Treatment of Flexor Tendon Injuries Abstract The goals of flexor tendon repair are to promote intrinsic tendon healing and minimize extrinsic scarring in order to optimize tendon gliding
Trang 1Treatment of Flexor Tendon Injuries
Abstract
The goals of flexor tendon repair are to promote intrinsic tendon healing and minimize extrinsic scarring in order to optimize tendon gliding and range of motion Despite advances in the materials and methods used in surgical repair and postoperative rehabilitation, complications following flexor tendon injuries continue to occur, even in patients treated by experienced surgeons and therapists The most common complication is adhesion
formation, which limits active range of motion Other complications include joint contracture, tendon rupture, triggering, and pulley failure with tendon bowstringing Less common
problems include quadriga, swan-neck deformity, and lumbrical plus deformity Meticulous surgical technique and early
postoperative tendon mobilization in a well-supervised therapy program can minimize the frequency and severity of these complications Prompt recognition of problems and treatment with hand therapy, splinting, and/or surgery may help minimize
recovery time and improve function In the future, the use of novel biologic modulators of healing may nearly eliminate complications associated with flexor tendon injuries
Tendon lacerations within the digital sheath are difficult to re-pair.1As a result of poor outcomes following primary tendon repair within the digital sheath (zone II), the area within the sheath contain-ing the flexor digitorum profundus (FDP) and flexor digitorum superfi-cialis (FDS) tendons has been re-ferred to as “no man’s land.”2In the 1960s, the development of stronger suture materials and improved su-ture techniques led to a renewed in-terest in primary repair within the digital sheath.3Primary repair is now the standard of care Despite these advances, outcomes have been rated fair or poor in 7% to 20% of patients
after flexor tendon repair.4,5A thor-ough knowledge of the basic science
of flexor tendon healing is essential for improving outcomes and for un-derstanding, recognizing, and manag-ing the various complications
Basic Science of Flexor Tendon Healing
Anatomy
Tendons are made up of spiraling bundles of mature tenocytes and pre-dominantly type I collagen In the distal palm and digits, the tendons are enclosed in a synovial sheath The synovial sheath enhances glid-ing of the tendons and is thickened
Soma I Lilly, MD
Terry M Messer, MD
Dr Lilly is Chief Resident, Department of
Orthopaedics, University of North
Carolina School of Medicine, Chapel
Hill, NC Dr Messer is Assistant
Professor, Department of Orthopaedics,
University of North Carolina School of
Medicine, Chapel Hill, NC.
None of the following authors or the
departments with which they are
affiliated has received anything of value
from or owns stock in a commercial
company or institution related directly or
indirectly to the subject of this article:
Dr Lilly and Dr Messer.
Reprint requests: Dr Messer, Wake
Orthopaedics, LLC, 3009 New Bern
Avenue, Raleigh, NC 27610.
J Am Acad Orthop Surg
2006;14:387-396
Copyright 2006 by the American
Academy of Orthopaedic Surgeons.
Trang 2in specific areas between the joints;
these thickened areas are called
pul-leys The pulleys enhance efficiency
of motion within the digit by
pre-venting tendon bowstringing and
maximizing tendon excursion Most
critical to this system are the A2 and
A4 pulleys, which are located over
the proximal and middle phalanges,
respectively6(Figure 1) The FDP and
FDS tendons are contained within
the digital flexor sheath
Flexor Tendon Healing
Tendon healing consists of three
phases: inflammatory, proliferative,
and remodeling.7The inflammatory
phase occurs during the first week
af-ter injury and involves migration of
fibroblasts and macrophages to the
injured area, with ensuing
phagocy-tosis of the clot and necrotic tissue
In the proliferative phase, which
lasts from weeks 1 through 3,
fibro-blasts proliferate, and there is
imma-ture collagen deposition and
neovas-cularization Finally, the remodeling
phase occurs in weeks 3 through 8
Collagen fibers become organized in
a linear manner parallel to the
ten-don Adhesion formation between
tendon and sheath is most clinically
evident during this last phase
Two mechanisms for healing
have been described in the literature:
extrinsic and intrinsic The extrinsic
mechanism is predominately
medi-ated by an influx of synovial fibro-blasts and inflammatory cells from the tendon sheath Healing also oc-curs via the intrinsic mechanism, in which fibroblasts and inflammatory cells from the tendon and epitenon invade the injured site The extrinsic mechanism is thought to predomi-nate early in tendon healing and in cases of digit immobilization; the in-trinsic mechanism becomes increas-ingly active after 21 days.8The
great-er prolifgreat-erative and inflammatory response of the synovial sheath, along with the greater cytokine reac-tivity and capacity for matrix degra-dation of synovial fibroblasts, favor the extrinsic pathway.8 Extrinsic healing produces increased collagen content at the injury site, but in a disorganized fashion Tendon heal-ing is likely a combination of both mechanisms, but the predominance
of extrinsic healing leads to scar for-mation and adhesions between the tendon and the surrounding sheath
Requirements for Tendon Healing
Requirements for tendon healing include motion and tension at the repair site, adequate tendon nutri-tion and vascular perfusion, mini-mal gap formation at the repair site, and a strong repair.9-12Early-motion protocols in animal flexor tendons resulted in a progressively greater
ul-timate tensile load over time than was the case in tendons managed with immobilization protocols.9 Early-motion protocols also helped avoid the loss of strength that occurs
in early phases of tendon healing.10 Additionally, both motion and ten-sion are needed to stimulate teno-cyte development and increase col-lagen amount and organization.11 Tendon nutrition is provided through vascular perfusion and sy-novial fluid diffusion Flexor tendon vascular supply originates from ves-sels in the proximal synovial fold, segmental branches of digital arter-ies through the vincular system, and the osseous insertion of the FDS and FDP tendons.13 Diffusion of nutri-ents through synovial fluid occurs via imbibition, in which fluid is forced through interstices on the surface of the tendon.14This process
is facilitated by the pumping mech-anism created by flexion and exten-sion of the digit
Gap formation as a result of cy-clic loading before tendon failure is seen routinely after flexor tendon re-pair.15The average gap is 3.2 mm.16 Gaps have previously been
associat-ed with adhesion formation and poor gliding.17Gelberman et al,12
howev-er, demonstrated that gap length has
no relationship to adhesion forma-tion, but it does have a negative ef-fect on the acquisition of tendon tensile properties during healing
In their canine study, repair gaps
>3 mm did not gain stiffness or strength from 10 to 42 days, but gaps
<3 mm had a 320% increase in stiff-ness and a 90% increase in strength over the same period.12
Techniques for maximizing ten-don repair strength comprise a large portion of flexor tendon research A strong repair is one that can with-stand early motion with minimal gap formation, thereby allowing suc-cessful tendon healing Well-accepted, established principles of tendon repair include using core su-tures of 3-0 or 4-0 nonabsorbable polyfilament material, an increased
Figure 1
Lateral view of the flexor tendon synovial sheath, including the palmar aponeurosis
(PA), five annular (A) pulleys, and three cruciform (C) pulleys The critical pulleys
are A2 and A4, located over the proximal and middle phalanges, respectively
(Reproduced with permission from Doyle JR: Anatomy of the finger flexor tendon
sheath and pulley system J Hand Surg [Am] 1988;13:473-484.)
