Contractures

Author(s): Adrian Cristian, MD, Ashish Khanna, MD, Richard Kim, MD

Originally published:09/20/2014

Last updated:09/20/2014

1. DISEASE/DISORDER:

Definition

Contractures are the chronic loss of joint mobilitycaused bystructural changes in nonbony tissue, including muscles, ligaments, and tendons. They develop when these normally elastic tissues are replaced by inelastictissues. This results inthe shortening and hardening of these tissues, ultimately causing rigidity, joint deformities, and a total loss of movementaround the joint.

Etiology

Contractures are a final common pathway for many conditions. The most frequent cause of contracture is immobilization, but they can be also be caused by muscle imbalance, heterotopic ossification,prolonged hypertonic spasticity, burns, and local trauma.

Epidemiology including risk factors and primary prevention

Currently, most epidemiologic information focuses on one single joint contracture; therefore, the epidemiology of joint contractures as a whole is limited. Additionally, the variance in definitions among studies used as diagnostic criteria results in a wide range of figures. However, it is clear that there is a high prevalence of major joint contractures.Overall, the prevalence has been reported to be between 15% and 70% in older adults.Patients with acquired brain injury developed contractures between 16% and 81%.3Children who have an obstetric brachial plexus injury were found to have a shoulder contracture 51% of the time.In institutionalizedolder adults, it was reported that 71% of those who were immobile were found to have a joint contracture, where all mobile patients were free from contractures.5Even with this data, the overall lack of epidemiologic data is a major hindrance to providingappropriate care and treatment for contractures.

Risk factors for contracture development include motor dysfunction (hemiplegia or tetraplegia), hypoxic ischemic injury (eg, stroke), spinal cord injury, and age.Overall, the primary risk factor for contracture development is immobility. Spasticityisa risk factor for later development, butparalysisisforemost.7

Patho-anatomy/physiology

Soft tissue changes that contribute to contractures begin very early after the onset of immobility. Protein synthesis within muscle fibers is reduced within 6 hours after a joint is immobilized. Shortening of muscle fibers occurs within 24 hours. After 48 hours, increased collagen infiltration of the perimysium appears. Chronic disuse also causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, further exacerbating baseline paresis.8

There is a reduction in longitudinal tension in muscles in patients with brain injury who have muscles and joints thatare immobilized for prolonged periods.9In animal models, only 24 hours of unloading caused a 60% shortening of muscle fiber length.10

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Most contractures begin with some insult to the body. For example, the body’s reaction to a painful joint is to immobilize it, placing it at risk for development of a contracture. Neurologic injuries increasing muscle tone or weakness cause a muscle imbalance, which results in a tonic contraction. In this way, many joint contractures are preceded by spasticity. Gone untreated, the spastic joint becomes immobilized and a contracture develops. In burns, direct thermal injury results in deformities of hands and limbs. Subsequent scar contraction of the skin crossing a joint can also result in immobility and contracture.

Specific secondary or associated conditions and complications

Associated conditions include spasticity, heterotopic ossification, degenerative joint disease, fracture, dislocation, and meniscal tears. Some contractures will result in abnormal positioning (eg,in a wheelchair, in bed), predisposing one to pressure ulcers. Generally, deconditioning and loss of function frequently results. This immobility further exacerbates or creates new contractures, resulting in a vicious cycle that increases disability.

2. ESSENTIALS OF ASSESSMENT

History

history should include the etiology of the contractures, its natural course, and its impact on the patient’s functionality. This includes pain, difficulties in mobility and transfers, activities of daily living (ADLs), and hygiene. Details regarding caregiver burden should be explored.

Physical examination

Ideally, the patient should be free from pain that may limit the examination. Inspect the patient for joint size, symmetry, and resting position comparedwith the contralateral side. A goniometer can measure residual range of motion and document changes over time. Joint deformities may also be present and palpable, and skin must be inspected for scars or thickening that may contribute to, or be the source of, contractures (eg, burns). Pressure ulcers may also be present. Skinfolds must be inspected frequently for opportunistic bacterial and fungal infections. A sensory examination must be performedbecause this will guide the choice of treatment modalities (eg, therapeutic heat). Altered proprioception and unilateral neglect should also be assessed.

The most important diagnostic element, however, is passive range of motion (PROM).Any muscle imbalance orweakness andan increase in tone should be noted. To rule out a true contracture in the presence of spasticity, prolonged passive stretch, with or without heat modalities, can overcome increased tone and result in further range of motion. PROM at slow, intermediate, and rapid speeds of stretch can further distinguish among hypertonicity, rigidity, and a true contracture.

