INTRODUCTION:
Plantar fasciopathy (PF) involves pain and structural changes at the proximal
insertion of the plantar fascia in the oscalcis. Thickening and degenerative tissue
findings are more common than inflammatory changes, so the term ‘plantar
fasciopathy’ should better define the disorder known as ‘plantar fasciitis’.
Chronic PF in our foot and ankle unit each year, although most cases are
possibly managed by primary healthcare practices and do not reach our clinic.
Frequently, patients do not look for primary health advice until symptoms are
already chronic. Most patients are not referred to the orthopaedic clinic until
their symptoms are recalcitrant.[1]
Plantar fasciitis is a progressive degenerative disorder of the plantar fascia of
the foot [17]. It has been associated with heel pain, falls, poor quality of life,
and disability.1,6,14,16,24
The 26-foot bones, tibia, and fibula make up the foot and ankle joint.
Talocalcaneal (subtalar), tibiotalar (talocrural), and transversetarsal joints
comprise the ankle joint complex. Locomotion and other daily activities depend
heavily on the ankle joint complex, which creates the kinetic connection that
allows the lower leg to interact with the ground.[2]
Foot movements have been frequently reported to result in the following three
fundamental planes: sagittal, frontal, and transverse [3]. The arch of the foot
includes the following three domes: one transverse dome and two longitudinal
domes. The ligaments and tendons in the foot support these arches created by
the tarsal and metatarsal bones.[4]
About 11-15% of all foot problems are significantly contributed by plantar
fasciitis, leading to frequent foot discomfort. Regular micro trauma or severe
stress to the fascia are the usual causes of plantar fasciitis [5]. This condition
causes extensive discomfort and stiffness in the feet. The band that connects the
calcaneus to the toes on the bottom of the foot is called the plantar fascia.
Persistent standing, overweight, excess foot pronation, jogging, and poor ankle
dorsiflexion are some risk factors that damage the plantar fascia [6]
The plantar fascia is a structure made up of fibrous and dense connective tissue,
which is located in the medial tuberosity of the calcaneus and the
metatarsophalangeal joints of each toe. It can be divided in three portions, called
the medial, lateral and central band, of which the latter is usually the largest,
and fulfils important functions within the biomechanics of the foot as it is the
support for the longitudinal plantar arch of the foot [1,2] (Figure 1).
Figure 1. Plantar fascia and plantar fasciitis (PF): (A) Frontal plane of the
plantar fascia with its different types insertions; (B) Posterior insertion of
plantar fascia in calcaneus.
PF is regarded as a degenerative condition (fasciosis) when symptoms persist
beyond 8 weeks, with the chronic stage defined after this time frame.[10]
[11].The diagnosis of PF is primarily clinical [12–14], but imaging techniques
such as ultrasound, electrography, or sonoelastography can confirm
characteristic plantar fascia thickening [15, 16] Typical ultrasound findings
include hypoechogenicity, increased tissue rigidity, and disruption of the normal
fibrillar pattern [17, 18].Conservative treatment is the first-line approach in
managing
PF, with surgical interventions reserved for cases refractory to conservative
therapies [19].
WHAT IS PLANTAR FASCIITISS?
Plantar fasciopathy (PF) involves pain and structural changes at the proximal
insertion of the plantar fascia in the oscalcis. Thickening and degenerative tissue
findings are more common than inflammatory changes, so the term ‘plantar
fasciopathy’ should better define the disorder known as ‘plantar fasciitis’.[1]
The plantar fascia is a band of connective tissue originating at the calcaneus and
inserting on the tendons of the forefoot and proximal phalanges with the
purpose of supporting the arch of the foot and acting as a shock absorber for
pressure placed on the foot.[1,2]
(A) The plantar fascia and the longitudinal arch of the
foot form a truss. (B) Dorsiflexion of the toes during the late stance phase of
gait tensions the plantar fascia around the metatarsal heads leading to an
increase in the height and stability of the longitudinal arch of the foot, this effect
is known as the “Windlass” mechanism. [23]
Pathogensis
Basically, In the 1990s, orthopaedic surgeons were worried about the
biomechanical complications that could follow plantar fasciotomy, particularly
lateral column destabilization and medial arch collapse [.16,17]
Classically, PF was thought to occur from a mechanical injury in which
excessive tensile strain within the plantar fascia produces microscopic tears
leading to chronic inflammation.[49]. However, current understanding is that PF
occurs through a degenerative rather than an inflammatory process, that is, a
“fasciosis,” rather than a fasciitis, where tensile strain is the key feature in the
pathogenesis.[49]
Traditionally, it was believed that plantar fasciitis is induced by mechanical
damage in which the plantar fascia was subjected to excessive tensile strain,
which caused tiny tears and persistent inflammation. According to current
theories, plantar fasciitis develops through a deterioration of fascia, which is
why it is sometimes referred to as fasciosis rather than fasciitis, where
maximum stress is the main factor in the etiology [7]
The risk factors associated with the onset of PF are intrinsic and extrinsic. The
intrinsic risk factors are associated with body characteristics and include
anatomic, functional and degenerative factors. The extrinsic risk factors are
associated with physical activities and include overuse, incorrect training and
inadequate footwear (Tab.I) [4]
TABLE 1: Principal risk factors associated with Plantar fasciitis.