Trang 3number of sutures crossing the
re-pair, and equal strength across all
strands In addition, certain locking
suture techniques (ie, transverse
limb of repair passed superficial to
the longitudinal component) have
been shown to increase repair
strength.18-20 A peripheral locking
epitendinous suture also should be
added to enhance repair strength.21
Complications
Adhesion Formation
Adhesion formation is the most
common complication following
flexor tendon repair Prevention of
adhesion formation is facilitated by
optimizing intrinsic healing Early
re-search reflected the belief that
ten-don healing depended on extrinsic
cellular ingrowth, which required
immobilization However, the ability
of tendons to heal by intrinsic
mech-anisms alone has since been well
documented.22Methods of adhesion
prevention can be divided into
me-chanical and biologic factors
de-signed to promote intrinsic healing
Mechanical Factors
Mechanical factors for preventing
adhesions include early
postopera-tive motion protocols, preservation
of sheath and pulley components,
partial FDS resection, and
atraumat-ic handling of the tendon and sheath
Motion, which leads to a
predomi-nance of intrinsic over extrinsic
healing, is critical to preventing
ad-hesions Three primary motion
pro-tocols are described in the literature:
passive, active, and synergistic In
1977, Lister et al23published the first
results of tendon repair using a
con-trolled passive motion protocol The
Kleinert splint was used to allow
ac-tive digital extension coupled with
passive digital flexion Good to
ex-cellent results were reported in 80%
of tendon lacerations in zone II.23
The splint has since been modified
by adding a midpalmar bar or pulley,
resulting in improved distal tendon
gliding and differential tendon
ex-cursion.24The addition of synergistic wrist motion (wrist flexion–finger extension combined with wrist ex-tension–finger flexion) also has been shown to improve overall tendon gliding and excursion.25
Early active motion protocols subsequently have been developed
to address concerns about
variabili-ty in tendon gliding with passive protocols Bainbridge et al26reported
on a consecutive series comparing controlled active motion with active extension–passive flexion protocols
Patients treated with controlled ac-tive motion acquired greater final motion.26 Other series using early active motion have reported good to excellent results ranging from 57%
to 92%, with rupture rates from 5%
to 46%.27-29These findings are com-parable to rates reported with pas-sive motion regimens Improved su-ture materials and techniques seem capable of withstanding the higher forces associated with active motion protocols.30-32 However, recent re-search in repaired canine tendon by Boyer et al33demonstrated no advan-tage with high-force rehabilitation in the accrual of either stiffness or strength compared with low-force rehabilitation
The synergistic motion regimen allows high tendon excursion with low force on the repair site.34This protocol consists of passive digit flion combined with active wrist ex-tension, followed by active wrist flex-ion combined with passive digit extension Zhao et al35 compared synergistic motion with passive mo-tion regimens in the management of canine flexor tendon repairs They noted fewer adhesions with the syn-ergistic motion group but reported el-evated gap formation in the motion group (30%) versus the passive group (6%).35Currently, agreement is uni-versal that repaired flexor tendons should be subjected to early mobili-zation; however, no single rehabilita-tion protocol is accepted by all
Preservation of sheath compo-nents is controversial When the
vas-cular source of nutrition is compro-mised because of trauma, the tendon sheath can maintain nutrition through imbibition until the vascu-lar system is reestablished.36 Preser-vation of flexor tendon sheath integ-rity may reduce adhesions through its positive effect on intrinsic heal-ing.37 However, sheath repair also may lead to impaired tendon gliding and increased resistance.17Another study compared sheath repair with excision and found no difference in final motion when early mobiliza-tion was done.38
Recently, resection of all or part of the FDS tendon has been suggested
as a method of decreasing gliding re-sistance of the FDP within the sheath.39Loss of the FDS tendon is not associated with significant func-tional compromise However, this technique was initially dismissed be-cause a considerable portion of the FDP blood supply is provided by cap-illaries emanating from the FDS ten-don In a cadaveric study, FDS resec-tion was found to be a viable opresec-tion for improving the gliding of a bulky FDP repair The authors did not dem-onstrate any advantage of complete resection versus partial resection.39 The use of meticulous surgical technique as a method for decreasing adhesion formation is well docu-mented Adhesion formation is known to be proportional to the amount of tissue crushing and to the number of surface injuries incurred
by the tendon and sheath during re-pair.4Accordingly, stiffness is more common in digits after crush injuries
as well as in those with concomitant neurovascular and bone injuries.40
Biologic Factors
Development of novel biologic factors to provide so-called scarless healing is an active area of re-search.22,41 Advances in this arena could lead to less reliance on postop-erative motion for adhesion preven-tion Methods currently under inves-tigation include mechanical barriers
to adhesion formation, as well as
Trang 4chemical and molecular modulation
of scar formation Many mechanical
barrier methods have been studied,
including silicone, alumina sheaths,
polyethylene, and
polytetrafluoro-ethylene, but none is in widespread
clinical use.22 ADCON-T/N
(Glia-tech, Cleveland, OH), a gelatin and
carbohydrate polymer, has shown
some potential.41In a recent
double-blind randomized study in which
ADCON-T/N was applied to the
tendon after repair, the authors
found no significant effect on final
motion; however, time to achieve
fi-nal motion was shorter with the use
of ADCON-T/N.41
