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“Not Plantar Fasciitis”: the differential diagnosis and management of heel pain syndrome
FOOT AND ANKLE
“Not Plantar Fasciitis”: the differential diagnosis and management of heel pain syndrome
degeneration, inflammation of the plantar bursa, nerve entrapment, local bony pathology and enthesitis caused by seronegative arthritis.1 The term Plantar Fasciitis is often used interchangeably with PHP. However, the distinction between true “Plantar Fasciitis” and many of the other conditions that cause PHP is not always clear. We therefore consider it more appropriate that patients presenting with symptoms of PHP have an initial diagnosis of heel pain syndrome (HPS) (Table 1).
Munier Hossain Epidemiology
Nilesh Makwana
HPS is not uncommon. It is estimated that 1 in 10 people will develop HPS during their lifetime.2 HPS is more common in middle-aged obese females and young male athletes.3 It is likely that the incidence is higher in the athletic population but not all suffering present for medical treatment. A number of risk factors
Abstract Plantar heel pain (PHP) is a common orthopaedic presentation, but our understanding of this symptom is still limited. Multiple risk factors have been proposed but few substantiated. Obesity and foot pronation are known risk factors, whilst running or standing for long periods probably also contribute. There, however, is no relationship between heel spurs and PHP. As well as plantar fasciopathy, a number of different conditions can also give rise to PHP. It may be helpful to consider the differential diagnoses in terms of the structures that are symptomatic: the plantar aponeurosis, other soft tissues, the calcaneum and the peripheral nerves. The pathophysiology of PHP is still unclear but could be multi-factorial. Histological specimens show evidence of degeneration in the plantar aponeurosis but not inflammation. Seronegative arthritis should be excluded in cases of bilateral PHP. A number of different treatment options have been tried but very few have been rigorously investigated. Indeed, the overwhelming majority of cases will improve on conservative treatment. Shock wave therapy and surgery may be of use in selected subsets of patients who do not respond to other modes of conservative treatment.
Differential diagnoses of heel pain syndrome Site Plantar aponeurosis
Sub diagnosis Insertional Non-insertional
Plantar aponeurosis rupture Plantar fibromatosis Enthesopathy Other soft tissues Fat pad atrophy Bursitis Flexor Hallucis Longus tendonitis Calcaneum Traumatic Stress fracture Infective Osteomyelitis Inflammatory Seronegative arthropathy Inflammatory bowel disease Gout Rheumatoid arthritis Neoplastic: benign Unicameral bone cyst Osteoid osteoma Intraosseous lipoma Aneurysmal bone cyst Giant cell tumour Neoplastic: malignant Metastatic tumour Osteogenic sarcoma Chondrosarcoma Ewing’s sarcoma Metabolic Osteomalacia Paget’s disease Hyperparathyroidism Neurological Baxter’s nerve entrapment Medial calcaneal nerve entrapment Tarsal tunnel syndrome S1 radiculopathy
Keywords heel pain syndrome; Plantar Fasciitis; plantar fasciopathy; plantar fasciosis; plantar heel pain
Introduction Plantar heel pain (PHP) is a common presentation in foot and ankle clinics. Although Plantar Fasciitis is the most common cause of PHP a variety of other conditions can also be implicated. Several mechanisms have been proposed for PHP: chronic inflammation and microtrauma of the plantar fascia, mechanical overload, periosteal inflammation, increased calcaneal intraosseous pressure, peripheral nerve entrapment, fat pad
Munier Hossain FRCS(Glasg) PG Cert MSc(Ortho Eng) MSc(Oxon) Associate Specialist at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK. Nilesh Makwana FRCSEd FRCS(Glasg) FRCS(Orth) Consultant Orthopaedic Surgeon at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK.
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Diagnosis e primary Plantar fasciopathy
Table 1
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described, only the central band is constant. It is triangular in shape and arises from the medial process of the calcaneal tuberosity (Figure 1). The band diverges distally at mid-metatarsal level into five separate strands that are attached at the forefoot onto the plantar skin, the base of the proximal phalanges (via the plantar plate), the metatarsophalangeal joints via the collateral ligaments and the deep transverse metatarsal ligaments. Proximally the PA has direct a fibrocartilaginous attachment to the calcaneum e an enthesis. In the fibrocartilaginous enthesis fibrous tissue is gradually replaced by uncalcified fibrocartilage, calcified fibrocartilage and finally bone. This extraordinary degree of osseous interdigitation is able to withstand very significant tensile and shear stress that is in direct proportion to the degree of calcification of the cartilage and the extent of interdigitation. The transitional arrangement is also helpful to evenly dissipate stress.10 Researchers have found that the fibres of the Tendo Achilles are in direct continuity with the fibres of PA.11 This finding may explain the association between HPS and tight heel cord (and therefore reduced ankle dorsiflexion).
have been proposed but there is scant evidence to substantiate these assertions. There seems to be general agreement that obesity and increased pronation are definite risk factors for HPS.4e6 Reduced ankle dorsi-flexion and prolonged standing have been proposed4 and refuted by the same authors.5 Increased age and reduced metatarsophalangeal joint extension may also play roles.4 Both Pes Cavus and Pes Planus have been implicated.7 It is suggested, but not proven, that extensive running, wearing poorly constructed shoes and running on hard surfaces can cause PHP.8 The association between PHP and heel spurs remains a subject of controversy. Although it is tempting to speculate that heel spurs may result from traction of the plantar aponeurosis (PA), it is important to be aware that in fact heel spurs are not located in the PA, but more dorsally in the Flexor Digitorum Brevis (FDB) muscle. A number of papers have reported a positive association between heel spur and PHP.4 However, most of these are retrospective case series and as such do not indicate causation. Heel spur is actually fairly common in the general population and the presence or absence of a spur has not been found to correlate with the patients’ symptoms.9
Nerves The posterior tibial nerve is located in the tarsal tunnel. It usually divides into its three terminal branches in the tarsal tunnel: the medial plantar nerve, the lateral plantar nerve and the medial calcaneal nerve. The medial calcaneal nerve innervates the medial side of the heel, the medial plantar aspect of the foot and the AH muscle, which is the medial most muscle of the superficial layer of the foot. The first branch of the lateral plantar nerve (Baxter’s nerve) is particularly at risk. This branch comes off of the lateral plantar nerve near its origin and travels to supply the rest of the superficial layer muscle of the foot and the QP muscle. The nerve also gives a sensory supply to the calcaneal periosteum. This nerve travels between the AH muscle medially and the QP muscle laterally and can become trapped between the deep fascia of AH and the medial head of the QP muscle.1
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Heel pain syndrome is common Obesity and increased foot pronation are known risk factors Reduced ankle dorsi-flexion and prolong standing have also been implicated, although the evidence is weak The common assumption of a positive association between heel spur and HPS remains unproven
Relevant anatomy Calcaneum An understanding of the local anatomy is helpful when considering the differential diagnoses of HPS. The posterior tuberosity of the calcaneum contributes to the bony architecture of the heel. The tuberosity has medial and lateral processes. The medial process gives attachment to the FDB, Abductor hallucis (AH) and the medial head of the Quadratus plantae (QP) muscles as well as the central band of the PA. The calcaneum is separated from the plantar skin by retrocalcaneal and plantar bursae and the heel fat pad. Plantar fat pad The plantar fat pad (PFP) is a complex multi-lobular fatty structure, whose anatomy and physiological role in HPS is poorly appreciated. The heel pad is uniquely designed to absorb shock and allow pain-free ambulation. The heel pad has a honeycombed structure and consists of fibroelastic septae extending from the calcaneum to the plantar skin. Enclosed between the septae are fat globules. Each fibroelastic chamber is further reinforced by diagonal and transversely running fibres. Plantar aponeurosis The PA is a fibro-aponeurotic structure, which is condensed deep fascia of the foot. Although a medial and lateral band has been
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Figure 1 Anatomy of the plantar aponeurosis.
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The PA shares a common origin with the muscles of the superficial layer of the foot The calcaneum is separated from the plantar skin by a complex honeycombed fibro-fatty fat pad that attenuates impact stress The PA has a fibrocartilaginous attachment to the calcaneum, which helps to dissipate stress Heel skin is supplied by the medial calcaneal nerve that, if compressed more proximally, may present with heel pain Baxter’s nerve is at risk of compression between the Abductor hallucis muscle and the medial belly of the Quadratus plantae muscle
Figure 2 Weight bearing loads the arch, compresses the struts and places tensile stress on the plantar aponeurosis.
