Phẫu Thuật Tạo Hình Grabb & Smith’s (Bản Cập Nhật – Kevin C. Chung)

avulsion, the FDP tendon retracts into the palm with disruption of the vincular system, and thus needs
urgent repair within 2 weeks from the time of injury. In type II avulsion, the FDP tendon retracts to the
level of the PIP joint, and can be repaired within 6 weeks from the time of injury, because of preservation
of some of the vincular blood supply. Type III injuries usually do not retract proximal to the A4 pulley
because of a large bony fragment; these may be repaired with a Kirschner wire or a screw. Pure tendon
lacerations in Zone 1, on the other hand, may require tendon-to-bone repair with or without a button if
the distal stump is less than 1 cm in length, otherwise it can be repaired primarily. In delayed
presentation of Zone 1 injuries outside of the time window for repair, DIP arthrodesis can be considered
in the setting of intact FDS function, understanding that the overall grip strength will be decreased.
FIGURE 76.7 Leddy classification of Zone 1 flexor tendon injuries.
Zone 2 flexor tendon injuries are more challenging because of the complex anatomy in this area. Care
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should be taken to preserve the A2 and the A4 pulleys when the lacerated tendons are passed through
them during the repair. The FDP tendon should be carefully pulled through the FDS tendons if it retracts
proximal to the chiasm. The proximal end of the FPL laceration in Zone 2 may retract to the thenar
musculature or even more proximally, which requires extension of the incision to the thenar eminence, or
a separate incision in the carpal tunnel or distal forearm, respectively. Milking the digit from proximal to
distal and wrist and MCP flexion can help to deliver the proximal tendon end near the laceration. If the
proximal FPL tendon cannot be retrieved readily, we prefer to make an incision at the wrist, radial to the
FCR tendon to find the proximal tendon end. A small feeding catheter is threaded into the sheath, taking
great care not to create a false path. The proximal tendon is then sutured to the catheter, which is used to
guide the tendon through the sheath. After tendon repair, gentle range of motion of the finger can detect
repair site gapping or catching at the edge of a pulley.
Flexor tendon injuries in Zones 3, 4, and 5 are repaired with similar techniques as those used in Zone 2
injuries, although epitendinous sutures may not be necessary because there is more room in these zones
for tendon excursion, which decreases the intensity of the adhesions. Furthermore, multiple structures are
cut in these zones, which require expedient repairs to keep the tourniquet time within 2 hours. Repairs in
Zones 3, 4, and 5 have less adhesion formation and better prognosis. Microsurgery may be needed for
concomitant nerve or arterial injuries at the time of tendon repair.
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Rehabilitation and Outcomes
After successful flexor tendon repair, a dorsal blocking splint is applied to maintain the wrist flexion at
20° to 30°, the MCP joint flexion at 50° to 70°, and PIP and DIP joints in full extension. Animal studies
have demonstrated that early protective motion promotes tendon healing. 31 The strength of the repair
determines the type of postoperative motion therapy. Studies have concluded that at least four core
strands are needed to create a strong enough repair to withstand the strain across the repair site from
light active motion (Figure 76.8). 22 Therapy should begin within a week of the surgery under the
guidance of an experienced hand therapist. Early motion rehabilitation protocol in the appropriate
patients helps to decrease intrasynovial adhesion formation and prevent digital stiffness.
FIGURE 76.8 Estimated strength to failure (in grams) for flexor tendon repairs with epitendinous sutures.
(Reproduced with permission from Strickland, JW. Flexor tendon injuries: I. Foundations of treatment. J Am Acad Orthop Surg. 1995;3:44-54.)
It has been well accepted that 3 to 5 mm of tendon excursion sufficiently prevents adhesion formation in
Zone 2 repairs. 32 Within this range, increased tendon excursion does not affect the tensile properties of
the repair site. 33 Similarly, increasing the level of applied force during rehabilitation does not affect the
ultimate strength of the repaired tendon. 34 A prospective randomized clinical trial demonstrated that the
active place-and-hold therapy improved finger active range of motion, compared to passive motion
therapy, although functional outcome scores were similar in both groups. 35
More rigorous active finger range of motion starts at 3 to 4 weeks postoperatively. The protective dorsal
splint is eventually discontinued around 6 to 8 weeks postoperatively. Individual digit strengthening is
gradually introduced at 10 weeks after surgery, and the patient may return to normal activities at 4 to
6 months after surgery. In pediatric patients and those who are unable to safely participate in an early
motion rehabilitation program, cast immobilization for 4 to 6 weeks is used to protect the repair. The cast
is applied to maintain the wrist in neutral, MCP joints at 70° of flexion, and IP joints in extension. Careful
initiation and progression of range-of-motion exercises with frequent monitoring are critical to achieve a
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good outcome.
Outcomes of flexor tendon repair surgery depends on multiple factors, including severity of initial injury,
timing and quality of the repair, patient’s underlying medical conditions that may affect tendon healing,
and the quality of postoperative rehabilitation. Majority of Zone 1 and Zone 2 repairs have good to
excellent outcomes, almost all Zone 3, 4, and 5 repairs have good to excellent outcomes.
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Complications
The most common complication after flexor tendon repairs is finger stiffness, which can be a result of
either tendon adhesion or IP joint contractures. Other complications, such as infection, skin flap necrosis,
and tendon rupture after repair, can also occur. These complications adversely affect the outcome and
should be addressed promptly.
Peritendinous adhesion can happen with crush injuries, inflammatory conditions, fractures, excessive
surgical manipulation during primary repair, tendon grafting, poor postoperative rehabilitation, and
wound complications. Based on the American Society for Surgery of the Hand guidelines, 36 the
postoperative total active motion (TAM) of the digit can be determined using the following formula:
A grading system categorizes the functional outcome based on the postsurgical TAM as a percentage of
the normal TAM of 260°. An excellent outcome is the recovery of 100% of the normal TAM; a good
outcome is the recovery of more than 75% of the normal TAM but less than 100%. A recovery of less than
75% but more than 50% is considered fair, and anything less than 50% is considered poor.
At 4 to 6 months after the flexor tendon repair surgery, if a patient’s digit function is no longer improving
with occupational therapy and there is still substantial limitation in the active motion but passive motion
has been restored, tenolysis followed by immediate mobilization may release the adhesion and help to
gain full or near full active range of motion. However, tenolysis is a complicated procedure that can result
in neurovascular injury, worsening stiffness, and even tendon rupture; therefore, it should be
recommended only for patients with fair or poor outcomes. These risks should be thoroughly discussed
with the patient preoperatively. Similarly, IP joint contractures are initially managed with passive
stretching exercises and static progressive splinting. Beyond 4 to 6 months after the index procedure, joint
releases to correct the contractures can be considered. Rupture within the first 3 weeks of the initial
tendon repair warrants an attempt for repeat repair, which has reasonable success. If the rupture occurs
more than 3 weeks after the primary repair, tendon reconstruction should be considered.
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Tendon Reconstruction
Single-stage flexor tendon grafting can be used to reconstruct flexor tendon injuries that have significant
segmental tendon loss or damage, or those that present late and outside of the time window for primary
repair, or ruptures that occur after primary repair but are not amenable to repeat repair. Graft donor sites
include the palmaris, plantaris, long toe extensors, extensor indicis proprius and extensor digiti minimi,
and toe flexors. Alternatively, the proximal FDS or FDP tendon can be used as a graft depending on
which motor source the surgeon chooses to keep to power the tendon graft. Patients with extensive
scarring, joint contractures not responsive to aggressive hand therapy, and incompetent pulleys need
two-stage reconstruction.
