Intrinsic Plus Hand 

Updated: Mar 15, 2019
Author: Bradon J Wilhelmi, MD; Chief Editor: Harris Gellman, MD 

Overview

Background

Contracture of the interosseous, lumbrical, or hypothenar muscles causes the fingers to stiffen and the hand to become deformed and functionally disabled.[1, 2, 3, 4, 5] Intrinsic plus hand is the result of imbalance between intrinsic muscles and comparatively weak extrinsic muscles. The frequency of intrinsic plus hand is not known.

The intrinsic plus position is otherwise known as the safe position for hand splinting. The hand can be immobilized in this position for long periods of time without developing as much stiffness as would occur if the digits were positioned differently. In the intrinsic plus position, the metacarpophalangeal (MCP) joints are flexed at 60-70°, the interphalangeal (IP) joints are fully extended, and the thumb is in the fist projection. The wrist is held in extension at 10° less than maximal.

The reason why intrinsic plus is the safe position is that in this position, the MCP joints are in flexion and the IP joints are in full extension. The MCP joints recover well from flexion, and the IP joints recover well from extension on the basis of differences in the shape of the metacarpal head, volar plate, and collateral ligament anatomy (see Anatomy).

Anatomy

Metacarpal head, proximal interphalangeal joints, and collateral ligaments

The metacarpal head is uniquely shaped in that it is ovoid in the sagittal plane, and it widens from the dorsal to the volar dimension. The collateral ligaments are eccentrically mounted dorsal to the axis of rotation of the MCP joint. This anatomy causes variable degrees of tightness on the collateral ligaments based on the position of the joint by a camlike effect. When the joint is in extension, the collateral ligaments are lax. In flexion, the collateral ligaments span a greater distance and are tight (see the image below).

The metacarpal head is uniquely shaped in that it The metacarpal head is uniquely shaped in that it is ovoid in the sagittal plane, and it widens from the dorsal to the volar dimension. The collateral ligaments are eccentrically mounted dorsal to the axis of rotation of the metacarpophalangeal joint. This anatomy causes variable degrees of tightness on the collateral ligaments based on the position of the joint by a camlike effect. When the joint is in extension, the collateral ligaments are lax. In flexion, the collateral ligaments span a greater distance and are tight.

In addition, the MCP joint is curved in two planes to permit abduction, adduction, and rotation, as well as flexion and extension in an abbreviated ball-and-socket configuration. In flexion, bone surface area contact is greater than in extension, producing a more stable joint.

Proximal IP (PIP) joint collateral ligaments originate close to the axis of rotation, providing a smaller change in length with joint position and providing lateral stability. The PIP joint ranges in only one plane, and its trochlear shape also adds to its lateral stability (see the image below).

Proximal interphalangeal (PIP) joint collateral li Proximal interphalangeal (PIP) joint collateral ligaments originate close to the axis of rotation, providing a smaller change in length with joint position and providing lateral stability. The PIP joint ranges in only 1 plane, and its trochlear shape also adds to its lateral stability.

Intrinsic musculature

The intrinsic musculature, composed of the interossei and the lumbrical muscles, acts on the hand to flex the MCP joints and extend the IP joints. The interossei also act to abduct and adduct the fingers.[6] There are seven interosseous muscles: four dorsal and three (or four) volar (palmar).[7] These muscles lie on either side of the metacarpals. The dorsal interossei are abductors, whereas the volar interossei are adductors.

Each dorsal interosseous muscle, except the one lying on the ulnar side of the middle finger, has two muscle heads, one superficial and one deep. The superficial head originates most dorsally and inserts by way of a medial tendon onto the lateral tubercle at the base of the proximal phalanx. Therefore, the superficial head abducts and weakly flexes the proximal phalanx.

The deep head of the dorsal interosseous muscle forms a lateral tendon or lateral band at the base of the proximal phalanx. These lateral bands are joined by the lateral slips of the extensor tendon to form the conjoined lateral band at the level of the PIP joint.

The conjoined lateral bands on either side of the finger then join at the distal end of the middle phalanx to form the terminal extensor tendon. The terminal tendon inserts onto the base of the distal phalanx and serves to extend it. Each lateral band at the level of the middle of the proximal phalanx sends off fibers, which arch dorsally to join each other on the dorsum of the finger. These fibers flex the proximal phalanx.

Oblique (spiral) fibers also originate from the lateral bands more distally and insert onto the lateral tubercles at the base of the middle phalanx. These oblique fibers extend the middle phalanx. Therefore, the deep head of the dorsal interosseous muscle acts to flex and weakly abduct the proximal phalanx and extend the middle and distal phalanges.

The volar interossei each only have one muscle head and form the ulnar lateral band of the index finger and the radial lateral band of the ring and little finger.

The hypothenar muscles function similarly to the interossei for the small finger. The abductor digiti quinti (ADQ) function is similar to that of the superficial head of a dorsal interosseous muscle. The flexor digiti quinti brevis (FDQB) functions similarly to the deep head of a dorsal interosseous muscle, forming the ulnar lateral band. The opponens digiti quinti (ODQ) is a third hypothenar muscle that serves to flex and supinate the fifth metacarpal.

