The Unfavorable Result in Plastic Surgery_ Avoidance and Treatment (2018, Thieme)

SECTION VIII THE HAND AND UPPER EXTREMITY
1166
of tendon fibers require awareness of the longitudinal and
horizontal configuration of the suture pass, but in reality
this detail does not alter the overall pull-out strength of
tendons significantly, largely because, as load is applied,
the configuration of these repairs changes dramatically.
Number of Strands
The number of strands has been a focus of attention in re­
cent years since Savage28 described his innovative technique
of using a single strand of material, passing between the
ends six times and thus potentially increasing load bearing
by a theoretical factor of three and assuming better load
sharing. In practice the load taken by each strand depends
on the clinical judgments on the length of each strand and
the amount of bedding-in of the suture into the soft ten­
don material. If one strand were to become extremely tight,
the overall effect would approximate a single-strand repair.
One way of allowing the forces in each strand to equilibrate
load is to perform the repair with one continuous suture. In
numerous patterns of placing the core suture have several
common characteristics (Fig. 61.9). The suture must grasp
the tendon material on either side of the divide, and a num­
ber of strands must cross the gap. Usually 2, 4, or 6 strands
are common, and the suture is tied and knotted, which is
important because knots of different materials may unravel
in variable ways under load. In addition, there is variability
of suture material tensile strength. Each of these character­
istics are discussed separately (Fig. 61.10).
Grasp
Early tendon repairs (e.g., Bunnell25) just passed through
the tendon from side to side with no specific attempt to en­
circle a few of the fibers in a grasp to lessen the risk of pull­
out. The Kirchmayer-Kessler pattern grasped at few fibers
at the four corners of a box-shaped configuration.26,27 Sav­
age and Risitano28 achieved a much more extensive grasp
by criss crossing the suture in addition to increasing the
number of strands. Concepts such as locking and ­grasping
Kirshmayr 1917
Cruciate 1999
Triple figure-of-eight 2009
Savage 1989
Lim-Tsai 1986
Bunnell 1918
“Lin” modified Kessler 1997
M-Tang 2003
Strickland 1995
Adelaide 2011
Fig. 61.9 Classic and current flexor tendon repairs. (Reproduced from Langer MF, Oeckenpöhler S, Kösters C, Herrmann K, Wieskötter B.
Nahttechniken für Beugesehnen der Hand. Der Orthopäde 2015;44(10):748-756.)

1167
Chapter 61 Flexor Tendon Injuries
gradable) sutures have been used. Round-bodied needles
have been advocated to prevent the edge of a cutting nee­
dle from weakening strands of materials touched by the
needle, but even the tip of a round-bodied needle can cause
damage. Cutting needles have also been advocated, because
they tend to cause less fraying of the tendon ends. To avoid
an unfavorable result, a departmental protocol should be
instituted to encourage all parties to be familiar with the
materials and their knot-holding properties.
Epitendinous Suture
The epitendinous suture was first used to smooth the re­
pair site to aid gliding. It has now been shown, at least in
ex vivo testing, to increase the strength of the repair (Fig.
61.11). A disadvantage of epitendinous sutures is that they
are generally continuous, and ex vivo testing has demon­
strated that once one loop detaches the whole suture un­
zips and slackens. Any increment in tensile strength is not
sufficient to change the rehabilitation protocol, and the ma­
jor role may be the smoothing effect on the tendon surface
preventing triggering of the repair on annular pulleys.
addition, compression at the repair site rather than gapping
can be introduced by staggering the repair (see Fig. 61.10).
Experimental studies have shown that areas of the tendon
subjected to high strain become acellular, largely because
of cell necrosis, and there is a theoretical argument that
multistrand repairs are likely to have more cell death and
inflammatory change, leading to swelling. Clinical evidence
of this has recently been reported with observations that
two-strand repairs typically rupture at 2 weeks from su­
ture failure, whereas multistrand repairs rupture as late as
8 weeks, probably related to failure of the tendon ends to
heal.29
Type of Suture and Knots
Very few of the sutures used for tendon repair have been
devised for this purpose, and there is no universal agree­
ment on suture choice. Commonly used sutures are mono­
filament polypropylene or braided polyester materials,
usually of 3–0 or 4–0 diameter (see Fig. 61.10). Stainless
steel wire is no longer commonly used, but fiberwire is a
strong, tendon-specific material. Even absorbable (biode­
Passive force
Active force with mild resistance
Active force with restricted flexion
Strong composite grip
Thumb pinch
Suture purchase
10 mm
7 mm
5 mm
3 mm
Epitendinous
4 core locking cruciate + epi
4 core locking cruciate
4 core Kessler + epi
4 core Kessler
2 core Kessler + epi
2 core Kessler
Suture configuration
Asymmetrical (4–0 x 4 core 10 and 5 mm bites)
Symmetrical (2–0 x 2 core 7.5 mm bites)
Symmetrical (4–0 x 4 core 7.5 mm bites)
Suture strands
8 strand
6 strand
4 strand
2 strand
Suture gauge
2–0
3–0
4–0
5–0
Suture material
Stainless steel
FibreWire
Ethibond
Prolene
Nylon
Tendon suture variable
Ultimate load to failure (Newtons)
0
10
20
30
40
50
60
70
80
90
100
110
120
130
140
Fig. 61.10 Factors that influence tendon repair strength.

SECTION VIII THE HAND AND UPPER EXTREMITY
1168
the back wall of the tendon before placing the core suture,
whereas others insert the core suture and then turn the ten­
don over to complete a circumferential epitendon suture.
Acute Pulley Management
Concern about the potential complication of bowstringing
has led to traditional teaching that the A2 and A4 pulleys
The ideal epitendinous suture should be simple to per­
form and should minimize the final tendon bulk while simul­
taneously affording some strength to the core repair. Locking
cross-stitch repairs are more difficult to perform and may risk
compromising the integrity of the core suture. For these rea­
sons, the continuous circumferential suture appears to be the
most common form of epitendinous repair in many centers
worldwide. Some surgeons insert the epitendinous suture in
Witzel 1887 Koch 1933
Halsted-Wade 1989
Kleinert “3 mm” 1973
Kleinert “2 mm” 1973
Kleinert 1973
Strickland 1993
Lembert-Lister 1977
Lin 1988
Mashada 1992
Silfverskiold 1993
Fig. 61.11 A variety of described peripheral repair techniques. (Reproduced from Langer MF, Surke C, Wieskötter B, Lötters E. Prinzipien der
Beugesehnenchirurgie. In: Towfigh H, Hierner R, Langer MF, Friedel R (Hrsg). Handchirurgie. Heidelberg: Springer; 2011.)

1169
Chapter 61 Flexor Tendon Injuries
pair at the time of wound closure can be expected never
to glide; hence the loss in range of motion from careful se­
lective venting of areas of impingement is preferable to a
stuck repair. This will be apparent at the completion of the
repair by passive, and preferably active, mobilization of the
digit, and directed venting may be required at this stage32
(Box 61.4).
Overall, whatever variables in suturing are chosen, the
best way to avoid an unfavorable result is to check the in­
tegrity of the repair by dynamic motion and to ensure that
there is no gapping, triggering on pulleys, or other obstruc­
tions. This can be verified by passively cycling the tendon
multiple times through its flexion–extension range or by
asking the patient to actively move the digits if wide-awake
anesthesia is being used.
Postoperative Rehabilitation
Many rehabilitation regimens are in use that include pas­
sive mobilization for several weeks then active, early active
mobilization, place and hold regimens, and combined pro­
tocols. A major factor that dictates success is how informed
and compliant with the rehabilitation regimen the patient is
(Box 61.5). Surgeons like to think that most failures of func­
tion do not arise from the surgery, but arise instead from
too much or too little mobilization. Given that ­ruptures
are much less common than “adhesion failures” (stiffness),
the risks are more on the side of insufficient movement,
which allows scar tissue to form in all of the tissue planes
that have been exposed. Many different regimens are in use
­internationally, but there are common principles. The aim
is to achieve some tendon glide and limited tendon load­
ing and to prevent secondary joint stiffness. All regimens
have periods of rest initially with passive, or limited active,
motion through a defined range, and load according to pro­
tocols.
Whatever the protocol, the patient will require educa­
tion and reeducation as to what to do, particularly in the
first weeks after the repair. This requires written protocols
or readily accessible video information and supervision by a
hand therapist who has agreed to a specific protocol for the
are to be preserved,31 and as a principle it seems appropri­
ate to preserve as much of the pulley system as possible.
However, it is necessary to fashion a window to perform
the repair. If access is sufficient to perform the repair be­
tween the A2 and A4 pulleys, the intervening cruciate and
A3 pulleys can be incised with little apparent detriment.
When access is needed within the A2 or A4 pulleys to re­
pair the tendon, the solutions are more controversial. In an
otherwise intact pulley system, the A4 can be vented com­
pletely with adjacent cruciates if required for glide32 (Fig.
61.12). Furthermore, there is clinical evidence to support
that partial venting of the A2 pulley to improve proximal
glide can be performed safely without an increased risk
of bowstringing.33 Tenorraphy results in a larger diameter
of the repaired tendon, which has a potential to impinge
upon the margins of a window cut in the tendon sheath.
The critical consideration is that a nongliding tendon re­
Box 61.4
Pitfalls for Pulley Venting
•• Excessive venting leading to bowstringing
•• Inadequate venting leading to triggering or
stuck repair
•• Venting in the event of an already compromised
pulley system
Steps to Avoid These Pitfalls
•• Performing on-table intraoperative passive and
active full range-of-motion testing to guide the
extent of pulley venting
•• Full assessment of the pulley system and vent
pulleys as recommended32
•• Venting pulleys intraoperatively after the repair
is performed
Pitfalls for Pulley Venting
and Steps to Avoid Them
Safe
Unsafe
Fig. 61.12 “Safe” and “unsafe” venting strategies. (Modified from Tang JB. Release of the A4 pulley to facilitate zone II flexor tendon repair.
J Hand Surg 2014;39(11):2300–2307.)

SECTION VIII THE HAND AND UPPER EXTREMITY
1170
major unfavorable results are rupture and stiffness or ad­
hesion, which often have their roots in both surgery and
rehabilitation.
Tendon Rupture
Rupture often occurs as a sudden and dramatic event, and
the patient is usually aware of a snap or jolt followed by an
inability to move the digit. The finger assumes an extended
posture and generally can be passively flexed. A provoking
factor is often identified, such as an attempt to grip, or the
rupture can occur at night. There may be a slower form of
failure in which motion is gradually lost, possibly related
to attenuation of the repair, with associated adhesions or
triggering. Many such progressive failures are primarily
caused by adhesions, but with secondary joint contracture.
This type of failure is characterized by a progressive loss of
motion over days or weeks, and the digit is held in a flexed
posture.
A ruptured or adherent tendon will not improve regard­
less of how much rehabilitation is offered. An urgent ultra­
sound is usually the best way to confirm the diagnosis, but
we now advocate early reexploration with wide-awake an­
esthesia so that the functional obstructions can be assessed.
This proactive approach allows the following:
1. A diagnosis
2. Liberation of the tendon from immature adhesions
3. Re-repair of the tendon before the tendon sheath col­
lapses or the tendon becomes adherent
4. Assessment of the full function and mechanical restric­
tions before closing the wound
This relatively simple proactive approach is beneficial for
both surgeon and patient, because it is likely to obviate the
need for secondary two-stage surgery.
Tendon ruptures that are brought to the surgeon’s at­
tention in a timely manner may be amenable to early re-
repair. Re-repair conducted within the first 48 hours has
been shown to result in good or excellent outcomes in only
half of the cases.
Immediate re-repair may not be appropriate for vari­
ous reasons, such as frayed tendon ends; an unfavorable
­surrounding soft tissue environment, such as infection; or
retraction of the proximal stump because of muscle contrac­
tion. A direct repair is deemed possible when inflammation
is minimal, as assessed by the quality of the surrounding
tissues. If the tissues are friable, this suggests that the ten­
don has been softened by matrix metalloproteinases and
is unlikely to hold sutures. Surgery should be delayed and
temporized by the insertion of a silicone rod, and two-stage
reconstruction is most likely necessary once the environ­
ment is more favorable. If, after débridement, the tendon
ends are healthy, a primary repair can be attempted and,
if needed, fractional lengthening of the intramuscular por­
tion of the tendon can be performed to release the tension
on the tendon repair. Overtightening a débrided shortened
tendon can be a problem if the tendons share a common
individual patient with knowledge of the pulley integrity,
the quality of the tendon, and the site of injury. The thera­
pist therefore requires access to a detailed operative record.
Rehabilitation with an early active motion regimen is
commonly initiated at day 4 or 5, because postoperative
edema is likely to increase the resistance to motion exer­
cises, and adhesions seem to develop around this stage.
The patient should see the therapist frequently during
the first 2 to 3 weeks, daily if insufficient progress is being
made, because the pattern of recovery is established at this
time. The repair needs to be protected to some extent for at
least 8 weeks and heavy loading for 12 weeks. Young chil­
dren can be statically immobilized with an expectation of
a good recovery in motion. Adults who fail to comply are
either too keen to return to work or too scared to move the
digit and need to be informed of the consequences imme­
diately. Recent results of protected “safe use” of the injured
hand in a short splint gives far better patient compliance,
because only the affected digit is protected as opposed to
the whole hand.14 Educating patients on safe use means they
are also less likely to be overly protective if they can use the
remainder of the functioning hand.
If nerves and tendons are divided or fractures and exten­
sor injuries also exist, there may be a conflict between post­
operative protocols, and a decision must be made regarding
which should dominate in the particular circumstances.
Managing the Unfavorable
Result in Flexor Tendon Repair
In the short term there are wound-associated factors that
predict a disappointing outcome, such as infection, hema­
toma, and damage to the surrounding structures, particu­
larly where skin cover is inadequate or there is bone and
joint injury that gives the tendon surgery little or no po­
tential to restore motion. However, focusing on the tendon
surgery alone, the range of outcomes is variable. The two
Box 61.5
Pitfalls of Rehabilitation
•• Poor patient engagement
•• Poor patient follow-up
Steps to Avoid These Pitfalls
•• Education
•• Structured, engaging rehabilitation
•• Simplified rehabilitation protocols
•• Dedicated rehabilitation facilities
•• “Safe use” education
Pitfalls for Rehabilitation
and Steps to Avoid Them

1171
Chapter 61 Flexor Tendon Injuries
this scenario, tendon reconstruction using a two-stage pro­
cedure is required.
The worst results can be expected from high-energy in­
juries, delayed healers, and infected patients whereby not
only is the digit compromised by adhesions, but fibrosis of
all the tissue gliding planes leads to restrictions in the range
of motion and joint stiffness. A stiff joint would prevent mo­
tion even if a complete tenolysis were performed.
In this setting, dividing the surrounding stabilizing
structures around the joint in a stepwise fashion should be
considered. Release should start with the check rein liga­
ments and passive motion tested on the operating table. If
incomplete motion is encountered, release of the volar plate
complex and accessory collateral ligaments should be per­
formed. However, such extensive surgery is rarely of long-
term benefit for patients.
For severe contractures, the total anterior tenolysis pro­
cedure may be performed as a salvage procedure if multiple
operations have failed to correct a hook finger. This involves
dissecting all volar structures off the periosteum and reposi­
tioning them to a more proximal position in relation to the
skeleton. Reconstruction or shortening may be required at
the fingertip.
A move toward wide-awake surgery enables on-table
testing that would benefit the surgical assessment of tenol­
ysis. Passive and active range of motion can be tested and
visualized intraoperatively by the surgeon, patient, and, if
available, therapists. Theoretically this would enable all par­
ties involved to appreciate the full potential of rehabilitation.
Reconstruction of a Failed Tendon
Repair
Options for the restoration of function after a failed tendon
repair depend upon the findings on exploration. Patients
will commonly require consent to a range of procedures in­
cluding tenolysis, re-repair, or one- or two-stage grafting35
(Box 61.6).
muscle belly because of the quadriga phenomenon. Fortu­
nately this problem is rare. To avoid rupture, the re-repair
should be technically sound with suture bites more than
1 cm from the tendon ends using at least a four-strand re­
pair with minimal handling of the suture. An alternative is
to insert a short bridge segment of tendon graft to replace
the section of unhealthy tendon.
Tendon Adhesions: The Problem of
Stiffness
Postoperative tendon adherence results in a reduced range
of motion in flexion, extension, or both. This is initially re­
lated to the posttraumatic response from injury and sur­
gery, which leads to an influx of inflammatory mediators
that encourage a widespread healing response.
Superimposed on this are the problems of joint stiffness
and adhesions in all of the gliding planes as the digits are ex­
posed to inflammatory mediators while being held in an un­
favorable position of flexion. Hand therapy aims to prevent
this with rehabilitation regimens, which at different stages
may disrupt, lengthen, or remodel adhesions.
Therapeutics to reduce tendon adhesions using lubri­
cants or antiadhesion molecules are gradually progressing
into the clinical field through randomized controlled trials
but are not yet widely available in clinical practice.
Adhesions form when the traumatized tendon adheres
to the sheath or other damaged tendon ends, thereby re­
stricting motion. The higher the energy transfer, the greater
the zone of injury, and the greater the range of tissues that
will be involved in the fibrosis process. When adhesions oc­
cur, tenolysis can be considered to restore active function
to the finger, but a prerequisite to this is that the passive
range of motion must be greater than the active range of
motion. Otherwise therapy should be instigated to try to
increase passive range. If adhesions are apparent early, we
prefer early exploration as described previously. Surgical
tenolysis once adhesions are well developed is a difficult
and often unsatisfactory procedure that requires explora­
tion of the original repair and separation of the tendon
from scar tissue, while attempting to preserve intact pul­
leys. Experimentally the optimum time to perform tenoly­
sis for mature adhesions is after 12 weeks, because before
this the tendon maybe more prone to rupture.34 Rupture
is a common complication after tenolysis, with rates of ap­
proximately 12%; therefore a modified rehabilitation regi­
men may be necessary. Preservation of important pulleys
to maintain functional excursion of the tendon should be
observed in the setting of an already compromised finger.
The separated pulleys are often weakened and prone
to rupture, allowing the scarred tendon to bowstring. An
assessment of the tendon and pulley tissue quality is essen­
tial, because it may be better to discard the scarred tendon
or excise the pulley and undertake a formal staged recon­
struction.
Tendon gapping is always accompanied by adhesions,
with nonunited tendon ends scarring upon the sheath. In
Box 61.6
•• Tenolysis
•• One-stage flexor tendon grafting
•• Two-stage flexor tendon reconstruction (using
Hunter’s rod technique35)
•• Tendon transfer
•• Interphalangeal joint arthrodesis in selected
cases of flexor digitorum profundus or flexor
pollicis longus rupture
•• Vascularized tendon transfer
•• Amputation
List of Options for Failed
Tendon Repair

SECTION VIII THE HAND AND UPPER EXTREMITY
1172
Advocates for the use of intrasynovial tendon grafts for
two-stage reconstruction stem from the principle under­
standing that it supplies a “like-for-like” to reconstruct the
FDP. Experimental studies in animal models show that an
intrasynovial tendon provides a smooth gliding surface for
the tendon to heal without adhesions.36 The Paneva-Holev­
ich is one such technique that provides for two-stage recon­
struction using intrasynovial tendon. At the time of primary
surgery, a silicone rod is inserted. The proximal stumps of
FDP and FDS are sutured together at the level of the lumbri­
cal origin. The second stage involves division of the FDS at
the musculotendinous junction and passing the proximal
end distally through the palm to replace the silicone rod
and reconstruct the FDP. With FDP injuries in patients who
wish to return to work quickly, it is sometimes appropriate
to perform arthrodesis of the DIP joint. In hands with a low
functional demand, such as those with rheumatoid arthritis,
it may be preferable to perform tendon transfers.
Other complications of tendon surgery are common and
include skin necrosis, which may heal by secondary inten­
tion and give rise to lumpy or contracted scars. Large skin
Primary tendon grafting is possible on the rare occa­
sion when a tendon is unsuitable for tenolysis or re-repair
but the sheath and surrounding tissues are well preserved.
It is more common to find extensive scarring, fibrosis, and
damage to the tendon sheath, which is unfavorable for this
technique. A two-stage reconstruction is the usual require­
ment. The first stage is to excise damaged tendon, recon­
struct pulleys as required, and insert a silicone tendon rod.
The biologic response is to form a “pseudosheath” or fibrous
capsule around the rod, which can later be used as a tendon
sheath. In the interim, therapy should commence to main­
tain a supple joint and protect the overlying soft tissues for
second stage repair. Secondary surgery requires a substan­
tial investment for all parties. It can only yield a positive
outcome in compliant patients who are willing to endure
extensive rehabilitation.
The second stage is commonly reconstructed with an ex­
trasynovial tendon graft. Options for donor tendon grafts are
commonly the palmaris longus, plantaris, extensor indicis
(which can be intrasynovial at the level of extensor retinacu­
lum), or toe extensors. FDS may also be used to graft the FDP.
a
b
Fig. 61.13 Composite tissue flexor tendon and sliding system transfer. (Image b is provided courtesy of Jean Claude Guimberteau.)

