Ovid: Chapman’s Orthopaedic Surgery

Editors: Chapman, Michael W.
Title: Chapman’s Orthopaedic Surgery, 3rd Edition
> Table of Contents > SECTION
III – THE HAND > Reconstructive Procedures > CHAPTER 65 –

Richard H. Gelberman
Michael J. Botte
R. H. Gelberman: Department of Orthopaedic Surgery, Barnes Hospital, St. Louis, Missouri, 63110.
M. J. Botte: Division of Orthopaedic Surgery, Scripps Clinic, La Jolla, California, 92037.
Acute compartment syndrome produces high interstitial
tissue fluid pressures that can reduce capillary perfusion below the
level necessary for tissue viability (1,3,7,8 and 9,11,22,26,29,35,36,58,59,68,81,93,97,98 and 99). If the compartment syndrome is sustained or untreated, ischemia results in irreversible muscle and nerve damage (12,19,23,25,28,33,34,35 and 36,40,64,70,74,77,79,86,87,96).
Muscle then undergoes necrosis, fibrosis, and contracture. Concomitant
nerve injury results in further muscle dysfunction, sensibility
deficits, or chronic pain. The result is a dysfunctional limb with
varying amounts of deformity, stiffness, or paralysis, known as
Volkmann’s ischemic contracture (4,5,10,13,25,30,31 and 32,37,39,40 and 41,44,45,46,47 and 48,50,51,56,61,62,63,64,65,66,67 and 68,71,72,74,75,76,77 and 78,80,81,84,85,90,91,92 and 93,97,100,101). See Chapter 13 on Compartment Syndrome.
In 1881, Richard von Volkmann first described this
condition, noting paralysis and subsequent limb contracture that
followed the application of tight, constricting bandages to an injured
limb (93). In 1922, Brooks described a similar condition and believed venous obstruction was a factor in the contracture formation (12). Arterial spasm or injury were subsequently indicated as causes by Leriche and Griffiths (32,49). In an attempt to prevent the contracture described by Volkmann, Bardenheur in 1911 discussed the use of forearm fasciotomy (2).
His “aponeurectomy” consisted of division of the deep antecubital and
forearm fascia. In 1922, Murphy also suggested fasciotomy as a means of
prevention of paralysis and contracture when pressure was increased
within a fascia-enclosed muscle space following hemorrhage or edema (65).
Although the pathogenesis was not clearly understood, in 1926 Jepson
objectively demonstrated the beneficial effects of early fascial
decompression of injured muscle (44).
Since these early reports, several investigators have
discussed the various aspects of ischemic contracture formation and
prevention, including the need for immediate fasciotomy, and the role
of median and ulnar nerve decompression and brachial artery
exploration. The operative


technique and appreciation of surgical anatomy evolved from reports by Benjamin (3), Eichler and Lipscomb (22), Henry (38), Eaton and Green (21), Whitesides et al. (98), Newmeyer and Kilgore (66), and Gelberman (24,25,26,27 and 28).
The relationships between increased tissue fluid pressure and myoneural
dysfunction, as well as the use of fasciotomy to prevent ischemic
contracture, are now well established (1,2,3,4 and 5,7,8,9,10,11,12 and 13,19,20,21,22,23,24,25,26,27,28 and 29,33,34,35 and 36,40,41,46,50,51 and 52,58,59,63,64,78,84,86,94,98,99).