Principal risk factors Causes
Intrinsic Anatomic risk Pes planus
Pes cavus
Overpronation
Leg-length discrepancy
Excessive lateral tibial
torsion
Excessive femoral
anteversion
Overweight
Functional risk Gastrocnemius and soleus
muscles tightness.
Achilles tendon tightness
Gastrocnemius, soleus and
intrinsic foot muscles
weakness.
Degenerative risk Aging of the heel fat pad
Atrophy of the heel fat pad
Plantar fascia stiffness
Extrinsic Overuse Mechanical stresses and
microtearing
Incorrect training A too-fast increase in the
distance, intensity, duration
or frequency of activities that
involve repetitive impact
loading of the feet
Inadequate footwear Poorly cushioned surface
Inappropriate replacement of
shoes
DIAGNOSIS
Diagnosis is clinical and patients suffering from PF typically present with ‘start-
up pain’, a sharp pain at the plantarmedial aspect of the heel on first walking in
the morning and after a period of rest that gets better after walking for a while.
[7]
A first approach to diagnose PF is the palpation of both the medial tubercle of
the calcaneus and proximal portion of the plantar fascia. For differential
diagnosis, ankle passive dorsiflexion, and ankle dorsiflexion/eversion test can
be performed to evaluate tarsal tunnel syndrome. Moreover, the Windlass test
can be performed to evaluate the plantar fascia loading, albeit this test is
characterized by low sensitivity [22]. These manipulations will trigger pain in
the subject [4],[11],[21]. The intrinsic and extrinsic risks associated with the
onset and progression of PF are also assessed (Tab. II).
Table II. Principal diagnostic elements for Plantar fasciitis.
Foot palpation Medial tubercle of the calcaneus
Proximal portion of the plantar fascia
Ankle passive dorsiflexion/eversion
and Windlass test
Evaluation of intrinsic and extrinsic Anatomic and functional examination
risks Physical activity
Imaging techniques Plain radiography
Bone scans
Ultrasonography, sonoelastography
Magnetic Resonance Imaging
Nerve conduction study
Blood analysis Inflammation markers
Imaging of diagnosis
Diagnostic imaging is not recommended for the initial evaluation of plantar
fasciitis.[21] However, magnetic resonance images, triple-phase bone scans, or
other imaging results may be required to rule out other considerations in the
differential diagnosis, particularly when 4 to 6 months of nonsurgical treatment
has failed or when the patient presents with atypical heel pain (Table).[12]
Table. Differential Diagnosis of Plantar Fasciitis 2,3,12-18
Diagnosiss History Physical Diagnostic
Examination Imaging
Findings
Skeletal Origin
Acute calcaneal High-energy Patients often Plain radiography
tuberosity/body axial overloading unable to
fracture through heel such ambulate; acute
as from a fall or ecchymosis and
MVA swelling of heel
Calcaneal stress Overuse injury Reproducible MR imaging,
fracture associated with pain with single-phase bone
sudden increase simultaneous scan
in athletic medial and
activity, deep, lateral
dull pain in compression of
calcaneal calcaneous
tuberosity (squeeze test")
worsened by
walking on hard
surfaces
Subtalar and Insidious lateral Pain, swelling, Plain radiography
talonavicular and medial heel and stiffness
arthritis pain, worsened by
respectively, and weight-bearing
relieved with rest activity
Soft Tissue Origin
Acute plantar Acute plantar Ecchymosis and Noncontrast MR
fascia rupture "pop" followed swelling in imaging
by severe heel plantar heel and
pain with foot midfoot, palpable
swelling mass under
medial arch may
exist
Fat pad atrophy Centrally located Deep pain with MR imaging
heel pain palpation of
worsened by medial aspect of
walking on hard heel
surfaces, most
common in
elderly patients
Insertional Posterior heelPoint tenderness Noncontrast MR
Achilles pain worsened by over posterior imaging
tendonitis ascending stairs tendon of foot,
or hills Achilles
contracture may
be present
Retrocalcaneal Pain in posterior Pain with passive Noncontrast MR
bursitis heel near dorsiflexion and imaging plain
calcaneal eversion of the radiography
insertion of foot
Achilles tendon,
common in
runners
Neurogenic Origin
Tarsal tunnel Pain radiating Plantar Electrodiagnostic
syndrome from the medial parasthesias studies, MR
malleolus into elicited by imaging, US
the foot, which tapping the: tibial
may worsen nerve behind the
throughout the medial malleolus
day, improves (Tinel sign),
with rest of plantar sensory
intrinsic foot loss or atrophy
muscles
LPN/MCN Plantar foot pain LPN tender over Electrodiagnostic
entrapment consistent lateral plantar studies, MR
throughout day aspect of foot, imaging, US
possible atrophy
of abductor digiti
minimi. MCN:
tender over