1173
Chapter 61 Flexor Tendon Injuries
(Fig. 61.13). Good functional results can be obtained from
such salvage techniques.
Conclusion
The key steps in avoiding an unfavorable result in flexor
tendon surgery are to establish a well-trained surgeon and
therapist team, to educate the patient about realistic out­
comes and the true length of recovery, and to give attention
to detail in the surgery and throughout the rehabilitation
period. Inevitably, the team will encounter unfavorable
results, and in general it is best to manage these proac­
tively with good documentation and root cause analysis
of the pitfalls that have arisen. These cases represent a
broad spectrum of etiologies; hence each will pose its own
unique challenges, and it is necessary to be aware of these
features and understand the biology of healing to guide
management. It is important that all centers critically look
at their practices to assess their shortcomings and improve
on them. Although they are not desired, the unfavorable
outcomes are the cases that surgeons learn the most from
and continue to evolve their practice.
defects may require secondary soft tissue reconstruction.
Rarer but devastating complications are wound infection
or, at its worst, purulent tenosynovitis. As prophylaxis we
routinely prescribe broad-spectrum antibiotics, because this
patient cohort is usually at high risk. Flexor sheath infections
despite antibiotic therapy are fortunately rare and display
the cardinal signs of a swollen digit, pain on passive exten­
sion, and tenderness on palpation. However, the finger may
not be held in flexion if the tendon has ruptured. Manage­
ment involves urgent repeated surgical débridement and
wash out until the infection has subsided. A staged ten­
don reconstruction can be considered, but if the infection
is severe, sepsis is likely to leave a stiff digit, and options
are limited and may include amputation or complex salvage
procedures. Salvage procedures include staged flap recon­
struction with pedicled flaps, such as an ulnar perforator
flap, or, if multiple digits are involved, a pedicled groin flap
with syndactyly release at a later date. Staged reconstruc­
tion of the tendons can then follow from this. Alternatively,
composite reconstruction can be performed using pedicled
or free ulnar-based vascularized composite tendon and slid­
ing system flaps to reconstruct the defects in one stage23,37
References
1. Lister GD, Kleinert HE, Kutz JE, Atasoy E. Primary flexor
tendon repair followed by immediate controlled mobili­
zation. J Hand Surg Am 1977;2(6):441–451
2. Sandow MJ, McMahon M. Active mobilisation following
single cross grasp four-strand flexor tenorrhaphy (Ad­
elaide repair). J Hand Surg Eur Vol 2011;36(6):467–475
3. Verdan CE. Primary repair of flexor tendons. J Bone Joint
Surg Am 1960;42-A:647–657
4. Tang JB. Flexor tendon repair in zone 2C. J Hand Surg [Br]
1994;19(1):72–75
5. Moiemen NS, Elliot D. Primary flexor tendon repair in
zone 1. J Hand Surg [Br] 2000;25(1):78–84
6. Masic A, Bertinetti L, Schuetz R, et al. Osmotic pressure
induced tensile forces in tendon collagen. Nat Commun
2015;6:5942
7. Enna CD, Ruby JR. Scanning electron microscopic
study of long flexors in human fingers. J Hand Surg Am
1981;6(4):329–335
8. Kastelic J, Galeski A, Baer E. The multicomposite structure
of tendon. Connect Tissue Res 1978;6(1):11–23
9. Jozsa L, Kannus P, Balint JB, Reffy A. Three-dimension­
al ultrastructure of human tendons. Acta Anat (Basel)
1991;142(4):306–312
10. Taylor SH, Al-Youha S, Van Agtmael T, et al. Tendon is
covered by a basement membrane epithelium that is
­required for cell retention and the prevention of adhesion
formation. PLoS One 2011;6(1):e16337
11. Wong JK, Lui YH, Kapacee Z, Kadler KE, Ferguson MW,
McGrouther DA. The cellular biology of flexor tendon ad­
hesion formation: an old problem in a new paradigm. Am
J Pathol 2009;175(5):1938–1951
12. Wong JK, Alyouha S, Kadler KE, Ferguson MW, Mc­
Grouther DA. The cell biology of suturing tendons. Matrix
Biol 2010;29(6):525–536
13. McDowell CL, Marqueen TJ, Yager D, Owen J, Wayne JS.
Characterization of the tensile properties and histologic/
biochemical changes in normal chicken tendon at the site
of suture insertion. J Hand Surg Am 2002;27(4):605–614
14. Wong JK, Peck F. Improving results of flexor ­tendon ­repair
and rehabilitation. Plast Reconstr Surg 2014;134(6):
913e–925e
15. Hardwicke JT, Tan JJ, Foster MA, Titley OG. A systematic
review of 2-strand versus multistrand core suture tech­
niques and functional outcome after digital flexor tendon
repair. J Hand Surg Am 2014;39(4):686–695.e2
16. Urbaniak JR, Cahil JD, Mortenson MD. Tendon Suturing
methods: analysis of tensile strength. AAOS Symposium
on Tendon Surgery in the Hand. St Louis: The C.V.Mosby
Company; 1974:70–80
17. Starnes T, Saunders RJ, Means KR Jr. Clinical outcomes of
zone II flexor tendon repair depending on mechanism of
injury. J Hand Surg Am 2012;37(12):2532–2540
18. de Jong JP, Nguyen JT, Sonnema AJ, Nguyen EC, Amadio
PC, Moran SL. The incidence of acute traumatic tendon in­
juries in the hand and wrist: a 10-year population-based
study. Clin Orthop Surg 2014;6(2):196–202
19. Caulfield RH, Maleki-Tabrizi A, Patel H, Coldham F, Mee
S, Nanchahal J. Comparison of zones 1 to 4 flexor tendon
­repairs using absorbable and unabsorbable four-strand
core sutures. J Hand Surg Eur Vol 2008;33(4):412–417
20. Lalonde DH. Wide-awake flexor tendon repair. Plast
­Reconstr Surg 2009;123(2):623–625
21. Lalonde D, Martin A. Epinephrine in local anesthesia in
finger and hand surgery: the case for wide-awake anes­
thesia. J Am Acad Orthop Surg 2013;21(8):443–447
22. Bruner JM. Surgical exposure of flexor tendons in the
hand. Ann R Coll Surg Engl 1973;53(2):84–94
23. Wong J, McGrouther DA. Minimizing trauma over ‘no
man’s land’ with flexor tendon retrieval. J Hand Surg Eur
Vol 2014;39(9):1004–1006
24. Mozafari N, Hosseini SN, Abdolzadeh M, Mozafari MA.
Parachute technique: a complimentary method in zone

SECTION VIII THE HAND AND UPPER EXTREMITY
1174
32. Tang JB. Release of the A4 pulley to facilitate zone II flexor
tendon repair. J Hand Surg Am 2014;39(11):2300–2307
33. Kwai Ben I, Elliot D. “Venting” or partial lateral release of
the A2 and A4 pulleys after repair of zone 2 flexor tendon
injuries. J Hand Surg [Br] 1998;23(5):649–654
34. Wray RC Jr, Moucharafieh B, Weeks PM. Experimental
study of the optimal time for tenolysis. Plast Reconstr
Surg 1978;61(2):184–189
35. Hunter JM, Salisbury RE. Flexor-tendon reconstruction in
severely damaged hands. A two-stage procedure using a
silicone-dacron reinforced gliding prosthesis prior to ten­
don grafting. J Bone Joint Surg Am 1971;53(5):829–858
36. Amiel D, Harwood FL, Gelberman RH, Chu CR, Seiler JG
III, Abrahamsson S. Autogenous intrasynovial and extra­
synovial tendon grafts: an experimental study of pro al­
pha 1(I) collagen mRNA expression in dogs. J Orthop Res
1995;13(3):459–463
37. Guimberteau JC, Bakhach J, Panconi B, Rouzaud S. A fresh
look at vascularized flexor tendon transfers: concept,
technical aspects and results. J Plast Reconstr Aesthet
Surg 2007;60(7):793–810
II tendon repair. Tech Hand Up Extrem Surg 2011;15(2):
78–81
25. Bunnell S. Repair of tendons in the fingers and descrip­
tion of two new instruments. Gynecology and Obstetrics.
1918;26:103
26. Kessler I, Nissim F. Primary repair without immobiliza­
tion of flexor tendon division within the digital sheath.
An experimental and clinical study. Acta Orthop Scand
1969;40(5):587–601
27. Kirchmayr L. Zur Technik der Sehnennaht. Zentralbl Chir
1917;40:906–907
28. Savage R, Risitano G. Flexor tendon repair using a “six
strand” method of repair and early active mobilisation. J
Hand Surg [Br] 1989;14(4):396–399
29. Vogelin E, Elliot D, Amadio P. IFSSH Scientific Committee
on Flexor Tendon Repair. 2015.
30. Silfverskiöld KL, May EJ, Törnvall AH. Tendon excur­
sions after flexor tendon repair in zone. II: Results with
a new controlled-motion program. J Hand Surg Am
1993;18(3):403–410
31. Doyle JR. Palmar and digital flexor tendon pulleys. Clin
Orthop Relat Res 2001; (383):84–96
Discussion by Jin Bo Tang
Flexor Tendon Surgery: Then and
Now
There are significantly fewer problems in flexor tendon
surgery than there were 30 to 40 years ago. In almost
all surgical units around the world, primary repair is
popular and outcomes are much better than they were
decades ago. Notably, excellent outcomes have been
reported in recent literature.1–4 In most patients, the
results of direct repair of tendon lacerations in zone II
are no longer unfavorable. In fact, some recent reports
show that outcomes of primary repair in zone II can be
as good as in other areas,1–4 though there is a greater
need for surgical expertise in this area than in other re­
gions. When repairing tendons in this area, surgeons
face much more delicate details than in other regions.5–7
However, generally good or excellent outcomes can be
expected if they carefully follow guidelines. In other
words, there is an established path to good and excel­
lent outcomes of zone II tendon repair, but it is a narrow
one, and a number of technical requirements must be
followed. In contrast, the outcomes of tendon repairs in
zones III through V can be quite good if surgeons focus
less on the details and feel free to select those methods
they deem proper.
Path to Satisfactory Zone II Primary
Repair: Technical Keys in Each Step
This section outlines the technical details of zone II pri­
mary flexor tendon repair. By closely following these
protocols, surgeons should be able to obtain good or
excellent outcomes. It is important that the surgeon not
neglect or omit any of these protocols, and understand
which details are important.
Timing of Primary Repair
The cut tendon can be repaired primarily a few hours
after injury or, if the wound is cleaned and closed im­
mediately, delayed primary tendon repair can take
place within 2 to 4 weeks. Because both lead to simi­
lar outcomes, primary repair is not always necessary.
However, the longer the tendon repair is delayed, the
greater the difficulty, especially when advancing the
retracted proximal tendon stump and in dealing with

1175
Chapter 61 Flexor Tendon Injuries
adhesions and collapsed or slightly fibrotic pulleys
or sheath. Therefore surgical repair within 2 weeks is
ideal.
Incisions
A zig zag incision about 2 cm in longitudinal length
is enough; a lengthy incision is not recommended. If
the proximal stump of the flexor digitorum profundus
(FDP) tendon is retracted, a small transverse incision
(smaller than 1.5 cm) is made in the distal palm to lo­
cate it and advance it to the cut area through gentle
progressive feeding of the tendon through the well-
preserved sheath toward the distal surgical incision.
Temporary Fixation
With the finger held in flexion by an operator or an as­
sistant, the proximal stump of the retracted tendon is
passed distally and visualized at the cut site, and the
end is then pulled with a forceps to keep it out of the
outlet of the sheath tunnel. At this time, a midsized
needle is inserted transversely through the skin to the
tendon from the side of the finger 2 to 3 cm proximal to
the skin wound to temporarily fix the tendon and ease
its tension during surgical repair. If the tendon ends are
ragged, trimming is necessary. This is easier to accom­
plish at this point because the proximal stump cannot
retract. Then the distal part of the finger is held semi­
flexed to allow approximation of the two tendon ends.
Repair Maneuvers
I use a 4–0 nylon suture to make a six-strand core su­
ture repair for any FDP tendon repair.6,7 The keys to
making a good surgical repair are listed in Box 61D.1.
Personal Preferences
It is not important to repair the flexor digitorum su­
perficialis (FDS) tendon. In most cases I do not repair it,
especially when a tendon is cut in the A2 pulley area.
Closure of the sheath is not important, nor are specific
repair configurations. Though I use the M-Tang re­
pair method or three groups of asymmetrical Kessler
repairs (see Fig. 61D.1), other methods can be used,
provided the surgeon makes sure that all the technical
points listed are met. The M-Tang method that I have
used for more than 10 years is very simple, because
with the looped suture, one pass of the needle in the
tendon carries two suture strands.5,6
Venting the Entire A4 or a Part of the A2
Pulley
After suturing the FDP tendon, the location and length
of injuries in the sheath (and pulleys) should be as­
sessed carefully. If the injury is at the A4 pulley area, this
pulley should usually be entirely vented (as described
in the chapter regarding the safe area and length for
venting the A4 pulley). If the tendon cut is in the area
of the A2 pulley or a little distal to it, the distal half or
distal two thirds of the A2 pulley should be vented.6 I
vent these two pulleys through a cut along the midline
of the pulleys using a scissors. In some cases with de­
layed primary repair I excise a part of the A2 pulley that
has collapsed or is fibrotic (see Fig. 61D.2). Because the
wound through which the tendon is lacerated is usu­
ally narrow, it is rare to have both A2 and A4 pulleys
Box 61D.1
Profundus Tendon Repair
•• Ensure the suture purchase is long enough
(at least 7–10 mm in each tendon end is
necessary).
•• If using a locking suture, the diameter of the
locks should be 2 mm or greater.
•• Use at least a 4-strand core suture
(preferably a 6-strand repair) to increase
the safety margin during early motion. An
M-Tang repair should be made with 4–0
looped sutures5,6,8 (Fig. 61D.1); a 6-strand,
3-group asymmetrical Kessler repair should
be made with a 4–0 Ethilon suture.
•• Ensure tension during the repair, and
ensure that the tendon ends are in tight
contact and, within the span of the core
suture, appear a little shortened (about 10%
shortening)9 or slightly rough, without being
too bulky or twisted, so the repair site is
pretensioned to resist gapping during early
tendon motion8,10 (Fig. 61D.2).
•• Add a simple peripheral suture to smooth
the junction site of the tendon ends. Only
4 to 6 runs of a simple running peripheral
suture using a 6–0 suture is necessary. A
large number of runs of the peripheral
suture is neither important nor necessary
when a 6-strand core suture is used. Some
surgeons do not use a peripheral suture with
a 6-strand repair; in that case, those core
sutures are pretensioned to prevent gapping.4
Keys to Making a
Good Flexor Digitorum

SECTION VIII THE HAND AND UPPER EXTREMITY
1176
involved. I do not suggest venting both A2 and A4 at the
same time or venting the entire A2 pulley.
Digital Extension–Flexion Test
Once the tendon repair is completed and an involved
major pulley is properly vented, a digital extension–­
flexion test (Fig. 61D.3) should be performed to ensure
the tendon does not gap when tensioned and that it
glides smoothly when pulled proximally.1,8 First, I fully
extend the repaired finger to see whether there are any
gaps between the two tendon ends at the repair site. Of­
ten gaps are seen at the repair site when fully extending
the finger after a four-strand core suture, but such gap­
ping does not occur if additional two-strand sutures are
added, to make the equivalent of a six-strand repair.
Second, the finger is flexed to confirm that the ten­
don glides smoothly.
Fig. 61D.1 Two suture methods. (a) The step-by-step repair method of the M-Tang repair. The first step is to make a four-strand
­U-shaped repair using one looped nylon suture; the second step is to insert an independent two-strand repair using another looped
suture. The six-strand M-Tang repair is thus completed. (b) Three groups of asymmetrical Kessler repairs.
M-Tang repair (6-strand)
a
Asymmetrical triple-Kessler repair (6-strand)
b

1177
Chapter 61 Flexor Tendon Injuries
No tension
Not recommended
10% tension
Recommended
20% tension
a
b
Shortening
Lateral venting
Midline venting
3
2
1
VENTING AND RESECTION
SUTURE TENSION
Fig. 61D.2 (a) Pretension of the repaired tendon is very important to preventing repair gaps. A 10% shortening of the repaired
tendon segment is recommended when making a core suture of the tendon. Tendon repairs without pretension can easily gap;
therefore it is not recommended. (b) Venting a major pulley is critical to reduce resistance to tendon gliding. The pulley can be
vented through a midline cut (1, preferred method) or a lateral cut (2). When the A2 pulley is embedded in adhesions, as often
seen in delayed primary repair, a part of the A2 pulley can be resected (3). (a Reproduced from Wu YF, Tang JB. Effects of tension
across the tendon repair site on tendon gap and ultimate strength. J Hand Surg Am 2012;37:906–912. b From Tang JB, Amadio P,
Guimberteau JC, et al. Tendon Surgery of the Hand, St Louis, MO: Elsevier, 2012.)
a
b
c
Fig. 61D.3 The three steps of the digital extension–flexion test. (a) Full extension of the repaired finger. (b) Digital flexion from
full extension to moderate flexion. (c) Digital flexion from moderate flexion toward almost full flexion.

SECTION VIII THE HAND AND UPPER EXTREMITY
1178
Finally, the finger is pushed to almost full flexion
to make sure the tendon repair site does not catch on
the rim of the proximal sheath or pulleys. If the proxi­
mal sheath or pulley prevents tendon gliding, further
venting is necessary. This is why a short-sheath inci­
sion (shorter than 1.5 cm) is important at the start of
this surgery; this leaves room for further venting at the
time of the digital extension–flexion test. The total al­
lowable length of the sheath to be opened or vented is
usually 2 cm. Beyond that length, tendon bowstringing
may become a problem; thus an extended sheath open­
ing should be avoided. The total opening or venting in
any sheath segment is kept within 2 cm.
It is not necessary to repair the cut sheath or keep
the sheath entirely closed. Leaving it partially open is
harmless, and venting a part of the major pulley is key to
good tendon gliding. The digital extension–flexion test
confirms the quality of the tendon repair and that the
sheath–pulley venting meets the needs of early, active
digital motion after surgery.
When the repair is performed with local anesthesia
without use of a tourniquet (i.e., a wide-awake surgical
setting11), this test is even more telling, because it rep­
resents intraoperative active digital motion. I use the
active extension–flexion test intraoperatively when I
perform wide-awake tendon repair.12
Failing the Digital Extension–Flexion Test
If the patient fails to pass this test, the repair should
be augmented with additional core suture strands and
additional tension over the suture strands. I have not
needed to add additional core sutures in my cases, but
because a strong surgical repair is necessary I do not
hesitate to use six- or eight-strand core sutures. Spend­
ing 5 to 10 extra minutes to add additional two-strand
core sutures will make early active motion much safer
in the coming weeks.
Closure of Incisions and Protection
After skin closure, the operated hand should be placed
in a short forearm splint from the fingertip to the lower
part of the forearm.8 A specific wrist position is not
essential; it can be neutral or slightly flexed at 20 to
30  degrees.8 The metacarpophalangeal joint is set at
30  to 40 degrees of flexion, and the interphalangeal
joints should be straight. There is no need for motion
in the first 3 days after surgery.8
Postoperative Therapy
I instruct the patient to move the joint starting on day
4 after surgery, with five to six exercise sessions per
day. In the first 4 weeks, in each session, passive mo­
tion of the finger for 20 to 30 repetitions (or more)
is undertaken first, through full finger extension
and flexion ranges to reduce joint stiffness, followed
by partial active finger flexion that covers the initial
one third to two thirds of the arc of active finger flex­
ion6,8,13 (Fig. 61D.4). The range of active finger flexion
is increased gradually from week 1 to week 3 or 4. This
is the key to the partial active flexion regimen, “Nan­
tong’s regimen”6 (or its variants).14 In the first 3 or 4
weeks, partial active flexion of the finger is sufficient
to enable the repaired tendon to glide, and full range
of passive motion should prevent finger joint stiffness.
From week 5, active flexion should be advanced to
reach full active flexion, and more exercise sessions
are added when necessary. The splint is discarded at
the end of week 6 or 7.
The early active motion method (Nantong’s regi­
men) is now the mainstay of therapy after primary
flexor tendon repair, except in children or when there
is severe hand trauma.6 Active flexion through the ini­
tial one-third to two-thirds range in the first 3 to 4
weeks after repair is quite safe and easily achievable,
and, most important, it encourages the tendon to glide
enough to prevent adhesions without risking repair
rupture, thus leading to fewer complications.6,8,13 This
regimen and its variants are now in popular use. Use
of such a regimen has been extended to rehabilitation
after secondary tendon grafting. A partial-range active
flexion regimen can be generally applied after tendon
repair or grafting. After tenolysis, full-range active flex­
ion must be implemented. Rubber band traction has
been abandoned, and now purely passive motion pro­
tocols and place-and-hold exercises are vanishing from
many units.
Avoiding Unfavorable Results
By using these step-by-step protocols, surgeons can
avoid unfavorable results.
Over the past 25 years, I have been advocating sev­
eral changes in primary flexor tendon repairs based on
biomechanical studies in my laboratory and the out­
comes of new methods in my patients.6,8,12,13,15 Around
2012, I felt that almost all the key elements for satis­
factory repair and outcomes had been investigated and
implemented into my practice. I could not think of any
missing technical points, but I had serious questions
about whether these protocols could be mastered eas­
ily by someone who is not an experienced hand surgeon
(i.e., a young surgeon, or someone whose practice cov­
ers only some hand cases). Therefore I chose two units
whose surgeons did not have extensive expertise and
whose cases had 6% to 8% rupture rates and below 70%

1179
Chapter 61 Flexor Tendon Injuries
good or excellent ratings by Strickland criteria.16 Such
outcomes are still typical in many units, indicating that
the techniques used in many units have not been up­
dated, and that appropriate surgical repair has fallen
behind.
I provided these surgeons with the same step-by-
step method listed in this discussion, along with edu­
cation regarding the detailed anatomy of zone II and
­illustrations showing an M-Tang repair method and the
area of pulley venting, together with videos demon­
strating digital extension–flexion tests. Those surgeons
confirmed they would do exactly as my protocols in­
structed. After 2.5 years, I asked the surgeons to follow-
up with their patients. They found that of more than
80 patients, none had experienced any rupture, and that
the good or excellent rate was 85 to 89%. They noted that
a few patients experienced adhesions that required te­
nolysis, and a few had minor joint stiffness that required
no further surgery. Overall, the improvement in these
two units has been dramatic.
I urge readers to consider meticulously following
the protocol outlined here, along with the accompany­
ing advice, and evaluate whether outcomes improve.
Local Injuries to Multiple Tissues: A
Lasting Challenge
Severe local trauma to the finger with severing of the
flexor tendon is still a largely unpredictable injury,
because local soft tissue loss or bony injuries and re­
sultant severe edema prevent early active motion. In
addition, patients who smoke or are noncompliant in
postoperative instructions do not usually obtain favor­
able outcomes.
Tendon defects in a patient with severe hand trauma
remain difficult to treat, and most require secondary
tendon grafting. Future efforts should be directed to­
ward these difficult cases.
If pulleys are destroyed, staged reconstruction is
necessary. However, such procedures take months, and
outcomes often are unsatisfactory or fall far short of
­expectations. At stage one, the pulleys should be recon­
structed, and a silicone tendon spacer should be placed
to stimulate formation of the sheath around it, followed
by the second stage of surgery 3 months later (and when
joints and soft tissues are supple) to replace the spacer
with a free tendon graft. This classic operation remains
at the very end of the salvage process for cases that are
complex or for which the outcomes of primary repair
are unfavorable.
Prerequisites for staged tendon reconstruction and
single-stage tendon grafting are listed in Box 61D.2.
Tenolysis is a common procedure for patients with
severe adhesions around the tendon, but this surgery
Box 61D.2
1. Normal passive motion of the finger joints
2. Good skin coverage
Indications for Single-Stage Tendon Grafting
•• The tendon has not undergone primary
repair, become frayed, or been impeded by
severe adhesions.
•• It has been at least 3 months after the onset
of trauma.
Indications for Pulley and Staged Tendon
Reconstructions
•• The tendon gliding bed has heavy scarring.
•• Important pulleys have been destroyed.
Prerequisites for Single
or Staged Tendon
Reconstruction
a
b
Fig. 61D.4 Partial active motion regimens (such as Nantong’s
regimen) after primary tendon repair in the digits. (a) Full pas­
sive flexion and extension should also be achieved before active
motion of the digits is initiated. (b) In the first 3 to 4 weeks after
repair, the early active flexion of the digits covers only the initial
one third or two thirds of the total flexion arc of the digits. The
active flexion exercise starts from day 4 after surgery.