Local biomechanics
rope”, or effectively shortens the PA and tightens it, thus elevating the medial arch by a windlass effect (Figure 3).12 During early stance phase there is coupled internal rotation of the leg and subtalar joint pronation. This “unwinds” the windlass and, as a result of elongation of the PA, lowers the arch via a “reverse windlass” mechanism. There is negative feedback in the system: lowering the arch tightens the PA that eventually prevents any further pronation. An adequately functioning windlass mechanism is essential to allow the foot to act as a propulsive lever. From heel strike to weight acceptance, subtalar joint pronation tenses the PA, which prevents excessive pronation and prepares the foot for supination from midstance onwards. Supination transforms the foot into a rigid lever ready for propulsion. From the foregoing discussion it is clear that excessive subtalar pronation during gait would prevent the medial arch from rising and affect the foot’s ability to propel forward.
Plantar aponeurosis Although the PA is thought of as being relatively inelastic, this premise is based on quasi-static tests performed on cadavers. Researchers have shown that the PA also has time-dependent visco-elastic properties, with a modulus of elasticity between 342 and 822 MPa.10 The PA supports the longitudinal arch of the foot. This was proved experimentally, with sectioning of the PA resulting in weakening of the arch.10 Plantar aponeurosis: truss and tie-beam: During static stance the biomechanical arrangement of the medial longitudinal arch has been likened to a truss, or more specifically, a uni-planar simple truss: a single triangular unit where the base is formed by the PA. Since the joints of this postulated truss are not fixed a better analogy may be a tie-bar connecting two compressive elements. It is useful to remember that the PA is the only element capable of elongation in this structure. Weight bearing transmits compressive force through the tarsi and the metatarsi. This tenses the PA, which resists further deformation of the arch (Figure 2). Variable elongation of the PA body can adjust the stiffness and height of the arch in response to the applied load. The clinical implication is that tension on the tie-beam may be higher in pes planus. Therefore, from a biomechanical point of view this lends credence to the clinical finding of increased risk of HPS in patients with foot pronation. The PA is also subject to tensile stress during different phases of the gait cycle. At the early part of stance phase, the longitudinal arch is lowered, which tenses the PA. Towards the end of the stance phase, the gastro-soleus complex lifts the heel off the ground for forward progression and generates a postero-superior torque on the calcaneus. The PA acts to counteract this torque, which places additional tensile stress upon itself.
Plantar heel pad Each heel strike generates a force through the heel pad of around 110% of the body weight. This can increase to 250% during running and the PHP is able to attenuate up to 80% of the strain to the lower leg. In comparison, insoles are able to attenuate less than 20% of the strain.13 It is therefore clear that a well cushioned heel is essential to absorb impact of heel strike. The PHP demonstrates visco-elastic behaviour under strain. The specialized macro and micro compartmentalized globular fat structure means that the fat cells are incompressible.14 The structure does not allow free fluid movement between the heel pad compartments. The fat globules in PHP are also specialized, with an altered ratio of saturated/unsaturated fat compared to normal
Plantar aponeurosis: the windlass mechanism: A windlass is a device designed to lift a heavy object by tightening a rope. It is proposed that the PA acts both as a windlass and reverse windlass. The anatomical basis for this analogy is that the PA has a broad insertion onto the forefoot. As such, dorsi-flexion of the metatarsophalangeal joints during terminal stance pulls or “winds” the PA over the metatarsal heads. This “shortens the
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Figure 3 Schematic diagram of a functioning windlass mechanism in the foot. Raising of the winch handle (hallux) results in shortening and tensioning of the rope and elevation of the arch.
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human adipose tissue.13 This means that the PHP has a lower viscosity compared to normal adipose tissue. There have been conflicting reports regarding the change in PHP thickness in HPS, with claims and counter-claims of thinning and thickening of the pad.14 However, it is agreed that loss of heel pad elasticity is a crucial factor in HPS.14 With ageing there is alteration in collagen and elastin content as well as changes in the thickness of the heel pad. This results in reduced shock absorbing capacity and could explain the increased risk of HPS with ageing.
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The plantar “fascia” is a fibro-aponeurotic structure Histological changes of the PA in HPS are suggestive of degeneration rather than inflammation Repetitive microtrauma is widely believed to initiate plantar fasciopathy but there is no strong evidence that supports this theory
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The PA is not inelastic, it has visco-elastic properties The PA supports the longitudinal arch of the foot The PA acts like a tie-beam and resists flattening of the arch on weight bearing A functioning windlass mechanism of the PA allows the foot to act as an efficient propulsive lever Excessive pronation of the subtalar joint prevents the arch from rising and turns the foot into an inefficient lever
The problem with “Plantar Fasciitis”: a misnomer
Figure 4 Area of tenderness: IPF: insertional PF, NIPF: non-insertional PF, MCN: medial calcaneal nerve compression, BN: Baxter’s nerve compression, TTS: tarsal tunnel syndrome, MM: medial malleolus.
The term “Plantar Fasciitis” implies that the plantar fascia is subject to inflammation. Actually the plantar fascia is not a fascia at all but a fibro-aponeurotic structure and there is no evidence that inflammation occurs in HPS. Current research indicates that “Plantar Fasciitis” may in fact be a degenerative condition. Classic signs of inflammation e swelling, erythema, leucocytic or macrophage infiltration e are absent. Histological analysis of resected specimens has instead shown tissue changes suggestive of chronic degeneration: myxoid degeneration and fibroblast necrosis, chondroid metaplasia, angiofibroblastic proliferation, collagen degeneration, altered ratio of Type III to Type I collagen, increased numbers of abnormal fibroblasts with mitochondrial defects etc.15 A number of authors have also found thickening of the PA in HPS, with a mean reported thickness exceeding 4 mm.16 It has therefore been suggested that a more appropriate term might be “Plantar Fasciosis” (PF) or “plantar fasciopathy”. It is widely believed that mechanical overload of the PA causes repeated microtrauma and, eventually, a mechanical type of PHP, although the actual evidence for this is tenuous.10 Mechanical stress, however, appears to be concentrated at the calcaneal attachment of the PA and could explain HPS. Some studies have shown the area of tendon most often affected in “degenerative” tendinopathy is not the area of the tendon that is subjected to the highest mechanical force.3 Such findings have led others to question repetitive trauma as a causative factor. Loss of the cushioning effect of plantar fat pad could be responsible in some patients. Researchers have found evidence that changes in heel pad thickness, especially with ageing, may result in loss of elasticity of the heel pad and HPS.17 There is certainly evidence of degeneration of the fat pad with ageing and this could explain the late onset of HPS in the nonathletic population.
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Clinical features Presentation Patients usually present with plantar heel pain. HPS is typically worse early in the morning, especially for the first few steps after arising, gets better after some time but returns towards the end of the day. Some patients with tarsal tunnel syndrome by contrast complain of pain that is worse in bed and is relieved by weight bearing. An appropriate clinical history should ascertain the
Baxter’s nerve Calcaneus
Quadraus plantae Abductor hallucis Flexor digitorum brevis
Plantar aponeurosis
Figure 5 Palpation of the medial border of heel will compress the Baxter’s nerve between the belly of AH and QP muscles.
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Useful clinical tests in HPS Tests Passive toe dorsi-flexion Silfverskiold’s test Resisted great toe flexion Dorsi-flexioneeversion test
Mechanism Tightens the Windlass mechanism and exacerbates pain Increased passive ankle dorsi-flexion with the knee flexed to 90 Strains the FHL and reproduces pain Dorsi-flexioneeversion of ankle with extension of MTP joints strains the tibial nerve and causes pain/dysaesthesia
Diagnosis Plantar fasciopathy Tight Tendo Achilles FHL tendonitis Tarsal tunnel syndrome
Table 2
Clinical examination A thorough clinical examination is essential. It may be useful to inspect the footwear first, provided they are not brand new, and observe the pattern of wear. One should specifically inspect for heel pad atrophy, pes planus or pes cavus, hindfoot deformity, overpronation during gait and check for ankle range of motion and posterior tibial tendon dysfunction. If ankle dorsi-flexion appears limited one should perform Silfverskiold’s test to assess if this is due to a tight gastrocnemius. Other tests that are of use include passive dorsi-flexion of the toes, which tightens the windlass mechanism and exacerbates the pain in PF. Resisted flexion of the toe will exacerbate HPS in case of Flexor Hallucis Longus (FHL) tendonitis (Table 2).
duration of symptoms, occupational activities, current footwear, any recent increase in activity etc. An enquiry into systemic health is also important, as bilateral HPS is likely to be due to spondyloarthropathy.8 Patients should be asked about any history of back pain, urethritis, uveitis, bowel disturbance etc. Unrelenting pain, even at rest, should alert one to the possibility of infection or tumour, whilst sensory disturbance suggests a neurological pathology. It is also useful to remember that patients may have multiple pathologies and present with a number of different presenting features. PF may be combined with entrapment of Baxter’s nerve or tarsal tunnel syndrome. There have been reports of a small series of patients presenting with a combination of PF, posterior tibial tendon dysfunction and tarsal tunnel syndrome.18 The authors postulated that the failure of both static and dynamic arch support led to traction injury to the posterior tibial nerve in these patients.
