounds of the ring and long finger were slow to heal, but they finally healed by
6 weeks postoperatively.
This case was complicated by the development of cellulitis in the ring fin-
ger 8 weeks postoperatively, which necessitated removal of the two percutaneous
K-wires, and a short course of IV antibiotics followed by oral antibiotics. After the
K-wires were removed, it was determined that the proximal phalanx fractures were
stable enough to tolerate motion at the interphalangeal joints of the long and ring
fingers. It was at this time that the severely stiff interphalangeal joints, the intrinsic
tightness, and the lack of active flexor tendon function were brought to the fore-
front as a therapy challenge.
Only 10 degrees of passive motion at the PIP joints was achieved on the first
day of mobilization and was slow to improve with range-of-motion exercises
S T I F F J O I N T S
177
Figure 28–5. A static-
progressive finger flexion
splint used to impart low-

load, long duration stress to
lengthen shortened tissues.
alone. There was no active PIP or distal interphalangeal (DIP) flexion as the
patient was now consistently contracting the lumbricals, which flexed the MP
joints and extended the PIP joints. He could not isolate use of the FDS and
FDP muscles as he had not used them functionally for weeks and they were
adherent at the digit level. An MP blocking splint, which facilitated flexion at
the PIP joints, was fabricated to retrain use of the long flexors (Fig. 28–4). A
biofeedback unit was used to assist in training the patient to contract the long
flexors and relax the lumbricals. Even though the patient had very little active
motion, due to adhesions on the long flexors, it was important to maintain mus-
cle strength and preserve independent function in preparation for a flexor tenol-
ysis when appropriate.
A static-progressive finger flexion splint was fabricated for the long and ring
fingers (Fig. 28–5). Wearing time was increased slowly, monitoring for any exten-
sion lag. After 2 weeks, the patient had gained 30 degrees of PIP flexion, and had
maintained full PIP extension. Wearing time was then increased to overnight (up
to 8 hours) and range of motion steadily improved.
By 4 months postinjury, the patient had nearly full passive PIP and DIP flexion,
but only 30 degrees of active PIP flexion and 0 degrees at the DIP joints. A flexor
tenolysis was required at 5 months postoperatively to restore active flexion. Imme-
diate active motion was performed, and as postoperative edema decreased and the
wounds healed, he was able to actively flex the middle and ring fingers to touch the
palm (Fig. 28–6). This amount of flexion was adequate to grasp most objects for
activities of daily living and tools for work.
Figure 28–6. Final outcome
demonstrating excellent com-
posite flexion of fingers.
C O N T R A C T U R E S
178

Figure 28–7. Static-
progressive splinting is also
used on larger joints such as
the wrist.
He returned slowly to his job as a cabinet maker after a course of strengthening
and reconditioning. Some of his tool handles were adapted for improved grasp and
custom gloves were required to accommodate the amputated digits.
Dia gnosis
Passive range-of-motion loss is the result of trauma and subsequent immobilization.
Adaptive shortening of tissues and scar formation are the main sources of loss of
joint flexibility and stiffness. All of these concepts apply in this case of near amputa-
tion with fractures and tendon lacerations. Besides exercises and stretching, several
splinting techniques are available to provide prolonged stretch of shortened tissues.
Splinting maintains the tissue elongation gained during therapy, home exercise pro-
grams, and functional use of the hand. Brand theorizes that the application of me-
chanical stress via splinting signals contracted tissue to “grow” or add cells while the
body absorbs redundant tissue.
Personal clinical experience and several studies have supported the use of low-load
prolonged stress to apply load and stress to achieve permanent length changes in tissue,
thereby increasing passive range of motion. Static-progressive splinting employs static
positioning of a joint at the end range, at low tension for periods of time adequate to en-
act lengthening or growth of shortened tissues (Figs. 28–5 and 28–7). Because the com-
ponents used in static-progressive tension lack the elasticity of those used in dynamic
splinting, the appropriately set tension of the splint does not continue to stress the tis-
sue beyond its current maximum length limit. It is well tolerated over long periods of
time–overnight, for example. It is especially important with revascularized digits that
tension be applied in a controlled fashion so as not to compromise blood flow. With the
splint components used in this case, tension could be altered for comfort and vascu-
lar status, in minute degrees via the MERIT static-progressive component (UE TECH,
Edwards, CO). A comfortable, well-tolerated splint with patient-controlled tension is

