I. Basic Science of Flexor and Extensor Tendons
A. Tendon structure
1. Tendons are organized groups of fascicles containing longitudinally oriented bundles of collagen (primarily type I) and fibroblasts called tenocytes.
2. Individual fascicles are covered by endotenon.
3. Epitenon covers groups of tendon fascicles.
4. Visceral and parietal paratenon line the surface of the tendon and the undersurface of the tendon sheath, respectively.
B. Flexor tendon nutrition
1. Perfusion of flexor tendons is accomplished by a network of vessels, including longitudinal vessels entering the tendon in the palm and extending down intratendinous channels, segmental vessels from the digital arteries that supply the tendon through the long and short vincula, and vessels that enter the tendon at their respective insertions.
2. In the relatively avascular watershed areas, particularly over the proximal phalanx, tendon nutrition is accomplished by synovial fluid diffusion via a process called imbibition.
3. An illustration of flexor tendon anatomy is shown in
Figure 1.
C. Extensor tendon nutrition
1. At the level of the wrist joint, extensor tendon nutrition is accomplished via diffusion from vessels in the mesotenon, which spans the length of the extensor retinaculum.
2. Distally, the extensor tendons are covered by paratenon.
3. Small segmental vessels from the paratenon supply the tendon distal to the retinaculum.
4. An illustration of extensor tendon anatomy is shown in
Figure 2.
D. Tendon healing
1. Phases of tendon healing
a. Inflammatory phase (injury to 7 days)—Fibroblast and macrophage migration to the site of injury leading to phagocytosis of clot and necrotic tissue. During this phase, repair strength is entirely due to the strength of the suture used.
b. Proliferative phase (weeks 1 to 3)—Neovascularization begins. An increasing number of fibroblasts deposit immature collagen (primarily type III), which is later replaced by type I collagen. Tendon repairs do not accrue tensile strength until the beginning of the remodeling phase.
[Figure 1. Lateral (A) and dorsal (B) views of a finger depict the components of the digital flexor sheath. The sturdy annular pulleys (A1, A2, A3, A4, and A5) keep the tendons closely applied to the phalanges. The thin, pliable cruciate pulleys (C1, C2, and C3) collapse to allow digital flexion. The palmar aponeurosis pulley (PA) adds to the biomechanical efficiency of the pulley system.]
[Figure 2. Finger extensor mechanism anatomy. A, Lateral view. B, Dorsal view. DIP = distal interphalangeal joint, MCP = metacarpophalangeal joint, ORL = oblique retinacular ligament, PIP = proximal interphalangeal joint, TRL = transverse retinacular ligament.]
c. Remodeling phase (weeks 3 to 12)—Collagen fibers become organized linearly, parallel to the tendon.
2. Mechanisms of tendon healing
a. Extrinsic tendon healing—Involves inflammatory cells and fibroblasts derived from the tendon sheath and predominates with immobilization of repaired tendon. Collagen deposition is disorganized.
b. Intrinsic tendon healing—Accomplished via inflammatory cells and fibroblasts derived from within the tendon and epitenon. The intrinsic mechanism predominates if motion rehabilitation is used postoperatively.
3. Growth factors and the biochemistry of tendon healing
a. Collagen synthesis
i. Collagen is synthesized by fibroblasts within tendon fascicles.
ii. The predominant collagen type in tendon is type I.
iii. Synthesis of collagen fibers includes both intracellular and extracellular processes.
iv. Posttranslational hydroxylation (in the ribosome) and glycosylation (in the golgi body) occur within the fibroblast.
v. Intermolecular cross-linking and triple helix formation occur within the cell as well.
vi. Fibril formation and intermolecular cross-linking occur within the extracellular matrix.
b. Binding of platelet-derived growth factor (PDGF) to receptors on the fibroblasts stimulates fibroblast proliferation and differentiation as well as collagen production.
c. Vascular endothelial growth factor (VEGF), a potent mediator of angiogenesis, is detectable at the tendon repair site early in tendon healing. Expression of VEGF peaks at 7 to 10 days. Subsequently, maximum vascular ingrowth occurs at 17 to 28 days.
d. Insulin-derived growth factor-1 (IGF-1) appears to increase cell proliferation at tendon repair sites and increases collagen content in repaired tendon.
e. Integrins, cell surface molecules that mediate the interaction between fibroblasts and their extracellular matrix, are upregulated for more than 2 weeks following tendon repair.