Ibuprofen and corticosteroids have
been investigated as possible
modu-lators of adhesion formation.42,43
Ibu-profen has been shown to improve
tendon excursion in animal models.42
Ketchum43 demonstrated that
al-though corticosteroids decrease the
strength and density of adhesions,
they are associated with smaller,
weaker tendons, diminished wound
healing, and decreased resistance to
infection These problems have
lim-ited their use in flexor tendon repair
New Research
Modulation of scar formation on
a molecular level is a new area of
research in tendon healing This
re-search has been directed toward
un-derstanding the role of cytokines
in tendon metabolism and
re-pair.22,44,45Two cytokines,
transform-ing growth factor-β(TGF-β) and
ba-sic fibroblast growth factor (bFGF),
have shown the most potential in
adhesion prevention.44,45TGF-βhas
been implicated in numerous
biolog-ic activities related to wound
heal-ing, such as fibroblast and
macro-phage recruitment, angiogenesis,
stimulation of collagen production,
downregulation of proteinase
activ-ity, and increased metalloproteinase
inhibitor activity.44
Chang et al45 demonstrated that
flexor tendons exposed to
transec-tion and repair exhibit increased
TGF-βin both tenocytes and
inflam-matory cells from the tendon sheath
These findings are significant be-cause TGF-β is thought to be in-volved in the pathogenesis of exces-sive scar formation Therefore, perioperative modulation of this cy-tokine may lead to decreased adhe-sion formation Three isoforms have been identified; the TGF-β1 isoform
is thought to be primarily responsi-ble for the proinflammatory and scarring activities.22The TGF-β3 iso-form demonstrates anti-scarring properties and acts as an inhibitor of scarring in injury models.22
Similar to TGF-β, bFGF has been implicated in early tendon healing.45 Basic FGF is a potent stimulator of angiogenesis and is able to induce migration and proliferation of endo-thelial cells in tissue culture In 1998, Chang et al45found that bFGF was upregulated in tenocytes, tendon sheath fibroblasts, and inflammatory cells from flexor tendons exposed to
a tendon wound environment With further research, modification of bFGF expression may also be useful
in postoperative adhesion reduction
Research into chemical modula-tion of cytokines has yielded 5-fluorouracil (5-FU) as a possible can-didate.46,475-FU is an antimetabolite that decreases scarring by an un-known mechanism Khan et al46 tested this drug in a rabbit model by treating the injured synovial sheath
of partially lacerated tendons with a 5-min application of 5-FU before
clo-sure A significant (P < 0.001) decrease
in the proliferative and inflammatory response of synovial fibroblasts was demonstrated There was also a
sig-nificant (P < 0.001) decrease in the
ex-pression of TGF-βin the treated tis-sue Others have reported the ability
of 5-FU to reduce postoperative adhe-sions in a chicken model.47 These findings are still experimental, how-ever, and have not yet been imple-mented in clinical practice
When adhesion prevention is un-successful, early recognition is crit-ical to ensure a good clincrit-ical out-come and prevent further progression
of stiffness Adhesion and tendon rupture present clinically with sim-ilar physical findings Both condi-tions may demonstrate loss of active flexion, but patients with adhesions have preservation of some residual active motion Imaging studies, such
as magnetic resonance imaging or ul-trasound, may be indicated to deter-mine the source of motion loss Mag-netic resonance imaging has been shown to be 100% accurate in distin-guishing adhesions from rupture.48 When adhesions are identified, ther-apy should be directed toward pro-grams that maximize differential mo-tion between the FDS and FDP tendons.25,26Splinting also may be a useful adjunct When therapy and splinting fail to produce effective re-sults, tenolysis may be indicated
Tenolysis
Flexor tenolysis is indicated when active range of motion (ROM) mea-surements do not improve within several weeks to months, despite strict patient compliance with splint-ing and ROM exercises.49Tenolysis should not be considered until the soft tissues have reached a state of equilibrium, with supple skin and subcutaneous tissues To achieve a good result, the digit must have min-imal joint contractures and near-normal passive ROM.17 Most sur-geons recommend waiting for 3 to 6 months after tendon repair or graft-ing before performgraft-ing tenolysis.49,50 When performing flexor tenoly-sis, a local anesthetic combined with intravenous sedation is
recommend-ed to allow the patient to perform active flexion in the operating room.50This intraoperative testing is critical to achieve a successful out-come A midlateral or Bruner zigzag incision is used to expose the length
of the tendon The neurovascular bundles are encountered at the ends
of the digital creases, and the sur-geon must take care to prevent iatro-genic injury to these structures The scarred tendon and its sheath are vi-sualized (Figure 2, A),51 the
Trang 5adhe-sions released, and the tendon
bor-ders identified A useful technique is
to pass a small elevator through
win-dows made in less critical parts of
the sheath (Figure 2, C) As much of
the pulley system as possible must
be preserved (Figure 2, B); when this
is not feasible, pulley reconstruction
or a staged tendon implant should be
considered If pulley reconstruction
requires protected mobilization,
however, the end result may be
com-promised Additionally, any
con-comitant procedure, such as tendon
lengthening or shortening, skin
grafting, osteotomy, or capsulotomy,
may have an adverse effect on the
outcome of flexor tenolysis.17At the
end of the procedure, the patient
should be placed in a splint that
per-mits immediate active ROM
Pa-tients for whom active ROM
im-proves in the first few weeks after
surgery tend to maintain these gains
Significant pain and little early im-provement in motion may be an in-dication for inserting an indwelling polyethylene catheter containing lo-cal anesthetic.50
