The Journal of Foot & Ankle Surgery 51 (2012) 509516

Contents lists available at ScienceDirect

The Journal of Foot & Ankle Surgery

journal homepage: www.jfas.org

Surgical Reconstruction and Mobilization Therapy for a Retracted Extensor Hallucis

Longus Laceration and Tendon Defect Repaired by Split Extensor Hallucis Longus
Tendon Lengthening and Dermal Scaffold Augmentation
Robert M. Joseph, DPM, PhD, FACFAS 1, Jessica Barhorst, DPT, PT 2
1
Perspective Advantage Solutions, LLC, Dayton, OH
2
Orion Physical Therapy Specialists, LLC, Dayton, OH

a r t i c l e i n f o a b s t r a c t

Level of Clinical Evidence: 4 A reconstructive technique and physical therapy protocol is presented for the treatment of extensor hallucis
Keywords: longus (EHL) lacerations with critical size defects caused by tendon retraction. The primary goal of treatment
foot was to restore EHL structure and function without the use of a bridging allograft or tendon transfer. The
hallux technique is performed by split lengthening the distal segment of the lacerated EHL and rotating the
injury
lengthened segment proximally 180 to bridge the tendon defect. The lengthened tendon is then sutured to
physical therapy
the proximal segment of the EHL. The EHL is then tubularized with an acellular dermal scaffold at the region of
reconstructive surgery
tissue adhesion tendon rotation to improve tendon strength, minimize the probability of tendon overlengthening or re-
rupture, and improve the tendon gliding motion, which can be compromised by the tendon irregularity
caused by rotation of the tendon. Postoperative range of motion therapy should be initiated at 3 weeks
postoperatively. A case report of this technique and postoperative mobilization protocol is presented. The
American Orthopaedic Foot and Ankle Society midfoot score at 3 and 6 months postoperatively was 90 of 100.
The patient regained active dorsiexion motion of the hallux without functional limitations, deformity, or
contracture of the hallux. The advantages of this technique include that a large cadaveric allograft is not
needed to bridge a critical size tendon defect and tendon lengthening provides a biologically active tendon
graft without the secondary comorbidities and dysfunction commonly associated with tendon transfer
procedures.
2012 by the American College of Foot and Ankle Surgeons. All rights reserved.

Extensor tendon injuries of the foot represent 1% of tendon injuries
(1). Extensor hallucis longus (EHL) lacerations are even less common,
and research on EHL lacerations has been limited to a small number of
case reports and series (1). EHL lacerations cause acute hallux
dysfunction and can result in a progressive contracture deformity of
the hallux (2). Lacerations are most commonly associated with
trauma; however, tendon ruptures have also been associated with
chronic disease, tendon overuse, steroid injections, and shoe gear
pressure (1,35). Acute surgical repair is recommended for most EHL
lacerations, with reports (1,610) of fair to good outcomes, as
described by Lipscomb and Kelly (Table 1) (9). In most reports, open
lacerations were explored and retracted tendons repaired through the
wound, with limited surgical dissection (1,11). The reports have
collectively suggested that direct tendon repair is most successful
Financial Disclosure: None reported.
Conict of Interest: None reported.
Address correspondence to: Robert M. Joseph, DPM, PhD, FACFAS, Perspective
Advantage Solutions, LLC, 305 Oakwood Avenue, Dayton OH 45409.
E-mail address: Footbiochemistry@hotmail.com (R.M. Joseph).
when the tendon retraction is minimal. Tendon retraction most
commonly occurs with lacerations in zones in which the ligamentous
and retinacular structures do not tether the EHL (Fig. 1) (1). For
example, lacerations in the midfoot, zone IV, are more prone to tendon
retraction and less amenable to simple repair than zone II lacerations,
near the extensor expansion of the hallux (1). Tendon retraction can
present a signicant intraoperative challenge when attempting to
identify and reapproximate the free tendon segments. Signicant
tendon retraction can prohibit direct repair altogether and require
large or secondary incisions to identify the remaining tendon and
restore tendon structure with grafting (12,13). Fascia lata, gracilus, and
peroneous tendon grafts have all been used to restore EHL structure
and function (12,13). Floyd et al (7) reported, in a case series, that 2 of
12 repairs required an additional incision to identify and reapprox-
imate retracted tendon segments. Currently, no clinical guidelines are
available to suggest when tendon retraction specically warrants
a second surgical incision. Historically, large second incisions and
extensive soft tissue dissection were ill advised with tendon repair
owing to the risk of complications from painful adhesion and scar
formation (6,10,14). Nonoperative care has historically been

1067-2516/$ - see front matter 2012 by the American College of Foot and Ankle Surgeons. All rights reserved.
doi:10.1053/j.jfas.2012.04.018
510 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
Table 1
Clinical outcomes of extensor hallucis longus laceration repair
Outcome Description
Good Normal function, strength, and pain free range of metatarsalphalangeal
joint motion compared with contralateral foot
Fair Active pain free range of motion of metatarsalphalangeal joint without
hallux dysfunction but with some weakness compared with
contralateral foot
Poor Failed repair with lack of hallux function, pain, and loss of active
extension of hallux
recommended instead of surgery when extensive surgical dissection is
necessary. However, more recent reports have contradicted older
recommendations by demonstrating improved hallux function after
EHL repair with grafting and tendon transfer procedures (1,6,12,15).
Hence, evidence is emerging that more extensive surgical approaches
can be more effective than previously believed, and primary repair
might be the favored treatment in most circumstances (1,12,1517).
Grafting and tendon transfer procedures are not without complica-
tions, however, and each procedure has inherent limitations (18).
Cadaveric allografts are compromised by the terminal sterilization
processes that render them devoid of living cells and unable to fully
integrate with the surrounding tissue (19,20). Allografts also pose the
risk of communicable disease; however, advances in donor screening
and graft sterilization have minimized these risks (21,22). Autografts
and tendon transfers from remote sites are associated with donor site
morbidity and potential functional decits at the site of harvest. Split
tendon lengthening procedures might have advantages to alternate
tendon bridging techniques in select circumstances when the
secondary functional and biologic limitations of tendon transfers and
allografts are a concern.
Neglected tendon lacerations are among the most complicated
tendon injuries to treat with the least predictable surgical outcome. A
host of factors complicate delayed tendon surgery, and the debate is
considerable regarding how much time is acceptable between the
point of injury and surgery (23). Those with neglected lacerations
Fig. 1. Zones of injury of extensor halluci longus tendon and corresponding surface
anatomy related to fascial structures that limit tendon retraction after injury.
often complicate their condition by underestimating the severity of
their injury and continuing with weightbearing activity on the injured
foot (16). Ankle motion with activity promotes tendon retraction,
increasing the complexity of surgery and the likelihood that grafting
or tendon transfer procedures will be necessary to restore tendon
structure and function (24). Neglected lacerations can also be asso-
ciated with greater tissue necrosis than acutely repaired lacerations.
