Important points for rehabilitation after flexor tendon laceration and repair

Figure 1-1 Author’s technique of flexor tendon repair in zone II. A, Knife laceration through zone II with the digit in full flexion. The distal stumps retract distal to the skin incision with digital extension. B, Radial and ulnar extending incisions are used to allow wide exposure of the flexor tendon system. Note appearance of the flexor tendon system of the involved fingers after the reflection of skin flaps. The laceration occurred through the C1 cruciate area. Note the proximal and distal position of the flexor tendon stumps. Reflection of small flaps (“windows”) in the cruciate-synovial sheath allows the distal flexor tendon stumps to be delivered into the wound by passive flexion of the distal interphalangeal (DIP) joint. The profundus and the superficialis stumps are retrieved proximal to the wound by passive flexion of the DIP joint. The profundus and superficialis stumps are retrieved proximal to the sheath by the use of a small catheter or infant feeding gastrostomy tube. C, The proximal flexor tendon stumps are maintained at the repair site by means of a transversely placed small-gauge hypodermic needle, allowing repair of the FDS slips without extension. D, Completed repair of both FDS and FDP tendons is shown with the DIP joint in full flexion. Extension of the DIP joint delivers the repair under the intact distal flexor tendon sheath. Wound repair is done at the conclusion of the procedure.

Figure 1-2 Blood supply to the flexor tendons within the digital sheath. The segmental vascular supply to the flexor tendons is by means of the long and short vincular connections. The vinculum brevis superficialis (VBS) and the vinculum brevis profundus (VBP) consist of small triangular mesenteries near the insertion of the FDS and FDP tendons, respectively. The vinculum longum to the superficialis tendon (VLS) arises from the floor of the digital sheath of the proximal phalanx. The vinculum longum to the profundus tendon (VLP) arises from the superficialis at the level of the proximal interphalangeal (PIP) joint. The cut-away view depicts the relative avascularity of the palmar side of the flexor tendons in zones I and II as compared with the richer blood supply on the dorsal side, which connects with the vincula.

Rehabilitation rationale and basic principles of treatment after flexor tendon repair

Anatomy

The anatomic zone of injury of the flexor tendons influences the outcome and rehabilitation of these injuries. The hand is divided into five distinct flexor zones (Fig. 1-3):

• Zone 1—from the insertion of the profundus tendon at the distal phalanx to just distal to the insertion of the sublimus

• Zone 2—Bunnell’s “no-man’s land”: the critical area of pulleys between the insertion of the sublimus and the distal palmar crease

• Zone 3—“area of lumbrical origin”: from the beginning of the pulleys (A1) to the distal margin of the transverse carpal ligament

• Zone 4—area covered by the transverse carpal ligament

• Zone 5—area proximal to the transverse carpal ligament

Figure 1-3 The flexor system has been divided into five zones or levels for the purpose of discussion and treatment. Zone II, which lies within the fibro-osseous sheath, has been called “no man’s land” because it was once believed that primary repair should not be done in this zone.

As a rule, repairs to tendons injured outside the flexor sheath have much better results than repairs to tendons injured inside the sheath (zone 2).

It is essential that the A2 and A4 pulleys (Fig. 1-4) be preserved to prevent bowstringing. In the thumb, the A1 and oblique pulleys are the most important. The thumb lacks vincula for blood supply.

Figure 1-4 The fibrous retinacular sheath starts at the neck of the metacarpal and ends at the distal phalanx. Condensations of the sheath form the flexor pulleys, which can be identified as five heavier annular bands and three filmy cruciform ligaments (see text).

Rehabilitation after flexor tendon repair

The rehabilitation protocol chosen (Rehabilitation Protocols 1-1 and 1-2) depends on the timing of the repair (delayed primary or secondary), the location of the injury (zones 1 through 5), and the compliance of the patient (early mobilization for patients who are compliant and delayed mobilization for patients who are noncompliant and children younger than 7 years of age). A survey of 80 patients with flexor and extensor tendon repairs determined that two thirds were nonadherent to their splinting regimen, removing their splints for bathing and dressing (Sandford et al. 2008).

REHABILITATION PROTOCOL 1-1 Rehabilitation Protocol after Immediate or Delayed Primary Repair of Flexor Tendon Injury: Modified Duran Protocol

Marissa Pontillo, PT, DPT, SCS

Postoperative Day 1 to Week 4.5

• Keep dressing on until Day 5 postoperative.