Despite the current appreciation for urgency in the
management of acute compartment syndrome, delays in treatment still
occur; these result in patients developing the full sequelae of
Volkmann’s ischemic contracture. The deficits can be devastating, and
management is challenging. Treatment can require a prolonged
rehabilitation program and/or operative management. A comprehensive
rehabilitation program includes active and passive exercises,
strengthening, splinting, desensitization, and pain management.
Operative management includes nerve decompression, infarct excision,
contracture release, myotendon lengthening, tendon transfers, or free
tissue transfers (4,5,10,13,14,15,16,17 and 18,21,22 and 23,25,30,31 and 32,37,39,40,41,42,43,44,45,46,47 and 48,50,51,53,54,55,56 and 57,60,61,62,63,64,65,66,67,68 and 69,73,74,75,76,77 and 78,80,81,82,83,84 and 85,88,89,90,91,92 and 93,95,97,100,101).
The following discussion reviews the general features of Volkmann’s
ischemic contracture, the classification of deformities, and the
methods of management.
Muscles and nerves are vulnerable to changes in oxygen
tension. Muscle undergoes necrosis after 4 hours of ischemia produced
experimentally by application of a tourniquet (33,34).
With prolonged ischemia, muscle necrosis leads to fibroblastic
proliferation within the muscle infarct. A variable amount of
longitudinal and horizontal contraction may progress over a 6- to
12-month period following the ischemic insult. The necrotic muscle
adheres to surrounding structures, fixes muscle position, and reduces
excursion and mobility. Limitation of muscle excursion may lead to loss
of joint motion with subsequent joint contracture.
Peripheral nerves in the vicinity can also be injured
from the original ischemic insult, as well as from subsequent
compression resulting from muscle fibrosis, or from the chronic stretch
of limb deformity. The developing fibrosis may surround, tether, or
impinge on adjacent peripheral nerves, leading to local compression.
Hyperflexion at the elbow or wrist can lead to secondary neuropathy of
the ulnar nerve or the median nerve, respectively. In addition to the
associated motor loss, neuropathy following ischemic contracture can
lead to paresthesias, loss of limb sensibility, and chronic pain.
The deepest compartments, especially those adjacent to
bone on the volar forearm, usually have the highest interstitial
pressure during an acute compartment syndrome (7,8,9 and 10,91,92).
Subsequent injury that leads to ischemic necrosis is most marked in
these deep compartments, more commonly involving the flexor digitorum
profundus and flexor pollicis longus (Fig. 65.1 and Fig. 65.2).
In the mildest contractures, only part of the flexor digitorum
profundus undergoes necrosis, usually to the ring and long fingers. In
severe contractures, all four digits are involved. The flexor digitorum
superficialis and pronator teres are generally less severely affected.
In the most severe cases, the wrist flexors, the wrist and digital
extensors, and the compartments proximal to the elbow may also undergo
varying degrees of fibrosis and contracture.
Figure 65.1.
The muscles affected in 16 cases of Volkmann’s contracture of the
forearm. (Adapted from Seddon HJ. Volkmann’s Contracture: Treatment by
Incision of the Infarct. J Bone Joint Surg Br 1956;38:152, with permission.)
Figure 65.2. Cross section of Volkmann’s contracture of the forearm. A: The shading represents the degree of involvement of the various muscles. The diagram is based on the data provided in Figure 65.1. B: Key to muscles. The plane of section is through the upper third of the forearm. E, EX, extensor; DIG, digiti; FL, flexor; POL, POLL, pollicis; L, longus; BREV, brevis; BR, brachio; ABD, abductor; C, carpi; R, radialis. (Adapted from Seddon HJ. Volkmann’s Contracture: Treatment by Incision of the Infarct. J Bone Joint Surg Br 1956;38:152, with permission.)
The frequent involvement of the deep flexors of the
forearm is attributed to their deep location, a factor that increases
their vulnerability to ischemia (79). These deep compartments, particularly the regions adjacent to bone, usually have the highest interstitial pressures (34).
With compression from within the compartment, the circulation to the
deep portions of the muscle belly are compromised, whereas collateral
circulation to the more superficial parts of the muscle is retained. In
the forearm, the most severe muscle damage usually occurs in the middle
third of the muscle belly, with more injury closer to bone, and less
injury toward the proximal and distal surfaces. When a compartment
syndrome remains untreated, swelling may eventually resolve, but the
injured, necrotic muscle becomes fibrotic. An ellipsoid section or cord
of cicatrix can develop within the muscle or group of muscles. The
characteristic deformity of ischemic contracture may take weeks or
months to completely develop. When the forearm, hand, and arm are
significantly involved, the deformity in the upper extremity often
consists of varying amounts of elbow flexion, forearm pronation, wrist
flexion, thumb flexion and adduction, digital metacarpophalangeal (MP)
joint extension, and interphalangeal joint flexion (Fig. 65.3).
The MP joint extension and proximal interphalangeal joint flexion give
rise to a “claw hand” deformity. The extremity may initially be
flexible, especially in milder cases. Chronic muscle imbalance and lack
of joint motion may ultimately lead to fixed deformity from secondary
joint capsule, ligament, and skin contracture.
Figure 65.3. A,B,C:
Upper extremity of a patient with severe ischemic contracture.
Unrecognized compartment syndrome developed after revascularization of
the extremity for a brachial artery injury. The deformity includes
hyperextension at the metacarpophalangeal joints and flexion at the
interphalangeal joints. The forearm muscle mass is fibrotic, with a
firm, “woody” consistency. Fixed myotendinous contractures exist that
involve the extrinsic flexor and extensor muscles. The elbow flexors
are also involved, with a fixed flexion deformity at the elbow and
associated fibrosis of the brachium. Patients with established ischemic
contracture often also show wrist flexion, forearm pronation, and
adduction or flexion of the thumb.
The pathomechanics of the ischemic claw-hand deformity
are complex. Although there may be an apparent similarity between the
ischemic contracture and the intrinsic muscle contracture in some
patients, the actual deformities are considerably different. Intrinsic
muscle contracture results in an intrinsic-plus deformity, with flexion
at the MP joints and extension at the proximal interphalangeal joints.
Volkmann’s contracture often leads to an intrinsic-minus deformity,
with hyperextension at the MP joints and flexion at the interphalangeal
joints. Although the two entities are associated and may occur
simultaneously, the resultant claw-hand deformity is determined by



of the more powerful extrinsic finger flexors. A paradoxical situation
of a claw-hand deformity with intrinsic tightness can exist (82).
The intrinsic contracture may not become apparent until the extrinsic
flexors have been released by a muscle slide, tendon lengthening, or
tenotomy. Only then does intrinsic tightness become evident.