SECTION VIII THE HAND AND UPPER EXTREMITY
1180
may not proceed as intended: Sometimes the surgeon
has to give up plans for tenolysis and proceed with
staged tendon reconstruction. Such a judgment is often
made intraoperatively, and the patient should give con­
sent for both plans before surgery.
Managing Difficult or Unfavorable
Situations in Flexor Tendon Surgery
There are a number of difficult problems and ongoing
challenges in flexor tendon surgery, and each has spe­
cific treatments for management.
Repair of a Finger with Only a Flexor
Digitorum Superficialis
When the FDP tendon is cut at zone II but the FDS is
functional, the surgeon should carry out the end-to-
end FDP tendon repair at primary or delayed primary
repair stages. However, if such a case comes to the
surgeon late and end-to-end repair is no longer an op­
tion, the surgeon should weigh carefully whether to
perform a tendon graft to restore FDP tendon function.
Tendon grafting to restore active flexion of the distal
interphalangeal joint carries the risk of damaging the
normal function of the FDS, and such a procedure is in­
dicated only in young, active patients who eagerly want
to actively flex the distal finger joint, which accounts
for only 15% of total finger flexion. The surgeon should
inform the patient about the possibility of damage to
FDS function if a tendon graft is being considered. If
the distal interphalangeal (DIP) joint is frail, alternative
treatments are tenodesis or arthrodesis of the DIP joint.
Tendon Repair or Reconstruction with a
Cutaneous Tissue Defect or Scar
A soft tissue defect and scar should be addressed
­before planning tendon surgery. Such a defect can be
­reconstructed with local flap transfers or soft tissue re­
arrangements to enable full passive motion of the joints.
Large scars in the skin should be resected and the result­
ing defects repaired. Tendon surgery is then planned a
few weeks or a few months later, when passive joint mo­
tion has been restored through rehabilitation.
Repair of Ruptured Primarily Repaired
Tendons
A primarily repaired tendon may occasionally be dis­
rupted during early active motion, which may occur
any time in the postoperative 1 to 6 weeks. Upon no­
ticing any loss of active digital flexion during reha­
bilitation, the surgeon should plan a re-repair of the
disrupted tendon as soon as possible. A strong repair
method must be used. After surgery, the partial active
motion regimen can still be used. Acceptable outcomes
of such re-repairs are reported in half of cases,17 but the
rest have tendon adhesions requiring tenolysis or sec­
ondary tendon grafting 3 months later. Such re-repairs
salvage function in half of cases without being deferred
to receive secondary surgical treatment.
Lacerations of Multiple Tendons at the
Proximal Palm or Carpal Tunnel
In the middle of the palm, repair of multiple tendon
structures is relatively easy. However, at or just distal
to the carpal tunnel, if multiple tendons or the median
nerve are injured, the tendons often retract to the fore­
arm, and the carpal tunnel has to be opened. Repairs
of these structures often lead to adhesions, and many
patients require tenolysis and neurolysis.
Tendon Repair in Digital Amputation
and Replantation
Tendon repairs with these more complex injuries is
more difficult, but the tendons should be repaired
primarily whenever possible. Major pulleys may need
venting to allow tendon gliding, and the FDS tendon
should not be repaired. A strong repair method should
be used in a FDP or flexor pollicis longus repair. Partial
active finger flexion should be encouraged from 1 to
2 weeks after surgery when survival of the replanted
digit is confirmed.
Defects in Multiple Flexor Tendons
Defects in multiple flexor tendons are usually treated
with tendon grafting more than 3 months after injury.
The availability of tendon donors is a concern. The pal­
maris longus tendons in both forearms are the first do­
nor site, followed by tendons from the lower leg. I have
used allograft tendons for such patients and found that
it worked well without foreign tissue reactions or rejec­
tion after 10 years of follow-up.
Repair of Tendons in Little Fingers
Either primary repair or secondary reconstruction of
the FDP tendon in the little finger is more challenging
than in other digits because of its small size. The pri­
marily repaired FDP tendon in this finger is more prone

1181
Chapter 61 Flexor Tendon Injuries
to disruption during early active motion, and adhesions
develop easily. The FDS tendon is absent in about 25%
of the little fingers; if it is present, it may be very thin.
The surgeon should not attempt to repair the FDS ten­
don in the little finger.
Treatment of Patients with Repeated
Tenolysis
Tendons may develop adhesions again after tenolysis. I
discourage repeating tenolysis more than once. If treat­
ment fails a second time, the patient should proceed
with tendon reconstruction. During the second tenoly­
sis, the surgeon should carefully determine whether
the tendon is frayed or the adhesions are very dense. If
so, the surgeon should give up the plan for the second
tenolysis and proceed to staged reconstruction. The pa­
tient should be informed about the possibility of plan
changes before surgery. The surgeon should also dis­
cuss with the patient the possibility of disappointing
outcomes, even after lengthy tendon reconstruction
efforts.
Active Flexion and Assessment
The methods discussed previously regarding Nantong’s
regimen are the most common form of active digital
motion after primary tendon repair and after tendon
grafting. However, after tenolysis full range of active
motion is encouraged from the first week, though it can
be started 2 to 4 days after surgery.
Regarding assessment after rehabilitation, digital
function may improve greatly in the first 6 months, and
improvement can be seen even 1 year later. The Strick­
land criteria16 remain the most popular. I recommend
them for evaluating all flexor tendon repairs. I also be­
lieve that more stringent criteria should be used for
primarily repaired patients. Some surgeons already use
such criteria in reporting outcomes.2,18 I designate a spe­
cific category for very unfavorable outcomes—“failure”6
(Table 61D.1).
Conclusion
•• Outcomes of primary repair of the tendon in zone
II can be as good as in other zones—provided the
surgeon carefully follows all the advice provided in
this discussion and meets all the requirements for
primary surgery repairs. The keys to primary tendon
repair in zone II have been provided here.
•• Severe multiple tissue trauma with tendon
injuries is a highly unfavorable situation and has
many challenges. These cases commonly require
secondary tendon grafting or staged reconstruction,
and outcomes are sometimes unfavorable.
•• Soft tissue defects should be addressed first, and
full passive motion of joints in the hand should be
restored before secondary tendon surgery.
•• A partial early active flexion protocol (such
as Nantong’s regimen) is recommended in
rehabilitation a few days after primary repair or
tendon grafting. This is a safe and efficient tendon
active motion protocol that avoids overburdening
the repaired tendons. However, full early active
motion should be initiated after tenolysis.
•• Surgeons should be particularly mindful in
treating patients whose FDS tendon is intact, when
attempting tendon repairs in the little finger, or
when repairing multiple structure lacerations at or
just distal to the carpal tunnel. Surgeries in these
patients may be difficult and the risks of adhesion
are higher.
•• Undeniably, flexor tendon surgery is technically
demanding. Surgeons should attend to details
in procedures relating to primary tendon repair.
Poor real-world outcomes after primary flexor
tendon repair usually relate to lack of mastery of all
technical details or failure to adhere to useful advice.
Table 61D.1 More stringent
criteria for outcomes of flexor
tendon repairs
Function grade
Return of motion (%)
Excellent
90–100
Good
70–89
Fair
50–69
Poor
30–49
Failure
<30
Note: Total active motion of the contralateral side is used as the
normal in calculating the percentage of return, or fixed values are
used as the normal. For zone II repairs, only the proximal interpha­
langeal (PIP) and distal interphalangeal (DIP) joints are included in
the evaluation, and 175 degrees is used as the normal. For zone III,
the metacarpophalangeal, PIP, and DIP joints are included and 260
degrees is used as the normal. This criteria can be used for zone I, IV,
and V flexor tendon repair, as well.
Source: From Tang JB. Indications, methods, postoperative motion
and outcome evaluation of primary flexor tendon repairs in Zone 2.
J Hand Surg Eur 2007;32:118–129.

SECTION VIII THE HAND AND UPPER EXTREMITY
1182
References
1. Tang JB. Outcomes and evaluation of flexor tendon
­repair. Hand Clin 2013;29(2):251–259
2. Moriya K, Yoshizu T, Maki Y, Tsubokawa N, Narisawa
H, Endo N. Clinical outcomes of early active mobili­
zation following flexor tendon repair using the six-
strand technique: short- and long-term evaluations.
J Hand Surg Eur Vol 2015;40(3):250–258
3. Moriya K, Yoshizu T, Tsubokawa N, Narisawa H, Hara
K, Maki Y. Outcomes of release of the entire A4 pul­
ley after flexor tendon repairs in zone 2A followed
by early active mobilization. J Hand Surg Eur Vol
2016;41(4):400–405
4. Giesen T, Sirotakova M, Copsey AJ, Elliot D. Flexor pol­
licis longus primary repair: further experience with
the tang technique and controlled active mobiliza­
tion. J Hand Surg Eur Vol 2009;34(6):758–761
5. Elliot D. Primary flexor tendon repair—operative re­
pair, pulley management and rehabilitation. J Hand
Surg [Br] 2002;27(6):507–513
6. Tang JB. Indications, methods, postoperative ­motion
and outcome evaluation of primary ­flexor tendon
­repairs in Zone 2. J Hand Surg Eur Vol 2007;32(2):
118–129
7. Wu YF, Tang JB. Recent developments in flexor ­tendon
repair techniques and factors influencing strength of
the tendon repair. J Hand Surg Eur Vol 2014;39(1):
6–19
8. Tang JB. Release of the A4 pulley to facilitate zone II
flexor tendon repair. J Hand Surg Am 2014;39(11):
2300–2307
9. Wu YF, Tang JB. Effects of tension across the tendon
repair site on tendon gap and ultimate strength. J
Hand Surg Am 2012;37(5):906–912
10. Tang JB, Amadio P, Guimberteau JC, Chang J. Tendon
Surgery of the Hand. St. Louis, Elsevier; 2012
11. Lalonde DH, Martin AL. Wide-awake flexor tendon
repair and early tendon mobilization in zones 1 and
2. Hand Clin 2013;29(2):207–213
12. Tang JB. Wide-awake primary flexor tendon repair,
tenolysis, and tendon transfer. Clin Orthop Surg
2015;7(3):275–281
13. Wu YF, Tang JB. Tendon healing, edema, and resis­
tance to flexor tendon gliding: clinical implications.
Hand Clin 2013;29(2):167–178
14. Tang JB, Chang J, Elliot D, Lalonde DH, Sandow M,
Vögelin E. IFSSH Flexor Tendon Committee re­
port 2014: from the IFSSH Flexor Tendon Commit­
tee (Chairman: Jin Bo Tang). J Hand Surg Eur Vol
2014;39(1):107–115
15. Savage R, Tang JB. History and nomenclature of mul­
tistrand repairs in digital flexor tendons. J Hand Surg
Am 2016;41(2):291–293
16. Strickland JW, Glogovac SV. Digital function follow­
ing flexor tendon repair in Zone II: A comparison of
immobilization and controlled passive motion tech­
niques. J Hand Surg Am 1980;5(6):537–543
17. Dowd MB, Figus A, Harris SB, Southgate CM, Foster AJ,
Elliot D. The results of immediate re-repair of zone 1
and 2 primary flexor tendon repairs which rupture.
J Hand Surg [Br] 2006;31(5):507–513
18. Zhou X, Li XR, Qing J, et al. Outcomes of the
six-strand M-Tang repair for zone 2 primary flexor
tendon repair in 54 fingers. J Hand Surg Eur Vol
2017;42(5):462–468

1183
Extensor tendons are located superficially and thus are
vulnerable to injury. Probably because surgical exposure is
simple, these injuries receive much less attention in publi­
cations than do flexor tendons, yet morbidity is deceptively
high. Unfavorable results are often related to loss of the del­
icate balance between the extrinsic and intrinsic extensor
systems, further complicated by morbid biologic changes
in adjacent uninjured structures proximate to the injured
tendon itself. These lead to stiffness with changes in the
volar plate, collateral ligaments, joint capsule, and even to
adjacent uninjured digits. Acceptance of a less than favor­
able outcome has thus almost become the norm for many
extensor tendon injuries, such as mallet and boutonnière
deformity and rheumatoid tendon ruptures. We contend
that this should not be the case.
This chapter emphasizes a number of commonly over­
looked management issues that lead to prevention of dete­
riorated function with adjacent, seemingly uninjured, struc­
tures, as well as addressing the injured tendon itself. The
surgeon needs to have an understanding of certain biologic
principles of healing and repair and of functional extensor
tendon anatomy before exploring each zone of extensor ten­
don injury in its specific detail.

Extensor Tendon Injuries
Wyndell H. Merritt and Collier S. Pace
CHAPTER
62
Summary Box
Unfavorable Results and Complications
Associated with Extensor Tendon Repair
•• Adverse effects on adjacent structures
•• Fibroplasia
•• Reflex sympathetic dystrophy
•• Complex regional pain syndrome/reflex
sympathetic dystrophy
•• Loss of flexion
•• Extensor tendon scar adhesions
•• Joint capsule extension contractures
•• Distal interphalangeal extension lag
•• Volar plate laxity
•• Volar plate contraction
•• General discomfort
•• Swan neck deformity
•• Extensor tendon rupture at the wrist, caput ulnae
(Vaughan-Jackson) syndrome
•• Splint-induced complications
○
○Dorsal skin pressure necrosis
○
○Inadequate positioning
•• Collateral ligament contraction
•• Failure to achieve bone union
•• Ankylosed joint
•• Dorsal bump
•• Boutonnière deformity
•• Clinical repair rupture
•• Infection

SECTION VIII THE HAND AND UPPER EXTREMITY
1184
As with any other tissues, tendon healing occurs in three
phases: (1) inflammatory, (2) proliferative, and (3) remodel­
ing.4 During the inflammatory phase, activated macrophages
target necrotic tissue and release chemoattractants, drawing
in tenocytes.5 The proliferative phase results from tenocyte–
macrophage collagen synthesis, starting several days after
injury. It is thus best to rest most injured hands in a splint
and bulky dressings for 3 to 5 days while surgical trauma
subsides and fibroblasts are mobilized. Initially, type III col­
lagen is deposited, but later type I collagen predominates
and the extracellular matrix becomes more organized, cross-
linked, and less responsive to therapy stretch. This remodel­
ing phase may continue for up to 1 year, and repaired ten­
dons never regain their original strength.6
Mechanical stress has a direct effect on tendon healing.
Too much stress can disrupt a healing tendon, whereas early,
protected motion results in increased vascularity and de­
oxyribonucleic acid (DNA) synthesis and overgrowth of epi­
tenon at the repair site, which is a phenomenon not seen in
immobilized healing tendons. This results in both increased
tensile strength and improved gliding function.7 Early ac­
tive motion also allows tendons to heal with fewer extrin­
sic adhesions.8 Although these observations are noted most
in studies on flexor tendons, they apply equally to extensor
tendons. These principles of protected early motion have
not been as rigorously applied to healing extensor tendons,
perhaps accounting for less well-studied outcomes in exten­
sor tendon injury.
Preserve Function in All Structures
The surgeon must focus not only on the healing tendon,
but also on the adverse response to injury of seemingly
uninjured adjacent structures9 (Fig. 62.2). This is best ac­
complished by early motion in such a way that repair is not
disrupted, emphasizing rigid fracture fixation and a pro­
tected tendon motion regimen, such as rubber band active
dynamic traction, short-arc controlled motion, and relative-
motion splinting.9,10 Relative-motion splinting allows early
protected active motion and minimally inhibits functional
use of the hand after repair of long extensor tendons, bou­
tonnière deformity, and sagittal band rupture. We also
advocate use of local anesthesia with epinephrine and no
tourniquet during surgical repair to ensure that the correct
extensor mechanism balance is restored and to verify by
Avoiding Unfavorable Results
and Complications in Extensor
Tendon Repair
Biologic Principles
There are three important biologic principles that, if ne­
glected, lead to unfavorable outcomes.
1. The hand should be considered as a “functioning
organ,” because any injury results in a response by the
entire organ.1
2. A challenge in hand surgery, with all types of injuries, is
to preserve function in all structures that may not have
been directly injured.2
3. Scar will most simulate the tissue to which it is jux­
taposed1 (the “one wound, one scar” enunciated by
Peacock3).
Response of the Entire Organ
An unfavorable result after extensor injuries commonly re­
sults from adverse effects on adjacent structures that are
not necessarily directly injured (Fig. 62.1). It is a miscon­
ception that structures composed of connective tissue (ten­
don, ligament, fascia, and the joint capsule) are biologically
inactive. Connective tissue develops a dramatic increase in
collagen synthesis and turnover, even greater than in skin
wounds, and continues at this level of activity long after
a similar skin injury would.2 This explains why swelling
and inflammation in the injured digit might continue for
months and why therapy can modify outcomes weeks or
even months after injury as long as it remains inflamed.
This is because the accelerated collagen turnover results
in a high level of uncross-linked collagen fibers that can be
modified in response to stretch stresses.
Activated macrophages in an injured digit may equally
involve the site of tendon laceration and the adjacent in­
tact collateral ligament or volar plate, resulting in fibropla­
sia. Structures that are closest to the site of injury undergo
the greatest change, but even the entire hand can respond
with swelling and generalized stiffness, seen at its most dra­
matic with reflex sympathetic dystrophy and complex re­
gional pain syndrome.
Fig. 62.1 This patient sustained an avulsion amputation of the index finger. Swelling and lack of use resulted in stiffness of the remaining
fingers with metacarpophalangeal joint extension contractures, even as distant from the amputation site as the little finger.