II. Diagnosis of Tendon Disruption
A. Examination of the injured hand
1. The examination should begin with observation of the resting position of the hand and assessment of the digital cascade.
2. Malalignment or malrotation of the digits may be a sign of underlying fracture.
3. A neurovascular examination should be obtained given the proximity of the tendons, particularly the flexors, to the digital neurovascular bundles.
4. Assessment of skin integrity on the dorsal and palmar aspects of the hand helps to localize potential sites of tendon injury.
5. Lacerations near joints must be carefully inspected for evidence of traumatic arthrotomy.
B. Examination of the flexor tendons
1. In the absence of flexor tendon disruption, wrist extension should cause passive flexion of the digits at the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints by means of tenodesis.
2. Maintenance of a digit in an extended position at the PIP or DIP joint with wrist extension indicates flexor tendon discontinuity.
3. Isolation of the flexor digitorum profundus (FDP) tendon of a digit is accomplished by gently maintaining the PIP joint in extension and asking the patient to flex the digit; failure to flex the DIP joint of the digit indicates an FDP injury.
4. Isolation of the flexor digitorum sublimis (FDS) tendons is accomplished by maintaining the adjacent digits in extension and asking the patient to flex the finger toward the palm; inability to flex the PIP joint of a digit with adjacent digits held in extension indicates an injury to the FDS tendon of that digit.
C. Classification of flexor tendon injuries—See
Figure 3.
1. Zone I is distal to the FDS insertion.
2. Zone II contains the tendons of both the FDS and FDP.
3. Zone III represents the palm.
4. Zone IV is the region of the carpal tunnel.
5. Zone V is over the distal forearm, distal to the musculotendinous junction.
D. Examination and classification of extensor tendon injuries—See
Figure 4.
1. Zones I and II extensor tendon injuries involve the terminal insertion of the extensor mechanism and result in the finger assuming a flexed posture of the DIP joint, or mallet finger.
a. The patient will be unable to actively extend the DIP joint.
b. Open injuries in this zone involve transection of the tendon, whereas closed injuries in this zone may involve a bony avulsion from the dorsal base of the distal phalanx and necessitate radiographic evaluation.
[Figure 3. The five zones of flexor tendon injury. Note the three zones of the thumb.]
2. Zone III injuries involve disruption of the central slip of the common extensor tendon. A positive Elson test (the inability to actively extend the PIP joint with the joint resting in 90° of flexion, or extension of the DIP joint with attempted PIP extension) indicates disruption of the central slip and triangular ligament, with potential volar subluxation of the lateral bands as well.
3. Zone V injuries—over the MCP joint; may involve damage to the sagittal bands.
a. Loss of active MCP extension and subluxation of the extensor tendons into the valleys between the MCP joints with MCP flexion may indicate damage to these structures.
b. Zone V is the region of the "fight bite" injury.
4. Extensor tendon injuries proximal to zone V—Examination involves having the patient attempt finger extension with the wrist held in slight flexion. Failure to maintain extension of the MCP joint indicates injury to the extrinsic extensors (extensor digitorum communis [EDC], extensor indicis proprius (EIP), and extensor digiti quinti [EDQ]) of the digit. The EIP and EDQ tendons lie ulnar to the EDC tendons of the given
[Figure 4. The extensor tendon zones of injury.]
digit. Injuries to the EDC tendons can be masked by these secondary digit extensors as well as the preservation of juncturae tendinum interconnecting the EDC tendons.
