FOOT AND ANKLE

“Not Plantar Fasciitis”: the degeneration, inflammation of the plantar bursa, nerve entrap-
ment, local bony pathology and enthesitis caused by seronega-
tive arthritis.1 The term Plantar Fasciitis is often used
differential diagnosis and interchangeably with PHP. However, the distinction between

management of heel pain true “Plantar Fasciitis” and many of the other conditions that
cause PHP is not always clear. We therefore consider it more

syndrome 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
Abstract that the incidence is higher in the athletic population but not all
Plantar heel pain (PHP) is a common orthopaedic presentation, but our suffering present for medical treatment. A number of risk factors
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
Differential diagnoses of heel pain syndrome
also contribute. There, however, is no relationship between heel spurs
and PHP. As well as plantar fasciopathy, a number of different conditions
Site Diagnosis e primary Sub diagnosis
can also give rise to PHP. It may be helpful to consider the differential
Plantar Plantar fasciopathy Insertional
diagnoses in terms of the structures that are symptomatic: the plantar
aponeurosis Non-insertional
aponeurosis, other soft tissues, the calcaneum and the peripheral nerves.
Plantar aponeurosis
The pathophysiology of PHP is still unclear but could be multi-factorial.
rupture
Histological specimens show evidence of degeneration in the plantar
Plantar fibromatosis
aponeurosis but not inflammation. Seronegative arthritis should be
Enthesopathy
excluded in cases of bilateral PHP. A number of different treatment
Other soft tissues Fat pad atrophy
options have been tried but very few have been rigorously investigated.
Bursitis
Indeed, the overwhelming majority of cases will improve on conservative
Flexor Hallucis Longus
treatment. Shock wave therapy and surgery may be of use in selected
tendonitis
subsets of patients who do not respond to other modes of conservative
Calcaneum Traumatic Stress fracture
treatment.
Infective Osteomyelitis
Inflammatory Seronegative
Keywords heel pain syndrome; Plantar Fasciitis; plantar fasciopathy;
arthropathy
plantar fasciosis; plantar heel pain
Inflammatory bowel
disease
Gout
Rheumatoid arthritis
Introduction Neoplastic: benign Unicameral bone cyst
Osteoid osteoma
Plantar heel pain (PHP) is a common presentation in foot and
Intraosseous lipoma
ankle clinics. Although Plantar Fasciitis is the most common
Aneurysmal bone cyst
cause of PHP a variety of other conditions can also be implicated.
Giant cell tumour
Several mechanisms have been proposed for PHP: chronic
Neoplastic: malignant Metastatic tumour
inflammation and microtrauma of the plantar fascia, mechanical
Osteogenic sarcoma
overload, periosteal inflammation, increased calcaneal intra-
Chondrosarcoma
osseous pressure, peripheral nerve entrapment, fat pad
Ewing’s sarcoma
Metabolic Osteomalacia
Paget’s disease
Munier Hossain FRCS(Glasg) PG Cert MSc(Ortho Eng) MSc(Oxon) Associate Hyperparathyroidism
Specialist at the Department of Trauma and Orthopaedic Surgery, Betsy Neurological Baxter’s nerve
Cadwaladr University Local Health Board, Wrexham Maelor Hospital, entrapment
Wrexham, UK. Medial calcaneal nerve
entrapment
Nilesh Makwana FRCSEd FRCS(Glasg) FRCS(Orth) Consultant Orthopaedic Tarsal tunnel syndrome
Surgeon at the Department of Trauma and Orthopaedic Surgery, Betsy S1 radiculopathy
Cadwaladr University Local Health Board, Wrexham Maelor Hospital,
Wrexham, UK. Table 1

ORTHOPAEDICS AND TRAUMA 25:3 198 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE
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 sug-
gested, 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 retro-
spective 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
Practice points
C Heel pain syndrome is common
C Obesity and increased foot pronation are known risk factors
C Reduced ankle dorsi-flexion and prolong standing have also
been implicated, although the evidence is weak
C 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 honey-
combed 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
ORTHOPAEDICS AND TRAUMA 25:3
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-meta-
tarsal 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 liga-
ments. Proximally the PA has direct a fibrocartilaginous attach-
ment 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 with-
stand 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 dorsi-
flexion).
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 super-
ficial 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 super-
ficial 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
Figure 1 Anatomy of the plantar aponeurosis.
199 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE

Practice points

C The PA shares a common origin with the muscles of the

superficial layer of the foot
C The calcaneum is separated from the plantar skin by
a complex honeycombed fibro-fatty fat pad that attenuates
impact stress
C The PA has a fibrocartilaginous attachment to the calcaneum,
which helps to dissipate stress
C Heel skin is supplied by the medial calcaneal nerve that, if
compressed more proximally, may present with heel pain
C 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
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 ten-
ses 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 longitu-
dinal 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.
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 supina-
tion 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 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 cush-
ioned heel is essential to absorb impact of heel strike. The PHP
demonstrates visco-elastic behaviour under strain. The special-
ized 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 compart-
ments. 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 Figure 3 Schematic diagram of a functioning windlass mechanism in the
metatarsophalangeal joints during terminal stance pulls or foot. Raising of the winch handle (hallux) results in shortening and
“winds” the PA over the metatarsal heads. This “shortens the tensioning of the rope and elevation of the arch.