1185
Chapter 62 Extensor Tendon Injuries
surgical handling with loss of paratenon (the important
tendon gliding surface) may result in tendon scar adhe­
sions.18 Likewise, a complex crushing injury with raw bone
surface and muscle denuded of dense connective tissue
will result in an “unfavorable scar” for gliding. Early protec­
tive motion tends to reduce cross-linking of adhesive colla­
gen in unfavorable scars and can produce a more favorable
gliding surface. On occasion, the surgeon may choose to
interpose a gliding surface for tendons, such as a vascular­
ized fascial flap, or create a more favorable scar bed with a
silicone rod spacer.
Functional Anatomy of Extensor
Tendons
Coordinated functional hand movement requires a balance
not only between long flexor and extensor tendons, but
also between the extrinsic and intrinsic extensor mecha­
nism. In addition, movement at one joint is affected by the
relative position of adjacent joints; for example, with the
wrist extended and stabilized, digital extensors are lax and
relaxed, enabling stronger finger flexion, which is the posi­
tion of grip strength.19 With the relative tenodesis across
the wrist, finger flexion is more difficult when the wrist
is flexed. This relative motion becomes important when a
number of tendons have a common muscle belly, as is the
case for both the extensor digitorum communis and flexor
digitorum profundus. Because of the common muscle ori­
gin, metacarpophalangeal (MCP) joint positioning in one
finger will affect adjacent fingers. This permits early ac­
tive motion by providing protection from a relative-motion
splint.20
direct intraoperative observation the protection afforded by
the relative-motion orthosis.11
There is a prolonged increased collagen turnover in
structures made of dense connective tissue beyond the
time taken for skin wounds to have matured. This colla­
gen response is greatest along the surfaces of the struc­
tures rather than within their deep substance. As much as
a 20-fold collagen increase may occur in the thin areolar
surface of the fascia within 5 days of simple laceration.10,12
This creates a “coat” of collagen that adheres to skin and af­
fects the mobility of the collateral ligament, joint capsule,
muscle fascia, and tendon once that added collagen has
become cross-linked.9 The most common unfavorable re­
sult of long extensor tendon repairs that are immobilized
postoperatively is loss of flexion and not of extension, most
likely related to remodeling of the uninjured joint capsule
collagen and the collateral ligaments.13 This complication
can be minimized by one of the early motion protocols that
have been espoused, three of which have been most studied
and popularized to include relative-motion extensor splint­
ing,14–16 active short-arc motion,9 and early passive motion
with dynamic extension outrigger splinting.17 The knowl­
edge and skills of a hand therapist are essential for a favor­
able outcome.
One Wound, One Scar
Peacock3 pointed out that after injury, a single viscous uni­
form scar develops between all injured collagen structures
to the full depth of the wound—bone, tendon, paratenon,
tendon sheath, and skin. Scars cannot regenerate into the
identical original biologic structures, but will show some
structural similarity to the adjacent tissue. Thus rough
Fig. 62.2 (a) This traumatically amputated hand was replanted. (b) The long-term result had a thumb adduction contracture, which could
possibly have been prevented by (c) a protective thumb web splint. (Reproduced from Merritt WH. Written on behalf of the stiff finger.
J Hand Ther 1998;11(2):74–79.)
a
b
c

SECTION VIII THE HAND AND UPPER EXTREMITY
1186
serts into the extensor mechanism of the index finger, usu­
ally found ulnar to the EDC index insertion. The extensor
muscles of the superficial and deep layers are innervated
by the posterior interosseous nerve (PIN), with the excep­
tion of ECRL, which is innervated before the take-off of the
PIN.22
As the tendons of the extensor muscles traverse the
wrist, they are contained within six extensor compart­
ments, numbered progressively from radial to ulnar (Fig.
62.3). The first extensor compartment, which runs along
the radial styloid, contains APL and EPB. A septum may be
present between the two tendons, and has been reported
to occur in 34% to 77.5% of cadaver specimens.23,24 When
overlooked, this structure can be responsible for a failure of
surgical ­release of de Quervain’s tenosynovitis. The second
extensor compartment contains ECRL and ECRB, which is
separated from the third compartment by Lister’s tubercle,
which has the EPL passing around its ulnar border before en­
tering the third compartment. Just proximal to the extensor
retinaculum, the musculotendinous junctions of the APL and
EPB cross over the radial wrist extensors. Pain and swelling
in this area can be caused by stenosing tenosynovitis, re­
ferred to as “intersection syndrome.”25 The fourth extensor
compartment contains EIP and EDC. The fifth compartment,
which lies dorsal to the distal radioulnar joint (DRUJ), con­
tains EDM, and the sixth compartment contains ECU.
There is much variation in extensor tendon anatomy,
especially between the retinaculum and the MCP joints. The
EDC, EIP, and EDM tendons may have multiple longitudinal
slips. The tendons of the EIP, EDC-index, and EDC-long are
usually single-tendon units. The EDC-ring has two or three
Extrinsic Extensor Tendons
The extrinsic extensor muscles can be divided into super­
ficial and deep layers. The superficial layer consists of, in
order of their innervation from proximal to distal:
•• Extensor carpi radialis longus (ECRL)
•• Extensor carpi radialis brevis (ECRB)
•• Extensor digitorum communis (EDC)
•• Extensor digiti minimi (EDM)
•• Extensor carpi ulnaris (ECU)
The ECRL, ECRB, and EDC originate from the lateral epicon­
dyle of the humerus and insert on the base of the second
metacarpal, base of the third metacarpal, and individual
finger extensor mechanisms, respectively. The EDM and
ECU originate below the elbow joint and insert into the
small finger extensor mechanism and the base of the fifth
metacarpal, respectively.21
The deep layer muscles originate further distally along
the interosseous membrane, consisting of, again in order of
their proximal to distal innervation:
•• Abductor pollicis longus (APL)
•• Extensor pollicis brevis (EPB)
•• Extensor pollicis longus (EPL)
•• Extensor indicis proprius (EIP)
The APL, EPB, and EPL insert on the base of the third meta­
carpal, the base of the thumb proximal phalanx, and the
base of the thumb distal phalanx, respectively. The EIP in­
Dorsal tubercle
Intertendinous
connections
Intertendinous
connections
Dorsal carpal
tendon sheaths
Extensor digiti minimi
Extensor carpi ulnaris
Extensor pollicis
brevis tendon
Abductor pollicis
longus tendon
Extensor carpi radialis
brevis tendon
Extensor carpi radialis
longus tendon
Extensor pollicis
longus tendon
Extensor indicis
tendon
Fig. 62.3 Anatomy of the extensor tendons over the dor­
sum of the hand, in their synovial compartments at the
wrist, and in the forearm. (Reproduced from Gilroy AM,
MacPherson BR. Atlas of Anatomy. 3rd ed. New York:
Thieme Medical; 2017.)

1187
Chapter 62 Extensor Tendon Injuries
There are wide variations in junctural anatomy. In 54% of
patients, the EDC to the small finger is absent and then is
represented by a type III junctura between the EDC-ring
and EDM.14
Extensor Mechanism at the
Metacarpophalangeal and Interphalangeal
Levels
At the MCP joint, the extensor mechanism fans out to form
a broad hood (Fig. 62.4). At the MCP level, the sagittal band
on either side of the central extensor tendon blends volarly
with the volar plate and flexor tendon sheath.29 This creates
a yoke around the base of the proximal phalanx and serves
as the mechanism by which the MCP joint extends, because
there is no direct insertion of the extensor mechanism to
the dorsum of the proximal phalanx.
Sagittal bands centralize and stabilize the EDC over the
MCP joint, so sagittal band rupture causes EDC tendon sub­
luxation into the adjacent web space, which results in MCP
joint extension lag. The long extensor trifurcates proximal to
the proximal interphalangeal (PIP) level into a central por­
tion and two lateral portions, which blend into the lateral
band proximal to the PIP joint (see Fig. 62.4a). Distal to the
PIP joint, the triangular ligament attaches to the two lateral
slips 61% of the time, and the EDC-small is absent in 54%
of cadaver specimens. The EDM usually has two slips and
can even have a slip that inserts on the ring finger exten­
sor mechanism in rare cases.26 There are many variations of
extensor anatomy, so the surgeon must be cautious when
evaluating these injuries and never assume the anatomy will
follow a specific textbook description.
Juncturae Tendinum
The juncturae tendinum are dense connecting bands from
one extensor tendon to another. They form between ad­
jacent tendons and so may mask a complete tendon lac­
eration, because an adjacent tendon may pull on the distal
lacerated tendon end and still effect finger extension. They
may connect the common extensors of the EDC as well as
the EDC-ring to the EDM. The EIP does not have juncturae.27
There are three subtypes of juncturae based on their thick­
ness28:
1. Type I is thin and filamentous.
2. Type II is thicker.
3. Type III has well-defined tendon slips that are thick
enough to be used as tendon grafts for pulley recon­
struction.14
Lateral band
Cut in central band
does not cause
boutonnière deformity
as long as lateral bands
remain dorsal to the axis
of rotation
Lumbrical tendon
Central band
Interosseus tendon
Lateral slip of EDC
a
Lateral band
Flexor digitorium
profundus (slack)
Cut in central band
Flexor digitorum sublimus
Lumbrical muscle (slack)
Interosseus muscle
Common extensor tendon
Interosseus tendon
Lumbrical tendon
Central band
b
Fig. 62.4 (a) Dorsal and lateral views of the extensor apparatus of the finger. The central long extensor trifurcates into the midline central
slip and lateral contributions to the lateral bands. (b) Insertions of the extensor mechanism: Winslow’s diamond encircles the proximal in­
terphalangeal joint, central slip, and lateral bands into a conjoined terminal tendon.
Continued

SECTION VIII THE HAND AND UPPER EXTREMITY
1188
Intrinsic Muscles
As seen previously, the long (extrinsic) and intrinsic exten­
sors are intimately associated as they blend over the exten­
sor hood of the digits. The intrinsic muscles join into this
extensor mechanism at the level of the MCP joint (where
they are the prime flexors through the transverse fibers),
although they are principally IP extenders in the extensor
mechanism. The lumbrical muscles originate from the ra­
dial side of the flexor digitorum profundus (FDP) to each
finger proximal to the A1 pulley. Their tendons cross volar
to the transverse metacarpal ligament. Lumbricals, inter­
ossei, and the long extensors (through their lateral tri­
furcations) all contribute fibers to form the radial lateral
band. Thus lumbrical tendons cross volar to the MCP joint
axis of rotation and functionally flex that joint. Distally, the
lateral bands extend dorsal to the PIP joint axis of rotation
and continue on to the DIP joint, resulting in both PIP and
DIP extension. With the PIP joint fully flexed, the DIP joint
cannot actively extend because of relaxation of the intrin­
sic mechanism due to being tethered by the central slip in­
sertion, unless the lateral bands are freed from the central
slip insertion and pathologically displaced volar (Elson)32
(see Fig. 62.18e, later in the chapter). The median nerve
innervates the lumbricals through the index and long fin­
gers, and the lumbricals to the ring and small finger are
bands (see Fig. 62.4c) and so stabilizes them in place. The
lateral bands separate normally during PIP flexion but are
restricted from too much lateral movement by the triangular
Winslow’s ligament, encircling the PIP joint and opening and
closing with flexion and extension, respectively, known as
“Winslow’s diamond” (see Fig. 62.4c).30 Separation and volar
positioning of the lateral band below the PIP axis of rotation
is necessary for a boutonnière deformity to develop. Not only
is the central slip disrupted, but there is also rupture or at­
tenuation of the triangular ligament and archiform hood fi­
bers. This explains why it sometimes takes time after a closed
boutonnière injury for the full deformity to develop. It also
explains why the Fowler procedure, which creates an isolated
division of the extensor central slip to reduce a swan neck
deformity, does not cause a boutonnière problem, and PIP
extension is preserved through the intact triangular ligament
and transverse and oblique fibers of the extensor hood.31 An
understanding of this extensor anatomy of the PIP joint is
critical to elucidating why relative motion flexor splinting
may be successful for boutonnière deformities.9 When the
MCP joint is placed in a greater relative flexion than adjacent
digits, greater tension is then exerted on the long extensor
and its effect on the interphalangeal joints through the intact
lateral bands (see Fig. 62.4b). Similarly, blocking the MCP
joint in the intrinsic paralyzed hand allows IP extension in
the fourth and fifth digits when the long extensors are acti­
vated (see Fig. 62.4d).
Lateral slips
Triangular ligament
Extensor digitorium
tendon
Extension
Flexion
c
d
Fig. 62.4, cont’d (c) Winslow’s diamond. (d) Even if cen­
tral slip is disrupted, or if there is intrinsic palsy from ulnar
nerve injury, blocking of the MCP joint will allow inter­
phalangeal extension through the extrinsic–intrinsic in­
terconnections of the lateral slips.

1189
Chapter 62 Extensor Tendon Injuries
PIP joint. Lateral bands then join dorsally to form the con­
joined tendon, which inserts on the dorsal base of the distal
phalanx. The dorsal positioning of the lateral bands to the
axis of rotation of the PIP joint is critical to normal finger
extension. If these lateral bands slip volar to the axis of rota­
tion, they then flex the PIP joint while continuing to extend
the DIP joint, resulting in a boutonnière deformity.
Stabilizing “Ligaments” of the Extensor
Mechanism
The triangular Winslow’s ligament serves to prevent volar
subluxation of lateral bands that cause boutonnière defor­
mity, while the transverse retinacular ligament prevents
dorsal subluxation by anchoring the lateral band to the
flexor sheath at the level of the PIP joint, preventing dorsal
migration of those lateral bands and thus preventing a swan
neck deformity30 (Fig. 62.5). Landsmeer’s oblique retinac­
ular ligaments (ORL) are the final extensor mechanism and
have uncertain purpose. They extend proximally from each
side of the distal conjoined tendon, passing volar and proxi­
innervated by the ulnar nerve (with the respective inner­
vations to the FDP tendon to those digits).
There are two rows of interosseous muscle, dorsal and
palmar. Four dorsal interossei abduct the index, long, and
ring fingers. Three palmar interossei adduct the index, ring,
and small fingers. All interosseous muscles originate from
the metacarpal of the finger on which they insert and re­
ceive innervation from the deep motor branch of the ulnar
nerve and function as flexors of the MCP joint. Their tendons
pass dorsal to the transverse metacarpal ligament and, in
concert with the lumbricals, extend the IP joint. Tendons
both insert on the base of the proximal phalanges to abduct
or adduct the finger and send fibers to the lateral bands,
which contribute to extension of the PIP and DIP joint.33
As the long extensor courses dorsal to the proximal pha­
lanx, it trifurcates, sending lateral branches to the radial
and ulnar side of the digit, contributing to the lateral bands,
and thus permitting interphalangeal extension by relative-­
motion flexion splinting for correction of a boutonnière de­
formity. The lateral bands then continue distally. They are
joined together by the triangular ligament just distal to the
Fig. 62.5 Anatomy of the extensor mechanism of the finger.
(a,b) The “restraining ligaments”: the triangular ligament,
transverse retinacular ligament, and oblique retinacular liga­
ment. (c) The delicate interweaving of the contributions of both
intrinsic and extrinsic systems, showing the extensor digitorum
communis lateral slip contribution into the intrinsic system.
Flexor
digatorium
profundus
t
d
Lumbrical
tendon
Flexor digitorium
sublimus
Extensor
tendon
Interosseous
tendon
Central band of the
extensor tendons
Interosseus
muscle
Long extensor
tendon
Lumbrical
muscle
Dorsal
expansion
hood
Central
band
Slips of long
tendon to
lateral bands
Conjoined
tendon
Triangular
ligament
Interosseus
muscle
Transverse
retinacular
ligament
Flexor
digitorum
profundus
Flexor
digitorum
superficialis
Lumbrical
muscle
Lateral band
c
a
b

SECTION VIII THE HAND AND UPPER EXTREMITY
1190
unique numbering system because the thumb has only one
IP joint (Fig. 62.6).
Managing Unfavorable Results
and Complications in Extensor
Tendon Repair
Mallet Deformity (Zones I and II)
A mallet deformity is the most common extensor tendon
injury and perhaps the most consistently undertreated.
Many suggest that even with treatment, there will be some
mild residual extension lag.38 The injury occurs when the
extended DIP joint is forcibly flexed, as with a jamming
baseball injury. There is a rupture of the distal conjoined
tendon or an avulsion fracture of the dorsal base of the
distal phalanx and, in rare instances, both.39 The intrinsic
imbalance leads to a hyperextension force transmitted
through the PIP joint, and the DIP joint droops, so the de­
formity resembles a mallet tool (Fig. 62.7).
The surgeon cannot be too casual in the treatment of
these injuries. Even without severe DIP extension lag, some
patients have inherent volar plate laxity at the PIP joint, so
secondary PIP joint hyperextension and discomfort may de­
velop. An unfavorable result from a mallet deformity is com­
monly not from the annoyance of the loss of DIP extension
but from the resultant swan neck deformity, leading to dif­
ficulty initiating PIP joint flexion and ultimately to that joint
becoming “locked” in extension.
Overwhelmingly, there is support for nonoperative
over surgical treatment for closed mallet deformities. This
is largely related to the complications of each form of treat­
ment. The reported experience in the treatment of 120 mal­
let fingers revealed that surgical repair had a 53% complica­
tion rate, compared with 45% when treated with splinting.40
However, splint-induced complications were nearly always
transient, whereas 76% of surgical complications were still
problematic at 38 months follow-up.
Thus nonsurgical over surgical treatment can certainly
help prevent potential complications. Even complications
that result from splinting can probably be avoided by taking
extra care in the approach to these patients. One potential
mally to the axis of the PIP joint, where they attach into
the lateral aspect of the proximal phalanx and flexor ten­
don sheath. Their functional significance has been debated.
Landsmeer suggested a tenodesis effect that results in syn­
chronized flexion and extension of the PIP and DIP joints.34
For example, with the PIP joint held in full extension, the
DIP joint can typically only passively or actively flex to 45
degrees or maximally to 60 degrees. However, with the PIP
joint in flexion and the ORL relaxed, 90 degrees of flexion at
the DIP joint is easily permitted. Landsmeer also suggested
that the extension of the DIP joint from a fully flexed posi­
tion was initiated as a result of ORL tenodesis in response to
the PIP joint extension, which pulls the ORL taut. However,
several authors have argued that the ORL is not involved in
active finger motion.35,36
Zones of Extensor Tendon Injury
The first congress of the International Federation of Societ­
ies for Surgery of the Hand reached a consensus regarding
anatomical classification of flexor and extensor tendon in­
juries in 1980.37 The extensor system was divided into nine
zones. In the fingers, extensor zones are numbered starting
distally at the DIP joint. Moving proximally, each zone is
numbered according to its relationship to the underlying
joint or phalangeal bone. Proximal to the MCP joint, ex­
tensor zones are delineated by the hand dorsum and the
extensor retinaculum, whereas the forearm is divided into
distal and proximal segments. The thumb extensors have a
VII
VI
V
III
IV
II
I
T-IV
T-III
T-II
T-I
T-V
Fig. 62.6 Extensor tendon zones of injury dorsal to (I) the distal in­
terphalangeal joints, (II) the middle phalanx, (III) proximal interpha­
langeal joint, (IV) the proximal phalanx, (V) the metacarpophalangeal
(MCP) joint, (VI) the hand, (VII) wrist (under the extensor retinacu­
lum), (VIII) the distal forearm, and (IX) the midforearm and proximal
forearm. These differ slightly for the thumb, which includes (T-I) an
interphalangeal joint, (T-II) the proximal phalanx, (T-III) the MCP joint,
(T-IV) the first metacarpal, and (T-V) the area between the carpo­
metacarpal joint and radial styloid.
Fig. 62.7 Chronic mallet deformity of DIP joint of middle finger has
led to a dysfunctional swan neck problem.

1191
Chapter 62 Extensor Tendon Injuries
reason for problems is the misconception that easily avail­
able commercial splints will fit any finger. An ill-fitting Stack
splint may be too tight and cause dorsal skin pressure ne­
crosis. Additionally, many Stack splints and padded alumi­
num splints will not maintain even a neutral DIP position,
because they may fit too loosely (Fig. 62.8).
The best extension that can be expected is that which
can be achieved during splinting. Poor outcome and mis­
management may be related to poor choice of a commercial
splint size, inadequate monitoring or miscommunication,
and patient noncompliance. For example, it is common for
a patient to insist on having been compliant with splinting
and yet “removed the splint only when showering,” or for a
patient to return with a Stack splint that has inadvertently
been replaced upside down (Fig. 62.9). One potential dis­
advantage of the Stack splint is that the plastic covers the
tactile volar distal finger pulp. It takes only 1.5 mm of ten­
don laxity or redundancy to create a 10-degree extension
DIP lag.41 It is essential to individualize patient management
because of the significant differences in DIP normal range of
motion among patients. Observation of the patient’s normal
Fig. 62.8 (a) A properly fitted Stack splint. (b) An improperly fitting Stack splint that is too large and has obvious (though partially disguised
by the splint) persistent flexion at the distal interphalangeal (DIP) joint. (c) An aluminum foam splint may be placed volar, but if the foam
is retained in the splint, the fingertip sinks into the foam, allowing DIP flexion even if the metal is bent into extension. (d) If the foam is cut
away, it allows a small amount of desirable DIP joint hyperextension. (e) A method of taping on a dorsally fitting aluminum foam splint.
(f) Because Stack splints are premade, they do not always fit precisely. (g) A custom-made thermoplastic splint fits better and allows slight
DIP joint hyperextension.
a
b
c
d
e
f
g
a
b
Fig. 62.9 (a) This patient returned to the office with the Stack splint
mistakenly applied upside down. (b) The mallet deformity persisted
because of the ineffective splinting.