The first stage in the two-stage reconstruction includes the placement of a silicone tendon implant in the
flexor tendon sheath, repair and/or reconstruction of the pulley system over the implant, and scar and
joint contracture release. This process promotes the formation of a pseudosheath over the silicone implant
in the next 3 months. During the second stage of the procedure, a tendon graft is passed through the
pseudosheath to replace the implant.
For either single-stage or two-stage flexor tendon grafting, the tendon graft is first repaired to the distal
phalanx either directly to the FDP tendon stump, or with a pull-through suture to secure the distal stump
in a drill hole in the distal phalanx and the suture tied over a button on top of the nail. After appropriate
tensioning, the proximal end of the tendon graft is repaired to the motor unit proximally to the remnant
FDS or FDP tendon stump. Early motion rehabilitation under close supervision of an experienced hand
therapist can be initiated in a similar fashion as that for primary repair, provided that the graft junctures
are strong.
In summary, flexor tendon injuries require early intervention. Understanding the biology of tendon
healing and the mechanics of the repair methods can direct treatment to improve functional outcomes. A
strong repair of the tendon ends with at least four-strand core sutures and an epitendinous suture
minimizes gap formation and creates a coaptation that tolerates early protective motion therapy to
promote healing and decrease adhesion formation. Chronic injuries are treated with tendon
reconstruction. Appropriately setting tension of the repair or reconstruction prevents the quadriga effect.
Modern surgical techniques, suture design, and postsurgical rehabilitation protocols have led to
satisfactory outcomes in these otherwise challenging injuries.
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Questions
1. A 20-year-old male presents at about 3 weeks after accidentally cutting his right index finger at the
distal interphalangeal joint. His clinical photo at presentation and initial radiographs are shown in
Figure 76.9. Upon finger exploration the distal tendon stump appeared to be 0.5 cm, and the
proximal tendon stump was found within the A4 pulley. Which of the following best describes his
injury and the treatment?
a. Zone 1 Leddy type 1 injury, primary repair with four-strand core sutures and an epitendinous
suture
b. Zone 1 Leddy type 2 injury, tendon-to-bone repair with nonabsorbable sutures tied over a
button
c. Zone 1 Leddy type 3 injury, tendon-to-bone repair with a suture anchor
d. Zone 2 injury, primary repair with four-strand core sutures and an epitendinous suture
e. Zone 2 injury, two-stage reconstruction
2. A 7-year-old girl presents with a laceration to the left index finger that occurred about 5 days
previously. Resting hand posture, initial radiographs, and photos from surgical exploration of the
finger are shown in Figure 76.10. What is the best treatment for her?
a. Tendon debridement
b. Tendon-to-bone repair with nonabsorbable sutures tied over a button
c. Primary repair with at least four-strand core sutures and an epitendinous suture
d. Single-stage reconstruction with a tendon graft
e. Two-stage reconstruction with a silicone rod followed by a tendon graft
3. A 32-year-old man presents with a nonfunctioning right small finger from an injury at the
proximal interphalangeal joint about 5 months ago. The clinical photo at presentation is shown in
Figure 76.11A, and Figure 76.11B–D are pictures from the surgical exploration of the finger, showing
the intact and competent tendon sheath. What is the best treatment for him?
a. Tendon excision
b. Tendon-to-bone repair of the injured tendon using a suture anchor
c. Primary repair with at least four-strand core sutures and an epitendinous suture
d. Single-stage reconstruction with a tendon graft
e. Two-stage reconstruction with a silicone rod followed by a tendon graft
4. A year after the surgery, the patient in question 3 developed loss of grip in his right small finger.
He is able to fully extend the small finger. However, when he attempted to make a fist, the proximal
and distal interphalangeal joints of the small finger extend instead. What is the likely cause of this
condition and what is the best treatment for him?
a. Adhesion causing stiffness; hand therapy and progressive static splinting to gain flexion
b. Rupture of the central slip; extension splinting at the proximal interphalangeal joint
c. Attritional rupture of the small finger FDP in the palm; end-to-side repair to the adjacent ring
finger FDP tendon
d. Quadriga effect; tendon lengthening
e. Progressive laxity in the tendon graft; lumbrical release
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FIGURE 76.9 Clinical photo and radiographs.
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FIGURE 76.10 Clinical and intraoperative photos, and radiographs.
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FIGURE 76.11 Clinical and intraoperative photos.
1. Answer: b. The clinical history, location of the laceration and proximal tendon stump, and the lack
of bony fragment on the radiographs suggest that this was a Zone 1 Leddy type 2 injury of the FDP.
The distal tendon stump was too short for primary repair, and therefore the best treatment was a
tendon-to-bone repair, which could be achieved with nonabsorbable sutures tied over a button or
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using a suture anchor.
2. Answer: c. The intraoperative photos suggest that this was an acute Zone 2 flexor tendon injury
with complete laceration of the FDP tendon, possibly also the FDS tendon. Tendon debridement is
only indicated for lacerations less than 50% of the tendon. Tendon-to-bone repair with nonabsorbable
sutures tied over a button is usually used to repair a Zone 1 injury. Tendon reconstructions are used
for more chronic injuries. This acute flexor tendon injury is best treated by primary repair using at
least four-strand core sutures and an epitendinous suture.
3. Answer: d. The clinical history and initial clinical photo suggest that this was a Zone 2 flexor
tendon injury involving both the FDP and FDS. Tendon excision will not restore finger flexion.
Tendon-to-bone repair with a suture anchor is usually used to repair a Zone 1 injury. The chronicity
of the injury makes the primary repair not appropriate because of degeneration of the tendon ends,
retraction of the proximal tendon stump, and scarring of the soft tissue. The intraoperative photos
demonstrate a competent pulley system, so the best treatment option among the choices is a single-
stage reconstruction with a tendon graft. Two-stage reconstruction is used when the tendon sheath is
so severely scarred that passing of a tendon graft is impossible.
4. Answer: e. The clinical scenario describes a lumbrical-plus finger, characterized by paradoxical
extension of the interphalangeal (IP) joints with active finger flexion, likely from progressive
lengthening of the tendon graft over time in this case. The lumbricals originate from the profundus
tendons and extend the IP joints while flex the metacarpophalangeal joints through pulling the
lateral bands. When there is laxity in the FDP tendon, the power of the proximal flexor muscle cannot
effectively pull the finger into flexion, and the lumbrical is pulled instead, causing extension of the IP
joints. The best treatment therefore is lumbrical release. Adhesions will not result in paradoxical IP
joint extension. Central slip rupture causes a Boutonniere deformity characterized by PIP flexion and
DIP extension. Attritional rupture of the small finger FDP can lead to a loss of finger flexor; however,
it will not result in paradoxical IP joint extension. The quadriga effect is a result of over shortening of
the FDP tendon during repair, limiting the ability of the adjacent fingers to fully flex, because the
FDP tendons to the long, middle, ring, and small fingers share a common muscle belly and the
shortest tendon determines the overall excursion.
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Acknowledgments
The work was supported by a Midcareer Investigator Award in Patient-Oriented Research (2 K24-
AR053120-06) to Kevin C. Chung. The content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institutes of Health.
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References
Lundborg, G, Myrhage, R, Rydevik, B. The vascularization of human flexor tendons within the digital synovial sheath region – structural
and functional aspects. 
 J Hand Surg. 1977;2(6):417-427.
Hagberg, L, Tengblad, A, Gerdin, B. Hyaluronic acid in flexor tendon sheath fluid after sheath reconstructions in rabbits: a comparison
between tendon sheath transplantation and conventional two stage procedures. Scand J Plast Reconst Surg Hand Surg. 1991;25(2):103-107.
