AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

Injuries to the flexor tendons of the hand are common. Each specific movement of the hand relies on the finely tuned biomechanical interplay of intrinsic and extrinsic musculotendinous forces. Considering the hand's role in labor, entertainment, art, literature, and passion, hand surgeons should fully define the normal and pathologic boundaries in each patient examined. With injuries that involve flexor tendons, fully defining the pathology is especially important. In this article, the management of the flexor tendon injuries is addressed specifically, with emphasis on history, physical examination, surgical repair, and rehabilitation. (Also, see the eMedicine article Hand, Tendon Lacerations: Flexors.)

For excellent patient education resources, visit eMedicine's Hand, Wrist, Elbow, and Shoulder Center. Also, see eMedicine's patient education articles Hand Injuries and Finger Injuries.

Frequency

Flexor tendon injuries are common.

Etiology

Flexor tendons can become disrupted from either open or closed injuries. Minor puncture wounds or lacerations over the flexor tendon can result in partial or complete transection. Open injuries are often associated with other neurovascular deficits. Closed injuries are frequently related to forced extension during active flexion of the finger. This type of avulsion injury, in which the flexor digitorum profundus (FDP) tendon ruptures at its insertion to the distal phalanx, is called Jersey finger. Flexor tendon rupture from chronic attrition may occur in rheumatoid diseases, Kienböck disease, scaphoid nonunion, a hamate fracture, or a Colles fracture.

Pathophysiology

The functional biomechanics of the flexor tendons depend on a number of factors, including an intact pulley system, synovial fluid, supple joints, and tendon excursion. The synovial fluid not only provides nutrients to the tendons but also is a constant source of lubrication, permitting frictionless gliding between the tendons. Adhesions between the tendons and other tissues restrict excursion. Stiff joints limit motion and function despite a normal tendon system.

The loss of the pulley system no longer prevents the tendons from gliding juxtaposed to the phalanges. The tendons bowstring away from the skeleton as the finger is flexed. This bowstringing increases the moment arm (a line drawn from the midaxis of the joint to the flexor tendon) of the tendon at that point. Greater excursion of the tendon and a greater amplitude of muscle contraction are required to obtain the same amount of finger flexion.

The clinical ramifications of tendon bowstringing are a weakened grip, incomplete flexion, and an ensuing stiffness of the joints. During normal tendon excursion, passive metacarpophalangeal (MCP) joint movement produces no relative motion of the flexor tendons. Distal interphalangeal (DIP) joint motion is 1-2 mm of FDP tendon excursion per 10º of joint flexion. Proximal interphalangeal (PIP) joint motion is 1-2 mm of FDP tendon and flexor digitorum superficialis (FDS) tendon excursion per 10º of joint flexion. Differential excursion is increased with a palmar bar or synergistic splints (wrist extension). The overall excursion of the FDS and FDP tendons is approximately 88 mm and 86 mm, respectively, to obtain total digit and composite flexion. Excursion of 2.5 cm is required for complete flexion of the fingers.

Treatment and hand rehabilitation are based on the understanding of the tendon-injury healing mechanism. Healing of the flexor tendon system has 4 stages: hemostasis, inflammation, proliferation, and remodeling.

• Hemostasis - Characterized by vasoconstriction, platelet deposition, and fibrin clot. The amount of clot may affect the ultimate repair by increasing the number of adhesions.
• Inflammation - Involves diapedesis of pro-inflammatory cells. Neutrophils and macrophages pass from the intravascular space to the extravascular space. Pro-inflammatory cytokines are released, and fibronectin is used as scaffolding for collagen deposition and vascular ingrowth. The inflammatory phase lasts approximately 0-7 days.
• Proliferation - Characterized by a marked rise in fibroblast proliferation occurring within 1 cm of the repair site. The proliferation phase lasts 2-28 days. The epitenon cells proliferate and migrate into the zone of injury. The epitenon cells are analogous to the epithelium of the skin, as these cells quickly cover the surface of the repair site in an attempt to restore a gliding surface. Collagen deposition rises markedly and rapidly as the fibroblasts proliferate. The vascular ingrowth can then migrate in via the collagen/fibronectin scaffolding.
• Remodeling - Marked by the increasing strength of the tendon repair. The collagen fibers increasingly reorientate to become parallel with the noninjured tendon fibers. The rate of collagen synthesis decreases. The clinical importance of the remodeling phase, which starts at approximately the sixth week, is that during this interval, active and passive range of motion (ROM) is mandated to promote tendon excursion and diminish local adhesions. During this time, the ROM of all digits is increased, external scar control and blocking exercises are initiated, and resting exercises and strengthening procedures can be started.