SECTION VIII THE HAND AND UPPER EXTREMITY
1192
not alter management, patients may “feel betrayed” to later
discover they had a previously undiagnosed fracture. A true
lateral finger radiograph will demonstrate whether the frac­
ture is associated with a volar subluxated joint (Fig. 42.10).
It is important to assess the degree of innate DIP and PIP hy­
perextension on the opposite, unaffected digit.
Rather than trying to fit a prefabricated Stack splint at
the time of acute injury when there is dorsal DIP swelling, it
is better to custom design a thermoplastic splint with some
DIP hyperextension. However, the surgeon must be cautious
with excessive hyperextension or dorsal finger contact pres­
sure, which could result in dorsal finger soft tissue necro­
sis. When seen in follow-up shortly thereafter, there may
be 10 to 15 degrees of DIP flexion within the splint because
loosening has occurred as swelling resolved. Adjustment
will be required. Initially, it may be wise to include the PIP
joint in the splint. This may need to be continued for pa­
tients who have innate PIP hyperextension laxity. This does
not necessarily mean total immobilization of the PIP joint but
merely blocking hyperextension, which can be done by add­
ing, for example, a figure-of-eight PIP orthosis (Fig. 62.11).
side suggests the amount of hyperextension that should be
used for immobilization.
Clinical Assessment and Acute
Management
The initial presentation in the emergency room may be
of a deceptively minor injury. A laceration of the DIP joint
may initially involve a partial extensor tendon laceration
that later propagates into a complete tendon disruption.
Any suspicious laceration should be explored (using local
anesthesia with epinephrine or with digital tourniquet),
and any finger that is suspected to have an extensor ten­
don injury should be protected with a finger extensor or­
thosis.
Dorsal DIP swelling from a closed injury may initially dis­
guise the extension lag of the mallet disruption. Furthermore,
it takes time for the imbalance to manifest between the ex­
trinsic and intrinsic systems and for the full-blown swan
neck problem to develop. All closed mallet injuries should
be radiographed. Approximately one third will have a distal
phalangeal fracture.42 Even if the results of the radiograph do
a
b
Fig. 62.10 Mallet fracture with joint subluxation in (a) the extended view and more obvious in (b) the flexed lateral view.
Fig. 62.11 (a) Some patients with pronounced proximal interphalangeal (PIP) hyperextension and mallet deformity need both a mallet
splint and a dorsal PIP-blocking splint. (b) A finger in PIP extension. (c) A flexed finger. (d) The PIP joint hyperextension can also be con­
trolled by a figure-of-eight splint.
a
b
c
d

1193
Chapter 62 Extensor Tendon Injuries
ment regimen makes intuitive sense: We immobilize the DIP
joint continuously, usually with some degree of hyperexten­
sion, based on the normal hyperextension of the opposite
side. After 6 weeks, there is gradual daytime splint wean­
ing and the splint is worn during all vigorous activities for
an additional 2 to 3 weeks, with nighttime splinting during
that additional 3 weeks. Mechanical stress across the heal­
ing tendon site strengthens that healing tendon, but in its
recently healed but not fully strengthened state, full activity
could lead to attenuation or rupture. Thus gradual resump­
tion of stress is warranted. If any extensor lag develops, full
­splinting is again instituted and often will correct the lag.
If the patient is unreliable, a longer duration of splinting or
even supplemental K-wire fixation may be instituted.
Finally, regarding management, temporary internal
­K-wire DIP immobilization has been suggested, but at least
one study has compared K-wire immobilization to an ex­
tension external orthosis in acute injuries treated within
2 weeks, with no significant outcome differences.47–49 In
­certain patients, the additional potential morbidity of a
.045 K-wire transarticular fixation, burying the wire beneath
the skin, may be justified and affords the possibility to wear
surgical gloves and to continue activity. An additional exter­
nal orthosis is recommended when ungloved. Tubiana50 rec­
ommended placing the K-wire obliquely across the joint to
minimize discomfort in the volar pulp and so that the wire
can be retrieved if it migrates proximally.
Late and Chronic Mallet Deformity
Patients may present long after the acute 2-week interval
since injury, which is the preferred time within which to
initiate splinting. This is because they initially misdiagnose
This is especially important for patients with delayed treat­
ment and secondary PIP hyperextension. They will not
recover full DIP extension while the PIP remains in abnor­
mal ­hyperextension.
Finally, with regarding clinical assessment, a mallet in­
jury should not be confused with a DIP extension lag that
may occur from tendon imbalance that results from subsid­
ence of a middle phalangeal angulated fracture (Fig. 62.12).
The mallet treatment would revolve around the most appro­
priate treatment for the phalangeal fracture itself or reefing
the lax extensor mechanism.
There is much debate regarding the most appropriate
orthosis for treatment of an acute closed mallet injury. A
controlled, randomized trial found no significant differ­
ences between groups who had a Stack splint, dorsal two-
part foam orthosis with a buckle over the DIP (“Mexican hat”
orthosis), or custom-made circumferential thermoplastic
(“thimble”) orthosis.43 These authors evaluated persistent
extension lag, patient satisfaction, and reported pain after
8 weeks of splinting. There were fewer complications with
the thermoplastic splint. Another study compared 12 weeks
of splinting using a dorsal padded aluminum orthosis, volar
padded aluminum orthosis, or custom thermoplastic ortho­
sis.44 In all groups, there was a resultant final extension lag
ranging from 9 to 16 degrees but no significant difference
between the groups.
Most reports recommend 6 to 10 weeks of extension
splinting with slight hyperextension of the DIP joint, fol­
lowed by 3 to 6 weeks of additional nighttime splinting, even
though a randomized trial of night splinting did not seem
to alter final outcomes.45 If the patient can lift the DIP joint
from a flat table position, and all dorsal DIP swelling and
erythema has resolved, the tendon is healed.46 Our treat­
Fig. 62.12 (a,b) This patient had a swan neck defor­
mity with a mallet droop to the distal interphalangeal
joint. (c) This problem is a result of middle phalangeal
foreshortening and extensor mechanism laxity from
an oblique fracture malunion. (d) Lateral radiographs
showed proximal interphalangeal hyperextension. (This
patient was treated by reefing the conjoined tendon.)
c
d
a
b

SECTION VIII THE HAND AND UPPER EXTREMITY
1194
least 6 to 12 months after injury to allow for a sufficiently
mature scar at the DIP that is strong enough to redistribute
forces that will extend the DIP joint. Furthermore, some pa­
tients spontaneously develop a sufficient degree of improve­
ment without surgery during that interval.55
Patients who present with a chronic mallet deformity
and who still desire definitive treatment or who have had
a splinting failure may potentially benefit from a surgical
tenodermatodesis (Fig. 62.13). This re-creates the original
defect by skin and tendon scar excision followed by immo­
bilization, usually with K-wire transarticular fixation and an
additional external orthosis. This technique was described
by Iselin et al.56 Provided that the DIP joint can be passively
extended, we have seen this procedure succeed as long as
20 years after the original injury. We prefer to place the
K-wire at the tip of the digit and leave it exposed where it
can be protected by a custom thermoplastic orthosis. This
not only facilitates later removal but also discourages prema­
ture ­patient removal of the splint. A simple surgical solution
for the patient with a very pronounced residual extension
lag at the DIP joint may be to perform an arthrodesis at the
DIP joint. However, this results in fusion of an essentially
normal joint.
Surgical Treatment of Mallet Injuries
The obvious indication for surgical repair is an already
open injury. However, there is some controversy regarding
this injury. McFarlane and Hampole57 recommended clos­
ing both skin and tendon in a single figure-of-eight suture
layer, if repair is done at all, and thereafter managing in the
same manner as that used for a closed injury with external
splinting. However, they also felt that if the tendon repair
would prove too flimsy, they would dress the skin wound
only, with the DIP joint immobilized in slight hyperexten­
sion. The results in these patients were no different in open
the injury as a “sprain” or think that the injury may resolve
on its own. Several reports give some comfort in nonethe­
less treating patients who present later with splinting. One
report found no more than 10 degrees of DIP extension lag
in 81% of 14 patients treated by orthosis within 2 weeks of
closed injury, compared with 80% of patients treated more
than 40 weeks after injury.51 There are a number of other
examples of successful late treatment by splinting even
with a 4-month or longer interval after injury.52,53 Success
with late splinting is more likely when there is still evi­
dence of potential tendon healing, evidenced by persistent
pain, swelling, and erythema and other signs of an ongoing
inflammatory response, regardless of the delay since injury.
In contrast, a patient with an asymptomatic late mallet
deformity who has no symptoms of inflammation is less
likely to remodel an already-attenuated but mature scar at
the site of tendon rupture. Patients must understand that
the outcome of treatment if delayed beyond 6 to 8 weeks
after injury is less predictable, especially if signs of ongoing
inflammation have resolved. However, an attempt at closed
splinting management is preferred.
When splinting has failed, the surgeon must resort to
different treatment options. Patients with only minor DIP
extension lag and no problems with PIP hyperextension may
be left untreated. If the patient is bothered only by compen­
satory PIP hyperextension and difficulty with the mechanics
of finger flexion, careful division of the central long exten­
sor attachment to the middle phalanx will redistribute the
balance between extrinsic and intrinsic tendon systems, al­
lowing greater tension along the lateral bands transmitted
to the distal phalanx and releasing the overpull on the cen­
tral extensor tendon (as described by Fowler31). This opera­
tion requires a careful approach beneath the extensor hood,
preserving the triangular ligament attachment between the
lateral bands, or else a boutonnière deformity will develop.54
The Fowler procedure should not be considered before at
Fig. 62.13 (a,b) This 70-year-old with chronic mallet deformity had both skin and extensor tendon redundancy. (c,d) Redundant skin was
excised elliptically, and dermatotenodesis sutures were placed. (e) K-wire fixation was then used for 6 weeks, followed by immobilization.
a
c
Skin redundancy
Tendon attenuation
Excision
b
d
e

1195
Chapter 62 Extensor Tendon Injuries
surface was involved and would not subluxate when less than
40% of the articular surface was involved.63 Others believe that
surgical correction and fixation should be performed any time
the fracture fragment is greater than one third of the joint
surface to avoid subluxation and later posttraumatic osteo­
arthritis.64 Sometimes, dynamic fluoroscopic imaging of the
DIP joint through extension and flexion may be necessary to
identify subluxation. When no subluxation is identified, we
prefer to manage the injury nonoperatively with a custom
thermoplastic splint regardless of fracture size.
A variety of surgical treatment options are available,
with no proven significant difference in outcomes among
any of them65 (Fig. 62.14):
•• Extension block pinning65–68
•• Open reduction internal fixation with pins68,69
•• Wires70–72
•• Screws73
•• Pullout wires or sutures39,74,75
•• Biodegradable arrows76
•• “Umbrella handle” technique77
•• Hook plates78,79
Of all these, extension block pinning is one of the more pop­
ular fracture reduction and treatment methods. The distal
phalanx is flexed and a K-wire is placed percutaneously
through the extensor tendon attached to the bone fracture
fragment, thus stabilizing and securing it to the middle
phalanx, followed by manual extension reduction of the
distal phalanx and longitudinal K-wire fixation across the
reduced DIP joint.80 The principles of this technique have
also been used by simply using an 18-gauge blunt needle
through a small incision, stabilizing the proximal fragment,
guiding this reduction under fluoroscopic observation, and
then finally using simple extension splinting in hyperex­
tension without K-wires for 6 to 8 weeks.81 This technique
of essentially nonoperative intervention may be used to
reduce the “bump” commonly seen after healing of non­
subluxated but widely separated fractures or dislocations.
It might even be used as a first attempt at treatment for
subluxated mallet fracture injuries.
Treatment of a Chronic Subluxated
Mallet Fracture
An especially difficult problem is treatment of a painful
late mallet deformity related to chronic nonunited fracture
subluxation. These patients present with pain and stiffness.
Some suggest proceeding directly to DIP joint fusion.
There are reports of successful surgical treatment of
these chronically presenting injuries. In a series of 19 pa­
tients with more than one-third joint surface involvement
who presented on average 57 days after injury, transtendi­
nous wiring was performed with the wire buried against
the volar surface (as described by Sonoda et al82), and the
fibrous tissue in the fragment gap was débrided to achieve
or closed injuries. Doyle58 also agrees with this approach.
The surgeon might not use braided sutures if the tendon
is repaired and should use a single-suture technique to
reduce infection complications.59 One other report recom­
mended 5–0 nylon for tendon repair or 4–0 continuous
monofilament or wire pullout (if there is inadequate distal
tendon stump for repair) with separate skin closure, along
with a transarticular K-wire fixing the DIP joint in slight
hyperextension, placed before the tendon repair.60
Our approach has been similar, relying on an initial
placement of a transarticular longitudinal wire with the
DIP joint in slight hyperextension, followed by repair of
skin and tendon with a single-suture closure if the tendon
is avulsed or badly crushed, or separate repairs if the ten­
don is a clean laceration. Management thereafter is similar
to that of the closed technique, with a custom thermoplas­
tic orthosis and removal of the K-wire at 6 weeks and a
gradual program of intermittent splinting and progressive
active flexion.
Treatment of Mallet Fracture
Avulsion fracture of the distal phalanx is reported to cause
mallet deformity in as many as 35% of cases and accounted
for two thirds of cases with late osteoarthritis 5 years af­
ter injury. In as many as 5% of closed mallet injuries, there
is an avulsion fracture of the distal phalanx. Two thirds of
those who had osteoarthritis 5 years later originally had an
associated fracture with a mallet injury.61 However, a de­
cision for surgical versus nonsurgical treatment remains
controversial. In general, fractures without DIP subluxation
are managed nonsurgically. However, it is debated whether
even the subluxated fractures and dislocations are better
managed nonoperatively,62 which may be preferable be­
cause of the increased complication rates in those managed
surgically.40
A study in a cadaver model, involving 29 fingers, showed
the DIP joint would subluxate if more than 52% of the joint
Fig. 62.14 Dermatotenodesis procedure for a chronic mallet defor­
mity with no fracture present.
b
a

SECTION VIII THE HAND AND UPPER EXTREMITY
1196
existing reduced range of motion may, for example, have
a poorer outcome by measurement but may actually be
pleased with their treatment results. A useful classification
of outcomes may be gleaned from the recommendation of
Patel et al,52 who compared the treated digit with the indi­
vidual’s contralateral finger (Table 62.1).
The Relative-Motion Concept
The relative-motion concept is addressed here because it
is pivotal to management of not only extensor tendon in­
juries of the dorsum of the hand, but also to sagittal band
injuries (zone V) and boutonnière problems (zone III). The
only differences are whether one uses the relative-motion
extension orthosis or relative-motion flexion orthosis. This
concept takes advantage of the “quadriga effect.”
Quadriga is a Roman description of a two-wheeled char­
iot drawn by four horses harnessed abreast and guided by
a charioteer with equidistant reins. The Greeks called it a
tethripon. Verdan coined the term quadriga effect in 1960
to explain the FDP imbalance that can occur after tendon
injury.85 Both the EDC and FDP function as single mus­
cle (“charioteer”) with multiple tendons of fixed lengths
(“reins”).86 The quadriga effect or syndrome describes a
complication that results in adjacent digits being unable to
flex to the palm, either because the repaired tendon is too
short and is able to flex because of weakness and lag in the
adjacent uninjured profundus tendons, or conversely inter­
phalangeal fusion in too much extension, causing inability
of adjacent digits to flex to the palm because of relative loss
of flexion to the fused digit.
bone contact, together with longitudinal K-wiring and ex­
ternal aluminum orthosis.83 Of these patients, 41% were
subluxated at the time of treatment. The average follow-up
extension lag was 7 degrees, and flexion ranged from 35 to
95 degrees, but in 21% either bone union failed or the joint
became ankylosed.
We prefer a nonsurgical attempt that was described
in a small series of 10 patients who presented 6 weeks to
6 months after sustaining a mallet fracture. Serial casting
was used with progressive manual reduction under fluoro­
scopic imaging, changing the cast once or twice per week,
until the mallet deformity was reduced and then immo­
bilized an additional 8 weeks84 (Fig. 62.15). Eight of ten
achieved bone union, and all remained stable. In our experi­
ence, this has proven to be a useful and safe technique that is
preferable to the morbidity of open reduction and fixation in
these late cases. It may, however, leave a dorsal bump where
the fracture unites. If this low-morbidity technique fails, the
surgeon may still resort to an open treatment.
Summary
It is surprising that such a common injury as a mallet finger
has so much controversy regarding indications for surgery,
types of orthoses, the variety of operations, and the length
of time for immobilization. An important reason why the
variety of treatment options have not shown any signifi­
cant differences may be because there are no standard­
ized treatment outcome measures and there is also a high
variability in the normal range of DIP flexion and natural
hyperextension among individuals. Older patients with
Fig. 62.15 (a) Initial radiograph. Even a chronic painful mallet finger with joint subluxation (3 months after injury) may be reduced (b) by
serial casting. (c–e) Bony union occurs with time, resulting in a stable distal interphalangeal joint. (c) After the third week of serial casting
and reduction. (d) After 6 weeks of serial casting and reduction. (e) Final reduction and union at 8 weeks of serial casting and reduction.
c
d
e
a
b

1197
Chapter 62 Extensor Tendon Injuries
when profundus and lumbrical relaxation is desired with
simultaneous increased long extensor force on the IP joints.
Boutonnière Deformity (Zone III)
Treatment results of established boutonnière deformity re­
main unfavorable, and this is the area of extensor tendon
injury recognized to need new and better treatment ap­
proaches to best preserve the delicate balance between the
extrinsic and intrinsic motor systems.9 Two important re­
cent developments that may enhance treatment outcomes
are use of the relative-motion orthosis to maintain mobil­
ity and wide-awake local anesthesia so that active function
can be assessed intraoperatively.9,11
Another problem with assessment and treatment of
acute boutonnière injury is that the deformity takes time
to evolve and so may be underestimated by both an unwary
emergency physician and patient. A patient with what ap­
pears to be a simple finger laceration or PIP joint sprain may
still be initially capable of normal range of motion with a
boutonnière rupture. When the patient returns later, there
may be a fixed PIP flexion contracture with DIP hyperexten­
sion, and the patient may never regain normal motion. It is
called the boutonnière deformity because the PIP “button­
holes” through the extensor hood; the central slip has lost
its insertion into the middle phalanx, and the lateral bands
relocate volar to the axis of rotation on each side of the PIP
joint (Fig. 62.17).
The diagnostic deception occurs when the lateral bands
may initially remain dorsal to the axis of PIP joint rotation
after central slip closed rupture or laceration. Later, the ex­
tensor hood fibers and triangular Winslow’s ligament at­
tenuation allows the lateral bands to migrate volarly. The
efforts of the lumbrical and interosseous muscles to extend
the PIP joint then actually cause PIP flexion and DIP hyper­
extension, the boutonnière deformity.
Next, the volar plate and palmar portion of the accessory
collateral ligaments and the dorsal DIP joint capsule remodel
and shorten, leading to a fixed boutonnière deformity. The
results of surgical treatment at this time are uncertain, and
this has led to a number of different proposed options. Thus
one can say that the best treatment of a boutonnière injury
is to prevent the deformity from forming and maturing in
This quadriga relationship can become an advantage,
allowing active motion during tendon healing by splinting
the MCP joints of the injured digit relative to adjacent digits.
When the MCP joint of the injured digit is placed in 15- to
20-degrees relatively greater extension than adjacent digits,
that long extensor tendon will have significantly less force
generated on it than adjacent extensor tendons, regardless of
interphalangeal or metacarpophalangeal active joint position,
provided the relative motion remains at 15- to 20-degrees
greater extension.20 Thus a relative-motion extension ortho­
sis (Fig. 62.16) is useful for extensor injuries at or proximal
to the MCP joints—long extensor tendon repair, sagittal band
rupture, caput ulnae syndrome—so that active motion can
be maintained while protecting the injured extensor com­
ponent.
In contrast, when the MCP joint is splinted in 15- to
20-degrees greater flexion, the quadriga effect is simulta­
neously present on both the volar (intrinsic and FDP re­
laxation) and dorsal (increased extensor force allowing IP
extension) surfaces. This is because the FDP of the splinted
digit is relaxed relative to adjacent FDP tendons. This also
relaxes the lumbrical muscle, which arises from that FDP
tendon, relaxing the downward pull on that digit’s lateral
band, while simultaneously increasing tension of that dig­
its’ long extensor tendon and its attachment to the lateral
bands through lateral slips of the common extensor tendon,
increasing pull on the IP joints. We call this the relative-mo­
tion flexion orthosis, and it is useful for boutonnière defor­
mity, protection of flexor tendon repair, and camptodactyly
Table 62.1 Comparison of the treated digit to contralateral normal fingera
Extension
Flexion
Pain
Cosmetic
Excellent
Equal
Equal
None
Satisfied
Good
<10° active extension lag
Equal
None
Satisfied
Fair
10–20° active extension lag
Equal
None
Dissatisfied
Poor
>20° lag/unimproved
Any restriction of flexion
May be present
Dissatisfied
aIn the classification by Patel et al.52
Fig. 62.16 Relative-motion extension splint for middle finger long
extensor repair at the MCP joint.

SECTION VIII THE HAND AND UPPER EXTREMITY
1198
A “pseudo-boutonnière deformity” may be mistaken for
this deformity and results from flexion contracture (see Fig.
62.19) of the PIP joint because of flexor tendon injury or vo­
lar plate or pulley disruption. In such a case, however, the DIP
joint can be passively flexed 45° to 60° (equal to the uninjured
side) while the PIP joint is maximally passively extended.
Anatomical Rationale for Boutonnière
Relative-Motion Flexion Splinting
The central long extensor trifurcates as it approaches the
PIP joint, with two lateral slips blending with the lateral
bands and a third central slip inserting into the proximal
middle phalanx. These lateral attachments between the
extrinsic tendon and intrinsic lateral bands remain intact
in the boutonnière injury, although the central slip is rup­
tured.
When one creates a large boutonnière defect in the ca­
daver laboratory by dividing the central slip, triangular liga­
ment, and arciform extensor hood fibers, thereby freeing
the lateral bands, longitudinal traction on the common EDC
muscle then causes the PIP joint to “buttonhole” into the
typical boutonnière posture. If one then places a relative-
motion flexion splint on the “affected” finger, with that digit
positioned in 15- to 20-degrees greater MCP joint flexion
than the others, longitudinal traction in the long extensor
muscle actually causes the lateral bands to centralize over
the dorsum of the PIP joint and bring about PIP extension
(Video 62.1).
We hypothesize this results from a simultaneous quad­
riga effect on both the flexor (FDP) and extensor (EDC) mo­
tor systems by laxity of tension on that digit’s lumbrical and
increased tension on the long extensor lateral band mecha­
nism—one relatively more lax and the other relatively more
taut than adjacent digits (Fig. 62.20). Although controversial,
Brand89 and Kaplan33 both regarded the lumbricals as the
principal interphalangeal extensors, because they have four
times greater excursion than the more powerful interossei
and a more volar angle of approach.90 Because lumbricals
the first place. This requires a high index of suspicion at the
time of initial injury and starting early relative-motion flex­
ion splinting for a closed injury in a compliant patient and
immobilization of the extended PIP joint in a young or non­
compliant patient.
For an acute open injury, surgery is necessary to repair
the extensor hood. Local anesthetic with epinephrine is ad­
ministered in the wide-awake patient so that the surgeon
can assess digital flexion and extension to ensure that the
proper delicate balance has been restored between extrinsic
and intrinsic systems, and this is then followed by relative-
motion flexion splinting.
Clinical Evaluation of the Boutonnière
Injury
If there is uncertainty that an acute boutonnière injury ex­
ists, the Elson test may be helpful87 (Fig. 62.18). The fin­
ger is held over the edge of a tabletop with the PIP joint
flexed. Extension of the PIP joint will intially be weak, be­
cause the central extensor tendon has lost its insertion into
the middle phalanx. At the same time, the DIP joint in this
finger position will have more extension resistance than
expected, because the lateral bands have lost their central
dorsal restraint. The surgeon can use a modification of this
Elson test32 (see Fig. 42.18d) in which the corresponding
opposite finger middle phalanx is placed abutting to the in­
jured finger middle phalanx and the PIP joint is fully flexed.
If the injured digit can extend the DIP joint, the diagnosis
is confirmed. This has the advantage then of also using the
opposite finger for comparison.
In chronic boutonnière deformity with a PIP flexion con­
tracture but mobile DIP joint, the Boyes’ test may be help­
ful88 (Fig. 62.19). The PIP joint is placed as forcibly as pos­
sible in passive extension, and the surgeon then assesses
resistance to passive flexion of the DIP joint. A boutonnière
deformity will respond with resistance, but when the PIP
joint is then flexed the DIP joint is easily passively flexed.
This is because the volarly subluxated lateral bands are lax
when the PIP joint is flexed and taut when it is extended.
Oblique retinacular ligament
Central tendon
Lateral bands above
axis of rotation
Lateral bands pass
below axis of rotation
Triangular Winslow’s
ligament attenuates
Fig. 62.17 Pathogenesis of boutonnière deformity with subluxation of lateral bands volar to the proximal interphalangeal joint axis of ro­
tation.