The lumbrical muscles arise from the flexor digitorum profundus (FDP) tendons in the palm and join the radial lateral band at the middle of the proximal phalanx. The lumbricals extend the PIP and distal IP (DIP) joints and assist in flexing the MCP joints.

Volar plate anatomy

Architectural differences exist between the volar plates of the MCP and IP joints. The MCP volar plate is composed of crisscrossing bands of fibers that collapse like an accordion on flexion and expand with extension.[8]

The IP volar plate is a more rigid cartilaginous structure that does not collapse but glides with movement. It is attached to the proximal phalanx only by the proximal checkrein ligaments; therefore, the rigid IP volar plate can slide proximally and distally with joint motion to protect the joint (see the image below).

Edema is the initial response to any insult to the Edema is the initial response to any insult to the hand and leads to adverse sequelae. Joint stiffness develops as intra-articular hematoma and fluid accumulate within the synovial space, distending the capsule. Increased fluid content within the articular capsule and collateral ligaments effectively shortens these structures, favoring extension.

Pathophysiology

Edema is the initial response to any insult to the hand and leads to adverse sequelae. Joint stiffness develops as intra-articular hematoma and fluid accumulate within the synovial space, distending the capsule. Increased fluid content within the articular capsule and collateral ligaments effectively shortens these structures, favoring extension. The fluid in the joint space also serves to hydraulically drive the MCP joints into extension.

In extension, the joint is able to accommodate this increased fluid capacity. As the MCP joints extend, the flexor tension on the IP joints increases and the extensor tension decreases. This causes the PIP and DIP joints to flex. The resultant late deformity is the intrinsic negative (or minus) hand, consisting of MCP joint extension, IP joint flexion, thumb adduction, and wrist flexion.

With injury, checkreins form at the IP joints (see the image below). Checkreins are collagenous bands connecting the lateral sides of the proximal volar plate to the assembly lines on the volar lateral surfaces of the phalanx. Assembly lines are the two ridges along the volar lateral surfaces of the phalanx, to which are attached volar ligamentous structures such as the flexor sheath, the Cleland and Grayson ligaments, and the oblique retinacular ligaments of Landsmeer.

With injury, checkreins form at the IP joints. Che With injury, checkreins form at the IP joints. Checkreins are collagenous bands connecting the lateral sides of the proximal volar plate to the assembly lines on the volar lateral surfaces of the phalanx. Assembly lines are the 2 ridges along the volar lateral surfaces of the phalanx to which are attached volar ligamentous structures, such as the flexor sheath, Cleland and Grayson ligaments, and the oblique retinacular ligaments of Landsmeer.

The volar plate pocket behind the MCP volar plate is smaller than that at the IP joint, and checkreins do not develop at the MCP joint (see the image above).[8]

Compartment syndrome is the usual cause of posttraumatic intrinsic contractures owing to edema and ischemia. Hematoma and edema fill the interosseous muscle compartment and are trapped by the firm dorsal and volar interosseous fascia.[9] Capillary compression and venous stasis add to the congestion. As the edema subsides, fibrosis develops.

Compressive circular dressings can also impede venous drainage and lead to the development of myostatic contractures in the interossei. Finally, muscle necrosis and fibrosis may ensue with cases of severe and prolonged deep-space edema of the hand.

Etiology

Excessive immobilization, trauma, inflammation, infection, tumor, central nervous system (CNS) disease, and joint destruction are all causes of joint stiffness and intrinsic contractures.[10, 11] Decreased blood supply to the hand as a result of injury or primary disease of the vessels of the upper extremity is a leading cause of intrinsic muscle contracture.

Prognosis

The prognosis for each patient is variable and depends on the severity of the contracture and the underlying cause of the contracture. The surgeon's objective is to restore structure and function to the contracted hand. The ultimate goal is to provide the patient maximal comfort and functional independence.

 

Presentation

Physical Examination

The test most commonly used to test for intrinsic contracture is the intrinsic tightness (Bunnell) test. The examiner holds the metacarpophalangeal (MCP) joints in extension while passively flexing the interphalangeal (IP) joints. The IP joints are then passively flexed with the MCP joints held in flexion.

If IP joint flexion is blocked or lessened when the MCP joint is extended in comparison with when it is flexed, the result is positive and there is tightness of the intrinsic muscles. In contrast, if extensor contracture is present at the proximal IP (PIP) joint, then PIP joint flexion is greater with MCP joint extension.

In some circumstances, the intrinsic tightness test may not be reliable in diagnosing intrinsic contracture. IP joint stiffness and capsular or intra-articular adhesions can mask underlying intrinsic muscle tightness. In these situations, IP joint flexion may be decreased regardless of the position of the MCP joint.

 

Workup

Imaging Studies

Radiography of the hands should be included as part of the workup for stiff joints. Although radiography is not helpful in diagnosing intrinsic contracture, it may be useful for ruling out other diagnoses or causes of a contracture.