typically able to produce the necessary elongation of adaptively shortened tissues,
thereby regaining passive range of motion lost via trauma, immobilization, and scarring.
Alterna tiv e Met hods of Management
There are alternatives to the splinting program used to overcome stiff PIP joints.
Table 28–1 describes the specific features of each and the advantages and disadvan-
S T I F F J O I N T S
179
Table 28–1 Alternative Methods of Management
Type of Management Advantages Disadvantages
Dynamic splinting: uses self-adjusting
resilient components such as rubber
bands, springs or elastic line to create
the mobilizing force.
Exerts tension upon one or more joints
moving into ever increasing passive
range of motion.
Useful in resolving contractures with
“soft” end feel.
Serial static splinting/serial casting:
Statically positions joint near end of its
elastic limit.
Useful in resolving contractures with
“hard” end-feel.
Static-progressive splinting:
Involves the use of inelastic
components such as Velcro tabs,
progressive hinges, or screws to
statically position joint(s).
Useful in resolving contractures with
“hard” or “soft” end-feel.

Maximize adhesion length in either
direction as patient can actively
move while in splint; however, this
ability to intermittently shorten
tissue thwarts the purpose of the
splint, which is to hold the joint at
end range
Allows active resistive motion in the
opposite direction of the dynamic
pull.
Well tolerated over long periods of
time because it holds tissue near the
end of its elastic limit and does not
stress beyond it.
Provides low-load, end range position-
ing, which facilitates relaxation and
lengthening of tissues.
Pressure is distributed over a large sur-
face area, which aids in comfort and
vascular flow.
Well tolerated over long periods of
time because it holds tissue near the
end of its elastic limit and does not
stress beyond it.
Provides low-load, end-range position-
ing, which facilitates relaxation and
lengthening of tissues.
Patient can make minute adjustments to
splint tension to accommodate range-
of-motion changes and for comfort.

Forces difficult to control, which can
lead to poor splint compliance and
inadequate wearing time to achieve
range-of-motion gains.
Tension of splint continues even when
tissue has reached its elastic limit,
potentially causing inflammation of
tissues.
Splint or cast must be remolded or re-
made to accommodate increases in
motion.
Active motion is unavailable at casted
joints; tendon adhesions may become
denser as patient cannot remove cast
for exercise.
Motion may be lost in the opposite
direction.
Active motion not possible in the splint.
Splint must be well made to distribute
pressure appropriately to allow long
wearing periods.
tages to consider when prescribing therapy for stiffness of any joint in the upper
extremity.
Complicat ions
Surgical complications in this case, as discussed previously, included an infection of
the ring finger at 8 weeks postoperatively and slow healing volar wounds, hindered
by the patient’s heavy smoking habit. Therapy complications included flexor tendon
adhesions, intrinsic tightness, inability to isolate lumbrical from long finger flexor
function, and PIP joint stiffness. Other potential complications include tendon rup-
ture and nonunion/malunion, but were not encountered in this case.

