30 years old football player with a Grade 2 ankle sprain

The patient arrived at our Hackney clinic one week after the accident.

A thorough medical history revealed no systemic issues. In addition to the presenting symptoms related to the ankle sprain that the patient wished to address, he had been experiencing symptoms of plantar fasciosis for over three months.

What is a lateral grade 2 ankle sprain?

A sprain occurs when there's damage to the collagen tissue, known as a ligament, which connects bones to a joint. Ligaments play a crucial role in stabilizing joints and proprioception. Sprains typically happen when a joint is suddenly pushed beyond its normal range of motion, stretching the inelastic fibers too far.

A lateral ankle sprain commonly involves the anterior talofibular ligament and the calcaneofibular ligament. The injury mechanism involves plantar flexion and inversion, first stressing the anterior talofibular ligament and then the calcaneofibular ligament. In this scenario, the Calcaneofibular (CFL) and posterior Talofibular ligaments (PTFL) are less likely to be injured. PTFL injuries are rare unless there's a talus dislocation associated with it.

The anterior talofibular ligament attaches to the front part of the outer ankle bone (lateral malleolus) and the neck of the talus.

On the other hand, the calcaneofibular ligament runs downward and backward from the lateral ankle bone to the outer surface of the heel bone (calcaneus). Its main job is to resist inward turning of the foot at the ankle and subtalar joints, especially when the foot is fully bent upward (dorsiflexed).

Together, these ligaments provide stability against inward turning of the foot across most ankle movements. About two-thirds of all lateral ankle ligament injuries involve damage to both of these ligaments.

The severity of a sprain is classified based on how much damage the ligament has sustained and whether it has caused instability in the joint:

  • Grade I: Minimal structural damage with slight local tenderness and no joint instability.

  • Grade II: Partial tearing of the ligament, causing visible swelling, tenderness, and moderate bleeding, with mild to moderate joint instability.

  • Grade III: Severe sprain with complete ligament rupture, significant swelling, and joint instability.

Patients typically experience pain, swelling, muscle weakness, difficulty walking, and sometimes, joint looseness at the initial presentation.

Which tissues could have been affected and caused additional pain in this patient?

The patient likely sprained their ankle while playing football by suddenly placing the foot in an inverted and plantarflexed position, causing a sudden lengthening and damage to the ligaments’ fibers. Consequently, the anterior talofibular and calcaneofibular ligaments are likely the primary source of symptoms, as the sprain resulted in tissue inflammation.

Over one week since the accident, these ligaments are now in the fibroplastic (proliferative) phase of healing, lasting about three weeks and characterized by activated and proliferating fibroblasts synthesizing new collagen and ground substance, responsible for scar tissue formation.

During this stage, collagen fibers initially create a loose mesh of fibrous connective tissue in the injured area, which is vascular and fragile and lacks cross-links between fibers. As time passes, vascularity decreases, cross-linking becomes established, and collagen fibers in the scar tissue are unorganized and randomly arranged, leaving the ligaments still weakened.

The patient is in a phase where inflammatory cells are still present within the ligament, and these inflammatory chemicals are pressing on nerve receptors, causing more pain. Additionally, swelling may occur, exerting extra pressure within the ligament and adjacent soft tissues (e.g., talocrural joint capsule), potentially causing additional pain.

Increased swelling within the ligaments will also reduce the capacity of inflammatory chemicals to leave the site, aggravating the symptoms.

With the stabilizers of the articular capsule of the talocrural joint being sprained and weakened, it might now be exposed to excessive loading and stretch, which could lead to deformation and inflammation of the capsule, causing pain.

These ligaments not only provide mechanical stability to the talocrural joint but also contain mechanoreceptors, such as free nerve endings and Ruffini endings. These receptors play a crucial role in proprioception, the body's ability to sense its position, motion, and equilibrium. By detecting changes in joint position and movement, these mechanoreceptors help activate the appropriate muscle responses to stabilize the joint, even subconsciously, thereby preventing excessive movement or injury.

Since the stabilizing effect of the ligaments has decreased, muscles such as Fibularis Longus, Fibularis Brevis, and Fibularis Tertius might be overstimulated to protect the area from excessive inversion (as their action is plantarflexion and eversion), while muscles such as Tibialis Anterior, the Extensor Hallucis Longus, and the Extensor Digitorum Longus will protect from excessive plantarflexion. This might lead to an increased resting tone in these muscles, potential ischemia, and pain in the lower leg.

Predisposing factor: 3 months duration plantar fasciosis symptoms.

The suffix -osis signifies an abnormal process, disease, or state without inflammation. The term ITIS should be reserved for injuries involving recent onsets accompanied by inflammation, as the suffix "itis" indicates acute inflammation.

Plantar fasciosis results from collagen degeneration of the plantar fascia at its origin, the calcaneal tuberosity of the heel, as well as the surrounding perifascial structures. It may also occur due to reduced blood supply to the tissues from the posterior tibial artery, which needs to pass under the Abductor Hallucis and retinaculum to supply the area around the calcaneus. Inappropriate footwear that extends and adducts the hallux places greater strain on the Abductor Hallucis, reducing blood flow to the calcaneal region, which may cause cellular death.

The plantar fascia normally stabilizes and locks the foot in supination before push-off. The plantar fascia is put under strain by the “windlass mechanism,” which occurs during push-off when the metatarsophalangeal joints are hyperextended. It is also stressed by hyperpronation of the foot, as the medial longitudinal arch collapses.

Biomechanical abnormalities of the foot may contribute to the development of plantar fasciitis. Excessive pronation and the resulting stretch and wringing of the plantar fascia during the stance phase can lead to straining of these tissues.

When plantar fasciosis is present, weight-bearing can become problematic, leading individuals to compensate by altering their gait and biomechanics. This compensation can result in increased stress on other structures of the foot and ankle. In this case, if the individual avoids weight-bearing on the affected foot, they may inadvertently subject the foot to abnormal forces. This altered biomechanical stress can predispose them to a lateral ankle sprain.

Furthermore, the avoidance of weight-bearing may increase the risk of a lateral ankle sprain during activities such as playing football. This combination of factors can contribute to the development of a grade 2 ankle sprain, potentially involving ligament damage and significant functional impairment.