An additional factor in the pathomechanics of upper
extremity deformity is the amount of peripheral nerve injury
superimposed on the muscle. Ischemic injury to the muscle usually
results in muscle contracture (from fibrosis of the necrotic muscle).
Nerve injury, conversely, results in muscle paralysis. Concomitant
median and ulnar neuropathy in the forearm or wrist therefore
contribute to intrinsic muscle weakness and, in turn, to an
intrinsic-minus deformity. The final clinical outcome is dependent on
the relative amount of extrinsic and intrinsic muscle contracture (from
muscle ischemia) and on the amount of extrinsic and intrinsic muscle
paralysis (from nerve injury) (9,10).
Several authors have classified contractures according to severity of involvement (4,50,63,80,91,100). The simplest classification, popularized by Seddon and Tsuge (80,91), describes mild, moderate, and severe involvement. This classification is useful for determining treatment options.
A mild or localized contracture is limited to a portion
of the deep extrinsic finger flexors, usually involving only two or
three fingers. Hand sensibility and strength are normal. The intrinsic
muscles are not involved, and fixed joint contractures are not present.
Most mild types of ischemic contracture are caused by fractures or
crush injuries to the forearm or elbow, and they usually occur in young
adults (40,91).
Moderate contracture, the classic type, primarily
involves the flexor digitorum profundus and flexor pollicis longus
muscles. Less frequently, the flexor digitorum superficialis, flexor
carpi radialis, and flexor carpi ulnaris are involved. The wrist and
thumb become flexed and the hand assumes a claw-hand deformity from
contracture of the long finger flexors.
Secondary compression neuropathies may develop at
specific locations where nerves pass beneath ligaments or fibrous
arcades or through contracted muscles. The median


is most frequently compressed, usually at the lacertus fibrosus,
pronator teres, or flexor digitorum superficialis, or within the carpal
tunnel. The ulnar nerve may be compressed within the cubital tunnel or
between the two heads of the flexor carpi ulnaris. The radial nerve is
rarely involved, but it may be compressed at the arcade of Frohse or
within the supinator muscle.

Most moderate contractures are caused by a supracondylar
fracture of the humerus. These fractures occur most commonly at 5 to 10
years of age (40,62,63,91).
Severe contractures affect forearm extensors as well as flexors (Fig. 65.3).
Complications, including loss of nerve function, malunion or nonunion
of forearm fractures, and cutaneous scarring and contracture, are often
encountered. The most common causes of severe contracture are prolonged
ischemia secondary to brachial artery injury, and prolonged external
compression secondary to drug overdose.
The treatment of mild contractures depends on the
severity of the deformity and the time interval between injury and
initiation of treatment. Contractures of the deep forearm flexors, with
normal hand sensibility and strength, may be treated conservatively.
Occupational therapy, including passive and dynamic extension
splinting, is designed to maintain wrist and interphalangeal joint
extension, to maintain or improve thumb web-space width, and to
strengthen weak thumb intrinsic muscles. Alternate the use of bivalved
pancake plaster casts or custom-molded synthetic orthoses with
low-profile digital extension, and thumb opposition splints. A C-bar
may be incorporated into the splint to maintain thumb position. In the
early stages, have the patient alternate passive and dynamic splints at
2-hour intervals during the day and, at night, wear extension splints.
Splinting techniques for Volkmann’s contracture have been described in
detail by Goldner (30). A satisfactory outcome
can be expected when mild contractures are treated soon after their
development using these techniques.
Tsuge recommends operative treatment for mild contractures that are encountered late (91,92).
If the contracture is limited to one or two digits and a cordlike area
is palpable, simple excision of the infarcted muscle or lengthening of
the involved flexor tendons is recommended.
  • Perform excision of the infarcted muscle through a curved, longitudinal incision on the palmar forearm.
  • Identify and protect the radial artery, median nerve, and ulnar artery and nerve.
  • Retract the flexor digitorum
    superficialis and flexor carpi radialis radially, and the flexor carpi
    ulnaris ulnarly, to expose the flexor digitorum profundus.
  • Isolate and excise the palpable, cordlike
    areas of indurated muscle. The flexor digitorum profundus of the ring
    and long fingers is most commonly affected.
  • If the contracture is localized to the
    pronator teres, this muscle may be excised. If the contracture and
    induration involve three or four digits, flexor tendon lengthening may
    be required.
  • Perform Z-lengthening of the involved tendons in the distal two thirds of the forearm.
  • Begin the Z-lengthening incisions
    proximally, near the musculotendinous junctions, to ensure adequate
    tendon length for satisfactory correction. Repair the tendons using 4-0
    nonabsorbable suture.
  • Following the surgery, immobilize the
    forearm in supination, the wrist in extension, and the digits in the
    corrected amount of extension.
The treatment of moderate to severe Volkmann’s contracture may be divided into four phases (25):
  • Release of secondary nerve compression
  • Treatment of contractures
  • Tendon transfers for substitution and reinforcement
  • Salvage procedures for the severely contracted or neglected forearm
Phase 1: Release of Secondary Nerve Compression
Following muscle infarct, nerves may become compressed
within a constricting cicatrix, or at specific anatomic locations where
space is minimal. Secondary compressive neuropathies require attention
in the earliest stages of treatment. Improvement of nerve function is
related to the severity and duration of compression, as nerves may
sustain compression for longer periods than muscle and still show some
reversibility, particularly in sensory function (11,79). When continuity is maintained, nerves may show signs of gradual recovery over a 12-month period (80,85).
If both fibrosis and contracture are severe, all three major forearm
nerves may become constricted. Careful clinical assessment is essential
before the first phase of treatment.
Median Nerve Decompression
Return of median nerve function is essential for
restoring a useful functional extremity. This nerve lies in the center
of the constricting cicatrix and may become compressed in four anatomic
regions: the lacertus fibrosus, the pronator teres, the proximal