Tissue necrosis can require extensive debridement that further
disrupts tenosynovium integrity and increases the risk of adhesion
formation (15,25,26). Delayed repair has also been associated with
limited tendon excursion and gliding within the tendon sheath (23).
Finally, extended periods of muscle disuse can result in progressive
brosis and degeneration of the muscle complex (27). These changes
compromise the normal physiologic tensionfunction relationship of
the myotendinous unit and compromise the surgeons ability to
restore muscle function (27). Each of these factors can present
unanticipated intraoperative scenarios that require more extensive
surgery than planned preoperatively, because the severity of these
factors cannot always be appreciated as well using magnetic reso-
nance imaging (MRI) and clinical examination as they can be intra-
operatively. Thus, it should be no surprise that nonoperative
treatment has been favored over surgery when clinical situations
unpredictably increase the operative risks of adhesion formation (6).
More recently, reports have related promising outcomes after delayed
treatment and the use of more extensive surgical procedures to repair
extensor tendon injuries (1,35,12,15,16). Although a general lack of
outcome data suggests a case by case rather than a routine approach
to surgically repairing neglected extensor tendon injuries, advance-
ments in surgical technique, biologic adjuncts, and postoperative
therapy protocols hold the promise of improved outcomes with
delayed surgery compared with those in the past.
Tissue scaffolds are surgical adjuncts used to re-enforce tendons
and promote healing (23,24). Biologic adjuncts have become more
common in foot and ankle surgery as the commercial markets for these
products have expanded. Scaffolds facilitate healing by providing
biologic factors, structural support, and a 3-dimensional matrix that
serves as a platform for tissue repair (28,29). The unique properties of
scaffolds are a function of the characteristics of the native tissues they
are derived from and the artifacts of processing (2933). Some of the
more common scaffolds used in tendon repair surgery are derived
from skin or visceral membranes (29,34). The variability in the thick-
ness, tensile modulus, and extracellular matrix composition of
commercially available scaffolds is signicant (29,35). A combination
of methods that physically alter, chemically treat, and enzymatically
modify the tissues is used to create the tissue scaffolds, but none are
able to precisely recapitulate the biologic and mechanical properties of
native tendon. Thus, most commercially available scaffolds have only
been approved by the Food and Drug Administration for soft tissue
augmentation and not as bridging grafts (29,36). GraftJacket (Wright
Medical Technology, Arlington, TN) an acellular human dermis-
derived scaffold, has been used to augment various soft tissues,
including skin, Achilles tendon, and rotator cuff (3740), and was used
with the technique described in the present report. Graft Jacket
(Wright Medical Technology) is reportedly well tolerated in patients
when used in the surgical repair of tendinous structures and elicits
a limited inammatory response (28). Studies have suggested histo-
logic evidence of tissue ingrowth and neovascularization within the
GraftJacket (Wright Medical Technology) (28). The primary concerns
of scaffold use in tendon surgery include prolonged inammation,
graft encapsulation, calcication, and adhesion formation that results
in pain, limited tendon excursion, and limited function (29,31,33,4143).
The optimal scaffold design and composition that maximizes biome-
chanical performance and tendon healing is unknown. Novel methods
and applications of natural, synthetic, and semisynthetic materials are
 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
an area of extensive research and initiatives in tissue engineering and
regeneration today.
The trends in outcome research suggest early mobilization therapy
plays a critical role in tendon healing and function (44). Early
mobilization promotes the preferred pathways of intrinsic tendon
healing associated with less adhesion formation than the extrinsic
pathways of repair that occur more prevalently with prolonged
immobilization (44). It is unclear, however, how the benets of early
mobilization might vary among tendons, depending on the injury site
and functional demands of the tendon (4547). Inconsistencies in
research protocols, tendon involvement, and injury location has made
answering questions such as these difcult and complicates the
translation of research into practical clinical protocols (47). The general
trend in research opinion, however, is that small tendon rehabilitation
consisting of active and passive mobilization can safely begin at 3 weeks
postoperatively for most patients and possibly as early as 48 hours
postoperatively (44,4850). The Norwich and Belfast mobilization
regiments of the hand begin mobilization at 48 hours postoperatively,
and research has suggested less adhesion formation and improved
tendon excursion with these protocols. However, these protocols have
been associated with slightly greater re-rupture rates than protocols
with longer periods of immobilization (51,52). The greater rates of
repeat injury might be related to tendon overloading during the rst 3
weeks of healing when the tendon substance is physically weakest and
tendon strength is more a function of surgeon technique and not
tendon healing (51,52). In addition, animal studies suggest that before 3
weeks, the gliding resistance of healing tendons is high and over-
aggressive mobilization during this period could promote, rather than
inhibit, adhesion formation, despite the benets of tendon loading,
which promotes intrinsic healing (44). Hence, caution is advised in
initiating therapy too early, regardless of the advancements in suture
techniques and available scaffolds that increase the immediate strength
of the repaired tendons (15,5356). Other factors believed to inuence
the efcacy of mobilization therapy include the frequency, duration,
rate, and total number of cycles of tendon motion with therapy.
However, the optimum conditions that promote tissue repair, strength,
and function have only begun to be examined (48,49,57). Basic science
and clinical studies have suggested that early protected motion of the
tendon with as little as 3 to 5 mm of tendon excursion might be suf-
cient to reduce adhesion formation in exor tendons and promote
intrinsic healing. It is reasonable to suspect that extensor tendon
rehabilitation could fair as well under similar conditions (48,58,59). In
canines, tendon repair strength and stiffness has been shown to
increase with rates of tendon motion of 60 daily cycles at 60 cycles/5
min compared with 60 daily cycles at 60 cycles/60 min, although
gliding friction was not shown to be affected by the rate of motion (48).
It has been speculated that a greater frequency of motion might
improve tendon strength and repair by assisting the synovial uid
diffusion that is essential for tendon health (44). Early tendon motion
has also been shown to improve tenosynovium healing (44).