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Site of tenderness The site of tenderness may be useful in informing the definitive diagnosis (Figure 4): the medial calcaneal tubercle is usually tender in PF but the calcaneal tuberosity may also be tender. Pain may also be present more distally over the central PA. We like to differentiate between the central pain and tenderness that is found in non-insertional PF and the medial calcaneal tenderness of insertional PF. In the case of plantar fibromatosis there may be a palpable nodule and pain/tenderness over the midpart of the PA. If there is compression of the Baxter’ nerve then pain is more proximal and dorsal. Palpating the medial aspect of the heel in line with the posterior border of the medial malleolus will compress the Baxter’s nerve between the AH and QP muscle and reproduce the symptoms (Figure 5). This is a useful sign, as patients with Baxter’s nerve compression usually do not complain of any sensory disturbance. Compression of the medial calcaneal nerve in the tarsal tunnel may also give rise to medial heel discomfort. This may also be associated with a positive Tinel’s sign and altered sensation of medial side of the heel. Tenderness, if present, is usually more posterior and dorsal to the area of tenderness in Baxter’s nerve compression. Diffuse pain and tenderness of the calcaneum is suggestive of a calcaneal stress fracture. Patients with plantar calcaneal bursitis or ‘Policeman’s heel’ present with burning, aching or a throbbing type of pain. The heel may or may not feel warm to touch, but is usually tender on direct compression. Pain due to PA rupture is more proximal and may be associated with a palpable gap.
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C C C
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Patients usually complain of heel pain immediately after waking up in the morning that gets better after a while but returns towards the end of the day Bilateral HPS is likely to be due to spondyloarthropathy Infection or tumour should be excluded if pain is unrelenting The medial calcaneal tubercle is tender in insertional plantar fasciopathy Tenderness over the medial aspect of the heel in line with the posterior border of the medial malleolus is suggestive of Baxter’s nerve compression Diffuse heel tenderness may suggest a calcaneal stress fracture
Investigations Blood tests Investigations may not always be necessary in routine practice. If symptoms are bilateral but there is no obvious previous systemic history then blood tests should be performed to rule out gout, spondyloarthropathy etc. However, blood tests, including HLA-B27, might be entirely normal in many patients with spondyloarthropathy.19 Plain radiology When radiology is performed a weight bearing lateral radiograph of the ankle should be the first investigation. This will help to rule out stress fracture or tumour (Figure 6a, b) but should not be performed in search of a heel spur.7,9,11 There are also reports
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Figure 7 Ultrasound shows thickening and hypo-echoic signal from the affected PA compared to the normal side.
diagnosis is unclear.7 Ultrasound is useful in detecting abnormalities of the PA (Figure 7). A thickened PA of more than 4 mm thickness, as well as areas of hypo-echoic abnormality within the PA, may be found in case of PF.20 The addition of Doppler may give additional information regarding local hyperaemia. Magnetic Resonance Imaging (MRI) MRI may be helpful in evaluating patients who have an atypical presentation, who fail conservative management or are suspected of other causes of heel pain, such as tarsal tunnel syndrome, ganglion, osteomyelitis or tumour.6 MRI is more useful to rule out other causes of HPS than to confirm a diagnosis of PF. Usual MRI findings include thickening of the plantar aponeurosis, periaponeurotic oedema, bone marrow oedema of the calcaneus, stress fracture, frank tear of the PA etc (Figure 8a, b). Electrophysiology Electromyography (EMG) and nerve conduction studies (NCS) can be performed and are useful for suspected tarsal tunnel syndrome. However, they are operator-dependent and Baxter’s nerve compression is difficult to examine with NCS. a Plain X-ray of the ankle shows a radio-lucent appearance of the calcaneum. b MRI demonstrates intraosseous cystic lesion with a peripheral rim of fat characteristic of intraosseous lipoma.
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Figure 6
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that a non-weight bearing lateral X-ray of the ankle has high sensitivity and specificity to rule out PF based on the assessment of the thickness of the PA and the quality of the fat pad.16 Periosteal reaction may be evident in infection or spondyloarthropathy.8 If there is strong suspicion of a stress fracture but X-ray is negative then further imaging is useful.
Treatment HPS is generally a self-limiting condition and an overwhelming majority are likely to report resolution of symptoms with conservative management alone.11 There is general agreement that if conservative treatment is started soon after the onset of HPS then this is likely to lead to improvement or recovery in most patients. However, the time to resolution is
Ultrasonogram Ultrasound examination is operator-dependent, but if available is considered by many to be the investigation of choice when the
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Get to know your radiologist If the diagnosis is unclear a discussion with the radiologist will help in planning appropriate modes of investigation
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a MRI scan showing incomplete stress fracture of the calcaneal tuberosity with surrounding bone oedema, sagittal section (blue arrow). b Stress fracture of calcaneum, coronal section. Figure 8
variable and around 10% of all cases fail to respond to conservative treatment.21 HPS can cause a significant deterioration in health related quality of life in patients with recalcitrant symptoms.22
friction massage have been tried, without any evidence of useful effect. Night splints are designed to prevent overnight ankle plantarflexion. Plantarflexion of the ankle relaxes the PA and allows it to contract. There is evidence that night splint is useful in improving symptoms although the strength of this recommendation is weak in view of poor internal validity of the studies.25 These studies also suggest that patient compliance with night splints is likely to be low.
A number of treatment options A number of different treatment modalities are available: rest, ice, heat, nonsteroidal anti-inflammatory drugs (NSAIDs), heel cushions, heel cups, magnetic insoles, taping, Achilles and plantar fascia-specific stretching exercises, night splints, walking cast, ultrasound, laser treatment, iontophoresis, steroid injections, extra-corporeal shock wave therapy and surgery.6 None have unequivocally proven benefit and very few have been assessed via well designed randomized controlled trials.23 Some of the interventions are assessed in combination with other interventions and this makes it difficult to comment on the usefulness of individual interventions. If there are modifiable external risk factors then these should be addressed. It is logical to advise patients to modify their physical activities, to change trainers or shoes if their own are less than ideal and to lose weight. A step-wise treatment approach is recommended: with simpler options tried first.
Physiotherapy Physiotherapy is recommended for tightness of the Tendo Achilles, and incorporates calf stretching as well as plantar fascia-specific stretching exercises. Tendo Achilles stretching is performed by leaning against a wall with the affected side is placed behind the normal side. The heels are kept firmly on the ground and knee fully extended on the affected side (Figure 9a). Passive extension of the metatarsophalangeal joints will specifically stretch the plantar aponeurosis. DiGiovanni et al were the first to publish the results of tissue specific plantar fascia-stretching exercise and found them to be superior to Achilles tendon stretching in a randomized trial.26 In a recently published study Rompe et al found plantar fascia-specific stretching (Figure 9b) to be superior to repeated low dose shock wave therapy for the treatment of acute symptoms of proximal PF at early follow-up, but there was no difference at 15 months.23 This study reinforces the generally agreed guideline that ESWT be used only in chronic cases.
