For an injury less than 3 weeks old, nonemergent repair is indicated unless there is active purulent infection.
An injury greater than 6 weeks old is a relative contraindication to attempt primary repair.
Multi-strand core suture technique with a running circumferential epitendinous suture is used
A red rubber catheter should be ready if retrieval is required.
The goal of repair and rehabilitation is a strong repair site that will not elongate beyond 3 mm with gentle active range-of-motion therapy designed to prevent adhesion formation.
Lacerations of the slips of the FDS require different suture techniques than do FDP lacerations.
Enter sheath between distal A2 and proximal A4.
Retrieve proximal stump: skin hooks, reverse Esmarch, Sourmelis, direct exposure.
Deliver distal stump by passive DIP flexion
Transfix tendons, once delivered through pulleys with 25-gauge needle.
Use a minimum of a four-strand core suture (4-0 FiberWire) technique with a running 6-0 Prolene epitendinous suture (nonlocked, deep bites into tendon).
Use graded active rehabilitation protocol under supervision of a qualified therapist.
Restoring digital function after flexor tendon injury continues to be one of the great challenges in hand surgery. In recent years, important advancements in our understanding of tendon anatomy, , biomechanics, nutrition, adhesion formation, and tendon repair techniques have led to enhanced results after flexor tendon repair. Despite the many gains, problems of stiffness, scarring, and functional impairment continue to frustrate the most experienced hand surgeons.
Appreciation of flexor tendon anatomy as well as the flexor retinacular sheath is critical to the surgeon’s ability to deal with flexor tendon injuries. The flexor digitorum profundus (FDP) arises from the proximal volar and medial surfaces of the ulna, the interosseous membrane, and occasionally the proximal radius. Along with the flexor pollicis longus (FPL), the FDP forms the deep muscle layer in the flexor compartment of the proximal forearm. In the midforearm, the muscle belly separates into a radial bundle and an ulnar bundle. In the distal third of the forearm, the radial bundle forms the index finger profundus tendon, and the ulnar bundle forms the profundus tendon to the ulnar three digits. The profundus tendons pass through the carpal canal, occupying the floor of the tunnel.
After traversing the carpal canal, the profundus tendons diverge to the digits. The lumbrical muscles originate at this level. The profundus tendons enter the flexor sheath deep to the superficialis tendons at the level of the metacarpophalangeal (MCP) joint. At the midproximal phalanx level, the profundus tendon becomes more palmar as it passes through the bifurcating superficialis tendon. It continues distally to insert into the palmar base of the distal phalanx.
The anterior interosseous branch of the median nerve innervates the FDP to the index and occasionally the long finger. The ulnar nerve innervates the FDP to the ring and small fingers.
The flexor digitorum superficialis (FDS) originates from two separate heads. The humeroulnar head arises from the medial humeral epicondyle and the coronoid process of the ulna. The radial head arises from the proximal shaft at the radius. In the proximal forearm, it occupies the intermediate layer of the flexor compartment superficial to the flexor profundus. In the middle third of the forearm, four separate muscles are identified. Four distinct tendons are seen in the distal third of the forearm. Presence of the small finger superficialis varies and may be absent in 21% of patients. At the carpal tunnel level, the long and ring finger superficialis tendons lie superficial and central to those of the index and small, which lie deeper and more peripheral.
At the level of the MCP joint, the superficialis tendon enters the flexor sheath palmar to the profundus tendon. At the proximal third of the proximal phalanx, the superficialis bifurcates around the profundus tendon. The two slips reunite deep to the profundus tendon at Camper’s chiasm, with 50% of fibers decussating and 50% remaining ipsilateral. The superficialis tendon then inserts through the radial and ulnar slips onto the proximal metaphysis of the middle phalanx. The median nerve provides sole innervation of the superficialis muscle.