During the course of mobilization therapy of the foot, the transi-
tion from nonweightbearing to weightbearing is a signicant mile-
stone. It is unclear, however, whether the weightbearing conditions of
the foot warrant special precautions compared with those for the
hand when resuming activity. This question is particularly difcult to
address given that most of the research on the effects of tendon
mobilization on healing has related to the exor tendon physiology of
the hand, less to the hand extensor physiology, and the least to the
foot extensor physiology. Clinical studies have reported ambulatory
protocols that range from immediate guarded weightbearing in a cast
to 6 weeks of immobilization with or without early mobilization,
suggesting signicant latitude in EHL tolerance to the functional
demands of the hallux while healing (4,5,9,18). Although no standard
clinical practice guidelines are available for postoperative
511
mobilization after EHL repair, the initiation of passive range of motion
at 3 weeks postoperatively has consistently been reported to be well
tolerated for most tendon injuries (15,60). Collectively, the combi-
nation of basic science and clinical research suggest mobilization
therapy promotes tendon healing and improved function.
Case Report
A 36-year-old female presented with a complete laceration of the
EHL tendon in April 2011 when a kitchen knife fell on the dorsum of
her foot. The patient presented 1 week after the initial injury with
a complaint of pain, a wound, inability to raise the great toe, and
difculty walking. The patients occupational demands included
extensive weightbearing, bending, and climbing activities as an
owner and operator of a domestic cleaning business. The patients
medical history included medically controlled hypertension and
tobacco use of 1 pack of cigarettes daily for the previous 15 years. The
physical examination revealed a noninfected, 2-cm laceration on the
dorsal aspect of the foot (Fig. 2). The patient was unable to dorsiex
the hallux and demonstrated a hallux extensor muscle strength of 0 of
5. Flexor strength and function were intact to the hallux, with
a muscle strength of 5 of 5. The nonweightbearing resting position of
the hallux was slightly inferior to the transverse plane alignment of
the lesser digits. The neurovascular status to the foot was intact.
Proximal retraction of the EHL was clinically noted to the level of the
anterior ankle joint as a palpable mass that was later conrmed on
MRI (Figs. 3 and 4). The patient initially deferred surgical treatment
and was treated with local wound care, tetanus immunization, and
immobilization with a walking brace (CAM boot), with instructions
for no weightbearing on the lacerated foot. However, 3 weeks after
the injury, the patient decided to pursue surgical care, at which point
MRI without contrast of the foot and ankle was obtained and
conrmed the isolated complete transection injury of the EHL tendon.
The tendon was lacerated at the level of the rst tarsal metatarsal
joint, and the proximal segment of the tendon had retracted to create
a 6-cm tendon gap (Figs. 3 and 4). No concomitant bone, ligament,
nerve, or secondary tendon injuries were noted on MRI. The period
from injury to surgery was 28 days.
Preoperative Planning
Although MRI is not necessary to diagnose EHL lacerations, it was
invaluable for preoperative surgical planning for the split tendon
lengthening repair technique. MRI was used to measure the EHL
tendon gap, evaluate the integrity of the lacerated tendon segments,
and calculate whether the distal EHL segment had sufcient length
that would tolerate split lengthening to bridge the gap caused by
tendon retraction. MRI showed approximately 7 to 8 cm of an intact
Fig. 2. Clinical presentation of laceration of extensor hallucis longus at the rst tarsal
metatarsal joint region with palpable retraction of the tendon to ankle level.
512 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
Fig. 3. Sagittal cross-section of T1-weighted magnetic resonance imaging scan obtained
3 weeks after initial injury demonstrating complete extensor hallucis longus laceration
with tendon retraction to the level of the anterior ankle. Region demonstrating 6-cm gap
between lacerated extensor hallucis longus segments (asterisk).
distal tendon segment that extended from the interphalangeal joint of
the hallux to the point of laceration at the level of the rst tarsal
metatarsal joint. A tendon gap of approximately 6 cm was estimated
between the lacerated tendon segments. The proximal portion of the
lacerated tendon was retracted to the level of the anterior ankle
beneath the extensor retinaculum. MRI also showed the extensor
hallucis brevis (EHB) tendon was approximately one half the diameter
of the EHL (Fig. 5).
Surgical Technique
Surgical repair was performed through a 12-cm linear incision
placed 2 cm medial to the original wound and parallel with the course
of the EHL. The incision extended from the interphalangeal joint of the
hallux to the anterior ankle. The ankle retinaculum was transected,
and the tenosynovial sheath of the EHL was evacuated of hematoma.
Care was taken to maintain the integrity of the tenosynovium for later
closure. The ends of the transected tendon were identied, and the
Fig. 4. Sagital cross-section of T2-weighted magnetic resonance imaging scan demon-
strating complete extensor hallucis longus laceration with tendon retraction to the level of
the anterior ankle. Magnetic resonance imaging scan obtained 3 weeks after initial injury.
Region demonstrating 6-cm gap between lacerated extensor hallucis longus segments
(asterisk).
devitalized tendon was excised. The distal segment of the lacerated
EHL was then incised longitudinally with an L-shaped incision along
the midline of the tendon. The incision began at the interphalangeal
joint of the hallux and was extended proximally to a point 1 cm distal
from the original laceration (Fig. 6). The incision was made in
a fashion similar to that described by Berens (13), who used a similar
technique to lengthen the EHB. The split portion of the tendon was
then rotated proximally 180 to increase the functional length of the
EHL and bridge the tendon gap (Fig. 7). Umbilical tape was used to
measure the length of tendon needed to bridge the tendon defect. The
rotated segment of the EHL was then sutured to the proximal stump of
the EHL using an overlay technique with 3.0 Prolene and a running
locking suture to secure the 2 tendon segments. Approximately
0.5 cm of the distal tendon segment was overlaid onto the proximal
tendon stump. The EHL was repaired with the hallux in a neutral
position and resting tendon tension, without evidence of tendon
bowstringing (10). The lengthened tendon was then reinforced with
4.0 Prolene suture at the point of tendon rotation to prevent further
propagation of tendon lengthening or tendon re-rupture (Fig. 7). This
region was then tubularized with an acellular dermal scaffold
(GraftJacket; Wright Medical Technology) to improve tendon
strength, minimize the probability of additional tendon lengthening,
and improve the tendon gliding motion compromised by tendon
irregularity and possible impingement caused by rotation of the
tendon (Fig. 8) (44,61). The tenosynovium was then repaired with
a running locking 5.0 Vicryl suture. Autogenous platelet-rich plasma
was inltrated between the repaired tendon and tenosynovium
during closure of the tenosynovium. The hallux was then brought
through the range of motion to ascertain smooth tendon excursion
without resistance. The skin was then closed in layers. A multilayered
compression dressing and nonweightbearing short leg cast were
applied to the lower extremity at the conclusion of the procedure.