Clinical

Careful attention to the patient's history and the mechanism of injury can often alert the hand surgeon to the extent of the pathology. Finger position at the time of injury is important. If the injury occurred while the finger was in flexion, the level of the tendon injury will be distal to the skin laceration. A finger that is injured in the extended position will have a tendon injury that closely corresponds to the skin laceration.

The natural resting position of the hand should be closely observed to determine whether the normal composite cascade of the fingers has been disrupted. In the uninjured hand, the composite flexion of the fingers increases from the radial to the ulnar side. The finger with a tendon disruption nests in a more extended position. If only the FDP tendon has been transected, the flexion of the MCP and PIP joints may be within the normal cascade but the DIP will be extended. A finger in which the FDS tendon and the FDP tendon are disrupted will lie flat in an extended position outside the normal cascade of fingers. A thorough, formal examination of the FDS and FDP tendons is important because testing these tendons may reveal partial lacerations. A partial laceration may present with pain when the patient attempts to flex against resistance. A thorough neurovascular examination is warranted to alert the surgeon to the possible need for microsurgical repair of the vessels or nerves.

The integrity of FDS and FDP tendons should be tested independently and in tandem. The examiner holds the other fingers in extension and stabilizes MCP and PIP joints. To test the FDP tendon, the patient is asked to flex the distal phalanx. To test the FDS tendon, MCP and PIP joints are released. Distal phalanges are kept extended, and the patient flexes the finger. The PIP joint and, to a lesser degree, the MCP joint should flex. About 20% of patients are missing an FDS tendon in the little finger. Thus, these patients have limited or no PIP flexion during testing. For flexor pollicis longus (FPL) testing, the thumb MCP joint is stabilized in neutral position. The patient is asked to flex the interphalangeal (IP) joint against resistance. A communication may exist between the FPL and the index FDP. The examiner stabilizes the other 3 digits. The patient opposes his or her thumb to the little finger MCP joint. Flexion of the index distal phalanx proves the existence of this anomalous communication.

Two additional ways exist to evaluate the integrity of the flexor tendon. Passively manipulating the wrist through flexion and extension results in extension and flexion of the digits, respectively. This test uses the tenodesis effect of the antagonistic tendons. Compression of the forearm flexion muscles also can be used to test the integrity of the flexor tendons in the hand. As the forearm is compressed, the digits are drawn into flexion. Transected tendons in the digits do not flex with this maneuver, nor do they extend and flex with the tenodesis test.

INDICATIONS

Section 3 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

See Surgical Therapy and Follow-up.

RELEVANT ANATOMY

Section 4 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

Flexor tendons of the forearm originate from the muscles based on the medial epicondyle and on the proximal radius and ulna. Flexor tendon muscle bellies have 3 layers: superficial, intermediate, and deep. The superficial layer consists of the pronator teres, which is the most radial of the superficial muscles. The flexor carpi radialis, palmaris longus, and flexor carpi ulnaris proceed in a radial-to-ulnar direction, respectively. The FDS is the only muscle of the intermediate layer. This muscle has 2 separate heads of origin: the radial head of the medial epicondyle and the ulnar head of the ulna and radial head from the brief muscular line of the radius. The 2 muscles of the deep layer are the FDP and the FPL. The FDP originates from the proximal two thirds of the ulna and from the interosseous membrane, and some element of the muscle may originate from the proximal radius. The FPL originates from the middle third of the radius and from the interosseous membrane.

The FDS and the FDP tendons travel through the carpal tunnel to insert in the fingers. The FPL is the most radial structure of the radial tunnel; it extends on the volar aspect of the first ray. The FDP tendon inserts into the base of the distal phalanx, whereas the FDS tendon inserts into the base of the proximal phalanx. At the level of the A1 pulley, the FDS tendon decussates to form the Camper chiasma. The FDP tendon extends through the chiasma from below the FDS tendon to become the more superficial tendon.