1199
Chapter 62 Extensor Tendon Injuries
Fig. 62.18 (a) Late boutonnière. This index finger boutonnière deformity was noted 6 weeks after a healed laceration over the dorsum of
the proximal interphalangeal (PIP) joint from a box cutter. (b) The Elson test shows weak PIP extension. (c) There is strong distal interpha­
langeal (DIP) extension (normally when the PIP is flexed, the DIP should not be able to extend). (d) The modified Elson test shows that the
DIP joint on the left is able to extend but the opposite finger (normal) cannot; this is the best clinical evaluation for an acute boutonnière
injury. (e) Modified Elson test. The loss of tethering when the central slip disrupts allows tightening of the lateral bands. (Image e is pro­
vided courtesy of Liz Begley.)
d
e
a
b
c
Fig. 62.19 (a) A positive Boyes’ test shows that when the middle phalanx is extended, passive distal interphalangeal (DIP) flexion meets with
resistance, but (b) when the proximal interphalangeal (PIP) joint is flexed, DIP flexion is easy. (c) In a patient with a PIP flexion contracture
and pseudo-boutonnière deformity, in this case (d) related to pulley rupture and flexor tendon bowstringing, keeping the PIP joint extended
as much as possible (e) still allows easy passive DIP joint flexion.
Cannot flex DIP joint with PIP
extended (boutonnière deformity)
a
DIP flexes easily when PIP is flexed.
b
c
Negative
Boyes’ test
e
Flexor tendons
torn from the
PIP volar plate
d

SECTION VIII THE HAND AND UPPER EXTREMITY
1200
originate from the FDP tendon, they are placed in relatively
less tension when in 15- to 20-degrees greater flexion in the
MCP flexion splint. This reduces the unfavorable volar pull
that would relocate the lateral bands volar to the axis of the
PIP joint rotation. On the extensor side, increased tension is
placed on the lateral bands through the lateral slips of the
long EDC extensor to that finger. The importance of the lat­
eral band pull through the lumbricals is evident in patients
with complete ulnar palsy who can extend their index and
middle interphalangeal joints through the median inner­
vated lumbricals. Furthermore, if the surgeon blocks the
MCP joints of the paralyzed ring and fifth digits in relatively
greater flexion, a patient with ulnar palsy can fully extend
both IP joints through the long extrinsic extensor contribu­
tions to the lateral bands (see Fig. 62.4c) when the index and
long digits are extended. This is ­because the long extensor
lateral slips connect to the intrinsic lateral bands, encircling
the PIP joint to rejoin distally into the conjoined ­tendon at­
tachment to the distal phalanx, and normally moves cen­
trally with PIP extension as described by Winslow, who
termed this a “tendinous rhombus,” later described as Win­
slow’s triangle30 (Fig. 62.21). Thus even with a large exten­
sor hood defect, disruption of the triangular ligament, and
absence of a central slip attachment, with relative-motion
flexion splinting these encircling components still provide
a centralizing force that occurs in the absence of a lumbrical
volar force as the proximal extrinsic extensor tendon pulls
with greater force than its unsplinted neighbors, tightening
the PIP encircling lateral bands over the PIP joint, a central­
izing force Lalonde91 calls “cinching.” (Video 62.2).
Fig. 62.21 Winslow’s diamond. In his 1732 description, Jacob Win­
slow pointed out that normal extension resulted in a medial pull of
the lateral bands via the extensor digitorum communis lateral slips,
whereas flexion of the PIP resulted in lateral displacement of the
lateral bands, restricted by the triangular Winslow’s ligament, a dy­
namic known as Winslow’s diamond.
Lateral slips
Triangular ligament
Extensor digitorium
tendon
Extension
Flexion
Lateral band
Flexor digitorium
profundus (slack)
Cut in central band
Flexor digitorum sublimus
Lumbrical muscle (slack)
Interosseus muscle
Common extensor tendon
Interosseus tendon
Lumbrical tendon
Central band
Fig. 62.20 When the finger is splinted at the metacarpophalangeal joint relative to the other fingers, both the flexor digitorum profundus
and lumbrical to that finger are relaxed as a result of the quadriga effect. Alterations also occur with increased relative tensions of the ex­
tensor mechanism. With that finger held flexed, the proximal extensor tendon pulls with greater force than its neighbors, tightening the
surrounding lateral bands, pulling down dorsally and centrally in the proximal interphalangeal (PIP) extended digit (“cinching”). (Modified
from an image by Juli Howell.)

1201
Chapter 62 Extensor Tendon Injuries
awake local anesthesia technique so that the surgeon can as­
sess active motion.11 It also provides an opportunity to test
relative-motion “protection” of the repair by placing a rib­
bon retractor on top of the repaired digit proximal phalanx
and beneath its neighbors and having the patient extend and
flex the digits under direct vision with the wound still open.
The postoperative relative-motion flexion protocol then
initially immobilizes the patient with the repaired digit in
15 to 20 degrees of greater MCP joint flexion for 3 to 5 days,
followed by active mobilization in a relative-motion flexion
orthosis, encouraging full active PIP flexion and extension
(Fig. 62.22). The patient is encouraged to resume preopera­
tive activities, but always in the splint. If there is concern
about the splint accidentally slipping off at night, a gutter-­
immobilizing resting night splint can be fabricated, again
with the injured digit in greater MCP joint flexion than ad­
jacent fingers. Intensive therapy is usually unnecessary,
and at 6 weeks additional therapy is typically not needed.
Follow-up visits ensure that functional range of motion is
maintained. Closed boutonnière rupture is managed in a
similar manner. If the patient develops increasing DIP joint
hyperextension compared with the opposite normal side,
an additional DIP dorsal blocking orthosis such as a small
figure-of-eight splint at the DIP joint may be required, with
attention paid to maintain full PIP extension in the relative-
motion flexion MCP orthosis. Our most common reason for
patient return to therapy was for repair of broken splints
for functional activity, leading our therapists to provide a
second prophylactic splint on the initial visit.
Treatment and Rehabilitation of an Acute
Boutonnière Injury
There are a variety of recommended protocols for treating
an acute boutonnière injury. After acute central slip re­
pair for a laceration or closed rupture of the central slip,
conventional treatment has used a gutter splint with both
PIP and DIP joints in extension for a few days until acute
swelling subsides, followed by a cylindrical nonremov­
able PIP extension splint, leaving the DIP free for active
and passive flexion to encourage dorsal repositioning of
the lateral bands. Some even recommend K-wire fixation
across the PIP joint to ensure its extended position is main­
tained. This PIP immobilization continues variably for 4 to
8 weeks, with those who favor the shorter 4-week period of
immobilization progressing to a PIP dynamic extension–
assisted splint. For this purpose, there are custom-made
coil orthoses as described by Wynn Parry92 and later modi­
fied by Maddy93 using Aquaplast (Qfix). Gradual weaning
from the splint is accomplished over 6 weeks, giving a min­
imum duration of 10 to 12 weeks of total splinting.
A more recent early active short arc-motion protocol has
been used by Evans.10 This allows early active limited motion
under supervision. There is a graded program of increased
motion. This protocol requires fairly intensive supervision
and a compliant patient.
There is thus a need for a simpler protocol that none­
theless reduces stiffness from prolonged immobilization. If
an open repair is necessary, this is best done with the wide-
Fig. 62.22 (a) A boutonnière deformity seen 1 week after injury. (b,c) Relative-motion flexion splinting of a border little finger digit also
keeps the index finger flexed for stability of the orthosis. Full active motion is encouraged, and most daily activities can be continued.
(d,e) Result at 6 weeks.
d
e
a
b
c

SECTION VIII THE HAND AND UPPER EXTREMITY
1202
sidered “excellent” and −30-degree extension to 80-degree
flexion was considered “good”94 (Table 62.2).
Discouraged by the poor results with surgery, we have
tried vigorously to avoid surgery in these chronic bouton­
nière patients. Serial casting is attempted until full PIP exten­
sion is achieved, if possible. Once PIP extension is maximized,
we then use relative-motion flexion splinting for 3 months
(Fig. 62.23). This is tolerated by patients because it is com­
patible with most functional hand use during that time. Even
in patients who have not been able to regain full PIP exten­
sion by preliminary serial casting, the improvement once all
splinting is discontinued has been maintained up to 3 years
later. We have had success with this regimen even in patients
presenting up to a year later with the PIP ­flexion contracture
of as much as −55 degrees, and in patients as old as 99 years.
All our patients treated in this manner achieved an excel­
lent outcome as categorized by Steichen and Strickland.94 Pa­
tients who have developed marked DIP hyperextension will
not achieve full PIP extension with a relative-motion flexion
orthosis unless DIP hyperextension is blocked (Fig. 62.24). If
we were unable to serially cast a patient to better than −30
contracture, we would favor a “wide-awake” reconstructive
procedure followed by 6 weeks of relative-motion splinting.
This has not yet ­happened (Video 62.3).
Sagittal Band Rupture (Zone V)
The long extensor tendon is central and stabilized dorsally
over the MCP joint by the sagittal bands on each side, which
attach volarly to the palmar volar plate. The MCP joint thus
extends through this lasso noose effect by lifting up on the
proximal phalanx, because there is no secure-enough ex­
tensor attachment directly to bone on the proximal pha­
lanx. If the “ring” is broken by sagittal band disruption, then
active extension fails from the flexed MCP finger position,
because the subluxated tendon is between the metacarpal
heads. However, the finger can often be held extended if
initially passively placed in this position, repositioning the
tendon centrally.
Treatment of the Chronic Boutonnière
Deformity
Chronic boutonnière deformity is plagued by generally
unfavorable results from a wide variety of described pro­
cedures. Although all protocols described for the acute
boutonnière injury will usually provide good results, late
correction of a chronic deformity with fixed PIP flexion
contracture is notoriously unpredictable in outcome. One
report showed disappointing results for patients treated
more than 8 weeks after the original injury.94 The four
worst prognostic outcome predictors were:
1. Inability to passively correct PIP contracture (70% poor
outcome)
2. Closed rupture treated several months later
3. Prior failed surgery
4. Older patients (older than 21 years, 45% poor result;
older than 45 years, 60% poor result)
The degree of PIP extension lag preoperatively was also
important, even when the flexion contracture was re­
solved through therapy and full passive extension could
be achieved. The best treatment results (65% good to ex­
cellent) were in patients who had active PIP extension to
at least −30 degrees, whereas those who could not actively
extend beyond −60 degrees had the worst results (86%
poor), even though full passive PIP extension was restored
through therapy. These authors thus recommend no sur­
gery for patients who had active PIP extension to −30
degrees or better and had full flexion, because one third
were actually worse after surgery. They also recommend
against operating on anyone who could not obtain absolute
full passive PIP extension after therapy because of a 92%
poor outcome, and were pessimistic about older patients
(those older than 33 years had 82% fair or poor results).
They developed a grading scale for outcome after surgery
for chronic boutonnière deformity in which PIP flexion of
90 degrees and extension to within −20 degrees was con­
Table 62.2 Results of surgical treatment of chronic boutonnière deformity:
analysis of prognostic factors
Preoperative extension
Good to excellent
Fair to poor
Passive
Active
−30 to −80°
−20 to −90°
−40 to −70°
< −40° extension, < −70° active flexion
Full
0-30°
65%
35% (17 patients)
Full
>30°
59%
41% (22 patients)
Not full extension
8%
92% (13 patients)
Note: Patients were not considered for operative treatment when they could actively extend to within 30 degrees of neutral, because the results of
­surgery were worse in one third. With even small increments of fixed flexion deformity, surgery was not considered, because the surgery proved
almost uniformly disastrous. Patients with injury of longer than 3-month duration had poor results. Of patients older than 45 years, 60% had poor
results. Of patients older than 33 years, 82% had fair or poor results.
Source: Data from Steichen JB, Strickland JW, Powell SG, et al. Results of surgical treatment of chronic boutonniere deformity: an analysis of prognos­
tic factors. In: Strickland JW, Steichen JB, eds. Difficult Problems in Hand Surgery. St Louis: CV Mosby; 1982:62–69.

1203
Chapter 62 Extensor Tendon Injuries
Fig. 62.23 (a) Chronic boutonnière deformity with fixed proximal interphalangeal (PIP) flexion contracture. (b) The deformity was initially
treated with 2 weeks of serial casting, which resulted in residual PIP contracture of −20 degrees, followed by 3 months of relative-motion
flexion splinting. He was able to continue work activities during this time. (c,d) Range of motion at the end of this treatment. (e,f) Range
of motion is still maintained 3 years later.
c
d
a
b
e
f
Fig. 62.24 (a) Late boutonnière deformity. (b) With relative-motion flexion splinting, the proximal interphalangeal (PIP) was almost cor­
rected, but distal interphalangeal (DIP) hyperextension persisted. (c,d) Splinting of the DIP joint as well with extension blocking restores
the extensor balance and allows full PIP extension.
c
d
a
b

SECTION VIII THE HAND AND UPPER EXTREMITY
1204
ticipated to regain full motion after this immobilization
treatment.
Chronic Sagittal Band Rupture
The patient may ignore the initial pain of a sagittal band
rupture and simply avoid full MCP joint flexion. At the time
of presentation, there may still be annoying extensor tendon
subluxation with MCP joint flexion, or the patient may have
passively manipulated the finger back into extension but
have chronic pain at the rupture site and reluctance to flex.
At this point, with established sagittal band rupture and no
further signs of inflammation, only surgical reconstruction
will correct the deformity. These procedures are designed to
recentralize the extensor tendon by restoring stabilization
to the ruptured sagittal band with a juncturae tendinum or
a strip of extensor tendon anchored to the extensor hood,
collateral ligament, intrinsic tendon, or bone.100–104 All these
procedures require a postoperative management protocol of
6 to 10 weeks of immobilization followed by extensive hand
therapy. Outcomes from these studies reveal that recurrent
extensor tendon subluxation is rare, but there may be loss
of full MCP joint flexion. Probably relative-motion exten­
sor splinting, if used with any of these treatments, would
reduce that morbidity of lost flexion. I (W.H.M.) found that
creating a tendon graft pulley into the metacarpal head pro­
vides stable centralization, permitting early active motion
with relative-motion extension splinting. However, the rela­
tive-motion extension postoperative management protocol,
regardless of the type of surgery used (free tendon graft, slip
of extensor tendon, or juncturae tendinum), permits imme­
diate active motion and hand use for most activities with
excellent range of motion at 6 weeks when the splint is dis­
continued. When reconstruction for sagittal band rupture
is performed using local anesthesia with epinephrine, the
value of using relative-motion extension splinting becomes
even more evident, because when protected with a splint
finger flexion does not cause repair disruption, whereas
when it is unprotected, disruption of the repair occurs (Fig.
62.25, Videos 62.4–62.6).
Human Bite (Zone V)
Lacerations of the MCP joint caused by fist contact with a
tooth are common and often present late because the cir­
cumstances surrounding the injury tend to delay seeking
medical attention. At this stage, the joint may be septic,
necessitating admission to the hospital, intravenous antibi­
otics, and surgical drainage. These infections may develop
quite rapidly.
When seen early with a suspicious injury, surgical ex­
ploration is necessary. The injury is misleading because the
fisted tendon puncture becomes proximal to the skin lacera­
tion once the fingers are extended. The wound is thoroughly
irrigated, antibiotic therapy is initiated, and the skin wound
is left open or repaired in a delayed fashion.
Open injuries that cause complete sagittal band disrup­
tion are rare. Closed injury is relatively common with forced
resistive activity, such as a tight grip with wrist flexion and
ulnar deviation while hitting a tennis ball or flicking a fin­
ger forcibly and hitting an object. This most often occurs
on the radial side of the middle or ring finger with subse­
quent painful subluxation of the tendon between the adja­
cent metacarpal heads on the uninjured ulnar side. This is
often painful when it occurs suddenly. However, rupture or
attenuation may also occur with inflammatory conditions
such as bulging from rheumatoid synovitis or chronic infec­
tion. Open injuries can be repaired, but if incomplete they
can be managed with splints. The sagittal band has been
described as having two layers: a thin superficial layer and
a thicker, deeper layer that envelops the extensor tendon.95
Degenerative ruptures are said to affect the superficial layer,
and traumatic ruptures affect both layers.
Acute Sagittal Band Ruptures
Patients with acute sagittal band ruptures are commonly
misdiagnosed, because often the extensor tendon is no
longer subluxated on presentation, the MCP joint is swol­
len, and they are reluctant to fully flex the MCP joint. The
MCP joint is, however, tender to palpation on the side of
the rupture. Pain is dramatically relieved within a few
days if tension is reduced on the affected digit by means
of relative-motion extensor splinting. The relative-motion
splint has been shown to reduce tension on the exten­
sor tendon, and pain reduction is much better than that
achieved with simple buddy taping, which many recom­
mend as a treatment option.20 However, with buddy taping
pain may persist for up to a year.96 Generally, the longest
duration to initiate nonoperative treatment successfully is
2 to 3 weeks after injury.97 However, if there are still signs
of inflammation (and hence of healing) with swelling, ery­
thema, and tenderness, nonoperative splinting is an option
that we have found successful even 6 weeks after injury in
these patients. Using relative-motion extension splinting,
a success rate of 57% has been reported in patients more
than 6 weeks after injury, but a 95% success rate is reported
for those treated within 3 weeks.98 Later than 4 weeks af­
ter injury, patients often have both decreased flexion and
extension of the MCP joint. In this case a relative-motion
extension splint can increase the normal range of motion;
splinting should be maintained for 6 weeks.14,99 We have
also used this technique to successfully treat patients with
rheumatoid arthritis who have a sagittal band rupture but
do not have associated digital ulnar deviation.
In noncompliant patients, closed sagittal band rupture
may require prolonged immobilization. Immobilizing the
digit in slightly greater extension than its neighbors re­
duces tension on the ruptured sagittal band, but the MCP
joint must be flexed 30 to 40 degrees to reduce the risk of
MCP joint extension contracture from collateral ligament
remodeling. A prolonged therapy program should be an­

1205
Chapter 62 Extensor Tendon Injuries
that then enabled motion, permitting tendon gliding of the
repaired tendon and allowing functional recovery and use of
the hand for most activities, even while the tendon is healing.
Initially, our cadaver studies revealed that combined full
composite flexion of both the wrist and fingers appeared to
place some tension on the repaired extensor tendon, and
we felt it wise to advise using a wrist splint in the first 3 to
4 weeks of rehabilitation along with the relative-motion fin­
ger splint. Others reported no clinical ruptures of repaired
tendons using only the relative-motion finger extension
splint.16,106 Others simply leave the wrist unprotected but
tell their patients not to make a clenched fist when the wrist
is flexed.107 Another suggestion is to use a wrist splint only
when intraoperative observation under wide-awake local
anesthesia with a ribbon retractor (placing that digit in rela­
tive extension) shows no tension on the repair with compos­
ite wrist and finger flexion.11
The long extensors change in cross-sectional morphol­
ogy from flat and thin at the MCP level to round and tubular
over the metacarpals and wrist. Thus core suture repair is
advised more proximally (such as Kessler, Becker, and aug­
mented Becker, Massachusetts General Hospital) for these
tendons. This is supplemented with a running epitenon su­
ture. However, early active protected motion seems far more
important than the suture technique itself, when even a sin­
gle simple 6–0 nylon repair holds up with relative motion
extension splinting on direct intraoperative observation.
For simple lacerations over the dorsum of the hand,
when the tendon ends have not retracted, repair can be done
with local anesthesia in the emergency room, observing
Long Extensor Injuries (Zones IV to VII)
Reported outcomes for extensor tendon injuries from the
wrist to the MCP joints are much more favorable than for
the more distal extensor tendon injuries already described.
However, morbidity may still be substantial. Clinical assess­
ment of these tendon lacerations can be deceptive when
the injury occurs proximal to the juncturae tendinum.
These communications may be flimsy or quite robust, de­
pending on individual variation. Pull through the juncturae
may afford enough extension by an adjacent digit that the
injury may be overlooked. Loss of full MCP joint hyperex­
tension and extension weakness against resistance are usu­
ally clues to the diagnosis. If accurate clinical assessment
may be masked by pain or swelling, ultrasound is quite
useful for diagnosing complete extensor tendon lacerations
and even for partial lacerations.105
All six extrinsic finger extensor muscles largely function
as a single motor unit with multiple tendons. Thus the rela­
tive-motion splint, through the quadriga effect, is excellent
for postoperative rehabilitation of these injuries. When the
MCP joint of the tendon of the injured finger is placed in
15- to 20-degrees greater extension than adjacent fingers,
this substantially reduces tension on the injured tendon.20
Beasley105 recognized this fact as early as 1981, when he im­
mobilized injured digits in relative extension, but he did not
recognize that this reduced tension persisted regardless of
finger position (Fig. 62.26). Flexor fisting causes the adjacent
extensor tendons to pull the EDC forward, maintaining less
tension on the splinted digit’s repair. It is this understanding
Fig. 62.25 (a) A patient with rheumatoid arthritis with sagittal band rupture and inability to actively extend the MCP joint of the middle
finger. (b) A tendon graft pulley anchored to bone is used to stabilize the extensor mechanism. (c) Postoperative rehabilitation in a relative-
motion extension splint. (d) Outcome 6 weeks after surgery.
c
d
a
b

SECTION VIII THE HAND AND UPPER EXTREMITY
1206
laceration, immobilization is the only alternative; the sur­
geon places the wrist in extension and 30 to 40 degrees of
MCP flexion, avoiding full extension of the MCP joints. How­
ever, whenever possible, a postoperative protected motion
protocol should be initiated as soon as permissible. A delay
of as little as 5 days before relative-motion splinting results
in substantially less final recovered finger motion, particu­
larly with regard to achieving MCP joint hyperextension.14
repair integrity with relative-motion simulation using a
tongue depressor (Fig. 62.27). If a border digit is affected,
then both the little and index fingers need to be placed in
a relative extended position to maintain splint stability.
When all six finger extensors have been divided, there is
no choice but to use a dynamic passive extension outrig­
ger splint for immobilization and postoperative rehabilita­
tion (Fig. 62.28a). In a noncompliant patient with extensor
Fig. 62.27 (a) A patient with a long extensor tendon laceration of the little finger. (b) The laceration was repaired in the emergency room;
the physician can assess the repair integrity with a tongue depressor in relative-motion extension mode. For this border digit, the index
finger is also kept extended. (c) The patient used a wrist splint for the first month. (d) During the last 2 weeks, the patient used only a hand
splint. (e,f) Range of motion at 6 weeks.
a
b
c
Lacerated fifth digit in
15 degrees of extension
d
e
f
Fig. 62.26 A relative-motion extension splint relaxes the repair regardless of metacarpophalangeal, proximal interphalangeal, and distal
interphalangeal position.