Postoperative Care and Mobilization Therapy
Phase I: Nonweightbearing on Operative Limb (weeks 1 to 3)
The patient remained nonweightbearing during the rst 3 weeks
postoperatively with the foot immobilized in a short leg cast with
a toe plate. A multilayered compression dressing was applied beneath
the short leg cast for edema control. The ankle was placed at 90 with
casting, and the hallux was placed in a neutral position.
Fig. 5. T1-weighted magnetic resonance imaging scan of the foot demonstrating
comparative diameters of the extensor hallucis brevis and extensor hallucis longus.
Transverse section of T1-weighted image of the forefoot showing the diameter of the
cross extensor hallucis longus measuring 4.5 mm (A) and extensor hallucis brevis
measuring 2.2 mm (B).
 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
Fig. 6. Split tendon lengthening of extensor hallucis longus tendon to be used as bridge
graft for repairing lacerated extensor hallucis longus and 6-cm tendon defect. The distal
segment of the lacerated extensor hallucis longus tendon was split lengthened from the
interphalangeal joint of the hallux (A) to a point 1.5 cm distal to the most proximal end of
that segment (B). The tendon was split lengthened along the midline of the tendon using
an L-shaped incision. The tendon was then rotated proximally 180 to bridge a 6-cm
tendon gap caused by proximal retraction of the lacerated tendon.
Phase II: Controlled Passive and Active Mobilization Therapy (weeks 4
to 7)
The patient began controlled passive and active mobilization
therapy and guarded weightbearing with a walking brace (CAM boot)
at 3 weeks postoperatively. Passive grade III dorsiexion and plan-
tarexion mobilization therapy for the rst metatarsalphalangeal and
interphalangeal joint was performed daily by the patient combined
with weekly physical therapy sessions as listed in Table 2 (62).
The patient was encouraged to weight bear with the brace to toler-
ation. The use of a xed ankle brace with the ankle xed at 90 , in
theory, limits EHL tendon excursion and thus reduces tendon stress
with activity compared with unrestricted ankle motion (63). The rigid
rocker bottom foot plate of the brace assisted in reducing excess
Fig. 7. Repair of 6-cm tendon defect in a lacerated extensor hallucis longus by split
lengthening remaining extensor hallucis longus. The procedure was performed by split
lengthening the distal segment of the lacerated extensor hallucis longus in a longitudinal
fashion along the midline of the tendon using an L-shaped incision. The tendon was
lengthened from the interphalangeal joint to a point 1.5 cm proximal to the laceration.
The split portion of the tendon was then rotated 180 proximally at point A to bridge a
6-cm tendon gap. The rotated tendon was then sutured to the proximal segment of the
lacerated extensor hallucis longus using 4.0 Prolene and a running locking suture tech-
nique at point B. Extensor hallucis longus was then re-enforced at the point of tendon
rotation (A) by tubularizing the tendon with 4.0 Prolene suture.
513
Fig. 8. Re-enforcement of split-lengthened extensor hallucis longus with a dermal scaffold
at the point of weakness caused by tendon rotation that enabled tendon lengthening. A split
lengthened extensor hallucis longus was used to repair a critical size defect in the lacerated
extensor hallucis longus. The defect was bridged by rotating the split tendon proximally.
Tendon rotation creates a point of weakness in the tendon that makes the tendon
susceptible to re-rupture or overlengthening. Tendon rotation also creates an irregularity in
the gliding surface of the tendon that increases the risk of tendon impingement and
adhesion formation. A dermal scaffold was tubularized around the extensor hallucis longus
in this region to re-enforce the tendon and provide greater continuity in the tendon gliding
surface to reduce the risk of tendon failure, impingement, and adhesion formation.
tension and strain on the EHL by restricting the plantarexion motion
of the hallux, similar to the splinting therapy used for after hand
surgery. The ability to participate in unrestricted hallux extension
with weightbearing enables controlled active EHL mobilization. This
phase of rehabilitation provided a combination of controlled passive
and active mobilization similar to the mobilization protocols used
for the hand such as the Belfast regimen. Unlike the hand regimens,
however, mobilization was begun at 3 weeks rather than 48 hours
postoperatively to mitigate the risk of tendon gapping and re-
rupture during the early phase of tendon healing when the tendon
is weakest.
Phase III: Weeks 8 to 10
At 8 weeks postoperatively, the patient transitioned from guarded
weightbearing in a xed ankle brace to regular shoe gear with the use
of a removable carbon ber footplate placed beneath the insole of her
shoe. The transition from a xed ankle brace to unrestricted ankle
motion in theory enables greater EHL tendon excursion with active
and passive mobilization. The use of a carbon footplate protects the
EHL from excess tension with hallux plantarexion while preserving
the potential benets of unrestricted ankle motion with mobilization.
Phase IV: Weeks 10 Onward
At 10 weeks postoperatively, the patient was transitioned from the
use of a carbon ber footplate with shoe gear to not using it with shoe
gear. The transition was gradual during a 2-week period at a recom-
mended schedule of reducing the use of the carbon ber footplate in
2- to 3-hour increments every 2 to 3 days.
Outcome
At 8 weeks postoperatively, the patient had regained unrestricted
active range of motion of the hallux and was allowed to return to
regular shoe gear without the carbon ber footplate. The patient
participated in a total of 5, 60-minute therapy sessions during a 35-day
period. The greatest improvement in postoperative hallux function
and rehabilitation occurred between weeks 6 and 8 postoperatively,
514 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
Table 2
Mobilization therapy protocol after surgical repair of extensor hallucis longus lacera-
tion and critical tendon defect
Therapy Performed by Physical Therapist
Warm up Stationary bike (6 min) or heat therapy (10 min)
Gastroc soleus muscle stretching (57 repetitions)  1 min
Talocrural joint mobilization (5 sets of 10 oscillations at end range
of motion (grade IV)
Subtalar joint mobilization (5 sets of 10 oscillations at end range
of motion (grade IV)
Manual hallux interphalangeal joint extension stretch
(5 repetitions  1 min)
Manual rst metatarsalphalangeal joint extension stretch
(5 repetitions  1 min)
First metarsalphalangeal joint mobilization (35 repetitions  10
oscillations; grade II-III)
Myofascial release plantar fascia (5 min)
Myofascial release/scar mobilization of hallux (5 min)
Cool down Cold therapy (10 min)
Self-guided Daily Therapy Performed by Patient
Therapy First metarsalphalangeal joint mobilization (35 repetitions  10
oscillations to toleration)
Gastroc soleus muscle stretching on slant board (3 repetitions  30 s)
Heel raises on reformer (23 sets of 10 repetitions)
Resistance band training (foot eversion/inversion, plantar exion/
dorsiexion (2  10 repetitions)
Single leg balance (4 sets of 10-s duration bilaterally)
Isometrics great toe extension with resistance (hold 35 s as
tolerated  3 sets)
Cool down Cold therapy (10 min)
Mobilization therapy consisted of daily therapy initiated by the patient under the
instruction of a physical therapist; patient-directed therapy was supplemented with
weekly mobilization therapy with a physical therapist. A total of 5 physical therapy
sessions were provided during a 35-day period; each session was 60 minutes and
began the third week postoperatively.