Suggested Readi ngs
Akeson WH, Ameil D, Avel M, et al. Effects of immobilization on joints. Clin
Orthop 1987;219:28–37.
C O N T R A C T U R E S
180
Akeson WH, Ameil D, Woo SL-Y. Immobility effects on synovial joints. The patho-
mechanics of joint contracture. Biorheology 1980;17:95–110.
Akeson WH, Ameil D, Woo SL-Y, et al. Collagen cross-linking alterations in joint
contractures: changes in the reducible crosslinks in periarticular connective tissue
collagen after nine weeks of immobilization. Connective Tissue Res 1977;5:15–19.
Ameil K, Woo SL-Y, Harwood FL, et al. The effect of immobilization on collagen
turnover in connective tissue: a biochemical-biomechanical correlation. Acta Or-
thop Scand 1982;53:325–332.
Brand PW. Clinical Biomechanics of the Hand. St. Louis: CV Mosby; 1985.
Bonutti PM, Windau JE, Abies BA, Miller FFI. Static progressive stretch to reestab-
lish elbow range of motion. Clin Orthop 1994;303:128–134.
Enneking WF, Horowitz M. The intra-articular effects of immobilization on the
human knee. J Bone Joint Surg [Am] 1972;54A:973–985.
Flowers KR, LaStayo P. Effect of total end range time on improving passive range of
motion. J Hand Ther 1994;7:150–157.
Flowers KR, Michlovitz SL. Assessment and management of loss of motion in or-
thopaedic dysfunction. In: Postgraduate Advances in Physical Therapy. Alexandria,
VA: APTA, 1988.
Light KE, Nuzik S, Personius W, Barstrom A. Low-load prolonged stretch versus
high-load brief stretch in treating knee contractures. Phys Ther 1984;64:330–333.
Schultz-Johnson KS. Splinting: a problem solving approach. In: Stanley BG,
Tribuzi SM, eds. Concepts in Hand Rehabilitation. Philadelphia: FA Davis; 1992.
Section VII
Tendon Injuries
A. Tenosynovitis

Flexor Stenosing Tenosynovitis: Trigger Finger and Thumb
Kevin D. Plancher
De Quervain’s Disease
Kevin D. Plancher
Flexor Carpi Radialis Tunnel Syndrome
Kevin D. Plancher
Flexar Carpi Ulnaris Calcific Tendinitis
Richard W. Barth
B. Tendon Repair
Acute Laceration of Flexor Tendons
Mark S. Rekant
Delayed Treatment of Flexor Tendons: Staged Tendon Reconstruction
Lawrence H. Schneider
Chronic Lacerations of Extensor Tendons
Angela A. Wang and Michelle Gerwin Carlson
Avulsions of the Flexor Digitorum Profundus
Donald M. Lewis and Randall W. Culp
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183
PEARLS
• To avoid recurrence of a trig-
ger finger, incise and excise a
part of the annular pulley.
• Early treatment and early
motion in patients with RA and
avoid releasing the A1 pulley.
• Multiple trigger fingers may be
a sign of flexor tenosynovitis
associated with RA, so avoid
releasing the A1 pulley.

PITFALLS
• To avoid nerve injury to the
thumb, utilize loupe dissection.
• Avoid releasing the A1 pulley
in patients with RA.
29
Flexor Stenosing Tenosynovitis:
Trigger Finger and Thumb
Kevin D. Plancher
His tory and Clinical Presentati on
A 45-year-old right hand dominant woman was seen in the office because her right
middle finger was stuck in her palm. She reported that her family physician gave her
an injection in that finger 6 months ago for her symptoms of clicking and pain over
the dorsal aspect of her proximal phalanx of her middle finger. She denies any symp-
toms of diabetes, rheumatoid arthritis, gout, or connective tissue disorders.
Phy sical Examination
On examination the patient actively initiated extension of her middle finger but
stopped with a short arc of motion because of pain. The patient withdrew her hand
when passive extension was attempted because of pain. The hand and all digits have
no signs of vascular compromise. The patient’s two-point sensory discrimination, as
determined by the Weber two-point discrimination test, using a dull pointed eye
caliper applied in the longitudinal axis of the digit without blanching the skin, is
within normal limits. A tender, palpable nodule is noted over the palmar surface of
the second metacarpophalangeal (MP) joint (Fig. 29–1).
Dia gnostic Studies
Anteroposterior (AP) and splay lateral radiographs reveal no osteophytes or evidence
of osteoarthritis. No soft tissue masses are noted.
Figure 29–1. A palpable mass seen
in the thumb pulley.
184