Physical therapy Heel cups and gel heel pads provide cushioning. They are also inexpensive and readily available. Foot orthotics may provide short-term benefit but are not useful over the long term.24 If a patient is deemed to require an orthosis (if they have pes planus or hindfoot varus/valgus) off-the-shelf orthotics should be tried. They are less expensive and there is no evidence that custom-made orthotics give better results.1 Orthotics support the medial longitudinal arch. Corrective orthotics can protect the foot from excessive pronation. There is no role for magnetic insoles.25 Taping of the foot is postulated to provide arch support but there is no strong evidence that it works.25 Ultrasound and deep
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Anti-inflammatory medication NSAID’s are often used in clinical practice and may be helpful to relieve acute symptoms of HPS but are unlikely to be effective alone and have not been adequately investigated. There is limited evidence to support the effectiveness of local corticosteroid injection. The rationale of injecting an anti-inflammatory agent in what is essentially a degenerate condition is not entirely clear. A recently withdrawn Cochrane review had found that steroid
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approach and placed deep to the PA. The medial approach is likely to be less painful than a direct plantar approach. Injecting deep to the PA ensures adequate spread of the corticosteroid preparation and reduces the risk of fat pad atrophy. Ultrasound guidance may prove to be an useful adjunct for accurate needle placement. Extra-corporeal Shock Wave Therapy (ESWT) ESWT involves the delivery of what are essentially rapidly pressurized sound waves. They are generated via a Lithotripsy unit that converts electrical energy into mechanical energy. ESWT can be of high or low energy. Local anaesthesia is usually required for high energy ESWT. ESWT application results in a positive pressure and a shock wave effect at the interface of two different types of tissues with different acoustic impedance.6 ESWT application also creates a tensile wave and a tissue cavitation effect. How ESWT works at tissue level is not fully understood but two different mechanisms have been proposed. It has been claimed that the deep tissue cavitation effect causes microrupture of capillaries, leakage of chemical mediators and promotion of neovascularization of the damaged tissue. The alternative theory is that ESWT works by depleting local sensory nerve fibres of substance P and calcitonin gene related peptide and thereby desensitises the area.23 ESWT is contra-indicated in bleeding diatheses. There have been a number of trials investigating its role but results are conflicting. This may be because of the heterogeneity of intervention and outcome measures employed. A Canadian Health Technology Assessment did not recommend the use of ESWT for PF.21 In the UK, the National Institute for Health and Clinical Excellence (NICE) recommends that ESWT should be used within a framework of audit after informed patient decision.27 ESWT is not recommended as a first line of management but textbooks recommend ESWT for symptoms lasting for more than 6 months where at least three different modes of conservative therapy have already been tried. In our practice we found ESWT useful for refractory cases of HPS. We are presently auditing our results. Surgery Open or endoscopic PA release may be suitable for a small subset of carefully selected patients in whom symptoms persist in spite of all other modes of conservative management. The procedure of choice is open partial PA release with simultaneous release of the Baxter’s nerve. The aim of surgery is to partially release the medial PA (<50%) and divide both superficial and deep fasciae of AH. Endoscopic PA release may appear to be attractive but there is concern that the procedure carries an unacceptably high rate of complications. Visualization is poor with the endoscopic technique and there is poor control of the extent of PA release. Other complications that have been reported include pseudoaneurysm of the lateral plantar artery and nerve injury. It is not possible to decompress Baxter’s nerve with the endoscopic technique and the American Orthopaedic Foot and Ankle Society (AOFAS) recommends that in case of suspected nerve compression endoscopic release should not be performed.8 It is not clear if the heel spur should be concurrently removed. Studies have reported complete/partial/no removal of the heel spur along with PA release.
a Tendo Achilles stretching: the stickman is leaning against the wall, keeping the front knee bent and the affected back knee completely extended, both heels are firmly on the ground. He should feel his calf muscles getting tight. b Plantar fascia-specific stretching is performed by passive extension of the toes until the PA feels taut. It is advisable to confirm that PA is correctly stretched by palpating the tension in the PA with the contralateral hand while stretching. Figure 9
injection had short-term benefit compared to control.2 This would suggest that the margin of benefit from corticosteroid injection is likely to be small. Nevertheless, corticosteroid injection remains a useful item in the orthopaedic armoury. There is a risk of fat pad atrophy and iatrogenic PA rupture with local corticosteroid injection. We suggest that the needle be introduced via the medial
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11 McPoil TG, Martin RL, Cornwall MW, Wukich DK, Irrgang JJ, Godges JJ. Heel pain e plantar fasciitis. J Orthop Sports Phys Ther 2008; 38: A1e17. 12 Hicks JH. The mechanics of the foot: the plantar aponeurosis. J Anat 1954; 88: 25e30. 13 Miller-Young JE, Duncan NA, Baroud G. Material properties of the human calcaneal fat pad in compression: experiment and theory. J Biomech 2002; 35: 1523e31. 14 Tong J, Lim CS, Goh OL. Techinque to study the biomechanical properties of the human calcaneal heel pad. The Foot 2003; 13: 83e91. 15 Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc 2003; 93: 234e7. 16 Osborne HR, Breidahl WH, Allison GT. Critical differences in lateral Xrays with and without a diagnosis of plantar fasciitis. J Sci Med Sport 2006; 9: 231e7. € € o € yu €ncu € Y, Ozg €rgen M, Dabak K. Effects of changes in 17 Ozdemir H, So heel fat pad thickness and elasticity on heel pain. J Am Podiatr Med Assoc 2004; 94: 47e52. 18 Labib SA, Gould JS, Rodriguez-Del-Rio FA, Lyman S. Heel pain triad (HPT): the combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome. Foot Ankle Int 2002; 23: 212e20. 19 Lehman TJA. Enthesitis, arthritis and heel pain. J Am Podiatr Med Assoc 1999; 89: 18e9. 20 McMillan AM, Landorf KB, Barrett JT, Menz HT, Bird AR. Diagnostic imaging for chronic plantar heel pain: a systematic review and metaanalysis. J Foot Ankle Res 2009; 2: 32. 21 Extracorporeal shock wave treatment for chronic plantar fasciitis. Canadian Agency for Drugs and Technologies in Health 2007; vol. 96. http://www.cadth.ca/media/pdf/E0009_chronic-plantar-fasciitispart1_cetap_e.pdf [accessed 19.12.10]. 22 Irving DB, Cook JL, Young MA, Menz HL. Impact of chronic plantar heel pain health related quality of life. J Am Podiatr Med Assoc 2008; 98: 283e9. 23 Rompe JD, Cacchio A, Weil Jr L, et al. Plantar fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar fasciopathy. J Bone Joint Surg Am 2010; 92: 2514e22. 24 Landorf KB, Keenan AM, Herbert RD. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Arch Intern Med 2006; 166: 1305e10. 25 Stuber K, Kristmanson K. Conservative therapy for plantar fasciitis: a narrative review of randomized controlled trials. J Can Chiropr Assoc 2006; 50: 118e33. 26 DiGiovanni BF. Tissue-specific plantar fascia stretching exercise enhances outcomes in patients with chronic heel pain. J Bone Joint Surg Am 2003; 85-A: 1270e7. 27 Extracorporeal shockwave therapy for refractory plantar fasciitis. National Institute for Health and Clinical Excellence. 2009. http:// guidance.nice.org.uk/IPG311 [accessed 19.12.10] 28 Riley G. Tendinopathydfrom basic science to treatment. Nat Clin Pract Rheumatol 2008; 4: 82e9.
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Although a myriad of treatment options are available very few have been assessed via well designed trials Plantar fascia-specific stretching exercise appears to be useful in an acute setting Steroid injection should be attempted via the medial approach, with the needle placed deep to the PA Ultrasound guided injection may assist accurate needle placement ESWT may be useful in chronic recalcitrant cases although how ESWT works are subject to speculation Surgery should only be attempted in a selected subset of patients after all modes of conservative therapy have been tried Open partial PA release and decompression of the Baxter’s nerve is the procedure of choice
Conclusion It will be useful if future trials include placebo or no treatment arms to investigate the self-limiting nature of HPS. More trials are also needed to better understand the doseeresponse relationship and the appropriate combination of energy, frequency and duration of treatment of ESWT to determine if this has a place in management plans. Advances in the future treatment of HPS are likely to come from improvements in our understanding of the pathomechanics of HPS. There is evolving interest in the role of metalloproteinase enzymes in tendinopathy in general and they may well have a role to play in HPS.28 Unlocking the cellular secrets of HPS may also help to advance more specific cell-based treatment options in future. A
REFERENCES 1 Lee T, Maurus PB. Plantar heel pain. In: Coughlin MJ, Mann RA, Saltzman CL, eds. Surgery of the foot and ankle. Philadelphia: Mosby Elsevier, 2007: 689e707. 2 Crawford F, Thomson CE. Interventions for treating plantar heel pain. Cochrane Database Syst Rev 2003; 3: CD000416. 3 Juliano PJ, Harris TG. Plantar fasciitis, entrapment neuropathies, and tarsal tunnel syndrome: current up to date treatment. Curr Opin Orthop 2004; 15: 49e54. 4 Irving DB, Cook JL, Menz HB. Factors associated with chronic plantar heel pain: a systematic review. J Sci Med Sport 2006; 9: 11e22. 5 Irving DB, Cook JL, Young MA, Menz HB. Obesity and pronated foot type may increase the risk of chronic plantar heel pain: a matched caseecontrol study. BMC Musculoskelet Disord 2007; 8: 41. 6 Puttaswamaiah R, Chandran P. Degenerative plantar fasciitis: a review of current concepts. Foot 2007; 17: 3e9. 7 Alvarez-Nemegyei J, Canoso JJ. Heel pain: diagnosis and treatment, step by step. Cleve Clin J Med 2006; 73: 465e71. 8 Buchbinder R. Plantar fasciitis. N Engl J Med 2004; 350: 2159e66. 9 Thomas JL, Christensen JC, Kravitz SR, et al. The diagnosis and treatment of heel pain: a clinical practice guideline e revision 2010. J Foot Ankle Surg 2010; 49: S1e19. 10 Wearing SC, Smeathers JE, Urry SR, Henning EM, Hills AP. The pathomechanics of plantar fasciitis. Sports Med 2006; 36: 585e611.