The FDP tendon flexes the distal phalanx and secondarily flexes the PIP joint and the MCP joint. The FDS tendon flexes the PIP joint and secondarily flexes the MCP joint.

The ulnar nerve supplies the flexor carpi ulnaris, the ulnar 2 FDP tendons (to the little and ring fingers), and the intrinsic muscles of the hand (except for the radial 2 lumbrical muscles, the opponens pollicis, and the abductor pollicis brevis). The median nerve supplies the remaining extrinsic flexors in the forearm, the radial 2 lumbrical muscles, and the thenar muscles (except for the deep head of the flexor pollicis brevis, which is innervated by the ulnar nerve).

The fibro-osseous canal is the tunnel in the digits where the flexor tendons are located. The metacarpals form the dorsal wall, and the annular pulley system and flexor sheath provide radial, ulnar, and volar coverage. The flexor synovial sheath of the fingers is present from the midpalm up to the level of the FDP insertion. The sheath for the thumb and index finger often proceeds down through the carpal tunnel and can join up in the distal forearm in a horseshoe bursa configuration. The annular and cruciform pulleys form an intricate constraining sheath to keep the tendons close to the bone, preventing bowstringing during their excursion to flex the MCP, PIP, and DIP joints.

Three cruciform pulleys (C1-C3) and 5 annular pulleys (A1-A5) exist. From a biomechanical vantage point, the A2 and A4 pulleys are considered the most important to the prevention of bowstringing. Flexor tendons have 5 different zones in the hand, as follows:

• Zone I contains only the FDP tendon and extends from the insertion of the FDP to the insertion of the FDS tendon.
• Zone II is the area once referred to as "no man's land." It is defined as the area extending from the insertion of the FDS tendon to the proximal end of the A1 pulley.
• Zone III is the zone of lumbrical origin in the palm.
• Zone IV is in the carpal tunnel
• Zone V is proximal to the carpal tunnel in the forearm.

Nutrition to the tendons is derived from 2 sources: intrinsic and extrinsic. Intrinsic nutrition occurs through vascular perfusion of the tendon. The 4 sources of vascular perfusion are as follows:

• Longitudinal vessels that enter the palm and extend down the intertendinous channels
• Vessels entering at the level of the proximal synovial fold in the palm
• Vincula (2 short and 2 long) harboring segmental branches from the digital arteries
• Osseous insertions

The internal vascularity of the tendon is primarily positioned in the septa of the endotendon separating the tendon fascicles. It should be noted that the vascular supply is mainly on the dorsal side of the tendons. The tendon in the area of the proximal phalanx also has a relatively poor blood supply. Extrinsic nutrition is provided by synovial fluid diffusion that occurs as synovial fluid is pumped into the tendon fibers during flexion and extension of the fingers.

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

Imaging Studies

• The injured hand should be radiographed to exclude any underlying fractures.
• Bodner and colleagues reported that ultrasonography and magnetic resonance imaging (MRI) can be used to accurately diagnose the complete disruption of annular pulley ligaments of the flexor tendons.¹

Other Tests

• See Clinical.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

Medical Therapy

The general principles of a tendon repair include the administration of intravenous (IV) antibiotics when indicated and the evaluation of the patient's tetanus immunization status.

Surgical Therapy

All flexor tendons should be repaired in the main operating room because, unlike many emergency departments, this arena is a controlled, sterile environment. Surgical exposure can be obtained through Brunner (volar zigzag) or lateral incisions. Hemostasis, irrigation, and debridement are of vital importance. Debris and nonviable tissue left within the wound are niduses for infection, which can severely compromise the final ROM of the finger.

The surgeon should handle only the lacerated edges of the tendon to avoid tendon bunching and trauma to the uninjured area of the tendon. Exposed knots and sutured ends may promote adhesion formation. One or 2 core sutures and a running epitendinous suture should be used. Early initiation of rehabilitation is important for an optimal result.