III. Primary Repair of Injured Flexor Tendons
A. General repair considerations
1. Partial tendon lacerations are repaired with a core suture when >60% of the tendon is disrupted.
2. Pain with resisted PIP or DIP flexion suggests a partial tendon injury. Small tendon flaps may be trimmed to avoid catching on the pulleys.
3. The strength of a flexor tendon repair at the time of repair is directly proportional to the number of suture strands across the repair site.
4. Most commonly, 3-0 or 4-0 core nonresorbable suture is used.
a. Four-core-strand repairs have nearly twice the strength of two-strand repairs.
b. Six- and eight-strand repairs, although strongest, are technically challenging and may result in excessive manipulation of the tendon ends, compromising nutrition to the tendon.
5. Epitendinous sutures improve tendon contour, enhance repair strength, and diminish gap formation in flexor tendon repairs. Most commonly, 6-0 monofilament suture is used.
6. Tension forces on tendons during digital flexion are greatest dorsally, hence dorsal to midline placement of repair sutures is recommended.
7. Preservation of the A2 and A4 pulleys is imperative to prevent bowstringing.
B. Specific considerations for zone I injuries
1. Zone I injuries may represent an avulsion of the FDP tendon insertion from the volar base of the distal phalanx or an avulsion fracture of the volar base of the phalanx. Such injuries, termed jersey finger injuries, are classified into three types:
a. Type I
i. FDP tendon is retracted to the palm.
ii. The vascular supply to the tendon is disrupted.
iii. Prompt surgical repair within 7 to 10 days of injury is recommended.
b. Type II
i. The FDP tendon retracts to the level of the PIP joint.
ii. Repair within several weeks can yield satisfactory outcomes.
c. Type III
i. Attached to a large avulsion fracture fragment, the FDP tendon retracts only to the level of the DIP joint.
ii. Similar to type II injuries, delayed repair can be successful.
2. Repair techniques include reinsertion of the FDP tendon using a suture anchor in the distal phalanx or by passing sutures that grasp the tendon dorsally through or around the phalanx and tying them over the nail plate. Larger bone avulsions are usually fixed.
C. Specific considerations for zone II injuries
1. Flexor zone II injuries involve lacerations to both the FDP and FDS tendons. Because of historically poor outcomes, this zone was once termed "no man's land," with some authors advocating late reconstruction with graft rather than acute repair. Modern repair techniques and advancements in postoperative rehabilitation have made primary repair of zone II injuries more successful.
2. Of particular importance in zone II is recreating the two-tailed insertion of the FDS tendon and restoring the passage of the FDP tendon through the chiasm between the two.
D. Rehabilitation after flexor tendon repair
1. Principles
a. Evolution of tendon rehabilitation protocols has followed development of stronger suture techniques, better understanding of tendon nutrition and healing, and greater understanding of tendon response to stress.
b. Motion of a repaired tendon unit leads to the predominance of intrinsic over extrinsic tendon healing and reduces adhesions.
2. Tendon motion rehabilitation protocols
a. Passive motion protocols: low force and low excursion
i. Kleinert technique—Uses a dorsal block splint with the wrist in 45° of flexion and elastic bands secured to the patient's nails and a more proximal attachment point. Once the interphalangeal (IP) joints are actively fully extended, recoil of the elastic bands flexes them down passively.
ii. Duran protocol—Uses a splint with the wrist in flexion (20°). Relies on the patient to alternately passively extend the DIP and PIP joints with the other joints of the finger flexed in an effort to draw the repaired FDS and FDP tendons away from the repair site. Patient compliance is a prerequisite.
b. Early active motion protocols: moderate force and potentially high excursion
i. Involve the generation of light muscle forces to either assist digit flexion or perform "place and hold" exercises with the digit.
ii. Most use a dorsal blocking splint limiting wrist extension to slight flexion or neutral.
iii. Although some evidence shows generation of increased tensile strength at the repair compared to passive protocols, risk of rerupture and gap formation are potential concerns.
c. Synergistic motion regimen: low force and high tendon excursion
i. Passive digit flexion is combined with active wrist extension, followed by active digit extension coupled with active wrist flexion.
ii. Tendon excursion by employing wrist motion is greater than that provided in an extension blocking splint.