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Acknowledgement The authors would like to thank Dr. HJ Patel, Consultant Radiologist, Wrexham Maelor Hospital for providing the radiological images.
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“Not Plantar Fasciitis”: the differential diagnosis and management of heel pain syndrome
degeneration, inflammation of the plantar bursa, nerve entrapment, local bony pathology and enthesitis caused by seronegative arthritis.1 The term Plantar Fasciitis is often used interchangeably with PHP. However, the distinction between true “Plantar Fasciitis” and many of the other conditions that cause PHP is not always clear. We therefore consider it more appropriate that patients presenting with symptoms of PHP have an initial diagnosis of heel pain syndrome (HPS) (Table 1).
Munier Hossain Epidemiology
Nilesh Makwana
HPS is not uncommon. It is estimated that 1 in 10 people will develop HPS during their lifetime.2 HPS is more common in middle-aged obese females and young male athletes.3 It is likely that the incidence is higher in the athletic population but not all suffering present for medical treatment. A number of risk factors
Abstract Plantar heel pain (PHP) is a common orthopaedic presentation, but our understanding of this symptom is still limited. Multiple risk factors have been proposed but few substantiated. Obesity and foot pronation are known risk factors, whilst running or standing for long periods probably also contribute. There, however, is no relationship between heel spurs and PHP. As well as plantar fasciopathy, a number of different conditions can also give rise to PHP. It may be helpful to consider the differential diagnoses in terms of the structures that are symptomatic: the plantar aponeurosis, other soft tissues, the calcaneum and the peripheral nerves. The pathophysiology of PHP is still unclear but could be multi-factorial. Histological specimens show evidence of degeneration in the plantar aponeurosis but not inflammation. Seronegative arthritis should be excluded in cases of bilateral PHP. A number of different treatment options have been tried but very few have been rigorously investigated. Indeed, the overwhelming majority of cases will improve on conservative treatment. Shock wave therapy and surgery may be of use in selected subsets of patients who do not respond to other modes of conservative treatment.
Differential diagnoses of heel pain syndrome Site Plantar aponeurosis
Sub diagnosis Insertional Non-insertional
Plantar aponeurosis rupture Plantar fibromatosis Enthesopathy Other soft tissues Fat pad atrophy Bursitis Flexor Hallucis Longus tendonitis Calcaneum Traumatic Stress fracture Infective Osteomyelitis Inflammatory Seronegative arthropathy Inflammatory bowel disease Gout Rheumatoid arthritis Neoplastic: benign Unicameral bone cyst Osteoid osteoma Intraosseous lipoma Aneurysmal bone cyst Giant cell tumour Neoplastic: malignant Metastatic tumour Osteogenic sarcoma Chondrosarcoma Ewing’s sarcoma Metabolic Osteomalacia Paget’s disease Hyperparathyroidism Neurological Baxter’s nerve entrapment Medial calcaneal nerve entrapment Tarsal tunnel syndrome S1 radiculopathy
Keywords heel pain syndrome; Plantar Fasciitis; plantar fasciopathy; plantar fasciosis; plantar heel pain
Introduction Plantar heel pain (PHP) is a common presentation in foot and ankle clinics. Although Plantar Fasciitis is the most common cause of PHP a variety of other conditions can also be implicated. Several mechanisms have been proposed for PHP: chronic inflammation and microtrauma of the plantar fascia, mechanical overload, periosteal inflammation, increased calcaneal intraosseous pressure, peripheral nerve entrapment, fat pad
Munier Hossain FRCS(Glasg) PG Cert MSc(Ortho Eng) MSc(Oxon) Associate Specialist at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK. Nilesh Makwana FRCSEd FRCS(Glasg) FRCS(Orth) Consultant Orthopaedic Surgeon at the Department of Trauma and Orthopaedic Surgery, Betsy Cadwaladr University Local Health Board, Wrexham Maelor Hospital, Wrexham, UK.
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Diagnosis e primary Plantar fasciopathy
Table 1
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described, only the central band is constant. It is triangular in shape and arises from the medial process of the calcaneal tuberosity (Figure 1). The band diverges distally at mid-metatarsal level into five separate strands that are attached at the forefoot onto the plantar skin, the base of the proximal phalanges (via the plantar plate), the metatarsophalangeal joints via the collateral ligaments and the deep transverse metatarsal ligaments. Proximally the PA has direct a fibrocartilaginous attachment to the calcaneum e an enthesis. In the fibrocartilaginous enthesis fibrous tissue is gradually replaced by uncalcified fibrocartilage, calcified fibrocartilage and finally bone. This extraordinary degree of osseous interdigitation is able to withstand very significant tensile and shear stress that is in direct proportion to the degree of calcification of the cartilage and the extent of interdigitation. The transitional arrangement is also helpful to evenly dissipate stress.10 Researchers have found that the fibres of the Tendo Achilles are in direct continuity with the fibres of PA.11 This finding may explain the association between HPS and tight heel cord (and therefore reduced ankle dorsiflexion).
have been proposed but there is scant evidence to substantiate these assertions. There seems to be general agreement that obesity and increased pronation are definite risk factors for HPS.4e6 Reduced ankle dorsi-flexion and prolonged standing have been proposed4 and refuted by the same authors.5 Increased age and reduced metatarsophalangeal joint extension may also play roles.4 Both Pes Cavus and Pes Planus have been implicated.7 It is suggested, but not proven, that extensive running, wearing poorly constructed shoes and running on hard surfaces can cause PHP.8 The association between PHP and heel spurs remains a subject of controversy. Although it is tempting to speculate that heel spurs may result from traction of the plantar aponeurosis (PA), it is important to be aware that in fact heel spurs are not located in the PA, but more dorsally in the Flexor Digitorum Brevis (FDB) muscle. A number of papers have reported a positive association between heel spur and PHP.4 However, most of these are retrospective case series and as such do not indicate causation. Heel spur is actually fairly common in the general population and the presence or absence of a spur has not been found to correlate with the patients’ symptoms.9
Nerves The posterior tibial nerve is located in the tarsal tunnel. It usually divides into its three terminal branches in the tarsal tunnel: the medial plantar nerve, the lateral plantar nerve and the medial calcaneal nerve. The medial calcaneal nerve innervates the medial side of the heel, the medial plantar aspect of the foot and the AH muscle, which is the medial most muscle of the superficial layer of the foot. The first branch of the lateral plantar nerve (Baxter’s nerve) is particularly at risk. This branch comes off of the lateral plantar nerve near its origin and travels to supply the rest of the superficial layer muscle of the foot and the QP muscle. The nerve also gives a sensory supply to the calcaneal periosteum. This nerve travels between the AH muscle medially and the QP muscle laterally and can become trapped between the deep fascia of AH and the medial head of the QP muscle.1
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Heel pain syndrome is common Obesity and increased foot pronation are known risk factors Reduced ankle dorsi-flexion and prolong standing have also been implicated, although the evidence is weak The common assumption of a positive association between heel spur and HPS remains unproven
Relevant anatomy Calcaneum An understanding of the local anatomy is helpful when considering the differential diagnoses of HPS. The posterior tuberosity of the calcaneum contributes to the bony architecture of the heel. The tuberosity has medial and lateral processes. The medial process gives attachment to the FDB, Abductor hallucis (AH) and the medial head of the Quadratus plantae (QP) muscles as well as the central band of the PA. The calcaneum is separated from the plantar skin by retrocalcaneal and plantar bursae and the heel fat pad. Plantar fat pad The plantar fat pad (PFP) is a complex multi-lobular fatty structure, whose anatomy and physiological role in HPS is poorly appreciated. The heel pad is uniquely designed to absorb shock and allow pain-free ambulation. The heel pad has a honeycombed structure and consists of fibroelastic septae extending from the calcaneum to the plantar skin. Enclosed between the septae are fat globules. Each fibroelastic chamber is further reinforced by diagonal and transversely running fibres. Plantar aponeurosis The PA is a fibro-aponeurotic structure, which is condensed deep fascia of the foot. Although a medial and lateral band has been
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Figure 1 Anatomy of the plantar aponeurosis.