The ideal repair is reliable, simple, and strong and does not impair healing. The optimal time for repair of the flexor tendons is within 24 hours of the injury. The longer the severed tendons have to develop adhesions and scar tissue, the smaller the possibility of restoring full function. Most repairs should be performed within the first 2 weeks following injury, since the tendon ends and tendon sheaths become scarred, and the musculotendinous units retract. Subsequent repairs after this time decrease the ultimate mobility of the fingers.

Repairs of the flexor tendon are performed under tourniquet control. Brunner or lateral (midaxial) incisions are used so that adequate exposure of the flexor fibro-osseous canal can be obtained. Care is taken not to breach the integrity of the neurovascular bundles, which can be quite superficial in the finger.

The location of the severed flexor tendon ends depends on the position of the finger at the time of injury. In a flexed finger, the flexor tendon is pulled proximally. The distal end of the flexor tendon is drawn distally as the finger assumes an extended position. The opposite is true for an extended finger, in which the distal flexor tendon end can usually be found at the site of the laceration.

The proximal tendon end retracts to a variable degree into the palm because of the muscle tension of the profundus and lumbrical muscles. The vincula to the tendons may prevent the proximal tendon from retracting during retrieval. The tendon can be retrieved with Jacob forceps or fine clamps, aided by milking the tendon proximally to distally. Alternatively, a pediatric feeding tube can be used to pull the tendon back into the wound. A counterincision in the palm must be made to find the proximal end of the severed tendons. Once identified, the feeding tube is introduced at the distal wound site through the fibro-osseous canal, to emerge through the palmar counterincision site. The feeding tube is sutured to the end of the tendon and pulled out distally, carrying with it the proximal end of the flexor tendon. The tendon is held in this position with a 25-gauge needle in the palm.

Disruption of the pulleys, especially A2 and A4, should be avoided. If the laceration is at these pulleys or if the repair is hindered because of the pulleys, then Z-plasties in the pulleys or partial releases may be required. The pulleys are repaired after the tendon is repaired. Shredded or mutilated pulleys may be reconstructed with a slip of the FDS tendon, tendon grafts, or extensor retinaculum grafts.

The initial intraoperative repair of flexor tendon injuries should follow the principles of all open wound management and consist of irrigation and debridement. All devitalized tissue is excised, the wound is thoroughly irrigated, and the vital structures are identified and isolated for repair. An atraumatic technique for tendon manipulation prevents further injury to the tendons and decreases the amount of adhesion formation. Every traumatic site along the tendon is another potential spot for adhesion formation. Delicate forceps, such as the Bishop-Harmon or Iris forceps, should be used to pick up the tendon at its severed end, although not along the sides of the tendon. The goal of the tendon repair is to coapt the severed ends without bunching or leaving a gap. Bunching of the repair may inhibit tendon excursion under the pulley system. A gap left at the repair site can either weaken the repair, which will subsequently be prone to rupture,  or  foster  an overabundance  of  adhesions,  limiting  excursion  of  the  tendon.

The suture material that is used to repair the severed tendon varies. The usual caliber of suture is either 3.0 or 4.0. Braided or monofilament sutures also have been used.

Strickland concluded that 6-strand repairs are stronger than 4-strand repairs, which, in turn, are stronger than 2-strand repairs.^{2, 3, 4, 5, 6} The tendon repair strength is thus proportional to the number of sutures that are placed across the repair site. A peripheral epitendinous suture permits an approximation of tendon ends and increases the repair strength.

Types of repairs

The various types of repair are listed below. This list illustrates the importance of a core suture followed by an epitendinous suture to complete the tendon repair.

• Commonly used techniques for end-to-end flexor tendon repair are as follows:
• • Kessler grasping suture
  • Tajima suture
  • Kessler-Tajima suture
  • Bunnell suture
  • Tsuge suture
  • Becker suture (bevel technique)
  • Double loop suture (Lee)
  • Interlock suture (Robertson)
  • Single-cross grasp 6-strand suture (Sandow)
  • Double-grasping single suture⁷
  • Double-grasping 2 sutures⁷
  • Six-strand suture using 3 suture pairs (Lim and Tsai)
  • Strickland suture
  • MGH suture
  • Indianapolis 4-strand suture
• Peripheral tendon (epitendinous) suture techniques are as follows:
• • Simple running suture
  • Running lock loop suture (Lin)
  • Cross-stitch epitendinous repair technique (Silfverskiold)
  • Halsted continuous horizontal mattress suture (Wade)
  • Horizontal mattress intrafiber suture (Mashadi and Amis)

A dorsal splint is recommended to keep the wrist in 30° of flexion and MCP joints in 50-70° of flexion. The PIP and DIP should be able to extend fully. In zone IV lacerations, the wrist is splinted in neutral position and MCP joints in 75-90° of flexion. When the FPL is injured, the wrist is flexed at 50° and the MCP and DIP are flexed at 15-20°.