with an American Orthopaedic Foot and Ankle Society midfoot score
improvement from 55 of 100 at 6 weeks postoperatively to 90 of 100 at
8 weeks postoperatively. The patient had no functional limitation of
the hallux; however, weakness in hallux extension strength was noted
compared with the contralateral hallux, an outcome similar to those
reported after alternate procedures (15,56). The patient experienced
a transient episode of tibial sesamoiditis at 10 weeks postoperatively
while transitioning from the use of the carbon ber footplate. The
sesamoiditis resolved uneventfully during the course of 2 weeks with
ice massage, nonsteroidal anti-inammatory use, and adjusting to
a more gradual course of discontinuing the use of the carbon ber
footplate. The nal assessment at 6 months postoperatively by one of
us (R.M.J.) showed an American Orthopaedic Foot and Ankle Society
Midfoot score of 90 of 100. Active metatarsalphalangeal joint dorsi-
exion range of motion was 50 on the operative foot and 72 on the
contralateral foot on discharge.
Discussion
Although tendon lengthening procedures have been described for
repair of Achilles tendon ruptures, similar concepts and techniques
have not been reported for repair of extensor tendon lacerations of
the foot (64,65). The split tendon lengthening technique reported in
the present study is the rst reported for delayed surgical repair of
a critical tendon defect caused by complete laceration and retraction
of the EHL. The rationale for the use of a split tendon lengthening
approach in this case was as follows. First, the size and location of the
defect was not amenable to direct anatomic repair. Second, a 6-cm
defect requires a large bridging graft. Split tendon lengthening avoi-
ded the donor site morbidity associated with harvesting an autograft
from a remote site. There are risks of disease transmission and pro-
longed inammatory response with cadaveric grafts. However, these
risks are obviated with the split tendon lengthening technique.
Finally, the patients pain and inability to dorsiex the hallux were
incompatible with the patients level of activity and not expected to
clinically improve with conservative care.
Several potential complications were considered before perform-
ing this procedure and should be evaluated on a case by case basis
before performing this procedure. The primary consideration is that
the resulting diameter of the split EHL might not be sufcient caliber
to withstand the biomechanical loading functions of the EHL muscle
tendon unit. This could result in re-rupture of the tendon. In instances
of subacute failure, the biomechanical load of the EHL distributed
across a smaller cross-sectional area of tendon could result in further
tendon lengthening during activity, limiting EHL power, tendon
excursion, and hallux function (66). The risk of these complications
was believed to be minimal in the present case, however, because the
split tendon was re-enforced with suture and a dermal scaffold (Figs. 7
and 8) (38). Furthermore, EHB tendon transfer has been shown to
effectively restore hallux function after laceration (14). The effective
diameter of the EHL after split lengthening in the present case was
effectively the same dimension as that of the EHB in our patient,
indirectly suggesting that the split EHL might also be sufcient to
restore hallux function as a bridging graft (Fig. 5) (15).
Adhesion formation is also an inherent risk of tendon repair
surgery, and this particular technique might impose an additional risk
owing to potential tendon impingement at the point at which the
tendon is rotated 180 . Tendon rotation creates an irregularity in the
tendon gliding surface that potentially impinges the tenosynovial
sheath (1,15,61). Impingement can physically interfere with tendon
excursion and/or promote adhesion formation by increasing the
friction between the tendon and tendon sheath (1). A number of
approaches have been used to improve continuity between the tendon
sheath and tendon, including grafting with retinaculum, fascia, para-
tenon, and synovium (44,6769). In the present case, a dermal scaffold
(GraftJacket; Wright Medical Technology) was tubularized around
the tendon in the region of rotation to improve the physical continuity
of the gliding surface of the tendon and reduce the friction between
the tendon and tenosynovium. GraftJacket (Wright Medical
Technology) has been used as a low-friction interpositional graft in
joint repair procedures (7072); however, its use as an interpositional
friction barrier between the tendon and tenosynovium has not been
previously reported.
Despite the benets of mobilization therapy for tendon healing,
few reports have been published of mobilization protocols for
EHL laceration rehabilitation (11). Compared with the mobilization
protocols of the hand, the timing, duration, frequency, and intensity of
hallux mobilization therapy has been poorly characterized in pub-
lished studies. The present study relates a detailed mobilization
protocol that was successfully used after repair of an EHL laceration
and critical defect. Our protocol differs from previously reported
mobilization protocols that have been used for less severe lacerations
treated by direct tendon repair (8,11). To date, little research is
available to provide guidance on how mobilization therapies might be
optimized to provide the greatest benets with the least risk of
tendon re-rupture after EHL laceration repair. However, recommen-
dations for the customization of hand therapy might have some
general relevance to the foot (59). For example, passive mobilization
protocols, characterized by low-stress, high-tendon excursion, have
been recommended for crush injuries to maximize adhesion
prevention and reduce the tendon stress that can result in tendon
re-rupture (59,63). Similar concepts applied to the foot might include
controlled passive metarsalphalangeal joint range of motion with the
ankle in a plantarexed position (59,63). It has been recommended
that a low-stress, low-tendon excursion protocol might be best for
simple hand tendon lacerations in patients with poor healing
 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
potential. Such a protocol could be likened to controlled passive joint
mobilization of the metatarsalphalangeal joint motion with the ankle
in a dorsiexed position (59,63). The general opinion of EHL laceration
rehabilitation, however, suggests a period of 3 weeks of immobiliza-
tion followed by passive mobilization therapy and advancement to
active mobilization against resistance (10). These recommendations
do not reect the current trend in hand research, suggesting early
active mobilization therapy improves tendon function and reduces
adhesion formation (57,59,7377). Although hand modalities such as
dynamic splinting have been applied to the foot with success, the
general advancements in hand rehabilitation have been slow to
inuence the tendon rehabilitation practices of the foot (75). This
might be from a general lack of research of extensor tendon injuries
of the foot and the consequential uncertainty of how the differences
between the weightbearing demands of the foot and the
nonweightbearing functions of the hand might compromise the
success of hand therapies applied to the foot (78).