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The PA shares a common origin with the muscles of the superficial layer of the foot The calcaneum is separated from the plantar skin by a complex honeycombed fibro-fatty fat pad that attenuates impact stress The PA has a fibrocartilaginous attachment to the calcaneum, which helps to dissipate stress Heel skin is supplied by the medial calcaneal nerve that, if compressed more proximally, may present with heel pain Baxter’s nerve is at risk of compression between the Abductor hallucis muscle and the medial belly of the Quadratus plantae muscle
Figure 2 Weight bearing loads the arch, compresses the struts and places tensile stress on the plantar aponeurosis.
Local biomechanics
rope”, or effectively shortens the PA and tightens it, thus elevating the medial arch by a windlass effect (Figure 3).12 During early stance phase there is coupled internal rotation of the leg and subtalar joint pronation. This “unwinds” the windlass and, as a result of elongation of the PA, lowers the arch via a “reverse windlass” mechanism. There is negative feedback in the system: lowering the arch tightens the PA that eventually prevents any further pronation. An adequately functioning windlass mechanism is essential to allow the foot to act as a propulsive lever. From heel strike to weight acceptance, subtalar joint pronation tenses the PA, which prevents excessive pronation and prepares the foot for supination from midstance onwards. Supination transforms the foot into a rigid lever ready for propulsion. From the foregoing discussion it is clear that excessive subtalar pronation during gait would prevent the medial arch from rising and affect the foot’s ability to propel forward.
Plantar aponeurosis Although the PA is thought of as being relatively inelastic, this premise is based on quasi-static tests performed on cadavers. Researchers have shown that the PA also has time-dependent visco-elastic properties, with a modulus of elasticity between 342 and 822 MPa.10 The PA supports the longitudinal arch of the foot. This was proved experimentally, with sectioning of the PA resulting in weakening of the arch.10 Plantar aponeurosis: truss and tie-beam: During static stance the biomechanical arrangement of the medial longitudinal arch has been likened to a truss, or more specifically, a uni-planar simple truss: a single triangular unit where the base is formed by the PA. Since the joints of this postulated truss are not fixed a better analogy may be a tie-bar connecting two compressive elements. It is useful to remember that the PA is the only element capable of elongation in this structure. Weight bearing transmits compressive force through the tarsi and the metatarsi. This tenses the PA, which resists further deformation of the arch (Figure 2). Variable elongation of the PA body can adjust the stiffness and height of the arch in response to the applied load. The clinical implication is that tension on the tie-beam may be higher in pes planus. Therefore, from a biomechanical point of view this lends credence to the clinical finding of increased risk of HPS in patients with foot pronation. The PA is also subject to tensile stress during different phases of the gait cycle. At the early part of stance phase, the longitudinal arch is lowered, which tenses the PA. Towards the end of the stance phase, the gastro-soleus complex lifts the heel off the ground for forward progression and generates a postero-superior torque on the calcaneus. The PA acts to counteract this torque, which places additional tensile stress upon itself.
Plantar heel pad Each heel strike generates a force through the heel pad of around 110% of the body weight. This can increase to 250% during running and the PHP is able to attenuate up to 80% of the strain to the lower leg. In comparison, insoles are able to attenuate less than 20% of the strain.13 It is therefore clear that a well cushioned heel is essential to absorb impact of heel strike. The PHP demonstrates visco-elastic behaviour under strain. The specialized macro and micro compartmentalized globular fat structure means that the fat cells are incompressible.14 The structure does not allow free fluid movement between the heel pad compartments. The fat globules in PHP are also specialized, with an altered ratio of saturated/unsaturated fat compared to normal
Plantar aponeurosis: the windlass mechanism: A windlass is a device designed to lift a heavy object by tightening a rope. It is proposed that the PA acts both as a windlass and reverse windlass. The anatomical basis for this analogy is that the PA has a broad insertion onto the forefoot. As such, dorsi-flexion of the metatarsophalangeal joints during terminal stance pulls or “winds” the PA over the metatarsal heads. This “shortens the
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Figure 3 Schematic diagram of a functioning windlass mechanism in the foot. Raising of the winch handle (hallux) results in shortening and tensioning of the rope and elevation of the arch.
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human adipose tissue.13 This means that the PHP has a lower viscosity compared to normal adipose tissue. There have been conflicting reports regarding the change in PHP thickness in HPS, with claims and counter-claims of thinning and thickening of the pad.14 However, it is agreed that loss of heel pad elasticity is a crucial factor in HPS.14 With ageing there is alteration in collagen and elastin content as well as changes in the thickness of the heel pad. This results in reduced shock absorbing capacity and could explain the increased risk of HPS with ageing.
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The plantar “fascia” is a fibro-aponeurotic structure Histological changes of the PA in HPS are suggestive of degeneration rather than inflammation Repetitive microtrauma is widely believed to initiate plantar fasciopathy but there is no strong evidence that supports this theory
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The PA is not inelastic, it has visco-elastic properties The PA supports the longitudinal arch of the foot The PA acts like a tie-beam and resists flattening of the arch on weight bearing A functioning windlass mechanism of the PA allows the foot to act as an efficient propulsive lever Excessive pronation of the subtalar joint prevents the arch from rising and turns the foot into an inefficient lever
The problem with “Plantar Fasciitis”: a misnomer
Figure 4 Area of tenderness: IPF: insertional PF, NIPF: non-insertional PF, MCN: medial calcaneal nerve compression, BN: Baxter’s nerve compression, TTS: tarsal tunnel syndrome, MM: medial malleolus.
The term “Plantar Fasciitis” implies that the plantar fascia is subject to inflammation. Actually the plantar fascia is not a fascia at all but a fibro-aponeurotic structure and there is no evidence that inflammation occurs in HPS. Current research indicates that “Plantar Fasciitis” may in fact be a degenerative condition. Classic signs of inflammation e swelling, erythema, leucocytic or macrophage infiltration e are absent. Histological analysis of resected specimens has instead shown tissue changes suggestive of chronic degeneration: myxoid degeneration and fibroblast necrosis, chondroid metaplasia, angiofibroblastic proliferation, collagen degeneration, altered ratio of Type III to Type I collagen, increased numbers of abnormal fibroblasts with mitochondrial defects etc.15 A number of authors have also found thickening of the PA in HPS, with a mean reported thickness exceeding 4 mm.16 It has therefore been suggested that a more appropriate term might be “Plantar Fasciosis” (PF) or “plantar fasciopathy”. It is widely believed that mechanical overload of the PA causes repeated microtrauma and, eventually, a mechanical type of PHP, although the actual evidence for this is tenuous.10 Mechanical stress, however, appears to be concentrated at the calcaneal attachment of the PA and could explain HPS. Some studies have shown the area of tendon most often affected in “degenerative” tendinopathy is not the area of the tendon that is subjected to the highest mechanical force.3 Such findings have led others to question repetitive trauma as a causative factor. Loss of the cushioning effect of plantar fat pad could be responsible in some patients. Researchers have found evidence that changes in heel pad thickness, especially with ageing, may result in loss of elasticity of the heel pad and HPS.17 There is certainly evidence of degeneration of the fat pad with ageing and this could explain the late onset of HPS in the nonathletic population.
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Clinical features Presentation Patients usually present with plantar heel pain. HPS is typically worse early in the morning, especially for the first few steps after arising, gets better after some time but returns towards the end of the day. Some patients with tarsal tunnel syndrome by contrast complain of pain that is worse in bed and is relieved by weight bearing. An appropriate clinical history should ascertain the
Baxter’s nerve Calcaneus
Quadraus plantae Abductor hallucis Flexor digitorum brevis
Plantar aponeurosis
Figure 5 Palpation of the medial border of heel will compress the Baxter’s nerve between the belly of AH and QP muscles.