1207
Chapter 62 Extensor Tendon Injuries
retain sufficient IP joint extension since the distal inser­
tion is quite broad (in contrast to the distal insertion of the
fingers), and a laceration may not be complete, with suf­
ficient lateral tendon preserved to produce IP joint exten­
sion. Because the initial emergency room examination may
be misleading, the patient may nonetheless subsequently
perceive that the thumb extension is not normal, and if the
surgeon asks the patient to attempt hyperextension of the
IP joint with the volar thumb flat on the table, the patient
will not be able to do so.
EPL is the most common spontaneously ruptured
tendon in the hand. It occurs most in patients with inflam­
matory rheumatoid arthritis but also is associated with
osteoarthritis and distal radius fractures. The last may be
related to attrition rupture on irregular fracture surfaces
or screw position but generally is believed to be a result
of interference with the tendon blood supply in the tight
third dorsal compartment with the additional constraint
of Lister’s tubercle. EPL rupture may occur in nondisplaced
distal radius fractures treated by simple splint immobiliza­
tion, after as late as 6 to 8 weeks after the fracture.110 Vas­
cular studies have confirmed that EPL is poorly vascularized
in this region.111 Patients who have painful EPL synovitis
should have the tendon relocated from Lister’s tubercle, re­
lieving pain and preventing rupture, with thumb function
remaining normal.
Tendon Repair
Sharp lacerations are repaired directly. However, the sur­
geon should be prepared for the fact that the proximal
EPL tendon often retracts far proximally and may have to
be sought through incision extension or through a coun­
terincision even as far back as proximal into the extensor
retinaculum. After attrition rupture of the EPL, it may be
necessary to place an interposition tendon graft or more
often to use a tendon transfer, most commonly an exten­
sor indicis proprius (EIP). Interestingly, after EIP transfer
the index finger is still able to extend independently with
its EDC muscle component.109 Tendon transfer is, of course,
necessary in a chronic situation when the proximal EPL
tendon has been retracted for some time and myostatic
elasticity and contractility are lost. Other options for ten­
don transfer are the APL and palmaris longus. As early as
1982, the value of local anesthesia for repair was pointed
out, enabling the surgeon to most effectively adjust the EPL
repair tension.110 This has been underscored more recently
with the popularization of wide-awake local anesthesia for
both EPL repair and EIP transfers.112
The ideal outcome of repair or tendon transfer should be
recovery of IP joint hyperextension and preservation of full
flexion. Often IP joint hyperextension is lost when treated
with postoperative immobilization alone. Dynamic splint­
ing is the best option to try to maintain both IP joint hy­
perextension and flexion in a compliant, motivated patient
(Fig. 62.28).
A delay in beginning motion seems even more detrimental
for recovery of extensor tendon lacerations than for flexors.
Outcome of Extensor Repairs
There is a wide variability in the method of outcome mea­
surement. This makes it difficult to contrast outcomes with
different treatment techniques. The most appropriate out­
come measurement would seem to be to compare the in­
jured hand range of motion with the uninjured side as a
percentage of total active motion and active extension and
flexion. Acknowledging this difficulty in comparing results,
similar outcomes at 6 months have been found when com­
paring the reports of the most commonly used postopera­
tive techniques of static splinting (total immobilization),
dynamic splinting, and short-arc motion.91
We nonetheless believe that relative-motion extension
splinting is the most preferable postoperative rehabilitation
protocol in compliant patients. We evaluated outcomes at
6 weeks rather than 6 months.14,15 At 6 weeks, flexion av­
eraged 97.8%, but in those who were splinted or operated
later than 5 days after injury, this was 89.5%, which is equal
to the 6-month result after management by immobilization
(86%).13,14 Others, however, have also found significant dif­
ferences in the measurement parameters of earlier recovery
of motion and much earlier return to work when comparing
relative-motion splinting with immobilization.16 This group
also did not include the wrist support component.
Average return to work in our series was only 18 days
compared with 2 to 4 months for other techniques of post­
operative rehabilitation.15,108 Our group did not exclude
those who were obliged to stay away from work because
they were not allowed to return while wearing an ortho­
sis, though they could conceivably actually have returned
to their line of duty. They nonetheless were able to continue
enjoying a variety of recreational activities even when wear­
ing their relative-motion orthosis. In our series of 180 pa­
tients treated with relative-motion extension splinting, the
average length of treatment was 7 weeks, number of ther­
apy visits was 8, and no patients developed clinical repair
rupture or developed complex regional pain syndrome.15 A
systematic review of 11 studies (371 patients) using relative-
motion orthosis protocols reported no tendon ruptures and
no pain syndromes.107
Thumb Extensor Tendon Injuries
Diagnosis and Functional Anatomy
Even after complete proximal laceration of the EPL tendon,
patients may have sufficiently preserved IP joint extension
to be considered to have normal function. The reasons may
be twofold. First, EPB has variable distal insertion, and sec­
ond, intrinsic thumb muscle function causes IP joint exten­
sion. However, these patients lack IP joint hyperextension.
Indeed, even a laceration directly over the IP joint may

SECTION VIII THE HAND AND UPPER EXTREMITY
1208
essentially a tendon injury that can be treated much as those
already described for more distal tendon zones. With more
proximal laceration, the repaired muscle does not have suf­
ficient strength to reliably allow early postoperative motion
protocols. Thus 3 to 4 weeks of initial immobilization is rec­
ommended. Passive dynamic extension outrigger splinting
can prevent distal stiffness and extension contractures (see
Fig. 62.28).
Extensor Injuries Accompanied by
Dorsal Soft Tissue Loss
When there is sufficient paratenon with intact extensor
tendons over the dorsum of the hand, thick split-thickness
skin grafts without meshing are preferable. If tendons are
abraded or repaired, a flap will be necessary.
Distant, staged pedicle flaps from the groin or abdomen
have been used, as well as free fasciocutaneous (such as an­
terolateral thigh flap) or muscle (such as latissimus dorsi
or rectus abdominis). These flaps are often too bulky and
require subsequent recontouring surgery. A radial forearm
fasciocutaneous turnover flap has also been described, pro­
vided the palmar arterial arch is intact as determined by the
Allen test. Even when the arch is incomplete, a radial artery
perforator flap may be used.123,124
However, the radial forearm fasciocutaneous flap leaves
an unsightly donor defect. This can be avoided by using a
fascia-only flap with overlying skin grafting, either as a turn-
over or free flap.125,126 The fascial flap may also be spread out
to potentially cover a larger surface area than a fasciocuta­
neous flap. Fascia and fat provide a better tendon gliding
surface than muscle. Thus the radial forearm fascia flap is
the “workhorse” for dorsal hand wounds. A temporoparietal
fascial free flap has also been described and has even been
suggested to be harvested endoscopically, leaving a poten­
tially inconspicuous scar.127–131
Complications
Many potential complications can occur after extensor ten­
don injuries and repair. Among the most common are ex­
tensor tendon adhesions that may lead to joint extension
contractures (limiting active finger flexion). By relaxing
tension on the next preceding joint by passive extension,
Forearm Extensor Injuries
(Zones VIII to IX)
Extensor tendon injuries in the forearm are relatively un­
common, making up only 1 to 2% of all reported extensor
tendon injuries.113,114 There are few published reports that
either guide the optimal form of management or provide
treatment outcomes.115,116
Clinical and Intraoperative Evaluation
These injuries may involve the muscle, musculotendinous
junctions, or tendon, depending on the forearm level of
injury. There may also be injury to the PIN. This nerve
rapidly branches out as it emerges from the distal edge of
the supinator, giving the last branch 7 to 9 cm proximal
to Lister’s tubercle. The surgeon should also identify lac­
erations to forearm sensory nerves (especially the lateral
antebrachial cutaneous, and particularly the superficial
radial sensory), which should in turn be repaired when­
ever possible to restore sensation and prevent painful
neuroma.
Repair Techniques
It is important to repair these injuries as soon as possible,
because myostatic contraction and remodeling of muscle
and fascia may be even more pronounced with these inju­
ries than further distally.
If the laceration is proximal in the muscle, then the mus­
cle should be repaired. However, the surgeon must search
for the proximal tendon end, which may have retracted
into the proximal muscle belly, because when available,
primary end-to-end tendon repair has the best chance at
being successful. The injured muscle can then be repaired
around this, because repaired muscle achieves better func­
tional regeneration than if simply left to scar and heal sec­
ondarily.117 Figure-of-eight absorbable sutures have been
recommended for muscle repair.118,119 Other repairs have
also been described.120,121 Augmentation of the muscle re­
pair with a fascia or tendon weave has also been recom­
mended.115,122 No one technique has yet been reported as
superior to the others.
Currently, these patients are not candidates for early ac­
tive motion protocols unless the wound is far distal and is
Fig. 62.28 (a) Dynamic extension outrigger splint for fingers. (b) Thumb dynamic extension splint.
a
b

1209
Chapter 62 Extensor Tendon Injuries
It is important to define the precise cause and the sever­
ity of the problem to design the most appropriate surgical
treatment. The most severely affected arthritic joint may
be treated by simple PIP fusion. Aside from that, surgical
correction will vary according to etiology. In patients with
mild deformity and little functional disturbance and no
pain, nonsurgical treatment is preferred. This can be ac­
complished by a figure-of-eight ring splint that prevents
DIP joint hyperextension and allows for flexion. These can
be aesthetically acceptable for chronic use when made of
silver rings.
If there is a relative intrinsic tightness secondary to MCP
joint flexion or volar subluxation, that problem must be cor­
rected first, such as with implant arthroplasty and relocation
of the MCP joint in rheumatoid arthritis. When the cause is
entirely related to intrinsic tightness, a release is performed
through a dorsal approach, resecting an approximate 1-cm
triangle of lateral band and extensor hood on each side of
the central tendon, distal to the transverse fibers. The tri­
angle of tissue is individually removed from distal to proxi­
mal, checking to see if the PIP joint resistance is adequately
released while the MCP joint is extended to determine the
amount to be resected (Video 62.7).
When a swan neck deformity is caused by imbalance
from a chronic mallet problem, late surgical repair of the
mallet can be performed with a dermatotenodesis.56 Post­
operatively, the DIP joint is maintained in extension with a
longitudinal K-wire for 6 weeks, and the PIP joint is mobi­
lized in a figure-of-eight or dorsal blocking splint, restricting
hyperextension of the joint.
A variety of methods have been described to provide a
volar tenodesis for volar PIP joint laxity. Lateral band trans­
location on the radial side can be accomplished through a
midlateral approach that longitudinally releases the lateral
band from the central slip and tethers it volar to the PIP axis
of rotation in a dorsally based flap of flexor sheath, effec­
tively reinforcing and maintaining the transverse retinacular
ligament function.132 Alternatively, the oblique retinacular
ligament function can be reproduced by creating a volar PIP
tenodesis either with a free tendon graft or with the ulnar
lateral band being divided proximally, separated from the
central slip, and passed volar to Cleland’s ligament, secur­
ing it to the flexor sheath.133 This lateral band reconstruction
should not be used if a mallet injury led to the swan neck
deformity, because its success is predicated on an intact ter­
minal insertion. If a mallet deformity is the cause, a free ten­
don graft (usually palmaris longus) can be used, attached to
the distal phalanx and then traveling subcutaneously around
the MCP joint and volarly to the contralateral side of the fin­
ger, where it is secured to the shaft of the proximal phalanx
through a bone tunnel.134 For all of these techniques, local
anesthesia with epinephrine and no tourniquet is important
to verify success intraoperatively.
When the PIP joint has a fixed hyperextension contrac­
ture, dynamic splinting or serial casting should be attempted
first. A surgical PIP dorsal capsule release may be required.
Ultimately, successful treatment of a dysfunctional swan
the surgeon can determine how much of the joint con­
tracture is produced by a more proximal tendon adhesion
versus an innate joint contracture itself. Tenolysis may best
be performed using the wide-awake local anesthesia tech­
nique for intraoperative assessment of complete resolution
of the problem by having the patient actively participate.
Occasionally, a joint capsulotomy may also be required.
This has the advantage also of the patient being able to
see that active range has been restored. When the patient
returns postoperatively, if motion is masked by pain and
swelling, then the recollection of the intraoperative range
of motion that was accomplished will facilitate ultimate re­
covery of range of motion.
Two additional complications of tendon injuries that
have not yet been fully discussed illustrate the principles of
careful clinical assessment so that a functionally directed
treatment protocol can be initiated. These are swan neck
deformity and caput ulnae syndrome (with spontaneous ex­
tensor tendon ruptures at the dorsum of the wrist).
Swan Neck Deformity
In a swan neck deformity there is an extrinsic–intrinsic ex­
tensor imbalance that results in PIP hyperextension with
the DIP in flexed posture. It may result from a variety of
causes, including trauma, inflammatory arthritis, and
central nervous spasticity. It may even result from a rela­
tive flexed position of the MP joint (as with a Dupuytren’s
contracture), leading to an imbalanced pull on the long ex­
tensors at the PIP joint. It is important to understand the
precise cause of the deformity to appropriately direct the
treatment. A functionally impairing deformity may result
through a variety of different pathways. Mallet injury, for
example, may create a similar intrinsic muscle imbalance
related to overpull of the central extensor slip, because the
lateral bands are retracted proximally. It may also result from
spastic intrinsic muscle contracture (stroke, cerebral palsy,
and Parkinson’s disease). Finally, when the PIP joint stabiliz­
ing structures are damaged (such as with flexor digitorum
superficialis laceration or rupture, or volar plate attenuation
or laxity), a swan neck deformity may also result.
Patients may notice a clicking as the lateral bands
subluxate around the PIP joint with flexion. With time, it
becomes more difficult to initiate PIP flexion from a hyper­
extended position, and this can progress to a PIP extension
contracture and even PIP arthritis. Thus, for example, in
rheumatoid arthritis, a swan neck deformity can be related
to five different potential causes that may occur in varying
combinations:
1. Rheumatoid rupture of the flexor digitorum sublimis
2. Synovitis of the volar plate and joint capsule causing
laxity
3. Synovitis of the DIP joint causing chronic mallet defor­
mity
4. Subluxation of the MCP joint and long extensor tendon
5. Intrinsic muscle or tendon contracture

SECTION VIII THE HAND AND UPPER EXTREMITY
1210
first described from tendon attrition on osteophytes in os­
teoarthritis but actually is a complication more common
in rheumatoid arthritis.136 It is treated, in the first instance,
by distal ulna (Darrach) resection. Distal ulna stabiliza­
tion and translocation of an extensor retinacular flap deep
to the extensor tendons shield them from further poten­
tial attrition on bone ends or osteophytes. If the ECU is
chronically ruptured, ECRL is transferred to the insertion of
the former to balance the wrist. Depending on how many
long finger extensors are ruptured, the surgeon can repair
those ruptured tendons to adjacent unruptured tendons or
if necessary perform a formal tendon transfer (generally
with flexor sublimis or flexor carpi radialis) to the finger
extensors.
To avoid tendon adherence postoperatively, the surgeon
may use a dynamic rubber band extension outrigger brace,
but we have successfully used the pan-type relative-motion
extensor MCP orthosis with the repaired fingers being placed
in 15- to 20-degrees greater extension than adjacent digits
for 6 weeks. Usually, the wrist is maintained at rest for the
first 3 weeks with both the fingers and wrist in a gutter ex­
tensor resting splint at night. Sometimes patients have dif­
ficulty recovering full MCP joint extension and a dynamic
extension splint can be added to the relative-motion splint
(Fig. 62.29, Video 62.8). This is maintained for 6 weeks. Tra­
neck deformity requires the PIP joint to be able to flex close
to 90 degrees, followed by temporary pinning of the PIP joint
and then a figure-of-eight dorsal blocking splint.135
Generally, the DIP extension lag with a swan neck defor­
mity is less bothersome than the PIP joint hyperextension.
Sometimes this DIP problem may correct postoperatively
once intrinsic balance is restored. However, if this DIP ex­
tension lag persists and is sufficiently bothersome, a central
slip Fowler tenotomy may restore the balance necessary to
bring the DIP joint to neutral.31 In the absence of this, DIP
fusion may be necessary.
Caput Ulnae (Vaughan-Jackson)
Syndrome with Extensor Tendon
Ruptures at the Wrist
Caput ulnae syndrome with wrist extensor tendon rup­
tures results from ulnocarpal synovitis and stretching of
those ligaments, leading to volar subluxation of the carpus
(or relative dorsal positioning of the distal ulna). In turn,
attrition ruptures of the long extensor tendons to fingers
may occur, starting first with the extensor digiti quinti
(EDQ) and then progressing sequentially in a radial direc­
tion to the EDC tendons of the fingers. This problem was
a
EDC
EDQ
EIP
b
Fig. 62.29 (a) All four extensor digitorum communis (EDC) tendons and the extensor digiti quinti (EDQ) ruptured in this 33-year-old pa­
tient with caput ulnae syndrome. (b,c) All four tendons are sutured to the remaining intact extensor indicis proprius (EIP) and reinforced
with proximal ruptured tendon stumps, which are also sutured to the EIP. Because she had wrist extension, her extensor retinaculum was
reconstructed to avoid bowstringing.
Proximal
tendon repairs
Distal
tendon repairs
Reconstructed
extensor retinaculum
Fingers
c
Continued

1211
Chapter 62 Extensor Tendon Injuries
complications of stiffness from immobilization not only in
the injured digits but also in adjacent, seemingly uninjured
digits. In reliable, adult patients, we recommend the wide-
awake local anesthetic technique to assess intraoperatively
that tendon balance has been restored and to evaluate in­
traoperative placement of relative-motion splinting, ensur­
ing integrity of the repair. Then the relative-motion protocol
is continued into the postoperative rehabilitation period.
This allows early active motion, immediately permitting
functional hand use and reducing morbidity. This can be
achieved with long extensor tendon repairs, as well as with
boutonnière, sagittal band, and Vaughn-Jackson problems.
ditional belief is that if the only remaining intact tendon is
the EIP, that alone is not sufficiently strong to extend the
remaining fingers to it if repaired.137 We have not found this
to be true if the proximal ruptured tendons are secured to
the EIP so that the combined strength is able to power all
four fingers.
Conclusion
Unfavorable results and morbidity after extensor tendon
injury and repair are most commonly related to difficulty
restoring the unique intrinsic–extrinsic balance and the
Fig. 62.29, cont’d (d,e) Alternating bracing with dynamic outrigger and relative extensor motion. (f,g) Long-term result.
f
g
d
e
References

1. Merritt WH. Written on behalf of the stiff finger. J Hand
Ther 1998;11(2):74–79

2. Merritt WH, Peacock EE Jr, Chvapil M. Studies on the
inductive capacity of canine fascia lata. Surgical Forum
XXVI. 1975; 26:553

3. Peacock EE Jr, Van Winkle WB: Wound repair. 2nd ed.
Philadelphia, London, Toronto: WB Saunders Co.; 368–
384

4. Voleti PB, Buckley MR, Soslowsky LJ. Tendon healing: re­
pair and regeneration. Annu Rev Biomed Eng 2012;14:
47–71

5. Gelberman RH, Steinberg D, Amiel D, Akeson W. Fibro­
blast chemotaxis after tendon repair. J Hand Surg Am
1991;16(4):686–693

6. Leadbetter WB. Cell-matrix response in tendon injury.
Clin Sports Med 1992;11(3):533–578

7. Gelberman RH, Manske PR, Akeson WH, Woo SL, Lund­
borg G, Amiel D. Flexor tendon repair. J Orthop Res 1986;
4(1):119–128

8. Wada A, Kubota H, Miyanishi K, Hatanaka H, Miura H,
Iwamoto Y. Comparison of postoperative early active
mobilization and immobilization in vivo utilising a four-
strand flexor tendon repair. J Hand Surg [Br] 2001;26(4):
301–306

9. Merritt WH. Relative motion splint: active motion after
extensor tendon injury and repair. J Hand Surg Am 2014;
39(6):1187–1194
10. Evans RB. Early active short arc motion for the repaired
central slip. J Hand Surg Am 1994;19(6):991–997
11. Lalonde DH. Extensor tendon repair of the finger. In:
Lalonde DH, ed. Wide Awake Hand Surgery. St Louis,
MO: CRC Press; 2016:209
12. Merritt WH, Johnson M, Diegelmann R. Studies of the
Biological Responses of Fascia to Injury. Downey, CA:
Plastic Surgery Research Council; 1977
13. Newport ML, Blair WF, Steyers CM Jr. Long-term results
of extensor tendon repair. J Hand Surg Am 1990;15(6):
961–966