plantar aspect of
medial arch, no
muscle atrophy
S1 radiculopathy: Radiating pain Diminished ankle Electrodiagnostic
traveling down jerk reflex and studies, MR
the posterior weakened plantar imaging, US
aspect of leg flexion of foot,
weakened toe
walking
Peripheral Risk factors for Decreased Electrodiagnostic
neuropathy peripheral sensation to studies, nerve
neuropathy; vibration, light biopsy,
gradual onset of touch, noncontrast MR
diffuse pain, temperature, and imaging, US
numbness or pain, hair loss,
tingling in foot smooth skin,
that may progress muscle atrophy,
to sharp, jabbing ulceration, and
pain progressive
clawing of toes
TREATMENT
Conversion treatment
The natural history of PF is often self-limited. However, the typical resolution
time is anywhere from 6 to 18 months and sometimes longer,[20] which can
lead to dissatisfaction of patient and physician. Most experts agree that early
recognition and management of PF leads to short course of treatment and
greater chance of success with conservative therapies.[6]
PF may be a disabling condition and frustrating for both the patient and the
orthopaedic surgeon. Despite the progress made with different conservative
treatments, controversy still exists on how to proceed with a patient suffering
from chronic PF. The most useful conservative treatment for PF is explaining to
patients that pain will possibly settle over time and managing patient
expectations. Some therapies focus on the proximal insertion of the fascia
(orthoses, injections, shock wave therapies) while others (night splints,
stretching) address the relationship between gastrocnemius tension and the
plantar fascia during weight-bearing activities
Orthoses and splints:
Mechanical treatments affecting loading of the plantar fascia have been
extensively used for the treatment of PF. Foot orthoses aiming to decrease
pronation and off-load the proximal insertion of the fascia have been studied.30
Nocturnal splints are applied to stretch the fascia to prevent morning stiffness
and pain.32 Several high-level studies support the use of night splints, but poor
patient toleranc may be an issue for compliance.32–35
Injections:
One or more injections of cortisone and local anaesthetics may result in
variable responses and duration of relief. Multiple injections may increase the
risk of rupture of the plantar fascia and fat pad atrophy. Controlled, randomized
clinical trials demonstrated low-quality evidence of moderate short-term
positive effects of cortisone injections when compared to a placebo, but they
usually lasted no more than 1 month.2,36Other injection therapies that have also
been shown to have short-term and variable benefits include hyperosmolar
dextrose, botulinum toxin A, and autologous blood.37–40
Platelet-rich plasma (PRP):
A recent systematic review of published literature for studies comparing PRP
injections and corticosteroid injections for PF shows PRP injections were
associated with improved pain and function at 3-month follow-up when
compared with corticosteroid injections.41 But there was no information
regarding either relative adverse event rates or costs. The authors concluded that
large-scale, high-quality, randomized controlled trials with blinding of outcome
assessment and longer follow-up were required.
Extracorporeal shock wave therapy (ECSWT):
Some well-designed Level-I clinical studies have shown ECSWT to be
effective in the treatment of PF.42–Radial shock wave is dispersed from the
applicator and does not concentrate on the tissue as FSW does. However, other
authors showed there was a considerably lower success rate of ECSWT in
patients with gastrocnemius shortening.27 There are also concerns regarding
availability and costs of this therapy, with different insurance companies not
covering ECSWT in our practice.
Strengthening exercises
Atrophy of intrinsic foot muscles has been associated with symptoms of PF in
runners by destabilizing the medial longitudinal arch.47 In a randomized
controlled single blind clinical trial, 83 patients with PF were allocated to one of
three treatment options – extrinsic and intrinsic foot muscles; abductor and
lateral rotator hip muscles; and stretching alone – for an 8-week period. All
three protocols led to improvements at 8-week follow-up in pain and function in
patients with PF.48
Stretching exercises
There is evidence that increased plantar fascia strain is associated with
increased calf tension.50 Calf-stretching exercises with eccentric loading,
widely considered to be the most effective conservative treatment for non-
insertional there is a growing trend towards the use of gastrocnemius release as
an isolated procedure to treat recalcitrant PF.
