Treating Arthrofibrosis of the Foot and Ankle
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Arthrofibrosis has had little description in the literature when concerning the foot and ankle. It has been referred to as fibroblastic proliferation on steroids. Arthrofibrosis by definition refers to joint pain, swelling, and stiffness that doesn’t allow adequate range of motion. For the purpose of this discussion, we will focus on the ankle, subtalar, and talonavicular joints. This condition is often secondary to trauma, infection, or post-surgical intervention and can include both intra-articular and extra-articular manifestations.1,2
Intra-articular adhesions (adhesion capsulitis) can result in fibrosis and scarring. Also, intra-articular fractures can lead to malalignment (resultant step-offs) and accelerated degeneration of joint cartilage. Extra-articular manifestations can also affect joint range of motion. Adhesions, periarticular fibrosis of supporting joint capsule, muscular contractions, and fascial contractions can greatly contribute to loss of joint motion. The patient often gives a history of joint pain and limitation of daily activity. Patients especially note problems with navigating stairs and sloped surfaces. Clinical features may include joint pain, swelling, stiffness, and decreased range of motion. Alteration of the gait cycle noted clinically as antalgia is common. We have found there is also typically a disconnect between the radiographic appearance and clinical scenario.
The pathophysiology for joint degeneration via arthrofibrosis begins with a synovial inflammatory response. This creates fibroblastic proliferation and deposition of extracellular matrix proteins. Metalloproteinases, designed to clear broken collagen, accumulate within the joint space. This then impairs blood flow, leading to decreased O2 delivery, and resulting in hypoxia. This causes the release of inflammatory cytokines, ie, transforming growth factor (TGF) beta, which is the transferring growth factor for platelet-derived growth factor (PGDF). This results in increased production of type II collagen, which greatly increases fibrosis by crosslinking the existing collagen fibrils.1
What You Should Know About Arthrofibrosis in the Ankle Joint
Approximately 40–73% of cases occur after an ankle fracture.1,2 Remaining cases occur often secondarily to more severe double ankle ligamentous injuries or involvement of the syndesmosis. Clinical symptoms include pain, decreased range of motion, stiffness, and difficulty performing activities of daily living. Radiographs of digital soft tissue imaging note loss of pre-talar (anterior capsule) and juxta-articular (posterior capsule) fat pads due to capsular shrinkage. Dynamic radiographic sequences under fluoroscopy note loss of joint motion in comparison to the contralateral ankle. Magnetic resonance imaging (MRI) on T1 images notes capsular and pericapsular thickening of > 3mm. Fluoroscopy-guided arthrography notes a decrease in joint capacity filling by obliteration of normal joint recesses and high back flow. Failure of open reduction and internal fixation (ORIF) of ankle fractures, especially trimalleolar, can lead to articular step-offs that alter contact motion. While most joint motion loss is intra-articular, extra-articular manifestations such as equinus must be evaluated and occur secondary to the healing process.2
Insights on Ankle Joint Management
Management of ankle joint arthrofibrosis includes physical therapy to increase range of motion and strength. One must undertake this with caution to avoid generation of inflammatory responses. Dynamic splinting with prolonged passive stretching 6–8 hours per day can allow stretching of the contracted connective tissues. Adjunctive corticosteroid injections may be of some help, but the literature indicates a success rate in approximately 20% of cases.3 Manipulation under anesthesia, commonly described in the knee and shoulder, has very little support in the existing literature in the ankle joint. Intra-articular injections of anakinra (an interleukin-1 antagonist) best known for inhibiting the inflammatory cascade and decreasing fibroblastic proliferation has recently been described; however, no long-term outcomes are noted.4
Surgical options include anterior chamber arthroscopy for anterior osteophytes and posterior chamber arthroscopy for posterior impingement lesions. Sugeons may also consider open arthrolysis with cheilectomy or circular external ring fixation with gradual distraction (arthrodiastasis) (Figure 1). One must address Achilles tendon lengthening and gastrocnemius recessions if contractures are present. Corrective intra-articular osteotomies for malleolar malalignment may apply in cases of intra-articular step offs. In advanced cases, we have found a total ankle replacement may become indicated if the hyaline articular cartilage is greatly damaged.