Functional assessment

Observing the patient ambulating, transferring, and performing ADLs characterizes the patient’s deficits and their impact on function. If bracing is used as a functional aid, it must be inspected for proper fit and pressure pointsbecause the contracture may have shifted, and the brace may need to be refitted.

Laboratory studies

Diagnosis is based largely on clinical examination. Thereare no blood markers orlaboratory studies that contribute to the diagnosis of a contracture. Other laboratory markers, including alkaline phosphatase, can be used to identify underlying conditions (eg, heterotopic ossification).

Imaging

Radiologic studies (eg, x-rays, bone scans) can be obtained to discern exacerbating pathology (eg, bony deformities, heterotopic ossification, fractures, dislocations, ankylosis). Magnetic resonance imaging and diagnostic ultrasound can be used to visualize soft tissue structures.

Supplemental assessment tools

There are no validated assessment tools in contractures; however, tools do exist for spasticity. Of the2 most common assessments, the Modified Ashworth Scale (MAS) and Tardieu Scale, it was found that the MAS frequently overestimated spasticity in the setting of a contracture, confounding it, whereas the Tardieu scale was better at differentiating the 2.11

Early predictions of outcomes

There are currently no validated prognostic indicators for contractures.

Environmental

Living with a contracture has a significant effect on one’s life. Complications range from hygiene issues in higher functioning individuals to debilitating contractures resulting in limited independence and being permanently bedbound.

Social role and social support system

Those with contractures can increase the burden to family members and caregivers in caring for patients.

Professional Issues

Because contractures are considered largely preventable, there are many professional issues that arise in their development. Among these are neglect in nursing homes and mismanagement of spasticity, including in children.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

The best treatment is to slow or prevent contracture formation. Clinically, this largely involves PROM and stretching exercises daily. However, new evidence-based research has made these longstanding interventions controversial. Recent Cochrane review articles have suggested that passive movements are not effective for the prevention and treatment of contractures,12 and stretch does not prevent or reverse joint contractures in people with neurologic conditions.13 However, many argue that these clinical trials did not provide a sufficient dose or have not combined modalities together.As such, PROM, proper positioning, and stretching are still the clinical mainstays of treatment and prevention.

Any weakness of musculature should be strengthened, particularly the antagonist of the contracted muscle, if applicable. Additional measures include the effective management of spasticity and edema, which can be prevented using massage, elevation, and compression garments.

At different disease stages

Once a contracture has developed, prolonged and continuous stretching of the joint is done through dynamic bracing or serial casting. After maximal stretching, an orthotic or cast is applied to fix the joint at that position. The device is removed every few days, and the process is repeated at an enhanced angle. Stretching can be further facilitated through therapeutic heating modalities. Heating the soft tissue structures around the joint improves elasticity, achieved through hot packs or therapeutic ultrasound. Hydrotherapy and parrafin baths can be used for smaller joints.Care should be taken in using such modalities, especially in patients who are unable to verbalize pain or heat intolerance.

Spasticity must be managed if it is thought to be maintaining the contracture. In truly fixed contractures that significantly impact function and have failed conservative therapy, surgical options are considered. These include surgical release of affected muscles, tenotomy or tendon lengthening, joint capsule release, or total joint replacement.

Coordination of care

The rehabilitation team consisting of a physiatrist,physical, occupational, and recreational therapists, and persons insocial work and case management function arethe unit to manage a patient’s contracture. This includes evaluation, therapeutic exercise, placement of adaptive equipment, andmanaging functional limitations as they pertain to participation restrictions and enhance quality of life.

Patient & family education

Patients and family should be educated regarding risk factors of contractures and strategies in prevention, including proper positioning andrange of motionexercises. Discussions are necessary about the sequelae of a joint contracture and treatment options available. Patient goals are discussed with the rehabilitation team and concerns addressed.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Prevention is key. Appropriate positioning in bed is a simple yet effective preventative measure. For example, one should avoid placing pillows under the knees while supine to prevent knee flexion contractures, and prone lying can force the hip into extension to prevent hip flexion contractures. Shoulderrange of motioncan be preserved with 30 minutes of positioning using a sling attached to the bed, holding the arms in maximal external rotation and abduction.14,15

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

In one animal model, radiofrequency treatments successfully treated underlying collagen contractures and helped in new collagen formation.16 In another study comparing speed and torque inrange of motionexercises using rats, high torque and long-duration static stretching were most effective.17

An injectable collagenaseenzyme derived from the bacteriaClostridium histolyticum(collagenase clostridium histolyticum)has been approved in the treatment ofDupuytren contracture.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

There is a lack of knowledge about the pathophysiology and disease course that lead to contractures.Because of the lack of standardization in assessment, quantification of disability, and evidence-based treatment, there remains a tremendous amount of individual interpretation without many unifying theories or clinical research studies. Clinical studies vary widely in what constitutes a contracture. Even still, evidence-based treatment options remain controversial, putting into question longstanding traditional interventions.