Doyle, JR, Blythe, WF. Anatomy of the flexor tendon sheath and pulleys of the thumb. J Hand Surg. 1977;2(2):149-151.
Chow, SP, Yu, OD. An experimental study on incompletely cut chicken tendons – a comparison of two methods of management. J Hand Surg.
1984;9(2):121-125.
Verdan, CE. Half a century of flexor-tendon surgery: current status and changing philosophies. Bone Joint Surg Am. 1972;54(3):472-491.
Bunnell, S. Surgery of the Hand. 2nd ed. Philadelphia, PA: JB Lippincott; 1948.
Tang, JB. Flexor tendon repair in zone 2C. J Hand Surg. 1994;19(1):72-75.
Zhao, C, Amadio, PC, Zobitz, ME, An, KN. Resection of the flexor digitorum superficialis reduces gliding resistance after zone II flexor
digitorum profundus repair in vitro. J Hand Surg. 2002;27(2):316-321.
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.
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Mason, ML, Allen, HS. The rate of healing of tendons: an experimental study of tensile strength. Ann Surg. 1941;113(3):424-459.
Potenza, AD. Tendon healing within the flexor digital sheath in the dog. Bone Joint Surg Am. 1962;44-A:49-64.
Potenza, AD. Critical evaluation of flexor-tendon healing and adhesion formation within artificial digital sheaths. Bone Joint Surg Am.
1963;45:1217-1233.
Lundborg, G. Experimental flexor tendon healing without adhesion formation – a new concept of tendon nutrition and intrinsic healing
mechanisms: a preliminary report. Hand. 1976;8(3):235-238.Elegant animal study to demonstrate intrinsic healing of tendons.
Gelberman, RH, Vandeberg, JS, Manske, PR, Akeson, WH. The early stages of flexor tendon healing: a morphologic study of the first
fourteen days. J Hand Surg. 1985;10(6 Pt 1):776-784.
Berglund, M, Hart, DA, Wiig, M. The inflammatory response and hyaluronan synthases in the rabbit flexor tendon and tendon sheath
following injury. J Hand Surg Eur Vol. 2007;32(5):581-587.
Gelberman, RH, Khabie, V, Cahill, CJ. The revascularization of healing flexor tendons in the digital sheath: a vascular injection study in dogs.
Bone Joint Surg Am. 1991;73(6):868-881.
Boyer, MI, Watson, JT, Lou, J, et al. Quantitative variation in vascular endothelial growth factor mRNA expression during early flexor tendon
healing: an investigation in a canine model. J Orthop Res. 2001;19(5):869-872.
Harwood, FL, Monosov, AZ, Goomer, RS, et al. Integrin expression is upregulated during early healing in a canine intrasynovial flexor
tendon repair and controlled passive motion model. Connect Tissue Res. 1998;39(4):309-316.
Manske, PR, Gelberman, RH, Lesker, PA. Flexor tendon healing. Hand Clin. 1985;1(1):25-34.
Taras, JS, Raphael, JS, Marczyk, SC, Bauerle, WB. Evaluation of suture caliber in flexor tendon repair. J Hand Surg. 2001;26(6):1100-1104.
Thurman, RT, Trumble, TE, Hanel, DP, et al. Two-, four-, and six-strand zone II flexor tendon repairs: an in situ biomechanical comparison
using a cadaver model. J Hand Surg. 1998;23(2):261-265.Biomechanical study in cadavers to demonstrate increased repair strength with increased
number of core sutures.
Strickland, JW. Flexor tendon injuries: I. Foundations of treatment. J Am Acad Orthop Surg. 1995;3(1):44-54.Classic review on flexor tendon
anatomy, biology, biomechanics, and treatment after injuries.
Osei, DA, Stepan, JG, Calfee, RP, et al. The effect of suture caliber and number of core suture strands on zone II flexor tendon repair: a study
in human cadavers. J Hand Surg. 2014;39(2):262-268.
Chung, KC. Operative Techniques: Hand and Wrist Surgery. 3rd ed. Philadelphia, PA: Elsevier; 2018.
Hotokezaka, S, Manske, PR. Differences between locking loops and grasping loops: effects on 2-strand core suture. J Hand Surg.
1997;22(6):995-1003.
Pruitt, DL, Aoki, M, Manske, PR. Effect of suture knot location on tensile strength after flexor tendon repair. J Hand Surg. 1996;21(6):969-973.
Lotz, JC, Hariharan, JS, Diao, E. Analytic model to predict the strength of tendon repairs. J Orthop Res. 1998;16(4):399-405.Biomechanical study
to establish the added repair strength with an epitendinous suture.
Merrell, GA, Wolfe, SW, Kacena, WJ, et al. The effect of increased peripheral suture purchase on the strength of flexor tendon repairs. J Hand
Surg. 2003;28(3):464-468.
Gelberman, RH, Boyer, MI, Brodt, MD, et al. The effect of gap formation at the repair site on the strength and excursion of intrasynovial
flexor tendons: an experimental study on the early stages of tendon-healing in dogs. Bone Joint Surg Am. 1999;81(7):975-982.Animal study
that established acceptable gap formation for tendon repair.
Leddy, JP, Packer, JW. Avulsion of the profundus tendon insertion in athletes. 
 J Hand Surg. 1977;2(1):66-69.Classification system of Zone 1
flexor tendon injury.
Gelberman, RH, Manske, PR, Akeson, WH, et al. Flexor tendon repair. J Orthop Res. 1986;4(1):119-128.
Duran, RJ, Houser, RG, Coleman, CR, Postlethwait, DS. A preliminary report in the use of controlled passive motion following flexor tendon
repair in zones II and III. J Hand Surg. 1976;1(1):75-83.Principles for the Duran Protocol after flexor tendon repair.
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Silva, MJ, Brodt, MD, Boyer, MI, et al. Effects of increased in vivo excursion on digital range of motion and tendon strength following flexor
tendon repair. J Orthop Res. 1999;17(5):777-783.
Boyer, MI, Gelberman, RH, Burns, ME, et al. Intrasynovial flexor tendon repair: an experimental study comparing low and high levels of in
vivo force during rehabilitation in canines. Bone Joint Surg Am. 2001;83-A(6):891-899.
Trumble, TE, Vedder, NB, Seiler, JG III, et al. Zone-II flexor tendon repair: a randomized prospective trial of active place-and-hold therapy
compared with passive motion therapy. Bone Joint Surg Am. 2010;92(6):1381-1389.Level I evidence comparing active place-and-hold with passive
motion therapy.
Kleinert, HE, Verdan, C. Report of the committee on tendon injuries (International Federation of Societies for Surgery of the Hand). J Hand
Surg. 1983;8(5 Pt 2):794-798.American Society for Surgery of the Hand determination of total active motion of the digit.
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C H A P T E R 7 7
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Extensor Tendon Repair and Reconstruction
Amir H. Taghinia and A. Samandar Dowlatshahi
Key Points
The extrinsic extensors of the digits are innervated by branches of the radial nerve and primarily
mediate metacarpophalangeal (MP) joint extension.
The intrinsic extensors of the digits are innervated by the ulnar and median nerves and primarily
mediate MP joint flexion and interphalangeal (IP) joint extension.
At the digit level, minimal tendon excursion translates into substantial change in joint position.
Redundancies in the extensor system, such as the juncturae tendinae, can initially mask injury.
Extensor injuries are classified by zones starting at the distal interphalangeal (DIP) joint (zone 1) and
sequentially progressing proximally.