The FPL originates from the proximal radius and interosseous membrane. In the proximal third of the forearm, it lies radial to the digital flexors in the flexor compartment’s deep layer. At the carpal tunnel level, the FPL lies on the radial floor. After traversing the carpal tunnel, it enters the palm by emerging between the adductor pollicis and the flexor pollicis brevis (FPB). The FPL is the only tendon that enters the thumb flexor sheath, and it inserts at the proximal palmar base of the distal phalanx. The anterior interosseous branch of the median nerve innervates the FPL.
The digital flexor sheath is a synovium-lined fibro-osseous tunnel. This system holds the flexor tendons in close opposition to the phalanges, ensuring efficient mechanical function in producing digital flexion. The flexor sheath is composed of synovial and retinacular tissue components, each with separate and distinct functions. The synovial component of the sheath consists of a visceral, or epitenon, layer that envelops the flexor tendon and a parietal, or outer, layer that lines the walls of the flexor sheath. These two layers are contiguous at the ends of the sheath, creating a double-walled, hollow tube that surrounds the flexor tendons. In the index, long, and ring fingers, the membranous sheath begins at the MCP joint and ends at the distal phalanx. At the thumb and small fingers, the synovial sheath continues proximally into the carpal tunnel as the radial and ulnar bursae, respectively. , The synovial sheath provides a low-friction gliding system and nutrition to the tendon.
The retinacular portion of the sheath is characterized by fibrous bands that overlie the synovial sheath in segmental fashion ( Fig. 35-1 ). Thickened transverse bands are termed annular pulleys , and thin flexible areas of criss-crossing fibers are termed cruciate pulleys . Stronger, broader annular pulleys provide mechanical stability to the system, ensuring optimal joint flexion for a given amount of tendon excursion. The more flexible cruciate pulleys permit flexibility to the system. The following pulleys have been identified: the palmar aponeurosis pulley, five annular pulleys, and three cruciate pulleys. The palmar aponeurosis pulley is formed from the transverse fibers , of the palmar aponeurosis. It is located at the beginning of the membranous sheath and is anchored on each side of the sheath by vertical septa that attach to the deep transverse metacarpal ligament. The first annular pulley (A1) arises from the volar plate of the MCP joint. The second annular pulley (A2) arises from the volar aspect of the proximal half of the proximal phalanx. The first cruciate pulley (C1) extends from the A2 pulley to the third annular pulley (A3), which arises from the volar plate of the proximal interphalangeal (PIP) joint. The fourth annular pulley (A4) arises from the middle phalanx and is connected proximally to the A3 pulley by the second cruciate pulley (C2). The fifth annular pulley (A5) arises from the volar plate of the distal interphalangeal (DIP) joint. It is connected proximally to the A4 pulley by the third cruciate pulley (C3). Not all of the elements of the flexor sheath can be identified as described, particularly A3 and A5, which can be indistinct or absent.
The pulley system of the thumb is distinct from that of the digits ( Fig. 35-2 ). One oblique and two annular pulleys have been identified. The first annular pulley of the thumb (A1) arises from the palmar plate of the MCP joint, and the second annular pulley (A2) arises from the palmar plate of the interphalangeal (IP) joint. The oblique pulley originates and inserts on the proximal phalanx in close association with the insertion of the adductor pollicis tendon.
Anatomic and clinical studies have demonstrated that the A2 and A4 pulleys are the most important components of the flexor sheath, their presence ensuring biomechanical efficiency of the system. The A3 and the palmar aponeurotic pulleys become important only when A2 and A4 have been damaged. The loss of all or portions of the pulley system may lead to flexor bowstringing. This leads to an increased mechanical moment arm, which can create late flexion contractures. In addition, increased flexor tendon excursions are required to produce full digital flexion. In the thumb, the oblique pulley is the most important. Loss of the thumb oblique pulley results in decreased IP joint motion. Incompetence of both the A1 and oblique pulleys of the thumb leads to a 30% loss of IP joint motion.