• At Day 5: replace with light dressing and edema control prn.

• Patient is fitted with dorsal blocking splint (DBS) fashioned in:

• 20 degrees wrist flexion.

• 45 degrees MCP flexion.

• Full PIP, DIP in neutral

• Hood of splint extends to fingertips.

• Controlled passive motion twice daily within constraints of splint:

• 8 repetitions of passive flexion and active extension of the PIP joint

Passive flexion and extension exercises of the proximal interphalangeal (PIP) joint in a dorsal blocking splint (DBS).

Passive flexion and extension exercises of the distal interphalangeal (DIP) joint in a dorsal blocking splint (DBS).

• 8 repetitions of passive flexion and active extension of the DIP joint

• 8 repetitions of active composite flexion and extension of the DIP and PIP joints with the wrist and MCP joints supported in flexion

4.5 Weeks

• Continue passive exercises as needed.

• Removal of DBS every 2 hours to perform 10 repetitions of each active flexion and extension of the wrist and of the digits

• May start intrinsic minus (hook fist) position and/or tendon gliding exercises

• Active wrist extension to neutral only

• Functional electrical stimulation (FES) with the splint on

5.5 Weeks

• Continue passive exercises.

• Discontinue use of DBS.

• Exercises are performed hourly:

• 12 repetitions of PIP blocking

• 12 repetitions of DIP blocking

• 12 repetitions of composite active flexion and extension

• May start PROM into flexion with overpressure

6 weeks

• Initiate passive extension for the wrist and digits.

8 weeks

• Initiate gentle strengthening.

• Putty, ball squeezes

• Towel walking with fingers

• No lifting or heavy use of the hand

10–12 weeks

• Return to previous level of activity, including work and sport activities.

In a comparison of early active mobilization and standard Kleinert splintage,Yen et al. (2008)found at an average 4-month follow-up (3 to 7 months) that those in the early active mobilization group had 90% of normal grip strength, pinch, and range of motion compared to 50%, 40%, and 40%, respectively, in those with Kleinert splinting.

Sueoka and LaStayo (2008) devised an algorithm for zone 2 flexor tendon rehabilitation that uses a single clinical sign—the lag sign—to determine the progression of therapy and the need to modify existing protocols for individual patients. They defined “lag” as PROM—AROM (active ROM) ≥15 degrees and consider it a sign of tendon adherence and impairment of gliding. Rehabilitation begins with an established passive ROM Protocol (Duran), which is followed for 3.5 weeks before the presence or absence of a lag is evaluated. The presence or absence of lag is then evaluated at the patient’s weekly or twice-weekly visits, and progression of therapy is modified if a lag sign is present (Rehabilitation Protocol 1-3).

REHABILITATION PROTOCOL 1-3 Zone 2 Lag Sign Algorithm

Background

Trigger finger is a painful snapping phenomenon that occurs as the finger flexor tendons suddenly pull through a tight A1 pulley portion of the flexor sheath. The underlying pathophysiology of trigger finger is an inability of the two flexor tendons of the finger (FDS and FDP) to slide smoothly under the A1 pulley, resulting in a need for increased tension to force the tendon to slide and a sudden jerk as the flexor tendon nodule suddenly pulls through the constricted pulley (triggering). The triggering can occur with flexion or extension of the finger or both. Whether this pathologic state arises primarily from the A1 pulley becoming stenotic or from a thickening of the tendon remains controversial, but both elements are usually found at surgery.

Clinical history and examination

Trigger finger most commonly occurs in the thumb, middle, or ring fingers. Patients typically present with clicking, locking, or popping in the affected finger that is often painful, but not necessarily so.

Patients often have a palpable flexor tendon nodule in the area of the thickened A1 pulley (which is at the level of the distal palmar crease). This nodule can be felt to move with the tendon and is usually painful to deep palpation.

To induce the triggering during examination, it is necessary to have the patient make a full fist and then completely extend the fingers because the patient may otherwise avoid triggering by only partially flexing the fingers.

Treatment

Spontaneous long-term resolution of trigger finger is rare. If left untreated, the trigger finger will remain a painful nuisance; however, if the finger should become locked, the patient may develop permanent joint stiffness. Historically, conservative treatment included splinting of the finger in extension to prevent triggering, but this has been abandoned because of stiffening and poor result.