Achilles tendinopathy, also work well for recalcitrant PF.51,52 A prospective,
randomized, double-blinded study compared two calf-stretching regimens for
PF and it was confirmed that Achilles stretching alone was an effective
treatment.53
Nerve decompression
Entrapment of the first branch of the lateral plantar nerve has been advocated as
a cause of PF in some patients with sensory and motor symptoms over the
abductor digiti quinti muscle.58 The release of the nerve is commonly
associated with plantar fascia release in recalcitrant PF.29
Low-level laser therapy
Low-level laser therapy (LLLT) utilized the absorption of laser light at the
electronic level without the generation of heat. It had been applied in a wide
range of treatments, including wound healing, inflammation, and pain
reduction.[32]. However, when comparing with ESWT, LLLT did not show
greater pain reduction.[33]
Therapeutic ultrasound
There was conflicting evidence about the effectiveness of therapeutic ultrasound
in treating PF. An RCT compared therapeutic ultrasound to sham ultrasound
and found that therapeutic ultrasound was no more effective than the sham
group,[34] Another RCT found no additional benefit of therapeutic ultrasound
when added to stretching exercise in treating PF.[36]
Dextrose prolotherapy
Dextrose prolotherapy is a type of regenerative injection and it is postulated that
it may decrease pain through the down-regulation of TRPV1 receptor.[47]
Dextrose prolotherapy was inexpensive and had been increasingly being used in
musculoskeletal disorders.[48] Due to the highly heterogeneous protocols in
previous studies, the optimal regimen of dextrose prolotherapy in treating PF
was still undetermined.[50]
Botulinum toxin A injection undetermined
Botulinum toxin A (BTX-A) had been used for the treatment of poststroke
spasticity and many chronic conditionsWhen comparing with other treatment,
an RCT showed the combination of BTX-A and plantar fascia stretching
exercises exhibited more rapid and sustained improvement than corticosteroids
injection over 6 months.[58] However, BTX-A did not achieve better pain relief
when compared with ESWT in another RCT.[59]
Radiofrequency nerve ablation
Radiofrequency nerve ablation (RFNA) of the calcaneal branches of the inferior
calcaneal nerve serves as another treatment option in patients with chronic heel
pain associated with PF. Several prospective interventional studies showed that
RFNA was an effective treatment in treating heel pain associated with PF,
especially for those patients who did not respond to other conservative
treatment options.[60-62]
Transcatheter arterial embolization
Transcatheter arterial embolization serves as a new intervention for
tendinopathy and enthesopathy that are refractory to traditional management. It
is hypothesized that chronic pain may partially result from neovascularization
and the accompanying neonerves, and embolization may block these pain
generators. Okuno et al. published case series in various musculoskeletal
diseases, and it seemed effective in a case with chronic PF.[63]
Ultrasound in Evaluation of Treatment Effect in Plantar Fasciitis
Apart from aiding the diagnosis of PF, ultrasound also plays an important role
in evaluating the treatment effect. Two studies showed that the reduction in
fascia thickness correlated with improvement in pain, and changing the
thickness of the plantar fascia is a valid objective measurement to evaluate the
effectiveness of treatment protocols.[67,68]
Sonoelastography in Plantar Fasciitis
In addition to traditional B-mode ultrasound, ultrasound elastography [Figure 4]
can also be utilized to evaluate PF. Ultrasound elastography has been utilized
widely in musculoskeletal diseases in the past two decades.
Two major techniques are used in musculoskeletal elastography, including
compression elastography and shear-wave elastography (SWE).[71]
Sonoelastography provides important diagnostic information beyond B-mode,
with typically lower tissue stiffness in symptomatic plantar fascia.[73]
Figure 4: Elastography of the plantar fascia
The plantar fascia comprises 3 bands of dense connective tissue, which
originate at the medial tubercle of the calcaneus and fan distally to insert into
the base of each proximal phalanx (Figure 1).3
Figure 1.
The plantar fascia supports the medial longitudinal arch by transmitting forces
between the heel and forefoot during the late stance to toe-off phases of gait.
Different approaches are available for the treatment of PF, including drug-,
instrumental-, physical-, and surgical-therapy. Furthermore, a growing number
of studies are exploring complementary and alternative strategies (Tab. III).
Table III. Principal treatment strategies for management of Plantar
fasciitis
Drugs NSAIDs
Instrumental Laser
Extracorporeal shock waves therapy
Iontophoresis
Ultrasound
Cryoultrasound
Low-dose radiotherapy
Physical Massage/manual treatments of soft
tissues
Osteopathic or manipulative
treatments
Stretching
Orthotic devices
Low-dye taping and kinesiotaping
Surgery Partial or complete fasciotomy
Radiofrequency microtenotomy
Ultrasonic tenotomy
Complementary and alternative Autologous whole blood and platelet-
strategies rich plasma injection
Botulinum toxin injection
Dehydrated amniotic membrane
injection