Flexor tendon excursion in the retinacular sheath zone in cadaveric specimens has been calculated. DIP joint motion produces excursion of the FDP on the FDS of 1 mm for every 10 degrees of DIP flexion. PIP joint motion produces excursion of the FDS and the FDP together of 1.3 mm for every 10 degrees of PIP flexion relative to the retinacular sheath. Recently, postrepair clinical motion studies have demonstrated that this calculated excursion decreases. DIP joint motion of 10 degrees produces excursion of the FDP of only 0.3 mm, and PIP motion of 10 degrees produces excursion of the FDP and superficialis of 1.2 mm. This may explain why DIP motion is often suboptimal after flexor tendon repair.
Flexor tendon nutrition appears to occur through both direct vascular supply (see Fig. 35-1 ) and synovial diffusion. Proximal to the digital sheath, a longitudinal blood supply originates from within the proximal muscle tissue and is carried distally through the peritenon. Within the sheath, transverse branches of the digital arteries passing through the vincular system add segmental blood supply. These branches include a proximal vessel to the vinculum longus superficialis, a proximal digital transverse artery, an IP transverse digital artery, and a distal transverse digital artery. As the transverse branches pass to the midline, they merge to carry palmarly into the tendons via the vincula. The vinculum profundus brevis is a short triangular pedicle supplying the profundus tendon near its insertion. A similar short vinculum supplies the superficialis tendon at the neck of the proximal phalanx, but here the vessels continue to form the vinculum longus to the profundus tendon. The superficialis receives additional blood supply from the vinculum longus superficialis at the base of the proximal phalanx. Both tendons receive additional blood supply from their distal osseous attachments. Throughout the sheath, vessels enter the tendon from the dorsal surface, with the palmar third remaining relatively avascular. This anatomic fact has led to the surgical technique of palmar placement of sutures within the tendon to preserve blood supply. Finally, an avascular watershed zone of the FDP has been identified between the longitudinal and vincular vessels at the midproximal phalanx level. ,
In addition to nourishment of the flexor tendons by vascular perfusion, experiments have demonstrated the importance of diffusional nutrition by the synovial fluid. Radioisotope tracer studies suggest a greater role of diffusion than perfusion. , In addition, strong evidence has demonstrated that the superficial layers of isolated segments of tendon can heal in an isolated synovial environment without direct vascularity. This finding has led some authors to recommend sheath repair to restore synovial fluid. The relative significance of these dual nutritional pathways in the normal and repaired flexor tendon has yet to be completely clarified. Recent studies suggest that synovial diffusion associated with neovascularization of the healing site in the absence of ingrowth of peripheral vessels may play a role in the nourishment of the healing tendon.
Flexor Tendon Healing
The subject of flexor tendon healing has traditionally been associated with controversy. Two theories have been proposed to help explain observed experimental phenomena. The first, the extrinsic healing theory, suggests that tendon healing occurs through cells extrinsic to the tendon through a fibroblastic response from surrounding tissue. This theory presupposes the necessity of surrounding peritendinous adhesions to allow complete healing of the tendon; thus, immobilization after flexor tendon repair was encouraged. Experimental clinical evidence of adhesions at the repair site has supported this concept. The sequence of healing by extrinsic mechanism begins with an inflammatory phase from 48 to 72 hours, formation of collagen fibers from 4 to 21 days, and scar remodeling after 21 days.
The second theory, intrinsic healing, suggests that healing is possible in the absence of cells and tissue extrinsic to the tendon. More recent experimental and clinical evidence to support this concept includes rounded ends of unrepaired tendons, tendon healing in the absence of adhesions, and in vitro healing of tendons in isolated, cell-free environments. Controlled mobilization of repaired tendons to allow healing but preventing peritendinous adhesions was the stated advantage of this healing theory. The sequence of intrinsic healing begins with the inflammatory phase, from 0 to 3 days after injury or repair with proliferation and thickening of epitenon cell layers. At 5 to 7 days, collagen formation and early vascular ingrowth ensue. A fibrous callus becomes visible by 10 days, and proliferation ingrowth of endotenon tenocytes occurs at 2 to 3 weeks.