Acute closed injuries of the digital extensor system are best treated with splinting; however, open
injuries usually require exploration and repair if the injury is substantial.
The mainstay of rehabilitation at the digital level (zones 1–4) remains static splinting; however, early
motion protocols have shown promising results in more proximal injuries (zones 5–8).
The extensor apparatus is a well-balanced system of interlinking tendons and fibroligamentous bands
that orchestrate the fine positional movements of each digit. As opposed to flexor tendons, extensors
exhibit minimal excursion, especially in the digits. Seemingly negligible position changes in the extensor
mechanism can translate into large degrees of motion in the digits. Thus, even minor disruptions of the
delicate balance of these tendons can cause significant functional deficits. Due to the superficial position
of extensor tendons, they are vulnerable to injury and exposure. Nevertheless, the phylogenetic evolution
of the extensor apparatus has led to interconnections and duplications that allow functional redundancy.
This 
 redundancy can compensate for acute injury to one of the parts and lead to misdiagnosis. Once
edema has subsided, and secondary support structures have fatigued, clinically significant deformity and
functional loss become evident. This combination of factors—redundancy and late manifestation—along
with significant anatomic variation in the extensor system makes accurate diagnosis difficult, but
crucially important.
After repair, the proximity of the tendons to bone, the high incidence of associated periosteal stripping
and capsular injuries, and the limited excursion of the extensors makes repair prone to adherence.
Furthermore, the mechanical strength of the repair and status of local soft and hard tissues may not allow
early mobilization. The stronger opposing action of the flexor system makes early rehabilitation even
more problematic. Although not always preventable, stiffness and adhesions can be minimized with
meticulous surgical technique and rational rehabilitation protocols. Associated injuries to the thin soft
tissue cover of the dorsum of the hand need to be treated concomitantly because they have a direct
impact on functional outcomes.
This chapter will discuss the anatomy and physiology of the extensor mechanism of the hand as well as
injury patterns, repair strategies, and rehabilitation protocols. The importance of an in-depth anatomical
understanding of this complex system cannot be overstated. Anatomy helps the reader to diagnose injury
patterns understand the logic behind repair and rehabilitation.
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Clinical Anatomy and Function
An appreciation of the fine mechanics and physiology of the extensor apparatus goes well beyond
descriptive anatomy. The system is composed of unsheathed extrinsic and intrinsic tendons aided by
retinacular structures and stabilized by periarticular constituents. Extension of the fingers follows a
slightly different mechanism than the thumb. Full finger extension occurs because of a coordinated
proximal to distal contraction of extrinsic and intrinsic muscles that set up an integrated series of
tenodesis actions via fibroligamentous interconnections. There is no better way to demonstrate the
tenodesis action of these interconnections than to passively flex the wrist. This action relaxes the long
digital flexors and stretches the extensors. Performing this passive tenodesis examination in an injured
hand is one of the best ways to diagnose an extensor tendon injury, especially proximal to the
metacarpophalangeal (MP) joint (Figure 77.1).
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FIGURE 77.1 Wrist tenodesis. This 2-year-old girl sustained a laceration on the dorsum of the small finger MP joint. In this age
group, assessing active motion is difficult. Relying on the tenodesis effect, maximal flexion of the wrist demonstrates lack of
extensor tone in the small finger (A), and exploration confirms a tendon laceration at zone 5 (B). C. Figure-of-eight braided
absorbable sutures were used to repair the tendon and the hand was immobilized in a cast for 3 weeks. D, E. Full active range
of motion is demonstrated 6 months after the repair with minimal hand therapy. Similar injuries in adults can be treated with
core and cross-stitch sutures with early mobilization.
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Extrinsic System
The extrinsic extensor muscles are so called because they are located outside the anatomic boundaries of
the hand. They are innervated by branches of the radial nerve or posterior interosseous nerve (PIN). The
radial nerve proper innervates (in order) the brachioradialis (BR), extensor carpi radialis longus (ECRL),
and (sometimes) extensor carpi radialis brevis (ECRB) muscles. BR is not a wrist or digital extensor—it
flexes the elbow. ECRL and ECRB are both wrist extensors (Table 77.1). BR and ECRL are innervated
above the elbow, whereas ECRB is innervated below the elbow. Thus, a radial nerve laceration at or
below the elbow is likely to maintain wrist extensor function.
TABLE 77.1
Extrinsic Extensors of the Hand and Wrist
Muscle
Origin
Insertion
Innervation
Function
Extensor
Compartment
Extensor carpi
radialis longus
(ECRL)
Lateral supracondylar ridge of
humerus
Dorsal base of
second metacarpal
Radial
nerve
Wrist extension and
radial deviation
2
Extensor carpi
radialis brevis
(ECRB)
Lateral epicondyle of humerus
Dorsal base of third
metacarpal
Radial
nerve
Wrist extension
2
Extensor carpi
ulnaris (ECU)
Lateral epicondyle of humerus and
posterior border of ulna
Dorsal base of fifth
metacarpal
PIN
Wrist extension and
ulnar deviation
6
Extensor digitorum
communis (EDC)
Lateral epicondyle of humerus
Finger extensor
shroud
PIN
Finger MP joint
extension
4
Extensor indicis
proprius (EIP)
Posterior surfaces and ulna and
interosseous membrane
Index finger extensor
shroud
PIN
Index finger MP joint
extension
4
Extensor digiti
minimi (EDM)
Lateral epicondyle of humerus
Small finger extensor
shroud
PIN
Small finger MP joint
extension
5
Abductor pollicis
longus (APL)
Posterior surfaces of ulna, radius,
and interosseous membrane
Base of thumb
metacarpal
PIN
Thumb abduction,
extension at CMC
joint
1
Extensor pollicis
brevis (EPB)
Posterior surfaces of radius and
interosseous membrane
Thumb extensor
shroud
PIN
Thumb MP joint
extension
1
Extensor pollicis
longus (EPL)
Posterior surfaces and ulna and
interosseous membrane
Thumb dorsal base
of distal phalanx
PIN
Thumb IP joint
extension,
retropulsion
3
CMC, carpometacarpal; IP, interphalangeal; MP, metacarpophalangeal; PIN, posterior interosseous nerve.
All other extrinsic extensor muscles are innervated by the PIN, a branch of the radial nerve. The
musculotendinous junctures of these tendons start at the mid to distal forearm. The most distal muscle
belly, which occasionally extends beyond the carpus, is the extensor indicis proprius (EIP). This is the last
muscle to receive innervation from the PIN, and thus the last to recover after a nerve injury. At the level
of the wrist, the tendons are stabilized by a synovial-lined sheath termed the extensor retinaculum. This
retinaculum is composed of horizontal fibers that form an overarching system of tunnels spanning the
dorsal wrist and acting as a pulley to prevent bowstringing. Vertical, fibrous septae separate the tunnel
into six individually numbered compartments (Figure 77.2).
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FIGURE 77.2 Illustration of the dorsal extensor system shows the extensor retinaculum covering the extensor tendons at the
wrist. Under the retinaculum, the extensors traverse six compartments numbered sequentially: (1) APL and EPB, (2) ECRL and
ECRB, (3) EPL, (4) EIP and EDC, (5) EDM, and (6) ECU. The juncturae tendinae connect the finger extensor tendons on the
dorsum of the hand; there are no juncturae that link to the thumb extensors. In most cases, the ring finger sends connections to
the middle and small fingers; but the connection between the index and middle fingers can be variable.
