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Treatment

Our motto for treating arthrofibrosis is “first, do no harm”.

We believe that specialised approaches are necessary to reduce the risk of further activating fibrosis, particularly for surgical and physiotherapy treatments where aggressive methods can cause worsening of the disease [1]. The fibrosis triggers to be avoided, as far as possible, include hypoxia, bleeding, and fat pad injury. In knees the infrapatellar fat pad (IFP or Hoffa’s fat pad) must be treated with great care. The fat pads present in other joints, such as the subacromial fat pad in shoulders [2], are also likely to generate pain and fibrosis due to chronic inflammation. 


Arthrofibrosis is a complex disease that, like other serious diseases, requires treatment by a team of professionals. Members of the team can include the areas of rheumatology, physiotherapy, surgery and psychology. Treatments may include medications, exercise, passive stretching [1] and psychological support, with surgery the “last resort” option. Non-prescription approaches include good sleep hygiene, massage, supplements, dietary approaches, meditation and stress reduction. 

 

The IAA recommendations are listed below under General, Surgery, Rheumatology and Physiotherapy.

General
Take-aways

  • Fibrosis is a serious disease and should be treated by a multidisciplinary team, in the same way other complex pathologies already are.

  • Arthrofibrosis patients must be treated differently to physiologically healing patients.

  • Early and appropriate treatment is essential to control arthrofibrosis onset and to prevent it from becoming permanent.

  • Chronic inflammation drives an ongoing, dysfunctional wound healing process. Treatment of this disease requires special attention during surgery and physical therapy.

  • Fat pads, such as the infra-patellar fat pad (IFP) are almost always involved in arthrofibrosis, but proper consideration is often not given to this during surgery and/or physical therapy.

  • Arthrofibrosis is frequently a consequence of a surgical procedure which triggers an inappropriate healing response itself.

  • Symptoms are highly variable and depend on the joint and tissues that are fibrotic. Signs instead are more consistent to a certain extent: restricted patellar mobility, joint range of motion (ROM) loss associated with stiffness, tissue thickening, hyper-reactive and tender hardened IFP. Others, such as redness, a warmer knee, and/or a central nervous system (CNS) sensitization might vary.

  • Do not over-treat - use as a-traumatic (minimal) surgery as possible, with only the necessary lysis of adhesions, not the removal of all scar tissue to restore the native anatomy - minimise cell damage.

  • Do not use a tourniquet unless absolutely necessary - avoid hypoxia.

  • Excellent control of bleeding using a cauterizing device and insufflation - avoid inflammatory and fibrotic mediators in blood.

  • Minimise pain using nerve blocks, placed before or immediately after surgery - minimalize the contribution of inflamed nerves that release substance P and other pro-inflammatory, pro-fibrotic mediators, permit immediate passive motion via continuous passive motion machine (CPM).

  • Do not use a rotary cutting tool/shaver - minimize cell damage and bleeding by ‘pulling tissues away’.

  • Immediate, gentle post-op use of a CPM - minimize adhesions and contractions recurrence.

Surgery
Recommen
dations

Rheumatology
Recommendations

  • Have early testing done by a rheumatologist to get the correct diagnosis

  • Actual evidence of inflammation may be relatively scant in low grade, indolent inflammation.

  • There may be more systemic features in the inflammatory process that need to be treated.

  • Good control of pain is important, there are many interactions between the nervous system and the immune system, so patients may need to see a pain specialist.

  • People with auto-inflammatory and auto-immune conditions, including diabetes, are at greatly increased risk of developing arthrofibrosis.

  • Early post-op medications to reduce inflammation and fibrosis may prevent the feedback lops that create chronic fibrosis.

  • Medications that may assist include metformin, Losartan, Pregabalin as well as a range of modern anti-inflammatory medications including anti-TNF-α antibodies and JAK inhibiters.

  • Good sleep, diet and stress reduction are important.

  • Do not try to force improvement, do things little and often to try to regain the overall joint ROM - minimize cell damage & inflammation.

  • Regaining muscle mass is not the goal like in a ‘classic’ post-operative knee rehabilitation plan. The joint needs to get back to its homeostasis (normality) first and foremost - minimize cell damage & inflammation.

  • Don’t attempt to force flexion or extension - minimize cell damage & inflammation.

  • In knees, use crutches for at least 6 weeks post-op, then carefully increase load using one crutch, and then none, as tolerated – minimise damage to the IFP and cautiously progress the joint load tolerance.

  • Extensive post-op use of a CPM machine, up to 12 hours a day, sometimes even overnight, with increases of only 1 degree in ROM at a time to avoid tearing tissue - reduce adhesions and contractions.

  • Strengthening of the muscles, for example, quadriceps, should not be attempted until the joint is no longer painful and inflamed. This can come later. Minimise damage to the IFP.

  • Use of biofeedback is helpful.

  • Blood flow restriction (BFR) should only be used well down the track after the joint has recovered, and then extremely carefully since hypoxia can re-stimulate myofibroblasts - minimise cell damage, fibrosis & inflammation.

  • Use careful, gentle physical therapy post-op or injury to avoid arthrofibrosis in the first place - don’t tell patients to push through the pain, listen and adapt the protocol to what their joint is able to tolerate.

Physiotherapy
Recommen
dations

Oral Medications

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Physiotherapy

Physiotherapy

Surgery

Surgical Scissors

Injections

Medical-Steroid-Injections

Prescription Free

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References

  1. Usher, K. M. et al. Pathological mechanisms and therapeutic outlooks for arthrofibrosis. Bone Research 7, doi:10.1038/s41413-019-0047-x (2019).

  2. Kirsch, J. R. et al. Minimally invasive, sustained-release relaxin-2 microparticles reverse arthrofibrosis. Science Translational Medicine 14, eabo3357, doi:10.1126/scitranslmed.abo3357.

Legal Disclaimer

The materials presented in this site are provided voluntarily as a public service. It is of a general nature, based on the scientific literature. The information and advice provided is made available in good faith but is provided solely on the basis that readers will be responsible for managing their own assessment of the matters discussed herein and that they should verify all relevant representations, statements and information. Please consult your doctor.

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