It has been estimated that the EHL contributes 15% of the dorsi-
exion strength of the ankle (79). This results in EHL forces that are
greater than the forces experienced by the independent extensor
digits of the hand. Hence, it is unclear whether the risk of tendon
gapping or re-rupture is greater in the foot than in the hand when
active mobilization is begun during the rst 3 weeks of tendon
healing when the tendon is weakest. Common hand mobilization
therapies such as the Belfast and Norwich regimens initiate active
mobilization therapy after the rst 48 postoperative hours. However,
early controlled action mobilization therapies can be associated with
re-rupture rates as great as 5.8% to 9.4% (51,52). With these protocols,
it is expected that the strength of surgical repair is sufcient to
withstand the biomechanical forces created by early active motion
(80). It is unclear whether these expectations hold true for the
tendons of the foot or in situations in which complex procedures such
as split tendon lengthening are used to reconstruct the tendons of the
foot. Until additional research of the extensor physiology of the foot is
conducted, we recommend caution when initiating active mobiliza-
tion therapies before the third postoperative week and even recom-
mend considering a delay of active mobilization therapy until 5 or
6 weeks postoperatively for repairs that are of tenuous quality. One
might also consider mitigating the risk of re-rupture by rst initiating
passive mobilization therapy and delaying active mobilization until
a patient comfortably demonstrates a favorable response to passive
mobilization. Finally, we recommend considering prolonged use of
bracing to reduce the risk of re-injury when the quality of the surgical
repair or a patients comorbidities suggest longer healing times might
be necessary for recovery. Braces that restrain ankle motion with the
foot in a neutral or dorsiexed position minimize EHL excursion and,
thus, the risk of excess tension, strain, and friction on the tendon that
can promote tendon gapping or re-rupture in the early stages of
tendon healing (63). Transitioning from ambulation with a xed ankle
brace to ambulation with a carbon ber footplate with a Morton
extension in the shoe gear increases EHL excursion with unconned
ankle motion but limits excess tension on the EHL by restricting
hallux exion. Thus, a carbon ber footplate could be a useful inter-
mediate adjunctive device to assist patients as they transition from
restricted to unrestricted activity after laceration repair.
The split tendon lengthening technique described in the present
report has several advantages compared with the cadaveric allograft and
tendon transfer procedures. The split tendon technique obviates the
need for a large bridging allograft, mitigating the potential for the pro-
longed host inammatory response associated with large biologic
implants. Split tendon lengthening also contributes viable tenocytes to
the repair site that are not contributed by cadaveric allografts owing to
graft sterilization. Thus, the preferred physiology of tendon healing
between 2 viable tendon segments is possible with a split tendon
515
lengthening procedure but not with allograft techniques in which
a viable tendon segment must heal to a nonliving allograft. The physi-
ologic consequences of a living tendon attempting to integrate with
a nonviable allograft are doubled if one considers that healing must
occur at 2 ends of the bridging allograft. Hence, allograft techniques
might have greater physiologic challenges and risk of complications
with tendon healing than split tendon lengthening procedures.
Although autografts and tendon transfers both consist of living tissue,
these procedures can be associated with donor site morbidity that
results in patient pain and dysfunction. The split tendon lengthening
approach minimizes these potential complications by using an extended
incision at the site of repair rather than a remote secondary incision.
In conclusion, EHL split lengthening could be an alternate tech-
nique for anatomically restoring tendon structure and function in
situations in which extensive tendon defects would otherwise require
a bridging allograft, free tissue autograft, or tendon transfer. The use
of a dermal scaffold to re-enforce the EHL repair was not associated
with functional limitations or excessive adhesion formation in the
case reported. Early mobilization therapy was believed to be an
essential component of the tendon rehabilitation process, and we
presented a mobilization therapy protocol as a reference protocol for
more extensive research and development of physical therapy
protocols specic for the EHL after laceration repair.
References
1. Al-Qattan MM. Surgical treatment and results in 17 cases of open lacerations of the
extensor hallucis longus tendon. J Plast Reconstr Aesthet Surg 60:360367, 2007.
2. Woodhams LE. A three-year follow-up study of hammer digit syndrome of the
hallux. J Am Podiatr Assoc 64:955966, 1974.
3. Mulcahy DM, Dolan AM, Stephens MM. Spontaneous rupture of extensor hallucis
longus tendon. Foot Ankle Int 17:162163, 1996.
4. Poggi JJ, Hall RL. Acute rupture of the extensor hallucis longus tendon. Foot Ankle
Int 16:4143, 1995.
5. Menz P, Nettle WJ. Closed rupture of the musculotendinous junction of extensor
hallucis longus. Injury 20:378381, 1989.
6. Grifths JC. Tendon injuries around the ankle. J Bone Joint Surg Br 47:686689,
1965.
7. Floyd DW, Heckman JD, Rockwood CA Jr. Tendon lacerations in the foot. Foot Ankle
4:814, 1983.
8. Skoff H. Dynamic splinting after extensor hallucis longus tendon repair: a case
report. Phys Ther 68:7576, 1988.
9. Lipscomb PR, Kelly PJ. Injuries of the extensor tendons in the distal part of the leg
and in the ankle. J Bone Joint Surg Am 37-A:12061213, 1955.
10. Scaduto AA, Cracchiolo A III. Lacerations and ruptures of the exor or extensor
hallucis longus tendons. Foot Ankle Clin 5:725736, 2000.
11. Bronner S, Ojofeitimi S, Rose D. Repair and rehabilitation of extensor hallucis
longus and brevis tendon lacerations in a professional dancer. J Orthop Sports Phys
Ther 38:362370, 2008.
12. Park HG, Lee BK, Sim JA. Autogenous graft repair using semitendinous tendon for
a chronic multifocal rupture of the extensor hallucis longus tendon: a case report.
Foot Ankle Int 24:506508, 2003.
13. Zielaskowski L, Pontious J. Extensor hallucis longus tendon repair using a fascia
lata allograft. J Am Podiatr Med Assoc 92:467470, 2002.
14. Wicks MH, Harbison JS, Paterson DC. Tendon injuries about the foot and ankle in
children. Aust N Z J Surg 50:158161, 1980.
15. Berens TA. Autogenous graft repair of an extensor hallucis longus laceration. J Foot
Surg 29:179182, 1990.
16. Franck WM, Olk A, Hennig FF. Combined rupture of the tibialis anterior and the
extensor hallucis longus tendonsdfunctional reconstruction. Arch Orthop Trauma
Surg 125:277280, 2005.