of the flexor digitorum superficialis, and the carpal tunnel. Sensory
and motor loss consistent with median neuropathy warrant aggressive
management for decompression.

  • Use an incision similar to that used for decompression of an acute forearm compartment syndrome (24) (Fig. 65.4).
    Begin the incision on the palmar aspect of the medial arm, about 2 cm
    proximal to the medial epicondyle. Extend it obliquely across the
    antecubital fossa to the mobile wad. Continue the incision
    longitudinally, curving slightly ulnarly to reach the palmar distal
    forearm. Extend the incision into the palm for carpal tunnel release.
    Locate the distal portion of the incision ulnar to the palmaris longus
    to avoid injury to the palmar cutaneous branch of the median nerve.
    Figure 65.4.
    The incision used for decompression of the median nerve in the forearm
    and hand. (Adapted from Gelberman RH, et al. Decompression of Forearm
    Compartment Syndromes. Clin Orthop 1978;134:225, with permission.)
  • Identify the median nerve in the proximal
    portion of the incision and trace it distally to the lacertus fibrosus.
    The lacertus fibrosus is a fascial extension of the biceps tendon and
    lies anterior to the median nerve at the elbow. Nerve compression
    occurs frequently in this area in the acute stages of a forearm
    compartment syndrome, and it may also occur in the later stages of
  • If signs of proximal median nerve
    compression are present, release the lacertus fibrosus. Incise the
    fascia of the lacertus fibrosus in a longitudinal fashion along the
    course of the median nerve to allow complete decompression and exposure
    of the nerve.
  • Continuing distally, the median nerve
    will pass between the two heads of the pronator teres muscle. Nerve
    compression can occur between these two heads. The ulnar head lies deep
    to the nerve, and the humeral head is superficial to the nerve. A
    tendinous band, which often lies along the deep head, may contribute to
  • Completely release the nerve throughout
    the entire length of its passage through the pronator teres. This often
    requires division of the humeral head of the pronator teres and
    division of any tendinous bands, deep or superficial, that may impinge
    on the nerve.
  • Distal to the pronator teres, the median
    nerve continues beneath and within the fascia of the flexor digitorum
    superficialis muscle, passing deep to the arch formed by the ulnar and
    radial origins. The nerve is most frequently compressed beneath the
    fibrous origin of this muscle (72).
  • Decompress the nerve by either incising
    the investing fascia or by dissecting the flexor digitorum
    superficialis from the underlying flexor digitorum profundus.
    Completely release the nerve from the investing fascia (72).
  • Despite the proximal location of muscle
    necrosis in Volkmann’s contracture, the incidence of median nerve
    compression in the carpal tunnel is high. Extend the incision for
    forearm decompression and expose the palmar fascia and transverse
    carpal ligament (24,87).
  • Incise these structures to decompress the median nerve decompression from the distal arm to the midpalm.
Ulnar Nerve Decompression
The incidence of ulnar nerve compression is much lower
than that of median nerve compression. It is often compressed at the
elbow as it passes between the ulnar and humeral heads of the flexor
carpi ulnaris. Decompress it if there are signs of ulnar neuropathy.
Radial Nerve Decompression
The radial nerve is rarely involved in compression
neuropathies following Volkmann’s contracture. Occasionally, however,
it may require decompression as it passes under the tendinous origin of
the supinator muscle (arcade of Frohse) or within the muscle itself.
Nerve compression is manifested by motor loss of the digital and thumb
extensors and the ulnar wrist extensors. Radial wrist extensor strength
and radial nerve sensibility remain intact, as these neural branches
arise proximal to the area of compression (10).
  • To decompress the radial nerve, make a
    straight, longitudinal incision on the proximal half of the posterior
    forearm along an imaginary line extending between the lateral
    epicondyle and the radial styloid.
  • Develop the interval between the extensor
    carpi radialis brevis and the extensor digitorum communis. This
    interval is most easily defined in the distal portion of the incision
    and should be developed here first and traced proximally.
  • Retract the extensor carpi radialis brevis radially and the extensor digitorum communis ulnarly.
  • Identify the supinator.
  • Identify the radial nerve proximally
    where it enters the supinator. The nerve may be found to be compressed
    by the tendinous bands of the arcade of Frohse, by a vascular leash
    that crosses the nerve transversely in this region, or by the supinator
    muscle itself. Carefully divide the appropriate structures to
    decompress the nerve (10).
Forearm nerve decompression should be undertaken as soon
as the patient’s condition permits. A nerve stimulator may be helpful
for verification of conductivity, especially