Although the function of each type of tendon healing continues to require clarification, in the clinical situation, tendons probably heal by a combination of extrinsic and intrinsic cellular activity. Theoretically, the more intrinsic healing occurs, the fewer peritendinous adhesions form. This concept forms the basis of controlled mobilization programs after tendon repair.
Zones of Injury
One must consider the level of injury when performing flexor tendon repair. Five anatomic zones of injury have been identified based on Verdan’s original description of the flexor tendon system ( Fig. 35-3 ). The level of injury should be recorded in relation to the position of tendon laceration in the sheath, with the finger in the extended position.
Zone I extends from the insertion of the FDS at the middle phalanx to that of the FDP at the distal phalanx. Injuries in this level may involve lacerations or avulsions of the FDP. Zone II involves that region in which both the FDS and FDP travel within the flexor sheath from the A1 pulley to the insertion of the FDS. This zone was termed “no man’s land” by Bunnell because of the poor prognosis associated with treatment of flexor tendon injuries at this level. A more descriptive term may be “some man’s land” because the more experienced hand surgeon can obtain satisfactory results with appropriate care. Zone III comprises the area between the distal border of the carpal tunnel and the A1 pulley of the flexor sheath. In addition to the common digital nerves, vessels, and both flexor tendons, the lumbrical muscles reside in this zone. Zone IV consists of that segment of flexor tendons covered by the transverse carpal ligament within the carpal tunnel. Injuries concomitant to the median and ulnar nerves may be associated with flexor tendon injuries in this zone. Zone V extends from the flexor musculotendinous junction in the forearm to the proximal border of the transverse carpal ligament. Associated neurovascular injuries may compromise results in this region as well.
The flexor tendon system in the thumb is predicated on only one flexor tendon. Zone I is at the insertion area of the FPL. Zone II coincides with the flexor retinaculum of the thumb, from the neck of the metacarpal to the neck of the proximal phalanx. Zone III is the area of the thenar muscles. Zone IV represents the area of the carpal canal. Finally, zone V is the anatomic area from the musculotendinous junction of the FPL to the transverse carpal ligament.
Knowledge of flexor tendon anatomy is necessary for diagnosing acute injury accurately. In the cooperative patient, diagnosis is usually not difficult. Because of the common muscle origin of the flexor profundi, FDS function can be assessed only by restraining the profundi by completely extending the other digits. An independently functioning superficialis is demonstrated by full flexion of the PIP joint of the affected finger. This test often is not applicable to the index finger because of the independent muscle belly of the FDP. The FDS to the index finger can be demonstrated through pulp-to-pulp pinch with the thumb and index finger.
Demonstration of index finger PIP joint flexion with the DIP joint fully extended or hyperextended confirms superficialis function to the index finger. As noted earlier, the presence of small-finger FDS varies and can be absent in 21% of patients. FDP function is demonstrated by means of active flexion of the DIP. Active flexion of the thumb IP joint indicates an intact FPL. If, when performing these tests, the patient demonstrates motion but experiences pain, the surgeon must entertain the possibility of partial flexor tendon injury.
In the uncooperative or unconscious patient or a child, additional diagnostic signs may be helpful. In the normal hand, a cascade of flexion of the digits is noted, increasing as one proceeds from the index to the small fingers. Abnormal posture or change in the normal cascade can indicate flexor tendon injury ( Fig. 35-4 ). In addition, squeezing the forearm musculature to demonstrate flexion of the digits may be helpful. Finally, assessing tenodesis of flexor tendons with the wrist in extension demonstrates loss of finger flexion if flexor tendons are severed.
The examiner is responsible for determining that the flexor tendons are intact before discharging the patient. If the examiner is uncertain, exploration of the wound under operating room conditions may be required. The actual level of tendon laceration depends on the position of the fingers when the injury occurred. If the injury occurred with the finger in extension, the skin wound and both tendons will be lacerated at the same level. In fingers injured in flexion, the tendon injury will be distal to the skin wound. In addition, the FDP will be lacerated at a level different from that of the superficialis tendon because of their different excursions.
