FOOT & ANKLE PAIN

The heel fat pad is a highly specialised and complex shock-absorbing structure comprising fibro-elastic septa that enclose fat globules within discrete compartments, collectively capable of absorbing the enormous compressive forces generated at heel strike during walking and running. With advancing age, repetitive high-impact loading, prolonged standing on hard surfaces and certain systemic conditions such as rheumatoid arthritis, the heel fat pad progressively atrophies — losing volume, elasticity and its shock-absorbing capacity. This leaves the calcaneal periosteum and subchondral bone relatively unprotected from impact forces. Heel fat pad syndrome is significantly more common in older adults (particularly those over 60), distance runners logging high weekly mileage and people who stand for long hours on concrete or other hard surfaces. It is frequently misdiagnosed as plantar fasciitis — the distinction is clinically important as the management differs substantially.

​

Symptoms include:
A deep, bruised, aching or burning pain directly under the centre of the heel that is present throughout standing and walking — not just with the first steps after rest as in plantar fasciitis. The pain is often described as "walking on a stone" or as though the protective padding has been worn away, because functionally it has been. Tenderness on direct pressure over the central heel pad, distinct from the medial calcaneal tubercle tenderness of plantar fasciitis. Pain that worsens progressively with longer periods of standing and walking, and that is notably worse on hard floors and in thin-soled shoes.

​

How we treat it:
Unlike most other musculoskeletal conditions where progressive loading is the cornerstone, heel fat pad syndrome requires a protection and offloading approach — the atrophied pad cannot be regenerated with exercise. Silicone heel cups are the primary treatment: they redistribute the plantar pressure across a wider area of the heel, reducing the peak pressure on the atrophied central fat pad and providing immediate and meaningful pain relief in the majority of patients. A comprehensive footwear assessment is essential — thin-soled, unsupportive footwear dramatically worsens fat pad syndrome and switching to shoes with adequate heel cushioning can alone produce substantial improvement. Activity modification reduces cumulative impact loading during the rehabilitation period, with guidance on safe walking distances and surfaces. Running biomechanics are assessed and corrected where an excessive rear-foot strike pattern is amplifying heel impact forces. Insoles with central heel cutouts — removing all pressure from the most painful area of the heel — can be effective for severe cases.

Calcaneal heel spurs are bony outgrowths (enthesophytes) that develop at the calcaneal enthesis — the bone-tendon or bone-fascia junction — in response to chronic tensile stress on the attaching soft tissue. They occur in two distinct locations: inferior heel spurs develop at the origin of the plantar fascia on the medial calcaneal tubercle and are found in association with plantar fasciitis; posterior heel spurs develop at the Achilles tendon insertion and are found in association with insertional Achilles tendinopathy. Both types are far more common than most people realise — they are present in approximately 15–25% of the general adult population on plain X-ray, and the vast majority of people who have them are entirely asymptomatic. When they do cause pain, it is almost always the surrounding inflamed or degenerated soft tissue driving the symptoms — not the bony spur itself.

​

Symptoms include:
Heel pain in the distribution of the associated soft tissue pathology — either plantar heel pain at the medial calcaneal tubercle (inferior spur and plantar fasciitis) or posterior heel pain at the Achilles insertion (posterior spur and insertional tendinopathy). Importantly, pain is not proportional to spur size — radiologically large spurs are frequently completely painless, while small spurs associated with actively inflamed soft tissue can be very painful. Most patients first become aware of their heel spur incidentally, when an X-ray ordered for heel pain reveals its presence.

​

How we treat it:
The heel spur itself does not require treatment in the vast majority of cases — it is the associated plantar fasciopathy or insertional Achilles tendinopathy that generates the pain, and treating this soft tissue pathology reliably resolves the pain regardless of the spur's presence. Shockwave therapy applied to the heel produces excellent and durable results for both inferior and posterior symptomatic heel spurs — it treats the degenerative soft tissue pathology at the enthesis and is supported by strong clinical evidence. Heel cushioning and footwear modification provide meaningful symptom relief during treatment. Patient education is one of the most valuable interventions we provide in this context: clearly explaining that the spur does not need surgical removal, that the pain is coming from the soft tissue and not the bone, and that conservative treatment produces excellent outcomes in the vast majority of cases — significantly reduces the anxiety and unnecessary treatment-seeking that heel spur diagnoses frequently generate.

Sever's disease — the most common cause of heel pain in children and adolescents aged 8–14 — is a traction apophysitis of the calcaneal growth plate (apophysis) at the posterior heel, where the Achilles tendon attaches. During periods of rapid skeletal growth, the calcaneal apophysis is significantly weaker than the surrounding mature bone, the Achilles tendon and calf muscles — creating a structural mismatch where the powerful traction forces generated during running and jumping repeatedly stress and irritate the vulnerable growth plate. Sever's disease is more common in boys than girls (reflecting their later skeletal maturity and longer window of apophyseal vulnerability), and is associated with high levels of physical activity in running and jumping sports. It affects both heels in approximately 60% of cases. It is a completely self-limiting condition that resolves fully with skeletal maturity when the apophysis fuses to the underlying calcaneus — typically between ages 14–16 in girls and 16–18 in boys.

