Plantar fasciitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Plantar fasciopathy is the commonest mechanical cause of plantar heel pain, but location and timing must fit. Ask the patient to point to the pain and describe first steps, warm-up, end-of-day recurrence and running or occupational load. Establish a training change, new shoes, barefoot hard-floor exposure, weight change, diabetes, inflammatory symptoms, osteoporosis risk, trauma, puncture, neurological symptoms and cancer history. Pain that is constant at rest or severe at night demands a different explanation.

Observe gait, shoes, arch, callus and swelling. Palpate the medial calcaneal tubercle and along the fascia, then compare the central fat pad, calcaneal squeeze, Achilles insertion, subtalar joint and tarsal tunnel. Passive dorsiflexion of the great toe tensions the fascia and may reproduce familiar origin pain. Measure ankle dorsiflexion with knee straight and bent to distinguish gastrocnemius contribution. Examine sensation, intrinsic power, pulses and the lumbar or inflammatory system when indicated.

Typical first-step pain and focal medial-origin tenderness are sufficient for diagnosis. Plain radiographs are appropriate after trauma, for suspected stress fracture, unusual bony tenderness or prolonged atypical symptoms. A plantar calcaneal spur reflects traction and age but frequently exists without symptoms. Ultrasound can show fascial thickening and guide a selected procedure; MRI is more sensitive for stress injury, tumour, deep infection and complex neurological or soft-tissue alternatives. Imaging must answer a question rather than confirm every case.

Explain the load-capacity model and favourable but slow course. Reduce only the provoking volume, such as running distance or continuous standing, while maintaining tolerable activity through cycling, swimming or shorter walks. Avoid telling the patient to rest until pain-free. Supportive cushioned shoes and avoiding prolonged barefoot hard-floor exposure often help. A temporary heel cup, low-dye taping or prefabricated orthosis can be tested against a specific walking goal; expensive custom devices are not automatically superior.

Stretch the plantar fascia directly by dorsiflexing the toes and massaging the taut band before first steps, and stretch gastrocnemius and soleus according to the measured restriction. Add slow calf raises and intrinsic-foot exercises, beginning bilaterally or with reduced range and progressing load, repetitions and walking or running exposure. Acceptable exercise discomfort should settle without a marked next-day increase. A night splint can reduce morning pain in selected patients but is useful only if tolerated and worn.

Topical NSAID or brief compatible systemic analgesia can support walking and exercise, but prolonged anti-inflammatory treatment does not rebuild tissue. Corticosteroid injection may reduce pain briefly, especially when ultrasound guided, yet risks fascial rupture, heel-pad atrophy, infection and glucose disturbance. Use only after diagnosis review and shared decision, not as first-line routine treatment or repeated series. Platelet-rich plasma has inconsistent evidence and should not be presented as a guaranteed biological repair.

Extracorporeal shockwave therapy is a specialist option for chronic symptoms after sustained conservative treatment. Surgery is rare and may include partial plantar release or gastrocnemius recession after the true pain generator, calf restriction and neurological alternatives have been reconsidered. Release can cause arch change, nerve injury and persistent pain. Return to running should advance duration before speed and hills, guided by first-step response and next-day load tolerance.

In pregnancy, footwear, stretching and activity measures are prioritised and systemic NSAIDs avoided according to gestation. In diabetes, inspect skin and protective sensation before taping, splints or heat and monitor glucose after steroid. Older adults need stress or insufficiency fracture considered. Anticoagulation increases injection bleeding and bruising; coordinate any procedure without unsupervised medicine interruption.