3. Immobilization protocols
a. Prolonged immobilization is reserved for children and patients unable to comply with the above motion protocols.
b. Casts or splints are applied with the wrist and MCP joints positioned in flexion and the IP joints in extension.
c. Initial casts are worn for 3 weeks and later changed to splints, allowing serially increasing degrees of wrist and MCP joint extension.
IV. Primary Management of Extensor Tendon Injuries
A. Extensor tendon injuries are most commonly repaired with core suture alone, with suture technique similar to that of flexor tendons.
B. Zone I (mallet finger)
1. Mechanisms of injury resulting in acute loss of active extension of the DIP joint can be blunt (eg, a baseball or football striking and forcibly passively flexing the DIP joint) or a sharp (laceration) injury to the terminal extensor insertion.
2. Most closed injuries are treated with full-time extension splinting of the DIP joint for 6 to 8 weeks, followed by several weeks of night splinting.
C. Zone III injuries (acute boutonniere deformity)
1. Acute loss of PIP extension results from injury to the central slip of the extensor apparatus at or just proximal to the level of the PIP joint.
2. Palmar PIP joint dislocations and lacerations over the dorsum of the PIP joint are the most common mechanisms.
3. Subsequent volar subluxation of the lateral bands causes DIP extension; this results in the boutonniere deformity.
4. Closed injuries and open injuries not associated with an extensor lag are usually treated with PIP joint extension splints with the DIP joint left free.
5. Surgical repair is advocated for open injuries when an inability to actively hold the PIP joint in the extended position is evident.
V. Tendon Repair Complications
A. Tendon adhesions
1. Despite advances in tendon repair rehabilitation, adhesion formation remains the most common complication following flexor tendon repair.
2. Factors associated with increased adhesion formation include repairs within the synovial flexor sheath, extensive crush injuries, excessive surgical manipulation, associated fractures and infections, and reconstructions of failed primary repairs.
3. Generally, older patients are more apt to develop adhesions.
4. If a significant difference exists between the active and passive motion of a digit despite dedicated efforts in therapy, adhesion release or tenolysis is considered.
5. Tenolysis
a. Indications—Ideal candidate for tenolysis is a patient with localized tendon adhesions, minimal to no joint contracture, and full passive digital motion who is motivated to perform immediate postoperative therapy.
b. Tenolysis combined with other procedures that would require postoperative immobilization (eg, nerve repair, bone grafting) is discouraged.
c. Generally, tenolysis is not performed before 3 to 6 months.
B. Tendon rupture
1. Predisposing factors include inadequate suture material, poor surgical technique, overly aggressive therapy, and noncompliance.
2. Reported rerupture rates average approximately 5%.
3. Acute recognition and timely exploration may allow revision repair under ideal circumstances.
4. Tendon reconstruction is preferred with late rupture and rupture associated with excessive scarring.
5. Rerupture occurs most frequently during the first 7 to 10 days postoperatively.
C. Joint contracture
1. Reported rates of contracture are as high as 17%.
2. Can be caused by scarring of the volar plate, bowstringing due to pulley incompetence, associated fractures, skin contractures, and tendon adhesion.
3. Early identification, therapy, and splinting can help in treatment of developing contracture.
4. Failure of nonsurgical methods warrants surgery when the degree of contracture limits function.
5. Surgical technique involves check-rein ligament release, sequential palmar-to-dorsal collateral ligament release, and volar plate release when necessary.
VI. Tendon Reconstruction
A. Principles
1. Neglected tendon injuries and late referrals of acute injuries are frequently complicated by contraction of the muscle-tendon unit as well as the presence of excessive scarring.
2. Under these circumstances and when acute tendon injury occurs with extensive or segmental destruction of the tendon, pulley system, or tissue bed, secondary reconstructive options are considered.