17. Kass JC, Palumbo F, Mehl S, Camarinos N. Extensor hallucis longus tendon injury:
an in-depth analysis and treatment protocol. J Foot Ankle Surg 36:2427, 1997.
18. Leung YF, Ip SP, Chung OM. A new method of functional tendon transfer for
the dysfunction of extensor hallucis longus. Foot Ankle Int 23:11241125,
2002.
19. Schefer SU, Schmidt T, Gangey I, Dustmann M, Unterhauser F, Weiler A. Fresh-
frozen free-tendon allografts versus autografts in anterior cruciate ligament
reconstruction: delayed remodeling and inferior mechanical function during long-
term healing in sheep. Arthroscopy 24:448458, 2008.
20. Chow SP, Hooper G, Chan CW. The healing of freeze-dried rabbit exor tendon in
a synovial uid environment. Hand 15:136142, 1983.
21. Buck BE, Malinin TI, Brown MD. Bone transplantation and human immunode-
ciency virus: an estimate of risk of acquired immunodeciency syndrome (AIDS).
Clin Orthop Relat Res 240:129136, 1989.
516 R.M. Joseph, J. Barhorst / The Journal of Foot & Ankle Surgery 51 (2012) 509516
22. Greenberg DD, Robertson M, Vallurupalli S, White RA, Allen WC. Allograft
compared with autograft infection rates in primary anterior cruciate ligament
reconstruction. J Bone Joint Surg Am 92:24022408, 1989.
23. Gelberman RH, Siegel DB, Woo SL-Y, Amiel D, Takai S, Lee D. Healing of digital exor
tendons: importance of the interval from injury to repairda biomechanical,
biochemical, and morphological study in dogs. J Bone Joint Surg Am 73:6675, 1991.
24. Rockwell WB, Butler PN, Byrne BA. Extensor tendon: anatomy, injury, and
reconstruction. Plast Reconstr Surg 106:15921603, 2000.
25. Lister G. Indications and techniques for repair of the exor tendon sheath. Hand
Clin 1:8595, 1985.
26. Gelberman RH, Ami D, Gonsalves M, Woo S, Akeson WH. The inuence of
protected passive mobilization on the healing of exor tendons: a biochemical and
microangiographic study. Hand 13:120128, 1981.
27. Meyer DC, Hoppeler H, von Rechenberg B, Gerber C. A pathomechanical concept
explains muscle loss and fatty muscular changes following surgical tendon release.
J Orthop Res 22:10041007, 2004.
28. Snyder SJ, Arnoczky SP, Bond JL, Dopirak R. Histologic evaluation of a biopsy
specimen obtained 3 months after rotator cuff augmentation with GraftJacket
matrix. Arthroscopy 25:329333, 2009.
29. Cornwell KG, Landsman A, James KS. Extracellular matrix biomaterials for soft
tissue repair. Clin Podiatr Med Surg 26:507523, 2009.
30. Gilbert TW, Sellaro TL, Badylak SF. Decellularization of tissues and organs.
Biomaterials 27:36753683, 2006.
31. Valentin JE, Badylak JS, McCabe GP, Badylak SF. Extracellular matrix bioscaffolds for
orthopaedic applications: a comparative histologic study. J Bone Joint Surg Am
88:26732686, 2006.
32. Brown B, Lindberg K, Reing J, Stolz DB, Badylak SF. The basement membrane
component of biologic scaffolds derived from extracellular matrix. Tissue Eng
12:519526, 2006.
33. De Deyne PG, Kladakis SM. Bioscaffolds in tissue engineering: a rationale for use
in the reconstruction of musculoskeletal soft tissues. Clin Podiatr Med Surg
22:521532, 2005.
34. Coons DA, Barber FA. Tendon graft substitutesdrotator cuff patches. Sports Med
Arthrosc 14:185190, 2006.
35. Derwin KA, Baker AR, Spragg RK, Leigh DR, Iannotti JP. Commercial extracellular
matrix scaffolds for rotator cuff tendon repair: biomechanical, biochemical, and
cellular properties. J Bone Joint Surg Am 88:26652672, 2006.
36. Aurora A, McCarron J, Iannotti JP, Derwin K. Commercially available extracellular
matrix materials for rotator cuff repairs: state of the art and future trends.
J Shoulder Elbow Surg 16(5 suppl):S171S178, 2007.
37. Lee MS. GraftJacket augmentation of chronic Achilles tendon ruptures. Orthope-
dics 27(1 suppl):s151s153, 2004.
38. Barber FA, McGarry JE, Herbert MA, Anderson RB. A biomechanical study of
Achilles tendon repair augmentation using GraftJacket matrix. Foot Ankle Int
29:329333, 2008.
39. Lee DK. A preliminary study on the effects of acellular tissue graft augmentation in
acute Achilles tendon ruptures. J Foot Ankle Surg 47:812, 2008.
40. Bond JL, Dopirak RM, Higgins J, Burns J, Snyder SJ. Arthroscopic replacement of
massive, irreparable rotator cuff tears using a GraftJacket allograft: technique and
preliminary results. Arthroscopy 24:403409, 2008.
41. Johnson KA, Rogers GJ, Roe SC, Howlett CR, Clayton MK, Milthorpe BK,
Schindhelm K. Nitrous acid pretreatment of tendon xenografts cross-linked with
glutaraldehyde and sterilized with gamma irradiation. Biomaterials 20:10031015,
1999.
42. Courtman DW, Errett BF, Wilson GJ. The role of crosslinking in modication of the
immune response elicited against xenogenic vascular acellular matrices. J Biomed
Mater Res 55:576586, 2001.
43. van Wachem PB, Brouwer LA, Zeeman R, Dijkstra PJ, Feijen J, Hendriks M,
Cahalan PT, van Luyn MJA. Tissue reactions to epoxy-crosslinked porcine heart
valves post-treated with detergents or a dicarboxylic acid. J Biomed Mater Res
55:415423, 2001.
44. Strickland JW. The scientic basis for advances in exor tendon surgery. J Hand
Ther 18:94110, 2005.
45. Strickland JW. Delayed treatment of exor tendon injuries including grafting.
Hand Clin 21:219243, 2005.
46. Carl HD, Forst R, Schaller P. Results of primary extensor tendon repair in relation to
the zone of injury and pre-operative outcome estimation. Arch Orthop Trauma
Surg 127:115119, 2007.
47. Talsma E, de Haart N, Beelen A, Nollet F. The effect of mobilization on repaired
extensor tendon injuries of the hand: a systematic review. Arch Phys Med Rehabil
89:23662372, 2008.