SECTION VIII THE HAND AND UPPER EXTREMITY
1212
33. Kaplan EB. Functional and surgical anatomy of the hand.
2nd ed. In: Kaplan EB, ed. Phila., Montreal: JB Lippincott,
Co.; 1965:209
34. Landsmeer JM. The coordination of finger-joint motions.
J Bone Joint Surg Am 1963;45(8):1654–1662
35. Bendz P. The functional significance of the oblique reti­
nacular ligament of Landsmeer. A review and new pro­
posals. J Hand Surg [Br] 1985;10(1):25–29
36. Harris C Jr, Rutledge GL Jr. The functional anatomy of the
extensor mechanism of the finger. J Bone Joint Surg Am
1972;54(4):713–726
37. Kleinert HE, Verdan C. Report of the Committee on Ten­
don Injuries (International Federation of Societies for
Surgery of the Hand). J Hand Surg Am 1983;8(5 Pt 2):
794–798
38. Stark HH, Boyes JH, Wilson JN. Mallet finger. J Bone Joint
Surg Am 1962;44-A:1061–1068
39. Zhang X, Shao X, Huang Y. Pullout wire fixation together
with distal interphalangeal joint Kirschner wire stabi­
lization for acute combined tendon and bone (double
level) mallet finger injury. J Hand Surg Am 2015;40(2):
363–367
40. Stern PJ, Kastrup JJ. Complications and prognosis of
treatment of mallet finger. J Hand Surg Am 1988;13(3):
329–334
41. Evans RB, Burkhalter WE. A study of the dynamic anato­
my of extensor tendons and implications for treatment.
J Hand Surg Am 1986;11(5):774–779
42. Okafor B, Mbubaegbu C, Munshi I, Williams DJ. Mallet
deformity of the finger. Five-year follow-up of conserva­
tive treatment. J Bone Joint Surg Br 1997;79(4):544–547
43. O’Brien LJ, Bailey MJ. Single blind, prospective, ran­
domized controlled trial comparing dorsal aluminum
and custom thermoplastic splints to stack splint for
acute mallet finger. Arch Phys Med Rehabil 2011;92(2):
191–198
44. Pike J, Mulpuri K, Metzger M, Ng G, Wells N, Goetz T.
Blinded, prospective, randomized clinical trial compar­
ing volar, dorsal, and custom thermoplastic splinting in
treatment of acute mallet finger. J Hand Surg Am 2010;
35(4):580–588
45. Gruber JS, Bot AG, Ring D. A prospective randomized con­
trolled trial comparing night splinting with no splinting
after treatment of mallet finger. Hand (NY) 2014;9(2):
145–150
46. Lalonde D, Merritt W. Extensor tendon injuries. Instruc­
tional course, ASPS annual meeting, Chicago, IL: 2014
47. Pratt DR. Internal splint for closed and open treat­
ment of injuries of the extensor tendon at the distal
joint of the finger. J Bone Joint Surg Am 1952;34 A(4):
785–788
48. Casscells SW, Strange TB. Intramedullary wire fixation
of mallet-finger. J Bone Joint Surg Am 1957;39-A(3):
521–526
49. Auchincloss JM. Mallet-finger injuries: a prospective,
controlled trial of internal and external splintage. Hand
1982;14(2):168–173
50. Tubiana R. Surgical repair of the extensor apparatus of
the fingers. Surg Clin North Am 1968;48(5):1015–1031
51. Garberman SF, Diao E, Peimer CA. Mallet finger: results
of early versus delayed closed treatment. J Hand Surg
Am 1994;19(5):850–852
52. Patel MR, Desai SS, Bassini-Lipson L. Conservative
management of chronic mallet finger. J Hand Surg Am
1986;11(4):570–573
14. Merritt WH, Howell J, Tune R, Saunders S, Hardy M.
Achieving immediate active motion by using relative
motion splinting after long extensor repair and sagittal
band ruptures with tendon subluxation. Oper Tech Plast
Reconstr Surg 2000;7(1):31–37
15. Howell JW, Merritt WH, Robinson SJ. Immediate con­
trolled active motion following zone 4-7 extensor ten­
don repair. J Hand Ther 2005;18(2):182–190
16. Hirth MJ, Bennett K, Mah E, et al. Early return to work
and improved range of motion with modified relative
motion splinting: A retrospective comparison with im­
mobilization splinting for zones V and VI extensor ten­
don repairs. Hand Ther 2011;16(4):86–94
17. Saldana MJ, Choban S, Westerbeck P, Schacherer TG. Re­
sults of acute zone III extensor tendon injuries treated
with dynamic extension splinting. J Hand Surg Am 1991;
16(6):1145–1150
18. Weeks PM, Ray RC. Management of Acute Hand Injuries,
A Biological Approach, 2nd ed. St. Louis: CV Mosby Co.;
1978:89
19. Netscher D. Extensor Tendon Injuries. In: Goldwyn RM,
Cohen MN, eds. The Unfavorable Result in Plastic Sur­
gery: Avoidance and Treatment. 3rd ed. Philadelphia:
Lippincott Williams & Wilkins; 2001
20. Sharma JV, Liang NJ, Owen JR, Wayne JS, Isaacs JE. Analy­
sis of relative motion splint in the treatment of zone VI
extensor tendon injuries. J Hand Surg Am 2006;31(7):
1118–1122
21. Wehbé MA. Anatomy of the extensor mechanism of the
hand and wrist. Hand Clin 1995;11(3):361–366
22. Bevelaqua AC, Hayter CL, Feinberg JH, Rodeo SA. Poste­
rior interosseous neuropathy: electrodiagnostic evalua­
tion. HSS J 2012;8(2):184–189
23. Leslie BM, Ericson WB Jr, Morehead JR. Incidence of
a septum within the first dorsal compartment of the
wrist. J Hand Surg Am 1990;15(1):88–91
24. Mahakkanukrauh P, Mahakkanukrauh C. Incidence of a
septum in the first dorsal compartment and its effects
on therapy of de Quervain’s disease. Clin Anat 2000;
13(3):195–198
25. Grundberg AB, Reagan DS. Pathologic anatomy of the
forearm: intersection syndrome. J Hand Surg Am 1985;
10(2):299–302
26. Von Schroeder HP, Botte MJ. Anatomy of the exten­
sor tendons of the fingers: variations and multiplicity.
J Hand Surg [Br] 1995;20(1):27–34
27. von Schroeder HP, Botte MJ, Gellman H. Anatomy of the
juncturae tendinum of the hand. J Hand Surg Am 1990;
15(4):595–602
28. von Schroeder HP, Botte MJ. Anatomy and functional sig­
nificance of the long extensors to the fingers and thumb.
Clin Orthop Relat Res 2001; (383):74–83
29. Rayan GM, Murray D, Chung KW, Rohrer M. The exten­
sor retinacular system at the metacarpophalangeal joint.
Anatomical and histological study. J Hand Surg [Br] 1997;
22(5):585–590
30. Winslow JB. Exposition Anatomique de la structure du
corps humain. Paris: Guillaume Desperezet, Jean Deses­
sarte; 1732
31. Bowers WH, Hurst LC. Chronic mallet finger: The use of
Fowler’s central slip release. J Hand Surg Am 1978;3(4):
373–376
32. Schreuders Ton AR. A modification of Elson’s test for the
diagnosis of an acute extensor central slip injury. Hand
Ther 2006;11(4):111–112

1213
Chapter 62 Extensor Tendon Injuries
74. Bauze A, Bain GI. Internal suture for mallet finger frac­
ture. J Hand Surg [Br] 1999;24(6):688–692
75. Damron TA, Engber WD, Lange RH, et al. Biomechani­
cal analysis of mallet finger fracture fixation techniques.
J Hand Surg Am 1993;18(4):600–607, discussion 608
76. Nelis R, Wouters DB. Is the use of biodegradable de­
vices in the operative treatment of avulsion fractures
of fingers, the so-called mallet finger advantageous? A
feasibility study with meniscus arrows. Open Orthop
J 2008;2(2):151–154
77. Rocchi L, Genitiempo M, Fanfani F. Percutaneous fixation
of mallet fractures by the “umbrella handle” technique.
J Hand Surg [Br] 2006;31(4):407–412
78. Lu J, Jiang J, Xu L, Xu W, Xu J. Modification of the pull-
in suture technique for mallet finger. Ann Plast Surg
2013;70(1):30–33
79. Toker S, Türkmen F, Pekince O, Korucu İ, Karalezli N.
Extension block pinning versus hook plate fixation for
treatment of mallet fractures. J Hand Surg Am 2015;
40(8):1591–1596
80. Ishiguro T, Itoh Y, Yabe Y, Hashizume N. Extension block
with Kirschner wire for fracture dislocation of the distal
interphalangeal joint. Tech Hand Up Extrem Surg 1997;
1(2):95–102
81. Miranda BH, Murugesan L, Grobbelaar AO, Jemec B. PBNR:
Percutaneous blunt needle reduction of bony mallet inju­
ries. Tech Hand Up Extrem Surg 2015;19(2):81–83
82. Sonoda A, Kishimoto H, et al. Treatment of chronic mal­
let fracture with tension wire fixation. J Jpn Soc Surg
Hand 2003;20(6):660–663
83. Lee HJ, Jeon IH, Kim PT, Oh CW, Deslivia MF, Lee SJ.
Transtendinous wiring of mallet finger fractures pre­
senting late. J Hand Surg Am 2014;39(12):2383–2389
84. Patel M. Chronic volar fracture subluxation of digital
distal interphalangeal joints. Presented at: the Annual
Meeting of the American Association for Hand Surgery;
1983; Miami, FL
85. Verdan C. Syndrome of the quadriga. Surg Clin North Am
1960;40:425–426
86. Leijnse JN, Walbeehm ET, Sonneveld GJ, Hovius SE, Kauer
JM. Connections between the tendons of the muscu­
lus flexor digitorum profundus involving the synovial
sheaths in the carpal tunnel. Acta Anat (Basel) 1997;
160(2):112–122
87. Elson RA. Rupture of the central slip of the extensor
hood of the finger. A test for early diagnosis. J Bone Joint
Surg Br 1986;68(2):229–231
88. Boyes JH. Bunnell’s surgery of the hand. 5th ed. Phila.: JP
Lippincott; 1970:441
89. Brand P. Mechanics of individual muscles at individual
joints. In: Clinical Mechanics of the Hand. CB Mosby Co.;
1985:288–289
90. Wang K, McGlinn EP, Chung KC. A biomechanical and
evolutionary perspective on the function of the lumbri­
cal muscle. J Hand Surg Am 2014;39(1):149–155
91. Lalonde D. Solving the chronic boutonniere. Presented at
the Philadelphia Hand Symposia, March 12, 2016. Phila­
delphia, PA.
92. Wynn Parry CB. Rehabilitation of the hand. 3rd ed.
St. Louis: CV Mosby; 1990
93. Maddy LS, Meyerdierks EM. Dynamic extension assist
splinting of acute central slip lacerations. J Hand Ther
1997;10(3):206–212
53. Brzezienski MA, Schneider LH. Extensor tendon injuries
at the distal interphalangeal joint. Hand Clin 1995;11(3):
373–386
54. Milford L. The Hand. In: Crenshaw AH, ed. Campbell’s
Operative Orthopaedics. 5th ed. St. Louis: CB Mosby Co.;
1971:105–106
55. Warren RA, Kay NRM, Ferguson DG. Mallet finger: com­
parison between operative and conservative manage­
ment in those cases failing to be cured by splintage.
J Hand Surg [Br] 1988;13(2):159–160
56. Iselin F, Levame J, Godoy J. A simplified technique for
treating mallet fingers: tenodermodesis. J Hand Surg Am
1977;2(2):118–121
57. McFarlane RM, Hampole MK. Treatment of extensor ten­
don injuries of the hand. Can J Surg 1973;16(6):366–375
58. Doyle JP. Extensor tendons—acute injuries. In: Green
DP, ed. Operative Hand Surgery. 2nd ed. New York/
Edinburgh/London/Melbourne:
Churchill
Livingston;
1988:1933
59. Lalonde D. Current practices in tendon management. In­
structional course. American Society of Hand Therapists
annual meeting, 2015, Denver, Colorado.
60. Elliot RA. Extensor tendon repair. In: May JW, Littler JW,
McCarthy JG, eds. Plastic Surgery: The Hand. Vol 1. Phi­
la.: WB Saunders; 1990:4573
61. Moradi A, Kachooei AR, Mudgal CS. Mallet fracture.
J Hand Surg Am 2014;39(10):2067–2069
62. Wehbé MA, Schneider LH. Mallet fractures. J Bone Joint
Surg Am 1984;66(5):658–669
63. Husain SN, Dietz JF, Kalainov DM, Lautenschlager EP. A
biomechanical study of distal interphalangeal joint sub­
luxation after mallet fracture injury. J Hand Surg Am
2008;33(1):26–30
64. Alla SR, Deal ND, Dempsey IJ. Current concepts: mallet
finger. Hand (NY) 2014;9(2):138–144
65. Hofmeister EP, Mazurek MT, Shin AY, Bishop AT. Exten­
sion block pinning for large mallet fractures. J Hand Surg
Am 2003;28(3):453–459
66. Lee YH, Kim JY, Chung MS, Baek GH, Gong HS, Lee SK. Two
extension block Kirschner wire technique for mallet finger
fractures. J Bone Joint Surg Br 2009;91(11):1478–1481
67. Pegoli L, Toh S, Arai K, Fukuda A, Nishikawa S, Vallejo IG.
The Ishiguro extension block technique for the treat­
ment of mallet finger fracture: indications and clinical
results. J Hand Surg [Br] 2003;28(1):15–17
68. Tetik C, Gudemez E. Modification of the extension block
Kirschner wire technique for mallet fractures. Clin Or­
thop Relat Res 2002;404(404):284–290
69. Fritz D, Lutz M, Arora R, Gabl M, Wambacher M, Pech­
laner S. Delayed single Kirschner wire compression tech­
nique for mallet fracture. J Hand Surg [Br] 2005;30(2):
180–184
70. Takami H, Takahashi S, Ando M. Operative treatment of
mallet finger due to intra-articular fracture of the distal
phalanx. Arch Orthop Trauma Surg 2000;120(1-2):9–13
71. Bischoff R, Buechler U, De Roche R, Jupiter J. Clinical re­
sults of tension band fixation of avulsion fractures of the
hand. J Hand Surg Am 1994;19(6):1019–1026
72. Jupiter JB, Sheppard JE. Tension wire fixation of avul­
sion fractures in the hand. Clin Orthop Relat Res 1987;
214(214):113–120
73. Kronlage SC, Faust D. Open reduction and screw fixation
of mallet fractures. J Hand Surg [Br] 2004;29(2):135–138

SECTION VIII THE HAND AND UPPER EXTREMITY
1214
injuries in the hand and wrist: a 10-year population-
based study. Clin Orthop Surg 2014;6(2):196–202
115. Regnard PJ, Trouilloud P, Obadia JF, Lucet A, Piganiol
G. Extensor tendon injuries. Presentation of a series of
ninety-nine cases. Ann Chir Main 1985;4(1):55–63
116. Dawson CK, Mudgal CS. Fascial augmentation tenorrha­
phy for extensor tendon lacerations in the forearm. Tech
Hand Up Extrem Surg 2012;16(2):72–74
117. Menetrey J, Kasemkijwattana C, Fu FH, Moreland
MS, Huard J. Suturing versus immobilization of
a muscle laceration. A morphological and func­
tional study in a mouse model. Am J Sports Med
1999;27(2):222–229
118. Hanz KR, Saint-Cyr M, Semmler MJ, Rohrich RJ. Exten­
sor tendon injuries: acute management and second­
ary reconstruction. Plast Reconstr Surg 2008;121(3):
109e–120e
119. Nolan WB. Extensor tendon injuries and reconstruction.
In: Mathes SJ, ed. Plastic Surgery, Volume VII: The Hand
and Upper Limb, Part 1. 2nd ed. Philadelphia, PA: Saun­
ders Elsevier; 2006:401–421
120. Julien TP, Mudgal CS. Anchor suture technique for mus­
cle belly repair. Tech Hand Up Extrem Surg 2011;15(4):
257–259
121. Chance JR, Kragh JF Jr, Agrawal CM, Basamania CJ. Pull­
out forces of sutures in muscle lacerations. Orthopedics
2005;28(10):1187–1190
122. Botte MJ, Gelberman RH, Smith DG, Silver MA, Gellman
H. Repair of severe muscle belly lacerations using a ten­
don graft. J Hand Surg Am 1987;12(3):406–412
123. Hansen AJ, Duncan SF, Smith AA, Shin AY, Moran SL,
Bishop AT. Reverse radial forearm fascial flap with radial
artery preservation. Hand (NY) 2007;2(3):159–163
124. Weinzweig N, Chen L, Chen ZW. The distally based ra­
dial forearm fasciosubcutaneous flap with preservation
of the radial artery: an anatomic and clinical approach.
Plast Reconstr Surg 1994;94(5):675–684
125. Merritt WH. Radial artery fascial free flap with vascular
donor reconstruction: A low-cost, versatile reconstruc­
tive choice. J Reconstr Microsurg 2006;22:A101
126. Demirkan F, Wei FC, Lutz BS, Cher TS, Chen IH. Reliability
of the venae comitantes in venous drainage of the free
radial forearm flaps. Plast Reconstr Surg 1998;102(5):
1544–1548
127. Hidalgo DA. Superficial and deep temporal facial free
flaps. In: Shaw WW, Hidalgo DA, eds. Microsurgery
and Trauma. Mt. Kisco, NY: Futura Pub. Co., Inc.; 1987:
237–243
128. Brent B, Upton J, Acland RD, et al. Experience with the
temporoparietal fascial free flap. Plast Reconstr Surg
1985;76(2):177–188
129. Chung KC, Cederna PS. Endoscopic harvest of temporo­
parietal fascial free flaps for coverage of hand wounds.
J Hand Surg Am 2002;27(3):525–533
130. Biswas G, Lohani I, Chari PS. The sandwich temporopa­
rietal free fascial flap for tendon gliding. Plast Reconstr
Surg 2001;108(6):1639–1645
131. Neumeister M, Hegge T, Amalfi A, Sauerbier M. The re­
construction of the mutilated hand. Semin Plast Surg
2010;24(1):77–102
132. Tonkin MA, Hughes J, Smith KL. Lateral band trans­
location for swan-neck deformity. J Hand Surg Am
1992;17(2):260–267
133. McKeon KE, Lee DH. Posttraumatic boutonniere and swan
neck deformities. J Am Acad Orthop Surg 2015;23(10):
623–632
94. Steichen J, Strickland J, et al. Results of surgical treat­
ment of chronic boutonniere deformity: An analysis of
prognostic factors. In: Strickland JE, Steichen JB, eds. Dif­
ficult Problems in Hand Surgery. St. Louis: CV Mosby;
1982:62–69
95. Ishizuki M. Traumatic and spontaneous dislocation of
extensor tendon of the long finger. J Hand Surg Am 1990;
15(6):967–972
96. Strauch RJ. Extensor tendon injury. In: Wolfe S, Peder­
son W, Hotchkiss R, Kozin S, eds. Green’s Operative Hand
Surgery. 6th ed. Philadelphia: Elsevier; 2011:180
97. Rayan GM, Murray D. Classification and treatment of
closed sagittal band injuries. J Hand Surg Am 1994;19(4):
590–594
98. Peelman J, Markiewitz A, Kiefhaber T, Stern P. Splintage
in the treatment of sagittal band incompetence and ex­
tensor tendon subluxation. J Hand Surg Eur Vol 2015;
40(3):287–290
99. Catalano LW III, Gupta S, Ragland R III, Glickel SZ, John­
son C, Barron OA. Closed treatment of nonrheumatoid
extensor tendon dislocations at the metacarpophalan­
geal joint. J Hand Surg Am 2006;31(2):242–245
100. Wheeldon FT. Recurrent dislocation of extensor tendons
in the hand. J Bone Joint Surg Br 1954;36-B(4):612–617
101. Elson RA. Dislocation of the extensor tendons of the
hand. Report of a case. J Bone Joint Surg Br 1967;49(2):
324–326
102. McCoy FJ, Winsky AJ. Lumbrical loop operation for luxa­
tion of the extensor tendons of the hand. Plast Reconstr
Surg 1969;44(2):142–146
103. Kilgore ES, Graham WP, Newmeyer WL, Brown LG. Cor­
rection of ulnar subluxation of the extensor communis.
Hand 1975;7(3):272–274
104. Carroll C IV, Moore JR, Weiland AJ. Posttraumatic ulnar
subluxation of the extensor tendons: a reconstructive
technique. J Hand Surg Am 1987;12(2):227–231
105. Beasley RW. Hand Injuries. In: Beasley RW, ed. Phila.:
WB Saunders Co.; 1981:254
106. Burns MC, Derby B, Neumeister MW. Wyndell merritt
immediate controlled active motion (ICAM) protocol fol­
lowing extensor tendon repairs in zone IV-VII: review of
literature, orthosis design, and case study—a multime­
dia article. Hand (NY) 2013;8(1):17–22
107. Hirth M, Howell J, O’Brien L. Relative motion orthosis in
the management of various hand conditions: A scoping
review. J Hand Ther 2016; 29(4):405-432
108. Soni P, Stern CA, Foreman KB, Rockwell WB. Advances in
extensor tendon diagnosis and therapy. Plast Reconstr
Surg 2009;123(2):52e–57e
109. Moore JR, Weiland AJ, Valdata L. Independent index ex­
tension after extensor indicis proprius transfer. J Hand
Surg Am 1987;12(2):232–236
110. Schneider L. Reconstruction in chronic extensor prob­
lems. In: Strickland JE, Steichen JB, eds. Difficult Prob­
lems in Hand Surgery. St. Louis: CV Mosby; 1982:51–52
111. Engkvist O, Lundborg G. Rupture of the extensor polli­
cis longus tendon after fracture of the lower end of the
radius—a clinical and microangiographic study. Hand
1979;11(1):76–86
112. Lalonde DH. Extensor tendon repair of the forearm. In:
Lalonde DH, ed. Wide Awake Hand Surgery. CRC Press;
2016:219
113. Patillo D, Rayan GM. Open extensor tendon injuries: an
epidemiologic study. Hand Surg 2012;17(1):37–42
114. de Jong JP, Nguyen JT, Sonnema AJM, Nguyen EC, Amadio
PC, Moran SL. The incidence of acute traumatic tendon