One complication of flexor teno-lysis is tendon or pulley rupture, which should be managed with a staged tendon reconstruction Other complications include postoperative edema and pain as well as inadver-tent neurovascular injury that may lead to loss of viability in a digit with marginal preoperative circula-tion Flexor tenolysis is a
technical-ly demanding procedure, and the postoperative rehabilitation is
equal-ly arduous Not all patients are can-didates for tenolysis The surgeon must evaluate how the loss of active motion will affect the patient’s needs and desires as well as the
abil-ity to perform activities of daily liv-ing and to return to his or her occu-pation The surgeon also must consider the sensory and circulatory status of the finger, the condition of the other digits, and the age and gen-eral health of the patient Patients who are noncompliant with therapy after their initial repair typically are poor candidates for tenolysis
Joint Contracture
Even with adherence to early-motion regimens, the reported rate of proximal interphalangeal (PIP) and distal interphalangeal (DIP) joint con-tracture is 17%.36Contractures may
be caused by unrecognized disruption
or scarring of the volar plate, tendon bowstringing secondary to pulley in-competence, concomitant fracture or neurovascular injury, prolonged heal-ing in a flexed position, collateral
lig-Figure 2
Flexor tenolysis is performed by identifying the scarred
tendon and sheath (A), followed by release of adhesions and careful preservation of the pulley system (B) C,
Re-lease may be facilitated by passing a small elevator or dental probe through windows in less critical portions of the sheath (eg, proximal to A2, or between A2 and A4 pulleys) (Reprinted from Strickland JW: Flexor tenolysis, in
Strickland JW [ed]: Master Techniques in Orthopaedic Surgery: The Hand Philadelphia, PA: Lippincott-Raven,
1998, pp 525-538 Illustrations copyright © Gary Schnitz and the Indiana Hand Center.)
Trang 6ament contracture, skin contracture,
or flexor tendon adhesions They also
may be secondary to inadequate
post-operative motion regimens and
dy-namic flexion splinting The latter
may be prevented through correct
po-sitioning of the wrist, hand, and
dig-its in the postoperative splint and
early motion Most postoperative
pro-tocols involve splinting the
metacar-pophalangeal (MCP) joint in flexion
(approximately 60°) with the
inter-phalangeal (IP) joints fully extended
Nonsurgical management of joint
contractures consists of early
iden-tification and modification of
splint-ing to allow greater PIP and DIP joint
extension A felt or foam block placed
inside a dorsal splint at the level of
the proximal phalanx, in addition to
increasing MCP joint flexion to relax
the intrinsic mechanism, will help
re-solve PIP joint contracture (Figure 3,
A) This method can be used with
buddy taping and active-assisted
tension exercises Static nighttime
ex-tension splinting and passive
exten-sion exercises with Velcro bands
applied to the splint to impart an
ex-tension force on the digit also may be
useful As the tendon continues to
heal and strengthen, finger splints (eg,
Joint Jack, Safety Pin) can be used
(Figure 3, B and C)
When nonsurgical management
of contractures is unsuccessful,
sur-gery should be considered No
abso-lute guidelines exist regarding the
degree of contracture that requires surgical release; rather, the decision for surgery is based on the patient’s functional limitations and goals
Preoperatively, the surgeon should attempt to determine whether the contracture is caused by extrinsic factors (eg, skin contracture, proxi-mal flexor tendon adhesions) or an intrinsic joint contracture When ex-trinsic factors are responsible, PIP joint extension will improve with MCP joint flexion PIP joint release should be performed only after all flexor tendon adhesions and skin contractures have been addressed
For PIP joint release, exposure is performed through a Bruner or mid-lateral incision The radial and ulnar neurovascular bundles are identified and protected The C1 portion of the flexor sheath is excised between the A2 and A3 pulleys, and the FDP and FDS tendons are exposed52(Figure 4, A) Flexor tenolysis is performed ini-tially; the checkrein ligaments are identified by passing a small hemo-stat or elevator volar to the trans-verse retinacular vessels as they en-ter the flexor sheath just proximal to the collateral ligament origin The checkrein ligaments are volar to the transverse retinacular vessels and can be divided sharply at this level
The transverse retinacular vessels should be preserved whenever possi-ble because they supply the tendon vincular system
When full passive PIP joint exten-sion cannot be obtained, release of the collateral ligaments is performed
at their insertion on the head of the proximal phalanx, beginning with the accessory collateral ligaments (Figure 4, B) Release of the
collater-al ligaments should be performed se-quentially, progressing from palmar
to dorsal, until full extension is achieved When full extension can-not be achieved, release of the volar plate may be necessary
Tendon Rupture
Rupture of a tendon repair is not
an uncommon problem In one study, a rupture rate of 4% was re-ported in 728 digital flexor tendon repairs (440 patients).53The authors were unable to identify the inciting factor in these failures Another se-ries reported a 5.7% rate of rupture
in digital flexor tendon repairs.19 Factors that predispose tendon re-pairs to rupture include inadequate suture material, poor surgical tech-nique, overly aggressive therapy, or early termination of postoperative splinting Patient noncompliance, such as removing the splint, lifting heavy objects, or attempting strong grasp, is a frequent cause of rup-ture.53
Tendon repairs are weakest be-tween postoperative days 6 and
18.35Although rupture is most com-mon during this period, it may be
Figure 3
Splints used to manage proximal interphalangeal (PIP) flexion contractures A, Dorsal forearm-based thermoplast splint with a felt block placed dorsally at the level of the PIP joint B, Joint Jack Finger Splint (Sammons Preston Rolyan, Bolingbrook, IL).