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Useful clinical tests in HPS Tests Passive toe dorsi-flexion Silfverskiold’s test Resisted great toe flexion Dorsi-flexioneeversion test
Mechanism Tightens the Windlass mechanism and exacerbates pain Increased passive ankle dorsi-flexion with the knee flexed to 90 Strains the FHL and reproduces pain Dorsi-flexioneeversion of ankle with extension of MTP joints strains the tibial nerve and causes pain/dysaesthesia
Diagnosis Plantar fasciopathy Tight Tendo Achilles FHL tendonitis Tarsal tunnel syndrome
Table 2
Clinical examination A thorough clinical examination is essential. It may be useful to inspect the footwear first, provided they are not brand new, and observe the pattern of wear. One should specifically inspect for heel pad atrophy, pes planus or pes cavus, hindfoot deformity, overpronation during gait and check for ankle range of motion and posterior tibial tendon dysfunction. If ankle dorsi-flexion appears limited one should perform Silfverskiold’s test to assess if this is due to a tight gastrocnemius. Other tests that are of use include passive dorsi-flexion of the toes, which tightens the windlass mechanism and exacerbates the pain in PF. Resisted flexion of the toe will exacerbate HPS in case of Flexor Hallucis Longus (FHL) tendonitis (Table 2).
duration of symptoms, occupational activities, current footwear, any recent increase in activity etc. An enquiry into systemic health is also important, as bilateral HPS is likely to be due to spondyloarthropathy.8 Patients should be asked about any history of back pain, urethritis, uveitis, bowel disturbance etc. Unrelenting pain, even at rest, should alert one to the possibility of infection or tumour, whilst sensory disturbance suggests a neurological pathology. It is also useful to remember that patients may have multiple pathologies and present with a number of different presenting features. PF may be combined with entrapment of Baxter’s nerve or tarsal tunnel syndrome. There have been reports of a small series of patients presenting with a combination of PF, posterior tibial tendon dysfunction and tarsal tunnel syndrome.18 The authors postulated that the failure of both static and dynamic arch support led to traction injury to the posterior tibial nerve in these patients.
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Site of tenderness The site of tenderness may be useful in informing the definitive diagnosis (Figure 4): the medial calcaneal tubercle is usually tender in PF but the calcaneal tuberosity may also be tender. Pain may also be present more distally over the central PA. We like to differentiate between the central pain and tenderness that is found in non-insertional PF and the medial calcaneal tenderness of insertional PF. In the case of plantar fibromatosis there may be a palpable nodule and pain/tenderness over the midpart of the PA. If there is compression of the Baxter’ nerve then pain is more proximal and dorsal. Palpating the medial aspect of the heel in line with the posterior border of the medial malleolus will compress the Baxter’s nerve between the AH and QP muscle and reproduce the symptoms (Figure 5). This is a useful sign, as patients with Baxter’s nerve compression usually do not complain of any sensory disturbance. Compression of the medial calcaneal nerve in the tarsal tunnel may also give rise to medial heel discomfort. This may also be associated with a positive Tinel’s sign and altered sensation of medial side of the heel. Tenderness, if present, is usually more posterior and dorsal to the area of tenderness in Baxter’s nerve compression. Diffuse pain and tenderness of the calcaneum is suggestive of a calcaneal stress fracture. Patients with plantar calcaneal bursitis or ‘Policeman’s heel’ present with burning, aching or a throbbing type of pain. The heel may or may not feel warm to touch, but is usually tender on direct compression. Pain due to PA rupture is more proximal and may be associated with a palpable gap.
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Patients usually complain of heel pain immediately after waking up in the morning that gets better after a while but returns towards the end of the day Bilateral HPS is likely to be due to spondyloarthropathy Infection or tumour should be excluded if pain is unrelenting The medial calcaneal tubercle is tender in insertional plantar fasciopathy Tenderness over the medial aspect of the heel in line with the posterior border of the medial malleolus is suggestive of Baxter’s nerve compression Diffuse heel tenderness may suggest a calcaneal stress fracture
Investigations Blood tests Investigations may not always be necessary in routine practice. If symptoms are bilateral but there is no obvious previous systemic history then blood tests should be performed to rule out gout, spondyloarthropathy etc. However, blood tests, including HLA-B27, might be entirely normal in many patients with spondyloarthropathy.19 Plain radiology When radiology is performed a weight bearing lateral radiograph of the ankle should be the first investigation. This will help to rule out stress fracture or tumour (Figure 6a, b) but should not be performed in search of a heel spur.7,9,11 There are also reports
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Figure 7 Ultrasound shows thickening and hypo-echoic signal from the affected PA compared to the normal side.
diagnosis is unclear.7 Ultrasound is useful in detecting abnormalities of the PA (Figure 7). A thickened PA of more than 4 mm thickness, as well as areas of hypo-echoic abnormality within the PA, may be found in case of PF.20 The addition of Doppler may give additional information regarding local hyperaemia. Magnetic Resonance Imaging (MRI) MRI may be helpful in evaluating patients who have an atypical presentation, who fail conservative management or are suspected of other causes of heel pain, such as tarsal tunnel syndrome, ganglion, osteomyelitis or tumour.6 MRI is more useful to rule out other causes of HPS than to confirm a diagnosis of PF. Usual MRI findings include thickening of the plantar aponeurosis, periaponeurotic oedema, bone marrow oedema of the calcaneus, stress fracture, frank tear of the PA etc (Figure 8a, b). Electrophysiology Electromyography (EMG) and nerve conduction studies (NCS) can be performed and are useful for suspected tarsal tunnel syndrome. However, they are operator-dependent and Baxter’s nerve compression is difficult to examine with NCS. a Plain X-ray of the ankle shows a radio-lucent appearance of the calcaneum. b MRI demonstrates intraosseous cystic lesion with a peripheral rim of fat characteristic of intraosseous lipoma.
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that a non-weight bearing lateral X-ray of the ankle has high sensitivity and specificity to rule out PF based on the assessment of the thickness of the PA and the quality of the fat pad.16 Periosteal reaction may be evident in infection or spondyloarthropathy.8 If there is strong suspicion of a stress fracture but X-ray is negative then further imaging is useful.
Treatment HPS is generally a self-limiting condition and an overwhelming majority are likely to report resolution of symptoms with conservative management alone.11 There is general agreement that if conservative treatment is started soon after the onset of HPS then this is likely to lead to improvement or recovery in most patients. However, the time to resolution is
Ultrasonogram Ultrasound examination is operator-dependent, but if available is considered by many to be the investigation of choice when the
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Get to know your radiologist If the diagnosis is unclear a discussion with the radiologist will help in planning appropriate modes of investigation
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a MRI scan showing incomplete stress fracture of the calcaneal tuberosity with surrounding bone oedema, sagittal section (blue arrow). b Stress fracture of calcaneum, coronal section. Figure 8
variable and around 10% of all cases fail to respond to conservative treatment.21 HPS can cause a significant deterioration in health related quality of life in patients with recalcitrant symptoms.22
friction massage have been tried, without any evidence of useful effect. Night splints are designed to prevent overnight ankle plantarflexion. Plantarflexion of the ankle relaxes the PA and allows it to contract. There is evidence that night splint is useful in improving symptoms although the strength of this recommendation is weak in view of poor internal validity of the studies.25 These studies also suggest that patient compliance with night splints is likely to be low.
A number of treatment options A number of different treatment modalities are available: rest, ice, heat, nonsteroidal anti-inflammatory drugs (NSAIDs), heel cushions, heel cups, magnetic insoles, taping, Achilles and plantar fascia-specific stretching exercises, night splints, walking cast, ultrasound, laser treatment, iontophoresis, steroid injections, extra-corporeal shock wave therapy and surgery.6 None have unequivocally proven benefit and very few have been assessed via well designed randomized controlled trials.23 Some of the interventions are assessed in combination with other interventions and this makes it difficult to comment on the usefulness of individual interventions. If there are modifiable external risk factors then these should be addressed. It is logical to advise patients to modify their physical activities, to change trainers or shoes if their own are less than ideal and to lose weight. A step-wise treatment approach is recommended: with simpler options tried first.
Physiotherapy Physiotherapy is recommended for tightness of the Tendo Achilles, and incorporates calf stretching as well as plantar fascia-specific stretching exercises. Tendo Achilles stretching is performed by leaning against a wall with the affected side is placed behind the normal side. The heels are kept firmly on the ground and knee fully extended on the affected side (Figure 9a). Passive extension of the metatarsophalangeal joints will specifically stretch the plantar aponeurosis. DiGiovanni et al were the first to publish the results of tissue specific plantar fascia-stretching exercise and found them to be superior to Achilles tendon stretching in a randomized trial.26 In a recently published study Rompe et al found plantar fascia-specific stretching (Figure 9b) to be superior to repeated low dose shock wave therapy for the treatment of acute symptoms of proximal PF at early follow-up, but there was no difference at 15 months.23 This study reinforces the generally agreed guideline that ESWT be used only in chronic cases.