3. The "reconstructive ladder of tendon reconstruction" includes tendon transfer, single-stage tendon reconstruction, and two-stage tendon reconstruction.
B. Tendon transfers
1. Preferred when the muscle belly powering a tendon is not functional or is significantly contracted; eg, using the FDS tendon of the ring finger to reconstruct a chronic distal flexor pollicis longus (FPL) rupture.
2. Common extensor tendon transfers include EIP to extensor pollicis longus (EPL) and end-to-side transfers of the EDC tendons.
3. Transfers are more frequently used for inflammatory and attritional ruptures.
C. Single-stage tendon grafting
1. Indications
a. Single-stage tendon grafting in the setting of a disruption of both FDS and FDP tendons is performed when repair is delayed and proximal muscle and tendon retraction has occurred.
b. In the setting of an intact FDS tendon with a disrupted FDP tendon, consideration must be given to the risk of compromising FDS function by inciting adhesion formation.
c. FDP reconstruction with an intact FDS tendon is often reserved for younger patients and those with specific vocational or avocational requirements for DIP flexion.
2. Graft choices
a. Intrasynovial donor grafts
i. Tendon grafts from intrasynovial sources are associated with less tissue necrosis, less expression of proinflammatory factor DNA, and better preservation of gliding.
ii. The second toe FDL has the longest segment of intrasynovial tendon.
b. Extrasynovial tendon grafts
i. Associated with increased adhesions, greater early cellular necrosis, and a rise in repair site DNA content.
ii. Common extrasynovial graft tendons include palmaris longus and plantaris, or toe extensors.
D. Two-stage flexor tendon reconstruction
1. Indications—Preferred in cases with severe crushing of adjacent soft-tissue structures including the pulley system, associated fractures requiring prolonged immobilization, and in cases of delayed or failed primary treatment where extensive scarring exists.
2. Technique
a. Stage 1
i. Silicone tendon implant rod introduced proximally, threaded distally through the remaining pulley system, and sutured to the FDP stump.
ii. The proximal portion of the rod is guided into the forearm in a plane between the FDS and FDP muscles.
iii. After stage 1, early passive motion within a dorsal blocking splint allows gliding of the tendon rod to develop an organized sleeve of fibrous tissue, forming a pseudotendon sheath.
b. Stage 2
i. Time interval between stages 1 and 2 is usually 3 months.
ii. In the second procedure, the tendon graft is sutured to the proximal edge of the implant and pulled distally through the newly developed sheath.
iii. The implant is removed and the distal insertion of the graft tendon is created.
iv. The graft tendon is then repaired to the tendon of the FDP, which remains in the distal forearm.
VII. Late Complications After Tendon Injury and Repair
A. Swan-neck deformity
1. Isolated loss of the FDS tendon within a digit rarely results in significant functional loss.
2. When combined with loss of integrity of the PIP volar plate, hyperextension of the PIP joint with flexion of the DIP joint results in the swan-neck deformity.
3. Tenodesis of the remaining stump of the FDS tendon to the proximal phalanx prevents this deformity.
B. Triggering
1. Triggering after flexor tendon repair (or following partial flexor tendon laceration) may occur due to impingement of the tendon repair site on the tendon sheath.
2. Occasionally, reduction tenoplasty may be indicated.
C. Lumbrical plus finger
1. Paradoxical extension of the IP joints of the injured digit with attempted flexion is termed the "lumbrical plus deformity."
2. Loss or lengthening of the portion of the FDP tendon distal to the lumbrical origin results in force transmission through the lumbrical tendon (and to the distal phalanx) rather than the flexor.
3. Via its insertion onto the radial band, the lumbrical tendon acts as an extensor of the IP joints.
4. Treatment involves release or excision of the lumbrical tendon.
D. Quadriga
1. Quadriga is the inability of uninjured fingers of the same hand to obtain full flexion.
2. Functional shortening of the FDP tendon causes quadriga.
3. Because the long, ring, and little fingers have a common muscle belly, the proximal excursion of the FDP tendons to these digits is only as far as the shortest tendon allows.