(Reproduced with permission from Shoshana, W. Ambani, SW, Chung, KC. Rheumatoid arthritis of the hand and wrist. In: Chung, KC , ed. Operative
Techniques in Plastic Surgery. Philadelphia, PA: Wolters Kluwer; 2019. Part 6, Figure 24-4.)
The extensor digitorum communis (EDC) is the shared extensor (with a common muscle belly) for all four
fingers. It travels through the fourth extensor compartment along with the EIP, the independent extensor
of the index finger. The EIP extends the index finger independently of the other digits, hence inviting its
moniker pointer finger. The only other independent finger extensor is the extensor digiti minimi (EDM)
(also named extensor digiti quinti) that is the sole tendon in the fifth extensor compartment. These two
independent tendons provide redundancy of finger extension, thus making them suitable for tendon
transfers. They typically lie ulnar to the EDC at the level of the MP joints.
At the distal metacarpal level, the extensors of the fingers are often connected by oblique tendinous
connections termed juncturae tendineae (see Figure 77.2). At the MP joint, the extrinsic tendons attach to
the sagittal bands, specialized retinacular fibers that encircle the MP joints and insert onto the volar plates
(Figure 77.3). These transverse laminar fibers provide radioulnar stability, effectively centralizing the
tendon over the convexity of the metacarpal head. The attachments of the extrinsic finger extensors onto
these structures make them effective extensors of the MP joints, which are not intuitive, because they do
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not directly insert onto the proximal phalanges. 1
FIGURE 77.3 Finger extensor apparatus. Dorsal (A) and lateral (B) anatomic illustrations of the finger extensor apparatus.
(Reproduced with permission from Smith, MD, Machol, JA IV, Chen, NC. Acute repair of extensor tendon injuries in zones I to VI. In: Chung, KC , ed.
Operative Techniques in Plastic Surgery. Philadelphia, PA: Wolters Kluwer; 2019. Part 6, Figure 41-1B and Figure 41-1C.)
Thumb extension is primarily mediated by the extensor pollicis longus (EPL). As it travels through the
third extensor compartment, it makes a sharp radial turn around Lister tubercle (a dorsal bony
prominence of the radius) and heads towards the thumb. This tendon forms the dorsal boundary of the
anatomic snuffbox. It facilitates thumb interphalangeal (IP) joint extension but its most direct action is
retropulsion (the act of lifting one’s thumb off a table while keeping the palm resting flat) (Figure 77.4).
The extensor pollicis brevis (EPB) and abductor pollicis longus (APL) travel through the first dorsal
compartment; their action is to extend the thumb MP and carpometacarpal (CMC) joints, respectively.
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FIGURE 77.4 Retropulsion. The ideal way to test the EPL is by asking the patient to rest the hand, palm down, on a flat
surface and lift the thumb.
There is significant variation in extrinsic extensor tendon anatomy. The more common variants and their
clinical relevance are outlined in Table 77.2.
TABLE 77.2
Surgically Relevant Anatomical Pearls
Anatomical Variant
Surgical Relevance
The first extensor compartment is partially divided by a fibrous septum
in 29% of the population, and by a bony septum in 5%. Complete
separation has been observed in 8.5% of cases.
During release of the first extensor compartment for de
Quervain’s syndrome, all subcompartments must be identified
and released
An extensor carpi radialis intermedius (ECRI) is present in 12% of
limbs, located either radial to ECRL or in between ECRL and ECRB
The ECRI can be used as a tendon graft or in tendon transfers
involving the radial wrist extensors
The EIP is absent in 4% of individuals. Its muscle belly extends further
distal than other extensor tendons. It is located ulnar and volar to EDC
of the index finger.
The EIP is often used for tendon transfers, either after EPL
spontaneous rupture or for opponensplasty. Anatomic
differences can help more easily localize the tendon.
An extensor medii proprius (EMP) is the middle finger equivalent of
the EIP and is present in 10% of individuals.
The EMP, if present, can be used for tendon transfers.
The extensor indicis et medii communis is a variant of EIP that inserts
onto the index and middle fingers.
The muscle belly can be hypertrophic to the point where it is
mistaken for a ganglion cyst. It can complicate a planned EIP
tendon transfer.
The extensor digitorum brevis manus muscle is an anomalous dorsal
muscle, present in 3% of hands, which arises distally on the wrist
between the index and middle finger metacarpals.
This muscle can be mistaken for a ganglion cyst.
The EDM is doubled in 72% of cases.
This redundancy allows the tendon to be used for tendon grafts
or additional tendon transfers.
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Intrinsic System
The intrinsic muscles originate and insert within the anatomic boundaries of the hand. For the extensor
apparatus, these muscles are the interossei and the lumbricals. There are seven interosseous muscles, four
dorsal, and three volar. They are all innervated by the deep branch of the ulnar nerve. In addition to
abducting (dorsal interossei) and adducting (volar interossei) the fingers, the interossei are the primary
flexors of the finger MP joints. They course dorsal to the deep transverse metacarpal ligament and insert
into the digital lateral bands (see Figure 77.3).
The lumbrical muscles are unique in that they originate from the finger profundus flexor tendons. There
are four lumbrical muscles in the hand, one for each finger, and they lie on the radial side of the
respective flexor tendon. They course volar to the deep transverse metacarpal ligament before attaching to
the radial lateral band of the respective finger. The median nerve innervates the lumbrical muscles of the
index and middle fingers, and the ulnar nerve innervates those of the ring and small fingers.
The intrinsic extensor tendons lie volar to the axis of rotation of the MP joint and dorsal to the axis of
rotation of the IP joints. Thus, they cause the MP joints to flex and the IP joints to extend. These
musculotendinous units are maximally stretched (taut) when the MP joint is passively extended and the
PIP joint is simultaneously flexed. They are maximally lax when the MP joint is passively flexed and the
PIP joint is extended (Figure 77.5). Intrinsic muscle action is also responsible for volumetric grip that
starts with coordinated MP joint flexion and simultaneous IP joint extension. 2 Patients with combined
lower median and ulnar nerve palsy are unable to perform volumetric grip, and instead initiate finger
flexion at the IP joints, curling the fingers towards the palm utilizing the extrinsic flexors.
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FIGURE 77.5 Intrinsic tightness. The intrinsic muscles flex the MP joints and extend the PIP joints of the fingers. In the passive
posture of maximal MP joint flexion and PIP extension, these muscles are fully lax. In contrast, the opposite passive posture of
maximal MP joint extension and PIP flexion puts them at peak stretch. When the intrinsic muscles are contracted or tight,
achieving this second posture is difficult. A. Intrinsic tightness can be demonstrated if the PIP joint cannot be easily flexed when
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the MP joint is held in extension. B. Flexing the MP joint and confirming normal PIP joint flexion rules out a problem with the PIP
joint.
The intrinsic muscles of the thumb are mainly involved in rotational motion. However, both the adductor
pollicis (ulnar) and the abductor pollicis brevis (radial) insert onto the EPL tendon at the MP joint level,
which along with the EPB, gives them the ability to extend the IP joint of the thumb at least to neutral,
thus potentially obscuring an EPL injury.
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Digital Extensor System
Just distal to the sagittal bands, the extrinsic extensor system splits into a central slip and two lateral slips
(see Figure 77.3). 3 Distal to this trifurcation, there is a crossing of fibers from the lateral bands to the
central slip and vice versa. The myriad of crisscrossing fibers create a contiguous coalescence of fibers
termed the extensor hood. The central slip then terminates as it inserts onto the dorsal base of the middle
phalanx.
The lateral slips pass on either side of the PIP joint and merge with the lateral bands forming the
conjoined lateral bands. These bands then course dorsally and join the triangular ligament on either side,
ultimately uniting to form the terminal tendon that inserts onto the dorsal base of the distal phalanx.