heavily scarred areas. Early return of sensibility and a decrease in
pain may be expected when decompression is undertaken in a timely
manner. Motor function return, although variable, can progress over
several days or weeks, depending on whether neuropraxia or axontemesis
is present. If nerves are irreparably damaged or have lost continuity
(neurotemesis), secondary excision of damaged segments and
microsurgical repair or reconstruction may offer some return of nerve
function. Alternatively, reconstruction may be accomplished with
appropriate tendon transfers.

Phase 2: Treatment of Contractures
Elbow flexion, forearm pronation, wrist flexion, digital
clawing, and thumb adduction are fixed deformities that develop over
time. Procedures used to help correct established forearm contractures
include infarct incision, flexor tendon lengthening or excision, and
flexor pronator slide. These procedures should be performed at the time
of, or subsequent to, nerve decompression.
Infarct Excision
Perform infarct excision 1 to 6 months after injury (Fig. 65.5) (52,80,91,92). Seddon recommends at least 6 months of preliminary splinting before contracture release (80).
Figure 65.5.
Excision of an infarct in the forearm, with preservation of the flexor
carpi ulnaris and ulnar neurovascular bundle. (Adapted from Seddon HJ. Rev Chir Orthop Reparatrice Appar Mot 1960;46:149, with permission.)
  • Excise the frequently encountered ellipsoid infarct through a long palmar forearm incision (80).
  • Excise fibrotic muscle and contracted
    scar tissue. The deep digital flexors and thumb flexor are usually most
    extensively involved. The pronator teres and pronator quadratus may be
    released or, if they are fibrotic, excised.
  • Gently manipulate the forearm and wrist
    into supination and extension, respectively, and immobilize in this
    corrected position following surgery.
Flexor Tendon Lengthening
Goldner has noted that infarct excision may not be
necessary and advocates Z-lengthening of the forearm flexors proximal
to the wrist (30). The flexor digitorum
profundus, flexor digitorum superficialis, flexor pollicis longus, and
pronator teres may be lengthened to accomplish digital and thumb
extension, and forearm supination (6,30). If severe forearm fibrosis is encountered and digital contracture is severe, excise the flexor digitorum superficialis.
The chief disadvantage of flexor tendon lengthening in
the forearm is further weakening of an already weakened muscle.
However, contracture release is usually functionally advantageous to
the maintenance of maximal strength. Tendon transfers, if needed, may
be performed at a later date.
Flexor Pronator Slide
The flexor pronator slide, first described by Page in 1923 (69), has gained wide acceptance (22,50,91,92). It has been shown to be more effective than infarct excision alone in obtaining a lasting correction (22).
  • Make a skin incision on the medial side
    of the elbow, 6 cm proximal to the medial humeral condyle and extending
    to the junction of the middle and distal thirds of the forearm.
    Separate the subcutaneous tissue from the deep fascia on the ulnar and
    radial sides of the incision.
  • Isolate the ulnar nerve at the level of the elbow and transpose it anteriorly.
  • Proceed with systematic, complete
    operative detachment of the origins of the flexor muscles of the
    forearm. Dissect the muscles subperiosteally using a scalpel.
  • Release the origins of the pronator
    teres, flexor carpi radialis, palmaris longus, and the humeral head of
    the flexor carpi ulnaris, and then detach the flexor digitorum
  • Detach the ulnar head of the flexor carpi
    ulnaris and the broad origin of the flexor digitorum profundus from the
    anterior aspect of the ulna.
  • Carry the dissection across the
    interosseous membrane and release the origin of the flexor pollicis
    longus from the anterior aspect of the radius.
  • Take care to avoid injury to the
    interosseous artery, vein, and nerves when detaching the flexors from
    the interosseous membrane.
  • Allow the muscles to slide distally 2–3 cm.
  • The incision may be extended distally and the palmar wrist capsule and pronator quadratus released. Although


    excision of the infarct and neural releases may be performed at the
    time of the flexor pronator slide, tendon transfers are performed
    secondarily (91,92).