C,Safety Pin Splint (Sammons Preston Rolyan)
Trang 7seen as late as 6 to 7 weeks after
sur-gery.36Timely surgical exploration is
indicated once tendon rupture is
identified When repair attenuation
is seen without obvious rupture and
<1 cm of scar is present, the scar can
be resected and the primary repair
revised When the scar is >1 cm, a
tendon grafting procedure should be
considered because excessive distal
advancement of the tendon can lead
to contractures and quadriga.36With
complete tendon rupture, the time
from the original repair influences
the course of action If the rupture
occurs in the early postoperative
pe-riod, the tendon may be primarily
re-paired When the rupture occurs 4 to
6 weeks after the original repair,
ten-don grafting or a staged
reconstruc-tion is recommended Staged
graft-ing is preferred when there is
significant scarring within the
sheath Pediatric urethral or vascular
dilators can be used to expand a
con-stricted but otherwise intact sheath,
thereby eliminating the need for a
two-stage reconstruction
Triggering
Triggering can occur after tendon
repair and is usually the result of the
repair site’s catching on a pulley or
sheath Causes of triggering include
a bulbous tendon repair or a tightly
repaired area of the tendon sheath
The surgeon should intraoperatively
assess tendon gliding to identify
ar-eas that may cause triggering or
re-strict gliding In the acute setting, a
partial tendon sheath excision or
re-lease may be used In contrast,
sheath repair may reduce triggering
of a bulky repair by acting as a
fun-nel Postoperatively, ultrasound or
massage may be helpful Once the
tendon is healed, a corticosteroid
in-jection may be indicated Reduction
tenoplasty may be considered when
nonsurgical measures fail; however,
this technique carries a risk of
ten-don rupture.54
Recent studies have addressed the
feasibility of partial sheath resection
to decrease triggering and gliding
re-sistance This problem is of particu-lar concern when it involves the A2
or A4 pulleys Tang et al55 found a decrease in gliding resistance with partial pulley release However, a ca-daveric study by Mitsionis et al56 demonstrated that, although exci-sion of up to 25% of both the A2 and A4 pulleys had no significant effect
on the efficiency of motion, it did not achieve the goal of decreasing sheath resistance
Partial Tendon Injury
Partial tendon lacerations can be challenging; if not managed
proper-ly, they carry the risk of triggering, entrapment, or secondary rupture.57 Repair has been recommended for lacerations involving >60% of the tendon substance.58In other studies, the authors reported that trimming digital flexor tendon lacerations in-volving >50% of the tendon sub-stance was not associated with
trig-Figure 4
A,Joint contracture release via excision of the C1 portion of the flexor tendon sheath between the A2 and A3 pulleys exposes the flexor digitorum superficialis
(FDS) and flexor digitorum profundus (FDP) tendons B, The checkrein ligaments
are released with subsequent release of the collateral ligaments from palmar to dorsal * = transverse retinacular vessels, DIP = distal interphalangeal, PIP = proximal interphalangeal (Reproduced from Idler RS: Capsulectomies of the metacarpophalangeal and proximal interphalangeal joints, in Strickland JW [ed]:
Master Techniques in Orthopaedic Surgery: The Hand Philadelphia, PA:
Lippincott-Raven, 1998, pp 361-379 Illustrations copyright © Gary Schnitz and the Indiana Hand Center.)