Indications and Contraindications
There has been controversy in the past over the efficacy of primary repair of flexor tendons, particularly in zone II, yet immediate or delayed primary repair is currently advocated for flexor tendon injuries with few exceptions. The advantages of primary repair over secondary grafting include less extensive surgery, decreased periods of disability, and restoration of normal tendon length.
Specific contraindications to immediate or delayed primary repair include severe contamination where infection is a possibility. In addition, loss of palmar skin overlying the flexor system generally precludes tendon repair, , although there have been some recent reports of concomitant tendon repair and soft tissue coverage procedures. Another contraindication to primary repair is extensive damage to the flexor retinaculum, where pulley reconstruction and one- or two-stage tendon reconstruction probably is required. Concurrent fracture or neurovascular injury, however, does not necessarily contraindicate tendon repair. If fracture stabilization can be obtained, then flexor tendon repair generally should ensue.
Researchers have effectively demonstrated that repair of both the FDP and the FDS rather than the FDP alone, even in zone II injury, provides the best result. The advantages of repairing and maintaining the FDS include maintenance of vincular blood supply to the FDP, retaining of a smooth gliding surface for the FDP, independent motion of the digit with stronger flexion power, and decreased possibility of hyperextension deformities of the PIP joint.
Schneider and colleagues demonstrated that tendon repairs delayed as long as 3 weeks after injury exhibited outcomes similar to those of tendons repaired more immediately. Although not statistically significant, repairs performed within the first 10 days after injury tended to be superior. Recent animal studies also have supported improved tendon excursion with early repairs. These studies demonstrate that, although tendon repair is not emergent, repair within the first few days after injury appears warranted.
Flexor tendon repair is ideally performed by trained surgeons who know the anatomy of the flexor tendon system and the potential pitfalls of surgical repair. Repair is generally accomplished under regional or general anesthesia in a bloodless field. Traditionally, a tourniquet has been used. Recently, Lalonde and coworkers reported using elective injection of lidocaine with epinephrine into the operative field in the office setting. This “wide awake” technique creates a relatively bloodless field, without the need for a tourniquet, allowing use of local anesthetic only. They report the risk of digital infarction is remote, with the benefit of observing the repair with the patient’s active movement. Despite the appeal of performing surgery in the office, I have no experience with this technique.
The use of 2- to 4-power loupe magnification decreases inadvertent nerve or vessel injury. Lateral or palmar zigzag (Bruner’s) incisions are performed, depending on the surgeon’s preference. The Bruner incision, our preferred approach, offers excellent exposure but can cause scarring over the palmar surface of the digit. , The midlateral incision is technically more demanding and may interfere with transverse digital branches supplying the vincula but has the advantage of decreased scarring over the flexor surface, which can lead to improved rehabilitation. Delicate use of instrumentation is required; pinching or crushing of the flexor tendon or sheath inevitably leads to suboptimal results. , We generally prefer to handle the tendon at its cut end only, avoiding grasping of the epitenon, which can create later epitendinous adhesions. Minimal debridement of tendon ends is not usually required but may be performed if necessary using a knife or nerve-cutting instrument. Many suture techniques have been described. Traditionally, many surgeons have preferred a modified Kessler grasping-type two-strand core stitch based on the studies by Urbaniak and others. Although 3-0 or 4-0 braided synthetic material placed in the volar third of the tendon has been the most popular core suture material, I prefer the more recently developed 4-0 FiberWire (Arthrex, Naples, FL) because it is stronger than braided synthetic suture of the same caliber and not too bulky when knotted. Most authors currently recommend a four-strand core repair, crossing the repair site with epitendinous suture augmentation to afford sufficient strength to support a program of early active motion rehabilitation. A