Grade	Preoperative Condition
1	Good: minimal scar with mobile joints and no trophic changes
2	Cicatrix: heavy skin scarring from injury or previous surgery; deep scarring from failed primary repair or infection
3	Joint damage: injury to the joint with restricted range of motion
4	Nerve damage: injury to the digital nerves resulting in trophic changes in the finger
5	Multiple damage: involvement of multiple fingers with a combination of the above problems

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).

Tendon Healing

The exact mechanism of tendon healing is still unknown. Healing probably occurs through a combination of extrinsic and intrinsic processes. Extrinsic healing depends on the formation of adhesions between the tendon and the surrounding tissue, providing a blood supply and fibroblasts, but unfortunately it also prevents the tendon from gliding. Intrinsic healing relies on synovial fluid for nutrition and occurs only between the tendon ends.

Flexor tendons in the distal sheath have a dual source of nutrition via the vincular system and synovial diffusion. Diffusion appears to be more important than perfusion in the digital sheath (Green 1993).

Several factors have been reported to affect tendon healing:

• Age—The number of vincula (blood supply) decreases with age.

• General health—Cigarettes, caffeine, and poor general health delay healing. The patient should refrain from ingesting caffeine and smoking cigarettes during the first 4 to 6 weeks after repair.

• Scar formation—The remodeling phase is not as effective in patients who produce heavy keloid or scar.

• Motivation and compliance—Motivation and the ability to follow the postoperative rehabilitation regimen are critical factors in outcome.

• Level of injury—Zone 2 injuries are more apt to form limiting adhesions from the tendon to the surrounding tissue. In zone 4, where the flexor tendons lie in close proximity to each other, injuries tend to form tendon-to-tendon adhesions, limiting differential glide.

• Trauma and extent of injury—Crushing or blunt injuries promote more scar formation and cause more vascular trauma, impairing function and healing. Infection also impedes the healing process.

• Pulley integrity—Pulley repair is important in restoring mechanical advantage (especially A2 and A4) and maintaining tendon nutrition through synovial diffusion.

• Surgical technique—Improper handling of tissues (such as forceps marks on the tendon) and excessive postoperative hematoma formation trigger adhesion formation.

The two most frequent causes for failure of primary tendon repairs are formation of adhesions and rupture of the repaired tendon.

Through experimental and clinical observation, Duran and Houser (1975) determined that tendon glide of 3 to 5 mm is sufficient to prevent motion-limiting tendon adhesions. Exercises are thus designed to achieve this motion.

Treatment of Flexor Tendon Lacerations

Partial laceration involving less than 25% of the tendon substance can be treated by beveling the cut edges. Lacerations between 25% and 50% can be repaired with 6-0 running nylon suture in the epitenon. Lacerations involving more than 50% should be considered complete and should be repaired with a core suture and an epitenon suture.

No level 1 studies have determined superiority of one suture method or material, although a number of studies have compared different suture configurations and materials. Most studies indicate that the number of strands crossing the repair site and the number of locking loops directly affect the strength of the repair, with six- and eight-strand repairs generally shown to be stronger than four-strand or two-strand repairs; however, the increased number of strands also increases bulk and resistance to glide. Several four-strand repair techniques appear to provide adequate strength for early motion.

Teno-Fix Repair

A stainless-steel tendon repair device (Teno Fix, Ortheon Medical, Columbus, OH) was reported to result in lower flexor tendon rupture rates after repair and similar functional outcomes when compared with conventional repair in a randomized, multicenter study, particularly in patients who were noncompliant with the rehabilitation protocol (Su et al. 2005, 2006). Active flexion was allowed at 4 weeks postoperatively. Solomon et al. (unpublished research) developed an “accelerated active” rehabilitation program to be used after Teno Fix repairs: Active digital flexion and extension maximum-attainable to the palm are started on the first day with the goal of full flexion at 2 weeks postoperatively. The anticipated risks with this protocol are forced passive extension, especially of the wrist and finger (e.g., fall on outstretched hand), and resisted flexion, potentially causing gapping or rupture of the repair.

FDP lacerations can be repaired directly or advanced and reinserted into the distal phalanx with a pull-out wire, but they should not be advanced more than 1 cm to avoid the quadregia effect (a complication of a single digit with limited motion causing limitation of excursion and, thus, the motion of the uninvolved digits). Citing complications in 15 of 23 patients with pull-out wire (button-over-nail) repairs, 10 of which were directly related to the technique, Kang et al. (2008) questioned its continued use. Complications of the pull-out wire technique included nail deformities, fixed flexion deformities of the distal interphalangeal (DIP) joint, infection, and prolonged hypersensitivity.

A more recent technique for FDP lacerations is the use of braided polyester/monofilament polyethylene composite (FiberWire, Arthrex, Naples, FL) and suture anchors rather than pull-out wires (Matsuzaki et al. 2008, McCallister et al. 2006). Reports of outcomes currently are too few to determine if this technique will allow earlier active motion than standard techniques.

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

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.

REHABILITATION PROTOCOL 1-2 Indianapolis Protocol (“Active Hold Program”)

(From Neumeister M, Wilhelmi BJ, Bueno Jr, RA: Flexor tendon lacerations: Treatment. http://emedicine.medscape.com/orthopedic_surgery)

• Indicated for patients with four-strand Tajima and horizontal mattress repair with peripheral epitendinous suture

• Patient who is motivated and compliant

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

• For the first 1 to 3 weeks, the modified Duran protocol is used. The patient performs repetitions of flexion and extension to the PIP and DIP joints and 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 to 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 distal palmar flexion crease. 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.

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

Trigger Finger (Stenosing Flexor Tenosynovitis)

S. Brent Brotzman, MD, and Theresa M. Kidd, BA

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).

REHABILITATION PROTOCOL 1-4 Rehabilitation Protocol After Trigger Finger Cortisone Injection or Release

After Injection

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

After Trigger Release Surgery

0–4 days	Gentle active MCP/PIP/DIP joint ROM (avoid gapping of wound).
4 days	Remove bulky dressing and cover wound with bandage.
4–8 days	Continue ROM exercises. Remove sutures at 7–9 days.
8 days–3 weeks	Active/active-assisted ROM/PROM MCP/PIP/DIP joints.
3 weeks +	Aggressive ROM and strengthening. Return to unrestricted activities.

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.

Flexor Digitorum Profundus Avulsion (“Jersey Finger”)

S. Brent Brotzman, MD

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.