Physical therapy Heel cups and gel heel pads provide cushioning. They are also inexpensive and readily available. Foot orthotics may provide short-term benefit but are not useful over the long term.24 If a patient is deemed to require an orthosis (if they have pes planus or hindfoot varus/valgus) off-the-shelf orthotics should be tried. They are less expensive and there is no evidence that custom-made orthotics give better results.1 Orthotics support the medial longitudinal arch. Corrective orthotics can protect the foot from excessive pronation. There is no role for magnetic insoles.25 Taping of the foot is postulated to provide arch support but there is no strong evidence that it works.25 Ultrasound and deep
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Anti-inflammatory medication NSAID’s are often used in clinical practice and may be helpful to relieve acute symptoms of HPS but are unlikely to be effective alone and have not been adequately investigated. There is limited evidence to support the effectiveness of local corticosteroid injection. The rationale of injecting an anti-inflammatory agent in what is essentially a degenerate condition is not entirely clear. A recently withdrawn Cochrane review had found that steroid
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approach and placed deep to the PA. The medial approach is likely to be less painful than a direct plantar approach. Injecting deep to the PA ensures adequate spread of the corticosteroid preparation and reduces the risk of fat pad atrophy. Ultrasound guidance may prove to be an useful adjunct for accurate needle placement. Extra-corporeal Shock Wave Therapy (ESWT) ESWT involves the delivery of what are essentially rapidly pressurized sound waves. They are generated via a Lithotripsy unit that converts electrical energy into mechanical energy. ESWT can be of high or low energy. Local anaesthesia is usually required for high energy ESWT. ESWT application results in a positive pressure and a shock wave effect at the interface of two different types of tissues with different acoustic impedance.6 ESWT application also creates a tensile wave and a tissue cavitation effect. How ESWT works at tissue level is not fully understood but two different mechanisms have been proposed. It has been claimed that the deep tissue cavitation effect causes microrupture of capillaries, leakage of chemical mediators and promotion of neovascularization of the damaged tissue. The alternative theory is that ESWT works by depleting local sensory nerve fibres of substance P and calcitonin gene related peptide and thereby desensitises the area.23 ESWT is contra-indicated in bleeding diatheses. There have been a number of trials investigating its role but results are conflicting. This may be because of the heterogeneity of intervention and outcome measures employed. A Canadian Health Technology Assessment did not recommend the use of ESWT for PF.21 In the UK, the National Institute for Health and Clinical Excellence (NICE) recommends that ESWT should be used within a framework of audit after informed patient decision.27 ESWT is not recommended as a first line of management but textbooks recommend ESWT for symptoms lasting for more than 6 months where at least three different modes of conservative therapy have already been tried. In our practice we found ESWT useful for refractory cases of HPS. We are presently auditing our results. Surgery Open or endoscopic PA release may be suitable for a small subset of carefully selected patients in whom symptoms persist in spite of all other modes of conservative management. The procedure of choice is open partial PA release with simultaneous release of the Baxter’s nerve. The aim of surgery is to partially release the medial PA (<50%) and divide both superficial and deep fasciae of AH. Endoscopic PA release may appear to be attractive but there is concern that the procedure carries an unacceptably high rate of complications. Visualization is poor with the endoscopic technique and there is poor control of the extent of PA release. Other complications that have been reported include pseudoaneurysm of the lateral plantar artery and nerve injury. It is not possible to decompress Baxter’s nerve with the endoscopic technique and the American Orthopaedic Foot and Ankle Society (AOFAS) recommends that in case of suspected nerve compression endoscopic release should not be performed.8 It is not clear if the heel spur should be concurrently removed. Studies have reported complete/partial/no removal of the heel spur along with PA release.
a Tendo Achilles stretching: the stickman is leaning against the wall, keeping the front knee bent and the affected back knee completely extended, both heels are firmly on the ground. He should feel his calf muscles getting tight. b Plantar fascia-specific stretching is performed by passive extension of the toes until the PA feels taut. It is advisable to confirm that PA is correctly stretched by palpating the tension in the PA with the contralateral hand while stretching. Figure 9
injection had short-term benefit compared to control.2 This would suggest that the margin of benefit from corticosteroid injection is likely to be small. Nevertheless, corticosteroid injection remains a useful item in the orthopaedic armoury. There is a risk of fat pad atrophy and iatrogenic PA rupture with local corticosteroid injection. We suggest that the needle be introduced via the medial
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11 McPoil TG, Martin RL, Cornwall MW, Wukich DK, Irrgang JJ, Godges JJ. Heel pain e plantar fasciitis. J Orthop Sports Phys Ther 2008; 38: A1e17. 12 Hicks JH. The mechanics of the foot: the plantar aponeurosis. J Anat 1954; 88: 25e30. 13 Miller-Young JE, Duncan NA, Baroud G. Material properties of the human calcaneal fat pad in compression: experiment and theory. J Biomech 2002; 35: 1523e31. 14 Tong J, Lim CS, Goh OL. Techinque to study the biomechanical properties of the human calcaneal heel pad. The Foot 2003; 13: 83e91. 15 Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc 2003; 93: 234e7. 16 Osborne HR, Breidahl WH, Allison GT. Critical differences in lateral Xrays with and without a diagnosis of plantar fasciitis. J Sci Med Sport 2006; 9: 231e7. € € o € yu €ncu € Y, Ozg €rgen M, Dabak K. Effects of changes in 17 Ozdemir H, So heel fat pad thickness and elasticity on heel pain. J Am Podiatr Med Assoc 2004; 94: 47e52. 18 Labib SA, Gould JS, Rodriguez-Del-Rio FA, Lyman S. Heel pain triad (HPT): the combination of plantar fasciitis, posterior tibial tendon dysfunction and tarsal tunnel syndrome. Foot Ankle Int 2002; 23: 212e20. 19 Lehman TJA. Enthesitis, arthritis and heel pain. J Am Podiatr Med Assoc 1999; 89: 18e9. 20 McMillan AM, Landorf KB, Barrett JT, Menz HT, Bird AR. Diagnostic imaging for chronic plantar heel pain: a systematic review and metaanalysis. J Foot Ankle Res 2009; 2: 32. 21 Extracorporeal shock wave treatment for chronic plantar fasciitis. Canadian Agency for Drugs and Technologies in Health 2007; vol. 96. http://www.cadth.ca/media/pdf/E0009_chronic-plantar-fasciitispart1_cetap_e.pdf [accessed 19.12.10]. 22 Irving DB, Cook JL, Young MA, Menz HL. Impact of chronic plantar heel pain health related quality of life. J Am Podiatr Med Assoc 2008; 98: 283e9. 23 Rompe JD, Cacchio A, Weil Jr L, et al. Plantar fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar fasciopathy. J Bone Joint Surg Am 2010; 92: 2514e22. 24 Landorf KB, Keenan AM, Herbert RD. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Arch Intern Med 2006; 166: 1305e10. 25 Stuber K, Kristmanson K. Conservative therapy for plantar fasciitis: a narrative review of randomized controlled trials. J Can Chiropr Assoc 2006; 50: 118e33. 26 DiGiovanni BF. Tissue-specific plantar fascia stretching exercise enhances outcomes in patients with chronic heel pain. J Bone Joint Surg Am 2003; 85-A: 1270e7. 27 Extracorporeal shockwave therapy for refractory plantar fasciitis. National Institute for Health and Clinical Excellence. 2009. http:// guidance.nice.org.uk/IPG311 [accessed 19.12.10] 28 Riley G. Tendinopathydfrom basic science to treatment. Nat Clin Pract Rheumatol 2008; 4: 82e9.
Practice points C
C
C
C
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C
Although a myriad of treatment options are available very few have been assessed via well designed trials Plantar fascia-specific stretching exercise appears to be useful in an acute setting Steroid injection should be attempted via the medial approach, with the needle placed deep to the PA Ultrasound guided injection may assist accurate needle placement ESWT may be useful in chronic recalcitrant cases although how ESWT works are subject to speculation Surgery should only be attempted in a selected subset of patients after all modes of conservative therapy have been tried Open partial PA release and decompression of the Baxter’s nerve is the procedure of choice
Conclusion It will be useful if future trials include placebo or no treatment arms to investigate the self-limiting nature of HPS. More trials are also needed to better understand the doseeresponse relationship and the appropriate combination of energy, frequency and duration of treatment of ESWT to determine if this has a place in management plans. Advances in the future treatment of HPS are likely to come from improvements in our understanding of the pathomechanics of HPS. There is evolving interest in the role of metalloproteinase enzymes in tendinopathy in general and they may well have a role to play in HPS.28 Unlocking the cellular secrets of HPS may also help to advance more specific cell-based treatment options in future. A
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Acknowledgement The authors would like to thank Dr. HJ Patel, Consultant Radiologist, Wrexham Maelor Hospital for providing the radiological images.
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