Follow-up

The key to success of flexor tendon repair is close adherence to a regimented hand therapy rehabilitation program. Complete immobilization is recommended for children younger than 10 years and for patients who are unable or unwilling to follow a controlled-motion protocol. Various protocols are available following flexor tendon repair. Each protocol must take into consideration the stress placed on flexor tendons before and after the repair.

Tensile stress on normally repaired flexor tendons is as follows:

• Passive motion - 500-750 g
• Light grip - 1500-2250 g
• Strong grip - 5000-7500 g
• Tip pinch, index FDP tendon - 9000-13,500 g

Edema and scar tissue increase the drag on a tendon, thereby increasing the force needed to carry out a given task. At the same time, the strength of the repair is variable over the course of the healing process. Initially rather strong, the repair strength decreases significantly between days 5 and 21.

The tendon is weakest during this period because of minimal tensile strength. Strength increases rapidly when tendon is stressed. Controlled stress is applied in proportion to increasing tensile strength. Stressed tendons heal faster, gain strength faster, and have fewer adhesions and better excursion. Tensile strength begins to gradually grow stronger at 3 weeks. Generally, blocking exercises are initiated 1 week after active ROM excursion (5 wk postoperatively).

Passive ROM in extension exercises start 2 weeks after active ROM excursion (6 wk postoperatively). Graded excursion strengthening starts 8 weeks postoperatively. If the digital nerve was repaired simultaneously, the PIP joint should be splinted at 30° of flexion in a dorsal-blocking splint. Extension may increase by 10° weekly, starting from the fourth week. No protocol allows forceful use of the hand until the end of the eighth postoperative week. The greatest achievement with ROM is seen between 12 and 14 weeks after surgery. Unrestricted motion and normal hand use are allowed 12 weeks after the repair. A plateau may be seen after 6-8 weeks.

The use of a dorsal-blocking splint places repaired tendons in a protected, shortened position to alleviate stress to anastomosis and prevents full, active extension. Rubber band traction maintains digits in a flexed position. Also, it extends splint restraint because flexors do not contract. Rubber bands pull digits back into flexion, alleviating any active flexor contraction. Rubber band traction provides tendon excursion to repaired tendons while minimizing stress. Tendon glide during the healing phase minimizes scar adhesions while promoting intrinsic tendon healing. The patient should be observed for fixed flexion contracture of the PIP joint. Three main protocol groups exist: active extension associated with rubber band flexion, controlled active motion, and controlled passive motion.

Injuries to zones I, II, and III

An early mobilization protocol is recommended. A well-motivated and reliable patient can initiate a Duran or Indianapolis protocol. Otherwise, the Kleinert protocol is applied, using rubber bands attached to hooks that have been glued to the patient's fingernails.

Modified Kleinert protocol

In the modified Kleinert protocol, pulleys are added at the level of the distal palm to obtain maximum DIP flexion. Rubber bands are removed at night. All patients are instructed to passively extend the PIP joint completely inside the splint to avoid flexion contractures.