At the PIP joint level, the transverse retinacular ligament tethers and stabilizes the extensor mechanism,
not dissimilar to the sagittal bands at the MP level. The oblique retinacular ligament (ORL, of Landsmeer)
arises from the lateral aspect of the flexor tendon sheath at the neck of the proximal phalanx (A2 pulley)
and passes volar to the axis of rotation of the PIP joint, inserting onto the extensor mechanism along the
middle phalanx. Although previously thought to link PIP and distal interphalangeal (DIP) motion, the
ORL has been found to be variably present and often attenuated—its role remains controversial. 3-5
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Extension Function
MP joint extension is primarily mediated by the extrinsic extensor tendons. Historically, it was thought to
be mediated by the sagittal bands as they lasso around the base of the proximal phalanx. However, more
recent evidence suggests that the extensor continuation to the extensor hood and middle phalanx is the
major mediator of MP extension. 6 Interphalangeal joint extension is more complex and requires the
interplay of both intrinsic and extrinsic systems (Figure 77.6).
FIGURE 77.6 Coordinating IP joint motion. A. When the MP joint is flexed, the extrinsic extensors are rendered tighter while
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the intrinsic interosseous-lumbrical system is lax and redundant. The lax structures are not able to generate significant force in
this situation. Thus, IP joint extension is mediated by the extrinsic system when the MP joint is flexed. In contrast, when the MP
joint is extended, the extrinsic system becomes lax and less effective. B. Meanwhile, MP joint extension tightens the intrinsic
tendons, thus making them better IP joint extensors. In summary, extensor action on the IP joints is mediated by the extrinsic
system when the MP joint is flexed and by the intrinsic system when the MP joint is extended.
Digital extensor tendon excursion is much wider at the forearm and wrist level than the digit. The
excursion of a common extensor proximal to the wrist is approximately 5 cm. The excursion of the
extensor mechanism at the PIP joint level is only a few millimeters, despite a PIP joint arc of motion of
100°. 7 Every millimeter of extensor tendon lengthening over the proximal phalanx leads to 12° of
extension deficit at the PIP joint. 8 Any small disturbance of this delicate balance causes deformity that
can be progressive and difficult to correct. Similar issues plague the DIP joint where each millimeter of
relative terminal tendon lengthening results in 25° of extension lag. 9
The interlinkages of the extensor mechanism have further pathophysiologic implications. Normal
function relies on individual tendons acting about the axis of rotation of multiple joints, and on
stabilization of joints between where the axial force is generated and where it is intended to act. If one
interlinkage is disrupted, this derangement causes (progressive) reciprocal deformity of adjacent joints.
This phenomenon is seen in boutonnière, swan-neck, and so-called zig-zag deformities, where
injury/deformity in one joint pathologically alters the position of an adjacent joint.
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Clinical Assessment
The clinical assessment of a patient with suspected extensor deficit or derangement requires thorough
knowledge of the anatomical and mechanical features of extensor function. Cross-functionality of the
extensor mechanism can mask serious injury that may manifest later as recalcitrant chronic deformity.
The best way to diagnose injury is to assess function distal to the level of the injury. This is especially
relevant in the hand, wrist, and forearm where retraction of the proximal tendon ends may obscure
visualization.
In the fingers, accurate diagnosis can be made by exploring an acute wound in the emergency room (ER).
Extensors in this area are superficial and will not retract much. However, one needs adequate lighting,
retraction, and hemostasis because small wounds with venous bleeding can obscure injury. When in
doubt, one should close the wound, apply a splint, and reexamine in a few days.
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Injury Patterns, Repair, and Rehabilitation
Extensor tendon injuries are classified based on location. Kleinert and Verdan 10 initially delineated these
zones from 1 to 8, and Doyle 11 later added a ninth zone for the muscular area of the mid to proximal
forearm. The zones start at the DIP joint and progress proximally. Odd numbers are over joints and even
numbers in between. There are separately numbered zones for the thumb (Figure 77.7).
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FIGURE 77.7 Zones of extensor muscle and tendon injury. These are numbered from I to IX starting at the DIP joint and
progressing proximally. Zone I is over the DIP joint, zone II is over the middle phalanx and so on. Zone IX is located in the
forearm proximal to zone VIII (not shown).
These zones are significant because they require different approaches for repair and rehabilitation. A
detailed outline of injury patterns and repair paradigms will follow. However, certain generalizations
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about rehabilitation are worth mentioning first. Rehabilitation of zone 1 and 2 injuries requires static
splinting for 6 weeks followed by night splinting and range of motion exercises. More proximal injuries
were traditionally treated by 3 to 4 weeks of static splinting followed by controlled motion. This approach
may increase adhesions particularly in those with multiple concomitant injuries that involve bone and
other soft tissue, as the tendon forms scars to adjacent structures during healing. Early controlled motion
using dynamic splinting has shown promising results for zone 4 to 7 injuries, and may be especially
suited for patients who are compliant and have associated bony and soft tissue injuries. 12-14 The idea is
that early controlled gliding of the tendon will break up impending adhesions while minimizing risk of
rupture. Dynamic splinting protocols are just as effective as early active motion protocols with less risk of
tendon rupture. 15,16 More proximal injuries in zones 8 and 9 carry the least risk of adhesions and can be
treated with static splinting for 3 to 4 weeks.
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Zone 1
Disruption of the terminal extensor tendon from the base of the distal phalanx results in a mallet finger
injury. The mechanism is either an open injury, or more commonly by closed rupture with or without
associated fracture of the distal phalanx. Sudden, resisted flexion of the DIP joint is the leading cause. The
terminal tendon usually inserts onto a thin area on the dorsal/proximal aspect of the distal phalanx. This
area corresponds to the dorsal ledge of the epiphysis prior to skeletal maturity.
The DIP joint is held in a flexed posture with decreased or absent active extension (Figure 77.8).
Compensatory hyperextension at the PIP joint (swan-neck deformity) can occur acutely in patients with
congenital or traumatic PIP volar plate laxity. Elderly patients with osteoarthritis can present with a
mallet deformity that is atraumatic.
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FIGURE 77.8 Type I (closed) bony mallet finger. A. Clinical posture of the digit after injury shows extension lag at the DIP joint.
B. A small bony fragment, still attached to the terminal tendon, has been separated from the distal phalanx. Most mallet injuries
present in this way with or without a small avulsion fracture.
Radiographs are necessary to rule out a fracture of the distal phalanx, and need to be appropriately
centered on the involved digit. The lateral view is critical, to assess joint congruity and subluxation.
Fractures are often missed on the anteroposterior view alone. Injuries presenting within 4 weeks of
trauma are considered acute; after 4 weeks, they are chronic. If left untreated, hyperextension of the PIP
joint can develop because of proximal and dorsal migration of the lateral bands, 17 creating the swan-neck
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deformity.
Doyle and others classified mallet finger injuries into four types. 11 Table 77.3 outlines this classification
and the treatment algorithm for each type of injury. Closed injuries without subluxation encompass the
great majority of mallet injuries (types I and IVb). These injuries are best treated with continuous
splinting of the DIP joint in extension for 6 weeks, followed by 2 weeks of night splinting. Splinting must
be continuous. If at any time the patient is to remove the splint (e.g., for hygiene), it must be rested
against a flat surface to ensure continuous extension of the DIP joint. Splinting in extreme hyperextension
or placing the splint too tightly can cause dorsal skin necrosis. Different types of splints (aluminum foam,
premade plastic, or custom-made thermoplastic) placed volar or dorsal have been used in the literature,
with comparable outcomes. 18,19 The main predictor of long-term extension lag appears to be compliance
with splinting. The authors recommend a dorsal aluminum foam splint with the DIP joint in slight
hyperextension. Active PIP joint motion is encouraged.