Dif ferential Dia gnosis
Tumors
Mass
Infection
Osteoarthritis with osteophytes
Trigger finger
Dia gnosis
Flexor Stenosing Tenosynovitis of the Right Middle Finger—“Trigger Finger”
The digital flexor sheath contains five discrete “annular bands” (A1 through A5 pul-
ley) (Fig. 29–2). These pulleys prevent bow-stringing of the flexor tendon and also
maximize its efficiency in relation to digital motion. Nutrition of the flexor tendon
sheath is dependent on perfusion from the surrounding tenosynovium rather than
the vincula system, which perfuses the flexor tendon distally through a small net-
work of vessels. The annular band and the tenosynovium are responsible for the
pathophysiology of trigger fingers and thumbs (Fig. 29–3).
When the normally thin flexor sheath becomes inflamed and thickened, it re-
duces the space that the tendon has to pass through. The tendon no longer glides
freely and the tendon itself may swell up in a balloon-like mass and prevent passage
of the tendon through the sheath. Forced movement at this point will drag the en-
larged portion (Fig. 29–4) of the tendon through the sheath, producing a snapping
Figure 29–2. The digital flexor sheath contains five discrete
“annular bands.”
Figure 29–3. The pathophysiology of the trigger finger.
Figure 29–4. The forced
movement drags the enlarged
portion of the tendon through
the sheath, producing a snap-
ping sensation. This is also
what can lead to the locking
of the finger.

F L E X O R S T E N O S I N G T E N O S Y N O V I T I S : T R I G G E R F I N G E R A N D T H U M B
185
sensation and may lead to locking of the finger in flexion. The first annular pulley
acts as a fulcrum about which the flexor tendon bends. This fulcrum has been pos-
tulated as causing focal tendon degeneration with sheath thickening and tendon
nodule development.
Nonsurgica l Managemen t
Conservative treatment includes modification of provocative activities in the work-
place and personal hobbies. Oral nonsteroidal antiinflammatory drugs (NSAIDs),
including cyclooxygenase (COX-II) inhibitors, and a steroid injection into the
area of primary pathology is indicated. Contraindications to injections or NSAIDs
include sensitivity to any of the materials or the presence of an infection. Using
a 27-gauge, a 1
1
⁄4-inch needle is used to inject 1.5 cc Celestone and 1.5 cc plain
Marcaine/lidocaine without epinephrine into the area of the proximal flexor sheath
and annular pulley. The needle should be placed at a 45-degree angle to the longitu-
dinal axis of the metacarpal at the proximal-most extension of the fibro-osseous
sheath, which is located just distal to the distal palmar crease (Fig. 29–5). The injec-
tion should not be forced, and if excessive force is required, then the needle should
be repositioned. Patients are encouraged to use their finger in a normal fashion after
the injection and should anticipate a decrease of triggering over the next 7 days.
Gentle manipulation by the surgeon once the digit is anesthetized will ensure that
the medication has moved proximally and distally throughout the fibro-osseous
tunnel. A successful injection is always noted when a fluid wave can be palpated
in the distal flexor sheath during the injection or when a “pop” is felt or heard with
injection of the finger. The patient attends a supervised occupational therapy pro-
gram for 6 weeks and schedules a follow-up appointment. If triggering occurs or if
the finger becomes irreducibly locked, surgical intervention is prescribed.
Surgical Management

Surgical management for a trigger finger is performed as an outpatient proce-
dure under local anesthetic. The area over the A1 pulley is anesthetized using 3 cc
of plain lidocaine solution. Limb exsanguination is maintained through an arm
tourniquet inflated to 250 mm Hg. Surgical exposure is performed through a
transverse incision at the distal palmar crease. Blunt dissection through the sub-
cutaneous fat allows exposure of the proximal portion of the fibro-osseous sheath
Figure 29–5. The injection
with the needle at 45 degrees
to the longitudinal axis of the
metacarpal at the proximal-
most extension of the fibro-
osseous sheath.