Trang 8gering or rupture.59 In a study by
Erhard et al60 that compared
trim-ming with repair of partial
lacera-tions, the lowest gliding resistance
was produced with trimming,
with-out a concomitant decrease in
ten-don strength
Pulley Failure and
Bowstringing
The A2 and A4 pulleys are
re-sponsible for preserving digital
mo-tion and finger strength (grip and
pinch power) Loss of the integrity
of these pulleys results in
bow-stringing, with loss of the A4 pulley
causing the greatest change in the
efficiency of tendon excursion,
work, and force.61Avoidance of
bow-stringing is the best management
strategy and may be facilitated by
performing tendon repair through
cruciate pulley windows, using
ex-ternal pulley rings for compromised
pulleys, and reconstructing pulleys
in a one- or two-stage procedure
when native tissue is
unsalvage-able36(Figure 5)
Many techniques for pulley
re-construction have been described,
such as Bunnell, Kleinert, Lister, and
Karev Nishida et al62 found that
Lister’s technique of using the
exten-sor retinaculum for pulley recon-struction had the least resistance to tendon gliding
Quadriga
Quadriga is the inability of unin-jured fingers of the same hand to ob-tain full flexion It manifests as a weak grasp on physical examination
This complication is caused by func-tional shortening of the FDP tendon
Shortening of one FDP tendon af-fects the function of the FDP ten-dons of adjacent fingers, causing overadvancement of the FDP ten-don, proximal tendon tethering or adhesions, and insertion of a short tendon graft Anatomically, quadriga occurs because the common FDP muscle belly to the middle, ring, and small fingers permits only as much proximal excursion in each digit as that of the shortest tendon Proper tendon tensioning during repair pre-vents this problem When quadriga occurs, tenolysis of the proximal ad-hesions or transection of the short-ened tendon will release the unin-jured profundi.7
Swan-neck Deformity
Swan-neck deformity consists of hyperextension at the PIP joint with
flexion at the DIP joint In flexor ten-don repair, common causes include isolated FDS rupture and volar plate injury This complication is infre-quent, however; loss of the FDS is usually associated with minimal functional deficit Careful attention
to and correction of volar plate inju-ries at the time of tendon repair pre-vents this problem Surgical man-agement of the hyperextension deformity may be facilitated through tenodesis with one slip of the FDS tendon
Lumbrical Plus Deformity
Lumbrical plus deformity is the paradoxical extension at the IP joints
of the injured digit with attempted forceful flexion Normally, PIP and DIP joint flexion occurs in conjunc-tion with simultaneous relaxaconjunc-tion of the lumbrical muscle (Figure 6, A) Paradoxical extension arises when the FDP distal to the lumbrical mus-cle is functionally too long or is not present Flexor tendon force is
there-by transmitted to the lumbrical and subsequently to the extensor mech-anism via the lateral bands before full digital flexion is reached (Figure
6, B) Other causes of lumbrical plus deformity include avulsion of the
Figure 5
A digit in which pulley reconstruction
necessitated a two-stage revision The
A2 and A4 pulleys were repaired using
excised flexor tendons sutured to the
retained tendon sheath edge combined
with a silicone rod tendon (Courtesy
of George S Edwards, Jr, MD, Raleigh,
NC.)
Figure 6
A,In normal finger mechanics, interphalangeal (IP) flexion occurs with concomitant
lumbrical relaxation B, In lumbrical plus deformity, extension of the IP joints
paradoxically is through the lateral bands once the limit of lumbrical relaxation is
reached (Reproduced with permission from Parkes A: The “lumbrical plus” finger J Bone Joint Surg Br 1971;53:236-239.)
Trang 9FDP tendon or amputation through
the proximal phalanx.63
Manage-ment involves lumbrical muscle
re-lease or placement of a tendon graft
of appropriate length
Summary
Despite advances in flexor tendon
surgery over the past 50 years,
com-plications continue to occur The
most common are adhesion
forma-tion and joint contracture
Achiev-ing optimal outcomes occurs
through meticulous surgical repair
using 3-0 or 4-0 polyfilament core
suture with a minimum of four
strands reinforced with an
epitendi-nous suture, a well-fitting splint,
early controlled mobilization, and
vigilant patient monitoring for
com-pliance with the rehabilitation
pro-gram Biochemical and molecular
advances in the research into
scar-less healing likely will lead to future
advances
References
Evidence-based Medicine:Level I/II
prospective studies include
referenc-es 16, 26, 27, 29, 30, 40, and 41 The
remaining references are
case-controlled reports or experimental
observations
Citation numbers printed in bold
type indicate references published
within the past 5 years
1 Verdan CE: Half a century of
flexor-tendon surgery: Current status and
changing philosophies J Bone Joint
Surg Am1972;54:472-491.
2 Bunnell S: Repair of tendons in the
fgers and description of two new
in-struments Surg Gynecol Obstet
1918;26:103-110.
3 Kleinert HE, Kutz JE, Ashbell TS,
Martinez E: Primary repair of
lacerat-ed flexor tendons in “no man’s land.”
J Bone Joint Surg Am1967;49:577.
4 Strickland JW: Development of flexor
tendon surgery: Twenty-five years of
progress J Hand Surg [Am] 2000;25:
214-235.
5 Saldana MJ, Chow JA, Gerbino P,
Westerbeck P, Schacherer TG:
Fur-ther experience in rehabilitation of
zone II flexor tendon repair with dy-namic traction splinting. Plast Reconstr Surg1991;87:543-546.
6 Doyle JR: Anatomy of the finger flexor tendon sheath and pulley system.
J Hand Surg [Am]1988;13:473-484.
7 Strickland JW: Flexor tendons—acute injuries, in Green DP, Hotchkiss RN,
Pederson WC (eds): Green’s Operative
Hand Surgery, ed 4 New York, NY:
Churchill Livingstone, 1999, vol 2,
pp 1851-1897.
8 Kakar S, Khan U, McGrouther DA:
Differential cellular response within the rabbit tendon unit following
ten-don injury J Hand Surg [Br] 1998;23:
627-632.
9 Gelberman RH, Woo SL, Lothringer
K, Akeson WH, Amiel D: Effects of early intermittent passive mobiliza-tion on healing canine flexor tendons.
J Hand Surg [Am]1982;7:170-175.
10 Aoki M, Kubota H, Pruitt DL, Manske PR: Biomechanical and histologic characteristics of canine flexor ten-don repair using early postoperative
mobilization J Hand Surg [Am]
1997;22:107-114.
11 Kubota H, Manske PR, Aoki M, Pruitt
DL, Larson BL: Effect of motion and tension on injured flexor tendons in
chickens J Hand Surg [Am] 1996;21:
456-463.