• At surgery, a half (dorsal-blocking) cast is applied with the wrist at 20-30° of flexion, MCP joints at 70-80° of flexion, and IP joints straight.
• After 1 week, the cast is removed and a thermoplastic splint is applied with the joints at the same angles. All digits stay in splint. The index finger may be left free if only the ring or small finger tendon is involved. Dynamic traction is applied, with the distal palmar pulley on the involved finger. The patient begins active extension from the dorsal-blocking splint against rubber band traction. He or she performs passive PIP and DIP motion within the restraints of the dorsal-blocking splint 4 times per day.
• After 2 weeks, sutures are removed. On intermittent days, the IP joints are positioned straight, with a dorsal-blocking splint only if fixed flexion contractures are developing.
• After 4 weeks, the patient begins active composite flexion and active extension out of splint. Dorsal-blocking continues between exercises.
• After 5 weeks, the dorsal-blocking splint is discontinued. The patient may initiate blocking exercises and functional electrical stimulation (FES) as necessary.
• After 6 weeks, the patient begins gentle passive extension. If necessary, a static extension splint is used for extrinsic flexor tightness.
• After 8 weeks, light strengthening exercises with a firm-but-squeezable foam ball (eg, Nerf ball), putty, or a hand helper are begun.
• After 12 weeks, the patient resumes normal activities.

Duran protocol

The Duran protocol is most frequently used and modified by hand therapists. If a flexion contracture develops, 2 options exist: initiation of the Kleinert technique or controlled passive extension of IP joints (with the more proximal joints in the protected position of full flexion).

• At surgery, a half (dorsal-blocking) cast is applied with the wrist at 20-30° of flexion, the MCP joints at 70-80° of flexion, and the IP joints straight.
• At 1 week, the cast is removed and a dorsal splint is placed. The wrist is held in 20° of flexion, and the MCP joints are held in relaxed flexion. With the MCP and PIP joints flexed, the DIP joint is passively extended. Then, with the DIP and MCP joints flexed, the PIP joint is extended. Thus, FDP and FDS tendon repairs diverge.
• After 4.5 weeks, the splint is removed and a wristband with rubber band traction is applied. While awake, the patient passively flexes all joints of the affected finger toward the palm and then actively extends the finger to the splint hood 15-25 times per hour.
• After 5.5 weeks, the patient begins active flexion with wristband removal.
• After 7.5 weeks, the patient begins resisted flexion.

Indianapolis protocol

The Indianapolis protocol is indicated for patients with 4-strand Tajima and horizontal mattress repair with an additional peripheral epitendinous suture. Patients should be motivated and understanding. Digits should have minimal or moderate edema and minimal wound complications.

Two splints are used, the traditional dorsal-blocking splint—with the wrist at 20-30° of flexion, MCP joints in 50° of flexion, and IP joints in neutral—and the Strickland tenodesis splint. The latter allows full wrist flexion and 30° of dorsiflexion, while digits have full ROM, and MCP joints are restricted to a 60° extension.

• For the first 1-3 weeks, the modified Duran protocol is used. The patient performs repetitions of flexion and extension to the PIP and DIP joints, as well as to the whole finger, 15 times per hour. Exercise is restrained by the dorsal splint. Then, the Strickland hinged wrist splint is applied. The patient passively flexes the digits while extending the wrist. The patient then gently contracts the digits in the palm and holds for 5 seconds.
• At 4 weeks, the patient exercises 25 times every 2 hours without any splint. A dorsal-blocking splint is worn between exercises until the sixth week. The digits are passively flexed while the wrist extends. Light muscle contraction is held for 5 seconds, and the wrist drops into flexion, causing digit extension through tenodesis. The patient begins active flexion and extension of the digits and wrist. Simultaneous digit and wrist extension is not allowed.
• After 5-14 weeks, the IP joints are flexed while the MCP joints are extended, and then the IP is extended.
• After 6 weeks, blocking exercises commence if digital flexion is more than 3 cm from the DPFC. No blocking is applied to the small finger FDP tendon.
• At 7 weeks, passive extension exercises are begun.
• After 8 weeks, progressive gradual strengthening is begun.
• After 14 weeks, activity is unrestricted.

Delayed mobilization in zone I-V injuries

Delayed mobilization in zone I-V injuries is indicated for patients who are unreliable, patients with a poor quality flexor tendon (as a result, for example, of a crush injury or a revascularization problem), children aged 10 years or younger, and patients with multiple anatomic structures involved other than flexor tendons.

• A dorsal-blocking splint is applied. The wrist is held at 30° of flexion, the MCP joints are held at 50° of flexion, and the IP joints are extended.
• At 3 weeks, active and passive motion exercises are performed within the restraints of the splint.
• After 4.5 weeks, active and motion exercises are performed outside of the splint. Protective splinting is continuous.
• After 6 weeks, the splint is discontinued and passive motion exercises are begun in extension.