Shear wave elastography has been studied as a means of achieving a quantitative evaluation of the condition of the intrinsic muscles of the hand.[12]

 

Treatment

Medical Therapy

Any injury to the hand can lead to intrinsic contracture.[13] Early recognition is essential. Efforts must be directed at decreasing edema in the injured hand. Limb elevation is crucial, and care must be taken to avoid applying compressive dressings such as Ace wraps or restrictive circular casts. If these conservative measures fail or if the surgeon notices persistent swelling and pitting edema, increasing median nerve hypesthesia, or poor capillary refill, a quantitative measurement of intracompartmental pressure may be obtained.

Surgical Therapy

Early and acute trauma: interosseus and adductor compartment release

When increased intracompartmental pressures do not respond quickly to conservative measures, the interosseous compartments should be released promptly. Most patients also require release of the adductor pollicis and carpal tunnel. When flexion of the metacarpophalangeal (MCP) joints is limited, Kirschner wires (K-wires) should be used to fix the MCP joints in 60° of flexion to stretch the collateral ligaments.

Late and mild posttraumatic intrinsic contracture: distal intrinsic release

Patients with mild intrinsic muscle contracture may be able to open and close their fingers normally, but they may have persistent limited flexion at the proximal interphalangeal (PIP) joint several months after an injury to the hand or wrist. These patients often have little to no MCP flexion contracture but limited PIP flexion.

In these instances, the edema of the hand causes the collateral ligaments to swell and tighten. Although the intrinsic contracture is mild, the swollen and tight collateral ligaments resist stretching, and the MCP joints are not pulled into flexion. The results of the intrinsic tightness test are positive. For these patients, distal intrinsic release is recommended. In this procedure, the lateral bands and oblique fibers of the distal third of the proximal phalanges are resected.[14]

Postoperatively, the MCP joints are splinted in extension (neutral) position for 3 weeks. The interphalangeal (IP) joints are ranged in active and passive flexion/extension exercises to avoid relapse of the deformity. Dynamic splinting in the MCP extension splint, otherwise known as the reverse knuckle-bender splint, is useful in this period.

Late posttraumatic intrinsic contracture with MCP and PIP joint contractures: muscle slide/release

With more severe ischemic contracture of the interossei and lumbricals, flexion contracture occurs at the MCP joints and extension contracture at the IP joints. With extensive edema of the hand, the contracted interossei overcome the resistance of the tightened collateral ligaments and pull the proximal phalanx into flexion. Secondary changes may include contraction of the volar plate and collateral ligaments of the PIP joints. The results of the intrinsic tightness test are positive, and the deformity of the hand is severe.

Extensive release of the dorsal aponeurosis is necessary to correct severe intrinsic muscle contractures that involve both the MCP and the PIP joints.[15] Muscle slide may be used if the interossei are fibrotic and tight but have retained some contractility. With more severe ischemic damage, the interossei are often necrotic and nonfunctional. Proximal intrinsic release is indicated, and the lateral tendons of all interossei, including the abductor digiti quinti (ADQ) tendon, are resected at the level of the MCP joints.

The volar plate is also freed of any attachments at the base of the proximal phalanx, and the accessory collateral ligaments may be resected at their insertion into the volar plate. K-wires may be inserted obliquely through the MCP joints to maintain them in maximal extension. If passive PIP joint flexion is still incomplete with the MCP joints in extension, the lateral bands are resected at the distal half of the proximal phalanx.

Postoperatively, the MCP joints are kept in extension for about 3 weeks. After this time, the K-wires usually are removed. Passive and active flexion/extension of the PIP joints should begin on the first postoperative day.

In a case report, Hamada et al described the use of a modified Ilizarov minifixator to correct severe intrinsic plus hand.[16]  Although they concluded that this technique could be recommended for severe or neglected hand contractures and deformities on the grounds that it was safe and less invasive, they did not strongly recommend it, and they cautioned that the success of the procedure depended to a large extent on postoperative management and careful evaluation of the hand disorder.

Spastic contracture of interossei: muscle slide

Patients with cerebral palsy, central nervous system (CNS) disease, or stroke may have spastic contracture of the interossei causing disability.[17, 18, 19] Often, intrinsic muscle spasticity is masked by extrinsic muscle spasticity and is seen several weeks after release of the extrinsic spasticity. After extrinsic release, the hand assumes the intrinsic plus position owing to its intrinsic contractures. The goal of treatment is not to remove the tightened muscles but to weaken them. This can be accomplished by means of muscle slide.

Muscle slide is accomplished via a dorsal approach to protect the palmar blood supply to the intrinsic muscles. The metacarpal origins of all interossei are released subperiosteally. The tendons of the ADQ and the flexor digiti quinti brevis (FDQB) are also usually transected.[20] The MCP joints are then extended and the PIP joints flexed, allowing the muscles to advance distally. The hand is then splinted in this claw position for a period of 3 weeks.

In a single-center retrospective review of 50 patients (54 hands) with CNS lesions and contractures of the wrist and extrinsic finger flexor and forearm pronator muscles, Thevenin-Lemoine et al found that the Page-Scaglietti technique (proximal release of extrinsic flexor and pronator muscles) yielded significant improvements in range of motion and function as evaluated according to the Zancolli and House classifications.[21]