12 Gelberman RH, Boyer MI, Brodt MD, Winters SC, Silva MJ: The effect of gap formation at the repair site on the strength and excursion of intrasy-novial flexor tendons: An experimen-tal study on the early stages of
tendon-healing in dogs J Bone Joint Surg Am
1999;81:975-982.
13 Ochiai N, Matsui T, Miyaji N, Merk-lin RJ, Hunter JM: Vascular anatomy
of flexor tendons: I Vincular system and blood supply of the profundus
ten-don in the digital sheath J Hand Surg
[Am]1979;4:321-330.
14 Weber ER, Hardin G, Haynes DW:
Synovial fluid nutrition of flexor ten-dons Presented at the 25th Annual Meeting of the Orthopaedic Research Society, San Francisco, CA, February 20-22, 1979.
15 Pruitt DL, Manske PR, Fink B: Cyclic stress analysis of flexor tendon repair.
J Hand Surg [Am]1991;16:701-707.
16 Silfverskiöld KL, May EJ, Törnvall AH: Gap formation during controlled motion after flexor tendon repair in zone II: A prospective clinical study.
J Hand Surg [Am]1992;17:539-546.
17 Boyer MI, Strickland JW, Engles D,
Sachar K, Leversedge FJ: Flexor ten-don repair and rehabilitation: State of
the art in 2002 Instr Course Lect
2003;52:137-161.
18 Hatanaka H, Zhang J, Maske PR: An
in vivo study of locking and grasping techniques using a passive mobiliza-tion protocol in experimental
ani-mals J Hand Surg [Am]
2000;25:260-269.
19 Tanaka T, Amadio PC, Zhao C, Zobitz
ME, Yang C, An KN: Gliding charac-teristics and gap formation for locking and grasping tendon repairs: A biome-chanical study in a human cadaver
model J Hand Surg [Am] 2004;29:
6-15.
20 Barrie KA, Tomak SL, Cholewicki J,
Merrell GA, Wolfe SW: Effect of su-ture locking and susu-ture caliber on fa-tigue strength of flexor tendon repairs.
J Hand Surg [Am]2001;26:340-346.
21 Lin GT, An KN, Amadio PC, Cooney
WP III: Biomechanical studies of run-ning suture for flexor tendon repair in
dogs J Hand Surg [Am]
1988;13:553-558.
22 Beredjiklian PK: Biologic aspects of
flexor tendon laceration and repair.
J Bone Joint Surg Am 2003;85:539-550.
23 Lister GD, Kleinert HE, Kutz JE, Atasoy E: Primary flexor tendon re-pair followed by immediate
con-trolled mobilization J Hand Surg
[Am]1977;2:441-451.
24 Chow JA, Thomes LJ, Dovelle S, Milnor WH, Seyfer AE, Smith AC: A combined regimen of controlled mo-tion following flexor tendon repair in
“no man’s land.” Plast Reconstr Surg
1987;79:447-453.
25 Horii E, Lin GT, Cooney WP, Lin-scheid RL, An KN: Comparative
flex-or tendon excursion after passive
mo-bilization: An in vitro study J Hand
Surg [Am]1992;17:559-566.
26 Bainbridge LC, Robertson C, Gillies
D, Elliot D: A comparison of post-operative mobilization of flexor ten-don repairs with “passive flexion-active extension” and “controlled
active motion” techniques J Hand
Surg [Br]1994;19:517-521.
27 Peck FH, Bücher CA, Watson JS, Roe A: A comparative study of two meth-ods of controlled mobilization of
flex-or tendon repairs in zone 2 J Hand
Surg [Br]1998;23:41-45.
28 Riaz M, Hill C, Khan K, Small JO: Long term outcome of early active mobilization following flexor tendon
repair in zone 2 J Hand Surg [Br]
1999;24:157-160.
29 Kitsis CK, Wade PJ, Krikler SJ, Parsons
NK, Nicholls LK: Controlled active motion following primary flexor ten-don repair: A prospective study over
Trang 109 years J Hand Surg [Br] 1998;23:
344-349.
30 Wada A, Kubota H, Miyanishi K,
Hatanaka H, Miura H, Iwamoto Y:
Comparison of postoperative early
ac-tive mobilization and immobilization
in vivo utilising a four-strand flexor
tendon repair J Hand Surg [Br] 2001;
26:301-306.
31 Tang JB, Wang B, Chen F, Pan CZ, Xie
RG: Biomechanical evaluation of
flex-or tendon repair techniques Clin
Orthop Relat Res2001;386:252-259.
32 Labana N, Messer T, Lautenschlager
E, Nagda S, Nagle D: A biomechanical
analysis of the modified Tsuge suture
technique for repair of flexor tendon
lacerations J Hand Surg [Br] 2001;
26:297-300.
33 Boyer MI, Gelberman RH, Burns ME,
Dinopoulos H, Hofem R, Silva MJ:
In-trasynovial flexor tendon repair: An
experimental study comparing low
and high levels of in vivo force during
rehabilitation in canines J Bone
Joint Surg Am2001;83:891-899.
34 Lieber RL, Silva MJ, Amiel D,
Gelber-man RH: Wrist and digital joint
mo-tion produce unique flexor tendon
force and excursion in the canine
fore-limb J Biomech 1999;32:175-181.
35 Zhao C, Amadio PC, Momose T,
Cou-vreur P, Zobitz ME, An KN: Effect of
synergistic wrist motion on adhesion
formation after repair of partial flexor
digitorum profundus tendon
lacera-tions in a canine model in vivo.
J Bone Joint Surg Am2002;84:78-84.
36 Taras JS, Gray RM, Culp RW:
Compli-cations of flexor tendon injuries.
Hand Clin1994;10:93-109.
