Joint Contracture

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Joint Contracture

Contracture around a joint can occur as a result of tissue trauma and subsequent scar formation, or joint immobilisation and resultant tissue adaptation, or as a combination of both.

Connective and periarticular tissues which surround a joint heal in a clearly defined and predictable manner. Healing by mitosis (cell division) is not always possible due to either the nature/capacity of the specific tissue or size of insult. Most frequently lost cells and structure are replaced by with scar tissue, often complicating complete recovery of function. Timeframes and success of healing may vary with size, location and nature of wound (accidental or surgical), and initial management.

Surgical wounds heal by first intention, healing rapidly with small degree of scarring and low risk of infection or complication (Knottenbelt, 2003). Degree of scarring is related to size and degree of the incision, and keyhole surgery is often preferred over open surgery as it limits tissue trauma, scarring and recovery time (apposition of edges). Open surgery to a joint is likely to result in some scarring as several structures are involved, and also contracture formation as postoperative ROM is likely to be restricted due to pain, functionally splinting the affected joint.

As scar tissue cannot fully replicate the strength of the tissue it has replaced. Surgical incisions therefore tend to be performed longitudinally to tissues tension lines rather than transecting them, as the tissue can then has potential to regain more dynamic and tensile strength. Adhesions formed can be broken, but this induces further inflammation and can thus further scar tissue formation and this occurrence is therefore best prevented (Johnston, 1985).

Joint contracture is mostly caused by immobilisation, either physical or physiological. Joint immobilisation is often used as a prescribed treatment following surgery or trauma, but can also occur as a result from any disease or situation which leads to limb disuse or recumbency. Contracture formation is therefore an adaptive reaction of affected tissues to diminished mechanical loading and altered joint position.

Relaxed tissues are more affected by immobilisation (Trudel et al., 1999), rationalising this as a response to lack of tension on the tissues. From a clinical standpoint; extension is most often the range that is lost first; quickly complicating successful weight bearing and locomotion.

Trudel and Uhtoff (2000) found that joint restriction in response to immobilisation was initially (48hrs) myogenic (muscle related) before becoming arthrogenic (joint related). The joint capsule responds to immobilisation by hypertrophy and proliferation of synovial cells, and normal pannus tissue is replaced with fibrocollagenous (scar) tissue. The fibrocollagenous tissue forms adhesions between the synovium folds (lax surface), the synovium and capsule, the synovium and cartilage (Schollmeier et al., 1994). Reduction in the number of synoviocytes causes a reduction in synovial fluid (Trudel et al., 2003), and together with the shrinking and thickened capsule this causes an increased intra-articular pressure, and proneness to capsular rupture.

Ligaments are not thought to be associated with contractures, unless they have been traumatised and are forming adhesions as part of their healing process. Ligaments have been shown to retain their cross-sectional area and viscoelasticity following immobilisation (Binkley and Peat, 1986), however collagen turnover becomes decreased and this is seen as a decreased frequency of small new collagen fibrils.

A joint contracture of the elbow will most likely prevent extension of the elbow, causing a dysfunction in the stance phase of gait of that limb. The limb might not even be weight bearing or reaching the ground. Likely to be affected is also extension for the shoulder if muscle belly of biceps has shortened (postural adaptation of non-weight bearing carriage of limb).

Degree of contracture is also dependent on the period of disuse and extent and location of the surgery/incision. Pre-operative/treatment disuse of the limb due to pain, and therefore limited use, will in itself cause changes to the joint structures and rage of movement.

Adaptations which have occurred over time are more difficult to affect than changes which are acute and still going through an active healing phase.

References

Binkley JM and Peat M (1986) The Effects of Immobilization on the Ultrastructure and Mechanical Properties of the Medial Collateral Ligament of Rats. Clinical Orthopaedics and Related Research 203, 301–308

Johnston DE (1985) Tendons, skeletal muscles, and ligaments in health and disease. In ‘Textbook of Small Animal Orthopaedics.‘ (Eds. Newton CD and Nunamaker DM) (International Veterinary Information Service: Ithaca)

Knottenbelt DC (2003)The pathophysiology of wound healing. In ‘Handbook of equine wound management.’ (Ed. Knottenbelt DC) pp 13-21 (WB Saunders: London)

Schollmeier G, Uhthoff HK, Sarkar K, Fukuhara K (1994) Effects of immobilization on the capsule of the canine glenohumeral joint. A structural functional study. Clinical Orthopaedics and Related Research. 304, 37-42

Trudel G, Jabi M, Uhthoff HK (2003) Localized and adaptive synoviocyte proliferation characteristics in rat knee joint contractures secondary to immobility. Archives of Physical Medicine and Rehabilitation. 84, 1350-6

Trudel G, Uhthoff HK (2000) Contractures secondary to immobility: is the restriction articular or muscular? An experimental longitudinal study in the rat knee. Archives of Physical Medicine and Rehabilitation 81, 6-13

Trudel G, Uhthoff HK, Brown M (1999) Extent and Direction of Joint Motion Limitation after Prolonged Immobility: An Experimental Study in the Rat. Archives of Physical Medicine and Rehabilitation 80, 1542-7

Zarzhevsky N, Coleman R, Volpin G, Fuchs D, Stein H, Reznick AZ (1999) Muscle recovery after immobilisation by external fixation. Journal of Bone and Joint Surgery (Br.) 81, 896-901

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