4. Loss of tendon excursion prevents full digital flexion in the adjacent digits, which manifests as weakness of grip.
VIII. Conditions Involving Tendinitis
A. Trigger finger
1. Characteristics/progression
a. Trigger digits, or stenosing tenosynovitis of the digits, is a common cause of hand pain and dysfunction.
b. A size mismatch between the flexor tendon and portions of the tendon sheath results in clicking or popping of the tendon through the sheath with attempted extension of a flexed digit.
c. Tendon thickening may result from bunching of tendon fibers at the level of the pulley as the angle of the tendon's course changes.
d. Fibrocartilaginous metaplasia of the tendon and pulley have been found in pathologic specimens.
e. With progression of the condition, manipulation of the digit to passively extend it may become necessary.
f. The most common site of triggering is the A1 pulley.
g. Systemic diseases including rheumatoid arthritis, amyloidosis, and diabetes mellitus are associated with an increased incidence of developing trigger digits.
h. The ring finger is the digit most commonly involved.
2. Treatment
a. Nonsurgical treatment includes activity modification, splinting, NSAIDs, and steroid injections.
b. Surgical intervention is indicated in cases of failed nonsurgical treatment and involves release of the A1 pulley.
B. de Quervain syndrome
1. Definition—Stenosing tendovaginitis of the first dorsal compartment of the wrist, which contains the abductor pollicis longus (APL) (palmar) and extensor pollicis brevis (EPB) (dorsal).
2. Nonsurgical management involves splinting and injections.
3. Surgical treatment
a. When performing surgical release of the first dorsal extensor compartment, the surgeon must appreciate the highly variable anatomy of the compartment and be sure to liberate all tendon slips (the APL usually has at least two) from their respective fibro-osseous compartments.
b. A separate EPB sheath or subsheath is frequently seen dorsally.
c. Injury to the adjacent dorsal radial sensory nerve must be avoided.
C. Intersection syndrome
1. Involves painful entrapment of the tendons of the second extensor compartment (extensor carpi radialis longus [ECRL] and extensor carpi radialis brevis [ECRB]) beneath the muscle bellies of the APL and EPB.
2. When the condition fails to respond to nonsurgical measures (splints, NSAIDs, injections, and rest), surgical release of the second extensor compartment, located 6 cm proximal to the radial styloid, is indicated.
Top Testing Facts
1. Tendon nutrition is via the vincula, intratendinous vessels, and perfusion at the site of insertion; avascular regions are nourished by imbibition.
2. Flexor tendon repair strength is proportional to the number of suture strands crossing the repair site.
3. Flexor tendon repair sites are most vulnerable to rerupture during the first 7 to 10 days postoperatively.
4. Flexor tendon injury in zone II involves the FDP and FDS tendons and is associated with a high risk of adhesion formation and poorer outcomes.
5. Preservation of the A2 and A4 pulleys is important to prevent tendon bowstringing.
6. Active wrist range of motion acts in synergy with passive digit motion to allow for low-force, high-excursion gliding.
7. Two-stage tendon reconstruction is preferred with segmental loss of tendon, disruption of the pulley system, and in cases of extensive tendon scarring.
8. Boutonniere deformity involves flexion of the PIP joint with extension of the DIP joint; swan-neck deformity involves hyperextension of the PIP and flexion of the DIP.
9. Zone V injuries as a result of a "fight bite" require joint inspection, debridement, and administration of antibiotics.
10. Fibrocartilaginous metaplasia is implicated in the pathogenesis of trigger finger.
Bibliography
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Boyer MI, Taras JS, Kaufmann RA: Flexor tendon injury, in Green D, Hotchkiss R, Pederson W, Wolfe S (eds): Green's Operative Hand Surgery. Philadelphia, PA, Elsevier, 1995, pp 219-276.
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Strickland JW: Flexor tendon injuries: II. Operative technique. J Am Acad Orthop Surg 1995;3:55-62.