TABLE 77.3
Doyle Classification of Mallet Injury
Type
Description
Treatment
Pearls and Pitfalls
I
Closed injury, with or
without small dorsal
avulsion fracture
8 wk continuous splinting with DIP in full
extension, PIP free.
If extensor lag is evident at
8 wk, then resume splinting
until extensor lag is resolved.
After 8 wk, initiate
splint weaning and
controlled active
motion under
therapist guidance.
Look for skin maceration and breakdown.
II
Open injury with
laceration to the terminal
extensor
Surgical tendon repair with running suture
incorporating skin and tendon, and transfixation of
DIP joint with axial or oblique 0.045 in K wire for
6 wk followed by night time splinting for 4 wk.
Beware of bulky suture material
that can become symptomatic
and extrude. The DIP joint is
invariably open and needs to be
washed out.
III
Open injury with loss of
skin and/or tendon
substance
Primary repair if possible. Positioning of DIP joint
in hyperextension is permissible if allows for
apposition of tendon ends. May require
homodigital or cross-finger flap for coverage with
or without tendon graft.
Consider staged reconstruction:
soft tissue, then tendon
reconstruction.
IV A
Transepiphyseal plate
fracture in children
(Seymour’s fracture)
Requires operative washout, reduction and
antibiotic coverage. Longitudinal K wire often
necessary.
Dislocated nailplate often
present. Untreated Seymour
fracture can lead to
osteomyelitis.
IV B
Hyperflexion injury with
20%–50% fracture of
articular surface
Operative and conservative methods of treatment
are acceptable based on current literature, even in
the presence of volar subluxation of the distal
phalanx. Operative treatment consists of extension
block pinning.
Patients are always advised that
they may have a permanent
dorsal bump with either
surgical or nonsurgical
treatment.
IV C
Hyperextension injury
with >50% fracture of
articular surface with early
or late volar subluxation
of distal phalanx
Residual extensor lag of 5° to 10° is common, despite adequate treatment and patient compliance (Figure
77.9). Erythema and swelling over the dorsal aspect of the DIP joint can last several months.
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FIGURE 77.9 Type II (open) mallet finger. A. Clinical posture of the digit shows a more significant extension lag than typically
seen in a closed mallet injury. B. Dorsal view demonstrates a healing laceration over the DIP joint. C. Repair was performed
with a running stitch and protected with a longitudinal pin. D. Three months postoperatively, the finger demonstrates mild
extension lag as can be seen often in these cases despite timely and adequate repair. Even a miniscule amount of tendon
lengthening in this area translates to significant extension lag.
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Chronic Mallet Injuries
There is no formal time cut off for closed treatment with splinting. Tenderness and inflammation over the
DIP extensor surface are considered to be relative indications for closed treatment, even several months
after injury. Surgical options include direct tendon repair with or without skin imbrication
(tenodermodesis), tendon rebalancing with a central slip tenotomy (Fowler tenotomy), ORL
reconstruction, or DIP joint arthrodesis.
Technique of skin imbrication/tenodermodesis: An elliptical wedge of skin and scarred tendon is excised.
20 The closure incorporates both skin and tendon as a single unit. A Kirschner wire maintains the
joint in full extension for 6 weeks.
Fowler tenotomy/central slip tenotomy: At least 6 to 12 months are required since injury to allow the
terminal tendon to mature. The principle underlying this procedure is a release of the central slip,
allowing the now centrally untethered lateral bands to move proximally and reduce the slack within
the extensor system distal to the PIP joint, correcting the extensor lag at the DIP joint. A boutonnière
deformity is prevented by keeping the triangular ligament intact. The release is performed from
underneath the extensor system via a midaxial incision. Passing a freer elevator underneath the
lateral bands ensures that any adhesions are released so that they can glide freely.
Spiral ORL reconstruction: This procedure links the position of the PIP joint to that of the DIP joint.
Performed with a tendon graft 21,22 or a lateral band, 23 it links the terminal tendon or distal phalanx to
the flexor tendon sheath or proximal phalanx, leading to a dynamic tenodesis (Figure 77.10).
FIGURE 77.10 Spiral oblique retinacular ligament reconstruction. A. The swan-neck posture of a mallet deformity is shown
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with lax lateral bands and PIP volar plate. B, C. The tendon graft is secured to the distal phalanx with a pull out suture that is
brought volarly and stabilized with a button. It is routed adjacent to the flexor sheath volar to the PIP joint, and then anchored to
the side of the proximal phalanx (Thompson) or the flexor sheath (Kleinman and Peterson). Extension of the PIP puts tension
on the graft, resulting in extension of the DIP. Flexion of the PIP relaxes the graft and allows flexion of the DIP.
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Posttraumatic Swan-Neck Deformity
A swan-neck deformity is flexion of the DIP joint with hyperextension of the PIP joint. It occurs after a
traumatic (untreated) mallet finger when the PIP volar plate is lax. It is important to ascertain whether the
deformity is primarily due to PIP joint laxity or DIP extension lag; this is done by blocking PIP
hyperextension and assessing active DIP extension. With PIP hyperextension blocked, if the DIP can be
actively extended fully, then the main problem is PIP laxity. Otherwise, the main problem is DIP
extension deficit. For PIP joint laxity, one should attempt conservative treatment with figure-of-eight
splinting. If that is not effective, then volar plate imbrication or FDS tenodesis may work. If the primary
issue is DIP extension deficit, then ORL reconstruction or Fowler tenotomy are advocated. Joints should
be supple before operative correction is attempted.
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Zone 2
These injuries are located over the middle phalanx and are usually sharp. They can involve the two
conjoined lateral bands and the triangular ligament that restrains them in the dorsal midline. Only one
lateral band is sufficient to achieve full extension of the DIP joint. If the injury involves less than 50% of
the extensor mechanism, then routine wound care and splinting for 7 to 10 days is sufficient treatment,
followed by active motion. If greater than 50% of the tendon is cut, then primary repair and a longer
period of immobilization is indicated. The extensor system at this level is thin and cannot carry a core
suture. A simple running nonabsorbable 5-0 suture can be augmented with a running cross-stitch (e.g.,
Silfverskiöld; Figure 77.11). PIP motion is permitted postoperatively. The DIP joint is held in extension for
6 weeks after which active motion can commence. Chronic zone 2 injuries can be treated with spiral ORL
reconstruction, as in chronic mallet injuries.
FIGURE 77.11 Extensor tendon repair techniques. A. The Silfverskiöld cross-stitch technique is demonstrated for a zone 2
injury. More proximal injuries can be repaired with 2 to 4 core sutures and augmented with the cross-stitch using a finer
monofilament suture (B). Repair of a T-2 thumb extensor injury is demonstrated with core Ethibond suture (green) and
Silfverskiöld cross-stitch (C).