When Arthrofibrosis Occurs Is Present in the Subtalar Joint
Intra-articular capsular and pericapsular thickening can occur with associated inversion injuries involving the cervical and interosseus ligaments of the subtalar joint. MRI, dynamic radiography, stress views, and anterior translation with inversion injuries may note restricted motion in comparison to the opposite extremity. Fluoroscopy-guided arthrography is helpful, noting significant filling defects of the anterior chamber (anterior and middle facets) and posterior chamber (posterior facet) components.
Intra-articular joint depression fractures without ORIF greatly disturb articular motion. With proper ORIF, disturbances of the periarticular capsular structures can still lead to significant joint motion loss. In our experience, extra-articular manifestations can present clinically as resultant protective peroneal spasm, which are tonic contractures that can lead to significant joint motion loss (Figure 2).
Managing Arthrofibrosis in the Subtalar Joint
Management of arthrofibrosis in the subtalar joint is similar to that for the ankle joint. Physical therapy, corticosteroid injections, arthroscopy, or open arthrolysis can be performed. Peroneal spasms may decrease by treating the source and may respond to intramuscular injections of local anesthetic. Most often, adjunctive peroneal tendon lengthening must take place in combination with treating the source of pain.
Understanding Arthrofibrosis of the Talonavicular Joint
Again, capsular and pericapsular injury are the primary sources of the restricted range of motion, swelling, and pain. These are often related to weight-bearing inversion injuries. Fluoroscopy-guided arthrography in comparison to the contralateral extremity is usually the best way to assess the condition. It can also be associated with tonic tibialis anterior muscle spasm attributed physiologically to the rest of the joint. own experience
Managing the Talonavicular Joint
Open arthrolysis may become a choice if physical therapy or intra-articular steroids fail. Tibialis anterior tendon spasm that is nonresponsive to joint treatments or intramuscular injections of local anesthetic may require adjunctive tibialis anterior tendon lengthening or split transfer along with resolution of the inflammatory source (Figure 3).
In Conclusion
The most common etiology of arthrofibrosis in the foot and ankle is following ankle fracture.2 Arthrofibrosis is also quite common following foot and ankle surgical procedures and not always correlated with surgical technique. Regardless of ideal alignment following reconstructive and corrective hindfoot and ankle surgical procedures, patients may continue to experience pain, stiffness, and loss of joint motion. It is important to take into consideration the contralateral extremity and obtain the appropriate imaging. Dynamic splinting, intra-articular corticosteroid injections, intramuscular injections with local anesthetics, and physical therapy are all reasonable considerations in the conservative management of this condition.
Current literature supports intra-articular injections with anakinra IL-1 antagonist having promising results in decreasing the inflammatory response associated with arthrofibrosis.4 Alternatively, arthroscopic and open procedures including arthrolysis with cheilectomy, arthrodiastasis with external fixator application, and tendon lengthening are all valid surgical options when conservative management fails. Addressing the equinus component to the deformity adjunctively either with Achilles tendon lengthening and/or gastrocnemius recession is essential. The literature is still out for debate regarding the effectiveness of surgical management.
Harry John Visser, DPM, FACFAS is the Director of SSM Health Podiatric Surgical Residency in St. Louis.
Jared Visser, DPM, FACFAS is an Attending Physician at SSM Health Podiatric Surgical Residency in St. Louis.
Omari Owens, DPM is a third-year resident at SSM Health Podiatric Surgical Residency in St. Louis.
References
1. Utsugi K, Sakai H, Hiraoka H, Yashiki M, Mogi H. Intra-articular fibrous tissue formation following ankle fracture: the significance of arthroscopic debridement of fibrous tissue. Arthroscopy. 2007;23(1):89–93.
2. Thomas B, Yeo JM, Slater GL. Chronic pain after ankle fracture: an arthroscopic assessment case series. Foot Ankle Int. 2005;26(12):1012–1016.
3. Cui Q, Milbrandt T, Millington S, Anderson M, Hurwitz S. Treatment of posttraumatic adhesive capsulitis of the ankle: a case series. Foot Ankle Int. 2005;26(8):602–606.
4. Brown CA, Toth AP, Magnussen B. Clinical benefits of intra-articular anakinra for arthrofibrosis. Orthopedics. 2010;33(12):877.