  • Postoperatively, immobilize the extremity
    for 2–3 weeks with the elbow at 90° flexion, the forearm supinated, and
    the wrist and digits extended.
The flexor pronator slide has been criticized for the
unpredictability of correction achieved, the risk of recurrence of
deformity with growth, and the resultant decrease in grip strength,
particularly at the distal interphalangeal joint (52,91,92).
Despite these criticisms, the procedure has gained popularity and has
been shown to be effective in achieving satisfactory to excellent
results in a large group of patients with moderate to severe
contractures (91,92).
Phase 3: Tendon Transfers for Substitution and Reinforcement
Among the most desirable functions to restore in
patients with Volkmann’s contracture are finger and thumb flexion and
thumb opposition. Tendon transfers are usually delayed until nerve
recovery has plateaued and the contractures have been corrected
maximally with mobilization and splinting, or with operative releases.
In 1947, Phalen and Miller described a series of tendon transfers
designed to provide digital flexion and thumb opposition (73).
Tendon Transfers
  • Transfer the extensor carpi radialis
    longus to the flexor digitorum profundus, and transfer the extensor
    carpi ulnaris, lengthened by tendon graft, to the thumb for opposition (71,73).
  • Excise the tendons of the flexor
    digitorum superficialis if they are nonfunctional. The extensor
    pollicis brevis may be used to reinforce the extensor carpi
    ulnaris–opponens transfer.
  • Alternative transfers to augment thumb opposition include the abductor digiti quinti opponensplasty described by Huber (42,52) and the extensor indicis proprius opponensplasty described by Zancolli (100) and Burkhalter et al. (14).
  • To reinforce thumb flexion, the brachioradialis may be transferred to the flexor pollicis longus (91,92).
  • When flexor tendons have been weakened
    severely by previous Z-lengthening, reinforcement by transfer of the
    extensor carpi radialis longus to the flexor digitorum profundus, and
    transfer of the extensor carpi ulnaris to the flexor pollicis longus,
    can be performed (30).
Phase 4: Salvage of the Severely Contracted or Neglected Forearm
The procedures of Phases 2 and 3 usually provide
satisfactory results, and further procedures are seldom necessary.
Occasionally, however, additional measures may be required for
satisfactory correction of the severely contracted or neglected
forearm. Operations that have proved useful include proximal or distal
row carpectomy, radial and ulnar shortening, wrist fusion, and digital
joint fusion.
Proximal or distal row carpectomy results in limb
shortening that allows wrist extension while maintaining flexibility.
In severe deformities, carpectomy may be performed before tendon
transfer. If adequate donor muscles are not available for transfer,
interphalangeal joint fusion can be performed. The stabilized limb can
then function as a hook, which is generally superior to a prosthesis,
especially if some sensibility is retained (30). Radial and ulnar shortening and wrist fusion are rarely indicated for the treatment or salvage of Volkmann’s contracture.
The hand deformity associated with Volkmann’s
contracture is complex, requiring a systematic approach. Intrinsic
contractures should be addressed only after extrinsic finger flexors
have been released. Fixed extrinsic contractures create a claw-hand
deformity (hyperextension of the MP joints and flexion of the
interphalangeal joints). Following extrinsic muscle release, intrinsic
tightness may become apparent. Complete release of intrinsic
contractures may not be desirable, since preservation of some MP joint
flexion will prevent recurrence of the claw-hand deformity. If the
intrinsic contracture is severe, the oblique fibers of the extensor
hood may be released to permit flexion of the interphalangeal joints (82).
Thumb-in-palm deformity often accompanies the claw hand
in Volkmann’s contracture. The deformity may be caused by both
intrinsic and extrinsic contractures. Flexion contracture at the
interphalangeal joint may be corrected with flexor pollicis longus
lengthening. Residual deformity following tendon lengthening is
attributable to intrinsic muscle contracture, joint contracture, or
skin contracture of the first web. Recommended procedures for
correction of a severe thumb-in-palm deformity include release of the
adductor pollicis, deepening of the thumb web space, fusion of the MP
joint or interphalangeal joint, or excision of the trapezium (6,30).
Thenar origin release (recession) and release of the first dorsal
interosseous muscle may also be necessary for additional correction (6,57).
The most significant hand disabilities may not be caused
by intrinsic contractures but rather by secondary problems from sequela
of extrinsic muscle contractures in the forearm or by associated
neuropathy. Loss of median and ulnar nerve sensibility, intrinsic
paralysis secondary to median and ulnar motor nerve paralysis, and
interphalangeal joint flexion deformity secondary to contracture of the
extrinsic flexors cause severe functional deficits. Proper management
of these problems, as described in


Phase 1 and Phase 2, should significantly improve hand function.