REFERENCES

1.Fergusson D, Hutton B, Drodge A. The epidemiology of major joint contractures: a systematic review of the literature.ClinOrthop Relat Res. 2007;456:22-29.

2.Gnass I, Bartoszek G, Thiesemann R, Meyer G. [Joint contractures in older age.A systematic literature review] [German].Z Gerontol Geriatr. 2010;43(3):147-157.

3. Pohl M, Mehrholz J. A new shoulder range of motion screening measurement: its reliability and application in the assessment of the prevalence of shoulder contractures in patients with impaired consciousness caused by severe brain damage.Arch Phys Med Rehabil. 2005;86(1):98-104.

4. Hoeksma AF, Ter Steeg AM, Dijkstra P, Nelissen RG, Beelen A, de Jong BA. Shoulder contracture and osseous deformity in obstetrical brachial plexus injuries.J Bone Joint Surg Am. 2003;85(2):316-322.

5. Selikson S, Damus K, Hamerman D. Risk factors associated with immobility.J Am Geriatr Soc. 1988;36(8):707-712.

6.Zafonte R, Elovic EP, Lombard L. Acute care management of post-TBI spasticity.J Head Trauma Rehabil. 2004;19(2):89-100.

7. Ada L, O’Dwyer N, O’Neill E. Relation between spasticity, weakness andcontracture of the elbow flexors and upper limb activity after stroke: anobservational study.Disabil Rehabil. 2006;28(13-14):891-897.

8. Gracies JM. Pathophysiology of spastic paresis. I: Paresis and soft tissue changes.Muscle Nerve. 2005;31(5):535-551.

9. Gracies JM. Pathophysiology of impairment in patients with spasticity and use of stretch as a treatment of spastic hypertonia.Phys Med Rehabil Clin N Am. 2001;12(4):747-768, vi.

10. McLachlan EM, Chua M. Rapid adjustment of sarcomere length in tenotomized muscles depends on an intact innervation.Neurosci Lett. 1983;35(2):127-133.

11.Patrick E, Ada L. The Tardieu Scale differentiates contracture from spasticity whereas the Ashworth Scale is confounded by it.Clin Rehabil.2006;20(2):173-182.

12.Prabhu RK, Swaminathan N, Harvey LA. Passive movements for the treatment and prevention of contractures.Cochrane Database Syst Rev. 2013 Dec 28;12:CD009331.

13. Katalinic OM, Harvey LA, Herbert RD, Moseley AM, Lannin NA, Schurr K. Stretch for the treatment and prevention of contractures.Cochrane Database Syst Rev. 2010 Sep 8;(9):CD007455.

14. Ada L, Goddard E, McCully J, Stavrinos T, Bampton J. Thirty minutes ofpositioning reduces the development of shoulder external rotation contractureafter stroke: a randomized controlled trial.Arch Phys Med Rehabil. 2005;86(2):230-234.

15. de Jong LD, Nieuwboer A, Aufdemkampe G. Contracture preventive positioning ofthe hemiplegic arm in subacute stroke patients: a pilot randomized controlledtrial.Clin Rehabil. 2006;20(8):656-667.

16. Choi S, Cheong Y, Shin JH, Jin KH, Park HK. Inflammatory effect of monopolar radiofrequency treatment on collagen fibrils in rabbit skins.J BiomedNanotechnol. 2013;9(8):1403-1407.

17. Moriyama H, Tobimatsu Y, Ozawa J, Kito N, Tanaka R. Amount of torque and duration of stretching affects correction of knee contracture in a rat model ofspinal cord injury.Clin Orthop Relat Res. 2013;471(11):3626-3636.

Author Disclosures

Adrian Cristian, MD
Nothing to Disclose

Ashish Khanna, MD
Nothing to Disclose

Richard Kim, MD
Nothing to Disclose

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