37 Peterson WW, Manske PR, Dunlap J,
Horwitz DS, Kahn B: Effect of various
methods of restoring flexor sheath
in-tegrity on the formation of adhesions
after tendon injury J Hand Surg
[Am]1990;15:48-56.
38 Gelberman RH, Woo SL, Amiel D,
Horibe S, Lee D: Influences of flexor
sheath continuity and early motion
on tendon healing in dogs J Hand
Surg [Am]1990;15:69-77.
39 Zhao C, Amadio PC, Zobitz ME, An
KN: Resection of the flexor digitorum
superficialis reduces gliding
resis-tance after zone II flexor digitorum
profundus repair in vitro J Hand
Surg [Am]2002;27:316-321.
40 Chow SP, Pun WK, So YC, et al: A
pro-spective study of 245 open digital
frac-tures of the hand J Hand Surg [Br]
1991;16:137-140.
41 Golash A, Kay A, Warner JG, Peck F,
Watson JS, Lees VC: Efficacy of ADCON-T/N after primary flexor tendon repair in zone II: A controlled
clinical trial J Hand Surg [Br] 2003;
28:113-115.
42 Kulick MI, Smith S, Hadler K: Oral ibuprofen: Evaluation of its effect on peritendinous adhesions and the breaking strength of a tenorrhaphy.
J Hand Surg [Am]1986;11:110-120.
43 Ketchum LD: Effects of triamcino-lone on tendon healing and function:
A laboratory study Plast Reconstr
Surg1971;47:471-482.
44 Chang J, Most D, Stelnicki E, et al:
Gene expression of transforming growth factor beta-1 in rabbit zone II flexor tendon wound healing: Evi-dence for dual mechanisms of repair.
Plast Reconstr Surg 1997;100:937-944.
45 Chang J, Most D, Thunder R, Mehrara
B, Longaker MT, Lineaweaver WC:
Molecular studies in flexor tendon wound healing: The role of basic fibro-blast growth factor gene expression.
J Hand Surg [Am] 1998;23:1052-1058.
46 Khan U, Kakar S, Akali A, Bentley G, McGrouther DA: Modulation of the formation of adhesions during the
healing of injured tendons J Bone
Joint Surg Br2000;82:1054-1058.
47 Moran SL, Ryan CK, Orlando GS, Pratt CE, Michalko KB: Effects of 5-fluorouracil on flexor tendon repair.
J Hand Surg [Am]2000;25:242-251.
48 Matloub HS, Dzwierzynski WW, Erickson S, Sanger JR, Yousif NJ, Muoneke V: Magnetic resonance im-aging scanning in the diagnosis of
zone II flexor tendon rupture J Hand
Surg [Am]1996;21:451-455.
49 Strickland JW: Flexor tenolysis.
Hand Clin1985;1:121-132.
50 Feldscher SB, Schneider LH: Flexor
tenolysis Hand Surg 2002;7:61-74.
51 Strickland JW: Flexor tenolysis, in
Strickland JW (ed): Master
Tech-niques in Orthopaedic Surgery: The Hand Philadelphia, PA: Lippincott-Raven, 1998, pp 525-538.
52 Idler RS: Capsulectomies of the metacarpophalangeal and proximal interphalangeal joints, in Strickland
JW (ed): Master Techniques in
Ortho-paedic Surgery: The Hand
Philadel-phia, PA: Lippincott-Raven, 1998,
pp 361-379.
53 Harris SB, Harris D, Foster AJ, Elliot D: The aetiology of acute rupture of flexor tendon repairs in zones 1 and 2
of the fingers during early
mobiliza-tion J Hand Surg [Br]
1999;24:275-280.
54 Seradge H, Kleinert HE: Reduction flexor tenoplasty: Treatment of stenosing flexor tenosynovitis distal
to the first pulley J Hand Surg [Am]
1981;6:543-544.
55 Tang JB, Wang YH, Gu YT, Chen F:
Ef-fect of pulley integrity on excursions and work of flexion in healing flexor
tendons J Hand Surg [Am] 2001;26:
347-353.
56 Mitsionis G, Bastidas JA, Grewal R, Pfaeffle HJ, Fischer KJ, Tomaino MM: Feasibility of partial A2 and A4 pulley excision: Effect on finger flexor
ten-don biomechanics J Hand Surg [Am]
1999;24:310-314.
57 Schlenker JD, Lister GD, Kleinert HE: Three complications of untreated par-tial laceration of the flexor tendon-entrapment, rupture, and triggering.
J Hand Surg [Am]1981;6:392-398.
58 Bishop AT, Cooney WP III, Wood MB: Treatment of partial flexor tendon lac-erations: The effect of tenorrhaphy and early protected mobilization.
J Trauma1986;26:301-312.
59 al-Qattan MM: Conservative man-agement of zone II partial flexor ten-don lacerations greater than half the
width of the tendon J Hand Surg [Am]
2000;25:1118-1121.
60 Erhard L, Zobitz ME, Zhao C, Amadio
PC, An KN: Treatment of partial lac-erations in flexor tendons by trim-ming: A biomechanical in vitro study.
J Bone Joint Surg Am 2002;84:1006-1012.
61 Rispler D, Greenwald D, Shumway S, Allan C, Mass D: Efficiency of the flexor tendon pulley system in human
cadaver hands J Hand Surg [Am]
1996;21:444-450.
62 Nishida J, Amadio PC, Bettinger PC,
An KN: Flexor tendon-pulley interac-tion after pulley reconstrucinterac-tion: A biomechanical study in a human
model in vitro J Hand Surg [Am]
1998;23:665-672.
63 Parkes A: The “lumbrical plus”
fin-ger J Bone Joint Surg Br
1971;53:236-239.