Lumbrical Bar Splint

nerve or possibly the lower cervical nerve roots (C8—T1) or inferior brachial plexus. Cervical nerve root compression typically results in neck pain with radicular symptoms down the arm. Weakness and atrophy would be expected in the thenar and hypothenar musculature, which are both innervated by the lower cervical and first thoracic nerve roots. A lesion of the lower brachial plexus (e.g., a Pancoast tumor of the lung apex) would result in similar findings. The ulnar nerve is most commonly compressed at the elbow (cubital tunnel syndrome) or at the wrist (ulnar tunnel syndrome). Intact function of the two ulnar flexor digitorum profundus tendons would point to a more distal lesion in the lower forearm or wrist.

Lastly, one must rule out other causes of peripheral nerve dysfunction such as a generalized peripheral neuropathy or hereditary motor-sensory neuropathy (Charcot-Marie-Tooth disease). Intrinsic atrophy with or without sensory loss may be seen in syringomyelia or motor neuron disease (amyotrophic lateral sclerosis, ALS). These typically result in symmetric disease. The history, physical findings, and corroborative electrical studies aid in localizing the nerve lesion and ruling out a more generalized disease process.

Diagnosis

The diagnosis is a low complete ulnar nerve palsy. The ulnar nerve innervates the four dorsal interossei, the three volar interossei, the two ulnar lumbricals, the hypo-thenar muscles and typically the deep head of the flexor pollicis brevis. It supplies sensation to the small finger and ulnar half of the ring finger.

A claw deformity develops due to imbalance between absent intrinsic (interossei and lumbricals) and intact extrinsic muscle function. The claw deformity is more pronounced in the ring and small fingers due to the intact index and middle finger lumbricals, which are innervated by the median nerve. Clawing is more significant in a low ulnar nerve palsy than a lesion at the elbow due to the intact flexor digitorum profundus tendons to the ring and small fingers. These tend to accentuate the flexion posture of the interphalangeal joints.

Loss of ulnar nerve function can be quite disabling. The intrinsic muscles are responsible for simultaneous flexion of the metacarpophalangeal (MP) joints and extension of the interphalangeal (IP) joints (the intrinsic-plus position). Although full finger flexion and extension is present, with intrinsic loss the fingers tend to roll up during flexion due to asynchronous motion of the MP and IP joints (MP flexion does not begin until IP flexion has been completed). IP joint extension requires contraction of the extrinsic extensor tendons (extensor digitorum communis). This leads to MP joint hyperextension and contributes to the claw posture.

The ability to place the hand around objects such as a glass or doorknob is lost. These activities requires the intrinsic-plus posture. All fine motor skills that require simultaneous MP flexion and IP extension, such as writing or threading a needle, are similarly impaired. Lastly, pinch and grip strength are markedly diminished due to loss of the interossei and hypothenar muscles.

Nonsurgical Management

Conservative treatment of ulnar nerve dysfunction relies on the use of external splints to block clawing of the digits. A lumbrical bar splint is commonly utilized for this purpose (Fig. 22—1). It is a static splint, usually made of Orthoplast by a hand

Figure 22—1. A lumbrical bar splint blocks metacarpophalangeal (MP) hyperextension in individuals with a claw deformity secondary to ulnar nerve dysfunction. This allows the long extensor tendons to extend the IP joints and corrects the claw deformity. It does not improve asynchronous digital flexion.

therapist, that fits over the dorsum of the metacarpal head and proximal phalanges. It does not improve grip strength or integrated MP and IP motion. It does, however, block MP hyperextension of the ring and small fingers, thereby correcting the claw deformity. This enables the extrinsic extensor tendons to fully extend the IP joints. It also prevents fixed proximal IP joint contractures from occurring.

Surgical Management

If a compressive neuropathy or isolated nerve disruption is identified, decompression or nerve repair is indicated. Unfortunately, with complete ulnar nerve transection, full recovery seldom occurs following repair. This is due to the mixed motor and sensory function of the ulnar nerve as well as the complex motor innervation of the many intrinsic muscles of the hand. Recovery is especially guarded in older individuals, in high lesions, and in nerve loss requiring grafts for reconstruction. Furthermore, motor end plates cannot be functionally reinnervated years after paralysis. In this setting, tendon transfers are the only option available to restore ulnar nerve function.