variety of multistrand core suture designs have been described, ranging from four to eight strands crossing the repair site. My preferred technique uses a single suture to create a four-strand repair as first described by Seiler ( Fig. 35-5 ). A four-strand cruciate flexor repair has been described by McLarney and colleagues and is similar to my preferred suture technique ( Fig. 35-6 ). Taras found that increasing suture caliber significantly increased the load to failure of core suture techniques. With 5-0 or 4-0 suture, the method of failure was suture rupture. With 3-0 and 2-0 suture, the failure was caused by suture pullout, clearly showing that repair technique with the modified Bunnell and double-grasping suture techniques securing the ends better than the modified Kessler technique. Recent studies have demonstrated that epitendinous suture significantly increases the repair strength. The epitendinous technique described by Silfverskiöld ( Fig 35-7 ), employing a cross stitch has shown excellent results in reducing gapping by 10% to 50% at the repair site. The superficialis tendon is preferably repaired with a four-strand core suture depending on the size of the tendon and the location of the laceration. A recent study by Tran and associates found that in vitro a four-strand Tajima technique with a Silfverskiöld epitendinous cross stitch was superior to a four-strand Tajima core suture with running locking epitendinous technique and capable of handling the rigors of an early active rehabilitation protocol.
Several techniques are available to atraumatically retrieve retracted tendon ends. With the wrist and MCP joints placed in maximal flexion, flexor muscle bellies can be milked manually to deliver the tendon ends. If this fails, alternatives are available. If a tendon end is visible in the flexor sheath, one may use a skin hook. The hooked end is slid along the surface of the sheath until it has passed the tendons, and the hook is then turned toward the tendons, engaging the most superficial one. As the instrument is pulled distally, the tendons follow. The tendons then can be held in position by a Keith or 25-gauge hypodermic needle placed through the skin and A2 pulley area for later repair.
Another common retrieval technique uses a red rubber urologic catheter, pediatric feeding tube, Hunter rod, or IV tubing, which is passed distal to proximal alongside the flexor tendons, which are left in situ. The catheter is sutured to both tendons 2 cm proximal to the A1 pulley through a second palmar incision. The catheter is advanced distally to deliver tendon ends into the repair site. A 25-gauge hypodermic needle is passed transversely through the skin and A2 pulley to maintain tendon position. Core sutures are then placed. The catheter tendon suture is then cut in the palm and withdrawn.
Another often-used technique uses a catheter that is passed from distal to proximal through the flexor sheath. A stitch is placed into the tendon end, and the other end of the suture is placed into the end of the catheter. The catheter and suture, followed by the tendons, are pulled distally through the flexor sheath. Further retraction of tendons is prevented again by transfixing them to the skin and A2 pulley with a 25-gauge hypodermic needle.
For all of these techniques, the anatomic relationship of the profundus to the superficialis tendons must be maintained. One anatomic point that can aid the surgeon in maintaining this orientation and preventing tendon twisting is the fact that the vincula insert on the dorsal surface of the tendons.
Every attempt is made to preserve all pulleys of the flexor retinacular sheath. Small surgical windows into the sheath often are required to identify tendon ends. Whether the sheath should be subsequently repaired is controversial. Theoretical support for repair includes tendon gliding and nutrition. To date, no clinical studies have documented superiority of repair versus resection of the sheath. , In addition, one prospective study comparing the two techniques demonstrated no superiority of sheath repair. Currently, we favor sheath repair when possible using 6-0 or 7-0 monofilament suture if there has been minimal loss of sheath substance and the repair can be performed easily without constriction of the sheath or the tendon repair.
Recently, a stainless steel device, TenoFix (Ortheon Medical, Columbus, OH) has been introduced for zone II flexor tendon repair. The authors reported similar results to a four-stranded core repair; however, smaller profundus tendons were unable to accommodate the device.