Key points

The classic symptom is medial plantar heel pain on the first steps after waking or sitting, easing with initial movement and returning after prolonged standing, walking or running.
High-yield examination findings are tenderness at the medial calcaneal tubercle and reproduction with passive great-toe dorsiflexion or the windlass manoeuvre.
First-line investigation is clinical assessment; routine radiographs, ultrasound and MRI are unnecessary in a typical presentation without red flags.
Use radiographs or MRI for a suspected fracture, inflammatory disease, mass or atypical persistent pain; a calcaneal spur is common and does not prove the pain source.
First-line management combines plantar-fascia-specific and calf stretching, progressive calf and intrinsic-foot loading, temporary load adjustment and supportive footwear over several months.
A heel cup, taping, prefabricated insole or night splint can be trialled as an adjunct when it improves function, but no device replaces exercise and load progression.
Consider shockwave treatment for persistent well-localised symptoms after a credible rehabilitation programme; corticosteroid injection offers limited short-term benefit with rupture and fat-pad risks.
Refer when red flags, neurological findings, diagnostic uncertainty or major disability persists despite six to twelve months of well-supported non-operative care.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Load-capacity mismatch

Running, prolonged standing or a sudden activity increase can exceed the plantar fascia's capacity at its medial calcaneal origin.

Restricted ankle dorsiflexion

Gastrocnemius or soleus tightness increases compensatory foot loading and tensile demand through the plantar fascia during stance and push-off.

Foot and footwear factors

A high or low arch, worn footwear, prolonged barefoot walking on hard surfaces and occupational standing can modify local stress without being sufficient alone.

Metabolic and systemic factors

Higher body weight, diabetes and inflammatory enthesitis alter tissue loading or biology and can influence persistence or change the underlying diagnosis.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Medial-origin microfailure
Repeated tensile demand at the medial calcaneal tubercle produces collagen disorganisation and degenerative repair rather than a simple acute inflammatory fasciitis.
2
Windlass loading
Great-toe dorsiflexion winds the fascia around the metatarsal head, raises the arch and tensions the painful origin during terminal stance.
3
Rest-start pain
After unloading, the sensitised fascia and calf-foot complex stiffen, making the first steps after sleep or sitting most painful before tissue warms.
4
Pain and gait adaptation
Avoiding heel contact shortens stride and shifts load to the lateral foot, forefoot, calf and opposite limb, creating secondary symptoms and reduced capacity.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

First-step pain

Medial heel pain is worst during the first steps after sleep or rest, then warms before recurring with prolonged load.

Medial calcaneal tenderness

Focal pain at the plantar-medial calcaneal tubercle follows the fascial origin rather than the centre of the heel pad.

Positive windlass provocation

Passive great-toe dorsiflexion tensions the plantar fascia and reproduces the familiar origin pain during weight-bearing or seated testing.

Stress-fracture pattern

Progressively continuous load pain, inability to walk and tenderness on medial-lateral calcaneal squeeze require fracture imaging.

Neuropathic pattern

Burning, tingling, sensory change or radiation with tarsal-tunnel provocation suggests tibial or branch nerve pain.

Inflammatory pattern

Bilateral heel enthesitis with long morning stiffness, psoriasis, uveitis or bowel inflammation warrants rheumatological assessment.

Red flags requiring action

A fall, sudden training increase or osteoporosis risk with diffuse calcaneal squeeze pain and inability to bear weight suggests stress or acute fracture.
Fever, puncture wound, ulcer, spreading warmth or immune compromise requires urgent soft-tissue and calcaneal infection assessment.
Unremitting night pain, weight loss, palpable mass or previous cancer requires imaging for tumour rather than a plantar-fasciitis label.
Burning, paraesthesia, intrinsic weakness or a positive tarsal-tunnel nerve provocation suggests neurological heel pain.
Bilateral heel pain with prolonged morning stiffness, psoriasis, uveitis or inflammatory bowel disease suggests enthesitis within spondyloarthritis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line clinical heel localisationFirst stepFirst line
Why
Confirm characteristic timing and medial fascial-origin tenderness and screen fracture, nerve, inflammatory and systemic alternatives.
Interpretation and limitations
First-step pain plus focal origin tenderness supports clinical diagnosis; diffuse, neural or rest pain changes the investigation pathway.
02
Plain calcaneal and foot radiographs
Why
Investigate trauma, bony tenderness, arthritis, tumour or prolonged atypical symptoms.
Interpretation and limitations
A spur is neither necessary nor sufficient for diagnosis, and early stress fracture can remain radiographically occult.
03
MRI for suspected stress or destructive disease
Why
Detect occult calcaneal stress injury, marrow infection, tumour or complex soft-tissue disease when suspicion persists.
Interpretation and limitations
MRI is not routine first-line confirmation; use it when the result changes protection, referral or source-control decisions.
04
Ultrasound for a focused fascial question
Why
Assess fascial thickness, tear or adjacent lesion and guide a selected injection or shockwave pathway.
Interpretation and limitations
Thickening supports but does not prove symptom causation, and imaging response is not the main functional outcome.
05
Targeted inflammatory and neurological tests
Why
Investigate bilateral enthesitis, systemic features, paraesthesia or weakness rather than typical mechanical pain.
Interpretation and limitations
Use history-led blood tests, electrodiagnosis or specialist imaging; indiscriminate panels have low diagnostic value.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Calcaneal stress fracture