Currently, nonoperative treatment involves injection of corticosteroids with local anesthetic into the flexor sheath. A meta-analysis of the literature found convincing evidence that combining lidocaine with the corticosteroid obtains results superior to those with corticosteroid alone(Chambers 2009). In a cost-minimization analysis, the use of two steroid injections before resorting to surgery was found to be the least costly treatment strategy compared to one or three injections before surgery and open or percutaneous release(Kerrigan and Stanwix 2009).

Our preference is 0.5 ml lidocaine, 0.5 ml bupivicaine, and 0.5 ml methylprednisolone acetate (Depo-Medrol) (Fig. 1-5). A single injection can be expected to relieve triggering in about 66% of patients. Multiple injections have been reported to relieve triggering in 75% to 85% of patients. Current reports indicate a success rate of 47% to 87% with this type of treatment. Systematic review of levels I and II studies in the Journal of the American Academy of Orthopedic Surgeons (Fleisch et al. 2007) indicates a success rate of 57%. Prognostic indicators of recurrence of trigger digits after corticosteroid injection include younger age, insulin-dependent diabetes mellitus, involvement of multiple digits, and a history of other tendinopathies of the upper extremity (Rozental et al. 2008).

Figure 1-5 A, Needle entrance points (dots) are located approximately one third distance from the distal palmar crease and two thirds the distance from the proximal distal crease. This corresponds to the center of the A1 pulley. B, Diagram depicts the location of the A1 pulleys in the fingers and the A2 pulley in the ring finger. Half of the A2 pulleys are located in the distal palm. C, A1 pulley of the thumb. D, Diagram depicts the optimal insertion point for the needle.

The risk of cortisone injection here is of inadvertent injection into the flexor tendon with possible tendon weakening or rupture. Ultrasound guidance has been reported to help avoid this complication and improve results (Bodor and Flossman 2009).

Physical therapy usually is not necessary to regain motion after cortisone injection because most patients are able to regain motion once the triggering resolves.

Surgery to “release” a trigger finger is a relatively simple outpatient procedure done with the patient under local anesthesia. The surgery involves a 1- to 2-cm incision in the palm overlying the A1 pulley to identify and completely divide the A1 pulley. Gentle active motion is initiated early, and return to unrestricted activities usually is possible at about 3 weeks (Rehabilitation Protocol 1-4).

Pediatric trigger thumb

Pediatric trigger thumb is a congenital condition in which stenosis of the A1 pulley of the thumb in infants causes locking in flexion (inability to extend) of the IP joint. It often is bilateral. Usually no pain or clicking occurs because the thumb remains locked. A recent report by Baek et al. (2008) indicates spontaneous resolution in 63% of cases. The rest require surgical intervention when the patient is around 2 to 3 years old to release the tight A1 pulley and prevent permanent joint flexion contracture.

Background

Avulsion of the flexor digitorum profundus (“jersey finger”) can occur in any digit, but it is most common in the ring finger. This injury usually occurs when an athlete grabs an opponent’s jersey and feels sudden pain as the distal phalanx of the finger is forcibly extended as it is concommitantly actively flexed (hyperextension stress applied to a flexed finger).

The resultant lack of active flexion of the DIP joint (FDP function loss) must be specifically checked to make the diagnosis (Fig. 1-6). Often the swollen finger assumes a position of extension relative to the other, more flexed fingers. The level of retraction of the FDP tendon back into the palm generally denotes the force of the avulsion.

Figure 1-6 With avulsion of the flexor digitorum profundus, the patient would be unable to flex the distal interphalangeal (DIP) joint, shown here.

(From Regional Review Course in Hand Surgery. Rosemont, Illinois, American Society of Surgery of the Hand, 1991, Fig. 7).

Leddy and Packer (1977) described three types of FDP avulsions based on where the avulsed tendon retracts: type I, retraction of the FDP to the palm; type II, retraction to the proximal interphalangeal (PIP) joint; and type III, bony fragment distal to the A4 pulley. Subsequently, a type IV injury was described in which a type III lesion is associated with a simultaneous avulsion of the FDP from the fracture fragment. Treatment is based on the anatomy of the injury.