Splinting the hand with a peripheral-nerve injury is both easy and difficult. The ease of splinting results from the readily recognizable and often identical deformities. Therefore, unlike many other hand injuries, the deformities resulting from isolated peripheral nerve paralysis are usually effectively splinted using standard splinting designs. The difficulty, however, in splinting peripheral nerve paralysis arises from the impossibility of building a static external device that substitutes for the intricately balanced muscles the splint attempts to replace.
Principles of Splints
The purposes common to all splints used for peripheral nerve injuries are as follows:
To keep denervated muscles from remaining in an overstretched position
To prevent joint contractures
To prevent the development of strong substitution patterns
To maximize functional use of the hand
Overstretching of Muscles
In all cases of isolated upper extremity peripheral nerve injury, the denervated muscle group will have normal unopposed antagonist muscles still present. These normal muscles will continuously overpower the denervated muscles and maintain them on constant stretch. A muscle undergoing reinnervation must first overcome this stretched position and achieve a normal resting length before it is able to contract enough to bring about joint motion. Short periods during which the unopposed muscles overpower the denervated muscles will not cause harm, but a denervated muscle constantly held in a stretched position decreases the potential for early return of normal muscle activity. A denervated muscle protected by appropriate splinting allows the earliest perception of returning motion. Properly executed splints will enhance returning muscle function instead of allowing substitution patterns.
Joints held continually in one position cannot experience the habitual movement of the capsular structures. Even without accompanying trauma, prolonged immobility will result in restriction of joint motion. To maintain motion, the joint must be frequently taken through its full range. It is not adequate to immobilize joints at one extreme at night and the other extreme during the day. Although positional splinting at night can be useful, it is the full active motion of joints during the day that maintains joint lubrication and accompanying soft tissue glide.
In an isolated peripheral nerve injury, there is no opposing force to the intact active muscle group and muscle imbalance is created. Without an external splinting constraint, the patient constantly reinforces the strength of the normal muscles and overpowers the denervated muscles. An excellent example is low median palsy, in which the intact flexor pollicis longus (FPL) and extensor pollicis longus (EPL) carry the thumb back and forth across the palm in an adducted position ( Fig. 34-1 ). With the opponens pollicis (OP) and abductor pollicis brevis (APB) absent, the extrinsic muscle pattern becomes dominant in the motor cortex. As the OP and APB are reinnervated, they have difficulty participating in thumb motion because the stronger extrinsic muscles continue to dominate. If substitution patterns are prevented, the patient is able to isolate and strengthen returning musculature earlier.
Functional Use of the Hand
A peripheral-nerve lesion with significant sensory loss prevents functional use of the hand even when a splint substitutes for absent muscles. The combination of sensory loss and motor imbalance in median and ulnar nerve lesions makes it impossible to use the hand normally. A splint can assist in maximizing function only when the sensibility returns to a functional level.
Cold intolerance is common with peripheral-nerve injuries, particularly during reinnervation. Protective neoprene mittens, gloves, or finger sleeves are helpful for patients in colder climates or for those who work in cold environments ( Fig. 34-2 ).
Splints should be kept as simple as possible. Bulky splints, if worn by the patient, will impede function of the hand rather than reinforce it. Early after the nerve injury, it is acceptable to cover a denervated sensory area with the splint. In cases of partial nerve laceration or returning sensibility, the tactile surfaces should be left free if possible.
Splints for peripheral-nerve injuries should not totally immobilize any joint. For example, splinting of the wrist in radial palsy with a static wrist immobilization splint prevents the returning wrist extensor muscles from gaining strength or excursion while in the splint.
Many peripheral-nerve injuries are associated with accompanying trauma to skin, tendon, bone, or vascular structures. Tension on the healing tissues must be avoided immediately after injury to allow adequate healing. Thereafter, glide of tendons and joint movement take precedence over splinting for the peripheral-nerve deformity. The peripheral-nerve splint will often restrict full tendon excursion. For example, in a laceration at the wrist involving the median and ulnar nerves and wrist and finger flexor tendons, the wrist must be held in some flexion immediately postoperatively to prevent tension at the repair sites. Only as wrist motion is gained and excursion of the flexor tendons is achieved will the claw deformity of the fingers be evident. The initial adherence of the flexor tendons at the wrist will create tenodesis of the finger flexors, providing a built-in splint. Only when the deformity becomes clinically evident should one splint for it. In longstanding denervation in which joint contractures have already developed, one must first splint to regain joint motion before splinting the dynamic deformity.