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Zone 3
As in mallet injuries, zone 3 injuries can be open lacerations or closed ruptures, the latter with or without
avulsion fracture of the middle phalanx. The injury may result in PIP joint extension deficit and DIP joint
hyperextension, the so-called boutonnière deformity. In the setting of an isolated (closed) central slip
injury, PIP joint extensor lag is usually not present at first. The intact lateral bands and triangular
ligament maintain an extension moment on the PIP joint due to their position dorsal to the PIP joint
rotation axis. However, the extension torque gets shifted completely to the lateral bands, and over several
weeks the restraining triangular ligament stretches out, thereby allowing volar translation and shortening
of the lateral bands. This in turn increases direct pull at the terminal extensor tendon, leading to
hyperextension of the DIP joint (Figure 77.12), and the boutonnière posture. 24,25 Concomitant injury to
adjacent structures may also be necessary to cause a boutonnière deformity. 26
FIGURE 77.12 Development of boutonnière deformity. A. The central slip is disrupted from the base of the middle phalanx
leading to all extensor forces being concentrated into the lateral bands. B. The lateral bands slip volarly and become flexors of
the PIP joint and hyperextensors of the DIP joint.
(Reproduced with permission from Shoshana, W. Ambani, SW, Chung, KC. Rheumatoid arthritis of the hand and wrist. In: Chung, KC , ed. Operative
Techniques in Plastic Surgery. Philadelphia, PA: Wolters Kluwer; 2019. Part 6, Figure 24-7A.)
A more reliable test for central slip disruption was suggested by Elson (Figure 77.13). 27 This test is found
to be the most sensitive test for diagnosing acute central slip disruption. 28 In clinical practice, the
aforementioned tests are difficult to perform in the acute setting because of pain and swelling. A digital
block may be helpful to do a proper Elson test. In suspected cases where the examination is inconsistent
or unreliable, the clinician should splint the PIP in extension and reexamine after a week once swelling
and pain have subsided.
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FIGURE 77.13 Elson test. With the finger held at 90° of PIP joint flexion against a right-angled surface (such as the end of a
table), active extension is tested. If the central slip is intact, the DIP joint should have very little active extension ability (flail). A.
This is because an intact central slip will draw the origin of the lateral bands distally. B. However, if the central slip is disrupted,
the proximal migration of the lateral bands stretches them and allows active DIP joint extension.
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Closed Central Slip Injury
Treatment of a closed central slip rupture with or without boutonnière deformity consists of splinting or
pinning the PIP joint in full extension for 6 weeks, followed by an additional 4 to 6 weeks of protective
splinting. The patient performs active DIP flexion and extension exercises to keep the lateral bands
gliding. In patients with a boutonnière deformity, active DIP flexion helps to pull the lateral bands back
into a more dorsal and central position thus correcting the deformity. When treated early in a compliant
patient, the injury will usually respond to this conservative approach.
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Closed Central Slip Injury with Associated Avulsion Fracture
Depending on the size of the fracture, these can also be treated closed. Larger fragments can be repaired
by Kirschner wire or screw fixation. In the presence of comminution, the fragment(s) can be excised and a
tendon-to-bone juncture performed.
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Open Zone 3 Injury
A traumatic PIP arthrotomy is usually present and requires joint irrigation. In cases where there is
minimal to no distal tendon, a suture anchor is employed or a trough can be created in the middle
phalanx for passing a suture. If there is sufficient tendon for repair, a cross-stitch suture with or without a
single-core suture is sufficient. A pin protects the repair for 6 weeks. Range of motion exercises can
commence after pin removal but night splinting should continue for another 3 weeks.
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Posttraumatic Boutonnière Deformity
This deformity refers to DIP joint hyperextension and PIP joint flexion. In addition to trauma discussed
earlier, arthritis, burns, and synovitis can also cause this condition via attenuation and rupture of the
central slip. The changes occur in three stages: dynamic imbalance (early), established tendon contracture
with supple joints (delayed), and fixed contracture (late/chronic). Passively correctable deformities should
initially be treated with splinting as even late treatment can allow realignment of the lateral bands. 29
Surgical treatment of chronic boutonnière deformity is extremely challenging. Supple joints are a
necessity before any surgical interventions; thus, fixed chronic cases should be treated with serial
splinting and stretching to maximize joint mobility. The distal Fowler tenotomy transversely divides the
extensor mechanism at the junction of the middle and proximal thirds of the middle phalanx while
preserving the ORL. This effectively creates a surgical mallet finger, decreasing tone at the DIP joint and
increasing tension at the PIP by allowing the extensor to slide proximally. A modification of this
procedure shifts the lateral bands dorsally and suturing them together over the PIP joint. 29 Lastly, Curtis
proposed a four-stage process to correct this deformity with reasonable outcomes. 30 The reconstruction
involves tenolysis, sectioning of the transverse retinacular ligament, distal Fowler tenotomy, and
advancement and reinsertion of the central tendon.
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Zone 4
The extensor mechanism in this zone is broad and the convexity of the proximal phalanx shields the
lateral bands, thus most injuries are partial. Surgical exploration is often necessary to diagnose the degree
of injury. Injuries that involve less than 50% of the extensor mechanism and/or those in which PIP active
extension is spared can be managed conservatively with range of motion exercises after the skin
laceration has healed. The choice of repair is variable and includes either figure-of-eight absorbable
sutures, or core sutures (2 or 4 of 4-0 or 5-0 nonabsorbable suture) augmented with a cross-stitch on the
dorsal surface. Similar to zone 3 injuries, the PIP joint should be splinted in extension for 4 to 6 weeks
while the DIP joint is exercised. Dynamic splinting can be considered in this zone. 31,32
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Zone 5
These injuries occur over the MP joint, are almost always open, and should be considered human bite
injuries unless proven otherwise. The classic fight bite occurs when the fully flexed MP joint forcefully
strikes human maxillary incisors. The teeth lacerate the skin, extensor tendon, and joint capsule before
inoculating the joint with oral flora. The finger then returns to its natural extended posture, sealing the
joint and catalyzing an impending septic arthritis. The clinician should be suspicious for those with
innocuous appearing injuries.
Primary tendon repair will be required after thorough joint irrigation. The lacerated tendon is proximal to
the area of skin injury. Flexing the joint recreates the multilevel injury tract and wash out all of the
inoculated tissues. Once identified, the tendon ends can be repaired with a two- or four-core (e.g.,
modified Kessler) suture followed by an epitendinous suture. If the sagittal bands are lacerated, they
should also be repaired to keep the tendon centralized. Radial sagittal band injuries are particularly prone
to subsequent subluxation. 33 The surgeon should obtain wound cultures and commence broad-spectrum
antibiotics. If there is frank septic arthritis, the wound and joint need to be opened widely, debrided,
irrigated, and left open to allow egress of purulence; and the tendon repaired secondarily once the
infection has resolved. Postoperative therapy should be tailored to the patient, mechanism, and extent of
injury.
In cases where the injury is not caused by human bite, the layers must be carefully identified and repaired
separately. Postoperative rehabilitation with intermittent-controlled active motion and relative motion
splinting is particularly useful in reliable, motivated patients (Figure 77.14).
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FIGURE 77.14 Zone 5 extensor tendon laceration. This 35-year-old carpenter sustained penetrating trauma to the dorsum of
his hand by a screwdriver. Extension deficit was evident preoperatively, but subtle. A. Intraoperative exploration revealed a
transected EDC tendon as well as injury to the shroud mechanism and traumatic MP joint arthrotomy. (B) Repair of the joint
capsule with 6-0 absorbable suture. Repair of extensor tendon with 4-0 nonabsorbable core suture (modified Kessler; C),
augmented with a 6-0 epitendinous suture (locking running; D). After repair, the patient is placed in an extension wrist splint and
a yoke splint with the affected digit in hyperextension relative to the neighboring digits. E, F. Controlled active motion begins
immediately with both splints in place. The wrist splint is discontinued at 3 weeks and the yoke splint at 6 weeks, followed by
strengthening and passive range of motion. This carpenter returned to work 3 days postoperatively.
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