There are many surgical procedures described to treat patients with intrinsic muscle paralysis. Tendon transfers are described to correct the claw deformity and integrated MP and IP joint motion, improve grip and pinch strength, and restore lateral deviation of the fingers (Fig. 22—2A). All require a motivated patient and full passive mobility of the digits. The choice of transfer depends on the age and needs of the patient, the availability of donor tendons, and the level of the palsy.

In this patient, a simple transfer was decided on that would correct the claw deformity and restore synchronous finger flexion. This was thought to be most appropriate for his functional demands. Loss of grip strength was not one of his complaints, and thus a transfer involving a wrist tendon was not chosen. The only way

Splint Claw DeformityClaw Hand Pancoast

Figure 22—2. (A) Preoperative claw posture of the hand. Note the minimal clawing of the index and middle fingers due to the intact radial two lumbrical muscles innervated by the median nerve. (B) Stiles-Bunnell transfer utilizing the flexor digitorum superficialis (FDS) tendon of the middle finger to correct the ring and small finger clawing and asynchronous flexion. The tendon has been longitudinally split. (C,D) Following transfer, the ulnar digits are rebalanced and digital motion is now synchronous without a claw posture.

Figure 22—2. (A) Preoperative claw posture of the hand. Note the minimal clawing of the index and middle fingers due to the intact radial two lumbrical muscles innervated by the median nerve. (B) Stiles-Bunnell transfer utilizing the flexor digitorum superficialis (FDS) tendon of the middle finger to correct the ring and small finger clawing and asynchronous flexion. The tendon has been longitudinally split. (C,D) Following transfer, the ulnar digits are rebalanced and digital motion is now synchronous without a claw posture.

to improve grip strength is to use a wrist motor-tendon unit, which adds power to the hand. This, however, requires the use of free tendon grafts to augment tendon length, and thus is a more complicated operative procedure.

A Stiles-Bunnell transfer was chosen, which utilizes a flexor digitorum superficialis (FDS) tendon to restore MP flexion and IP extension and redistribute balance within the hand (Fig. 22—2B). The FDS has excellent amplitude and force with little functional morbidity as a donor. As this patient had a low ulnar nerve palsy with only ring and small finger clawing, a single FDS tendon from the middle finger was transferred.

Through a palmar incision, the FDS was harvested and split longitudinally. These were then passed through the lumbrical canals (palmar to the MP joints) and sutured into the lateral bands of the extensor mechanism of the ring and small fingers. When the wrist was passively flexed and extended intraoperatively, the ulnar digits no longer assumed a claw posture.

Postoperatively, the patient was placed in a short arm dorsal blocking splint with the wrist in 20 to 30 degrees of flexion and the MP joints in ~60 degrees of flexion for 3 weeks. Active flexion and extension of the fingers was allowed within the limits of the splint. A hand-based lumbrical bar splint was then worn for an additional 2 weeks. At 5 weeks postoperative, the patient had regained synchronous digital flexion and extension without clawing (Fig. 22—2C,D). Functional use was encouraged.

Suggested Readings

Brand PW. Tendon transfers for correction of paralysis of intrinsic muscles of the hand. In: Hunter JW, Schneider LH, Mackin EJ, eds. Tendon Surgery of the Hand. St. Louis: Mosby; 1987:439-499.

Burkhalter WE. Ulnar nerve palsy. In: Gelberman RH, ed. Operative Nerve Repair and Reconstruction. Philadelphia: JB Lippincott; 1991:729-746.

Hastings H, Davidson S. Tendon transfers for ulnar nerve palsy: evaluation of results and practical treatment considerations Hand Clin 1988;4:167-178.

Omer GE. Ulnar nerve palsy. In: Green DP, Hotchkiss RH, Pederson WC, eds. Green's Operative Hand Surgery. 4th ed. Philadelphia: Churchill Livingstone; 1999: 1527-1541.

Smith RJ. Tendon transfers to restore intrinsic muscle function to the fingers. In: Smith RJ, ed. Tendon Transfers of the Hand and Forearm. Boston: Little, Brown; 1987:103-133.

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Responses

  • feorie
    How to make static anticlaw splint?
    6 years ago
  • ONNI KULMALA
    How to correct wrist ulnar deviation with splint?
    6 years ago
  • Grimalda
    What is a lumbrical bar splint?
    5 years ago
  • robert
    What is the purpose of the hypothenar bar in a wrist immobilizer?
    3 years ago
  • belisarius
    What is the function of lumbrical bar in hand splint?
    3 years ago
  • Hamid
    How many hours a day should a patient wear a lumbrical bar splint?
    2 years ago
  • Robinia
    What is alumbrical artery?
    1 year ago

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