Treatment of Acute Flexor Tendon Injuries
In zone I, distal to the FDS insertion, only the FDP tendon is injured. The patient maintains PIP joint flexion but loses DIP flexion. Although adequate finger function can be maintained without repair in some circumstances, early direct repair is desirable. This is particularly true as one proceeds from the radial (precision grip) to the ulnar (power grip) side of the hand. In addition, the small finger superficialis is absent in a significant percentage of individuals, necessitating repair of the lacerated FDP tendon in that digit. With early repair, digital function can be near normal.
If more than 4 weeks have elapsed since the injury, direct repair usually cannot be performed due to FDP muscle contracture and degeneration of the lacerated ends of the tendon. Another pitfall in zone I is injury to the normally functioning FDS caused by excessive surgical manipulation. Finally, the surgeon must not advance the profundus tendon more than 1 cm at this level of injury to accomplish repair. This leads, particularly in the ulnar three digits, to unacceptable flexion contractures of the affected digit as well as incomplete flexion of the neighboring digits—a condition termed quadrigia syndrome .
Three patterns of laceration occur in zone I. The first occurs when the short vincula of the FDP remain intact. Although this pattern is rare, the FDP remains just proximal to its insertion. Direct repairs can be performed late with this pattern of injury. The second pattern presents with the long vincula of the FDP intact. The severed end of the tendon lies at the FDS decussation. The prognosis for early repair is good. The third laceration pattern occurs when the FDP retracts into the palm, rupturing both vincula and resulting in loss of vincular blood supply. This type of repair requires more extensive surgical dissection and early repair. When this pattern of injury is diagnosed late, alternative treatments such as observation, tendon graft, DIP tenodesis, and arthrodesis must be entertained.
Surgical Technique in Zone I Injuries
A volar zigzag incision from the PIP joint crease to distal to the DIP joint is utilized. Every effort is made to preserve the A4 pulley. If only a short distal stump of FDP remains, opening the tendon sheath at the C3-A5 pulley level may be required. If the proximal FDP stump has retracted to the level of the PIP joint, a window at the C2 pulley may be fashioned to retrieve it. If the proximal profundus has retracted to the level of the palm, the zigzag incision may be extended proximally, or a separate transverse incision in the palm proximal to the A1 pulley may be required. Retracted proximal FDP tendon ends are retrieved atraumatically as described previously. If the injury is recent, the FDP may be passed through the FDS decussation. In older lacerations, one slip of the superficialis may be sacrificed to facilitate passage of the FDP through a tight flexor sheath. Under no circumstances should a normal FDS be completely excised to repair the FDP.
Every effort is made to repair to the distal tendon stump to avoid overadvancement. As previously discussed, the FDP is not advanced more than 1 cm to permit repair. If the repair catches at the end of the A4 pulley, a small portion of the sheath may be vented.
If the distal stump is extremely short or nonexistent, the tendon must be repaired to the distal phalanx ( Fig. 35-8 ). One develops a periosteal flap at the base of the distal phalanx, carefully avoiding the palmar plate of the DIP joint. The cortex is prepared with a curette to provide a bleeding bone surface that will encourage tendon-to-bone healing. A synthetic monofilament suture, such as 2-0 Prolene, is inserted into the tendon in “unlocked” fashion to facilitate later removal. The ends of the suture are threaded onto a Keith needle. Regardless of whether a short FDP stump is present, I fasten the sutures using an “around-the-bone” technique. With the use of a needle holder, the Keith needles are passed around both sides of the distal phalanx to emerge through the middle third of the nail plate. Effort should be made to avoid the germinal nail matrix; the ideal point of exit through the nail plate should be 3 to 4 mm distal to the lunula and approximately 2 mm from the midline. The Keith needles are withdrawn, and the sutures are tied directly over the nail. The pullout suture is removed 6 weeks after initial repair. Alternatively, a bone anchor is reported to have been used at the distal phalanx level for this injury. The length of the bone anchor must avoid the nail bed. The use of a bone anchor technique has been reported to make no significant difference in outcome versus pullout suture technique without the morbidity of this method.