Injury in zones IV-V

• At surgery, a half (dorsal-blocking) cast is applied with the wrist at 30° of flexion, the MCP joints at 50° of flexion, and the IP joints at full extension.
• After 3-5 days, the cast is removed, and a dorsal-blocking splint is applied at the same angles. The splint may vary depending on which tendon is injured (wrist vs digital tendon). Passive ROM is begun within splint restrains.
• At 3 weeks, active ROM is begun within splint restraints. FES is initiated a few days after the initiation of active ROM.
• After 4 weeks, active ROM outside of the splint is begun.
• After 6 weeks, splint use is discontinued, and passive extension is begun.

Flexor pollicis longus injury

• At surgery, a dorsal-blocking cast is applied with the wrist in 20° of flexion, the MCP and IP joints in 15° of flexion, and the carpometacarpal (CMC) joint in palmar abduction.
• The dynamic or static protocol used in injuries to zones I-V is used.

Excursion/differential gliding

Hook and fist positions produce more gliding of the FDP tendon than of the FDS tendon. In the rooftop (angle) and straight fist positions, FDS tendon excursion exceeds that of the FDP tendon. The greatest excursion for the FDS tendon is in the straight fist position, and the greatest excursion for FDP tendon is in the full fist position. Maximum gliding between the FDP and FDS tendons is in the hook position. The straight, fist, and hook positions provide maximum differential gliding for both flexors. When the hand is held in the fist position for a sustained period, the 2 flexors require the greatest amount of muscle contraction.

COMPLICATIONS

Section 7 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

The most common complication of flexor tendon laceration is the development of adhesions, which causes stiff joints. Factors that promote adhesion formation are trauma to the tendon and sheath, bleeding in the tendon sheath, foreign material in the tendon and sheath, tendon ischemia, digital immobilization, the loss of the tendon sheath or pulleys, gap formation following tendon repair, and prolonged edema. Factors that suppress adhesion formation are tendon mobilization, tendon stress, and minimal tendon or sheath trauma. Flexor contractures of IP joints after the initiation of an early hand therapy rehabilitation program require prompt protocol modification. Greater joint extension and dynamic splints are recommended.

Rupture of the tendon repair is most common between the seventh and tenth postoperative day. If the clinical diagnosis of a digital flexor tendon rupture is uncertain, MRI can be used for this evaluation. This noninvasive tool can be very helpful in the early postoperative period, when active flexion is not possible to aid in the clinical diagnosis of tendon rupture. Also, MRI can be used to differentiate adhesions from tendon rupture as the cause of immobility. Other possible complications of flexor tendon laceration are skin flap compromise, injury to neurovascular structures and the development of reflex sympathetic dystrophy (RSD), bowstringing of the tendon, infection, and permanent contractures.

OUTCOME AND PROGNOSIS

Section 8 of 9  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

So and colleagues conducted a prospective study to compare 5 different evaluation systems for flexor tendon repair.⁸ They reported significant discrepancies among the evaluation methods. Currently, no universally accepted evaluation method exists for flexor tendon repair.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• References

1. Bodner G, Rudisch A, Gabl M, et al. Diagnosis of digital flexor tendon annular pulley disruption: comparison of high frequency ultrasound and MRI. Ultraschall Med. Aug 1999;20(4):131-6. [Medline].
2. Strickland JW. Opinions and preferences in flexor tendon surgery. Hand Clin. Feb 1985;1(1):187-91. [Medline].
3. Strickland JW. Results of flexor tendon surgery in zone II. Hand Clin. Feb 1985;1(1):167-79. [Medline].
4. Strickland JW. Flexor tendon repair. Hand Clin. Feb 1985;1(1):55-68. [Medline].
5. Strickland JW. Flexor tendon injuries. Part 1. Anatomy, physiology, biomechanics, healing, and adhesion formation around a repaired tendon. Orthop Rev. Oct 1986;15(10):632-45. [Medline].
6. Strickland JW. Flexor tendon surgery. Part 1: Primary flexor tendon repair. J Hand Surg [Br]. Aug 1989;14(3):261-72. [Medline].
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Article Last Updated: Oct 19, 2007