The deformity of established Volkmann’s ischemic
contracture remains a challenging problem despite the available methods
of management. Advances in the free transfer of vascularized muscle,
nerve, and skin have offered potential additional methods of
reconstruction (15,16,17 and 18,43,88).
One of the early uses of these techniques for reconstruction of
Volkmann’s contracture was the transfer of the lateral head of the
pectoralis major to the flexor forearm, reported by Chien et al. in
1977 (15). Subsequently, Taylor and Daniel
achieved satisfactory results with a free vascularized superficial
radial nerve graft transfer to an irreparably damaged median nerve (89).
Chuang et al. have obtained an 80% success rate in free muscle transfer
in nine patients undergoing 10 transfers for Volkmann’s contracture (16,17 and 18).
As free tissue transfer has become more popular, reconstruction of
forearm muscles has now included the use of the gracilis, rectus
femorus, latissimus dorsi, or pectoralis muscles (15,16,17,18,43,53,54 and 55,60).
The early results of these procedures are promising, especially in
their role in the reconstruction of severe or neglected Volkmann’s
contracture in which few adequate donor muscles are available for
tendon transfer.
Each reference is categorized according to the following
scheme: *, classic article; #, review article; !, basic research
article; and +, clinical results/outcome study.
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# 4. Benkeddache Y, Gottesman H, Hamdani M. Proposal of a New Classification for Established Volkmann’s Contracture. Ann Chir 1985;4:134.
+ 5. Blout WP. Volkmann’s Ischaemic Contracture. Surg Gynecol Obstet 1950;90:244.
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# 7. Botte MJ, Gelberman RH. Compartment Syndrome and Ischemic Contracture. In: Nickel VL, Botte MJ, eds. Orthopaedic Rehabilitation, 2nd ed. New York: Churchill Livingstone, 1992.
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# 11. Boyes JH. Bunnell’s Surgery of the Hand. Philadelphia: JB Lippincott, 1970.
! 12. Brooks
B. Pathological Changes in Muscle as a Result of Disturbances of
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+ 13. Bunnel S. Ischemic Contracture Local in the Hand. J Bone Joint Surg Am 1953;35:88.
+ 14. Burkhalter WE, Christensen RC, Brown P. The Extensor Indicis Proprius Opponensplasty. J Bone Joint Surg Am 1973;55:725.
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# 16. Chuang DCC. Function Free Muscle Transplantation. In: Peimer CA, ed. Surgery of the Hand and Upper Extremity. New York: McGraw-Hill, 1996:1901.
+ 17. Chuang
DCC, Chen HC, Wei FC, et al. Compound Functioning Free Muscle Flap
Transplantation (Lateral Half of Soleus, Fibula and Skin Flap). Plast Reconstr Surg 1992;89:335.
+ 18. Chuang
DCC, Strauch RJ, Wei FC. Technical Consideration in Two-stage Function
Free Muscle Transplantation (FFMT) Reconstruction of Both Flexor and
Extensor Function of the Forearm. Microsurgery 1994;15:338.
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# 20. Doyle JR. Anatomy of the Upper Extremity Muscle Compartments. Hand Clin 1998;14:343.
+ 21. Eaton RG, Green WT. Epimysiotomy and Fasciotomy in Treatment of Volkmann’s Ischemic Contracture. Orthop Clin North Am 1972;3:175.
# 22. Eichler GR, Lipscomb PR. The Changing Treatment of Volkmann’s Ischemic Contractures from 1955 to 1965 at the Mayo Clinic. Clin Orthop 1967;50:215.
* 23. Finochietto R. Volkmann’s Contracture of the Intrinsic Muscles of the Hand. Bol y Trab Soc Cir (Buenos Aires) 1920;4:31.
+ 24. Gelberman RH, Zakaib GS, Mubarak SJ, et al. Decompression of Forearm Compartment Syndromes. Clin Orthop 1978;134:225.
# 25. Gelberman RH. Volkmann’s Contracture of the Upper Extremity: Pathology and Reconstruction. In: Mubarak SJ, Hargens AR, eds. The Compartment Syndrome and Volkmann’s Contracture. Philadelphia: WB Saunders, 1981.
# 26. Gelberman RH, Garfin SR, Hergenroeder PT, et al. Compartment Syndromes of the Forearm: Diagnosis and Treatment. Clin Orthop 1981;161:252.