ORTHOPAEDICS AND TRAUMA 25:3 200 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE

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.
Practice points
C The plantar “fascia” is a fibro-aponeurotic structure
C Histological changes of the PA in HPS are suggestive of
degeneration rather than inflammation
C Repetitive microtrauma is widely believed to initiate plantar
fasciopathy but there is no strong evidence that supports this
theory

Practice points

C The PA is not inelastic, it has visco-elastic properties

C The PA supports the longitudinal arch of the foot
C The PA acts like a tie-beam and resists flattening of the arch
on weight bearing
C A functioning windlass mechanism of the PA allows the foot to
act as an efficient propulsive lever
C 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,
The term “Plantar Fasciitis” implies that the plantar fascia is MCN: medial calcaneal nerve compression, BN: Baxter’s nerve compres-
sion, TTS: tarsal tunnel syndrome, MM: medial malleolus.
subject to inflammation. Actually the plantar fascia is not
a fascia at all but a fibro-aponeurotic structure and there is no
Clinical features
evidence that inflammation occurs in HPS. Current research
indicates that “Plantar Fasciitis” may in fact be a degenerative Presentation
condition. Classic signs of inflammation e swelling, erythema, Patients usually present with plantar heel pain. HPS is typically
leucocytic or macrophage infiltration e are absent. Histological worse early in the morning, especially for the first few steps after
analysis of resected specimens has instead shown tissue arising, gets better after some time but returns towards the end of
changes suggestive of chronic degeneration: myxoid degenera- the day. Some patients with tarsal tunnel syndrome by contrast
tion and fibroblast necrosis, chondroid metaplasia, angiofibro- complain of pain that is worse in bed and is relieved by weight
blastic proliferation, collagen degeneration, altered ratio of Type bearing. An appropriate clinical history should ascertain the
III to Type I collagen, increased numbers of abnormal fibro-
blasts 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 Fas-
ciosis” (PF) or “plantar fasciopathy”. It is widely believed that Baxter’s nerve
mechanical overload of the PA causes repeated microtrauma Calcaneus
and, eventually, a mechanical type of PHP, although the actual
evidence for this is tenuous.10 Mechanical stress, however,
Quadraus
appears to be concentrated at the calcaneal attachment of the plantae
PA and could explain HPS.
Abductor
Some studies have shown the area of tendon most often hallucis
affected in “degenerative” tendinopathy is not the area of the
Flexor digitorum
tendon that is subjected to the highest mechanical force.3 Such brevis
findings have led others to question repetitive trauma as a caus-
ative 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 Plantar aponeurosis
There is certainly evidence of degeneration of the fat pad with
ageing and this could explain the late onset of HPS in the non- Figure 5 Palpation of the medial border of heel will compress the Baxter’s
athletic population. nerve between the belly of AH and QP muscles.

ORTHOPAEDICS AND TRAUMA 25:3 201 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE

Useful clinical tests in HPS

Tests Mechanism Diagnosis

Passive toe dorsi-flexion
Silfverskiold’s test
Resisted great toe flexion
Dorsi-flexioneeversion test
Tightens the Windlass mechanism and Plantar fasciopathy
exacerbates pain
Increased passive ankle dorsi-flexion with the Tight Tendo Achilles
knee flexed to 90
Strains the FHL and reproduces pain FHL tendonitis
Dorsi-flexioneeversion of ankle with Tarsal tunnel syndrome
extension of MTP joints strains the tibial nerve
and causes pain/dysaesthesia

Table 2

duration of symptoms, occupational activities, current footwear, Clinical examination

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.
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).
Practice points

C Patients usually complain of heel pain immediately after

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.
waking up in the morning that gets better after a while but
returns towards the end of the day
C Bilateral HPS is likely to be due to spondyloarthropathy
C Infection or tumour should be excluded if pain is unrelenting
C The medial calcaneal tubercle is tender in insertional plantar
fasciopathy
C 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
C 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

ORTHOPAEDICS AND TRAUMA 25:3 202 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE
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.
Figure 6
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 Peri-
osteal reaction may be evident in infection or spondyloarthrop-
athy.8 If there is strong suspicion of a stress fracture but X-ray is
negative then further imaging is useful.
Ultrasonogram
Ultrasound examination is operator-dependent, but if available is
considered by many to be the investigation of choice when the
ORTHOPAEDICS AND TRAUMA 25:3
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 abnor-
malities 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, peri-
aponeurotic 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.
Practice points
C Get to know your radiologist
C If the diagnosis is unclear a discussion with the radiologist will
help in planning appropriate modes of investigation
Treatment
HPS is generally a self-limiting condition and an over-
whelming 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
203 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE
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 deteri-
oration in health related quality of life in patients with recal-
citrant symptoms.22
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 injec-
tions, 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.
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
ORTHOPAEDICS AND TRAUMA 25:3
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 recom-
mendation 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.
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.
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
204 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE
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
ORTHOPAEDICS AND TRAUMA 25:3
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 con-
flicting. This may be because of the heterogeneity of inter-
vention 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 deci-
sion.27 ESWT is not recommended as a first line of manage-
ment 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 simulta-
neous 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. Visualiza-
tion 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.
205 Ó 2011 Elsevier Ltd. All rights reserved.
 FOOT AND ANKLE
Practice points
C Although a myriad of treatment options are available very few
have been assessed via well designed trials
C Plantar fascia-specific stretching exercise appears to be useful
in an acute setting
C Steroid injection should be attempted via the medial
approach, with the needle placed deep to the PA
C Ultrasound guided injection may assist accurate needle
placement
C ESWT may be useful in chronic recalcitrant cases although how
ESWT works are subject to speculation
C Surgery should only be attempted in a selected subset of
patients after all modes of conservative therapy have been tried
C 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 98: 283e9.
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Acknowledgement
The authors would like to thank Dr. HJ Patel, Consultant Radiol-
ogist, Wrexham Maelor Hospital for providing the radiological
images.
206 Ó 2011 Elsevier Ltd. All rights reserved.