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The basics about intrinsic contractures of the hand.

Posted on: 07/28/2014
The hand is a very intricate and complicated feature of the human body. There are many small structures, including tendons, ligaments and muscles that run through the hand and fingers. When these structures don’t move properly the result can be mild to severe disability from weakness of grip strength, inability to grasp objects and difficulty with general hygiene.

Intrinsic contracture is a diagnosis that specifically refers to small muscles with origin and insertion in the hand called interossei and lumbricals. There are seven interossei muscles, four on the dorsal or backside of the hand and three on the volar or palm side. There are four lumbricals, which originate from one of the long finger flexor tendons. These muscles course through the fingers to act as flexors of the MCP and extensors of the PIP. With this case these muscles become stiff and contracted causing imbalance in the forces that help us open and close our fingers. This results in stiffness, deformity and even dislocation of the fingers. In severe cases the resultant deformity is where the base of the finger (metacarpophalangeal or MCP joint) is flexed or bent while the middle finger joint (proximal interphalangeal or PIP joint) is extended or straight.

Intrinsic contractures can result from several causes. This can include trauma, spasticity, loss of blood supply, rheumatoid arthritis or even as a result of a medical procedure.

With a traumatic injury, such as a fracture, the primary problem is edema and immobilization, which can lead to adhesions and stiffening of the tendons and muscle bellies over the course of the recovery. Other injuries causing a fibrotic muscle can result from a loss of blood flow as with compartment syndrome or a vascular injury. Blood loss can also result from bandages or casts that are too tight, however this is less common today.

Spasticity is a condition where the neuron controlling the muscle is injured as with a stroke, traumatic brain injury or cerebral palsy. In this case there may be other contractures present as well.

Rheumatoid Arthritis is another common cause of intrinsic contracture. In these such cases the impaired muscle function can be the result of adhesions, muscle spasm from inflammation, or contraction due to decreased movement. Often in this population there are several factors including joint instability, and drifting of the fingers in the ulnar direction (towards the pinky finger).

Assessment and evaluation of these cases is based on the history of the injury as well as measurements for both active movements and passive movements of all the joints in the hand. This is important to distinguish between joint or muscle contracture. Often there will be testing of multi-joint motion to further evaluate the complicated balance of the many structures in the fingers and hand. There may also be radiographs to evaluate bony deformity, fracture, or joint instability. Testing for joint instability may also include laboratory testing for signs in the blood stream for rheumatic signals in cases with no obvious cause.

The most conservative and first line of management is nonsurgical. This will include proper care following trauma to reduce effects of swelling and immobilization. Quite often hand therapy protocols will be utilized to assist in reducing these effects and will usually include stretching and progressive splinting. With spastic patients, often optimizing their medications can improve on intrinsic function.

Surgeries are also common to treat intrinsic contractures, and there are many types that are chosen based on the specific case. Some of the many surgical options are to release tendons, release or partial release of the passive structures of the joints; or the procedures can be more complicated and include tendon repositioning, lengthening of the muscles, moving the location of the muscles, or even cutting off the nerve supply.

References:
Rick Tosti, MD, et al. Intrinsic Contracture of the Hand: Diagnosis and Management. In Journal of the American Academy of Orthopaedic Surgeons. February 2013. Vol. 21. No. 10. Pp. 581-591.

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