​

Symptoms include:
Posterior heel pain at the back and bottom of the heel — over the calcaneal apophysis — that develops during and after physical activity, particularly running, jumping and kicking. Pain that may cause a limp during or after sport in more severe cases. A strongly positive calcaneal squeeze test — compressing the sides of the posterior heel between the examiner's fingers firmly reproduces the pain and is the most reliable diagnostic clinical finding. Pain with standing on tiptoe (heel raises). Symptoms that are typically worse during and immediately after activity and ease with rest, and that often flare significantly during growth spurts when the Achilles tendon-to-bone length discrepancy is at its greatest.

​

How we treat it:
Sever's disease is managed with intelligent, activity-preserving load management — not complete rest, which is both unnecessary and counterproductive to the child's physical and social wellbeing. The first step is identifying a tolerable activity level that keeps symptoms manageable while maintaining meaningful sport participation, and building from there. During acute flares, we reduce the volume and intensity of jumping and high-speed running — the most provocative activities — while maintaining lower-intensity training, games participation and non-impact activities such as swimming and cycling where possible. Gastrocnemius and soleus stretching is addressed systematically, as calf muscle tightness — which dramatically increases during growth spurts as the bone grows faster than the muscle-tendon unit — directly amplifies the traction force on the apophysis. Progressive calf and lower limb strengthening builds the muscle's ability to absorb and attenuate the forces transmitted to the apophyseal attachment. A simple 5–10 mm heel raise — either in both shoes or as an insole insert — temporarily reduces the Achilles traction force on the apophysis and provides quick and meaningful pain relief. A patellar (infrapatellar) strap worn around the lower leg can provide additional symptom control during sport participation. Ice applied to the posterior heel for 10–15 minutes after activity reduces post-exercise soreness. Thorough, age-appropriate education for both the child and their family about the self-limiting nature of the condition, its expected timeline and the safety of continued sport participation is one of our most valued contributions — it significantly reduces the anxiety that this diagnosis often generates.

Medial tibial stress syndrome (MTSS) — universally known as shin splints — is a diffuse periosteal stress reaction along the posteromedial border of the tibia, caused by repetitive tibial bending forces that exceed the bone's capacity for adaptive repair and remodelling. It is the most common running injury in new runners and military recruits beginning a running program, accounting for up to 35% of running injuries in these populations. MTSS is not simply "muscle soreness" — it represents genuine bone stress, and it exists on a continuum that, if the loading stimulus is not appropriately reduced, can progress to a frank tibial stress fracture. Accurate differentiation between MTSS and tibial stress fracture is therefore clinically important and influences management significantly.

​

Symptoms include:
A diffuse, aching or burning pain along the inner border of the lower leg — typically extending over a broad area of 5 cm or more along the posteromedial tibia — that is present during running and eases with rest. Tenderness to palpation along this same broad segment of the posteromedial tibial border, which is a key clinical differentiator from tibial stress fracture (where tenderness is localised to a single focal point). The absence of pain at rest in the early stages, with pain only during and after running. Symptoms that are typically worst at the start of a run, improve during the middle of the run, and return after stopping. Progressive worsening if training loads are not modified. Focal point tenderness, night pain or pain at rest should always prompt urgent MRI to exclude stress fracture.

​

How we treat it:
An immediate reduction in running load is the essential first intervention — continuing to run through MTSS without load modification reliably results in progression to stress fracture. We design a structured walk-run program that progressively re-exposes the tibia to impact loading at a rate that allows bone adaptation, rather than the abrupt load increases that caused the injury. Hip abductor and calf strengthening corrects the biomechanical deficits — excessive knee valgus, rearfoot overpronation and weak hip abductors — that increase the tibial bending moment during running and are consistently identified in runners with MTSS. Running gait assessment addresses crossover gait (where the feet land across the midline, increasing tibial torsion forces) and overstriding (where the foot lands too far in front of the body, increasing impact loading). Bone stress nutrition is systematically reviewed — calcium and vitamin D intake, total energy availability and any features of relative energy deficiency in sport (RED-S) that may be reducing the bone's capacity for adaptive repair. When symptoms are atypical, progress is slower than expected, or focal tenderness is identified, we coordinate MRI or bone scan with the patient's GP to exclude stress fracture before returning to running. Most runners with MTSS achieve a full return to their pre-injury training volume within 4–8 weeks with this approach.