Pain becomes more continuous with loading, calcaneal squeeze is positive and risk follows training increase, low bone density or systemic bone disease.

Heel-fat-pad syndrome

Central plantar tenderness and a bruised sensation on hard floors localises beneath the heel rather than at the medial fascial origin.

Tarsal tunnel or Baxter nerve

Burning, paraesthesia, nerve provocation or weakness points to tibial or branch compression rather than isolated fascial tenderness.

Inflammatory enthesitis

Bilateral or multiple enthesis pain with prolonged morning stiffness and extra-articular features supports formal spondyloarthritis assessment.

Infection or tumour

Systemic illness, skin portal, night pain, mass or destructive imaging requires urgent investigation and must not be dismissed as resistant fasciopathy.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First-lineMake a clinical diagnosisFirst stepFirst lineFirst-step medial heel pain and focal fascial-origin tenderness occur without red flags.

1Map pain precisely and reproduce it at the medial calcaneal origin with palpation and gentle windlass loading.
2Check calcaneal squeeze, fat pad, Achilles, tarsal tunnel, ankle dorsiflexion, skin, sensation and pulses.
3Explain the slow favourable course and avoid routine imaging or assigning causation to an incidental heel spur.
4Agree walking, work or running outcomes and begin footwear, stretching and progressive loading care.

02Stepwise rehabilitationIncrease plantar-calf capacityMechanical plantar fasciopathy limits first steps, standing, walking or running.

1Reduce provoking load temporarily and provide supportive cushioned footwear, with taping, heel cup or prefabricated insole only if helpful.
2Perform plantar-fascia-specific stretching before first steps and address gastrocnemius and soleus restriction.
3Progress calf raises and intrinsic-foot loading from tolerable bilateral work to unilateral, heavier and task-specific exposure.
4Use first-step and next-day symptoms to dose return, advancing duration before speed, hills and repeated impact.

03AtypicalInvestigate the competing diagnosisTrauma, squeeze pain, rest symptoms, neurological signs, systemic inflammation, infection or mass is present.

1Protect and image suspected calcaneal fracture, using MRI when initial films are normal but clinical concern remains high.
2Route a hot breached or systemically unwell heel through urgent infection and diabetic-foot pathways.
3Investigate nerve distribution, lumbar findings or tarsal-tunnel mass when burning and sensory changes dominate.
4Refer inflammatory enthesitis or oncological features without delaying behind prolonged empirical fasciopathy treatment.

04PersistentEscalate only after diagnosis reviewEscalationMajor function remains limited after several months of adhered-to loading, flexibility and footwear treatment.

1Reassess location, exercise dose, calf restriction, stress fracture, nerve disease and inflammatory features.
2Consider ultrasound or MRI only for a specific unresolved question and selected shockwave treatment in a specialist pathway.
3Discuss steroid injection cautiously as short-term symptom care with rupture, fat-pad, infection and glucose risks.
4Reserve surgical referral for severe symptoms after six to twelve months of credible non-operative treatment and informed risk discussion.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

May reduce pain enough to perform first-step stretching and progressive calf-foot loading.