48. Takai S, Woo SL, Horibe S, Tung DK, Gelberman RT. The effects of frequency and
duration of controlled passive mobilization on tendon healing. J Orthop Res
9:705713, 1991.
49. Gelberman RH, Nunley JA, Osterman AL, Breen TF, Dimick MP, Woo SL. Inuences
of the protected passive mobilization interval on exor tendon healing:
a prospective randomized clinical study. Clin Orthop Relat Res 264:189196, 1991.
50. Gelberman RH, Botte MJ, Spiegelman JJ, Akeson WH. The excursion and defor-
mation of repaired exor tendons treated with protected early motion. J Hand
Surg Am 11:106110, 1986.
51. Langley C, Hobbby J. Focus on exor tendon repair. J Bone Joint Surg Br
89-B:13961401, 2010.
52. Elliot D, Moiemen NS, Flemming AF, Harris SB, Foster AJ. The rupture rate of acute
exor tendon repairs mobilized by the controlled active motion regimen. J Hand
Surg Br 19:607612, 1994.
53. Kim HM, Nelson G, Thomopoulos S, Silva MJ, Das R, Gelberman RH. Technical and
biological modications for enhanced exor tendon repair. J Hand Surg Am
35:10311037, 1994.
54. Taras JS, Raphael JS, Marczyk SC, Bauerle WB. Evaluation of suture caliber in exor
tendon repair. J Hand Surg Am 26:11001104, 2001.
55. Barrie KA, Wolfe SW, Shean C, Shenbagamurthi D, Slade JF, Panjabi MM. A
biomechanical comparison of multistrand exor tendon repairs using an in situ
testing model. J Hand Surg Am 25:499506, 2000.
56. Mowlavi A, Schall J, Wilhelmi BJ. Extensor hallucis longus tenorrhaphy by using the
Massachusetts General Hospital repair. J Foot Ankle Surg 43:412418, 2004.
57. Groth GN. Current practice patterns of exor tendon rehabilitation. J Hand Ther
18:169174, 2005.
58. Gelberman RH, Woo SL, Lothringer K, Akeson WH, Amiel D. Effects of early
intermittent passive mobilization on healing canine exor tendons. J Hand Surg
Am 7:170175, 1982.
59. Pettengill KM. The evolution of early mobilization of the repaired exor tendon.
J Hand Ther 18:157168, 2005.
60. Paoloni J, De Vos RJ, Hamilton B, Murrell GA, Orchard J. Platelet-rich plasma
treatment for ligament and tendon injuries. Clin J Sport Med 21:3745, 2005.
61. Al-Qattan MM, Posnick JC, Lin KY. Triggering after partial tendon laceration. J Hand
Surg Br 18:241246, 1993.
62. Maitland GD. Manipulationdmobilisation. Physiotherapy 52:382385, 1966.
63. Refshauge KM, Taylor JL, McCloskey DI, Gianoutsos M, Mathews P, Fitzpatrick RC.
Movement detection at the human big toe. J Physiol 513(Pt 1):307314, 1998.
64. Demirel M, Turhan E, Dereboy F, Yazar T. Augmented repair of acute tendo Achilles
ruptures with gastrosoleus turn down ap. Indian J Orthop 45:4552, 1998.
65. Takao M, Ochi M, Naito K, Uchio Y, Matsusaki M, Oae K. Repair of neglected
Achilles tendon rupture using gastrocnemius fascial aps. Arch Orthop Trauma
Surg 123:471474, 2003.
66. Maquirrriain J. Achilles tendon rupture: during surgical repair and rehabilitation.
Yale J Biol Med 8:289300, 2011.
67. Oei TS, Klopper PJ, Spaas JA, Buma P. Reconstruction of the exor tendon sheath:
an experimental study in rabbits. J Hand Surg Br 21:7283, 1996.
68. Liu AM, Lu SB. Reconstruction of sheath with fascial graft in exor tendon repair:
an experimental study. J Hand Surg Br 16:179184, 1991.
69. Eiken O, Holmberg J, Ekerot L, S algeback S. Restoration of the digital tendon
sheath: a new concept of tendon grafting. Scand J Plast Reconstr Surg 14:8997,
1980.
70. Burkhead WZ Jr, Krishnan SG, Lin KC. Biologic resurfacing of the arthritic
glenohumeral joint: historical review and current applications. J Shoulder Elbow
Surg 16(5 suppl):S248S253, 2007.
71. Bhatia DN, van Rooyen KS, du Toit DF, de Beer JF. Arthroscopic technique of
interposition arthroplasty of the glenohumeral joint. Arthroscopy 22:570, 2006.
72. Adams JE, Merten SM, Steinmann SP. Arthroscopic interposition arthroplasty of
the rst carpometacarpal joint. J Hand Surg Eur 32:268274, 2007.
73. Panchal J, Mehdi S, ODonoghue JM, O'Sullivan ST, OShaughnessy M, OConnor TP.
The range of excursion of exor tendons in zone V: a comparison of active vs
passive exion mobilisation regimes. Br J Plast Surg 50:517522, 1997.
74. Chesney A, Chauhan A, Kattan A, Farrokhyar F, Thoma A. Systematic review of
exor tendon rehabilitation protocols in zone II of the hand. Plast Reconstr Surg
127:15831592, 2011.
75. Newport ML, Tucker RL. New perspectives on extensor tendon repair and impli-
cations for rehabilitation. J Hand Ther 18:175181, 2005.
76. Howell JW, Merritt WH, Robinson SJ. Immediate controlled active motion
following zone 47 extensor tendon repair. J Hand Ther 18:182190, 2005.
77. Milner C, Russel P. Upper limb: focus on extensor tendon injury. Bone and Joint
Website. Available at: http://www.boneandjoint.org.uk/content/focus/extensor-
tendon-injury. Accessed May 21, 2012.
78. Gott M. Tendon phenotype should dictate tissue engineering modality in tendon
repair: a review. Discovery Medicine Website, July 26, 2007. Available at: http://
www.discoverymedicine.com/Michael-Gott/2011/07/26/tendon-phenotype-should-
dictate-tissue-engineering-modality-in-tendon-repair-a-review/. Accessed August
7, 2011.
79. Wolfgang M, Alexander O, Friedriech F. Combined rupture of the tibialis anterior
and extensor hallucis longus tendonsdfunctional reconstruction. Arch Orthop
Trauma Surg 125:277280, 2005.
80. Silfverskiold KL, May EJ, Tornvall AH. Gap formation during controlled motion
after exor tendon repair in zone II: a prospective clinical study. J Hand Surg Am
17:539546, 1992.