Specific Nerve Lesions
It is easiest to understand the deformity of a pure lesion of the three primary upper extremity peripheral nerves: ulnar, median, and radial. Combined nerve injuries, especially when associated with other injuries, require more skill to determine treatment priorities, although the splinting principles are the same.
Laceration of the ulnar nerve at the wrist (low ulnar palsy) results in denervation of the majority of the intrinsic muscles of the hand ( Fig. 34-3 ). The ulnar nerve innervates all of the hypothenar muscles: abductor digiti minimi, flexor digiti minimi, and the opponens digiti minimi. The ulnar border of the transverse metacarpal arch is lost. Absence of the dorsal and volar interossei muscles creates the inability to abduct and adduct the fingers, causing loss of the fine manipulative power of the hand. In addition to the loss of the interossei, the ring and little fingers also lose function of the lumbricales, removing any intrinsic muscle balancing force in these two digits. The extrinsic muscles dominate.
The resulting deformity is clawing of the ring and little fingers. The intrinsic muscles normally flex the metacarpophalangeal (MP) joint and extend the interphalangeal (IP) joints. When they are absent, there are no prime flexors of the MP joint. Because there is no intrinsic muscle control in these digits, the tension of the long flexors is opposed only by the extrinsic extensors, which primarily extend the MP joints ( Fig. 34-4 ). In this claw position, both the lumbricales and the interossei are held in a stretched position. The patient can flex the MP joints actively, but only after the IP joints are fully flexed. The greatest functional loss is the inability to open the hand in a large span to grasp objects and the inability to handle small objects with precision.
The loss of the powerful adductor pollicis and the deep head of the flexor pollicis brevis removes one of the key supports of the thumb MP joint during pinching. The thumb may demonstrate Froment’s sign: extension or hyperextension of the MP joint with hyperflexion of the IP joint. Splinting cannot easily assist this deformity because stabilizing the thumb is difficult without restricting other essential mobility.
The goal in splinting ulnar palsy is to prevent overstretching of the denervated intrinsic muscles of the ring and little fingers. The ring and little finger MP joints must be prevented from fully extending ( Fig. 34-5 ). Any splint that blocks the MP joints in slight flexion prevents the claw deformity by forcing the extrinsic extensors to transmit force into the dorsal hood mechanism of the finger. This extends the IP joints in the absence of active intrinsic muscle pull ( Fig. 34-6 ). The dorsal block should be molded carefully to distribute pressure over the dorsum of each proximal phalanx and should end exactly at the axis of the proximal interphalangeal (PIP) joint.
A bulky splint that blocks the MP joints will impede function of the hand. In isolated low ulnar palsy, two thirds of the palmar surface of the hand has intact median nerve sensibility. Ulnar palsy splints should cover a minimal surface of the palm. Total finger flexion must also remain unimpeded. Early after injury, the MP joint block can be incorporated into the immobilization splint that prevents tension on the nerve and tendon repairs at the wrist. When wrist movement is allowed, a small molded thermoplastic splint (see Fig. 34-6 ) or leather splint can be applied ( Fig. 34-7 ).
Some authors advocate a spring wire splint with a coil at the axis of the MP joint that allows full MP extension and follows the joint through the full MP flexion. This splint construction is challenging because the tension of the spring must be exact. It must be strong enough to block MP extension when the patient attempts finger extension while also following the arc of the proximal phalanx when the MP joint flexes. Therapists who apply a dynamic force for MP flexion (e.g., the Bunnell knuckle-bender splint ) are missing the concept of blocking MP hyperextension. In such a splint, the patient hyperextends actively against the force of the rubber bands, which gives resistance and proprioceptive input to the extrinsic extensors, strengthening them. Unless one is able to construct a coil splint with precise tension, it is recommended that static splinting that prevents the MP joint from hyperextending be applied.
Ulnar palsy splints will not create flexion contractures of the MP joint. Every time the splint is removed for skin care, the extrinsic extensor will still hyperextend the MP joint.
High ulnar palsy lesions are commonly a result of trauma at or above the elbow. In addition to the muscles previously mentioned in low ulnar palsy, the flexor digitorum profundi (FDP) of the ring and little fingers and the flexor carpi ulnaris are absent in a high lesion ( Fig. 34-8 ). With absence of the FDP and all intrinsic muscles to the ring and little fingers, clawing in the high ulnar nerve lesion is rarely present. As reinnervation of the FDP occurs, clawing becomes evident and splinting becomes mandatory rather than optional. The same MP hyperextension restriction splint is used for both the high and low ulnar palsy lesions (see Fig 34-5 ). In a high lesion, the patient must maintain full passive IP flexion of the ring and little fingers when the FDP is absent.