Topical diclofenac gel

Use 2–4 g of diclofenac 1.16% gel over intact medial-heel skin at each application, up to three or four applications daily for a brief trial within the licensed maximum.

Avoid broken or neuropathic uninspected skin and NSAID hypersensitivity, account for other NSAIDs and pregnancy, and stop if local dermatitis develops.

Provides temporary analgesia during a severe mechanical flare while load treatment begins.

Short-course oral naproxen with protection when suitable

If symptoms prevent rehabilitation and risks are acceptable, use naproxen 250–500 mg orally twice daily with food briefly and add omeprazole 20 mg once daily during treatment when gastroprotection is indicated.

Check gastrointestinal, renal, hepatic, blood-pressure and cardiovascular hazards, frailty and antithrombotic treatment; never combine NSAIDs, and apply the restrictions on use from 20 weeks of pregnancy.

Can provide short-term relief in carefully selected persistent disease but does not restore load capacity.

Plantar-fascial corticosteroid injection

If exceptionally selected after prolonged conservative care, use one ultrasound-guided dose under a trained local protocol around, not within, the diseased fascial origin and avoid scheduling routine repeats.

Discuss fascial rupture, heel-pad atrophy, skin change, infection, bleeding and transient hyperglycaemia; avoid with infection, poor skin, uncontrolled diabetes or uncertain diagnosis.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Chronic heel pain

Symptoms can persist for many months, limiting walking, work, exercise and sleep despite the generally favourable long-term course.

Altered gait and deconditioning

Protective limping transfers load to forefoot, knee, hip and opposite side and reduces calf and general fitness.

Fascial rupture and fat atrophy

Corticosteroid injection can weaken the fascia or atrophy the heel pad, replacing one pain generator with a more difficult structural problem.

Treatment burden

Repeated scans, passive devices and unproven procedures can reinforce fear and cost without restoring progressive walking and calf-foot capacity.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record first-step pain, continuous standing time, walking distance and one work or running target rather than tenderness alone.
Review plantar-fascia and calf stretching technique, ankle dorsiflexion, calf-raise load and next-day response every several weeks.
Inspect footwear wear pattern, heel cushioning, taping or orthosis comfort and skin, especially with diabetes or neuropathy.
Reopen fracture, neurological, inflammatory or malignant assessment if pain becomes continuous, nocturnal, swollen or neurologically associated.
After injection, monitor glucose where relevant and provide urgent advice for a new snap, arch pain, bruising, numbness or infection.
Progress running or occupational impact gradually and maintain calf-foot strength after pain improves to reduce recurrence.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

The spur is often innocent

Calcaneal spurs occur in people without pain and can persist after recovery, so they should not drive invasive treatment.

First steps reveal tissue behaviour

Rest-start pain that warms with movement is much more characteristic than undifferentiated constant heel pain.

Squeeze tests bone

Medial-lateral compression of the calcaneus stresses its body; marked pain should redirect attention from fascia to stress injury.

Stretch both linked tissues

Direct toe-dorsiflexion stretching targets the fascia, while knee-straight and knee-bent calf work addresses different ankle restrictions.

Orthoses are an adjunct trial

A device earns continued use by improving walking or loading, not by being custom made or changing a static footprint.

Injection can trade pain generators

Fascial rupture or fat-pad atrophy may be harder to treat than the original fasciopathy, making repeated corticosteroid unattractive.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing plantar fasciitis from any heel pain without checking first-step timing and exact medial-origin tenderness.
02
Reassuring from a normal early radiograph despite stress-fracture risk and positive calcaneal squeeze.
03
Treating a calcaneal spur as the cause of pain or an automatic surgical target.
04
Prescribing rest, insoles or analgesia without progressive calf and plantar-foot loading.
05
Repeating corticosteroid injections without discussing fascial rupture and heel-pad atrophy.
06
Missing nerve, inflammatory, infectious or malignant disease when symptoms are burning, bilateral, hot or nocturnal.