+ 27. Gelberman RH, Szabo RM, Mortensen WW. Carpal Tunnel Pressures and Wrist Position in Patients with Colle’s Fractures. J Trauma 1984;8:747.
# 28. Gelberman RH. Acute Carpal Tunnel Syndrome. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: JB Lippincott, 1991:939.
# 29. Gellman H, Buch K. Acute Compartment Syndrome of the Arm. Hand Clin 1998;14:385.
# 30. Goldner JL. Volkmann’s Ischemic Contracture. In: Flynn JE, ed. Hand Surgery. Baltimore: Williams & Wilkins, 1975.
# 31. Goldner L. Intrinsic and Extrinsic Contractures of the Hand Due to Ischemic and Nonischemic Causes. In: Jupiter J, ed. Flynn’s Hand Surgery. Baltimore: Williams & Wilkins, 1991:913.
+ 32. Griffiths DV. Volkmann’s Ischemic Contracture. Br J Surg 1940;28:239.
! 33. Hargens AR, Romine JS, Sipe JC, et al. Peripheral Nerve Conduction Block by High Muscle Compartment Pressure. J Bone Joint Surg Am 1979;61:192.
! 34. Hargens
AR, Evans KL, Hagen PL, et al. Quantitation of Skeletal-Muscle Necrosis
in a Model Compartment Syndrome. Presented at a meeting of the
Orthopedic Research Society, Dallas, TX, February 1978.
! 35. Hargens
AR, Akeson WH, Mubarak SJ, et al. Kappa Delta Award Paper. Tissue Fluid
Pressures: From Basic Research Tools to Clinical Applications. J Orthop Res 1989;7:902.
# 36. Hargens AR, Mubarak SJ. Current Concepts in Pathophysiology, Evaluation, and Diagnosis of Compartment Syndrome. Hand Clin 1998;14:371.
+ 37. Harris CJ, Riordan DC. Intrinsic Contracture in the Hand and Its Surgical Treatment. J Bone Joint Surg Am 1954;36:10.
# 38. Henry AK. Extensile Exposure, 2nd ed. London: Churchill Livingstone, 1973.
+ 39. Hill RL, Bortrkes B. Volkmann’s Ischemic Contracture in Hemophilia. Am Surg 1936;103:444.
+ 40. Holden CE. The Pathology and Prevention of Volkmann’s Ischemic Contracture. J Bone Joint Surg Br 1979;61:296.
# 41. Hofmeister EP, Shin AY. The Role of Prophylactic Fasciotomy and Medical Treatment in Limb Ischemia and Revascularization. Hand Clin 1998;14:457.
# 42. Huber E. Hiltsoperation ber Medianers-lahmung. Dtsch Z Chir 1921;162:271.
+ 43. Ikuta Y, Kubo T, Tsuge K. Free Muscle Transplantation by Microsurgical Technique to Treat Severe Volkmann’s Contracture. Plast Reconstr Surg 1976;58:407.
! 44. Jepson PN. Ischemic Contracture. Experimental Study. Am Surg 1926;84:785.
+ 45. Jorge J. Retraction Ischejique de Volkmann. Rapport d’Albert Monchet. Bull Mem Soc Nat Chir 1925;51:884.
# 46. Kadiyala RK, Waters PM. Upper Extremity Pediatric Compartment Syndromes. Hand Clin 1998;14:467.
+ 47. Landi A, DeSantis G, Torricelli P, et al. CT in Established Volkmann’s Contracture in Forearm Muscles. J Hand Surg 1989;14B:49.
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+ 50. Lipscomb PR. The Etiology and Prevention of Volkmann’s Ischemic Contracture. Surg Gynecol Obstet 1956;103:353.
# 51. Lister G. The Hand: Diagnosis and Indications. Edinburgh: Churchill-Livingstone, 1977.
# 52. Littler JW. The Hand and Upper Extremity. In: Converse JM, ed. Reconstructive Plastic Surgery. Philadelphia: WB Saunders, 1977.
+ 53. Manktelow RT, Mckeen NH. Free Muscle Transplantation to Provide Active Finger Flexion. J Hand Surg 1978;3:416.
+ 54. Manktelow RT, Zuker RM, Mckee NH. Functioning Free Muscle Transplantation. J Hand Surg 1984;9A:32.
+ 55. Manktelow RT, Zuker RM. The Principles of Functioning Muscle Transplantation: Applications to the Upper Arm. Ann Plast Surg 1989;22:1275.
# 56. Massart R. La Maladie de Volkmann. Rev Orthop 1935;22:385.
* 57. Matev I. Surgical Treatment of Spastic “Thumb-in-palm” Deformity. J Bone Joint Surg Br 1963;45:703.
* 58. Matsen FA III, Winquist RA, Drugmire RB Jr. Diagnosis and management of Compartmental Syndromes. J Bone Joint Surg Am 1980;62:286.
+ 59. Matsen
FA III, Wyss CR, Drugmire RB Jr, et al. The Effects of Limb Elevation
and Dependency on Local Arteriovenous Gradients in Normal Human Limbs
with Particular Reference to Limbs with Increased Tissue Pressure. Clin Orthop 1980;150:187.
# 60. Mckee NH, Kuzon WM Jr. Functioning Free Muscle Transplantation: Making It Work. What Is Known? Ann Plast Surg 1989;23:249.
+ 61. Meyerding HW. Volkmann’s Ischemic Contracture. JAMA 1930;94:394.
+ 62. Meyerding HW. Volkmann’s Ischemic Contracture Associated with Supracondylar Fracture of Humerus. JAMA 1936;106:1139.
+ 63. Mubarak SJ, Carroll NC. Volkmann’s Contracture in Children: Etiology and Prevention. J Bone Joint Surg Br 1979;61:285.
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+ 65. Murphy JB. Myositis. JAMA 1914;63:1249.
+ 66. Newmeyer WL, Kilgore ES Jr. Volkmann’s Ischemic Contracture Due to Soft-tissue Injury Alone. J Hand Surg 1976;1A:221.
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+ 72. Peacock EE, Madden JW, Trier WC. Transfer of Median and Ulnar Nerves During Early Treatment of Forearm Ischemia. Ann Surg 1969;169:748.
+ 73. Phalen
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